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Yr4: Cancer Care > Oncological Emergencies > Flashcards

Oncological Emergencies Flashcards

1
Q

What are oncological emergencies?

A

Group of conditions, that occur as a direct or indirect result of cancer or it’s treatment that are potentially life threatening

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2
Q

State some common oncological emergencies you need to know

A
  • Neutropenic sepsis
  • Metastatic spinal cord compression
  • Hypercalcaemia of malignancy
  • Superior vena cava obstruction syndrome
  • Tumour lysis syndrome
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3
Q

Define neutropenia

Define mild, moderate & severe neutropenia

A
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4
Q

State some possible causes of neutropenia

A
  • chemotherapy and other immunosuppressive drugs (e.g. clozapine, carbimazole)
  • stem cell transplantation
  • infections (e.g. HIV, EBV, hepatitis)
  • bone marrow disorders e.g. aplastic anaemia
  • myelodysplastic syndromes
  • SLE (mechanisms include circulating antineutrophil antibodies)
  • rheumatoid arthritis (e.g. hypersplenism in Felty’s syndrome)
  • nutritional deficiencies
  • haemodialysis
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5
Q

Define neutropenic sepsis

A

Neutrophil count of < 0.5 * 109in a patient who is havingsystemic anticancer treatment (SACT) and has one of the following:

  • a temperature higher than 38ºC or
  • other signs or symptoms consistent with clinically significant sepsis
  • *NICE “It is defined as a temperature of greater than 38°C or any symptoms and/or signs of sepsis, in a person with an absolute neutrophil count of 0.5 x 109**/L or lower.”*
  • *NOTE: you should suspect in all chemotherapy patients who become unwell as some chemo patients cannot mount a fever (e.g. if on corticosteroids)*
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6
Q

Answer true or false to the following statements:

  • Newer biological/targeted therapies and radiotherapy have more propensity to cause neutropenia
  • Therapy for haematological malignancies may cause lower neutrophil count and a greater duration of neutropenia
A
  • FALSE; less propensity to cause neutropenia
  • TRUE
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7
Q

All pts who are receiving SACT are at risk of neutropenic sepsis however there are some factors that can increase risk; state some of these

A
  • Prolonged neutropenia (>7 days)
  • Severity of neutropenia
  • Significant comorbidities (COPD, DM, renal/hepatic impairment)
  • Aggressive cancer
  • Central lines (potential source of infection)
  • Mucosal disruption (potential source of infection)
  • Hospital inpatient (risk of catching infection increased)
  • Age (infants and >60yrs)
  • Corticosteroids (further immunosuppression)
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8
Q

State some signs & symptoms of neutropenic sepsis

A
  • Pt may report “feeling generally unwell” and nurses may say “patient is just not right”
  • Fever
  • Tachycardia >90
  • HYPOTENSION < 90 systolic= URGENT
  • RR > 20
  • Symptoms related to a specific system e.g. cough, SOB, line, mucositis (always check mouth, lines etc…)
  • Drowsy
  • Confused
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9
Q

State some of the most common organisms and sources of infection in neutropenic sepsis

A

Common Organisms

  • 80% arise from endogenous flora. Most common causative organisms are gram positive cocci: Staphylococcus aureus, Staphylococcus epidermis, enterococcus and Streptococcus (pneumoniae & pyogenes)
  • Less commonly: E-coli, Klebsiella, pseudomonas
  • MRSA & VRE (vancomycin resistant enterococcus) are increasingly prevalent

Common Sources

  • GI tract is most common source (SACT has greatest impact on rapidly dividing cells; epithelial cells in GI tract renew every 2-4 days so are greatly affected. Impairs barrier in GI tract allowing bacteria to spread. Think about mucositis in mouth)
  • Other sources include: central lines, breaks in skin, other usual sources of infection e.g. cellulitis
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10
Q

Blood cultures are often negative in neutropenic sepsis; true or false?

A

True; source often only identified in 20-30% of pts

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11
Q

Discuss the management of neutropenic sepsis

A
  • Prompt A-E assessment & investigations within that
    • IV access
    • Bloods: FBC (with differential), U&E’s, LFTs, clotting screen, CRP, ABG/lactate, central & peripheral blood cultures
    • Cultures/swabs: urine dipstick and M,C&S, sputum sample, wound etc…. Also other investigations e.g. CXR
  • Escalate SpR/consultant
  • Sepsis 6
    • Antibiotics: IV Tazocin (piperacillin/tazobactam) 4.5g TDS within an hour. If evidence of line or tunnel infection add in IV vancomycin. If severe penicillin allergy give IV meropenem 1g TDS
    • Oxygen
    • IV fluids
    • Consider catheterisation for monitoring of urine output
    • (Bloods)
    • (Lactate)
  • Consider escalation of care (e.g. ICU)
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12
Q

How long do we usually give abx for in neutropenic sepsis?

