TBI HEAD injury Anaesthesia hshushuwjjeh

TBI HEAD INJURY ANAESTHESIA CONSIDERATION

1. ROLE OF ANAESTHETISTS IN HEAD INJURIES PRESENTOR: DR.M.Sai Mahitha , MODERATORS: DR.Rukmini , Dr.Archana Dr.Lavanya

2. Worldwide, Traumatic Brain Injury (TBI) is a leading cause of morbidity and mortality in young adults. Seen in age groups of 5-35yrs. Anesthesiologists are involved in the care of patients with TBI in various situations, including but resuscitation and stabilization in the emergency department (ED), sedation and anesthesia for diagnostic imaging, craniotomy or decompressive craniectomy , extracranial surgery, and intensive care management

3. PATHOPHYSIOLOGY PRIMARY AND SECONDARY INJURIES The primary injury : initial injury( physical or mechanical ) on the brain parenchyma and skull produces an inflammatory cascade including cerebral edema, axonal injury, and decreased CPP Secondary injuries : consequence of the primary injury which leads to electrolyte abnormalities, hypoxemia, glycemic imbalance, hypotension, loss of auto regulation, increased ICP, and hyper or hypo carbia .

4. TBI may also be classified according to whether it is blunt or penetrating. Penetrating injury may vary depending on site, depth, and energy, but is generally fatal if it bilaterally traverses the midbrain. Although initial mortality from penetrating injury is higher , outcome in survivors of both groups are similar.

5. Evaluation of TBI Patients Focused history and physical examination. HISTORY TAKING SHOULD INCLUDE Neurological state (consciousness, pupillary response) and vital parameters at the scene and during transport Estimated blood loss Nature of treatment at scene and in transit Use of airbags, seat-belts, crash-helmets Time, place, mechanism, vehicle speed (in relation to the accident) Past medical history Suspected influence of drugs or alcohol

6. Physical examination: careful airway assessment thorough neurological examination (baseline sensation, motor function, and the presence of new FND)  degree of TBI & CSI During first assessment: recognize critical signs of other trauma related injuries such as bleeding, pneumothorax, cardiac tamponade , etc.

7. Determine the level of consciousness according to the Glasgow Coma Scale

8. Examine the pupils for size, symmetry, and reaction to light.

9. Cervical Spine Injury (CSI) after TBI Early assessment of cervical spine integrity is essential to rule out a hidden cervical spine fracture, especially in the TBI patient. Studies show correlation between CSI and poor GCS. Maintain a high degree of suspicion for CSI in a TBI patient especially with a low GCS . O/E of the cervical spine look for tenderness along the spine, a “gap” or “step” deformity in the continuity of the spine, other mass effect due to edema, hematoma, or muscle spasm

10. IMAGING IN CSI PATIENTS Improves efficiency in treating TBI patients. There are two well established guidelines for obtaining cervical spine radiographic imaging of TBI patients. The National Emergency X-Radiography Utilization Study (NEXUS) and the Canadian C Spine Rule.

11. The NEXUS study concluded that a patient was at low risk for CSI if none of the following five clinical criteria are present: Low risk criteria for CSI (NEXUS) If following are absent: 1. Midline cervical tenderness 2. Focal neurological deficits 3. Altered mental status 4. Evidence of intoxication 5. Distracting injury present diverting attention from neck pain

12. CANADIAN C-SPINE RULE

13. Securing the Airway If radiographic study cannot be done (hemodynamic instability or airway emergency) unstable cervical spine is assumed until proven otherwise. Prevention of further neurological injury is critical. Maintaining spinal alignment, protecting the spinal cord, and stabilizing the cervical spine. Cervical collar may stabilize the spine BUT, interferes with Laryngoscope. So removal of only anterior portion of the cervical collar is recommended, leaving the posterior portion.

14. MANUAL-IN-LINE-STABILIZATION

15. The use of MILI has less impact obtaining a view of the vocal cords during direct laryngoscopy compared to immobilization with axial traction utilizing a cervical collar, tape, or sandbag Historically, practitioners preferred nasotracheal intubation with flexible bronchoscopy or a surgical airway due to the possibility of spinal injury during oral intubation. Complications : 1.Suspected basal skull fracture  endotracheal tube inserted blindly may find path to the brain. 2.Trauma to the nares and epistaxis  impair visualization of Vocal cords.

16. Therefore, OROTRACHEAL INTUBATION AFTER RAPID SEQUENCE INDUCTION AND DIRECT LARYNGOSCOPY WITH MILI IS SAFEST CHOICE . If airway management history or assessment reveals a possible challenging intubation, an awake fiberoptic intubation should be performed instead ADVANTAGES if done by experienced practitioner :maintains the cervical spine in a neutral position & preserves airway reflexes.

