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Head injuries

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  • Diastatic Skull Fracture The skull of infants and children are not completely solid until they grow older. The skull is composed of jigsaw-like segments (cranial fissures) which are connected together by cranial sutures. Skull fractures that separate the cranial sutures in children prior to the closing of the cranial fissures are termed "diastatic skull fractures". Cribiform Plate Fracture The cribiform plate is a thin structure located behind the nose area. If the cribiform plate is fractured, cerebral spinal fluid can leak from the brain area out the nose. Can cause damage to the nerves and blood vessels that pass through the opening at the base of the skull
  • Fractures occurring in posterior cranial fossa – temporal bone. Figure 63-2 Basilar fractures allow cerebrospinal fluid to leak from the nose and ears. Adapted from Hickey, J. V. (2003). The clinical practice of neurological and neurosurgical nursing (5th ed.). Philadelphia: Lippincott
  • Halo sign: testing for CSF when blood is mixed with possible CSF. Place drop of fluid on white pad – blood will coalesce and CSF will leave a yellowish ring if possible.
  • Otorrhea signifies a tear in the dura
  • Periorbital ecchymosis Nerve damage for the sense of smell or eye functions may occur.
  • Of clients admitted to ER, 50% have evidence of alcohol or substance abuse. Most are male< 30 years of age.
  •    Mechanism of Injury.   The brain is somewhat mobile within the spiny interior of the skull. Under normal circumstances the delicate brain is protected from contact with the spiny contours of the skull. This protective barrier is known as cerebrospinal fluid. It surrounds the brain, and under normal circumstances, cushions the brain from contact with its hard, spiny shell.      However, when the head is subjected to violent forces, such as those exerted in: automobile accidents;  violent shaking or whiplash;  forceful falls and blows; the brain may sustain permanent damage. Such damage results from the delicate brain being forcibly rotated and battered within the spiny skull, also known as, the brain vault. During such episodes brain tissue is ripped, torn, stretched, battered and bruised.  Such battering is followed by bleeding, swelling and bruising of brain tissue.  Sometimes the brain can recover from such insults without any apparent consequences.  In other cases the resultant difficulties can last a lifetime. 
  • Concussion: ( a sudden transient mechaincal head injury with disruption of neural activity and a change in loc) May experience only dizziness and feel “dazed”. Retrograde amnesia Treatment involves observing patient for headache, dizziness, lethargy, irritability and anxiety. Client should resume normal activities slowly and the following should be watched for: difficulty in awakening or speaking, confusion, severe headache, vomiting or weakness on one side of the body. May or may not show up on CAT scan. Can cause diffuse axonal type injury resulting in permanent or temporary damage Blood clot can occasionally occur causing death Months to years to heal
  • Contusion: Depends on which areas of the brain damaged – cerebral hemispheres, brain stem (RAS) If widespread injury, abnormal eye movement and motor function, increased intracranial pressure and herniation - poor outcome. May have residual damage, seizures
  • The image below shows a lateral view of the brain with contusions (hemorrhagic necrosis) at the frontal poles, and along the temporal lobes.
  • Diffuse Axonal Injury There is extensive tearing of nerve tissue throughout the brain. This can cause brain chemicals to be released, causing additional injury. Experiences immediate coma, decerebrate & decorticate posturing, and global edema The tearing of the nerve tissue disrupts the brain’s regular communication and chemical processes. This disturbance in the brain can produce temporary or permanent widespread brain damage, coma, or death. A person with a diffuse axonal injury could present a variety of functional impairments depending on where the shearing (tears) occurred in the brain.
  • Hematomas . often have delayed effects as the subsequent swelling of the brain causes increased intracranial pressure, distortion and herniation of the brain. Signs and symptoms depend on size of area affected and the speed with which the hematoma develops.
  • Locations of intracranial hemorrhages.
  • Epidural hematomas occur between the skull and the dura. Occurs in 10% head injuries and usually associated with skull fracture Often caused by a rupture or lacerations of the menigeal artery that leads to continuous bleeding, separation of dura from skull and compression of brain. Usual sequence is loss of consciousness, client awakens followed by change in LOC, change in pupil reactivity and eye movement paralysis on same side as hematoma., then coma.
  • Onset of symptoms is somewhat slower because bleeding is venous.
