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Brain Injury Dr. Shema Dr.


Case presentation:
‡ NA ‡ 18 Y/O ‡ Muganda ‡ From Nsambya ‡ DOA-17/9/2010 ‡ NOK- N B(mother) PC: Vomiting Cut wound on head all 2ry to being knocked by a motorcycle while crossing the road. No h/o ENT bleeding ROS-unremarkable PMH-index admission, no chronic illnesses, no known drug allergies. PSH- unremarkable FSH-un employed,BF a 6/12 baby

O/E: FGC, mild pallour,not jaundiced, afebrile CNS: semi comatose, PEARL, GCS-12/15 CVS:PR-72 regular BP-130/80mmhg HS-Normal RS: RR-18bpm, not in distress, normal air entry PA: N fullness, soft, non tender, no organomegally, N bowel sounds Dx: closed moderate head injury

Inv: Skull xray Ct scan-open head injury and cerebral oedema but no increased ICP Hb gp n xmatch Mgt: Sts T.T 0.5mls stat Caps ampiclox 500mg qid x5/7 i.V mannitol 100ml 8hrlyx3/7 i.M diclo 75mg stat Follow up: 2nd day-no photophobia c/o- severe frontal headache up to date and vomits. GCS-15/15,BP-110/70mmhg,PR-78bpm

1. Cerebral Trauma
Objectives: ‡ Define primary and secondary injury
± Discuss types of each

‡ Discuss evaluation of head injured patients ‡ Discuss management of head injured patients
± Medical ± Surgical

‡ Understand concept of brain death

secondary injury 1. Secondary damage (after the original incident) -e.g.Primary vs. Primary damage (at the time of impact) impact) 2. brain edema. hypoxia. hypotension« .

Primary injuries .

Classification of primary injuries .

Linear fracures: Most common type. Surgery (to elevate bone fragments) is indicated if significant cosmetic deformity or if there is an underlying hematoma with significant mass effect. B. Heal expectantly Depressed skull fracture: As with linear skull fractures. .Skull fractures A. depressed fractures are usually treated non-operatively.

. Role of antibiotics controversial. May have blood behind tympanic membrane on otoscopy or bloody discharge from ear. Delayed facial palsy (from swelling of VII in petrous bone) may occur. If tympanic membrane is disrupted. May have hearing loss which is usually conductive (secondary to blood/CSF in middle ear) and less often sensorineural (from disruption of inner ear). Patients present with Battle·s sign (bruise at mastoid) or Racoon·s eyes (periorbital ecchymosis). Complete resolution with expectant management in vast majority of cases.Basal skull fracture Basal skull fracture: Most commonly extends through petrous bone. may have CSF otorrhea.

directly below area of impact on the skull. the patient has ´contra-coupµ frontal contusions. opposite side of the brain from area of direct impact.Brain contusions Occipital fracture Contusions: May be ´coupµ i. the patient fell backwards.e. slamming the frontal lobes into the frontal bones. or ´contracoupµ i. In the above example. . The brain ´bouncedµ inside the skull. sustaining a linear skull fracture to the occiput.e... Thus.

outside of the brain) ± Epidual ± Subdural ‡ Acute ‡ Chronic ‡ Intra-axial (i. involves brain paranchyma) ± Intracerebral hematoma .Hematomas ‡ Extra-axial (i.e..e..

dilated pupil.Epidural hematoma Epidural hematoma: Young patient. Excellent outcome if surgical intervention (craniotomy) is prompt. followed by brief ´lucid intervalµ. Classic presentation is loss of consciousness. hemiparesis). . often a child or teenager. Classically caused by a linear fracture of the squamous temporal bone that disrupts underlying middle meningeal artery. in contrast to subdural hematoma which is venous.g. then rapid neurological deterioration with localizing deficits (e. The epidural hematoma is ARTERIAL in origin.

