Primary and secondary head injury EDH and SDH
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Management of EDH and SDH
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Primary and secondary head injury EDH and SDH
- 1. DIFFERENCE BETWEEN PRIMARYAND SECONDARY HEAD INJURY MANAGEMENT OF EDHAND 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 ◦ RTAapprox. 50% cases ◦ Motorcylist and pedesticians most common victims
- 5. Basic Anatomy Scalp Skull Meninges Dura Mater Arachnoid Pia Mater Brain Tissue CSF and Blood
- 15. 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.
- 16. 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
- 17. 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”
- 18. 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
- 19. 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
- 21. The MONROE KELLIE doctrine “the total volume of the intracranial contents remain constant”
- 22. Brain Herniation
- 23. MECHANISM OF HEAD INJURY BLUNT INJURY High Velocity Low Velocity PENETRATING INJURY Gunshot Sharp instruments
- 24. MECHANISM OF HEAD INJURY Scalp injury Skull fractures : a) Vault fracture b) Base of skull fracture Intracranial injury : a) Focal lesions Extradural hematoma Subdural hematoma Subarachnoid hematoma Intracranial hematoma b)Diffuse lesions Contusions (multiple) DAI
- 25. MECHANISM OF HEAD INJURY SCALP INJURY Cephal-Hematoma Subgaleal Hematoma Scalp laceration
- 26. MECHANISM OF HEAD INJURY Vault : Linear/stellate Depressed/non depressed Open/closed
- 27. 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
- 28. Signs of Head injury
- 29. INTRACRANIAL LESIONS Extradural hematoma(EDH) Collection of blood & clot between duramater 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
- 30. 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
- 32. Treatment options ◦ Two treatment options ◦ Immediate surgical intervention ◦ Initial conservative , close clinical observation with possible delayed evacuation
- 33. 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.
- 35. 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
- 36. MEDICAL THERAPIES FOR HEAD INJURY ◦ Head end elevation – 30 degrees ◦ Intravenous fluids: Maintain normovolemia Hypotonic saline should not be used ◦ Serum sodium levels monitored daily ◦ HYPERVENTILATION ◦ Barbiturates
- 37. Acute subdural Hematoma(SDH) Between duraand arachnoid Disruptionof cortical vesselsor brain laceration produces hematoma Associated with significant primary injury Mortality rateas high as 40% in some series
- 38. • Hyperdense concave lesion spreading across brain. • Midline shift disproportionate to size of lesion
- 39. 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
- 40. 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- Headache, 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
- 41. Acute on chronic SDH Chronic SDH will more recent hemorrhage in dependant (posterior) areas. Treatment is Burr hole evacuation rather than craniotomy
- 42. 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
- 43. APPROACH TO A PATIENT WITH HEAD INJURY ◦ History ◦ Initial Assessment ◦ Primary Survey ◦ Secondary Survey
- 44. 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
- 45. Primary Survey ◦ Ensure adequate oxygenation and circulation ◦ Exclude hypoglycaemia ◦ Check pupil size and and response, GCS asap
- 46. GCS
- 47. Airway maintenance with cervical spine protection Breathing and ventilation
- 48. Circulation ◦ Maintain MAP >90mmhg- adequate ◦ Hematocrit >30% ◦ Isolated intracranial injuries do not cause hypotension ◦ LOOK FOR THE CAUSE OF HYPOTENSION
- 49. Disability ◦ Pupilary size ◦ Motor function ◦ Injury level Constricted? narcotics? Sluggish/dilated? mid brain ICP Unilateral dilation? pressure on CNIII Fixed and Dilated? herniation
- 50. SECONDARY SURVEY Examination of Head to toe ( Log roll to check whole spine) Glasgow Coma Scale Detailed Neurological Examination
- 51. SECONDARY SURVEY HEAD: Inspetion and palpation of scalp Battle sign , Raccoon eye , Panda eye Hemotympanum, CSF rhinorrhoea Complete examination of all cranial nerve
- 52. 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.
