1. By ABDULRAHMAN J. SABBAGH MBBS, FRCSC National Neurosciences Institute (NNI), King Fahad Medical City (KFMC). Wednesday, May 28, 2015 1

2. How many Stars are there in our Galaxy?

3. TBI Arguably the most common Cranial condition that Neurosurgeons deal with Decline in mortality from severe TBI: – 50% 1970s to 36% 1980s to 27% 1990s to 15% 2000s – EMS, Critical Care, CTs In the USA a brain injury occurs every 7s and result in death every 5 min TBI accounts for 1/3 of all trauma related deaths 50,000 patients die / year 80,000 patients suffer long-term disability Motor vehicle crashes account for 50% Two times greater in men than women 3

4. Outcome of TBI Death : 30 -36% Persistent vegetative state : < 5% Severe Disability : 15% Moderate Disability : 14 – 20% Good Outcome : 25%

5. GCS 5 Patients with Glasgow coma scores of 8 or below require oral endotracheal intubation.

6. CLASSIFICATION OF TBI 6

7. Head Injury Severity Scale (HISS) 7 Stein SC et al. Brain Inj. 1995 Jul;9(5):437-44. The Head Injury Severity Scale (HISS): a practical classification of closed-head injury.

8. MILD TBI 80% of all TBI Are skull x-rays helpful? 3% of pts with mild TBI deteriorate How could I know if my pt is in the 3%? Classification of mild TBI: – Admission GCS – Duration of LOC – Post traumatic amnesia – Focal neurological deficits 8

9. MILD TBI (cont’d) Category 0: GCS=15, No LOC, No PTA, No risk factors D/C Home Category 1: GCS=15, LOC < 30min, PTA < 60min, No RF CT HEAD Category 2: GCS=15 with RF Category 3 GCS=14 with or without RF RF: ambiguous accident, continued PTA, clinical signs of skull #, H/A, Vomiting, Focal deficit, age 60, coagulation dis, high speed accident 9

10. MODERATE TBI 10% of all TBI pts seen in ER 10% will deteriorate CT head in all cases Admission VS/NVS F/U CT 10

11. SEVERE TBI GCS < 8 Will typically be evident by CT ICU required The worse the GCS the worse the prognosis In this regard the motor component of GCS is more important than the other 2 11

12. SCALP INJURY 5 Layers – Skin – Connective tissue – Galea Aponeurotica – Loose areolar tissue – Pericranium Bruising Laceration 12

13. SKULL #S Fracture patterns depend on: – Thickness – Morphology – Composite nature of the bone Types – Linear – Depressed (open or closed) – Basilar or Basal 13

14. LINEAR SKULL #S Most common Direct impact to the cranium From a broad surface Separation of the # edges (diastasis) Thinnest areas of the skull Squamous portion of temporal bone and damage of middle maningeal artery - epidural hematoma 14

15. DEPRESSED SKULL # Small surface area of the object Punched inwards CSF leakage Open (laceration of scalp) Infection Seizures Ping Pong ball 15

16. DEPRESSED SKULL # Surgical intervention when … – > 8-10 mm depression (or greater than the thickness of skull) – Deficit related to underlying brain – CSF leak – Compound # – Cosmetic region

17. BASAL SKULL # Direct trauma to Mastoid (Battle’s sign) Occipital Supraorbital (Raccoon eyes) Indirectly to Cribriform plate CSF leak Rhinorrea Otorrea Cranial nerves Carotid artery 17

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19. SDH More common than EDH In acute form are associated with other significant brain injuries Cerebral contusion (67%) Highest Mortality rate 60-70%. (acute SDH) Can be subdivided into Acute - less than 3 days Subacute - 3 days to 3 weeks Chronic - after 3 weeks 19

20. SDH Surgical intervention when … – Symptomatic – SDH thickness > 1cm (5mm in Peds) – Midline shift > 5mm Positive Displacement Factor or shift out of proportion – Midline shift > SDH thickness Timing of Sx – Early : 0 – 4 Hrs from injury – Late : > 4 Hrs

21. Natasha Richardson (1963-2009) 21

22. EDH An acute lesion Commonly seen in frontal or temporal region 75-90% of patients with epidural hematomas will have fractures. Middle meningeal artery (85%) Post fossa ones are flattened “Lucid interval” “Kernohan’s phenomenon” 22

23. EDH

24. TRAUMATIC SAH Most common lesion from closed head injury. Significant SAH always associated with cortical contusions. Block arachnoid villus causing hydrocephalus. 24

25. TRAUMATIC INTRACEREBRAL CONTUSIONS Contusions classified into: Coup Conter-coup Fracture contusions Frontal and temporal contusions are the predominant ones regardless of the site of impact. 25

