Lymphoma nursing: Hodgkin and non-Hodgkin reference for nursing students

Lymphoma is the third most common hematologic malignancy in the United States, with approximately 90,000 new cases diagnosed each year. Unlike leukemia — which originates in the bone marrow — lymphoma arises from lymphocytes within the lymphatic system itself: the lymph nodes, spleen, thymus, and extranodal lymphoid tissue. The result is a disease that presents primarily as lymphadenopathy, often with systemic constitutional symptoms, and is staged and treated according to the extent of nodal and extranodal involvement.

There are two broad categories. Hodgkin lymphoma (HL) is distinguished by a single pathognomonic finding — the Reed-Sternberg cell — and carries a favorable prognosis, with 5-year survival around 87%. Non-Hodgkin lymphoma (NHL) is a far larger and more heterogeneous group, encompassing more than 60 distinct subtypes ranging from indolent diseases managed for years without treatment to some of the most rapidly fatal malignancies in oncology.

For the nurse caring for these patients, the two diseases share overlapping priorities — lymph node assessment, neutropenic precautions, tumor lysis syndrome surveillance, and chemotherapy management — while diverging significantly in pathophysiology, staging, and specific treatment toxicities. This reference covers both, with the clinical depth needed for NCLEX preparation and the nursing detail required for clinical practice.

Hodgkin lymphoma

Pathophysiology and the Reed-Sternberg cell

Hodgkin lymphoma originates from a clonal expansion of an abnormal B-lymphocyte precursor. The defining pathological finding is the Reed-Sternberg cell — a giant, binucleated or multinucleated cell with large, prominent “owl eye” nucleoli. These cells constitute only a minority of the tumor mass; the surrounding inflammatory infiltrate (eosinophils, plasma cells, lymphocytes, macrophages) makes up most of the tissue. The Reed-Sternberg cell and its variants are the histological requirement for a diagnosis of Hodgkin lymphoma. No other malignancy produces them. For NCLEX: Reed-Sternberg cell = Hodgkin lymphoma, always.

Age distribution

HL has a bimodal age distribution — a pattern distinctive among lymphomas. The first peak occurs in young adults aged 15–35 years, making it one of the most common malignancies in this demographic. A second, smaller peak occurs after age 55. The classic presentation in a young patient with painless cervical or supraclavicular lymphadenopathy and constitutional symptoms should prompt immediate evaluation.

Ann Arbor/Lugano staging

Staging drives treatment intensity in HL. The Ann Arbor system, updated as the Lugano classification for lymphomas, uses four stages:

• Stage I: Involvement of a single lymph node region or a single extralymphatic site
• Stage II: Two or more lymph node regions on the same side of the diaphragm; or localized extranodal extension with nodal involvement on the same side
• Stage III: Lymph node regions on both sides of the diaphragm; may include the spleen
• Stage IV: Diffuse or disseminated extranodal involvement (liver, bone marrow, lung parenchyma)

Each stage is further classified as A (no B symptoms) or B (B symptoms present). Bulky disease — typically a mediastinal mass greater than one-third the thoracic diameter — is an additional modifier that influences treatment intensity.

B symptoms

B symptoms are three constitutional symptoms that, when present, indicate systemic disease activity and confer a worse prognosis:

• Fever greater than 38°C (100.4°F) without infectious cause
• Drenching night sweats requiring a change of clothing or bedding
• Unintentional weight loss greater than 10% of body weight within the preceding 6 months

Nurses must assess for all three at every encounter with a lymphoma patient. The presence of B symptoms upstages the clinical picture and intensifies treatment. The absence of all three = “A” designation.

ABVD chemotherapy

First-line treatment for HL is the ABVD regimen — four drugs given in combination, typically every 28 days for 2–6 cycles depending on stage:

Bleomycin pulmonary toxicity: priority nursing assessment

Bleomycin-induced pulmonary toxicity (BPT) is a potentially life-threatening complication that requires proactive assessment before each chemotherapy cycle. The mechanism is direct oxidative damage to pulmonary endothelial and epithelial cells, progressing to interstitial fibrosis if not caught early.

