Oncological Emergencies Flashcards

1
Q

What is neutropenic sepsis as described by NICE?

A

A neutrophil count of 0.5 × 10^9 per litre or lower, plus one of the following:

  • Temperature ≥ 38°C OR
  • Other signs or symptoms consistent with significant sepsis
  • Patient undergoing systemic anticancer treatment (SACT)
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2
Q

What are some of the causes of neutropenia?

A

Recent chemotherapy

  • Malignant bone marrow infiltration
  • Extensive radiotherapy
  • Bone marrow failure secondary to non-malignant disease (e.g. aplastic anaemia)
  • Hypersplenism
  • Megaloblastic anaemia
  • Drug-induced (e.g. clozapine)
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3
Q

What are some of the RFs for neutropenic sepsis?

A
  • Patients over the age of 60
  • Advanced malignancy
  • Previous neutropenic sepsis
  • Mucositis
  • Poor performance status
  • Significant co-morbidities (the risk increases further in the presence of multiple co-morbidities)
  • Indwelling central venous catheters
  • Corticosteroids (causes immunosuppression)
  • Prolonged hospital admission
  • Severe or prolonged neutropenia
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4
Q

What are some of the clinical signs of neutropenic sepsis?

A
  • Hypotension: URGENT ATTENTION – involve outreach and consider escalation above ward care
  • Fever
  • Reduced urine output
  • Altered conscious level or confusion/ impaired MMSE
  • Mottled/ashen appearance
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5
Q

What investigations should be performed for neutropenic sepsis?

A

Bedside investigations

§Urinalysis: to look for urinary tract infection

§ECG: should be performed in all acutely unwell patients.

§Capillary blood glucose: to exclude hypoglycaemia.

Laboratory investigations

  • Baseline blood tests (FBC, U&E, coagulation, CRP, LFTs): white cells may be low or raised and CRP may also be raised. Serum lactate, Group and save,
  • Cultures (central and peripheral); urine
  • ABG
  • Microbiological cultures: wounds, urine, stool, sputum, and line tip (if indwelling line infection suspected).
  • Viral respiratory swab: if viral respiratory infection suspected.

Imaging

§Chest X-ray: to look for evidence of pneumonia.

§High-resolution chest CT: if fungal pneumonia is suspected.

§Abdominal ultrasound or CT abdomen: if biliary or abdominal infection suspected.

Other investigations: Bronchoalveolar lavage: if an atypical chest source is suspected, such as Pneumocystis jirovecii.

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6
Q

How is neutropenic sepsis managed?

A
  • The sepsis six care bundle should be completed.
    • Pharmacological
      • 1st line : IV piperacillin with tazobactam (tazocin). Some guidelines may also recommend the administration of gentamicin
      • 2nd line (e.g. penicillin allergy) may include IV meropenem (dependent on local guidelines)
  • Other:
    • Additional anti-microbial cover (e.g. teicoplanin) for gram-positive organisms may be required for patients with indwelling central venous catheters.
    • Anti-fungal treatment may be considered when the fever persists beyond 4 – 6 days
    • Granulocyte-colony stimulating factor: Recombinant granulocyte-colony stimulating factor (G-CSF) may be used for both prophylaxis and treatment of neutropenia to reduce the risk of neutropenic sepsis.
      • Consider in patients who are profoundly septic/neutropenic
      • Mechanism: stimulates bone marrow to produce neutrophils and may form part of specific chemotherapy regimens. E.g. filgrastim
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7
Q

What are some of the complications of neutropenic sepsis?

A
  • Single or multi-organ failure (e.g. renal failure, heart failure and acute respiratory distress syndrome)
  • VTE (e.g. PE), DIC, Opportunistic or hospital-acquired infections, Delirium, Psychological complications (e.g. anxiety regarding future infections and chemotherapy treatment)
  • Delays in chemotherapy leading to worse cancer outcomes
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8
Q

What cancers are most commonly associated with metastatic spinal cord compression?

A
  • lung, prostate, breast, myeloma, melanoma.
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9
Q

What is the incidence of MSCC?

A
  • 3–5% of cancer patients have spinal metastases.
  • ~15% of those with advanced cancers develop metastatic spinal cord compression
  • 10% of patients with spinal mets develop MSCC
  • Incidence may be as high as 19% in breast/prostate/lung cancer
  • Breast, prostate and lung account for > 60% of cases
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10
Q

How does MSCC arise?

A
  • Collapse or compression of a vertebral body due to metastases (common), direct extension of a tumour into vertebral column (rare).
  • 10% by direct tumour (paraspinal mass) extension into the vertebral column
  • Compression of cord initially causes oedema, venous congestion and demyelination which are reversible
  • Prolonged compression -> vascular injury, cord necrosis and permanent damage
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11
Q

Where (location) does MSCC arise?

A
  • 30-50% have > 1 area involved
  • Below L2 vertebra =cauda equina compression of peripheral nerves and not spinal cord
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12
Q

What are some of the signs and sx of MSCC?

