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MED-SURG
TRAUMATIC BRAIN INJURY
| Term | Definition 1 | Definition 2 | Time Frame | Density on CT | Treatment | Mortality | Causes |
|---|---|---|---|---|---|---|---|
| TRAUMATIC BRAIN INJURY | ● Major cause of death and disability ● 10% of all deaths in the US are caused by injury and about half of traumatic deaths involve the brain ● Men are affected 3-4 times as often as women | motor vehicle accidents, fall, sports and recreation, violence | |||||
| Head injury | leading cause of death among people under the age of 24 years | ||||||
| CAUSES OF TBI ● Falls: | 28% | ||||||
| CAUSES OF TBI ● Motor Vehicle - Traffic: | 20% | ||||||
| CAUSES OF TBI ● Struck by/ against: | 19% | ||||||
| CAUSES OF TBI ● Assault: | 11% | ||||||
| CAUSES OF TBI ● Unknown: | 9% | ||||||
| CAUSES OF TBI ● Other: | 7% | ||||||
| CAUSES OF TBI ● Pedal cycle (non MV): | 3% | ||||||
| CAUSES OF TBI ● Other transport: | 2% | ||||||
| CAUSES OF TBI ● Suicide: | 1% | ||||||
| Glasgow Coma Scale (GCS) | pagod na q kakalagay dito tignan mo na lang ya | ||||||
| CLINICAL CATEGORIZATION OF RISK FOR INTRACRANIAL INJURY | ● LOW RISK FOR INTRACRANIAL INJURY ● MODERATE RISK FOR INTRACRANIAL INJURY ● HIGH RISK FOR INTRACRANIAL INJURY | ||||||
| LOW RISK FOR INTRACRANIAL INJURY | ● Asymptomatic ● Headache ● Dizziness ● Scalp hematoma, laceration, contusion or abrasion | ||||||
| LOW RISK FOR INTRACRANIAL INJURY RECOMMENDATION: | ○ Observation at home with discharge instructions ○ CT scan & skull x-ray not recommended | ||||||
| MODERATE RISK FOR INTRACRANIAL INJURY | ● History of change or loss of consciousness on or after injury ● Progressive headache ● Alcohol or drug intoxication ● Posttraumatic seizures ● Unreliable or inadequate history ● Age <2 years old ● Vomiting ● Post traumatic amnesia | ● Signs of basilar ● Signs of basilar skull fracture ● Multiple trauma ● Serious facial injury ● Possible penetration or depressed skull fracture ● Suspected child abuse ● Significant subgaleal swelling | |||||
| MODERATE RISK FOR INTRACRANIAL INJURY RECOMMENDATION: ○ Brain CT scan at the ER | ■ 8-46% of this patient may have silent hematomas ■ Skull x-ray not recommended unless CT scan is not available | ||||||
| MODERATE RISK FOR INTRACRANIAL INJURY RECOMMENDATION: ○ Observation at home if: | ■ Normal cranial CT ■ Initial GCS >14 ■ No high-risk criteria ■ No other moderate risk signs except for LOC ■ There is a responsible sober adult that can observe patient ■ Reasonable access to an ER anytime ■ No complicating circumstances | ||||||
| HIGH RISK FOR INTRACRANIAL INJURY | ● Depressed level of consciousness ● Focal neurologic findings ● Decreasing level of consciousness ● Penetrating skull injury or depressed fractures | ||||||
| HIGH RISK FOR INTRACRANIAL INJURY RECOMMENDATION: | ○ Cranial CT scan ○ Admit ■ Emergency surgery for deterioration ■ Pag sa level of sensorium something emergency something | ||||||
| SKULL FRACTURES | ● Important markers of potentially serious injury but rarely cause problems by themselves ● Prognosis depends on the nature and severity of underlying brain injury than on the severity of the skull injury | ||||||
| SKULL FRACTURES TYPES: | linear, depressed or comminuted | ||||||
| Open/compound fracture: | if the scalp is lacerated over the fracture | ||||||
| Skull Fractures - LINEAR | ● 80% of skull fractures ● Most common in the temporoparietal region ● Generally, do not require surgical intervention and managed conservatively | ||||||
