Management of head injury

Robust presentation on basic management of head injury for medical students, resident doctors, Nurses and other allied professionals

1. MANAGEMENT OF HEAD INJURY BY DR GEORGE OWUSU (Registrar NSU)

2. OUTLINE Introduction Relevant anatomy of the Head Definitions Epidemiology Aetiology Classification Pathogenesis Specific entities Assessment/ Treatment of head injured patient Conclusion

3. INTRODUCTION The head contains vital structures responsible for the control of the cognitive, physical and psychosocial functions of man. Injuries to these vital organs may alter the proper function of man with several debilitating impairments and even death.

4. RELEVANT ANATOMY OF THE HEAD

5. DEFINITIONS INJURY: Exchange of energy between the environment and tissue that exceeds the resilience of the tissue resulting in disruption of the structural and physiological integrity of the tissue Head injury is a pathophysiological event in which there is exchange of energy between the cranium, its content and covering that exceeds the resilience of those tissues either in isolation or in combination.

6. DEFINITIONS Traumatic brain injury (TBI) is a non-degenerative, non-congenital, insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical and psychosocial functions with an associated diminished or altered state of consciousness.

7. EPIDEMIOLOGY Trauma is one of the leading causes of death and head injury is the commonest cause of death in trauma patients (50%). Estimated about 500,000 to 1 million cases of head injury occur yearly. Common between age 15 - 45 years. More in males than females 4:1

8. AETIOLOGY Road traffic accidents 60% Falls 20-30 % Violence 10 % Sport 10 %

9. CLASSIFICATION Based on severity Closed and Open (penetrating) Primary and Secondary Focal and diffuse Based on aetiology Based on location of the lesion

10. CLASSIFICATION BASED ON SEVERITY USING THE GLASGOW COMA SCORE:

11. CLASSIFICATION

12. CLASSIFICATION CLOSED VS OPEN (Penetrating) Open (penetrating) head injuries involve breach of the cranium (fracture) and dura mater with communication to the external environment.

13. CLASSIFICATION PRIMARY AND SECONDARY: Primary injuries are defined as immediate injuries to neurons from transmission of force of impact (from initial impact) Secondary injuries are subsequent neuronal damage due to the sequelae of trauma.

14. CLASSIFICATION FOCAL AND DIFFUSE BRAIN INJURY

15. PATHOGENESIS

16. PATHOGENESIS MONROE-KELLIE DOCTRINE: Auto-regulation occurs to maintain the Cerebral Perfusion pressure and cerebral blood flow. CPP= MAP – ICP (works within 50-150mmHg) The pressure-volume relationship between the ICP, volume of CSF, Blood and brain tissue and cerebral perfusion pressure known as the Monroe Kellie Doctrine

17. SPECIFIC INJURIES Soft tissue injuries laceration Subgaleal haematoma/ cephal haematoma Skull fractures Concussion Diffuse axonal injury Intracranial haemorrhages Epidural haemorrhage Subdural haemorrhage Subarachnoid haemorrhage Contusion Intraparenchymal/ intraventricular haemorrhage

18. LACERATIONS Easily recognized The most minor type of head trauma. Scalp is highly vascular, presents with profuse bleeding. Major complication is infection. Apposition with sutures.

19. SUBGALEAL/ CEPHAL HAEMATOMA Subgaleal haematoma Occurs following rupture of emissary veins. Collection between galea aponeurotica and periosteum. Can cross suture lines Rare but lethal. (cephal haematoma are subperiosteal and do not cross suture lines.

20. SKULL FRACTURES Linear skull fracture break in the continuity of bone without alteration of relationship of part cause- Low velocity injuries Depressed Inward indentation of skull cause- powerful blow

21. SKULL FRACTURES Comminuted skull fracture multiple linear fractures with fragmentation of bones into pieces. Compound skull fracture Injury to the skull and surround tissues and neurovascular bundles.

