A 75 year old woman, with a history of hypothyroidism and essential hypertension,
underwent a screening colonoscopy for the first time in her life. It is worth noting
that the patient was asymptomatic. Colonoscopy revealed two polyps which were deemed
endoscopically unresectable: one at the cecum and one at 40 cm from the anus. Both were
biopsied, and a marking with India ink was made distal to the lesion at 40 cm in order
to easily locate it at surgery. Both biopsies showed tubulovillous adenoma with areas of
high grade dysplasia.
Further workup, including complete blood count, liver enzymes, CEA levels, chest x-ray
and abdominal CT, was normal.
It was decided to proceed to surgery. We initially attempted to perform a laparoscopic
resection, but due to severe intra-abdominal adhesions a conversion to open laparotomy
was made. At laparotomy, a dark discoloration was seen at the distal transverse colon,
about 100 cm from the anus, with no tattooing noted distally. It is worth noting that
the transverse colon was in contiguity with the descending colon. Due to the discrepancy
between the area of tattooing according to the colonoscopy report and the tattooed
segment visualized at laparotomy, the possibility of inadvertent transmural injection
was considered, and as a result we performed a complete dissection of the left colon and
sigma, which enabled us to palpate the small lesion in the descending colon. A subtotal
colectomy was performed in order to remove of both colonic lesions. Primary functional
end to end anastomosis between the terminal ileum and the sigmoid colon was
constructed.
During examination of the surgical specimen the cecal lesion was easily found, while the
more distal lesion was seen at the descending colon. The India ink marking was in the
transverse colon. It was apparent that the inaccurate marking was a result of a
transmural injection of India ink through the wall of the descending colon into the
transverse colon. The surgical margins of resection appeared to be free of tumor.
Postoperatively the patient made an uneventful recovery. Upon histologic examination of
the surgical specimen the distal lesion turned out to be a moderately differentiated
adenocarcinoma that invaded the submucosal layer, without involvement of the muscular
layer (T1). The cecal lesion was a tubulovillous adenoma with areas of high grade
dysplasia. The proximal, distal and radial margins of resection were free of tumor, as
were all 13 examined lymph nodes (N0).


A 20-year-old male was brought in by the EMS as an activated level 1 trauma. The patient had sustained multiple gunshot wounds to the abdomen.
On arrival the patient was alert and oriented to time and place. The patient was also complaining of abdominal pain. Primary survey revealed a patent airway, bilateral air entry on auscultation, questions answered appropriately, and movement of all his extremities. There was one wound on either side of the mid anterior abdomen as well as on the left suprapubic region and left buttock. However within a span of few minutes the patient became progressively more lethargic and obtunded. The decision was made to emergently intubate the patient and transfer to the OR. Volume resuscitation was started, with 1 liter of normal saline (NS) being given and massive transfusion activated. Initial labs showed WBC 9.19 × 103/μL, Hgb 10.3 g/dL, Hct 31.1%, Plt 102 × 103/microliter, Na 146 mEq/L, K 4.5 mEq/L, Cl 102 mEq/L, CO2 19 mEq/L, BUN 10 mg/dL, Cr 1.4 mEq/L, ALT 272 IU/L, AST 185 IU/L, ALP 51 IU/L, and TPR 0.6 ng/mL. Pre-op blood gases showed a pH of 6.8, paCO2 of 56 mm Hg, and HCO3 of 9.3 mmol/L.
An exploratory laparotomy was performed emergently. Injuries to the right colic artery, 1st jejunal branch of mesentery, and 3rd portion of the duodenum were found as well as two “through and through” injuries to the small bowel and a complete transection of the descending colon that involved “fecal spillage.” The two small bowel injuries were resected and the devitalized tissue surrounding the descending colon transection was also excised. Considering the physiological status of the patient intraoperatively a damage control surgery was performed, the bowel ends were stapled, obvious bleeders were addressed, contamination was controlled, and the was abdomen packed. The abdomen was left open and covered by an Abthera wound vacuum. Post-op chest and abdominal X-rays were taken, seen in Figures and , and the patient was transferred to the ICU for further resuscitation and stabilization of hemodynamics.
The patient was returned to the OR 3 days later. An exploratory laparotomy was performed along with one jejunojejunal anastomosis, one side to side ileocolic anastomosis, both hands sewn, closure of the mesenteric rents, and closure of the abdominal fascia. The skin was closed with staples. The patient tolerated the surgery well. The patient was reprepped and draped. A right subclavian central line was placed on second attempt after the first attempt resulted in the catheter being bunched up in the vein with brief period of arrhythmia. The patient experienced a brief period of hypotension and a chest X-ray was ordered which did not show any hemothorax or pneumothorax. The right IJ was guide wired by pulling the line back, clamping it with a hemostat and dividing it, and then going down the central lumen with a guide wire. A Mahurkar catheter was placed into the right IJ vein. Both the subclavian and the IJ dialysis lines were secured and sterile dressings applied prior to transferring the patient.
The patient developed nonsustained runs of ventricular tachycardia 3 days after the second operation, visible in . The EKG on admission was sinus tachycardia. Cardiology was consulted. The electrolytes were checked and with the exception of magnesium which was 1.1 mEq/L, the rest of the electrolytes were within normal range. The magnesium was replaced. The ventricular tachycardia persisted despite electrolyte replenishment and amiodarone drip was started. The amiodarone was changed to lidocaine but the patient continued to have runs of ventricular tachycardia. Four days post-op the source of the patient's arrhythmia remained a mystery until a chest X-ray revealed a piece of what was suspected to be a fractured central catheter, seen in . The catheter fragment had lodged itself within the inferior vena cava and the right atrium. All lines and tubes connected to the patient including the EKG leads were disconnected to make sure it is not superimposed image causing confusion. A Chest CT imaging was performed which confirmed the suspicions produced by the chest X-ray, shown in .
Interventional radiology was consulted and plans for immediate retrieval were made. A fluoroscopy guided percutaneous intervention resulted in retrieval of the 10 cm catheter fragment via a triple loops snare, demonstrated in Figures and . The removed catheter fragment was briefly inspected and can be seen in . The procedure was performed without any complications and the patient was found to tolerate it well. Repeat chest imaging confirmed successful removal of the catheter fragment, as seen in . No further ventricular tachycardia was observed during several days of continued monitoring while the patient was in the hospital recovering from his other injuries.


A 21-year-old Syrian male seeking asylum in Switzerland was referred to our tertiary centre with a history of a constantly sore throat causing sleep deprivation. Furthermore, he complained about increased pain on swallowing food and fluids. He reported that he had been wounded by a bullet eight months before in Syria, where he had been part of a Kurdish armed force. According to the patient, the bullet had glanced off a wall and had entered his right upper pharynx after perforating his left eye. After being hit, the patient suffered from anterograde amnesia covering one day. However, he was not provided appropriate medical treatment and the bullet was not removed. On the third day after the incident, the patient had been able to eat again despite serious pain and intermittent vomiting. Subsequently, the general condition improved but the patient suffered from a permanent foreign body sensation with pain behind the pharynx. Over several months he noticed a gradual, caudal migration of the symptoms.
Upon clinical examination, a foreign body was palpable through the mouth, just lateral to the right tonsil in the parapharyngeal space. The patient was found to have phthisis bulbi (i.e., a shrunken eye ball that lost its function) on the left side. Routine laboratory testing revealed a microcytic hypochromic anaemia and an iron and vitamin B12 deficiency. Serum lead, assayed during a workup for anemia, was noted to be normal. CT of the head and neck area showed a metallic object measuring 19 mm × 7 mm located in the right parapharyngeal space at the level of the second cervical vertebra (), along with an old dislocated fracture of the left medial orbital floor ().
The patient underwent uneventful transoral extraction of the bullet under general anaesthesia (). The extracted bullet proved to be a steel core, with a diameter between 6.7 mm and 6.8 mm at the base (). The core was deformed and bent approximately 45°. The tip and the jacket were torn off. The entire bullet fragment measured 19 mm in length.
The patient was discharged one day after surgery in good condition. His throat pain resolved completely within a month.


In 2009, a 62-year-old male patient was referred to the Radiation Oncology Department of the Burdenko Neurosurgical Institute. He had been previously treated with consecutive surgical resections of a right-sided cranio-orbital meningioma in 1998, 2000, 2001, and 2009. All histological investigations showed a typical WHO Grade I meningioma with an infiltrative growth pattern. At the time of admission, he had headaches, facial deformity, right eye displacement, right eye movement restriction, right-sided ptosis, and right-sided facial hypoesthesia. Signs of intracranial hypertension were identified with an eye fundus study. Informed patient consent was obtained for treatment.
MRI with contrast enhancement revealed right-sided extended calvarial, skull base, and facial meningioma. The tumor caused calvarial, skull base, and facial hyperostosis, infiltrated chewing muscles, and thickened meninges and periosteum, up to 15 mm. Due to massive unilateral meninges thickening, septa pellucida displacement was found.
The patient was treated with the CyberKnife. Tumor volume composed 1085 cc. Due to hyperostotic changes of the skull, the target included both soft tissue (702 cc) and bone components (383 cc). The following treatment regimen was chosen: 35 Gy total median dose in 7 fractions with 48-72 hours interfraction interval. Two conic collimators with 50 and 25 mm aperture diameter were chosen for treatment delivery. The acceptable treatment plan was generated after several cycles of alternation of iterative and simplex algorithms (Table ). It contained 271 beams. The mean dose was 35.3 Gy. The dose of 31.5 Gy was achieved at the 72% isodose line, encompassing 95% of the target volume (Figure ). Irradiation was performed from August 19 to September 2, 2009. During treatment time, and several days after, the patient was administered dexamethasone (up to 16 mg daily) and acetazolamidum.
During the month after treatment, mild acute adverse reactions were detected. The following reactions were noticed: alopecia (Grade 2 CTCAE 4.02), skin hyperemia (Grade 1, CTCAE 4.02), and oral mucositis (Grade 2 CTCAE 4.02). All reactions regressed spontaneously or with a short course of medications.
The patient was followed for six years after his treatment with consecutive MRI studies and clinical evaluations. No late reactions were detected during this period. After treatment, the patient noticed headaches ceasing and partial regression of his facial deformation. Follow-up neuro-ophthalmological evaluation six months after treatment detected regression of the intracranial hypertension signs.
Follow-up images revealed tumor shrinkage six years after the treatment (Figure ). Tumor shrinkage was obvious with image fusion performed with iPlan software (BrainLab, Germany). Target volume diminished from 1085 cc to 901 cc (for 17%). Simultaneously, the soft-tissue component decreased from 702 cc to 518 cc (for 26%).


