Adrenal Cancer (ACC): Symptoms, Causes, Treatment & Nursing Care

In everyday hospital language, “adrenal cancer” usually means adrenocortical carcinoma, a primary epithelial malignancy of adrenal cortical origin rather than metastatic disease seeding the gland or a benign cortical adenoma. Tumour cells retain variable steroidogenic machinery, so some lesions flood the circulation with glucocorticoids, androgens, or mineralocorticoids, while others grow silently until compressive symptoms or systemic spread appear.

Natural history is dominated by locoregional aggressiveness and late metastases. Even after macroscopically complete resection, multidisciplinary teams watch for recurrence because radiological cure is uncommon in high-stage groups without adjuvant strategies. Nurses anchor care on hormone consequences, treatment toxicities, and rapid recognition of sepsis or adrenal collapse when steroid bridges are imperfect.

ENSAT (European Network for the Study of Adrenal Tumours) staging translates tumour size, invasion beyond the adrenal, nodal involvement, and distant metastasis into four ordinal stages that guide trial eligibility, intensity of mitotane discussion, and surveillance cadence. Pathologists also comment on nuclear grade (for example Ki-67 index) because proliferative markers influence prognosis independent of anatomic stage.

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*Exact definitions follow the published ENSAT framework—apply the version your tumour board cites because borderline interpretations (e.g., periadrenal fat involvement) change staging calls.

Presentations split between hormone-driven syndromes and mass effects. Because features overlap with common conditions (obesity, depression, primary hypertension), timeline and objective endocrine data separate ACC from mimics.

Hormone-excess patterns

• Cushingoid change: proximal weakness, purple striae, hyperglycaemia, infections, mood lability.
• Androgen excess: hirsutism, virilisation, libido change—track alongside DHEA-S or androgen panels per protocol.
• Mineralocorticoid effect: hypokalaemia, alkalosis, refractory hypertension—align with hypertension symptoms surveillance.

Local or systemic progression

• Deep abdominal pain, early satiety, palpable mass, or venous obstruction.
• Fatigue, cachexia, or unexplained weight loss disproportionate to intake.

Most ACC appears sporadic. Germline cancer-predisposition variants (for example TP53 in Li-Fraumeni syndrome, Lynch mismatch-repair genes, Beckwith-Wiedemann spectrum) explain a minority but mandate genetic counselling when family or paediatric context fits. Chronic stimulation from an adenoma does not “turn into” ACC often; instead, new radiographic growth or biochemical surges in a previously stable lesion should trigger referral.

Risk-aware practice

• Document ionising radiation exposure relevant to field-specific second cancers when constructing histories.
• Screen first-degree relatives when known hereditary syndromes surface.

Clinical assessment

Combine tempo of symptoms, hormone phenotype, performance status, and antecedent imaging. Pain assessment scores help quantify visceral progression or bone involvement.

Laboratory investigations

• Screens for hypercortisolism (overnight 1 mg dexamethasone suppression where appropriate, late-night salivary cortisol, or 24-hour urinary free cortisol per pathway).
• Serum electrolytes, renal panel, and glucose—mirrored in the comprehensive metabolic panel when services bundle tests.
• Haematologic baselines: complete blood count and platelet count before mitotane or cytotoxics.

Imaging & pathology

Thin-slice adrenal-protocol CT defines size, fat content, centripetal enhancement, and invasion. MRI helps characterise lipid-poor lesions or venous extension. Expert histopathology (often including IHC) distinguishes ACC from adenoma, pheochromocytoma, or metastasis. Biopsy is not automatic—multidisciplinary tumour boards weigh seeding risk.

1. Stabilise critical hormone or metabolic derangements (potassium, glucose, blood pressure, infection).
2. Confirm diagnosis with imaging + pathology strategy agreed at MDT.
3. Stage with ENSAT-aligned reporting and document distant sites.
4. Resect if R0/R1 resection is realistic; otherwise enrol in neoadjuvant or palliative systemic plans.
5. Adjuvant mitotane or surveillance follows risk strata per published multidisciplinary guidance.
6. Re-image on defined intervals; escalate early for performance decline or new pain.

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All regimens follow supra-regional protocols; nurses focus on safe delivery, monitoring, and flagging toxicity.