A
  • Back pain ~95%. – earliest and most common
  • Nocturnal pain and pain with straining.
  • Spinal or radicular pain (8/10)
  • Red flag: cervical/thoracic pain.
  • Other: limb weakness, difficulty walking, sensory loss, bowel/bladder dysfunction
  • Sensory loss in the saddle area
  • Neurological signs: depend on the level of the lesion.
    • Lesions above L1 – usually UMN signs in the legs and a sensory level.
    • Lesions below L1 - usually cause LMN signs in the legs and perianal numbness. Tendon reflexes tend to be increased below the level of the lesion and absent at the level of the lesion

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13
Q

What features can be seen of MSCC on clinical examination?

A
  • Spasticity (increased tone, clonus and hyperreflexia in limbs below level of MSCC
  • Plantar reflexes up going (not cauda equina)
  • Sensory loss with well defined dermatonal level
  • Palpable bladder (urinary retention)
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14
Q

How is MSCC managed?

A
  • Admit for bed rest with log rolling – lie pt flat
  • Ix: Urgent (within 24h) MRI of whole spine.
  • Pharmacological: Dexamethasone 16mg/24h PO + PPI (unless? lymphoma) for prophylatic gastroprotection and blood glucose monitoring.
  • Thromboprophylaxis (compression stockings, LMWH: Consider if reduced mobility
  • Urgent referral to clinical oncology/cancer MDT
  • Radiotherapy is the commonest treatment and should be given within 24 hours of MRI diagnosis.
  • Decompressive surgery (Balloon kyphoplasty) Treatment of choice if fit and good prognosis (>3/12)
    • Prognostic indicators: Multiple myeloma, lymphoma, or breast, prostate or renal cancers
      • Good motor function at presentation
      • Good performance status
      • Limited comorbidity
      • Single-level spinal disease
      • Absence of visceral metastasis
      • Long interval from primary diagnosis
      • Also for biopsy or stabilisation
  • Urinary cathetarisation
  • Supportive: Good nursing care; care re pressure areas; Analgesia; Laxatives; Bladder care; Monitor BMs; VTE prophylaxis; Physiotherapy; Occupational therapy
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15
Q

In which cancers is metastatic hypercalcaemia most commonly seen?

A
  • Most common in SCC (lung, H&N, kidney, cervix).
  • Also seen in breast cancer and multiple myeloma
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16
Q

How does hypercalcaemia arise?

A
  • Tumour secretion parathyroid hormone-related peptide (PTHrP) (80%)
  • Osteolytic metastases with local release of cytokines (20%)
  • Tumour production of 1,25 dihydroxy vitamin D (lymphoma)
17
Q

What are some of the signs and sx of hypercalcaemia?

A
  • Weight loss, anorexia, nausea, polydipsia, polyuria, constipation, abdominal pain, dehydration (thirstiness) , weakness, confusion, seizure, coma.
  • Severe; N&V, ileus, delirium, coma and death
18
Q

How is hypercalaemia managed?

A
  • Aggressive rehydration: IV 0.9% Normal Saline – several litres
  • Bisphosphonates (if EGFT≥30 IV pamidronate 60-90mg or IV zolendronic acid 4mg
    • Can cause renal failure so must make sure properly rehydrated first
    • Takes 5-7 days to work
    • Denosumab for refractory hypercalcaemia
  • Calcitonin produces a more rapid (2h) but short-term effect and tolerance can develop. Long-term treatment is by control of the underlying malignancy.
19
Q

What is SVCO?

A
  • Reduced venous return from head, neck, and upper limbs.
  • Due to extrinsic compression (most common), or venous thrombosis
  • SVC Syndrome with airway compromise requires urgent treatment.
20
Q

What are some of the most common causes of SVCO?

A
  • >90% of svc syndrome results from malignancy (extrinsic compression)

Most common cancers: lung cancer (80%) – Occurs in 10% SCLC cases and 2% of NSCLC cases, lymphoma (10%), metastatic (eg breast), thymoma, germ cell.

  • Other malignancies: metastatic seminoma, Kaposi’s sarcoma, breast cancer
  • Aortic aneurysm
  • Mediastinal fibrosis
  • Goitre
  • SVC thrombosis
21
Q

What are some of the symptoms of SVCO?

A
  • SOB (50%), Swelling of face and neck (40%) , Trunk and arm swelling (40%)
  • Orthopnoea, stridor, plethora/cyanosis, oedema of face and arm, cough, headache, engorged neck veins (non-pulsatile ↑JVP), engorged chest wall veins.
  • Headache and lethargy
22
Q

What are some of the key sign(s) of SVCO?

