Oncologic Emergencies — Viva Defence

Long Case Viva Defence

The scenario

A 66-year-old man, a lifelong smoker, presents to the emergency department with a two-week history of progressive facial swelling, a one-week history of dyspnoea and a dry cough, and a three-day history of confusion. On examination he has facial and periorbital oedema, distended and non-pulsatile neck veins that do not fall with inspiration, prominent collateral veins over the anterior chest wall, and upper limb oedema. He is clubbed. He has a right upper lobe collapse on the chest radiograph. His observations are heart rate 108, blood pressure 132/78, respiratory rate 24, oxygen saturation 92 per cent on room air, temperature 37.1 degrees. His chest CT confirms a right upper lobe mass with mediastinal lymphadenopathy compressing the superior vena cava. His bloods show sodium 118 mmol per litre, potassium 4.0 mmol per litre, urea 6.0, creatinine 80, corrected calcium 3.0 mmol per litre, albumin 32. His serum osmolality is 250, urine osmolality 360, urine sodium 55. The parathyroid hormone is suppressed and the parathyroid hormone-related peptide is elevated. A bronchial biopsy confirms small cell lung cancer. [1]

Opening statement (SASPOP)

"This is Mr R, a 66-year-old lifelong smoker presenting with a two-week history of superior vena cava obstruction and a three-day history of confusion from metabolic derangement, in the setting of a newly diagnosed small cell lung cancer. He has three concurrent oncologic problems: (1) superior vena cava obstruction from the right upper lobe mass and mediastinal nodes, for which he needs symptom control and definitive cancer treatment; (2) severe symptomatic euvolaemic hyponatraemia (sodium 118) from syndrome of inappropriate antidiuretic hormone — small cell lung cancer is the classic cause — which I am correcting carefully to avoid osmotic demyelination; and (3) hypercalcaemia of malignancy at 3.0, a PTHrP-mediated humoral hypercalcaemia, which is contributing to his confusion. The unifying solution is treatment of the small cell lung cancer with chemotherapy, to which it is highly responsive. My immediate management is airway and breathing support, careful correction of the hyponatraemia with 3 per cent saline to a safe ceiling, intravenous fluids and zoledronic acid for the hypercalcaemia, a tissue diagnosis — which I already have — and urgent oncology review for the chemotherapy that will relieve the SVC obstruction and the SIADH. I am involving the palliative care team for symptom control and goals-of-care discussions." [1]

Problem list (numbered, prioritised)

1. Superior vena cava obstruction from the right upper lobe mass and mediastinal nodes — symptomatic and progressive.
2. Severe symptomatic SIADH (sodium 118 with confusion) from ectopic ADH production by the small cell lung cancer.
3. Hypercalcaemia of malignancy (corrected calcium 3.0, PTHrP-mediated) contributing to the confusion.
4. Newly diagnosed small cell lung cancer — the unifying diagnosis and the target of definitive therapy.
5. Hypoxaemia (oxygen saturation 92 per cent) from the right upper lobe collapse and the SVC-related venous congestion.
6. The communication and goals-of-care conversation, given the prognosis of extensive-stage small cell lung cancer. [1]

Integrated management plan

Pillar 1 — The SVC obstruction: "He is not stridulous and his observations are stable, so this is not an immediate airway emergency requiring a stent. I would sit him upright, give supplemental oxygen, and proceed to definitive treatment of the small cell lung cancer — small cell is chemosensitive and responds to platinum-etoposide within days to weeks, which will relieve the obstruction. The Rowell and Gleeson systematic review establishes that the priority is a tissue diagnosis and treatment of the underlying cancer [7]. I have the biopsy, so I would start the chemotherapy urgently. If he develops stridor, cerebral symptoms, or haemodynamic compromise, I would arrange urgent endovascular stenting for rapid relief. I would avoid upper-body central lines (use a femoral route if a line is needed) and anticoagulate if thrombosis is documented."

