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A 35-year-old woman was referred to our hospital with liver masses in an ultrasound study that was requested because of vague upper abdominal pain. She also mentioned mild nausea that started one month earlier. Medical history revealed three normal vaginal deliveries and she was receiving medroxyprogesterone acetate injections every 3 months for contraception.\nThe patient’s physical examination was normal as well as her laboratory tests, which included complete blood count (CBC), liver biochemical tests, tumor markers, sedimentation rate (ESR), and C-reactive protein (CRP) (). Esophagogastroduodenoscopy (EGD) was done, which showed only Los Angeles grade B reflux esophagitis.\nThe initial ultrasound study showed three hypoechoic subcapsular nodules with maximum diameters of 25 mm in the right hepatic lobe in a background of normal liver parenchyma (). Abdominal and pelvic computed tomography (CT) with intravenous/oral contrast revealed two hypodense lesions of 10 and 12 mm diameters in the anterior segment of the right hepatic lobe and one 25 mm diameter lesion with more density in the posterior segment of the right hepatic lobe. Red blood cell single photon emission computed tomography (RBC-SPECT) was performed to rule out hemangioma (). Ultrasound guided liver biopsy was done to make a definite diagnosis. Two 1×10 mm biopsy specimens were sent for histopathological study. Hematoxylin and eosin stained (H&E) sections of liver specimens showed multiple foci of proliferating bile ducts composed of bland cuboidal cells and duct formation in the fibrotic and inflamed portal spaces. Bile duct proliferation was compatible with BDA (). Immunohistochemical (IHC) staining was done for CK7 and P53, which showed positive for CK7 and negative for P53.\nAs no risk factors were known to have a relationship with BDA, the patient was advised to discontinue medroxyprogesterone. A proton pump inhibitor was started to treat the esophagitis. She was then followed up for two years by routine laboratory tests and ultrasonography performed by an expert sonographer. Gradual size reduction of the lesions was reported. Liver parenchyma was normal in ultrasound after 16 months. Because magnetic resonance imaging (MRI) has more accuracy in detecting small hepatic lesions (less than 2 cm), liver MRI was performed in the 22nd month, which showed no hepatic lesion (, ). |
A 50 year-old male, with a history of coronary arterial bypass grafting 14 years back, presented with shortness of breath and dry cough. An X-ray revealed a large mass in the left hemithorax adjacent to the heart silhouette. A chest CT demonstrated the presence of a mass with smooth edges, in middle mediastinum next to the heart and partially intrapericardial (Fig. ). The mass was of heterogeneous density and of 11 cm size. Presence of atelectasis at the left lower lobe abating the mass was clearly seen. Based on clinical and radiologic evidence, we did proceed with CT guided FNA of the mass. The cytology findings revealed inflammatory lesion. Laboratory tests were normal. Based on patient symptoms, history and the presence of a mass potentially compressing the cardiopulmonary structures in vicinity, we decided to offer exploratory surgery for diagnosis and treatment.\nStandard hemodynamic monitoring and general anesthesia were followed by positioning, prepping and draping patient in left lateral decubitus position. An anterolateral left thoracotomy was carried out and entrance in the hemithorax was made without any challenge. The mass was assessed and found to be leaning medially on the surface of the lateral wall of the left ventricle, including the pericardial layer and had smooth edges which didn’t infiltrate the lung (Fig. ). We started dissecting the mass from its smooth capsule, making it through all its layers. An old and degraded piece of surgical swap was visualized (Fig. ). The surgical swap was removed along with the capsular layer of this mass. Patient tolerated the procedure very well and blood loss was minimal. A chest tube was inserted in the left hemithorax and chest wall was closed following standard procedures.\nIn the immediate post-operative phase, patient improved steadily and on day four was discharged home symptom-free. In the long-term follow -up, patient was found to remain without symptoms. |
We report the case of a 40-year-old healthy male with a history of hypertension and migraine who presented to the ED with a persistent headache and fever for five days. Review of systems was negative for changes in vision, speech, focal weakness, or numbness of the extremities. He did have a rash on the right lateral thigh and gluteal region. He reported that he was undergoing treatment for shingles infection with some improvement in the vesicular rash. There was no skin involvement on the left side. He did not report any history of recent travel or sick contacts. The physical exam did not show focal neurological signs and skin findings limited to the above description.\nCT head non-contrast showed no acute intracranial hemorrhage, territorial infarct, or mass effect. The confusion, headache, and fever necessitated a lumbar puncture, which was performed. CSF analysis revealed elevated white blood cell count with lymphocytic predominance (121 nucleated cells (lymphocytes 71%)), elevated red blood cells (RBC 5 (reference range <2); likely from traumatic tap), mildly elevated protein (106 mg/dL; reference range 15-45 mg/dL), and normal glucose level (51 mg/dL reference range (40-71 mg/dL). These findings were consistent with aseptic meningitis. Gram stain of the CSF was negative. There was no bacterial growth of the CSF culture. Polymerase chain reaction (PCR) for VZV was performed, which was positive. Despite the CSF glucose level being low-normal when compared to serum glucose at that time, the CSF/serum glucose ratio was 0.3, which is abnormal. The patient was treated with intravenous acyclovir 750 mg every eight hours for 21 days.\nLyme serologies were checked on the patient on admission, and he was positive for IgM antibodies, which was followed up with a positive confirmatory blot (positive for p39, p41). The result was equivocal, so qualitative Lyme PCR was sent out. In the interim, he was also started on doxycycline 100 mg twice daily for 14 days for empiric. It was unlikely that the patient had two primary CSF infections as per the infectious disease consulting service, even though the Lyme could appear consistent with lymphocytic meningitis. The repeat Lyme serologies were negative for both IgM and IgG, and the Lyme DNA qualitative PCR was negative. A CD4 count was also checked as it is unusual for multidermatomal VZV to occur in immunocompetent patients. The absolute CD4 count was 1437 (reference range 430-1800 cells/uL) with a CD4/D8 ratio of 4.1 (reference range 0.8 to 3.9). HIV was checked, which was negative for the HIV-1 p24 antigen and HIV-1/HIV-2 antibodies.\nThe patient followed on discharge three weeks later in the outpatient infectious disease clinic. At that time, the patient still had complained of mild headaches. He also endorsed a history of a red circular, discrete rash on his right lower extremity prior to his recent hospitalization for aseptic meningitis. A vesicular rash persisted on his right lateral thigh, although there was improvement along the gluteal region. At this point, the acyclovir duration was extended for one week, and the patient transitioned from intravenous to oral acyclovir therapy at 1 g three times per day. |
The patient is a 57-year-old man (height, 173.5 cm; weight, 61.7 kg), and the remaining teeth in his lower jaw were 1, 2, and 3 on the right side and 1, 4, and 5 on the left side. The patient had chronic apical periodontitis and severe periodontal disease. There was teeth movement, and it was difficult to preserve them. We planned to extract these teeth and place six implants (Figure ).\nA physician had suspected the presence of VWD when the patient was aged 21 years, but no detailed testing or treatment was performed. The family history was not relevant, and the patient was on no current medications.\nIn terms of preoperative chest findings, the chest X-ray was normal (Figure ) with a normal cardiothoracic ratio of 42%, and there were no particular issues. Blood test results are shown in Table . The platelet count, a hemostatic factor, was 360,000/µl, the activated partial thromboplastin time was 35.4 s, and the prothrombin time was 11.7 s; all were within normal limits. However, coagulation factor VIII was 49%, VWF activity was 24%, and VWF antigen was 26% indicating that the coagulation factor was lower than normal. Based on detailed testing carried out by our hospital's hematology department, the patient was diagnosed with Type 1 VWD, in which there is a quantitative decrease in the VWF.\nThere was nothing of particular note in terms of family history. Implants in the upper jaw had already been placed at a different hospital, and there had been some difficulty stopping the bleeding when the teeth were extracted. In this case, after consulting with the hematology department, we decided that surgery would be possible by transfusing heat-treated factor VIII concentrate (Confact F®), which contains VWF. This transfusion was done to prevent abnormal bleeding during surgery. Furthermore, considering the risk of bleeding due to fluctuations in hemodynamics, with the patient's consent, we planned to carry out tooth extraction and implant placement under local anesthesia with intravenous sedation.\nOne hour before entering the operating room, 1500 units of Confact F® were transfused. In terms of transfusion volume, although we planned to carry out implant placement, it was determined that the amount of bleeding would not differ greatly from that of tooth extraction alone, so we used 25 IU/kg, basing our calculations on those published in the New England Journal of Medicine (Table ). Immediately before surgery, we took another blood sample. We confirmed that VWF activity was 127% and that coagulation factor VIII had increased to 104%. We then proceeded with the surgery. Considering that fluctuations in hemodynamics during surgery promote bleeding, intravenous sedation was performed to stabilize circulation. Oxygen (2 L/min) was administered transnasally, and cefmetazole sodium (1 g) was administered preoperatively to prevent infection. During the operation, we used midazolam iv and propofol (1% Diprivan Injection kit®) target-controlled infusion for continuous intravenous sedation. Also, 2% Xylocaine Dental® with epinephrine 1:80,000 was used for local anesthesia. The operation time was 3 h and 37 min, the anesthesia time was 4 h and 16 min, and blood loss was 405 ml. Although it was a little difficult to stop bleeding during the operation, we completed the procedure with no major problems. No postoperative complications, such as bleeding, were observed, and the prognosis was favorable. One week after the operation, evaluation of the coagulation factor VIII and VWF activity revealed that they had decreased to 48% and 23%, respectively, which were close to their preoperative values (Table ). |
A 54-year-old Caucasian man presented with epigastric pain associated with nausea without fever or respiratory symptoms. He had a known history of Bochdalek hernia diagnosed two years prior. Medical records indicated that our patient was seen previously by a thoracic surgeon who recommended nonoperative treatment. It was not known if the extent of herniated viscera had worsened in the interim as imaging studies were not available. A physical examination was significant for diminished breath sounds over his right thorax; his abdominal examination was benign. Laboratory data revealed mild leukocytosis with normal serum chemistry and liver-associated enzymes. Radiographic evaluation with axial CT confirmed a massive hernia of Bochdalek with multiple displaced organs into his right thorax (Figure and Figure ). Initial management included nasogastric decompression and intravenous fluid resuscitation with the presumptive diagnosis of bowel incarceration. After 24 hours, our patient was then taken to the operating theater for repair of the hernia. Given the size of the defect, the surgical approach was a thoracoabdominal incision to allow simultaneous access to both his abdominal and thoracic cavities. At surgery, near complete agenesis of his right hemidiaphragm was noted. Following reduction of his stomach, omentum and bowel, the liver was noted to be grossly abnormal with a macronodular appearance. Further examinationination confirmed acute cholecystitis of the displaced gallbladder (Figure ). Nearly his entire liver was situated in his lower thorax with its bilio-vascular pedicle stretched as it was pulled into his chest. Following cholecystectomy, a liver biopsy was taken prior to reducing his liver and other organs back into his abdomen. His diaphragm was reconstructed with expanded polytetrafluoroethylene (e-PTFE; 0.2 mm, WL Gore and Assoc., Flagstaff, AZ) (Figure ). Due to concern for loss of domain and the possible development of abdominal compartment syndrome (ACS), a smaller prosthetic patch was used to close the abdominal fascia to decrease the risk of abdominal hypertension. The right lower lobe of his lung was noted to be hypoplastic; malrotation of the bowel was not observed. Our patient was extubated after surgery and nasogastric decompression was used for 48 hours prior to advancement of oral intake. Postoperatively, our patient was monitored for the development of abdominal hypertension with transurethral bladder pressure measurements for 24 hours []. Fortunately, there were no concerns for ACS and our patient had an unremarkable postoperative recovery. At follow-up one year later, our patient noted significant improvement in his activity level as compared to his preoperative state and chest radiography confirmed acceptable separation of his chest and abdominal cavities without recurrence (Figure ). The liver biopsy returned with the diagnosis of NRH (Figure ). The pathogenesis of NRH is unknown, but thought to be due to hepatic blood flow disturbances []. |
A previously healthy 34-year-old Korean female was admitted to a regional hospital for fever, myalgia and severe headache that had started 2 weeks ago. Brain MRI showed a high T2 signal intensity change and diffuse swelling of the right temporal lobe, insula and hippocampus (Fig. ). Lumbar puncture showed lympho-dominant pleocytosis. The patient was started on intravenous (iv) dexamethasone and acyclovir under a high suspicion of viral encephalitis.\nShe was transferred to our institution 4 days later due to persistent headache despite treatment. A noncontrast computed tomography (CT) brain scan taken at our institution showed a hemorrhagic transformation of the right temporal lobe, which was not observed on the initial MRI (Fig. ). Follow-up lumbar puncture showed 510 white cells per mm3 (82% lymphocytes), 144 mg/dL protein and 61 mg/dL glucose. CSF culture studies were negative for bacteria, fungi and tuberculosis. PCR of the CSF confirmed the presence of HSV1. The patient was free of neurological symptoms, with a Glasgow Coma Scale of E4M6V5, and was admitted for close observation and continuation of iv acyclovir. Corticosteroid treatment was discontinued upon her admission. On day 3 of hospitalization, the patient presented with a sudden onset of vomiting and severe headache. Brain CT showed an increased amount of temporal lobe hemorrhage and a leftward shift in the midline (Fig. ). Mannitol was administered but did not seem to have a significant effect. The patient became increasingly drowsy, and her right pupil became dilated. She underwent emergency right decompressive craniectomy, expansile duraplasty and ICP monitor insertion. Postoperative brain CT showed alleviation of midline shifting (Fig. ). The patient recovered fully 5 days after the surgery. Apart from mild intermittent headache and dizziness, she did not show any other significant clinical symptoms, including neuropsychological problems. There were no significant neurologic deficits upon neurological examinations performed by the attending neurosurgeon and neurologist. The patient was discharged after completion of 2 weeks of acyclovir and returned 2 months later for cranioplasty. She was followed up 3 more times after cranioplasty. She was stable, without any neuropsychological problems or neurologic deficits, and was able to successfully return to work as a public official. |
A 61-year-old Hispanic male with a history of undifferentiated schizophrenia was admitted to the intensive care unit after a rapid response team evaluated him in the psychiatric unit for a syncopal episode.\nThe patient was being managed in the psychiatry floor for agitation and aggressive behavior and had been there for 5 weeks before this presentation. Patient had multiple psychiatry admissions for similar reasons. At baseline, the patient was unable to speak in meaningful sentences but responded by answering “yes” or “no” to goal-directed questions.\nThe patient was on levothyroxine for hypothyroidism, which was well controlled with free thyroid-stimulating hormone of 1.20 for 2 weeks before the current presentation. He also had seizure disorder, which was being treated with divalproex sodium extended release 1,000 mg daily, and levetiracetam 750 mg twice daily.\nThe patient was being treated with clozapine for his schizophrenia. The treatment of the patient was started with clozapine 5 weeks back during the current psychiatric admission, and dose gradually increased to 150 mg everyday in the morning and 150 mg everyday in the evening. His evening dose was increased to 175 mg everyday in the evening 5 days before this presentation. He had glaucoma for which he was receiving dorzolamide/timolol eye drops. He was not on any other medications. He was given a regular diet and was encouraged to take plenty of fluids and fibers. He did not have any surgical history.\nThe patient was apparently well until the day of this presentation when the patient was noted to walk around the nursing station and appeared as if about to fall and developed a syncopal episode. The vitals were temperature 98°F (36.6°C), blood pressure 86/54 mmHg, pulse 127 beats/min, regular, respiratory rate 16 breaths/min, and oxygen saturation 100% while breathing ambient air. Intravenous access was obtained and normal saline of 500 mL bolus was administered. The patient became responsive within few minutes and tried to get up. He was moving all his limbs and did not appear to have any focal motor deficits. No seizure activity was noted. He was confused, agitated, and unable to provide any history. The patient was transferred to the intensive care unit.\nPhysical examination was significant for abdominal distension with hypoactive bowel sounds. Rectal examination revealed hard impacted stool in the rectal vault. Stool qualitative guaiac test was performed, which was negative.\nThe complete blood count revealed leukocyte count of 17,300/mm3 with neutrophil differential of 52% with absolute neutrophil count (ANC) of 9,000/mm3 with band neutrophils of 12%. Prior to the syncopal episode, the weekly leukocyte counts after the initiation of clozapine were as follows:\nWeek 1 – Leukocyte count 7,100/mm3 with neutrophil differential of 45% (ANC, 3,195/mm3). Week 2 – Leukocyte count 6,600/mm3 with neutrophil differential of 61% (ANC, 4,026/mm3). Week 3 – Leukocyte count 5,400/mm3 with neutrophil differential of 65% (ANC, 3,510/mm3). Week 4 – Leukocyte count 5,200/mm3 with neutrophil differential of 60% (ANC, 3120/mm3). Week 5 – Leukocyte count 6,500/mm3 with neutrophil differential of 67% (ANC, 4,355/mm3).\nHemoglobin was 18.6 g/dL, the baseline range was 13–14 g/dL. Comprehensive metabolic panel was significant for elevated blood urea nitrogen (BUN)/creatinine of 34/1.4; however, baseline BUN/creatinine range was 13.0–17.0/0.8–1.0. Liver function tests were within normal limits. Sodium, potassium, magnesium, and phosphorous were normal. Serum bicarbonate was low at 18 mmol/L with low serum chloride of 100 mmol/L and elevated anion gap of 17. Serum lactic acid was elevated at 115.4 mg/dL. Serum total protein, albumin, globulin, and creatine kinase were normal. Serum valproic level was 60 µg/mL, serum clozapine level was not available.\nElectrocardiogram revealed sinus tachycardia without any acute ST-T segment changes. Serum troponin I was normal.\nUrinalysis revealed high specific gravity, with no bacteria or elevated nitrate. Urine toxicology was negative.\nChest X-ray () was significant for elevated hemidiaphragm with low lung volumes and clear lung fields. Abdominal X-ray () revealed large amount of fecal content in the colon and dilated small bowel suggestive of bowel obstruction from fecal impaction. The patient was started on broad spectrum antibiotics after pan cultures were obtained and intravenous fluids were administered; however, he had a rapid decline in clinical status with worsening hypotension. Surgical evaluation was requested for possible surgical intervention of bowel obstruction; however, he was deemed to be too unstable for any surgical intervention. He was being managed as per surviving sepsis guidelines for septic shock. He developed cardiac arrest and unfortunately expired within 12 hours of presentation. The blood culture revealed Escherichia coli within 24 hours. Urine culture revealed no growth.\nThe patient did not have a prior history of constipation or fecal impaction, or any other risk factors for constipation. He was described as being minimally communicative, often mumbling incoherent words, and disorganized and aggressive at times. |
A 5-year-old boy weighing 20 kg having the history of seizures, mental, and motor retardation referred to our clinic for upper gastrointestinal endoscopy due to the recurrent respiratory tract infections and gastric reflux. He was the second son of a married couple. His parents were not relative. He was born at full term with cesarean section delivery, weighing 2800 g.\nThe weight of the baby at birth was 2800 g with a cranial circumference of 40 cm an Apgar score 6 and 8 at 1 and 5 min, respectively. There was no coiling of the umbilical cord or amniotic fluid turbidity at the time of the birth. Echocardiography showed good heart contractility. No kidney, heart, or immune system abnormalities were found. The metabolic screening tests; serum lactate and ammonium were within normal limits. The color of the baby's hair was blonde, eyes were light blue.\nHe was drowsy, hypotonic, hyporeflexic with no finger grasp. To investigate the possible dysmorphic syndrome magnetic resonance (MR) was performed. MR imaging of the brain showed macrocephaly with corpus callosum agenesis. He had seizures, myoclonic jerks, macrocephaly, global development delay, and cataract. Neurologic examination revealed a hypotonic infant with the inability to stand unsupported. He was unable to blink his eyes, smile, or frown. Gastroesophageal reflux disease was diagnosed owing to repeated lower respiratory tract infections. He was using long-term multiple antiepileptic drugs and had a cataract in one eye.\nThe patient was scheduled for upper gastrointestinal endoscopy. Preoperative routine laboratory investigations and hormone profile were normal. After preoperative stabilization and written informed consent from the parents, deep sedation was planned.\nIn the operating room, the routine monitors were attached and intravenous (IV) access established with a 24 G cannula. Sedation was accomplished with dexmedetomidine IV 0.5 μg/kg/h. He received nasal oxygen breathing spontaneously. Oxygen saturation was maintained between 97% and 100%. Body temperature, heart rate, noninvasive blood pressure, O2 saturation, and end-tidal CO2 were stable during the procedure and postoperative period. |
An 89-year-old male presented from a nursing home with potential seizure-like activity witnessed by his daughter. He had an extensive medical history that included colon cancer status post colectomy with ileostomy placement and significant resection of the small bowel secondary to small bowel obstruction caused by adhesions. Furthermore, he suffered from malnutrition and chronic electrolyte abnormalities, given his short bowel syndrome secondary to multiple resections.\nThe daughter noticed her father became unresponsive hence initiated bedside cardiopulmonary resuscitation (CPR) for two minutes until emergency medical services (EMS) arrived. Upon arrival to the emergency department (ED), the patient was noted to have a serum magnesium level of 0.6 mg/dl, and an EKG revealed a prolonged QTc of 590 ms, as noted in Figure .\nTwo grams of magnesium sulfate IV push was administered, and the patient was then transferred to the intensive care unit (ICU). Later that afternoon, the patient’s QTc began to normalize, and his magnesium was then 2.5 mg/dl. Given that he appeared medically stable and had no capacity issues at the hospital, he was placed back in the ED for ICU holding.\nThe following morning, the patient began having intermittent episodes of TdP as noted on telemetry. His QTc prolonged again to 573 ms (Figure ); however, his serum magnesium remained normal.\nHe was given additional magnesium along with IV metoprolol and two bolus doses of amiodarone. He required defibrillation for these episodes of TdP each time, at which point cardiology was consulted. The episodes of TdP were successfully terminated each time, and magnesium level never dropped below normal. Cardiology recommended using isoproterenol if episodes of TdP were to recur. He remained stable throughout the day until later that evening, when the patient became unresponsive and lost his pulse as he developed another episode of TdP witnessed by the ICU team (Figure ).\nImmediate defibrillation was successful in attaining a normal sinus rhythm, and isoproterenol was initiated for the following 24 hours. As per cardiology, we maintained the patient’s potassium above 4 mg/dl and magnesium above 2 mg/dl, which required recurrent replacement throughout admission. The patient did not develop any arrhythmias on isoproterenol and appeared stable once removed from it after the 24 hours was complete. Around midnight, the patient developed another brief episode of TdP; however, it spontaneously converted back to sinus rhythm and did not require defibrillation. Isoproterenol was added back at half dose, and the following morning, cardiology recommended for permanent pacemaker (PPM) placement in the management of persistent TdP. The patient agreed and had a successful placement of his pacemaker the following morning with a higher rate setting, given his propensity to develop arrhythmia. Following pacemaker placement, the patient no longer developed episodes of TdP. With exception to when he first arrived in the ED, his magnesium level never dropped below 1.8 mg/dl and mostly stayed above 2 mg/dl. His QTc normalized to 406 ms following PPM placement (Figure ).\nThe patient was stable for transfer out of the ICU to the telemetry floor. He did not develop any arrhythmias the rest of admission and was then discharged back to the nursing home in stable condition six days later. |
The patient is a 19-year-old man, a seasonal agricultural worker daily in contact with sheep, living in Burgundy and with no history of travel neither abroad nor in the south of France during the previous months. At the end of September 2016, the patient performed farm work in contact with sheep when he had an ocular traumatism caused by a fly. Three hours after the ocular traumatism, the patient complained of a painful right eye discomfort, with sensation of moving foreign. Upon arrival at the department of ophthalmic emergency of the University Hospital Center of Dijon within hours of the onset of the first symptoms, the clinical examination showed a red and irritated conjunctiva in the right eye with the observation of mobile and translucent larvae in the conjunctival fornix. The rest of the ophthalmologic examination was normal. Eight larvae were extracted using Bonn hook forceps under local anesthesia. All larvae were sent to the Parasitology-Mycology Laboratory of the University Hospital Center of Dijon for identification.\nThe parasitological diagnosis allowed the identification of stage 1 Oestrus ovis larvae (L1). Indeed, the macroscopic examination revealed larvae of white color and about 1 mm length. Microscopically, these larvae were composed of eleven metameres, each of these displaying 4 rows of spines (Fig. a). The cephalic segment had two large black buccal hooks (Fig. b), while the posterior segment consisted of two tubercles, each containing about ten curved spines (Fig. c) which is concordant with the morphological description of L1 Oestrus ovis larvae in the literature [].\nAt the first visit, the patient received a local treatment based on the administration of oxybuprocaine and antiseptics (Biocidan®) as eye drops. The curative treatment consisted of the mechanical removal of all of the eight larvae present at the level of the conjunctiva using a forceps, as mentioned before. Subsequently, the treatment was supplemented by the administration of antiseptic eye drops (i.e. desomedine) and antibiotics (i.e. ofloxacin). Removal of the larvae resulted in rapid relief and no complication was further reported. |
A 27-year-old woman with a history of obesity and asthma was admitted to hospital with a diagnosis of H1N1 influenza A pneumonia and acute respiratory distress syndrome (ARDS). After a prodrome of nonproductive cough and chest tightness, she presented to the emergency department with worsened shortness of breath and subsequently required intubation and mechanical ventilation for hypoxic respiratory failure. On the day of admission, a nasopharyngeal sample was positive for influenza A by reverse transcriptase-polymerase chain reaction (RT-PCR). She had not received seasonal influenza or 2009 H1N1 pandemic flu vaccinations prior to her illness.\nAntiviral therapy with oseltamivir was administered for a 10-day initial course. Given a persistently positive RT-PCR for influenza A in 3 samples over 3 weeks and worsening of her ARDS despite the course of oseltamivir, she subsequently received the investigational antiviral agent peramivir intravenously after consent was obtained from her family. The patient's severe ARDS required treatment with a course of intravenous methylprednisolone and neuromuscular paralysis to facilitate appropriate mechanical ventilation. On day 11 of her hospitalization, the patient developed acute oliguric renal failure and required hemodialysis for several weeks. Tracheostomy was performed approximately one month into her hospitalization.\nFive weeks into her hospitalization, as her sedation was lightened in the context of improved oxygen requirements, the patient was found to have altered mental status and quadriparesis. The next day, she became unarousable with nonreactive pupils, absent corneal reflexes, and absent motor response to noxious stimuli. An unenhanced head computed tomography (CT) showed diffuse cerebral white matter edema, with posterior fossa edema causing effacement of the fourth ventricle and obstructive hydrocephalus. The CT also showed a small intraparenchymal hemorrhage in the left occipital lobe. The patient was urgently transferred to the Neuroscience Intensive Care Unit at our Neurosurgical Center, where a ventriculostomy was placed.\nMagnetic resonance imaging (MRI) of the brain illustrated diffuse abnormal T2/FLAIR hyperintensities with swelling in the gray matter and subcortical white matter throughout the bilateral cerebral hemispheres, cerebellum, brainstem, and thalami (Figures –). There was also evidence of edema in the bilateral lentiform nuclei and posterior limb of the internal capsules. There were signs of tonsillar herniation and upward cerebellar herniation. Diffuse leptomeningeal enhancement and patchy parenchymal enhancement were present throughout the bilateral cerebellar hemispheres, right basal ganglia, and the left ventromedial thalamus. Multiple areas of microhemorrhage were seen on gradient echo sequences at the gray-white junction in the cerebrum and cerebellum. The CT and MRI findings were consistent with a diagnosis of ANE [].\nCerebrospinal fluid (CSF) obtained from the patient's ventriculostomy showed 7 white blood cells per microliter (97% polymorphonuclear leukocytes, 3% lymphocytes), protein level of 78 mg per deciliter, and glucose level of 65 mg per deciliter. Molecular analyses of the CSF and serum samples were negative for the virus.\nAfter treatment of the patient's obstructive hydrocephalus by ventriculostomy, no clinical improvement was observed. Given the possibility of an inflammatory or parainfectious etiology for the patient's acute necrotizing meningoencephalitis, treatment with intravenous immunoglobulin was begun and steroid therapy was restarted. Despite these treatments, her neurological examination continued to deteriorate and the patient progressed to brain death.\nPostmortem examination revealed evidence of severe influenza pneumonia and advanced interstitial pneumonitis with fibrosis. The brain showed extensive and widespread edema, necrosis, and hemorrhage (Figures –). Multiple brain regions demonstrated diffuse edema, venous congestion, and multifocal areas of hypoxic ischemic neuronal injury. The internal capsule and basis pontis demonstrated intravascular fibrin thrombi surrounded by cellular debris with early necrosis. Beta-amyloid precursor (beta-APP) immunostains in these regions demonstrated widespread axonal injury associated with the vascular lesions. The thalamus showed venous congestion and parenchymal hemorrhage without associated inflammation. The corpus callosum had small necrotic foci with a macrophage response and also showed evidence of marked axonal injury on the beta-APP immunostains. The cerebellar hemispheres were necrotic with associated hemorrhage (), and the basilar leptomeninges were congested.\nMolecular analyses of multiple samples of postmortem brain tissue were negative for the virus. |
A 46-year-old Caucasian male patient was referred to the acute eye casualty department with a 10-day history of bilateral floaters and blurring of vision. Although ophthalmic history was unremarkable, previous medical history identified an acute episode of jaundice 6 months before presentation. Medical investigations at this point identified a raised alkaline phosphatase (>900), and magnetic resonance cholangiopancreatography confirmed a diagnosis of PSC. There was no history of inflammatory bowel disease (IBD) and his autoantibodies and hepatitis screen were all noted to be normal. He had previously been of good health and was a keen amateur bodybuilder. However, due to family commitments, he had given up this hobby 9 months preceding his attendance. He was local to the area, with no history of travel abroad. He smoked 5 cigarettes a day, and there was no history of alcohol intake. He was not on any medication at the time of presentation. His mother suffered from inflammatory arthropathy and his sister from multiple sclerosis.\nOn examination, the unaided logarithm of the minimum angle of resolution (logMAR) visual acuity (VA) in the right eye (RE) was 0.38 and the left eye (LE) 0.30. He had a bilateral nongranulomatous uveitis, extensive posterior synechiae, and normal intraocular pressures. There was a limited fundal view with vitreous cells noted in each eye. This was indeed more marked and active in the RE with an associated hyperemic optic disc. The LE revealed occlusive retinal vasculitis of the superior retinal vasculature [Figures and ]. This subsequently progressed to involve the right retinal vasculature upon the patient's next clinic attendance 5 days later, however, due to significant anterior chamber inflammation, fundal photos were not possible for this eye. There was no macular involvement in either eye, as was confirmed by optical coherence tomography. Systemic examination revealed possible early clubbing but was otherwise unremarkable.\nThe patient was commenced on hourly topical steroids with cycloplegic agents in each eye pending urgent investigations. The results of these showed a normal erythrocyte sedimentation rate and C-reactive protein, negative septic screen, and normal chest X-ray. There was mild thrombophilia, but this was much reduced from his inpatient tests, 6 months previously. Blood tests including angiotensin-converting enzyme, antineutrophil cytoplasmic antibodies, antinuclear antibodies, HIV, syphilis screen, herpes simplex virus, herpes zoster virus, immunoglobulin G4, and alpha-fetoprotein were all noted to be negative or within normal parameters. He was subsequently commenced on oral prednisolone 60 mg a day and omeprazole 20 mg a day and referred for a gastroenterology, rheumatology, and tertiary uveitis center review with a planned fundus fluorescein angiogram and review in our own department.\nAt 1-week follow-up, the anterior chamber in each eye was quiet, with some of the posterior synechiae showing release and improved pupillary dilation. The patient unfortunately did not attend the tertiary uveitis appointment due to the distance he needed to travel. Unaided logMAR VA improved to −0.10 RE and −0.14 LE. The vitritis and vasculitis continued to settle with a reducing regime of oral steroids. With time, topical medication was discontinued and the posterior segment was stabilized with residual vascular occlusion evident in the left superior retina (ghost vessels). With the last recorded vision 6 months after initial attendance, of logMAR −0.10 in the RE and −0.14 in the LE, neovascularization at this point had not been seen. |
A 48-year-old Caucasian woman was admitted to our hospital with presyncope, nausea, and palpitations. An electrocardiogram (ECG) showed new, complete atrioventricular (AV) block (Fig. ). A permanent pacemaker was implanted, which resulted in resolution of her symptoms. Her serum troponin levels were within normal range. She subsequently developed intermittent watery diarrhea without blood or mucus and was passing 10–15 bowel movements per day. The patient reported having painful, recurrent oral and genital ulcers for the previous 10 months. She also had intermittent large joint swelling and tenderness during this period. Furthermore, she had had an episode of redness of her eyes 2 months before her first admission that had lasted for 2 weeks, consistent with uveitis. She had been admitted 3 weeks before her current presentation with chest pain due to pericarditis. An ECG at that time showed normal sinus rhythm (Fig. ), while an echocardiogram showed small pericardial effusion. At that time, tender swelling of her right knee joint was observed. Her physical examination also revealed numerous mucosal ulcers in her mouth and on the labia minora. Her past medical history included 40 pack-years smoking and a right lower limb deep venous thrombosis when she was pregnant with her second child.\nHer clinical examination did not reveal any evidence of extraintestinal manifestation of inflammatory bowel disease. Of note, her pathergy test result was negative. The results of her autoimmune screen, including rheumatoid factor, antinuclear antibody, anti-double-stranded DNA, anti-cyclic citrullinated peptide antibody, and extractable nuclear antibodies, were negative. Her human leukocyte antigen (HLA)-B51 was negative, but she had genotype HLA-B35 in her blood. Stool microscopy and culture did not reveal any pathogens. An endoscopic evaluation showed a large ulceration in the terminal ileum that did not appear typical of Crohn’s disease. Her histopathological examination showed changes consistent with vasculitis but no granulomas or transmural inflammation. A computed tomographic enterogram showed no other areas of ulceration or evidence of Crohn’s disease. On the basis of this patient’s oral and genital ulceration, documented evidence of synovitis, vasculitic ulcer in the gastrointestinal tract, and an episode of ocular inflammation and no evidence of another inflammatory disease, a diagnosis of BD was made. She was commenced on prednisolone 50 mg with a slow tapering course, as well as sulfasalazine 500 mg twice daily that was later increased to 1 g twice daily, to which she responded with resolution of her diarrhea and mucosal ulceration. She continued to be in remission during once-monthly and then thrice-monthly clinical follow-up. |
