Traumatic Head injuries
Benjamin W. Wachira
Outline
• Basic Sciences – Mechanism of injury and
Physiology of ICP regulation
• Independent Predictors of Poor Outcomes
• Complications
Primary Injury
 Acute traumatic intracranial injuries include
Primary injury which occurs during the initial
insult, and results from displacement of the
physical structures of the brain.
Secondary Injury
• Secondary injury is defined as post-traumatic
insults to the brain arising from extracranial
sources and intracranial hypertension.
Cerebral Blood Flow
• Brain metabolism is dependent on a constant
delivery of oxygen and glucose as well as the
removal of "waste" products through a
constant Cerebral Blood Flow
Cerebral Blood Flow
• Cerebral blood flow is equal to the cerebral
perfusion pressure (CPP) divided by the
cerebrovascular resistance (CVR): CBF = CPP /
CVR
Cerebral Perfusion Pressure
• Cerebral perfusion pressure (CPP) is defined as
the difference between mean arterial and
intracranial pressures.
• The Brain Trauma Foundation now
recommends that the CPP target after severe
TBI should lie between 50–70mmHg.
Intracranial Pressure
Clinical Correlate
• A reasonable estimate of CPP can be made in
head injured patients who are not sedated:
– Drowsy and confused: (GCS 13-15)ICP=20
mmHg,
– Severe brain swelling (GCS <8) ICP=30
mmHg
Clinical Correlate
• Thus in a confused, restless and drowsy
patient It would be reasonable to estimate his
ICP to be 20 mmHg.
• A drop in SBP to 80 mmHg drops MAP to
65 mmHg and therefore CPP falls to less than
45 mmHg.
Cerebral Vascular Resistance
• CVR is controlled by four major mechanisms:
• Pressure autoregulation
• Chemical control (by arterial pCO2 and pO2)
• Metabolic control (or 'metabolic
autoregulation')
• Neural control
1. Pressure Autoregulation
• In the normal brain, when the MAP is
between 60 and 150 mm Hg, cerebral vessels
work to maintain desirable CBF through their
ability to constrict and dilate. This is termed
“autoregulation.”
cont…
• When the MAP is less than 50 mm Hg or
greater than 150 mm Hg, the arterioles are
unable to autoregulate and blood flow
becomes entirely dependent on the blood
pressure, a situation defined as pressurepassive flow.
Vasodilatory Cascade
cont..
• This process can only be broken by increasing
the blood pressure to raise CPP, inducing the
vasoconstriction cascade.
Vasoconstriction Cascade
2. Chemical Control
3. Neuronal Control
• Cushing Reflex - is a hypothalamic response to
ischemia, usually due to poor perfusion in the
brain.
cont…
• The ischemia activates the sympathetic
nervous system, causing an increase in the
heart's output by increasing heart rate and
contractility along with peripheral constriction
of the blood vessels.
cont…
• The increased blood pressure also stimulates
the baroreceptors (pressure sensitive
receptors) in the carotids, leading to an
activation of the parasympathetic nervous
system, which slows down the heart rate,
causing the bradycardia
Cerebral Vascular Resistance
Mechanisms of Secondary Brain Injury
• Mechanisms that lead to secondary brain
injury are:
– Hypoxia
– Hypotension
– Increased intracranial pressure
– Hypercarbia
– Acidosis
1. Hypoxia
2. Hypotension
3. Raised Intracranial Pressure
Brain Herniation
Signs of Herniation
• GCS of three to five.
• Abnormal posturing - a characteristic
positioning of the limbs indicative of severe
brain damage.
• One or both pupils may be dilated and fail to
constrict in response to light.
• Vomiting can also occur due to compression of
the vomiting center in the medulla oblongata.
Medical Therapy For Increased ICP
• The indication for treatment of elevated ICP
with hyperosmolar therapy is for short-term
treatment while further diagnostic procedures
(CT scan of the brain) and interventions (such
as treatment of mass lesion found on CT scan)
are performed.
