16.1 | Malignancy-related hypercalcaemia |
- About: causes polyuria and dehydration and delirium. Seen in 10–20% of all adults with cancer. Also see Section 5.5.
- Causes: solid tumours, such as lung or breast cancer tumours. Multiple myeloma and other haematological malignancies.
- Aetiology: PTH-related peptide increases renal calcium reabsorption. Humoral hypercalcaemia due to circulating tumour secreted factors. Osteolytic hypercalcaemia due to primary or secondary bone lesions.
- Clinical: severe dehydration, bone pain, anorexia, N&V. Signs of underlying malignancy.
- Investigations: FBC, ↑urea, ↑creatinine, ↑Ca, PTH, PTH-related peptide, CXR. Serum immunoglobulins, Bence–Jones protein, skeletal survey.
- Management: palliate selected patients. If severe, rehydrate with 3–6 L NS over 24 h. Close watch on renal function and level of calcium and cardiac status. Once rehydrated repeat calcium and consider renal function before PAMIDRONATE 30–90 mg IV or ZOLEDRONATE 4 mg IV infusion over 15 min. Also see Hypercalcaemia, Section 5.5 for further detail.
16.2 | Tumour lysis syndrome |
- About: seen with treatment of chemosensitive malignancies and death of neoplastic cells. Potential AKI, seizures and arrhythmias.
- Aetiology: seen with bulky tumours, high turnover, chemosensitive. Cell death causes ↑↑LDH, ↑uric acid, pre-chemotherapy or impaired renal function.
- Chemotherapy for malignancies: acute leukaemias (ALL, AML, APML, CLL/CML with blast crisis). High-grade non-Hodgkin lymphomas, Burkitt’s lymphoma. Breast cancer, small cell lung cancer, sarcomas.
- Clinical: vague, lethargy, N&V. Carpopedal spasm (low Ca), seizure, arrhythmias (high K).
- Investigations: FBC: watch Hb, WCC and platelets. U&E: AKI, ↑urea, ↑creatinine. Cell lysis: ↑uric acid, ↑LDH, ↑phosphate, ↑K and low Ca. ↑CRP: increase can suggest infection/inflammation/malignancy. ECG and telemetry to detect effects of high K. ↑lactate, ABG: ↑anion gap metabolic acidosis. Coagulation screen: rarely a coagulopathy can develop such as DIC.
- Management: prevent with hydration with IV fluids if needed. Central line if needed (4–5 L per day). Cardiac monitoring for ↑K. Standard replacement for K/Ca/Mg. Monitoring bloods 2–3 times daily for 48–72 h after chemotherapy initiation. Hyperuricaemia: ALLOPURINOL 300 mg 8 h (reduce if CKD/AKI) started prior to treatment or RASBURICASE. Some patients with renal impairment may need to be on dialysis prior to the initiation of therapy. Urinary alkalinisation with NaHCO3 to maintain a urine pH >7.0 can help clearance of uric acid.
16.3 | Hyperviscosity syndrome |
- About: increased plasma viscosity due to increased cells (red and white cells) or large proteins, e.g. immunoglobulins.
- Causes: Waldenstrom’s macroglobulinaemia, myeloma (increased IgM, IgA, IgG), immunoglobulin M (IgM) paraproteins. Leukaemias (WCC >100), myeloproliferative diseases, polycythaemia and thrombocytosis. Eisenmenger’s syndrome.
- Clinical: visual disturbances, bleeding (GI bleeds, mucous membranes, epistaxis, retinal haemorrhage), neurological manifestations, e.g. stroke/TIA, vertigo and hearing loss.
- Investigations: FBC, U&Es, LFT, ESR, Ca. PPE: monoclonal band, urinary Bence–Jones protein. CT brain: if stroke/TIA, CXR: if breathless.
- Management: ABC, IV access and ensure well hydrated, treat infection. Treat the underlying condition. Acutely may consider phlebotomy with simultaneous infusion of isovolaemic fluid for RBC/WCC excess. Plasma exchange is the gold standard treatment.
16.4 | Brain tumour |
- About: primary or secondary. Variation in behaviour – some benign, others grow slowly over years, some very rapid. Histology can help plan treatment.
- Causes: primary: usually single (primary CNS lymphoma often multifocal). Metastatic: single or multiple (10 times commoner than primary). Most are intradural. Leptomeningeal disease with adenocarcinomas.
- Risk: primary brain: radiation, HIV/AIDS, genetics – von Hippel–Lindau disease, tuberous sclerosis, Li–Fraumeni syndrome, and neurofibromatosis. Secondary: smoker and lung cancer, breast lumps, skin melanoma, renal mass, haematuria, etc.
- Differential: stroke (ischaemic and haemorrhagic), abscess, inflammatory, infection, PML.
- Clinical: seizures, morning headache, vomiting, ↑ICP, papilloedema, cognitive, behavioural changes. Focal neurology dependent on site, e.g. weakness, cerebellar signs, hemianopia, personality change. May present as stroke, e.g. with subcortical hypodensity or with a haemorrhage. Leptomeningeal spread more insidious with cranial nerve palsies, headache.
- Signs of an extracranial primary malignancy: lung: weight loss, cough, hoarseness, Horner’s syndrome. Breast lump, Paget’s disease of nipple, localised nodes. Testicular mass. Haematuria, renal mass: renal cell tumour. Anaemia: gastrointestinal primary. Skin pigmentation: look for melanoma.
- Investigations: bloods: FBC: anaemia from gut malignancy, U&E, LFT, Ca, ALP: liver metastases. CT brain + contrast: usually a well demarcated hypodense lesion which enhances with ring appearance often sited at grey–white matter border, or even within the dura, with associated vasogenic oedema. In adults most are in the cerebral hemispheres with a minority in the posterior fossa. Look for hydrocephalus. Melanomas, renal cell carcinomas, lung tumours and choriocarcinomas and anticoagulated tend to bleed. MRI head with gadolinium: FLAIR, T1 and T2 with contrast can confirm lesion. CXR: lung tumour or lung metastases. CT chest abdomen pelvis for primary malignancy. PET scan: specialist use only. Brain biopsy:
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