TRAUMATIC BRAIN INJURY( BTF GUIDELINES AND MANAGEMENT)

Dr. Devawrat Buche, MDFNB Fellow ( CCM )

Level of evidence

• Level I : derived from good quality RCTs• Level II : data from clinical studies, prospective

or retrospective, based on reliable data. Includes observational, cohort , prevalence and case control studies.

• Level III : data from observational prospective or retrospective studies. Includes case series , case reports , case registeries and expert opinions.

Level of recommendations

• Level I : based on strongest evidence of effectiveness, reflect principles of patient management that reflect a high degree of clinical certainty

• Level II : reflect moderate degree of clinical certainty

• Level III : degree of certainty not established.

TBI : Etiology and Demographics

• Vehicular accidents : most common• Falls, assaults, industrial accidents• “silent global epidemic”

• Incidence studies show 2 peaks : 1. Second to third decade - M:F ( 2: 1)2. Seventh to ninth decade – M: F ( 1:1)

Patterns of Injury

• Range : mild to severe• Can be : blunt or penetrating• Majority are minor ( 70- 80 % ), but have

significantly high poor outcomes due to secondary insults

• 20 – 30 % are major injuries : approx. 10 % are dead on arrival, rest may have prolonged ICU stay and disability.

TBI : Pathophysiology of Brain injury

A. PRIMARY BRAIN INJURY

• include all types of injury to the brain parenchyma and vasculature.

• Primary injuries that are associated with adverse outcome :

1. traumatic subarachnoid haemorrhage 2. nonevacuable mass lesions, particularly in

posterior fossa.

B. SECONDARY BRAIN INJURY• characterised by a reduction in cerebral substrate

availability and utilisation.• The factors shown to independently worsen

survival following traumatic brain injury : 1. Hypotension ( systolic BP < 90 mm Hg )2. Hypoxia ( O2 saturation < 90 % , or Pa O2 < 50 mm

Hg )3. Hypoglycaemia4. Hyperpyrexia ( temperature > 39 degree celcius )5. Prolonged hypocapnia ( Pa CO 2 < 30 mm Hg ).

• may occur during initial resuscitation, transport AND in the ICU.

• may initiate or propagate pathophysiological processes

• damage neurons already susceptible

CEREBRAL BLOOD FLOW FOLLOWING TBI

• Autoregulatory mechanisms are disturbed following TBI

• 3 distinct patterns are observed :

1. Hypoperfusion phase :

• Cerebral blood flow is reduced in the first 72 hours following injury - global and regional ischaemia.

• autoregulation is impaired : cerebral blood flow is largely dependent on systemic blood pressure.

• Resultant neuronal ischaemia - ‘cytotoxic’ cerebral oedema and increased intracranial pressure

2. THE HYPERAEMIC PHASE• autoregulatory mechanisms may start to recover - improved

cerebral blood flow.• During this phase, medical therapies directed at maintaining

adequate cerebral perfusion pressure may result in cerebral hyperaemia and increased intracranial pressure.

• result in ‘vasogenic’ cerebral oedema. • persist for a variable period, up to 7–10 days post injury• occurs in 25–30% patients.

3. THE VASOSPASTIC PHASE• In 10–15%, with severe primary and secondary injuries or

those with significant traumatic subarachnoid haemorrhage• a vasospastic phase • complex of cerebral hypoperfusion due to arterial vasospasm,

post-traumatic hypometabolism and impaired autoregulation.

TBI MANAGEMENT

• Primary survey ( examination ) with resuscitation

• Secondary survey ( head to toe examination )• Brain specific resuscitation• Imaging modalities• ICU management

PRIMARY SURVEY

The initial emphasis is directed : • at assessing and controlling the airway• ensuring adequate oxygenation and ventilation• establishing adequate intravenous access and correcting

hypotension. “A-B-C-D”

Neurological assessment and brain-specific treatment should follow only after cardiorespiratory stability has been establishedResuscitative measures should go hand in hand with the primary examination

A : Airway assessment• All head-injured patients should be assumed to

have a potential cervical spine injury - should be immobilised in a rigid collar

• Only jaw thrust for airway patency : NO HEAD TILT OR CHIN LIFT

• Early oral intubation : in traumatic coma, marked agitation, significant extracranial trauma

• Intubation should be done with RSI using MILS.• ET tube placement to be confirmed with etCO2

monitoring.