22. SKULL FRACTURE ACCORDING TO LOCATION Frontal fracture Temporal fracture Parietal fracture Posterior fossa fracture Orbital fracture Basal skull fracture

23. TEMPORAL BONE FRACTURE Boggy temporal muscle because of extravasation of blood Oval shaped bruise behind the ear in mastoid region (battle sign) CSF otorrhoea

24. PARIETAL BONE FRACTURE Deafness CSF Otorrhoea Bulging of tympanic membrane by blood or CSF Facial paralysis

25. ORBITAL FRACTURE Periorbital ecchymosis(RACCO-ON EYES) Optic nerve injury

26. BASAL SKULL FRACTURE CSF Otorrhoea , rhinorrhoea Bulging of tympanic membrane Battle’s sign Facial paralysis Tinnitus , vertigo

27. TEST TO DETERMINE CSF LEAKAGE Method 1 Check for presence of glucose Dextrostrip / Tes -Tape strip If blood is present in the fluid, the test will be unreliable.

28. TEST TO DETERMINE CSF LEAKAGE Method 2( halo ring sign). Allow leaking fluid drip onto an absorbent material ( white pad/towel). Observes the drainage Within a few minutes the blood coalesces into center and a yellowish ring encircles the blood.

29. CONCUSSION A temporary neuronal dysfunction following non-penetrating head trauma Deficits resolves over minutes to hours COLORADO GRADING SYSTEM: Grade 1: Head trauma patients with confusion only Grade 2: Patients with Amnesia Grade 3: Patients who lose consciousness

30. DIFFUSE AXONAL INJURY Caused by damage to axons throughout the brain, due to rotational acceleration and then deceleration.

31. DIFFUSE AXONAL INJURY

32. EPIDURAL HAEMORRHAGE Accumulation of blood between the skull and dura Arterial bleed in 85% (middle meningeal artery) Has a classic , three stage clinical presentation probably seen in 20% of cases Ipsilateral 3 rd nerve palsy with contra -lateral hemiparesis (uncal herniation) Delayed epidural haematoma may occur in 9 to 10% of epidural haematomas

33. EPIDURAL HAEMORRHAGE Shows as bright (hyperdense) blood clot on cranial CT Biconvex shaped, well defined borders and does not cross suture lines.

34. EPIDURAL HAEMORRHAGE Open craniectomy is done for evacuation of congealed clots and haemostasis Criteria for conservative management: Clot volume < 30cm 3 Clot thickness <1.5cm GCS >8 Good outcome in 85-90 % of patients with rapid intervention Mortality is about 20%

35. SUB-DURAL HEMATOMA Subdural hematoma occurs from bleeding between the dura mater and the arachnoid layer of the meninges. Results from venous bleeding (bridging veins) Types acute subdural hematoma subacute subdural hematoma Chronic subdural hematoma

36. ACUTE SUBDURAL HAEMORRHAGE It develops within 24-48 hrs after head trauma Commonly related to acceleration deceleration injury The size of hematoma determines the patient clinical presentation Decreasing level of consciousness from drowsy and confused to unconsciousness Headache Ipsilateral pupil dilation Contra-lateral hemiparesis

37. ACUTE SUBDURAL HAEMORRHAGE On head CT scan, the clot is bright or mixed-density crescent-shaped (lunate) M ay have a less distinct border and crosses sutural lines Does not cross the midline

38. ACUTE SUBDURAL HAEMORRHAGE Open craniotomy for evacuation of clot and decompression is indicated for: Clot thickness > 1cm or smaller hematomas that are symptomatic Midline shift >5cm GCS drop by two or more points from time of injury to hospitalization Prognosis for functional recovery is worse than EDH, due to associated primary brain injury from high energy impacts

39. SUBACUTE SUBDURAL HAEMORRHAGE Usually occurs within 2-14 days of the injury The alteration in mental status as hematoma develops Progression depends on the size and location of hematoma Presents as Iso-dense clot on cranial CT scan.

