Antonios H. Tzamaloukas

Hyperosmolar Coma: Cellular Dehydration and the Serum Sodium Concentration

Excerpt Nonketotic hyperosmolar coma is a syndrome found mostly in diabetic patients with marked hyperglycemia; the relative pathogenetic roles of hyperglycemia, hyperosmolality, and cellular (espe...

Acid-base disorders in hyperglycemia of insulin-dependent diabetic patients on chronic dialysis

The authors studied hyperglycemia occurring in insulin-dependent diabetic patients on chronic dialysis to determine the types of associated acid-base disorders, their treatment, and any differences from hyperglycemia in diabetic patients with intact renal function. Eighty-eight episodes of serum glucose greater than 25 mmol/L were observed, 23 in hemodialysis patients and 65 in patients on continuous peritoneal dialysis. Treatment consisted of low-dose insulin in 77 episodes and low-dose insulin plus saline in 11; no base was administered. Seventeen episodes (19%) presented with ketoacidosis. Arterial blood gas determinations were carried out at presentation in 37 of the episodes without ketoacidosis. Of these, 12 had respiratory alkalosis, six had respiratory acidosis and severe pulmonary edema, 14 had other single or mixed acid-base disorders, and only five had normal acid-base status. Insulin corrected the ketoacidosis in all instances and both pulmonary edema and respiratory acidosis in five of six instances. In eight cases metabolic alkalosis developed during treatment, without external acid loss. At the completion of treatment respiratory alkalosis was present in half the cases. No difference was noted between patients treated with hemodialysis or peritoneal dialysis. Insulin alone is sufficient for the management of hyperglycemia in dialysis patients. Certain acid-base disorders persist, but do not need further treatment. Hyperglycemia in patients on dialysis is characterized by infrequent development of metabolic acidosis and frequent presentation with respiratory alkalosis, by respiratory acidosis that is corrected by insulin, and by metabolic alkalosis developing during treatment without external cause.

Plasma Potassium Changes in Anuric Hyperglycemia Treated with Insulin

We followed sequentially the plasma potassium concentration in five, essentially anuric, hyperglycemic patients with no known abnormality of potassium metabolism and treated only with insulin. Acid-base balance, external potassium and fluid balance, and weights did not change during observation. The following changes in plasma potassium concentration (ΔK) were noted: In initial hyperkalemia (three patients) ΔK was −1.8±0.1 mmo l/l (P<0.005). In normokalemia (one patient) δK was −1.3 mmol/l. In hypokalemia (one patient) δK was +0.1 mmol/l. The correlation between the starting potassium concentration and the change in potassium concentration was −0.88 (p = 0.05).Conclusions: When only parenteral insulin is used for treatment and acid-base balances and body weights do not change during treatment in anuric hyperglycemia: a) The change in potassium concentration is dependent on the starting plasma potassium concentration, b) hyperkalemic patients will drop their plasma potassium concentration toward normal, and c) hypokalemic patients may not need potassium replacement.

Asystole Associated with Lidocaine Use in a Hyperkalemic Patient during Advanced Cardiac Life Support

A case report of fatal asystole associated with use of lidocaine in a hyperkalemic patient is presented. The patient was a 61–year-old man with a rapidly increasing serum potassium level related to acute renal failure. Ventricular tachycardia with a pulse developed twice, for which lidocaine was administered according to the American Heart Associations ACLS protocol. Both episodes were immediately followed by asystole, the second of which was terminal. Available information suggests that this phenomenon can be explained by a synergistic effect on membrane responsiveness and conduction velocity. Thus, extreme caution should be exercised in the use of lidocaine when ventricular tachycardia complicates severe hyperkalemia.