UPDATES IN TRAUMA RESUSCITATION. Traumatic Brain Injury. Pre-hospital Care 4/3/2016. Leading Causes of Death Following Injury?

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1 UPDATES IN TRAUMA RESUSCITATION Deborah M. Stein, MD, MPH Chief of Trauma, R Adams Cowley Shock Trauma Center Leading Causes of Death Following Injury? #1 Traumatic Brain Injury #2 Hemorrhage #3 Sepsis/MODS Traumatic Brain Injury is the leading cause of death and disability in all persons ages 1-44 Pre-hospital Care O 2 Sat Mortality Severe Disability Patients with suspected severe TBI should be monitored.for hypoxemia (<90%) or hypotension (<90 mmhg) Secondary Insults >90% 14.3% (3/21) 4.8% (1/21) 60-90% 27.3% (6/22) 27.3% (6/22) <60% 50% (3/6) 50% (3/6) Number of Patients % Total Patients Good or Moderately Disabled Outcome (%) Severely Disabled or Vegetative Dead Total Cases Hypoxemia Hypotension Neither Both Brain Trauma Foundation. Guidelines for Prehospital Management of Traumatic Brain Injury, 2 nd Edition; Chesnut, et al. J Trauma. 1993;34:216. Stochetti, et al. J Trauma. 1999;40:764. 1

2 Prehospital Intubation Prehospital Intubation Pros Oxygenation Ventilation Treat cerebral edema/impending herniation Prevent airway obstruction Prevent aspiration Long distance transport/better access to appropriate facility Cons Training Time Intubation failure RSI meds given Risk of pneumonia Hyperventilation Von Elm, et al. Br J Anaesth Prehospital Intubation Prehospital Intubation Von Elm, et al. Br J Anaesth Von Elm, et al. Br J Anaesth Prehospital Intubation What to do? An airway should be established, by the most appropriate means possible, in patients with severe TBI (GCS <9) with the inability to maintain an adequate airway, or with hypoxemia not corrected by supplemental oxygen Confirmation of placement of the tube in the trachea should include lung auscultation and ETCO 2 determination. Patients should be maintained with normal breathing rates (ETCO mmhg) and hyperventilation (ETCO 2 <35 mmhg) should be avoided unless the patient shows signs of cerebral herniation. Other prehospital interventions? Multicenter, double-blind, randomized, placebo-controlled clinical trial A single 250-mL bolus of 7.5% saline/6% dextran 70 (hypertonic saline/dextran), 7.5% saline (hypertonic saline), or 0.9% saline (normal saline) initiated in the outof-hospital setting. This study was terminated by the DSMB after randomization of 1331 patients, having met prespecified futility criteria. There was no difference in 6-month neurologic outcome among groups with regard to proportions of patients with severe TBI (GOSE 4) (hypertonic saline/dextran vs normal saline: 53.7% vs 51.5%; difference, 2.2% [95% CI, 4.5% to 9.0%]; hypertonic saline vs normal saline: 54.3% vs 51.5%; difference, 2.9% [95% CI, 4.0% to 9.7%]; P=.67). Brain Trauma Foundation. Guidelines for Prehospital Management of Traumatic Brain Injury, 2 nd Edition; Among patients with severe TBI not in hypovolemic shock, initial resuscitation with either hypertonic saline or hypertonic saline/dextran, compared with normal saline, did not result in superior 6-month neurologic outcome or survival. Bulger E, et al. JAMA

3 Initial Management Signs of Herniation o o ABCs Who to intubate? GCS <9 or mgcs <5 Loss of laryngeal reflexes Ventilatory insufficiency Hypoxemia Hypercarbia Deteriorating level of consciousness Agitation??? Dilated and unreactive pupils mgcs of 1 or 2 Decrease in GCS of >2 points Bradycardia and hypertension Treatment Osmolar therapy Hyperventilation Burr holes Surgical decompression Who Needs a Neurosurgeon? Who Needs a Neurosurgeon? o o o Unilateral pupillary abnormality Rapid decline of GCS Lateralizing signs SDH >10 mm or shift >5 mm regardless of GCS OR With a GCS <9 should undergo surgical evacuation if the GCS score decreased between the time of injury and hospital admission by 2 or more points asymmetric or fixed and dilated pupils ICP exceeds 20 mm Hg Brain Trauma Foundation and The American Association of Neurologic Surgeons. Management of Severe Brain Injury Who Needs a Neurosurgeon? EDH >30 cm3 regardless of GCS <30 cm3 can be managed nonoperatively and with less than a 15- mm thickness and with less than a 5-mm MLS in patients with a GCS score >8 without focal deficit Who Needs a Neurosurgeon? IPC any lesion >50 cm3 should be treated operatively OR Parenchymal mass lesions and signs of progressive neurological deterioration referable to the lesion, medically refractory ICH, or signs of mass effect on CT scan should be treated operatively GCS 6-8 with frontal or temporal contusions greater than 20 cm3 with MLS 5 mm and/or cisternal compression Brain Trauma Foundation and The American Association of Neurologic Surgeons. Management of Severe Brain Injury Brain Trauma Foundation and The American Association of Neurologic Surgeons. Management of Severe Brain Injury

