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Box 5.4 Packed redcells
Indication Symptomatic/ severe anaemia or severe haemorrhage
Immunology Needs ABO and Rh(D) compatibility between donor and recipient
Volume
220– 320mL (RBCs are ‘packed’ to achieve 770% haematocrit)
Donor Each unit from one donor
Shelf life 35d at 4°C; must be used within 4h once removed from fridge
Whole blood is seldom used in non- military settings. All blood is leucocyte depleted.
Box 5.5 Platelets
Indication
Immunology Rh(D) compatibility more important than ABO, but not crucial
Volume
Donor Typically pooled from four donors but apheresis from one
Shelf life 5d at room temperature— must be kept agitated
Symptomatic thrombocytopenia (E p. 427)
7300mL (unit will raise platelet count by 20– 40 × 0
donor becoming more popular
9
)
Box 5.6 Fresh frozen plasma(FFP)
Indication Massive blood transfusion, replacement of coagulation factor
Immunology Rh(D) compatibility more important than ABO, but not
Volume
Donor Each unit from one donor
Shelf life – 2yr at– 30°C; must be used within 4h once thawed
deciency, multiple coagulation deciencies (with severe
bleeding), disseminated intravascular coagulation (DIC)
crucial
7250mL; adult dose is 0– 5mL/ kg (usually 3–4units)
423TRANSFUSION OF BLOOD PRODUCTS
Box 5.7 Cryoprecipitate(cryo)
Indication Contains brinogen, von Willebrand factor, and factors VIII,
Immunology Rh(D) compatibility more important than ABO, but not crucial
Volume 250mL (adult dose 500mL; 2units)
Donor Each (250mL) unit from ve donors
Shelf life – 2yr at– 30°C; must be used within 4h once thawed
0
Knowing when to transfuse can be dicult; see guidelines at Mhttp:// www.b- s- h.org.uk
Because of the presence of serum antibodies, compatibility is reversed for non- red cell blood
products so AB becomes the universal donor and O the universal recipient. Rh(D) status is unaected:Rh(D) −ve recipients should receive Rh(D) −ve blood products if possible.
XIII; used in DIC and massive transfusion
424 CHAPTER5 Haematology
Consent for blood product transfusion
If a transfusion is required, patients and/or their carers should be given
verbal
and written information explaining:
• The reason for the transfusion
• The risks and benets
• The transfusion process
• Any transfusion needs specic to them
• Any alternatives that are available
• That they cannot donate blood after receiving a transfusion.
The discussion should be thoroughly documented in the notes. If a patient
is unable to consent, check for a valid advanced directive. Competent patient refusal or a refusal on a valid advanced directive are contraindications
to transfusion.
In emergency situations where it is not possible to have this discussion with
a patient or their carers, the information should be given retrospectively.
Following a blood transfusion
It takes 76– 2h after a transfusion for the concentration of the RBCs to
settle; FBC taken before this is likely to give an inaccurate value.
Discharge Include details of transfusions and any adverse events on the dis-
charge letter.
The Jehovah’s Witness and blood products
Most patients welcome open discussion about sensitive issues that could
aect their care and Jehovah’s Witnesses are no dierent. The individual
wishes of the patient must always be respected. Timely discussion about
acceptable practice and the possible utility of alternative treatments allows
healthcare professionals to plan and provide better patient care. In general:
Acceptable treatments These include non- blood volume expanders (saline,
Hartmann’s, glucose, gelatins (Gelofusine
®
), starches (Voluven®), dextrans),
agents which control haemorrhage (recombinant factor VIIa (NovoSeven
tranexamic acid), and agents which stimulate red cell production (recombinant erythropoietin; check preparation is free from human albumin), IViron.
Unacceptable treatmentsThese are treatments which involve the transfu-
sion of donor whole blood, packed red cells, white cells, FFP, and platelets. Preoperative autologous (self- donated) blood can sometimes be
considered acceptable.
Treatments which individuals may consider These include blood salvage
(intraoperative and postoperative), haemodilution, haemodialysis, and cardiac bypass (pumps must be primed with non- blood uids). Some fractions
of plasma or cellular components may be considered acceptable by some
individuals (cryoprecipitate, albumin, immunoglobulins, clotting factors, and
haemoglobin- based O
liver) as well as bone and tissue may also be accepted.