| Skull Fractures - DEPRESSED | ● One or more fragments of bone are displaced inwards, compressing on the underlying brain | ||||||
| Criteria to elevate depressed fractures: | ○ >8-10 mm depression ○ Deficit related to underlying brain ○ CSF leak ○ Open depressed fracture | ||||||
| Skull Fractures - COMMINUTED | ● Multiple, shattered-bone fragments which may or may not be displaced | ||||||
| Skull Fractures - BASILAR | ● Fracture of the orbital roof, sphenoid bone, base of the occipital bone or petromastoid portion of the temporal bone ● May be linear, comminuted or depressed ● Skull x-ray < CT with bone windows | ||||||
| Basilar Skull Fractures signs: | ○ CSF otorrhea or rhinorrhea ○ Hemotympanum or laceration of EAC (External Auditory Canal) ○ Battle's sign & Raccoon's sign ○ CN injury (7,8,1,2,6) ○ Delayed meningitis | ○ Avoid NGT ○ Prophylactic antibiotics | |||||
| Otorrhea | - CSF leaks from ears | ||||||
| Rhinorrhea | - CSF leaks from nose | ||||||
| Battle’s sign | - ecchymosis | ||||||
| Basilar Skull Fractures Surgery done when: | ○ Traumatic aneurysm ○ Post Traumatic carotid-cavernous fistula ○ CSF fistula ○ Meningitis or brain abscess ○ Post Traumatic facial palsy ○ Cosmetic | ||||||
| TRAUMATIC BRAIN INJURY | ● Concussion ● Contusion ● Contrecoup injury ● Diffuse axonal injury (DAI) | ||||||
| Concussion | brief altered consciousness at the moment of impact | ||||||
| Contusion | focal parenchymal hemorrhage in areas where sudden head deceleration causes the brain to impact on bony prominence | ||||||
| Contrecoup injury | in addition to the injury to the brain directly, the force imparted to the head may cause the brain to be thrust against the skull opposite to the blow, resulting in contusion | ||||||
| Diffuse axonal injury (DAI) | a primary lesion of rotational acceleration/deceleration head injury; Cause prolonged altered consciousness following head injury in the absence of a space occupying lesion on CT | ||||||
| CEREBRAL CONCUSSION | ● Brief alteration of consciousness (e.g.<6 hours), may be unconscious or dazed ● No gross or microscopic parenchymal abnormalities ● No or minimal CT/MRI abnormalities ● Confusion, retrograde or anterograde amnesia, loss of consciousness | ● Due to transient functional disruption of the reticular activating system, caused by rotational forces on the upper brainstem | |||||
| DIFFUSE AXONAL INJURY | ● Comminuted skull fractures ● Traumatic coma lasting more than 6 hours ● No other causes of coma is identified by CT or MRI ● Single most important cause of persistent disability after traumatic brain damage | ● Widespread microscopic and macroscopic axonal-shearing injury ● Patients may remain unconscious for days, months or years and those who recover may be left with severe cognitive and motor impairment | |||||
| BRAIN SWELLING | ● Post Traumatic brain swelling is a poorly understood phenomenon that may result from several different mechanisms ○ Increased cerebral blood volume resulting from abnormal vascular dilatation ○ True cerebral edema | ○ True cerebral edema ■ Both vasogenic and cytotoxic cerebral edema can occur within hours of head injury | |||||
| Vasogenic: | extra CSF, it happens with intracranial tumors | ||||||
| Swelling of Cytotoxic edema: | intracellular | ||||||