A 56-year-old African man, from Guinea-Bissau, received a kidney from a deceased donor with 4 HLA mismatches in April 2013. The aetiology of his chronic kidney disease was unknown and he had been on haemodialysis for five years. In 2012, he suffered acute upper gastrointestinal bleeding; an endoscopy showed no lesions.
The recipient presented 0% panel reactive antibodies (PRA) and no anti-HLA class I and II antibodies; donor and recipient were both cytomegalovirus (CMV) IgG positive.
He received initially basiliximab and the maintenance immunosuppressive regimen was achieved with tacrolimus, mycophenolate mofetil (MMF), and prednisone.
Immediate diuresis and progressive improvement of renal function (creatinine 1.34 mg/dL at discharge) were observed in the postoperative period.
In October 2013, unexpectedly, the serum creatinine level increased to 2.57 mg/dL. Doppler ultrasonography showed no alterations. A renal allograft biopsy revealed interstitial fibrosis and tubular atrophy grade II, assumed as toxicity of calcineurin inhibitor. His medication was switched to everolimus and serum creatinine levels slowly decreased until serum creatinine of 1.8 mg/dL.
In March 2014, the patient was admitted due to anasarca (serum creatinine of 3.28 mg/dL and proteinuria of 395 mg/day). New renal allograft biopsy was carried out and showed no additional changes. Anti-HLA class I and II antibodies remained negative. mTOR inhibitor was stopped, and the patient was, once again, treated with calcineurin inhibitors with no improvement of renal function.
In May 2014, the patient was admitted due to anuria with significant deterioration of renal function (serum creatinine of 6.9 mg/dL), haematochezia, and anaemia (haemoglobin: 7.5 g/dL), requiring 5 units of packed red blood cells. Extremities swelling due to bilateral oedema and diffuse, ill-defined thickening of the skin and deeper tissue of the limbs were also present. No mucosal lesions were identified.
Colonoscopy showed haemorrhagic patches in the colon and the rectum (). Histology confirmed proliferation of spindle cells with vascular spaces slit and positivity for CD-31 and HHV-8, confirming gastrointestinal KS. A skin biopsy revealed cutaneous involvement of KS. The investigation of graft failure was inconclusive, immunosuppressive therapy was progressively stopped, and haemodialysis was started.
In few days, the patient had substantial clinical deterioration with multisystem organ failure, leading to death in June 2014. No necropsy was allowed.


We present a case of a 62-year-old male with 42-year history of small intestinal CD diagnosed at the age of 20, requiring two small bowel resection surgeries during this course of time. Our patient was solely on prednisone therapy for an extended period of time and switched to AZA (150 mg daily) for the last 21 years with relatively well controlled symptoms. During routine follow-up screening tests, he was incidentally found to have left lobe liver mass and was diagnosed with HCC for which he received left lobe hepatectomy at the age of 58. The AZA dose was reduced to 50 mg daily.
On subsequent follow-up, four years after the initial resection, he was found to have liver mass and was admitted to the hospital for further evaluation. On presentation to hospital, the patient appeared well without any evidence of jaundice or stigmata of chronic liver disease. Preoperative blood work including liver profile and viral hepatitis markers was entirely normal: AST 18 U/L (<37 U/L), ALT 16 (<60 U/L), albumin 3.5 g/dL (3.5–5 g/dL), bilirubin 0.8 mg/dL (0.3–1.2 mg/dL), and INR 1.0, alpha-fetoprotein 10.3 ng/mL (<6.1 ng/mL), prothrombin time 13.3 seconds, and platelet count 210/μL.
Triple phase contrast enhanced CT of abdomen showed solitary mass in the segment 5 of the right lobe measuring 2.2 × 1.6 × 2.1 cm, with arterial enhancement and early wash out in the venous phase, and no evidence of lymphadenopathy or extrahepatic metastasis (Figures and ).
The decision toward surgical excision of the tumor was made. Patient underwent laparoscopic resection of segment 5 with no postoperative complications. Microscopically, the resected mass showed moderately differentiated hepatocellular carcinoma without evidence of microvascular invasion ().
There was no postoperative adverse events and AZA was discontinued and patient was kept on oral budesonide.


A 55-year-old male presented to the emergency department with left lower limb painless swelling and redness which started gradually over two weeks prior to presentation. He stated that he usually does not stay immobilized for a long period of time and there was no recent history of immobilization or surgeries. He denies any trauma to his left lower limb. His medical background includes obstructive sleep apnea. He has never been a smoker and his family history was negative for thromboembolic events or other hematological disorders. On physical examination, there were swelling and redness in his left lower limb extending from the foot to the upper thigh. Warmth was also noted compared to the right lower limb. The rest of the physical exam was unremarkable, there was no evidence of injury or venous stasis.
Biochemical and haematological investigations were normal. Venous Doppler ultrasound showed DVT extending from the common femoral vein at the level of the left groin to the popliteal vein at the level of the knee and a second DVT in the deep profunda vein.
Giving the extent of the thrombosis, CT of the chest and abdomen was considered to rule out further extension of the clot or suspected malignancy. CT revealed absent infrarenal IVC () associated with multiple para-aortic collaterals and tortuous dilatation of the inferior mesenteric vein. It also confirmed the presence of acute thrombosis involving the left external iliac and left common and superficial femoral veins.
Treatment was started initially with therapeutic dose of Enoxaparin. After that, he was started on Warfarin and required life-long anticoagulation. Following daily measurement of the calf and thigh circumference, his DVT had resolved. After discharge, life-long Warfarin was continued and he was advised to use elastic stocking. No recurrence of DVT has occurred at three and six months of follow-up. Thrombophilia studies, including lupus anticoagulant, cardiolipin antibody, antithrombin III, antinuclear antibody, factor V Leiden, and prothrombin gene mutation, were normal. However, his proteins C and S activity was low. As thrombophilia studies were done after initiating treatment, low activity level of anticoagulant proteins (proteins C and S) could be attributed to treatment with Warfarin [].


A 31-year-old female, two months postpartum, presented to the Oral and Maxillofacial Surgery Department at New York Presbyterian Hospital/Columbia University Medical Center (CUMC/NYPH; New York, NY). The patient's chief complaint was of a large, persistent growth of her left maxillary gingiva that presented during her first trimester of pregnancy. She reported the growth to her obstetrician who was monitoring it and advised her to wait until after her pregnancy before seeking consultation with oral surgery. The patient reported frequent bleeding from the site.
On physical exam, she had a left cheek swelling with a large red-purple lesion of the left maxillary buccal gingiva (). The lesion was soft and spongy in texture and easily bled upon manipulation. The lesion extended to the palatal gingiva. The patient also had a left facial port-wine stain, adjacent to the oral lesion, which had been present since birth. The port-wine stain was not limited to the lip, as it involved the facial skin of her left cheek. Intraorally, the left maxillary vestibule displayed hypervascular markings.
Given the clinical appearance of the oral lesion and that it presented during pregnancy, a clinical diagnosis of pregnancy tumor was rendered. Sturge-Weber syndrome, a disorder often associated with facial port-wine stains, had been ruled out due to a lack of other clinical symptoms characteristic of the syndrome, such as neurologic and ocular abnormalities [–].
A panoramic radiograph depicts interproximal bone loss between teeth numbers 24 and 25 (international nomenclature) and tooth number 24 is mesially displaced (). A computed tomography (CT) angiogram revealed a 3.9 × 1.7 cm hypervascular lesion in the left buccal space with a principal arterial blood supply from the left facial branch of the left external carotid artery. No major arteriovenous shunting was demonstrated.
The patient met with an interventional neuroradiologist in preparation for surgery to evaluate the lesion's vascular nature. Preoperative elective embolization of particular branches of the left internal maxillary artery was successful. Branches of the facial artery were spared during embolization to prevent tissue ischemia and necrosis and poor wound healing.
Under general anesthesia, the lesion was excised (). The most prominent sublesion of the left posterior maxillary buccal gingiva was excised in full thickness fashion along with a cuff of healthy tissue. The anterior and palatal sublesions were also excised in full thickness fashion along with a cuff of healthy tissue. Although there was significant interproximal bone loss involving teeth numbers 24 and 25 (international nomenclature), they were nonmobile and, therefore, maintained. Peripheral ostectomy was performed to remove any remaining soft tissue in-growths and vascular channels. The flap was closed primarily without tension. The excised specimens were sent for histopathologic review.
Histopathologic analysis revealed endothelial proliferation, chronic inflammatory cells, and anastomosing vascular channels, all consistent with an oral pyogenic granuloma or pregnancy tumor (). Immunohistochemistry staining for GLUT-1 was negative, which ruled out a hemangioma [].
The patient was followed closely and initially did well. Three weeks after surgery, the patient complained of new bleeding from the surgical site. Six weeks after surgery, the patient developed a recurrent lesion (). Teeth numbers 24 and 25 (international nomenclature) were now grossly mobile and the mesial aspect of tooth number 26 (international nomenclature) displayed a >10 mm probing depth. In preparation for excision of the recurrent lesion, the patient underwent a repeat angiogram. Palatal branches of the left ascending pharyngeal artery, a proximal branch of the left carotid artery, were successfully embolized. Under general anesthesia, the patient underwent excision of the recurrent lesion along with extraction of teeth numbers 24, 25, and 26 (). Histopathologic review confirmed a recurrent pyogenic granuloma. The patient was fitted with a removable intermediate prosthesis (). The prosthesis provided esthetic and functional benefits while permitting hygiene and surveillance for recurrence.
At most recent follow-up, the patient is 11 months' post-excision of the recurrent lesion and reports being 5 months' pregnant. On monthly examinations, she continues to show no evidence of disease.


