Head injury


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Laith Ali Jebur
Baghdad University
Alkindy College Of Medicine

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Head injury

  1. 1. 1 HEAD INJURY by Zainulaabdeen Saad Laith Ali M.B.CH.B Baghdad University Alkindy College Of Medicine
  2. 2. Introduction  Trauma is the third most common cause of death.  Head injury contributes significantly to the outcome in over half of trauma-related deaths.  It is the most common cause of death in young adults (age 15–24 years)  Males > females.  Account for 3.4% of all presentations  incidence = 450 cases /100 000/ year.  About 4 million people experience head injury annually.  around 500 000 children with head injury attend hospital every year and head injury admissions account for nearly 10% of all pediatric hospital admissions.  Head injury associated with traumatic brain injury (TBI) occurs with an incidence of 20–40 cases per 100 000 population per year.  Road traffic accidents (RTAs) are the most common cause of TBI followed by falls and assaults. 2
  3. 3. Pathological processes  Direct trauma  Cerebral contusion  Intra-cerebral shearing: The rotational injury will cause shear forces that result in tearing of axons and myelin sheaths  petechial hemorrhages.  Cerebral edema  intracranial hemorrhage  Hydrocephalus: either communicating or non-communicating 3
  4. 4. Classification  Glasgow Coma Scale (Eye, Verbal, Motor) for adults & children • Minimal • Mild • Moderate • Severe • Critical  Blunt (closed) vs. penetrating (open) • Penetrating: Low or high velocity 4
  5. 5. Glasgow Coma Scale 5 The Glasgow coma scale gives a numerical value to the three most important parameters of the level of consciousness—opening of the eyes, best verbal response and best motor response Best eye opening Spontaneous To speech To pain Non 4 3 2 1 Best verbal response Oriented Confused Inappropriate words Incomprehensible sounds Non 5 4 3 2 1 Best motor response * Obey command Localizes pain Withdrawal Abnormal flexion (decorticate) Abnormal extension (decerebrate) Non 6 5 4 3 2 1
  6. 6. Children's Glasgow Coma Scale Ocular response Spontaneous 4 To speech 3 To pain 2 Verbal response Smiles, orientated to sounds, follows objects, interacts Cries but consolable, inappropriate interaction Inconsistently inconsolable, moaning Non 1 6 4 Motor response Infant moves spontaneously or purposefully Infant withdraws from touch 3 Infant withdraws from pain Inconsolable, agitated 2 No verbal response 1 Abnormal flexion to pain for an 3 infant (decorticate response) Extension to pain (decerebrate 2 response) No motor response 1 5 6 5 4
  7. 7. Glasgow Coma Scale… Cont.  If the patient is not eye opening or obeying commands in response to verbal stimuli, then a painful stimulus must be applied. Where?  The best possible score is 15/15 and the worst possible score is 3/15.  The best score is obtained during the examination. E.g.  Written as E V M  A patient who is eye opening to painful stimuli, saying occasional words and flexing to pain has a GCS of ??  If a patient is intubated then the verbal score is ‘T’. E.g. 7T/15 7
  8. 8. Classification.. Morphological  Scalp injuries  Skull fractures • Skull vault fractures (openclosed, linearcomminuted, depressed nondepressed, Ping-Pong fracture) • Skull base fractures  Brain injuries • Direct injury (primary) 1. Focal:  Cerebral Contusion  Intracranial Hemorrhage (EDH, SDH, SAH, ICH, IVH)  Direct trauma to cranial nerves or blood vessels 2. Diffuse: Concussion and Diffuse Axonal Injury • Indirect injury (secondary) ?? 8
  9. 9. Scalp injury  laceration or bruising  Scalp is characterized by high vascularity (children may develop shock) but if you faced shocked adult you should seek another cause or underlying major injury  Scalp hematoma include 3types: • Sub-cutaneous • Sub-aponerotic • Sub-pericranial 9
  10. 10. Vault fractures  A skull vault fracture is considered significantly depressed if the inner table fragments are depressed by at least the thickness of the skull.  A depressed fracture  may cause focal neurological signs.  Many patients never lose consciousness  intracranial hematoma  progressive neurological deterioration.  If the depressed fracture is compound  risk of infection. 10
  11. 11. Diastatic skull fracture  occur when the fracture line transverses one or more sutures of the skull causing a widening of the suture.  Usually seen in infants and young children  can also occur in adults (the lambdoid suture) 11
