Approachtotraumaticbraininjury 100608045123-phpapp01
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Approachtotraumaticbraininjury 100608045123-phpapp01 Approachtotraumaticbraininjury 100608045123-phpapp01 Presentation Transcript

  • OUTLINES• Introduction• Definition• Pathophysiology• Severe head injury• Minor head injury• Second impact syndrome• Cerebral herniation
  • INTRODUCTION• Traumatic brain injury (TBI) encompasses a broad range of pathologic injuries to the brain of varying clinical severity that result from head trauma.• MVC ---- young• Fall ---- elderly View slide
  • ETIOLOGY MVA approx. 28-50%• Falls 20-30% (infants, children, elderly)• Assaults 9-10%• Sports and recreational - 10-20% View slide
  • DEFINITIONSHead injury:Injury is clinically evident on physical examination.Traumatic brain injury:Not always clinically evident.
  • CLASSIFICATION• Clinical severity scores• Neuroimaging scales   Leading Cause - MVA approx. 28-50%  0-20%
  • • PROGNOSIS — Cohort studies have suggested that patients with severe head injury (GCS ≤8) have about a 30 percent risk of death and only about 25 percent achieve long-term functional independence.
  • Specific outcome predictors include :•GCS at presentation (especially the GCS motor score)•CT findings (subarachnoid hemorrhage, cisternal effacement, midlineshift)•Pupillary function•Age•Associated injuries•Hypotension•Hypoxemia•Pyrexia•Elevated ICP•Reduced CPP•Bleeding diathesis (low platelet count, abnormal coagulation
  • PATHOPHYSIOLOGY• primary brain injury• secondary brain injury.
  • PRIMARY BRAIN INJURY• occurs at the time of trauma.• Common mechanisms include direct impact, rapid acceleration/deceleration, penetrating injury, and blast waves.• The damage that results includes a combination of focal contusions and hematomas, as well as shearing of white matter tracts (diffuse axonal injury) along with cerebral edema and swelling.
  • Diffuse axonal injury• Shearing mechanisms lead to diffuse axonal injury (DAI), which is visualized pathologically and on neuroimaging studies as multiple small lesions seen within white matter tracts.• present with profound coma without elevated intracranial pressure (ICP), and often have poor outcome.• Involves the gray-white junction in the hemispheres
  • Epidural hematomas• Typically associated with torn dural vessels such as the middle meningeal artery• are almost always associated with a skull fracture• are lenticular-shaped• tend not to be associated with underlying brain damage
  • Subdural hematomas• result from damage to bridging veins• Are crescent-shaped• are often associated with underlying cerebral injury
  • Subarachnoid hemorrhage• can occur with disruption of small pial vessels• commonly occurs in the sylvian fissures and interpeduncular cisterns.• may also extend into the subarachnoid space.
  • Intraventricular hemorrhage• Is believed to result from tearing of s ubependymal veins, or by extension from adjacent intraparenchymal or subarachnoid hemorrhage.
  • SECONDARY BRAIN INJURYa cascade of molecular injury mechanisms :•Neurotransmitter-mediated excitotoxicity causingglutamate, free-radical injury to cell membranes•Electrolyte imbalances•Mitochondrial dysfunction•Inflammatory responses•Apoptosis•Secondary ischemia from vasospasm, focalmicrovascular occlusion, vascular injury
  • Examples:•hypotension•hypoxia -- decrease substrate delivery of oxygen andglucose to injured brain•fever•seizures -- may increase metabolic demand•hyperglycemia
  • CUSHINGS REFLEX• is seen in only one third of cases of life-threatening increased ICP.Triad of:• hypertension• bradycardia• diminished respiratory effort
  • Prehospital• The primary goal of prehospital management for severe head injury is to prevent hypotension and hypoxia• Early endotracheal intubation is generally recommended for patients with a GCS of 8 or less if performed by well-trained personnel.• If this expertise is not available, bag-mask ventilation is recommended.
  • Prehospital• In a meta-analysis of clinical trials and population- based studies, hypoxia (PaO2 <60 mmHg) and hypotension (systolic BP <90 mm Hg) were present in 50 and 30 percent of patients respectively and were each associated with a higher likelihood of a poor outcome: hypoxia
  • Prehospital• Prevention of hypotension -- isotonic crystalloids.• Studies of hypertonic saline in the prehospital setting have not suggested benefit.• Saline is preferred over albumin; the latter was associated with increased mortality in one randomized study of patients with TBI .
