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Chapter5
Haematology
Anaemia 44
Transfusion of blood products 420
Clotting disorders 426
Anticoagulation 428
413
414 CHAPTER5 Haematology
Anaemia
$ Reduced red blood cell (RBC) mass, usually conveniently approximated as reduced haemoglobin concentration (eg ♂ <30g/ L, ♀
<5g/ L
RBC production, increased RBC destruction, RBC loss) with clues found
in abnormalities of RBC size and shape (Box5.).
Think about Most likely Haemorrhage, chronic blood loss (iron- deciency
anaemia), anaemia of chronic disease, renal failure;
deciency (coeliac disease, Crohn’s disease, partial gastrectomy, pernicious anaemia, elderly, alcoholism), haemoglobinopathy (E p. 414),
haemolysis, alcoholic liver disease, malignancy/ lymphoma/ myeloma,
myelobrosis, hypothyroidism;
Ask about Evidence of hypoperfusion Dizziness (especially on standing),
SOB (exertional/ at rest), chest pain, palpitations;
staxis, haematemesis, haemoptysis, haematuria, menorrhagia, melaena,
PR bleeding). See E Table7.8 for symptoms seen in bloodloss;
toaetiology
FH Haemoglobinopathy; DH NSAIDs, trimethoprim, anticonvulsants,
atypical antipsychotics; SHAlcohol, vegetarianism, dietaryfads.
Obs Resting iHR or postural BP d suggest compromise.
Look for Pallor (conjunctiva, nail beds, tongue), glossitis, mouth ulcers,
hepatomegaly, splenomegaly, lymphadenopathy, jaundice; CVS Bruits,
signs of active bleeding, signs of heart failure; PNS Peripheral neuropathy; CNSOptic atrophy; PRMelaena/ blood; GU Haematuria.
Investigations blds FBC (E p. 594) (with MCV— Table5.), blood
lm, iron, ferritin, TIBC and transferrin saturation, serum vitamin B
folate,
LDH, serum electrophoresis;
cancer and to help explainSOB;
colonoscopy, bone marrow biopsy. See Table5.2.
Treatment
Asymptomatic anaemia
• Look hard for a cause; exclude malignancy, eg in patients>40yr
• Assess diet (vitamin B
Symptomatic anaemia or Hb<80g/ L
Consider blood transfusion if anaemia and/ or symptoms are acute
(E p. 421). The key is identifying the precipitatingcause.
). Causes easily divide into three basic mechanisms (reduced
2Worrying features Hb <80g/ L, SOB, iHR, dBP, dizzy, fainting,
lethargy, palpitations, chest pain, dGCS/ agitation.
OtherFolate/ vitamin B
Dilutional Pregnancy, uid resuscitation.
Any bleeding (eg epi-
Weight loss, change in bowel habit, abdominal cramps; PMHor
2
reticulocyte count, DAT (Box 5.2), CRP, ESR, U+E, LFT, TFT,
ECGIf CVS symptoms; CXRIf suspicion of
OtherUrine Bence Jones protein, OGD,
:meat, eggs, milk; folate:leafy greens, legumes;
iron:meat, legumes, greens) and consider oral supplements (eg vegans).
2
Clues
and
2
2
Note since 203 UK NHS laboratories report Hb in g/ L, notg/ dL.
2
Always send before any transfusion, since transfusion may derange results.
Table5. Mean cell volume (MCV) indierent forms ofanaemia
MCV <76fL MCV 77– 95fL MCV >96fL
Iron deciency Pregnancy Vitamin B
Thalassaemia Haemorrhage Alcohol
Haemoglobinopathies Haemol ysis Liver disease
Sideroblastic anaemia Renal failure Thyroid disease
Malignancy Myelodysplasia
Anaemia of chronic
disease
Bone marrow failure
deciency
Antifolate drugs (eg
methotrexate)
/ folate
2
Table5.2 Laboratory ndings indierent forms ofanaemia
Iron TIBC Ferritin MCV
Iron deciency
Chronic disease
Haemolysis
Note:ferritin is a non- specic acute phase protein, as is CRP, so will subsequently be raised in
many hospitalized patients irrespective of theirHb.
