Head Injury Principles of Management

Head Injury Principles of Management

Head Injury

Head injury is defined as any trauma to the head other than superficial injuries to the face. Any trauma victim with altered consciousness must be considered to have a brain injury. The primary injury is due to irreversible mechanical injury, but secondary injury which leads to cerebral ischemia, results from raised intracranial pressure (The pressure within the rigid skull), hypotension, hypoxia, anemia, seizures, hypoglycemia and hyperthermia. Prevention and correct management of these complications improves outcome from head injury.

Principles of Management

The main aim of assessment and management of head-injured patients is to maintain adequate cerebral blood flow (is the flow of blood through the brain, important for delivery of oxygen and removal of "waste" products) and to avoid cerebral ischemia and hypoxia. In patients with head injury the normal autoregulation of cerebral blood flow (CBF) is lost and CBF becomes proportional to cerebral perfusion pressure (CPP, is the difference between mean arterial pressure and intracranial pressure), which in turn is directly determined by both the mean arterial pressure (MAP) and the intracranial pressure (ICP): CPP = MAP - ICP

Autoregulation

Autoregulation is a protective mechanism that maintains a constant CBF in the presence of a changing CPP and reflects the ability of cerebral arterioles to constrict or relax in response to changes in perfusion pressure. This response normally requires 1 to 3 minutes to develop, so a rapid increase or decrease in MAP causes a brief period of cerebral hyperperfusion or hypoperfusion, respectively. Autoregulation maintains CBF relatively constant between a CPP of 50 and 150 mm Hg in normotensive, healthy individuals

The cranium is a rigid structure with a fixed capacity, which contains 80% brain, 10% blood and 10% CSF. These structures are all non-compressible; therefore an increase in the volume of any of these contents, unless coupled by a decrease in volume of another, results in an increase in ICP. The main mechanisms of maintaining CPP are to ensure adequate MAP (by the use of fluids and vasopressors) to prevent excessive rises in ICP. In normal individuals the ICP is 0 -10mmHg and this is largely determined by autoregulation of CBF (i.e. the amount of blood in the cranium). Vasoconstriction or vasodilatation of cerebral vessels occurs in response to changes in MAP, PaO2, and PaCO2. Although these responses may be obtunded in head injury, prevention of secondary brain injury involves manipulation of these variables. An increase in PaCO2 causes vasodilatation and an increase in CBF, which may increase ICP; a decrease in PaCO2 causes vasoconstriction leading to decreased CBF and ICP. Thus inappropriate hyperventilation may cause ischemia. A fall in PaO2 causes vasodilatation with a consequent rise in ICP.

Assessment and General Management of Head Injury

Initial Assessment: Patients presenting with significant head injury may have multiple injuries. The history of the mechanism of injury is useful in determining the potential extent of the head injury and is also an indication of the likelihood of other injuries. Brain injury may be worsened by airway or circulatory compromise; use the "ABCDE" approach to identify and treat life-threatening injuries early. Once the patient has a secure airway, is adequately oxygenated and has a stable cardiovascular system, where available consideration should be given to transfer or to a neurosurgical unit or better facility or hospital to manage patient.

Airway: The main concern is whether the patient is able to protect their airway and therefore whether intubation is necessary. Indications for intubation include:

  • GCS ≤ 8 (Table 6.1)
  • Risk of raised ICP (Table 6.2) due to agitation (i.e. sedation required)
  • Inability to control/protect the airway or loss of protective laryngeal reflexes
  • A fall of 2 or more points in the motor component of the GCS
  • In order to optimize oxygenation and ventilation
  • Seizures
  • Bleeding into mouth/airway
  • Bilateral fractured mandible

Breathing: Hypoxemia is associated with a significant increase in mortality. Targets for gas exchange should be a PaO2 100mmHg and a PaCO2 in the low-normal range -35-39mmHg. Prolonged hyperventilation is not recommended since cerebral vasoconstriction and ischemia may result, however short bursts of hyperventilation (a few minutes) may help to control episodes of high ICP.

Table 6.1 Glasgow coma score

The basic level of consciousness is rapidly noted in the primary survey, while a more complete neurologic examination is performed as part of the secondary survey to assess the presence of traumatic, brain, spine, or spinal cord injuries. A critical part of this evaluation is calculation of a patient's Glasgow Coma Score (GCS): Mild GCS = 13-15 Moderate GCS 9-12 and severe head injury=GCS ≤8

Circulation: The loss of the autoregulation of CBF can result in a reduction in oxygen delivery.

Maintenance of the MAP and CPP is essential; resuscitation and treatment of life threatening circulatory instability should take precedence over neurosurgical interventions. This may require surgery for hemorrhage control.

Use fluids, and where necessary vasopressors, to achieve a MAP greater than 80- 90mmHg. This figure is recommended as a guide until ICP monitoring is established, and assumes that the ICP is 20mmHg and therefore ensures a CPP of at least 60-70mmHg (since CPP = MAP - ICP). Once ICP monitoring is established then treatment is targeted at maintaining CPP 60-70mmHg.

A urinary catheter allows monitoring of urine output and fluid balance and is necessary if mannitol or other diuretics are used.

Table 6.2 Signs of Increased ICP and Management

Signs Suggestive of Increased ICP
  • Headache
  • Dizziness
  • Loss of consciousness
  • Confusion
  • Hypertension and bradycardia
  • Nausea
  • Vomiting
  • Focal weakness or paresthesia
  • Other focal neurological signs
  • Change or asymmetry pupils
Measure to Reduce ICP
  • Elevation of the head of the bed to 30º
  • Good neck alignment - head in the neutral position
  • Administer mannitol 0.5-1g/kg or furosemide 0.5-1mg/kg
  • Avoid hyperthermia, but do not actively induce hypothermia.
  • Thiopentone infusion can be used to reduce the cerebral metabolic rate to a basal level.
  • Hyperventilation can be used to reduce the PaCO2 as a temporary measure
  • If ICP remains raised is to perform a decompressive craniotomy.

Last modified: Sunday, 20 November 2016, 10:54 AM