17. PRIMARY RESUSCITATION AIRWAY BREATHING Maintain SPO2 > 90% Maintain PaO2 > 60mmHg Maintain PCO2:35-40mmHg Obtain CXR Check ABG CIRCULATION Prevent hypotension Aim SBP> 90mmHg Resuscitation with isotonic crystalloid Inotropes (adrenaline) if needed

18. Indication for intubation : Unable to maintain airway GCS ≤ 8 Loss of protective laryngeal reflexes. Unstable facial bone # Bleeding into mouth Seizures

19. Ventilation in TBI Securing the airway by intubating our patient has three specific goals: prevention of aspiration of gastric contents prevention of hypoxia and Prevention of hypercarbia . Hypoxia has direct correlation to poor outcomes in TBI patients

20. Monroe-Kellie doctrine The Monroe-Kellie hypothesis states that the cranial compartment is incompressible, and the volume inside the cranium is fixed. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another.

21. INTRAOPERATIVE MANAGEMENT

22. Anaesthesiologists play critical role during induction of anesthesia, positioning of patient, take measure to prevent excessive heat loss, maintainence of anesthesia, fluid therapy, supplementary drug therapy, monitoring during anesthesia, apply techniques to reduce intra-cranial pressure and normotensive BP, recovery of anesthesia & post- operative care. Goals of anesthetic management: I) maintain CPP II) treat increased ICP III) provide optimal surgical conditions IV) avoid secondary insults

23. The patient will require to be anesthetised , even when consciousness is already impaired, to minimize the risk of secondary brain damage due to induced raised ICP. Rapid sequence induction and intubation is the recommended technique using a combination of sedative with low cardio pressant effects (e.g. midazolam), analgesic (fentanyl) and muscle relaxant ( e.g.succinylcholine ) agents

24. 1. INTRAOPERATIVE MONITORING AND INTRAVENOUS ACCESS: Standard ASA monitors, an arterial line and adequate intravenous access are essential in the management of TBI patients. One very important consideration: placement of these lines should not delay the start of the surgical intervention. Placement of two large bore (>/=18 gauge) . If difficult IV then proceed to central line, (the femoral vein is most appropriate in order to avoid trendelenburg positioning )  fail, then tibial or humeral intra-osseous lines should be placed Temperature monitoring (lower esophageal= tympanic membrane)

25. Intra-cranial pressure(ICP ) Intracranial pressure (ICP) is the pressure inside the skull and thus in the brain tissue and cerebrospinal fluid (CSF). ICP is measured in millimeters of mercury(mmHg) and, at rest, is normally 7–15 mmHg for a supine adult. ICP monitoring can be done by placing intra parenchymal probe or intra ventricular catheter and ICP maintained <20mmHg .

26. MANAGEMENT OF ICP The Brain Trauma Foundation states that ICP > 20 mmHg is associated with increased mortality and worse outcomes . The fastest way to decrease ICP > 20 mmHg is to allow CSF drainage from a CSF drain if present. elevate the patient’s head and maintain the neck in a neutral position, to improve venous blood return. slow administration of 0.25-1 gm /kg of mannitol in stable patients over fifteen minutes (not rapidly)  ICP reduction, a transient increase in oxygen transport, and increase in CBF.

27. monitor and replace urinary loses to prevent intravascular volume depletion and hypotension when mannitol is administered  otherwise there will be adverse effect on kidney due to hypo perfusion. Rebound increase in ICP can occur due to worsening of vasogenic edema (damaged blood brain barrier) . Hyperventilation: Hyperventilation decreases CBF: Hyperventilating to PCO2 26mmHg decreases CBF by 31% and CBV by 7% thus maintaining normal ICP. CBF 90% of control at 4 hours of hyperventilation.

28. BLOOD PRESSURE MANAGEMENT: Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP) . Normal CPP > 50 mm Hg If CPP decreases, brain parenchyma oxygenation can be further compromised in TBI patients. Treatment should focus on keeping CPP within normal range and also decreasing ICP. MAP should be maintained >90mmHg throughout treatment to maintain CPP >70mmHg.

29. FLUID RESUSCITATION IS MAINSTAY OF THERAPY (hypertonic saline solutions optimal, no ideal IVF). Hypotonic fluids should be avoided isotonic or hypertonic fluids alone should be used Glucose-containing solutions should not be used in large quantities. Higher mortality of albumin is used for resuscitation.

30. COAGULOPATHY AND HEMOGLOBIN LEVEL TBI may produce coagulopathy through the systemic release of by-products from neuronal death such as tissue factor and phospholipids  impairs coagulation reactions, platelet function  disseminated intravascular coagulation. Exacerbated by colloid infusion Coagulation parameters should be measured immediately in acute TBI patients. Any abnormal values should be identified and corrected. INR in TBI patients should be maintained less than or equal to 1.4 Platelet count maintained above 75,000 Hemoglobin levels should be maintained at or above 7 g/dl to avoid a decrease in brain oxygen delivery

31. TBI patients may also develop endogenous acute coagulopathy (EAC) due to activation of the protein C pathway(25% of major trauma patients) EAC is characterized by anticoagulation derangement and hyper fibrinolysis  not reflected by standard coagulation tests ( aPTT and PT/INR). Therefore, once multiple injuries are found and the patient is unstable despite crystalloid infusion, balanced transfusion of blood products should be considered early, possibly without waiting for lab results. Balanced transfusion involves the use of plasma, platelets and packed red blood cells (1:1:1), with the aim to effectively reconstitute whole blood.

