What are the goals of secondary brain injury prevention?

Goals of Secondary Brain Injury Prevention

The primary goals of secondary brain injury prevention are to control intracranial pressure (ICP), maintain adequate cerebral perfusion pressure (CPP), and promptly correct systemic insults including hypoxia, hypotension, and hypercapnia to prevent further neurological damage and improve survival. 1

Core Physiological Targets

Intracranial Pressure Management

• Maintain ICP below 20 mmHg as the fundamental threshold to prevent herniation and secondary ischemic injury 1
• ICP monitoring is essential after severe traumatic brain injury, particularly following decompressive craniectomy where postoperative increases may occur due to secondary bleeding, new collections, or increased brain edema 1
• Elevated ICP contributes to secondary injury through multiple mechanisms including ischemia, edema, herniation, and altered cerebral metabolism 1

Cerebral Perfusion Pressure Optimization

• Target CPP between 60-70 mmHg in adults when multimodal monitoring is unavailable 1
• CPP below 60 mmHg is associated with poor neurological outcomes, while CPP above 70 mmHg increases the risk of respiratory distress syndrome without improving outcomes 1
• CPP exceeding 90 mmHg worsens neurological outcomes due to aggravation of vasogenic cerebral edema 1
• The optimal CPP strategy depends on cerebral autoregulation status: patients with impaired autoregulation benefit from ICP-focused management (lower CPP around 60 mmHg), while those with preserved autoregulation benefit from CPP-focused management (higher CPP around 70 mmHg) 1

Prevention of Systemic Insults

Hypotension Prevention:

• Maintain systolic blood pressure >110 mmHg to prevent secondary cerebral insults and preserve cerebral blood flow 2, 3
• Maintain mean arterial pressure (MAP) >90 mmHg, especially in the first period after injury 4, 5
• The combination of hypotension (MAP <45 mmHg) and hypoxemia carries approximately 75% mortality 2, 3

Oxygenation Management:

• Prevent and promptly correct hypoxemia (SaO₂ <90%) as it significantly worsens neurological outcomes 2, 3
• Target PaO₂ ≥13 kPa (approximately 98 mmHg) to prevent hypoxic secondary injury 2
• Even brief periods of hypoxia can exacerbate secondary brain injury and should be avoided 2
• The brain is extremely sensitive to oxygen deprivation, with SaO₂ below 80% causing altered consciousness even in healthy individuals 2

Ventilation Control:

• Target PaCO₂ of 4.5-5.0 kPa (approximately 34-38 mmHg) to maintain normocapnia 2
• Avoid prolonged hypocapnia as it is not recommended for routine treatment of intracranial hypertension 1
• Hyperventilation (PaCO₂ not less than 4 kPa or 30 mmHg) should only be used short-term when there is evidence of raised ICP with impending herniation 2
• Prolonged severe hypocapnia (25 ± 2 mmHg for 5 days) does not improve outcomes and may worsen cerebral ischemia through excessive vasoconstriction 1

Osmotherapy for Acute ICP Crisis

Use mannitol 20% or hypertonic saline at a dose of 250 mOsm, infused over 15-20 minutes, to treat threatened intracranial hypertension or signs of brain herniation after controlling secondary brain insults. 1

• Osmotherapy produces maximum ICP reduction after 10-15 minutes with effects lasting 2-4 hours 1
• At equiosmotic doses, mannitol and hypertonic saline have comparable efficacy 1
• Mannitol induces osmotic diuresis requiring volume compensation, while hypertonic saline causes hypernatremia and hyperchloremia 1
• Prophylactic administration of hypertonic saline in patients without evidence of intracranial hypertension is not superior to crystalloids 1
• Monitor fluid, sodium, and chloride balances when using osmotic agents 1

Temperature Management

Control fever and consider targeted temperature control (TTC) to prevent secondary brain injury, though its role in improving long-term outcomes remains uncertain. 1

• Hyperthermia increases the risk of complications and is associated with unfavorable clinical outcomes including death 1
• TTC can modulate cerebral metabolism and ICP, but appropriate indications, targets, and duration in severe TBI are not yet definitively established 1
• Temperature control targets should be individualized based on perceived risk of secondary brain injury and fever etiology 1

Fluid Management

Use 0.9% saline as the crystalloid of choice as it is isotonic in terms of osmolality and prevents increases in brain water 2

• Avoid hypo-osmolar fluids such as 5% dextrose in water, which may worsen cerebral edema 1
• Mild fluid restriction is appropriate, but avoid hypovolemia as brain-injured patients do not tolerate it well 2

Positioning and Basic Measures

Position the patient with 20-30° head-up tilt to optimize cerebral perfusion while minimizing intracranial pressure 2

• Neutral head and neck position is recommended to prevent intracranial hypertension and facilitate venous drainage 1, 4, 5
• Factors that exacerbate raised ICP including hypoxia, hypercarbia, and hyperthermia should be treated promptly 1

Metabolic Control

Maintain normoglycemia as both hyperglycemia and hypoglycemia worsen cellular damage 4, 5

• Hyperglycemia with reduced ATP leads to ischemic acidosis 4, 5
• Hypoglycemia enhances decomposition of phospholipids and release of fatty acids, worsening cellular damage 4, 5

Monitoring Strategy

Implement multimodal monitoring beyond ICP/CPP when available to optimize cerebral blood flow, oxygen delivery, and substrate supply 6

• Standard ICP/CPP monitoring may be insufficient to prevent all secondary injury 6
• Consider brain tissue oxygen (PbtO₂), cerebral microdialysis, and transcranial Doppler to detect subtle secondary insults 6, 7
• Continuous CNS monitoring helps detect secondary cerebral insults early and provides online feedback for therapeutic interventions 7

Critical Pitfalls to Avoid

• Avoid early prognostication as it can lead to self-fulfilling prophecy bias where negative test results influence premature withdrawal of care 2, 8
• Never allow even brief periods of hypoxia or hypotension as these dramatically worsen outcomes, particularly when combined 2, 3
• Do not use prolonged hyperventilation as routine ICP management, as it may worsen cerebral ischemia 1
• Avoid CPP targets above 70 mmHg in routine care due to increased risk of respiratory complications without neurological benefit 1
• Do not rely on single monitoring parameters; secondary insults may be subtle and remain undetected by usual systemic monitoring alone 7

Evidence of Effectiveness

Implementation of protocols focused on detection and correction of secondary insults like hypoxia and hypotension is associated with improved outcomes for brain-injured patients 2

Secondary injuries were documented in approximately 90% of patients who died after traumatic brain injury, but unlike primary injuries, these are potentially preventable with adequate therapy 4, 5

With organized trauma centers and adequate intensive care focused on preventing secondary injury, mortality from traumatic brain injury has decreased from 50% in 1970 to approximately 30% currently 4, 5