d i d d
d d n or i n
i d i n
Box 5. Abnormalities onthe peripheral blood lm
(E OHCM1p. 324)
Acanthocytes Irregularly shaped RBCs (liver disease)
Anisocytosis RBCs of various sizes (megaloblastic anaemia/ thalassaemia)
Blast cells Nucleated precursor cells (myelobrosis/ leukaemia)
Howell– Jolly bodies Nuclear remnants in RBCs (post- splenectomy)
Hypochromic Pale RBCs (iron- deciency anaemia)
Left shift Immature white cells (infection or marrow inltration)
Leukaemoid reaction Reactive leucocytosis (infection/ burns/ haemolysis)
Poikilocytes Variably shaped cells (iron or vitamin B
Reticulocytes Immature RBCs (haemorrhage/ haemolysis)
Right shift Hypersegmented neutrophils (megaloblastic anaemia and
Rouleaux Clumping of RBCs (infection/ inammation)
liver disease)
deciency)
2
415ANAEMIA
K Box 5.2 Direct and indirect antiglobulintests
(E OHCM p. 332‘An approach to haemolytic anaemia’, which also
explains the antiglobulin tests in more detail.)
The direct antiglobulin test (DAT) (Coomb’s test) is an essential part of
any haemolysis screen as it detects the presence of auto antibodies on
RBCs (is haemolysis caused by auto immune destruction of RBCs?).
The indirect antiglobulin testscreens the serum antibodies against donor
RBCs. It is used in pre natal testing and before blood transfusion.
416 CHAPTER5 Haematology
2Anaemia secondary toblood loss(Ep. 482.)
SymptomsChest pain, palpitations; may be history of peptic ulcer, recent
surgery, trauma, epistaxis, haematemesis, melaena, or menorrhagia.
Signs iHR, dBP, postural BP drop, iRR, dGCS/ restlessness, shock,
pallor, sweating, cold, clammy; look at the wound site or catheter bag
for haematuria if post- op; PR:melaena. See Table5.3.
Investigations bldsInitially may be normal; Hb, MCV, U+E (iurea out of pro-
portion to icreatinine in upper GI bleed), LFT, clotting, G+S/ X- match; once
stable recheck Hb, reticulocytes; OGD/ colonoscopyIf suspect GI source.
Acute treatment(Ep. 482.)
• Lay at, elevate legs if hypotensive; giveO
• IV access, take bloods, give rapid IV infusion (L 0.9% salineSTAT)
• If bleeding site is obvious, apply rm pressure and elevate
• Contact your senior— treat the cause (eg return to theatre if bleeding
from operationsite).
Table5.3 Measuring haemoglobin inacute bloodloss
3Measurement of haemoglobin does not accurately estimate the volume of
blood loss in the rst few hours after haemorrhage.
Acute Hb concentration may be normal initially, with red cells and
Intermediate With IV uid resuscitation Hb and clotting factors are diluted,
Late Homeostasis regulates the volume of uid in the intravascular
plasma lost in equal proportions. With IV uids or normal
haemodilution a fall in Hb becomes evident
unmasking loss of RBCs. Even in absence of IV therapy, salt and
water retention occurs, resulting in a natural haemodilution
compartment and the Hb often rises as the ‘clear’ uid (colloids/
crystalloids) is eliminated. Without IV therapy Hb may remain
low until erythropoiesis generates more RBCs
Anaemia ofchronic disease(EOHCM1 p. 326.)
CausesInfection (eg TB, endocarditis), rheumatoid arthritis, malignancy,
liver failure, most chronic diseases.
SymptomsFatigue, SOBOE, lethargy; may have very few symptoms/ signs.
Investigations n MCV, dTIBC/ serum iron, n/ iferritin.
TreatmentTreat underlying disease; consider EPO in renal failure or malignancy.
Haemolytic anaemia
Causes Acquired Autoimmune, microangiopathic,
extracorporeal circuit, blood transfusion incompatibility, drugs, toxins,burns;
Hereditary Haemoglobinopathy, G6PD deciency, red cell membrane disorder (eg spherocytosis).
