Traumatic Brain Injury/ Head injury Management/ Approach to Head injury

Traumatic Brain Injury/ Head injury Management/ Approach to Head injury according to latest guidelines from Traumatic brain injury foundation

1. Traumatic Brain injury Dr Sushil G yawali MS resident

2. Severity of TBI Mild: GCS 13-15 Moderate: GCS 9-12 Severe: GCS <9 associated injuries to internal organs, limbs, or the spinal cord.

3. Traumatic Brain injury Primary Injury: at time of trauma ( contusion,laceration , fracture, axonal injury) Secondary Injury: develops subsequent to initial injury (edema, hypoxemia, ischemia, vasospasm, hematoma, HCP, seizures, features of raised ICP)

4. Severe TBI: Initial Evaluation The injured brain is especially vulnerable to secondary insults in the first 24 hours The primary goal: prevention and treatment of hypotension and hypoxia, two systemic insults known to be major causes of secondary injury after TBI

5. Approach Primary survey Airway with C Spine protection Breathing Circulation with control of hemorrhage Disability/Neurological assessment: GCS Exposure and environment control Secondary Survey Brief history, AMPLE Head to toe; pupil investigation Reassess vital sign plan

6. Intubation GCS score <9, unable to protect airway, low Sats<90% despite supplemental Oxygenation or clinical signs of cerebral herniation . Evidence of aspiration Both hypoventilation and hyperventilation should be avoided following intubation.

7. Neuroimaging CT scan is the preferred in the acute phase of head injury; for lifesaving neurosurgical interventions NCCT scan: skull fractures, ICH, and cerebral edema Current guidelines recommend head CT in all TBI patients with a GCS < 15 Follow-up CT scan: if clinical deterioration Evolution of CT findings is common and may indicate an alternative treatment

8. In the absence of clinical deterioration, repeat imaging in 6 hours is reasonable in patients with a hematoma present on the initial scan, particularly in patients with a GCS < 9.

9. Intensive Care Management A principal focus of critical care management for severe TBI is to limit secondary brain injury. A imed at ICP management and maintenance of cerebral perfusion, optimizing oxygenation and BP and managing temperature, glucose, seizures, and other potential secondary brain insults. Other extracranial traumatic injuries are managed simultaneously

10. Level of Recommendation determined by the assessment of the quality of the body of evidence, rather than the class of the included studies. Level I : based on a high-quality body of evidence. Level II A : moderate-quality body of evidence. Level II B and II I :low-quality body of evidence . 189 publications used for evidence—5 Class 1, 46 Class 2, 136 Class 3 studies, and 2 meta-analyses.

11. Fluids Isotonic fluids (NS) to maintain euvolemia . RL, plasmalytes : relatively hypotonic and may worsen cerebral edema . ( SMART ICU trial 2018 ) NS prefered over albumin (SAFE trial 2004 ) Electrolyte imbalances are common in TBI and should be regularly assessed along with other laboratory parameters .

12. Blood pressure The avoidance of hypotension Autoregulation : Fall in SBP results in vasodilation and increase flow to brain Autoregulation can fail to maintain brain perfusion in severe TBI

13. Recommendation Level III Maintaining SBP at ≥100 mm Hg for patients 50 to 69 years old or at ≥110 mm Hg or above for patients 15 to 49 or over 70 years old may be considered to decrease mortality and improve outcomes.

14. Ventilation Definitive airway protection Hypoxia should also be avoided, and maintain PaO2 >60 mmHg Under normal conditions, PaCO2 is the most powerful determinant of cerebral blood flow (CBF) and, between a range of 20 mm Hg and 80 mm Hg, CBF is linearly responsive to PaCO2.

