Head injury-          

              pathophysiology & medical management:

 

Dr. A. Vincent Thamburaj,   

Neurosurgeon, Apollo Hospitals,  Chennai , India.


Head injury remains a serious cause of mortality and morbidity. From the moment of the trauma, a cascade of events takes place and several different pathological events are set in motion. These events are poorly understood. However, these events interact and determine the final outcome. The patients' age and associated medical factors do play an important role.  

PATHOPHYSIOLOGY:

Axonal damage:

This occurs in various degrees in all head injuries due to movement of the brain within the cranium as seen in acceleration-deceleration injuries. Additionally, there are changes at the subcellular level.

Diffuse axonal injury is thought to be responsible for prolonged coma in patients without a mass lesion. In increasing severity the damage may be graded as follows:

grade 1- damage in the white matter of the hemispheres, 

          the corpus callosum, the brainstem, and the cerebellum.

grade 2-also a focal lesion  in the corpus callosum.

 

 

 

medial temp.lobe

  corpus callosum

       thalamus

       grade 2 axonal injury, hyperdense lesions-MRI T2 

grade 3- in addition a focal lesion in the dorsolateral part of the rostral brainstem.

The damage extend centripetally from the cortex to the brainstem as the injury force increases; the direction of the acceleration is also important. Sagittal acceleration only occasionally produces grade 1 damage. Coronal acceleration (lateral movement)  has a high incidence of diffuse axonal damage. Oblique acceleration causes intermediate type. A higher grade is related deeper and more prolonged coma as well as more severe residual neurological deficit.

At first there is progressive accumulation of organelles associated with axonal thickening and later large ball- or club- like swellings. Ultimately, they lose contact with the distal segment resulting in axonal disruption. Myelin sheath breaks down followed by phagocytic cell reaction. 

Histological post-mortem studies reveal axonal retraction balls in short (days) survivors, large numbers of microglial stars formed by reactive astrocytes in intermediate (weeks) survivors and signs of demyelination of the tracts in the longest (months) survivors. 

Vascular damage:

Structural cellular changes, and changes in autoregulation occur following injury. 

Endothelial lesions in the pial arterioles appear in the form of a baloon or bleb; they burst into the lumen and crater-like lesions are formed. Abnormal permeability of the vascular wall to macromolecules with perivascular leakage. There is dilatation of arterioles immediately after injury. There is a decrease in vasoconstrictor response to hypocapnia and in severe injury the ability to react is lost. Hyperaemic responses to arterial hypoxia are reduced as well. These changes impair CBF.

Brain ischaemia:

Mass lesions, arterial injuries, vasospasm, increased ICP, loss of autoregulation, and brain swelling can interact resulting in ischaemia. A CBF below the threshold for infarction (18ml/100gms/minute) creates ischaemia with loss of neuronal activity. The extent of damage depends on severity and duration of ischaemia. After decompression of a mass, there is sudden reperfusion and there a risk of  increased ICP and edema in some, especially after a long period of compression as often seen in delayed decompressive surgery.

Brain edema:

The post traumatic edema is predominately vasogenic due to ischaemia; cytotoxic edema may compound the problem. There is blood brain barrier breakdown and leakage of plasma constituents extracellularly. In addition, cell swelling also occurs as a result of inadequate Na+ K+ pumps and influx of Na+ into the cells.

Increased intracranial pressure:

This may be a result of various processes and in turn may aggravate different processes. The volume of the mass lesion, changes in CSF absorption, changes in CSF volume, compliance of the brain tissue, and the cerebrovascular volume and pressure determine the ICP.

Brain herniation:

Rapidly expanding lesions soon block CSF spaces causing pressure gradients in the parenchyma. Eventually, there is a descent and herniation of the medial temporal lobe in the supratentorial lesions and cerebellar tonsils in the infratentorial lesions. Herniation causes interruption of CSF passage and distortion of the brainstem and compressive ischaemia. This results in further raise in ICP and deterioration of the patient.

Biochemical changes:

Following head injury, neurochemical processes evolve gradually in time and lead to structural damage. A detailed understanding is still awaited. 

There is an increase in extracellular K+  and release of neurotransmitters, especially the the excitatory aminoacids (EAA) such as glutamate; this, in turn, leads to further massive increases in the k+ efflux and the Ca++ influx. Ca++ can activate proteolysis that will breakdown the cytoskeleton. Phospholipase C activity is markedly increased; there is release of arachidonate from tissue phospholipid sources. The arachidonate gets converted into the endoperoxide prostaglandin G2 (PGG2) by cyclooxygenase. PGG2 gets converted to prostaglandin H2 (PGH2) by prostaglandin hydroperoxidase (PGH); in the presence of suitable cosubstrates such as NADH or NADPH; oxygen radical superoxide is produced in the wall of cerebral vessels. Superoxide can react with hydrogen peroxide (H2O2) in the presence of iron and form the extremely reactive hydroxyl radical (OH) which can react with almost every molecule found in living cells.

