Haematology Nursing Guide – GCC Nurse Exam Prep

Blood Disorders Overview

Full Blood Count (FBC) Interpretation

Parameter	Normal Range (Adult)	Clinical Significance
Haemoglobin (Hb)	M: 130–175 g/L \| F: 120–160 g/L	Low = anaemia; monitor trends not single value
MCV	80–100 fL	Classifies anaemia (micro/normo/macrocytic)
MCH	27–33 pg	Amount of Hb per RBC; low in IDA
MCHC	315–360 g/L	Hb concentration per RBC; elevated in hereditary spherocytosis
WBC Differential	4–11 ×10⁹/L total	Neutrophils (1.8–7.5), Lymphocytes (1–4), Eosinophils (<0.5)
Platelets	150–400 ×10⁹/L	<100 = thrombocytopenia; <50 = significant bleed risk; <20 = spontaneous bleeding risk
Reticulocytes	0.5–2.5%	High = bone marrow responding (haemolysis/acute blood loss); Low = hypoproliferative cause

Anaemia Classification by MCV

Microcytic (MCV <80 fL)

IDA – Iron deficiency anaemia (most common worldwide)
Thalassaemia – alpha or beta; very prevalent in GCC
Sideroblastic anaemia – ring sideroblasts on marrow biopsy
Anaemia of chronic disease – can be microcytic in severe/prolonged cases

⚠IDA vs thalassaemia trait: both microcytic but ferritin normal/high in thalassaemia; use Mentzer index (MCV/RBC count: <13 suggests thalassaemia)

Normocytic (MCV 80–100 fL)

Anaemia of chronic disease (ACD)
Haemolytic anaemia – raised LDH, low haptoglobin, raised bilirubin
Aplastic anaemia – pancytopenia + hypocellular marrow
Acute blood loss
Renal anaemia – low EPO production

Macrocytic (MCV >100 fL)

B12 deficiency – neurological symptoms (subacute combined degeneration), vegans at risk
Folate deficiency – pregnancy demand, methotrexate, phenytoin
Liver disease
Hypothyroidism
Drugs – hydroxyurea, azathioprine, alcohol

Iron Studies Interpretation

Test	IDA	ACD	Iron Overload	Notes
Ferritin	↓ Low	Normal/↑ High	↑↑ Very high	Acute phase reactant – may be falsely elevated in inflammation, infection, malignancy
Serum Iron	↓ Low	↓ Low	↑ High	Diurnal variation – sample in morning
TIBC	↑ High	↓ Low/Normal	↓ Low	Total iron binding capacity reflects transferrin
Transferrin Saturation	↓ <16%	↓ Low	↑ >45%	Gold standard for functional iron deficiency assessment

Iron Deficiency Anaemia (IDA) – Nursing Management

Causes

Blood loss – menorrhagia (most common in women), GI bleeding (PUD, colorectal cancer), haematuria
Malabsorption – coeliac disease, post-gastrectomy, IBD
Increased demand – pregnancy, lactation, rapid growth in infancy/adolescence
Inadequate intake – rare in isolation; dietary assessment important

Treatment & Nursing Considerations

Oral iron: Ferrous sulfate 200 mg TDS (65 mg elemental iron per dose). Take on empty stomach. Vitamin C enhances absorption
Counselling: Dark/black stools expected (reassure patient), constipation common (increase fluids/fibre, consider laxative), nausea (take with food if severe – reduces absorption)
Duration: Treat for 3 months after Hb normalises to replenish stores
Response: Reticulocyte rise at 7–10 days; Hb rise ~10 g/L per week

⚠ IV Iron (Ferinject/Monofer/Cosmofer): Indicated when oral iron not tolerated, malabsorption, IBD, pre/post surgery, non-compliance, or rapid correction needed. ANAPHYLAXIS RISK – administer only where resuscitation equipment and trained staff available. Test dose may be required (product-specific). Monitor for 30 minutes post-infusion. Hypersensitivity reactions can be delayed. Document batch number.

GCC Relevance

The GCC population has among the highest rates of haemoglobinopathies globally. National premarital screening programmes (UAE, Saudi Arabia, Qatar, Kuwait, Bahrain, Oman) screen couples for sickle cell and thalassaemia traits to reduce trait × trait marriages and affected offspring. Nurses play a key role in pre-test counselling and result communication.

