1. MBARARA UNIVERSITY MANAGEMENT OF TRAUMATIC BRAIN INJURY PRESENTED BY: OGWANG TOM 2020/MNS/014/PS Date: 11/6/2021. E-mail: ogwangtom1@gmail.com

2. Objectives: 1.To describe brief anatomy of brain. 2.To define Traumatic head injury. 3.Describe classification of TBI. 4.Describe the injury types in TBI. 5.To describe the management of TBI. 6.List the complications of TBI.

3. ANATOMY OF THE BRAIN

4. The brain is composed of three parts: the brainstem, cerebellum, and cerebrum The CEREBRUM is the largest part of the brain and is composed of right and left hemispheres. The cerebrum is divided into four lobes: frontal, parietal, temporal, and occipital It performs higher functions like interpreting touch, vision and hearing, as well as speech, reasoning, emotions, learning, and fine control of movement. The CEREBELLUM is located under the cerebrum. Its function is to coordinate muscle movements, maintain posture, and balance. The BRAINSTEM includes the midbrain, pons, and medulla. It acts as a relay center connecting the cerebrum and cerebellum to the spinal cord. It performs many automatic functions such as breathing, heart rate, body temperature, wake and sleep cycles, digestion, sneezing, coughing, vomiting, and swallowing. Ten of the twelve cranial nerves originate in the brainstem *The diencephalon appears at the upper end of the brain stem, situated between the cerebrum and the brain stem. It is made up of four distinct components: the thalamus, the hypothalamus, the epithalamus and the pituitary gland

7. Ventricles Ventricles are hollow cavities of the brain They contain the cerebrospinal fluid (CSF), which circulates within the brain and spinal cord There are 4 ventricles in the human brain There are 2 lateral ventricles, known as right and the left ventricle, which are located within the cerebral hemisphere. The lateral ventricles are the largest ventricles of the brain Function of the ventricles is the production, as well as the circulation of cerebrospinal fluid

10. Definition. Traumatic brain injury (TBI) is defined as blow or jolt to the head or a penetrating head injury that disrupts the function of the brain

11. Primary Brain Injury – Cellular Level Primary Cellular Injury “Neurotransmitter Storm” Massive Depolarization of Brain Cells Glutamate Calcium NMDA Disruption of normal cellular processes: Protein Phosphorylation Microtubule Construction Enzyme Production Membrane and Cytoskeleton Breakdown Cell Death Oxygen Free Radical Pathway Activation Lipid Peroxidation Cell Membrane Dysfunction Cell Lysis Nitric Oxide Synthase High Nitric Oxide Levels Intracellular Signaling Processes

12. Primary Brain Injury Occurs at the time of trauma. Common mechanisms include: Direct impact Rapid acceleration /deceleration Penetrating injury Blast waves They all result from external mechanical forces transferred to intracranial contents. The damage that results includes a combination of: Focal contusions and hematomas Shearing of white matter tracts (diffuse axonal injury) Cerebral edema and swelling

13. Secondary Brain Injury Injury to the brain subsequent to the original traumatic event Common causes of secondary injury: Cerebral edema Hypotension Respiratory depression that may lead to hypoxemia Electrolyte imbalance **End result is decreased O2 delivery to brain and further death of nerve cells**

14. Head Injury classifications. 1.Severity 2.Blunt (closed) or penetrating (open) 3.Injury type eg concussion, extradural haematoma

15. Severity of traumatic brain injury Mild GCS 13-15Moderate GCS 9-12Severe GCS <9

16. Glasgow Coma Scale (GCS) Eye OpeningOpens spontaneously4 Responds to verbal command3 Responds to pain2 No eye opening1 VerbalOriented5 Disoriented4 Inappropriate words3 Incomprehensible speech2 No verbal response1 MotorObeys commands6 Localizes to pain5 Withdraws to pain4 Flexion to pain (Decorticate posturing)3 Extension to pain (Decerebrate posturing)2 No motor response1

17. Mild Brief or no loss of consciousness Signs of concussion Nausea and vomiting Headache Fatigue Dizziness Poor recent memory Unable to form new memories following the injury (less than 1 hour) GCS = 13 - 15

18. Moderate Coma less than 24 hours Unable to form new memories following the injury (less than 24 hours). GCS = 9 - 12 SEVERE Coma more than 24 hours Unable to form new memories following the injury (longer than 24 hours). GCS = 3 – 8 (Less than 9).

