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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.
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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. |
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medial temp.lobe |
corpus callosum |
thalamus |
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grade 2 axonal
injury, hyperdense lesions-MRI T2 |
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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.
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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. |
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Pneumocephalus |
Traumatic SAH |
bil. hgic.
contusions |
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Some of the traumatic lesions which require intensive medical
care. |
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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.
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