by Vigor Arva, Gregor Prosen
A 79-year-old man was brought to the emergency department (ED) by his wife. She complained that the patient had general weakness and was feeling ‘unwell’ for the last two days. He had a history of dementia, diabetes, renal failure, and hypertension. He was on diabetic and antihypertensive medication.
On examination, his vital signs were as follow HR 115/min, BP 135/90 mmHg, RR 17/min, and afebrile with normal oxygen saturation. He was confused and disoriented, but there was no other deficits or localizing signs on neurological exam. He was clinically dehydrated with dry oral mucosa. Lab results showed a serum sodium concentration of 160 mEq/L, with elevated glucose, creatinine, urea, and osmolality. Point of care ultrasound demonstrated a small and almost totally-collapsed inferior vena cava. Upon further history taking, the patient’s wife reported that he had not been drinking much for the last few days, even though he did not complain about thirst.
Critical Bedside Actions and General Approach
Hypernatremia should be excluded in any patient who presents with altered mental status, particularly, the very young or old and those with abnormal basal cognition.
Once diagnosed, the next step is to assess for volume status and acuity of symptoms, as they influence treatment plan. It is considered acute if symptoms develop within 48hrs, and chronic if it is longer. Then, the cause should be determined and treated.
Hypernatremia usually results from relative water losses, and rarely secondary to sodium overload. The causes can be categorized into the following three groups:
A. Hypernatremia with hypovolemia: Often found with dehydration and fluid losses such as heatstroke, excessive sweating, burns, and gastrointestinal losses with diarrhea and vomiting
B. Hypernatremia with euvolemia: Occurs mostly as a result of ADH deficiency, diabetes insipidus, reset of osmostat, hypothalamic dysfunction, primary hypodipsia, renal diseases, drugs and alcohol (e.g., lithium, amphotericin, phenytoin, aminoglycosides)
C. Hypernatremia with hypervolemia: Can occur because of iatrogenic causes infusion of hypertonic sodium solutions (3% saline, or large volumes of sodium bicarbonate), ingestion of salt water or large amounts of salt, Cushing’s and Conn’s syndrome
Diabetes insipidus (DI) refers to an absolute or relative antidiuretic hormone (ADH) deficiency. Absolute ADH deficiency occurs in the setting of inadequate ADH secretion and is called central DI. Relative ADH deficiency occurs in lack of renal response to ADH and is called nephrogenic DI.
Malignant diseases, trauma or surgery on the pituitary, infiltrative diseases, familial diseases or idiopathic conditions may cause central DI. Chronic renal insufficiency, tubulointerstitial diseases, polycystic kidney disease, hypercalcemia, hypokalemia, lithium toxicity, or familial diseases may cause nephrogenic DI.
Symptomatic hypernatraemia (e.g., polyuria and polydipsia, lethargy and weakness) with an inappropriately low urine osmolality (<300 mOsm/kg) should suggest DI in the ED. The formal diagnosis requires a water deprivation test, which is often not performed in the ED given the long duration required.
Central and nephrogenic DI are further distinguished by the response to desmopressin (synthetic ADH). With desmopressin, urine osmolality will rise to more than 800 mOsm/kg in patients with central DI, while this rise is absent in nephrogenic DI.
Psychogenic polydipsia can be distinguished from DI by water restriction. Following water restriction, urine osmolality will rise in psychogenic polydipsia and remain unchanged in DI.
History and Physical Examination Hints
The signs and symptoms of hypernatremia are nonspecific including lethargy, irritability, restlessness, hyperactive reflexes, and increased muscle tone. Severe symptoms usually occur after the serum Na has risen acutely above 158 mEq/L, and may include seizures, coma or even death.
Rapid and severe hypernatremia developing over minutes and hours can result in brain hemorrhage, due to the accompanying rapid decrease in brain volume causing ruptures of cerebral veins. It is also associated with hypocalcemia, for unclear reasons.
If the hypernatremia is chronic, the brain can adapt by generating intracellular osmogenic compounds, or idiogenic osmoles, which increases the osmolality in the cells and thus maintaining brain volume by resisting shrinkage.
Patients should be asked about their fluid and salt intake, urine output, and concurrent medical and medication history. The patient’s caregiver should be interviewed, especially if the patient is mentally altered, to see if there are mental or behavioral changes (e.g., excessive water intake).
Patients should be examined for their volume status by checking skin turgor, capillary refill, looking for edema and raised jugular venous pressure, measuring heart rate, blood pressure and looking for a postural drop, mental and neurological status.
