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I HAVE A PATIENT WITH HYPONATREMIA. I HAVE A PATIENT WITH HYPERNATREMIA

How do I determine the cause?

HYPONATREMIA

CHIEF COMPLAINT

PATIENT image

Mr. P is a 66-year-old man who comes to the emergency department with a chief complaint of an inability to urinate. Shortly after arrival he has a generalized seizure. Initial labs reveal a serum sodium concentration of 122 mEq/L.

image What are the symptoms of hyponatremia? What is the differential diagnosis of hyponatremia? How would you frame the differential?

CONSTRUCTING A DIFFERENTIAL DIAGNOSIS

As noted in Chapter 1, the first task when evaluating patients is to identify their problem(s). Mr. P’s problems clearly include seizure, marked hyponatremia, and inability to urinate. While other causes of seizures must be considered, the hyponatremia clearly requires evaluation because it is severe, potentially life-threatening, and likely to have caused the seizure.

Hyponatremia is the most common electrolyte abnormality in hospitalized patients and associated with an increase in mortality that is profoundly modified by the underlying cause of hyponatremia. It is defined as a serum sodium concentration < 135 mEq/L and is classified as mild (130–135 mmol/L), moderate (125–129 mmol/L), or profound (< 125 mmol/L).

Symptoms of Hyponatremia

The adverse effects and manifestations of hyponatremia depend on its severity and rapidity of development. Acute hyponatremia (defined as developing within the prior 48 h) leaves the brain hypertonic relative to the hypotonic serum. This osmotic gradient drives water into the brain’s astrocytes, resulting in cerebral edema and CNS symptoms. Acute hyponatremia may cause seizures, brain damage, brainstem herniation, respiratory arrest, rhabdomyolysis and death. Symptoms occur at much more modest degrees of hyponatremia than in patients with chronic hyponatremia. Seizures can occur even at sodium levels above 120 mEq/L. On the other hand, in chronic hyponatremia (most cases), CNS adaptations occur. Astrocytes decrease their intracellular osmolality, decreasing the osmotic flux of water into the brain in turn causing less cerebral edema. Therefore, symptoms tend to develop when hyponatremia is more severe than in patients with acute hyponatremia. Seizures and herniation are much less frequent. Typically, patients with chronic hyponatremia and serum sodium levels > 130 mEq/L are asymptomatic. Symptoms associated with profound hyponatremia (< 125 mEq/L) include nausea (44–49%), vomiting (27–30%), gait disturbance (31%), headache 27%, confusion (14–30%), seizures (5%), and coma.

Before reviewing the differential diagnosis of hyponatremia, it is useful to briefly review the pathophysiology of normal water handling, antidiuretic hormone (ADH), and then hyponatremia. ADH plays a key role in water handling.

In health, dehydration increases the serum sodium and osmolality and triggers ADH release. This causes water channels (aquaporins) to be inserted into the luminal membrane of the collecting ducts, promoting water reabsorption. This restores normal osmolality and sodium concentration. Conversely, excessive water ingestion lowers the serum sodium and osmolality suppressing ADH secretion and results in the removal of the aquaporins. This prevents water reabsorption, promotes its excretion and restores the normal osmolality and sodium concentration.

Hyponatremia occurs when water accumulates in excess ...

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