4 ICP Monitoring Who should get monitored?? Severe head injury with abnormal CT GCS 3-8 after resuscitation GCS 3-8 after resuscitation with a normal CT scan and two or more Age > 40 years Unilateral or bilateral posturing SBP < 90 mmhg ICP Monitoring Treatment should be initiated with ICP >20 mmhg Brain Trauma Foundation and The American Association of Neurologic Surgeons. Management of Severe Brain Injury Brain Trauma Foundation and The American Association of Neurologic Surgeons. Management of Severe Brain Injury To Monitor or Not to Monitor To Monitor or Not to Monitor A combination of ICP values, clinical, and brain CT findings should be used to determine the need for treatment Brain Trauma Foundation and The American Association of Neurologic Surgeons. Management of Severe Brain Injury Monroe-Kellie Doctrine Blood ~12% Brain tissue ~64% Management of Cerebral Edema Brain Tissue Compartment CSF Compartment CSF ~8% Intracranial volume is constant and the skull is non-distensible and noncompressible Any increase in the volume of one component of the intracranial cavity causes : a decrease in the volume of other component an increase in pressure within the intracranial cavity Blood Compartment Sedation Temperature Management Blood Pressure Management Hyperventilation Decompressive laparotomy Increase intra-abdominal pressure Increase intra-thoracic pressure Inhibit cerebro-venous outflow Increase ICP 4

5 Therapeutic hypothermia SCI and Hypothermia 35 ASIA A cervical SCI Hypothermia was delivered in 5.76 (±0.45) hours from injury (excluding 4 cases with delayed admission) Modest hypothermia to 33 C for 48 hours 15/35 patients (43%) improved at least one AIS grade at latest follow up (±1.03) months Dididze M, et al. Spinal Cord SCI and hypothermia Therapeutic Hypothermia for TBI RCTs of hypothermia for severe TBI can be divided into Those trials in which hypothermia was used to treat raised ICP Started in the first 24 h after injury but continued through the peak period of raised intracranial pressure (3 5 days) or until intracranial hypertension was resolved 4/5 studies reported a decrease in mortality rate or in the percentage of patients having a poor recovery Jiang JY, Yu MK, Zhu C. J Neurosurg Jiang JY, Xu W, Li WP, et al. J Cereb Blood Flow Metab Qiu W, Zhang Y, Sheng H, et al. J Crit Care Yan Y, Tang W, Den Z, et al. J Clin Neurosci Those trials where used as a neuroprotectant (like cardiac arrest) and reached C in the first 10 h after injury and continued for a predefined h, irrespective of intracranial pressure all failed to show improved outcome with hypothermia treatment. Hansebout RR and Hansebout CR. J Neurosurg Spine Therapeutic Hypothermia for TBI Therapeutic Hypothermia for TBI Enrollment from Outcome was poor in 31 of 52 patients in the hypothermia group and 25 of 56 in the normothermia group (RR 1.08, 95% CI ; p=0.67) 12 patients in the hypothermia group died compared with eight in the normothermia group (RR 1.30, 95% CI ; p=0.52) The trial was terminated for futility at interim analysis Clifton GL, et al. Lancet Neurol Georgiou AP, Manara AR. Br J Anaesthesia

