Hematology Oncology

A

• Acute Chest Syndrome in Sickle Cell Disease — Antibiotics, Bronchodilators, and (Exchange) Transfusion

  New pulmonary infiltrate plus fever and/or respiratory symptoms in sickle cell disease. Provide oxygen, antibiotics (cover atypicals), incentive spirometry, and bronchodilators; transfuse simple or exchange based on severity and Hb; involve hematology early.
• Anticoagulant Reversal — Life Threatening Bleeding

  Life-threatening bleeding on anticoagulation requires immediate hemostatic resuscitation, identification of the anticoagulant and last dose, control of the bleeding source, and targeted reversal when the expected benefit exceeds thrombosis risk. Use 4-factor PCC plus IV vitamin K for warfarin, idarucizumab for dabigatran, and andexanet alfa or PCC for major factor Xa inhibitor bleeding when appropriate.

D

• Deep Vein Thrombosis — Diagnosis & Anticoagulation

  Deep vein thrombosis is thrombus formation in the deep venous system, most often in the lower extremity, with the principal acute danger of pulmonary embolism and the longer-term risk of post-thrombotic syndrome. Diagnosis should use a structured pretest probability strategy with D-dimer and compression ultrasonography rather than symptoms alone. Most confirmed proximal DVTs require therapeutic anticoagulation unless bleeding risk is prohibitive. Selected isolated distal DVTs at low risk for extension can b
• Disseminated Intravascular Coagulation — Diagnosis & Treatment

  DIC is a consumptive coagulopathy from systemic activation of coagulation (sepsis, malignancy, trauma, obstetric). Diagnose with clinical context and labs (↑PT/INR, ↑aPTT, ↓fibrinogen, ↑D‑dimer, thrombocytopenia). Treat cause; provide targeted blood products; consider heparin in chronic DIC.
• Disseminated Intravascular Coagulation — Treat Cause and Support

  Disseminated intravascular coagulation is an acquired systemic activation of coagulation that produces widespread thrombin generation, consumption of platelets and clotting factors, secondary fibrinolysis, microvascular thrombosis, organ injury, and bleeding. It is always secondary to an underlying disorder such as sepsis, major trauma, obstetric catastrophe, malignancy, or severe tissue injury. Treat the cause immediately, trend platelets, PT/INR, aPTT, fibrinogen, and D-dimer, and use blood products for c

F

• Febrile Neutropenia — Risk Scores, Broad‑Spectrum IV Antibiotics, and Antifungal Escalation

  Defined as fever with ANC <500 (or expected). Start broad‑spectrum IV antibiotics within 60 minutes of presentation. Use MASCC/CISNE scores to triage for inpatient vs outpatient therapy; add antifungal coverage if persistent fever after 4–7 days or earlier if instability or imaging suggests fungal disease.
• Febrile Neutropenia — Risk Scores, Early Antipseudomonal Coverage, and Disposition

  Fever with ANC <500 (or expected to decline) after chemotherapy. Obtain cultures quickly and start an antipseudomonal β‑lactam within 60 minutes; add MRSA coverage only with specific indications. Use MASCC/CISNE for risk and consider outpatient oral therapy for low‑risk patients.

H

• Hemolytic Anemia — DAT‑Positive vs DAT‑Negative Evaluation

  Differentiate immune from non‑immune hemolysis using DAT and peripheral smear; treat underlying cause and initiate corticosteroids for warm AIHA; urgent support for severe hemolysis.
• Heparin‑Induced Thrombocytopenia — 4Ts & Anticoagulation

  Suspect HIT with platelet drop 5–10 days after heparin; use 4Ts score; stop all heparin and start non‑heparin anticoagulant while confirming diagnosis.
• Heparin‑Induced Thrombocytopenia — 4Ts Score, PF4 Testing, and Non‑Heparin Anticoagulation

  Immune‑mediated thrombocytopenia with thrombosis risk 5–10 days after heparin exposure. Use 4Ts score for pretest probability, stop all heparin, send PF4 immunoassay with functional testing as needed, and start a non‑heparin anticoagulant while awaiting confirmatory testing.
• Hodgkin Lymphoma — Initial Workup & Staging

