Introduction to neurosurgery & traumas Dr Waleed Dabbas Neurosurgery Department

1. Introduction to neurosurgery & traumas Dr Waleed Dabbas Neurosurgery Department College of Medicine Al Balqa University Al Salt- Jordan

2. Neurosurgery • Specialty in brain and spine • Subspecialties: Neurotrauma Neurooncology Cerebrovascular Functional Skull base Neuroendocraniology and spinal surgery

3. Neurotraumas • Head injuries • Spinal injuries

4. Just keep your head away and contemplate

5. We do not like to see this????

6. introduction • 300/100 000/y • Of these 9/100 000 die • Some are inevitable others are potentially preventable • Causes: • MVA most common in young males. Contributes 60% of deaths from head injuries • Falls • Assaults • Domestic accidents • Sport injury • Gun shot

7. continued • Primary impact is un preventable • Aim of management is to: - minimise further brain damage from secondary complications -Maintain adequate CPP - Lower ICP

8. Cerebral perfusion pressure • Normal ICP is less than 10 mm Hg, around 135 mm H2O, High ICP if >15 • Best measured by EVD that is connected to ICP monitor • Cerebral perfusion pressure is :MAP-ICP • CPP ranging between 60-100 mm hg • MAP= diastolic+1/3 systolic • Cerebral blood flow CBF= CPP CVR

9. CPP= MAP-ICP

10. Aetiology • Brain injury occurs at the time of impact and as a result development of secondary complications • Primary involves the initial mechanical injury due to local deformation and energy transformation. • Secondary encompass a cascade of biochemical and cellular processes which are initiated by primary process which may cause ongoing cellular damage or even death

11. Primary damage 1- brain contusion and laceration • Coup and counter coup • Frontal and temporal

12. continued 2-diffuse axonal injury • This type occurs as a result of shearing injury • Causing tearing of axons • Mild to severe • Mild :Concussion • Severe usually causes corpus callosum, mid brain, and SCP contusions. • CT may be normal but patient in moribund condition

13. Secondary brain damage May be preventable Occurs at any time after initial impact 1-Intracranial haematomas Epiduarl haematomas: from MMA, less likely from venous source or fracture site Takes biconvex shape. Mortality rate 10%. If deteriorates 40-50%

14. continued Sub dural haematomas Classified to Acute: • from rupture bridging veins. • concavo-convex shape. • high mortality rate 60%. • Usually associated with intracerebral contusions and shearing injury that increases the morbidity and mortality rate

15. continued subacute : Iso dense on CT scan, Symptoms appear within 4-21 days. Chronic: More than 3 w Usually in infants and olds Hypo dense on CT scan .

16. continued 2- brain oedema Very common after head injury may be fatal if left untreated Vasogenic type. increases ICP. 3-CONING OR BRAIN HERNIATION Central and lateral. Subfalcine transtentorial or diencephalic ,tonsillar. Due to increase in ICP from brain swelling or supratentorial haematomas as a result of space occupying lesion.

17. Brain herniation syndromes The shift of brain structures goes through weak points which are the orifices inside the skull which is a rigid box that does not expand in a response to this shift • Classified to: • Central or rostro-caudal • Lateral

18. TYPES • Subfalcine or cingulate herniation: which is the mid line shift: due to space occupying lesion that shifts the ipsilateral structure to opposite underneath the interhemispheric falx. • If continues it ends with transtentorial herniation Trans tentorial herniation: • Lateral or uncal: common • The uncus of the temporal lobe herniates through the tentorial opening. Causing mid brain compression

19. S&S • Earliest sign is decline in GCS. If proceeds it causes 3rd CN palsy then contralateral hemiplegia. At this stage brain herniation might be reversible but if it continues it end with pontine or medullary syndromes which are irreversible • Central or diencephalon as in mid line structure lesions or bilateral hemispheric lesions. • It causes rapid decline in GCS rather than causing the classic syndrome before it Takes the same stages

20. Tonsillar herniation Posterior fossa lesions that cause herniation of the cerebellar tonsils via the foramen magnum Causing significant medullary compression and sudden death Up ward herniation may also occur at the same time through the tentorial herniation • Other types :Transcraniotomy herniation

21. END RESULT 4-cerebral ischemia Caused by progressive rise in ICP, hypoxia or hypotension

22. OTHERS 5- infection 2-5% as seen in compound depressed #, or basal skull # 6-Epilepsy immediate after trauma early within a week in 5% late after a week in 5% more common with ICH, depressed #, severe head injury at 20-25%

23. Classifications of head injury 1-According to severity • Mild GCS13-15 • Moderate 9-12 • Severe <9 2-According to morphology .Scalp injuries • Cut and lacerated wounds • Degloving wounds

24. .skull Vault: • Linear: a crack within the bone without displacement • Depressed: displacement of bone fragment inwards • Either compound or simple

25. Comminuted: fragmented bone without displacement Base: • Anterior fossa • Middle fossa • Posterior fossa .Intracranial Extra-axial EDH SDH SAH