15. Acute hypercarbia may increase ICP, and hypocarbia may precipitate cerebral ischemia; ETCO2 monitoring With Hyperventilation PaCO2 decreases, leading to cerebral vasoconstriction, resulting in decreased cerebral blood volume and ICP. H yperventilation-induced vasoconstriction may also cause secondary ischemia and may thereby worsen outcomes

16. Transient hyperventilation to treat cerebral herniation : can be used to reduce ICP temoparily but avoided in acute phases 24-28 hrs ( PaCO2<30mmHg) Hyperventilation can also increase extracellular lactate and glutamate levels that may contribute to secondary brain injury

17. Recommendation Level II B Prolonged prophylactic hyperventilation with PaCO2 of 25 mm Hg or less is not recommended.

18. Prior (3rd) Edition Recommendation Not Supported by Evidence Meeting Current Standards 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 when cerebral blood flow (CBF) is often critically reduced. If hyperventilation is used, jugular venous oxygen saturation (SjO2) or brain tissue O2 partial pressure (BtpO2) measurements are recommended to monitor oxygen delivery.

19. Anesthetics , Analgesics, and Sedatives For prophylaxis or control of intracranial hypertension and seizures. Depressed cerebral metabolism and oxygen consumption is said to be neuroprotective in some patients. Anesthetics and sedatives, such as barbiturates, may also improve coupling of regional blood flow to metabolic demands resulting in higher brain oxygenation with lower CBF and decreased ICP from decreased CBV.

20. Side effects: hypotension and decreased cardiac output, as well as increased intrapulmonary shunting, which may lead to hypoxia. These may give rise to a paradoxical decrease in CPP, which may negate the benefits of decreased ICP. In addition, anesthetics such as propofol have been associated with hyperkalemia , metabolic acidosis, myocardial failure, rhabdomyolysis , and death.

21. Recommendation : Level II B Administration of barbiturates to induce burst suppression measured by EEG as prophylaxis against the development of intracranial hypertension is not recommended. High-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment. Hemodynamic stability is essential before and during barbiturate therapy. 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.

22. Steroids E xperimental evidence accumulated that steroids were useful in the restoration of altered vascular permeability in brain edema , reduction of cerebrospinal fluid production, attenuation of free radical production, and other beneficial effects in experimental models. Glucocorticoids were found to be beneficial to patients with brain tumors when administered in the perioperative period.

23. Recommendation 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

24. Seizure prophylaxis Post-traumatic seizures (PTS) : early within 7 days of injury or late after 7 days following injury. Post-traumatic epilepsy (PTE) is defined as recurrent seizures more than 7 days following injury. In patients with severe TBI, the rate of clinical PTS may be as high as 12%, while that of subclinical seizures detected on EEG may be as high as 20% to 25%.

25. Risk factors The risk factors for early PTS : (GCS) ≤10; immediate seizures; post-traumatic amnesia lasting > 30 minutes; linear or depressed skull fracture; penetrating head injury; subdural, epidural, or intracerebral hematoma; cortical contusion; age ≤65 years; or chronic alcoholism. Risk factors for PTE : severe TBI and early PTS prior to discharge; acute ICH or cortical contusion; posttraumatic amnesia lasting longer> 24 hours; age >65 years; or premorbid history of depression.

26. Recommendation 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 , when the overall benefit is felt to outweigh the complications associated with such treatment. However, early PTS have not been associated with worse outcomes. At the present time there is insufficient evidence to recommend levetiracetam over phenytoin regarding efficacy in preventing early post-traumatic seizures and toxicity.

27. Levetiracetam vs phenytoin (Lin Zhao, MM et al Metaanalysis 2018 ) LEV prevention of seizures was associated with early seizure rates that were lower than the PHT-prolonged course of treatment. There is no statistically significant difference in the efficacy and safety profile of PHT and LEV in cases of traumatic BI.

28. Osmotic therapy For those who are clinically symptomatic from cerebral edema or have documented ICP elevation that does not respond to initial measures such as CSF drainage, analgesia, and sedation NaCl 3% infusion to achieve a Na goal of 145 to 155 mEq /L in patients with elevated ICP. In addition, 30 mL bolus doses of 23.4 percent NaCl , administered over 10 minutes,(intermittent bolus) to treat acute ICP elevations.