| BRAIN HERNIATION | ● SUBFALCINE HERNIATION ● UNCAL OR TRANSTENTORIAL HERNIATION ● CEREBELLAR TONSILLAR HERNIATION | ||||||
| SUBFALCINE HERNIATION | ● Cingulate gyrus is pushed under the falx ● compression of the anterior cerebral artery and frontal lobe infarction ● Weakness of the lower extremity | ||||||
| UNCAL OR TRANSTENTORIAL HERNIATION | ● Displacement of the medial temporal lobe, including the uncal gyrus, into the tentorial opening ● Injury to outer fibers of ipsilateral oculomotor nerve ● Creasing of contralateral cerebral peduncle (Kernohan's notch) | ● Compression of the posterior cerebral artery ● Lateral flattening of the midbrain ● Rising intracranial pressure and hydrocephalus (aqueduct and 3rd ventricle) | |||||
| CEREBELLAR TONSILLAR HERNIATION | ● Downward displacement of the inferior medial parts of the cerebellar hemisphere (mainly the ventral paraflocculus or tonsilla) through the foramen magnum, behind the cervical cord | ● Episodic tonic extension and arching of the neck and back and extension and internal rotation of the limbs ● Nape pain and stiff neck ● Paresthesias in the shoulders ● Respiratory disturbance and cardiac irregularity ● Coma ● Respiratory arrest | |||||
| DELAYED DETERIORATION | ● 15% of patients who are normal initially will deteriorate in a delayed fashion ● 75% of delayed deterioration are secondary to hematomas (EDH,SDH, contusion) | ○ Posttraumatic diffuse cerebral edema ○ Hydrocephalus ○ Tension pneumocephalus ○ Seizure ○ Metabolic abnormalities ○ Vascular event (carotid dissection, SAH) ○ Meningitis | |||||
| HEMORRHAGIC CONTUSION | ● Traumatic intracerebral hemorrhage ● Considered as high density area on CT ● Occur in areas where sudden deceleration of the head causes the brain to impact on bony prominences in coup or contrecoup fashion | ● Follow-up CT often show minimal or no encephalomalacia | ○ Surgical decompression may sometimes be considered if herniation threatens | ||||
| DELAYED TRAUMATIC INTRACEREBRAL HEMORRHAGE (DTICH) | ● Usually occur within 72 hours after the trauma ● "Talks and deteriorate" ● Due to local or systemic coagulopathy, hemorrhage in necrotic brain tissue, coalescence of micro hematomas ● Same treatment but outcome poor | ||||||
| THE MENINGES | ● Dura mater ● Arachnoid mater ● Pia mater | ||||||
| EPIDURAL HEMATOMA | ● Epidural - above the dura mater (“epi” - above) ● 1% of head trauma ● Rare before age 2 or after age 60 ● A temporoparietal skull fracture disrupts the middle meningeal artery as it exits its bony groove at the pterion, causing bleeding | ● 85% arterial bleeding (MMA), rest MMV or dural sinus ● 70% occur laterally over the hemisphere with epicenter at the pterion | |||||
| EPIDURAL HEMATOMA PRESENTATION: | ○ Brief posttraumatic LOC ○ Lucid interval (several hours only) ○ Obtundation, contralateral hemiparesis, anisocoria | ||||||
| EPIDURAL HEMATOMA EVALUATION: ○ Plain skull x-ray | ■ No fracture in 40% | ||||||
| EPIDURAL HEMATOMA EVALUATION: ○ CT scan | ■ High density lenticular shape adjacent to skull ■ Uniform density & sharply defined ■ Mass effect is frequent | ||||||
| EPIDURAL HEMATOMA EVALUATION: ○ Mortality | ■ 20-55% (higher if with ASDH) | ||||||
| EPIDURAL HEMATOMA MEDICAL TREATMENT: | ○ Small (<1 cm maximum thickness ○ Subacute/chronic ● Minimal symptoms ● No evidence of herniation | ||||||
| EPIDURAL HEMATOMA SURGICAL TREATMENT: | ○ Any symptomatic EDH ○ Acute asymptomatic EDH >1cm thick ○ Pediatrics | ||||||