A
  • Pemberton’s test: elevation of the arms to the side of the head causes facial plethora/cyanosis.
  • Others:
    • Thoracic vein distension (65%)
    • Neck vein distension (55%)
    • Facial oedema (55%)
    • Increased RR (40%)
    • Plethora 15%, Cyanosis 15%, Arm oedema 10%, Advanced stages, Laryngeal stridor, Drowsy, Coma and death
23
Q

What investigations can be performed to work out the underlying cause with SVCO?

A
  • CXR Is there a mass?
  • CT with contrast
    • Extensive collateralization
    • Intraluminal thrombus of SVC
    • Evidence of extrinsic compression
24
Q

How is SVCO managed?

A
  • Prop up. Assess for hypoxia (pulse oximetry, blood gas): Give 02 if needed.
  • Pharmacological: Dexamethasone 16mg/24h. CT is used to define the anatomy of the obstruction.
  • Surgical: Balloon venoplasty and SVC stenting provide the most rapid relief of symptoms
    • Stenting: can be use if not radio or chemotherapy sensitive. 95% response rate. Symptomatic relief only
  • Oncological management: Treat with radiotherapy or chemotherapy depending on the sensitivity of the underlying cancer.
    • Small cell: chemotherapy + radiotherapy
    • Non-small cell: radiotherapy
    • Chemotherapy: Used for SCLC, lymphoma and teratoma response rate >70%.
25
Q

What is tumour lysis syndrome?

A
  • Oncological emergency due to turnover of high cell mass malignancies resulting in severe metabolic derangement
  • Occurs when the rapid destruction of malignant cells releases intracellular contents
  • Chemotherapy for rapidly - proliferating tumours (leukaemia, lymphoma, myeloma) leads to cell death and ↑urate, ↑K+, ↑phosphate, ↓ calcium, AKI (uric acid and/or calcium phosphate crystals in the renal tubules)
26
Q

What metabolic derangements can be seen with tumour lysis syndrome?

A

HIGH: ↑urate ↑K+, ↑phosphate

LOW:↓ calcium

AKI (uric acid and/or calcium phosphate crystals in the renal tubules)

27
Q

How does tumour lysis syndrome present?

A
  • Lymphoproliferative malignancy + chemotherapy, radiotherapy or corticosteroids
  • Can occur spontaneously
  • Normally 12-72h hours post chemo
  • GI upset, oedema, fluid overload, haematuria, symptoms of metabolic derangements
28
Q

What are some of the RFs for tumour lysis syndrome?

A
  • Large tumour burden
  • LDH > 1500 IU
  • Extensive marrow involvement
  • High tumour sensitivity to chemotherapeutic agents
  • ALL, Burkitt lymphoma
  • Chemotherapy – cisplatin, etoposide, fludarabine, intrathecal methotrexate, paclitaxel, ritiuximab, radiation, interferon, corticosteroids, tamoxifen
29
Q

What are some of the tumours that cause TLS?

A
  • Poorly differentiated lymphomas, e.g. Burkitt lymphoma and high-grade non-Hodgkin lymphomas
  • Haematological malignancies: Leukemia, e.g. acute myeloid leukemia (AML), transformed chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL)
  • Some fast-growing solid tumours such as hepatocellular carcinoma, hepatoblastoma, testicular cancer, small cell lung cancer, breast cancer and neuroblastoma
30
Q

What clinical signs may be seen on examination in a patient with tumour lysis syndrome?

A
  • Clinical features: including nausea, diarrhoea, muscle weakness, tetany, arrhythmias, seizures and sudden death (Requires appropriate prophylaxis and early recognition and treatment)
  • Haematuria -> oliguria -> anuric
  • Heart failure
    • Cardiac arrhythmia/arrest
    • Peaked T waves, QTc derangement
    • Primary presentation of malignancy
    • ‘Spontaneous tumor lysis’

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31
Q

How is tumour lysis syndrome managed?

A
  • Prevent with hydration and uricolytics, eg:
    • Rasburicase (Synthetic uricase -> degrades uric acid to allantoin (water soluble)
    • Allopurinol (Xanthine oxidase inhibitor -> less hyperuricemia)
  • Increasing renal clearance -> dialysis

Management of complications

  • Hyperkalaemia: (1) membrane stabilisation -> calcium gluconate; (2) shift of K+ intracellularly -> insulin, 50% dextrose, salbutamol (3) reduction of K+ load -> resonium, diuretics, dialysis
  • Hyperphosphataemia. Mx: phosphate binders, dialysis, low phosphate diet
  • Hypocalcaemia. Mx: calcium gluconate
32
Q

How does raised ICP present?

A
  • Headache (worse in the morning, when coughing or bending over)
  • N+V
  • Papilloedema
  • Fits
  • Focal neurological signs
33
Q

How is raised ICP managed (Ix and mx)?

A
  • Ix: urgent CT/ MRI (for diagnosis of expanding mass, cystic degeneration, haemorrhage within a tumour, cerebral oedema, hydrocephalus due to a tumour or blocked shunt
  • Mx: dexamethasone, mannitol (for relief of cerebral oedema)