sodium-bicarbonate and Cerebral-Hemorrhage

Insulin-dependent diabetes mellitus in poor control, alcohol intake associated with extracellular fluid volume contraction, or hypoglycemia may each lead to an increased rate of production of ketoacids. Generally, several days of illness are required before ketoacidosis becomes severe. Two clinical examples are presented to suggest that a severe degree of ketoacidosis may develop over a short period of time, literally overnight. In both examples, there was the ingestion of a modest amount of ethanol. From a quantitative analysis of factors that may influence the rate of production and removal of ketoacids, the following were deduced. Contributing factors to the very rapid development of maximal ketoacidosis could include the absence of a lag period for the conversion of ethanol to acetyl-coenzyme A in the liver and an impaired ability of the brain and kidneys to oxidize ketoacids, especially if these ketoacids are produced very rapidly and/or if less metabolic work is performed by these organs. In special settings, ketoacidosis may develop more rapidly than is generally appreciated.

Topics: Adult; Alcohol Drinking; Cerebral Hemorrhage; Diabetic Ketoacidosis; Humans; Insulin; Keto Acids; Male; Sodium Bicarbonate; Sodium Chloride; Time Factors

After more than 25 years of experience with sodium bicarbonate, the following conclusions may be in order: 1. It is not certain that the net effect of administration of this agent to patients with metabolic acidosis is positive, other than when given as replacement for renal or gastrointestinal bicarbonate losses. 2. Adequate oxygenation and ventilation must be ensured before it is given. 3. Profound fluctuations in blood pressure and cerebral blood flow, intracranial bleeds, and compromise of oxygen delivery to tissues all have been found to be possible adverse effects of sodium bicarbonate infusion. Because hyperosmolarity and sodium content are important factors, the commercially prepared solutions (0.9 or 1M) should be diluted 1:2 to 1:4 with water and given over not less than several minutes--if it is to be given at all. 4. Current recommendations for dose, dilution, and rate of administration, including those mentioned above, are largely arbitrary. If sodium bicarbonate were a newly proposed treatment for hypoxic metabolic acidosis, one would recommend that carefully conducted prospective laboratory and clinical trials be done before giving it to sick patients. As it is in widespread use, one can only reiterate that if it is to be given, it should be used with extreme caution.

Topics: Acidosis; Animals; Bicarbonates; Cerebral Hemorrhage; Female; Humans; Hydrogen-Ion Concentration; Infant, Newborn; Infant, Newborn, Diseases; Osmolar Concentration; Oxygen Consumption; Pregnancy; Respiratory Distress Syndrome, Newborn; Sodium; Sodium Bicarbonate

Topics: Acidosis; Bicarbonates; Blood Component Transfusion; Brain; Cerebral Hemorrhage; Female; Fluid Therapy; Hemorrhage; Humans; Infant, Newborn; Magnetic Resonance Imaging; Scalp; Sodium; Sodium Bicarbonate; Tomography, X-Ray Computed; Vacuum Extraction, Obstetrical

In a population of 225 very low birthweight infants born over a 21 month period the cerebroventricular system was scanned by ultrasound. One third of the infants developed a periventricular haemorrhage; in 41% of infants the haemorrhage was detected before an hour of age and 66% of all haemorrhages occurred within the first 24 hours. Statistically significant associations with periventricular haemorrhage included vaginal delivery, endotracheal intubation and intravenous sodium bicarbonate when this was administered in the first 24 hours. In a stepwise regression analysis, however, these and other potentially significant variables added little to the total accountable variance. A similar analysis of perinatal factors and mortality revealed that decreasing gestation was the major association with death.

Topics: Bicarbonates; Cerebral Hemorrhage; Delivery, Obstetric; Female; Humans; Hydrocephalus; Infant, Low Birth Weight; Infant, Newborn; Intubation, Intratracheal; Male; Pregnancy; Sodium Bicarbonate; Ultrasonography

Topics: Animals; Asphyxia Neonatorum; Bicarbonates; Blood-Brain Barrier; Cerebral Hemorrhage; Glycerol; Humans; Infant, Newborn; Osmolar Concentration; Prognosis; Sodium Bicarbonate

