(see relevant section)

• Vaso-occlusive crisis (VOC)
• Acute chest syndrome (ACS)
• Fever and sepsis
• Osteomyelitis 
• Acute anaemia
• Acute stroke and other CNS complications
• Acute hepatobiliary complications
• Priapism
• Acute renal failure
• Blood transfusion
• Hydroxycarbamide

Symptoms and signs

• Severe pain (usually in extremities, back or abdomen)
• Dehydration
• Enlarged liver or spleen
• Bone pain
• Low grade fever (<38°C) even in absence of infection

History

• Is pain similar to that of a sickle cell crisis or is it different in any way?
• Analgesia already taken for current episode?
• Any precipitating factors - infections, dehydration, stress, exercise, temperature extremes?
• Any complicating factors:
  • shortness of breath/cough/chest pain?
    • if YES consider ACS
  • headache/neurological symptoms
    • if YES undertake full neurological examination see Acute stroke and other complications
  • abdominal pain/priapism
  • features to indicate infection
  • assess features of other non sickle related presentations
• Previous SCD admissions and complications?
• Other medical history
• Use age-appropriate pain score

Observations/examination

• Temperature, pulse, BP, respiratory rate and oxygen saturations on air
• Hydration status
• Enlarged liver or spleen
• If neurological symptoms/headache – full neurological findings 
  
  • fever – low grade temperature <38°C can occur in absence of infection

Investigations

• FBC and reticulocyte count
  
  • check whether Hb and reticulocyte count similar to patient’s baseline 
  • reticulocytopenia may indicate virus-induced bone marrow aplasia - send parvovirus serology
• Group and screen (G&S) 
  
  • in new patients, obtain full red cell phenotype
• U&E, LFT, CRP
• If fever or relevant symptoms or signs, septic screen (including blood cultures, MSU, throat swab)
• If chest or abdominal signs - CXR 
• If O₂ saturations <95% or concerns re acute chest syndrome - ABG
• If new to trust - Hb electrophoresis
• If abdominal signs - CXR, abdo XR +/- USS
• If diarhoea/abdominal pain on desferrioxamine (Desferal^®) chelation - screen Yersinia on blood and stool and stop desferrioxamine
• If history of trauma or unexplained swelling - consider X-ray (not indicated routinely)

Analgesia

• Select pain assessment tool (PAT)
• Document pain assessment score using appropriate tool 
• Administer first dose of analgesia within 30 min of presentation to clinical area
• Ensure drug, dose and administration route are suitable for severity of pain and age of patient
• Refer to patient’s individual care plan if available
• Not all patients require opioid analgesia (although many do)
• Offer a bolus of strong opioid to all patients presenting with:
  
  • severe pain
  • moderate pain not relieved by analgesia already taken

Non-opioid and weak-opioid analgesia

• If no contraindications, offer all the following regularly:
  
  • paracetamol 1 g oral 6-hrly
  • if well hydrated and eGFR ≥30 mL/min, ibuprofen 400 mg oral 8-hrly or alternative NSAID
  • dihydrocodeine 30-60 mg oral 4-6 hrly (maximum 240 mg/24 hr) or tramadol 50-100 mg 6-hrly (maximum 400 mg/24 hr)
• Review doses in presence of renal impairment 

Opioid analgesia for severe pain

• Opiate naïve with weight ≤50 kg; morphine 2.5-5 mg SC/oral usually 2-4 hrly
• Opiate naïve with weight >50 kg; morphine 5-10 mg SC/oral usually 2-4 hrly
• Non-opiate naïve; morphine 5-10 mg SC/oral usually 2-4 hrly
• Do not use pethidine for treating pain in an acute sickle cell episode (associated with seizures, muscle abscesses and contractures). Named patient basis only
• Avoid IV morphine to limit need for canulation and preserve (often difficult) venous access. SC morphine is just as efficacious as IV for most patients
  
  • if IV morphine indicated on individual patient plan - give morphine 0.1-0.15 mg/kg IV (maximum 10 mg) over 5 min up to every 2 hr
• Consider patient controlled analgesia (PCA) once initial pain under control

Auxiliary medications

• Ensure regular laxatives prescribed
• Prescribe antiemetics e.g. ondansetron 8 mg 12-hrly
• Prescribe PRN antipruritic medication e.g. loratadine 10 mg once daily 

