Patho physiology and mechanism of head injuries .pptx

Trauma can be defined as an injury to any part of the human body as a result of energy transfer from an inflicting source.
Trauma management is based on the principles of Advanced Trauma Life Support(ATLS) guidelines to rapidly identify and treat life threatening injuries during primary survey.

1. PATHO PHYSIOLOGY & MECHANISM OF HEAD INJURY

2. Trauma can be defined as an injury to any part of the human body as a result of energy transfer from an inflicting source. Trauma management is based on the principles of Advanced Trauma Life Support (ATLS) guidelines to rapidly identify and treat life threatening injuries during primary survey.

3. Primary Survey: The primary survey aims to identify and manage the most immediately life threatening pathologies first and follows cABCDE . The cABCDE of trauma care: c-Control of massive external haemorrhage A-Airway with cervical spine protection B-Breathing and ventilation C-Circulation and haemorrhage control;apply a pelvic binder and do no remove until a pelvic fracture is excluded D-Disability(neurological status) E-Exposure(assess for other injuries)

4. All severely injured patients require a detailed top-to-toe examination after life-threatening injuries have been identified and managed during the primary survey. Patients may be intubated and unresponsive at this point, limiting the accuracy Patients may be intubated and unresponsive at this point, limiting the accuracy of clinical examination of clinical examination. SECONDARY SURVEY

5. Head injury accounts for 3 to 5% of emergency department attendances. Road traffic accidents are the leading cause of head injury,responsible for upto 50% of cases. Other common mechanism of injury include falls and assault. TRAUMATIC BRAIN INJURY

6. At the tissue level brain injuries are the result of either direct transmission of energy or the accumulation of blood within the cranium. Energy transmitted to the cranium and the underlying brain tissue can cause direct injury both at the location of contact and on the contralateral side. Mechanism of Brain Injuries

7. COUP&COUNTER COUP INJURY

8. Traumatic brain injury can be considered as the combination of primary injury sustained on impact and secondary injury developing in the following hours and days. The primary brain injury process cannot be reversed or corrected and the outcome after TBI is dictated by how well secondary injury is prevented. PATHO PHYSIOLOGY

9. The mainstay of preventing secondary brain injury consists of maintenance of acceptable cerebral perfusion and subsequent oxygenation. Cerebral perfusion and intra cranial pressure: Normal cerebral blood flow is about 55ml/min for every 100 grams of brain tissue. Ischaemia starts when this rate drops below 20ml/min and even lower levels will result in infarction unless promptly corrected.

10. Flow depends on cerebral perfusion pressure(CPP) which is the difference between mean arterial pressure(MAP) and the intra cranial pressure(ICP) CPP(75-105 mmHg)= MAP(90-110 mmHg)-ICP(5-15 mmHg) In normal brain,variation in vascular tone maintain a constant CBF across a range of MAP between 15 and 150 mm of Hg and a corresponding range of CPP-the process of cerebral autoregulation

11. Autoregulation can be impaired in the context of trauma,so that MAP and ICP must be actively regulated in these patients to maintain proper perfusion. Intra cranial pressure: A continuous supply of oxygenated blood is essential for brain survival. Rised ICP can compromise cerebral perfusion resulting in cycle of secondary brain injury and swelling.

12. Alexander monro observed in 1782 that the cranium is a rigid box containing a nearly incompressible brain. Any expansion in the contents especially hematoma and brain swelling,maybe initially accommodated by exclusion of fluid components,venous blood and cerebro spinal fluid. Further expansion is associated with exponential rise in ICP. The Monro -Kellie Doctrine and Herniation Syndromes

13. Uncontrolled increase in ICP results in cerebral herniation. Typically herniation of uncus of the temporal loop over the tentorium results in pupil abnormalities usually occurs 1 st on the side of expanding hematoma.

14. Cerebellar tonsillar herniation through the foramen magnum compresses medullary vasomotor and respiratory centers,classically producing cushing’s triad. 1)Hypertension 2) Bradycrdia 3)Irregular respiration The patient is then said to be in coning and brain stem death will result without immediate intervention.