Presentation is usually decreased level of consciousness and associated localizing neurological findings (dilated pupil.Subdural hematoma. hemiparesis). . patient may not have a skull fracture. acute Acute subdural: Usually an adult with a history of significant trauma. Surgical outcome typically poorer than epidural hematoma. Emergent craniotomy indicated if subdural is large enough to cause mass effect/neurological deficit. Unlike epidual hematoma.

chronic Chronic subdural: Typically elderly patients with underlying brain atrophy. Most chronic SDH·s are able to be evacuated with simple burr hole drainage (because chronic blood is liquefied). Superficial cerebral veins tethered to inside of skull get ´strechedµ and leak small amounts of blood chronically. Often no history of significant trauma. Often have no lateralizing findings on clinical exam.Subdural hematoma. fib found on the Floor at home . Especially at risk are patients on anticoagulants. 82 yo male on warfarrin for a.

Surgery (craniotomy) is indicated if significant mass effect causing progressive neurologic deficit.Intracerebral hematoma Intracerebral hematoma: Traumatic intracerebral hematomas may be acute or the result of hemorrhagic conversion of a brain contusion. Most small ICH·s are treated non-operatively. Tiny hemorragic contusions are called ´petechial hemorrhagesµ .

Concussion: ± ± ± ± ‡ ‡ Brief loss of consciousness or altered level of consciousness No focal neurological findings Normal CT scan Often have post-concussion syndrome Headache.Diffuse brain injury 1. Repeated concussions require abstinence from sports for period of time. nausea. . malaise that lasts days-weeks Symptomatic management ± Avoid sports until symptoms subside.

Diffuse axonal injury ± ± ± ± Severe brain injury resulting from high speed accelerationdeceleration. therefore CT may appear completely normal MRI may disclose small petechial hemorraghes or contusions. usually around midline structures such as corpus callosum Very poor prognosis .Diffuse brain injury 2. Diffuse shearing of axons changes are at microscopic level.

Secondary injury .

Classification of secondary injuries .

Intracranial pressure (ICP) ‡ Normal = about 10 mm Hg (wide range) ‡ Abnormal > 20 mm Hg ‡ Grave > 40 mm Hg .



Brain herniation .

Cerebral perfusion pressure (CPP) ‡ More important than ICP in preventing secondary injury ‡ CPP is basically the arterial inflow pressure to the brain minus the venous outflow pressure from the brain ± ICP ~ venous outflow pressure because CSF is absorbed into venous blood CPP = Mean arterial pressure ICP To prevent secondary injury. neurosurgeons try to keep: CPP > 70 mm Hg ICP < 20 mmHg MAP > 90 mm Hg .

Cerebral blood flow (CBF) ‡ More important than CPP in preventing secondary injury ± However. therefore we use CPP as a rough guide to CBF ‡ CBF is normally tightly controlled by a process known as autoregulation CBF = CPP CVR ‡ Normal = 50 ml/100g/min ‡ EEG fades < 25 ml/100g/min ‡ Cell death < 10 ml/100g/min *NB: CVR = cerebral vascular resistance . it is difficult to measure CBF.

Mechanisms that govern autoregulation become disturbed in head injured patients Normal zone of autoregulation In altered autoregulatory response. greater CPP is required to maintain the same CBF .

Evaluation and management of head injured patients .

breathing and circulation.First thing. . and then«««««. remember ABC Airway.

as in neurological THIS IS IMPORTANT ² YOU NEED TO KNOW THE GLASGOW COMA SCALE!!!!!!! .D = deficit or disability.

Tentorial (uncal) herniation Classically presents with: Ipsilateral IIIrd nerve palsy (dilated pupil. deviated ´down and outµ) Contralateral hemiparesis (from compression of ipsilateral cerebral peduncle) False-localizing hemiparesis = Kernohan·s phenomenon (from compression of contralateral cerebral peduncle against the tentorium) .