  • Prehospital• Patients with TBI should be assumed to have a spinal fracture• precautions taken to stabilize and immobilize the spine during transport.
  • Emergency department• Assessment is done according to the ATLS protocol• Adequate oxygenation (PaO2 >60 mm Hg)• Blood pressure support (systolic BP >90 mm Hg)• Vital signs including heart rate, blood pressure, respiratory status (pulse oximetry, capnography), and temperature require ongoing monitoring.
  • Emergency department• A neurologic examination should be completed as soon as possible• Neurologic status should be continuously assessed. Deterioration is common in the initial hours after the injury.
  • Emergency department• The patient should be assessed for other systemic trauma.• evaluate and manage increased intracranial pressure• A complete blood count, electrolytes, glucose, coagulation parameters, blood alcohol level, and urine toxicology should be checked if indicated
  • Neuroimaging • Computed tomography (CT) is the preferred imaging modality in the acute phase of head trauma• should be performed as quickly as possible• CT scan will detect skull fractures, intracranial hematomas, and cerebral edema
  • Neuroimaging• Risk stratification
  • RISK GROUP FOR THE PRESENCE OF ICI IN HEAD TRAUMA JAMA,SEPT.28,2005. Low risk for ICI. MODERATE OR HIGH RISK No loc • LOC No PTA (post-traumatic amnesia) • PTA Absence of moderate and high risk criteria. • Depressed level of consciousnessThe following have not been found to be predictive of • Progressive , severe headache injury: • Severe nausea or vomiting Headache • Alcohol or drug intoxication Dizziness • Age <2 yrs Scalp hematoma, laceration or abrasion. • Post-traumatic seizure • Focal neurological deficit • Sign of skull # • Possible penetrating injury • h/o hemophilia or warfarine use.
  • CANADIAN CT RULE, LANCET 2001 CT Head Rule is only required for patients with minor head injuries with any one of the following:High risk (for neurological intervention)● GCS score <15 at 2 h after injury● Suspected open or depressed skull fracture● Any sign of basal skull fracture (haemotympanum, ‘raccoon’ eyes,cerebrospinal fluid otorrhoea/rhinorrhoea, Battle’s sign)● Vomiting two episodes● Age 65 yearsMedium risk (for brain injury on CT)● Amnesia before impact >30 min● Dangerous mechanism (pedestrian struck by motor vehicle,occupant ejected from motor vehicle, fall from height >3 feetor five stairs)
  • COMPARISON OF THE CANADIAN CT HEAD RULE ANDTHE NEW ORLEANS CRITERIA IN PATIENTS WITHMINOR HEAD INJURY• Design, Setting, and Patients In a prospective cohort study (June 2000-December 2002) that included 9 emergency departments in large Canadian community and university hospitals, the CCHR was evaluated in a convenience sample of 2707 adults who presented to the emergency department with blunt head trauma resulting in witnessed loss of consciousness, disorientation, or definite amnesia and a GCS score of 13 to 15. The CCHR and NOC were compared in a subgroup of 1822 adults with minor head injury and GCS score of 15.• JAMA. 2005;294:1511-1518.
  • COMPARISON OF THE CANADIAN CT HEAD RULE ANDTHE NEW ORLEANS CRITERIA IN PATIENTS WITHMINOR HEAD INJURY• Results Among 1822 patients with GCS score of 15, 8 (0.4%) required neurosurgical intervention and 97 (5.3%) had clinically important brain injury. The NOC and the CCHR both had 100% sensitivity but the CCHR was more specific (76.3% vs 12.1%, P<.001) for predicting need for neurosurgical intervention. For clinically important brain injury, the CCHR and the NOC had similar sensitivity (100% vs 100%; 95% confidence interval [CI], 96%-100%) but the CCHR was more specific (50.6% vs 12.7%, P<.001), and would result in lower CT rates (52.1% vs 88.0%, P<.001). The values for physician interpretation of the rules, CCHR vs NOC, were 0.85 vs 0.47. Physicians misinterpreted the rules as not requiring imaging for 4.0% of patients according to CCHR and 5.5% according to NOC (P = .04). Among all 2707 patients with a GCS score of 13 to 15, the CCHR had sensitivities of 100% (95% CI, 91%-100%) for 41 patients requiring neurosurgical intervention and 100% (95% CI, 98%-100%) for 231 patients with clinically important brain injury.