Pillar 2 — The SIADH: "The sodium of 118 with confusion is a medical emergency. I would give intravenous 3 per cent saline — 100 mL over 10 minutes, repeated up to three times if he seizes or remains deeply confused — with a target of raising the sodium by no more than 4 to 6 mmol in the first 6 hours and no more than 8 to 10 mmol in 24 hours, to avoid osmotic demyelination. I would check the sodium every 2 to 4 hours during the active correction. Once his confusion improves and the sodium is above 120, I would restrict his fluids to 800 to 1000 mL per day. The definitive treatment is the chemotherapy, which will suppress the ectopic ADH production and often resolves the SIADH within weeks. I would avoid over-rapid correction with a vaptan in the acute phase." [1]

Pillar 3 — The hypercalcaemia: "I would give intravenous normal saline — guided by his volume status and his (normal) renal function — and then zoledronic acid 4 mg over 15 minutes. The calcium will fall over 48 to 72 hours. For the first 48 hours, while the zoledronic acid takes effect, I would add subcutaneous calcitonin 4 to 8 IU per kg every 12 hours as a rapid bridge [6]. The PTHrP-mediated mechanism is confirmed by the low phosphate (if present), the suppressed PTH, and the elevated PTHrP. I would continue zoledronic acid or denosumab monthly as part of his supportive care."

Pillar 4 — The small cell lung cancer: "Extensive-stage small cell lung cancer is treated with platinum-based chemotherapy (cisplatin or carboplatin with etoposide), with the addition of atezolizumab or durvalumab (an anti-PD-L1 checkpoint inhibitor) in the first-line setting per the IMpower133 and CASPIAN trials, which improved overall survival. Prophylactic cranial irradiation is considered for limited-stage disease in complete response, and is debated in extensive-stage disease. He would be referred to a medical oncologist for the regimen and the staging (a CT chest, abdomen and pelvis, and an MRI or CT of the brain for staging)." [1]

Pillar 5 — Hypoxaemia and supportive care: "Supplemental oxygen, treat any infection, DVT prophylaxis, and symptom control (analgesia, antiemetics). I would involve the palliative care team early, both for symptom control and for the goals-of-care conversation, given the prognosis of extensive-stage small cell lung cancer (median survival 12 to 13 months with modern therapy)." [1]

Pillar 6 — Communication and goals of care: "I would speak with Mr R and his family in plain language about the diagnosis, the prognosis, and the treatment plan. I would frame the chemotherapy as both the treatment of the cancer and the relief of the three emergencies (the SVC obstruction, the SIADH, and the hypercalcaemia), and I would be honest about the prognosis and the goals of care. I would document the agreed plan and review it at every transition." [1]

Probing questions the examiner would ask

Q: Why are you not stenting his SVC immediately? [1]

A: "Because he is not stridulous, has no cerebral symptoms, and is haemodynamically stable. The priority in the stable patient is a tissue diagnosis and treatment of the underlying cancer — small cell lung cancer responds to chemotherapy within days to weeks, and the chemotherapy is also his definitive systemic therapy. Stenting is reserved for severe or life-threatening obstruction (stridor, cerebral symptoms, haemodynamic compromise) or for obstruction refractory to cancer-directed therapy. Stenting before a tissue diagnosis is appropriate only when rapid relief is essential. If his obstruction worsens or he develops stridor while awaiting the chemotherapy, I would stent him [7]."

Q: He develops a seizure while you are correcting the sodium. What do you do? [1]

A: "I would give intravenous lorazepam 4 mg to terminate the seizure, then give 100 mL of 3 per cent saline over 10 minutes to raise the sodium rapidly enough to terminate the cerebral oedema. I would continue the hypertonic saline to a ceiling of a 4 to 6 mmol rise in the first 6 hours and no more than 8 to 10 mmol in 24 hours. The seizure is the hallmark of severe hyponatraemia and mandates hypertonic saline — the rate of correction must be controlled to avoid osmotic demyelination, which is the devastating complication of over-rapid correction." [1]

Q: How would your management change if the biopsy had shown a non-small cell lung cancer rather than small cell? [1]

