Lung cancer nursing: assessment, interventions, and NCLEX review

Lung cancer is the leading cause of cancer-related mortality in the United States, responsible for more deaths each year than colorectal, breast, and prostate cancers combined. The American Cancer Society estimates approximately 234,000 new diagnoses and 125,000 deaths annually. Despite advances in targeted therapy and immunotherapy that have transformed outcomes for select patients, overall 5-year survival remains around 25% — a reflection of how frequently the disease is caught at advanced stage.

Two biologically distinct categories drive nearly all cases. Non-small cell lung cancer (NSCLC) accounts for roughly 85% of diagnoses and encompasses several subtypes with different molecular drivers, locations, and treatment responses. Small cell lung cancer (SCLC) makes up the remaining 15% — a neuroendocrine malignancy defined by explosive growth, early metastasis, and a dramatic but short-lived initial response to chemotherapy.

Nurses encounter lung cancer patients across virtually every clinical setting: oncology units, ICUs managing acute respiratory failure, emergency departments evaluating superior vena cava syndrome, palliative and hospice settings, and primary care offices. Whether managing post-thoracotomy chest tubes, monitoring immunotherapy toxicities, or supporting a patient through a first prognosis conversation, the nurse’s clinical foundation in lung cancer pathophysiology, staging, and treatment directly affects patient outcomes. This reference covers that foundation with the clinical detail needed for NCLEX preparation and practice.

Quick reference: NSCLC vs SCLC

Types and pathophysiology

Adenocarcinoma

Adenocarcinoma is the most common lung cancer subtype overall (~40% of cases) and the most common in non-smokers — though smoking remains a risk factor. It arises from peripheral glandular cells and typically presents as a peripheral mass or ground-glass opacity on imaging. Adenocarcinoma is the subtype most frequently driven by targetable oncogenic mutations: EGFR mutations (most common in Asian non-smoking women), ALK rearrangements, ROS1 fusions, KRAS mutations, and BRAF mutations. Identifying these mutations is essential before initiating therapy because they predict response to specific targeted agents.

A distinct variant — adenocarcinoma in situ (formerly bronchioloalveolar carcinoma) — grows along alveolar walls without destroying architecture, can present with production of large volumes of thin secretions, and may be multifocal.

Squamous cell carcinoma

Squamous cell carcinoma (SCC) arises from bronchial epithelial cells and is strongly associated with cigarette smoking. It is a central tumor — arising near the carina or proximal bronchi — and is prone to cavitation (a thick-walled cavity visible on imaging). SCC is the subtype most associated with hypercalcemia of malignancy, caused by tumor secretion of parathyroid hormone-related protein (PTHrP), which mimics PTH and drives calcium release from bone. PTHrP-mediated hypercalcemia is termed humoral hypercalcemia of malignancy — distinct from hypercalcemia caused by direct bone metastasis. Clinically: confused, constipated, hypercalcemic patient with a central cavitating lung mass = squamous cell until proven otherwise.

Large cell carcinoma

Large cell carcinoma is a diagnosis of exclusion — poorly differentiated tumors that lack the features of adenocarcinoma, squamous cell, or SCLC on light microscopy. These tumors are aggressive, peripherally located, and have a poorer prognosis than adenocarcinoma or SCC. Molecular testing often reveals actionable mutations (KRAS, STK11, KEAP1). Large cell neuroendocrine carcinoma (LCNEC) is a specific subtype with neuroendocrine features and behavior closer to SCLC.

Small cell lung cancer (SCLC)

SCLC originates from neuroendocrine Kulchitsky cells within the bronchial epithelium. It is almost exclusively found in heavy smokers. The hallmarks: central location, rapid doubling time (~30 days), early and widespread metastasis (brain, liver, bone, adrenal glands), and a paradoxical initial response to chemotherapy — tumors may shrink dramatically — followed by rapid relapse with resistance.

SCLC staging uses a simplified two-stage system:

• Limited disease (LD): Tumor confined to one hemithorax and draining lymph nodes, encompassable within a single radiation field. Treated with concurrent chemoradiation.
• Extensive disease (ED): Beyond one hemithorax, including malignant pleural effusion. Treated with chemotherapy ± immunotherapy; radiation is palliative.

