Oncological Emergencies Flashcards
Oncological emergencies
Neutropenic sepsis Metastatic spinal cord compression Hypercalcaemia of malignancy SVCO Tumour lysis syndrome
Nice definition of neutropenic sepsis
Patient undergoing systemic anticancer treatment (SACT)
Temp > 38
Neutrophil count < 0.5*10^9/L
Causes of neutropenic sepsis
Suspect in all chemo patients who become unwell - some cannot mount fever (corticosteroids)
Typically occurs 10 days post chemo
Newer biological/targeted therapies and RT have less propensity
Haematological malignancy treatment have deeper nadir so greater duration of neutropenia
Clinical features of neutropenic sepsis
Fever Tachycardia > 90 Hypotension < 90 systolic = urgent RR > 20 Symptoms related to specific system - cough - SOB Drowsy Confused
Risk factors for neutropenic sepsis
Prolonged neutropenia - harsher chemo Severity of neutropenia Significant comorbidities - COPD, DM, renal/hepatic impairment Cancer uncontrolled/progressive Central lines Mucosal disruption Inpatient
Responsible pathogens for neutropenic sepsis
80% arise from endogenous flora
- staph aureus
- staph epidermis
- enterococcus
- streptococcus
Increasing frequency of gram +ve cocci - indwelling plastic catheters
MRSA and VRE (vancomycin resistant enterococcus) increasing prevalence
Source only identified in 30% of patients - BC often negative
Ix for neutropenic sepsis
Blood counts - FBC - U+Es - LFTs - Lactate - CRP Cultures - blood - central and peripheral - urine - sputum Swabs - lines - wounds ABG CXR
Prevention of neutropenic sepsis
Patient education - written and oral information - how and when to contact 24 hour specialist oncology advice/emergency care Consider abx prophylaxis Consider future chemo cycles - dose reduction (palliative care) - prophylactic GCSF (curative/adjuvant) - consider stopping treatment
Mechanism of malignant spinal cord compression
Usually caused by collapse or compression of vertebral body that contains metastatic disease (arterial seeding)
10% causes by direct tumour (paraspinal mass) extension into vertebral column
Compression of cord initially causes oedema, venous congestion and demyelination - reversible
Prolonged compression -> vascular injury, cord necrosis - permanent damage
Site of compression in MSCC
10% cervical
70% thoracic
20% lumbar and sacral - below L2 = cauda equina compression
Incidence of MSCC
5% of all cancer patients
- 15% of advanced cancer patients
Commonly breast, prostate and lung
23% will have no previous Ca diagnosis
Presentation of MSCC
> 90% have back pain
- vertebral met, root compression, compression of long tracts of spinal cord
- prolonged often 2-3/12
- spinal or radicular pain
- exacerbated by straight leg raising, coughing, sneezing, straining
- worse after period of lying down
Limb weakness
Sensory level
Bladder and anal sphincter dysfunction
Diminishing performance status/generally unwell
Examination findings of MSCC
Acute onset, flaccid paralysis
Progressing over time
- spasticity - increased tone, clonus and hyperreflexia
- plantar reflexes upgoing
- sensory loss with well defined dermatomal level
- palpable bladder
Immediate mx for MSCC
If pain suggestive of spinal mets - MRI within 1 week Signs of MSCC - MRI within 24 hours Admit Bed rest with log rolling Dexamethasone 16mg + PPI Adequate analgesia
Definitive mx for MSCC
Admit patient - bed rest with log rolling
IV DEXAMETHASONE
Adequate analgesia
Surgical decompression - if fit enough and good prognosis
Local radiotherapy
Supportive care of MSCC
Good nursing care - pressure areas Analgesia Laxatives Bladder care Monitor BMs VTE prophylaxis Physiotherapy Occupational therapy
MSCC prognosis
Dictated by timing
- 80% of patients ambulatory at presentation remain so
Radiosensitive tumour types have improved functional capacity
