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Sickle cell anemia Pathophysiology Anaesthesia considerations Anaesthesia management Management of Sickle cell crisis

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sickle cell anemia pathophysiology diagram sickling

This diagnostic image is an annotated echocardiogram in the parasternal long-axis view, functioning as a pathophysiology diagram to illustrate cardiac involvement in Sickle Cell Anemia (SCA). The image labels three primary cardiac chambers with their associated clinical and functional abnormalities. The Right Ventricle is annotated with increased right ventricular pressure. The Left Ventricle is associated with increased extra-cellular volume and left ventricular diastolic dysfunction, suggesting interstitial myocardial fibrosis or edema. The Left Atrium highlights increased left atrial stiffness, decreased reservoir strain, and increased positive strain rate. Centrally, a four-way arrow signifies the interrelated nature of these dysfunctions, culminating in decreased exercise capacity. This educational visual demonstrates how diffuse myocardial changes in SCA lead to impaired chamber compliance and global functional impairment. It is intended for intermediate to advanced medical learners focusing on cardiology, hematology, or the systemic manifestations of hemoglobinopathies.

This diagnostic image is an annotated echocardiogram in the parasternal long-axis view, functioning as a pathophysiology diagram to illustrate cardiac involvement in Sickle Cell Anemia (SCA). The image labels three primary cardiac chambers with their associated clinical and functional abnormalities. The Right Ventricle is annotated with increased right ventricular pressure. The Left Ventricle is associated with increased extra-cellular volume and left ventricular diastolic dysfunction, suggesting interstitial myocardial fibrosis or edema. The Left Atrium highlights increased left atrial stiffness, decreased reservoir strain, and increased positive strain rate. Centrally, a four-way arrow signifies the interrelated nature of these dysfunctions, culminating in decreased exercise capacity. This educational visual demonstrates how diffuse myocardial changes in SCA lead to impaired chamber compliance and global functional impairment. It is intended for intermediate to advanced medical learners focusing on cardiology, hematology, or the systemic manifestations of hemoglobinopathies.

A medical pathophysiology diagram illustrating the oxidative stress cascade in Sickle Cell Disease (SCD) and its progression to vascular pathology. The diagram follows a vertical flow starting with a sickled red blood cell (RBC) undergoing HbS auto-oxidation and polymerization, leading to the generation of reactive oxygen species (ROS) such as H2O2, ferrylHb, and hemichromes. This triggers a central event of RBC hemolysis, characterized by membrane lipid oxidation, protein aggregation, and the release of pro-oxidant microparticles and L-arginase. Downstream pathways depict the systemic consequences, including the activation of platelets and the TLR4-linked inflammatory pathway, adhesion of SCD RBCs to endothelial cells and leukocytes, and a significant decrease in nitric oxide (NO) bioavailability. The lower section highlights the depletion of the antioxidant system and the oxidative modification of blood components into ADMA, AGEs, and ALEs. The cascade culminates in clinical manifestations such as vasoconstriction, endothelial dysfunction, and thrombosis, collectively summarized as SCD vascular pathology. This illustration is designed for advanced medical education regarding the molecular mechanisms of hematologic disorders.

A medical pathophysiology diagram illustrating the oxidative stress cascade in Sickle Cell Disease (SCD) and its progression to vascular pathology. The diagram follows a vertical flow starting with a sickled red blood cell (RBC) undergoing HbS auto-oxidation and polymerization, leading to the generation of reactive oxygen species (ROS) such as H2O2, ferrylHb, and hemichromes. This triggers a central event of RBC hemolysis, characterized by membrane lipid oxidation, protein aggregation, and the release of pro-oxidant microparticles and L-arginase. Downstream pathways depict the systemic consequences, including the activation of platelets and the TLR4-linked inflammatory pathway, adhesion of SCD RBCs to endothelial cells and leukocytes, and a significant decrease in nitric oxide (NO) bioavailability. The lower section highlights the depletion of the antioxidant system and the oxidative modification of blood components into ADMA, AGEs, and ALEs. The cascade culminates in clinical manifestations such as vasoconstriction, endothelial dysfunction, and thrombosis, collectively summarized as SCD vascular pathology. This illustration is designed for advanced medical education regarding the molecular mechanisms of hematologic disorders.