For further information The Hospital Liaison Committee for Jehovah’s
carriers). Transplants including solid organ (heart,
2
Witnesses has several centres all over the country run by Jehovah’s
Witnesses. Hospital switchboard will have contact details of your local
representatives though there is also a 24h contact service for urgent
advice for patients and healthcare professionals (020 837 345); nonurgent enquiries can be sent via email to hid.gb@jw.org.
®
),
3Transfusion reactions
$ In the UK, blood products (except white cell products) are leucocyte
depleted to reduce the risk of transfusion reaction.
• These are potentially fatal, so must be managed urgently (Table 5.9)
• ABO incompatibility and bacterial contamination may be seen within
minutes of starting the transfusion
• Low- grade pyrexia is common during a transfusion, though a rapid rise
in temp at the start is worrying.
Investigations blds FBC, U+E, bilirubin, LDH, blood lm, direct anti-
globulin test, clotting, repeat G+S and crossmatch (check blood group),
antibody screen, blood cultures, mast cell tryptase (if anaphylaxis suspected); Urine Free haemoglobin; CXR If signs of heart failure; Retain
blood bag Re- check identiers and return bags to laboratory.
Table5.9 3Acute transfusion reactions (E OHCM1p. 345)
Features Diagnosis Management
≥of:
• Temp rise>2°C
• Chest/ abdopain
• SOB
• iHR/ dBP
• Agitation
• Flushing
• iHR/ dBP
• Bronchospasm
• Cyanosis
• Oedema
• Temprise <2°C
• Shivering
• Urticaria
• ±itemprise
<2°C
• ±iitch
• SOB
• Cough
2
Likely Haemolytic transfusion
reaction (ABO incompatibility)
OR
2Bacterial contamination
(
irisk with platelets)
Likely anaphylaxis
2
Likely febrile non-haemolytic
transfusion reaction
Likely mild allergic reaction Observe closely to exclude
With uid
overload
(raised JVP,
basal lung
crackles)
No uid
overload
Likely transfusion
associated
circulatory
overload (TACO)
Possible transfusion-
associated acute
lung injury (TRALI)
Stop transfusion.
senior help.5L/ min O
L 0.9% saline STAT (via
new giving set), take bloods,
catheterize and monitor urine
output, check ECG, antibiotics
± treatment for DIC
Stop transfusion.
senior help
adrenaline (epinephrine) 0.5mg
(0.5ml of :000) IM, L 0.9%
saline STAT (via new giving
set), take bloods, catheterize
and monitor urine output
Slow transfusion. Give
paracetamol g/ 6hPO.
Monitor obs (HR, BP,temp).
Call for senior help if no
improvement or worsening
anaphylaxis. Slow transfusion.
Inform senior. Monitor
obs (HR, BP,temp), give
chlorphenamine 0mg STAT IV
Slow transfusion. 5L/ min
O
and sit upright. Consider
2
furosemide 40mg STAT IV,
catheterize, bedside CXR.
Call for senior help if no
improvement or worsening
Call for senior help. 5L/ min
O
and sit upright. Seek urgent
2
critical care input
Call for
Call for
. 5L/ min O2,
,
2
425TRANSFUSION OF BLOOD PRODUCTS
426 CHAPTER5 Haematology
Clotting disorders
(E pp. 478–9 Hypotension emergencies; E p. 482 Hypovolaemicshock;
E p. 595 Causes of deranged clotting prole.)
Bleeding disorders(E OHCM1p. 340.)
Haemophilia A $ Factor VIII deciency; X- linked recessive, but 30% of
cases have no FH due to new mutation. Presentation Bleeding in child-
hood, usually haemarthrosis; Investigations iAPTT (corrects with the
addition of normal plasma) and dfactor VIII; Treatment Avoid NSAIDs
and IM injections. Seek senior help early, and call the haematologist if
patient is bleeding. Factor VIII is replaced using recombinant or plasma
products.
Haemophilia B (Christmas disease) $ Factor IX deciency; X- linked reces-
sive. Clinically treat in the same fashion as haemophiliaA.
von Willebrand disease $ Mild but common (/ 000) autosomal domin-
antly inherited coagulopathy associated with deciency of von Willebrand
factor (vWF). Presentation Mucocutaneous bleeding and menorrhagia;
Investigations iAPTT; PT and platelets normal; specialist specic assays;
Treatment Not usually required unless problematic bleeding. Tranexamic
acid, desmopressin, and vWF clotting factor concentrates have a role.
3Disseminated intravascular coagulation
$ Pathological activation of the clotting cascade results in formation of
microvascular thrombi and multiorgan failure. Consumption of brinogen,
platelets, and clotting factors results in haemorrhagic complications.
