Head Injury Overview
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Traumatic Brain Injury Head Injury Neurotrauma
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Head Injury Overview
- 1. HEAD INJURY DR. DHAVAL SHUKLA, MCh ASSOCIATE PROFESSOR DEPARTMENT OF NEUROSURGERY NIMHANS, BANGALORE. NIMHANS
- 2. Epidemiology • Incidence 150/ 100000 • Prevalence 97/ 100000 • Mortality 20/ 100000 • Case fatality 10% • Burden of casualty 40% NIMHANS
- 4. Intracranial Pressure ICP • Normal values < 10 - 15mmHg for adults and older children • 3 to 7 mm Hg for young children • 1.5 to 6 mm Hg for term infants • ICP can be subatmospheric in newborns • ICP values > 20 - 25 mm Hg require treatment • Sustained ICP > 40 mm Hg indicate severe, life-threatening intracranial hypertension. NIMHANS
- 5. Cerebral Perfusion Pressure (CPP) • CPP = MAP - ICP • Normal cerebral blood flow (CBF) with a CPP ranging from 50 to 150 mm Hg • CPP < 50 mm Hg CBF falls passively with CPP • After injury the ability of the brain to pressure autoregulate may be absent or impaired and, even with a normal CPP, CBF can passively follow changes in CPP NIMHANS
- 6. Raised ICP in TBI • Intracranial hematoma: EDH, SDH, Contusions • Cerebral edema • Hyperemia • Hypoventilation • Increased intrathoracic or intra-abdominal pressure • Hydrocephalus NIMHANS
- 7. Secondary raised ICP • 30% of patients • 3 to 10 days after trauma • Delayed hematoma • Hypoxia • Hypotension • Vasospasm • Hypoventilation • Hyponatremia NIMHANS
- 8. ICP WAVES • Lundberg A waves: Plateau waves – Amplitude > 50 mm Hg lasting 5 to 20 min. – Accompanied by increase in MAP • Lundberg B waves: Pressure pulses – Amplitude 50 mm Hg and lasting 30 sec. to 2 min. NIMHANS • Lundberg C waves: – Amplitude 20 mm Hg and frequency of 4 – 8/ min.
- 10. NIMHANS
- 11. Age distribution Age groups (years) NIMHANS Percentage
- 12. Cause Etiology NIMHANS Percentage
- 13. Alcohol • 24% regular consumers • 15% under influence of alcohol NIMHANS • More severe injuries • Multiple intracranial hematomas • Delirium and withdrawal • Liver dysfunction
- 14. Concussion • Transient loss of brain function due to blow on head • Orientation, Immediate memory, Concentration • Grade 1: __ Transient Confusion __ No Loss of Consciousness __ Concussion Symptoms < 15 min. • Grade 2: __ Transient Confusion __ No Loss of Consciousness __ Concussion Symptoms > 15 min. • Grade 3: __ Any Loss of Consciousness, Brief or Prolonged NIMHANS
- 15. Unconsciousness NIMHANS • Concussion • At time of impact – Worsening – Improving • Delayed • Lucid interval • Amnesia
- 16. Seizures • Generalized tonic clonic or focal • Status epilepticus in 10 – 15% • Postictal unconsciousness NIMHANS • Immediate – No significance • Early – Severe injury
- 17. Other symptoms NIMHANS • Vomiting – Raised ICP • ENT bleeding – Skull base #
- 18. Examination • A – Airway Wounds • B – Breathing ENT bleeding • C – Circulation CSF leak • D – Disability • E – Exposure • F – Foley/ family • G – Gastric tube NIMHANS
- 19. Breathing NIMHANS Cheyne-Stokes Neurogenic hyperventilation Apneusis Ataxic breathing Apnea
- 20. Associated injuries NIMHANS Percentage Sites
- 21. Glasgow coma score (GCS) NIMHANS • Post resuscitation • Best response • Swollen eye • Aphasia • Endotracheal intubation • Quadriplegia
- 22. Pain response DO NOT PINCH NIMHANS
- 23. (GCS) NIMHANS Eye Response • 4 - eyes open spontaneously • 3 - eye opening to verbal command • 2 - eye opening to pain • 1 - no eye opening • ES - eye swollen
- 24. (GCS) Motor Response • 6 - obeys commands • 5 - localizing pain • 4 - withdrawal from pain • 3 - flexion response to pain • 2 - extension response to pain • 1 - no motor response NIMHANS
- 26. (GCS) Verbal Response • 5 - oriented • 4 - confused • 3 - inappropriate words • 2 - incomprehensible sounds • 1 - no verbal response • VT - endotracheal tube NIMHANS
- 27. Severity Severity NIMHANS Percentage
