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A 27-year-old female patient reported to the department of periodontics with a chief complaint of tooth sensitivity and exposure of root surface in relation to lower front tooth.\nOn examination, her oral hygiene status was fair and in the lower right central incisor area, gingiva was red in color with Grade I bleeding on probing. Miller's class II gingival recession was seen [] in relation to 41 and attached gingiva was inadequate in relation to this tooth. Grade I mobility was also present and attachment loss was 6 mm in relation to 41 []. Probing depth was 2 mm. Many mucogingival problems such as recession, loss of attached gingival, and traumatic injuries are a result of vigorous brushing.[] In this female patient of 27 years, the reason was faulty tooth brushing.\nIOPA revealed crestal bone loss in relation to 41 in mesial aspect []\nRoutine hemogram revealed the parameters in their normal range.\nFull mouth scaling, root planing, and polishing in relation to 41 area was performed. Patient was motivated to improve her oral hygiene status, chlorhexidine mouth rinse 0.2% was advised after phase 1 therapy [].\nSurgical phase: Stage I: Gingival augmentation with free soft tissue graft\nSurgical procedures were performed three weeks following phase 1 therapy. After disinfecting with 0.12% chlorhexidine mouth rinse, local anesthesia was given to the recipient site and donor site (palatal site). The first part of surgery involved preparation of the recipient site apical to recession area. A horizontal incision along the mucogingival junction extending one tooth mesially and distally from affected area was placed using a no:15 bard parker blade []. A tin foil template of the recipient site was prepared and was placed over the recipient site to facilitate the placement of incision [Figures and ]. Free soft tissue graft was harvested from the palate [ and ] and was adapted to the recipient site []. Sutures were placed using 5-0 catgut and periodontal dressing was placed to protect the surgical site [Figures and ]. An acrylic stent was positioned at the donor site to protect the wound [] and necessary instructions were given to the patient. Mechanical plaque control was avoided in the surgical site and dressing was removed after 10 days. Significant increase in the width of attached gingiva was appreciated in about 4 weeks and around 1 mm reduction in the recession height was observed []. A recall check up was done after 3 months.\nSurgical phase II: Root coverage with lateral sliding flap\nAfter three months healing period, root planing was performed in relation to 41 area [. The surgical site was anesthetized. Preparation of the recipient site was carried out [ and ]. A partial thickness flap as wide as the defect was reflected [ and ]. vertical incision was continued horizontally [] and cut back incision was given to relieve the tissue tension []. The flap was moved laterally to cover the exposed root []. This flap was then secured with sutures (black braided silk size 3-0) and the site was protected by periodontal dressing [Figures and ]. Mechanical plaque control was avoided in surgical site for 10 days following surgery. Patient was advised the necessary instructions. Increase in the attached gingival width after the 1st surgical procedure [] in relation to 41 and the root coverage achieved around 4 mm after 2nd surgical phase [] could be appreciated. |
A case of a 10-year-old boy was referred to emergency department because of an abrupt onset of aggravating abdominal pain and vomiting. The boy was generally healthy except for that he was newly diagnosed with ADHD and started the use of methylphenidate (Ritalin) for the past three weeks at a dose of 30 mg daily. Physical examination on admission revealed that the boy looks suffering and afebrile and has diffuse tenderness of abdomen without rebound and no dyspnoea. Laboratory tests showed high level of serum amylase 5824 U/L (amylase normal value: 30–110 U/L), high level of lipase 1950 U/L (normal value: 10/140 U/L), high levels of liver enzymes, AST 1259 (normal range 5–43), ALT 769 (normal range 5–40), and normal levels of electrolytes, cholesterol, triglycerides, bilirubin. There was no metabolic acidosis. Ultrasound of abdomen () showed edematous and enlarged pancreas, big amount of free fluid in the abdomen (), thickened gallbladder wall up to 6 mm without intraluminal stones (), and no intrahepatic or extrahepatic biliary dilatation. There was no anamnestic familial history of pancreatitis.\nThe boy was admitted to intensive care unit with the diagnosis of acute pancreatitis and was started workup to investigate the etiology which revealed no alcohol use, transesophageal ultrasound (EUS) followed by magnetic resonance cholangiopancreatography (MRCP) () no biliary stone or any congenital or acquired malformation, and normal levels of immunoglobulins which excluded autoimmune pancreatitis. Other possible causes such as viral, bacteria, and parasites screening were all negative.\nThe boy was treated with intravenous rehydration and fasting with nasogastric tube. The boy improved slowly and discharged with the diagnosis of idiopathic pancreatitis from hospital after one week in good condition, free of symptoms, and with normalization of laboratory tests. Three weeks later, the boy was readmitted to the hospital again with more severe similar clinical scenario, received the same palliative treatment, and discharged after two weeks with good condition. After 5 days he was readmitted again to the hospital with the same clinical presentation of severe pancreatitis. This admission lasted for one week and on discharge the family reported on the use of Ritalin and therefore it was recommended to stop taking Ritalin.\nThe boy is now free of symptoms for one year and half after stopping taking Ritalin. |
A 39-year-old Hispanic Male with no past medical history presented to the emergency department with palpitations and a rapid heart rate. His symptomology was associated with lightheadedness and chest pain radiating to his left shoulder. He remained hemodynamically stable and coherent throughout his hospital course. The patient had experienced palpations for years, but previous evaluations demonstrated an inconclusive etiology. As part of initial management, the standard 12-lead electrocardiogram (ECG) was obtained which revealed sinus tachycardia with occasional premature ventricular complexes (Fig. ). A repeat ECG 2 h later showed a heart rate of 213 bpm and a right bundle branch block (RBBB) with left axis deviation, suggesting a phenomenon from the left ventricle (Fig. ). Echocardiogram showed mild tricuspid regurgitation, mild mitral regurgitation, and normal left ventricle systolic function with an ejection fraction of 60–65%, ruling out any significant structural defects (Fig. ).\nQuestion: What is the likely electrophysiology which contributed to the ECG findings and symptomology?\nRe-entrant circuit arising from the posterior fascicle and extending apically Decreased AV conduction associated with digoxin toxicity Ventricular tachycardia originating from the right ventricle Spontaneous transition from premature atrial complexes to atrial fibrillation\nAnswer: (A) Re-entrant circuit arising from posterior fascicle and extending apically.\nThe ECG findings suggest a morphology associated with an idiopathic QRS Belhassen tachycardia. Given this finding, this arrhythmia was likely due to an ectopic focus within the left ventricle causing a re-entrant tachycardia arising from the posterior fascicle and extending apically along the inferoposterior septum in an anterograde fashion, Choice A . As the cardiac conduction system generates subsequent electrical impulses, standard ventricular activation from the Purkinje fibers to the ventricles is no longer preserved as a consequence of the aforementioned ectopic focus. It is believed that this re-entry tachycardia stems from abnormal Purkinje fibers because of its dependence on the slow conduction of calcium in partial depolarization . This is significant because Purkinje fibers are targeted and guide therapy in acute management of Belhassen tachycardia through the use of verapamil. It is known that idiopathic ventricular tachycardias depend on slow entry calcium in partially depolarized Purkinje fibers, thus making verapamil the ideal first-line treatment. 12 mg of IV Adenosine was used initially, but the arrhythmia was refractory to such treatment allowing us to confirm our diagnosis of fascicular tachycardia. It should be emphasized that Belhassen tachycardia is refractory to beta blockers, adenosine, and vagal maneuvers because its pathway is not cAMP mediated, unlike other adenosine-sensitive ventricular tachycardias.\nTreatment involved chemical cardioversion with intravenous verapamil for the patient's incessant paroxysmal tachycardia. His heart rate of 213 beats per minute was concerning as this was not only an extremely rapid heart rate that contributed to his initial symptomology, but was also a very rare phenomenon in fascicular ventricular tachycardias. Catheter ablation was offered, but the patient opted for chronic long-term oral verapamil and follow-up in the clinic. This case highlights an atypical presentation of Belhassen ventricular tachycardia in which a heart rate greater than 200 bpm and a QRS that intermittently dropped below 120 msec were seen . |
A 33-year-old woman, gravida 3, para 3, non-obese and with no chronic diseases, underwent TLmRH as curative treatment for clinical stage IA1 cervical cancer. Two months later, she presented to our department with abdominal pain and genital bleeding after her first sexual intercourse after surgery from the previous day.\nWe sutured the vaginal cuff with absorbable sutures during initial surgery. We performed colpotomy with ultrasonic device and monopolar device in both cases.\nBoth patients were immediately diagnosed with VCD (Figure ). The prolapsed organ was found to be the intestine and it remained within the vagina without evisceration out of the vagina. The color of the intestine was normal, indicating that there was no ischemia present. After washing of the prolapsed intestine, we pushed back the prolapsed intestine, with sterilized gauze to prevent herniation outside of the vagina until operation. Vaginal approach repair (repair from the vaginal cavity), open approach repair, or laparoscopic approach repair were treatment choices. Suturing from the vagina could shorten vaginal length. To prevent recurrence, we thought it would be better to suture the peritoneum. We already resected the vagina about 2 cm in the initial surgery in both cases; thus, we would like to avoid further shortening. We thought that the open approach should be avoided considering its invasiveness if we could safely avoid this complication laparoscopically. Thus, we initially employed total laparoscopic repair.\nThe ureter was separated from the paravaginal tissue during initial cancer surgery, losing its normal anatomical position. This may cause ureteral damage during repair (Figure ). Thus, in order to avoid ureteral injury and to create a tight suture, the vaginal wall was separated by 1.0 cm, to the extent that concrete vaginal cuff suture could be made (Figure ), and suturing was complete (Figure ). The peritoneum was sutured to prevent recurrence, hematoma, and infection. The postoperative course was good. The cuff remained intact at 1-, 2-, 3- and 6-month examination. We suggested that sexual intercourse is safe 6 months after surgery.\nInterviews conducted on these cases after the 6-month examination revealed that normal sexual intercourse was performed without troubles in both cases. |
A 7-year-old boy from overseas was referred to us with corrosive stricture esophagus. The child had ingested corrosive 2 years back. This was followed by more than twenty attempts at esophageal dilatation in Pakistan and India at several centers. After each session of dilatation, he was able to take liquids for 4-6 weeks. In the last attempt at dilatation, he had developed a diverticulum with failure of even a guidewire to go through the stricture. Unfortunately, throughout these 2 years of endoscopic attempts, he had no significant nutritional support and was weighing (7 years, 14 kg) less than the third centile for his age.\nThe child was evaluated with a contrast swallow and esophagoscopy. The stricture was long with multiple pseudodiverticula. The thinnest guidewire (0.18 mm, Terumo) was not negotiable across the stricture. Since he had arrived in dehydrated emaciated state, he was kept on intravenous fluids for a week. This was followed by laparoscopic feeding gastrostomy, and he was nutritionally built up for the procedure for 1 week.\nA week later, he was taken up for laparoscopic transhiatal esophagectomy and esophageal substitution with stomach. After endotracheal intubation and general anesthesia, the child was placed at the foot end of the table in low lithotomy position. The camera port was placed at the umbilicus and pneumoperitoneum created at a pressure of 10 mmHg. Two working ports were placed on the right and the left iliac fossa in the midclavicular line at the level of the umbilicus. The procedure was started with mobilization of the gastrostomy and closure of the gastrostomy site by intracorporeal suturing. The gastrostomy site at the left hypochondrium was used for retraction of the liver to aid in transhiatal dissection. There were dense adhesions around the esophageal hiatus of the diaphragm. The diaphragmatic crura were divided and scarred, and fibrosed esophagus was dissected from mediastinal adhesions.\nThe retromediastinal dissection was challenging due to dense postcorrosive ingestion adhesions and loss of tissue planes. During the difficult dissection at the lower end of the esophagus, a small tear was inadvertently created in the left hemidiaphragm. The small rent in the diaphragm was closed with interrupted sutures. The lower two-third of the esophagus was mobilized by the transhiatal route. The cervical esophagus was exposed through the neck incision and the upper esophagus mobilized, and entire esophagus was delivered through the neck wound.\nThe stomach and duodenum were mobilized by the division of short gastric vessels with kocherization and ligation of the left gastric artery. The posterior mediastinal gastric transposition was completed with the esophagogastric anastomosis in the neck.\nThe child was ventilated for 48 h and contrast swallow was done on the 7th day which showed wide patent neck anastomosis, no leak, and prompt gastric emptying []. He was started on semisolid diet, which he began to tolerate without any symptom. Later in the evening, he started developing progressive respiratory distress. The child was placed on oxygen by mask and close monitoring. A chest X-ray on the same evening revealed a diaphragmatic hernia with hugely dilated colon [].\nIn view of the high risk of strangulation and gangrene of the herniated loop of large bowel, he was taken up for surgery immediately. Laparoscopy was done through the same port sites used for transhiatal esophagectomy and esophageal substitution. The hiatal access was difficult with omentum, small bowel and large bowel adhesions blocking the approach to the hiatal area. Gentle traction and separation of adhesion led to definition of the hiatus, demonstrating snugly fitting lower end of the stomach. In the parahiatal region, the central tendon had a small rent where the repair of the iatrogenic injury had given way allowing colon to migrate up. The hugely dilated and obstructed, congested transverse colon was reduced back into the abdomen. The diaphragmatic defect was repaired by intracorporeal interrupted mattress suturing. Postoperative period was unremarkable with quick recovery and he was discharged 2 days later. He remains well on follow-up 1-year after surgery having gained significant weight. |
A 62-year-old female patient was referred by her oncologist for a routine dental evaluation. The patient’s medical history revealed a cutaneous melanoma of the left dorsum diagnosed six years before she was referred to our dental service. The tumor was primarily treated by surgery and developed two local recurrences (one and three years following surgery, respectively), which were also managed by surgical resection. Disease progression was identified five years after the first treatment and confirmed by a computed tomography (CT), which revealed multiple organ involvement including the lungs, skin (subcutaneous nodules on the dorsum) and bone (osteolytic lesions in the iliac and femur bones, ribs, vertebrae, sternum and scapula).\nThe patient was undergoing a palliative treatment protocol based on dacarbazine, zoledronic acid and radiotherapy in the lumbar region (total dose of 20 Gy) and in the left supraclavicular fossa (total dose of 36 Gy) when she was referred to our dental facility. An extraoral clinical examination identified a pigmented subcutaneous nodule on the patient’s dorsum, measuring 5 cm in diameter, and scarring from the previous surgical resections.\nThe patient’s chief complaint was the loss of the dental crown of her upper left incisor. She denied oral pain or the existence of any relevant oral soft tissue lesion. Intraoral soft tissue examination revealed a nodule with an ulcerated surface and areas of telangiectasia, on the posterior left lateral border of the tongue, measuring approximately 1 cm in diameter, adjacent to a partial edentulous mandibular area (Fig. A). Based on the clinical features of the tongue lesion and on the patient’s medical background, the diagnostic hypothesis included metastatic melanoma, squamous cell carcinoma and fibrous hyperplasia.\nAn incisional biopsy was performed under local anesthesia. The histopathological analysis showed nests and solid sheets of non-pigmented atypical cells with an epithelioid phenotype infiltrating the sub-epithelial connective tissue. A high mitotic index was observed (Fig. B). Tumor cells displayed diffuse immustaining for S100 protein. Other melanocytic markers such as HMB-45 and Melan-A were negative. (Fig. C).\nAfter the diagnosis of a metastatic lesion on the tongue, the patient was referred back to the clinical oncologist who maintained her in a palliative protocol of chemotherapy with cisplatin, dacarbazine and vinblastine (CVD). Unfortunately, the patient died due to disease progression four and a half months after the diagnosis of tongue metastasis. |
Patient 1 was a 38 years-old male. In May 2010, this patient was diagnosed with glioma soon after an episode of seizures. MRI showed intra-axial expansive and infiltrative lesions that were cortical and subcortical, and which affected the anterior half of the right temporal lobe and extending from the pole to the Sylvian fissure superiorly and to the right parahippocampal gyrus, posteriorly, and medially. Partial surgical resection was performed in August 2010 and the first pathologic diagnosis was astrocytoma grade II. He underwent chemotherapy with TMZ at a dose of 2,000 mg with cycles every 28 days for 5 days in the years 2011–2013, with no tumor regrowth until the beginning of 2015. At this time, he underwent MRI, which was used to compare the discrete extension of the signal alteration areas, especially the subinsular regions. In March 2015, he resumed chemotherapy with TMZ at a dose of 100 mg/day and the patient then lost 12 kg of body weight, which was associated with anorexia, insomnia, and depression. In May 2015, he suffered a seizure requiring hospitalization. In June 2015, the patient resumed the old chemotherapy regimen with TMZ (2,000 mg every 28 days for 5 days), and a follow-up with MRI; however, the tumor size continued to increase. In January 2016, the neuro-oncology team decided to discontinue treatment with TMZ considering the risk/benefit and planned a surgical re-approach. This was followed by chemoradiation and lasting 6 cycles of PCV associated with CBD. The CBD dosage was ranging from 300 to 450 mg/day.\nDuring chemoradiation, the patient had an excellent clinical performance, practiced sports and had few symptoms of fatigue and/or nausea.\nAt 1 month after the end of chemoradiation, control MRI (Figure ) was characterized by exacerbation and the ultra-precocious phenomenon of PSD with increased edema and inflammatory disease characterized by extensive areas of contrast enhancement associated with tissue hypoperfusion (not shown). MRI controls demonstrated the progressive reduction of these findings.\nThe result of a pathological study after the first surgery was astrocytoma grade II with Ki67 staining of 5%. After the second surgery, he progressed to GBM grade IV (Figure ), related to increased cellularity, frequent mitosis, presence of micronecrosis, microvascular proliferation/endothelial, Ki67 staining of 30%, and loss of ATRX expression. Biomolecular marker analysis indicated IDH-1 mutated and MGMT methylated. |
A 50-year-old female reported to nephrology outpatient department with complaints of the right upper abdominal discomfort of 6 months duration. The pain was dull aching type with no radiation elsewhere. There was a history of intermittent hematuria with the abdominal discomfort. There was no history of colicky abdominal pain, lithuria, weight loss, anorexia, or jaundice in the past. She was postmenopausal with none significant medical or surgical history. She hailed from a remote village in central India and was sheep rearer by occupation. She consumed mixed diet and belonged to low socioeconomic strata. General examination revealed palor while on abdominal examination right kidney was palpable with bosselated surface and was nontender. There was no renal angle tenderness or hepatosplenomegaly.\nComplete hemogram showed anemia (hemoglobin - 6.5 g/dl) with normal leucocyte and platelet count. Her renal and liver function test was normal. An ultrasound examination of abdomen and pelvis showed a multiloculated cystic lesion of size 6 cm × 7 cm × 13 cm size with daughter cysts in the right kidney. Other viscera were found to be normal. The patient was hospitalized and transfused two units of blood. After adequate hydration, she was subjected to contrast-enhanced computed tomography of abdomen. It showed a well-defined multilocular peripherally enhancing cystic lesion with mixed internal attenuation and peripherally arranged daughter cysts and curvilinear calcification []. The cystic lesion replaced almost entire right kidney causing enlargement and architectural distortion measuring 5.5 cm × 7 cm × 13.5 cm with no contrast excretion. Rest of the examination was normal. Serology was not done due to nonavailability at our center. A final diagnosis of primary right renal hydatid cyst was arrived at.\nThe patient was started on tablet albendazole 10 mg/kg/day in two divided doses with fatty meal and hematinics. Urology consultation was sought, and the patient was explained about the need of right total nephrectomy in view of nonfunctioning right kidney. The patient was discharged and later admitted after 4 weeks of oral albendazole therapy. Extraperitoneal right nephrectomy was performed. Specimen showed a large thick walled cyst with numerous daughters’ cysts in the kidney []. Gross examination of the nephrectomy specimen showed chalky white external surface of kidney with distorted calyces. Multiple cystic cavities with attached cyst wall were noted. Multiple pearly white tissues contained gelatinous material suggestive of hydatid cysts.\nHistopathologic examination showed sclerosed glomeruli, thyroidization of tubules and thickened arterioles. There was marked chronic inflammatory infiltrate in the interstitium including eosinophils, lymphocytes, and giant cells. Cysts specimens showed scolices with hooklets and thus final diagnosis of hydatid cyst with chronic pyelonephritis was arrived. The patient was discharged on day 5 after an uneventful postoperative course. Oral albendazole was continued for another 4 weeks on discharge. The patient is on regular follow-up in outpatient department in health and normal renal function test. |
A 20-hour-old full-term male neonate presented to us with complaints of an externally visible, beating heart over the chest wall and difficulty in respiration. The neonate was delivered at home by a normal vaginal delivery and had a birth weight of 2.5 kg. He was the first issue of his 28-year-old mother. The antenatal history was unremarkable and there was no history of exposure to any unusual infection or drug. Antenatal ultrasonography had been done by a local practitioner but the deformity was not detected, probably due to lack of experience. There was no family history of any congenital abnormality. At the time of presentation, the neonate had peripheral cyanosis and there was history of difficulty in breathing and of vomiting since birth. The beating heart, covered with a serous membrane, was visible in the middle of the chest wall. The lower half of the sternum and the upper abdominal wall was deficient and was covered with a thin membrane. The umbilical cord was attached at the lower part of the abdominal wall defect near the epigastric region and the abdomen was scaphoid []. Other than this, no external deformity was found in any other part of the body. Chest movement on the left side was absent and no air entry could be made out on auscultation. X-ray of the chest revealed a left-sided diaphragmatic hernia with mediastinal shift. Echocardiography showed interventricular septal and pericardial defects. Blood gas analysis revealed severe respiratory acidosis and dyselectrolytemia. The neonate was resuscitated and put on mechanical ventilation (pressure-limited, time-cycled). Continuous nasogastric aspiration and broad spectrum antibiotics were started. Appropriate measures were taken to correct hypothermia and dehydration. We tried to correct the acidosis and electrolyte imbalance, but the neonate did not show any improvement either clinically or on blood gas analysis and expired before any surgical intervention could be undertaken. Autopsy was not done. |
A 34-year-old, non- smoker male was admitted, in September 2007, to the Department of Pulmonary Medicine, as a follow through case of border line lepromatous leprosy. He had complaints of breathlessness, loss of appetite with cough with expectoration for last two and half months and skin lesions over face, forearm and dorsum of hands with exfoliative skin lesions over fore arm for last two months and recurrent haemoptysis for last 25 days. He was on medication, tab. Dapsone 100 mg daily, tab. Clofazimine 500 mg daily and cap, Rifampicin 600 mg, once a month, for the last nine months. He had also taken oral Prednisolone for more than three months duration about six months back, for neurological complications. There was no past history of tuberculosis as per information provided by the patient. Clinical examination revealed multiple hypo pigmented skin lesions varying in size from 2 to 4 cms over the trunk with thickened left ulnar nerve and nodular lesions over face, forearm and dorsum of hands [Figure and ] and exfoliative skin lesions over fore arm []. His resting pulse rate was 102/min and blood pressure was 112/74 mmHg and his respiratory rate was 26/min. His general examination revealed no significant abnormality. His respiratory system examination revealed coarse crepts localized to left infraclavicular and axillary areas. Initially he was put on symptomatic treatment for hemoptysis. Subsequently, his chest X-ray showed a large cavity with a mass filled opacity confined to left upper zone and fibrotic changes in right upper zone []. Computed tomography of thorax revealed fibro-consolidation with cavitation in the anterior segment of left upper lobe, fibrotic nodule in both anterior and posterior segments of right the upper lobe []. Thus a possibility of aspergilloma with other possibilities was raised. The clinical examination of the rest of the system revealed no abnormality.\nHis blood biochemistry revealed total leucocyte count: 10,200/cmm, DLC: P 66 %, L 34 %. His PPD was 2219 mm induration. His sputum for AFB on three consecutive days was positive. Thus a diagnosis of pulmonary tuberculosis was confirmed. For leprosy, patient consulted the skin department, was diagnosed with borderline lepromatous leprosy (on the basis of slit skin smear) with type-II Lepra reaction (biopsy of nodular lesion revealed diffuse sheets of foamy macrophages centered around adenexal structures with heavy infiltration of lepra bacilli suggestive of Erythema Nodosum Leprosum). He was advised to stop Dapsone and started oral Prednisolone, Thaliodomide and Clofazimine.\nThus a final diagnosis of borderline leprosy with type-II lepra reaction with concomitant pulmonary tuberculosis was made. The patient was referred to DOTS clinic and started on category-I treatment. The oral prednisolone was subsequently tapered and stopped while the other antileprotic drugs continued. The patient's general condition improved and was on regular follow-up. |
Our patient was a 40-year-old right-handed woman with a previous history of recurrent deep vein thrombosis (DVT), reportedly related to oral contraceptive use and not managed medically. Otherwise, her past medical history was unremarkable for stroke risk factors. She awoke one morning complaining of dizziness and shortly thereafter began to act strangely, including missing a step while walking and getting into a low-impact collision while driving her son to work. She was alert and speaking clearly following this event, and her son suggested that she walk the short distance home. A couple of hours later, the patient was dysarthric and confused. She was subsequently found with evidence of trauma likely due to falls, including contusions on her feet, shin, and face for which she was not able to provide a history. Her initial Glasgow Coma Scale (GCS) was documented to be between 8 and 10 by Emergency Medical Services.\nUpon arrival at the ED, our patient’s GCS deteriorated to 6 (motor 4, eyes 1, verbal 1) and she was temporarily intubated. Neurological exam was significant for subtle anisocoria with right pupil dilation, but both pupils were equally reactive to light and there was no gaze deviation. Initial medical workup including lumbar puncture and electroencephalography was unremarkable. CT head without contrast showed no acute intracranial abnormalities. A repeat CT head with angiogram performed the same day were also unremarkable. Finally, a brain MRI with angiogram the following day demonstrated evidence of acute infarcts in the bilateral thalami and midbrain (Fig. ) with angiographic findings suggestive of occlusion of the right artery of Percheron (Fig. ). Unfortunately, our patient was past the time window for thrombolysis. She was managed conservatively and then admitted to a local rehabilitation centre for post-stroke rehabilitation once medically stable. Investigations for stroke etiology, including coagulopathy screen, ultrasound for DVT, and transthoracic echocardiogram with contrast bubble study for intracardiac shunting, were unremarkable. A thorough vasculitis workup was not performed given the lack of evidence of brain angiitis on imaging or clinical signs of a systemic rheumatologic disease.\nShe was ultimately transferred to an Acquired Brain Injury (ABI) Rehabilitation Program 59 days following her initial presentation. Her admitting neurological examination revealed slightly reduced left-sided strength in both her upper and lower extremity without other focal neurological deficits. Meanwhile, significant cognitive impairment was identified, specifically involving her memory and executive functioning. Regarding functional status, she was using a wheelchair regularly for safety and cognitive reasons but was physically able to perform transfers and climb stairs with supervision, she was alert but not oriented, she was occasionally incontinent of urine, and she displayed lack of judgement and some impulsiveness. A trial of neurostimulants (amantadine up to 100 mg BID and methylphenidate up to 15 mg BID) aimed at improving her cognition did not lead to any functional benefit.\nAs an inpatient on the ABI unit, our patient underwent several days of standardized neuropsychological assessment at four months following her initial event. A battery of tests was administered over several sessions, which assessed her intellectual functioning, processing speed, attention, working memory, visuospatial function, memory, and executive functioning. She was noted to have a profound memory deficit, with performance in the lowest percentile on nearly all tests of immediate recall, delayed recall, and recognition (i.e. she was unable to recall or recognize either verbal or visual information after delays of approximately 20 to 30 min). While she tended to perform in the low average to average range on tests of working memory, she could not encode these memories into long-term storage. Moreover, consistent with a severe anterograde and retrograde amnesic syndrome, she self-reported an inability to form any new episodic memories or recall any events which occurred before her stroke, including the inability to recall memories of her childhood. While she also performed poorly on tests of executive function, it was difficult to determine the true extent of these deficits as her ability to perform these tasks and learn from feedback may have been confounded with her memory deficits. Importantly, her relatively intact basic attention, working memory, and social skills made it extremely difficult for those around her to determine the extent of her memory impairments. At 1 year follow-up, the patient’s neuropsychological assessment showed mild improvement in her visual memory functioning, but her other memory scores remained weak and consistent with her previous assessment (Table ). Prior recommendations including 24-h supervision, repetition of information, provision of one-step instructions, and gradually increasing physical and mental activity were still being employed by her family with good tolerance of these strategies. |
A 43-year-old male patient was admitted with a complaint of moderate, gradually progressive headache and occasional episodes of vomiting that had been going on for 6 months. The patient’s history did not suggest any neurological cause. Powers in the right upper limb and lower limb were 4/5 and 3/5, respectively. No other neurological deficit other than this was found. The patient’s brain tomography showed lobulated contour image in the cerebrospinal fluid (CSF) density which formed a compression on the level of right lateral ventricular anterior horn of the left frontal region. The lesion had airfluid levels on the lateral ventricles and air particles on subarachnoid spaces. The rupture was evaluated in favor of cystic mass. The ventricular system had a dilated appearance ().\nPreoperative magnetic resonance imaging of the brain showed a lobulated, well-defined mass lesion in the anterior horn of the left lateral ventricle, which included hyperintense material hypointense on T1 () sequences and hypointense material hyperintense on T2 sequences (). The lesion had a size of 30 × 50 mm, it had a lobulated contour and it was hyperintense. The lesion compressed the left lateral ventricle anterior horn and minimal periventricular ooze with obstructive hydrocephalus was observed on FLAIR sequences (). The patient’s lesion was completely removed with left frontal craniotomy, duraplasty and tisselian tissue adhesive. The tumor was avascular and pearly white and it covered the left lateral ventricle anterior horn. Postoperative contrast negative computed tomography showed near-total excision of the lesion and resolution of hydrocephalus. The patient’s postoperative recovery was normal. Six months later, at his follow-up, the patient was found to have improvement in his hemiparesis as well.\nThe lesion was confirmed to be epidermoid as a result of histopathological examination. Parts of pearly white fragmented tissue were presented for formalin fixation and paraffin sectioning. The hematoxylin and eosin stained slide showed numerous anucleated squamous cells which did not show any presence of identifiable basal germinal cells. Skin adnexal tissues such as sebaceous glands, hair follicles or mucinous gland were observed. Overall features were consistent with epidermoid cyst. |
A 63-year-old man presented with hematuria and urinary obstruction symptoms. He came to the hospital four times each with presence of gross hematuria. Moreover, the patient suffered from frequency and nocturia at least for six months. Physical examination revealed enlargement of prostate, but there was no palpable nodule on the digital rectal examination. PSA was normal and there was also no evidence of hepatomegaly or splenomegaly.\nThe first transurethral resection of the prostate (TURP) and biopsy was done for him, but pathologic results showed the evidence of BPH. After 28 days, the patient was admitted again due to gross hematuria. Rectal examination was normal. Pelvic CT-scan revealed a big clot in bladder without any lymphadenopathy. There was a significant heterogeneity in prostate. In second TURP, clot evacuation and biopsy were performed on more than 15 different areas of prostate. During the next 2 weeks, the patient underwent 3 other trans-urethral coagulation and clot evacuations due to hematuria.\nHowever, laboratory tests such as prothrombin time (PT) , partial thromboplastin time (PTT), clotting time (CT), bleeding time (BT) and platelet count were normal. After 15 days hematuria was stopped and was not repeated. Sections from prostate show foci of hemorrhage, and ).\nThe first transfusion was 2 units of PC during the second surgery. The second transfusion was 2 units of PC and 2 FFP, two days later. The consecutive third and fourth transfusions were done two days later during which the patient received 3 units of FFP, and 3 units of whole blood.\nImmunohistochemistry studies demonstrate CD20-positive in 90% of lymphoid cells and in the lymphoepithelial lesions (), CD5-positive in background lymphocytes, CD43-positive in 90% of lymphoid cells, CD3-positive in background lymphocytes, CK and PSA markers are negative in neoplastic cells. Further evaluation and examination such as bone marrow biopsy, abdominal and pelvic CT-scan did not show other involvement.\nIn the last fallow up, around eight months after discharging, the patient was alive and asymptomatic. Moreover, there is no evidence of other organ involvement. |
Revision laparotomy due to septic condition one day after radical right hemicolectomy showed an extensive infarction of the small bowel in a fifty-one year old woman as seen in . She had mesenteric venous thrombosis involving the ileum and the jejunum probably due to compromised blood flow in the superior mesenteric vein. The proximal part of the jejunum of about 80 cm (segment I), was slightly congested but appeared to be vital. The other part of the smaller intestine up to the ileocolic anastomosis (segments II and III) was congested and viability was highly questionable. The colon (segment IV) looked normal. Aiming to avoid short bowel syndrome, we decided to use LDF and spectrometry to save as much bowel as possible (O2C device, LF-2 probe, LEA Medizintechnik GmbH, Germany).\nIn this unknown situation we used general threshold values recommended by the manufacturer (microvascular haemoglobin concentration <90 units, microvascular flow >10 units, microvascular haemoglobin oxygenation >10%). At the time of measurement positive end-expiratory pressure was 5 mmHg, the patient was eucapnic and without hypoxia, her mean arterial blood pressure was 80 mmHg, the haematocrit was 34 percent, 30 micrograms norepinephrine per minute was administered and she had received pantoprazole, metamizole, midazolam, fentanyl, propofol, atracurium, metronidazole, cefuroxime, and imipenem.\nStarting our measurements at the proximal part of the jejunum and proceeding stepwise towards the terminal ileum, we defined the cut margin just before the recommended threshold values were reached as seen in . The viable colon was used for reference measurement. Instead of 80 cm we could preserve 190 cm of small bowel. A split stoma was constructed to avoid primary anastomosis.\nAfter operation lactate ion levels decreased to normal values, the stoma remained vital and no further surgical intervention was required. No long-term parenteral nutrition was needed.\nThe histological examination showed the haemorrhagic ischemic necrosis reaching to the cut margin as near as 5 mm (). |
