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A 72-year-old woman was admitted to hospital because of chronic respiratory disease for approximately 2 months. Her major symptoms included dry cough and nocturnal fever (to 38°C). Her outpatient record indicated that she was prescribed amoxicillin by her general practitioner but no improvement was obtained. She had no history of infection with mycobacteria or contact with an elephant. Results of physical examination were unremarkable. The patient's tuberculin test was negative. Routine laboratory testing on admission revealed an elevated C-reactive protein (CRP) of 34 mg/L, and an erythrocyte sedimentation rate of 45 mm/hr. The chest X-ray examination showed a diffuse shadow in the right apex suggestive of pulmonary tuberculosis. The initial microbiological examination of bronchial lavage by the hospital laboratory revealed the presence of small coccobacillary acid-fast organisms. The bronchial lavage specimen was cultured on Löwenstein-Jensen medium for mycobacterial isolation. Since the growth of the isolate on Löwenstein-Jensen medium was slower than that for the majority of rapidly growing mycobacteria, and due to apical pulmonary lesions the patient was misdiagnosed as having tuberculosis and entered into the TB Register. After one month of antituberculosis therapy, the patient discontinued treatment due to extreme weakness and severe abdominal pain. Meanwhile the isolate was referred to our laboratory for definitive identification. Further investigation on repeated specimens revealed that the infecting micro-organism was a rapidly growing mycobacteria. The patient's treatment was changed from the antituberculosis regimen to a combination therapy consisting of amikacin and ciprofloxacin. After two months of treatment she recovered and has remained well ever since.\nThe conventional identification and drug susceptibility of the Iranian isolate, namely, ‘M202’ was achieved according to the standard procedures described previously. The conclusive identification included molecular testing, i.e. the PCR restriction fragment length polymorphism analysis (PRA algorithm) of the hsp653 and direct sequencing analysis of almost full length of 16S rDNA and 16S–23S internal transcribed spacer (ITS) as well as partial sequencing of hsp653 and rpoB genes. The GenBank accession numbers of M. elephantis determined in this work are as follow: GU142921, HM229788-90 for 16S rDNA, rpoB, hsp65 and ITS genes, respectively.\nBased on the phenotypic characteristics, M202 was a scotochromogenic rapidly growing mycobacterial species which grew at 37°C and 45°C as well as on Löwenstein-Jensen medium with 5% NaCl. It was positive for the key biochemical tests including catalase, nitrate, urease, tween hydrolysis and tellurite reduction tests. It was resistant to rifampicin but susceptible to amikacin, clarithromycin, ciprofloxacin, ethambutol, isoniazid, doxicyclin, streptomycin, cefoxitin, sulfamethoxazol and imipenem. The main microbiological traits of the Iranian isolate resembled those of the human clinical strains of M. elephantis characterized by Turenne et al. and Tortoli et al.\nIn PRA method the isolate exhibited a unique pattern that was distinct from the previously published patterns as well as from those in our in-house library.\nThe 16S rDNA, rpoB and hsp65 gene sequences of the isolate showed 100%, 98.7% and 96.2% similarities with those of the validly published reference strains of M. elephantis, respectively. The hypervariable signature sequences of 16S rDNA of M202 were identical to those of the type strain of M. elephantis (Figure ). The ITS sequence of M202 was unique compared with those of other validly published mycobacteria. |
A 62-year-old Caucasian woman presented to the emergency department with a history of progressive muscular weakness associated with nausea, vomiting, and diarrhea. At baseline, the patient was independently ambulating with a walker. However, she started to have a gradual bilateral upper and lower extremities weakness for two weeks before her presentation. As a result, she became dependent on her roommate to perform daily living activities (i.e., bathing, dressing, toileting, transferring, and feeding). She also reports an associated history of diarrhea three to four times a day since the onset of her symptoms. She reports a history of weight loss, poor appetite, polyuria, polydipsia, memory impairment, decreased visual acuity, and hearing loss on review of systems. She denied any history of shortness of breath or chest pain. The patient stated that she has been drinking 8-10 cans of 16 oz of Pepsi cola every day. The past medical history is remarkable for chronic obstructive pulmonary disease (COPD), history of abdominal trauma with subsequent splenectomy, gastroesophageal reflux with esophagitis and hiatal hernia status post failed Nissan fundoplication, alcohol abuse, and longstanding multiple psychiatric disorders treated with different antipsychotics and antidepressants. The patient stated that she had not taken any of her home medications for more than two weeks before the presentation. In addition, she reports a 20 pack-years history of cigarette smoking and lived with a roommate who has been busy lately and did not provide sufficient support to the patient.\nOn physical examination, vital signs were normal; the patient looked cachexic and dehydrated with dry skin and mucous membranes. She was also confused with impaired remote memory and appeared in poor hygiene as she could not shower or sanitize her excreta for three to four days due to weakness. Neurological examination showed normal cranial nerves, a decreased strength in the upper and lower extremities (3/5 and 2/5, respectively), and normal sensation to soft touch. On abdominal examination, the patient was noted to have a midline surgical incision with reducible umbilical hernia, no abdominal tenderness was elicited, and she had normal bowel sounds.\nInitial laboratory workup was remarkable for profound hypokalemia; serum potassium was 1.6 mmol/L (ref range: 3.5-5.0) with an elevated troponin of 2.63 ng/mL, brain natriuretic peptide (BNP) of 570 pg/mL, and total creatine kinase (CK) 1,391 U/L. Other electrolytes were normal, she had a serum sodium of 144 mmol/L, magnesium of 2.2 mg/dl, phosphorous of 2.7 mg/dl and calcium of 8.9 mg/dl. Furthermore, blood tests for complete blood count (CBC), creatinine, blood urea nitrogen (BUN), thyroid-stimulating hormone (TSH), free T4, lipid and coagulation profiles were unremarkable for any abnormalities. Liver function showed an elevated aspartate transaminase (AST) of 55 U/L (ref range: 0-41) but normal alanine aminotransferase (ALT) and alkaline phosphatase. Electrocardiogram on presentation showed a prolonged QT-interval (QTc 583 ms) with U-wave and ST-segment depression on lateral leads (Figure ).\nTherefore, an echocardiogram was done on the day of admission, and it showed a moderate to a severe reduction in the left ventricular ejection fraction (estimated LVEF of 30%-35%) associated with apical and anterior wall akinesia. It also showed moderate mitral and mild tricuspid valve regurgitations (Video ). The patient was started on IV heparin infusion for presumed non-ST elevation myocardial infarction.\nHypokalemia was corrected with intravenous and oral potassium chloride replacements. The serum potassium level returned to a normal value of 4.0 mmol/L on the third day of the hospital stay. After correcting hypokalemia, the follow-up EKG showed resolutions of ST-depression, improved QT-prolongation (QTc of 463 ms) and disappearance of U-wave (Figure ).\nFurther cardiac workup was negative for any evidence of myocardial ischemia on a nuclear stress test. Additionally, serum troponin level decreased to 0.53 ng/ml from 2.63 ng/ml on presentation.\nUnfortunately, her hospital course was complicated with a sudden onset of bilateral visual loss, associated with decreased sensation on the left lower extremity and persistent weakness of bilateral upper and lower extremities. MRI brain showed diffusion abnormalities of bilateral posterior temporal lobes (Figure ) and the left cerebellum (Figure ) consistent with acute ischemia.\nTherefore, she underwent trans-esophageal echocardiogram to rule out left ventricular thrombus formation. It showed resolutions of left ventricular wall motion abnormalities with moderate to severe dilatation of the left atrium and no visualized thrombus in the left atrial appendage. Also, it showed an intact atrial septum, and no interatrial shunt on agitated saline bubble study (Video ).\nHence, the patient was diagnosed with reversible TTS associated with in-hospital complication of thromboembolic stroke.\nThe patient was treated with anticoagulation and aspirin, IV heparin infusion was switched to oral rivaroxaban (xarelto) 20 mg daily, in addition to aspirin 324 mg daily for outpatient anticoagulation. On discharge, the serum level of potassium remained at a normal range with dietary replacement. She was discharged to a skilled nursing facility followed by cardiology and neurology clinics for further evaluation and management. |
A 37 years-old unmarried premenopausal female presented in the emergency of our hospital with complaints of bleeding from ulcerative lesion in the left breast for a couple of hours. The patient had history of ulcer in the left breast for past 2–3 weeks which developed over the underlying huge breast lump. The lump was present for past 5 months but rapidly grew over the last 3 months to current size. There was no history of coagulopathy, trauma, chronic liver disease or history of similar illness in first degree relatives. The patient attained menarche at the age of 15 years. She is a non-smoker and denies history of contraceptive use or alcohol intake.\nOn examination in our emergency there was severe pallor with tachycardia. However the blood pressure was maintained. There was an oozing ulceration in upper outer quadrant of the left breast with underlying huge lump measuring 15 × 15 cm occupying the upper outer, lower outer and upper inner quadrants with deformed shape of the breast (a). The skin surrounding the ulcer was erythematous and edematous. Axilla did not show lymphadenopathy.\nBefore the development of breast lump, the patient had itchy lesion at the same site. The patient unfortunately attributed all these events to that itchy lesion and sought help late. There was no history of headache, shortness of breath, abdominal distension or bone pain.\nOn investigating the patient, she was severely anemic with hemoglobin of 5 gm% with normal total and differential counts. Coagulation parameters and liver function tests were normal. Chest X-ray showed no evidence of metastasis other than dense breast shadow on left side due to huge breast lump(a).\nMammogram revealed homogeneous radiodense lobulated mass occupying whole of left breast with subcutaneous thickening on the background of dense breast (b). Ultrasound (USG) of abdomen and pelvis did not reveal any abnormal findings. Trucut biopsy from the breast mass showed necrotic areas with fibrocollagenous tissue with proliferation of oval to elongated spindle cells showing mild degree of atypia.\nAfter discussion about the possibility of metaplastic versus malignant phyllodes tumor, the patient underwent modified radical mastectomy (MRM). Histopathological examination showed maximum tumor size of 14 cm with increased stromal cellularity, loss of stromal-epithelial balance and frequent mitoses more than 45 per 10 high power fields () typical of malignant phyllodes. All the resected margins, nipple and areola were free of tumor. Lymphovascular and perineural invasions were not identified. Seventeen axillary nodes retrieved were free of tumor.\nPostoperatively patient gained weight and was doing well. Three months after surgery, the patient started developing progressively increasing headache, nausea and vomiting for which she got admitted in our center. There was no local recurrence. However on further investigations, she had a huge cystic lesion with mural nodule in her brain (b,c,d). Contrast enhanced computed tomography (CECT) of chest, abdomen and pelvis showed lesions in lower lobe of left lung (a) of size 3.9 × 3.6 cm of +40 Hounsfield unit (HU) in posterobasal segment and right adrenal gland () of 5.8 × 5.1 cm of +30HU with significant enhancement in post-contrast images. Functional evaluation for the adrenal mass with urinary metanephrines and serum cortisol was negative. Patient refused biopsy from right adrenal gland and lung, but while preparing for burrhole biopsy from brain, patient succumbed to the disease. The patient underwent serial ultrasound of abdomen and pelvis during hospital stay which showed increase in size of 4 cm of adrenal mass in 15 days (tumor velocity). |
We report a rare case of a 79-year-old diabetic female with well-differentiated keratinizing SCC arising in a vaginocutaneous fistula secondary to polypropylene mesh-related complications. Except for diabetes, medical history is negative for diseases associated with chronic inflammation such as arthritis, asthma, atherosclerosis, autoimmune diseases, and cancer.\nThe patient underwent an anterior Prolift synthetic mesh kit placement and trans-obturator tape (TOT) mid-urethral sling procedure in 2008 for pelvic organ prolapse and stress urinary incontinence. One-year post-procedure, she developed symptoms of pain and chronic drainage from her right inguinal and groin area with malodorous discharge from her vagina.\nDue to persistent worsening symptoms, the patient was referred to our urogynecology clinic in May of 2018, and examination showed extensive vaginal mesh erosion with a chronic draining sinus from where the mesh arms would have been placed. Her vaginal epithelium was atrophic, with a large area of visualized mesh erosion through the apex of the vagina and the anterior vagina wall. A fistula tract measuring approximately 2 cm in diameter with minimal discharge and minimal fibrinous material was noted overlying the right intertriginous region, lateral to the labia majora (Figure ).\nMRI at that time revealed a stable fistula extending from the right vaginal cuff through the right anterior pelvic and thigh musculature and terminating at the skin lateral to the right labia (Figure ). Subsequent cystoscopy revealed no bladder involvement.\nThe patient underwent surgery in the form of transvaginal excision of the Prolift mesh and TOT sling with dissection through the medial obturator membrane and muscle to facilitate the excision of the mesh from the left and right sides (Figure ).\nHer surgery was complicated by a left ureteral transection, which was immediately recognized and corrected by performing a left ureteroneocystostomy and placement of a left double-J stent. Cultures taken at the time of surgery grew Escherichia coli, Proteus mirabilis, and Corynebacterium species. The patient was initially treated with intravenous piperacillin/tazobactam followed by a complete course of 14 days of oral amoxicillin/clavulanate.\nFive months post-surgery she continued to have persistent drainage from the sinus tracts in the right lateral inguinal region. MRI imaging revealed a persistent vaginocutaneous fistula with a tract length of 9 cm extending from the right vaginal cuff to the right obturator and adductor muscles to the left medial thigh. Although not obvious on imaging, it was suspected she had retained mesh (Figure ).\nShe then underwent another procedure with excision of right upper inner thigh soft tissue involved in multiple chronic draining sinuses and removal of the remaining portion of trans-obturator sling, which was involved with the chronic draining sinuses. Cultures taken at the time of surgery grew Providencia rettgeri, Trueperella bernadine, Enterococcus faecalis, and Bacteroides fragilis. Inpatient parenteral antibiotics were administered for the multi-organism culture under the direction of the infectious disease specialist. She was discharged on oral amoxicillin/clavulanate. The pathology report revealed skin and soft tissue with acute and chronic inflammation reactive changes. No malignant changes were noted.\nThe patient continued with a non-healing wound in the right upper thigh with subsequent MRI (three months post-surgery) showing a vaginal cutaneous fistula with signs of osteomyelitis of the pubic rami (Figure ).\nShe then underwent another debridement and excision of the fistulous tract. Cultures grew Corynebacterium striatum and Bacteroides fragilis, and she completed six weeks of vancomycin, ceftriaxone, and Flagyl. She experienced resolution of her symptoms for about one month subsequent to this surgery. Despite chronic suppression with antibiotics as recommended by the infectious disease specialists, her postoperative course was complicated and required readmission due to complaints of increased pain and discharge from her chronic genital tract fistula. She was then evaluated by a multidisciplinary team including gynecology, orthopedics, and plastic surgeons for consideration of a more radical surgical intervention to excise the entire fistulous tract and alleviate her symptoms. She declined further surgical intervention.\nIn October 2020 (12 years from her mesh placement and two years from her initial presentation), another MRI examination revealed continued expansion and enhancement throughout the chronic pelvic fistula concerning for squamous malignancy. Persistent edema and patchy enhancement in the right pubic ramus were noted, which reflected osteomyelitis (Figure ). Subsequent ultrasound-guided biopsy of the right pubic mass revealed a well-differentiated keratinizing SCC.\nGiven these findings a multidisciplinary team approach to her management was again taken and the patient was referred to a radiation oncologist, medical oncologist, and an orthopedic surgeon. Subsequent staging in November, with a positron emission tomography (PET) scan, demonstrated slight interval growth of hypermetabolic vaginal mass extending through the right obturator foramen, hypermetabolic right obturator, external iliac, and inguinal lymph nodes indicating possible reactive, secondary chronic infection or lymph node metastasis. DNA mismatch repair deficiency was not found; therefore, pembrolizumab was not an option. Radical surgery with internal hemi-pelvectomy removing the superior and inferior pubic rami on the right side, obturator foramen, vessels, and nerves with portions of the bladder wall and vaginal wall was discussed with the patient. She again declined any surgical intervention and remained undecided about conservative management with chemoradiation. She opted to continue chronic suppression with antibiotics. |
A 39-year-old female was admitted to Shaoxin Hospital on December 1, 2008 due to lower abdominal pain and discomfort for a duration of four days. Prior to admittance, the patient experienced lower abdominal pain with no obvious incentive, continuing perineum radiation pain with nausea, but without vomiting, and syncope once for ~30 sec. No chills, fever or other particular discomfort were noted and the patient had no history of surgery, trauma or radiotherapy. A physical examination revealed pain, a flat abdominal area and mild lower abdominal tenderness, but no rebound tenderness. A 6×5-cm tender mass was palpated in the left ovarian area. An ultrasound examination revealed a 6.9×4.6-cm mixed echo mass in the left side of the pelvic cavity; irregular dark areas and free dark areas were observed in the surrounding area of the mass and in the Pouch of Douglas, with cloudy areas of light (). The laboratory examination revealed no abnormalities in the blood, urine, stool, blood coagulation ability, biochemistry or tumor marker levels. Laparoscopic surgery was performed under intravenous anesthesia with endotracheal intubation on December 4, 2008. A 6×5-cm mass was identified on the greater omentum, located posterior to the annex and next to the left side of the uterus. The tumor was completely resected. Intraoperative frozen pathological observations revealed a malignant omentum tumor. Therefore, an omentum resection was performed. No remarkable abnormalities were identified in the abdominal cavity following a careful investigation. The microscopical examination of the paraffin sections revealed that the tumor had no capsule, but was intertwined with the greater omentum. The tumor cells were of various sizes and shapes. Dark stained nuclei and pathological karyokinesis were observed in the cells. The tumor cells were exhibiting infiltrating growth into the greater omentum (). Large amounts of tumor sclerotin were observed among the tumor cells (). Heterogeneous multi-core tumor giant cells and chondroblastoma islands were also observed. The cells were positive for vimentin and CD99 expression, but negative for cytokeratin (CK), calretinin (CR), epithelial membrane antigen (EMA), CD117, CD34, CD68, smooth muscle actin (SMA) and desmin expression by immunohistochemistry. The tumor recurred at three months post-surgery (). Chemotherapy was performed, including vincristine (1.4 mg/m2 i.v. on day 1), cyclophosphamide (750 mg/m2 i.v. on day 1) and doxorubicin (50 mg/m2 i.v on day 1) for 6 cycles; however, the patient demonstrated a poor response. The patient succumbed to systemic failure with lung metastases on June 30, 2009. |
The second case refers to a 48-year-old woman, a busy manager with a history of depression and sleep disturbance. She has had three terminations of pregnancy and one delivery by cesarean section. She smokes approximately ten cigarettes per day and has high cholesterol serum levels. She takes several medications: a selective serotonin reuptake inhibitor (escitalopram), two benzodiazepines (delorazepam and clonazepam), and a statin. She reports a four-year history of urinary symptoms: daily UUI episodes, mild stress urinary incontinence (SUI), and two episodes of nocturia per night. She wears pads every day. The urology consultation revealed some degree of pelvic pain, especially during vaginal examination. The urine dipstick was negative and there was no PVR. No specific causes of the symptoms such as urine tract infection were identified. The patient also complained of mild dyspareunia and occasional constipation. The urine culture turned out to be sterile, with no blood in urine, and the pelvic ultrasound scan and urine cytology were also negative. The cystoscopy, which was performed as a result of the presence of storage symptoms and to rule out a bladder tumor in this current smoker, was normal.\nIn OAB patients, it is of utmost importance to consider all comorbidities. Anxiety and depression may play a role, feeding a vicious circle. Moreover, medications to treat neurological or psychiatric disorders can influence OAB and be responsible for side effects [, ]. Gastrointestinal disorders are frequently associated with OAB, such as constipation in this case, but patients rarely raise the topic. An overlap exists between irritable bowel syndrome and OAB [].\nThe patient was prescribed a β3 agonist, pelvic floor muscle training (PFMT) and bladder retraining. Four months later, she noticed some degree of improvement, but had stopped the treatment as she felt that she had no time for PFMT. She was not compliant with the bladder drill either, and soon stopped the β3 agonist because she did not sense any real improvement. She also felt that she did not have the time to complete a bladder diary. She was prescribed fesoterodine 8 mg for three months. In parallel, her general practitioner asked for vaginal and urethral culture swabs, which were negative. After three months, her urinary urgency improved, but she said that the few remaining episodes of urgency were “killing her life” and that she did not want to be on pills for her whole life. Therefore, she refused to continue the treatment and requested an “easy fix”. Her reaction highlights the need for careful consideration of the consequences of incontinence in terms of QoL. A publication from Vaughan et al. [] reported that OAB and incontinence synergize to reduce QoL, especially in the domains of sleep, elimination, usual activities, discomfort, distress, vitality, and sexual activity.\nConsistent efficacy on urgency symptoms with a significant decrease in UUI and urgency episodes has been reported with fesoterodine at doses of 4 and 8 mg compared to placebo () [, , , ]; however, some patients may react differently. Patient satisfaction is an important driver of treatment success []. Patient expectations should be considered carefully in the context of OAB management. The achievement of patients' goals was measured in the Study Assessing FlexIble-dose fesoterodiNe in Adults (SAFINA study) [], a 12-week multicenter open label study with 331 OAB adults, using the Self-Assessment Goal Achievement (SAGA) questionnaire. Fesoterodine treatment resulted in 81.3% of patients declaring that their goals were “somewhat achieved/achieved” or that the result “exceeded/greatly exceeded their expectation”.\nOur case patient had very specific expectations; she refused to have an implant (neuromodulation), saying “I'm not going to be an android!” She accepted botox injections, and so a first set of injections was performed under local anesthesia. She found the injections “a little painful” and “a big annoyance”, but at the one-month follow-up visit after botox injection she reported no more UUI episodes and an improvement in frequency and the number of urgency episodes, as well as in QoL. Even though she stated that she did not like the idea of being a patient for the rest of her life, she accepted subsequent injections.\nThe clinical points that can be learned from this case are as follows:All OAB cases are different, and a thorough evaluation is mandatory to adequately address each case. It is important to assess other aspects, such as functional and psychological disorders that may influence symptoms, and to consider nonneurogenic OAB as a multifactorial disease. The major goal of initial therapy is to meet the patient's expectations regarding the reason for their visit, to improve their satisfaction, and their QoL. Due to fesoterodine's characteristics and flexible dosage, improvement of symptoms and achievement of the patients' goal are usually high with this medication. When patients have specific requirements, all options should be discussed and the patient's agreement obtained. A customized approach is a crucial factor for treatment success. OAB management should be personalized; beware of a simplistic application of a standardized treatment algorithm. |
The patient, a 31 year old healthy male Caucasian, who was an anesthesiologist, from São Paulo in Brazil, identified symptoms like gingival recession, dentine hypersensitivity and mobility in teeth 31 and 41, greater than its original physiology, went to a general dental practitioner for dental health care. The professional carried out an extra-coronal splinting in the lower anterior teeth, and gave him a referral to consult the Periodontology Department of the UNESP- Araçatuba, São Paulo, Brazil. In the anamnesis questionnaire, the patient informed that there was no previous specific periodontal treatment, neither was he taking any medication for at least 3 months prior to this study, and denied any pre-existing systemic conditions or significant history of harmful habits.\nHowever, the patient revealed a nasal obstruction and chronic mouth breathing condition, which induced an altered maxillary arch development with a high narrow vault. Clinical and radiographic assessments were obtained, with a similar protocol used by Page et al. (2002) [] and Repeke et al. (2012) []. The patient also submitted to standard protocols, for the evaluation of the hematological and endocrine markers, as used by Repeke et al. (2012) []. Microbiology tests were carried out, by employing the methodology applied by Page et al. (2002) []. Concerning the dental occlusion conditions, a significant deflective premature contact in the centric relation was verified. The premature contact deflected the mandible forward and away from the centric relation, to the maximum intercuspation causing an effective and deleterious contact in the anterior teeth.\nThe posterior premature contact was, adjusted in the centric relation, in order to stabilize the mandible, and to eliminate a deleterious contact in the anterior teeth. No eccentric movements were defective. The patient also had anxiety and constant stress development because of his work, and realized that several times, an unconscious centric bruxism occurred during the daytime and, that after sleeping time, he felt pain around his temporo-mandibular joint, mainly, when he was under stress. In the clinical examination, the patient did not present any probing depth ≥ 3mm or bleeding on probing, however, an extensive clinical attachment loss ranging from 4mm to 7 mm, was verified in the maxilla and the mandible that were principally in the posterior teeth buccal side. The patient presented a satisfactory oral hygiene, no apparent detectable bacterial plaque, calculus, and periodontal inflammation (Fig. ). A Full-mouth radiographic survey, showed a generalized and horizontal alveolar bone loss, however interproxial bone no present significant loss when compared with bone loss of the buccal side (Fig. ).\nResults from a complete blood count demonstrated no significant findings. The levels of total hydroxyproline, ALP, calcium, calcitonin, urine calcium, PTH (parathyroid hormone), DHEA (dehydroepiandrosterone), FSH (follicle-stimulating hormone), LH (luteinizing hormone), glycemia, total cholesterol, HDL (highdensity lipoprotein), LDL (low-density lipoprotein), triglycerides, type I urine, CRP (C reactive protein) and bone densitometry were completely normal, confirming the findings of previous studies carried out by Repek et al. (2012) []. The sub-gingival plaque samples harvested from the sites with the deepest probing depths were, cultured for putative anaerobic periodontal pathogens and analyzed in the commercial Microbiology Testing Laboratory. The samples were negative for Aggre-gatibacter actinomycetemcomitans, Porphyromonas gingivalis, Bacteroides forsythus, Peptostreptococcus micros, Eubacterium sp., Campylobacter rectus, and for enteric the bacteria, while the Fusobacterium sp., and Prevotella intermedia, accounted for 2.0% and 3.1% of the flora, respectively. The spirochetes were not observed, using the dark field microscopy. To obtain information about possible previous periodontal infection, blood sample was drawn and serum antibodies titers to antigens of putative periodontal pathogens, were measured using, standard techniques. Titers were not elevated to any of the putative periodontal pathogens tested. Results relative to values for sera from periodontally normal controls set at 100 Enzymes-Linked Immunosorbent Assay (ELISA) units, demonstrated no elevation of titers to antigens of the putative periodontal pathogens tested, and were: A. actinomycetemcomitans = 0; P. gingivalis = 3 and B. forsythus = 31. The data of all the microbiologic analysis, confirm the findings of Page et al. (2002) []. The patient was advised to seek psychological treatments, so that he could be able to control his emotional disorder, and, an otorhinolaryngologist to treat his nasal obstruction. Oral hygiene procedures were reviewed, occlusal adjustment and a maxillary night guard were constructed. The patient’s protocol control was similar to the one established by Page et al. (2002) []. The patient was under professional control every 3 months, however, a treatment plan to treat recession by subepithelial gingival graft was not instituted, since the etiologic factors which induced bone loss and clinical attachment loss, were not well defined. Throughout one year and six months of observation, the patient maintained his teeth, and they were free from significant microbial deposits, as the gingival aspect was reasonably free of inflammation, and the interproximal alveolar bones were stable and without periodontal pocket progression. The results were similar to the results achieved by Page et al. (2002) [] and Repeke et al. (2012) []. However, the loss of the periodontal attachment progress was moderate in the buccal aspect of some teeth, and was predominant in premolars and canines in spite of the treatment instituted. At this time, the patient had difficulty in controlling his emotional disorder under systematic stress. |
A 16-year-old girl was admitted to the hospital because of headache and vomiting for 20 days, which aggravated with decreased vision for 3 days. Twenty days ago, she had headache, nausea and vomiting, no fever, no obvious cause, and no improvement after infusion therapy (cephalosporins) at the local clinic. The patient had frequent vomiting and poor appetite. She went to the gastroenterology department for treatment, but her symptoms still aggravated after symptomatic treatment. In the past 3 days, she had blurred vision and progressive vision loss, accompanied by unconsciousness, so she was transferred to our hospital for emergency treatment. She had always been in good health, no history of hepatitis or tuberculosis, no history of trauma surgery, no history of food or drug allergy, no history of exposure to toxic substances, full-term delivery, and no family history.\nHer vitals on admission were: temperature 36.8 °C, pulse 72 beats/min, respiratory rate 19/min, blood pressure 106/71 mm Hg. She was wheeled into the ward, physical examination cooperation. There was no yellow staining or bleeding spots on the skin mucosa, no swelling of superficial lymph nodes, and no positive signs on cardiopulmonary and abdominal examination. Neurological examination revealed that somnolence; poor memory; the right side of the eye fissure was small; the pupils of both sides were unequal with the diameter of the right side 5mm, insensitive to light reflection, and the diameter of the left side 4mm, slow to light reflection; both eyes move freely in all directions, no nystagmus, and no blurred vision. Bilateral frontal stria and nasolabial groove were symmetrical; the tongue was in the middle. She could speak clearly; and pharyngeal reflex existed. Muscle strength and muscle tension of the limbs were normal; bilateral tendon reflex was negative; bilateral deep sensation, shallow sensation and ataxia movement examination were normal; and pathological signs were negative; neck stiffness (five transverse fingers), bilateral Kernig’s sign and Brudzinski’s sign were positive.\nThe head computed tomography (CT) and electroencephalogram (EEG) were normal. Abdominal CT showed gallstones, small kidney stones. Blood routine revealed: white blood cell (WBC) 14.4 × 109/L, neutrophil granulocytes (NE) 12.53 × 109/L, lymphocytes (LY) 1.08 × 109/L, red blood cell (RBC) 4.79 × 1012/L, hemoglobin (Hb) 145 g/L, hematocrit (HCT) 40.7, platelets (PLT) 280 × 109/L; erythrocyte sedimentation rate (ESR) 4 mm/h; myocardial enzyme spectrum, liver and kidney function, electrolyte and coagulation function were normal. Brain MRI plain scan: bilateral hippocampus, right thalamic abnormal signal, high possibility of virus infection, the supratentorial ventricle slightly enlarged. Lumbar puncture examination results: CSF pressure was greater than 400 mm H2O (1 mm H2O = 0.0098 kPa); CSF routine: light yellow, sight turbidity, no clot, Pan’s test (Pandy) positive, total cells number 20 × 109/L, WBC count 13 × 109/L; Cryptococcus neoformans polysaccharide antigen (LA) negative (-), no acid-fast bacilli, no cryptococcus; CSF biochemistry: protein 4.97 g/L (high), Cl 105.2 mmol/L (low), glucose 4.98 mmol/L (high), lactate dehydrogenase (LDH) 34 U/L, high-sensitivity C-reactive protein (hsCRP) 0.37 mg/L, adenosine deaminase (ADA) 0.41 U/L. Viral antibody examinations showed: cytomegalovirus (CMV)-IgG positive (+), Rub-IgG positive (+), herpes simplex virus (HSV)I-IgG positive (+), the others were negative. Serum tumor marker results showed no abnormalities.\nAfter admission, she was treated with antiviral therapy (ganciclovir), nerve nutrition, dehydration, decreasing intracranial pressure therapy (mannitol, glycerol fructose, albumin, and furosemide), electrolyte supplementation and nutritional support. On the second day of admission, the patient’s vision dropped to a sense of no light, and she could not distinguish day from night. For the patient’s vision loss, we consulted the ophthalmology. Examination of the ophthalmoscope found that the edge of the nipple was unclear, the physiological depression disappeared, the retinal vein was filled with distortion, and the retinal edema around the nipple was turbid. According to the condition, the cranial hypertension syndrome was considered; and the pupils were unequal, considering the formation of cerebral edema and cerebral palsy. It was needed to relieve the craniocerebral pressure urgently, but the patient’s intracranial pressure was extremely high, direct lumbar puncture and drainage of CSF would have the risk of developing cerebral hernia, which is life-threatening. After we consulted the neurosurgery and considering the cause of high blood pressure syndrome, emergency Ommaya sac implantation was done, with drainage of light yellow CSF about 300 mL per day. The patient’s cranial hypertension was relieved, and the patient’s visual acuity gradually recovered after treatment.\nAfter standard antiviral treatment for half a month, there was no decrease in CSF drainage. The pathogenic test results of the CSF sent to Huada Gene Company showed that no related gene fragments were found in viruses, bacteria, fungi, tuberculosis or parasites. In order to find out the cause, fresh CSF was repeatedly sent for examination, and enhanced magnetic resonance examination was performed. The cytology of CSF showed heterogenous cells with prominent malignant features. The cells were scattered and varied in size, the cell membrane was malformed, the ratio of nucleus to cytoplasm was significantly unbalanced, the nucleoli were active, and the nucleoli accounted for the majority of chromatin. Enhanced magnetic resonance imaging showed extensive enhancement of the leptomeningeal, especially in the brainstem and tentorium cerebellum, as shown in .\nCSF cytology and enhanced MRI results confirmed the diagnosis of meningeal carcinoma. According to the classification of central nervous system tumors of the WHO in 2016 [, ], the results were consistent with DLGNT with high malignancy. After we consulted the oncology department, chemotherapy was suggested, but the patient’s condition was gradually progressing, spinal cord metastasis occurred as follows: decreased lower extremity sensation, decreased muscle strength, and urinary retention. Finally, the patient’s family gave up further treatment. |
A 15-year-old female patient (bodyweight 50 kg, height 160 cm) presented with syncope. Severe arterial hypertension was diagnosed (178/147 mmHg left arm, 102/83 mmHg left leg). She reported previous episodes of exercise independent headaches and nose bleeds. Auscultation revealed no cardiac murmurs, but an accentuated second heart sound and reduced pulses in the lower limbs. There were no clinical signs to suggest Alagille or William’s syndrome or clinical evidence of neurofibromatosis. Blood tests showed normal inflammatory markers and normal creatinine. The urine dip showed no markers for blood or protein. No regular medication was taken at the time she presented. The electrocardiogram showed normal sinus rhythm, no significant signs of left ventricular (LV) hypertrophy or abnormal repolarization. Echocardiography detected a severe concentric LV hypertrophy (14 mm diastolic septal diameter, 15 mm diastolic diameter of the LV posterior wall) and a long hypoplastic segment in the abdominal aorta with massive arterial collateralization. Cardiac catheterization confirmed the diagnosis of a midaortic syndrome with a minimum diameter of <1.5 mm and a gradient of 50 mmHg between the aortic arch and the femoral arteries (Figure ). The narrow part began directly under the diaphragm above the truncus coeliacus and continued down to the bifurcation of the arteriae iliacae including the renal arteries, with reversed flow in the caudal aorta up to the renal arteries. Because of the extraordinary length of the hypoplastic segment of 23 cm, we decided for a stepwise interventional therapy with a paclitaxel covered balloon. No additional computed tomography scan or magnetic resonance imaging (MRI) was performed. Consultation with our surgeon, supported the interventional approach. The proposed procedure was reviewed and approved by our institutional review board, extensively discussed with the patient’s family, and informed consent was obtained before proceeding.\nAfter balloon interrogation of the long stenotic abdominal aorta using a 6 × 20 mm Tyshak balloon (NuMED Inc., Hopkinton, NY, USA) to differentiate between rigid stenosis and hypoplastic parts, serial balloon dilation with a 7 × 40 mm paclitaxel covered In.Pact balloon (Medtronic, Minneapolis, MN, USA) (3 µg/mm2 Paclitaxel on the balloon) was performed (Figure ) from end to end of the stenosis. Planned redilations, to stepwise improve the aortic compliance and reduce the risk of dissection, were performed after 2, 4, and 8 months with Elutax balloons ranging from 8 mm to 12 mm diameter (Aachen Resonance, Düsseldorf, Germany) (2 µg/mm At the end of the last interventional procedure, a mild endothelial lesion at the former narrowest point of the aorta was noticed (Figure ). This lesion healed and after 2.7 years MRI showed a stable and adequate result (Figure ). Today the girl is in unrestricted physical condition. The blood pressure has markedly improved (139/64 mmHg right arm and 127/65 mmHg right leg) under therapy with atenolol and amlodipine.\nThe patient and patient’s family consented to the publication of this case’s history and the images presented. |