Monitoring

• Assess analgesia effectiveness 30 min after administration
  
  • consider repeating/increasing dosage according to efficacy 
• 30 min and 1 hr after analgesia, monitor;
  
  • full observations 
  • sedation score 
  • pain score
• Assess pain every 30 min until satisfactory pain relief achieved, then monitor at least every 4 hr (use pain score) 
• Monitor patient observations 4-hrly; or more frequently if clinical concerns 
• If respiratory rate <8 per min, patient unrousable or cyanosed - manage as opioid-induced respiratory depression 
  
  • stop all opiods
  • call for urgent medical assistance
  • administer naloxone 80 microgram IV as slow IV bolus. Further doses may be required. See Naloxone guideline in surgical guidelines and call emergency response team

Fluid replacement

• Encourage oral fluids 2-3 L/day
• IV fluids should only be used if patient is dehydrated or unable to drink
• Ensure accurate fluid balance chart maintained
• Do not canulate veins in ankles/feet as high risk of leg ulceration 
• If unable to give orally, give glucose (4%) and sodium chloride (0.18%) 1 L by IV infusion over 
  3 hr; 
• then follow IV fluid maintenance guideline

Oxygen therapy

• Of doubtful use if patient is not hypoxic
• Monitor pulse oximetry with regular readings on air and on oxygen (if in use)
• If O₂ <95% on air;
  
  • urgent medical review - ?acute chest syndrome ?opiate-induced respiratory suppression ?infection/PE/other
  • start oxygen 2-4 L/min by mask/nasal canulae - see Hypoxaemia guideline
  • if O₂ <95% on air, check ABG 
  • increase frequency of observations 
• If SpO₂ cannot be maintained >94%, discuss with haematology team and critical care team 

Blood transfusion (see transfusion section or regional guidelines for further details)

• Not indicated in uncomplicated painful crisis
• No evidence it shortens duration of crisis
• Baseline Hb often 60-90 g/L in HbSS patients. Transfusion may cause harm through hyperviscosity
• Do not exceed 10-20 g/L above baseline (or baseline if steady state >100g/L) especially if HbS >30%
• Discuss with haematology team before any transfusion
• Ensure special blood requirements met (extended phenotype matched, HbS negative)
  
  • link closely with transfusion laboratory 

Antimicrobials

• If temperature >38°C undertake septic screen and start sepsis pathway
  
  • focus antibiotics to likely source of infection - see trust guidelines
• If no active infection, continue prophylactic antimicrobials (if routinely taking)

Infection control alerts

• Check IC alert
• If IC alert not available, check previous 12 months of microbiology reports
• If MRSA present, treat as tagged for MRSA. See MRSA management guideline
  
  • if ESBL, MGNB, CARB present, treat as tagged for ESBL. See ESBL/MGNB/CARB management guideline

Thromboprophylaxis

• Unless contraindicated, give thromboprophylaxis
• see VTE prophylaxis guideline

Supportive treatment

• Offer incentive spirometry
• Folic acid 5 mg once daily
• Ensure antiemetics/laxatives prescribed

Ongoing Management

• Monitor patients closely
  
  • to determine the effectiveness of analgesia, using a pain-scoring tool
  • assess vital signs including sedation score for adverse effects of analgesia 
• Use incentive spirometry to reduce basal atelectasis 
• Haematology team may discuss patients with difficult pain management with specialist haemoglobinopathy team (Sandwell and West Birmingham Hospitals) or acute pain team
  
  • no role for palliative care input 

Discharge following VOC and follow-up

• Discharge home when pain controlled by oral medication
• Provide 3-4 days' supply of analgesia
• Schedule timely follow-up review in red cell clinic
• Before leaving hospital ensure information given (NICE quality standard 2014) on how to: 
  
  • access specialist support
  • get extra medication 
  • manage any side effects of treatment
  • See intranet > haematology > Patient information leaflets > SCD Care following discharge

• Acute life-threatening complication of SCD
• Characterised by breathlessness, hypoxia, fever and new onset pulmonary infiltrates in CXR 
  
  • leading cause of premature mortality in SCD 
  • third most common cause of death in adults
  • mortality 3% even with optimal care
• Early recognition and prompt escalation with specialist support is essential
• Discuss urgently with haematologist
• Have low threshold for involvement by local critical care outreach services

