1. Traumatic Head injuries
Benjamin W. Wachira

2. Outline
Basic Sciences – Mechanism of injury and Physiology of ICP regulation
Independent Predictors of Poor Outcomes
Complications

3. 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.
The spectrum of injuries include isolated fractures of the cranium, subarachnoid haemorrhage, subdurals, epidurals, hemorrhagic, and bland contusions.

4. Secondary Injury
Secondary injury is defined as post-traumatic insults to the brain arising from extracranial sources and intracranial hypertension.
It is a result of ongoing cellular damage from the release of calcium, excitatory amino acids, and other neurotoxins in response to impaired cerebral blood flow, oedema, or increased intracranial pressure.

5. 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

6. Cerebral Blood Flow
Cerebral blood flow is equal to the cerebral perfusion pressure (CPP) divided by the cerebrovascular resistance (CVR): CBF = CPP / CVR

7. 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.
Aggressive attempts to maintain CPP > 70mmHg should be avoided because of the risk of ALI

8. Intracranial Pressure
The principle constituents within the skull are brain (80%), blood (12%) and CSF (8%). The total volume is 1600ml. 
Normal ICP ranges from 0-15mmHg
In 1783 Alexander Monro noted that the cranium was a rigid box containing a nearly incompressible brain. He observed that any increase in one of the component contents (brain, blood and CSF) required accommodation by displacement of the other elements.

9. 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

10. 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.
45mmHg is significantly below the critical value of 50-70 mmHg with a significant risk of causing cerebral ischaemia and a poor cerebral outcome. 
Maintenance of a SBP of >90mmHg maintains a CPP above 50mmHg

11. 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

12. 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.”
MAP = DBP + 1/3 PP

13. 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 pressure-passive flow.
A similar situation is present in traumatised brain, though autoregulation may still be functioning in up to 69% patients with head injuries

14. Vasodilatory Cascade
In this situation if CPP falls below the critical value of 50 mmHg, the patient will have inadequate cerebral perfusion. Autoregulation will cause cerebral vasodilatation leading to a rise in brain volume. This in turn will lead to a further rise in ICP and induce the vicious circle described by the vasodilatation cascade which results in cerebral ischaemia.

15. cont..
This process can only be broken by increasing the blood pressure to raise CPP, inducing the vasoconstriction cascade.
This explains why the maintenance of arterial blood pressure at adequate level by careful monitoring and rapid correction if it falls is so important.

16. Vasoconstriction Cascade

17. Chemical Control
Carbon dioxide causes cerebral vasodilation. As the arterial tension of CO2  rises, CBF increases and when it is reduced vasoconstriction is induced.
 Low arterial oxygen tension also has profound effects on cerebral blood flow. When it falls below 50 mmHg (6.7 kPa), there is a rapid increase in CBF and arterial blood volume.

18. Neuronal Control
Cushing Reflex - is a hypothalamic response to ischemia, usually due to poor perfusion in the brain.

19. 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.
This accounts for the rise in blood pressure, ensuring blood delivery to the brain.

20. 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

21. Cerebral Vascular Resistance

22. Mechanisms of Secondary Brain Injury
Mechanisms that lead to secondary brain injury are:
Hypoxia
Hypotension
Increased intracranial pressure
Hypercarbia
Acidosis

23. Hypoxia
Low arterial oxygen tension also has profound effects on cerebral blood flow. When it falls below 50 mmHg (6.7 kPa), there is a rapid increase in CBF and arterial blood volume.

24. Hypotension
BTF - At Present, a defining level of Hypotension is unclear. Hypotension defined as a single observation of an SBP of less than 90mmHg must be avoided if possible or rapidly corrected in Severe TBI

25. Raised Intracranial Pressure
CPP = MAP - ICP
During the initial stages of rising intracranial pressure due to a mass lesion, cerebrospinal fluid and venous blood are displaced from the cranium buffering the change in pressure.
However, once the point of compensatory reserve has been reached, rapid elevation of the ICP occurs .
The pressure changes within the skull are drawn in the classical curve Fig. 2 which indicates an increase in volume with little change in pressure until a certain point is reached when a further small change in volume results in a large increase in pressure: 1-2 compensation phase; 3-4 decompensation phase.

26. Brain Herniation Supratentorial masses may cause;
displacement of the cingulate gyrus under the falx cerebri resulting in subfalcine herniation. This can cause compression of the anterior cerebral artery and subsequent ischaemia and infarction.
causes the uncus of the medial temporal lobe to herniate from the middle cranial fossa medially and downwards through the tentorial incisura compressing the oculomotor nerve and the midbrain giving you an oculomotor nerve palsy and contralateral hemiparesis.
Uncal herniation can also compress the posterior cerebral artery leading to occipital lobe infarction and obstruction to the flow of cerebrospinal fluid through the aqueduct of Sylvius causing hydrocephalus.
Compromise of the reticular activating system of the midbrain contributes to the impairment of consciousness.
Transtentorial herniation may also stretch perforating branches of the basilar artery causing secondary ‘Duret’ haemorrhages in the brainstem.