  12. 12. Skull base fractures Anterior cranial fossa fracture  It may cause tearing of the basal dura resulting in a fistula into the frontal, ethmoid or sphenoid sinuses causing CSF rhinorrhea.  An intracranial aerocele is proof of a fistulous connection.  They are often occult radiologically but diagnosed clinically.  Subconjunctival hemorrhages  Periorbital hematomas or ‘raccoon eyes’ indicate subgaleal hemorrhage and not necessarily a base of skull fracture  Anosmia  Nasal tip paraesthesiae  CSF rhinorrhoea: may be difficult to diagnose. early stages: CSF needs to be differentiated from a bloody nasal discharge how??. Late: ddx. Allergic rhinitis  CSF rhinorrhoea diagnosed by: • Testing for sugar or B2-transferrin • CSF isotope scans • High-resolution CT scan  CSF rhinorrhoea may not become apparent for a few days after the head injury or CSF leakage may cease 12
  13. 13. 13
  14. 14. Skull base fractures… Cont. Middle cranial fossa fracture  Longitudinal: • CSF otorrhea or rhinorrhea how?? • Haematotympanum • Ossicular disruption • Conductive hearing loss • Carotid cavernous fistula • Epistaxis  Transverse: • Battle sign • Sensorineuralhearing loss • 7th&8th cranial nerve palsies • Vertigo and nystagmus Posterior cranial fossa fracture  Bruising over suboccipital  cranial nerve injuries 14
  15. 15. The double ring sign  the fluid from ear or nose placed on filter paper and a "halo" or double ring may be seen. 15
  16. 16. Cerebral contusion  the coup or contre-coup  Sudden acceleration/deceleration  brain slides forwards and backwards over the ridged cranial fossa  The inferior frontal lobes and temporal poles are the commonest affected areas.  Contusion may lead to intracerebral hematoma  mass effect  focal neurological deficit  hemiparesis  speech disorder  memory abnormalities  visual dysfunction 16
  17. 17. Epidural hematoma  Hematoma that accumulates in the space between bone and Dura  It is nearly always associated with a skull fracture  The most common site is temporal bone (thinnest + MMA)  They are not always arterial  The force required to sustain a skull fracture can be surprisingly small  The classical presentation of an EDH is initial injury followed by a lucid interval (headache but is fully alert and orientated with no focal deficit) After minutes or hours a rapid deterioration occurs. Why?? 17
  18. 18. Subdural hematoma Acute subdural hematoma  SDH accumulates in the space between the Dura and the arachnoid.  Disruption of a cortical vessel or brain laceration  SDH is nearly always associated with a significant primary brain injury.  Patients with SDH usually present with an impaired conscious level from the time of injury, but further deterioration can occur. Why?? Chronic subdural hematoma  it is usually occur in the elderly (esp. anti-coagulant or antiplatelet)  There is usually but not always a history of minor head injury in the weeks or months prior to presentation.  small bridging veins tear and cause a small acute SDH, which is clinically silent. As the hematoma breaks down it increases in volume, leading to a mass effect on the underlying brain. 18
  19. 19. Subarachnoid haemorrhage  trauma is by far the commonest cause of subarachnoid haemorrhage overall.  Headache (sudden onset of a severe headache of a type not previously experienced by the patient)  Diminished conscious state  Meningism (Neck stiffness, vomiting, photophobia, fever)  Focal neurological signs  Fundal changes • Subhyaloid haemorrhage • Retinal haemorrhage • Papilloedema 19
  20. 20. Intracerebral hemorrhage  Traumatic intracerebral haematomas occur as a result of a penetrating injury (such as a missile injury) or a depressed skull fracture, or following a severe head injury  60% from small contusions coalesce to form larger hematoma.  Transtentorial Herniation lead to midbrain bleed.  The Commonest sites for ICH are anterior temporal and inferior frontal lobes (impact against lateral sphenoid bone/ floor of ant fossa). 20
  21. 21. Intraventricular hemorrhage  hemorrhage into ventricle may occur from tearing of the choroid plexus at the time of injury or rupture of intracerebral clot into the ventricle.  It occurs particularly in childhood and is usually part of an overwhelming head injury. 21
  22. 22. Cranial nerves  The cranial nerves may be injured by: • direct trauma by the skull fracture • movement of the brain • cerebral swelling.  The olfactory nerves  The optic nerve  The oculomotor nerve (direct trauma or by brain herniation)  The sixth cranial nerve  Facial paralysis  The eighth nerve (Vertigo and nystagmus) 22