Haemoglobinopathies

Sickle Cell Disease (SCD)

Pathophysiology

SCD is caused by a point mutation (GAG→GTG) in the beta-globin gene producing abnormal haemoglobin S (HbS). Under deoxygenation, HbS polymerises, causing RBCs to adopt a rigid sickle shape. These cells occlude small vessels (vaso-occlusion), causing ischaemia and pain, and are haemolysed prematurely (haemolytic anaemia).

HbSS

Most severe – sickle cell anaemia

HbSC

Milder; retinal complications common

HbS/β-Thal

Severity depends on β-thal type

HbAS

Sickle trait – usually asymptomatic

SCD Complications & Nursing Management

Vaso-Occlusive Crisis (VOC)

Presentation: Severe bone/joint/abdominal pain, no objective findings
Triggers: Cold, dehydration, infection, stress, hypoxia
Analgesia ladder: Paracetamol 1g QDS → NSAIDs (ibuprofen 400 mg TDS) → Weak opioid (codeine) → Strong opioid (morphine IV/SC, oxycodone)
Fluids: IV/oral hydration 2–3 L/day – avoid over-hydration
Warmth: Warm packs to painful areas (cold worsens sickling)
Oxygen: Only if SpO₂ <95% – routine O₂ not recommended
Monitoring: Pain score hourly; opioid side effects; respiratory rate

Acute Chest Syndrome (ACS) – EMERGENCY

⚠ACS = new pulmonary infiltrate + one of: chest pain, fever, SpO₂ fall, respiratory distress. Leading cause of death in SCD adults.

Immediate O₂ to maintain SpO₂ >95%
Antibiotics: co-amoxiclav + clarithromycin (atypical cover)
IV fluids – avoid overload (worsens pulmonary oedema)
Incentive spirometry (prevents atelectasis)
Simple transfusion (Hb <60 g/L) or exchange transfusion (rapidly worsening – preferred)
Escalate immediately to haematology + ITU review if deteriorating

Other Acute Complications

Stroke: Silent cerebral infarction common in children. Transcranial Doppler (TCD) screening annually in children 2–16; elevated velocity triggers prophylactic transfusion programme (maintain HbS <30%)
Aplastic Crisis: Parvovirus B19 infects erythroid precursors → reticulocytopenia → rapid Hb fall. Treat with transfusion; isolate from immunocompromised patients (infectious)
Splenic Sequestration: Acute trapping of blood in spleen; most common in children under 5. Presents as acute hypotension + rapidly enlarging spleen + falling Hb. Emergency transfusion. Risk of recurrence → prophylactic splenectomy
Priapism: Painful prolonged erection; treat with hydration, analgesia, aspiration ± transfusion. Urological emergency if >4 hours

Disease-Modifying Therapy

Hydroxyurea (hydroxycarbamide): Stimulates HbF production (HbF dilutes HbS, reduces polymerisation). Reduces VOC frequency by ~50%, ACS risk, transfusion requirement. Monitor: FBC (myelosuppression), creatinine. Teratogenic – contraception counselling essential
Prophylactic penicillin V: Lifelong in all SCD patients (functional asplenia → encapsulated organism susceptibility). Pneumococcal, meningococcal, Hib vaccinations
Folic acid 5 mg daily: Haemolytic anaemia increases folate demand
Bone marrow transplant: Potential cure; best outcomes in children with matched sibling donor
New therapies: Voxelotor, crizanlizumab, gene therapy (emerging)

Thalassaemia

Classification & GCC Prevalence

Type	Genotype	Clinical Features	GCC Relevance
Alpha thalassaemia trait	--/αα or -α/-α	Mild microcytosis; usually asymptomatic	High prevalence in Saudi Arabia, Oman, UAE
Haemoglobin H disease	--/-α	Moderate haemolytic anaemia; splenomegaly	Intermittent transfusions may be needed
Beta thalassaemia trait	β/β⁺ or β/β⁰	Mild microcytic anaemia; clinically well	Carrier rate up to 4–5% in some GCC regions
Beta thalassaemia major	β⁰/β⁰	Severe anaemia from 6 months, hepatosplenomegaly, bone deformity, growth retardation	Premarital screening targets trait × trait