Oxygen radicals can mediate the vascular consequences and vasogenic brain edema after injury. Other effects are lipid peroxidation, release of Ca++ stores, inhibition of enzymes, mitochondrial destruction, DNA damage and disruption of cytoskeleton.  

MEDICAL MANAGEMENT:   

On arrival, and initial resuscitation, basic bedside investigations are done, including ECG, chest x-ray. An ultra sound scanning of the abdomen  to rule out a silent visceral injury is advisable. Appropriate x-rays to rule out a bony injury and x-rays of the cervical spines should be carried out in all patients, even in those with no obvious cervical injury. 

CT scan of the brain is the imaging of choice in all head injuries. Skull x-rays have become redundant these days. 

MRI of the spines is indicated when there is a suspicion of a spinal injury.  

Further management of head trauma is aimed to prevent secondary insults to the brain in addition to attempting to provide optimum conditions for recovery from the primary injury, providing adequate cerebral blood flow and oxygenation.

 

 

 

    Pneumocephalus

     Traumatic SAH

  bil. hgic. contusions

   Some of the traumatic lesions which require intensive medical care.

Following initial assessment and investigations, the patients may be grouped into four groups for the purpose of planning further care: 

Group 1:

Patients with transient loss of consciousness, but are alert without neurological deficit at presentation.

The neurosurgeon must exercise clinical judgment. Age and systemic illnesses and alcohol intoxication may be considered. It is safer to admit them for observation, as there is 1-3% risk of delayed deterioration despite a normal CT.

Group 2:

Patients with impaired consciousness or a focal neurological deficit; they may follow a simple command. GCS score may be between 12-9.The initial CT brain may be normal.

They require admission for strict observation.

ICP monitoring may be considered if they have a non-surgical lesion in the CT scan, especially if they require urgent surgical intervention for an associated injury.

It is prudent to repeat the CT after a day in this group.

Group 3:

Patients who are unable to follow even a simple command and those with a GCS score of less than 8 fall in this group.

Immediate intubation and controlled positive pressure ventilation may be considered. CT scan and other investigations should be carried out immediately and appropriate measures taken. 

Anti edema measures may be considered in the waiting period.

Those who do not require surgical intervention must be ventilated.

Careful monitoring of the patient’s status is the foundation of intensive care.

Lately, bedside measurement of CBF, metabolism, and electrical activity has become a routine in some centers. Serial clinical examination is still the most comprehensive method of assessing the progress of the patient. 

a) Respiratory care:

Neurogenic pulmonary edema is being increasingly recognized lately in severe head injury. Hypothalamic injury resulting in sympathetic discharge, systemic hypertension, left sided heart failure and pulmonary hypertension and edema is blamed. In addition there appears to be a centrally mediated effect on alveolar capillary endothelium that increases its permeability.

Hypoxia is common even in those with no obvious cause for the decreased ventilation.This has been termed ‘central neurogenic pulmonary insufficiency’. Post-concussion apnea resulting in military atelectasis, incipient neurogenic pulmonary edema, and pharyngeal dysfunction with aspiration are the possible causes.

Associated thoracic injury, and aspiration are other possible causes. Fat embolism, more often seen with long bone fractures, occurs in other disease states as well. DVT and pulmonary embolism are to be kept in mind.

Adult respiratory distress syndrome may develop as a result of the above conditions, compounding the problem. 

Removal of any inciting factors and ventilatory care are the mainstay.

It is a good practice to obtain ABG analysis immediately on arrival as the pulse-oxymeter may be deceptive and administer supplemental oxygen to the injured.

The decision to ventilate the patient depends on whether the patient is :

a)  conscious or unconscious with no other significant injury.

b)  able to maintain adequate airway with good cough reflex, and without stridor or not. 

c)  able to maintain optimal oxygenation (spO2>95% and pO2 of 100-120mmHg and pCO2 of 28-33 mmHg, but< 45 mmHg) on his own or not. 

d)  normotensive or not.

Patients with stridor require  an airway, oro/naso pharyngeal.

If the pO2 is <60mmHg and /or pCO2 >40mmHg, and in those with GCS of <8 (irrespective of ABG parameters), endotracheal tube and ventilation is preferred. 

If the patient requires to be ventilated, slow rates and large tidal volumes (12 breaths a minute and 10ml/kg of tidal volume) are recommended to ensure adequate venous drainage and re-expand atelectatic areas. PO2 must be maintained between 100-140 mmHg as higher pO2 induces cerebral vasoconstriction PCO2 must be maintained between 28-35mmHg and lesser pCO2 will compromise CBF. It is  important to maintain the cerebral perfusion pressure (CPP= MAP - ICP)) of 70-100 mm Hg. Concommitent use of ICP monitor and arterial pressure monitor is essential for the same.