SCLC is the lung cancer subtype most associated with paraneoplastic syndromes, produced by ectopic hormone secretion from the neuroendocrine tumor cells:

• SIADH: Ectopic ADH → free water retention → dilutional hyponatremia. Symptoms: headache, confusion, seizures in severe cases. Management: fluid restriction, monitor serum sodium, consider hypertonic saline only for severe symptomatic hyponatremia.
• Cushing’s syndrome: Ectopic ACTH → bilateral adrenal hyperplasia → cortisol excess. Presents with hypokalemia, hyperglycemia, hypertension, and metabolic alkalosis. Unlike pituitary Cushing’s, the typical fat redistribution and striae may not be prominent because onset is rapid.
• Lambert-Eaton myasthenic syndrome (LEMS): Autoantibodies (anti-VGCC) attack presynaptic voltage-gated calcium channels → impaired acetylcholine release → proximal limb weakness. Key distinction from myasthenia gravis: in LEMS, strength briefly improves with repeated muscle use; in MG, strength worsens. Absent or reduced deep tendon reflexes are characteristic.

Clinical presentation

Early disease

Lung cancer is frequently asymptomatic in its early stages. Many early-stage tumors are discovered incidentally on chest imaging obtained for other reasons — a pre-operative CXR, trauma CT, or cardiovascular workup. This is the rationale for low-dose CT (LDCT) lung cancer screening in high-risk individuals: current USPSTF guidelines recommend annual LDCT for adults aged 50–80 with a 20+ pack-year smoking history who currently smoke or quit within the past 15 years.

Pulmonary symptoms

As the tumor grows, pulmonary symptoms emerge:

• Cough — new persistent cough or a significant change in a chronic smoker’s cough. The most common presenting symptom.
• Hemoptysis — blood-streaked sputum to frank hemorrhage. Any hemoptysis in a smoker warrants urgent investigation.
• Dyspnea — from airway obstruction, pleural effusion, or parenchymal involvement.
• Wheezing — unilateral, fixed wheezing (unlike the diffuse wheeze of asthma) suggests endobronchial obstruction.
• Chest pain — pleuritic or dull, suggests chest wall or pleural involvement.

Constitutional symptoms

Weight loss, anorexia, fatigue, and night sweats appear in more advanced disease and carry prognostic significance. Unintentional weight loss of ≥5% over 6 months is a marker of poor prognosis.

Location-specific presentations

Central tumors (SCC, SCLC) obstructing a mainstem or lobar bronchus cause:

• Post-obstructive pneumonia — recurrent pneumonia in the same lobe or segment. A pneumonia that does not resolve or recurs in the same location demands imaging and bronchoscopy.
• Stridor — high-pitched inspiratory sound from large-airway obstruction; requires urgent airway assessment.

Pancoast tumor (superior sulcus tumor): A tumor in the apex of the lung that invades the chest wall, brachial plexus, and sympathetic chain. The classic triad:

1. Horner’s syndrome — ptosis (drooping eyelid), miosis (constricted pupil), anhidrosis (absent sweating) on the ipsilateral face. Caused by disruption of the cervical sympathetic chain (T1 stellate ganglion).
2. Shoulder and arm pain radiating into the ulnar distribution — from brachial plexus invasion.
3. Ipsilateral hand muscle wasting — from C8-T1 nerve root involvement.

Superior vena cava (SVC) syndrome: Compression or invasion of the SVC by a right-sided mediastinal tumor (most common cause: SCLC or right upper lobe NSCLC) obstructs venous drainage from the upper body. Signs and symptoms:

• Facial, neck, and arm edema (often worse in the morning after lying flat)
• Plethora and facial flushing
• Distended neck and chest wall veins (collateral circulation)
• Headache, visual changes, confusion (from increased intracranial pressure)
• Dyspnea and cough

SVC syndrome is an oncologic emergency. Nursing priority: elevate the head of bed 30–45°, apply supplemental oxygen, maintain IV access in the lower extremities (upper extremity IV lines are contraindicated — poor drainage), notify the physician immediately. Definitive treatment is radiation therapy, chemotherapy, or endovascular stenting.

