1. Name: David Ramirez

Age: 29 years Gender: Male Mechanism of injury: High-speed MVA, front-end collision; unrestrained driver

EMS reports that the patient was found unconscious, slumped over the steering wheel. Airbag deployed. Windshield starred. No obvious external bleeding.

EMS noted:

Initial GCS 9 (E2 V2 M5)

Hypotension that briefly improved after fluid bolus

Worsening level of consciousness en route

One episode of projectile vomiting

Pupils unequal (R 5 mm sluggish, L 3 mm reactive)

During transport, the patient extended both arms and legs rigidly in response to painful stimulus.

PAST MEDICAL HISTORY

No chronic illnesses reported

No previous neurological issues

Prior appendectomy

Occasional alcohol use (friends stated he had "two beers earlier")

Medications

None prescribed

Midline shift of 7 mm

Signs of brain herniation

Cerebral edema

C-Spine CТ

No fracture noted, but swelling present

The patient suddenly extends his arms and legs rigidly after painful stimulation. What does this indicate?

A. Infuse 1 unit of platelet: Platelet transfusion is indicated for thrombocytopenia or active bleeding related to low platelet counts. Acute adrenal insufficiency does not involve platelet depletion or coagulation defects. This intervention does not address the underlying hormonal crisis.

B. Restrict daily fluid intake: Clients with acute adrenal insufficiency are at risk for hypovolemia and hypotension due to aldosterone deficiency. Fluid restriction would worsen dehydration and circulatory collapse. Fluid replacement is typically required rather than restriction.

C. Admin hydrocortisone sodium: Acute adrenal insufficiency requires immediate glucocorticoid replacement to restore cortisol levels. Hydrocortisone sodium provides both glucocorticoid and some mineralocorticoid effects, helping stabilize blood pressure and metabolism. Prompt administration is critical to prevent adrenal crisis complications.

D. Give oral spironolactone: Spironolactone is a potassium-sparing diuretic and aldosterone antagonist. In adrenal insufficiency, aldosterone levels are already low, making this medication inappropriate. Its use could worsen hyperkalemia and hypotension.

A. Increased protein diet: Increasing protein intake can raise ammonia levels because protein metabolism produces nitrogenous waste. In cirrhosis, impaired hepatic detoxification limits conversion of ammonia to urea. Excess protein may worsen hepatic encephalopathy symptoms.

B. Decreased sodium diet: Sodium restriction is commonly used to manage ascites and edema in cirrhosis. While important for fluid balance, it does not directly reduce ammonia production or levels. This intervention addresses volume status rather than encephalopathy risk.

C. Decreased protein diet: Reducing dietary protein lowers ammonia generation from intestinal breakdown of amino acids. This approach helps decrease neurotoxic ammonia accumulation when hepatic clearance is compromised. Protein intake is often temporarily restricted during episodes of elevated ammonia.

D. Increased carbohydrate diet: Carbohydrates provide an alternative energy source and can help prevent protein catabolism. While beneficial as part of overall nutrition, increasing carbohydrates alone does not directly reduce ammonia production. It is supportive rather than primary management for hyperammonemia.