B. BREATHING • Ventilation with 100% oxygen, 6–10 mL/kg tidal

volumes until blood gas analysis is available.• Oxygenation maintained at least 80– 100 mmHg

and the ventilator adjusted to achieve a normal arterial carbon dioxide tension (35– 40 mmHg).

• Non-depolarising muscle relaxants and narcotics facilitate ventilation in the immediate post-intubation period in combative patients.

• Empirical hyperventilation during initial resuscitation is not indicated. ( Level II evidence ).

C. CIRCULATION

• Prompt restoration of circulating blood volume - euvolaemia is critical.

• Early arterial monitoring and central venous catheter placement for volume replacement and administration of blood and drugs is essential. The placement of these lines must not delay volume resuscitation.

• Blood transfusion should be commenced as soon as possible in actively bleeding patients with early administration of coagulation factors where appropriate.

• Crystalloid, specifically normal saline, is recommended for fluid resuscitation of patients with traumatic brain injury.

• Hypertonic saline ( 3% NS) : may have a role as a small-volume resuscitation, although there is no evidence of reduced mortality when used in the pre-hospital period.

• Vasopressors : may be used to maintain blood pressure once correction of hypovolaemia is underway.

D. DISABILITY ( NEUROLOGICAL ASSESSMENT)a. Level of consciousness• The ATLS® recommends AVPU scale:Awake VerbalPainUnresponsive • provides a rapid and practical grading of

function with severe head injuries

• The Glasgow Coma Scale (GCS) • the most widely accepted and understood scale.• it provides an overall assessment of neurological function, derived from

three parameters: eye opening, verbal response and motor response.• The best responses in the GCS components should be recorded

following cardiorespiratory resuscitation prior to surgical intervention. 14–15 indicates a mild injury, 9–13 a moderate injury and 3–8 is classified as severe (traumatic coma)

• In severely injured patients or those who are intubated or with ocular or facial trauma, the motor response is the most useful.

• If the initial GCS score is reliably obtained and not tainted by prehospital medications or intubation : approximately 20% with the worst initial GCS score will survive and 8%-10% will have a functional survival.

b. Pupillary responses• Pupil size and reactivity are important . • The pupillary function should always be assessed and recorded at the same time as the

GCS, particularly prior to the administration of narcotics, sedatives or muscle relaxants. • abnormalities of pupil size and reactivity may indicate compression of the third cranial

nerve, suggesting raised intracranial pressure or impending herniation, particularly when associated with lateralising motor signs and depressed consciousness.

The recommendations for evaluation/ interpretation of pupillary light reflex are :

1. Pupillary light reflex for each eye should be used as a prognostic parameter.2. The duration of pupillary dilation and fixation should be documented.3. A pupillary size greater than 4 mm is recommended as the measure for a dilated pupil.4. A fixed pupil should be defined as no constrictor response to bright light.5. Right or left distinction should be made when the pupils are asymmetric.6. Hypotension and hypoxia should be corrected before assessing pupils for prognosis.7. Direct orbital trauma should be excluded.8. Pupils should be reassessed after surgical evacuation of intracranial hematomas.

c. Motor function• Document the motor response of the GCS• In addition , decerebrate or decorticate

posturing, hemiparesis or lateralising signs, paraparesis and quadriparesis should be documented concurrently.

2. SECONDARY SURVEY ( “HEAD TO TOE” EXAMINATION )• The principles outlined in the initial assessment form the basis for prioritising

interventions in the secondary survey. • Extracranial causes of hypoxia such as pulmonary contusion or

haemo/pneumothorax must be excluded and promptly treated. • Haemorrhage – both externally from fractures or lacerations and internally from

major vascular disruption or visceral injuries – must be aggressively treated until circulatory stability is achieved.

• There is no place for ‘permissive hypotension’ in head-injured patients as has been advocated in selected cases of penetrating trauma.