An 83-year-old woman suddenly became aware of impairment in her eyesight and visual field of the left eye. She was admitted to the ophthalmology department in our hospital because she did not experience any improvement with observation. During an eyesight examination, abnormal vision was confirmed in her left eye.\nThe patient had a history of lung cancer for which she had undergone surgery 10 years ago and arrhythmia for which she had a pacemaker implanted 5 years ago.\nComputed tomography (CT) images showed a neoplastic lesion with contrast enhancement and an indistinct boundary, which had invaded to the maxillary sinus and orbital cavity. The principal site of the lesion was the left pterygopalatine fossa. In addition, the images also showed bone destruction of the lateral wall of the maxillary sinus because of exclusion and invasion of the lesion at its outer side (). Magnetic resonance imaging (MRI) could not be performed because the patient had a pacemaker.\nEyesight examination test showed that the best corrected visual acuity (BCVA) of the left eye was 0.2. The visual field test showed enlargement of the blind spot. The soluble interleukin-2 receptor (sIL-2R) level was a little high at 576 U/mL (normal range: 145 U/mL–519 U/mL); however, abnormalities pertaining to inflammation markers, tumor markers, and collagen disease markers were not noted during another blood test.\nWe performed a biopsy of the lesion to obtain a definitive histopathological diagnosis. First, the uncinate process was removed, and then the maxillary ostium was opened. The tumor mass was removed from a part of the maxillary sinus and the pterygopalatine fossa.\nHematoxylin-eosin (HE) staining of the biopsied specimen showed dense infiltration of small lymphocytes, which possessed equally sized round nuclei with a fine chromatin pattern. There was also an admixture of small numbers of plasma cells and eosinophils. The lymphocytic infiltration did not reveal nodularity or lymphoepithelial lesions of the sinonasal gland (). Immunohistochemistry showed both CD3-positive T-cells and CD79a-positive B-cells infiltrated to the lesion (). Among the plasma cell, there was no predomination for kappa- or lambda-positive ones. IgG4-positive plasma cells were scarcely encountered. Proliferation of ALK-positive myofibroblasts or CD21-positive follicular dendritic cells was not demonstrated. In situ hybridization for EBV-encoded RNA (EBER) gave negative results. Additional immunohistochemical analysis was performed to analyze the proliferative capacity of the lesion using Ki-67 and P53. The Ki-67 labeling index was approximately 10–15%, and P53-positive lymphocytes were hardly seen (). Furthermore, positive signals of CD34 were restricted in blood vessels (). These data showed mixed infiltration of mature T- and B-cells with a low proliferative capacity.\nTo examine the possibility of lymphoproliferative disorders, multiplex PCR-based clonality assays as to VH-JH region of immunoglobulin heavy chain (IgH) and T-cell receptor gamma (TCRγ) were conducted using genomic DNA extracted from the formalin-fixed paraffin-embedded tissue samples and BIOMED-2 primer sets []. As shown in , definite results suggesting malignant lymphoma were not obtained. From these histological, immunohistochemical, in situ hybridization, and multiplex PCR findings, we diagnosed the lesion as IPT that was not suitable for known neoplastic conditions, such as inflammatory myofibroblastic tumor or EBV-positive inflammatory follicular dendritic cell tumor.\nThe clinical course after biopsy included steroid pulse therapy according to the following protocol: 1 g of methylprednisolone sodium succinate for 3 days, followed by prednisolone, for which the dosage was gradually reduced from 40 mg to 10 mg and finally to 5 mg. However, no apparent vision recovery was observed during eyesight examination. Subsequently, we decided to administer radiotherapy. The patient received a total of 40 Gy radiotherapy, which was very effective, and her left eye vision recovered with a BCVA of 0.7.The CT images after steroid therapy showed no change in the lesion (); however, after radiotherapy, almost the entire lesion disappeared ().\nThe patient is well and free of disease after the therapy for three years. |
A 3 year old boy presented at our heart centre with a cardiac murmur that had been noticed first 2 weeks prior to admission. The mother described a mildly limited physical activity most likely due to asthmatic bronchitis. There was no history of chest pain, oedema, cyanosis, or loss of consciousness. On physical examination, he presented in a good general condition. His pulse rate was 150 bpm and regular, and the blood pressure was 75/50 mmHg. A 2/6 mid-systolic murmur was audible above the heart apex. No definite splitting of the second heart sound was detected. The lungs were clear on auscultation with good bilateral air entry. No hepatosplenomegaly. There was no peripheral oedema. His haemoglobin was 6.9 mmol/l, the haematocrit 33 %. White blood cell counts and differentiation, platelet count, creatinine, ASAT, C-reactive protein, coagulation parameters were within normal limits. The electrocardiogram was unrevealing. Chest X-ray films showed a slightly increased size of the heart silhouette and moderately increased pulmonary vascular markings.\nTransthoracic echocardiography disclosed a tumor in the left atrium that arose with a stalk from the upper part of the interatrial septum reaching a size of 3×3×2 cm. In diastole the tumor prolapsed through the mitral valve into the left ventricle (Figures and ).\nThe tumor had a flaccid structure and slipped partially with the blood flow back and forth through the mitral valve into the left ventricular inflow and outflow tract. The moving images convey the impression of potential embolization.\nThe patient was immediately referred to surgery for excision of the tumor. The operation was performed under cardiopulmonary bypass. The left atrium was opened. There was a 3×3×2 cm colloid mass originating from the atrial septum. The tumor had macroscopically the shape of a sea anemone. Histopathological examination revealed a typical papillary fibroelastoma. The tumor was fully resected including its attachment, and the defect in the atrial septum was closed by a pericardial patch. The postoperative course was uneventful. |
A 57-year-old man presented with a long history of groin pain for several years. There was no history of trauma or injury to groin. The pain exacerbated by walking and prolonged sitting. Since last few months his pain had increased with loss of movement at the hip. Physical examination revealed slight asymmetry in the region of the iliac bone compared with the contralateral side, with no signs of inflammation or palpable mass. Hip range of motion was decreased with flexion limited to 90°, and abduction of 15°. Patient walked with Trendelenburg gait possibly because of pain. Conventional radiographs of the hip () revealed the presence of a bony protuberance at the right anterior inferior iliac spine, several centimeters in length close to the right acetabulum, with no signs ofjoint degeneration. Suspecting a giant osteochondroma which could be in the process of malignant transformation we performed a magnetic resonance imaging (MRI) which showed the existence of a bone tumor with benign appearance, but excluding the osteochondroma as a diagnostic possibility, because there was no peripheral cartilage. Subsequently a CT scan () revealed a bony lesion (6 cm long and 3 cm thick) with a well-defined cortical bone and a heterogeneous zone in the junction with the ilium suggesting a pseudo- articulation. With these studies we could establish the diagnosis of pelvic digit instead of an osteochondroma.\nInitially, non-steroidal anti-inflammatory medications were prescribed with no symptomatic improvement. Surgical excision of the pelvic rib was planned with consent of the patient. Anterior approach to the hip (Smith-Petersen) was used. Tensor fascia latae and gluteus minimus required to be partially detached to completely expose the ‘rib’ till the base. The ‘rib’ was resected from its base and samples send for histopathology (). Histopathological examination showed the presence of corticomedullary structure similar to a rib, with no accompanying cartilage; this finding was consistent with a pelvic digit.\nThe pain disappeared gradually after surgery, and a year later the patient remains asymptomatic, with an improvement in flexion (130°) and abduction (35°) of the hip; the radiograph () shows no radiological signs of recurrence after one year (). |
A 66-year-old Japanese man who had no past medical or medication history complained of gross hematuria and visited a nearby hospital in October 2013. He had no habit of drinking alcohol or smoking tobacco. He was diagnosed as having a right renal tumor and underwent right nephrectomy laparoscopically. The pathological diagnosis was right renal cell carcinoma (RCC), clear cell carcinoma, pT1bN0M0, v1 (Fig. ). One and half years later, lymph node swelling was detected at hepatic portal region and he underwent lymphadenectomy. The pathological diagnosis was a metastasis from RCC. Two years after diagnosis, he was suspected of lung metastases and started treatment with interferon α. Three years later, the multiple lung metastases grew larger and were determined as progression despite interferon α therapy. At this point, he was referred to our hospital in October 2016. There were no abnormalities on physical examination and his vital signs were normal. He started treatment with sunitinib 50 mg/day on a schedule of 4 weeks on treatment and 2 weeks off; however, adverse events including grade 3 thrombocytopenia (platelet count, 49,000/μL), gum swelling, and hoarseness became intolerable 2 weeks after starting sunitinib. Four weeks after cessation of sunitinib 50 mg/day, he was started on a dose of sunitinib 25 mg/day on a schedule of 2 weeks on and 1 week off. Computed tomography (CT) findings in January 2017 revealed that his lung metastases had shrunk; however, he continued to experience the same adverse events. Therefore, the dose of sunitinib was further reduced to 12.5 mg/day on a schedule of 2 weeks on and 1 week off. CT findings in May 2017 revealed new metastases in the pleura, diaphragm, and the right paracolic gutter (Fig. a, b). As a result, the treatment was changed from sunitinib to axitinib and he started treatment with axitinib at 10 mg/day; however, adverse events including gum swelling, dysphonia, hypertension, diarrhea, and thrombocytopenia became intolerable (Fig. ). Two weeks after cessation of the drug, the dose of axitinib was gradually reduced from 6 mg/day to 4 mg/day. CT findings in September 2017 revealed the metastases had diminished in size and lung metastases were maintained at a diminished size (Fig. c, d); however, the adverse events could not be controlled and he discontinued axitinib treatment. His adverse events improved after discontinuation of axitinib; however, CT findings in December 2017 revealed the size of metastases had increased again (Fig. e, f). Consequently, he was started on fourth-line therapy with nivolumab (3 mg/kg every 2 weeks) and did not experience any adverse events. However, after he had received eight cycles of nivolumab, his metastatic lesions had grown, peritoneal dissemination appeared in his pelvic region, and pleural effusion appeared (Fig. g, h), so nivolumab was discontinued. After giving a detailed explanation of treatment options to our patient, he decided to rechallenge with axitinib 4 mg/day. However, adverse events including gum swelling and dysphonia became intolerable. After that, the dose of axitinib was reduced to 2 mg/day, and he experienced relief of adverse symptoms except for hoarseness. CT findings in August 2018 revealed metastases in lungs, pleura, diaphragm, and the right paracolic gutter had diminished in size (Fig. i, j). He has been continuously receiving a low dose of axitinib at 2 mg/day for 10 months with metastases maintained at reduced size. |
A sixty-year-old man was admitted to a hospital because he had fever, dyspnea, cough, and chest pain. The clinical and laboratory exams and chest X-ray confirmed pneumonia. The patient completely recovered after an antibiotic treatment.\nThe patient reported more than 25 years of alcohol abuse as well as smoking two packs of cigarettes a day and recent hospitalization due to acute pancreatitis. His family history was unremarkable for neoplasms and congenital diseases. Before this hospitalization, he was examined because of suspicion on thyroid gland disease. Also, for some time, he has been taking medications for chronic heart failure disease. He stated slow growth of a neck mass in the last 20 years. Physical examination showed a bilateral enlargement of the retroauricular, occipital, and upper back areas. Patient was 178 cm tall and weighted 76 kg his body mass index was normal (24.0 kg/m2). Laboratory blood analysis revealed elevated concentrations of aspartate aminotransferase (195 U/L), alanine aminotransferase (290 U/L), gamma glutamyltransferase (440 U/L), and C-reactive protein (24.3 mg/L). The blood triglycerides and cholesterol were within normal range. All other laboratory findings were in reference ranges. Based on clinical presentation and patient's history of long time alcohol abuse, the working diagnosis of Madelung's disease was established. The confirmation was made by magnetic resonance imaging (MRI). A cervicothoracic MRI showed an accumulation of large, bilateral subcutaneous masses of nonencapsulated adipose tissue in ventral and lateral regions of the neck and especially in a suboccipital region, pushing against the atrophic neck muscles typical of Madelung's disease (). Excision biopsy of the neck adipose mass confirmed adipose tissue mass without malignant transformation. The patient did not have any respiratory or other symptoms associated with Madelung's disease, and therefore, the surgical treatment was not performed. The patient was advised to cease alcohol consumption and to visit the doctor regularly in order to monitor progression of the disease. |
The patient was a 24-month-old Hispanic male who presented to our Endocrinology-Genetics Clinic for a follow-up evaluation due to his history of failure to thrive and short stature (Figs , ). He was the third child born to his parents and was delivered at 38 weeks of gestation to a 32-year-old mother via spontaneous vaginal delivery. The pregnancy was complicated by diet-controlled gestational diabetes. His birth weight was 3.3 kg (25%ile) and birth length 47 cm (7%ile), both appropriate for gestational age. He was identified with undescended testes after birth. The only postnatal issue was jaundice that required 2 days of phototherapy. Family history was significant for one older male sibling with poor weight gain beginning at age 2 years until age 5, which subsequently resolved without medical intervention. Genetic testing was not indicated on the sibling after evaluation by the genetics team. No other family history of syndromic conditions, recurrent pregnancy losses, abnormal short stature, or learning disabilities. His father’s height was 152 cm and his mother’s height 144 cm, resulting in a mid-parental height of 154.5 cm (0.1%ile). Despite recommendations for parental genetic testing, neither parent has the financial means nor health coverage to do so.\nAt 4 months of age, the patient began to display poor weight gain in absence of vomiting or diarrhea. No febrile illnesses or difficulty swallowing. He was breastfed until 8 months of age, then transitioned to regular formula without difficulty. He was also started on pureed table foods without problem. At 10 months of age he was referred to pediatric gastroenterology due to lack of appropriate weight gain. He was started on fortified milk and foods. Sweat test, CBC and electrolytes were reassuring. At 12 months of age he was followed weekly for weight checks. At 16 months of age he was admitted when noticed dropping his weight from 7.2 to 7.0 kg from the previous week, and had intensive workup for failure to thrive.\nDue to suspicion of abnormal facial features, the genetics service was consulted. On examination he appeared small for his age, but was interactive. He had hypertelorism with innercanthal distance 3.5 cm (above +2SD), down-slanting palpebral fissures, flat midface and philtrum, low set ears, upturned nose and overlapping toes. He also had a 2/6 systolic murmur. The rest of the exam was unremarkable. Transthoracic echocardiogram, plasma amino acids, urine organic acids, ammonia, lactate, thyroid stimulating hormone, free thyroxine and celiac screen were negative for abnormalities. Chromosomal microarray and karyotype was ordered, which demonstrated 47,XYY (Figs , ). The karyotype finding was incidental, as it would not explain his facial features and growth difficulties. At the follow-up clinic visit at age 18 months, his presentation was more suspicious for NS, so a NS genetic panel was ordered. The gene test was conducted via Sanger sequencing of the tyrosine phosphatase non-receptor type 11 gene (PTPN11) gene, which detected one pathogenic mutation: c.922A > G; p.Asn308Asp. The p.Asn308Asp has been reported in many patients with NS and is estimated to account for about 30% of cases []. He had subsequent evaluation for related renal, cardiac, ophthalmologic and audiological abnormalities, which were reassuring.\nWith a confirmed diagnosis of NS and in the presence of poor growth, he was evaluated by pediatric endocrinology at age 24 months. Insulin-like growth factor-1 (IGF1) and insulin-like growth factor binding protein 3 (IGFBP3) were 61 ng/mL (30–122) and 1810 ng/mL (972–4123), respectively. He was demonstrating low normal growth velocity at 8 cm/year. The option of starting growth hormone (GH) treatment was discussed, though deferred due to parent’s preference and questionable benefit to starting it at this age for growth failure. The clinical team recommended continued observation while on a high caloric diet. |
An 88 year old 63 kg woman, presented to the University of Arizona Medical Center after she tripped and fell at her home. She complained of left hip and wrist pain. Patient denied any past medical or surgical history. She was not on any medications and had no known drug allergies. Physical examination revealed tenderness on palpation of the left hip with deformity and tenderness over the ipsilateral wrist. Radiographs confirmed a nondisplaced left intertrochanteric femur fracture and an ipsilateral dorsal bending distal radius fracture. She was neurovascularly intact in bilateral upper and lower extremities.\nInformed consent regarding closed reduction and splinting of the distal radius fracture were discussed with patient and family, all consenting. The 22 gauge needle was inserted dorsally 3 cm proximal to fracture site, at a 30 degree angle. The needle was advanced to the fracture site once the skin was penetrated. A flash of blood was present. Over a thirty second interval, a 20 mL mixture of lidocaine 1% and bupivacaine 0.25% was infiltrated into the fracture hematoma. Neither anesthetic contained epinephrine. Within 15 seconds following the completion of injection, the patient became difficult to arouse, responding only to sternal rub. She developed mild tonic clonic movements of her upper and lower extremities lasting 15 seconds. Vital signs remained stable. Electrocardiogram showed no abnormalities. Approximately one minute after completion of injection, patient began responding verbally. At approximately 5 minutes post injection, patient was awake, alert, and oriented. She did not recall the events surrounding the injection. She underwent closed reduction of her distal radius fracture and a sugar tong splint was applied. She was admitted to the medicine service, underwent cephalomedullary nail fixation of her femur the following day, and was discharged from the hospital to inpatient rehabilitation on hospital day 4. Upon 2 and 6 week follow up, she had no neurologic sequelae. |
A 62-year-old woman presented to our hospital in November 2016 complaining of intermittent nausea, vomiting, and diarrhea and multiple masses in the liver found on routine abdominal computed tomography (CT) imaging.\nThe patient underwent right-sided modified radical mastectomy including lymphadenectomy with nipple and areola preservation 4 years ago at a local hospital. No lymph node metastases were detected. Postoperative pathology revealed poorly-differentiated NEC of the right breast with a size of 1.5 cm × 1.5 cm × 1 cm. Immunohistochemical staining revealed expression of chromogranin A (CgA), synaptophysin (Syn), and hormone receptors [estrogen receptor (ER) and progesterone receptor (PR)]. Staining for human epidermal growth factor receptor 2 (HER-2) was negative. The Ki-67 index was 50%-75%. Curative resection was followed by four cycles of adjuvant chemotherapy with the pirarubicin and paclitaxel regimen. The patient had been receiving endocrine therapy after operation and regular follow-up every 3 mo.\nThe patient had a free previous medical history.\nThe patient dined any personal and family history.\nThe physical examination revealed no obvious abnormalities.\nLaboratory examination revealed no obvious abnormalities.\nAn initial imaging evaluation by enhanced abdominal CT revealed multiple masses in the liver, with the largest one measuring about 8.4 cm × 6.3 cm. Chest CT showed a mass on the right front chest wall and a small nodule in the upper lobe of the right lung.\nThe liver lesions were further evaluated by abdominal magnetic resonance imaging (MRI), which revealed multiple masses in the liver with the largest one measuring about 8.8 cm × 6.7 cm. A whole body bone scan revealed increased bone metabolism in the second anterior rib on the right, which was considered local bone invasion caused by chest wall masses combined with previous chest CT findings.\nFurther clinical work-up including upper endoscopy and colonoscopy did not reveal further pathological findings, not providing any evidence of another possible primary tumor.\nThe pathological consultation performed at our hospital of the primary breast lesion showed an NEC in the right breast with no metastases in the axillary lymph nodes. Immunohistochemical staining revealed expression of Syn, CgA, and hormone receptors (ER > 50%, slightly weaker expression of PR). Staining for HER-2 was negative. The Ki-67 index was approximately 50%.\nThis patient underwent a liver and chest wall biopsy at our hospital. Liver and bone metastases of the NECB were detected. Immunohistochemical analysis of a biopsy taken from the lesion in the liver and chest wall showed an NEC with positive expression of CgA and Syn as well as strong expression for ER (> 95%). The expression of O6-methylguanine DNA methyltransferase (MGMT) and somatostatin receptor SSTR2 was negative. The Ki67 index was approximately 70% (Figure ). |
A 20-year-old male patient presented to the emergency department with nausea and upper abdominal pain after food intake. His past medical history included an appendectomy, overweight and ~20 kg weight loss in the past 3 years through exercise and dieting. After weight loss, he developed recurrent episodes of vomiting and mild abdominal pain. At that time, vomiting was variable, with episodes occurring once a week to up to three times a day and happened mostly after meals. It was also accompanied by mild depression. Bowel movements were regular and no other symptoms were acknowledged.\nWith this history, he attended to a physician consultation. Clinical examination was unremarkable, laboratory tests including an upper endoscopy appeared normal at that time. Considering his history and the fact that he had concerns about his body and shape, without any apparent physical dysfunction, an eating disorder was contemplated for which he received 2 years of psychological support. After treatment the vomits and weight loss, to some extent, were controlled. However, he stated that his eating patterns had significantly changed during these years as he mostly ate mushy blended food with liquids; and that even after the treatment pain persisted.\nAt the time of the assessment in the emergency room, clinical examination revealed dehydration, and abdominal examination revealed periumbilical pain without any tenderness or masses. Laboratory exams revealed anemia and stomach distention was noted on abdominal x-ray. An upper endoscopy was performed revealing a tortuous duodenum in its second and third portions and an extrinsic compression that partially limited the pass of the endoscopy at this point. Due to these findings, surgical consultation was required. A contrast-enhanced CT showed a narrowing at the SMA origin without signs of obstruction (Fig. A). An angiotomography with a vascular reconstruction (Fig. A) later revealed a 20.5° aortomesenteric angle (Fig. B) and 5.26 mm of aortomesenteric distance (Fig. C).\nWilkie’s syndrome was diagnosed and, given the particularities of this case, a conservative treatment was discarded since the bulimia treatment to gain weight over the last 2 years was not effective. Instead, a surgical treatment was decided.\nAt laparoscopy, a dilated stomach and duodenum were encountered. The jejunum was identified at the ligament of Treitz, and a segment of jejunum 25 cm distal to the ligament of Treitz was mobilized and attached with a 2-0 absorbable suture to the duodenum. A side to side duodenojejunostomy was performed using a 45-mm linear stapler. The common enterotomy was closed with an absorbable suture without any complications.\nFrom there, the patient had good clinical development. Bowel sound and flatus were present from the third postoperative day and sips of liquids were initiated, attaining good oral tolerance. He was discharged on the seventh postoperative day.\nOn follow up controls patient is well, 4 months after surgery he started to gain weight (Fig. B), and had overcome his depression. |
A 42-year-old, gravida 3, para 2, Korean woman was referred to the Department of Emergency Medicine at Samsung Medical Center in November, 2014, for abdominal pain and fever. Her past medical history was unremarkable, although she had received myomectomy in 2010 and total abdominal hysterectomy in 2011 at another university hospital due to symptomatic uterine leiomyoma. Unfortunately, the registered medical chart or pathology slides of her previous operation specimens were not available. Therefore, we could not review the previous slides of her previous operation.\nShe had been suffered from abdominal pain since one month ago. Otherwise, there were no urinary or gynecologic symptoms. Even though, she had fever at first, her vital signs relatively stable as follows: systolic and diastolic blood pressure 127 and 76 mmHg, pulse rate 96 beats per minutes, respiratory rate 20 breaths/min, and body temperature 39.1℃. Laboratory test showed no definite abnormal results except for elevated C-reactive protein (25.93 mg/dL). Blood and urine culture results revealed no growth of microorganisms. Routine urine human chorionic gonadotropin (hCG) test for childbearing age women was not performed, because she already had hysterectomy.\nOn magnetic resonance imaging and computed tomography (CT) for the abdomino-pelvic region, there were 9-cm-sized soft tissue like lesion in the midline lower abdominal wall () and another 6.6-cm-sized lesion in the right side of the pelvic cavity which formed a fistula with the distal sigmoid colon. Otherwise, there were no definite abnormal findings on imaging studies.\nThe presumed diagnosis was desmoid tumor or mesenteric sarcoma. Urgent exploratory laparotomy was performed for surgical resection and pathologic confirmation. Midline lower abdominal wall mass was removed by wide excision (). Through exploration, we identified that the distal sigmoid colon was perforated with massive inflammatory changes and had a fistula connected with the right-side pelvic mass. This mass with the distal sigmoid colon fistula was removed through the Hartmann's procedure. Furthermore, there were three nodular lesions in the sigmoid mesentery and a 4-cm-sized tumor in the terminal ileum, therefore, the general surgeon removed all of these notable masses. Resected tumors were suspected to malignant tumors of mesenchymal origin by frozen section biopsy during surgery.\nGrossly, tumors were tan-yellow colored soft masses with necrotic changes. Microscopically, tumors were composed of nests and cords of epithelioid cells with moderate to marked atypia. Peri-tumoral hyaline material and geographic tumor necrosis were observed. Mitotic rate was 12 per 10 high power fields (HPFs) and Ki 67 labelling index was up to 50%. Immunohistochemically, the tumor cells were positive for β-hCG, human placental lactogen (hPL), inhibin-α, and p63 (). The immunohistochemical staining results are summarized in . Collectively, the histologic features and the immunohistochemical results were compatible with ETT in the final pathologic diagnosis.\nShe received intensive post-operative care in the intensive care unit for 2 days and was discharged 20 days later, uneventfully. Her serum β-hCG level was not checked before surgery because there were no clues based on which we could suspect ETT. After pathologic confirmation, her β-hCG level was checked on the post-operative fifteenth day and the value was 1.3 mIU/mL. Fortunately, even though large multiple masses had been existed in her abdominopelvic cavity before surgery, there was no residual tumor or distant metastasis on CT scan which was done at post-operative seventh days. Considered imaging studies, β-hCG results and ETT's chemoresistant nature, she did not need adjuvant chemotherapy.\nTwo months after surgery, her β-hCG level was checked at the outpatient clinic and it was 0.6 mIU/mL. Three months later, CT scan of her chest and abdomino-pelvis showed no recurrent or remarkable lesion. Nine months later, there was no evidence of recurrence on serum β-hCG and imaging studies. |
We describe the case of a 34-year-old gravida II para l woman, with a gestational age of 26 + 3 weeks at admission, who had a relatively healthy 4-year-old child with her 40-year-old husband of non-consanguineous marriage. She had been on injectable contraception for 2 years and had regular menses for 6 months before the pregnancy. She had antenatal care at a local health center and was vaccinated with tetanus toxoid once and supplemented with iron for 3 months. She was screened for retroviral infection, hepatitis, and syphilis and it was documented nonreactive. She had no anatomic scan at early gestation. She came to Felege Hiwot Referral Hospital with the chief complaint of severe and persistent headache of a day’s duration which was occipital in location associated with blurred vision and generalized body swelling of 1 week’s duration. She had no other danger signs in pregnancy. Her past gynecologic history, medical history, and surgical history were uneventful. She is Amhara by ethnicity. She had no known family history of hereditary or chromosomal disorders.\nHer blood pressure at admission was 180/120 mmHg and pulse rate was 84 beats per minute; her respiratory rate was 22 breaths per minute and she was afebrile. She had pink conjunctiva and non icteric sclera, 24 weeks-sized gravid uterus, no abdominal tenderness, no organomegaly, no sign of fluid collection in her abdomen, and the fetal heart beat was positive. She had no vaginal bleeding or discharge. She had pedal and pretibial edema. She was conscious and oriented to person, place, and time. Her deep tendon reflex was +2 and her motor and sensory examinations showed no motor or sensory problems. Other parts of systemic examinations were normal.\nHer hypertension was controlled with intravenously administered hydralazine 5 mg two doses at our emergency department. In her complete blood count her white blood cells were 7300 cells/micL, hemoglobin of 13.4 g/dl, and platelet count was 169,000 cells/micL. Urine protein dipstick was +2, and liver and renal function tests were done: serum glutamic pyruvic transaminase (SGPT) 89 IU/L (elevated), serum glutamic oxaloacetic transaminase (SGOT) 102 IU/L (elevated), alkaline phosphatase (ALP) 229 IU/L, and lactate dehydrogenase (LDH) 288 IU/L. Total bilirubin was 0.24 mg/dl, albumin was 3.49 g/dl, blood urea and nitrogen was 12 mg/dl, serum creatinine was 0.69 mg/dl, and oral glucose tolerance test was in the normal range. Obstetric ultrasound showed a singleton, alive, intrauterine pregnancy with average gestational age of 26 weeks, there was a single large ventricle with partially formed midline structure (see Fig. ), amniotic fluid index was 13.4 cm, placenta was located anteriorly at the body of the uterus, and the presentation was breech; the fetus had normal four chambers of heart with normal outflow tract.\nAfter blood pressure was controlled (it took 2 hours), she was admitted with the diagnosis of late second trimester pregnancy and preeclampsia with severity feature plus semilobar HPE. Seizure prophylaxis for preeclampsia was given (magnesium sulfate according to World Health Organization guideline), methyldopa 500 mg orally every 8 hours was added, and she was counselled about options of management; the high incidence of associated anomalies, severe morbidities of survivors, and poor prognosis were discussed. Termination was decided and done with misoprostol 100 microgram every 3 hours at the third dose with outcome of 1.1 kg male, alive neonate. On examination of the neonate, there was cebocephaly, hypotelorism, single patent nostril which enabled nasogastric tube 6F, micropenis (8 mm), and unilateral right hand polydactyly with agenesis of middle phalanges of the fifth finger. There was rigidity involving all extremities which resisted extension and flexion (see Figs. , and ).\nAfter basic neonatal care was given (cord tied, airway cleaned, and newborn dried), he was transferred to our neonatal intensive care unit (NICU) but he died 20 minutes after admission to NICU. Immediate cause of death was not known. Following his death, further investigations were not possible for cultural reasons. At third postpartum day, maternal blood pressure was 130/90 mmHg, pulse rate was 78 beats per minute, and respiratory rate was 20 breaths per minute. Her complete blood count showed white blood cells of 12,000 cells/micL, hemoglobin was 11 g/dl, and platelet count was 122,000 cells/micL. Liver function tests showed SGPT of 35 IU/L, SGOT of 12 IU/L, ALP of 359 IU/L, and LDH of 254 IU/L; total bilirubin was 0.56 mg/dl, blood urea and nitrogen was 22 mg/dl, and serum creatinine was 0.8 mg/dl. After she was counselled to have preconception care and prenatal screening in next pregnancy, she was sent home relatively healthy. She was well at postpartum visits and methyldopa was discontinued at seventh postpartum day. |
A 49-year-old woman with a history of transsphenoidal pituitary adenoma surgery visited the outpatient clinic owing to microcalcification detected on a screening mammogram in 2016. Physical examination showed nonspecific findings with no palpable lesions. Breast ultrasonography showed a probably benign hypoechoic lesion measuring 7 mm at the 2 o'clock position in her right breast. Magnification mammography showed several grouped microcalcifications with amorphous features in the upper outer and inner quadrants of the right breast, and they classified as a Breast Imaging Reporting and Data System category 4a lesion. She had undergone a stereotactic biopsy using an 11-gauge needle with the vacuum-assisted breast biopsy system. The biopsy revealed low-grade ductal carcinoma in situ. Additional magnetic resonance imaging showed multicentric suspicious masses with suspicious enhancement in the upper, central, and medial areas of the right breast. Suspicious non-mass enhancement was observed in the upper inner to the central areas of the left breast, suggesting malignant involvement. Other preoperative evaluation including chest X-ray, electrocardiogram, and laboratory tests showed no significant abnormalities.\nUnder general anesthesia, the patient was placed in a supine position with a shoulder pad under the ipsilateral chest wall. The ipsilateral arm was straightened to the head and fixed to an arm board ().\nA 6-cm vertical skin incision was made in the anterior axillary line, and a sentinel lymph node biopsy was performed. Radioisotopes and the indigo carmine dye were used for the detection of sentinel lymph nodes. After the sentinel lymph node biopsy, a subcutaneous skin flap was prepared through that incision toward the nipple-areolar complex using electrocautery under direct vision. An intraoperative frozen section was performed to confirm a negative tumor margin. After undermining a subcutaneous skin flap to the nipple-areolar complex from the axilla, the Modified Chung's retractor (external retractor) () [] was placed under the skin flap with a table mount lift to maintain the working space.\nA dual-channel 30-degree down telescope was placed on the central arm. Fenestrated bipolar forceps and a permanent cautery spatula were placed on both sides of the scope. During the procedure, ProGrasp forceps were placed on the left side of the spatula to retract and counter-retract the breast parenchyma. The da Vinci Xi Surgical System® (Intuitive Surgical, Sunnyvale, USA) was used for this surgery ().\nBreast boundaries were marked using 0.5 mL of indigo carmine injections every 2 cm before robotic dissection. Using the robotic arms, superficial subcutaneous tissue was dissected below the nipple-areolar complex to the breast borders, including the outer, inner, upper, and lower margins. The first assistant checked the state of the flap by observing the degree of illumination (visual inspection). The deep layer was subsequently dissected from the lateral margin of the pectoral muscle fascia to the entire deep layer of the retromammary tissues. Full mobilization of the breast parenchyma was completed, and the specimen was removed through the axillary incision.\nAfter specimen removal, manual inspection of the subcutaneous flap was performed. Manual inspection revealed that the skin flap in the upper area was slightly thicker than 5 mm. Additional subcutaneous flap shaving was performed using Metzenbaum scissors. Using the robotic arms, the plastic surgeons inserted the tissue expander through the axillary incision. Two drain tubes were inserted—one inside and the other outside the pectoralis pocket.\nThe total operation time was 409 minutes. The console time was 132 minutes for mastectomy and 25 minutes for reconstruction. The remaining time included waiting for the sentinel node biopsy results, constructing the skin flap, docking the robots, awaiting the arrival of the plastic surgery team, and skin incision closure. Intraoperatively, her urine output was 2,280 mL and mild hypotension was observed, which were suspicious for central diabetes insipidus. Desmopressin was administrated in the recovery room, and she was referred to the intensive care unit for early postoperative care. However, her postoperative electrolyte levels and osmolality tests showed no evidence of central diabetes insipidus, and she could be transferred to the general ward on postoperative day 1. She was discharged without any other postoperative complications on postoperative day 9.\nHer final histopathological examination revealed two foci of invasive ductal carcinoma measuring 1.1 cm and 0.8 cm with extensive intraductal components. The maximum dia-meter of the invasive and in situ carcinoma was 3.2 cm. No axillary lymph node metastasis was identified. Immunohistochemical evaluation showed positive estrogen receptor and negative human epidermal growth factor receptor 2 expression. The Ki-67 index, which was calculated using the Roche iScan (Ventana, Tucson, USA) and the Ki-67 (30-9) antibody was 13.7%. The superficial margin of the primary specimen showed small foci (<1–2 mm) of abutting carcinoma, and tissues of additional flap shavings after removal of the primary breast specimen were not available to examine the final histopathological features. Thus, postoperative radiation was recommended by the multidisciplinary team at our hospital. Although she refused to undergo the OncotypeDx™ (Genomic Health, Redwood City, USA) test, systemic chemotherapy was not recommended by the multidisciplinary team. Endocrine therapy using tamoxifen was initiated 3 weeks postoperatively. Intensity-modulated radiation therapy was performed for 14 days, and the total dose of radiation administered was 3,400 cGy. Follow-up studies including breast ultrasonography and mammography performed for 1-year postoperative routine surveillance showed no recurrence. |
A 51-year-old male weighing 131 kilograms (kg) presented to the emergency department (ED) via ambulance with altered mental status and slurred speech after undergoing cervical epidural injection with two milliliters (mL) of 2% lidocaine (40 milligrams [mg]) under fluoroscopic guidance in an ambulatory setting. He became unresponsive during the injection with subsequent brief convulsive activity for which he was given 2 mg of midazolam. Emergency medical services was called and found him obtunded with shallow breathing and low oxygen saturations requiring ventilation assistance. On arrival to the ED his breathing was spontaneous and erratic with low oxygen saturations. He remained somnolent with slurred speech, unable to answer questions appropriately or follow commands. Preparations were made for intubation given altered mental status and low oxygen saturations; however, oxygen saturations and mental status improved within the first 10 minutes of arrival and ultimately intubation was not required.\nOn cardiopulmonary monitor he was noted to have an irregularly irregular heart rhythm. Electrocardiogram showed atrial fibrillation with a rate of 82 beats per minute. Hemodynamically he was stable. He converted to normal sinus rhythm 20 minutes later. He reported no history of atrial fibrillation. Within 60 minutes of ED arrival the patient’s mental status was back to baseline without recollection of the events that had occurred after the start of the procedure. He only had chest wall pain, possibly from sternal rub or from any bystander chest compressions that may have been performed when he became unresponsive. Imaging studies obtained included the following: chest radiograph, computed tomography (CT) of the head, CT angiogram of the head and neck, and CT of the chest with intravenous contrast. No pertinent imaging abnormalities were identified. Serum/plasma levels of lidocaine and its primary active metabolite, monoethylglycinexylidide (MEGX) were obtained 15 minutes after patient arrival. Both levels returned undetectable. The patient was observed overnight in the hospital and remained asymptomatic and without any further dysrhythmia. He was discharged home the following day on aspirin 325 mg daily and with a referral to outpatient cardiology. |
