Blood components and transfusion reactions

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Information about Blood components and transfusion reactions

Published on February 4, 2014

Author: drasimrana



Basically made for ICU nurses to help them understand different kinds of blood transfusion reactions and how to diagnose and manage them in ICU

Dr. Muhammad Asim Rana MBBS, MRCP(UK), FCCP, SF-CCM , EDIC Critical Care Medicine

• Bed no 1 is a 68 yrs old chronic case for tracheostomy and the Hb% is 8.5 • ENT and Ansthesia has demanded Hb% of 10.0 • What will you do?

PRBCs Ideal for patients requiring red cells but not volume replacement. Increase O2 carrying capacity • Transfusion trigger (HCT<30% ; HB<10g/dl) • 1 Unit increases 3% HCT or 1g/dl • Shelf life =42 d (1-6 ℃)

• Bed no 14 Medical ICU, a 35 yrs old female case of Sickle Cell Anemia has been admitted with chest pain and cough, has anemia Hb% is 6.0, your consultant advised therapeutic exchange. • What will be your plan?

• Bed no 34 surgical ICU, a 25 yrs old male victim of RTA admitted with severe abdominal injury with ruptured spleen and tear in liver is admitted post OR. • His Hb% pre OR was 3.0 he received 10 PRBCs in OR as he was massively bleeding during surgery • Came hypotensive, hypothermic, oozing from wounds and active bloody out put from drains • What will be your plan?

• His resuscitation started with PPF, Hessteril and PRBCs but his bleeding is not stopped • GS has no plan to re-explore him • His labs showed that he is in severe DIC • Why? • What is the solution now?

• Bed no 50 surgical ICU, a 55 yrs old male ESRD on haemodialysis admitted post fixation of his fracture femur. • You found he has a constant ooz from the incision so that his Hb% dropped to 6.0 • What will be your plan? • What is the cause of constant oozing in this pt?

• Bed no 23 a 65 yrs old female, case of hydrocephalus due to TBM is going for EVD insertion and you see that she has very low platlets around 30,000 (thrombocytopenia) • What will be your plan? • What is the risk in this pt?

• Consists of formed elements (cells) suspended & carried in plasma (fluid part) • Total blood volume is about 5L • Plasma is straw-colored liquid consisting of H20 & dissolved solutes • Includes ions, metabolites, hormones, antibodies

PRBCs Ideal for patients requiring red cells but not volume replacement. Increase O2 carrying capacity Transfusion trigger (HCT<30% ; HB<10g/dl) 1 Unit increases 3% HCT or 1g/dl Shelf life =42 d (1-6 ℃) Platelets Thrombocytopenia (< 5,000) Platelet dysfunction Each unit increase 5,000 PLTs after 1hr FFP ( initial therapeutic dose : 10-15 ml/kg ) and used in Isolated factor deficiencies Reverse warfarin therapy Correction of coagulopathy associated with liver disease Massive blood transfusion with microvascular bleeding (>1 BV/ 24 hrs or > 50 % BV within 3 hrs or > 150 ml/min) Antithrombin III deficiency TTP ( Thrombotic thrombocytopenic purpura )

Christian Zagado (1665) First human blood transfusion Dr. James Blundell, a British obstetrician (1825) Austrian Karl Landsteiner (1900) Discovery of ABO type Oswald Hope Robertson US Army Capt 1916 First Blood Bank World War 1

Erythrocytes (RBCs) • RBCs are flattened biconcave discs • Shape provides increased surface area for diffusion • Lack nuclei & mitochondria • Each RBC contains 280 million hemoglobins 13-9

• Have nucleus, mitochondria, & amoeboid ability • Granular leukocytes help detoxify foreign substances & release heparin • Include eosinophils, basophils, & neutrophils • Agranular leukocytes are phagocytic & produce antibodies ,Include lymphocytes & monocytes 13-10

• Are smallest of formed elements, lack nucleus • Are fragments of megakaryocytes • Constitute most of mass of blood clots • Release serotonin to vasoconstrict & reduce blood flow to clot area • Secrete growth factors to maintain integrity of blood vessel wall • Survive 5-9 days 13-12

• Constitute 7-9% of the plasma • Three types : albumins, globulins, & fibrinogen Albumin accounts for 60-80% • Creates colloid osmotic pressure that draws H20 from interstitial fluid into capillaries to maintain blood volume & pressure Globulins carry lipids. Gamma globulins are antibodies Fibrinogen serves as clotting factor Serum is fluid left when blood clots 13-8

 Whole Blood;  Blood Component;RBC PLT FFP Leukocyte concentrate  Plasma Substitutes; Use of whole blood is considered to be waste of resources Indications • Acute massive blood loss; • Anaemia and hypoalbuminemia • Overwhelming Infection • Dysfunction of Coagulation;

 Approach Route: PVL, CVL  Filtration before Transfusion  Velocity of Transfusion: 5-10ml/min  Double Check: Name, Type and Cross-match  Storage Time  Pre-heat  No any other Medication  Observation during / after Transfusion

• The pt of bed 1 is receiving 2 units of PRBCs for possible tracheostomy. After his 1st unit of blood he developed a temp of 38.3 °C (101.0°F). He has no other symptoms. On exam he appears anxious but his vital signs are stable with BP 120/70mmHg, HR 80bpm RR18 Sat O2 98% on Room Air he has no skin rash and his urine color is amber What is your diagnosis? How would you manage this patient ?