15. The severity of head injury is classified according to the post resuscitation Glasgow Coma Scale(GCS) score. In particular the motor score that is the best predictor of neurological outcome. Classification of Head Injuries

16. Ensure adequate oxygenation and circulation Exclude hypoglycemia Check people size and response and GCS score as soon as possible Check for focal neurological defecits before intubation if possible Examination: Primary Survey

17. During secondary survey special attention has to be paid to head,neck and spine. Head: Examination should include inspection and palpation of scalp for any evidence subgaleal hematoma and scalp lacerations, which may bleed profusely and potentially overlie scalp fractures. Examine the face for evidence of fractures especially to the orbital rim,zygoma and maxila . Secondary Survey

18. Clinical evidence of skull based fracture may include battle’s sign. Hemotympanum or overt bleeding from the ear if the tympanic membrane has ruptured and CSF rhinorrhoea or otorrhoea are also highly suggestive of fracture of the base of skull.

19. Neck and Spine: Studies have demonstrated an incidents of cervical fracture of upto 10% in association with moderate and severe TBI. A peripheral nerve examination with documentation of limb tone,power , reflexes and sensation needs to be performed early to identify spinal pathology. Cervical collar should be used in patients for stabilization of c-spine. Priapism is a strong predictor of severe cord injury even in intubated patients.

20. In general, patients with isolated head injuries and without ongoing defcits can be safely discharged from the emergency department, provided they meet suitable criteria. Patients who do not meet all the discharge criteria will need admission for a further period of observation and/or brain imaging. Early computed tomography (CT) imaging is desir -able in patients with a persistent reduced conscious level, focal defcits , suspected fractures or risk factors for intracranial bleed Minor and Mild Head Injury

21. Concussion is defned as the alteration of consciousness as a result of closed head injury but is generally used to describe mild head injury without imaging abnormalities: loss of consciousness at the time of injury is not a prerequisite. Key features include confusion and amnesia. The patient may be lethargic, easily distractable , forgetful, slow to interact or emotionally labile. Concussion,post concussive syndrome

22. Postconcussive syndrome is a loosely defned constellation of symptoms persisting for a prolonged period after injury. Patients may report somatic features such as headache, dizziness and disorders of hearing and vision.

23. Resuscitation is performed according to Advanced Trauma Life Support (ATLS) guidelines, beginning with management of the airway with cervical spine control and proceeding to assess and manage breathing and circulation. Includes FRACTURES EXTRA DURAL HEMATOMA ACUTE SUB DURAL HEMATOMA CHRONIC SUB DURAL HEMATOMA MODERATE AND SEVERE TRAUMATIC BRAIN INJURY

24. 5.TRAUMATIC SUB ARACHNOID HEMORRHAGE. 6.CEREBRAL CONTUSION 7.DIFFUSE AXONAL INJURY .

25. Can follow relatively minor trauma with brief loss of consciousness. Followed by a lucid interval and then sudden deterioration. Lentiform lesion on CT. Require immediate transfer to a neurosurgical unit for evacuation. EXTRA DURAL HEMATOMA

26. It is encountered in two broadly distinct contexts. First,high energy injury mechanisms can result in the rupture of cortical surface vessels with significant associated primary brain injury. This results in an expanding hematoma with rapid deteoration and development signs of rised ICP without lucid interval. In second group of patients,older and often anti coagulated,a lower energy injury leads to venous bleeding around the brain. Since the dura is not as adherent to the brain as it is to the skull subdural blood is free to expand across the brain surface giving a diffuse concave appearance. ACUTE SUBDURAL HEMATOMA

27. Common in the elderly especially those on anti coagulants. Clinical deficits result from osmotic of a deegrading clot over days or weeks. Appears as diffuse hypodense lesion on CT. Burrhole drinage is usually preffered . CHRONIC SUBDURAL HEMATOMA

28. Trauma is the commonest cause of sub arachnoid hemorrhage and this is managed conservatively. It is not usually associated with significant vasospasm,which characterises aneurysnal sub arachnoid hemmorhage . SUB ARACHNOID HEMORRHAGE

29. Contusions are common and are founded predominantly where the brain is in contact with the irregularly ridged inside of the skull i.e,at the inferior frontal lobes and temporal poles. Contusions appear heterogeneous on CT reflecting their composition of injured brain matter interspersed with acute blood. Contusions rarely require surgical intervention but may warrant delayed evacuation to reduce mass effect. CEREBRAL CONTUSIONS

30. THANK YOU