Multiple myeloma nursing: CRAB criteria, treatment, and NCLEX tips

Multiple myeloma is a malignancy of clonal plasma cells in the bone marrow that produce a single abnormal monoclonal immunoglobulin known as the M-protein. As the malignant plasma cell clone expands, it crowds out normal hematopoiesis, secretes cytokines that activate osteoclasts, and floods the circulation with paraprotein that damages the kidneys. The clinical syndrome is summarized by the CRAB criteria: hyperCalcemia, Renal impairment, Anemia, and Bone lesions. Multiple myeloma accounts for approximately 1.8% of all new cancer diagnoses in the United States and represents about 10% of hematologic malignancies, with a median age at diagnosis of 69 years.

Understanding myeloma nursing care requires an integrated grasp of the disease biology, the diagnostic workup, the modern treatment regimens, and the long list of treatment-related toxicities. This reference covers each in turn and ends with a focused NCLEX section.

Pathophysiology: clonal plasma cells and the M-protein

Plasma cells are the terminally differentiated B-lymphocytes responsible for producing immunoglobulins. In multiple myeloma, a single plasma cell acquires genetic abnormalities (commonly translocations involving the immunoglobulin heavy chain locus on chromosome 14, or trisomies of odd-numbered chromosomes) and proliferates clonally in the bone marrow. Every cell in the resulting clone produces the same immunoglobulin molecule – the monoclonal protein, or M-protein – which appears as a sharp spike on serum protein electrophoresis.

Three interrelated mechanisms drive the clinical syndrome:

1. Marrow infiltration. Clonal plasma cells replace normal erythroid, myeloid, and megakaryocytic precursors. The most common hematologic finding is normocytic, normochromic anemia. Thrombocytopenia and neutropenia appear in advanced disease. For the broader nursing framework on marrow-replacement anemia, see the anemia nursing reference.

2. Osteoclast activation. Myeloma cells secrete RANKL, MIP-1α, and other cytokines that stimulate osteoclasts and suppress osteoblasts. The result is uncoupled bone resorption – lytic lesions, diffuse osteopenia, pathological fractures, and the release of calcium into the bloodstream that produces hypercalcemia.

3. Paraprotein toxicity. The M-protein and excess free light chains are filtered by the glomerulus and overwhelm proximal tubular reabsorption. Light chains precipitate with Tamm-Horsfall protein in the distal tubule to form characteristic cast nephropathy (“myeloma kidney”). Hyperviscosity from very high paraprotein levels can also impair microcirculation. The nursing approach to acute kidney injury in this setting overlaps with the broader AKI nursing reference.

The combination of these three mechanisms produces the CRAB syndrome that defines symptomatic disease.

CRAB and SLiM-CRAB diagnostic criteria

The International Myeloma Working Group (IMWG) defines active multiple myeloma by clonal plasma cells of at least 10% on bone marrow biopsy (or a biopsy-proven plasmacytoma) plus one or more myeloma-defining events. The traditional myeloma-defining events are the CRAB criteria, and the IMWG expanded these in 2014 to include three biomarkers of imminent end-organ damage – the SLiM criteria. Together, these are now the SLiM-CRAB framework.

MGUS, smoldering myeloma, and active myeloma

Multiple myeloma exists on a continuum that begins decades before symptomatic disease.

Monoclonal gammopathy of undetermined significance (MGUS) is a premalignant state defined by an M-protein <3 g/dL, clonal plasma cells <10% on marrow biopsy, and no end-organ damage. MGUS is found in about 3% of adults over 50 and progresses to multiple myeloma at a rate of approximately 1% per year. Patients are followed with periodic SPEP and clinical assessment.

Smoldering multiple myeloma (SMM) sits between MGUS and active disease: M-protein ≥3 g/dL or clonal marrow plasma cells 10–60%, but no CRAB criteria and no SLiM biomarkers. Risk of progression is roughly 10% per year for the first five years, then declining. High-risk SMM (M-protein ≥2 g/dL, marrow plasmacytosis ≥20%, light chain ratio ≥20) is sometimes treated with lenalidomide on protocol.

Active multiple myeloma requires clonal marrow plasma cells ≥10% (or a plasmacytoma) plus at least one CRAB or SLiM biomarker. This is the threshold for initiating systemic therapy.

