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A 20-year-old Caucasian man was brought to the emergency department (ED) after having a suicidal attempt. He had a long history of depression and obsessive/compulsive disorder and came to Virginia with the stated intent to buy a gun because the gun laws were lenient in Virginia, and the intent of buying the gun was to kill himself. However, he did not buy a gun but did attempt suicide by cutting his wrists, then tying a rope around his neck, tying the other end of the rope to a tree, getting in his car, and driving away. The patient then got out of the car, walked to a nearby building, complained that he could not breathe, and then subsequently collapsed. When EMT arrived, he was intubated at the scene and then transferred to the hospital by air care. Upon arrival and evaluation in the ED, he was noted to have massive subcutaneous emphysema in the neck (). The anesthesiologist present at the bedside felt that the endotracheal tube was not in the correct position, therefore, he decided to change the endotracheal tube with a new tube. The patient went under portable chest X-ray,and the radiologist mentioned that tip of tracheal tube is at thoracic inlet (). The patient then went to radiology and had a CT scan of the head, neck, and chest which showed that the endotracheal tube is entering through the oropharynx, but in the hypopharynx, the tube appears to enter into the left piriform sinus, at which it would appear to leave the airway in the soft tissues of the neck on the left side and to reenter the trachea at the thoracic inlet. As visualized on the coronal images, the endotracheal tube had bypassed the area of vocal cords and upper trachea. This implies a disruption of the airway. There is diffuse subcutaneous air within the neck dissecting bilaterally and anteriorly as well. The endotracheal tube cuff is inflated. This may lie within the airway at approximately the level of the thyroid gland (). The patient underwent bronchoscopy which did confirm that endotracheal tube eventually reentered the trachea distal to where it was coarse outside the trachea. Later he underwent an esophagography performed under fluoroscopy guidance, followed by an EGD in the operating room, which showed an additional rupture of the esophagus.\nDuring his hospitalization, the patient underwent a crico-tracheal reanastomosis, open reduction and internal fixation of the cricoid fracture, direct esophageal repair and tracheostomy placement. An MRI of the cervical spine detected a prevertebral soft tissue swelling at the level of C2-C3 which could potentially represent a ligamentous injury to the C-spine but could also represent soft tissue swelling related to the nature of the injury.\nThis patient was admitted to the ICU, where his course was complicated by sepsis and multiple infections. The patient was transferred to the intermediate critical care (IMC) and then psychiatric unit where they transferred patient to a partial day program in New York on the hospital day 74. He had an appointment with a psychiatrist and with a pulmonologist after leaving the hospital. |
The authors report a case of a 29-year-old Saudi woman who was G4T2P0A1L2 at 21 weeks of gestation. She was free from medical illness and she had had no previous surgical procedures. She is a housewife; she never smoked tobacco or drank alcohol, and she had no history of recent travel to endemic or pandemic areas. She was referred based on an antenatal ultrasound finding that showed multiple fetal anomalies. This ultrasound had been conducted at another hospital for evaluation and management. Her past obstetrical history was uneventful with two normal term vaginal deliveries and a history of first trimester unexplained miscarriages. She is married to a first-degree cousin working in a governmental institute; there is no history of genetic or congenital anomaly in either of their families.\nHer current pregnancy was spontaneous with no history of illicit drug use or exposure to infection or radiation. Her initial early antenatal scan diagnosis showed suspicion of possible fetal diaphragmatic hernia and required further validation which was not possible at the maternal–fetal medicine (MFM) unit at the hospital which also did not have available sonographic specialists. During her first antenatal visit at 21 weeks + 0 day of gestation, the results of her anatomy scan revealed a single viable fetus with estimated fetal weight (EFW) on 50th percentile with normal biometry measurements.\nFurther detailed anatomy scan findings revealed a male fetus with both kidneys appearing small in size, hyperechoic dysplastic, both ureters were dilated, urinary bladder looked abnormal in shape with thickened bladder wall, and umbilical cord at fetal insertion side appeared thickened. In addition, the diaphragm was seen clearly separating the chest from the abdominal compartments with no evidence of diaphragmatic hernia. Both feet were clubbed and open hands were seen with no other anomalies or any soft marker seen (see Fig. .) Based on the multiple fetal structural anomalies discovered, the couple was counseled about the scan findings and advised for further workup, such as: perinatal invasive testing; toxoplasmosis, other (syphilis, varicella-zoster, parvovirus B19), rubella, cytomegalovirus, and herpes (TORCH) screening; and fetal echocardiogram to exclude syndromic or chromosomal causes. This would support reaching a better diagnosis and allow for further discussion on the options available such as the continuity of the pregnancy or termination based on the severity of the fetal condition (see Table ).\nOur patient had some social issues and was also following her condition in another institute and only revisited our center at 32 weeks and 4 days of gestation. At our center another follow-up scan revealed a single viable fetus, cephalic in presentation, anhydramnios with normal head and femoral length biometry. Unfortunately, the abdominal circumference (AC) was not taken due to the extremely distended abdominal wall that prevented any further visualization by ultrasound. The right kidney measured 3.4 × 1.1 cm with a small cyst, the left kidney measured 2.9 × 1.3 cm with bilateral hugely dilated ureter and urinary bladder (mega cyst) (see Fig. ).\nTORCH screen test results were non-reactive. Amniocentesis was performed and showed normal chromosomal results. A fetal echocardiogram allowed for limited examination due to anhydramnios; however, no obvious cardiac anomalies were noted. Lungs appeared compressed due to severely distended abdomen from the progressively enlarged urinary system, otherwise no other abnormal findings noted. The couple was counseled by the MFM team about the worsening condition from the recent scan findings and were told about the poor fetal prognosis and the high mortality rate, secondary to severe lung compression with the presence of anhydramnios which would lead to lung hypoplasia and cause fetal demise.\nIt was explained that the entire urinary system was affected with severe dilatation causing severe abdominal wall dilatation and for this reason measuring fetal AC had been difficult antenatally. Options were discussed with the couple:Termination of pregnancy to avoid obstetrical complication during labor which is fetal abdominal dystocia as it was difficult to measure the abdominal wall antenatally with the severe progressive renal system dilation with advancing gestational age versus To wait until term pregnancy while knowing the poor fetal prognosis\nFurthermore, antenatal interventions were offered to the couple including tapping of the fetal bladder and ureters prior to induction of labor and to then send the amniotic fluid sample for further genetic testing. Our patient’s case was initially discussed by a multidisciplinary team which included a perinatologist and a neonatologist before finally making a combined agreement and alignment with the couple who decided to terminate the pregnancy; a caesarian section would be preserved for maternal indication and comfort care post-delivery to born infant were also explained.\nAt 32 weeks and 5 days of gestation, tapping of the fetal bladder and ureter was performed and samples of amniotic fluid were sent for whole exome sequencing (WES) test; however, unfortunately, after waiting a few weeks for the results, no results could be determined due to a laboratory error.\nOur patient underwent induction of labor to terminate the pregnancy and delivered vaginally a male neonate with Apgar score of 2 in 1 minute and 5 in 5 minutes, weighing 1800 grams without any complications. The vital signs revealed blood pressure of 90/60, pulse 100 beats /minute, and temperature of 36 °C. Clinical examination of the newborn revealed distended abdomen and thin wrinkled skin, retracted chest, cryptorchidism, and clubbed feet; no facial anomalies were noted and the features were most likely to be suggestive of PBS (see Fig. ). The newborn died 2 hours post-delivery.\nThe placenta was sent for a histopathology examination as a part of the workup and the result revealed normal findings.\nA postmortem examination was not offered to the couple since this is not conducted in the center. The couple was counseled prior to discharge regarding future pregnancy plans, despite low reoccurrence. It was also highlighted to them the importance of having early prenatal testing in a center in which there were well-trained sonographers and a high risk in pregnancy unit available. They were also informed about the lack of result of WES test due to laboratory error and they were fine. |
This 73-year-old white man had not previously been known to specialist mental health services and had in fact not seen his general practitioner (GP) for over three decades. His family reported that he had periods of depression during his late teenage years, when he left the merchant navy after only a few weeks, and in the third and fourth decade of his life. He neither sought nor received any treatment for these episodes. He never married, had no children, and did not work after leaving the navy. He lived alone following the death of his cohabiting parents and relied heavily on his siblings and nieces for assistance with food shopping and house maintenance. Notably, his mother had a history of recurrent depression with inpatient psychiatric admissions requiring ECT.\nThe patient’s family report him having always been different in personality. He struggled in social settings, found it hard to make friends, and had never been in a romantic relationship. He was obsessional about routine and was known as a child to pace and exhibit repetitive actions when anxious. He also had very specific and intense interests, such as obsessively learning the Latin names of plants. He had not previously been diagnosed with a childhood or developmental mental disorder. His only medical history consisted of a tonsillectomy and childhood scarlet fever. He took no regular medication, did not smoke cigarettes, and consumed no alcohol, and there was no recreational drug use. He was not known to the social care service and had no forensic history.\nAt the start of the current episode, the patient was referred for an urgent mental health consultation by his GP owing to concerns about his mental state over the preceding few weeks. He had retreated into his bedroom and was not washing himself or eating. He was noted to be unkempt, thin, and frail. He displayed objective signs of depression and reported feeling lonely. He stated that he had suicidal thoughts but denied intent. He was noted to speak quietly but was repetitive with short responses. He was not fully orientated to time or place, and his attention was notably poor when tested. He was admitted to a psychiatric ward for older people for a period of assessment. His GP found no acute physical cause for his symptoms, and on admission no abnormalities were detected on all initial investigations, including a battery of blood tests. There were no positive findings on physical examination and specifically no focal neurology. His observations showed hypertension with a blood pressure of 160/72 mmHg, but were otherwise unremarkable.\nA long inpatient admission began, which would eventually last 16 months as summarized in a timeline shown in Fig. . Despite being admitted informally, he was soon deemed to lack mental capacity to consent to admission and was detained under the UK Mental Health Act 1983 (amended 2007). His clinical presentation included tearfulness, poor eye contact, reduced content of speech, frequent pacing, expression of thoughts of self-harm, and mimicking stabbing motions on himself. He wrote about a wish to die in his diary on the ward, although the content of this was disjointed. Collateral history from his family was received regarding his premorbid personality and level of functioning. It was concluded that he was experiencing severe depression on a background of autistic spectrum disorder. He was commenced on mirtazapine and then risperidone, which were titrated to effect, with sertraline added as a second antidepressant. During his initial assessment, the diagnosis of hebephrenic schizophrenia was considered. This was excluded after his family confirmed that prior to the current episode he had functioned relatively well, showering independently and preparing his own meals, for example, and his speech and behavior were not disorganized.\nDuring the early weeks of his admission, the patient progressively became mute. He attempted to eat inanimate objects such as soap bars and continued to pace relentlessly. He also became intermittently incontinent of urine and feces. He was reviewed by the department for neurological sciences who excluded conditions such as motor neuron disease, and a negative autoantibody screen helped to exclude a diagnosis of limbic encephalitis. Dementia was suspected, and a brain computed tomography (CT) scan was attempted, but the patient did not tolerate this. Due to the importance of excluding an organic brain disorder, a repeat CT brain scan was organized but this time using conscious sedation with oral lorazepam (2 mg pre-scan). This resulted in an unexpected, sudden, and dramatic clinical response within minutes. The patient began speaking fluently and coherently for several hours, until his presentation of mutism, increased motor activity,and agitation returned. The use of lorazepam for conscious sedation, and the subsequent clinical response, was interpreted as a positive lorazepam challenge, and a syndrome of catatonia was confirmed. A trial of 0.5 mg lorazepam four times per day was commenced; however, the dose was reduced and then stopped altogether within days owing to severe sedation and frequent falls.\nFollowing the unsuccessful trial of oral lorazepam, our patient was commenced on bilateral, twice weekly ECT (Somatics Thymatron System IV). After nine treatments, there were some signs of improvement, with brief and short episodes of speaking and increased writing in his diary. With ongoing ECT, his mutism became more intermittent, and this revealed disordered thought form. A diagnosis of schizophrenia was revisited as a possible contributing factor to his catatonia, with risperidone replaced by aripiprazole. Although still showing some signs of improvement after 24 ECT treatments, the patient continued to constantly pace and remained mute most of the time.\nNotably, CT brain imaging and later magnetic resonance imaging (MRI) findings included mild generalized cerebral atrophy, including mild bilateral hippocampal volume loss, but no specific features of neurodegenerative disease, Creutzfeldt–Jakob disease, or cerebral amyloid angiopathy.\nFollowing continued failure to significantly improve with ECT, antipsychotic medication was suspended owing to its possible effect on the poor response to ECT in catatonia, as has been reported previously [, ]. Sertraline and mirtazapine were also stopped to exclude serotonin syndrome as a potential cause of his restlessness. Zolpidem, which has previously been suggested as a treatment for catatonia [], was then trialed for 2 weeks but provided no benefit. Following completion of 35 treatments of ECT, the patient remained mostly mute and displayed continued psychomotor agitation. However, his presentation then changed markedly to become rigid and unresponsive to external stimuli, demonstrating stupor. He continued to be mute and demonstrated repetitive teeth clenching (stereotypy) with negativism. He scored 16 on the Bush–Francis Catatonia Rating Scale. This deterioration in presentation prompted a further trial of lorazepam, initially given intravenously under close monitoring in a local general hospital.\nAs before, the first dose of lorazepam provided marked but temporary improvement in symptoms, as the patient started to talk fluently, and his rigidity disappeared. He was again trialed on regular intravenous then oral lorazepam, cautiously increased from 0.5 mg twice daily to 6 mg daily. Unfortunately, the patient developed aspiration pneumonia and remained in the general hospital for treatment of this. His prognosis was thought to be very poor, and his lorazepam was stopped owing to the risk of respiratory depression. He was deemed too unfit for anesthetic to undergo further ECT. At this point, he was transferred back to our psychiatric hospital for end-of-life care, with his family in agreement.\nSomewhat remarkably, shortly after transfer, he became slightly more alert and was able to be fed by staff, although he remained largely stuporous. As a last resort, he was re-referred for further ECT twice weekly. He again showed initial noticeable improvement with a repeat Bush–Francis Catatonia Rating Scale scored at 8. We postulate that the improved effect of ECT at this time may have been related to previous cessation of concurrent antipsychotic medication. Nonmedical treatment was also offered through intensive physiotherapy, including hydrotherapy and passive stretching to reduce the risk of permanent strictures.\nDespite a further 15 treatments of ECT, there was no sustained benefit in psychomotor presentation. It had already been established that our patient could not tolerate high-dose benzodiazepines. By this time, the patient was confined to his water chair and would communicate briefly verbally, but he still required full nursing care for toileting, feeding, changing, and transferring. He often looked anxious, and the team considered medication for symptomatic relief. Sertraline was restarted to treat potential underlying depression, and low-dose diazepam was used for anxiety, with olanzapine added as an adjunct. There was no change in presentation 1 month after cessation of ECT, and a best-interests decision was made with his family not to trial further treatment and to transfer him to a nursing home for full-time care.\nThe patient remained in a stable condition for many months in the nursing home, before sadly dying following sepsis due to bullous pemphigoid 2 years after his initial presentation. |
A 45-yr-old man presented with a painful ulcerative lesion on his right elbow. The patient had been treated for herpes zoster 4 yr before and erythematous 1-cm sized painful nodule was noted on his upper arm in the following years. His past medical history was not specific and he had worked as a carpenter for 20 yr. The nodular lesion developed into ulcerative lesion pregressively and finally became a dry, black, escharous lesion with a maximal diameter of 6 cm (). The surrounding skin was erythematous. Neither purulence nor odor was noted, and no localized axillary or generalized lymphadenopathy was observed. Laboratory studies revealed unspecific results, except a mildly elevated white blood cell count. The patient did not exhibit any sensory or motor deficits in his upper extremities, although movement resulted in intermittent pain.\nThree-dimensional (3-D) upper extremity computed tomographic (CT) angiography of the lesion revealed a skin defect at the posterolateral aspect of the distal humerus and a low attenuated lesion 3 cm in size that was located intramuscularly and showed rim enhancement. A candidate recipient artery, a 1-2 mm-sized branch of the brachial artery, was marked. Magnetic resonance imaging (MRI) examination showed a chronic inflammatory change of the skin at the subcutaneous fat defect portion and infectious myositis at the triceps muscle (). The possibility of squamous cell carcinoma could not be ruled out. Diagnostic skin punch biopsy demonstrated chronic active inflammation with ulceration and necrosis with regenerating epithelia, but failed to show any microorganism on direct microscopy or in culture.\nWe planned surgical resection of the necrotic skin ulcer and free flap coverage. The necrotic and infected central tissue extending into the subcutaneous fat was removed, and a 2-3 cm rim of non-necrotic, erythematous skin was also removed as the surgical margin (). The lateral side of the triceps muscle and periosteum was also partially excised. No bony involvement was seen on the gross view but elbow joint external capsule was exposed. The wound bed was severely scarred owing to chronic inflammation. We dissected the profunda brachii artery and the vein between the biceps and triceps brachii muscles as a recipient vessel. After identification of the perforator using Doppler sound, a 13×8 cm-sized ipsilateral thoracodorsal perforator flap was designed and elevated. After flap transfer, we performed arterial microanastomosis first between the radial collateral artery and thoracodorsal artery. Finally, we did venous anastomosis between each of vena commitantes.\nOne week postoperatively, permanent pathology with Gomori methenamine silver (GMS) and periodic acid-Schiff (PAS) staining confirmed chronic active inflammation and extensive necrosis with numerous fungal hyphae showing septation and branching consistent with Aspergillus species (, ). Tissue cultures grew A. fumigatus. After surgery, the patient was started on amphotericin B (20 mg/day) IV for 5 days and switched to oral itraconazole (200 mg q 12 hr) medication. The wound went on to heal satisfactorily, and there has been no evidence of recurrent disease at 2 yr of follow-up (). |
A 64 year-old male with no significant past medical history other than hypertension presented with progressive gait imbalance and slurred speech over a period of 2 - 3 weeks. He denied any history of recent travel outside of urban Philadelphia, any sick contact or other constitutional symptoms. His social history was significant for smoking of one pack of cigarettes per day for about 30 years. He denied any history of hereditary neurodegenerative disorders in his family. Significant findings on neurologic exam included a severe gait imbalance, truncal ataxia, and dysarthria. A Brain MRI demonstrated a prominent enhancement along the inferior surface of the cerebellum along with diffuse white matter changes. A CT scan of the chest showed a large mass lesion involving the right upper lobe with mediastinal extension (). The patient underwent a CT guided fine needle aspiration (FNA) from the mediastinal mass, and transbronchial biopsy of the right lung lesion. The pathology was consistent with small cell lung cancer with endocrine features ().\nA lumbar puncture was performed to rule out leptomeningeal carcinomatosis. Cerebrospinal fluid (CSF) analysis demonstrated WBC 5, RBC 300, protein 85 mg/dL and glucose 60 mg/dL. It was not remarkable for any viral encephalitides such as Herpes or west Nile and CSF cytology was also negative for any atypical or malignant cells. The patient underwent a brain and dural biopsy to rule our leptomeningeal carcinomatosis. We performed biopsy instead of less invasive methods like MR spectroscopy because MRI findings like leptomeningeal enhancement was concerning for direct neoplastic seeding. In addition, other radiographic findings like white matter changes which are less typical seen in a paraneoplastic syndrome, made us to proceed a brain biopsy. The pathology was negative for any metastatic lesion or any leptomeningeal involvement. It showed normal cortical grey and white matter cells with no significant pathologic changes.\nExtensive laboratory work up was performed to rule out collagen vascular disorders or any possible infectious or metabolic etiologies. Based on history and clinical findings, our impression was paraneoplastic cerebellar degeneration due to the small cell lung cancer. Among onconeuronal antibodies, CSF anti-Hu antibody came back positive which confirms our diagnosis. We thought the white matter changes found on brain MRI were nonspecific and most likely caused by chronic small vessel changes due to long standing hypertension.\nSystemic chemotherapy and plasmapheresis were initiated immediately. However; the patient rapidly deteriorated and became encephalopathic. The family decided to discontinue any further medical treatment based on his will prior to his altered mental status, hence he was discharged to a hospice care facility afterwards. |
A 50-year-old man was referred to our department with the chief complaint of discomfort on the right side of his neck. He had no medical history. He had initially become aware of pain on the right side of his neck three years before visiting our department. He first consulted with the oral and maxillofacial department of a local hospital. Computed tomography (CT) at that hospital showed styloid process prolongation; however, the patient reported mild discomfort upon follow-up. The discomfort on the right side of his neck worsened, and he was referred to our hospital for the treatment of his neck symptoms.\nThe patient had no systemic disease at the initial visit. He was aware of the discomfort of the right side of his neck when he turned his head (). A rigid bone-like structure was palpable in the right submandibular region. In addition, panoramic radiography revealed an elongated right styloid process beyond the mandibular plane (). CT showed styloid process prolongation on both sides (). The length of the styloid process was 60 mm on the right side. Calcification of the minor horn of the hyoid bone and the styloid process' tip was also observed. Moreover, prolongation of the right superior cornu of the thyroid cartilage was observed, with a length of 23.2 mm. The cervical symptoms might have been due to the extension of the superior thyroid cartilage angle. Still, the discomfort that occurred during the neck rotation coincided with the tip of the styloid process. The patient was diagnosed with symptoms of styloid prolongation .\nSurgical trimming of the elongated styloid process with an extraoral approach was performed under general anesthesia. A skin incision was made in the submandibular region, and detachment was performed to reveal the intermediate tendon of the digastric muscle. A styloid process was observed near the hyoid bone. After the detached surrounding area, the styloid process was resected using an ultrasonic bone scalpel (). The stylohyoid ligament was attached to the tip of the styloid process and, consequently, resected (). The postoperative course was eventful, and the patient's neck discomfort dissipated. Eight years after the operation, the cervical symptoms did not recur. |
A 43-year-old woman presented with vomiting and abdominal pain and had no previous medical history. The patient began experiencing abdominal distension 3 months prior, with intermittent abdominal pain and nausea developing after the first month. As symptoms persisted, the patient consulted the nearby clinic and underwent upper and lower gastrointestinal endoscopy and abdominal CT scan. Findings suggested ileal intussusception, and the patient was referred to our department for detailed examination.\nThe abdomen was flat and soft, and did not show tenderness or rebound tenderness. There were no palpable abdominal masses or Dance signs.\nAbdominal contrast CT scan showed edematous thickening of the distal ileum (), and we observed intussusception developing from a tumor lesion, with fat in the same site (). Mild dilation was observed in the upper gastrointestinal tract, and there were no obvious regions of poor contrast. Based on these findings, the patient was diagnosed with intussusception of the ileum. As there were no findings suggesting gastrointestinal obstruction or impeded blood flow in the intestinal tract, the patient was scheduled for naval single-incision laparoscopically-assisted partial ileectomy.\nLaparoscopy was performed by making a vertical incision measuring 3 cm in the navel. A wound retractor was inserted, and we laparoscopically observed the peritoneum via the suspension method until we located the lesion. The intestinal tract was brought out through the incision, and a mass was palpable in the lumen about 50 cm from the end of the ileum. An inversion in the opposite side of the upper gastrointestinal mesentery was thought to be the base of the mass, and we removed approximately 8 cm of the ileum, including this section ().\nExamination of the mass showed protruding, raised lesions from the opposite side of the ileal intestinal mesentery to the intestinal lumen, which was considered to be an MD inversion. Furthermore, despite observing erosion at the top and sides of the diverticulum, no tumor or ectopic tissues were observed macroscopically ().\nHistopathological examination revealed a full-thickness true diverticulum (), and an aggregation of tall columnar epithelium, mucosal glands and islets of Langerhans were observed at the tip (). Due to these findings, we concluded that the patient had ectopic pancreas with Heinrich Classification I [].\nThe patient recovered well, resumed eating 3 days after surgery and was discharged 9 days after surgery. |
We report a clinical case of a 75-year-old woman, with a history of breast cancer who undergone surgery 7 years ago, presenting bone metastases in different areas. The lesion was found by a routine mammography 7 years ago and she was operated few months after the discovery. After 7 years of clinical silence from the diagnosis, the patient was submitted to a positron emission computed tomography (PET/CT) that showed multiple predominantly lytic lesions in several skeletal segments, especially to the left iliac wing and ipsilateral acetabulum, at the level of the right scapula and L4 and D10 vertebra. This result led to a palliative radiant treatment at the level of the L4 vertebrae with a total dose of 30 Gy in 10 fractions (3 Gy/fraction) provided with a 6 MeV flash technique. After 2 months from the treatment, a total body CT was performed and it confirmed the previous lesions seen in the PET/CT and showed new lesions to the vertebra from D1 to D5. A further CT few months later pointed out an unchanged condition but there was also a worsening of the lytic lesions in D3 and D4, confirmed by an MRI 1 month later (). In February 2016, this woman arrived at our structure for a palliative treatment for the pain she felt at the level of her back and right scapula. We visited the patient and evaluated the pain level in the different sites through a numeric scale of evaluation (Karnofsky scheme) and an objective examination. After evaluating her clinical conditions and viewing the radiological exams, we decided to treat firstly the D2-D6 vertebra with a total dose of 30 Gy in 10 fractions (3 Gy/fraction) and then the scapula with a singular dose of 8 Gy provided with a 6 MV flash technique, where the patients felt the stronger pain, and not to treat the other lesions in areas where the pain was minimal or not existent. This way we save the opportunity to treat them when the patient will become symptomatic. |
The patient is a 48-year-old man brought to the Emergency Department in March 2019 from a nursing home with new right-sided facial droop. The patient had baseline cognitive impairment with left-sided weakness and visual field deficit from previous strokes. He was last known well the day earlier before he went to bed the previous night. He did not have any new arm or leg weakness. His past medical history was significant for antiphospholipid syndrome, NBTE of his aortic valve status post aortic valve replacement with Trifecta bioprosthetic valve 5 years back, occipital stroke with residual inferior visual field deficits, and multiple prior pulmonary embolisms and deep vein thromboses with inferior vena cava filter placement. He had previously failed warfarin and rivaroxaban and was on apixaban 10 mg two times daily. He had failed warfarin at another hospital as his international normalized ratio was never therapeutic from suspected Protein C or Protein S deficiency. Therefore, he was placed on rivaroxaban in September 2014. He was changed to apixaban during a hospitalization for a stroke in June of 2015 while on rivaroxaban. He was on apixaban 5 mg two times daily with last dose an hour prior to presentation. On examination, his temperature was 97.2°F and he was noted to have bilateral inferior visual field deficits from previous stroke. He performed one task correctly, answered one question correctly, had flattened nasolabial fold with asymmetry while smiling, and loss of fluency with National Institute of Health Stroke Scale of 4. Rest of the examination was unremarkable.\nHe was deemed not a candidate for recombinant tissue plasminogen activator as he had received apixaban an hour prior to presentation. A stat computed tomography of head showed encephalomalacia along bilateral superior and posterior parietal lobes with age indeterminate areas of low attenuation along the superior left frontal lobe extending to the cortex which were concerning for infarcts. Diffusion-weighted magnetic resonance imaging of the brain showed acute versus subacute punctate foci of hyperintensity within the left medial occipital lobe and bilateral superior parietal lobules along with remote infarcts involving the superior middle frontal gyri, left frontal opercular regions and extending into bilateral occipital regions. Magnetic resonance angiogram of the head and neck did not show any hemodynamically significant stenoses in intracranial circulation, cervical carotids, and vertebral arteries. Electrocardiogram showed sinus rhythm with first-degree AV block. He was started on aspirin 81 mg daily and atorvastatin 40 mg daily. Hematology was consulted who recommended lifelong anticoagulation with enoxaparin 104.3 mg two times daily based on his weight.\nGiven history of aortic valve endocarditis and replacement and concern for embolic phenomenon, transesophageal echocardiogram (TEE) was performed. It showed a well-functioning stented bioprosthetic aortic valve with trace aortic insufficiency and no evidence of thrombus or vegetation. However, a 0.7 × 1.1 cm mass noted on the tip of anterior mitral valve leaflet and 0.7 × 0.9 cm mass was noted on the tip of the posterior mitral valve leaflet with findings consistent with NBTE (). He had moderate to severe, central mitral regurgitation (MR) and an intact interatrial septum with no evidence of a shunt by color Doppler or with injection of agitated saline. The left atrial appendage appeared normal. The mitral valve and bioprosthetic aortic valve were noted to have been functioning well at an outside hospital transthoracic echocardiogram (TTE) report a few years back. Other significant lab results are presented in . IgG B2 Glycoprotein 1 Antibody and IgG Cardiolipin Antibody were elevated consistent with his history of antiphospholipid syndrome. Mitral valve endocarditis was managed conservatively with anticoagulation. He was discharged to a subacute rehab on subcutaneous enoxaparin 100 mg two times daily.\nPatient had a subsequent hospitalization 3 months later with a fever of 100.9°F and a low hemoglobin of 6.7 g/dl (reference range: 14–17.5 g/dL). He was noted to have hemolytic anemia with reticulocytes of 10.9% (reference range: 0.5–2.0%), mild lactose dehydrogenase elevation of 287 IU/L (reference range: 140–271 IU/L), and elevated indirect bilirubin of 1 mg/dL (calculated by subtracting direct from total bilirubin). His direct Coombs test was positive for warm autoantibody IgG and C3 complement. His fecal occult blood test was negative. He received blood transfusion as necessary with goal hemoglobin > 7.0 g/dl and was started on intravenous methylprednisone that was tapered to hydrocortisone due to his adrenal insufficiency. Two out of 2 of his blood cultures from admission came back positive for Enterococcus faecalis which cleared on the sixth day of admission with antibiotics. Patient had a chronic indwelling Foley’s catheter. Source of bacteremia was urine which grew >100,000 CFU/mL E. faecalis and >100,000 CFU/mL Escherichia coli. The patient was placed on intravenous vancomycin and ceftriaxone. Vancomycin was later changed to daptomycin due to persistent bacteremia. TTE showed focal thickening and calcification of the mitral valve leaflets and subvalvular apparatus, a small density on the atrial side of the mitral valve and moderate to severe mitral regurgitation. TEE further showed 0.6 × 0.5 cm and 0.4 × 0.3 cm masses attached to the tip of the anterior and posterior MV leaflets, respectively, with moderate to severe, central MR (). No obvious vegetation was noted in the aortic valve. Given persistent bacteremia and severe MR, patient underwent redo sternotomy and mitral valve replacement with 27 mm Edwards bioprosthesis. Endocarditic breakdown of mitral valve was observed but no real vegetation was noted during the procedure. Histologic examination of the mitral valve was consistent with vegetation, but bacterial, fungal, and anaerobic cultures were negative for definitive organisms. Post-operative stay was uneventful, and patient was discharged on IV daptomycin to complete a 6-week course.\nThe patient was hospitalized a month later with right temporal occipital intraparenchymal hemorrhage measuring 4.4 × 3.8 × 3.2 cm with adjacent edema but no midline shift. This was thought to be due to hemorrhagic conversion of prior stroke. Hemorrhagic stroke was managed conservatively by holding enoxaparin for 4 days and starting levetiracetam for seizure prophylaxis. He was again hospitalized a month and a half later with 3.8 × 3.4 × 2.7 cm large right cerebellar hematoma with mass effect on the fourth ventricle without hydrocephalus (). Patient passed away later the same day thought to be from brain herniation. |
A 14-year-old boy presented to our outpatient clinic because of right knee pain that had been present for the previous 2 months. There was persistent pain in the medial side of the right knee, and the pain was worse on knee flexion while weight-bearing. Conservative treatment performed in a local clinic did not improve the symptoms. The patient participated in Hapkido, but had no specific trauma history.\nOn physical examination, there was medial joint line tenderness. There was no joint effusion or limitation of the range of motion. There were no palpable soft tissue mass lesions on the medial side of the knee.\nThere were no abnormal findings on plain radiography. MRI revealed a huge intrameniscal cyst located in the central parenchyma of the posteromedial corner of the MM, and a very thin meniscal parenchymal layer between the cyst and the upper and lower surfaces of the meniscus (Fig. , Pre op.). However, it could not be clearly identified whether the thinness of the parenchyma was caused by a pressure effect or a loss of degenerated meniscal substance due to cystic fluid. In addition, one sagittal slice on MRI revealed a vertical tear in the red-white zone of the upper surface of the MM (Fig. , Pre op.). Therefore, the tear was classified as a stage 2B meniscal tear using the Stoller and Crues 3-stage MRI classification of meniscal degeneration. The presence of such a tear accompanied by a huge intrameniscal cyst is very unusual [–]. Arthroscopy was performed to identify and treat the lesions identified on MRI as an intrameniscal cystic lesion and suspected meniscal tear. On the posteromedial portion of the MM, arthroscopy revealed a small vertical longitudinal meniscal tear in the red-white zone of the upper surface of the MM (Fig. ). Arthroscopic probing also confirmed the presence of a cystic lesion inside the meniscus.\nAs the patient was only 14 years old, we decided to preserve the meniscus through suturing as the primary operation. However, because the lesions were chronic, it was expected that simple arthroscopic repair alone would not achieve a successful outcome. Thus, we decided to also perform open meniscal repair with cystic debridement by directly accessing the intrameniscal cyst through a skin incision. A small vertical skin incision was made over the medial joint line, and the subcutaneous tissue of the posteromedial corner of the knee was dissected to expose the posteromedial capsule behind the medial collateral ligament. Under arthroscopic translumination assistance, the joint capsule was transversely incised just proximal to the upper surface of the MM to prevent iatrogenic meniscal injury. The upper surface of the MM was identified, and the meniscal cyst was exposed through an additional small transverse incision of the meniscocapsular junction (Fig. a). A meniscal rasp and a curette were used to debride the cyst wall through the open incision. Open meniscal repair was performed with vertical sutures using 0 vicryl (Polyglactin 910; Ethicon, Somerville, NJ, USA) to close the surgically opened intrameniscal cyst (Fig. b). Two inside-out horizontal meniscal sutures were placed using no. 2–0 FiberWire meniscal repair needles (Arthrex, Naples, FL, USA) and zone-specific cannulas (Linvatec, ConMed, Largo, FL) (Fig. c). Figure d shows a simplified illustration of the suture repairs performed for the intrameniscal cyst and the tear of the upper surface of the MM. Biopsy was not performed.\nRange of motion exercise was started immediately after the surgery. The patient was only permitted to walk with crutches to restrict weight-bearing until 6 weeks postoperatively. Weight-bearing was then gradually increased. Full weight-bearing was permitted from 3 months postoperatively. Return to daily sports activity was allowed at 6 months postoperatively. The patient was regularly followed up, and consented to undergo MRI at 3 months, 6 months, 1 year, 2 years, 3 years, and 4 years postoperatively. Over time, the high signal intensity where the meniscal cyst was located slowly disappeared (Fig. , Post op.)\nAt 4 years postoperatively, MRI showed a normal meniscus (Fig. , Post op.) There was no recurrence of symptoms, and the International Knee Documentation Committee 2000 subjective knee score was significantly improved from 42 points preoperatively to 93 points at 4 years postoperatively. The patient reported that he did not feel any discomfort during daily life and exercise. |