Clinical presentation

• In 50% cases preceded by 24-72 hr history of more typical VOC
  
  • increased risk in postpartum and post-operative periods
• Patients may appear well compensated initially, followed by rapid deterioration - have low threshold for escalation
• Symptoms include:
  
  • chest pain - especially sternal or rib pain 
  • shortness of breath
  • increasing oxygen requirement
  • fever
• On examination
  
  • hypoxia
  • tachycardia
  • dullness to percussion
  • crackles, bronchial breathing, wheeze or reduced air entry 
• Hypoxia is a particularly important sign
• Closely monitor and rapidly escalate patients if:
  
  • fall in SaO₂ of 3% from baseline, or 
  • SaO₂ <95% on air 
  • consider other contributors to hypoventilation e.g. inadequate pain relief, opioid induced narcosis

Investigations

• If SpO₂ <95% on room air, ABG 
• Room air ABG unless
  
  • patient in obvious respiratory distress
  • if oxygen stopped briefly and SpO₂ saturations fall to <85% 
• FBC and reticulocytes - fall in baseline Hb of >10 g/L or a fall in platelets predict morbidity
• Renal function, liver function and CRP 
• G&S: inform blood bank that patient has sickle cell anaemia to allow appropriate products to be requested 
• CXR - note changes may lag behind clinical picture. Bilateral infiltrates are typical of ACS
• Sputum for MC&S
• Respiratory viral PCR (either swab or nasopharyngeal aspirates as per local protocols)
• Atypical serology (on presentation and repeated at 3 weeks)
• Urinary legionella and pneumococcal antigen
• Blood cultures in febrile patients

Potential precipitants and differential diagnosis

• Respiratory infections 
  
  • identifiable as a precipitant in 38% of cases
• Pulmonary embolism
  
  • can co-exist or precipitate chest crisis
  • history is usually of more sudden onset
  • patient recognises pain as not typical of sickle cell
  • D-dimer is invariably raised
  • consider CTPA or VQ if there is clinical suspicion of PE 
• Patients with pre-existing respiratory disease
  
  • patient with asthma at increased risk of ACS
• Fluid overload in at risk populations 
  
  • consider if cardiac disease, renal impairment, transfusion associated fluid overload (TACO)

Severity assessment

• Increased morbidity seen with following features:
  
  • increasing oxygen requirement
  • increasing respiratory rate 
  • decreasing platelet count 
  • fall in Hb from baseline of 10 g/L 
  • neurological symptoms 
  • multi-lobar involvement on CXR

Management

• Contact on-call haematologist early in any patient suspected of ACS
• Regular observations
  
  • to include pulse rate, blood pressure, respiratory rate and pulse oximetry
  • at least 4-hrly or as per EWS
  • more frequently if on PCA or clinical concerns
• Analgesia as per VOC guidance 
• IV crystalloid until patient able to maintain hydration orally
  
  • monitor fluid balance every 24 hr
• Give parenteral antibiotics to all patients with ACS
  
  • refer to local microbiology protocols for severe community acquired pneumonia
  • ensure atypical organisms are covered
• Physiotherapy
  
  • refer all patients for same day evaluation by chest physiotherapist
  • offer all patients incentive spirometry to aid lung expansion
• Thromboprophylaxis with low molecular weight heparin 
  
  • unless absolute contraindication
• Transfusion - may be life-saving 
  
  • involve haematology specialist from outset
  • if at risk of further deterioration - initiate transfusion early 
  • consider early top-up in hypoxic patients with severe anaemia (Hb<70g/L) to prevent futher deterioration 
• If deteriorating patient or Hb >90 g/L, exchange transfusion - discuss with haemoglobinopathy co-ordinating centre to arrange
  • undertake in HDU setting

• Patients with SCD are at increased risk of severe infections due to functional asplenia
  
  • sources of infection are chest, urine, osteomyelitis, indwelling central venous access devices (CVAD) and hepatobiliary 
• Complete sepsis 6 - See Sepsis guideline
• Low grade temperature <38°C can occur with vaso-occlusive crisis in the absence of infection
• If temperature ≥38°C and/or suspected sepsis ensure
  
  • full clinical review 
  • septic screen: cultures of blood, urine, and any other potential sites of infection
  • CXR
  • if there is a history of travel to an endemic region, malaria screen 
• Antibiotics as per local antibiotic guideline 
  