• • Most common, usually benign without sequelae Concerning because initial presentation is similar to more adverse reactions. i.e. fever, chills +/- mild dyspnea. 15% will have a recurrence in the future with subsequent transfusion • Management • • • Discontinue transfusion, rule out hemolysis i.e. check labels, repeat type and cross match, coombs test Antipyretics +/- meperidine for chills and rigors Although antihistamine premedication is widely used there are no evidence to support that their use actually prevents reaction.

• A 35-year-old woman with sickle cell disease, she is receiving 2 units of PRBC. Her 1st unit of blood was transfused without events but 5minutes into her 2nd unit, She complains of new flank pain and fever. On exam she appears very anxious, diaphoretic and in acute distress, she is febrile to 38.8C with BP 100/60mmHg, HR101/m RR 22/m, Pulse Ox 98% 0n RA She has no skin rash but is oozing out of IV sites and her urine color is now reddish brown. Labs: elevated Bun/creat, increased PTT, PT and decreased HCT. What is the diagnosis and how would you manage this patient?

• Medical emergency • Occurs due to rapid transfused RBC destruction by preformed recipients Abs • Mostly due to ABO incompatibility • Most common causes are clerical or procedural errors • Complications includes DIC, shock, ARF secondary to ATN Clinical presentation • Classic presenting triad of Fever, flank pain and reddish brown urine from hemoglobinuria are rarely seen • DIC may be presenting mode • Positive Direct Coombs

• People with Type A blood make antibodies to Type B RBCs, but not to Type A • Type B blood has antibodies to Type A RBCs but not to Type B • Type AB blood doesn’t have antibodies to A or B • Type O has antibodies to both Type A & B • If different blood types are mixed, antibodies will cause mixture to

• If blood types don't match, recipient’s antibodies agglutinate donor’s RBCs • Type O is “universal donor” because lacks A & B antigens • Recipient’s antibodies won’t agglutinate donor’s Type O RBCs • Type AB is “universal recipient” because doesn’t make anti-A or anti-B antibodies • Won’t agglutinate donor’s Insert fig. 13.6 •

Management 1. Stop transfusion, alert blood bank to start search for clerical error since another patient may be at risk , repeat type and cross matching 2. Supportive care; ABC +/-pressors 3. Cardiac monitoring because of risk of hyperkalemia 4. Infuse N/S to maintain BP and promote diuresis, avoid LR and dextrose because calcium in LR will promote clotting in IV line and dextrose will increase hemolysis. Maintain urine output >100-200ml/hour 5. With DIC early heparinization 10u/kg/hr may be beneficial

life threatening emergency •Occurs within a few seconds to minutes following transfusion •Characterized by rapid onset of anaphylaxis •Can occur with all blood products •Incidence ; 1 in 20-50 thousand •Presence of class specific IgG and anti IgA abs in patients who are IgA deficient •Treatment: Epinephrine , ABC +/- pressor

After 3days of treatment, he had improved however, he developed a cough and a temperature of 38.3°C , with increasing FiO2 requirement O/E, BP is 120/80 mm Hg. There is no rash . he is tachycardic . Oxygen saturation is 80% on FiO2 of 85%, and a blood gas study shows an arterial PO2 of 45 mm Hg. A chest radiograph reveals diffuse opacifications of both lungs. Which of the following is the most likely cause for this patient's reaction? 1. Pulmonary embolism 2. Antileukocyte antibodies 3. Allergy to donor plasma proteins 4. Circulatory overload

• New acute lung injury occurring during or within 6 hour of blood product transfusion • 1 case for every 1000-2400 units transfused with 6-9% mortality rate • Abs against HLA Clinical presentation • Acute onset of respiratory distress (hypoxemia) during or shortly after blood transfusion. • Fever, tachycardia, tachypnea, +/-hypotension • In intubated pts; elevated peak airway pressures, pink frothy airway secretion • CXR bilateral patchy alveolar infiltrates, normal cardiac picture Management • Mostly supportive with abrupt resolution in symptoms within a few days • A majority of patients may require mechanical ventilation

Immune mediated transfusion reactions • Febrile non hemolytic transfusion reactions • Acute and delayed hemolytic reactions • Anaphylactic transfusion reaction • Urticarial transfusion reaction • Post-transfusion purpura • GVHD • TRALI (Transfusion Related Acute Lung Injury)

• Physical reactions: thermal i.e. heat or cold induced • Infectious; Hepatitis B/C, malaria, HIV, CMV, West Nile virus • Chemical; citrate toxicity, hypo/hyperkalemia, iron overload • Acute hypotensive reaction: mediated by bradykinins and occurs in patients with faulty bradykinin metabolism on ACE I • Osmotic injury

• Transfusion reactions are mostly due to documentation errors and can range from benign reactions to life threatening emergencies • Early detection, discontinuation of transfusion and instituting supportive care are key to management. • Reporting of all reactions helps to improve standard practices and reduce future occurrences.

Dr. Asim Rana

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