  23. 23. Cerebral concussion  It results from closed injury to the brain  slight brain distortion &temporary cerebral dysfunction without organic structural damage.  Temporary LOC (<24 H)  Autonomic abnormalities)  Retrograde short-term amnesia  temporary lethargy  Irritability  Cognitive dysfunction. 23
  24. 24. Diffuse Axonal Injury Moderate Diffuse Axonal Injury  It is caused by the same mechanism as concussion.  In addition to minute bruising of brain tissue.  It is characterized by unconsciousness or persistent confusion, loss of concentration, disorientation, retrograde & antegrade amnesia, visual and sensory disturbances, mood or personality changes. Sever diffuse axonal injury  The brain injury occurs as a result of mechanical shearing at the gray /white mater interface, following sever acceleration –deceleration that lead to disruption & tearing of axon myelin sheath  The patient presents with prolonged loss of consciousness without space occupying lesion, cushing’s reflex, decorticate or decerebrate posturing. 24
  25. 25. Non specific clinical features Increased intracranial pressure  Compresses brain tissue  Herniates brainstem • Headache – most common – generalized in nature • Nausea – vomiting (projectile) • Blurring of vision • Papilledema • Hypertension • Bradycardia • Ataxia • Cranial nerve paralysis 25
  26. 26. Non specific clinical features Brain Injury  Frontal Lobe Injury: Alterations in personality  Occipital Lobe Injury: Visual disturbances  Cortical Disruption: • Reduce mental status • Amnesia (Retrograde or Antegrade)  Focal Deficits: Hemiplegia, Weakness, Decorticate posturing or Seizures  Cushing’s Reflex (Increased BP, Bradycardia, Erratic respirations)  Vomiting (with nausea, Projectile)  Body temperature changes  Changes in pupil reactivity 26
  27. 27. Missile injuries  The cranial injury is directly proportional to the velocity of the missile. (high-velocity or lowvelocity)  The energy dissipated by the missile equals MV2 where M is the mass and V the velocity of the missile.  Three categories: • Tangential • Penetrating • Through-and-through  The primary missile frequently fragments and can cause further secondary missiles from fragments of bone or metal.  The missile causes cerebral damage via three mechanisms: • mechanical laceration • the shock wave • Cavitation  The pathological processes ??  The high intracranial pressure resulting from the cavitation may result in death from failure of the respiratory and cardiac centers in the brainstem. 27
  28. 28. Management  The key aspects in the management of patients following head injury involve: • Accurate clinical assessment of the neurological and other injuries. • Determination of the pathological process involved. • The concept that a change in the neurological signs indicates a progression or change in the pathological processes.  Management include the 3 phases of ATLS: 1. Primary survey 2. Secondary survey 3. Definitive care 28
  29. 29. 1. Primary Survey:  It includes initial assessment & resuscitation of the patients. A. Airway and cervical spine: • Remove any oropharyngeal obstruction • Control airway by jaw thrust or chin lift • Insertion of oropharyngeal airway • Endotracheal intubation which is indicated in: - Depressed level of consciousness GCS <7 - Severe maxillofacial trauma • Tracheostomy • The cervical spine should be immobilized 29
  30. 30. 1. Primary Survey: ..Cont. B. Breathing: - Inspect chest wall for symmetrical movement - Give O2 - Seal off open chest wounds - Relieve tension pneumothorax if present - Ventilation if necessary as in flail chest or severe head injury 30
  31. 31. 1. Primary Survey: ..Cont. C. Circulation: - Ensure adequate circulating volume ( skin color, BP, pulse) - Control external hemorrhage - Put IV line by 2 large bore cannulas, take blood sample for grouping & cross matching - Replacing fluids: NS 0.9% or RL (isotonic) 31
  32. 32. 1. Primary Survey: ..Cont. D. Disability: - Assess CNS injury by GCS - Assess pupillary size and reactivity • The pupillary size is recorded in mm and the light response as present, sluggish or absent • Anisocoria or an asymmetrical sluggish response may suggest partial third nerve dysfunction on the side with the larger or sluggish pupil, implying uncal herniation (reactive at first remain but subsequently will become sluggish and then become fixed and dilated). • As the intracranial pressure increases this same process commences on the contralateral side. • Pitfalls in the examination of pupillary responses: (periorbital bruising, traumatic mydriasis) differentiate 32