A 31-year-old right-handed female was admitted to the emergency department because of headache associated with visual disturbance. She had no previous history of headache and no known vascular risk factors but she used an oral contraceptive pill. On admission, she reported a 9-hour progressive pulsatile headache, with nausea and photophobia, followed by a sudden left visual field defect. Neurological examination documented left homonymous hemianopia. A head computed tomography (CT) scan was judged to be normal (fig. ). She was treated with paracetamol and metoclopramide with subjective improvement followed by hospital discharge. The next day, the patient was observed at an outpatient consultation and subsequently admitted in the neurology ward because the headache had worsened and she felt weakness and numbness of the left limbs. She also recalled a history of thoracic rash 1 month before and she reported having had varicella at the age of 7 years. Neurological examination at that time revealed slight drowsiness, mild left hemiparesis, left hemihypesthesia and homolateral homonymous hemianopia. A new CT scan showed an ischemic infarct on the territory of the right posterior cerebral artery (fig. ) and contrast administration excluded dural sinus venous thrombosis. Cervical and transcranial ultrasound did not disclose significant abnormalities, namely vasospasm. She was started on acetylsalicylic acid 150 mg and simvastatin 20 mg i.d.\nTwo days after admission, the neurological picture worsened with acute onset of left central facial palsy, visual and tactile inattention and worsening of the left motor deficit. A new CT scan showed enlargement of the ischemic lesion with involvement of the right thalamus (fig. ) and new areas of infarction involving different arterial territories, further depicted on MRI (fig. ). MR angiography showed an occlusion of the right posterior cerebral artery 5 mm after its origin (fig. ). Transthoracic and transesophageal echocardiography and Holter ECG were within the norms, as were the of laboratory blood tests (including HIV antibodies). Clinical deterioration continued with further motor compromise, and although no cardiac or large vessel embolic source had been documented, facing neurological worsening, acetylsalicylic acid was substituted by low molecular weight heparin (60 mg subcutaneously twice a day) 6 days after admission. The patient remained stable for a week, but then a new episode occurred, with headache and slight drowsiness associated with hemorrhagic transformation involving the thalamus but sparing the cortical territory of the posterior cerebral artery (fig. ). Anticoagulation was stopped immediately.\nBecause of the medical history of recent VZV reactivation, it was then hypothesized that the stroke could be secondary to VZV vasculopathy. However, at that time, evidence of increased intracranial pressure contraindicated the lumbar puncture. Acyclovir and prednisolone were started empirically (acyclovir 750 mg three times daily, and prednisolone 60 mg once a day for 21 days), with slow but steady improvement. Digital subtraction angiography (DSA) showed narrowing at the origin of the right posterior cerebral artery and demonstrated an irregular lumen of the posterior segment of the pericallosal artery with beading-like pattern appearance (fig. ). She underwent a lumbar puncture 11 days after initiation of therapy (27 days after admission). Cerebrospinal fluid (CSF) protein content was slightly increased (48 mg/dl), glucose 59 mg/dl, and a discrete mononuclear pleocytosis was detected (6 cells). VZV-DNA was not detected by polymerase chain reaction, but there was an increased CSF/serum ratio of VZV IgG (3.3), confirming intrathecal production of anti-VZV antibodies.\nMotor function improved, but the patient was discharged with persistent left homonymous hemianopia and spatial inattention, unable to walk without assistance [modified Rankin scale (mRS) score 4]. After antiviral therapy, she restarted acetylsalicylic acid 150 mg once a day. On the 6-month follow-up, only a mild to moderate paresis of the left limbs was present. Hemianopia also, improved but an incomplete deficit of the left visual field persisted. The patient was able to walk unassisted and look after her own affairs (mRS score 2). |
A 5-year-old male was brought by his grandmother with a history of recurrent abnormal body movement and shaking of his body. It was initially misconstrued as seizure or dystonic reaction without the loss of consciousness for 3 days. It was of abrupt onset and a fluctuating pattern. The client had no history of drugs usage such as antipsychotic or antiemetic that could cause abnormal body movement or dystonia. There were intervals of normal movement and behavior. He was said to be having 4–5 episodes of abnormal body movements per day. There was no history of muscle spasm, tongue thrusting, stridor, or dysphonia. There was no history of seizure at any time. There was no history of use of anticonvulsant at any time and electroencephalogram done was normal. The physical and neurological examination done on him was normal. His cognitive functions and psychometric evaluation done withdraw a person test was normal. Laboratory results, including a full blood count, blood film for malaria parasite, and blood chemistry (serum calcium, sodium, potassium, and bicarbonate), were essentially normal. He was sleeping well and was fully interactive and energetic in the ward. The child was initially managed as a case of dystonia; even though, no history of the use of drug that can cause dystonia. He was placed on iv fluid and diazepam 2.5 mg twice daily for 2 days. On the 3rd day, repeated abnormal body movement persisted even while walking without any fall. There was curiosity to look at malingering as a diagnosis in the child despite his age because of abnormal movement and gyration while walking without any fall which is not consistent with features of seizure disorder, pseudoseizure, or dystonia. The need to consider interaction with the child was encouraged to explore a positive outcome. The child was then instructed to display that movement voluntarily, and to our amazement, he was able to display the movement repeatedly and was able to abort the movement voluntarily. He was able to repeat this symptom and abort severally when instructed. Further history at this point revealed that child and grandmother had frequented kind of syncretic churches where worshippers fall into a state of religious trance, during which they gyrate their bodies rhythmically while delivering “spiritual” messages. On close discussion with the child, he revealed his perceived passion for the body movement learnt from the spirit-filled worshiper in the church and the attention he gets from the grandmother when displaying such movement. Adopting a nonjudgmental approach and gentle persuasion, the client was encouraged to tell the full story, and he expressed the passion he has for such movement and dance. He enjoyed mimicking the abnormal body movement because of the attention he gets from the grandmother any time he displayed it. |
A male patient aged 51 years was admitted to our hospital on March 15, 2016 with a complaint of blurred vision in the right eye for 4 h after dizziness and vomiting. He felt dizzy when he got up and then symptoms of nausea and vomiting appeared. After he sit back and rested immediately, he felt decreased vision in his right eye. He has no history of trauma and eye diseases. His vision acuity was 20/20 in both eyes after the physical examination just 1 month ago. He was healthy with no history of systemic diseases, such as high blood pressure, diabetes, and heart disease. Normal development of his body, without signs of Marfan syndrome, Marchesani syndrome, and homocystinuria.\nNo abnormality was found by general physical examination. His vision acuity was hand moving (HM) in right eye and 20/25 in left eye. The intraocular pressure in the right eye and the left eye was 20 mmHg (1 mmHg = 0.133 kPa) and 18 mmHg, respectively. Conjunctival congestion was noticed in right eye, however, the cornea is clear. The lens dislocated into the anterior chamber. The pupil was 6 mm in diameter and the light reflex was delayed. A small amount of vitreous body was seen behind the pupil (Fig. ) and the retina was not clear. The left eye was normal. The patient was diagnosed as lens dislocation in right eye and perforned the surgery of lens removal combined with anterior vitrectomy after 48 h. The operation was succeed, but the corneal edema was obvious after surgery since the lens contacted with the corneal endothelia for long time. After treatment for 1 week, the cornea recoverd transparent and the anterior chamber was clear. The pupil diameter returned to normal after 1 month and the retina turned out to be normal (Fig. ). The contralateral eye was normal when checked and no abnormality of the lens and the zonular fiber was found (Figs. , and ). His physical examination included the cardiac color ultrasound, the aortic doppler, and the brain magnetic resonance examination, was totally normal. His hands and somatotype were also normal (Fig. ). His right vision was still HM (no improvement when corrected) and the IOP was 16 mmHg on the day of hospital discharge (one week after surgery). After 1 month, his corrected vision acuity was improved to 20/25 and the secondary intraocular lens suture fixation was performed 3 months later. |
A 55 year old lady admitted with bilateral neck swelling with an 8 year history of a lump on the left side of the neck and a 15 month history of the right sided lump. She had a past medical history of breast cancer in 1998.\nOn examination both lumps were palpable below the angle of the mandible and medial to it, they were mobile, not attached to the overlying skin, non tender and of normal colour and temperature. She had no evidence of cranial nerve involvement or endocrine abnormalities and no issue with blood pressure control.\nCarotid Duplex US showed a normal left common carotid artery but the left internal carotid and external carotid artery were splayed with evidence of a mass between the vessels, suspicious of a chemodectoma. The mass was 3 cm in diameter and appeared vascularised, fed by branches of the ECA. See Figure .\nThe left mass was excised through a subadventitial dissection. The diagnosis of carotid body tumour was confirmed by histology, which revealed features consistent with a paraganglioma. Immunohistochemistry demonstrated that the mass was S100 positive, Ki67 low.\nThe right common carotid was normal but the right internal carotid artery and right external carotid artery were splayed by a soft tissue mass of 2.5 cm diameter. CT neck was carried out which revealed that the right sided mass extended superiorly to enlarge the jugular foramen and there was an intracranial component. See Figure , , .\nShe had a full work-up with serological and urinalysis combined with a CT abdomen to rule out the presence of concomitant glomus tumours.\nAs CTA yielded inadequate visualization of the distal end of the CBT, MRI brain was performed which demonstrated a well defined enhancing lesion measuring 1.8 cm in diameter extending from localised posterolateral to the right carotid sheath and extending from the level of the carotid sheath up to the jugular foramen.\nThe right sided CBT was excised and postoperatively she developed a right vocal cord palsy and dysphagia particular for solids. This has resolved gradually. |
A 13-year-old Sri Lankan boy presented to our medical unit with a sudden onset tonic-clonic convulsion of the right arm with secondary generalization resulting in loss of consciousness lasting about 10 minutes. He developed two similar focal fits after admission of which the durations were about 5 minutes each. When further questioning from the parents, it was revealed that he had developed sore throat and fever 2 weeks prior to admission and were resolved with treatment including an oral antibiotic. He was fever free for about one week but he complained of recurrent frontal headaches. He had not noticed any gross hematuria, dysuria or decreased urine output prior to admission. On the day of admission the patient had developed repeated episodes of vomiting and, increased sleepiness. He also noticed to have transient visual disturbances which he explained as distorted sizes of the images. The patient also gave a history of an infected wound over right ankle that he had 2 weeks back, which was healed by the time of admission.\nOn admission he was drowsy but rousable with a Glasgow coma scale (GCS) of 13/15. He had mild periorbital swelling, without clinically detectable dependant edema. His throat was not inflamed and his thyroid gland was normal. He didn’t have any signs of meningeal irritation or any focal neurological signs. His blood pressure was 130/80 mmHg on admission with a significant protein urea detected by dipstick. Within 2 hours his blood pressure raised up to 200/100 mmHg and he was admitted to the intensive care unit (ICU) for close monitoring and further management. While in the ICU intravenous antihypertensive drugs were used to control the blood pressure. Later blood pressure was controlled with oral antihypertensive medications. His urinalysis reported as moderately field full red cells with dysmorphic red cells of 15% suggestive of hematuria of glomerular origin and occasional pus cells but no cellular casts. His anti streptolysin O titre (ASOT) reported as more than 200 U/mL and was considered significant, urine and the throat swab cultures were sterile. He had normal serum creatinine and electrolytes; however his blood urea was elevated up to 26.7 mmol/L despite adequate hydration. His serum protein was low. Diagnosis of acute PSGN was made and he was started on intra venous (IV) penicillin.\nDuring the second day of ICU his urine output started declining to less than 0.5 mL/kg/h. His peri orbital swelling worsened and developed bilateral plural effusions and ascites. He was started on IV furosemide and strict fluid balance was maintained. His blood urea started to rise despite adequate hydration but other renal functions including serum creatinine remained normal. He underwent ultrasound scan of the abdomen on day-2 of the admission and showed ultrasonic evidence of acute renal parenchymal disease, ascites and bilateral plural effusions. Blood picture was suggestive of acute bacterial infection but the blood cultures and throat swab cultures were sterile. He underwent 24 hour urine collection and found to have sub-nephrotic range protein urea of 0.6 g/24 h. An urgent electro encephalogram (EEG) was done on admission and showed changes suggestive of encephalopathy secondary to recurrent fits, he was started on sodium valproate and phenytoin sodium by the neurologist.\nA contrast-enhanced computed tomography (CT) of brain done on day-3 and revealed non-enhancing low-attenuating areas in fronto -parietal regions (Figure ). There was no abnormal meningeal enhancement or focal lesions. A T2 weighted image of magnetic resonance imaging (MRI) was taken on day-10 of the admission and found to have linier sub-cortical hyper intensities in both parietal regions which was consistent with the radiological diagnosis of PRES. MRI findings were less intensive than CT finding suggesting recovery of the cerebral insults during that period (Figure ). As cerebral vascuitis was also a possibility, erythrocyte sedimentation rate (ESR), anti nuclear antibody (ANA) and anti neutrophil cytoplasmic antibody (ANCA) were done and found to be negative. After 5 days of ICU stay followed by 2 days of inward stay, patient's blood pressure was well controlled with oral captopril. He had a satisfactory urine output without diuretics and no clinical or biochemical evidence of acute kidney injury. His hematuria was settling and he was seizure free. His vision had returned to normal. He was discharged with the antihypertensive and anti-epileptics and planned to be reviewed weekly in the outpatient clinic. After 3 weeks, his hematuria had totally resolved according to repeat urinalysis and antihypertensive drug was gradually tailed off whilst patient was normotensive. He underwent a repeat MRI scan 3 weeks later and the above radiological manifestations disappeared, thus it was reported as normal. |
A 30-year-old woman presented with gradually increasing weakness of both upper and lower limbs. She reported having had a similar episode twice previously, most recently 2 months ago; and at all of these occasions, she had documented hypokalemia and she was managed by a local physician with parenteral and oral administration of potassium chloride that improves her condition on these occasions. Resting after exercise or eating did not precipitate the weakness and there was no family history of similar illness. Patient also had complaints of recurrent oral ulceration, photosensitivity, hair loss, loss of appetite, easy fatigability, pain in multiple joints and she experienced this pain almost throughout the day, but it was worse in the morning. The patient also had significant morning stiffness and daytime fatigue. All these symptoms were present since 6 months. She had also off and on low grade fever over 3 months before admission but she had no burning in the urine, cough and abdominal pain or vomiting, pruritus, dryness of mouth, difficulty in swallowing, gritty or sandy sensation under eyelids and Reynaud's phenomenon. On the day of admission, the patient also complained of difficulty in swallowing solid food and inability to speak loudly but there was no history of visual blurring, diplopia, facial asymmetry, sensory, bladder, or bowel complaints. She had a clear sensorium with no history of seizures, involuntary movements, root pains, or band-like sensation over the trunk. She did not give a history of prior drug intake, colicky abdominal pain and recent vaccination.\nSix months before her current presentation, the patient had progressive weakness in all four limbs; it started in one limb, but progressed to all four limbs within a few hours and her past medical record and history given by her husband revealed that she was conscious and oriented at the onset of weakness. Her eye movements were normal and there was no facial asymmetry and seizure at the onset of weakness. At current admission to our hospital in physical examination, blood pressure was 130/80 mm Hg; Pallor was present. There was no edema, icterus and lymphadenopathy. Musculoskeletal and neurological examination revealed muscle strength was poor (flicker 1/5) in all the muscle groups. Deep tendon reflexes were intact and planter reflex was flexor bilateral. Laboratory investigations done revealed blood urea 28 mg/dl, serum creatinine 1.3 mg/dl, hypokalemia 2.2 mmol/L, hyperchloremic metabolic acidosis (chloride 112 mEq/L, arterial blood pH 7.279) and alkaline urine (urinary pH 7.5). Radiograph of the abdomen did not show any nephrocalcinosis. Ultrasonography of the abdomen revealed right nephrolithiasis with bilateral normal size kidney and normal liver size and echotexture. In view of the normal anion gap acidosis (12.4 mmol/l), alkaline urine (urinary pH 7.5), low serum potassium (2.2 mmol/l), absence of Fanconi's syndrome, positive urinary anion gap (46 mmol/l), the diagnosis of dRTA was made. Type 2 RTA was excluded, as her 24 h urinary excretion of phosphate and uric acid was normal with no glycosuria. Renal biopsy was deferred in view of normal renal function and no active sediment in urine routine microscopy. The patient was started on oral potassium and bicarbonate supplementation. Oral hydroxychlroquine and a short course of steroid were also given. Her biochemical parameters corrected with treatment and she attained blood urea of 24 mg/dl, serum creatinine 1.0 mg/dl, potassium 3.9 mEq/L, chloride 95 mEq/L and arterial blood pH of 7.332. She had continued on the oral supplements with sodium bicarbonate (500 mg twice daily) and oral hydroxychloroquine 200 mg twice a day and had been asymptomatic on regular follow-up []. |
A 62-year-old male reported to our hospital with an asymptomatic swelling in the right lower half of the face with reduced mouth opening since two weeks. History revealed that this was the 3rd time that such a swelling had appeared in the buccal region over a span of 8 years. The first episode 5 years before involved a previous history of pus discharge with a diagnosis of buccal space infection treated by incision and drainage. The buccal swelling had regressed on its own upon a second occurrence 2 years back. The patient has been a known diabetic since a year and on regular medication. A detailed medical examination was performed in which the patient was screened for anomalies of the skin, eyes, skeletal system, endocrine system, nervous system, and any other developmental disorders, ruling out any syndromic association.\nOn examination, gross asymmetry on the right side of the face was evident. A large ovoid submucosal swelling (6 × 6 cm in size) was observed extraorally, extending superoinferiorly from the level of the right lateral canthus of the eye to 1 cm below the corner of the mouth and anteroposteriorly from the corner of the mouth to the mandibular ramus (). The borders of the lesion were ill-defined on palpation. The consistency of the swelling varied from being soft to firm. Overlying skin was normal. There was no history of any pain, fever associated with the swelling. Submandibular and cervical lymphadenopathy was absent. Paresthesia or palsy of the right side of the face or swelling of the right parotid gland was not noted.\nIntraorally, the ovoid swelling presented as a slight elevation of the buccal mucosa without any obliteration of the buccal vestibule. It extended from 1 cm from the commissure of lip to 1 cm short of the pterygomandibular raphae. The buccal mucous membrane appeared stretched and glistening without any signs of inflammation. Mouth opening was restricted due to the size of the lesion.\nComputed tomography revealed a well-defined lesional mass with cystic areas involving the buccal space. Intracystic loculation was visible with a pus-like dense cystic content. Erosion of the posterior buccal cortex was evident with no perforation of the maxillary bone. The maxillary antral wall was compressed (Figures –).\nA clinical diagnosis of a nonspecific chronic abscess with spread of infection was made and the lesion was treated under GA through an intraoral approach. An incision was made on the buccal mucosa and the lesion was excised in toto along with a safe margin of a fibrous tissue cuff. The lesion shelled out easily without any involvement of the buccinator muscle nor of any bony component. On surgical exposure, the lesional mass was well circumscribed with a fibrous outer covering. The lesion looked lobulated as the mass had herniated into the pterygomaxillary space (Figures and ).\nThe excised lesion resembling a leathery pouch was present completely within the soft tissue in the buccal space. It was not attached to the buccinator muscle nor was it attached to any bony component of the maxilla or related to the parotid gland or duct.\nThe specimen obtained was 4.8 × 4.5 cm in size, creamish brown in colour with a firm consistency with an irregular surface. Multiple samples were routinely processed and stained with hematoxylin and eosin ().\nA differential of a large dermoid or epidermoid cyst, a parasitic cyst, and a cyst of inflammatory origin was considered.\nMicroscopically, the tissue sections showed a cystic lumen lined by parakeratinized epithelium of uniform thickness. The basal cells were cuboidal to columnar in shape exhibiting nuclear palisading. The spinous layer was thin and the parakeratin layer showed surface corrugations. Some areas were lined by flattened, stretched epithelium whereas other areas exhibited numerous infoldings of the epithelium into the connective tissue wall. The epithelium connective tissue interface was smooth and flat with no rete ridges. Underlying fibrous connective tissue was thin and mature with fibrocytes and fibroblasts with few odontogenic rests. Areas of haemorrhage and blood vessels were evident in the stroma. No daughter cysts, epithelial islands, skeletal muscle tissue, or any appendages were present in the connective tissue wall (Figures and ).\nA diagnosis of an extragnathic KCOT of the buccal region was made taking into account mainly the histologic features supported by the clinical and CT (radiologic features). Regular patient follow-up is carried out every 6 months with no evidence of recurrence in 24 months.\nThe lesional tissue was immunostained with Ki-67 (Biogenex) to assess the mitotic activity of the cystic lining to reveal the proliferative potential of the lesion as compared to conventional intraosseous KCOT. An interesting finding was that almost all the basal cells and only few suprabasal cell nuclei stained positive for Ki-67. A converse of this finding is generally observed in most conventional intraosseous KCOTs wherein a larger number of suprabasal cell nuclei stain positive for Ki-67 as opposed to the nuclei of the palisading basal cells (Figures and ). |
A 10-year-old male patient reported to the Department of Pedodontics and Preventive Dentistry with his mother, with a chief complaint of pain in the left lower back tooth region since 7 days. The pain was dull and intermittent in nature. No significant medical and family history was obtained. There was no significant past dental history and no history of orofacial trauma. On general physical examination, patient was apparently well. On intraoral examination, left and right mandibular permanent first molars were carious and left and right mandibular primary second molars were grossly decayed. Root stumps of left and right mandibular primary first molars were present. In maxillary arch, left and right primary second molars were grossly decayed. During intraoral examination, it was found that permanent mandibular right central incisor had a large crown with horn-like projection on the lingual surface of tooth (). The permanent mandibular right central and lateral incisors were provisionally diagnosed to be fused as lateral incisors were not visible in the oral cavity. Two-thirds part of the crown of tooth was erupted in oral cavity and was rotated from its normal position (). Intraoral periapical () and mandibular occlusal radiographs were taken (). Both the radiographs revealed fusion of only crown of permanent mandibular right central and lateral incisor teeth with two separate roots. Fused teeth showed two pulp chambers with two root canals. An inverted “V“-shaped radiopaque structure arising from the cingulum of teeth superimposed on affected crowns of teeth. This horn-like projection consisted of enamel and dentin with pulp chamber, which confirmed the presence of a talon cusp. After examination and confirmation of diagnosis of all the carious teeth, necessary treatment was rendered to the child. The fused teeth were clinically asymptomatic and the talon cusp neither irritated the tongue during speech or mastication nor did it interfere with occlusion. As there was no clinical problem associated with the fused teeth, clinical findings were explained as both parents and patient were unaware of the related condition, reassurance of the patient was done, and pit and fissure sealants were applied on the fused teeth to prevent any decay or further problem. Patient was scheduled for extraction of grossly carious teeth and root stumps. All the carious teeth were restored (). Patient was kept on regular follow-up for examination of fused teeth. |
A 68-year-old man with a past medical history of clinically asymptomatic dilated cardiomyopathy and alcohol abuse was diagnosed with metastatic BRAF wild-type melanoma metastatic to lymph nodes and small bowel in June of 2011 and subsequently treated with 4 doses of ipilimumab between July and September of 2011.\nApproximately one month after the last dose of ipilimumab the patient developed dyspnea upon exertion in addition to upper and lower extremity edema, leading to hospitalization for heart failure exacerbation in November of 2011. An initial echocardiogram revealed enlargement of the left ventricle with an EF of 46 %, thickening of the mitral valve, and severe mitral regurgitation, mild to moderate tricuspid regurgitation with severe pulmonary hypertension. Coronary artery disease was ruled out by nuclear cardiac stress test. He was treated with diuretics, beta blocker, and ACE inhibitor with symptomatic improvement and normalization of the volume overload. The etiology was initially attributed to ethanol (ETOH) abuse, however a repeat echocardiogram in December of 2011 performed after strict abstinence from ETOH showed worsened EF (25–30 %), which prompted a right and left heart and coronary catheterization as well as cardiac biopsy. Coronary artery disease was definitively ruled out and measurements of right heart pressures suggested elevated right atrial, right ventricle, and pulmonary artery pressure. A cardiac biopsy was nonspecific but ruled out acute myocarditis. Corticosteroids were not administered and the patient’s performance status only slowly improved over months.\nRestaging imaging following completion of ipilimumab treatment demonstrated clear progressive disease. Subsequent oncologic treatment was complicated by multiple hospitalizations due to recurrent cellulitis however the patient was eventually treated with temozolomide chemotherapy. Over the course of 18 months, the patient developed long-term disease stabilization. The patient is alive more than five years following diagnosis of metastatic melanoma. While an association of heart failure exacerbation and treatment with ipilimumab was not definitively established, the close temporal relation, absence of clear other exacerbating etiologies and long-term survival of the patient suggest an immune-mediated etiology triggered by ipilimumab as the most likely culprit of the heart failure. |
A 76-year-old male patient diagnosed ambulant with acute ruptured aortic type B dissection was referred to our ICU. He presented with severe tearing pain that migrated from his back and then to his abdomen. He had a history of hypertension, diabetes and hyperlipidemia. Physical examination upon arrival revealed blood pressure of 82/55 mmHg. The patient complained distress and vomiting. Three dimensional reconstruction of the CT angiography showed a dissecting and acute ruptured aneurysm from 1 cm beyond the left subclavian artery with a diameter reaching 4 cm at the largest part. There was also distinctive left side hematothorax (Figure ). Fortunately, all abdominal arteries were feeded by the true lumen with no signs of abdominal malperfusion. Laboratory examination showed highly increased lactate level while haemoglobin was decreased. Based on the severe hemorrhagic shock, the patient was immediately transferred to our hybrid OR. Under general anaesthesia the patient needed high dose inotropic support and showed poor oxygenation despite high pressure ventilation. Our interventional team, consisting of two angiologists and one heart surgeon, decided to release the left pleura due to a 4cm left side mini thoracothomy in the 4th intercostal space and overall delivered three litre fluid hematoma.\nSimultaneously the left femoral artery was surgically accessed and a transversal arteriotomy was performed. A 5F sheath was inserted percutaneously through the right brachial artery, through which a 5F pigtail catheter was directed for angiographic monitoring of the endovascular graft position. After administering 5,000 units of heparin we inserted the delivery system through the arteriotomy in the left common femoral artery. Valiant Captiva (34-34-200 mm) stent prosthesis was positioned and expanded in order to exclude aneurysm completely. At the end of the procedure, angiography was used to demonstrate the correct location of the stent and regular perfusion of the aorta and its branches.\nWith moderate inotropic support, the patient was administrated to our ICU. Furthermore the patient received a cerebrospinal fluid drainage system immediately after arriving on ICU. It was used for spinal cord protection within the next 3 days.\nThe post interventional course was complicated by renal failure and neurologic morbidity necessitating tracheotomy. Computed tomographic scan showed mild ischemia in the area of the left middle cerebral artery. We suppose that the meanwhile low flow during stenting procedure was causal for renal und neurologic impairment. Fortunately all neurologic deficits resolved moderate within the next days. On post interventional day 20 the patient was transferred to a neurologic rehabilitation. He has been followed up regularly and was free of neurologic symptoms after six months. Three dimensional reconstructions of the control- CT scan showed regular stent expansion without any endoleak (Figure ).\nThe suitable treatment strategy for acute descending aortic dissection has long been a matter of debate and continues to be a challenge []. High mortality rates in surgical treatment (25-50%) of complicated acute type B dissections, directed surgeons to search for other treatment modalities. Implementation of endovascular techniques has provided new therapeutic options []. Initial series and subsequent multicenter trials demonstrated technical feasibility and a low rate of complications even in high-risk patients with acute type B dissection.\nHowever, treatment of acute aortic dissections by endovascular grafting itself carries some risks. Leakage can occur in approximately 25% of patients. Rarely, the stent graft may not plug the aortic wall adequate and may dislocate. In 8% of patients embolic material may originate from an atherosclerotic basis and corrupt the blood flow of the spinal cord, leading to paraplegia. There is furthermore the risk for abdominal malperfusion. In this situation fenestration of the dissection membrane is recommended in several publications.\nThe most serious circumstance is rupture of the dissected aorta. In most of these cases the blood loss is very high and occurs into the left pleura. Without sufficient treatment strategies in specialized centres it leads directly to subsequent hemorrhagic shock and highly increased morbidity and mortality. This case illustrates that optimal treatment strategies are necessary to avoid serious complications. In our case, hemorrhagic and pulmonary shock due to ruptured aneurysm requires simultaneous thoracotomy and endovascular stent implantation. While opening the left pleura and release hemorrhagic effusion, stent grafting was performed during sufficient circulation and mechanical ventilation. |
The patient is a 56-year-old woman who presented to the emergency room with a chief complaint of a 6-hour history of worsening ‘cramping, burning’, right lower quadrant abdominal pain aggravated by movement with occasional radiations to the low back. She tested positive for COVID-19 11 days prior. The patient reported mild residual nausea and diarrhea but denied other associated symptoms. Past medical history included restless leg syndrome and hypertension. Past surgical history was significant for laparoscopic hysterectomy 3 years prior and ovarian cystectomy in her teenage years. The patient had three previous vaginal deliveries, and her last menstrual period was 7 years prior. Vitals signs were stable in the emergency department. Physical examination demonstrated isolated abdominal tenderness in the right lower quadrant with no distension or rebound tenderness. Pertinent labs included mild hypokalemia and mild thrombocytopenia. An abdominal and pelvic computed tomography (CT) with contrast showed inflammatory changes and fluid along the right gonadal vein with no definite thrombosis; the right ovary was not distinctly identified. A transvaginal Doppler ultrasound revealed appropriate arterial flow with questionable visualization of the right ovary, no visualization of the left ovary and a small amount of free fluid in the pelvis. A transabdominal pelvic ultrasound was able to identify a relatively enlarged right ovary with irregular borders and a normal left ovary. Considering the patient’s clinical presentation and high index of suspicion for ovarian torsion, surgical intervention was recommended, and the patient consented for diagnostic laparoscopy.\nIntraoperatively, surgical access to the abdomen was obtained and an initial survey of the pelvis demonstrated surgically absent uterus and bilateral fallopian tubes, normal appearing left ovary and a necrotic, indurated right ovary without evidence of torsion. The distal right ovarian vessels and surrounding local tissues appeared indurated with evidence of thrombus ~2-cm cephalad to the ovary extending down to the ovary. These findings suggested an ongoing thrombotic process localized to the ovary as there was no evidence of active infection or involvement of neighboring structures. The area of induration correlated with previously noted findings on the CT scan. A bipolar cautery and cutting device was used to dissect through the mesovarium and infundibulopelvic ligament. Once the thrombus was identified, care was taken to dissect above and excise the thrombus along with the ovary. The specimen was sent for pathologic analysis, which demonstrated a blood clot within a dilated vessel. Postoperatively, the patient reported resolution of her abdominal pain, tolerated oral intake well and was started on heparin. Her hospital course was uneventful, lasting 2 days. The patient was discharged on an anticoagulation regimen of 5 mg apixaban BID tapered to 2.5 mg BID after 6 months. Six months postoperatively, the patient was doing well without recurrence or need for further surgical intervention. |
A 16 year-old non-obese Hispanic girl with approximately a seven-week history of migraine headache presented to our emergency department in the early summer of 2000 with a sudden onset of left hemiparesis. Her previous migraine episodes were accompanied by nausea and photophobia but were neither associated with aura nor complicated by neurological deficits. There was no family history of migraine or stroke. She did not smoke and had never used oral contraceptives, hormonal treatment or illicit drugs. She had been otherwise healthy. Earlier on the day of presentation, the patient experienced an aura of tingling in her left hand that rapidly progressed to involve her left face and leg. The patient subsequently developed a complete left hemiplegia. One hour after the onset of symptoms, the patient was found to also have a complete left hemisensory loss. Her symptoms resolved completely as she was undergoing a head computed tomography (CT) scan and CT angiography, both of which were normal. There was no evidence of cerebral vasculopathy. Following the CT angiography the patient developed another episode of transient left hemiplegia that rapidly improved but left a residual mild pronator drift. Fluid-attenuated inversion recovery MRI of the brain was performed two and a half hours after onset of her initial symptoms and revealed increased signal intensity in the right basal ganglia extending into the posterior limb of the right internal capsule, most consistent with an acute ischemic infarct (Fig. ). Diffusion-weight MRI and apparent diffusion coefficient confirmed the presence of an ischemic infarct (images not shown). The patient was started on intravenous heparin to maintain a partial thromboplastin time of 60-80 seconds. Evaluation for a possible coagulopathy prior to initiation of heparin, inborn error of metabolism and mitochondrial disorders was unremarkable. A trans-esophageal echocardiogram revealed no evidence of a patent foramen ovale, thrombus, or other structural abnormality. Approximately six hours after the onset of hemiplegia, the patient developed a right temporal pulsatile headache associated with left arm tingling which rapidly resolved. Migrainous infarction was considered and the possibility of vasospasm responsible for the reversible sensory deficit was raised. The patient was started on nimodipine 30mg via parental route every 6 hours for 48 hours followed by verapamil 80 mg daily for presumed cerebral vasospasm. The doses of nimodipine and verapamil were carefully titrated to avoid hypotension. By the following day, her headache and left pronator drift had resolved completely. After her discharge, the patient continued to have episodic headaches with left arm numbness that were often triggered by salty and greasy food. The diagnosis of migraine with aura was thus made. The verapamil dose was increased to 120 mg daily and the patient was advised to refrain from any offensive food. In addition, valproic acid was added to the patient’s migraine prophylaxis regimen and she has remained headache free and has no additional neurological deficits for at least four years of follow-up. |
A 53-year-old male patient presented with a tetraparesis after the accident. He first woke up in a hospital after the accident. After 1 day, he was brought to a hospital in Germany for diagnosis and treatment.\nThe patient had a reduced muscle strength on examination. It is shown in . The muscles of the right side of his body were weaker than the left side. Furthermore, the right hip flexors were not affected as much as the muscles in the other segments below C5. The anal sphincter was floppy but could be activated to a minor degree from the right side. Clinical testing on the muscle strength showed that the patient had spared muscle movement below the level of the injury and could not move against gravity on one half of his body. The other half was not effected in this way. In conclusion, the right part of his body has to be classified as American Spinal Injury Association (ASIA) C, while the left part of his body can be classified as ASIA D.\nThe patient has to be checked for injuries of the vertebrae, the spinal cord and the soft tissue of his dorsum. Fractures can be assessed using X-ray or computed tomography (CT) of the spine. The CT imaging should be preferred if available because it is not possible to display the complete spine using X-ray. Especially the cervicothoracic junction is often superimposed by the shoulders. The biggest advantage of the CT is the possibility to create multiplanar reconstructions of different planes of the spine. Magnetic resonance imaging (MRI) is necessary to evaluate whether the patient has a direct or indirect (swelling/edema/bleeding) injury of the spinal cord or soft tissue injury. There are also patients who have a neurological deficit but no radiographic evidence for a trauma. This is called SCIWORA (Spinal Cord Injury Without Radiographic Abnormalities).\nThe patient initially received a CT, which showed an avulsion of the anterior inferior margin of the 6th cervical vertebra. Additionally there were fractures of the transverse processes of the 6th and 7th cervical vertebra, the 1st thoracic vertebra and rib fractures from the 4th to the 8th rib on the left side. To evaluate the soft tissue damage and the injury of the spinal cord, he also underwent an MRI. A discoligamentous lesion between C5 and C6, as well as a swelling of the spinal cord was detected and is shown in .\nThe patient received no methylprednisolone because he arrived more than 8 hours after the injury happened. The intervertebral disc between the cervical vertebras 5 and 6 was removed and the vertebras were joined. During this surgery, a suprapubic fistula of the bladder was applied to allow the urination.\nTo reduce the influence of the secondary injury the patient received an experimental therapy with an initial intrathecal application of erythropoietin (EPO). From the first postsurgery day until the 58th postsurgery he was treated with subcutaneous injections of EPO, granulocyte colony-stimulating factor (G-CSF) and vitamin C every 3–5 days and regular control of his laboratory values. |
