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Head injury
 

Head injury

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  • Intracranial problems include injuries and increased ICP.
  • Majority of head injury deaths occur immediately from direct trauma or from massive hemorrhage and shock. Deaths occurring in a few hours are caused by progressive worsening of head injury or from internal bleeding. Note of changes in neuro status and surgery are critical in prevention of deaths at this point. Deaths 3 weeks or more after injury result from multisystem failure.
  • Can be like fainting all the way to unarousable, all ranges in between. Not a diagnosis or disease, but manifestation of many pathophysiologic processes: trauma, metabolic disturbances, mass lesions, infections. Care focuses on determining and correcting cause, maintaining function, protection from injury and hazards of immobility
  • Scalp is very vascular and bleeds freely when lacerated. Children may develop shock from briskly bleeding scalp wound. Head injuries are common in child abuse. Suspect abuse when no clear explanation of cause, if story is inconsistent with injury, or suggests child performed activity not age-appropriate. Pay attention to setting. If abuse suspected, follow procedures for your area. As a general rule, if you have an adult patient with a scalp injury who is in shock, look for another cause for shock (such as internal bleeding). However, do not underestimate blood loss from a scalp wound. Most bleeding from scalp can be easily controlled in field with direct pressure if your exam reveals no unstable fractures under wound.
  • IMAGE: Scalp laceration. Notice linear fracture on visible skull. Skull injuries can be linear nondisplaced fractures, depressed fractures, or compound fractures. Suspect an underlying skull fracture in adults who have a large contusion or darkened swelling of scalp. Very little can be done for skull fractures in field except to avoid placing direct pressure upon an obvious depressed or compound skull fracture. Open skull fractures should have wound dressed, but avoid excess pressure when controlling bleeding.
  • Basilar skull fracture indicated by any of following: Bleeding from ear or nose Clear or serosanguineous fluid running from nose or ear Swelling and/or discoloration behind ear (Battle’s sign) Swelling and discoloration around both eyes (raccoon eyes) Battle’s sign can occur from immediately following injury to within 1–2 hours postinjury. Raccoon eyes are a sign of anterior basilar skull fracture. Through thin cribriform plate in upper nasal cavity and allow spinal fluid and/or blood to leak out. Raccoon eyes with or without drainage from nose are an absolute contraindication to inserting a nasogastric tube or nasotracheal intubation.
  • In a brain injury via acceleration, the skull moves directly away from the blow. The brain rapidly changes from a stationary to a moving state. The injury to the brain results in bruising from impact, as well as cellular damage due to the sudden change in motion.
  • When the brain becomes injured because of a sudden stop in motion, it is an injury of deceleration. An example is when the child’s head hits a car windshield. Here, the skull stops immediately, but the brain continues moving toward the point of impact resulting in cellular damage.
  • Coup and contracoup injuries, also referred to as cerebral contusion, result from a rapid, violent movement of the brain. In a coup injury, the brain is damaged at the impact site. In contracoup, the injury occurs on the side directly opposite the impact.
  • IMAGE: Knife impaled in skull. IMAGE: X-ray of gunshot to head. Tissue destruction is seen in light area. NOTE: Reference to Mechanism of Injury (from Scene Size-up lecture). Remember: Velocity injuries (missiles) cause additional damage due to the shock wave of expanding tissues (temporary cavity). Penetrating objects in skull should be secured in place (impaled object) and patient transported immediately. Unless there is a clear entrance and exit wound in a perfectly linear path, assume that bullet may have ricocheted and is lodged in neck near spinal cord.
  • Forces that can cause a skull fracture can also cause a brain injury. Treat brain injury with adequate oxygenation and maintain perfusion.
  • Major trauma includes contusions and lacerations, usually with closed injuries. Contusion frequently at site of fracture. Coup-contrecoup occurs because of mass movement of brain inside skull. Injury at site of direct impact of brain on skull and opposite side from injury.