| ACUTE SUBDURAL HEMATOMA | ● Magnitude of impact damage is higher: more lethal ● Often associated with underlying brain injury ● Also occurs in patients receiving anticoagulants | ||||||
| 2 common causes of traumatic ASDH: | ○ Accumulation around parenchymal laceration; No lucid interval, focal signs later ○ Bridging or surface vessel torn off due to violent head motion; Brain injury may be less severe, lucid interval may occur with later rapid deterioration | ||||||
| ACUTE SUBDURAL HEMATOMA ● CT scans: | ○ Crescent-shaped mass of increased signal adjacent to inner table ○ More diffuse, less uniform & less dense | ○ Surgery: ASH >1cm at thickest point ○ Non-surgical: <1cm thickness ○ Surgery may increase brain injury if there is severe swelling with herniation through the craniotomy ○ A large craniotomy flap is often required | ○ 50-90% (higher on aged/anticoagulant) ○ Variables: ■ Mechanism of injury (motorcycle highest) ■ Age: >65 y.o. , 82% mortality ■ Neurological exam on admission (poorer GCS, poorer outcome/higher mortality) ■ Postoperative ICP: >45 mmHg, all dead | ||||
| CATEGORY: ● Acute | 1-3 days | Hyperdensity | |||||
| CATEGORY: ● Subacute | 4 days - 3 weeks | Isodense | |||||
| CATEGORY: ● Chronic: | 3 weeks - 4 months | Hypodensity | |||||
| CHRONIC SUBDURAL HEMATOMA | ● Generally, occur in the elderly (mean age: 63 yrs) ● Head trauma is only identified in <50% ● Hematoma thickness tends to be larger in older patients due to a decrease in brain weight & increase in subdural space | ||||||
| CHRONIC SUBDURAL HEMATOMA Risk Factors: | alcoholism, seizures, coagulopathies, CSF shunts & patient at risk of falls | ||||||
| CHRONIC SUBDURAL HEMATOMA Pathophysiology: | Start as acute subdural, blood evoke an inflammatory response & in-growth of new capillaries & fibrinolytic enzymes & liquefaction of blood clot | ||||||
| CHRONIC SUBDURAL HEMATOMA Clinical presentation: | ○ Minor symptoms: headache, confusion, language difficulties or TIA like symptoms ○ Degrees of coma, hemiplegia or seizures | ○ Seizure prophylaxis (short term) ○ Reverse coagulopathies ○ Surgical evacuation indicated for: ■ Symptomatic lesions ■ Maximum thickness of >1 cm | |||||
| CHRONIC SUBDURAL HEMATOMA Outcome: | ○ There is improvement once pressure is reduced close to zero (removal of 20% of the collection) ○ Patient with higher pressure tend to have more rapid brain re-expansion & clinical improvement | ○ Residual fluid collections are common on CT even after 10 days, they are only treated if patient deteriorates or do not improve or there is an increase in volume | |||||
| GUNSHOT WOUNDS TO THE HEAD | ● Accounts for the majority of penetrating head injuries ● Ultimately fatal | ||||||
| GUNSHOT WOUNDS TO THE HEAD Primary injury due to: | ○ Injury to soft tissue: scalp & facial injuries, bacteria dragged intracranially, pressure waves from gas combustion ○ Comminuted fracture of bone: 2ry missiles | ○ Cerebral injuries from missile: direct path & shockwave ○ Depend on muzzle & impact velocity | ○ General measures: ABC ○ Radiographic evaluation: Skull x-ray & CT ○ Medical treatment ■ Mannitol: for medical decompression ■ Prophylaxis w/ anti seizure medications ■ Antibiotics ■ Tetanus toxoid ○ Surgical: for less severe injured pts only | ||||
| GUNSHOT WOUNDS TO THE HEAD Goals of surgery: | ■ Debridement, hemostasis, evacuation of hematoma, remove bullet if possible |
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avemaria