SignsMild jaundice, murmurs, lymphadenopathy, hepatosplenomegaly.
Investigations ibilirubin (unconjugated), reticulocyte count >85×0
>2%), iLDH, dhaptoglobin, iurobilinogen, direct/ Coombs antiglobulintest.
TreatmentThis depends upon the cause. Often steroids, immunosuppres-
sion ±splenectomy if autoimmune, treat precipitating cause if acquired.
3
Microangiopathic haemolytic anaemia refers to destruction of red cells within capillaries. Schistocytes
(fragmented red cells) are seen on a blood lm. Causes include disseminated intravascular coagulation
(DIC, E p. 426), HELLP syndrome (E p. 501), thrombotic thrombocytopenic purpura (TTP), and
haemolytic uraemic syndrome(HUS).
2
3
mechanical heart valves,
9
/ L (or
Iron- deciency anaemia
Iron Found in most diets containing adequate meat, legumes, or greens; Causes
GI loss (gastroduodenal ulcer, oesophageal varices, IBD, malignancy), menorrhagia, poor diet, malabsorption syndromes, intestinal helminthiasis;
Symptoms
Abdominal pain, melaena or haematochezia, dysphagia, haemoptysis, haematemesis, diarrhoea; menorrhagia, epistaxis;
itis, angular stomatitis; PR Blood/ melaena;
Signs Pallor, koilonychia, gloss-
Investigations bld lm (microcytic,
hypochromic with anisocytosis and poikilocytosis), blds dserum iron, dferritin,
iTIBC; Stool Check for faecal occult blood;
OGD ±colonoscopy; CT Abdo iffrail;
Video capsule endoscopy if suspect small bowel pathology; Treatment Find and
treat the cause. Iron supplements (eg ferrous sulfate 200mg PO given for 3/2
to replenish stores; NB OD or alternate-day dosing gives good replacement
and fewer SE: change in bowel habit, nausea, epigastric pain). IV iron preparations available for those unable to tolerate or absorb PO iron. 2IV iron is
contraindicated in sepsis. Transfusion is considered a last resort (Ep. 420).
$ Treatment with oral iron raises Hb by 70g/ L per week at best.
Failure to respond may reect poor compliance due to side eects.
Folate/ folic acid (vitamin B9) deciency
Folate Found in green vegetables, nuts, liver, yeast. Body stores are small
and depleted within weeks if dietary intake becomes inadequate;
Causes
Malabsorption Alcohol, coeliac disease, Crohn’s disease, tropical sprue;
irequirement Pregnancy, DM, lymphoma, malignancy; Drugs Anticonvulsants,
trimethoprim, methotrexate;
SignsGlossitis; Investigations bldsvitamin B
tion (Ep. 322);
Treatment Treat the cause; folic acid 5mg/ 24h PO for 4mth.
Symptoms Breathlessness, fatigue, headaches;
, folate, iMCV, look for malabsorp-
2
For chronic haemolysis give long term. 2First exclude and treat any concurrent
vitamin B
deciency as this may worsen vitamin B2 deciency neuropathy.
2
$ If planning pregnancy, folate should be taken 0.4mg/ 24h PO until 2/
40 to reduce risk of foetal neural tube defects.
Vitamin B2 deciency
Vitamin B
Found in liver, kidney, sh, chicken, dairy products, eggs. Extensive total
2
body stores and recycling from enterohepatic circulation means nutritional deciency may take several years to manifest in the absence of other GI pathology:
suspect pathologyif d vitamin B2; Causes Poor dietary intake, pernicious anaemia,
malabsorption (as for folate deciency), stomach/ bowel resection, Crohn’s
disease, nitrous oxide abuse;
Symptoms Sensory neurological decit, autoimmune
disorders (eg vitiligo, infectious mononucleosis, Addison’s disease), dementia;
Signs Sore mouth (glossitis, angular cheilosis, mouth ulcers), neurological defects
(peripheral neuropathy, optic atrophy), jaundice;
folate, iMCV, bloodlm; Specic tests for pernicious anaemia Intrinsic factor and
gastric parietal cell antibodies
4
; Treatment Dietary advice, hydroxocobalamin mg/
Investigations blds Vitamin B
72h IM for 2wk, then mg/ 3mth IM as maintenance dose. Oral cyanocobalamin
50–50mcg/24h can be given as maintenance if dietary cause. Don’t delay as
early treatment may help prevent long- term neurological sequelae.