A 29-year-old Saudi male with SCD, was referred from the general surgery service to improve his poor physical condition. He was severely crippled and bed bound for 8 years with severe bilateral knee and hip dysfunction secondary to complications of SCD. Past history included an admission to hospital 8 years before for fever, swelling and severe pain of the right knee. Needle aspiration, as well as irrigation and debridement, was performed and the patient was diagnosed with septic arthritis. Since then he had developed progressive joint stiffness involving the dorsal and lumbar spines as well as the lower extremity.\nOn physical examination his knee range of motion (ROM) bilaterally was almost nonexistent with the knees held in full extension. His hips ROM was also severely limited, with no ROM. Loss of hip flexion was noted to result in the most severe functional loss with the hips fixed in full extension, adduction of 15° and 50° of external rotation. He required a 2-person assist as well as a walker to weight bear however he was unable to mobilize.\nSerial radiological studies were done. Radiological investigations demonstrated severe avascular necrosis and ankylosis of the hip (\n) and severe erosion of the articular surfaces of the knees as well as ankylosis (\n). Computed tomography (CT) scan of the hips and knees showed similar findings as that of the X-rays. Shoulders and spine X-ray were done for further assessment. Gallium bone scan demonstrated no evidence of active osteomyelitis. Our patient had a proper preoperative evaluation and blood transfusion to prevent adverse outcomes and sickle cell complications postoperatively\n. We took him to surgery for bilateral cementless total hip replacement (THR) in one session.\nThe patient was operated on with an aim to provide movement at the hips and knees and to recover his ability to sit, stand, transfer, balance and improves personal hygiene. Bilateral THR was done successfully (\n). The procedures were performed utilizing the Harding lateral approach. Particular attention was paid to padding bony prominences and skin care in view of his poor skin condition. Intraoperatively, the bone was noted to be very fragile. The patient was kept in the intensive care unit for two days post operatively for observation and pain control. Post bilateral THR, the patient had marked improvement of hip flexion bilaterally permitting easy functional sitting. Post surgery physiotherapy resulted in great improvement in his general physical activity.\nLeft total knee replacement (TKR) was performed one month after the THR (\n). Intraoperatively, the bone quality was noted to be severely deficient. The quadriceps muscle was adherent to the femur and atrophied; therefore, V-Y quadricepsplasty was done. Soft tissue was mobilized carefully around the joint prior to component insertion. Intraoperatively, knee flexion approached 50°. Post-left-TKR rehabilitation was severely restricted secondary to poor bone quality. This prevented adequate ROM exercises and function, and ROM gains at the knee were minimal. Poor bone quality also limited the ability for the patient to progress to functional lower extremity weight-bearing activities. Postoperatively, rehabilitation, patient education, transfer training and functional rehabilitation were carried out. This allowed the patient to transfer safely and independently from bed to wheel chair without much pain, and improved the quality of life by changing the patient’s functional ability and allowing the freedom to mobilize independently with a wheelchair. |
A 65-year-old woman with aortic regurgitation following infectious endocarditis had undergone twice aortic valve replacement procedures within 2 months. After the second operation, more than 3 weeks were required before she could be weaned from intensive treatment, including artificial ventilation and sedative drug administration. Following recovery from heart failure, sedative drug administration was discontinued. The patient's clouded consciousness persisted for several days, but she did not show signs of epilepsy. At that time, a computed tomography (CT) scan of the brain showed a diffuse lacunar infarction but no distinct lesion. As the patient's consciousness increased, she complained of intense pain and allodynia originating from the neck and radiating to her left hand. The patient was treated with oral nonsteroidal anti-inflammatory drugs, but no favorable effects were observed. Her pain worsened, and she consulted our pain clinic 3 months after the second operation. She showed no signs and symptoms of neurological complications, except for pain and allodynia, before and after the cardiovascular surgeries.\nDuring the first examination at our pain clinic, she complained of spontaneous burning pain and severe allodynia from her neck to her hand; her left hand was swollen, pale, and hot. We diagnosed her condition as complex regional pain syndrome (CRPS) [] and began treatment, although the initiating injury was unknown. Because she was being administered anticoagulant therapy, many of the available neural blockades could not be used, except for a regional intravenous nerve blockade (Bier block, with 20 mL of 0.5% lidocaine). This neural blockade was performed 4 times per week concurrently with oral administration of a tricyclic antidepressant, nortriptyline (20 mg); this treatment resulted in the gradual reduction of pain and allodynia, which allowed the patient to receive physiotherapy. One month after treatment, pain and allodynia symptoms were nearly eliminated and swelling had also diminished. Additionally, her upper limb motor disturbance was significantly improved.\nOne hour after the 18th Bier block, the patient suddenly experienced a major epileptic seizure and lost consciousness during physiotherapy. This was the first time in the patient's life that a seizure episode had occurred. Intravenous administration of diazepam followed by thiamylal was used to control the seizure. An emergency CT scan of the brain showed no distinct lesions, which was confirmed by magnetic resonance imaging (MRI). The following day, the patient regained consciousness and complained of burning pain and severe allodynia localized in her left upper limb; subsequently, there was a recurrence of other CRPS symptoms (swelling, skin temperature escalation, and paleness). Despite regular intravenous administration of phenytoin, seizures occurred several times over the following 3 days, which occasionally required additional administrations of intravenous diazepam or thiamylal, and consciousness was again lost. When the patient was partially asleep due to intravenous anticonvulsants, she executed escaping movements for noxious stimulations on various healthy body parts but did not respond to noxious and tactile stimulations on the left upper limb, suggesting an absence of hyperalgesia and allodynia. After 3 days, her consciousness was fully recovered and no seizure episodes occurred. The patient had no further complaints of burning pain or allodynia. SPECT examinations, using 99m-Tc-hexamethyl-propylene amine oxime (HMPAO), were performed during the seizure period and 10 days later (). The first image, obtained during a seizure, showed relative hyperperfusion in the right parietal lobe and both thalami and relative hypoperfusion in the left frontal and parietal lobes (Figures and ), which improved after 10 days (Figures and ). Electroencephalography (EEG) examinations were also carried out immediately following a seizure and 2 weeks later. EEG readings immediately following a seizure showed irregular and sporadic spiked waves in the left temporal lobe, followed by spikes in both the temporal lobes. Clinically, the patient showed an intermittent left upper limb spasm, although obvious epileptic discharges were not noted on EEG readings after the 3-day seizure episodes. Although postictal EEG readings occasionally displayed irregular spiked waves in the left posterior parietal and temporal lobes, the patient did not show epileptic symptoms. Clinical symptoms suggested that spiked waves were not related to the intermittent left upper limb spasm. On the basis of the SPECT and EEG findings, our neurologist diagnosed the patient as having temporal symptomatic epilepsy focused in the right parietal lobe. Her recovery was uneventful, and pain and allodynia nearly disappeared, although her skin color remained pale and her hand remained hot.\nWe obtained her consent to report her progress in accordance with the Declaration of Helsinki. |
A 59-year-old male without any known health problems was admitted to Sisli Hamidiye Etfal Training and Research Hospital General Surgery Department with a complaint of right upper quadrant abdominal pain and a weight loss of 8 kg in one month period. There were no special features at his medical history. On physical examination, there was a mild right upper quadrant abdominal tenderness on deep palpation. Abdominal ultrasound revealed a mass with 130 × 74 mm diameters, originating from the left lobe of the liver extending to the midline, with multiple thick septas and intense cystic lesions containing echogenic areas identified. Also another 3 cm cystic mass with similar ultrasonographic features was detected at the posterior right lobe of the liver. Magnetic resonance imaging (MRI) was performed for the patient. According to the MRI findings, there was a cystic lesion in the left lobe of the liver with a diameter of 11.5 cm at the widest spot. In the first plan the mass was thought to be a degenerated hemorrhagic adenoma but a metastatic tumor was unable to rule out. MRI images are shown in . Upper and lower gastrointestinal endoscopy was performed but no primary tumor was detected.\nLaboratory analyses were in normal range while CA19-9 was 29.69 U/mL. Because of the presence of a malignant disease which cannot be ruled out, it was decided that a surgical excision should be performed.\nAccording to the intraoperatively assessment, 10 cm mass was identified in the left lobe of the liver and excised by performing left hepatic lobectomy. The patient was hospitalised for recovery for 4 days and then discharged.\nPathological evaluation showed a 7 × 6 cm cystic, dark brown mass in the 13 × 9 cm liver tissue obtained from left hepatectomy. According to immunohistochemical consideration HMB45, S100 and pCEA were strongly positive; CK8, CK18, CD34, and Glypican 3 were negative for the tumor (). In light of the present findings, the lesion has been considered as the liver metastasis of malignant melanoma. |
This 69-year-old woman was found to have a large mass destroying her sphenoid sinus when she lost vision in her right eye eight years prior to current presentation (). During the surgical removal of tumor, there appeared to be a chance of injuring the internal carotid artery (ICA). We therefore performed preoperative catheter angiography and balloon test occlusion. The anterior communicating artery was widely patent on the balloon test occlusion, and no vascular abnormalities, including aneurysm, were identified by the catheter angiography (). She underwent gross-total resection of the tumor at that time without any adverse event, and a pathological examination confirmed the diagnosis of chondrosarcoma. She subsequently underwent cranial radiation therapy (total dose of 59.4 Gy) as adjuvant treatment. She was clinically monitored throughout the next eight years with serial magnetic resonance imaging (MRI). During this time, she demonstrated no new neurological deficit except slight cognitive decline, and none of the MRIs showed any sign of residual or recurrent tumor ().\nThe patient presented to the emergency room due to severe headache and a slightly drowsy mentality, and computed tomography (CT) revealed intracerebral hemorrhage and subarachnoid hemorrhage (). The patient underwent catheter angiography, which revealed an aneurysm of the anterior communicating artery and luminal narrowing and irregularity in the petrous and lacerum segments of the right ICA ().\nWe suspected that the anterior communicating artery aneurysm had ruptured and attempted endovascular treatment with coil embolization. However, the tortuosity of the bilateral A1 segments of the anterior cerebral arteries (ACAs) and the broad neck of the aneurysm made the endovascular treatment difficult. We stopped the endovascular treatment and surgically clipped the aneurysm. During the microsurgery, the wall of the aneurysm was very rubbery, and the surgical clip slipped from the neck of the aneurysm. After several surgical clipping attempts, the neck of the aneurysm was clipped, and a booster clip was used to reinforce the primary clip. The patient's immediate postoperative neurological state was the same as baseline. CT angiography performed ten days after surgery revealed the small, residual neck of the aneurysm, but the patient's state was stationary (). At 14 days after surgery, the patient's mental state worsened, and a CT revealed rebleeding from the aneurysm; catheter angiography demonstrated that the clips had slipped from the aneurysm (). We performed emergency surgery using a contra-lateral craniotomy and confirmed that the clips had slipped from the aneurysm; new clips were applied around the aneurysm neck. The patient's neurological state immediately after the 2nd operation was deeply drowsy. However, three days after the 2nd operation, the patient became semicomatose, and CT and catheter angiography revealed rebleeding and the slip of the clips, respectively. After the repeated failure of surgical clipping, we performed endovascular trapping from the right distal A1 to the aneurysm (). After the procedure, the final catheter angiogram showed complete obliteration of the aneurysm and intact flow of the bilateral A2s ().\nAfter the endovascular treatment, her neurological state was semi-comatose, and we continued conservative management. One month after the endovascular treatment, there was massive bleeding from her nasal cavity, and catheter angiography showed a rupture of the lacerum segment of the right ICA, suggesting carotid blow out syndrome (). We performed endovascular coil embolization of the ruptured site in the lacerum segment of the right ICA as a life-saving procedure (). The patient did not recover from the semi-comatose state and was discharged home in a bed-ridden state. |
The patient is a 57-year-old female with history of hypertension, hypercholesterolemia, and mitral valve regurgitation. She presented with multiple episodes of syncope over the prior few months. Each episode was transient and was provoked by rotating her head toward the right. All episodes were self-limiting with none resulting in permanent neurological injury.\nAn extensive workup was conducted including computed tomography (CT), CT angiography, magnetic resonance imaging and angiography, and digital subtraction angiography of the head and neck. Rotational dynamic angiography revealed a dominant right VA that became occluded at the level of C5/6 with head rotation to the right side. The vertebral flow was reestablished by neutralizing or turning the head to the left [Figure and ]. The patient also had a hypoplastic left VA and fetal posterior communicating arteries bilaterally. Thus, her entire posterior circulation was primarily dependent on the right VA. Cervical spine CT showed that she had extensive degenerative changes and spondylosis including auto-fusion between C2 and C3 as well as at C6 and C7 [].\nThe cause of the patient's syncope was determined to be hemodynamic insufficiency as the result of intermittent compression of the V2 segment of the VA at the level of C5/6.\nThe patient was taken to the operating room under general anesthesia and placed in the supine position with a shoulder roll placed in the interscapular region. Her neck was slightly extended. Baseline somatosensory and motor evoked potentials were obtained and continuously monitored throughout the duration of the procedure. A standard approach to the anterior cervical spine was performed utilizing an incision parallel to the anterior border of the sternocleidomastoid muscle.\nThe longus coli were dissected partially on the left side and more extensively on the right side, exposing the transverse processes of C5 to C7. The VA was identified as it entered the transverse foramen at C6, and the anterior bar of the transverse foramen at C5 and C6 was removed to decompress the artery. A partial discectomy and resection of the uncovertebral joint at C5–C6 on the right was performed. A fibrous band encasing the VA was identified and subsequently released. After the sectioning of the fibrous sheath, the VA began to expand and pulsate more prominently. An intraoperative ICG angiography demonstrated that the VA was patent during head rotation []. This was also confirmed by an intraoperative right VA dynamic angiogram []. The patient remains free of symptoms at 6-month follow-up. |
A 50-year-old male patient reported to our department with chief complaint of a proliferative swelling in upper labial gingiva since 3-4 months. About 6 months back the right maxillary central and lateral incisors exfoliated and 2 months later patient noticed a small swelling at the same region which attained the present size. It was not associated with pain or any other symptoms.\nIn his medical history, it was noticed that the patient had abdominal discomfort and vomiting on having food from 3 years which had increased since last 10 months. He had undergone endoscopy of upper gastrointestinal tract 3 years back which revealed chronic Helicobacter pylori associated gasritis for which he was on oral medication (proton pump inhibitors) till date. Patient was a chronic bidi smoker since 30 years.\nThere were no significant extraoral findings; also, no significant cervical lymphadenopathy was noticed. An intraoral examination revealed a single, oval proliferative lesion with well-defined borders on the anterior right maxillary labial aspect measuring about 4 × 5 cm extending anterioposteriorly in relation to right first premolar to left central incisor and superioinferiorly from the depth of the labial sulcus up to crest of the ridge []. The color of the lesion was pinkish white with a pebbly irregular surface. When palpated the lesion was soft, painless and pedunclated with a stalk of about 4 cm diameter.\nAt the initial visit patient had bouts of vomiting associated with abdominal pain, hence he was admitted and symptomatically treated. Incisional biopsies were performed from both mesial and distal aspects of the oral lesion and were sent for histopathologic examination which revealed dysplastic glandular epithelial cells arranged in the form of ductal and papillary pattern []. The cells were tall columnar exhibiting dysplastic features in the form of nuclear and cellular pleomorphism, nuclear hyperchromatism, prominent nucleoli and numerous mitotic figures [] suggestive of metastasis of adenocarcinoma of gastrointestinal tract.\nDue to history and current complaint of vomiting and abdominal discomfort, a repeat endoscopy was advised.\nResults of upper gastrointestinal endoscopy revealed a proliferative growth at cardia extending into lesser curvature []; multiple biopsies were taken from the lesion. Biopsy report revealed fragments of gastric mucosa showing intestinal metaplasia. Few other segments showed tumor cells arranged in glands, sheets and papillary projections []. The cells were round to oval with hyperchomatic and vesiculated nuclei, multiple nucleoli, moderate amount of amphophilic cytoplasm and exhibited numerous mitotic figures [] suggestive of moderately differentiated gastric adenocarcinoma.\nLater, on comparison of both reports, a similar origin that is the gastric adenocarcinoma was evident. Hence, it was concluded that the lesion seen in the oral cavity was a secondary metastasis from gastric adenocarcinoma. The case was discussed with tumor board and was decided for palliative chemotherapy. |
A 35-year-old female patient was presented to our center for TV replacement due to stenosis. At the age of 11 years, the patient suffered from endocarditis supported by a small ventricular septal defect. At that time, the ventricular septal defect was closed and a mechanical tricuspid valve (SJM, 28 mm) implantation and epicardial single chamber pacemaker implantation due to concomitant third degree AV block without escape rhythm were performed. At the age of 17 years, the abdominal pacemaker was replaced, due to battery depletion (Biotronik). Six months later, a second surgery followed with replacement of the dysfunctional mechanical valve for a 27 mm Porcin-Baxter biological TV. Another PM replacement (Medtronic) was performed at the age of 27 years, again, due to battery depletion. At the age of 30 years, the abdominal pacemaker was explanted and a two chamber transvenous ICD (Medtronic Egida DR) was introduced, as the patient suffered a syncope during documented sustained ventricular tachycardia. The ICD lead was implanted passing the tricuspid valve into the right ventricle. Six years later, severe TV stenosis developed, caused by an ICD lead, that stuck to the posterior leaflet of the biological valve and ventricular myocardium, and the TV had to be replaced a third time. To avoid future TV dysfunction due to lead related complications, we discussed several options with the patient. These included first TV replacement in combination with epicardial pacemaker leads and a subcutaneous ICD (S- ICD, EMBLEM™ Boston Scientific) or alternatively placing a pacing lead in the coronary sinus in combination with an S- ICD. As the patient disagreed on both options, despite a higher risk of TV dysfunction by placing another transvenous ICD lead through the TV, we discussed another option and opted for a lead sparing replacement of the TV. The TV ring was cut open on both sides beneath the original ICD lead, and the TV prosthesis was excised. A new bioprosthetic valve was implanted, leaving the ICD lead outside the ring of the new TV prosthesis. As the lead was stuck to the former TV annulus and posterior ventricular wall, no further fixation of the lead was needed. The new valve (SJM biological 28 mm) was implanted using 14 Coreknots (Figures , , ).\nThe postoperative course was unremarkable, and the patient was dismissed on the 11th postoperative day/postoperative day 11. Follow-up after 4 months showed a well functioning TV prosthesis without stenosis or regurgitation and no deterioration in pacing or sensing parameters. No artifacts or other hints to a lead dysfunction were recorded (Table ). |
A 46 year old Caucasian man with a previous diagnosis of stage T4b melanoma of the scalp 8 months prior, presented with a 2 week history of left hemiparesis and headaches (Fig. a). Magnetic resonance imaging (MRI) demonstrated 5 hemorrhagic metastatic brain lesions. Given his subacute hemiparesis and the presence of a metastatic lesion in the right motor strip, he had an awake craniotomy for removal of this lesion, which was confirmed to represent MBM by pathology. His hemiparesis improved and he did not receive brain radiation to the cavity or other intracranial lesions as planned. He was admitted 1 month later after his primary surgery with altered mental status and interval increase in his intracranial lesions. The right anterior frontal lesion now measured 3.6 cm (increased from 2.9 cm at presentation) with significant surrounding edema and associated localized brain compression. He had surgery for removal of this metastasis and again due to poor social support did not receive radiation. He came back within several weeks with headache, nausea, vomiting, and ataxia. Imaging again demonstrated progression of his intracranial lesions with compression of the fourth ventricle causing hydrocephalus by the left cerebellar lesion. He underwent a third craniotomy for resection of this symptomatic lesion and he was kept in the hospital to initiate brain radiation (Fig. b). Approximately 1 week after his last surgery, he began dabrafenib and trametinib. At his 2 month follow up, his MRI showed significant improvement in previously resected and previously radiated intracranial masses and no new intracranial masses. Six months after his last craniotomy, MRI demonstrated an increase in size of all lesions. The patient was also evaluated by oncology and it was determined he was not taking his chemotherapeutics as directed. Salvage whole brain radiation (30 Gy) was initiated the following month and he was started on immunotherapy (nivolumab and ipilimumab). Three months later the patient expired (Fig. a). Overall survival from his primary diagnosis was 18 months and survival from MBM diagnosis was 12 months.\nGiven the unique opportunity to study metachronous brain metastases in a patient who was treatment naïve at the time of surgeries, genomic, transcriptomic and proteomic profiling was performed as approved by our institutional review board. From the DNA sequencing data, the variant allele frequencies of all four tumors (i.e. the primary skin lesion and 3 BMs) were used to generate a phylogeny illustrating the evolutionary history of the tumors and the relative order in which single nucleotide variants (SNVs) and copy number variants (CNVs) occurred. Most SNVs and CNVs were shared by all samples, but a SMARCA4 mutation and deletion of 12q were shared by all BM and not the primary tumor (Fig. c).\nWe next used a proteogenomics approach to identify overlapping features amongst the DNA sequencing panel, transcriptome and proteome of all samples. 326 features overlapped between gene, transcript and protein in all 3 omic data sets and 8187 overlapping features were identified in both the proteomics and RNA sequencing data sets (Additional file : Fig. 1A). Substantial overlap was not seen in comparisons of gene transcripts to proteins between the primary tumor and each respective metastasis. Minimal overlap was observed between metastatic tumor comparisons (Additional file : Fig. 1B).\nTo identify differentially expressed proteins amongst the tumors, we filtered protein expression by fold change (> 2) and p values (< 0.05). Using these cutoffs, significantly differential proteins that were down regulated or upregulated were represented in blue or red respectively. A large number of significantly different proteins were observed between the primary and each respective metastatic tumor but fewer differences in protein expression were present between the metastatic tumors, especially metastatic BM 2 versus 3 (Fig. a). RNA transcript profiles demonstrated similar trends as the protein expression (Fig. b).\nHierarchial clustering of significantly expressed gene transcripts and proteins demonstrated (protein expression: fold change ≥ 2 and p value < 0.05, RNA transcripts: probability > 0.90) that the primary tumor clustered separately from the metastatic tumors. Within the metastatic tumor cluster, BM 2 and 3 were the most similar (Fig. c). Ingenuity Pathway Analysis (IPA) was performed on the proteomics dataset to identify canonical pathways up and downregulated in the metastatic tumors. The nine most significant pathways downregulated in the metastatic tumors were predominately involved in immune response (Fig. a). On the other hand, the nine most significant canonical pathways increased in the metastatic tumor biopsies were most frequently associated with coagulation and G-protein signaling (Fig. b). The three significant pathways with the greatest z-score were G beta gamma signaling, CXCR4 signaling, and thrombin signaling (Fig. b). All three of these pathways were associated with GNAO1, GNAS, GNAZ, GNG5, PIK3CG, PRKD1, and PRKD3. Gene expression levels of top proteins identified in upregulated pathways from the metastatic samples were queried in the cancer genome atlas (TCGA). Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit γ (PIK3CG) was identified in multiple upregulated pathways for the metastatic brain tumors and gene expression was significantly increased in metastatic melanoma samples in comparison to primary melanoma from TCGA data (Fig. c). PIK3CG is in the P2Y purigenic receptor signaling pathway and the protein level was upregulated in all three metastatic tumors as compared to the primary tumor (Fig. d). To validate this finding, we then performed immunohistochemistry (IHC) on histopathological tissue sections. All four tumors were histologically similar on hematoxylin and eosin staining (Fig. a, c, e, g). PIK3CG protein levels were significantly increased in metastatic tumors in comparison to the primary by proteomics. IHC confirmed no PIK3CG staining was present in the primary tumor and focally and weakly positive staining was present in all metastatic tumors (Fig. b, d, f, h). |
A 26-year-old man presented in May 2017 with one month of left hip pain. He began physical therapy but the following month sustained an intertrochanteric femur fracture while getting out of bed. This was treated with intramedullary fixation. Follow-up imaging revealed a progressive lytic lesion of the proximal femur with cortical erosion and soft tissue mass. Biopsy found this to be an epithelioid hemangioma with atypical features and extension into extraosseous soft tissue. He underwent radical resection of the proximal femur and total hip arthroplasty in October 2017. Follow-up imaging from 2/2018 showed a subtle lesion in the ischium which was not recognized at the time (Fig. ).\nX-ray imaging in May 2018 showed stable instrumentation but increasing lysis of the left ischium (Fig. ). This was followed up two weeks later with an MRI of the pelvis and CT angiogram, which revealed a 7.4 cm lobulated expansile mass involving the ischium, inferior pubic ramus, and posterior acetabular column. This was thought to be recurrence of his epithelioid hemangioma, and he was scheduled for embolization of the ischial lesion.\nHe was referred to us for consideration of systemic treatment and we saw him in August 2018. By this time, he was experiencing worsening pain in his left buttock with sitting and activity. With prior case reports of successful use of propranolol in treatment of benign hemangiomas, including two recent examples of benefit in epithelioid hemangioma, we initiated monotherapy of oral propranolol 40 mg twice daily with close follow-up. He tolerated this well. After 4 weeks of treatment, the patient reported that his pain had stabilized and the lesion appeared unchanged on CT. Because of his clinical improvement and radiographic stability, he did not undergo embolization. By 5 months of therapy on January 2019 he had resolution of his pain and imaging again demonstrated no progression of the mass. He continues on propranolol to date (4/2019); imaging after 10 months on treatment shows increasing sclerosis of the mass (Fig. ). |
An otherwise healthy 66-year-old woman presented with a 4 cm diameter mass in the left thyroid lobe, which she had had for 2 months, and underwent a thyroidectomy at a peripheral hospital in September 2011. No preoperative imaging study was performed other than a color ultrasonography. Intraoperative frozen section revealed a papillary thyroid carcinoma, and the patient underwent a thyroid lobectomy without lymph node dissection. Intraoperative exploration revealed that the musculature of the cervical esophagus was involved with tumor. Elaborate efforts were made to remove the tumor en bloc; cervical esophageal perforation was identified intraoperatively and closed primarily with three number 4 silk sutures. The patient developed hoarseness, aspiration, swelling on the left side, discharge from the incision line, and high fever on the first postoperative day. Oral intake was withheld; intravenous nutrition and antibiotics were administered. Esophageal barium X-radiography on the seventh postoperative day revealed severe stenosis of the cervical esophagus 2 cm below the inlet (Figure \n), which was subsequently verified by a transnasal gastroscope. Although the endoscope could not pass the stenosis, a nasogastric tube was successfully inserted for enteral nutrition. Wound drainage was maintained for 2 weeks. Daily drainage of a mixture of abscess and saliva was 80 to 150 ml from the 1st to the 7th postoperative day. The drainage diminished slowly and the wound healed; the drain was removed on the 14th postoperative day. On the 10th postoperative day, the patient began to complain of dysphagia and could not swallow any saliva. The nasogastric tube was removed and gastrostomy was performed for long-term nutrition 2 weeks later. An interhospital consultation was obtained for further diagnosis and management 2 months after the operation, when complete dysphagia persisted. Computed tomography demonstrated a stricture of the cervical esophagus with a length of 3 cm just 2 cm below the inlet, without residual tumor or lymph node metastasis. Fiberscopy revealed a complete stenosis of the esophagus. Fiberscopic dilation was attempted but failed because the smallest fiberscope could not pass the esophageal lesion.\nAfter informed consent was obtained from the patient and her family, the patient was taken to surgery. Intraoperative exploration found that the anterior wall of the cervical esophagus was sutured to its posterior wall and that the esophagus was completely closed by granulation and fibrotic tissue 2 cm below the inlet; the recurrent laryngeal nerve had been transected during the initial surgery. A cervical esophagectomy with preservation of the larynx was performed that resulted in a circumferential defect of 6 cm length, starting at the esophageal inlet. A tubed radial forearm free flap of 12 × 7 cm2 was used to reconstruct the circumferential esophageal defect. The donor artery was anastomosed end-to-end to the transcervical artery and the accompanying vein was anastomosed end-to-side to the internal jugular vein. Postoperative recovery was uneventful. The patient was given a trial of water oral intake on the 7th postoperative day without any discomfort and subsequently began a liquid diet. One month later, she tolerated a normal diet. Subsequently, the patient underwent radioactive iodine ablation. Barium radiography 6 months after the operation demonstrated that the reconstructed cervical esophagus was widely patent and smooth, with a diameter of 2.5 cm (Figure \n). |
An 89-year-old fit female with a history of chronic back pain and an appendectomy during her youth completed using a McBurney incision presented with a one-day history of spontaneous pain in her right flank without any fever, chills, or other symptoms. At the time of her admission, she was not in distress, she was not febrile, and her vital signs were within normal values. On clinical examination, there was swelling with a red area measuring 12 cm × 4 cm and tenderness of the right flank around her appendectomy scar. Crepitus could be felt diffusely on her right and left flanks and the periumbilical and epigastric regions upon palpation. Blood test showed the presence of mild inflammation, with a CRP value of 7 mg/l (within normal values) and an elevated white blood cell count of 18 G/l. The rest of the laboratory results were normal. Emergency ultrasonography was unhelpful because of air interference. An abdominal CT scan () showed diffuse subcutaneous abdominal emphysema extending to the pelvis on the left side that was more pronounced on the right inguinal fossa with a bowel loop in contact with the abdominal wall. An emergency laparotomy centered on the McBurney incision showed feces and pus within the subcutaneous compartment. Furthermore, at the level of the aponeurosis of the external oblique muscle, an inflammatory diverticulum could be seen fistulizing between the lumen of the sigmoid colon loop and the necrotic subcutaneous tissue. We subsequently diagnosed intraoperatively a subcutaneous abscess and emphysema with an enteroparietal fistula caused by a ruptured sigmoid diverticulum in an incisional hernia. The necrotic tissues were excised, and the punctiform sigmoid colon fistula was closed. Revision of the rest of the sigmoid showed important adhesions between the sigmoid colon and the parietal peritoneum of the right flank and between the caecum and the sigmoid colon, respectively. The sigmoid colon also showed diffused diverticulosis with no inflammation. The cutaneous and subcutaneous tissues were left open and dressed with a negative pressure-assisted closure device on postoperative day 1. The patient received intravenous antibiotherapy for two weeks with quinolones and a third-generation cephalosporin at first which was then switched to aztreonam due to an allergic reaction. Bacteriological studies showed polymicrobial digestive bacteria (i.e., Escherichia coli, Streptococcus equinus, and Enterococcus). Subsequently, there was good clinical and biological evolution. At two weeks postoperation, she was reoperated on for closure of the wound. She was discharged from the hospital three weeks after her initial surgical intervention with the indication to continue antibiotics for a total of four weeks. |
A 74-year-old male patient was admitted to our hospital in March 2017 to undergo liver resection to treat a malignant hepatic lesion diagnosed with CT and PET and a fine-needle biopsy positive for squamous carcinoma. The hepatic tumour discovered during follow-up for a previous bladder cancer submitted to endoscopic surgery three years before measured 22 mm in diameter and was located in the VIII Couinaud's segment [] of the liver in association with three smaller hypodense liver lesions with a focal dilatation of peripheral biliary tree ().\nThe case is discussed with radiologists, oncologists, and pathologists of our hospital. Even if the lesion had been the single site of disease; due to the proximity/doubtful infiltration of the lesion to the biliary tree, we decided to submit the patient to an explorative staging laparotomy and possible palliative surgery.\nOur internal protocol states that during the preadmission every patient who is a candidate for a liver resection is subjected to a routine liver function test with ICG to determinate the most appropriate surgical procedures []: 0,5 mg/Kg ICG are routinely injected intravenously up to seven days before surgery to evaluate the ICG retention rate at 15 min (R15). In our case 45 mg of ICG was intravenously administrated to test hepatic function, ten days before the surgery (patient R15 = 8.9).\nThanks to the ICG property of being fluorescent with the light emitted from the photodynamic eye of the laparoscopic system in our possession, it is possible to visualize the lesion during the surgical procedure. To this target, timing of administration and dose of ICG are key points.\nSeveral studies have demonstrated that the effective dose of ICG depends on the timing of injection; in particular, if the function liver test had been performed more than 7 days before surgery it would have been necessary to administer an adjunctive dose (0,1 mg/Kg) the day before []. In this case, it was necessary to administrate an adjunctive dose of ICG the day before the surgery (9 mg of ICG injected intravenously). After laparotomy, exploration of the abdominal cavity, and exposure of the liver, we easily confirmed the superficial lesion in the VIII Couinaud's segment. The liver surface has been analysed with the fluorescent imaging system. The fluorescing tumour has been clearly identified and defined on the liver surface, as shown in . We have also identified that a large area of fluorescent parenchyma that gets from the peripheral of the lesion up to the portal pedicle such as the neoplasia would interest the right biliary tree in the form of neoplastic lymphangitis (). This datum was not preoperatively known.\nA right hepatectomy would have been the oncologically correct surgical procedure due to the infiltration of right biliary duct. Considering the probable metastatic nature of the lesion, the absence of a clearly primary lesion, the age, the comorbidities, and the small size of residual liver, we have decided to perform an atypical segmental resection of S8 associated with cholecystectomy and lymphadenectomy of the hepatic pedicle nodes, including the area of impaired biliary excretion.\nAt the histological examination, the lesion, the lymph nodes of the hepatic pedicle region, and the right biliary branch, respectively, resulted in hepatic metastases from squamous cell carcinoma and sites of metastatic location. As expected the resection margin was interested by neoplasia.\nIn particular, the histological examination showed the following:Macroscopical exam: the neoplasia, in a site, appears to be in contact with the resection margin Microscopical exam: parenchymal hepatic section that showed metastatic localization of squamous carcinoma moderately differentiated. The neoplasia interest the surgery resection margin.\nIn this case, fluorescent imaging has revealed a fluorescing ring around the hepatic metastasis (). The fluorescence of the cholestatic area was shown on the cut surface (). |
A 30-year-old woman visited the hospital due to right lower quadrant pain over the period of 1 week. A laparoscopic myomectomy was performed 4 years ago because of a broad ligament leiomyoma, which was about 10 cm in size. Laboratory findings included a routine blood examination, and a C-Reactive Protein (CRP) test, with tumor markers all found to be within normal ranges. The pelvic Magnetic Resonance Imaging (MRI) scan showed some nodules at the posterior margin of the bladder that were considered to be endometriosis, and some pelvic effusion that was significant on the right side. It was also noted that there was a mass shadow at the lower right ureter (medial to the iliopsoas muscle), with distention of the lower right ureter (Fig. ). The patient also underwent computed tomography (CT) scans to enable the practitioners to observe the size of the abdominal mass and its surroundings. The CT images revealed a region occupying the middle right ureter that was considered to be a retroperitoneal aggressive fibroma, which led to severe hydronephrosis on the right kidney and upper ureter, and a right pelvic effusion (Fig. ). After more detailed examinations were conducted, there were no obvious abnormalities detected in the brain, heart, liver, gallbladder, spleen, pancreas or blood. The color Doppler ultrasound demonstrated that there was a hypoechoic mass next to the right iliac vessels that was closely related to the adjacent ureter. This resulted in severe hydronephrosis of the right kidney and a right upper ureteral dilatation (Fig. ). Ndzengue et al. [] reported a case of a pelvic desmoid tumor simulating a uterine leiomyoma recurrence. The patient that presented at our hospital had a history of uterine leiomyoma. We subsequently organized a multidisciplinary consultation to determine the next stage of her treatment plan. According to the patient’s surgical history, the next step would be determined after reviewing the results of the last surgical pathological wax, because the pathological nature of the retroperitoneal mass was uncertain.\nConsequently, a laparoscopic pelvic tumor resection with assistance from a Da Vinci robot was successfully conducted. A local peritoneal protuberance was observed in the right iliac vascular area. The parietal peritoneum was incised above the mass and it was carefully freed along the edge of the mass. The size of the tumor was about 6.0 cm × 5.0 cm × 3.0 cm. It had invasively grown and it was wrapped around the right ureter and the right ovarian arteries and veins. It was stuck to the psoas muscle and the iliac vessels. According to preoperative preparations and intraoperative conditions, a decision was made to cut off the right ureter, the right ovarian arteries and veins, and completely remove the tumor and the two masses that were located in front of the broad ligament on the right hand side of the uterus. The sizes of the masses were approximately 1.5 cm × 1.0 cm × 1.0 cm. The right ureter was anastomosed and put into a double J tube. A pathological diagnosis of an intraoperative frozen sample determined that it was a spindle cell soft tissue tumor, and the two masses were leiomyomas. Postoperative pathology tests of the pelvic mass determined that it was aggressive fibromatosis that had invaded the ureteral wall (Fig. ). The uterine surface nodules were also leiomyomas. Microscopically, the tumor cells were arranged sparsely in a spindle shape with blood vessels of different sizes found in the interstitial tissue. Immunohistochemical findings were found to be partially positive for smooth muscle actin (SMA) and desmin, and less than 5% ki-67 of positive cells were seen in the lesion. A detailed re-examination was performed 3 months after the initial surgery, to determine the structure and function of the ovaries. The transvaginal color Doppler ultrasonography was able to determine that the ovaries were normal in size with several follicular echoes. The blood supply to the right ovary was good. There were no obvious abnormalities in the uterus or pelvic cavity (Fig. ). The pelvic MRI and the CT scan of the whole abdomen determined that there were no abnormal lesions in the pelvis. Simultaneously, the endocrine function of the patient’s ovaries was found to be normal, and she was able to self-maturate after removing the double J tube. |