Assessment before each ABVD cycle:

• Oxygen saturation at rest and with ambulation
• Respiratory rate and work of breathing
• Ask directly about new dry cough, dyspnea on exertion, or dyspnea at rest since the last cycle
• Auscultate lung fields — fine inspiratory crackles are an early sign
• Review PFT trends and diffusing capacity for carbon monoxide (DLCO) if available

Risk factors that increase BPT risk: Cumulative bleomycin dose greater than 200–400 units, renal impairment (bleomycin is renally cleared), prior chest radiation, age over 40, and supplemental oxygen use — including during surgery. Alert the anesthesia team to bleomycin exposure before any operative procedure; high intraoperative FiO2 can precipitate acute pulmonary toxicity.

If BPT is suspected — any new respiratory symptom in a patient on bleomycin — stop the infusion, notify the provider, and obtain a chest X-ray and CT. Bleomycin is typically discontinued permanently once pulmonary toxicity is identified. The condition can progress to pulmonary fibrosis even after drug discontinuation.

Radiation therapy in HL

Involved-site radiation therapy (ISRT) is often used after chemotherapy in Stage I–II disease. Mediastinal involvement is common in HL, and mediastinal radiation carries late effects that nurses must understand for long-term survivorship monitoring:

Cardiac late effects: Pericarditis, accelerated coronary artery disease, cardiomyopathy, and valvular disease can manifest years to decades after mediastinal radiation. HL survivors are at substantially elevated lifetime cardiovascular risk — monitor blood pressure, lipids, and glucose at each visit; educate about cardiac symptom recognition.

Pulmonary late effects: Radiation pneumonitis (onset 4–12 weeks post-radiation) and pulmonary fibrosis (months to years later). Monitor for dyspnea, cough, and declining exercise tolerance in HL survivors.

Secondary malignancy risk: Breast cancer risk is significantly elevated in women who received chest radiation before age 30 (particularly mantle field radiation in older protocols). Annual mammography begins 8–10 years after radiation or at age 40, whichever comes first.

SVC syndrome in bulky mediastinal HL

Bulky mediastinal disease can compress the superior vena cava, impairing venous return from the head, neck, and upper extremities. Signs include facial and upper extremity edema, neck vein distension, facial plethora, dyspnea, and headache that worsens when lying flat or bending forward. SVC syndrome is an oncologic emergency. Nursing priorities: elevate the head of bed to 45 degrees, avoid all IV access and blood pressure measurement in upper extremities, notify the provider immediately, and prepare for urgent imaging and emergent radiation or systemic therapy. See oncology nursing reference for the full SVC management framework.

Non-Hodgkin lymphoma

B-cell vs T-cell lineage

NHL arises from lymphocytes at various stages of maturation. Approximately 85% are B-cell lymphomas; the remaining 15% arise from T-cells or NK cells. This distinction matters clinically because B-cell NHL responds to rituximab (an anti-CD20 monoclonal antibody) while T-cell NHL does not express CD20 and requires different treatment strategies.

NHL subtypes: aggressive and indolent

The most clinically important distinction in NHL is tempo — aggressive (fast-growing, requires immediate treatment) versus indolent (slow-growing, often managed with observation in early stages).

R-CHOP regimen

R-CHOP is the standard first-line treatment for aggressive B-cell NHL (particularly DLBCL) and is also used in follicular lymphoma when treatment is required. It combines a targeted monoclonal antibody (rituximab) with five conventional chemotherapy drugs.

Rituximab infusion reactions: detailed protocol

Rituximab reactions range from mild cytokine release (chills, fever, flushing) to life-threatening anaphylaxis. Distinguishing the two guides management:

Cytokine release syndrome (infusion-related): Most common type. Onset typically within the first 30–120 minutes of infusion. Features: fever, chills, rigors, headache, nausea, mild urticaria. Management: stop infusion, administer antihistamine and acetaminophen as ordered, and restart at 50% of the rate when symptoms resolve. Usually manageable; reaction severity decreases with subsequent infusions.

Anaphylaxis: True IgE-mediated hypersensitivity. Features: bronchospasm, stridor, severe hypotension, angioedema, loss of consciousness. Management: stop infusion immediately, administer epinephrine 0.3–0.5 mg IM into the outer thigh, call a rapid response, establish large-bore IV access, administer normal saline bolus, diphenhydramine, and corticosteroids per protocol. Do not restart infusion. The patient will require a desensitization protocol for future rituximab administration.