• Target mean arterial pressure should be estimated in the context of the patient’s premorbid blood pressure. Higher pressures may be necessary in hypertensive or elderly patients.

• The early use of vasoactive drugs such as epinephrine or norepinephrine may be necessary to achieve this.

• An approach of ‘damage-control surgery’ is recommended in patients with traumatic brain injury to minimise secondary insults. In the initial 24–48 hours following injury, only life- or limb-threatening injuries should be addressed, following which patients should be transferred to the ICU for stabilisation and monitoring. Thereafter, semiurgent surgery such as fixation of closed fractures or delayed plastic repairs may be done.

• Patients with severe traumatic brain injury undergoing prolonged emergency surgery should have intracranial pressure monitoring placed as soon as possible.

3. BRAIN SPECIFIC RESUSCITATION A. Hyperventilation• Prophylactic hyperventilation is not recommended ( Level II evidence ).• Ventilation-induced reductions in PaCO2 result in marked reductions in cerebral

blood flow and consequently in intracranial pressure: HARMFUL IN HYPOPERFUSION PHASE.

• Reductions of PaCO2 to levels ≤ 30 mmHg may be considered prior to urgent imaging or surgery for evacuation of a mass lesion as a temporary measure ( Level III evidence ).

• In patients who are normoventilated , well oxygenated and are normotensive, but with signs of herniation, hyperventilation can be used as a temporary measure and discontinued when signs of herniation resolve. Hyperventilation can be administered as :

20 breaths / min : adult 25 breaths / min : child 30 breaths / min : infant less than 1 year.

• Capnography is used, the goal being etCO2 of 30 – 35 mm Hg.

• If hyperventilation is used, jugular venous saturation or brain tissue oxygen tension measurements are recommended ( Level III evidence ).

B. Osmotherapy

• An intact blood–brain barrier is necessary .

1. MANNITOL• Following intravenous administration of mannitol, an immediate plasma-expanding effect that

reduces haematocrit and viscosity ensues, which temporarily increases cerebral blood flow. • exerts an osmotic effect over a narrow range of plasma osmolality (290– 330 mosm/L• Mannitol will enter the brain where the blood–brain barrier is damaged, thereby potentially

increasing cerebral oedema by increasing brain osmolality.• It is a potent osmotic diuretic that may compromise haemodynamic stability by inducing an

inappropriate diuresis in a hypovolaemic patient.• Given the high risk with minimal benefit during resuscitation, the routine use of mannitol is

not recommended in the absence of raised intracranial pressure. The use should be restricted in those with signs of transtentorial herniation or neurological deterioration not attributable to extracranial causes( Level III evidence ).

• Similarly to hyperventilation, mannitol is considered as an option only in resuscitated patients with unequivocal signs of raised intracranial pressure prior to imaging or evacuation of a mass lesion.

• Although doses are frequently quoted as 0.25–1.0 g/kg, lower doses are equally as effective as higher doses in terms of improving cerebral perfusion and are associated with a lower incidence of side-effects ( Level II evidence ).

2.Hypertonic saline (3% solution) • exerts similar osmotic plasma-expanding effects to mannitol.• These solutions do not exert an osmolal gap so serum sodium reflects serum osmolality

allowing easier titration.

C. Emergency surgical decompression ( Burr holes)

• In areas without immediate access to CT scanning - surgical evacuation may be life-saving in selected patients with a strong clinical probability of an expanding mass lesion

• These include patients with low-velocity injuries to the temporal region with an associated skull fracture and developing lateralising neurological signs.

4. IMAGING

A. CT Scan

• CT scanning is now standard in all patients following traumatic brain injury.• moving the patient to a radiological suite must be done only when initial

assessment and resuscitation are complete and the patient is stable enough to be transported by appropriately trained and equipped personnel.

• Indications : all patients with a history of loss of consciousness or traumatic coma (GCS < 8) combative patients where clinical assessment is masked by associated

alcohol, drugs or extracranial injuries; these patients may require endotracheal intubation, sedation and ventilation to facilitate completion of CT scanning

to exclude a cervical spine injury.