SignsBleeding + petechiae with signs of underlying precipitant (Box 5.8).
Investigations blds dplatelets, iPT/ INR, iAPTT, dbrinogen, ii D- dimer.
General treatment Request urgent senior help (most likely ITU) and discuss
with haematologist. Treat underlying cause (most commonly sepsis), supportive measures for BP, acidosis, hypoxaemia, and maintain normothermia.
Blood transfusion for anaemia (may exacerbate coagulopathy).
Correction of coagulopathy With FFP, platelets, cryoprecipitate (rich in
brinogen), or factor concentrates as advised by the haematologist.
Further pharmaceutical management is controversial; see local policy.
ComplicationsMassive haemorrhage, end- organ failure, death (DIC is an
independent predictor of mortality in trauma or sepsis).
2Box 5.8 Common precipitantsofDIC
• Septicaemia (Gram– ve > Gram+ve)
• Disseminated malignancy
• Incompatible blood transfusion reactions
• Obstetric emergencies
• Liver failure
• Severe trauma/ burns.
Thrombocytopenia
$ Often an incidental nding, but patients may present with bleeding (gums,
epistaxis) or easy bruising. Spontaneous bleeding tends not to occur until
platelet counts <20 × 0
Causes dproduction (eg aplastic anaemia, leukaemia), iconsumption
9
/ L.
(eg immune thrombocytopenic purpura (ITP), haemolytic– uraemic
syndrome), and drug- induced (eg amiodarone, carbamazepine).
Treatment Primarily identication and reversal of cause, with guidance by
a haematologist. Avoid IM injections. Platelet transfusion is indicated in
some situations E p. 422.
2Consider heparin- induced thrombocytopenia (HIT) if occurs 4– 4d
after commencing heparin (Box 5.9).
K Box 5.9 Heparin- induced thrombocytopenia(HIT)
The development of procoagulant antibodies in those receiving heparin
(unfractionated > LMWH) may lead to thrombocytopenia with thrombosis. Risk factors include recent heparin exposure (within 00 days)
and recent orthopaedic or cardiovascular surgery. Perform a baseline
FBC and consider HIT in those with dplt >30% and/ or new thrombosis
within 4– 4d of starting heparin. Diagnosis is conrmed by heparindependent platelet-activating antibodies to platelet factor 4. Discuss any
suspected cases with haematology.
Patients must be anticoagulated with
a non-heparin agent (eg argatroban or DOAC); platelet transfusion is
contraindicated.
427CLOTTING DISORDERS
428 CHAPTER5 Haematology
Anticoagulation
$ Anticoagulants are used to prevent thrombotic events in those at risk
of thrombosis or to prevent clot propagation after a thrombotic event
has occurred. DOACs are often recommended over warfarin when
possible. Generally parenteral routes (eg heparin) are preferred in the
acute setting, with oral dosing used for longer- term therapy.
Table5.0 Anticoagulant treatment options
Uses Notes
VTE* TP** ACS CVA
Heparin
(unfractionated,
Box 5.0)
Heparin
(low
molecular
weight:
LMWH)
Fondaparinux SC
Warfarin PO
Dabigatran PO
Apixaban PO
Rivaroxaban PO
Edoxaban PO
All anticoagulants should be avoided in patients with active bleeding or at high risk of bleeding.
Seek specialist advice in patients with renal failure, liver failure, and haemophilia.
*VTE:venous thromboembolism (PE/ DVT treatment and prevention of recurrence);
**TP:thromboprophylaxis— see below;
‡
Licensed for TP only in hip/ knee orthopaedic surgical patients; ‡‡Licensed in atrial brillation
AF;
in absence of mitral valve disease or replacement and with ≥ risk factor:eg previous CVA/ TIA/
PE/ DVT, diabetes, CCF, HTN, age≥75yr.