19. Blunt (closed) Is when there is no communication between the brain and environment. Penetrating (open) is when there is communication between the brain with the environment. Any head injury involving bleeding from the nose and ears is considered open head injury even if there is no wound being seen out.

20. Level of Recommendation Level I : high-quality (Evidence from Clinical trial research conducted in a wide / very large study sites. Level II A : moderate-quality (Clinical trial done in a few study sites). Level II B and III: low-quality; (Evidence from research which clinical trial). The levels are primarily based on the quality of the body of evidence as follows

21. Assessment History Examination Investigations

24. Head Injury - History Patient details – age / details Mechanism & timing Vomiting Seizure Severe / persisting headache Pre-traumatic amnesia Past medical history Medications (especially anticoagulants) Social history

25. Head Injury - Examination GCS Pupils General behavior Suspicion of skull fracture (depressed / basal) Neurological examination Neck examination Other injuries as indicated

26. Wound Exploration Need managed correctly – ensure cleaned adequately Boggy Swelling = Higher risk of skull fracture. Consider depressed skull fracture / compound injury in all open wounds May bleed +++

27. Head Injury Types Contusion Subdural hematoma Extradural hematoma Traumatic subarachnoid haemorrhage Skull fracture Concussion Scalp laceration

28. Cerebral Contusion Bruising to the brain surface Usually caused by trauma of brain being thrown around inside the skull Often accompanied by cerebral oedema Contusions size and oedema can increase post injury Peak risk for swelling is days 3-5 post injury Increase risk of seizure activity

29. Subdural Haematoma Blood gathers between the inner layer of the dura mater and the arachnoid mater. Usually resulting from tears in bridging veins which cross the subdural space Venous bleed Subdural haemorrhage may cause an increase in intracranial pressure (ICP) which can cause compression of and damage to delicate brain tissue

30. Subdural Haematoma Tear in a “Bridging Vein” Caution: Alcohol dependant patients Elderly patients Anti-coagulant usage

31. Extradural Haematoma Extradural hematoma is when bleeding occurs between the tough outer membrane covering the brain and the skull. Arterial bleed.

32. Concussion A concussion is a mild traumatic brain injury caused by a blunt jolt or blow to the head. The sudden movement causes the brain to bounce around or twist inside the skull. This leads to stretching and damaging of brain cells and causes chemical changes in the brain.

33. Concussion Concussion is regarded as a traumatic brain injury Can result from a direct or indirect blow to the head LOC is not required. Children are more vulnerable. Symptoms can evolve over minutes or hours after the event. Helmets / scrum caps do not protect against concussion Not just sport.

34. Head Injury - Investigation Complete blood count CT scan Blood sugar X - ray Urinalysis Stool analysis HIV Blood slide for malaria parasite

35. Scope of the guideline PART I: TREATMENTS PART II: MONITORING PART III: THRESHOLDS

36. PART I : TREATMENTS DECOMPRESSIVE CRANIECTOMY PROPHYLACTIC HYPOTHERMIA HYPEROSMOLAR THERAPY CEREBROSPINAL FLUID DRAINAGE VENTILATION THERAPIES ANESTHETICS, ANALGESICS, AND SEDATIVES STEROIDSNUTRITION INFECTION PROPHYLAXIS DEEP VEIN THROMBOSIS PROPHYLAXIS SEIZURE PROPHYLAXIS

37. Decompressive Craniectomy Cerebral edema primary injury secondary injury DC : relieving elevated intracranial pressure variations in surgical techniques timing patient populations

38. Decompressive Craniectomy Recommedations Level II A Bifrontal DC is not recommended to improve outcomes as measured by the Glasgow Outcome Scale–Extended (GOS-E) score at 6 months post-injury in severe TBI patients with diffuse injury (without mass lesions) Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury.[Erratum appears in N Engl J Med. 2011 Nov 24

39. Decompressive Craniectomy Recommedations Level II A A large frontotemporoparietal DC (not less than 12 x 15 cm or 15 cm diameter) is recommended over a small frontotemporoparietal DC Jiang JY, Xu W, Li WP, et al. Efficacy of standard trauma craniectomy for refractory intracranial hypertension with severe traumatic brain injury: a multicenter, prospective, randomized controlled study. J Neurotrauma. 2005 Qiu W, Guo C, Shen H, et al. Effects of unilateral decompressive craniectomy on patients with unilateral acute post-traumatic brain swelling after severe traumatic brain injury. Crit Care. 2009

40. Hypothermia Remove the patient from cold Remove wet clothes Cover with the blanket. Provide warm drinks. Use warm or dry compresses.

