The incidence of head injury in the world is declining due to developments in highway engineering, automobile innovations and creation of awareness among the public. But the Indian situation is different. Illiteracy, inadequate or dilapidated roads, huge population and insufficient facilities, lead to increase in head trauma cases and death rate is much higher.
In India, every one minute one accident takes place and in every eight and half minutes one accidental death. Our patient reaches the hospital almost four hours late. On the spot treatment is not available and transportation is inadequate and ill equipped.
The survival chances are better than before, due to advancement of newer diagnostic tools, advance management and well equipped ICU – which mitigate the bad effects of head injury, if patients reach on time.
Mechanisms of injury
The complex clinical injury pattern observed with head trauma can be attributed primarily to two phenomena: contact and inertial forces. These two phenomena cause damage to the brain and skull by causing deformation, strain of the bony or soft tissue that can result in either a functional or structural derangement.
1) Linear fracture
A linear fracture is caused by a hard impacting object, with most of the energy from the object used to deform the skull locally. Little energy is used to move or accelerate the skull.
2) Depressed fracture
Depressed fracture is caused by small, hard impactors that create concentration of stresses and strains immediately beneath the impact point. If the force is substantial, all bone under the impact is damaged and skull perforation occurs.
3) Basilar fracture
It is either due to direct impact or the propagations of stress waves through the skull as a result of the remote impact. Basilar fractures may occur as a consequence of impact to facial bones as well. The thin basilar skull is susceptible to remote contact effects.
Focal brain injury
1) Epidural haematoma
It is a more complex form of linear fracture. Due to bleeding from fracture site or during the fracture, underlying dural vessels get torn and bleeding leads to hematoma formation. Sometimes, even without fracture, local skull bending caused by impact is sufficient to tear vessels.
2) Coup contusions
Under the impact point, coup contusion arises principally from the local skull bending or fracture caused by impact. This in turn, subjects the underlying cortical and pial vascular network to strain, that, if excessive, causes bleeding at or near the brain surface. Damage is likely to occur when the skull is rebounding from the impact and the vessels are experiencing tensile strain.
3) Contrecoup contusions
Cavitation and initial loading are the two phenomena that lead to contrecoup contusion. The most important is the translational or angular head motion, where brain moves toward the impact site and creates an area of negative pressure opposite to the point of loading. The negative pressure may in turn cause damage by exceeding the tensile strength of water, which is the primary fluid component of the brain. Cavitation has little support.
4) Intermediate coup contusions
This is nothing but vascular disruption of brain surfaces that are not adjacent to the skull. It is due to impact generated stress waves, like intermediate contusion of the cingulated gyrus can be due to interactions with the falx as well inferomedial temporal lobe.
5) Intracerebral haematoma
Large traumatic haematoma is uncommon and most of the time is associated with cortical contusions. Single hematoma without contusion is due to acceleration induced tissue strains deep within the brain.
6) Tissue tear haemorrhage
They are multiple areas of intracerebral damage to blood vessels and axons occurring in association with diffuse axonal injury. They are a part of diffuse axonal injury that results in prolonged coma.
7) Subdural haematoma
This is tearing of the parasagittal bridging veins located along the superior margin of the brain. It results entirely from inertial force and not from contact.
Diffuse brain injury
Cerebral concussion is produced by inertial forces. Angular and rotational motions of head cause the classic widespread disruption of brain function that occurs in concussion. In this type of injury, most o the strain is insufficient to cause structural damage.
2) Diffuse axonal injury
Axonal damages are the main cause of prolonged traumatic coma, considering more severe type of cerebral concussion and no caused by contact but due to angular and rotational acceleration of head. The damage occurs in white matter axon connecting t two hemispheres in high-speed vehicular injury. The lesion occurs in four places corpus callosum, basal ganglia, cervico-medullar junction, and brain stem.
1) Skull X–rays
X-rays are almost obsolete in diagnosing a case of head trauma. The standard views are AP, Lat, and Towne’s. In X-rays one can see the depressed fracture, linear fracture or pneumocephalus only.
2) CT scan brain
Since, the advent of CT Scan, this is the primary diagnostic tool in a case of head trauma, rather a gold standard. CT Scan is mandatory in a case of unconsciousness for 10 minutes, confused or altered sensorium, compound depressed fracture, pupillar asymmetry, focal neurological deficit or bleeding from orifices.
