Outline Basic Sciences Mechanism of injury and Physiology of ICP regulation Independent Predictors of Poor Outcomes Complications Primary Injury Acute traumatic intracranial injuries include ID: 775205
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Slide1
Traumatic Head injuries
Benjamin W. Wachira
Slide2Outline
Basic Sciences –
Mechanism of injury and Physiology of ICP regulation
Independent Predictors of Poor Outcomes
Complications
Slide3Primary 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.
Slide4Secondary Injury
Secondary injury
is defined as post-traumatic insults to the brain arising from
extracranial
sources and intracranial hypertension.
Slide5Cerebral 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
Slide6Cerebral Blood Flow
Cerebral blood flow is equal to the cerebral perfusion pressure (CPP) divided by the cerebrovascular resistance (CVR): CBF = CPP / CVR
Slide7Cerebral 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.
Slide8Intracranial Pressure
Slide9Clinical 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
Slide10Clinical 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.
Slide11Cerebral Vascular Resistance
CVR is controlled by four major mechanisms:
Pressure autoregulation
Chemical control (by arterial pCO
2
and pO
2
)
Metabolic control (or 'metabolic autoregulation')
Neural control
Slide12Pressure 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.”
Slide13cont…
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
pressure-passive flow.
Slide14Vasodilatory Cascade
Slide15cont..
This process can only be broken by increasing the blood pressure to raise CPP, inducing the vasoconstriction cascade.
Slide16Vasoconstriction Cascade
Slide17Chemical Control
Slide18Neuronal Control
Cushing Reflex - is a hypothalamic response to ischemia, usually due to poor perfusion in the brain.
Slide19cont…
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.
Slide20cont…
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
Slide21Cerebral Vascular Resistance
Slide22Mechanisms of Secondary Brain Injury
Mechanisms that lead to secondary brain injury are:
Hypoxia
Hypotension
Increased intracranial pressure
Hypercarbia
Acidosis
Slide23Hypoxia
Slide24Hypotension
Slide25Raised Intracranial Pressure
Slide26Brain Herniation
Slide27Signs 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.
Slide28Medical 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.
Slide29Medical Therapy For Increased ICP
Slide30Hypercarbia
Hypercarbia
Slide31Hyperventilation to Reduce ICP
Thus hyperventilation can lead to a mean reduction in intracranial pressure of about 50% within 2-30 minutes.
When PaCO
2
is less than 25 mmHg (3.3kPa) there is no further reduction in CBF.
Slide32Hyperventilation 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 (over-perfusion) if the PaCO
2
is returned rapidly to normal levels
Slide33Contributing Events In The Pathophysiology Of Secondary Brain Injury
Slide34Independent Predictors of Poor Outcome
Age
Head CT intracranial diagnosis
Pupillary reactivity
Post-resuscitation GCS
Presence or absence of hypotension.
Slide351. 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.
Slide362. 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.
Slide372. 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
Slide382. 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
Slide393. 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)
Slide404. Pupillary Reactivity
The parasympathetic, pupilloconstrictor, light reflex pathway mediated by the third cranial nerve is anatomically adjacent to brainstem areas controlling consciousness.
Slide414. 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.
Slide425. 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.
Slide436. 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.
Slide446. 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.
Slide45Complications
Skull base fracture – CSF leak
Depressed skull fractures – infection risk
Pneumocephalus
Slide46Complications
Traumatic subarachnoid haemorrhage
Chronic subdural haematoma
Epilepsy
Slide47Complications
Hydrocephalus
Cranial nerve trauma
Concussion
Post-traumatic encephalopathy after repeated injury
Slide48Slide49Summary
Slide50References
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