Head injury

 Head injury

Pathology of head injury The Monreo-Kelly  doctrine confirms that the skull cannot easily accommodate an increase in volume of its contents without a significant rise in intracranial pressure (ICP) .cerebral perfusion pressure (CPP)equals the systemic arterial pressure(SAP)minus the ICP this relationship is fundamental and explains the pathophysiology of brain injury .brain injury causes swelling .this volume increase causes a rise in ICP and thus a fall inCPP resulting in brain ishaemia . deterioration in cerebral function causes respiratory failure resulting in reduced PaO2 and rise in PaCO2 , which both
causes cerebral vasoconstriction ,further aggravating ischaemia . this lead to infarction which causes more brain swelling .if this vicious cycle is not interrupted ,the inevitable outcome is death , as total brain failure occurs when ICP=SAP,and the CPPis zero ,a rise in the ICP results in displacement of parts of the brain . in earlier phases this is seen as midline shift . later stages result in herniation of the cingulate lobe under the adjacent falx (subfacial herniation),the uncus through the tentorial hiatus to compress the oculomotor nerve and mid brain ,and the cerebellar tonsil through the foramen magnum compressing the medulla oblongata . there are terminal events mechanism of brain injury trauma may either injury the brain ,or the extracerebral vessels .rupture of extra cerebral vessels results in intracranial bleeding , indirectly causing further brain injury .trauma severe enough to cause brain injury usually also result in skull fracture .however ,skull fracture in not requisite for either direct brain injury or intracranial bleeding .brain injury may occur at the site of the trauma (coup injury).acceleration of the brain away from the source of injury with an abrupt stop at the opposite side also results in injury (contre-coup injury) as 1-intracranial bleeding .extra cerebral bleeding occurs in the extradurl or subdural space .intra cerebral bleeding results from coup or contre-coup injury .all result in haemtomas that raise the ICP .1- cerebral contusion injuries range from mild contusion to large intracerebral haemtoma mild contusion resolve .large haemtoma are acute space occupying lesions ,and need to be evacuated 2- extradural haemtoma .the thin pteryon anterior to the ear fractures easily and rupture of underlying middle meningeal artery may result .a compact haematoma lying between the periosteal layer of te dura mater and the inner table of the skull results .the classical sequence of
events is loss of consciousness as a result of the blow , followed by some recovery (the so - called lucid phase) before consciousness is lost again .ct scan shows characteristic convex haematoma .treatment is by craniotomy ,evacuation of haemtoma ,and clipping of the bleeding artery .small extra dural haematomas may result from blood oozing from skull fractures 3- acute subdural haematoma .this is far more common than extra dural haematoma .it result from bleeding communicating veins in the less restricted subdural space ,and thus develops rapidly .prompt evacuation is required 4- chronic subdural haematoma .the elderly are prone to develop subdural haematoma .cerebral atrophy places the communicating veins under tension and these rupture easily .because of cerebral atrophy , there is a greater space for blood accumulate . the haematoma may remain undiscovered for a long time as the content alters ,it becomes osmotically active ,slowly expanding ,and presenting as a chronic confusional state 2- direct parenchymal injury . the brain has a layered structure .a force applied to the parenchyma causes shearing stresses and the layers may move over each other .this direct parenchymal disruption is impossible to visuzlize by any means and may occur without any appreciable intracranial bleeding .the prognosis is poor Evolution of clinical signs .with cortical disruption .convulsions may occurs the level of consciousness reduce and there may be Cheyne-Stokes respiration .as corticospinal tracts are disrupted contralateral weakness occurs .with involvement of the midbrain ,hyperventilation may occur.the ipsilateral pupil becomes fixed and dilated . with the involvement of the upper pontine respiratory centre , the respiratory pattern develops with episodes of hyperventilation separated by periods of apnea.if the lower pons is involved there may be prolonged inspiration and expiration .blood pressure elevation and bradycardia signify involvement of medullary cardiovascular regulatory centre.Evaluation of clinical signs conscious level may be rapidly evaluated using the Glasgow Coma Scale (GCS) the highest score possible is 15 and the lowest is three .this serves to assess neurological state in standard terms and seconds to monitor the progress of a patient following a head injury and to identify quickly any deterioration in condition .external examination reveal sign of a brain skull fracture as blood or CSF from the ear ,Battle,s sign (bruising around the mastoid area), bilateral periorbital haematoma (panda eyes)or haemotympanum the Glasgow Coma Scale1-motor response divided into six as obeying commands =6 localizing to pain =5 withdrawal to pain =4 flexsion to pain =3 extension to pain =2 no movement =1 2- verbal response divided into five as orientated =5  confused =4   inappropriate  speech =3  incomprehensible sound =2 no verbal response =1 , 3-eye opening divided into fourth as spontaneous eye opening = 4 eyes open to request =3 eyes open to pain =2 no eye opening =1

tags:head,injury