A 58-year-old man presented to the Department of Advanced General Dentistry, Dankook University College of Dentistry in 2017 for comprehensive dental treatment. The patient was diagnosed with amyotrophic lateral sclerosis (ALS) after a spinal cord injury nine years prior to presentation in a traffic accident and no medication was prescribed. He was 178 cm tall and weighed 44 kg. He was unable to walk because of weakness of the lower limbs, and therefore presented in a wheelchair. He could not hold his head up because of atrophy of his neck muscles. There was a clear general decline in bodily function and he demonstrated slurring of speech, although communication was possible. He could not blink his eyes on instruction or freely swallow saliva because of dysphagia (). During the year prior to presentation, his dysphagia had become increasingly severe, resulting in aspiration pneumonia and admission. After that, he was taking a sticky liquid meal. There was no sensory deficit on examination.\nOral examination revealed the presence of proximal caries in the maxillary right first, second, and third molar and second premolar, and generalized periodontitis (). A treatment plan including extraction, root canal treatment, and periodontal treatment was established. We decided to proceed with dental treatment under general anesthesia in the outpatient unit because the risk of reflux and lung aspiration due to the patient's swallowing dysfunction was expected to be high.\nThe patient had a history of severe hypotension after propofol infusion during general anesthesia induction performed at this center 4 years ago. A 4-hour dental treatment was performed while under general anesthesia with stable vital signs after atropine and ephedrine administration. Pre-anesthesia blood test and chest X-ray results were normal.\nOn the day of treatment, the patient presented after 8 hours of fasting and entered the operating room without receiving premedication. The patient was placed in a supine position on the dental chair and electrocardiography (EKG), non-invasive blood pressure monitoring (NIBP), and pulse oximeter monitoring were performed. An electroencephalogram (EEG)-entropy device (Entropy EasyFit Sensor disposable, Datex Ohmeda E-Entropy Module, GE Healthcare, Finland) was attached to the forehead of the patient to determine the anesthetic induction procedure and intraoperative anesthetic depth. The patient's initial vital signs were as follows: BP = 88/58 mmHg, heart rate = 82 beats/min, SpO2 = 98%, and electrocardiogram was normal.\nA face mask was used to administer 4 L/min oxygen and nitrous oxide gas. After the patient's loss of consciousness, an 18-gauge intravenous catheter was inserted into the right arm and Hartman solution was administered. Next, 4% sevoflurane gas was added to maintain O2-N2O-sevoflurane (4 L/min-4 L/min-4% volume, respectively) via a face mask. A muscle relaxant (atracurium, 25 mg) was also administered via the intravenous line. The patient's BP dropped to 32/21 mmHg and the waveform as seen using the pulse oximeter was lost. In the EKG, sinus bradycardia (less than 40 beats/min) was persistent and the carotid pulse was lost. The end tidal CO2(ETCO2) dropped to 10 mmHg and our team diagnosed PEA (). Since PEA is a cardiac arrest, our team performed cardiopulmonary resuscitation (CPR) according to the Advanced Cardiopulmonary Life Support (ACLS) guidelines []. The anesthetic gas was immediately turned off and the patient was placed in the Trendelenburg position with 100% oxygen. Tracheal intubation was then performed with a 6.5-mm internal diameter endotracheal tube (Sewon Medical Corporation, Cheonan-si, Korea). After placement of the endotracheal tube, chest compression was applied at a rate of at least 100 compressions per minute continuously without pause for ventilation. The ventilation was given at 1 breath every 6 seconds (10 breaths per minute). Fluid was full dropped via the intravenous line and 0.5 mg epinephrine (0.01 mg/kg) was administered.\nAfter 2 minutes of chest compressions, our team rechecked the vital signs of the patient. The blood pressure was 82/56 mmHg. The SpO2 and EKG graph showed a normal pattern. We judged that return of spontaneous circulation (ROSC) had been achieved, stopped CPR, and carefully monitored the patient. After confirming that the vital signs of the patient were stable, dental treatment was started. Anesthesia was maintained with 2 L/min O2, N2O, and 2% sevoflurane. During the treatment, blood pressure was maintained as low as 60–80/40–55 mmHg. The other vital signs were maintained as follows: heart rate, 75–95 beats/min; SpO2, 98%; and EEG-Entropy, 30–40. Ventilation was maintained for 2 hours without significant changes in BP or ETCO2. After completion of the treatment, intubation was removed after confirming that the patient's consciousness and spontaneous breathing were fully returned. Using a facial mask, 100% oxygen was administered and the patient was transferred to the recovery room. The oxygen saturation of the patient was stable and measured more than 95% when breathing atmospheric air, and there was no pattern of respiratory distress. The patient recovered after about an hour in the recovery room and returned home with his wife. |
A mother of a girl of 4 years old reported to the pediatric clinic of School of Dentistry in Araraquara (State University of São Paulo) complaining about the aesthetic involvement caused by the absence of primary mandibular incisors of the child. The mother of the patient said during the anamnesis the following statement: “My daughter did not smile anymore and every time she did it, she put the hand in front of the mouth”, which demonstrated the social and mental involvement that the absence of teeth was causing.\nDuring clinical examination, besides the absence of mandibular incisors, the absence of upper lateral incisors was noted (). The patient was caries-free and had no history of trauma or even any conical tooth, deciduous teeth impacted or delay in eruption of them. In view of those clinical findings, a panoramic radiograph was requested to detect the absence of permanent teeth especially. The analysis of panoramic radiograph detected the agenesis of permanent teeth as lower incisors, upper lateral incisors, and upper and lower premolars (). Moreover, the patient had no clinical signs of any syndrome or disorder like ectodermal dysplasia or Down syndrome, which are usually syndromes related with oligodontia in primary dentition.\nThe treatment plan involved the installation of an adhesive partial denture for restoring only the lower incisors due to the lack of space for construction of an upper dental prosthesis (Figures and ). The choice of an adhesive prosthesis was due to the difficulty of the patient's adhesion to use a removable appliance.\nIn the first appointment, the clinical procedure was carried out as follows: upper and lower molding, interocclusal record in wax, and confection of partial dental prosthesis with lower incisors. The partial prosthesis had rods made of metallic steel wire located on each side of their lateral extremity (). These rods were designed to be fixed into the lingual surface of the canine and into the first deciduous molar lower with composite resin.\nIn the second appointment, the partial prosthesis was installed as follows: etching acid of the enamel of canine and first deciduous lower molars with 35% phosphoric acid for 15 seconds, the enamel was rinsed and dried to apply only the Scotchbond Multi-purpose Plus adhesive (3 M/ESPE, USA) according to the manufacturer's directions, and finally, the rods of partial prosthesis were bonded to the surface of these teeth with a thick layer of Z250 (3 M/ESPE, USA) and the occlusion was checked. demonstrated the final result of this case. Adequate care with adhesive dental prosthesis and oral hygiene was given to the mother of the patient. |
A 53-year-old Caucasian British woman originally presented to her local hospital in 2002 with shortness of breath secondary to atrial fibrillation. During the admission, chest radiography revealed widespread pulmonary nodular infiltrates, and a subsequent computed tomography (CT) scan confirmed the presence of widespread pulmonary metastases, most marked in the lower lung fields (Figure ). The CT scan also demonstrated extensive retroperitoneal and para-aortic lymphadenopathy and hepatic abnormalities consistent with metastases, but no obvious primary site for the disease (Figure ).\nBefore admission, our patient had no symptoms of liver dysfunction and her medical history was otherwise unremarkable. She had no family history of malignancy. Routine haematology, clotting, serum biochemistry and liver function tests, hepatitis screen and tumour markers were all within normal limits. After the standard medical management for atrial fibrillation was completed, a CT-guided biopsy of the predominant hepatic lesion was performed.\nHistological examination of the biopsy confirmed the presence of an infiltrating tumour with pleomorphic elongated cells that stained positively with the vascular markers Factor VIII, CD31, and CD34. These morphological and immunohistochemical features were consistent with the diagnosis of HEH. In the presence of disseminated disease, surgical management was not indicated, and our patient was referred to the oncology team for ongoing management.\nIn response to radiological evidence of disease progression, first-line therapy with interferon was commenced in accordance with the dosing recommendations published in an earlier case report []. A CT scan performed after three months therapy demonstrated stable disease; however, as our patient was experiencing significant interferon-related side effects, the treatment was discontinued. After a six-month break from therapy, there was evidence of disease progression within the spleen seen on an updated CT scan, and the decision was taken to explore treatment with thalidomide.\nStarting initially at 100 mg per day, the dose of the drug was increased at weekly intervals up to 400 mg. Treatment was well tolerated and currently remains at 400 mg daily, more than seven years later. During this period, our patient has had regular restaging by CT scans; the disease has remained stable in the lungs and liver by Recist criteria, but with the development of calcification within the predominant liver lesion (Figure Figure ). At present, our patient continues to have no symptoms of the disease, and throughout the course of treatment has not had any treatment-related toxicity that has required either hospitalization or dose reduction. |
Patient 2 is a 78-year-old male who was experiencing persistent lower urinary tract symptoms despite combined medical therapy with alpha blockade and 5-alpha reductase inhibitors. His medical history included coronary artery disease status post-coronary artery bypass grafting and percutaneous coronary intervention, and a history of pneumonia. Preoperative cystoscopy revealed enlarged median and lateral lobes, as well as severe trabeculations of the bladder with a TRUS measuring a 41 cc prostate. HoLEP was carried out utilizing a two-incision technique. Upon completion of morcellation, it was noted that the patient's abdomen was distended, but his peak airway pressures were normal, the abdomen was soft, and the catheter drainage was noted to be clear. In addition, there was no suspicion for a significant mismatch between irrigation used and fluid output collected in the drainage system.\nGiven the previous similar presentation in Case 1 with no suspicion of bladder injury, we suspected that the patient had extraperitoneal extravasation of the saline irrigation through a capsular perforation as occurred in Case 1. The decision was made for the patient to be awakened, extubated, and transferred to the recovery room where he was further monitored. A stat noncontrast abdominal CT scan was performed that revealed a moderate amount of free fluid in the pelvis and upper abdomen; the fluid in the pelvis and lower abdomen was distributed in the extraperitoneal region with no evidence of hematoma (). The patient remained hemodynamically stable and was transferred to the floor with continuous bladder irrigation. The patient was given a 40 mg dose of Lasix ∼8 hours after the operation was completed. Overnight, there were no acute events. On POD 1, the patient's abdomen was soft and significantly less distended. The Foley catheter drained 3950 cc of urine overnight without evidence of hematuria. The patient was discharged with a catheter on POD 1. The patient had his catheter removed on POD 9. A postoperative CT cystogram revealed no evidence of leak with resolution of the pelvic and perivesical fluid (). Thirty grams of benign prostate tissue was removed on final pathology analysis. The patient was noted to have a bladder neck contracture seen on cystoscopy 4 months after his procedure for which he underwent cystourethroscopy and laser incision of bladder neck contracture. |
The patient was a 7-year-old boy born with tracheoesophageal fistula (TEF) with esophageal atresia. Fistula division and primary anastomosis of the esophagus was attempted on the third day after birth in another hospital. However, because of long gap atresia, he underwent cervical esophagostomy and feeding gastrostomy. Two years later, he underwent an Ivor Lewis operation, pyloroplasty, and feeding jejunostomy. However, leakage from the anastomosis site occurred and re-anastomosis was attempted on the 7th postoperative day. However, the leakage could not be controlled and the patient became hemodynamically unstable due to septic shock. Therefore, reposition of the gastric conduit in the abdominal cavity and a cervical esophagostomy were performed (). After a difficult recovery period, he was transferred to our hospital with a body weight of 12 kg at age 2. He was followed up for 5 years with the expectation that he would grow with jejunostomy feeding. However, he suffered from severe growth retardation and his body weight was just 15 kg when he became 7 years old. He was referred to our clinic for corrective surgery. When he visited our clinic, he had not been able to eat food by mouth since his birth.\nHe underwent esophageal reconstruction with colon interposition via a substernal route. The transverse and descending colon pedicled with a left colic artery was harvested and anastomosis in the isoperistaltic direction was performed. The cervical esophagus was recovered from an esophagostomy and proximal anastomosis with the colon was made. Distal anastomosis was made to the upper body of the remnant stomach. A substernal route was chosen because of the history of multiple operations in the posterior mediastinum. On the 7th postoperative day, an esophagogram revealed that the proximal and the distal anastomoses were intact and the distal passage was good (). Postoperative diet training was difficult because he did not know how to swallow food. However, the amount of oral intake increased gradually, and on the 23rd postoperative day, he was discharged without symptoms of dysphagia. Seven months after the operation, his body weight became 18 kg and he can now tolerate a regular diet.\nThe patient was a 13-month-old girl born with tracheoesophageal fistula with esophageal atresia, type C. An attempt at primary anastomosis in other hospital failed due to long gap atresia. She also underwent fistula division, cervical esophagostomy and feeding gastrostomy on the third day after birth.\nAfter the first operation, duodenal atresia was found and an additional gastrojejunostomy was performed. She visited our clinic for esophageal reconstruction with a weight of 7.4 kg, which was below the 3rd percentile of the growth curve. Nutritional support had been maintained by gastrostomy tube only when she visited our clinic. Preoperative CT scans showed malrotation of the bowel with whirling of mesenteric vessels, the small bowel aggregated in the right side of the abdomen, and the large bowel aggregated in left side. However, an angiogram of the superior mesenteric artery and inferior mesenteric artery demonstrated normal arcades to the marginal arteries.\nShe underwent esophageal reconstruction with the colon via a substernal route at 13 months of age. The left colon, pedicled with a left colic artery, was used in the isoperistaltic direction. On the 9th postoperative day, an esophagogram demonstrated no leakage at the proximal or distal anastomoses. Diet training was also difficult because she initially refused oral feeding. On the 25th postoperative day, she was discharged without dysphagia. Eight months after the operation, stenosis at the proximal anastomosis site occurred and endoscopic balloon dilatation was attempted twice. At 22 months after the colon interposition, surgical widening of the proximal anastomosis site was performed. She is now on a regular oral diet. |
A fifteen-year-old boy sustained a trivial injury to his left knee while turning on weight-bearing knee joint. He presented with severe pain and a swelling around knee joint and inability to bear weight on injured limb. On examination, flexed attitude of knee joint was evident. Tenderness over lateral femoral condyle was detected with restricted movements. No instability was detected. All ligament tests were normal. Routine AP and lateral radiographs showed large osteochondral fracture of lateral femoral condyle (Figures and ). CT scan with 3D reconstruction was done to understand the anatomy of the fracture and to rule out any associated injuries (Figures , , , and ).\nThe patient was investigated as the force of injury was inadequate to cause a traumatic fracture. The serum vitamin D levels were 13.8 ng/mL (normal = above 80 ng/mL) and serum testosterone level of 0.93 ng/mL along with alkaline phosphatase levels increased to 187 from normal range of 40–120. Hence we felt this was a pathological fracture.\nWe decided on open reduction and internal fixation of the fracture as with arthroscopy introducing Herbert's screws perpendicular to fracture site was not possible. An anterior midline skin was taken. Skin flap was elevated mainly on lateral side to aid exposure. A lateral parapatellar arthrotomy was done. There was inadequate exposure with this approach (). Though the anterior aspect of the fractures fragment was clearly visible, posterior part of the fractured fragment and its bed on femoral condyle were not visible enough to perform anatomical reduction, neither in flexion nor extension. The space obtained by this exposure was not enough to accommodate instrumentation to put Herbert's screws in direction perpendicular to fracture direction. We discussed on table the option of excision of infrapatellar fat pad and came to conclusion that it would expose the anterior part of fracture more clearly but visualisation of posterior aspect would still be inadequate.\nHence, to obtain good exposure for anatomical reduction and rigid fixation as well as to get space for use of instrument of definite fixation, Z-plasty of quadriceps apparatus was done (, modification of Coonse and Adam's approach). With Z-plasty, posterior part of lateral femoral condyle was seen clearly () and fracture bed was nicely visible (). Anatomical reduction of fracture was done and fracture was fixed temporarily with 1.2 mm K-wires (). Definite and stable fixation with Herbert's screws was done () following the AO principles for intra-articular fractures. Postfixation quadriceps was securely sutured ().\nImmediate postoperative radiographs were done. Good anatomic reduction with stable fixation achieved (). The patient was immediately mobilised in bed as quadriceps apparatus was securely fixed. Patient was encouraged to do active movements of the knee joint and was advised nonweight bearing for three months postoperatively. At one year follow up patient managing all activities including sports without any deficiency or weakness of quadricep muscles. Radiographs shows good healing without any articular cartilage or subchondral bone changes (Figures and ). |
A 52-year-old male patient was admitted with complaints of hoarseness and bloody sputum. The patient has 30 pack/years of smoking history. In thoracic computerized tomography (CT), a mass lesion with irregular contours was observed surrounding aortic arc and the left main bronchus in the mediastinum and causing a loss of calibration in the left pulmonary artery (). Fiberoptic bronchoscopy performed under conscious sedation with midazolam revealed mucosal infiltration at the orifice of the upper division of left upper lobe having a tendency for bleeding, almost fully obstructing the orifice. Also lingular segment was almost fully obstructed and constricted at an advanced level. Mucosal biopsies were obtained from these areas and the procedure was terminated by the control of minor bleeding. After approximately one hour, sudden massive hemoptysis developed (about 600 cc in 15 seconds). The patient was urgently taken to the operation room and was intubated by rigid bronchoscope. Fluid replacement, inotropic agents, fresh frozen plasma, and erythrocyte infusion were given. The lumen was observed to be covered with coagulum starting from the trachea inlet. After cleaning the coagulum, active hemorrhage was observed from the entrance of the left main bronchus. The sterile gauze impregnated with epinephrine (0.2%) was placed towards the distal part of the left main bronchus using rigid forceps to occlude the area which origin of the bleeding. In the meantime, cardiac massage was applied for 5 minutes due to cardiac arrest. After stabilization of the patient, the right bronchial tree was carefully cleaned from bleeding residues and bleeding control was ensured. Patient was intubated and transferred to the intensive care unit. The patient was connected to mechanical ventilator under mild sedation for 24 hours. The condition of the patient was stable and approximately 50 cc bleeding occurred through the orotracheal tube in 24 hours. The next day, rigid bronchoscopy both for removing the gauze and for ensuring long-term control over bleeding was done. The gauze at the distal part of the left main bronchus was removed carefully with a forceps. The bleeding was observed to continue massively from the mucosal infiltration area obstructing the upper division. The lesion invaded the mediastinal and main vascular structures so that surgical procedure could not be performed. A silicone Y stent, 14 × 10 × 10 mm in size, was planned to be placed, for bleeding control, in the left main bronchus of the patient who was not suitable for the embolization which we do not have in our hospital and not suitable to be transported to another center due to high risk. The leg of the stent extending to the left main bronchus was closed up to carina level, the inlet of the upper lobe bronchus, by applying bronchial stapler and the leg of the stent extending to left lower lobe bronchus was cut and placed in appropriate size, so that 5 mm remains (). After ensuring that bleeding did not continue following placement of the stent, the procedure was terminated. The patient was observed in the intensive care unit for a day. He was extubated at the 4th hour of his follow-up. Pathological examination of biopsy specimens revealed non-small cell lung cancer. The patient receiving palliative chemotherapy concomitant with radiotherapy is followed with stent without hemoptysis in the 3rd month. No complication due to the stent was observed in two sessions of fiberoptic bronchoscopy within this period of time. |
A 30-year-old adult male presented to the trauma ward with a history of accidental fall followed by stampede over his left elbow and had pain, swelling, and deformity over his left elbow region.\nOn clinical examination, his elbow was in 20° flexed attitude, forearm in supination and a hollow depression present on posterior aspect of forearm (), with loss of olecranon prominence. The left upper limb was swollen with blisters over the forearm region (). Stretch pain was present; radial pulse was not palpable. There were finger and thumb drop. The dorsiflexion of wrist was possible.\nPlain radiography showed anterior dislocation of the elbow (). Preoperatively, brachial and ulnar arterial flow was not recordable with Doppler, but monophasic response was present in radial artery.\nClosed reduction was done under intravenous sedation in the minor operating room, and the elbow joint was found to be stable post reduction. The reduction maneuver being traction at wrist and counter traction at the arm, mild flexion and posterior displacement of forearm. The postreduction radiograph () and computed tomography () showed congruent reduction. This was done immediately following closed reduction. As there was severe swelling and the distal vascularity insufficient, an attempt of closed reduction was done before the vascular surgeon assessed the limb vascularity, in the idea to reduce the ischemia time and that the compression of the neurovascular structures by the dislocated bony parts, could be temporarily relieved by closed reduction of the elbow joint before contemplating over open reduction or any vascular procedure.\nAfter reduction, radial pulse was still absent and vascular surgeon assessment revealed clinically absent distal pulses but monophasic flow in radial artery on a hand-held Doppler probe showing no significant improvement in the vascularity of the limb even after closed reduction.\nA primary exploration of the brachial artery was planned. Intraoperatively, the brachial artery was found to be lacerated (). Long saphenous vein was harvested from the ipsilateral leg and used as a bypass graft at the injured level of brachial artery. The posterior interosseous nerve was found to be intact but with a minimal contusion. In addition, a prophylactic fasciotomy () of the forearm was done.\nThe limb was immobilized in an above elbow slab with 90° flexion and forearm in mid-prone position. Split skin graft was done for the fasciotomy wound 1 week later. Limb was immobilized () for 3 weeks and active mobilization started thereafter. At 3 months follow-up, there was complete recovery of wrist and finger movements. The elbow range of movement was from 0° to 100° ( and ). |
The patient, a 57-year-old woman, had no significant history of traumatic injuries or psychiatric or movement disorders. Involuntary movement of the right ear had gradually developed at 53 years of age, and involuntary movement of the left ear had developed two months later. Initially, the movements were intermittent; bilateral ear movements had developed gradually, and became continuous with significant pain in the right auricle and posterior neck. She was diagnosed with focal auricular dystonia and received oral medicines including clonazepam (3 mg), pain medications (NSAID and tramadol hydrochloride), repetitive botulinum toxin injections (5–10 IU) into the right posterior auricular muscles, and occipital nerve blockers (lidocaine). However, these treatments were not effective in reducing pain and involuntary movements of the ear. She discontinued anticholinergic drugs due to side effects including dry mouth, sleepiness, and dizziness. Although botulinum toxin injections into the anterior auricular and/or superior muscle were partially effective for involuntary movement of the right auricle, she discontinued botulinum toxin injections due to high associated costs and unpredictable effects. She was ultimately referred to our hospital for surgical treatment evaluation. Her ear movements were predominantly on the right side. Involuntary muscle contractions were confirmed in the right anterior and superior auricular muscles of the right auricle (). In the left auricle, the main involuntary muscle contraction was confirmed to be in the superior auricular muscle (). She exhibited no voluntary control over these ear movements, and could not suppress them; significant pain was only present in the right auricle. There were no synchronous and rhythmic movements between the two ears. Involuntary movements were not confirmed during sleep and were mild in the morning. Her brain MRI showed no abnormalities; electromyography was not performed. Before the onset of the auricular movements, she had not taken any oral medications. We diagnosed her with focal auricular dystonia. Although we suggested deep brain stimulation, the patient rejected the implantation of a mechanical device. Since involuntary movements and pain were predominantly present on the right side, we decided to perform left pallidothalamic tractotomy after the patient provided written informed consent for the surgery.\nT2-weighted brain MRI was used to identify a potential surgical target, while brain lab elements were used for stereotactic planning. The target was 9 mm lateral, 0.5 mm posterior, and 3.5 mm inferior to the midpoint of the anterior and posterior commissures. The surgery was performed under local anesthesia. A Leksell neurogenerator and monopolar radiofrequency electrode (1 mm diameter, 4 mm insulated tip) were used to perform macrostimulation and lesioning. Macrostimulation at the target (100 µs, 133 Hz, and 1–3.5 mA) induced no abnormal sensory or motor responses. We made two contiguous lesions and a 3 mm withdrawn point at 70ºC/40 seconds. Immediately following lesioning (on the day of the surgery), bilateral ear movements had ceased (). The right auricular pain was completely resolved, while that in the posterior neck was not. Post-operative brain MRI showed a coagulated lesion located on the intended target (). There were no significant complications, although the patient continued to complain of discomfort in the left auricle despite no visual observations of involuntary movements 3-months postoperatively. |
A 63 years old lady carried out a complex re-laparotomy for a postoperative small bowel occlusion after a radical cystectomy because of urothelial carcinoma. The procedure lasted 3 h because of thick adhesions that needed to be cleared. At the end of the procedure, total blood loss was 2 litres, and two Units of Packed Red Blood Cells (PRBC) were infused. During the surgical procedure, a central venous catheter was placed in the internal jugular vein by ultrasound-guided puncture of the vessel, but an inadvertent puncture and cannulation of the right subclavian artery occurred before catheter placement. Because of the ultrasound-guided procedure, the anesthesiologist thought to have cannulated the carotid artery and applied local pressure for a few minutes. Two hours later, when the patient was in the Intensive Care Unit (ICU) around midnight, a chest X-ray to check the correct position of the central venous catheter revealed a massive hemothorax (), while the patient was hypotensive and responder to crystalloids and blood infusions. A chest drain was inserted without any substantial output but a small amount of clotted blood. The patient rapidly worsened, despite appropriate resuscitation with 10 U of PRBC, 8 U of Fresh Frozen Plasma (FFP), 3 U of cryoprecipitate and 1 U of platelets from apheresis. A second chest X-Ray to check tube position revealed a tension hemothorax (). The team in charge of the patient, comprising the anesthesiologist that did the general anaesthesia for the surgical procedure, made the diagnosis of suspected subclavian artery perforation and tension hemothorax with both hypovolemic and obstructive shock. The team decided to bring the patient in the hybrid room to control the likely bleeding for the right subclavian artery. While the patient has been positioning on the angiographic table, the ECG monitor showed severe bradycardia, with a heart rate of 30 and an impending cardiac arrest with a systolic blood pressure of 30 mmHg. An emergency thoracotomy to decompress the right chest was then performed via a V space incision, and five litres of blood under pressure were drained from the right pleural space, with a rapid improvement in the vital signs. During the endovascular procedure, the general surgeon left the thoracotomy open to allow a continuing suction in the pleural space to prevent the accumulation of clots. The endovascular procedure was conducted by the vascular surgeons and lasted 40 min, confirming the massive leak from a significant defect in the subclavian artery () and consisted in a 7 x 37 mm covered stent placement in the subclavian artery at the origin of the vertebral artery. The stent was expanded with a balloon taking care of not injuring the already damaged vessel (). The patient had a transient improvement, but in the next few hours, a hemodynamic instability again occurred, even if responsive to blood infusion. A CT scan revealed a leakage from the stent, because of retrograde revascularization of the vertebral artery (). A new endovascular procedure, with more pronounced balloon dilatation of the stent, definitely controlled the bleeding. ) The patient slightly improved after an open surgical debridement of the pleural space from clots and blood, given the absence of an output from the two large drains that were in place. In the next few days, the patient went back to the ward and made a gradual full recovery with no neurological or vascular defects (). |
The donor was a 35-year-old male, Maastricht category III, who died after cardiac arrest (DCD) due to intracranial haemorrhage secondary to trauma. The right kidney was sent to another centre first and declined due to vascular damage. It then went through the fast-track scheme and was accepted by our team at Guy's Hospital. Once we had the kidney, the initial evaluation showed a right kidney, with three veins in a single cava patch, three renal arteries, the main artery with aorta patch that is 8 cm long, a small lower pole artery, which was sectioned during retrieval surgery at approximately 1 cm from its origin, and a third small mid-lower pole artery. The ureter had bifid renal pelvis.\nDuring bench surgery the kidney was well perfused well with Soltran solution. From the three veins in the single cava patch, it was decided to ligate the posterior branch in order to allow the single patch to be more mobile. The small mid-lower pole artery was already damaged and was deemed unreconstructable and was therefore tied off. The main artery was left with a 1 cm aortic patch. The lower pole damaged artery was reconstructed using tubularised aorta patch to a total length of 5 cm. No additional donor vessels had been sent.\nAlthough the inferior epigastric artery is sometimes preferred for this kind of reconstruction, in this case, it would probably have been too small for the reconstruction; also, the availability of a long and healthy aortic patch and the fact that during benching we did not know the status of the recipient vessels made us decide to take this approach.\nThe reconstruction was carried out with an aorta patch that is 5 cm in length that was part of the main artery patch of the organ. Using an 8 ch Nelaton bladder catheter as a mold a 5 cm long aorta segment was tubularised using 3 7-0 Prolene interrupted stiches in the distal area to avoid stenosis and Prolene 7-0 continuous suture in the rest of the patch to minimize bleeding risk. After construction of the tubulised aorta, E-E anastomosis to the damaged polar artery was done with interrupted 7-0 Prolene (Figures – showing steps of the vascular reconstruction).\nThe recipient was 68-year-old male, with past medical history of ESRD secondary to IgA nephropathy on peritoneal dialysis and no other medical issues nor surgical procedures. After a detailed discussion with the patient, regarding the benefits and the risks due to the surgery and donors/organ characteristics, the patient was happy to proceed and signed the consent.\nTransplant surgery was performed in the right iliac fossa with an extraperitoneal approach to the iliac vessels. The common cava patch was anastomosed to the recipient's external iliac vein. The main artery was anastomosed to the common iliac artery. Finally the reconstructed artery with the tubulised patch anastomosed the external iliac artery. After completion of all three vascular anastomoses the kidney was reperfused (Figures , , and ). The ureter was anastomosed to the bladder over a double J stent. A Robinson drain was left and wound was closed. The cold ischemic time was 27 hours and 15 minutes and warm ischemic time was 75 min.\nThere were no immediate postoperative complications. The first ultrasound was performed two hours after finishing the surgery in the recovery ward, showing good perfusion of the kidney.\nAfter 48 hours a second ultrasound was performed. The presence of a superficial haematoma within the subcutaneous tissues and slightly reduced perfusion within the interpolar region was reported; otherwise appearance of the transplant kidney was satisfactory.\nHaemoglobin fell from 11.2 (preoperatively) to 6.4 gr/dl. A decision to transfuse two units of blood cells and a relook surgery was reached. There was subcutaneous and perigraft haematoma and no active bleeding. The three vascular anastomoses were identified, both arteries, main and reconstructed, had good thrill, and the vein was soft and had good outflow. A new drain was left at the surgical site and wound closure was performed.\nThree days later, the ultrasound was repeated showing that the right iliac fossa transplant kidney had normal cortical thickness and appearance. There was no pelvicalyceal dilatation. The previously demonstrated superficial collection was no longer present. There was satisfactory global vascularity. The sampled interlobular and arcuate vessels demonstrate normal flow with resistive indices between 0.65 and 0.8. The two renal arteries and veins had normal spectral waveforms, with a final impression of normal appearances of right iliac fossa transplant kidney.\nUreteric stent was removed at week 4 after transplant. Three months after transplantation the patient was stable and had no dialysis requirements with creatinine of 187. |
A 36-year-old male was admitted to the emergency room of our hospital with a primary complaint of blindness of the right eye for 2 days after head injury. The patient's head was hit by a heavy object 2 days before, which resulted in pain and blindness of the right eye. The patient was transferred to our hospital after treatment for a duration of 2 days in another hospital which was unsuccessful. General examination indicated that the patient was alert, but bruises and swelling were present around the right eyelid. The right eye showed no light perception, and the pupil was dilated and fixed with no reflex to direct and indirect light signals. The left eye appeared normal. No otorrhea or rhinorrhea of the cerebrospinal fluid was observed. No other symptoms were found during neurological examination. A computed tomography (CT) scan of the head and orbit showed a fractured right frontotemporal bone with a small right frontal epidural hematoma in addition to multiple fractures of the right frontal temporal bone, right orbital lateral wall, right anterior and lateral maxillary sinus, right zygomatic arch, right alisphenoid and sphenoid body, left nasal bone, and nasal septum (Fig. ). A head computed tomography angiography (CTA) scan demonstrated that the walls of the left carotid had a rough appearance, combined with ∼30% local stenosis. As an antiplatelet therapy, Bayaspirin was given orally at a dose of 100 mg/d. The next morning, approximately 12 hours after the CTA scan, when the patient woke up, he was found unconscious. The patient's left upper and lower limbs muscle strength was reduced to 3. A head CT scan revealed an infarction of the right brain; moreover, a head CTA scan demonstrated no visualization of the right carotid artery. The digital subtraction angiography (DSA) showed no visualization of the right internal carotid artery (ICA); however, blood circulation was compensated by the left ICA. During angiography, blood vessels in the right hemisphere demonstrated slow image development. The posterior cerebral circulation could partially compensate for the defect; however, this angiography development was also on the slow side. Given the infarction and compensatory circulation, this patient was given no further treatment, except for symptomatic support and rehabilitation therapy. Three months later, the patient was given a modified Rankin Scale (mRS) score of 3. |