This educational graphic illustrates the molecular and cellular pathophysiology of sickle cell disease (SCD) leading to vaso-occlusion. The diagram is divided into a microscopic anatomical illustration and a high-magnification scanning electron micrograph. Steps A through D depict the hemoglobin S (HbS) polymerization process: (A) individual deoxygenated hemoglobin tetramers, (B) aggregation of hemoglobin molecules, (C) formation of long, rigid hemoglobin polymers or strands, and (D) the resulting transformation of a flexible biconcave red blood cell into a rigid, crescent or sickle-shaped erythrocyte. A corresponding scanning electron micrograph (labeled D) highlights the characteristic elongated, spicular morphology of a sickled cell. Section E shows a cross-section of a small bifurcating blood vessel where these rigid, abnormally shaped cells are aggregating, causing mechanical obstruction (vaso-occlusion) of the lumen. This process demonstrates the mechanism behind tissue ischemia and subsequent complications such as osteonecrosis in SCD patients. The content is suitable for medical students and clinicians studying hematology and musculoskeletal pathology.

This educational graphic illustrates the molecular and cellular pathophysiology of sickle cell disease (SCD) leading to vaso-occlusion. The diagram is divided into a microscopic anatomical illustration and a high-magnification scanning electron micrograph. Steps A through D depict the hemoglobin S (HbS) polymerization process: (A) individual deoxygenated hemoglobin tetramers, (B) aggregation of hemoglobin molecules, (C) formation of long, rigid hemoglobin polymers or strands, and (D) the resulting transformation of a flexible biconcave red blood cell into a rigid, crescent or sickle-shaped erythrocyte. A corresponding scanning electron micrograph (labeled D) highlights the characteristic elongated, spicular morphology of a sickled cell. Section E shows a cross-section of a small bifurcating blood vessel where these rigid, abnormally shaped cells are aggregating, causing mechanical obstruction (vaso-occlusion) of the lumen. This process demonstrates the mechanism behind tissue ischemia and subsequent complications such as osteonecrosis in SCD patients. The content is suitable for medical students and clinicians studying hematology and musculoskeletal pathology.

This pathophysiology diagram illustrates the signaling pathway of endothelial cell (EC) activation and apoptosis, particularly in the context of sickle cell disease (SCD) interactions with the vascular wall. The process begins with 'Inflammation' triggering the release of mediators including VEGF, IL-8, ET-1, and chemokines. These factors upregulate adhesion molecules on vascular ECs, specifically ICAM-1, VCAM-1, and E-selectin (represented by colored chevron icons). Activation of these molecules converges on the NF-̄Κβ signaling hub. This pathway facilitates the recruitment and interaction of homozygotic SS red blood cells (RBCs) and leukocytes (white blood cells). The subsequent cascade leads to the secretion of inflammatory cytokines, notably IL-8, IL-1, and TNF-α. The final stage of this inflammatory loop is the induction of apoptosis in normal endothelial cells, shown as a cluster of fragmented cells. The diagram serves as a model for understanding vaso-occlusive mechanisms and potential therapeutic targets like NF-̄Κβ inhibition in hematological disorders.

This pathophysiology diagram illustrates the signaling pathway of endothelial cell (EC) activation and apoptosis, particularly in the context of sickle cell disease (SCD) interactions with the vascular wall. The process begins with 'Inflammation' triggering the release of mediators including VEGF, IL-8, ET-1, and chemokines. These factors upregulate adhesion molecules on vascular ECs, specifically ICAM-1, VCAM-1, and E-selectin (represented by colored chevron icons). Activation of these molecules converges on the NF-̄Κβ signaling hub. This pathway facilitates the recruitment and interaction of homozygotic SS red blood cells (RBCs) and leukocytes (white blood cells). The subsequent cascade leads to the secretion of inflammatory cytokines, notably IL-8, IL-1, and TNF-α. The final stage of this inflammatory loop is the induction of apoptosis in normal endothelial cells, shown as a cluster of fragmented cells. The diagram serves as a model for understanding vaso-occlusive mechanisms and potential therapeutic targets like NF-̄Κβ inhibition in hematological disorders.

