Oncological emergencies Flashcards
What are some common presenting complaints in acute oncology?
- Fever - NS
- SOB - PE, effusion, NS, collapse, ascites
- Hypotension - NS, PE, tamponade
- Face swelling - SVCO
- Leg weakness - cord compression
- Mental deterioration - hypercalcaemia, RICP
- Renal failure - obstruction, sepsis, drugs (NSAID, methotrexate, cisplatin), metabolic
- Haemorrhage - tumour prison, thrombocytopenia, DIC
- Bone pain - #, painful mets
- Acute abdomen - obstruction, perforation
- Jaundice - obstruction, parenchymal liver destruction by tumour/drugs
Define neutropenic sepsis
Temp >38 for more than 1h, or any signs/sx of sepsis in someone with neuts <0.5
Febrile neutropenia: a one off reading >38.5/>38 for >1h, rapidly leads to NS
Only find a source in a minority
In practice treated when neuts <1, as they are likely to go down more
RF for neutropenic sepsis
Chemotherapy (biological/targeted lower risk but still a risk) esp 7-14 post chemo, prolonged neutropenia >7d (in haem cancer treatment), more severe neutropenia, co-morbidities like DM/renal impairment, uncontrolled cancer, central lines (G+ cocci), mucosal disruption, hospital inpatient
CF of neutropenic sepsis
- Sx of a specific infection (not always)
- Fever (some dont get cos of steroids)
- Non-specific: nausea, diarrhoea, drowsy, dyspnoea
- Sepsis red flags: responsive to pain/not responsive, acute confusional state, BP<90 (or drop >40), HR>130, RR>25, sats<92 OA, rash/mottled/ashen/cyanotic, oliguric, lactate > 2, recent chemotherapy
Workup for neutropenic sepsis
- Sepsis 6 protocol - take BC, lactate + urine output, give fluids Abx and oxygen if need
- other bloods, line culture, sputum, urine, CXR
- Abx: follow local guideline remembering allergy + renal impairment. E.g. Tazocin + Gentamicin for synergistic effect. Continue until neuts >0.5 and apyrexial for >24h
- GCSF: consider in profound neutropenia, but not for myeloid disorders as increases abnormal cells
How is neutropenic sepsis prevented?
- Pt education about signs + when to go to A+E/acute oncology
- Abx prophylaxis sometimes given
- Prophylactic GCSF
- Adv neutropenic diet: low in contamination so avoid all uncooked veg + most fruits, rare meat, fish, undercooked eggs, food from buffets/deli counters, soft cheeses
Pulmonary embolism
Due to coagulopathy of cancer + chemo
CF: unexplained dyspnoea, exacerbations from multiple small emboli, hypoxia
Ix: CTPA
Prophylactic LMWH given to all immobilised pt (warfarin ineffective in CoC)
Metastatic spinal cord compression
Cause: collapse/compression of a vertebral body that has mets, or less commonly a para-spinal mass.
Course: compression causes oedema + venous congestion + demyelination, if not reversed get cord necrosis + permanent damage
CF: back pain (usually for a couple of months), spinal/radicular pain exacerbated by movement/SLR/straining, limb weakness (these occur in most); may also have a sensory level weakness and sphincter dysfunction. A/w deterioration
- Acute onset - flaccid paralysis
- More insidious - spasticity, up going planters, sensory loss at a well defined dermatomal level, palpable bladder cos of retention
- If below L2 vertebra is cauda equina compression - may present without leg weakness, doesn’t cause a sensory level weakness, doesn’t cause up going planters. LMN signs rather than UMN
Prognosis: lowered if non-ambulatory at presentation, sphincter function lost, NSCLC + sarcomas
M:
- MRI within 24h + admit + bed rest
- Dexamethasone + PPI (unless suspect lymphoma-wait for biopsy )
- Surgery if fit + no visceral mets + good PS
- Radiotherapy within 24h of diagnosis: majority have this as they have extensive disease. Relieves compression by causing cell death + relieves pain + stabilities neuro deficit
Define hypercalcaemia
Above 2.65mmol/L
Mild - 2.65-3
Moderate 3-3.4
Severe >3.4 or if symptomatic
Mostly occurs in disseminated disease, esp breast/lung/kidney/myeloma
Why does hypercalcaemia develop?
- Cancer causes: PTHrp causing osteoclasts to resorb bone + more renal absorption (majority), can also be excessive bone destruction from osteolytic mets + cytokine release, and in lymphoma some types produce 1, 25-dihydroxyvitamin D (more intestinal absorption + bone resorption)
- Non-cancer causes: primary hyperparathyroidism (commonest cause, excessive PTH secretion usually due to a single parathyroid adenoma, increases renal reabsorption + mobilises from bone + increases 1,25VD so more intestinal absorption), less commonly drugs like lithium/vitD/thiazides, granulomatous diseases, CKD stages 4/5 (low Ca - parathyroid hypertrophy), thyrotoxicosis (excessive osteoclast activity), VIPoma
How does hypercalcaemia present in cancer pt?