  • Neurologic emergency, usually caused by fracture crossing a major artery in the dura. Arterial tear develops rapidly and under high pressure: unconscious at scene, brief lucid interval, decreased LOC. HA, N/V. acute arterial bleeding has these typical signs: unconscious at scene, regains consciousness briefly, then nonresponsive. May have venous or arterial origin. Subdural hematoma usually venous in origin, much slower to develop mass large enough to produce symptoms, may be acute, subacute, chronic. Chronic develops over weeks or months after minor head injury, peak incidence in 60s and 70s, brain atrophy causes tension on structures, may tear. Head trauma only 60-70% of cases. Intracerebral hematoma usually from rupture of vessels in frontal and temporal lobes at time of injury.
  • Initial response of injured brain is to swell. Bruising or injury causes vasodilatation with increased blood flow to injured area, and thus an accumulation of blood that takes up space and exerts pressure on surrounding brain tissue. There is no extra space inside skull. Swelling of injured area increases intracerebral pressure and eventually decreases blood flow to brain that causes further brain injury. Increase in cerebral water (edema) does not occur immediately, but develops over hours. Only significant opening through which pressure can be released is foramen magnum at base, where brain stem becomes spinal cord.
  • Manifestations usually brief, patient usually discharged to notify if symptoms persist or behavior changes noted. Family should be taught to notify if decreased level of consciousness
  • Post-concussion syndrome: 2 weeks to 2 months after concussion. Persistent HA, lethargy, personality and behavior changes, short attention span, decrease short term memory, changes in intellectual ability. May be the beginning of a more serious, progressive problem.
  • LOC reflects the integrity of the brain as a whole, even subtle changes can be significant. Excess sleepiness can indicate increased ICP is developing. Evaluate LOC and compare with previous findings: include arousability, content of consciousness, speech. Determine the level of stimulus needed to arouse the patient (verbal, touch, shaking?) Content of consciousness: orientation Ability to follow commands: stick out your tongue, let go of my fingers Speech: clear, coherent, slurred, garbled, aphasic, incomprehensible sounds, no effort to speak Report changes immediately!
  • Brain itself is insensitive to pain. HA often continuous, but worse in the morning, straining or movement may exacerbate.
  • Nonspecific sign of IICP.
  • Compression of oculomotor nerve result in dilation of pupil, sluggish or no response to light, inability to move eye upward, ptosis of eyelid. A fixed, unilaterally dilated pupil indicates herniation of the brain. Signs of dysfunction of other cranial nerves are: blurred vision, diplopia, changes in extraocular eye movements.
  • Motor ability is controlled by nerve tracks originating in the frontal lobes of the brain, with fibers passing through the brain stem to the spinal cord before going to the muscles of the body. Distortion of brain tissue along these pathways can cause motor dysfunction. Patient may exhibit localization to painful stimulus or withdraw from it. Motor strength and tone are assessed in all 4 exxtremities. Decorticate posturing now called abnormal flexion, decerebrate posturing now called abnormal extension.
  • It may be difficult to identify IICP as cause of a coma, loss of consciousness confuses signs, makes it difficult to see the progress of IICP. Studies to identify the presence and cause of IICP. MRI and CT have revolutionized diagnosis of IICP, can differentiate many conditions that can cause IICP.
  • Because of confusion and ambiguity about terms describing altered states of consciousness, GCS developed in 1974. 3 areas assessed respond to definition of coma as inability to speak, obey commands, or open eyes with verbal or painful stimulus. Specific responses are given a number, can be graphed to see if patient is stable, improving, deteriorating. Nurse responsibility is to elicit the best response on each of the scales, higher scores mean higher level of brain functioning. Fully alert person is 15, 8 or less indicates coma. GCS is specific and structured, saves time by using number ratings rather than lengthy descriptions, can discriminate between different or changing states. GCS assess arousal aspect of consciousness.
  • Always assess circulation and respirations first! Other neuro assessments are pupillary checks, extremity strength testing, corneal reflex testing.
  • Mannitol is an osmotic diuretic, used to increase serum osmolarity so fluid is drawn into vascular space from interstitial space in cells, then excreted by kidneys. Has greatest effect on normal brain tissue, decreases bulk. Use in-line filter when administering mannitol because it tends to precipitate into crystals. Indwelling catheter necessary due to rapid diuresis, need for accurate monitoring, minimize patient activity. Anticipate effects in 5-15 minutes, lasting for several hours.