  Classical HL: obtain PET‑CT, stage with Ann Arbor, document B symptoms, and plan ABVD‑based therapy with consideration of bulky disease and interim PET adaptation.
• Hypercalcemia of Malignancy — Fluids, Calcitonin, and Anti‑Resorptives

  Cancer‑related hypercalcemia requires isotonic fluids, short‑term calcitonin for rapid reduction, and anti‑resorptives (IV bisphosphonates or denosumab) for sustained control; add dialysis for severe/renal failure. Treat underlying malignancy and limit calcium/vitamin D.
• Hypercalcemia of Malignancy — Fluids, Calcitonin, and Bisphosphonate/Denosumab

  Treat symptomatic or severe hypercalcemia with aggressive IV saline, calcitonin for rapid effect, and IV bisphosphonate (zoledronic acid/pamidronate) or denosumab for sustained control; stop exacerbating drugs and treat the underlying malignancy.

I

• Immune Thrombocytopenia (ITP) — First‑ and Second‑Line Therapy

  Diagnosis of exclusion; treat when platelets <30k or bleeding; first‑line corticosteroids or IVIG; second‑line TPO‑RA, rituximab, or splenectomy.
• Immune TTP — ADAMTS13, Plasma Exchange, Steroids, and Caplacizumab

  Suspect iTTP with MAHA and thrombocytopenia; send ADAMTS13 urgently and begin plasma exchange plus high-dose steroids immediately; add caplacizumab when iTTP is likely to reduce time to platelet recovery and relapses.
• Indolent Non‑Hodgkin Lymphoma — Watchful Waiting vs Treatment

  Many indolent NHLs (e.g., follicular) can be observed initially. Treat when GELF criteria or symptoms present; prefer anti‑CD20‑based regimens; monitor for transformation.
• Iron Deficiency Anemia — Workup & IV Iron

  Diagnose with ferritin and iron studies; identify bleeding sources; treat with oral or IV iron depending on severity/tolerance; replete stores and monitor response.

M

• Malignant Spinal Cord Compression — Emergency Care

  Back pain with neurologic deficits in cancer patients requires urgent MRI, high dose steroids, and oncology and surgical consultation for decompression and radiotherapy.
• Malignant Spinal Cord Compression — Steroids and Oncologic Urgency

  Metastatic spinal cord compression is an oncologic emergency caused by tumor in the vertebral column or epidural space compressing the spinal cord or cauda equina. New severe spinal pain, radicular pain, weakness, gait change, sensory loss, or bladder/bowel dysfunction in a patient with cancer requires urgent assessment. Give dexamethasone 16 mg promptly when neurologic signs or symptoms of cord compression are present unless contraindicated, obtain whole-spine MRI as soon as possible and within 24 hours, a
• Malignant Spinal Cord Compression — Steroids, MRI, and Urgent Decompression/Radiation

  Back pain with neurologic deficits in cancer patients is an emergency. Give dexamethasone promptly, obtain MRI whole spine, and coordinate urgent surgical decompression and/or radiotherapy based on stability, radiosensitivity, and prognosis.
• Myelodysplastic Syndromes — Risk Stratification & Treatment

  Heterogeneous clonal disorders with cytopenias and risk of AML transformation. Diagnose with marrow morphology and cytogenetics/molecular profiling. Use IPSS‑R/IPSS‑M to stratify risk and guide therapy from supportive care to HMA or transplant.

N

• Neutropenic Fever — Initial Management

  Febrile neutropenia is fever in a patient with severe chemotherapy-related or disease-related neutropenia and is an oncologic emergency because bacteremia can progress rapidly with minimal localizing signs. Empiric antibacterial therapy with an antipseudomonal beta-lactam should begin within about 1 hour of triage after cultures are obtained when feasible. Risk stratification identifies a small group suitable for carefully selected outpatient oral therapy, while unstable patients, profound or prolonged neut

P

• Paroxysmal Nocturnal Hemoglobinuria — Hemolysis, Thrombosis & Complement Inhibition

  Paroxysmal nocturnal hemoglobinuria is an acquired clonal stem-cell disorder caused by PIGA mutations that produce deficiency of GPI-anchored complement regulators such as CD55 and CD59. The result is complement-mediated intravascular hemolysis, cytopenias, and a distinctive risk of thrombosis, diagnosed by high-sensitivity flow cytometry and treated with complement inhibition when clinically significant.