The second patient was a 39-year-old white female with peripheral arthritis and inflammatory back pain related to spondyloarthritis. She received NSAIDs, sulfasalazine, and methotrexate successively, all of which were ineffective. She developed infections under adalimumab. Due to persistent back pain, pamidronate was started in August 2009. She received six pamidronate infusions, 60 mg monthly, leading to progressive improvement. Three weeks after the third infusion, she complained of abdominal pain with elevated serum lipase (184 UI/L; N < 60) and AP was seen on injected CT scan of the abdomen (CTSI 2). Microlithiasis was observed on abdominal ultrasound and the patient thus underwent laparoscopic cholecystectomy surgery. She had two other episodes of AP without receiving pamidronate and a nonmalignant caudal pancreatic tumor was then diagnosed in 2010 (glucagonoma). This tumor was removed by surgery and pamidronate treatment was restarted in 2011. Five days after the third infusion, she again had AP diagnosed on a CT scan of the abdomen (). This patient had neither dyslipidemia, nor IBD, nor a history of alcohol intake. PTH serum level was normal. The ABPP was permanently withdrawn. No new episode of AP after pamidronate cessation was observed in either of these two patients.\nThe safety profile of pamidronate is well described, with acute-phase reaction following its administration but no evident abdominal organ toxicity []. Drug-induced pancreatitis is a rare cause of AP, estimated at between 0.1 and 2% of all AP [, ]. Most of the information available on drug-induced AP comes from single case reports with varying levels of evidence []. Our two patients had no predisposing factors for AP and the other usual causes of AP were excluded (alcoholism, hypertriglyceridemia, hypercalcemia, IBD, trauma, and surgery). The first patient had a past history of AP with no identified cause while the second had microlithiasis and a pancreatic tumor, but despite cholecystectomy and pancreas surgery, she experienced another episode of AP after pamidronate was reintroduced. In these two cases, there was a clear temporal relationship between the pamidronate infusions and the development of AP (ten days for the first patient, three weeks and five days for the second). In the second case, a rechallenge of the drug caused a recurrence of AP. According to the Badalov classification of drugs that induce AP, pamidronate may be considered as a class Ib drug with a high level of causality []. Our two patients scored +5 and +7, respectively, on the Naranjo probability scale for drug causality assessment []. One case of suspected pancreatitis has been reported with alendronate, also with a possible causality []. ABPPs do not diffuse specifically to the pancreas and a direct toxic effect thus seems unlikely. Our two patients had no systemic reaction and a hypersensitivity reaction was therefore not evident. Conversely, ABPPs can modulate the immune system and the production of proinflammatory cytokines []. In a mouse model of induced pancreatitis, macrophage ablation by liposome encapsulated bisphosphonates may worsen pancreatic inflammation []. However, our two patients developed other flares of AP without concomitant pamidronate infusion and we cannot therefore exclude the hypothesis of a spontaneous recurrence for the episodes following pamidronate infusions. Alternatively, pamidronate may have played a role as a triggering factor in these patients with previous history of pancreatic damage and thus made a new recurrence more likely. The mechanisms explaining drug-induced pancreatitis are in general poorly understood [] and collecting data about all drug-induced pancreatitis, including ABPPs, should help to better identify the contributing factors of such an adverse event. |
A 3-year-old male was brought in the outpatient clinic because of hyperemia and progressive proptosis of the right eye for one month. There was no history of head trauma and no family history of connective tissue disease. He has no symptoms of increased intracranial pressure or signs of neurologic or cranial nerve deficits. An initial noncontrast computed tomography scan showed a dilated right SOV and exophthalmos of the right orbit, a finding that prompted a referral to the neuroendovascular service. Initial workup was a right transfemoral arterial angiography under general anesthesia. The right internal carotid angiography showed a direct type of CCF at the level of C4 and the draining veins are the SOV anteriorly and the inferior petrosal sinus (IPS) posteriorly [Figure and ]. There was no cortical venous reflux. Patient is negative for any connective tissue disorder after a genetic analysis. Due to the progressive ophthalmologic problem, the patient underwent coil embolization through the transvenous approach.\nEndovascular procedure was started aseptically with patient under general anesthetics. A 4F sheath was inserted through the right transfemoral artery to the right internal carotid artery (ICA) to obtain a baseline angiography. Road-map images were done during the procedure. Injections into the contralateral ICA and vertebral artery were done to check the retrograde filling of the carotid siphon through the anterior communicating artery and posterior communicating artery and showed a poor collateral flow of the right ICA. Activating clotting time was elevated by intravenously infusing 1000 units heparin. Another 4F catheter was inserted through the left transfemoral vein going to the right internal jugular vein (IJV) into the right IPS, then into the cavernous sinus, and eventually into the right SOV using a Prowler-plus micro catheter (Cordis) with GT 0.012, 45° angle microguide wire. A total length of 276 cm from 28 coils were detached and densely packed from the right SOV to the cavernous sinus. Post-embolization angiography and plain skull X-rays showed dense coiling and complete disappearance of AV shunts, which signifies total occlusion of the fistula and preservation of the patency of the right ICA [Figures and , and ]. The vital signs were stable in the entire duration of the procedure. He was monitored in the neurosurgery intensive care unit for 24 hours post-embolization. A gradual improvement of the chemosis on the right eye was noted and was discharged after a week without complication. On one-month follow-up, exophthalmos and chemosis on the right eye have completely resolved. |
An 88-year-old man was referred to our hospital for emergent massive hemoptysis. His medical history was remarkable for chronic heart failure, moderate mitral regurgitation, atrial fibrillation, and chronic kidney disease. He was undergoing treatment with apixaban and pilsicainide for atrial fibrillation. He was severely hypoxic (SpO2: 80 under O2 15 L/min by oxygen mask) and hypotensive (systolic blood pressure: 80 mmHg) on admission. In the emergency department, we performed intubation into the right main bronchus through guided bronchoscopy; this was followed immediately by right side one-lung ventilation as portable chest radiography showed consolidation in the left upper lung. Bronchoscopy showed that the trachea was almost obstructed by haemorrhage and haematoma. He experienced cardiopulmonary arrest immediately after the airway was maintained. However, spontaneous circulation was restored by cardiopulmonary resuscitation. Contrast computed tomography (CT) demonstrated an aortic aneurysm at the aortic arch, which penetrated the upper lobe of the left lung (Fig. A,B). We suspected that it would be difficult to perform emergent surgery because of the patient’s poor general condition. Furthermore, we believed that there was no indication for endovascular stenting due to the following reasons: (1) the root of the left brachiocephalic artery was close to the penetrating portion of the aneurysm, at a distance of 12 mm. Thus, there might have been a high risk of obstructing blood flow to the brachiocephalic artery; (2) a risk of aortic injury might have been induced by stenting because the aortic arch was highly calcified. He was admitted to the intensive care unit, and we controlled blood pressure using nicardipine and discontinued anticoagulation therapy and performed platelet and fresh frozen plasma (FFP) transfusion for haemostasis. Bleeding from the APF decreased gradually due to astriction by haematoma. On the 17th hospital day, we performed bronchoscopy for the suction of haematoma, except in the bronchi of the left upper lobe, and adjusted the intubation tube for conversion to bilateral lung ventilation. On the 18th hospital day, we performed endobronchial occlusion with EWS to prevent fatal hemoptysis despite the risk of atelectasis. We inserted the EWS into each target bronchus with haematoma, with consideration of the risk of re-bleeding due to the removal of the haematoma. EWS sizes were as follows: (B1 + 2a: 7 mm; B1 + 2b: 7 mm; B3b + c: 7 mm; and B3: 7 mm) (Fig. A). B1 + 2c did not undergo EWS insertion because this bronchus was not responsible for bleeding on CT findings. There was no massive hemoptysis after bronchial occlusion with the EWS; subsequent mild hemosputum was controlled by a haemostatic drug. The patient was successfully extubated on the 22nd hospital day and was discharged on the 47th hospital day without complications and free from oxygen. Radiography showed that EWS had promptly fixed each bronchus (Fig. B). |
A 73 y/o man with no smoking history and a diagnosis of RA was referred to the pulmonary clinic for multiple pulmonary nodules in a peri-lymphatic pattern (). Patient was noted to have progressive pulmonary nodules that have been increasing in size ().\nHis rheumatologist planned to start him on TNF-alpha inhibitors for his RA and wanted to evaluate for infections and malignant causes prior to proceeding with the treatment. He was asymptomatic and denied any respiratory complaints. At the time of presentation, he was being treated with leflunomide, hydroxychloroquine and sulfasalazine. Pt is a Navy veteran with exposure to asbestos while he was in the Navy. Following his discharge from the Navy, he worked 10 years overseeing production of plastic and metal parts for guided radar systems. He then transitioned to working in residential construction, hanging, siding and replacing windows. He also worked on restoring brick on old houses by stripping off paint for about 5 years.\nPulmonary function test (PFT) revealed mild obstructive ventilator defect with FEV1/FVC 66%, FEV1 of 3.13L, 94% predicted. He underwent bronchoscopy with transbronchial biopsies of the right upper lobe nodules. Pathology revealed a necrotic tissue () with central silica crystals visualized under polarized light which was consistent with silico-anthracotic nodules. The biopsies were negative for malignancy. There was no evidence of infection on bronchoalveolar lavage. His AFB and fungal cultures were also negative.\nThree years following his biopsy, the patient presented with lower extremity edema and dyspnea on exertion. He was found to have worsening renal failure with subsequent renal biopsy showing a mixture of minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS). The staining was negative for amyloid and no silica deposits were identified. He also underwent right heart catheterization that showed mild pulmonary hypertension with mean PAP of 33. CT chest did not show worsening or progression of the nodule |
A 74-year-old woman presented to our hospital with a mass on her scalp, which she had for 40 years. When she first noticed the mass and she applied caustic soda at a beauty shop, about 40 years prior and in the last 3 years the mass had rapidly grown showing ulceration. The patient had a complex medical history of hypertension, arrhythmia, and thyroid cancer after total thyroidectomy. Further, she was maintained on oral nifedipine for hypertension. Clinical assessments revealed a firm, fixed, protruding mass measuring about 2.0×3.0×0.5 cm in size with ulceration and pigmented nodular lesions (). The clinical diagnosis was nevus with pyogenic granuloma, and the lesion surgically excised. Gross examination revealed the tumor to be a fibrogranuloma. However, since the patient had previously applied caustic soda on the lesion and ulcer was observed overall, the frozen biopsy was decided to perform during surgery.\nWe performed duplicate tissue excision and frozen biopsy to confirm cell malignancy and local invasion (). The first simple excision and frozen biopsy during surgery revealed a poroid hidradenoma with atypia and abundant tumor cells at the anterior and posterior resection margins but not at the right and left sides (). Since this biopsy could not rule out basal cell carcinoma, we performed wide excision with a safety margin of 5 mm (). Then, the surgical wound was directly closed without complications. The pathology report confirmed poroid hidradenoma with cell atypia and free of all resection margins. Histopathologically, there was a well-circumscribed neoplasm composed of small dark poroid cells and larger paler cuticular cells with clear cytoplasm and no connection to the overlying epidermis ().\nOn immunohistochemistry, the tumor stained positive for high molecular weight cytokeratin and epithelial membrane antigen and negative for membrane-bound carcinoembryonic antigen, low molecular weight cytokeratin, CK20, and CD34.\nAt 1-year follow-up, she remains asymptomatic and without evidence of recurrence. The surgical wound healed uneventfully leaving only a scar and little alopecia (). |
The patient is an 80-year-old woman, who presented to the hospital with fever and productive cough with yellowish expectoration of 2 days duration. She also had lethargy over the same period and had sick contacts in the form of two daughters who both had recently recovered from a “flu-like” illness. She was known to have bronchial asthma treated with seretide 25/250 two puffs ON + PO monteleukast 10 mg ON, hypertension treated with PO losartan 50 mg BD, type 2 diabetes mellitus controlled with PO linagliptin 5 mg OM and a previous right thalamic ischemic stroke 5 years ago for which she was on PO clopidogrel 75 mg OM and PO simvastatin.\nThe patient had a total of two admissions to the medical ICU. The patient was initially admitted to general ward for treatment of possible pneumonia and asthma exacerbation and started empirically on intravenous amoxicillin/clavulanic acid but had worsening shortness of breath and hypoxia in the ward requiring intubation and transfer to medical ICU for invasive ventilatory support.\nShe was put on volume control mode ventilation with a tidal volume (TV) of 8 mL/kg ideal body weight and started on light sedation with intravenous propofol (30 - 50 mg/h) and fentanyl (30 - 50 µg/h) infusions post-intubation for comfort. She was given intravenous (IV) hydrocortisone 100 mg × q6h and inhaled bronchodilators for her asthma. Antibiotics were escalated empirically to IV meropenem. On day 2 of ICU stay, propofol and fentanyl infusions were discontinued and she was switched to pressure support mode of ventilation. She was given a total of 10 days of carbapenem cover. She required a slow wean from the ventilator over the next few days and was extubated to non-invasive ventilation (NIV) on day 7. Trials to wean her off NIV were unsuccessful.\nThe patient required re-intubation for decompensated type 2 respiratory failure after 2 weeks of weaning trials in the wards. She was put on pressure-regulated volume-controlled (PRVC) mode ventilation and started on low-dose fentanyl and propofol infusions for sedation and analgesia. Serial chest X-rays (CXRs) done were suggestive of hospital-acquired pneumonia and the patient was treated with empiric IV antibiotics (piperacillin + tazobactam) and inhaled bronchodilators (salbutamol/ipratropium) with IV steroids for possible asthma exacerbation.\nOn day 3 of her second ICU stay, the patient required increasing doses of sedation due to agitation. Sedation and analgesia were increased gradually from 50 mg/h of propofol to 100 mg/h of propofol. Fentanyl was also increased from 30 to 100 mg/h. Paradoxically, on increasing her sedation and analgesia, the patient was noted to have episodic severe discordant breathing with prolonged expiratory phase with breath-holding with severe ventilator desynchrony. Peak airway pressures were high (> 50 cm H2O) and generated TVs were low (about 50 - 100 mL) despite increasing pressure limits on the ventilator. No wheezing was heard on auscultation of her chest and plateau airway pressure remained low (15 - 20 cm H2O). The endotracheal tube was patent and airway secretions were minimal. Repeat CXR done did not show any evidence of pneumothorax or new infiltrates. Electrocardiogram (ECG) and cardiac enzymes performed did not show any acute changes. Multiple ventilatory modes were tried (pressure control, volume control, PRVC) without any improvement in ventilation. Because of extremely low TVs, the ventilator was changed to exclude a leak which was less likely given the high airway pressures. She was empirically treated with IV steroids and also given multiple puffs of bronchodilator with no significant improvement. End-tidal carbon dioxide tracing showed rising trend and serial arterial blood gas showed worsening respiratory acidosis (pH 7.27, pCO2 52.9). She was put on increasing doses of sedation (propofol 150 mg/h and fentanyl 160 µg/h). She responded well to boluses of muscle relaxants with subsequent improvement in ventilation and lowering of airway pressures dramatically. A magnetic resonance imaging (MRI) of the brain was done and did not show any central cause for the hypercarbia.\nFrom day 3 to 4, an attempt was made to wean down the propofol infusion. However, all efforts at weaning off the propofol infusion were met by repeat episodes of ventilator desynchrony, low minute volumes and breath-holding. Each episode of high peak pressure and low minute volumes was evaluated systemically. There was no response to bronchodilators, no worsening of the CXR and no pneumothorax. These episodes were aborted with small boluses of propofol of 10 - 20 mg. At this time, a diagnosis of possible fentanyl-induced chest wall rigidity was considered and the patient was taken off fentanyl and continued on propofol infusion. IV dexmedetomidine infusion was started for the patient with the propofol infusion. A dramatic improvement in breathing pattern was noted. There were no more episodes of ventilator asynchrony, low TVs and high airway pressures. The propofol infusion was weaned down with the dexmedetomidine infusion. If there were episodes of agitation, they were briefly aborted with boluses of propofol. The patient was switched to pressure support mode ventilation the next day with no further episodes of desynchrony.\nBecause of prolonged ventilation and difficulty in weaning as a result of deconditioning for repeated ICU admission, the patient underwent an elective tracheostomy. She was given low-dose IV fentanyl peri-tracheostomy and tolerated it well without any further respiratory distress. Further ICU stay was uneventful and she was gradually weaned off the ventilator completely and transferred out of ICU. |
The 25-year-old male was referred to Department of Periodontics, Saveetha Dental College, Chennai, Tamil Nadu, India, with a complaint of periodontal abscess in relation to 11. On examination, the patient was systemically healthy and had not taken any long-term antiinflammatory medications or antibiotics.\nOn periodontal examination and radiographic evaluation, the patient presented with an intrabony defect extending up to apical third of right maxillary central incisor (number 11) with a probing depth of 8 mm using William's periodontal probe [Figures and ]. The patient did not present with pain in relation to number 11 tooth and had no pain on percussion. There was positive electric pulp test response suggesting the concerned tooth was vital. The diagnosis was made to be localized chronic periodontitis with periodontal abscess.\nInitial therapy consisted of incision and drainage of the abscess, with antibiotic regimen for 5 days followed by oral hygiene instructions, which were repeated until the patient achieved an O’leary et al. plaque score of 20% or below.[] Scaling and root planning of the teeth were performed.\nFour weeks following Phase 1 therapy, a periodontal re-evaluation was performed to confirm the suitability of number 11 tooth for this periodontal surgical procedure. Clinical measurements were made using William's periodontal probe with graduation to a precision of 1 mm.\nBlood sample was taken on the day of the surgery according to the PRF protocol with an REMI 3000 centrifuge and collection kits. Briefly, 6 ml blood sample was taken from the patient without an anti-coagulant in 10 ml glass test tubes and immediately centrifuged at 3000 rpm for 12 min. A fibrin clot was formed in the middle of the tube, whereas the upper part contained cellular plasma, and the bottom part contained red corpuscles. The fibrin clot was easily separated from the lower part of the centrifuged blood. The PRF clot was gently pressed between two sterile dry gauges to obtain a membrane which was later minced and added to the xenogenic graft material (OSSEOGRAF™).\nAn intrasulcular incision was made on labial and lingual aspect of the tooth of right anterior maxillary teeth (number 11, 12, 13) along with two vertical incisions, extending to the muco gingival junction in relation to the distal aspect of number 13 and 11. A full thickness trapezoidal flap was raised, and inner surface of the flap was curetted to remove the granulation tissue. Root surfaces were thoroughly planed using hand instruments and ultrasonic scalers. The right maxillary central incisor demonstrated a circumferential intrabony defect is extending distally to affect right maxillary lateral incisor, after removing granulation tissue thoroughly, the intrabony defect was found to extend in buccal and apical aspect.\nBriefly, minced PRF was mixed with xenograft (OSSEOGRAF™) and was applied to the defect walls and root surfaces []. The xenograft with PRF was then condensed using amalgam condensers. The flap were repositioned to their presurgical levels and sutured with silk utilizing an interrupted technique [].\nAfter the operation, the patient was prescribed systemic antibiotics (amoxicyllin 500 mg tid, 3 days), nonsteroidal antiinflammatory drug (combiflam tid, 3 days) and 0.12% chlorhexidine rinse (twice a day for 4 weeks). Sutures were removed after 7 days. Clinical healing was normal with neither infectious episodes nor untoward clinical symptoms. The patient was seen at 1st week, 2nd week, 1st month, 3rd and 6th month [].\nPeriapical intraoral radiographs were obtained from the periodontal defect site at baseline and 6 months after surgery []. The radiographs were obtained with paralleling technique using film holders. To standardize, putty index was made, and patient was asked to bite on it along with that of the holder.\nIn this case report, the reduction in pocket depth and gain in clinical attachment were found after 6 months of follow-up []. These are the important clinical outcomes for any periodontal regenerative procedures. Radiographs revealed improved bone fill in the intrabony defect compared to measurements at baseline. |
A 13-year-old girl diagnosed the previous year with CVID in the setting of pneumonia, low serum immunoglobulin levels, and absent antibody responses to immunizations, presented with worsening dyspnea. Whole exome sequencing did not reveal an underlying genetic explanation for the immune deficiency. A chest CT scan at the time of CVID diagnosis revealed only mediastinal lymphadenopathy. She was placed on monthly IgG replacement therapy and did well until she reported gradual worsening of dyspnea over 3 months. The dyspnea first manifested during competitive sports and progressed to an inability to walk up a single flight of stairs. Pulmonary function testing results () showed a restrictive pattern, and she was unable to complete the maneuvers for diffusing capacity of the lungs for carbon monoxide (DLCO). A follow-up chest CT scan revealed mediastinal and hilar lymphadenopathy, peripheral interlobular septal thickening, peripheral consolidation, and ground glass opacities (). Bronchoalveolar lavage obtained by bronchoscopy did not show any evidence of infection. Specific testing included bacterial, fungal, mycobacterial, and viral cultures along with PCR assays for influenza, respiratory syncytial virus, parainfluenza, human metapneumovirus, adenovirus, cytomegalovirus, Epstein-Barr virus, human herpes virus-8, and Pneumocystis jirovecii. She underwent a right lower lobe wedge resection biopsy via thoracoscopy. The biopsy () showed non-caseating granulomatous inflammation with aggregates of small lymphocytes, scattered multinucleated giant cells, scattered foci of organizing pneumonia, interstitial fibrosis focally in the subpleural space but not prominent or diffuse, and airway luminal compromise from adjacent lymphoid hyperplasia, confirming the diagnosis of GLILD.\nShe was treated with 4 doses of rituximab 375 mg/m2 given 4–6 months apart, based on clinical symptoms and pulmonary function testing, and azathioprine 50 mg daily for 18 months as IgG replacement therapy was continued. She responded well to the new therapy regimen with complete resolution of exercise intolerance and normalization of pulmonary function testing parameters (). She also had remarkable improvement of the CT scan abnormalities () with the follow up CT scan after completion of therapy demonstrating resolution of all abnormalities. |
The third case is of a 68-year-old Irish woman who presented to the MMUH in April 2016 with acute laryngitis. She had a background of bipolar affective disorder which had been stable for the past 30 years on monotherapy with lithium. There had been a recent history of lithium toxicity secondary to a deterioration of her renal function, which had been managed at her local psychiatric hospital. After the episode, she had been restarted on a low dose of lithium as well as a low dose of valproate.\nOn presentation to the MMUH she was initially treated jointly by the ear, nose, and throat (ENT) team and medical team and was managed in an ICU environment due to respiratory compromise. She had no oral intake for multiple days. Once stabilized she was transferred to an acute medical ward but an acute onset confusional state with bizarre behavior was noted over a period of 2 days. Due to her psychiatric history the Liaison Psychiatry service was consulted. On review she was severely thought disordered and confused. She was only able to produce a word salad and showed echolalia. She had motor retardation, increased tone, negativism, and posturing on examination. The impression was that she was suffering from acute catatonia. Brain imaging did not reveal acute abnormalities. She was diagnosed as having bipolar I disorder with catatonia as per DSM-5 (Table ).\nAdvice was given to treat her with paliperidone. Her mental state improved slightly as a result, but she remained severely thought disordered and confused for 2 weeks. Eventually, lithium was cautiously reintroduced under close monitoring of her renal function. The reintroduction of lithium was well tolerated and she improved significantly over a 2-week period. At discharge she was no longer thought disordered, she was well orientated, and back to her fully independent baseline. She continues to live independently to date. |
This is a case of a 59-year-old morbidly obese female with situs inversus totalis who presented for a laparoscopic sleeve gastrectomy. Her BMI was 38 (height 4 ft 11.5 inches, weight 188.2 pounds), and she had a lifelong history of morbid obesity and obesity-related comorbidities, including obstructive sleep apnea requiring a continuous positive airway pressure machine, an elevated hemoglobin A1c (5.8) and a fasting blood glucose increasing her risk of developing diabetes mellitus, and degenerative joint disease which significantly impacted her ability to exercise. The main challenges she identified in losing weight involved eating carbohydrate rich foods, overeating during meals and limited activity due to musculoskeletal pain. The patient had made multiple attempts to lose weight through commercial dieting programs but had been unsuccessful. The patient also completed a six-month medically supervised diet through her primary care provider, which also included working closely with a bariatric registered dietician, following a strict diet of about 1800 calories/day and performing modified exercise, about 120 minutes/week. Despite these intense medical weight loss efforts, she was unable to maintain a healthy weight. The patient was motivated to try bariatric surgery after she witnessed the significant weight loss success her daughters had from this intervention. Her greatest hope from the bariatric surgery was to be healthier and to alleviate her obesity-related comorbidities.\nThe patient’s surgical history included cesarean section and evacuation of an ectopic pregnancy. She was a former smoker, quitting over 25 years ago, and has no other history of substance or alcohol use. Family history is positive for obesity, diabetes, hypertension, coronary artery disease and hypercholesterolemia. She did not take any medications, including supplements, except for Ibuprofen 800 mg 1–3/daily for musculoskeletal pain.\nThe patient underwent a comprehensive evaluation and treatment plan prior to the surgery including: psychiatric evaluation and clearance, nutritional consultation with a registered dietician, education about bariatric surgery and pre/post op expectations, routine preoperative labs, UGI, esophagogastroduodenoscopy (EGD), pulmonary function analysis, and a cardiovascular exam. Situs inversus totalis was confirmed with abdominal X-ray and CT, and echocardiogram. Pre-procedural evaluation with UGI revealed mild gastroesophageal reflux observed to the level of the distal one-third esophagus and small sliding-type hiatal hernia. EGD revealed normal esophagus and duodenum. Stomach biopsy was obtained for antral gastritis, and no helicobacter organism was identified. Abdominal ultrasound confirmed fatty liver disease. Pulmonary function analysis including spirometry, lung volumes and diffusion was normal. A pre-procedural cardiovascular exam was performed due to dextrocardia to exclude other structural cardiac abnormalities. 2-D echocardiography with M-mode demonstrated a left ventricular ejection fraction of 60%, no structural abnormalities in the aortic, pulmonic, tricuspid and mitral valve, or right and left atrium and ventricles. Color Doppler and continuous and pulse wave Doppler demonstrated mild pulmonic regurgitation and mild tricuspid regurgitation.\nThe patient discontinued the Ibuprofen more than one month before her surgery and began a low-calorie liquid diet two weeks prior to surgery. On the day of surgery, preoperative antibiotics, Cefazolin, were given within 60 minutes before the first incision. Prior to induction, the patient received 5000 units of heparin subcutaneously and sequential compression device (SCD) boots were placed for deep vein thrombosis (DVT) prophylaxis. No beta-blockers were administered. The patient was placed in the supine position and general anesthesia was induced. A Foley catheter was placed and the patient was supported with positioning devices including: arms on padded arm boards, gel pad under left axilla, footboard with gel pads, hover mat and a bariatric safety belt over patient’s thighs. The abdomen was then prepped and draped in the standard surgical fashion.\nA Veress needle was used in the right upper quadrant to access the abdomen and insufflation was created to 15 mmHg. Veress was removed and replaced with a 5 mm trocar and the scope was placed. Additional trocars were placed in the following position: right and left 5 mm lateral trocars, right and left 12 and 15 mm supra-umbilical trocars. The placement of all retractors and graspers was adjusted accordingly to the mirror image anatomy of the intraabdominal organs. The primary surgeon was positioned on the left side of the patient and the assisting surgeon on right side of the patient. Situs inversus totalis was confirmed with the majority of the liver oriented to the patient’s right, spleen on the right, greater curvature of the stomach on the right and gallbladder on the left.\nThe operating table was placed in the reverse Trendelenburg position. The patient’s right-sided half of the liver was retracted cephalically using a Nathanson retractor to expose the vicinity of the esophageal hiatus. The peritoneum over the cardia was incised using the Ethicon Harmonic scalpel, and the plane between the cardia and the left crus of the diaphragm was opened to expose the right diaphragmatic crus. No hiatal hernia was present. A point 5 cm proximal to the pylorus along the greater curvature of the stomach was marked corresponding to the incisura angularis just proximal to the crow’s foot of Latarjet’s nerve. The vessels along the greater curvature and all the short gastric vessels were sealed and divided using the Ethicon Harmonic scalpel, freeing the greater curvature and the fundus of the stomach. A 42-French bougie was placed and oriented towards the antrum along the lesser curvature (Figure ). The stomach was stapled and divided alongside the tube in a vertical fashion towards the angle of His (Figures -).\nAn Ethicon Echelon Flex triple staple line power stapler with a total of one black, three green, and one gold staple loads was used. All staple loads were 60 millimeters in length with staple line bio-absorbable reinforcement. Hemostasis at the external staple line was achieved (Figure ). The stomach was removed from the abdomen via the left-sided 15 mm trocar (Figures , ). Intraoperative endoscopy was performed using a 5 mm Olympus Ultrathin gastroscope revealing no areas of stenosis, internal staple line bleeding, nor staple malformation or leak seen. Total operation time was 108 minutes. There were no post-operative complications.\nPost-operative care included pain management and DVT prophylaxis with SCD, heparin and early ambulation four hours post-surgery. A UGI was performed on post-op day 2 with normal findings for a post-bariatric surgery evaluation and clear fluids were started. The patient was discharged on post-op day 3 without any complications. Upon discharge, the patient had a treatment plan that was previously discussed that included instructions for diet and medications, including vitamin supplementation and antacids. At her three-month follow-up, the patient was still without complications and very pleased with her weight loss of 46.2 lbs, weighing 142 lbs (BMI 29). |
A 33-year-old unrestrained male driver involved in a head-on, high-speed motor vehicle collision presented to Johnson City Medical Center in Johnson City, Tennessee as a level 1 trauma alert in February 2016. He was intubated in the field and per the emergency medical services report was initially hypertensive and tachycardic during transport. Vitals upon arrival on assist control ventilation were temperature (T) 95.3°F, heart rate (HR) 106 beats per minute, blood pressure (BP) 89/60 mmHg, and oxygen saturation (O2 sat) 100%. During primary survey, the patient was scored Glasgow Coma Scale 3T with multiple orthopedic injuries and a distended abdomen. Massive transfusion protocol was initiated. The patient became increasingly hypotensive with only transient improvement in mean arterial pressure. He was emergently transported to the operating room (OR) and underwent multiple small and large bowel resections, secondary to blunt force perforation and mesenteric bleeding. He was left in discontinuity and returned to the OR 24 hours postoperatively for creation of primary anastomoses and abdominal closure. At time of initial and subsequent operation, the adrenal hemorrhage was unknown, and with no evidence of expanding retroperitoneal hematoma this area was not explored. During the early resuscitation period, the patient exhibited both transient tachycardia and hypertension documented as HR 110 beats per minute and BP 165/67 mmHg on the morning of postoperative day 1. CT scan was obtained after initial stabilization and illustrated few small punctate cerebral hemorrhages, single non-displaced facial fracture, multiple extremity fractures, thoracic spinous process fractures, multiple rib fractures, and a hematoma of the right adrenal gland approximately 2.2 x 3.5 cm in size.\nDespite overall improvement with resuscitation and routine postoperative care, the patient continued to exhibit persistent hypertension and tachycardia even with administration of continuous intravenous (IV) sedatives such as fentanyl and midazolam. Additional medications, including oxazepam and quetiapine, were added as clinical findings were thought to be concurrent with intermittent idiopathic episodes of agitation, but this only led to mild improvement. Pain control was also reassessed, and subjective patient reports indicated adequate management. Around hospital day 7, metoprolol was added to medication regimen, but despite increased dosage it only displayed a limited effect on hemodynamic state during the next 24 hours. The patient’s BP was continuously elevated with systolic blood pressure averaging 200 mmHg. IV sedation was switched to propofol in an attempt to alleviate persistent hypertensive urgency. At this time, work-up was also significant for the development of fever with worsening leukocytosis. The patient was 7-10 days postoperative and at high risk for possible intra-abdominal abscess or leak of intestinal anastomosis. Abdominal CT was obtained with overall unremarkable results showing stable right adrenal hematoma, development of small bilateral pleural effusions, and expected postoperative inflammatory changes.\nDue to inadequate BP control, a continuous IV esmolol drip was started and both plasma and urine metanephrines were ordered. Labs illustrated plasma metanephrines at 0.26 and normetanephrine at 1.89 nmol/L (normal reference range 0-0.49 and 0-0.89 nmol/L, respectively). Urinary metanephrines were also elevated at 227 and normetanephrines at 1,159 μg/g (normal 0-300 and 0-400 μg/g, respectively) []. Esmolol drip was weaned within the next few days with addition of both clonidine and metoprolol. Vital signs at this time were documented around BP 170/80 mmHg and HR 120 beats per minute, and two days later recorded at BP 151/86 mmHg and HR 103 beats per minute. Recollection of labs, one week after initial values, showed persistently elevated urinary metanephrines and normetanephrines at 333 and 878 μg/g, respectively. BP was still elevated at this time but able to be controlled on oral agents alone; therefore, clonidine dose was tapered over the next few days. Maximum BP and HR values were recorded at 140/90 mmHg and 95 beats per minute, respectively, approximately one month into hospital stay. As the patient had otherwise recovered well from recent traumatic injuries, he was placed on a tapered dose of oral metoprolol (12.5 mg twice daily) and discharged home. The patient did not present for scheduled post hospital outpatient follow-up. The patient however did subsequently present to the hospital for unrelated reasons one month later (almost two months after initial admission date). At this presentation to the ED, there was no evidence of persistently elevated BP or HR, and repeat CT abdomen did not show any residual adrenal hemorrhage. Due to lack of follow-up, no further outpatient testing of metanephrines was able to be completed. |
A 64-year-old man, who had experienced sudden weakness and numbness in the left lower extremity for 4 weeks, visited our emergency department for evaluation and treatment. Over several days, his gait disturbance gradually worsened and the numbness had extended to the left upper chest region. There was no evident traumatic episode before admission. A physical examination conducted at presentation revealed gait disturbance with spasticity. He was able to stand by himself, but needed a crutch for walking. A neurological examination showed motor weakness of left lower extremity (Grade IV). In addition, sensory disturbances of vibration and positional sensation were present on the left side below the T4 dermatome. Impaired perception of pain and temperature stimuli were also noted on the right side below the T4 dermatome. Brown-Séquard syndrome of the cervicothoracic or thoracic spine was then suspected. Plain radiographs of the cervical spine showed multiple degenerative changes. Accordingly, magnetic resonance imaging (MRI) of the whole spine was performed. Sagittal T2-weighted MR images revealed a left-sided cystic extradural lesion at the C7-T1 junction (), and axial images showed that the extradural cystic lesion markedly compressed the spinal cord (). The lesion appeared homogenously isointense on T1 weighted images and exhibited heterogeneous high signal intensity on T2 weighted images. Under a presumptive diagnosis of a cystic lesion in the lower cervical spine, emergent surgery was performed. Because there were additional osteophytes causing cord compression at C4-5 and C5-6, modified expansive laminoplasty of C5-6 and a laminectomy of C7 followed by complete removal of the extradural cyst were performed. The lesion was homogeneous, bright yellow in color, firm in consistency, and slightly adherent to dura mater, and contained a small amount of serous fluid. Pathological examination showed the cyst to be composed of fibrous connective tissue and to have a distinct synovial cell lining with focal calcification (). The diagnosis was confirmed as a synovial cyst. Immediately after surgery, motor power and impaired sensation were improved. At his 6-month follow-up, he was able to walk without any assistance and returned to work. At his 8-month follow-up, no recurrence of symptoms, except for mild numbness, was evident. |