A 24-year-old primipara (height 138 cm, weight 42 kg, non-pregnant weight 37 kg) was scheduled for cesarean section at 37 weeks and 1 day due to cephalopelvic disproportion. A diagnosis of CCD was made at birth, although gene examination has not been performed. She underwent tonsillectomy under general anesthesia in middle school and dilatation and curettage under sedation with intravenous anesthesia 2 years ago. Both of these procedures were performed uneventfully. At prenatal checkups conducted at 28 weeks gestation, the fetus also had short limbs and cranial defects, suggesting both the patient and the fetus were suspected of having skeletal dysplasia. Preanesthetic examination demonstrated a hypoplastic right clavicle, patent fontanelles, dental malalignment, and a high palate. Because thoracoabdominal radiography and magnetic resonance imaging (MRI) revealed no abnormalities in the spinal cord or vertebra, spinal and continuous epidural anesthesia was planned for cesarean section and postoperative analgesia.\nAfter inserting an epidural catheter from the L1/2 intervertebral space, 1.5 mL of 0.5% hyperbaric bupivacaine was injected via the L3/4 intervertebral space for spinal anesthesia. Because the highest level of sensory blockade was the L1, 6 mL of 2% mepivacaine was administered from the epidural catheter, which extended analgesia to the T4 level bilaterally. Cesarean section was completed uneventfully, and a newborn weighing 2394 g with Apgar scores of 8 and 9 at 1 and 5 min, respectively, was delivered. The total amount of intraoperative blood loss, including amniotic fluid, was 2186 g. The operation and anesthesia lasted 59 and 83 min, respectively. The patient was discharged without any complications. The child was diagnosed with CCD based on their postnatal radiography and clinical findings.\nCCD is a systemic bone disease, which is characterized by delayed ossification of skeletal structures, hypoplastic clavicles, delayed closure of the fontanelles, delayed eruption of the second dentition, and a short stature. Its hereditary form is inherited in an autosomal dominant manner, and the causative gene is located on chromosome 6p21, which encodes runt-related transcription factor 2 (one of the transcription factors in the runt domain-containing gene family) [].\nPatients with CCD exhibit various features, including a high palate, dental malalignment, and micrognathia as well as spinal or vertebral abnormalities such as scoliosis or spondylosis. These anomalies make ventilation, intubation, and neuraxial anesthesia difficult. Imaging examinations should be performed before neuraxial anesthesia in patients with CCD [–]. We evaluated this patient using MRI before CSEA. Furthermore, we prepared the equipment required for the difficult airway management such as bronchofiberscope and supraglottic airway devices in case the CSEA had an insufficient effect and general anesthesia was required. Fiberoptic intubation in a patient with CCD was reported because direct laryngoscopy visualized only the posterior commissure []. Furthermore, thoracic hypoplasia due to the absence or underdevelopment of the clavicles or ribs can cause postoperative respiratory failure [, ]. As the present case did not have any abnormal findings in the spine, we could perform spinal-epidural anesthesia without any problems.\nIn pregnant women complicated with CCD, delayed ossification of the pubic bone causes symphysiolysis and a contracted pelvis, which often require cesarean section. The reported frequency of cesarean section in such women is 69% []. Although regional anesthesia is frequently selected for pregnant women with CCD, the anesthetic level of single-shot spinal anesthesia can be unpredictable due to their short stature and spinal abnormalities. In our case, single-shot spinal anesthesia failed to provide sufficient analgesia levels and epidural analgesia was required. Furthermore, if a newborn has CCD, careful monitoring of its airway and respiratory status are required immediately after delivery []. |
A 9-year-old female, right hand dominant, presented to our institution with a one-year history of left middle finger pain and palpable growing masses. The patient was first evaluated by her pediatrician. Plain radiographs were performed by her pediatrician and the report stated no significant findings. Her past medical history is significant for hypothyroidism which is being treated with levothyroxine. Magnetic resonance imaging (MRI) was performed to further evaluate the masses. The study demonstrated multiple hypodense masses and seven identifiable masses, on the volar aspect of the proximal, middle, and distal phalanx of the left middle finger (Figures and ).\nThree months after obtaining the MRI, the patient was seen in the clinic for evaluation by the orthopaedic hand service. Physical examination revealed mild swelling and tenderness throughout her left middle finger; however, no sensory deficits were noted, and brisk capillary refills were present. Three palpable small masses could be felt throughout the volar aspect of her finger. Bluish discoloration could be seen over some of these masses (). The range of motion of her finger was significantly limited due to pain and swelling: 0–10 degrees in proximal interphalangeal joint, 0–15 degrees in distal interphalangeal joint, and 0–30 degrees in metacarpophalangeal joint. There were no enlarged lymph nodes found on physical examination. The patient denied recent weight loss, fevers, chills, fatigue, or trauma. A decision was made to perform an excisional biopsy to identify the masses through histological examination.\nThe patient initially underwent excisional biopsy of two of the masses that were abutting each other. Definitive diagnosis was not obtainable from the initial frozen section. The third mass was located more proximal and a decision was made to not excise this lesion until a definitive diagnosis could be made. Tissue was submitted for further histological examination. Standard sections revealed a cellular process including giant cells and mononuclear stromal cells within a collagenous matrix (). Hemosiderin deposition and clusters of xanthomatous cells were also identified (Figures and ). These findings were consistent with GCTTS. Two months after the initial surgery, a decision was made to excise the remaining masses. Five additional lobular masses were identified intraoperatively and resected (Figures and ). Permanent sections from the remaining masses were consistent with GCTTS and histologically analogous to the previous biopsy.\nAt this time, the patient is two years from her second surgery. She denies any pain and has full range of motion of her left middle finger. Her incisions are well healed and no foci of recurrence are noted at this time (). |
A 20-year-old, left-handed man was playing rugby when he tackled another player, gripping his rugby shirt. Immediately he suffered pain on his left middle finger but was able to complete the remainder of the game. Afterwards his finger had swollen and he was unable to bend it fully. He presented to his local emergency department where the extent of the injury was not recognised; he was provided with neighbour strapping and given follow up in his local orthopaedic clinic for 1 week after the injury. On examination at orthopaedic follow up, he was unable to flex the distal interphalangeal joint (DIPJ) and had very weak flexion at the proximal interphalangeal joint (PIPJ). Passive movement was maintained at the DIPJ but he had a restricted passive range of motion at the PIPJ. An initial diagnosis of a closed rupture of the FDP tendon was made and the patient referred to a hand specialist who counselled the patient for exploration and tendon repair or reconstruction.\nSurgical exploration was performed on day 14 after his injury and under anaesthesia tenodesis revealed no flexion at the PIPJ or DIPJ. Initially, a Brunner’s incision was performed opening the A5 pulley where a rupture of the FDP tendon was identified. It was not possible to milk the retracted FDP tendon so the initial incision had to be extended proximally to the A1 pulley and the FDP was identified and delivered. However, a continued restricted movement at the PIPJ led to opening of the A3 pulley where a complete rupture of the FDS tendon was revealed (). The FDS tendon was not repaired as it was found to be swollen and the vinculae damaged; instead, the FDS was trimmed to facilitate repair of the FDP. The FDP tendon was threaded back through the residual pulleys and finally secured to the distal phalanx using a dorsal pull through technique.\nThe patient was splinted in the Edinburgh position and was commenced on an active range of motion protected with a dorsal splint. Unprotected movement of the finger was allowed from 8 weeks. He was reviewed in the outpatient clinic at 4 months where he had full movement at the PIPJ and an arc of 20° to 70° of flexion at the DIPJ (). The patient reported Disabilities of the Arm, Shoulder and Hand score of 0 and he had successfully returned to work and sport. |
We examined a 30-year-old male with a sudden, painless visual loss in his right eye that lasted for 3 h. Nine years ago, he had been treated with scatter laser photocoagulation for an ischemic type of upper branch retinal vein occlusion (BRVO) in the left eye. At that time, he was diagnosed with homocysteinemia with the homozygous C677T mutation in the methylenetetrahydrofolate reductase gene. After a detailed systemic workup, he was put on warfarin sodium. On examination, his best-corrected visual acuity (BCVA) was hand motions in the right eye and 20/30 in the left eye. A slit-lamp examination was unremarkable in each eye. The intraocular pressure was 15 mm Hg in both eyes. Dilated fundoscopy revealed tortuous and dilated retinal veins with 360° scattered retinal hemorrhages as well as a clearly demarcated pale retina in the distribution of the upper temporal artery in the right eye and scattered laser spots with macular retinal pigment epithelium changes in the left eye (fig. ). Our fundus autofluorescent image clearly depicted the extent of the infarcted area (fig. ), and fluorescein angiography demonstrated that the peripheral retina was well perfused in the right eye (fig. ). Optic coherence tomography (OCT) showed the presence of subretinal fluid and the ganglion cell layer infarct in the right eye (fig. ). The diagnosis was simultaneous CRVO and upper BRAO in the right eye. After a prompt digital ocular massage and a 20% mannitol infusion, an anterior chamber paracentesis was immediately performed. However, no visual improvement was noted following the procedure. Two weeks later, a dexamethasone intravitreal implant (Ozurdex, Allergan Inc., Irvine, Calif., USA) was injected into the right vitreous cavity to at least alleviate the CRVO-related concomitant macular edema, as the patient still had a visual acuity of hand motions in the right eye. Visual acuity gradually improved in the following weeks with a remarkable decrease in the central macular thickness, and no postoperative injection-related complication was observed. Six months after the operation, the retinal anatomy appeared to be dramatically improving (fig. ), and his BCVA was found to be 20/25. His visual field defect contracted with time in the right eye (fig. ). |
The patient, a 54-year-old man, was admitted to the hospital because of "a space-occupying lesion in the right kidney for 2 d upon ultrasound examination".\nHis past history was unremarkable.\nHis family history was unremarkable.\nHis physical examination on admission was unremarkable.\nThe results of a hemogram, blood biochemistry, and tumor markers were in the normal range.\nComputed tomography (CT) showed the mass as a soft tissue density shadow with a diameter of approximately 6.8 cm in the right renal pelvic area. The density was not uniform, and the boundary was not clear. It extended into the renal sinus and showed uneven enhancement (Figure ), which manifested as partial deformation, a disappearance of the pelvis and calyces of the lower pole of the right kidney, and delayed enhancement of the left right renal parenchyma. No enlarged lymph nodes were observed behind the peritoneum. Ultrasound images showed a cystic solid mass of approximately 6.8 cm × 6.5 cm that was visible in the right kidney, which had an unclear boundary and irregular shape. Color Doppler flow imaging (CDFI) revealed dotted blood flow signals in the periphery and interior. CEUS revealed that, after the mass injection of the contrast agent, the right renal cortex began to enhance at 9 s, the renal mass began to enhance at 11 s, and the mass began to peak at 28 s. The mass subsided more rapidly than the renal cortex, and the right renal mass showed "slow in and fast out" hyperenhancement (Figure ). The cystic solid masses were in the renal medulla, pelvis, and calyces, and they had a size of 6.8 cm × 5.5 cm × 5.5 cm. The abundant tumor cells were of spindle cell type, and a small number of tubules were observed among spindle cells through pathological examination. No tumor cells were found at the ureteral resection margin. Immunohistochemistry showed that the lesion was positive for SYT genome rearrangement, B-cell lymphoma-2 (Bcl-2), Vimentin, Pax-8, and CK7, and negative for smooth muscle actin (SMA), soluble protein-100, epithelial membrane antigen, CD99, and Pax-2. PRSS was diagnosed according to its imaging manifestations and pathological results (Figure ). |
The first case of post-transplant Malaria in Spain was a 30-year-old man who had received a liver transplant [] in 2005. Three weeks after the transplant, the patient presented with fever, shivers and hypotension. Molecular tests confirmed the presence of P. vivax. The donor had lived in Colombia up to 2004 and had suffered from malaria in 2001; however, he had been asymptomatic since the initial treatment. A further four patients who had received organs from the same donor remained asymptomatic, but in two of the four thick blood smear tests showed malaria parasites and they were treated with anti-malarials.\nIn 2005, there were two other cases of post-transplant malaria, both from the same Bolivian donor. Two women who had received transplants (kidney and heart respectively) developed fever a number of weeks after the procedure. Peripheral blood studies identified P. vivax.\nIn 2013, a 50-year-old man received a heart transplant [] and 2 weeks later he developed fever and abdominal pain due to a splenic infarction. A peripheral blood analysis revealed intracellular parasites consistent with P. falciparum. The donor originally came from Mali and had arrived in Spain a year before, although it was not known if he had travelled subsequently. Another four patients received organs from the same donor, one of whom developed fever and the subsequent blood test was positive. A further patient—though asymptomatic—had a positive antigen test. Anti-malarial treatment was administered to both patients. The other two organ recipients, though not presenting symptoms and with negative blood smears, were given anti-malarial prophylaxis.\nThe last reported case was in 2014 [] when a 52-year-old male who had received a kidney transplant presented a month afterwards with symptoms that were initially diagnosed as a urinary infection. A blood smear test showed the presence of P. ovale. The donor was Equatorial Guinean in origin and had travelled there recently. The other patients who received organs from the same donor were asymptomatic but nevertheless received anti-malarial treatment. |
A 10-year-old boy was admitted to our hospital with progressive vertigo, nausea, and vomiting for 17 days. Neurological examination indicated left hemiparesis and multiple cranial nerves palsy of right third, sixth, seventh, and bilateral ninth, tenth. Computed tomography and magnetic resonance imaging (MRI) revealed a partially thrombosed giant aneurysm of the BA trunk without any sign of bleeding. Mass effect on the brainstem was prominent, and the aneurysm measured 40 mm on MRI (Fig. –). Selective vertebral with 3-dimensional rotational angiography confirmed the giant fusiform, probably dissecting basilar aneurysm, which originated approximately 0.5 cm distal to the both anterior inferior cerebellar arteries and apparently ended in both posterior cerebral arteries (PCAs), and neither of the superior cerebellar arteries can be found. At bilateral internal carotid artery injection, there was no filling of both PCAs over the circle of Willis. The first digital subtraction angiography was conducted in other hospital; the balloon occlusion test and carotid compression test were not performed. After multidisciplinary discussion, it was decided that the best solution was to overlay two or three Enterprise stent (because it was impossible to obtain a high-density mesh stent, such as Silk or Pipeline) from the proximal BA to PCA P1 segment to divert the blood flow direction and then fill the patent portion of aneurysm with minimum coils, and hoping that the mass effect could be limited to least extent. The alternative treatment based on the collateral circulation checking, if the patient has sufficient collaterals over the posterior communicating arteries, was that the proximal basilar trunk be occluded by coils, if not, a superficial temporal artery to PCA bypass surgery is needed preceding BA occlusion.\nThe procedure was performed under general anesthesia. The patent portion of aneurysm is 39.7*20.8 mm (Fig. –). First, an attempt was made to catheterize the distal BA and left PCAs with a microcatheter (Headway 17, MicroVention, Inc. 75 Columbia, Ste A. Aliso Viejo, California 92656, USA) through the aneurysm, but this proved impossible because of the volume of the aneurysm and the pulsations in the sac. Therefore, bilateral carotid compression test was performed separately. A retrograde filling of the left posterior communicating artery (PCoA) and internal carotid artery was seen on the vertebral artery (VA) injection and left carotid compression, proving the functionality of the circulus of Willis on the left (Fig. –). Then, we decided to partially embolize the patent portion of aneurysm and occlude the BA above both anterior inferior cerebellar arteries. Assistance with temporal occlusion of the proximal BA by Hyperform 7*7 mm balloon (ev3 Inc. 9600 54th Avenue N.Plymouth, MN 55442- 2111 USA), the patent portion of aneurysm was partially embolized with coils (Axium, two 25mm*50 cm, one 20mm*50 cm, and one 18mm*44 cm, ev3 Inc), and then the mid-BA was occluded by coils (Axium, one 4mm*12 cm, hydrocoil, one 3mm*10 cm, and one 2mm*6 cm, ev3 Inc) above the level of the origin of the anterior inferior cerebellar arteries (Fig. ). Final angiographic evaluation confirmed total exclusion of the blood flow from BA to aneurysm (Fig. ), and bilateral PCAs were filled through left PCoA at the left internal carotid artery injection (Fig. –). The patient has had aspirin 100 mg and clopidogrel 50 mg for 4 days before treatment. After endovascular therapy, clopidogrel 50 mg were given continuously for 3 days combined with low-molecular-weight heparin calcium injection (GlaxoSmithKline, 0.4 ml, q12h) for 1 week. Follow-up MR in the next week confirmed the thrombosis of the aneurysm with an increase in the mass effect on the brainstem (Fig. –). Slight aggravation of symptoms was found in the patient after endovascular treatment for 2 weeks. After that, gradual improvement of the neurological deficits was observed, and all symptoms resolved within 3 months. The 3-month MRI revealed significant reduction in the size of the aneurysm and in the mass effect on the brainstem (Fig. –). MRI at 7- and 23-month showed further shrinkage of the aneurysm (Fig. –). Magnetic resonance angiography at the next week (Fig. –) and at 23-month (Fig. –) show the collateral circulation over the left PCoA supplying bilateral PCA and top of BA, and exclude any kind of endoleak situation. |
A 17-year-old male presented with recurrent rhythmic movement since the age of five. He repetitively tapped his brow or chin with the right fist only during sleep. The duration of this rhythmic movement ranged from 10 seconds to five minutes. Sometimes he repetitively punched the brow hard enough to render skin reddish discoloration. This behavior recurred almost every day. Upon admission, video-EEG monitoring demonstrated that the patient struck his brow with the right fist for one minute during the light sleep. The frequency of tapping during the monitoring was 2 Hz. There was no EEG change. Previously, under the impression of frontal lobe complex partial seizure, various ant-epileptic drugs including oxcarbazepine, zonisamide, levetiracetam and clobazam had been administered to control this symptom without any significant improvement. With the diagnosis of the rhythmic movement during sleep, clonazepam was prescribed before night time sleep. The dose of clonazepam was increased up to three mg per day. Clonazepam could not alter the symptom and induced only daytime drowsiness as an adverse event. Levodopa 250 mg plus carbidopa 25 mg were administered as a therapeutic challenge. Surprisingly this rhythmic movement increased dramatically in intensity and duration. The patient more or less violently punched his brow for four or five hours every night. With the hint of aggravating symptom by dopamine-agonist, haloperidol was chosen. One mg of haloperidol could markedly suppress the symptom to one-tenth degree in the intensity and duration compared with the symptom of the initial presentation. To avoid long-term adverse events, haloperidol was switched to pimozide two mg just before the night time sleep. After five days of administration, the rhythmic movement was completely disappeared for the following two months. The symptom reappeared after two months. However, the intensity was very mild and the duration was very short, which the parents could not notice the movement without careful observation for a whole night. |
The second case involves a 30-year-old Deaf, Hispanic male who presented to the Emergency Department after his mother reported that the he was behaving oddly and not taking his risperidone. Per reports, the patient was talking to his mother about going places in a UFO and exhibiting disorganized and illogical behaviors. He was subsequently placed under a Baker Act by the emergency room physician who documented that the patient was exhibiting auditory hallucinations. Initially an interpreter was brought to the hospital prior to his admission. Per the ASL-interpreter, the patient stated that he felt “fine and not crazy” and that all of these events are happening because his mother does not “understanding Deaf culture.” He also conveyed that he did not like to take his meds because they interfered with him being able to drink alcohol and caused drowsiness.\nUpon initial psychiatric interview an interpreter was not present as the hospital only agreed to set periods of time for the interpreter. As an effort to communicate, questions were prepared for the patient to answer via written responses. highlights a portion of the questions and answers that were constructed. From the responses he maintained bizarre delusions but denied current SI, HI, or AVH. When the ASL-interpreter arrived, the patient appeared jovial and yearned to express himself. The interpreter stated she had difficulties reading his rapid signing at first and had to have him slow down several times. However she did note that this was a common occurrence when addressing Deaf individuals.\nWith the interpreter's assistance, the patient was answering questions logically with a linear thought process. He reported that he had been diagnosed with schizophrenia as a teenager after having several interpersonal issues with his mother. She is Spanish speaking only and he stated that she has never fully understood how to communicate effectively with him. He had been taking risperidone for several years but was tired of continuing with the medication due to the side effects of drowsiness and weight gain, which he was never able to fully discuss with his psychiatrist. Patient reported he was in an ASL school and learning a career in massage therapy. After meeting a girlfriend there he began to develop a sense of independence that he reported his mother disapproved of. This caused an altercation that he reports his mother misinterpreted which precipitated his admission.\nThe patient continued to express that he was abducted by aliens as a child and could understand their language, but besides this he expressed no other psychotic processes. He was observed for two days without medications and remained calm/cooperative but was unable to participate in most activities due to limitations of the interpreter availability. After a family session was completed the patient was discharged home with plans to follow up with his community psychiatrist. The patients' diagnosis was changed to delusional disorder upon his discharge. |
A 51-year-old male with a history of nonischemic cardiomyopathy with a left ventricular assist device was admitted for expedited heart transplant evaluation. The evaluation included an elective colonoscopy in light of a family history of colorectal cancer in his mother who died at age 61 from the disease. The patient had his first screening colonoscopy at age 45 and was diagnosed with benign polyps, which were removed, and left-sided diverticulosis. The procedure was uncomplicated and he was advised to repeat a colonoscopy in five years.\nThe patient was without GI symptoms at the time of his colonoscopy. He denied tobacco, alcohol, or illicit drug use. His medications included amiodarone, aspirin, famotidine, levothyroxine, lisinopril, metoprolol, sildenafil, and intravenous heparin as well as torsemide, acetaminophen, docusate sodium, and melatonin as needed. On examination, he had a left ventricular assist device port entering at the upper abdomen, but otherwise the abdomen was soft and nontender to palpation with normal bowel sounds and no appreciable masses or ascites.\nThe patient underwent a standard bowel preparation which included a clear liquid diet the day prior to the procedure and 20mg of Dulcolax with 4 liters of polyethylene glycol the night prior to the procedure. Monitored anesthesia care sedation was administered with propofol. The colonoscopy was performed at night without difficulty with good bowel preparation. Abdominal pressure was briefly required to maneuver around the splenic flexure. The colonoscope was advanced to the cecum with identification of the appendiceal orifice and ileocecal valve. Findings included multiple sigmoid and descending colon diverticula and two, small (<5mm) sessile polyps that were removed using cold forceps.\nThe night of the procedure the patient had no pain or nausea and ate dinner and breakfast the following morning without incident. He then developed epigastric abdominal pain in the midmorning approximately 12-14 hours after the procedure and had one episode of nonbloody, nonbilious emesis following lunch. On physical examination, he was afebrile with a blood pressure of 104/89mmHg, heart rate of 68 beats per minute, and oxygen saturation of 100% on room air. Abdominal examination was notable for mild distension and moderate tenderness to palpation in the epigastric region without guarding or rebound tenderness and decreased bowel sounds. Laboratory examination revealed an elevated lipase of 2275 U/L and amylase of 1141 U/L. Additional abnormal laboratory findings included an elevated aspartate aminotransferase of 105 U/L, alanine aminotransferase of 94 U/L, and total bilirubin of 1.4 μmol/L (normal prior to the procedure). An abdominal X-ray did not reveal an obstructive bowel gas pattern or evidence of free air. A computed tomography (CT) scan of the abdomen/pelvis revealed diffuse edematous changes of the pancreas with surrounding inflammatory stranding in the bilateral paracolic gutters, extending superiorly to the perihepatic region and inferiorly to the pelvis (). The constellation of symptoms, labs, and imaging were suggestive of an episode of acute pancreatitis.\nThe patient was treated conservatively with bowel rest, intravenous fluids, and analgesics as needed. Over the next three days his symptoms and abdominal examination improved and his diet was advanced to a regular diet. The lipase normalized to 15 U/L. |
In June 2018, a 62-year-old healthy Caucasian woman underwent a standard follow-up magnetic resonance imaging (MRI) of subpectorally placed textured anatomical breast implants [Allergan (Dublin, Ireland)] in situ for 26 years after cosmetic augmentation. She had never experienced any complaints related to the breast implants. In 1990, she was treated for a basal cell carcinoma on her left shoulder but has no other comorbidities except for past tobacco use. Her eldest son was diagnosed with non-Hodgkin’s lymphoma at age 12. In August 2018, the patient started experiencing pain and Baker grade III capsular contraction of the right breast. Control MRI showed breast implant leakage. Explantation of both implants in January 2019 showed bilateral leakage after which symptoms went into remission. About three months later our patient noted an erythematous area on the lateral side of the inframammary fold of the right breast (, ). She recalled that the scar of this breast had been swelling increasingly followed by leakage of some serous fluid out of the scar. Although not ill she was prescribed oral antibiotics (amoxicillin clavulanate) for one week, without alleviating symptoms. Ultrasound echography of the right breast showed “snowstorm sign”, suggestive for residual silicone after leakage. Subsequently, the siliconomas and old scars were removed under local anesthesia and send for pathological assessment. The pathology report stated that the skin contained some macroscopic cystic abnormalities filled with a mucous substance. Microscopically extensive fibrosis was observed with round nucleate inflammatory cell infiltration, multinucleated giant cell macrophages and foreign material, likely silicone. Yet, the discomfort and inflammatory response continued to exist for which another MRI was made. This showed bilateral subpectoral residual silicone particles, with the largest silicone pocket of about 2,3 × 1,5 cm in the left breast (, ). In June 2019, revision surgery was performed in order to remove the siliconomas. Several superficially located siliconomas were excised on the right side on the right side. On the left, a thickened capsule was found containing a substantial amount of silicone. Therefore, a partial capsulectomy was performed simultaneously removing the substance. Histopathology and immunohistochemical analysis showed monotonous small cell B-lymphocytic infiltration (CD20+, CD5+, CD23+, ALK-) in both capsules, highly suggestive for CLL/SLL (a–e). Breast implant associated anaplastic large cell lymphoma (BIA-ALCL) was considered but excluded as CD30 tested negative. Microbiology tested positive for Staphylococcus epidermidis. After diagnosis, the hematology department was consulted for systemic medical workup and further guidance. Complete blood count (CBC) indicated a mild hypogammaglobulinemia (0.32 g/L IgM and 5.6 g/L IgG) and leukocytosis (10.5 × 109/L). In the peripheral blood there was an absolute number of 0.04 10e9/L (CD19+, CD20+, CD5+, Lambda+, CD23+, CD43+, CD45+, and CD200+) monoclonal B-cells. Abdominal ultrasound was made to investigate the spleen and abdominal lymph nodes while thoracic X-rays were made to assess the mediastinum and hilar lymph nodes; no significant abnormalities were reported. Subsequent bone marrow biopsy showed cell-rich tissue with large fields of atypical lymphocytes and grumulee pattern. Additionally, a low percentage of monoclonal B-cells (0.04 × 10e9/L) in the peripheral blood after explantation of the breast implants suggested either CLL/SLL localized in the bone marrow and periprosthetic capsule or induced by the prosthesis material. Time between follow-up appointments will gradually be extended to six months if the lymphoma remains in remission. No additional treatment was necessary. Follow-up CBC and immunophenotyping will take place every three months (or earlier in the case of new symptoms) and will be extended to six months if the lymphoma remains in remission. Bone marrow biopsy may be utilized in the future to follow-up on disease activity and the effect of explantation. |
A 29-year-old Japanese woman in her second pregnancy was being treated for pregnancy-induced hypertension and preeclampsia with a drip infusion of magnesium sulfate at 30 weeks 2 days gestation. The dose of continuously infused magnesium sulfate was 0.1 g/h on day 1, 0.5 g/h on day 2–5, and 1.0 g/h on day 6–12. The dose was increased to 2.0 g/h to control an imminent preterm delivery on day 12, just before an emergency transfer to our hospital. During this treatment, maternal serum magnesium levels were not monitored. The mother had no medical conditions or any intake of other medications within these 12 days, which could have influenced blood potassium concentration.\nOn admission to our hospital, the patient could not mobilize independently because of hypotonia caused by severe hypermagnesemia and hypocalcemia (Table ). On the same day, she delivered a male infant through vaginal birth. Her laboratory analysis at 7 h before and 7 h after delivery showed that the serum concentration of potassium, sodium, and creatinine ranged from 4.3 to 6.0 mmol/L, 133 to 128 mmol/L, and 0.85 to 0.95 mg/dL, respectively. These levels returned to within normal ranges at 5 days after delivery.\nThe male infant was born at 32 weeks gestation weighing 1268 g and with Apgar scores of 8 at 1 min and 9 at 5 min. He was immediately admitted to the neonatal intensive care unit in our hospital. There was no evidence of respiratory distress syndrome on chest radiograph, and he had a stable microbubble test. His heart rate was 130 beats per minute, and the arterial blood pressure was 42/22 mmHg, with normal contraction of the left ventricle confirmed by echocardiographic examination. His muscle tone was determined to be within the normal range by two expert neonatologists. The size and shape of both kidneys on ultrasonography were within the normal range, and his first urine was observed at 2 h after birth.\nLaboratory data showed that his venous blood potassium concentration was 6.4 mmol/L at 2 h after birth and reached 7.0 mmol/L at 4 h after birth even though he had sufficient urine output (Table , Fig. ). Glucose-insulin combined therapy was administered for 54 h with an insulin infusion rate between 0.9 units/kg/day and 1.9 units/kg/day to maintain his serum potassium concentration below 6.0 mmol/L. All blood samples were obtained from a catheter inserted directly into the right radial artery. During the therapy, he was not given potassium. His urine output was 4.1 mL/kg/h during the first 8 h, 6.2 mL/kg/h during the next day, and 3.3 mL/kg/h during the third day after birth with insufficient urinary potassium excretion (Table ).\nLaboratory analysis of his umbilical blood also showed hypermagnesemia at birth, which gradually subsided (Table , Fig. ). The serum calcium concentration remained over 7.3 mg/dL with intravenous drip administration of calcium sulfate. Although transient hyponatremia was observed at 6 h after birth, it recovered in 24 h without sodium administration.\nAfter resolution of NOHK, the neonate’s serum concentrations of potassium and magnesium were within the normal range. He was discharged from our hospital at 72 days after birth with no clinical complications and had normal growth and development at 3 years of age. |
On a freezing cold morning, a 71-yr-old male of Han nationality who was retired, but worked as a community volunteer, was brought to the neurology emergency with a history of sudden onset of left-sided weakness and difficulty in speaking while he was performing road patrol. Approximately an hour and a half had elapsed since the onset of symptoms before he was brought to the emergency room.\nAs for the past medical history, he had undergone a surgical procedure involving left kidney, left ureter and bladder for treatment of transitional cell carcinoma of bladder, approximately 8 months ago. One month after the surgical procedure, the results of laboratory investigations, such as complete blood count, kidney and liver function tests were within normal limits. There was no history of common risk factors of atherosclerosis, such as hypertension, diabetes mellitus, coronary artery disease and smoking.\nHe was conscious, had pallor, the blood pressure was 150/80 mmHg and the blood sugar level was 6.5 mmol/L. Chest and cardiac examination was unremarkable. The neurological examination demonstrated a left-sided hemiparesis with clumsy speech. The muscle strength of the left limb was grade III and the left Chaddock’s sign was positive. The patient’s upper and lower extremities were very cold, and the finger tip oxygen saturation was 76 %. However, the arterial blood gas analysis revealed the oxygen saturation of 94 % without supplementary oxygen.\nA computed tomography (CT) scan of the brain revealed absence of hemorrhage, hence the diagnosis of acute ischemic stroke was highly probable. Routine blood test revealed a haemoglobin of 58 g/L, platelet count of 124 × 109/L,white blood cell count of 7.55 × 109/L, however, the number of red blood cells, hematocrit, mean corpuscular volume could not be measured due to the interference by agglutinated erythrocytes. The low level of hemoglobin combined with presence of pallor suggested severe anemia. On coagulation study, d-dimmer was found to be 19.17 mg/L and fibrin degradation product (FDP) was found to be 101.2 mg/L, indicating secondary fibrinolysis.\nDue to the low level of hemoglobin, intravenous thrombolysis was contraindicated and the patient was hospitalized and treated with gastrodin. On the same day, the neurological symptoms of the patient dramatically recovered with the recovery of strength in the left limb (grade V), and the development of relatively clear speech. During this time, the patient was kept in a warm room where the temperature was maintained at 24 °C. However, the patient complained of severe back pain and passage of dark colored urine. Urine examination revealed the presence of hemoglobinuria, on the basis of which we suspected acute intravascular hemolysis.\nThe direct Coombs test was performed, which was negative for anti-globulin immunoglobulin G, but positive for anti-C3d, indicating the possibility of autoimmune hemolytic anemia. To rule out the possibility of connective tissue disease, tests for antinuclear antibody (ANA), antineutrophil cytoplasmic antibodies (ANCA), and antibodies to a spectrum of extractable nuclear antigens (ENA), such as smooth muscle (Sm), ribonucleoprotein (RNP), Sjogren's syndrome A (SSA), Sjogren's syndrome B (SSB), DNA topoisomerase I (Scl70), and histidyl-tRNA synthetase (Jo-1) were performed, which were found to be negative. To rule out multiple myeloma, serum and urine protein electrophoresis was performed, which were negative. The cold agglutinins were positive with a titer more than 1:1000. The abdominal enhanced computer tomography (CT) revealed no signs of relapse of bladder cancer. The cranial magnetic resonance imaging (MRI) showed the presence of acute infarction in the area of right basal ganglia and corona radiata (Fig. ).\nOn magnetic resonance angiography (MRA), we could not demonstrate severe stenosis of intracranial internal carotid artery; however, there was mild to moderate stenosis of the left posterior cerebral artery (Fig. ). The extracranial internal carotid artery was found to be normal on carotid sonography.\nBased on the above mentioned findings, a diagnosis of the cold agglutinin disease and ischemic stroke were made. The patient was transfused with 2 units of the washed red blood cells, and received corticosteroids, sodium bicarbonate and intravenous fluid therapy. After one day of corticosteroid therapy the back pain was dramatically relieved. The urine of the patient became progressively less dark. After one week of therapy, the titer of cold agglutinins decreased to < 1: 10 and the patient’s symptoms completely disappeared. |
A 32-years-old female presented with complaints of redness, watering, photophobia, and diminution of vision in the left eye with duration of two weeks. She disclosed a history of a similar attack in the left eye one year previously. She had a visual acuity of 20/20 in the right eye and count fingers close to face in the left eye. Examination of the right eye did not reveal any abnormality. There was mild conjunctival congestion in the left eye. Slit lamp biomicroscopy showed corneal edema, medium-sized keratic precipitates, cells (++) and flare (++). Fluorescein staining of the cornea did not reveal any epithelial defect. There was a marked decrease of corneal sensation in the left eye. A diagnosis of keratouveitis due to recurrent herpes simplex virus infection in the left eye was considered. She was placed on prednisolone acetate (1%) suspension four times daily, atropine sulfate (1%) thrice a day, and oral acyclovir 400 mg twice-daily. At one week follow-up, there was decrease in her symptoms. The visual acuity in the left eye improved to counting fingers at three meters. Slit lamp biomicroscopy revealed mild corneal edema, decrease keratic precipitates, cells (+) and flare(+). She was advised to continue the same treatment. At three weeks, she felt symptomatically better, but complained of diffuse loss of hair from scalp. There was no history of drug eruptions. Her visual acuity in the left eye was 20/200. Slit lamp biomicroscopy revealed residual corneal opacity and few old keratic precipitates in the left eye. Examination of the scalp revealed a diffuse hair loss and no drug eruptions []. The color and the texture of the hair were normal.\nOral acyclovir was discontinued, and topical prednisolone was reduced to thrice a day for two weeks and then twice a day for two weeks. A follow up after three months of discontinuation of oral acyclovir revealed hair re-growth in the affected area on her scalp []. Examination of the left eye revealed a corneal opacity, and she was advised to undergo penetrating keratoplasty for the left eye. The patient was not on any other oral, topical or over-the-counter medication. In addition, she did not receive any holistic, natural or home remedies during this period. Patient was moderately-built and did not suffer from any nutritional deficiency. She had not been pregnant recently. In addition, she did not have any other systemic problem that may lead to hormonal imbalance. She did not suffer from lupus erythematosus, hypothyroidism, hyperthyroidism, syphilis, sarcoidosis, HIV infection or any systemic malignancy. |