A

Usually have empirical IV antibiotics for 5 days; may switch to oral after 48hrs if risk if low

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13
Q

If after 48hrs blood cultures were negative but pts is still pyrexia and neutropenic, what would you need to consider?

A
  • Repeat cultures
  • Discuss with microbiology
  • Consider alternative abx e.g. meropenem
  • Consider adding vancomycin if line in place and not already started
  • Consider possibility of fungal infection
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14
Q

Following initial management of neutropenic sepsis, what further management may be considered?

A
  • GCSF (granulocyte colony stimulating factor):not routinely used but may consider in pts who are profoundly septic or neutropenic
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15
Q

Discuss some preventative measures for neutropenic sepsis

A
  • Patient education: written & verbal information. Ensure know what to look out for and know how to contact 24hr specialist oncology advice or other emergency care
  • Antibiotic prophylaxis with fluoroquinolones
  • Prophylactic GCSF
  • Consider dose reduction for future chemotherapy
  • Consider stopping treatment
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16
Q

State some possible causes of neutropenia

A

There are multiple possible causes of neutropenia such as cytotoxic chemotherapy and other immunosuppressive drugs, stem cell transplantation, infections, bone marrow disorders such as aplastic anaemia and myelodysplastic syndromes, and nutritional deficiencies

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17
Q

Discuss the prognosis of neutropenic sepsis

A
  • Significant cause of cancer-treatment related mortality
    • 5% pts with solid tumours
    • 11% haematological malignancies
  • Deterioration can be very rapid so prompt recognition and treatment can be life saving
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18
Q

How long after chemotherapy does neutropenic sepsis usually occur?

A

7-10days post chemo

*any pt on cancer treatment always helpful in history to ask when had their last lot of treatment

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19
Q

Define malignant/metastatic/neoplastic spinal cord compression (MSSC)

A

Compression of the dural sac and its contents at the level of the cord or the cauda equina

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20
Q

For MSSC, discuss:

  • How many pts are affected my MSSC each year/how common it is
  • What % of pts presenting with MSSC have no previous cancer diagnosis
A

How common is it?

  • 4000 cases per year in UK
  • 5% of pts with all cancer develop MSSC
  • 15% of pts with advanced cancer develop MSSC

23% of pts presenting with spinal metastases have no previous cancer diagnosis

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21
Q

What is the most common mechanism for compression of dural sac and its contents in MSSC?

A
  • 80-85% caused by collapse or compression of vertebral body that contains metastatic disease
  • 10% by direct tumour (paraspinal mass) extension into the epidural space- especially common in lymphoma
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22
Q

MSSC can happen with any cancer however it more common with certain cancers; state these cancers

A

The following make up 60%:

  • Lung
  • Breast
  • Prostate

Other common causes:

  • Lymphoma
  • Myeloma
  • Renal
  • Thyroid
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23
Q

Which part of spine is most commonly affected by MSSC?

A

Thoracic spine

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24
Q

Which part of spine is most commonly affected by MSSC?

A

Thoracic spine

*30-50% have more than 1 area involved

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25
Q

State the symptoms of MSSC- highlighting the most common symptoms

A
  • Back pain (>90%):
    • often first symptom and been present for some time- commonly 2-3/12
    • Pain is poorly responsive to analgesia
    • Radiates around chest (band-like) or down legs
    • Worse after period of lying down e.g. at night
    • If radicular (nerve root) component may be exacerbated be neck flexion, straight leg raise, coughing, sneezing, straining & have radicular pain (burning, shooting, numb)
  • Motor symptoms (>75%):
    • Reduced power
    • Difficulty with standing, walking, stairs, often symmetrical
    • May have poor truncal balance if affecting high cervical region
  • Sensory loss (>50%):
    • Pt may not report this and it may only become apparent when examined
    • Ensure check perianal area
  • Sphincter dysfunction:
    • Urinary hesitancy, frequency, retention leading to overflow
    • Faecal incontinence
  • Diminishing performance status/generally unwell
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26
Q

State signs/what you may find on clinical examination of a pt with MSSC

A

**NOTE: neurological signs depend on level of lesion. Above L1 usually result in UMN signs and below L1 causes LMN signs/cauda equina signs. Tendon reflexes tend to be increased below the level of lesion and absent at the level of lesion.