Diagnostic workup

A complete myeloma workup integrates serum, urine, marrow, and imaging studies. Each test answers a specific question.

Serum protein electrophoresis (SPEP) and immunofixation

SPEP separates serum proteins by charge into albumin, alpha-1, alpha-2, beta, and gamma fractions. The M-protein produces a tall, narrow “M-spike” in the gamma region (or occasionally beta). Immunofixation electrophoresis (IFE) is then performed to identify the heavy chain class (most commonly IgG, then IgA; rarely IgD or IgM in myeloma) and the light chain type (kappa or lambda). The combination of SPEP plus IFE is the cornerstone of diagnosis.

Urine protein electrophoresis (UPEP) and Bence Jones proteins

When clonal plasma cells produce excess free light chains, the small molecules (~22 kDa) pass through the glomerulus and appear in the urine. These free light chains in urine are called Bence Jones proteins. Standard urine dipsticks detect albumin but miss Bence Jones proteins, which is why a 24-hour urine collection with UPEP and immunofixation is required. About 15% of myeloma patients have light chain–only disease and produce no detectable serum M-spike, making UPEP indispensable.

Serum free light chain (sFLC) assay

The sFLC assay quantifies kappa and lambda free light chains in serum and reports the kappa-to-lambda ratio. A skewed ratio reflects clonal light chain production. The sFLC is more sensitive than UPEP for low-burden disease and is one of the SLiM biomarkers when the involved-to-uninvolved ratio exceeds 100.

Bone marrow biopsy

A bone marrow aspirate and core biopsy quantify clonal plasma cells. Active myeloma requires ≥10% clonal plasma cells. Cytogenetic studies by fluorescence in situ hybridization (FISH) identify high-risk abnormalities including del(17p), t(4;14), t(14;16), and gain(1q), which feed into the R-ISS staging system.

Imaging

Plain skeletal surveys are now considered insensitive and have largely been replaced by whole-body low-dose CT as the modern first-line imaging modality per IMWG recommendations. Whole-body MRI is preferred for detecting marrow infiltration and focal lesions before lytic destruction is visible. PET-CT is useful for assessing solitary plasmacytomas and monitoring treatment response.

Supporting labs

A complete myeloma panel includes CBC (for anemia, thrombocytopenia), basic metabolic panel (for calcium and creatinine), LDH, beta-2 microglobulin, serum albumin, and quantitative immunoglobulins. Beta-2 microglobulin reflects tumor burden and renal function; combined with albumin, it forms the basis of the original International Staging System.

Staging: ISS and R-ISS

The International Staging System (ISS) uses two routinely available labs – beta-2 microglobulin and albumin – to define three prognostic stages. The Revised ISS (R-ISS), published in 2015, incorporates serum LDH and high-risk cytogenetics by FISH for improved prognostic resolution.

For NCLEX purposes, the high-yield association is: beta-2 microglobulin and albumin = ISS staging in multiple myeloma.

Treatment regimens

Modern myeloma therapy is built around three classes – proteasome inhibitors, immunomodulatory drugs (IMiDs), and anti-CD38 monoclonal antibodies – with autologous stem cell transplant for eligible patients and CAR-T cell therapy for relapsed disease.

Induction therapy

The current standard induction backbone is the VRd regimen: bortezomib (Velcade), lenalidomide (Revlimid), and dexamethasone. In transplant-eligible patients, the addition of daratumumab to produce Dara-VRd (D-VRd) has become the preferred quadruplet regimen based on the PERSEUS and GRIFFIN trials, which demonstrated deeper responses and improved progression-free survival. Patients typically receive four to six cycles of induction before stem cell collection.

Autologous stem cell transplant (ASCT)

After induction, eligible patients undergo high-dose melphalan conditioning followed by reinfusion of their own previously collected hematopoietic stem cells. This is autologous transplant – not allogeneic, because the donor cells come from the patient themselves. ASCT remains a standard of care for fit patients up to approximately age 70–75, though chronological age alone does not exclude eligibility. Allogeneic transplant is reserved for highly selected younger patients with high-risk relapsed disease and is rarely performed.

Maintenance therapy

After ASCT, patients receive long-term lenalidomide maintenance (typically until progression or intolerance), which prolongs progression-free and overall survival. High-risk patients may receive bortezomib-based maintenance.