IV
✓ ✓ ✓ ✓
SC
✓ ✓ ✓ ✓
✓ ✓ ✓
✓ ✓
✓ ✓
✓ ✓
✓ ✓
✓ ✓
‡
✓ ✓
‡
‡
†
CVA:prevention of stroke and systemic embolism in eg
†
Also used in arterial thrombus;
risk of HIT (Box 5.9); to
reverse, stop infusion ± full
reversal with protamine
Lower risk of HIT (Box 5.9);
preferred option in pregnancy;
monitor anti- factor Xa levels
only in those at risk of bleeding;
partial reversal with protamine
Preferred option in ACS;
monitoring not required; no
specic reversal agent— discuss
with haematology
In use since 954; E pp. 429–30
‡‡
Routine monitoring not
‡‡
required; idarucizumab
✓
can be used to reverse
‡‡
✓
dabigatran. Andexanet alfa
‡‡
can be used to reverse
apixaban and rivaroxaban
2
K Box 5.0 Unfractionated heparin
This has a rapid onset of action, a short half- life (0.5– 2.5h, but longer in
hypothermia), and is reversible with protamine (mg protamine over
0min IV neutralizes 700units unfractionated heparin within 5min).
This makes it the best, if cumbersome, option for situations where effective but rapidly reversible anticoagulation is desired (eg patients with
metallic valves awaiting surgery or at risk of bleeding). Administration
is by bolus followed by a continuous infusion set at a rate determined
according to 6h measurements of the APTT— check your local policy.
2
Exceptions to this include those with active cancer and a DVT or PE, in whom longer- ter m
therapy with LMWH is more eective than warfarin.
Venous thromboprophylaxis (VTE prophylaxis)
$ Each patient will have a documented VTE assessment in their notes which
should be completed on admission to hospital. Risk factors are highlighted
here and this guides prophylactic treatment according to local policy.
In medical patients Consider if mobility signicantly reduced for ≥3d, or
ongoing reduced mobility and one or more risk factors of:age >60yr,
3,4
active cancer, dehydration, obese, PMH or FH of DVT/ PE, known
thrombophilia, on COCP/ HRT, signicant active medical comorbidity.
In surgical/ trauma patientsConsider if one or more of above- mentioned
risk factors, or if one or more of:signicantly reduced mobility, total anaesthetic time >90min, pelvic/ lower limb surgery lasting >60min, signicantly reduced mobility, acute inammatory or intra- abdominal condition.
Bleeding risk Balance benets of thromboprophylaxis against bleeding
risk, including any active bleeding, falls risk, acquired or inherited
bleeding disorders, concurrent use of anticoagulants (eg warfarin),
LP/ epidural/ spinal anaesthesia within the previous 4h or within the
next 2h, acute stroke, thrombocytopenia, uncontrolled hypertension
(≥230/ 20mmHg).
Treatment In addition to good hydration and early mobilization, where
benets outweigh bleeding risk, oer pharmacological therapy. In most instances this will be with LMWH (eg enoxaparin 40mg/ 24h SC or 20mg/
24h if eGFR <30mL/ min). Alternatives include fondaparinux (accelerates
breakdown of activated factor Xa), rivaroxaban, edoxaban, or apixaban
(direct activated Xa inhibitors), and dabigatran (thrombin inhibitor)— see
Table 5.0. Compression stockings oer less eective prophylaxis but
are used for those in whom pharmacological therapy is contraindicated
(avoid in those with vascular disease or stroke).
Direct factor Xa inhibitor Apixaban, rivaroxaban, edoxaban
Direct thrombin inhibitor Dabigatran, argatroban (IV)
429ANTICOAGULATION
Direct acting oral anticoagulants (DOACs)
DOACs are increasingly used for VTE prophylaxis following orthopaedic surgery and have largely superseded warfarin for the treatment of VTE and
non-valvular AF. Warfarin must still be used for patients with antiphospholipid
syndrome or metallic heart valves, and may be more suitable for patients with
severe renal impairment or a high risk of GI bleeding. They unreliably aect PT/
APTT. The direct factor Xa inhibitors can be monitored using anti-factor Xa
levels (only in certain situations—discuss with haematologist). See Box 5..
K Box 5. Monitoring anti-factor Xa levels
The plasma anti-Xa assay can be used to monitor patients receiving
LMWH and the direct factor Xa inhibitors (apixaban, rivaroxaban,
edoxaban). Routine monitoring is not required, but a haematologist may
request monitoring for patients with marked obesity, pregnancy, or severe renal impairment. Therapeutic targets vary—discuss with the lab.
3
NICE guidelines available at Mnice.org.uk/guidance/ng89
4
Age >35yr if pregnant or up to 6wk post partum.
430 CHAPTER5 Haematology
Warfarin
$ Antagonizes the vitamin K- dependent synthesis of factors II, VII, IX,
and X.Warfarin slows clot formation, as measured by theINR.