A 57-year-old Caucasian woman presented with a large non-tender submandibular mass. The lesion had been present for about 25 years with a slow increase in size. Our patient's medical history was unremarkable. A physical examination revealed a giant painless, movable, semi-hard elastic mass in her right submandibular region measuring about 8×6 cm. Fine needle aspiration cytology was suggestive of a PA. Contrast-enhancement computerized tomography confirmed a giant well-defined mass without cystic changes in her right submandibular region (Figure ). No lymph node swelling or other tumorous lesions were detected. Submandibular tumor extirpation was performed under general anesthesia.\nImmediately after removal, samples were obtained in the surgery room following a topographic scheme (Figure ). Group 1 comprised six samples from the periphery of the tumor, adjacent to the subcutaneous tissue; group 2 comprised six samples from the periphery of the tumor, adjacent to the floor of the mouth; and for group 3, the tumor was opened along the midline, and six deep samples were extracted from the center of the tumor.\nHalf of the samples in each group were fixed in 4% buffered formalin, processed and embedded in paraffin according to routine procedures, for histological and immunohistochemical analysis. The remainder of the samples of fresh material for each group were immediately submitted for DNA flow cytometry. The rest of the surgical specimen was routinely studied in the Department of Pathology and diagnosed as a benign PA.\nSamples of each group were minced with a scalpel in phosphate-buffered saline solution. Single nuclear suspensions were prepared by filtering through a 50-μm nylon mesh. The DNA contents were measured in a Cytomics FC500 (Beckman Coulter Inc., Fullerton, CA, USA) flow cytometer. DNA histograms of at least 10, 000 nuclei were plotted. The DNA-diploid cell population corresponding to surrounding normal tissue from the same location was used as an internal reference standard for the identification of DNA-aneuploid clones. The percentages of the cell cycle phases as well as the DNA indices of the aneuploid clones were calculated using the Modfit 5.2 software package. DNA histograms were classified as diploid if there was a single G0-G1 peak and aneuploid if additional G0-G1 peaks were present. The ratio of aneuploid G0-G1 peak values to diploid G0-G1 peak values was expressed as a DNA index. All specimens had a G0-G1 peak coefficient of variation of no more than 4%. The following were taken as cytometric variables: DNA ploidy, DNA index, and S-phase fraction. The cases with DNA indices between 0.9 and 1.10 were considered as DNA diploids, and those less than 0.9 or greater than 1.10 as DNA aneuploids.\nHalf of the paraffin-embedded samples of all three groups were routinely stained with hematoxylin and eosin. The rest of the paraffin samples were submitted to the labeled-polymer method of immunohistochemistry using antibodies against α-smooth-muscle actin (α-SMA), cytokeratin (CK) AE1/AE3, CK 8, protein 53 (p53), protein 63 (p63) and antigen Ki67.\nThe histogram of Group 1 samples presented a single peak in the G0-G1 area. The cell nuclei population was 5.91% in the G2 region and 91.30% in the G1 area. The proportion of cells in the S-phase was 2.78% and the coefficient of variance (CV) was 3.70%. Samples of this group were considered as being DNA diploid (Figure ). Group 2 samples also exhibited a DNA diploid pattern with an 88.26% nuclei population in the G1 region and 8.80% in the G2 area. The S-phase fraction was 2.95% and the CV was 3.04% (Figure ). Group 3 samples showed DNA aneuploidy: 48.70% of the cell population was considered diploid with 4.18% in the G2 region, 91.27% in the G1 area and a CV of 2.17%, whereas 51.30% of the cells analyzed presented an aneuploid pattern with 10.53% in the G2 region, 89.03% in the G1 area and a CV of 7.08%. The total aneuploid S-phase was 0.44% and the total S-phase fraction was 2.45% (Figure ).\nHistological analysis of Group 1 and Group 2 samples showed ductal structures, cords and islands of polygonal cells without atypia, sheets and strands of hyaline or plasmacytoid cells in a myxoid stroma. These findings were consistent with PA (Figure ). On immunohistochemistry, slight positivity was observed in the ductal cells with CK AE1/AE3 and CK 8 (Figure ). The non-luminal cells strongly expressed α-SMA (Figure ). Occasional cells were positive with proliferation antigen Ki67 and no expression was observed with p53 (Figure ). Otherwise, myoepithelial cells showed high positive nuclear staining for p63 (Figure ).\nGroup 3 samples exhibited an unusual histological pattern. These hypercellular areas were composed of blocks of round to ovoid epithelial cells without the 'reminiscent' myoepithelium. The epithelial cells were round with pale eosinophilic cytoplasm and round to oval nuclei. Nuclear pleomorphism or atypia, malignant luminal cells and necrotic foci were not observed (Figure ). The immunohistochemical study showed strong expression of CKs AE1/AE3 and CK 8 in most of the epithelial cells (Figure ). p63 and α-SMA staining were seen to a lesser degree than in the Group 1 and 2 samples (Figure ) whereas expression of antigen Ki67 was more intense (Figure ). p53 was expressed in a few epithelial cells (Figure ). |
A 69-year-old male visited the emergency room due to chest tightness and dyspnea that had occurred 3 days prior. Four years before this visit, the patient had undergone aortic valve replacement, ring mitral annuloplasty, and reconstruction of an aortic annular defect due to infective endocarditis using bovine pericardium.\nHe showed the symptoms of cardiac tamponade. Echocardiography and computed tomography revealed a large amount of pericardial effusion and a 16-mm cavity at the anterolateral wall of the left ventricle. The cavity had no communication with the nearby pericardial space and had the continuity of parietal pericardium. The myocardial wall motion around the cavity was normal. To stabilize vital signs, we performed pericardial centesis. The old bloody pericardial effusion was drained and there was no progressive bleeding.\nCoronary angiography showed 30% tubular stenosis in the left anterior descending artery and 40% focal stenosis in the proximal left circumflex artery. Magnetic resonance imaging (MRI) showed an aneurysmal change of the left ventricle from the base to the middle and anterior wall. Considering the surrounding myocardium of pseudoaneurysm was normal, pseudo-pseudoaneurysm or intramyocardial abscess was suspected ().\nSurgery was performed under cardiopulmonary bypass and cardiac arrest. In gross, we couldn't indentify the site of the pseudo-pseudoaneurysm, so we palpated the ventricular base between the left anterior descending artery and the ramus intermedius to identify the thinnest ventricle wall and incised it. After removing the inner thrombus, we identified a defect 1 cm in diameter in the endocardium and a 3×2-cm defect in the epicardium. There was no evidence of infection, so it was diagnosed as a pseudo-pseudoaneurysm. We performed patch closure of the defect using a prosthetic bypass graft in horizontal mattress sutures with pledgets (). The patient's postoperative vital signs were stable, and postoperative echocardiography showed no abnormal cardiac wall motion. With the exception of temporary pleural effusion in the left thoracic cavity, no complications occurred, and the patient was discharged on the thirteenth postoperative day. There was no evidence of abnormal cardiac wall motion or recurrence of the cardiac aneurysm in the follow-up echocardiography one month post-operation. |
A 40-year-old Hispanic man with a past medical history of human immunodeficiency virus (HIV) was brought to the emergency department complaining of right upper extremity (RUE) weakness and numbness for four days with associated bitemporal headache and generalized fatigue. The patient reported first time use of intranasal cocaine and heroin, after which he lost consciousness and woke up approximately four hours later with new onset RUE and headache. His cluster of differentiation 4 (CD-4) count was reported above 500 cells/mm3 and viral load (VL) was undetectable. The patient did not have any known CNS complications in the past.\nOn physical examination, his blood pressure was 151/97 mm Hg and pulse was 82 and regular. He was alert and cooperative. His cranial nerves were intact. His motor exam, however, was abnormal in the RUE with 3/5 arm strength and wrist drop; the strength and tone of the other extremities were normal throughout. Deep tendon reflexes were normal bilaterally, but his gait could not be evaluated. His sensory function decreased to pin sensation at the RUE and normal sensation was noted in the rest of the extremities and face. Laboratory testing was normal except for an elevated creatinine of 6.9 mg/dl, creatine phosphokinase (CPK) of 7855 IU/l, alanine transaminase (ALT) of 139 IU/l, and aspartate transaminase (AST) of 109 IU/l. Urine toxicology was positive for metabolites of cocaine and heroin. Magnetic resonance imaging (MRI) of the brain was done and it revealed two areas of increased T2/FLAIR signal within the medial aspect of both basal ganglia, measuring 16 mm in the right and 12 mm on the left involving each globus pallidus and the genu of the internal capsule, as can be seen in Figures -. His chest radiography was normal, computerized tomography (CT) of the brain, as can be seen in Figure , and cervical spine were normal. His electrocardiogram was normal.\nIn the subsequent days, his kidney function and rhabdomyolysis improved. The patient remained fully awake, alert and oriented, but the weakness of his RUE persisted. The patient decided to leave against medical advice despite full explanation of the risk of leaving.\nThe patient was contacted over the phone and he informed us that he followed up with his primary care physician and reported improvement of the weakness. He received physical therapy and was independent in all activities of daily living and functional mobility. His only limitation was a moderate decrease in fine motor coordination of the RUE. |
A 20-year-old female patient was referred to our hospital with abdominal pain, nausea and vomiting. Physical examination revealed mild hypotension and a distended, tender abdomen. Her vital signs were a temperature of 37.9°C, a heart rate of 98 beats per minute and a blood pressure of 97/49 mm Hg. Laboratory studies found a white blood cell count of 12,250/mm3. A computed tomography scan showed notable dilatation of the sigmoid colon with intraperitoneal fluid (fig. ). An emergent laparotomy revealed dilatation of the sigmoid colon, breakdown of the serosa and muscularis propria of the sigmoid colon with impending perforation, and intra-abdominal hemorrhage caused by breakdown of the mesenterium of the sigmoid colon (fig. ). As the rest of the intestine was normal, resection of the sigmoid colon with Hartmann's pouch and an end colostomy were performed. The macroscopic appearance of the resected colon showed strong alteration of the bowel wall, with some areas showing a complete lack of the lamina muscularis propria (fig. ). Histological findings of the resected specimen showed mucosal necrosis with leukocytic infiltration (fig. ). The postoperative course was uneventful, and the patient was discharged from the hospital 1 month after entry. Careful physical examination showed joint hypermobility, translucent skin with venous prominence and facial structure abnormalities (crooked nose and large eyes). Because of the uncommon intraoperative and clinical findings, there was a high suspicion of connective tissue disorder. Genetic analysis using cDNA extracted from the patient's fibroblasts by a reverse transcriptase polymerase chain reaction direct sequencing method showed a nucleotide change at c.2150 G>A on exon 32 (GenBank ID: NM_000090.3) as the reference. This nucleotide change resulted in the amino acid change of glycine at position 717 to aspartate within the triple helix region of COL3A1 (Gly717Asp), which confirmed a diagnosis of vEDS (fig. ). No specific therapy has been shown to delay or prevent further complications. Lifelong close follow-up should be continued in this patient. |
A 50 year-old male, with a history of coronary arterial bypass grafting 14 years back, presented with shortness of breath and dry cough. An X-ray revealed a large mass in the left hemithorax adjacent to the heart silhouette. A chest CT demonstrated the presence of a mass with smooth edges, in middle mediastinum next to the heart and partially intrapericardial (Fig. ). The mass was of heterogeneous density and of 11 cm size. Presence of atelectasis at the left lower lobe abating the mass was clearly seen. Based on clinical and radiologic evidence, we did proceed with CT guided FNA of the mass. The cytology findings revealed inflammatory lesion. Laboratory tests were normal. Based on patient symptoms, history and the presence of a mass potentially compressing the cardiopulmonary structures in vicinity, we decided to offer exploratory surgery for diagnosis and treatment.\nStandard hemodynamic monitoring and general anesthesia were followed by positioning, prepping and draping patient in left lateral decubitus position. An anterolateral left thoracotomy was carried out and entrance in the hemithorax was made without any challenge. The mass was assessed and found to be leaning medially on the surface of the lateral wall of the left ventricle, including the pericardial layer and had smooth edges which didn’t infiltrate the lung (Fig. ). We started dissecting the mass from its smooth capsule, making it through all its layers. An old and degraded piece of surgical swap was visualized (Fig. ). The surgical swap was removed along with the capsular layer of this mass. Patient tolerated the procedure very well and blood loss was minimal. A chest tube was inserted in the left hemithorax and chest wall was closed following standard procedures.\nIn the immediate post-operative phase, patient improved steadily and on day four was discharged home symptom-free. In the long-term follow -up, patient was found to remain without symptoms. |
A 62-year-old female patient admitted to our clinic because of recent fatigue, shortness of breath, abdominal distention, and pain in the right upper quadrant. In her history, she had a liver wedge resection 3 years ago with AE found in the biopsy material. On physical examination, the liver was 5 cm palpable under the right rib, the spleen was non-palpable, and Traube's space was clear. Tension ascites and collateral veins in an upward flow direction were noted on the abdomen. Respiratory sounds were decreased at the bases of both lungs and dullness was found with percussion.\nHemoglobin was 8.3 g/dl in the whole blood count. Except for low albumin levels (2.1 g/dl), all other biochemical tests were normal. There was no flow viewed in the left hepatic vein and inferior vena cava on abdominal portal Doppler ultrasound. The portal vein was 16 mm, and the splenic vein was 15 mm in diameter and hepatofugal flow was noted. On contrasted abdominal CT, there was a 54×70×45 mm-sized cystic lesion in left lobe of the liver extending towards the posterior mediastinum with irregular calcifications that invaded the diaphragm, esophagus, and pericardium. It was occluding the inferior vena cava and left hepatic vein at the level where the hepatic veins poured into the inferior vena cava. Secondary to inferior vena cava occlusion, the azygos vein and the hemiazygos vein appeared to be dilated. There was bilateral pleural effusion (). A grade 1 esophageal varix was observed on upper endoscopy. The inferior vena cava was found to be occluded at the L1 level with venography. It was determined that the venous return was provided by the azygos, hemiazygos system, and the collaterals (). In the performed echocardiography, the entrance of the inferior vena cava into the right atrium was normal.\nWith paracenthesis, the intraperitoneal fluid was turbid and total leucocyte number was 410/mm3 (10% neutrophils, 90% lymphomonocytes). The intraperitoneal fluid was exudate in character (serum acid albumin gradient was 0.2 g/dl) and protein was 5.1 g/dl. There was no other pathology found in the Gram staining and culture of the intraperitoneal fluid.\nAccording to these findings, the patient was diagnosed with secondary Budd-Chiari Syndrome (BCS) development due to AE. The patient was given 15 mg/kg albendazole (800 mg/day) for treatment. |
An 83-year-old female with a past medical history of rheumatoid arthritis (on DMARD's), asthma, depression, gastroesophageal reflux disease (GERD), and lumbar spondylosis, as well as a past surgical history of right posterior total hip arthroplasty (1999), bilateral total knee arthroplasties (2003, 2012), and right shoulder hemiarthroplasty (2010), presented with five days of right hip pain and inability to ambulate after bending down. In the emergency department, initial radiographs revealed a right posterior hip dislocation, as well as chronic appearing fractures of the right greater trochanter and left inferior public rami (). Her right lower extremity was shortened, internally rotated, and adducted. A propofol-induced conscious sedation was performed by the emergency physician and closed reduction was attempted by an experienced orthopaedic resident. The reduction maneuver involved hip flexion, traction, adduction, and internal rotation followed by external rotation and abduction. After three attempts, post reduction radiographs were significant for a right inferior obturator hip dislocation (). The patient tolerated the procedure and was neurovascularly intact distal to her hip. Computed tomography (CT) was performed, which confirmed a persistently dislocated femoral head with intrapelvic migration through the right obturator foramen (Figures and ). Having failed three attempts at closed reduction, the patient was taken to the operating room for open reduction and revision arthroplasty.\nUsing a posterolateral approach, the femoral head was found to be locked inferior and posterior to the acetabulum. Manual traction was utilized to successfully extricate the femoral component from within the obturator ring. Both the femoral and acetabular components were stable; however, a large amount of posterior wear was noted on the liner, which was exchanged for a constrained component. A greater trochanteric hook plate with cerclage cables was then utilized for the fixation of the greater trochanteric fragment (). Excellent stability with a full range of motion was noted.\nPostoperatively, the patient was weight bearing as tolerated, with standard posterior hip precautions including an abduction pillow. Aspirin 325 mg BID was used for deep vein thrombosis (DVT) prophylaxis. Although the patient initially did very well, she developed urosepsis six months after the index procedure, leading to an acute right periprosthetic septic hip with Proteus mirabilis. Radiographs showed greater trochanteric escape from the hook plate (). She then underwent irrigation and debridement with greater trochanter excision and hook plate removal (). The patient was discharged with 6 weeks of ceftriaxone antibiotics via a peripherally inserted central catheter and has since been doing well with no further dislocations. |
A 62-year-old woman was referred to us with suspicion of pulmonary hypertension, due to PA dilatation, in Department of Chest Diseases. Her complaint was shortness of breath during last 3 months. She had been told that she had a congenital heart disease. In physical examination, 3/6 systolic ejection murmur, best heard at left side, was observed. Other physical findings were normal. Electrocardiography (ECG) was in sinus rhythm. No ischemic ST-T changes were observed. There was a widened mediastinum in chest X-ray.\nIn transthoracic echocardiography, left ventricular measurements and functions were normal. Right ventricle was nearly dilated. There was main pulmonary artery dilatation (46 mm) and moderate pulmonary valvular stenosis (maximum gradient 46 mmHg, mean gradient 30 mmHg). Systolic pulmonary artery pressure (PAP) could not be measured with Doppler echocardiography because of pulmonary stenosis. Echocardiographic images could not be shown as figure due to poor echocardiographic imaging. To evaluate any other congenital anomalies and measure PAP and gradients, coronary angiography and right-sided cardiac catheterization were planned.\nDuring coronary angiography, left coronary ostium was located normally, and selective left coronary angiography demonstrated the normal left main, LAD, and dominant left circumflex (Cx) arteries. An anomalous RCA, as a separate branch, arose from the proximal of LAD after the first septal perforator and coursed anterior to the right ventricular outflow tract to gain the right atrioventricular sulcus (Figures and ). The RCA could not be cannulated in the right sinus of Valsalva. Aortagraphy showed no coronary ostium originating from the right sinus of Valsalva (). No significant stenosis could be observed in any of the coronary arteries. Right ventricular angiograms revealed evidence of doming of the calcified pulmonic valve with a large poststenotic dilatation involving the main pulmonary artery and its branches (). Systolic PAP pressure was 14 mmHg, and systolic right ventricular pressure was 47 mmHg. Peak-to-peak pulmonary gradient was observed 33 mmHg. Qp/Qs was calculated as 1,1.\nIn order to evaluate PA, pulmonary computed tomographic angiography was planned. Diameters of main PA, right and left PA, were 45 mm, 28 mm, and 32 mm, respectively (). There was no dissection or another anomalies. Multislice coronary computed tomographic (cCT) angiogram was planned to evaluate course of RCA. Mechanical compression of the anomalous RCA between the aorta and pulmonary artery might be related ischemia. But, it could not be performed due to technical insufficiency in our hospital. Therefore, exercise stress test was planned to determine presence of ischemia. During the stress test, ischemic signs were not observed.\nPatient was evaluated by cardiothoracic surgeons for surgical treatment. They suggested conservative management and followup because of low PAP pressures and moderate pulmonary stenosis. It was suggested orally a β-blocker (50 mg of metoprolol) and aspirin (100 mg) treatment due to minimal coronary heart disease. During 6 months followup, no clinical and hemodynamic changes were observed in the patient. |
A 69-year-old man developed a sudden epigastric pain. He was presented at this hospital as an emergency outpatient. Six years earlier, he underwent laryngoesophagopharyngectomy, bilateral lymph node dissection for hypopharyngeal cancer, and esophageal reconstruction with a free jejunum flap. On physical examination, the abdomen was flat and soft with tenderness in the epigastric region, but no sign of peritoneal irritation. Blood biochemistry findings revealed elevated values: creatinine, 1.16 mg/dl; lactate dehydrogenase, 364 U/l; and creatine phosphokinase, 622 U/l.\nAbdominal contrast computed tomography (CT) revealed twisted mesentery with the small intestine around the point of torsion (whirl sign) and the superior mesenteric artery as the axis. Contrast enhancement was weakened in the same area of the small bowel (Fig. ). Given this information, we suspected small bowel volvulus and performed emergency surgery on the same day.\nA 5-mm camera port was placed in the umbilicus and 5-mm ports in the lower and right lower abdomen. During laparoscopic examination, the upper jejunum adhered to the small bowel close to the terminal ileum with overlapping of the small bowel. The entire part from the upper jejunum to the terminal ileum was twisted clockwise with the superior mesenteric artery and vein as the axes and the adhesion site as the starting point. There were areas of poor color enhancement throughout the twisted section of the small bowel (Fig. ). We laparoscopically separated the adhesion between different sections of the intestinal tract and traced the bowel from the small bowel in the region of the ligament of Treitz toward the anus to confirm the absence of adhesions or torsion up to the terminal ileum. The color of the small bowel improved; hence, the surgery was completed without resecting any part of the intestine.\nPostoperatively, the patient made good postoperative recovery, resumed oral intake on day 2, and was discharged on day 5 after surgery. No recurrence has been reported 1 year postoperatively. |
In June 1997, a 52-year-old man without any medical history was referred to the department of gastroenterology because of gastric subepithelial tumor. Esophagogastroduodenoscopy (EGD) demonstrated 1 cm sized subepithelial tumor on the proximal antrum anterial wall (). Biopsies showed chronic gastritis only. He was admitted and diagnostic endoscopic mucosal resection was done (). The pathologic finding was diffuse aggregation of monomorphic lymphoid cells without any large cell or small cell component in the submucosal layer (). Immunohistochemical staining showed atypical lymphoid cells that were positive for pan B and lamda, but negative for pan T, bcl-2 and kappa. Ki-67 labeling index was 5%. These findings suggested his diagnosis was low-grade MALT lymphoma. Abdomen and pelvic computed tomography (CT), chest CT, bilateral bone marrow examination and F-18-fluorodeoxyglucose positron emission tomography (PET) were done and there were no involvement of disease. Although rapid urease test (RUT), serologic test for H. pylori, urea breath test (UBT) and H. pylori culture of gastric mucosa were all negative, he took triple regimen of H. pylori eradication including clarythromycin, amoxicillin, and proton-pump inhibitor (PPI) for 14 days. After the H. pylori eradication was completed, subtotal gastrectomy was done. In the pathologic review of surgical specimen, there were no residual tumor cells. We performed esophagogastroscopy, abdomen and pelvic CT and PET every 6 months for 2 years and then we performed the same examination every 12 months for 4 years. He had been followed without evidence of disease recurrence for 6 years, after which he stopped visiting our hospital. In May 2007, he was referred to our hospital again complaining of throat pain and neck mass. Neck CT showed multiple enlarged lymph nodes in bilateral cervical nodes (). The largest diameter of the involved lymph node was 6 cm. Excisional biopsy showed diffuse infiltration of large atypical lymphoid cells (), which were positive for CD 20, but not for CD 3, CD10, CD 56, ALK-1, or CD 21. Ki-67 labeling index was 90%. These findings suggested DLBCL. EGD and full staging evaluation showed no involvement of other site. He was diagnosed with stage IIA DLBCL and received three cycles of systemic chemotherapy including rituximab, cyclophospamide, doxorubicin, and vincristine (R-CHOP), followed by 3,600 cGy radiotherapy. He achieved and maintained complete remission until recent days. |
A 35-year-old man underwent ACL reconstruction of the right knee with hamstring tendons and partial lateral meniscectomy for a meniscal tear. Magnetic resonance imaging scan showed moderate osteoarthritic changes and a subchondral cyst in the central portion of the lateral femoral condyle (). At arthroscopy, he was found to have degenerative chondral changes in the lateral compartment, mainly on the tibial side. The medial meniscus showed evidence of previous partial meniscectomy that had been performed six years previously. He responded well initially and underwent a physiotherapy rehabilitation program.\nAt six weeks after surgery, he presented with a two-day history of pain and swelling in the knee. He did not report any locking or giving way, or a new injury. Clinically, he had a severe effusion in the knee, but he was able to bear weight with some discomfort. He had a limited range of movement with only 10°-90° of knee flexion; further movements were restricted by pain. The arthroscopic portals were well healed. Plain radiographs showed no chondrocalcinosis. Although he was apyrexial, the inflammatory markers were raised, with the erythrocyte sedimentation rate and C-reactive protein levels at 110 mm/hr (normal range, 1 to 7 mm/hr) and 130 mg/L (normal range, 0.1 to 6 mg/L), respectively. He underwent an arthroscopic joint washout of the knee. The graft was found to be intact (), and there was no chondrocalcinosis of the menisci. He had no new arthroscopic findings in terms of degenerative changes. The synovial fluid was straw-colored and grew no organisms or culture but was positive for calcium pyrophosphate crystals on microscopic examination. The fluid was obtained at the time of washout, as given the amount of swelling and raised inflammatory markers, it was considered more appropriate to improve the patient's symptoms even if the diagnosis proved not to be septic arthritis.\nHe was treated with non-steroidal anti-inflammatory drugs (Diclofenac) and his pain improved. Unfortunately, he did not follow the full postoperative physiotherapy rehabilitation and did not attend clinic appointments. One year later, he presented with continuing pain in the knee. A further arthroscopy at that time was performed to debride the knee and alleviate the pain, which showed the graft had incorporated well but degenerative changes had progressed to involve both the lateral and patellofemoral compartments (). |
A 30 year-old non-smoking Caucasian G3P1011 presented for initial prenatal assessment at six weeks gestation. The conception was established without medical assistance. The patient had no significant medical or surgical history. She underwent an uncomplicated curettage for missed abortion four years before presentation and an uneventful term vaginal delivery occurred two years later.\nTransvaginal ultrasound at seven weeks gestation revealed a dichorionic-diamniotic twin pregnancy. At 18 weeks gestation no growth discordance was noted, but cervical length was two cm with funneling. Based on these findings, the patient was counseled about maternal and neonatal risks associated with twin pregnancy, particularly the risk of preterm labor due to cervical shortening. Although rescue cerclage was offered to the patient, this option was declined. She was therefore placed on bedrest for two weeks with follow-up ultrasonography for assessment of cervical length.\nAt 192/7 weeks gestation the patient experienced abdominal cramping and non-purulent blood-tinged vaginal discharge. The patient remained afebrile. She was hospitalized and placed on bed rest in Trendelenburg position after sterile speculum exam found the cervix two cm dilated with protruding "hourglass membranes".\nOne day later, amniotic membranes had fully retracted and were no longer visible above a closed cervix. Microscopic examination of vaginal fluid found occasional clue cells. External monitoring identified occasional uterine contractions; heart rates at ~150/min were measured for both twins. The patient was again counseled about the implications of preterm labor at this early stage, and the uncertainty of preventing further cervical dilation. After consideration of all therapeutic options (including cerclage), the patient elected tocolysis with a view to save her pregnancy. A 4 g loading dose of magnesium sulfate was administered intravenously, followed by a maintenance dose of 2 g/h. Oral metronidazole (500 mg) was given every 8 h, and 500 mg ampicillin was given intravenously every 6 h after a 2 gm loading dose according to hospital protocol. Additionally, oral indomethacin (50 mg) was given every 6 h for 3 days. Just as the magnesium sulfate was initiated, the patient experienced spontaneous rupture of membranes and prolapse of umbilical cord of twin A was noted several hours later. Fetal demise was confirmed approximately 1 h later, but there was no evidence of labor or infection over the next 24 h. After discussing the potential dangers of prolonged rupture of membranes, retention of dead fetus, maternal sepsis, the potential for prolonged hospitalization, need for hysterectomy and risk of death, the patient elected to continue limited oxytocin augmentation in an attempt to deliver twin A and salvage twin B. The risk of losing both fetuses was carefully discussed, and the patient agreed with this management approach despite the acknowledged uncertainty of outcome.\nAfter 8 h of oxytocin therapy, a stillborn female fetus (319 g) was delivered. The placenta remained in situ and the umbilical cord of twin A was divided and ligated near the cervix with 3-0 chromic gut suture. Oxytocin was immediately discontinued. Monitoring of twin B confirmed stable heart tones and appropriate fetal movement throughout delivery of the non-viable twin. Intravenous ampicillin and metronidazole were continued postpartum but MgSO4 was not reinitiated. Immediately following delivery of twin A, sterile speculum exam found a closed cervix with the umbilical cord completely retracted in utero. Maternal vital signs remained stable and she was discharged home one week later on full bed rest, preterm labor precautions, and oral amoxicillin-clavulanate (875 mg) twice daily × 5 d.\nAt 25 weeks gestation, 12 mg betamethasone was administered intramuscularly with an additional dose 24 h later. There was no evidence of infection or coagulopathy at biweekly clinical evaluations, which included serial ultrasounds until 34 weeks to assess cervical length. Formal biophysical profiles (BPP) began at 28 weeks, when the estimated fetal weight was 1250 g and the BPP score was 8/8. At this time mild uterine irritability was detected and 5 mg oral terbutaline was given every 4 h until 34 weeks. Uterine activity was reduced following oral terbutaline therapy.\nSpontaneous labor began at 35 1/7 weeks. At readmission, the cervix was 5 cm dilated with intact membranes and vertex presentation. Epidural anesthesia was established, an amniotomy was performed, and the patient had a normal progress of labor. She delivered a viable male infant weighting 2894 g (1 and 5 min Apgar 9 and 9, respectively) over an intact perineum. Approximately 5 min later, two placentas were delivered spontaneously (Figure ). The postpartum course was uncomplicated; mother and baby were discharged home in stable condition 48 h later. |
A 46-year-old female presented to the orthopaedic outpatient clinic of our level 1 trauma center one month after sustaining bilateral femur fractures in a motor vehicle accident. These injuries were treated at an outside hospital by locked plating of the right distal femur fracture, and by antegrade intramedullary interlocking nail fixation of the left femoral shaft fracture. She presented for a second opinion experiencing progressive left groin pain in the absence of an additional trauma, resulting in wheelchair dependency. The physical examination revealed healed surgical incisions on bilateral lower extremities, and impaired active and passive range of motion to the left hip secondary to significant pain. Neuromuscular examination of the distal left lower extremity was within normal limits. She had a leg-length discrepancy with shortening of the right leg secondary to multiple previous surgical procedures, which included a right total hip arthroplasty (THA) after acetabular fracture fixation, ipsilateral sacro-iliac joint fusion, and right-side distal femur plate fixation (Figure ). The patient also demonstrated a right-sided foot drop. Radiographic evaluation revealed a displaced basicervical femoral neck fracture adjacent to the piriformis entry point of an antegrade femoral interlocking nail. This implant was effectively stabilizing a transverse midshaft femur fracture, with early signs of callus formation (Figure ). After discussing all treatment options, the patient underwent closed reduction of the femoral neck fracture on a traction table, and revision fixation of both fractures was performed with a reamed cephalomedullary nail (Stryker Gamma 3™, Mahwah, NJ) through a greater trochanter starting point. Postoperative radiographs revealed an adequate cumulative tip-apex distance of <25 mm, however, the reduction appeared to be in slight varus of the hip (Figure ).\nAt two-week follow-up, the patient was ambulating with weight bearing as tolerated on crutches. All surgical incisions were healed and staples were removed. Six weeks later, she reported progressive worsening of left hip pain without additional hip trauma. She was no longer able to bear weight on the left leg and had resumed use of a wheelchair for 3 weeks. Physical examination demonstrated no indication of infection, but any motion of her left hip was extremely painful. Radiographs revealed a failure of fixation of the basicervical femoral neck fracture, with “cut-out” of the lag screw through the femoral head. The midshaft femur fracture was continuing to heal uneventfully (Figure ).\nGiven the unsalvageable damage to the femoral head and acetabulum she was converted to a total hip arthroplasty (THA). The procedure was performed without complications, using non-cemented acetabular cup and press-fit stem components (Zimmer, Warsaw, IN). The stem of the arthroplasty appears to have been placed in slight varus position (Figure ). On postoperative day one, the patient mobilized with physical therapy and noted a significant leg-length discrepancy, with the left leg approximately 3.5 cm longer than the right, as confirmed by full-length standing X-rays (Figure ). The patient was offered a revision THA to partially correct the leg length discrepancy. She agreed and a revision THA was performed, including proximal femoral shortening and revision of acetabular and femoral components resulting in a near equal leg length (Figure ). The patient subsequently sustained an acute anterior dislocation of her left THA revision at one week after discharge from the hospital, possibly related to the shortening procedure (Figure ). The dislocation was successfully managed by closed reduction under general anesthesia. The intraoperative exam revealed that the hip was stable in full flexion and abduction, but unstable in extremes of extension or adduction. The THA dislocation was successfully managed in a hip abduction orthosis for 6 weeks. The patient had no further complications or adverse events, and presented with an acceptable outcome at one-year follow-up in our orthopaedic clinic. |
A 30-year-old gravida 3, para 2, abortus 1 Ethiopian mother was admitted to the labor and delivery ward with a diagnosis of latent first stage of labor and grade-2 meconium-stained amniotic fluid, at cervical dilation of 3 cm and at a gestational age of 40 weeks plus 1 day. She presented with pushing-down pain and passage of liquor of 12 hours duration. She had no history of shortness of breath or history of cough. She had no headache or blurry vision. Her past medical, surgical, family, and psychosocial history was unremarkable. She had no history of prior hospital admission. Upon physical examination at the time of admission, her blood pressure was 140/85 mmHg, pulse rate was 88–92 beats per minute, and respiratory rate was 20 breaths per minute. A diagnosis of preeclampsia was considered, and she was worked up for that. Her complete blood count (CBC) profile was normal with hematocrit of 42%. Her liver enzymes were also normal. Urine protein was negative.\nIn the second stage of labor, cesarean section was done for an indication of fetal bradycardia, with the outcome being 3200 g alive male neonate with an Apgar score of 7/10 and 8/10 at minutes 1 and 5, respectively. There was postpartum hemorrhage (PPH) due to uterine atony and uterine incision extension, which was managed with a combination of medical management of PPH, compression sutures, and extension repair. She was transfused with two units of blood postoperatively.\nFour hours into her postpartum period, she started to experience shortness of breath and her oxygen saturation was 85% on atmospheric oxygen. Her blood pressure was 130/80 mmHg, and her pulse rate was 115 beats per minute. Chest osculation revealed bilateral basal crackles. With a diagnosis of pulmonary edema (caused by preeclampsia), 80 mg of Lasix was given parentally, resulting in a good response. She was taken off oxygen on the following day. Her pulse rate was also in the normal range. Her posttransfusion hematocrit was reported as 24%.\nFive days later, she again developed shortness of breath of sudden onset. With severe hypoxia and impending respiratory failure—her oxygen saturation was down to 70% with atmospheric air—pulmonary thromboembolism was considered, and chest computed tomography (CT) scan was considered shortly after she was evaluated by an internal medicine senior resident. She was already on 10 L of 100% oxygen via face mask. Within an hour, while being prepared for imaging and as she was about to be started on empirical anticoagulation therapy, she went into respiratory failure (she could not maintain her saturation with 15 L of 100% oxygen via face mask). Her CBC profile was updated and revealed a hematocrit of 26% and WBC count of 14,400. Her updated liver enzymes and renal function test was otherwise normal.\nShe was instantly admitted to the intensive care unit (ICU) and put on a mechanical ventilator with the same suspected diagnosis. Meanwhile, a differential diagnosis of heart failure was made, considering the overall course of her medical condition. She was provided 40 mg of Lasix intravenously. She produced adequate urine. Her updated hematocrit was 26.3%. Bedside chest ultrasound and echocardiography was done subsequently. Bilateral pleural effusion was observed with the chest ultrasound, but fluid analysis was unremarkable. The echocardiography findings were severe mitral stenosis (mitral valve area of 0.9 cm2) and mild pulmonary hypertension.\nWith a revised tentative diagnosis of New York Heart Association classification (NYHA) Class IV congestive heart failure secondary to severe mitral stenosis, her Lasix dosage was escalated to 40 mg intravenously three times per day. The patient showed a remarkable improvement. She was extubated after 48 hours of stay in the ICU. She was fully conscious and communicating well when she was transferred to the medical ward for full recovery. Her oxygen saturation was 93% on atmospheric air. The same standing dose of Lasix was continued. |