A 34-year-old male with a past medical history of MS was brought into the emergency department by Emergency Medical Services after being found unresponsive by his mother with three pill bottles at his side. The bottles were an empty bottle of valacyclovir, an empty bottle of temazepam and a bottle of dalfampridine still containing some pills. His mother gave the history that the patient was under multiple social stressors of late. Other than MS, the patient was diagnosed with insomnia and had no other pertinent past medical history. His current medications were valacyclovir, temazepam, dalfampridine (4-AP) and a tysabri IV infusion (all part of his MS treatment regimen).
The initial vital signs were as follows: Blood pressure: 155/82mmHg; Heart rate: 106/min; Respiratory rate: 24/min; Temperature: 97.4ºF; O2 sat: 97% 2L NC. The bedside glucose was 144mg/dl. The patient appeared extremely tremulous, was awake, but not responding to questioning nor following simple commands. He responded to tactile stimulation by localizing to the pain. He did not appear to have any focal deficits. His pupils were 4 mm, equal and reactive and his mucous membranes were moist. His heart sounds were tachycardic, with no murmurs. The patient had clear breath sounds bilaterally and no retractions. The abdomen had normoactive bowel sounds. The skin was diaphoretic with piloerection.
Intravenous access was established, labs were drawn and the patient was given two liters of normal saline. Soon after arrival, the patient lost consciousness, his oxygen saturation decreased to below 90% and he began to have a tonic-clonic seizure. The patient was administered boluses of lorazepam, to a total of 8 mg, without effect in seizure resolution. He was intubated and subsequently placed on a lorazepam and propofol infusion for sedation. He was loaded with one gram of phenytoin and 300mg phenobarbital and then placed on a phenobarbital infusion. Clinically the patient continued to have frequent, recurrent seizures.
The patients lab values on arrival were significant for a white blood cell count of 31.1×103/mcL, a sodium of 143mEq/L, potassium 3.1mEq/L, chloride 107mEq/L, bicarbonate of 24mEq/L, a blood urea nitrogen of 15mg/dL and a creatinine of 1.2mg/dL. The anion gap was 12. The lactic acid was 3.4mg/dl. Total creatinine kinase was 99 units/L. Liver function tests and coagulation studies were all within normal limits. Ethanol, acetaminophen and salicylate levels were all negative. A urine toxicology screen was positive for benzodiazepines. An arterial blood gas showed pH 7.22, pCO2 65, pO2 127 and HCO3 26.6 (performed immediately after intubation). Computerized tomography of the brain and chest x-ray were both normal. The electrocardiogram showed a sinus rhythm at 88 beats per minute with normal QRS and QT intervals. Drug levels were sent for 4-AP and valacyclovir. The 4-AP level resulted at 530ng/mL (therapeutic: 25 to 49ng/mL). The valacyclovir level was 7.5mcg/mL (therapeutic 2.0–4.0mcg/mL).
The patient was admitted to the intensive care unit (ICU) and while he was there he continued to have seizures. While in the ICU the patient had two electroencephalographs (EEGs) performed. The EEG on hospital day 2 showed epileptiform activity and the other EEG was performed on hospital day 7 and was indicative of epileptiform encephalopathy.
The patient stopped seizing on hospital day 3. The patient was extubated on hospital day 12. He was discharged, with normal mental status and neurologic exam to an inpatient psychiatric facility.


The patient was an 89 year-old man who presented to the emergency department (ED) with one week of hemoptysis. He described that twice per day he would “feel warm liquid in my mouth, gag, and spit up clots of blood.” He denied a history of coughing, vomiting, or postnasal drip. His medical history was significant for coronary artery disease, hypertension, and chronic kidney disease. He was not taking anticoagulants. He had never smoked or consumed excess alcohol. His vitals on arrival included a temperature of 36.7 degrees Celsius, pulse of 82 beats per second, blood pressure at 135/64mmHg, respiratory rate 18 breaths per minute, and an oxygen saturation of 97% of room air. Laboratory data included hemoglobin 12.5gm/dL, platelets 131K/mm3, INR 1.0, PT 14.5 seconds. After obtaining a chest plain film with normal findings, a head, neck, and chest computed tomography was performed in the ED, which showed no evidence of masses, vascular malformations, or pulmonary embolism. Esophagogastroduodenoscopy showed mild duodenitis but no gastric ulcers or esophageal varices. After bronchoscopy failed to identify a source of bleeding, the patient was discharged as his symptoms seemed to have resolved during his hospitalization.
Two days later the patient presented to the ED again with bleeding from the mouth. Otolaryngology was consulted and fiberoptic nasopharyngoscopy was performed, revealing normal nasal mucosa and no bleeding from the pharynx. However, upon asking the patient to protrude his tongue, a 0.5cm, non-bleeding, pedunculated varix was observed in the left vallecula. At this point the patient’s hemoglobin had decreased to 10.7gm/dL. The patient underwent direct laryngoscopy with microscope and yttrium aluminum garnet laser cauterization, followed by cold steel resection ( and ). The pathology report was varix with acute thrombus. The patient was discharged the next day after overnight observation for bleeding.
The patient’s post-operative course was complicated by a need to return to the operating room on post-operative day 10 due to bleeding from the surgical site. There was no evidence of recurrence of his varix and the bleeding was managed with suction cautery. Again, the patient was monitored overnight, demonstrated no further bleeding, and was discharged. The patient has remained well since.


A 57-year-old woman was admitted for painful lower leg ulcers. Past history included subcutaneous injection of esthetic filler material in the lower legs 20 years ago, hypothyroidism and HIV infection on highly active antiretroviral therapy (HAART: raltegravir, abacavir, lamivudine). Viral load was negative and CD4 cells were 600/μl. One year before admission, bilateral torpid lower leg ulcers developed after minor trauma and progressively expanded. She was treated with diclofenac.
On admission blood pressure was 190/88 mmHg (previously normal) and she had extensive necrotic ulceration and edema in both lower legs. Key lab results were serum creatinine 1.5 mg/dl (previously 1.0 mg/dl), serum albumin 3.5 mg/dl, serum cholesterol 139 mg/dl, complement factor 3 (C3) nadir 63 mg/dl, normal C4, polyclonal hypergammaglobulinemia, urinary albumin:creatinine ratio 2082 mg/g, urinary protein:creatinine ratio 3557 mg/g and urinary sediment containing 20–40 red blood cells/high power field. ANCA, ANA, and anti-GBM were negative. Ulcer cultures grew Group A streptococcus pyogenes.
Kidney biopsy (two cores; 9 and 11 mm long) containing 26 glomeruli, 2 of them completely sclerosed, disclosed diffuse proliferative glomerulonephritis characterized by glomerular hypercellularity due to mesangial proliferation and endocapillary leukocytic infiltration (Fig. ). Trichrome staining revealed subepithelial fuchsinophilic deposits. Jones silver stain did not show spikes or basement membrane reduplication (Fig. ). Coarse mesangial and peripheral capillary loop staining for C3 was seen on immunofluorescence (Fig. ), without IgG, IgA or IgM deposition. Round translucent, non-birefringent microspherical bodies (30–35 μm) resembling adipocytes were identified within some capillary lumens (Figs. and ). Microspheres were also seen in a globally sclerosed glomerulus (Fig. ). In the tubulointerstitial compartment, intratubular red blood cell casts, acute tubular damage and patchy interstitial lymphocytic infiltrates were noted. Vessels showed arteriolar hyalinosis and moderate myointimal hyperplasia. Ultrastructural study revealed subepithelial deposits (‘humps’) (Fig. ).
Treatment included local debridement, antibiotics and angiotensin converting enzyme inhibitors. Estimated glomerular filtration rate, C3 and microhematuria normalized at month 3, 5 and 12, respectively, while albuminuria progressively improved over the next 12 months (Fig. ). One year after the initial admission, angiotensin converting enzyme inhibitors had been stopped and serum creatinine was 0.9 mg/dl, estimated glomerular filtration rate 94 ml/min/1.73 m2, urinary albumin:creatinine ratio 188 mg/g and urinary sediment contained no red blood cells/high power field.


A 77-year-old man, with well-controlled hepatitis B virus (HBV) by entecavir (HBsAg positive, HBsAb negative, HBcAb positive, HBeAg negative, and undetectable HBV-DNA), was diagnosed with a primary HCC and was treated with radiofrequency ablation (RFA) in January 2010 at the previous hospital. Ten months later, he was admitted to our hospital because of the intrahepatic recurrences and then treated with RFA and with partial hepatectomy. One year later, he had a recurrence at the needle site of RFA on the chest wall and local resection was performed. However, he showed multiple and bilateral lung metastases with local recurrence at the chest wall, whereas there was no viable lesion in the liver. At that time, liver function was categorized as Child-Pugh class A with normal range of blood counts, electrolytes, and renal functions. Sorafenib was introduced 400 mg twice a day (total 800 mg/day), and there was no significant adverse event 1 week after the administration. Just after 1 month, when we checked, he is in a good general condition only with slight hand rubefaction that does not influence the treatment continuation and his laboratory data are without unexpected values (the serum total bilirubin 1.4 mg/dl, AST 33 IU/L, ALT 24 IU/L); he had general fatigue and appetite loss, and those symptoms gradually worsened despite improvement of the skin reaction. Two months after the induction of sorafenib, the symptoms aggressively worsened, and the laboratory data demonstrated significantly worsened liver functions in the serum bilirubin value (total bilirubin 28.6 mg/dl, direct bilirubin 20.4 mg/dl), transaminase values (AST 1611 IU/L, ALT 1098 IU/L), and other liver enzymes (Table ), without significant evidence of HBV reactivation. By computed tomography, there is no significant finding such as intra- and extra-biliary duct dilatation and intrahepatic recurrence. Therefore, the fatal liver dysfunction was diagnosed due to sorafenib-related adverse event. We stopped the intake of sorafenib and treated with stronger Neo-Minophagen C and ursodeoxycholic acid. While serum transaminase values decreased in response to the above treatments, the serum bilirubin level did not change. As a next therapeutic approach, we started hyperbaric oxygen therapy (HBOT) every business day from day 8. HBOT was provided with a monoplace hyperbaric chamber. He was accommodated for about an hour and a half in the chamber, where the ambient pressure with pure oxygen increased two times higher than the local atmospheric pressure in 10 to 15 min; it was maintained for 60 min and was relieved back to the atmospheric pressure gradually in the same or more time spent than the increasing time. Thereafter, the serum bilirubin level started to decrease depending on the number of times of HBOT, and he could sustain himself with oral take (Fig. ). Interestingly, the serum bilirubin levels failed to decrease during the weekend without HBOT. For example, while gradual decrease of the serum total bilirubin level was observed in the interval only on weekdays between days 15 (18.9 mg/dl) and 18 (17.4 mg/dl), there is no change of the bilirubin level in the interval including a weekend between days 18 and 22 (17.7 mg/dl). This tendency was observed during the prominent hyperbilirubinemia. A liver biopsy was performed, and the microscopic findings demonstrated cholestasis, degeneration, and necrosis in hepatocytes with lymphocyte infiltration (Fig. ). On day 43 from the start of treatment, although a phenobarbital was administered in addition to HBOT in anticipation of further improvement in bilirubin level, an additional phenobarbital treatment seemed to be not effective. After 2 months of treatment, serum bilirubin level was around 3 mg/dl and he was discharged and restarted to treat HCC with tegafur/uracil leucovorin, but as progression of the lung metastases, he died 1 year after discharge.