Medical Therapy For Increased ICP
4. Hypercarbia
Hypercarbia
Hyperventilation to Reduce ICP
• Thus hyperventilation can lead to a mean
reduction in intracranial pressure of about
50% within 2-30 minutes.
• When PaCO2 is less than 25 mmHg (3.3kPa)
there is no further reduction in CBF.
Hyperventilation to Reduce ICP
• Acute hypocapnic vasoconstriction will only
last for a relatively short time (5 hours) due to
a gradual increase in CBF towards control
values leading to cerebral hyperaemia (overperfusion) if the PaCO2 is returned rapidly to
normal levels
Contributing Events In The
Pathophysiology Of Secondary
Brain Injury
Independent Predictors of Poor
Outcome
1.
2.
3.
4.
5.
Age
Head CT intracranial diagnosis
Pupillary reactivity
Post-resuscitation GCS
Presence or absence of hypotension.
1. Age
• There is an increasing probability of poor
outcome with increasing age, in a stepwise
manner with a significant increase above 60
years of age.
2. Head CT Intracranial Diagnosis
• Initial CT examination demonstrates
abnormalities in approximately 90% of
patients with severe head injury.
• Prognosis in patients with severe head injury
with demonstrable pathology on initial CT
examination is less favorable than when CT is
normal.
2. Head CT Intracranial Diagnosis
• Individual CT characteristics found to be
particularly relevant in terms of prognosis
were:
– Compressed or absent basal cisterns
measured at the midbrain level.
– tSAH
• Blood in the basal cisterns
• Extensive tSAH
2. Head CT Intracranial Diagnosis
• Individual CT characteristics found to be
particularly relevant in terms of prognosis
were:
– Presence and degree of midline shift at the
level of the septum pellucidum
– Presence and type of intracranial lesions
3. Head CT Intracranial Diagnosis
Marshall Classification of Diffuse Brain Injury
• Grade 1 = normal CT scan (9.6% mortality)
• Grade 2 = Basal cisterns present, shift < 5mm
(13.5% mortality)
• Grade 3 = Basal cistern compressed/ absent,
shift <5mm (34% mortality)
• Grade 4 = Shift > 5mm (56.2% mortality)
4. Pupillary Reactivity
• The parasympathetic, pupilloconstrictor, light
reflex pathway mediated by the third cranial
nerve is anatomically adjacent to brainstem
areas controlling consciousness.
4. Pupillary Reactivity
• Pupillary size (<4mm) and light reflex (>1 mm)
are indirect measures of dysfunction to
pathways subserving consciousness and, thus,
an important clinical parameter in assessing
outcome from traumatic coma.
5. Post-Resuscitation GCS
• If the initial GCS score is reliably obtained and
not tainted by prehospital medications or
intubation, approximately 20% of the patients
with the worst initial GCS score will survive
and 8%-10% will have a functional survival.
6. Presence or Absence of
Hypotension
• A systolic blood pressure less than 90 mm
Hg was found to have a 67% PPV for poor
outcome and, when combined with
hypoxia, a 79% PPV.
6. Presence or Absence of
Hypotension
• A single episode of hypotension (SBP <90
mm Hg) is associated with doubling of
mortality and increased morbidity when
compared to similar patients without
hypotension.
Complications
• Skull base fracture – CSF leak
• Depressed skull fractures – infection
risk
• Pneumocephalus
Complications
• Traumatic subarachnoid haemorrhage
• Chronic subdural haematoma
• Epilepsy
Complications
•
•
•
•
Hydrocephalus
Cranial nerve trauma
Concussion
Post-traumatic encephalopathy after
repeated injury
Summary
References
• An Evidence-Based Approach To Severe
Traumatic Brain Injury – Emergency Medicine
Practice; December 2008 Volume 10, Number
12
• Head Injury - A Multidisciplinary Approach;
Edited by Peter C. Whitfield Consultant Neurosurgeon
and Honorary Clinical Senior Lecturer South West
Neurosurgery Centre Derriford Hospital Plymouth
Hospitals NHS Trust Plymouth, UK