Spontaneous Cholesterol Embolism Leading to Small Bowel Obstruction and Perforation.

A spontaneous occurrence of cholesterol embolization syndrome causing small bowel obstruction and perforation is a highly scarce event. In this article, we report a case of spontaneous cholesterol embolism resulting in small bowel obstruction and perforation in a 52-year-old male with multiple cardiovascular and medical comorbidities. In our patient, the source was an eccentric left lateral atherosclerotic plaque from the abdominal aorta that was identified using computed tomography. A distal occlusion in numerous small intestinal arteries due to cholesterol embolism was confirmed on biopsy after surgical resection. (Level of Difficulty: Intermediate.).

Cerebral Salt Wasting Syndrome Following Right Occipital Craniotomy in a Patient With Metastatic Lung Adenocarcinoma.

Cerebral salt wasting syndrome (CSW) is characterized by excessive natriuresis leading to hyponatremia and hypovolemia. It is commonly encountered among patients who have undergone brain trauma or subarachnoid hemorrhage. The occurrence of CSW after neurosurgical procedures has been frequently reported in the pediatric age group; however, it is a rare phenomenon in adults. We describe the case of a 59-year-old female who developed symptoms of polyuria and polydipsia after a right occipital craniotomy.

Infected Hemodialysis Arteriovenous Fistula with Distant Explosive Pleuritis: A Rare Phenomenon.

BACKGROUND The management of patients with end-stage kidney disease can be accomplished with hemodialysis via a surgically created arteriovenous fistula. An arteriovenous fistula has an advantage because of the ability to serve as permanent access for hemodialysis over several months to years; however, it has a disadvantage because of its associated vascular and infectious complications. An infectious complication such as explosive pleuritis, which is usually due to respiratory infections, in the setting of an infected arteriovenous fistula site infection, is extremely rare. CASE REPORT A 36-year-old man with a past medical history of IgA nephropathy on hemodialysis with a left forearm arteriovenous fistula presented to the Emergency Department because of left flank pain. Despite no recent history or evidence of a respiratory tract infection, he developed explosive pleuritis within 48 h. The presence of Group A Streptococcus at the arteriovenous fistula site coincided with Streptococcus pyogenes infection. The pleural effusion was drained and he was treated with antibiotics. He recovered and was eventually discharged home. CONCLUSIONS Explosive pleuritis, although less frequent, is almost always secondary to respiratory tract infections. An arteriovenous fistula site infection may be the source of infection of an internal organ if no apparent source is identified.

A Real Neglected Problem With a Grave Prognosis: Nephrogenic Ascites.

Nephrogenic ascites is described as a clinical condition of refractory ascites in patients with end-stage renal disease (ESRD) on renal replacement therapy. This entity was first described in 1970. Many nephrologists do not believe in nephrogenic ascites. The underlying etiologies can be multifactorial including a combination of poor nutrition, inadequate dialysis and ultrafiltration, increased peritoneal membrane permeability, and overall uremia. The nephrogenic ascites is a rare syndrome and is often associated with a grave prognosis especially if it is not diagnosed early and treated. In the present study, we report a 27-year-old woman with past medical history of diabetes type 1 (diagnosed at age 11), ESRD secondary to diabetic nephropathy on hemodialysis (diagnosis in December 2017), bilateral diabetic retinopathy, ovarian cyst, hypertension, and anxiety who presented to the emergency department for evaluation of intractable abdominal pain, nausea and vomiting for 2-day duration. She was found to have large ascites. Diagnostic paracentesis was done and found to be exudative with serum ascites albumin gradient (SAAG) of 0.7. After detailed workup, hepatic, cardiac, infectious and malignant causes for ascites were ruled out. The diagnosis of ascites of nephrogenic origin was made. Given the patient's situation and her inability of self-care, she is not a good candidate for intra-abdominal dialysis. The patient has been treated conservatively with salt/fluid restriction and intensive hemodialysis with ultrafiltration.

Development of glomerulonephritis during anti-TNF-alpha therapy for rheumatoid arthritis.

BACKGROUND: Treatment of rheumatoid arthritis with anti-tumour necrosis factor alpha (TNFalpha) agents may lead to autoantibody formation and flares of vasculitis, but renal complications are rare. METHODS: We report the clinical and pathologic findings in five patients with longstanding rheumatoid arthritis (duration of rheumatoid arthritis, 10-30 years; mean, 23 years) who developed new onset of glomerular disease after commencing therapy with anti-TNFalpha agents (duration of therapy, 3-30 months; median, 6 months). RESULTS: At presentation, three patients were receiving etanercept, one adalimumab and one infliximab. Two subjects presented with acute renal insufficiency, haematuria, nephrotic-range proteinuria, positive lupus serologies, and hypocomplementemia, and renal biopsies showed proliferative lupus nephritis. Two individuals presented with new onset renal insufficiency, haematuria and proteinuria, and renal biopsies showed pauci-immune necrotizing and crescentic glomerulonephritis. One of these subjects, who had anti-myeloperoxidase autoantibodies, also developed pulmonary vasculitis. The fifth patient presented with nephrotic syndrome and renal biopsy findings of membranous glomerulonephritis, associated with immune complex renal vasculitis. A pathogenic role for anti-TNFalpha therapy is suggested by the close temporal relationship with development of glomerular disease, and by the improvement in clinical and laboratory abnormalities after drug withdrawal and initiation of immunosuppressive therapy in most cases. CONCLUSIONS: Rheumatoid arthritis patients receiving anti-TNFalpha agents may develop glomerulonephritis via the induction of rheumatoid arthritis-related nephropathy or de novo autoimmune disorders.