A 59-year-old woman was admitted to our hospital with locally advanced lung adenocarcinoma. Chest computed tomography (CT) showed a tumor in the right upper lobe that had invaded the middle lobe and S6 segment, as well as hilar lymphadenopathy (#12u and #11 s) without mediastinal lymph node swelling (cT2aN1M0). An ESL procedure (right upper, middle lobectomies and S6 segmentectomy) that preserves the basal segment with a double-sleeve technique was considered in order to avoid a right pneumonectomy in this patient. Since successful ex situ auto-transplantation after a pneumonectomy for locally advanced lung cancer has been reported [, ], the Dokkyo Medical University Hospital Ethics Committee approved our protocol (#26030) for an operation including a back-table procedure and auto-lung transplantation after a pneumonectomy for locally advanced lung cancer to examine its merits. Such an auto-lung-transplantation protocol was performed in the present case for curative resection and basal-segment preservation. Consent to participate and to publish this study was obtained from the patient before surgery.
We initially performed a 5th intercostal posterolateral thoracotomy. After administration of intravenous heparin and prostaglandin E1, the pulmonary artery and vein were clamped, and the right pneumonectomy was completed. For a venous anastomosis between the lower pulmonary vein of the graft and upper pulmonary vein of the body, the pulmonary veins were dissected as distal as possible for the upper pulmonary vein and proximal as possible as for the lower pulmonary vein (Fig. ). Following completion of the pneumonectomy, the excised lung was irrigated with a cold low-potassium phosphate-buffered dextran glucose solution (EP-TU solution; Cell Science & Technology Institute, Sendai, Japan) to protect the lung graft from ischemia-reperfusion injury during preparation of the graft of the basal segment as a back-table procedure. At the same time, another surgeon performed a mediastinal lymph node dissection to shorten the operation time. Thereafter, basal segment auto-transplantation was performed in the order of bronchus, pulmonary artery, and pulmonary vein anastomosis. Finally, the basal pulmonary vein of the graft was anastomosed to the upper pulmonary vein orifice. The operation time was 359 min and blood loss was 305 g.
The postoperative course was uneventful and no ischemia-reperfusion injury was observed, and the patient was discharged from the intensive care unit 1 day after the operation. The pathological diagnosis was pT2aN2M0 adenocarcinoma. Following surgery, the patient received adjuvant chemotherapy with carboplatin and nab-paclitaxel. At 9 months after the operation, she had returned to normal life without recurrence of the primary disease.
We have performed ESL for 37 patients with locally advanced non-small cell lung cancer at our hospital. Thirty-two of those were considered to have a good risk for undergoing a pneumonectomy, while the others had compromised cardio-pulmonary function. Thirteen underwent a basal-segment preserving ESL, for whom the operation time was 334 ± 75 min and blood loss was 445 ± 394 g. Operation time and blood loss for patients who underwent auto-transplantation preserving the basal segment were similar to those who underwent a usual ESL procedure preserving the basal segment (Fig. ). Thus, our complicated protocol using auto-transplantation does not increase operation time or blood loss.


A 29-year-old woman with 2 years of primary infertility resulting from male factor infertility (oligoasthenospermia) and abnormal karyotype [45,XY, rob [, ] (q10;q10)] underwent PGD-ICSI treatment at the Center for Reproductive Medicine, Renji Hospital, Shanghai. During her first ART treatment cycle, stimulation was performed with daily administration of 150 units of recombinant follicle stimulating hormone (rFSH) (N.V.Organon, Netherlands) according to a standardised long protocol with Triptorelin 0.05 mg daily downregulation (Ferring, Germany). Following hCG trigger, 17 oocytes were collected, of which eight cleavage stage embryos were biopsied. Following fluorescent in situ hybridization (FISH), two normal euploid embryos were diagnosed, of which one was selected for transfer. The embryo selected had undergone single cell biopsy at the 10 cell stage and was subsequently transferred on day 4.
The woman successfully conceived, as confirmed by a hCG level of 2610 IU/L on day 15 post-transfer. Routine two-dimensional (2D) transvaginal ultrasound (US) by a reproductive medicine specialist on day 29 following transfer reported a single gestational sac (37 × 21 × 37 mm) with three yolk sacs and three foetal poles, all with heart beats. The TVU was repeated by the same doctor on day 35 post-transfer reporting a single gestational sac (52 × 19 × 40mm) with three viable foetuses with crown rump lengths (CRL) of 10.5, 8.1 and 10.0 mm. The couple was informed about the increased maternal and foetal risks with this condition and were counselled about the possibility of a foetal reduction procedure.
After consideration, the couple decided to undergo foetal reduction at the prenatal diagnosis centre (PDC) of the First Maternal and Infant Hospital of Shanghai. At 13 + 2 weeks of the pregnancy, an abdominal US was performed by a foetal medicine specialist in fact revealed the presence of a MCQA pregnancy with four equal sized viable foetuses (CRL of 82, 83, 82 and 82 mm), all with nuchal translucency measurements within normal range. The woman subsequently underwent selective foetal reduction via use of radiofrequency ablation on two occasions, at 16 + 3 and 17 + 4 weeks of gestation. In the absence of any definitive evidence, reduction of only one foetus at a time was performed, with the assumption that it may reduce the risk of miscarriage in the remaining foetuses. The procedures were uncomplicated, and two healthy twin girls were delivered by elective Caesarean Section at 35 + 6 weeks of gestation, weighing 2060 and 1985 g. The placental specimen along with the two selectively reduced foetuses confirmed a MCQA pregnancy (Fig. ).


A 34-year-old lady with 7 years of secondary infertility due to tubal factor underwent conventional IVF treatment at the University ART unit, Prince of Wales Hospital, Hong Kong. She had a previous first trimester miscarriage in 2007 and a right ectopic pregnancy in 2008, at which time she had a salpingectomy. Subsequent investigations including a laparoscopy confirmed blockage of the contralateral tube and evidence of endometriosis. During her first ART cycle, stimulation was performed with daily administration of 225 units of human menopausal gonadotrophin (hMG) (Serono, Aubonne/Switzerland) according to a standardised antagonist protocol with Ganirelix 0.25 mg downregulation (Merck Serono, Germany). Following hCG trigger, 14 mature oocytes were collected, of which 12 were fertilised, yielding 6 viable blastocysts (i.e. Gardner grading of BB grading or above) on day 5. No assisted hatching was performed, and a single expanding blastocyst (i.e. increasing blastocoel cavity with thinning of the zona pellucida and differentiation of the inner cell mass) was transferred to the patient on day 5. The remaining blastocysts were all cryopreserved following appropriate consent.
The woman successfully conceived, as confirmed by an hCG level of 154 IU/L on day 9 post-transfer. Routine 2D transvaginal US 23 days following transfer was suspicious of monochorionic twin or triplet pregnancy; therefore, a 3D US was performed on the same day demonstrating clearly a single gestational sac with three yolk sacs and three foetal poles (CRL of 4.5, 3.1 and 3.0 mm) (Fig. ). On day 36 following transfer, 3D US confirmed a MCTA pregnancy (Fig. ). The couple was informed appropriately regarding the increased maternal and foetal risks of higher order monozygotic gestations and was counselled regarding the possibility of a foetal reduction procedure.
After being reviewed by the foetal medicine team of the Prince of Wales Hospital, an US at 11 + 5 weeks showed all three CRLs of the triplets to be within normal range, although the nuchal translucency was increased in one of the triplets (3.6 mm versus 2.3 and 1.2 for the other two). The couple subsequently decided to proceed with selective foetal reduction via use of radiofrequency ablation, which was successfully performed for the triplet with the thickest nuchal translucency at 14 + 1 weeks of gestation. The procedure was uncomplicated, and the remaining twins are well at the time of writing this article.


This 26 year old non-smoker woman presented with a spontaneous pneumothorax at 3 months ago. The pneumothorax was treated by simple aspiration resulting in adequate clinical and radiological improvement. However, 3 months later, she presented with further pneumothorax. She had no signs of tuberculosis, rheumatic disease and other background diseases. A lung HRCT scan showed extensive cystic air spaces throughout both lungs on suspicion of lymphangioleiomyomatosis (LAM) (Fig. ). In view of her age a thoracoscopic lung biopsy was performed in July 2013. At operation there were numerous cystic areas within all lobes of the right lung and she had a large apical bulla. There were no post-operative complications and the lung remained fully expanded. Histology of the lung showed smooth muscle, staining for desmin, HMB-45, β-catenin, SMA, ER, and PR, within the lung, alveolar walls and blood vessels not in keeping with LAM. However, there are diffuse pulmonary interstitial cholesterol clefts surrounded by lymphocytes, without the formation of granulomas (Fig. ).


In 2009, a 27-year-old woman was admitted to our psychiatric department. She had been found by emergency response firemen, sitting with her 8-month-old twin babies on the window ledge of her 9th floor apartment tossing personal effects into the air.
The patient had no prior personal or family psychiatric history. She was of Algerian origin and had arrived in France 18 months earlier. Her husband was unemployed, drug-dependent, and was rarely present at home. It had been her first pregnancy, and she had given birth to two girls via caesarean section, due to uterine haemorrhage during the 35th week of amenorrhoea.
Upon admission, an examination found fluctuating psychomotor agitation, anxiety, emotional lability, and impulsivity. The patient had incoherent speech, persecutory delusions, auditory hallucinations, and was disoriented in time and space. According to her family, symptoms had appeared three months earlier and had progressively worsened. She was not known to be taking any medications nor did she suffer from substance abuse. Considering the clinical picture and because of the presence of classical risk factors (first-time mother with multiple births associated with obstetrical complications, recent immigration, father of the children barely present), post-partum psychosis was firstly suspected even though the delayed onset of psychiatric symptoms 5 to 8 months after birth was longer than what is usually admitted for such a diagnosis []. As a consequence, oral risperidone 2 mg daily and cyamemazine 30 mg daily were introduced. Forty-eight hours later, symptoms worsened, and the patient presented with permanent auditory hallucinations, psychomotor instability, as well as aggressive behaviour alternating with mutism, negativism, stereotypic gestures and diffuse rigidity with catalepsy. A vesperal aggravation was noted. According to DSM-IV [] and DSM-5 [] criteria, catatonia was diagnosed. Oral lorazepam was introduced and progressively increased until 12.5 mg daily. Because the clinical picture worsened and to avoid an evolution towards malignant catatonia, antipsychotics were stopped and complementary investigations were conducted.
Electroencephalography (EEG) showed a widespread slowing of background activity without sharp-waves, suggestive of encephalopathy. Brain imaging including CT-scan, magnetic resonance imaging (MRI) scan, and single photon emission computed tomography (SPECT-scan) were all normal. The patient was euthyroid but had elevated titres of anti-thyroglobulin (TGAB) and anti-thyroperoxidase (TPOAB) antibodies (200 and 10 times compared to normal, respectively). Cerebrospinal fluid (CSF) examination revealed normal cell count, protein, and glucose levels. CSF cultures were negative and TGAB and TPOAB titres in the CSF were normal. Thyroid echography showed a heterogeneous gland without any sign of inflammation. No other abnormality was found from further testing, including blood tests for regular auto-immune disorders, serological tests for herpes simplex virus, cytomegalovirus, viral hepatitis B and C, human immunodeficiency virus, syphilis, as well as blood sampling for vitamins B 12, PP, and ceruloplasmin.
Hashimoto’s encephalopathy (HE) was suspected given the association of high concentrations of anti-thyroid antibodies and the presence of an otherwise unexplained neuropsychiatric condition. Although medication with risperidone 2 mg daily, cyamemazine 30 mg daily, and eventually lorazepam 12.5 mg daily, was ongoing, no clinical amelioration was observed. Therefore, oral prednisolone was introduced at 60 mg daily. It was quickly followed by a dramatic improvement of the clinical picture; within 72 h, the patient was again oriented in time and space, and auditory hallucinations, as well as catatonia, disappeared. A follow-up EEG returned normal. Corticosteroid treatment was maintained at a dosage of 60 mg daily for a month before being progressively decreased and stopped within a year. In 2013, after three years of follow up, the patient still remained free of any psychiatric symptom.


