Traumatic brain Injury (TBI)
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Traumatic brain Injury (TBI)

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  • It is our duty for continuation of care of traumatic patient after they have been well stabilized by the first responder and under Emergency careTherefore it is also our duty to update ourself and to have repetitive revision regarding the best care for TBI patientAs we know TBI pt have high mortality and the need for the best intervention is needed Which may improve the survival rate and patient outcome exponencially depend on our good knowledge, skills and judgements
  • 60MMhG = 90-
  • Limited period of timeFurther increase in ICP- eventual ischemia will damage the vital centres leads to deathFurther increase in ICP – cause brain herniation as pressure inside the skull is so great that it forces brain tissue downward causing severe brain damage
  • Regulation of cerebral blood flowCO2 concentrationH+ concentrationO2 concentrationSubstances released from astrocyte
  • Sudden ceasation of blood supply to brain – can cause unconciousness for 5 to 10 secs
  • Axonal tissue is more susceptible to the injury than vascular tissue
  • There is experimental evidence that the extent of ‘primary injury’ may be modulated by subsequent management, andIschemia, re-perfusion and hypoxia, to areas of ‘at risk’ brain in the period after the initial injury
  • It may also be a surrogate marker for marked hypercapnia, which would be expected to lower cerebral perfusion pressure. Animal work suggests that, in rats, the combination of hypoxia and percussive trauma leads to a small increase in oedema formation when compared with the percussive trauma alone
  • , though the limits of PaCO2 vary between guidelines.
  • increase cerebral metabolic rate, enhance neurotransmitter release and are associated with rises in ICP.

Traumatic brain Injury (TBI) Traumatic brain Injury (TBI) Presentation Transcript

  • Traumatic Brain Injury (TBI)Dr Nor Hidayah Zainool AbidinInternational Islamic University of Malayia(IIUM)Hospital Sultan Abdul Halim
  • Morbidity and mortality impact…• leading cause of death among adult < 45 yrand in children (1–15 yr).• Mild TBI– good prognosis providing treatable complicationsare not missed.– Overall mortality - 0.1% (missed intra-cranialhaemorrhage)– around 50% of survivors have moderate or severedisability
  •  more severe TBI prognosis is much worse. Approximately 30% with GCSscore <13 will ultimately die. Mortality for those with GCS <8 after resuscitation maybe as high as 50%. Patient with GCS <12 around 8% will die within thefirst 6 h, 2% within the first hour. Long-term outcome among survivors - only around20% will make a good recovery on the (GOS)
  • • Skull is a rigid box – fixed volume• About 1600ml – 1700mlSKULLBrainCSFBlood
  • Brain Edema• Traumatized brain tissue and damage capillarywall  brain edema compress vasculature decrease blood flow – brain ischemia• Ischemia – arteriolar dilatation – increasecapillary pressure  cause more edema
  • • And increase 1 of the 3 components must becompensated with a decrease of volume ofanother componentSKULLBrainBlood CSF
  • • for a certain period of time• A critical point – no further compensation canoccur lead to exponencial rise in ICP causingsecondary brain damageInrease ICP will reduce CPPCPP = MAP –ICP
  • Cushing’s Reflex• Increase MAP• Falls in pulse rate– Reflexs from increasing blood pressure• Rise in respiratory rate– With further ischemia, body attemp to incrase oxygenation byincreasing respiratory rate
  • Physiology of Human brain• Normal blood flow 50-65ml/100g/min• 750-900ml/min• 2 % of body weight• 15% of resting cardiac output
  • • 150 ml of skull volume occupied by CSF• Formed at rate of 500ml/day• Normal pressure in CSF system = 150mm H2O(10mmHg)• Ranging 65 mmH2O-195 mmH2O
  • Brain metabolism• 2% of total body weight• 15% of total body metabolism• 7.5 times the average metabolism in non-nervous system tissue• Most excess metabolism occur in the neuron – transport sodiumand calcium ions for proper ionic different to conduct actionpotentials• During high level of brain activity – neuronal metabolism can be ashigh as 100-150%No anaerobic activityNeuronal activity depends on second to second delivery of O2 from the bloodGlucose delivery – not dependant on insulin
  • Types of brain injury• the initial, mechanical forces• in shearing and compressionof neuronal, glial, andvascular tissue.PrimaryDamage• further physiological insults• may start at the time ofinitial mechanical insult.SecondaryDamage
  • Primary Damage1. Diffuse injuriesConcussion• Mildest form• Temporary LOC• Confusion• Headache, dizziness,nausea, ringing in theearsDiffuse axonal injury• Prolonged coma• 44% of head Injuries –coma damage inprimarily microscopicand scatteredthroughout the brain• Autonomic dysfunction(high fever, sweating mhypertension)