S

• Sickle Cell Acute Chest Syndrome — Antibiotics, Bronchodilators, and Transfusion Strategy

  New pulmonary infiltrate with fever and/or respiratory symptoms in sickle cell disease. Provide oxygen, incentive spirometry, pain control, antibiotics, and transfusion (simple vs exchange) based on severity; avoid fluid overload and treat concomitant VOC.
• Sickle Cell Disease — Acute Crisis & Disease‑Modifying Therapy

  Manage acute pain crises, prevent complications (ACS, stroke), and use disease‑modifying therapy (hydroxyurea, transfusions; selected newer agents). Vaccinate and provide comprehensive care.
• Sickle Cell Vaso Occlusive Crisis — Analgesia and Complications

  Sickle cell vaso-occlusive pain is an acute ischemic pain syndrome requiring rapid individualized analgesia, assessment for acute chest syndrome and other complications, and careful supportive care. Treat pain promptly, use NSAIDs selectively, avoid routine transfusion for uncomplicated pain, and escalate evaluation whenever fever, hypoxemia, chest symptoms, neurologic deficits, severe anemia, or atypical pain is present.
• Superior Vena Cava Syndrome — Oncologic Emergency

  Superior vena cava syndrome results from obstruction of venous return from the head, neck, and upper extremities, most often from thoracic malignancy or intravascular devices. Most cases permit rapid diagnostic imaging and tissue diagnosis before definitive therapy; airway compromise, cerebral edema, or hemodynamic instability requires urgent endovascular and multidisciplinary intervention.

T

• Transfusion Thresholds in Adults — Restrictive Strategy

  Red blood cell transfusion decisions should combine hemoglobin concentration with active bleeding, hemodynamics, ischemic symptoms, comorbidity, and patient goals. For most hemodynamically stable hospitalized adults, evidence supports a restrictive strategy near 7 g/dL, with higher individualized thresholds in selected cardiovascular and perioperative populations and a distinct approach to acute myocardial infarction.
• Tumor Lysis Syndrome — Prevention & Management

  Oncologic emergency from rapid cell lysis causing hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. Prevent with risk stratification, vigorous hydration, and urate‑lowering therapy; manage electrolyte derangements promptly; dialyze if refractory.
• Tumor Lysis Syndrome — Prevention & Treatment

  Tumor lysis syndrome is an oncologic emergency caused by rapid release of intracellular potassium, phosphate, and nucleic acids after tumor-cell breakdown, producing hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, acute kidney injury, seizures, arrhythmias, and death. Prevention in high-risk patients relies on vigorous but individualized hydration, frequent laboratory monitoring, and urate-lowering therapy. Established or high-risk TLS may require rasburicase and urgent nephrology support for
• Tumor Lysis Syndrome — Prevention and Treatment

  Identify high risk hematologic malignancies, start aggressive hydration, control uric acid with allopurinol or rasburicase, and manage electrolytes; dialyze when refractory.
• Tumor Lysis Syndrome — Prevention, Rasburicase vs Allopurinol, and Renal Protection

  High‑grade hematologic malignancies carry TLS risk at chemo initiation. Stratify risk; give aggressive hydration, allopurinol for low‑moderate risk, or rasburicase for high‑risk or established hyperuricemia. Monitor electrolytes closely; treat hyperkalemia/hyperphosphatemia; consider early dialysis for AKI.
• Tumor Lysis Syndrome — Risk Stratification, Hydration, and Uric Acid Control

  TLS arises after cytotoxic therapy (or spontaneously) in high-burden hematologic malignancy. Prevent with aggressive isotonic fluids, strict monitoring of potassium, phosphate, calcium, uric acid, and renal function, and early uric acid–lowering therapy (rasburicase for high risk).
• Tumor Lysis Syndrome — Risk Stratification, Rasburicase/Allopurinol, and Renal Support

  Rapid tumor cell breakdown after cytotoxic therapy (or spontaneously) causing hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. Risk‑stratify, start aggressive hydration, give allopurinol for prevention or rasburicase for treatment, and monitor electrolytes/renal function closely; initiate dialysis when refractory.