A 56-Year-Old Man With A Long History Of Alcohol Use ✓ Solved

A 56-year-old man with a long history of alcohol use is admitted to th

A 56-year-old man with a long history of alcohol use is admitted to the hospital after he had a seizure that was witnessed by his wife. The patient is obtunded, swollen, and jaundiced. Temperature is 36.8°C (98.3°F), pulse rate is 104/min and regular, respirations are 18/min, and blood pressure is 104/62 mmHg. On physical examination, auscultation of the chest shows diminished breath sounds. Examination of the abdomen shows firmness of the right upper quadrant, palpable hepatomegaly, and protruberance of the umbilicus. Results of laboratory studies of serum include the following: Creatinine 0.8 mg/dL, Sodium 108 mEq/L, Potassium 3.5 mEq/L, Blood urea nitrogen 4 mg/dL. Which of the following is the most appropriate initial management?

Sample Paper For Above instruction

Introduction

The management of hyponatremia, especially in the context of cirrhosis and ascites, poses significant clinical challenges. Hyponatremia, defined as a serum sodium level below 135 mEq/L, can lead to neurological disturbances such as seizures if corrected too rapidly. This case involves a patient with a history of alcohol use presenting with hyponatremia, neurological symptoms, and signs suggestive of advanced liver disease. Understanding the pathophysiology of hyponatremia in cirrhosis is essential to determine the most appropriate initial management.

Clinical Presentation and Pathophysiology

The patient's presentation includes obtundation, seizure, jaundice, hepatomegaly, and abdominal distention. These signs point toward decompensated liver disease with probable cirrhosis. Laboratory findings reveal a critically low serum sodium level of 108 mEq/L, which is symptomatic and warrants urgent correction. Cirrhosis-associated hyponatremia often results from impaired water excretion due to elevated antidiuretic hormone (ADH) levels, secondary to decreased effective arterial blood volume caused by splanchnic vasodilation. As a result, water retention exceeds sodium retention, leading to dilutional hyponatremia.

The patient's clinical signs need to be interpreted in this context. Diminished breath sounds and abdominal findings suggest possible complications like ascites, which further exacerbate circulatory dysregulation. The low serum sodium level, along with neurological symptoms (seizure), indicates the urgency to correct hyponatremia to prevent further neurological deterioration.

Management Principles in Hyponatremia

The management of hyponatremia depends on severity, symptoms, volume status, and underlying cause. In symptomatic hyponatremia, especially with seizures, rapid correction using hypertonic saline (3% NaCl) is generally indicated. However, overcorrection poses a risk for osmotic demyelination syndrome. Therefore, careful administration with close monitoring is essential.

In cases where hyponatremia is associated with cirrhosis, the approach includes addressing underlying circulatory dysfunction, restricting free water intake, and carefully administering hypertonic saline if symptomatic. Diuretics may be used cautiously to manage ascites but are not the initial treatment for hyponatremia itself.

The serum BUN of 4 mg/dL and creatinine of 0.8 mg/dL suggest preserved renal function, ruling out renal failure as the cause of hyponatremia. The sodium level of 108 mEq/L warrants urgent correction, especially given the presence of seizures.

Why Not Other Options?

- Emergent hemodialysis (A): Not indicated unless renal failure is present.

- Fluid restriction (B): Part of the general management of SIADH and cirrhotic hyponatremia but not sufficient in emergencies with neurological symptoms.

- Intravenous administration of 5% dextrose in water (D): Would worsen hyponatremia by introducing free water.

- Intravenous administration of diltiazem (E): Used for hypertension or arrhythmias, not hyponatremia.

Most Appropriate Initial Management

The most suitable initial management in this scenario is the cautious administration of hypertonic saline (3% NaCl), which rapidly corrects serum sodium in symptomatic hyponatremia, especially seizures, while minimizing risks of demyelination.

Conclusion

In this patient presenting with symptomatic hyponatremia and neurological symptoms, the immediate priority is to restore serum sodium safely. Hypertonic saline infusion, under close monitoring, is the most appropriate initial intervention to prevent further neurological compromise and stabilize the patient.

References

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