Metastatic symptoms

NSCLC commonly metastasizes to the brain, bone, liver, and adrenal glands. SCLC spreads to virtually every organ. Metastatic symptoms:

• Bone metastases: Localized bone pain, pathologic fractures, hypercalcemia (from bone resorption)
• Brain metastases: Headache (often worse in morning), seizures, focal neurologic deficits, altered mental status
• Liver metastases: RUQ pain, jaundice, elevated liver enzymes, ascites in advanced disease
• Lymphadenopathy: Supraclavicular lymph nodes are a common site of spread; Virchow’s node (left supraclavicular) is a classic finding

Diagnostic workup

Imaging

• Chest X-ray (CXR): Often the first imaging obtained. May reveal a peripheral coin lesion, hilar mass, widened mediastinum, atelectasis, or pleural effusion. A normal CXR does not exclude lung cancer.
• CT chest/abdomen/pelvis with contrast: Standard staging workup. Characterizes tumor size, location, mediastinal lymph node involvement, and distant metastases. CT is the primary tool for T and N staging.
• PET scan (FDG-PET/CT): Identifies metabolically active sites of disease for M staging. Distinguishes active tumor from scar tissue. Required for curative-intent surgical planning to exclude occult distant metastases. Not useful for brain metastases (normal brain uptake is high).
• Brain MRI with contrast: Required when brain metastases are suspected or before curative surgery (brain mets would change management to Stage IV).

Tissue diagnosis

No treatment decision should be made without pathologic confirmation:

• Bronchoscopy with BAL and biopsy: Best for central, endobronchial tumors. Allows direct visualization, washings, brushings, and forceps biopsy. Endobronchial ultrasound (EBUS) can sample mediastinal lymph nodes.
• CT-guided transthoracic needle biopsy: Best for peripheral tumors accessible from the chest wall. Higher pneumothorax risk (~15–30%); post-procedure: monitor for respiratory distress, obtain post-procedure CXR, ensure supplemental oxygen available.
• Video-assisted thoracoscopic surgery (VATS): Minimally invasive surgical biopsy. Used when bronchoscopy and CT-guided biopsy are non-diagnostic or when a resectable peripheral nodule requires both diagnosis and treatment.
• Mediastinoscopy / mediastinotomy: Surgical sampling of mediastinal lymph nodes for staging when non-invasive methods are inadequate.

Molecular and biomarker testing

All patients with non-squamous NSCLC (and squamous in non-smokers) should undergo comprehensive molecular testing on tumor tissue. This is standard of care and directly determines treatment:

• EGFR mutations — present in ~15% of US NSCLC (higher in Asian populations). Predict response to EGFR tyrosine kinase inhibitors (erlotinib, gefitinib, osimertinib).
• ALK rearrangements — ~3–7% of NSCLC. Predict response to ALK inhibitors (crizotinib, alectinib, brigatinib).
• ROS1 fusions — ~1–2%. Predict response to ROS1 inhibitors (crizotinib, entrectinib).
• PD-L1 expression (IHC) — determines immunotherapy eligibility. PD-L1 ≥50% qualifies for first-line pembrolizumab monotherapy. Lower expression may still benefit from combination chemo-immunotherapy.
• KRAS G12C — ~13% of adenocarcinomas; targetable with sotorasib or adagrasib.
• BRAF V600E — ~2–4%; treated with dabrafenib + trametinib.

Staging

NSCLC — TNM staging (8th edition AJCC/UICC):

SCLC staging:

• Limited disease (LD): Disease within one hemithorax, can be enclosed in a tolerable radiation field. Concurrent platinum-etoposide chemotherapy + thoracic radiation. Prophylactic cranial irradiation (PCI) for patients achieving complete response (reduces brain metastasis rate).
• Extensive disease (ED): Disease beyond one hemithorax or malignant effusion. Platinum-etoposide + atezolizumab (PD-L1 inhibitor). Palliative thoracic radiation if needed for symptom control.

Treatment overview

Surgery

Surgical resection is the cornerstone of curative-intent treatment for early-stage NSCLC. SCLC is almost never resectable at diagnosis.

• Lobectomy: Removal of one lobe of the lung. The preferred operation for Stage I–II NSCLC; preserves more lung function than pneumonectomy.
• Pneumonectomy: Removal of an entire lung. Reserved for tumors involving the main bronchus or crossing lobar boundaries. Higher morbidity and mortality; significant functional consequence.
• VATS (video-assisted thoracoscopic surgery): Minimally invasive lobectomy. Equivalent oncologic outcomes to open thoracotomy with faster recovery, less pain, and shorter hospitalization.
• Sublobar resection (segmentectomy, wedge resection): For patients with limited pulmonary reserve who cannot tolerate lobectomy; acceptable for tumors ≤2 cm.

