Anesthesia and Traumatic Brain Injury: A Case Report

Traumatic brain injury is the leading cause of death and disability among persons in the United States.1 Acute traumatic brain injury is often accompanied by increased intracranial pressure among other detrimental effects requiring optimal management through medical and surgical treatments. The surgical measures in current common practice include external ventricular drain insertion and decompressive craniectomy.2 Anesthesia care is aimed to maintain acid/base balance, regulate ICP, prevent coagulopathies and provide adequate fluid replacement.2

1 ANESTHESIA AND TRAUMATIC BRAIN INJURY: A CASE REPORT by Cheryl Howard, RN, MS A capstone project submitted in partial fulfillment of the requirement for the degree of Master of Science in Nurse Anesthesia Westminster College December, 20142 Keywords: ICP, disseminated intravascular coagulopathy (DIC), acid/base balance, decompressive craniectomy, shock Abstract Traumatic brain injury is the leading cause of death and disability among persons in the United States.1 Acute traumatic brain injury is often accompanied by increased intracranial pressure among other detrimental effects requiring optimal management through medical and surgical treatments. The surgical measures in current common practice include external ventricular drain insertion and decompressive craniectomy.2 Anesthesia care is aimed to maintain acid/base balance, regulate ICP, prevent coagulopathies and provide adequate fluid replacement.2 Case Report A 15-year-old, 62 kg, 165 cm caucasian female suffered an acute traumatic brain injury after being ran over by a truck while sunbathing in her driveway. The patient suffered a respiratory and cardiac arrest in the field and was intubated in route to the hospital. Upon admission to the emergency department, patient presented with blood hemorrhaging from her nares and ears. Tympanic membranes could not be visualized. Obvious depression was noted on the top of her head. The patients' blood pressure was 55/35 mmHg with a heart rate of 124 bpm with no evidence of resuscitation. Ecchymosis surrounded both eyes and pupils were fixed and dilated to 8 mm. Oropharynx exhibited bloody discharge. Lungs were clear to 3 auscultation bilaterally; heart sounds regular, lower extremities without lesions or deformities. Blood gas in the Emergency Room showed a pH of 7.36, CO2 27, PO2 323, and lactic acid of 6.4. Chemistry panel showed sodium 137, potassium 4.0, chloride 112, CO2 22, blood urea nitrogen 8, creatinine 1.27 with a glucose of 256. Bilirubin was 0.3, aspartate transaminase 27, alanine transaminase 18, alkaline phosphatase 60, lipase 113. Pro thrombin was 15; hemoglobin 8.6, hematocrit 28.0 and platelet count 269,000. Cat scan evaluation showed significant cranial fractures with marked intracranial injury. Cerebral edema was present with intraparenchymal hemorrhaging. Patient presented with circulatory shock as well as hemorrhagic shock. Patient received multiple blood products in route to the hospital. The patient was taken immediately for an emergency decompressive craniectomy. Upon entrance into the operating room the patient was connected to the breathing circuit with volume control ventilation and was placed on 100% oxygen. Patient was hyperventilated with tidal volumes between 500-600 ml, respiratory rate of 12 and peak inspiratory pressures of 23. Patient had a right subclavian central line in place with Levophed infusing. A femoral line was placed and intra-arterial BP monitored. Mannitol was administered. Two large bore 16g IVs were present in bilateral antecubitals with Normal Saline infusing. No sedation was necessary. Patient was kept normothermic with a temperature of 35.9. Patient's blood gas was monitored throughout the procedure. Two ampules of bicarbonate were administered for acute acid/base imbalance. The patient went into DIC and was started on the massive transfusion protocol where she received several blood products including 5 units of fresh frozen plasma, 2 units of 4 cryoprecipitate, 2 units of platelets and 9 units of PRBCs. Patient was started on drips of Epinephrine, Levophed, Vasopressin and Insulin, which she required upon returning to the ICU. Upon arrival to the ICU patient was hemodynamically stable with O2 saturations in the high 90s on 80% FiO2. Patient continued to be unresponsive and did not require sedation. Discussion Early trauma related mortality is typically secondary to head injury (40%-50%), hemorrhage (20%-40%), which is then worsened with coagulopathy.3 Coagulopathy is present in 65% of patients requiring massive transfusion because of hemorrhage secondary coagulation and platelet consumption as well as physical loss.3 The patient exhibited hemorrhagic shock and was placed on the massive transfusion protocol that in retrospect may have contributed to the patient's transition into disseminated intravascular coagulation. Coagulopathy after hemorrhage is thought to be a secondary event because of a triad of depletion and dilution of coagulation factors, acidosis and hypothermia.3 Disseminated intravascular coagulation diagnosis is often based on clinical symptoms such as presence of bleeding and laboratory findings as in this particular case study. Current data and research supports the decision made in this case study to use early and aggressive coagulation factor replacement through transfusion of plasma, platelets and cryoprecipitate products.3 The anesthetic administered is in accordance with current practice and literature. 