By scan one can diagnose parenchymal lesion, extraparenchymal lesion or extracranial lesion. Fracture of skull as well secondary effect of brain injury like cerebral oedema, ischemia, infarcts, midline shift and hydrocephalus can also be diagnosed by CT scans.
Follow up scan can say the sequelae of head injuries like communicating hydrocephalus, cerebral atrophy, encephalocele and porencephaly. But the diffuse axonal injury lesions are not well demonstrated by CT scans. With CT one can see only swelling or focal hemorrhages.
3) MRI scan
MRI is good for diffuse axonal injury, as it shows hyperintense lesion on T2 weighted images at white-grey interface or deep in the white matter, corpus callosum and the brain stem. MRI again is a better investigating tool, if there are non-hemorrhagic lesions.
The other investigations like angiography, pneumoencephalogram, radionuclide scanning are almost obsolete in diagnosing head injury cases.
The concept of primary and secondary brain damage had changed the treatment of severe head injury. Primary head injury can be prevented but cannot be cured. Improvement in management like prompt resuscitation, transport, treatment of associate injuries, and rapid cranial imaging and surgery or drug therapy for ischemia may prevent secondary injury and affect the final outcome.
The pathophysiologic sequences of secondary injury are potentially treatable or preventable. Following severe traumatic brain injury, those cells that were not mechanically damaged are likely to become deranged due to cellular ionic and metabolic alterations. Early development of cerebral ischemia, within the first few hours of injury, is the common pathway for the secondary injury and subsequent neuronal degeneration.
The mechanisms involved in ischemic brain damage are primarily those related to calcium overload, excessive acidosis and increased production of free radicals. There are variable levels of perfusion; the complete ischemic areas will undergo a brief period of anaerobic glycolysis resulting in lactic acid production. Area of incomplete ischemia also undergoes anaerobic metabolism due to inadequate oxygen supply.
In spite of pharmacological advancement, hypothermia is one of the mode for preventing secondary brain damage. A moderate hypothermia of surface cooling up to 32-33o C limits secondary brain damage by reducing cerebral metabolism, stabilizing cell membranes and suppressing high levels of excitatory amino acids. Hypothermia can be done either by cooling blankets or gastri lavage by cold water.
Management before reaching the hospital
On site management: The airway should be kept free. Shock should be treated with intravenous fluid, and any bleeding should be stopped with pressure bandages. The head should be elevated by thirty degrees to enhance venous drainage and this in turn reduces the ICP.
In the ambulance: The patient should be transported gently like a log on the stretcher, unless and until spinal injury is ruled out. For unconscious patients, lateral position is best to avoid asphyxiation caused by the tongue. Oxygen should be administered. Blood pressure should be recorded, intra-venous fluid should be given started and (if a trained medical personnel is available) vasopressure medicine can be started for maintaining the blood pressure. If the ambulance has ventilation facilities, intubation and ventilation should commence if there is a respiratory problem.
Management on reaching the hospital
As soon as the patient reaches the in emergency room, the first priority is the complete restoration of pathophysiology.
This constitutes checking the airway and respiratory problems, immobilisation of the cervical spine, checking the circulation and examining for haemorrhages and other neurological tests including the Glasgow coma scale.
• Systemic examination of the whole body should be carried out by the emergency room medical officers.
• C T scan examination with other radiological examinations especially trauma series should be conducted.
• Monitoring for vital signs including CVP should be done routinely and SOS for arterial pressure.
• Comprehensive management required.
• Diffuse axonal injury should be treated accordingly.
• Intracranial hemorrhages or depressed fractures need surgery and should be performed accordingly.
• Any other hemorrhages like haemothorax or haemoperitoneium should be treated at the earliest.
• If the patient’s condition deteriorates, it needs further imaging and should be treated accordingly.
Criteria for admission of head injury in the hospital
• Decreased level of consciousness
• Neurological signs and symptoms including headache and vomiting
• Difficulty in assessment after alcohol or post ictal stage
• Skull fracture or CT scan findings like contusions or other findings
• Elderly patient and children below the age of twelve years must be kept under observation
• Other medical conditions like diabetes, high BP or blood coagulation disorder or on medicine
Preventive measures can reduce the incidence of serious accidents, like rigorous enforcement of speed restriction, automatic camera recording, enforcing helmets for two-wheeler riders, seat belts for car passengers and urban ‘traffic calming’ by speed breakers. The ‘No drinking and driving campaigns’ and surprise breath test conducted by the police have helped in reducing the number of road accidents.