Relapsed and refractory disease

Most myeloma patients eventually relapse. Salvage options include:

• Carfilzomib (Kyprolis) – a second-generation proteasome inhibitor.
• Pomalidomide – a third-generation IMiD active after lenalidomide failure.
• Daratumumab or isatuximab – anti-CD38 monoclonals.
• Belantamab mafodotin – an antibody-drug conjugate targeting BCMA, notable for ocular toxicity (corneal microcyst-like deposits, blurred vision, dry eye) requiring REMS-mandated ophthalmologic monitoring before each dose.
• Selinexor – an oral selective inhibitor of nuclear export, used in heavily pretreated disease.
• Venetoclax – a BCL-2 inhibitor with selective activity in patients with t(11;14) translocation.

CAR-T cell therapy

Two BCMA-directed chimeric antigen receptor T-cell products are approved for relapsed/refractory myeloma:

• Idecabtagene vicleucel (ide-cel, Abecma) – approved for patients after at least four prior lines of therapy (and now moved earlier in the treatment sequence).
• Ciltacabtagene autoleucel (cilta-cel, Carvykti) – with deeper and more durable responses in heavily pretreated patients.

CAR-T therapy involves apheresis to collect autologous T cells, lymphodepleting chemotherapy (fludarabine + cyclophosphamide), and infusion of the engineered product. Two specific toxicities define the post-infusion nursing window: cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). Both are discussed in detail in the nursing priorities section below.

Nursing priorities and interventions

Bone disease and pathological fracture risk

Lytic bone lesions are the most common presenting feature of multiple myeloma, found in approximately 80% of patients at diagnosis. Vertebral compression fractures, rib fractures, and femoral neck fractures occur with minimal trauma. Nursing assessment includes a focused musculoskeletal exam at every visit, with particular attention to new back pain (which may herald a vertebral fracture), inability to bear weight, or radicular pain (suggesting cord compression).

Fall precautions are essential. The bedside checklist includes bed in low position, call light within reach, non-slip footwear, adequate lighting, and a clear path to the bathroom. Patients with vertebral involvement should not lift more than 5–10 pounds, should avoid bending and twisting at the waist, and should use proper body mechanics for transfers. Symptomatic vertebral compression fractures may be treated with kyphoplasty or vertebroplasty – percutaneous cement augmentation procedures that stabilize the vertebra and provide rapid pain relief.

Spinal cord compression is an oncologic emergency. Sudden new back pain with neurologic deficit (weakness, numbness, bowel or bladder dysfunction) requires immediate MRI of the entire spine, high-dose dexamethasone, and urgent radiation oncology or neurosurgical consultation.

Bisphosphonate therapy and osteonecrosis of the jaw

All myeloma patients with bone disease should receive a bone-modifying agent to reduce skeletal-related events. The two options are:

• Zoledronic acid (Zometa) – an IV bisphosphonate given every 3–4 weeks (often de-escalated to every 12 weeks in stable disease per the CALGB 70604 trial).
• Denosumab (Xgeva) – a RANKL inhibitor given subcutaneously, preferred in renal impairment because it is not renally cleared.

The signature toxicity of both agents is osteonecrosis of the jaw (ONJ). ONJ presents as exposed bone in the maxilla or mandible, often after a dental extraction, and can be severely disabling. Prevention is the nursing priority:

1. A complete dental examination and any necessary extractions or invasive dental work should be completed before initiating bone-modifying therapy.
2. During therapy, patients should maintain meticulous oral hygiene and avoid invasive dental procedures whenever possible.
3. Any new oral pain, mucosal lesion, or exposed bone requires prompt dental consultation.

Bisphosphonates require monitoring of renal function (zoledronic acid is renally cleared and dose-adjusted by creatinine clearance) and serum calcium (transient hypocalcemia can occur, especially with denosumab). Patients should receive supplemental calcium and vitamin D unless hypercalcemic.

Hypercalcemia management

Hypercalcemia of malignancy in myeloma is driven primarily by osteoclast-mediated bone resorption and is exacerbated by dehydration and immobility. The classic symptom mnemonic is “stones, bones, groans, thrones, psychiatric overtones”: kidney stones, bone pain, abdominal pain (with constipation), polyuria, and altered mental status. Severe hypercalcemia (calcium >14 mg/dL) can produce shortened QT interval, arrhythmia, and coma.