- 28. Pupils NIMHANS
- 30. Neurological deficits NIMHANS • Optic nerve – With local injury • Facial nerve – UMN / LMN – Ear bleed • Limb movements – Hemiplegia contralateral to pupillay dilatation – Hemiplegia ipsilateral to pupillay dilatation • Kernohan’s notch
- 31. Treatment - Airway • Hypoxia doubles mortality • pO2 > 60 mm Hg or SaO2 >90% • Endotracheal intubation – GCS < 8 – Maxillofacial injuries – Restless patient requiring heavy sedation – Status epilepticus NIMHANS
- 32. Treatment - Breathing • No prophylactic hyperventilation • Mechanical ventilation NIMHANS – Coma GCS < 8 – Severe raised ICP – Uncontrolled status epilepticus – Awaiting surgery
- 33. Treatment - Circulation NIMHANS • 16 or 18G iv cannula • 500 ml NS • Maintain SBP > 90 mm Hg • Hypotension doubles mortality • Do not give dextrose containing fluids • Foley’s catheterization
- 34. CT scan NIMHANS • Bradycardia • Vomiting • Severe headache • Neuro. deficits • Early seizures • Skull fracture • CSF leak • Extremes of age • Alcohol consumption • Loss of consciousness
- 35. CT scan classification Focal Diffuse Normal Minor Swelling Shift NIMHANS
- 36. MRI • After clinical stabilization • If CT scan is normal and patient is uncosncious • 25 days after injury for prognostication • Limited use only for research • T1, T2, FLAIR and T2* NIMHANS
- 37. Lab investigations • CBC with platelet count NIMHANS • RBS • Urea/ creatinine • Na+/ K+ • PT/ APTT • Blood group/ cross match
- 38. Monitoring NIMHANS Hourly • Pulse rate < 60 bpm • BP < 90 mm Hg • GCS > 2 score deterioration • Pupils Asymmetry • Limb movement Paucity
- 39. Treatment • Head of bed elevation • Normal blood pressure NIMHANS • Normal oxygenation • Normal temperature • Normal blood glucose
- 40. Indications for ICP monitoring GCS: 3–8 (after resuscitation) 1. Abnormal admission head CT scan 2. Normal admission head CT scan plus two or more of the following a. Age > 40 yrs. b. Motor posturing c. Systolic blood pressure < 90 mm Hg NIMHANS
- 41. Complications of ICP monitoring • Infection: 5% to 14% – Antibiotic-coated catheters has been shown to reduce the risk for infection from 9.4% to 1.3%. • Hemorrhage: 1.4% • Malfunction, obstruction, and malposition NIMHANS
- 42. Goals of ICP treatment 1. Maintain ICP at less than 20 to 25 mm Hg. 2. Maintain CPP at greater than 60 mm Hg by maintaining adequate MAP. 3. Avoid factors that aggravate or precipitate elevated ICP. NIMHANS
- 43. NIMHANS
- 44. Mannitol NIMHANS • Available as 20% • Max. dose 5 ml/ kg • BP should be normal • Decorticate or decerebrate posturing • Rapid deterioration of GCS
- 45. Hypertonic saline (HS) • 3% to 23.4% HS as effective as mannitol • Advantage over mannitol – Hypovolemic and Hypotensive patients NIMHANS • Adverse effects – Hematologic • bleeding secondary to decreased platelet aggregation and prolonged coagulation time – Electrolyte abnormalities • Hypokalemia and hyperchloremic acidosis Hyponatremia should be excluded before administering hypertonic saline, to reduce the risk for central pontine myelinolysis
- 46. Barbiturates NIMHANS • Pentobarbital – Loading dose 10 mg/kg – 5 mg/kg every hour for 3 doses – Maintenance 1 to 2 mg/kg/h • Titrated to a serum level of 30 to 50 mg/mL or until EEG shows a burst suppression pattern • Barbiturate coma in patients with refractory intracranial hypertension increases twofold greater chance of controlling the ICP
- 47. Barbiturates NIMHANS • Mechanism: – Coupled reduction in CBF and CMRO2, with an immediate effect on ICP – Retention of CO2 reactivity by brain • Complications: – Hypotension 58% – Hypokalemia 82% – Respiratory 76% – Infections 55% – Hepatic 87% – Renal dysfunction 47%
- 48. Hypothermia • Cerebral metabolism reduced by 5-7% for each oC reduction – Decreased glucose & O2 consumption • Prevents cell injury leading to apoptosis – Inhibition of caspase activation – Prevents mitochondrial dysfunction – Decreased excitatory neurotransmitters – Modification of intracellular ion concentration – Modification of intracellular acidosis NIMHANS