  • Drug therapy to reduce cerebral metabolism, decreases cerebral blood flow and ICP. High dose barbiturates (probably phenobarb) decrease metabolism, decrease ICP, reduce cerebral edema, produce more uniform blood supply to brain. May use Dilantin, seizures increase ICP. Infuse within 1 hour, tends to precipitate, don’t infuse with dextrose.
  • Must meet nutritional needs, regardless of state of consciousness or health. Early enteral feeding following brain injury improves outcomes. Patient with IICP is in hypermetabolic and hypercatabolic state, needs glucose for metabolism of injured brain. Need nutritional replacements within 3 days after injury. May need added salt, minerals, free water to meet fluid needs. Malnutrition promotes continued cerebral edema!
  • Controversy about whether patients should be in state of moderate dehydration: may be effective to reduce cerebral, fluids restricted to 65-75% of normal. But---hypovolemia may result in decreased CO and BP, may have impact on cerebral perfusion and oxygen delivery to brain, dehydrated patients do not respond well to vasoactive drugs. May use 5% dextrose in water for piggyback meds, .45% or .9% NS for IV solution
  • Base ventilatory support on basis of gases, be aware if moderate hyperventilation is desired. Disturbances have adverse effect on ICP. Especially monitor: glucose, sodium, potassium, osmolality.

Head injury Head injury Presentation Transcript

  • Head Injury Dr Mohamed EL Hady. Senior Neurosurgeon Specialist K S H
  • Head Injury 44% 5% 21% 11% 6% 12% 1% CARS MOTORBIKES DOMESTIC WORK SPORTS OTHER CAUSES UNKNOWN Causes
  • Head Injury  Any trauma to the  Scalp  Skull  Brain  Head trauma includes an alteration in consciousness.
  •  Common major trauma  4 million people experience head trauma annually  Severe head injury is most frequent cause of trauma death  At Risk population  Males 15-24 males 2x as likely as women  Infants  Young Children  Elderly Head Injuries
  • Head Trauma  Usually signifies craniocerebral trauma  Includes alteration in consciousness  High potential for poor outcome  Death at injury  Death within 2 hours after injury  Death 3 weeks after injury
  • Consciousness  State depends on intact cerebral hemispheres  Reticular activating system (RAS) in the brain stem midbrain hypothalamus and thalamus  Impairment on conscious level occurs due to any lesions in the cerebral hemispheres or in the (RAS)
  • RAS is located in brain stem RAS
  • Unconsciousness  An abnormal state in which patient is unaware of self or environment  Can be for very short time to long term coma  Care is designed to  Determine the cause  Maintain bodily functions  Support vital functions  Protect patient from injury
  • Different Types of Injury Head Injury Cranial Injury Brain Injury
  • Head Injuries Scalp wound • Highly vascular, bleeds briskly  Shock: child may develop  Shock: adult another cause • Management  No unstable fracture: direct pressure, dressings  Unstable fracture: dressings, avoid direct pressure 10Head Trauma -
  • Skull fracture • Linear nondisplaced • Depressed • Compound Suspect fracture • Large contusion or darkened swelling Management • Dressing, avoid excess pressure • Before operating Head Injuries 11Head Trauma -
  • Cranial Injury  Trauma must be extreme to cause fracture  Linear  Depressed  Open  Impaled Object
  •  Basal Skull  Unprotected  Spaces weaken structure  Relatively easier to fracture
  • Cranial Injury  Basal Skull Fracture Signs  Battle’s Signs  Retroauricular Ecchymosis  Associated with fracture of auditory canal and lower areas of skull  Raccoon Eyes  Bilateral Periorbital Ecchymosis  Associated with orbital fractures
  • Basilar Skull Fracture Battle’s sign Raccoon eyes 15Head Trauma -
  • Raccoon eyes
  • Cranial Injury  Basilar Skull Fracture  May tear dura  Permit CSF to drain through an external passageway  May mediate rise of ICP  Evaluate for“Halo” sign
  • Mechanism of injury Non- missile or closed head injury Acceleration – decelaration Coup - counter coup
  • 191919 Acceleration o Direct blow to the head o Skull moves away from force o Brain rapidly accelerates from stationary to in- motion state causing cellular damage Acceleration 19
  • 202020 Deceleration o Head impacts to a stationary object (e.g., car windshield) o Moving skull stops motion almost immediately o However, brain, floating in cerebral spinal fluid (CSF), briefly continues moving in skull towards direction of impact, resulting in significant forces that damage cells Deceleration 20
  • 212121 Coup/Contracoup Injury resulting from rapid, violent movement of brain is called coup and contracoup. This action is also referred to as a cerebral contusion. o Coup: an injury occurring directly beneath the skull at the area of impact o Contracoup: injury occurs on the opposite side of the area that was impacted Coup injury Contracoup injury 21
  • Direct Brain Injury Types  Coup  Injury at site of impact  Contrecoup  Injury on opposite side from impact
  • Mechanism of injury Missile or penetrating injuries
  • Crainial Injuries Penetrating trauma 24Head Trauma - Bullet fragments
  • Head Trauma - 26 Forces that cause skull fracture can also cause brain injury.
