A client with a severe traumatic brain injury is exhibiting signs of dysphagia.
What should the nurse do first to ensure safe feeding?

Evaluating a cervical spine injury for neurogenic shock requires knowledge of autonomic nervous system disruption. Specifically, loss of sympathetic tone below the level of injury must be identified. Differentiating neurogenic shock from spinal shock involves assessing hemodynamic parameters and thermoregulation.

Choice A rationale

Neurogenic shock involves loss of sympathetic vascular tone, causing massive vasodilation and hypotension. Unchecked parasympathetic activity leads to bradycardia. Normal heart rate is 60 to 100. Warm, pink skin results from peripheral blood pooling due to vasodilation.

Choice B rationale

Hyperactive reflexes are characteristic of the later stages of spinal cord injury after spinal shock resolves. They do not indicate the acute hemodynamic collapse seen in neurogenic shock, which specifically targets the cardiovascular regulatory systems.

Choice C rationale

Loss of sensation and movement defines spinal shock or the initial cord injury itself. While present in neurogenic shock, these findings are not specific to the autonomic failure that characterizes the life-threatening hemodynamic instability of shock.

Choice D rationale

Spasticity occurs due to upper motor neuron damage after the initial period of areflexia. This is a chronic or subacute finding and is not associated with the acute cardiovascular distributive failure seen in neurogenic shock.

The clinical presentation of asterixis and lethargy in liver failure indicates hepatic encephalopathy. Knowledge of nitrogenous waste metabolism and the pharmacological action of osmotic laxatives is necessary to address the buildup of neurotoxic ammonia levels within the systemic circulation.

Choice A rationale

Vitamin K is essential for synthesizing clotting factors II, VII, IX, and X in the liver. While liver failure causes coagulopathy, this intervention does not address the neurological symptoms caused by elevated ammonia or metabolic encephalopathy.

Choice B rationale

Historically, protein restriction was used to limit ammonia production. However, modern guidelines emphasize maintaining adequate protein intake to prevent muscle wasting and malnutrition, which can actually worsen the clinical outcomes and metabolic status in cirrhotic patients.

Choice C rationale

Lactulose is a synthetic disaccharide that acidifies colonic contents. This converts ammonia into ammonium, which is poorly absorbed and excreted via stool. It is the gold standard for reducing neurotoxic ammonia levels in hepatic encephalopathy.

Choice D rationale

Sodium restriction is primarily utilized to manage fluid retention and ascites in portal hypertension. While important for volume control, it does not directly impact the cerebral edema or neurotoxicity associated with the presence of asterixis.