Post-operative nursing priorities:

• Chest tube management: assess drainage character and volume, maintain patency, ensure water-seal integrity, monitor for air leak (bubbling in water-seal chamber)
• Respiratory assessment: hourly oxygen saturation, breath sounds bilaterally, work of breathing
• Incentive spirometry: begin in the PACU, 10 breaths per hour while awake; prevents atelectasis
• Pain management: adequate analgesia is essential — undertreated pain prevents deep breathing and coughing
• DVT prophylaxis: early ambulation, compression stockings, pharmacologic prophylaxis per protocol
• Position: head of bed 30–45° to optimize diaphragmatic excursion
• After pneumonectomy: position on the operative side to prevent mediastinal shift; NO clamping of the chest tube without specific MD order (the space fills with serosanguinous fluid intentionally)

Radiation therapy

• Stereotactic body radiation therapy (SBRT): High-dose, precisely targeted radiation delivered in 3–5 fractions. First-line for Stage I NSCLC in patients who are not surgical candidates. Highly effective for small peripheral tumors.
• Conventional fractionated radiation: Used with concurrent chemotherapy for Stage III unresectable disease.
• Prophylactic cranial irradiation (PCI): Standard in limited-stage SCLC achieving complete or good partial response; reduces brain metastasis rate by ~25%.
• Palliative radiation: For bone pain, hemoptysis, airway obstruction, or brain metastases. The goal is symptom relief, not cure.

Chemotherapy

Targeted therapy

Targeted therapy is indicated only for NSCLC with a specific actionable mutation — not for unselected patients.

• EGFR inhibitors: Erlotinib (Tarceva), gefitinib, osimertinib (Tagrisso — preferred third-generation agent, penetrates CNS). Common toxicities: acneiform rash (paradoxically, rash correlates with drug efficacy), diarrhea, mucositis, paronychia, interstitial lung disease (rare but serious). Nursing: educate patients that rash does not require stopping the drug; teach skin care; report dyspnea or new respiratory symptoms immediately (possible drug-induced pneumonitis).
• ALK inhibitors: Crizotinib (first-generation), alectinib, brigatinib, lorlatinib (newer agents with better CNS penetration). Toxicities vary by agent: crizotinib → visual disturbances, nausea, bradycardia, hepatotoxicity; alectinib → constipation, myalgia, photosensitivity.
• KRAS G12C inhibitors: Sotorasib (Lumakras), adagrasib. Toxicities: diarrhea, nausea, hepatotoxicity.

Immunotherapy (checkpoint inhibitors)

PD-1/PD-L1 checkpoint inhibitors have transformed lung cancer treatment. By releasing the “brake” on T-cell activity, they restore anti-tumor immune responses. Used in NSCLC and increasingly in SCLC.

• PD-1 inhibitors: Pembrolizumab (Keytruda — first-line monotherapy if PD-L1 ≥50%, or in combination with chemo), nivolumab (Opdivo)
• PD-L1 inhibitors: Atezolizumab (Tecentriq), durvalumab (Imfinzi — consolidation after Stage III chemoradiation)

Immune-related adverse events (irAEs) are the defining nursing challenge of checkpoint inhibitor therapy. Because these agents upregulate immune activity globally, any organ system can be affected. The pattern: new or worsening symptom in an immunotherapy patient → think irAE first.

Key irAEs in lung cancer patients:

• Pneumonitis: Most feared irAE in lung cancer (pre-existing lung pathology increases risk). Symptoms: new or worsening dyspnea, cough, fever. Management: hold drug, high-dose corticosteroids (prednisone 1–2 mg/kg/day), CT imaging, pulmonology consult. Severe cases require hospitalization and IV methylprednisolone.
• Colitis: Diarrhea (watery or bloody), abdominal cramping. Management: hold drug, corticosteroids, GI consult; infliximab for steroid-refractory cases.
• Hepatitis: Elevated transaminases, bilirubin. Monitor LFTs each cycle. Grade 3–4: hold drug, high-dose steroids, hepatology consult; mycophenolate for refractory cases.
• Endocrinopathy: Thyroiditis (most common), hypophysitis (pituitary inflammation → deficiency of multiple pituitary hormones including ACTH → adrenal crisis risk), primary adrenal insufficiency, type 1 diabetes. Monitor TSH, free T4; educate patients on adrenal insufficiency symptoms.
• Dermatitis: Rash, pruritus, rarely Stevens-Johnson syndrome. Most cases are mild and managed with topical steroids.
• Myocarditis: Rare but potentially fatal. New chest pain, dyspnea, or arrhythmia in an immunotherapy patient requires urgent ECG and troponin.