A 20 year old female, G2P0, presented to the emergency department at the end of her 17th week of amenorrhea with violent abdominal pain. Her first pregnancy was marked by the appearance of an intense pelvic pain occurring at 18 weeks in the context of hemorrhagic shock.\nDuring laparotomy, the amniotic membranes were discovered bulging into the abdominal cavity from a breach in the ruptured left rudimentary uterine horn in what was discovered to be a pseudo-unicornuate uterus. Treatment consisted of ablation of the left rudimentary horn, with excision extending to its junction with the right hemi-uterus. The current pregnancy was unbooked at presentation. Its evolution was marked by the appearance of pelvic pain at 17 weeks gestation. There was no bleeding but the patient was noted to have malaise and fatigue. On clinical examination, the blood pressure was 90/50 mm/Hg, pulse was 100 bpm, and there was mucocutaneous pallor. The abdominal examination showed pelvic guarding, and both flanks were dull to percussion. The gynaecological exam found a bulky uterus with cervical excitation and pelvic peritonism. Physical assessment revealed a hemoglobin of 6 g/dl. Ultrasound scan showed a uterus of normal structure with an empty cavity, placenta, and a non-viable pregnancy of 17 week's gestation outside the myometrium. They also noted a large intra-peritoneal effusion, suggesting an abdominal pregnancy ().\nAn urgent lower midline laparotomy was carried out together with simultaneous resuscitation of the patient. The surgical findings included a hemoperitoneum of two liters, a full thickness rupture of the uterine wall measuring 6 cm involving the remaining hemi-uterus, and a dead foetus with a placenta showing no sign of placental insertion in the abdomino-pelvic cavity (). After extraction of the foetus and placenta, repair of the hemi-uterus was carried out by way of interrupted stitches in two layers. The post operative course was uncomplicated and the patient was discharged on the 7th post-operative day. |
A 14-month-old African American boy presented to our hospital during the winter with hand stiffening that started on the day of presentation. His mother noticed that his hands were stiff and bent inward while he was playing. He had no fever, seizure-like activity, upper respiratory symptoms, vomiting, nor diarrhea. His medical history was significant for atopic dermatitis (AD) since the age of 3 months and a recent diagnosis of iron deficiency anemia. His diet, in addition to breast milk, was limited to rice, chicken, potatoes and broccoli; all of which have low vitamin D content. He had an even more restricted diet due to presumed food allergies to dairy products, eggs, wheat, soy, almonds and peanuts, which were based on elevated allergen-specific IgE levels. He was taking iron supplements, but no other medications. He had no developmental regression, but he was still unable to walk or to even pull himself up to stand. He could crawl but fatigued quickly. The patient was born full-term and the pregnancy was complicated by maternal gestational diabetes, hypothyroidism and vitamin D deficiency. A physical examination revealed an alert child with normal vital signs and no dysmorphic features. He weighed 10.5 kg (60th percentile) and his length was 77 cm (25th percentile). He had diffuse xerosis on his cheeks, trunk and flexural areas. His hands were stiff and contracted, but there were no visible skeletal deformities such as joint widening or genu varum. He had mild hypotonia; he was able to sit unassisted and to stand briefly with support but could not walk. His reflexes were normal with no fasciculations, and the remainder of the examination was unremarkable. The laboratory findings shown in in addition to radiography findings () were consistent with calcipenic rickets, most likely a consequence of his vitamin D and calcium deficient diet. A further consequence of his limited diet was microcytic anemia due to iron deficiency as was evident by his complete blood counts and iron studies. Aspartate transaminase (AST) and alanine transaminase (ALT) were 137 and 90 U/L, respectively (normal < 45), and his albumin, total bilirubin, γ-glutamyl transferase levels, electrolytes, and renal function were normal. A liver ultrasound was obtained due to ALT and AST elevation, and it was normal. His alkaline phosphatase isoenzyme was found to have originated in the bone as was expected. His ALT and AST mild elevation were likely due to muscle spasms and not due to liver etiology, and they normalized later. Celiac serology antibodies were normal, ruling out the concern for malabsorption. Electrocardiography (ECG) showed a sinus rhythm with prolonged QTc interval of 480 milliseconds (normal < 445), which was consistent with his hypocalcemia.\nThe patient was admitted to the hospital and received serial intravenous (IV) and oral replacement of calcium with vitamin D supplementation, which gradually corrected his hypocalcemia and hypophosphatemia. This was done initially in the intensive care unit with close monitoring until the ECG changes resolved. His AD was managed with emollient and topical steroids. The family met with a nutritional specialist and were educated on proper diet and provided with an AD action plan. On the third day of his hospitalization, the patient developed a fever with erythema and mild swelling of his right arm at the site of the peripheral IV catheter. The ultrasonography showed basilic vein thrombosis, and a new IV catheter was placed in the left arm. Broad spectrum antibiotics were started after obtaining a blood culture, which later grew methicillin-sensitive Staphylococcus aureus and his antibiotics were adjusted to IV cefazolin. He had a similar presentation at the site of his peripheral IV catheter in the left arm 4 days later and ultrasonography also showed left basilic thrombosis. A thrombophilia screen including protein S, protein C, cardiolipin antibodies, antithrombin III, factor V Leiden and prothrombin gene mutation were all normal. He was started on subcutaneous low molecular weight heparin (LMWH) to prevent further clotting. The patient was discharged home after 11 days to continue calcium and vitamin D supplements for his rickets and oral cephalexin and subcutaneous LMWH for his superficial septic thrombophlebitis. |
A 62 year-old male had displayed bradykinesia and tremor of his right limbs for one year, during which he was able to perform limited fine movements such as dressing himself, lacing up his shoes and brushing his teeth. His tremors were aggravated by nervousness and relieved when asleep. He had had a history of hypertension and took a daily dose of 5 mg amlodipine. The patient had no history of any other chronic illnesses and was not on any other type of medication. Neither the electrocardiogram nor the Holter monitor showed any abnormalities. His baseline recumbent-upright blood pressure (BP) and heart rate (HR) were normal prior to treatment with piribedil, as shown in Table . He was diagnosed with PD based on the Movement Disorder Society clinical diagnostic criteria []. Initially, he received dopamine replacement therapy of 50 mg piribedil per day. Although there was no significant improvement in symptoms neither did he feel any discomfort. Therefore, starting the first dose change of piribedil, he added extra 50 mg to his dose. About two hours later after the first change in dose, the patient experienced symptoms of dizziness and sweating; he collapsed half an hour later. Whilst in a sitting position, the patient’s BP and HR were measured immediately. The BP reading was 85/48 mmHg and HR was 45 beats/min. His symptoms continued for the duration of the day with sitting BP fluctuating between 80–95 mmHg to 45–68 mmHg. Because his head computerized tomography examination found no abnormalities, the patient received 500 mL of 0.9% sodium chloride solution, after which his symptoms improved. Due to adverse drug reactions (ADRs), the patient was started on a second dose change of piribedil, i.e. an extra dose of 25 mg piribedil was to be taken in the afternoon in addition to the existing 50 mg taken in the morning. After two and a half hours, the patient experienced dizziness, sweating, nausea and vomiting, with a BP reading of 70/45 mmHg and a HR of 47 beats/min when sitting. His BP recovered to 105/65 mmHg and HR to 60 beats/min after elevating his lower limbs and resting for 20 mins. As a result of these incidences, the patient was switched to pramipexole to replace piribedil. After taking pramipexole 0.125 mg or 0.25 mg three times a day (tid), the symptoms of hypotension and bradycardia disappeared but a reduced amplitude of his right arm swing was still observed. Finally, after the pramipexole dose was increased to 0.375 mg tid, the patient showed marked improvements in motor symptoms. The changes in BP and HR are shown in Fig. . |
We present the case of a 65-year-old male with no previous smoking or supplemental oxygen history who presented to the emergency department after a routine clinic visit that showed desaturation into the 70s. Past medical history was insignificant except for recent hospital admission the week prior that entailed a recent bilateral embolic stroke followed by a left carotid endarterectomy with 80% stenosis bilaterally, as well as a viral infection with influenza type B treated with Tamiflu. Initial evaluation upon admission revealed acute hypoxemic respiratory failure without hypercapnia. CT chest showed significant bilateral consolidation in the mid to lower lobes correlating with a bilateral pneumonia secondary to recent viral illness (). Meropenem and Levaquin were started, followed by vancomycin as the patient continued to require more oxygen and non-invasive ventilation over the following three days. This included high-flow-nasal cannula (HFNC) initially, with advancement to Vapotherm to maintain the patient’s oxygenation status. Initial laboratory work revealed a white blood cell (WBC) of 13.3 (high of 23 during admission), erythrocyte sedimentation rate (ESR) of 88, and c-reactive protein (CRP) of 8.8. The respiratory viral panel was negative, and tests for other possible causes, including fungal and autoimmune causes, were negative.\nThe patient underwent an endobronchial ultrasound (EBUS) bronchoscopy where the obtained samples were negative for source of infection from cytology, Gram stain, and sputum findings. The findings from EBUS bronchoscopy also included respiratory macrophages and inflammatory cells. Following this procedure, there was increasing concern for noninfectious organizing pneumonia as other diagnoses had been excluded. The patient was then started on IV steroids, and IV antibiotics were discontinued. In addition, nightly continuous positive airway pressure (CPAP) was added as there was also a concern of undiagnosed obstructive sleep apnea (OSA) as a contributing factor to the patient’s hypoxia. An echocardiogram with bubble study was additionally performed out of concern for possible shunting that could be worsening the patient’s oxygenation status, as the patient also had recent bilateral embolic stroke, but none was noted. The patient’s oxygen requirements began to slowly improve following this regimen over the course of several days, although an extended stay was required due to slow oxygen titration needs. An interval CT chest showed an improvement of consolidation as well. The patient’s oxygen status on the day of discharge remained at 2L on nasal cannula (NC) and he required supplemental oxygen upon discharge. The patient was also transitioned to per os (by mouth) (PO) steroids with instructions for slow taper upon discharge and to have close follow up with both his primary care provider (PCP) and pulmonologist, and referral for sleep study to evaluate for OSA workup. Follow-up CT chest after discharge showed significant resolution of consolidation (). |
A 35-year-old male presented to the Department of Otorhinolaryngology with a pigmented mass over the left retromolar trigone that existed for six months. The patient had a history of occasional paroral bleeding for the past three months and loosening of the upper last molar tooth for two months. He had consulted with a dentist for the same and was advised topical medication for two months. He was then referred to the Otorhinolaryngologist as the symptoms failed to respond to the treatment. Physical examination revealed a pigmented proliferative mass involving the gingival surface of the retromolar trigon, extending laterally to the buccal mucosa and gingivobuccal sulcus and superiorly to the alveolar process of the maxilla (). No palpable cervical lymphadenopathy was detected in the patient. A contrast-enhanced computed tomography (CECT) scan revealed a soft tissue mass in the left retromolar trigone (RMT) space. This mass involved the maxillary alveolus and palate without erosion of the palatal bone ().\nAll routine hematological and biochemical investigations were found to be normal. The incisional biopsy of the lesion indicated intact squamous epithelium and diffuse infiltration of the subepithelium by spindle-shaped tumor cells with prominent nucleoli. Immunohistochemistry showed strong positivity for Melanin A and S-100 in the tumor cells ().\nThe CECT scan of the whole abdomen and chest was found to be normal. Written informed consent of the patient were taken for surgical excision after the nature of the lesion, treatment options, prognosis of the disease, and the possibility of the need for adjuvant chemoradiation was explained to him and his family. Wide local excision along with left segmental mandibulectomy and infrastructural maxillectomy was performed (). The tumor was 5.6 × 3.5 × 4.9 cm in size and weighed 62.2 g (). The defect was reconstructed with pectoralis major myocutaneous flap, spreading from the palatal margin to the floor of the mouth ().\nThe patient was started on Ryle's tube feeding 24 hours after the surgery and was discharged seven days after the surgery. Histopathological section was suggestive of malignant melanoma with tumor-free resected margin with absence of lymphatic/ bony involvement. The patient was advised for postoperative radiotherapy, considering the grave prognosis of the disease. He has been on regular follow-up for the past 24 months and found asymptomatic without the recurrence of the disease (). |
A 30-year-old Indian man who migrated to the USA from India 3 years prior to this presentation with a past medical history of psoriasis, not on any medications presented to the emergency department (ED) with sudden onset constant abdominal pain for 5 days. The pain was in the right and left upper quadrant, spasmodic in nature, 5/10 in intensity, not radiating and no aggravating or relieving factors. The abdominal examination did not reveal any guarding, or any other abnormality. In the ED, he was evaluated with a complete blood count, metabolic panel, urinalysis, computed tomography (CT) abdomen and pelvis, and right upper quadrant ultrasound, all of which were negative except for leukocytosis 17.9 (4.5 - 11 ×103/µL). He was discharged from the ED with a prescription for pantoprazole and tramadol.\nThe patient returned to the ED 2 days later with persistent abdominal pain associated with nausea, vomiting and inability to tolerate an oral diet. At this time, he also reported maculopapular rash that he noticed on both legs which started at the same time with abdominal pain. He reported rash extended to his calves. He was admitted for further evaluation and underwent endoscopy which showed non-bleeding small gastric ulcer with multiple duodenal erosions (). He was treated symptomatically and discharged on pantoprazole. On day 12 (since the onset of pain), the gastric biopsy came back positive for HP () and he was started on triple therapy (clarithromycin, amoxicillin and lansoprazole) for HP.\nThe patient completed the 2 weeks of triple therapy; however, abdominal pain persisted. The rash continued to spread to involve the thighs, flanks, around the umbilicus, and extensor surfaces of arms (, ). The patient came back to the ED on day 27 (since the onset of symptoms) with the same symptoms after finishing triple antibiotic therapy. The patient was again admitted and underwent extensive immunological workup including rheumatoid factor, C-reactive proteins, anti-nuclear antibodies, total complement level, C3, C4, IgA level, ANCA IgG level, myeloperoxidase antibody, serine protein 3, anti-DNA antibody and erythrocyte sedimentation rate, which were all within normal limits. He underwent repeat endoscopy which showed healed gastric ulcer. Skin rash continued to worsen to involve almost all extensor surfaces of both legs (). A skin biopsy of the skin rash was obtained while the patient was treated symptomatically with narcotics to control the pain. The patient was eventually discharged with pain medications and instructed to follow-up as an outpatient. The skin biopsy eventually came back positive for leukocytoclastic vasculitis (). HSP diagnosis was made by exclusion since patient did not have connective tissue disorders based on immunological workup, no history of drug ingested prior to symptoms. At that point, the patient was started on prednisone 40 mg daily and improved drastically on the following day of starting steroids. Patient continued on steroids taper for 8 weeks. Rash as well as abdominal pain resolved completely. |
A 33-year-old man presented to the dental office with the complaint of an absent lower canine on the left side. The patient had no other symptoms and was classified as ASA I. The clinical examination revealed the absence of dental element 33. In light of the above, a computed tomography (CT) scan was requested, and transmigration of the left lower canine in the midline in the mentonian region, in the horizontal and vestibular position, was diagnosed, as shown in .\nDue to the unfavorable position of the dental element, orthodontic treatment was contraindicated, establishing surgical extraction as the preferred mode of treatment [, ]. The patient underwent surgery under local anesthesia (articaine 4% 1 : 100,000) with bilateral blocks of the lower alveolar nerve, complemented by a vestibular canine-to-canine infiltration terminal. During surgery, a horizontal incision was made 5 mm below the mucogingival line extending from canine to canine, as shown in . The tissue was then detached, allowing partial visualization of the impacted tooth.\nThe surrounding tissue was then separated from the tooth and odontosection was carried out using a piezoelectric apparatus in order to minimize the trauma, as can be seen in .\nAfter extracting the tooth, curettage and synthesis maneuver were performed in the internal musculature and in the superficial plane, both using an absorbable suture thread (Monocryl 5.0) as shown in .\nAt the end of the surgical procedure, the patient received counselling regarding postoperative care. Antibiotic was prescribed (Amoxicillin 500 mg every 8 hours for 7 days) with an anti-inflammatory (Meloxicam 7.5 mg every 12 hours) and analgesic (Dipyrone Sodium 500 mg every 6 hours for three days). The patient underwent 5 laser therapy sessions during the recovery period and returned after 7 days to remove the sutures. At this presentation, there was no complaint of pain or paresthesia and no evidence of infectious symptoms. |
A 42-year-old healthy man was evaluated initially elsewhere for acute right-sided headache followed by visual loss of the right eye with pain on eye movement. Best-corrected visual acuity was 20/400 in the right eye and 20/20 in the left eye, with a right relative afferent pupillary defect. The right eye had 30% red desaturation and an inferonasal visual field defect. Optic disc edema was not detected, and a brain magnetic resonance imaging (MRI) without contrast was unremarkable. After 5 days of deteriorating vision, the patient was prescribed 40 mg prednisone daily.\nThe patient was then referred to our clinic for progressive visual loss and persistent pain with eye movement in the right eye. At initial presentation, 7 days after onset of symptoms, vision in the right eye was hand motion temporally with a relative afferent pupillary defect. The optic nerve had mild edema with blurring of the superior margin. Orbit MRI with contrast revealed enhancement of the right optic nerve and sheath (), as well as nonspecific periventricular, deep, and subcortical white matter lesions. The patient was started on intravenous methylprednisolone 1 g daily, with a plan to assess clinical response frequently, as the MRI optic nerve and sheath enhancement suggested an inflammatory component.\nRepeat examination at 11 days after the onset of symptoms demonstrated narrowing of the visual field of the right eye to hand motion in a small temporal island and persistent right afferent pupillary defect. The right optic nerve head was diffusely edematous without hemorrhage (), and the left optic nerve head was normal with a 0.5 cup-to-disc ratio (). A systemic workup for inflammatory etiologies was unremarkable, including anti-aquaporin-4 antibody, anti-neutrophil cytoplasmic antibodies, angiotensin-converting enzyme, rapid plasma reagin, and fluorescent treponemal antibody, as well as Leber hereditary optic neuropathy genotyping, chest X-ray, and cerebral spinal fluid analysis. Due to lack of improvement in vision, intravenous methylprednisolone was discontinued after 8 days and the patient was started on oral prednisone 60 mg daily for 1 week, with a taper of 40 mg daily for 1 week, followed by 20 mg daily for 1 week.\nThree weeks after the onset of symptoms, the right eye vision was still hand motion only in the superotemporal quadrant. The right optic nerve head showed persistent edema and the left optic nerve remained normal (). Goldmann visual field (GVF) showed severe constriction of the visual field, with a small superotemporal and superonasal island of vision remaining (). Repeat MRI showed enhancement of the right optic nerve extending to the optic canal (). Given the progressive clinical course and the lack of significant improvement with intravenous corticosteroids, atypical optic neuritis with perineuritis, ischemic optic neuropathy, and malignant optic glioma were considered. After discussing the case in a multidisciplinary meeting, the decision was made to observe closely and continue prednisone with the aforementioned taper, with the option of an optic nerve or sheath biopsy should the patient’s condition worsen further.\nSeven weeks after the onset of symptoms, the vision in the right eye had improved to 20/400; repeat GVF showed expansion of the superior field (), eye pain resolved, and a repeat MRI found decreased right optic nerve enhancement (). The patient eventually admitted to intermittent use of several over-the-counter sexual enhancement supplements throughout the course of his steroid treatment without disclosing the exact amount or frequency, which he had discontinued prior to his clinical improvement. Four months after onset of visual loss, his headache and pain with eye movement had resolved. GVF showed improved sensitivity in the superior field and a persistent inferior defect in the right eye (). Visual acuity of the right eye was 20/200, at which point it remained stable. |
A 37-year-old Caucasian male with a known history of aplastic anemia (AA), presented to a rural hospital after a ground level fall. AA was diagnosed 10 months earlier after he was investigated for pancytopenia. A bone marrow biopsy showed cellularity of only 10% and the presence of a small paroxysmal nocturnal hemoglobinuria clone (less than 0.2%). He received standard combination treatment for AA with cyclosporine 225 mg orally twice daily, horse anti-thymocyte globulin (ATG) 40 mg/kg daily for 4 consecutive days, and prednisone 1 mg/kg daily. His other medications included daily Pantoloc 40 mg orally, daily Valtrex 500 mg orally, and daily Dapsone 50 mg orally for Pneumocystis jirovecii prophylaxis due to a reported allergy to trimethoprim/sulfamethoxazole. He had recently quit smoking and denied alcohol use but actively used other recreational drugs, including marijuana, cocaine, and methamphetamine. He was unemployed. He had no known other medical co-morbidities and was taking no other medications prior to developing AA. The etiology of AA was felt to be idiopathic because he had no improvement after an initial trial of sobriety. AA improved following immunosuppressive therapy and, although human leukocyte antigen typing was performed, a subsequent bone marrow transplant was deferred not only because of the medical therapeutic response but also due to his ongoing recreational drug use. Although he was no longer transfusion dependent a month after starting immunosuppressive therapy, his treatment compliance waned overtime due to regular ongoing recreational drug use of cocaine and methamphetamines. He routinely used unsterilized tap water for illicit drug injections, but he denied other exposure to fresh or salt water sources at home or in the community.\nOn presentation to the emergency department he was not in distress, with a heart rate of 90 bpm and a blood pressure of 116/59. Severe pallor was noted upon examination, as well as a petechial rash and mild ecchymoses (Fig. ). The rest of his physical assessment was normal, including a neurological examination. Admission bloodwork revealed severe pancytopenia with hemoglobin of 22 g/L, a platelet count of 1 × 109/L, a white blood cell count of 3.7 × 109/L, and an absolute neutrophil count of 0.2 × 109/L (reticulocytes were not sent at admission, but 2 weeks into his hospitalization his absolute reticulocyte count was 12 × 109/L with a reticulocyte percentage of 0.5). All other admission blood work was normal, including liver function tests (total bilirubin 9 μmol/L (reference < 21 μmol/L), alanine aminotransferase 13 μmol/L (reference < 41 μmol/L), alkaline phosphatase 66 U/L (reference 30–130 U/L)) and renal function tests (creatinine 63 μmol/L (reference 59–104 μmol/L), glomerular filtration rate 120 mL/min (reference < 59 mL/min)). He was stabilized and transferred to a tertiary care center where he was restarted on treatment for relapsed AA with a regimen that included cyclosporine (5 mg/kg/day) and prednisone 30 mg daily in addition to five doses of ATG. He remained transfusion dependent throughout his hospitalization.\nOn day 10 after admission, he developed generalized, mild (3/10), colicky abdominal pain with an associated fever > 38.5 °C. He was started empirically on piperacillin-tazobactam (PTZ) 3.375 gm intravenously every 6 hours. Two sets of blood cultures, each consisting of an anaerobic and aerobic BacT/Alert bottle (bioMérieux, Laval, Quebec), were collected peripherally and from his central line. E. coli grew in each bottle set at 10 and 11 hours, respectively. He then developed watery, non-bloody bowel movements, 3–4 times a day, associated with rectal pain. Real-time PCR for Clostridium difficile A/B toxin on a stool sample was negative. Computerized tomography of the abdomen and pelvis was also unremarkable. Repeat blood cultures were negative at 24 and 48 hours after the initial positive set. He improved dramatically after 7 days of intravenous PTZ and was stepped down to oral ciprofloxacin 500 mg orally twice daily to complete a further 7 days of therapy.\nOn day 19 of admission he developed acute continuous severe (9/10), non-radiating dull rectal pain, associated with a high-grade fever (40.4 °C). Vancomycin 1.5 g intravenously every 12 hours and metronidazole 500 mg orally twice daily were empirically started and ciprofloxacin was continued in the same dosage. Blood cultures that were collected from peripheral venipuncture and a peripherally inserted central catheter line grew A. hydrophila at 11 hours. The peripherally inserted central catheter line was immediately removed the next day (day 20 after admission). The same day he also began to complain of vague, mild, bilateral leg pain. Delayed serum sickness due to recent ATG administration was considered a possible cause for his new symptoms because clinical examination did not show erythema, edema, or deformities on either of his legs. However, sustained bacteremia was diagnosed by recovery of A. hydrophila from repeat blood cultures (i.e., one anaerobic and aerobic bottle set from two peripheral venipunctures) positive after 11 and 16 hours of incubation. Bilateral leg pain steadily worsened in intensity (10/10) over the next 48 hours, and the area of distribution of pain extended to the lateral aspect of the right thigh although physical examination remained unremarkable. Creatinine kinase was increased at 470 U/L (normal range for males, 0–195 U/L). Ultrasound venous Doppler of both legs also showed no evidence of deep venous thrombosis. However, magnetic resonance images of both legs showed extensive bilateral patchy multi-compartment muscular and fascial inflammatory changes highly concerning for NF (Fig. , ).\nUrgent initial surgical debridement was performed that evening. An extensive four-compartment fasciotomy, debridement, and myomectomy were performed on both legs. Extensive ‘dishwater’ purulent material was found in multiple compartments of both legs, including (1) the superficial posterior compartment between the gastrocnemius and soleus muscles, and (2) the lateral deep compartment. There was also clinical evidence of severe muscle necrosis of the tibialis anterior muscles in the anterior compartment of both legs. He was admitted to the Intensive Care Unit post-operatively. After consultation with the Infectious Diseases service and review of the antibiotic susceptibility profile of the previously isolated A. hydrophila strain, antibiotics were changed to meropenem 1000 mg intravenously every 8 hours and clindamycin 600 mg intravenously every 8 hours. High dose intravenous immunoglobulin (2 g/kg) was also given. All prior antibiotics were discontinued.\nGram stain of tissue samples from the right tibialis anterior muscle showed no neutrophils but that gram-negative bacilli were present, and subsequently grew a heavy amount of A. hydrophila. Gram stain and anaerobic culture from the right vastis lateralis muscle also did not show the presence of neutrophils or organisms but grew scant amounts of A. hydrophila. A genus-level identification as Aeromonas was obtained for all isolates from blood and tissue samples by matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry using a VITEK MS (bioMérieux, Laval, Quebec, Canada); since this technique has an accuracy of identification rate of 80–90% for species-level identification of Aeromonas [], all isolates were also analyzed using in-house bi-directional 16S rRNA gene cycle sequencing of the V1-V3 (approximately first 500 bp), as previously described []. Broth microdilution susceptibility panel testing was performed and interpreted using published guidelines []. All isolates were multidrug resistant to ampicillin, ceftriaxone, ciprofloxacin, and trimethoprim/sulfamethoxazole but susceptible to meropenem and tetracycline. The isolates were confirmed to produce an extended-spectrum β-lactamase (ESBL) using published guidelines and the Mast Disc Test (Mast Group Ltd., Merseyside, UK) []. Production of an AmpC β-lactamase was shown by resistance to cefoxitin disk (30 μg) testing and the Mast Disc test (Mast Group Ltd.).\nTwo additional extensive surgical procedures for removal of necrotic tissue from both legs were undertaken in the next 24 hours. Bilateral above-knee amputations were performed during the last debridement as a life-saving measure because of extensive rapid progression of bilateral leg necrosis, and the patient’s rapid clinical deterioration with severe unremittent hemodynamic instability during the operation. Post-operatively, he required aggressive resuscitation for septic shock in the Intensive Care Unit with intractable hyperkalemia and severe acidosis, and anuric acute kidney failure (creatinine 210 μmol/L; normal range for males, 50–120 μmol/L). Despite all therapeutic interventions, the patient went into cardiac arrest and passed away within 2 hours after the final surgery.\nPost-mortem examination at autopsy revealed findings related to the underlying AA, and evidence of septic shock secondary to extensive bilateral lower limb necrotizing myofasciitis. The bone marrow was markedly hypocellular and there was splenic enlargement at 331 g. The heart was enlarged (536 g). Cardiomegaly was likely a compensatory response to the AA due to the absence of atherosclerotic and hypertensive cardiovascular disease. In keeping with the patient’s severe septic shock, there was marked centrilobular necrosis of the liver, as well as petechial hemorrhages of the skin, heart, pleural surfaces, kidneys, and liver capsule. Histologic examination of skin and muscle from the left thigh showed necrosis of the muscle and deep subcutaneous adipose tissue, admixed with dense collections of gram-negative bacilli (Fig. , ). However, in keeping with the AA, there was notably an absence of an acute inflammatory response. |
A 45-year-old woman from Achefer, near Bahir Dar, northwestern Ethiopia, presented to the emergency department of our hospital on February 18, 2020, with a complaint of generalized fatigue for 18 years and worsening abdominal pain, vomiting, and diarrhea of 1 month duration. The history dated back 18 years to the birth of her seventh child in home delivery, following which she experienced excessive vaginal bleeding due to delayed expulsion of the placenta. She had lost consciousness following the vaginal bleeding and had been treated locally by traditional healers and survived. After the delivery, she had failed to lactate and remained amenorrheic and could not conceive, but had no any gynecological evaluation. She also complained of progressive generalized fatigue and decreased work capacity, preventing her from doing her routine activities. She had experienced repeated abdominal pain, nausea, vomiting, and diarrhea as well for the past 6 years and had repeatedly visited a nearby clinic and was managed for dyspepsia and gastroenteritis but with no lasting improvement. In addition, she had associated weight loss, anorexia, dizziness, cold intolerance, myalgia, arthralgia, and progressive loss of axillary and pubic hair. These symptoms had worsened over the past month, and she had developed generalized weakness and extreme fatigue even at rest and experienced excessive sleepiness. She also had mild to moderate intermittent headache, but otherwise no blurring of vision or diplopia She had no history of head trauma, surgery, or irradiation, and no history of polyuria or polydipsia on physical examination, and she was conscious but sleepy. Her blood pressure was 90/60 mmHg, pulse rate 86 beats per minute, respiratory rate 24 breaths per minute, and temperature of 36.9 °C. She had mild epigastric and periumbilical tenderness. She had dry, coarse skin and sparse axillary and pubic hair. Examination of other systems was unremarkable. Laboratory findings showed the following: white blood cell count 2590 cells/μL, hematocrit 26.9%, mean corpuscular volume (MCV) 81.3 fl, creatinine 1.2 mg/dL, normal liver function tests, sodium 126 mEq/L, potassium 2.52 mEq/L (repeat 4.2 mEq/L), random blood sugar 113 mg/dL, total cholesterol 152 mg/dL, triglyceride 86 mg/dL, and low-density lipoprotein (LDL) 161 mg/dL. Brain magnetic resonance imaging (MRI) revealed an empty sella turcica, as shown in Fig. . As the clinical manifestations related to the patient’s previous obstetric history suggested Sheehan’s syndrome, relevant available hormone studies were performed (Table ). After all these tests were performed, she was diagnosed with Sheehan’s syndrome presenting with imminent adrenal crisis.\nThe patient was rehydrated with one bag of normal saline (NS), and started on prednisolone 2.5 mg in the evening/5 mg in the morning and subsequently levothyroxine 75 μg/day to be titrated based on clinical response. She was strictly instructed on the nature of her illness and was told to take these medications for the rest of her life. She was referred to an endocrine clinic and discharged. On subsequent clinical assessment, abdominal pain, nausea, vomiting, and diarrhea had subsided; her appetite had returned and she had started to gain weight. |
Case was a 38-year-old Latin American female with a family history of cardiac disease, arterial hypertension, pulmonary, and testicular cancer. The patient was diagnosed 2 years prior to evaluation with borderline personality disorder and had positive tobacco and alcohol use, reaching inebriation at least once every 15 days. The patient presented depressive symptoms with labile mood for the first time at 18 years of age. At 21 years old, she was diagnosed with postpartum depression after symptoms of isolation, anhedonia, and emotional lability augmented. She had two suicide attempts at age 24 and 28, both of which were followed by the hospitalization of the patient. Since age 24, she had received several antidepressants intermittently (mainly fluoxetine and sertraline), with poor improvement of symptoms. Two months ago, depressive symptoms increased, and she started fluoxetine 40 mg daily by herself. Poor symptomatic response was achieved, and she continued with anhedonia, hopelessness, sleeping problems, irritability, and anxiety.\nThe patient was conscious and oriented. She complained of occasional tachycardia and lower limb paresthesia while being stressed, as well as acid reflux with every meal, leading to a diminishment in daily food intake; additionally, the patient appears to be sleepy and tired. At the time of assessment and treatment, the patient had suspended medication without physician supervision.\nThe patient was assessed with the same scales and inventories as in previous cases. The MADRS showed moderate depression (score of 28 points), and the BDI indicated the presence of severe depression (score of 42 points). Meanwhile, the BAI indicated the presence of severe anxiety (score of 37 points), as well as the presence of insomnia (score of 10 in AIS). Finally, the MMSE indicated no impairment; however, the score is on a limit cut-off value (score of 24 points).\nReassessment was performed after 15 sessions of HFLI TMS, showing an improvement in all measures. The BDI (score of 9 points) demonstrated a reduction of depressive symptoms, reaching minimum levels of depression, while the MADRS (score of 10 points) score reduction reached mild depression levels. The BAI also indicated a minimum presence of anxiety (score of 5 points), and the AIS (score of 7 points) showed a minimum presence of insomnia symptoms. Finally, the cognitive score improved by five points (MMSE = 29 points), which could indicate that baseline evaluation could be influenced by concurrent MDD. The changes in the scales were corroborated by the self-report of the patient.\nBefore and after changes in scales for the three subjects are presented in . |
A 54-year-old man was admitted to the Department of Surgery at our hospital following abnormal abdominal CT findings. He had no complaints, such as upper abdominal pain or abdominal distension. He presented with comorbidities of neurogenic bladder due to spinal cord injury and sleep apnea syndrome. His past history included previous surgeries for appendicitis and renal stones in the left kidney. The laboratory data showed normal findings. Abdominal contrast-enhanced CT revealed a tumor in the hepatoduodenal ligament, measuring 40 mm, with enhancement at its margin in the arterial phase; the enhancement was prolonged in the delayed phase (Fig. a, b). The boundary between the tumor and the caudate lobe of the liver was unclear. The abdominal magnetic resonance imaging (MRI) showed that the tumor was hypointense on T1-weighted images and both hypo- and hyperintense on T2-weighted fat-suppression images (Fig. a, b). Moreover, the contrast MRI showed that the margin of the tumor was enhanced in the arterial phase (Fig. c). The boundary between the tumor and the liver was clear; hence, the tumor was considered an extrahepatic lesion. Positron emission tomography (PET) revealed localized accumulation of fludeoxyglucose (FDG) (5.9 F) in the hepatoduodenal ligament tumor (Fig. ). The biopsy was difficult to perform due to the location of the lesion. Although no preoperative diagnosis was made, surgical intervention was planned for an accurate diagnosis. The patient underwent 5-port laparoscopic surgery for tumor resection. Perioperatively, the tumor was found to be located on the left side of the portal vein and on the ventral side of the inferior vena cava (Fig. a–c). The tumor was surrounded by a fibrous capsule and did not infiltrate the other organs. In the operative technique used, the proper hepatic artery and common hepatic artery were taped at three sites (Fig. d). Each tape was used for traction in order to proceed with smooth and safe tumor resection. The total operative time was 273 min, and the total intraoperative blood loss was minimal. Macroscopic examination of the specimen showed an elastic, hard tumor measuring 40 × 30 mm with a smooth surface and fibrous capsule (Fig. ). The cross-section of the tumor was milky white in color. Histopathologically, the peripheral nerve was near the tumor. The tumor was mainly composed of spindle cells and hypercellular (Antoni type A) and hypocellular (Antoni type B) areas (Fig. a). Immunohistochemical staining revealed that the tumor was strongly positive for S-100 protein (Fig. b), but had an extremely low Ki-67 positive rate. The patient was diagnosed with low-grade schwannoma. The postoperative course was uneventful, and the patient was discharged on postoperative day 5. |