  • Bleeding directly into the brain tissue Often caused by things that stab wounds, bullet wounds, and may be caused by systemic hypertension. May be difficult to treat surgically because of location. Rx includes supportive care, management of ICP, fluids, electrolytes, and anti-hypertensives.
  • Oculocephalic (Doll’s Eye reflex) Only done on unconscious patients, & never in unconscious pts with ? C-spine injury Is movement of the eyes in the direction opposite to that in which the head is moved. Abnormal reaction: eyes remain in fixed position in skull when head is turned. The reflex is absent or impaired in patients with brain stem problems. Oculovestibular (caloric test) Only performed if oculocephalic responses are absent. Tests CN III, IV, VI, & VII Instillation of ice water or warm water should result in deviation of eyes either toward (ice water) or away (warm) from irrigated ear. Absence of movement indicates brain death. Do not perform in conscious Pt. or ruptured tympanic membrane.
  • Change in vital signs is a late manifestation! Ongoing monitoring for changes is imperative!!
  • Read and know the care of clients post-craniotomy!
  • Ongoing assessment: Level of consciousness and responsiveness with the Glasgow Coma Scale. Level of cognitive functioning (example pg 1683, Smeltzer & Bare) Vital Signs Other neurologol signs
  • Because the GCS is based on client’s ability to respond and communicate, you would not use it under the following conditions: Client is Intubated Eyes are swollen shut Client is unable to speak English Blindness Aphasic Paralyzed or hemiplegic
  • The total of the 3 scores can range from 3-15. Example: client who is unresponsive to painful stimuli; does not open eyes; & has complete muscle flaccidity has a score of 3. A score of less than 7 is interpreted as coma. Neuro assessment sheets will include along with the Glasgow Coma: Voluntary motor control - In the cooperative alert client voluntary motor is assessed for symmetry vs. symmetry – right and left side. 2) Cranial nerve function pupils EOMS Blink reflex Facial symmetry 3) Vital signs including temperature & respiratory pattern 4) Speech – clear, slurred, rambling, aphasic
  • IICP is associated with decreased LOC, hypercapnia, and potential for PE. Hypotonic solutions move water into the cell!
  • Goals of ICP Monitoring: Maintain CPP 50-70mmHg Maintain ICP < 20 Monitor for evanta (rebleed, herniation)
  • Sedation to reduce metabolic demand
  • It acts by increasing osmotic pressure of the glomerular filtrate, inhibiting reabsorption of water and electrolytes. This elevates blood osmolality, drawing fluid from the interstitial spaces & brain cells into the blood. Diuresis is expected.
  • Transcript

    • 1. Head Injuries Zafar Iqbal Sr. LecturerJinnah College of Nursing Karachi
    • 2. Head Injury Causes Causes – Motor vehicle accidents Motor vehicle accidents – Firearm-related injuries Firearm-related injuries – Falls Falls – Assaults Assaults – Sports-related injuries Sports-related injuries – Recreational accidents Recreational accidents
    • 3. Road Traffic Crashes
    • 4. Sports injuries
    • 5. Assaults(Sickle injuries)
    • 6. MECHANISM BLUNT INJURY  High Velocity  Low Velocity PENETRATING INJURY  Gunshot  Sharp instruments
    • 7. Head Injury High potential for poor outcome Deaths occur at three points in time after injury: – Immediately after the injury – Within 2 hours after injury – 3 weeks after injury
    • 8. Types of Brain Injury
    • 9. Types of Head Injury  Scalp injury : minor injury resulting in laceration, abrasion & hematoma  Skull injury : may occur with or without damage to brain.  Brain injury
    • 10. Head Injuries Closed or blunt: blunt object damages the brain and its coverings without actually perforating the skull or dura. Penetrating: when the skull and brain are directly lacerated by an object such as a bullet, or piece of bone. Coup-Contrecoup Injuries : same blow causes injury on opposite sides of the brain.