Nursing principle for irAEs: the earlier they are caught and treated, the better the outcome. Teach patients to report any new symptom — even one that seems unrelated to cancer.

Nursing priorities

Airway management

Airway compromise is an immediate life threat in lung cancer. Priorities:

• Assess breath sounds bilaterally each shift; report absent or markedly diminished unilateral sounds
• Position with head of bed elevated (30–45°) to reduce work of breathing and improve diaphragmatic excursion
• Ensure suction equipment is at the bedside for patients with hemoptysis or excessive secretions
• Humidified supplemental oxygen to prevent mucosal drying and secretion thickening
• Administer bronchodilators as ordered (short-acting beta-2 agonists for bronchospasm)
• Facilitate secretion mobilization: chest physiotherapy, mucolytics, encourage coughing and deep breathing

Dyspnea management

Dyspnea is the most distressing symptom reported by lung cancer patients and correlates strongly with anxiety and depression.

• Monitor SpO2 and titrate O2 to maintain saturation ≥90% (or per individualized goal in palliative patients)
• Teach pursed-lip breathing to reduce respiratory rate and improve gas exchange
• Fan therapy: a cool airflow fan directed at the face stimulates trigeminal nerve receptors and reduces perception of dyspnea — evidence supports this as an adjunct
• For refractory dyspnea in palliative patients: low-dose opioids (morphine) are evidence-based for symptom relief and do not hasten death at analgesic doses
• Anxiolytics (lorazepam) for dyspnea-associated panic and anxiety, particularly in the palliative setting
• Reduce exertional demands: space activities, allow rest periods, plan care around the patient’s best functional periods

Pain management

Lung cancer pain arises from multiple mechanisms — tumor invasion of pleura, ribs, or brachial plexus; bone metastases; post-thoracotomy incision; or neuropathic pain from Pancoast syndrome.

• Assess pain systematically using a validated scale at each assessment
• WHO analgesic ladder: non-opioid (NSAIDs, acetaminophen) → weak opioid → strong opioid; do not skip rungs without clinical justification
• Titrate opioids to effect; reassess regularly; anticipate bowel regimen (stimulant laxative + stool softener with every opioid prescription)
• Neuropathic pain (Pancoast/brachial plexopathy, bone mets with nerve compression): gabapentin, pregabalin, tricyclic antidepressants as adjuvants
• Bone metastases: bisphosphonates (zoledronic acid) or denosumab to reduce skeletal-related events; radiation for painful bone lesions
• For nerve block candidacy (intercostal, paravertebral): refer to pain management / anesthesia

Hemoptysis

Hemoptysis ranges from blood-streaked sputum to massive (≥200–600 mL/24 hours) and life-threatening hemorrhage.

• Position the patient with the affected (bleeding) side down — prevents blood from flooding the unaffected lung
• Ensure suction is immediately available at the bedside
• Apply supplemental oxygen and monitor SpO2 continuously
• Establish IV access; have type and screen available for massive hemoptysis
• Notify the physician immediately; massive hemoptysis requires emergent bronchoscopy, embolization, or surgical intervention
• Keep the patient calm — anxiety increases respiratory rate and worsens hemoptysis

Chemotherapy toxicity management

Cisplatin (nephrotoxicity — the priority):

• Pre-hydrate with 1–2 L of normal saline over 2–4 hours before infusion
• Post-hydrate with an additional 1–2 L NS after infusion
• Monitor serum creatinine, BUN, and electrolytes (magnesium, potassium, sodium) — cisplatin causes renal magnesium wasting
• Ensure urine output ≥100 mL/hour during hydration period
• Nausea management: 5-HT3 antagonists (ondansetron, palonosetron) + dexamethasone + NK1 antagonist (aprepitant) — cisplatin is highly emetogenic; inadequate antiemetic prophylaxis is a common failure point
• Monitor for peripheral neuropathy (cumulative): tingling and numbness in feet and hands, loss of proprioception