The nursing approach to severe hypercalcemia follows a stepwise sequence:

1. Aggressive IV hydration with isotonic saline – typically 200–300 mL/hour initially, titrated to urine output and volume status. Restoring intravascular volume promotes calciuresis and is the first and most important intervention.
2. Calcitonin (4 IU/kg SC or IM every 12 hours) – provides rapid but short-lived calcium reduction within 4–6 hours; tachyphylaxis develops within 48 hours.
3. IV bisphosphonate (zoledronic acid 4 mg IV) – produces durable calcium reduction within 48–72 hours.
4. Loop diuretics (furosemide) – only after volume repletion is achieved, and primarily to manage volume overload in patients with cardiac or renal impairment. Loop diuretics are no longer first-line for hypercalcemia management.
5. Continuous cardiac monitoring for arrhythmia in severe hypercalcemia.

Avoid thiazide diuretics (which cause calcium retention) and calcium-containing fluids.

Renal impairment

Approximately 20–40% of patients have some degree of renal impairment at diagnosis. The pathology is dominated by light chain cast nephropathy (“myeloma kidney”), with smaller contributions from hypercalcemic nephropathy, amyloid deposition, and direct plasma cell infiltration.

Nursing interventions to protect renal function:

• Aggressive hydration – maintain urine output at 2.5–3 L/day to clear light chains and prevent cast formation.
• Avoid nephrotoxic agents – withhold NSAIDs, aminoglycosides, and IV iodinated contrast whenever possible. If contrast cannot be avoided, ensure pre- and post-procedure hydration.
• Drug selection – bortezomib is preferred over lenalidomide in patients with creatinine clearance <30 mL/min because it is hepatically metabolized and not renally cleared. Lenalidomide requires significant dose reduction in renal impairment.
• Treat the underlying disease – the most effective renal-protective intervention is rapid disease control with anti-myeloma therapy, which reduces the light chain burden.

For broader nursing management of acute kidney injury, see the AKI nursing reference.

Anemia and fatigue

Anemia in myeloma is multifactorial: marrow infiltration by clonal plasma cells, inflammatory cytokine suppression of erythropoiesis, renal failure with reduced erythropoietin production, and treatment-related myelosuppression. Hemoglobin <10 g/dL meets the CRAB criterion.

Management options include packed red cell transfusion for symptomatic anemia (typical threshold Hb <7–8 g/dL or symptomatic at higher values), erythropoiesis-stimulating agents (ESAs such as epoetin alfa or darbepoetin) when appropriate, and aggressive treatment of the underlying disease. Nursing care emphasizes activity pacing, energy conservation, fall prevention in fatigued patients, and patient education on signs of worsening anemia.

Immunocompromise and infection prevention

Multiple myeloma produces a state of immunoparesis: the clonal plasma cell expansion suppresses normal polyclonal immunoglobulin production, leaving patients severely deficient in functional antibodies even when total immunoglobulin levels appear normal. Add chemotherapy-induced neutropenia, and patients face a substantial infection risk – with infection being the leading cause of early mortality in newly diagnosed myeloma.

Standard prophylaxis includes:

• Acyclovir or valacyclovir for HSV/VZV prophylaxis in patients receiving proteasome inhibitors (bortezomib and carfilzomib both cause significant zoster reactivation).
• Trimethoprim-sulfamethoxazole for Pneumocystis jirovecii (PCP) prophylaxis in patients receiving high-dose dexamethasone or daratumumab-based therapy.
• Intravenous immunoglobulin (IVIG) for patients with recurrent serious infections and documented hypogammaglobulinemia.
• Vaccinations – pneumococcal, annual influenza, COVID-19, and shingles (recombinant zoster vaccine, Shingrix – live vaccines are contraindicated). Vaccination should be completed before significant immunosuppression when feasible.

Nursing patient education focuses on early recognition of infection: any fever ≥38.0°C, new cough, dysuria, or skin lesion warrants prompt clinical evaluation. Patients should receive a thermometer and clear written instructions to call the oncology team for fever rather than waiting.

