Prescribing blood products

Question 1

• Indications for red cell transfusions
• Storage
• What levels of hb to use

Answer 1

• Contains rbcs
• For chronic anaemia
• Stored for 35 days frozen
• Need to transfuse as soon as leaving fridge within 4 hours. If removed from fridge >30 mins + unused then dispose
• 1 unit can increase hb by 10g/l
• If <70g/l for healthy, 80 with cvs disease, 90 if bleeding from critical source like eye
• All tested for HIV, hep B/C, syphillis
• Emergency O D - red cells whilst waiting for specific red cells. If Rh- can be given Rh+ as they haven’t be alloimmunised before but reserved for critical situations
• Benefits and risks?????

Question 2

• Indications for platelet transfusion
• Storage
• What platelet levels to give

Answer 2

• To prevent bleeding in thrombocytopenia in reversible bm failure such as DIC or haemorrhagic stroke
• Store at room temp 20-24C
• Shelf life of 3 days
• Transfusion within 30 mins of commencement

Question 3

Indications for FFP, cyroprecipitate, prothrombin complex concentrate

Answer 3

FFP (clotting factors):

• For non-specific coag defects in bleeding patient which inc clotting times (INR/APTT>1.2) - massive haemorrhage, DIC, liver disease haemorrhage
• There are only red cell antibodies in this not antigens, should still be ABO compatible
• Shelf life of 3 years stored frozen at -25C and once thawed used within 4 hours
• Do a clotting screen before and after

Cryoprecipitate:

• Corrects low fibrinogen (<1.5, <2 if obstetric haemorrhage), vwf, factor 8 hence used for acute haemorrhage and haemophilia
• Shelf life of 3 years stored frozen at -25C and once thawed used within 4 hours

PCC: factors 2, 7, 9, 10

• For warfarin reversal and for inherited deficiencies

Question 4

Who requires special blood components

Answer 4

Irradiated (prevents transfusion assoc graft vs host disease) - hodgkins lymphoma, some chemo drugs such as fludarabine, or other drugs cladribine, alemtuzumab, bm transplant, acquired T cell immunodef

CMV - intrauterine transfusion, elective transfusions in preg, granulocyte transfusion
- Normally causes glandular fever but in immunocomp can cause fatal pneumonitis and disseminated CMV infection

If they are really immunocompromised any lymphocytes in donor blood can overpower pts own lymphocytes

Question 5

Massive blood loss:

• Definition
• Management

Answer 5

• 40% blood loss of total blood volume or a rate of >150ml/min

1. Wide bore peripheral cannula
2. Send for emergency bloods (g&s, crossmatch, fbc, clotting inc fibrinogen, lfts)
3. Resus via IV fluids + aim for BP
4. SENIOR STAFF
5. Oxygen
6. Give 4 units blood - can use emergency O- until specific one comes
7. If on warfarin give PCC
8. If trauma and <3 hours give tranexamic acid 1g over 10 mins then IV infusion over 8 hours
9. Arrest bleeding via pressure, elevation, surgical intervention

Question 6

Alternatives to blood transfusions

Answer 6

Iron - diet, supplements, IV iron
Erythropoiesis stimulating agents but not if HTN
Tranexamic acid prevents bleeding
Intraop and post op cell salvage

Question 7

Benefits of transfusion
Risks of transfusion

Answer 7

• Symptomatic treatment - treats anaemia
• To replace blood loss
• To prevent further bleeding
• Viral illnesses like HIV, and bacterial infection
• Risk of allergic or haemolytic reaction
• Risk of vCJD
• Risk of receiving unsuitable blood

Question 8

Complications (and management) of blood transfusion

Answer 8

Immunological:

1. ABO mismatch: also known as acute hemolytic reaction. A reaction caused by transfusing wrong blood type destroying rbcs by recipients preformed antibodies by hemolysis which can cause AKI. Presents usually within an hour with urticaria, hypotension and fever and haemoglobinuria. Bloods (low hb, low serum haptoglobin, high LDH/bilirubin, + direct antiglobulin test confirms diagnosis). Stop transfusion (keep IV access in!!), fluid resus saline, o2, A-E. Prolonged oliguria and shock are poor prognostic signs.
2. Delayed haemolytic transfusion reactions: a patient has been sensitised to a rbc antigen and has very low ab levels and hence neg pretransfusion tests. May take 1-4 weeks where slight fever/assymp, slight jaundice. As they get destroyed hematocrit dec, LDH inc, bilirubin inc, + direct antiglobulin test. Usually unidentified and sudden drop in hb to pretransfusion level
3. Transfusion related acute lung injury TRALI: a form of acute resp distress syndrome ARDs caused by anti HLA and antigranulocyte ab in donor plasma agglutinate and degranulate recipient granulocytes within the lung causing pul oedema - dyspnoeic + crackles on examination. High mortality. Need high flow oxygen, urgent cxr and need intensive care
4. Anaphylaxis: presents as hypotension. Stop transfusion and treat as per anaphylactic guidelines epinephrine 0.5ml of 1:1000 solution sc and 0.9% saline. If history of allergies then antihistamine prophylactically
5. Non haemolytic febrile transfusion reactions: an unpleasant but non life threatening reaction, which can occur without hemolysis. Ab directed against wbc HLA in donor or cytokines release of cytokines during storage. Temperature can increase of >1C, chills, headaches, back pain. Need to stop transfusion (investigate for acute hemolytic reaction) and give antipyretics (paracetamol), anti histamines (chlorphenamine)

