Dr. Amitava Ray

MODERATE TO SEVERE HEAD INJURY

Table of Contents

The Glasgow Coma Score

The Glasgow Coma Score was initially developed by Jennett and Teasdale in Glasgow to standardise the assessment of head injuries. They realised that the system would have to be easy to administer without any special training, reproducible and accurately convey the seriousness of the injury. Published in 1974, it was soon adopted in clinical practice. It has remained unchanged except the motor response, where ‘flexion’ has been replaced by flexion (or abnormal flexion) and withdrawal (or normal flexion) increasing the total score from 14 to 15, with 3 being the lowest score. It is based on the best response of the eyes, speech and motor system to speech or pain. There are a few instances that Glasgow Coma Score may not accurately predict the severity of injury, but on the whole it is the best bedside predictor of head injury outcome and is still used extensively in the management of head injured patients.

Eye Response

Motor Response

Verbal Response

Head Injury Grading

Head injuries are graded according to the Glasgow Coma Score – a score of

  • 13 – 15 is mild
  • 9 – 12 is moderate and
  • less than 8 – 3 is severe.
  • The lowest score on the scale is 3.

Head Injury - Early Management

As soon as a patient is wheeled into the emergency room, the trauma team will attend to them. The trauma team is usually a multi-disciplinary group of anaesthetists, surgeons, orthopaedic surgeons, neurosurgeons, trauma nurses and trauma technicians who perform specific pre-rehearsed roles to optimise outcome. They will initially assess the extent of injury after securing the airway (breathing pipe) making sure that the lungs are being adequately ventilated. The neck (cervical spine) is almost immediately placed in a collar to prevent any further injury. If the airway is compromised, a tube may be inserted into the trachea (windpipe) to ensure adequate air entry into the lungs. The patient may also be placed under a drug induced coma. The blood pressure, pulse, respiratory rate are checked along with the GCS and pupillary reaction to light (a non-reacting large pupil is a sign of severe injury and needs an emergency neurosurgical consultation). Routine blood tests are performed. Blood is arranged for transfusion, if required. Sometimes, if bleeding into the abdomen is suspected a diagnostic peritoneal lavage may be performed (a small cut is made in the abdomen and then washed out with saline to see if there is any blood).

CT Scan In Head Injury Management

The CT scan is vital in the diagnosis of the type injury- intracranial haemorrhage, skull fracture, or contusions of the brain parenchyma. The scan even provides an indirect measure of the pressure inside the cranium. Following trauma, haemorrhage can occur in one or several compartments of the brain- in the layers of the scalp outside the bony cranium, between the dura and the skull or extradural haemorrhage, between dura and the brain or subdural haemorrhage, within the brain parenchyma or intracerebral haemorrhage or even within the CSF filled ventricles in the middle of the brain or intraventricular haemorrhage. At times, as a result of high velocity accidents, there are multiple, punctate haemorrhages in the substance of the brain commonly known as diffuse axonal injury (DAI). There is now an established link with long term neurodegenerative disease and DAI. 

The decision to operate or to manage the patient without surgery is almost exclusively dependent on the findings of the scan. As the cranium is considered to be a closed box, any increase in volume of one of the components will result in an increase in intracranial pressure which can ultimately prove fatal. Clinically, this manifests with a headache, vomiting and drowsiness- drowsiness progressing to coma as the pressure increases. On the scan, there are several indicators that point to an increase in intracranial pressure- the most commonly used being ‘shift’- or the displacement of the midline structures on the brain caused by an expanding lesion. Usually, a threshold of 1 cm is used as an approximate guide to decide when to intervene surgically.

Skull Fracture

A blow to the head can result in a fracture of the skull. Depending on the type of blow, skull fractures can be closed (covered by skin) or compound (the overlying skin is cut or lacerated, exposing the fracture to the air). Compound fractures pose an increased risk of infection and l CSF (cerebrospinal fluid) leak. A leak of CSF may also occur at the base of the brain in basal skull fractures. Here, the fluid leaks into the back of the mouth and throat,or may come out through the nose or ear increasing the risk of infection from bacteria normally present in the mouth and nose. This increases the chances of meningitis. (this is different from the childhood meningitis for which a vaccine is available). Fractures may also be displaced – where the two edges of the bone are not in continuity- or commonly a depressed skull fracture. Here a fragment of bone is driven inward which in turn can tear the meninges (covering of the brain) or contuse the brain per se. This usually is part of a compound injury. Simple linear fractures- fractures that are not displaced and not compound usually heal on their own. In a very small percentage of patients however, the fracture may tear a major artery on the surface of the dura (the outer layer of the meninges that cover the brain) leading to extradural haemorrhage (see below).

What Happens With The Patient In ICU?

The management of the patient in ICU revolves around minimizing secondary brain damage caused by hypoxia (lack of oxygen), hypotension (low blood pressure causing decreased perfusion of tissues), prevention of fits / seizures and ensuring adequate nutrition for the head injured patient.

