salicylates and Diabetic-Ketoacidosis

Cerebral edema is a potentially life-threatening complication shared by diseases of different etiology, such as diabetic ketoacidosis, acute liver failure, high altitude exposure, dialysis disequilibrium syndrome, and salicylate intoxication. Pulmonary edema is also habitually present in these disorders, indicating that the microcirculatory disturbance causing edema is not confined to the brain. Both cerebral and pulmonary subclinical edema may be detected before it becomes clinically evident. Available evidence suggests that tissue hypoxia or intracellular acidosis is a commonality occurring in all of these disorders. Tissue ischemia induces physiological compensatory mechanisms to ensure cell oxygenation and carbon dioxide removal from tissues, including hyperventilation, elevation of red blood cell 2,3-bisphosphoglycerate content, and capillary vasodilatation. Clinical, laboratory, and necropsy findings in these diseases confirm the occurrence of low plasma carbon dioxide partial pressure, increased erythrocyte 2,3-bisphosphoglycerate concentration, and capillary vasodilatation with increased vascular permeability in all of them. Baseline tissue hypoxia or intracellular acidosis induced by the disease may further deteriorate when tissue oxygen requirement is no longer matched to oxygen delivery resulting in massive capillary vasodilatation with increased vascular permeability and plasma fluid leakage into the interstitial compartment leading to edema affecting the brain, lung, and other organs. Causative factors involved in the progression from physiological adaptation to devastating clinical edema are not well known and may include uncontrolled disease, malfunctioning adaptive responses, or unknown factors. The role of carbon monoxide and local nitric oxide production influencing tissue oxygenation is unclear.

Topics: Altitude Sickness; Animals; Brain Edema; Capillaries; Diabetic Ketoacidosis; Humans; Ischemia; Liver Failure, Acute; Renal Dialysis; Salicylates

Altered level of consciousness describes the reason for 3% of critical emergency department (ED) visits. Approximately 85% will be found to have a metabolic or systemic cause. Early laboratory studies such as a bedside glucose test, serum electrolytes, or a urine dipstick test often direct the ED provider toward endocrine or metabolic causes. This article examines common endocrine and metabolic causes of altered mentation in the ED via sections dedicated to endocrine-, electrolyte-, metabolic acidosis-, and metabolism-related causes.

Topics: Acidosis; Aged; Child; Consciousness Disorders; Cushing Syndrome; Diabetic Ketoacidosis; Ethylene Glycol; Female; Glucose Metabolism Disorders; Humans; Hyperammonemia; Inappropriate ADH Syndrome; Metabolic Diseases; Methanol; Pregnancy; Salicylates; Thyroid Diseases; Water-Electrolyte Imbalance

The roles of changes in cellular redox, interorgan lactate flux and balance, and quantitative aspects of lactate metabolism in the pathogenesis of lactic acidosis are discussed. Altered metabolism of pyruvate is central to the development of lactic acidosis and hyperlactatemia. Lactic acidosis occurs as a result of a relative or absolute imbalance in lactate production and utilization. Lactate utilization for oxidative purposes and for the resynthesis of glucose is essential for the maintenance of acid-base balance. Because of its role in lactate homeostasis the liver may play a central role in acid-base balance. Impairment of hepatic utilization of lactate may produce lactic acidosis.

Topics: Acidosis; Animals; Diabetic Ketoacidosis; Dichloroacetic Acid; Ethanol; Homeostasis; Humans; Hypoglycemia; Kidney; Lactates; Liver; Liver Diseases; Neoplasms; Phenformin; Renal Dialysis; Salicylates; Seizures; Vasodilator Agents

Topics: Child, Preschool; Diabetic Ketoacidosis; Diagnosis, Differential; Female; Humans; Poisoning; Salicylates

Improvements in nuclear magnetic resonance (NMR) technology are generating an expanding variety of medical applications. In this investigation I have used high-field proton NMR to identify and quantity endogenous and ingested substances in human serum. After addition of a small amount of 2H2O and a reference compound to a 0.4-mL specimen, spectra were recorded for 3 min in Fourier-transform mode, with use of presaturation to suppress the extremely intense H2O peak. Compounds detected at clinically significant concentrations include glucose, alcohols, acetone, organic acids, and salicylate. Less than 1 mmol/L of some of these substances could be detected. For serum containing 20--500 mg of added methanol per liter, peak area was a linear function of concentration (r = 0.998). High-field proton NMR, despite the drawback of expensive, sophisticated instrumentation, offers some unique advantages for clinical chemistry: it permits rapid, specific, nondestructive measurement of several compounds simultaneously, including some that may be inconvenient to measure by conventional means.

Topics: Acidosis; Adult; Aged; Blood Chemical Analysis; Blood Glucose; Diabetic Ketoacidosis; Ethanol; Humans; Lactates; Magnetic Resonance Spectroscopy; Male; Methanol; Phenobarbital; Salicylates

All patients in stupor or coma should undergo blood chemistry studies, including blood gases. The anion gap and serum osmolality must be calculated in all patients. An indwelling catheter to monitor urine content and volume is essential. Electrocardiogram monitoring is indicated in all significant metabolic acidosis, especially for evaluation of intracellular potassium effect and arrhythmias. Repeated arterial monitoring of blood gases and electrolytes is essential with the use of flow sheets. Sodium lactate and Ringer's solution should never be given in an emergency care area. Large doses of insulin (100+ units intravenously) are not necessary or indicated in diabetic ketoacidosis and may be contraindicated and dangerous especially in HHNKC. Intravenous or intramuscular regular insulin after urine tests for glucose and ketones alone should not be given. Urine dilution of serum ketones is useless, and serum dilution may be grossly misleading and contraindicated: arterial studies are much more reliable.

Topics: Acidosis; Blood Glucose; Diabetic Ketoacidosis; Diagnosis, Differential; Electrolytes; Emergencies; Ethylene Glycols; Humans; Hypoglycemia; Lactates; Metabolic Diseases; Methanol; Salicylates; Uremia

Topics: Acidosis; Aged; Alcoholic Intoxication; Alkalosis; Alkalosis, Respiratory; Arrhythmias, Cardiac; Coma; Diabetic Ketoacidosis; Diagnosis, Differential; Encephalitis, Arbovirus; Humans; Male; Myocardial Infarction; Poisoning; Salicylates; Stomach Neoplasms; Sweating

Topics: Acidosis; Acute Kidney Injury; Adrenal Insufficiency; Alkalosis; Alkalosis, Respiratory; Carbohydrates; Dehydration; Diabetic Ketoacidosis; Electrolytes; Heat Exhaustion; Humans; Hyperkalemia; Hypernatremia; Hypokalemia; Hyponatremia; Nutritional Requirements; Parenteral Nutrition; Potassium Deficiency; Proteins; Pyloric Stenosis; Salicylates; Shock; Sodium; Vitamins; Water Intoxication

Topics: Acetone; Biguanides; Diabetes Complications; Diabetes Mellitus; Diabetic Ketoacidosis; Diet Therapy; Glucose Tolerance Test; Glycosuria; Holidays; Humans; Hypoglycemia; Hypoglycemic Agents; Insulin; Insulin Secretion; Interpersonal Relations; Prediabetic State; Salicylates; Sports; Travel

Topics: Diabetes Complications; Diabetic Ketoacidosis; Diagnosis, Differential; Humans; Poisoning; Salicylates