  • Brain Injury  As defined by the National Head Injury Foundation  “a traumatic insult to the brain capable of producing physical , intellectual, emotional, social and vocational changes.”
  • Focal brain injury Brain contusion Bruises on the brain
  • Brain contusion  Contusion – bruising of brain tissue  Has area of necrosis infarction and hemorrhage  Often from coup - contrecoup injury  Seizures are common after contusion
  • Focal brain injury •Blood between skull and duramater •Arterial bleed •period of lucency •relatively uncommon •present in 1% of all head-injured patients Epidural hematoma
  • Focal brain injury  Epidural hematoma  Comes from bleeding between dura and inner surface of the skull  Will be unconscious, then awake, and then deteriorate ( lucid interval )  Headache, nausea and vomiting  Needs surgical intervention to prevent brain herniation and death
  • Focal brain injury Subdural hematoma > Between the dura mater and the piaarachnoid mater > Occurring in approximately 30% of severe head injuries
  • Subdural Hematoma - - - Usually bleeding is from veins, so bleeding is GENERALLY slower than epidurals  CAN be from arteries and these require IMMEDIATE removal  Administration of anticoagulants is one of the causes of CHRONIC TYPES esp. in the elderly.
  • Focal brain injury Intracerebral hematoma Can even appear 24 hours following initial insult
  • Traumatic Subarachnoid Hemorrhage  Most common CT finding in moderate to severe TBI  If isolated head injury, may present with headache, photophobia and meningismus  The outcome depends on the Size of bleed  Timing of CT  Nimodipine reduces death and disability by 55%
  • Traumatic Subarachnoid Hemorrhage
  • Brain Injury Response to injury • Swelling of brain  Vasodilatation with increased blood volume  Increased ICP • Decreased blood flow to brain  Perfusion decreases  Cerebral ischemia ( hypoxia) 39Head Trauma -
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  •  Cushing’s Reflex  Increased BP  Bradycardia  Irregular respirations Signs & Symptoms of Brain Injury Vomiting  Without nausea  Projectile Body temperature changes Changes in pupil reactivity Decorticate posturing
  •  Pathophysiology of Changes  Frontal Lobe Injury  Alterations in personality  Occipital Lobe Injury  Visual disturbances  Cortical Disruption  Reduce mental status or Amnesia  Retrograde  Unable to recall events before injury  Antegrade  Unable to recall events after trauma  “Repetitive Questioning”  Focal Deficits  Hemiplegia, Weakness or Seizures Signs & Symptoms of Brain Injury
  • Minor Head Trauma  Concussion –patient may not lose consciousness  Will be a brief change in LOC, patient may not remember the event and will have headache  Post-concussion syndrome is 2 weeks to 2 months after injury
  • Post Concussion Syndrome  Persistent headache  Lethargy  Personality changes  Short attention span  Decreased short-term memory  When patient is discharged after concussion nurse should instruct family on what to watch for and when to call Dr.
