EpidemologyHead injury Number One Killer in Trauma 25% of all trauma deaths 50% of all deaths from MVC 200,000 people every year inthe world live with thedisability caused by theseinjuries
Indian Head Injury Foundation India – highest rate of head injuries in the world Yearly 1,00,000 lives lost with 1 million suffering fromsevere head injury 1 out off 6 trauma victim dies in India ; in USA thefigure is 1 out off 200 RTA (road traffic accidents) most common causefollowed by falls and assault Motorcylist and pedesticians most common victims ofRTAs
In the year 2050India will have the highest number of automobiles onthe planet , overtaking USA
Etiology Road traffic accidents (RTA) – most common cause Falls Sports injury Assault Gun shot wounds to head
Basic Anatomy Scalp Skull Meninges Dura Mater Arachnoid Pia Mater Brain Tissue CSF and Blood
Dictates that “the total volume ofthe intracranial contents MUSTremain constant”The MONROE KELLIE doctrine
Brain Physiology Brain Metabolism :1.Brain oxygen consumption (CMRO2, cerebralmetabolic rate for oxygen) – 3.5 ml per 100 g per min2.90% of energy from blood glucose Cerebral blood flow (CBF) :CBF is 55 ml per 100g per minautoregulated over mean arterial pressure range of 50 -150 mm of Hg
Intracranial Pressure The pressure of the brain contents within the skull isintracranial pressure (ICP) The pressure of the blood flowing through the brain isreferred to as the cerebral perfusion pressure (CPP) The pressure of the blood in the body is the mean arterialpressure (MAP) Cerebral Perfusion Pressure (CPP) can be determined bythe following formula:CPP = MAP - ICP
Primary Brain Injury :-occurs at the time of impact- mechanical damage which is irreversible- causes permanent mechanical cellular disruptionand microvascular injury.-includes 1) cerebral contusions2) diffuse axonal injuries (DAI)3) cerebral lacerationsPATHOPHYSIOLOGY
Secondary Brain Injury occurs at some time after the moment of impact often preventable Prevention of secondary brain injury results inimproved neurological outcome after head injury may make the difference between independentsurvival and dependent survival/death.
Brain suffers from traumaticinjuryBrain swelling or bleedingincreases intracranial volumeRigid cranium allows no room forexpansion of contents so ICPincreasesPressure on blood vessels withinthe brain causes blood flow to thebrain slowlyCerebral hypoxia and ischemiaoccursIntracranial pressure continuesto rise. Brain may herniateCerebral blood flow decreases
Basilar skull fractures Usually diagnosed on CT imaging or on clinicalevidences Clinical signs include Battle sign ,Raccoon Eyes andCSF leak. May or may not be associated with seventh and eighthcranial nerve injury
INTRACRANIAL LESIONSEpidural hematoma Collection of blood & clot b/n dura mater and bones ofthe skull Source Middle Meningeal ArteryDural Venous Sinuses C/F Brief loss of consciousness, headache,drowsiness, dizziness ,nausea, vomitting Rapid clinical deterioration
Classical presentation seen only in 1/3 rd cases On CT scan lentiform hyper dense lesion betweenskull and brain Associated with mass effect on underlying brain withor without midline shift. Overall mortality rate 18% in all cases but only 2% inisolated EDH
Acute subdural Hematoma Accumulates in space between dura and arachnoid Disruption of cortical vessels or brain lacerationproduces hematoma A/w significant primary injury- patients present withimpaired conscious level from the time of injury CT scan –hyperdense concave lesion spreading acrossbrainmidline shift disproportionate to size of lesion Mortality rate as high as 40% in some series
Subarachnoid Hemorrhage Trauma is most common cause followed by Aneurysms Rarely aneurysmal hemorrhage immediately precedestrauma. Most can be managed conservatively