A 72-year-old Caucasian female patient was referred to the respiratory clinic with a 6-month history of exertional breathlessness. She gave a history of yearly chest infections, particularly in winter months. She, however, had no history of childhood respiratory problems or any significant respiratory symptoms during her adult life. She had a 30-pack-year smoking history but she quit 25 years prior to presentation. She worked as a nursing auxillary at a local hospital and had no prior asbestosis. She was on a 1 mg maintenance dose of prednisolone for polymyalgia rheumatica. Otherwise, she had no significant medical condition and was not on any regular medications. Her exercise tolerance was unlimited and she enjoyed a good health.\nHer O2 saturation was 95% on room air and her spirometry showed obstructive pattern with FEV1 1.14L (55%), FVC 2.09L (83%) and FEV1/FVC ratio 54%.\nAn initial chest radiograph 2 years prior to presentation suggested an increased radiolucency of the left lung but this was not investigated further (). Serial CXRs 2 years later showed a relatively unchanged appearance of the left hemithorax with progressively increased opacification in the periphery of the middle and lower zones, and accompanying reduction in lung volume, on the right side ().\nThe patient underwent a contrast-enhanced CT of the chest in view of the repeated chest infections and lack of complete resolution to rule out the possibility of an adenocarcinoma in situ or endobronchial lesion, respectively. Cross-sectional imaging was also carried out to assess the possibility of an underlying bronchiectasis in the presence of the recurrent chest infections and to further assess the interstitial changes seen on the CXR on the right side.\nHer CT showed hypoplastic left pulmonary artery (; arrow), attenuated peripheral pulmonary artery branches on the left (: arrows), hyperinflated left lung with air trapping and cystic bronchiectasis of the lingua and left lower lobe (). Features were in keeping with the diagnosis of Swyer-James-MacLeod syndrome (SJMS). Interestingly, the right lung was small in size with evidence of subpleural reticulation, traction bronchiectasis and ground-glass opacification suggesting an underlying pulmonary fibrosis (). The oligaemia of the left lung is shown as reduced FDG uptake () on PET CT, which was done to investigate a different pathology.\nSputum culture grew pseudomonas species and bronchoalveolar lavage from the right lung showed mixed cellularity with 22% eosinophils and a 36% neutrophils. |
A 61-year-old gentleman presented to our urology outpatient department with complaints of painless progressive swelling in the perineal area for the past 2 years. The swelling was around 3 cm in size to begin with and progressively increased in size to the present size of 10 cm over the last 2 years. Patient reported difficulty in sitting due to swelling. He also developed LUTS in the form of straining at urine, poor stream, intermittency, incomplete emptying, and increased daytime frequency for the past 2 months. He also complained of increasing constipation for the past 2 months. There was no history suggestive of neurofibromatosis type 1 or type 2. His general physical examination was unremarkable. Abdominal examination revealed a palpable firm swelling in the suprapubic area of size 10 × 5 cm. Examination of the perineum showed a firm immobile nontender 12 × 10 cm lump behind the scrotum with extension towards right gluteal area (). Posteriorly the perineal lump was going up to 2 cm beyond the anal verge. On digital rectal examination (DRE), the lump had occluded majority of the rectal lumen. However, the rectal mucosa was free over the lump. Superior limit of the lump could not be felt on DRE. Prostate was not felt separately from the lump. His investigations revealed normal blood workup, with blood urea 27 mg%, serum creatinine of 0.7 mg%, and serum PSA of 0.940 ng/mL. USG pelvis and abdomen showed 12 × 10.9 cm heterogenous mass inferior to bladder with internal vascularity with anechoic areas suggestive of necrosis. Bladder was pushed anteriorly and superiorly by the mass. There were no upper tract changes. MRI abdomen showed a heterogenous solid pelvic mass on T1 image, 25 × 15 cm, which was probably arising from prostate, as prostate was not visualized separately (). Mass had central hyperintense areas on T2 image likely necrosis with increased perilesional vascularity. The mass was seen extending up to pelvic inlet superiorly and abutting the lateral pelvic wall, compressing the sigmoid colon and bladder with ill-defined planes between them (Figures and ). The fat planes with iliac vessels were well defined. Uroflowmetry showed mild obstructive pattern. Patient underwent a TRUS guided biopsy (12 cores) from the mass, which suggested a diagnosis of benign schwannoma. Thus, with a working diagnosis of giant abdominoperineal benign schwannoma, the patient was taken up for laparotomy with tumor excision. Using meticulous dissection, it was possible to safely separate the mass from iliac vessel, sacrum, small bowels, and pelvic side walls. The pelvic plexus was also well preserved. Due to very large size of the tumor and its dumbbell shape, it could not be extracted from the abdomen itself, so a perineal incision was made and the perineal part of dissection completed from below (Figures and ). But the tumor was densely adhered to the middle third of rectum and to bulbar urethra. In view of suspicious nature of the mass, the involved rectal wall and urethral wall were removed. The large gut continuity was restored using anal pull through and coloanal anastomosis. The urethral defect was repaired primarily. Suprapubic and perurethral catheters were placed and a diversion loop ileostomy to protect the anastomosis was also fashioned. Postoperative recovery of the patient was uneventful. The stoma started functioning from 2nd postoperative day and the patient was orally allowed. Per urethral catheter was removed on 7th postoperative day and suprapubic catheter was clamped. Patient voided well per urethrally and suprapubic catheter was also removed on postoperative day nine. Patient was discharged home on post op day ten with advice to follow up regularly. Subsequently final histopathology report was suggestive of low grade malignant peripheral nerve sheath tumor in view of presence of spindle shaped nuclei, occasional verocay bodies with mitotic counts of 2 to 3 per 10 HPF, and areas of infarction (Figures and ). IHC was positive for vimentin and S-100 (). All margins of specimen were free of tumor. Patient is currently doing well and is under followup in our outpatient department. He is planned for ileostomy closure. |
This 54-year-old female was referred to the Neurofibromatosis outpatient clinic of the Oral and Craniomaxillofacial Surgery Department for treatment of numerous cutaneous tumors that preferentially covered her trunk and extremities. On admission, the patient described the tumors to be painless and disfiguring. Besides the cutaneous tumors the patient sought advice for treatment of a painful region of her left small finger (Figure 1 ). For some time the ulnar side of the distal phalanx of this finger had become very touch-sensitive. There was neither a tumor visible nor any other pathological alteration of the skin. However, the finger could not be examined by palpation. The suspected diagnosis was initially a glomus tumor [] or a non-palpable nodular PNF.\nMRI at 3T revealed numerous, popcorn-like, contrast-absorbing, hyperintense formations on T2-weighted images, up to 1.2 x 1.9 cm² in size located on the palmar side of the left hand (Figure 2 ). These small lesions mainly affected the metacarpal bones II and III. MRI also showed a sharply defined lesion of max. 1 cm in diameter in the subcutaneous layer at the level of the radiocarpal joint and distal to first digit that reached to the tendons of the extensor musculature. The bony structures showed a homogeneous signal. The findings were interpreted as disseminated subcutaneous and cutaneous neurofibromas of the entire left hand. Structures were found on the distal phalanx of the left small finger whose intensity pattern corresponded to that of the other lesions.\nDuring surgery for the excision and vaporization of numerous neurofibromas of the trunk and extremities, the pain sensitive finger region was also explored. After incision of the skin, no tumor was visible. Therefore, a circumscribed subcutaneous excision was taken as a tissue sample and examined histologically.\nThe tissue findings confirmed cutaneous neurofibromas for the numerous nodules excised from the trunk and extremities. Surprisingly, there was no evidence for a glomus tumor in the tissue sample of the finger. Smaller neurofibromas were differentiable in this tissue sample. Within the corium as well as in the subcutaneous adipose tissue there were some clustered Vater-Pacini (VP) corpuscles. Next to the corpuscles several small nerve fibers were present. Diagnosis of VP neuroma was made (Figure 3 ).\nThe nerve fibers were positive for S100 and neurofilament. S100 immunoreactivity was especially strong in the center of the corpuscle. The perineurium of the nerve fascicles and the lamellae of the corpuscles expressed epithelial membrane antigen (EMA).\nThe healing process of the wounds was inconspicuous. The patient noticed that the sensations of pain had diminished significantly in the area of the small finger soon after surgery. |
An 87-year-old woman, with senile dementia, diabetes mellitus, hypertensive diastolic heart failure and chronic renal disease presented at the Accident and Emergency Department with jaundice (total bilirubin 15.8 mg/dL, direct 12.4 mg/dL), significant bile duct dilatation at ECHO examination and obstructing cholangitis. Since 1987, when she has had an open cholecystectomy for symptomatic cholecystolithiasis, she was known to have three calcified asymptomatic hydatid cysts. One cyst was located at the spleen and another at the left liver lobe, both heavily calcified. The third one, that was barely calcified radiologically, was at the periphery of the right liver lobe, about 45-50mm in diameter. An ERCP performed the next day visualized at least five round bile duct contents (), which proved to be, after sphincterotomy and debriment of the bile duct, hydatid cyst remnants. A 10F plastic stent was inserted and broad spectrum antibiotics were initiated. Bilirubin level dropped to a total of 5.31 mg/dL (direct 4.95 mg/dL) on day 3 of admission.\nOn the third day of hospitalization, the patient developed dyspnea, tachypnea and clinical signs of right pleural effusion and ascitic fluid. An emergency CT scan of the thorax and abdomen was performed that revealed a large right pleural effusion with atelectasis (which proved to be reactive after laboratory analysis), a small left effusion and a large diffuse peritoneal effusion around the liver and down to the pelvis. Air was present inside the right hepatic lobe hydatid cyst, consistent with a biliary tree communication and the antecedent sphincterotomy (). The CT scan suggested a simultaneous free intraperitoneal cyst rupture. Due to the concomitant biliary tree communication, not only hydatid cysts and remnants, but also bile leak, was probably the cause of patient’s large effusions.\nAfter thorough discussion with the patient’s family and considering her poor general status and possible technical difficulties, a minimal invasive approach was selected. After a second ERCP that removed the plastic stent and another debridement that confirmed an efficient sphincterotomy and a clear duct, a subdiaphragmatic drainage was placed radiologically. Albendazole at a dose of 15 mg/kg/day was initiated.\nPeritoneal fluid drainage gradually fell from 300 cc to about 50 cc/day over a two-week period. X-ray chest film showed a complete resolution of the pleural effusions () and CT scan revealed the absence of ascites (). After 3 months of albendazole, the drainage tube was extracted and patient remained both clinically and radiologically improved at the first monthly scheduled follow-up. |
Mrs. SM, an 80-year-old woman admitted to the surgical unit for a gluteal abscess, was referred for psychiatric evaluation. The referring physician said that the patient believed that her deceased son was still alive. She had two sons and a daughter, who provided the psychiatric history. The deceased son was her favorite, but her relationship with other family members was depleted. When he was in his twenties, he was accused of fraud at his workplace, following which he developed depressive symptoms. At 10 days later he committed suicide by consuming poison, leaving separate notes for his mother and sister. When taken to the morgue, the patient claimed that he was not dead. The suicide note was not shown to her.\nOver the next few months, the patient displayed behaviors indicating that she believed her son was alive. She maintained his room and belongings exactly as before. She often rushed up to the terrace at the sound of airplanes and would say that her son was returning home. The above behaviors persisted for the next 35 years. Her self-care, sleep and appetite were unchanged. Her daughter reported that during the current admission the patient had been looking for her son among the medical interns.\nPatient was an emotionally restrained person who was not demonstrative about her affection for her children. There was a family history of suicide in her paternal uncle, sister and her son as described above and depression in her grandson.\nOn mental status examination, her higher mental functions were intact. When asked about her son she said she could not talk about him, but requested us to arrange for his return.\nBased on the history and examination, we considered differential diagnoses of delusional disorder and atypical bereavement. The family refused any psychiatric intervention for her. She passed away 2 months later. Her daughter subsequently presented to us with depression. |
An 80-year-old male patient with known diabetes mellitus and essential hypertension presented with a stroke (bilateral thalamic, left occipital, and brain stem), which left him quadriplegic, bedridden, and dysphagic. To support nutrition, nasogastric tube feeding was initiated and continued for 3 weeks. There was no improvement in his dysphagia and a prolonged need for nutrition was recognized. A decision to insert a PEG tube was taken at a joint multidisciplinary meeting of the nutritionist, gastroenterologist, and primary team physician.\nA 20-Fr (6.7-mm) tube was inserted using the pull-through technique, and the position of the bumper was confirmed endoscopically in the body of the stomach. No immediate technical difficulties or postprocedural complications were encountered. His vital signs and complete blood count remained stable before and after the procedure, as shown in Table .\nTen days later, the patient developed bleeding per rectum, which initially was intermittent, bright-red blood mixed with stool. As this was not associated with any instability of his vital signs or change in complete blood count, an elective colonoscopy was requested. However, 48 h later the rectal bleeding became profuse, with passing of large clots. Apart from tachycardia, the blood pressure remained stable, as shown in Table . On examination, the abdomen was soft with normal bowel sounds and no distention or tenderness. A rectal examination revealed fresh red blood with no palpable mass. His hemoglobin level dropped from 13.4 to 9.6 mg/dL, and his white cell count increased to 18.3 × 109/L. Due to ongoing significant rectal bleeding with clots, it was decided to perform an endoscopy, starting with a gastroscopy to rule out an upper gastrointestinal source and then proceeding to colonoscopy.\nUpper endoscopy showed no evidence of upper gastrointestinal bleeding, and the PEG tube was noted to be in situ with no evidence of bleeding or any blood until the second part of the duodenum (Fig. ). Colonoscopy showed blood clots in the rectum up to the transverse colon, where a white glistening foreign body was noted. The PEG tube was clearly identified after cleaning and washing to be traversing the transverse colon (Fig. ).\nDue to ongoing bleeding, the patient underwent urgent exploratory laparoscopic surgery. The PEG tube was found traversing the anterior abdominal wall and the stomach, with the transverse colon interposed. Segmental transverse colon resection was performed, with removal of the PEG tube and placement of a new one.\nFollowing the operation there was no more rectal bleeding, and the patient tolerated feeding through the PEG tube without any complications. |
Case B: A 54-year-old male, biomedical researcher, spouse of a physician, often feeling tired. He had temporarily been on hypertension drugs and discontinued. He appeared to have a busy workaholic lifestyle, tried to get 40 min of cardiovascular exercise 3 times a week, but not always regular. Slow deep breathing of 3 rounds of 20 breaths each made him feel much better. Two months later, he reported that he had benefitted very much by daily such practice, no longer feeling tired, was sleeping better, and had a feeling of wellness.\nKey organ systems C (communication energy), IA (normalized area), and E (entropy) before and after the intervention for the two cases are noted in .\nindicates that these two cases of tiredness are very different. While both have improvement in the C of Respiratory system, Thorax Zone, hypothalamus (a stress indicator), and immune system with deep breathing, Case A is an endocrine communication imbalance arising from worries (mental health) while Case B is simply the case of an overworking stressed workaholic.\nThe last three columns confirm that the change in the respiratory system and immune systems are incidental (with increased IA or total energy) and not the active driver in both cases (since entropy does not reduce). However, change in hypothalamus, indicative of stress reduction, is a common driver for both. Further, in Case A, the endocrine and nervous systems respectively with a 30% and 27% drop in entropy (increased coherence) and increased IA are the most active drivers while the cardiovascular system also contributes similarly but with lesser impact. However, in Case B, the drop in E in the thoracic zone respiratory activation along with hypothalamus indicates that the key driver is a lack of good breathing and building of stress from a workaholic way of life.\nIn these cases, the data suggest that it is coherence (reduced E) for pituitary functionality that through metabolism drives weight loss.\nCases C (Diabetic going off insulin): This is a case of a 66-year-old woman who is a chronic diabetic, becoming slightly arthritic in the knee, who was asked to lose weight to help reduce weight on her knees and for overall improvement. She had been coming regularly for weekly chair-based yoga to a wellness clinic in 2015. No changes were perceptible in 2 months. On measuring with EPI, the lowest C was pancreas. She was asked to do (gentle and slow) forced exhalation (Kapalbhati) for 15 min. The C for pancreas thereafter showed significant improvement [], and the patient reported feeling very good. She continued the practice of 15 min of Kapalbhati twice a day religiously, lost 16 lbs in 6 weeks, and after 3 months, her doctor took her off Lantis (Insulin). She continued with metformin.\nHer pituitary C – indicates metabolic control – had not shown any remarkable change staying in stable C zone (4.72), but she experienced remarkable weight loss. This puzzle is explained by the drop in entropy (E) for pituitary indicating increased coherence in the metabolic communication. |
In December 2017, a 73-year-old man was admitted with a 2-month history of pain in the back and right side of the chest associated with dry cough, and inability to walk for the last 1 month. He had a 50-year history of smoking and a 10-year history of chronic obstructive pulmonary disease (COPD). He was diagnosed with pulmonary TB based on positive T-spot and Xpert tests and computed tomography (CT)-scans at a local hospital 1 month ago. He was administered anti-TB treatment for 1month, comprising the empirical therapy using pyrazinamide, isoniazid, rifampicin, and ethambutol. Recent signs were weight loss and severe asthenia.\nTo investigate the patient's pain, a chest CT scan was performed, which revealed significant osteolytic destruction at the bodies of the 5th and 6th thoracic vertebrae and thoracic pedicles, with swelling of the soft tissue (Fig. ). It was suspected that the destruction and the swelling of soft tissue were due to TB with cold abscess, resulting in paraplegia. The chest scan showed tiny, wide spread, and discrete pulmonary opacities with bilateral pleural effusion, and a lump in the lower lobe of the left lung which was suspected to be an inflammatory granuloma. There was 1 thoracic aortic aneurysm (116 mm × 40 mm) at the aortic arch, 1 saccular pseudoaneurysm (67 mm × 32 mm) in the descending thoracic aorta, another saccular pseudoaneurysm (69 mm × 34 mm) in the descending thoracic aorta above celiac trunk, 1 abdominal aortic aneurysm (112 mm × 33 mm) and 1 right iliac aneurysm (58 mm × 16 mm) (Fig. ). A diagnosis of multiple tuberculous mycotic aneurysms of the aorta was made. Considering the patient's condition, surgery was not attempted. He underwent endovascular repair using microcore stent graft at our hospital. The surgical procedures are described below. The femoral artery was incised, and a microcore stent was implanted into the diseased artery. The stent covered a region ranging from the proximal normal aortic docking site to the site above the celiac trunk. The stent was not allowed to cover the openings of the major branches of the abdominal aorta, such as the celiac trunk, superior mesenteric artery, and bilateral renal arteries. Since the aneurysm involved important branches of the abdominal aorta, provisional observation was necessary. The procedures were performed under general anesthesia. Hemodynamic imaging of the distribution of wall pressure of blood flow in the aorta using computational fluid dynamics (CFD), was obtained before and after surgery in accordance with the preoperative and postoperative CT images in the digital imaging and communications in medicine (DICOM) format. On post-operative day 14, the patient was discharged without complications. The patient was in a stable condition and was transferred to a local hospital for continuation of the treatment of pulmonary infection and TB. Following transfer to the local hospital, the respiratory function deteriorated due to aggravated pulmonary infection. The patient was admitted to the Intensive Care Unit for type 1 respiratory failure and pulmonary infection. However, he could not survive the infection. |
A 24-year-old male presented in August 2017 with transient memory loss and paresthesia of the left lower limb. The patient was right handed with no tobacco intoxication and occasional alcohol intake. The patient’s main medical history was a known right arterial thoracic outlet syndrome diagnosed in Nov 2016 after a 3 days episode of cold and painful right hand during the night, and Raynaud’s syndrome when he was playing table tennis.\nHe underwent in January 2017 a CT angiography of the supra-aortic arteries that showed an extrinsic compression of the right subclavian artery with mild stenosis of the retro-scalar subclavian artery, associated to a typical post-stenotic dilatation with no thrombus inside. Ultrasound examination of the supra-aortic arteries depicted a focal occlusion of the termination of the right humeral artery. Upper limb electroneuromyography was normal. Cervical spine and chest X ray did not show a cervical rib. Cervical CT scan showed anterior synostosis of the 1st and 2nd rib. Due to the occlusion of the right humeral artery and the post-stenotic dilatation on the right subclavian artery, it was decided to plan a surgery of the first rib associated with an arterial bridging for Sept 2017. On the day before admission in our unit in August 2017, the patient had an episode of transient memory loss and paresthesia of the left lower limb. The episode lasted for 30 min. He decided to present himself to the emergency room. The neurological exam was normal. There was a difference of arterial pressure between the right arm (101/67 mmHg) and the left arm (127/78 mmHg). MRI of the brain revealed acute right PCA territory infarction (Fig. ), with no visible arterial occlusion. CT angiography revealed the presence of a 24.1 mm thrombus in the post-stenotic aneurysm sac (Fig. ).\nAn ultrasound examination of the supra-aortic arteries (Fig. ) confirmed the post-stenotic dilatation and showed the presence of a small mobile thrombus on the distal wall the aneurysm, 5 cm away from the ostium of the right vertebral artery. Doppler shows retrograde reflux lasting about 0.45 s. During this reflux, the average maximum speed is − 12.8 cm / sec. The reflux can be therefore estimated to be 5.76 cm (12.8 × 0.45). The distance separating the edge of the mobile thrombus from the ostium of the right vertebral artery was 5 cm.\nBlood cell counts and inflammatory markers were normal. Thrombophilia and vasculitis tests were negative. Electrocardiogram showed sinus rhythm with no arrhythmia during 1 week of telemetry. A trans-thoracic and trans-esophageal echocardiography was normal.\nAn enoxaparin treatment was started at curative dose. The thrombus disappeared after one week follow up. The patient underwent the surgery as planned in Sept 2017 with resection of the first rib, anterior scalenectomy and bridging of the aneurysm via a supra and sub-clavicular approach.\nThe patient always remained asymptomatic. |
A 62-year-old woman presented with a one-month history of sudden painless visual loss in the right eye. On examination, best corrected visual acuity (BCVA) was 20/20 in both eyes. Intraocular pressure was 21 mmHg in both eyes. Dilated funduscopic examination in the right eye revealed retinal emboli inferior to the optic disc obstructing a small arteriole associated with retinal ischemia (Figures and ). The left eye was unremarkable. There was no prior past ocular history. The patient had hypertension and hypercholesterolemia and had an extensive smoking history.\nFluorescein angiography revealed delayed retinal perfusion along the inferior arcade in the right eye (Figures and ). Optical coherence tomography showed normal foveal contour with inner retinal ischemia and thickening, consistent with an acute inferotemporal branch retinal artery occlusion (). The patient was started on Latanoprost at nighttime in the right eye to lower the intraocular pressure in hopes to increase reperfusion of the retina. An extensive cardiovascular workup was done, and significant carotid artery stenosis of less than 70% was found. She was started on plavix and aspirin by her cardiologist. The patient continued with BCVA 20/20 OU vision and persistent highly refractile peripapillary emboli; retinal ischemia resolved. Her OCT showed inner retinal atrophy (Figures and ).\nUnexpectedly, the patient presented with a three-day history of sudden painless visual loss OD a year and a half after her initial presentation. BCVA was counting fingers (CF) in the right eye. Fundus exam revealed new superotemporal retinal ischemia associated with two new emboli. OCT demonstrated thickening and hyperreflectivity of the inner retinal layers consistent with an acute BRAO OD (). The patient refused fluorescein angiography at that time. Urgent workup revealed worsening stenosis to 80% in her right common carotid artery. The vascular surgery referral prompted a right carotid endarterectomy with a carotid stent placement approximately two months following her presentation with acute vision loss.\nAfter endarterectomy, vision in the right eye improved from counting fingers to 20/200 and 20/250 at 2 months and 6 months, respectively. Postoperatively, retinal whitening resolved and reduced intraretinal edema was noticed (). One year after endarterectomy, visual acuity was 20/30. The retinal swelling had resolved (). |
A 30-year-old man presented to our Trauma unit with penetrating abdominal trauma. He had no known background medical or surgical history. Of note were two gunshot wounds - one thoracoabdominal in the 8th intercostal space on the right and a second wound over the right buttock. He came in haemodynamically unstable with a blood pressure of 60/40 mmHg pulse of 100 beats per minute. He was resuscitated according to the ATLS® principles of Primary and Secondary survey. The arterial blood gas showed severe metabolic acidosis. Fluid resuscitation and massive transfusion protocol were initiated per standard of care. The patient was taken to theatre for an emergency damage control laparotomy by the Trauma surgeon and a senior trauma registrar (resident).\nHaemoperitoneum, gross faecal contamination and multiple hollow viscus injuries were confirmed at laparotomy. Bleeding from the bowel mesentery and the bowel ends was controlled first, without any overt bowel blood supply changes. Minor contusion of the second part of the duodenum (AAST Grade I) was noted at laparotomy, requiring no intervention []. Extensive caecal and transverse colon injuries (AAST Grade V), not amenable to repair, were noted. A right hemicolectomy was performed with a GIA stapler resulting in the typical ‘clip-and drop’ of the bowel ends []. The patient was transfused four units of packed red blood cells, four fresh frozen plasma units, and one mega unit of platelets intra-operatively. The abdomen was left open with a temporary vacuum-assisted abdominal closure, with a plan to return to theatre for definitive surgery.\nHe was transferred postoperatively to the trauma intensive care unit (ICU) for continued resuscitation and close monitoring. Given gross contamination, broad-spectrum antibiotics were continued in ICU. He still required vasoactive support to maintain acceptable mean arterial pressures. His acidosis corrected within 24 h of his ICU admission, although he still had features of Systematic Inflammatory Response Syndrome (SIRS) as evidenced by ongoing pyrexia and persistent tachycardia. A planned relook laparotomy was performed on day 2. The abdomen was noted to be clean at relook. The transverse colon stump was intact, all the remaining bowel was viable, and an end ileostomy was fashioned.\nDay 3 post-operation, he developed an acute kidney injury and mild hypoglycaemia attributed to possible systemic sepsis. His antibiotics were escalated to a carbapenem as per the trauma unit protocol. A septic workup (blood cultures, Chest X-rays etc.) was done, including a 1,3 Beta D glucan assay (Fungitell®). The BDG result was significantly raised (500 pg/ml), highly suggestive of invasive fungal sepsis. As per our local micro-biogram, he was started on an antifungal cover using Fluconazole at 800 mg daily. He showed good clinical improvement and was successfully weaned off a ventilator and extubated on day 5 post-operation.\nPreviously well-perfused ileostomy became necrotic on Day 7 post-operation. At this stage, the patient had been off vasoactive medication for more than 5 days. A relook on demand was performed in theatre. Multiple segments of patchy necrosis and ischaemia starting 160 cm from the duodenal jejunal flexure (a, b) were discovered. No surgical, mechanical explanation or complications could be elicited for the cause of bowel ischaemia. This finding was unusual and surprised the surgical team. Small bowel resection of necrotic bowel was done, and specimens sent off for histology. Unfortunately, in our setting, the frozen section is not available after hours. The necrosis was associated with features of early perforation in some regions.\nThe pathology report confirmed a diagnosis of mucormycosis on the segment of resected small bowel that was submitted for histopathological examination. Serosal fibrinopurulent exudate and a site of perforation were identified macroscopically and features of haemorrhagic infarction. Haemotoxylin and eosin (H&E) sections were representative of small bowel wherein transmural necrosis, perforation and acute serositis were confirmed. Large areas of mucosal necrosis containing fungal hyphae were present (). The hyphae were large, non-septate, lacked parallel walls and demonstrated acute angle branching, including 90-degree angle branching, morphologically consistent with mucormycosis. Transmural invasion by the hyphae with extensive angioinvasion was also demonstrated ().\nAt this stage, we had histological evidence of mucormycosis. This was despite negative screening for common associated medical conditions in this patient. Workup for Diabetes mellitus, Tuberculosis, Human immune deficiency virus and hypertension were all negative. There were no immunosuppressive medications identified in the history provided or administered during his stay with us before this development. The patient continued to have a turbulent course and required a further two relooks. He demised despite additional antimicrobial support and escalating antifungal therapy to include Amphotericin B therapy. Low dose physiological intravenous steroids were introduced for refractory hypotension towards the end. |
Case 1: A 10-year-old girl was diagnosed as having scoliosis with Prader Willi syndrome at the age of 2 years. She received brace treatment from 5 to 10 years of age. We performed stage 1 posterior short fusion from T7 to L1 for her preoperative major curve Cobb angle of 100 degrees and angle of trunk rotation (ATR) of 40 degrees at the age of 10 years. Preoperative height was 117 cm, weight was 25.3 kg, and body mass index (BMI) was 18.5 kg/m2. Her height was equivalent to that of a child of 6 years and 8 months. Although, Y cartilage was closed, Risser grade was 0 and she was before the first menstruation before the first surgery. So, we judged that there was a possibility of growing yet, and 2 staged surgery was applied. Surgical time was 205 minutes and blood loss volume was 150 g. Postoperative Cobb angle of the major curve improved to 63 degrees. Postoperative ATR improved to 13 degrees. Postoperative brace therapy was continued to prevent a crank shaft phenomenon. We performed stage 2 posterior spinal fusion from T2 to L4 for her preoperative major curve Cobb angle of 89 degrees and ATR of 28 degrees at the age of 14 years. Preoperative height was 122 cm, weight was 38.8 kg, and BMI was 26.0 kg/m2. Her height was equivalent to that of a child of 7 years and 7 months. Risser grade was 3 before the second surgery. Surgical time was 316 minutes and blood loss volume was 800 g. Postoperative Cobb angle of the major curve improved to 46 degrees. Postoperative ATR improved to 20 degrees. Thoracic height (T1-12) had improved from 160 to 206 mm and spinal length (T1-S1) had increased from 240 to 320 mm at the final follow-up (Fig. ). Forced vital capacity improved from 0.5 L before surgery to 0.88 L afterwards. Preoperative SRS-22 domain scores were 4.2, 4.0, 2.0, 4.4, and 3.65 for function, pain, self-image, mental health, and subtotal, respectively, which were ameliorated at the final follow-up at 4.0, 4.6, 2.8, 4.2, and 3.9, respectively. There were no severe perioperative complications. |
A 78-year-old male with multiple comorbidities, including hypertension, hyperlipidemia, and type II diabetes mellitus, presented to our emergency setting with complaints of recurrent bouts of abdominal pain and fluctuating fevers for the previous two weeks. The patient reported that the pain is a new manifestation of a previously dull aching pain that had waxed and waned over the last decade. His description alluded to a pain that was sharp and intermittent with localization in the right upper quadrant. He could not attribute the intermittent nature of his predicament to any aggravating or relieving influences. The pain was associated with fluctuating low-grade fevers (99°F-100°F), anorexia, and an associated 13-pound weight loss, which culminated in a visit to our clinical setup.\nFurther interrogation disclosed that the patient underwent a laparoscopic cholecystectomy in 2003. The ensuing year was relatively pain-free but was followed by recurrent bouts of right upper quadrant pain, albeit less upsetting than his current presentation. He was subsequently diagnosed in 2005 with gallstone spillage. The patient chose conservative treatment for his abdominal pain, rather than invasive interventions, which included the administration of acetaminophen and non-steroidal anti-inflammatory drugs (NSAIDs). This treatment modality was sufficient for the duration of a decade. He presented to another medical facility with similar complaints of fever and abdominal pain in 2016. A computed tomography (CT) scan of his abdomen disclosed the presence of a necrotic phlegmon, which was subjected to aspiration. Its composition included a combination of fibrous material, granulation tissue, and inflammatory infiltrate. The aspiration provided considerable relief of symptoms and he was discharged on a gabapentin prescription that was well-tolerated and produced sustained amelioration of his pain, with only occasional wavering with respect to his baseline.\nThe initial assessment showed an elderly gentleman, who was alert and well-orientated but under considerable distress due to the abdominal pain and accompanying chills. He had a fever of 104°F, a heart rate of 120 beats per minute, a blood pressure of 95/70 mm Hg, and a respiratory rate of 19 per minute. An abdominal exam revealed a non-protuberant, soft, and tender abdomen with marked sensitivity in the right upper quadrant. He had perceptible bowel sounds, an absence of dullness on percussion, and a clear rectal vault. Pertinent initial laboratory investigations included an elevated white blood cell (WBC) count of 16,900/µL, C-reactive protein (CRP) of 6.5 mg/dL, and a random blood glucose (RBG) of 280 mg/dL. The patient subsequently underwent a whole body CT scan, which revealed a large 19-cm sub-diaphragmatic, right retroperitoneal abscess, which was inferior and posterior to the right hepatic lobe (Figure ).\nIn lieu of these findings, the patient was admitted and started on a combination of intravenous fluids, intravenous (IV) vancomycin and piperacillin-tazobactam due to an underlying suspicion of sepsis secondary to a hepatic and/or perihepatic liver abscess caused by a lack of gallstone retrieval following his cholecystectomy. He was subsequently subjected to a percutaneous CT-guided drain placement, which allowed for the evacuation of approximately 700 mL of grossly purulent material and provided prompt pain relief. The fluid sample was sent for a gram stain, culture, and a bilirubin assay. The gram stain of the abscess fluid revealed branching gram-positive rods concerning for Actinomyces, Nocardia, and Streptomyces; therefore, the patient remained on IV vancomycin and piperacillin-tazobactam, with the addition of trimethoprim-sulfamethoxazole (TMP-SMX) to the antibiotic regimen. Remarkably, the culture growth was positive for Propionibacterium and ampicillin-sulbactam was added to the list of antibiotics. Two days later, the patient was shifted to the intensive care unit (ICU) following unrelenting fever and persistent tachycardia, even after his abdominal drain placement was supplemented with vigorous antibiotic and antipyretic therapy. His ICU stay was complicated by episodes of dyspnea, tachypnea, and pleuritic chest pain, while a chest auscultation unveiled a decrease in breath sounds at the right basal region. A repeat CT scan confirmed the reduction in the size of the abscess and showed a new right-sided pleural effusion, which explained the patient’s breathing difficulties (Figure ).\nThe patient underwent an ultrasound-guided chest tube placement, which evacuated 10 mL of purulent fluid, followed by two doses of lytic therapy with tissue plasminogen activator (tPA) via the catheter. The following morning, he described an aggravation in his pleuritic chest pain, and an episode of shortness of breath, whereby, the oxygen saturation dipped to 90%. A new chest CT scan was ordered, which showed an interval increase in the right basilar opacity with a moderately sized pleural effusion (Figure ).\nHe was subsequently upgraded to a larger catheter via a CT-guided approach that evacuated a total of 900 mL of purulosanguinos fluid. The patient tolerated subsequent lytic therapies well and showed vast clinical improvement following this procedure, with a reduction in dyspnea, pleuritic chest pain, and fever, as well as a down-trending of his inflammatory markers.\nA repeat CT scan was performed on the 10th day of admission, which revealed a near-complete resolution of his right-sided pleural effusion, and a decrease in his right-sided retrohepatic intrabdominal abscess (Figure ).\nThe chest drain was removed and the patient was subsequently discharged with a transhepatic drainage catheter, daily intravenous ampicillin-sulbactam, and acetaminophen, as needed for pain control. The patient was shifted to oral amoxicillin-clavulanate a month after the resolution of his pain, fever, and stabilization of inflammatory markers. The transhepatic percutaneous drain was left in place in order to allow for the formation of a chronic drainage tract, with hopes of localizing the perpetrating gallstones at its base.\nTwo months after discharge, the patient underwent a procedure for upsizing the drain in order to accommodate for a choledochoscope into the abscess cavity and the maturing sinus tract. He subsequently underwent an abscess cavity endoscopy, whereby a catheter and scope were advanced into the cavity for exploration. An abscess catheter study was performed through the existing catheter and showed no filling defects, after which the catheter was removed and an endoscope was inserted for direct visualization of the main cavity, as well as the two “fingers” branching out of the abscess cavity. Two small stones were expelled after flushing the main cavity multiple times. Following the expulsion of the gallstones, a replacement catheter was advanced into the cavity and a second catheter study was performed to rule out the possibility of any other stones. The patient tolerated this intervention well and had no further drainage from the intra-abdominal drain.\nFollowing a lack of drain output and resolution of symptoms after his last endoscopic procedure a month ago, the patient's intra-abdominal drain was removed. The patient is currently stable and is being followed as an outpatient to date. |
