deamino-arginine-vasopressin and Hyperkalemia

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Deamino Arginine Vasopressin; Humans; Hyperkalemia; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Membrane Potentials; Morpholines; Osmolar Concentration; Potassium; Randomized Controlled Trials as Topic; Sodium; Spiro Compounds; Survival Rate; Tolvaptan; Water-Electrolyte Imbalance

Hemorrhage in trauma is a significant challenge, accounting for 30% to 40% of all fatalities, second only to central nervous system injury as a cause of death. However, hemorrhagic death is the leading preventable cause of mortality in combat casualties and typically occurs within 6 to 24 hrs of injury. In cases of severe hemorrhage, massive transfusion may be required to replace more than the entire blood volume. Early prediction of massive transfusion requirements, using clinical and laboratory parameters, combined with aggressive management of hemorrhage by surgical and nonsurgical means, has significant potential to reduce early mortality.. Although the classification of massive transfusion varies, the most frequently used definition is ten or more units of blood in 24 hrs. Transfusion of red blood cells is intended to restore blood volume, tissue perfusion, and oxygen-carrying capacity; platelets, plasma, and cryoprecipitate are intended to facilitate hemostasis through prevention or treatment of coagulopathy. Massive transfusion is uncommon in civilian trauma, occurring in only 1% to 3% of trauma admissions. As a result of a higher proportion of penetrating injury in combat casualties, it has occurred in approximately 8% of Operation Iraqi Freedom admissions and in as many as 16% during the Vietnam conflict. Despite its potential to reduce early mortality, massive transfusion is not without risk. It requires extensive blood-banking resources and is associated with high mortality.. This review describes the clinical problems associated with massive transfusion and surveys the nonsurgical management of hemorrhage, including transfusion of blood products, use of hemostatic bandages/agents, and treatment with hemostatic medications.

Topics: Acidosis; Antifibrinolytic Agents; Bandages; Blood Coagulation Disorders; Blood Transfusion; Cause of Death; Critical Care; Deamino Arginine Vasopressin; Factor VIIa; Factor VIII; Fibrinogen; Hemorrhage; Hemostatics; Humans; Hyperkalemia; Hypocalcemia; Hypothermia; Military Medicine; Recombinant Proteins; Resuscitation; Risk Factors; Transfusion Reaction; United States; Wounds and Injuries; Zeolites

Ion-regulating renal function and influence of vasopressin and its analogues on the rate and selectiveness of the urinary potassium excretion were investigated after short-term parenteral and oral potassium loading. In experiments with Wistar rats it was shown that increase in volume of orally administrated 1.25% KCl solution from 1 to 5 ml per 100 g body weight led to the proportional rise in potassium excretion. Hyperkalemia was already observed at 5 min after parenteral potassium loading, potassium excretion reached the maximum after administration of 2 ml of KCl solution per 100 g body weight. Kaliuresis induced by oral potassium load was higher and faster than after parenteral load and was followed by increase in diuresis, urinary sodium and magnesium excretion. Desmopressin and 1-deamino-Arg4-vasotocin prevented rise of diuresis, natriuresis and magniuresis under these conditions; 1-deamino-Arg4-vasotocin and vasopressin stimulated urinary potassium excretion during first 30 min after loading. After parenteral potassium load vasopressin analogues did not affect urinary potassium and sodium excretion. The data obtained suggest the participation of the gut in regulatory signal transduction to the kidney after potassium entering and prevention of significant changes in the internal environment.

Topics: Administration, Oral; Animals; Antidiuretic Agents; Deamino Arginine Vasopressin; Female; Hyperkalemia; Injections, Intraperitoneal; Intestinal Mucosa; Kidney; Natriuresis; Potassium; Rats; Rats, Wistar; Signal Transduction; Sodium; Vasotocin; Water-Electrolyte Balance

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3-6.9 mmol/l), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mmol/l), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/h), high plasma aldosterone level (32-100 ng/dl), and normal glomerular filtration rate (131 ml/min/1.73 m2). During the hyperkalemic period, urine was highly acidic (pH 4.6-5.0), urinary NH4 excretion (10-13 microEq/min) and urinary net acid excretion (19-24 microEq/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, the maximal tubular HCO3 reabsorption was markedly diminished (19.8 mmol/l glomerular filtrate), and the fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized was 20%. Urine minus blood PCO2 increased normally during NaHCO3 infusion (31 mm Hg), and the urinary pH remained maximally low (less than 5.3) when the buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while the urinary pH remained maximally low (4.9-5.2), the maximal tubular HCO3 reabsorption returned to normal values (24.8 mmol/l glomerular filtrate), and FE HCO3 at normal plasma HCO3 was 1%. Nasal insufflation of 1-desamino-8-D-Arginine Vasopressin (dDAVP) resulted in an acute normalization of the renal handling of K and in an increase in net urinary acid excretion. We conclude that: the effect of dDAVP on renal handling of K may be explained by the reversal of the distal chloride shunt and/or an increase in luminal membrane conductance to K; the distal acidification seems to be normal which in the event of distal chloride shunt impairing distal hydrogen secretion might be explained by the presence of systemic acidosis which is a potent stimulus of hydrogen secretion, and metabolic acidosis in the steady state was accounted for by the diminution of bicarbonate reabsorption and ammonia production in the proximal tubule secondary to chronic hyperkalemia.

Topics: Acid-Base Equilibrium; Acidosis, Renal Tubular; Adult; Aldosterone; Deamino Arginine Vasopressin; Drug Resistance; Humans; Hyperkalemia; Kidney; Male; Potassium; Renin-Angiotensin System; Syndrome

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3 to 6.8 mM), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mM), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/hr), high plasma aldosterone (32 to 100 ng/dl), normal GFR (131 +/- 2.5 ml/min/1.73 m2). During hyperkalemic period, urine was highly acidic (pH 4.6 to 5.0), urinary NH4 excretion (13 mumoles/min) and urinary net acid excretion (24 mumoles/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, maximal tubular HCO3 reabsorption (Tm HCO3) was markedly diminished (19 mmoles/liter GF), fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized, was 20%. Urine-minus-blood PCO2 increased normally (31 mmHg) during NaHCO3 infusion, and urinary pH remained maximally low (less than 5.3) when buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while urinary pH remained maximally low (4.9 to 5.2), Tm HCO3 returned to normal value (24.8 mmoles/liter GF), and FE HCO3 became nil. The renal handling of K was improved with acute NaHCO3 loading and normalized after DDAVP nasal insufflation.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acidosis, Renal Tubular; Adult; Aldosterone; Deamino Arginine Vasopressin; Humans; Hyperkalemia; Male; Syndrome