Chronic subdural Hemorrhage Usually occurs in elderly on anti coagulant or antiplatelet agents h/o minor head injury in weeks or months prior topresentation Small bridging veins tear and cause small clinicallysilent ASDH ,when hematoma breaks down andincreases in size mass effect is produced c/f- headache, cognitive impairment, focalneurological deficit and seizures. CT scan – acute blood (0-10 days) = hyperdense- sub acute blood (10-14 days) = isodense- chronic blood (>2 weeks) =hypodense
Acute on chronic SDH Chronic SDH will more recent hemorrhage independant (posterior) areas. Treatment is Burr hole evacuation rather thancraniotomy
Cerebral contusions Coup and counter coup injuries Most commonly affecting inf frontal fossa andtemporal lobes CT appears heterogeneous with mixed areas of highand low density Rarely require immediate surgery Observation for 48-72 hrs
Concussion Temporary & brief interruption of neurological functionafter minor head injury Due to shearing / stretching of white matter fibres at thetime of impact or temporary neuronal dysfunction C/o headache, confusion, amnesia CT/MRI cannot detect 3 grades (Colorado Grading)grade I- symptoms for 15 mins no LOC , only confusiongrade II-symptoms for > 15 mins ,no LOC, amnesiagradeIII- LOC present Medical opinion should be sought in Grade II and III
DAI Diffuse Axonal Injury Disruption of axons in white matter and brainstem Injury occurs immediately and is irreversible Seen after MVC or shaken baby syndrome Usually have persistent sequlae e.g. cognitiveimpairment, spasticity etc. 90% pts with severe DAI will be vegetative CT usually normal MRI with multiple, diffuse abnormalities Hemorrhagic spots classically seen over corpuscallosum, dorsolateral midbrain.
This is early triage mostly done by paramedics Core of ATLS system and constitutes ABCDE of traumacarePRIMARY SURVEY
Airway maintenance with cervical spine protection
Intubation with Cervical inline stabilization Breathing and ventilation : Intubation precautionsPre-medicate with Lidocaine, 1mg/kg IV 2 minutesprior to attempt Laryngoscopy produces an ICP Spike
MANAGEMENT OFMILD HEAD INJURY (GCS14 -15) History General Examination Limited Neurologic Examination C-spine and other X-rays as indicated CT scan?? Discharge with advice
Patient can be discharged if following criteria are metbefore discharge1.GCS must be 15/152.no focal neurological deficit3.accompanied by responsible adult4.verbal and written advice given
Aim is prevention of secondary brain injury Achieved by avoidance of hypoxia and hypotension CT scan after complete stabilization of patient. Early neurosurgery consult if intracranial hematomaseen Measures to reduce ICP (reverse Trendelenburg) i.e.head up position by 20-30 degrees ? ICP monitoring Mannitol during transport.MANAGEMENT OF MODERATE HEADINJURY(GCS 9-12)
MANAGEMENT OF SEVERE HEAD INJURY(3 -8 ) Primary Survey and Resuscitation Secondary Survey and ‘AMPLE’ history Admit to facility – neurosurgical care Neurologic Re-evaluation Eye opening Motor response Verbal response Pupillary reaction
CT scan only after hemodynamic stabilization Medical therapy for raised ICP Immediate neurosurgeon opinion If needed surgical management
MEDICAL THERAPIES FOR HEAD INJURY Head end elevation – 30 deg Intravenous fluids: Maintain normovolemia Hypotonic/glucose containing fluidsshould not be used Serum sodium levels monitored daily
Mannitol 0.25-1g/kg Osmotic agent- dec ICP, maintains CBF,CPP and brainmetabolism Dec ICP within 6 hrs. Expands volume, O2 carrying capacity. Diuretic effect- net intravascular volume is reduced.
Furosemide To reduce ICT in conjunction with mannitol Dose 0.3 to 0.5 mg/kg Never use in Hypovolemia
Hypertonic Saline Improves CPP and brain tissue O2 levels Decreased ICP by 35% (8-10 mm HG) CPP increased by 14% MAP remained stable Greatest benefit in those with higher ICP and lower CPP Repeated doses were not associated with rebound,hypovolemia or HTN 30 mL of 23.4% over 15 minutes
HYPERVENTILATION No role as prophylaxis in 24 hrs. Reducing PaCO2 cerebral vasoconstriction Maintain PaCo2 25 – 35 mmhg Last resort for reducing ICP TEMPORARY MEASURE ONLY.