Two brothers presented to us, both with similar symptoms. Our first patient was an eight-year-old male who presented with an inability to stand or walk since the past two months, along with bilateral foot deformities. According to his father, the patient had developed a difficulty in walking and in climbing stairs, accompanied by frequent falls - about six months back. Gradually, he had lost the ability to walk even with support and was mainly confined to his bed-although he could sit up and crawl.\nThe patient’s intelligence was unaffected by the illness; he had no history of trauma, fever, fits, incontinence, or syncope and did not display vision, speech, or hearing abnormalities. A detailed review of the gastro-intestinal, genitourinary, respiratory, and cardiovascular systems showed no abnormality. The patients’ parents were first cousins, albeit unaffected by the disease themselves. However, out of five siblings, two of the patient’s sisters (12 and 14 years of age) and one brother (five years old) were affected by a similar illness. The patient had had an unremarkable birth history, had reached all the relevant milestones timely and was said to be taking a nutritionally adequate diet. As per the parents, all his vaccinations were complete and the past medical history was clear.\nOn general examination, the patient was well oriented in time, place, and person with his vitals, height, and weight all within the normal ranges. Regarding system-wise examination, the central nervous system examination showed no signs of wasting or abnormal tone in the upper limbs, the power in both the upper limbs was 4/5, and the deep tendon reflexes were normal when elicited. However, the bulk of both the lower limbs was decreased, with the right lower limb being slightly more wasted than the left. The tone was decreased as well and power in both the lower limbs was 2/5. The deep tendon reflexes of the lower limbs were absent. On further examination, Babinski sign was negative and the pupils were bilaterally and equally, reactive to light. The gait of the patient could not be assessed as he could not stand. However, there were no signs pointing towards cerebellar or cranial nerve dysfunction and mental functions and speech proved to be intact. On sensory examination, a higher threshold to pain and temperature was noted.\nOn examination of the musculoskeletal system, the patient had marked wasting in the anterior compartments of both legs. He demonstrated a bilateral foot drop with pes cavus (Figure )-more pronounced on the left side - and his feet were kept in a plantar, fixed position in the relaxed state. Contractures on the knees and Achilles tendon were seen. The upper limbs did not show any marked abnormality other than contractures over the interphalangeal joints of the fingers, with the skin prominently thicker there. The examinations of all the other systems were unremarkable.\nAs per laboratory investigations: the complete blood count, electrolytes, and creatine-phosphokinase levels were all within the normal ranges. The nerve conduction velocities were markedly decreased. A sural nerve biopsy was carried out and a subtotal reduction in myelin fibers was noted, along with focal endo-neuronal edema. No granuloma formation or inflammatory component could be identified. Based on the clinical, hereditary, and investigative findings, the patient was diagnosed with CMT disease, type 2.\nIn terms of management, no specific medical treatment is available, but the patient was referred to the orthopedic and rehabilitation departments to manage the foot deformity.\nOur second patient, brother of the first patient, was a five-year-old male who presented with difficulty in walking and frequent falls since the past two months. Gradually, his condition had progressed and his distal weakness had worsened, due to which he had been unable to walk without support since the past two weeks. Unlike his brother, the patient could still walk with support, although by dragging his feet. There was no significant difference in the history and examinations of this patient when compared to his brother and similar investigations were carried out, wherein the sural nerve biopsy showed nerve bundles with adequate myelin. Based on the above information, a diagnosis of CMT disease was made here as well and the child was similarly referred to the orthopedic and rehabilitation departments.\nConcerning the apparent autosomal recessive mode of inheritance, the parents of the boys were counseled accordingly regarding the implications of having more children in future and the manner in which their children could further propagate the condition. Additionally, they were counseled to bring in their affected daughters with reportedly similar symptoms for an evaluation and any possible rehabilitation as well, even though the parents described their status as nonambulatory. |
An ill-appearing 19-year-old male with the one-year history of asthma presented to the emergency room with non-specific symptoms including fatigue, dyspnea, numbness in the right leg, nausea, vomiting, and dizziness. Two months prior to presentation, he had a sinus surgery and within few days after this surgery, he developed cough and dyspnea, so he was admitted to outside hospital for possible pneumonia. He was treated with cefuroxime, Tamiflu, and oral prednisone. He improved momentarily with steroids. Two weeks later, he returned to the outside hospital complaining of right foot plantar numbness and dyspnea, he was discharged home on Levaquin as they thought he may have some residual sinus disease left. One week later he was seen by a pulmonologist at outside hospital and they noticed that one of the cultures grew staph, hence started on Bactrim. He took Bactrim for three days and his mother noticed that he developed some mental status changes, hence Bactrim was stopped. After this, no more symptom of mental status change was noticed. Over the next few weeks, the patient noticed tachypalpitations, continued to have fatigue, shortness of air, and fatigue so the family decided to come to our hospital's emergency department for further workup. While in the emergency room, he was found to be in atrial fibrillation with the rapid ventricular response and elevated troponins. The patient spontaneously converted into sinus rhythm within 10 minutes. His vital signs were stable except for tachycardia with a heart rate of around 100 beats per minute. Physical examination was unremarkable with a normal sensation on right leg and foot. He was admitted to cardiac intensive care unit for further workup due to elevated troponin.\nSalient laboratory values and electrocardiogram\nThe patient’s initial complete blood count was remarkable for white blood cell of 28,800/ul with eosinophil count of 12,960/ul (45%) in spite of the use of low-dose oral corticosteroids for a few days prior to admission. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were both elevated at 35 and 4.14, respectively. His admission troponin was 16.28. His initial electrocardiogram (ECG) showed atrial fibrillation with a heart rate of 161 beats per minute, non-diagnostic Q waves in the inferior leads, T-wave inversions in the inferior leads and no significant ST segment changes noted (Figure ). His repeat ECG 10 minutes later when he converted to sinus rhythm showed sinus tachycardia with a heart rate of 100 beats per minute, Q and T changes as noted earlier, as well and no significant ST segment changes noted (Figure ). Other labs, including TSH, UDS, BNP, lactate, and renal function, were unremarkable. Rheumatological workup including anti-nuclear antibody (ANA), perinuclear antineutrophil cytoplasmic antibody (p-ANCA), cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA), rheumatoid factor, myeloperoxidase (MPO) antibody, serine protease antibody 3, and anti-cyclic citrullinated peptide (anti-CCP) IgG was inconclusive. However, the patient’s IgE and IgG were both markedly elevated. Several infectious causes, such as histoplasma, coccidioides, strongyloides, cytomegalovirus (CMV), human immunodeficiency virus (HIV), tuberculosis (TB), Epstein-Barr virus (EBV), hepatitis B, and hepatitis C, were explored and all were negative.\nImaging\nTransthoracic echocardiogram revealed an ejection of 55% with some apical hypokinesis. The transesophageal echocardiogram showed no evidence of endocarditis, thrombus, shunt, or atherosclerosis. Computed tomography angiography (CTA) of the chest with and without contrast showed moderate mediastinal and bilateral hilar adenopathy in addition to bilateral axillary lymphadenopathy, bilateral peribronchial thickening, and patchy ground-glass opacities most predominantly in the posterior lower lobes. There was no evidence of pulmonary embolism (Figure ). Cardiac magnetic resonance (CMR) showed several areas of delayed enhancement within the left ventricular myocardium and decreased perfusion in the mid to apical septal and inferior segments throughout the apex. It also revealed a small pericardial effusion and minimal hypokinesis of the lateral apical wall (Figures -). Due to the abnormal myocardial enhancement, a CT of the heart with coronary CTA was ordered which showed normal coronary artery anatomy with no evidence of stenosis, calcified plaque, or soft plaque (Videos -). Due to his reported neurologic symptoms, CT of the head without contrast was ordered and showed two areas of low-attenuation within right frontal white matter. MRI of the head was subsequently performed which showed many small bilateral punctate infarcts throughout cerebrum and a few additional ones in the cerebellum.\nBiopsies\nA bone marrow biopsy showed normocellular bone marrow for age and no concern for dysplasia; however, both the bone marrow biopsy and peripheral blood smear showed marked eosinophilia with leukocytosis. Several transbronchial cryobiopsies were taken from the left lower, upper lobes and lingula of the lung which showed patchy areas of eosinophilic venulitis with dense eosinophilic infiltrates involving many of the small venules. This process was happening in the background of chronic bronchiolitis with abundant eosinophils within small airways, smooth muscle hypertrophy, and goblet cell metaplasia (which suggests asthma). All these findings taken into consideration together suggested EGPA (Figure ).\nThe patient was initially started on 1000 mg of intravenous methylprednisolone for three days and then 1 mg/kg/day of oral prednisone for several months with a gradual taper. He was also started on cyclophosphamide for three to six months. Additionally, due to the patient’s young age, arrangements for sperm preservation were made prior to starting cyclophosphamide. The patient responded well to the treatment and at his one-month rheumatology follow-up, the patient continued to improve. His troponin-I reduced to 0.08 at one month visit. |
A 28-year-old man without previous medical history was brought to the emergency department of the hospital with worsening dyspnea, chest pain, and coughing developed following penetrating chest trauma by a nail gun which happened 5 hours earlier. He was repairing a sofa at his home using this gun when a nail was misfired to his chest accidentally. Upon primary survey, the patient's airway was intact, he was tachypneic, and had reduced lung sound at left hemithorax. He had a blood pressure of 110/70 mm Hg and heart rate of 94 beats per minute and his heart sounds were muffled but regular S1-S2 were barely heard. He had a GCS score of 15/15. Upon chest inspection, a clean circular puncture wound was noted in the third intercostal space of the left hemithorax at the midclavicular line (). According to the hemodynamic stability, he underwent chest CT scan and it revealed a nail as a sharp hyperdense foreign body that penetrated the chest wall and passed through the lower lobe of the left lung and then entered the pericardium, and finally the anterior aspect of the left ventricle (LV) reaching LV cavity. Also, patchy ground glass opacities at left lower lobe was noted which pertained to hemorrhage (, , , , ). Transthoracic echocardiography was performed and chest CT scan observation was confirmed and revealed pericardial effusion. Considering clinical and imaging findings, the patient underwent midline sternotomy. After opening the pericardium, the gush of blood was completely evacuated and controlled by Teflon felt-supported suture and to impede the left anterior descending artery involvement, Teflon-felt wrapping repair was performed in horizontal mattress manner (Video-2). After cardiac suturing, the nail was extracted from the left lung, and the chest wall (). Regarding surgery assessment, transesophageal echocardiography was done and confirmed no evidence of further intraventricular dissection, ventricular septal rupture or any residual defect. There was no postoperative complication and he was extubated on postoperative day 2 and the drain output progressively diminished and was removed serially. The patient was discharged 4 day's after admission. His outpatient follow-up, 2 weeks after surgery was uncomplicated. |
A 55-year-old male with only a remote medical history of seizure disorder on levetiracetam presented to the emergency department (ED) complaining of a generalized and bilateral headache graded a 2-3/10 for the past six days prior to admission. He had generalized fatigue, a loss of sense of taste, and double, blurry vision since this time period. He had exposure to a family member who was COVID-19 positive prior to symptom onset. He denied any other medical history including hypertension or diabetes mellitus (hemoglobin A1c on admission was 5.8%) and denied any significant family or social history. In the ED, he was evaluated by the neurologist and ophthalmologist. Physical exam revealed a blood pressure of 122/79 mm Hg, heart rate of 89 beats per minute, respiratory rate of 16 breaths per minute, oxygen saturation of 98% on room air, and temperature of 98 degrees Fahrenheit. His pupils were reactive to light bilaterally but noted to have left sided ptosis and diplopia on all fields of gaze except to the left. His visual acuity was 20/50 in both right and left eyes. He was noted to have 10% reduction of adduction and elevation in his left eye. Facial nerve sensation was intact in all branches and facial strength was symmetric. There was no evidence of pupil or orbital involvement on slit lamp or fundal ophthalmologic examination. He was also noted to have mild bilateral lower extremity sensory deficits with intact proprioception which he claimed to be chronic due to an old injury several years prior to this admission. He had no other sensory or neurological deficits on physical examination. He was determined to be COVID-19 positive using reverse transcription-polymerase chain reaction (RT-PCR). Complete blood count and comprehensive metabolic panels were all within normal limits. A computed tomography (CT) scan of the head without contrast was emergently obtained but was unremarkable (Figure ).\nFurther testing with CT angiography and magnetic resonance imaging (MRI) of the brain and neck were also unremarkable without any signs of nerve compression, masses, or aneurysms (Figure ).\nHe was admitted for further observation and was treated supportively for COVID-19 and third cranial nerve palsy. On day 3 of hospitalization, his symptoms gradually improved and he was discharged with outpatient neurologic and ophthalmologic follow-ups. One week after discharge his symptoms continued to improve and ultimately his ptosis and diplopia completely resolved. |
A male neonate was born via low transverse Cesarean section to a 27-year old gravida 2, para 2 mother at 39 weeks and zero-day gestation. Apgar scores were 8 and 9. Past medical history and family history were noncontributory. The prenatal and perinatal periods were uneventful, and the nursing staff expressed that no instrumentation was used for delivery that may have resulted in a known birth trauma. Deviation of the lower lip to the left side while crying, suggesting right-sided muscle weakness, was noted at the time of delivery (Video , Figure ). This, however, did not interfere with the boy’s ability to latch or breastfeed. Initial physical examination was otherwise in accordance with delivery of a healthy male neonate with no focal neurological deficits. Follow-up examination at 28 hours was unchanged except for a new well-demarcated swelling of the left posterior parietal region (Figure ). Further clarification was sought regarding the use of instrumentation during delivery as the swelling strongly suggested the presence of cephalohematoma. The appearance of a potential left-sided cephalohematoma along with right-sided lower lip weakness and no obvious birth trauma raised concern for other potential congenital malformations, including the remote possibility of an intracranial lesion. Non-contrast magnetic resonance imaging (MRI) of the head confirmed cephalohematoma with no intracranial abnormalities (Figures , ). The patient was later discharged at 53 hours of life after passing both hearing and critical congenital heart disease screenings.\nThe patient was diagnosed with right-sided ACF due to CHDAOM along with an idiopathic cephalohematoma. At the time of discharge, the parents elected to receive care at an affiliated primary care office in the locality. In communicating with the providers at the affiliated health facility, the report was that the baby had remained clinically stable. The facial asymmetry showed progressive but slow improvement, and as previously noted it did not seem to affect the patient’s ability to feed normally. He had regained birth weight by the two-week well child visit. |
A 58-year-old African American male with a history of non-ischemic cardiomyopathy who underwent orthotopic heart transplantation 5 years ago presented with increasing shortness of breath, dizziness, and generalized weakness. Six months prior to this presentation he had been diagnosed with cryptococcal meningitis. His initial treatment consisted of amphotericin B and flucytosine, after which he was maintained on chronic suppressive fluconazole therapy. The opportunistic infection also prompted a reduction in his maintenance immunosuppression. Specifically, his mycophenolate mofetil dose was reduced from 750 mg BID to 500 mg BID, and his cyclosporine dose from 125 mg BID to 75 mg BID. His cyclosporine trough was 90 ng/mL on admission, and 142 ng/mL on discharge ().\nFive months prior to presentation he began to notice bilateral hand numbness and tingling, and, two weeks prior to presentation, he developed imbalance. During his evaluation, the patient was noted to be in atrial flutter with rapid ventricular response, which was initially rate controlled with diltiazem. An echocardiogram performed at that time revealed normal left and right ventricular size and systolic function, with normal diastolic function.\nWhile in the hospital he developed progressive dysphagia, gait instability, and profound weakness of his bilateral lower extremities. Head CT and brain MRI were unremarkable. Lumbar puncture revealed clear, colorless fluid with an elevated protein level of 147 mg/dL, a normal glucose level of 67 mg/dL, and 5 nucleated cells/mL (within normal limits) of which 85% were lymphocytes. The patient also underwent nerve conduction studies and an electromyogram, which showed conduction block and prolonged distal latencies, suggestive of IDP. Consistent with this diagnosis, he also had a positive IgM antibody to Trisulfated Heparan Disaccharide (TS-HDS). As treatment for IDP, he underwent four sessions of plasmapheresis and was initiated on high-dose oral dexamethasone. The patient had significant improvement in his neurologic symptoms and was discharged one week later to a physical rehabilitation facility.\nWithin two weeks, the patient was readmitted to the hospital with anasarca. On admission, an echocardiogram demonstrated reduced RV systolic function with an RV tissue doppler S′ of 0.05 m/s, impaired LV diastolic function, and mild global LV systolic dysfunction with an averaged left ventricular outflow tract time-velocity integral (VTI) of 13.75 cm (LVOT VTI was 19.0 cm two weeks earlier). His cyclosporine trough level was 53 ng/mL on admission (). Diuresis was attempted with IV furosemide, but the patient rapidly developed acute renal failure. He subsequently underwent a right heart catheterization and endomyocardial biopsy to further evaluate his heart failure (). Given his elevated right-sided filling pressures, reduced cardiac output, and poor renal function, he was initiated on continuous infusions of dobutamine and furosemide. Endomyocardial biopsy showed ISHLT grade 1R chronic inflammation with strong capillary endothelial immunostaining for C4d, consistent with pAMR2 [] (). DSA against HLA DR53 was detected with a mean fluorescence intensity (MFI) of 5991.\nThe patient was treated with 3 sessions of plasmapheresis followed by intravenous immunoglobulin (IVIG) at a cumulative dose of 1 gram/kilogram. His outpatient immunosuppressive regimen was also continued. After completing plasmapheresis, the patient had a significant improvement in his anasarca and renal function, and his furosemide and dobutamine drips were successfully weaned. A follow-up echocardiogram obtained prior to discharge showed improved systolic and diastolic function. Prior to discharge, the anti-DR53 MFI was reduced to 2585, a 57% reduction compared to initial DSA. At an outpatient follow-up visit one month after discharge, the patient was doing well, without heart failure symptoms and only mild residual weakness. Approximately one month after his follow-up appointment, the patient died suddenly at home (). An autopsy was not performed. |
A 67-year-old man was admitted to our hospital because of liver dysfunction during a screening examination. Enhanced abdominal computed tomography (CT) revealed a hypervascular mass of 35 mm in diameter in the descending portion of the duodenum (Fig. ), and the left three sections of the liver were occupied by multiple cystic tumors with contrast enhancement of the cystic wall, 13 cm in diameter (Fig. ). A duodenal tumor was identified on gastrointestinal endoscopy (Fig. ), and a biopsy revealed a NET. The serum levels of insulin, gastrin, and glucagon were within normal ranges. CT did not initially reveal evidence of pancreatic invasion between the tumor and the pancreas; however, irregularities of the duodenal wall and swelling of the lymph nodes around the pancreatic parenchyma were observed. Thus, the patient was diagnosed with non-functional duodenal NET with multiple liver metastases, T2N1M1 stage IV (UICC 8th). In addition, CT revealed the anatomical variation of the CHA, which branched from the SMA and ran fully through the head of the pancreatic parenchyma (Fig. , Additional file Figure S1). The CHA branches into the left hepatic artery (LHA), the middle hepatic artery (MHA), and the right hepatic artery (RHA) (Fig. a, b). Furthermore, a developed gastric arterial arcade, 4 mm in diameter, was found between the left gastric artery (LGA) and the right gastric artery (RGA). The RGA was branched from a distal portion at a distance of 10 mm from the root of the LHA (Fig. ). Incidentally, we did not observe stenosis of the celiac axis due to compression by the median arcuate ligament. We planned PD and left trisectionectomy with caudate lobectomy combined resection of the tp-CHA with the preservation of the gastric arterial arcade in order to maintain arterial flow of the remnant liver, preserving the route of the celiac artery to the right posterior hepatic artery (RPHA) via the gastric arterial arcade from the LGA to the RGA, LHA, and RHA. If the hepatic arterial flow could not be maintained by this route, the preservation of the tp-CHA by separating from pancreatic parenchyma or arterial reconstruction using radial artery graft between CHA and RHA was planned. Four weeks after percutaneous transhepatic portal embolization, surgery was carried out.\nAfter laparotomy, the gastric arterial arcade was exposed and encircled, and the LHA, RHA, and proper hepatic artery (PHA) were encircled (Fig. ). The LHA was divided at the distal side of the origin of the RGA. The MHA and the right anterior hepatic artery (RAHA) were also divided. The left portal branch and the right anterior portal branch were divided (Fig. ). The liver was transected, and the left hepatic duct and right anterior hepatic duct were divided. The left trisections and caudate lobe were anatomically resected. After clamping the PHA, the hepatic arterial signals of the RPHA via the gastric arterial arcade were confirmed by intraoperative Doppler ultrasonography (Fig. ). After trisectionectomy and caudate lobectomy, PD was performed. The pancreatic head was dissected from the SMA after the upper jejunum was divided. The pancreas was divided in front of the SMV. Finally, the specimen was only connected by the tp-CHA and the common hepatic duct (CHD) (Fig. ). The hepatic arterial signals of the RPHA was maintained after clamping the PHA. The PHA and the origin of CHA were divided, and the tp-CHA was taken out with the pancreatic head (Fig. ). The CHD was divided, and the specimen was removed (Fig. ). Reconstruction was performed via modified Child’s method. The operative time was 1072 min and the intraoperative blood loss was 3052 ml, and red blood cell transfusion was performed (1680 ml).\nPostoperatively, the patient developed pancreatic fistula (Clavien-Dindo IIIa) and biliary leak (Clavien-Dindo IIIa), and these complications were treated conservatively. There were no signs of hepatic ischemia. The patient was discharged on postoperative day 39. The pathological diagnosis was duodenal neuroendocrine tumor G2 with multiple liver metastases. The Ki-67 labeling index was < 20%, and staining for chromogranin A and synaptophysin were positive. There was no evidence of invasion of the pancreatic parenchyma; however, the duodenal tumor was confined to the MP layer, and one of the 25 examined lymph nodes was positive, and moderate lymphovascular invasion was observed. The final diagnosis was pMP, med, INFa, ly1, v2, pPM0, pDM0, and pEM0. The patient has shown no recurrence in the 22 months since the operation. Enhanced abdominal CT at 4 months after surgery revealed the blood flow of the RPHA via the gastric arcade (Fig. ).\nOver the years, several authors have described variations in the hepatic arterial anatomy; a CHA arising from the SMA—called the hepatomesenteric type—is a rare clinical entity. Yang et al. and Hiatt et al. reported that this condition was observed in only 31 of 1324 patients and 15 of 1000 patients, respectively [, ]. A CHA passing through the pancreatic head parenchyma, tp-CHA, is even rarer; Yang et al. [] reported that among 31 patients with the hepatomesenteric type, only 3 had this condition.\nWhen PD is scheduled in such patients with tp-CHA, it is important to maintain the arterial supply to the liver. Surgeons should preoperatively determine whether to preserve or perform combined resection of the tp-CHA. Tp-CHA preservation was selected in several previous reports [, , ]. This surgical procedure is technically feasible; however, there is a risk of a positive surgical margin or insufficient lymph node dissection and a tendency for increased intraoperative blood loss during the separation of the pancreatic parenchyma. If the tp-CHA is resected, reconstruction is usually necessary in order to maintain the hepatic arterial flow. Previous reports [, , ] have described successful arterial reconstruction after CHA resection during PD; however, such procedures are associated with an increased risk of thromboembolism, which can lead to a fatal outcome, especially in HPD []. In contrast, when collateral circulation develops, surgeons can perform combined resection of the tp-CHA, preserving the collateral circulation without arterial reconstruction. Several reports have recommended preoperative embolization of CHA in order to maintain the hepatic arterial flow through enlarged collateral arteries []. Although preoperative embolization can increase the liver arterial flow through collateral arteries, it is not routinely recommended because of the risk of complications, which includes the migration of embolic material [, ].\nA developed gastric arcade or pancreaticoduodenal arcade is frequently seen in patients with the stenosis of the CHA due to factors such as compression by the median arcuate ligament []. There are only a few cases in which the hepatomesenteric trunk and the tp-CHA and the association between the tp-CHA and the development of a gastric arterial arcade have not been reported. On the other hand, Miyamoto et al. reported the case of a patient with pancreatic head cancer with a CHA arising from the SMA who underwent radical PD combined with the resection of the CHA, in which the hepatic arterial flow was maintained via the gastric arterial arcade []. In this report, the patient did not have a developed gastric arterial arcade; however, the hepatic arterial flow via the gastric arterial arcade was sufficient and hepatic ischemia was not detected after the operation. Considering this case, even if the patients with tp-CHA do not have a developed gastric arterial arcade, surgeons may be able to preserve hepatic arterial flow via the gastric arterial arcade alone. If the hepatic arterial flow via the gastric arterial arcade alone is adequate after clamping the PHA, the combined resection of the tp-CHA can be considered, even if the gastric arcade is not developed before surgery. In cases in which the hepatic arterial flow is not adequate, the preservation of the tp-CHA or arterial reconstruction should be considered.\nWhen performing HPD, a PD-first procedure before hepatectomy is generally performed, as this approach is anatomically rational []. However, in the present case, performing hepatectomy after PD carried a risk of the arterial supply to the liver being reduced during hepatectomy. Had we chosen a PD-first procedure and the hepatic arterial flow not been maintained after CHA resection, it would have been necessary to perform arterial reconstruction before liver transection. This method is associated with a risk of injury to the reconstructed artery and thrombosis during liver transection. Given the above, we opted to perform hepatectomy before PD in our patient with a tp-CHA undergoing HPD.\nIn the procedure for separating the tp-CHA from the pancreatic parenchyma entirely, the surgeon should be concerned about the increasing rate of hemorrhage, surgery time, and the risk of injury to the tp-CHA. The surgical reconstruction of the hepatic artery when performing HPD is also associated with a high degree of risk. The association between tp-CHA and gastric arterial arcade was recognized on preoperative CT scans; the development of this collateral circulation may have the potential to prevent ischemia-related liver complications. From these points of view, the preoperative identification of the developed arcade of the gastric arteries helps in planning an appropriate operative procedure, and this procedure seems to be a viable and simple option. To our knowledge, this is the first report of PD combined with resection of a tp-CHA without preoperative embolization. Furthermore, this is also the first report of HPD for a patient with a tp-CHA. The preoperative identification of the developed arcade of the gastric arteries helps in planning the appropriate operative procedure when PD is scheduled for patients with a tp-CHA. |
A previously healthy 34-year-old Korean female was admitted to a regional hospital for fever, myalgia and severe headache that had started 2 weeks ago. Brain MRI showed a high T2 signal intensity change and diffuse swelling of the right temporal lobe, insula and hippocampus (Fig. ). Lumbar puncture showed lympho-dominant pleocytosis. The patient was started on intravenous (iv) dexamethasone and acyclovir under a high suspicion of viral encephalitis.\nShe was transferred to our institution 4 days later due to persistent headache despite treatment. A noncontrast computed tomography (CT) brain scan taken at our institution showed a hemorrhagic transformation of the right temporal lobe, which was not observed on the initial MRI (Fig. ). Follow-up lumbar puncture showed 510 white cells per mm3 (82% lymphocytes), 144 mg/dL protein and 61 mg/dL glucose. CSF culture studies were negative for bacteria, fungi and tuberculosis. PCR of the CSF confirmed the presence of HSV1. The patient was free of neurological symptoms, with a Glasgow Coma Scale of E4M6V5, and was admitted for close observation and continuation of iv acyclovir. Corticosteroid treatment was discontinued upon her admission. On day 3 of hospitalization, the patient presented with a sudden onset of vomiting and severe headache. Brain CT showed an increased amount of temporal lobe hemorrhage and a leftward shift in the midline (Fig. ). Mannitol was administered but did not seem to have a significant effect. The patient became increasingly drowsy, and her right pupil became dilated. She underwent emergency right decompressive craniectomy, expansile duraplasty and ICP monitor insertion. Postoperative brain CT showed alleviation of midline shifting (Fig. ). The patient recovered fully 5 days after the surgery. Apart from mild intermittent headache and dizziness, she did not show any other significant clinical symptoms, including neuropsychological problems. There were no significant neurologic deficits upon neurological examinations performed by the attending neurosurgeon and neurologist. The patient was discharged after completion of 2 weeks of acyclovir and returned 2 months later for cranioplasty. She was followed up 3 more times after cranioplasty. She was stable, without any neuropsychological problems or neurologic deficits, and was able to successfully return to work as a public official. |
This 11-year-old boy presented with 3 days history of progressively increasing radicular pain over the sacrogluteal region bilaterally; left side more than the right side, along with lower limb weakness and sensory impairment in both lower limbs. He also developed urinary retention and was catheterized elsewhere 1 day prior to his presentation. On examination, his cranial nerves and upper limbs were normal. He had asymmetrical lower limb weakness with the left side worse than the right. His sensory examination also revealed an asymmetrical sensory impairment in the lower limbs with the upper limit being D12 dermatome. Both knee jerk and ankle jerk were absent with plantars not being elicitable. His muscle tone and bulk were normal. He did not have any neurocutaneous markers, palpable lymph nodes or spinal deformity. With this presentation and neurological examination, a diagnosis of spinal cord pathology with clinical localization to cauda equina was made. An emergency magnetic resonance imaging (MRI) of the lumbosacral spine with screening was performed, which showed a well-defined sausage shaped intradural lesion at L2, L3 level, without evidence of any other central nervous system (CNS) lymphomas. The lesion was iso-intense in T1- and T2-weighted images []. He underwent emergency L2, L3 laminectomy and excision of intradural extramedullary lesion. The lesion was removed piecemeal. Intra-operatively the lesion had some attachment to the anterior dura. Total removal was carried out, with coagulation of the anterior dura.\nPost-operatively he had total relief of pain and his motor power improved by one Medical Research Council grade and sensations were slowly improving. Histoplathological examination of the tumor revealed a dense infiltration of round cells admixed with cells with a large eosinophilic cytoplasm and vesicular nucleus with prominent nucleolus, which was consistent with non-Hodgkin's lymphoma []. The diagnosis was confirmed by immunohistochemistry showing CD20 positivity. Detailed investigation was carried out to stage the disease, which included complete hematological examination, including bone marrow aspiration and computerized tomography of the chest and abdomen. All the above investigations were normal.\nOn follow-up after 1 month he had received radiotherapy to the local area of 32 Gy in 20 fractions and was on chemotherapy; cyclophosphamide, hydroxydaunomycin, oncovin-vincristine, and prednisone regimen. Post-operative MRI showed total excision of the lesion []. At 1 year follow-up, he was having near normal power, normal sensations, and normal bladder control. |
An 8 days old male neonate was born to an Asian mother through vaginal delivery at 37 weeks of gestation, weighed 2,380 g, and had APGAR scores of 9 and 10 at 1 and 5 min, respectively. He was admitted to our hospital with a 2 days history of fever of up to 39°C but did not have respiratory or gastrointestinal symptoms. The infant's family denied any medical history and TB contact. His physical examination at admission documented smooth respiration, clear breathing sound, and no hepatosplenomegaly. The complete blood count indicated a total white blood cell count of 17,500/μL with 69% neutrophils, 20% lymphocytes, 9% monocytes, and 2% eosinophils. The C-reactive protein level was 7.3 mg/dL. The findings of the cerebrospinal fluid (CSF) analysis were normal. Bacterial cultures of the blood, urine, and CSF were negative. Intravenous antibiotics, namely cefotaxime and ampicillin, were administered after admission on the basis of suspicion of neonatal fever. Despite the administration of the antimicrobial combination therapy, the fever persisted and the neonate developed abdominal distension when he was 12 days old. Abdominal radiography exhibited nonspecific dilated bowel loops. Because no improvement in the condition of the patient was observed after changing antibiotics, infection caused by some virus and other atypical pathogen, including Mycobacterium tuberculosis, was considered. Tests for herpes simplex virus, Epstein–Barr virus, cytomegalovirus, hepatitis B virus, rubella, Chlamydia trachomatis, and Toxoplasma gondii were all negative. The repeat C-reactive protein level was elevated to 14.4 mg/dL. Coagulopathy with 323.7 μg/mL of abnormal fibrin degradation product and more than 20 mg/L of D-dimer were also noted. Antibiotics were switched to vancomycin and ceftazidime empirically. Chest radiography displayed only increased right lung field infiltration when the infant was 12 days old (), and chest computed tomography (CT) imaging exhibited a large amount of right pleural effusion with mild inflammatory changes in the right lower lobe when the infant was 15 days old (). Pleural effusion drainage was suggested but refused by his parents at that time. Gastric lavages for acid-fast staining and culture were examined when the infant was 20 days old after his parents agreed to further testing, and one of the three acid-fast stains of gastric lavages yielded few acid-fast bacilli. Repeat chest and abdomen CT imaging performed when the infant was 24 days old indicated patchy consolidation in the right upper lung, multiple new nodules in both the lungs, moderate pleural effusion, and multiple low-density nodules in the spleen and hepatic hilar region without hepatomegaly (). Subsequently, pigtail catheter insertion for pleural effusion drainage was performed. The findings of pleural fluid analysis indicated a total white blood cell count of 10,800/μL with 6% neutrophils, 57% lymphocytes, and 37% mesothelial cells; a total protein level of 4.6 g/dL, a lactic dehydrogenase level of 250 IU/L, and a glucose level of 164 mg/dL. TB infection was strongly suspected. The neonate was administered isoniazid (15 mg/kg/day), rifampicin (15 mg/kg/day), and pyrazinamide (20 mg/kg/day) when he was 24 days old. After initiating anti-TB treatment, the neonate's symptoms and signs subsided gradually. Finally, both gastric lavage and pleural effusion cultures showed M. tuberculosis complex.\nThe neonate's mother was 33 years old, gravida 1, para 1. Her Group B streptococcus test was negative. She had been healthy with no previous medical history and TB contact history; however, she developed a mild dry cough 1 week after delivery, experienced persistent general weakness, and was admitted to our medical intensive care unit because of altered mental status 24 days postpartum. Laboratory examinations indicated leukocytosis, thrombocytopenia, coagulopathy, acute hepatic failure, and acute renal failure. The HIV serology test was negative. A chest X-ray exhibited a miliary TB pattern (). A chest CT image displayed diffuse interlobular and intralobular septal thickening with ground-glass opacities (). Because her neonate was highly suspected to have TB infection at that time, acid-fast staining and TB polymerase chain reaction (PCR) of the sputum were performed. Both tests were strongly positive. The mother was administered anti-TB therapy immediately, but she died 3 days after hospitalization. M. tuberculosis infection was confirmed through sputum culture. |
An 85-year-old woman presented with a bulky tumor in the collecting system of a congenital solitary left kidney. Her past medical history includes significant chronic obstructive pulmonary disease with a 2 pack-day smoking history more than 50 years. She has a history of recurrent low-grade non-muscle invasive bladder cancer (NMIBC) for the last 7 years for which she received intravesical BCG treatments. Her last recurrence in the bladder was 3 months prior showing non-invasive low-grade urothelial carcinoma.\nLaboratory tests revealed normal renal function including serum creatinine of 0.69 mg/dl. A computerized tomography (CT) scan with a urographic phase demonstrated lobulated urothelial thickening of the left renal pelvis without hydronephrosis (Fig. ). CT imaging of the chest did not identify metastatic disease.\nThe patient underwent flexible ureteroscopy and nephroscopy with ureteral washing and biopsy. A sessile tumor greater than 2 cm was visualized in the renal pelvis towards the upper pole infundibulum. Two adequate specimens were obtained in order to determine the disease grade and were consistent with low grade urothelial carcinoma.\nAfter a detailed discussion with the patient about the risks, benefits, and possible complications of KSS, the patient elected to undergo percutaneous treatment with laser ablation of the UTUC in her solitary kidney. Prior to the procedure, a lower pole percutaneous nephrostomy tube was successfully placed under sedation by Interventional Radiology.\nThe patient was positioned in prone split leg position. We cystoscopically confirmed that there was no tumor recurrence in the bladder. A guidewire was passed through the nephrostomy tube, ureteroscopically grasped with a nitinol basket and was taken out to achieve through-and-through access. After placing a 12.7 French ureteral access sheath under fluoroscopy, we visualized the renal pelvis again using the ureteroscope and dilated the percutaneous tract with a balloon dilatator under direct vision and placed a 28 French Amplatz sheath, which allowed the introduction of a 24 French continuous-flow cystoscope (Richard Wolf, CITY) with normal saline for irrigation. Importantly, the ureteral access sheath was left to optimize drainage, provide low pressure in the renal pelvis, and limit any tumor seeding in the bladder.\nAfter systematic exploration of the collecting system, the boundaries of the large sessile tumor were visualized, and the renal pelvis mass was vaporized with the 532 nm laser in a systematic manner with continuous irrigation of normal saline through the cystoscope. GreenLight XPS LBO 180W laser console (Boston Scientific, Malborough, MA) was used with an extended application (EA) 600 micron side-fire fiber (Boston Scientific, Malborough, MA). The mass was vaporized using a setting of 40 watts; to coagulate any bleeders, the power was set at 20 watts. Care was taken to stay in near-contact with the mass during vaporization, using visible bubbles as feedback of efficient vaporization and hemostasis of the tumor bed without charring tissue. The hemostasis was achieved effectively in a very short duration at low power. Total energy used during the procedure was 39,515 J. After satisfactory tumor ablation, an 8-French nephroureteral catheter was inserted under fluoroscopic and cystoscopic guidance to maintain adequate urinary drainage.\nThe patient was discharged home on postoperative day 2 with the nephroureterostomy catheter open to drainage. The catheter was subsequently clamped and removed two weeks later without complications. Follow up included cystoscopy and CT urogram at 3 months. CT urogram demonstrated focal thickening in the upper pole urothelium without obvious recurrence. Ureteroscopy was performed at 6 months which demonstrated minimal residual or recurrent disease (5 mm in upper pole calyx) that was successfully ablated (thulium laser). Excellent treatment response was observed throughout the remaining collecting system. At the same time two small papillary low-grade bladder tumors were resected, followed by intravesical gemcitabine. The patient is now at 8 months of follow up and remains well, with plans for ongoing cross sectional imaging, cystoscopic and ureteroscopic follow up. Throughout the treatment, we did not observe any deleterious consequences to renal function. In the accompanying video (Additional file ), we present our technique for KTP Green-light laser vaporization of UTUC via a percutaneous approach. |