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sickle cell disease anesthesia perioperative management

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Sickle Cell Anemia: Complete Clinical Review

1. PATHOPHYSIOLOGY

Genetic Basis

Sickle cell disease (SCD) is an autosomal recessive hemoglobinopathy caused by a single nucleotide mutation in the β-globin gene on chromosome 11 - an adenine to thymidine transversion at codon 6 (A6T), resulting in substitution of glutamic acid by valine at position β6. The resulting abnormal hemoglobin is called HbS.
  • HbSS (sickle cell anemia): homozygous - most severe; >85% HbS, Hct 18-28%
  • HbSC disease: compound heterozygous HbS + HbC; moderate severity (~50% HbS)
  • HbS β-thalassemia: variable severity
  • Sickle cell trait (HbAS): carrier; 35-40% HbS; benign clinically (sickle only at SpO₂ ~40%)
(Goldman-Cecil Medicine, p.1719; Barash Clinical Anesthesia 9e, p.1895)

Molecular Mechanism of Sickling

Pathophysiology of sickle cell disease showing HbS polymerization, cell heterogeneity, hemolysis, vaso-occlusion, and nitric oxide depletion
Under conditions of deoxygenation, HbS molecules polymerize into rigid fiber-like chains called tactoids that distort the normal biconcave RBC into the characteristic crescent/sickle shape. This sickling-desickling cycle repeats with each pass through the capillary bed. Key steps:
  1. Deoxygenation in capillaries → HbS polymerization → sickle shape
  2. Return to lungs → reoxygenation → polymer deaggregation (reversal)
  3. If transit is delayed → persistent sickling → membrane damage → vaso-occlusion
Factors that worsen polymerization:
  • Low pO₂ / low pH (acidosis)
  • High temperature
  • Dehydration (elevated intracellular HbS concentration)
  • Low HbF levels
Factors that inhibit polymerization:
  • Presence of HbF (fetal hemoglobin) - critical protective effect
  • HbA (in heterozygotes)
  • Hydroxyurea (increases HbF production)
(Goldman-Cecil, p.1719)

Downstream Pathological Mechanisms

The sickling cascade causes injury through multiple overlapping mechanisms (as detailed in Barash Table 24-22):
MechanismConsequence
Microvascular obstructionTissue ischemia and infarction
RBC + platelet adhesion to endotheliumVascular inflammation, thrombosis
Hemolysis with free Hb releaseNitric oxide (NO) scavenging → vasoconstriction
Arginase release from lysed RBCsDepletes L-arginine (NO substrate) → further NO deficiency
Reactive oxygen species (ROS) generationOxidative stress, endothelial injury
Leukocyte activationCytokine release, inflammatory cascade
Reperfusion injuryActivates endothelium after ischemia
Reticulocyte adhesion ligandsAugment RBC-endothelial interactions
The net result: reduced NO bioavailability → impaired vasodilation → skewed toward vasoconstriction, platelet activation, and upregulation of adhesion molecules (ICAM-1, VCAM-1, E-selectin). (Goldman-Cecil, p.1719)

Consequences of Chronic Hemolysis

  • RBC lifespan reduced from 120 days → 12-17 days
  • Chronic hemolytic anemia (Hb typically 6-9 g/dL in HbSS)
  • Compensatory bone marrow hyperplasia
  • High reticulocyte count; elevated LDH, bilirubin; low haptoglobin
  • Functional asplenia (auto-infarction of spleen in childhood) → immunocompromised state

2. MULTISYSTEM COMPLICATIONS

SystemComplications
HematologicHemolytic anemia, aplastic anemia, leukocytosis, alloimmunization
PulmonaryAcute chest syndrome (ACS), pulmonary hypertension (10%), asthma (50%), fibrosis, pulmonary infarction, sleep apnea
CardiacCardiomegaly, LVH, RV dilation, diastolic dysfunction, cor pulmonale, cardiomyopathy
NeurologicStroke (cerebral infarct - adolescents; hemorrhagic - adults), hemorrhage, aneurysm, meningitis
RenalPapillary necrosis, inability to concentrate urine, glomerular sclerosis, renal failure, hematuria
MusculoskeletalPainful vaso-occlusive crises, avascular necrosis, osteomyelitis, bone infarction, dactylitis
SpleenAuto-infarction, hyposplenism, acute sequestration crisis
HepatobiliaryJaundice, cholelithiasis, hepatitis, cirrhosis, cholestasis
OcularRetinopathy, vitreous hemorrhage, vision loss
GUPriapism, renal failure, infections
PsychosocialDepression, anxiety, chronic pain disorder, opioid dependence
(Barash Clinical Anesthesia 9e, Table 24-23)