Peripheral neuropathy

Bortezomib and thalidomide both cause dose-dependent peripheral sensory neuropathy. Symptoms typically begin with distal paresthesias and may progress to painful neuropathy, sensory loss, and gait instability. Subcutaneous bortezomib administration (rather than IV) and weekly (rather than twice-weekly) dosing significantly reduce neuropathy incidence.

Nursing assessment at each visit should include:

• A focused symptom review using validated tools (numbness, tingling, pain, weakness).
• Examination of vibration sense, light touch, and proprioception.
• Functional assessment – buttoning a shirt, walking heel-to-toe, reaching for objects.
• Fall risk assessment, especially in older adults.

Dose modification is indicated for grade 2 neuropathy with pain or grade 3 neuropathy. Symptomatic management includes gabapentin or duloxetine for painful neuropathy and physical therapy for gait training. Educate patients to inspect their feet daily, wear well-fitting footwear, and report new or worsening symptoms promptly.

Hyperviscosity syndrome

Very high serum paraprotein concentrations (typically with IgM in Waldenström macroglobulinemia, but occasionally with IgA or IgG in myeloma) increase blood viscosity and impair microcirculation. The classic triad is mucosal bleeding, visual disturbance (blurred vision, “sausage-link” retinal veins), and neurologic symptoms (headache, dizziness, confusion, seizure). Severe hyperviscosity is an oncologic emergency requiring plasmapheresis to mechanically remove the paraprotein, followed by initiation of disease-directed therapy. Nursing assessment for new headache, visual change, or epistaxis in any myeloma patient with very high paraprotein should prompt immediate evaluation.

DVT/VTE prophylaxis with IMiDs

Lenalidomide, thalidomide, and pomalidomide all increase venous thromboembolism risk, particularly when combined with high-dose dexamethasone. The IMWG recommends VTE risk stratification at the start of every IMiD-based regimen:

• Low risk (no risk factors): aspirin 81–325 mg daily.
• High risk (prior VTE, immobility, central venous catheter, obesity, comorbid cardiac or renal disease, surgery, erythropoietin use, or high-dose dexamethasone): low molecular weight heparin (LMWH) or therapeutic anticoagulation. Direct oral anticoagulants (DOACs) are increasingly used.

Nursing education includes signs of DVT (unilateral leg swelling, pain, warmth) and pulmonary embolism (sudden dyspnea, chest pain, tachycardia, hypoxia). For broader nursing management, see the DVT nursing reference.

REMS programs for IMiDs

All three IMiDs are regulated under Risk Evaluation and Mitigation Strategy (REMS) programs because of severe teratogenicity (thalidomide is among the most potent human teratogens known). Requirements:

• Prescriber, pharmacy, and patient enrollment.
• Patient counseling and signed acknowledgment.
• For females of reproductive potential: two negative pregnancy tests before initiation, monthly pregnancy testing during therapy, and use of two reliable forms of contraception (or complete abstinence) starting four weeks before therapy through four weeks after the last dose.
• For males: barrier contraception during therapy and for four weeks after the last dose; no sperm donation.
• Limited dispensing quantities.

Nursing role includes verifying REMS enrollment, performing or arranging pregnancy testing, reinforcing contraception counseling, and ensuring no doses are dispensed outside the program.

Daratumumab and the blood bank

Daratumumab and isatuximab bind CD38, which is also expressed on red blood cells. The drug coats the patient’s red cells and produces a positive indirect antiglobulin test (a false-positive antibody screen) that interferes with pretransfusion compatibility testing. This interference can persist for up to six months after the last dose.

Nursing actions before initiating an anti-CD38 monoclonal:

1. Type and screen the patient before the first infusion. Phenotype the patient’s red cells if possible.
2. Notify the blood bank that the patient will be receiving daratumumab so the laboratory can prepare alternative crossmatch protocols (typically dithiothreitol treatment of reagent cells, or genotyping).
3. Document daratumumab use prominently in the chart and provide the patient with a wallet card.
4. Ensure appropriate infusion-reaction prophylaxis – steroids, antihistamines, acetaminophen, and montelukast – before the first dose, with slow titration of the infusion rate.

CAR-T cell therapy nursing

After CAR-T infusion, two distinct toxicity syndromes dominate the early monitoring period.