Emergency Diagnostic Tests and Interpretation
Serum sodium level (Normal reference: 135-145 mEq/L) and serum osmolality (Normal reference: 275-295 mOsm/L) should be checked. Both can be done at the bedside. Other electrolytes (mainly potassium and calcium) should be checked. Patients urine output and urine osmolality should be measured.
Total body water (TBW) deficit can be calculated as a function of sodium concentration:
TBW deficit = TBW x [(serum sodium/140) – 1]
Average total body water is obtained by multiplying the patient’s body mass by 0.6. However, this holds mostly for children and adult men. A multiplier of 0.5 for elderly men and adult women and 0.45 for elderly women should be preferred.
Emergency Treatment Options
Following the initial ABC evaluation, hypernatremic patients with hemodynamic instability should be resuscitated with intravenous fluids. The aim at this point is to address the underlying hypovolemia and tissue hypoperfusion. Unless this is corrected, the body’s normal response is to increase the sodium concentration even further to maintain intravascular volume, which will worsen the hypernatremia. Fluid resuscitation can be achieved using normal saline (0.9%) or Ringer’s lactate.
After stabilizing the patient, proceed to evaluate for and treat the underlying cause of hypernatremia (e.g., fever, new medicine, gastrointestinal disturbances and DI).
In patients with acute hypernatremia (symptoms occurring <48hrs), it is relatively safe to correct sodium at a rate of 1mEq/L/hr, with correction of the total water deficit in 24 hours. This is because the brain did not have enough time to produce idiogenic osmoles, lowering the risk for cerebral edema.
In patients suspected of having chronic hypernatremia, the sodium should be corrected gradually, and no more than 0.5 mEq/hr or 10-12 mEq/day. Rapid overcorrection can result in cerebral edema, especially in children. Oral rehydration with water may be the safest option.
Sodium concentration in different solutions
- 0.9% NaCl: 154 mmol/L
- Ringer’s Lactate: 130 mmol/L
- 0.45% NaCl: 77 mmol/L
- 5% Dextrose in water (D5W): 0 mmol/L
To determine the volume and rate of correction, one can calculate it manually using the formulas given above. There are also several free online calculators available as well, such as the one by Medcalc.
Patients with known central DI should be given desmopressin (DDAVP) which should improve symptoms. Initial doses are 1 – 2 micrograms. The dose should be up-titrated if necessary.
Pediatric, Geriatric, Pregnant Patient, and Other Considerations
Infants can develop hypernatremia if they are not given adequate fluids, or are given hypertonic fluids. Older children can also develop hypernatraemia with volume depletion following after severe diarrhea or vomiting.
Pregnant patients may develop hypernatremia if vomiting secondary to hyperemesis gravidarum is severe. Cases of gestational diabetes insipidus have been documented and should not be confused with polyuria that can normally occur during pregnancy.
Hypernatremia is common in the elderly. The causes are likely multi-factorial and inter-related, including the decrease in thirst sensation, polypharmacy, and pre-existing co-morbidities.
Patients with symptomatic hypernatremia should be admitted for evaluation and treatment, as the free water deficit is generally replaced gradually. Those with severe neurological symptoms will require admission to a closely monitored unit.
Hemodynamically stable and asymptomatic patients with mild hypernatremia from benign causes may be discharged with advice and follow up with the primary physician.
References and Further Reading
- Tintinalli JE, Stapczynski JS. Tintinalli’s emergency medicine : a comprehensive study guide. 7th ed. New York: McGraw-Hill Medical; 2011.
- Marx JA, Hockberger RS, Walls RM, Adams J, Rosen P. Rosen’s emergency medicine : concepts and clinical practice. 7th ed. Philadelphia: Mosby/Elsevier; 2010.
- Westafer JFL. Hypernatremia [Internet]; 2011. Podcast. Available from: http://foamcast.libsyn.com/foamcastini-2-hypernatremia
- Cadogan M. Hypernatraemia. Life in the fast lane 2011; http://lifeinthefastlane.com/investigations/hypernatraemia/. Accessed 29.04, 2016. – link (last updated 2017)
- Wyatt JP. Oxford handbook of emergency medicine. 3rd ed. Oxford; New York: Oxford University Press; 2006.
- Aleksandrov N, Audibert F, Bedard MJ, Mahone M, Goffinet F, Kadoch IJ. Gestational diabetes insipidus: a review of an underdiagnosed condition. J Obstet Gynaecol Can. 2010;32(3):225-231.