A previously healthy 57-year-old woman, with no significant past medical history, presented to the surgical department of our hospital for definite management of a primary pancreatic leiomyosarcoma, after being treated with adjuvant chemotherapy.\nOne year before her last admission, she was initially admitted to our emergency department due to abdominal pain, fatigue, and weight loss. She was totally healthy prior to these symptoms. She then underwent magnetic resonance imaging (MRI) that was indicative of a pancreatic head lesion along with possible metastatic liver lesions, superior mesenteric vein occlusion, and portal vein infiltration (Fig. a, b). The decision was to undergo an endoscopic ultrasound (EUS) biopsy in order to determine the exact nature of the lesion. EUS report was indicative of pancreatic leiomyosarcoma.\nMultidisciplinary team’s decision was to use gemcitabine- and docetaxel-based chemotherapy as up-front treatment to assess tumor response. Follow-up CT scan and magnetic resonance imaging (MRI) after the completion of chemotherapy regimen showed downsizing of the pancreatic mass, as well as downsizing of suspicious for malignancy segment III liver lesion (Fig. c, d).\nBased on the response to chemotherapy, tumor characteristics, and physical status of the patient, multidisciplinary team’s decision was to proceed to surgical exploration. Due to local expansion of the pancreatic tumor, its relation with the superior mesenteric and portal vein, and the underlying SMV thrombosis, excision of the pancreatic tumor was not feasible. Intraoperatively, a small piece of tumor was excised in order to be sent for histopathology. Surgeon’s decision was to ablate the tumor with irreversible electroporation (Fig. ). Metastatic liver lesions were identified with the use of intraoperative ultrasound. Segment III liver lesion was resected, while smaller lesions of the right lobe were ablated using microwave ablation.\nThe patient had an uneventful postoperative recovery and complete resolution of her symptoms. Histopathological examination of pancreatic lesion as well as segment III liver lesion revealed sarcomatous tissue of high cellularity with fascicular pattern, increased mitotic activity, and diffuse cytoplasmic immune reactivity for SMA, desmin and h-Caldesmon, and chromagen DAB (Figs. and ). Surprisingly enough, pathological report of a smaller liver lesion was indicative of angiomyolipoma staining positive for HMB45 and Melan-A. The lesion was a benign hamartomatous, circumscribed but unencapsulated hepatic mass composed mainly by mature lipocytes and limited mesenchymal component (smooth muscle cells), showing no marked atypia and thick-walled vasculature. Myoid component was positive for ΗΜΒ-45 and Melan-A. Based on the histopathological report, tumor board decided that the patient should be treated with adjuvant therapy for leiomyosarcoma after surgery. A regimen with anthracycline and olaratumab was used for 3 months. Follow-up imaging in 6 and 12 months showed no progression of the disease (Fig. a–d). |
A woman in her early twenties presented to her ophthalmologist with complaints of visual disturbances and “light spots” beginning to obscure her vision. The patient had a long history with this ophthalmologist for corrective lenses. Her ophthalmologist determined she had bilateral papilledema and referred her to a neuro-ophthalmologist for evaluation. The neuro-ophthalmologist saw the patient on her eighth day of symptoms. Now, “steady brightness” was blocking her view in her right eye and she experienced color desaturation. The left eye did not appear to have any visual changes. The patient had a normal BMI and reported no history of being overweight, headaches, tinnitus, or previous visual disturbances. She had a 4-month history of polycystic ovarian syndrome (PCOS) for which she was being treated with a progestin and estrogen birth control.\nUpon examination, papilledema was noted in both eyes as well as a 2+ right relative afferent pupillary defect. No cranial nerve deficits were noted. The patient had a 20/20 visual acuity, and a visual field test was performed. A severe peripheral visual field deficit was noted in the right eye with a mean deviation on the Humphrey scale of −26.10 dB using a Central 24-2 Threshold Test (). The normal mean deviation should be between −1 and −2 db. The left eye was at baseline. The patient was admitted to the hospital for expedited vision workup. An MRI with and without contrast showed slight dilation of the optic nerve sheath, as well as an incidental small right frontal developmental venous sinus anomaly, but otherwise unremarkable (). No tumor or thrombosis was noted on the MRI.\nSeveral tests were completed including a complete blood count, metabolic panel, routine coagulation panel, and neuro hypercoagulative panel. All results were within normal limits except for her Vitamin A which was elevated at 88 µg/dL with no known reason or dietary explanation. A lumbar puncture was performed 9 days after the initial presentation with an opening pressure of 41 cm of water. In total, 19 mL of cerebrospinal fluid (CSF) was drained and the closing pressure was 18 cm. The CSF was determined to be normal. The patient was also evaluated for systemic disorders and endocrine disorders, and all tests were negative. The patient was given the diagnosis of papilledema with secondary optic neuropathy and Vitamin A toxicity. |
A 54-year-old male patient presented with a two-day history of severe left-sided, lower back pain which disappeared with the appearance of left-sided lower limb pain felt deep inside the whole lower limb and described by the patient as intense internal pressure (VAS 8/10). On examination, power was 5/5 with no sensory deficit and normal reflexes. The patient received NSAID painkillers and active bed rest was advised. However, on the patient's insistence, a lumbar spine X-ray and MRI were done which showed mild IVD protrusion. The patient was reassured and sent home. A week later the patient presented to the ER with an 18-hour history of heaviness and difficulty in raising the left foot when walking, with numbness along the lateral part of the leg and dorsum of the foot. The pain was moderate (VAS 5/10). No sphincter-related symptoms were observed. According to the patient, the decreased pain caused the delay in presentation, against the instructions on first evaluation. On examination of the foot dorsiflexion was 2/5 (movement on gravity alleviation) with decreased sensation along the left L5 dermatome. There were normal reflexes and sphincters. The patient underwent immediate, new lumbar MRI which showed a large disc sequester with disc migration. His status was fully explained; he was admitted and underwent microdiscectomy L4/5.\nThe initial back pain lasted for 2 days, mostly caused by stretching and pressure on the weakened annulus fibrosis. This type of pain disappears or decreases once the annulus opens and nucleus pulposus leaks to the spinal or root canal. Initial left lower limb pain is a typical description of painful radiculopathy where mass pressure and inflammatory irritation of the nerve root and dorsal root ganglion cause neuropathic pain. This is different from nociceptive and referred pain types. Dorsal root ganglion hosts the cell bodies of sensory nerves with bidirectional connections (to the periphery and spinal cord). Injury to the nerve root motor fibers causes weakness.\nThe majority of patients with lumbar disc and radicular pain improve with conservative treatment. Surgical indications are acute or progressive motor weakness, sphincter dysfunction, intractable pain not responding to analgesia, and pain affecting patient daily life, not responding to 6 weeks of conservative treatment in the absence of acute surgical indications. In all cases, there should be a correlation between the clinical picture and MRI findings. In the current case, the patient has left L5 nerve root symptoms and signs (dorsiflexion weakness, normal reflexes, and dermatologic radiculopathy). The expected IVD prolapse occurred on either the left posterior-lateral L4/5 or left extreme lateral L5/S1 disc. Although there is a debate about dermatologic sensory distribution in root-originating symptoms and variations in clinical presentation (i.e., the L4/5 disc causing S1 root symptoms via compressing the root in higher position, groin pain with lower lumbar discs due to paravertebral sympathetic ganglion pathway entering at L1 or L2 nerve), we presented the commonly encountered scenarios. |
A 77-year-old woman presented with abdominal pain and anorexia for the past month. Her history was otherwise noncontributory. The clinical examination revealed tenderness in the right upper abdominal quadrant and rebound tenderness in the lower abdomen. Blood tests demonstrated elevated transaminase and lipase levels (aspartate aminotransferase 75 IU/L; normal 7 to 38 IU/L, lipase 63 U/L; normal 7 to 60 U/L). The level of carbohydrate antigen 125 was elevated at 279.5 U/mL. The serum concentrations of carcinoembryonic antigen, carbohydrate antigen 19-9 and alpha-fetoprotein were within the normal limits. Abdominal computed tomography () and magnetic resonance imaging (MRI) () revealed the presence of a large (about 10 × 5 cm) mass arising from the tail of the pancreas that had invaded the spleen and the adjacent bowel loop. The wall of the tumor was slightly enhanced after administering intravenous contrast medium. No regional lymphadenopathy, ascites, or metastasis was demonstrated on MRI. We performed s distal pancreatectomy with s splenectomy. On the operative field, the pancreatic mass had invaded the adjacent colon and posterior wall of the stomach. Therefore, a left hemicolectomy and partial resection of the stomach were performed together. The patient had an uneventful recovery and she was discharged on postoperative day 11. She refused any additional adjuvant chemotherapy. She was lost to follow-up and died due to pneumonia 3 months after surgery.\nA tumor (14 × 7.7 cm) was located in the tail of the pancreas () and had invaded the colonic submucosa. The cut surface of the tumor was yellowish-white and showed signs of hemorrhage and fibrosis ().\nThe resected specimen was fixed in 20% formalin, and tissue blocks prepared from the tumor were embedded in paraffin. The sections were stained with hematoxylin and eosin for light microscopy. Immunohistochemical studies using avidin-biotinylated peroxidase complex were performed. Antibodies against cytokeratin 19, vimentin, and CD68 were used.\nHistologically, the tumor was composed of two major cell types: atypical mononuclear round cells and abundant osteoclast-like multinucleated giant cells with central nucleoli. The atypical cells showed eosinophilic and partially granular cytoplasm, anisokaryotic, hyperchromatic nuclei, and prominent nucleoli (). There were many mitotic figures (). These atypical cells were generally distributed among the osteoclast-like giant cells without any epithelioid structures. The osteoclast-like giant cells lacked features of atypia and they occasionally showed phagocytosis of the atypical cells.\nAn immunohistochemical examination showed positive staining for vimentin () and CD68 and focal staining by cytokeratin 19 and actin. No staining of C-kit, desmin, CD34 and bcl-2 was observed. The tumor was diagnosed as an undifferentiated carcinoma with osteoclast-like giant cells of the pancreas. |
The patient is a 47-year-old Caucasian female who presented to the Emergency Department of an academic tertiary-care hospital in the Midwestern United States with complaint of left-sided weakness of the upper and lower extremities and right gaze preference three weeks after a right pontomedullary infarct complicated by Posterior Reversible Encephalopathy Syndrome (PRES) [that initial infarct had been treated in a different state]. Imaging revealed an acute infarct in the posterior limb of the right internal capsule without hemorrhagic transformation and an acute punctate infarct in the right parietal subcortical white matter with corresponding diffusion restrictions, as well as remote evidence of subcortical chronic diffuse microhemorrhages (). The Psychiatry Consultation & Liaison service was consulted on hospital day 2 after the patient reported, “I want to strangle myself with my oxygen cord.”\nOn initial evaluation, the patient reported history of anxiety treated previously by her primary care physician (PCP). She reported she had been frustrated with her medical condition but really did not intend to harm herself. She reported fluctuating mood since her initial stroke and had “good days and bad days.” She denied prior history of inpatient or outpatient psychiatric care or prior suicide attempts. She was oriented to person and place, but not time, was able to state the days of the week forwards, but not backwards, and endorsed visual hallucinations during her hospitalization. This presentation was felt to be consistent with delirium, and she was started on quetiapine 25 mg.\nFollowing a six-day medical admission, the patient was discharged to the acute inpatient rehabilitation unit housed within the hospital. Extensive diagnostic studies did not reveal an underlying etiology for the strokes, which were thought to be due to uncontrolled hypertension.\nPsychiatry was reconsulted by the rehab physicians for management of problematic behaviors. The patient exhibited ego-dystonic behaviors for which she would later apologize including repeatedly climbing out of bed, shouting for nursing assistance without clear need for help, shoving her fist into her mouth to induce vomiting, and periodic, purposeless screaming. These behaviors were disruptive to staff and other patients on the unit. While initially conceptualized as residual hyperactive delirium, her behaviors persisted and continued testing for underlying causes of delirium including electrolyte derangement, occult infection, new or evolving cerebrovascular event, or excess medication burden which were unrevealing\nAfter 60 days of acute rehab, she had reached maximal benefit of that intervention and continued exhibiting behaviors incompatible with nursing home disposition. The patient was then transferred to the university's geriatric psychiatry inpatient unit on an involuntary mental health commitment for behavioral management.\nIneffective medication trials prior to transfer included quetiapine (25 mg at bedtime and 25 mg several times daily as needed), mirtazapine (7.5 mg at bedtime), olanzapine (initial trial of 2.5 mg at bedtime and 2.5 mg several times daily as needed and a second trial of 15 mg and 2.5 mg several times daily as needed), buspirone (15 mg TID), divalproex (initial trial of 750 mg at bedtime and a second trial of 500 mg TID with lactulose and levocarnitine for hyperammonemia), melatonin (9 mg at bedtime), propranolol (40 mg QID), trazodone (150 mg at bedtime), gabapentin (200 mg several times daily as needed), dextromethorphan (20 mg BID, given as Robitussin), and clonazepam (0.5 mg AM and 1 mg PM).\nThroughout this period, the patient remained intermittently apologetic for her behaviors. Orientation was typically attuned to person, sometimes place, and generally not to month or year. She consistently denied depressed mood, anxiety, visual hallucinations, auditory hallucinations, paranoia, suicidal ideation, or homicidal ideation. Thought process remained concrete and perseverative with limited spontaneous speech output and paucity of thought content. Language remained intact without evidence of aphasia. Recent and remote memory were difficult to assess formally due to behavioral disturbance, but she had difficulty remembering recent details of her hospital course and remote details of her life prior to moving to her current city. She required staff assistance for completion of toileting, dressing, and feeding. She had deficiencies in executing complex motor tasks, such as getting out of bed, and was frequently found diagonal in bed with a limb tossed over the side-rail. These deficiencies were in excess of the residual motor effects of her strokes and suggestive of alterations in visuospatial skills, executive function, and planning. Her aberrant vocalizations did not appear goal-oriented and were not ameliorated by staff presence. This presentation persisted and was thought to represent a new cognitive baseline meeting diagnostic criteria for major vascular neurocognitive disorder with behavioral disturbance.\nNonpharmacological strategies including music, sensory stimulation, one to one time with staff, and frequent repositioning were tried without improvement in her symptoms. Additional ineffective medication trials following transfer to inpatient psych included fluoxetine (60 mg per day), retrial of dextromethorphan with fluoxetine as an enzymatic inhibitor (again to 20 mg BID), retrial of quetiapine (up to 600 mg total per day), haloperidol (5 mg several times daily as needed IM), oxycodone (5 QID), lorazepam (up to 6 mg daily), carbamazepine (200 TID), and chlorpromazine (50 QID). Throughout these trials, the patient continued to exhibit frequent periods of severe psychomotor agitation requiring vest restraint and purposeless screaming alternating with periods of oversedation following medications. Other than providing intermittent sedation, no particular combination of medications proved effective in treating the target symptoms.\nAt this point, having exhausted all reasonable behavioral and pharmacologic options, the inpatient psychiatric team recommended ECT as a last intervention prior to pursuing a palliative approach. Medical Ethics was consulted and felt ECT to be consistent with her previously articulated beliefs and wishes.\nThe patient was formally evaluated by the ECT service and, given her incapacity to consent, a court order was obtained for the procedure. She underwent an acute course of bitemporal ECT using a MECTA Spectrum 5000Q machine. She received methohexital and succinylcholine as anesthetic and relaxant agent, respectively. A dose-titration method was used to determine stimulus intensity. She received treatments at 50% over seizure threshold with the following parameters: pulse width: 1 millisecond, frequency: 20 Hz, duration: 2 sec. Treatments were given three times per week. She was maintained on chlorpromazine (50 mg QID) and lorazepam (1 mg QID) during the treatments. Following the sixth ECT treatment, the patient rarely engaged in purposeless yelling, and remained quiet most of the day, experienced normalization of her sleep wake cycle, but still exhibited purposeless movements and psychomotor agitation requiring a vest restraint at night.\nFollowing the third week of ECT treatments, she was consistently having low scores on the Pittsburgh Agitation Scale (PAS) and had minimal requirements for as needed medications for agitation []. While she still required a vest restraint overnight, her psychomotor agitation had improved dramatically. She resumed feeding herself with her right arm and tolerated pureed foods for the first time in six months. Following an acute course of 16 treatments, ECT was tapered to twice weekly and she started sertraline 25 mg in preparation for further decrease in ECT frequency. She remained stable and was successfully discharged to a nursing home with continuation of ECT as an outpatient. Following the expiration of the original court order for ECT, outpatient ECT was discontinued and the patient's family chose to not pursue a renewal of the order for continued treatment. She received 29 treatments in total. Nursing home staff reported that her behaviors remained in control after stopping ECT and she was thereafter able to return home with her parents. |
A 26 year old otherwise healthy, G1P0 female at 13 weeks gestation was admitted to medical intensive care unit after she experienced cardiac arrest at home. She had reported shortness of breath earlier that day and then collapsed. During initial paramedic evaluation, she was pulseless and found to be in pulse less electrical activity (PEA). She was successfully resuscitated with return of spontaneous circulation (ROSC) in approximately 7 min and was brought to the hospital. Emergency department (ED) evaluation revealed the patient to be nonresponsive, and she was immediately intubated. Her exam was remarkable for cold and cyanotic extremities, without palpable distal pulses but strong femoral pulse. Shortly after her arrival to ED, the patient became pulse less again needing resuscitation and ROSC on 2 occasions.\nInitial blood work was remarkable for severe metabolic acidosis (HCO3 of 10) and elevated troponin I (2.77 ng/ml, normal range 0–0.34 ng/ml). EKG showed right bundle branch block while bedside 2 D echocardiogram demonstrated right heart strain pattern. Bedside ultrasound (USG) showed no significant free fluid with live intrauterine gestation. Bilateral lower extremity compression venous dopplers of the entire venous system were negative for any evidence of deep venous thrombosis. She underwent computerized tomography (CT) of the chest which revealed a nearly occlusive thrombus in the bilateral lower lobar arteries extending into the segmental arteries (Fig. ). The main pulmonary arterial trunk was noted to be enlarged with evidence of right heart strain (Fig. ). Head CT scan was negative for any acute intracranial abnormalities. She was administered intravenous tissue plasminogen activator (TPA) (50 mg after ROSC the second time) in the ED with improvement in her hemodynamics. Hypothermia protocol was concurrently initiated. She was subsequently transferred to medical intensive care unit on unfractionated heparin (UFH), bicarbonate and norepinephrine drips. The patient was extubated two days following and was gradually weaned off blood pressure support. UFH drip was titrated based on aPTT and 6 days later she was transitioned to LMWH (dalteparin 10,000 units subcutaneously once daily in view of her insurance issues). She had aggressive supportive care and after a 2 week hospital stay, she was discharged to rehabilitation facility on Dalteparin. A month later dalteparin was changed to enoxaparin 55 mg (1 mg/kg) s/q twice daily (monitored with anti Xa levels).\nAt approximately 20 week’s gestation, the patient had a fetal ultrasound that revealed singleton gestation with massive hydrops, fetal contractures and ventriculomegaly/hydranencephaly. It was presumed that these findings were secondary to early hypoxic injury and she was counseled about poor prognosis. During her 25th week gestation, the patient noted worsening abdominal pain with associated headaches, lightheadedness and weakness. She had elevated blood pressures and was suspected to have mirror syndrome. Enoxaparin was discontinued 24 h prior to the planned procedure with initiation of UFH drip. The patient underwent elective induction of labor with palliative care services. The infant died shortly after delivery. The patient experienced increased vaginal bleeding secondary to retained products of conception and underwent dilatation and curettage with achievement of hemostasis. Enoxaparin at previous dosage (55 mg s/q twice daily) was restarted 24 h after the delivery without any major or untoward complication. Platelet count and anti-Xa levels were checked while the patient was on enoxaparin. Anti-Xa levels were in therapeutic range (0.8–1, goal 0.6–1.0 IU/ml) and platelet counts remained within normal limits.\nIn order to identify the cause of her VTE the patient had further work up including thrombophilia testing and CT chest, abdomen/pelvis. Thrombophilia testing revealed the patient to be wild type for Factor V and Prothrombin gene. Protein C and S antigen levels were normal. Antithrombin activity was initially low (71, normal range 75–125 % ACT) at the time of initial VTE but subsequently normalized (107). Antiphospholipid antibody testing including lupus anticoagulant, anti-cardiolipin antibodies and beta 2 glycoprotein I antibodies was negative. CT chest, abdomen and pelvis showed constellation of imaging findings compatible with heterotaxy syndrome. These included left-sided superior vena cava (SVC) draining into the left coronary sinus, hemiazygous vein drains into left SVC, absent azygous vein, absent (interrupted) inferior vena cava (IVC) below the hepatic IVC with persistent left IVC which drains into left coronary sinus, polysplenia, bilateral left lung and benign hepatic hemangioma (Fig. ).\nThe patient completed 6 month duration of anticoagulation with LMWH and was subsequently placed on ASA 81 mg. Prior to discontinuation of anticoagulation therapy the patient had CT pulmonary angiogram which showed normal diameter of the main pulmonary artery without any evidence of acute or chronic pulmonary emboli. She is currently stable on low dose ASA and is into her third year after the VTE without any recurrence. She has had no further pregnancies. |
A 41-year-old previously healthy woman presented to the hospital with dyspnea on exertion and dry cough for 1 week. A computed tomography (CT) scan of the chest revealed small mediastinal lymph nodes. The patient was discharged on a tapering dose of oral steroids and albuterol inhalation with a follow-up outpatient appointment with a pulmonologist. An endobronchial ultrasound-guided biopsy of the mediastinal lymph nodes was performed 1 week later. The patient had worsening dyspnea and was again admitted to the hospital. She denied any orthopnea or paroxysmal nocturnal dyspnea. On admission, the physical examination, including chest auscultation, was unremarkable. Initial basic blood work, including complete cell count and metabolic profile, revealed no abnormalities. Her serum cardiac brain natriuretic peptide level was elevated at 1,500 U/L, along with mild elevation of cardiac troponin. The chest radiograph was unremarkable. A CT scan of the chest revealed new small nodular opacities with a tree in bud appearance in the peripheral centrilobular area (). Subsequent transthoracic echocardiogram revealed extremely elevated right ventricular systolic pressures with flattening of the interventricular septum and severely high pulmonary artery pressures, suggestive of acute cor pulmonale from severe pulmonary hypertension. Within a day of admission, the patient's dyspnea worsened and she required high-flow oxygen. Meanwhile, mediastinal lymph node biopsy revealed signet ring cell poorly differentiated adenocarcinoma (), and mucicarmine staining confirmed mucin secreting signet ring cells (). A CT scan of the abdomen was performed to look for the primary tumor, and revealed a diffusely thickened stomach wall with enhancement consistent with diffuse gastric cancer (), in accordance with the signet ring adenocarcinomatous cells observed in the lymph node biopsy. At that time, the patient's plasma prothrombin time was elevated at 80 seconds, and further testing showed a plasma D-dimer level of more than 5,000 µg/L with a low fibrinogen level of 100 mg/dl, suggestive of disseminated intravascular coagulation (DIC). The CT scan appearance of the chest, acute severe right-sided heart failure from severe pulmonary hypertension, and DIC were characteristic of PTTM. Accordingly, the patient was started on empiric anticoagulation with heparin and intravenous corticosteroids for PTTM based on anecdotal case reports. The patient was scheduled to receive chemotherapy for the gastric adenocarcinoma; however, the hypoxia worsened and the patient required ventilator support. Unfortunately, she rapidly progressed to death within an hour due to extreme hypoxia and cardiac arrest. The patient's family declined autopsy.\nSince diffuse gastric cancer is associated with hereditary diffuse gastric cancer (HDGC), it was important to know if the patient's three daughters were at risk. The updated guidelines recommend testing for cadherin 1 (CDH1) gene mutation in a patient's blood when the diagnosis of diffuse gastric cancer occurs at the age of 40 years or less. Thus, we decided to test for the CDH1 genetic mutation in the patient's stored blood. Fortunately, the test came back negative, ruling out HDGC in principle. |
A 57-year-old man presented to the A&E with loss of consciousness due to a motorcycle collision 9 h prior. Upon initial examination, the patient had a GCS of E4M6V5. The patient had no other symptoms that required inpatient care. The patient also had no history of bloody discharge from the external auditory meatus. The patient's past medical examination shows no other history of past illness and surgery. He reported family history shows the patient's parents died due to heart attacks. Further examination with a head CT scan revealed minimal PNC forming in the right frontal region (, ). The patient was first admitted to the A&E then requested for discharge against medical advice after 5 days of inpatient care.\nTen days later, the patient then came to the outpatient clinic, complaining of severe headache and rhinorrhea developed, prompting the patient to return for re-examination. The patient exhibited right-sided hemipharesa with a GCS of E2V2M4 on the second visit. A second CT scan revealed massive PNC far more severe than evident in the previous CT scan (). Bone reconstruction showed a right frontal linear fracture ().\nThe final assessment concluded that the patient suffered from a tension PNC. An operation was then performed to drain the PNC and seal the cranial defect. The operation was performed via a bicoronal incision. A burr hole in the calvarium was created at the highest convexity to release the PNC, and the cranial defect was closed using a pericranial rotational flap (). The diameter of the defect was measured, and a flap with the same diameter was drawn adjacent to the defect. The pericranium was sacrificed to obtain clear margins, and the underlying bone was drilled.\nHe was given an intravenous broad-spectrum antibiotic ceftriaxone (1 g, administered for 5 days) and analgesics drugs (ketorolac, 30 mg intravenous if necessary, not exceeding 5 days). Post-operative was unremarkable, with discharge and rehabilitation taking 6 days for a total of 7 days of inpatient care. Post-operation, the patient's headache and rhinorrhea decreased. The patient was followed up every 3 days for the first week. Sutures were removed 2 weeks post-operative. The patient was then observed every 2 weeks for 3 months. Complaints were minor, consisting of mild headaches. The wounds healed with minimal scarring, and the cosmetic outcome for the craniofacial fracture was acceptable to the patient. |
A 38-year-old African American male with a history of hypertension and alcohol, cocaine, and tobacco use presented with recurrent abdominal pain. Three days prior, he was admitted with abdominal pain and hypertensive urgency. Cocaine and cannabinoids were found in his urine. A computed tomography (CT) scan of the abdomen with IV contrast demonstrated atherosclerosis of the aortoiliac system. With conservative management, the patient was diagnosed with cocaine-induced vasospasm and was discharged after two days.\nThe following day, he returned with recurrence of his abdominal pain and reported continued cocaine use. He described his symptoms as crampy in nature localizing to the upper right and left quadrants. He denied any associated nausea, vomiting, diarrhea, melena, or hematochezia. On arrival, his blood pressure was 190/120 mmHg. His abdomen was soft and flat with diffuse abdominal tenderness to soft and deep palpation with no guarding, organomegaly, rebound tenderness, or peritoneal signs.\nResults of laboratory tests revealed a serum lactic acid of 2.7 mmol/L. A CT angiogram (CTA) of the abdomen and pelvis revealed a SISMAD within the proximal-to-mid SMA with a 3 cm thrombosis of the proximal false lumen and distal false lumen patency; 70% stenosis of the proximal SMA was noted secondary to this process (). There was no evidence of abdominal ischemia. He was admitted to a medical/surgical floor with telemetry and was treated with conservative management. In addition to pain control and bowel rest, his home amlodipine 5 mg daily and hydrochlorothiazide 12.5 mg daily were restarted with the addition of as-needed hydralazine for a strict systolic blood pressure target of <140. In conjunction with the vascular surgery team, he was started on antiplatelet monotherapy with aspirin 325 mg daily. Two days after presentation, a repeat CT angiogram showed stabilization of the SMA dissection and the patient was safely discharged. The patient did not have any further abdominal imaging after discharge. |
A 66-year-old female with a history of type 2 diabetes mellitus and systemic hypertension presented to the emergency room with sudden painless visual decrease in the right eye. She had no history of intraocular surgery, injections, or laser photocoagulation. Visual acuity in the right eye was hand motion and in the left eye was 20/25. Intraocular pressure was 20 mmHg in OD and 13 mmHg in OS. Slit lamp examination was unremarkable with no iris neovascularization and mild nuclear sclerosis. Fundus examination in the right eye was not possible due to dense vitreous hemorrhage, while the left eye had 0.3 cup/disc ratio, mild nonproliferative diabetic retinopathy with dry macula, and no peripheral lesions. B scan ultrasound was performed in the right eye and reported vitreous hemorrhage and an exudative retinal detachment inferotemporally extending from the far periphery into the macula with dense subretinal opacities [].\nA 23-gauge three-port PPV was performed with careful examination of the peripheral retina and shaving of the vitreous base. Significant subretinal hemorrhage was found involving the temporal and inferotemporal retina extending from the periphery into the macula until the perifoveal area []. 0.3 ml of 25 µg/0.1 ml of TPA was injected into the subretinal space with a 41-gauge needle in an area of attached retina superior to the subretinal hemorrhage, and eventually, this bleb joined and diluted with the subretinal hemorrhage. Air–fluid exchange was performed, and sulfur hexafluoride 20% was injected into the eye [].\nThe patient was followed up closely, and once the gas disappeared, the vitreous hemorrhage recurred. This likely occurred from the subretinal hemorrhage liquefying and entering the vitreous cavity through the puncture site of the 41-gauge needle. A second vitrectomy was performed to washout the vitreous cavity, and endolaser was applied in the peripheral retina over the areas with pigmentary changes and residual subretinal hemorrhage.\nPostoperative visual acuity in the right eye improved to 20/100 in the early stages. Follow-up visits have shown cystoid macular edema (CME) in the right eye that is being managed with intravitreal anti-vascular endothelial growth factor agents []. |
A 33-year-old gentleman, working as a school counsellor, with no family history of mental illness, previously diagnosed as bipolar disorder in 2018, was brought to the emergency department of a general hospital after his colleagues called the Emergency Medical Services when they found him in a confused state in his apartment. In the emergency department, he presented with altered level of consciousness and displayed disorganized and agitated behavior in terms of entering a female cubicle and trying to take another patient's mobile phone, damaging an intravenous drip stand, taking a hook from the wall and damaging the tap of an oxygen supply, which was managed by physical and chemical restraints. His manager reported that he was absent from work for three days and that he found anabolic steroids in his apartment. He was then transferred to the psychiatric inpatient unit for further management, with a provisional diagnosis of substance-induced confusion.\nAt the beginning of his admission, his mental state examination was significant for labile affect, irrelevant speech, derailment, flight of ideas, and persecutory delusions. He was on high risk one-to-one observations precautions and nursing team have reported disorganized behavior in terms of eating cigarettes, tried to burn his genitals with cigarettes, jumping over the nursing station, unable to dress himself, tried to use the female nursing staff washroom, talkativeness, and disturbed sleeping pattern, in addition to altered level of sensorium throughout the day. He also mistook the female occupational therapist for his mother and tried to kiss her feet. Otherwise, he did not display hallucinatory behavior, grandiose delusions, or elated mood. He was vitally stable and he had a BMI of 29. Physical examination was unremarkable except for testicular atrophy. He also reported taking tadalafil 20 mg for erectile dysfunction.\nPast psychiatric history is significant for 1 similar episode in 2018 for which patient was admitted in a psychiatric hospital under the impression of bipolar disorder and was discharged on sodium valproate 2 g daily, olanzapine 20 mg daily, haloperidol 5 mg twice daily, and procyclidine 5 mg BID. He took the medications for 3 months and stopped them because of sedation and weight gain. Collateral history obtained from parents were negative for manic symptoms.\nSubstance use history is positive for anabolic steroids. He took 5 courses of injectable testosterone propionate and cyprionate, and trenbolone acetate from the age of 21 for bodybuilding purposes. Last had the injectable in May 2019. He described 1 course as 100 to 200 mg daily for 90 days. One month prior this admission he used to take metandienone tablets 20 mg daily.\nComplete blood count, comprehensive metabolic panel, lumbar puncture, computed tomography of the brain were unremarkable. Urine toxicology screen was negative for amphetamines, cannabis, cocaine, and opiate. HIV and syphilis screening were negative. Endocrinology work-up is illustrated in Table . He was managed as a case of anabolic steroids induced delirium. Treatment comprised mainly antipsychotics, although at the start of his presentation in the emergency department he necessitated multiple as needed parenteral benzodiazepines and antipsychotics. He was discharged on Haloperidol 7.5 mg and Quetiapine 700 mg daily and left to his home country. A timeline chart of pharmacological management is shown in Figure . |
A 44-year-old Japanese woman with a 6-year history of insulin-dependent diabetes mellitus and an 11-year history of central diabetes insipidus presented with a pain in the genital area worsening over 2 weeks, general fatigue, and loss of appetite. Two months earlier, patient underwent a urinary catheter insertion as a management for urinary frequency, but it was removed during the previous hospital stay, a month before her recent hospitalization, for possible urinary infection. She has had frequent hospital admissions (6 times/year) and was hospitalized 3 months before her recent admission because of edema of the pelvic area and lower limbs. The patient developed diabetes mellitus after undergoing total pancreatectomy for nesidioblastosis, a surgical procedure which involved the removal of patient’s pancreas including the spleen and gallbladder. Her sister was also diagnosed with idiopathic central diabetes insipidus; thus, a family etiology was suspected. The patient had a surgery for suspected tongue cancer 2 years ago and was also suspected of non-alcoholic steatohepatitis with episodes of hepatic encephalopathy. Although she was on multiple medications including subcutaneous insulin injections and desmopressin tablets, her glycemic and hydration status were poorly controlled.\nFour days prior to the present admission, she visited a gynecologist for her inguinal pain. No uterine tenderness or exudate was observed, and she was prescribed gentamicin and lidocaine ointments for possible local infection. She developed edema in the pelvic area with loss of appetite, and her home doctor consulted the university department 1 day before the present admission.\nUpon admission, the patient appeared weak but was alert and had low-grade fever (37.4 °C) under a regular use of acetaminophen (1500 mg/day) and diclofenac (75 mg/day). Her blood pressure was not significantly different from previous measurements (88/42 mmHg) but a sinus tachycardia (heart rate 125/min) was noted. She complained of continuous abdominal pain and tenderness in all four quadrants. No abdominal guarding or rigidity was observed, but she had severe edema in the pelvic and bilateral femoral areas without necrotic skin discoloration. Laboratory investigations revealed a white cell count of 16,310/μL with neutrophilia (90.8%), elevated C-reactive protein of 22.18 mg/dL, and no serum sodium or potassium abnormalities. Serum aspartate aminotransferase and alanine aminotransferase were elevated at 466 U/L and 148 U/L, respectively. The patient’s international normalized ratio was high (2.26), but disseminated intravascular coagulation score did not meet the criteria. The patient’s HbA1c level was 8.8%, and blood sugar at admission was 316 mg/dL. She had low serum albumin concentration (1.7 g/dL), elevated serum ammonia concentration (154 μg/dL), and elevated lactate level (10.3 mmol/L). No ketonuria was noted, but significant pyuria was observed.\nThe abdominal ultrasound was unrevealing; thus, an intravenous treatment with ceftriaxone (1 g every 8 h) was initiated empirically after obtaining the blood and urine culture samples. A CT scan performed the following morning revealed the presence of air in the soft tissue of the inguinal and pelvic areas, such as pectineal and psoas major muscles (Fig. ). Immediate infectious and surgical consultations were made, and the antibiotics were changed to meropenem (1 g every 8 h), vancomycin (1 g every 12 h), and clindamycin (600 mg every 8 h). Gram-positive cocci and gram-positive rods were found in the initial blood cultures. In the evening of hospital day 2, a surgical debridement of the extraperitoneal pelvic tissue with colonostomy was performed, and the CT image after the operation suggested a complete resection of the affected tissue. However, hypernatremia (a serum Na concentration of 160 to 170 mEq/L) ensued as the use of nasal desmopressin could not effectively control the patient’s central diabetes insipidus after the operation.\nNo bacteria could be cultured from the debridement tissues (Table ). The blood culture isolates were finally identified as Streptococcus constellatus using superoxide dismutase A sequencing and C. ramosum by 16S ribosomal DNA sequencing []. The minimum inhibitory concentrations (MICs) of various antibiotics were tested using Etest for C. ramosum [] and the broth microdilution method [] except imipenem and meropenem (Etest) for S. constellatus (Table ). These results were interpreted using the Clinical & Laboratory Standards Institute M11-A8 document [] for C. ramosum and M100-S24 document for S. constellatus. Both strains were susceptible to penicillin, meropenem, and clindamycin. Despite the continued use of susceptible antibiotics and intensive care, disseminated intravascular coagulation and pancytopenia developed, and the patient died on hospital day 8. |