NCLEX distinction: The question will ask what to do first when a patient receiving rituximab develops chills, fever, and urticaria. The answer is stop the infusion — before administering any medication.

CNS prophylaxis in high-risk DLBCL

The CNS is a sanctuary site where the blood-brain barrier limits drug penetration. In high-risk DLBCL — defined by the CNS-IPI score incorporating LDH, performance status, stage, extranodal sites, kidney/adrenal involvement, and age — prophylactic intrathecal methotrexate (IT-MTX) or high-dose IV methotrexate is given to reduce the risk of CNS relapse (which otherwise approaches 10–15% in high-risk cases). Nursing assessment for CNS involvement includes monitoring for new headache, cranial nerve changes, vision changes, leg weakness, and any new neurological symptom.

Tumor lysis syndrome

Tumor lysis syndrome (TLS) is the most acute metabolic emergency in lymphoma. It occurs when rapid cell death — spontaneous or chemotherapy-induced — floods the bloodstream with intracellular contents faster than the kidneys can clear them. In lymphoma, TLS risk correlates with tumor burden, proliferation rate, and sensitivity to initial chemotherapy.

Burkitt lymphoma carries the highest TLS risk of any lymphoma, driven by a Ki-67 proliferation index near 100% and extreme sensitivity to first-dose chemotherapy. DLBCL with bulky disease is the next highest risk. The TLS framework in leukemia-nursing applies directly here — both diseases share the same metabolic cascade and management principles; see leukemia nursing for the full TLS protocol including rasburicase dosing, allopurinol dosing, and hemodialysis indications.

TLS prevention: the nursing priorities

• Aggressive IV hydration beginning 24–48 hours before chemotherapy: target urine output ≥2 mL/kg/h; this is the single highest-yield TLS preventive intervention
• Rasburicase (recombinant urate oxidase): preferred in high-risk patients including Burkitt lymphoma and bulky DLBCL; converts existing uric acid to the soluble allantoin, rapidly reducing uric acid levels; contraindicated in G6PD deficiency (causes severe hemolysis)
• Allopurinol (xanthine oxidase inhibitor): used in moderate-risk patients; prevents new uric acid formation but does not reduce existing levels; start 1–2 days before chemotherapy
• Labs every 4–6 hours during high-risk period: potassium, phosphate, calcium, uric acid, creatinine, BUN
• Continuous cardiac monitoring during acute risk window

Lymph node assessment

Lymph node evaluation is a foundational nursing skill for lymphoma assessment and monitoring. A thorough lymph node exam guides staging, identifies treatment response, and detects relapse.

Palpation technique: Examine all major nodal chains systematically — cervical (anterior and posterior), supraclavicular, axillary, epitrochlear, inguinal, and femoral. Use the pads of the second and third fingers in a circular motion. Assess each node for:

• Size: Nodes greater than 1 cm in diameter are suspicious. Nodes in the axilla can normally be up to 1.5 cm.
• Consistency: Rubbery nodes (characteristic of lymphoma) versus soft/shotty (reactive) versus stony-hard (more typical of metastatic carcinoma)
• Mobility: Mobile nodes (more common in reactive lymphadenopathy) versus fixed/matted (more concerning for malignancy or infection spreading to overlying tissue)
• Tenderness: Tender nodes often suggest infectious or inflammatory cause; non-tender nodes are more typical of lymphoma
• Location: Supraclavicular nodes are always abnormal in adults — report immediately; mediastinal and retroperitoneal involvement is assessed by imaging

Documentation: Record size in centimeters (two dimensions), location, consistency, mobility, and tenderness at each assessment. Changes from baseline guide provider decision-making.

Splenomegaly and hepatomegaly

Lymphoma infiltrating the spleen or liver presents as organomegaly with distinct nursing implications:

• Splenomegaly: Left upper quadrant fullness or pain, early satiety (stomach compression), left shoulder pain (Kehr’s sign from diaphragmatic irritation). Nursing: palpate gently — never percuss forcefully; position patient on their right side for comfort; educate to avoid contact sports and heavy lifting; report any sudden severe left upper quadrant pain (splenic rupture). See thrombocytopenia management if splenic sequestration is causing platelet suppression: thrombocytopenia nursing reference.
• Hepatomegaly: Right upper quadrant discomfort, jaundice if bile duct compression is significant; monitor LFTs. Hepatic lymphoma infiltration can impair drug metabolism — report any abnormal LFT trend before chemotherapy cycles.