Thalassaemia Major – Transfusion Programme

Regular red cell transfusions every 3–4 weeks to maintain pre-transfusion Hb >90–100 g/L
Leukodepleted, extended matched red cells (to reduce alloimmunisation)
Monitor for transfusion reactions; document carefully
Splenomegaly and hypersplenism may increase transfusion requirements → splenectomy considered

Iron Chelation Therapy – Critical Nursing Role

Each unit of blood delivers ~200–250 mg iron; no physiological excretion mechanism exists
Deferasirox (Exjade/Jadenu): Oral, once daily. Side effects: GI upset, renal impairment, hepatotoxicity. Monitor U&E, LFTs monthly
Desferrioxamine (DFO): SC infusion 8–12 hours 5–7 nights/week. Compliance is the biggest challenge – patient education essential
Deferiprone: Oral TDS; risk of agranulocytosis – weekly FBC monitoring
Serum ferritin target <1000 µg/L; cardiac MRI T2* for cardiac iron monitoring
Iron overload consequences: cirrhosis, diabetes, cardiomyopathy, endocrine failure (growth, puberty)

Bleeding Disorders

Haemophilia

Haemophilia A & B

Haemophilia A: Factor VIII deficiency; ~1 in 5,000 male births
Haemophilia B: Factor IX deficiency (Christmas disease); ~1 in 25,000 male births
Inheritance: X-linked recessive; female carriers may have mildly reduced factor levels and bleed

Severity	Factor Level	Bleeding Pattern
Mild	5–40%	Surgery/major trauma only
Moderate	1–5%	Minor trauma, occasional spontaneous
Severe	<1%	Spontaneous bleeds: joints, muscles

Bleeding Patterns & Complications

Haemarthroses: Knees, ankles, elbows most common; acute: hot, swollen, painful joint; chronic: haemophilic arthropathy (irreversible joint damage)
Muscle haematomas: Iliopsoas (presents as hip flexion + groin pain, can compress femoral nerve)
Intracranial haemorrhage: Most life-threatening; any head injury = treat first, scan second
Inhibitor development: Alloantibodies to infused factor; most common in severe HA (20–30%). Requires ITI therapy or bypass agents (rFVIIa/FEIBA)

Haemophilia Treatment

Factor Replacement Therapy

Recombinant FVIII (rFVIII): Standard treatment for HA; dose = (target % − current %) × weight × 0.5
Recombinant FIX (rFIX): For HB; dose = (target % − current %) × weight × 1.0 (longer half-life)
Prophylaxis: Regular infusions 2–3×/week in severe haemophilia to prevent haemarthroses
On-demand: Treat bleeds as they occur (less preferred)
Extended half-life products: PEGylated/Fc-fusion products allow less frequent dosing

DDAVP & Non-Factor Therapies

DDAVP (desmopressin): IV/SC/intranasal; releases stored FVIII from endothelial Weibel-Palade bodies. Effective in mild HA (raises FVIII 3–6×). Not effective in HB. Test dose before relying on it (variable response). Side effects: fluid retention, hyponatraemia, facial flushing, tachycardia
Emicizumab (Hemlibra): Subcutaneous weekly/fortnightly/monthly. Bispecific antibody mimicking FVIII function. Effective for HA with and without inhibitors. Revolutionised prophylaxis. Monitoring: anti-Xa levels if using concurrent bypass agents (TMA risk with aPCC)
Tranexamic acid: Adjunct; antifibrinolytic; useful for mucosal bleeds, dental procedures

Von Willebrand Disease (VWD)

Most common inherited bleeding disorder – affects ~1% of population. VWF is a multimeric plasma protein essential for platelet adhesion and as a carrier for FVIII.

Type	Description	Treatment
Type 1 (most common, ~75%)	Partial quantitative deficiency of VWF	DDAVP usually effective; tranexamic acid for mucosal bleeds
Type 2 (qualitative defect)	Subtypes 2A/2B/2M/2N – structural/functional abnormality	VWF concentrate (DDAVP contraindicated in 2B – may cause thrombocytopenia)
Type 3 (rare, severe)	Near-complete absence of VWF	VWF concentrate; FVIII may also be low

ⓘVWD symptoms: easy bruising, epistaxis, menorrhagia, prolonged bleeding post-surgery/dental. Clotting screen: normal PT, prolonged/normal APTT, reduced VWF antigen and activity (ristocetin cofactor assay).