29. Hypertonic saline Vs Mannitol Advantage: volume depletion and hypovolemia do not occur, which makes this agent safer in the trauma patient with ongoing blood loss, hypovolemia , or hypotension. Hypertonic saline has a reflection coefficient of 1.0 (compared with 0.9 for mannitol ), and is therefore less likely to leak into brain tissue. Potential adverse effects include circulatory overload and pulmonary edema , and an increased chloride burden, which may result in a non-anion gap metabolic acidosis

30. Mannitol : in boluses of 0.25 to 1 g/kg every four to six hours as needed. Judicious use as mannitol use: leakage into brain tissue in patients with disruption of the BBB, with consequent reversal of the osmolar gradient and rebound cerebral edema .

31. hyperosmolar agents should be weaned slowly after prolonged use to prevent a reversal in the osmotic gradient and consequent rebound cerebral edema .

32. Recommendation L evel I, II, and III Although hyperosmolar therapy may lower ICP, there was insufficient evidence about effects on clinical outcomes to support a specific recommendation, or to support use of any specific hyperosmolar agent, for patients with severe traumatic brain injury.

33. Recommendations from the Prior (3rd) Edition Not Supported by Evidence Meeting Current Standards Mannitol is effective for control of raised intracranial pressure (ICP) at doses of 0.25- 1 g/kg body weight. Arterial hypotension (SBP<90) should be avoided. Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or progressive neurological deterioration not attributable to extracranial causes.

34. Monitoring Serial measurement of electrolytes, often at 4-6hrs intervals, to prevent excessive elevation of sodium and chloride levels, and to detect and correct other derangements such as hypokalemia .

35. Venous thromboembolism prophylaxis Patients with TBI are at increased risk of VTE. Up to 54% incidence DVT without prophylactic treatment3 and a 25% incidence in patients with isolated TBI treated with sequential compression devices Due to hypercoagulability resulting from the primary brain injury, prolonged periods of immobilization, and focal motor deficits Age, subarachnoid hemorrhage , Injury Severity Score >15, and extremity injury were predictors of DVT Reiff et al. demonstrated a 3-4fold increase in the DVT risk in TBI despite use of mechanical and chemoprophylaxis.

36. Safe when initiated within 24 -48 hours of injury in TBI patients with stability demonstrated on repeat imaging Mechanical prophylaxis: intermittent pneumatic compression stockings, boots and Chemoprophylaxis: either UFH or with enoxaparin following admission in most TBI patients with stability confirmed on repeat imaging.

37. Recommendation Level III LMWH or low-dose UFH may be used in combination with mechanical prophylaxis. However, there is an increased risk for expansion of intracranial hemorrhage

38. Antifibrinolytic : Tranexamic acid B enefit is highly time dependent in mild to moderate injury, but not in patients with severe injury M oderate TBI within 3 hours of injury; safe and is associated with decreased mortality. Tranexamic acid 1 g stat and then TDS

39. CRASH3 Trial (Lancet 2019) A benefit for tranexamic acid in moderate TBI randomized 9202 TBI patients with GCS <13 or any evidence of intracranial bleeding on CT scan within 3 hours of injury to tranexamic acid or placebo The benefit of tranexamic acid was highly time dependent in patients with mild to moderate injury, but not in patients with severe injury.

40. Glucose management Both hyper- and hypoglycemia a/w worsened outcome, aggravation of secondary brain injury. Several mechanisms : increased tissue acidosis from anaerobic metabolism, free radical generation, and increased blood-brain barrier permeability. target a range of 140 to 180 mg/ dL , no aggressive control

41. Temperature management Fever is associated with worse outcome, aggravating secondary brain injury . Fever also worsens ICP control through an increase in metabolic demand, blood flow, and blood volume. Maintain Normothermia

42. Prophylactic Hypothermia neuroprotective effects, ability to reduce intracranial pressure. risks, including coagulopathy and immunosuppression , and profound hypothermia bears the additional risk of cardiac dysrhythmia and death.