  • if source unknown - broad-spectrum antibiotics to include coverage for pneumococcus and gram negative organisms, including Salmonella
  • if blood cultures become positive admit for parenteral antibiotics
• If well with isolated temperature rise consider outpatient management
• Admit to hospital if: 
  
  • acute painful crisis (severe that cannot be managed with home analgesia) 
  • suspected ACS (chest pain, breathlessness/increasing oxygen requirements, pulmonary infiltrates on CXR) 
  • dehydration, vomiting 
  • requirement for supportive care, e.g. IV fluid or oxygen 
  • unreliable compliance/support
  • consider if indwelling catheter

• Clinical presentation similar to vaso-occlusion 
  
  • pain, localised tenderness, warmth, swelling, fever and leucocytosis 
  • note bone pain more likely VOC than osteomyelitis
• Increased incidence in SCD from infection of infarcted bone
• Usually due to salmonella (especially non-typical serotypes such as Salmonella typhimurium, Salmonella enteritidis), followed by Staphylococcus aureus and gram-negative enteric bacilli
• If pain persists beyond typical VOC, or pain is atypical and fever continues, investigate:
  
  • blood cultures
  • bone biopsy/aspiration in selected cases - positive result confirms diagnosis
  • imaging - plain X-rays and MRI are not sufficiently discriminating to differentiate 
• Discuss management with haematologist and orthopaedic surgeon
  
  • broad spectrum antibiotics to cover salmonella and staphylococcus pending culture results
    
    • if organism isolated, tailor choice of antibiotic 
  • continue antibiotics for 6 weeks
  • drainage for fluid accumulation that does not respond to antibiotics

• Patients with SCD have a variable degree of anaemia 
  
  • due to ongoing intravascular and extravascular haemolysis
  • tolerate anaemia well in the steady state
  • may become symptomatic of anaemia if rapid, significant fall in Hb - usually of at least 20 g/L
• Worsening anaemia may develop due to: 
  
  • increased haemolysis e.g. infection, VOC, G6PD deficiency, transfusion reaction 
  • reduced erythropoiesis e.g. parvovirus infection, medications
  • blood loss e.g. bleeding
  • sequestration of blood e.g. spleen sequestration (commoner in milder phenotypes), liver sequestration
• May be multiple co-existing causes for acute anaemia 
• Take into account history of bleeding, infection, travel, malaria risk, medications e.g. hydroxycarbamide, organomegaly, transfusion 
• Investigations to include:
  
  • reticulocyte count
  • LFTs including unconjugated bilirubin
  • direct Combs test (DCT)
  • G6PD assay (in steady state)
  • malaria screen (if relevant travel history)
  • parvovirus serology (?positive IgM)
  • infection screen
  • clinical examination for rapidly enlarging painful splenomegaly/hepatomegaly

• Adults with SCD at risk of both acute ischaemic and haemorrhagic stroke 
  
  • risk of acute ischaemic stroke increasing with older age
• Acute presentations can include: 
  
  • headache
  • seizures
  • focal neurological signs
  • visual impairment
  • altered consciousness 
  • acute deterioration in cognition
• Emergency neuroimaging required in adults presenting with symptoms of transient ischaemic attack (TIA) or stroke 
• Urgent review by neurologist and haematologist 
  
  • manage in hyperacute stroke unit with access to multidisciplinary support from a haemoglobinopathy specialist centre, vascular interventional neuroradiology, neurology and neurosurgery
  • urgent red cell exchange recommended for patients with a sickle related acute ischaemic stroke - target HbS <30%
  • in older patients with risk factors for non-sickle stroke, discuss requirement for thrombolysis with multidisciplinary team (including haemoglobinopathy coordinating centre)
  • consider other causes of stroke seen in young adults without SCD - e.g. thrombophilia, CNS infection, illicit drug use, arterial dissection, congenital heart disease
• Headache - common symptom and in most cases do not indicate significant CNS pathology
  
  • consider possibility of intracranial haemorrhage, central venous thrombosis, CNS infection and ischaemic stroke 

• Painful and prolonged (>4 hr) penile erection unrelated to sexual stimulus
• This is an emergency - urgent urological and haematological input required
  
  • can impact significantly on erectile and sexual function
  • delayed therapy of acute priapism can lead to impotence
• Lifetime incidence of priapism high 
  
