19/02/2026
SECONDARY BRAIN INJURY IN RTA
Secondary brain injury results from disturbance of brain and systemic physiology by the traumatic event. It is defined as subsequent or progressive brain damage arising from events developing as a result of the primary brain injury. Hypotension and hypoxia are the two most acute and easily treatable mechanisms of secondary injury. Secondary injury can occur minutes, hours, days or even weeks after the initial injury and the damage can be averted or lessened by appropriate clinical management.
Pathophysiology:
• An acute CNS insult can trigger any of the following resulting in secondary brain injury
• Disruption of physiological(homeostatic) measures:
o Blood brain barrier disruption, cerebral vasodailation, neuronal depolarization and release of excitatory neurotransmitters……..> cerebral edema…increase ICP
o Mitochondrial dysfunction…..> impaired cerebral metabolism….> neuronal cell death
o Stress induced hyperglycemia….> endothelial dysfunction of cerebral blood vessels…..> cerebral vasoconstriction or vasodilation……> cerebral hypoxia or cerebral hyperaemia
o Loss of cerebral autoregulation of cerebral blood flow causes increase risk of brain injury secondary to critical care measure
o Injury to hypothalamus and/or pituitary ………> neurogenic fever and central diabetes insipidus
o Initiation of reparative responses: activation of inflammatory cascade…….> hyperthermia and hyperglycemia
Types of secondary brain injury:
• Intra cranial hematomas
• Cerebral edema
• Ischemia
• Infection
• Epilepsy/seizures
• Metabolic/endocrine disturbances.
Causes of secondary brain injury:
• Haematoma
• Contusion
• Diffuse brain swelling
• Systemic shock
• Intracranial infection
• Secondary injury can result from complications of the injury. These include
o Ischemia
o Cerebral hypoxia
o Hypotension
o Cerebral edema
o Changes in the blood flow to the brain
o Raised intracranial pressure (the pressure within the skull). If intracranial pressure gets too high, it can lead to deadly brain herniation, in which parts of the brain are squeezed past structures in the skull.
• Other secondary injury include :
o Hypercapnia
o Acidosis
o Meningitis
o Brain abscess
• Alterations in the release of neurotransmitters can cause secondary injury. Imbalances in some neurotransmitters can lead to excitotoxicity, damage to brain cells that results from overactivation of biochemical receptors for excitatory neurotransmitters (those that increase the likelihood that a neuron will fire).
• Another factor in secondary injury is loss of cerebral autoregulation, the ability of the brain's blood vessels to regulate cerebral blood flow.
• Other factors in secondary damage are breakdown of the blood–brain barrier, edema, ischemia and hypoxia.
• Ischemia is one of the leading causes of secondary brain damage after head trauma.
Signs of secondary brain injury:
• Severe, frequent headaches
• Vision problems or loss of visual stability
• Memory loss or difficulty with short-term memory
• Insomnia or hypersomnia
• Dizziness or fainting
• Moodiness, acute depression, or personality changes
• Changes in eating habits
• Sudden seizures or convulsions
• Sensory deficits (loss of smell and hearing)
• Hypersensitivity to light and/or noise
• Slurred speech, inability to communicate, inability to understand what others are saying
Measures to prevent secondary brain injury:
• Oxygenation and ventilation: Oxygenation and ventilation Avoid hypoxia, hyperoxia, hypocapnia, and hypercapnia in patients with acute CNS insult.
• Control of PaO2 (oxygenation):
o Target: Normoxia or mild hyperoxia
Target PaO2: > 60 mm Hg
Target oxygen saturation (SpO2): > 92-94%
o Measures to achieve target oxygenation:
Avoid hypotension
Oxygen therapy
- Administer supplemental oxygen only if SpO2 is < 92%
- Use the lowest FiO2 possible to maintain normoxia
Airway management: if necessary, intubate (rapid sequence intubation) according to local hospital protocols
- Carefully consider intubation induction agents: Ketamine 2 usually preferred if no signs of ICP
- See improving oxygenation in mechanically ventilated patients for further details.
o Hypoxia and hyperoxie can worsen neurological outcome and should be avoided. Routine use of supplemental oxygen in nonhypoxic patients is of no clinical benefit in the prevention of secondary brain injury.
• Control of PaCO2 (ventilation):
o Target PaCO2:35-45 mmHg (normocapnia)
o Measures to achieve target ventilation:
No signs of increased ICP: Prophylactic hyperventilation is not recommended
Signs of increased ICP or signs of cerebral herniation syndromes present: Consider short-term hyperventilation to attain mild hypocapnia (PaCO2 between 30-35 mm Hg).
- Ventilation strategy for elevated ICP for suggested initial ventilator settings.
- ICP management
o Hypercapnia (including permissive hypercapnia) and long-term hypocapnia worsen neurological outcome in patients with acute CNS insults and should be avoided. Hypocapnia should only be used as a temporizing measure for patients with signs of cerebral herniation syndromes while simultaneously initiating definitive management fort ICP.