Often non-specific
N+V, confusion, bone pain, polydipsia, polyuria, dehydration, constipation, ileus, delirium, coma, death, AKI
Severity relates to rate of increase rather than absolute
Management of hypercalcaemia
- Up to 3.2: conservatively rehydrate at least 24h with saline, furosemide to enhance renal excretion of calcium
- Above 3.2: aggressive rehydration + IV bisphosphonates (e.g. pamidronate, work by interfering with osteoclast resorption, usually well-tolerated but ensure well hydrated as can impair kidneys and sometimes causes low calcium/phosphate)
Superior vena cava obstruction
Obstructed blood flow through SVC
- Most due to extrinsic compression, or can be mediastinal lymphadenopathy (mets or lymphoma), in children T cell ALL + NHL are a cause
- Occ can be benign from a thrombus due to a CVC, or fibrosis from radiotherapy
CF: usually gradual onset but can be acute with dyspnoea (50%), oedema of face/neck/trunk/arms (40%), sensation of choking, feeling of fullness in head, headache, lethargy, dilated veins, Pemberton sign (worse when lift arms above head)
Ix: CXR, CT contrast
M: steroids (often given but no evidence), stent for rapid relief of sx, radiotherapy to shrink, chemo good in SCLC/lymphoma/teratoma, sometimes anticoagulation
What are the features of tumour lysis syndrome?
Hyperkalaemia
Hyperphosphataemia
Hyperuricaemia
Hypocalcaemia
May lead to AKI + cardiac arrhythmias (high K+ + phosphate and low Ca - peaked T wave, QTc derangement, syncope, SCD)
CF: often vague with N+V, lethargy, diarrhoea/anorexia, nephropathy from high urate (haematuria, anuria)
What are the causes of tumour lysis syndrome?
- Treatment triggers a massive breakdown in cells esp in haem and bulky chemo-responsive tumours, esp when start chemo, commonest in high grade lymphoma + leukaemia (thus commonest in children/YA)
- More likely if pt has pre-existing chemo dysfunction, pre-treatment high rate, hypovolaemia e.g. if on diuretics, pre-treatment LDH is raised, urinary tract is obstructed
Laboratory vs clinical TLS?
- Lab: abnormality in two or more of the values 3d before/7d after chemo - high uric acid, high potassium, high phosphate, low calcium
- Clinical: lab TLS plus one out of high serum creatinine, arrhythmia or seizure
How do you prevent TLS?
- Pre-hydration
- Monitor electrolytes + fluid balance
- Allopurinol to reduce risk of TLS in low-risk pt, it reduces uric acid production (xanthine oxidase inhibitor)
- Rasburicase in high risk pt, degrades uric acid as is a synthetic uricase
How do you treat TLS?
- Vigorous hydration
- Rasbirucase IV - degrades uric acid to a water soluble metabolite
- For hyperkalaemia: calcium gluconate (heart protection + insulin-dextrose infusion (drive K+ into cells) + fluids
- To reduce phosphate: oral phosphate binders e.g. calcium carbonate
- Sodium bicarbonate if not using rasburicase, it works by alkalinising urine so more phosphate + potassium excreted (also dont use if pH of urine >7 already)
- Haemodialysis if persisting
Brain metastases causing RICP
Often lung, kidney, melanoma, bowel, or primary brain
CF: headache, N+V, seizures, weakness, speech/vision/memory defect, change in personality
MRI head best, CT head may show oedema
M: dexamethasone + PPI to reduce oedema, surgery or stereotactic radio for solitary lesions, whole brain radio for palliative
Bowel obstruction
Can be same causes as normal like strictures/adhesions, or cancer obstruction or cancer infiltration of nerves causing gut paralysis
M: may have drip + suck, may have surgery, may have stent, may have hyoscine butyl bromide (buscopan-reduces cramps) or octreotide (reduce oedema) or steroids
Hyperviscosity
V high haematocrit, WCC + plts
Usually untreated leukaemia or cos of high paraproteins in myeloma
Rare
CF: hypoxia, confusion, headache, vision disturbance, lung infiltrate, papilloedema, HF, priapism
M: plasmapheresis
Malignant bile duct obstruction
Causes cholestatic jaundice
Usually palliative, endoscopic stent insertion into biliary tree helps re-establish flow
Signs of MSCC based on location
Lesions above L1 usually result in upper motor neuron signs in the legs and a sensory level.
Lesions below L1 usually cause lower motor neuron signs in the legs and perianal numbness.