  • 2. Focal injuriesExtradural Hematoma• Inner surface of the skull anddura mater• Caused by tear in MMA andits braches• Excellent prognosis if treated• May have Lucid interval afterinitial injuryAcute Subdural Hematoma• Fall or strong decelerationforces• High mortality (70%)• Seen In about 30% of TBI• Early evacuation improvesoutcome• Poor prognosis because ofunderlying brain damage•Bruise of the brainShearing force of the cortexSwelling of the brainUnconcious for some timeAccompanied bu subpial and subarachnoid hemorhagesIntracerebral hemotoma maybe presentContussionHemorrhages
  • SecondaryInsultsHypoxiaHypercapniaandhypocapniaHyperglycemiaHypotension
  • Secondary Injury1/3 of patients who die after TBI will talk orobey commands before their death suggesting that the initial injury per se is notlethal, even with diffuse axonal injury, but theconsequences are.The secondary injury is amenable to treatmentThe early management of TBI is thereforedirected towards minimizing progression ofinjury
  • Risk factors for poor outcome• Secondary insultsamenable forintervention– Hypotension– Hypoxia– Hyperglycaemia– Hypercapnia andhypocapnia• Fixed risk factors - mayprovide prognosticinformation, but cannotbe influenced bysubsequent care.– Mechanism of injury– Age, gender, and genetics– Pupillary signs– Glasgow coma scale– CT findings
  • Mechanism of injury• Penetrating injuries have a worse outcome than blunttrauma, when other factors are taken into account.– more likely to present with a lower GCS and die early.• Non-accidental injury in children , 5 yr is associatedwith worse outcome, which may be in part because ofa higher rate of cerebral infarction in this group.• Pedestrians & pedal cyclists fare worse > vehicleoccupants in MVA• Ejection from the vehicle > significant intra-cranialinjury
  • Age, gender, and genetics• The age of the patient influences both thelikelihood of TBI and the prognosis.• TBI has a bimodal incidence distribution;young adult males comprise the largest peak– motor vehicle accidents– lcohol-associated trauma• second smaller peak in the elderly• women > brain swelling and intra-cranialhypertension
  • Pupillary signs• Pupil size and reactivity can be affected by avariety of mechanisms associated with headinjury– Trauma to the eye– 3rd nerve damage – at any point of its course– Mid brain and pontine dysfunction– Drug administration• May provide prognostic information
  • • Pupillary constriction is mediated via aparasympathetic pathway by the third nerve andits nuclei in brain stem• Third nerve palsy initially -> mydriasis then loss ofreactivity to light.– compression of the nerve• Unilateral  the consensual light reflex (oppositeeye constricting in response to bright light)should still be present.• Optic nerve injury  impair both the direct andindirect responses– lead to fixed or sluggish pupils, which may displayspontaneous fluctuations
  • • Bilaterally fixed pupils occur in around 20–30% of patientswith severe head injury (GCS _8) after resuscitation:– 70–90% of these patients will have poor outcome(vegetative or dead) when compared with around 30%with bilaterally reactive pupils.• Unreactive pupils are associated with the presence ofhypotension, lower GCS, and closed basal cisterns on CT.• The underlying pathology influences the prognostic value ofunreactive pupils:– patients with epidural haematoma fare better than thosewith subdural haematoma.• Unilaterally unreactive pupils have an outcome intermediatebetween bilaterally reactive and unreactive pupils.– Pupil asymmetry is associated with an operable masslesion in around 30% of patients
  • Glasgow coma scale• The relationship between field GCS and survival is non-linear, with a steep relationship between GCS 3 and 7,followed by a shallower decline in mortality between GCS 8and 15• Relationship between field GCS and functional outcomeappears to be approximately linear• post-resuscitation GCS vs mortality &functional outcome ingeneralized TBI– a sharp decrease in mortality as GCS increases from 3 to 8,– a shallower decrease between 8 and 15.• The change in GCS may also be prognostic, withdeterioration in GCS predicting the need for evacuation oftraumatic subdural haematoma.
  • CT Brain• The incidence of abnormalities on CTincreases with severity of head injury.– minor head injuries- 2.5–8%– severe TBI- 68–94%• CT brain linked to poor outcome:– mid-line shift– compression of the basal cisterns– traumatic sub-arachnoid haemorrhage (SAH),
  • Marshall CT Classification
  • SecondaryInsultsHypoxiaHypercapniaandhypocapniaHyperglycemiaHypotension
  • Hypotension• hypotension were separately and additively associatedwith increased mortality.• a single episode of hypotension during the period frominjury through resuscitation  doubling of mortalityand a parallel increase in morbidity in survivors.• The duration and number of episodes of hypotensionare correlated with mortalityThe precise mechanism for the enhancedsusceptibility of the injured brain to hypotension isnot clearbut up to 90% of head-injured patients have beenfound to have evidence of ischaemic damage atautopsy
  • Hypoxia• Association between observed early hypoxia ,SpO2< 90% or kPa 7.9 kPa (60 mm Hg)] andpoor outcome.• The association is not as strong as forhypotension• Hypoxia may be a marker of the severity ofbrain or systemic injury, or it may be asecondary insult to the at risk brain.