6 Therapeutic Hypothermia for TBI RCT of adults with an ICP > 20 mm Hg despite stage 1 treatments to standard care (control group) or hypothermia (32 to 35 C) plus standard care 387 patients in 18 countries from Final nail in the coffin for therapeutic hypothermia? Stage 3 treatments were required to control intracranial pressure in 54% of the patients in the control group and in 44% of the patients in the hypothermia group A favorable outcome (GOS-E score of 5 to 8, indicating moderate disability or good recovery) occurred in 26% of the patients in the hypothermia group and in 37% of the patients in the control group (P=0.03). Andrews PJD, et al. N Engl J Med 2015 Post-cardiac arrest therapeutic hypothermia Post-cardiac arrest therapeutic hypothermia The Hypothermia after Cardiac Arrest Study Group. NEJM Bernard, et al. NEJM Nielsen N, et al. NEJM So now what? Other interventions? VS 6

7 Other Interventions? Other interventions? A nested, randomized, placebo controlled trial. The mean total hemorrhage growth was 5.9 ml (SD 26.8) and 8.1 ml (SD 29.2) in the tranexamic acid and placebo groups respectively (adjusted difference 3.8 ml (95% CI 11.5 to 3.9)). New focal cerebral ischemic lesions occurred in 6 (5%) patients in the tranexamic acid group versus 12 (9%) in the placebo group (aor 0.51 (95% CI 0.18 to 1.44); ns) There were 14 (11%) deaths in the tranexamic acid group and 24 (18%) in the placebo group (aor 0.47 (0.21 to 1.04); ns). This trial shows that neither moderate benefits nor moderate harmful effects of tranexamic acid in patients with traumatic brain injury can be excluded. CRASH-2 Collaborators. BMJ Population is aging Frequency of use of anticoagulants Third-party payers and patients spent $900 million in 2007 on adult outpatient prescriptions for anticoagulant drugs Used one or more anticoagulants in % of Americans aged 75 and older 6% of Americans between the ages of 65 and million Americans aged 18 and older used a blood thinner in AHRQ, Correction of coagulopathy 7

8 Reversal of Warfarin PCCs Advantages over FFP PCC are more effective than FFP at correcting INR The mean correction time was shorter with PCC than with FFP Compared with FFP, PCC were associated with significantly reduced clinical progression of intracerebral hemorrhage and greater and quicker (four to five times) reduction in INR Including a RCT and meta-analysis Smaller volumes of PCC are required to reverse anticoagulation Concentration of clotting factors in PCC is approximately 25 times higher than that in human plasma PCC are quicker to prepare than FFP, as they can usually be stored at room temperature Franchini M and Lippi G. Blood Transfus Makris M, et al. Thromb Haemost Cartmill M, et al. Br J Neurosurg Huttner HB, et al. Stroke Fredriksson K, et al. Stroke Imberti D, et al. Pathophysiol Haemost Thromb Leissinger CA, et al. Am J Hematol Vigué B, et al. Intensive Care Med PCCs Adverse events include immediate allergic reactions thromboembolic complications The primary safety concern with PCC has been their association with thrombogenic events such as stroke, MI, PE, DIC and DVT Actual rates % depending on product used Coagulopathy in TBI Meta-analysis of 34 studies Overall prevalence of 32.7%. The presence of coagulopathy after TBI was related both to mortality (OR 9.0; 95%CI: ) unfavourable outcome (OR 36.3; 95%CI: ) Franchini M and Lippi G. Blood Transfus Ansell J, et al. Chest Leissinger CA, et al. Am J Hematol Harhangi BS, et al. Acta Neurochirurgica Role of PCC Direct thrombin inhibitor All patients with TBI with coagulopathy without warfarin therapy who received PCC (25 IU/kg) in conjunction with FFP or FFP alone The groups (PCC + FFP vs FFP alone) were matched using propensity score matching 222 patients (PCC + FFP, 74; FFP, 148). Mean INR on presentation was 1.92 ± 0.6. PCC + FFP therapy was associated with an accelerated correction of INR (P =.001) and decrease in overall PRBC (P =.035) and FFP (P =.041) administration Factor XA inhibitors Craniotomy was performed in 26.1% of patients (n = 58). Patients who received PCC + FFP therapy had faster time to craniotomy (P =.028) compared with patients who received FFP therapy alone. Joseph B, et al. Neurosurgery