41. Prophylactic Hypothermia Hypothermia bears risks Coagulopathy Immunosuppression Cardiac dysrhythmia Death

42. Prophylactic Hypothermia Recommendations Level II B Early (within 2.5 hours), short- term (48 hours post-injury) prophylactic hypothermia is not recommended to improve outcomes in patients with diffuse injury Clifton GL, Valadka A, Zygun D, et al. Very early hypothermia induction in patients with severe brain injury (the National Acute Brain Injury Study: Hypothermia II): a randomised trial. Lancet Neurol. Feb 2011

43. Hyperosmolar Therapy Administration of hypertonic or hypotonic intravenous solutions Hypertonic saline and Mannitol : Osmotic diuretic of the brain. Care must be taken as Hypertonic saline can cause Central pontine myelinolysis ((CPM) is a neurological condition involving severe damage to the myelin sheath of nerve cells in the pons (an area of the brainstem) Mannitol; Diuretic effect is undesirable in hypotensive patient

44. Hyperosmolar Therapy Recommendations Recommen dations from the Prior (3rd) Edition Mannitol is effective for control of raised intracranial pressure (ICP) at doses of 0.25 - 1 g/kg body weight Arterial hypotension (systolic blood pressure <90 mm Hg) should be avoided Restrict mannitol use prior to ICP monitoring -signs of transtentorial herniation -progressive neurological deterioration

45. Cerebrospinal Fluid Drainage External ventricular drainage (EVD) : controversy EVD closed position : monitor intracranial pressure (CP) open position : drainage of CSF

46. Cerebrospinal Fluid Drainage Recommendations Level III An EVD system zeroed at the midbrain with continuous drainage of CSF may be considered to lower ICP burden more effectively than intermittent use Nwachuku EL, Puccio AM, Fetzick A, et al. Intermittent versus continuous cerebrospinal fluid drainage management in adult severe traumatic brain injury: assessment of intracranial pressure burden. Neurocrit Care. Aug 2013 Use of CSF drainage to lower ICP in patients with an initial Glasgow Coma Scale (GCS) <6 during the first 12 hours after injury may be considered Griesdale DE, McEwen J, Kurth T, Chittock DR. External ventricular drains and mortality in patients with severe traumatic brain injury. Can J Neurol Sci. 2010

47. Ventilation Therapies Definitive airway protection Risk of pulmonary aspiration Compromised respiratory drive and function Transient hyperventilation (respiratory alkalosis due to rapid correction of imbalance of sodium and Ca ions. The goal for severe TBI patients Normal ventilation and normal partial pressure of carbon dioxide in arterial blood (PaCO2) ranges from 35-45 mm Hg. Cerebral blood flow : The brain’s metabolic demands Low PaCO2 : low CBF  cerebral ischemia High PaCO2 : cerebral hyperemia  high intracranial pressure (ICP)

48. Ventilation Therapies Older studies : cerebral hyperemia > cerebral ischemia  suggest hyperventilation Recent studies : cerebral metabolic rate is variable Cerebral ischemia has been largely documented after severe TBI High prevalence of cerebral ischemia suggests safety in providing normal ventilation

49. Ventilation Therapies Recommendations Hyperventilation is recommended as a temporizing measure for the reduction of elevated intracranial pressure (ICP) Hyperventilation should be avoided during the first 24 hours after injury If hyperventilation is used monitor oxygen delivery venous oxygen saturation (SjO2) brain tissue O2 partial pressure (BtpO2)

50. Ventilation Therapies Recommendations Level II B Prolonged prophylactic hyperventilation with partial pressure of carbon dioxide in arterial blood (PaCO2) of 25 mm Hg or less is not recommended Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. Nov 1991

51. Anesthetics, Analgesics, and Sedatives Important for prophylaxis or control of intracranial hypertension and seizures Barbiturates example phenobarbital have a long history of being used to control intracranial pressure (ICP) Side effects : hypotension and decreased cardiac output, increased intrapulmonary shunting ( involves blood flow through areas of lung with excessive perfusion for the amount of ventilation).