A 55-year-old male patient presented with the gradual painful loss of vision in the left eye for 4 months associated with rapidly progressive proptosis. Best corrected visual acuity in right eye was 20/40 and no perception of light in left eye. Left eye pupil was dilated and not reacting to light, cataractous lens with proptosis of 4 mm. Single well-defined yellow-red, elevated partially spherical, firm mass with diameter 1.5 cm in superonasal quadrant without any conjunctival and episcleral adhesion was noted []. The anterior border was 4 mm superior to the limbus and the posterior edge could not be visualized. B-scan ultrasonography of the left eye revealed hyperechoic lesion superiorly, sub-Tenon's fluid, hemorrhagic choroidal detachment. The right eye was within normal limits. The patient was a diagnosed case of laryngeal carcinoma with a history of laryngectomy 1.5 years back followed by three cycles of chemoradiation. The patient had no other significant past medical or surgical history.\nComputerized tomography showed a well-defined homogeneous isodense mass in the superior part of orbit extending till optic nerve base; complete infiltration of the sclera was seen along with ill-defined heterogeneous mass in vitreous cavity s/o left eye vitreous or choroidal hemorrhage. No bony erosion was noted [].\nPositron emission tomography (PET) scan showed the left eye scleral hyperplastic lesion along with weekly metabolic thoracic node with no other systemic lesions. In view of a single metastatic focus after consultation with a medical oncologist plan for the left eye, enucleation was made. The patient underwent left eye enucleation. Histopathological examination (HPE) revealed an invasive poorly differentiated malignant tumor of squamous differentiation with full-thickness choroidal and scleral invasion and conjunctiva free of tumor [Fig. and ]. The optic nerve was free of tumor. Immunohistochemistry was positive for CK5/6 (specific for squamous epithelial differentiation) and negative for Vimentin. HPE of incision biopsy laryngeal mass (poorly differentiated squamous cell carcinoma) was compared and diagnosis of metastasis was confirmed.\nThe patient underwent repeat chemotherapy with cisplatin and external beam radiation for left eye orbit of 54 Gy in 27 divided fractions. He developed multiple systemic metastasis 6 months posttreatment and expired a year after diagnosis of orbital metastasis. |
A 43-year-old man with a history of cocaine and amphetamine use and no medical contact since childhood presented to an outside hospital with severe, acute-onset, tearing back and flank pain. On initial evaluation his blood pressure was 240/130 mmHg with a heart rate of 100 beats per minute and he was noted to have an altered mental status. Computerized tomography (CT) angiography at the outside hospital demonstrated a descending aortic dissection. He received an intravenous labetalol bolus followed by continuous infusions of esmolol and nitroprusside. He was transferred to our institution for further management.\nOn arrival, the heart rate was 91 beats per minute and noninvasively measured blood pressure was 139/66 mmHg in both arms. The radial, dorsalis pedis, and posterior tibialis pulses were full and equal bilaterally. Laboratory evaluation was notable for potassium of 5.9 mmol/L, creatinine of 1.57 mg/dL, lactic acid of 2.9 mg/dL, white blood cell count of 20.17 × 103/µL, and a mild troponin-T elevation at 0.06 ng/mL (Table ). The electrocardiogram showed sinus rhythm at a rate of 63 beats per minute with left axis deviation as well as an R wave in aVL measuring 14 mm, consistent with left ventricular hypertrophy. Urine toxicology screen was positive for amphetamines, tetrahydrocannabinol, and opiates (the latter had been administered prior to transfer).\nReview of the CT obtained at the hospital of first presentation revealed a descending aortic dissection that began distal to the origin of the left subclavian artery and extended to both iliac arteries (Fig. ). The left renal artery received blood supply from the false lumen, which compressed the true lumen at the site of the right renal artery takeoff. There was lack of contrast enhancement of the left kidney consistent with malperfusion. Enhancement of the right kidney was normal.\nFollowing multidisciplinary evaluation, consensus was reached that the time for surgical intervention to preserve the left kidney had passed. It was noted that the right kidney appeared to be perfused and the left kidney had a warm ischemic time of approximately 12 h. Given the duration of warm ischemic time and lack of evidence of other limb or visceral malperfusion, surgical intervention was deemed unlikely to be beneficial and intensive medical management was recommended. Medical therapy was selected with careful monitoring of renal function and visceral and extremity perfusion. The infusions of esmolol and nitroprusside were uptitrated and the patient was given hydromorphone and fentanyl for pain. He was intubated for airway protection in the setting of altered mental status and was monitored in the cardiac intensive care unit with goal heart rate <60 beats per minute and goal systolic blood pressure 100–120 mmHg.\nDespite control of heart rate and blood pressure, the urine output declined to <20 cc/h and creatinine rose to 2.9 mg/dL within the first 24 h. It was felt that expansion of the false lumen with compression of the true lumen was leading to malperfusion of the right kidney. In addition, he was noted to have diminished pulses in the right foot. After multidisciplinary consultation, the decision was made to proceed with aortic fenestration with the goal of decompressing the false lumen to restore flow to the right kidney (Fig. , Movie 1). The right renal artery pressure was lower than the proximal aorta pressure with a peak gradient of 50 mmHg and mean gradient of 22 mmHg. Intravascular ultrasound (IVUS) of the aortic true lumen showed it to be severely compressed in the suprarenal segment with a dynamic component. Fenestration was performed using a Pioneer® Plus catheter (Medtronic CardioVascular, Santa Rosa, CA) and dilations across the dissection flap were performed with 10 and 14 mm balloons. Intravascular ultrasound showed an expanded true lumen and a patent right renal artery. The urine output increased to 60 cc/h over the next 4 hours.\nDespite the initial improvement in renal function, the urine output again declined to <30 cc/h with progression to anuria over the subsequent 8 h. The patient was taken back to the catheterization laboratory 12 h after the first procedure. IVUS of the aorta showed that in the thoracic aorta the true lumen was widely patent but in the sub-diaphragmatic segment at the level of the visceral vessels the true lumen became quite small before enlarging again in the infrarenal aorta. An endovascular endarterectomy from T11 to the aortic bifurcation was undertaken (Fig. ) with restoration of flow to the right renal artery. Urine output post-procedure was 400 cc/h for the next hour and then returned to baseline.\nThe remainder of the hospital course was complicated by ventilator-associated pneumonia, right internal jugular vein thrombosis, and new-onset left arm weakness with magnetic resonance imaging of the brain demonstrating likely embolic infarcts in the right middle cerebral artery territory. The patient was successfully extubated and transitioned to oral medications to control the blood pressure and heart rate. No embolic source was found and the left arm weakness had markedly improved by discharge on hospital day 20. The creatinine, which had peaked at 3.36 mg/dL on hospital day three, had declined to 1.3 mg/dL by discharge. At follow-up, the patient was compliant with a stable regimen of metoprolol, hydrochlorothiazide, lisinopril, and amlodipine to maintain a normal blood pressure and had not used cocaine or amphetamines since discharge. The creatinine stabilized between 1.3 and 1.5 mg/dL. Contrast enhanced CT scan performed three and a half months after discharge (Fig. ) demonstrated a stable dissection beginning immediately distal to the left subclavian artery and extending to the distal thoracic aorta without involvement of the great vessels. The upper pole of the left kidney was infarcted and atrophied. The proximal abdominal aortic dimensions remained stable at 3.3 × 3.3 cm. |
An 81-year-old male presented for consideration of vertebral augmentation due to diagnosis of stage IV, metastatic prostate adenocarcinoma, and worsening back pain. Lupron therapy was initiated at diagnosis four months prior. Docetaxel treatment was planned for six cycles but was subsequently stopped after the first cycle secondary to side effects. No radiation therapy was previously given. PSA level was 120.73 at diagnosis and 0.6 before radiofrequency ablation.\nAt the first appointment, the patient reported mild back pain and required a walker but was able to ambulate without difficulty. He did have pain upon palpation of the thoracolumbar junctional level. He did not have any neurologic deficit at presentation. Computed tomography (CT) scans showed 40% compression deformity of T12. Magnetic resonance imaging (MRI) showed pathologic involvement of T12 and L1 and metastatic involvement of the epidural component, resulting in 40% spinal canal stenosis (Figure ). At this time, vertebral augmentation was recommended although it was believed the epidural component would not be addressed and Radiation Oncology would need to be consulted. In a short period of two months, the patient’s condition deteriorated where he was wheelchair bound due to severe pain, not controlled with NSAIDS or opioids. In addition, repeat studies showed further tumor infiltration involving T11, prompting augmentation of T11, in addition to T12 and L1.\nThe procedure was performed under monitored anesthesia care (MAC) and fluoroscopic guided imaging. Under this image guidance, 10-gauge introducer needles were advanced into the T11, T12, and L1 vertebral levels using a bilateral transpedicular approach (Figure ). A drill and osteotome were used to create cavities at the anterior aspect of the vertebral bodies. Bilateral 17-gauge bipolar radiofrequency probes were advanced into the vertebral cavities and simultaneous application of radiofrequency energy was performed as part of the protocol for volumetric ablation of the vertebral bodies. These were done in serial at T11, T12, and L1 vertebral bodies for approximately 15 minutes for each level. Lastly, methylmethacrylate was injected into the vertebral bodies of T11, T12, and L1 (Figure ) for vertebral stability. No complications occurred during the surgery and the patient was discharged the same day.\nThe patient reported no pain at the three-week follow-up and he was able to ambulate without assistance and continued to increase daily activities. He also no longer required any pain medication. He continued to be pain-free at the eight-week follow-up and repeat MRI showed stable vertebral changes and complete resolution of epidural disease at the T12 and L1 level (Figure ). At nine-months post-op, the patient still had no pain and returned back to his normal activities. |
A 46-year old female patient, who had been suffering from autoimmune thyroid disease for eight years, presented at our clinic with an acute exacerbation of GO. Clinical examination revealed a convergent strabismus fixus with severe hypotropia of both eyes (Fig. ). The patient complained of increasing loss of eyesight and heavy retrobulbar pain. Visual acuity had deteriorated significantly from 0.6/0.5 to 0.1/0.1 within 3 months. A contrast enhanced orbital MRI scan showed distinct swelling of all extraocular muscles with bilateral compression of the optic nerve (Fig. ). There was no history of comorbidities except nicotine abuse. Laboratory tests showed a euthyroid biochemical status with TSH within the normal range, but elevated levels of Anti-Thyroid Peroxidase Antibody, Anti-Thyroglobulin Antibody and Thyroid Receptor Antibody. The patient’s daily medication comprised of 200 μg L-Thyroxin and 200 μg Selenium. Over many years, the patient had shown only mild to moderate symptoms of GO, but following a thyroidectomy, the symptoms had recently worsened dramatically. Since the disease could not be controlled by high-dose systemic glucocorticoid therapy, bilateral three wall orbital decompression had been performed twice previously. In the first step, the medial orbital wall had been resected via an endonasal approach. Due to ongoing findings as before, two months later partial resection of the orbital floor and fenestration of the lateral orbital wall via a combined transconjunctival/transcaruncular approach with piezosurgery had been performed. In addition, high-dose systemic glucocorticoid therapy was conducted prior to surgery and for the first two months after surgery. Glucocorticoid medication had to be gradually reduced until zero because the patient suffered from an upcoming depression and Cushing syndrome. Orbital radiotherapy for the treatment of thyroid eye disease had been considered as a therapeutic option, but the rapid progress of the disease with the growing risk of dysthyroid optic neuropathy forced us to act more quickly than orbital radiotherapy could perform []. Since the patient increasingly suffered from loss of vision and heavy pain attacks because of medial caudal squinting, we decided to correct the hypo- and esotropia surgically by releasing and repositioning the insertion points of the inferior and medial rectus muscle. Acute surgery was the last remaining treatment option.\nOperations on the left and right eye were performed consecutively with an interval of one week. The eye with the lower vision (left side) was chosen first. A forced duction test showed a complete fixation of the bulb. We opted for a transconjunctival approach (limbal incision) combined with lateral canthotomy to gain access to the dorsal part of the inferior part of the eye bulb. The insertion of the inferior rectus muscle was localized and then circuited with a squint hook (Fig. ). A non-absorbable polyethylene suture (Mersilene 4.0, Ethicon, U.S.) was placed at the anterior rim of the muscle before the muscle was detached from the outer bulb. This release in tension immediately resulted in the spontaneous elevation of the bulb. Lengthening of the muscle with an interposition graft (e.g. fascia lata) was not possible because of the deep retraction of the muscle. Instead, the polyethylene thread loop was directly fixed to the sclera at the former muscle insertion area, placing the muscle 12-15 mm dorsally with regard to its original fixation position. By marking of the original muscle insertion point with a non-absorbable polyethylene suture, an option could be preserved for a more precise muscle readaption at a later stage. Subsequently, the same procedure was carried out with the medial rectus muscle. Less tension allowed direct refixation of the muscle to the sclera without bridging by the polyethylene suture. The bulb was freely movable and remained vertically and horizontally in a primary position (Fig. ). Despite a significant exophthalmos, passive eyelid closure could easily be performed. The significant conjunctival contraction caused by the long-term hypotropia meant that only partial conjunctival wound closure with a polyglactin suture (Vicryl 7.0, Ethicon, U.S.) was possible. No postoperative complications occurred under the postoperative systemic antibiotic medication with Clindamycin of 3x600mg per day over three days supplemented by local application of Neomycin eye ointment for one week. Surgery of the right eye was conducted in the same manner (Fig. ) and under the same perioperative protocol one week later. Additionally, two mucosal grafts of 3.0 × 1.5 cm were harvested bilaterally from the inner cheek to be used for the bilateral reconstruction of the conjunctiva. The intraoral donor sites were closed primarily by using Vicryl 3.0 (Ethicon, U.S.). Starting from extreme eso- and hypotropia, the operation succeeded in repositioning the bulbs into the vertical and horizontal primary position with no restriction of passive movements. Three months postoperatively, the patient was free of pain and had a visual acuity of 0.3/0.6. Visual field testing (Goldmann perimetry) showed only slight concentric bilateral restrictions. Surprisingly, the patient did not suffer from diplopia despite the persistent restriction of active ocular mobility and a moderate bilateral exotropia (Fig. ).\nFollow-up examinations of the patient will be performed at close intervals, including ophthalmological check-ups and the testing of thyroid blood parameters. Contrast enhanced orbital MRI scans will allow the measurement of extraocular muscle volume, as described by Kolk et al. []. Orbital MRI scans were performed preoperatively and three months postoperatively (Fig. ) and the volumes of the extraocular muscles were calculated by using manual segmentation (Osirix Imaging software 5.9) (Table ). During this time interval, the total extraocular muscle volume increased from 24.91cm3 to 29.29cm3. Together with the ongoing high levels of thyroid-specific antibodies (Anti-Thyroid Peroxidase Antibody, Anti-Thyroglobulin Antibody and Thyroid Receptor Antibody), this indicated that the patient was still in an active stage of GO. Volumetric measurements of the extraocular muscles, based on follow-up MRI scans, will help to monitor the course of the disease. Further squint surgery, in terms of a precise readaption of the extraocular muscles, will be postponed to the future, when a more stable stage of the systemic autoimmune disease will be reached. |
A 3-year-old boy was admitted to the hospital with a 1-week old soft tissue injury with accompanying infection on the dorsum of his right hand. The child's right hand was crushed by wheels, resulting in bicycle-spoke injuries 1 week before he was brought to the hospital. An external hospital diagnosed “metatarsal 2–5 fractures of the right hand, distal segmental mutilation of the right middle finger, soft tissue defect on the right dorsal hand (5 × 7 cm) with extensor tendon defects in the fore, middle, ring, and little fingers of the right hand.” Treatments at the other hospital included a reduction of metacarpal fractures with Kirschner wire internal fixation, stump repair of the right middle finger, and debridement of the dorsal hand. However, most of the extensor tendons of the right fore, middle, ring, and little fingers were crushed and lost. Postoperatively, granulation tissue growth was poor, and the wound was infected. To further repair the dorsal hand defects, the child was transferred to our hospital at 1-week post injury. Upon physical examination, the boy presented with the soft tissue defects of the right dorsal hand (5 × 7 cm) with extensor tendon defects in the fore, middle, ring, and little fingers of the right hand. Granulation and necrotic tissues were observed on the wound surface (Fig. A). The child underwent a reduction of the metacarpal fractures with a Kirschner wire internal fixation following stump repair of the right middle finger. X-ray examination showed that the fractures were well reduced with proper fixation of the Kirschner wire.\nUnder general anesthesia, the upper limbs of the boy were wrapped with tourniquets. After routine surgical disinfection, the wound on the dorsal hand was thoroughly debrided and expanded to remove necrotic tissue followed by labeling of the damaged tendons (extensor tendons of the right fore, middle, ring, and little fingers). The dorsal hand defect was then covered with a vacuum sealing drainage (VSD) device fixed at the edge and was sealed with a semi-permeable membrane. Continuous suction using negative pressure was then performed. After 1 week, the VSD device was removed, and the wound was relieved (Fig. B). After 3 days of dressing changes (once a day), the wound surface before surgery was ruddy with well and uniformly growing granulation tissue and no sign of infections (Fig. C and D). Therefore, combined transfer of the dorsal foot flap and tendon at stage I was planned under general anesthesia (Fig. A–C).\nFirst, the distal and proximal ends of the extensor tendon in each finger were separated from the dorsal hand, and the length of tendon defects was measured. The ipsilateral dorsal foot served as the donor. The axial lead of the flap was defined along the dorsal plantar artery. A composite flap graft was designed based on the size of the dorsal hand defect with the distal end to the toe web, the proximal end to the extensor retinaculum, and both sides to the 1st and 5th metatarsal bones. The dorsal plantar artery and its accompanying veins were exposed between the extensor hallucis longus and the extensor digitorum longus. The dorsal plantar artery was carefully separated up to the deep plantar branch and dorsal digital branch, followed by isolation of the superficial peroneal nerve up to the medial and middle dorsal cutaneous nerves. The nerves were ligated at the base of the 1st metatarsal bone space; the deep plantar branch and accompanying vein of the dorsal plantar artery were cut off. The flap was separated from the distal end to protect the tendon of the extensor digitorum longus. Intraoperative exploration of the extensor digitorum brevis tendon with complete aponeurosis was performed at the metatarsophalangeal joint. The flap was further cut off toward the proximal end. According to the length of the tendon defect, the extensor digitorum brevis tendon was correspondingly cut off at the proximal end. Moreover, the dorsal artery and its accompanying vein, as well as the medial dorsal cutaneous nerve of the superficial peroneal nerve, were used as needed.\nThe radial artery and its accompanying vein and superficial branch of the radial nerve were subsequently separated at the anatomical snuffbox of the wrist. The separated flap was placed on the wound surface of the dorsal hand, followed by anastomosis between the dorsal foot artery and its accompanying vein, and the radial artery and its accompanying vein, between the medial dorsal cutaneous nerve of the superficial peroneal nerve and the superficial branch of the radial nerve, and between the 2 ends of the extensor digitorum brevis tendon and the extensor digitorum tendon (Fig. D). Afterward, the tourniquet was released and the anastomosed blood vessels were observed to pulsate properly. The flap color and temperature gradually returned to normal, and the capillary response was normal. Finally, the mid-thickness skin flap of the ipsilateral thigh was used to cover the wound of the donor site. Postoperatively, the child's hand was fixed in a functional position with a plaster cast. In addition to conventional methods such as warming, fluid replacement, anti-infection, anti-spasmodic and anti-coagulant, and improved microcirculation, a small dose of phenobarbital (Lumina, 3 mg/kg)[ was administered via pump injection to keep the child in a lethargic state. The child had a wakeful response to command and could complain of the site of pain with a white value scored 3.[ Vital signs were closely monitored post operation. The flap survived till 2 weeks after the operation (Fig. A and B). X-ray examination at 6 weeks showed that the metacarpal fracture healed well. The Kirschner wire was removed and rehabilitation exercise for hand function was gradually performed. During the 6-month follow-up, the shape of the dorsal hand flap was satisfactory, and the skin color was nearly normal. Protective sensation was restored, and the tendon graft functioned well in vivo. Satisfactory outcomes were achieved in the flexion and extension of each finger. The donor site on the dorsum of the foot healed well without ptosis of the toes. |
A thin 75-year-old woman was transferred to Kyungpook National University Hospital with a complaint of chest wall pain resulting from her chest being stepped on while she was lying down supine. Her initial systolic blood pressure and heart rate were 137 mm Hg and 73 beats/min, respectively. She was mentally alert. Her hemoglobin level was 11.8 g/dL, and electrocardiography revealed a normal sinus rhythm. An initial chest computed tomography (CT) scan revealed a right hemothorax, multiple rib fractures, and a sternum fracture. There was an approximately 1.2-cm right pulmonary artery (PA) blind pouch that was suspicious for a rupture, 4 cm apart from the main pulmonary trunk, accompanied by diffuse bronchial anthracofibrosis (). The patient was immediately transferred to the operating room for surgical repair with normothermic heart- beating cardiopulmonary bypass (CPB). The injured right PA was approached through a median sternotomy. CPB was established by arterial cannulation of the ascending aorta near the aortic arch and bicaval venous cannula without venting. Upon opening of the right PA, an approximately 1.5-cm ruptured area of tissue was present at the distal superior aspect of the right PA before branching (). Proximal and distal clamping of the PA was not performed due to lack of space, and the field of view was secured using a pediatric intracardiac sucker. After removing the injured tissue and hematoma, the black-pigmented enlarged calcified lymph node was visible next to the injured tissue. PA angioplasty was performed along the healthy PA borders with bovine pericardium with 6-0 Prolene in a running fashion (). After definite deairing before closing the PA, routine closure was performed. The total operative time was 123 minutes, and the CPB time was 37 minutes.\nThe patient’s postoperative course was uneventful, and the patient was extubated following usual procedures, without any adverse events. On postoperative day (POD) 10, CT revealed a patent PA and no evidence of pseudoaneurysm (). The patient was discharged on POD 20 without complications and was placed on a routine outpatient follow-up schedule.\nThe patient provided written informed consent for publication of clinical details and images. |
A 24-year-old male patient with a history of D-TGA with VSD who underwent Rastelli repair at age three and subsequently lost to follow-up was admitted for worsening dyspnoea on exertion and fatigue for 1 month duration.\nTransthoracic echocardiography (TTE) revealed severe left ventricular (LV) dysfunction with ejection fraction (EF) of 25% with a 1.5 cm LV thrombus ( and Videos 1–3). The RV was moderately dilated with severe systolic dysfunction and suprasystemic RV pressure. The RV was markedly hypertrophied with an apical RV thrombus as well. There was moderate pulmonary regurgitation and critical homograft stenosis () with mean and peak gradients of 42 and 79 mmHg, respectively.\nOver the course of the hospitalization, he developed cardiogenic shock requiring inotropic support and intravenous vasodilators. He was deemed not a candidate for advanced therapies given history of incarceration and poor social support, and was at prohibitive surgical risk. After multi-disciplinary discussion and discussion with the patient, it was felt given his young age, an attempt at a high-risk transcatheter pulmonary valve replacement (TPVR) was warranted, understanding that there is no surgical or transplant back-up.\nThe patient was taken to the cardiac catheterization lab and underwent intubation given he was unable to lie flat. Vascular access was obtained and as angiography was being performed the patient suffered cardiac arrest. As cardiopulmonary resuscitation (CPR) was performed the patient underwent peripheral cannulation of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) with a 24 Fr venous cannula and an 18 Fr arterial cannula and ultimately he achieved return of spontaneous circulation after several rounds of CPR and defibrillation.\nOnce the patient was stabilized the pulmonary conduit was crossed using a 4 Fr angled glide catheter and a wholey wire as it was too critically stenosed to allow a wedge catheter to cross. Haemodynamics were tenuous when dilating the conduit despite being on ECMO support. Serial dilations of the conduit were performed with 6.0 and 8.0 mm × 40 mm Charger balloons at 16 atm (). The wholey was exchanged with a Lunderquist wire over the glide catheter into the distal left PA for better support. An 18 Fr curved sheath was then advanced into the RV and the conduit was further serially dilated with a 12 through 20 mm VIDA balloons () with angiography ruling out rupture or contrast extravasation, and coronary angiography during homograft balloon dilation without any evidence of coronary compression. The sheath was advanced further across the conduit, and a 10-Zig 4.5 mm Cheatham Platinum (CP) stent crimped onto a 20 mm Balloon-in-Balloon (BIB) was used to stent the conduit (), which was post-dilated with 22 and 24 mm VIDA balloons to reach a stent diameter of 20 mm. Transcatheter pulmonary valve replacement with a 22 mm Melody valve over a 22 mm ensemble was then performed within the CP stent ( and ). Pulmonary angiogram post-deployment showed no regurgitation (, ), and invasive gradient of <5 mmHg ().\nGiven significant improvement in haemodynamics immediately post-TPVR, the patient underwent ECMO weaning and decannulation the same day. Intra-aortic balloon pump insertion was performed first to safely transition off ECMO support. Post-procedural transoesophageal echocardiogram revealed a well-seated Melody valve with no pulmonary insufficiency and a gradient of 4 mmHg.\nThe patient recovered well and he was started on a heart failure medication regimen and ultimately discharged home. The intracardiac thrombi resolved with anticoagulation during the hospital stay and anticoagulant was discontinued. He had a follow-up TTE 5 months later demonstrating improved LVEF to 35%, moderate RV dysfunction ( and , ), and mean and peak gradients across the Melody valve of 22 and 40 mmHg, respectively. |
A 67-year-old male chronic smoker with medical history significant for chronic obstructive pulmonary disease was admitted for imaging guided biopsy of a 1.2 cm left lower lobe lung nodule found recently on a computed tomography (CT) scan of the chest. The nodule was highly suspicious for primary lung malignancy. The patient was placed in a prone position and lung parenchyma in the posterior lateral left chest was visualized. Under CT guidance, a 19-gauge guide was advanced into the left lower lobe and two separate 20-gauge core biopsy specimens were obtained from the mass. There was no hemorrhage or immediate post procedure complication. However, towards the end of the procedure, the patient started complaining of sudden onset of chest pain and became unconscious. No palpable pulses were identified. A code blue was called and cardiopulmonary resuscitation was begun according to Advanced Cardiovascular Life Support guidelines. The patient subsequently demonstrated ventricular fibrillation which responded to defibrillation shock and epinephrine. The patient had three cycles of chest compressions, one dose of epinephrine, and a shock of 200 J. He was successfully resuscitated and intubated for mechanical ventilation. A CT scan of the chest was obtained immediately after the resuscitation and it demonstrated development of a small anechoic area in the left cardiac ventricle consistent with air embolus (Figure ).\nThe vital signs recorded at the time were as follows: blood pressure of 130/80 mmHg, pulse rate of 90 beats per minute, respiratory rate of 18 breaths per minute, and normal oxygen saturation of 92% on room air. The patient was admitted to the intensive care unit. Bedside transthoracic echocardiogram (TTE) did not reveal evidence of an air embolus. Additionally, no cardiac wall motion abnormalities were noted. The patient remained hemodynamically stable for 24 hours, and he was successfully weaned off from the mechanical ventilator next day and discharged home in a stable condition. |
A 90-year-old man was admitted to our emergency department after a simple fall from his bed (height ∼1 m). He had wanted to get out of bed independently and had forgotten that he needed his walker. There was no mention of prodromal symptoms leading to the fall. He was found on the floor by caretakers after a call for help and was unable to get up. He was unable to explain how he fell. His medical history was remarkable for obesity (body mass index, 35), cardiac ischemia, Parkinson’s disease and chronic renal insufficiency. Before hospital admission, he resided in a convalescent home and he mobilized with the aid of a walker. Clinical examination revealed external rotation of both legs and pain on passive movement of both sides of the hips. Motor and sensory functions were intact. Plain radiographs of the pelvis showed bilateral slightly displaced intertrochanteric fractures of both femoral bones (Fig. ). In the AO classification of trochanteric femoral fractures classified as type 31.A3 [], a reverse oblique fracture with the fracture line passing between the minor and major trochanters, with an abduction of the proximal fragment due to the pull of the abductor muscles. There were no signs of osteoporosis or osteopenia due to decreased mobility nor did the patient have any signs of an underlying malignant illness on chest X-ray. The glomerular filtration rate was 34 with slightly increased serum values of urea (13.6 mmol/l) and creatinine (152 µmol/l). Surgical treatment was discussed with the patient and his family, and informed consent was obtained. Under general anesthesia both fractures were treated by bilateral intramedullary nailing using the extended Stryker Gamma3 intramedullary nail fixation (Kalamazoo, MI) in one surgical session. The extended gamma nails were locked statically leaving the possibility to convert them to the dynamic state at a later point in time. Intraoperative radiographs (Fig. ) confirmed correct placement of the gamma nails. The combined surgical procedure lasted 4 hours and 21 minutes with an estimated blood loss of 200 ml and without occurrence of hypotension, bradycardia or decreased oxygen saturation. The patient was able to mobilize, fully bearing weight, supervised by a physical therapist within 4 days postoperatively. He was ready to be discharged back to his convalescent home 9 days postoperatively with improved kidney function (glomerular filtration rate of 51). |
A 30-year-old woman was admitted to the hospital in 1994 for hematuria. A papillomatous bladder tumor was diagnosed and removed during a transurethral resection. Histological examination showed a papillomatous transitional epithelium without cellular atypia. There was no evidence of infiltrative growth in the subepithelial connective tissue. This case was reviewed and graded according to the World Health Organization (OMS)/International Society of Urological Pathology (ISUP) Consensus Classification of Urothelial Neoplasms of the Urinary Bladder[] as a low grade papillary urothelial carcinoma. During the following (12 months (1995), 48 months (1999), 72 months (2001), 108 months (2004), and in 2006) a recurrent bladder tumor was resected. Histologically, the tumor showed the similar pattern. An infiltrative growth pattern was not seen on any occasion, and increasing cellular atypia with time did not occur.\nOn December 2007, a right ovarian tumor and a nodule of the left ovary were discovered and surgically removed. At the same time, some small papillomas of the urinary bladder were endoscopically removed. Macroscopically, the right ovary was changed into a monolocular cyst with a diameter of 30 cm, containing a bright yellow serous fluid. The outside of the cyst was smooth but the inside was partly covered with several papillomatous vegetations (). Microscopic examination (Fig. , ) showed a cyst with endoluminal papillae covered by transitional epithelium, practically indistinguishable from the urinary bladder tumors (Fig. , ), without stroma infiltration. These findings were similar to the proliferating Brenner tumor of ovary. The nodule of the left ovary showed close histological similarity with the previously described ovarian mass.\nThe uterus was normal. Immunohistochemical studies demonstrated that the ovarian Brenner tumor and the multiple recurrent urothelial carcinoma of bladder stained diffusely positive for cytokeratin 7, but both of these tumors were negative for cytokeratin 20 (Fig. , and Fig. , ). The patient's post-operative course has been free of recurrence of the bladder tumor for 7 months. |
BB is a 34-year-old married woman with 3 children from the urban part of Oman. She approached the unit at the present hospital with her husband and her female siblings who helped provide us with anamnestic data. According to them, BB went through clouded sensorium which lasted for a short duration. The distress was accompanied by abrupt onset of inappropriate emotions, trouble in concentrating, suspiciousness, and spending a lot more time alone than usual; episodes that tended to reappear monthly throughout her adult life. The family attributed her distress to ethnopathology. She had been taken to a traditional healer who recommended dietary changes, herbal medicine and attributed her behavior to an ‘invading evil spirit’.\nDuring these episodes, she had had poor self-care, hygiene, oral intake and a disturbed sleep pattern. She had once woken up at midnight to sprinkle her children with water. During exacerbation of her distress, she became suspicious of her husband and the female domestic servant. She displayed odd mannerisms and stereotypical behavior along with rituals of cleaning and washing. On one occasion, she had escaped from the house and was found wandering aimlessly in the neighborhood. At the time, it was also reported that she had been improperly dressed, in a manner that is deemed to be socially immodest in a rural, conservative society.\nA protracted interview with her husband and siblings indicated that her distress tended to occur at the onset of menstrual flow. Her symptoms continued until the end of menstrual flow. She had a patchy memory of her state of clouded sensorium. She stated that she often felt tired and dysphoric during a certain time of the month which she attributed to stress at work.\nPremorbid, there was no indication that BB had experienced any adverse life events during her childhood. She completed 12 years of education and later enrolled herself in a higher education institution to distinguish herself as a teacher. She has 11 siblings with no evidence of mental illness in the family. Her menses began at age 12.\nBB denied having consumed any mind-altering substance including tobacco or its rejuvenated forms or alcohol. A routine urine drug screening did not reveal the presence of any illicit substances in her system.\nPhysical examination was unremarkable and her medical workup—including hormonal study, brain CT scan, and EEG—was inconclusive. The clinical team suggested that the respondent displayed manic episodes with psychotic symptoms or according to ICD-10, the client’s distress might be parallel to a manic episode, unspecified (F309)/brief psychotic disorder (F24). CIDI did not indicate the presence of typical manic (F30), Bipolar affective disorder (F31), schizophrenia or other psychotic disorders (F20, F22, F23, or F25).\nHer distress subsided immediately upon admission and she was discharged with antipsychotic olanzapine (5 mg) for which she was compliant. Following up a week later, she was deemed suitable for protracted psychometric evaluation. Her intellectual and neuropsychological functioning are depicted in Fig. . BB scored 21 on the [] which implied the presence of moderate depressive symptoms. Six months later, still compliant to prescribed medication (olanzapine 5 mg), she reported two episodes of relapse but with less intense symptoms. The two episodes of relapse once again coincided with menstruation and subsided with the end of her menstrual flow. |
The patient’s course is outlined in Fig. .
A 58-year-old, previously healthy, white female presented to her primary care provider (PCP) with the desire to remove a right posterior scalp cyst for cosmesis. This non-inflamed, non-draining, painless, 1–2 cm cyst had been present for close to 10 years without change in size or fluctuance. The cyst was initially drained by the PCP, but, when it recurred 6 months later, the PCP excised the cyst and sent the specimen for routine pathology. The initial read of the tissue sample was high-grade invasive carcinoma with squamous features and arising in association with a PTT. Based on the pathology, the PCP referred the patient to a plastic surgeon for a more definitive excision of the lesion and repair of the defect. The lesion was excised with negative margins and pathology read as invasive high-grade squamous cell carcinoma (SCC). Eight months post resection, the lesion recurred locally along with a palpable right posterior cervical lymph node (LN). A positron emission tomography (PET) scan at that time demonstrated hypermetabolic activity in the posterior occiput and in a posterior neck LN. Fine needle aspiration (FNA) of both the primary scalp lesion and LN were completed, and pathology was reported as SCC, similar to the primary lesion.