A 38-year-old male patient came to the Urgent Trauma Center after being hit in the chest by a bull. Symptoms were mild pain on the right lower ribs posteriorly without visible contusion marks and without cardiorespiratory compromisation. According to the patient’s medical history he had never had any respiratory symptoms or condition before the incident. A chest X-ray was performed and while there was no sign of broken ribs, pleural effusion or pneumothorax, there was a big, sharply marked, round shadow present on the right lung. Laboratory tests (complete blood count, C-reactive protein, renal function and coagulation parameters), thorax and abdominal ultrasound were performed immediately without any pathological finding. Urgent thorax computed tomography (CT) scan was performed and the radiologist described a dense sharply marked formation filled with fluid sized 10.6 × 11.1 × 11.6 cm in contact with the right main bronchus (Fig. ). The patient was admitted, a bronchoscopy was performed and there was no intraluminal evidence of tumor. A pulmonologist was called in, who then recommended an ultrasound or a CT-guided thoracic puncture considering the formation to be an intrapulmonary hematoma and, less likely, a primary lung tumor or an echinococcal cyst. CT-guided transthoracic puncture was performed and the substance was sent for a cytological analysis which showed that the formation is most likely a pleomorphic adenoma but could also be a hamartoma and required histopatholological verification. From the admittance and during his hospital stay the patient was stable and asymptomatic. The operation procedure was scheduled as soon as the cytological analysis was completed. Right lateral muscle-sparing thoracotomy was performed. Macroscopic examination showed a large reddish capsulated tumor with a smooth surface, clearly demarked from the surrounding lung parenchyma. There were no macroscopic pathological findings on the pulmonary lobes. During the extirpation, surgical resection of the tumor from the right main bronchus was done using the ultracision. The tumor was extirpated and we noticed that the capsule on the extirpated tumor was not intact. A small portion of the tumor was still on the right main bronchus. The resection of the remaining tumor was performed, after which the right main bronchus seemed to have macroscopically clear resection margin (Fig. ). Hilar station lymphadenectomy was performed and the nodes were sent with a tumor for an intraoperative histopathological analysis showing no malignancy. Postoperative recovery was uneventful. Results of the final histopathological analysis verified it was truly a pleomorphic adenoma. Considering this result, the patient was sent to do a salivary gland CT-scan which did not show any pathological finding. After the operation a positron emission tomography (PET) CT was performed, which did not show any local or distant metastasis. Since the PET CT did not show any bone metastasis we did not consider a bone scan necessary.


A 61-year-old female 50-pack-year smoker with severe COPD, advanced emphysema, chronic hypoxia on home oxygen secondary polycythemia, non-insulin-dependent diabetes mellitus, hypertension, dyslipidemia, and a stable, untreated renal cell carcinoma presented with an incidental finding of a left-upper-lobe (LUL) nodule on a chest x-ray performed during a COPD exacerbation. Apart from the chronic dyspnea from her underlying lung disease, the patient was asymptomatic with good functional capacity (Eastern Cooperative Oncology Group score 1). Physical exam was unremarkable. Signed informed patient consent was obtained.
Further imaging characterized an apical-posterior spiculated noncalcified 1.7 cm FDG-avid LUL pulmonary nodule, with no evidence of nodal involvement or metastatic disease (Figure ). Despite initial benign bronchoscopic LUL washing and brushing cytology, fine needle aspiration (FNA) biopsy of the mass demonstrated small-cell carcinoma (cT1a, cN0, cM0, Stage IA).
Given her poor pulmonary function (FEV1 of 0.39 pre-bronchodilator and 0.5 post-bronchodilator, DLCO of 37% predicted), the patient was deemed not to be a candidate for combined chemoradiotherapy. Chemotherapy proceeded with the standard regimen of four cycles of cisplatin and etoposide. CT performed two weeks following chemotherapy completion demonstrated only partial response of the primary lesion, and the patient was offered adjuvant radical irradiation for the residual LUL tumour. An SBRT technique was selected to minimize pulmonary toxicity. Starting eight weeks following the last cycle of chemotherapy, 48 Gy, prescribed to 95% of the PTV, were delivered in four fractions over two weeks by dynamic conformal arcs. Prophylactic cranial irradiation (25 Gy in 10 fractions) was also administered. The patient tolerated this treatment well and interval post-treatment imaging has demonstrated a sustained complete response.
Fifteen months after her initial diagnosis, the patient presented with a COPD exacerbation and hyponatremia. A CT scan revealed a new 2 cm peripheral right-upper-lobe (RUL) pulmonary nodule with FNA cytology demonstrating atypical epithelial cells, suspicious for NSCLC (not further histologically characterizable, given the limited FNA sample; cT1a, cN0, cM0, Stage IA) (Figure ). A right middle lobe collapse was noted and was ascribed to mucus bronchial plugging secondary to the patient’s underlying lung disease, rather than malignant obstruction.
The RUL NSCLC was treated with SBRT (48 Gy in four fractions), which the patient tolerated well (Figures -). Post-treatment imaging is pending to assess disease response.


A 34-year-old man was diagnosed with pulmonary tuberculosis (TB). Mycobacterium tuberculosis (susceptible to rifampicin and isoniazid) was cultured from his sputum. After commencing the intensive phase of TB treatment (rifampicin, isoniazid, pyrazinamide and ethambutol) his TB symptoms improved. He tested HIV seropositive and his CD4 count was 34 cells/ml. He commenced antiretroviral therapy (ART) with stavudine, lamivudine and efavirenz two weeks after starting TB treatment. Four days after ART initiation he developed a dry cough, worsening shortness of breath, central cramping abdominal pains, and recurrence of drenching night sweats.
He was admitted to another hospital and was treated with high-dose cotrimoxazole and prednisone 80 mg daily for a presumptive diagnosis of Pneumocystis jiroveci pneumonia (which in our opinion was an incorrect diagnosis). ART was temporarily interrupted then restarted. He initially responded to this therapy, but symptoms worsened five days after he had completed a 14-day course of prednisone. Over the next few days, he developed progressively worsening shortness of breath as well as orthopnoea, paroxysmal nocturnal dyspnoea and pedal oedema. He was then referred to our facility, four weeks after the initiation of ART.
On admission, he was in severe cardiogenic shock. His peripheries were cold and radial pulses were not palpable. His systolic blood pressure, detectable only on palpation, was 60 mmHg. He had a regular heart rate of 130 beats/min. His apex beat was laterally displaced, diffuse and hypokinetic, his jugular venous pressure was elevated 10 cm and there was a third heart sound. On chest auscultation there were extensive bilateral coarse crepitations. He had tender hepatomegaly.
A chest radiograph showed worsening of the right mid-zone infiltrate that had been present prior to ART and was related to his pulmonary TB, as well as a marked increase in the cardiothoracic ratio . Echocardiography confirmed a globally dilated heart with a fractional shortening of 13%. The ECG on presentation showed sinus tachycardia with a heart rate of 122 beats/min . The QRS axis was –30 degrees, there was evidence of both left atrial and left ventricular hypertrophy by Cornell criteria, the QTc interval was prolonged at 453 ms, and there were widespread non-specific T-wave abnormalities. No other QRS or ST-segment abnormalities were noted.
A cardiac magnetic resonance image (MRI), performed after the patient was stabilised, showed no evidence of focal inflammation in the myocardium. The left ventricular ejection fraction was 15% on the MRI. Renal function was normal, haemoglobin was 10.6 g/dl, white cell count was 2.3 × 109/l, platelet count was 163 × 109/l and thyroid stimulating hormone level was 3.16 mU/l (normal range = 0.49–5.66). There was no history of significant ethanol abuse to suggest alcoholic cardiomyopathy.
Two diagnoses were made. Firstly, we made a diagnosis of paradoxical TB-associated immune reconstitution inflammatory syndrome (TB-IRIS). This was supported by his initial diagnosis of drug-susceptible pulmonary TB, his response to TB treatment prior to ART and then recurrence of TB symptoms associated with worsening of the pre-existing infiltrate of TB on the chest radiograph soon after ART commencement. Secondly, the patient had presented with severe acute heart failure four weeks after starting ART, coincident with the development of TB-IRIS. The cause of his heart failure was unclear and our considerations regarding the aetiology are discussed below.
He was transferred to the high-care unit and commenced on a dobutamine infusion, and once his blood pressure had improved over the next few days, furosemide, enalapril and spironolactone were introduced and the dobutamine weaned. His ART was stopped and he was recommenced on prednisone 100 mg daily initially. TB treatment was continued. Broad-spectrum antibiotics (ampicillin plus amikacin) were prescribed to cover the possibility of a bacterial pneumonia, but a blood culture was negative. He was also prescribed intravenous thiamine. Carvedilol was added later. ART was re-introduced after two weeks.
During the next two months, two attempts at weaning prednisone resulted in a return of his night sweats, dyspnoea, dry cough and worsening of his pre-existing infiltrates but not worsening of heart failure. On both occasions, he had rapid symptomatic improvement after reintroduction of high-dose prednisone. At evaluation three months after initial presentation, he was able to walk two kilometres on the flat, had no signs of heart failure and a repeat echocardiogram measured his fractional shortening as 22%. Prednisone was gradually weaned and he received six months in total. After six months on ART his CD4 count was 359 cells/ml, his HIV viral load was undetectable and his sputum TB culture was negative.


A 64-year-old woman presented to the emergency department after falling when she tripped on a rock while doing yard work. Physical examination revealed an open deformity of the left forearm (). Radial pulse was palpable, sensation was intact, and she had normal range of motion of the fingers. While awaiting radiographs, bedside ultrasound was performed ().
Ultrasound revealed intact radius and ulna and a large linear foreign body. The wooden foreign body was removed at the bedside () and patient was admitted for observation and intravenous antibiotics.