A 50-year-old alcoholic male with a history of schizophrenia presented in profound shock to the Denver Health Emergency Department with stab wounds to the left thorax. 1.5 liter of blood was aspirated with an emergent pericardiocentesis and the patient underwent resuscitative anterolateral thoracotomy in the ED. The emergency thoracotomy was performed in the standard fashion, with an incision made along the left fifth intercostal space extending across the sternum. After cardiac repair and hemostasis, the incision was closed primarily. At ten days post-operatively, the patient developed a thoracotomy wound infection that cultured positive for methicillin resistant staphylococcus aureus. Despite appropriate antibiotics, the infection necessitated radical debridement of involved bone (lower part of the sternum and rib), cartilage and soft tissue. Vacuum-assisted closure device (KCI, USA, San Antonio, TX) was placed after each debridement. The wound after two debridements measured approximately 20 × 8 cm, and extended deep to the pericardium (Figure ). Location of the EDT wound however precluded use of pectoralis major or latissimus dorsi muscle flaps due to the inadequate reach of these flaps. A CT angiography of the internal mammary vasculature was performed to explore the potential use of a superiorly based rectus abdominis muscle flap for the wound reconstruction. However, it revealed interruption of the contrast medium in the internal mammary vasculature at the level of the right seventh rib (Figure ) and left fifth-seventh rib (Figure ). Therefore, a free tissue transfer by using the right-sided rectus abdominis muscle flap was carried out for wound reconstruction. The deep inferior epigastric vessels, the vascular pedicle of the flap, were anastomosed to the right internal mammary vessels in the third-forth intercostal space proximal to the transection level for restoration of perfusion [] (Figure , , and ). The surface of the muscle flap was skin grafted. The flap took successfully and the patient healed without further complications (Figures , , and ). |
A 28-day-old female baby was presented to the surgical emergency of our institution with abdominal distension, bilious vomiting, constipation and reluctance to feed for 3 days. Few antenatal scans available gave no abnormality in the fetus. The baby was a product of spontaneous vaginal delivery at term. The baby initially tolerated feeds during the first week of life, but developed vomiting thereafter. The frequency of vomiting had increased to 4-5 times a day over three weeks. Three days prior to the presentation, she developed abdominal distension, bilious vomiting after every feed and constipation.\nOn clinical examination, abdomen was distended with visible gut loops. On palpation, no mass lesion was present. The bowel sounds were absent and digital rectal examination revealed an empty rectum. Provisional diagnosis of intestinal obstruction was made and patient was investigated. Patient was initially resuscitated with intravenous fluids. Naso-gastric tube was passed and antibiotics started. Abdominal radiograph performed showed multiple air fluid levels. Ultrasound showed massive gaseous distension of the intestinal loops obscuring other viscera. Laboratory tests were within normal limits. The patient underwent exploratory laparotomy which showed a stenosis of mid-ileum causing small bowel obstruction (Fig. 1). A dark brown colored cyst was present in the pelvis having a grayish nodular thickening on one side (Fig. 2). The cyst was freely floating in the peritoneal cavity; not attached to the surrounding structures.\nFurther exploration revealed absence of left sided ovary. Moreover, left sided fimbrial end of fallopian tube was freely floating in the abdomen. \nSome fibers of connective tissue were present between the fimbrial end and the uterine end of the fallopian tube and the portion in between was absent (Fig. 3). Right sided ovary and fallopian tube were normal.\nResection and ileo-ileal end to end anastomosis was performed for ileal stenosis. Cyst was eviscerated and sent for histopathology which revealed a benign ovarian cyst with hemorrhagic fluid inside. Post operative recovery was uneventful. Patient visited us for 6 months and then never returned. |
A 30-year old male was involved in a motor vehicle accident and suffered from multitrauma including fractures of the processus spinosi of the cervical vertebra 7 and thoracic vertebrae 1 and 2, fracture of the processus transversi of the thoracic vertebrae 8 to 11, fractures of the right olecranon, the left clavicle and a third-degree open right tibial fracture with severe soft tissue defect exposing the tibial fracture zone (Schatzker C). At first entry to the combined center of traumatology and reconstructive surgery an external fixation was performed combined with a plate osteosynthesis (LCP proximal tibial plate 3,5/6, Johnson&Johnson Synthes) to ensure limb salvage. In a second procedure the osteosynthesis was planed to be replaced by a coated tibial nail (e.g. PROtect expert tibial nail, Johnson&Johnson) after the coverage of the vacuum sealed soft tissue defect and a 6-week antibiotic therapy to avoid chronic infection with subsequent osteomyelitis. Prior to the subsequently discussed operation, an attempt to cover the defect was made by performing a free ALT flap with end-to-end anastomosis to the posterior tibial artery, but ended with flap necrosis due to arterial embolism triggered by the massive intima damage in spite of temporary therapeutic anticoagulation. The decision to make an end-to-end anastomosis within the primary injury zone is debatable, even though a preoperative CT angiography showed sufficient flow of the posterior tibial artery. The clotted posterior artery was ligated after removal of the ALT flap.\nNegative wound pressure therapy (NPWT) was used for coverage and preconditioning of the 8 x 18 cm soft tissue defect (Figure 1 ). Preceding the free LD flap an AV loop system (AV loop marked * in Figure 2 ) was constructed by the vascular surgery department on the popliteal P3 segment. The patient was thus ready to have the defect covered by means of a free LD flap with microvascular connection to the AV loop and simultaneous split skin coverage plus a monitor island (marked *) for better flap observation (Figure 3 ) after 7 days of Doppler monitoring the AV loop. The flap showed no signs of low perfusion or infection. The monitor island was disconnected during a bedside procedure on the 7th postoperative day before starting flap training via dangling of the leg. The donor sites on the left thigh and back showed no signs of seroma, wound dehiscence or inflammation.\nThe patient underwent early physiotherapy for remobilization. Customized compression garments were worn for 6 weeks for flap remodeling. He was discharged to outpatient care on the 63rd day in a healthy condition with good scarring. The initial care was performed by the outpatient unit with weekly follow-up visits and short-term visits after 2 and 8 weeks (Figure 4 and Figure 5 ), 6 months (Figure 6 and Figure 7 ) and 1.5 years post-surgery (Figure 8 and Figure 9 ). Given full weight bearing, the patient did not complain of any disturbance. A contrast CT performed at week 16 post discharge confirmed the efficacy of the AV loop (Attachment 1 ). Figure 5 , Figure 6 , Figure 7 and Figure 8 show the patient standing and able to walk with no crutches. The X-rays (Figure 10 ) one year after bone fixation showed no sign of bone infection or pseudarthrosis after removal of the external fixator. No further surgical procedures were performed due to good overall patient satisfaction and adequate aesthetic outcome. |
A 45-year-old otherwise healthy woman with a diagnosis of spinal cord injury due to falling down the stairs about 13 h ago was admitted to our hospital. She wasn’t on any medication. Based on CT-scan findings her injuries included C5-6 dislocation causing severe cord contusion and compression with the manifestation of motor and sensory loss. The patient underwent neurosurgical intervention in order to fix the cervical dislocation and prevent vertebral compression. After the operation she was admitted to our ICU with BP = 99/45 mmHg and o2 saturation = 100%. On physical exam she has no active bleeding, clear respiratory sounds without distress and her force of left upper limb was 3/5. Her lab data and hemodynamic parameters were presented in . On day 1 of injury the patient developed hypotension (BP = 99/45 mm-Hg) and bradycardia (HR = 50 bpm). We maintained euvolemia based on frequent bedside echocardiography. According to our hospital protocol continuous infusion of methylprednisolone 100 mg/24 h was administered on day 1. Despite adequate hydration she still had bradycardia and hypotension, so dopamine was initiated to optimize blood pressure and heart rate. On day 2, because of continuing bradycardia, aminophylline infusion (10 mg/h) was administered.\nOn day-3after the injury, the patient was successfully weaned off dopamine, and midodrine was started (2.5 mg BD) and the dose was titrated to 5 mg three times a day. And 5 days later, aminophylline drip was discontinued because the patient’s HR was stable on 76 bpm without aminophylline. The patient did not have any further episodes of bradycardia or hypotension, so there was no need to start theophylline instead of aminophylline. Her BP was about 130/70 on midodrine, so we did not discontinue midodrine. No serious adverse effects including arrhythmia or central nervous system side effects were observed during therapy. She also received citalopram for improving her depression, melatonin for insomnia, ipratropium bromide and salbutamol and N-acetylcysteine, pregabalin for neuropathic pain, pantoprazole and prophylactic dose of enoxaparin.\nSubsequently the patient was transferred to the neurosurgery ward and after one week, she was successfully discharged from the hospital on midodrine without any bradycardia or hypotension while she was paraplegic. She was advised to increase her salt and water intake and was appointed for our clinic to follow up on her BP, HR, and possibly tapering down of midodrine. |
The blind and painful right eye of a 38-year-old man was eviscerated in September 2016. The patient stated that his right eye had been blind since early childhood due to a unilateral congenital anomaly complicated by secondary glaucoma. He received the diagnosis of SO in January 2017 after he experienced visual loss in his only seeing (left) eye. At the time of diagnosis, the patient was admitted to the hospital and meticulously investigated for possible infectious and noninfectious causes to rule out other uveitic entities, but without any positive findings. At that time, his best-corrected visual acuity was 6/10. Slit-lamp examination yielded some vitreous cells in the left eye. Fundoscopy showed a few scattered pigmented chorioretinal scars and discrete yellowish round choroidal lesions throughout the left fundus (). Fluorescein angiogram delineated the active lesions as early hypofluorescent () with late staining. Left macular contour was normal on optical coherence tomography (OCT) examination (). He was started on oral prednisolone (64 mg) for 2 weeks with gradual tapering of 8 mg per week. Despite initial visual improvement, he experienced another episode of visual decline while taking 32 mg of prednisolone. His best-corrected visual acuity decreased to 2/10 and he had grade 4 vitreous haze according to the Miami grading. Fundus examination showed marked yellowish-white discoloration of the macula with some evidence of intraretinal hemorrhage ( and ). He was hospitalized and treated with pulse methylprednisolone 1 g (250 mg 4 times daily) for 3 days. Following pulse therapy, 64 mg oral prednisolone and 150 mg (50 mg 3 times daily) azathioprine were co-administered. Two weeks after the completion of pulse therapy, his visual acuity was still 2/10 despite a significant reduction in vitreous haze. Fluorescein angiogram and OCT demonstrated type 2 choroidal neovascularization (). Five intravitreal 2 mg aflibercept injections were given within a period of 8 months. His final visual acuity was 6/10 with a stable-looking macula ( and ) and he was continued on a treatment regimen of 150 mg azathioprine and 8 mg prednisolone daily. |
A 36-year-old healthy male presented to the Department of Periodontology, Faculty of Dental Sciences, Siksha 'O' Anusandhan University, for the treatment of severe GR in relation to the upper left first molar. On clinical examination, the patient had Miller Class III GR with the absence of keratinized gingiva of the offending tooth. The tooth presented with an attachment loss of 7 mm with no pocket. Grade III furcation involvement was present on mesial and the buccal aspect of the tooth []. The tooth was vital and nonmobile. Considering the tooth being nonmobile vital, with acceptable amount of bone support, and patient's willingness to save the tooth, it was decided to cover the GR in relation to left first maxillary molar using PBFP graft.\nPatient-signed informed consent was taken prior to the procedure. The phase I initial therapy of plaque control was carried out including proper oral hygiene instructions. The use of PBFP was planned to cover the tooth root and augment the final width of the keratinized mucosa coronal to the recession.\nAfter administering local anesthesia (2% lignocaine HCL with 1:200,000 epinephrine), a 2 cm horizontal incision was made at the highest point of the vestibule extending backward from above the upper left second molar tooth []. Blunt dissection was carried out through the buccinators and loose surrounding fascia by an artery forceps, which allowed the PBFP to be exposed into the mouth [].\nA full-thickness envelope flap was raised using a sulcular incision in the recipient site extending anteriorly up to canine tooth region. The recipient site was prepared, including thorough debridement of the teeth roots and furcation defect.\nThe body of the PBFP and the buccal extension were gently mobilized by blunt dissection, ensuring not to disrupt the delicate capsule and vascular plexus and to preserve the base as wide as possible. The PBFP was made to easily spread over the maxillary roots as far anteriorly as the premolar tooth region. The PBFP was adapted and secured tightly against the maxillary roots by use of resorbable vicryl sling sutures [].\nThe vascularized flap was advanced, secured, and immobilized to the buccal surface of the upper first molar and premolar teeth with the help of interrupted silk sutures ensuring the flap being free of tension []. The patient was given antibiotics and analgesics and was instructed to be on a soft diet. The patient was advised to refrain from toothbrushing in the treated area for 6 weeks and was instructed to rinse with chlorhexidine (0.12%) mouthwash twice daily for 2 weeks.\nPostoperative healing was uneventful. Loose ends of the sutures were removed after 14 days in order to speed up the healing process. Clinical healing was normal with neither infectious episodes nor untoward clinical symptoms. The patient was followed up till the end of the 6th month. In week 1, the color of PBFP changed to reddish pink. At the end of the 4th week, shrinkage of PBFP and discrete areas of epithelialization were seen on its surface.\nAn attachment gain of 6 mm was observed at the end of the 6th month with increased width of keratinized gingiva []. |
A 54-year-old male patient with Han nationality was presented in the Department of Urology of a tertiary hospital, because of a cyst in the right kidney. The cyst was found 5 years ago during a physical examination, and it was left untreated until recently it became obviously bigger. The patient reported a past history of hypertension for 2 years, whose highest record was 140/90 mmHg. He had taken bisoprolol 2.5 mg qd for treatment. No history of other disorders was reported.\nThe preoperation computed tomography (CT) showed that the middle and low pole of the right kidney had elliptical cystic which had low density with clear border and no enhancement. And there was also an adrenal nodular hyperplasia presented in the left adrenal (). And the patient also had a ++++ leukocyte esterase urinalysis result which equaled ≥500 WBC/mL. The diagnoses of the patient were 1) acquired renal cyst, 2) benign adrenal tumors, 3) hypertension, 4) urinary tract infection.\nThe patient undertook a selective operation during which surgeons performed a renal cyst incision with flexible ureteroscope. After general anesthesia, Storz ureteroscope was placed through the urethra. According to preoperative CT image localization, laser (1.0 J × 20 Hz) was used to incise the mucosal wall of the bulging collecting system. There were loose tissues and no clear cyst wall. Ultrasound-guided puncture of right kidney cyst was performed. The incision was about 1.5 cm without bleeding. Double-J tube and catheter were indwelled after the operation.\nAt postoperation day (POD) 2, patient suffered from abdominal distension and pain, with the drop of blood pressure and hemoglobin. Bedside color Doppler ultrasonography showed that a moderate echo mass was in front of psoas major muscle about 5 cm from the lower pole of right kidney. Renal artery embolization was performed successfully under local anesthesia, and renal artery branch hemorrhage was found during the operation ().\nThree days later (POD 5), the patient’s hemoglobin was 79 g/L. He suffered from tachycardia and atrial fibrillation. Four units of suspended red blood cell and 400 mL plasma were transfused. Since the symptom of cardiac and pulmonary insufficiency caused by abdominal distention, diaphragmatic elevation and compression of the lungs cannot be relieved, the patient undertook the removal of the retroperitoneal hematoma. After the operation, he was moved to intensify care unit (ICU).\nBecause of the renal artery hemorrhage and the damage of the right renal structure, the patient suffered from perirenal and retroperitoneal hematoma. The efficient drainage helped with the reducoin of the hematoma and suspected urinary fistula. Four times of CT results before and after the invasive operations are shown in . However, since the cyst incision operation, the inflammatory markers were high, which included body temperature, blood neutrophile granulocyte count (NEUT) and C-reaction protein, suggesting an infection statue of the patient ().\nThe steadily high levels of inflammatory markers necessitated anti-infective agents. The timeline of the invasive operations, symptoms and anti-infective medicine prescriptions is shown in . At POD 3–4, cefimazole was prescribed when the patient was in the urology ward. When he was moved to ICU, the drug was changed into cefoperazone/sulbactam for 3 days. Nevertheless, the cephalosporin prescripts seemed not helpful to his symptoms. At POD 8–17, meropenem and linezolid were used instead of cephalosporin. The symptoms and CT results gradually improved (). During these days, all the bacteria cultures of drainage and blood yielded a negative result. However, some pin-point colonies were detected on the Columbia blood agar (CBA) plate and chocolate agar (). The Gram stain failed to reveal any identifiable shapes of a typical bacterium. And the identity of the colonies could not be resolved with commonly used bacterial identification methods available in our laboratory. By the time, meropenem and linezolid seemed effective since his condition gradually improved though the infective pathogens were unknown. At POD 14, the drainage was sent for next-generation-sequencing (NGS). The result showed a M. hominis infection (, ), which was reported to the attending doctor at POD 17. The anti-infective agents were changed empirically to fosfomycin and levofloxacin. And the prescript was changed to azithromycin after the sensitivity test result was reported. It was kept the same until the inflammatory markers regained their normal levels and CT results showed this treatment was effective (). The patient was fully recovered and discharged at POD 39.\nAfter been discharged from the hospital, the patient was called to come back to do a CT scan as follow-up evaluation. He simply dismissed the requirement and did not come back so far.\nThe result of NGS showed that the most prominent pathogen was M. hominis which had the highest reads count and the estimated copy number and designed as M. hominis strain X (). The genomic sequence of the strain X was reconstructed. According to the sequence of strain X and the data download from NCBI BLAST, a phylogenetic tree was constructed with maximum likelihood method by MEGA 7.0. The phylogenetic tree used HF559394.1 Mycoplasma cynos C142 as outgroup. The closest strain to strain X was CP009652.1 M. hominis ATCC 27545 and CP011538.1 M. hominis strain sprout ().\nThe anti-infective drug sensitivity test was done with M. hominis IST (BioMerieux, France), which is a widely applied commercial Mycoplasma culture, detecting and drug sensitivity test kit with satisfying sensitivity and specificity,. The result is show in . And the strain X had resistance to quinolones, clarithromycin and erythromycin. The sensitivity to azithromycin was intermediate. |
A 71-year-old man with progressive angina was found to have severe stenosis in the circumflex artery and complex CTO of the left anterior descending artery (, Supplementary ). Coronary artery bypass surgery was offered to the patient but declined. He underwent uncomplicated stenting of the circumflex artery, followed by staged CTO recanalization of the LAD. A guidewire was passed relatively easily across the occlusion into the true lumen of the distal LAD beyond the bifurcation. Antegrade wiring of the diagonal artery was difficult. An epicardial collateral from the distal right coronary artery was used to access the diagonal branch retrograde, and this wire was steered into the antegrade guide catheter and externalized (). Both the LAD and diagonal were dilated with 3.0 mm noncompliant balloons. The diagonal was stented into the proximal LAD, and the distal LAD was rewired. The distal LAD was dilated through the stent struts to allow passage of stents into the distal LAD (Culotte technique). The distal LAD was stented using four everolimus drug-eluting stents. The stents were postdilated with 3.0 mm noncompliant balloons in the diagonal and distal LAD and 4.0 mm noncompliant balloon in the proximal LAD. Within the distal-most stent in the distal LAD, the balloon had a persistent waist until an inflation pressure of 12 ATM. At that point, the balloon suddenly expanded. Angiography revealed contrast filling of the right ventricle (RV), with the appearance of one or two focal jets of contrast extravasation at the location of the rigid lesion in the distal LAD, consistent with iatrogenic LAD-RV fistula (, Supplementary ). Of note, the flow beyond the stents in the distal LAD was not seen, likely due to shunt flow and “coronary steal.” The patient remained hemodynamically stable and was asymptomatic, and it was elected to manage the fistula conservatively. Serial echocardiograms revealed only trace pericardial effusion. He was discharged in stable condition.\nApproximately three weeks after the CTO procedure, the patient was presented to the emergency department with chest pain and dyspnea. He described several episodes of “tearing” sensation in the chest. Blood pressure and heart rate were 123/69 mmHg and 64 beats per minute, respectively. A 12-lead ECG revealed inferior T wave inversion. Troponin I was elevated to 0.06 ng/mL. Urgent coronary angiography was performed, which revealed patent stents in the proximal LAD and diagonal branch. LAD-RV fistula appeared relatively unchanged compared to during the CTO procedure (). The right coronary artery was normal and provided a very faint collateral to the apical LAD. Left ventriculography in the left anterior oblique projection revealed no evidence of a ventricular septal defect. The patient developed profound hypotension of unclear etiology during angiography. A right heart catheterization revealed normal filling pressures, normal cardiac output and ratio of pulmonic to systemic flow (Qp:Qs) 1.7. A transthoracic echocardiogram revealed preserved ejection fraction and normal left ventricular wall motion with turbulent flow signals at the LV and RV apex throughout the cardiac cycle (Supplementary ). There was no pericardial effusion. The patient was transferred to the cardiac intensive care unit in stable condition.\nHeart team evaluation was undertaken, and it was decided to perform coil embolization of the distal LAD. A standard 6 French left coronary guide catheter was used to advance a ProGreat (Terumo Medical Corp., Somerset, New Jersey) guidewire and 2.8 French catheter into the distal LAD. This was used to deploy two Ruby (Penumbra, Inc., Alameda, California) coils at the distal end of the stent.\nThere was still persistent shunt flow, so two Tornado (Cook Medical, Bloomington, Indiana) coils were subsequently deployed. Angiogram of the LAD confirmed complete cessation of flow into the distal LAD and absence of shunt flow (, Supplementary ). Hemodynamics postprocedure demonstrated a 20 mmHg increase in systolic blood pressure and normalization of Qp:Qs. A follow-up echocardiogram revealed the obliteration of apical shunt flow, normal left ventricular ejection fraction, and no left ventricular wall motion abnormalities. Creatine kinase eight-hour postprocedure was normal. The patient was discharged home in stable condition. At follow-up, one month later, the patient remained asymptomatic. |
Woman 52 year old with severe grade III APLD came in consultation. She was also aware of her familiar condition. Liver transplantation was offered to her in another center but she refused. Previous MRI from another center showed multiple giants cysts compromising the whole abdominal cavity. Cysts reached hypogastric area and both inferior quadrants. Higher segments of the liver seemed to be respected. Globulous deformation of the abdomen was clearly observed. Despite aesthetic and mild abdominal pain symptoms were not as significant as they were in her two sister so she did not want to underwent liver resection too. However she kept coming to consultation every six months.\nTwo years later she came back presenting jaundice with serum levels of FAL>1700 mg/dl. Bilirrubin 9,8/7,9 mg/dl. New MRI showed cyst compression of the hepatic pedicle including common bile duct and portal vein ( A and 3B)\nSurgery was soon programed and approach was discussed. We decided laparoscopic approach but being aware room will be very reduced even after pneumoperitoneum. We decided to start by performing aspiration and evacuation of the big lower and anterior cysts to intend reducing the mass and make new space for the laparoscopic procedure. By performing this gesture followed by several fenestration and partial cysts resections space was increased within the abdominal cavity so laparoscopic liver resection could be then performed. Once gallbladder was located, we then identified two cysts that seemed to be responsible for hepatic pedicle compression. Fenestration was done and, then, intra-operative cholangiogram showed no further compression of the common bile duct with adequate passage of contrast to duodenum. Standard cholecystectomy was completed and later laparoscopic left lateral sectionectomy was done in association with several more cyst fenestration. Post-operative course was un-eventful and patient was discharged at 6th day with decreasing levels of FAL and bilirubin. Late follow up imaging control are still to come. |
The case in question involves a 44-year-old male who sustained a crush injury to both lower extremities after being run over by a large utility vehicle. In the trauma bay, he was noted to have a degloving injury of the distal right lower extremity in combination with an open fracture and non-pulsatile bleeding. Biphasic pedal signals were identified bilaterally during resuscitation. Plain films revealed open displaced fractures to right metatarsals 2-4 and displaced right medial malleolar and tibial metaphysis fractures with a spiral fracture of the proximal fibula as shown in Figure . His MESS score was 6, and Gustilo-Anderson score was 3b, which are not predictive of needing amputation but do predict an elevated risk of complication. The patient did undergo computed tomography angiography (CTA) of the extremities, which showed three-vessel runoff to the level of the malleolus with a transection of the dorsalis pedis. The orthopedic surgery team took the patient to the operating room where he underwent debridement of nonviable tissues with reduction of the fractures and placement of a negative pressure wound therapy system. Postoperatively the patient’s extremity was warm with palpable dorsalis pedis pulse. During rounds on hospital day three, the patient was noted to have a cool and pulseless foot distal to the malleolus, which is suggestive of ischemia. Therefore, the patient was taken urgently to the operating room by trauma surgery service. His preoperative wound is shown in Figure .\nIn the operating room, the dorsalis pedis artery was exposed at the level of the ankle as identified by Doppler signals. This was exposed distally until a complete transection was identified 2 cm distal to the ankle. The distal portion was identified proximal to the webspace. Necrotic tissues were resected, and the vessel underwent embolectomy to restore brisk bleeding from the proximal segment before flushing and systemic heparinization. Distal greater saphenous vein was dissected, and an 8-cm segment was utilized to create a reversed interposition graft with spatulation of the ends. Fasciotomies were performed in the forefoot, and hematomas were evacuated from the compartments due to the presence of compartment syndrome. The wounds were packed with gauze, and, given the lack of nearby viable tissue for complete coverage, the exposed vessels and anastomosis were covered with IntegraTM (Integra LifeSciences, Princeton, NJ) before wrapping in bismuth-laden petroleum gauze and dry gauze. Postoperative images of the patient’s revascularized wound are shown in Figure .\nPostoperatively, the patient’s graft was maintained on a heparin infusion. His distal digits remained ischemic, but the patient had palpable pulses distally. Given the concern for continued ischemic insult with disruption of the microvasculature due to crush injury, the patient underwent hyperbaric therapy. Postoperative pictures of the wound are shown in Figure . Despite attempts to salvage the forefoot with continued hyperbaric therapy and serial debridement, the patient did require transmetatarsal amputation as shown in Figure on the 19th hospital day before and after IntegraTM placement. The residual foot (and ankle) has remained viable and functional. |
In June of 2017, a 23-year-old man with progressive back pain was presented to our hospital. In his history of present illness, the patient stated he has been experiencing a paroxysmal and severe back pain for approximately 2 months. The pain in his back could reach 7 points using visual analog scale (VAS) and could not be alleviated with rest and hot compresses. Initially, the patient attributed the pain to his overwork and thus did not seek medical attention. The patient denied experiencing any other constitutional symptoms. Upon further questioning, he denied history of any injury or underlying diseases. No pertinent family history was identified, including, hypertension, cancer, and congenital birth difficulties.\nOn physical examination, the patient showed pressure pain and percussion pain in his thoracic region, normal sensation to pin-prick and fine-touch of bilateral lower extremities and exhibited a 5/5 strength in bilateral lower extremities. Deep tendon reflexes revealed normal for both knee jerk and Achilles tendon reflexes bilaterally. Ataxia was absent. Cranial nerves, mini-mental, and the rest of the neurological exam showed no abnormalities. Routine laboratory tests were ordered, including electrolytes, liver and kidney function tests, tumor markers, and complete blood count. The results of the laboratory studies were almost within normal range. Preoperative assessments included electrocardiogram, echocardiogram, and chest X-ray. Plain radiographs of the spine showed an evident soft tissue mass sized 7.3 × 5.2 cm in thoracic spinal region penetrating into the right thoracic cavity and compressing lower lobe of the right lung (Fig. A and B). Chest enhanced computed tomography was performed to assess pleural involvement of the giant mass and revealed the density of soft tissue measuring 7.5 × 7.0 × 5.5 cm, obvious bony destruction in the left pedicle of T7, and pleural involvement caused by the thoracic mass. Spinal magnetic resonance imaging (MRI) was ordered to visualize the thoracic lesions, to assess the stability of the vertebral column and pleural involvement, and to aid in the formulation of the surgical approach. The internal multiple calcifications were observed on computed tomography (CT) scan, and the enhanced CT scan revealed that the solid part of the tumor was slightly enhanced (Fig. A–H). MRI of the thoracolumbar spine revealed widespread abnormal and irregular signals at T7 caused by the component of the mass, with increased marrow infiltration of the lateral vertebral body and the 7th rear rib, as well as mild bony destruction secondary to the epidural component of the large mass in the left T7 vertebral and paravertebral regions, which presented as a solid tumor (Fig. A–H). Tumor infiltrated through the T7 vertebral bodies into the right pedicles and posterior elements (Fig. A–H). Extraosseous spread into the right aspect of the epidural space extending posteriorly, resulting nerve root compression (Fig. A–H). Bone scintigraphy indicated the skeletal abnormality of right side of the T7 vertebrae and the right 7th posterior rib, with high suspicion of benign tumor (Fig. ).\nAfter a detailed assessment, posterior thoracic spinal canal decompression, complete tumor resection, pleural defect repair, and T4 to T10 internal fixation were performed to alleviate the symptoms caused by the giant tumor and subsequently stabilize the vertebral spine. Because of the size and location of the giant lesion and the extent of the involvement, the risk of surgical intervention is exceedingly high.\nAfter successful anesthesia, the patient was placed in a prone position for dorsal access to the thoracic spine. In brief, posterior circumferential decompression, tumor resection, and T4 to T10 internal fixation were performed. For the posterior approach, the paraspinal muscles were detached gently on each side after a midline longitudinal incision was made over the spinous processes from T4 to T10. The pedicle entry points were exposed by step-by-step bilateral dissection. At first, the pedicles of T4, T5, T9, T10, and the right pedicles of T7 were fixed by routine screw preparation and placement needles. C-arm fluoroscopy showed that the location of pedicles was accurate and the position was satisfactory. Then, the pedicle screws were placed bilaterally, followed by pedicle screw insertion. The heads and proximal region of the right 7th rib were exposed by dissection and resected. The tumor was located at the right paravertebral region of T7, involving the vertebral body and the right pedicle of T7. During the operation, the root of right 7th rib, the right transverse costal process joint, and the right paravertebral region were involved by the tumor. The tumor was oval in shape and hard in texture, sizing 7.5 × 7.0 × 5.5 cm (Fig. A and B). Moreover, the tumor invaded the parietal and visceral pleura and adhered to the adjacent pulmonary lobe. T6 to T8 spinous processes and interspinous ligaments were removed, then the right laminae of T6, T7, and T8 vertebrae were resected. Subsequently, the dural sac was exposed and protected. The proximal segments of the right 6, 7, 8, and 9 ribs were resected and the intercostal vessels and nerves were ligated. The transverse costal process joints and the right vertebral body of T7 were all resected. The tumor was then turned up and the adhesion of the tumor, the pleura, and the right lung was carefully separated. Finally, the giant tumor was completely removed. There was a partial pleural defect and a local air leak in the right lung, thus lung repair and visceral pleura repair were performed by a thoracic surgeon. There was no air leakage in the expansion process of the lung, and the repair was satisfactory. Because the patient did not exhibit hemodynamic instability to the placement of the pedicle screws, fixation using a screw-rod system was employed. Visual inspection using the intraoperative fluoroscopy showed optimal position of all pedicle screws. After spinal operation, 1 thoracic tube was placed between the 5th and 6th ribs of the right axillary midline, and closed drainage bottle was connected to the right thoracic cavity. The incision was closed. Intraoperative blood loss was approximately 2940 mL, thus we used erythrocyte 6 U and plasma 800 mL. Postoperatively, the patient was referred to the intensive care unit and transferred to general ward the next day. An x-ray after the surgery confirmed the correct positioning of the implants and no signs of displacement of the screws and rods (Fig. A and B). The postoperative pathology report confirmed a BFH with negative margin. Pathological result was positive for CD68 indicating epithelial origin. Biopsy samples were positive for S-100, smooth muscle actin (SMA), with 1% Ki-67 positive nuclei (Fig. A–I).\nOne week after the operation, the VAS score of his back pain improved to 0-1 points compared to the preoperative status, 7 points. Following wound healing and removal of thoracic drainage tube, the patient underwent rehabilitation therapy and was monitored as an outpatient. The postoperative 2-year follow-up visit showed no tumor progression and no new symptoms. |