***Remember. GCS less than (or equal to) 8 = INTUBATE (for airway protection) .


best verbal response is groaning. Right hemiparesis and dilated left pupil.Case example 65 to woman. Eyes open to pain. . alcoholic. fell down. does not follow commands but localizes pain on the left.

and postop .Same patient. comparing pre.

Mannitol ‡ Indications for mannitol ± Signs of herniation (e.. fixed or dilated pupil.g.25-1 gm/kg ‡ Hypovolemia should be avoided by fluid replacement with normal saline . hemiparesis) ± Progressive neurological deterioration ± ICP > 20mmHg ‡ Intermittent boluses more effective than continuous infusion ‡ Effective doses: 0.

Hypertonic (3%) saline ‡ Head injured patients often develop hyponatremia. ± Some studies claim hypertonic saline is more effective than mannitol at lowering ICP . usually not secondary to SIADH ‡ An increase in serum sodium concentration significantly decreases ICP and increases CPP ‡ Many centers now using hypertonic saline in patients with an exhausted response to mannitol.

Hyperventilation ‡ Chronic prolonged hyperventilation therapy (PaCO2 of 25 mm Hg or less) is discouraged in current practice ± Has negative effect on autoregulation curve. CSF drainage. and osmotic diuretics (see second teir therapies) . paralysis. and ultimately. cerebral blood flow ‡ Mild hyperventilation (PaCO2 30-35 mm Hg) may be necessary for ± brief periods when there is acute neurological deterioration ± longer periods if there is high ICP refractory to sedation.

Glucocorticoids ‡ Not recommended for head injury on the basis of randomized controlled trials (Class I evidence) .

seizure within 24 hrs after injury . penetrating head injury.g. depressed skull fracture.Anti-Seizure Prophylaxis ‡ Phenytoin or carbamazepine ‡ May be used to prevent early post-traumatic seizure (i. hematoma.. cortical contusion. seizures occuring up to 7 days post-injury) in high-risk patients: ± e.e. GCS < 10.

contusion.ICP monitoring ‡ Requires surgical placement of either an external ventricular drain or a parenchymal device ‡ Indicated for most patients with severe head injury (GCS 3-8). especially if CT scan shows an abnormality such as a hematoma. edema or compressed basal cisterns .

tight spine collar) Sedation +/.General measures to control ICP ‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡ Avoid hypotonic intravenous fluids (hypotonic fluids contribute to cerebral edema) Control body temperature (prevent hyperthermia) Seizure prophylaxis Elevate head of bed Avoid jugular venous outflow obstruction (e.g.pharmacological paralysis Adequate O2 Maintain adequate blood pressure (CPP > 70 mm Hg) .

Treatment algorithm for elevated ICP ‡ ± ± ‡ ± ± ± ± 1st tier therapies: CSF drainage (if external ventricular drain in place) Mannitol and/or hypertonic saline 2nd tier therapies Barbiturates (if pt is hemodynamically stable) Hypothermia Hyperventilation Decompressive craniectomy (controversial) .

negative calorics. Angiogram. positive apnea test (no respirations despite PaCO2 > 60mmHg) ± Requires independent assessment by 2 physicians to make the diagnosis (usually a neurosurgeon or neurologist + the ICU attending) ‡ Questionable cases require ancillary testing (e. but patient is legally dead ‡ Must pass a rigorous clinical protocol to make this diagnosis. no metabolic disturbance.g..Brain death ‡ Heart continues to beat.g. no drugs that depress the central nervous system. cerebral blood flow studies. no hypothermia. no response to pain. organ donor card) and/or next-of-kin . EEG) ‡ Patients that meet criteria for brain death are candidates for organ donation ± Requires consent of patient (e. including: ± Fixed dilated pupils. no corneal response. negative doll s eyes. no spontaneous respirations.

And finally . An example of the ³Saskatoon epidemic´! .

27 yo man stabbed in the head with a knife. The knife handle was removed. .








Postop ² mild hemiparesis (resolved by 6 weeks) .

Thank you for listening! Any comments? .