9 NOAC Reversal Role of PCC Options Activated charcoal Dialysis (for pradaxa) 4-factor PCCs Novel reversal agents While 4-factor PCCs may have potential to reverse bleeding with NOACs based on their ability to increase levels of factors II, VII, IX, and X, there are insufficient data to conclude that reversing NOAC effect based on laboratory test results correlates with improved clinical outcomes Small number of case reports and studies performed on animals or healthy human volunteers in which laboratory coagulation parameters were monitored before and after PCC administration Sarick TC, et al. American Heart Journal. In Press Role of PCC Reversal of anticoagulants 3 NOAC-specific reversal agents: (1) andexanet alfa a recombinant, modified human factor Xa that is being developed as a direct factor Xa reversal agent (2) idarucizumab a fully humanized antibody fragment (Fab) that binds dabigatran with high affinity and specificity The FDA gave idarucizumab (Praxbind) (both Boehringer Ingelheim) accelerated approval on October 16, 2015 for use in patients who require emergency surgery or other urgent procedures or who have life-threatening or uncontrolled bleeding (3) PER977 (ciraparantag) a water-soluble small-molecule nonspecific reversal agent. in preclinical testing and during testing with edoxaban in healthy male volunteers, it rapidly reversed the effect of multiple anticoagulants, purportedly via hydrogen bonding a broad-spectrum reversal agent for anticoagulants including LMWH, UFH and NOACs Currently in Phase 2 clinical trials Sarick TC, et al. American Heart Journal. In Press Frontera JA, et al Neurocritical Care All bleeding stops eventually Hemorrhage is the leading cause of potentially preventable death 9

10 Hemostasis Hemostasis Microscopic level The arrest of bleeding by vasoconstriction coagulation Macroscopic level The arrest of bleeding by surgical means The physiologic process whereby bleeding is halted The hemostatic mechanisms have several important function: Maintain blood in a fluid state while circulating within the vascular system Arrests bleeding at the site of injury by formation of hemostatic plug Ensure the removal of the hemostatic plug when healing is complete Hemostasis Hemostasis The components of normal hemostasis include: Blood vessels Platelets Plasma coagulation factors and their inhibitors The fibrinolytic system When a blood vessel is wounded: Vasoconstriction minimizes vessel diameter and slowing bleeding Primary hemostasis Platelets bind to collagen in the exposed walls of the blood vessel to form a hemostatic plug Occurs within seconds Secondary hemostasis (coagulation) Complex cascade of coagulation factors, ultimately resulting in the transformation of fibrinogen, into polymerized fibrin making a clot Takes several minutes Hemostasis Normal Hemostasis Is a Balance The objective of the hemostatic system is to preserve intravascular integrity by achieving a balance between hemorrhage and thrombosis Bleeding to Death Trauma Major Surgery Hemophilia Blood coagulation Anticoagulation Fibrinolysis Antifibrinolysis Vascular tone and blood flow Endothelial cells and platelets Clotting to Death Stroke MI Thrombosis Adapted from Lawson JH, et al. Semin Hematol

11 In-hospital mortality % 4/3/2016 TRAUMATIC HEMORRHAGE Lethal Triad Hemorrhage Hypothermia Acidosis Vicious bloody cycle Coagulopathy Acute Coagulopathy of Traumatic Shock (ACoTS) Coagulopathy Following Trauma Tissue Injury Hemorrhage COAGULOPATHY Dysfunction Loss, Consumption, Dilution Dysfunction Hypothermia Acidosis Genetics Anticoagulants Hess JR, et al. J Trauma Admission INR and mechanism of injury in trauma patients admitted directly from the scene of injury with ISS > 15 as predictors of in-hospital mortality at R Adams Cowley Shock-Trauma Center N = 5605 Blunt injury Penetrating injury INR <1 INR INR INR INR INR >2.2 Admission INR Dutton and Hess, Unpublished data. Can we resuscitate the bleeding trauma patient better? Damage Control / Hemostatic Resuscitation 3 main components Hypotensive resuscitation Minimizing crystalloid Blood product ratios 11