A 70-year-old female patient was scheduled for abdominal aortic aneurysm resection and reconstruction. She had undergone general anesthesia for surgery of purulent cervical spondylitis about 6 years ago without any adverse event. The height of the patient was 142 cm, and the weight was 54 kg.\nA catheter was inserted into the thoracic vertebrae 9–10 epidural interspace to enable analgesia prior to sedation using propofol. Anesthesia was induced with continuously injected remifentanil at a rate of 0.15–0.3 mg/kg/h, and propofol was started intravenously at a target plasma concentration of 3 μg/ml using a target-controlled infusion (TCI) pump, followed by 40 mg of rocuronium bromide for endotracheal intubation. Anesthesia was maintained with 70% nitrous oxide, 30% oxygen, and propofol continuously injected at a target plasma concentration of 1–2 μg/ml.\nThe abdominal aortic aneurysm, which measured 4.9 cm in diameter, was observed from the infrarenal artery to the level of bifurcation of the inferior mesenteric artery (IMA), while the renal artery and iliac artery were not clamped. The peripheral anastomosis to the aorta was possible above the IMA. The operation time was extended significantly beyond the scheduled time in order to control bleeding due to a lumbar vein injury, and the anesthesia lasted 5 h 38 min. Total blood loss was 3424 ml, 1159 ml in the blood loss was returned by the autologous blood collection device, and 6 units of red cell concentrates mannitol-adenine-phosphate were used. However, abdominal aortic aneurysm resection and reconstruction were performed routinely, and the patient’s hemodynamic condition was stable throughout the anesthesia course. We confirmed adequate arousal after the surgery, and the endotracheal tube was removed in the operating room, after which the patient was transferred to the recovery room.\nOn the second post-operative day, oliguria was prolonged, and her respiratory frequency exceeded 45 times with respiratory distress appearing due to pulmonary edema. Therefore, we decided that re-intubation and a ventilator were necessary, and propofol was used for sedation. Prior to endotracheal intubation, 30 mg of propofol was injected, and sedation was maintained with propofol at a rate of 50 mg/h using an infusion pump instead of a TCI pump.\nFrom the following day, a fever of 39.7 °C and a decrease in blood pressure appeared. Blood tests showed that platelets had dropped to 26,000/μl, and creatinine phosphokinase (CPK) had risen to 57220 U/l. A blood gas analysis during propofol infusion showed pH 7.40, PCO2 23.4 mmHg, HCO3 14.2 mmol/L, base excess − 9.0 mmol/L, anion gap 22.0 mmol/L, and lactate 1.5 mmol/L. No significant elevation of lactate or acidosis was observed. Metabolic acidosis may have been compensated by mechanical ventilation (Table ).\nWe suspected intestinal ischemia and severe infection, and immediately started treatment for disseminated intravascular coagulation, stopping using epidural anesthesia. Colonoscopy revealed mild ulcers but no intestinal necrosis, myocardial infarction was denied from echocardiographic findings, and skeletal muscle necrosis was negative according to clinical findings. Thereafter, a fever of 41.1 °C and high CPK persisted, and her hemodynamics were disrupted, so we finally stopped propofol infusion to maintain her blood pressure. Continuous hemodiafiltration (CHDF) was started for the oliguria due to deterioration of the renal function.\nFrom the day after the propofol infusion was stopped, the fever decreased to 36.8 °C, CPK started to decease, and the hemodynamics improved dramatically (Fig. ). Two weeks later, her respiratory condition improved, and the ventilator was able to be removed. The urine volume and renal function had been stable, and hemodialysis was able to be discontinued. However, the patient suffered from prolonged consciousness disorder. Neither computed tomography (CT) nor magnetic resonance imaging (MRI) of the brain revealed any particular lesions causing prolong consciousness disorder other than a small area of cerebral infarction in the subacute phase. Concerning the continuation of consciousness disorder, an electroencephalogram was conducted, which suggested the possibility of seizures; however, the details were unclear. After two more weeks, the level of consciousness gradually improved, and speech and spontaneous movement became apparent.\nAfter normalization of CPK and improvement of the general condition, re-examinations were performed, including CT and MRI; however, no disease other than PRIS causing an increase in CPK or a disruption of hemodynamics was suspected. Immediately after the injection of propofol was stopped, her condition improved, which eventually prompted our diagnosis.\nTen months after the operation, the patient’s communication level had improved, but hemiplegia remained due to cerebral infarction and muscle weakness due to disuse, so she was transferred to a rehabilitation hospital for functional recovery. |
A 34 year-old woman with no history of diabetes presented to her local ER in March 2015 with chest pain. Family history was negative for diabetes. A chest X-ray revealed a left lung mass confirmed on subsequent chest CT to be a left upper lobe mass measuring 5.2 × 3.7 × 3.8 cm with left hilar and AP window lymphadenopathy. A bone scan on 3/19/15 was negative for osseous metastases. She underwent bronchoscopy with sampling of the level 4 L, 7 and 11 L lymph node stations. Samples from stations 7 and 4 L were negative for malignancy, but the 11 L station contained tumor cells consistent with high grade adenocarcinoma. A full body staging PET-CT revealed significant FDG avidity in the primary tumor and the left hilar and AP window nodes, without evidence of distant metastatic disease. A brain MRI on 3/31/15 did not reveal metastatic disease. She underwent a staging mediastinoscopy and bronchoscopy, with a total of 19 nodes sampled from 4R, 4 L and 7 lymph node stations, all negative for malignancy. The patient subsequently underwent treatment with concurrent chemotherapy and radiation therapy for unresectable stage IIIA NSCLC (carboplatin and pemetrexed – 4 cycles, given every 3 weeks from April 2015–June 2015). Follow-up CT imaging on 11/3/15 revealed treatment response in the thorax and a new soft tissue lesion near the right acetabulum concerning for a metastatic implant (1.8 × 2.3 cm). A CT guided biopsy of the right gluteal mass revealed metastatic adenocarcinoma. Molecular testing of the metastatic gluteal lesion identified a TP53 mutation, however, activating EGFR, ALK and ROS1 mutations were not present. A restaging PET-CT scan and brain MRI obtained December 2015 showed the metastasis to the right gluteal region as the only active disease site. The patient subsequently opted for systemic therapy with nivolumab. She received her first treatment with nivolumab 170 mg (3 mg/kg) on 12/14/15 and a second dose on 12/28/15, with no acute complications.\nTwo weeks after the second nivolumab treatment, the patient presented to a local ER with abdominal pain, nausea and weakness progressively worsening over 3 days. Laboratory evaluation revealed diabetic ketoacidosis (DKA), with a plasma glucose 739 mg/dL, venous pH of 7.12, CO2 11, AG 30, and urine ketones > 80 mg/dL. She was admitted to the ICU for IV fluids, continuous insulin infusion and frequent lab monitoring. A hemoglobin A1c level on 1/12/16 was 7.1% (normal range 4.6–6.1%). C-peptide levels on 1/16/16 (while BG 377 mg/dL) and 1/18/16 (while BG 423 mg/dL), were < 0.1 ng/mL (normal range 0.8–3.85). Further evaluation to establish the diagnosis of autoimmune diabetes (Type 1), provided the following results: glutamic acid decarboxylase 65 (GAD-65) antibody > 30 U/ml (normal < 1.0); tyrosine phosphatase islet 2 antibody (IA-2) 6.1 U/ml (normal < 0.8); insulin autoantibody (IAA) 0.4 U/ml (normal < 0.4). HLA genotyping was homozygous for A30 and DR9. (Table ) Other endocrine testing showed: normal hypothalamic-pituitary-adrenal function with morning ACTH 24 pg/mL (normal 6–50) and cortisol 10 ug/dL (normal 6.7–22.6); subclinical hyperthyroidism with slightly suppressed TSH 0.21 uIU/mL (normal 0.34–5.6), FT4 1.41 ng/dL (normal 0.58–1.64). Thyroid stimulating immunoglobulins and thyroid autoantibodies obtained after hospitalization were negative.\nDue to the rare development of autoimmune diabetes in this patient, we obtained consent to retrieve and test a small amount of serum previously collected prior to therapy with nivolumab and the onset of autoimmune diabetes. The frozen specimen was tested for diabetes related autoantibodies with the following results: GAD65 Ab > 250 IU/ml (normal < 5.0); IA- 2 Ab 6.2 U/ml (normal < 0.8); IAA < 0.4 U/ml (normal < 0.4); zinc transporter isoform 8 (ZnT8) antibody 64 U/mL (normal <15). Interestingly, three of the four diabetes related autoantibodies were positive 8 months prior to the initiation of treatment with nivolumab and before the onset of diabetes. ZnT8 Ab measured 13 months after diagnosis of diabetes had decreased below the cutoff for positivity (<15) (Table ).\nGlycemic control proved challenging with severe instability of glucose and frequent and unpredictable hypoglycemic and/or ketoacidosis episodes. Over the course of 11 days, the patient’s glucose was gradually controlled with a basal-bolus insulin regimen recommended by endocrinology, and the patient was discharged. Unfortunately the patient had multiple re-admissions due to hyperglycemia and DKA over the ensuing month, ultimately requiring placement of an insulin pump. Despite intensive visits with her endocrinologist and diabetes educators, the patient found the insulin pump too difficult to use, eventually discontinuing it and resuming multiple daily injections. While she continues to have erratic blood sugars with frequent hypoglycemia and hyperglycemia, she has become more adept at managing her diabetes and has not been hospitalized for her diabetes. The current plan is to try to obtain a continuous glucose monitor to help manage the extreme glucose variability.\nAt the time of follow up with medical oncology in March 2016, the patient was clinically improved with near resolution of pain in the right gluteal region. Re-staging CT Chest/Abdomen/Pelvis with contrast in April 2016 revealed a significant treatment response, with decrease in the size of the primary left upper lobe mass and resolution of the gluteal mass. Given these results, her treatment holiday was continued. Re-staging CT scans in October 2016 revealed no definite evidence of disease. At the time of initial manuscript preparation, she is feeling well, on no antineoplastic therapy. |
A-56-year old Hispanic female with idiopathic pulmonary arterial hypertension (PAH) for 13 years was stable (WHO class II) on subcutaneous treprostinil for 8 years. In 1999, diagnostic right heart catheterization had shown elevated right atrial (mean 20 mmHg) and pulmonary artery (PA) pressure (145/42 mmHg) with normal pulmonary capillary wedge pressure (10 mmHg). The patient began complaining of fatigue, lethargy, and dyspnea on minimal exertion in January 2007 and was admitted in February for syncope, anorexia, abdominal pain, jaundice, and decreasing urine output. An echocardiogram revealed right ventricular hypertrophy with severe tricuspid regurgitation (TR) and preserved right ventricular (RV) systolic function. In May 2007 she was admitted to an outside hospital for persistent symptoms and resistant volume overload. Physical examination demonstrated jaundice, ascites, and right heart failure. Her jugular venous pressure was 18 cm H2O. A systolic RV heave was present. There was a 3/6 holosystolic murmur at the left sternal border, a loud pulmonary component of the second heart sound and an RV S4 gallop. The patient was moderately hypotensive (systolic blood pressure of 80 mmHg), and room air oxygen saturation was 93%. An echocardiogram demonstrated severe TR with a flail anterior leaflet (), which was not previously noted. Estimated PA pressure had fallen to 2/3 of systemic (). M-mode echocardiography demonstrated diastolic leftward septal motion consistent with RV volume overload (). RV systolic function was unchanged, and there was no TV annular dilation.\nRetrospective review of hepatic function aroused suspicion for acute decompensated RV failure with congestive hepatopathy occurring several months earlier, possibly related to the flail tricuspid leaflet. Upon review of an echocardiogram performed three months prior, the flail tricuspid leaflet was indeed found to be present. Because of the temporal relationship between the severe TR and worsening symptoms as well as RV failure and hepatic dysfunction despite preserved RV systolic function, it was felt that tricuspid valve (TV) failure alone could explain the patient's symptoms and that TV repair or replacement might benefit the patient.\nThe patient was continued on subcutaneous treprostinil (46 ng/kg/min) and treated with diuretics and digoxin then transferred to our institution for evaluation for possible lung transplant and/or TV surgery. Repeat right heart catheterization demonstrated elevated right atrial pressures (V = 35 mmHg, mean = 21 mmHg), moderately elevated PA pressure (64/29 mmHg), pulmonary capillary wedge pressure at upper limits of normal (mean 16 mmHg), decreased cardiac index by thermodilution (1.7 L/min/m2), and elevated pulmonary vascular resistance (7.1 Wood Units). Chest CT demonstrated marked dilation of the main and proximal branch pulmonary arteries with mural calcification and a moderate pericardial effusion. Ventilation/perfusion scan showed low probability for thromboembolism. Laboratories showed platelet count of 58000/μL, total bilirubin of 3.3 mg/dL, serum creatinine of 1.2 mg/dL, and albumin of 3.1 g/dL. Repeat echocardiogram with agitated saline demonstrated excellent biventricular systolic function, absence of tricuspid annular dilation, and late (>5 cycles) right-to-left shunting suggesting a pulmonary right-to-left shunt. The patient received empiric steroids for possible idiopathic thrombocytopenic purpura after other etiologies were excluded, with improvement of her platelet counts. The patient also developed recurrent atrial flutter.\nBecause of her hyperbilirubinemia and thrombocytopenia, she was felt to be a poor candidate for lung transplantation. It was concluded that without TV surgery, the patient's long-term outcome would be poor and that surgery was indicated. The recommendation was buttressed by the presence of normal RV systolic function with normal TV tissue Doppler systolic annular velocity () and the abrupt clinical deterioration suggesting sudden disruption of valve integrity leading to poorly tolerated severe TR. The patient was presented with the option of high-risk surgical intervention and consented to TV surgery.\nTwo weeks later the patient underwent TV replacement. Treprostinil was held immediately prior to surgery. Intraoperative inspection of the TV revealed ruptured chordae with a flail, prolapsing anterior leaflet, and normal annular size. A patent foramen ovale was not present. Valve repair was not performed due to friability of the subvalvular apparatus and concern regarding longevity of repair given her pulmonary hypertension. A stented 27 mm Magna (Edwards Life Sciences) bioprosthesis was selected for TV replacement. Right atrial MAZE cryoablation and ligation of the left atrial appendage were also performed. PA systolic pressure increased to 90 mmHg postvalve replacement (preintervention baseline 65 mmHg). The patient was successfully weaned from cardiopulmonary bypass on intravenous epinephrine, dopamine, milrinone, inhaled nitric oxide (40 parts per million), and intravenous prostacyclin (20 ng/kg/min). Total cardiopulmonary bypass time was 106 minutes, and aortic cross-clamp time was 81 minutes.\nCatheterization on postoperative day 1 demonstrated PA pressure of 90/32 mmHg and improved cardiac index of 2.7 L/min/m2 and a pulmonary vascular resistance of 6.7 Wood units. Repeat echo demonstrated decreased RV size, normal systolic function, and mild high pressure TR. She was extubated on postoperative day 4 and discharged from the intensive care unit 10 days postoperatively. She was transitioned from intravenous prostacyclin to subcutaneous treprostinil (20 ng/kg/min) and oral sildenafil (20 mg twice daily). She was discharged on postoperative day 15 on the above medications as well as digoxin, prednisone, spironolactone, bosentan, and furosemide. She was seen in clinic three months postoperatively and had returned to her baseline functional status (WHO class II). The jaundice, ascites, hypoalbuminemia, RV failure, and liver abnormalities had resolved. |
A 2-year-old Japanese boy was hospitalised with a 2-day history of fever and neck swelling. He had visited a nearby hospital the previous day and had been prescribed clarithromycin. However, the neck swelling increased rapidly, and he was referred to our hospital. On admission, his temperature was 37.5°C and blood pressure was 118/80 mmHg. Physical examination revealed bilateral tonsillitis and swelling of the left posterior pharyngeal wall, and a mildly tender soft mass on his left posterior neck. Laboratory tests revealed a white blood cell count of 14,840 cells/μL and C-reactive protein level of 1.70 mg/dL. Emergency neck computed tomography (CT) angiography showed an enhanced abscess cavity posterior to the left retropharyngeal space, and a low-density area surrounded by an area without contrast enhancement in the posterior neck (Figure ). The latter was suspected to be a deep neck infection secondary to the retropharyngeal abscess. Based on these findings, we performed surgical incision and drainage under general anaesthesia. After induction of anaesthesia, we used a gag to hold the mouth open, and examined the patient’s oral cavity to locate the exact site of swelling in the left posterior pharyngeal wall (Figure ). After aspirating 1 mL of purulent fluid by needle puncture, we made an incision over the abscess and washed the abscess cavity with physiological saline. Culture of the abscess fluid was positive for penicillin-resistant Streptococcus pneumoniae (PRSP). We also percutaneously punctured the mass on the posterior neck, and drained approximately 10 mL of clear yellowish lymph, but no pus. Rapid cytology showed that this fluid contained mostly protein-like substances and lymphocytes. The mass was no longer palpable after drainage, and no further surgery was performed. The patient was placed under observation with postoperative administration of meropenem (450 mg) and clindamycin (150 mg). On postoperative day 3, his laboratory test results showed improvement, and the antibiotic therapy was changed to ceftriaxone sodium hydrate (700 mg) based on the sensitivities of the cultured organisms. There were signs of improvement in the pharynx, but the mass on the posterior neck had recurred. Repeat neck CT angiography showed a low-density area in the posterior neck, and signs of improvement in the posterior pharyngeal wall. Subsequent magnetic resonance imaging (MRI) angiography showed an area with low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, and an area of low signal intensity surrounded by an area of high signal intensity on post-gadolinium images (Figure ). The lesion in the posterior neck was diagnosed as a cystic lymphangioma based on the MRI findings and the results of the needle-puncture biopsy culture. Although repeat CT on postoperative day 7 showed slight asymmetry between the left and right retropharyngeal spaces, the patient was discharged as there was no observable asymmetry of the posterior pharyngeal wall, and the posterior neck mass continued to decrease in size. He was followed up at our outpatient clinic for a year, and there was no recurrence of the lymphangioma during that time. |
A 22-year-old woman was admitted to our hospital with a history of intermittent colicky right hypochondrial pain not relieved by any medications for the past 3 months. Initially, she was given proton pump inhibitors, but her pain was not relieved. She had no other symptoms. Her past medical and family histories were not significant. The result of her clinical examination was normal. Upper gastrointestinal (GI) endoscopy showed globular swelling at the medial wall of D2 (Fig. ). The ampulla was situated at the summit of swelling.\nComputed tomography (CT) with oral contrast agent showed dilation of the intramural part of the common bile duct (CBD). A cyst of size 2.4 × 2.3 cm was noted in the second part of the duodenum (Fig. ). On the basis of the above findings, it was reported as type 3 choledochal cyst. The patient was further investigated with magnetic resonance imaging, which showed dilation of the intramural part of the distal CBD. A 2.4 × 2.3 cm cyst was noted in the ampullary region, again consistent with a type 3 choledochal cyst (Fig. ). Then the patient was planned for endotherapy, but owing to difficulty, it could not be negotiated into the ampulla. Finally, the patient was referred to the surgical gastroenterology department for operative management. After multidisciplinary team discussion, an abdominal ultrasonogram (USG) was done, which showed a clear thick wall cyst measuring 4.6 × 2.6 cm between the second part of the duodenum and the head of the pancreas with gut signature (Fig. ). Opening of the CBD into the duodenum was seen just distal to the cystic lesion. There was active peristalsis noted all around the cyst, suggestive of duodenal duplication cyst.\nAfter the diagnosis was confirmed, the patient was taken for elective laparotomy. Intraoperative findings were a 5 × 3-cm cyst over the medial wall of the duodenum extending proximal and distal to the ampulla and displacing it posteriorly (Fig. ). The cyst was communicating with the ampulla by a small opening in its medial wall (Fig. ). So, cyst secretions were drained via the ampulla, which avoided retention of cystic fluid. Part of the cyst wall was shared with duodenal musculature. Upon needle aspiration, the cyst wall contained bile due to communication with the ampulla. The duodenum was Kocherized, and a longitudinal duodenotomy was made for about 5 cm. Partial excision of the cyst was done (Fig. ) because it was closely associated with the ampulla. Marsupialization of the remaining cyst wall was done. The duodenotomy was closed horizontally. Feeding jejunostomy (FJ) was done using a modified Witzel method. A flank drain was kept in place. The postoperative period was uneventful. The patient was started on oral medications on the third day after surgery. The FJ tube was removed after 6 weeks. Histopathology showed the cyst wall was lined by duodenal mucosal epithelium with focal areas of ulceration and composed of tall columnar cells with goblet cells on either side of a common (shared) muscular layer. The submucosa showed lymphoid aggregates with Brunner glands. The common muscular layer showed congested vessels. Histopathological features were suggestive of duodenal duplication cyst (Fig. ). At her 9-month follow-up visit, the patient had no complaints. |
A 49-year-old woman presented with breathlessness on exertion with gradual onset over the previous one month; there was no other significant past medical history. Cardiac and respiratory examinations were normal, and the 12-lead electrocardiogram (ECG) was inconspicuous. Two-dimensional echocardiography showed an anomalous left main coronary artery (LMCA) arising from the main pulmonary artery (MPA), moderate left ventricular dysfunction, an ejection fraction of 40%, and mild mitral regurgitation. The coronary angiogram revealed anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA). Multislice computed tomography (CT) coronary angiography revealed an ALCAPA from the posterior wall of the MPA, which bifurcated into the left anterior descending (LAD) artery and the left circumflex artery. The right coronary artery (RCA) was tortuous, dilated, and a rising from the aorta (). The patient was otherwise healthy and had an uneventful life history (from childhood to adulthood), without any evidence of arrhythmic or syncopal attacks.\nThe patient underwent coronary artery bypass grafting (CABG) with closure of the LMCA opening from inside the MPA. Surgery was performed with both invasive arterial and pulmonary artery pressure monitoring. After sternotomy and opening of the pericardium, we observed the RCA arising from the aorta, which was hugely dilated, tortuous, and the LMCA was arising from the lateral aspect of the MPA ( ). It was not possible to mobilize the LMCA for reimplantation to the aorta, therefore we planned a CABG with closure of the left main orifice of the LMCA. The left internal mammary artery (LIMA) was harvested and cardiopulmonary bypass (CPB) was established with right atrial and aortic cannulation. After aortic cross clamping, cardioplegia was given by two methods: root cardioplegia was given in the aorta for the RCA and followed by left main ostial cardioplegia after opening the MPA ( ). The LIMA was grafted to the LAD and the reversed saphenous vein was grafted to the second obtuse marginal artery. The left main ostium was closed with 6-0 Prolene sutures from inside the MPA. Aortic cross clamp was released, CABG completed, the patient was weaned from CPB, and the chest was closed. The patient was transferred to the intensive care unit with minimal inotropes, stable hemodynamics, and an isoelectric ECG. Extubation occurred on the morning of the next day (postoperative day 1). On postoperative day 2, the patient had atrial fibrillation with a fast ventricular rate, which required amiodarone infusion, oral beta-blockers, and oral digoxin for rate control. After 72 hours (i.e., postoperative day 5), the patient converted to normal sinus rhythm and was maintained with oral amiodarone and beta-blockers. On postoperative day 8, a CT coronary angiogram was performed, which showed blood flowing through the bypass grafts and no communication between the MPA and LMCA (). |
We present a 75-year-old white female with refractory CML, diagnosed in 2004, who has gone through multiple BCR/ABL inhibitors, namely imatinib, nilotinib, and dasatinib, currently on bosutinib 300 mg daily for 5 years who has achieved hematological remission but has never achieved complete molecular response (CMR).\nThe patient was found to have elevated white blood cell (WBC) count in June of 2004. Subsequent bone marrow aspirate and biopsy were diagnostic for CML. Therapy was initiated with imatinib and was effective until 2007 when her WBC count started to rise again. She was then started on nilotinib 400 mg, to which she responded but again subsequently regressed, with her WBC count going from 13,500 to 40,000/mL. Dasatinib was started, which the patient did not tolerate, and was stopped after 1 month due to cardiac symptoms which the patient described as her heart feeling like it was going to “flop out.” At this point in time, she was placed on interferon-α, but it was stopped due to side effects.\nShe was seen by our center in 2012 and had recently been placed back on imatinib 800 mg, which was subsequently lowered to 600 mg a day, as well as hydroxyurea. A bone marrow biopsy done in January of 2012 showed chronic-phase CML. Until then, no mutational analysis had been done to evaluate her drug resistance to TKIs. At this time, she also developed pericardial and pleural infusion, most likely from imatinib, and underwent a pericardial window placement in the same month.\nFollow-up with mutational analysis was negative, and it was decided to retry dasatinib, as she had progressed through imatinib and nilotinib. Dasatinib 50 mg daily was started with close monitoring and plans to use pulse steroids and diuresis if fluid buildup should develop. She developed a cough relieved by steroids with no effusions present. In March 2013, she was tolerating dasatinib, and her dose was increased to 50/100 mg every other day. BCR/ABL PCR done at this time was 31.83%. BCR/ABL continued to be stable, but no decline in levels was noted. Bone marrow biopsy in May 2013 was negative for BCR/ABL, but the PCR was still concerning. It was decided to try a course of ponatinib at 15 mg daily. After initiation of therapy, she had a decrease in her platelet counts. She was switched to bosutinib in January 2014 due to ponatinib being taken off the market. After the switch to bosutinib, her BCR/ABL clones once again started to increase. A switch back to dasatinib was offered, but the patient was reluctant, and it was decided to continue on bosutinib.\nAt this point, it was decided not to monitor her BCR/ABL levels as she was not a transplant candidate. The focus was on hematological remission alone. Since that time, the patient's only major complaint with bosutinib has been some bouts of diarrhea, and even this has mainly been when dosage increase was attempted. BCR/ABL levels rose from 44% in 2015 to 65% in February of 2016. Kinase domain mutation analysis was negative again. BCR/ABL decreased from 65 to 52.3% in May 2016. At this time, her bosutinib was increased from 300 to 500 mg every day due to another rise in BCR/ABL. This elevated dose caused an increase in diarrhea, and it was dropped down to 300 mg as it was previously. Since that time in 2016, her BCR/ABL waxed and waned, but she continued in hematological remission. Currently, she is still on bosutinib 300 mg daily with plans to add interferon-α if disease progression is observed. |
A 35-year-old pregnant woman (G2P1), at 33 weeks of gestation, presented to the emergency department of our hospital reporting fluid leakage from the vagina. Her pregnancy so far was low risk. She was not on any regular medications, did not have any known allergies, and was a nonsmoker. Vaginal speculum examination revealed amniotic fluid leakage from the cervical os, and a diagnosis of preterm rupture of membranes was made.\nA transabdominal ultrasound examination revealed a normally grown fetus. Polyhydramnios was noted, with the deepest vertical pool measuring 10 cm. In addition, we noted small bowel dilatation, with a maximum diameter of 25 mm (Figure ). These findings were compatible with fetal jejunal atresia. Detailed ultrasound examination demonstrated no other fetal malformations. A nuchal translucency scan at 12 weeks had shown a low risk for chromosomal abnormalities, and the anomaly scan at 22 weeks was normal.\nThe parents were counseled in detail about the diagnosis of fetal intestine atresia, the possible association with other abnormalities, and the postnatal management and prognosis. An amniocentesis was offered at 33+1 weeks for the exclusion of chromosomal abnormalities, and the parents were also tested for cystic fibrosis. The procedure was performed the following day at 33+2 weeks, and the results (karyotype, array-based comparative genomic hybridization [CGH]) were normal.\nAt 34+5 weeks of gestation, she delivered a female neonate (2,680 g) by cesarean section because of initiation of labor with a history of a previous cesarean section. After birth, the neonate was examined by an expert neonatologist who found a mild abdominal distention with palpable distended loops of bowel. Appropriate medical treatment and parenteral nutrition were started the same day. The newborn underwent X-ray imaging according to the instructions of the neonatal team, and the following surgical management confirmed the diagnosis of jejunal atresia (Figure ). Multiple atresias were found in approximately 70 cm of the jejunal. Following the confirmation of diagnosis, the entire section of the small bowel was resected and end-to-end anastomosis was performed. The condition of the infant after the operation was excellent and she was discharged after three weeks. |
We present a 56-year-old white male presenting with a history of acute myocardial infarction with high tobacco and alcohol consumption. The patient refers to risky sexual behaviors, but no use of IV drugs. He went to an ophthalmology consultation because of a progressive decrease in visual acuity (VA) of the right eye (RE), in the last few months, without pain or inflammatory signs. Fundoscopy revealed dispersed preretinal hemorrhage and yellowish exudates. CMV retinitis was established as the main diagnostic hypothesis in the context of a possible HIV infection. HIV serology was requested, and a positive result was found. The patient was referred for an Internal Medicine consultation. While waiting for an appointment, he presented a rapidly progressive worsening of his VA and resorted to the Emergency department. Upon observation, he maintained alterations in the retinography of the RE, with worsening of pre-retinal hemorrhage and yellowish exudates, with no other findings (Figure ). The left eye was not affected (Figure ).\nHe was admitted to the Internal Medicine department, assuming the diagnostic hypothesis of CMV retinitis as the first manifestation of HIV infection and starting IV ganciclovir empirically.\nAn etiological study was performed, showing positive CMV serology for acute infection with positive IgM and IgG and confirmation of HIV type 1 infection by the western blot technique, with a viral load of 13076 copies/mL and decreased CD4+ T lymphocytes (155cel/μL). Confirmed CMV and HIV-1 infection, with criteria of AIDS, in stage C, according to the classification proposed by CDC Atlanta for patients infected with HIV. He started HAART with tenofovir, emtricitabine and efavirenz, and Pneumocystis jirovecii pneumonia prophylaxis. Other opportunistic infections, as well as manifestations of CMV infection in other organs, were ruled out. The sexual partner's HIV infection was excluded. The patient was discharged maintaining the therapy mentioned above.\nFollow-up consultation revealed good therapeutic adherence, with the slow recovery of lymphocyte populations and a sustained decrease in viral load.\nOphthalmology follow-up one month after treatment showed an improvement in retinal bleeding and exudates. Two months later, the retinography (Figure ) and the widefield retinography (Figure ) show a total resolution of bleeding and exudates but no full VA recovery was achieved due to chronic vitritis and tractional retinal detachment. Vitrectomy was not indicated at the moment by the ophthalmology department due to necrosis and tractional detachment.\nThree months Internal Medicine follow-up shows clear immunological improvement with T lymphocytes CD4+ 333 cel/µL and viral load 96 copies/mL. Pneumocystis jirovecii pneumonia prophylaxis was discontinued, maintaining HAART, valciclovir, and serial ophthalmology follow-ups. |
A 71-year-old man presented with a several-month history of reproducible transient dizziness on leftward head rotation, with no neurological deficit, thus indicative of BHS. Magnetic resonance angiography (MRA) showed no pathological abnormality; he exhibited bilateral VAs merging into the basilar artery, and the left VA was dominant (). However, digital subtraction angiography (DSA) showed variants of the bilateral vertebral arteries; the right PICA originated from the right VA at the atlas–axis level and ran vertically into the spinal canal (), whereas the left VA ran into the spinal canal at the atlas–axis level without passing through the atlas' foramen transversarium (). Leftward head rotation at 45° did not induce dizziness, but dynamic DSA showed stenosis of the right VA at the level of the axis (). At 60° head rotation, which induced dizziness, occlusion of the right PICA was revealed (). Computed tomography angiography (CTA) on leftward head rotation showed that the PICA was severely compressed in the narrow space surrounded by the atlas and axis, and that the right VA was compressed at the axis level (). Notably, the occipital articular facet did not shift during the head rotation, which was compensated by atlantoaxial hyper-rotation in the form of atlantoaxial rotary subluxation. Thereafter, the extracranial PICA, together with the C2 nerve root and perivascular venous plexus, ran through a narrow tunnel surrounded by bone components of atlas and axis during head rotation. The compression of the PICA was mainly considered responsible for causing the BHS in the patient. However, the concomitant VA stenosis may have resulted in poor blood supply into the PICA.\nThe dizziness was restrictive to the patient's daily activities; therefore, he underwent surgery to decompress the right PICA and VA via a posterior approach (). A 6-cm linear skin incision was made on the back of the neck, with 3 cm laterally to the right at the level of the axis–atlas. The posterior arch of the atlas was identified following dissection between the splenius capitis and semispinalis capitis muscles. Posterior cervical muscles were preserved, including the ones originating from the atlas and axis. The right VA was identified by Doppler on the cranial side of the atlas's arch. The posterior wall of the atlas transverse foramen was removed, and the VA was dissected from the canal of transverse foramen and surrounding connective tissues, enabling the VA to shift posteriorly. Bleeding from the venous plexus was controlled by bipolar coagulation with an oxidized cellulose-based hemostatic sheet. Following resection of the right posterior arch from the transverse foramen to the spinal canal, the PICA in the C2 root sheath was identified by Doppler. By opening the sheath, the intra-sheath PICA was identified running in parallel with the C2 nerve root, and it was dissected to be totally free between the VA and dural sac. There was no fibrous band compressing the PICA.\nThe postoperative course was uneventful. The patient had no dizziness during head rotation, thereby freeing him from the dizziness-associated life restriction. On postoperative MRA at 60° leftward head rotation, compression of the right VA and PICA had disappeared (). BHS did not recur without any thrombotic therapy for 3 months after the surgery. |
The second patient was a 69-year-old woman involved in a high speed car crash where she was rear ended and pushed into oncoming traffic and hit again. She was evaluated at the scene by EMS where she was initially a Glasgow Coma Scale (GCS) score of 13 but had a witnessed ventricular fibrillation arrest, underwent cardiopulmonary resuscitation, two doses of epinephrine, shocked three times, and had bilateral thoracic needle decompression before return of spontaneous circulation (ROSC) was obtained. She was taken to the closest hospital where the needle decompression was replaced with bilateral tube thoracotomies. The initial hospital had access to a limited amount of blood and blood products for transfusion (3 units of pRBC and 2 units of FFP). The patient was given all of this in addition to 1 unit pRBC and 1 unit FFP that Maine Life Flight carried. The patient was sent with emergent aeromedical transport to our hospital for further management in critical condition and extremely tenuous from a hemodynamic standpoint.\nOn initial evaluation in our ED, the patient had palpable femoral pulses, with an initial heart rate of 127 and blood pressure of 103/72 and a GCS score of 10T (M6, E3, V1T). Shortly after arrival, she had a second witnessed arrest in our trauma bay with ROSC after a single round of chest compressions and 1 dose of epinephrine. After this, given her overall clinical picture including her prearrest GCS and blunt mechanism, in combination with a negative Extended Focused Assessment with Sonography in Trauma (E-FAST), bilateral chest tubes, and a chest X-ray () without significant thoracic hemorrhage, the decision to move to REBOA was made in the midst of the arrest. The Prytime 7 French sheath was placed into the right CFA under ultrasound guidance rapidly and without difficulty and the REBOA catheter inserted. RAO was used intermittently in Zone 3 to support and improve blood pressures (with balloon inflation) and conserve blood flow to the heart, lungs, and brain as the Massive Transfusion Protocol was instituted, and the patient responded hemodynamically. With clear chest wall trauma, lung contusions, negative E-FAST, and a pelvic film with a binder on that did not demonstrate overt pelvic displacement () and multiple cardiac arrests of uncertain etiology, our decision was that the patient was better served by, and stable for (with REBOA in and able to provide RAO if needed) CT scan rather than empiric exploratory laparotomy. Imaging revealed numerous rib, spine, and pelvic fractures without signs of vertical shear or open book morphology which would be helped by pelvic binding, external fixation or packing in addition to minimal pelvic hematoma without extravasation of contrast. At that time, the patient had stabilized, although was still requiring vasopressors (vasopressin and norepinephrine), and did not require intermittent RAO any longer. After stabilizing hemodynamically, the patient became responsive and followed commands prior to being moved from the ED to the ICU. Intermittent RAO was also used to minimize further hypoperfusion injury to the myocardium. The patient did have a mildly elevated troponin at 0.69 but a normal echo in the trauma bay once stabilized; overall given the traumatic injury, this is consistent with a blunt myocardial injury. However, given her stabilization and subsequent lack of arrhythmias once resuscitated, the argument could be made that this may also have represented as a type II non-ST-elevation myocardial infarction in the setting of the overall response to injury and acute blood loss anemia.\nWe were ultimately able to appropriately resuscitate the patient in our ICU while leaving the REBOA catheter in place (high Zone 3 but not inflated) overnight (). Should our resuscitative efforts have failed, we would have been able to immediately gain RAO and proceed to surgery. After stabilization and normalization of her initial metabolic derangements, the patient was able to undergo extensive repair of her injuries (). The patient required 19 days in the ICU with 12 days on mechanical ventilation and was discharged neurologically intact on hospital day 25. The tone and course of our resuscitation would have been much different if the patient had undergone RT. REBOA allowed us to safely obtain imaging information that steered us toward the ICU and controlled resuscitation and away from surgery which would not have found an obvious source for her hemorrhagic shock. The REBOA system was used not as a bridge to surgery, but as an adjunct to hemostatic resuscitation and facilitated a higher percentage of circulating blood volume to be directed at her heart and brain during the initial resuscitation. |
A 23-year-old gentleman presented with a spiral fracture of his right femur after being assaulted with a hammer (Figure ). He was treated with a femoral interlocking nail. Within 12 weeks, the fracture united and he regained full function of the limb (Figures , ). Five months later, he had pain and swelling around his right knee. The plain radiograph showed a destructive lesion of the femoral metaphysis at the tip of the nail and the two locking screws (Figures , ). Bone scan showed increased radiotracer uptake seen at the fracture site and the distal femoral meta-epiphysis region as well as its extra-osseous component (Figure ). Biopsy confirmed the diagnosis of osteosarcoma. There was no evidence of metastases on staging prior to commencement of chemotherapy, which was approximately eight months after the initial injury. He underwent three cycles of neoadjuvant chemotherapy and responded well. The neoadjuvant therapy used was according to the modified European Osteosarcoma Intergroup (EOI) Protocol consisting of a two-hour infusion of cisplatin 100 mg/m2 (total of three divided doses) administered on day one to day three and doxorubicin 25 mg/m2 administered over 24 hours via intravenous infusion on day one to day three. Total femur with distal quadriceps resection was performed to achieve a wide and adequate margin given previous surgery contamination. Intra-operatively, there was no evidence of soft tissue infiltration or contamination neither at the fracture site nor at the entry point for reaming and nail insertion (Figures , ). The limb was reconstructed with total femur endoprosthesis and motorized latissimus dorsi flap. Post-surgery, the patient was subjected to both chemotherapy and radiotherapy. The remaining three cycles of the same chemotherapy regime as neoadjuvant were administered four weeks following the surgery. Local radiation of 60 centigray (cGy) was given to the entire femur to minimize local recurrence of oncological contamination from the initial interlocked nailing surgery.\nDuring his most recent follow-up, he was 60 months post-operation, free of disease, and ambulating without aid with a knee extension lag of 20 degrees due to the weakness of the quadriceps. Retrospective analysis of the initial knee radiograph following trauma revealed evidence of cancellous changes at the distal femoral metaphyseal region (Figures , ). However, the patient did not complain of any symptoms prior to the injury he sustained. The fracture united well, and there was no evidence of bony destruction within the medullary cavity despite contamination from the previous cancerous area. Final histopathology confirmed that there was no evidence of marrow and proximal soft tissue infiltration. |