The relationship between hyperosmolality and intracranial hemorrhage as well as brain dysfunction was studied. Hyperosmolality was induced by continuous infusion of hyperosmotic solutions, such as 7% sodium bicarbonate (1,666 mOsm/1), 4.64% sodium chloride (1,666 mOsm/1), 20% glucose (about 1,200 mOsm/1), 20% mannitol (about 1,200 mOsm/1), and 10% glycerol with 0.9% sodium chloride and 5% fructose (about 2,000 mOsm/1). 1) Intracranial hemorrhage was observed without exception after the rabbits had died of hyperosmolality due to the infusion of these agents. The intracranial hemorrhage was mostly subdural hemorrhage in the subtentorial region. 2) The plasma osmolality just before death varied according to the agents administered and was lowest in the case of 7% sodium bicarbonate with a level of 441 mOsm/1. 3) The plasma osmolality in the case of 10% glycerol was higher than the case of 20% mannitol at the death. 4) The arousal reaction was suppressed by hyperosmotic solutions which contain sodium ions, and when the plasma osmolality surpassed 320 mOsm/1, dysfunction of the CNS began to appear. 5) The evoked muscular discharges caused by stimulation of the midbrain reticular formation were suppressed only by the administration of 7% sodium bicarbonate, so this result is related to alkalosis.

Topics: Animals; Arousal; Bicarbonates; Cerebral Hemorrhage; Electric Stimulation; Electroencephalography; Electromyography; Evoked Potentials; Glucose Solution, Hypertonic; Glycerol; Mannitol; Mesencephalon; Muscle Contraction; Osmolar Concentration; Rabbits; Reticular Formation; Saline Solution, Hypertonic; Sodium Bicarbonate; Water-Electrolyte Balance

Studies on the correlation between hyperosmolality and brain damage, especially intracranial hemorrhage, were carried out on young and newborn rabbits following infusion with 7% sodium bicarbonate. 1) All the young rabbits injected with 7% sodium bicarbonate died of hyperosmolality at over 380 mOsm/L (the mean was 462 mOsm/L) after drip infusion at the rate of 20-60 ml/kg/hr. Young rabbits under a 10% hypoxic environment died even at the 350 mOsm/L level (the mean was 392 mOsm/L) during infusion of 7% sodium bicarbonate. Half of the case of newborn rabbits injected with 7% sodium bicarbonate at 10 ml/kg, intraperitoneally, had intracranial hemorrhage at 335 mOsm/L. When the hyperosmolality reached 392 mOsm/L (50 ml/kg), intracranial hemorrhage was observed in all cases. 2) The main cause of death in young and newborn rabbits was subdural hemorrhage in the subtentorial region. Intraventricular hemorrhage was observed in about 40% of the cases of young and newborn rabbits. 3) The blood pH was elevated by the drip infusion, but when the hyperosmolality reached about 400 mOsm/L, the blood pH began to fall. At the same osmolality, pCO2 showed a marked elevation. It is likely that the decrease of the blood pH was caused by the elevation of pCO2 and the outflow of H+ from intracellular compartments resulting from the hyperosmolality. These results apparently indicate that fatal intracranial hemorrhage was induced by hyperosmolality and was enhanced by the combination of hypoxia and immaturity.

Topics: Animals; Bicarbonates; Blood; Cerebral Hemorrhage; Osmolar Concentration; Rabbits; Sodium Bicarbonate

Four cases of the iatrogenic nondiabetic hyperosmolar state are presented. The clinical presentation, biochemical findings and management are discussed. No hypertonic solution should be infused at a rate above the level of patient tolerance; irrigation of a hollow viscus with a hypertonic solution should be avoided, and salt should not be used as an emetic. Patients under stress are particularly prone to this condition, largely because of the high circulating cortisol levels. The use of corticosteroids, salt-containing solutions in excess of patient requirements, water depletion and intravenous nutrition in the absence of careful biochemical monitoring, are all factors which may precipitate the hyperosmolar state in the critically ill.

Topics: Acid-Base Imbalance; Adult; Aged; Bicarbonates; Cerebral Hemorrhage; Citrates; Female; Glucose Solution, Hypertonic; Humans; Hyperglycemia; Hyperglycemic Hyperosmolar Nonketotic Coma; Hypernatremia; Iatrogenic Disease; Male; Middle Aged; Osmolar Concentration; Saline Solution, Hypertonic; Seizures; Sodium Bicarbonate