1 HEAD INJURY TODD D. ALEXANDER, M.D.

2 OBJECTIVES To review the spectrum of specific types of head injuryTo understand the management principles of severe head injury in the emergency room and ICU To understand some of the issues regarding concussion and athletic head injury

3 CASE STUDY A 9 year boy was playing on the railroad tracks and was struck by a train.  He was intubated in the field and brought by emergency transport to the hospital.  He was found to be lethargic but arousable with a large open wound on the right side of his scalp and an obvious skull defect.  There were no other injuries and his vital signs were stable. 

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7 OUTLINE Epidemiology Pre-hospital Management ER ManagementNeurologic Assessment Focal vs. Diffuse Brain Injuries A. Focal Injuries 1. Epidural Hematoma 2. Subdural Hematoma a. Acute b. Chronic 3. Skull Fractures 4. CSF Leaks B. Penetrating Injuries 1. Missile 2. Nonmissile

8 OUTLINE VI. ICU Management A. ICP management 1. Philosophy2. ICP monitoring a. Indications b. Technques c. Treatment threshold 3. ICP lowering measuares a. Hyperventilation b. Mannitol c. Barb Coma d. Craniectomy e. Lobectomy B. Steroids in head injury Antiepileptics in head injury General critical care Brain Death Minor head injury Concussion Second impact syndrome Athletic head injury Case study

9 EPIDEMIOLOGY Trauma causes 150,000 death/year – 50% due to head injuryPeak incidence in young adults age 15-24 Most common cause is transport related followed by falls – urban areas: assaults and firearms

10 PREHOSPITAL MANAGEMENTTransportation: into of helicopters, paradoxical mortality figures Airway management: effect of hypoxia on outcome Hypotension and fluid resuscitation: rapid resuscitation Spine immobilization: 5-10% of head injured patients have associated spine and/or spinal cord injury

11 ER MANAGEMENT ABC’S CT scan (non-infused)Non infused head CT is the diagnostic cornerstone of head CT Routine skull x-rays – historic relic (special indications) ER burr holes – historical relic except in extremely unusual circumstances

12 ER MANAGEMENT (continued)Airway: GCS≤8 intubate, sedation in the borderline patient, advantages, disadvantages Fluid resuscitation: hypotension to be strictly avoided ICP management: papillary changes or lateralizing sign mannitol, hyperventilation Seizures: single seizure in the first 24 hours – no Rx, Rx of status epilepticus

13 NEUROLOGICAL ASSESSMENTGlasgow Coma Scale Eye opening: 4 Best verbal response: 5 Best motor response: 6 Pupilary exam: herniation syndrome, pathophysiology, false localizing sign

14 FOCAL VS. DIFFUSE BRAIN INJURYFocal: contusion (coup, contracoup), hemorrhage/hematoma (epidural, subdural, intracerebral, petechial) Diffuse: concussion, diffuse axonal injury

15 EPIDURAL HEMATOMA Radiographic diagnosis PathophysiologyClinical presentation – “lucid interval” Significance – “talk and die” Management Special cases (delayed, asymptomatic, posterior fossa, vertex)

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18 SUBDURAL HEMATOMA Radiographic diagnosisAcute vs. chronic subdural hematoma Pathophysiology Clinical features Management Special cases (isodense subdural)

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24 SKULL FRACTURES Linear Comminuted Depressed “ping-pong”Compound fractures Fractures involving the frontal sinus Basilar skull fracture Growing fracture – post traumatic leptomenigneal cyst

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27 CSF LEAK Diagnosis Significance CSF otorrhea CSF rhinorrheapneumocephalus

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29 MISSILE PENETRATING HEAD INJURYGunshot wounds to the head are perhaps the most lethal traumatic injury Epidemiology – public health crisis Ballistics (and missile characteristics): KE=mv2  emphasis on velocity; dividing point at 1000ft/second

30 MISSILE PENETRATING HEAD INJURY (continued)Management: initial evaluation, controversies regarding aggressiveness of debridement Differences in series: military, suburban, urban, rural, suicide, American, European, gang-related violence infection

31 MISSILE PENETRATING HEAD INJURYCSF leak Traumatic aneurysm formation Post traumatic epilepsy

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35 NON MISSILE PENETRATING WOUNDS TO THE BRAINRare in western practice because of ready availability of hand guns South Africa has world’s largest experience Clinical picture can be confusing or misleading especially when only a trivial scalp wound is present

36 NON MISSILE PENETRATING WOUNDS TO THE BRAINIncidence of vascular lesions high – aggressive investigation Pencil injuries  BEWARE!

