1. Rahul Mutneja Rick Klinger Sonia Dhillon

2. Patient is a 79 year old male who initially presented to an outside hospital with generalized seizure like activity which lasted approximately 2 minutes, following which the patient became unconscious. He was intubated for AMS and his CT head showed a suspected left temporal mass. The patient was then transferred to HH for further management.

3. PMH: Lyme disease 20 years back alcohol dependence PSH: cholecystectomy Benign neck tumor removal versus ?thoracic tumor Allergies: NKDA SH: daily smoker since age of 10, divorced, 3 children, did not have a PCP and had not seen a doctor for >10 years.

4. Hospital Course He was started on Keppra and his MRI showed moderate chronic ischemic changes with no mass. He did well and was extubated on 5/13/14. During his hospitalization he complained of shortness of breath at rest and on minimal exertion and lower extremity edema and orthopnea, all of which were chronic complaints. Cardiology and pulmonary were consulted. His Echo showed an EF of 65% with grade 1 diastolic dysfunction. BNP = 381, and negative cardiac enzymes. His SOB was though to be due to likely CHF and COPD and was managed with lasix and nebulizers with improvement.

5. Patient was getting ready for discharge on the afternoon of 5/20 when he felt dizzy and was found to be hypotensive in 80’s SBP. First recorded hypotensive episode was at 12:18 PM with BP of 86/52 mmHg. 1:06PM: Fluid resuscitation was attempted with 250 cc of NS. The patient continued to be hypotensive after the fluid bolus. 3:15PM-3:30PM: a rapid response was called. The patient complained of feeling weak and tired and had abdominal pain. 3:30PM: Patient was transferred to the ICU and was noted to be hypotensive, with a pulsatile epigastrium and tender left abdomen. A retroperitoneal v/s a ruptured AAA was considered and a stat H/H was sent, fluid resuscitation started, a central line and an A-line placed. 4:00-6:00PM: H/H reported as 7.1 and 22.7, Surgery called stat, a stat abdominal ultrasound was done, vascular surgery was called. In the mean time patient was resuscitated with 3 L NS, 3 vials of 5% 250cc albumin, 6 units of FFP, 12 PRBC, 2 platelet concentrates.,2 gm of calcium gluconate 6:10PM: Patient went to OR. He had a arteriography, and placement of a aortic balloon occluder. Patient was found to have a large AAA(6.5 - 7cm preoperatively on the USG) with extension upto the renal arteries and repair was not possible without compromising the renal arteries and this was discussed with the family and it was decided not to go ahead with the surgery and the patient was transferred back to 11i where he died at 8:30PM.

6. Hematocrit drop

7. Massive Transfusion Guidelines Purpose Standard approach to resuscitation Help coordinate efforts between blood bank and primary team Optimize the transfusion approach in face of hemorrhagic shock

8. Massive Transfusion Guidelines Population: Considered massive if replacing at least one blood volume (70-80ml/kg) in 12-24 hour period for life threatening bleed

9. Identification of potential patient Criteria Immediate life threatening bleed AND Clinician judgement that MTP is needed OR 3 of 4 indicators considered risk of shock/coagulopathy Tachycadic or hypotensive Base deficit of > 6 or Lactate >4 mmol/l INR >1.5 Hemoglobin <9 g/dl

10. Massive Transfusion Principles Avoid overuse of crystalloids (to minimize dilutional coagulopathy) Avoid and treat Hypothermia (use fluid warmer and Bair hugger if needed) Avoid and treat Acidosis (pH<7.2 treat with bicarbonate) Treat low iCal for hemostatic and hemodynamic effects

11. Blood Bank Role Notify Transfusion Service Medical Director Transport blood to pt Immediately prepare 1 st unit Begin prep of next unit upon previous unit being transported RBCs of less than 21 days age are preferentially used Transfusion physician is available for bedside assistance

12. Implementation of MTP Blood packs by Pt Wt and protocol <3kg: 1 unit of PRBC, plasma, platelets 3-20kg: 2 units of PRBCs, plasma, platelets 21-40kg: 5 units of PRBCs, plasma, platelets >40kg: 5 units of PRBCs, plasma, platelets

13. Massive Transfusion Protocol Labs upon initial evaluation: Blood gas, lactate, Hgb, iCal, Chem 7, INR/PT Type and Screen, CBC, Fibrinogen Labs q 1 hour until MTP stops: Blood gas, lactate, Hgb, iCal, chem 7, INR/PT CBC, Fibrinogen