27. 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.
Ipsilateral pupil dilatation occurs as the parasympathetic fibers, which are located around the outer aspect of the third nerve, are compressed by the uncus. This leads to dysfunction of the parasympathetic fibers with subsequent unopposed sympathetic responds. This will dilate the ipsilateral pupil. Contralateral hemiparesis occurs with compression of the ipsilateral cerebral peduncle. Since the cortical spinal tracts decussate (cross over) below the mid brain in the level of pons, the hemiparesis is contralateral.
 In some cases, an ipsilateral hemiparesis can occur with a contralateral dilated pupil or oculomotor paresis.  This occurs when the lateral translation of the brainstem is so great as to push the midbrain and cerebral peduncles all the way across the perimesencephalic cistern, so that the opposite (contralateral) third nerve and peduncle are pressed against the opposite tentorial edge.  This phenomenon is called a Kernohan’s notch

28. 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.

29. Medical Therapy For Increased ICP
Mannitol works to reduce ICP by 2 mechanisms.
The first, which begins within minutes of infusion, is by expanding plasma volume, thereby reducing the hematocrit and blood viscosity, leading to increased cerebral blood flow and oxygen delivery.
The second, which takes 15 to 30 minutes, is through an osmotic effect from a gradient between the plasma and neuronal cells, causing net movement of water out of the cells. As an osmotic agent, diuresis will ensue and hypotension can result if the patient is not kept euvolemic.
Hypertonic saline (HTS) has gained recent attention as a potential therapy for the management of both hypotension and elevated ICP. Based on animal models, the theoretical advantage of HTS (usually 3% or higher) over standard concentrations of saline (0.9%) is that cerebral edema is less likely to result from aggressive resuscitation. This effect is due to a shift of free water out of the CNS due to the higher osmolality of the surrounding vasculature. The same effect is also present in the rest of the body, leading to fluid shift out of the interstitium and into the vasculature, improving blood pressure and cardiac output.

30. Hypercarbia Hypercarbia
Carbon dioxide causes cerebral vasodilation. As the arterial tension of CO2  rises, CBF increases and when it is reduced vasoconstriction is induced.
Hypercarbia

31. 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.
Therefore there is no advantage in inducing further hypocapnia as this will only shift the oxygen dissociation curve further to the left, making oxygen less available to the tissues.

32. 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 (over-perfusion) if the PaCO2 is returned rapidly to normal levels

33. Contributing Events In The Pathophysiology Of Secondary Brain Injury

34. Independent Predictors of Poor Outcome
Age
Head CT intracranial diagnosis
Pupillary reactivity
Post-resuscitation GCS
Presence or absence of hypotension.

35. 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.
The significant influence of age on outcome is not explained by the increased frequency of systemic complications or intracerebral hematomas with age.

36. 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.

37. 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
Mortality is increased two- to threefold in the presence of compressed or absent basal cisterns.
tSAH is a frequent occurrence in severe head injury (26%-53%).
Mortality is increased twofold in the presence of tSAH.
Presence of blood in the basal cisterns carries a PPV to unfavorable outcome of approximately 70%.

38. 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
Presence of midline shift is inversely related to prognosis; Class I evidence shows a PPV of 78% to poor outcome in the presence of shift greater than 5mm in patients over 45 years of age.
Presence of mass lesions has a PPV of 78% to unfavorable outcome; Mortality is higher in acute subdural hematoma than in extradural hematoma.

39. 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)

40. 4. Pupillary Reactivity
The parasympathetic, pupilloconstrictor, light reflex pathway mediated by the third cranial nerve is anatomically adjacent to brainstem areas controlling consciousness.

41. 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.

42. 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.
The motor component is generally regarded as the most accurate predictor of outcome.

43. 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.

44. 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.

45. Complications Skull base fracture – CSF leak
Depressed skull fractures – infection risk
Pneumocephalus
This places the patient at risk of meningitis while the CSF leak continues; prophylactic antibiotics does not significantly reduce this risk.
Since 90% of cases seal spontaneously within 2 weeks, neurosurgical intervention is not usually considered until this time has elapsed. An exception is a fracture of the posterior wall of the frontal sinus where a persistent leak is likely. Early anterior fossa repair is normally considered in such cases.
The role of antibiotics in the management of compound depressed skull fractures has not been studied in randomized controlled trials.
The ‘Infection in Neurosurgery’ working party of the British Society for Antimicrobial Chemotherapy recommended the use of a 5-day course of i.v. co-amoxiclav or a i.v. cefuroxime + p.o. or rectal metronidazole.

46. Complications Traumatic subarachnoid haemorrhage
Chronic subdural haematoma
Epilepsy
Post-traumatic seizures are classified into;
immediate (during the first 24 hours after injury),
early (within 7 days of injury) and
late (more than 7 days after injury). Late seizures are often referred to as ‘unprovoked seizures’.
The overall risk of seizures at 5 years was;
0.7% for mild injuries;
1.2% for moderate injuries and
10% for severe injuries.
The 30-year cumulative incidence was 2.1%, 4.2% and 16.7% for these groups, respectively.
None of the trials have demonstrated a reduction in the incidence of late seizures or any improvements in outcome following phenytoin prophylaxis.

47. Complications Hydrocephalus Cranial nerve trauma Concussion
Post-traumatic encephalopathy after repeated injury

49. Summary

50. 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