Cytokine release syndrome (CRS) is a systemic inflammatory response from massive T-cell activation and cytokine release (especially IL-6). Onset is typically within 1–14 days after infusion. CRS is graded by the ASTCT consensus criteria:

• Grade 1: fever ≥38.0°C without hypotension or hypoxia.
• Grade 2: fever with hypotension responsive to fluids, or hypoxia requiring low-flow oxygen.
• Grade 3: fever with hypotension requiring vasopressors, or hypoxia requiring high-flow oxygen.
• Grade 4: life-threatening – multiple vasopressors, mechanical ventilation, organ failure.

Tocilizumab (anti-IL-6 receptor monoclonal antibody) is the first-line treatment for grade 2 or higher CRS. Corticosteroids are added for refractory or severe CRS. Nursing care during CRS includes continuous vital sign monitoring, telemetry, hourly assessments, fluid resuscitation, and ICU transfer when grade 3 develops.

Immune effector cell-associated neurotoxicity syndrome (ICANS) is a distinct neurologic syndrome that can occur with or without preceding CRS. Manifestations include confusion, dysphasia (with the classic early sign being difficulty writing a simple sentence – the immune effector cell-associated encephalopathy [ICE] score), tremor, seizures, and in severe cases coma and cerebral edema. ICANS is graded by the same ASTCT framework using the ICE score, level of consciousness, seizure activity, motor findings, and elevated intracranial pressure.

ICANS is treated primarily with corticosteroids (dexamethasone or methylprednisolone). Tocilizumab is generally not effective for ICANS because it does not penetrate the central nervous system well. Nursing care includes serial ICE scoring at least every 8 hours during the at-risk period (typically the first 30 days), neurologic checks, seizure precautions, and fall precautions.

The key NCLEX distinction: CRS is fever-driven and treated with tocilizumab; ICANS is neurologic and treated with corticosteroids.

Differentiating myeloma from other hematologic malignancies

Multiple myeloma, the leukemias, and the lymphomas are all hematologic cancers and frequently appear together on NCLEX questions. The differentiation table below highlights the high-yield exam features.

For deeper dives, see the leukemia nursing reference, the lymphoma nursing reference, and the broader oncology nursing reference.

Patient education priorities

Effective myeloma patient education should be reinforced at each visit. The core teaching points:

• Signs of infection – fever ≥38.0°C, new cough, dysuria, or skin breakdown require immediate clinical contact. Hand hygiene, avoidance of crowds during nadirs, and food safety.
• Bone protection – avoid heavy lifting and high-impact activity; use proper body mechanics; report new or worsening bone pain; do not stop bone-modifying therapy without contacting the team.
• Dental care – maintain meticulous oral hygiene; avoid invasive dental procedures while on bisphosphonates or denosumab; report any new oral pain, exposed bone, or non-healing lesion.
• DVT awareness – on IMiD-based therapy, watch for unilateral leg swelling, calf pain, sudden shortness of breath, or chest pain.
• Hydration – maintain at least 2–3 liters of fluid daily to support renal clearance of light chains, unless restricted for cardiac reasons.
• Medication adherence – emphasize adherence with oral agents (lenalidomide, ixazomib, pomalidomide, selinexor) and the importance of REMS counseling and pregnancy precautions where applicable.
• Avoid NSAIDs – ibuprofen, naproxen, and similar agents are nephrotoxic and should not be used for myeloma bone pain. Acetaminophen and prescribed opioids are the appropriate analgesics.
• Vaccination – encourage non-live vaccines (pneumococcal, annual influenza, COVID-19, recombinant zoster) and avoid live vaccines while immunosuppressed.

NCLEX tips: multiple myeloma

1. CRAB defines active disease. HyperCalcemia, Renal impairment, Anemia, Bone lesions. Memorize the four letters – at least one CRAB or SLiM criterion is required (in addition to ≥10% clonal marrow plasma cells) to diagnose active multiple myeloma.

2. M-spike on SPEP = monoclonal protein from clonal plasma cells. The tall, narrow peak in the gamma region of serum protein electrophoresis is the most recognizable diagnostic finding.

3. Bence Jones proteins = free light chains in urine. Standard urine dipstick misses them; a 24-hour urine with UPEP and immunofixation is required.

4. Pathological fracture risk is highest priority. With known lytic lesions or vertebral involvement, the priority nursing action is fall precautions, lifting restrictions, and prompt evaluation of any new back pain (vertebral fracture or cord compression).