  • Clinical Manifestations of head injury  Change in level of consciousness is the most sensitive and important indicator of neuro status  May be pronounced or subtle  Early signs may be nonspecific: restlessness, irritability, generalized lethargy
  • Clinical Manifestations  Headache  From compression on the walls of cranial nerves, arteries and veins  Worse in the morning  Straining and movement makes worse
  • Clinical Manifestations  Vomiting  NOT preceded by nausea- “unexpected”  May be projectile
  • Clinical Manifestations  Ocular signs  Pupil changes are from pressure on third cranial nerve  Pupils become sluggish, unequal. This is because of brain shift. May also be pressure on other cranial nerves
  • Clinical Manifestations  Decrease in motor function  May have hemi paresis or hemiplegia  May see posturing – either decorticate or decerebrate  Decerebrate – more serious from damage in midbrain and brainstem  Decorticate – from interruption of voluntary motor tracts
  • Decerebrated and Decorticted
  • Diagnostic Tests  CT  MRI  Transcranial Doppler studies  Looking for vasospasm  EEG  No lumbar puncture if there is IICP because sudden release of pressure can cause brain to herniate  ABG’s – keep O2 at 100% and PCO2 as related to ICP (25-35)
  • Diagnostic Tests  Cervical spine x-ray  You must see from 1 – 7 to see that they have no injury  Glasgow Coma Scale (GCS)
  • Glasgow coma scale  First described in 1974 by Graham Teasdale and Bryan J. Jennett Lancet 1974, 2:81
  • Glascow Coma Scale  Used to document assessment in three areas  Eyes opening  Verbal response  Motor response  Normal is 15 and less than 8 indicates coma
  • Glasgow coma scale
  • Minor Head Injury: 13-15 Moderate Head Injury: 9-12 Severe Head Injury (Coma): <= 8 Categorize of head injury
  • Other Assessment  Assess bodily function including respiratory,and circulatory  Pupil checks – are pupils equal and how they react to light  Extremity strength  Corneal reflex test
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  • Principles of emergency management  First priority is -  Ventilation  Circulation  Stabilize cervical spine  Limited time for initial evaluation of neurological status  Treatment of hemorrhagic shock takes precedence over neurosurgical procedures
  • Emergency Management-Initial  Airway  Stabilize cervical spine  Oxygen administration  IV access (2 large bore catheters), LR or NS  Control external bleeding with pressure  Assess for rhinorrhea, otorrhea, scalp wounds  Remove clothing
  • Secondary Trauma Survey  After patient relatively stable  Look for coexisting other organ injuries  Complete neurological examination  Severity of head injury classified by GCS score.
  • Drug Therapy  Mannitol – Rapid short acting diuretic that decreases ICP. Decreases total brain water content  Watch fluids and electrolytes closely  Don’t give in cases of renal failure or if serum osmolality increased
  • Drug Therapy  Barbiturates – causes decrease in metabolism and ICP. Causes reduction in cerebral edema and blood flow to brain.  Watch for hangover effects and drowsiness. Side effects make it harder to check LOC. Watch for constipation – do not want patient straining. Skeletal muscle paralyses may be used (Pavulon) Antiseizure drugs - Dilantin
  • management  Treatment principles  Prevent secondary injury in the brain  Timely diagnosis  Surgery if necessary  Craniotomy  Craniectomy  Cranioplasty  Burr-hole
  • Nutrition  Patient need higher amounts of glucose to survive.  Will need nutritional support quickly.  Watch sodium if on Mannitol – may need to give additional salt.  Also may need additional free water if dehydrated
  • Nutrition  Fluid balance is controversial  Do not want too dry  Keep normavolemic  Give saline either .45% or normal saline – not glucose to help prevent additional cerebral edema
  • Laboratory Work  ABGs regularly  Electrolytes daily
  • Rehab  Most head trauma requires rehab  Some rehab units do coma management  Patient may have trouble swallowing and need speech therapy  Patient may agitate easily and act out sexually  May be a flight risk and have to be in a locked ward until passes through the agitation phase
  • Elderly  At risk for head trauma from falls  Be alert if patient has fallen and is taking anticoagullants