  • Hyperglycemia• Severe TBI leads to a marked sympathetic andhormonal response levels of catecholaminesinversely related to the severity of injury.• Hyperglycaemia is common after TBI and isassociated with severity of injury• Has poor outcome for both early mortality andfunctional recovery in adults and children.• Approximately 50% of patients present withblood glucose >11.1 mmol l and peak levelsgreater than this in the first 24 h after admissionare associated with a significantly worse mortality
  • Hypercapnia and hypocapnia• Hypercapnia is more likely to occur in the setting ofmultiple trauma• Hypercapnia  secondary insult– Significant association between hypercapnia and poor outcome.• As a consequence of these findings, hyperventilation haspreviously been used in the initial and ongoingmanagement of TBI.• However, cerebral blood flow in the first few hours afterinjury has been shown to be reduced to less than half ofnormal (~25 ml 100 g min vs ~50 ml 100 g min)• Various studies have demonstrated both physiologicalderangements and worse outcome paCO2 < 4 kPa (30 mmHg)] if aggressive indiscriminate hyperventilation is used.
  • • Hypercapnia  cerebral vasodilatationincrease cerebral blood volume  increaseintracranial pressure (ICP)  reduce cerebralperfusion.• reduced cerebral blood flow and oxygendelivery, where intracranial hypertension isnot a problem, it is possible– that hypercapnia may be of benefit throughimprovements in cerebral blood flow
  •  General principles1. Arterial pressure maintenance2. Mannitol3. Ventilatory support4. Glycaemic control5. Imaging6. Other injuries7. Seizures
  •  maintenance of adequate and stable cerebralperfusion adequate oxygenation avoidance of hyper- and hypocapnia avoidance of hyper- and hypoglycaemia, avoiding iatrogenic injury.
  •  The American guidlelines◦ maintaining SAP >90 mm Hg and avoidance ofhypotension◦ the severe TBI guidance advocates MAP >90 mmHg. The European guidelines◦ SAP >120 mm Hg , MAP >90 mm Hg, The UK transfer guidelines◦ MAP >80 mm Hg
  •  Preferable Isotonic solution (normal saline) Avoids◦ Hartmann’s solution is hypotonic◦ Glucose containing fluids are usually hypotonic,lead to hyperglycaemia Colloids - need to deliver large volumes offluid and blood is not available Anaemia should be corrected and someevidence exists to suggest that the optimalhaemoglobin is 100gms/l.
  •  Suggesting that administration of high dosemannitol (1.4 g kg) is associated withimproved outcome after traumatic braininjury. 1.5g/kg over 20 mins Rapid administration cause hypotension andtranssient hyperkalaemia
  •  For patients who are able to maintain their own airway,supplemental oxygen therapy is always recommended. For patients unable to maintain oxygenation or their ownairway then tracheal intubation may be required. Avoid Hyper- and hypocapnia◦ The American guidance suggests a lower limit of around 4.6 kPa,◦ The UK guidance (4.5–5.0 kPa)◦ The EBIC guidelines suggest a lower P (4.0–5.0 kPa). Problem during transfer of patient Risk of hyperventilation during manual begging orportable ventilator setting As no Et CO2 monitoring
  •  CT is the preferred modality for initialassessment of TBI CT is more sensitive for SAH More severe TBI  a clear indication for CT ofthe head.
  •  Around 5% of patients with moderate-severeTBI  cervical spine injury Conversely, around 1/3 patient with cervicalspine injury suffer moderate- severe headinjury CT cervical spine should be carried out at thesame time
  •  Head injury is the cause of death in aroundone-third of patients dying after trauma, andmajor extra-cranial injuries are found in 50%of patients with severe TBI significant extra-cranial injury  significantlyhigher mortality for TBI patient Control of haemorrhage still apply forpatients with TBI to prevent hypotension
  •  Incidence of early (1 week) seizure of 4–25%. Various factors increase seizure risk :◦ GCS <10◦ cortical contusions◦ depressed skull fracture◦ epidural, subdural, or intracranial haematoma◦ penetrating head wound,◦ seizure within 24 h of injuryRisk of increase ICP
  • Americanguideline•anti-epileptics as atreatment option toprevent early seizuresin high-risk patients.UK•Not mentioned