Severe Hyperchloremic Acidosis Research Articles

Empagliflozin-associated postoperative mixed metabolic acidosis. Case report and review of pathogenesis

BackgroundEuglycemic diabetic ketoacidosis associated with SGLT2 inhibitors is a rare, relatively new and potentially fatal clinical entity, characterized by metabolic acidosis with normal or only moderately elevated glycemia. The mechanisms are not fully understood but involve increased ketogenesis and complex renal metabolic dysfunction, resulting in both ketoacidosis and hyperchloremic acidosis. We report a rare case of fatal empagliflozin-associated acidosis with profound hyperchloremia and review its pathogenesis.Case presentationA patient with type 2 diabetes mellitus treated with empagliflozin underwent an elective hip replacement surgery. Since day 4 after surgery, he felt generally unwell, leading to cardiac arrest on the day 5. Empagliflozin-associated euglycemic diabetic ketoacidosis with severe hyperchloremic acidosis was identified as the cause of the cardiac arrest.ConclusionsThis unique case documents the possibility of severe SGLT2 inhibitor-associated mixed metabolic acidosis with a predominant hyperchloremic component. Awareness of this possibility and a high index of suspicion are crucial for correct and early diagnosis.

Experimental protocol for metabolic acidosis induction by intravenous administration of hydrochloric acid in sheep

ABSTRACT The aim of this study was to assess the magnitude and duration of blood and urine changes and the side effects of hyperchloremic acidosis induced by the intravenous administration of hydrochloric acid in sheep. Five healthy, crossbred adult ewes, with a mean body weight of 44±2.9kg were used. The hydrochloric acid solution was administered intravenously at a rate of 25mL/kg/h for 4 hours continuously. Venous blood and urine samples were collected and pH values, blood carbon dioxide partial pressure, bicarbonate, base excess, strong ion difference, anion gap, total concentration of nonvolatile buffers, creatinine, plasma L-lactate, plasma and urine sodium, potassium, and chloride were determined. The experimental protocol induced severe hyperchloremic acidosis at the end of the infusion, with a decreased plasma strong ion difference. The fractional excretion of sodium and chloride remained increased during 4 hours after the infusion. Aciduria was observed at approximately 24 hours. Twenty-four hours after the infusion, the animals showed mild and compensated metabolic acidosis. This protocol was effective in inducing severe and long-lasting hyperchloremic acidosis and did not cause serious side effects. Therefore, this protocol can be used safely in adult sheep for studies on the treatment of this condition.

Isotonic Fluid Absorption during Hysteroscopy Resulting in Severe Hyperchloremic Acidosis

oped rapidly, and signs suggestive of pulmonary edema were present on auscultation. Only then, approximately 30 min after the start of the hysteroscopy, was a deficit in distending fluid balance of almost 7.5 l noticed; it was unidentified before despite the presence of a systembased warning system. Because fluid overload was suspected as the most likely diagnosis, intravenous furosemide (20 mg) was given to enhance diuresis, and the hysteroscopy was discontinued. Laboratory investigations revealed a hyperchloremic metabolic acidosis enhanced by a small respiratory component (fraction of inspired oxygen, 1.0; pH, 7.12; HCO3 , 15.5 mmHg; base excess, 13.3 mM; partial pressure of carbon dioxide, 48.7 mmHg; partial pressure of oxygen, 185.2 mmHg; sodium, 141 mM; potassium, 3.2 mM; chloride, 122 mM; anion gap, 3.5 mM). There were also signs of dilutional coagulopathy (international normalized ratio, 1.4; activated partial thrombin time, 59 s). Fifty milliliters intravenous sodium bicarbonate, 8.4%, and 20 mmol potassium chloride were given as a part of corrective treatment. In the absence of signs of respiratory compromise, the laryngeal mask was removed when the patient was awake. She was agitated and somewhat confused, and her blood pressure was 150/90 mmHg. An additional dose of intravenous furosemide (20 mg) was administered. On arrival in the intermediate care unit, an oxygen saturation of 98% was achieved with 10 l oxygen via facemask. Within 4 h, the patient’s condition improved, and all hemodynamic and laboratory values were within the normal range; in particular, the laboratory indices of hyperchloremic acidosis had disappeared (chloride, 110 mM; pH, 7.42; base excess, 1m M).

Saline-induced Dilutional Acidosis in a Maintenance Hemodialysis Patient

A patient with end-stage renal disease developed severe hyperchloremic acidosis (venous serum total CO2 level of 10 mmol/L) after treatment with 16 L of isotonic saline. Analysis of this case and published literature indicates that dilutional acidosis may result when very large volumes of isotonic saline are administered intravenously, especially in patients with impaired or absent renal function.