• Blood pressure and cerebral perfusion pressure:
o Blood pressure control after acute CNS insult is complex and the optimal treatment goals are yet to be established. The main aim is to maintain cerebral perfusion pressure (CPP) between 60-70 mm Hg by maintaining mean arterial pressure (MAP) between 65-100 mm Hg.
o Avoid hypovolemia and hypervolemia when resuscitating a patient with an acute CNS insult. Hypovolemia decreases cerebral perfusion, worsens cerebral ischemia, and may potentiate thiromboses in the injured tissue. Hypervolemia worsens cerebral edema.
o Hypotensive patients:
Hypotension should be avoided in all patients with depressed consciousness as it decreases CBF, thus worsening neurological outcomes and increasing the mortality risk
Target: SBP> 90 mm Hg or mean arterial pressure (MAP) > 80 mm Hg
Treatment:
- IV fluid resuscitation: isotonic saline typically preferred
- Vasopressor therapy (see vasopressors): phenylephrine e preferred in patients with TBI and vasodilatory shock
- Identify and treat the underlying cause.
o Hypertensive patients:
The SBP threshold at which to administer antihypertensives and target SBP differ according to the etiology of the acute CNS insult.
Ischemic stroke
Intracranial hemorrhage (including TBI):
- Target SBP: 140-180 mm Hg
- Timing: Initiate treatment as soon as possible in patients with SBP > 180 mm Hg
- Commonly used antihypertensive agents: Nicardipine, Labetalol, Sodium nitroprusside
• Blood sugar:
o Blood glucose should be checked at presentation and serially monitored. Strict blood glucose control is recommended as hypoglycemia or hyperglycemia worsen the neurological outcome after an acute CNS insult
o Target blood sugar: normoglycemia
In nontraumatic acute CNS insult: 140-180 mg/dL
In traumatic brain injury: 80-180 mg/dL (21123)
o Treatment:
Hypoglycemic patients (blood glucose < 60 mg/dL):
Hyperglycemic patients (blood glucose > 180 mg/dL):
Avoid dextrose-containing solutions in the resuscitation of nonhypoglycemic patients with an acute CNS insult.
• Seizure prophylaxis and treatment:
o Seizure prophylaxis: Prophylactic administration of anticonvulsants is not routinely recommended. Seizure prophylaxis for the first 7 days after injury is recommended in patients with severe traumatic brain injury: Consider seizure prophylaxis in patients with ICH or SAH at high risk for seizures.
o Seizure treatment: Seizures detected clinically or on EEG should be managed with anticonvulsants.
o Suggested anticonvulsants:
Levetiracetam
Phenytoin
o Because seizures may be clinically inapparent in comatose patients or those on neuromuscular blockers. continuous EEG monitoring is recommended in this group of patients.
• Electrolyte abnormalities:
o Sodium disorders and hypokalemia are the most common electrolyte abnormalities seen after an acute CNS insult.
Disorders of sodium balance
o General considerations:
Identify and treat the underlying cause.
Sodium disturbances are often self-limiting in patients with brain injury.
o Hyponatremia:
Acutely symptomatic patients: prompt treatment with gradual correction (see Treatment in hyponatremia and SIADH)
Asymptomatic patients: Supportive treatment strategy is usually appropriate.
o Hypernatremia:
Severe elevation (> 160 mEq/L): gradual correction
Mild-moderate elevation (up to 160 mEq/L): consider gradual correction
Symptomatic hypernatrernia should be corrected gradually to minimize the risk of cerebral and pulmonary edema. Symptomatic hynonetreria should be corrected gradually to minimize the risk of central pontine myelinolysis :
o Disorders of potassium balance:
Hypokalemia
Hyperkalemia
• Neurogenic fever and targeted temperature management: Neurogenic fever:
o Noninfectious fever after an acute CNS insult is likely caused by injury to the hypothalamic thermoregulation centers. It is seen in up to 37% of patients with TBI; may also occur after stroke or neurosurgical intervention.
o Management: targeted temperature management. In patients with acute CNS insults, fever should be aggressively treated as it is associated with a poor neurological outcome and increased risk of mortality.
• Targeted temperature management (TTM):
o Controlled maintenance of a target body temperature aimed to prevent secondary brain injury after an acute CNS insult.
o Target body temperature: differs according to the inciting events
Indications for controlled normothermia (36-37.8°C/96,8-100°F)
- TBI
- Hemorrhagic stroke
- Ischemicstroke
- Neurogenic fever
Indication for moderate therapeutic hypothermia (33°C/91.4°F): postcardiac hypoxic ischemic encephalopathy
o Measures to achieve TTM:
Physical/surface cooling: may be local (e.g., head cooling with a cooling helmet) or general (e.&-. with cooling blankets/pads)
Endovascular cooling leg., rapid IV infusion with cold normal saline)
Pharmacological hypothermia (for therapeutic hypothermia): hypothermia-inducing drugs (eg. cannabinoids, opioids)
Antipyretics (eg.. acetaminophenz)
• Other:
o Intracranial pressure (ICP) Set:
Target. Maintain ICP below 20-22 mm Hg
Treatment: ICP management.
Monitoring. ICP is not routinely monitored, but patients should be observed for signs of raised ICP.
o Patient positioning:
Patients without features of raised ICP or hypoxia: supine position with no elevation of the head. Patients with features of raised ICP or those at risk of aspiration or airway obstruction: head end elevation to 30°
o Transfusion:
Red cell transfusion: Transfuse packed red cells if Hb