4
Gastric parietal cell antibodies sensitive (+ve in >90% with autoimmune gastritis, the end result
of which is pernicious anaemia), but not specic (+ve in 5– 0% of healthy indi viduals). Intrinsic
factor antibodies are specic but less sensitive (+ve in 50– 70%).
417ANAEMIA
2,
418 CHAPTER5 Haematology
Leukaemia(Table5.4; E OHCM1pp. 352–57.)
Table5.4 Epidemiology ofcommon forms ofleukaemia
Type Patient Prognosis
Acute Lymphoblastic (ALL) 2– 4yr
Myeloid (AML) Old >young, post- chemo 20% 5yr survival
Chronic Lymphocytic (CLL) >40yr, often male 85% 5yr survival
Myeloid (CML) Middle aged 75% 5yr survival
>60yr
Children 85% cure
Elderly <20% cure
Symptoms Recurrent/ unusual infection, easy bruising, bleeding, joint pain,
bone pain, malaise, weakness, abdo pain, weight loss, night sweats;
petechiae, bruises, bleeding (check gums), lymphadenopathy, signs of infection, hepatosplenomegaly, focal neurology;
Investigations bldsFBC (anaemia,
iWCC, look at dierential), blood lm, U+E, LFT, iLDH, iurate, clotting; Biopsy Bone marrow;
Treatment Acute Antibiotics, blood and platelet
transfusions; Long- term Chemoradiotherapy, bone marrow transplant or
observation;
Complications Infection, bleeding (DIC), hyperviscosity, tu-
mourlysis syndrome (Ep. 397).
Lymphoma(Table5.5; E OHCM1pp. 358–61.)
Table5.5 Basic epidemiology oflymphoma
Type Patient Prognosis
Hodgkin’s Young adults or elderly, often male ~80% 5yr survival
Non- Hodgkin’s Any age, especially the elderly 50–60% 0yr survival
Symptoms Enlarged non- tender lumps, fever, night sweats, infection,
itching, tiredness, weight loss, malaise, weakness, occasionally pain with
alcohol.
Signs Pale, lymphadenopathy (Box 5.3), hepatosplenomegaly;
Investigations bldsFBC, blood lm, U+E, LFT, Ca
2+
, LDH,urate; CXR CT/
MRI Chest/ abdo/ pelvis; BiopsyLymph node (Reed– Sternberg cell seen
in Hodgkin’s) and bone marrow;
oids, bone marrow transplant;
Treatment Chemoradiotherapy, ster-
Complications Infection, bone marrow
failure, SVC obstruction (Ep. 297).
Paraproteinaemia$ Several diseases can cause an excess of a single (clonal)
immunoglobulin including myeloma (E p. 411). Elderly patients may get a mono-
clonal gammopathy of undetermined signicance (MGUS) distinguished from
myeloma on the basis of paraprotein levels <30g/ L, with <0% plasma cells on
bone marrow biopsy and no evidence of end- organ damage. MGUS will progress to myeloma in <2% patients/ year. In Waldenström’s macroglobulinaemia,
iIgM from a lymphoplasmacytic lymphoma may lead to hyperviscosity.
Box 5.3 Causes oflymphadenopathy
InfectionLocal infection, EBV, CMV, hepatitis, HIV, TB, syphilis, toxoplas-
mosis, Bartonella (‘cat- scratch’ disease), fungal;
leukaemia, metastases;
AutoimmuneSLE, rheumatoid; OtherSarcoidosis,
MalignancyLymphoma,
amyloidosis,drugs.
5
5yr survival decreases with increasing age, see Mcancerresearchuk.org for more information.
5
Signs Pallor,
Myeloproliferative disease(OHCM1 Ep. 362.)
