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Chapter 2: Electrolyte Disorders

A 52-year-old man with history of chronic alcohol (ETOH) abuse, chronic obstructive pulmonary disease (COPD), hypertension (HTN), and previous gastrointestinal (GI) bleed presented to the emergency department (ED) with 3 to 4 days of altered mental status. He was lethargic and drowsy but communicating appropriately when aroused. His girlfriend reported decreased food intake but excessive beer consumption of approximately 30 cans in the past 3 days.

On physical exam, he was afebrile. His blood pressure was 120/80 mmHg, his pulse was 80 beats/min, his respiratory rate was 20 breaths/min, and his oxygen saturation was 93% on room air. He appeared disheveled but not dehydrated. He had no pupillary abnormalities, and deep tendon reflexes were normal with no focal neurologic deficits. In addition, he had palmar erythema and a few spider angiomas on the chest.

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Labs:
Hematocrit 44%
White blood cells 6.9 × 103 μL
Platelets 142 × 103 μ/L
Blood urea nitrogen 3 mg/dL
Serum osm 98 mOsm/kg
urine Na 6 mmol/L
Thyroid-stimulating hormone 0.5 mIμ/L
International normalized ratio 1.0
Sodium 107 mEq/L
Chloride 69 mEq/L
Potassium 4.0 mEq/L
Creatinine 0.4 mg/dL
Urine osm 97 mOsm/kg
Alcohol level 268 mg/dL
Albumin 2.4 g/dL

What is the most likely cause?

A. Hypovolemia

B. Syndrome of inappropriate antidiuretic hormone secretion

C. Pseudohyponatremia

D. Poor solute intake

D. Poor solute intake

Hyponatremia from poor solute intake (beer potomania) is secondary to water intoxication with relatively low solute intake. ADH secretion will be (appropriately) negligible and urine osmolality will be maximally dilute. In a patient whose diet is comprised of mostly beer, there will be a very low solute intake (< 250 mOsm/day). Hence, despite a maximally dilute urine (50 mOsm/L), the maximum urine volume will be 5 Liters before the patient will be unable to excrete additional free water (250 mOsm ÷ 50 mOsm/L = 5 Liters)., Introduction of more solute will lead to a brisk aquaresis, which causes rapid correction of sodium and places the patient at risk for osmotic demyelination syndrome. Patients typically have a low serum osmolarity (although it can be high if there is an acute alcohol load), low urine sodium, and low urine osmolarity. In some patients with beer potomania, loss of the urea concentration gradient can impair some of the dilution capacity, but urine osmolality should still be relatively low. Hyponatremia in alcoholics also can be caused by hypovolemia, pseudohyponatremia from hypertriglyceridemia, SIADH, cerebral salt wasting syndrome, and CHF. Clues for diagnosis are history of ETOH abuse, binge drinking, and poor dietary intake.

Choice A is incorrect since he shows no evidence of hypovolemia by vital signs, physical exam, or renal indices. Choice B is incorrect, since urine osmolality is less than 100. Pseudohyponatremia (choice C) is incorrect, as his serum osmolality is truly low, which suggests hypotonic hyponatremia.

A 52-year-old man with history of chronic alcohol (ETOH) abuse, chronic obstructive pulmonary disease (COPD), hypertension (HTN), and previous gastrointestinal (GI) bleed presented to the emergency department (ED) with 3 to 4 days of altered mental status. He was lethargic and drowsy but communicating appropriately when aroused. His girlfriend reported decreased food intake but excessive beer consumption of approximately 30 cans in the past 3 days.

On physical exam, he was afebrile. His blood pressure was 120/80 mmHg, his pulse was 80 beats/min, ...

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