Traumatic brain injury

A summary of head injury and traumatic injury diagnosis and management. For any medical student or healthcare provider.

1. TRAUMATIC BRAIN INJURY Wanjau George kariuki Alicen Jeruto Kiprop

2. Outline. Introduction Epidemiology. Aetiology Pathophysiology Classification. Management complications

3. Introduction. Head injury- trauma to the head Traumatic brain injury- An alteration in brain function, or other evidence of brain pathology, caused by an external force 1.

4. Epidemiology. Is a major public health concern worldwide. 69 million people are estimated to sustain TBI each year 2. Head injury following road traffic collision is more common in LMICs, and the proportion of TBIs secondary to road traffic collision is likewise greatest in these countries

5. epidemiology Of Head Injuries In Kenya 3 1979-1985 (pre- ct scan era) Mortality 16 % in adults and 1.4% in children . The male to female ratio was 7:1. in adults and 1.1:1 in children . Most of the TBI in adults in the pre-CT scan period were due to either road traffic accidents (46%) or assaults (40%), Children falls from a height being most frequent (50%) followed closely by road traffic accidents (42%).

6. epidemiology Of Head Injuries In Kenya 3 1999-2009 CT scan era The male to female ratio in patients with severe TBI (GCS 8 and below) was 8:1 while the overall mortality was 57% 

7. Aetiology. Road traffic accidents – commonest- about 48-53% Falls – 20-28% Sports and recreation activities- 3-9% Assault

8. Pathophysiology. Normal cerebral blood flow is 55mL/100 gm /min If this rate drops below 20 mL/100 gm /min infarction will result The flow rate is related to cerebral perfusion pressure ( CPP) CPP (75–105 mmHg) = MAP (90–110 mmHg) − ICP (5–15 mmHg). Monro -Kellie Doctrine Skull is a confined rigid space contains the brain, CSF and blood The sum of the Intracranial volumes of blood, brain, CSF is constant , and that an increase in any one of these must be compensated by an equal decrease in another, otherwise pressure will rise. Once ICP rises, it results decreased CBF and eventually brain herniation

9. Classification. According to Severity Morphology Mechanism of injury

10. Severity. Depending on GCS Minor- GCS15 with no LOC Mild-14/15 with LOC Moderate-9-13 Severe- 3-8

11. Mechanism of injury. Missile injury damage is the result of an object entering the cranial cavity and dissipating energy through the brain. Damage is often focal and the extent relates to the velocity of the missile . High velocity vs low velocity Non-missile injury rapid deceleration and acceleration which causes the brain to move within the cranial cavity and to come into contact with bony protuberances within the skull. This results in contusions, lacerations, and shearing strains within the brain substance. The acceleration/deceleration forces rather than actual impact against the skull are the critical factors in producing brain injury

12. Morphology. Primary injury - occurs at the time of impact Secondary brain injury- occurs as a result of events after the initial injury. Causes of secondary injury Hypoxia: PO2<8kPa Hypotension : systolic blood pressure (SBP) < 90 mmHg Raised intracranial pressure (ICP): ICP > 20 mmHgLow cerebral perfusion pressure (CPP): CPP < 65 mmHg Pyrexia Seizures Metabolic disturbance

13. Primary brain injury. Contusion Diffuse axonal injury concussion

14. Cerebral contusion. Occurs at the time of injury as the result of contact between the brain and bony protuberances of the skull base. Have a characteristic distribution- orbital surface of frontal lobes, frontal poles, around the Sylvian fissure, temporal poles, and undersurface of temporal lobes. They occur on the crests of gyri but commonly extend into subcortical white matter.

15. Cerebral contusion. rarely require immediate surgical treatment. must be admitted for observation as these lesions will tend to mature and expand for 48–72 hours following injury. delayed surgical evacuation to reduce the mass effect

16. Diffuse axonal injury. Most common cause of coma after head injury. Widespread axonal injury occurs as a result of shear and tensile strains . Least severe- in the parasagittal white matter of the cerebral hemispheres. Moderately severe- least + focal lesions in the corpus callosum. Very severe- discrete lesions are found in the dorsolateral quadrants of the rostral brainstem.

17. Concussion. Concussion is transient loss of consciousness following non-penetrating closed head injury without gross or microscopic brain damage.

18. Indications for CT-Scan (NICE) GCS <13 at any point GCS 13/14 at 2 hrs. Neurological deficits. Suspected skull fracture. Seizures. More than 1 episode of vomiting. Urgent CT scan if Age>65. Coagulopathy. Dangerous mechanism of injury. Anterograde amnesia.