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41 ICP MANAGEMENT Overall goal – prevent secondary injuryCushing’s triad – only in 33% Hypertension Bradycardia Respiratory irregularity Good ICP management requires an ICP monitor

42 INDICATIONS FOR ICP MONITORINGGCS 3-8 (severe head injury) after cardiopulmonary resuscitation and an abnormal CT scan Severe head injury with a normal CT scan in the following situations: Age> 40 years Unilateral or bilateral motor posturing SBP <90 mmHg

43 INDICATIONS FOR ICP MONITORING (continued)Specialized indications even in the conscious patient: need for sedation/paralysis e.g. severe lung contusion, (ARDS) or prolonged operation is necessary

44 ICP MONITORING TECHNIQUESVentricular catheter connected to an external strain gauge is most accurate, low cost, and reliable (also allows for therapeutic CSF drainage) Fiberoptic (Camino) devices placed in ventricular catheters provide similar benefits at higher costs

45 ICP MONITORING TECHNIQUES (continued)Intraparenchymal fiberoptic ICP monitors are 2nd best option Subarachnoid, subdural, and epidural monitors are currently less accurate

46 INTRACRANIAL TREATMENT PRESSURE THRESHOLDMost recommended treatments be initiated if ICP> mmHg (controversial) pure CPP-based therapy in which higher ICPs may be accepted in the face of adequate CPPs (>70 mmHg) is no longer recommended goal is CPP 50-70 greater than 70 is associated with increased risk of ARDS

47 ICP LOWERING MEASURES HyperventilationMannitol (lasix, urea, hypertonic saline) Mild head elevation - controversial and neck positioning Sedation Paralysis IV lidocaine for suctioning

48 ICP LOWERING MEASURES (continued)Pentobarbital coma Decompressive craniectomy Cerebral lobectomy **Never get into a cycle of managing ICP elevation without ruling out a surgically evacuable lesion

49 HYPERVENTILATION Mechanism Severe hyperventilation can be HARMFULPCO2 < 25 mmHg are to be avoided Prophylactic hyperventilation, especially in 1st 24 hrs when CBF is low, is to be avoided

50 HYPERVENTILATION (continued)General goal is intensive ICP management – PCO2 around mmHg Jugular venous oxygenation monitoring is now being used by some physicians to guide the use of hyperventilation Brain tissue oxygenation monitoring is being utilized

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52 MANNITOL Intermittent boluses appear to be more effective than a continuous infusion Effective doses: gram/kg With ongoing use must monitor serum osmolarity and discontinue if >320 mOsm Must maintain euvolemia and K+

53 BARB COMA Remains controversialTheoretical benefit in decreasing metabolic demand Proven to lower ICP Problems: Hypotension (many advocate Swan-ganz catheter) Inability to follow neurologic exam – can only follow ICP May produce more vegetative and comatose survivors who would have other wise expired

54 BARB COMA (continued) Should never be used prophylactically or indiscriminately; must determine the salvagability of the patient Must follow protocol of high does intravenous pentobarbital therapy; strictly speaking, “pentobarbital coma” requires continuous EEG monitoring for burst suppression

55 STEROIDS IN HEAD INJURYThe use of glucocorticoids is not recommended for improving outcome or reducing ICP in patients with severe head injury

56 STEROIDS IN HEAD INJURY (continued)Six major studies of glucocorticoids in severe head injury have been conducted that evaluate clinical outcome and/or ICP None of these studies showed a substantial benefit of glucocorticoid therapy in these patients

57 ROLE OF ANTIEPILEPTICS IN HEAD INJURYProphylactic use of anticonvulsants is not recommended for preventing late post traumatic seizures; thus prophylaxis beyond one week is not recommended

58 ROLE OF ANTIEPILEPTICS IN HEAD INJURY (continued)Prophylactic use during first week should be in patients with identified risk factors: GCS<10 Contusion Depressed skull fracture Hematoma of any kind Seizure in the 1st 24 hours Penetrating head injury

