Traumatic brain injury assessment (anesthesia).pptx

Slide contains various assessment necessary for TBI patients

1. Injury assessment Adequate exposure and examination of extent of injury Physical exposure increases risk of hypothermia Maitain Resuscitation bay and OT at near body temp., warm IV fluids and Blood products, Under body warmers Team Efficiency required in identifying Life threatening injuries, assessment completed within 20 mins of patient arrival

2. FAST examination Focused Assessment with Sonography for Trauma) Performed at bedside – free fluid in perihepatic and perisplenic spaces, pericardium, and pelvis Free fluid in theses areas + two of the following: penetrating injury, SBP <90 mm Hg, or HR > 120 bpm High mortality and TIC and requirement of massive transfusion

3. Resuscitation Hemorrhage (ACS) Class I - <15% of circulating volume, no change in HR, BP, IV fluids not required if bleeding promptly controlled Class II - prompts sympathetic responses; 15% to 30%, DBP increases d/t vascoconstriction , HR increases to maintain CO. IV fluids indicated. Class III- 30% to 40%, Compensatory mechanisms of vasoconstriction and tachycardia- not sufficient, metabolic acidosis. Blood transfusions necessary Class IV- Life threatening, >40%, unresponsive and profoundly hypotensive, aggressive blood-based resuscitation (damage control resuscitation) ,TIC , massive transfusion

4. Trauma induced Coagulopathy Common and independent risk factor for death Upto 25 % patients -shortly after injury and before any resuscitative efforts Global tissue hypoperfusion appears to play a key role During hypoperfusion  the endothelium releases thrombomodulin and activated protein C, prevents thrombosis Thrombomodulin binds thrombin  prevents thrombin from cleaving fibrinogen to fibrin. This complex activates protein C inhibits extrinsic coagulation pathway through effect of cofactors V and VIII

5. Effects of hypoperfusion on coagulation parameters:- (1) progressive coagulopathy as base deficit increases; (2) increasing plasma thrombomodulin and falling protein thromboplastin times; and (3) early-onset TIC and increase mortality.

6. Mechanism of hyperfibrinolysis in tissue hypoperfusion. Tissue plasminogen activator (tPA) released from the endothelium cleaves plasminogen to initiate fibrinolysis. Activated protein C ( aPC ) consumes plasminogen activator inhibitor-1 (PAI-1) when present in excess, and reduced PAI-1 leads to increased tPA activity and hyperfibrinolysis.

7. TIC not solely related to impaired clot formation, fibrinolysis equally important component as a result of plasmin activity on an existing clot Tranexamic acid administration is associated with decreased bleeding during cardiac and orthopedic surgeries

8. Hemostatic resuscitation Early coagulopathy of trauma is associated with increased mortality Military conflicts in the 2000s -provided ample opportunities for developing updated transfusion protocols damage control resuscitation (DCR) - administration of red blood cells, fresh frozen plasma, and platelet units (1:1:1) in military setting Administering blood products in equal ratios early in resuscitation- accepted approach for preventing or correcting TIC.

9. Type O-negative blood- depending on urgency Patient receiving uncrossmatched O negative- greater risk of requiring massive transfusion If >8U used, persist use of O – ve blood, reverting to native blood type  risk of transfusion reaction

10. The PROMTT study, conducted across 10 U.S. level 1 trauma centers, 2013 severe injury and resulting hemorrhagic shock increase the probability of trauma-induced coagulopathy (TIC), often necessitating massive transfusion and heightening mortality risk. role of activated protein C in TIC and advocates for blood-based resuscitation over crystalloid-based methods for managing hemorrhagic shock.

11. Point-of-care functional clotting studies are extremely useful for guiding Blood product use Thromboelastography (TEG) and rotational elastometry (ROTEM) identify the specific deficiencies assess the rate of clot formation and clot stability,interactions between the coagulation cascades, platelets, and the fibrinolytic system

12. Potential hazards from aggressive administration of blood products: blood-borne diseases transfusion-related acute lung injury (TRALI) -presence of HLA antibodies in donor plasma is the principal TRALI risk factor-> blood from only anti- HLA negative transfusion-associated circulatory overload (TACO)-> when blood products > patients CO

13. Massive transfusion protocols “Massive transfusion is defined as the replacement of one blood volume (approximately 70 mL/kg) in less than 24 hours, or the administration of more than 10 units of packed red blood cells (PRBCs) in an hour or less” Clinical evidence supports need and benefit of established Massive transfusion protocols improves survival from trauma, reduces total blood product use in the 1 st 24 h of injury, reduces acute infectious complications and decreases postresuscitation organ dysfunction

14. Definitive trauma interventions critical initial issues impacting anesthetic management of trauma patients include the adequacy of the airway and vascular access, the ability of the patient to tolerate anesthesia, prevention of hypothermia, access to adequate blood bank supplies, and avoidance of crystalloids and vasopressors until hemorrhage is controlled.

