Spontaneous haematomas and haematochezia due to vitamin C deficiency in a haemodialysis patient.

A man in his 50s with dialysis-dependent end-stage renal disease, several weeks history of progressive skin bruising and acute-onset gastrointestinal bleeding presented to the emergency department following a syncopal event during routine haemodialysis owing to profound hypotension. He was found to have a severe normocytic, normochromic anaemia requiring several blood transfusions. He followed a diet lacking fruits and vegetables and stopped taking renal multivitamins. All parameters of coagulation were unremarkable, but serum vitamin C level was undetectable, supporting a diagnosis of scurvy. Although typically associated with individuals who are at risk of malnourishment, such as those with alcohol use disorder, malabsorption, and those who experience homelessness, scurvy should be considered in patients receiving renal replacement therapy as vitamin C is removed during haemodialysis.

Utility of Hypertonic Saline and Diazepam in COVID-19-Related Hydroxychloroquine Toxicity.

BACKGROUND: Hydroxychloroquine (HCQ) poisoning is a life-threatening but treatable toxic ingestion. The scale of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (COVID-19) and the controversial suggestion that HCQ is a treatment option have led to a significant increase in HCQ use. HCQ poisoning should be at the top-of-mind for emergency providers in cases of toxic ingestion. Treatment for HCQ poisoning includes sodium bicarbonate, epinephrine, and aggressive electrolyte repletion. We highlight the use of hypertonic saline and diazepam. CASE REPORT: We describe the case of a 37-year-old man who presented to the emergency department after the ingestion of approximately 16 g of HCQ tablets (initial serum concentration 4270 ng/mL). He was treated with an epinephrine infusion, hypertonic sodium chloride, high-dose diazepam, sodium bicarbonate, and aggressive potassium repletion. Persistent altered mental status necessitated intubation, and he was managed in the medical intensive care unit until his QRS widening and QTc prolongation resolved. After his mental status improved and it was confirmed that his ingestion was not with the intent to self-harm, he was discharged home with outpatient follow-up. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: For patients presenting with HCQ overdose and an unknown initial serum potassium level, high-dose diazepam and hypertonic sodium chloride should be started immediately for the patient with widened QRS. The choice of hypertonic sodium chloride instead of sodium bicarbonate is to avoid exacerbating underlying hypokalemia which may in turn potentiate unstable dysrhythmia. In addition, early intubation should be a priority in vomiting patients because both HCQ toxicity and high-dose diazepam cause profound sedation.

Topiramate and metabolic acidosis: an evolving story.

Topiramate is an anticonvulsant that is being increasingly used for a number of different off-label indications. Its inhibition of carbonic anhydrase isoenzymes can lead to metabolic acidosis, elevated urine pH, reduced urine citrate, and hypercalciuria, thereby creating a milieu that is ripe for calcium phosphate stone formation. In this review, we describe a case of topiramate-induced metabolic acidosis. We review the frequency of metabolic acidosis among children and adults, as well as the mechanism of hyperchloremic metabolic acidosis and renal tubular acidosis in topiramate users. Finally, we describe the long-term effects of topiramate-induced metabolic acidosis, including nephrolithiasis, nephrocalcinosis, and bone degradation. Patients who are prescribed topiramate should be carefully monitored for metabolic derangements, and they may benefit from alkali supplementation, or in extreme cases, discontinuation of the drug altogether.

The calcium-alkali syndrome.

The milk-alkali syndrome was a common cause of hypercalcemia, metabolic alkalosis, and renal failure in the early 20th century. It was caused by the ingestion of large quantities of milk and absorbable alkali to treat peptic ulcer disease. The syndrome virtually vanished after introduction of histamine-2 blockers and proton pump inhibitors. More recently, a similar condition called the calcium-alkali syndrome has emerged as a common cause of hypercalcemia and alkalosis. It is usually caused by the ingestion of large amounts of calcium carbonate salts to prevent or treat osteoporosis and dyspepsia. We describe a 78-year-old woman who presented with weakness, malaise, and confusion. She was found to have hypercalcemia, acute renal failure, and metabolic alkalosis. Upon further questioning, she reported use of large amounts of calcium carbonate tablets to treat recent heartburn symptoms. Calcium supplements were discontinued, and she was treated with intravenous normal saline. After 5 days, the calcium and bicarbonate levels normalized and renal function returned to baseline. In this article, we review the pathogenesis of the calcium-alkali syndrome as well as the differences between the traditional and modern syndromes.

Pulmonary invasive mucormycosis in a patient with secondary iron overload following deferoxamine therapy.

Mucormycosis (zygomycosis) is an acute and often fatal opportunistic fungal infection. Predisposing factors in the development of mucormycosis are nonspecific and include hyperglycemia, hematologic malignancies, neutropenia, pharmacologic immunosuppression, solid organ or bone marrow/stem cell transplantation, burns, trauma, malnutrition, and intravenous drug use. Mucormycosis has also been described in patients with iron and aluminum overload, patients on dialysis, and patients receiving iron chelating therapy. We describe a 75-year-old man with myelodysplastic syndrome and iron overload secondary to multiple red blood cell transfusions who had been treated with deferoxamine chelation therapy. He was admitted to the hospital for atrial fibrillation, developed multiple organ failure, and died. Pulmonary invasive mucormycosis was demonstrated at autopsy. This case further documents an association between invasive mucormycosis, iron overload, and deferoxamine therapy.

Collapsing focal segmental glomerulosclerosis following treatment with high-dose pamidronate.

Collapsing focal segmental glomerulosclerosis (FSGS) is a distinct clinicopathologic entity seen most commonly in young African American patients who present with renal insufficiency and nephrotic syndrome. The only epidemiologic factor previously linked to collapsing FSGS is HIV infection. Here clinicopathologic findings are reported for a distinctive population of seven patients, who were older, Caucasian, and HIV negative and developed collapsing FSGS during active treatment of malignancy (multiple myeloma in six patients and metastatic breast carcinoma in one). Although oncologic treatment regimens included vincristine for four patients, doxorubicin for five patients, cisplatin for two patients, and total-body irradiation for one patient, the only agent common to all patients was pamidronate (Aredia). All patients had normal renal function before the administration of pamidronate. Patients began therapy with pamidronate at or below the recommended dose of 90 mg, intravenously, monthly, which was increased to 180 mg monthly in two patients and 360 mg monthly in three patients. Patients received pamidronate for 15 to 48 mo before presentation with renal insufficiency (mean serum creatinine, 3.6 mg/dl) and full nephrotic syndrome (mean 24-h urinary protein excretion, 12.4 g/d). Pamidronate, which is a member of the class of bisphosphonates, is widely used in the treatment of hypercalcemia of malignancy and osteolytic metastases. At the recommended dose of 90 mg, intravenously, monthly, renal toxicity is infrequent; however, higher doses have produced nephrotoxicity in animal models. The temporal association between pamidronate therapy and the development of renal insufficiency, the use of escalating doses that exceed recommended levels, and the distinctive pattern of glomerular and tubular injury strongly suggest a mechanism of drug-associated podocyte and tubular toxicity. These data provide the first association of collapsing FSGS with toxicity to a therapeutic agent.