With a working diagnosis of locally advanced SCC, the patient’s care was referred to a tertiary care center. There, a dermatopathologist re-evaluated the previous biopsy specimens and altered the diagnosis from SCC to MPTT (Fig. ). Subsequently, the patient was referred to a head and neck surgeon for modified radical posterior neck and lymph node dissection. Intraoperative findings uncovered the presence of nodal metastases to the posterior neck with extranodal extension, extensive perineural invasion of the spinal accessory nerve, and jugular venous invasion of the MPTT. After surgery, the case was discussed at a multi-disciplinary tumor board, and a common |
A 60-year-old man with a past history of RCC (clear cell type, G2, T1b N0 M0 Stage I) treated by a right nephrectomy in June 2015 was required to have a follow-up examination at 6-month intervals after surgery, without the use of an anticancer agent. In January 2018, a routine gastrointestinal endoscopy found an ulcerative lesion of approximately 10 mm diameter in the greater curvature of the gastric body (Fig. ). An endoscopic ultrasonography (EUS) of this lesion showed the first three sonographic layers were blurred, which suggested submucosal invasion. An endoscopic biopsy of the lesion exhibited clear cytoplasm with prominent nucleoli, which was histologically compatible with metastasis to the stomach of the patient’s known RCC. On the other hand, computed tomography (CT) incidentally detected a well contrast-enhancing round-shaped mass in the fundus of the gallbladder (Fig. ). Additional ultrasonography revealed a sessile polypoid lesion, and gallbladder stone and wall thickening were not observed. Although these findings were lacking conclusive evidence of diagnosis whether the gallbladder tumor was primary or metastatic, the circumstantial evidence potentially pointed to the tumor as a metastasis from the patient’s known RCC. 18F-Fluoro-deoxyglucose positron emission tomography combined with CT (FDG-PET/CT) was performed as a preoperative workup to detect other possible remote metastasis. However, specific FDG uptake was not shown, even in the gastric and gallbladder tumors. The blood examination was unremarkable.\nIn February 2018, a gastric wedge resection via laparoscopic and endoscopic cooperative surgery (LECS) technique was applied to the gastric tumor, and laparoscopic cholecystectomy to the gallbladder tumor was simultaneously performed (Fig. ). The operation lasted 190 min with little intraoperative blood loss. Intraoperative pathologic diagnosis was not performed in this case. The hospitalization period after surgery was not eventful, and the patient was discharged on postoperative day 7. Histological examination confirmed that the tumors of the stomach and gallbladder were both metastatic RCC. Immunohistochemical staining was strongly positive for CAM 5.2 and vimentin, supporting the diagnosis. Macro- and microscopic findings are shown in Fig. . Thereafter, the patient required examination every 3 months without the use of anticancer agents and has survived without relapse to 12 months after the surgery. |
A young 16-year-old male patient presented to the neurosurgical outpatient department from neurorehabilitation ward with history of rhinorrhea, difficulty in talking, and inability to control his urine and bowel for two days. He suffered multiple episodes of on-and-off watery rhinorrhea since the last three days. He was involved in motor vehicular accident (passenger) two weeks back and sustained extradural hematoma (EDH) and multiple skull fractures, including the left frontoparito temporal bone, left orbit without globe injury, and skull base. He underwent evacuation of EDH and recovered, and he was shifted to rehabilitation with a Glasgow coma scale (GCS) score of 15 without any neurological abnormalities.\nHe was admitted to the neurosurgical ward for observation. He was awake, and pupils were equal and reactive to light. No neurological deficit was observed, but he was aphasic. Rhinorrhea was diagnosed as CSF leak and started on ceftriaxone after taking the CSF for culture and sensitivity.\nHis computer tomography (CT) and magnetic resonance imaging scans showed massive intraventricular pneumocephalus with ventricular distension (frontal and lateral) but failed to locate the exact site of CSF leak and demonstrated the skull base fracture. We started to nurse him in a flat position, supplemented with oxygen by face mask (6 to 8 L/minute), and shifted him to the neuro high dependency unit for close neurological monitoring.\nOn day two, he neurologically deteriorated and became confused, and his GCS decreased to 8/15. His pupils became unequal (left 5 mm and right 2 mm), and an urgent CT brain done showed increased left lateral ventricular distension due to pneumoventricle and still distended frontal ventricle with significant brain edema (). The patient was pushed to the operating theater, and EVD was inserted. Gush of air with pressure came out during the procedure, and he was shifted to the surgical intensive care unit. In the six hours postoperative period, he was awake and still aphasic, but his pupils were equal and reactive to light. EVD continued to drain air, and he remained hemodynamically stable.\nOn day three, the patient started to murmur simple words, and supportive care was continued. By day four, he was awake and started to speak with normal articulation. The follow-up CT brain on day four showed decreased distension of the lateral ventricle with a decreased amount of pneumocephalus ().\nPneumoventricle was completely resolved completely by day five. His speech was normal, and he regained bowel and bladder control. EVD was removed by day seven, and on day eight, he was discharged home to be followed up in neurosurgical outpatient clinics. |
An 8-month-old female infant had coronary reimplantation at age 3 months for ALCAPA. Postsurgical ejection fraction showed early improvement with subsequent deterioration. A diagnostic left heart catheterization performed as part of a heart transplant evaluation revealed severe ostial stenosis of the LMCA. She was referred for PCI of the left main coronary artery to relieve her heart failure and preempt transplant. Her physical exam was significant for congestive heart failure and failure to thrive. The patient's echocardiogram showed markedly depressed left ventricular function. A cardiac computed tomography angiography (CTA) and initial diagnostic nonselective root aortogram demonstrated stenosis of the LMCA at the site of ALCAPA reimplantation. Selective left coronary angiogram revealed severe kinking of the reimplanted LMCA at the ostium ().\nThe procedure was performed in the Pediatric Cardiology interventional suite after extensive discussion and planning with Pediatric and Adult Interventional Cardiology, Pediatric Cardiac Anesthesia, Pediatric Cardiothoracic Surgery, and Pediatric Cardiac Radiology. General anesthesia and a femoral arterial approach were utilized. An ascending aortic root angiogram was obtained in 2 planes to assess the ostial left main stenosis. Due to the small size of the infant aorta, a 6 Fr JR-4 guide was reshaped to engage the left main coronary artery. A BMW wire was used to cross the lesion. Since the infant left main coronary artery was small but was expected to grow with age, a somewhat larger (3.0 × 8 mm Vision bare metal) stent was carefully implanted in the proximal LMCA at less than nominal pressure to avoid distal dissection. A poststent angiogram showed that the stent had moved during implantation and missed the ostium with residual stenosis of the LMCA origin. Hence, a 3.5 × 8 mm Vision bare metal stent was placed into the LMCA ostium overlapping with the previous stent distally and protruding 1-2 millimeters in the aorta proximally. The ostium and aortic overhanging portion of the stent were postdilated producing proximal flaring. The final angiogram confirmed excellent stent position and normal flow ().\nThe patient tolerated the procedure well and was discharged home on dual antiplatelet therapy (DAPT) with aspirin and clopidogrel one day after PCI. She was followed in Cardiology clinic post-PCI and noted to have no change in her ventricular function. Nevertheless, she continued to do well clinically until six months post-PCI, at which time she demonstrated failure to thrive and required admission for initiation of continuous milrinone infusion. The left main stent was widely patent with normal Doppler flow signals as visualized by echocardiography (). She was listed as status 1A for orthotopic heart transplantation (OHT) and underwent transplantation one year post-PCI, at age 20 months. |
An 80-year-old man with known cervical canal stenosis due to ossification of the cervical posterior longitudinal ligament was transferred to an emergency room soon after a falling accident. The patient was alert and had complete tetraplegia, sensory deficits below the C4 cervical sensory level, and progressive restrictive respiratory failure that required assisted ventilation, and, eventually, a tracheostomy. Cervical spine magnetic resonance imaging showed cervical cord compression that was worse at the C3–C4 intervertebral level, and an intramedullary high signal at C3 and C4 vertebral levels, and the patient was managed conservatively. During the conventional weaning process of trials of intermittent spontaneous breathing in the ICU, an unexpected cardiac arrest made both the patient and medical staff reluctant to proceed with further weaning. Fifty-eight days after cervical cord injury, the patient was transferred to our hospital for further rehabilitation. He was fully conscious and received pressure-support mechanical ventilation with back-up rates of 16 breaths. He had total tetraplegia below shoulder girdle muscles with a preserved sensation from C2 to C3 on both sides, and a urinary obstruction. The limbs and trunk were stiff with contracture, and muscle stretch reflexes of the limbs were abolished. Neurological level of injury was C3 according to the ISNCSCI, with a total sensory score of four. There was no sensory sacral sparing, while the deep anal pressure was preserved, and the American Spinal Injury Association scale graded B. Chest roentgenogram and computerized tomography showed bilateral, widespread atelectasis. The patient occasionally showed signs of pulmonary infection. Intensive pulmonary care and rehabilitation, including physical support for expectoration, mechanically assisted removal of tracheal secretions (CoughAssist E70®, Philips Japan, Tokyo), ventilator muscle training, and management of the spasticity of the abdominal wall, resulted in the improvement of the roentgenological findings. His expiratory tidal volume (VT) measured 150 mL.\nAlthough the neurological status according to the ISNCSCI was unchanged, the patient was willing to be weaned from mechanical ventilation as his general condition improved. After informed consent was given, we attempted automated weaning from mechanical ventilation using IntelliVent®-ASV on and after 131 days of injury. IntelliVent®-ASV (Hamilton Medical AG, Switzerland) is a closed-loop ventilation mode that adjusts the pressure support in terms of the percentage of the ideal minute volume (%MV). The ideal MV (100%MV) is calculated from the patient’s height and gender. Based on Otis’ equation [], adaptive support ventilation will select the best VT–respiratory rate (RR) coupling for the optimal work of breathing. IntelliVent®-ASV has interrelated functions: an auto-adjustment for carbon dioxide (CO2) elimination, an auto-adjustment for oxygenation, an auto-weaning tool named Quick Wean (QW), and a spontaneous breathing trial (SBT). The setting of the target %MV is automated based on either the monitored end-tidal CO2 or monitored spontaneous breathing rate. The auto adjustment of fraction of inspiratory oxygen or positive end-expiratory pressure is based on the monitored oxygen saturation fraction of hemoglobin with a pulse oximeter (SpO2) []. The QW mode is an optional automated weaning, and progressively reduces the pressure support, monitors for readiness-to-wean criteria, and provides the option to automatically conduct a fully controlled SBT. In the QW mode, when the spontaneous rate is less than the upper limit of the predicted target range, %MV is automatically decreased gradually to the selected level. To facilitate the recovery of VT by means of the loading work on respiratory muscles, we set the level of support to 70%MV for the QW mode. When spontaneous breathing satisfied the pre-determined conditions of oxygenation and ventilation for 1 min, the SBT mode was used. We operated the SBT mode during the day from 9:00 a.m. to 6:00 p.m.\nIn the QW mode, the duration of 70%MV and SBT time (25%MV) increased gradually (Figs. and ). Twenty-two days after the introduction of the QW and SBT modes in association with intensive pulmonary rehabilitation, SBT was running almost fully during the daytime. At this time, the expiratory VT was increased to 350 mL from 150 mL upon admission to our hospital. Thereafter, we withdrew the pressure support ventilation during the nighttime 39 days after the introduction of the auto-weaning mode, and the patient’s weaning process was completed. |
The present case report is about a 40-year-old female patient with the complaints of a swelling in the mandibular angle region of 5 months duration she was referred to our department by her oncologist with the differential diagnosis of osteomyelitis or osteogenic sarcoma. On palpation a hard, non-tender, localized, round swelling of size 4 cm × 3 cm on left angle-ramus region was felt []. There were no palpable regional lymph nodes. Oral cavity examination did not reveal the existence of any ulcer, fistula or wound except missing lower left first molar.\nHer medical history revealed a modified radical mastectomy 2 years back for invasive ductal carcinoma of the left breast. The tumor was positive for c-erbB-2(HER-2/neu) assay with score 3 plus in immunohistochemistry. Hence, she was on adjuvant hormone therapy.\nA panoramic radiograph showed a retained root remnant of left mandibular first molar, carious second molar and an area of rarefaction on left angle region with indistinguishable margin [].\nSerial axial and coronal computed tomography (CT) scan of mandible (1 mm-thick slice) showed destructive lesion on left angle of mandible extending in to the ramus []. Features like Codman triangle and sunray appearance were seen in the margins of the lesion and minimum soft-tissue component were seen adjacent to it [ axial view, coronal view].\nThe CT scan differential diagnosis included chronic osteomyelitis, osteogenic sarcoma and secondary metastasis. A fine-needle aspiration cytology (FNAC) revealed loosely cohesive group of epithelial cell having increased N: C ratio and hyperchromatic nuclei in adenoid pattern []. It was diagnosed as infiltration from poorly differentiated adenocarcinoma, possibly of mammary ductal origin.\nA full body radionuclide scan was carried out and it was suggestive of skeletal metastases. A technetium-99m-methylene diphosphonate bone scan located a region of increased radioisotope uptake in the ramus of mandible on the left side as well as in the T-2 and T-10 vertebrae [].\nThe patient was referred back to her oncologist for further treatment since it was not amenable to surgical management. |
In October 2007, a 14-year-old Asian female was referred for an ophthalmological evaluation for posterior uveitis and was referred to our outpatient clinic due to decreased visual acuity. She had a history of a severe sore throat 9 months previous and subsequent proteinuria. Her initial corrected visual acuity was 20 / 30 in the right eye and 20 / 25 in the left eye. The anterior segment and lens were clear in both eyes. Cells measuring 3+ right eye and 2+ left eye were found in the vitreous. Dilated fundus exam revealed blurred disc margins with disc swelling in both eyes (). Fluorescein angiography demonstrated retinal vasculitis sparing the posterior pole in both eyes (). Laboratory findings showed a mild elevation of white blood cells to 6,990/mm3. Results for tuberculin skin test and serological testing for syphilis, human immunodeficiency virus, hepatitis C virus, hepatitis B virus, toxoplasmosis, cytomegalovirus, varicella zoster virus, and herpes simplex virus were all negative. The chest radiograph showed nothing significant. Elevated anti-streptolysin O (ASO) of 630 IU/mL (normal <200) and an acute phase reactant erythrocyte sedimentation rate 16 mm/hr was noted. Urinalysis and serum chemistries showed no evidence of proteinuria, and renal function was normal.\nAfter starting steroid eye drops and oral steroid (prednisolone 1 mg/kg), her symptoms and visual acuity improved, as did the vitritis and disc swelling. Topical and oral steroids were slowly tapered. In January 2008, her corrected visual acuity improved to 20 / 20 in both eyes. Fluorescein angiography demonstrated that retinal vascular leakage was improved, and steroid treatment was stopped.\nAfter 3 weeks, the patient visited our clinic with visual loss and infection in the right eye. In the inferior of the right eye, an anterior chamber cell score of 4+ and posterior synechiae were noted. Vitreous cells were also noted. After starting oral steroid therapy, she recovered. Her best corrected visual acuity was 20 / 20 in both eyes. Over the 1-year follow up, there was no recurrence. |
A 31-year-old man was seen in neuro-ophthalmology consultation for double vision and suspected internuclear ophthalmoplegia. He had a past medical history of chronic intermittent diarrhea starting 3 years prior to presentation. Following extensive investigations including multiple colonoscopies, his condition was diagnosed as irritable bowel syndrome and medically managed with cholestyramine and diphenoxylate/atropine daily. One year prior to presentation, he developed abdominal pain and leucocytosis for which he underwent a laparotomy for small bowel obstruction. The distal small bowel and cecum were resected, whereby the procedure revealed chronic ruptured appendicitis without any evidence of inflammatory bowel disease. A few months later, he underwent right nephrectomy due to possible congenital atrophic right kidney, discovered during the investigation of recurrent UTIs for a year. As a child, he had a normal developmental history and academic performance.\nOne year prior to presentation, he developed intermittent horizontal binocular diplopia that was present in all directions of gaze and had increased in duration 6 months prior. He saw an ophthalmologist who noted bilateral limitation of adduction of each eye and suspected internuclear ophthalmoplegia. He therefore underwent MRI of the brain, which was initially reported to represent advanced multiple sclerosis but after later review was interpreted as a diffuse leukoencephalopathy, as shown in Figure . A neuro-ophthalmology consultation was then requested to clarify the etiology of his double vision.\nAt the neuro-ophthalmology consultation, he appeared cachexic and weighed 46 kg and was 177 cm tall (BMI 14.7 kg/m2). He reported no family history of neurological or oculomotor syndromes except a grandfather with Parkinson disease. He had normal afferent visual function with a visual acuity of 20/20 in each eye and normal Humphrey visual field testing. Dilated fundus examination was normal. External examination revealed bilateral ptosis with recruitment of the frontalis muscles. There was a large exotropia of 40 prism diopters (PD) in the primary position. The exotropia was fairly comitant, measuring 35 PD in both left and right gaze. He had diffuse limitation of extraocular movements, as shown in Figure . Neurological examination revealed diffuse muscle atrophy, particularly in the proximal upper and lower limbs with relative sparing of his distal leg, forearm, and hand muscles. There was moderate weakness (4/5 on the Medical Research Council scale) in proximal upper and lower limb muscles, with normal distal strength. He had reduced vibration sensation at the big toes, which normalized by the ankle. Joint position sense was normal and sensation to pinprick was normal throughout. Nerve conduction studies and electromyography demonstrated a mixture of a diffuse predominantly axonal, but mixed axonal and demyelinating, sensory-motor peripheral neuropathy, along with evidence of a proximal myopathy (small motor unit potentials with early recruitment in proximal muscles).\nHe saw his gastrointestinal specialist and additional bloodwork including those measuring vitamin levels was performed. He was found to be anemic with a hemoglobin of 129 g/L (normal 140–180 g/L) and deficient in magnesium at 0.40 mmol/L (normal 0.70–1.10 mmol/L), calcium at 2.13 mmol/L (normal 2.20–2.62 mmol/L), 25-hydroxy vitamin D at 14 nmol/L (normal 25–200 nmol/L), and vitamin B12 at 212 pmol/L (normal 222–652 pmol/L). His parathyroid hormone levels were elevated at 9.9 pmol/L (normal 1.3–7.6 pmol/L), while his albumin was normal at 42 g/L. He continued supportive treatment and vitamin supplementation to correct these deficiencies. Diphenoxylate/atropine was discontinued due to low energy and fatigue, and he was started on loperamide 2 mg as needed up to twice daily. |
A 50-year-old man presented with progressive left wrist pain and swelling, following a trauma one year back, in which he fell on his left upper extremity. He was operated by percutaneous pinning for the extra-articular lower end radius fracture. Post operative period was uneventful but then patient started developing pain and fullness over the operated wrist on removal of the cast 6 weeks post-operatively with loosening of pins, which were removed. Patient continued to have fullness with gradual & progressive loss of wrist movement. Patient was treated on the lines of CRPS by local physician with non-steroidal anti-inflammatory agents. No improvement was observed and the stiffness and pain progressively worsened for the last 9 months. Past medical history was non-significant. He had no history of tuberculosis (TB) or any other immune-suppressive disease. There was neither any family history of TB infection nor of any rheumatic or autoimmune disease. He had been immunized with BCG vaccine at birth. Constitutional symptoms such as fever, anorexia, fatigue and weight loss were absent. He was not receiving any regular medications. When seen in our institute, he had considerable pain and severely restricted range of motion of the left wrist. The rest of the musculoskeletal examination was normal.\nRoutine laboratory investigations including biochemical tests, complete blood cell count were all normal apart from an elevated ESR (42 mm in 1st hour; normal: <20 mm in 1st hour) and CRP (8.93 mg/L; normal: <5 mg/L). Serological tests for Anti-Nuclear Antibodies (ANA) and hepatitis viruses were negative. Tumour markers and HIV test, as well as test for Brucella antibodies were also negative. The result of tuberculin skin test (5 tuberculin units) was strongly positive with induration of 17 mm diameter. His chest x-ray was normal with no evidence of any active pulmonary disease.\nAn antero-posterior radiograph of the left wrist indicated soft tissue swelling, loss of joint space, gross articular destruction with erosion and cavities throughout the carpus, distal ulna and radius with destruction of the proximal row of carpal bones. Diffuse osteoporosis of the carpal bones was also observed (). A CT scan of the wrist showed total disappearance of bony trabeculae with marked osteoporosis and cortical cysts associated with erosions in the carpal, metacarpal bones, as well as in the ulna and radius. A diagnosis of osteoarticular TB was made depending on the clinical, radiological and pathological (biopsy) findings and he was started on anti-tubercular treatment and wrist arthrodesis performed using a wrist joint spanning plate and cancellous bone graft. Over a three-month period thereafter; his symptoms and functional disability regressed, ESR returned to normal. |
A 21-year-old Asian man visited our hospital with fever, dyspnea, and hemoptysis. He was healthy except for obesity and he was college student (music major).\nThe patient was referred to our hospital while intubated and on oxygen. He underwent elective liposuction surgery under general anesthesia at a local medical center 8 hours before his admission. His body mass index was 32.5 kg/m2. A preoperative evaluation showed no abnormalities and the intraoperative period was uneventful. However, 1 hour after extubation, he became breathless and the hypoxia worsened to oxygen saturation of 50%. Hemoptysis was observed and fever developed. He showed impaired mental state and was transferred to the emergency center of an adjacent hospital. He was immediately intubated and required mechanical ventilation. After chest computed tomography (CT) was performed, he was referred back to our hospital with suspected acute respiratory distress syndrome (ARDS).\nOn evaluation in the emergency center of the adjacent hospital, dyspnea and decreased mentality were observed (Glasgow Coma Scale score 10). After intubation, pinkish and frothy endotracheal secretions were identified, suggestive of pulmonary hemorrhage.\nWhen the patient visited our hospital, his initial vital signs showed blood pressure 111/60 mm Hg, heart rate 119 beats per minute, respiratory rate 20 cycles per minute, and body temperature 37.0℃. However, several hours after arrival, his blood pressure decreased to 64/50 mm Hg, for which an infusion of norepinephrine was started. His initial oxygen saturation was 76% on monitoring. Both pupils responded normally to light and no abnormalities were noted in the conjunctivae and sclerae. Forty hours after the onset of dyspnea, a petechial rash was identified on the left upper chest wall and left axillary region. On auscultation, rales were heard on both upper lung fields and heart sounds were regular with no murmur. Abdominal palpation revealed no signs of hepatomegaly or splenomegaly. Several wounds from the liposuction surgery were clear without signs of infection.\nAt the first visit to our hospital, the patient was intubated and oxygen was supplied by manual Ambu bagging. Initial arterial blood gas analysis showed pH 7.430, PaCO2 29.8 mm Hg, PaO2 57.7 mm Hg, HCO3- 19.4 mmol/L, and SaO2 91.1%. There was bilateral diffuse haziness on a chest radiograph (), and a chest CT similarly showed bilateral diffuse airspace opacities and interlobular septal thickening (). Integration of the patient history, radiologic findings, and symptoms of hemoptysis and pinkish secretion from the endotracheal tube was strongly suspicious of ARDS due to diffuse alveolar hemorrhage by FES. Initial laboratory parameters showed a total leukocyte count 6,400/mm3 (neutrophils, 89.7%; lymphocytes, 8.8%; monocyte, 1.4%), hemoglobin 17.0 g/dL, platelets 187,000/mm3, and C-reactive protein 0.45 mg/dL. All other blood chemistry parameters were within normal limits. The patient's coagulation profile was checked after transfer to our hospital. Prothrombin time was 14.5 seconds (international normalized ratio, 1.35) and the serum D-dimer level was 2.37 mg/L (normal range, <0.80 mg/L). Other investigations included urinalysis and microbiology testing. Fat globules were not detected in the urine and the final blood and sputum culture results revealed no isolated pathogenic organisms. The basic cardiac rhythm on electrocardiography was regular sinus tachycardia. On transthoracic echocardiography (TTE) to evaluate the cause of hypotension, right ventricular enlargement and signs of pulmonary hypertension were noted suggestive of right ventricular failure accompanied by FES. Dilation of the left ventricle with decreased contractile function (ejection fraction, 47%) was also noted.\nUnder the impression of fulminant FES, supportive care was provided that consisted of mechanical ventilation and prophylactic antibiotics. Several hours after hospital arrival, the patient's condition was aggravated by a systolic blood pressure decrease to 64 mm Hg and fever of 39.1℃. The operative wounds were clear and no other sources of infection leading to septic shock were found. Therefore, there seemed to be a low probability of septic shock. Acute heart failure in fulminant FES is thought to be a cause of hypotension. Norepinephrine was started and continuously infused to maintain blood pressure.\nThree days after admission, the patient's medical condition and mentality had improved and the norepinephrine infusion was ceased. His respiratory function gradually recovered and he was successfully weaned from the ventilator on day 6. A repeat chest CT on day 10 revealed much clearing of the bilateral alveolar opacities (). A subsequent echocardiographic evaluation performed on day 13 revealed a normalized left ventricular chamber size and recovered left ventricular contractile function to the lower normal limit. The right ventricular systolic pressure was decreased to 28 mmHg, indicating resolution of the pulmonary arterial hypertension. The patient showed no more symptoms except for a yellowish sputum and was discharged 14 days after admission. |
Mrs. A. is a 37-year-old woman who was admitted to the Neurosurgery Clinic of the University of Pisa. An MRI brain scan revealed a hydrocephalus for a shunt obstruction. The patient had already been treated with surgery and radiotherapy at the age of 30. At that age, during the postpartum period, the patient developed tingling and muscle weakness with abnormal gait. She complained also of a transient demoralization, with loss of energy and apathy, impaired concentration and generalized anxiety. The concomitant severe muscle weakness prompted her general practitioner to prescribe a brain scan. The CT scan revealed the presence of a thalamic glioblastoma for which Mrs. A. was successfully treated with surgery and radiotherapy. A mild left hemi paresis persisted localized in the left hand and leg that improved in few months with physiotherapy. After this event, she was euthymic for 2,5 years, and the mood/anxiety symptoms presented during the postpartum period were considered as secondary to the glioblastoma. Two and a half years after surgery-radiotherapy treatment, she suffered from psychomotor retardation, energy loss, drowsiness, and impaired concentration and memory. In a few days she became comatose. An MRI scan revealed a post-radiation hydrocephalus that was successfully treated with a ventricular-peritoneal shunt placement. She maintained a good physical condition for 5 years. Then, Mrs. A. presented again with psychomotor retardation, apathy and loss of energy. The MRI brain scan revealed a recurrence of the hydrocephalus for a shunt obstruction. The patient was hospitalized and successfully treated with a ventricular-peritoneal shunting replacement. Two days after the shunt replacement, MRI scan revealed the resolution of the hydrocephalus, with a marked reduction of the right lateral ventricles and the re-expansion of the underlying and adjacent brain structures. She was discharged from the Neurosurgery Clinic. Two days after dismissal, she unexpectedly became hyper-talkative and irritable. She developed a subtotal insomnia, with grandiosity, flight of ideas, and persecutory delusions. Two days after, she was referred to the Psychiatric Clinic of the University of Pisa. The neurological assessment was negative (except for a mild residual left hemiparesis localized in the left hand and leg); blood investigations were unremarkable. A neurosurgical clinical consultation and a CT brain scan confirmed the successful ventricular-peritoneal shunting replacement. The patient met the diagnostic criteria for a manic episode with psychotic symptoms. She was treated with typical and atypical antipsychotics (Haloperidol 3 mg/daily and Quetiapine 600 mg/daily) combined with the antiepileptic drugs already prescribed by neurosurgeons (Phenytoin 200 mg/daily and Gabapentin 600 mg/daily). The episode remitted in 7 days, and Mrs. A. was discharged. |
An 81-year-old Caucasian male was referred after he noticed sudden onset of floaters in the right eye followed by rapid loss of vision 4 h after receiving his 6th IVT bevacizumab injection for macular edema caused by central retinal vein occlusion according to records provided by the referring physician. His past ocular history was significant for cataract surgery with implantation of an in-the-bag posterior chamber IOL OU 19 years ago, and disciform scar in the left eye secondary to neovascular age-related macular degeneration. He denied history of high myopia and the emmetropic IOL power in the right eye was +20 D. His past medical history was significant for atrial fibrillation with CHA2DS2-VASC score of 5 (2 for age, 1 each for hypertension, congestive heart failure, and type 2 diabetes) for which he was on warfarin for stroke prophylaxis with international normalized ratio maintained between 2.5 and 3 []. His systemic medications included 81 mg aspirin/day for stable ischemic heart disease and other medications for hypertension, oral hypoglycemic agents, and high cholesterol. His visual acuity at presentation was hand motions in the right eye and 20/400 in the left. The intraocular pressures were normal OU. The anterior segment examination showed a well-centered PCIOL with open capsules from prior YAG capsulotomies OU. The dilated fundus examination of the right eye showed dense vitreous hemorrhage (VH) without any view of the optic nerve or retina. The left eye showed a normal nerve and a disciform scar in the macula. An ultrasonography of the right eye showed vitreous opacities but no RD.\nThe patient underwent a 25-g pars plana vitrectomy 8 days after the onset of symptoms and after withholding warfarin for 3 days without bridging with low-molecular-weight heparin (online suppl. Video; for all online suppl. material, see ) []. The international normalized ratio was 1.6 (subtherapeutic) on the day of surgery. After clearing the VH, a round retinal hole with surrounding retinal hemorrhages was noted at the inferotemporal periphery in the same region as the site of last IVT injection. The retinal break was treated with endolaser (Fig. ). The patient had an uneventful recovery with return of vision to 20/30 three months after surgery. Dilated fundus examination showed a well-lasered break at the inferotemporal periphery and scattered retinal hemorrhages consistent with old central retinal vein occlusion (Fig. ). |
Absence of retinal vessel pulsation was noted in a twelve-year-old boy during a routine ophthalmology assessment. He had presented with bilateral congenital glaucoma as an infant requiring surgical correction and hence long-term ophthalmology screening. At the age of eighteen months he had a right seventh nerve palsy that lasted 4 months and subsequently resolved; at the age of two years he developed acute, unexplained cardiac failure with evidence of dilated cardiomyopathy. He was commenced on digoxin, captopril, and frusemide and his cardiac contractility gradually recovered. The underlying cause of cardiomyopathy was never determined.\nBetween the ages of four and ten years he attended school full time. He had reduced stamina and a long history of calf claudication with a claudication distance of 200 m. He reported recurrent episodes of chest and left arm pain but no unexplained fevers and no cutaneous lesions. His growth parameters were normal (weight and height 50th centile for his age and sex). On examination, he had absent femoral, popliteal, dorsalis pedis, posterior tibialis, and brachial and radial pulses bilaterally. Centrally located abdominal and renal flank bruits were noted. Routine laboratory markers of inflammation (white cell count, erythrocyte sedimentation rate, C reactive protein) were normal, as were routine haematological and biochemistry panels. Antinuclear and antineutrophil cytoplasmic antibodies were negative. Peripheral blood cytokine analysis (TNF alpha, IL-6, and IL10) was normal; in addition he had a normal circulating endothelial cell (CEC) count of 20 cells per mL of whole blood []. It was noted however that he had a reversed CD4 : CD8 ratio (32% : 40%, resp.).\nMultiple radiological investigations were undertaken to assess for on-going active large vessel vasculitis and/or late stenotic sequelae. Radiological investigations collectively revealed widespread arterial disease with occlusion of the subclavian, common iliac, and proximal tibial and peroneal arteries (Figures , , and ). On computer tomography (CT) angiography, and conventional catheter digital subtraction arteriography the descending abdominal aorta was irregular and tapered distal to the renal arteries with severe proximal bilateral renal artery stenosis (). The abdominal aorta was thread-like up to the level of the common iliac arteries with some irregular calcific plaque demonstrated on the CT scan (Figures and ). He had an extensive collateral circulation throughout his arterial tree supplying his limbs.\nA half body PET-CT (positron emitting tomography, PET) was performed using fludeoxyglucose (FDG) that showed no uptake of FDG in the large vessels. Echocardiogram showed slight left ventricular impairment with a normal aortic arch, confirmed on angiography, and the coronary arteries appeared normal although selective coronary arteriography was not undertaken.\nThe clinical history, symptoms, absence of acute phase response, and imaging appearances were compatible with a large vessel vasculitis, currently inactive and in the late stenotic phase of the disease. The exact time of disease onset was unknown. The only positive investigation was a reversed T cell (CD4 : CD8) ratio, and with no FDG uptake on PET-CT, the presence of extensive arterial stenotic lesions, absence of acute phase response including normal peripheral blood cytokines, normal CECs, and aortic intramural calcification, we considered the disease to be in the late fibrotic/stenotic stage. It was therefore felt that immunosuppression was unlikely to confer any benefit. Since there was no obvious angioplasty/revascularisation target; management consisted of a careful and graded return to activity and lifestyle advice to minimise conventional cardiovascular risk factors in the future.\nAt the age of 14 years he collapsed suddenly; resuscitation attempts were unsuccessful. Postmortem examination revealed severe left ventricular hypertrophy and 70% occlusion of the coronary arteries. The abdominal aorta was narrowed with a patchy and sparse chronic inflammatory cell infiltrate and evidence of active inflammation within the vasa vasorum of the distal aorta. There was marked intimal fibrosis with calcification and collateral vessels, as noted on previous imaging. |
An 11-year-old boy presented with complaints of frequent cough and fever since the age of 5 years. The child was initially investigated elsewhere and diagnosed as a case of pulmonary tuberculosis. He had received antitubercular treatment for 1 year. After temporary relief, his symptoms recurred and the sputum showed presence of acid fast bacilli. The child was restarted on antitubercular treatment, which was administered for 2 years. Radiological investigations revealed the presence of a left intrathoracic mass. The child underwent thoracotomy and biopsy elsewhere. The biopsy was suggestive of inflammatory myofibroblastic tumor of the lung. The child was started on prednisolone but remained symptomatic. Subsequently, the child was referred to our institution for definitive treatment. His general condition was good and there was no evidence of respiratory distress. On examination, the movements of the chest wall were diminished on the left side. The left hemithorax was dull on percussion and the air entry was absent. The right side was normal. Chest radiograph showed the presence of a homogenous opacity in the left hemithorax with large areas of calcification in the hilar region. A contrast enhanced CT scan of the chest revealed a large soft tissue mass in the left lung with dense calcification and collapse of the lung. The child underwent thoracotomy; there was a soft tissue mass arising from the left lung and densely adherent to the pericardium, aorta, and thymus. Large mediastinal lymph nodes were present and the left pulmonary vein and artery were encased by the mass. Complete excision of the mass along with the involved pericardium and left pneumonectomy was performed. The child suffered a cardiac arrest during surgery but was revived immediately. Postoperatively, the child required ventilator support for 7 days. The child was subsequently discharged in a stable condition with no neurological deficit. The histopathological examination confirmed the diagnosis of inflammatory myofibroblastic tumor []. |
A 18-years-old male, working in the screen-printing industry for the last 4 years, presented with complaints of numbness in both feet and impaired ground sensations in both feet for one and a half years. Within 9 months of the onset, the numbness progressed up to the knees. After another 3 months, he developed numbness in both hands up to the wrist. For about a month prior to presentation, he started experiencing dizziness, diplopia on looking towards both side, and oscillopsia. He also had a sense of lassitude, lack of interest in his work and excessive sleepiness. There was a change in his voice as if drunk. He was spending more time and even sleeping in his workshop for the last one month. His symptoms further worsened and he developed imbalance while walking and needed support to walk. For the past 1 week, he was bed bound. He denied fever, rash, joint pains, use of alcohol, drug abuse and glue-sniffing. Four of the seven people working with him had similar sensory complaints in their limbs but of variable magnitude.\nPhysical examination revealed desquamation of the skin over his palms. Higher mental functions, visual acuity, field of vision, color vision and both fundii were normal. He had cerebellar dysarthria, bilateral lateral rectus palsy, downbeat nystagmus and bilateral lower motor neuron facial palsy. All other cranial nerves were normal. All his limbs were hypotonic with normal power, and besides brisk knee jerks, all other reflexes were absent. Sensations of touch and pain were diminished in a glove-stocking distribution, while vibration was diminished in both lower limbs up to the level of the anterior superior iliac spine and in both upper limbs up to the level of radial styloid process. Joint position sensation was impaired in both lower limbs. Romberg's sign was positive.\nHis hemogram, and biochemical profile for blood sugar, LFT, blood urea, creatinine, serum electrolytes, acid base levels, thyroid profile, calcium, phosphorus were normal. Cerebro spinal fluid (CSF) examination was normal. C reactive protein (CRP) and rheumatoid arthritis (RA) factor, antinuclear antibody (ANA), double stranded DNA (ds-DNA), cytoplasmic antineutrophil cytoplasmic antibodies (c-ANCA), perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA), anti Ro, anti-La antibodies, HIV, Hepatitis B surface antigen (HBsAg), anti hepatitis C virus (HCV) were negative. Roentgenogram of Chest, electro cardiogram (ECG) and ultra sound examination of abdomen were normal. Urinary 2, 5-HD levels [qualitative] were high.\nNerve conduction studies [] revealed prolonged distal latency in both common peroneal (CP) and posterior tibial (PT) nerves, decreased CMAP amplitude of left CP, and both PT nerves, and partial conduction block [distal/proximal amplitudes and % drop; Right CP: 6.7/3.2 mV (52.2%); Left PT: 3.0/1.5 mV (50.0%)] in right common peroneal and left posterior tibial nerves. There was slow conduction in both common peroneal and posterior tibial nerves. The F wave was prolonged in both lower limb nerves along with chronodispersion of 6. 7 ms [normal ≤6 ms], in bilateral posterior tibial nerves. Temporal dispersion was not encountered in any of the studied nerves. Sensory nerve conduction studies revealed decreased Sensory nerve action potential (SNAP) amplitudes in both median and ulnar nerves while sural and superficial peroneal SNAPs, on both sides, were not recordable. However, dorsal ulnar cutaneous SNAPs were normally recorded. Needle Electromyography (EMG) revealed changes of chronic denervation in extensor digitorum brevis, and first dorsal interosseous, bilaterally. Grade one fibrillations were recorded from right Tibialis anterior and left Flexor digitorum sublimus. EMG of quadriceps, medial gastrocnemius, brachioradialis, pronator teres, biceps, deltoid, on both sides, was normal. The pattern evoked VEP revealed prolonged P100 latency (left: 137 ms; right: 144 ms.; normal, ≤104.5 ms) [Figure and ] Brain stem evoked responses were within normal limits. Somatosensory evoked potential recording with stimulation of the median nerve revealed normal N 20 latency on both sides while P37 with stimulation of the posterior tibial nerve could not be recorded, from either side. Facial nerve study revealed normal distal latencies, while the CMAP amplitude was comparatively low on the left side (left, 2.7 mV; right, 3.9 mV, normal, ≥1.0 mV). Blink reflex study on stimulation of the supraorbital nerve revealed normal latency of R1 and R2, on both sides. However, the difference in latency between Ipsilateral R2 and Contralateral R2 was 6.15 ms [normal, <5.0 ms], on the left side [] and 2.4 ms, on the right side. R/D ratio [R1/direct facial nerve latency] was 3.70 [normal, 2.6-4.6]. magnetic resonance imaging (MRI) brain was normal. Biopsy of the right sural nerve showed loss of large diameter myelinated fibers with no evidence of inflammation or fibrosis []. The patient was managed symptomatically. By the seventh day of his admission, his downbeat nystagmus had resolved completely and by the 10th day, both the 6th and 7th nerve palsies disappeared. Ataxia also showed marked improvement in the first week, however, tandem walking remained impaired even at the end of two and a half months. The deep tendon jerks remained the same. On 70 days of follow up, his electrophysiological evaluation revealed normalization of the blink reflex study []. The R/D ratio was 3.21. There was improvement in P100 latency [left: 114 ms; right: 120 ms Figure and ], non recordable sensory potentials in both sural and superficial peroneal nerves and decreased SNAP amplitude in both median and ulnar nerves. The distal latencies of both lower limb nerves [Rt. CP 9.6 ms; Lt. CP 10.6 ms; Rt. PT 9.75 ms; Lt. PT 10.50 ms] had further prolonged with F wave showing chronodispersion in right common peroneal [6.30 ms] and left posterior tibial nerves [9.70 ms] along with prolonged minimal latency, in all the motor nerves studied of both upper and lower limbs.\nThe chemical analysis of the liquid used in his place of work revealed n-hexane. Suitable instructions were given, regarding the handling of n-hexane, to the patient and his co-workers. |
