Neurology 5: Increased Intracranial Pressure Portal
Head trauma causes increased intracranial pressure. Injury occurs with the primary insult (which accounts for 50% of the deaths associated with head injury) and also secondary insult. Secondary injury refers to delayed insults, both systemic and intracranial, which can be attributed to initial traumatic injury. When secondary complications occur, they are associated with increased mortality. Early intervention and management are necessary entities to preserve uninjured brain tissue. Because the cranial vault is a fixed space occupied by three components (brain—86%, blood—4%, and CSF—10%), to maintain normal intracerebral pressure a change in volume in any one of these components will result in a compensatory change in one or both of the remaining two.
Physiologic compensation is accomplished by displacement/absorption of CSF and decreasing cerebral blood flow. These compensatory mechanisms are rapidly exhausted by the individual, resulting in a rapid rise in intracranial pressure. The elevation of intracranial pressure without an equivalent rise in systemic mean arterial pressure (MAP) results in decreased cerebral perfusion pressure (CPP) and the risk of brain ischemia. Without assisting in the compensatory mechanism, through the treatments listed, herniation of the brain ensues.
The goal in the first several minutes to hours after head injury must be to prevent/limit the amount of secondary insult sustained. The most effective measures are listed below:
Positioning
Maintain alignment of head, neck, and thorax to promote venous return routed primarily through internal jugulars. Use caution with immobilization devices. Elevation of the head remains controversial. In the stabilization phase, proper alignment is more effective than raising the HOB. Additional data suggests elevation beyond 30 degrees may actually further complicate by decreasing arterial flow and CPP.
Hyperventilation
Hyperventilation in the field or during resuscitation (before ICP monitoring) should be reserved for patients demonstrating specific signs of intracranial hypertension such as evidence of herniation or progressive neurological deterioration not attributable to extracranial sources.
Decreased PCO2 causes cerebral vasoconstriction thereby decreasing cerebral blood flow and decreasing intracranial pressure. Ideal PCO2 levels to treat increased intracranial pressure are 30 to 35. Levels < 30 cause excessive vasoconstriction and secondary ischemia and should not be used. Continuous ETCO2 monitoring is helpful. Abrupt cessation of hyperventilation may cause rebound cerebral vasodilitation and increased intracranial pressure. Monitoring with serial blood gases and intracranial pressure devices should be initiated as soon as possible.
Hyperventilation should not be used prophylactically (ie, in the absence of measured intracranial hypertension or clinical signs highly suggestive of elevated intracranial pressure). When used for the treatment of documented intracranial hypertension, it should generally be reserved for intracranial pressure problems that are refractory to treatment modalities with more favorable risk benefit ratio (eg, establishment of an adequate CPP, cerebrospinal fluid drainage, sedation, neuromuscular blockade, mannitol).
It is important to note that the term hyperventilation does not mean simply increasing the rate of ventilation. The PCO2 levels can also be affected by changes in tidal volume (TV). PEEP (positive end expiratory pressure) increases intrathoracic pressure thereby causing a decreased venous outflow from the cranial vault and a decreased venous return to the heart.
Airway Protection
Generally patients with increased intracranial pressure require intubation, preferably by rapid sequence intubation. The need to control ventilation and oxygenation in the patient with neurological decline/compromise is paramount to optimize outcome. Glasgow Coma Scale of less than 8 is a common numeric for the practitioner to calculate a need for intubation. Neuromuscular blockade and sedation/analgesia must be utilized with patients requiring control of airway. Neurological assessment must be judicious and documented when this is utilized. Maintain PCO2 30 to 35. Use RR and TV to decrease PCO2. Maintain adequate oxygenation. RR>12 essentially hyperventilating; TV 10 to 12 mL/kg of body weight—start at low end and work up as needed. Remember PEEP will increase intrathoracic pressure and cause hypotension, which could lead to decreased CPP. Consider all factors.
Diuresis
Osmotic and loop diuretic therapy are widely utilized to decrease intracranial pressure. Mannitol is an osmotically active agent that reverses the osmotic gradient in brain tissue and shifts water from the brain to the blood. Administer mannitol 1 g/kg load IV over 15 minutes through a filter. Monitor BP frequently, especially if the patient has multiple injuries. Use extreme caution if considering the use of mannitol for increased intracranial pressure in a patient in hypovolemic shock because it can lead to cardiovascular collapse. If possible, consult with a neurosurgeon prior to use of mannitol.
Mannitol increases the extracranial osmolarity and creates a blood-brain osmotic gradient that pulls fluid from the uninjured cranial extracellular spaces to the extracranial circulation. The blood viscosity is decreased and microcirculation is improved. Hyperosmolar treatment of elevated intracranial pressure increases the normal serum Osm of 290 to 300 to 320 mOsm/L.
Osmolity less than 300 is ineffective; osmolity greater than 320 results in renal and neurologic dysfunction. The serum osmolality goal is to achieve a hyperosmolar state of 300 to 315. Loop diuretics (Lasix 0.5 mg/1kg) may be used to further dehydrate patients and reduce CSF production.