12 Hypotensive Resuscitation Hypotensive Resuscitation Injection of a fluid that will increase blood pressure has dangers in itself If the pressure is raised before the surgeon is ready to check any bleeding that might take place, blood that is sorely needed may be lost. - Cannon, JAMA 1919 Prospective trial comparing immediate and delayed fluid resuscitation in 598 adults with penetrating torso injuries who presented with a prehospital systolic blood pressure 90 mm Hg Randomization in field to fluid or no fluid Therapy continued to OR door Results Among the patients who received delayed fluid resuscitation, 203/289 (70 %) survived vs.193/309 (62 %) who received immediate fluid resuscitation (p = 0.04). Bickell, et al, NEJM Hypotensive Resuscitation Type of Fluids This trial was performed to assess the feasibility and safety of controlled resuscitation (CR) versus standard resuscitation (SR) in hypotensive trauma patients. RCT CR patients received 250 ml of fluid if they had no radial pulse or an SBP lower than 70 mm Hg and additional 250-mL boluses to maintain a radial pulse or an SBP of 70 mm Hg or greater. The SR group patients received 2 L initially and additional fluid as needed to maintain an SBP of 110 mm Hg or greater. The crystalloid protocol was maintained until hemorrhage control or 2 hours after hospital arrival Intensive care unit free days, ventilator-free days, renal injury, and renal failure did not differ between the groups. At 24 hours after admission, there were 5 deaths (5%) in the CR group and 14 (15%) in the SR group (adjusted odds ratio, 0.39; 95% CI, ). Among patients with blunt trauma, 24-hour mortality was 3% (CR) and 18% (SR) with an adjusted odds ratio of 0.17 ( ). Crystalloid Colloid Blood products Schreiber MA, et al. J Trauma and Acute Care Surgery Fluid administration - Guiding Principle Evils of Crystalloid Any fluid which does not clot or carry oxygen should be suspect. -Richard Dutton, MD Kasotakis, et al. J Trauma Acute Care Surg

13 Mortality % 4/3/2016 Traumatic Injury Evils of Crystalloid Inflammation Fluid Administration Catabolism Direct Tissue Injury Post-Capillary Hypertension Endothelial cell damage Capillary Interstitium Increased hydrostatic pressure Decreased hydrostatic pressure Increased edema Organ dysfunction Decreased oncotic pressure Increased oncotic pressure Disrupted lymphatics Stein DM and Scalea TM. Adv Surg Bradley M, et al. Amer Surg Evils of Crystalloid Effect of FFP : RBC Ratio on Overall Mortality in 252 Massively Transfused Trauma Patients (long term outcomes) 65% Chi Square RB: p=0.006 RG: p<0.001 BG: p= % n=31 n=56 20% n= :22-1:4 1:3.9-1:2.1 1:2-1: FFP : RBC Ratio Borgman MA, et al. J Trauma Randomized patients to 1:1:1 vs 1:1:2 No significant differences were detected in mortality at 24 hours or 30 days Exsanguination was significantly decreased in the 1:1:1 group More patients in the 1:1:1 group achieved hemostasis No differences in complications Holcolmb, et al. JAMA

14 Pre-hospital blood administration? Hypothesized that prehospital transfusion of thawed plasma and/or RBCs would result in improved patient coagulation status on admission and survival. Dilution is inevitable when giving blood products Whole blood Donation 500 ml (Hct 38% 50%; Plts150 K 400 K; Plasma coagulation activity100%) Prehospital plasma and RBC transfusion was associated with improved early outcomes negligible blood products wastage not an overall survival advantage Large multicenter trial just concluded 1 Unit PRBC (335 ml, Hct 55%) 150 ml anticoagulant added; centrifuged 1 Unit Plasma (275 ml, coagulation activity 80%) 1 Unit Platelets (50 ml, 5.5 x plts) Holcolmb, et al. Prehosp Emerg Care Patient Receives 650 ml fluid Hct 29%, Plts 88 K, 65% coagulation activity Whole Blood? Fibrinolysis Acute coagulopathy of trauma is characterized by a systemic anticoagulation and hyperfibrinolysis In approximately 2-10% of patients Occurs early (<1 hour) More respiratory failure More renal failure Spinella PC, et al. J Trauma Cotton BA, et al. Ann Surg More likely to require massive transfusion A strong independent predictor of mortality Brohi K, et al. Curr Opin Crit Care Kashuk JL. Ann Surg Ives C, et al. J Am Coll Surg TXA TXA Many criticisms TXA is associated with a 1.5% reduction in 28-day all-cause mortality in adult trauma patients with signs of bleeding Overall modest effect on the overall population: All-cause mortality was significantly reduced from 16.0% to 14 5% (NNT, 67). The risk of death caused by bleeding overall was significantly reduced from 5.7% to 4 9% (NNT, 121). In adult trauma patients with severe hemorrhagic shock (SBP <= 75 mm Hg), with known predictors of fibrinolysis, or with known fibrinolysis by TEG (LY30 > 3%) Only administer TXA if less than 3 hours from time of injury CRASH-2 Trial Collaborators. Lancet Napolitano L, et al. J Trauma Acute Care Surg