    • 11. Skull Fractures Linear Skull Fracture: is a break in the continuity of the bone, appear as thin lines on X-ray. Depressed Skull Fracture - The broken piece of skull bone is pressed towards or embedded in the brain. Comminuted and Compound Skull Fracture - The scalp is cut and the skull is splintered, multiple fractures. Basilar Skull Fracture The skull fracture is located at the base of the skull and may include the opening at the base of the skull
    • 12. Skull Fractures
    • 13. Basilar fractures
    • 14. Some Signs of SkullFractures – CSF or fluid draining from ear (“halo” sign) – Blood behind tympanic membrane – Raccoon Eyes: periorbital ecchymoses – Battles Sign: bruise over mastiod process – Cranial nerve and inner ear damage
    • 15. Battles’ sign  Often occurs in fractures at base of skull (posterior cranial fossa).  Large "black and blue mark" looking areas below the ear, on the jaw and neck.  It may include damage to the nerve for hearing.  CSF Otorrhea: cerebral spinal fluid may leak out of the
    • 16. Raccoon Eyes  The skull fracture produces "black and blue" mark looking areas around the eyes.  CSF Rhinorrhea: cerebral spinal fluid may leak into the sinuses and out of nose.
    • 17. Otorrhea
    • 18. Traumatic Brain Injury
    • 19.  Traumatic brain injury (TBI) isAn insult to the brain, caused by an external physical force, that may produce physical, intellectual, emotional, social and vocational changes. Major causes of TBI motor vehicle accidents, falls, acts of violence, sports & recreational injuries, blows to head, child abuse (shaken baby syndrome).
    • 20. Mechanisms of BrainInjury  Acceleration injury occurs when the immobile head is struck by a moving object.  Deformation injury : the force results in deformation and disruption of the impacted part, (skull fracture)
    • 21. Mechanisms Cont’d Deceleration injury : head is moving and hits an immobile object (car accident-hitting steering wheel) Acceleration-deceleration injury : moving object hits immobile head and then head hits immobile object. Associated with rotation injury where brain is twisted in the skull (whiplash).
    • 22. Injuries  Blunt  Penetrating  Coup- Contrecoup
    • 23. Types of Brain Injury Concussion: is a head trauma that may or may not result in loss of consciousness (for 5 minutes or less) and retrograde amnesia. Contusion: is a severe injury in which the brain is bruised resulting in swollen brain tissue, areas of hemorrhage, infarction, necrosis, edema. Results in loss of consciousness and symptoms of shock.
    • 24. Concussion May experience only dizziness and feel “dazed”. Retrograde amnesia Treatment involves observing patient for headache, dizziness, lethargy, irritability and anxiety. Client should resume normal activities slowly and the following should be watched for: difficulty in awakening or speaking, confusion, severe headache, vomiting or weakness on one side of the body. May or may not show up on CAT scan. Blood clot can occasionally occur causing death Months to years to heal
    • 25. Contusion Depends on which areas of the brain damaged – cerebral hemispheres, brain stem (RAS) Can cause diffuse axonal type injury resulting in permanent or temporary damage If widespread injury, abnormal eye movement and motor function, increased intracranial pressure and herniation - poor outcome. May have residual damage, seizures
    • 26. Contusion resulting innecrosis
    • 27. Diffuse Axonal Injury:severe widespread injury to axons in the cerebral hemispheres, corpus collosum and brain stem.
    • 28. Diffuse Axonal Injury Extensive tearing of nerve tissue throughout the brain causing the release of chemicals, causing additional injury. Immediate coma, decerebrate & decorticate posturing, and global edema The tearing of the nerve tissue disrupts the brain’s regular communication and chemical processes producing temporary or permanent widespread brain damage, coma, or death. A person with a diffuse axonal injury could present a variety of functional impairments depending on where the shearing (tears) occurred in the brain.
    • 29. IntracranialHemorrhage Intracranial hematomas are collections of blood that develop within the cranial vault. Three kinds: epidural, subdural & intracerebral
    • 30. Types of CerebralHemorrhage
    • 31. Meninges Epidural Scalp Hematoma: mostly arterial Skull (blood collects Dura matter b/t the skull & Arachnoid the dura mater of the brain) Pia Brain tissue grey white
    • 32. Subdural hemorrhage - usuallyScalp venous (bloodSkull collects b/t theDura matter dura & the arachnoid mater). May be classified as acute, subacute or chronic.
    • 33. Acute & Subacute SubduralHematoma Usually result from brain or blood vessel laceration Symptomatic within 24 to 48 hours of injury Symptoms include loss or variable levels of consciousness, headache, irritability, increasing signs of increased ICP (increased BP, decreased pulse, slowing respiratory rates) Requires prompt treatment!
    • 34. IntracerebralHematomaBleeding directlyinto the braintissue.
