Unnikrishnan Pillai

Severe propylene glycol toxicity secondary to use of anti-epileptics.

Propylene glycol toxicity presenting as high anion gap metabolic acidosis and osmolar gap has been extensively reported in literature, and most of them are secondary to intravenous lorazepam infusion. However, propylene glycol is used as a solvent in a number of medications that are frequently utilized in critical care setting, and hence one should be aware that the toxicity is possible from a variety of medication. Phenobarbital and phenytoin are one of those, and we hereby report a novel case of propylene glycol toxicity secondary to phenobarbital and phenytoin infusion in a patient with refractory status epilepticus. Furthermore, our patient had end-stage renal disease, which we think could have been an important precipitating factor for the toxicity. Because most of the symptoms from propylene glycol toxicity can mimic sepsis—which is very common in critical care unit patients—this life threatening scenario could be easily missed. Regular monitoring of osmolar gap is an easily available intervention in the at risk patients.

Immunoglobulin A Nephropathy: A Review of Current Literature on Emerging Pathophysiology

Abstract:Immunoglobulin (Ig) A nephropathy is one of the most common causes of glomerulonephritis worldwide. Its prognosis can be totally different in various patient populations, ranging from asymptomatic slow progression to end-stage renal disease in as much as 40% of patients in few months to years. This disease process can be idiopathic, or it can be associated with a variety of disease processes. Various risk stratification scoring systems are available, which can predict the long-term outcome. New evidences are also emerging that IgA nephropathy is an autoimmune disease with a known antigen, galactose-deficient IgA1, which can elicit an autoantibody response and formation of immune complexes that are deposited in the mesangium.

Colchicine-induced myopathy in a tacrolimus-treated renal transplant recipient: Case report and literature review

Renal transplant recipients are prone to develop drug toxicities because of polypharmacy and drug-drug interactions. Colchicine is often used for the treatment of gout in these patients as nonsteroidal medications are contraindicated. In addition, patients are often on corticosteroids and frequent, periodic, dose escalation for gouty flare may lead to side effects. Colchicine-induced myopathy has been very well described in the literature. Several cases of colchicine toxicity have been reported in cyclosporine-treated patients due to a drug-drug interaction. We report a 62-year-old African American renal transplant recipient who had been doing well on tacrolimus-based immunosuppression and was started on colchicine (0.6 mg twice daily) for gouty flare. A few days later, he was found to have a 4-fold increase in aspartate aminotransferase and an elevated creatine phosphokinase. Although this interaction is very well known with cyclosporine, it has not yet been reported in patients on tacrolimus.

A Rare Case of Hyperammonemia Complication of High-Protein Parenteral Nutrition

Hyperammonemia is a metabolic derangement that can be potentially fatal. Primary hyperammonemia due to urea cycle enzyme deficiency is usually discovered in neonates but rarely can present in adulthood. Late-onset manifestations of urea cycle disorders can go unnoticed, until they become life threatening. The authors report a 28-year-old man who developed hyperammonemia in the hospital following parenteral nutrition (PN), leading to cerebral edema, which was fatal despite resolution of the hyperammonemia with cessation of PN and the use of continuous renal replacement therapy.

Downhill varices secondary to HeRO graft-related SVC syndrome.

Tunneled hemodialysis catheters are well‐documented causes of benign central vein stenosis, which can be associated with proximal or downhill esophageal varices due to shunting of blood flow from the upper portion of the body through the esophageal venous plexuses. A majority of these cases remain asymptomatic. As a result, studies are largely limited to symptomatic patients, with incidence rates ranging from 16% to 29%. Recently, Hemodialysis Reliable Outflow (HeRO) graft has been introduced as an effective alternate hemodialysis access in catheter‐dependent patients, especially in the presence of significant central venous occlusion. It differs from a conventional arteriovenous graft (AVG) by the fact that its venous outflow end is in the right atrium via one of the central veins, bypassing any significant occlusion upstream. Lower intervention rates and reduced incidence of bacteremia make it comparable to conventional tunneled catheters. However, the incidence of central vein occlusion and associated complications with HeRO grafts is unknown. We present the first case of gastrointestinal bleeding from downhill esophageal varices secondary to HeRO – graft‐related SVC occlusion.