15 TXA PCCs Purified and viral-inactivated factors II, VII, IX, and X Beriplex, Octaplex, Kcentra, Cofact Kcentra was approved by FDA on April 30, 2013 Retrospective observational study The TXA group had lower unadjusted mortality than the no-txa group (17.4% vs 23.9%, respectively; P=.03) This benefit was greatest in the group of patients who received massive transfusion (14.4% vs 28.1%, respectively; P=.004) TXA was also independently associated with survival (odds ratio=7.228; 95% CI, ) and less coagulopathy (P=.003). Morrison JJ, et al. Arch Surg PCCs Franchini and Lippi. Blood Transfus Freeze-dried plasma Does not require freezing or thawing Can be deployed far forward And for NOACs Measuring coagulopathy TEG/ROTEM Conventional Clotting studies: PT PTT INR Platelet count Fibrinogen Is there a better way? Whiting and DiNardo. Am J Hematology. 2014;89:228 15

16 TEG/ROTEM TEG/ROTEM Whiting and DiNardo. Am J Hematology Whiting and DiNardo. Am J Hematology TEG in Trauma TEG in Trauma 1974 major trauma activations, all had admission r-teg and CCTs. Correlated r-teg values with their corresponding CCTs for transfusion requirements. r-teg correlated with CCTs. When controlling for age, injury mechanism, RTS, base excess and hemoglobin ACT-predicted RBC transfusion α-angle predicted massive RBC transfusion better than PT/aPTT or INR (P < 0.001) α-angle was superior to fibrinogen for predicting plasma transfusion (P < 0.001) MA was superior to platelet count for predicting platelet transfusion (P < 0.001) LY-30 documented fibrinolysis. Holcomb JB, et al. Ann Surg Holcomb JB, et al. Ann Surg Anatomic Hemostasis QuikClot Granular zeolite powder that absorbs water producing an exothermic reaction that promotes clot formation Has been shown to reduce blood loss and improve mortality in a lethal femoral artery and vein laceration injury in swine and in a grade V liver injury model QuikClot is not biodegradable, and it must be debrided from wounds after hemorrhage control QuikClot ACS+ Has been re-engineered to stay cooler on contact Costs about $20 per application Pusateri J, J Trauma Alam H, J Trauma

17 Tourniquets Tourniquets 1916, the Journal of the Royal Army Medical Corps called tourniquets the "invention of the devil" Cons The majority of external hemorrhage can be controlled by direct pressure. Previously tourniquets have been used inappropriately when not clinically indicated Preventing arterial blood flow to a limb will result in ischemia Reperfusion injury may also result from tourniquet An incorrectly applied tourniquet will actually cause increased hemorrhage A policy of periodic loosening of a tourniquet in an attempt to reduce limb ischemia has often led to incremental exsanguination and death. A properly applied tourniquet is painful Tourniquets - Military Tourniquets Beginning in 2004, the U.S. Army Institute of Surgical Research began studying mechanical tourniquets. A paper detailing the benefits and strongly advocating their use appeared in 2008 in Journal of Trauma Injury, Infection, and Critical Care. Since then, C-A-T devices have become standard military issue and all soldiers are trained to use them. Numerous studies of military and civilian casualties have demonstrated benefit Indications For Use Extreme life-threatening limb hemorrhage, or limp amputation/mangled limb with multiple bleeding points, to allow immediate management of airway and breathing problems. Life threatening limb hemorrhage not controlled by simple methods. Point of significant hemorrhage from a limb is not peripherally accessible due to entrapment (unable to provide direct pressure.) Major incident or multiple casualties with extremity hemorrhage and lack of resources to maintain simple methods of hemorrhage control. Bulger, et al. Pre Hosp Emerg Care Kragh, et al. Milit Med Lewis, PC. J Emerg Nursing Lee, et al. Emerg Med J Pelvic Hemorrhage Pelvic Fracture Hemorrhage 17

18 Pelvic Fracture Hemorrhage Consensus: A pelvic binder is a treatment intervention rather than a packaging intervention and should be applied early Operative Intervention Scott, et al. Emerg Med J 2013 The only weapon with which the unconscious patient can immediately retaliate upon the incompetent surgeon is hemorrhage. - Halstead Damage Control Surgery Damage Control One of the major advances in surgical technique in the past 20 years The principles of damage control go against the most standard surgical teaching practices - that the best operation for a patient is one, definitive procedure. Patients with major exsanguinating injuries will not survive complex procedures such as formal liver resection It is well recognized that multiple trauma patients are more likely to die from their intra-operative metabolic failure that from a failure to complete operative repairs 18

