Rahul Mutneja Rick Klinger Sonia Dhillon. Patient is a 79 year old male who initially presented to an outside hospital with generalized seizure like activity.

M&MRahul Mutneja

Rick KlingerSonia Dhillon

CASE: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.

PMH: Lyme disease 20 years back alcohol dependencePSH: cholecystectomy Benign neck tumor removal versus ?

thoracic tumorAllergies: NKDASH: daily smoker since age of 10, divorced, 3

children, did not have a PCP and had not seen a doctor for >10 years.

Hospital CourseHe 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.

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.

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Massive Transfusion GuidelinesPurpose

Standard approach to resuscitationHelp coordinate efforts between blood bank

and primary teamOptimize the transfusion approach in face of

hemorrhagic shock

Massive Transfusion GuidelinesPopulation:

Considered massive if replacing at least one blood volume (70-80ml/kg) in 12-24 hour period for life threatening bleed

Identification of potential patientCriteria

Immediate life threatening bleed ANDClinician judgement that MTP is needed OR3 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

Massive Transfusion PrinciplesAvoid 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

Blood Bank RoleNotify Transfusion Service Medical DirectorTransport blood to ptImmediately prepare 1st unitBegin prep of next unit upon previous unit

being transportedRBCs of less than 21 days age are

preferentially usedTransfusion physician is available for bedside

assistance

Implementation of MTPBlood 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

Massive Transfusion ProtocolLabs upon initial evaluation:

Blood gas, lactate, Hgb, iCal, Chem 7, INR/PTType and Screen, CBC, Fibrinogen

Labs q 1 hour until MTP stops:Blood gas, lactate, Hgb, iCal, chem 7, INR/PTCBC, Fibrinogen

Complications of Massive Transfusion

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

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

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

Acute ComplicationsCoagulopathy 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 timeHemodilution 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

Delayed ComplicationsDelayed

Delayed hemolytic transfusion reactionsTransfusion-related immuno-modulationTransfusion-transmitted diseasesPost-transfusion graft-vs-host diseasePost-transfusion purpura

Strategies to Reduce the Complications Associated with MTHypothermia

Warm the roomSurface warm the patient with heating

blankets, heating lampsHeat and humidify inspired gases for

ventilatorsWarm all IV fluids and blood products when

administered

Strategies to Reduce the Complications Associated with MTCoagulopathy & Thrombocytopenia

Transfuse PRBC-FFP-Platelets in 1:1:1 ratioRecombinant factor VIIa as indicated

Electrolyte AbnormalitiesMonitor K, Ca, Mg serum concentrations and

correct accordinglyAcid-Base Disorders

Sodium bicarbonate for severe metabolic acidosis with hemodynamic instability or renal failure

Strategies to Reduce the Complications Associated with MTInfection

Maintain high index of suspicion to allow for early diagnosis and appropriate treatment

TRALIMinimize transfusions once hemorrhage is

controlledConsider using PRBCs with a shorter storage time

Multiple Organ FailureSupportive Care

Take Home PointsEarly recognition of life threatening

conditions associated with hypotensionAppropriate resuscitation to be initiated in a

timely mannerEarly surgical /vascular surgery consultUse of massive transfusion protocol early in

the ressusscitation.

Thank you