  • majority of cases first episode occurs before aged 20 yr
• Stuttering priapism
  
  • short episodes (<4 hr) of recurrent or intermittent ischaemic priapism 
  • self-limiting but can lead to a more sustained or fulminant episode
• Fulminant priapism
  
  • acute ischaemic event requiring emergency treatment
  • early recognition and initiation of treatment may achieve detumescence 
• Assess:
  
  • duration of episode
  • presence of pain
  • previous priapism and treatment
  • any trauma
  • medications including analgesia
  • recreational drugs
  • other complication of SCD
• Initial management includes:
  
  • exercise e.g. going up and down stairs
  • adequate pain relief
  • hydration
  • encourage to empty bladder
  • offer etilefrine if available (alpha adrenergic agent)
• Early urgent urological review for consideration of surgical intervention
  
  • penile aspiration of stagnant blood under anaesthesia to decompress the corpora carvenosum potentially followed by shunt procedure
  • aim is to relieve penile ischaemia and to preserve erectile function
  • results are however variable
• Transfusion
  
  • no evidence for efficacy
  • consider before surgery

• May be due to:
  
  • vaso-oclusion
  • gall stone complications
  • infection
  • unrelated diseases
• Manage in partnership with haematology, gastroenterologists, upper GI surgeons and microbiologists with experience of SCD
• Imaging to include:
  
  • ultrasound - to look for gallstones in the gallbladder and/or common bile duct 
  • magnetic resonance cholangiopancreatography (MRCP) - if ultrasound has not detected common bile duct stones but bile duct dilated and/or liver tests abnormal

Gallstones

• Common in SCD
• Complications may develop due to: 
  
  • infection and inflammation of the gall bladder and biliary duct (acute cholecystitis, gallbladder empyema, ascending cholangitis) 
  • obstruction of biliary ducts 
  • acute pancreatitis
• Management to include:
  
  • early antibiotics in view of infection risks - broad spectrum including cover for salmonella species and anaerobic organisms
  • if symptomatic (occurs in 20%) refer for laparoscopic cholecystectomy
  • if common bile duct stones refer for bile duct clearance (ERCP) then laparoscopic cholecystectomy 
  • elective cholecystectomy appropriate after acute complications settle - more urgent treatment indicated in some instance
  • preferentially use laparoscopic route as fewer postoperative complications and shorter length of stay 
  • if asymptomatic, inform of gallstone complications and manage as per general population

Jaundice

• Present in patients with SCD - baseline degree individual to patient 
• Elevation in baseline bilirubin can occur with:
  
  • haemolysis - often exacerbated in VOC
  • consider delayed transfusion reaction and hyperhaemolysis
  • obstructive causes such as gallstones, biliary sludge
  • intrahepatic cholestasis
• Intrahepatic cholestasis is an uncommon but severe form of sickle hepatopathy due to intrasinusoidal sickling and intracanalicular cholestasis
• Acute presentation can include:
  
  • severe right upper quadrant pain
  • acute hepatomegaly
  • coagulopathy
  • extreme hyperbilirubinemia (mainly conjugated) but moderately elevated liver enzymes
• Some patients can progress to acute hepatic failure
• Exclude other causes of liver dysfunction through USS/Magnetic Resonance Cholangiopancreatography (MRCP) imaging
• Biopsy is relatively contraindicated in acute hepatopathy in SCD due to the risk of bleeding and other complications
• Early exchange transfusion can improve outcome and reduce mortality

• ARF can be precipitated by: 
  
  • dehydration
  • sepsis
  • drugs e.g. NSAIDs, intravenous contrast
  • in the context of multi-organ failure 
  • on the background of chronic renal failure (either from sickle related nephropathy or other aetiologies) 
• ARF may be due to 
  
  • pre-renal aetiologies (e.g. dehydration)
  • intrinsic renal pathology
  • or post renal causes
• Management of ARF 
  
  • follow similar principles as in other patient groups
  • careful fluid balance and close monitoring of renal function in all patients
  • jointly with renal physician
• Haematuria 
  
  • consider renal papillary necrosis (vaso-occlusion of vasa- recta)
  • may cause clot colic
  • offer conservative management - hydration 

General principles

• All patients should carry a transfusion card with details: 
  