19 Acute Coagulopathy of Traumatic Shock (ACoTS) Tissue Injury COAGULOPATHY Genetics Dysfunction Hemorrhage Loss, Consumption, Dilution Dysfunction Hypothermia Acidosis Damage Control Surgery First question: Do I need to do Damage Control? How do you know? When you open the abdomen and say oh s*~t Anticoagulants Hess JR, et al. J Trauma Damage Control Surgery Damage Control Surgery Technique is also used for Orthopedic injuries Major vascular injuries Thoracic injuries Etc. Pelvic fracture Angiography 19

20 Pelvic fracture hemorrhage Hybrid ORs Noncompressible hemorrhage Non-compressible bleeding accounts for approximately 85% of preventable deaths on the battlefield, 80% of which include acute hemorrhage within the abdomen/torso. Abdominal hemorrhage involves injury to the spleen, liver, or retroperitoneal vasculature Is typically non-compressible, meaning that it cannot be treated by external compression or the application of tourniquets or topical dressings. Proximal Aortic Control Aortic Occlusion Balloon (REBOA) Advantages to aortic occlusion prior to laparotomy: 1. Continued cerebral/coronary perfusion 2. Avoid catastrophic CV collapse with laparotomy 3. Proximal aortic control decreases blood loss Ledgerwood AM, et al. J Trauma

21 Brenner ML, et al. J Trauma Acute Care Surg REBOA REBOA Moore LJ, et al. J Trauma Acute Care Surg REBOA 2016 REBOA FDA-approved 7 French Arterial Pressure Monitoring Prophylactic No Guide wire No Fluoroscopy* Current Literature Translational research shows improved physiology compared to EDT Clinical research demonstrates: SBP increases significantly after REBOA May or may not change survival May or may not improve outcomes Currently used in select centers by ACS with minimal complications Major complications have been published (outside USA) ACS do not need extensive training to perform REBOA 21

22 REBOA REBOA in the field? Unanswered questions Physiology Anatomy Patient selection Procedure Technology Training Outcomes Credentialing How London Air Ambulance saved life of cyclist who lost leg in skip lorry crash A young cyclist who was miraculously saved by Air Ambulance medics and hospital surgeons after being run over by a skip lorry today told how she felt lucky to be alive. Victoria Lebrec, 24, only survived because a London s Air Ambulance doctor performed a life-saving procedure successfully at the roadside for only the second time in the world to stop her bleeding to death. 05 January 2015 Noncompressible hemorrhage Emergency Preservation and Resuscitation Arsenal Foam System Treatment consists of an injection of two liquid polymers that react upon combining to create a foam that expands rapidly through actively flowing blood to compress the injury and control bleeding. Once the patient reaches definitive surgical repair, the material can be removed by the surgeon. Protection and preservation of the organism during circulatory arrest of 2h or longer for transportation and control of bleeding during pulselessness followed by delayed resuscitation. Could allow survival from otherwise lethal insults Rago A, et al. J of Trauma Rago A, et al. J Trauma Acute Care Surg Peev MP, et al. J Trauma Acute Care Surg Duggan M, et al. J Trauma Acute Care Surg EPR Studies 22

23 Mean Arterial Pressure (MAP, mmhg) 4/3/2016 EPR Studies EPR Studies Exsanguination Cardiac Arrest (Tty 10 o C) Final OPC 90 min 120 min 5 Brain Death 4 Coma 3 Severe Disability 2 Moderate Disability 1 Normal Behringer, CCM, Prolonged HS->arrest, PHCA EPR-I (hypo-12h) EPR-II (hypo-36h) Overall Performance Category CPR 5 Dead 4 Coma 3 Severe disability 2 Moderate disability 1 Normal Wu et al. Circulation, EPR Human Trial yo Signs of life (pulse, respirations, reactive pupils, or spontaneous movement) present within 5 min of ED arrival or in the ED Remains pulseless after OCCPR and no response to clamping aorta EPR Human Trial Final gasp Lose pulse Open chest Emergency Preservation Transport to OR Hemostasis <60 min Time MAP Tty Tympanic Temperature (Tty, o C) Trauma Aortic flush Delayed resuscitation 23

24 Thank you! 24