• The most important role of CT scanning is prompt detection of intracranial mass lesions such as extradural or subdural haematomas.

The degree of brain injury may be quantified by radiological criteria as follows: • DI I (diffuse injury) : No visible intracranial pathology seen on CT scan

• DI II (diffuse injury): Cisterns are present with midline shift 0–5 mm and/or Lesion densities present

No high- or mixed-density lesion >25 mm May include bony fragments and foreign bodies

• DI III (swelling) : Cisterns are compressed or absent with midline shift 0–5 mm No high- or mixed-density lesion >25 mm

• DI IV (shift) : Midline shift >5 mm• No high- or mixed-density lesion >25 mm

• Evacuated mass lesion : Any lesion surgically evacuated

• Non-evacuated mass lesion : High- or mixed-density lesion >25 mm, not surgically evacuated.

• These criteria are important for providing an index of injury severity, providing criteria for intracranial pressure monitoring, comparing the progression of injuries with subsequent scans and providing an index for prognosis.

The evidence in literature with respect to prognostic outcomes are as follows :

• Initial CT abnormalities seen 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.

• In patients with a normal CT on admission, outcome is primarily related to concomitant extracranial injuries.

• The absence of abnormalities on CT at admission does not preclude the occurrence of raised ICP, and significant new lesions may develop in 40% of patients.

• patients with diffuse injuries were found to have an intermediate prognosis ( BETTER OUTCOME ) when compared to patients with epidural or subdural hematomas.

• While acute subdural hematomas with low GCS scores had a high mortality, diffuse injuries with higher GCS scores showed a low mortality and a high incidence of good recovery.

With regards to midline shift on CT scan the evidence based conclusions are as follows :

• Presence of midline shift is inversely related to prognosis; however, interaction with the presence of intracranial lesions and other CT parameters exists.

• PPV of 78% to poor outcome in the presence of shift greater than 5 mm in patients over 45 years of age. ( Class I evidence )

• PPV of 70% to unfavorable outcome at midline shift greater than 1.5 cm. ( Class II evidence )

• Presence of midline shift is indicative of increased intracranial pressure. The degree of midline shift has not been well studied and authors report widely differing values.

• The value of shift seems less important than other CT parameters, because the degree of shift is also influenced by the location of intracerebral lesions and the presence of bilateral abnormalities.

• the presence and degree of midline shift as seen on the admission CT scan can be significantly altered on subsequent investigations, following the evacuation of mass lesions

III ) Regarding hematomas/ intra or extra cranial lesion the conclusions were as follows : • Extracerebral and intracerebral lesions occur frequently in

comatose patients with head injury.• Presence of mass lesions has a PPV of 78% to unfavorable

outcome (Class II Evidence).• Presence of mass lesions in patients over 45 years of age

carries a PPV of 79% to poor outcome as defined by the categories dead and vegetative.

• Mortality is higher in acute subdural hematoma than in extradural hematoma.

• Diffuse injuries have better outcome than epidural/ subdural hematomas.

• Hematoma volume is correlated to outcome.• Intraparenchymal lesions are ill defined.

B. MRI• Magnetic resonance imaging provides accurate details of

parenchymal damage, specifically small collections and non-haemorrhagic contusions.

• The information provided is not significantly better than that obtained from CT scanning to warrant routine use of MRI in the acute phase of injury.

• MRI has an emerging role in prognostication at a later stage in management.

C. X Rays • In areas without immediate access to CT, X-rays should

focus on identifying injuries or confirmation of placement of lines and tubes post resuscitation

5. INTENSIVE CARE MANAGEMENT

A. CARDIOVASCULAR SYSTEM MANAGEMENT• Accurate measurement of systemic blood pressure is essential and should be measured via

an arterial catheter ( Level II evidence ).• Therapy should be titrated to MAP in accordance with the patient’s premorbid blood

pressure , i.e., in older patients, higher mean arterial pressure (e.g. 70–80 mmHg) may be necessary ( Level II evidence ). .

• Volume status should be assessed using clinical criteria including pulse rate, right atrial and mean arterial pressure, urine output serum sodium and osmolality, urea and creatinine.