A 27-year-old Latino man with a past medical history of type I diabetes and chronic low back pain of 3 years’ duration presented to the local emergency department for evaluation of acute worsening of the low back pain rendering him unable to bear weight. Computed tomography (CT) and magnetic resonance imaging (MRI) of his lumbar spine demonstrated lytic bone lesions involving the fourth lumbar (L4) vertebral body and right iliac crest. Conservative management over a period of 1 week at a local hospital failed to provide pain relief. Subsequently, he was transferred to our institution for further management.\nOn review of symptoms, he described experiencing “shock-like” pain, which originated at the lateral aspect of his right hip with radiation to his right knee. Pain was accompanied by paresthesia along the medial aspect of his right lower leg and worsened with lumbar spine flexion and extension. He rated the pain at 4 using the Numeric Rating Scale (NRS; 0 = no pain, 10 = worst possible pain). He was unable to maintain an upright position due to pain. Chronic difficulties with initiation of urination and constipation were also reported. The right lower extremity pain was reproduced on physical examination by right straight leg raising test to 30 degrees above the horizontal and left straight leg raising test to 45 degrees. Repeat lumbar spine MRI with and without contrast at our institution revealed interval increase in size of the indeterminate destructive lesions at the L4 vertebral body with pathologic fracture, the L4 spinous process, and the right iliac bone, compared to the outside MRI of his lumbar spine from 10 days prior. New enhancement along the right aspect of the cauda equina extending cephalad from L4 was also evident (Fig. ).\nWhile awaiting further assessments, he was started on scheduled orally administered acetaminophen 1000 mg every 6 hours, scheduled orally administered pregabalin 150 mg twice daily, 5% lidocaine patch, and orally administered oxycodone 10 mg every 4 hours as needed. However, these medications provided inadequate pain relief, and he still could not maintain an upright position.\nA core biopsy of the right iliac bone lesion revealed a vascular proliferation composed predominantly of well-formed capillary channels lined by epithelioid endothelial cells that appeared to protrude into the vascular lumina (Fig. ). These lesional cells contained rounded-to-lobated nuclei and abundant deeply eosinophilic cytoplasm. The background stroma contained a prominent inflammatory infiltrate composed of eosinophils, lymphocytes, and scattered plasma cells. By immunohistochemistry, the lesion was positive for FosB, which is expressed in a subset of EHs. These histologic and immunohistochemical findings confirmed the diagnosis of an EH.\nGiven the morbidity of a surgical approach, the decision was made to treat the tumor with radiotherapy alone. A photon intensity-modulated radiotherapy (IMRT) arc therapy plan was generated with two planning target volumes (PTVs): a high-dose volume (PTV 4500), which comprised the gross tumor volume (GTV), with a prescription dose of 45 Gy in 10 fractions; and a low-dose volume (PTV 4000), which comprised the volume of a 1 cm radial expansion from the GTV, with a prescription dose of 40 Gy in 10 fractions (Fig. ). A low-dose clinical target volume (CTV) 4000 was generated with a 0.5 cm radial expansion of GTV. For PTV 4500, the finalized treatment plan achieved a D95% (the minimum dose covering 95% of the target volume) of 100.5% of the prescription dose, with a V100% (the minimum target volume receiving 100% of prescription dose) of 97% and a V95% of 99.6%, and V115% (the maximum target volume receiving 115% of the prescription dose) of 0 ml. A V95% of 99.9% and a V100% of 99.5% were achieved for PTV 4000 and CTV 4000, respectively. The dose-limiting structures included: cauda equina, V30Gy (the maximum target volume receiving 30 Gy) = 6.3 ml and D0.03ml (the maximum dose received by 0.03 ml of the target volume) = 39.82 Gy; small bowel, V19.5Gy = 4.97 ml, D0.03ml = 26.04 Gy; colon, D0.03ml = 28.97 Gy; and bladder wall D0.03 ml = 9.31 Gy.\nThe radiotherapy was delivered in ten consecutive daily treatments starting on day 9 of an 18-day hospital stay. Our patient reported his worst pain of 7/10 on day 10, and he had improvement in both pain and paresthesia on day 11. On day 12, he had resolution of urinary retention and was able to ambulate. He was able to discontinue narcotic analgesics on day 15. He was subsequently discharged with pregabalin, acetaminophen, ibuprofen, and lidocaine patch for pain management on day 18 at the completion of the 10-day course of radiotherapy with no adverse effects from radiation therapy.\nAt a 3-month follow-up after completing radiotherapy, he reported mild right knee pain; however, he was able to ambulate with conservative management. MRI of his lumbar spine with and without contrast demonstrated the lesions at L4 vertebral body, L4 spinous process, and right iliac bone were stable in size with decreased enhancement, and there was less enhancement and tissue within the epidural space and right neural foramen (Fig. ). |
In November 2010, a 61 year old Moroccan housewife was diagnosed with a stage IV poorly differentiated serous ovarian adenocarcinoma (peritoneal, mediastinal and retroperitoneal lymph node metastasis). The patient had a medical history of diabetic neuropathy and hypertension. Her family history noted a sister and a niece who were respectively diagnosed with pancreatic cancer and breast cancer. A retroperitoneal lymph node biopsy was performed to obtain tumor tissue for histological diagnosis. Given the spread of the disease it was decided to administer chemotherapy first. Since she had a contraindication to taxane-based regimens because of her peripheral neuropathy, the patient received 3 cycles of Cyclophosphamide 600 mg/m\n2 and Carboplatin AUC 5 in the first cycle and AUC6 in the subsequent cycles, every three weeks. The response assessment with PET-FDG after the third cycle showed partial response. One and a half months after the third cycle of chemotherapy, she underwent debulking surgery. The treatment was completed by two additional cycles of chemotherapy of the same combination.\nThree months after the end of treatment, a CT scan showed progressive disease in the mediastinal and abdominal lymph nodes. The patient received Liposomal Doxorubicin 40 mg/m\n2 q4w, as second line chemotherapy. The response assessment after three cycles showed disease progression. Since the patient had been asymptomatic, it was decided to wait and see.\nFour months later, in January 2012, the patient presented with skin erythema and edema of the right breast. The clinical examination found ipsilateral supraclavicular lymph node swelling. The patient also complained of a diarrhea, which was resistant to standard treatments. Breast MRI showed breast and chest edema with multiple non-specific contrast uptakes giving the aspect of a homogeneous enhancement. The patient underwent sigmoidoscopy that revealed extended ulcerations of the lining of the rectum (\n). The breast and rectal biopsies showed a positive staining of PAX8 by immunohistochemistry (\n). Both lead to a diagnosis of metastasis from the known serous ovarian neoplasia. The patient was treated by topotecan as third line chemotherapy Topotecan 4 mg/m\n2 days 1, 8, 15; every 28 days. Unfortunately the disease progressed dramatically after two cycles. The patient died in March 2012, 18 months after the initial diagnosis, 3 months after the diagnosis of the breast metastasis. |
A 50-year-old woman with bilateral breast cancer underwent a bilateral DIEP free flap procedure. Preoperative thoracoabdominal computed tomography angiography showed that both inferior epigastric arteries were patent. No abnormality was detected in her preoperative laboratory tests, which included prothrombin time, activated partial thromboplastin time, and a complete blood cell count.\nIn the surgical procedure, the right deep inferior epigastric flap was designed to be larger than its counterpart because the right breast was larger than the left breast. A 20×15 cm right DIEP flap was elevated using two medial row and two lateral row perforators. The weight of the flap was 589 g. Then, a 13×15 cm left DIEP flap was elevated using one medial row and one lateral row perforator. The elevated flap weighed 387 g. Each elevated flap was inserted into the side of each breast ().\nThe flaps were monitored at intervals of every 3 hours for the first 48 hours, and every 6 hours from 48 to 96 hours post-surgery. The patient was kept on absolute bed rest for 48 hours, after which ambulation was allowed. Until postoperative day 5, no adverse events were observed, and the flap remained soft. In the early morning of postoperative day 6, however, the patient complained of chest discomfort and, during a dressing change, a dark skin color change was found at the flap site (). It was difficult to decide whether to revise or remove the flap. Because multiple perforator dissection had been performed and there was a high likelihood of an intact perforator, flap revision was planned. In the flap revision, the pedicle vein was fully obstructed by a thrombus, and no venous outflow was detected. Even upon removal of the intravenous thrombus using a Fogarty catheter, venous outflow was not restored. Additionally, the superficial inferior epigastric vein (SIEV) was fully obstructed, and even after urokinase injection, no outflow was detected. A short perforator vein stump, which was dissected in the initial operation, was found at the flap, and slow venous outflow was identified. No other intact vein pedicle was present; therefore, it was decided to use this vein stump as a vessel for anastomosis. The vein stump and 8 cm of the initial pedicle vein graft were first ligated in retrograde fashion (). Then, 55 IU of urokinase (Green Cross Corp., Yongin, Korea) was injected into the arterial branch and, a few moments later, venous outflow was detected through the ligated vein. The third rib was then fully removed using a rongeur to avoid venous congestion caused by mechanical compression. Subsequently, the vein graft was anastomosed to the internal mammary vein. Flap perfusion was restored after the anastomosis ().\nThe congested flap site was rubbed with heparin gauze every 2 hours after the flap revision. Rubbing was discontinued on postoperative day 4 because flap congestion had begun to improve. On postoperative days 7 and 8, hyaluronidase was injected into the subcutaneous layer of the flap site, and by this point, the flap skin color had almost fully recovered (). The patient was discharged on postoperative day 8, and follow-up was performed at an outpatient clinic (). |
A 79-year-old man underwent open hepatectomy for a hepatocellular carcinoma 4.3 cm in diameter. One year later, abdominal computed tomography revealed a locally recurrent tumor 1.5 cm in diameter and a giant incisional hernia measuring approximately 15 × 6 cm on the supraumbilical midline. Consequently, the incisional hernia was repaired using a free fascia lata graft patch after repeat hepatectomy. During the surgery, the fascia lata was harvested from the left thigh. An incision approximately 12 cm long was made on the lateral side of the thigh to allow for the dissection of subcutaneous tissue and harvest a piece of fascia lata measuring 16 × 8 cm. After the hepatectomy, the skin and subcutaneous tissues were dissected down to the level of the anterior rectus sheath on both sides of the defect, exposing the native fascia along the edge of the defect. After suturing 2 cm of the top and bottom edges of the native fascia lata, the fascia lata graft was used to reconstruct the remaining defect, which measured 12 × 6 cm. For placement of the graft, the fascia lata was sutured superficial to the edge of the defect with minimal overlap (interpositional graft) () [].\nTwo years later, the patient was readmitted because of recurrent tumors measuring 3.0 and 1.0 cm in the S5 and S7 subsegments of the liver, respectively. Preoperative magnetic resonance imaging (MRI) revealed the implanted fascia lata graft above the sheath of the rectus abdominis as an interpositional graft (). Repeat hepatectomy was performed. A ventral midline incision was made and the skin and subcutaneous tissues were dissected down to the level of the fascia, which was white and hard, similar to an implanted fascia lata graft (). The fascia lata graft had survived well and become incorporated into the native fascia. We incised this fascia lata graft in the same way as for a normal laparotomy (). After limited hepatectomy had been performed, the midline abdominal fascia, including the fascia lata graft and the skin, was closed in layers with interrupted suture and skin staples, respectively. The patient was discharged on postoperative day 11 with no wound-related morbidity or hernia recurrence. Three months after surgery, MRI revealed that the resutured fascial graft had healed completely to the same state as that evident preoperatively, and the patient is doing well for 11 months after surgery without hernia recurrence. |
A four-year-old female child was brought with the history of drooping of left upper eyelid along with hypo tropic globe since birth. Clinical examination revealed severe variable ptosis in the left eye with hypotropia of around 15 degrees with an esotropia of around 15 degrees in the primary gaze. [] Duction movements in the left eye for elevation and abduction were severely restricted, whereas for depression and adduction there was mild to moderate limitation. On attempted up gaze, there was perverted convergence in the left eye. [] Rest of the anterior and posterior segment examination was essentially within normal limits.\nBased on these clinical findings a diagnosis of congenital fibrosis of extraocular muscles was made and the patient was planned for intraoperative forced duction test (FDT) for inferior rectus (IR) followed by the recession of 4.5 mm or more if tight and medial rectus recession of 4.0 mm with intraoperative adjustment. During surgery due to severely tight IR, following insertion of the muscle hooks [] for suture passage a sudden give away or sudden loss of tension within the muscle was felt. [] The muscle tendon appeared thinner now with the loss of tension within it, thus it was confirmed as intraoperatively pulled into two of the rectus muscle. Immediately a search for the posteriorly snapped muscle fibers was carried out; however, a definitely expected muscle bulk/fibers could not be retrieved because of the small orbit, thus further surgical intervention was abandoned and the patient was kept under close follow up postoperatively. During subsequent visits at the end of 6 weeks, hypotropia was significantly improved but the perverted convergence was persistent. A second surgical intervention consisting of medial rectus transposition to superior rectus insertion was performed to alleviate this innervational abnormality along with esodeviation. This was taking advantage of the innervation to MR coming during attempted elevation, along with a recession of 3 mm because of its tightness. After the second surgical intervention, a significant improvement in hypotropia and the perverted convergence was achieved with a residual deviation of fewer than 5 degrees along the horizontal and vertical meridian. [] |
We present a case of a 73-year-old male with a history of alcohol use and smoking, arterial hypertension, diabetes mellitus type 2, hypertrophic cardiomyopathy, and Bence Jones monoclonal gammopathy with no surgical or trauma history. He presented to the emergency department with symptoms of abdominal distention and pain for 48 h as well as several months of watery diarrhea and defecation urgency. Physical examination revealed abdominal distension with shifting dullness and a positive fluid wave as well as a palpable mass on the left flank. He was admitted to the General Medicine Service for detailed investigation. Abdominal ultrasound revealed large volume abdominal ascites and portal vein in the high limit of normality []. Paracentesis was performed which was negative for malignant cells. Serum-ascites albumin gradient was 15 g/L, which indicates portal hypertension as the origin of ascites. Blood tests revealed normal tumor markers except an elevation of CA-125. Computed tomography (CT) abdomen and pelvis with contrast showed wall thickening of the descending and sigmoid colon with edematous wall and extensive collateral formation in the inferior mesenteric artery (IMA) territory []. Optical colonoscopy revealed edema in the left colon corresponding to the wall thickening seen on CT scan, but no mass lesions were seen endoscopically, and no biopsy was performed []. CT angiography of the abdomen and pelvis confirmed a large arterial malformation involving the IMA [].\nTreatment was initiated with diuretics, and the patient had a slight improvement in symptoms. Subsequently, the patient underwent selective microcoil embolization of IMA branches supplying the splenic flexure, descending colon and sigmoid, selectively excluding the superior hemorrhoidal artery []. After embolization, there was a significant decrease in the size of the palpable mass on physical examination. The patient was observed postembolization for pain management followed by laparotomy 24 h later. Intraoperative findings revealed 3 litres of ascites as well as a swollen left colon with swollen epiploic appendices and a very congested mesentery obliterating retroperitoneal planes. A large draining vein within the transverse mesocolon level was observed []. A left colectomy was performed from the transverse colon to the upper rectum with transverse colorectal anastomosis. There were no complications during the postoperative period, and the patient was discharged after 6 days. The pathological specimen revealed significant vascular proliferation and collateral formation within the mesentery and congestive changes in the mucosa secondary to a large AVM []. |
A 74-year-old male patient was admitted to our hospital in March 2017 to undergo liver resection to treat a malignant hepatic lesion diagnosed with CT and PET and a fine-needle biopsy positive for squamous carcinoma. The hepatic tumour discovered during follow-up for a previous bladder cancer submitted to endoscopic surgery three years before measured 22 mm in diameter and was located in the VIII Couinaud's segment [] of the liver in association with three smaller hypodense liver lesions with a focal dilatation of peripheral biliary tree ().\nThe case is discussed with radiologists, oncologists, and pathologists of our hospital. Even if the lesion had been the single site of disease; due to the proximity/doubtful infiltration of the lesion to the biliary tree, we decided to submit the patient to an explorative staging laparotomy and possible palliative surgery.\nOur internal protocol states that during the preadmission every patient who is a candidate for a liver resection is subjected to a routine liver function test with ICG to determinate the most appropriate surgical procedures []: 0,5 mg/Kg ICG are routinely injected intravenously up to seven days before surgery to evaluate the ICG retention rate at 15 min (R15). In our case 45 mg of ICG was intravenously administrated to test hepatic function, ten days before the surgery (patient R15 = 8.9).\nThanks to the ICG property of being fluorescent with the light emitted from the photodynamic eye of the laparoscopic system in our possession, it is possible to visualize the lesion during the surgical procedure. To this target, timing of administration and dose of ICG are key points.\nSeveral studies have demonstrated that the effective dose of ICG depends on the timing of injection; in particular, if the function liver test had been performed more than 7 days before surgery it would have been necessary to administer an adjunctive dose (0,1 mg/Kg) the day before []. In this case, it was necessary to administrate an adjunctive dose of ICG the day before the surgery (9 mg of ICG injected intravenously). After laparotomy, exploration of the abdominal cavity, and exposure of the liver, we easily confirmed the superficial lesion in the VIII Couinaud's segment. The liver surface has been analysed with the fluorescent imaging system. The fluorescing tumour has been clearly identified and defined on the liver surface, as shown in . We have also identified that a large area of fluorescent parenchyma that gets from the peripheral of the lesion up to the portal pedicle such as the neoplasia would interest the right biliary tree in the form of neoplastic lymphangitis (). This datum was not preoperatively known.\nA right hepatectomy would have been the oncologically correct surgical procedure due to the infiltration of right biliary duct. Considering the probable metastatic nature of the lesion, the absence of a clearly primary lesion, the age, the comorbidities, and the small size of residual liver, we have decided to perform an atypical segmental resection of S8 associated with cholecystectomy and lymphadenectomy of the hepatic pedicle nodes, including the area of impaired biliary excretion.\nAt the histological examination, the lesion, the lymph nodes of the hepatic pedicle region, and the right biliary branch, respectively, resulted in hepatic metastases from squamous cell carcinoma and sites of metastatic location. As expected the resection margin was interested by neoplasia.\nIn particular, the histological examination showed the following:Macroscopical exam: the neoplasia, in a site, appears to be in contact with the resection margin Microscopical exam: parenchymal hepatic section that showed metastatic localization of squamous carcinoma moderately differentiated. The neoplasia interest the surgery resection margin.\nIn this case, fluorescent imaging has revealed a fluorescing ring around the hepatic metastasis (). The fluorescence of the cholestatic area was shown on the cut surface (). |
Written informed consent was obtained to report the case. A 34-year-old G2P1 pregnant woman diagnosed with AS presented at the obstetric outpatient clinic at 18 weeks of gestation. She experienced back pain when she was 25 years old; these symptoms made walking difficult during her first pregnancy at 31 years old. Following her first vaginal delivery, she was able to walk although pain persisted to a lesser degree than during pregnancy. Radiography revealed osteosclerosis of the posterior surface of cervical vertebrae and osteoarthritis of the right hip with joint space narrowing (Figure ). The initial diagnosis of AS was made at 33 years of age.\nPain was managed by the administration of nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen. After the present pregnancy was diagnosed, only acetaminophen continued to be administered, but pain increased during the present pregnancy. She complained of right hip pain, with a visual analog scale (VAS) score of 7/10. A dosage of 5 mg of oral prednisolone was administered daily from 18 weeks of gestation, and thereafter, the symptoms temporarily improved to 0/10 on the VAS. Unfortunately, the symptoms relapsed at 31 weeks of gestation. At 32 weeks of gestation, she complained of restricted neck mobility with difficulty gargling, restricted lumbar mobility that caused difficulties in bending her back, and restricted right hip joint mobility with a limitation of 10º of abduction, which also affected internal and external hip rotation. Peripartum management was discussed and planned by obstetricians and anesthesiologists. Given that only hip abduction and rotation, but not flexion, were limited, it was considered that an attempt of vaginal delivery would be possible when spontaneous labor occurred. However, if an emergency cesarean section (CS) was necessary during labor owing to other obstetric complications such as nonreassuring fetal status, special anesthesia management may be required because of the possible failure of spinal anesthesia due to calcified spinal ligaments and difficult tracheal intubation and airway management for general anesthesia. In such cases, the preparation of awake fiberoptic intubation or supraglottic airway device insertion should be considered.\nAt 38 weeks of gestation, the patient was admitted to our hospital because of membrane rupture. Labor analgesia was not provided. Oxytocin administration was required due to prolonged second stage of labor. Vacuum delivery with episiotomy left of the midline, which was opposite to the restricted right hip joint, was performed due to fetal bradycardia at birth. A healthy baby with a weight of 3358 g was successfully delivered. Both mother and neonate had a good postpartum course. Prednisolone and NSAIDs were started after pregnancy. |
A 55-year-old male presented to the emergency department with left lower limb painless swelling and redness which started gradually over two weeks prior to presentation. He stated that he usually does not stay immobilized for a long period of time and there was no recent history of immobilization or surgeries. He denies any trauma to his left lower limb. His medical background includes obstructive sleep apnea. He has never been a smoker and his family history was negative for thromboembolic events or other hematological disorders. On physical examination, there were swelling and redness in his left lower limb extending from the foot to the upper thigh. Warmth was also noted compared to the right lower limb. The rest of the physical exam was unremarkable, there was no evidence of injury or venous stasis.\nBiochemical and haematological investigations were normal. Venous Doppler ultrasound showed DVT extending from the common femoral vein at the level of the left groin to the popliteal vein at the level of the knee and a second DVT in the deep profunda vein.\nGiving the extent of the thrombosis, CT of the chest and abdomen was considered to rule out further extension of the clot or suspected malignancy. CT revealed absent infrarenal IVC () associated with multiple para-aortic collaterals and tortuous dilatation of the inferior mesenteric vein. It also confirmed the presence of acute thrombosis involving the left external iliac and left common and superficial femoral veins.\nTreatment was started initially with therapeutic dose of Enoxaparin. After that, he was started on Warfarin and required life-long anticoagulation. Following daily measurement of the calf and thigh circumference, his DVT had resolved. After discharge, life-long Warfarin was continued and he was advised to use elastic stocking. No recurrence of DVT has occurred at three and six months of follow-up. Thrombophilia studies, including lupus anticoagulant, cardiolipin antibody, antithrombin III, antinuclear antibody, factor V Leiden, and prothrombin gene mutation, were normal. However, his proteins C and S activity was low. As thrombophilia studies were done after initiating treatment, low activity level of anticoagulant proteins (proteins C and S) could be attributed to treatment with Warfarin []. |
A 29-year-old multiparous female at 35 weeks and 6 days of gestational age arrived at our obstetrical triage unit in extremis with the chief complaint of abdominal pain. She was transported to the hospital by her male partner who provided the history. The abdominal pain was of abrupt onset approximately 1.5 hours prior to arrival and was mainly epigastric in origin. The partner observed a single episode of emesis en route and the gradual onset of confusion. The patient's prenatal course had otherwise been unremarkable. A physical examination revealed a lethargic and confused gravid female in apparent distress. The fundal height was 35 cm and the abdomen was diffusely tender. There was evidence of involuntary guarding and an absence of rebound tenderness. The systolic blood pressure was 60 mmHg as determined by palpation, pulse was 150 beats per minute, and body temperature was 38.2°C. She was able to localize pain and respond to simple commands. The obstetric history was significant for two prior uncomplicated spontaneous vaginal deliveries, one at term and one late preterm. An ultrasound study of the abdomen was performed at the bedside and showed a singleton fetus with a fetal heart rate of 70 beats per minute and free peritoneal fluid. The cervix was 3 cm dilated by digital examination, the membranes were intact, and there was no evidence of significant vaginal bleeding.\nTwo large bore intravenous lines were placed and aggressive fluid replacement was undertaken with normal saline. The systolic blood pressure improved modestly to 70/30. The fetal bradycardia persisted despite aggressive volume replacement, oxygen supplementation via nasal cannula, and position changes. An emergent exploratory laparotomy with cesarean delivery under general anesthesia was performed for the indications of suspected intra-abdominal hemorrhage and nonreassuring fetal heart tones. At the time of initial evaluation, the most likely cause of the patient's symptoms was assumed to be uterine rupture. A Pfannenstiel incision was used to access the abdomen. Upon entering the peritoneal cavity, 1500 mL of hemoperitoneum was encountered. A viable female infant was delivered through a low transverse hysterotomy and transferred to the neonatologist for resuscitation. The hysterotomy site was closed and the abdomen and pelvis were packed with laparotomy sponges to control the hemorrhage and identify the source of bleeding. The packs were removed from the pelvis in a stepwise fashion. The uterus and accompanying pelvic structures were intact and were not the source of hemorrhage. Upon removing the packs from the upper abdomen, brisk bleeding was encountered following removal of the packs in the left upper quadrant. An intraoperative consultation was obtained from a general surgeon who created a midline vertical incision extending to the xiphoid. The lesser sac was opened revealing copious blood clot and a peripancreatic hematoma. Heavy bleeding from this area was encountered stemming from the spleen. A splenectomy and distal pancreatectomy were performed with cessation of bleeding. Intraoperatively, she received six units of packed red blood cells, four liters of crystallized fluids, four units of fresh frozen plasma, and one pack of pooled platelets after an estimated three-liter blood loss. She received two prophylactic doses of Cefazolin. Her abdomen was closed after a Jackson Pratt drain was placed, and she was transferred to the Intensive Care Unit.\nPostoperatively, broad spectrum antibiotics were administered empirically for 6 days for leukocytosis and persistent fever to 38.2°C. A discrete source of infection was not identified. Appropriate vaccinations were administered to Haemophilus influenza, seasonal influenza, pneumococcus, and meningococcus. She was discharged home in stable condition on hospital day 8 with one week of oral antibiotics. The patient's long-term course was complicated by a pancreatic fistula that resolved with conservative management. Final pathology revealed a 165-gram spleen measuring 10.8 × 6.8 × 4.5 cm with a large aneurysm of the main splenic arterial branch.\nThe neonate was born with APGARS 0 and 2, an arterial blood gas pH of 6.507, pCO2 of 176, and a base excess of −29.4. The neonate was resuscitated, intubated, and given head cooling measures for suspected hypoxic ischemic encephalopathy. An MRI of the head showed multiple brainstem infarcts. The neonate had multiple procedures performed to include tracheostomy and percutaneous gastrostomy. The infant was with severe neurologic impairment at one year of age. |
A 47 year old male with one year history of exertional dyspnea & palpitation was admitted with complaints of syncopal attacks of sudden onset. He denied any head ache, chest pain, palpitation, edema legs, persistent fever, weight loss or loss of appetite.\nHe had been seen at the trauma center 4 years ago following a bike accident. X-Ray at that time showed a lytic lesion in the distal end of the right femur with destruction of the lateral cortex and break in the anterior and posterior cortex of the lateral condyle with extension of the lesion to the distal femoral articular surface and a pathological fracture and periosteal reaction along the lateral aspect of distal femur (Figure ). CT scan of right lower femur showed expansile lytic lesion noted in the lateral condyle of femur with associated soft tissue mass noted extending out side the cortical margins with calcific densities and bony fragments within (Figure ).\nA biopsy was sent from lytic lesion of fractured lower end of femur. A curettage followed by cement application with cancellous leg screw was done. After 15 days bone cement removal, bone grafting and internal fixation with condylar blade plate was performed. Post operatively patient had minimal restriction of right knee flexion. Clinical and radiological follow up showed healing of the lesion. Cut section of the curettage material consisted of multiple hemorrhagic and tiny grey white focal areas. Microscopy showed bony trabeculae and a tumour composed of sheets of mononuclear stromal cells and many scattered multi nucleated osteoclast like giant cells (Figure ). Histologic diagnosis was Giant cell tumor of the bone.\nHe had multiple spotty pigmentations (lentigines) on his trunk for several years (Figure ). He also had been noted to have swelling of submandibular region requiring three times surgical excisions for the recurrence of the mass (Figure ) which was pathologically confirmed to be a poorly circumscribed lesion composed of myxoid nodule containing thin walled capillaries along with spindle shaped or stellate fibroblasts. The features were suggestive of superficial angiomyxoma (Figure ).\nHis cardiac exam showed normal sinus rhythm at 84 beats per minutes and blood pressure of 130/80 mmHg. Mitral first heart sound was slightly accentuated, but the pulmonic sound was normal. Grade-I diastolic murmur was heard over the mitral area. Opening snap was absent. Lungs were clear and chest radiograph showed slight cardiomegaly. Trans-thoracic Echo cardiography revealed an intra-cardiac tumour attached to inter atrial septum, which was almost filling the left atrium & obstructing the mitral inflow. Moderate amount of mitral regurgitation was present (Figure ). Coronary angiogram showed normal epicardial coronary arteries.\nPatient underwent surgical excision of left atrial myxoma under cardiopulmonary bypass through right atrial approach. When a finger was introduced through the right atrial appendage a firm, smooth, egg sized tumour was encountered. The mitral valve was normal in structure and function. It was excised under vision. The patient had an uneventful recovery without neurologic or renal damage with significant relief of clinical symptoms. Follow up Echocardiography after 6 months showed no evidence of any intra cardiac recurrence.\nPathological examination of the tumour revealed a solitary mass weighing 50 gms & measuring 6.5 × 4.5 × 2.5 cms. Externally the tumour appeared congested, shining with myxoid areas (Figure ).\nMicroscopically it was a hypocellular myxoid tumour with small polygonal, spindle & ovoid tumour cells (Myxoid cells) with round to oval nucleus, scanty eosinophilic cytoplasm, arranged in strands, along with large " Lipidic" cells having abundant vacuolated, clear cytoplasm arranged around thin walled blood vessels in perivascular pattern. Focal nesting of tumour cells was seen. Stroma showed extensive myxoid change. Hemosiderin laden macrophage, focal dense lymphocytic infiltrate, plasma cells, mast cells were also seen (Figure ). |
A 56-year-old man was hospitalized because of pain and numbness in his left hand since he slipped a week earlier. He had no medical history of diabetes or hypertension. He had a thirty pack-year smoking history. In the physical examination, we found that the motor and sensory functions of his left hand were normal. However, his radial artery had no pulsation. His laboratory data, including anti nuclear antibody, anti-neutrophil cytoplasmic antibody, and rheumatoid arthritis factor, were within normal limits. However, the laboratory analysis showed decreased protein C and S concentrations (protein C antigen, 57%; protein S antigen, 19%). The diagnostic work-up to determine the degree of lesion included a computed tomography (CT) angiography, which showed an intraluminal lesion of the left upper extremities vessel. In the CT scan, the deep brachial and radial artery of the left hand was occluded (). Coincidently, we stumbled across a mass lesion on the aortic arch. For the evaluation of the incidental mass lesion, we performed a chest CT scan and transthoracic echocardiography. The ascending aorta and the aortic arch had intact intima and a normal size (). In transthoracic echocardiography, we found a floating mass in the lesser curvature of the aortic arch (). We decided to surgically remove this floating mass because of the risk of peripheral embolization, including thrombectomy for the brachial and radial artery occlusion of the left arm. We inserted arterial cannulation in the left femoral artery. A median sternotomy was performed, a venous cannula was inserted in the RA auricle, extracorporeal circulation was begun, and the central temperature was decreased to 25℃. The patient was then in total circulatory arrest. An incision was made in the aortic arch, and the 3.0-cm intraaortic mass was completely removed (). The mass had no definite stalk, and its attachment site in the aorta was relatively normal. A histopathologic examination revealed the mass to be a fibrin thrombus. We also removed the thrombus of the left upper extremities through the brachial artery. In the postoperative peripheral angiography, the brachial artery and the radial artery showed good blood flow (). One week later, the patient recovered without complications and was discharged on the regimen of warfarin. |
The patient was an 18-year-old female who referred to Rheumatology Clinic in Alzahra Hospital. She was complaining from low back pain and paravertebral muscle spasm since two weeks prior to admission. The pain was mainly localized in the right side of her waist and this sudden onset of the pain made her troubles walking. Three days later, she found the pain radiating to her left ear and her lower left molar teeth. At this time, she got aware of a painless huge mass in the left side of her neck. She complained from weight loss about 3 kg over 6 months but she denied any fever or other constitutional symptoms. Increasing pain and the mass in the left side of her neck caused her seek for medication. On admission, she was stable and afebrile. Her left radial pulse was undetectable, but other pulses were completely normal. No sign of ischemia was present on her limbs. A soft and pulsatile mass was observed in the left side of her neck. On auscultation, vascular bruit was audible on the carotid arteries. No positive finding was detected in neurological examination, and fundoscopic evaluation of the eyes was also normal. Left and right arm blood pressures were 80/60 and 120/80 mmHg, respectively. Right and left foot had equal pulse pressure (120/80 mmHg). The laboratory data is summarized in .\nColor Doppler of carotid arteries showed a left common carotid artery aneurysm with dimensions of about 15×17×21 mm with increased intima and media wall thickness in site of dilation. Computed tomography (CT) angiography revealed aneurysmal dilation at mid common carotid in a length of about 4 cm. Diameter of aneurysm at the most dilated portion was about 15 mm. In addition, diameters proximal and distal to aneurysm were 5 mm and 4 mm, respectively. Left carotid distal to aneurysm was well visualized. Rest of carotid and vertebral arterial system showed normal caliber with no significant stenosis. No definite plaque formation was identified. In the region of aortic area, left vertebral artery was arising from the aortic arch. Left subclavian artery was not visualized. There was also narrowing at the origin of right subclavian artery ().\nThe chest radiography, abdominal sonography, and thyroid gland sonography were normal. Echocardiographic findings were compatible with trivial mitral and tricuspid regurgitation. Based on these vascular data, unequal arm blood pressure, leukocytosis and elevated ESR, the diagnosis of the Takayasu's arteritis was made.\nHeparin infusion was started for the patient (2500 units every 3 hours) followed by oral warfarin therapy. She received prednisolone tab (50 mg) daily (in divided doses). She was also treated with infusions of monthly 700 mg cyclophosphamide pulse. After 6 cyclophosphamide pulses, a significant improvement was seen, constitutional symptoms vanished, neck mass was reduced 50% in size, and ESR got the normal range.\nThe left radial artery found to have a weak pulse. Totally, she received 6 pulses of cyclophosphamide within six months. Then, she was treated with 15 mg intramuscular methotrexate per week, 1 mg oral folic acid daily, and 80 mg aspirin daily. In addition, prednisolone was tapered. Like any other patient on chronic corticosteroids, to prevent osteoporosis, she was prescribed with calcium, vitamin D, and a bisphosphonate and perform weight-bearing exercises. Modifiable risk factors for atherosclerosis especially hypertension, smoking, inactivity, diabetes, and hyperlipidemia should be treated maximally. |
A 68-year-old male presented to the oral oncology outpatient department with a swelling over the right side of the mandible of one month's duration. A comprehensive history was taken, and the patient revealed a history of extraction of multiple teeth on the same side, after which the swelling started insidiously. It was soon accompanied by intermittent episodes of pain, which was of a pricking nature and radiated upwards along the jaw and to the ear on the same side. The patient was prescribed analgesics and anti-inflammatory medications, which provided temporary pain relief but there was no decrease in the swelling. The patient also complained of excessive salivation for two weeks. The patient had a habit of smoking 10 - 15 cigarettes a day for more than 25 years with occasional alcohol consumption. There was a negative history of chewing tobacco in any form.\nClinical examination revealed a bony hard swelling of the right side of the mandible, approximately 5 x 4 cm in maximum dimension, extending from the angle of the mandible to 2 cm short of the midline. The swelling was tender on palpation, with defined edges, and was fixed over the bone. No crackling or crepitus was elicited and the overlying skin was unremarkable. However, paraesthesia of the skin over the ipsilateral chin and lower lip was elicited.\nOn intraoral examination, no abnormality of the oral mucosa was detected and the patient was edentulous. Tenderness was elicited on palpating the alveolar mucosa on the right side, up to the retromolar region. The neck was palpated; however, no significant cervical nodes were found. An orthopantomogram was taken which showed a large radiolucency with irregular borders extending from the lower right canine region to the right angle of the mandible (Figure ).\nClinical findings and previous biopsy reports were correlated and the diagnosis was inconclusive. The lesion was provisionally diagnosed as an intraosseous malignancy of the mandible. The oral pathologist suggested an excisional biopsy for confirmation of the lesion and the patient was planned for surgery.\nThe proposed treatment plan was a segmental mandibulectomy of the affected area and intraoperative frozen section, followed by reconstruction using a reconstruction plate. Segmental resection of the mandible from 42 regions up to the right sub-condylar region was performed under general anaesthesia, and the intraoperative frozen section finding was still inconclusive (Figure ).\nThe excised specimen was sent for histopathological examination. Reconstruction was carried out with a contoured stainless-steel reconstruction plate and a watertight primary closure was achieved (Figure ).\nThe postoperative period was initially uneventful. However, on the fifth postoperative day, the patient had a purulent discharge from the submental region, with gaping of the surgical wound at the retromolar region intraorally. Culture and sensitivity testing from swabs taken were positive for Pseudomonas growth, and intravenous antibiotics were prescribed accordingly. With antibiotic therapy, the patient recovered from the infection and there was satisfactory wound healing.\nThe final histopathology report was suggestive of a high-grade malignancy of epithelial origin (metastatic adenocarcinoma/renal cell carcinoma). Positron emission tomography (PET) scan revealed well-defined, thick-walled cavitary lesions in the superior segment of the right upper lobe and the anterior segment of the right lower lobe of the lung (Figure ).\nThe patient was referred to an interventional radiologist and a Tru-Cut® (MeritMedical, Jordan, UT) biopsy was performed, which confirmed the malignant growth in the right lobe of the lung. The patient is currently undergoing palliative chemoradiotherapy for the primary tumour of the lung (oral Gefitinib, 250 mg, and 10 fractions of radiotherapy). |
