Primary and secondary head injury EDH and SDH

Management of EDH and SDH

1. DIFFERENCE BETWEEN PRIMARY AND SECONDARY HEAD INJURY MANAGEMENT OF EDH AND SDH Presenter- Dr Ravi Bhushan jha Rajeev Sir GangaRam Hospital New Delhi Moderater - Dr Srikrishna Das

2. Agenda Basic anatomy Head injury and its types Mechanism of Head injury EDH and SDH Management to a patient

3. Epidemology of Head injury 25% of all trauma deaths 50% of all deaths from RTA

4. Indian Head Injury Foundation India – highest rate of head injuries in the world Yearly 1,00,000 lives lost with 1 million suffering from severe head injury 1 out off 6 trauma victim dies in India RTA approx. 50% cases Motorcylist and pedesticians most common victims

5. Basic Anatomy Scalp Skull Meninges  Dura Mater  Arachnoid  Pia Mater Brain Tissue CSF and Blood

6. Head Injury Any Trauma to Scalp , skull or Brain Traumatic Brain Injury(TBI)- A non degenerative , non congenital insult to brain from an external mechanical force possibly leading to permanent or temporary impairment of cognitive , physical and psychosocial functions with an associated altered state of consciousness.

7. Head Injury Pathophysiologically :  Primary Brain Injury : - occurs at the time of impact -mechanical damage which is irreversible - causes permanent mechanical cellular disruption and microvascular injury. -includes 1) cerebral contusions 2) diffuse axonal injuries (DAI) 3) cerebral lacerations

8. Head Injury Secondary Brain Injury -occurs over a period of time ( from hours to days) after the moment of impact - Includes cascade of cellular , chemical , tissue or blood vessel changes -Largely preventable and treatable “In an ideal world no secondary brain damage would occur”

9. Causes of secondary brain damage Extracranial causes: Hypoxia Hypotension Hyponatremia Hyperthermia Hypoglycemia Intracranial Causes: Hemorrhage EDH SDH ICH IVH SAH Swelling Infection Meningitis Brain abscess

10. Causes of secondary brain damage If the extracranial insults are associated with intracranial lesions- Penumbra becomes the primary target of hypoxemia or ischemia. Higher levels of CPP are associated with better outcomes from head injury

11. Volume Pressure curve

12. The MONROE KELLIE doctrine “the total volume of the intracranial contents remain constant”

13. Brain Herniation

14. MECHANISM OF HEAD INJURY BLUNT INJURY High Velocity Low Velocity PENETRATING INJURY Gunshot Sharp instruments

15. MECHANISM OF HEAD INJURY Scalp injury Skull fractures : a) V ault fracture b) Base of skull fracture Intracranial injury : a) F ocal lesions Extradural hematoma Subdural hematoma Subarachnoid hematoma Intracranial hematoma b)Diffuse lesions Contusions (multiple) DAI

16. MECHANISM OF HEAD INJURY SCALP INJURY Cephal - Hematoma Subgaleal Hematoma Scalp laceration

17. MECHANISM OF HEAD INJURY Vault : Linear/stellate Depressed/non depressed Open/closed

18. MECHANISM OF HEAD INJURY Basilar skull fracture Usually diagnosed on CT imaging or on clinical Clinical signs include Battle sign ,Raccoon Eyes and CSF leak. May or may not be associated with seventh and eighth CN injury

19. Signs of Head injury

20. INTRACRANIAL LESIONS Extradural hematoma(EDH) Collection of blood & clot between dura mater and bones Source : Middle Meningeal Artery Dural Venous Sinuses Clinical feature: Brief loss of consciousness, headache, Nausea , Vomiting Lucid interval Rapid clinical deterioration Contralateral hemiparesis

21. Extradural hematoma(EDH) Classical presentation seen only in 1/3 rd cases On CT scan lentiform hyperdense lesion between skull and brain Associated with mass effect on underlying brain with or without midline shift. Overall mortality rate 18% in all cases but only 2% in isolated EDH

22. Treatment options Two treatment options Immediate surgical intervention Initial conservative , close clinical observation with possible delayed evacuation

23. Burr hole A burr hole is placed on the side of the dilating pupil. In the absence of a CT scan, the burr hole is placed 2 finger widths anterior to the tragus of the ear and 3 finger widths above the tragus of the ear.

