Starvation ketoacidosis and refeeding syndrome

Starvation ketoacidosis (SKA) is a rarer cause of ketoacidosis. Most patients will only have a mild acidosis, but if exacerbated by stress can result in a severe acidosis. We describe a 66-year-old man admitted with reduced consciousness and found to have a severe metabolic acidosis with raised anion gap. His body mass index (BMI) was noted to be within the healthy range at 23 kg/m2; however, it was last documented 1 year previously at 28 kg/m2 with no clear timeframe of weight loss. While his acidosis improved with intravenous fluids, he subsequently developed severe electrolyte imbalance consistent with refeeding during his admission. Awareness of SKA as a cause for high anion gap metabolic acidosis is important and knowledge of management including intravenous fluids, thiamine, dietetic input and electrolyte replacement is vital.

Atypical Euglycemic Ketoacidosis in a non-diabetic Patient due to acute pancreatitis

We describe the case of a previously healthy 40- year-old Female with a known medical history of essential hypertension (HTN). She did not have past medical history of Diabetes Mellitus. She presents to the emergency department with sudden onset of severe shortness of breath that began shortly after non-bilious, non-bloating emesis. She also reported low-grade fever, nausea, cough, abdominal pain, pleuritic chest pain, and generalized weakness. She was found to have acute pancreatitis. She was diaphoretic. She had Kussmaul breathing. She was subsequently admitted to the intensive care unit (ICU) for severe metabolic acidosis. The cause of her metabolic acidosis and clinical presentation was found to be the acute pancreatitis which very rarely can be the cause of euglycemic ketoacidosis.

Ethylene Glycol Intoxication Requiring ECMO Support

Ethylene glycol is commonly used in antifreeze, and ingestion of even a small amount can result in acute kidney injury, severe metabolic acidosis, and neurological injury. When cases are recognized early, treatment involves administration of alcohol dehydrogenase inhibitors to prevent conversion to toxic metabolites of glycolate, glyoxolate, and oxalate. In later presentations with more severe renal injury, hemodialysis may be required for clearance of toxic metabolites and supportive care for renal failure. We present the first reported case of severe ethylene glycol intoxication requiring support of extracorporeal membrane oxygenation (ECMO) due to refractory cardiopulmonary collapse.

Renal Tubular Acidosis Type I with Prominent Hypokalemia and Nephrolithiasis as a Presentation of Sjögren’s/Systemic Lupus Erythematosus Disease

Female patient, suffering from nephrolithiasis, at the age of 32 was admitted for renal colic caused by a stone obstructing UP junction with left hydronephrosis. Nephrostomy was placed, resulting in brisk diuresis. Severe metabolic acidosis with normal anion gap and urine pH of 6.5 was noted. Potassium level dropped to extremely low level (1.6 mEq/L), causing muscle paralysis and respiratory failure, necessitating mechanical ventilation. The patient was treated by potassium chloride infusion, followed by correction of severe metabolic acidosis by sodium bicarbonate. Diagnosis of distal type renal tubular acidosis type I (dRTA) was made based on normal anion gap metabolic acidosis, alkaline urine, hypokalemia, and nephrolithiasis. Five years later, the patient presented with severe hypoxia, lung opacities, and bronchiolitis obliterans organizing pneumonia which was confirmed by bronchoscopy with lung tissue biopsy. Concurrently, the patient presented with dry mouth, pruritus, skin rash with hypocomplementemia, elevated anti-DNA, anti-Ro, and anti-SmAb. Diagnosis of overlap Sjögren’s/systemic lupus erythematosus disease was done and treatment by hydroxychloroquine, prednisone, and azathioprine was started. Possible presence of Sjögren’s syndrome should be considered in adult patients with unexplained dRTA.

Identifying prognostic factors of severe metabolic acidosis and uraemia in African children with severe falciparum malaria: a secondary analysis of a randomized trial

Background Severe metabolic acidosis and acute kidney injury are major causes of mortality in children with severe malaria but are often underdiagnosed in low resource settings. Methods A retrospective analysis of the ‘Artesunate versus quinine in the treatment of severe falciparum malaria in African children’ (AQUAMAT) trial was conducted to identify clinical features of severe metabolic acidosis and uraemia in 5425 children from nine African countries. Separate models were fitted for uraemia and severe metabolic acidosis. Separate univariable and multivariable logistic regression were performed to identify prognostic factors for severe metabolic acidosis and uraemia. Both analyses adjusted for the trial arm. A forward selection approach was used for model building of the logistic models and a threshold of 5% statistical significance was used for inclusion of variables into the final logistic model. Model performance was assessed through calibration, discrimination, and internal validation with bootstrapping. Results There were 2296 children identified with severe metabolic acidosis and 1110 with uraemia. Prognostic features of severe metabolic acidosis among them were deep breathing (OR: 3.94, CI 2.51–6.2), hypoglycaemia (OR: 5.16, CI 2.74–9.75), coma (OR: 1.72 CI 1.17–2.51), respiratory distress (OR: 1.46, CI 1.02–2.1) and prostration (OR: 1.88 CI 1.35–2.59). Features associated with uraemia were coma (3.18, CI 2.36–4.27), Prostration (OR: 1.78 CI 1.37–2.30), decompensated shock (OR: 1.89, CI 1.31–2.74), black water fever (CI 1.58. CI 1.09–2.27), jaundice (OR: 3.46 CI 2.21–5.43), severe anaemia (OR: 1.77, CI 1.36–2.29) and hypoglycaemia (OR: 2.77, CI 2.22–3.46) Conclusion Clinical and laboratory parameters representing contributors and consequences of severe metabolic acidosis and uraemia were independently associated with these outcomes. The model can be useful for identifying patients at high risk of these complications where laboratory assessments are not routinely available.

Critical care management of hydrofluoric acid burns with a negative outcome

Hydrofluoric acid is a highly corrosive acid widely used in various industries. When in contact with skin it causes local and systemic reactions due to the generation of fluoride ions. Severe burns are associated with high mortality rates, approaching 100%. We present a 21-year-old man with 15% full thickness burns, severe metabolic acidosis, hypoxia and electrolyte disturbances. The burns were treated with topical and subcutaneous injections of calcium gluconate, and the patient was given intravenous fluid, calcium chloride, magnesium and insulin-glucose infusions. Continuous renal replacement therapy was initiated due to the severity of the systemic toxicity. Extracorporeal membrane oxygenation was considered as it plays a vital role when conventional therapies fail. Our patient suffered multiple cardiac arrests and cardiopulmonary resuscitation was conducted several times but despite extensive efforts, he did not survive.