52. Anesthetics, Analgesics, and Sedatives Recommendations Level II B Administration of barbiturates to induce burst suppression as prophylaxis against the development of intracranial hypertension is not recommended Ward JD, Becker DP, Miller JD, et al. Failure of prophylactic barbiturate coma in the treatment of severe head injury. J Neurosurg. Mar 1985

53. Anesthetics, Analgesics, and Sedatives Recommendations Level II B High-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment Eisenberg HM, Frankowski RF, Contant CF, Marshall LF, Walker MD. High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. J Neurosurg. Jul 1988

54. Anesthetics, Analgesics, and Sedatives Recommendations Level II B Although propofol is recommended for the control of ICP, it is not recommended for improvement in mortality or 6-month outcomes Caution is required as high-dose propofol can produce significant morbidity Kelly DF, Goodale DB, Williams J, et al. Propofol in the treatment of moderate and severe head injury: a randomized, prospective double-blinded pilot trial. J Neurosurg. Jun 1999

55. Steroids Steroid examples are betamethasone and dexamethasone are used for; The restoration of altered vascular permeability in brain edema Reduction of cerebrospinal fluid production Attenuation of free radical production Glucocorticoids benefit for patients with brain tumors when administered in the perioperative period. However, studies of severe TBI patients failed to find a benefit.

56. Steroids Recommendations Level I The use of steroids is not recommended for improving outcome or reducing ICP In patients with severe TBI, high-dose methylprednisolone was associated with increased mortality and is contraindicated Edwards P, Arango M, Balica L, et al. Final results of MRC CRASH, a randomised placebo- controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet. Jun 2005

57. Nutrition The complex interaction of the body with nutritional support is magnified during illness, particularly after severe traumatic brain injury (TBI) Seminal work from the 1980s demonstrated that severe TBI was associated with increased energy expenditure early after injury

58. TBI patient’s are in a hypermetabolic state. There is evidence suggesting malnutrition increases mortality rates in TBI patients. NGT necessary if patient cannot protect their airway. May even need G-tube if recovery is prolonged and mental status is poor.

59. Infection Prophylaxies Severe traumatic brain injury can increase a patient’s susceptibility to infection The use of mechanical ventilation Invasive monitoring Patients undergoing intracranial pressure (ICP) monitoring have related infection rates as high as 27%.

60. Infection Prophylaxis For external ventricular drains (EVDs) prophylactic intravenous (IV) antibiotics reduces infection rates or increases the risk of drug- resistant organisms Ventilator associated pneumonias (VAP) may be as high as 40%, and associated with longer exposure to mechanical ventilation The occurrence of VAP represents a significant morbidity

61. Infection Prophylaxis Recommendations Level II A Early tracheostomy is recommended to reduce mechanical ventilation days No evidence early tracheostomy reduces mortality or the rate of nosocomial pneumonia Bouderka MA, Fakhir B, Bouaggad A, Hmamouchi B, Hamoudi D, Harti A. Early tracheostomy versus prolonged endotracheal intubation in severe head injury. J Trauma. Aug 2004 Sugerman HJ, Wolfe L, Pasquale MD, et al. Multicenter, randomized, prospective trial of early tracheostomy. J Trauma. Nov 1997

62. Infection Prophylaxis Recommendations Level II A The use of povidone-iodine (PI) oral care is not recommended to reduce VAP and may cause an increased risk of ARDS Seguin P, Tanguy M, Laviolle B, Tirel O, Malledant Y. Effect of oropharyngeal decontamination by povidone-iodine on ventilator-associated pneumonia in patients with head trauma. Crit Care Med. May 2006 Seguin P, Laviolle B, Dahyot-Fizelier C, et al. Effect of oropharyngeal povidone-iodine preventive oral care on ventilator-associated pneumonia in severely brain-injured or cerebral hemorrhage patients: a multicenter, randomized controlled trial. Crit Care Med. Jan 2014

63. Infection Prophylaxis Recommendations Level III Antimicrobial-impregnated catheters may be considered to prevent catheter-related infections during EVD Wang X, Dong Y, Qi XQ, Li YM, Huang CG, Hou LJ. Clinical review: Efficacy of antimicrobialimpregnated catheters in external ventricular drainage - a systematic review and meta-analysis. Crit Care. 2013 Ratilal BO, Costa J, Sampaio C, Pappamikail L. Antibiotic prophylaxis for preventing meningitis in patients with basilar skull fractures. Cochrane Databse Syst Rev. Aug 2011. PMID: 21833952.