• Pulmonary artery catheterisation for the measurement of cardiac output is not recommended.

i ) Fluid management• Euvolaemia is essential throughout intensive care management; both dehydration and fluid

overload should be avoided.• NS is the resuscitation fluid of choice for patients with traumatic brain injury. • The use of albumin is associated with increased mortality due to increased intracranial

pressure. • Hypotonic crystalloids such as compounded sodium lactate (Ringer’s lactate or Hartmann’s

solution) should be avoided.• Maintenance fluids should be restricted at maintaining normal serum sodium (140–145

mmol/L) and osmolality (290–310 mosmol/L).• As a general principle, glucose-containing solutions are not recommended; however, these

may be required if patients become hyperosmolal (>320 mosm/L).

ii ) Vasopressor therapy

• The early use of vasopressors during the hypoperfusion phase. • Norepinephrine is currently regarded as the initial agent of

choice • Vasopressin is commonly used as a catecholamine sparing agent

or as a primary vasopressor - role in traumatic brain injury has not been established and is not recommended.

• Hypotension is repeatedly found to be one of the most powerful predictors of outcome and is generally the only one that is amenable to therapeutic modification.

• A single recording of a hypotensive episode is generally associated with a doubling of mortality and a marked increase in morbidity from a given head injury.

• The estimated reduction in unfavorable outcome that would result from the elimination of hypotensive secondary brain insults is profound.

B. RESPIRATORY SYSTEM MANAGEMENT• Monitoring of ventilatory parameters includes measurement of tidal

volumes, respiratory rates, and inspiratory and expiratory airway pressures as well as the continuous measurement of arterial oxygen saturation.

• Hypoxia ( PaO2 < 60 mmHg or SpO2 < 90% ) should be avoided ( Level III evidence ).

I ) Ventilation• The majority of patients with severe head injury will require mechanical

ventilation to ensure adequate oxygenation and to maintain normocapnia (36– 40 mmHg).

• PEEP is recommended at low levels (5–10 cmH2O). Higher levels may compromise systemic blood pressurein hypovolaemic patients.

• Weaning from ventilation should commence once intracranial pathology has stabilised – that is, resolution of cerebral oedema on CT scan and control of intracranial hypertension.

• Trials of extubation should be carefully considered so that subsequent hypoxic episodes do not occur, as these are potent secondary insults.

• Patients with slow recovery of adequate consciousness should be considered for early tracheostomy.

II ) Neurogenic pulmonary edema• It is a clinical syndrome that occurs in some patients with

severe head injury and correlates with severity of injury. • pathophysiological process is complex - primarily related

to centrally mediated sympathetic overactivity. • It is characterised by sudden onset of clinical pulmonary

oedema, hypoxia, low filling pressures, poor lung compliance and bilateral lung infiltrates, usually within 2–8 hours following brain injury.

• usually self-limiting and treatment is primarily supportive, aimed at ensuring adequate oxygenation and ventilation.

• requires endotracheal intubation and mechanical ventilation with the administration of PEEP.

C. CENTRAL NERVOUS SYSTEM MANAGEMENT

The Brain Trauma Foundation guidelines recommend intracranial pressure monitoring in patients with traumatic coma (severe head injury: GCS < 8 following non-surgical resuscitation) with any of the following: ( Level II evidence ).

• abnormal CT scan• diffuse injury II–IV or high- or mixed-density lesions >25 mm3• normal CT scan with two or more of the following features:– age >40 years– unilateral or bilateral motor posturing– significant extracranial trauma with systolic hypotension (<90 mmHg ).

• Intraventricular catheters are the gold standard. may also employ subdural bolts, epidural catheters and manometry.

• Coagulopathy is a relative contraindication to intracranial pressure monitoring.• Treatment should be initiated with ICP threshold above 20 mm Hg ( Level II

evidence ).

Cerebral blood flow can be indirectly assessed by : • Jugular bulb oximetry : Jugular venous saturation <

50 % is a treatment threshold ( Level III evidence ).• Transcranial Doppler Cerebral metabolism and function can be assessed by : • Electroencephalography ( EEG )• Evoked potentials ( visual, auditory, somatosensory,

motor ) • Cerebral microdialysis• Functional CT scans.