19. Intracranial hematomas.

20. Extradural hematoma Aka epidural hematoma. Is a neurosurgical emergency Common in young people In < 30 yrs. – 40% - associated with skull # In > 30 yrs. – almost all associated with skull # 20% associated with subdural hematoma

21. Extradural hematoma Temporal region most affected as the pterion is thin and it overlies a large vessel. 1 Classical presentation( of patients) Injury›››› lucid interval(headache but otherwise normal) ›››› rapid deterioration as a result of brain compression There may be no primary brain injury with an EDH. Mortality – 20-55% With early treatment – 5-10%  

22. Extradural hematoma CT scan shows lentiform ( lens shaped or biconvex) hyperdense lesion between the skull and brain. There may be an associated mass effect on the underlying brain, with or without a midline shift . Areas of mixed density may be seen in a lesion that is actively bleeding.

23. Extradural hematoma. Surgical management is evacuation via a craniotomy

24. Acute subdural hematoma. Accumulates between dura and arachnoid mata Due to disruption of cortical vessels or brain laceration Almost always associated with primary brain injury

25. Acute subdural hematoma. Pts. present with impaired level of consciousness from the time of injury which may deteriorate as the hematoma expands. Mortality with treatment is as high as 40%

26. Acute subdural hematoma. The CT appearance of an ASDH is hyperdense ( acute blood ) but the haematoma spreads across the surface of the brain(concave)

27. Acute subdural hematoma. The treatment of an ASDH is usually evacuation via a craniotomy. Small haematomas with little mass effect may be managed conservatively in. It may be inappropriateto perform surgery on cases with a very poor prognosis: factors best GCS pupillary reactivity Age presence of anticoagulants

28. Chronic subdural hematoma. Common in elderly esp those on antiplatelet/anticoagulant therapy. Hx of minor head trauma days,weeks,months Clinical features of CSDH include headache , cognitive decline focal neurological deficits seizures. exclude hypoxic, metabolic and endocrine disorders

29. Chronic subdural hematoma. Treatment of a CSDH and most acute-on-chronic subdural haematomas is evacuation via burr hole(s) rather than craniotomy. This is an important distinction as burr holes can be easily performed under local anesthetic in an elderly patient with extensive comorbidity

30. Ct findings- subdural hematoma

31. Intra-cerebral haemorrhage Haemorrrhage within the brain tissue Two main types Intraparennchymal Intraventricular causes Hypertensive vasculopathy (70-80%) Ruptured AVM Blood dyscrasias .

32. Management.

33. Supportive Measures . Endotracheal intubation for patients with GCS<8 and poor airway protection. Cautiously lower blood pressure to a MAP less than 130 mm Hg, but avoid excessive hypotension. Rapidly stabilize vital signs, and simultaneously acquire emergent CT scan. Maintain euvolemia , using normotonic rather than hypotonic fluids, to maintain brain perfusion without exacerbating brain edema Avoid hyperthermia. Facilitate transfer to the operating room or ICU.

34. Decrease cerebral edema. Modest passive hyperventilation to reduce PaCO2 Mannitol , 0.5-1.0 gm /kg slow iv push Furosemide 5-20 mg iv Elevate head 20-30 degrees, avoid any neck vein compression Sedate and paralyze if necessary (struggling, coughing etc will elevate intracranial pressure)

35. Surgery. Surgical Evacuation of hematoma: No surgical intervention if collection <10ml unless; The GCS score decreases by 2 or more points between the time of injury and hospital evaluation The patient presents with fixed and dilated pupils The intracranial pressure (ICP) exceeds 20 mm Surgical decompression hematoma >10mm or >5mm midline shift Hematoma>30mls

36. Types of surgery. Burr-hole Craniotomy -bone flap is temporarily removed from the skull to access the brain Craniectomy –in which the skull flap is not immediately replaced, allowing the brain to swell, thus reducing intracranial pressure Cranioplasty -surgical repair of a defect or deformity of a skull.

37. Mild head injury Discharge after history, physical examination and a period of observation. (hours) Must met the following criteria before discharge GCS 15/15 with no neurological deficits In the company of an adult. Not under influence of drugs/ alcohol. Verbal and written advice on head injury given (symptoms that should prompt a revisit) CT-scan done***

38. Complications. Neurological deficits or death Seizures Obstructive Hydrocephalus Spasticity Urinary complications Cushing’s ulcer Neuropathic pain Deep venous thrombosis Pulmonary emboli Cerebral herniation Aspiration pneumonia

39. Glasgow outcome score

40. References. Oxford Textbook of Surgery Merck Manuals- Professional Version Bailey and Love Uon online repository.

41. The end