5 Other potential complications resulting from traumatic brain injuries include an acute and abrupt increase in intracranial pressure leading to detrimental effects. Intracranial pressure monitoring is critical in patients who have experienced a traumatic brain injury.2 The cat scan of the head is the primary investigation that can show clinically non-obvious abnormalities associated with increased risk of developing an increase in intracranial pressure. In this particular case, the cat scan was utilized immediately upon arrival to the Emergency Room, which is supported by this particular research. The mainstay of intracranial pressure management is medical and includes head elevation, adequate oxygenation, fluid resuscitation, sedation, muscle relaxation, mild hyperventilation to reduce cerebral blood volume and cooling.2 Mannitol effectively lowers the intracranial pressure minutes after administration, however must be used carefully.4 The patient was hyperventilated and placed in beach chair position to aid in the intracranial pressure management, which correlates directly with this particular research. The patient's intracranial pressure was surgically managed by performance of a decompressive craniectomy. Decompressive craniectomies are 1 of 2 most commonly used methods in controlling intracranial pressure.2 The patient's initial blood pressure in the Emergency Room was 55/35mm Hg with no evidence of resuscitation. According to the Journal of Neurotrauma, secondary insults after traumatic brain injury increase morbidity and mortality, and the combination of traumatic brain injury plus hemorrhagic shock is particularly deleterious. Hypotension with a systolic BP < 90 mm Hg worsened outcomes after a traumatic brain injury.5 Management priorities in trauma patients are to ensure adequate ventilation, oxygen 6 delivery, hemorrhage control and to restore tissue perfusion to vital organs.6 The patient was treated with normal saline, albumin and several blood products as supported by research. Controversy as to the optimal resuscitation fluid in traumatic brain injuries is still being discussed, however, characteristics of the ideal resuscitation fluid include small infusion volumes to minimize cerebral edema, prevention of acute causes of mortality, and attenuation of secondary injury5 as practiced in this case. Traditional acute resuscitation solutions may include lactated ringer's solution, Hextend, or alternative colloid products.5 Isotonic crystalloids; particularly lactated ringers may require larger volumes to maintain desired blood pressure. Discussion has resulted as to the comparison of albumin versus saline in traumatic brain injury victims. A recent study suggested that the use of albumin in patients with traumatic brain injuries increased mortality versus saline, but no mechanism for the increased mortality seen with colloid use was presented.5 Current research shows different strategies for control of bleeding in trauma patients. Prevention of further bleeding, transfusion of packed red blood cells, hemoglobin-based transfused triggers, transfusion of allogeneic blood cells, fresh frozen plasma, platelets, and coagulation factors are all current treatments, most of which were utilized in this case study.6 Unfortunately this case resulted in mortality. However, the result was specific to the trauma itself and not due to the anesthetic managed. It is apparent that the anesthetic 7 administered was within the standards of current research and practice. In summary, lessons learned include the role of rapid fluid replacement, intracranial pressure & coagulopathy management, initiation of protocols and surgical interventions to optimize treatment. Unfortunately research is inconclusive and studies would support a variety of methods for fluid replacement, management of ICP and other complications resulting from a TBI. The conduct in this particular case was in accordance with current literature and would go to show that it is up to the anesthesia provider to carefully evaluate the situation and perform the optimal anesthetic for each individual patient. 8 References 1. Thurman, D, Alverson, C, Dunn, K, Guerrero, J, & Sniezek, J. Traumatic Brain Injury in the United States: A Public Health Perspective. Retrieved from http://journals.lww.com/headtraumarehab/Abstract/1999/12000/Traumatic_Brain_Injury_in_the_United_States__A.9.aspx 2. Li, LM, Timofeev, I, Czosnyka, M, Hutchinson, P, Surg, The Surgical Approach to the Management of Increased Intracranial Pressure After Traumatic Brain Injury. Anesthesia & Analgesia. 2010; 111(3): 736-748. doi: 10.1213/ANE.0b013e3181e75cd1 3. Shaz, BH, Dente, CJ, Harris, RS, Macleod, JB, Hillyer, CD. Transfusion Management of Trauma Patients. PMC US National Library of Medicine National Institute of Health. 2009; 1760-1768. doi: 10.1213/ane.0b013e3181a0b6c6 4. Nagelhout, JJ, Plaus, KL. Nurse Anesthesia (4 ed.). St. Louis, Missouri: Darlene Como; 2010 5. Exo, JL, Shellington, DK, Bair, H, Vagni, VA, Keri, J, Ma, L, Cochanek, PM. Resuscitation of Traumatic Brain Injury and Hemorrhagic Shock with Polynitroxylated Albumin, Hextend, Hypertonic Saline, and Lactated Ringer's: Effects on Acute Hemodynamics, Survival, and Neuronal Death in Mice. Journal of Neurotrauma, 2010; 2403-2408. doi:10.1089/neu.2009.0980 6. Theusinger, OM, Spahn, DR, Ganter, MT. Transfusion in trauma: why and how should we change our current practice? Current Opinion in Anaesthesiology, 2009; 305-312. Retrieved from http://journals.lww.com/co-9 anesthesiology/Abstract/2009/04000/Transfusion_in_trauma__why_and_how_should_we.26.aspx Mentor: Chris Torman, CRNA, MAE [e-mail]