pituitrin and Diabetic-Ketoacidosis

Blindness caused by ischemic optic neuropathy in the hospital setting occurs perioperatively and in critically ill patients, but its etiology remains ill defined. We describe four critically ill patients who developed blindness within 1 mo of one another. Three cases occurred outside of the operative arena. Potential risk factors for the development of ischemic optic neuropathy, such as use of vasopressors, venous congestion, and hypotension, are described.

Topics: Accidents, Traffic; Blindness; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Diverticulitis; Female; Flail Chest; Hemothorax; Humans; Intensive Care Units; Lung Injury; Male; Middle Aged; Myasthenia Gravis; Myocardial Infarction; Optic Nerve Injuries; Optic Neuropathy, Ischemic; Pancreatitis; Pelvic Bones; Prone Position; Risk Factors; Sepsis; Spinal Fractures; Vasopressins

Topics: Diabetic Ketoacidosis; Humans; Vasopressins

Topics: Adolescent; Blood Glucose; Child; Child, Preschool; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Humans; Lipids; Potassium; Sodium; Vasopressins

Concentrations of the antidiuretic hormone, arginine vasopressin, were measured in 28 patients with severe hyperglycemia to determine if abnormalities in hormonal regulation of water excretion could contribute to the extreme dehydration of uncontrolled diabetes mellitus. Vasopressin levels were markedly elevated in both nonketotic and ketotic patients, indicating that vasopressin deficiency plays no role in the polyuria that accompanies hyperglycemia. Instead, the observed increases in vasopressin represent an ineffective effort to conserve water in the face of an overwhelming solute diuresis caused by the glucosuria. The reasons for such marked elevations in plasma vasopressin in these diabetic patients are multifactorial. Both groups of diabetic patients had evidence of hypovolemia, which was sufficient in magnitude to stimulate vasopressin release. Furthermore, nausea provided an independent stimulus to vasopressin secretion in many patients. Osmotic stimulation might have resulted from the large fraction of unidentified plasma solutes, but this factor alone was not sufficient to explain the markedly increased concentrations of vasopressin. Whether such elevations in vasopressin could have metabolic and/or hemodynamic effects in uncrontrolled diabetes remains to be established.

Topics: Adolescent; Adult; Aged; Blood; Blood Glucose; Blood Pressure; Diabetes Mellitus; Diabetic Ketoacidosis; Female; Humans; Male; Middle Aged; Osmolar Concentration; Renin; Sodium; Urea; Urine; Vasopressins

Four cases of cerebral edema associated with therapy for diabetic ketoacidosis are reported. One patient had an inappropriate ADH-like syndrome at the time of onset of clinical symptoms of cerebral edema; he survived. The remaining patients had hyponatremia at or near the time of onset of clinical symptoms of cerebral edema, and they subsequently died. The literature is reviewed and some aspects of therapy, which might be casually related to cerebral edema observed in association with therapy of diabetic ketoacidosis, are discussed.

Topics: Blood; Brain Edema; Child; Child, Preschool; Diabetic Ketoacidosis; Female; Hormones, Ectopic; Humans; Hyponatremia; Infusions, Parenteral; Insulin; Male; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

Topics: Adult; Blood Glucose; Dehydration; Diabetes Mellitus; Diabetic Coma; Diabetic Ketoacidosis; Diabetic Retinopathy; Glucose; Humans; Hyperglycemia; Hypothalamo-Hypophyseal System; Iatrogenic Disease; Insulin; Male; Pituitary Hormones, Anterior; Stress, Physiological; Vasopressins

Topics: Acidosis; Antidiuretic Agents; Blood Chemical Analysis; Blood Glucose; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Diabetic Ketoacidosis; Humans; Vasopressins; Water-Electrolyte Balance