Immune Thrombocytopenic Purpura (ITP)

Pathophysiology & Diagnosis

Autoimmune destruction of platelets by IgG autoantibodies (anti-GPIIb/IIIa most common)
Diagnosis of exclusion: platelet <100 ×10⁹/L with no other identifiable cause
Acute ITP: children, usually post-viral, self-limiting
Chronic ITP: adults, >12 months duration
Symptoms vary with platelet count: <50 = bruising/petechiae; <20 = spontaneous mucosal bleeds; <10 = ICH risk
Bone marrow biopsy if age >60 or atypical features (normal/increased megakaryocytes)

ITP Treatment Ladder

1st line: Prednisolone 1 mg/kg/day (4–6 weeks taper). Side effects: hyperglycaemia, hypertension, osteoporosis, immunosuppression. Monitor BM/BP/glucose
IVIG: 1 g/kg IV over 1–2 days; rapid platelet rise (48–72 hours); effect temporary (3–4 weeks). Used for active bleeding or pre-procedure. Headache common – infuse slowly
Rituximab: Anti-CD20; 375 mg/m² weekly × 4. Response in ~60%. Monitor for PML (rare), hepatitis B reactivation
TPO receptor agonists: Eltrombopag (oral) / romiplostim (SC weekly). Stimulate platelet production. Long-term use. Risk of bone marrow fibrosis (rare)
Splenectomy: Removes primary site of platelet destruction and antibody production. 60–70% long-term remission. Pre-splenectomy vaccinations mandatory (pneumococcal, meningococcal, Hib)

Heparin-Induced Thrombocytopenia (HIT)

⚠ HIT is a prothrombotic emergency – NOT just low platelets. Immune-mediated; IgG antibodies against PF4-heparin complexes activate platelets → paradoxical thrombosis despite low platelet count.

Feature	Detail
Timing	Platelet fall typically 5–10 days after heparin initiation (or within 24 hours if prior heparin exposure)
Platelet fall	Drop >50% from baseline (even if still in normal range)
Thrombosis	DVT/PE, arterial thrombosis, skin necrosis at injection sites
4Ts Score	Thrombocytopenia + Timing + Thrombosis + no oTher cause → Low/Intermediate/High probability
Diagnosis	HIT antibody ELISA (high sensitivity); functional assay (SRA – high specificity)
Action	STOP ALL heparin immediately (including heparin flushes, LMWH). Switch to argatroban (IV direct thrombin inhibitor) or fondaparinux (SC). Do NOT give warfarin until platelet >150

Thrombophilia & Anticoagulation Monitoring

Inherited Thrombophilias

Condition	Mechanism	Prevalence	VTE Risk
Factor V Leiden	Resistance to APC; FVa not inactivated	4–8% Caucasian (heterozygous)	3–8× (het); 50–80× (homo)
Prothrombin gene mutation G20210A	Elevated prothrombin levels	2–3% Caucasian	2–4× increased
Protein C deficiency	Impaired inactivation of FVa and FVIIIa	0.2–0.5%	7–10× increased
Protein S deficiency	Cofactor for protein C	0.1–0.3%	5–10× increased
Antithrombin deficiency	Reduced inhibition of thrombin + FXa	0.02–0.05%	10–50× increased (highest risk)

ⓘThrombophilia testing: do NOT test during acute VTE, acute illness, or while on anticoagulation (warfarin falsely reduces protein C/S; heparin/DOAC affects antithrombin/anti-Xa assays). Test 3 months after event and off anticoagulation.

Antiphospholipid Syndrome (APS)

Diagnostic Criteria (Revised Sapporo/Sydney)

Clinical: arterial or venous thrombosis, or pregnancy morbidity (recurrent miscarriage/late pregnancy loss)

Laboratory (must be positive on 2 occasions ≥12 weeks apart):

Lupus anticoagulant (LA) – prolonged APTT not corrected by mixing study; most thrombogenic
Anticardiolipin antibodies (aCL) – IgG/IgM; titre >40 GPL/MPL
Anti-β2-glycoprotein I antibodies – IgG/IgM; titre above 99th percentile

⚠Triple positivity (all 3 positive) carries the highest thrombotic and obstetric risk. Target INR 2–3 with warfarin for VTE; some arterial APS managed at INR 2.5–3.5. DOACs are generally NOT recommended in high-risk APS (inferior to warfarin in triple-positive patients per TRAPS trial).