K.J., a 26-year-old male, first presented at the Drug Prevention and Treatment Centre with his wife in November 1997. They both asked to be treated for heroin addiction. Before admission they had been treated once as out-patients without success. He first used heroin a year later, in 1995, intravenously from the start, beginning with half a gram once a week; six months later his dose had increased to a gram a day. By then he was shooting up daily. He had never had any physical illness. Once he was hospitalized because of overdose, although opiate antagonist medication was not necessary. The concentration in the blood of morphine, the catabolite of heroin, was 0.05 mg/l. At the time of admission no internal medicine or neurological disorder could be found, while dysthymia and emotional lability were observed in the psychiatric state without psychotic symptoms or disorientation. Laboratory tests showed no abnormality. Detoxification with clonidine was followed by rapid relapse. He was never abstinent for longer than a week.\nHis wife recounted that on January 8, 1999, the day before his death, they had decided to begin withdrawal the following day. Next day, January 9, the wife remained at home and K.J. set out for work. What happened after that can be reconstructed from the forensic medical report and from information given by drug-using friends. On the way to work K.J. changed his mind and, breaking his promise to his wife, went to the dealer and bought a dose of heroin. He met other drug-using friends there who had bought heroin from the same dealer that day and later told the author that the heroin purchased then did not differ in quality from the usual. K.J. did not return home with the heroin purchased as he did on other occasions but went to the public toilet in the pedestrian underpass at the Népliget Metro station where he injected the same quantity (0.5 gram) that he had taken the previous day in the accustomed place, at home with his wife. The authorities called out were unable to help and pronounced him dead. A syringe half filled with a yellowish-brown fluid and a sooty spoon were found beside the body. The fluid in the syringe was heroin, while the metabolite of heroin, 6-0-acetylmorphine, and morphine-3-0-glucuronid were found in the blood and urine.\nThe autopsy found numerous traces of punctures by injection needles of various age on both upper limbs, the left side of the neck and the lower limbs. Traces of an infected but healing needle puncture were found inside the right elbow. Examination of the internal organs showed signs of general, very acute circulatory failure: acute congestive plethora of the organs, cerebral oedema, heightened brain pressure, cerebellar inclusion, acutely inflated lungs. The concentration in the blood of morphine, the catabolite of heroin, was 0.05 mg/l. The dose did not differ from the accustomed, daily dose. Other substances (alcohol, benzodiazepines, barbiturates) were not found. Heroin 'overdose' was given as the cause of death. |
A 67-year-old male patient had a history of smoking with a smoking index of 800. He had quit smoking for more than 1 year. He had a long-term history of hypertension and cerebral infarction. He regularly took his antihypertensive drugs, and his blood pressure was controlled. In January 2017, the patient accidentally found a mass in the right neck, accompanied by swelling and discomfort in the right upper extremity, which was not taken seriously at the beginning. Later, masses occurred in the right axillary fossa in succession. The patient was treated in a local hospital in April 2017. Enhanced neck and thoracic computed tomography (CT) showed 1) multiple enlarged lymph nodes (the maximum was 3.2×2.4 cm) in the right neck, right supraclavicular region, right axillary fossa, and right tracheal and esophageal sulcus and 2) nodule in the posterior segment of right upper lung (0.63×0.78 cm). Pathological puncture of the right supraclavicular lymph node showed metastatic, poorly differentiated adenocarcinoma. Positron emission tomography (PET)/CT did not find a clear primary tumor, and the clinical diagnosis was “metastatic poorly differentiated adenocarcinoma with unknown primary site.” The patient then received 6 cycles of TP (taxanes/cisplatin) regimen in the hospital. Partial remission (PR) of target lesions was assessed after 3 cycles of chemotherapy, and no significant change in the nodules in the right upper lung was seen. One month after the last chemotherapy, the lymph nodes in the right neck and right axillary region showed a progressive increase, indicating progression of the disease.\nIn October 2017, the patient was transferred to our department for treatment. The Eastern Cooperative Oncology Group (ECOG) score was 2 points. The patient was fatigued and had poor appetite. He lost 5 kg of weight. Physical examination revealed signs of anemia and multiple enlarged lymph nodes in the right neck and right axilla, with the largest one fused into a hard, painless mass, about 3 cm in diameter, with poor mobility. No obvious positive signs were found in other systems. PET/CT showed 1) multiple nodular soft tissue density shadows in the right neck, right upper and lower clavicular regions, right axilla and mediastinum, besides increased fluorodeoxyglucose (FDG) metabolism (SUVmax =10.8), which was considered as metastatic lymph nodes (); 2) nodular shadows in the posterior segment of the right upper lung, with not-so-high FDG metabolism (); and 3) multiple cerebral infarctions, splenomegaly, and multiple cysts in the left kidney. Laboratory tests indicated normal liver and kidney function; normal white blood cell, neutrophil, and platelet count; hemoglobin 87 g/L; and serum CEA 41.35 ng/mL (normal, <5 ng/mL). Clinical diagnosis indicated 1) metastatic adenocarcinoma in the right neck, right clavicular region, right axillary fossa, and mediastinal lymph nodes with unknown primary site (stage IV); 2) anemia (moderate); 3) hypertension of grade 2 (very high-risk group); 4) multiple cerebral infarctions; and 5) multiple cysts in the left kidney. The patient was poorly tolerant to further chemotherapy and had a willingness to seek targeted therapy. Thus, a second biopsy of the lymph nodes in the right neck was performed to obtain real-time pathology of the tumor tissue. Moreover, peripheral blood and freshly punctured tumor tissues were taken to perform the next-generation sequencing (NGS)-based multigene panel analysis (Burning Rock Biotech, Guangzhou, China) to reveal possible drug targets. The results of histopathological and immunohistochemical (IHC) diagnoses were consistent with those of metastatic poorly differentiated adenocarcinoma (–): CK7 (2+), TTF-1 (–), CK5/6 (–), and p63 (–). The targeted NGS analysis of neck metastatic carcinoma revealed EGFR mutation (–), ALK fusion (–), ROS1 fusion (–), BRAF mutation (–), RAS mutation (–), MET gene amplification (9.12 times) (), NTRK1 gene c.339-2A > C mutation (+) [at a mutant allele frequency (MAF) of 16.17%] (), Cyclin D1 (CCND1) gene amplification (4.75 times) (), and TP53 gene R249S mutation (at a MAF of 11.54%). Tumor mutation burden was moderate. The tumor was microsatellite stable. However, targeted NGS of ctDNA only identified NTRK1 (at a MAF of 0.42%) () and TP53 gene mutation (at a MAF of 0.39%). IHC was performed against MET to verify the findings of the gene test, and the results indicated that the protein staining was positive and the expression level was high (2+ to 3+) (,). Anti-MET-amplification therapy with crizotinib (250 mg, twice daily) was recommended in November 2017 on the basis of the molecular findings, accessible drugs in China, and treatment willingness of the patient. After 1 week of medication, the patient’s clinical symptoms ameliorated significantly and promptly. Scans demonstrated a complete response (CR) after 1 month of treatment (), and the tumor markers returned to normal levels. During the administration of crizotinib, the main AEs were grade II creatinine elevation, grade I localized edema, and a new cyst in the right kidney (). Considering the decrease in creatinine clearance and long-term history of chronic hypertension, the dose was reduced by half (250 mg, once daily) for maintenance after 2 months of medication, and treatments for protecting the kidneys were combined. Tumor was excellently controlled until the patient died of tumor progression in September 2018, with a progression-free survival (PFS) and OS time of 8.5 months and 10.0 months, respectively, from the initiation of crizotinib. The treatment using half-dose crizotinib was well tolerated, with a good quality of life and without deterioration in renal complications. |
A 51-year-old woman presented with fatigue, nausea, and vomiting for three days. She was diagnosed with metastatic melanoma to pelvic nodes in July 2014 and was treated with ipilimumab (anti-CTLA-4) in combination with nivolumab (PD-1 inhibitor) between September 2014 and April 2015, receiving a total of 4 cycles of combination therapy and 9 cycles of nivolumab monotherapy with an initial mixed response followed by slow progression of disease. In April 2015 she was enrolled on a study of radiation (to pelvic mass) in combination with pembrolizumab (PD-1 inhibitor), receiving a total of 9 cycles of pembrolizumab with no toxicities. In December 2016 she was found to have new brain metastases and in January 2017 pembrolizumab was added. The day following her second dose of pembrolizumab, she developed fatigue and nausea and began having intermittent vomiting and diarrhea. Abdominal CT scan demonstrated diffuse colitis. Infectious studies including C. difficile antigen, stool culture, viral PCR, and ova and parasites exam were all negative. She was started on methylprednisolone 2m/kg/day. Over four days of hospitalization, her abdominal pain worsened and she developed melena, which progressed to bright red blood per rectum. She was given infliximab at 10mg/kg. Repeat imaging performed 48 hours later due to severe abdominal distension showed large amounts of free air with gaseous distention of large and small bowel loops, consistent with perforation in the context of colitis with ileus. She was taken to the operating room for emergent bowel resection and a perforation site was identified at the transverse colon. The resected transverse colon serosa was congested and dusky with site of perforation identified (). The colonic mucosa revealed diffusely edematous folds as well as confluent areas of yellowish exudate and multifocal ulcers (). Histologic sections confirmed the presence of transmural necroinflammation and multifocal ulceration (Figures and ). The findings were of a fulminant colitis with multifocal ulceration and perforation. No evidence of metastatic melanoma to the bowel was identified. |
The index case was a 62-year-old female from Indore, Madhya Pradesh, India, with no significant comorbid illness except for well-controlled bronchial asthma of 25 years. She presented to us in May 2014 with history of recurrent episodes of nonmassive streaky hemoptysis since 2010. She had such episodes of hemoptysis manifesting every 6–8 months, lasting for 10–14 days and subsiding each time with a week to 10 day course of ciprofloxacin prescribed by her physician. She had no fever or respiratory distress. There was no history of loss of weight or appetite.\nShe was evaluated for these complaints in 2011 at AIIMS, New Delhi. Chest radiograph done at AIIMS revealed presence of “Air Crescent” sign suggestive of a fungal ball inside a lung cavity in the left upper lobe. Serum and bronchoalveolar lavage (BAL) galactomannan were not in detectable range. Sputum and BAL analysis did not yield any acid-fast Bacilli. Her serum immunoglobulin E (IgE) titer was 100, and Aspergillus-specific IgE was not detectable. Left upper lobectomy was planned, but the patient was not willing for any procedure and was discharged on request. She continued to have such symptoms every 6–8 months and was treated by her physician with ciprofloxacin.\nShe approached our cardiovascular surgery unit in May 2014 with persistent but increasing frequency of symptoms. Computed tomography scan of the chest confirmed the presence of a lung cavity in the left upper lobe with an organized mass within the cavity suspicious of a fungal ball [].\nHer renal and liver functions were within normal range, erythrocyte sedimentation rate (ESR) was 64, and HIV ELISA was nonreactive. With the working diagnosis of aspergilloma with manifest troublesome hemoptysis, left upper pulmonary lobectomy was done, and the excised tissue and lung cavity was sent for histopathological analysis. Histopathology of the cavitary tissue revealed lung parenchyma with cavity lined by necrotic material surrounded by neutrophils, lymphocytes, plasma cells, and histiocytes with presence of sulfur granules with Splendore-Hoeppli phenomenon in the cavitary lining []. No breach or invasion of respiratory lining was noted, ruling out invasive aspergillosis. Gram-stain was equivocal, but silver stain for fungi was negative. No acid-fast Bacilli were detectable. Charcot-Leyden crystals were seen in abundance and a final impression of botryomycosis was made.\nTissue culture from the cavitary specimen revealed heavy growth of pan-sensitive Pseudomonas aeruginosa []. During postsurgery, she was asymptomatic and hence was not started on any specific antibiotic therapy. She had a week-long asymptomatic postoperative stay in the hospital and was discharged. |
A 25-year-old male was working with braided cable under tension at a local construction site when the cable, approximately 2 inches in diameter, snapped without warning and perforated his right cheek, penetrating his right temporal and right parietal lobe. After shortening the cable to 1.5 feet at the construction site, emergency medical services brought the patient to our Level I trauma center. He was transported wearing a cervical spine collar in the sitting position. On arrival, he was awake and alert, unable to speak, and mildly agitated. His initial vital signs were a blood pressure of 159/67 mmHg, heart rate of 54 beats per minute, respiratory rate of 18 breaths per minute, and a pulse oximetry reading of 97% on 15 liters of oxygen. The remainder of his primary and secondary surveys revealed no further injuries.\nBecause of the position of the cable through his jaw and upward into his brain, the patient was unable to open his mouth more than two centimeters. In the trauma bay he became more agitated and began to pull at the cable that protruded 1.5 feet outside of his mouth. We decided to sedate and intubate him to facilitate further evaluation and treatment of his injuries. After 30 mg of etomidate and 100 mg of succinylcholine administered intravenously, blood and construction site debris was suctioned from his oropharynx, and he was intubated using the GlideScope Portable GVL and a 7.5 endotracheal tube on the first attempt.\nThe patient was taken for an IV-contrasted computed tomography of his brain, face, and neck to assess vascular injury and define the extent of damage ().\nThe patient was taken to the operating room for cable removal, neck exploration, facial nerve exploration, right temporal craniotomy, and tracheostomy. He was found to have a cranial nerve XII paralysis, right temporal and parietal lobe traumatic brain injury and intraparenchymal hemorrhage, intraventricular hemorrhage, right cochlea damage, and some general soft tissue damage. On post-operative day 3, he was transferred to the floor on a liquid diet. On post-operative day 7 he was diagnosed with bacterial meningitis after developing a headache, fever, and neck rigidity. On post-operative day 13 he was discharged on oral antibiotics to a rehabilitation facility. |
An obese 33-year-old male patient with no significant past medical history presented to the emergency room (ER) complaining of left-leg pain after a recent COVID-19 infection. He had tested positive nearly three weeks earlier and had remained asymptomatic, not requiring hospitalization. Repeat testing on admission via antigen and polymerase chain reaction (PCR) was negative. He developed acute onset severe pain and swelling in the left leg and foot nearly one week before presentation, which progressed to numbness. He did not seek medical attention previously until the current presentation when his pain became unbearable. Five days before arriving at the ER, he also had a motor loss of the toes and ankle. The patient denied any coughing, had no shortness of breath or chest pain. The patient was afebrile and vital signs were stable on presentation. On physical exam, the patient had positive Homan’s sign and palpable cord of the left lower extremity with minimal swelling. The right and left dorsalis pedis (DP) and posterior tibial (PT) pulses were palpable. The popliteal pulses were palpable on the right side and noted to be monophasic on the left. The femoral pulses were palpable bilaterally. The left foot was noted to be cool in temperature with diminished sensation at the level of the ankle. The patient also had a foot drop, was unable to flex the ankle, minimal toe flexion/extension, and early mottling of the skin was noted. The rest of the physical exam was within normal limits.\nUltrasound of the left lower extremity showed evidence of acute deep venous thrombosis in the popliteal (partial) and gastrocnemius (nearly occlusive) veins. Subcutaneous edema and rouleaux flow were seen throughout the extremity. Nearly occlusive arterial thromboses were also discovered throughout the distal femoral, popliteal, posterior tibial, anterior tibial, and peroneal arteries with very low flow velocities to absent flow overall (Figure ). More proximally, triphasic waveforms were observed with moderately reduced velocities through the common femoral, deep femoral, proximal, and mid-femoral arteries. Heparin infusion was immediately started. Vascular surgery was consulted, and the patient was taken to the operating room for an open thrombectomy of the superficial femoral artery, popliteal, anterior tibial, posterior tibial, and peroneal arteries under general anesthesia. Heparin infusion was maintained throughout the procedure and the patient was also heparinized using 100 U/kg heparin which circulated for three minutes before the activated clotting time (ACT) was measured. The ACT was maintained between 250-300 throughout the procedure. Despite appropriate anticoagulation, he had recurrent thromboses. The posterior tibial artery lost signal within a few minutes of closing and was reoccluded. These tibial vessels were subsequently reopened, and he underwent repeat thrombectomy. After the re-thrombectomy, the patient developed signs and symptoms of impending respiratory failure with oxygen saturations dropping down to the low 70s despite a 100% fraction of inspired oxygen (FiO2) and tachycardia. As such, the patient was intubated. The posterior tibial artery was reoccluded, but there was a signal in the dorsalis pedis. However, because the patient was deemed to be in danger of significant decompensation, a third thrombectomy was not attempted.\nPost-operatively, the patient developed worsening respiratory failure, increased work of breathing, and apparent ST elevation on the monitor. EKG confirmed an inferior ST segment elevation myocardial infarction (STEMI) with reciprocal anterior ST depression (Figure ). Unfortunately, the doppler signal of the anterior tibial artery was also lost around the same time. He was taken emergently to the cardiac catheterization lab and was deemed unstable for return to the OR for another attempt at tibial thrombectomy.\nIn the cardiac catheterization lab, he was found to have triple vessel disease; percutaneous coronary intervention was attempted but was unsuccessful. The ejection fraction based on the left ventriculogram was 20%. He experienced atrial flutter during the procedure requiring chemical cardioversion with amiodarone. He was noted to have a possible left apical and right mural thrombus both of which were confirmed on a subsequent echocardiogram. His left foot remained cold and pulseless. Patient remained on a heparin gutta (gtt) (heparin infusion 25,000 units in 500 mL 0.45% NaCl continuous at 0-30 units/kg/hr, titrated per protocol while monitoring activated partial thromboplastin time [aPTT]). Clopidogrel (Plavix) 300 mg per os (PO) was administered once after the patient sustained a STEMI and then continued at 75 mg PO daily thereafter. The patient demonstrated signs of heparin resistance as he could not reach goal aPTT despite maximal heparin gtt with a mean activated partial thromboplastin time of 55.7 seconds and an average anti-Xa assay of 0.24 IU/mL. Argatroban infusion was initiated at 2 mcg/kg/min and aPTT level within 24 hours of initiating argatroban was 114.8 seconds, achieving the therapeutic range indicated for anticoagulation. His left foot was not deemed salvageable and given his poor overall condition, ongoing hypercoagulability, and mortality risk, a guillotine amputation of the left foot just proximal to the ankle was performed. No arterial inflow was present. An acute clot was extracted from the posterior tibial artery with the restoration of pulsatile inflow. The clot was also extracted from the anterior tibial artery with the return of weak inflow.\nFour days following the STEMI, the patient developed pulseless ventricular tachycardia and was successfully resuscitated and started on amiodarone. While he remained on mechanical ventilation, he required intermittent pressor therapy for undifferentiated shock. Three days later, the patient was successfully extubated and transferred out of the ICU and began to work with physical therapy. One week later, the patient developed recurrent acute hypoxemic respiratory failure, requiring re-intubation, and he was transferred back to the ICU. Anticoagulation with warfarin was initiated after bridging with fondaparinux. Three days later, the patient was extubated and then three days thereafter, he again went into acute respiratory distress, requiring BiPAP. Despite attempts at non-invasive ventilation using BiPAP, he became somnolent and required intubation, and transition to full mechanical ventilatory support was altered and he was intubated. During the peri-intubation period, the patient lost pulse and went into pulseless electrical activity and advanced cardiac life support (ACLS) protocol was initiated. Thirty minutes of ACLS was completed and a cardiac ultrasound thereafter showed no cardiac movement with the presence of a ventricular thrombus. The patient was pronounced dead.\nHematology-oncology was consulted during the hospitalization to investigate potential underlying etiologies of the patient’s hypercoagulability, given his young age and unusual clotting symptoms. Further lab workup to investigate causes of hypercoagulopathy included antiphospholipid antibodies, anticardiolipin antibodies, beta 2 microglobulin antibody, lupus anticoagulant, and factor II DNA analysis that all resulted negative. Flow cytometry testing for paroxysmal nocturnal hemoglobinuria was also collected and the results were negative. Janus Kinase 2 (JAK2) kinase mutation looking for evidence of polycythemia vera or other myeloproliferative disorders was also negative. Other hypercoagulable syndromes more related to venous clotting, specifically with factor V Leiden, prothrombin gene mutation, protein C deficiency, protein S deficiency, and antithrombin III deficiency were worked up (although it was expected that the antithrombin III level was not reliable, as the patient remained on heparin in the setting of acute clotting) and no test came back positive. Screening for underlying connective tissue disorders/rheumatologic disorders was conducted inclusive of the antinuclear antibody (ANA), rheumatoid factor, and serum protein electrophoresis (SPEP) with quantitative immunoglobulins. This extensive workup for hypercoagulability, while the patient was hospitalized, was non-diagnostic, suggesting COVID-19 syndrome of hypercoagulability as the most probable etiology in the post-acute infection setting.\nThe patient also notably had elevated blood glucose levels during his hospitalization ranging in the 200s. An A1C was then obtained and resulted to be 12.0%. Though the patient had not been formally diagnosed with diabetes, his hemoglobin A1c (HbA1C) and elevated blood glucose readings in the hospital confirmed the diagnosis of type 2 diabetes. His blood glucose levels were controlled in the inpatient setting with sliding scale insulin. |
A 23-year-old male was admitted to the hospital with the complaint of intermittent twitching of the muscles on the right side of his face. First, the muscles over the right side of his mouth and lower eyelid were affected 1 month before being admitted to the hospital. Then, it spread to all of the muscles on the right side of his face. Upon admission to the hospital, these involuntary spasms occurred repetitively within 10–15 minute intervals for a day. The spasms were also observed during physical examination []. There was no alteration of consciousness or associated involuntary movements of any other body parts of his body during the spasms. The neurological examination was normal. He had no history of convulsion, neurotrauma or developmental delay in childhood. There was no family history of neurological disease.\nMagnetic resonance imaging (MRI) of the brain was requested. It revealed a well-demarcated cyst (hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging without contrast enhancement) in the right cerebellopontine cistern. This cyst had diameters of 28 mm and 25 mm in its largest portion on transverse images. It caused shifting of the pons and medulla to the left side and compression of the right cerebellar peduncles and fourth ventricle. To differentiate between the epidermoid cyst and the arachnoid cyst, diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) mapping were done. It was hyperintense on DWI and slightly hypointense on ADC relative to the brain [].\nThe results of the laboratory tests including hemogram, biochemical tests, and tumor markers were normal. Audiogram showed normal hearing patterns. EEG results were also normal. The patient was informed about his disease and advised to have neurosurgery treatment option. He was operated with the retrosigmoid (lateral suboccipital) approach in an external neurosurgery department. The diagnosis was also confirmed histologically. Only a slight hypophonia was noted during the outpatient clinic visit 15 days after the operation. HS completely disappeared after the surgery. The patient remains asymptomatic during 18 months postoperative follow-up. |
A 46-year-old male with a history of severe developmental delay, hydrocephalus, and seizure disorder presented to the hospital with blunt head trauma after a ground level fall. Work-up revealed bilateral acute subdural hematomas for which an external ventricular drain was placed. Despite intensive care management, the patient deteriorated to brain death. He was subsequently evaluated for organ donation. Abdominal computerized tomography (CT) scan () revealed an “elongated structure with metallic components in the upper portion of the IVC that extends into the right atrium.” There was no medical history of a prior procedure, or symptoms, to explain the incidental finding. The radiologist's interpretation and presumptive diagnosis were a retained atrial pacing wire.\nHe subsequently underwent procurement for organ donation after brain death. At the time of cross-clamp, the previously identified foreign body was transected when the right atrium was incised for exsanguination. During the back-table dissection, it was apparent that the foreign body had eroded into the posterior wall of the IVC, extending down the retrohepatic IVC (Figures and ). It also created a calcified reaction at the junction of the suprahepatic IVC and right atrium, adjacent to the left hepatic vein (LHV) and middle hepatic vein (MHV). We removed the foreign body () and performed a venoplasty () of the posterior wall of the IVC and of the common wall of the LHV and MVH, so that the outflow of the LHV and MHV was not compromised after transplant. We discovered that the foreign body was, most likely, a fractured CVC due to the overall appearance and interval markings.\nThe liver recipient was a 65-year-old woman with cirrhosis due to alcohol abuse; her Na-MELD score was 40 at the time of transplant. She underwent caval-sparing total hepatectomy and deceased donor liver transplantation via piggyback technique: the donor suprahepatic IVC was anastomosed to a common orifice of the recipient's right and middle hepatic veins. We did not alter our immunosuppressive therapy or prophylactic antibiotic regimen. Additionally, we did not initiate any anticoagulants or antiplatelet agents beyond our standard postoperative protocol. Postoperative imaging showed normal velocities and waveforms on ultrasound () and unremarkable appearance on axial CT () of the hepatic vein anastomosis. The patient otherwise had an uneventful postoperative course and has had stable allograft function with no venous outflow issues for >8 months after transplant. There were no reported complications in the other organ recipients. |
The case was a 31-year-old man who had not undergone computed tomography (CT) or ultrasound examinations even though his father had VHL disease and died of a brain tumor at 58 years of age. He was aware of a testicular mass, and contrast-enhanced CT revealed multiple testicular cysts, multiple pancreatic cysts, and bilateral renal tumors. In addition, retinal hemangiomas and cerebellar hemangioblastomas were found on magnetic resonance imaging (MRI), and the patient was diagnosed with VHL disease.\nMultiple renal tumors with increased vascularity were found in both kidneys. The largest tumor was 60 mm in diameter and located in the right kidney (A and B). He had no venous tumor thrombus, lymph node metastases, or distant metastases. His serum creatinine level was 0.74 mg/dl. The tumor was too large to perform partial nephrectomy, and axitinib administration was started at a dose of 6 mg/day and increased to 10 mg/day after 1 month. Three months later, the largest tumor had shrunk to 48 mm in diameter, and it exhibited diminished vascularity (C and D). The axitinib dose was increased to 14 mg/day, and treatment was continued for an additional 2 months. After 6 months of axitinib treatment, partial right nephrectomy was performed when the tumor diameter was 44 mm. We resected the largest tumor and two additional tumors simultaneously. The pathological diagnosis was clear cell carcinoma, pT1b, Fuhrman grade 1, and negative surgical margins with necrotic tissues indicated the efficacy of axitinib therapy (). The patient's post-operative serum creatinine level was 0.96 mg/dl. He had hematuria in 1 month after the surgery, and transarterial embolization was performed for the pseudoaneurysm.\nTwo months after surgery, several small tumors remained in the left kidney (largest diameter, 10 mm). To prevent tumor growth, 6 mg/day axitinib was started. Six months after surgery, the dose of axitinib was decreased to 4 mg/day, and treatment has continued at this dose. CT and MRI have revealed no signs of tumor growth or metastasis during 3 years of follow-up (). Grade 2 hand-foot syndrome, hypertension, and hypothyroidism as adverse events were controlled by oral calcium channel blockers and levothyroxine. |
A 42 year old man presented with a history of forgetfulness, behavioral abnormalities, and difficulty in walking for 6 months. The first symptom was gradual onset of forgetfulness to recent events which gradually progressed to difficulty in carrying out office duties. He developed a change in behavior in the form of decreased interest, irritability, and agitation. Over the next 2 months, his family members noted progressive unsteadiness while walking. Over the next 3 months, he developed sudden shock-like jerky movements which started in the upper limbs and gradually progressed to involve the lower limbs as well. These jerky movements were precipitated by a sudden noise. During the course of illness, he developed features of bulbar dysfunction and features of emotional lability. He had a significant family history on his maternal ancestry of multiple family members developing similar symptoms.\nAt presentation, he was conscious, and higher mental function examination revealed reduced attention span and impairment of recent memory and executive functions. Remote memory was relatively preserved. He had a moist voice with features of bulbar dysfunction. All deep tendon reflexes were normal with bilateral flexor plantar responses. He had cogwheel rigidity involving all the four limbs and signs of cerebellar dysfunction in the form of gait ataxia and intention tremor. Multifocal stimulus-sensitive myoclonic jerks were present with a frequency of 3–5/min. Given these clinical symptoms and his family history, a possibility of familial CJD was entertained.\nThe patient's hemogram; liver, kidney, and thyroid function tests; serum Vitamin B12 levels; and cerebrospinal fluid (CSF) studies were normal. Thyroid peroxidase antibody test was negative. CSF protein 14-3-3 was negative. Diffusion-weighted imaging magnetic resonance imaging sequence of the brain revealed bilateral symmetric hyperintensities in caudate nuclei and insular cortices []. His electroencephalogram (EEG) revealed continuous generalized slowing without any periodic discharges. Blood samples of the patient and his younger brother and children were sent to the Centers for Disease Control and Prevention, China, for evaluation.\nHe and two of his family members (younger brother and younger son) were found to have D178N mutation in PRNP gene. The polymorphism of the 129th amino acid was V/V, while the polymorphism of 219th amino acid was E/E in all of them. The samples from other three family members (daughters and elder son) were found normal with normal sequencing of PNRP gene. The polymorphism of the 129th amino acid was M/V in all.\nThe patient was treated with supportive care. He died after 13 months of symptom onset. |
An 8-month-old male child was referred to our service with a history of membrane formation on the upper and lower palpebral conjunctiva of both eyes since 2 months after birth. Hemophilus influenzae was cultured from the conjunctival smear. Examination under general anesthesia revealed firmly thickened, sessile membrane and papillomatous lesion on the upper and lower tarsal conjunctiva in both eyes []. There was no involvement of the bulbar conjunctiva and cornea in both eyes, and the membranes and papillomatous lesions were excised. Postoperatively, the patient was treated with corticosteroid and antibiotic eye drops. Histological examination of the membrane was suggestive of LC []. Three months after the surgery, membrane and papillomatous lesion recurrence was noted in both eyes. The patient was started with CsA 2% drops in olive oil, four times daily. Local tolerability was excellent. The patient complained of a mild burning and sensation of a foreign body in the eye for a few minutes after application of the CsA drop. Excision of the membranes together with amniotic membrane (AM) transplantation for conjunctival reconstruction was decided upon. Before surgery, the ethics committee of our department approved the treatment, and the family provided written informed consent. The human AM was prepared according to Tseng et al.'s method.[] The new membrane and papillomatous lesion were excised under general anesthesia. The AM epithelium was secured up to the conjunctival edge at the mucocutaneous junction and the fornices with 8-0 polyglactin sutures in both upper and lower tarsal conjunctiva []. Two months postoperatively, the AM had dissolved. Topical application of CsA 2% four times daily was continued for 6 months. The patient was examined monthly for the first 6 months and then quarterly by the same ophthalmologist. At the end of 40 months follow-up, the membrane had resolved, leaving moderate residual conjunctival scarring on the upper and lower conjunctiva in both eyes []. |
A 74-year-old man presented to our ER with shortness of breath. He had a recent history of air and car travel lasting seven hours. His past medical history was remarkable for DVT, prostate cancer, obstructive sleep apnea, hypertension, and chronic kidney disease stage 1. His examination was unremarkable except for mild tachycardia and hypoxemia at rest. Laboratory studies showed an elevated D-dimer, troponin, and BNP. An occlusive thrombus extending from the mid-thigh to the mid-calf on the right was seen on a Doppler study. A CT angiogram of the chest was not performed due to high creatinine but ventilation-perfusion scan showed a high probability for pulmonary embolism. Trans-thoracic echocardiography (TTE) revealed a large mobile mass extending from the right atrium through the tricuspid valve into the right ventricle (). Right ventricle was mildly dilated with decreased systolic function.\nA retrievable IVC Tulip filter was placed. After consultation with cardiology, pulmonary medicine, and cardiovascular surgery, it was decided to pursue surgical exploration with thrombectomy. The presence of the right atrial mass was confirmed by TTE prior to surgery. Right atrial exploration demonstrated no masses. A 2 cm incision was made in the pulmonary artery and a large thrombus was removed from the orifice of the left pulmonary artery (). Pathologic examination showed laminated thrombus confirming diagnosis of pulmonary embolism.\nPostoperatively in the ICU, the patient needed cardio-pulmonary resuscitation for pulseless electrical activity on two separate occasions within hours of surgery. Next four days, he required high degree of supportive care with pressors, ionotropes, mechanical ventilation, and inhaled epoprostenol. A repeat TTE showed severely decreased right ventricular systolic function. A CT scan of the chest showed extensive bilateral pulmonary emboli. The patient was liberated from mechanical ventilator on postoperative day eight. Thrombophilia panel was positive for lupus anticoagulant. He was discharged home on hospital day seventeen with a plan of indefinite anticoagulation. |
A 93-year-old man with a history of severe aortic stenosis, coronary artery disease, hypertension, and cognitive impairment presents to the hospital for a transcatheter aortic valve replacement (TAVR), as recommended by his cardiologist. His wife has been anxious to try any modality that might reverse his functional decline. The patient is a poor historian, and she provides a list of her concerns which include generalized weakness, dyspnea on exertion, nausea, and sweats. After reviewing the patient’s medical records, it was noted that he had been hospitalized three times over the past 6 months for these complaints.\nA transthoracic echo reveals an aortic valve mean gradient of 60 mmHg, aortic valve area of 0.63 cm2, and ejection fraction of 61%. A left heart catheterization shows severe left circumflex disease but no change compared to one performed 5 years ago. As a member of the cardiac team, the geriatrician evaluates the patient and is asked to assess the patient’s dementia given concerns expressed by the interventional cardiologist and cardiac nurses.\nThe patient is pleasant and can engage in simple conversations with the geriatrician consultant. Further questioning reveals a lack of understanding as to why he has been hospitalized. He states that his heart is “fine.” The geriatrician notices the patient’s inability to unwrap a muffin before eating it and has to remove the wrapper so the patient can eat it. No acute findings are seen on brain imaging, and there is no evidence of delirium or depression.\nThe patient’s wife, who is his health care agent, reports noticing a progressive decline in his cognition starting at the age of 80 years. He currently requires 24-h care, is dependent in all of his instrumental activities of daily living (IADLs), and needs assistance with several basic activities of daily living (ADLs). The patient scores 11 out of 30 on a Montreal Cognitive Assessment (MOCA) test (), consistent with severe dementia.\nIn light of the patient’s functional and cognitive limitations from his severe dementia, and the uncertainty that his physical symptoms are due to aortic stenosis, the cardiology team and geriatrician consultant concur that TAVR is not appropriate in this patient. A family meeting held with the patient’s wife and children leads to a plan that includes close follow-up with his cardiologist and increased services to assist with his dementia care. |