The patient is a 76-year-old male with a history of chronic hepatitis B with well-compensated cirrhosis. Nine years prior to admission, he underwent nonanatomic left lateral liver resection for a 2 cm well-differentiated hepatocellular carcinoma using a “sandwich technique.” This involved anchoring two Teflon felt pledgets to the resection margin anteriorly and posteriorly with running Ethibond (Ethicon Inc., Cincinnati, OH) polyester sutures. This method was chosen to expedite the procedure and minimize bleeding in an elderly, cirrhotic patient. He recovered uneventfully although a year later he required percutaneous radiofrequency ablation in the left medial segment for a 1.1 cm nonlocal recurrence of hepatocellular carcinoma.\nNine years after resection, he complained of early satiety and a 10-pound weight loss. An esophagogastroduodenoscopy (EGD) revealed the Teflon felt within the lumen of the duodenal bulb with cleanly ulcerated mucosa. This had not been evident on EGD or CT scan () four and two years prior, respectively. The mesh could not be removed endoscopically as it was quite adherent and there were concerns that the base was still sutured to a cirrhotic liver. However, the endoscope was able to move distally past the mesh indicating the absence of complete obstruction by the mesh.\nFour hours after the EGD, the patient presented to the emergency department with severe abdominal pain and nausea. CT scan showed that the mesh was partially attached to the left medial segment of liver and passed transmurally into the lumen of the adjacent stomach and duodenum (). Much of the mesh appeared to line the anterior wall of the distal stomach and first portion of the duodenum. There was no evidence of perforation or abscess; however, there was also a distal small bowel obstruction unrelated to this mesh. Comparison with serial imaging for his hepatocellular cancer showed that the migration of this mesh likely occurred within the previous year. Shortly after admission, he developed transient bacteremia and hemodynamic instability requiring intensive care unit monitoring and resuscitation. Because of his cardiac arrhythmias, cirrhosis with borderline thrombocytopenia, and poor nutritional state, he was managed conservatively with nasogastric tube decompression, total parental nutrition, and broad-spectrum antibiotics.\nHis small bowel obstruction was not strangulated and resolved several days later. After 21 days, his nutritional parameters returned to normal and he had no evidence of sepsis or active infection. He then underwent an exploratory laparotomy and the lesser curvature and antrum of the stomach were densely adherent to the residual left medial segment of liver. There was concern of either causing bleeding at the cirrhotic liver edge and/or disrupting a significant portion of the anterior stomach, which might require an extensive gastrectomy. It was decided to approach this with a 4 cm gastrotomy on the posterior aspect of the stomach through which the mesh was visualized. The majority of the mesh was easily delivered from the first portion of the duodenum through the gastrotomy. A small point of fixation on the lesser curve towards the left lobe of the liver of the mesh was sharply divided and the base suture ligated. Two segments of mesh (12.5 × 0.8 cm) with attached sutures were then removed entirely and the posterior gastrotomy closed. A thick adhesive band in the small bowel of the right lower quadrant was identified as the likely site of the previous bowel obstruction though no dilated loops were seen. The patient tolerated the procedure without complication and was started on a diet on the fifth postoperative day. After receiving a cardiac pacemaker for his arrhythmias, he was discharged on postop day 10. |
A 32-year-old lady presented to the emergency department (ED) with symptoms of dyspnea, chest pain, cough, and subjective fevers since three days. The patient was reportedly in good health before she received a dose of intramuscular naltrexone for the treatment of alcohol and opiate dependence on the day of symptom onset. The patient had been smoking cigarettes consistently for the past six years. On arrival, she was noted to be hypoxic, and oxygen supplementation was initiated through a nasal cannula. Examination was pertinent for tachypnea and bilateral crackles. The patient was afebrile. While in the ED, she was placed on a non-rebreather mask because of worsening hypoxia. Chest X-ray showed diffuse bilateral pulmonary infiltrates (Figure ). A CT angiogram of the chest was ordered, which was negative for pulmonary embolism but showed diffuse bilateral pulmonary infiltrates as well (Figures , ). Initial laboratory data were pertinent for elevated WBC count with mild peripheral eosinophilia (700 cells/microliter). Levofloxacin was administered intravenously for the treatment of suspected community-acquired pneumonia.\nThe patient was admitted to the medicine service and was started on intravenous methylprednisolone for the management of suspected AEP secondary to injectable naltrexone given the temporal relationship between administration of the medication and onset of symptoms. Bronchodilator therapy was initiated for wheezing. Antibiotics were discontinued upon admission. The patient’s oxygen requirements improved. Pulmonology consultation was requested, and the patient underwent bronchoscopy. BAL studies showed predominance of lymphocytes (62%) followed by neutrophils (32%) with no eosinophils, which was not suggestive of AEP. However, histology of the lung biopsy sample showed the presence of eosinophils in the lung parenchyma consistent with drug-induced eosinophilic pneumonitis (Figure ). HIV viral load testing and hepatitis C serology were negative, BAL bacterial cultures (including tuberculosis) remained sterile, and the BAL fungal culture grew rare yeast, which were considered to be contaminants. BAL fluid testing for Pneumocystis jirovecii was negative as well. The patient’s hypoxia resolved with steroid therapy. The patient was discharged with a course of oral prednisone, albuterol inhaler, and outpatient pulmonology follow-up. |
A 41-year-old, nonsmoker, married man works in a college with no past relevant family or medical history. He had blurry vision and headache, and after 2 hours he developed generalized tonic-clonic seizure. He was brought to the local emergency department where benzodiazepine and 2 antiepileptic drugs loading doses failed to stop his seizures. Midazolam boluses as a continuous infusion over 5 days were then administered. Although the medications’ doses were increased, his seizure was drug resistant. He was then intubated, and propofol, midazolam, fentanyl in addition to the maintenance medication valproic acid, phenobarbitone, levetiracetam, and phenytoin were administered.\nHe was given empirical antibiotics although the workup findings of CT scan and brain MRI performed at the local hospital he first presented in were normal, including the lumbar puncture which only showed slightly elevated white blood cells with normal protein and glucose levels.\nAfter 2 weeks, he was transferred to a tertiary center Emergency Department due to his deteriorated status. He was comatose and was having intermittent twitching of the face and upper extremity. He was transferred immediately to the intensive care unit and epilepsy service. Head CT, MRI and neck magnetic resonance angiography and venography (MRA/MRV), in addition to cerebral angiography showed no abnormality detected except for a parasagittal hematoma (, ) which improved after 2 weeks although the patients status remained the same. Although he was already on midazolam, propofol, and fentanyl, he had a prolonged seizure that lasted more than 10 minutes. He continued having in between seizures activities while he was being kept intubated and ventilated on tracheostomy with ketamine and thiopental. Continuous EEG showed initially generalized spikes and waves every 1-2 seconds () for >48 hours, and NORSE was diagnosed. Then, anesthesia induced burst suppression pattern was observed ().\nWork-up excluded Anti-NMDA receptor encephalitis and revealed elevated Antiphospholipid antibody (APA) including antiB2 Glycoprotein I. Lumbar puncture yielded clear cerebrospinal fluid, 6 white blood cells, with normal glucose and protein content. Bacterial, fungal cultures, cryptococcal antigen, cytology and whole-body pet scan in addition to para-neoplastic work-up all showed negative findings including voltage-gated potassium channel (VGKC), AMPA, GAD 65, LGI1. The APA levels remained elevated on 2 occasions.\nAnti-β2 glycoprotein-I antibodies result was (50–100 U/mL) (IgG&IgA) and our normal laboratory value is <20U/mL. Antiphospholipid syndrome was diagnosed and heparin started. He continued to have episodic right arm and leg jerks with right facial twitching.\nMultiple intravenous doses of benzodiazepine and a loading dose of phenytoin, valproic acid, levetiracetam, midazolam, thiopental, phenobarbitone, fentanyl, and ketamine infusion were administered. Moreover, a trial of 5 days induced hypothermia ended up with insufficient seizure suppression.\nHe was then put on a treatment plan which included pulse intravenous steroid, immunoglobulin, plasma exchange and rituximab which showed no immediate response. The doses were as follow :- IVIg 0.4g/kg for 5 days, steroid 1g for 5 days, and Rituximab 1g/once, 2 doses given within a 2 week interval. Over the following 8 months, levetiracetam 2g intravenously twice daily, lamotrigine 200mg nasogastric twice daily, and phenobarbital 110mg twice daily were administered and suppressed the seizures completely.\nA third head CT and MRI () after 8 months showed complete resolution of the hematoma. All anesthetic agents were then tapered off gradually while his seizures remained controlled, and he was eventually extubated. After approximately 8 months of ICU admission, he was discharged to the regular floor.\nDuring the neuropsychologist’s evaluation, the patient was neat and mostly cooperative, although slightly aggressive. The patient showed neurocognitive decline, affected temporal orientation to day, date and year, slowed motor activity, labile mood, constricted affect, distracted attention and memory, and orientation impairment. Although his speech was impoverished, he had some insight of his illness, lack of words and difficulty in articulation. Although visual hallucinations were present, he did not have any suicidal or delusional thoughts. He was then being monitored in the same tertiary center for few months and then discharged with phenobarbital, tegretol, lamictal, and levetiracetam to a rehabilitation center with residual moderate to severe cognitive decline without any focal neurological deficits.\nAfter 7 months of following up and being evaluated by the rheumatology and epilepsy service, he remained seizure free, and neurological examination showed nystagmus bilaterally and intact cranial nerves. However, psychiatric assessment’s remarkable findings were euphoric mood, cognitive impairment, poor planning, and macropsia with positive illusion picture.\nDuring his routine outpatient follow up, a mental status assessment was conducted and it was reported that his appearance was disheveled, his speech was tangential, and his eye contact was intense with slowed motor activity and labile affect. He was easily distracted and had an irritable mood. In addition, his behavior was agitated with grandiose and paranoid delusions along with visual and auditory hallucinations. Furthermore, he was aggressive, homicidal, and had self-harm thoughts with short-term memory and orientation to place, object, and person. Schizophrenia psychosis was then diagnosed in the outpatient clinic after 9 visits over the course of a year. He started treatment with regular psychiatric follow-up at the local hospital in his town. |
A 74-year-old woman, admitted for planned total knee arthroplasty, was seen in consultation by the general surgery service because of a massive preperitoneal hematoma. The patient had a past medical history of Graves' disease treated surgically at the age of 20, mitral valvuloplasty for mitral regurgitation 17 years previously, and pacemaker implantation for sick sinus syndrome 16 years previously. The patient was treated with warfarin after valvuloplasty because of a previous left atrial thrombus.\nFive days prior to consultation, she was admitted to the orthopedic surgery service for a planned total knee arthroplasty. Since she was currently receiving warfarin, the warfarin was stopped and heparin given as bridging anticoagulation therapy. Anticoagulation was well controlled in the outpatient setting, with a prothrombin time international normalized ratio (PT-INR) of 2.00 before admission. Three days prior to consultation, she began receiving subcutaneous teriparatide using a 32-gauge, 4 mm needle. After the first injection of teriparatide in the right lower abdomen, she noticed right sided back pain. On that day, the PT-INR was 2.00; however, the activated partial thromboplastin time (aPTT) was prolonged at >100 seconds. On the day of consultation, she became hypotensive which responded to an intravenous bolus of normal saline. She denied any history of abdominal trauma prior to admission. On physical examination, her right lower quadrant was distended and tender, with an injection scar in the central area (). The aPTT was continuously prolonged at >100 seconds. Abdominal computed tomography (CT) scan with intravenous contrast was obtained, which revealed a massive preperitoneal hematoma and hemoperitoneum (Figures and ). No apparent extravasation was detected; however, bleeding from the hypogastric vessels was suspected based on the location of the hematoma. Based on these findings, the general surgery service was consulted. A massive preperitoneal hematoma with hemoperitoneum due to subcutaneous teriparatide injection was suspected. Since the patient was hypotensive, urgent surgery was undertaken, and McBurney's incision was made. When the preperitoneal space was opened, uncoagulated blood spontaneously flowed out. Blood in the peritoneal cavity had not coagulated and was easily aspirated. There was no apparent bleeding site in the abdominal cavity. We ligated the right hypogastric vessels and closed the wound. Her postoperative course was uneventful and she underwent total knee arthroplasty 10 days later. |
A 24-year-old woman underwent a successful laparoscopic gastric bypass on June 2008 for super morbid obesity (body weight 166 kg, body mass index 61.7). She did not subsequently take vitamin supplements. She developed frequent episodes of vomiting and abdominal pain. The differential diagnoses of symptoms include nutritional deficit and internal hernia. In the following 4 months, she lost 32 kg, her weight falling from 166 to 134 kg. Approximately 5 months after the surgery, she noticed muscle weakness in her lower limbs and experienced difficulty in walking and standing. The symptoms worsened progressively and she developed generalized weakness and ultimately became bed-ridden. Five weeks later, she was transferred to the rehabilitation unit of our hospital. She could not move her ankles and feet, and the strength of her hips was only grade 2 according to the five-point scale of Medical Research Council of the Great Britain. The strength of the upper limbs was grade 3 in proximal arms and grade 1 in distal hands. Foot drop and wrist drop developed and there was marked distal limb muscle atrophy [Figures and ]. The laboratory findings were within normal ranges, including complete blood cell counts, creatinine kinase, liver function, renal function, vitamin B12, thyroid stimulating hormone (TSH), and serum electrolyte levels. Magnetic resonance imaging (MRI) of the cervical spine without contrast enhancement was normal []. Electromyography was done to confirm the clinical suspicion of neuropathy; it showed the presence of sensorimotor axonal polyneuropathy. According to the clinical presentation, thiamine deficiency was suspected – also called neuropathic beriberi. Two months after she had become bed-ridden, intravenous replacement therapy with vitamin B complex was started: 1 ml of B-complex was given once daily (containing 100 mg of thiamine, 5 mg of riboflavin, 5 mg of pyridoxine, 50 mg of nicotinamide, and 5 mg of sodium pantothenate). She experienced mild improvement during her hospitalization. |
Case 1: Ms. K, a 70-year-old woman who immigrated to the US at the age of 53, began complaining of watery eyes, chest pain, lower back and joint pain, leg cramps, and weakness. She harbored delusions of being afflicted with high blood pressure, uterine cancer, blood cancer with bone metastasis, brain cancer with extensive metastasis, and believed that her brain was "shrinking."\nShe first visited a cardiologist in 2013, complaining of intermittent episodes of chest pain over six months. An electrocardiogram (EKG) at the time showed bradycardia, a first-degree atrioventricular (AV) block and a left bundle branch block. At her sixth visit with the cardiologist, she mentioned non-specific somatic complaints, which she said were because of a "hematological problem." Five months later, she was evaluated for “renal hypertension” and imaging studies showed a renal cyst. While she did not follow up with the nephrologist, she continued to make hospital visits for persistent chest pain. A full medical workup was completed and found to be normal at every ER visit. Medical records from a prior ER visit revealed that she had made claims that the Russian military entered her residence and stole her urine, resulting in the disappearance of her kidneys.\nMs. K was brought to the ER by the police after she showed up with a can of gasoline and matches at her primary doctor's office and threatened to burn it down. She was irate and claimed that all of her doctors, in the US and in her home country, were concealing the fact that she had oncological issues. She vehemently denied any psychiatric illness, stating that these diagnoses appeared on her records as a result of a rumor started by an envious former colleague. She explained that because she had been a former practicing neurologist in her home country, she was confident that she had cancer. Upon repeated questioning, she admitted that in a final bid to receive the medical attention that she was rightfully due, she had devised the plan to burn down the doctor’s office.\nWhile in the psychiatric inpatient unit, she remained somatically preoccupied and reported abdominal pain, lower back pain, and weakness, which she attributed to the metastatic spread of uterine cancer to her spine. Radiological imaging confirmed no evidence of uterine cancer, though a thickened endometrium was reported with recommendations for further testing by tissue sampling. Because Ms. K’s ability to make rational and reasonable decisions about her psychiatric and medical treatment was compromised by her delusions, the team sought and was granted a court order allowing them to treat her over her objection. |
A 76-year-old female patient presented at the emergency department with dyspnea, a productive cough, and a fever for several days. She had experienced exacerbations of congestive heart failure for the previous 20 years and had a permanent cardiac pacemaker that had also been initially inserted about 20 years earlier due to sick sinus syndrome with atrial fibrillation. She also had dementia, and a history of multiple incidents of cerebral infarction and its complications.\nAt the emergency department, her blood pressure was 112/72 mmHg, pulse rate was 101/min with an irregular rhythm, and body temperature was 36.5℃. On examination, she appeared tachypneic (respiratory rate, 28/min) and her breathing sounds were reduced over the left lung field. The arterial oxygen saturation in room air was 92%. The other laboratory findings were not notable. Chest radiography revealed opacification of the whole left lung field, thought by a physician of the emergency department to be unilateral pleural effusion (). Therefore, after local anesthesia and under sterile conditions, a 16F catheter (Prime-S; Sungwon Medical, Cheongju, Korea) was inserted into the 6th left intercostal space in the anterior axillary line without image guidance.\nShortly after insertion, blood was draining in a pulsatile way from the catheter. However, she was hemodynamically stable with a blood pressure of 132/78 mmHg and a heart rate of 98/min. After clamping the catheter, contrast-enhanced computed tomography (CT) of the chest was performed () and showed that severe cardiomegaly with displacement of the heart to the left with atelectasis (originally thought to be massive pleural effusion). The catheter had been inserted anterolaterally into the sixth intercostal space on the left and was within the left ventricle, exiting the ventricle through the aortic valve with the tip of the catheter located in the ascending aorta. Transthoracic echocardiography revealed mild aortic regurgitation with a small amount of pericardial effusion without hemodynamic significance.\nOpen mini-thoracotomy with chest tube insertion was performed under general anesthesia the next day. The previous catheter was carefully pulled out without myocardial repair. Although the removal of the catheter was successful and well tolerated by the patient, the hospital course was complicated by pneumonia and long-term mechanical ventilation. About a month after the complication, the patient died from pneumonia with septic shock. |
A 28-year-old woman initially presented with blurry vision that developed over the span of approximately one month. The blurry vision was initially most prevalent on horizontal gaze but progressed to include vertical gaze. It resolved with closure of one eye. She reported a history of gradually worsening headache over the past several years. Her headaches both worsened in intensity and increased in frequency, until it was quite debilitating and occurred daily. She described the headache as an intense pressure in both the front and back of her head. She also noted a “whooshing” sound in her right ear. She denied any nausea or vomiting and had not had any syncope, numbness, weakness, facial droop or slurred speech. Furthermore, she had no history of bladder or bowel dysfunction.\nHer medical history was pertinent only for obesity with a body mass index (BMI) of 39. On physical exam she was noted to have papilledema. Her neurological exam was unrevealing with the exception of a subtle sixth cranial palsy.\nA magnetic resonance image (MRI) was obtained which showed a T1 hypointense and T2 hyperintense cystic lesion arising from the pineal gland measuring 2.0 x 1.1 cm in the sagittal plane with mild mass effect on the tectum and partial effacement of the cerebral aqueduct (Figures , ). The lesion demonstrated a thin rind of contrast enhancement and had thin enhancing internal septations. The lateral ventricles were mildly enlarged. There was no restricted diffusion and no loss of gray white differentiation. Cine flow study noted cerebral spinal fluid (CSF) flow through the cerebral aqueduct. Based on the radiographic images, the most likely diagnosis was an atypical pineal cyst.\nGiven the rapidity of the vision changes, the decision was made to pursue surgical intervention. An endoscopic third ventriculostomy (ETV) with pineal cyst fenestration was performed without complication. A computed tomography (CT) scan obtained post-operatively noted questionable decompression of the lateral ventricles but the patient reported no improvement in symptoms (Figure ). Ophthalmologic evaluation noted worsened papilledema. At this time the patient underwent a lumbar puncture, which noted an opening pressure of 32 cm H2O. Subsequent catheter venography noted severe stenosis of the right transverse sinus associated with a 9 mm Hg trans-stenosis gradient (Figure ). Placement of a venous sinus stent obliterated the pressure gradient (Figure ).\nAt six-month follow-up, her blurred vision, headaches and papilledema had all resolved. She reported complete resolution of her symptoms and plans were made for continued annual follow-up to monitor symptoms and ensure patency of the stent. |
The patient was a 48-year-old male and had a body weight of 95 kg. He was admitted to the hospital on August 31, 2019 for memory impairment and nonspecific dizziness that persisted for 4 months.\nThe preoperative laboratory results were normal, and the chest computed tomography (CT) scan showed no evidence of a pathology. Upon examination, the patient was found to be a little drowsy but was able to obey commands. His vital signs at the time of admission were as follows: blood pressure of 104/66 mmHg, pulse rate of 97 beats per minute, respiratory rate of 24 breaths per minute, and temperature of 36.7°C. His Glasgow coma scale score was 15/15. His vital signs were all within normal ranges. The rest of the neurological and respiratory examination findings were found to be unremarkable. A CT scan of the head showed an intraventricular mass attached to the anterior third of the septum pellucidum and Monro's foramen and enlargement of the left lateral ventricles (Figure ). A magnetic resonance image confirmed an intraventricular cystic tumor 1.9 cm in diameter without enhancement with gadolinium (Figure ). Furthermore, active left lateral ventricle hydrocephalus was present. A colloid cyst was considered the primary diagnosis.\nWith the patient in the supine position and the head turned 10 to 15 degrees to the opposite side, a curvilinear skin incision that was 12 cm long was made around Kocher's point, which was located 1 cm in front of the palpated coronal suture and 3 cm from the midline (along the midpupillary line). A craniotomy that was 5 cm long and 4 cm wide was performed to expose the main part of the middle frontal gyrus. After the cortical surface was coagulated, a soft catheter (Medtronic, Minneapolis, Minnesota, USA, #27703 or 26026) was used for the initial accurate ventricular entry. The catheter was aimed at the ipsilateral external auditory meatus in the coronal plane and the contralateral medial canthus in the sagittal plane. The cerebrospinal fluid (CSF) flow was visualized after the catheter was advanced 4 cm. After the operative corridor was created along this catheter, the left lateral ventricle was opened, and the tumor was revealed. The color of the tumor was milky white, and it appeared to be similar to a peeled lychee. Only a tiny vessel of the tumor adhered to the roof of the third ventricle. The tumor did not adhere to the fornix. The vessel was coagulated while care was taken to prevent heat damage or direct trauma to the fornix. The entire tumor wall was removed in a gross fashion. The same catheter was then left in the left ventricle. The surgery lasted two hours, and anesthesia was induced for three hours. The patient exhibited stable vital signs during the surgery.\nAfter the operation, the patient was conscious and was admitted to the intensive care unit (ICU) at 1:00 p.m., where the patient did not suffer convulsions. Starting at 2 pm, the urine volume of the patient exceeded 250 ml per hour for 10 hours. At the 5th hour after the operation, the urine volume was as high as 700 ml. During the 10 hours, after the administration of 12 units of posterior pituitary injection (Anhui Hongye Pharmaceutical Co., Ltd), the patient's urine volume returned to normal. Since then, the patient's urine volume did not exceed 200 ml per hour.\nAt 8:00 p.m., a high fever occurred, and the patient’s body temperature reached 38.8°C. At 10:00 p.m., his body temperature reached 39.6°C. Physical cooling and antipyretic drugs were administered, showing favorable results. Six hours later, his temperature was normal, 37°C.\nAt the 19th hour after the operation, the head CT scan showed no intracranial hemorrhage, but the length of the catheter in the brain was close to 7 cm, and the tip of the catheter was located at the right cerebral peduncle (Figure ).\nAt the 20th hour after the operation, the catheter was removed. On day 1 after surgery, the morning (8:00) ACTH level was 1.2 pg/ml (normal, 7.2-63.4 pg/ml), and the cortisol concentration was 0.09 µg/dL (normal, 4.26-24.85 µg/dL). Following stabilization, the patient was transferred to the general neurological ward. He was discharged home with no neurological deficits on day 11. The final histologic diagnosis was subependymoma of WHO grade I.\nTwo months later, his ACTH level was normal, and he never needed to take prednisone again (Figure ). He has been working as a taxi driver again for three months and has not experienced headache, fatigue or dizziness. |
A 63 years old man, operated 10 years ago for an inguinal hernia, underwent a chest CT scan in the context of a chronic cough. There were no parenchymal abnormalities except a moderate left pleural effusion (liquid density 10 Hounsfield unity). We incidentally found a round 25 mm diameter mediastinal mass adjacent to the descending aorta. Its upper pole was at the carina. (, ). It displaced the esophagus to the right (). The lesion was enhanced with contrast agent to the same degree as the aorta, which revealed that this lesion was vascular the findings were mimicking a saccular aneurysm of the descending thoracic aorta. However, this lesion seemed to be separate from the descending aorta, without any communication. Instead, small tubular structure emanating from the descending aorta was identified in the space between the descending aorta and feeding the mass (). This was interpreted as being the left bronchial artery. On the basis of these findings, a definitive diagnosis of mediastinal bronchial artery aneurysm was made.\nThis aneurysmal sac was partially thrombosed. It was 15 mm distant from the ostium of the left bronchial artery and extended to the hilar branches (). There was no sign of rupture or fissuration. The patient was asymptomatic with no history of pulmonary infection or trauma or CT evidence of atherosclerosis. There was also no history of vasculitis or radiotherapy. After a multidisciplinary consultation including interventional radiologist, thoracic surgeon and pulmonologist, a collegial decision to treat this aneurysm with a transtarterial embolization was taken. After a selective catheterization using a 1,4 French microcatheter (), we embolized using Onyx* the aneurysmal sac and also the hilar branches and the left bronchial artery proximal to the aorta to ensure the occlusion of the inflow and the outflow and prevent the recurrence Immediate control was satisfying showing a total exclusion of the aneurysm (). |
An eight-year-old female patient who suffered from tooth trauma half a year ago was treated in the local general hospital. Recently, she came to Department of Pediatric, School of Stomatology, the Fourth Military Medical University for treatment, with the chief complaint of recurrent swelling of the gum in the anterior teeth region and occlusal pain. Intraoral clinical and X-ray examination showed that the neck of the crown oftooth 21 was broken at the 1/3 position, white filling was seen on the fracture surface, probing (–), knocking (+), and no obvious loosening of the tooth was found (). Periapical radiograph showed that the apical foramen with tooth 21 was open with periapical shadow and the pulp chamber was wide.\nAccording to the treatment plan, the tooth was sterilized, triple antibiotic paste (main components were metronidazole, ciprofloxacin and minocycline) was sealed, and the status of the periapical region was observed. After the inflammation was eliminated, apexification was performed. After root development was completed at the age of ten, the root canal was treated and the defect of the tooth was repaired. The tooth will be permanently repaired when the child grows up into an adult.\nAt a follow-up visit, we found that the periapical shadow in the tooth gradually became smaller. Apexification was performed using Vitapex (). Six months later, X-ray radiography showed that there was radiolucency in the root canal, the length of root increased and the apical barrier formed. Under the rubber dam isolation, the length of the root canal was measured and the root canal was prepared. The root canal was initially prepared with #10 and #15 K filings, then prepared with nickel-titanium instruments, and washed with 5.25% sodium hypochlorite and normal saline alternately. The root canal was filled with cold gutta-percha (). During the filling of the root canal, multiple radiographs from various angles showed that radiolucency still existed in the root canal ().\nCone-beam computed tomography (CBCT) showed that the roots were bifurcated in the middle third of the root in the mesiodistal direction, and there were two apical foramina in the apices. The root canals were explored and dredged under the microscope. We found that in the middle third of the root in the mesiodistal direction, a thin layer of canal wall divided the root canal into two independent canals. The root canals were measured again for their lengths, prepared with nickel-titanium instruments, and sealed with calcium hydroxide for two weeks before the next visit. Under the rubber dam isolation, the root canals were washed with 5.25% sodium hypochlorite and normal saline and dried, and the master gutta-percha cone was fitted. The root canals were filled with the vertical compression technique. After the operation, the quality of the filling was evaluated on a periapical radiograph (). Finally, Z350 composite resin was used to repair the tooth.\nThe patient was followed-up at three, six, and 12 months after endodontic treatment. Clinical examination showed that the tooth had no percussion pain, the sinus was completely healed, gingival tissue was normal, periodontal probing depths were 2–3 mm, and there was no abnormal loosening. Periapical radiography showed that there was no periapical radiolucency with 21, no external absorption in the root and the periapical periodontal ligament was continuous. |
A 39-year-old man presented to our clinic with nausea and headache. He reported that these symptoms had waxed and waned for five years and were aggravated for three weeks before admission. His medical history revealed that he had been diagnosed with a pituitary microadenoma at the age of thirty four with symptoms of polyuria, polydipsia, and severe headache. Initial sellar MRI showed a pituitary microadenoma with stalk deviation and thickening (). An anterior pituitary function test revealed minimal elevation of prolactin (20.2 ng/mL) with no other significant abnormalities. He began to take lisuride hydrogen maleate, which decreased his serum prolactin level. Although intranasal vasopressin therapy significantly relieved the polyuria and polydipsia, his headache did not subside, and, thus, intermittent low-dose steroid therapy was performed based on clinical evidence suggesting that corticosteroids can treat migraine and cluster headache []. Interestingly, his headache responded effectively to steroid therapy, and the size of the pituitary mass was decreased with improvement of stalk deviation as compared to the initial sellar MRI ().\nAfter discharge, the patient had a symptom-free period of three years with intermittent steroid therapy. However, nine months before the current admission, his headache recurred with severe olfactory-induced emesis. These symptoms did not respond to steroid therapy as previously. Due to the enlargement of the pituitary tumor on the follow-up sellar MRI, gamma knife radiosurgery was performed (), but his symptoms aggravated.\nWhen readmitted because of progressive worsening of the symptoms, he was presenting with general weakness and weight loss of 13 kg during the previous six months (from 66 kg to 53 kg) without sign of dehydration, skin rash, or pigmentation. Galactorrhea was not observed. The testes retained a normal size and consistency, but beard was decreased. His visual field was intact, and there was no focal neurologic abnormality.\nThe patient's serum creatinine level was 1.3 mg/dL, and serum calcium was 12.1 mg/dL. His 24-hour urinary calcium was above normal (484.77 mg/day). Parathyroid hormone (PTH) was lower than normal (5.7 pg/mL), while PTH-related peptide (PTHrP) was normal (1.1 pmol/L). The level of 1,25-dihydroxyvitamin D was lower than normal (3.3 pg/mL), while the level of 25-hydroxyvitamin D was normal (11.5 ng/mL). A thyroid function test revealed normal levels of free T4, T3 (free T4 1.64 μg/dL, T3 204 ng/dL) and low level of TSH (0.06 μU/mL). Thyrotropin binding inhibitory immunoglobulins (TBII) was 13.9%. Combined pituitary stimulation tests were consistent with panhypopituitarism. The results of a tuberculin skin test and interferon-gamma release assays for latent tuberculosis infection were negative. The level of angiotensin converting enzyme (ACE) was normal (17 U/L). There was no evidence of infectious disease.\nHis follow-up brain MRI indicated that the lesion initially regarded as a pituitary microadenoma had become larger (13 mm) with contrast enhanced T1-weighted images. In addition, the mass was extended into the right cavernous sinus and caused narrowing of the internal carotid artery, as confirmed by the digital subtraction cerebral angiography (). Thickening of the pituitary stalk with deviation to the left also reappeared (). After a thorough radiologic review of previous MRI findings and the clinical and laboratory data, we determined that the pituitary lesion was the result of an inflammatory disease, such as neurosarcoidosis or lymphocytic hypophysitis.\nSurgical biopsy for diagnostic confirmation was postponed due to the small size of the mass and stenosis of the right cavernous internal carotid artery, both of which could cause serious surgical complications. Instead, high-dose steroid therapy was planned to resolve the impending obstruction of the internal carotid arteries and severe headache with the presumptive diagnosis of neurosarcoidosis.\nSaline hydration lowered the patient's serum creatinine level to 1.0 mg/dL, but hypercalcemia was not easily corrected even after several days of adequate hydration. Oral administration of 300 mg hydrocortisone rapidly corrected the hypercalcemia to 8.0–9.0 mg/dL, and the symptoms of headache and olfactory-induced emesis were also relieved. Given the characteristic findings of the sellar MRI and the resolution of the patient's hypercalcemia after steroid therapy, panhypopituitarism, and central diabetes insipidus, neurosarcoidosis of the pituitary gland was strongly suggested.\nAfter three months of prednisolone therapy with dose tapering, an apparent reduction in size of the infiltrating pituitary lesion was observed on sellar MRI (). After nine months, the patient's combined pituitary stimulation tests showed improvement of the anterior pituitary function with no need for hormone replacement therapy. The patient is currently taking desmopressin and oral calcium carbonate. Sellar MRI at forty-eight months revealed no evidence of recurrence (). |