Causes of hypercalcaemia
Normal range 2.2-2.6
Most common in squamous cell cancers (lung, H+N, kidney, cervix), multiple myeloma and breast cancer
Humoral cause - 80%
- production of PTH-related protein and increased vitamin D3 (lymphoma)
- increased bone resorption and renal reabsorption
Bone invasion - 20%
- osteolytic metastases with local release of cytokines
- increased bone resorption and calcium release form bone (local bone destruction)
Symptoms of hypercalcaemia
Nausea Thirsty Constipated Confused Anorexia Polydipsia and polyuria Fatigue and weakness Poor concentration Drowsy
Mx of hypercalcaemia
Rehydration - 24hrs of normal saline
Bisphosphonates
- pamidronate or zoledronic acid
- can cause renal failure so ensure rehydrated
- takes 4 days to work
Systemic treatment of malignancy
Likely to recur in future - monitoring with 2-4 weekly blood tests
Define tumour lysis syndrome
Metabolic emergency that presents as severe electrolyte abnormality
Massive tumour cell lysis -> release of large amounts of potassium, phosphate and uric acid into systemic circulation
- hyperuricemia
- hyperkalaemia
- hyperphosphatemia
- AKI - uric acid or calcium phosphate crystals
- hypocalcaemia
Risk factors for tumour lysis syndrome
Risk greatest for haematological malignancies
Bulky chemo-responsive tumours
Most common with high grade lymphomas and leukaemia
Generally following initiation of cytotoxic therapy
Patient specific factors
- pre-existing renal dysfunction/nephropathy
- pre-treatment hyperuricaemia
- hypovolaemia
- pre-treatment diuretic use
- pre-treatment LDH high
- urinary tract obstruction from tumour
Presentation of tumour lysis syndrome
3-7 days post chemo N+V Diarrhoea Anorexia Lethargy Haematuria -> oliguria -> anuric Heart failure Cardiac arrhythmia/arrest - peaked T waves, QTc derangement Primary presentation of malignancy
Features of SVCO
Compression or obstruction of SVC
90% extrinsic compression
- intrathoracic primary lung cancer or mesothelioma
Occurs in 3-8% of cancer patients
Clinical features of SVCO
Breathlessness Swelling of face + neck Trunk and arm swelling Sensation of choking Feeling of fullness Headache Lethargy Chest pain Cough Dysphagia Cognitive dysfunction Hallucinations Seizures Stridor Coma
Ix for SVCO
CXR Chest CT with contrast - extensive collateralisation - intraluminal thrombus of SV - evidence of extrinsic compression
Mx of SVCO
Steroids - DEXAMETHASONE Stent - if not radio or chemo sensitive - 95% response rate - rapid relief of symptoms Anticoagulation if thrombus Chemo - SCLC, lymphoma and teratoma Radiotherapy
Symptom relief in SVCO
Sit upright Opioids Benzodiazepines O2 Psychological and emotional support
Causes of SIADH
Tumour cells secreting ADH - commonest in SCLC Drug related - SSRIs - Pneumonia Meningitis/encephalitis Alcohol
Clinical features of SIADH
Hyponatraemia with intracellular cellular oedema Anorexia N+V Drowsiness Confusion Seizures Coma
Ix for SIADH
Serum Na < 130
Low plasma osmolality < 270
Urine osmolality > plasma osmolaltiy
Mx of SIADH
Anti-cancer treatment
Fluid restrictions
Demeclocycline
Prevention of tumour lysis syndrome
Allopurinol - 2 days prior
IV fluids - 1 day prior
K+ levels monitored every 2 hours for the first 8-12 hours of treatment
Mx of tumour lysis syndrome
Rasburicase - recombinant urate oxidase
Causes of MSCC
Collapse of a vertebral body containing metastatic disease
Direct tumour expansion causing pressure on the spinal cord
Metastatic lesions in the vertebral bodies causing compression
Mx of neutropenic sepsis
IV TAZOCIN - within 1 hour
- if still febrile after 48 hours switch to meropenem + vancomycin
Fluid resuscitation
Consider catheterisation for urine monitoring
Consider G-CSF in patients with extreme sepsis/neutropenia
