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Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
Management of head injury
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Management of head injury

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  • 1. MANAGEMENTOFHEAD INJURYMonday 26th September,2011STATE HOUSE MEDICAL CENTRE,ASO ROCK ABUJA.
  • 2. CONTENTS Definition Overview Classification Pathophysiology Presentation Investigations Treatment Follow-up
  • 3. DEFINITIONStrictly defined as alteration in the integrity of the head resulting from an impact.Hence, there may be both extracranial and intracranial components.However, the terms traumatic brain injury and head injury are often used interchangeably in the medical literature.
  • 4. Head and brain
  • 5. OVERVIEW• Traumatic brain injury (TBI) continues to be an enormous public health problem, even with modern medicine in the 21st century.• the most common causes include motor vehicle accidents , falls, assaults, sports-related injuries, and penetrating trauma.• Motor vehicle accidents account for almost half of the TBIs,and motorcycle-related head injuries deserve special mention in this regard.
  • 6. OVERVIEW• Head injury data are difficult to compare internationally for multiple reasons, including inconsistencies and complexities of diagnostic coding and inclusion criteria.• AGE: Approximately half of the patients admitted to a hospital for head injury are aged 24 years or younger.• SEX: Men are nearly twice as likely to be hospitalized with a brain injury than women.
  • 7. CLASSIFICATION• Closed or Open.• Diffuse or Focal.• Coup or contrecoup.• Mild, Moderate or Severe.• Non-haemorrhagic or Haemorrhagic (extradural,subdural,subarachnoid ,intraparenchymal or intraventricular).• Concussion,Contusion or Diffuse axonal• Primary or Secondary
  • 8. Vascular structures involved inbrain injuries
  • 9. PATHOPHYSIOLOGY• Brain is contained within the skull, a rigid and inelastic container. Hence,only small increases in volume within the intracranial compartment can be tolerated before pressure within the compartment rises dramatically.• V i/c = V b + V cf + V d(Monro-Kellie equation).
  • 10. PATHOPHYSIOLOGY• Vi/c=1,500mls,Vb=87%,Vcf=3%,Vd=10%.• A second crucial concept in TBI pathophysiology is the concept of cerebral perfusion pressure (CPP),which is the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP).• CPP = MAP – ICP• Autoregulation of Cerebral blood flow occurs in non-injured brain over MAP:50-150mmHg.
  • 11. PATHOPHYSIOLOGY• Secondary brain injury results from: Systemic hypotension, Hypoxia, Elevated ICP, or the biochemical changes.• The treatment of head injury is directed at either preventing or minimizing secondary brain injury.
  • 12. PRESENTATION• Initial clinical evaluation: involves a thorough systemic trauma evaluation referred to as the advanced trauma life support (ATLS) guidelines.• After patient has been resuscitated and stabilized, attention may then be directed to a focused head injury evaluation.
  • 13. PRESENTATION• Elicit the type and mechanisms of the injury: prognostic value.• Altered consciousness: even a questionable loss of consciousness can be a marker of severe neurological injury.• Bleeding from sites including orifices• Seizures• Vomiting
  • 14. PRESENTATION• The presence of prior head injuries.• Remote or active drug or alcohol use: may raise the risk of intracranial bleeding and cloud the mental status assessment.• Present anticoagulant therapy .• Carefully consider past psychiatric disease and a premorbid history of headaches.
  • 15. PRESENTATION• The neurologic assessment begins with ascertaining the GCS score.• Cranial nerves characterisation • Pupillary reflexes • Ocular movement • CN VII palsy • Hearing loss • Dysphagia•
  • 16. PRESENTATION• Motor examination:Focal signs indicate localized contusion or, more ominously, an early herniation syndrome.  Flexor or extensor posturing-extensive intracranial pathology or raised intracranial pressure.  Spasticity or flaccidity more unusually,  Akinesia and rigidity.  Tremors and dystonia  Postural instability and imbalance
  • 17. PRESENTATION• Sensory examination: Corneal reflex• Primitive reflexes-despite their presence in some healthy elderly patients,they are useful when multiple,and can correlate with cognitive deficits.• Bedside Cognitive Testing:n the acute setting, attention and orientation are important.
  • 18. INVESTIGATIONS Laboratory Studies  PCV/FBC  E/U/Cr  Arterial blood Gases  Alcohol level  Drug screens Imaging Studies  Skull Xrays:largely replaced by CT scanning.Fractures may be visible.
  • 19. INVESTIGATIONS• Computerised Tomography Scanning:The standard CT scan for the evaluation of acute head injury is a noncontrast scan that spans from the base of the occiput to the top of the vertex in 5-mm increments.• Three data sets are obtained from the primary scan, as follows: (a) bone windows, (b) tissue windows, and (c) subdural windows.
  • 20. INVESTIGATIONS• Extradural haematoma-biconvex,Subdural- crescent,Subarachnoid-filling of gyri over convex brain surfaces.• Magnetic Resonance Imaging:has a limited role in the evaluation of acute head injury because of its long acquisition times and the difficulty in obtaining MRIs in persons who are critically ill.It is superior to CT scan for helping identify diffuse axonal injury (DAI) and small intraparenchymal contusions.
  • 21. TREATMENT Mild head injuries :analgesics and close monitoring for potential complications such as intracranial bleeding. Moderate and Severe head injuries:There is significant secondary injury :  Prevention of hypoxia: Oxygen therapy  Control of elevated intracranial pressure. Mannitol,hyperventilation,CSF diversion,
  • 22.  Hypothermia,Hypertonic saline,Barbiturate coma,Decompressive craniectomies.Steroids have no role . Maitenance of perfusion:Ringer’s lactate,paediatric saline,monitoring of blood pressure,vassopressors. Seizures:anticonvulsants Agitation:Paralytics,sedation. Nutrition:Enteral or parenteral feeding. Correction of dyselectrolytaemia:Hyponatramia,Hypomagnesaese mia.
  • 23. COMPLICATIONS Insomnia Cognitive decline Posttraumatic headache Posttraumatic depression Posttraumatic seizures Hydrocephalus Deep vein thrombosis Heterotopic ossification
  • 24. COMPLICATIONS Posttraumatic seizures Hydrocephalus Deep vein thrombosis Heterotopic ossification Spasticity Gastrointestinal complications:cushing’s ulcers. Gait abnormalities
  • 25. FOLLOW-UP A putative diagnosis of mild head injury does not necessarily mean a favourable outcome. 80% of patients with mild head injury recover completely. Patients could develop Alzheimer’s disease subsequently.
  • 26. THANKYOUALL

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