Warfarin Monitoring

INR Targets

Indication	Target INR	Range
AF, DVT/PE prophylaxis/treatment, APS	2.5	2.0–3.0
Mechanical mitral valve	3.0	2.5–3.5
Mechanical aortic valve (bileaflet low-risk)	2.5	2.0–3.0
Recurrent VTE on anticoagulation	3.0	2.5–3.5

Over-Anticoagulation Reversal

INR	Bleeding	Action
5–8	None/minor	Omit 1–2 doses; restart lower dose
5–8	Minor	Vitamin K 1–5 mg oral
>8 or 5–8	Minor with risk factors	Vitamin K 5 mg oral (IV 1–3 mg for faster effect)
Any	Major/life-threatening	4-factor PCC (Beriplex/Octaplex) + Vitamin K 5–10 mg IV slow infusion
Any	Life-threatening (no PCC)	FFP 15 mL/kg (slower, volume load)

ⓘWarfarin interactions: Hundreds documented. Key interactions to know: CYP2C9 inducers (rifampicin, carbamazepine, St John's Wort – reduce INR); CYP2C9 inhibitors (fluconazole, amiodarone, ciprofloxacin, metronidazole, omeprazole – raise INR). Always check BNF/pharmacy before adding any new medication. Consistent vitamin K dietary intake (dark leafy greens) important.

DOAC Monitoring

Monitoring Principles

No routine coagulation monitoring required (designed for fixed dosing)
Dabigatran: Prolongs TT and APTT; dilute thrombin time (dTT/Hemoclot) for quantitative level
Apixaban/Rivaroxaban/Edoxaban: Drug-specific anti-Xa calibrated assay for level measurement
When levels needed: Urgent surgery, bleeding, renal impairment, extremes of weight, suspected non-compliance, drug interactions
Monitor renal function: eGFR annually (3–6 monthly if borderline). Dose adjustment/contraindication if eGFR <15–30 (product-specific)

DOAC Reversal Agents

Idarucizumab (Praxbind): Monoclonal antibody fragment; specific antidote for dabigatran. 5 g IV in 2 × 2.5 g doses. Immediate and complete reversal. Approved for life-threatening bleeding or urgent surgery
Andexanet alfa (Ondexxya): Modified FXa decoy; reverses apixaban and rivaroxaban. Given as IV bolus + infusion. High dose vs low dose regimens based on last dose timing/drug
4-factor PCC: Non-specific but used when specific agents unavailable. May have partial efficacy
Activated charcoal: If ingestion within 2–3 hours

Heparin Monitoring

Heparin Type	Monitoring Test	Target	Special Circumstances
Unfractionated heparin (UFH) IV	APTT	1.5–2.5× control (typically 60–100 seconds)	4-hourly until stable, then 12-hourly; anti-Xa if APTT unreliable (e.g., lupus anticoagulant)
LMWH (enoxaparin, dalteparin)	Anti-Xa level (4 hours post-dose)	Treatment: 0.5–1.0 IU/mL (BD) or 1.0–2.0 IU/mL (OD)	Required in: morbid obesity (BMI >40), weight <50 kg, pregnancy, eGFR 15–30 mL/min
UFH platelet monitoring	Platelet count	Baseline then Day 5–10	4Ts score if >50% fall; STOP if HIT suspected

Bone Marrow & Stem Cell Transplant Nursing

Bone Marrow Failure

Aplastic Anaemia

Definition: Pancytopenia (Hb↓, neutrophils <0.5 ×10⁹/L in severe, platelets <20 ×10⁹/L) with hypocellular bone marrow biopsy
Causes: Idiopathic (most common ~70%); drugs (chloramphenicol, carbamazepine, gold); viral (EBV, parvovirus B19, hepatitis-associated); PNH (paroxysmal nocturnal haemoglobinuria); inherited (Fanconi anaemia)
Severity: Non-severe, severe (SAA), very severe (VSAA) based on neutrophil count and marrow cellularity
Treatment <40 years + matched sibling donor: Allogeneic HSCT (curative)
Treatment >40 or no donor: Immunosuppression with ATG (anti-thymocyte globulin) + ciclosporin ± eltrombopag. Response assessed at 3–6 months
Supportive care: Transfusions (judicious – preserve future transplant), G-CSF, GCSF, antifungals, neutropenic precautions

