Kembara Xtra - Medicine - Hypernatremia
Serum sodium (Na) concentration >145 mEq/L, which often denotes a hypertonic state The equilibrium between total body water (TBW) and total body Na is reflected in the Na concentration. Water relative to sodium deficiency is the cause of hypernatremia. Hypernatremia typically comes from net water loss or, less frequently, from main Na gain. Dehydration is defined as hypernatremia from water loss. Hypovolemia is defined as concurrent water and salt loss. Patients who can acquire water and have functioning thirst mechanisms won't experience hypernatremia. Epidemiology Incidence: More prevalent in the very young and elderly; occurs in 1% of elderly hospital patients; seen in roughly 9% of ICU patients Pathophysiology and Etiology Due to the potent impact of the thirst mechanism, hypernatremia usually only affects patients who do not have easy access to water, such as babies, patients who are intubated, people who have changed mental status, or people who have hypodipsia. The most frequent cause of hypernatremia is water loss that is out of proportion to salt loss. Excessive water loss is caused by the factors listed below: - Transdermal loss due to burns or profuse perspiration (examples include illness, newborns exposed to radiant heaters, heat exposure, and intense exercise). - Loss of urine Nephrogenic diabetes insipidus (DI) (congenital or caused by renal dysfunction, hypercalcemia, hypokalemia, or medication-related, such as lithium) and Central DI (caused by head injury, stroke, or meningitis) are two types of diabetes insipidus. Post-ATN diuresis - Gastrointestinal loss Osmotic diuresis: glucose, urea, and mannitol Enterocutaneous fistula Osmotic diarrhea: lactulose, malabsorption, and some forms of infectious diarrhea NG suction and vomiting Because of inadequate water intake, disorders of the thirst mechanism (such as cerebral lesions, intrinsic hypodipsia, and chronic volume enlargement in mineralocorticoid excess) can cause hypernatremia. Hypernatremia is less frequently brought on by excess Na (an increase in total body Na). Excess total body Na may originate from the following condition: - IV infusion of hypertonic NaCl or NaHCO3 for the treatment of metabolic acidosis, hyperkalemia, or brain damageIngestion of sea water, excessive use of NaHCO3 antacids, improper preparation of newborn formula and tube feeding, and an abundance of Na in dialysate solutions Acute hypernatremia can cause the cerebral veins to burst, which can result in focal intracerebral and subarachnoid hemorrhages as well as potentially irreparable neurologic impairment. Genetics Some types of DI may run in families. Risk factors include: infants and children; elderly patients (who may also exhibit a diminished thirst response to osmotic stimulation via an unknown mechanism); patients who are intubated or have altered mental status; acute gastrointestinal illness; poorly controlled diabetes mellitus; prior brain injury; surgery; diuretic therapy, particularly loop diuretics; and lithium therapy. Treatment and/or prevention of the underlying cause Keep patients well-hydrated, properly mix newborn formula, and never salt any purchased infant formula. Gastroenteritis, altered mental status, burns, and head damage are associated conditions. presenting the history Head injury, fever, heat exposure, polyuria, nausea, vomiting, diarrhea, and polyuria all have a history of causing water loss or impairing thirst. Neurologic symptoms frequently occur: - Mild: anorexia, thirst Moderate symptoms include confusion, myalgia, twitching muscles, tiredness, and irritability. - Severe: seizure (particularly if hypernatremia develops quickly), coma Severe symptoms are likely to occur with sudden rises in plasma Na levels or at concentrations >160 mEq/L. The severity of symptoms correlates with the rate of the increase in Na as well as the degree of hypernatremia. clinical assessment Tachycardia, hypotension, orthostatic hypotension, dry mucous membranes, and poor skin turgor are indications of water or volume loss. Lethargy, weakness, tremor, focal impairments (in situations of intracerebral bleeding/lesion), disorientation, coma, and seizures are examples of neurologic abnormalities. Differential diagnosis, hyperosmotic coma, salt intake, hypertonic dehydration, hypothyroidism, and Cushing syndrome are all possible diagnoses. Initial test results from the laboratory and imaging Blood tests for sodium, potassium, BUN, creatinine, glucose, calcium, and osmolality (and, if necessary, serum lithium) Hemoglobin/hematocrit levels (which could be higher than normal due to hemoconcentration) Na and osmolality in urine Low urine osmolality: DI is suggested by urine osmolality (typically 300 mOsm/kg) serum osmolality. The causes of intermediate urine osmolality (300 to 800 