A 78 year-old woman complained of a gradually progressive gait abnormality, beginning with difficulty initiating steps after rising from a chair. Her symptoms progressed steadily over four years, to include shuffling during forward walking and FoG with both gait initiation and passage through doorways. She felt that her freezing was significantly improved by the use of a rolling walker. She noticed that her right leg tended to freeze more than the left, but denied resting tremor or stiffness. She also denied falls (including backward), other coordination difficulties, autonomic complaints, and numbness or weakness. Upper limb functioning was normal. A previous trial of levodopa (up to 800 mg daily) did not alleviate her symptoms. Medical history included non-insulin dependent diabetes mellitus, uncontrolled hyperlipidemia, and remote 3 pack-year cigarette exposure. She denied exposure to neuroleptics.
Examination revealed an oriented woman with normal language. Concentration was intact to complex backward spelling; executive function was intact to bedside Luria sequence testing. More detailed testing, however, revealed visuospatial and executive function deficits (clock drawing, box drawing, and Trails Part B), with a MOCA score of 22/30. Cranial nerves were normal. Tone and strength were normal. Resting tremor and bradykinesia were absent, including in the lower extremities. Proprioception was intact in the toes; coordination was normal. The right patellar reflex was brisk with crossed adduction; other reflexes were normal. Unassisted gait was wide based with freezing upon standing and prominent freezing with both straight walking and turning (see Additional file : video segment 1). The right foot was more affected by freezing with a pattern consisting of several small right steps with the right foot followed by one l step with the left. Walking with trekking poles resulted in dramatic improvement of gait and lessening of freezing (see Additional file : video segment 2). Despite significant gait impairments, standing balance in quiet stance was intact with normal postural sway, even on a foam surface.
Objective measures of gait from body-worn inertial sensors [] showed significant asymmetry of right and left lower leg angular velocity during forward walking, caused by a peculiar pattern of multiple, small right steps followed by a singular left step (“floor scanning”). This phenomenon was only related to this case, and not seen in healthy control subjects, idiopathic PD or vascular parkinsonism (Fig. vs. , , and ). The areas shaded in light blue (Fig. vs. ) highlight this interesting non-reciprocal, floor scanning gait pattern. The red shaded areas highlight separate FoG episodes during turning.
MRI of the brain showed a lesion in the anterior corpus callosum (Fig. ). It restricted diffusion but did not have an apparent diffusion coefficient (ADC) correlate to suggest acute infarct; nor did it enhance. Additional subcortical white matter changes were present in anterior periventricular and centrum semiovale regions, and were slightly more marked on the left (Fig. and ). MRI of the thoracic spine showed mild degenerative changes only. A DaT scan was not performed. Probabilistic tractography derived from diffusion tensor imaging revealed interhemispheric fiber loss in regions of the corpus callosum responsible for connecting the dorsal premotor (PMd) and pre-supplementary motor areas (pre-SMA) (Fig. ). For representative control data, see Fig. and .


A 64-year-old female with past medical history of hyperlipidemia, osteoporosis, and diverticulosis presented to the emergency department with worsening, debilitating lower back pain of one-month duration. Further history revealed anorexia, low-grade fever, sweating, and shortness of breath for about 3 weeks and 10 pounds of weight loss. One month earlier, she visited the emergency department for right lower quadrant pain and was discharged with the diagnosis of diverticulitis. Laboratory test at that time did not reveal anemia, hypercalcemia, or decreased renal function. An abdominal computed tomography done at that time revealed incidental splenomegaly at 14.5 cm. Further evaluation was deferred to her primary care physician. At this presentation in the emergency department, the vital signs were stable, and she was pale and cachectic. Abdominal examination revealed rigidity, distention, tender splenomegaly, and Grey Turner's sign. Neurologic examination of lower extremities revealed weakness and numbness with hyperreflexia. The rest of the physical examination was unrevealing. Laboratory investigation showed the following: white blood cells of 13.8 × 1000/μL, haemoglobin of 9 g/dL, and platelets of 101 × 1000/μL. The peripheral smear showed rouleaux formation and plasma cells less than 10%. Earlier laboratory findings showed mild normocytic anemia, thrombocytopenia, and normal white blood count. Internal hemorrhage was greatly suspected given the clinical and laboratory findings. Other laboratory tests were significant for a creatinine of 2.5 mg/dL and a total calcium level of 9.0 mg/dL. Urinalysis was positive for blood and protein, 511 mg/dL. Prothrombin time was slightly elevated 14.2 sec and a normal activated partial thromboplastin time. Biochemical tests revealed a low total protein at 6.5 g/dL and serum albumin was low at 2.7 g/dL. Serum LDH was elevated at 240 U/L (60–160 U/L). Quantitative D-dimer was more than 0.5 mg/L (reference value is less than 0.5 mg/L). Fibrinogen was normal with a value of 194 mg/dL (193–423 mg/dL). Quantitative immunoglobulin showed an increased IgG at 2187 mg/dL and decreased IgA and IgM levels. Serum and urine immunofixation identified a monoclonal IgG lambda. CT abdomen revealed interval worsening of splenomegaly to 20 cm, multiple enlarged lymph nodes, and retroperitoneal haemorrhage extending from the left kidney to the left inguinal region. MRI of lumbar spine done emergently as the lower extremities showed progressive paralysis revealed critical long segment spinal cord compression extending from the T12 to L5 level secondary to medullary canal haemorrhage (Figures and ).
The patient was transferred to the ICU for developing severe haemorrhagic shock. Based on the clinical and laboratory data the diagnosis of multiple myeloma versus plasma cell leukaemia was considered. Plasma cell leukaemia was excluded as the peripheral blood showed less than 20% plasma cells which is the major criteria for diagnosing this condition. The cause of retroperitoneal bleeding in the absence of a bleeding disorder, vascular disease, and anticoagulant medications was considered to be related to the basic disease of multiple myeloma. Given the emergent and rapidly worsening condition, the patient was started on high dose corticosteroids and supportive measures including vasopressors and blood products including packed red blood cell, fresh frozen plasma, and platelets transfusion. The patient haematocrit and platelets count continued to drop precipitously. In 5 days, the hematocrit dropped from 9 g/dL to 5.6 g/dL and the platelets dropped from 101 × 1000/μL to 56 × 1000/μL despite supportive measure with blood products. Haematological consult was obtained. Due to the poor clinical status, bone marrow biopsy was deferred. Also, neurosurgery consultation was obtained to evaluate the developing cord compression. She was deemed to be a very poor surgical candidate. The ICU course was complicated with DIC confirmed by PT of 24 sec (9–12 sec), PTT of 47 sec (25–35 sec), and fibrinogen of 75 mg/dL (193–423 mg/dL), worsening acute kidney injury with creatinine increasing from 2.5 mg/dL to 5.5 mg/dL, and acute hypoxic respiratory failure requiring endotracheal intubation due to severe refractory anemia leading to high output cardiac failure, and the chest X-ray revealed bilateral pulmonary vascular congestion and prominent left-sided pleural effusion. Finally, seven days after admission, her code status was changed to do-not-resuscitate per her family and healthcare proxy, given her refractory illness and poor prognosis. In the same day, she developed cardiac arrest and expired. Autopsy was obtained and gross evaluation revealed large blood clot in the left pelvis and retroperitoneal space measuring 40 cm in greatest dimension and weighing 1060 g indicating that the most likely cause of death was a haemorrhagic shock probably due to underlying bleeding diathesis secondary to platelets dysfunction. Microscopic evaluation confirmed the diagnosis of multiple myeloma with more than 60% CD138 and lambda light chain positive plasma cell in the bone marrow (Figures and ). Also, microscopic evaluation of the spleen revealed heavy infiltration of plasma cells. Microscopic evaluation of the kidneys revealed light chain casts consistent with Bence Jones protein. Congo red staining was negative ruling out amyloidosis.


A 54-year-old Caucasian woman with open angle glaucoma and a history of suboptimal medical therapeutic compliance owing to an intolerance to drops was referred to our Ophthalmology Department. She was severely obese (body mass index 37 kg/m2) and had type 2 diabetes but was using insulin with good metabolic control. Her best corrected visual acuity (BCVA) in both eyes was 1.0. Her IOP was 35 mmHg without the use of medication, though she achieved values of 18 mmHg in her right eye and 16 mmHg in her left eye with the use of tafluprost once daily. No changes were identified in an examination of her anterior segment. The papillary cup was 0.3 in her right eye with a temporal notch and her left eye had a normal appearance.
Our patient’s compliance to medical therapy continued to be poor, because she blamed her drops for coughing and dyspnea attacks. Without the use of drops, her IOP values remained consistently in the 30s. After continuous non-compliance with several other ocular medications, surgery was discussed as an alternative treatment option. The risks and potential complications of surgery were explained to our patient. No signs of cornea or ocular media opacity, retinal hemorrhage, macular or peripheral detachments, or other contraindications were observed in either eye. Our patient decided to opt for surgery. Her right eye was operated on first with an uneventful mitomycin C trabeculectomy (0.3 mg/ml, 3 minutes).
On the first postoperative day, our patient presented with a diffuse, functioning, and non-leaking filtration bleb, associated with a well-formed anterior chamber, and an IOP of 8 mmHg, with a normal appearance on fundoscopy. Two weeks postoperatively she complained of decreased visual acuity; her BCVA was 20/32 and her IOP was 10 mmHg without medication. Fundoscopy exhibited multiple superficial, flame-shaped retinal hemorrhages located centrifugally from the optic disc associated with optic disc edema (Fig. ). There was no evidence of choroidal effusion. A fundus examination of her left eye was unremarkable.
Optical coherence tomography (OCT) revealed folding of the macular retina associated with a small detachment of the neurosensory retina (Fig. ). The angiographic pattern showed macular microaneurysms associated with fluorescein diffusion, peripapillary hemorrhages, and late optic disc leakage, without ischemic areas or neovascularization (Fig. ). One month later the overall fundoscopic changes resolved spontaneously (Fig. ). Given this situation, a suspected diagnosis of DR was proposed. Other possible diagnoses were retinal venous occlusion or Valsalva retinopathy, but these were considered unlikely given the diagnostic results pattern. Subsequent follow-up visits were satisfactory, with our patient maintaining a steady IOP of 8–14 mmHg without medication. The peripapillary hemorrhages and optic disc edema spontaneously recovered during the second postoperative month, and our patient’s BCVA reached 20/25.
Three months later, she underwent an uncomplicated left eye trabeculectomy with mitomycin C (0.3 mg/ml, 3 minutes). No postoperative hypotony was registered. On the first postoperative day, the anterior chamber was formed, the bleb was diffuse, her IOP was 8 mmHg, and results from fundoscopy were normal, without choroidals. The pattern of clinical evolution of this eye was similar, with decreased vision complaints 10 days after surgery (her BCVA was 20/32). Her IOP was 9 mmHg, with no medication. A fundus examination revealed identifiable multiple peripapillary retinal hemorrhages, optic disc swelling, and macular edema (Fig. ). OCT revealed macular folding and neurosensory retinal detachment (Fig. ). Choroidal striation, optic disc leakage, and signs of macular microangiopathy and epitheliopathy were visible on angiography (Fig. ). The localized hemorrhages and sectorial optic disc edema reduced progressively and her macular edema recovered spontaneously during the first postoperative month (Fig. ). Her left eye IOP on the last follow-up visit was 16 mmHg without hypotensive medication and her BCVA was 20/25.
Given the occurrence of the same pattern in the contralateral eye, our patient’s complete medical history was reviewed again, with inquiries about possible hypertensive peaks, usual medication, and frequent Valsalva maneuvers. A summary infectious test was performed to rule out any possible systemic causes of bilateral papillitis. Results for the infectious study were negative.