A 24-year-old female patient reported to the Outpatient Department of our hospital complaining of swelling associated with pain on the left side of the face since 1 month. Initially the swelling was about peanut size, which gradually increased to present size, and was associated with pricking and localized pain. Medical history revealed blurred vision and lacrimation for the past 1 week. Her dental history revealed surgical excision of a tumor in 2007 and subsequent recurrent lesion at the same site in 2013 which was again operated.\nAt present, extra-oral examination revealed a solitary diffuse swelling in the left infraorbital region of the face measuring approximately 4 cm × 4 cm, extending mediolaterally from the medial canthus of the eye to frontozygomatic region and superioinferiorly from the lower eyelid to 1 cm above the left corner of mouth obliterating the nasolabial fold []. Skin over the swelling was normal with no visible sinus tracts. On palpation, all the inspectory findings were confirmed. The swelling was bony hard with mild tenderness and no local rise in temperature. Intraoral examination showed deficient maxilla and the absence of teeth in relation to 14–28 region [].\nComputerized tomography revealed a comminuted fracture of the lateral wall of the left orbit with an asymmetric outline of the globe. The posterior wall of left orbit was also incomplete with little soft tissue masses seen protruding into its posterio-lateral aspect. Part of soft tissue was seen extending toward the anterior wall of left maxillary sinus which was completely effaced. Two metal plates were seen, supporting the anterior lateral wall of the left maxillary antrum as artifacts. These plates were presumed to be placed in the previous surgeries [].\nOn reviewing the dental history, clinical and radiological features, a provisional diagnosis of recurrent ameloblastoma of the left infraorbital region was given. The tumor was surgically excised with normal tissue margins surrounding the lesion and the excised specimen was sent for histopathological examination.\nMicroscopic examination revealed a nasociliary epithelium with adjacent tumor area composed of small round cells arranged in lobular pattern separated by fibrovascular stroma. These tumor cells are arranged in pseudorosettes and glandular patterns, and showed round to oval hyperchromatic nucleus with few presenting salt and pepper chromatin pattern. The adjacent bone tissue is infiltrated by these tumor cells along with new bone formation (osteoid). The stroma is fibro-cellular and -vascular with focal areas of neurofibrillary matrix, giant cells and mitoses [].\nBased on clinical, radiological and histological findings, a final diagnosis of olfactory neuroblastoma was established. For the confirmation of the diagnosis, immunohistochemistry with a panel of markers was performed [ and ], establishing the diagnosis as olfactory neuroblastoma. With the suspicion about the former treated pathologies, past records of the patient were reevaluated and subjected to histopathological and immunohistochemical examination. Histopathology revealed the characteristic features of olfactory neuroblastoma and was confirmed immunohistochemically with the marker neuron-specific enolase (NSE) which showed strong positivity []. The patient was referred to the cancer institute for adjuvant radiotherapy. |
A 34-year-old female who has no previous clinical illness presented in 2000 with a large irregular mass, estimated clinically to be around 5 × 6 cm by physical examination, involving the right breast while she was lactating. There were no other signs or symptoms. FNA was done to rule out breast cancer, and the specimen showed few foamy macrophages and rare clusters of ductal cells, with focal secretory lactational changes. Based on that, it was determined that the specimen was negative for malignancy. The tumor continued to grow, and in June 2004, FNA of the right breast was repeated and showed large staghorn-shaped sheets of uniform ductal cells with no cytologic atypia along with myoepithelial cells. There were fragments of fibrotic stroma and bare nuclei scattered in a bloody background, and so, a diagnosis of fibroadenoma was made. Two months later, the patient underwent excision of the tumor in another healthcare facility. Examination of the slides showed an overgrowth of epithelial and stromal components in pericanalicular and intracanalicular patterns with irregular large cystic spaces showing protruding leaf-like structures (). The stromal cells showed plump elongated slightly dysmorphic nuclei with occasional prominent nucleoli. Other areas showed significant cellular growth of the stromal spindle cells which appeared to be arranged in long intersecting fascicles and growing in herringbone pattern (). Within the spindle cell growth, extracellular mucin was noted. One focus showed an exclusive spindle cell growth which was moderately atypical with plump elongated hyperchromatic nuclei. Numerous mitosis was found, up to 20 in 10 high power fields in this focus. Entrapped epithelial ductal elements were occasionally seen in other areas exhibiting ductal epithelial hyperplasia. These features were consistent with malignant phyllodes tumor with stromal fibrosarcomatous overgrowth. The patient subsequently underwent mastectomy as the margins were focally involved. During the procedure, a mass measuring around 3-4 cm was found in the most posterior aspect of the breast and there was some indication that it may have invaded the pectoralis major muscle. All the breast tissue, the tumor, and some of the muscle fibers were removed. On gross examination, there were multiple tumor masses in the inner lower and outer upper quadrants, the largest being 3 cm. On microscopy, there was proliferation of atypical spindle and elongated plump cells with pleomorphic nuclei and occasional prominent nucleoli. Extracellular mucin was also identified. The atypical stromal cells formed herringbone fascicular growth pattern reminiscent to fibrosarcoma and numerous mitosis averaging around 14 mitosis in 10 high power fields. No residual phyllodes tumor elements were identified. The tumor nodules had a well-demarcated margin with focal infiltration of surrounding breast and adipose tissue. No lymphovascular invasion, necrosis, or heterologous differentiation was seen. All surgical margins and muscle fibers were not involved by the tumor. The skin and nipple did not show any involvement either. All these histological features were identical to those identified in her previous lumpectomy except that there was more pronounced atypia and no residual epithelial component of phyllodes tumor identified. No lymph nodes were identified. A year later, the patient began to suffer from acute bouts of pancreatitis and was admitted several times for this. In March of 2006, abdominal CT was performed and showed a heterogenous low attenuation soft tissue mass involving the head and body of the pancreas and was extending upwards. The celiac vessels and its branches were going through this mass but did not show any significant narrowing. There was obvious atrophy of the pancreatic tail and dilatation of the pancreatic duct. The mass was in contact with the anterior aspect of the inferior vena cava (IVC) with no clear fat plane in between (). Biopsy of the pancreatic mass showed uniform proliferation of elongated spindly cells which had coarse chromatin and mild to moderate nuclear pleomorphism. Some cells had plump hyperchromatic nuclei. Numerous mitotic figures were identified (). The background showed variable amounts of collagen and stroma with focal areas of myxoid appearance. Immunohistochemical staining showed strong positivity for vimentin; however, the cells were negative for actin, S100, and cytokeratin (). These findings were consistent with metastatic fibrosarcoma of the pancreas secondary to her primary breast lesion. Due to the location, extent, and nature of the condition, the case was deemed unresectable. Chemotherapy was initiated; and in the little chance that the tumor shrunk enough, the possibility of resecting the metastasis would be entertained. In January 2007, the patient presented to the ER with severe epigastric pain, where she collapsed, was hypotensive, and subsequently admitted. On examination, a tender mass in the epigastric area was felt. Urgent CT of the abdomen and pelvis with and without contrast showed a pseudoaneurysm in the splenic artery measuring around 3.5 cm. There was also expansion of the retroperitoneal mass and blood in the intraperitoneal cavity. There was heterogenous enhancement in the liver most probably indicating liver infarct. In addition, there were areas of the IVC which had markedly thinned wall and areas suspicious for active bleeding, especially from the proximal splenic artery (). The pancreatic fibrosarcoma had grown and eroded branches of the celiac artery with bleeding pseudoaneurysm along with infarct of the liver, spleen, and adjacent organs. The patient continued to be hypotensive with abdominal distention due to severe intra-abdominal bleeding and developed multiorgan failure and hemorrhagic shock leading to her death. |
A 54-year-old female patient with a past medical history significant for diabetes presented to the emergency department with worsening abdominal pain. The day before she underwent a diagnostic colonoscopy for complaints of chronic diarrhea (2 months) where a transverse colon adenomatous polyp was resected, and several mucosal biopsies were obtained.\nThe patient reported that the abdominal pain started suddenly about 4–5 h after the colonoscopy. She described the pain as being colicky and intermittent, occurring every hour, lasting for about 15 min, and then resolving on its own. She reported that overnight the pain worsened to the point that she sought medical care the next morning when we (the gastrointestinal team) were consulted by the emergency department. Additionally, she noticed that she had some red mucus in her stools on the morning of presentation.\nHer vital signs in the emergency department were stable with a blood pressure of 128/72 mm Hg, a pulse of 83 bpm, and a respiratory rate of 16/min with normal oxygen saturation. Physical examination showed a nondistended abdomen, with mild tenderness over the right upper quadrant without any palpable masses. Her blood work was significant for a white cell count of 13, lactate of 1.2, and a normal metabolic profile.\nIn the emergency department, the patient had an abdominal X-ray, and a CT of the abdomen with intravenous contrast which showed a transverse colo-colonic intussusception (Fig. , , ) with partial obstruction.\nThe patient was seen by the surgical team who deemed her not to be obstructed and opted for conservative management with intravenous fluids and nil per os. On the following day, the patient reported that her symptoms had rapidly improved and subsequently had an abdominal X-ray that showed spontaneous resolution of her intussusception (Fig. ). She was started on a liquid diet which was advanced without any complications. She was discharged on the third day of stay after she had had a normal bowel movement. She followed up with her gastroenterologist who ordered an MRI 2 months after discharge, which was unremarkable (Fig. ). |
A 63-year-old woman presented with abdominal pain and diarrhea for two weeks. The patient had undergone transabdominal ultrasonography at a local hospital, and the procedure incidentally demonstrated a dilatated main pancreatic duct in the pancreatic tail; she was then referred to our hospital for further evaluation. There was no personal or family history of pancreatic disease. A physical examination revealed no unusual findings. No elevation of the levels of serum amylase and lipase and such tumor markers as carbohydrate antigen 19-9 (CA 19-9) were noted on the laboratory tests.\nContrast-enhanced pancreas computed tomography (CT) showed a moderate dilatation of the main pancreatic duct in the pancreatic tail without an obstructive mass (). No peripancreatic fatty infiltration or lymph node enlargement was noted. Magnetic resonance (MR) imaging with MR cholangiopancreatography (MRCP) was performed to exclude any lesion that could cause obstruction proximal to the dilated main pancreatic duct. The unenhanced and gadolinium-enhanced pancreas MR images () showed an enhancing mass in the dilated main pancreatic duct of the pancreatic body, which resulted in obstruction and dilatation of the upstream main pancreatic duct, and this caused chronic pancreatitis. MRCP showed a filling defect due to an intraductal mass with dilatation of the upstream main pancreatic duct with no dilatation of the downstream main pancreatic duct (). An endoscopic retrograde pancreatogram () showed a filling defect of the contrast media due to a mass in the dilated, yet patent main pancreatic duct. No hypersecretion of mucin was noted.\nUnder the impression of a mass confined to the main pancreatic duct of the pancreatic body, the patient underwent a subtotal pancreatectomy. Macroscopically, the tumor was 2.5 cm in the maximum diameter and it filled the lumen of the main pancreatic duct (). Microscopically, the tumor was confined to the main pancreatic duct with focal stromal invasion and the tumor had an intraductal nodular appearance with a monotonous tubular growth pattern, and there was no papillary projection or mucin hypersecretion. On the immunohistochemical staining, the tumor cells were diffusely positive for MUC-1 and p53, and they were negative for MUC-2 and MUC-5AC. The final diagnosis was a T1N0M0 stage ITC. |
A 29-year-old female presented with nausea, vomiting, diarrhea, and abdominal pain. Her past medical history was significant for bilateral retinoblastoma. Her right eye was enucleated at four months, and one year later retinoblastoma was identified in the contralateral eye. She underwent external beam radiation and chemotherapy with vincristine and cyclophosphamide for three years. At age 12 she developed osteosarcoma of the right femur for which she received adriamycin, ifosphamide, and methotrexate for one year, with subsequent limb salvage surgery with allograft. At age 29, she presented to our hospital and underwent imaging that demonstrated a vascular mass in the posterior bladder with incidental findings of fibroid uterus and right ovarian cyst. Exploratory laparoscopy, cystoscopy with biopsy, and pelvic washing revealed a bladder neoplasm consistent with high-grade leiomyosarcoma. Gynecologic evaluation showed an endometrial polyp with simple hyperplasia without atypia in the curettage specimen and rare atypical malignant cells suggestive of either an adenocarcinoma or a spindle cell neoplasm. Further radiological surveys of the chest, abdomen, and pelvis did not reveal any metastatic disease, although a bone scan showed a moderate focus of activity in the right proximal humerus; this was subsequently consistent with enchondroma.\nThe patient underwent a radical cystectomy with ileal conduit and simple hysterectomy. The cystectomy specimen showed a tan, partially necrotic papillary tumor with edematous and focally hemorrhagic surrounding mucosa. The tumor did not extend throughout the bladder wall, and there was no connection between the posterior wall of the bladder and the anterior aspect of the uterus. The hysterectomy specimen revealed multiple leiomyomatous lesions in the anterior and posterior uterine walls and cervix that varied from small microscopic lesions to up to 3.2 cm in largest diameter.\nHistopathological analysis demonstrated two distinct leiomyosarcomas: one arising from the urinary bladder, the other from the uterus. These were established to be unrelated, representing two independent primary sarcomas. The bladder leiomyosarcoma was high-grade with mitotic figures averaging 80/10 high power fields. The tumor was positive for Rb, p53 (1-2%) and negative for estrogen receptor (ER) and progesterone receptor (PR) and had a higher MIB-1 (Ki-67) proliferation marker count (50%) (Figures and ). In contrast, the uterine leiomyosarcoma was low-grade, well differentiated with a lower mitotic count (10/10 high power fields). It arose in a background of diffuse leiomyomatosis that extensively involved the myometrium. This leiomyosarcoma was positive for ER and PR and negative for Rb marker MIB-1 count which confirmed the increased but lower proliferative activity, as compared to the bladder leiomyosarcoma (10–15%) (Figures and ). Additional confirmatory markers for leiomyosarcoma included vimentin (+), smooth muscle actin (+), desmin (−), S-100 (−), CD117 (−), melanoma marker (−), and CD10 (−).\nAll other specimens including pelvic lymph nodes received were without malignancy, and all resection margins were free of tumor. The patient has undergone follow-up for seven years and remains cancer-free. |
A 21-year-old girl reported to the hospital along with her father with a chief complaint of enlarged gums and early loss of lower 1st molar along with pus discharge from various sites in the oral cavity [].\nDetailed history of the patient revealed that enlargement and pus discharge started when the girl was 15 years and was preceded by mobility of her teeth. It was also revealed that the girl left her school at the age of 17 years as she was not able to catch up with her peer group in her studies although she was normal but slightly sluggish in her other day-to-day activities. One peculiar finding which was reported was that the girl lacked the desire to eat. Her father reported that the girl was not able to eat properly as she had mobile teeth and pain in her gums.\nOn examination, the girl looked absolutely normal except that she looked slightly younger than her reported age and had a pale appearance. To rule out any psychiatric abnormality, consultation was taken from the Department of Psychiatry. They diagnosed the patient with borderline mental depression based on Hamilton Depression Rating Scale but suggested no treatment other than counseling (i.e., cognitive behavioral therapy [CBT]). CBT is in fact an established treatment, and majority of the cases of mental depression responded well to the same even in the absence of any antidepressant. Also to rule out possibility of any syndrome and variation in her skeletal and mental age, full body radiographs of her right hand and wrist, right shoulder, right hip joint, right pelvis, right ankle, right elbow, and right knee were advised by her physician and the findings were negative [].\nA complete blood count was advised which revealed reduced hemoglobin. The red blood cells which showed the presence of mild anisocytosis, normocytes, microcytes, pencil cells, hypochromia, and occasional polychromatic macrocytes were also seen. Hence, the patient was diagnosed with dimorphic anemia with neutrophilia.\nDiffused gingival enlargement was present with superimposed gingival inflammation, and multiple sites with periodontal abscesses were also noticed in the region of upper canines and lower molars. Increased probing pocket depths and moderate-to-severe clinical attachment loss with vertical bone defects were present throughout the oral cavity at various sites []. A peculiar finding was that in addition to the involvement of mandibular 1st molars and incisors, there was a severe loss of attachment and vertical bone defects in relation to various maxillary and mandibular teeth []. The amounts of microbial deposits were inconsistent with the severity of periodontal tissue destruction. There was also pathological mesial migration of mandibular left 2nd molar. A few carious teeth were also present. On microbiological investigation, it was revealed that there were elevated proportions of Aa but the Aa antibody titers were found to be normal.\nBased on the patient's history, general physical and oral examination, a diagnosis of GAP associated with pubertal gingival enlargement and periodontal abscesses was made, with mental depression and dimorphic anemia as the systemic manifestations of GAP.\nA detailed treatment plan was made which included restoration of carious teeth, treatment of periodontal abscesses, and thorough supra- and subgingival scaling. An orthodontic consultation was also advised to restore the deranged occlusion. It was advised to undertake orthodontic therapy after the periodontal condition of the patient was stabilized. The patient and her father were given detailed oral hygiene instructions and were motivated for better plaque control. Chlorhexidine digluconate mouthwash (0.12%) was prescribed to further aid in plaque control. Systemic antibiotics (amoxicillin and metronidazole, 250 mg of each thrice daily) were prescribed for 8 days. After the initial periodontal treatment which consisted of regular recalls every alternate day for the 1st week, the patient was recalled after 2 weeks for evaluation of the response to treatment.\nA re-evaluation at 3rd week from the initial periodontal therapy showed a reduction in probing depths and absence of gingival abscesses and no bleeding on probing. There was marked improvement in patient's mental status and hematological reports. Since the patient was improving and showing signs of gain in clinical attachment levels [ and ] and her father was inclined to avoid periodontal surgery, she was put on supportive periodontal therapy and was advised to recall every month for the next 6 months. |
A 61-year-old married man referred to the orthopedic clinic of our hospital, complaining of inability to extend his left hand fingers and wrist. The patient was admitted in the orthopedic ward. He reported a gradual onset of pain and tingling sensation in the affected extremity with three week duration; however, the night before admission while watching TV he had rested his hand under his head for a long period of time. In the morning, he found that he was unable to extend the wrist and fingers of his left hand. The patient had no history of chronic metabolic or inflammatory diseases, diabetes, hypertension or sensory-motor and balance disturbances; in addition, he did not have any history of trauma. He did not report a history of smoking or use of a specific medication. Clinical examinations revealed normal systemic functions. Examination of the affected extremity revealed complete motor palsy of the extensors of the wrist and fingers. The sensation of the dermatome of the distal radial nerve to the wrist was nonexistent. The pulse, temperature and color of the affected extremity were completely symmetrical and normal compared to the unaffected extremity. Laboratory examinations: Plain radiographs of the affected extremity did not reveal any signs of previous fractures, foreign bodies or masses with external pressure. Electromyography revealed poor and absent nerve impulse conduction of the radial nerve in relation to movement and sensation, respectively. In addition, evaluation of brachioradialis, extensor carpi radialis longus and extensor muscles of the fingers showed very poor or absent motor unit action potential (MUAP). In summary, electromyography demonstrated severe lesion of the radial nerve of the left extremity in the proximal area of the arm, along with significant axonal loss without any evidence of regeneration in the muscles mentioned.\nSurgery was done under general anesthesia and tourniquet control and the radial nerve was explored. The surgical findings were two sausage-shaped areas at the distal third of the nerve (). A neuroma (1.5 cm in length) was excised and the two ends of the nerve were coapted under magnification using 6-0 prolene suture. The limb was placed in a splint at 60 degrees flexion with the shoulder in adduction. The excised nerve segment was submitted for pathological evaluation, which yielded a diagnosis of neuroma (). The patient achieved complete recovery of upper extremity movements after 9 months. |
A 39-year-old non professional soccer player arrived in our Emergency Department complaining of pain in his anterior thigh near the insertion of the rectus femoris on the anterior inferior iliac spine (AIIS), which happened during a football match; he referred a feeling of snapping in the same zone.\nThe patient walked with the help of two crutches because he was unable to weight bear freely due to pain.\nAn evident hematoma in the region mentioned above was noticeable.\nOn physical examination there was pain due to manual pressure, a deficit of strength in hip flexion against manual resistance and a gap in the AIIS region which was clinically palpable. For this reason we suspected a lesion/avulsion of proximal rectus femoris.\nAn ultrasound study confirmed our suspicion and showed the presence of hematoma at the myo-tendinous junction with fascial blood layers and tendon rupture of the proximal rectus femoris ().\nFurthermore, magnetic resonance imaging (MRI) performed 7 days later confirmed the diagnosis and showed a lesion of the myotendinous junction characterized by partial lesion of the direct head and total lesion of the indirect head of the tendon with retraction of 1.5 cm associated to edema and hematoma ().\nIn that moment the patient got better. He did not use crutches, he had less pain during his daily life and he had less pain both in manual pressure and in tests against manual resistance.\nIn the face of this clinical improvement we decided to not consider the surgical option and to treat the patient with ultrasound guided PRP injections and a specific rehabilitation program, which was initially based on isometric exercises and, later, on eccentric work exercises and it was always accompanied by tecartherapy.\nAn autologous blood sample of the patient was taken by the Transfusion Center of the University Hospital of Parma. From this sample, 3 stocks of PRP were obtained. The injections were done 10, 20 and 30 days after injury (5 ml of PRP and 1 of thrombin) under ultrasound guidance.\nFollowing the first infiltration the patient reported a progressive improvement in symptoms and a progressive decrease in pain.\nFifteen days after the end of the infiltrative cycle another evaluation showed the absence of pain and the patient referred to walk freely without limitations in his daily life, even if a deficit of strength against manual resistance was present ().\nWe therefore planned a new MRI and clinical evaluation 45 days after the end of the infiltrative cycle.\nIn the meantime, the patient continued the rehabilitation program, including concentric exercises against elastic resistance.\nAt the final clinical check the patient did no longer complain of pain. There was no more gap in the AIIS region, the range of motion was 0°-130° bilaterally and there was no deficit of strength against manual resistance. The MRI confirmed the advanced stage of healing as no longer hematoma was appreciable and edema had almost completely disappeared ( and 5).\nThe patient returned to his sports activity without any problems 90 days after injury. |
A 72-year-old man underwent upper endoscopy for epigastric discomfort, which revealed mucosal erosion on the posterior wall of the middle body of the stomach (Fig. a), an elevated lesion on the duodenal bulb (Fig. b), and a raised tumor on the antrum of the stomach (Fig. c). A histopathologic examination of the mucosal erosion on the posterior wall of the middle body of the stomach and elevated lesion on the duodenal bulb showed that small atypical lymphoid cells proliferated diffusely and occasional lymphoepithelial lesions were also present. Immunohistochemically, the lymphoid cells were positive for CD20 and BCL2, while they were negative for CD10. Moderately differentiated adenocarcinoma was revealed in the antrum of the stomach. Abdominal computed tomography (CT) showed a tumor 2 cm in size in the antrum of the stomach and no signs of lymph node or liver metastasis. Based on these examinations, the initial diagnosis was gastric and duodenal MALT lymphoma with early gastric cancer. The urea breath test showed H. pylori infection. To avoid postoperative MALT lymphoma remnants and shorten the resection range of the duodenum, H. pylori eradication therapy, which was expected to reduce gastric and duodenal MALT lymphoma lesions, was thus performed.\nOne month after performing eradication therapy, the second upper endoscopy revealed no improvement in the gastric or duodenal mucosa, and an area of strong redness with a shallow recess just below the cardia of the stomach (Fig. d). Poorly differentiated adenocarcinoma was revealed in the cardia of the stomach. The preoperative diagnosis was gastric and duodenal MALT lymphoma with two gastric cancers. One month after the last upper endoscopy, total gastrectomy with proximal duodenum resection using intraoperative upper endoscopy and regional lymph node dissection was performed. No improvement in either the gastric or duodenal mucosa was observed by intraoperative endoscopy. Three cancer lesions found in whole tissue sections of a resected specimen after fixation were examined according to the 15th edition of Japanese Classification of Gastric carcinoma (Fig. ). In lesion A, measuring 3 × 3 cm and located in the cardia, cancer cells arranged in small nests and cords had proliferated and invaded the subserosal layer (por2, T3) (Fig. a). In lesion B, measuring 1 × 1 cm and located in the small curvature of the middle corpus, cancer cells arranged in well-formed glands had proliferated and remained in the lamina propria (tub1, T1a) (Fig. b). In lesion C, measuring 2.5 × 1.5 cm and located in the small curvature of the antrum, cancer cells arranged in fused glands had proliferated and remained in the lamina propria (tub2, T1a) (Fig. c). Of the 60 perigastric lymph nodes, 1 showed metastatic carcinoma (N1). In both the posterior wall of the middle body of the stomach (Fig. d, e) and the duodenal bulb (Fig. g, h), small atypical lymphoid cells proliferated diffusely and deeply from the lamina propria to the submucosa, and occasional lymphoepithelial lesions were present. Immunohistochemically, the lymphoid cells were positive for CD20 and BCL2 and negative for CD10, and lymphoepithelial lesions were highlighted by CAM5.2 (Fig. f, i). The morphological features and immunohistochemical staining patterns supported the diagnosis of gastric and duodenal MALT lymphoma. No MALT lymphoma lesions were detected outside the range of green and purple frames in Fig. .\nWe diagnosed the disease as stage IIB (T3N1M0) gastric cancer (the 15th edition of Japanese Classification of Gastric carcinoma) and stage I gastric and duodenal MALT lymphoma (Lugano classification). The patient was discharged 11 days after surgery and received adjuvant chemotherapy (S-1 100 mg/day/body). |
A 41-year-old man presented with a 1-month history of abdominal pain. His previous medical and familial histories were unremarkable. Unenhanced transverse CT scan of the abdomen revealed an ill defined, lobulated mass that measured about 13 × 12 × 7 cm in size and it appeared as a heterogeneously low attenuated mass with numerous areas of coarse calcification. It was located in the left side of the retroperitoneal space and involved the body and tail of the pancreas (). Contrast-enhanced CT was performed after mechanical injection of 130 cc of nonionic iopromide (300 mg/ml of iodine) into the antecubital vein at a rate of 2.65 ml/sec. After initiating infusion of contrast material, we used scanning delays of 30 seconds before starting to obtain the arterial phase images. Imaging in the portal venous phase was performed after a scanning delay of 70 seconds from the initiation of infusion of contrast material. On the contrast-enhanced transverse CT scan obtained during the portal venous phase, subtle enhancement was noted in only the periphery of the mass and most of the mass remained without enhancement (). The contrast-enhanced coronal reformatted image showed the ill defined necrotic low attenuated mass with obliteration of the splenic vein by the mass, and there was the development of multiple collateral veins (). Portal venography via the celiac axis also showed tumor invasion to the splenic vein (). The patient underwent exploratory laparotomy and mass excision was done. The specimen was revealed to be a large, firm, fixed hypervascular mass arising from the pancreas, and it occupied the left upper quadrant of the abdomen. A large multilobulated mass that measured 15 cm in maximum diameter was located in the body and tail of the pancreas, and it was attached to the spleen and transverse colon (). Microscopically, the chondroid zone was surrounded by proliferation of undifferentiated cells with abrupt transition (). The pathological diagnosis was extraskeletal mesenchymal chondrosarcoma arising from the pancreas with invasion to the splenic vein. |
A 55-year-old gentleman, presented with complaints of pain over the left knee joint and inability to weight bear over his left leg for the past ten 10 months. The patient was apparently normal ten10 months ago, when he had a history of slip and fall from 10 feet height at his workplace in the month of January 2017 and sustained close injury to his left knee. The patient developed pain and inability to weight bear over his left leg. The patient initially underwent native splinting for 6 months following the injury. As patient was not relieved of his symptoms following native splinting, patient came to Sri Ramachandra Medical College Porur for further management With complaints of pain, deformity, and unable to bear weight on left leg (). There is no history of fever, loss of appetite or any other bone injury. The patient is not a known case of diabetic mellitus, Hypertension hypertension cardiac disease tuberculosis asthma epilepsy. The patient is not a smoker or an alcoholic. Examination revealed left lower limb appears to be shorter than the right lower limb. Muscle wasting was noted over the thigh and calf region. Healed abrasion scar present over the anterior aspect of the knee joint and the distal aspect of the leg. Dilated veins present over the posterolateral and the medial aspect of the knee joint. No popliteal fossa fullness was noted. Tenderness present over medial and lateral jointline Swelling present over the anterior aspect of knee joint. Bony mass is palpable over the anteromedial and lateral aspect of the knee. Broadening and thickening present over the anterior, medial, and lateral aspect of the knee joint. Abnormal mobility was noted. The Range range of Movement movement of the knee was 20 to –70°° with fixed flexion deformity of 20°. Further movements were painful. There was no neurovascular deficit noted. Radiographs showed comminuted malunited proximal tibia with depression over the medial condyle 1-2 cm and fracture line extending to the lateral and posterior condyle of tibia (). Computed tomography CT of the knee revealed that the whole of the medial condyle was depressed by more than >2 cm and the fracture line was extended into the medial and posterior condyle. (Figs. and )). There was no fracture line noted over the metaphyseal region of the shaft of the tibia. Knee joint showed significant osteoarthritis changes. Intraoperatively, we found that the articular cartilage was found to be completely damaged and there was a coronal split of the tibial plateau. The depressed medial condyle was raised and fixed with the help of of cannulated cancellous screw from the medial aspect of the tibia. (Figs. and ). He was operated upon using a total knee prosthesis – Smith and Nephew Genesis II system with long stem tibial component and cruciate retaining femoral component. Then, appropriate femoral femoral cuts were made and and size 6 left cemented, nonmodular Genesis II cruciate retaining femoral component with Genesis II long slotted stem placed. An appropriate tibial cut made and Genesis II left nonporous tibial base plate placed. Size 5-613mm Genesis II dished articular insert was was placed. Movements of the knee joint were checked intraoperatively and were as found found to be satisfactory. Six 6 weeks postoperatively (), the patient could walk freely without a stick and had no pain. The knee was stable and had a full range of movement. |
A 55 year old man was referred to our department for surgical management of a substernal goiter. He had a 7 year history of a slowly growing anterior neck mass, associated during the last year with a dry cough, shortness of breath, dyspnea, dysphonia, palpitations and sweating. He was followed by an endocrinologist for hyperthyroidism, for which he was placed on neomercazole for thyroid suppression. Physical examination showed an enlargement of the thyroid gland; it was bilateral, irregular and non adherent. The inferior pole of the goiters left lobe was not palpated because of its extension through the thoracic inlet. Chest X-ray showed that upper mediastinum was enlarged and the trachea right deviated. An ultrasound examination of the neck had revealed a multinodular goiter which the left lobe extends inside the thorax. CT scan of the chest (Figure ) demonstrated a large multinodular goiter which left lobe measuring 20 × 5,2 × 4,4 cm, it enlisted in the anterior mediastinum laminating the trachea and displacing it to the right. Its lower pole down into the middle mediastinum and arrives below the carina. The diagnosis of substernal goiter was made, and the patient consented for total thyroidectomy through Transcervical approach, and if necessary transthoracic approach. At first, a thyroidectomy was performed via standard neck approach. The presumed intrathoracic part of the goiter was easily extracted after ligation-section of the inferior left pedicle. After excision of the goiter we found that the left lobe was well encapsulated and measured 12 cm in length, this remark was inconsistent with CT findings. The digital exploration followed by axial mediastinoscopy of the anterior mediastinum noted the presence of a residual mediastinal mass. Total median sternotomy was then performed. Intraoperative findings revealed that the mass was totally separated from the cervical goiter and its blood supply was independent from thyroid vessels. This mediastinal mass had macroscopic similarities with the cervical goiter (Figure ). It derived its blood entirely from thoracic vessels, especially from the ascending aorta. The patient had an uneventful postoperative recovery and was discharged from hospital after 6 days. He was put on daily thyroid substitution. The histopathological examination showed the same diagnosis of multinodular colloid goiter with no malignancy in the two specimens. Eighteen months after surgery, the patient was asymptomatic and disease free. |
The patient's clinical history started when she was 13 years old and presented with a generalized tonic–clonic seizure, which lead to a magnetic resonance imaging (MRI) of the brain with the subsequent diagnosis of multiple intracerebral CVs: a left frontal intraparenchymal one (35 mm in diameter) and a left posterior temporal one, both within the parenchyma (23 mm in diameter), and an intraventricular one (30 mm in diameter). Despite the best medical treatment, the epilepsy was not well controlled and the patient had up to three to four epileptic attacks per week. This case was discussed several times at our multidisciplinary meeting, as well as with the patients and the parents. The final decision was to remove the largest and the apparently symptomatic CV, and this decision was guided by a video-EEG (electroencephalogram). The left frontal CV was removed at the age of 14 years, with epilepsy symptoms being temporarily improved. Unfortunately, after 10 months, she started to complain of epilepsy again, with a clinical absence type behavior, pointed for temporal lobe origin type of seizures. Thus, a few months later, the left posterior temporal lesion was removed as well. The second operation gave very good medical results in terms of seizures control. The episodes dropped to one or two focal seizures per year. The third lesion, the intraventricular one, was followed up with a yearly MRI scan. At the age of 21, because the lesion had increased in size (∼8 mm) and because of the patient's desire, we decide to remove it using a transcranial interhemispheric approach. The operation was uncomplicated, and the patient was discharged home a week after the procedure. At that stage, no other lesions were present, and in the following 10 years, the follow-up MRI scans did not show any recurrence or new CVs. When she was 32 years old, on the yearly follow-up scan, a newly developed lesion was identified. This lesion, suspicious for CV, was small (6 mm) and located within the septum pellucidum. Because of its small size, the location, and the absence of symptoms, a conservative treatment option was followed. Unfortunately, the lesion doubled in size in the following 18 months and therefore the patient was very adamant about having it removed (\n). We were a bit reluctant because the patient was completely asymptomatic and had not had any epileptic attack for 10 years. Upon neurologic examination, she presented no issues. Finally, we took the decision to remove the lesion and we started to discuss how to approach it. We were wondering whether to use the same interhemispheric approach with the possibility of encountering scar tissue or if it was better to use a new surgical route such as a transcortical one. Finally, we decided to use something completely different and we opted for a transcortical endoscopic approach.\nWith the patient in the supine position through a single burr hole, placed slightly more laterally in relation to Kocher point, a purely endoscopic approach was performed and the lesion was completely removed (\n). A rigid endoscope was used and guided by the neuronavigation. Upon inspection, the lesion (\n) presented with two veins attached to it (one rostral and the other caudal). The removal began with the coagulation and dissection of the septum pellucidum superior to the CV location. After accurate coagulation and section of the caudal vein, using endoscopic forceps allowed the creation of a “pedunculated” CV. The insertion of an endoscopic rongeur in the space between the peel-away cannula and the endoscope allowed keeping the CV in place, avoiding its fluctuation in the ventricles. This maneuver allowed the exposition and easy dissection of the rostral vein, which, eventually, was coagulated and cut. The CV was then freed from the surrounding tissue and finally removed. An external ventricular drainage was precautionary left in the right ventricle just for 24 hours.\nThe histological examination revealed multiple dilated and congested vascular spaces lined by the endothelium, confirming the diagnosis of a CV.\nThe postoperative course was uneventful, and the patient was discharged home 2 days later. Serial follow-up MRI scans did not show any new or recurrent lesion at 5 years follow-up. |
Presenting complaints
A 66-year-old Caucasian male presented to the ED with memory loss, altered mental status, and agitation. He was brought to the ED by police after bystanders noticed him sitting in the car with his pets for two hours at a gas station. Initially, he did not recall that he had pets with him when he was picked up and claimed he was at a contest before arriving at the ED. Two days later, he was able to recall being in the car with his pets and claimed he was picked up by the police for leaving his animals unattended, but he had no recollection of how, when, and why he was at the gas station. The patient claims he lives with his wife, who died two days prior to presentation, and mother, who died a few years earlier. He says he just saw them leave the room while he was being seen in the hospital. He had no recollection of his wife’s death or the earlier phone call. The patient reports a remote history of hitting his head while playing soccer back in college, approximately 40 years ago, and was hospitalized for about a month. However, he could not remember whether he had any complications from the episode of head trauma.