64. Deep Vein Thrombosis Prophylaxis 54% incidence of DVT without prophylactic treatment 25% incidence in patients with isolated TBI treated with sequential compression devices

65. Deep Vein Thrombosis Prophylaxis Significant risk for VTE due to Hypercoagulability resulting from the primary brain injury Prolonged periods of immobilization Focal motor deficits Non pharmacologic Vs Pharmacologic prevention.

66. Deep Vein Thrombosis Prophylaxis Recommendation Low molecular weight heparin (LMWH) or low-dose unfractionated heparin may be used in combination with mechanical prophylaxis Increased risk for expansion of intracranial hemorrhage. Kwiatt ME, Patel MS, Ross SE, et al. Is low-molecular-weight heparin safe for venous thromboembolism prophylaxis in patients with traumatic brain injury? A Western Trauma Association multicenter study. J Trauma Acute Care Surg. Sep 2012 Mohseni S, Talving P, Lam L, Chan LS, Ives C, Demetriades D. Venous thromboembolic events in isolated severe traumatic brain injury. J Emerg Trauma Shock. Jan 2012 Scudday T, Brasel K, Webb T, et al. Safety and efficacy of prophylactic anticoagulation in patients with traumatic brain injury. J Am Coll Surg. 2011 Daley MJ, Brown CV. Late venous thromboembolism prophylaxis after craniotomy in acute traumatic brain injury Am Surg 2015

67. Seizure Prophylaxis Post-traumatic seizures (PTS) are classified as; Early < 7 days of injury late > 7 days following injury Post-traumatic epilepsy (PTE) is defined as recurrent seizures > 7 days following injury.

68. Seizure Prophylaxis Glasgow Coma Scale (GCS) score of ≤10 Immediate seizures Post-traumatic amnesia lasting longer than 30 minutes Linear or depressed skull fracture Penetrating head injury Subdural, epidural, or intracerebral hematoma Cortical contusion Age ≤65 years Chronic alcoholism The risk factors for early PTS include:

69. Seizure Prophylaxis Severe TBI and early PTS prior to discharge Acute intracerebral hematoma or cortical contusion Post traumatic amnesia lasting longer than 24 hours Age >65 years or premorbid history of depression Risk for PTE (Post-traumatic epilepsy)

70. Seizure Prophylaxis Seizure prophylaxis for PTS refers to the practice of administering anticonvulsants to patients following TBI

71. Seizure Prophylaxis Recommendations Level II A Prophylactic use of phenytoin or valproate is not recommended for preventing late PTS Phenytoin is recommended to decrease the incidence of early PTS (within 7 days of injury) Inaba K, Menaker J, Branco BC, et al. A prospective multicenter comparison of levetiracetam versus phenytoin for early posttraumatic seizure prophylaxis. J Trauma Acute Care Surg. Mar 2013 Dikmen SS, Machamer JE, Winn HR, Anderson GD, Temkin NR. Neuropsychological effects of valproate in traumatic brain injury: a randomized trial. Neurology. Feb 2000 Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N Engl J Med. Aug 1990

72. Part II : Mornitoring Intracranial pressure monitoring Cerebral perfusion pressure monitoring Advanced cerebral monitoring Brain Tissue Oxygen (PbrO2) Monitoring Transcranial Doppler and Microdialysis. Jugular Bulb Monitoring of Arteriovenous Oxygen Content Difference(AVDO2)

73. Intracranial pressure monitoring

74. Critical Pathway for Treatment of Intracranial Hypertension in the Severe Head Injury Patient (Treatment Option) *Threshold of 20-25 mmHg may be used. Other values may be substituted in individual conditions. May Repeat Mannitol if Serum Osmolarity < 320 mOsm/L & Pt euvolemic High dose Barbiturate therapy Hyperventilation to PaCO2 < 30 mmHg Monitoring SjO2, AVDO2, and/orCBF Recommended Other Second Tier Therapies NO YES NO YESNO YESNO Carefully Withdraw ICP Treatment Consider Repeating CT Scan YES Second Tier Therapy Intracranial Hypertension? Hyperventilation to PaCO2 30 - 35 mmHg Intracranial Hypertension? Mannitol (0.25 - 1.0 g/kg IV) Intracranial Hypertension? Ventricular Drainage (if available) Intracranial Hypertension?* Maintain CPP  70 mmHg Insert ICP Monitor