43. either early after injury and prior to ICP elevation, in which case it is termed “ prophylactic, ” or as a treatment for refractory intracranial pressure elevation, typically referred to as “ therapeutic

44. Recommendation ( Level IIB ) Early (within 2.5 hours), short-term (48 hours post-injury) prophylactic hypothermia is not recommended to improve outcomes in patients with diffuse injury

45. Nutritional support TBI itself causes an intrinsic increase in metabolism and requirement for caloric support There is some evidence that early enteral nutrition may decrease rates of pneumonia (VAP) as well as mortality following TBI

46. Recommendation Level II A • Feeding patients to attain basal caloric replacement at least by the 5 th day and, at most, by the 7 th day post-injury is recommended to decrease mortality. Level II B • Transgastric jejunal feeding is recommended to reduce the incidence of ventilator associated pneumonia.

47. Infection Prophylaxis Severe TBI increase a patient’s susceptibility to infection because of necessary mechanical ventilation to prevent airway obstruction, aspiration, and consequential hypoxia, in addition to invasive monitoring. Infection risks such as ventilator associated pneumonias (VAP) and central line-associated bacteremias are increased in all critically ill patients

48. Data prior to the 2011 CDC definitions show that VAP in TBI may be as high as 40%, and it is strongly associated with longer exposure to mechanical ventilation. The occurrence of VAP represents a significant morbidity and is associated with factors such as hypoxia, fevers, hypotension, and increased ICP, known to worsen the TBI patient’s hospital course. In (CDC) definition, possible VAP requires a positive culture, purulent respiratory secretions, or positive results on one of several tests.

49. Recommendation Level II A Early tracheostomy is recommended to reduce MV days when the overall benefit is felt to outweigh the complications associated with such a procedure. However, there is no evidence that early tracheostomy reduces mortality or the rate of nosocomial pneumonia. The use of povidone -iodine (PI) oral care is not recommended to reduce VAP and may cause an increased risk of ARDS Level III Antimicrobial-impregnated catheters may be considered to prevent catheter-related infections during EVD.

50. Timing of Tracheostomy Early tracheostomy has been proposed to decrease the incidence of pneumonia in critically ill patients. Two RCTs, with small numbers of subjects (n=62 and n=67) and different definitions of early (3-5 days and 5-6 days), found no differences in pneumonia rates or mortality in severe TBI patients undergoing early tracheostomy compared with patients with later tracheostomy . Bouderka , 2004: Early tracheostomy (5 or 6 days) vs. prolonged ET Sugerman , 1997 Early (3-5 days) vs. late (10-14 days) tracheostomy

51. Cerebral perfusion pressure Autoregulation between 50-150mmHg MAP Disrupted in one third severe TBI cases ‘pressure passive’ associated with secondary brain injury surrogate measure for the delivery of nutrients to the brain. Increase MAP can lead to elevated ICP due to increased cerebral blood volume and hyperemia , while drops in MAP may be associated with hypoperfusion and ischemia.

52. TBI management includes CPP monitoring in the “bundle” of care best managed with efforts to lower ICP, rather than by elevating MAP with vasopressors ; hypertension is more likely to worsen cerebral edema when protective autoregulation is impaired

53. Recommendation Level II B Management of severe TBI patients using guidelines-based recommendations for CPP monitoring is recommended to decrease 2-week mortality. The recommended target CPP value for survival and favorable outcomes is between 60 and 70 mm Hg. (Whether 60 or 70 mm Hg is the minimum optimal CPP threshold is unclear and may depend upon the patient’s autoregulatory status.)

54. ICP Management Initial treatment —Head of bed (HOB) elevation to 30° to permit adequate venous drainage from the brain while not compromising cerebral perfusion Optimization of venous drainage: keeping the neck in neutral position, loosening neck braces if too tight

55. In Impending cerebral herniation : ET intubation, 30 ° - 45 ° head elevation Brief hyperventilation to a pCO2 approx 30 mmHg (ETCO 2 25 to 30 mmHg), as a lifesaving measure bolus dose osmotic agent : transiently reversing cerebral herniation . Mannitol /Hypertonic Saline

56. ICP and CPP monitoring — Indications for ICP monitoring in TBI are GCS score ≤8 and an abnormal CT scan with evidence of mass effect from lesions such as hematomas, contusions, or swelling. ICP monitoring in severe TBI patients with a normal CT scan may be indicated if any two present : age >40 years, motor posturing, S BP< 90mmHg