Allogeneic HSCT (Haematopoietic Stem Cell Transplant)

Donor Types & Conditioning

Sibling donor: 25% chance of HLA-identical sibling; best outcomes
Matched unrelated donor (MUD): 10/10 or 9/10 HLA match via registries (e.g., Anthony Nolan, DATRI); higher GVHD risk than sibling
Haploidentical: 50% matched (parent/child/sibling); post-transplant cyclophosphamide protocol
Myeloablative conditioning (MAC): High-dose chemotherapy ± TBI; destroys marrow completely; for younger/fitter patients
Reduced intensity conditioning (RIC): Lower doses; relies more on graft-versus-tumour/disease effect; for older/comorbid patients

HSCT Timeline & Phases

Day -7 to 0 (Conditioning): Chemotherapy ± TBI. Severe mucositis, nausea, alopecia, hepatotoxicity, haemorrhagic cystitis (cyclophosphamide – ensure mesna co-administration, vigorous hydration)
Day 0 (Stem cell infusion): Preserve cells at -196°C; DMSO cryoprotectant causes garlic/sweetcorn odour; monitor for anaphylaxis, haemolysis, cardiac dysrhythmia during infusion
Day +1 to +14 (Aplasia): Critical period; absolute neutrophil count (ANC) at nadir; risk of bacteraemia, fungal infection (aspergillus), viral reactivation (CMV, EBV, HSV)
Day +14 to +21 (Engraftment): ANC >0.5 ×10⁹/L for 3 consecutive days = engraftment. Engraftment fever occurs. Chimerism testing (donor vs recipient DNA %)
Day +30 to +100 (Early post-transplant): Acute GVHD, infections, organ toxicities
Day >100 (Late): Chronic GVHD, secondary malignancy, endocrine dysfunction, infertility

Graft-Versus-Host Disease (GVHD)

Acute GVHD (aGVHD)

Donor T-cells attack recipient tissues. Classic triad of skin, gut, liver involvement.

Organ	Presentation	Grade 4 (Severe)
Skin	Maculopapular rash (palms/soles first)	Bullae, desquamation (>50% BSA)
Gut	Diarrhoea, N&V, cramping	Diarrhoea >2 L/day; severe pain, bleeding
Liver	Raised bilirubin, alkaline phosphatase	Bilirubin >256 µmol/L

Treatment: Methylprednisolone 2 mg/kg/day IV. Steroid-refractory: ruxolitinib, extracorporeal photopheresis

Nursing: Daily weights, accurate fluid balance, strict skin assessment (grade every shift), stoma output if applicable, nutritional support (TPN if severe gut GVHD), pain management, rectal biopsy care

Chronic GVHD (cGVHD)

Occurs >Day 100; multi-organ; resembles autoimmune disease
Skin: Sclerosis, lichen planus-like lesions, dyspigmentation, contractures
Eyes: Sicca syndrome (dry eyes); artificial tears, sunglasses outdoors
Mouth: Lichen planus, xerostomia, difficulty eating; topical steroids, dental hygiene critical
Lungs: Bronchiolitis obliterans – progressive airflow obstruction; spirometry monitoring
Gut/Liver: Malabsorption, cholestatic jaundice
Treatment: Systemic steroids + calcineurin inhibitors; ibrutinib, ruxolitinib for steroid-refractory
Nursing: Patient education on signs, sun protection (photosensitivity), vaccination schedule, infection prophylaxis (PCP, aciclovir, penicillin)

Veno-Occlusive Disease (VOD) / Sinusoidal Obstruction Syndrome (SOS)

⚠ VOD/SOS is a life-threatening post-conditioning complication. Endothelial injury → occlusion of hepatic sinusoids → post-hepatic portal hypertension. Onset typically Days +7 to +21.