32. GLYCEMIC CONTROL The presence of hyperglycemia might produce an increase in neuronal metabolism and increase neuronal death after TBI. These events occur due to: increased tissue acidosis through anaerobic metabolism, creation of free radicals increased blood brain barrier permeability. Blood glucose concentration should not be >180mg/dl.

33. THERMOREGULATION : it is important to remember that fever worsens the severity of brain injury by increasing cerebral metabolic rate. early hyperthermia after TBI has been found to be a possible predictor of paroxysmal sympathetic hyperactivity. The final BTF recommendation is to avoid hyperthermia and to maintain normothermia with antipyretics and surface cooling devices

34. GENERAL PRINCIPLES A smooth anaesthetic technique is essential to avoid increase in arterial & venous pressure and changes in CO2 concentration. Maintanance of hypnosis with either an inhalational agent or infusion of propofol . Patient must be transferred to post-operative room with no residual neuro -muscular blockade or opioid induced respiratory depression as both produce critical increase in ICP.

35. Management protocol

36. INDUCTION Propofol is indicated as a sedative agent in the TBI patient with a secure airway. Advantage : quick onset and offset of action that facilitates neurologic assessment also decreases neuronal oxidative stress. Caution : sympathetic blockade resulting in hypotension. Complication : propofol infusion syndrome(infusion>= 4 mg/kg/ hr )

37. Muscle relaxants: As RSI is commonly done in TBI  Succinylcholine is the neuromuscular blocking agent of choice  transient increase in ICP. Despite this potential side effect, the benefit of its rapid onset and duration of action and the prevention of coughing during direct laryngoscopy greatly outweighs its negative effect. This side effect can be prevented by administering defasciculating dose of a non-depolarizing muscle relaxant or by using rocuronium 0.9-1.2mg/kg. It will achieve same intubating conditions like succinylcholine at 60-90 seconds however muscle paralysis might last for 30 to 40 minutes.

38. Opioids are used to suppress airway reflexes, decrease required dose of induction agents and inhalation anesthetic maintenance as well as to blunt the sympathetic response to direct laryngoscopy. Fentanyl, sufentanil , and remifentanil are commonly used in TBI patients. Careful opioid titration should be observed to avoid hypotension secondary to a reduction in sympathetic tone and potential histamine release from these agents

39. MAINTENANCE OF ANESTHESIA Opioids do not further increase ICP, blunt the sympathetic response during intubation and surgical stimulation and prevent hypertensive response that would further increase ICP. Intravenous and inhalation anesthetics can be used safely Intravenous anesthetics such as sodium thiopental, etomidate , midazolam and propofol decrease CBF,CBV,CMRO2 and ICP under controlled ventilation conditions. They achieve these effects by producing cerebral vasoconstriction and acting at the neurons’ GABA receptors to open chloride channels.

40. Dexmedetomidine , alpha 2 receptor agonist, it exerts its effects in the locus coeruleus . Despite its sedative and anxiolytic action it preserves adequate respiratory function when compared with benzodiazepines or narcotics. This property makes it an ideal agent in the non intubated TBI patient. In ICU setting dexemedetomidine has proved to decrease the incidence of delirium. It suitable alternative to propofol for sedation purposes

41. Inhalation Anesthetics (IAs) produce “ uncoupling effect ” that may lead to increase ICP. Sevoflurane is the volatile agent of choice & best avoiding enflurane as it is associated with seizure activity at high doses. This effect can be avoided by titrating IAs to levels below 1 Minimal Alveolar Concentration (MAC) . At a dose of 0.5 MAC, CMR suppression–induced reduction in CBF predominates, and net CBF decreases in comparison with the awake state. At 1 MAC, CBF remains unchanged; CMR suppression and vasodilatory effect are in balance. Beyond 1 MAC, the vasodilatory activity predominates, and CBF significantly increases, even though the CMR is substantially reduced

42. While nitrous oxide is the only inhalation anesthetic that produces an increase in CMRO2, the rest, isoflurane , sevoflurane and desflurane decrease CMRO2 (H>D>I>S) Therefore, the use of nitrous oxide should be avoided in TBI patients. The literature currently finds no difference in outcomes between the use of inhalation anesthetics and intravenous anesthetics or the combination of both in the intraoperative and perioperative care of TBI patients there is no ideal anesthetic, BTF clinical guidelines should be followed while administering anesthesia to this group of patients, especially avoiding hypoxemia,PaO2 below 60 mmHg, oxygen saturation below 90%, hypercarbia and hypotension, (systolic blood pressure below 90 mmHg)

43. EXTUBATION & RECOVERY Stormy extubation with laryngospasm, coughing and bucking are extremely unwanted during recovery of head injury patient after surgical intervention. It is probably most reliably avoided by deep extubation . If recovery is prolonged airway management can be assisted by insertion of a laryngeal mask or simple Guedel airway tube.

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