Non immunological:

1. Transfusion associated circ overload TACO: High osmotic load of blood product draws volume into intravasc space over course of hours causing overload. Presents with dyspnoea and features of fluid overload (crackles) esp common in people with cardiac failure/renal impairment. Need a CXR and treat with oxygen and IV diuretics. For prevention if at risk can be prescribed 20mg furosemide during transfusion, observed during infusing slowly and if signs of HF then stop and treatment for HF
2. Transmission of infection: small risk of getting hepb/c (any product), hiv, syphilis (fresh blood and platelets, infective donors are seroneg early in disease), CMV (via wbcs in blood (not fop, ab not tested in donor as doesn’t cause disease in immunocompetent individuals), malaria (if latent in donor, storage doesn’t render it safe), vCJD. Freezing decreases risk.

Question 9

Autoimmune haemolytic anaemia:

• Definition
• Pathophysiology
• Symptoms
• Signs
• Investigations
• Investigations for severe anaemia
• Management
• Causes of non autoimmune

Answer 9

Autoimmune haemolytic anaemia

• Definition: destruction of rbcs causing anaemia. Autoimmune is extravascular meaning occurs in RES and free hb not released into systemic circ
• Pathophysiology: occurs when ab created against patients rbcs leading to destruction.

Warm is more common IgG mediated where spleen phagocytosis where hemolysis occurs at normal to above normal temps, usually idiopathic. Associated with CLL, non hodgkins lymphoma, HIV/EBV, SLE

Cold (also known as cold agglutinin disease) is IgM mediated when at lower temps <10C, ab attach to rbcs and cause them to clump which activates immune system to destroy them, this is due to lymphoma, leukaemia, SLE, infections (EBV, CMV, HIV)

• Causes of non autoimmune haemolytic anaemia: acquired (alloimmune (transfusion reactions, hemolytic disease newborn, prosthetic valve related), inherited (here’d spherocytosis/elliptocytosis, thalassemia, sickle cell)
• Symptoms: fatigue, weak, dyspnoea, nausea, weight loss, dark urine (hemoglobinuria)
• Signs: anaemia, splenomegaly (filled with destroyed rbcs), jaundice, fever
• Investigations: fbc (normocytic anaemia, inc reticulocyte count (destruction leads to inc EPO stimulating bm to produce more erythrocytes inc immature rbcs), LDH, LFTS (inc unconj bilirubin), serum haptoglobin), blood film (schistocytes which are abc fragments), direct Coombs test + in autoimmune
• Investigations for severe anaemia: bloods (fbc, reticulocyte count, iron profile, creatinine, tfts, lfts (if inc bilirubin then hemolysis), ldh (marker of cell turnover, u+es, haptoglobin), peripheral blood film, hb electrophoresis, uss spleen, bm biopsy
• Management: in general, prednisolone, if not responding then transfusion, ritiximab or azothoprine long term, splenectomy
  If warm pred 1mg/kg/day, then if not other immunosuppression or splenectomy
  If cold kept patient warm and blood warmer transfuse blood, ritux if not working

Monitoring: if acute then via vital signs if outpatient then via bloods

Question 10

Describe the coagulopathy associated with:

• liver disease
• renal disease
• massive blood loss
• disseminated intravascular coagulation

and management of them

Answer 10

• DIC:

Triggers such as infection (sepsis) and non infectious (malign, burns) leads to release proinflamm cytokines in a systemic inflammatory response or there is increased expression of procoag factors leading to intravasc activation of coal cascade causing aggregation of platelets within small bv leading to microvascular thrombosis which can lead to tissue ischaemia hence multi organ failure. At the same time there is reduction in circumstances coag factors such to consumptive coagulopathy leading to thrombocytosis increasing risk of spontaneous bleeding such as haemorrhage
Need to do bloods (fbc (platelets dec), coag screen (pt/inr inc, apt inc), fibrinogen, d dimer, blood cultures). Then treat underlying disorder and supportive (platelet transfusion if bleeding (if coag results inc then FFP), or others if low fibrinogen, therapeutic heparin if thrombosis prominent (unfractionated if high risk bleeding)

• Liver disease

Fibrosis leads to decreased production of clotting factors 7, 9, 10, 11, fibrinogen and also decrease in anti clotting proteins. There will be bruising and deranged coag tests (