Anemia in lymphoma patients can arise from marrow infiltration, autoimmune hemolysis, or anemia of chronic disease. See anemia nursing reference for transfusion thresholds and erythropoiesis-stimulating agent management.

Neutropenic precautions

Lymphoma patients — particularly during active chemotherapy — develop profound neutropenia from marrow suppression. The absolute neutrophil count (ANC) is the key parameter:

• ANC <1,000/µL: Initiate neutropenic precautions
• ANC <500/µL: Severe neutropenia — highest infection risk

Neutropenic fever protocol

Definition: Temperature ≥38.3°C (101°F) on a single measurement, OR ≥38°C (100.4°F) sustained for one hour, in a patient with ANC <500/µL. This is a medical emergency.

The neutropenic patient may have no localizing signs of infection — no induration, no purulent drainage, no cough — because neutrophils mediate the inflammatory response that produces these signs. A single temperature spike may be the only clue that the patient is septic.

Nursing response:

1. Obtain at least two sets of blood cultures from different sites (one from central line if present, one peripheral) — obtain before antibiotics, but do not delay antibiotics more than 15 minutes to get cultures
2. Obtain urinalysis and urine culture; chest X-ray
3. Notify provider immediately
4. Anticipate broad-spectrum IV antibiotics (piperacillin-tazobactam, cefepime, or meropenem depending on risk stratification) — target initiation within 60 minutes of fever recognition
5. Monitor vital signs every 1–2 hours; assess for signs of evolving sepsis (hypotension, tachycardia, altered mental status)

For the full sepsis recognition and bundle management framework, see sepsis nursing.

Protective precautions

Standard neutropenic precautions for lymphoma patients during chemotherapy:

• Private room for single-patient isolation
• Strict hand hygiene — most effective single intervention for preventing healthcare-associated infection
• No fresh flowers or plants — potting soil and standing water harbor Aspergillus and gram-negative bacteria
• No raw or unwashed produce — source of Pseudomonas and other pathogens; cooked or properly washed produce only
• Screen all visitors for respiratory symptoms or active infection; no ill visitors
• Avoid rectal temperatures, suppositories, enemas, and any procedure that disrupts mucosal barriers
• Meticulous oral care — mucositis creates a portal of entry for bacteremia; saline or chlorhexidine rinses per protocol
• Sterile technique for central line care and dressing changes

G-CSF support: Filgrastim or pegfilgrastim is often administered 24–72 hours after R-CHOP and ABVD cycles to shorten the duration of neutropenia. Administer subcutaneously. The primary side effect is bone pain from marrow expansion — acetaminophen is usually adequate for management. Monitor CBC until ANC recovery.

CAR-T cell therapy

Chimeric antigen receptor T-cell (CAR-T) therapy is a cellular immunotherapy used for relapsed or refractory B-cell NHL — primarily DLBCL — after two or more prior lines of treatment. It involves harvesting the patient’s own T-cells via leukapheresis, genetically engineering them to express a receptor targeting CD19 (expressed on B-cells), manufacturing them in a laboratory over 2–4 weeks, and then infusing them back into the patient after lymphodepleting chemotherapy. Currently approved CAR-T products for B-cell NHL include axicabtagene ciloleucel (axi-cel), tisagenlecleucel (tisa-cel), and lisocabtagene maraleucel (liso-cel).

CAR-T therapy is high-yield on NCLEX due to two specific toxicities that require ICU-level nursing vigilance.

Cytokine release syndrome (CRS)

CRS is the most common serious complication of CAR-T therapy, occurring in up to 90% of patients to some degree. It results from massive immune activation as the engineered T-cells expand and attack CD19-expressing cells, releasing inflammatory cytokines (IL-6, IFN-γ, TNF-α) systemically.