57. EVD, connected to a strain gauge transducer is the most accurate and cost-effective method of ICP monitoring and has the therapeutic advantage of allowing to CSF drainage to treat rises in ICP An ICP goal ≤22 mmHg is recommended as the threshold that predicts survival and favorable outcome following TBI

58. Recommendation Level II B • Management of severe TBI patients using information from ICP monitoring is recommended to reduce in-hospital and 2-week post-injury mortality

59. Recommendations from the Prior (3rd) Edition Not Supported by Evidence Meeting Current Standards ICPshould be monitored in all salvageable patients with a (TBI) (GCS 3-8 after resuscitation) and an abnormal computed tomography (CT) scan. An abnormal CT scan of the head is one that reveals hematomas, contusions, swelling, herniation , or compressed basal cisterns. ICP monitoring is indicated in patients with severe TBI with a normal CT scan if two or more of the following features are noted at admission: age over 40 years, unilateral or bilateral motor posturing, or SBP

60. Cerebrospinal fluid drainage I n patients with a ventricular catheter, drainage of CSF is generally the first intervention for lowering ICP. EVD in a closed position allows for monitoring of ICP, while in an open position drainage of CSF Drainage may be continuous or intermittent, with a limited volume of CSF drained in response to elevations in ICP above goal. Based on observational data, guidelines recommend continuous CSF drainage for better control of ICP compared with intermittent drainage

61. EVD in patients with severe TBI remains a controversial topic. Continuous drainage is particularly recommended in patients with a GCS score < 6 in the first 12 hours. Caution :excessive drainage can lead to ventricular collapse and malfunctioning or occlusion of the catheter in the setting of cerebral edema and small ventricles

62. Csf drainage: Changes from Prior Edition This new topic, which was added to the 4th Edition as Cerebrospinal Fluid (CSF) drainage, is a potential treatment to lower intracranial pressure.

63. Recommendation 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 . Use of CSF drainage to lower ICP in patients with an initial (GCS) <6 during the first 12 hours after injury may be considered.

64. Refractory ICP elevation may be managed with decompressive craniectomy , barbiturate coma, or hypothermia.

65. Surgical Treatment Indications for emergency surgery after severe head injury are based upon neurologic status (GCS) and CT findings such as large hematoma volume or thickness and evidence of mass effect including midline shift

66. Epidural hematoma Surgical guidelines recommend evacuation of EDH > 30 mL in volume regardless of a patient's GCS score; emergency surgical evacuation in acute EDH and coma (GCS score ≤8) who have pupillary abnormalities ( anisocoria )

67. Subdural hematoma Acute SDH >10 mm in thickness or associated with midline shift >5 mm on CT should be surgically evacuated, regardless of the patient's GCS score . In addition, if the GCS ≤8 or if the GCS score has decreased by ≥2 points from the time of injury to hospital admission, and/or if the patient presents with asymmetric or fixed and dilated pupils, or intracranial pressure (ICP) measurements are consistently >20 mmHg.

68. Intracerebral hemorrhage Surgical evacuation of a traumatic ICH in the posterior fossa is recommended when there is evidence of significant mass effect (brainstem compression, obliteration of the fourth ventricle, effacement of the basal cisterns, or obstructive hydrocephalus)

69. For traumatic ICH involving the cerebral hemispheres , surgical indications are not as clearly defined. Consensus surgical guidelines recommend craniotomy with evacuation if the hemorrhage exceeds 50 cm in volume, or if the GCS score is 6 to 8 in a patient with a frontal or temporal hemorrhage greater than 20 cm with midline shift of at least 5 mm and/or cisternal compression on CT scan

70. Penetrating injury Superficial debridement and dural closure to prevent CSF leak is generally recommended. Small entry wounds can be treated with simple closure. Aggressive debridement and removal of deep foreign bodies such as bone or bullet fragments have not been shown to be effective in preventing delayed infection. The use of prophylactic broad-spectrum antibiotics is routine in this setting and is believed to have contributed to the reduced incidence of infection