5. Hypercalcemia management sequence: hydrate first, then bisphosphonate. Aggressive isotonic saline hydration is the first intervention. Calcitonin provides rapid bridge therapy. IV zoledronic acid produces durable calcium reduction. Loop diuretics are used only after volume repletion.

6. Bortezomib and peripheral neuropathy. Assess for distal numbness, tingling, and pain at every visit. Subcutaneous and weekly dosing reduce risk versus IV twice-weekly. Hold or dose-modify for grade 2 with pain or grade 3 neuropathy.

7. Daratumumab – alert the blood bank before the first infusion. Anti-CD38 binds CD38 on RBCs and produces false-positive antibody screens that interfere with crossmatching for up to six months. Type and screen first, notify the lab, document prominently.

8. Lenalidomide and thalidomide are teratogenic – REMS is mandatory. Two negative pregnancy tests before starting, monthly during therapy, two reliable forms of contraception, and four-week washout before and after therapy. Thalidomide STEPS program is the strictest.

9. DVT prophylaxis is required with IMiD-based regimens. Aspirin for low-risk patients; LMWH or therapeutic anticoagulation for high-risk patients. Education on calf swelling, sudden dyspnea, and chest pain.

10. Infection risk in myeloma is from immunoparesis. The malignant clone suppresses production of normal polyclonal antibodies, leaving patients functionally hypogammaglobulinemic even when total immunoglobulins look normal. This is why infection is the leading cause of early mortality.

11. ONJ prevention requires dental clearance before bisphosphonate. Complete dental exam and any extractions before initiating zoledronic acid or denosumab. During therapy, avoid invasive dental procedures and maintain oral hygiene. Report new oral pain or exposed bone immediately.

12. Hyperviscosity syndrome – think mucosal bleeding, visual changes, headache. Acute treatment is plasmapheresis. The classic triad in question stems is epistaxis or gingival bleeding, blurred vision, and headache or confusion.

13. Bortezomib is preferred over lenalidomide in renal impairment. Bortezomib is hepatically metabolized and not renally cleared, making it the proteasome inhibitor of choice when creatinine clearance is low. Lenalidomide requires significant dose reduction in renal impairment.

14. CRS vs ICANS with CAR-T. CRS is the inflammatory syndrome – fever, hypotension, hypoxia – treated with tocilizumab. ICANS is the neurologic syndrome – confusion, dysphasia, seizure – treated with corticosteroids. Tocilizumab does not cross the blood-brain barrier and is not used for ICANS.

15. ISS staging uses beta-2 microglobulin and albumin. Stage I: β2M <3.5 and albumin ≥3.5. Stage III: β2M ≥5.5. R-ISS adds LDH and high-risk cytogenetics (del(17p), t(4;14), t(14;16)).

16. Avoid NSAIDs and IV contrast. Both worsen myeloma renal injury. Use acetaminophen and prescribed opioids for bone pain. If contrast cannot be avoided, ensure aggressive pre- and post-procedure hydration.

17. Stem cell transplant in myeloma is autologous, not allogeneic. High-dose melphalan conditioning followed by reinfusion of the patient’s own previously collected stem cells. Allogeneic transplant is rarely performed in myeloma.

Clinical sources and further reading

This reference draws on guidelines and recommendations from the International Myeloma Working Group (IMWG), the National Comprehensive Cancer Network (NCCN) Guidelines for Multiple Myeloma, the American Society of Clinical Oncology (ASCO), the National Cancer Institute (NCI), and standard hematology-oncology nursing references including the Oncology Nursing Society (ONS) chemotherapy and immunotherapy guidelines.

For related nursing topics, see:

• Leukemia nursing reference – AML, ALL, CML, CLL with tumor lysis syndrome and neutropenic precautions.
• Lymphoma nursing reference – Hodgkin and non-Hodgkin lymphoma, ABVD/R-CHOP nursing.
• Oncology nursing reference – overarching framework for oncologic emergencies, neutropenic precautions, and chemotherapy administration.
• Anemia nursing reference – classification, diagnostic workup, and transfusion thresholds.
• AKI nursing reference – stages, prerenal/intrinsic/postrenal differentiation, nephrotoxic agent avoidance.
• DVT nursing reference – risk stratification, prophylaxis, and anticoagulation management.