  33. 33. 1. Primary Survey: ..Cont. D. Disability: - Eye movements: disorders of ocular movement occur following head injury (injury to an muscle or its nerve supply, or due to disturbance of the conjugate gaze centers and pathways) - Focal neurological signs: • Hemiparesis • The decerebrate posture (upper brainstem injury) • The decorticate posture (cerebral white matter and basal ganglia) 33
  34. 34. 34
  35. 35. 1. Primary Survey: ..Cont. E. Exposure: - Remove all clothes in order not to miss hidden injury. - Prevent cooling (if hypothermia occurred: warm fluids, blankets and heating mattress) F. Foley's catheter G. Gastric tube: Care should be taken when passing gastric catheters nasally in the presence of maxillofacial injury or suspected base of skull fracture. 35
  36. 36. 1. Primary Survey: ..Cont. • Adjuncts to the primary survey • Blood samples for full blood count (FBC), coagulation studies, plasma chemistry (urea and electrolytes and, sometimes, toxicology or other case-specific indices), transfusion screening (group and cross-match, etc.) • 12-lead electrocardiography (ECG) monitoring • arterial blood gases and pulse oximetry. • X ray to the skull, lateral cervical spine anteroposterior chest and anteroposterior pelvis. 36
  37. 37. 1. Primary Survey: ..Cont. • Admission to hospital: the indications are: - Confusion or impaired conscious level - Skull fracture - Neurological signs or symptoms as fits or headache - Difficulty in assessing the patient - Persistent nausea or vomiting >4h. - Complicating medical condition - Lack of responsible adult - No adequate home care. • Any patient who has suffered a head injury must be observed for at least 4 hours. 37
  38. 38. 1. Primary Survey: ..Cont. • Other: - Bed rest with head of bed elevated 20-30 - Make a chart for the patient and check vital signs - Neurological check - NPO until become alert - Isotonic IV fluid - Mild analgesics - Anti-emetic (infrequently) 38
  39. 39. 39
  40. 40. 2. Secondary Survey: 40  Review the patient`s history using AMPLE (Allergy, Medications, Past medical history, Last meal, Events related to injury).  Examination from head to toe.  Neurological evaluation.  Diagnostic studies.  Re-evaluation of the patient especially of the vital signs and urinary output.  Analgesia.
  41. 41. Review the patient`s history using AMPLE   Taking a history in head injury Mechanism of injury  Loss of consciousness or amnesia  Level of consciousness at scene and on transfer  Evidence of seizures  Probable hypoxia  Pre-existing medical conditions  Medications (especially anticoagulants)  Illicit drugs and alcohol 41
  42. 42. Examination from head to toe: head, neck, chest, abdomen, neurological and limbs 42 Neurological examination should be repeated frequently and recorded every 2 hours in stable patient and 15 minutes in unstable patient. Detailed examination of the head: First, look and feel the scalp. There may be evidence of external head injury such as scalp laceration, which may be a cause of significant external blood loss. Palpation of a scalp laceration may reveal an underlying skull fracture with or without a CSF leak. Look for clinical evidence of skull base fracture:
  43. 43.  Bilateral periorbital bruising (Raccoon eyes),(Panda eyes) 43
  44. 44. Battle’s sign (bruising over the mastoid) 44
  45. 45. CSF rhinorrhea or otorrhea, or haemotympanum 45
  46. 46. 46  Bleeding from an ear may result from local trauma or from a skull base fracture with a perforated tympanum. A skull base fracture may be associated with a facial or vestibulocochlear cranial nerve injury.  Examine the eyes: • injury to the conjunctiva or cornea. • Re-examine the pupils • hyphaema or retinal detachment • Examine eye movements: gaze paresis. dysconjugate gaze or roving eye movements suggest midbrainor brainstem dysfunction.  Assess the facial skeleton for evidence of orbital ridge, zygomatic or maxillary fractures.
  47. 47. 47  A peripheral nerve examination should record limb tone, evidence of motor weakness or sensory loss, and reflexes.In those patients with an associated spine injury it is important to document neurological deficits, particularly if the patient is likely to be moved to the operating theatre or to intensive care where such an assessment will not be possible for some time afterwards.