71. Depressed skull fracture Elevation and debridement are recommended for open skull fractures depressed greater than the thickness of the cranium or if there is dural penetration, significant intracranial hematoma, frontal sinus involvement, cosmetic deformity, wound infection or contamination, or pneumocephalus

72. Refractory intracranial hypertension Decompressive craniectomy may be lifesaving in patients with refractory elevations of ICP

73. Decompressive Craniectomy A craniectomy of sufficient size can rapidly relieve intracranial hypertension. Potentially lifesaving in patients who have failed medical therapy. A "primary" or prophylactic craniectomy is performed in anticipation of elevated ICP, most often at the time of hematoma evacuation, or life-threatening intracranial hypertension. A "secondary" or therapeutic decompressive craniectomy is performed to control proven ICP elevation (measured using invasive monitoring) that is refractory to medical therapy.

74. 2016 update Level IIA 1. “ Bifrontal DC is not recommended to improve outcomes as measured by the GOS-E score at 6 months post-injury in severe TBI patients with diffuse injury (without mass lesions), and with ICP elevation to values > 20 mm Hg for more than 15 minutes within a 1-h period that are refractory to first-tier therapies. However, this procedure has been demonstrated to reduce ICP and to minimize days in the intensive care unit (ICU). 2. A large FTP DC (not less than 12 × 15 cm or 15 cmdiameter ) is recommended over a small FTP DC for reduced mortality and improved neurologic outcomes in patients with severe TBI.”

75. DECRA trial RCT that compared bifrontotemporoparietal DC to initial medical management for refractory raised ICP, 15 tertiary care hospitals in Australia, New Zealand, and Saudi Arabia between December 2002 and April 2010. This study found poorer GOS-E scores for patients in the DC group than those in standard care at 6 months postinjury , and lower ICP and fewer ICU days for patients in the DC group. Despite randomization, the proportion of patients in the DC group with reactivity in neither pupil on admission was higher (27% vs. 12%, p=0.04) than in controls. Planned baseline covariate adjustment did not change the results, but post hoc adjustment for this difference in pupil reactivity at admission resulted in outcome differences that were no longer significant. Based on this, the authors reported that “…the overall effect size did not change, although the harmful effect of craniectomy was no longer significant. A beneficial effect of craniectomy was excluded.”

76. 2020 update findings of the RESCUEicp study (Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension ) as well as the recently published 12-mo outcome data from the DECRA ( Decompressive Craniectomy in Patients With Severe Traumatic Brain Injury) trial.

77. New recommendation Level IIA–to improve mortality and overall outcomes 1. NEW–Secondary DC performed for late refractory ICP elevation is recommended to improve mortality and favorable outcomes. 2. NEW–Secondary DC performed for early refractory ICP elevation is not recommended to improve mortality and favorable outcomes. 3. A large FTP DC (not less than 12 × 15 cm or 15 cm in diameter) is recommended over a small FTP DC for reduced mortality and improved neurological outcomes in patients with severe TBI. Level IIA–for ICP control 4. NEW–Secondary DC, performed as a treatment for either early or late refractory ICP elevation, is suggested to reduce ICP and duration of intensive care, though the relationship between these effects and favorable outcome is uncertain.

78. 1. Decompressive Craniectomy 2. Prophylactic Hypothermia 3. Hyperosmolar Therapy 4. Cerebrospinal Fluid Drainage 5. Ventilation Therapies 6. Anesthetics , Analgesics, and Sedatives 7. Steroids 8. Nutrition 9. Infection Prophylaxis 10. Deep Vein Thrombosis Prophylaxis 11. Seizure Prophylaxis Monitoring 12. Intracranial Pressure 13. Cerebral Perfusion Pressure 14. Advanced Cerebral Monitoring 15. Blood Pressure

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80. Management of Coagulopathy Approximately one-third of patients with severe TBI demonstrate a coagulopathy , associated with an increased risk of hemorrhage enlargement, poor neurologic outcomes, and death. release of TF and brain phospholipids into the circulation inappropriate intravascular coagulation and a consumptive coagulopathy Pt on warfarin : prothrombin complex concentrate (PCC) and vitamin K /FFP Platelets: maintain >75000/cc ( insufficient evidence)