Dehydration due to osmotherapy causes metabolic acidosis which may stimulate respiration in  under sedated patients on a ventilator and reduce the pCO2  to less than desired to normalise the pH, which will compromise the CBF. Metabolic acidosis is the earliest sign of dehydration before it shows up in serum urea and creatinine levels. Dehydration must be avoided. 

Mini heparin and antiembolic stockings help to prevent DVT.

b) Cardiovascular care:

Severe head injury induces induces hyperadrenergic state resulting in hyperdynamic cardiovascular and metabolic response and arrythmias and signs of myocardial ischemia

Cerebrovascular autoregulation is frequently deranged in association and may interact with CVS abnormalities to affect CBF. Hypotension leads to cerebral ischemia. Systemic hypertension may lead to cerebral hyperemia and swelling.

Meticulous attention to CVS function is thus important. Sustained systolic hypertension above 160mmHg must be treated. Propranolal is an appropriate agent. Sodium nitroprusside, because of its cerebrovascular dilatory effect, causes cerebral swelling. Some advise fluid restriction. But, it is preferable to maintain a state of normovolemia with isotonic crystalloid or colloidal solutions.  

c) Fluid and electrolytes care:

Both pathophysiological processes and therapeutic maneuvers may lead to a number of electrolyte abnormalities. Sodium is the most important one. Serum electrolytes and osmolality should be checked frequently and attended to appropriately. 

d) Hematological care:

Anemia reduces the oxygen carrying capacity of the blood; however, the oxygen carrying capacity also depends blood flow, which increases with a fall in blood viscosity (hematocrit). In fact, the oxygen delivery increases until an hematocrit of about 33%. Hematocrit below 30% should be corrected with blood transfusions.

Coagulopathy due to release of brain thromboplastin and damage to cerebrovascular endothelium is often seen. Disorders range from abnormalities in lab findings to full blown disseminated intravascular coagulation.

Measurement of hemoglobin, thromboplastin time, partial thromboplastin time, platelet count, fibrinogen levels, and fibrinogen degradation products are widely used.

Treatment is not satisfactory; obviously the underlying cause should be eliminated. Blood loss should be corrected along with fresh frozen plasma and platelets. Low dose heparin may help. 

e) Gastrointestinal care:

Problems of gastritis to frank ulceration are associated with head injuries, especially in the first week. About 10% of them have significant bleeding. Pathogenesis is not clear. Vagal stimulation due to diencephalic or brainstem injury, adrenergic surge have all been blamed. 

Cimitidine (500mg I.V) is effective; concurrent antacids help. 

f) Seizures:

About 5% of the head injured patients have seizures in the immediate post injury period. Debate continues on prophylactic anti convulsants; most surgeons use them in severe head injury.

Acute control and status epilepticus are attended to appropriately. 

g) Infections:

Meningitis results from open or penetrating wounds, CSF fistulae, ICP monitoring, and operative procedures. Meningitis complicating basilar fractures within 72 hours of injury is commonly due to streptococcus pneumoniae. Meningitis from open wounds or CSF leaks or following craniotomy often results from staphylococcus aureus or gram negative bacillus or both. Staphylococcus aureus and epidermidis are the common organisms in meningitis following ICP monitoring.

Strict aseptic precautions during procedures, and use of appropriate antibiotics help. 

h) Nutrition: 

Starved head injured patients lose sufficient N2 to lose weight by 15% per week.

Major head injury alone may provoke a hypermetabolic state as seen in multiple trauma and burns. Concurrent injuries, fever, sepsis, seizures, and posturing may further aggravate.

The aim is to optimize the nutritional support until homeostasis is re-established as the illness subsides. Overfeeding is to be avoided. For periods longer than few days, the help of a qualified dietician is mandatory.

i) Increased ICP control:

It is widely accepted that increased ICP is a cause and an effect of brain injury. There are conditions in which patients have severe neurological deficit with out increased ICP. In the absence of a mass lesion, increased ICP is seen only in 30% of diffuse brain injuries.

It is the main concern of medical management.

j) Cerebral protection:

Since secondary damage seems to be due to a cascade of of biochemical reactions, there are multiple possibilities of pharmacological intervention. Various clinical trials are initiated and conducted on the brain protective effect in the head injured of several different pharmacological agents.

Nimodipine in high doses (60mgm every 4 hour) is reported  to have beneficial effect on injured brain. Some studies  lately have found no benefit. NMDA and AMPA antagonists are being tried to counteract glutamate excitotoxicity on experimental basis. Free radical scavengers such as steroids, mannitol, barbiturates, vitamin C and E have been used in various combinations.

Hypothermia reduces CMR, edema formation, release of glutamate, excitatory transmitters, ion exchange, blood coagulation, and the concentration of lactate and leukotrienes. It is reduced in some centers with good results.

Group 4:

The patients in this group show no brainstem activity (brain death).

The neurosurgeon’s role becomes a social one, comforting the family.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


 

from Peer Reviewed Resources only

 

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