26. continued Intra-axial Brain contusions and lacerations Brain haematomas Intra ventricular haemorrhage Head injuries may also be closed or open Open: Basal skull factures and compound depressed fractures Or as seen in penetrating injuries mainly in war time

27. Management

28. That includes

29. Concepts of Initial assessment for traumas 1-Rapid primary survey 2-Resuscitation 3- Adjunct to primary survey /resuscitation 4-Detailed secondary survey 5-Adjuncts to secondary survey 6-Re evaluation 7-Definite care

30. Primary survey • Get IV access, send bloods • A: airway check for obstruction. ETT • B: breathing oxygenate, check respiratory movements. ?ventilation • C: circulation BP, pulse. Control bleeding, restore volume • D: disability GCS, Pupillary response, focal deficits • E: exposure Completely undress patient, protect from hypothermia

31. Resuscitation • GOALS • Achieve normovolemia and hemodynamic stability • Compensate for the internal fluid fluxes from the interstitial and intracellular compartment • Improve the microvascular blood flow • Normalise oxygen delivery to cells • Parameters: • BP,PR,RR,O2 sat, urine output, pulse pressure, perfusion.

32. ICP • Skull is a rigid contains: • brain: 1200-1600 ml +150 ml of ECF • CSF: 130- 150 ml • blood: 100-150 • They are incompressible and in balance • Monro Kellie doctrine; pressure volume curve

33. Monro- Kellie Doctrine

34. Adjuncts Treatment • ECG • Urinary output • Catheters • Pulse oximeter and PCO2 • ABGs

35. Secondary survey Proceed to secondary survey when • primary completed • ABCDEs are reassessed • Vital function returning to normal

36. Key components to secondary survey • History: • A M P L E • Observational at scene, initial clinical observation, progress. • Physical examination: • head to toe • Tubes and fingers in every orifice • Complete Neuro exam,: • palpate for spine tenderness • Musculoskeletal checks • Special diagnostic tests • Keep hard neck collar on • Re evaluation to minimise missed injuries • Pain killers as appropriate

37. Points to get in head injuries • Mechanism of injury • Circumstances of injury • LOC • PTA • Headache and vomiting • Seizures • Weakness • CSF leak • Spine pain • Other symptoms

38. Examination • 1- level of consciousness GCS (E4 V5 M6). • take the best response. Lowest score 3 highest 15, if intubated (ETT) give 1 • 2-Pupillary reaction: • unresponsive unilaterally implies pathology of ipsilateral 3ed N. herniation • Anisocoria may be physiological if mild • 3-Focality: • asymmetric response implies intracranial event • 4-Signs of head trauma • 5-Signs of basal skull #: CSF leak, raccoon eyes, sub conjunctival bleed, battle’s sign .

39. Imaging in trauma • Initial trauma series • Lateral c- spine x-ray • CXR • Pelvis • Abdominal U/S if handy • CT Scan brain, c-spine as routine • In multiple trauma chest, abdomen and pelvis should be included • Angiography in vascular injuries mainly in pelvis • MRI in spinal trauma

40. Indications for CT and admission • LOC or PTA >5 minutes • Hx of epilepsy • GCS <15 or decline in GCS • Neurological deficits • CSF leak • Positive radiological findings • Social indication?

41. Treatment mild and moderate injuries, linear, comminuted Observation: Basal skull #: observation, antibiotics ? CSF leak ceases within 3-10d in 90-95% If continues drainage or dural repair may be needed Compound depressed #: craniectomy and antibiotics EDH: needs craniotomy if thickness more the 1 cm. or if causing mass effect

42. CONTINUED SDH: usually associated with other injuries that require craniotomy vs craniectomy + ICP monitor Post traumatic epilepsy: treatment is controversial Anticonvulsants usually phenytoin loading and maintenance may be given to patients at risk.

43. Management of severe head injury Coma implies: inadequate airway control ICP is usually elevated Hemodynamics are unstable Aim to maintain adequate cerebral perfusion pressure to maintain the integrity of neurons

44. What brain needs • Rest • Oxygen • Glucose

45. Treatment Intubate Oxygenate Keep head up at 30 EVD for ICP monitor and CSF drainage Mannitol is effective bolus or infusion Lasix may help Steroids are controversial Anticonvulsants in high risk patients SBP must be >100 O2 sat >98% PCO2 32-35 Temperature <37

46. Continued • Barbiturates for refractory ICP in salvageable patients. Needs enough experience before getting used due to serious side effects • craniectomy: Is an effective surgical method for ICP control in certain cases

47. Consequences • Death

48. How brain responds

49. ICP=MAP= ZER0= DEATH • Any increase in intracranial constituents results in subsequent compensatory responses to maintain normal ICP • Failure of compensatory mechanisms results in rise of ICP and reduction in CPP and subsequent herniating syndromes and eventually brain death • CBF is zero when ICP = MAP

50. ICP Waves