3. ANAESTHESIA CONSIDERATIONS

Why SCD Patients Are High-Risk

Patients with SCD are among the most complex surgical patients due to multiorgan dysfunction, chronic anaemia, increased infection risk from functional asplenia, and the risk of triggering perioperative crises. Sickling occurs at SpO₂ as high as 85% in homozygous disease. (Barash, p.1895)

Preoperative Assessment

History:
  • Frequency, severity, and pattern of vaso-occlusive crises
  • Previous acute chest syndrome episodes
  • Prior stroke or neurological events
  • History of OSA, pulmonary hypertension
  • Opioid tolerance and pain management history
  • Response to prior anaesthetics
  • Current medications (especially hydroxyurea)
  • Vaccination status
Examination & Investigations:
  • Full blood count (CBC) + reticulocyte count
  • Serum creatinine (renal function)
  • ECG
  • Chest X-ray
  • Echocardiogram - indicated for all but minor procedures; screen every 1-3 years (NT-proBNP >159 pg/mL or 6MWT <333 m suggests pulmonary hypertension)
  • Type and screen (even for low-risk procedures given risk of hemolytic crisis)
  • Liver iron content by MRI every 1-2 years in patients receiving repeated transfusions (not ferritin alone)
  • Arterial blood gases if indicated
(Miller's Anesthesia 10e, p.3985; Miller's Anesthesia 10e, p.4338)
Organ-Specific Concerns:
  • Pulmonary: Pulmonary hypertension independently predicts mortality. ACS is the leading cause of death.
  • Cardiac: LVH, diastolic dysfunction common. Symptoms overlap between SCD and pulmonary hypertension.
  • Renal: Loss of concentrating ability → prone to dehydration. CKD affects drug dosing.
  • Neurologic: Prior stroke may affect regional anaesthesia decision and positioning.
  • Immune: Functional asplenia → susceptible to encapsulated organisms; ensure vaccinations up to date.

Preoperative Optimization

Fasting/Dehydration: Minimize fasting periods. Schedule as an early morning case. Consider IV fluids perioperatively if prolonged fast needed. Patients may benefit from admission the day before surgery.
Transfusion Strategy (pre-operative):
  • Low-risk surgery (<30-60 min; superficial): no transfusion needed, or observe; if on hydroxyurea with Hb >9 g/dL, no transfusion required
  • Intermediate-risk surgery (most intra-abdominal, head/neck, orthopaedic): simple transfusion to target Hb >10 g/dL (>100 g/L); as effective as exchange transfusion for reducing HbS to <30% in this setting
  • High-risk surgery (cardiac, neurosurgery, major vascular, transplant): exchange transfusion to reduce HbS concentration to <30%; also required if baseline Hb already >10 g/dL (simple top-up would cause hyperviscosity)
  • Red cell exchange (RCE) regardless of Hb level recommended for HbSS patients undergoing high-risk surgery
Key principle: Goal of transfusion is to dilute HbS-containing cells, not merely correct anaemia. High alloimmunization rates in SCD mean cross-matching can take time - plan early with the blood bank.
Liaison with Hematology: Designate a lead hematologist (as per UK Association of Anaesthetists 2021 guidelines). Liaise with the sickle cell service team before surgery. Do NOT operate during an active crisis except for emergencies. (Miller's Anesthesia, p.3985-3986)

4. ANAESTHESIA MANAGEMENT

Intraoperative Principles

The core principle is: technique matters less than meticulous avoidance of sickling triggers.
AVOID the "5 Hs":
  • Hypoxia - maintain SpO₂ >95%; use supplemental oxygen
  • Hypothermia - active warming; warm IV fluids; monitor temperature
  • Hypovolaemia/dehydration - maintain normovolaemia with IV fluids
  • Hypotension - rapid treatment; hypoperfusion is a sickling trigger
  • Acidosis - avoid hyperventilation-induced alkalosis paradoxically; target normal pH; avoid metabolic acidosis
Additional triggers to avoid:
  • Stasis/venous stasis - careful positioning, avoid vena caval compression
  • Infection
  • Hypothermia