UG was a pretty seventeen-year old girl in March 2003 when she was interviewed by a locally trained interviewer. She looked, however, visibly ill and strained -quite unlike a normal happy young woman. She complained of constant headache and pain in her eyes. UG's PTSD diagnosis was confirmed within a two-week period by an expert using the CIDI.\nUG did not wait to be offered treatment, but came herself to the project centre and requested for help. In her own words, "I have been to all the doctors but they have done nothing for me. All they give me are painkillers. I had to drop out of school because of my headaches and pain in my eyes." When the treatment protocol was explained to her, she was enthusiastic about relating her experiences and readily gave her assent. Her mother was quick to give her consent. She said she would try anything that would help her daughter. In her own words, ' My daughter has not been her real self for a long time.'\nAt the beginning of NET 1, UG drew a picture of the Somali flag. Asked to explain, she said she loved her homeland and hoped to go back there one day when there was peace. While laying her lifeline, UG included a happy family life in Somalia till the age of 4, her arrival in Uganda after a long and difficult flight itinerary and being accepted as a refugee by the UNHCR as the flowers in her life. The stones in her life represented the worst event, when her older brother was killed, her sister was severely injured and her two younger brothers were lost, never to be seen again, to date. Other stones symbolised flight difficulties such as extreme hunger, and a failure to access a solution for her headaches and eye pain, which she has had since the worst event.\nIn subsequent NET sessions, UG talked in detail about these events. Excerpts from her story read:\nI was born on August 26th 1986 in Mogadishu.... I had six brothers, two younger than me and two sisters older than me. We were a very happy family. As a big family, we conversed a lot and made jokes. We were very happy with our father. He made us laugh and brought us presents whenever he went anywhere. This was a happy time till I was 4 years old...\nOne day,... we heard guns and bullets firing and we were excited. My father ran from work and picked up the other children from school and came back home with them. Some people came to chase us away from our house because we were a minority clan (Madiban). They were from the Hawie (Habrigidir). They were men, very many. They told us to leave everything and flee from the house. They did not beat us. I was still a child, with a soft head. I heard the bullets and started vomiting and fell down. My mother picked me up and put me on her back. We all left the house...\nOn the way, we met very many militia men dressed as army men. They told us to lie down on the ground. I was still crying. The rest were silent. One of them knocked me with the butt of the gun on the soft part of my head. Then I kept quiet. They wanted to kill everyone...\nThey put us in a house for security purposes. A heavy gun was shot near the house. There was another house near our house. They shot this house and the fragments reached our house. Some people were killed in our group, including my brother. He was older than me. He was called Mahad. He was in his school uniform. He fell down on his stomach. I did not see him fall but I saw the blood. My sister Khadija was lying down when the fragments hit her. I did not see any blood, but the fragments went into her stomach and she was hurt in her stomach. My father thought she was dead, but people said she was still alive and she was still talking. He went to her and told her to get up. She could not get up. My father carried her to the hospital. Two of my brothers, Abdirahman aged four years, and Abdirasaq aged three years, disappeared in that group as everyone ran away. They were my two younger brothers. My dead brother Mahad was left there. We never saw my two brothers who disappeared again. So many other people died as well...\nAfter one year, we came back to Mogadishu. We found our father and sister in the hospital. They first stayed in the hospital for some time, then moved to a house. My sister had been operated on. My father had become a bit deaf because of the gunshot.\nWe decided to leave Somalia and go somewhere else more secure. We left Somalia with nothing. My mother, my father, my injured sister Khadija, and the other six children...\nWe went to Kampala. My mother was advised to go to the UNHCR and got a mandate. My sister Shamso and my cousin sister Fardosa also got separate mandates.... In 1997, we were resettled in Nakivale camp...\nI hit my head down and I felt the pain of the gun again. I was not hurt but I got a terrible headache for three days. I went to the doctor but I did not get any assistance except Panadols and eyedrops. Since then, I was unable to go to school because the headaches increased. My eyes had begun paining from birth, but they increased with the headaches.\nI am still here but I hope for a better future and a happier life e.g. to be resettled elsewhere, to have an education, to have a happy family of my own and to make contact with my lost loved ones.\nAmong her hopes and aspirations for the future, UG hoped to trace her missing brothers under the auspices of the Red Cross, as well as re-enter the education system. She also hoped to one day have a happy family of her own\nIn the final picture at the end of therapy, she drew a happy family inside a nice house, living in peace.\nUG had a CIDI pre-test sum-score of 16; immediately after treatment, this reduced to 12 in the CIDI post-test and 1 at the nine-months follow-up. The nine months follow-up found UG no longer in the camp but in Kampala, the capital city of Uganda. She looked happy and cared about her appearance. She said she had no more headaches, and little eye problems. In her own words, "I feel like a newborn child," she told the blind evaluator. She had moved away from the camp to explore possibilities for further education, resettlement and to seriously try to trace her brothers. She also reported joining other adolescents when they were out to socialize. "My biggest dream is to play soccer myself, but as a girl, I would never be allowed. But at least I go and cheer to the boys when they play." She says her family members, especially her mother, have all noticed the difference in her and keep commenting on the improvements she has made. She is more like any healthy young woman. |
A 51-year-old female with a history of rheumatoid arthritis and a 10.5-pack-year smoking history presented with an aspergilloma in her right lung. After failing medical management, she was treated with a right pneumonectomy at an outside institution. This was complicated by BPF and empyema of the pneumonectomy cavity. She underwent two additional thoracotomies requiring rib resection, and placement of serratus anterior and later latissimus dorsi flap to close the fistula. Seven months following her last operation, she presented to us with stridor, persistent cough, and dysphagia, concerning for postpneumonectomy syndrome. Review of last computed tomography (CT) imaging from three months after the pneumonectomy revealed a multiloculated pleural space, with air fluid levels in the pneumonectomy cavity. An updated CT scan showed interval progressive rightward mediastinal shift with nearly complete obliteration of the pneumonectomy cavity by the heart (Fig. ). A bronchoscopy was performed, which demonstrated narrowing of the left mainstem bronchus (Fig. a) and stenosis of the lower lobe bronchial orifice due to external compression of the airways. Results of a previous complex right-sided BPF with two areas of disrupted bronchial staple line were noted (Fig. b).\nThe patient elected to proceed with operative correction of her postpneumonectomy syndrome. A thoracotomy in the fifth intercostal space was performed and dense adhesions in the chest with rotation of mediastinal structures were faced. Upon entering the pleural space, a small loculated serous fluid collection was encountered. To rule out an infected field, the pleural rind and fluid samples were sent for intraoperative gram stains, which returned negative. Cultures were also submitted. The mediastinum was mobilized from the chest wall, taking care to avoid damage to the muscle flaps, which had previously sealed the BPF. As a result, only the mid and inferior portion of the mediastinum was mobilized. A saline immersion test was performed to ensure the integrity of the muscle flap seal over the right mainstem bronchus. The implants were sized based on measuring the amount of saline instilled in the chest, and close hemodynamic monitoring of arterial and central venous pressures. Before placing the implants, the thoracotomy was closed temporarily after placement of implant sizers, monitoring hemodynamics to ensure there was no right heart compression. Two implants (250 mL and 100 mL) were placed into the pleural cavity, and the thoracotomy was closed. The postoperative recovery was uneventful. The patient was discharged on post-operative day 5. She noted complete resolution of her stridor, cough, as well as dysphagia four weeks post-operatively. Her post-operative chest radiograph showed partial medialization of the inferior mediastinum with persistent rightward deviation of the proximal trachea (Fig. ). At time preparation of this manuscript, the patient continues to have full resolution of symptoms at fourteen months following surgery. |
A 54-year-old woman presented to the emergency department with a four-day history of right upper quadrant abdominal pain. She described the pain as constant and sharp in nature. The pain radiated to the right shoulder and was associated with nausea and two episodes of vomiting. She reported having previous similar episodes of this pain over the previous year that occur after fatty meals but the pain was milder and had spontaneous resolution. The patient noticed slight yellowish discoloration of her skin and eyes. The patient noticed a dark urine and pale stool. In addition, he recently developed a generalized pruritus. Her past medical history is remarkable for a long-standing gastroesophageal reflux disease which is well-controlled with proton-pump inhibitors. Of note, the patient does not drink alcohol and does not have any history of recreational drug use. There was no history of recent travel.\nUpon presentation, she was icteric and her pulse rate, blood pressure, temperature, and respiratory rate were observed to be 112 beats per minute, 124/68 mmHg, 37.9° C, and 13 breaths per minute, respectively. The abdominal examination revealed a tenderness in the right upper quadrant with a positive Murphy sign. There were no clinical signs of peritonitis and no stigmata of liver disease were observed. Her basic hematological and biochemical investigations revealed a hemoglobin level of 13.5 g/dL, a leucocyte of 12.0 × 103/μL with a left shift (85% neutrophils), a total bilirubin of 2.1 mg/dL with a direct bilirubin of 1.2 mg/dL, a gamma glutamyl transferase of 200 U/L, and her levels of urea and electrolytes were normal. The urinalysis revealed no abnormalities. An ultrasonography of the abdomen was further performed to confirm the diagnosis of obstructive jaundice. A dilated common bile duct (8 mm) with the presence of a small stone was observed. Pericholecystic fluid and several gallbladder stones with acoustic shadow were found.\nGiven the aforementioned clinical and imaging findings, the patient was started on conservative treatment and intravenous ceftriaxone 1 g daily. She demonstrated clinical and laboratory improvement within 48 hours. The patient was prepared for a laparoscopic cholecystectomy. The surgery was performed under general anesthesia and four ports were inserted to carry out the procedure. A diagnostic exploration was performed after establishing the pneumoperitoneum and introducing the trocars. It revealed the presence of a gallbladder duplication (Figure ).\nMeticulous dissection was performed. The cystic artery and both cystic ducts were ligated. Both gallbladders and their cystic ducts were resected (Figure ).\nIntra-operative cholangiogram showed no evidence of choledocholithiasis. The total operation time was 90 minutes and the estimated blood loss was 50 ml. The patient tolerated the procedure well and was discharged on the fourth postoperative day. She remained symptom-free at one-month follow-up. |
We report the case of a 39-year-old man who was diagnosed with congenital lymphangiomatosis at the age of 12 when he underwent diagnostic intra-abdominal lymph node excision.\nWhen he went to a consult due to the impressive scrotal volume and penian deformity, the patient could not have sexual intercourse, could not maintain proper local hygiene and had walking problems. He required the administration of a treatment with antidepressants ().\nPhysical examination revealed a marked enlargement of the scrotum with the thickening and the loss of the elasticity of the peno-scrotal skin and subcutaneous tissue. Moreover, a little difference between the circumferences of the legs was visible, probably as a result of lymphatic disorder. The patient was in good condition without changes in laboratory tests.\nAbdominal and testicular ultrasound, chest and abdomino-pelvin CT did not show changes except for the global thickening of the peno-scrotal skin and subcutaneous tissue and important hydrocele on both sides ().\nAfter a preoperative discussion with the patient (presenting him all the possible treatment options and related side effects) and considering important skin troficity changes, we decided to form a mixed surgical team urology – plastic and reconstructive surgery.\nThe surgical technique\nUsual preoperative procedures were performed. After a spinal anesthesia the procedure began with the midline scrotal skin incision. Both vaginal testes and spermatic cords were isolated. Incision, excision and inversion of both vaginalis were performed; each vaginalis contained about 1,500mL of milky-like lymphatic fluid. The exceeding skin and subcutaneous tissue (with an infiltrated, boarded aspect) were removed. The penile skin was also excised immediately above Buck’s fascia. The remaining skin was used for the “new” scotum and a midline suture simulating the scrotal raphe was performed. The skinless penile shaft was covered with a split-thickness skin graft harvested from the anterior surface of the thigh. The scrotum was drained on both sides with a continuous drainage tube. An occlusive dressing consisting of a mild compression bandage which ensured adequate contact of the graft with the recipient bed and an indwelling urinary catheter were placed. |
A 30-year-old male was admitted to our hospital with complaints of a 3-day history of severe headache and high fever. On admission, he presented with disorientation, and his body temperature was higher than 39°C. Blood examination showed a white blood cell count of 12,200 cells/mm3 and C-reactive protein of 1.22 mg/dl. A computed tomography scan revealed subarachnoid hemorrhage (SAH) with intracerebral hematoma, predominantly in the anterior interhemispheric fissure, and intraventricular hematoma []. Initial digital subtraction angiography (DSA) demonstrated a fusiform aneurysm with an irregular shape on the left pericallosal artery, 4.5 mm in maximum diameter []. He had cardiac noise on chest examination by stethoscope, and cardiologists finally diagnosed mitral insufficiency by further study. The detection of Staphylococcus haemolyticus in the blood culture led to a definite diagnosis of infective endocarditis (IE). Thus, the fusiform aneurysm of the left ACA was considered to be associated with this IE, and it was diagnosed as infectious cerebral aneurysm. He was initially treated with high-dose intravenous antibiotics (cefazolin 8 g/day and gentamicin 120 mg/day). However, follow-up DSA performed 20 days after the onset revealed the enlargement of the aneurysm to 14 mm in maximum diameter and vasospasm of the left pericallosal artery []. We decided to perform surgery to prevent recurrent bleeding from the growing aneurysm. The left paracentral artery originated from the dome of this aneurysm, which would perfuse a motor area of the right lower limb []. Thus, the aneurysm could not be occluded without revascularization.\nLeft frontal craniotomy was performed, and a proximal side of the A2 segment was initially found within the anterior interhemispheric fissure. We distally followed the ACA, and subsequently observed an old SAH. Then, we found the distal part of the A3 segment before approaching to the aneurysm. Considering the risk of premature rupture, we decided to create a bypass in advance of the dissection of the aneurysm. A frontal branch of the left STA, 8 cm in length, was harvested, and this STA was used as an interposition graft to reconstruct the left ACA in an end-to-side manner: Left callosomarginal artery (proximal side) – STA graft – left pericallosal artery (distal side) [Figure and ]. Then, the origin of the left paracentral artery was cut and anastomosed to the STA graft in an end-to-side manner []. The patency of the graft was confirmed by indocyanine green video angiography. After the creation of the bypass and trapping the parent artery, we went into a hematoma cavity and found the infectious aneurysm. We dissected the aneurysm from the surrounding tissue and then resected the aneurysm. Postoperative magnetic resonance imaging showed no ischemic or hemorrhagic complications, and postoperative DSA revealed the patency of the interposition graft [Figure and ]. The postoperative course was uneventful, and the patient manifested no neurological deficits. The patient was thereafter treated for IE by a cardiologist.\nHematoxylin-eosin stained sections and Elastica–Masson stained sections of the resected aneurysm corresponded to the features of an infectious cerebral aneurysm []. A rupture of an arterial wall adjacent to the aneurysm had the appearance of a pseudo-aneurysm. The vascular media had become fibrotic, and the smooth muscle was thin. The vascular intima was globally hypertrophic and partially disappeared []. No bacteria were detected in these sections, but the adventitia was invaded by many inflammatory cells []. |
A 37-year-old female presented to the emergency room at our institution with intractable abdominal pain and fever. She has a history of dysuria and hematuria for 10 months, which at the time prompted an MRI demonstrating an abdominal wall mass with extension into the bladder. Outside biopsy was reported as “inflammation”. She was initially treated with antibiotics. A cystoscopy was performed and a transurethral bladder biopsy showed acute and chronic cystitis and Von Brunn nests. Cytology report indicated presence of atypical urothelial cells and she was then referred to the urology service due to suspicion for malignant neoplasm. Follow up CT scan imaging demonstrated a heterogeneous ill-defined enhancing soft tissue density in the space of Retzius inseparable and compressing the anterior aspect of the urinary bladder measuring 11.3 × 4.5 × 12.8 cm with a peripherally enhancing loculated collection measuring 4.7 × 6.0 × 3.0 cm along with marked thickening of urinary bladder . As strong suspicion for malignant lesion persisted, a repeat percutaneous biopsy was done that again demonstrated infiltrative granulation tissue and chronic inflammation.\nAs the patient’s symptoms continued to progress, including persistent hematuria diagnosis was uncertain despite multiple percutaneous and transurethral biopsies, she was referred to Surgical Oncology team for multidisciplinary management. As there were still concerns for neoplastic malignant process vs desmoid vs pseudoinflammatory neoplasm, the multidisciplinary team recommendations were to offer operative management in coordination with the surgical oncology and urology teams with an intention to provide larger tissue for definitive diagnosis to guide extend of surgery, which would include complete bladder removal with construction in the form of ileal conduit, abdominal wall resection with abdominal wall reconstruction if malignancy were to be confirmed intraoperatively.\nIntraoperative cystoscopy demonstrated an ulcerated infiltrative tumor into the dome of the bladder. Intraoperative frozen biopsies did not provide definite diagnosis and suggested spindle cell neoplasm, possible of urachal origin but malignancy could not be confirmed, thus the decision was to proceed with palliative resection including abdominal wall resection with en bloc resection of pelvis tumor, partial cystectomy and partial oophorectomy, as the mass was found to have invaded the abdominal wall below the umbilicus as well as the ipsilateral ovary and ureter. There was significant thickened white tissue within the muscles and extending to posterior rectus sheath. . However, near the bladder the abnormal thickened tissue extended from the dome of the bladder over the urethra. Decision was made to avoid creation of an ileal conduit and rather perform a partial cystectomy and await definitive diagnosis. An incidental Meckel’s diverticulum was found and resected.\nThe final pathology showed an ill-defined pale-tan markedly fibrotic area measuring 8.5 × 5 × 5 cm extending from the mucosa. The mucosal and submucosal aspect of the bladder showed markedly necrotic aspects. The abdominal rectus muscles were grossly present in the specimen and were focally involved by the fibrotic area. The abdominal wall mass was predominantly reactive fibrous tissue with acute and chronic inflammation and fibrosis without evidence of malignant neoplasia. The mass contained low-grade spindle cell proliferation with abundant inflammation, granulation tissue, and chronic abscess. The mass had connections to the bladder suggesting urachal origin. The muscularis layer was noted to have attached granulation tissue. Left partial oophorectomy yielded unremarkable parenchyma with attached reactive fibrous tissue containing chronic inflammation and hemorrhage.\nThe frozen section demonstrated an ill-defined pale-tan markedly fibrotic area measuring 8.5 × 5 × 5 cm extending from the bladder mucosa. The mucosal and submucosa of the bladder showed markedly necrotic aspects. The abdominal rectum muscles were grossly present and were focally involved by the fibrotic area ().\nThe patient’s final pathology was discussed in multidisciplinary tumor board and recommendations were to treat her with NSAIDS to attempt control residual disease if symptoms returns or progression occurs. A post-op MRI 10 months later showed resolving residual inflammation. She is recommended to remain on NSAIDs and close follow up and monitoring her with imaging. |
A 46-year-old Bahraini female diagnosed as premature ovarian failure at the age of 29 years treated with hormonal replacement therapy presented with a history of epigastric abdominal pain and vomiting at the age of 37 years. Biochemical and radiological assessment showed features of acute pancreatitis in terms of elevated pancreatic enzyme level, and CT abdomen finding showed edematous pancreas with normal ductal system. It was attributed to hormonal replacement therapy after thorough investigation. Although the patient had stopped the implicated medications, she still had recurrent attacks of acute pancreatitis.\nSince there was no obvious cause found for her recurrent episodes of pancreatitis, autoimmune pancreatitis was suspected.\nThen, she underwent endoscopic ultrasound in 2015 which revealed mass swelling at the duodenal ampulla, and biopsy was taken. The biopsy showed ampullary adenoma with high-grade dysplasia (Figures and ).\nThen, the patient decided to go abroad for further assessment where she underwent Whipple's procedure and histopathology confirmed the presence of ampullary adenoma with high-grade dysplasia.\nUnfortunately, she continued to have recurrent episodes of pancreatitis despite the removal of the ampullary adenoma.\nIn 2016, while she was admitted under care of a surgical team for another episode of pancreatitis, she was reviewed by the rheumatology team to rule out autoimmune condition. Therefore, IgG4 level was tested (1.49 g/L (149 mg/dl)). The biopsy was reassessed and found to have increased IgG4-positive plasma cells around 30–40 per high-power field with the background of adenoma with high-grade dysplasia. Accordingly, she was diagnosed to have both IgG4-related disease and ampullary adenoma.\nShe was started on oral prednisolone 0.5 mg/kg and rituximab therapy with significant improvement over 1 year of follow-up as the pancreatitis attacks have reduced from around once in every month to around once in every 3 to 4 months after 3 months of rituximab therapy, and currently she remained attack free for around one year. |
A 73-year-old woman with no previous comorbidities or family history of hematological disorders or hypercoagulability was admitted to the Infectious Disease Clinic due to suspected HFRS and dehydration. Two weeks prior to disease onset, she had been exposed to bank voles while cleaning out a cabin. For 6 days following disease onset, she had been ill with fever, chills, weakness, low urine production, and difficulties eating and drinking. The patient had positive serology for Puumala virus thereby confirming the HFRS diagnosis. Laboratory tests taken the day before admission revealed thrombocytopenia (platelet count: 48 × 10\n9\n/L), impaired renal function (creatinine: 278 μmol/L), and leucocytosis (white blood cell count: 14 × 10\n9\n/L). Upon admission to the hospital, the platelet count had increased to 61 × 10\n9\n/L and creatinine increased to 370 μmol/L indicating clinical progression to the oliguric stage of HFRS. However, the platelet levels decreased to 12 × 10\n9\n/L on days 8 to 9. The treating physicians decided to transfuse platelets on days 8, 9, and 10 due to the high risk of spontaneous bleeding. Despite transfusion with three platelet units, the patient remained severely thrombocytopenic with platelet counts below 50 × 10\n9\n/L during days 8 to 13. The case is summarized in\n. Criteria for disseminated intravascular coagulation (DIC) were fulfilled from day 8 (see\nfor an overview of criteria).\nOn day 13 (2 days after the last platelet transfusion and a platelet count of 27 × 10\n9\n/L), the patient falls ill with abdominal pain which increases in severity during the evening. An abdominal computed tomography (CT) shows congestion and ischemia in the terminal ileum due to a thrombus in the superior mesenteric vein (SMV) reaching up to the portal vein (PV). The hematologist advised against thrombolysis due to thrombocytopenia in combination with a known mild VHF, which could increase the risk of bleeding. A national coagulation expert is consulted for further advice, who recommends anticoagulant treatment with heparin in a “careful” dose. Heparin at a dose two-thirds the national recommended dose is initiated with the aim of APTT 1.5 times the baseline value (40–50 s). The patient therefore receives a bolus dose of 4,000 units heparin followed by transfusion of 24,000 units heparin per day. The following day (15), the patient has gastrointestinal bleeding and a decrease in hemoglobin values from 100 to 89 g/L. According to the surgeon consultant, the stasis caused by the SMV and PV thrombus damages the intestinal mucosa leading to the observed gastrointestinal bleeding. Heparin is therefore continued in the same careful dose and the patient receives one unit red blood cells (RBCs) that day and the following day (16). The following criteria had to be fulfilled before mesenteric phlebography and thrombolysis via catheter could be considered: (1) platelet levels greater than 100 × 10\n9\n/L, (2) no bleeding, and (3) the patient can tolerate a full-dose heparin. On day 19, the patient fulfilled these criteria and underwent mesenteric phlebography via interventional radiology. Using the percutaneous transhepatic route to the PV, a hydrolyser 7F, double lumen, over-the-wire thrombolysis (Hydrolysis, Cordis Europe NV, Roden, the Netherlands) was used to perform a mechanical thrombolysis of the PV followed by pharmacological thrombolysis with tPA (Actilyse infusion: 0.8 mg/hour). A notation from the surgery department states that the previous heparin treatment aiming for 1.5 times APTT had been unsuccessful in decreasing the size of the SMV and PV thrombus. A control angiography 6 hours postsurgery shows that the thrombus distally in the SMV has been removed. There is still a thrombus between the portal and the splenic vein; therefore, the catheter is moved further into the area of thrombosis and thrombolysis by Actilyse administration is continued. At this time, there is no contrast leakage as a sign of hepatic bleeding. The patient stays in the intensive care unit (ICU) with local hydrolysis via the catheter. The following day (20), the patient becomes hypotensive with systolic blood pressure down to 75, and has signs of peritonitis. The levels of the fibrin degradation product D-dimer increases to 20 mg/L and fibrinogen decreases to 0.69 g/L. A CT thorax/abdominal scan shows an ongoing expanding hepatic intraparenchymal arterial bleeding. In addition, the CT scan shows presence of pulmonary emboli. Since the patient has a propensity for bleeding and thromboembolism, arterial intervention via the femoral artery into the aorta and then out into the common hepatic artery with coiling was not an option. Instead an emergency surgery procedure is performed with ligation of the right hepatic artery in the hepatoduodenal ligament, which stops the bleeding. In addition, the anticoagulant therapy is discontinued that day and the patient is tended in the ICU in a respirator. On day 21, the anticoagulant therapy is readministered at a low dose. The patient is extubated on day 22 and the anticoagulant therapy is increased to a target of APTT 60s due to remaining portal thrombi and peripheral pulmonary emboli. On the evening of day 25, the patient develops acute dyspnea, and oxygen saturation decreases to 88% with 4 L of oxygen and tachycardia. A CT pulmonary angiography shows pulmonary emboli in the right and left pulmonary arteries and peripherally in the pulmonary lobe arteries. The patient is transferred that evening to the ICU with heparin treatment at a target of APTT 85s. An ultrasound of the peripheral extremities (day 26) shows bilateral deep vein thrombosis in the posterior tibial veins. Since the APTT remains difficult to adjust (ranging from over 180s to the therapeutic target of 80s) and the propensity to develop thrombosis despite anticoagulation, it is decided to change the treatment from heparin to low-molecular-weight heparin (Fragmin 16,000 IU/day) on day 32. After day 55, the patient receives warfarin as prophylaxis against further thromboses and is discharged to her home on day 61. To rule out other causes for the thromboembolic complications, she was tested and found negative for activated protein C resistance. |
A 58-year-old male patient was referred by a doctor to the dental office, presenting with a woody edema that affected the right side of the hemiface, with accompanying reddish colour and painful symptoms, which started 1 week ago. The patient did not have any other illness or any medically compromised disease.\nOn clinical examination, the region was hyperthermal and without a fluctuant point []. During palpation, the presence of the salivary calculus was evident. When milking the parotid gland to stimulate salivation, a purulent secretion was observed []. Ultrasonography of the region and cone beam computed tomography were requested to confirm the diagnosis [Figure –].\nStimulating mouthwash therapy, associated with the milking movements of the gland, was used to exteriorize the stone. However, the infection did not improve and the patient's medication was changed to amoxicillin trihydrate and potassium clavulanate 875 mg, with one tablet taken every 12 h.\nAfter 4 days of follow-up, it was possible to observe a change in the texture of the site, which started to show a fluctuation point. The patient was instructed to perform external heat compresses. After 3 more days, extraoral drainage was performed with subsequent placement of a Penrose drain [Figure and ]. A large amount of bloody, purulent fluid was observed during the drainage. The surgical site was divulsed and the salivary calculus was not found. The drain was left in place for 2 weeks. The dressing was changed every 2 days, and rifocin and iodine were applied externally to the region. The drain was removed and the surgical site was divulsed a second time, allowing for identification of the salivary calculus and subsequent removal. The edges of the site were sutured, and the patient was monitored until completely healed []. Throughout this process, the patient's blood samples were tested in the laboratory on alternate days, and the patient took the prescribed medication.\nThe patient was followed for 6 months [], with a minimal scarring and no noteworthy change. |
An 11-year-old boy presented to the outpatient department with headache and vomiting in August 2011 []. CT scan showed a contrast enhancing isodense space occupying lesion with areas of calcification in right frontal cortex with surrounding edema (). Craniotomy was done and part of the lesion was sent for squash cytology. The smear appeared cellular showing discohesive sheets and clusters of pleomorphic oval to polygonal cells with abundant eosinophilic cytoplasm some showing cytoplasmic vacuolation and marked nuclear atypia in a background of necrosis and hemorrhage. A suggestion of atypical teratoid/rhabdoid tumour was made. A near total excision of the space occupying lesion in the right parietooccipital region was done and sent for histopathologic examination. Grossly, the specimen was received as multiple irregular gray white soft tissue fragments ranging from 0.5 × 0.5 cm to 4 × 3 × 2 cm. External surface appears irregular and nodular. Cut surface appears variegated with gray tan areas, glistening areas, cystic areas, and hemorrhagic areas. Few areas of calcification are also seen ().\nHematoxylin and eosin stained tissue sections revealed a highly cellular neoplasm composed of predominantly spindle shaped cells with pleomorphic oval to elongated hyperchromatic nuclei (). The cells are arranged in interdigitating fascicles and herring bone pattern in few foci and with frequent mitoses of 2–10 per high power field. There are also foci showing deep staining round cells arranged in small clusters and rosettes with areas of necrosis and hemorrhage and no reticulin fibers present.\nA differential diagnostic consideration of (1) gliosarcoma with leiomyosarcomatous differentiation and (2) teratoma with malignant transformation was made.\nImmunostaining for Vimentin showed cytoplasmic positivity in 70% of the cells. Smooth muscle actin showed focal weak positivity in 30% of the cells. Immunostaining for S100, epithelial membrane antigen, was found to be negative and glial fibrillary acidic protein was scanty positive; Ki67 proliferation index was 10–15% and P 53 protein was positive (Figures , , , , , and ). A final diagnosis of gliosarcoma was then made.\nThe patient was given external beam radiotherapy 66 Gy at 2 Gy in 33 fractions and 6 cycles of chemotherapy with temozolomide 200 mg per day for 5 days every 28 days (). The post-treatment MRI scan showed a residual focal area of brain edema and granulomatous calcified lesion with reactivation 2.5 × 2.5 cm; the lesion is hypointense in T1W and hyper in T2W (). On examination his performance score according to Eastern Cooperative Oncology group is 2, he has a scar on the right side scalp consistent with the previous surgery, his cognition is good, and he has mild difficulty in talking and mild weakness in the left lower limb. He is on regular follow-up with us and has survived for 30 months (Figures and ). |
On May 3, 2011, at 10 AM, a 50-year-old female was admitted to an outpatient department hospital at Mahad in the district of Raigad. She complained of insomnia, suffocation, fever, severe whole-body pain, and malaise over the past 4 days. On April 30, she had been examined by her family doctor. She received an unidentified injection, acetaminophen tablets, and oral chloroquine. There was no improvement of symptoms.\nSince she additionally complained of chest pain, she was admitted to the Intensive Care Unit (ICU) on May 2, where her pain was attributed to unstable angina. She was closely monitored and was given nasal oxygen, intravenous fluids, a nitroglycerin drip and furosemide. In addition, a treatment with low-molecular-weight heparin 60 mg every 12 h digoxin, aspirin, clopidogrel and statin was started. There was no clinical improvement. On the 3rd day, the ICU doctor transferred her to a tertiary care hospital for further cardiac investigation to rule out ischemic cardiomyopathy.\nInstead of going to Mumbai, the relatives brought the patient to the clinic at Mahad. On admission, she was fully conscious. She presented with a history of mitral valve replacement in 1994. She complained of excessive thirst and being unable to drink water for 2 days. While examining her, we asked for a glass of water. Simple by hearing the word water (Pani in vernacular language), she suddenly developed severe laryngeal spasm [, ]. This repeated laryngeal spasm in response to the word “water” confirmed that she was suffering from rabies. We asked her and the relatives regarding any history of a dog bite. She reported that 4 months ago, a furious dog had bitten four persons from her village. All of them were treated with immunization as exposure prevention by the government hospital. All the four are healthy at present. The furious dog had caught her sari (cloth), and with its claws, it caused multiple abrasions at her right foot. She cleaned the blood and the abrasions by rubbing it with her sari. She and her relatives believed that only the bite of a dog can cause the disease and hence avoided postexposure rabies immunization though it is free and freely available at the primary health center, which is 5 km away from her village. However, she reported that instead of visiting the hospital, she visited a Tantrik (village healer) who gave her some herbal medicine.\nHer blood pressure was 140/80, she had no signs of myocardial failure, a grade 3/6 systolic murmur was heard at over the aortic root area, and an ejection click of the mitral valve was heard over the apex. The respiratory rate was 14/min and no pathological breathing sounds were heard over her chest. Her body temperature was 99°F. There was no any neurological deficit except laryngeal spasm.\nAs major symptom, she described that she experienced tingling and numbness and heaviness in her right lower limb. Troponin T was negative, and serum sodium was 128 mEq/l. Electrocardiogram showed a heart rate of 75 beats/min with minor ST-T changes []. Hemoglobin level was 14.6 g/dl, leukocyte count was 11,100 cu.mm, and blood sugar was 105 mg/dl.\nShe was isolated in a dark room. Very carefully, we placed a nasogastric feeding tube. She was given intravenous fluids, intravenous atropine 3 mg, magnesium sulfate (MgSO4) 2 g, midazolam 1 mg/kg body weight, and sustained acting zolpidem 12.5 mg through the nasal tube. The next day she developed a mixed form of delirium with being fully conscious in-between (lucid interval). She still occasionally developed laryngeal spasms. On the 3rd day, she presented with tachycardia, delirium, internuclear ophthalmoplegia, and plantar flexion, and the strength in all limbs was grade 5/5, but she had no neck rigidity. Moist rales were heard over the chest, and she became tachypnoeic. At 3 AM on the 4th day, she developed pulmonary edema and massive hematemesis and died of respiratory arrest. She was conscious till death. No attempt to resuscitate her was initiated following the decision of seniors and relatives. |
A 69-year-old female Japanese patient suffered from narrow stool and was determined to have a 15-mm superficial lesion with central depression in the rectosigmoid colon (Fig. ). Invasive carcinoma was suspected and biopsy of the lesion confirmed well-differentiated adenocarcinoma. Positron-emission tomography—computed tomography showed no metastasis. We planned laparoscopic surgery, and CTA was performed to investigate the local vascularity. Unexpectedly, this revealed an approximate 5-cm stenosis from the infrarenal abdominal artery to the root of the inferior mesenteric artery (IMA) and collateral circulations, although the patient had no complaint of angiostenosis symptoms (Fig. ).\nWe observed no blood vessel wall thickness at the narrow segment and only a little calcification, then we diagnosed middle aortic syndrome (MAS). Although we did not detect the overswelling of the inferior epigastric artery that is usually seen in this condition as the collaterals to the legs, the IMA communicated with the collateral circulation branched from the superior mesenteric artery and gastroduodenal artery, such that blood flow to below the narrow segment was expected to be due to IMA reflex. Furthermore, deficiency of left colic artery (LCA) meant that the bloodstream to below the narrow segment depended only on collateral circulation, namely, curative colectomy with vascular ligation blocked blood flow to the legs.\nThe patient exhibited no hypertension, leg numbness, coldness, or intermittent claudication—but further examinations revealed the following low ankle brachial index (ABI) values: 0.69 in the right and 0.66 in the left. From this information, we anticipated a low ability to preserve blood flow to the legs and decided that vascular reconstruction was needed. Angiography revealed that the collateral circulation flowed to the IMA, as expected from the CTA (Fig. a). We chose to perform stent reconstruction because it is simple and less invasive, and because a properly placed stent would make blood flow obstruction unlikely in the event of obstruction of the IMA root. A self-expandable stent was placed in the narrow segment, and we verified the pressure gradient improvement above and below the narrow segment (Fig. b). ABI was improved to 1.02 in the right and 0.95 in the left.\nEight days after vascular reconstruction, we performed single-incision laparoscopic anterior resection. We started SLC with a 2.5-cm vertical incision in the umbilicus (Fig. a). We ligated IMA with a vascular clip and then completed CME (Fig. b). The colon was resected with sufficient distal and proximal margins from the tumor and then anastomosed. We did not need additional trocar (Fig. c). The patient showed no symptoms of leg ischemia, although ABI fell to 0.88 in the right and 0.77 in the left. The patient was received 20,000 unit/day heparin administration after stenting until 3 h prior to surgery and restarted heparinization 15,000 unit/day 3 days after surgery. Cilostazol and aspirin were started 7 days after surgery; then, the heparinization was ended the next day of administering antiplatelet drugs. The patient was discharged on the tenth day after operation with no complications. Histological examinations revealed the tumor to be moderately differentiated adenocarcinoma with invasion to the submucosa (T1) and no lymph node metastasis (N0). No distant metastasis was found (M0) at the time of surgery, and the histological staging of the tumor was stage I. The root of the IMA was histologically examined to determine whether any vascular lesion existed, revealing slight inner wall thickness and calcification, but otherwise no other remarkable findings. |