15. Anesthetic Induction and maintainance Severely injured, conscious, and oriented trauma arriving for Emergency surgery  abbreviated interview and examination Consent for BT and intraoperative awareness documentation Ot should be warm. IV fluid warmers and rapid infusion devices Presumed Full stomachs – risk of aspiration, C-collar for C-spine stabilization difficulty in intubation. Alternative airway devices and adequate suction devices

16. IV access – peripheral access ma be impossible due to profound hypotension and hypovolemia  Subclavian , I-O device inserted For induction of GA- severely injured Pt -profound hypotension following even modest doses (0.25–0.5 mg/kg IV) of propofol Etomidate preserves sympathetic tone, safer than propofol Ketamine- given at 10mg boluses until pt is unresponsive Scopolamine- 0.4mg IV- for profoundly Hemodynamically unstable- but concious pt- risk of collapse

17. Emphasize on blood products rather than crystalloids for fluid management MTP should be requested and followed All fluids should be warmed , except for platelets Replace ionized Ca++ during rapid infusion Vasopressors avoided until control of bleeding source A-line helpful but not mandatory – should not delay surgery

18. Damage control surgery intended to stop hemorrhage and limit contamination of the abdominal compartment Definitive repair of complex injuries is not part of DCS Identification and control of injured blood vessels and solid organs Hollow viscus injuries are addressed with resection, stapling Anesthesia team must speak up the need of pausing surgical procedure to allow resuscitation Compression or packing of bleeding area until restoration of acceptable SBP

19. If unsuccessful  compression of aorta– direct feedback to effectiveness of transfusion Breif episode of bradycarda /asystole may accompany direct aortic compression When transfusions are ineffective- interrupt operation, combined decision to pack bleeding areas, possible transfer to intervention radiology or Critical care unit

20. Key component of DCS- planned reoperation once patient is more stable Bowel continuity restored , or colostomy performed later Abdominal fascia not definitively closed- occlusive dressing over a wound vacuum sponge  prevention of abdominal compartment syndrome, respi compromise and multi organ failure

21. Traumatic brain injury Any trauma patient with an altered level of consciousness must be considered to have a traumatic brain injury (TBI) until proven otherwise Maintain Cerebral perfusion pressure and oxygenation GCS for assessment of TBI in nonsedated , non paralyzed Declining motor score  progressive neurological deterioration  prompt evaluation and intervention

22. Categorized as Primary and secondary:- Primary brain injuries are directly related to trauma. subdural hematoma; epidural hematoma; intraparenchymal hemorrhage; and nonfocal , diffuse neuronal injury disrupting axons of the central nervous system Elevate ICPs, compromising CBF

23. Acute subdural hematoma is the most common brain injury prompting emergency intervention- a/w highest mortality Result of disruption small bridging veins between skull and brain Morbidity and mortality- related to size of the hematoma and the magnitude of the midline shift of intracranial contents.

24. Epidural hematoma occurs when the middle cerebral artery or other cranial vessels are disrupted. < 10% of neurological trauma emergencies initially conscious, followed by progressive unresponsiveness and coma Emergency decompression if- supratentorial lesion >30ml and infratentorial lesion > 10 ml

25. Intraparenchymal injuries d/t rapid deceleration of the brain within the skull, usually involving the tips of the frontal and temporal lobes 20% of neuro emergencies Associated with edema, necrosis, and infarcts surrounding areas of damaged tissue Diffuse neuronal - rapid deceleration or movement of brain tissue of sufficient force to disrupt neurons and axons- more common in children Extent of injury- serial MRI- greater the extent higher the mortality and disability severity

26. Secondary brain injuries are considered potentially preventable injuries Systemic hypotension, hypoxia, hypercapnia and hyperthermia  negative impact on morbidity and mortality as it contributes Cerebral edema and ICP Hypoxemia-single most important parameter correlating with poor neurological outcome- correct at the earliest Hypotension (MAP <60) treated aggressively with fluids, vasopressors, or both in the presence of isolated head injury

27. Management of severe head trauma in the presence of other severe injuries and hemorrhage creates a difficult resuscitation dilemma control of life-threatening hemorrhage takes precedence over neurosurgical intervention

28. Management consideration for Acute TBI In the absence of an intracranial clot requiring surgical evacuation, medical interventions are the primary means of treating elevated ICP Normal cerebral perfusion pressure (CPP=MAP – ICP) ~ 80 -100 mm Hg ICP monitoring is not required for conscious and alert patients Interventions for reducing ICP are indicated when readings are higher than 20 to 25 mm Hg

29. Current Brain Trauma Foundation guidelines recommend maintaining CPP between 50 and 70 mm Hg and ICP at less than 20 mm Hg for patients with severe head injury.

30. Cerebral blood flow (CBF) is influenced by arterial carbon dioxide concentration: Cerebral vasoconstriction occurs with decreased arterial CO2, reducing CBF and ICP. Conversely, cerebral vasodilation happens with increased arterial CO2, elevating CBF and ICP.

31. Hyperventilation effectively reduces ICP in TBI by promptly altering CBF, but it should be cautiously applied in hemodynamically unstable patients due to the risk of neurological ischemia. Osmotic diuretic therapy with intravenous mannitol reduces brain edema and ICP by drawing fluid from brain tissue into the vascular system, requiring close monitoring of plasma osmolality and serum electrolytes.

32. Barbiturate coma lowers cerebral metabolic rate and ICP, but its use is limited in hemodynamically unstable patients due to associated hypotension, necessitating vasopressor support to maintain cerebral perfusion pressure (CPP). Fluid therapy with crystalloid is preferred over colloid in isolated TBI to avoid exacerbating brain edema and ICP, as albumin-based resuscitation has been linked to higher mortality rates in TBI patients.