$ Neoplastic diseases of myeloid progenitor cells with potential to
transform to AML, including CML, as wellas:
• Polycythaemia (rubra) vera (iHct; plethora, thrombosis)
• Essential thrombocytosis (iplatelets; thrombosis or bleeding)
• Myelobrosis (marrow brosis; marrow failure, splenomegaly).
Pancytopenia $ dHb, dplts, and dWCC (E OHCM1p. 348).
Marrow failure Aplastic anaemia, malignancy, myelodysplasia, brosis;
Other Hypersplenism, SLE, infection (eg TB, AIDS), vitamin B
ciency;
Investigations blds FBC, reticulocytes, blood lm, vitamin B
bone marrow
biopsy; TreatmentAddress underlying cause; may need RBC/
/ folate de-
2
, folate;
2
plt transfusions.
Sickle- cell disease and trait(E OHCM1 p. 336.)
6
$ Point mutation in haemoglobin β- chain gene causes mutant Hb with
tendency to polymerize under low oxygen tension. Resultant RBC deformities and increased endothelial adherence lead to haemolysis, vasoocclusive crises, and microinfarcts.
With heterozygote frequencies as high as 30%, all patients with an AfricanCaribbean background must be screened for haemoglobinopathies before
elective surgery. Labs may have dierent protocols, but normally take 7h
to get results back. 2 Alert anaesthetist if you suspect sickle-cell disease on
your pre- op assessment;
ibilirubin; history of sickle cell crises; hyposplenism;
Normal Hb, usually healthy;
Homozygote Haemolytic anaemia, ireticulocytes,
Heterozygote (trait)
Complications Vaso- occlusive crises with se-
vere pain in long bones or acute abdomen; thromboses elsewhere may
lead to splenic infarction, stroke, priapism, or myocardial and renal
microinfarcts; sickle chest syndrome with chest pain, tachypnoea, and pulmonary inltrates is an emergency requiring ICU involvement; parvovirus
B9 infection may lead to failure of erythropoiesis and aplastic anaemia.
Acute treatment 2Contact haematologist. Encourage supportive treat-
ment during crises, with opioid analgesia, vigorous IV hydration, warming,
O
± broad- spectrum antibiotics; exchange transfusion in severe crises.
2
Chronic Hydroxycarbamide ± crizanlizumab may reduce frequency and se-
verity of crises. Hyposplenism (due to splenic infarction) results in greater
susceptibility to infection:penicillin prophylaxis, pneumococcal vaccination
(5yrly), and meningococcal vaccination (single dose) should be oered,
along with early identication and treatment of infections.
Thalassaemia(E OHCM1 p. 338.)
6
$ Genetic diseases of impaired production of dierent Hb chains with
wide variety in severity and named after the defective globinchain.
Common in Mediterranean, Arabian, and Asian populations.
(homozygote) and α- thalassaemia cause severe anaemia that requires
major
transfusion (E pp. 420–25).
β
- thalassaemia minor (heterozygote) causes a
β
- thalassaemia
mild anaemia (>90g/ L, MCV <75fL) that hardly ever requires treatment.
Treatment Repeated transfusions with chelation therapy to combat iron
overload; splenectomy reduces transfusion requirements.
419ANAEMIA
6
For information on the NHS Sickle Cell and Thalassaemia antenatal and neonatal screening pro-
grammes, see Msct.screening.nhs.uk
420 CHAPTER5 Haematology
Transfusion ofblood products
$ The understanding of blood groups and safe blood transfusion
underpinned the huge advances in medicine and surgery of the 20th century.
Blood bank samplesIt is essential to take two blood bottles (separ-
ated in time) and
transfusion protocols (usually hand- labelling). Always check ID against the
patient’s wristband. Human error is the main cause of complications.
Group and save (G+S) Blood is analysed for ABO (Table5.6) and
Rh(D) grouping and for common red cell antibodies. 2Any further transfusion >72h after an initial transfusion will require a fresh G+S sample,
since new antibodies may have formed.
Crossmatch (X- match) Blood is analysed as for G+S, then fully
screened for any antibodies against a compatible stored blood product.
