5.2 Traumatic Brain Injury (TBI) and Intracranial Pressure (ICP) Management

Traumatic Brain Injury (TBI) and Intracranial Pressure (ICP) Management

Pathophysiology of Brain Injury: Primary vs. Secondary

Managing traumatic brain injury (TBI) in transport medicine requires understanding the distinction between primary and secondary brain injury. Primary brain injury occurs at the moment of impact and represents the mechanical disruption of neural tissues, such as diffuse axonal injury, contusions, and subdural or epidural hematomas.

The primary goal of critical care transport is to mitigate secondary brain injury, which represents the physiological and biochemical cascades that occur hours after the trauma. It is driven by systemic insults that worsen cerebral ischemia. The Brain Trauma Foundation (BTF) highlights the 'H Bombs' of TBI as preventable causes of secondary injury:

• Hypoxia: A single episode of hypoxia (SpO2 < 90% or PaO2 < 60 mmHg) doubles TBI mortality.
• Hypotension: A single systolic blood pressure reading of < 90 mmHg (or < 100-110 mmHg based on age) doubles mortality.
• Hyperventilation: Routine hyperventilation causes vasoconstriction, reducing cerebral blood flow to ischemic levels.
• Hypoglycemia/Hyperglycemia: Hypoglycemia causes cellular energy failure, while hyperglycemia exacerbates cerebral lactic acidosis.

The Monroe-Kellie Doctrine and ICP Target Ranges

The Monroe-Kellie Doctrine describes intracranial dynamics. The skull is a rigid, non-compliant bony vault. Its internal volume is constant and comprises three components:

1. Brain Parenchyma: ~80% of volume.
2. Cerebral Blood Volume (CBV): ~10% of volume.
3. Cerebrospinal Fluid (CSF): ~10% of volume.

Because volume is fixed, an increase in any component must be offset by a decrease in the others. Compensatory mechanisms include displacing CSF into the spinal canal and shunting venous blood out of the skull via the jugular veins. Once these reservoirs are exhausted, even a minute volume increase leads to an exponential rise in Intracranial Pressure (ICP).

• Normal ICP: 5 to 15 mmHg.
• Pathological ICP: > 20 mmHg.
• Treatment Threshold: Guidelines recommend initiating ICP-lowering therapies when ICP exceeds 22 mmHg.

Cerebral Perfusion Pressure (CPP) Calculations and Targets

Cerebral Perfusion Pressure (CPP) is the net pressure gradient driving blood flow to the brain, calculated as: CPP = MAP - ICP (or CPP = MAP - CVP if CVP is higher than ICP). MAP is calculated as: MAP = DBP + 1/3(SBP - DBP).

• Target CPP: The optimal range is 60 to 70 mmHg.
• CPP < 50 mmHg: Results in critical cerebral ischemia, leading to tissue infarction.
• CPP > 70 mmHg: Should be avoided, as it can cause hyperperfusion, exacerbate cerebral edema, and increase the risk of acute respiratory distress syndrome (ARDS) due to systemic fluid loading.

Hyperosmolar Therapy: Mannitol vs. Hypertonic Saline

When a patient exhibits signs of elevated ICP, hyperosmolar therapy is indicated to draw water out of the swollen brain tissue.

Mannitol (20% solution)

Mannitol is an osmotic diuretic that acts via a rheological effect (decreases blood viscosity, causing reflex vasoconstriction and lowering ICP) and an osmotic effect (draws water from the brain parenchyma into the intravascular space for renal excretion).

• Dose: 0.25 to 1.0 g/kg IV bolus over 10-20 minutes.
• Administration: Must be run through a 0.22-micron in-line filter because mannitol can crystallize at room temperature.
• Contraindications: Hypotension (SBP < 90 mmHg) is a strict contraindication, as the osmotic diuresis will worsen hypovolemia and cause cardiovascular collapse. It is also contraindicated in renal failure.

Hypertonic Saline (HTS - 3% or 23.4%)

Hypertonic Saline draws water out of brain tissue without causing profound diuresis. It expands intravascular volume, increases MAP, improves cardiac output, and restores normal neuronal membrane potentials.

• Dose (3%): 250 to 500 mL IV bolus, or run as an infusion at 1 to 2 mL/kg/hr.
• Dose (23.4%): 30 mL slow IV bolus over 10 to 20 minutes (the 'hypertonic bullet') via a central line.
• Preference: HTS is the agent of choice in hemodynamically unstable or hypotensive patients, as it supports blood pressure while lowering ICP.

Carbon Dioxide Management and Ventilation Limits

Carbon dioxide (CO2) is a potent regulator of cerebral blood flow (CBF). Cerebral blood vessels are highly sensitive to changes in PaCO2:

• Hypercapnia (PaCO2 > 45 mmHg): Causes cerebral vasodilation, increasing CBV and elevating ICP.
• Hypocapnia (PaCO2 < 35 mmHg): Causes cerebral vasoconstriction, reducing CBV and lowering ICP. However, excessive vasoconstriction can reduce CBF to ischemic levels.

Ventilation Guidelines

• Routine Hyperventilation: Strictly contraindicated in TBI. The target PaCO2 is 35 to 45 mmHg (ETCO2 35-45 mmHg) to maintain normocapnia.
• Impending Herniation: Brief, mild hyperventilation is indicated only during active brain herniation (e.g., sudden unilateral pupillary dilation, Cushing's triad, or decerebrate posturing). The target PaCO2 is 30 to 35 mmHg (ETCO2 30-35 mmHg). Hyperventilation should be discontinued as soon as the acute crisis is resolved or hyperosmolar therapy takes effect.

Target Vital Signs and Systemic Resuscitation

To optimize perfusion, the transport clinician must adhere to strict physiological targets:

• Oxygenation: Maintain SpO2 >= 90% (ideally 94-98%) and PaO2 >= 60 mmHg.
• Systolic Blood Pressure (SBP): Maintain SBP >= 100 mmHg for patients aged 50-69 years, and >= 110 mmHg for patients aged 15-49 or >70 years.
• Mean Arterial Pressure (MAP): Maintain MAP >= 80 mmHg. If fluid resuscitation fails, vasopressors (typically Norepinephrine) should be initiated.
• Sedation and Analgesia: Adequate sedation (Propofol or Midazolam) and analgesia (Fentanyl) are critical to decrease cerebral metabolic demand (CMRO2) and prevent ICP spikes. Propofol is favored due to its short half-life, allowing for rapid neurological reassessment.