40. CHRONIC SUBACUTE HAEMORRHAGE It develops over weeks or months after seemingly minor head injury. Accumulation of blood breakdown products The peak incidence of chronic SDH is in 50-60 Years of age Clinical manifestations- progressive alteration in level of consciousness, headaches, seizures, contralateral hemiparesis

41. CHRONIC SUBDURAL HAEMORRHAGE Presents as hypodense lesions on cranial CT scan May however have areas of hyperdensity from recurrent bleeds ‘ acute on chronic SDH’

42. CHRONIC SUBDURAL HAEMORRHAGE Chronic SDH > 1cm or any symptomatic SDH should be surgically drained and irrigated via: Burr hole drainage Open craniotomy PREVENTION OF ACCUMULATION: Subdural or subgaleal drain left in place for 1 -2 days Mild hydration and bedrest with head of bed flat may encourage brain expansion. High level of inspired oxygen to draw out Nitrogen from cavity

43. SUBARACHNOID HAEMORRHAGE Bleeding occurs between the arachnoid and pia mater CAUSES: Rupture of Berry aneurism Trauma (fracture at the base of the skull leading to internal carotid aneurysm) CLINICAL FEATURES: Explosive headache, “worst headache of my life” nausea and vomiting, decreased LOC or coma. Signs of meningeal irritation

44. SUBARACHNOID HAEMORRHAGE Increased attenuation is seen in the CSF Spaces over the cerebral hemisphere on cranial CT scan

45. CONTUSION Bruise of the brain Breakdown of small vessels and extravasation of blood into the brain. Rarely cause significant mass effect due to small amount of blood (developing oedema may cause mass effect). May progress to frank haematoma within first 24 hours.

46. CONTUSION May occur in brain tissue opposite site of impact ‘ contre -coup injury’ Results from deceleration of the brain against the skull. Contusion appears as bright areas (hyperdense) on cranial CT scan.

47. INTRACEREBRAL HAEMORRHAGE Also known as intra-axial haemorrhage (occuring in brain tissue) There are two main types Intraparenchymal haemorrhage Intraventricular haemorrhage Causes: Hypertensive vasculopathy (70-80%) Ruptured Aneurism Trauma- 16%

48. INTRACEREBRAL HAEMORRHAGE CLINICAL FEATURES: Rapidly progressive severe headache, building over several minutes, often accompanied by focal neurological deficits, nausea and vomiting, decreased level of consciousness . Also depending on site of haemorrhage: Basal ganglia/ internal capsule -hemiparesis, dysphasia Cerebellum –ataxia, vertigo Pons – cranial nerve deficits, Coma Cerebral Cortex – hemiparesis, hemisensory loss, hemianopsia , dysphasia

49. INTRACEREBRAL HAEMORRHAGE INDICATIONS FOR CRANIOTOMY: Clot volume > 50cm 3 Clot volume > 20cm 3 with neurologic deterioration (GCS 6-8) Associated midline shift > 5mm Basal cistern compression

50. ASSESMENT/ TREATMENT OF HEAD INJURED PATIENT A T L S protocol Air way and cervical spine control Breathing and ventilation Circulation Dysfunction of the C N S Exposure in a controlled environment

51. HISTORY TAKING Mechanism of injury Loss of consciousness or amnesia Level of consciousness at scene and on transfer Evidence of seizures History of vomiting, Lateralizing sign Pre-existing medical conditions Medications (especially anticoagulants) Illicit drugs and alcohol

52. CLINICAL FEATURES Loss of consciousness/ Disorientation Features of raised ICP Vomiting Headache Coma Bleeding from craniofacial orifices Periorbital ecchymosis ( racoon eyes, panda eyes) Mastoid bruising (battle’s sign) Subconjuctival haemorrhage Lateralizing signs Focal weakness Focal seizure Unilateral dilatation of a pupil

53. PHYSICAL EXAMINATION Glasgow Coma Score Pupil size and response Signs of skull fracture Bilateral periorbital edema (raccoon eyes) Battle’s sign (bruising over mastoid) Cerebrospinal fluid rhinorrhoea or otorrhoea Haemotympanum or bleeding from ear Full neurological examination: tone, power, sensation, reflexes