Ordering blood products forelective useFollow local guidance on
what to order for each operation, to prevent waste. AG+S is sucient
since a subsequent X- match can usually be done within45min.
How many units to transfuse Depends upon the clinical situation. In
general, expect unit to result in a Hb rise of 70g/ L (if no ongoingloss).
2Ordering blood products foremergency useA daily occurrence
in most hospitals. Ensure blood bottle and form are labelled fully, with the
quantity, type of blood product(s) needed, and your location. Phone the
haematology lab and arrange a porter to collect the blood products. In
extreme emergencies blood can be issued without a full X- match, but this
carries a greater risk of transfusion reactions (Table 5.7). Activate the
major haemorrhage protocol if necessary (Ep. 479).
Checking blood products Checking before blood products are given
to a patient requires sta who must be trained in local transfusion proto-
8
cols.
Electronic scanning of barcodes is increasingly used. Conrm and
check the patient’s ID against their wristband and the compatibility label
on the blood product. Next check their details on each bag and the form.
Table5.6 ABO blood groups … Do you knowyours?
Blood group Serum antibodies UK frequency Comment
O Anti- A, Anti- B 44% Universal donor
A Anti- B 45%
B Anti- A 8%
AB None 3% Uni versal recipient
See the National Blood Service website:Mwww.blood.co.uk for how to donate blood and
read up- to- date information on blood stocks in theUK.
Table5.7 Options forcrossmatching ofpacked redcells
O- negative Universal donor. Often stored in the ED, theatres, or blood
Group- specic
Full crossmatch
7
For those who nd transfusion protocols overly burdensome, the UK transfusion incident reports
available at Mwww.shotuk.org make sobering reading.
8
See Mtransfusionguidelines.org and Mb-s-h.org.uk for UK national transfusion guidelines.
label them at the bedside according to your hospital’s
bank. Does not rst require a specimen from patient
ABO and Rh(D) status specic. Takes 75min
ABO, Rh(D) status and antibody tested. Takes 745min
7
Thinking about whento transfuse
Why not transfuse?Besides the fact that blood products are expensive and
have limited availability, they carry signicant risks (Table5.8).
Table5.8 Complications ofblood and blood product transfusion
Immunological Non- immunological
Anaphylaxis
Urticaria
Alloimmunization
Incompatibility
Haemolytic transfusion reactions
Non- haemolytic transfusion
reactions
Transfusion- associated lung injury
Transfusion triggers Have varied over the years. NICE
Transmission of infection:
• Bacteria (staph/ strep)
• Viruses (HIV, HCV, CMV etc)
• Parasites (malaria etc)
• Prion (vCJD)
Fluid overload— TACO (transfusionassociated circulatory overload)
Iron overload (repeated transfusions)
9
recommends a restrictive RBC transfusion threshold of 70 g/ L in hospitalized haemodynamically stable adults. The threshold is higher (80 g/ L) for patients undergoing
orthopaedic or cardiac surgery and those with pre- existing CVS disease.
These values may feel very low, but there has been no demonstrable benet
to the majority of elective transfusions while the risks of exposing the patient to potentially serious complications of transfusion remain veryreal.
Before transfusion Ensure the cause of anaemia is known, or appropriate
investigations including serum vitamin B
sent. This is easy to forget, but measurements made post transfusion will
/folate/ iron studies have been
2
include a contribution from the donor and lead to missed deciencies.
Irradiated blood products
Exposure to irradiation will inactivate any lymphocytes in cellular blood
products; this prevents any donor lymphocytes from mounting a transfusion- associated graft- versus- host disease (TA- GvHD). Immunocompromised patients have an increased risk of TA- GvHD, it is rare if
immunocompetent. Non- cellular products (such as FFP or cryoprecipitate,
see Boxes 5.6 and 5.7) do not need irradiation;
Indications Include current
or previous Hodgkin’s lymphoma, recent HSCT, intrauterine transfusion,
most congenital immunodeciencies, and certain drug-induced immunosuppression (purine analogues, alemtuzumab for haematological disorders,
ATG). HIV/AIDS is
not an indication for irradiated blood. Always discuss
with blood bank (in advance if possible). Be specic when describing the
indication as timing of irradiation can be important. Hyperkalaemia can be a
problem if RBCs transfused >24h after irradiation.