26. ICH Surgical intervention when … – Progressive neurological deterioration – Refractory high ICP – GCS 6 – 8 – Frontal or temporal contusions >20 cm 3 – Midline shift > 5mm – Any lesion >50 cm 3

27. DAI Arises from rotational injury forces (angular acceleration). Microscopic axonal injury – the sudden acceleration shear forces can disrupt axons – Eosinophilic spheres (retraction balls) Grossly: – DAI shows minimal gross alteration. SEVERITY – Mild: coma 6 – 24 Hrs – Moderate: coma > 24 Hrs without decerebrate posturing – Severe: coma > 24 Hrs + decerbrate posturing and flaccidity – CLINICAL HALLMARK – prolonged loss of consciousness. – occurs immediately after the injury. – no correlation with external trauma or skull fractures. 27

28. QUIZ 23 YO F LHD, FELL DOWN THE STAIRS, NO LOC, IN ER: OPENS EYES SPONTANEOUSLY, OBEYS, CONFUSED 47 YO M RHD, MVC, LOC @ SCENE. IN ER: OPENS EYES TO PAIN, MOANING, WITHDRAWS WITH LT. SIDE BUT NOT MOVING RT. 28

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32. Late complications of TBI Posttraumatic SZ Communicating Hydrocephalus Postconcussive Syndrome – Cluster of Symptoms (organic / psychological) H/A, dizziness, visual disturbance, anosmia, hearing difficulty Difficulty concentrating Emotional difficulties, insomnia, loss of libido

33. Approach to Trauma History: – Age, Sex – Time & Place of Injury – MECHANISM of INJURY – Assessment @ Scene ABCs GCS Pupils – Vomiting, Aspiration, SZ – Drugs (Dose, time), ETOH – PMHx – Other Casualties

34. Approach to Trauma Primary Survey: – A: Airway (+ Full Spine Precautions) – B: Breathing – C: Circulation – D: Disability (Neuro Assessment) GCS, Pupils, H&N + EENT, DRE – E: Exposure Resuscitation (F: Fluids, Foley if not c.i.) Secondary Survey: – System by System – Radiographs, Peritoneal Lavage, CT Definitive Care

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37. PUPILS Unilateral Dilated: CN III compression secondary to tentorial herniation Traumatic Mydriasis Bilateral Dilated: Inadequate brain perfusion, bilateral CN III compression Bilateral Miotic: Drugs, metabolic encephalopathy, Pontine lesion Unilateral Miotic: Injured sympathetic pathway (e.g. carotid sheath injury)

39. Symptoms develop slowly – headache – neurologic symptoms related to the specific part of the brain that is infected – altered mental status – seizures – Fever and stiff neck occur in less than one- third of cases. Fever – Additional symptoms vomiting, nystagmus, nystagmus poor balance, uncoordinated movements.

40. Conclusion GCS Mechanism of Injury Don’t forget the Spine ! Utilization of resources Timely Disposition

42. Brain abscess is a collection of pus and infected material coming from: – Local ear infection, dental abscess paranasal sinuses mastoid air cells of the temporal bone mastoid Post op, post skull # – remote ( lung, heart, kidney etc.) lungheartkidney

43. Diagnosis (CT) + (MRI) Biopsy +/- Evacuation Other tests – blood cultures – X rays of the chest – a physical exam of the ears, sinuses, and teeth. – A test for human immunodeficiency virus (HIV)immunodeficiency

44. CT Brain pre & post contrast (Brain abscess)

45. Cerebeller abscess

46. Axial T2-weighted MRI in a patient with a right frontal abscess Axial T1-weighted MRI in a patient with a mature cerebral abscess of the right frontal lobe

47. Anterior view of a chest radiograph in a patient with thick-walled right lung abscess. The patient later developed a brain abscess

48. Treatment intravenous antibiotics, chosen to match the infecting bacterium if known, or to cover a wide spectrum of possibilities if not. Treatment usually continues for six to eight weeks.antibiotics Aspiration surgery For patients with many sites of infection, aspiration or surgical removal is not done because of the increased difficulty and risk of the procedure. For these patients, antibiotic therapy alone is used. Steroid treatment is controversial, but may be indicated in some cases.

49. Prognosis Fatal in about 20% of cases. Half of those who survive have some residual neurological deficit There are several reasons why patients with brain abscess can have a poor prognosis. – Wrong diagnosis or antibiotics. – Diffuse infection – Fungal infection difficult to diagnose. – The location of the abscess may be deep within the brain, or the infection may have moved into many locations within the brain. complications can – Coma – Permenan deficit – Seizures Infants and neonates have worse prognosis than adults – I.Q. usually < 80 The prognosis depends largely on the clinical presentation and rapidity of progression.

50. Prevention Brain abscess may be preventable by prompt and aggressive treatment of the infections which give rise to it, especially sinus and ear infections.