  48. 48. Superficial and Deep tendon reflexes: 48  DTR’s exaggerated after TBI due to cortical disinhibition  Decreased / absent after Spinal cord injury  Asymmetric DTR’s means unilateral brain/spine injury  Superficial (lost/decreased) in corticospinal dysfunction and helpful in localizing lesions  Plantar response: Normal reflex Positive Babinski Intact descending corticospinal inhibition Interrupted inhibition pathways
  49. 49. Brainstem Reflexes 49 Facial palsy unilateral 7 n injury -Basilar skull fracture Corneal reflex Rostral Pontine function Dolls eye maneuver Vestibuloocular function Ice water caloric test ( never in awake child) COWS normal response Coma – same side deviation Stuporous/obtunded – nystagmus to contralateral rapid component Gag and cough reflex 9,10 CN + brainstem swallowing centers Periodic( Cheyne-stokes) hemispheric/diencephalic injury to as caudal as upper pons Apneustic ( prolonged respiratory plateau) Mid- caudal pons injury Ataxic breathing( irregular stuttering resp) Medullary respiratory generator center.
  50. 50. Diagnostic studies:  Skull X Ray - It includes lateral and anteroposterior view Indications: o period of LOC has occurred or impaired conscious level (GCS < 15) o Amnesia o scalp swelling or laceration o history of high-energy injury o persistent headache or vomiting o significant maxillofacial injuries 50
  51. 51. Findings  fracture ( linear or depressed ) 51
  52. 52. 52  pineal shift (calcified structure)  air-fluid level  pneumocephalus  foreign body
  53. 53. 53  Spinal X-Rays: Cervical , thoracic & lumbar .  Brain CT scan:  Indications??  It may show a fracture or hematoma and also provide information about scalp soft tissue injury and cerebral contusions.  CT is the most accurate radiological method for demonstration of brain haemorrhage, Because of the clear distinction between blood (high attenuation) & surrounding brain.
  54. 54. 54
  55. 55. 55
  56. 56. 56  MRI of the brain: • is more sensitive than CT scan but is not appropriate for acute head injury so it useful after the patient has stabilized. It is used to evaluate brain stem injuries & small white mater changes ( punctate hemorrhage in the corpus callosum & diffuse axonal injury).  MRI is less sensitive in detection of acute haemorrhage because it appear isointense to the brain.
  57. 57. 57
  58. 58. MRI T1&T2, hyperacute haemtoma 58
  59. 59. Hyper acute SDH 59
  60. 60. 60  Angiography: The primary need is to determine whether or not intracranial hemorrhage is occurring and, if it is, whether bleeding is from severance of the artery, from laceration of brain substance or from rupture of cortical veins. Intracerebral hematoma. slight shift of anterior cerebral artery and depression of left middle cerebral artery.
  61. 61. 61 Arrows point to concave outline of chronic unilateral subdural hematoma.
  62. 62. Re-evaluation of the patient especially of the vital signs and urinary output.  62 Pulse oximetry is a useful real-time measure of oxygenation and is sensitive to sudden changes in the patient’s ventilation and airway Analgesia:  it is very important to provide relief of pain in the initial management. Pain and anxiety can produce changes to the vital signs, and it is important that adequate relief be provided.
  63. 63. 3. Definitive care 63  Scalp laceration: • ‘spurting’ arteries should be controlled with haemostatic clips prior to the application of a sterile bandage . • The hair should be shaved • The skin sutures should approximate the cut edges of the skin and avoid excessive tension . • clean scalp lacerations can nearly always be closed with local anaesthetic infiltration. • if the scalp wound has resulted in loss of soft tissue the wound may need to be extended to provide an extra ‘flap’ of healthy tissue so that the skin edges can be approximated without tension.
  64. 64. 64  Scalp hematoma:  Minor hematoma with intact skin left for natural absorption  Hematoma is evacuated if it is of significant size or there is signs of infection.  Depressed vault fractures:  Compound fracture :prophylactic antibiotics and surgery under GA.  Closed fracture: there is no urgency in elevating the bone fragments, provided there is no underlying intracranial complication.  There is controversy over whether a depressed fragment might lead to epilepsy due to continued pressure on the brain so Prophylactic anticonvulsant medication .
  65. 65. Indications of elevation:  CT scan show that the dura might have been penetrated  significant brain compression  The fracture is compound  Cosmetic, such as a frontal fracture in a young child.  Simple linear fracture:  Require no specific neurological treatment  Patient should have CT scan & admitted for 48 hrs.  Linear fracture of the temporal bone require frequent observation . 65
  66. 66.  Base of skull fracture: 66 A.Anterior cranial fossa: frontal craniotomy with repair of the dural defect should be performed if:  CSF leakage continues for more than 5 days. indicating the fistula is not trivial.  intracranial aerocele  episode of meningitis. B.Middle cranial fossa: Unlike fractures of the anterior cranial fossa the leakage nearly always settles and the fistula does not usually provide a route of infection.