Clinical presentation: Fever (often the first sign, typically within 1–7 days of infusion), hypotension, tachycardia, hypoxia, and in severe cases, capillary leak syndrome with pulmonary edema and multi-organ dysfunction. Graded 1–4 by the American Society for Transplantation and Cellular Therapy (ASTCT) criteria.

Nursing assessment: Temperature, blood pressure, oxygen saturation, and heart rate every 4 hours — or every 1–2 hours in the immediate post-infusion period. Report any fever within the first 14 days after CAR-T infusion as potential CRS.

Management:

• Grade 1 (fever alone): supportive care, monitoring, antipyretics
• Grade 2 (fever + hypotension responsive to IV fluids or low-flow O2): tocilizumab (IL-6 receptor antagonist) 8 mg/kg IV — this is the first-line CRS treatment; corticosteroids (dexamethasone) added for refractory cases
• Grade 3–4 (ICU-level hemodynamic/respiratory support required): tocilizumab + high-dose corticosteroids + ICU transfer; vasopressors and mechanical ventilation may be required

NCLEX key: CAR-T → CRS → tocilizumab is the treatment. Tocilizumab blocks IL-6 signaling, which is the central driver of CRS cytokine storm.

ICANS (immune effector cell-associated neurotoxicity syndrome)

ICANS is a delayed neurotoxicity that typically develops 5–14 days after CAR-T infusion, sometimes after CRS has resolved. The mechanism is not fully elucidated but involves cytokine-mediated disruption of the blood-brain barrier with endothelial activation and neuroinflammation.

Clinical presentation: Ranges from mild (confusion, word-finding difficulty, handwriting deterioration, tremor, expressive aphasia) to severe (seizures, motor deficits, cerebral edema, coma). The immune effector cell-associated encephalopathy (ICE) score — a 10-point bedside neurocognitive assessment — is used to grade ICANS severity.

Nursing assessment: Perform baseline and daily ICE score assessments. Monitor for: new confusion, changes in level of consciousness, difficulty following commands, expressive aphasia, agitation, seizure activity, headache, and changes in handwriting (ask the patient to write a standard sentence at baseline and compare daily). Report any neurological change promptly — ICANS can progress rapidly to cerebral edema.

Management:

• Grade 1: observation, monitoring
• Grade 2–4: corticosteroids (dexamethasone or methylprednisolone) are first-line; tocilizumab is NOT used for isolated ICANS (it does not cross the blood-brain barrier effectively and may worsen neurotoxicity in some contexts)
• Seizure prophylaxis with levetiracetam is given prophylactically in most CAR-T protocols
• Grade 4 (cerebral edema): ICU, neurosurgery consultation, high-dose corticosteroids, anti-edema measures

The NCLEX distinction between CRS and ICANS: CRS = systemic (fever, hypotension, hypoxia) → tocilizumab. ICANS = neurological (confusion, aphasia, seizure) → corticosteroids. Both require ICU monitoring. ICANS can occur concurrently with or after CRS.

ICU monitoring requirements for CAR-T patients:

• Continuous telemetry for at least 72 hours post-infusion (CRS can cause arrhythmias)
• Neurological assessments every 4–8 hours including ICE score
• Daily CBC to monitor for cytopenias from lymphodepleting chemotherapy and ongoing CAR-T-related marrow suppression
• LFTs, renal function, ferritin, CRP, LDH as inflammatory markers — elevated ferritin (>10,000 µg/L) correlates with severe CRS/hemophagocytic lymphohistiocytosis
• Strict fall precautions for any degree of neurological involvement
• Patients must remain near the treating institution for at least 4 weeks after infusion per FDA REMS requirements

NCLEX tips: lymphoma

1. Reed-Sternberg cells = Hodgkin lymphoma. Pathognomonic. Giant binucleated cells with “owl eye” nucleoli on lymph node biopsy = HL, every time. No other malignancy.

2. B symptoms = fever/sweats/weight loss = worse prognosis in both HL and NHL. Fever >38°C + drenching night sweats + >10% weight loss = Stage B disease.

3. Ann Arbor Stage IV = extranodal involvement. Liver, bone marrow, and lung parenchyma involvement = Stage IV. Stage III = nodes on both sides of the diaphragm.

