Monitor Patient with Increased ICP
For acute patients with/at risk for raised intracranial pressure, additional monitoring is required as follows (report changes promptly to physician):
- Monitor core Temperature q 1 h. Continuous monitoring should be considered if cooling blankets and/or neuromuscular blockers are in use.
- Obtain order for acetaminophen and cooling blanket for T > 38. If fever is severe, review with physician other strategies such as sedation or neuromuscular blockade.
- Lower temperature of cooling blanket gradually to avoid shivering.
- Wrapping arms and legs in blankets may reduce shivering.
- Neuromuscular blockers may help to reduced temperature and block shivering, but may cause rapid drop in temperature.
- Monitor BP and HR carefully. Treat hypotension and hypovolemia promptly.
- Maintain euvolemia.
- Monitor blood gases q 6 h and prn during acute phase. Keep PaCO2 35-40 (or lower if ordered) and PaO2 > 80-90 unless otherwise ordered. Unlike other ventilated patients, PaCO2 is the target, not the pH.
- If mannitol is ordered or hypertonic saline is used, measure serum electrolytes and osmolalities q 6 h as ordered. Notify Neurosurgeon if serum osmolality >320 (mannitol) or hypertonic saline (>340), of if serum sodium is > 156 with hypertonic saline.
- Monitor for increased/dilute urine output. Obtain order for serum and urine electrolytes and osmolality to assess for Diabetes Insipidus.
- Correct hyper/hyponatremia slowly (.5-1 mmol/L/hr of change in either direction (unless neurological death has been diagnosed and organ donation is being pursued).
- Monitor carefully for signs of seizure activity.
- Monitor blood sugar closely. Avoid hyper or hypoglycemia. Review target glucose with physician if insulin is required for an increase in the lower limit range.
- Monitor for seizure activity. Prophylactic anticonvulsants may be ordered for patients with injuries most likely to cause seizures.
Hypothalamus dysfunction can cause neurogenic fever and/or Diabetes Insipidus (DI). Fever is associated with a poor neurological outcome and increases the brains oxygen consumption. Shivering increases metabolic rate and heat production, and promotes vasoconstriction that reduces heat loss. Sedation and Neuromuscular Blockade can lower temperature by decreasing heat production (due to muscle activity).
DI is diagnosed by presence of polyuria, low urine osmolality, high serum osmolality and hypernatremia. It can cause severe and lethal dehydration. Acute DI following severe brain injury is associated with very poor outcome.
Hypercarbia, acidosis, hypoxemia or hypotension can trigger a sympathetic rise in cerebral blood flow. Increased cerebral blood volume can increase ICP. Patient triggered hyperventilation may be a sign of increased ICP.
Hypotension and/or hypovolemia can decrease cerebral blood flow. A rise in BP may be a sign of increased ICP as the body attempts to maintain cerebral perfusion pressure (CPP). Hypertension with widening pulse pressure (increased systolic and decreased diastolic pressure), bradycardia and irregular respirations or apnea suggestions brainstem herniation (Cushings Triad). Urgent intervention is needed.
Hyponatremia can induce seizures (critical threshold <120 mmol/L; critical level may be higher in patient with brain injury). Rapid correction of low sodium (blood is hypotonic) can cause Central Pontine Myelinolysis (potentially fatal). Rapid correction of hypernatremia can cause cerebral edema. Rapid sodium changes cause rapid changes in osmolality.
Calculate Serum Osmolality =
2 (Na) + urea + glucose
Excessive mannitol use can produce dehydration. Dehydration can increase CSF production and ICP. The goal is to maintain euvolemia.
The brain is totally dependent upon glucose as a source of energy. Hypoglycemia causes energy depletion in the brain. Hyperglcyemia is associated with poor neurological outcomes. Careful monitoring is important.
Seizures increase brain metabolic rate and can lead to ischemic injury if not treated promptly.