MANAGEMENT OF HEAD INJURIES

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Presentation transcript:

MANAGEMENT OF HEAD INJURIES KEVIN HENSHAW BSc.(Hons.) Cert.Ed RODP

OBJECTIVES TO BE AWARE OF THE PROBLEMS ASSOCIATED WITH DEALING WITH PATIENTS WITH AN ACUTE HEAD INJURY WITHIN THE PERI-OPERATIVE AREA TO HELP MAINTAIN HOMEOSTASIS IN THE HEAD INJURED PATIENT

BACKGROUND Approximately 1 Million patients annually 50% of trauma-related deaths from severe head injury 1% OF ALL UK DEATHS 85% OF ALL SEVERELY HEAD INJURED PATIENTS REMAIN DISABLED AFTER 1yr ONLY 15% RETURN TO WORK AFTER 5yrs

Assessment Glasgow Coma Scale (GCS) GCS 13-15 (Mild) 80% GCS 9-12 (Moderate) 10% GCS 3-8 (Severe) 10%

The Glasgow Coma Scale (GCS) was developed by Teasdale and Jennett in 1974 Glasgow Coma Score The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. It is composed of three parameters : Best Eye Response, Best Verbal Response, Best Motor Response, as given below : Best Eye Response. (4) No eye opening. Eye opening to pain. Eye opening to verbal command. Eyes open spontaneously. Best Verbal Response. (5) No verbal response Incomprehensible sounds. Inappropriate words. Confused Orientated   Best Motor Response. (6) No motor response. Extension to pain. Flexion to pain. Withdrawal from pain. Localising pain. Obeys Commands.

PATHOLOGY SCALP lacerations, contusions or abrasions CRANIUM simple or compunded,depressed or planar, base or vault

PATHOLOGY UNDERLYING BRAIN Primary (result of impact) Secondary (result of non homeostatic factors)

PRIMARY Intra-cranial haematoma (intracerebral,extradural or subdural) Contusion (coup or contre-coup to impact site) Diffuse axonal (result of mechanical shearing following deceleration)

NORMAL BRAIN IMAGE

EXTRA DURAL HAEMATOMA Extradural haemorrhage Results from rupture of one of the meningeal arteries that run between the dura and the skull. The middle meningeal artery is most commonly affected. Usual cause is a skull fracture

ACUTE SUB DURAL HAEMATOMA Subdural haemorrhage More common than extradural haemorrage Associated with sudden jarring or rotation of the head Shears and tears the small veins which bridge the gap between the dura and cortical surface of the brain

TRAUMA

TRAUMA

TRAUMA

SECONDARY RESULT OF: Ischaemia Cerebral oedema Infection Tonsillar or tentorial herniation ALL EXACERBATE ORIGINAL HEAD INJURY!!!

INTRA CEREBRAL ABCESS

NORMAL AUTOREGULATION OF CBF IS LOST IN SEVERE HEAD INJURY MAKING THE INJURED BRAIN MORE SUSCEPTIBLE TO : HYPO-OR HYPER VOLAEMIA HYPOXIA HYPERCAPNEA

INTRACRANIAL PRESSURE MONRO-KELLIE DOCTRINE ‘CRANIUM IS CLOSED BOX’ ‘Contents are incompressible, increase in one constituent or an expanding mass within the skull results in an increase in intracranial pressure’

FACTORS INFLUENCING OUTCOME NORMOTENSION: Single episode of hypotension can have catastrophic effect (systolic <90mm Hg) Initial treatment –fluid resuscitation Vasopressors – epinepherine MAP of 70mm Hg

FACTORS INFLUENCING OUTCOME NORMOXIA: Hypoxemia (Spo2<90%) decreases prognosis possibly by four fold increase in mortality (Spo2<60%) O2 maintenance needs to be balanced against any other factors egg PEEP & chest trauma

FACTORS INFLUENCING OUTCOME NORMOCAPNIA: Hyperventilation (PaCO2 <25 mm Hg) should be avoided for first 24h after Head Injury. Hyperventilation results in vasoconstriction, reduced CBF. First 24h CBF reduced by 50% hyperventilation may result in further cerebral ischemia

FACTORS INFLUENCING OUTCOME NORMOTHERMIA: Increased body and brain temp’ increases CBF Cerebral metabolism and O2 utilisation Increase in ICP

TRAUMA REMEMBER: AIRWAY BREATHING CIRCULATION CERVICAL SPINE (until patient is awake treat as potentially unstable)

QUESTIONS