  • COMPARISON OF THE CANADIAN CT HEAD RULE ANDTHE NEW ORLEANS CRITERIA IN PATIENTS WITHMINOR HEAD INJURY• Conclusion For patients with minor head injury and GCS score of 15, the CCHR and the NOC have equivalent high sensitivities for need for neurosurgical intervention and clinically important brain injury, but the CCHR has higher specificity for important clinical outcomes than does the NOC, and its use may result in reduced imaging rates.•
  • SELECTION OF ADULT FOR CT SCAN.• Guideline published by NICE, National Institute for health and Clinical Excellence.• Recommended by Royal college of surgeon.
  • NICE GUIDELINEIf the patient presents out of hours and :• 1- is >65 yrs• 2-has h/o amnesia >30 minutes• 3-the presence of dangerous mechanism of injury, It is acceptable to admit for overnight observation with CT scan the next morning, unless CT scan is required with 1 hr in the presence of the above listed finding.
  • ELEVATED INTRACRANIAL PRESSURE (ICP)• associated with increased mortality and worsened outcome• Efforts to evaluate and manage increased intracranial pressure (ICP) should begin in the emergency department.• Patients with severe TBI (GCS ≤8) and clinical symptoms suggesting possible impending herniation from elevated ICP (unilateral or bilaterally fixed and dilated pupil(s), decorticate or decerebrate posturing, bradycardia, hypertension, and/or respiratory depression) should be treated urgently
  • ELEVATED INTRACRANIAL PRESSURE (ICP)Simple techniques should be instituted as soon aspossible:•Head of bed elevation to 30 degrees•Optimization of venous drainage: keeping the neck inneutral position, loosening neck braces if too tight•Monitoring central venous pressure and avoidingexcessive hypervolemia
  • HYPERVENTILATION • guidelines recommend avoiding hyperventilation, especially in the acute phase (the first 24 to 48 hours) following TBI. Mild to moderate hyperventilation can be considered at later stages, but PaCO2 of less than 30 mmHg should be avoided
  • HYPOCAPNIA AND THE INJURED BRAIN: MORE HARM THAN BENEFIT.• OBJECTIVES: Hypocapnia is used in the management of acute  brain injury and may be life-saving in specific circumstances, but it  can produce neuronal ischemia and injury, potentially worsening  outcome. This review re-examines the rationale for the use of  hypocapnia in acute brain injury and evaluates the evidence for  therapeutic and deleterious effects in this context. hypocapnia can  cause or worsen cerebral ischemia. The effect of sustained  hypocapnia on cerebral blood flow decreases progressively  because of buffering; subsequent normocapnia can cause  rebound cerebral hyperemia and increase intracranial pressure.  Hypocapnia may also injure other organs. Accidental hypocapnia  should always be avoided and prophylactic hypocapnia has no  current role. • Crit Care Med. 2010 May;38(5):1348-5
  • HYPOCAPNIA AND THE INJURED BRAIN: MORE HARM THAN BENEFIT.• CONCLUSIONS: Hypocapnia can cause harm and  should be strictly limited to the emergent management of  life-threatening intracranial hypertension pending  definitive measures or to facilitate intraoperative  neurosurgery. When it is used, Paco2 should be  normalized as soon as is feasible. Outside these settings  hypocapnia is likely to produce more harm than benefit.• Crit Care Med. 2010 May;38(5):1348-5
  • Osmotic therapy• The intravascular injection of hyperosmolar agents creates an osmolar gradient, drawing water across the blood-brain barrier.• Mannitol is administered in boluses of 0.25 to 1 mg/kg• Monitoring of serum osmolality, fluid balance, renal function, and electrolytes
  • Hypertonic saline• Hypertonic saline is being used increasingly in this setting, but with varying volumes and tonicity (3 to 23.4 percent) and either as a bolus or continuous infusion
  • Hypertonic saline• Two small studies compared mannitol and hypertonic saline in patients with TBI
  • Hypertonic saline• In one study, nine patients received two treatments each of 200 mL 20 percent mannitol and 100 Ml of 7.5 percent saline with 6 percent dextran-70 solution (HSD) in a random order .• Median ICP reductions were greater with HSD than mannitol infusion (13 versus 7.5 mm Hg).
  • Hypertonic saline• In another study, 20 patients were randomly assigned treatment with either 20 percent mannitol or 7.5 percent hypertonic saline solution, each given as a dose of 2 mL/kg.• The mean number and duration of recurrent elevated ICP episodes were higher in patients treated with mannitol than with hypertonic saline.