mOsm/kg) include partial DI, osmotic diuresis, and hypovolemia. - High urine osmolality (>800 mOsm/kg) may indicate salt consumption or extrarenal water loss. Low urine sodium levels (10) typically indicate volume depletion, but they can also result from dilution when combined with excessive urine production from DI. - Osmotic diuresis may be the cause of intermediate urine Na. - Consuming salt is suggested by high urine Na. Tests in the Future & Special Considerations Antidiuretic hormone (ADH) stimulation distinguishes between central and nephrogenic DI; in nephrogenic DI, urine osmolality does not rise in response to ADH or desmopressin. To rule out cerebral abnormalities in individuals with central DI or hypodipsia using head CT/MRI Management The underlying cause of hypernatremia must be addressed in addition to the water deficiency. As the speed of correction relies on the severity of the symptoms and the rate at which hypernatremia develops, ascertain the length of the hypernatremia. Acute hyponatremia is a relatively rare condition that can result from salt consumption, extreme hyperglycemia, or acute DI. - Infuse D5W at 3 to 6 mL/kg/hr to reduce serum Na by 1 to 2 mEq/L/hr. - Check serum Na every 1 to 2 hours to ensure correction is occurring at the required rate. – D5W infusion should be decreased to 1 mL/kg/hr once serum Na falls to 145 mEq/L until serum Na returns to normal. – In 24 to 48 hours, try to cure hypernatremia. Chronic hypernatremia (lasting more than 48 hours): Delay fast correction to avoid cerebral edema. Check serum Na every 4 to 6 hours to assess whether the correction is occurring at the required pace. D5W infusion at 1.35 mL/kg/hr. Correct at a rate of no more than 0.5 mEq/L/hour or 10–12 mEq/L/day. Infusion rates frequently need to be changed to allow for persistent water losses. Hyponatremia combined with hypernatremia Before treating hypernatremia, treat severe volume loss with isotonic IV fluids: - Once hemodynamic stability is achieved, 0.45% saline can be used to treat hypovolemia and hypernatremia simultaneously because every 2 mL of this solution contains 1 mL of saline and 1 mL of water. When hypernatremia and hypervolemia coexist, hypervolemia can be treated with diuretics while hypernatremia is being corrected. However, concurrent diuretic use will increase urinary water losses and may call for higher water replenishment. If you have mild hypernatremia, think about oral water replacement. Dialysis is an option if acute kidney damage and conventional treatment have failed. High infusion rates of D5W may generate hyperglycemia. Hyperglycemia-induced osmotic diuresis may increase urinary water losses and require higher water replenishment. First Line of Medicine Instead of using medications, most treatments use hypotonic IV fluids or water. Medication may be used to treat DI Desmopressin acetate (DDAVP), a centrally injected analgesic, should be administered parenterally to patients with acute symptoms and intranasally or orally for chronic therapy. - Free water replacement: To prevent glycosuria when administering large amounts of water in DI, use 2.5% dextrose in water. - For chronic but not acute treatment, sulfonylureas/thiazide diuretics may be considered. Nephrogenic DI should be treated with NSAIDs and diuretics. - Amiloride hydrochloride 5 to 10 mg PO BID Second Line: Hydrochlorothiazide 25 mg PO BID or Indomethacin 50 mg PO TID A number of case reports and case series have demonstrated the effectiveness and safety of employing continuous renal replacement therapy (CRRT) to treat hypernatremia in critically ill patients with CHF and severe burns. NSAIDs should be taken into consideration in nephrogenic DI. Referral A nephrology referral would be advantageous if there was underlying renal involvement brought on by hypernatremia. Admission The following criteria must be met before a patient can be discharged: stabilization of the blood Na level and relief of symptoms in a symptomatic patient with serum Na >155 mEq/L. Patient Follow-Up Monitoring Daily weight, electrolytes, and blood glucose for a time after correction Periodic monitoring of urine osmolality and urine output in DI Regular neurologic assessments throughout acute correction Ensure sufficient nourishment throughout the acute phase of the condition. After the acute phase has passed, the patient may consider a sodium-restricted diet. Patients with nephrogenic DI need to limit their salt intake and consume a lot of water. The majority of patients recover, however neurologic damage is possible. Complications include: CNS thrombosis/hemorrhage; seizures; and chronic hypernatremia, which has a greater death rate if it persists for longer than two days. Serum Na >180 mEq/L (>180 mmol/L): frequently causes lingering CNS injury
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