A 35 year old G2, P2 female presented with a two hour history of retrosternal chest discomfort radiating to the jaw, associated with nausea and diaphoresis. She was 7 months post-partum and had no underlying cardiovascular risk factors. On physical examination, the heart rate was 84 bpm with a blood pressure of 115/70 mm Hg. The jugular venous pressure, heart sounds and breath sounds were within normal limits. The initial EKG demonstrated evidence of an acute inferior ST elevation myocardial infarction (STEMI). On coronary angiography, there was evidence of a distal dissection of the left second obtuse marginal (OM2) coronary artery, with no percutaneous options for repair (Figure\nA). During the patient’s admission to CCU, the cardiac enzyme levels including creatine kinase and high sensitivity troponin T peaked at 1340 U/L and 3702 ng/L, respectively. Transthoracic echocardiography (TTE) demonstrated mild hypokinesis of the basal inferior wall with a left ventricular ejection fraction of 50-55%. As the hematologic and connective tissue disease work-up was negative, the patient was diagnosed with an acute inferior STEMI secondary to spontaneous dissection of the OM2. The patient was appropriately discharged on dual antiplatelet therapy including ASA and Clopidogrel including beta blockade with Metoprolol.\nOne month later, the patient returned with diplopia and numbness of her left arm and face. Computed tomographic angiography demonstrated a focal 8 mm long dissection of the right vertebral artery in its V1 segment with mild associated aneurysmal dilatation (Figure\nB). No other abnormalities were present in the angiogram and repeat TTE was within normal limits. With the diagnosis of spontaneous dissection in two separate vascular territories, including the coronary and vertebral arteries, the patient was investigated with genetic testing to rule out any underlying collagen disorders including Ehlers Danlos and Marfan syndrome, which was within normal limits. The patient was subsequently started on anticoagulation therapy to prevent future spontaneous dissections. |
A 2-year-old healthy boy underwent an office-based surgical circumcision by his physician. During the procedure, profound bleeding was observed that was not controlled by applying direct pressure. The physician attempted to control the bleeding by multiple deep suturing; the bleeding was stopped successfully and the patient was discharged home. During the postoperative period, the child had progressive painful and difficult voiding with only few drops of urine after straining. During this period the child was prescribed painkillers for his discomfort and no additional evaluation was done. After about a week he was referred to a district hospital with fever (temperature=38.1C), agitation, vomiting, urinary retention, and significant abdominal distension. Abdominal examination showed decreased bowel sounds, dull percussion, and severe guarding. Urgent abdominopelvic ultrasound revealed large volume of free fluid in the abdomen and pelvis, with small amount of urine in the bladder. The initial lab tests also showed leukocytosis with left shift and increased blood creatinine and blood urea nitrogen. Catheterization with a 6-Fr feeding tube failed because it did not pass beyond the subcoronal urethra. The patient underwent emergency midline laparotomy with the diagnosis of acute abdomen and the fluid was drained. A small intraperitoneal bladder rupture was noticed at the dome of bladder. The gastrointestinal tract was inspected precisely and was intact. The diagnosis of intraperitoneal bladder rupture with urinary ascites was made probably due to near-total urethral obstruction. The rupture site was repaired in two layers and a suprapubic cystostomy catheter was fixed.\nTwo months later, the patient was referred to our center for further evaluation and treatment. Antegrade voiding cystourethrography (VCUG) was performed via the suprapubic catheter that showed terminal urethral obstruction (). Urethroscopy was attempted under general anesthesia that failed due to complete obstruction at 1 cm from the meatus.\nDecision was made to explore the area and to repair the urethra. Through a circumferential incision, distal urethra was elevated from the corpus spongiosum. A 3-Fr ureteric catheter also did not pass the obstructed part (). A 5-mm fibrotic tissue was encountered at the site of obstruction (). The corpus spongiosum was dissected free from the corpora cavernosa to prevent iatrogenic chordee after end-to-end urethral anastomosis. The obstructed fibrotic part of urethra was completely resected and an end-to-end urethral anastomosis was performed along with spongioplasty over an 8-Fr silicon catheter in two layers; dartos pedicled flap was used to cover the site of anastomosis. The postoperative period was uneventful and the patient was discharged home with suprapubic and urethral catheter. The urethral catheter was removed seven days following the surgery. The suprapubic catheter was removed four weeks after the surgery following normal urethral voiding and normal ultrasound. A VCUG was performed six weeks after the surgery that showed normal bladder and urethra with acceptable voiding per urethra (). During a 2.5-year follow-up period, the patient was asymptomatic with normal renal function, ultrasound, and voiding pattern. He had a maximum flow rate of 15.3 ml/sec in uroflowmetry study. |
Case 2 (male, nine days old, Dongxiang minority nationality from Linxia Dongxiang autonomous county,Gansu Province) was admitted to our hospital on the 25th of August 2013 due to the presence of a skin sore on the occipital site and exudation for five days, as well as having a fever for one day. The parents placed a tile wrapped in a towel under the neonate’s occipital site with the intention of changing his rounded occipital head shape to a flat occiput. Five days prior, the parents observed that the occipital site was pale, which was followed by the presence of a sore and exudation. Improvement was not achieved after treatment in a local clinic, and the lesion size gradually increased to exposure of the occipital bone. The neonate came from a first pregnancy with full-term normal delivery. The examination on admission included the following: Temperature, 38.5 °C; Respiration rate, 28 times/min; Pulse, 156 beats/min; Weight, 3 kg. The neonate showed normal development, modest nutritional status, normal skin color, normal head size, and no abnormalities upon heart and lung examination. There was a 2.8 cm × 1.8 cm size skin defect in the middle of the occipital site, where the occipital bone was exposed and the occipital periosteum was absent. The color of the occipital bone was normal with an irregular lesion edge. There was the presence of purulent secretion, tenderness was apparent, and the skin color around the lesion site was normal with no swelling (Fig. ). After systemic support, control of wound infection and preoperative preparation, occipital debridement and bilateral sliding skin flap transposition were performed to cover the exposed skull on the 30th of August 2013 (Fig. ). Routine hemostasis, infection control and further systemic support were given, and a dense sponge-made head frame was used to avoid occipital pressure. Lesion dehiscence was observed after stitches were removed nine days later (Fig. ); therefore, local suturing was undertaken on the 11th of September 2013. The stitches were removed nine days later, and the wound was healed. The patient was discharged on the 22nd of September 2013 (Fig. ). |
A 49-year-old man with a history of acromegaly was admitted to our hospital with the concern of recurrent shortness of breath and dyspnea on exertion during the previous 2 years, and he had experienced an episode of presyncope 2 weeks prior without any further evaluation. He was a chef in a local restaurant for almost 30 years. He had no family history of any diseases and no past history of hypertension, diabetes mellitus, sleep apnea, or sudden cardiac death. He did not smoke or consume alcohol. The patient provided a history of stereotactic radiosurgeries twice in a decade or so and adherence to treatment with a somatostatin analog (octreotide given 40 mg once per month through intramuscular injection) at the time of diagnosis 20 years before. The patient was overweight and moderately nourished. He was 1.85 m (73 inches) tall, weighed 134 kg, and had a body mass index of 39 kg/m2. His blood pressure was 110/60 mmHg, and his heart rate was 92 beats/min with sinus rhythm. He had distinct skeletal features that included prominent superciliary arches and nose bridge, enlargement of the tongue and lip, and large hands and feet. Cardiac auscultation revealed irregular premature beats and pathological third heart sound, and a systolic murmur was discovered over the apex and aortic area. Bilateral extensive borders of cardiac dullness were noted. His physiological reflexes were present without any pathology. An electrocardiogram demonstrated sinus rhythm with wide (160 ms) QRS duration of left bundle branch block (LBBB) (Fig. ). The patient’s condition was classified as New York Heart Association (NYHA) stage III–IV.\nOn admission, magnetic resonance imaging showed pituitary macroadenoma. Given the symptoms described, we arranged blood testing of myocardial injury markers showing an elevated brain natriuretic peptide level of 740 pg/ml indicating cardiac failure (Table ). Hormone laboratory tests performed subsequently demonstrated excessive secretion of GH and IGF-1, twofold greater than the reference normal upper limit, which was consistent with pituitary macroadenoma (Table ). Other routine analyses of liver and renal function were roughly normal.\nA Holter monitor was ordered for underlying arrhythmias to explain the patient’s dyspnea, chest discomfort, and presyncope. It demonstrated sinus rhythm with an average heart rate of 68 beats/min, frequent ventricular premature beats, and nonsustained ventricular tachycardia (up to 2200 ms) (Fig. ).\nA chest x-ray showed a cardiothoracic ratio (CTR) of 78%. Echocardiography showed diffuse impairment of left ventricular (LV) systolic motion, reaching an LVEF of 16%. We noted hypertrophy of the ventricular septum at 18 mm, ventricular dilation, with LV diameter of 72 mm. The right ventricle and atrium and the left atrium were also dilated with moderate mitral regurgitation and mild tricuspid regurgitation. There was no associated systolic anterior motion (SAM) of the mitral valve. Dyssynchrony of the biventricular systolic motion was apparent.\nGiven an exertional component to the symptoms together with echo presentations in order to better exclude ischemic cardiomyopathy, coronary angiography was performed, which showed normal coronary arteries without stenosis, and left ventriculography applied simultaneously revealed an EF of 20% with diffuse LV hypokinesis.\nGiven the patient’s previous medical history of acromegaly, the absence of obstructive coronary artery imaging findings or segmental dyskinesia, family history of hypertrophic cardiomyopathy (HCM), symmetric hypertrophy, as well as absence of SAM of the mitral valve, acromegaly-induced cardiomyopathy was confirmed, which was absolutely opposed to coronary heart disease (CHD) and HCM.\nThese results indicated that it was probably not a case of hereditary cardiomyopathy; therefore, we diagnosed the patient as having secondary dilated cardiomyopathy due to acromegaly, even taking it a step further progressing to congestive heart failure secondary to acromegaly-induced dilated cardiomyopathy.\nChronic excess of GH and IGF-I secretion affects cardiac morphology and performance [], so etiological treatment for acromegaly-induced cardiomyopathy is crucial to suppressing GH secretion or blocking GH action for the sake of reversing acromegaly-induced cardiomyopathy. The mainstay of treatment acknowledged globally is surgical resection of the pituitary adenoma [], which was unfortunately considered high-risk given our patient’s cardiac condition (NYHA stage III–IV). Although stereotactic radiosurgery combined with somatostatin analogs and GH antagonists administrated previously were effective in suppressing hormones, they could not help his cardiac function. Therefore, we carefully administered diuretics, vasodilators, angiotensin-converting enzyme inhibitor (ACEI), β-blockers, and spironolactone for management of heart failure following the current guidelines []; in the meantime, octreotide (200 μg/day) was administered for the control of GH excess. After good compliance of pharmacotherapy and a regular medical examination regimen for nearly half a year, the serum GH and IGF-1 concentrations decreased from 32.50 ng/ml to 1.98 ng/ml and 627.00 ng/ml to 229.10 ng/ml, respectively, but the patient was hospitalized again because of uncontrollable cardiac failure. Accompanied by the normalization of GH and IGF-1 levels, the patient’s cardiac function did not seem to take a favorable turn upon readmission. Though echocardiography showed a recovered EF value from 16% to 28%, a significant ventricular mechanical dyssynchrony was detected as formerly. Electrophysiological study was performed using a nonaggressive stimulation protocol, which revealed a nonsustained ventricular monomorphic tachycardia []. In the presence of overt ventricular dyssynchrony, complete LBBB, LVEF< 35%, inducible ventricular tachycardia, and symptomatic heart failure despite guideline-directed medical therapy, surgical indication was rarely assessed by neurosurgeons, and stereotactic radiosurgery together with pharmacotherapy produced infinitesimal effects. Therefore, we boldly recommended cardiac resynchronization therapy with defibrillator (CRT-D) implantation based on device implantation official guidelines [, ]. The patient underwent CRT insertion finally and was discharged to home 5 days later, pharmacotherapy continued as usual (Fig. ).\nTelephone follow-up was arranged, and the patient claimed symptom improvement following the device insertion 1 month later and was basically back to normal life. We required that he return for follow-up at 1 month, 3 months, and 6 months after the interventional therapy. The patient has been followed in our outpatient clinic for nearly half a year now. During his last visit, echocardiography identified improved LVEF of 54%, and a chest x-ray showed reduced CTR of 60%. The patient was in NYHA functional class II (Fig. ). |
A 74-year-old Japanese woman noticed a tender lump in her right breast. She immediately went to a breast clinic to get a breast cancer screening. She had no family history of breast and ovarian cancer. After a month, she was referred to our institution with suspicion of metaplastic breast carcinoma with a core needle biopsy at the breast clinic. Physical examination revealed a hard, tender, and 25-mm mass in the upper outer quadrant of her right breast and a palpable lymph node in her right axilla. Mammography indicated an indistinct mass on the mediolateral oblique view and the craniocaudal view. Ultrasound (US) showed an 18 × 16-mm, irregular-shaped, and hypoechoic mass with a suspicion of a spread to the nipple inside the duct (Fig. a) and several swollen lymph nodes in levels I to II (Fig. b). Magnetic resonance imaging (MRI) detected enhancement of a 17 × 17-mm indistinct mass surrounded with a non-mass enhanced segmental lesion toward the nipple side spreading a maximum of 74-mm range, which had no interaction with the chest bone, muscles, and breast skin, in the right breast tissue (Fig. ). Invasive carcinoma with multiple axillary lymph node metastases was strongly suspected on clinical examination and imaging. Histological evaluation of the biopsy for the mass revealed a tumor with the growth of oval and spindle-shaped cells and multinucleated giant cells, the infiltrating lymphocyte into the breast tissue, and hyalinization in the stroma. The multinucleated giant cells stained positively for CD68. A part of the oval and spindle mononuclear cells stained weakly positive for CD68. These tumor cells stained negatively for estrogen receptor (ER), progesterone receptor (PgR), and human epidermal growth factor receptor 2 (HER2). There was a focal hemorrhage without necrosis. Few non-epithelial atypical cells were observed in the breast duct, but no atypical epithelial cells consistent with breast cancer were detected. GCT of the breast, breast cancer with OGCs, and giant cell-rich sarcomas should have to be considered as differential diagnoses, and the pathological findings suggested most GCT. Fine needle aspiration biopsy for the swollen lymph node revealed only normal lymphocyte, even though metastatic lymph node was strongly suspected on US. However, we could not rule out the possibility that the biopsy tissue showed a part of malignant tumor with OGCs and biopsy for the lymph node was false negative, because there was a gap between the clinical presentation, such as a tender mass suggesting rapid growth and multiple lymphadenopathies, and the pathological presentation of biopsy tissue. To obtain further evidence of malignancy, the tumor was sampled using a vacuum-assisted US-guided biopsy again. The result was the same as the prior biopsy. After discussing the treatment plan with the patient, we performed mastectomy and sentinel lymph node biopsy according to a surgical procedure for node-negative breast cancer with a wide ductal spread. The resection tissue histologically revealed similar findings to the biopsy specimen. The tumor was composed mainly of oval and spindle mononuclear histiocyte-like cells and multinucleated giant cells (Fig. ). The mitotic figure of these cells did not stand out. There was no evidence of malignancy, and only intraductal epithelial hyperplasia around the tumor, which did not fill the criteria of ductal carcinoma in situ (DCIS). No sentinel lymph nodes contained malignant cells, and we concluded the lymphadenopathies were a response to the inflammation around the tumor. Immunohistochemically, a high proportion of the multinucleated giant cells stained positively for CD68 (Fig. ). A part of the oval and spindle mononuclear cells stained weakly positive for CD68. These cells were negative for CK OSCAR, GATA-3, and MGB1 (Fig. ). These findings were consistent with the GCT of the breast. The patient received no adjuvant therapy because GCT-ST is usually considered as a benign tumor. She is being followed up with regular clinical examinations without any symptoms of recurrence after 1 year past from surgery. |
A 17-year-old boy with the features of KT syndrome presented to the Clinic of Ophthalmology of Erzurum Region Education and Research Hospital with the complaint of low vision in the right eye. His mental status was adequate to communicate without trouble. Ocular alignment was orthophoric, and extraocular muscle movements were not limited. Corneal topography revealed normal pattern bilaterally. His best corrected visual acuity (BCVA) was hand motion in the right eye and 20/20 in the left eye. Anterior segment examination revealed mature cataract in the right eye () and normal findings in the left eye. Funduscopic examination was within normal limits in the left eye. There was no determined retinal detachment but increased choroidal thickness in ocular ultrasonography scan of the right eye.\nAccording to the history obtained from his parents, he was born following uncomplicated vaginal delivery. The parents reported a congenital cutaneous vascular malformation on his face with the color of purple at birth. Family history was negative for KT syndrome and other phakomatoses. During the physical examination, port-wine stains were noted over the right side of his face (), ankle, and toes (). His face was asymmetric and his head was larger on the right side. Leg lengths were symmetrical, although he had skin hypertrophy. The hair and teeth were appearing normal. The remaining of general and neurological examinations was within normal limits. Psychomotor development was apparently normal. Electrocardiogram, leg X-rays, and heart, abdominal, and pelvic ultrasound examinations were normal.\nCranial magnetic resonance imaging (MRI) studies showed cortical atrophy discordant to his age (), asymmetric vascular dilatations in the right hemisphere (), hypertrophy in the right periorbital soft tissue (), and choroidal plexus ().\nThe patient received an uncomplicated cataract surgery under sub-Tenon's local anesthesia by phacoemulsification for the right eye. His BCVA in the right eye improved to 20/200 after the surgery. After removing cataractous lens, we were able to examine the fundus that revealed severe vitreoretinopathy () and choroidal hemangioma (). Fundus fluorescein angiography findings revealed dilated retinal vessels (), neovascularization, leaking (), and ischemia in the right eye. The funduscopic examination () and fundus fluorescein angiography () findings were within normal limits in the left eye. |
A 55-year-old Japanese woman was referred to our hospital because of hepatic tumors detected by abdominal ultrasonography during a screening examination. Her medical and family history was unremarkable; her occupational and residential history showed no apparent exposure to asbestos. She received no medical drugs, and neither smoked tobacco nor drank alcohol. On admission, her general status was unremarkable; her temperature was 36.2 °C and her blood pressure was 110/70 mmHg with a regular heart rate of 80/minute. A physical examination revealed no abnormal findings; neurological examinations were unremarkable. All laboratory data, including levels of the serum tumor markers carcinoembryonic antigen, cancer antigen 19-9, alpha fetoprotein, protein induced by vitamin K absence or antagonist-II, and cancer antigen 125 were within normal ranges (Table ). An abdominal enhanced CT scan revealed four hypervascular, round hepatic tumors. One tumor, which was 32 mm in diameter, was in contact with the lateral liver segment and the hepatic hilus; the other three tumors were in contact with the diaphragm and measured 7 mm in segment 4, 17 mm in segment 7, and 15 mm in segment 8 (Fig. a–d). There was no pleural effusion or ascites, and no other nodular lesions in her chest or abdomen were observed. Similar to the CT findings, magnetic resonance imaging (MRI) revealed a tumor of lower intensity than the liver on T1-weighted images, and with higher intensity than the liver on T2-weighted and diffusion-weighted images (Fig. a–c). Upper and lower gastrointestinal endoscopic examination findings were normal. We hypothesized that the tumor arose from her liver, and diagnosed our patient as having multiple hepatic hemangiomas, at first. However, imaging findings were not typical of hepatic tumor: all tumors were on the edge of the liver and the tumor margins were clear. Moreover, the tumor in segment 7 appeared continuous with the diaphragm with similar high-density contrast medium (Fig. d). We then performed CT angiography to obtain further details.\nCT findings during arterial portography showed enhancement in none of the tumors (Fig. a and b), but CT during hepatic arteriography revealed strong enhancement in the tumor in the lateral segment and that this tumor was fed by the left gastric artery. In contrast, the remaining three tumors had no enhancement and were fed by the right inferior phrenic artery (Fig. c and d). Imaging findings indicated that the liver was not the origin of these tumors. Moreover, all tumors exhibited increased uptake of 18F-fluorodeoxyglucose, with a standardized uptake value of 7.8 with positron emission tomography (PET)-CT (Fig. ). We considered these tumors to be peritoneal malignant tumors, preoperatively, and performed surgical resection. Laparotomy revealed that the tumor in the lateral segment was clearly in contact with the hepatoduodenal ligament, and that the other three tumors were on the diaphragm (Fig. a–c). We performed tumorectomy with left liver lobectomy (Fig. ) and partial diaphragmatic resection. Histopathological and immunohistochemical examinations of the resected specimens were positive for CD34, CD31, D2-40, and calretinin, which confirmed epithelioid mesothelioma (Fig. a–h). Our patient was not given any medication except a general drip infusion and prophylactic antibiotics; she was discharged 10 days after surgery without complications. CT and PET-CT revealed no recurrence 20 months after surgery without adjuvant therapy. |
A 72-year-old man was diagnosed 12 years ago as suffering from idiopathic PD. He has been taking dopaminergic treatment with a fair symptomatic control. His past medical history was significant for coronaropathy, pacemaker, and hemochromatosis. At the age of 64, the patient started to complain of increasingly invalidating, chronic back pain during movement of the lower lumbar region. This back pain was progressively associated with bilateral radicular leg pain and weakness. Clinical examination revealed motor function impairment at level L4/L5 with a leg motor scale score of 3 out of 5. He first presented at an orthopaedic surgery department where he had undergone L3–L5 laminectomies for degenerative lumbar stenosis. Surgery had only a limited and temporary benefit. Indeed, the patient reported six months postoperatively low back and right radicular leg pain recurrence with foot drop. Motor function remained impaired with a marked hypoesthesia along L4 dermatome. Electromyography revealed right L4, L5, and S1 irritation.\nMedical treatment and epidural cortisone injections remained unsuccessful over the years. Lumbocrural pain and neurological impairment were progressively associated with thoracolumbar kyphosis.\nThree years postoperatively, the patient was referred to our institution. Extensive radiological assessment was realized with analysis of previous imaging compared to new ones. Plain radiographs revealed a combination of an extensive discovertebral destruction with L2 degenerative collapse associated with paravertebral hypertrophic ossifications. Lesions developed at the upper limit of the laminectomized area (Figures and ). Dynamic X-ray imaging revealed the extent of the spinal instability. CT scan showed a severe lateral dislocation of the L2/L3 joint associated with a reduced local kyphosis angle ().\nThe progressive onset of associated destructive and constructive radiological phenomena provided arguments for an osteoarthropathy and raised suspicions of Charcot spine. Firstly, investigations focused on differential diagnosis and etiological research. Blood tests and cultures including serologic test for syphilis were performed. There was no evidence of infection or an inflammatory syndrome. Nevertheless, the hypotheses of a chronic vertebral osteomyelitis or a tumoral process were explored. A CT-guided vertebral biopsy was consequently performed. Cultures proved negative. Histological examination revealed the presence of fibrous tissue with sequestered bone but no signs of malignancy. Screening for the HLA B27 gene was negative. Investigations concluded that the patient had a neurological osteoarthropathy with an isolated PD.\nFurther surgery was decided in order to decompress and stabilize the spine. The patient underwent decompression and transforaminal lumbar interbody fusion (TLIF). First laminectomy at L3 was performed; then, each L3/L4 nerve root was decompressed. Foraminotomy and bilateral facetectomy provided access to the L2/L3 intervertebral disc. A vacuum disc phenomenon was noted at this level. Discectomy was thus reduced to a minimum. Finally, disc space was replaced by intersomatic bone graft. The fusion from L1 to L4 was performed using pedicle screws, rods, and a posterolateral bone graft. The patient was placed in a thoracolumbosacral orthosis during 3 months. Afterwards, the patient's condition improved progressively. Three months postoperatively, he had a significant pain relief and complete weakness recovery. At the 5-year follow-up examination, clinical outcome was satisfactory and radiological assessment confirmed that the bony union was achieved and that a solid and stable fusion of the spine was obtained (). |
A 15-year-old teenage boy initially presented in a district hospital, with a swelling at the right side of his neck, without any significant clinical symptoms. Although full details of the work-up performed at the time are not available, he was diagnosed with a branchial cleft cyst and was offered surveillance with follow-up imaging. Eight years later, he visited our unit. Physical examination revealed a painless palpable well-defined mass () within the right carotid triangle with positive Fontaine and Kocher I signs []. There was no palpable lymphadenopathy. An ultrasound scan was performed depicting a solid mass of mixed echogenicity in the right carotid triangle echogenicity in the left carotid triangle. This was suspected to be neurogenic in origin because of its location. A digital subtraction angiography (DSA) () followed, which revealed a 60x35mm protruding mass in the right carotid bifurcation, causing local compressive effects and posterior displacement of the vessels. The patient was admitted in our unit in order to be treated surgically. During the operation a large CBP was identified as seen in . The tumor was classified as Shamblin II and was completely excised. Histopathology study showed a 3 cm carotid body paraganglioma with characteristic “zellballen” growth pattern and cell nests surrounded by prominent fibrovascular stroma, with no evidence of malignancy (). The patient had an unremarkable recovery and was discharged home on the second POD.\nThe surgical technique adopted in both patients consisted of an oblique incision along the sternal head of the left sternocleidomastoid muscle under general anesthesia. Our strategy was to expose, dissect, and isolate the proximal common carotid artery using a vascular tape. The ansa cervicalis was also exposed early in the operation. The carotid bifurcation was exposed in a caudocranial approach. The proximal external and the proximal internal carotid arteries were isolated and controlled with vessel loops. Dissection was extended to the level of the digastor muscle in order to expose and control the distal internal carotid artery. During this process, the hypoglossal nerve was identified and preserved, by following the ansa cervicalis. The external carotid artery was cross-clamped temporarily. Finally, the tumor was removed with sharp dissection from the bifurcation with meticulous technique in order to avoid injury to the internal carotid artery and the cranial nerves. The reported plane of dissection reported as a white interface plane between the tumor and the vessels was not identified in the first patient as the tumor was severely adhering to the vessel wall and was typically found in the second patient. Following the removal of the CBP, the carotid sheath and platysma were approximated and the skin closed with a continuous subcuticular suture, after performing meticulous hemostasis (Figures and ).\nBoth patients had an annual postoperative follow-up with cervical ultrasound and carotid duplex ultrasonography with no evidence of local recurrence. Familial disease was excluded clinically, by screening the patient's first degree relatives with ultrasound imaging. |
We present the case of a 75-year-old female patient, previously fit and well, who presented with the extremely rare finding of an ascending colon schwannoma. She was already under surveillance colonoscopy by the gastroenterologists because of her strong family history of bowel cancer.\nPrevious colonoscopy, 4 years prior, had found several benign polyps. On recent colonoscopy, a 2 cm submucosal lesion within the ascending colon was identified and thought to be a lipoma (Figure Xa and Xb). Biopsies taken at the time were found to be benign with only oedematous large bowel mucosa seen, however these were superficial and no submucosal tissue was present (Figs –).\nIn view of this CT Colonoscopy was performed, alongside a CT Chest examination. This showed a 12 mm lesion arising from the lateral wall of the ascending colon. It appeared rounded and mural-based, and displayed irregular peripheral enhancement post-contrast. It did not conform with a lipomatous lesion, with an average internal density of approximately 40 HU. No other colonic lesions were demonstrated, and no locoregional adenopathy or distant metastases were identified.\nBased on the endoscopic and radiological findings, the differential diagnoses included the other rare causes of submucosal tumours like GIST, GI autonomic neural tumour, leiomyoma, leiomyosarcoma, lymphoma, schwannoma and metastatic melanoma.\nThe case was discussed at the MDT and the multidisciplinary team felt that this was not a lipoma and warranted excision. The patient underwent an uncomplicated laparoscopic right hemicolectomy with an uneventful post operative course and was discharged on Day 6.\nMacroscopically, there was a bump on the lateral wall close to the distal resection margin. The bump was firm to the touch.\nMicroscopically, there was an unencapsulated, round tumour centred on the submucosa and muscularis propria. The tumour was composed of fascicles of spindle cells, including some palisading of nuclei (Verocay bodies), however, no significant atypia and no mitoses are seen. The tumour was strongly positive for S100. A diagnosis of Schwannoma was made.\nAs the postoperative histology showed complete resection and benign pathology, no further treatment was required. These tumours are noted to have a good prognosis.\nThe patient visited the clinic after four weeks and had recovered well. She was informed of the reassuring histopathology report and was advised to follow her surveillance colonoscopies as before. |
A 75-year-old female presented acutely with a history of sudden onset paraesthesia and ischemic rest pain involving the left foot and ankle. Motor function was retained, capillary and superficial venous return were reduced, the foot was cold, and there were no palpable pedal pulses. The calf remained soft to palpate. There was no history of palpitations or arrythmia, and the patient was in sinus cardiac rhythm both clinically and on electrocardiography. Plain chest radiography and computed tomography angiography (CTA) excluded a proximal arterial source of embolism. Furthermore, there was no previous trauma, (local or systemic) infection or inflammation, collagen, connective tissue or genetic syndromes, or arteritis; nor was there a family history of aneurysmal disease. Positive cardiovascular risk factors included hypercholesterolaemia and hypertension. Baseline haematological and biochemical analyses were normal, as were the renal and liver function. The creatinine kinase was within normal limits. The right foot was well perfused with a palpable PTA pulse.\nCTA demonstrated no significant stenosis in the supragenicular vessels bilaterally. On the symptomatic left side, the tibioperoneal trunk (TPT) and anterior tibial artery (ATA) were patent proximally, with the ATA and peroneal artery occluding in the distal calf. The dorsalis pedis was occluded; however, the plantar arteries reconstituted. Dominant flow to the foot was via the PTA, which occluded in the distal calf (). These findings were considered reflective of embolic disease within the left-sided tibial arteries. The asymptomatic right leg demonstrated dominant flow to the ankle via the PTA. The ATA and peroneal arteries occluded in the midcalf.\nDue to the acute nature of the patient's symptoms, emergent thromboembolectomy of the popliteal and tibial arteries was performed via a medial approach to the distal popliteal artery. Selective thromboembolectomy using Fogarty catheters for each tibial artery was unsuccessful. Urokinase was also injected into each tibial artery without effect. Subsequent exposure of the dominant PTA at the ankle demonstrated a thrombosed 10mm diameter aneurysm. A PTA thrombectomy was performed and subsequent angiography demonstrated flow to the foot via the aneurysmal PTA (). The aneurysm was opened and demonstrated a mixture of old, organised, and fresh thrombus (). The PTA aneurysm was excised and thrombectomy established adequate inflow and backflow to the excised PTA segment. The PTA was repaired using an interposition long saphenous vein graft (). Postoperatively, the PTA pulse was present, the foot had brisk capillary refill, and motor and sensory function normalised. Follow-up at 16 months demonstrated the patient to have a well perfused left foot with a palpable PTA pulse.\nAlthough the patient's contralateral foot was asymptomatic, she opted to have this repaired electively considering the aneurysmal right PTA aneurysm was the single arterial supply to the foot. Repair was performed via excision of the 8mm PTA aneurysm and a spatulated primary end-to-end PTA anastomosis. Completion angiography was satisfactory, and the right foot was well perfused with a palpable PTA pulse postoperatively. Histopathology of the right-sided PTA aneurysm demonstrated findings consistent with atherosclerotic degenerative aneurysmal disease. Specifically, there was intimal thickening, extensive lamina disruption, and broad areas of media replaced by collagenous fibrous tissue, with calcification of the media. There was no inflammation or mural necrosis seen. |
A 39-year-old Chinese female was referred to our hospital with a 5-year history of a slow growing mass in the left upper abdomen and an 18-month history of surgical incision exudation. The painless mass was found incidentally with an initial diagnosis of pancreatic cyst 5 years previously, and the palliative bypass procedure of cystojejunostomy was performed. However, due to the increasing size of the mass, the patient underwent a laparotomy 2 years later. This revealed a pancreatic tumor which was inoperable because of the major adhesion surrounding the neoplasm, stomach, greater omentum, mesentery and abdominal wall. Some of the anastomotic stoma tissue was excised for pathological examination, and a diagnosis of noninvasive MCN with intermediate-grade dysplasia was made. After 18 months, the surgical incision began to produce exudate. On admission to hospital, physical examination revealed a single, deep-seated, painless mass and two incisional sinuses with exudation in the left upper abdomen, without tenderness or muscular tension. Laboratory investigations were unremarkable, and serum levels of carbohydrate antigen 19–9 and carcinoembryonic antigen were within normal ranges. Abdominal ultrasonography and computer tomography scan revealed a 7.8 cm × 7.3 cm, heterogeneous hypoechoic or low-density mass with poorly defined margins in the tail region of the pancreas, compressing other adjacent organs. The mass was composed of several large loculi with an irregular thickening of the cyst wall and papillary excrescences projecting into the cystic cavity (Figure ). Splenomegaly was also found. The patient underwent a distal pancreatectomy and splenectomy, during which a pseudo-encapsulated cystic mass adhering to the greater curvature of stomach and distal duodenum was observed. The pancreatic parenchyma in the region of the cyst was completely atrophied, and the previously performed anastomosis was obliterated. After an uneventful postoperative recovery, the patient remained symptom-free without recurrence during the 14-month follow up.\nThe resected neoplasm measuring 7.8 cm × 7.3 cm × 6.5 cm presented as a round mass with a fibrous pseudocapsule of variable thickness. In cross-section, the specimen revealed a multilocular tumor with cystic spaces ranging in size from a few millimeters to 1.3 centimeters in diameter, and containing grey–tan cloudy gelatinous material. The internal surface of the lumina showed multiple papillary projections and mural nodules. The spleen was intumescent and free of tumor invasion.\nThe specimen that was resected at the anastomotic stoma 3 years previously showed two distinct components: an inner epithelial layer and an outer cellular ovarian-type stromal layer. The columnar mucin-producing epithelium with pseudopyloric-type intracellular mucin and goblet cells formed small papillary projections – local pseudostratifications with crowding of slightly enlarged nuclei that are oriented perpendicular to the basement membranes. The columnar cells with bland uniform histological pattern and minor architectural atypia, were characterized by basally located nuclei and abundant supranuclear mucin which was positive for periodic acid Schiff with diastase and Alcian blue stains. Crypt-like invaginations were found focally (Figure A). The ovarian-type stroma, characteristic subepithelial tissue, was composed of densely packed spindle-shaped cells with elongated nuclei and sparse cytoplasm. Hypocellular and hyalinized connective tissue was present in variable amounts accompanied by focal lymphocytic infiltration. In addition to the typical features of MCN as discussed above, there were some unusual findings, including extensive pronounced squamous metaplasia and an obviously decreased stroma in the complete resection specimen (Figure B). Squamous epithelium combined with the top glandular epithelium excreting mucin. The stratified squamous epithelium formed papillary excrescences with sparse hyalinized fibrovascular stromal cores that protruded into cysts. The tumor-to-stromal interfaces were smooth with no invasion by the tumor cells. The squamous epithelium in the basal layer exhibit moderate pleomorphism and contain large hyperchromatic nuclei with a high nucleus to cytoplasm ratio, and mitotic figures are more abundant than usual, but they never reached the level of that seen in carcinoma. The abundant cytoplasm was mostly eosinophilic but occasionally clear. Cytoplasmic borders between tumor cells were distinct. Intercellular bridges were easily identified in the vast majority of tumor cells, and keratinization was not a prominent feature. Abundant ectatic vessels and focal neutrophils and eosinophils were observed in the rare stroma of the glandular element region. The tumor has a relatively well-demarcated pushing border.\nIn terms of immunohistochemistry (IHC), the epithelial component with squamous differentiation was strongly immunoreactive with high molecular weight cytokeratin (HCK, 34βE12) and CK5/6 (Figure A), while the glandular epithelial cells were strongly positive for low molecular weight CK (LCK, 35βH11) (Figure B). CK14 was expressed in some basal cells, but not in all of the squamous epithelium (Figure C). Some cells in the micropapillary proliferation architectures were immunoexpressed with CK20 (Figure D), while both squamous epithelium and glandular epithelium were negative for CK20. The expression of P63 was diffusely positive for the squamous cells with a tendency for intense positivity in the basilar part, but it was negative for the glandular epithelium. P53 positivity was found in the area of squamous epithelium (approximately 35% stained tumor cell nuclei), while glandular epithelium was negative (i.e. <10% stained tumor cell nuclei). The distinctive fusiform ovarian-type stroma showed positive staining for smooth muscle actin, CD10 (Figure E), estrogen receptor and progesterone receptor (PR) (Figure F). (All antibodies from Dako).\nElectron micrography of the squamous differentiated region demonstrated some tonofibril intracytoplasm and a few intercellular desmosomes arranged on the lateral sides of plasma membranes. |