59 OTHER CRITICAL CARE ISSUESH2 blockers Aggressive control of fever Control hyperglycemia PEEP Nutrition: timing, route Fluid/electrolyte disorders: SIADH Cerebral salt wasting DI

60 BRAIN DEATH Brain death exam Philosophy: organ donation vs. non-organLegal issues Beware in children “Lazarus Phenomenon”, spinal cord reflexes

61 BRAIN DEATH EXAM No response to deep pain Absent brain stem function:Fixed pupils Absent corneal reflexes Absent oculocephalic Oculovestibular reflexes No gag reflex No spontaneous respirations on apnea test (paCO2>60 mmHg, O2 sat>80%)

62 BRAIN DEATH EXAM (continued)Vital signs: Core temp > 90ºF (32.2ºC), SBP>/=90mmHg Confirmatory tests: EEG CBF Cerebral angiogram

63 SEQUELAE OF HEAD INJURYPost traumatic epilepsy: early and late Hydrocephalus Intellectual impairment Neurobehavioral disorders Cranial nerve injuries Infection Metabolic disorders

64 CONCUSSION DefinitionTraumatically induced alteration of mental status with or without loss of consciousness Hallmarks are confusion and amnesia

65 CONCUSSION (continued)Frequently observed signs Vacant stare (befuddled facial expression) Delayed verbal and motor responses Inability to focus attention Disorientation Slurred or incoherent speech Gross observable discoordination Emotionality out of proportion to circumstances (appearing distraught, crying for no apparent reason) Memory deficits Any period of loss of consciousness

66 CONCUSSION (continued)Presence or absence of loss of consciousness (LOC is important to document) Duration of LOC has been found to be of questionable value and often inaccurate Length of post traumatic amnesia has been found to be a more reliable indicator of concussion severity

67 CONCUSSION (continued)Multiple grading symptoms have been developed to classify the severity of the concussion Cantu Colorado Medical Society Jordan Ommaya Nelson Roberts Torg Virginia Neurological Institute

68 SECOND IMPACT SYNDROMEThe most serious of post-concussive complications is a potentially fatal condition that can occur after a seemingly trivial second head injury First described in 1973, the term was coined by Saunders and Harbaugh in 1984 JAMA article

69 SECOND IMPACT SYNDROME (continued)An athlete suffers an initial concussion followed by a second often trivial head injury before the 1st injury has resolved fully (usually within 1 week) After the second head injury within minutes the player displays signs of elevated intracranial pressure including dilated pupils, posturing, respiratory arrest and coma proceeding to death Demise occurs more rapidly than usually seen with an epidural hematoma

70 SECOND IMPACT SYNDROME (continued)The pathophysiology is believed to involve sub clinical brain swelling from the initial traumatic insult which makes the brain more susceptible to a second injury It is postulated that the first insult disturbs the brain’s autoregulatory mechanisms with consequent vascular congestion and poor brain compliance

71 ATHLETIC HEAD INJURY Athletes differ from the general population who may only sustain a single concussion in their lifetime and are not asked to return to an environment where they are subjected to possible additional head injuries

72 FOOTBALL IS THE WORST OFFENDER IN ORGANIZED AMERICAN SPORTS8 deaths occur annually 15% risk of minor head injury for high school football players 200,000 concussions annually

73 NEUROPSYCHOLOGICAL TESTINGUsually testing reverts to normal baseline in 7-10 days after uncomplicated concussion Athletes who sustained two or more concussions have long term deficits in speed of information processing and executive functioning

74 NEUROPSYCHOLOGICAL TESTING (continued)Computer based software programs are now available that eliminate some of the limitations of paper and pencil testing Most widely used is IMPACT – Immediate Post-Athletic Concussive Cognitive Testing (many NFL, NHL, Div. I Colleges and High Schools using currently)

75 RETURN TO PLAY In most community settings, neuropsychological testing with baseline studies on file is not realistic Guidelines offer the physician a reference in making decisions about return to play

76 RETURN TO PLAY (continued)Several return to play guidelines have been published The different guidelines have minor differences in the duration of time off All guidelines agree that no athlete should return to play who has post concussive symptoms

77 RETURN TO PLAY (continued)Physician must remember that the guidelines are just that and do not replace individual clinical judgement Two main goals of guidelines: Prevent cumulative injury Prevent rare but frightful second impact syndrome