Hypernatremia acute

Improper proportioning of dialysate, due to either human or mechanical error, is still an important cause of neurological abnormality in dialysis patients (Bleumle, 1968). The usual effect of such dialysate abnormalities is the production of either hypo- or hypernatremia. Both of these abnormalities of body fluid osmolality can lead to seizures and coma, although different mechanisms are involved. In acute hypernatremia, there will be excessive thirst, lethargy, irritability, seizures, and coma, with spasticity and muscle rigidity. In acute hyponatremia there is weakness, fatigue, and dulled sensorium, which may also progress to seizures and coma,... 

Serum sodium in acute-onset hypernatremia may be lowered... 

When acute overuse or chronic misuse of saline or stimulant laxatives is suspected, it may be necessary to check for electrolyte disturbances (e.g., hypokalemia, hypernatremia, hyperphosphatemia, or hypocalcemia). 

Hypernatremia is a serum sodium concentration greater than 145 mEq/L (145 mmol/L) and can occur in the absence of a sodium deficit (pure water loss) or in its presence (hypotonic fluid loss).19 The signs and symptoms of hypernatremia are the same as those found in TBW depletion. Symptoms of hypernatremia are evident with a serum concentration greater than 160 mEq/L (160 mmol/L) and usually consist of thirst, mental slowing, and dry mucous membranes. Signs and symptoms become more profound as hypernatremia worsens, with the patient demonstrating confusion, hallucinations, acute weight... 

Sodium phosphate is available as a nonprescription liquid formulation and by prescription as a tablet formulation. When taking these agents, it is very important that patients maintain adequate hydration by taking increased oral liquids to compensate for fecal fluid loss. Sodium phosphate frequently causes hyperphosphatemia, hypocalcemia, hypernatremia, and hypokalemia. Although these electrolyte abnormalities are clinically insignificant in most patients, they may lead to cardiac arrhythmias or acute renal failure due to tubular deposition of calcium phosphate (nephrocalcinosis). Sodium phosphate preparations should not be used in patients who are frail or elderly, have renal insufficiency, have significant cardiac disease, or are unable to maintain adequate hydration during bowel preparation. 

The polyuria which often accompanies lithium treatment is normally compensated for by drinking water, but when consciousness is impaired severe hypernatremia may develop. When any acute illness (particularly if associated with gastrointestinal symptoms) occurs or when new medication is given, lithium blood levels should be closely monitored, and the lithium dose adjusted. 

Volume resuscitation is the cornerstone of management of lithium toxicity (Table 3) [124, 125]. Patients with underlying lithium-induced diabetes insipidus may initially present with volume depletion. It must be borne in mind, however, that hypernatremia [125] is a potential complication, especially in those with underlying diabetes insipidus. Forced saline diuresis is expected to increase lithium clearance by decreasing proximal tubular reabsorption. With normal renal function, lithium can be cleared at a rate of 10-40 mL/min [125]. The excretion of lithium can be further increased acutely by using acetazolamide and/or loop diuretics [124,125]. 

Mannitol, the most commonly employed osmotic diuretic, is a large polysaccharide molecule. It is often selected for use in the prophylaxis or treatment of oliguric ARF. It is not absorbed from the gastrointestinal tract and, therefore, is only administered i.v. with its elimination dependent on the GFR (within 30 to 60 min with normal renal function). Mannitol is distributed within the plasma and extracellular fluid spaces and produces an increase in the serum osmolality and expansion of the circulating volume. It is not generally used for the treatment of edema because any mannitol retained in the extracellular fluid can promote further edema formation. Furthermore, acute plasma volume expansion may challenge individuals with poor cardiac contractility and can precipitate pulmonary edema. Mannitol is commonly administered for the treatment of cerebral edema consequent to head trauma or to hypoxic-ischemic encephalopathy in neonatal foals. Because mannitol promotes water excretion, hypernatremia is a potential complication in patients that do not have free access to water (Martinez-Maldonado Cordova 1990, Wilcox 1991). 

Hypernatremia (plasma Na >150 mmol/L) is always hyperosmolar, Symptoms of hypernatremia are primarily neurological (because of intraneuronal loss of H2O to the ECF) and include tremors, irritability, ataxia, confusion, and coma. As with hyponatremia, the rapidity of the development of hypernatremia wiU determine the plasma Na value at which symptoms occur. Acute development may cause symptoms when Na reaches 160 mmol/L, although in chronic hypernatremia, overt symptoms may not occur until Na exceeds 175 mmol/L. In chronic hypernatremia, the intracellular osmolality of CNS cells wiU increase to protect against intracellular dehydration. Because of this, rapid correction of hypernatremia can cause dangerous cerebral edema, as CNS cells will take up too much water if the ICF is hyperosmotic when normonatremia is achieved. ... 

Appropriate follow-up care of patients with acute diarrhea is based on successful restoration of fluid losses. The clinical signs and symptoms (see Table 111-1) that led to the diagnosis also can indicate adequate rehydration and should be assessed frequently. Because oral rehydration therapy is now preferred, routine laboratory testing often is unnecessary. Electrolytes should be measured in those receiving parenteral fluids, when oral replacement fails, or when signs of hypernatremia or hypokalemia are present. Follow-up stool samples to ensure complete evacuation of the infecting pathogen may be necessary only... 

Observational studies The use of tolvaptan in short- and long-term studies in heart failure and hyponatremia has been reviewed [82 ]. In an open extension study in 4133 patients with heart failure who were followed for a mean of 10 months, 111 patients with hyponatremia took oral tolvaptan for a mean of 701 days dry mouth, thirst, and hypernatremia were more common in those who took tolvaptan the incidences of hypotension and renal failure were comparable in the two groups [83 ]. The most common adverse events that were assessed by the investigator as being potentially related to the use of tolvaptan were pollakiuria ( = 11) thirst (n = 10) fatigue (n = 6) and dry mouth, polydipsia, polyuria, hypotension, hypernatremia, dizziness, headache, peripheral edema, and acute renal failure (four patients each) [84 ]. 

Overhydration does not occur with normally functioning kidneys. It is rare even with chronic kidney disease. In acute kidney disease, overhydration may be preceded by hypernatremia. This is suggested by the fact that in the early stages of the edema, the plasma sodium levels are low. 

The diuretic (subacute) phase of acute toxicant-induced renal failure is characterized by hypokalemia, hypernatremia, hyperphosphatemia, decreas urine specific gravity, and a normal blood urea nitrogen (BUN) level. The immature ceiis of the recovering tubule lack the ability to control potassium and sodium balance through the normal sodium pump and exchange mechanisms, producir dilute urine. Because urea is freely filtered, the BUN level may be kept within a normal rar because of the high rate of filtration artd formation of dilute urine. 

---