  • Acute onset flacid paralysis
  • Spasticity (increased tone, clonus & hyperreflexia in limbs below level of MSSC due to impairment of UMNs)
  • Up-going plantar reflexes (UMN lesion)
  • Sensory loss with well defined dermatomal level
  • Palpable bladder if in urinary retention
  • Cauda equina:
    • Lower back pain
    • Saddle anaesthesia
    • Reduced anal tone
    • Bladder/bowel dysfunction (painless urinary retention)
    • Erectile dysfunction
    • Bilateral sciatica
    • Weakness or paralysis
    • Reduced sensation/paraesthesia affected area
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27
Q

What key investigation would you do in suspected MSSC?

A

Urgent MRI (within 24hrs)

*NOTE: if cannot have MRI e.g. due to OOH then would do CT if

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28
Q

If someone has back pain suggestive of spinal metastases but no features of MSSC when should they have an MRI?

A

Within 1 week

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29
Q

Discuss the initial management of MSSC

A

Emergency requiring urgent admission and MRI within 24hrs:

  • High dose PO dexamethasone (16mg) + PPI unless ?new lymphoma diagnosis)
  • Analgesia
  • Bed rest with log rolling

**REMEMBER: if giving cancer pts steroids must always give PPI

Also require supportive care:

  • Laxatives
  • Bladder care (e.g. catheterisation)
  • VTE prophylaxis
  • Physiotherapy (later date after further managment)
  • Occupational therapy (later date after further management)
30
Q

Discuss the further management of MSSC following results of MRI (4)

**HINT: consider what the management would be if pt had no motor function for >48hrs

A

Treatment options following initial management include:

  • Surgery: relieve pressure, remove tumour & stabilise spine
  • Balloon kyphostomy: inject bone cement into vertebral body to restore vertebral height and correct angular deformity
  • Radiotherapy: relieves compression of spine & nerve roots by causing cell death in rapidly dividing tumour tissue
  • Urgent chemotherapy: may be used for very sensitive tumours e.g. lymphoma, SCLC

If pt has >48hrs with no motor function they would be for best supportive care with 1# radiotherapy for pain

Many will require supportive care:

31
Q

Surgery is the treatment of choice, offering a good prognosis, if the patient is fit enough; state some features/characteristics that would make a pt a good candidate for surgery

A
  • 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
32
Q

If radiotherapy is used to treat MSSC, discuss:

  • How soon after confirmation of diagnosis it should be given
  • How it is given
  • Benefits
A
  • Within 24hrs of confirmation of diagnosis
  • Pt usually supine, targets abnormal area + 1-2 vertebra each side
  • Benefits:
    • Relieve compression
    • Relieve pain
    • Stabilise neurological deficits
    • Increase life expectancy (months)
33
Q

Surgery is the treatment of choice for MSSC if pts are fit enough; however, what treatment do most pts end up having?

A

Majority of pts have radiotherapy as at this point they have extensive disease & poor physiological reserve

34
Q

Discuss the prognosis of MSSC

A

Prognosis/odds of recovery depend on stage at presentation:

  • 80% those who are ambulatory at presentation remain so
  • < ⅓ of non-ambulatory pts regain strength to walk
  • Loss of sphincter function= poor prognostic sign

In terms of mortality…

  • Those who don’t recover mobility survive ~ 1-3/12
  • Those who are able to walk 5-8/12
  • Myeloma/lymphoma longer
35
Q

Why is prompt treatment of MSSC so important?

A
  • Compression of cord initially causes oedema, venous congestion & demyelination; all of which are reversible
  • Prolonged compression can lead to vascular injury, necrosis and permanent damage
36
Q

What’s the normal range for corrected calcium?

A

2.2-2.51mmol/L

37
Q

Which cancers is hypercalcaemia of malignancy most common in?

A

Common cancers: breast, SCC (squamous cell carcinoma), renal, myeloma, lymphoma

  • ***Occurs most often in disseminated disease*
  • ***Affects about 20% all cancer pts*
38
Q

There are two main mechanisms for hypercalcaemia of malignancy; describe each and state which is most common

A

Occurs most often in disseminated disease (2% all cancer pts). 20% of cases do NOT have bone metastases.

Humoural cause (80%)

  • Chemical agents released by tumour disrupt normal calcium homeostasis e.g. PTHrP, overproduction vitamin D etc…

Bone invasion (20%)

  • Osteolytic metastases with local release of cytokines leading to bone resorption & calcium release from bone
39
Q

State symptoms & signs of hypercalcaemia of malignancy

A

Often non-specific and severity relates to rate of increase in calcium:

  • Nausea
  • Thirst
  • Constipation (ileus if severe)
  • Confusion (delirium if severe)
  • Anorexia
  • Polyuria
  • Fatigue
  • Weakness
  • Poor concentration/drowsy
  • Bone pain

Can lead to coma & death.