75. Intracranial Pressure Monitoring Recommendations Level II B Management of severe TBI patient using information from ICP monitoring is recommended to reduce in-hospital and 2-week post-injury mortality (Farahvar A, Gerber LM, Chiu YL, Carney N, Hartl R, Ghajar J. Increased mortality in patients with severe traumatic brain injury treated without intracranial pressure monitoring. J Neurosurg. Oct 2012;117(4):729-734. PMID: 22900846. )

76. Cerebral perfusion pressure monitoring CPP = MAP – ICP MAP measured at the level of the heart ICP at the level of the foramina of Monro, or the external auditory meatus

77. Cerebral Perfusion Pressure monitoring Recommendations Level IIB CPP monitoring is recommended to decrease 2-week mortality Gerber LM, Chiu YL, Carney N, Hartl R, Ghajar J. Marked reduction in mortality in patients with severe traumatic brain injury. J Neurosurg. Dec 2013

78. Advanced Cerebral Monitoring Brain Tissue Oxygen (PbrO2) Monitoring Transcranial Doppler and Microdialysis Jugular Bulb Monitoring of Arteriovenous Oxygen Content Difference(AVDO2)

79. Advanced Cerebral Monitoring Brain Tissue Oxygen (PbrO2) Monitoring

80. Oxygen tension in brain tissue (brain PtiO 2 ) is as close to a gold standard of cerebral oxygenation as we have at the bedside. Brain PtiO 2 can be directly measured using a small flexible microcatheter (<0.5 mm in diameter) that is inserted usually into the frontal white matter and fixed onto a special bolt.

81. Advanced Cerebral Monitoring Transcranial Doppler and Microdialysis Transcranial Doppler uses ultrasound to examine the arteries, measure blood flow, and look for signs of vasospasm. Microdialysis to measure brain metabolism (Glucose, lactate, pyruvate, and glutamate) is not common outside of research settings.

82. Advanced Cerebral Monitoring Transcranial Doppler

83. Because the bones of the skull block most of the transmission of ultrasound, regions with thinner walls (called insonation windows), which offer the least distortion to the sound waves, must be used for analyzing.skull For this reason, recording is performed in the temporal region above the cheekbone / zygomatic arch, through the eyes, below the jaw, and from the back of the headcheekbone zygomatic arch it is still useful for diagnosis of arterial occlusions in patients with acute ischemic stroke, especially for middle cerebral artery

84. Advanced Cerebral Monitoring Jugular Bulb Monitoring of Arteriovenous oxygen content difference (AVDO2) Measure oxygen saturation of venous blood from brain and calculate Arteriovenous oxygen content difference

85. Advanced Cerebral Monitoring Level III Jugular bulb monitoring of arteriovenous oxygen content difference (AVDO2), as a source of information for management decisions, may be considered to reduce mortality and improve outcomes at 3 and 6 months post-injury Cruz J. The first decade of continuous monitoring of jugular bulb oxyhemoglobin saturation: management strategies and clinical outcome. Crit Care Med. Feb 1998 Le Roux PD, Newell DW, Lam AM, Grady MS, Winn HR. Cerebral arteriovenous oxygen difference: a predictor of cerebral infarction and outcome in patients with severe head injury. J Neurosurg. 1997 Robertson C. Desaturation episodes after severe head injury: influence on outcome. Acta Neurochir Suppl (Wien). 1993 Robertson CS, Gopinath SP, Goodman JC, Contant CF, Valadka AB, Narayan RK. SjvO2 monitoring in head-injured patients. J Neurotrauma. Oct 1995

86. Part III : Thresholds Blood pressure (BP) Intracranial pressure (ICP) Cerebral perfusion pressure monitoring (CPP) Advanced cerebral monitoring (ACM).