  • Sedation• The use of sedative medications and pharmacological paralysis are often used in patients with severe head injury and elevated ICP.• sedation may lower ICP by reducing metabolic demand.• Barbiturate coma has been used traditionally in this setting. However, there is little clinical data to support its use:
  • Sedation• a randomized trial of 73 patients with severe TBIConclusion : pentobarbital coma was associated with more effective ICP control compared to control treatment, but not improved 30-day mortality.
  • Cerebral perfusion pressure• Cerebral autoregulation is disrupted in about a third of patients with severe TBI• Patients with impaired cerebral autoregulation are described as "pressure-passive".
  • Cerebral perfusion pressure (CPP)• The difference between mean arterial pressure and ICP• CPP target is 60 mmHg, avoiding CPP >70 mm Hg and <50 mm Hg• Achieved by optimizing ICP first and then MAP (with volume expansion, pressors) second. 
  • Cerebral perfusion pressure• According to guidelines published in 2007, the recommended CPP target is 60 mm Hg, avoiding levels below 50 mm Hg and above 70 mm Hg .• In children these thresholds may be lower, 40 to 65 mm Hg .• Patients with more severely impaired autoregulation in particular may be more likely to respond to efforts to lower ICP
  • TEMPERATURE MANAGEMENT • Fever worsens outcome• Induced hypothermia has been a proposed treatment for TBI based upon its potential to reduced ICP as well as to provide neuroprotection and prevent secondary brain injury• Induced hypothermia has been shown to be effective in improving neurologic outcome after ventricular fibrillation cardiac arrest.
  • Therapeutic hypothermia• A systematic review of 12 randomized controlled trials of mild-to-moderate hypothermia (32 to 33ºC) following TBI noted a small but significant decrease in the risk of death (RR 0.81, 95% CI 0.69-0.96) or poor neurologic outcome (RR 0.78, 95% CI 0.63-0.98) among more than 500 patients treated with hypothermia.• borderline benefits for death and neurologic outcome as well as an increased risk for pneumonia .
  • Therapeutic hypothermia• therapeutic hypothermia treatment should be limited to clinical trials, or to patients with elevated ICP refractory to other therapies
  • GLUCOCORTICOIDS• The use of glucocorticoid therapy following head trauma was found to be harmful rather than beneficial.
  • A RANDOMISED PLACEBO-CONTROLLED TRIAL OFINTRAVENOUS CORTICOSTEROID IN ADULTS WITHHEAD INJURY-OUTCOMES AT 6 MONTHSMRC CRASH is a randomised controlled trail of the effect ofcorticosteroids on death and disability after head injury.Method: randomly allocated 10,008 adults with head injuryand a Glasgow Coma Scale score of 14 or less, within 8 h ofinjury, to a 48-h infusion of corticosteroid(methylprednisolone) or placebo. Data at 6 months wereobtained for 9673 (96.7%) patients. The risk of death washigher in the corticosteroid group than in the placebo group(1248 [25.7%]vs 1075 [22.3%]deaths; relative risk 1.15, 95%CI 1.07-1.24; p=0.0001), as was the risk of death or severedisability (1828 [38.1%]vs 1728 [36.3%]dead or severelydisabled; 1.05, 0.99-1.10; p=0.079).•Lancet 2005 Jun 21;365
  • A RANDOMISED PLACEBO-CONTROLLED TRIAL OFINTRAVENOUS CORTICOSTEROID IN ADULTS WITHHEAD INJURY-OUTCOMES AT 6 MONTHSThere was no evidence that the effect of corticosteroidsdiffered by injury severity or time since injury. Theseresults lend support to our earlier conclusion thatcorticosteroids should not be used routinely in thetreatment of head injury.•Lancet 2005 Jun 21;365
  • REFRACTORY INTRACRANIAL HYPERTENSION• treatment options include• Hyperventilation• barbiturate coma• induced hypothermia• decompressive craniectomy.• Hyperventilation should be avoided in the first 24 to 48 hours and should not exceed PaCO2 <30 mm Hg
  • Antibiotic Prophylaxis•Infection may occur as a complication of penetratinghead injury, open skull fractures, and complicatedscalp lacerations.•Prophylactic antibiotics may be used in thesecircumstances•are not recommended in patients with otorrhea orrhinorrhea from a basilar skull fracture
  • PEDIATRIC HEAD INJURIES• Falls are the most common mechanism• motor vehicle crashes• pedestrian and bicycle accidents• Projectiles• assaults• sports-related trauma• abuse
  • POST TRAUMATIC SEIZURE• impact seizure: Secondary to traumatic depolarization Little morbidity  Immediate: within 24 huors  Early: < 1 wk post injury  Late: > 1 wk post injury
  • POST TRAUMATIC SEIZURE• occur in fewer than 5 % of mild or moderate TBI• more common with more severe TBI• 50% occur within the first 24 hours• 25% occur within the first hour.• The earlier a seizure begins -- generalized• after the first hour -- simple partial or focal with secondary generalization.