40
Q

What investigations should you do if you suspect hypercalcaemia of malignancy?

A
  • ECG
  • Bloods:
    • U&E
    • Bone profile
    • LFTs
    • PTH
    • Vitamin D
    • Bicarbonate
41
Q

Discuss the management of hypercalcaemia of malignancy

A
  • First, rehydrate using IV 0.9% NaCl (~3L over 24hr or 2L if risk of fluid overload)
  • Stop any drugs that may worsen hypercalcaemia or its symptoms (e.g. thiazides, lithium, vitamin D, calcium supplements)
  • After at least 24hrs of fluids, give IV bisphosphonates: IV pamidronate or zoledronic acid
  • Manage associated symptoms e.g.:
    • Antiemetic for N&V: haloperidol (1st line biochemical cause)
    • Laxatives for constipation: e.g. movicol or lactulose
  • If hypercalcaemia continues options include:
    • Repeat dose of bisphosphonates (if hypercalcaemic at day 7)
    • Denosumab for refractory hypercalcaemia (monoclonal antibody against RANLK that reduces osteoclast differentiation, activity and survival; hence reduces bone resorption. SC injection which once established is every 4 weeks)
    • Calcitonin is occasionally used in severe hypercalcaemia to temporarily lower the calcium level prior to onset of action of Zolendronic acid
  • Systemic treatment of malignancy

??? if corticosteroids may be beneficial if vitamin D mediated

42
Q

UHL guidelines for asymptomatic hypercalcaemia with calcium <3mmol/L

A
43
Q

Why must you rehydrate for 12-24hrs prior to giving bisphosphonates in treatment of hypercalcaemia of malignancy?

A

Bisphosphonates can impair renal function/cause renal failure so must ensure properly hydrated first

Always seek advice if significant renal impairment

44
Q

How long do bisphosphonates take to work (in hypercalcaemia of malignancy)?

A

Up to 4 days

*Max effect after 4-7 days

45
Q

What monitoring is required in pts with hypercalcaemia of malignancy?

A

Immediate/first week monitor:

  • U&E’s (renal func)
  • Bone profile (calcium)

Hypercalcaemia is likely to recur in future so may need 2-4 weekly blood tests to monitor. Some pts need regular bisphosphonate infusions.

46
Q

Discuss the prognosis of hypercalcaemia of malignancy

A

Most pts who have hypercalcaemia have disseminated disease and many die in <3/12

  • Solid organ malignancy= 52 day prognosis
  • Haematological malignancy= 362 day prognosis
47
Q

State some potential complications of hypercalcaemia of malignancy

A
  • Bisphosphonate induced flu-like syndrome
  • AKI
  • Coma
  • Acute pancreatitis

Other side effects of bisphosphonates: acute osteonecrosis of jaw, hypocalcaemia if given to pts with critical vit D deficiency

48
Q

What is superior vena cava syndrome/obstruction?

A

Obstruction of blood flow through SVC either due to extrinsic compression (90%) or intraluminal occlusion of the SVC (this may be a thrombus or tumour invasion); it leads to interrupted venous return from the head, thorax and upper extremities to the right atrium.

*SVCO most commonly occurs due to malignancy however can be benign and due to occlusion of SVC by thrombus; number of benign cases has increased due to use of central venous catheters. BMJ says 65% are due to malignancy.

49
Q

What % of all cancer pts will go on to develop SVCO?

A

2-5%

50
Q

State some malignancies that are more likely/common to cause SVCO; highlight two most common

A
  • Intrathoracic primary lung cancer (80%)- commonly small cell due to central position
  • Lymphoma (non-Hodgkin’s) ***Consider in younger pts
  • Mesothelioma
  • Metastases in lung
51
Q

State some signs & symptoms of SVCO

A

*NOTE: Presentation with airway obstruction is serious, although rare in current clinical practice

  • Dyspnoea
  • Headache
  • Confusion
  • Blurred vision
  • Lethargy
  • Swelling of face, neck & upper limbs
  • Distended neck & chest veins
  • Cyanosis
  • Hoarse voice
  • Stridor
  • Conjunctival swelling
  • Periorbital oedema
  • Papilloedema
  • Pulseless jugular venous distension
52
Q

Discuss what investigations you would do for SVCO

Would you do these before starting treatment for SVCO?