Choice of Anaesthetic Technique

  • All anaesthetic techniques are acceptable provided the above principles are respected
  • Regional/neuraxial anaesthesia is preferred where feasible:
    • Superior perioperative pain control (important in opioid-tolerant patients)
    • Resulting vasodilation may reduce sickling tendency
    • Spinal anaesthesia for caesarean section associated with less blood loss and reduced postoperative opioid requirement
    • Note: Treat hypotension from spinal quickly to avoid hypoperfusion
    • Avoid epinephrine in local anaesthetic solutions (vasoconstriction)
  • General anaesthesia: acceptable; all standard agents are suitable; maintain normothermia, normoxia, normocarbia

Positioning

  • Avoid high-risk positions that promote venous stasis: prone position, lithotomy for extended duration
  • Avoid vena caval compression (especially in pregnant patients)
  • Careful extremity positioning to prevent circulatory compromise

Tourniquets

  • Avoid tourniquets if possible - cause distal metabolic acidosis and regional hypoxemia → promote sickling
  • If absolutely required for surgical success, may be used with extreme caution; ensure adequate exsanguination before inflation

Contrast Media

  • Use iso-osmolar or hypo-osmolar contrast agents; hyperosmolar contrast can precipitate sickling

Monitoring

  • Standard ASA monitoring + temperature probe
  • Pulse oximetry is essential (target SpO₂ >95%)
  • Consider arterial line for high-risk procedures
  • Urine output monitoring

Fluid Management

  • Maintain normovolaemia - both hypovolaemia (sickling) and hypervolaemia (pulmonary oedema in impaired cardiac function) are harmful
  • Use balanced crystalloids; avoid hypotonic solutions

Postoperative Care

  • Continue supplemental oxygen until fully awake and SpO₂ stable
  • Optimal multimodal analgesia (opioids + NSAIDs + regional) - note: avoid NSAIDs in renal dysfunction
  • Prevent dehydration, hypothermia, hypoxia, acidosis
  • Incentive spirometry - reduces risk of ACS
  • Venous thromboprophylaxis - indicated
  • Monitor Hb and renal function
  • Acute chest syndrome can develop 2-3 days postoperatively - requires supportive treatment
  • Careful sedation monitoring if opioids used
(Miller's Anesthesia 10e, pp.4339-4340; Barash Clinical Anesthesia 9e, pp.1897-1898)

5. MANAGEMENT OF SICKLE CELL CRISIS

Types of Sickle Cell Crisis

TypeKey FeatureReticulocytesCommon Cause
Vaso-occlusive (VOC)Pain; ischemic infarctionNormal/elevatedDehydration, infection, hypoxia, cold, stress
HemolyticAcute drop in Hb + HctElevated (reticulocytosis)Accelerated hemolysis
AplasticAcute drop in HbLow/absentParvovirus B19 (>90% of cases)
SequestrationAcutely enlarged spleen + Hb ≥2 g/dL below baselineVariableRapid splenic trapping of RBCs
Acute Chest Syndrome (ACS)New pulmonary infiltrate + fever/respiratory symptoms-Infection (Chlamydia, Mycoplasma), fat embolism, infarction
(Miller's Anesthesia Pediatric Critical Care, p.11439)

A. Vaso-Occlusive Crisis (VOC) / Painful Crisis

Precipitants: infection, dehydration, acidosis, hypoxia, cold exposure, stress, alcohol
Clinical presentation: severe musculoskeletal pain; dactylitis in children <2 years; multifocal pain in adults. Any organ can be affected.
Management:
1. Analgesia (priority):
  • Mild-moderate pain: oral NSAIDs (if renal function normal) + oral opioids (oxycodone, morphine, hydrocodone)
  • Moderate-severe / hospitalized:
    • IV opioids: morphine or hydromorphone as first-line
    • Use fentanyl if hepatic or renal dysfunction
    • Patient-controlled analgesia (PCA) with as-needed breakthrough doses; schedule if not using PCA
    • Ketamine (low-dose) if poor opioid response (sub-anaesthetic, anti-hyperalgesic)
    • NSAIDs (with adequate renal function) for opioid-sparing effect
    • Epidural analgesia for severe VOC
2. Hydration:
  • IV fluids for dehydration; avoid fluid overload
  • Goal: maintain normovolaemia (specific fluid type/volume evidence is limited)
3. Oxygen:
  • Supplemental O₂ for SpO₂ <95%; goal SpO₂ >95%
  • Incentive spirometry to prevent ACS
4. Address precipitants:
  • Treat underlying infection with appropriate antibiotics
  • Rewarm if cold exposure
5. Transfusion:
  • Not routinely indicated for simple VOC alone
  • Consider if associated severe anemia, ACS, or organ dysfunction
(Harriet Lane Handbook 23e, p.482-483)