  • ABO group, extended red cell phenotype, Rh phenotype and 
  • existence of any red cell alloantibodies (current and historic) 
• Transfusion history is important, particularly if care is a different hospital 
  
  • liase with transfusion laboratory at primary hospital to obtain transfusion history
• Advise transfusion laboratory/blood bank that transfusion is for a patient with SCD
• Discuss with haematology to determine if simple top-up or exchange transfusion needed 
• Determine post-transfusion target Hb and HbSS
• Record and document transfusion triggers and indications 
• Monitor closely both during and after completion of transfusion for:
  
  • immune haemolytic transfusion reaction (IHTR)
  • delayed haemolytic transfusion reaction (DHTR) and 
  • hyper haemolysis
• All patients to have annual viral screening for Hepatitis B, C and HIV 1 and 2 

Venous access

• Simple top-up transfusion: single peripheral venous cannula 
• Manual exchange transfusion: 2 separate large bore venous access
  
  • one for transfusion and inlet port (wide bore needle grey/orange) and 
  • another for venesection (vascath: femoral/central neck line) 
• Automated red cell exchange: femoral line/vascath - double lumen 
• Long-term transfusion programme: consider port-a-cath 

Top-up transfusion

Indications

• Severe anaemia (Hb <50 g/L) owing to: 
  
  • hepatic or splenic sequestration
  • red cell aplasia or haemolysis
• Severe anaemia when decrease in Hb >20% from baseline in a symptomatic patient (heart failure, dyspnoea, hypotension and marked fatigue)
• Transfuse to baseline Hb (patient’s Hb in steady state)
• Consider when exchange transfusion indicated and starting Hb <50 g/L 
• Discuss with haematologist

Exchange transfusion

Indications

• Severe chest syndrome 
• New ischaemic stroke
• Multi-organ failure
• Consider in priapism
• Do not initiate exchange transfusion before discussing with haematologist

Targets

• To reduce HbS to <30%
• To maintain Hb <100 g/L
  
  • note: haematocrit of donor blood is approximately double that of patient
• To maintain steady blood volume throughout procedure

Venous access

• Ideally, identify 2 ports for venous access; 1 for venesection, the other for transfusion
  
  • in emergency, consider a central line, or arterial line (e.g. on ITU)
• Exchange transfusion is performed isovolaemically (equal quantities in and out)
• Ensure patient well hydrated before exchange
  
  • prehydrate with sodium chloride 0.9% 500 mL if Hb >80 g/L

Method

• Procedure and regimen will depend on investigations and must be discussed with haematologist 

• Licenced for use in SCD
• Commenced by dedicated red cell team
• Continue hydroxycarbamide during admissions unless cytopenia (see below) or toxicity suspected 
• Reduces frequency of VOC, ACS, need for blood transfusion, hospitalisation and mortality in adults with SCD
• Works by increasing Hb F levels, reducing surface expression of adhesion molecules, reducing bone marrow production of neutrophils and reticulocytes, improving red cell rheology, and improving nitric oxide availability
• Indicated in adult patients if:
  
  • SS/Sβ 0 with ≥3 moderate to severe pain crises in a 12 month period 
  • SS/Sβ 0 who have a history of severe and/or recurrent ACS
  • SS/Sβ 0 who have sickle associated pain or severe symptomatic anaemia that interferes with quality of life or activities of daily living
  • consider in SCD with genotypes other than SS/Sβ 0 who have recurrent acute pain, acute chest syndrome or episodes of hospitalisation; or for other indications on a case-by-case basis
• Contraindicated in pregnancy 
• Dose dictated by weight, clinical response, blood test monitoring
• Side effects include cytopenia, hyperpigmentation of nails/skin, GI toxicity including diarrhoea and constipation, nausea and vomiting, skin rash, alopecia, oral ulcers, azoospermia/oligospermia
• Offer male patients sperm cryopreservation before commencing treatment
• Prescribed by secondary care (unless formulary agreement with primary locally)
• Monitoring bloods 8-12 weekly bloods once dose established, to include FBC, reticulocytes, U&E, LFT
• Stop hydroxycarbamide if any of the following apply:
  
  • neutrophils <1.0 x 10⁹/L
  • platelets <80 x 10⁹/L
  • reticulocytes <1% 
  • Hb 30 g/L below baseline
  • Hb >120 g/L or rise >30 g/L above baseline
• Link with red cell team regarding recommencement (with dose reduction)