This is accomplished in the following ways

  1. Intubation and ventilation: In the severely head injured patient, the tongue tends to fall backwards and block the airway. The safest way to ensure that the breathing tube remains patent at all times is to insert an endo-tracheal tube into the trachea  or breathing pipe through the mouth or nose. Patients are usually given  sedation to prevent the gag-reflex from being triggered. Hypoxia, or the lack of oxygen has a profound deleterious effect on the outcome in head injury, which makes airway management an essential part of the treatment
  2. Fluids and ionotropes: Fluids are often administered to make sure the daily requirement is met, but also to replace the loss of blood that may have taken place. Blood loss that causes a drop in blood pressure is not a sign of head injury per se but is seen often enough because of other injuries that are present- ie chest or abdomen being the most common. In spite of fluid replacement the use of ionotropes like dopamine and adrenaline (epinephrine) may be required at times to make sure that the blood pressure is high enough to ensure adequate perfusion. Inadequate perfusion will cause tissue hypoxia that will further aggravate the damage. 
  3. Drugs to reduce swelling: Intravenous mannitol and 3% normal saline are used to control rising intracranial pressure. By increasing the osmolarity of the blood, it is presumed that the tissue oedema (brain swelling) will be reduced by osmosis. While this may be true for the initially, caution needs to be exercised while administering hypertonic fluids after the first 48-72 hours as there is a distinct possibility that the salts will leak out of the damaged vessels and accumulate in the injured area of the brain, and increase swelling. 

Barbiturate induced coma is neuroprotective and can be used with EEG (electroencephalography) monitoring to decrease the ICP and improve outcome. 

  1. Anticonvulsants. Seizures on impact are a common symptom in head injury and will probably affect 1 in 10 individuals. Some of these will continue in the immediate post injury phase. A percentage of these seizures will be silent and will be picked up only on EEG. As seizures in the early post injury phase are associated with a poorer outcome, anti-seizure medication in the form of Phenytoin and Carbamazepine have been traditionally prescribed. Nowadays, newer anticonvulsants like Levetirecetam or Lacosamide have been used.   However, the early use of anticonvulsants do not decrease the incidence of delayed seizures and so should be stopped soon after discharge from hospital. The incidence of delayed seizures is directly related to the severity of injury with the incidence ratio (incidence in post head injured patients/ normal controls) increasing from 1.5 in minor head injury to 17 in major head injury. Age more than 65 years, subdural hematoma, contusions of the brain, loss of consciousness or amnesia for more than a day increase the risk of delayed seizures. 
  2. Antibiotics: prophylactic antibiotics may be used to cover infection from contaminated wounds or other injuries (like penetrating injuries to the bowel) but have shown to have no role in the prevention of infection in base of skull fractures with a leak of CSF. In fact, some studies have shown the administration of prophylactic antibiotics encourages growth of antibiotic resistant organisms that increase the morbidity and mortality of meningitis.
  3. Steroid: Steroids used to be routinely used in the management of head injury, However, the CRASH trial (Corticosteroid Randomisation After Significant Head Injury) has shown death from all causes and severe disability is more likely in patients who have had methylprednisolone (steroid)  and is now contraindicated.

Neurosurgical Interventions In The Head Injured Patient

Depending on the nature of injury, there are several neurosurgical interventions that may take place.

  1. Insertion of a pressure monitor: If there is a significant amount of brain injury, swelling of the brain 24-72 hours after the injury may become a serious problem. The swelling results in the rise of pressure inside the cranium, which can be accurately measured by a pressure monitor. Pressure monitors can be fiber-optic, pneumatic, strain gauge, micro-transducing or a CSF drainage device connected to an external drainage system. They may be placed via a hole in the skull (usually with a twist drill) in the subdural or subarachnoid spaces, or in the brain parenchyma or the ventricles and serve a similar purpose. The ventricular monitors are probably the most difficult to place, but most accurate.  
  2. Burr holes: Burr holes are not commonly done on acute head trauma as a definitive procedure. However, in the elderly, where there is an increased gap between the skull vault and the brain (due to age related atrophy of the brain) minor slip and falls or bumps to the head can cause a leak of venous blood into the subdural space. This happens gradually, often over weeks and months, with acute (white on a CT scan) liquefying to the gray color of the brain on the scan, or sometimes darker- or a chronic subdural hematoma.  Burr holes are curative in most of these cases. 
  3. Craniotomy: A craniotomy is an opening in the skull through which access to the brain is obtained. It is usually performed using power tools- like a craniotome that produces a smooth cut of bone that can be replaced after surgery. In trauma, a craniotomy helps the surgeon evacuate the blood clot and also stop the source of bleeding. 
  4. Craniectomy: Sometimes, surgery is performed to decrease the pressure inside the skull, in the absence of an operable blood clot or a blood clot that is not significant when compared to the degree of shift. This is usually the case when medical measures fail to decrease the rising intracranial pressure. In this case a large portion of the skull (more than 11 cm in length) is opened along with the underlying dura mater. The swollen brain herniates out through this large deficit, thus decreasing the pressure inside the skull. Clinical trials have now shown that this operation does improve outcome in trauma.

Predictors Of Outcome In Head Injury

Head injury can cause death or lifelong impairment in cognitive and social functioning. Factors that are shown to correlate with poor outcomes include a poor GCS after resuscitation, pupillary asymmetry, traumatic subdural or subarachnoid hemorrhage, hypoxia or hypotension at presentation in ER and the inability to control intracranial pressure in spite of optimal medical therapy. Data from the Traumatic Coma Data Bank found people with an initial GCS of 3 had a 78% mortality. The overall prognosis for patients with severe head injury (GCS 3-8) were: good recovery 27%, moderate disability 16%, severe disability 16%, vegetative 5% and mortality 36%. The long term side effects seen in all head injured patients include headache, loss of concentration, memory loss, imbalance and difficulty in walking and in severe cases of repeated head injury Parkinson’s Disease, dementia  and other neurodegenerative conditions  are not exclusive to the moderate and severely head injured group.

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