- 49. Hypothermia • Suppresses inflammatory processes • Decreases free radical production • Reduces vascular permeability – Reduced brain oedema • Helps maintain cell membrane integrity • Prevents hyperthermia NIMHANS
- 50. Hypothermia • 13 studies involving 1321 patients in last 15 years – All reported a reduction in ICP – Most observed improved neurological outcome especially in patients with low GCS (4-7) on admission – Results however not significant NIMHANS • Adverse effects – Hypotensive episodes and bradycardia more common – Low magnesium – Insulin resistance
- 51. Decompressive Craniectomy (DECRA) • Less time with raised ICP • Fewer interventions for increased ICP • Fewer days in ICU • Worse scores on the GOS • Greater risk of unfavorable outcome • Rates of death at 6 months similar NIMHANS
- 52. Antibiotics • Not routinely required • For contaminated depressed fracture • Endotracheal intubation NIMHANS • Cefotaxime 1 gm tid
- 53. Risk of seizures NIMHANS Percentage Severity
- 54. Anticonvulsants NIMHANS • Phenytoin – Loading 18 mg/ kg iv in 100 ml NS over 30 min – Maintenance 5 mg/ kg/ day • 10 – 14 days for prophylaxis • Continue as case of epilepsy in early PTS
- 55. Pharmacological Neuroprotection • Pre-clinical and clinical data are disconnected • Need adequate pre-clinical TBI models • Virtually no early phase trials in TBI • Dosing • Duration of treatment • Time of treatment initiation NIMHANS
- 56. Design Problems • Weaknesses in study design • Insufficient power/sample size • Inadequate outcome measures or lack of sensitivity of the outcomes measure • Too small effect sizes • Too variable population NIMHANS
- 57. Facts • No single measure can capture the multidimensional nature of TBI outcome • Combination of drugs are needed for the treatment of TBI NIMHANS • Current Trials – Progesterone (SYNAPSE) – Citicoline (COBRIT) – Erythropoetin
- 60. Surgery for EDH NIMHANS Surgery Any GCS • Volume > 30 cc • Volume > 20 cc – Basitemporal – Posterior fossa Conservative • Volume <20 cc • Thickness < 15 mm • Midline shift< 5 mm • GCS > 8 • No deficits Craniotomy with hitch stitches
- 61. Surgery for acute SDH NIMHANS Any GCS • Thickness > 10 mm • Midline shift > 5 mm Thickness < 10 mm Midline shift < 5 mm • GCS < 9 • Deteriorated by 2 GCS • Pupillary asymetry Craniotomy with or without bone flap replacement and duraplasty
- 62. Surgery for cerebral contusions NIMHANS Volume > 50 cc • Any GCS Volume > 20 cc • GCS 6 – 8 • Progressive deterioration • Failure of medical treatment • Midline shift > 5 mm • Cisternal compression Craniotomy with evacuation of lesion Decompressive craniectomy and bone flap placement in abdominal wall
- 63. Surgery for posterior fossa lesions • Neurological dysfunction or deterioration • Distortion or obliteration of IV ventricle • Cisternal compression • Hydrocephalus Suboccipital craniectomy and evacuation NIMHANS
- 64. Surgery for depressed fracture NIMHANS Surgery • Compound (open) • Thickness > cranium Nonoperative • No dural breach • No significant hematoma • < 1 cm • No infection • No cosmetic deformity • No pneumocephalus Elevation with debridement Duraplasty Antibiotics
- 65. Glasgow outcome scale (GOS) GOS Favorable Unfavorable NIMHANS Good Recovery Upper Lower Moderate Disability Severe Disability Vegetative State Death Upper Lower Upper Lower
- 66. Outcome assessment Periods of improvement • 3 months - 66% • 6 months - 90% • 12 months - 95% NIMHANS
- 67. NIMHANS
- 68. Prevention If treatment is duty then prevention is responsibility Helmet • Not compulsory for pillion riders • 60% compliance • <5% at time of injury • 6 times increase in mortality without helmet • Myths – baldness, headache, neck injury, decreased vision NIMHANS etc.