IV ) Brain specific therapy• Brain-specific or ‘targeted’ therapy is directed at maintaining cerebral perfusion

pressure and minimising intracranial pressure. • The Brain Trauma Foundation guidelines recommend a range of cerebral perfusion

pressure of 60 mmHg ( 50 – 70 mm Hg ) ( Level III evidence ).• CPP less than 50 mm Hg should be avoided ( Level III evidence ). a. During the hypoperfusion phase ( 0 – 72 hrs ) : a target cerebral perfusion pressure of at least 60 mm Hg is maintained. Osmotherapy or hyperventilation should be used only if cerebral perfusion pressure is maintained at an appropriate level and the patient is adequately monitored.However, aggressive attempts to maintain CPP above 70 mm Hg with fluids and vasopressors should be avoided because of the risk of ARDS ( Level II evidence ).Assessment of adequacy of the response to augmentation of cerebral perfusion pressure is made by intracranial pressure trends, CT scan appearance and neurological assessment.

b. During the hyperemic phase ( 3- 7 days ) , 25–30% of patients will develop clinical signs of raised intracranial pressure and persistent cerebral oedema on CT scan due to vasogenic cerebral edemaA target cerebral perfusion pressure target of 40–60 mmHg is recommended.Intracranial pressure should be maintained at < 20– 25 cmH2O.

The strategies to control / decrease raised ICP are :

• Surgical evacuation : prompt detection and evacuation of mass lesion causing raised intracranial pressure is the most effective method of relieving intracranial hypertension.

• CSF drainage : through an intraventricular catheter is an effective

method of reducing intracranial pressure. If present, these catheters should be placed 5–10 cm above the head and opened for drainage every 1–4 hours.

• Osmotherapy : There is no evidence that osmotherapy or induced

dehydration improves outcome or is more effective in cytotoxic than vasogenic cerebral edema.

Mannitol or hypertonic saline should be used only in patients with validated intracranial hypertension who are euvolaemic, haemodynamically stable, with a serum osmolality <320 mosm/L.

• Hyperventilation : The routine prolonged use is associated with a worse outcome than patients ventilated to normocapnia. This is probably due to reduction of cerebral blood flow and secondary brain ischaemia. Current evidence-based guidelines do not recommend the use of routine hyperventilation.

• Hypothermia : Currently, hypothermia is regarded as a ‘second

tier’ option in patients with refractory intracranial hypertension but, on current evidence, cannot be recommended.

• Preliminary findings from pooled data indicates that greater decrease in mortality risk is seen when target temperatures are maintained for more than 48 hours ( Level III evidence ).

• Barbiturate coma : barbiturates reduce cerebral metabolism and reduce intracranial pressure, but no definitive studies have shown a benefit in clinical trials.

• Prophylactic barbiturate administration to achieve burst suppression on EEG is not recommended ( Level III evidence ).

• High dose barbiturates are administered to control elevated ICP refractory to maximal standard medical and surgical therapy. Hemodynamic stability is essential before and during the barbiturate therapy ( Level III evidence ).

• Steroids : Steroid use is not recommended for reducing ICP or improving

outcomes (MRC CRASH Trial, Lancet 2005 ). In moderate or severe head injury, high dose methylprednisolone is associated with high mortality and is contraindicated ( Level I evidence ).

• Decompressive craniotomy : • mainly been used in patients with refractory intracranial hypertension

without evacuable mass lesions.• However, a large randomised-controlled trial of early decompressive

craniectomy in patients with diffuse traumatic brain injury and early intracranial hypertension demonstrated an increase in unfavourable neurological outcome in survivors.

• Seizure prophylaxis : • Seizures are infrequent following traumatic brain injury and usually

present at the time of injury.• These should be treated with anticonvulsants (e.g. diazepam,

midazolam) when they occur.• Anticonvulsants are indicated to decrease the incidence of early

posttraumatic seizures ( within 7 days). However, early PTS are not associated with worse outcomes ( Level II evidence ).