CounsellingAdvise the patient of the risks and benets of therapy and dis-
cuss the need for compliance with INR monitoring. Discuss large number
of drug interactions and the need to inform doctors of warfarin therapy
before starting any new medication (Ep. 72).
LoadingInitiate according to local guidelines. LMWH is usually continued
until INR is within the therapeutic range.
Target INRThis will generally be in the range 2– 3. In those with prosthetic
heart valves, or previous thromboembolism while on warfarin, higher
targets (range 3– 4) may be required, despite increased bleedingrisk.
Treatment durationTreatment is lifelong for most indications (or until risks
>benets). In DVT/ PE, treatment should be reviewed at 3mth, and early
cessation considered where a clear, temporary provocative factor can
be identied.
Stopping warfarin Stopping for a procedure may require no additional
cover (low- risk indications eg AF) or cover with heparin (LMWH or
unfractionated according to local policy). 2Never stop anticoagulation in
patients with cardiac stents or metallic valves without consultation with
cardiologists. Metallic mitral valves carry a much higher risk of thrombus
formation than valves in the higher pressure aortic position.
Discharging patients Discharging requires suitable anticoagulation service
follow- up to be in place, with current dosing documented (eg UK ‘yellow
book’).
For management of raised INR when on warfarin, see Box 5.2.
2Box 5.2 Management ofraisedINR on warfarin
No bleeding
INR5– 8
• Withhold –2
doses of warfarin
• Reduce
subsequent
maintenance dose
INR>8
• Stop warfarin
• PO vitamin K –5mg
• Repeat dose of
vitamin K if INR
remains high after 24h
Minor bleeding
INR5– 8
• Stop warfarin
• IV vitamin K –3mg
• Repeat dose of
vitamin K if INR
remains high after 24h
INR>8
• Stop warfarin
• IV vitamin K –3mg
• Repeat dose of
vitamin K if INR
remains high after 24h
Major bleeding
• Stop warfarin
• Give vitamin K 5mg
STAT IV
• Consider factors II,
VII, IX,andX
• Prothrombin
complex
concentrate
(eg Beriplex
Octaplex
if prothrombin
complex unavailable.
Always look for cause of raised INR. If required, warfarin can be restarted when INR <5.
®
), FFP
®
/
Chapter6
Skin andeyes
2Rash emergency 432
Rash 433
Bacterial infections causing a rash 434
Viral infections causing a rash 436
Fungal infections causing a rash 438
Infestations causing a rash 438
Chronic inammatory rashes 439
Other causes of rash 440
Skin lumps 442
Skin cancers 444
Leg ulcers 446
2Acute red eye emergency 448
Sudden visual loss 45
Gradual visual loss 452
Other visual disturbances 453
431
432 CHAPTER6 Skin andeyes
2Rash emergency
3Call for senior help early if patient unwell or deteriorating.
•
5L/ min O
•
Monitor pulse, BP, put on debrillator ECG leads ifunwell
• Obtain a full set of
• Take
•
Examine patient: skin examination and condensed CVS, RS,abdo
• Establish likely causes and rule out
• Look for the ndings listed in Table 6. which may aid diagnosis.
Table 6. Features ofserious causes ofrash
Finding Life- threatening diagnoses to consider
Shock (iHR, dBP) Meningococcal septicaemiaEp. 435
Wheeze/ SOB
Purpura
Postoperative
Following drug
administration
Mouth involvement
if short of breath, O2 sats <94%, orunwell
2
observations including temp, BP,andRR
history if possible/ check notes/ ask wardsta
seriouscauses
Allergic reaction/ anaphylaxisEpp. 474–5
Necrotizing fasciitisEp. 435
Toxic epidermal necrolysis (TEN) E p. 440
Allergic reaction/ anaphylaxis E pp. 474–5
Meningococcal septicaemia (Fig.6.) E p. 435
Necrotizing fasciitisEp. 435
Allergic reaction/ anaphylaxis E pp. 474–5
Allergic reaction/ anaphylaxisEpp. 474–5
Erythema multiforme majorEp. 440
TEN/ Stevens– Johnson syndrome (SJS) E p. 440
Allergic reaction/ anaphylaxisEpp. 474–5
Erythema multiforme majorEp. 440
TEN/ SJSEp. 440
Meningococcal septicaemia E p. 435
Fig.6. Meningococcal septicaemia in a young infant with purpura.
Reproduced from Lewis- Jones, S.Paediatric Dermatology 200, with permission
from Oxford UniversityPress, 978099208388.