A 64-year-old woman presented to the emergency room for muscular pain and headache after a slip down the stairs. Her initial blood pressure was 240/100 mmHg, but it decreased to 200/100 mmHg after resting. She had a history of hypertension for 13 years, and her blood pressure had become less responsive to medication, including calcium channel blocker, beta-blocker, angiotensin receptor blocker, and diuretics. After pain control, she was referred to the department of cardiology for her high blood pressure. For evaluation of uncontrolled hypertension, blood chemistry, Venereal Disease Research Laboratory (VDRL) test, serum renin and aldosterone assay, urinalysis, and electrocardiogram (ECG) were performed. All of these test results were normal except left ventricular hypertrophy (LVH) in ECG. Echocardiogram for LVH was performed and showed increased left ventricular mass (134 g/m2) and dilated left atrium (anteroposterior diameter 45.3 mm). The results of the subcostal four-chamber view imaging of the abdominal aorta revealed small-caliber abdominal aorta (Figure A) with marked flow acceleration (peak velocity =5.1 m/s) (Figure B). At this point, the patient’s blood pressure in the upper and lower extremities was measured. The blood pressure at her right upper extremity was 200/120 mmHg, left upper was 205/110 mmHg, right lower was 100/70 mmHg, and left lower was 110/75 mmHg. Aortic stenosis after branching to left subclavian artery was suspected. Subsequent aortic angiogram (Figure C) with aortic pressure measurement showed 88 mmHg systolic pressure gradient at the mid thoracic aorta. The pressure gradient of the aortic arch for both carotid arteries and renal artery was normal. Subsequently, bypass surgery between the ascending aorta and abdominal aorta was carried out successfully. Currently, the patient is taking beta-blockers and diuretics, and her blood pressure is stable without the use of other antihypertensive medication.


A 60-year-old woman was referred to the hospital because of substernal chest pain. She also experienced slowly progressive exertional dyspnea for 3 years. She had a history of hypertension for 10 years with an uncontrolled blood pressure, in spite of administration of multiple antihypertensive medications. Upon admission, her blood pressure was 167/67 mmHg and her heart rate was 68 bpm. Her ECG revealed LVH and following echocardiogram revealed LVH and left atrial enlargement with normal regional wall motion and global systolic function of the left ventricle. However, in subcostal view, the caliber of the abdominal aorta was diminished with increased systolic flow velocity. These findings suggested stenosis of the aorta. Subsequent aorta imaging study revealed stenosed thoracoabdominal aorta. The patient was also found to have multiple stenoses in the coronary arteries and both carotid arteries. During the screening test, ankle brachial index on both legs was decreased (right, 0.53; left, 0.57); the renin level was 19.37 ng/mL/h at supine position, and the VDRL test was not reactive. A diagnosis of Takayasu arteritis was made based on the results of the imaging studies, and other causes of stenosed aorta could be ruled out. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level were mildly elevated (ESR, 38 mm/h; CRP, 8.19 mg/L), indicating active inflammation, and therefore, a steroid therapy was initiated. Percutaneous intervention for coronary arteries and carotid arteries was performed, and aortic bypass surgery will be considered after stabilization of vascular inflammation.


The third case is a 61-year-old woman who presented with cardiac murmur and uncontrolled hypertension despite multiple antihypertensive drugs. At first visit, physical examination revealed high brachial systolic blood pressure of 200/25 mmHg, increased pulse pressure, bounding pulse, and loud to-and-fro murmur at the anterior and back of thorax. Aortic regurgitation was suspected. The results of laboratory test including renin, aldosterone, and VDRL were in normal range. Following echocardiography showed marked LVH and moderate to severe aortic regurgitation (Figure A,B). Similar to the case 1 result, the subcostal view revealed small-caliber abdominal aorta with high aortic flow velocity, which suggested aortic stenosis. Subsequent aortogram and carotid angiogram showed complete occlusion of the proximal left common carotid artery and narrowed descending thoracic aorta and proximal portion of the abdominal aorta with normal lower extremity. Aortic bypass surgery with aortic valve replacement was recommended, but the patient refused surgery.


A 66-year-old man presented to the clinic with a history of acute onset right lower quadrant abdominal pain, hematuria, and flank pain. General physical examination revealed no significant findings. The patient's family history revealed his mother had both thyroid and colon cancer, though the details of each were unknown.
Initial laboratory findings included mild iron deficiency anemia with elevated white blood cell count, increased BUN and creatinine, and a urine analysis positive for blood and protein. Abdominal CT scan revealed a hypervascular multilocular solid renal mass that had compromised Gerota's fascia and was occupying the right renal vein. Also noted on CT scan was an enhancing partially necrotic solid nodule within the left mesentery, as well as multiple diminutive ill-defined hepatic lesions.
The patient then underwent a right radical nephrectomy with tumor thrombectomy and retroperitoneal lymph node dissection. During intraoperative inspection of the mesenteric region, an ileal mass was encountered, and an en bloc resection was performed with primary anastomosis and ultrasound-guided liver biopsies.
Evaluation of the nephrectomy specimen revealed a 7 cm Fuhrman grade 2 clear cell RCC invading the renal vein with lymphovascular invasion and clear surgical margins without invasion of Gerota's fascia or the renal sinus (T3aN0M0) (). The resected small bowel specimen demonstrated a 2.5 cm ileal mass with multiple foci of intermediate grade neuroendocrine carcinoma (G2 with 12 mitoses per high-power field) seen in penetrating the serosal surface of the bowel with both lymphovascular and perineural invasion. Interestingly 2/15 mesenteric lymph nodes, 8/13 paracaval nodes, and 3 mesenteric nodules were positive for neuroendocrine carcinoma (T4N1M0). Liver biopsy revealed the presence of localized hemangiomas. Following successful resection of both tumors, his brain MRI; CT of the chest, abdomen, and pelvis; and octreotide scan found no evidence of additional metastatic disease. Preoperative 24-hour urine for 5-HIAA was mildly elevated but postoperative repeat was normal. The patient recovered well after surgery and continues to follow up regularly with no signs of reoccurrence in 20 months after surgery.


A 61-year-old man presented with constant dull right lower quadrant pain associated with fatigue and malaise. Initial CT scan showed an enlarged appendix and a partially exophytic, enhancing mass located in the upper pole of the left kidney with an enlarged para-aortic lymph node (). The patient then underwent appendectomy; pathology findings showed a low-grade appendiceal mucinous neoplasm. After recovery, the patient was then referred to the urology service for assessment and treatment of the left renal mass.
Initial examination of the patient revealed an asymptomatic well-developed man. Besides a past medical history of hypertension, the patient was otherwise healthy. Upon physical examination, findings included bilaterally descended testes, left grade II varicocele, and lack of lymphadenopathy or hernia. The patient's family history was insignificant. The patient's CBC and serum chemistry panel were normal. Urinary analysis found 3 RBCs per high-power field but was otherwise normal.
The patient then underwent left-sided robotic-assisted partial nephrectomy with para-aortic lymphadenectomy. Histological findings of the renal mass confirmed a 3 cm Fuhrman grade 3, clear cell RCC limited to the renal parenchyma with negative margins. Resection of lymph nodes revealed 0/6 perihilar and 1/14 para-aortic nodes with metastasis. He was, therefore, staged as a T1aN1M0. Following removal of tumors, the patient recovered without complication. A follow-up CT scan was performed four months postoperatively and showed no evidence of metastasis. The patient is currently in good health and has no evidence of disease at four-month follow-up.


A 36-year-old female initially presented for evaluation of a left supraclavicular neck mass. The patient underwent fine needle aspiration of the mass, which revealed adenocarcinoma favoring renal cell. CT scan of the chest, abdomen, and pelvis revealed a large left renal mass 9 cm in diameter. The scan incidentally also detected a possible filling defect in the transverse colon. The patient underwent colonoscopy, and a mass was visualized and biopsied. Histological examination found the mass to be positive for invasive adenocarcinoma.
Physical examination of the patient revealed an overweight woman with a past medical history of hypertension. The patient denied any changes in bowel habits or urinary complaints other than intermittent left flank pain. The patient reported that her family history was negative for cancer or polyps. General physical examination revealed a small nodule palpable in the left supraclavicular region of the patient's neck. Laboratory findings were normal except for presence of iron deficiency anemia.
The patient then underwent left radical nephrectomy with periaortic lymphadenectomy and extended right hemicolectomy. Histological examination of the left kidney confirmed a 7.5 cm Fuhrman grade 4, clear cell RCC limited within Gerota's fascia with no lymphovascular invasion. The tumor was present in 5/5 periaortic lymph nodes that were resected (T2aN1Mx). The resected large bowel specimens demonstrated tubular adenoma present in the cecum and hepatic flexure; also noted was moderately differentiated invasive adenocarcinoma extending into the submucosa of the transverse colon (T1N0M0) (). Microsatellite instability staining was ordered; results were positive for hereditary nonpolyposis colorectal cancer (HNPCC). Given this patient's negative family history of colon cancer, this was likely a spontaneous mutation. The patient developed chylous ascites and peritonitis with acute kidney injury postoperatively and returned to the operating room for evacuation of fluid and ileostomy placement. She eventually recovered following a cardiac diet (low fat, low cholesterol, and high protein) with peritoneal drainage and octreotide.
She was started on sunitinib postoperatively but failed therapy after developing bilateral malignant pleural effusion and malignant disease progression and was subsequently given temsirolimus.
After one month, postoperative CT scan revealed local recurrence in the kidney bed, suggesting highly aggressive cancer. Imaging also found enhancing enlarged supraclavicular lymph nodes extending cranially along the jugular chain and caudally into the mediastinum. This finding was strongly suggestive of metastatic disease. PET scan was performed and confirmed diffuse nodal metastasis throughout the thorax and neck. She then underwent chest wall biopsy and pleurodesis using video-assisted thoracoscopic surgery, the results of which confirmed malignant RCC. The patient died approximately one year following initial resection.