Extensive Deep Venous Thrombosis in a Patient with Neurolept Malignant Syndrome despite Being on Prophylaxis

The risk of venous thromboembolism (VTE) in patients with Neuroleptic malignant syndrome (NMS) and those on antipsychotic medications is well established. We present here a case whereby the patient had NMS and developed extensive deep venous thrombosis (DVT) despite being on standard DVT Prophylaxis. Our case illustrates that empiric intravenous heparin for the initial few days after the onset of NMS may be considered in those with high risk of VTE, as in such patients standard DVT prophylaxis may not be sufficient. To standardize as to which patients with NMS would be at the highest risk of VTE while on standard DVT prophylaxis, the role of a standardized scoring system and a double-blind randomized trial in the future would probably be beneficial.

Resistant hyponatremia and hypokalemia treated successfully with nephrectomy

Persistent hyponatremia and hypokalemia in the setting of hypertension may be a manifestation of an underlying hyperreninemic state. We present here a case of a patient who presented with a constellation of hypertension with severe polydipsia, subnephrotic proteinuria, with resistant hyponatremia and hypokalemia. Workup revealed an elevated plasma renin activity and elevated plasma aldosterone. Magnetic resonance imaging of the renal vasculature revealed complete occlusion of the right renal artery and a nuclear medicine renal scan showed a split renal function of 87% for the left kidney and 13% for the right kidney. The use of angiotensin receptor blockers (ARB) and angiotensin-converting enzyme (ACE) inhibitors was contraindicated due to a history of angioedema. Nephrectomy of the ischemic kidney was thus planned, and it resulted in a dramatic and complete resolution of his laboratory abnormalities and hypertension.

Intracranial capillary hemangioma mimicking a dissociative disorder

Capillary hemangiomas, hamartomatous proliferation of vascular endothelial cells, are rare in the central nervous system (CNS). Intracranial capillary hemangiomas presenting with reversible behavioral abnormalities and focal neurological deficits have rarely been reported. We report a case of CNS capillary hemangioma presenting with transient focal neurological deficits and behavioral abnormalities mimicking Gansers syndrome. Patient underwent total excision of the vascular malformation, resulting in complete resolution of his symptoms.

Coagulopathy and spontaneous hemorrhage in a patient with nephrotic syndrome.

Patients with nephrotic syndrome, particularly those with membranous nephropathy tend to be in a hypercoagulable state and often present with thromboembolic phenomena. The association of nephrotic syndrome with a bleeding diathesis however is much less common and the etiologies less well recognized. We report a patient who presented with coagulopathy and recurrent spontaneous hemorrhage in association with nephrotic syndrome. The case highlights key diagnostic and therapeutic challenges and strategies: 1) work up to establish a unifying etiology for both nephrotic syndrome and the bleeding disorder; 2) decision making to obtain a tissue biopsy, select the site of biopsy and understand the relative yields for each site; 3) recognizing the risk and managing peri-procedural bleeding; and 5) developing a treatment strategy with the lowest risk of possible complications. Our patient underwent a kidney biopsy without any complications and a definitive diagnosis of AL amyloidosis was reached. He was treated with anti-plasma cell chemotherapy followed by autologous stem cell transplant with resultant complete hematologic response, improved coagulation parameters, and no further bleeding.

Ectopic ACTH and cisplatin toxicity--a diagnostic dilemma.

Ectopic Adrenocorticotropic hormone (ACTH) causes 20% of ACTH-dependent Cushing syndrome and can often be the primary manifestation of an underlying malignancy, most commonly small cell lung cancer. This syndrome is characterized by the rapid onset and progression of Cushing syndrome with hypertension, hyperpigmentation, hypokalemia, and metabolic alkalosis. Cisplatin, a common chemotherapeutic agent used in the treatment of lung cancer, can sometimes present with electrolyte abnormalities, which can mimic ACTH-dependent Cushing syndrome. We present an atypical case of ectopic ACTH syndrome related to an underlying small cell lung cancer, with a background of cisplatin-related tubulopathy.