87. Blood pressure Threshold Level III SBP at ≥100 mm Hg for patients 50 to 69 years old SBP ≥110 mmHg for patients 15 to 49 or over 70 years old to decrease mortality and improve outcomes Berry C, Ley EJ, Bukur M, et al. Redefining hypotension in traumatic brain injury.Injury. Nov 2012

88. Intracranial Pressure Recommendations Level II B Treating ICP above 22 mm Hg is recommended because values above this level are associated with increased mortality(Level2B) Sorrentino E, Diedler J, Kasprowicz M, et al. Critical thresholds for cerebrovascular reactivity after traumatic brain injury. Neurocrit Care. 2012

89. Intracranial Pressure Recommendations Level III A combination of ICP values and clinical and brain CT findings may be used to make management decisions Chambers IR, Treadwell L, Mendelow AD.Determination of threshold levels of cerebral operating characteristic curves: an observational study in 291 patients. J Neurosurg. Mar 2001

90. Cerebral perfusion pressure (CPP) Recommendations Level II B cerebral perfusion pressure (CPP) value for survival and favorable outcomes is between 60 and 70 mm Hg. Allen BB, Chiu YL, Gerber LM, Ghajar J, Greenfield JP. Age-specific cerebral perfusion pressure thresholds and survival in children and adolescents with severe traumatic brain injury. Pediatr Crit Care Med. Jan 2014

91. Cerebral perfusion pressure (CPP) Recommendations Level III Avoiding aggressive attempts to maintain CPP > 70 mm Hg with fluids and pressors may be considered because of the risk of adult respiratory failure Johnnson U, Nilsson P, Ronne-Engstrom E, Howells T, Enblad P. Favorable outcome in traumatic brain injury patients with impaired cerebral pressure autoregulation when treated at low cerebral perfusion pressure levels. Neurosurg. Mar 2011

92. Advanced Cerebral Monitoring Thresholds Recommendations Level III Jugular venous saturation of <50% may be a threshold to avoid in order to reduce mortality and improve outcomes Robertson C. Desaturation episodes after severe head injury: influence on outcome. Acta Neurochir Suppl (Wien). 1993

93. Take Home Message Prolonged prophylactic hyperventilation is not recommended Ventilation therapy Administration of barbiturates as prophylaxis against the development of intracranial hypertension is not recommended High-dose barbiturate administration is recommended to control refractory elevated ICP Propofol is not recommended for improvement in mortality or 6-month outcomes Anesthetic agent

94. Take home massage Intracranial pressure monitor should be monitored but in low technology setting CT scan and clinical examination can be used Cerebral perfusion pressure monitoring is recommended Jugular Bulb Monitoring of Arteriovenous Oxygen Content Difference(AVDO2) monitoring is recommended to reduce motality Monitoring

95. Take home massage SBP at ≥100 mm Hg for patients 50 to 69 years SBP ≥110 mm Hg for patients 15 to 49 or over 70 years old ICP > 22 mmHg should be treated CPP should be maintained 60-70 mmHg Aggressive volume and pressors to maintain CPP > 70 mmHg should be avoided Jugular venous saturation of the brain <50% should be avoided Thresholds

96. Common Motor Problems ______________________________________________________ Apraxia Ataxia Coordination problems Paresis or paralysis Orthopedic problems Spasticity Balance problems Impaired speed of movement Fatigue

97. Sensory/Perceptual Problems ______________________________________________________ Visual deficits field cuts tracking (moving and stationary objects) spatial relationships double vision (diplopia) Neglect Auditory deficits Tactile deficits

98. Cognitive/Communication Problems _______________________________________________________ Executive functions Memory Attention Concentration Information processing Sequencing Problem solving Comprehension of abstract language Word retrieval Expressive language organization Pragmatics

99. Social/Emotional Problems _______________________________________________________ Irritability Impulsivity Disinhibition Perseveration Emotional lability Insensitivity to social cues Low frustration tolerance Anxiety Withdrawal Egocentricity Denial of deficit/ lack of insight Depression Peer conflict Sexuality concerns High risk behavior

100. Behavioral Problems ______________________________________________________ Deficits (all types) may lead to challenging behaviors non-compliance aggression confrontational behavior lack of initiative withdrawal

101. Impact on Learning ______________________________________________________ Orientation and Attention to Activity Starting, Changing, and Maintaining Activities Taking in and Retaining Information Language Comprehension and Expression Visual-Perceptual Processing Visual-Motor Skills Sequential Processing Problem-Solving, Reasoning, and Generalization Organization and Planning Skills Impulse or Self-Control Social Adjustment and Awareness Emotional Adjustment Sensorimotor Skills

102. Thank you for your attention