Paclitaxel (hypersensitivity — the priority):

• Premedicate as ordered: dexamethasone (IV or PO 12 and 6 hours before, or IV 30–60 min before), diphenhydramine 50 mg IV, and an H2 blocker (ranitidine or famotidine) 30–60 min before infusion
• Monitor continuously during first 10–15 minutes of infusion: flushing, urticaria, dyspnea, chest tightness, hypotension indicate hypersensitivity reaction — stop infusion immediately, maintain IV access, notify MD, administer rescue medications per protocol
• Peripheral neuropathy: cumulative dose-dependent; assess sensation and proprioception at each visit
• Myelosuppression: nadir at 8–11 days; monitor CBC

Checkpoint inhibitors (irAEs — any new symptom matters):

• Baseline organ function before initiating: TSH, LFTs, creatinine, CBC, blood glucose
• Monitor labs each cycle: LFTs, TSH, creatinine
• Educate patients extensively: report any new symptom (rash, diarrhea, cough, joint pain, fatigue) because irAEs can develop at any time, including months after completing therapy
• Grade irAEs per CTCAE criteria: Grade 1–2 = may continue with close monitoring and supportive care; Grade 3–4 = hold or permanently discontinue, initiate high-dose corticosteroids

Nutrition

Malnutrition is present in 30–80% of lung cancer patients at diagnosis and worsens with treatment.

• Assess weight at each visit; ≥5% loss over 6 months is clinically significant
• Recommend high-calorie, high-protein diet (1.2–1.5 g protein/kg/day)
• Encourage small, frequent meals; large meals worsen dyspnea by elevating the diaphragm
• Nutritional supplements (Ensure, Boost, Carnation Breakfast Essentials) for patients unable to meet needs through diet alone
• Manage anorexia: megestrol acetate (appetite stimulant), dexamethasone (short-term); mirtazapine for combined anorexia and depression
• Mucositis from chemoradiation: soft, cool, non-acidic foods; avoid spicy and coarse textures; prescription mouthwash per protocol; assess mucous membranes daily
• Refer to registered dietitian for patients with significant weight loss or treatment-related nutritional challenges

Psychosocial support

Lung cancer carries a unique burden — the strong association with smoking can lead to stigma, self-blame, and guilt, even in patients who never smoked. These dynamics affect care engagement and quality of life.

• Screen for depression and anxiety at diagnosis and at regular intervals (PHQ-9, GAD-7)
• Normalize emotional distress — a lung cancer diagnosis is one of the most devastating a patient can receive
• Address stigma directly and without judgment; smoking cessation remains beneficial even after diagnosis and should be supported, not weaponized as blame
• Facilitate early palliative care integration — evidence shows that early palliative care referral improves quality of life, reduces unnecessary aggressive end-of-life interventions, and — in landmark NSCLC studies — was associated with longer median survival
• Assess caregiver burden; family members and partners carry enormous weight and benefit from their own support resources
• Social work referral for financial concerns, transportation, insurance navigation, and community resources

Oncologic emergencies related to lung cancer

NCLEX tips

• NSCLC vs SCLC exam shortcut: NSCLC = No Small Cell = ~85% = Surgical candidate (early stage). SCLC = Small Cell = ~15% = Surgery is NOT a primary option (almost always metastatic at diagnosis). SCLC is Specifically Chemo/radiation.

• SCLC paraneoplastic syndromes — memorize three: SIADH (hyponatremia, fluid restriction), ectopic ACTH/Cushing’s (hypokalemia, hyperglycemia, hypertension), Lambert-Eaton (proximal weakness that improves with use — opposite of MG).

• Squamous cell = hypercalcemia: The association is PTHrP (parathyroid hormone-related protein), not direct bone invasion. Exam question pattern: lung cancer + confusion + constipation + elevated calcium = squamous cell carcinoma → check serum calcium → aggressive IV hydration + bisphosphonate.

• Pancoast tumor triad: Horner’s syndrome (ptosis + miosis + anhidrosis — ipsilateral face) + shoulder/arm pain + hand weakness. Location = lung apex. Mechanism = invasion of stellate ganglion and brachial plexus (C8-T1).