A 14-year-old boy presented in neurology emergency, with history of progressive quadriparesis since 1 year. Weakness was initially confined only to upper limbs and in another 2 weeks involved the lower limbs. Over next 3 months, he lost the ability to walk, became bed bound and required assistance for all his activities of daily living. During this period, there was severe, diffuse loss of muscle mass in whole body. About 3 weeks prior to reporting, he developed severe breathlessness and nasal twang in voice along with nasal regurgitation of food and fluids .\nOn examination he was restless. There was fever with tachycardia and tachypnea. Accessory muscles of respiration were active and paradoxical respiratory movements were present. The single breath count was between seven and ten. Cognition was intact. There was paralysis of 9th, 10th, 11th, and 12th cranial nerves. Gross wasting of limb and trunk muscles was present. There was grade 3/5 power at both hip and knee joints with bilateral foot drop, grade 2/5 power at both shoulder and elbow joints with bilateral wrist drop. Severe weakness of trunk and neck muscles along with generalized hypotonia and areflexia was present. Sensory examination revealed impairment of posterior column sensations. Systemic examination was unremarkable.\nHematology and serum biochemistry were normal. The serum creatine phosphokinase was normal (110 U/L) and needle EMG did not show any myogenic potentials. Nerve conduction studies [] showed prolonged distal latencies, conduction block, decreased conduction velocities, prolonged F-wave, and decreased motor action potentials of the median, ulnar and common peroneal nerves, suggesting demyelinating type of neuropathy. Electrophysiologically definite and clinically typical CIDP was considered as per the revised criterias published by the Peripheral Nerve Society and by the European Federation of Neurology.[]\nThe chest X-ray revealed elevated domes of diaphragm suggesting bilateral phrenic nerve palsy which was later confirmed by fluoroscopy. Cerebrospinal fluid examination showed elevated proteins (120 mg/dL) and five lymphocytes. The vasculitis and hepatorenal profile, Venereal Disease Research Laboratory test, and Human Immunodeficiency Virus serology were negative. Serum electrophoresis was negative for M band and there was normoblastic erythropoiesis in bone marrow aspiration smear.\nHe was immediately intubated and ventilated by manual AMBU ventilation. A course of intravenous immunoglobulin was given, along with antibiotics. After ensuring adequate control of infections he was started on oral corticosteroids (1 mg/kg body weight). Due to financial constraints he remained on continuous AMBU ventilation for 6 weeks, after which he required it only intermittently (4-5 hrs/day) to maintain adequate oxygen saturation. Relatives of the patient were trained to provide accessory care like nutrition, physiotherapy of chest and limbs, throat suction, and care of tracheostomy tube under supervision of respective experts. Later they were also trained to use an ambubag device and ventilate the lungs at rate of 15- 16 /min. After 2 months of hospital stay there was a significant improvement in respiratory effort and motor power, he could stand and walk with minimal assistance. He remained on tracheostomy care and required domiciliary, intermittent AMBU ventilation. Over another 2 months patient was completely weaned from the AMBU ventilation and his tracheostomy tube was removed. Oral corticosteroids were tapered and withdrawn. Presently, the patient can breathe normally and perform all activities of daily living independently. |
A 51-year-old male with a permanent IVC filter that had been inserted approximately 20 years ago when the patient developed a DVT during a hospitalization for severe non-ischaemic cardiomyopathy, was transferred to our medical intensive care unit for shock and acute renal failure. Following the IVC insertion, he had been treated with warfarin for one year and had been on anti-platelet therapy since.\nHe had been admitted to the hospital three days prior to transfer after presenting with progressive bilateral lower extremity pain and decreased sensation in his gluteal region. Acute bilateral DVTs involving the common femoral and popliteal veins were diagnosed. Over 48 h, despite receiving unfractionated heparin, he developed anuric renal failure and shock. Placement of a right internal jugular dialysis catheter was complicated by airway compromise due to a retropharyngeal haematoma necessitating endotracheal intubation. The heparin infusion was discontinued and the patient was transferred to our hospital.\nOn arrival, his mean arterial pressure was 71 (104/53) mmHg while on norepinephrine, vasopressin, and phenylephrine. Arterial blood gas analysis showed a pH of 7.06, partial pressure of carbon dioxide (PaCO2) of 28 mmHg, partial pressure of oxygen (PaO2) of 312 mmHg, and a lactate of 16 mmol/L. The platelet count was 31 K/μL. Examination was notable for tense bilateral lower extremity oedema. Dorsalis pedis pulses were detectable with Doppler ultrasound. An abdominal computed tomography (CT) showed dilation of the distal IVC suggesting thrombosis (Fig. A). Transthoracic echocardiography showed a 25% ejection fraction with no right ventricular dilation or strain. The IVC was collapsible proximal to the hepatic veins. Lower extremity ultrasound confirmed acute bilateral DVTs involving the external iliac and femoral veins. Laboratory evaluations excluded thrombophilia, heparin-induced thrombocytopenia and thrombotic thrombocytopenic purpura. Infusion of 5 L of isotonic fluid and continuous renal replacement therapy led to a reduction in the vasopressor requirement, a reduction in lactate to 2.0 mmol/L, and pH/PaCO2 normalization. However, the lower extremity oedema progressed with development of bullae and purple skin discolouration (Fig. B). Dorsalis pedis pulses became undetectable, consistent with compartment syndrome due to PCD.\nCatheter-directed thrombolysis, surgical thrombectomy, and fasciotomy were deemed to be contraindicated due to ongoing shock, severe cardiomyopathy, the retropharyngeal haematoma, and persistent thrombocytopenia thought to be the consequence of platelet consumption. Unfractionated heparin was restarted and, within 24 h, lower extremity pulses were again palpable. However, there was a progressive rise in creatinine phosphokinase to 44,000 IU/L and an increase in lactate to 5.8 mmol/L despite continued vasopressor support and continuous dialysis. His family decided to pursue palliation and withdrawal of life-supportive measures. Post-mortem examination confirmed an occluding thrombus at the level of the IVC filter with extension to the internal and external iliac veins (Fig A, B). The autopsy did not identify an underlying malignancy. |
A 63-year-old, right-handed man presented with a 6-month history of gait deterioration, requiring a walker. For the 3-4 weeks prior to presentation, he had also experienced a new onset of memory difficulties and subtle trouble with word finding, as well as mild headaches and declining vision. Of note, the patient had a history of spinal cerebellar atrophy (SCA). The patient's neurologic exam was remarkable for mild dysmetria, dysdiadochokinesia, and a positive Romberg sign, in addition to subtle fluent dysphasia and memory dysfunction.\nAn MRI scan revealed a left temporal lobe mass measuring 3.5 cm × 2 cm abutting the temporal horn of the lateral ventricle (). Notable T2 signal prolongation was observed, extending from the ventricle to more anterior and superior portions of the temporal lobe. Mass effect was present, with mild effacement of the ventricle and minimal midline shift. Radiological signs secondary to the SCA were also observed, including cerebellar atrophy with enlargement of the foramina of Luschka bilaterally, as well as a fourth ventricular enlargement.\nA craniotomy for tumor resection was recommended to the patient in order to achieve a tissue diagnosis, alleviate neurologic symptoms, and extend survival given the presumptive diagnosis of high grade glioma.\nThe surgical technique of the authors is generally to use a twilight-awake-twilight model of anesthesia for these cases. The patient is fully off sedation for the entirety of the intradural portion of the case during which time the patient undergoes cortical mapping followed by continuous interaction with the neurophysiology team including reading flashcards, performing recall exercises, and answering simple questions. In this particular case, a temporal craniotomy was performed in the standard fashion centered over the middle temporal gyrus. Frameless image guidance was used to guide the placement of the bone flap, which was approximately 3 cm in diameter. Cortical mapping of the exposed temporal lobe did not reveal any changes in speech functions. The tumor was cannulated through the middle temporal gyrus using a previously described method [] (). Resection through the endoscopic port was relatively uneventful, except for two instances of fluency changes that occurred during tumor resection. Both were easily reversed by adjustment of the port trajectory. An aggressive resection was achieved. Pathological examination was consistent with glioblastoma multiforme (GBM).\nPostoperative MRI scan demonstrated a 93.3% volumetric resection of the tumor, with minimal residual tumor noted in the anteroinferior margin of the tumor bed (). Postoperative recovery was uneventful, with the patient being discharged from the hospital on day 3.\nAt a one week postoperative followup, the patient was observed to have slight horizontal nystagmus that was noted postoperatively. He reported that his vision seemed to be improving. The patient did slur his speech on occasion; however, this was consistent with his baseline speech preoperatively. No new impairments of language or cognition were noted secondary to the surgery. The patient was undergoing speech and physical therapy and had been referred for radiation therapy and chemotherapy due to his GBM diagnosis.\nAfter 7 months, the patient had an MRI showing multifocal enhancement within the dominant hemisphere. MR spectroscopy was suggestive of multifocal tumor progression. The patient was subsequently treated with two cycles of avastin. At the 9-month followup, the patient has been noted to have improved T2 and FLAIR images consistent with the avastin effect. On the neurological exam, the patient was mildly dysarthric as had been noted prior to surgical intervention. The patient continued to demonstrate mild abnormalities with word finding but could recall 3/3 words in 5 minutes when given categorical clues. The patient had no other new motor, sensory, or cognitive defects noted on exam. |
L.S., a 39 years-old female professional dancer, came to visit 4 years ago reporting bilateral swelling and pain on the medial part of the hindfoot along the posterior tibial tendon and on the lateral sides of the ankle joints. It was impossible for her to dance because of these symptoms. At the clinical examination she presented with bilateral rigid deformity of the hindfoot, calcaneus valgus, forefoot abduction, and medial arch disappearance ().\nHeel lifting experiment was positive. Routine X-ray included the anterior-posterior and latero-lateral films of the feet, assessing the severity of flat foot, osteoarthropathy and checking for other deformities and abnormalities. Radiological measurement of Meary angle, Kite angle and Pitch angle were altered ().\nAAFD was classified as type III according to Johnson and Strom classification () modified by Myerson.\nMRI examination was performed in order to understand the condition of posterior tibial tendon. After clinical and instrumental evaluation, the patient underwent Grice subtalar arthrodesis. Surgery was firstly performed on the left foot (the most symptomatic side) in December 2017. After spinal anesthesia and antibiotic prophylaxis with cefazoline, a thigh tourniquet was applied and regular iodine alcohol disinfection was used. A lateral incision was performed over the sinus tarsi: synovitis and severe cartilage degeneration were seen. After debridement and decortication of the articular surfaces, an autologous corticocancellous graft was harvested from the ipsilateral proximal tibia. The graft was prepared to appear suitable, positioned in a slightly vertical position into the sinus tarsi and then stabilized with 2 k-wires under fluoroscopic control ( and ).\nSurgery lasted 90 minutes (tourniquet has been maintained for 74 minutes) and the patient was discharged 2 days later. The limb was immobilized in a plaster cast and weight bearing was not allowed on the affected foot for 50 days. The cast and k-wires were removed 40 days after surgery and progressive weight bearing was permitted 10 days later. The rehabilitation program started with active and passive mobilizations, progressive strengthening and resistive exercises, electrotherapy and pulsed electromagnetic field therapy. X-rays performed at 2 months showed articular fusion and good osteointegration of the graft into the subtalar joint. The patient was satisfied and returned to dance 5 months after surgery with no referred pain or limitations. Because of good functional and painless long-term results, Grice subtalar arthrodesis was performed with no complication on the contralateral foot in June 2020. The surgical procedure was identical to the first time. Through lateral incision over the sinus tarsi decortication of articular surface was performed in the same way. An autologous corticocancellous graft was harvested from the ipsilateral proximal tibia, positioned into the subtalar articulation and fixed with 2 k-wires ().\nThe patient followed the same postoperative protocol (plaster cast and no weight bearing for 50 days) and follow-up. The results have been comparable with those obtained after the first intervention and finally the patient fully resumed her work 3 months after surgery. Follow-up at 8 months from second surgical procedure showed good radiological and functional outcomes ( and ).\nNowadays there are no limitations of strength and of range of motion on both sides and no pain has been reported.\nHindfoot valgus deformity and abduction of the forefoot have been reduced and the patient returned to dance with no referred pain or limitations. |
A 42-year-old male patient presented with new onset seizures with two episodes of seizure over 20 days. He also complained of severe intermittent headaches for 2 weeks. There was no history of fever. The patient did not have any other significant systemic complaints. Neurologic examination did not reveal any significant abnormality. There were no focal neurologic deficits.\nRoutine blood investigations were within normal limits and there was no evidence of electrolyte imbalance. A CSF analysis revealed increased proteins (73 mg%). CSF was negative for HIV antibodies and CSF culture was sterile.\nA contrast-enhanced CT scan was performed taking 3 mm axial sections from base of skull to the vertex after injecting 30 ml if iv contrast, on a 6 slice Seimens Somatom scanner. There was dilatation of both lateral ventricles and the third ventricle with associated subependymal transudation of CSF. A subtle well-defined rounded lesion was noted within the third ventricle. The lesion was of CSF density and showed a punctate enhancing focus within. The fourth ventricle was normal []. There were no obvious neuroparenchymal lesions. The cranial vault appeared normal. A provisional diagnosis of third ventricular neurocysticercosis was made and the patient was referred for an MRI.\nMRI of the brain was performed using a 1.5T Seimens Avanto magnet with a standard head matrix coil. Standard T1 and T2- weighted images were acquired. In addition, a fluid inversion recovery (FLAIR) sequence was also obtained.\nMRI revealed dilatation of the lateral and third ventricles with subependymal transudation of fluid. A cystic structure was seen within the third ventricle, distending it []. Furthermore, an eccentric mural nodule of intermediate signal intensity was identified. This nodule was thought to represent the scolex.\nA diagnosis of third ventricular cysticercosis causing obstructive hydrocephalus was made.\nThe patient was then taken for surgical evacuation of the cysticercus. A right parietal approach was taken with the plan of approaching the third ventricle through the right lateral ventricle. However, during ventriculostomy, no lesion was seen within the third ventricle. A VP shunt was placed in situ to decompress the hydrocephalus and the procedure was abandoned. An endoscopic third ventriculostomy was not attempted due to lack of adequate expertise and equipment.\nMRI of the brain was repeated to locate the cysticercus. The third ventricle did not reveal the neurocysticercus []. The cysticercus was now seen to have migrated into the occipital horn of the right lateral ventricle []. However, the hydrocephalus was seen to have decreased in severity compared to the previous scan.\nThe patient then received antihelminthic therapy and a repeat MRI performed after 2 months did not reveal any evidence of neurocysticercosis. |
We present a case of a nine-year-old, previously healthy boy, presenting to the emergency department of a tertiary care hospital with complaints of severe frontal headache for the last two weeks but more for the last two days. Headache was associated with nausea, vomiting, photophobia, and pain in both eyes. There was no history of fever, jerking movements, or trauma. The child had no past medical or surgical history. He achieved all developmental milestones normally and was doing well at school. His examination revealed a fully conscious and oriented child with a heart rate of 77 per minute and blood pressure of 159/112 mm Hg. Power was 5/5 on both sides, all cranial nerves were intact, and no sensory loss was observed. There were no meningeal signs but there was right side papilledema. The rest of the exam was normal. His blood investigations, including blood glucose, full blood count, serum creatinine, and electrolytes, were normal. MRI of the brain was done, after initial symptomatic management. MRI showed left temporal, extra-axial collection measuring 5.40 × 4.10 cm of CSF-like intensity compatible with arachnoid cyst and bilateral frontoparietal subdural enlargement compatible with subdural hygroma ().\nWithin an hour of ED admission the child's frequency of vomiting increased along with mild drowsiness. At that point Cushing's reflex was positive with heart rate was 64/minute and blood pressure of 177/110 mm Hg. The child was referred to the neurosurgery team and the subdural hygromas were drained through bilateral frontal burr holes. Left temporal arachnoid cyst was partially drained through left temporal craniotomy. A left subdural-peritoneal shunt was placed for drainage of any future collection. Drained CSF was xanthochromic and negative for malignant cells. CSF culture showed no growth. Histopathology of cyst confirmed radiological diagnosis of arachnoid cyst. Final diagnosis of left temporal arachnoid cyst with spontaneous subdural hygroma was made as the child presented symptomatically in the absence of any history of trauma. Postoperatively the child recovered uneventfully and was discharged on the 7th postoperative day. Any medium term CT scan was not performed. |
A 12-year-old girl presented with a 2-year history of repeated swelling and purulence behind the right earlobe and neck. The patient reported no earache, otorrhea, hearing loss, halitosis, fever, cough, or swallowing discomfort. She visited a local hospital and was diagnosed with a second branchial fistula associated with infection. The redness and swelling of the neck could not be completely cured by antibiotics.\nUpon presentation to our hospital, the skin behind the right earlobe was congestive and scabbed. A small hole was present at the right incisura intertragica (). The fistula extended to the deep surface of the parotid gland. Another fistula was seen behind the lower aspect of the right mandibular angle and at the leading edge of the middle segment of the sternocleidomastoid muscle (). The fistula coursed upward and forward (i.e., inward). Another internal fistula was found above the right pharyngopalatine arch (). Contrast agent was injected into the external fistula and an enhanced computed tomography scan was performed. The fistulas were examined on the computed tomography images (). Contraindications were excluded before surgical treatment, which was performed under general anesthesia. During the operation, the upper segment of the fistula was found to be in close contact with the cartilage of the external auditory canal. The fistula was explored successively in the parotid parenchyma, the deep surface of the main facial nerve, and the superficial surface of the posterior belly of the digastric muscle. The fistula then diverged at the lower neck behind the mandibular angle. The lower end extended into the external neck fistula, and the deep part advanced forward and inward through the surface of the vagina vasorum, the stylohyoid muscle, and the superficial surface of the hypoglossal nerve (). This fistula was found to end in the oropharynx. The fistula was completely removed (), and no complications such as facial paralysis were observed. |
A 54-year-old Nigerian woman was referred to our department for further evaluation of abdominal pain. She had no remarkable past medical history and no history of alcohol consumption, smoking and drugs. She underwent endoscopic examination during a routine checkup. Upper GI endoscopy was performed and revealed a small submucosal lesion of about 1.2 × 1 cm in diameter, located on the lesser curvature of the gastric antrum. The esophagus, duodenum and the remaining parts of the stomach were normal. Upon hospitalization, physical examination, biochemical parameters were completely normal. Endosonography demonstrated a homogeneous, hypoechoic, clearly demarcated 1.2 × 1 cm mass, which was confined to the submucosal layer and above the muscularis propria (). It was challenging to confirm the diagnosis. Because the tumor was relatively small in size, it was considered for endoscopic resection.\nHypertonic saline-epinephrine solution was injected to distinct the tumor from the muscularis propria layer and prevent bleeding. The tumor was lifted with placement of elastic bands over tissue to produce mechanical compression over the lower end of the tumor () and cut electrically with a high-frequency snare inserted, and submucosal resection was done. No post procedural complication, such as bleeding or perforation. The excised specimen showed complete removal of the lesion. Cross-sections showed the tumor to be well-defined, homogeneous, solid and of yellowish color.\nIn the resected specimen, the tumor measured 1.2 × 0.6 × 0.5 cm in diameter. Histologic appearance showed submucosa to contain a lesion which is circumscribed and composed of nets and fascicles of cells with abundant granular cytoplasm and vesicular nuclei. Wisp of collagen is seen intersecting the lesion (). The granules were positive for periodic acid-Schiff stain, and also were immunoreactive to NSE and S-100 (). The diagnosis of GCT was made. The post procedure recovery was uneventful. She remained asymptomatic and no recurrent disease was observed after a 1-year follow-up. |
A 27-year-old woman, recently bereaved due to the death of her 6-month-old daughter, came to the emergency with the sudden onset of drowsiness that lasted for 4 hours. She had no history of poisoning or drug overdose. On her physical examination, a clear observation of pinpoint pupils, bradycardia, bronchorrhea, and the drooling of saliva raised strong suspicions of organophosphate poisoning, which is usually one of the most common types of poisoning in developing countries.\nHer treatment started with the administration of intravenous atropine and pralidoxime based on her physical examination findings. A few hours later she developed seizures for which she was administered intravenous benzodiazepine. Despite treatment, the seizures continued. She was given multiple antiepileptic drugs, none of which controlled the seizures. She was then intubated due to her condition of having refractory status epilepticus and the electrolytes were normal. She was put under 24-hour EEG monitoring, which showed continuous seizure activity. CSF studies along with brain imaging to point towards any infectious or ischemic etiology for her condition were found to be negative. Meanwhile she remained on intravenous atropine and pralidoxime. Her seizures were controlled after 3 days of treatment. When intravenous administration of atropine and pralidoxime was stopped, the seizures recommenced within a few hours. Her intravenous anesthetic dose was increased and she was put on a combination of five antiepileptic medications. Based on her examination findings and clinical parameters, the treatment combo of intravenous atropine and pralidoxime was restarted. She continued to have seizures for 6 days. Finally her seizures were controlled after 10 days via application of intensive intravenous anesthetic agents, antiepileptic medications, and atropine infusion. The application of antiepileptic medications, atropine, and intravenous anesthetic agents was gradually tapered. The patient was extubated after a few days and remained well afterwards. She was discharged home on prescription of oral levetiracetam and phenytoin with neurology follow-ups. |
A 30-year-old white man was admitted to his local hospital after he was found unconscious in his home. His past medical history included a history of drug abuse, bipolar disorder and chronic hepatitis C. He had no history of headaches. The family reported that he was last seen when he returned home the same morning about 5 hours prior to admission. Before he went to bed, he had told them that he was assaulted on his way home, and had been beaten and kicked several times to the head. There was no reported loss of consciousness. His only complaint before he went to bed was of a mild headache. Five hours later a family member called for an ambulance, as he was not responding adequately to speech or other stimuli.\nIn the emergency department he had a Glasgow Coma Scale (GCS) [] score of 8 and anisocoria with a slight right-sided pupillary dilatation. He had bruises on his face and thorax, as well as a periorbital swelling. There were no signs of cerebrospinal fluid (CSF) rhinorrhoea or otorrhoea. He was otherwise clinically stable with normal vital parameters (blood pressure 125/60mmHg, regular heart rate/pulse 75/minute, oxygen saturation 100 %). The initial examination performed by a trauma team included X-ray imaging of his thorax and pelvis, that were found normal, as well as ultrasound of his abdomen, which showed no sign of free fluid. Imaging with computed tomography (CT) of his head revealed a 10cm×4cm expansive epidural lesion in the right temporoparietal region causing significant anteromedial compression of the right lateral ventricle and a midline shift of 7mm (Fig. and ). The lesion had the attenuation values of air (−1000 Hounsfield units), and there were no signs of intracranial bleeding. There were no signs of herniation. CT also demonstrated a communication between the right mastoid sinus and the epidural space, and a fracture was suspected (Fig. ). He was immediately intubated and transported by helicopter at sea level to the nearest neurosurgical department, located approximately 180km away, where an emergency burr hole evacuation was performed to equalize the pressure. He experienced immediate recovery and was extubated the same day. In the evening he had a full GCS score of 15. On examination there were no neurological deficits. A postoperative control CT the first postoperative day showed a small epidural bleed in the compartment that previously was filled with air, but the majority of the epidural air was removed and the midline was normalized (Fig. ).\nThe following days he deteriorated and consecutive CT scans demonstrated increasing air entrapment. An indication for more invasive surgery was found, and a craniotomy with cranialization and sealing of the mastoid sinus with autologous musculature, an absorbable fibrin patch (Tachosil®) and fibrin glue (Tisseel®) was performed, to prevent further air entrapment. The dura was intact, and there was no leakage of cerebrospinal fluid. During the procedure several bony defects were found in his mastoid bone, and a mucosal membrane arising from the mastoid sinus found adherent to his skull and dura mater (that is, a mucocele) was removed.\nHe recovered quickly from this procedure, and postoperative CT scans were satisfactory, with re-expansion of the dura, resolution of the midline shift, and only minor residuals of the epidural air. He was discharged from the hospital 15 days after admission.\nUnfortunately, 4 weeks later he deteriorated again, and complained of increasing headaches and diplopia. Renewed CT scans revealed increasing entrapment of the residual air, and a second surgery was performed. The same procedure was repeated, and a recanalization of the defect in the bone was found. Again, thorough sealing was obtained with bone wax, a fibrin patch and fibrin glue, and this time it ultimately turned out to be successful. The latest follow-up CT scan performed 4 months later was still found to be satisfactory. |
A 91-year-old female patient visited our hospital. She was in good condition and walked very well for her age. While she was getting on a bus, she lost her footing and fell backwards onto the ground. She was unable to walk because of severe back pain, but the initial physical examination did not show neurologic deficit. She did not complain of sensory decrease and the lower extremity motor grade was more than grade 4 on both lower legs. The initial plain radiographic study showed a fracture at the anterosuperior portion of the thoracic eleventh (T11) vertebral body (). Also, we suspected oblique fractures at the spinous processes of T9 and T10 vertebrae, and therefore conducted computed tomography (CT) to confirm fracture characteristics as we diagnosed (). The L2 vertebral body fracture was diagnosed as an old compression fracture. Because the fracture involved the posterior column, which are spinous process fractures, magnetic resonance imaging (MRI) was required. On MRI, acute benign fracture was shown at the anterosuperior portion of the T11 vertebral body with hemorrhage of the fracture site (). Hemorrhage within the disc was also seen at the T10 to T11 space. The posterior column including spinous process and interspinous ligament had high signal intensity on T2-weight MRI. The ALL was disrupted with the bony fragment attached. Although the interspinous ligament showed a high signal, the signal intensity within the spinal cord was not increased.\nConsidering the patient's age and the absence of neurologic deficit at the initial phase, conservative management was chosen. Also, bony lesion, vertebral body and spinous process fractures, were more prominent than soft tissue lesions, and we expected only bony union. On day two of hospitalization, we applied thoraco-lumbo-sacral orthosis and started standing physical therapy including tilt table. On seventh day, follow-up plain radiographic showed slightly reduced the fracture site of the T11 vertebra (). Until day 19, she could stand for 20 minutes but couldn't walk by herself. She did not complain of any neurologic change until then.\nOn day 20 of hospitalization, she complained of lower extremity weakness, and general lower extremity motor grade was decreased to grade 1 or 2. Sensory functions may have also been slightly decreased. She said the symptoms gradually aggravated over the last three days and she couldn't remember any significant event before the appearance of the neurologic deficit. Knee jerk and ankle jerk of both lower legs were accelerated. Ankle clonus and babinski sign were positive. We immediately conducted a follow-up plain X-ray and MRI (). The fracture was not more displaced compared to previous imaging, but the intervertebral disc of T10 to T11 space was extruded with superior migration, compressing the spinal cord with compressive myelopathy.\nWe immediately did surgical decompression (spinous process resection and total laminectomy from T9 to T12), pedicle screws instrumentation and then fusion of T9 to T12 with morcellized allograft (freeze-dried human allograft) and demineralzation bone matrix (). Operation finding showed the dura of the spinal cord was intact. We couldn't remove the herniated disc for fear of further spinal cord injury. Three days after operation we started again standing physical therapy. Three months following surgery, she regained lower extremity motor strength to the grade 4. She could walk with a walker. |
Patient “FT” is a 7-month-old girl with a history of d-transposition of great vessels with side-by-side vessels and a single coronary artery arising anteriorly and coarctation of the aorta. She initially underwent an arterial switch and coarctation repair with augmentation of the aortic arch in the newborn period. Three months later, she presented with severely elevated right ventricular pressures and was found to have hypoplasia of the neopulmonary valve with subvalvular obstruction. She underwent infundibular resection with the placement of a 9 mm pulmonary homograft conduit from RV to PA with right PA angioplasty. The native connection to the pulmonary arteries was left open.\nAt a routine follow-up visit four months later, the patient's mother reported feeding intolerance with solids only, with frequent gag initiation. The patient was also noted to have mild tachypnea and fussiness when she was supine and constantly wanted to be held in upright position. On physical examination, her oxygen saturation was 98% on room air. There was a Grade II/VI to-and-fro murmur heard best at the left upper sternal border. The chest radiograph revealed widening of the anterior mediastinum in the region of the PA []. Transthoracic echocardiography showed normal biventricular function and a large fluid collection anterior to the RV []. A subsequent cardiac magnetic resonance imaging (MRI) demonstrated a large PSA in the anterior mediastinum related to the RV-PA conduit measuring 5.5 cm × 3.3 cm × 7.1 cm in transverse, anteroposterior, and superoinferior dimensions, respectively []. The neck of the aneurysm measured 1.5 cm × 2.5 cm. The ascending aorta was displaced posteriorly secondary to its mass effect. She underwent open heart surgery the next day. Cardiopulmonary bypass was achieved through cervical incision. The right common carotid artery and internal jugular vein were heparinized and cannulated. Once the patient was cooled to 22 degrees, sternotomy was done. During her previous surgery, a Gore-Tex membrane was placed which basically served as the anterior portion of the capsule of the PSA. This membrane was removed which revealed a massive PSA extending from the base of diaphragm to the innominate vein and included the entire homograft. The native connection from the RV to the pulmonary arteries was still patent. There was stenosis of the origin of the right and left pulmonary arteries. The entire capsule of PSA was excised and replaced with a 15 mm pulmonary homograft. The patient did well thereafter and was discharged on postoperative day 8 with a normal echocardiogram on the day of discharge. |
A 16 year and 7-month-old African American female, who participates in multiple sports including cheer, softball, and competitive volleyball, presents with 5 months of worsening atraumatic bilateral anterior leg pain. She normally trains 6 h per day and 4 days per week. Initially, her pain only occurred with sports-related activities; however, after a recent 3-day volleyball tournament, her pain acutely worsened, yet improved with rest.\nShe denied prior history of stress fractures, multiple previous fractures, and a family history of bone diseases, such as osteogenesis imperfecta. She is otherwise healthy with menarche at age 11 and reported normal cycles. The mother reported the patient had no dietary concerns but could be eating healthier. The patient had a normal BMI, with no concerning signs of metabolic or hormonal abnormalities.\nAfter obtaining radiographs and a physical exam, the patient was found to have bilateral multiple anterior cortex mid-tibial diaphyseal stress fractures. Three focal lucencies were noted over the anterior cortex of the right mid-tibial diaphysis and one over the left with bilateral cortical thickening and periosteal reaction ().\nBone metabolic labs and bilateral lower extremity CT scans were obtained. The patient's serum calcium was normal at 9.4 mg/dL, but her 25-hydroxy vitamin D resulted low at 17 ng/mL, and she was diagnosed with vitamin D deficiency. All other labs were noted to be within normal limits. She was started on high-dose vitamin D at 50,000 IU weekly for 8 weeks, and was referred to a registered dietician for consultation. CT scan of the bilateral lower extremities demonstrated additional smaller lucent defect in the left anterior cortex proximal to the stress fracture noted on x-ray.\nThe atypical nature of multiple stress fractures and a low vitamin D level were concerning for possible prolonged healing. After extensive discussion with the patient and parents regarding activity level and risks of operative management, they wished to proceed with surgery for a potentially faster return to competitive volleyball in hopes of obtaining collegiate scholarships. She first underwent a transpatellar tendon reamed intramedullary nailing of the more symptomatic left tibia with proximal and distal locking screws (). She underwent IM nailing of the contralateral tibia 6 weeks later. She attended physical therapy shortly after the right tibial procedure, focusing on a sport-specific return to play. Three and a half months after surgery, she reported the pain had dramatically improved and was cleared to gradually return to sports. Improvement in radiographic appearance of the linear lucencies was appreciated. At the 1-year post-operative follow-up, the patient had returned to full sports (HSS Pedi-FABS = 23) and reported minimal anterior knee pain with impact-related activities. She transitioned her vitamin D supplements to 1,000 IU QD, and her most recent 25-hydroxy vitamin D level was noted to be normal at 41 ng/mL (). |
A 36-year-old male presented to the outpatient department with a history of low backache for the past one year, associated with typical claudication symptoms, left-sided unilateral numbness, and paresthesia of the foot. He gave no history of radicular pain, but he complained of progressive reduction in claudication distance. He had experienced a sudden deterioration in gait along with urinary incontinence, following a trivial traumatic fall, one week before presentation. There was no history of constitutional features. On examination, he had a bilateral high-stepping gait due to foot drop. Symmetrical weakness of both the L4 and L5 roots (MRC grade 0/5) and partial weakness of the S1 root (MRC grade 3/5) was noted with nondermatomal sensory disturbances. Deep tendon reflexes of the lower limbs were absent bilaterally. Though anal tone was normal, saddle anesthesia was present. Postvoidal ultrasonogram of the urinary bladder revealed a residual urine volume of 250 ml, thus confirming a neurogenic bladder.\nPlain radiography of the lumbar spine did not show any gross feature of instability and was inconclusive (). Magnetic resonance imaging (MRI) of the lumbar spine revealed a solitary intraspinal posterior epidural lesion of 1.8 × 1.5 × 0.5 cm at the L2-L3 level with heterogeneous signal intensities and adjacent epidural fatty hypertrophy contributing to severe canal stenosis (3 mm). The cauda equina was severely compressed and was almost not visible (). Owing to the heterogeneous signal intensities, computerized topography (CT) was performed which revealed the presence of an osseous lesion attached to the right L2 inferior articular process causing severe secondary canal stenosis (). Considering the recent-onset neurological deficit, the patient was advised surgical decompression and excision biopsy at the earliest. The patient was positioned prone on a Relton Hall frame under general anesthesia. A standard midline posterior approach was employed and L2 and L3 lamina were exposed. The spinous process was removed and using a motorized burr, a rectangular trough was created surrounding the lesion. The lamina was thinned out using a burr to avoid further insult to the dural sac, and then using a Kerrison ronguer, laminectomy was completed all around the lesion under microscopic guidance (). A small osteotome was used to remove the attachment on the right side which required partial removal of the facet joint. The lesion was then held, and the adherent soft tissues beneath the lesion were removed, resulting in en bloc removal and complete decompression of the cauda equina. Fusion was performed, as the procedure involved partial facet joint resection. The lesion was sent for histopathological examination. There were no adverse events or postoperative complications. The patient was mobilized with bilateral orthoses, and bladder training was initiated.\nAt 4 weeks, there was an improvement in his urinary symptoms, and by 12 weeks partial neurological recovery (MRC grade 3/5 motor power) in bilateral L4 and L5 was observed. The S1 root power increased by one grade (MRC grade 4/5). His gait improved thereafter, and he was able to return to his normal activities by 6 months with further neurological improvement by 1 grade in all roots.\nThe gross specimen measured 2 cm × 1.5 cm × 1.5 cm. It was greyish white in color and firm to hard in consistency (). It had a well-defined capsule and had the feel of particulate materials on cut sections. Histopathological examination revealed the presence of bone, cartilage and ligamentous tissue, and zones abutting all these composed of mature adult-type encapsulated adipose tissue (Figures and ). This confirmed the diagnosis of benign osteolipoma. |