24. Surgical management of Acute (EDH) Indications: Volume greater than 30cc should be evacuated regardless of GCS Volume less than 30cc or < 15mm thickness or < 5mm midline shift or GCS > 8 may be managed non-operatively Timing Any patient with acute EDH with GCS<9 / anisocoria should undergo operation “as soon as possible” Methods No preferred surgical method Neurosurgery 58:S2 1-62, 2006

25. MEDICAL THERAPIES FOR HEAD INJURY Head end elevation – 30 degrees Intravenous f luids : Maintain normovolemia Hypotonic saline should not be used Serum sodium levels monitored daily HYPERVENTILATION Barbiturates

26. Acute subdural Hematoma(SDH) B etween dura and arachnoid Disruption of cortical vessels or brain laceration produces hematoma Associated with significant primary injury Mortality rate as high as 40% in some series

27. Hyperdense concave lesion spreading across brain. Midline shift disproportionate to size of lesion

28. Surgical management of Acute SDH   Indications: SDH with thickness > 10mm or midline shift > 5mm should be evacuated regardless of GCS GCS < 9 should have ICP monitoring Thickness < 10mm or < 5mm midline shift should be evacuated if GCS drops 2 or more points from injury to admission, pupillary function is abnormal, or ICP> 20 mm Hg Timing “As soon as possible”   Methods Craniotomy with or without bone flap removal/ duroplasty

29. Chronic subdural Hemorrhage Usually occurs in elderly on anti coagulant or anti platelet agents H /o minor head injury in weeks or months prior to presentation C/f- H eadache, cognitive impairment, focal neurological deficit and seizures. CT scan: acute blood (0-10 days) = hyperdense sub acute blood (10-14 days) = isodense chronic blood (>2 weeks) =hypodense

30. Acute on chronic SDH Chronic SDH will more recent hemorrhage in dependant (posterior) areas. Treatment is Burr hole evacuation rather than craniotomy

31. Comparision EDH Usually accidental injury Middle meningeal artery Lentiform Donot cross sutures SDH Usually non accidental Bridging veins and dural venous sinuses Cresentic Cross sutures

32. APPROACH TO A PATIENT WITH HEAD INJURY History Initial Assessment Primary Survey Secondary Survey

33. History Bystanders and paramedics Preinjury state Mechanism and energy involved in injury Consciousness after injury Length of time taken for extrication Past medical history- Anticoagulant , Antiplatelet Signs of RICP

34. Primary Survey Ensure adequate oxygenation and circulation Exclude hypoglycaemia Check pupil size and and response, GCS asap

35. GCS

36. Airway maintenance with cervical spine protection Breathing and ventilation

37. Circulation Maintain MAP >90mmhg- adequate Hematocrit >30% Isolated intracranial injuries do not cause hypotension LOOK FOR THE CAUSE OF HYPOTENSION

38. Disability Pupilary size Motor function Injury level  Constricted?  narcotics?  Sluggish/dilated?  mid brain ICP  Unilateral dilation?  pressure on CNIII  Fixed and Dilated?  herniation

39. SECONDARY SURVEY  Examination of Head to toe ( Log roll to check whole spine)  Glasgow Coma Scale  Detailed Neurological Examination

40. SECONDARY SURVEY HEAD: Inspetion and palpation of scalp Battle sign , Raccoon eye , Panda eye Hemotympanum, CSF rhinorrhoea Complete examination of all cranial nerve

41. SECONDARY SURVEY Neck and spine: 10% associated with TBI Cervical spine injury must be excluded In high velocity injury( RTA , Fall from height) thoracic and lumber spine injury be must be excluded.

42. Severity of head injury Head injury classification using GCS score Minor head injury GCS 15 with no LOC Mild head injury GCS 14 or 15 with LOC Moderate head injury GCS 9-13 Severe head injury Gcs 3-8

43. History GPE Neurological examination CT scan ?? Discharge with advice

44. MANAGEMENT OF MILD HEAD INJURY ( GCS14 -15) Before discharge- Criteria 1.GCS must be 15/15 2.No focal neurological deficit 3.Accompanied by responsible adult 4.Verbal and written advice given

45. Phineas Gage: Neuroscience’s Most Famous Patient

46. THANK YOU 20 march 2018 World Head injury awarenss day