Hypertonic saline is an osmotic agent with a higher concentration of sodium and a lower concentration of water than blood. By reducing water content in an injured brain, hypertonic saline can reduce mass effect as well as control intracranial pressure, leading to a decrease in secondary brain injury.
Hypertonic saline has the advantage of improving intravascular volume and maintaining/improving MAP and CPP.
To treat acute intracranial pressure elevations, hypertonic saline can be administered in bolus form. Give a highly concentrated dose (30 mL of 23.4% NaCl) through a central line over approximately 15 minutes. The bolus dose can help decrease ICP and improve cerebral perfusion. If a central line is not available, 150 cc of 5% hypertonic saline can be delivered via a peripheral line over 30 minutes. Consult early with your neurosurgeon regarding the use of hypertonic saline.
PEDS: Hypertonic saline has been used safely and effectively in children with traumatic brain injury. It is particularly beneficial in treating refractory increases in ICP in pediatric patients. Follow your facility’s protocol.
Fluid Administration
Maintain CPP (do not allow MAP to fall below 50 for more than 1 hour). Treat concomitant injury with judicious fluid treatment when possible.
Adequate CPP must be maintained but regulation of fluids is difficult without invasive monitoring devices (Swan Ganz, arterial line, and intracranial pressure). The complete equation utilized in intensive care settings is CPP=MAP-ICP (cerebral perfusion pressure=mean arterial pressure minus intracranial pressure).
This requires an arterial line and an intracranial pressure monitor. If central line placement is possible, measurement of CVP can be helpful to determine need for fluid resuscitation with multiple trauma. In the absence of invasive monitoring, the MAP can be calculated. (MAP=diastolic BP + 1/3 [systolic BP minus diastolic BP]). The normal range of MAP is 80 to 100 mm Hg. If the MAP remains below 50 mm Hg for more than an hour, renal damage and inadequate coronary/cerebral perfusion are likely to occur.
The normal intracranial pressure is 10; pressures > 20 for several minutes are potentially damaging, > 40 for any length of time are generally irreversible and fatal.
Many head-injured patients are hypertensive related to catecholamine release with pain, hemorrhage, and stress. Judicious use of fluids and potential need for anti-hypertensive therapy must be monitored.
Control of Stimulation/Stressors
Paralytic/Sedative/Analgesic Therapy
When
the patient has been stabilized and intubated and disposition awaits,
it may be necessary to use neuromuscular blockade (NMB) agents to
facilitate complete cooperation of patient with ventilatory efforts.
Weigh the options and evaluate the need. Careful monitoring of the BP
and HR are the measurements that can be predictors of continued increases in intracranial pressure.
Cushing’s
Response is a form of CNS ischemic response, resulting specifically
from increased intracranial pressure. Clinically the patient develops:
- Widened pulse pressure from an increased systemic BP
- Reflex bradycardia
- An abnormal respiratory pattern
Norcuron is a long-acting NMB paralytic medication that does not have hemodynamic effects; therefore it does not confuse the picture with changes in VS. Dosage initially (0.1 mg/kg IV), subsequent dosages one half of previous dose due to its cumulative effect. Sedation and/or analgesia must always be utilized with paralytic agents. Versed and morphine are commonly utilized. Consideration of need for analgesia or sedation in hypertensive patients should precede initiation of anti-hypertensives such as Nipride or Lopressor.
Hypothermia
Temperature control systems in the hypothalamus continually receive input from the body. Thermoregulation is often impaired in altered consciousness states . . . generally causing hyperthermia. Efforts to maintain normal temperature in order to avoid increasing cerebral metabolism, which increases cerebral blood flow and volume, can be utilized after the stabilization period. Moderate therapeutic hypothermia is 34°C (93°F). It is currently used primarily to treat intractable intracranial pressure. Prevent shivering and monitor for cardiac dysrhythmias. Temperature is continuously monitored with an internal device connected to a cooling/warming blanket.
Anticonvulsant Therapy
Post-traumatic seizures will increase intracranial pressure and may potentiate secondary brain injury. The treatment for seizures in this scenario is Dilantin or Cerebyx as necessary. Patients with severe traumatic brain injury, penetrating injuries, major depressed fractures should be loaded intravenously with phenytoin if mg/kg body weight. Treatment should continue for 7 days and then be discontinued.
Controversial Therapies
Barbiturates and steroids. Both have fallen in and out of favor over the years as treatment for traumatic brain injury. Steroids completely failed to produce the desired result of decreasing intracranial pressure and cerebral swelling. Steroids are contraindicated in traumatic brain injury but may be considered with metastatic disease as the cause. Barbiturates may be prescribed for patients with increased intracranial pressure refractory to more conservative management. Appropriate monitoring considerations and neurological consult are highly recommended.
Investigational Interventions
Pharmacological agents are currently being evaluated for patients with severe brain injury. Although not widely utilized and definitely not administered in the stabilization phase, one should be aware of their presence and anticipate future implications for treatment of brain injury. Oxygen free radical scavengers, membrane stabilizers, calcium channel blockers, and glutamate antagonists are several examples.
Reference
Mortimer DS, Jancik J. Administering hypertonic saline to patients with severe traumatic brain injury. J Neurosci Nurs. 2006;38:142-146.