In June 2016 a 54-year-old white woman was admitted for treatment of her chronic major depressive episode in the course of a major depressive disorder as well as panic disorder. She complained of severely depressed mood, loss of pleasure and interest, loss of drive and energy, disturbed sleep, and increased weight. The current depressive syndrome began approximately 5 years before admission. Her first episode occurred 36 years ago at the age of 18. Moreover, she had spontaneous and situationally induced panic attacks with severe avoiding behavior that did not allow her to leave the house by herself for at least 2 years. She lives with her husband (married for 22 years) in a house and has two adult children.\nShe has hypertension, which is treated with 5 mg ramipril, and adiposity. Between the age of 10 and 16 she sleepwalked once a month. No other physical illness is known.\nTen years ago a therapy with doxepin, venlafaxine, and lithium was started. Episodes of dysfunctional eating at nighttime made their first appearance in the course of this treatment. Observed by her husband approximately once or twice a week she had nightly eating and SRE, mostly without any recall in the morning. During these episodes, she ate large amounts of unusual foods (glass jars of marmalade, several bars of chocolate, and so on), brought food into her bed, and gained approximately 20 kg in the last years. SRE started with a frequency of approximately once a week and continued after the cessation of drug treatment. From 2015 to 2016 she took doxepin once or twice a week when she felt sleepless. Besides this she was on no other medication. During these nights with intake of doxepin she noticed SRE events. She became aware of the nightly eating through food wrappings in her bed and her husband confirmed the consumption through observance. Her body mass index (BMI) was 48.8 kg/m2 at admission to our hospital. She had normal blood values except for cholesterol (217 mg/dl), C-reactive protein (CRP; 17.4 mg/l; permanently until discharge), gamma-glutamyltransferase (GGT; 44 U/l), and blood glucose (123 mg/dl). Urine analysis was within normal limits. Her blood pressure was 140/90 mmHg under medication with ramipril 5 mg. An electroencephalogram (EEG), electrocardiogram (ECG), and thyroid scintigraphy showed no pathological result. A magnetic resonance imaging (MRI) was refused on the basis of her panic disorder and accompanying anxieties.\nA head, eye, ear, nose, and throat physical examination was within normal limits. A chest examination was clear to auscultation bilaterally. An examination of her heart was notable for a normal S1, S2, and it was without rubs, murmurs, or gallops. Her pulse was 84 beats/minute. Her abdomen was soft, obese, with no organomegaly, and normoactive bowel sounds in all quadrants. A neurologic examination revealed that all her cranial nerves were grossly intact. Her strength was 5/5 throughout with 2+ reflexes. Her sensation to fine touch was intact throughout.\nIn our hospital, SRE continued under antidepressant treatment with sertraline plus doxepin. Under therapy with 150 mg sertraline, 50 to 100 mg melperone, and 150 to 300 mg bupropion the frequency of nighttime eating increased to at least once a night (Fig. )\nWith regard to sleep disorders, in the presence of severe adiposity, we found evidence for a moderate sleep apnea syndrome with an apnea–hypopnea index of 6.9 per hour in polygraphy. She complained about an irresistible urge to move her legs almost exclusively during nighttime, with temporary relief from this urge during movements, but had no sensations of pain or other unpleasant sensations and, therefore, did not completely fulfil the criteria for restless legs syndrome.\nIn order to treat SRE we added 50 mg agomelatine, which is in accordance with reports of treatment of a similar disorder, nighttime eating []. During the following 14 nights, SRE completely vanished and reoccurred after stopping agomelatine for a week. Then we added 4 mg melatonin extended release and again, immediately, SRE vanished and she lost 3 kg of weight in the following 3 weeks. Her BMI fell to 46.5 kg/m2 and she lost 6.1 kg in total at discharge from our hospital. A follow-up 2 months after discharge showed a further reduction of her BMI to 45.7 kg/m2. At the second follow-up 10 months after discharge we found that she remained well until 5 months after discharge and then developed a further episode of major depression mainly attended by avoidance behavior. She refused complementary individual and group psychotherapy as well as her support group. A voracious appetite emerged during the day and she consumed a huge amount of fast food through which she gained weight up to a BMI of 49.4 kg/m2. Nightly eating occurred up to once a week from that time on but never again reached a level of seven times a week as in August 2016. |
A 66-year-old male with a history of hypertension arrived at the emergency department with cardiac arrest. On arrival, he was comatose and electrocardiography confirmed that his heart had stopped. Thus, cardiopulmonary resuscitation (CPR) was continued. The emergency medical service providers accompanying the patient reported that they had been dispatched to the scene after receiving a call about an explosion in a building. When they arrived at the site, they discovered two unconscious people lying on the floor. One of the two was our patient. With the patient not having received any bystander CPR, the emergency medical service providers promptly initiated CPR, and inserted a laryngeal mask airway before transporting him to our emergency medical center. It took about 20 minutes to get to the hospital.\nThe patient’s initial arterial blood gas analysis showed the following results: pH 6.63, partial pressure of carbon dioxide 201.6 mmHg, partial pressure of oxygen 8.9 mmHg, capillary oxygen saturation 3.0%, and bicarbonate 20.6 mmol/L. After receiving six minutes of CPR at the emergency department, the patient had a return of spontaneous circulation. Electrocardiography directly after the return of spontaneous circulation showed atrial fibrillation, but no remarkable ST segment changes. The results of bedside Focused Abdominal Sonography for Trauma, and transthoracic echocardiography, were normal. Portable chest radiograph showed no active lung lesions. His non-enhanced brain computed tomography showed no evidence of acute intracranial hemorrhage. After starting a mechanical ventilation, serial arterial blood gas analysis findings improved rapidly. Carbon dioxide concentration decreased rapidly, and it returned to normal within half an hour ().\nLater, police officers visited the emergency room to check the patient’s condition. They showed a closed-circuit video of the explosion, and informed the medical staff about what had happened in more detail. A closed-circuit camera was not installed in the room where the explosion had occurred, but a camera was located in the passageway directly outside the room. They did not have information on the dimensions of the room, or the characteristics of the tank that had exploded but specified that the tank contained carbon dioxide. On being informed of the explosion, two supervisors approached the room in which the explosion had occurred, without wearing any protective equipment, but they did not enter it. Within a few seconds, they became unconscious and collapsed to the ground without any warning.\nEven though the patient recovered spontaneous circulation within 26 minutes, he failed to restore his mental function in the emergency department, and started showing jerking movements, which raised the possibility of a seizure from carbon dioxide toxicity or hypoxic brain damage. After consulting with a neurologist, the patient underwent a portable electroencephalogram (EEG), which showed generalized epilepsy (). He was admitted to the intensive care unit (ICU) under the care of the pulmonology department. EEG and diffusion magnetic resonance imaging were recommended after neurology department consultation a few days after ICU admission. A portable EEG, done three days after the patient’s ICU admission, showed severe diffuse cerebral dysfunction (). Diffusion magnetic resonance imaging, performed two days later, showed that he had hypoxic brain damage (). A chest radiograph, taken the same day revealed increased haziness in the left lower lung field, indicating the presence of pneumonia (). C-reactive protein levels, measured daily for patient monitoring, gradually increased. After starting antibiotics, C-reactive protein level soon decreased to within the normal range. A follow-up EEG, done 6 days after his admission showed no significant interval change (). As the patient’s mental function had not improved, his family requested that he be transferred to another hospital for supportive care. The patient was transferred to a neighboring hospital on the seventh day of his hospitalization. |
Our patient is a 59-year-old female with a significant past medical history of hypertension, iron deficiency anemia, and tobacco dependence amounting to a 40-pack-year smoking history. She initially presented to her primary care physician (PCP) with a 6-month history of generalized fatigue with associated symptoms of anorexia and a 20-pound unintended weight loss. Fearing the possibility of a lung cancer, her PCP obtained a computed tomography (CT) scan of the chest, which showed a 3-mm nodule in the right lower lobe of the lungs, multiple heterogeneous hepatic lesions, the largest of which measured 7.2 × 5.6 cm, and a hypoattenuating lesion measuring 4.8 × 3.1 cm at the tail of the pancreas (Fig. ). A follow-up CT scan of the abdomen and pelvis re-demonstrated these findings with multiple enlarged periaortic lymph nodes. At the same time, her laboratory test revealed elevated liver transaminases and cancer antigen 19-9 level. An ultrasound-guided core biopsy of the liver was performed and histology confirmed liver lesions to be small-cell carcinoma, poorly differentiated. Positron emission tomography (PET) scan showed uptake consistent with malignancy in the liver and pancreas, but no PET-avid lesions were seen anywhere else.\nAfter discussing the diagnosis and treatment options with the patient, she elected to proceed with palliative chemotherapy. She was started on a standard regimen of carboplatin and etoposide. Restaging scans after two cycles showed great response with some reduction in the sizes of both the hepatic and pancreatic lesions. The subsequent imaging after 6 cycles showed a stable disease. She was at this time referred to a tertiary teaching hospital where she was evaluated for a clinical trial but was found ineligible to participate. Unfortunately, repeat CT scan of the abdomen and pelvis 2 months after completing 6 cycles of palliative chemotherapy showed disease progression with increase in the sizes of the previously seen hepatic lesion and new metastatic lesions. She was subsequently started on topotecan. A restaging scan performed after cycle 2 of second-line palliative chemotherapy showed further disease progression (Fig. ). She had a good ECOG performance status of 1. We reviewed the treatment goals and options with the patient once again. We introduced the idea of a trial of nivolumab based on preliminary results of CheckMate 32 studies showing favorable outcomes for the treatment of recurrent SCLC and she welcomed the idea. A repeat CT scan after 5 weeks and 4 doses of nivolumab treatment showed a reduction in size of the largest hepatic lesion from 7.2 × 6.6 cm to 4.8 × 3.7 cm and the number of hepatic metastases. Similarly, the pancreatic tail mass was decreased in size from 3.7 × 3.5 cm to 3.6 × 2.4 cm (Fig. ). |
A 55-year-old female with a history of renal cell carcinoma of the left kidney metastatic to the bony pelvis, lungs, mediastinum, and spleen presented to the emergency department with shortness of breath, pleuritic chest pain, and left scapular pain. She presented to the same emergency department one week prior with pleuritic chest pain but was discharged home after pulmonary embolism was ruled out.\nShe was diagnosed with renal cell carcinoma of the left kidney five years prior after presenting with gross hematuria. At that time, she underwent left radical nephrectomy. One year later, she developed a metastatic lesion in the bony pelvis for which she underwent radiation therapy. She as treated with pazopanib for two years with stable disease but stopped due to gastro-intestinal toxicity. Therapy was switched to nivolumab, which was discontinued after six months due to grade four pancreatitis and grade two rash. Eight months prior to her current presentation, she underwent radiation treatment to metastatic lesions in the left pubic symphysis and spleen. The patient initiated therapy with cabozantinib, a tyrosine-kinase-inhibitor used to treat renal cell carcinoma, three months prior to her current presentation.\nOn physical examination, she was wheezing in all lung fields and hypoxemic requiring supplemental oxygen. She had prior 12-pack-year smoking history but no formal diagnosis of chronic obstructive pulmonary disease (COPD). A chest x-ray revealed a small left pleural effusion and left basilar atelectasis. Laboratory workup, including complete blood count, renal and hepatic panels, and troponin, was unremarkable. An electrocardiogram (ECG) revealed sinus tachycardia without signs of ischemia. CT was not repeated due to her negative CT angiogram one-week prior. Given radicular and left scapular pain, an MRI of the spine was done, which revealed no pathologic metastases in the thoracic or lumbar spine but did reveal a new sacral lesion. Given her progressive stridor, she underwent laryngoscopy, which revealed a normal upper airway. A bronchoscopy showed significant trachea-bronchomalacia and thick purulent secretions in the left upper lobe, lingula, and right upper lobe.\nTwo days after admission, repeat chest X-ray revealed near complete opacification of left lung and large pleural effusion, a remarkably different radiograph from admission (Figure ).\nSubsequent CT chest revealed a large left pleural effusion with partial loculation as well as partial atelectasis of the left upper lobe and complete atelectasis of the left lower lobe. A right perihilar metastasis and perisplenic metastases were reported. The study was negative for pulmonary thromboembolism.\nThoracentesis revealed cloudy straw colored exudative effusion. A four French pigtail catheter was placed. Approximately 400 milliliters of yellow-green fluid was immediately drained. Pleural fluid studies revealed a white blood cell count of 33,000/μL (97% neutrophils), pH of 6.44, LDH of 4760 U/L, and an amylase of 394 U/L. She was started on vancomycin, cefepime, and metronidazole for presumed empyema. Pleural fluid cultures showed heavy growth of lactobacillus species, heavy growth of anaerobic gram negative cocci, and moderate growth of Candida krusei. Antimicrobial therapy was subsequently narrowed to ertapenem and anidulafungin. Given lack of improvement and continued significant chest tube output over the following week, further CT imaging was obtained, revealing a gastro-pleural fistula (via the left diaphragm and superior posterolateral stomach) with associated complex pleural effusion containing contrast material and gas (Figure ). This process abutted the known splenic metastases.\nAn esophagogastroduodenoscopy (EGD) revealed a 1.5-cm fistula in the posterolateral stomach that opened to the pleural space (Figure ).\nEndoscopic suturing was attempted to close the fistula with limited success (partial closure noted on imaging, with methylene blue dye taken via mouth visualized in the chest tube drainage catheter on water seal; Figure ).\nFor complete closure, the authors attempted a novel approach utilizing a venting gastrostomy tube and chest tube to water seal to facilitate closure of the fistula over the ensuing six weeks. Enteral feeding via jejunostomy tube to aid closure of the fistula was employed. The patient was continued on ertapenem and anidulafungin. She was also initiated on a proton pump inhibitor. She was discharged to a rehabilitation facility with plans to repeat imaging and methylene blue swallow in six weeks.\nUnfortunately, CT scans after six weeks showed that the fistula remained patent. A second attempt was made at endoscopic closure, which was again unsuccessful. One month later, during a hospitalization for electrolyte abnormalities, the patient decided to pursue elective surgical repair of the fistula in hopes of regaining the ability to resume normal oral intake. Four months after her initial presentation, she underwent laparoscopic surgery for fistula repair. The surgeon visualized extensive radiation fibrosis involving the stomach, spleen and retro-peritoneum. Given these findings and to avoid splenic bleeding, they pursued a conservative surgery whereby they stapled the stomach to ligate the gastro-pleural fistula anatomically. This approach is novel and was successful in our patient. A fluoroscopic upper GI series with oral contrast three days after surgery demonstrated no leakage of contrast outside of the GI tract or into the pleural space, and CT five days after surgery revealed no evidence of communication between the stomach and pleural space (Figure ).\nShe tolerated an oral diet. Gastrostomy tube, jejunostomy tube, and chest tube were removed without complication. |
A 38-year-old Caucasian woman, 35 weeks into her first pregnancy, presented to the emergency department for acute right-sided hip pain which precluded weight-bearing. Her right leg was shortened and externally rotated - there was no bruising or evidence of trauma.\nThe patient’s history was significant for hereditary thrombophilia (Factor V Leiden) and secondary anemia. Hip radiography revealed an unstable, displaced, right-sided femoral neck fracture with no evidence of osteonecrosis (Figure ). The decision to administer radiography, in this case, was based on the American College of Radiology guidelines, which cite an absence of in-utero deterministic effects of ionizing radiation effects after 27 weeks of gestation. Unfortunately, it was not possible to evaluate the symptoms of the patient with MRI at this time due to the coronavirus disease pandemic-induced stress on the healthcare system of our country.\nThe patient denied falls or trauma during the pregnancy, nor was there any history of smoking, alcohol abuse, use of glucocorticoids, or presence of rheumatologic/oncologic disease. Additionally, the patient was not malnourished, she underwent routine antenatal care, and took multivitamins. Serologic tests for inflammatory markers, as lab tests for serum calcium, phosphate, alkaline phosphatase, parathyroid hormone, vitamin D, and D-dimer returned normal.\nDuring multidisciplinary rounds, it was decided that delaying surgery was the best course of action out of fear of causing either mechanical or fluoroscopy-induced damage to the fetus during total hip arthroplasty. Five days later the patient experienced premature rupture of membranes, which was managed with emergency cesarean section (C-section) - no complications were encountered and a healthy 2300 g female was successfully delivered. Three days later the patient was transferred to our orthopedic surgery department for the treatment of the fracture. The significant degree of displacement (grade IV) of the fracture lasting over one week precluded open reduction with internal fixation due to fears of femoral head necrosis. During our literature review, we encountered a similar case of femoral neck fracture with grade IV displacement that was treated with open reduction internal fixation - despite restoration of blood flow to the femoral head within 15 hours, the authors still encountered femoral head necrosis with collapse six months later []. Given the considerable delay between symptom presentation and treatment, we decided the case warrants total hip arthroplasty instead of native hip salvage. Hemiarthroplasty was considered but was ultimately discarded as the conversion rate to total hip arthroplasty in young patients remain relatively high and the fracture was subsequently treated with a total uncemented prosthesis (Figure ), consisting of a 50 mm cup with 32 mm ultra-high-molecular-weight polyethylene insert and a 32 mm head with a 4 mm ceramic insert (Link Inc., Hamburg, Germany). Postoperative radiography confirmed prosthesis placement (Figure ); antibiotic and anticoagulant prophylaxis was initiated with ampicillin/sulbactam and enoxaparin sodium, respectively.\nThree days after the intervention the patient developed moderate abdominal pain without fever and accelerated intestinal transit, which both worsened over the next four days. Given the clinical presentation, there was a high index of suspicion for infection with Clostridium difficile (C. diff), although the diagnosis was ambiguous as the enzyme immunoassay (EIA) for the C. diff-specific antigen glutamate dehydrogenase was positive, while EIA for exotoxin A and B were negative. Due to exacerbation of symptoms and development of moderate hypokalemia (2.9 mEq/L), empiric treatment with metronidazole was began and marked rapid improvement. The patient was discharged five days later. |
An otherwise healthy 2-year-old African-American female presented to the emergency department with episodic abdominal pain for 12 hours. There were no bloody stools, diarrhea, or vomiting. There were no symptoms of recent upper respiratory infection. Physical exam showed a nontender abdomen without palpable mass.\nAn abdominal ultrasound identified ileocolic intussusception in the right and transverse colon (B and C). Color Doppler signal was present within the intussusception, and there was no entrapped fluid or lead point mass. A supine radiograph identified a tubular mass in the expected location of the transverse colon representing the intussusception (A). There was no preprocedural pneumoperitoneum.\nPrior to the reduction attempt, an intravenous catheter was placed, surgical consult was obtained, a nurse accompanied the patient to the fluoroscopy suite to monitor the patient during reduction, and written consent for reduction was obtained from the patient's mother, who also accompanied the patient. The patient was not sedated.\nA lubricated 20 Fr Foley catheter (E) was inserted into the anus and the retention balloon was inflated with 30 mL of air in the rectum under fluoroscopic visualization. Hand-sphygmomanometer insufflation of air through the catheter through a 3-way connector with a pressure release valve in supine and prone positions was capable of reducing the intussusception to the ileocecal valve under fluoroscopic guidance but air could not be refluxed into the terminal ileum. Air leaks prevented further reduction as intracolonic pressures approached 80 mm Hg, and the patient expelled the catheter with the balloon inflated despite manual pressure held on the tube and buttocks. Residual intussusception at the ileocecal valve was confirmed with ultrasound. An external tape plug and anal occlusion disc were then placed around the exterior side of the Foley catheter, the internal balloon was inflated with 30 mL of air, and the catheter was taped to the buttocks. Again, air leaks at 80 mm Hg disallowed further reduction, and the patient expelled the catheter.\nNext, a lubricated 30 Fr double balloon-tipped catheter () was placed per rectum (F). The internal balloon inflated with 50 mL air, and the external balloon inflated with 70 mL air (the maximum volumes recommended by the manufacturer). During insufflation the patient expelled the catheter 3 times and the procedure was concluded. A filling defect remained at the ileocecal valve (G) and there was no post-procedural pneumoperitoneum. Total procedural time was 1 hour. The patient was admitted for observation. Surgery consultation recommended repeating ultrasound if symptoms of episodic abdominal pain recurred. The patient resumed a normal diet and activities.\nEighteen hours later after the patient experience repeated symptoms of episodic abdominal pain, ultrasound identified recurrence of the ileocolic intussusception in the ascending colon (A and B) without lead point mass, entrapped fluid, or absence of Doppler signal.\nThe patient received 5 mg intravenous lorazepam per mother's preference for sedation, and was returned to the fluoroscopy suite after obtaining consent for intussusception reduction, again accompanied by her mother and a nurse for intraprocedural monitoring. A lubricated 30 Fr double balloon-tipped catheter was placed per rectum. The internal was balloon inflated in the rectum under fluoroscopy with 50 mL water and external balloon inflated with 70 mL air. Hand-sphygmomanometer insufflation with the patient in the prone position achieved sustained intracolonic pressures of 80-100 mm Hg with a notable reduction in rectal air leakage. Air was refluxed into the terminal ileum (E) and there was no filling defect at the ileocecal valve. There was no post-procedural pneumoperitoneum. Total procedural time from insertion to removal of the catheter was 5 minutes. The patient was discharged home the same day and has had no further procedures or symptoms as of this writing. |
A 65-year-old male, presented with crescendo angina on minimal exertion and was diagnosed with a non-ST elevation myocardial infarction. He had a background history of type 2 diabetes mellitus (T2DM), ischaemic heart disease with a previous myocardial infarction 11 years prior, hypercholesterolaemia, hypertension and a long-standing history of smoking.\nA preoperative transthoracic echo (TTE) revealed left ventricular hypertrophy with an ejection fraction of 75%, no mitral or aortic valve abnormalities and trivial tricuspid regurgitation. He was scheduled for a coronary artery bypass graft (CABG) procedure 5 days after his initial presentation. TOE is used routinely at our institution for all cardiac procedures as part of routine monitoring and patients are consented for its use.\nThe procedure was complicated surgically by poor targets for revascularization leading to a longer-than-expected case. Following an apparently easy and what was described as an atraumatic placement of the TOE probe, the anaesthetist had difficulty obtaining clear TOE images. The transgastric views in particular were noted as being unusual and a second cardiac anaesthetist was called on for assistance. The TOE probe was removed and reinserted presumably in an attempt to improve image quality and exclude any previously undetected damage on the TOE probe transducer that could explain the poor image quality. On removal of the probe, it was noted that there was fresh blood on the probe and further blood was suctioned from the pharynx. On reinsertion, it was still not possible to obtain good-quality views and the transgastric views in particular were still noted to be abnormal.\nAfter the initial attempt post revascularization to separate from cardiopulmonary bypass failed, the decision was made to go back on to bypass to initiate further cardiac support. The patient stabilized after insertion of an intra-aortic balloon pump (IABP) and initiation of 0.1 µg/kg/min of adrenaline for transfer to the intensive care unit (ICU) post-operatively. Total theatre time was more than 9 h. On arrival in ICU, the attending anaesthetist noted their concerns regarding the problems with obtaining TOE images and the possibility of oesophageal injury.\nThe patient was taken back to theatre later that night for a re-exploration and a clot was discovered and removed from the chest. He required further blood and products post-operatively with an increased adrenaline requirement on return to ICU. The diagnosis of oesophageal perforation was made the next morning following a failed attempt at nasogastric tube (NGT) placement and after appropriate further investigation. A gastroscopy performed in the ICU revealed an undiagnosed hiatus hernia and an oesophagogastric perforation.\nThe oesophagogastric perforation was initially managed conservatively with the placement of a covered gastric stent. Unfortunately, the patient became septic after a few days and developed a ventilator-acquired pneumonia, most likely due to the ongoing free reflux post stent placement. A follow-up chest CT scan revealed that a collection had developed around the perforation. Thirteen days post CABG, he returned to theatre for a thoracotomy and drainage of the peri-oesophageal collection.\nThe patient’s time in ICU continued to be complicated as he developed a right hemiparesis, required ongoing inotropic support, failed attempts at extubation and remained dependent on the IABP support. His pneumonia continued to worsen with ongoing subclinical aspirations. Despite drainage of the peri-oesophageal collection, he developed worsening sepsis and passed away in ICU on day 25 post surgery.\nThis case highlights the potentially devastating consequences of an oesophageal perforation following the use of TOE. The inability to obtain clear TOE images (transgastric in particular), and the presence of fresh blood on removal of the TOE probe, should alert the clinician to a potential oesophageal perforation as part of their differential diagnosis. In this case, the undiagnosed hernia may have further contributed to the difficulty obtaining good TOE images. In addition to pre-existing patient risk factors, as discussed below, excessive TOE probe manipulation and the need for a prolonged period of cardiopulmonary bypass (CPB) are further risk factors for TOE-associated oesophageal perforation. Despite the prompt diagnosis of oesophageal perforation and the institution of appropriate management, the associated risks of oesophageal perforation are brought to the attention of the reader. In this case, despite the early diagnosis, the patient unfortunately did not recover after surgery. |
A 79-year-old female with past medical history of hypertension and hyperlipidemia presented with progressively worsening dyspnea on exertion and dry cough for 1 month. Electrocardiogram (ECG) showed normal sinus rhythm and left axis deviation. TTE revealed a large mobile echodensity in the right ventricular outflow tract (RVOT) measuring 6 × 2 cm (). The peak RVOT velocity was elevated at 4.2 m/s, consistent with significant RVOT obstruction. The right ventricle was mildly enlarged and hypokinetic. CT angiogram of the chest showed intraluminal mass in the RVOT extending into the right pulmonary artery, with smaller filling defects in the distal segmental branches ().\nBased on the clinical scenario, pulmonary thromboembolism was a possibility, and the patient was started on heparin infusion. However, the patient’s dyspnea on exertion could also have been attributed to RVOT obstruction which is rarely reported in the setting of PE. Furthermore, the well circumscribed appearance of the mass on TTE was more characteristic of a tumor. In addition, the right ventricular remodeling with global hypokinesis was consistent with right ventricular pressure overload rather than the characteristic McConnell’s sign seen in PE.\nFurther workup included a cardiac magnetic resonance imaging (MRI) which showed an enhancing RVOT mass concerning for sarcoma or other malignancies. PET scan revealed these lesions to be hypermetabolic, increasing suspicion for malignancy. The decision was made for surgical resection of the mass. The patient underwent an incomplete surgical resection of the cardiac mass with positive tumor margins. Pathology confirmed undifferentiated intimal pleomorphic sarcoma with 90% tumor infiltrating immune cells positive for programmed death-ligand 1 (PD-L1). Postoperative complications included cardiogenic shock and acute kidney injury from which patient recovered and underwent physical rehabilitation. She was started on immunotherapy with pembrolizumab to target PD-L1+ tumor cells.\nAlthough the patient was clinically improving, a 4-month follow-up of chest CT revealed a new solid 12 mm right suprahilar pulmonary nodule concerning for metastatic disease. The decision was made to monitor the patient clinically with continued course of pembrolizumab immunotherapy and interval follow-up imaging. Further advancement in her disease or symptomatology would require consideration for a multidisciplinary treatment approach including surgical resection if appropriate, combined with chemotherapy and/or radiation therapy. |
The third case is a 50-year-old female with a past medical history significant for COPD, CHF, and seizure disorder who was initially admitted at the end of March 2020 for a COPD exacerbation. Imaging done at this time, as seen in , did not show any significant acute processes. At this time, her COVID-19 PCR test was negative by DSL. She presented to the emergency department in mid-April for a worsening cough and was tested once again for COVID-19, which was negative by DSL. A week later, she was admitted for worsening shortness of breath, wheezing, and worsening cough; now, she tested positive for COVID-19 via PCR by DSL and discharged two days later. During the short admission, the patient never required oxygen supplementation and was considered safe for discharge, due to mild symptoms and clinical diagnosis more indicative of acute COPD exacerbation, not requiring COVID-related treatments. One and a half weeks later, she presented to the emergency department again for worsening shortness of breath and discharged three days later; DSL COVID-19 test was negative at this time. She was admitted once again in June 2020 for three days of worsening shortness of breath secondary to a COPD exacerbation, and COVID-19 testing during this time was negative by DSL. At the beginning of July, she once again presented to the emergency department for worsening shortness of breath and was admitted for two days, testing positive for COVID-19 via PCR by CSI. Chest X-ray done during this admission was concerning for airspace disease, including pulmonary edema as seen in . With concern for acute COPD and CHF exacerbations, the patient was started on pertinent treatments including diuretics, empiric clarithromycin, and IV steroids. The patient was discharged on a prednisone taper and clarithromycin. Due to the mildness of her respiratory symptoms, she was not started on COVID-related treatments. The patient once again never required oxygen supplementation during the short hospital stay. |
A fit and well, non-smoker, 23-year-old male motorbike courier was referred to the senior author (DC) for the management of a neglected patellar tendon rupture, 10 weeks following a low-speed road traffic collision.\nPre-operatively, lateral radiographs of both knees were performed in order to estimate the Insall–Salvati ratio and use the measurement from the uninjured side as a guide during the reconstruction. The Insall–Salvati ratio measured 1.0. The patient was consented for a patellar tendon reconstruction using hamstring graft and possible Z lengthening of the quadriceps tendon.\nThe patient was placed under general anaesthesia in a supine position on the operating table and intravenous antibiotic prophylaxis was administered. Tourniquet ischemia was not applied as this may have caused tethering of the quadriceps, preventing adequate assessment of patellar height. During the examination under anaesthetic no restrictions of patellar mobility were identified and it was possible to bring the patella distally to its appropriate position. An anterior midline skin incision was made, with adequate exposure to allow for the anatomy to be fully defined. The ruptured patella tendon was identified and it was apparent that the tendon had ruptured off the distal pole of the patella. The scar tissue at the level of the rupture was excised to expose healthy tendon edges. An assessment of the ability to recreate the Insall–Salvati ratio was confirmed at this stage and the patella was mobilized distally without significant tension from the quadriceps. The pes anserinus was identified and the semitendinosus and gracilis tendons were harvested with an open tendon stripper, achieving maximum length of the tendon grafts and leaving the tendons attached distally at their tibial insertion. The free tendon edges were cleaned of remaining muscle and soft tissue and prepared with whipstitch sutures. Two transosseous tunnels were subsequently drilled following the general principles as described by Ecker et al.\n; first, a 5.5 mm transverse tunnel through the patella, just distal to the mid-patellar level and then a 4.5 mm oblique tunnel behind the tibial tubercle, beginning proximally on the lateral aspect and extending distally to the medial aspect (). With the knee in full extension, a FiberWire suture (Arthrex, Florida, USA) was passed through the tibial and patellar tunnels and tensioned to bring the patella distally. The suture was used to set the height of the patella, using the previously calculated Insall–Salvati ratio of the uninjured knee. This was confirmed using C-arm image intensifier with the knee at 30° of flexion (). The free end of the semitendinosus tendon was passed medio-laterally through the oblique tunnel behind the tibial tubercle using the whipstitch and a suture passer. It was then passed latero-medially through the transverse patellar tunnel, again using a suture passer. The free end of the gracilis tendon was then passed medio-laterally through the transverse tunnel in the patella. The remaining tendons were then overlapped and sutured to each other. The tendon edges at the site of the original tendon rupture were also sutured (Ethibond suture, Ethicon, Gargrave, UK). After the repair was completed, the knee could be flexed to 90° passively without any gapping at the rupture site and the final patellar height was assessed at 60° of knee flexion and found to be symmetrical to the uninjured side. The wound was closed in layers (Vicryl and Monocryl sutures, Ethicon, Livingston, UK), after repair and reefing of the injured extensor retinaculum.\nPostoperatively, the knee was immobilized in a plaster cast at 20° of flexion. The patient was discharged the second postoperative day, not weight bearing. At the two-week follow-up, the cast and sutures were removed and the knee was placed in a hinged brace allowing flexion from 0 to 20°. Quadriceps isometric exercises were initiated at this stage. Further follow-up appointments were arranged at two weekly intervals with a 20° increase of the knee flexion on every occasion, ultimately achieving 120° of flexion in 12 weeks. At the three-month follow-up, initiation of weight bearing was permitted along with closed chain knee exercises under the supervision of a physiotherapist. At the six-month follow-up, the patient was able to walk unaided and without a limp. He had full active knee extension and 130° of flexion, achieving pre-injury functional levels, including return to sport. His Lysholm knee score was 87 points. |
An 81-year-old female presented with 6 months of left knee pain, instability and swelling after a ground-level fall. The patient had a history of primary left total knee arthroplasty to treat rheumatoid arthritis performed in 1988. She otherwise had no pertinent past medical history. The patient reported severe pain with weight-bearing and knee flexion, and had been taking anti-inflammatory medication as needed, and has been using a cane for ambulation. She denied any constitutional symptoms indicative of infection. On physical exam, the patient had a slight joint effusion and passive range of motion from 5 degrees to 100 degrees. The knee was unstable on varus and valgus testing, in extension, mid flexion, and 90 degrees of flexion. There was slight joint line tenderness medially and laterally as well as palpable crepitus and grinding when ranging the knee.\nKnee radiographs revealed amorphous densities in the posterior capsule and the suprapatellar recess consistent with the “cloud sign” () and curved radiodensities around the distal femur and joint capsule both medially and laterally, consistent with the “bubble sign” (). There was severe osteolysis with loosening of both the femoral implant and tibial base plate. A knee arthrocentesis was done in clinic, with significant amounts of black-tinged fluid aspirated (). Infection was ruled out with joint fluid analysis resulting in a WBC count of 406 and PMN % of 6. Bloodwork was obtained, with CRP and ESR levels within normal range. Given the severe pain, evidence of implant aseptic loosening and high clinical suspicion for metallosis, the recommendation was made for the patient to undergo left revision total knee arthroplasty.\nDuring the operation, there was extensive necrotic black material overlying the entire knee joint after arthrotomy (). A complete synovectomy was performed at the medial and lateral gutters and suprapatellar and infrapatellar regions to remove metallic debris (). The patellar button was noted to be a metal-backed. The tibial polyethylene liner was found to be severely worn but it was not fractured or worn through at any area. The femoral component had evidence of aseptic loosening as well as severe distal femoral osteolysis. After component removal, there was evidence of severe osteolysis of both posterior condyles and extensive metal debris overlying the femoral canal (). Similarly, there was evidence of severe osteolysis underneath the tibial baseplate with bone resorption into the proximal tibial metaphysis after the tibial component was removed ().\nClose inspection of the implants revealed metallic wear secondary to grinding on both the femoral component () and metal backed patella (), as well as along the lateral surface of the tibial plate (). After irrigation and debridement, most of the metal debris was removed. The revision implants included long press-fit diaphysis fitting stems in both the femur and tibia and a varus-valgus constrained component with tibial and femoral wedges used to reconstitute the bone loss and restore the anatomical joint line. An oxidized zirconium femoral component was used to prevent repeat metallic wear (Smith & Nephew, Memphis, TN). The patellar component was removed in its entirety and not replaced due to insufficient bone stock to support a new patella button (Figs and ).\nIntraoperative joint fluid analysis was again negative for infection, with WBC count 243 and PMN % of 10. Histologic examination of the periprosthetic tissues demonstrated extensive fibrosis () with multiple histiocytes () and multi-nucleated giant cells () consistent with the diagnosis of metallosis.\nThe patient was allowed to be weight-bearing as tolerated with an unlocked Bledsoe brace. She was able to ambulate and perform range of motion exercises with physical therapy and was discharged on postoperative day 3. At 6 weeks follow-up, her incision was healed, she was ambulating well without an assistance device, and her range of motion was 0-110 degrees. The knee was stable to varus and valgus stress. |
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