He presents with selective remote and recent memory loss. He approximates answers to questions about the number of children he has, wives ever married in the past, and events that led to his present hospitalization. He cannot answer questions promptly. The patient drinks alcohol occasionally and has a history of occasional marijuana use during young adulthood. He smoked 1.5 packs/day of cigarettes for 17 years and stopped five years ago. Past medical history reveals a history of memory problems with an onset of 18 months ago. He states that his problem prevented him from being able to work the machines at his job, causing him to take a leave of absence. A few months before present |
A 32-year-old, previously healthy, African American man presented to an emergency department 45 minutes after the acute onset of left facial droop and right-sided weakness (Fig. ). A thorough history confirmed an episode 1-week prior, during which he developed sudden onset of dizziness associated with nausea and vomiting that resolved within hours. He denied any past medical or surgical history and was taking no medications. He has no family history of tumors. In the emergency room, his vital signs were within normal limits. His physical examination was significant for a left facial droop and right hemiparesis. Auscultation of his chest revealed a regular rate and rhythm with no appreciable murmur. No additional significant findings were noted. Stroke protocol was initiated. A chest X-ray was normal and an electrocardiogram showed normal sinus rhythm. A head computed tomography (CT) scan was negative for signs of intracranial hemorrhage. He was subsequently started on tissue plasminogen activator (tPA) therapy. Magnetic resonance imaging (MRI) of his brain demonstrated a right basal ganglia infarct and an old left cerebral infarct. A carotid ultrasound was negative. TTE demonstrated a 1 cm by 1 cm mass on the posterior leaflet of the mitral valve with a moderate mitral regurgitation In addition, TTE revealed a questionable mass on the left coronary cusp of the aortic valve. These findings were confirmed with TEE (Fig. ), which verified no sign of endocarditis and no atrial septal defect. A complete hypercoagulable workup was negative. Stroke protocol continued with the working diagnosis of cerebrovascular accident secondary to emboli from the mitral valve mass. Within 24 hours, he regained function of the right side of his body and had complete resolution of symptoms. He was diagnosed as having transient ischemic attack (TIA) and discussion was undertaken regarding surgical excision of his mitral valve mass.\nA median sternotomy was performed and cardiopulmonary bypass was employed via aortic and bicaval cannulation with full anticoagulation. His aorta was cross-clamped and his heart arrested with retrograde cardioplegia. The aortic valve was examined through an ascending aortotomy and all three valve leaflets appeared normal. A left atriotomy was made and the mass was easily identified on the posterior mitral valve leaflet adjacent to the mitral valve annulus (Fig. ). The mass was excised and a frozen section confirmed globular myxoma cells with abundant eosinophilic cytoplasm consistent with myxoma. The valve leaflet was reconstructed with an autologous pericardium patch and the annulus was supported using a running DeVega-type suture. The valve appeared normal and was tested; no regurgitation was noted. His left atrium and aorta were closed. His aorta was unclamped, after aggressive venting and de-airing maneuvers, and his heart returned to normal sinus rhythm with successful weaning from cardiopulmonary bypass. Anticoagulation was reversed with protamine and his chest was closed after placement of drains and pacing wires. At the conclusion of the operation, TEE confirmed appropriate mitral valve function and normal aortic valve with no evidence of a mass and no regurgitation at either location. |
A 44-year-old male initially presented with pain in his lower extremity. He visited a nearby hospital that referred him to our institute where a working diagnosis of a bone tumor was made. The plain radiograph shows an osseous lesion on the left posterior pelvis. Computed tomography (CT) depicted an osseous lesion arising from the left sacral ala. The osseous lesion was covered by a layer with intermediate signal intensity on the T1 weighted image and high signal intensity on the T2 weighted image from magnetic resonance imaging. The diagnosis from the image was an osteochondroma, which was covered by a cartilaginous cap. The maximum size of the tumor was ~6 cm and the thickness of the cartilaginous cap was <2 cm (). The histology of the needle biopsy of the cartilaginous cap showed a proliferation of chondroid tissue without atypia, suggesting an osteochondroma.\nOn diagnosis of the osteochondroma, a resection was performed. With the patient in the lateral position, a skin incision was made along the iliac crest to the contralateral paravertebral muscle, with a distal convex shape at the sacrum. The distal multifidus muscle was detached from the lamina of the sacral and lumber vertebrae. The posterior ilium and vertebrae were exposed, and the tumor was resected. Following resection, a vertebral fusion between L5 and S1 was performed using pedicle screws (). No complications associated with the operation appeared. The pathological diagnosis of the resected material was osteochondroma. The patient was able to walk without a crutch though dull back pain existed 6 months after the surgery with the degree of the pain getting worse. Image analysis 11 months after the initial operation revealed new cartilaginous nodules. The distal multifidus muscle on the tumor side was still thin, but the distal multifidus muscle on the non-tumor side was morphologically almost normal ().\nA needle biopsy of the new tissue revealed no atypical cartilaginous tissue. However, taking into consideration the clinical course, chondrosarcoma was diagnosed. Surgery was performed with almost the same incision, but the incision was extended to the distal sacrum (). The multifidus muscle was removed from the distal sacrum in the same way as in the primary operation (). The tumor compressed the L5 nerve root and was resected in several blocks. The pathological diagnosis of the resected material was a chondrosarcoma arising from the osteochondroma (). The pain was relieved postoperatively. |
A 31-year-old female, 2 weeks postpartum, presented with complaint of chest pain for 3 days. On admission, she was found to have ST segment elevation in leads I and aVL on the electrocardiogram (EKG). The patient was taken to cardiac catheterization laboratory for intervention. Coronary angiography showed spontaneous dissection of the left anterior coronary artery (LAD), and a drug-eluding stent was placed from mid to distal LAD (). During the procedure, she had 3 episodes of ventricular tachycardia requiring shock with return of spontaneous circulation. Postprocedure she complained of frontal and occipital headaches. Computed tomography (CT) angiogram of the head and neck showed long segment stenosis of the mid and distal right cervical internal carotid artery (ICA) consistent with dissection. Mild luminal irregularities of the mid to distal left cervical internal carotid artery suggesting 50% stenosis were noted (). Since the patient did not complaint of neurologic deficits, no carotid interventions were performed. Given the involvement of multiple vessels, fibromuscular dysplasia (FMD) was suspected and a duplex ultrasound of the renal artery was done, which showed borderline mid right and mid left renal artery peak systolic velocity to aortic velocity ratio, which confirmed the diagnosis of FMD. The patient was sent home on aspirin and ticagrelor with plan to follow-up as an outpatient.\nThe patient returned within 48 hours with complaints of chest pain and worsening headaches. EKG showed ST elevation in leads I, aVL, and V2-V4. Coronary angiography showed dissection of left main artery and left circumflex ( and ), which were difficult to stent. The patient eventually underwent coronary artery bypass surgery (CABG). A repeat CT angiogram of the head and neck showed new diffuse narrowing of the left cervical ICA consistent with a dissection and a pseudoaneurysm. A new pseudoaneurysm was noted in the right cervical ICA and the right vertebral artery ( and ). No neurologic deficits were present during readmission and intervention was deferred. Unfortunately, the patient developed an apical thrombus in the left ventricle and warfarin was initiated along with aspirin prior to hospital discharge. |
A 14-year-old boy with morbid obesity and no known prior psychiatric history underwent sleeve gastrectomy. Prior to the surgery, he weighed 167 kilograms with a body mass index (BMI) of 54.5. Within a few months postoperatively, he weighed 70 kilograms with a BMI of 22.8. The patient’s substance use disorder started at the age of 15, one year after the bariatric surgery. Of note, the patient's parents were separated and he lived with his mother and siblings. None of his family members or relatives had a history of substance use disorder. He initially started using fenethylline (marketed under the brand name Captagon), as it was a common substance used by his peers at school. He started with two tablets daily and increased his use gradually up to 15 tablets daily. He started smoking cannabis a year later, at the age of 16, starting with one cigarette per day and increasing his use gradually until reaching a peak of 20 cigarettes per day. The patient started drinking alcohol occasionally at the age of 16 as well, and it soon became an issue of excessive use on a daily basis. The patient drank different types of alcoholic beverages. He reported incidents of fainting in relation to alcohol use but had never experienced withdrawal. He mentioned that he started using alcohol as a way to reduce his use of other substances. Two years later, at the age of 18, the patient started using methamphetamine, which caused him to develop paranoid ideation, auditory hallucinations, severe insomnia, and aggressive behavior. The patient was admitted to an inpatient psychiatric unit for a few days and was started on haloperidol 3 mg orally twice daily, benztropine 2 mg orally twice daily, and quetiapine 50 mg orally as needed for insomnia. His psychotic disorder improved with the cessation of substance use and the treatments initiated on the inpatient side. After his discharge, he unfortunately relapsed and continued to use the aforementioned substances.\nAfter arranging for close follow-up, the patient voluntarily presented to the rehabilitation center, motivated to stop using all substances, as he was legally and financially burdened by this disorder. He was incarcerated twice for substance use-related criminal charges. He was also motivated to start a new life and to enroll again in higher education, as he dropped out of school previously due to his polysubstance use disorder. The patient has thereafter been involved in a rehabilitation and relapse prevention program, which included inpatient admissions as needed to the rehabilitation center, involvement in individual and group therapy, occupational therapy, and addiction counseling. |
A 45-year-old, right-hand-dominant, male desk worker presented to us with the chief complaint of inability to make a fist following an episode of injury when he was trying to get up from his chair and felt a popping sensation in his ring finger. At first, he ignored the pain and took some over the counter pain killers. After around 3 weeks of injury when the pain subsided, he noticed that he is not able to actively flex his ring finger completely. The medical history was not significant and there was no history of steroid use. On palpation, there was no tenderness along the ring finger, but there was swelling on the volar aspect around the middle phalanx. When asked to make a fist, his ring finger remained extended at the DIP joint (). However, passive flexion was possible at DIP joint and range of motion at proximal interphalangeal (PIP), and metacarpophalangeal joints were within the normal range. We ordered radiographs of the hand in AP and oblique views with special focus on the ring finger and found that a fractured fragment from the distal phalanx was lying there in front of the middle phalanx (). 2 days after his visit, he was posted for surgery. The volar incision was used and the ring finger FDP tendon was found attached to the bony fragment. After a careful freshening of the margins, the bony fragment along with the attached tendon was reduced anatomically, and fixation was achieved using two K-wires (, , , , , and ). The patient was kept in a finger splint till 2 weeks when sutures were removed, and the wires were taken out at 3 weeks, and he was allowed active extension and passive flexion of the DIP joint. Gradually, he was allowed to pinch and grasp when the strength improved at 6 weeks. He was followed regularly every month initially and thereafter at 3 monthly intervals to a total of 1 year. At present, he is able to make a complete fist and is able to do all his routine activities without any difficulty (, , and ). |
A 42-year-old female presented with the general medical history of SLE for approximately 16 years, who was on steroid-type drugs for her illness. Commonly, the differential diagnosis of SLE is systemic rheumatic diseases or the other rheumatologic disorders such as polymyalgia rheumatica. As a result of long-term use of steroid drugs, the patient who also had rheumatoid arthritis, experienced bone loss and had implanted the hip area []. In the first implant installation operation, the patient was paralyzed by 55cm on the right foot because of inadequate surgery, therefore the patient is routinely on physiotherapy with infrared light lamp. A family history of the same disease was observed, which means there are genetic factors that play a role. The patient was a workaholic woman, and always active in social activities and nongovernmental organizations.\nThe patient also had experienced discomfort in the area around the TMJ, the feeling of stiffness in the joints, and occasionally there was pain, but still did not let it interfere with her daily activities. An occlusal splint was made for this patient. The patient used an occlusal splint to overcome the disorder in the joint. The occlusal splint used was the one for stabilization, which was used for approximately 6 months.\nThe patient was asked for prior approval as a subject in this case report, and she had stated her approval. Then a written informed consent was taken from her and ethical approval for this study was obtained from the institute. She was photographed on the area around the right and left TMJ with infrared thermography camera, with the specification resolution of visible image 0.3 megapixels. Temperature measurement was carried out on the area around the joint, TMJ in front of tragus, the masseter on its insertion (the angle and the lateral lower surface of the mandible ramus), insertion of temporal muscle to the coronoid process above the zygomatic arch, glabella point as a point that has no temperature rise as it was expected [].[]\nPhoto capture was done at picture capture 30%. Seen the area temperature around the right joint was 34.6°C and left joint temperature at 34.1°C []. An identifiable image of the infrared that was visible appears at the right side TMJ. The temperature was more diffuse than in the left joint, also reaches the cheek area (masseter and temporalis muscle), when compared infrared image between the right and the left joint.\nIn another photo capture, from some captures taken, it was also found that the right TMJ was higher in average temperature than the left joint. When viewed in the visible infrared light, there was also a slight difference, seen in the left joint of heat that looks more spread in the area of the side head toward the back, whereas for the right TMJs, infrared image was more diffuse in the area of the side head and the front []. |
A 25-year-old male patient presented with complaints of pain and redness in the right eye for 1 month. He had taken a short course of oral steroids 15 days ago. He was better while on oral steroids but the symptoms reappeared on discontinuing them. He also gave a history of visualizing a white floater in front of the right eye since a week.\nOn examination, his visual acuity was 6/6 in both the eyes. Ocular examination of the right eye revealed a live, long, white coiled, and highly motile worm in the anterior chamber []. The conjunctiva was slightly congested but rest of the ocular examination was unremarkable. Systemic examination did not reveal any abnormality.\nPatient gave no history of fever, subcutaneous nodules, or any localized swelling in or around the eye. There was no history of travel to endemic areas.\nComplete blood picture and erythrocyte sedimentation rate were within normal limits with no evidence of eosinophilia. Peripheral blood smear was unremarkable, and no microfilariae were seen. Chest x-ray was also normal. Patient was immediately taken up for surgical removal of the worm from the anterior chamber as delay could have lead to posterior migration of the worm. However, in the operating room (OR) no worm could be visualized in the anterior chamber. Henceforth, we performed gonioscopy and a detailed fundus examination under mydriasis but the worm could still not be localized. The patient was then made to lie prone and after half an hour the worm reappeared in the anterior chamber. The pupil was constricted with pilocarpine to prevent the posterior migration of the worm and patient was again taken to the OR.\nA side port incision was made in the nasal quadrant. The worm began to migrate toward the incision with the egress of the aqueous. The intact live worm was recovered from the side port incision itself and preserved in water and sent for identification.\nOn examination, the specimen was found to be an immature female nematode measuring 10 mm, with a maximum width of 290 μm. The worm was rounded at both the ends. The worm had a thick cuticle with longitudinal ridges and circular annulations giving the external cuticle a beaded appearance []. Paired reproductive tubes were visualized at the lower cut end of the worm []. Based on the morphological characteristics, the worm was identified as female adult Dirofialria repens. The images were sent to the Parasitology Division, CDC Atlanta, where the diagnosis was confirmed. |
A 2-year-old malnourished girl presented to our outpatient department with erythematous scaly plaque over left upper arm. She also had bony swellings over nose, fingers, left foot, and back for the past 1 year. The child was highly irritable and pale looking and as per the parents, suffered from intermittent low-grade fever. History revealed that the girl was delivered as a healthy baby of an apparently healthy mother in a hospital setting. She was in perfect health at birth with a normal birth weight. BCG vaccine as a part of national immunization protocol was given to the baby at the age of 6 weeks. She received other vaccines on time. As reported by the parents the vaccination was followed by development of an erythematous papule over the arm, which ulcerated after 1 month. However, the ulcer never actually healed completely in spite of various topical medications. The ulcerated lesion kept increasing in size slowly for the next 3 to 4 months; finally, developing into a large plaque of size 5 cm × 8 cm []. The lesion was painless. At around 1 year of age however, the parents noted appearance of multiple bony swellings involving fingers, foot, root of nose, and vertebral column. [Figures –] The swelling over the fingers was painful and associated with ulceration and discharge. The skin overlying foot and back swelling was relatively normal, except for mild ichthyotic changes. Throughout this period, the plaque over the arm kept on increasing in size slowly.\nApart from the skin and bone changes, the child also suffered from low-grade intermittent fever and loss of appetite. However, there was no history of chronic cough, hemoptysis; neither there was any symptoms of gastrointestinal or central nervous system involvement. There was also no history of contact in the family or neighborhood. The child had been treated with oral and intravenous antibiotics on several occasions over the past year but the symptoms persisted.\nOn examination, the child was found to be malnourished. Her body weight was 8 kg, which was around 70% of the expected weight for a child her age. She was pale, irritable, and her body temperature was 98.7 F. The plaque over the left arm was 5 cm × 8 cm in size at the time. It was erythematous, indurated, and scaly with a raised and irregular border. There was central atrophy with areas of scarring and surrounding xerotic skin. At the root of the nose, a hard swelling was seen but with no surface changes. Tender bony swellings were also seen over left middle finger and right thumb with overlying scaly, erythematous plaque. A diffuse swelling could also be felt over dorsum of left foot, which was firm and tender. Similar such swelling was seen over the upper back in midline. No lymphadenopathy was noted however, with spleen and liver apparently normal, the child was otherwise normal.\nLaboratory investigations showed normocytic normochromic anemia (Hemoglobin- 8.3 gm%), raised white blood cell count and a raised ESR. Mantoux test was done and was positive (9 mm × 10 mm). X-ray of the bones revealed lytic lesions in the involved areas [Figures and ]. USG of whole abdomen and the chest X-ray were within normal limits. ELISA for HIV was negative.\nAt this moment, in consultations with her pediatrician we had two differential diagnoses: Langerhans cell histiocytosis (LCH) or disseminated tuberculosis following BCG vaccination.\nTo establish the diagnosis, a skin biopsy was taken from the plaque and histopathology was done. Under light microscopy, tuberculoid granulomas were seen with giant cells in the dermis []. Ziehl-Neelsen stain for acid-fast bacilli was negative, and so was Periodic acid–Schiff stain for fungus. We also did the special immune-stain for CD1a. However, the immune-stain came negative ruling out LCH.\nTo avoid delay in treatment, the child was admitted and started on a trial of standard antitubercular drugs, with a provisional diagnosis of disseminated BCG infection. In the meantime, a culture was done for Mycobacterium, but it came out to be negative with no growth seen after 8 weeks. However the child responded very well to the treatment. Furthermore, to further establish the diagnosis, a polymerase chain reaction (PCR) sample was sent. The PCR showed positivity for Mycobacterium tuberculosis complex (MTC) [].\nThe case was diagnosed as disseminated tuberculosis with multiple skin and bony involvement, initiated by BCG vaccination.\nThe child was kept admitted to the department of Pediatrics and her treatment on standard antitubercular drugs were continued. Improvement was noted in her general condition too, soon after start of the treatment. The fever subsided and appetite returned to normal gradually. Cutaneous lesions as well as bone swellings started to regress. After 6 months of treatment, lesions had resolved completely with only residual scarring and deformity for which she was referred to department of Orthopedics [Figures –]. |
The patient was a 30-year-old female, with a past history of a traffic accident, which resulted in tetraplegia and autonomic dysreflexia as sequelae of trauma to the neck region. Since the accident, the patient had experienced repeated attacks of severe renal colic and urinary tract infections. These attacks were associated with episodes of hypertension and headache.\nThe patient was admitted to the intensive care unit to receive epidural anaesthesia after new repeated severe attacks of abdominal pain. During observation at the intensive care unit, the electrocardiogram monitor showed an apparent narrow QRS tachycardia with a QRS frequency of 150 to 180/min. She received repeated metoprolol injections 2 to 5 mg which had a doubtful effect. A few hours later, the apparent tachycardia worsened and the QRS frequency increased to 200 to 300/min. Her blood pressure was normal. The arrhythmia was interpreted as rapid atrial fibrillation by the managing internal medicine team, who administered intravenous sotalol 40 + 20 + 20 mg, which had no apparent effect on the arrhythmia.\nThe 12-lead surface ECG showed irregular narrow QRS complex tachycardia (). Two rhythms with two different QRS complex morphologies were noted in the same ECG. The first rhythm was irregular and had a frequency of 250 to 300/min (the rapid rhythm). The second was regular with a frequency of 130/min (the slower rhythm). The patient was very anxious, panic-stricken, and quivering all over. Because the initial drug treatment was ineffective, and the arrhythmia was at times apparently regular, further evaluation of the case by esophageal ECG recording was performed and repeated adenosine injections were administered ().\nThe esophageal ECG recording was made under chaotic circumstances. The patient did not like having the electrode in her esophagus. The esophageal electrode was inserted deeply in the esophagus and then pulled back very slowly while recording the ECG, including the esophageal lead, at a paper speed of 50 mm/sec and an amplification of 10 mm/mV. Adenosine 5, 10, and 15 mg were administered via the jugular vein. It was not possible to conclude what the esophageal ECG showed at the moment of examination, and the adenosine had no effect on the rapid tachycardia. A decision was made to perform electrical cardioversion. For anesthetic induction, sodium pentothal was administered. Surprisingly, the "resistant arrhythmia" terminated abruptly during sodium pentothal administration, and the ECG showed regular sinus tachycardia thereafter ().\nUpon review of the esophageal ECG recording (), P waves were noted before every QRS complex of the slower rhythm; this P wave was unrelated to the rapid rhythm. After identification of P waves in the esophageal ECG recording, a closer review of the 12-lead surface ECG () also revealed P waves before every QRS complex of the slower rhythm. Injection of adenosine 10 mg intravenously via the jugular vein reduced the slower rhythm to about 45 to 50 beats/min, and adenosine 15 mg caused further slowing (total block) of the slower rhythm, with the maximum recorded R-R interval of 3.5 seconds (). Even the blocked P waves can be seen clearly in leads V2 to V6 in the same figure (asterisk) continuing through the rapid rhythm. No change in the rapid rhythm was seen during or after bolus adenosine administration. We concluded that the slower rhythm was, in fact, the regular cardiac (native) rhythm and the rapid rhythm, which did not respond to antiarrhythmic drugs but disappeared completely after sodium pentothal injection, was most probably an extracardiac artefact, mimicking atrial fibrillation.\nFortunately, the purported rapid "arrhythmia" relapsed about 30 minutes after terminating the sodium pentothal. Blood pressure monitoring showed a normal, regular tracing, with a frequency that corresponded to the slower rhythm of about 130/min. Once again, the patient was shaking all over. Palpation of the radial pulse and cardiac auscultation revealed a regular rhythm with a frequency corresponding to the blood pressure tracing and the slower rhythm on the ECG monitor. The body movements and the apparent rapid arrhythmia disappeared completely after administration of 5-mg intravenous diazepam. Thus the rapid "arrhythmia" was diagnosed as an ECG artefact due to tremulous, quivering body movements. |
The second case is a 75-year-old Irish woman with a psychiatric history of bipolar affective disorder, stable for several years on olanzapine and valproate, enabling her to lead an independent lifestyle. There was no history of cognitive impairment. She suffered from multiple medical conditions including: atrial fibrillation, type 2 diabetes mellitus, obstructive sleep apnea, and a recent mitral valve repair complicated by postoperative delirium.\nShe was admitted medically to a rural Irish hospital in November 2015 for management of a raised INR. During the admission she developed sudden onset left-sided weakness and altered levels of consciousness, as well as rigidity and one isolated temperature spike. The concern was raised that she may be or might have been suffering from neuroleptic malignant syndrome and her neuroleptics were stopped as a precaution (Table ). She was transferred to the intensive care unit (ICU) in the MMUH in Dublin with a suspicion of neuroleptic malignant syndrome or encephalopathy. Computed tomography (CT) brain imaging was normal at the time. As neuroleptic malignant syndrome was suspected, olanzapine was stopped. However, her creatinine kinase levels were normal as was her body temperature. Hence, neuroleptic malignant syndrome was deemed to be unlikely. An electroencephalogram during admission showed changes suspicious of encephalopathy and MRI imaging showed no acute abnormality. A working diagnosis of metabolic encephalopathy was established but extensive investigations yielded no cause for the encephalopathy.\nDue to prolonged altered levels of consciousness and unexplained altered mental state, the Liaison Psychiatry service was consulted in January 2016.\nOn examination, she responded with a mouthed single word greeting, but made no other attempt at verbal interactions. She inconsistently followed the examiner with her gaze, but stared out of the window for most of the examination. On physical examination she presented with waxy resistance to passive movement and psychomotor retardation. The impression was that these features were most likely related to a catatonic exacerbation of her bipolar affective disorder, in the absence of an organic explanation. She was diagnosed as having bipolar I disorder with catatonia as per DSM-5 (Table ).\nDelirium was raised as a differential diagnosis (Table ), but she had been reviewed in September 2015 by the Liaison service, when she was delirious after her valve replacement and her presentation was distinctly different on that occasion.\nShe was initially treated with intravenously administered lorazepam, but became drowsy, with a significant drop in Glasgow Coma Scale (GCS). As such the treatment was abandoned. Instead, olanzapine was cautiously reintroduced, which led to a significant improvement in her mental state within days. On follow-up review, she was mildly confused but engaged well at interview, and was euthymic with no evidence of thought disorder or movement disturbance. Subsequently she was discharged back to her own home. She was not reviewed at 6-month follow-up as she was living in a rural area and was followed up in her local service.\nOf note, in 2017, the same patient was readmitted to the MMUH ICU, from the same peripheral hospital, in a very similar state to the presentation in November 2015. Again her neuroleptics had been stopped when she was acutely unwell and she developed typical traits of acute catatonia. She was trialled on lorazepam, which she did not tolerate and reinstitution of her neuroleptics brought no improvement. The therapy was then escalated to electroconvulsive therapy (ECT), to which she had a dramatic response and significant improvement of her mental state. |
A 53-year-old man presented to the outpatient department with complaints of an intermittent headache and a right swollen ankle, which became worse after activity. His history included a craniocerebral trauma related to a fall during alcohol intoxication. In the first quarter of 2015, during the removal of cranial epidural hemorrhage, percutaneous catheterization of central veins via the right femoral vein was attempted because of the need for intravenous infusion. After the surgery, the patient was sent to the intensive care unit for postoperative care. A few days later, the patient was discharged home; he demonstrated a slight weak muscular tension in his right upper extremity and had difficulty in speaking extended sentences. Approximately 1 and a half months after the surgery, the patient was re-examined by CT. The CT scan showed that 1 guidewire had ascended in the superior vena cava and the heart. Despite this finding, the hospital was unable to perform the surgery to remove the guide wire, and the doctors suggested that he should have a follow-up visit in every few months. The patient ignored the guide wire, took no medication, and continued to lead a normal life. In January 2016, the patient received another CT scan which revealed that the guide wire had arrived at the cerebrum. However, the patient did not have any symptoms of discomfort. The doctors suggested that the patient should go to a better hospital for further treatment.\nAt this point, the patient presented with swollen ankle and headaches, and as a result, he wished to have the guidewire removed. The patient then underwent a comprehensive CT scan, which revealed that the guide wire had broken into 2 segments. One segment (with a diameter and length of 2.0 mm and 535 mm, respectively) had arrived at the right brachiocephalic vena cava, and the other segment (with a diameter and length of 1.2 mm and 323 mm, respectively) had arrived at the cerebrum (Figs. and ). Both the diameter and the length are measured by CT (General Electric Company) and its post-processing platform. The CT scan demonstrated that the core wire had punctured the vascular wall of the aortic arch between the left common carotid artery and the left subclavian artery to reach the cerebrum (Figs. –). There was no obvious thrombus on the ultrasonography. The vascular surgeons, neurosurgeons, and radiologists determined that the risks of surgery to remove the guide wire were high; the patient refused surgery due to worry about the risks outline to him. He was advised to take anticoagulants, avoid strenuous exercise, return for a follow-up visit once every 3 months, and visit the emergency department if his headaches became more painful. The follow-up has for last 5 months by phone message, but the patient did not come to the outpatient department again. The patient has survived for almost 4 years with the guide wire present in his circulation. |
A 14-year-old female, studying in class 9, belonging to a nuclear family presented to the emergency department with a history of recurrent episodes of vomiting of 1 year duration, headache from 3 months and was admitted to medicine ward. Since relevant tests and investigations ruled out organic causes, she was referred to the department of psychiatry. The patient was apparently alright 1 year ago, she was bullied by her classmates on regular basis over her appearance. Over time, she started to feel sad and raised the concern to her mother but was not taken seriously. She started to have episodes of vomiting which was insidious in onset. It was not associated with nausea, frequency gradually progressive in nature. The vomiting episodes were immediately after consumption of food and water 2–3 times per day. The vomitus was nonbile stained, nonblood stained, consisting of recently ingested food particles, and not relieved on any medications. The vomiting also developed even after her eating her favorite dishes. No history of fever, pain abdomen, or loose stools. Previously, she had consulted multiple physicians, hospitalized twice previously, and relevant testes such as endoscopy done which showed low-grade gastroesophageal reflux disease but never showed significant improvement on any interventions. The patient also complained of headache which was insidious in onset. The patient also complained of headache which was insidious in onset, throbbing type and lasting for few hours. There were no aggravating or relieving factors. On detailed interview, the patient reported to be fine irrespective of her vomiting episodes although she had missed 1 year of her school and was losing weight. There was no personal distress to her. She considered herself to have been overweight and that her ideal weight is 30 kg. She also believed since she was dark skinned and if she lost weight her friends would stop making fun of her. She also reported that she used to throw away the food at times, before the onset of the vomiting to lose weight. The vomiting was never self-induced. No history of any psychiatric illness in the family. Patient's birth and development history is unremarkable. Academically, the patient was good in her studies. She had sound sleep and also had a good appetite. On general physical examination, she was found to be moderately built but poorly nourished. Systemic examination was within normal limits. Her body mass index (BMI) was 16.6 kg/m2, which is above the 3rd percentile and below the 15th percentile. She was managed successfully with Selective serotonin reuptake inhibitors, supportive psychotherapy, and psychoeducating the patient and the mother and is maintaining the improvement on follow-ups. |
Thirty seven years old male with no known chronic medical illness presented with history of four months left sided nasal blockage and discharge associated with left facial pain and two episodes of large amount of epistaxis from left nostril which stopped spontaneously. No history of ear symptoms, blurring of the vision and neck swelling noted.\nOn endoscopic examination, the left nasal cavity was occupied by the mass but did not extend to nasopharynx (Figure ). The mass was polypoidal and pinkish in appearance and bled minimally with touch and suction. Both fossa of Rosen Muller were clear. Moderate deviation of nasal septum to the right side noted but no mass seen in right nasal cavity.\nPunch biopsy from two different parts of the mass performed for histopathological examination and reported as inverted papilloma. Also CT scan done and reported as followings: heterogeneous soft tissue mass seen in left maxillary sinus and nasal cavity with no extension to nasopharynx (Figure ). Erosion of medial and posterolateral wall of left maxillary sinus noted. No intra cranial or orbital extension reported. Posterior extension to the left infratemporal space with intact pterygopalatine fossa was seen. The features were consistent with aggressive left maxillary soft tissue tumor such as inverted papilloma.\nOperation was decided and done as left open partial maxillectomy and complete excision of the tumor. After incision of the skin and raising the flap, osteotomy was performed as removal of frontal process of maxilla and medial wall of maxillary sinus. Then the lacrimal sac was exposed and distal end of lacrimal duct was cut. Intraoperatively, a big mass seen that occupied whole left nasal cavity and maxillary sinus. During the first step of resection of the tumor, bleeding occurred and was secured by packing for about half an hour. The tumor was removed from posterolateral wall of maxilla to the left infratemporal fossa and from posterior wall of maxilla until left pterygopalatine fossa. Inferiorly, the mass was resected from floor of the maxillary sinus and erosion of hard palate was noted. In addition, superior turbinate was removed and ethmoidectomy and sphenoidectomy conducted. There was no tumor seen inside the sphenoid sinus. The left frontal sinus was opened as well and clear antrum with polypoidal mucosa was noted.\nFinally, the bleeding secured. The amount of intraoperative blood loss was estimated as 700 ml. The cavity was packed by PIPP that was kept for one week duration. The patient was discharged 9 days after operation. Post-operative histopathology report was: co-existing of inverted papilloma and angiofibroma.\nCurrently, patient is asymptomatic with no sign of recurrence noted clinically (Figure ) and in post-operative CT scan. He is under regular three monthly follow up. |