Barbiturates Effective in reducing ICP – refactory to other measures Not used in presence of hypotension/hypovolemia
Surgical Management of SpecificHead injuries Various guideline followed Guidelines For Surgical Management of TraumaticBrain Injury Published in 2001 All new reports and literature regularly updatedthrough Neurosurgical Evidence Based MedicineCentre ,University Of Washington.
Depressed skull Freacture Indications of operative treatment1.gross wound contamination2.significant intracranial hematoma3.gross cosmetic deformity4.frontal sinus involvement5.dural penetration6.depression > 1cm7.wound infection8.pneumocephalus Elevation and debridement – method of choice
Fracture Skull Base With CSF leaksno acute surgery required for CSF leakfor first 72 hrs observation (elevation of head)if leak persiststemporary CSF diversion (lumbar drainage orventriculostomy)Still leak persists surgery to be done Exploration of floor of frontal fossa with closure ofdural defect
EDH Absolute indications of surgery (regardless of GCS)1. > 30 ml vol of hematoma2. > 15 ml thickness of blood clot3. midline shift >5 mm4. anisocoria ( > 1mm) If GCS <8 = immediate surgery If GCS > 8 = as soon as possible If size less than above but GCS <8 = surgery If size less than above but GCS >8 =nonoperativemanagement can be done Mean time of EDH for reexpansion is 8 hrs -36 hrs.
SDH Absolute indication of surgery1. > 10 mm thickness of blot clot2.Midline shift > 5mm If size less than above but GCS <8 along with1. GCS decreased by 2 from time of injury toadmission2. Pt. with asymmetric or fixed dilated pupils3.ICP >20 mm of Hg If size less than above and GCS >8 = non operativetreatment. If planned surgery should be within first 4 hrs Craniotomy with duraplasty with or without bone flapremoval
Posterior Fossa Lesions No monitoring possible because of location Guidelines for evacuation1. > 3cm clot on CT scan2. any size of clot with ASDH or EDH
Penetrating Brain Injury Meningitis and abscess most common complicationsfollowed by Seizures If grossly contaminated wound then craniotomy anddebridement required Small clean wounds with no scalp devitalization can bemanaged conservatively If open sinus suspected repair should be done If dural injury suspected repair should be done.
Burr hole Pentrator Burr hole bit Bone rongeur Scalpel
ProcedureA burr hole is placed onthe side of the dilatingpupil.In the absence of a CTscan, the burr hole isplaced 2 finger widthsanterior to the tragus ofthe ear and 3 finger widthsabove the tragus of the ear.
A vertical incision is made approximately 3cm long, centered over the entry point allthe way down to the temporalis muscledividing the fibers of the muscle vertically.The periosteum is then cut in the samemanner.
The outer table of the skull is drilled with thepenetrator
If there continues to be excessive bleedingthrough the hole, packing the wound shouldbe tried with Gel foam or by cutting off a pieceof temporalis muscle and stuffing it into thehole.
Decompressive Craniectomy Controversial Used in patients without focal lesion and raised ICPwho are refractory to maximum medical management The operation involves removing a large section ofskull and opening the dura, allowing the swollen brainto expand underneath the scalp The bone flap is stored and can be replaced 3–6months later when the patient has made a goodneurological recovery and the brain swelling hasresolved
Long term sequelae of Head Injury Neurorehabilitation Neuropsychology – after minor head injuries such asheadache, dizziness, impaired short term memory,concentration etc. Seizures –prophylactic anticonvulsants cant prevent longterm seizures Delayed CSF leak –CT cisternography or CT isotope studiescan be done
Seizure Disorder 2% Early post-traumatic incidence Increased to 30% in children, alcoholics and withintracranial hematoma Prophylactic antiepileptics reduce early occurrence Use not supported by the literature Concussion- Brief LOC - Vertigo - Nausea- Dizziness - Headache - Vomiting- Photophobia - Cognitive/Memory dysfunction
Concussion Up to 80% may have symptoms at 3 months 15% may have symptoms at 1 year Persistence of these symptoms is termed PostconcussiveSyndrome 85-90% recover after 1 year Risk factors:- Female - Litigation - Low socioeconomic status