Cytomegalovirus (CMV)- negative blood products
CMV is very common (>50% of adults in the UK are CMV +ve). New
CMV infection in immunocompromised individuals can be fatal, hence
products from CMV −ve donors should specically be requested for immunosuppressed patients who are known to be CMV−ve.
Indications
Include intra uterine/ neonatal transfusions and transfusions during pregnancy. Organ transplant patients do not require CMV−ve products.
9
NICE guidance on blood transfusion:Mguidance.nice.org.uk/ng24
421TRANSFUSION OF BLOOD PRODUCTS
422 CHAPTER5 Haematology
Red cell transfusion
Indications To correct symptomatic/ severe anaemia; replace loss in
haemorrhage; triggers E p. 421. Generally a unit of RBC raises adult
Hb by 0g/ L. See Box5.4.
Contraindications Absolute Patient refusal (eg Jehovah’s Witness E p. 424);
Relative Pernicious/ macrocytic anaemia, heart failure/ uid overload.
Prescribing Ensure patient consent is well documented. Consider age, body
weight, comorbidities (particularly CCF), uid status, and symptoms when
deciding the rate of administration. Assess risk of Transfusion Associated
Circulatory Overload (TAC O) and consider concurrent IV furosemide
(20–40mg) STAT for high-risk patients; some hospitals have a mandatory
TACO checklist that must be completed before transfusion. If the patient
is hypovolaemic from haemorrhage then each unit of blood should be infused quickly (STAT to 30min), though for more elective transfusions each
unit can be administered at 2– 3h.
Transfused bloodMust be given through a dedicated giving set with an in- line
lter; changed every 2h. Any size of IV cannula may be used; for rapid
infusion use larger- bore cannulae. Blood should not be left unrefrigerated
for >4h (if >30min it cannot be returned to the bloodbank).
Monitoring of the patient Including HR, BP, RR, and temp is required. Obs
should be taken no more than 60min prior to the start of transfusion, 5min
into the transfusion, and when the transfusion ends. Asmall rise in temp
and HR are common. E p. 425 for transfusion reactions. Close monitoring
requirements may strain nursing stang levels and aect safety, hence only
urgent transfusions should be performed out ofhours.
Platelet transfusion
$ Always discuss with a haematologist regarding transfusion triggers as timings and platelet limits are complex.
Indications Prophylaxis inbone marrow failure ifplts <0 × 0
procedures to prevent associated bleeding (eg if plts <20 × 0
venous line, if <50 × 0
if plts <50 × 0
9
for liver biopsy/major surgery); major haemorrhage
9
; specic clinical conditions (eg platelet disorders) as pre-
0
9
; prior to invasive
scribed by haematologists. Since transfused plts have a short half-life (which
may be further reduced in pathological thrombocytopenia E p. 427), time
the transfusion as close to the procedure as possible. See Box5.5.
Contraindications HIT (Ep. 427), TTP.
3Massive blood transfusion
$ Major haemorrhage is dened as loss of one circulating blood volume
in 24h, loss of 50% blood volume in 3h, or loss of >50mL/min, though
this can be dicult to assess in an acute scenario.
2Call for senior help early for any patient with suspected haemorrhage.
Consider Reversal of anticoagulation, direct pressure or tourniquet, sta-
bilization of fractures, endoscopic, surgical, or obstetric intervention.
Tranexamic acid is given in some cases.
Activate themajor haemorrhage protocol(E p. 479). Major haemorrhage
packs typically contain RBC, FFP, and platelets ± cryoprecipitate. RBCs
and FFP are usually transfused in : ratio via a uid warmer.
Assess bloods frequently, if APTT/PT >.5 give FFP, if brinogen <.5g/L
give cryoprecipitate, if plts <50 x 0 give platelets. Aim Hb >80, beware hyperkalaemia and hypocalcaemia.
9
for central