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M&M. Rahul Mutneja Rick Klinger Sonia Dhillon. CASE:. - PowerPoint PPT PresentationTRANSCRIPT
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