A: "The SVC obstruction would be managed the same way in the stable patient — treat the underlying cancer, reserving the stent for severe obstruction. The difference is the cancer treatment: non-small cell lung cancer is treated with chemo-radiotherapy for locally advanced disease, or with immunotherapy and chemotherapy for metastatic disease, guided by the PD-L1 status and the molecular profile (EGFR, ALK, ROS1, KRAS). The SIADH is far less common in non-small cell lung cancer (it is the hallmark of small cell), so if he had non-small cell with a sodium of 118 I would look hard for another cause of the hyponatraemia — a drug, an adrenal insufficiency, a gastrointestinal loss — before attributing it to the cancer. The hypercalcaemia, however, is more common in non-small cell (particularly squamous cell, the classic PTHrP-secreter) than in small cell." [1]

Q: What is the prognosis, and how does it shape your management? [1]

A: "Extensive-stage small cell lung cancer has a median survival of about 12 to 13 months with platinum-etoposide and an anti-PD-L1 agent, and a 5-year survival of under 10 per cent. This shapes my management in two ways. First, the three emergencies are potentially reversible with the chemotherapy, so I treat them aggressively — the goal is symptom relief and the best possible quality of the remaining time. Second, I involve the palliative care team early, not for end-of-life care but for symptom control, prognostic framing, and family support throughout the illness trajectory. If he deteriorates despite the chemotherapy or if he declines further treatment, the goal shifts to comfort care with a dignified death, supported by palliative care." [1]

Q: What is the role of prophylactic cranial irradiation in this patient? [1]

A: "Prophylactic cranial irradiation reduces the incidence of brain metastases and improves survival in limited-stage small cell lung cancer in complete response after chemoradiotherapy. In extensive-stage disease, its role is debated: it reduces brain metastases but the survival benefit is less clear in the era of effective systemic therapy and MRI surveillance. The EORTC trial showed a survival benefit in extensive-stage disease, but more recent studies question the magnitude in patients who receive regular MRI surveillance and salvage radiotherapy at the time of metastasis. The decision is made with the oncologist and the patient, weighing the small survival benefit against the cognitive late effects of whole-brain radiotherapy." [1]

Communication and shared decision-making

"I would sit with Mr R and his family in a quiet room and speak in plain language. I would explain that the cancer in his lung has caused three problems — the swelling in his face and arms, the low sodium that made him confused, and the high calcium — and that the chemotherapy I am recommending will treat the cancer and all three of these problems. I would be honest that this is an extensive-stage small cell lung cancer, that the chemotherapy can control the disease for a period but is unlikely to cure it, and that the aim is to give him the best possible quality of the time he has. I would ask what matters most to him now, whether there are things he wants to do or people he wants to see, and I would build the treatment plan around his priorities. I would involve the palliative care team for symptom control and family support, and I would document the shared decisions and review them as his clinical picture evolves." [1]

Short Case Discussion — Focused neurological examination of suspected malignant spinal cord compression

Instruction: "This patient with known prostate cancer has new back pain and difficulty walking. Examine his neurological system and present your findings." [1]

Systematic examination routine

1. End of bed — observe for a urinary catheter, pressure areas, a walking aid, the posture, the ability to rise from the chair, and any obvious wasting or fasciculation.
2. Gait — assess for an antalgic, a foot-drop, a spastic (scissoring), or an ataxic gait; the gait is a sensitive screen of the motor and sensory pathways.
3. Tone in the legs — spasticity (an upper motor neuron lesion, the cord), hypotonia (acute shock), or normal.
4. Power in the legs — grade each muscle group on the Medical Research Council 0 to 5 scale, comparing proximal and distal, and looking for a pyramidal pattern (flexors weaker than extensors in the leg).
5. Reflexes in the legs and the plantar responses — hyperreflexia and extensor plantars (an upper motor neuron lesion), hyporeflexia (acute cord shock, or a cauda equina lesion), and a reflex level that may localise the lesion.
6. Sensation — test the modalities systematically (light touch, pinprick, vibration, joint position), and look for a sensory level (a band below which sensation is reduced) which is the cardinal sign of a cord lesion. Map the level on the trunk (T4 at the nipple line, T6 at the xiphoid, T10 at the umbilicus, L1 at the inguinal ligament).
7. Sphincter tone and perineal sensation — a rectal examination for anal tone and perineal sensation; saddle anaesthesia and a lax anal tone indicate a conus or cauda equina lesion.
8. Examine the spine for tenderness, a gibbus, and a step in the thoracic or lumbar spine.
9. Complete the examination — the upper limbs (if the lesion is cervical), the blood pressure for autonomic dysfunction, and the skin for pressure areas. [1]