A 45-year-old lady presented with complaints of diminished vision for distance and near in the right eye for the past 3 months. She had no other ocular complaints. On examination, the best-corrected visual acuity was counting fingers at 2 m in the right eye and 20/20 N6 in the left eye. Anterior segment evaluation, intraocular pressures, and ocular motility were normal in both eyes. No proptosis was noted. Right eye fundus showed a serous retinal detachment with underlying diffuse, subretinal yellowish-cream colored infiltrates whereas the left eye was normal []. The infiltrates were largely situated on and around the posterior pole with the periphery being uninvolved. The vitreous cavity was clear with no signs of inflammation. Fundus fluorescein angiography showed hypofluorescence during the arterial phase and progressive hyperfluorescence during the subsequent phase. Pin-point discrete leakages were seen from the multiple lesions in the late phase along with disc leakage []\nA clinical diagnosis of choroidal metastasis was made, and a detailed systemic history was elicited in order to localize a primary tumor. Her systemic history was significant: She gave a history of frequent headaches and a six month history of menorrhagia. A metastatic screening in the form of ultrasound of the abdomen, liver function tests, serum lactate dehydrogenase, and a gynecological consult were requested. Gynecological examination revealed an ulcerative mass arising from the cervix measuring approximately 4 cm × 4 cm × 3.5 cm, which bled on touch. A biopsy of the mass was performed which confirmed the diagnosis of poorly differentiated adenocarcinoma of the cervix with perivascular and perineural invasion. High resolution computed tomography (CT) scans of the chest showed multiple pleuroparenchymal metastatic nodules [Fig. and ]. Positron emission tomography CT–(PET-CT) scan was performed which showed a bulky uterine cervix with increased metabolic activity. Multiple, hypermetabolic enhancing right supraclavicular, retropectoral, and mediastinal lymph nodes were noted. Multiple, hypermetabolic pleuroparenchymal lung nodules were also seen []. Hypermetabolic erosive lesions were seen involving the left parietal skull and a hypermetabolic lytic lesion seen in the subtrochanteric shaft of the left femur. A diagnosis of the International Federation of Gynecology and Obstetrics (FIGO) Stage IVb (American Joint Committee on Cancer staging–T3a N1 M1) adenocarcinoma of the cervix was made. In view of disseminated metastasis, she was advised for palliative chemotherapy and whole body radiation. She, however, declined treatment and succumbed to respiratory complications 2 months after diagnosis. |
In a 58-year-old man with a history of arterial hypertension and mild hypercholesterolaemia, an aortic ectasia was detected during an echocardiogram performed to evaluate for hypertension-related preclinical cardiac damage and, due to this finding, echocardiographic follow-up was suggested. Three years later, the patient was admitted for coronary angiography (CA) after the computed tomography (CT) finding of a suspected occlusion of the LM with collateral circulation from RCA to LAD and Cx (). The indication for CT consisted of providing a more precise evaluation of the ascending aorta tracts which were not adequately explored by echocardiography. The patient was asymptomatic despite an active lifestyle and the physical examination was unremarkable. Cardiac auscultation revealed that cardiac sounds were rhythmic and no additional sounds (3rd or 4th sound) or bruits were audible; peripheral pulses were palpable, and no vascular bruits were heard as well as no clinical signs of heart failure were observed. Electrocardiogram was normal. Echocardiogram showed left ventricular concentric remodelling with normal systolic function (ejection fraction 65%), dilatation of the ascending aorta (45 mm) and a tricuspid aortic valve with mild aortic regurgitation. Routine laboratory tests were within normal limits.\nCA showed LMCA as demonstrated by contrast injection into the left sinus of Valsalva (). The left coronary artery was retrogradely supplied from the RCA through Rentrop 3 grade coronary collaterals whose calibre was similar to that of the target left-sided vessels (). No obstructive coronary artery disease (CAD) was detected. In order to exclude potential myocardial ischaemia, a technetium-tetrofosmin cardiac single-photon emission computed tomography (SPECT) was performed during maximal exercise-stress testing, which did not show a perfusion defect (). During weekly Heart Team meetings, preventative CABG was not deemed to be indicated since the patient was asymptomatic, without evidence of inducible ischaemia. The patient was discharged with targeted medical therapy to prevent atherosclerosis of this single coronary artery. Clinical follow-up with periodic transthoracic echocardiograms was planned; however, with the plan to follow-up earlier in the case of new symptom development. At 9-month follow-up, the patient was asymptomatic and in a stable clinical condition. |
A 42-year-old woman presented with a 3-month history of bloody discharge from the urethra and lower back pain. Physical examination performed showed no remarkable changes on admission. She did not show urinary dysfunction. Laboratory data of the blood were within normal limits. Serum levels of tumor markers were not evaluated. Cytological examination of the urine sediment was highly suggestive of adenocarcinoma. Computed tomography (CT) and magnetic resonance imaging (MRI) showed a tumor (diameter, 47 mm), which involved the urethra entirely []. There were no remarkable changes in the gynecological system and no swelling was observed in the intra-abdominal and intrapelvic lymph nodes. Cystourethroscopy showed two diverticula fenestrated in the urethral wall. Whitish papillary and villous lesions were observed in both diverticula []. Specimens of biopsy and TUR histologically suggested CCA, but were indeterminate for malignancy. The patient underwent total cystourethrectomy and partial resection of the vaginal wall. Grossly, the tumor extended around the entire urethra and anterior vaginal wall. Final diagnosis of the resected tumor was CCA stage III pT3N0M0.\nThe Papanicolaou-stained specimens showed a small number of papillary or spherical clusters of atypical cells with many benign urothelial cells and squamous cells in the background [Figure and ]. A few neutrophils and lymphocytes were seen, but no necrotic debris was seen. The nuclei of the atypical cells showed an increase in the chromatin content with fine to granular pattern and irregular contours []; the nucleoli were prominent. Most of the atypical cells had a moderate amount of cytoplasm that was lightly stained light green; however, some atypical cells showed clear, abundant cytoplasm that formed spherical clusters resembling “mirror balls” []. These findings suggested a malignant tumor of the urinary system and favored adenocarcinoma.\nThe biopsy and TUR samples showed that the tumor comprised papillo-tubular lesions []. The epithelial cells covering the tumor were cuboidal and single layered, and some of these cells showed a “hobnail pattern.” Most of the cells had eosinophilic cytoplasm, except for a few that had clear cytoplasm. The cells with a clear cytoplasm were positive for periodic acid-Schiff reaction. The epithelial cells showed relatively mild cytological atypia and did not invade the stroma. Mitotic figures were observed at a frequency of 10/10 high-power fields. Necrotic debris was frequently observed in the lumen of the tubular structures. In immunohistochemistry, the tumor cells were positive for cytokeratin (CK) 7 [SP52, ready-to-use (RTU) prediluted, Ventana Medical Systems, Tucson, AZ, USA], epithelial membrane antigen (EMA) (E29, RTU prediluted, Nichirei Bioscience, Tokyo, Japan), and carbohydrate antigen (CA) 125 (M11, 1:25, Dako, Glostrup, Denmark), and were also focally positive for CD15 (80H5, RTU prediluted, Immunotech, Marseille, France)\n[]. The tumor cells were negative for CK 5/6 (D5/16 B4, 1:50, Dako), CK 20 (SP33, RTU prediluted, Ventana Medical Systems), carcinoembryonic antigen (12-140-10, RTU prediluted, Leica Microsystems, Milton Keynes, UK), thrombomodulin (1009, 1:50, Dako), uroplakin III (AU1, RTU prediluted, Nichirei Bioscience), prostate-specific antigen (polyclonal, Dako), calretinin (5A5, RTU prediluted, Leica Microsystems), estrogen receptor (6F11, 1:50, Leica Microsystems), and progesterone receptor (312, 1:50, Leica Microsystems). Histological findings suggested diagnosis of CCA, although definite diagnosis of the malignancy could not be elicited because of absence of stromal invasion in both biopsy and TUR samples. In the surgically resected specimens, clear atypical cells with papillo-tubular structure invaded almost all layers of the urethra and vaginal muscular layer. The final definite diagnosis was CCA.\nThe Ki-67 labeling index of these tumor cells was approximately 20% [] and approximately 5% of the tumor cells showed strong p53 positivity in the nucleus. |
We report a 57-year-old male with history of extensive prior tobacco use, nonischemic cardiomyopathy, and an Eastern Cooperative Oncology Group (ECOG) performance status (PS) of 3. After successfully completing his initial evaluation, he was deemed cancer-free and eligible for cardiac transplantation. Due to severe heart failure despite standard medications, he received mechanical cardiac support with an LVAD. Three months after surgery for the LVAD, he was noted to have mediastinal widening on a chest X-ray performed for dyspnea and cough. CT scans showed mediastinal lymphadenopathy without evidence of disease outside the chest (Figures and ). Renal and liver functions were within normal limits. The patient underwent mediastinoscopy and the pathologic examination was consistent with SCLC. Due to headaches and distended neck veins, he was evaluated for superior vena cava syndrome. The patient was removed from active consideration for cardiac transplantation. After extensive discussion with patient and his family, chemotherapy was administered while hospitalized for close monitoring. He received carboplatin (area under the curve (AUC) 5) on day 1 and intravenous (IV) etoposide 100 mg/m2 on days 1–3. Patient received IV dolasetron 100 mg for 30 minutes on days 1–3 and IV prochlorperazine 10 mg every 6 hours as needed. The patient did not receive any prophylactic antibiotics. Carboplatin was used instead of cisplatin due to concerns over aggressive hydration and inducing volume overload. The radiation oncologist had an extensive discussion with the patient and the multidisciplinary team including the LVAD manufacturer and provided the information about the risks, benefits, and complications of concurrent radiation treatments. The patient ultimately decided not to pursue any radiation treatment.\nThe treatment course was complicated by cellulitis, neutropenic fevers with pseudomonas aeruginosa infection, and protracted nausea and vomiting. The patient was treated with prolonged IV antibiotics course including aztreonam and ciprofloxacin. The patient received oral dolasetron 100 mg on day 4 and subcutaneous pegfilgrastim 6 mg on day 4 after completion of chemotherapy. Anticoagulation with warfarin was started. Although the renal function remained within normal limits, the patient developed signs of worsening overload with left-sided pleural effusion and peripheral edema. Subsequently he became weaker with weight loss of about 25 pounds. After his first cycle of chemotherapy, the patient elected not to receive further chemotherapy and workup. Patient was discharged home under hospice care and passed away about 6 months after the administration of chemotherapy. |
A 59-year-old man presented to the urgent care clinic at the School of Dentistry complaining of an upper lip mass for one-year duration. The mass started out as a small bump and had grown steadily since then. 3 months prior to his presentation, a draining parulis developed on the mass. The patient had no history of systemic symptoms such as fever, chills, weight loss, or fatigue. He was aware of a dark-colored “dead tooth” for several decades in the area of concern but denied any previous history of swelling in the area. The patient had recently moved to the United States from Nigeria and had previously been without access to adequate dental care. The patient said that a doctor in Nigeria told him that the lesion was likely cancerous.\nOn exam, there was a large, painless, fibrous, exophytic mass in the anterior maxillary labial vestibule (Figures and ). The base of the mass approximated the apex of tooth #8. A yellow purulent material was observed draining from the parulis (). Tooth #8 was discolored and was confirmed to be nonvital on pulp testing. There was a significant gap between teeth #7 and 8. Tooth #8 was displaced medially and was extruded relative to the adjacent dentition.\nA periapical radiograph revealed a large unilocular radiolucency associated with the apex of tooth #8 (). Cone-beam computed tomography again demonstrated a large cystic-appearing defect in the anterior maxilla with perforation of the buccal and palatal cortices . The lesion extended to the nasal floor on the ipsilateral side.\nThe patient was referred to the oral surgery department for excisional biopsy. After tooth #8 was removed, an incision was made around the base of the stalk that connected the mass to the labial and alveolar mucosa. Sharp dissection was used to free the mass, and the specimen was sent for histopathologic analysis. The mass communicated with a cystic lesion of the maxilla. The cyst was enucleated with a curette and also sent for pathology. Perforation of the cyst through the buccal and palatal cortices was noted during the procedure. Slight undermining of the wound margins allowed for closure with resorbable sutures.\nAt the patient's one-week follow-up (), he was doing very well. He reported minimal pain, no neurosensory disturbances, and no systemic or local symptoms of infection. He and his family were very relieved to learn that the lesion was benign. He was happy with his appearance after having the mass removed. |
A 51-year-old Moroccan Berber man was referred to our hospital with a history of three months of intermittent painless total gross hematuria, frequency and urgency. The medical and familial histories were unremarkable. Ultrasonography revealed a grade II left hydronephrosis and circumferential thickening of the urinary bladder wall. A computed tomography (CT) scan showed a diffuse neoplasm of the urinary bladder with no lymph node enlargement or distant metastases (Figure ). Cystoscopic examinations revealed nonpapillary sessile tumors occupying almost the whole of the bladder wall (Figure ), and the left side of the trigone obstructing the left ureteral meatus. Transurethral resection of the lesion was realized incompletely because of the diffuse character of the tumor. Histopathological specimen examination found a poorly differentiated mucin-secreting adenocarcinoma of the signet-ring cell type (Figure ).\nWe performed a complete gastrointestinal endoscopic evaluation and analysis of tumor markers to exclude an extravesical primary tumor site, but no other primary site was found. The tumor was therefore treated as a primary signet-ring cell carcinoma of the urinary bladder.\nThe patient underwent radical cystectomy with an ileal conduit and bilateral pelvic lymphadenectomy. Histopathological examination of the surgical specimen reported adenocarcinoma composed of signet-ring cells with an abundant mucin pool that was invading the perivesical adipose tissue and one lymph node (<2cm) staging the tumor at pT3bN1M0. Adjuvant chemotherapy was then performed with four cycles of cisplatin, a 100mg/m2 on day 1 and gemcitabine 1000mg/m2 on days 1 and 8 combination, every 21 days. The patient was followed up every six months, and a thoracoabdominal CT scan was done every six months. He was free from metastasis, the quality of life was good without symptoms of pain or renal dysfunction, and he achieved weight recovery soon after finishing his chemotherapy. Eighteen months postoperatively, the patient presented with pelvic and back pain. Multiple metastases to spine, lung and pelvis were noted on a thoracoabdominal CT scan. The patient refused to be enrolled in any additional protocol and died four months later due to respiratory distress. |
A 28-year-old female with insignificant past medico surgical history presented with one day of acute onset pain in the periumbilical region that later migrated and confined to the RIF. She had associated intermittent fever, nausea, and loss of appetite. She did not have any urinary symptoms, bowel irregularities, or gynecological complaints. Abdominal examination was performed by two senior surgeons at two different occasions; the same day had findings of guarding and rebound tenderness at RIF. Hematological tests showed polymorphonuclear leukocytosis with left shift. Biochemical tests and urinalysis were normal. Urinary pregnancy test was negative. Abdominal radiographs were unremarkable. USG could not visualize appendix and was inconclusive except for probe tenderness in RIF. CT scan of the abdomen could not be done due to unavailability. A clinical diagnosis of acute appendicitis was made assigning an Alvarado score of 9/10. Laparotomy was performed using the Lanz incision in RIF. Intraoperatively appendix was found to be normal without evidence of inflammation or infection in RIF. In view of symptoms and signs, a possibility of other pathology was thought. Walking the bowel proximally up to 3 feet (1 m) did not show a Meckel's diverticulum or any other small bowel lesions. There were no obvious mesenteric lymph nodal enlargement and pelvic organs looked pristine. Approaching closure, just when the medial edge of the incision was retracted superomedially, a hemorrhagic lesion seemed to appear little deeper in the mid abdomen. Therefore, the incision was extended transversely from the medial edge to explore further. Entire bowel was explored and this revealed an ulcerated lesion measuring 7 × 5 cm arising from the antimesenteric border of the ileum 8 feet (2.5 m) from ICJ with localized interloop hemoperitoneum and inflammatory exudates as shown in . Resection of ileal segment containing the lesion was performed followed by restoration of bowel continuity and peritoneal toileting. The lesion was subsequently reported to be an ulcerated malignant ileal GIST.\nHistopathologically, gross examination confirmed the operative findings, and the cut section revealed a nodular lesion protruding out of the serosal surface measuring 7 × 5 cm along with 2 lymph nodes each measuring 2 × 1 cm.\nMicroscopically, the growth from the ileum had villous lining epithelium with focal ulceration. The submucosal region had a circumscribed nodule with proliferation of loosely cohesive spindle cells; some of which were arranged in vague storiform pattern and others in long fascicles. There were areas with epitheloid cells forming small anastomosing nests and cords. The areas in between these showed skenoid fibers along with focal areas of hemorrhage, infarction, and congestion as shown in . The mitotic figures were seen (8/50 high-power field). The lymph nodes were microscopically identified to be reactive, and the resected margins of the ileum were free of tumor.\nBased on tumor size and mitotic activity, possibility of a malignant GIST was suggested along with immunohistochemical analysis (CD117 and CD34) for further confirmation. The patient had an uneventful recovery and was discharged on the 8th postoperative day. She was advised to review a week later at the outpatients but failed to report. All possible contacts were used to trace her, but she remained inaccessible and lost to follow-up. |
A 74-year-old woman visited our station with squamous cell carcinoma (SCC) on the right buccal mucosa. Her past medical history included chronic obstructive airways disease, hypertension, and diabetes mellitus. The patient is a current smoker, with a history of 20 pack-years. Preoperative chest radiography, electrocardiogram, full blood count, and serum biochemistry were within the normal range. After being diagnosed with SCC as a result of incisional biopsy, the patient underwent the resection of SCC on the right buccal mucosa of the mandible, modified radical neck dissection, and primary reconstruction with a fibula-free flap. Tourniquet pressure was 300 mm/Hg, and its application time was 60 min. Total on-table time was approximately 7 h. Upon admission to the SICU after the 7-h operation, hypothermia and hypotension were noted. On the first postoperative day, the patient exhibited oliguria and proteinuria and elevation of CK, AST, ALT, and LDH. Together with the nephrology and neurology staff, we tried to figure out our patient’s symptoms and clinical findings. We thought that her clinical picture was based on an impression in which acute renal failure was diagnosed as secondary to rhabdomyolysis. Thus, she was managed with high-dose loop diuretic therapy. Additionally, we gave her hepatotonic to recover her liver function. The patient was supplemented with 150 to 250 mL/h of lactated Ringer’s solution and 0.9% NaCl. When the volume was full, urine output of above 100 mL/h was maintained by 20 mg intravenous injection with furosemide.\nHer urine output for the first hour is at 20 mL/hour, but after the medication, her urine output began to improve on day 4 with a corresponding reversal in the serum creatinine. After postoperative day 4, the muscular enzyme showed a downward trend. We treated the patient with medication and hydration, and then the result became favorable. In the end, she was able to recover fully from the symptoms. Figures and show the change in serum enzyme levels during hospitalization (Figs. and ). |
A 75-year-old Sri Lankan female with a background of hypertension and ischemic heart disease presented with a history of pain, blurring of vision, photophobia, and redness of her left eye of about 6-h duration. She admitted that she received the first dose of zoledronic acid 4 mg in 100 mL normal saline intravenously over a period of 15 min on the previous day. She denied any history of trauma, fever, or headache.\nShe was diagnosed with post-menopausal osteoporosis 2 years ago after having a dual-energy X-ray absorptiometry (DEXA) scan when she presented with mechanical lower back pain. She was initiated on oral alendronate 70 mg weekly along with calcium and vitamin D supplements. She had been taking them regularly since then without reporting any side effects. In spite of good adherence to treatment, she failed to be symptom free and had continued to experience intermittent mechanical lower back pain. Subsequently, she underwent a repeat DEXA scan which showed a T-score of −5.1 over her lower lumbar vertebra with no significant improvement compared to the previous T-score. Accordingly, the clinical team decided to switch her to zoledronic acid as a substitution for oral alendronate and she was given 4 mg of zoledronic acid in 100 mL of normal saline as an intravenous infusion over a period of 15 min on the day before admission.\nPhysical examination revealed a hyperemic conjunctiva on the left eye with best corrected visual acuity of 6/9 and 6/6 on left and right eye, respectively. Intraocular pressure was 14 mmHg in the right eye and 10 mmHg in the left eye. Slit-lamp examination of left eye revealed conjunctival hyperemia, fine few keratic precipitates, cells and flare in the anterior chamber () with normal posterior segment. Her right eye was normal. There was no evidence of proptosis, periorbital edema, ptosis, or ophthalmoplegia. Rest of the general and systemic clinical examinations was unremarkable with a blood pressure of 130/80 mmHg. Her initial investigations showed elevated C-reactive protein (CRP) (84.4 mg/L) and erythrocyte sedimentation rate (ESR) (65 mm at the first hour) with no significant abnormalities detected in rest of the basic investigations. A diagnosis of acute non-granulomatous anterior uveitis of the left eye secondary to zoledronic acid was made and she was started with topical prednisolone. She was also evaluated for any other conditions that may cause acute anterior uveitis. Subsequent investigations (complete blood count, angiotensin-converting enzyme level, X-ray chest, rheumatoid factor, human leukocyte antigen B27 (HLA-B27), perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA), cytoplasmic ANCA (c-ANCA), and serology for infective causes, namely, Epstein–Barr virus, Cytomegalovirus (CMV), human immunodeficiency virus (HIV), Venereal Disease Research Laboratory test (VDRL), and polymerase chain reaction (PCR) for Varicella zoster) did not show any abnormalities.\nShe responded well clinically to the treatment and achieved complete resolution of symptoms by the end of 2 weeks along with the normalization of CRP to 3.1 mg/L. Thereafter, she had been followed at the ophthalmologic clinic for 6 months, during which she never experienced recurrence of any similar episodes. At the 6-month review, she was asymptomatic and findings on ophthalmological examination showed persistent and complete resolution of ocular signs (). |
A 29-year-old woman came to the emergency room with massive hemoptysis, producing more than 300 mL of fresh blood. Approximately 6 weeks prior, she had developed sudden massive hemoptysis for the first time. Before the initial event, she did not have any previous medical history or medication history. She had gone to a neighboring hospital, and then undergone endoscopic hemostasis.\nFor further evaluation and management, she was referred to our hospital. On physical examination, the patient was afebrile, blood pressure was 100/70 mm Hg, heart rate was 80 beats per minute, respiratory rate was 20 breaths per minute, and oxygen saturation 98% on room air. Head and neck examination showed normal dentition with no lymphadenopathy. Chest examination showed clear breath sounds bilaterally with decreased air entry in the left lower lobe. Abdominal and cardiac exams were unremarkable. The results of a complete blood count were normal, except for hemoglobin (11.0 g/dL). An arterial blood gas analysis showed pH 7.41, pCO2 34 mm Hg, and PO2 79 mm Hg. Chest radiograph had no abnormal findings.\nShe experienced persistent dry cough with expectoration of more than 200 mL blood at once, and her hemoglobin level decreased from 11.0 g/dL to 9.5 g/dL. For management of massive hemoptysis, thoracic aortogram and left bronchial angiogram was performed, and it revealed aberrant bronchial artery with tortuous dilatation arising from the T9 vertebrae level of descending thoracic aorta and parenchymal blush of left upper lobe (). Left aberrant bronchial artery was selected, and spinal artery branch was seen on bronchial angiography. Selective catheterization was performed for stabilization of the microcatheter within the bronchial artery and safe positioning in the bronchial circulation beyond the origin of spinal cord branches, an approach that prevents severe complication. Left aberrant bronchial artery embolization was performed successfully using a 3 mm×2 cm stainless steel platinum coil (Tornado; Cook Medical Inc., Bloomington, IN, USA). This procedure resulted in control of the hemoptysis, and no procedure-related complications occurred. She was discharged.\nOn her second visit, her hemoglobin level was 11.7 g/dL; however, her follow-up hemoglobin level dropped to 9.6 g/dL and revealed a blood pressure of 92/46 mm Hg and a pulse rate of 73 per minute. Chest radiograph showed focal increased parenchymal opacities on left lower lung field, and multidetector computed tomographic angiography (MDCTA) showed a dilated left bronchial artery arising from thoracic aorta, a finding that was suggestive of the bleeding focus due to blood clots in left upper lobar lingular segment, left lower lobar, and segmental bronchus (, ). Left aberrant bronchial artery arteriography still showed tortuous dilatation and marked parenchymal contrast stain. It was difficult to achieve a selective and stable catheterization within the bronchial artery. Moreover, angiographic findings showed subintimal dissection of the origin site of the left aberrant bronchial artery and extravasations of contrast medium. Therefore, selective catheterization of the bronchial artery was stopped. Subsequently, she was admitted to the intensive care unit for close monitoring. The patient developed further hemoptysis with acute worsening of oxygenation.\nSurgery was deemed the procedure of choice in the treatment of massive recurrent hemoptysis. The patient underwent left upper lobectomy, and histopathologic examination of the resected specimen showed intra-alveolar hemorrhage with vascular congestion. The operation and the postoperative period were uneventful and the patient was discharged from the hospital after 5 days in good clinical condition. She has been well since then without any hemoptysis. |
A 29-year-old man presented with a half-month history of paroxysmal upper abdominal pain that gradually evolved into continuous pain and was accompanied by the urge to defecate. He went to the local hospital on June 9 where he underwent the following diagnostic investigations: upper abdominal computerized tomography (CT) scan, routine blood tests, gastroscopy, and colonoscopy. No abnormalities were observed on CT. The results of routine blood tests are shown in Table . Gastroscopy revealed gastritis, whereas colonoscopy showed a normal colonic mucosa (Fig. ). After symptomatic treatment, the patient experienced slight relief from the pain.\nOn June 16, the pain worsened; it was persistent and accompanied by the urge to defecate. He defecated once a day, and his stools were characterized as loose and non-bloody. He often experienced abdominal distention and heartburn, and he had not lost any weight recently. For further evaluation and treatment, he was admitted into our hospital (the affiliated hospital of Jining Medical College) on June 18, 2020. The patient's medical history did not reveal any past diseases, and he had no history of drug abuse or food allergy. The physical examination was unremarkable.\nThe results of the routine blood tests performed on June 18 are shown in Table . On June 19, the appendiceal ultrasound showed normal results, whereas the chest CT scan findings indicated bronchitis. Magnetic resonance cholangiopancreatography did not reveal cholangiectasis or cholecystitis. The results of the liver function test, kidney function test, serum calcium, serum electrolyte test, blood glucose, urine routine test, and antinuclear antibody spectrum were all normal. In addition, no parasitic ovum was found in the stool ova and parasites test. However, the fecal occult blood test was positive.\nThe initial diagnosis that was considered was gastritis and a disorder of the gastrointestinal function. Hence, we administered omeprazole, otilonium bromide, and probiotics along with other symptomatic and supportive treatments. However, the abdominal pain gradually worsened to the point where spasmolytics and pain reliever (tramadol hydrochloride and 654-2) were not effective anymore.\nOn June 21, the enhanced CT scan showed diffuse thickening of the jejunum wall which was suspected to be due to inflammation, although the presence of a tumor could not be ruled out completely (Fig. ). The blood routine tests in Table were repeated, and the results revealed an eosinophil count of 1.22 × 109/L, which was higher than the previous results. In addition, the ratio of eosinophils was 12.2% higher than that of the previous results. Thus, we arrived at a diagnosis of EE. On June 22, an enteroscopy was performed, which showed gastritis, congestion of the duodenal and jejunal mucosa, and partial erosion of the mucosal membrane, especially in the descending part of the duodenum (Fig. ). Biopsy specimens were obtained from the descending duodenum, horizontal segment of the duodenum, and jejunum. In all biopsy specimens, the pathological findings showed acute and chronic inflammation accompanied by eosinophilic infiltration (>20 eosinophils/ high-power field [HPF]) (Fig. ). On June 23, bone marrow examination was performed, and the results revealed a slightly higher ratio of eosinophils with a preserved cellular morphology (Fig. ). The subsequent flow cytometry did not reveal abnormal lymphocyte phenotypes (Fig. , Tables and ).\nBased on the clinical manifestations, CT scan and enteroscopy images, pathological findings, and the results of bone marrow examination and flow cytometry, we considered EE as the most likely diagnosis. On June 24, we initiated dexamethasone 10 mg IV infusion per day for 3 consecutive days; the abdominal pain was resolved on the first day. Three days later, we reduced the dose of dexamethasone to 7.5 mg per day for 2 days. After 5 days since initiating dexamethasone, the patient was discharged from our hospital, and oral prednisolone (30 mg per day) was prescribed. On the day of discharge, we repeated the routine blood test and found that the eosinophil count and EO ratio derived ratios returned to the normal ranges (0.11 × 109/L and 0.8%, respectively) (Table ). But before the steroid giving to the patient, eosinophil counts were 1.22 × 109/L, and EO ratio was 12.2%, they were both higher than normal (Table ). Since our patient had no history of food allergy, we did not modify the patient's diet.\nAfter the patient was discharged, we informed him to taper the dose of prednisolone by 5 mg per week. On July 6, he returned to our hospital for a follow-up. He was asymptomatic and underwent routine blood tests, with the results shown in Table . The eosinophil count and EO ratio were 0.64 × 109/L and 3.2%, respectively, which were both normal. During the follow-up, he had been taking prednisolone 20 mg per day. During the following month, the dosages of steroids were gradually tapered until discontinuation. The total dosage taken for each steroid was 45 mg and 735 mg for dexamethasone and prednisolone, respectively. On October 12, a telephone follow-up revealed that he had completely stopped taking steroids and had no obvious symptoms. The results of the repeat routine blood tests are shown in Table . The eosinophil counts and EO ratio were 0.15 × 109/L and 1.8%, respectively. |
A 13-month-old boy, with consanguineous parents, was referred to the Pediatric Emergency Department of our hospital with partial-complex seizure. Clinical evaluation revealed normal neurological development and no focal deficits. No iris nevi or Lisch nodules were evident on ophthalmological examination. Prominent café-au-lait skin lesions were observed on the patient's neck and midchest [Figure -]. His father and brother had similar dermatologic signs, the latter having died at the age of 6 years due to T-cell acute lymphocytic leukemia. He also had an older brother who died owing to congenital heart disease []. MRI of the brain showed an isolated lesion in the left mesial-temporal lobe []. Microsurgical total removal of the lesion was performed. Histological diagnosis confirmed a typical cavernous hemangioma. The patient had an uneventful postoperative course and was discharged after four days. Outpatient consultations were performed routinely.\nAt the age of 4 years he presented with a 7-day history of progressively worsening headache, vomiting, and gait ataxia. Ophthalmological evaluation revealed papilledema. MRI scans showed supratentorial hydrocephalus associated with a posterior fossa tumor in the left cerebellar hemisphere displacing the brainstem []. Thorough neuroimaging screening of the neuroaxis showed no other lesions at that time. Gross total resection was achieved by suboccipital craniotomy. Histological examination of the tumor revealed a nodular medulloblastoma grade IV (WHO). The patient underwent radiotherapy and chemotherapy. Five years later, control MRI scans confirmed no recurrence of the lesion, however showed multiple and asymptomatic radiation-induced cavernous hemangiomas []. At the age of 10 a massive recurrence of the medulloblastoma was observed in the posterior fossa associated with severe hydrocephalus []. Initially, an endoscopic third ventriculostomy was performed uneventfully. A surgical resection was attempted with the aim of reducing the lesion. In spite of aggressive adjuvant treatment, the child died 3 months later due to infiltration of adjacent brain stem and clinical complications [Figure , ]. |
A 45-year-old Caucasian man was referred to the Head and Neck Department at San Raffaele Hospital in 2018 with pigmented lesions of the maxillary gum that expanded up to the hard palate. He reported that a small pigmented macule had appeared on the maxillary gum, near the right central incisor, five years before. At that time, his dentist performed a biopsy that reported a benign melanotic macula. In April 2018, a new ulcerated pigmented lesion appeared on the central part of the hard palate, and upon examination in the Oral Pathology Unit, the maxillary gum macula was enlarged, involving the mucosa of both sides of the upper gum and hard palate. In particular, the anterior labial gum pigmentation extended interdentally and became continuous with a large black pigmented lesion in the hard palate, with a central ulceration (). A new biopsy was then taken, with a histologic section showing a mucosal lentiginous malignant melanocytic lesion (S100+, SOX 10+), infiltrating and focally submucosal ().\nMRI showed an increased signal in both T1WI and in T1 C+ in the central area of the hard palate with thickening of the mucosa by 3–4 mm (). No bone infiltration was seen; on the other hand, PET/CT (Positron emission tomography/Computed tomography) revealed positive cervical lymph nodes, but no distant metastasis (). TNM staging was cT3, cN1, cM0 stage IV. Histological mapping before major surgery was performed, and samples, taken from the mucosa of the hard palate and maxillary gum, were positive for MM in situ, with two areas of infiltrating MM in correspondence with the central part of the hard palate and upper gum. The case was discussed with the multidisciplinary team (MDT), which agreed with a program of transoral hard palate–upper gum mucosectomy associated with resection of a cuff of the bone of the upper dental arch (from 1.5 to 2.3 teeth) and the central hard palate, where the invasive MM was previously mapped (). Bilateral MRND (modify radical neck dissection) and temporary tracheotomy were also performed. Theoretically, no reconstruction would have been needed because second-intention healing of oral mucosa was possible. Nonetheless, the MDT recommended postoperative radiotherapy (PORT) that cannot be done on demucosized bone, and which is done within 6 weeks after surgery. The reconstruction of surgical gap was performed successfully with a hybrid reverse-flow submental island flap (SIF). In particular, the upper gum–hard palate osteo-mucosal defect was restored with a hybrid reverse-flow SIF with facial nerve-sparing: the facial artery was cut in the proximity of the mandibular branch of the facial nerve, the flap was tunnelized under the nerve and through the buccinator muscle up to reach the cheek mucosa just in front of the Stensen duct papillae. Venous drainage was restored through the interpositioning of the venous graft of external jugular vein between facial vein abutments with a double microanastomosis.\nMicroscopic examination of the surgical sample confirmed the diagnosis of infiltrating MM of the hard palate; bone and lymph nodes were free of disease. Pathological TNM staging was pT3, pN0 stage III.\nThe final esthetic result was highly satisfactory in term of scars, oral reconstruction, and facial nerve function (); healing was reached within 3 weeks, and the patient succeeded in undergoing postoperative radiotherapy within the time required (66 Gray, ended in January 2019) with no local adverse events. However, even if adjunctive therapy helped in reducing hair bearing of the reconstructive flap, tailored laser ablation sessions were scheduled, with resolution of local impairment ( and ).\nAt the time of writing (28 months after surgery), radiological and clinical follow-up is negative. The patient has undergone a prosthodontist evaluation, which performed a mobile prosthesis to be anchored to the lateral teeth of the surgical defect (). |
An 8-month-old female infant had coronary reimplantation at age 3 months for ALCAPA. Postsurgical ejection fraction showed early improvement with subsequent deterioration. A diagnostic left heart catheterization performed as part of a heart transplant evaluation revealed severe ostial stenosis of the LMCA. She was referred for PCI of the left main coronary artery to relieve her heart failure and preempt transplant. Her physical exam was significant for congestive heart failure and failure to thrive. The patient's echocardiogram showed markedly depressed left ventricular function. A cardiac computed tomography angiography (CTA) and initial diagnostic nonselective root aortogram demonstrated stenosis of the LMCA at the site of ALCAPA reimplantation. Selective left coronary angiogram revealed severe kinking of the reimplanted LMCA at the ostium ().\nThe procedure was performed in the Pediatric Cardiology interventional suite after extensive discussion and planning with Pediatric and Adult Interventional Cardiology, Pediatric Cardiac Anesthesia, Pediatric Cardiothoracic Surgery, and Pediatric Cardiac Radiology. General anesthesia and a femoral arterial approach were utilized. An ascending aortic root angiogram was obtained in 2 planes to assess the ostial left main stenosis. Due to the small size of the infant aorta, a 6 Fr JR-4 guide was reshaped to engage the left main coronary artery. A BMW wire was used to cross the lesion. Since the infant left main coronary artery was small but was expected to grow with age, a somewhat larger (3.0 × 8 mm Vision bare metal) stent was carefully implanted in the proximal LMCA at less than nominal pressure to avoid distal dissection. A poststent angiogram showed that the stent had moved during implantation and missed the ostium with residual stenosis of the LMCA origin. Hence, a 3.5 × 8 mm Vision bare metal stent was placed into the LMCA ostium overlapping with the previous stent distally and protruding 1-2 millimeters in the aorta proximally. The ostium and aortic overhanging portion of the stent were postdilated producing proximal flaring. The final angiogram confirmed excellent stent position and normal flow ().\nThe patient tolerated the procedure well and was discharged home on dual antiplatelet therapy (DAPT) with aspirin and clopidogrel one day after PCI. She was followed in Cardiology clinic post-PCI and noted to have no change in her ventricular function. Nevertheless, she continued to do well clinically until six months post-PCI, at which time she demonstrated failure to thrive and required admission for initiation of continuous milrinone infusion. The left main stent was widely patent with normal Doppler flow signals as visualized by echocardiography (). She was listed as status 1A for orthotopic heart transplantation (OHT) and underwent transplantation one year post-PCI, at age 20 months. |
A 67-year-old female with a past medical history of rheumatic mitral stenosis, non-ischemic dilated cardiomyopathy with chronic left ventricular systolic dysfunction, chronic renal insufficiency, and breast cancer (in remission) presented reporting weeks of progressive symptoms and with signs of right-sided heart failure. She had undergone both implantation of a single-chamber ICD in 2008 and bioprosthetic mitral valve replacement in 2012.\nAt the time of her presentation in 2012, the patient complained of increasing fatigue, lower extremity swelling, and abdominal distension. She had had multiple previous hospital admissions for symptomatic heart failure, and had been treated with diuresis and therapeutic paracenteses. A transthoracic echocardiogram revealed severe tricuspid regurgitation, with evidence of impingement from the RV defibrillation lead. A cardiovascular surgeon was consulted, and the patient was taken for tricuspid valve replacement. During surgery, the defibrillator lead was found to be compressing the septal leaflet, and its removal was deemed required for bioprosthetic valve replacement. The lead was cut immediately distal to the SVC coil and left in position in the right atrium. A bipolar epicardial RV pacing lead was subsequently implanted and placed in a pocket in her left upper abdominal quadrant. Epicardial patch(es) placement unfortunately was not performed. Postoperatively, the patient was noted to have developed complete atrioventricular block and atrial flutter. Her ventricular rhythm was maintained via temporary epicardial pacing wires placed at the time of her surgery. The electrophysiology service was consulted with regards to permanent pacing and defibrillation options.\nThe patient was ultimately brought to the electrophysiology laboratory for dual-chamber ICD placement. The pre-existing left infraclavicular pocket was accessed. The RV ICD, which had been cut intraoperatively, was detached and the old ICD generator was explanted. Brief attempts to remove this lead using manual traction proved unsuccessful, so it was instead capped and left in situ. A new single-coil ICD lead (Durata™ 7122Q Defibrillation Lead; Abbott Laboratories, Chicago, IL, USA) was then placed in the right atrium as close to the tricuspid valve, and thus the RV, as possible ( This lead was placed to serve as an atrial pace/sense lead and the “distal RV” ICD coil. A subcutaneous coil (Medtronic 6996SQ; Medtronic Inc., Minneapolis, MN, USA) was implanted via the left infraclavicular pocket and tunneled posterolaterally to provide a vector towards the left ventricle. The leads were attached to a dual-chamber ICD (2357-40C Fortify Assura™ DR; Abbott Laboratories, Chicago, IL, USA). Ventricular defibrillation safety margin testing was performed. The shocking configuration was set can/subcutaneous coil (cathode) to right atrium coil (anode) (). Ventricular fibrillation (VF) was induced twice. There was appropriate sensing, and the patient was successfully defibrillated each time with 25 J. |
A 70-year-old Caucasian female was evaluated for a one month history of progressively worsening low back pain and weakness. She had no gastrointestinal tract complaints. Her past medical history was significant for multiple basal and squamous cell cancers, as well as Merkel cell carcinoma 5 years previously, at which time she presented with a lump in her left groin. After local resection, she was treated with radiation and carboplatin. There was no recurrence and a subsequent abdominal CT (computed tomography) scan 3 years later showed no evidence of metastatic disease. The primary site was thought to be an inguinal lymph node.\nOn physical exam she had a 5 mm mobile lymph node in the left supraclavicular area. There were no focal neurological deficits. Stool tested guaiac negative. Labs revealed hemoglobin 7.1 g/dL, hematocrit 21.1%, iron level 15 mcg/dL, total iron binding capacity 330 mg/dL, and transferrin saturation 5%, consistent with severe iron-deficiency anemia. A contrast enhanced abdominal CT scan showed bulky retroperitoneal adenopathy encompassing the renal arteries, aorta, inferior vena cava as well as circumferentially thickened loop of small bowel in the left hemiabdomen (Figure ). A small bowel series was negative. The decision was made to perform a colonoscopy.\nThe findings at colonoscopy (Figure ) revealed a semi-sessile ascending colon polyp measuring approximately 1 cm in size. The polyp was smooth and pale, with regular margins, and normal surrounding mucosa. It was resected as a single piece using hot snare polypectomy technique, and all tissue was recovered into a sterile trap and submitted for routine histology. Post-resection appearances suggested complete removal of all polypoid mucosa. Pathological examination of the specimen showed a small blue cell neoplasm involving both the mucosa and submucosa (Figures , , and ). The tumor cells were relatively small with scanty cytoplasm and hyperchromatic round nuclei. Immunostain for cytokeratin 20 showing perinuclear dot like cytoplasmic and surface positivity. Immunostaining for endocrine markers chromogranin and synaptophysin showed strong cytoplasmic positivity. The findings are typical of MCC and were similar to the patient’s previous groin tumor. The patient was diagnosed with stage IV MCC based on the presence of a distant metastasis.\nThe patient was treated with 4 cycles of cisplatin and etoposide (VP-16). Five months later, a CT of the abdomen showed increase in abdominal lymphadenopathy and a midjejunal small bowel mass that was felt to represent a metastatic focus. She received an additional 8 cycles of chemotherapy with cyclophosphamide, doxorubicin and vincristine and a follow-up positron emission tomography scan showed resolution of the previous multifocal lymphadenopathy in the chest, abdomen, and pelvis with no new lesions. |