- 53. 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
- 54. ◦ History ◦ GPE ◦ Neurological examination ◦ CT scan ?? ◦ Discharge with advice
- 55. 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
- 56. Phineas Gage: Neuroscience’s Most Famous Patient
Hinweis der Redaktion
- About 3 decades ago trauma was not considered as a disease , however there is a paradigm shift in consensus. Becoz trauma is preventable and frequently predictable, it is subject to same epidemiology as disease. By defining and addressing trauma as a disease we can develop interventions with potential to reduce impact and incidence.
- Majority of head injury patients are presently managed by emergency services that do not have knowledge of specialised of pathophysiology of treatment. It is the reason that the traditional division of primary and secondary damage remains useful.
- Includes cascade of cellular , chemical , tissue or blood vessel changes that contributes to further destruction of brain tissue.
- classification of secondary brain damage has traditionally been into extra- and intracranial
- penumbra of functionally impaired but potentially viable tissue
- Uncontrolled increase in icp results in cerebral herniation.
- Dr monro in 1783 observed that cranium is a rigid box containing a nearly incompressible brain
- Cushings reflex= physiological nerveous response to RICT resulting in cushings triad increased BP irregular breathing and bradycardia Seen in terminal stage of acute head injury and indicate imminent brain herniation
- Vault= space in skull within neurocranium occupied by brain
- With extradural hemorrhage, the time from first recorded deterioration in level of consciousness to operation was less than 2 hours on average in patients who made a good recovery or who were only moderately disabled.
- Pentrator Burr hole bit Bone rongeur Scalpel
- No role as prophylaxis in 24 hrs. Reducing PaCO2 cerebral vasoconstriction Maintain PaCo2 25 – 35 mmhg Last resort for reducing ICP TEMPORARY MEASURE ONLY Barbiturates Effective in reducing ICP – refactory to other measures Not used in presence of hypotension/hypovolemia Phenytoin- Loading18 – 20 mg/kg
- Most common type of intracranial lesion High morbidity and mortality patients present with impaired conscious level from the time of injury
- acute subdural hemorrhage the time from injury to operation strongly influenced outcome, delays of more than 4 hours from injury being the most significant.
- Patients with acute SDH and GCS < 9 should have ICP monitoring Acute blood is too viscus to evacuate through burr hole
- 2-3 weeks after acute Small bridging veins tear and cause small clinically silent ASDH ,when hematoma breaks down and increases in size mass effect is produced
- Bystanders and paramedics may provide vital information Preinjury- fits, alcohol , chest pain
- Cushing’s Triad –bradycardia , htn , abnormal respiration
- Pre-medicate with Lidocaine, 1mg/kg IV 2 minutes prior to attempt Laryngoscopy produces an ICP Spike . Though one would assume that the ICP mediated effects of lidocaine stem from its local anesthetic effect, there are other proposed mechanisms of ICP reduction via the IV route. Lidocaine injected IV has been shown in models to induce cerebral vasoconstriction leading to a decrease in cerebral blood volume and thus ICP . Furthermore, IV lidocaine leads to sodium channel inhibition and thus a reduction in cerebral activity and metabolic demands [3, 4], as well as excitotoxicity , leading to a potential ICP reduction effect.
- Subgaleal hematoma, laceration Midbrain or brainstem dysfunction –gaze paresis
- In 1848, Gage, 25, was the foreman of a crew cutting a railroad bed in Cavendish, Vermont. On September 13, as he was using a tamping iron to pack explosive powder into a hole, the powder detonated. The tamping iron—43 inches long, 1.25 inches in diameter and weighing 13.25 pounds—shot skyward, penetrated Gage’s left cheek, ripped into his brain and exited through his skull, landing several dozen feet away. Though blinded in his left eye, he might not even have lost consciousness, skull, the tamping iron and a mask of his face made while he was alive are the most sought-out items at the Warren Anatomical Museum on the Harvard Medical School campus.