Metabolic effects of urinary diversion of exocrine secretions in pancreatic transplantation.

We have compared the metabolic consequences of two forms of exocrine drainage for pancreaticoduodenal transplant, duodenojejunostomy (DJ) and duodenocystostomy (DC). DC offered the advantage of avoiding opening of the recipient small intestine with its potential for wound sepsis, as well as a reliable method for early detection of pancreatic rejection as measured by an abrupt fall in urinary amylase and bicarbonate concentration. However, DC led to a large urinary loss of bicarbonate with a concomitant mild metabolic acidosis. During periods of renal dysfunction, the patients with DC developed severe hyperchloremic acidosis. Use of DC for pancreatic exocrine diversion may require patients to take supplemental bicarbonate even with a well-functioning renal transplant.

Rhabdomyolysis and Myoglobinuria

A 44-year-old woman had severe hyperchloremic acidosis and hypokalemia. She had paralysis, muscle tenderness, and myoglobinuria. There was no history of previous muscle abnormality. In this case, the rhabdomyolysis appeared to be the result of potassium deficiency without concurrent drug therapy.

Rhabdomyolysis and myoglobinuria. Association with hypokalemia of renal tubular acidosis.

A 44-year-old woman had severe hyperchloremic acidosis and hypokalemia. She had paralysis, muscle tenderness, and myoglobinuria. There was no history of previous muscle abnormality. In this case, the rhabdomyolysis appeared to be the result of potassium deficiency without concurrent drug therapy.

The relationship of acidosis and growth retardation

Young male albino rats were subjected to the following procedures: Group IA, unilateral nephrectomy; Group IB, unilateral nephrectomy and 4 per cent ammonium chloride in the diet; Group II, 4 per cent ammonium chloride and 0.1 per cent acetazolamide in the diet; Group III, 13 per cent carbon dioxide in the ambient air; Group IV, 0.4 per cent acetazolamide in the diet. Pair-fed controls were maintained under normal conditions. These various regimens produced acidosis which was hyperchloremic in Groups IB, II, and IV and hypochloremic in Group III. In Groups IB, II, and III, retardation of growth as manifested by weight gain and femur length was produced. This retardation in growth was not necessarily proportional to the degree of acidosis. In Group IV, in spite of severe hyperchloremic acidosis, no growth retardation was produced during the experimental period of 40 days. The results of these experiments seem to indicate that acidosis may bear some relationship to retardation of growth. However, more problems are created than are solved by this work. Studies of hormone regulation of growth, tissue analyses, accurate studies of intake and loss of metabolites, and calorimetric studies of acidotic rats and patients all remain to be done in order to elucidate the basic mechanisms reponsible for the retardation of growth produced in these experiments and observed in renal disease. Young male albino rats were subjected to the following procedures: Group IA, unilateral nephrectomy; Group IB, unilateral nephrectomy and 4 per cent ammonium chloride in the diet; Group II, 4 per cent ammonium chloride and 0.1 per cent acetazolamide in the diet; Group III, 13 per cent carbon dioxide in the ambient air; Group IV, 0.4 per cent acetazolamide in the diet. Pair-fed controls were maintained under normal conditions. These various regimens produced acidosis which was hyperchloremic in Groups IB, II, and IV and hypochloremic in Group III. In Groups IB, II, and III, retardation of growth as manifested by weight gain and femur length was produced. This retardation in growth was not necessarily proportional to the degree of acidosis. In Group IV, in spite of severe hyperchloremic acidosis, no growth retardation was produced during the experimental period of 40 days. The results of these experiments seem to indicate that acidosis may bear some relationship to retardation of growth. However, more problems are created than are solved by this work. Studies of hormone regulation of growth, tissue analyses, accurate studies of intake and loss of metabolites, and calorimetric studies of acidotic rats and patients all remain to be done in order to elucidate the basic mechanisms reponsible for the retardation of growth produced in these experiments and observed in renal disease.

Severe hyperchloremic acidosis of unusual etiology

Summary The occurrence of severe hyperchloremic acidosis associated with depletion of potassium and with rickets in a child with an imperforate anus and a rectourethral fistula is reported. Data are presented suggesting that the primary cause of the acidosis was the loss of bicarbonate ions as the result of a change in the composition of the urine as it passed through the colon. Following reparative surgery, the ability of the patient to acidify the urine in response to ammonium chloride was normal. These considerations strongly suggest that the pathogenesis of the acidosis was entirely extrarenal.