Head Injury PDF - Medical Guide

- Bruising of the mastoid process (back ear) (indication of Head Injury fracture of middle cranial fossa) - CSF leak: Primary vs. Secondary Br...

- Bruising of the mastoid process (back ear) (indication of Head Injury fracture of middle cranial fossa) - CSF leak: Primary vs. Secondary Brain injury - Otorrhea (from ears) vs. - Rhinorrhea (clear fluid leaks from nose) Primary Injury: result of the initial damage - Often 1st sign of bleeding or CSF leakage - Opening into brain - Ex. contusions, lacerations, damage to blood vessels, - Complication: acceleration/decerleration injury, or foreign object penetration - Infection - esp. Open fracture - Hemorrhage - esp. depressed Secondary Injury: damage evolves after the initial insult - CN injury - 1,2,3,4,5 - Caused by cerebral edema, ischemia or chemical changes associated with trauma (similar to SCI due to system responses Mechanism of Injury - Major occurrences due to direct contact (can have rotation forces) & Primary Injury acceleration-deceleration head motion - Brain surface is not smooth it’s rough so when there is force movement in brain there might be shearing the tissue that can lead to contusions & hematomas - Coup-contrecoup Injuries Skull fractures - Coup: contusion at site of external force impact - Contrecoup: injury on opposite side of brain from rebound Simple fracture (linear) - break in bone against skull Brain Injury Types: Focal vs. Diffuse Depressed - Bone is fragmented 조각 & embedded into brain tissue - Complication: epidural hematoma - bleeding (tear in the artery) Diffuse Injuries - Surgery required Concussion Basilar - fracture at base of skull - Involves acceleration-deceleration forces - Racoon eyes (periorbital ecchymosis) - Microscpic changes in neurons (as well as in the supportive tissue) - blood from cranial cavity (head) leaks into orbits (eye) - All within 24 hour time frame - Battle sign - Often see temporary interruption of brain function  - Often involves immediate brief loss of consciousness- 1-2sec Patho - May have amnesia - if mild, might have amnesia with no - Diffuse microscopic damage to axons, disconnenction and swelling neurological manifestations or residual damage - Axons sheared/streched won’t function properly and - Usually recover within 24 hours damaged will cause swelling/cellular edema (get disconnections) Diagnostics - White matter accelerates/decelerates faster than grey - Sometimes nothing; depends on nature of presenting matter cuz of density (white matter is more dense) manifestations - Try not to do CT b/c a lot of radiation might just observe for 24 Manifestation hours to make sure it no worsening - Most often it can affect cerebral hemispheres, brainstem and lead to - CT does not show concussion (only show bleeding in the brain) immediate coma - Leading to decorticate posturing (abnormal flexion of arms Manifestations and extension of legs - may persist for months - Post concussion syndrome Diagnostics - Dizziness, - Won’t show on CT or X-Ray - headache - Cannot tx because nerve cell can’t regenerate - Irritability - Only thing that can be done is supportive care - Insomnia - Poor concentration and memory Complication Diffuse Axonal Injury (DAI) - Post traumatic dementia (in small area of the brain) - Persistent vegetative state (seen more often) Caused - By sudden deceleration or acceleration leading to rotational forces Focal Injuries that shear, stretch or tear nerve cells Contusion - Bruise on surface of brain Caused - Blunt force trauma Can be Patho - Single or multiple hits (coup-countrecoup) - Tear in middle meningeal artery (a quick bleed - artery faster than - Frontal, temporal lobes most susceptible vein) leads to collection of arterial blood - May have tiny hemorrhages and edema within - Leads brain tissue compression Manifestation Classic Pattern - Severity depends on location adn size (often have edema & often - Brief loss of consciousness followed by lucid period(LOC) then rapid develop hematoma) unconsciousness - Ipsilateral (same side) pupil dilation Treatment - Cranial nerve do not cross over - Observe for any progression & prevent any secondary brain injury - Contralateral (oppsite side) hemiparesis 마비 (ie. ischemia) Diagnosis Complications - CT Scan - classic presentation - Edema - Hemorrhage Treatment - Increase ICP & herniation - Urgent surgery to evacuate 대피 hematoma - if large contusion & a lot of edema are at risk of increase ICP Prognosis Hematomas - Good if tx - If untreated Caused - Increase ICP - Vessel injury & bleeding - Brain herniation / death Types 2.Subdural Hematoma (SDH) Collection of blood btw Dura & arachnoid (below dura) 1.Epidural Hematoma (EDH) - collection of blood btw Skull & dura Patho - Tear in bridging vein (slow bleed) occurring when brain moves Caused (accel/decler) suddenly in relation to skull - Leads to collection of venous blood - Trauma or depressed fracture  - Develops slower than EDH 3.Traumatic Intracerebral Hematoma(ICH) Collection of blood in brain tissue SDH Classifications Caused Acute: - Servere motion of brain or by contusion that develops into - Manifestations within 24 hrs of injury hematoma - Progresses rapidly - Higher risk of death due to cerebral edema, increase ICP Can be Sub Acute: - Single or multiple hits (coup-countrecoup) - Manifestations occur 2 - 10 days after injury - Frontal, temporal lobes most susceptible - May have some improvement but will deteriorate if SDH not - More frequently in elderly, alcoholics (due to vessel is friable) removed Manifestation Chronic: - Depend on size and location - Manifestations may not appear for