The patient was a 34-year-old African American US-born single female. At the time of the investigation she was unemployed and lived temporarily with her mother, who had a history of paranoid schizophrenia. The patient was brought to the psychiatry emergency room by ambulance for evaluation of aggression. Upon presentation, the patient described an altercation with her mother's landlady, hitting her numerous times in the face with a closed fist. The patient started the altercation because she felt that the landlady practiced voodoo and had cursed her, causing her hair to fall off. She described an overwhelming rage prior to the physical assault. The patient did not show any remorse for her actions: “I hate her,” “I did the right things,” and “She is evil” are examples of statements made by the patient. Collateral information from the patient's mother revealed that the patient had not been compliant with her medications. She refused to follow up with outpatient care after the last inpatient admission ten months previously. The patient denied auditory hallucinations but appeared to be internally preoccupied. She denied visual and tactile hallucinations, thought insertion, and thought broadcasting. She reported an unchanged pattern of sleep and appetite, which she described to be “good.” Prior to this episode, the patient had been under economic and emotional stress. She lost her job as a nurse aide five months earlier and had not been able to secure another job since then. The patient broke up with her fiancée ten months previously after cutting her fiancée's stepfather's face following verbal altercation. There was no symptom suggestive of mania, seizure disorder, head trauma, loss of consciousness, cerebrovascular accident, Parkinson's disease, anxiety, or other organic brain disorder. The patient denied use of nicotine, alcohol, and other psychoactive substances currently or in the past. The patient had her first inpatient psychiatry admission for acute exacerbation of paranoid schizophrenia and FAS ten months earlier. She was then treated with risperidone tablets with improvement including change in accent on discharge, when she was less psychotic. The patient had a family history of sickle cell disease (brother had sickle cell disease) and schizophrenia (brother, mother, and uncle had schizophrenia). Birth and developmental history were unremarkable. There were no reported behavioral or learning disabilities, and the patient denied being a victim of emotional, physical, or sexual abuse. She had some college education and worked as a nurse aide up till five months prior to presentation to the hospital.
Mental status examination showed a middle-aged, well-groomed, dark-haired woman with poor eye contact and in no apparent distress. The patient was tangential and preoccupied with “voodoo” and was deeply paranoid of her neighbors and her mother's landlady. Auditory hallucinations were not elicited, and she denied suicidal ideation at the time of evaluation. The patient continued to endorse homicidal ideation towards her mother's landlady. She was awake, alert, orientated in time, place, and person, and attentive and had good concentration but had poor impulse control. Her insight and judgment were impaired. Immediate recall and short- and long-term memory were intact.
The physical examination of the patient showed no significant pathological findings. Laboratory investigations were unremarkable. Electroencephalogram showed no seizure activity. Structural magnetic resonance imaging (MRI) and MR angiography of the head were both unremarkable.
The patient presented with a British-like accent, despite never having lived in Britain, and was therefore investigated by a speech therapist. There was no phonetic problem or grammatical errors, but there was a problem with prosody, including prominence of the pitch of the words and syllables. The patient's pitch range was narrow, as she sparingly expressed any emotions during speech. Her speech was monotonous, hesitant, and of low volume. She substituted “th” for “f” and “w” for “wh” as well as “t” for “d” and “ai” for “ei.”
The patient was diagnosed according to DSM-V criteria with paranoid schizophrenia, chronic condition with acute exacerbation, and in addition FAS. The diagnosis of schizophrenia was made based on disorganized speech, specifically tangentiality, paranoid delusions, and grossly disorganized behavior, which lasted for more than ten months and affected the level of functioning, specifically with regard to interpersonal relations and occupation. This was determined not to be due to illicit drug use or known medical illness.
The patient was discharged from the previous hospitalization ten months earlier with a prescription of disintegrating tablets of risperidone. However, she was not compliant with this compound after discharge and also refused to take it during the second hospital admission described here. The patient agreed to take olanzapine tablets to address her psychosis. She was offered a readily dissolvable formula, as we had concern she was “checking” her medications to spit out after administration. However, the patient refused to take any other medication than conventional olanzapine tablets. The olanzapine serum concentration could not be controlled, because the patient became more delusional and refused further blood work. The patient continued to have psychotic symptoms and her foreign accent remained unchanged. She refused augmentation with any other antipsychotic medication because of paranoia. In the course of treatment, the patient continued to endorse homicidal ideation, paranoid ideation towards her mother's landlady, and still spoke in a British accent. In view of unremitting psychotic symptoms, she was transferred to a long-term psychiatric inpatient facility.


A 60-year-old male was admitted to our hospital with a complaint of right lower abdominal pain. The patient did not have same symptoms before, and he only had a medical history of asthma. The laboratory data on admission showed a slightly elevated WBC count of 9,300/μl and a CRP level of 1.0 mg/dl, but the tumor marker levels (CEA, CA19-9) were almost within the normal limits. Abdominal computed tomography (CT) demonstrated a 15-cm large cystic mass, like a dilated intestine, and fluid collection was observed inside.
The cystic mass was adhered to the ileum, but there was no definite communication to the ileum. The feeding arteries of the cyst were communicating branches from the upper mesentery artery, and the lymph nodes around the cyst were slightly swollen (Figure a,c). At the small-bowel follow-through exam, the cyst did not come out, but it did exclude normal intestine (Figure b). There were not significant findings during a colonoscopic examination.
Based on these findings, we diagnosed the cyst as an ileal duplication and decided to perform surgery in order to prevent a recurrence of abdominal pain and lethal complications, such as bleeding or perforation.
We employed a four-port laparoscope-assisted resection of the duplicated ileum and segmental resection of the normal ileum. An umbilical port was used for a mini-laparotomy with a zigzag skin incision (Figure a). The cyst’s stalk was attached to the base of the mesentery of the terminal ileum, approximately 40 cm from the ileocecal junction (Figure b,c). After resection of the cyst, a side-to-side anastomosis of the ileum was made with a stapler.
The resected specimen showed an ileal duplication of 18 × 7 cm in diameter, filled with purulent matter with some ulcers inside (Figure a). The histological findings showed that it had a mucus gland inside, like intestinal epithelium, and was covered with two layers of smooth muscle. There was no communication between the duplication and normal ileum, but they had a common muscle layer (Figure b,c).
The postoperative period was uneventful without any asthma attack, and the patient was discharged on the 13th postoperative day.


A 65-year-old Hispanic man with a significant past medical history of disseminated cutaneous coccidioidomycosis infection, hiatal hernia, and portal hypertensive gastropathy presented to the emergency room after a 5-day history of worsened shortness of breath associated with diffuse abdominal pain. The patient was in his normal state of health until approximately 5 months prior to admission when he began to notice a rash in the T4-T9 dermatome. At that time, the patient was diagnosed with disseminated cutaneous coccidioidomycosis. Over the course of the next 5 months, he began to experience abdominal pain and was seen in the outpatient clinic. Referral for abdominal ultrasound during this time demonstrated normal hepatic portal vein, hepatic artery, and IVC (Inferior Vena Cava) flow on color Doppler. A CT scan of the abdomen 1 month prior to admission showed moderate ascites, with a new-onset 2.02-cm nodule on the left lower lobe, left pleural effusion, splenomegaly, and ascites, and esophagogastroduodenoscopy showed grade 1 esophageal varices, diffuse portal hypertensive gastropathy, and a sliding hiatal hernia. Liver biopsy was subsequently done, which showed mild inflammatory activity and fibrosis.
On the day of admission, the patient’s vital signs were stable, and physical exam showed diminished breath sounds with rales bilaterally, abdominal distention with moderate fluid shift, caput medusa, umbilical protrusion, tenderness in all 4 quadrants, 15-cm liver span, splenomegaly, and a positive fluid wave. CBC(Complete Blood Count) displayed marked pancytopenia. The patient denied any history of alcohol abuse or recent travel.
On day 2, the patient continued to complain of abdominal pain and shortness of breath. Physical examination showed oxygen saturation of 88% with worsening ascites and still positive for rales. Repeat imaging of the abdomen was done on day 2 of admission, which confirmed ascites and pleural effusion that was previously reported (). A thoracentesis and paracentesis helped relieve the patient’s symptoms ( and ). Pleural fluid was exudative. Paracentesis confirmed a SAAG(Serum Ascites Albumin Gradient) score of 1.2, suggesting portal hypertension. Microbiology of both body fluids showed no evidence of infection. CT and ultrasound of the abdomen were positive for ascites and splenomegaly but negative for cirrhosis. Considering thrombosis as a possible cause of portal hypertension, reevaluation of the ultrasound showed patent hepatic vasculature, including the portal vein, hepatic vein, and splenic vein (). Laboratory results showed pancytopenia, elevated alkaline phosphatase levels, elevated GGT(Gamma-Glutamyl Transferase) levels, and elevated 5′ nucleotidase. Given the results, splenic causes of pancytopenia were considered.
On day 4, symptoms persisted. A peripheral blood smear showed pancytopenia and the presence of dacrocytes, elliptocytes, echinocytes, and anisocytosis. Hematology/Oncology was consulted and recommended flow cytometry of the bone marrow aspirate and a bone marrow biopsy. Both were completed and pending. On day 5, the patient complained of abdominal pain again, but denied shortness of breath and maintained an oxygen saturation above 94%. A therapeutic paracentesis was done, which relieved the abdominal pain.
Flow cytometry of the bone marrow showed a small population of monotypic B cells of uncertain clinical significance and T cells with minor immunophenotypic alterations but no abnormal myeloid cell populations. Furthermore, JAK-2 kinase was negative; B cells were positive for CD 20 and negative for CD 5, 10, and 11c ( and ). Subsequently, bone marrow biopsy showed a hypercellular marrow with trilineage hyperplasia, mild eosinophilia, focal mild reticulin fibrosis, and mild increase in iron and was positive for a monoclonal B cell population (). These findings were consistent with SMZL. These results, in addition to the lack of hepatic congestion and/or cirrhosis, led to the diagnosis of noncirrhotic portal hypertension.
The patient no longer complained of shortness of breath throughout the rest of the hospitalization. Abdominal pain slowly returned; however, it remained stable and was controlled with acetaminophen with codeine. On day 14, the patient was discharged. To obtain a second opinion regarding hepatosplenomegaly and portal hypertension, the patient was referred to an outside gastroenterologist for a higher level of care. The patient was also advised to follow with his primary care physician within 4 weeks.