15. Acute Complications Acute hemolytic transfusion reactions Typically occurs very soon after transfusion, ABO compatibility Rapid destruction of donor RBCs by host antibodies (IgG, IgM) Most severe rxns occur when group A blood  group O recipient Fever, hypotension, hematuria, DIC Febrile non-hemolytic transfusion reactions Associated with fever but not directly hemolysis Antibodies directed against donor leukocytes and HLA antigens TRALI Acute lung injury that occurs within 6 hours of transfusion Acute Hypoxemia, bilateral pulmonary infiltrates on CXR and no evidence of left atrial hypertension Recent study of ICU population: 8% of transfused patients developed TRALI and that the risk was increased almost 3 fold for patients who received either FFP or platelets

16. Acute Complications Hypocalcemia Stored blood anticoagulated with citrate – binds Ca Each PRBC = 3 gms of citrate Healthy adult liver can metabolize 3 gms every 5 mins Transfusion rates greater than 1 unit every 5 min or impaired hepatic function from either hypothermia or pre-existing liver disease may lead to hypocalcemia Regularly monitor iCal Citrate Toxicity – tetany, muscle tremors, prolonged QT interval, decreased cardiac contractility, and hypotension Tx: Intravenous calcium Hypokalemia, Hyperkalemia Potassium concentration of plasma increases in stored blood, 7-77 mEq/L, with higher concentrations seen with increased duration of storage K increased with irradiation and reduced by washing Hyperkalemia less common in adults, typically associated with patients who have underlying renal insufficiency, ARF, or severe tissue injury HypoK- restoration of ATPase pump, co-infusion of K poor solutions – cryst, Plts, FFP

17. Acute Complications Alkalosis and Acidosis Storage of blood in citrate phosphate dextrose adenine solution = pH 7.0, older blood pH decreases Citrate is metabolized to bicarbonate, it is common in pts who require MT frequently develop a metabolic alkalosis. Therefore presence of a metabolic acidosis in pts who require MT is an indicator of tissue hypoperfusion Temporizing measures with sodium bicarb may be appropriate Acidosis may exacerbate coagulopathy – eg. pH 7.4  7.0 reduces the activity of factor VIIa by than 90% - Thrombin generation, the primary engine of hemostasis, is thus profoundly inhibited by acidosis Hypothermia Exposure, infusion of cold fluids/blood products, opening of body cavities, decreased heat production, and impaired thermoregulatory control Decreased citrate metabolism/hepatic metabolism/drug clearance/production of clotting factors Dilutional coagulopathy Dilutional thromobocytopenia

18. Acute Complications Coagulopathy and Thromobocytopenia Dilutional/Consumptive coagulopathy and Thrombocytopenia leading to impaired hemostasis 25% to 30%of severely injured patients are coagulopathic upon arrival in the ED Early coagulopathy associated with increased mortality Most labile clotting factors – V and VIII deteriorate with blood storage over time Hemodilution is inevitable, even 1:1:1 ratio of PRBC:Plasma:Plts is not equivalent to whole blood as there is significantly reduced platelet count and coagulation activity

19. Delayed Complications Delayed Delayed hemolytic transfusion reactions Transfusion-related immuno-modulation Transfusion-transmitted diseases Post-transfusion graft-vs-host disease Post-transfusion purpura

20. Strategies to Reduce the Complications Associated with MT Hypothermia Warm the room Surface warm the patient with heating blankets, heating lamps Heat and humidify inspired gases for ventilators Warm all IV fluids and blood products when administered

21. Strategies to Reduce the Complications Associated with MT Coagulopathy & Thrombocytopenia Transfuse PRBC-FFP-Platelets in 1:1:1 ratio Recombinant factor VIIa as indicated Electrolyte Abnormalities Monitor K, Ca, Mg serum concentrations and correct accordingly Acid-Base Disorders Sodium bicarbonate for severe metabolic acidosis with hemodynamic instability or renal failure

22. Strategies to Reduce the Complications Associated with MT Infection Maintain high index of suspicion to allow for early diagnosis and appropriate treatment TRALI Minimize transfusions once hemorrhage is controlled Consider using PRBCs with a shorter storage time Multiple Organ Failure Supportive Care

23. Take Home Points Early recognition of life threatening conditions associated with hypotension Appropriate resuscitation to be initiated in a timely manner Early surgical /vascular surgery consult Use of massive transfusion protocol early in the ressusscitation.

24. Thank you