54. INVESTIGATIONS BASELINE INVESTIGATIONS Full blood count SE/U/Cr Urinalysis ± grouping and cross match blood SPECIFIC INVESTIGATIONS Skull and C-spine X-ray Cranial CT Scan Bain MRI Transcranial doppler

55. INVESTIGATIONS COMPUTERISED TOMOGRAPHY: CT scan is considered the best diagnostic test to evaluate for cranio -cerebral trauma because it allows rapid diagnosis and intervention in the setting The National Institute for Health and Clinical Excellence (NICE ) criteria:

56. TREATMENT The goal of treatment is to: Prevent secondary brain injury Control and maintain the intracranial pressure (maintain ICP below 20mmHg and CPP between 50-70mmHg) Prevent other attending complications Return to normal function. Severe head injured patients/ those with intracranial haemorrhage, contusion or diffuse axonal injury are managed in the ICU

57. TREATMENT TO PREVENT SECONDARY BRAIN INJURY (especially from hypotension and hypoxia) Maintain systolic blood pressure >90mmHg PaO 2 < 60mmHg and O 2 saturation < 90% should be avoided. M onitor blood glucose Monitor temperature Prevent occurrence or recurrent early post-traumatic seizures

58. TREATMENT Prophylactic anticonvulsant Prophylactic anticonvulsants is not recommended in all patients Some risk factors for seizure Cortical contusion Depressed skull fracture Subdural hematoma Intracerebral hematoma Penetrating head wound Seizure within 24 h of injury

59. TREATMENT CONTROL OF INTRACRANIAL PRESSURE: Nurse in 30 o head up position (head of bed) Ensure cervical spine immobilisation device does not obstruct jugular venous flow ICP Monitors: for patients with GCS <8, Patients with abnormal cranial CT findings Post operative patients. Initiate treatment of ICP when >20mmHg

60. TREATMENT CSF drainage External ventricular drain, ventriculostomy Sedation and pharmacologic paralysis Using barbiturates Use of mannitol and other diuretic agents 0.25- 1g/kg every 4-6 hours (monitor serum osmolality - 320mOsm/kg) Hyperventilation to PaCo2 of 30-35mmHg (cranial vasoconstriction) Decompressive craniectomy

61. TREATMENT PREVENTION OF OTHER COMPLICATIONS: Peptic Ulcer prophylaxis with proton pump inhibitors Compression stockings or antithrombotic pumps for prophylaxis against DVT Nutrition: feeding should be initiated within 7 days of injury (high calorie, high protein diet) Care for unconscious patients (bladder, bowel,breathing,bedsores,bones,basal metabolic demands)

62. Treatment IV fluid ( N/S, D/S, P/S) Analgesic Tetanus prophylaxis 30 o head up to encourage venous drainage Anticonvulsants if needed ( phenytoin , carbamazepine , phenobarbitone ) Intubate if G C S is less than 8 and the patient should be transfer to ICU Early nutritional rehabilitation of this patients – Enteral preferred Care to prevent aspiration pneumonia by ensuring NG tube is in place.

63. SURGICAL TREATMENT INDICATIONS FOR OPERATIVE MANAGEMENT: For space occupying haematomas Based on clot volume Midline shift >5mm Smaller haematomas in treacherous positions Eg posterior pituitary fossa Patients with diffuse cerebral oedema with recalcitrant raised ICP for decompressive craniectomy Patients with open, depressed skull fractures with or without sinus involvement.

64. SURGICAL OPTIONS Burr-hole- opening into cranium with a drill Craniotomy- bone flap is temporarily removed from the skull to access the brain Craniectomy – Excision into the cranium to cut away a bone flap Cranioplasty – surgical repair of a defect or deformity of a skull

65. REHABLITATION Ambulatory and Home Care Nutrition Bowel and bladder management Seizure disorders Family participation and education Physiotherapy

66. PREVENTION Health Promotion Prevent car and motorcycle accidents To Wear safety helmets Legislation Enforcement of safety laws

67. CONCLUSION The sequelae of a head injured patient ranges from a lifetime of potential neurological impairments and disabilities, with a critical burden of care on the patient and immediate community at large. Care should be taken to avoid occurrence.