First-line curative pathway

• Open or minimally invasive radical adrenalectomy with en-bloc removal of invaded tissue when feasible.
• Perioperative stress-dose glucocorticoids even if preoperative cortisol was normal—the remaining axis may be inadequate.

Adjuvant and advanced disease

• Mitotane: adrenalolytic agent with narrow therapeutic window—requires therapeutic drug monitoring, neurocognitive surveillance, and gastrointestinal support.
• EDP-M (etoposide, doxorubicin, cisplatin) and other combinations per ESMO–EURACAN-era pathways for metastatic disease.
• Focal radiation for painful bone or brain metastases when radiotherapy teams agree benefit outweighs toxicity.

• Pre-op: document baseline cortisol syndrome severity, optimise potassium, involve anaesthesia early.
• Post-op day 0–5: watch for expanding drain output, ileus, wound infection, and need for stress steroid taper schedules.
• Surveillance: typical restaging involves cross-sectional imaging every 3–6 months for high-risk cohorts—confirm exact dates in MDT letters.
• Mitotane: teach nausea management, dizziness precautions, and when to withhold dose pending drug levels.
• Refer sooner if new neuropathy, rising LFTs beyond expected, or cyclical vomiting emerges on therapy.

• Hormone storm, hypokalaemic arrhythmia, hyperglycaemic hyperosmolar crisis.
• Postoperative adrenal insufficiency or iatrogenic crisis if steroid cover stops abruptly.
• Venous thromboembolism in prolonged bed rest or hypercortisolism.
• Chemotherapy myelosuppression, febrile neutropenia, mucositis.

There is no population screening analogous to cervical or colorectal programmes. Prevention in practice means genetic counselling for at-risk families, vigilant follow-up when syndromic features emerge, and prompt referral of enlarging adrenal masses or accelerating biochemistry so teams can intervene before unresectable invasion.

Outlook depends tightly on stage, margin negativity, Ki-67 index, symptom control, and response to mitotane or chemotherapy. Localised, completely resected disease offers the longest intervals, whereas widespread metastatic ACC still behaves aggressively despite modern combinations—communicate uncertainty honestly while highlighting active trial options.

Shift work rarely exposes teams to large ACC volumes—lean on tumour board minutes and named clinical nurse specialists for clarifications. Translate dense endocrine jargon into intake/output, orthostatic checks, and medicine times the bedside can action.

• Blood pressure (lying and standing when steroid tapering or dehydrated).
• Heart rate, temperature, oxygen saturation, pain scores.
• Point-of-care or laboratory glucose at clinically appropriate intervals.
• Strict intake/output if diuretics or mitotane diarrhoea coexist.
• Mental status checks when cortisol swings or opioid doses change.

• Thunderclap headache, focal neurology, or seizure—rule intracranial catastrophe.
• Refractory vomiting with abdominal rigidity—surgical review for perforation or haemorrhage.
• SpO₂ <92% on previously stable patients, or new pleuritic pain with hypoxia—consider thromboembolism or effusion.

Invoke the medical emergency or oncology acute pathway when mean arterial pressure drops >20 mmHg below personal baseline despite fluids, potassium falls <3.0 mmol/L with ectopy, glucose exceeds local hyperglycaemic crisis thresholds, or NEWS2 rises sustained. Bring recent drug levels (mitotane), steroid chart, and imaging discs to senior review.

Pre-treatment

• Establish vascular access adequate for contrast, resuscitation, and chemotherapy as planned.
• Provide culturally competent teaching on hair loss, fertility preservation referrals, and work-leave documentation where relevant.

Active therapy

• Anti-emetic timing tied to chemotherapy protocols; mouth care for stomatitis risk.
• Infection precautions when neutrophil counts fall—observe neutropenic fever bundles.

Evaluation

• Compare weight, grip strength, and sleep quality visit-to-visit as patient-reported outcome proxies.

These NCLEX-style clinical judgment practice items focus on the nursing priorities for this condition — recognise cues, escalate red flags, take safe action and evaluate outcomes (NCSBN Clinical Judgment Measurement Model) — through Priority FIRST, SATA, deterioration trends, multi-patient triage, ordered response, matrix matching and cloze drops on the topic of adrenocortical carcinoma evaluation (functional vs non-functional, imaging features, ENSAT staging), peri-operative steroid management and mitotane stewardship.