A 42-year-old man, a known case of type 2 diabetes mellitus, presented with a generalized painless blurring of vision in the left eye for four days. It was associated with left periorbital swelling and eye redness. He had a fever with a left leg abscess for four days prior to eye symptoms. He was treated with an oral antibiotic for the leg abscess.\nOn examination, he was not toxic-looking and afebrile. His vital sign was stable with a blood pressure of 120/84 mmHg and the pulse rate was 84 beat per minute. Visual acuity of the right eye was 6/9 and the left eye was hand movement. There was a positive relative afferent pupillary defect on the left eye.\nLeft eye examination showed periorbital swelling with generalized redness (Figure ). The conjunctiva was injected with chemosis at the lateral part and mild corneal haziness centrally. There was a presence of whitish fibrin covering the pupil and the height of the hypopyon was 1.5 mm with cells 4+ in the anterior chamber (Figure ). The pupil was round, 3 mm in size, and reactive to light. Intraocular pressure was 17 mmHg. There was a mild restriction of eye movement in all directions. The fundus view was obscured by the presence of fibrin in the pupillary area. B-scan ultrasound showed severe vitritis with multiple loculations. Right eye examination was normal, with no features of diabetic retinopathy.\nLeft leg examination showed a large abscess at the anterior shin, measuring 8 cm x 6 cm (Figure ). The area of the abscess was red in color, warm, painful on palpitation, with mild to moderate fluctuation. There was no punctum or open sore over the abscess area. There was no other abscess on other parts of the body. The lung was clear, with a normal cardiovascular system. There was no hepatosplenomegaly and no lymphadenopathy.\nCapillary blood sugar was 12.0 mmol/L at presentation, and the total white blood cell count was 18.9 x 109/L with predominantly neutrophils (80%). Urine full examination microscopy examination (UFEME) was normal with no growth. Chest X-ray and ultrasound abdomen showed normal findings.\nHe was treated as left eye endogenous endophthalmitis secondary to left leg abscess. Intravitreal vancomycin 2 mg/0.1 ml with ceftazidime 2 mg/0.1 ml injections were given to the left eye. Vitreous specimens for culture and sensitivity did not yield any growth. He was also started with intravenous ceftazidime 1 gm TDS and gutt. moxifloxacin hourly to the left eye. Incision and drainage were done for the left leg abscess. About 15 ml of yellowish pus was drained during the procedure. Pus and tissue culture did not grow any organism.\nHe was given multiple intravitreal antibiotic injections but there was no improvement. In view of the poor clinical response, trans pars plana vitrectomy was performed. Despite that, his left visual acuity dropped to non-perception of light (NPL). His vitreous sample taken during vitrectomy finally showed non-sporulating fungal hyphae (Figure ). His general eye condition improved (Figure ) after administration of oral fluconazole 200 mg BD and topical amphotericin B hourly to the left eye. However, his left eye remains NPL. There was a resolution of periorbital swelling and chemosis with full extraocular muscle movement. The hypopyon was resolved with contracted fibrin and mild anterior chamber reaction. The oral fluconazole was continued to be completed for six weeks and the topical amphotericin B was tapered down slowly within three months. |
A 46-year-old man, in good general health, with an implant placed 5 years before, wanted to have his maxillary incisor diastema closed (Fig. ). Clinical and radiological examination showed a correctly osseointegrated implant replacing the right maxillary central incisor and healthy soft tissues. The orthodontic treatment plan goal was to reduce the maxillary and mandibular incisor protrusion and the setup revealed, as the implant could not be moved by orthodontic treatment, a severe malposition without any possibility for a new prosthetic restoration. Esthetic rehabilitation required repositioning or implant removal.\nThe treatment management was, first, to correct the mandibular incisor protrusion with the avulsion of the right mandibular central incisor, which was necrotic with a very dark enamel. Then, the lower jaw space and the maxillary anterior diastema had to be closed, and finally, the implant had to be relocated or removed.\nOrthodontic preparation to close the maxillary incisor diastema and the mandibular extraction space was done with a .018x.025 stainless steel wire (SSW) excluding the implant on the maxilla, and with a .019x.025 SSW in the lower arch.\nAfter teeth alignment, it was confirmed that the position of the implant was unfavorable for a new prosthetic rehabilitation (Fig. ). Despite good implant osseointegration and an adequate prosthetic crown, an OBS technique was proposed to the patient. Ultrasonic cuts were made on the palatal side for implant relocation with an antero-posterior movement. Immediately after flap closure, orthodontic forces were applied with an elastic chain between the implant and the archwire associated with 4.5 oz. intermaxillary elastics to pull the implant towards the palatal direction (Fig. ). Elastics were changed by the patient twice a day, and, elastic chain reactivation was performed by the orthodontist, every week in the first month, then every 15 days. After 3 months, the implant crown was aligned with adjacent incisors, and the relocation result was stabilized by 3 additional months with a .021x.025 SSW. (Fig. ). The prosthetic crown was preserved and a fixed retainer was bonded to the anterior upper arch. At 18 months post-treatment, teeth alignment and esthetic results were stable (Fig. ). |
A 39-year-old woman, who had been taking medication of quetiapine as an antipsychotics for depression, experienced mild dysarthria and visited the department of neurology in our hospital. Her symptom was diagnosed as drug-induced lip dyskinesia, which disappeared in a week. Screening head magnetic resonance imaging (MRI) at this time revealed stenosis of the left MCA with no brain parenchymal lesions (), why she was consulted to our department. We performed angiography, confirming moderate M1 portion stenosis (Figures and ). SPECT showed no apparent laterality in CBF, thereby we decided to observe her with no treatment.\nSeven months later, the patient experienced mild weakness and numbness in her right hand and visited our department. Although MRI showed no apparent ischemic change in her brain, arterial spin labelling (ASL) of MRI detected the decrease of CBF in the left cerebrum (), which was thought to well correspond for her symptoms. She was admitted and treated with an antiplatelet agent. Two weeks later, she still complained of numbness in her right hand; thereby, we decided to perform left STA-MCA anastomosis to prevent deterioration of her symptoms. Preoperative SPECT showed no apparent laterality in CBF (). On operation, left temporal craniotomy was performed, and the parietal branch of the STA was anastomosed with the M4 portion on the temporal lobe (Figures and ). The intraoperative course was uneventful, and the patient recovered from anesthesia without any new neurological symptoms\nPostoperatively, her speech was normal until postoperative day 1 (POD1). On POD2, she exhibited mild speech disturbance, which worsened day by day finally resulting in complete motor aphasia on POD6. Her comprehension was kept normal. On POD3, generalized convulsion occurred, which ceased quickly by diazepam, and levetiracetam was initiated. On the same day, she presented with mild weakness of right upper extremity, which improved gradually and disappeared on POD7. MRI and CT showed no ischemic or hemorrhagic changes, but ASL and SPECT revealed remarkable increase of CBF in the left cerebrum (Figures and ), by which the symptoms were diagnosed as CHPS. Despite the treatment with strict blood pressure and the administration of edaravone and minocycline, complete motor aphasia remained unchanged on POD21. MRI showed no abnormality except slightly hypointense changes on T2 weighted images and FLAIR (). At this point, the patient was discharged partly because of the request from the patient, and we continued to follow her in outpatient visit. One month after the surgery, the patient started to utter words that were not fluent, when SPECT and MRI showed normalization (). Thereafter, the improvement of her speech was slow, and totally more than three months was taken for full recovery after the surgery. |
A 66-year-old man presented to the emergency department after being struck by a cyclist. He complained of left-sided chest, shoulder/hip pain, and post-traumatic amnesia. He had a past medical history of hypertension, hypercholesterolaemia, and chronic, residual, Stanford Type A AD, which was repaired in 2014. On examination, he was haemodynamically stable with a brachial blood pressure of 115/71 mmHg, no significant blood pressure differences between arms, a respiratory rate of 22 breaths per minute, and a pulse oximeter saturation of 95% on 2 litres nasal prong oxygen. He had a tender left chest wall posteriorly and laterally, with extensive subcutaneous emphysema over his chest wall and neck bilaterally. He had reduced air entry in his left chest. His had dual heart sounds without murmurs. A computed tomography (CT) scan of his chest showed a comminuted left clavicle fracture, left rib fractures from the second to the ninth, with flail segments from the third to the ninth, and a moderate left pneumothorax ( and ). The sixth posterior rib fracture was only 13 mm away from the aorta ( and A). The CT also demonstrated that the residual AD had increased in size since the original diagnosis in 2014. A CT of his brain and facial bones showed no new intracranial pathologies or fractures.\nA 28-gauge French intercostal catheter was inserted into the patient’s left fifth intercostal space and connected to an underwater seal. The water in the water seal displayed oscillations. The patient was started on high flow nasal prongs at 30 L/min with 30% oxygen and intravenous morphine patient-controlled analgesia. On day 1 of his admission, he was able to perform an incentive spirometry of approximately only 250 mL. After discussion of the patient’s condition and clinical history with a cardiothoracic surgeon, it was decided that SSRF would not be performed in the posterior sections. Owing to the patient’s poor respiratory output and persistent pain, the decision was made to perform SSRF on the anterior rib fractures.\nThe patient underwent surgical stabilisation of his fractures on day 6 post-admission. He had a general anaesthetic with double lumen endotracheal tube for single lung ventilation. The patient was positioned in the left lateral position with a left flexed arm. A horizontal subpectoral incision was performed over the sixth rib. The anterior fractures were identified and lung adhesions to fractured ribs were mobilised gently.\nIntraoperative thoracoscopy was performed with extreme care. Whilst using intraoperative thoracoscopy to identify the relative positions of the posterior rib fractures and the AD site, it was crucial to carry out the procedure with precision and meticulous care owing to the risk of AD rupture. The anterior third to seventh ribs were reduced, plated, and screwed. A paravertebral block was inserted under direct vision.\nThere were several technical challenges related to this SSRF process. Intensive general anaesthesia monitoring was necessary because of the complex issues involved. The patient’s blood pressure needed to be constantly monitored, steadied, and maintained because of the major risk of AD rupture. The monitoring needed to be done both intraoperatively and postoperatively. Whilst manipulating the rib fractures of the flail segment anterolaterally, meticulous care was needed to avoid further posterior rib or rib fragment displacement towards the AD site.\nAfter fixation, two 19 French intercostal catheters were inserted before closing. The thoracic wall muscles and subcutaneous fat were approximated with 2-0 Vicyrl and the skin was closed with subcuticular 3-0 Monocryl. The patient was monitored in the high dependence unit for 2 days with no complications. On day 7 of admission, the left clavicle was fixed with surgical plating. Functional lung expansion improved substantially (>50%) on day 8 of his admission, which corresponded to day 2 after SSRF. On day 10 of his admission, corresponding to day 4 after SSRF, he was able to perform incentive spirometry adequately (1200 mL). He was discharged on day 14 of his admission with no opioid analgesia and without supplemental oxygen. He was followed up in an outpatient clinic after 4 weeks, where his pain was demonstrably well controlled (0/10 at rest and 3/10 on exertion), and his chest X ray and chest CT revealed good expansion of his chests with plates and screws in situ (B). |
A 64-year-old, 87 kg female presented for clipping of a 4 mm wide neck unruptured saccular anterior communicating artery aneurysm which was discovered incidentally during the evaluation of headaches and memory difficulties. Her past medical history was significant for remote breast carcinoma, hypertension, obstructive sleep apnea, and gastroesophageal reflux disease. She was a lifelong nonsmoker and notable preoperative medications included aspirin, furosemide, and propanolol. Preoperative imaging had no evidence of prior infarcts. After induction of anesthesia, a right internal jugular central venous catheter and radial arterial catheter were placed and maintenance of anesthesia was performed with a combination of 0.5 MAC sevoflurane, propofol 50 mcg/kg/min, and remifentanil 0.125 mcg/kg/min infusions. Mannitol 1 gram per kilogram for a total of 80 grams was administered. The neurosurgeon placed an 80 cm closed-tip, barium impregnated lumbar drainage catheter with a 0.7 mm inner diameter (Medtronic USA, REF 46419) at the L3-4 level prior to the start of surgery.\nThe surgery commenced and was progressing unremarkably. Prior to opening of the dura, 20 mL of CSF was drained over 15 minutes per neurosurgeon request. After dural opening and during dissection of the aneurysm, the surgeon requested the lumbar drain to be opened allowing further drainage of CSF. After approximately 15 minutes, the blood pressure sharply increased over the course of 1 to 2 minutes from a baseline systolic blood pressure of 130 mmHg to over 205 mmHg with an associated decrease in heart rate from 60 bpm to 50 which resolved over the course of minutes. This acute hypertension was treated with a number of interventions including 250 mg propofol and 1 mcg/kg remifentanil boluses aimed at treating light anesthesia as well as a bolus of 7.5 mg labetalol. At the time of the hypertensive event, the propofol, remifentanil, and Sevoflurane dosing had been stable and unchanged for over an hour. There was also no change in the level of surgical stimulation at this time as the dura had been incised and the neurosurgeons were using the operative microscope to expose the aneurysm. After the aneurysm was successfully clipped, the lumbar drain was closed and the surgery was completed without further episodes of hypertension. A total of 60 mL of CSF was drained via the lumbar drain during the case in addition to the losses from the surgical field.\nAt conclusion of the operative procedure, the patient remained comatose and unresponsive despite an hour in the operating room awaiting emergence from anesthesia. A postoperative head CT was obtained prior to transport to the intensive care unit which demonstrated mild cerebral edema and borderline inferior transtentorial herniation, but no significant hemorrhage or focal abnormalities. She was then transported to the Neurocritical Care Unit intubated and ventilated. Initial arterial blood gas analysis on arrival to the ICU did not reveal a cause to her delayed emergence (pH 7.35, pCO2 47 mmHg, pO2 323 mmHg, glucose 204 mg/dL, and sodium 137 mEq/L). She did not receive any benzodiazepines during the case, but did receive 50 mcg of fentanyl on induction and 1 gram of levetiracetam in addition to the propofol, remifentanil, and Sevoflurane maintenance. Initial neurological exam demonstrated midline and equal 4 mm pupils which were reactive to light bilaterally. She withdrew to painful stimuli in all four extremities. On postoperative day (POD) 1, her mental status continued to be depressed with a Glasgow Coma Scale of 7T (E2:V1T:M4). That day, an MRI was obtained which revealed bilateral thalamic infarctions on the diffusion weighted imaging which can be seen in . Supportive care was continued and over the course of several days, her mental status slowly improved to GCS of 10 (E4:V1:M5) on POD 5. This allowed for safe extubation that day. She continued to improve and was alert and oriented to person, place, time, and situation with some memory and attention difficulties by POD 16. A timeline of her in-hospital recovery can be found in . She was discharged home with referrals for home physical, occupational, and speech therapy on POD 19. She continued her gradual neurological improvement and by over a year postoperatively, Neurology records indicated she was living independently and her Montreal Cognitive Assessment score had recovered to a normal 27/30. |
A 19-year-old young man had a two-year history of exertional dyspnea, lower limb edema, periodic chest pain, and jaundice. The patient was in NYHA classes II and III with his symptoms progressively worsening over time. His past medical history indicated the successful balloon angioplasty and stenting for coarctation of the aorta (COA) at the age of 15, which left an arterial hypertension and no significant residual COA, and in the follow-up periods. His clinical evaluation based on the chest X-ray findings showed cardiomegaly, particularly, in the right ventricle and pulmonary congestion (). Laboratory data showed that he had a mild increase in the serum creatinine (Cr), bilirubin (BIL), and nonalcoholic fatty liver disease (NAFLD). Furthermore, transthoracic echocardiographic examination (TTE) indicated that the patient had a large VSD and prolapse of the noncoronary cusp of the aorta into the VSD due to severe aortic regurgitation. Left ventricular (LV) ejection fraction (EF) index was about 40%, left ventricle end diastolic diameter (LVEDD) was 75 mm, and left ventricle end systolic diameter (LVESD) was 55 mm. The catheterization prior to surgery indicated that Qp/Qs was 2.2. Also his pulmonary artery pressure was estimated to be 60 mm Hg and the pulmonary artery pressure to aortic pressure ratio was 0.7.\nAfter his complete evaluation, surgery was recommended. After initiating the cardiopulmonary bypass machine and arresting the heart function, a significant aortic valve insufficiency with perforation of the right and left aortic cusps in the base segment was observed. In addition, prolapse of the noncoronary aortic cusp into the large subarterial VSD was seen. The right coronary sinus of valsalva showed an aneurysmal formation that was attached to the right ventricle with a short tract. Also, there was a mild dilation of the aortic root and the ascending aorta. The aortic leaflet was also thin and perforated, and its excision was sent for a further pathological examination (). After removing the aneurysmal sac of the right coronary artery, the defect that was created in the right ventricle (RV) was closed with a small piece of patch. Furthermore, the VSD was repaired using a Gore-Tex patch and the aortic valve replacement was performed with a St. Jude mechanical aortic prosthetic valve. Weaning the patient from cardiopulmonary bypass was successful, and the patient was discharged 1 week later after the recovery. In the follow-up period, echocardiography tests showed that the patient had no residual VSD, and a good hemodynamic status of the prosthetic valve was also observed. |
A baby girl was born at 39 weeks via normal spontaneous delivery to a 26-year old G2P0 who presented in labor and was Group B streptococcus (GBS) positive by record. The mother had artificial rupture of membranes approximately one hour prior to delivery with meconium stained amniotic fluid. Full-term female weighed 2700grams and was crying. There was adequate respiratory effort, however with poor tone and color. APGAR scores were 6, 8 at 1 and 5 minutes respectively.\nAfter birth, she remained persistently hypoglycemic and was transferred to the Neonatal Intensive Care Unit (NICU) for management of hypoglycemia and possible sepsis. Empirical antibiotic treatment was begun at this time. Further physical examination revealed a sacral dimple, newborn jaundice, and bilateral congenital hip dislocation. The patient was given ampicillin/gentamicin over a 48-hour period during which time sepsis was ruled out. An abnormal abdominal x-ray was obtained and surgery was consulted for evaluation of NEC. The patient was slow to gain weight in the NICU and had difficulty in tolerating oral or gavage feeds. Due to episodes of bilious aspirate, the patient underwent an upper gastro-intestinal (UGI) study on 10th day of life which showed a dilated duodenum and dilated loops of bowel with no evidence of malrotation. On day of life 22, the patient appeared mottled, and had a distended abdomen. Plain films suggested portal venous gas, as well as pneumatosis. At the operation, approximately 120cm of small bowel was necrotic. Approximately 10cm of jejunum distal to the ligament of treitz was left intact as well as approximately 10cm of ileum with a competent ileocecal valve and colon. A jejunostomy and ileostomy were created.\nAfter surgery the patient was briefly started on trophic feeds but was never fed much orally. On day of life 45, the patient underwent G-tube placement and closure of her stoma. During her extensive hospital stay, the patient was found to be hypothyroid. Additionally, a CMA yielded a 123kB deletion in the region of the 15q13.3. The patient is currently one year old and is tolerating a greater amount of her energy intake orally and is being weaned off her TPN. |
A 74-year-old male patient underwent left total knee arthroplasty (TKA) at our institution for degenerative knee osteoarthrosis. He had an uneventful postoperative course with no history of delayed wound healing or persistent drainage. Four years later, he presented with a 2-month history of a gradually developing painless swelling over the anterior aspect of the operated knee; the swelling was associated with a small sinus that was extruding a straw-coloured fluid. He had no history of fever, decreased appetite, or weight loss. He had no other musculoskeletal, respiratory, or systemic symptoms of note. He had no history of antecedent trauma, recent travel, or contact with infectious diseases. The patient is a known hypertensive, but the blood pressure was well controlled with treatment, and he is otherwise healthy. He is a retired teacher with no history of involvement in activities requiring excessive kneeling. He is ambulatory in his community and can walk comfortably with the assistance of a cane.\nThe patient's general physical examination results were within normal limits; positive physical findings were limited to the involved knee. There was an anterior knee swelling involving mainly the prepatellar area, approximately 7 cm in diameter, fluctuant, and not tender to palpation, with minimal surrounding erythema; the erythema was present mainly at the punctum. The punctum was draining a yellowish discharge on pressure (). There was no bony tenderness at the patella, distal femur, or proximal tibia. There was no detectable knee effusion, instability, or crepitus. The range of motion was well preserved (5–110°), as it was a prosthetic knee. It was only painful at the end of flexion as this movement compressed the prepatellar bursa.\nPlain radiographs of the knee showed a prepatellar soft tissue swelling (). There were no obvious bony changes, osteolysis, or loosening at the bone-prosthesis interface. Needle aspiration of the prepatellar bursa yielded 50 mL of slightly turbid straw-coloured yellowish fluid that was sent as per our protocol for cell count determination, microcrystal analysis, Gram staining, and Ziehl–Neelsen (ZN) staining for acid-fast bacilli (). Cultures for aerobic and anaerobic bacteria, Mycobacterium tuberculosis, Brucella, and fungi were requested.\nConsidering the patient's age, chronic presentation, and the presence of sinus, he was admitted with a diagnosis of infected prepatellar bursitis. The primary aims of admission were wound dressing, awaiting aspiration results, and further work-up. Aspiration results revealed normal cell counts, no crystals, and no organisms on Gram stain. To our surprise, ZN stain revealed acid-fast bacilli consistent with typical tuberculous infection; the bacterium was confirmed on culture 6 weeks later as Mycobacterium tuberculosis-sensitive to rifampicin, isoniazid, ethambutol, and streptomycin. Cultures for bacteria, Brucella, and fungi were negative. Aspiration was repeated and yielded similar results. The blood work-up showed normal total and differential white blood cell count and slight elevation of both erythrocyte sedimentation rate (ESR) (80 mm/hr; normal: 30–70 mm/hr) and C-reactive protein (CRP) (8 mg/L; normal: 0–4 mg/L). Tuberculin skin test revealed a negative result (<5 mm induration at 72 hrs), and further work-up including chest radiograph and echocardiogram revealed no evidence of systemic disease. A triple three-phase bone scan displayed normal uptake both at the bone-prosthesis interface and at the patella. An infectious disease consult was obtained. The patient was started on rifampicin (600 mg/day), isoniazid (300 mg/day), pyrazinamide (1500 mg/day), and ethambutol (800 mg/day) for 2 months and continued on the same dosage of rifampicin and isoniazid to complete a 6-month course.\nThree weeks later, the swelling significantly subsided in size and the sinus healed; therefore, the patient was discharged. He was reviewed at 6-week intervals at both the orthopaedic and infectious disease clinics for clinical progression and for any side effects of the medication. At the most recent 6-year follow-up, he was doing well with no evidence of local recurrence or prosthetic loosening (). |
The presented patient is a 70-year-old woman with a history of Stage IIIA thymic carcinoma. She was originally diagnosed in September 2009 and was treated with cisplatin/etoposide chemotherapy (four cycles) and concurrent radiation, followed by surgical resection of the primary tumour which yielded clear margins. The pathology of the resected tumour demonstrated a thymic neoplasm favouring thymic carcinoma with squamoid features [World Health Organization histologic classification (WHO) Type C]. In July 2014, the patient developed recurrent disease with bone and pleural metastases. She declined systemic chemotherapy due to toxicity concerns, but accepted therapy with sunitinib, a tyrosine kinase inhibitor, which was discontinued, 1 year later, in July 2015, due to intolerance. She subsequently received palliative radiation therapy to areas of disease progression. In September 2018, the patient presented with progressive disease in the spine for which she underwent decompressive laminectomy at the level of T7–T8. The surgical pathology favoured metastatic thymoma (WHO Type B3), despite the original findings in 2009 favouring thymic carcinoma. She had no signs or symptoms of autoimmune disease and recovered normally from surgery. The patient received post-operative radiation therapy to the thoracic spine.\nIn April 2019, positron emission tomography–computed tomography (CT) imaging revealed new bone and lung metastases. Patient was extensively counselled regarding treatment options but decided against chemotherapy due to previous toxicities and associated poor quality of life. The original pathology was re-examined and determined to be most consistent with thymic carcinoma. The tumour tissue exhibited high PD-L1 expression with a tumour proportion score of 70%. After discussion of potential risks and benefits, immunotherapy was initiated with pembrolizumab (200 mg), with intravenous delivery every 3 weeks.\nSixteen days after the first dose of pembrolizumab, the patient reported to the emergency department with exertional dyspnoea and was admitted to the hospital. Vital signs on admission indicated a heart rate (HR) of 100 b.p.m., blood pressure (BP) of 154/78 mmHg, respiratory rate (RR) of 22 rpm, and an oxygen saturation (O2Sat) of 92% (on room air); a physical exam had a non-contributory cardiovascular examination. A chest computerized tomography angiography revealed a left lower lobe pulmonary embolism (). Electrocardiography on admission showed biphasic T waves in the septal leads. The reported troponin T levels peaked at 0.271 ng/L (normal: 0.0–0.29 ng/L) (not measured with high-sensitivity assay). Echocardiography revealed mild left ventricular (LV) hypertrophy with normal LV ejection fraction of 63%. The right ventricle was normal in size and function. Measured right ventricular systolic pressure was 50 mmHg. The patient was treated with therapeutic enoxaparin (80 mg, subcutaneous, every 24 h) and continued low-dose aspirin previously started at the emergency department (81 mg, per oral, once daily). The patient was discharged in stable condition 2 days later.\nThree days following discharge, the patient was readmitted to the hospital, presenting with dyspnoea, orthopnoea, and weakness. Vital signs on readmission indicated an HR of 87 b.p.m., BP of 158/93 mmHg, RR of 32 rpm, and O2Sat of 95% (on room air); a physical exam was within normal limits. However, her troponin T during this presentation had increased to 10.50 ng/L (normal: 0.0–0.29 ng/L). In addition, the patient developed severe respiratory failure and was intubated and placed on supportive mechanical ventilation. Electrocardiography revealed a new right bundle branch block, with T-wave inversions in I and aVL, poor R-wave progression, ST elevation in precordial leads, and Q waves in anterolateral leads suggestive of anterior myocardial infarction (). Limited echocardiography showed preserved LV ejection fraction and probable anterior wall hypokinesis with compensatory hyperdynamic posterior wall. Lab studies indicated mild peak troponin T levels of 10.50 ng/L (not measured with high-sensitivity assay), creatine kinase levels of 1667 U/L, and creatine kinase muscle/brain levels of 107 U/L. Myocarditis was suspected, likely secondary to the ICI therapy. The patient received methylprednisolone (1 g per day, intravenously, for 3 days), and subsequently switched to oral prednisone, and enoxaparin (80 mg, subcutaneous, every 24 h) was continued.\nSubsequently, the patient was found to be in complete heart block with ventricular escape rhythm between 20 and 30 b.p.m. and severe respiratory failure. The patient was placed on intravenous isoproterenol drip and underwent coronary angiography, right/left heart catheterization, and urgent temporary pacemaker placement. The coronary angiography revealed normal coronary artery anatomy ().\nA right heart catheterization showed pulmonary artery pressure of 24/16 mmHg (mean: 18 mmHg), and pulmonary capillary wedge pressure of 12 mmHg. At that time, an endomyocardial biopsy (EMB) was performed, and the patient was treated with pulse-dose steroids using methylprednisolone (1 g per day, intravenously, for 3 days). A dual-chamber pacemaker was subsequently placed due to intermittent complete heart block with asystole. The EMB revealed mild myocyte hypertrophy with diameters in the 30–40 µm range. Lipofuscin granules were observed in the perinuclear region of myocytes. Abundant lymphocytosis, consistent with myocarditis, was reported. Three of the seven tissue samples exhibited the presence lymphocytes and macrophages. No giant cells or eosinophils were present. Trichrome staining indicated early interstitial fibrosis and endocardial fibrosis in areas of inflammatory infiltration. There was no evidence of endocardial fibroelastosis, glycogen storage, or iron depletion. Amyloid was also not present ().\nAlthough the patient had been intubated emergently upon admission to the floors due to severe bradycardia and respiratory failure, she was unable to be weaned from mechanical ventilation due to persistent hypercapnia. After neurology consultation, testing for muscle-specific tyrosine kinase (MuSK) and acetylcholine receptor (AChR) antibodies was performed, which were positive for AChR binding and blocking antibodies. The patient was determined to have de novo MG given the lack of previous signs or symptoms, although an exacerbation of subclinical MG could not be excluded. Pyridostigmine (60 mg, every 6 h) was initiated and the patient received five plasmapheresis sessions. Methylprednisolone (1 gr per day, intravenously, for 3 days) followed by oral prednisone (1 mg/kg per day) was administered. The use of intravenous immunoglobulin (IVIG) was avoided in this patient, due to her recent thromboembolic event. Because IVIG increases blood viscosity in vitro and in vivo, it should generally be avoided in high-risk patients due to potential for cardiovascular and cerebrovascular thromboembolism. On Day 13 of hospitalization, the patient was extubated to non-invasive ventilation via bilevel positive airway pressure (BiPAP) treatment with successful weaning to nasal cannula oxygen.\nAfter 50 days of hospitalization, the patient’s respiratory status progressively improved, and she was discharged home in stable condition with home BiPAP treatment during sleep. Prior to discharge, a chest CT, without contrast, was performed approximately 6 weeks after pembrolizumab treatment to evaluate the disease status. The CT results showed improvement with significant decrease or resolution of all measurable sites of metastatic disease in the lungs (). |
The patient’s course is outlined in Fig. .
A 58-year-old, previously healthy, white female presented to her primary care provider (PCP) with the desire to remove a right posterior scalp cyst for cosmesis. This non-inflamed, non-draining, painless, 1–2 cm cyst had been present for close to 10 years without change in size or fluctuance. The cyst was initially drained by the PCP, but, when it recurred 6 months later, the PCP excised the cyst and sent the specimen for routine pathology. The initial read of the tissue sample was high-grade invasive carcinoma with squamous features and arising in association with a PTT. Based on the pathology, the PCP referred the patient to a plastic surgeon for a more definitive excision of the lesion and repair of the defect. The lesion was excised with negative margins and pathology read as invasive high-grade squamous cell carcinoma (SCC). Eight months post resection, the lesion recurred locally along with a palpable right posterior cervical lymph node (LN). A positron emission tomography (PET) scan at that time demonstrated hypermetabolic activity in the posterior occiput and in a posterior neck LN. Fine needle aspiration (FNA) of both the primary scalp lesion and LN were completed, and pathology was reported as SCC, similar to the primary lesion.
With a working diagnosis of locally advanced SCC, the patient’s care was referred to a tertiary care center. There, a dermatopathologist re-evaluated the previous biopsy specimens and altered the diagnosis from SCC to MPTT (Fig. ). Subsequently, the patient was referred to a head and neck surgeon for modified radical posterior neck and lymph node dissection. Intraoperative findings uncovered the presence of nodal metastases to the posterior neck with extranodal extension, extensive perineural invasion of the spinal accessory nerve, and jugular venous invasion of the MPTT. After surgery, the case was discussed at a multi-disciplinary tumor board, and a common |
The patient was a 61-year-old man with multiple left rib fractures (1–6 ribs), left pneumothorax, left lung contusion, and left thoracic subcutaneous emphysema due to a fall injury. The examination showed a partial depression in the left front rib and abnormal breathing (see Fig. ).\nAdmission chest CT examination: 1–6 rib fractures on the left side (of which 3, 4 ribs are long comminuted fractures (see Fig. )); left pneumothorax, left traumatic wet lung; a small amount of liquid pneumothorax on the left side.\nPatient was given early chest straps, multiparametric monitoring, analgesia, and oxygen therapy. The chest pain was still severe. The visual analogue scale scored 7–8 points for the pain at rest and 9 points for the cough.\nPhysical examination revealed that the left chest wall was recessed and abnormally breathed. The CT scan of the rib showed a long comminuted fracture of 3 and 4 ribs. The key to successful operation was the reduction and fixation of these two rib fractures. A preoperative CT scan was performed to reconstruct the 3D model based on the scan results (see Fig. ), and 3D printing technology was used to prepare 3 and 4 rib models (see Fig. ). The three D print models of each fracture segment of the two ribs were adherently reconstructed.\nThe two rib metal plates were separately shaped according to the reconstruction model (see Figs. and ).\nThe patient is scheduled to have a open reduction and internal fixation of 3–6 rib fracture. After general anesthesia, right side lying position, small incision about 8 cm was performed under the edge of 4th rib underarm. The skin was sequentially incised and the subcutaneous tissue was freed layer by layer. The front of the latissimus dorsi muscle and the anterior serratus were exposed. The tunnel was established on the 3rd and 4th rib surfaces from the back of the chest and small muscles to the back of the scapula. The special long hooks lifted the scapula and exposed the scapular operation space. With assistance of endoscope, the electrocautery is useful to expose 3 cm outside the outermost fracture lines of the 3 and 4 ribs. The locking plate was molded on the surface of the third rib before operation, and the broken end of the non-fracture at the anterior and posterior portions of the third rib was well fitted. The distance between the two ends of the metal bone plate exceeded the fracture line to 3 nail holes distance. Under the thoracoscope, the metal plate and the ribs were temporarily fixed with long-angled forceps. The MIPO system was used to drill the holes. Two screws were implanted and locked at both ends to firmly fix the metal plate. In turn, each fracture segment was reset and drilled and secured to a metal plate. The fourth rib is fixed in the same way. Intraoperative image (Figs. , and ). 5, 6 rib fractures given to fix the ribs, not the content of this article, not elaborated. Sufficient to stop the bleeding, the wound was given to leave a negative pressure drainage tube. After a routine thoracoscopic probe of the chest cavity, a closed thoracic drainage tube was placed posterior to the 7th intercostal space and the incision was closed layer by layer. After the chest wall is well-shaped. Three days after surgery review the map (Fig. ). |
A 12-year-old boy with Xq24 deletion syndrome presented with symptoms of intermittent intestinal obstruction 8 wk after primary surgery.\nThe child was symptomatic with a distended abdomen, refusal of feeds, and episodes of abdominal pain. Furthermore, he presented with large gastric residuals that became bilious in the next week.\nEight weeks previously, he presented with suspected intestinal bleeding without further symptoms. US, abdominal MRI, endoscopy, and laparoscopy did not reveal the cause of the chronic bleeding. Specialized angiographic MRI was suspicious for a small intraluminal vascular tumour in the ileum. Limited laparotomy and meticulous palpation of the small bowel enabled the identification of the tumour in the lower ileum. Limited small bowel resection and primary anastomosis were performed. Further clinical investigation of the whole small and large bowel did not reveal any further pathological findings. Histopathological examination showed a venous malformation (2.5 cm × 2.0 cm) at the transition of the jejunum to the ileum. The following clinical course was uneventful. The boy was discharged on the 5th postoperative day.\nExcept for Xq24 deletion syndrome, there was no other personal or family history of acute or chronic disease.\nOn physical examination, the patient showed a distended abdomen and abdominal pain. The examination of the heart, lungs, and further organ status showed no abnormalities. Due to his Xq24 deletion syndrome, he showed psychomotor delay, intellectual disability, and a characteristic craniofacial dysmorphism.\nLaboratory findings showed slightly elevated C-reactive protein (0.3 mg/dL) and normal findings across the rest of the blood panel.\nThe abdominal US showed pendulum peristalsis and free fluid in the abdominal cavity, and a plain abdominal X-ray showed some air fluid levels (Figure ). A gastrointestinal contrast study was performed, which revealed distended small bowel loops (maximum diameter of 50 mm) and narrow segments of the large intestine. There was appropriate intestinal transit, with the presence of contrast in the jejunal and ileal loops after 1 h of administration. The contrast agent arrived at the terminal ileum and caecum at 2 h of intestinal transit. Due to the inconclusive results, we performed MRI, which revealed a distended duodenum and small bowel loops with multiple intraluminal air fluid levels and thickened walls but with no signs of obstruction (Figure ). |
A 64-year-old, 87 kg female presented for clipping of a 4 mm wide neck unruptured saccular anterior communicating artery aneurysm which was discovered incidentally during the evaluation of headaches and memory difficulties. Her past medical history was significant for remote breast carcinoma, hypertension, obstructive sleep apnea, and gastroesophageal reflux disease. She was a lifelong nonsmoker and notable preoperative medications included aspirin, furosemide, and propanolol. Preoperative imaging had no evidence of prior infarcts. After induction of anesthesia, a right internal jugular central venous catheter and radial arterial catheter were placed and maintenance of anesthesia was performed with a combination of 0.5 MAC sevoflurane, propofol 50 mcg/kg/min, and remifentanil 0.125 mcg/kg/min infusions. Mannitol 1 gram per kilogram for a total of 80 grams was administered. The neurosurgeon placed an 80 cm closed-tip, barium impregnated lumbar drainage catheter with a 0.7 mm inner diameter (Medtronic USA, REF 46419) at the L3-4 level prior to the start of surgery.\nThe surgery commenced and was progressing unremarkably. Prior to opening of the dura, 20 mL of CSF was drained over 15 minutes per neurosurgeon request. After dural opening and during dissection of the aneurysm, the surgeon requested the lumbar drain to be opened allowing further drainage of CSF. After approximately 15 minutes, the blood pressure sharply increased over the course of 1 to 2 minutes from a baseline systolic blood pressure of 130 mmHg to over 205 mmHg with an associated decrease in heart rate from 60 bpm to 50 which resolved over the course of minutes. This acute hypertension was treated with a number of interventions including 250 mg propofol and 1 mcg/kg remifentanil boluses aimed at treating light anesthesia as well as a bolus of 7.5 mg labetalol. At the time of the hypertensive event, the propofol, remifentanil, and Sevoflurane dosing had been stable and unchanged for over an hour. There was also no change in the level of surgical stimulation at this time as the dura had been incised and the neurosurgeons were using the operative microscope to expose the aneurysm. After the aneurysm was successfully clipped, the lumbar drain was closed and the surgery was completed without further episodes of hypertension. A total of 60 mL of CSF was drained via the lumbar drain during the case in addition to the losses from the surgical field.\nAt conclusion of the operative procedure, the patient remained comatose and unresponsive despite an hour in the operating room awaiting emergence from anesthesia. A postoperative head CT was obtained prior to transport to the intensive care unit which demonstrated mild cerebral edema and borderline inferior transtentorial herniation, but no significant hemorrhage or focal abnormalities. She was then transported to the Neurocritical Care Unit intubated and ventilated. Initial arterial blood gas analysis on arrival to the ICU did not reveal a cause to her delayed emergence (pH 7.35, pCO2 47 mmHg, pO2 323 mmHg, glucose 204 mg/dL, and sodium 137 mEq/L). She did not receive any benzodiazepines during the case, but did receive 50 mcg of fentanyl on induction and 1 gram of levetiracetam in addition to the propofol, remifentanil, and Sevoflurane maintenance. Initial neurological exam demonstrated midline and equal 4 mm pupils which were reactive to light bilaterally. She withdrew to painful stimuli in all four extremities. On postoperative day (POD) 1, her mental status continued to be depressed with a Glasgow Coma Scale of 7T (E2:V1T:M4). That day, an MRI was obtained which revealed bilateral thalamic infarctions on the diffusion weighted imaging which can be seen in . Supportive care was continued and over the course of several days, her mental status slowly improved to GCS of 10 (E4:V1:M5) on POD 5. This allowed for safe extubation that day. She continued to improve and was alert and oriented to person, place, time, and situation with some memory and attention difficulties by POD 16. A timeline of her in-hospital recovery can be found in . She was discharged home with referrals for home physical, occupational, and speech therapy on POD 19. She continued her gradual neurological improvement and by over a year postoperatively, Neurology records indicated she was living independently and her Montreal Cognitive Assessment score had recovered to a normal 27/30. |
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