several weeks - If large: increase ICP - Bleed is slow - May lead to brain herniation - Some may even forgot about injury - Onset is often insidious (happens right away w/o forewarning signs) - Can still be functional - Some neurological deficits & headaches Manifestation Treatment - Low level of consciousness - If able to be evacuated can do surgery but if not the prognosis is not - drowsy ,confusion, apathy(acute) so good - Headache/ Both epidural & subdural have low LOC but w/ SDH don’t have lucid period Diagnosis - CT scan Secondary Brain Injury brain is “high maintenance”➙ depend heavily on supply; uses 20% of O2, Treatment 1/6th of blood flow (cardiac output), high need for glucose & ALSO depends - Surgery to evacuate SDH on waste removal through venous circulation (CO2); w/slow blood flow wastes cannot leave Patho - Fluid escapes from capillaries into ECF; more fluid and plasma proteins leaving brain cells 1. Brain suffers traumatic injury 2. Brain swelling or bleeding & increase ICP Cytotoxic 3. Rigid cranium allows no room for expansion of contents so increase ICP 4. Pressure on blood vessels w/n brain causes blood to brain to slow Caused: cytotoxic edema; cells and impaired Na/K pump(loss ATP, cell 5. Cerebral hypoxia & Ischemia occur swelling) 6. ICP continues to rise; brain herniate (only hole out is foramen magnum) - Na into cell which H2O follow = more fluid = edema = rupture 7. Cerebral blood flow ceases 중단 8. Neurologic death Manifestation - Focal neurological deficits - Further injury to the brain occring after intial injury - LOC changes - First 72 hrs crucial - Increased ICP - Ischemia is most common cause of secondary injury Diagnosis Excitatory Amino Acid Injury (Excitotoxicity) - CT/MRI Patho Treatment 1. Prolonged ischemia depletes ATP & leads to the inappropriate release of - Mannitol glutamate - Dexamethasone 2. Excess calcium to enters cells triggering the calcium cascade - when excessive calcium triggers the release of harmful levels of neurotransmitters like glutamate, causing damage to neurons and contributing to neurodegenerative diseases such as stroke, Alzheimer's, and Parkinson's. 3. Calcium cascade leads to cell injury & death / protein damage Intracranial Pressure (ICP) Cerebral Edema - Determined by pressure-volume relationships of cranial contents - ICP can increase of one of these other components decrease - Normally the Monro-Kellie Hypothesis maintains a normal ICP 2 types - Brain tissue / Cerebrospinal fluid (CSF) / Blood - The total volume of these three components must Vasogenic remain constant because the skull cannot expand. If Caused: failure of BBB (blood-brain barrier); become more permeable one of these components increases in volume, the  other components must decrease to maintain a Cushing Reflex (triad) Late sign in H.I. stable intracranial pressure (ICP). Otherwise, ICP will increase, leading to potential damage to brain tissue - Compensatory response that attempts to provide adequate CPP in due to compression. the presence of rising ICP - Impact of ICP varies due to compliance of brain tissue - Only happens late in head injury - Compliance refers to the brain's ability to adapt to changes in volume within the skull without a significant increase in Manifestation pressure. - Hypertension - Widening pulse pressure = cushing reflex Cerebral Perfusion Pressure (CPP) directly - Cause in ICP: Increased ICP reduces cerebral blood flow, which the body tries to counteract by raising systemic blood affected by ICP pressure to maintain perfusion to the brain. As a result, the CPP=MABP-ICP (ICP usually zero) systolic pressure rises significantly, widening the pulse As ICP increase CPP decrease = leads to hypoxia & ischemia (impairs cerebral pressure. perfusion) - Bradycardia - HTN stimulates baroreceptors in aortic arch which activates PNS to slow HR Increased ICP Consequences of untreated ICP Brain Herniation - Obstruct cerebral bloodflow - Increase ICP pushes the brain out of position - Destory brain cells (neurons) - Brain tissue is compressed into: - Displace brain tissue (hernitaion) - Center of the brain - Damage brian structures - Aganist bone - Aganist rigid folds of the dura mater Earliest sign - Compression of CN III (oculomotornerve) is nearly sign - Decrease in LOC Late sign Signs of Deteriorating Brain Function - Cushing reflex (triad) - Level of consciousness - Motor Responses - Pupilary Light Responses - Respiratory Patterns Treatment - Brainscan - EEG (electroencephalogram) - Observation & Close monitoring (Always do GCS) Have to do brainstem testing to see if any of the cranial nerves are working - Adequate airways & oxygenation and have to do it TWICE (6 hrs later to make sure ther is no reflexes - Has to do with LOC (if GSC less than 8 get ready to intubate) - Manage ICP (osmotic generators like mannitol & dethamexazone) - Surgery if hematoma - Family supports - Rehab Diffuse dont show up in CT scan - negative No test on penetrating brain Persistent Vegatative State (PVS) - Absence of awareness of self and surroundings Ischemia leads to excitatory amino - Inability to interact with others - Absence of sustained or reproducible voluntary behavioural No test on prognosis responses - Lack of language comprehension - Suffcient brainstem and hypothalmus function to sustain life (but still function) - Bowel and bladder incontinence - Intact cranial nerve and spinal cord reflexes (and sleep wake cycles) - Manifestations must persist for 1 month - Required total nursing care Brain Death - Irreversible loss of function of brain - Must be due to irreversible cause Diagnosis - Cerebral angiography