A 45 years old female was admitted for nausea, vomiting and anorexia, and this had all started 6 months previously. For her past history, she was diagnosed with hypertension 10 years ago, she was diagnosed as having IgA nephropathy 5 years ago and she was taking beta-blocker, Cozaar and angiotensin converting enzyme inhibitors. There was no significant family history. The vital signs were normal at the time of admission. On the abdominal physical examination, a hard and mobile mass the size of a baby's fist was palpated in the upper abdomen and this was associated with pain. Any other special findings were not detected on the physical examination. The results of the general blood tests that included tumor markers were all normal.\nOn gastroduodenoscopy, the mucosa of the body of the stomach was not well spread, and the gastric folds were thicker and harder than normal, and so we suspected this to be Borrmann's type 4 stomach adenocarcinoma that showed hypertrophic gastric lesions, and then a biopsy was performed (). On the abdominal computed tomography, similarly, the layering of the stomach wall was lost and the pattern that the stomach was not well spread suggested linitis plastica corresponding to Borrmann's type 4 stomach adenocarcinoma ().\nOn gastroduodenoscopy and ultrasonography, the greater curvature of the stomach wall showed diffuse thickening, and the thickness was observed to be approximately 10 mm. Particularly, the 2nd layer was thickened and heterogeneous low echo contrast was primarily seen, and these findings corresponded to hypertrophic gastric disease or type 4 advanced stomach cancer. When performing a gastroduodenal barium enema, we observed that the entire stomach wall was thickened and the stomach space was narrowed. In addition, there was the loss of peristaltic movement.\nGastric cancer was suspected and so endoscopic biopsy performed, but cancer cells were not detected. Nonetheless, several imaging findings and the clinical symptoms strongly suggested stomach cancer. Thus, endoscopic mucosal resection of the stomach wall was performed for making the diagnosis (). After the mucosal resection of the hypertrophic lesions of the greater curvature and the anterior wall of the body, tissues were taken by biopsy forceps from the area determined to be the submucosal layer and histological tests were performed. Nevertheless, cancer cells were not detected on the histological tests, and only the thickening of epithelial cells was observed ().\nStomach cancer was strongly suspected and surgery was recommended. However, the patient refused to undergo surgery without a definite histological diagnosis. Ambulatory follow-ups were planned and the patient was discharged. During the follow-up observation, the clinical symptoms of the patient deteriorated, and surgery was again recommended. The patient agreed to undergo surgery and laparotomy was performed. During laparotomy, adhesion or ascites was not detected. In addition, there were no findings of metastasis to other organs within the abdominal cavity and the rectal shelf, and dissemination in the peritoneum was not observed. The stomach wall was thickened overall, and the local enlargement of lymph nodes in the vicinity of the stomach was observed, so total gastrectomy, extended lymphadenectomy and Roux-en-Y esophagojejunostomy were performed. The stomach disease was diagnosed as poorly differentiated type 4 advanced stomach cancer by the postsurgical pathohistological tests. The mucosa layer was thickened to 5~9 mm, and most of the cancer cells were found as a pattern that initiated from the submucosal layer and then it spread (). This was the diffuse type according to Lauren's classification. Tumor had penetrated and invaded the serous layer. Cancer cell metastasis was detected in 23 of the 35 resected lymph nodes and the final disease stage was determined to be stage IIIc (T4aN-3bMo) according to the AJCC TNM staging system (7th ed).\nAfter surgery, the patient was discharged without any special complications. Combination chemotherapy with TS-1 and cisplatin was initiated from 4 weeks after surgery. However, anorexia and severe bone marrow suppression developed during the 4th cycle, and so currently, the chemotherapy has been interrupted and the patient is under ambulatory follow-up observation. |
We report a case of a 57 year old male with metastatic melanoma who developed multiple severe immune related adverse effects attributed to pembrolizumab including arthritis, ocular hypotony and pulmonary fibrosis. Four years ago, he was diagnosed with cutaneous melanoma of the upper back measuring 4 mm in thickness associated with ulceration and two positive sentinel lymph nodes. The pathological staging was pT4bN2a. This was treated with wide local excision and regional lymph node clearance. The patient's medical history includes deep vein thrombosis and depression. He is a non-smoker. He did not receive adjuvant treatment and was monitored clinically.\nTwo years later, he developed metastatic recurrence with cutaneous nodules of melanoma and Positron Emission Tomography (PET) scan demonstrated fluorodeoxyglucose (FDG) avid intrathoracic and intraabdominal lymphadenopathy. Archival tissue analysis did not demonstrate mutations in BRAF gene. He was treated with pembrolizumab (200 mg IV every 3 weeks) and attained complete metabolic response on subsequent PET scans after 3 months of treatment. He continued to receive maintenance pembrolizumab for a total of 32 doses until cessation. After the first 3 months of treatment, he developed arthritis predominantly affecting the small joints of the hands bilaterally, which was associated with mild functional impairment. However, this responded well to low dose glucocorticoids (prednisolone 5 mg daily). The patient was also noted to have developed grade 1 asymptomatic pneumonitis findings on chest CT imaging after 12 months of treatment. These findings were not present at baseline and monitored on serial scans.\nAfter 20 months of treatment and 2 weeks after his last dose, the patient developed reduced vision in the right eye with visual acuity down to <20/200. This was preceded by a work-related blunt trauma injury to his right eye 1 week prior. He was referred to a tertiary eye hospital and exploratory surgery performed excluded a globe rupture. Ophthalmological examination revealed profound ocular hypotony (0 mmHg in right eye) with minimal inflammation. His left vision remained unaffected at this time. Multiple tests and ophthalmological procedures were performed to reverse the hypotony (these will be detailed in a separate ophthalmological report); however, the effect was minimal. Pembrolizumab was ceased thereafter.\nTwo weeks later, the vision in his left eye started to deteriorate to a visual acuity of only hand movements on the right and counting fingers on the left. Ophthalmological examination confirmed bilateral profound hypotony of 1 mmHg in both eyes, along with fundus changes consistent with hypotony but there was still minimal ocular inflammation. Repeat PET scan excluded recurrence of metastatic disease. He received high dose intravenous and oral steroids and further intraocular surgeries to re-pressurize the eyes, however the response was modest with minimal improvement in vision. It was found intraoperatively that the ciliary processes were pale and atrophic. Despite best efforts, the best attained visual acuity was hand movements in the right eye and 20/120 in the left eye.\nTen months after the cessation of pembrolizumab, the patient developed respiratory symptoms of dyspnoea on exertion, dry cough and progressively worsening exercise tolerance. This was on the background of low-grade inflammatory changes consistent with mild pneumonitis on his prior imaging. High resolution CT chest demonstrated volume loss, asymmetrical interstitial lung markings with honeycomb pattern greater on the left and in predominant subpleural distribution consistent with pulmonary fibrosis. Transthoracic echocardiogram demonstrated normal left ventricular function and moderate pulmonary hypertension (RVSP 47 mmHg). Pulmonary function test demonstrated moderately severe restrictive ventilatory defect and reduced diffusion capacity of lung for CO of 49% predicted. Six-minute walk test demonstrated exertional hypoxia corrected with supplemental oxygen. Bronchoscopy did not yield any infective pathogens. There were no laboratory findings suggestive of connective tissue disorders. A course of oral glucocorticoids provided limited effect. The antifibrotic agent, nintedanib was commenced but resulted in only moderate symptomatic improvement in respiratory symptoms and caused gastrointestinal toxicity with diarrhea despite dose reductions. At the time of this report, the patient remains in complete remission from melanoma, 18 months after treatment cessation. However, he remains severely affected by the adverse effects of severe visual impairment and progressive pulmonary fibrosis. |
A 6-year-old previously healthy Caucasian girl presented with history of pain and swelling in her left knee for 5 weeks. Her symptoms began while on holiday with her family in South Africa, when she fell while running. She developed pain and swelling of the left knee and was unable to weight bear. Her parents took her to the local emergency room, where she was found to have a swollen left knee, a small superficial abrasion over the knee, but no other external injuries. There was no radiological evidence of fracture. In the first few days following the fall, she had a low-grade fever and brief decrease in appetite. Management was conservative, with analgesics and a splint for 2 weeks. Her systemic symptoms resolved but the knee swelling and pain persisted.\nOn returning to Canada, three weeks after the fall, she was taken to our hospital's emergency room where repeat X-ray showed prepatellar soft tissue swelling and superior pole changes at the patella that could represent either a healing fracture or a normal variant. Rest and nonsteroidal antiinflammatory treatment were recommended.\nThere was slow improvement in the next few days but upon resuming physical activities the left knee pain and swelling worsened. She was seen in the orthopedic clinic at the BC Children's Hospital, where a large left knee effusion was found with no overlying redness; there was limited range of motion and mild quadriceps wasting. The complete blood count showed haemoglobin of 109 g/L, white blood count of 6.9 × 109/L, platelets of 528 × 109/L, ESR of 66 mm/hr, and CRP of 28 mg/L. Repeat X-ray showed marked soft tissue swelling anterior to the knee as well as within the knee joint and a possible healing fracture at the superior pole of the patella. Subsequent MRI of her left knee showed a large effusion, a radial tear of the medial meniscus, and a bipartite patella that was felt to be a normal variant with no evidence of fracture.\nShe was subsequently referred to the paediatric rheumatology team by the paediatric orthopaedic consultant, five weeks after her initial fall, for evaluation of suspected chronic arthritis. At that time, she had persistent left knee swelling and limp as well as pain with weight bearing. She was otherwise well and had remained afebrile. On examination, she was a cheerful and well-appearing child with a normal general physical examination. On musculoskeletal examination the sole abnormality was involving the left knee, which was warm and had a large effusion. There was a flexion deformity of 20 degrees and attempts at further extension were very painful. A differential diagnosis of early juvenile idiopathic arthritis versus chronic atypical septic arthritis was considered.\nA knee aspiration and synovial biopsy were done under radiological guidance. The synovial fluid showed 27,450 × 106/L white cells which were predominantly neutrophils. The biopsy showed evidence of acute and chronic inflammation with few Gram-positive bacteria on Gram stain. The acid-fast bacilli stain was negative. Cultures from the joint grew only Bacillus pumilus, as determined by mass spectrometry (BioTyper 3.1 software with the database update 5627, Bruker MicroFlex LT, Milton, ON) with a score of 2.281; no other species had high scores, including the closely related B. safensis. The B. pumilus was considered likely to be a contaminant. The patient was commenced on oral cephalexin for empirical coverage of common possible causes of septic arthritis after consulting with the Infectious Diseases team.\nHowever, joint swelling and pain worsened and laboratory testing showed a WCC of 9.1 × 109/L, an ESR of 35 mm/hr, and a CRP of 12 mg/L. A week after the initial aspiration, she underwent an arthroscopy which resulted in the release of a large amount of pus under pressure. A culture again grew B. pumilus identified by mass spectrometry, and a 16S rDNA sequence confirmed a Bacillus species, not cereus or anthracis. Susceptibility testing showed sensitivity to ciprofloxacin, vancomycin, septra, and imipenem.\nInfectious Diseases reconsultation was requested, and the team recommended treatment with intravenous vancomycin. The knee swelling and pain improved steadily while on antibiotic therapy with a rapid decrease of the CRP. The patient developed neutropenia after 2 weeks of treatment that was attributed to vancomycin, and therefore she was switched to oral ciprofloxacin for an additional 4-week course. Her neutropenia resolved and she continued to improve. At the time of last assessment, 5 months after the initial fall, she was fully functional and parents denied any restriction of activities. Her left knee had almost full range of motion with no tenderness or effusion. The ESR and CRP had normalized. |
A 71-year-old woman presented with ten-day history of general weakness and muscle pain. The patient was on Simvastatin 40 mg daily for approximately 10 years without any complaints of side effects, especially no muscle pain or muscle fatigue.\nIn the year 2000, the patient was diagnosed with ER positive and HER-2 negative breast cancer. The patient underwent a surgical resection followed by adjuvant local radiation therapy of the pectoral region. In 2012 the patient had local recurrence of the tumor and was treated with a total mastectomy, followed by adjuvant treatment with aromatase inhibitors, which acts by facilitating key steps in the production of estrogen []. In 2017 the patient developed thoracic back pain and Magnetic Resonance Imaging (MRI) of the spine revealed four bone metastases in thoracic and lumbar vertebrae. A whole body positron emission tomography (PET) excluded additional metastases. 1 month later the patient was prescribed Palbociclib 125 mg daily for 21 days and Fulvestrant 500 mg on day one and 14 receiving 1 cycle of treatment. Prior to initiation of the first cycle of Palbociclib, the patient was in good condition with no complaints of myalgia, normal gait function, full bladder control and the light back-pain was managed with paracetamol and tramadol.\nAfter 3 days of Palbociclib treatment the patient experienced onset of mild myalgia worsening over 7 days to pronounced muscle pain and severe proximal muscle weakness. After 10 days she could not raise her arms above shoulder level, she had difficulty getting up from a sitting position, and progressive impairment of walking that within 10 days resulted in complete loss of gait function and ability to stand upright without aid. Additionally, the patient experienced dark colored urine. There were no sensory complaints or sphincter dysfunction.\nNeurological examination showed weakness of neck flexors and mainly proximal muscle weakness in both upper and lower limbs; shoulder abduction medical research council (MRC) grade 3, elbow flexion / extension grade 4, and bilateral hip flexion MRC grade 2. There was no independent gait function, and the patient was confined to a wheelchair. The patient could stand when assisted but could not walk. Cranial nerve examination, sensory evaluation and reflexes were unremarkable. The patient was initially admitted at a local emergency department under suspicion of metastatic spinal cord compression, but MRI of the spine showed, beside the known vertebral metastases, no sign of cord compression or myelopathy. Six days later the patient was transferred to our neurology department at a tertiary center for the suspicion of myositis. Simvastatin, Palbociclib, and Fulvestrant were immediately discontinued. At that time the patient had received Palbociclib daily for 21 days.\nBlood samples showed increased creatine kinase (CK) 13,000 U/L on arrival at the neurology department increasing to above 22,000 U/L during day three to five reaching a plateau, and slowly decreasing to near normal on day 14. Plasma-myoglobin was elevated as well (10,400 μg/L) and decreased subsequently under treatment. Creatinine levels were low and glomerular filtration stayed within normal range throughout (Table ). A diagnostic panel for detection of myositis-specific and myositis-associated autoantibodies was not contributive (Table ).\nA muscle biopsy was obtained from the left vastus lateralis muscle. In hematoxylin and eosin (HE) stain the biopsy showed no signs of cell necrosis. No mononuclear cell infiltration verified in the macrophage and CD8+ stains, and no HLA-ABC positive fibers were found. There were no ragged-red fibers on trichrome staining and all fibers had normal cytochrome oxidase (COX) staining. There were no regenerated fibers in vimentin staining and biopsy showed type 2 atrophy (Fig. A).\nAn MRI of the lower extremities showed edema in multiple muscle groups (Fig. B). The right leg showed edema at the level of the adductor magnus, vastus intermedius, proximal vastus lateralis, distal vastus medialis and biceps femoris muscle. The left leg showed edema at the level of the vastus lateralis and biceps femoris. The MRI Short-TI Inversion Recovery (STIR) signal was abnormal at the left vastus lateralis indicating muscular necrosis (Fig. B).\nTo prevent kidney injury, the patient was hydrated with 4 l saline i.v., and a trial of intravenous immunoglobulin (IVIG) 0,4 g/kg over 5 days was initiated under suspicion of an autoimmune etiology for the muscle injury. This was initiated before autoantibody and muscle biopsy results were available.\nThe patient recovered gradually over 2 weeks. One month after hospitalization the patient had regained cane-assisted gait and was discharged to outpatient rehabilitation. Approximately one-year after hospitalization, the patient was seen at the neuromuscular outpatient clinic, showing no signs of neuro-muscular deficit.\nA blood sample was obtained after discharge, and genetic analyses revealed heterozygous presence of the common SNP rs4149056 in the SLCO1B1 gene. |
A 38-year-old Caucasian male with a history of severe alcohol and tobacco use disorder and no other prior psychiatric or medical history was admitted as a transfer from an outside hospital’s emergency department to our inpatient psychiatry unit after a suicide attempt by hanging while under the influence of alcohol. He had spent his day at a company party and then spent time with family before going to his garage to do mechanical work, as he regularly does. Throughout the day, he had consumed a significant amount of alcohol, which he suspects was about 18 beers, slightly more than his typical 10-15 beers daily, though he reported that drinking as much as 18 beers was not unusual for him. While working in his garage that night, he sent his significant other concerning text messages and she went to check on him. She found him cyanotic in the face while hanging with a rope around his neck. She likely saved his life as she removed the rope from his neck and called emergency medical services who brought him to our hospital. The patient reported being amnestic to these events and only being aware of them as his significant other had reported them to him.\nThroughout the patient’s hospitalization, he was pleasant and cooperative with care. A thorough psychiatric review of systems did not reveal any conditions, except for alcohol use disorder (severe) and tobacco use disorder (severe). He said that he has been using both substances for more than 20 years. Collateral information was obtained from the patient's fiancée, who said that he has been drinking daily for some time. He continually denied any ability to recall the suicide attempt and was distraught regarding the event, especially related to the thought of leaving his significant other and two children without their partner and father, respectively. In conversations, he did admit to increased stress at work due to a promotion many months before, which he attributed to an increase in the amount of alcohol he was drinking as well as increased stress due to having an infant daughter. He noted that the amount of alcohol he had consumed was greater than he typically had been drinking but that he had not previously had a “blackout” with this amount of alcohol. Another possibility considered was amnesia secondary to traumatic asphyxiation or head injury; however, the patient did not demonstrate any cognitive or functional deficits during his inpatient hospitalization nor any signs of this on physical examination. The patient's laboratory value for ethanol was 0.182, and his urine drug screen was negative. He denied any history of illicit and prescription drug abuse.\nDuring the course of evaluation, he noted that he had begun varenicline for cigarette cessation one week ago. He had twice previously used varenicline for the cessation of cigarettes in the past, but both of those times he had also quit alcohol simultaneously. He had relapsed on both occasions, and therefore this time he decided to try quitting only cigarettes with varenicline. In our review of varenicline’s literature, it was notable that what had occurred to our patient was similar to the warning on the prescriber’s information packet, namely unusual and/or aggressive behavior (in this case, toward the self) and amnesia related to the event.\nDuring his stay, the patient was started on the Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol, but consistently scored 0 during all assessments. He was started on disulfiram and nicotine replacement therapy while hospitalized, which were both well-tolerated. His hospitalization was otherwise uneventful, and he was discharged three days later. |
The patient's clinical history started when she was 13 years old and presented with a generalized tonic–clonic seizure, which lead to a magnetic resonance imaging (MRI) of the brain with the subsequent diagnosis of multiple intracerebral CVs: a left frontal intraparenchymal one (35 mm in diameter) and a left posterior temporal one, both within the parenchyma (23 mm in diameter), and an intraventricular one (30 mm in diameter). Despite the best medical treatment, the epilepsy was not well controlled and the patient had up to three to four epileptic attacks per week. This case was discussed several times at our multidisciplinary meeting, as well as with the patients and the parents. The final decision was to remove the largest and the apparently symptomatic CV, and this decision was guided by a video-EEG (electroencephalogram). The left frontal CV was removed at the age of 14 years, with epilepsy symptoms being temporarily improved. Unfortunately, after 10 months, she started to complain of epilepsy again, with a clinical absence type behavior, pointed for temporal lobe origin type of seizures. Thus, a few months later, the left posterior temporal lesion was removed as well. The second operation gave very good medical results in terms of seizures control. The episodes dropped to one or two focal seizures per year. The third lesion, the intraventricular one, was followed up with a yearly MRI scan. At the age of 21, because the lesion had increased in size (∼8 mm) and because of the patient's desire, we decide to remove it using a transcranial interhemispheric approach. The operation was uncomplicated, and the patient was discharged home a week after the procedure. At that stage, no other lesions were present, and in the following 10 years, the follow-up MRI scans did not show any recurrence or new CVs. When she was 32 years old, on the yearly follow-up scan, a newly developed lesion was identified. This lesion, suspicious for CV, was small (6 mm) and located within the septum pellucidum. Because of its small size, the location, and the absence of symptoms, a conservative treatment option was followed. Unfortunately, the lesion doubled in size in the following 18 months and therefore the patient was very adamant about having it removed (\n). We were a bit reluctant because the patient was completely asymptomatic and had not had any epileptic attack for 10 years. Upon neurologic examination, she presented no issues. Finally, we took the decision to remove the lesion and we started to discuss how to approach it. We were wondering whether to use the same interhemispheric approach with the possibility of encountering scar tissue or if it was better to use a new surgical route such as a transcortical one. Finally, we decided to use something completely different and we opted for a transcortical endoscopic approach.\nWith the patient in the supine position through a single burr hole, placed slightly more laterally in relation to Kocher point, a purely endoscopic approach was performed and the lesion was completely removed (\n). A rigid endoscope was used and guided by the neuronavigation. Upon inspection, the lesion (\n) presented with two veins attached to it (one rostral and the other caudal). The removal began with the coagulation and dissection of the septum pellucidum superior to the CV location. After accurate coagulation and section of the caudal vein, using endoscopic forceps allowed the creation of a “pedunculated” CV. The insertion of an endoscopic rongeur in the space between the peel-away cannula and the endoscope allowed keeping the CV in place, avoiding its fluctuation in the ventricles. This maneuver allowed the exposition and easy dissection of the rostral vein, which, eventually, was coagulated and cut. The CV was then freed from the surrounding tissue and finally removed. An external ventricular drainage was precautionary left in the right ventricle just for 24 hours.\nThe histological examination revealed multiple dilated and congested vascular spaces lined by the endothelium, confirming the diagnosis of a CV.\nThe postoperative course was uneventful, and the patient was discharged home 2 days later. Serial follow-up MRI scans did not show any new or recurrent lesion at 5 years follow-up. |
An 18 years old male was referred to the regional cardiac centre following admission to a peripheral hospital with exertional syncope during weight lifting exercises. He had no significant past medical history and he was not taking any regular medication. There was a history of sudden cardiac death in his family.\nThe patient's resting electrocardiogram had shown features consistent with left ventricular hypertrophy and repolarisation abnormalities ().\nHis full blood count, kidney function and inflammatory markers were all normal.\nEchocardiography was performed, and the findings were consistent with a HCM phenotype with interventricular septal hypertrophy in excess of 3cms. Stress testing demonstrated a good exercise capacity but an absolute absence of systolic blood pressure increase. In view of the patient's risk factors for SCD he was counselled with regards to the benefits of ICD therapy. Due to his young age and concerns about the potential for complications during long term endovascular device therapy a subcutaneous Cameron Health ® ICD (S-ICD) was advised and implanted under general anaesthesia.\nIn preparation for the implant the patient underwent assessment of his surface ECG QRS morphology as per Cameron Health's recommended protocol to guard against over sensing of T waves and under sensing. The patient was discharged home on beta blockade and the device set with a VF detection zone of 240bpm.\nThe patient was re-admitted to hospital one month following implantation, because of a conscious shock from the device. This had been associated with presyncope. The logged arrhythmia downloaded from the device demonstrated atrial flutter (). Device interrogation demonstrated three episodes of flutter in total, only one of which received inappropriate shock therapy. The conscious shock was attributed to the over sensing of flutter waves as short RR intervals.\nAn attempt was made to perform a flutter ablation during this admission, this was not successful because it was not possible to produce cavo-tricuspid isthmus bidirectional block. The device was re-programmed and the setting was changed a VF zone at >250 beats per minute. The patient was loaded with oral amiodarone in addition to the pre existing bisoprolol prescription.\nHe was re-admitted to hospital three months later following an S-ICD discharge; this occurred without any preceding symptoms. Interrogation of the device demonstrated four logged episodes in the VF zone, three of which were atrial flutter associated with over sensing of flutter waves, the fourth episodes demonstrated over sensing of both P waves and T waves whist in sinus rhythm () The device sensing configuration was changed from the primary vector to the secondary vector in an attempt to eliminate the over sensing in sinus rhythm that was felt to be positional.\nEchocardiography done a month before admission had shown HCM with massive bi-atrial enlargement and pulmonary hypertension (). On review of previous echocardiograms this had been present previously.\nThe patient was referred to the national HCM clinic and it was advised that the device should be changed for an endovascular device. It was decided not to attempt a further flutter ablation.\nThe patient was admitted for a fourth time following syncope and a subsequent conscious ICD shock. Device interrogation for logged events showed episodes of polymorphic VT () and atrial flutter. The polymorphic VT had been undetected and not treated. The shock had been delivered once again in response to over sensing of a flutter wave.\nDuring this admission S-ICD was explanted and implanted with conventional ICD. |
A 71-year-old female with a history of peripheral neuropathy of unknown etiology presented with a one-year history of intermittent pallor of both hands which was precipitated with cold objects. She fell from a chair onto her elbows and hands one year earlier, but no fractures or dislocations were sustained. There was no history of rest or claudication pain and no prior instrumentation of the vessels. She had no family history of autoimmune or hypercoagulable conditions and no history of smoking, alcohol, or illicit drug use.\nOn examination, her blood pressure was 120/60 mmHg on the right arm and 100/50 mmHg on the left, pulse 86 beats per minute, and respiratory rate 18 breaths per minute. Her radial pulses were reduced bilaterally. There were no sensory deficits in her bilateral upper extremities and no palmar atrophy. Other aspects of her clinical examination were unremarkable. There was no pallor or cyanosis of the palms of her hand at the encounter. However, prior photos taken showed marked pallor of the distal fingers of the palms of both hands (Figures and ). Laboratory investigations including autoimmune screen, ESR, CRP, and prothrombotic panels were unremarkable. HIV testing was negative. Echocardiography was normal with an ejection fraction of 65–70%. CT angiography showed a focal right brachial artery stenosis and a short segment 2 cm occlusion of left brachial artery with distal reconstitution by muscular collateral branches. She further underwent conventional angiography which showed tapered high grade stenosis of the proximal right brachial artery () and on the left a short focal tapered occlusion, with likely dissection of the left brachial artery reconstituted with collateral muscular branches ().\nTreatment was undertaken on the right with low pressure balloon angioplasty across the affected segment. After angioplasty there was modest improvement in luminal diameter with no extravasation of contrast and a 5 mm × 5 cm Viabahn covered stent was inserted and then postdilated with 4 mm mustang balloon. Repeat angiography showed excellent positioning of the stent and no residual stenosis. Runoff angiogram showed widely patent runoff arteries (). A stent was applied to the focal dissection on the left and a 5 mm mustang angioplasty balloon was advanced across the occluded segment and used for low pressure balloon angioplasty. The occluded segment was stented with 2 overlapping stents, 5 mm × 2.5 cm Viabahn stents. The stents were postdilated with a 5 mm mustang balloon. Poststent angiogram showed good poststenting positioning and no residual stenosis and unimpeded flow of contrast to the hand (). There was no evidence of embolic phenomenon. There were no postprocedural complications and dual antiplatelet therapy with aspirin and clopidogrel was commenced. Five months later the patient remained asymptomatic without further episodes of hand pallor. |
A 36-year-old man visited our department with a mass on his right cheek, measuring 1×1 cm lateral to the oral commissure. He had undergone surgical correction for right ZM complex fracture with bone defect at ZM buttress and right inferior orbital wall fracture due to road traffic accident 6 years prior. The bone defect was filled with β-TCP bioceramic powder (PolyBone, Kyungwon Medical Co. Ltd., Seoul, Korea). The mass had appeared 5 years prior along with signs of inflammation of the adjacent skin, such as redness and tenderness (). Initially, excisional biopsy through direct skin incision under local anesthesia was performed with a preliminary diagnosis of infected epidermal cyst. However, the mass was calcified and had a sinus tract (). The tract was not completely removed as it extended into the deep tissue. Biopsy results revealed chronic inflammation around the calcified fragments. Computed tomography (CT) with contrast enhancement revealed that the sinus tract was connected to the ZM bone defect site (). Bone formation was not seen at the defect site and remnant calcified granules were found above the defect.\nFurther surgical resection under general anesthesia was performed to remove the sinus tract and remnant granules completely. Intraoral approach with right upper buccogingival incision was used to reveal the fibrous sinus tract connecting the defect to the subcutaneous tissue. The tract was excised from the superficial fat tissue, and resected in an en bloc pattern with the help of a guide probe (). Dense adhesive tissue at the defect was also completely removed and curettage of the fine granules filling the ZM defect was performed with copious saline irrigation. The fine granules were connected to skin through the sinus and covered by a cystic wall, which isolated it from the adjacent bony structures. The Stensen's duct was intact. Histopathological examination revealed that it was a foreign body reaction with chronic inflammation of the sinus tract and that the tiny granule was degenerated bony spicules and calcification materials (). The surgical wound healed without any complication and no recurrence was noted. |
A 63 years old lady carried out a complex re-laparotomy for a postoperative small bowel occlusion after a radical cystectomy because of urothelial carcinoma. The procedure lasted 3 h because of thick adhesions that needed to be cleared. At the end of the procedure, total blood loss was 2 litres, and two Units of Packed Red Blood Cells (PRBC) were infused. During the surgical procedure, a central venous catheter was placed in the internal jugular vein by ultrasound-guided puncture of the vessel, but an inadvertent puncture and cannulation of the right subclavian artery occurred before catheter placement. Because of the ultrasound-guided procedure, the anesthesiologist thought to have cannulated the carotid artery and applied local pressure for a few minutes. Two hours later, when the patient was in the Intensive Care Unit (ICU) around midnight, a chest X-ray to check the correct position of the central venous catheter revealed a massive hemothorax (), while the patient was hypotensive and responder to crystalloids and blood infusions. A chest drain was inserted without any substantial output but a small amount of clotted blood. The patient rapidly worsened, despite appropriate resuscitation with 10 U of PRBC, 8 U of Fresh Frozen Plasma (FFP), 3 U of cryoprecipitate and 1 U of platelets from apheresis. A second chest X-Ray to check tube position revealed a tension hemothorax (). The team in charge of the patient, comprising the anesthesiologist that did the general anaesthesia for the surgical procedure, made the diagnosis of suspected subclavian artery perforation and tension hemothorax with both hypovolemic and obstructive shock. The team decided to bring the patient in the hybrid room to control the likely bleeding for the right subclavian artery. While the patient has been positioning on the angiographic table, the ECG monitor showed severe bradycardia, with a heart rate of 30 and an impending cardiac arrest with a systolic blood pressure of 30 mmHg. An emergency thoracotomy to decompress the right chest was then performed via a V space incision, and five litres of blood under pressure were drained from the right pleural space, with a rapid improvement in the vital signs. During the endovascular procedure, the general surgeon left the thoracotomy open to allow a continuing suction in the pleural space to prevent the accumulation of clots. The endovascular procedure was conducted by the vascular surgeons and lasted 40 min, confirming the massive leak from a significant defect in the subclavian artery () and consisted in a 7 x 37 mm covered stent placement in the subclavian artery at the origin of the vertebral artery. The stent was expanded with a balloon taking care of not injuring the already damaged vessel (). The patient had a transient improvement, but in the next few hours, a hemodynamic instability again occurred, even if responsive to blood infusion. A CT scan revealed a leakage from the stent, because of retrograde revascularization of the vertebral artery (). A new endovascular procedure, with more pronounced balloon dilatation of the stent, definitely controlled the bleeding. ) The patient slightly improved after an open surgical debridement of the pleural space from clots and blood, given the absence of an output from the two large drains that were in place. In the next few days, the patient went back to the ward and made a gradual full recovery with no neurological or vascular defects (). |
A 78-year-old male patient reported with a complaint of swelling on left side of the face () and difficulty in mouth opening since 4 months with associated paresthesia of the same region for the past 2 months.\nHe revealed productive cough and exertional dyspnoea for the past 4 years and was under steroid inhalers. Patient had habit of smoking 5-6 chuttas per day for the past 50 years. Clinical examination revealed diffuse swelling over left body and angle of the mandible. Skin over the swelling was smooth with no surface changes. On palpation it was firm in consistency and slightly tender. There was also a palpable lymph node in the left sub mandibular region which was 2 × 1.5 cm in size, hard in consistency, nontender, and not freely movable. Intraoral examination revealed decreased mouth opening with inter incisal distance of 24 mm, restricted jaw movements, and grade 2 mobility in relation to 36, 37, and 38. Considering history and clinical picture provisional diagnosis of malignant neoplasm involving left body and angle of mandible was considered. Differential diagnosis of metastatic jaw tumor, osteosarcoma, and chondrosarcoma was given. Panoramic and PA skull radiographs revealed radiolucency with irregular borders at the left body and ramus of the mandible till the condylar head ().\nTMJ tomography showed osseous destruction involving left condyle. Radiographically differential diagnosis of gorhams disease and metastatic jaw tumor were considered. Considering history of persistent cough chest radiograph was taken which revealed homogeneous opacity involving the entire mid- and lower zones of the left lung ().\nThe patient was referred to radiologist for CT chest and mandible. CT chest revealed 12 × 7 × 6 cm mixed dense lesion in left lung with bronchial stenosis and distal collapse (). Axial sectional study of CT mandible revealed osteolytic areas involving the left body extending from 46 region of mandible encroaching the entire ramus till the condylar head with adjacent soft tissue mass ().\nAs metastatic work up abdominal ultrasound scan was done which revealed no evident pathology. Later whole body scan was performed showing metastasis in the mandible and left submandibular lymph node. Hematological findings showed raised ESR. Serum calcium, phosphorus, alkaline, and acid phosphatase were done to rule out fibro osseous lesions which were under normal limits. Incisional biopsy was done from jaw tumor which revealed infiltrating epithelial islands with dysplastic features like cellular pleomorphism, nuclear hyperchromatism, increased nuclear cytoplasmic ratio, mitotic figures, keratin pearls, and dense inflammatory cell infiltrate suggestive of squamous cell carcinoma ().\nCytological smear from lung tumor showed few discrete atypical epithelial cells with eosinophilic cytoplasm and irregular hyperchromatic nuclei with evident keratinisation suggestive of squamous cell carcinoma (). FNAC was performed from left submandibular lymph node which revealed squamous dysplastic islands suggestive of squamous cell carcinoma ().\nConsidering clinicoradiographic features and histopathological findings final diagnosis of mandibular metastasis with primary squamous cell carcinoma of lung was given and patient was referred to oncologist for further evaluation. Sadly patient expired within 4 months after discovery of metastatic lesion in the mandible. Consent was taken from patient's son regarding publication. |
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