B. Acute Chest Syndrome (ACS)

Definition: new pulmonary infiltrate on CXR + one or more of: fever, respiratory symptoms, chest pain, hypoxia
Importance: leading cause of death and second most common complication in SCD. ~50% initially present with pain before respiratory symptoms appear.
Common causes: Chlamydia pneumoniae, Mycoplasma pneumoniae (most common pathogens), pulmonary fat embolism from bone marrow necrosis, pulmonary infarction/thrombosis
Management:
  • Admission (all cases)
  • Oxygen to maintain SpO₂ >95%
  • IV antibiotics: IV cephalosporin (cefuroxime or cefotaxime) + oral macrolide (covers atypical organisms)
  • Analgesia + IV fluids (see VOC management above)
  • Incentive spirometry
  • Transfusion:
    • Simple transfusion for moderate illness
    • Exchange transfusion for severe ACS or unresponsive cases
  • Avoid transfusion if no other indication (risk of volume overload)
  • Diuretics if fluid overloaded
  • Respiratory support (non-invasive or mechanical ventilation) if severe
  • High-dose dexamethasone is controversial
(Miller's Pediatric Critical Care, p.11440)

C. Aplastic Crisis

Cause: Parvovirus B19 infection in >90% of cases (suppresses erythropoiesis)
Features: Acute drop in Hb below baseline, absent reticulocytes (distinguishes from hemolytic crisis), often with viral prodrome
Management:
  • Admission; isolate (parvovirus is contagious - risk to immunocompromised contacts)
  • IV fluids
  • Simple transfusion if severe anemia
  • Parvovirus serology + PCR for confirmation
  • Self-limiting (erythropoiesis recovers within 7-10 days)

D. Splenic Sequestration Crisis

Features: Acutely enlarged spleen + Hb ≥2 g/dL below baseline; rapid onset; can cause hemodynamic instability
Management:
  • Admit; serial abdominal examinations
  • IV fluid resuscitation (aggressive)
  • Transfusion - cautious (release of sequestered RBCs on recovery can cause hyperviscosity)
  • May require splenectomy for recurrent episodes or hemodynamic instability

E. Admission Criteria (Harriet Lane)

Admit if:
  • Fever ≥40°C, WBC >30,000 or <5,000, Hb <5 g/dL, platelets <100,000, abnormal SpO₂, infiltrate on CXR
  • Signs of ACS, stroke, or organ complications
  • Pain not manageable in outpatient setting
  • Aplastic crisis
  • Splenic sequestration

Long-Term Disease-Modifying Therapy

DrugMechanismUse
HydroxyureaIncreases HbF productionReduces VOC frequency/severity, ACS, transfusion requirements
VoxelotorIncreases HbS-oxygen affinityReduces sickling and hemolysis
CrizanlizumabAnti-P-selectin antibodyReduces VOC
L-glutamineReduces oxidative stressReduces ACS
Bone marrow transplantCurativeSevere SCD in eligible patients
Gene therapyEmerging curativeUnder investigation
(Barash Clinical Anesthesia 9e, p.1897)

Quick Reference: Anaesthesia Checklist for SCD Patients

Pre-op: ✅ Liaise with hematologist ✅ Echo if any respiratory/cardiac symptoms or before intermediate/high-risk surgery ✅ Type & screen early; plan transfusion strategy ✅ Minimize fasting; schedule early morning ✅ Do not operate during active crisis (unless emergency)
Intra-op: ✅ Maintain SpO₂ >95% ✅ Maintain normothermia (active warming) ✅ Maintain normovolaemia ✅ Avoid acidosis ✅ Avoid prolonged tourniquets ✅ Prefer regional techniques where feasible ✅ Avoid epinephrine in local anaesthetics ✅ Use iso-osmolar contrast
Post-op: ✅ Supplemental O₂ ✅ Incentive spirometry ✅ Multimodal analgesia ✅ DVT prophylaxis ✅ Monitor for ACS at 48-72 hours
Sources: Miller's Anesthesia 10e (pp.3985-3986, 4337-4340, 11439-11440) | Barash Clinical Anesthesia 9e (pp.1895-1898) | Goldman-Cecil Medicine (pp.1719-1720) | Harriet Lane Handbook 23e (pp.482-483)
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