• Prophylactic use of phenytoin or valproate is not recommended for preventing late post traumatic seizures ( Level II evidence ).

• Levetiracetam is as effective as phenytoin in preventing early posttraumatic seizures. However, levetiracetam monotherapy was associated with increased frequency of abnormal EEG findings.

D. SEDATION, ANALGESIA AND MUSCLE RELAXATION

• During the initial resuscitation phase, sedation should be titrated to cause the least effect on systemic blood pressure.

• short-acting narcotics such as fentanyl are useful. As narcotics affect pupillary responses, these must be documented before administration. Short-term muscle relaxants such as vecuronium/ rocuronium are useful to control combative patients.

• During the intensive care phase - patient sedated as lightly as possible to allow clinical assessment of neurological function and to facilitate mechanical ventilation.

• Propofol should be used with caution in haemodynamically unstable patients, however, as it is a potent negative inotrope.

• The prolonged use of propofol is associated with tachyphylaxis and significant caloric loading from the lipid vector. Concerns have been raised about myocardial depression and sudden cardiac death, particularly if large doses are administered.

• Propofol is recommended for control of ICP, but not for improvement in mortality or 6 month outcome. High dose propofol can produce significant morbidity ( Level III evidence ).

• The prolonged use of MR is associated with polyneuromyopathies.

E. METABOLIC AND NUTRITION MANAGEMENT• Hyperglycaemia is common following severe head injury and is usually

centrally mediated and transient.• Blood sugar levels should be maintained within normal limits with insulin

infusions, between 140 – 180 mg/ 100 ml, hypoglycaemia should be avoided.• Core temperature should be routinely monitored as hyperthermia has been

identified as a cause of secondary injury. Normothermia (core temperature at 37oC) is recommended.

• Early enteral feeding is recommended. Placement of a nasogastric and/or enteral feeding tubes in head-injured patients is usually via the oral route.

• By Day 7 post injury, the patient should be fed enough to achieve full caloric replacement ( Level II evidence ).

F. STRESS ULCER PROPHYLAXIS• Head-injured patients are at no more risk than other critically ill patients for

developing stress ulceration.• H2 antagonists or proton pump inhibitors should be used in ventilated

patients until enteral feeding is established, following which they may be ceased.

G. THROMBOPROPHYLAXIS• The use of anticoagulants such as fractionated or low-molecular-weight heparins

is advocated with mechanical compression devices. However, there is increased chance of expansion of intracranial bleed. ( Level III evidence ).

• elastic stockings or pneumatic calf compressors are of unproven effectiveness, but provide a reasonable alternative. ( Level III evidence ).

• Patients who develop deep-vein thrombosis and who cannot be anticoagulated should be considered for inferior vena caval filters.

• The use of anticoagulants in head-injured patients with proven pulmonary embolism will depend on the relative risk to the patient’s life.

H. ANTIBIOTIC PROPHYLAXIS• Periprocedural antibiotics for intubation should be administered to reduce the

incidence of pneumonia. However there is no mortality / outcome benefit. ( Level II evidence )

• Routine ventricular catheter exchange or prophylactic antibiotic use for ventricular catheter placement is not recommended to reduce infections. ( Level III evidence ).

• Early extubation in qualified patients can be done without increased risk of pneumonia. ( Level III evidence ).

MISCELLANEOUS MEASURES

a. Tracheostomy : Early tracheostomy should be performed to reduce mechanical ventilation days. However it does not reduce mortality or rates of nosocomial pneumonia ( Level II evidence ).

b. Hyperbaric oxygen therapy : In people with traumatic brain injury, while the addition of HBOT may reduce the risk of death and improve the final GCS, there is little evidence that the survivors have a good outcome. Currently the therapy is not recommended and awaits further clinical trials.

c. Glycerol, cetycholine , etc. : not recommended

6. OUTCOME AND PROGNOSIS• Outcomes are difficult to quantify. • mortality is an easy end-point to measure,

functional outcome is an equally important measurement as psychosocial recovery and rehabilitation often take extended periods of time.

• Increasing age is a strong independent factor in prognosis with a significant increase in poor outcome above 60 years of age.

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