Key physical signs the patient may demonstrate

• A spastic gait and bilateral leg weakness (a pyramidal pattern).
• Hyperreflexia in the legs with extensor plantar responses (an upper motor neuron lesion).
• A sensory level on the trunk (the cardinal localising sign).
• A palpable bladder (urinary retention from the sphincter involvement).
• Spinal tenderness at the level of the compression. [1]

Presentation template

"I examined Mr R, a 66-year-old man with prostate cancer, who has a spastic gait and bilateral leg weakness. On examination the tone is increased in the legs, the power is grade 4 of 5 proximally and 3 of 5 distally in a pyramidal distribution, the reflexes are brisk bilaterally with extensor plantar responses, and there is a sensory level at T8 on the trunk. There is a palpable bladder and saddle anaesthesia is absent. These findings are consistent with a thoracic spinal cord lesion — in the setting of known prostate cancer, malignant spinal cord compression until proven otherwise. My immediate management is intravenous dexamethasone 16 mg and an urgent MRI of the whole spine, followed by urgent neurosurgical and clinical oncology review." [1]

Discussion questions

Q: What is the significance of the sensory level? [1]

A: "A sensory level is the cardinal sign of a spinal cord lesion — it localises the lesion to a segment at or above the level of the sensory loss, because the spinothalamic fibres cross and ascend a segment or two above the entry level. A level at T8 on the trunk points to a lesion at approximately T6 in the cord. The level, together with the motor and reflex findings, allows me to request the MRI at the correct anatomical focus — though I would still scan the whole spine because multiple levels of disease are common in prostate cancer metastases [4]."

Q: How do you decide between surgery and radiotherapy? [1]

A: "The Patchell trial established that for selected patients — a single compressive level, spinal instability, bone retropulsion into the canal, or neurological deterioration despite steroids or radiotherapy — direct decompressive surgery plus radiotherapy is superior to radiotherapy alone: 84 per cent of the surgery group were ambulatory versus 57 per cent, and the benefit was greatest in patients who were non-ambulatory at presentation [5]. Patients with multiple compressive levels, a very poor performance status, a life expectancy under 3 months, or complete paraplegia for more than 24 to 48 hours are generally managed with dexamethasone and palliative radiotherapy. The decision is made with the neurosurgeon, the radiation oncologist, and the patient [4]."

Q: What is the role of the steroid, and what dose do you use? [1]

A: "Dexamethasone reduces vasogenic oedema around the cord, relieving pain and often improving the neurological deficit within hours, and is given immediately on suspicion — before the MRI. The standard regimen is 16 mg intravenously as a loading dose, then 16 mg daily in divided doses, tapered during radiotherapy. Higher doses (up to 96 mg) have been used but increase complications without clear additional benefit [4]. The complications are hyperglycaemia, immunosuppression, psychosis, gastritis, and fluid retention — I monitor the blood glucose, give a proton pump inhibitor, and review the dose daily."

Q: What if the MRI shows cord compression but the patient has a performance status of 4 and a life expectancy of weeks? [1]

A: "The goals of care shift. If the patient is at the end of life and the family and the patient (where possible) have agreed on a comfort-focused approach, the management is dexamethasone (for symptom relief and a modest chance of preserving ambulation for the remaining time), palliative radiotherapy if it can be tolerated and delivered, and a strong palliative care input for pain, sphincter management, pressure area care, and family support. The surgery would not be offered because the harm (a major operation in a dying patient) outweighs the benefit. The decision is made with the patient and family, the oncologist, the palliative care team, and sometimes an ethics consultation, and is documented and reviewed." [1]