• Horner’s syndrome components: Remember the three: Ptosis (drooping lid), Miosis (small pupil), Anhidrosis (no sweating) — ipsilateral to the lesion. Anhydrosis vs anhidrosis: the “h” is often dropped. Any question with a lung mass + ipsilateral facial changes = Pancoast tumor.

• SVC syndrome priority intervention: Head of bed up (elevate) + IV access in LOWER extremity. The question may say “where do you place the IV” — answer is lower extremity. Upper extremity IV lines are contraindicated because venous return from upper body is compromised.

• SVC syndrome vs SVCS emergency trigger: It becomes an emergency when there is airway compromise (stridor, inability to swallow, altered mental status from elevated ICP). Notify the physician, position upright, O2, prepare for emergent radiation or stenting.

• Cisplatin nursing priority = hydration: The stem will describe a patient receiving cisplatin and ask the priority nursing action. Answer: ensure adequate IV hydration (1–2 L NS pre and post). Secondary: monitor creatinine and urine output. Cisplatin is the most nephrotoxic common chemotherapy agent.

• Paclitaxel = premedicate for hypersensitivity: Dexamethasone + diphenhydramine + H2 blocker before every dose. If question asks what to do when a patient develops flushing, dyspnea, and urticaria during a paclitaxel infusion: stop the infusion first, then assess and notify.

• Checkpoint inhibitor principle for NCLEX: Any new symptom in a patient on pembrolizumab, nivolumab, or atezolizumab is an irAE until proven otherwise. The exam will test whether you recognize that: (a) diarrhea = possible immune colitis; (b) new cough/dyspnea = possible immune pneumonitis; (c) jaundice = possible immune hepatitis. Action: hold the drug, notify the MD, prepare for high-dose steroids.

• Immune pneumonitis is the highest-risk irAE in lung cancer: Patients already have compromised pulmonary reserve. New dyspnea on immunotherapy → stop drug, chest CT, high-dose steroids. Do not assume it is tumor progression without imaging.

• Post-thoracotomy positioning: Head of bed 30–45° to optimize ventilation. After lobectomy, the patient may be positioned on either side. After pneumonectomy, position on the operative side (the empty hemithorax) to prevent mediastinal shift toward the remaining lung.

• Pneumonectomy chest tube: Unlike a standard chest tube, the pneumonectomy space tube is NOT attached to suction and should NOT be clamped without a specific physician order. The space fills with serosanguinous fluid intentionally. If a student nurse clamps it: call the MD immediately.

• Malignant pleural effusion priority nursing action: Position for comfort (usually sitting up or affected side up) + prepare for thoracentesis. After thoracentesis: check breath sounds bilaterally, obtain CXR, monitor SpO2 — pneumothorax is a complication.

• SCLC staging distinction: Limited disease = one hemithorax, can be covered in one radiation field. Extensive disease = beyond that boundary or malignant effusion. This distinction drives treatment: LD gets concurrent chemoradiation; ED gets chemo ± immunotherapy.

• Spinal cord compression — back pain = emergency: In a patient with known lung cancer, new back pain is a potential spinal cord compression until proven otherwise. Exam action: notify the physician, prepare for urgent MRI, administer corticosteroids (dexamethasone) as ordered. Do NOT perform straight leg raise testing.

• Post-obstructive pneumonia pattern: Recurrent pneumonia in the same lobe or segment in a smoker should trigger investigation for an obstructing endobronchial lesion. The NCLEX question may describe a patient with “three pneumonias in the right lower lobe in one year” — next action is CT chest and pulmonology referral.

Related nursing resources

For related clinical content, see the following references on this site:

• Oncology nursing reference — comprehensive oncology nursing overview including myelosuppression management, neutropenic precautions, and chemotherapy safety
• Pleural effusion nursing — thoracentesis procedure, nursing assessment, and management of malignant and transudative effusions
• Pneumonia nursing — post-obstructive pneumonia, CAP vs HAP, antibiotic management, respiratory nursing priorities
• ARDS nursing — acute respiratory distress syndrome, lung-protective ventilation, and ICU respiratory nursing
• COPD pathophysiology — COPD overlap with lung cancer (shared risk factors, spirometry, smoking cessation)