  67. 67. 67 C.posterior cranial fossa It is rare and occur in only 5% of all skull base fractures. However, they require special attention because of their high mortality rate. The three most important complications associated with posterior skull base fractures are:  Brain stem compression due to mass effect (eg, epidural hematoma, or intracerebellar hematoma)  Acute hydrocephalus due to occlusion of the 4th ventricle  Craniocervical instability due to occipital condylar fractures
  68. 68. 68  Cerebral contusion:: rarely require immediate surgical treatment.  Epidural hematoma: immediate surgical evacuation via a craniotomy.  Acute subdural hematoma: is usually evacuation via a craniotomy.  Chronic subdural hematoma: evacuation via burr hole(s) rather than craniotomy.  Subarachnoid haemorrhage: Traumatic subarachnoid haemorrhage is managed conservatively.  Intracerebral hemorrhage: Significant hematoma needs craniotomy with incision of hemisphere at the most superficial area & evacuation of the clot.  Pressure & Structural Displacement: A sustained ICP of > 20 mmHg is associated with poor outcome.  Missile injury: Admission, Antibiotics,Imaging, surgery.
  69. 69. Burr Hole(s) 69
  70. 70. Minimal – Mild Head Injury   criteria must be met before discharge: 70 GCS of 15/15 with no focal neurological deficit.  the patient must be accompanied by a responsible adult.  verbal and written head injury advice must be given.  Some patients are at significant risk of intracranial haematoma and require CT.  If there has been a period of LOC, or if the patient is drowsy, then the following measures should be instituted to minimize the development of cerebral swelling:  Elevation of the head of the bed 20°  Mild fluid restriction to 2–2.5 l/day in an adult.
  71. 71. Moderate - Severe head injury 71  The patient has a clinical assessment and CT scan as described previously.  If the CT scan shows an intracranial haematoma causing shift of the underlying brain structures then this should be evacuated immediately.  If there is no surgical lesion, or following the operation, the management consists of: A. Careful observation using a chart with the Glasgow coma scale. B. Measures to decrease brain swelling. C. Temperature control. D. Nutrition. E. Routine care of the unconscious patient including bowel, bladder and pressure care.
  72. 72. Birth injury 72  Birth trauma is a frequent cause non accidental head injury.  Chronic subdural haematomas occur in approximately 20% of battered children.  The violent shaking of the immature brain might be sufficient to rupture bridging veins or cause shearing at the grey/white interface without evidence of external trauma.  If an inadequate history is provided in such a setting, it is important to screen for a coagulopathy, examine the fundi for retinal haemorrhage, arrange a skeletal survey and when appropriate involve a pediatrician and social services.  MRI now plays an important role in determining the chronicity of cerebral injuries
  73. 73. 73 NOW, what are the complications of head injury??
  74. 74. Early:  Meningitis  Hyperpyrexia  Syndrome of inappropriate anti-diuretic hormone secretion (SIADH)  Spinal Injury  Death 74
  75. 75. Late  Post-concussional syndrome.  Amnesia.  Epilepsy  Death 75
  76. 76. Outcome 76 Glasgow Outcome Score (GOS) 5 Good recovery light damage with minor neurological and psychological deficits 4 Moderate disability No need for assistance in everyday life, employment is possible but may require special equipment 3 Severe disability Severe injury with permanent need for help with daily living 2 Persistent vegetative state Severe damage with prolonged state of unresponsiveness and a lack of higher mental functions 1 Death
  77. 77. Rehabilitation  77 The major groups of disabilities resulting from a head injury are: 1. impairment of motor function—hemiparesis, quadriparesis, ataxia, poor coordination 2. speech disturbances—dysphasia, dysarthria 3. impairment of special senses—vision, hearing 4. cognitive disturbance—memory impairment, intellectual disability, personality change. So:  Limb contractures and pressure sores are avoided by frequent patient turning, physiotherapy and the use of splints.
  78. 78. 78  Orthotic devices will assist hemiplegic patients to walk.  The speech therapist may provide valuable assistance for patients with dysarthria and swallowing difficulties.  Although the perceptual problems may resolve with time and rehabilitation, the problems associated with cognitive disturbances and alteration of personality may persist.  Family counselling and support is essential to help the relatives understand and cope with these long-term disabilities.
  79. 79. 79