    • 35. Diagnostic Tests CT or MRI: data on structural causes such as tumor or hemmorhage. -Metabolic – will be unremarkable LP: infection or bleeding (cloudy or bloody) EEG: structural or metabolic, seizure activity Lab tests: LFTs, kidney function, glucose levels, toxicology, ABGS
    • 36. Diagnostic Tests for Abnormal Reflexes Oculocephalic reflex response – abnormal if eyes remain in fixed position when head turned Oculovestibular reflex response – absence of eye movement when water instilled in ear = brain death
    • 37. * Level of consciousness is *the single most importantindicator of neurologicalfunction and change*
    • 38. Medical Management Prompt recognition and treatment of hypoxia & acid-base disorders (why?) Control of increasing ICP resulting from increased cerebral edema and expanding hematoma Surgical treatment – Burr holes – Craniotomy
    • 39. Burr holes
    • 40. Craniotomy (Pre)
    • 41. Craniotomy
    • 42. Craniotomy
    • 43. Post Head Injury Observe for 24 hrs Take to emergency if any of following:: – decreasing LOC (confusion, drowsy) – loss of consciousness/inability to wake – vomiting – convulsions – bleeding or drainage from ears/nose – weakness or loss of sensation in arm or leg – blurring of vision/slurring of speech – changes in pupil
    • 44. Nursing Assessment: Brain Injury ABCDs Maintaining airway History if possible Determine LOC, ability to respond to verbal commands, reactions to tactile stimuli, status of reflexes. Glasgow Coma scale Fluid and electrolyte balance Monitoring/managing potential complications
    • 45. The Glasgow Coma ScaleThe Glasgow Coma Scale (GCS) is a universally used neurological assessment tool to assess degree of consciousness impairment. CGS measures eye, verbal, and motor response. It is an excellent scale to measure arousal. It is less helpful related to content measurement. Know the difference b/ content & arousal
    • 46. GLASGOW COMA SCALE SCORE (GCS)Eyes 1 Closed at all times 2 Opens to pain 3 Opens to voice command A score of 10 or less 4 Open spontaneously indicates a need forMotor 1 No response emergency 2 Extension (decerebrate) attention 3 Flexion posturing (decorticate) 15 (top score) 4 Flexion withdrawal 5 Localizes painful stimulus A score less than 7 6 Obeys commands is interpreted asVerbal 1 No response coma 2 Incomprehensible sounds 3 Inappropriate words 4 Disoriented and converses 5 Oriented and converses
    • 47. Nursing Diagnoses – Altered Tissue Perfusion – Risk for Suffocation/Aspiration – Altered Oral Mucous Membranes – Risk for Impaired Skin Integrity – Risk for Contractures – Altered Nutrition: Less than Body Requirements – Fluid volume deficit – Risk for Injury – Altered family processes
    • 48. Nursing management – Maintaining the airway – Protecting the patient – Fluid balance – Mouth care, skin and joint integrity – Corneal integrity – Thermoregulation
    • 49. Emergency Care ABCs Airway maintenance, intubation with oxygenation (PO2 > 90mmHg), mild hyperventilation – avoid hypercapnia. Ensure adequate fluid however avoid lowering the blood osmolarity. Initial neuro assessment and Glasgow Coma Scale Etiology of the brain injury will dictate further evaluation & treatment
    • 50. Emergency Care Cont’d osmotic diuretics (mannitol IV) steroids (controversial) vasoactive medication (100-150mmHg systolic) elevate HOB (30 degrees) sedate as needed (barbituates IV) drain CSF (keep ICP < 20) maintain fluid status (normal serum Na &
    • 51. Nursing Management Cont’d Administer prescribed meds to reduce ICP: barbituates, mannitol analgesics, narcotics Maintain fluid balance with NaCl or RL solution Avoid noxious stimuli (explain) Maintain cerebral perfusion pressure >70mmHg Maintain normal body temperature – avoid hyperthermia
    • 52. Osmotic Diuretic (Mannitol) Reduces cereberal edema by osmotic dehydration. Preferred b/c it is confined to extracellular space & does not normally cross an intact blood brain barrier. Carefully monitor vitals, CVP, B.P, intake & output, catheter patency, signs of fluid overload, eye response /acuity & electrolyte imbalance?? Why?? NOTE: If blood-brain barrier is damaged the medication enters the brain and increases swelling!!