- 69. No head injury is so trivial that it can be ignored Nor so serious that life can be despaired off NIMHANS
Editor's Notes
- Hyperemia owing to vasomotor paralysis or loss of autoregulation Hypoventilation that leads to hypercarbia with subsequent cerebral vasodilation Hydrocephalus resulting from obstruction of the CSF pathways or its absorption Increased intrathoracic or intra-abdominal pressure as a result of mechanical ventilation, posturing, agitation, or Valsalva’s maneuvers
- Lundberg C waves: amplitude 20 mm Hg and a frequency of 4 to 8 per minute; they are seen in the normal ICP waveform, but high-amplitude C waves may be superimposed on plateau waves
- Flow chart summarizing various pathophysiological events involved in cerebral ischemic and traumatic insults. Four phases of injury are indicated that divide the spectrum of processes into immediate, acute, subacute, and ultimate outcome. As indicated, similar pathomechanisms are considered to participate in the structural and functional abnormalities associated with cerebral ischemia and trauma. Degrees of involvement as well as temporal profiles of these events are important in determining whether they play a dominant role in cell death and injury. As in any type of injury, injury severity and the presence of secondary injury mechanisms impact on the robustness of these pathological events. It should be emphasized that there are generally more similarities in terms of pathogenesis between cerebral ischemia and trauma than there are differences. J Cereb Blood Flow Metab, Vol. 24, No. 2, 2004
- American Academy of Neurology guidelines
- Different abnormal respiratory patterns are associated with pathologic lesions (shaded areas) at various levels of the brain. Tracings by chest-abdomen pneumography, inspiration reads up. (A) Cheyne-Stokes respiration is seen with metabolic encephalopathies and with lesions that impair forebrain or diencephalic function. (B) Central neurogenic hyperventilation is most commonly seen in metabolic encephalopathies, but may rarely be seen in cases of high brainstem tumors. (C) Apneusis, consisting of inspiratory pauses, may be seen in patients with bilateral pontine lesions. (D) Cluster breathing and ataxic breathing are seen with lesions at the pontomedullary junction. (E) Apnea occurs when lesions encroach on the ventral respiratory group in the ventrolateral medulla bilaterally. (From Saper, C. Brain stem modulation of sensation, movement, and consciousness. Chapter 45 in: Kandel, ER, Schwartz, JH, Jessel, TM. Principles of Neural Science. 4th ed. McGraw-Hill, New York, 2000, pp. 871–909.
- Motor responses to noxious stimulation in patients with acute cerebral dysfunction. Levels of associated brain dysfunction are roughly indicated at left. Patients with forebrain or diencephalic lesions often have a hemiparesis (note lack of motor response with left arm, externally rotated left foot, and left extensor plantar response), but can generally make purposeful movements with the opposite side. Lesions involving the junction of the diencephalon and the midbrain may show decorticate posturing, including flexion of the upper extremities and extension of the lower extremities. As the lesion progresses into the midbrain, there is generally a shift to decerebrate posturing (C), in which there is extensor posturing of both upper and lower extremities. (From Saper, C. Brain stem modulation of sensation, movement, and consciousness. Chapter 45 in: Kandel, ER, Schwartz, JH, Jessel,
- Ocular reflexes in unconscious patients. The left-hand side shows the responses to oculocephalic maneuvers (which should only be done after the possibility of cervical spine injury has been eliminated). The right-hand side shows responses to caloric stimulation with cold or warm water (see text for explanation). Normal brainstem reflexes in a patient with metabolic encephalopathy are illustrated in row (A). The patient shown in row (B) has a lesion of the right side of the pons (see Figure 2–8), causing a paralysis of gaze to that side with either eye. Row (C) shows the result of a lesion involving the medial longitudinal fasciculus (MLF) bilaterally (bilateral internuclear ophthalmoplegia). Only abducens responses with each eye persist. The patient in row (D) has a lesion involving both MLFs and the right abducens nucleus (one and a half syndrome). Only left eye abduction is retained. Row (E) illustrates a patient with a midbrain infarction eliminating both the oculomotor and trochlear responses, leaving only bilateral abduction responses. Note that the extraocular responses are identical to (C), in which there is a bilateral lesion of the MLF. However, pupillary light responses would be preserved in the latter case. (From Saper, C. Brain stem modulation of sensation, movement, and consciousness. Chapter 45 in: Kandel, ER, Schwartz, JH, Jessel, TM. Principles of Neural Science. 4th ed. McGraw-Hill, New York, 2000, pp. 871–909. By permission of McGraw-Hill.)
- %; colonization of the device is more common than clinical infection [25]. A study found no significant reduction in infection rate in patients undergoing prophylactic change of monitors before day 5, compared with those whose catheters were in place for 5 days or more [26]. Factors that are not associated with infection are insertion of the catheter in the neurologic ICU, previous catheter insertion, drainage of CSF, and use of steroids. In a group of patients who had prolonged ventricular drainage of 10 days or more, a nonlinear increase in daily infection rate was observed over the initial 4 days but remained constant, despite prolonged catheter use [27].
- also creates an osmotic force to draw water from the interstitial space of the brain parenchyma into the intravascular compartment in the presence of an intact blood–brain barrier, reducing intracranial volume and ICP. Mannitol is contraindicated in hypovolemic patients because of the diuretic effects, whereas hypertonic saline augments intravascular volume and may increase blood pressure, in addition to decreasing ICP.
- . Although routine use of barbiturates in unselected patients has not been consistently effective in reducing morbidity or mortality after severe head injury [63,64], a randomized multicenter trial showedthat instituting
- Reilly PL and Bullock R. Head injury pathophysiology and management. (2nd Edition) , Hodder Arnold; London 2005; pp 444
- http://www.crash2.lshtm.ac.uk/Risk%20calculator/index.html