Diagnosis (EBMT 2016 criteria)

Hyperbilirubinaemia (>34 µmol/L)
Weight gain >5% from baseline
Painful hepatomegaly
±Ascites detected on ultrasound
Hepatic venous pressure gradient elevation on Doppler

Treatment & Nursing

Defibrotide: IV 6.25 mg/kg QDS; enhances endogenous fibrinolysis; funded in severe VOD. Infuse over 2 hours. Monitor closely for bleeding
Nursing: Daily weights (same time, same scales), accurate fluid balance (hourly in severe), abdominal girth measurement, restrict sodium intake, diuretics cautiously, avoid hepatotoxic drugs, pain assessment
Severity: Mild/Moderate/Severe/Very severe; mortality >80% in very severe without treatment

Protective Isolation & Neutropenic Care

Environmental Controls

HEPA-filtered positive pressure single room (12+ air changes/hour)
Visitors restricted and screened (no colds, no recent live vaccines, no children with recent illness)
No fresh flowers or potted plants (aspergillus risk)
Surfaces and equipment cleaned with sporicidal agents
Staff: surgical/FFP2/N95 mask, gloves, apron as per local policy

Neutropenic Diet & ANTT Practice

Low microbial/neutropenic diet: No raw salad/vegetables, no raw eggs, no unpasteurised dairy, no raw/undercooked meat/fish, well-cooked foods only
Avoid pepper (Aspergillus contamination risk)
Bottled/filtered water if institutional policy
ANTT (Aseptic Non-Touch Technique): Meticulous for all IV access, blood sampling, wound care
Central venous catheter (CVC/PICC/Hickman) care: dressing changes, daily inspection, flush protocols
Oral care: 4-hourly mouthwashes, soft toothbrush, treat mucositis (pain scoring, gelclair, morphine PCA)
Temperature monitoring: neutropenic fever ≥38°C on one occasion or ≥37.5°C twice in 1 hour → blood cultures × 2 sites → broad-spectrum antibiotics within 60 minutes

GCC Context & Exam Preparation

GCC-Specific Haematology Context

Disease Prevalence in the GCC

Country	HbS Trait Prevalence	Beta-Thal Trait
Saudi Arabia (Eastern Province)	~4%	~1–4%
Bahrain	~2.6%	~1.5%
Oman	~2–5%	~2–3%
UAE	~1–2%	~2–3%
Qatar	~1–2%	~1.5%
Kuwait	~1.5–2.5%	~1–2%

ⓘThe GCC has among the highest global burdens of haemoglobinopathies. Consanguineous marriages (prevalent in some communities) increase risk of homozygous disease in offspring.

National Premarital Screening Programmes

Saudi Arabia (NPSP): Mandatory since 2004; screens for SCD, thalassaemia, and infectious diseases. Counselling mandatory; marriage not prohibited even if both carriers
UAE: Pre-marital and pre-employment screening; Abu Dhabi Thalassaemia programme
Bahrain: Mandatory pre-marital and prenatal screening
Qatar: Premarital screening; national registry
Nurse role: Pre-test counselling, sample collection, result communication, genetic counselling referral, patient education on carrier status vs disease, reproductive options (IVF/PGD available)

BMT Programmes in GCC

Saudi Arabia: King Faisal Specialist Hospital (KFSH&RC, Riyadh) – one of the largest BMT programmes in the Middle East; significant thalassaemia and SCD transplant volume
UAE: Cleveland Clinic Abu Dhabi, Sheikh Khalifa Medical City
Qatar: Hamad Medical Corporation (HMC) – expanding BMT services
Oman: SQUH Sultan Qaboos University Hospital BMT unit
GCC patients often travel for MUD transplants to European/US centres when matched local donor not found

DHA/DOH/SCFHS Examination Tips

GCC exams heavily test sickle cell and thalassaemia nursing management
Know Hydroxyurea mechanism and counselling in detail
Know VOC analgesia ladder doses and monitoring parameters
Iron chelation compliance and side effects commonly examined
GVHD grading and nursing management appears regularly
Distinguish HIT management (stop heparin, NOT warfarin)
ITP treatment order and IVIG timing for urgent platelet rise
DOAC reversal agents and indications
Neutropenic fever management: blood cultures first, then antibiotics within 60 minutes

Sickle Cell Crisis Assessment Tool

Rate the patient's current status to generate a management pathway.

Pain Score (NRS): 5 / 10

SpO₂

Temperature

Chest Symptoms

Recent Admissions in Past 6 Months