4. ABVD = Hodgkin lymphoma. R-CHOP = aggressive NHL (primarily DLBCL). Knowing which regimen belongs to which disease is an NCLEX staple.

5. Bleomycin → pulmonary toxicity. Before each ABVD cycle, assess oxygen saturation, respiratory rate, and ask specifically about new cough or dyspnea. Report any respiratory symptom — bleomycin may be permanently discontinued.

6. Rituximab → infusion reaction highest risk on the first dose. Premedicate with acetaminophen + diphenhydramine + methylprednisolone. Stop infusion immediately if fever, chills, urticaria, bronchospasm, or hypotension develop. Restart at 50% rate when mild symptoms resolve.

7. First action with rituximab reaction = stop the infusion. Always stop the drug first before treating the symptoms. This applies to any IV medication reaction.

8. Follicular lymphoma → watch and wait in low-burden asymptomatic disease. Observation without treatment is evidence-based. The correct NCLEX answer for asymptomatic Stage I–II follicular lymphoma is not to initiate chemotherapy.

9. DLBCL = most common aggressive NHL. When a question presents aggressive NHL, DLBCL is the most likely diagnosis. R-CHOP × 6 cycles is standard.

10. Burkitt lymphoma = highest TLS risk among lymphomas. Ki-67 ~100% means near-total proliferative activity — every tumor cell is dividing. Aggressive hydration and rasburicase before chemotherapy are mandatory.

11. TLS electrolyte pattern = K↑ PO4↑ Ca↓ uric acid↑. Three values rise (potassium, phosphate, uric acid); calcium falls. Memory device: three “hypers” plus one “hypo.”

12. Rasburicase is contraindicated in G6PD deficiency. It causes acute hemolysis in G6PD-deficient patients. Screen before use. Allopurinol is the alternative.

13. CAR-T → CRS → tocilizumab is the treatment. The IL-6 receptor antagonist tocilizumab is first-line for Grade 2+ CRS. Corticosteroids are added for refractory cases.

14. ICANS (immune effector cell-associated neurotoxicity syndrome) → corticosteroids, not tocilizumab. ICANS is the neurological complication of CAR-T (confusion, aphasia, seizures). Treatment is dexamethasone/methylprednisolone. Tocilizumab does not treat ICANS.

15. Neutropenic fever = medical emergency. Blood cultures before antibiotics, but do not delay antibiotics more than 15 minutes for cultures. Broad-spectrum IV antibiotics within 60 minutes of fever identification.

16. Supraclavicular lymph nodes are always abnormal in adults. Any supraclavicular node in an adult requires immediate evaluation. It is never a normal finding.

Summary

Lymphoma nursing bridges two distinct diseases — Hodgkin lymphoma and non-Hodgkin lymphoma — with overlapping assessment priorities but substantially different clinical profiles. HL’s defining feature is the Reed-Sternberg cell; its treatment with ABVD is effective but demands bleomycin pulmonary toxicity monitoring before every cycle. Favorable prognosis (87% 5-year survival) and a young patient population make long-term survivorship — cardiac and pulmonary late effects from radiation — a nursing priority that extends well beyond the acute treatment phase.

Non-Hodgkin lymphoma encompasses a spectrum from the indolent follicular lymphoma (where watch-and-wait is evidence-based) to Burkitt lymphoma (where near-100% proliferation rate creates the highest TLS risk in oncology). R-CHOP is the workhorse regimen for aggressive B-cell NHL, and rituximab infusion reaction management is a core NCLEX and clinical competency. For relapsed or refractory B-cell NHL, CAR-T therapy introduces two new toxicities — CRS and ICANS — that require ICU-level monitoring, rapid recognition, and protocol-driven treatment.

Across all lymphoma subtypes, three nursing priorities remain constant: lymph node assessment to monitor disease activity, TLS prevention and surveillance during cytotoxic treatment, and neutropenic fever recognition and immediate response.

For related hematologic malignancy content, see leukemia nursing for the complete TLS management protocol, ANC calculation, and shared bone marrow suppression framework. For general chemotherapy safety, oncologic emergencies, and supportive care, see oncology nursing reference. For thrombocytopenia from marrow infiltration, see thrombocytopenia nursing reference. For anemia of malignancy and transfusion management, see anemia nursing reference.