A 9-year-old female leucoderma patient presented to the stomatology department of a public hospital in Rio de Janeiro, Brazil. She complained of small nodules in the left parotid region that had developed over the course of 2 years. Her main complaint was of recurring periods of worsened symptoms characterized by the exacerbation and remission of gland volume that was possibly triggered by occasional otolaryngologic infections or unrelated to these infections. These symptoms suggest juvenile recurrent parotitis. Facial panoramic radiography revealed the presence of multiple circular radiopaque masses in the left parotid region (Fig. ). The ultrasound revealed increased volume of the left parotid, with imprecise borders, heterogeneous echotexture with hypoechoic and hyperechoic areas within it. These features were suggestive of an inflammatory process associated with calcifications in the parenchyma of the gland. CT scan revealed a dense mass in the left parotid; it was heterogeneous and included calcifications in its center (Fig. ). Because of the association between the patient’s clinical history, her clinical presentation, and the imaging findings, the possible origin of the calcified materials was questioned. There was evidence of sialoliths or dystrophic calcification associated with recurrent inflammation/infection. Sialoliths are typically symptomatic because of their association with secondary bacterial infections, which are generally treated with systemic antibiotic therapy. Spontaneous remission of bacterial sialadenitis associated with sialoliths is not expected. In addition, sialoliths generally observed as oval-shaped calcified masses or fusiforms on imaging. Because of the pediatric nature of this case, the clinical conduct selected to treat this patient was clinical follow-up and the use of imaging and functional assessments of the gland affected every 6 months or when any signs and/or symptoms appeared. After 48 months, the patient is asymptomatic, without periods of exacerbation of the condition. Recent ultrasound (Fig. ) demonstrates an improvement in the inflammatory aspect of the gland. Clinical and imaging follow-up will be maintained. |
A 26-year-old Thai woman presented with a foreign body in her left orbit that had been retained for 8 months. Eight months previously, she had sustained a gunshot injury to her left eye. There was only a small wound on her left eyelid (Fig. ); she had normal eye movement, a normal visual field, and no pain. A plain radiograph was performed at that time; it detected a round-shaped metallic foreign body located medially in her left eye globe. She was then diagnosed as having a retained foreign body in her left orbit and she was advised to have clinical observation. However, 8 months later, she developed pain in her left eye without any sinonasal symptoms. After discussion about the risk of surgery and retention of an orbital foreign body, an ophthalmologist referred her to our department for the minimally invasive procedure option of removal of the foreign body using an endoscopic transnasal approach. On examination, the movements of her left orbit were not restricted and there was normal visual acuity (20/20) with no proptosis or chemosis. A computed tomography (CT) scan of her left orbit revealed a round-shaped metallic foreign body in the medial intraconal space, and lateral attachment of posterior ethmoid sinus, measuring 6 mm (Fig. ). A transnasal endoscopic approach, with navigator assistance (Brainlab), was used to remove the bullet. Uncinectomy and anterior-posterior ethmoidectomy were performed. The location of the intraconal metallic foreign body was confirmed with a navigator system, then part of the lamina papyracea was removed and the periorbita incision was done. The defect was enlarged and the fibrotically encapsulated bullet was found lying in the orbital fat (Fig. ). The fibrotic capsule was dissected, and the bullet was delivered through her left nostril with probes and curetted (Fig. ). No intraorbital bleeding or damage to any soft ocular structures was noted. A relative afferent pupillary defect was found in her left eye during removal of the foreign body, but it resolved and no postoperative complications were observed. |
A-79-year old man presented to our tertiary oculoplastic and adnexal clinic with a five-month history of gradually increasing painless left proptosis associated with a reduction in visual acuity, double vision, swollen left cheek, and nasal congestion. The patient had no significant medical or family history.\nVisual acuity (VA) was 6/6 in the right eye and 6/18 in the left eye. Ishihara colour plates test was full at 17/17 in the right eye, and diminished to 12/17 in the left eye. No pupillary defect was noted. Optic disc appeared normal on dilated fundoscopy. Exophthalmometry illustrated a 4 mm left-sided nonaxial proptosis. Diplopia was demonstrated in all positions of gaze, but was more pronounced on down gaze and adduction. Nasal endoscopy revealed normal mucosa; however his left nostril was obstructed by the medialisation of the medial antral. There was no apparent lymphadenopathy on palpation or areas of numbness on his face.\nAn urgent CT scan was performed showing a large maxillary mucocele eroding through the inferior orbital ridge and causing superolateral displacement of the globe. The medial antral wall was eroded with the mass projecting into the nasal cavity (). There was no enhancing soft tissue to suggest the presence of malignancy.\nFunctional endoscopic sinus surgery was performed to drain the maxillary mucocele and 50 mL of thick yellow mucus was expressed, which was sent to pathology. This intervention induced an orbital decompression and preservation of optic nerve function. The mucosa appeared healthy and histology confirmed no evidence of malignancy.\nWithin one month his left visual acuity and colour vision returned to normal with a VA of 6/6 bilaterally and 17/17 bilaterally with the ishihara colour test plates. He also had complete resolution of diplopia and proptosis. Postoperative CT scans show remodelling of the orbital floor () and therefore further reconstruction surgery to the orbital floor was not performed.\nTwo years later, the patient shows no evidence of recurrence of his mucocele. He has no ophthalmic symptoms or signs, and his occasional nasal symptoms are controlled with saline douches. |
A 32-year-old female had sudden-onset severe headache associated with vomiting. The patient was admitted in the emergency department. On admission, computed tomography (CT) brain was performed, which revealed a hemorrhagic lesion in the right parieto-occipital region []. The patient was then referred to the neurosurgery department for further management.\nOn admission to the neurosurgery unit, the patient's Glasgow Coma Scale score was 15/15, and the patient had no neurological deficit. The patient was married and had two children. The patient had a medical termination of pregnancy 2 years back. At the time of admission, the patient's last menstrual period was 15 days back. No other significant history was present. Chest X-ray revealed no abnormality. Ultrasonography (USG) abdomen revealed chronic calculus cholecystitis. No other abnormality was detected on abdominal USG. Antiepileptics and antiedema measures were started.\nOn the basis of clinical presentation and CT brain findings, a working diagnosis of the vascular lesion was made. A CT angiogram brain was performed, which did not reveal any vascular etiology []. Cerebral digital subtraction angiography (DSA) was then performed, which did not show any arteriovenous malformation (AVM) or aneurysm []. A contrast magnetic resonance imaging (MRI) brain with MR spectroscopy (MRS) was performed, which revealed a hemorrhagic lesion []. MRS findings were inconclusive possibly due to hemorrhage []. No abnormality was detected on contrast-enhanced CT (CECT) abdomen and chest.\nA craniotomy was planned with the aim of achieving a tissue-based diagnosis and gross total excision of the lesion. The craniotomy was performed, which revealed a superficial cortical lesion with areas of hemorrhage. No feeding vessels or unexpected hemorrhage were encountered during the procedure. Gross total excision of the hemorrhagic lesion was performed. The patient had uneventful intraoperative and postoperative course. Postoperative contrast MRI was performed, which showed some residual tumor [].\nHistopathological examination and immunohistochemistry revealed choriocarcinoma []. Serum beta-human chorionic gonadotropin (β-hCG) level was estimated on postoperative day 4, which was found to be highly elevated []. The case was discussed in the institute's tumor board meeting regarding further management, and chemotherapy was started. The patient received cisplatin, etoposide, and bleomycin combination chemotherapy and whole-brain radiotherapy. The patient is without any neurological deficit at 4-month follow-up, with serum β-hCG values within reference interval []. |
A 30-year-old male presented to us with the complaints of gradually progressive dysphagia mainly to solids for 4 months’ duration. He denied any history of significant weight loss, vomiting, acute abdominal pain, abdominal distension, hematemesis, melena, dyspnea on exertion, facial puffiness or peripheral edema. The patient denied any history of addiction. On physical examination, his vitals were stable with pulse rate of 90/min and blood pressure of 120/70 mm Hg. Rest of the abdominal and respiratory examinations were within normal limits.\nOn further evaluation, his hematological and biochemical parameters were within normal limits. Upper GI endoscopy revealed a well-defined submucosal lesion which was bulging into the esophageal lumen involving the right antero-lateral wall of the distal esophagus just above the gastro-esophageal junction (). The overlying mucosa was normal and there was mild luminal narrowing but gastroscope could be negotiated across this narrowing. Ultrasonography of the abdomen was unrevealing. Further contrast-enhanced computed tomography (CT) imaging of the thorax revealed a 3.5 × 2.3 × 3 cm well-defined homogenous hypodense cystic lesion involving the right antero-lateral wall of the distal thoracic esophagus with likely possibility of submucosal or intramural lesion (). The patient was then subjected to EUS which revealed a 3.3 × 2.8 cm homogenous hypoechoic lesion without any vascularity involving the distal esophagus wall (). The lesion was intramural in location as muscularis propria was seen to go around the lesion. It could be easily identified as a duplication cyst rather than a bronchogenic cyst as there was absence of cartilage and the lesion was in close proximity to the esophageal lumen. In view of imaging finding consistent with that of duplication cyst, fine-needle aspiration (FNA)-guided fluid aspiration was not attempted in this patient in view of high risk of introducing infection. In view of the cyst being symptomatic, the patient underwent complete surgical excision of the cyst with exteriorization of the base. On histopathology, the lesion showed features consistent with esophageal duplication cyst. At present, the patient is asymptomatic on 6-month follow-up. |
A 32-year-old man was admitted to our hospital with appetite loss. He had a history of traumatic transverse cervical spinal cord injury at the C5 level due to suicide attempt at the age of 18. As a result of cervical spinal cord injury, he was paralyzed in the lower body. Contrast-enhanced computed tomography (CT) revealed a late-onset traumatic diaphragmatic hernia with strangulated ileum (Fig. ). The small intestine, transverse colon, and omentum were displaced into the left thoracic cavity, and some portions of these organs showed a decrease in blood flow. Left lung collapse and a compressed right lung with mediastinal shift were evident. The patient underwent emergency surgery. After replacing the incarcerated organs to their original positions, scattered areas of necrosis were identified in the small intestine, transverse colon, and omentum (Fig. ). By using interrupted sutures with non-absorbable 1–0 monofilament, the diaphragmatic orifice was closed. Wedge resection with primary closure was performed for the colonic necrosis in two places. Partial resection, 45 cm long, with end-to-end anastomosis was performed for the small intestine. The necrotic omentum was removed (Fig. ). In addition, a gastrostomy tube was placed since delayed initiation of oral intake was expected. The patient developed severe septic shock postoperatively. Treatment-resistant critical hypotension with non-compensatory tachycardia developed, likely due to parasympathetic nervous system damage related to the cervical spinal cord injury. On postoperative days (POD) 3 and 6, cardiac arrest occurred. Fortunately, he was rescued by cardiopulmonary resuscitation with administration of large doses of vasopressin and catecholamine. However, peripheral vasoconstriction, increased intra-abdominal pressure, and ischemia of the gastrointestinal tract developed, which resulted in colonic anastomotic leakage with diffuse peritonitis, abdominal wound dehiscence, and collapse of gastrostomy on POD 6 (Fig. ). The patient was unable to undergo surgical repair because of his poor general condition with continuing severe septic and neurogenic shock. Therefore, he underwent AVS through the open abdominal wound and it was the first procedure at the intensive care unit. The procedure of AVS was as follows: 1. the open wound and peritoneal cavity were rinsed with normal saline and necrotic and/or contaminated tissues were debrided (Fig. ); 2. wound dressing materials (DUOACTIVE® ConvaTec, New Jersey, USA) for protecting healthy skin around the open wound were patched along the abdominal wound in piecemeal fashion so as to adjust dressing materials to the complicated shape of the wound (Fig. ); 3. two drainage tubes with multiple side holes, up to 30 cm from the tip, were placed in the abdominal cavity through the open abdomen and the enteric contents were suctioned through the drainage tubes using a Continuous Suction Unit MERA Sacuum (Senko Medical Instrument Manufacturing CO, Tokyo, Japan) set to 50–75 mmHg continuous negative pressure; and 4) the entire wound was filled with saline-moistened gauzes and covered with polyurethane drape (Fig. ). The colonic anastomotic leakage showed gradual healing over the course of 2 months, followed by contraction and closure of wound dehiscence (Fig. ). Because the gastric fistula remained, a gastrostomy balloon catheter was placed through the gastric fistula. The patient resumed oral intake on POD 112 and left the hospital on POD 190 with the gastrostomy balloon catheter and without incisional hernia. |
A 56-year-old female presented to the emergency room with a three-day history of right hip pain. She reported decreased range of motion and difficulty ambulating. She denied constitutional symptoms or fever. She had undergone intra-articular steroid injection of her right hip three days prior. Review of systems was otherwise unremarkable. Her past medical history was relevant for hereditary spherocytosis with splenectomy at age 14 and chronic right hip osteoarthritis. Her only medication was celecoxib as needed. She denied any drug allergy. She was unaware of her immunization history. She worked as a flight attendant, denied smoking or recreational drug use, and had not recently travelled outside of Canada. On initial examination she was afebrile and her vital signs were within normal limits. On examination of her right hip she had limitation of internal rotation with reproducible pain, but her physical exam otherwise was unremarkable. Her initial investigations showed elevation in C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) at 22.9 mg/L and 25 mm/hr, respectively. Her white blood cell count was not elevated. An X-ray of her right hip showed severe joint space narrowing with osteophytosis consistent with severe osteoarthritis. Arthrocentesis was performed and synovial fluid samples were directly inoculated onto solid culture media, including blood agar and chocolate agar. Two of three samples also underwent cytospin centrifugation and direct Gram stain. Gram-negative bacilli were observed in one sample though heavy neutrophils were observed in both. Synovial fluid analysis for cell count and chemistry was not performed due to insufficient sample. She was admitted to hospital for 24 hours of observation and was subsequently discharged with instructions to return to hospital if her symptoms worsened or if cultures subsequently grew a pathogenic organism.\nThree days later she was seen in a follow-up clinic. In the interim she had developed a fever (38.3°C), had chills, and had worsening right hip pain. Repeat physical examination showed deterioration in range of motion at her right hip with significant pain. Cardiovascular examination was unremarkable with no appreciable murmur. Synovial fluid cultures from the initial arthrocentesis were now growing Haemophilus parainfluenzae with colonies observed on solid media within 24 hours of inoculation. She received one dose of ceftriaxone and subsequently underwent right hip arthrotomy with synovectomy and irrigation. The Infectious Disease service was consulted the following day. The organism was susceptible to ceftriaxone and cefuroxime and resistant to ampicillin and ciprofloxacin (). Blood cultures and intraoperative tissue cultures did not demonstrate growth, likely due to the administration of antibiotics prior to collection. The patient was treated with intravenous ceftriaxone and was subsequently discharged with outpatient follow-up for home intravenous antibiotics. Ongoing pain, difficulty ambulating, and persistently elevated inflammatory markers necessitated a prolonged, nine-week course of antimicrobial therapy (). At the time of treatment discontinuation, she reported pain and her functional ability had not yet returned to baseline. She is currently awaiting evaluation for total hip arthroplasty. |
A 47-year-old premenopausal Caucasian woman presented in December 2009 during a multidisciplinary tumour board for nonpalpable lesions. Mammography revealed microcalcifications and gentle densities suspicious for invasion in the area of 6 × 8.6 cm in her left breast (Figure ). An ultrasound showed indistinct hypoechoic lesions with posterior acoustic shadows. A core biopsy revealed high grade DCIS with calcifications. Due to the extensive microcalcifications, the patient was recommended to undergo a mastectomy and immediate breast reconstruction with expander implant. The surgery was performed on 23 March 2010. The mastectomy specimen weighed 238 g and measured 13 × 12 × 3 cm. Grossly, in the upper lateral quadrant of the breast a suspicious area was found. The suspicious focus measured around 2 cm in the largest diameter and consisted of somewhat harder yellow-whitish tissue of granular appearance. In the other parts, the breast tissue was mainly fatty without macroscopically suspicious changes. Careful sampling of the suspicious area and surrounding parenchyma was performed. Altogether, 12 tissue blocks were taken from that area. Besides, one paraffin block was taken from each quadrant and central part of the breast. Microscopic examination revealed massive, high grade DCIS with multiple foci of microinvasion that measured up to 0.1 mm in the largest diameter. Deeper sections from the paraffin blocks with microinvasion were also performed, but no invasive focus ≥1 mm was found. DCIS was located mainly in the upper lateral quadrant but multicentric foci of DCIS were present in all breast quadrants. The dimension of the DCIS was approximately 8 cm. Surgical margins were free (the basal margin was 6 mm). Tumour cells were negative for oestrogen (expressed in less than 1% of cells) and progesterone receptors (0%). Testing for HER2 status was not performed. In the pathologist’s opinion, the invasive clusters were too small for a reliable determination of HER2 status. Isolated tumour cells were found in the two sentinel lymph nodes. No adjuvant systemic therapy was recommended. The patient was regularly checked by a plastic surgeon from March to June 2010. In the meantime, filling of the expander implant with saline was performed. In June 2010 the patient went back to her work. On 23 September 2010, the replacement of the temporary implant for the permanent silicone prosthesis was performed. Blood count, electrolytes, urea and creatinine were in a normal range at that time. Laboratory liver function tests were not performed. She was examined for the last time by the plastic surgeon on 11 October 2010 when the sutures were removed and the wearing of an elastic bra was recommended. On 23 November 2010, the patient was referred to our institution after having been hospitalised for two weeks in a regional hospital due to the general deterioration of her health. Upon referral, she was icteric and in Eastern Cooperative Oncology Group performance status 3. Laboratory tests revealed leucocytosis, hypercalcaemia, deterioration of the liver and renal function and elevated tumour markers. Laboratory results upon referral were: leukocytes 14.8 × 109/L, haemoglobin 121 g/L, platelets 167 × 109/L, creatinine 145 μmol/L, urea 12 mmol/L, calcium 3.78 mmol/l, alkaline phosphatase 7 μkat/L, gama glutamil transferase 14 μkat/L, total bilirubin 95 μmol/L, direct bilirubin 84 μmol/L, aspartate transaminase 8.7 μkat/L, alanine transaminase 1.9 μkat/L, lactate dehydrogenase 7.9 μkat/L, albumins 26 g/L, C-reactive protein 69 mg/L, procalcitonin 4.1 μg/L, carcinoembryonic antigen 37000 μg/L, CA 15–3 432 kU/L and ammonium ion 187 μmol/L. An abdominal ultrasound was performed and showed ascites and an enlarged liver with diffuse lesions suspicious for metastases. A sample of ascites was sent for cytopathological examination. No malignant cells were found in the specimen. The hepatorenal failure progressed rapidly and the patient died on 29 November 2010. An autopsy was performed.In the autopsy a massive and diffuse infiltration of the liver with breast cancer metastases was found (Figure A). On immunohistochemical staining, tumour cells were negative for oestrogen and progesterone receptors and highly positive for HER2 (Figure B). The fluorescent in situ hybridization deoxyribonucleic acid probes score was over 10 (Figure C).\nWe report a highly aggressive course of DCISM in a premenopausal woman. She was treated with a mastectomy, sentinel lymph node biopsy and immediate breast reconstruction with implant. Tumour cells in microinvasive foci were hormone receptor negative and of unknown HER2 status. The sentinel lymph nodes showed no macrometastases but isolated tumour cells. The patient received no adjuvant systemic therapy. Eight months after the surgery she died from hepatic failure without her previously known breast cancer progressing. The autopsy revealed diffuse liver metastases with HER2-positive and hormone receptor negative breast cancer.\nDespite the increasing incidence of DCIS as a consequence of widespread use of screening mammography, the incidence of DCISM remains low and accounts for around 1% of all breast cancers []. In general, the prognosis of DCISM is good and thought to be intermediate between pure DCIS and an early stage invasive cancer (T1a). Only a few reports present the local and distant recurrence rate and long-term outcome of patients with DCISM [,,,]. The heterogeneous definitions of microinvasion that were used in the past make clinical outcomes difficult to compare. In studies in which the current American Joint Committee on Cancer definition of microinvasion was used, the 5-year local relapse rate was between 0% and 3% and 5-year distant relapse free survival almost 100% [,,]. The worst distant relapse free survival was reported by Parikh et al. In a group of 72 patients the 10-year distant relapse free survival was 97.9% [].\nWe are currently still lacking a reliable test to accurately predict outcomes. Among prognostic factors for the outcome in DCISM, the number of microinvasive foci, metastases to the sentinel lymph node, high Ki-67, negative oestrogen receptor status, and HER2 overexpression were found [,]. The number of microinvasive foci is probably higher in more extensive DCIS. The size and extent of DCIS lesions are often only an estimate []. Quantifying the size of a DCIS lesion is difficult and precise measurement is often impossible. Still, an estimation of the DCIS size is clinically very important. According to the College of American Pathologists guidelines for examining specimens from patients with DCIS, microscopic examination of the entire area affected by DCIS is recommended but is very often impractical if DCIS is larger than 4 (even 2) cm []. In such a case, there is always a possibility of undetected areas of invasion if the area affected by DCIS is not completely examined. As well, smaller invasive foci could be missed because they can be present deeper in that part of the paraffin block that was not histologically examined. It is difficult for the pathologist to find all possible foci of microinvasion in very extensive DCIS. The multifocality of microinvasive disease is in correlation with positive sentinel nodes [,].\nIn invasive breast cancer, axillary lymph node metastases are the most powerful prognostic factor for relapse and survival. The risk of sentinel lymph node metastases among patients with DCISM has been reported to be between 0 and 20% []. It is crucial to identify a very small subset of microinvasive cancer patients with macrometastases, which could benefit from adjuvant systemic therapy []. In case of a positive sentinel node, an axillary dissection should be performed [,,]. In case of positive axillary nodes, adjuvant systemic therapy with tamoxifen in hormone receptor positive tumours, and with chemotherapy in hormone receptor negative tumours could be offered. In invasive breast cancer, micrometastases but not isolated tumour cells were associated with additional positive nodes upon axillary dissection and with distant recurrence []. Most authors agree that a sentinel node biopsy should be performed although some believe it could be omitted due to a low rate of positivity [,]. The outcome is generally very good with few local and even fewer distant relapses [,]. At present, the significance of lymph node micro- or macrometastatic disease on overall survival in DCISM is unclear and needs to be ascertained with further studies. Colleoni et al. reported increased Ki-67 as a significant prognostic factor for disease free survival in DCISM [].\nHER2 overexpression was present in 77% of locally relapsed tumours after breast-conserving therapy for DCIS (with or without radiation therapy in European Organisation for Research and Treatment of Cancer trial 10853) []. A clinical implication of HER2 status in DCIS is unclear. On the contrary, HER2 overexpression in even small invasive cancers is correlated with poor prognosis. Roses et al. found HER2 status to be a predictor for the transition from in situ to invasive breast cancer []. However, there are some technical constraints on HER2 testing as a certain volume/number of malignant cells in a cluster should be found for reliable testing. One of the on-going trials in HER2-positive DCIS involves the testing of a single application of neoadjuvant trastuzumab in <1 cm DCIS before surgery. The second trial is a phase III National Surgical Adjuvant Breast and Bowel Project B43 trial comparing adjuvant radiotherapy with or without two doses of adjuvant trastuzumab in HER2-positive DCIS after breast-conserving surgery []. There are also promising results of clinical studies with HER2-pulsed autologous dendritic cell vaccine administered before surgical resection of high-risk HER2-positive DCIS [,]. The results of those trials will hopefully show more insights into the biology of HER2-positive DCIS and DCISM.\nMori et al. evaluated almost 400 tumour specimens of patients who were diagnosed with either DCIS, DCISM or T1a breast cancer. The comedo type and ER negative/HER2-positive type were found more frequently in DCISM than in either DCIS or T1a tumours. The co-expression of HER2 and 14.3.3 zeta could be important since HER2 overexpression plays a role in the process of first invasion and 14.3.3. zeta in the reduction of cell adhesion [].\nOur patient had many potential risk factors for relapse. She had a very extensive DCIS in the whole breast with more than one microinvasive focus within DCIS. DCIS was of a comedo subtype. She had no micro- or macrometastases but isolated tumour cells were present in the sentinel lymph node, which suggested a more aggressive disease. Tumour cells were negative for oestrogen and progesterone receptors. HER2 status was not determined due to an unreliable result determined on a scant sample. The patient received no adjuvant systemic therapy. The number of invasive foci and the extent of DCIS could be very suspicious of many microinvasive foci. In that specific case, we did not consult a pathologist for the additional counting of invasive foci. Following this case, the general practice at our institution has changed. If a pathologist finds more than 5 microinvasive foci (where the sum of the sizes is at least 5 mm) we discuss adjuvant chemotherapy with the patient. |
A 31-year-old woman with a history of left common iliac vein thrombosis presented with symptomatic lower abdominal and left groin superficial varicosities associated with itching, swelling, and discomfort. Vital signs revealed a blood pressure of 114/80 mmHg and pulse of 72 beats/minute. Physical examination confirmed the presence of large tortuous varicosities at the lower abdomen and left groin (). The patient had previously been diagnosed with left common iliac vein thrombosis during her first pregnancy, 10 years earlier, that was only managed with enoxaparin injections. Over the next few years, she developed lower abdominal and left groin varicosities that worsened significantly during her second and third pregnancies without confirmed recurrent deep vein thrombosis (DVT). The patient denied leg swelling prior to the DVT event. She also denied any history of abdominal trauma, other thromboembolic events, or family history of vascular anomalies. Computed tomography (CT) venography revealed compression of the left common iliac vein by the right common iliac artery without evidence of acute thrombosis, indicating a diagnosis of May-Thurner syndrome- (MTS-) related anatomy ().\nCatheter-based venography with hemodynamic pressure measurements confirmed May-Thurner anatomy with sequelae of chronic DVT in the left iliac vein and cross-pelvic drainage via pelvic and abdominal wall varices (). Successful recanalization was performed using percutaneous transluminal angioplasty with stenting of the left common iliac vein (20 mm x 55 mm Wallstent) and left external iliac vein (14 mm x 60 mm Protege). The patient was managed with apixaban (5 mg twice daily) for three months and clopidogrel (75 mg daily) for one month that was changed to aspirin (81 mg daily) in the long term. A 3-month follow-up CT venogram indicated a patent left iliac vein stent. However, the patient continued to present with painful, though slightly improved, lower abdominal and left groin varicosities.\nGiven these persisting symptoms, we performed successful stab phlebectomy of the large superficial abdominal varicosity. We also treated the deeper feeding branch and groin varicosities with ultrasound-guided sclerotherapy using a sclerosing foam (two injections of 1 cc of 3% sotradecol mixed with 2 cc of room air). The procedure resulted in complete resolution of the symptomatic lower abdominal and left groin varicosities (). The patient did very well at 6- and 12-month follow-up visits while on aspirin, and a repeat CT venogram indicated a patent left iliac vein stent. |
A 46-year-old Hispanic male with a known history of type 2 diabetes mellitus presented with 2 days history of acute epigastric abdominal pain with associated postprandial nausea and vomiting. His other medical conditions include hypertension, hyperlipidemia, diabetic neuropathy and seizure disorder. On examination, he was thin built with body mass index (BMI) of 20.1, and vital signs revealed mild tachycardia and hypotension. Remainder of the exam was unrevealing. Pertinent labs revealed creatinine of 1.4 mg/dl, hemoglobin 10.3 g/dl, albumin 1.5 g/dl, prealbumin 4.7 mg/dl and normal liver function tests. Patient had similar symptoms intermittently for the last 2 years. In the past, his symptoms were attributed to gastroparesis due to his long-standing diabetes mellitus. He had multiple CT scans of abdomen done during this period but most of them were without contrast. These scans were either normal or showed mild gastric distension at times which was thought to be secondary to gastroparesis. Of the several scans, he had one CT abdomen with IV contrast approximately one year prior to this presentation, this revealed mild gastric and proximal duodenal dilatation but there was no evidence of duodenal obstruction. He had an upper GI endoscopy recently and this revealed dilated stomach and duodenum along with pyloric and proximal duodenal circumferential ulceration and was treated with proton pump inhibitors. Due to his intermittent symptoms he had poor oral-intake and had a weight loss of about 15 lbs in the last few months (Figs –).\nPatient was admitted for possible gastroparesis exacerbation and peptic ulcer disease. He was treated with intravenous fluids and Pantoprazole. Supportive care with fluids normalized his renal functions but not his abdominal pain, hence CT abdomen with IV contrast was undertaken. This revealed dilatation of stomach and proximal duodenum and decompression of rest of the duodenum and small bowel. The aortomesenteric distance was measured at 3.1 mm and narrowed aortomesenteric angle of 14°. All these findings along with his symptoms were consistent with SMA syndrome.\nGastric decompression with nasogastric tube was done and Gastroenterology and General surgery were consulted. He underwent upper gastrointestinal endoscopy which revealed distended stomach and proximal duodenum with presence of food but no evidence of ulceration as seen few weeks ago. Endoscope could not be advanced into distal duodenum.\nPatient was given total parental nutrition for about 3 weeks. His nutritional status improved as seen by improvement in his albumin (from 1.5 to 2.5 g/dl) and prealbumin (from 4.7 to 21.5 mg/dl). Patient felt better and gained weight but continued to have abdominal pain, nausea and vomiting when challenged with diet. Due to lack of improvement with conservative management, patient was taken to operation room by general surgeon and underwent open gastrojejunostomy. Intraoperatively, decreased amount of intrabdominal fat was seen. Patient did well postoperatively and was tolerating diet well prior to discharge. |
This 77 year old woman was being prepared for an aortic valve replacement and tandem aorto-coronary bypass graft surgery. Under general anesthetic, the anesthetist used a Site-Rite 3 (Bard Access systems, Salt Lake City, UT, USA) ultrasound unit while attempting to access the right internal jugular vein for venous sheath placement. This attempt failed.\nThe anesthetist then used the same ultrasound unit attempting to access the right subclavian vein for venous sheath placement. Following what was presumed to be successful ultrasound guided venous access, an 8.5 F sheath was implanted. The anesthetist noted an arterial wave-form arising from the sheath tracing. It was presumed that the subclavian artery, beneath the mid-portion of the clavicle, had been inadvertently catheterized. The sheath was left in situ due to concerns about uncontrollable arterial bleeding if it was extracted without the ability to directly compress the arterial puncture site.\nThe cardiovascular surgeon performed aortic valve replacement and aorto-coronary bypass surgery. Consultation with a peripheral vascular surgeon was sought. The peripheral vascular surgeon suggested that rather than perform a complicated surgical procedure to extract the sheath, i.e. an extensive anterior chest wall dissection and resection, that interventional radiology be consulted about angiography and the possible placement of a stent-graft in the infraclavicular subclavian artery. The cardiovascular surgeon consulted the interventional radiology team.\nThe patient was transferred to the angiography suite directly from the operating room and remained under general anesthetic. Consent for the procedure was obtained from the patient's family.\nRight femoral artery access was achieved and a 6 F groin sheath was placed for angiographic imaging. Injections of the right innominate artery demonstrated a normal infra-clavicular subclavian artery. The 8.5 F sheath was situated with the tip just downstream from the origin of the right common carotid artery within the proximal right subclavian artery. (figure ) Further angiographic images were obtained in other projections. In addition, the 8.5 F sheath was directly injected with contrast agent in order to determine the exact location of the sheath. Early (figure ) and delayed (figure ) angiographic images were acquired.\nIt was determined that the 8.5 F sheath had actually entered via the ventral aspect of the right subclavian artery just downstream of the origin of the right common carotid artery and had not punctured the more distal infra-clavicular subclavian artery as suspected by the clinical team. There was no evidence of spasm or extravasation of contrast at the site of the catheter entrance into the subclavian artery, or elsewhere. Despite the very proximal entry point of this catheter into the subclavian artery the cardiovascular surgeon had not been able to directly visualize it, or palpate it, during the surgical exploration of the mediastinum.\nRight sided pelvic angiography was performed to ensure that the pelvic arterial anatomy would accommodate the placement of a stent-graft. There were no pelvic or distal aortic impediments to stent-graft placement.\nThe 6 F right femoral artery sheath was removed and a 12 F right common femoral artery sheath was implanted to accommodate the stent-graft. An exchange length Amplatz guide wire was situated with the tip in the right axillary artery. A 70 mm long/12 mm diameter Wallgraft endoprosthesis (Boston Scientific, Natick, MA, USA) was successfully implanted in the right subclavian artery while the 8.5 F sheath in the subclavian artery was simultaneously extracted.\nImmediate post-implantation angiography demonstrated a patent stent-graft and acute occlusion of the right internal mammary artery and the right vertebral artery. There was no evidence of contrast extravasation and no clinical evidence of subclavian artery bleeding. (figure ) The patient remained hemodynamically stable. The right groin sheath was extracted and groin hemostasis was achieved. The patient was transferred to the Intensive Care Unit (ICU) for further care. Right arm and right leg pulses were all palpable and there was no clinical evidence of hemorrhage.\nThe patient spent 3 days in the ICU and was then discharged to the ward. She recovered with no evidence of peripheral vascular or neurologic sequelae. She was discharged from hospital to further convalesce 3 days after leaving the ICU. |
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