  • POST TRAUMATIC SEIZURE• Early seizures increase the risk of post-traumatic epilepsy by fourfold, to more than 25 %• anticonvulsants are not helpful in the prevention of post-traumatic epilepsy
  • Concussion• any traumatically induced disturbance of neurological function and mental state, occurring with or without actual loss of consciousness.• significant but self limited symptoms including loss of consciousness, amnesia, and altered mental status• Normal CT
  • Concussion• The hallmarks of concussion are confusion and amnesia, often without preceding loss of consciousness
  • Postconcussion syndrome• may result from brain injury or from trauma involving head and neck structures.• include headache, dizziness, neuropsychiatric symptoms, and cognitive impairment• typically develop in the first days after mild traumatic brain injury (TBI) and generally resolve within a few weeks to a few months.
  • Second impact syndrome• Diffuse cerebral swelling is a rare but generally fatal complication of mild head injury.• The cause is hypothesized to be disordered cerebral autoregulation causing cerebrovascular congestion and malignant cerebral edema with increased intracranial pressure.• when diffuse cerebral swelling occurs after a second concussion, while an athlete is still symptomatic from an earlier concussion.
  • Return to play• Despite this uncertainty, the suggestion that a second impact may be a risk factor for this severe complication,• has led to the development of several guidelines that address concussion severity and return to play for athletes.
  • Post-traumatic headaches• Headaches occur in 25 to 78 % of patients after mild TBI• According to the International Headache Society (IHS) criteria, the onset should be within seven days after the injury.• some suggest that three months seems a more reasonable latency for onset than does seven days..
  • Post-traumatic epilepsy• Mild TBI is associated with a twofold increase in the risk of epilepsy for the first five years after injury• Seizures occurring within the first week -- are not epilepsy
  • cranial nerve injuries• The risk of injury to other cranial nerves increases with the severity of brain injury, but these are known to occur with mild TBI.
  • Cumulative neuropsychological impairment•  There is some evidence that repeated concussions can cause cumulative neuropsychological deficits (ie, increasing severity and duration of mental status abnormalities after each separate incident).
  • HERNIATION SYNDROMESUncal:• Compression of the uncus on the tentorium• CN3 palsy: dilated, fixed pupil; abnormal EOM• This may initially present as anisocoria and a sluggish pupil• Contralateral hemiparesis develops with pressure of the peduncle against the tentorium• Decerebrate posturing eventually ensues
  • HERNIATION SYNDROMESCentral Transtentorial• Caused by an expanding lesion at the vertex or frontal pole,• Begins as altered LOC, bilateral weakness and pinpoint pupils• Symptoms progress to midpoint pupils, altered respiratory patterns (Cheyne-Stokes) and bilateral decorticate/decerebrate posturing
  • HERNIATION SYNDROMESCerebellotonsillar• Tonsils herniate through foramen magnum• Sudden respiratory and cardiovascular collapse• Flaccid quadriplegia is the most common motor problem• Pinpoint pupils can be seen due to pontine dysfunction• Mortality exceeds 70%
  • HERNIATION SYNDROMESUpward transtentorial• Less common• Usually due to an expanding posterior fossa lesion• Pinpoint pupils due to pontine compression• Downward conjugate gaze with no vertical eye movements• Rapid decline in LOC
  • Warning signs should prompt the caregiver to seek immediatemedical help:•Inability to awaken the patient•Severe or worsening headaches•Somnolence or confusion•Restlessness, unsteadiness, or seizures•Difficulties with vision•Vomiting, fever, or stiff neck•Urinary or bowel incontinence•Weakness or numbness involving any part of the body
  • CONCLUSION• Traumatic brain injury is the leading cause of mortality and severe morbidity.• Early neurosurgical consultation improve the outcome• Early recognition and management of head injury• Early recognition and management impending herniation syndrome
  • CONCLUSION• Be familiar with low and high risk criteria for ICI minor head injury in adult and peadiateric age group• Prevention is better than the cure