A
  • CXR: mediastinal mass, mediastinal shift
  • Chest CT with contrast: mediastinal mass, extensive collateralisation, intraluminal thrombus of SVC, evidence of extrinsic compression
  • ABG (for saturations)

Chest CT with contrast is investigation of choice. If very high clinical suspicion of SVCO sources say can start dexamethasone.

Need to do investigations prior to treatment to be sure of cause??? CHECK

53
Q

Discuss the immediate management of SVCO

A

First-line treatment consists of securing the airway and relief of obstructive symptoms:

  • A-E assessment
  • Escalate
  • Sit upright
  • Give oxygen
  • Dexamethasone 16mg + PPI
  • Opioids
  • Benzodiazepines

*Cochrane review found no evidence to support use of steroids but they are frequently prescribed. Assess the severity of SVCO to see if need steroids?

54
Q

Discuss the further management/definitive treatment of SVCO

A
  • Percutaneous vascular stenting: most effective means of overcoming SVCO in early stages; rapid response but doesn’t treat cause.
  • Anticoagulation if thrombus
  • Chemotherapy (used for SCLC, lymphoma, teratoma. Response rate >70%)
  • Radiotherapy (used for other malignant causes. Response rate ~60%)
55
Q

Discuss the prognosis of SVCO

A
  • Prognosis partly depends on underlying condition
  • Most pts have improvement in symptoms following treatment (**in patients with non-small cell lung cancer resistant to chemotherapy and radiotherapy, development of SVC syndrome is associated with poor prognosis and median survival of <6 months)
  • Recurrence of symptoms can occur at a later date
56
Q

Define tumour lysis syndrome (include trigger, pathophysiology & biochemical picture)

A

Oncological emergency characterised by metabolic and electrolyte abnormalities; it can occur after the initiation of any cancer treatment (usually occurs after chemotherapy) but can also occur spontaneously or in some occasions after steroids alone. It is caused by rapid breakdown of large numbers of cancer cells resulting in the release of large amounts of intracellular content (potassium, phosphate, uric acid) into the bloodstream resulting in hyperuricaemia, hyperphosphataemia, hyperkalaemia and hypocalcaemia.

57
Q

Which cancers is TLS most commonly associated with?

A

Risk of TLS is greatest with haematological malignancies e.g. high grade lymphomas and leukaemia

58
Q

State some risk factors for TLS

A
  • Haematological malignancy
  • Large tumour burden/bulky disease
  • Chemosensitive tumours
  • Recent chemotherapy
  • Pre-existing renal disease
    • Nephrotoxic medications (may cause or worsen renal impairment)
  • Urinary tract obstruction from tumour
  • Dehydration
  • Pre-treatment LDH high
  • Pre-treatment hyperuricaemia
  • High circulating WCC
59
Q

When, if occurring after chemotherapy, does TLS occur?

A

Normally 3-7 days post chemotherapy

60
Q

State signs & symptoms of TLS

A
  • Nausea & vomiting
  • Anorexia
  • Diarrhoea
  • Lethargy
  • Muscle weakness & cramps
  • Parasthesia
  • Haematuria
  • Oliguria or anuria
  • Hypertension or hypotension
  • Fluid overload
  • Lymphadenopathy (malignancy)
  • Splenomegaly (malignancy)
61
Q

Alongside signs & symptoms of TLS already discussed, how may TLS present?

A
  • Acute renal failure
  • Cardiac arrhythmias
62
Q

Explain how TLS can lead to AKI and hypocalcaemia

A
  • Release of intracellular contents (potassium, phosphate, uric acid)
  • Uric acid leads to acute urate nephropathy which leads to AKI
  • Phosphate binds to calcium causing hypocalcameia
  • Calcium phosphate crystals can deposit in kidneys and worsen AKI
63
Q

What investigations would you do if you suspect tumour lysis syndrome?

A
  • U&Es (potassium, calcium, phosphate, urea, creatinine, eGFR): renal function & electrolytes
  • Uric acid: raised
  • LDH: raised
  • ECG: arrhythmias due to hyperkalaemia and/or hypocalcaemia
64
Q

What grading system is used for TLS? (less important to know)

What do we mean when we talk about laboratory and clinical TLS?

A

Cairo & Bishop grading system

Laboratory tumor lysis syndrome: abnormality in two or more of the following, occurring within three days before or seven days after chemotherapy.

  • uric acid > 475umol/l or 25% increase
  • potassium > 6 mmol/l or 25% increase
  • phosphate > 1.125mmol/l or 25% increase
  • calcium < 1.75mmol/l or 25% decrease

Clinical TLS= patient meets two or more criteria for laboratory diagnosis and has an additional clinical complication attributed to the abnormalities such as:

  • renal insufficiency (serum creatinine 1.5x ULN)
  • cardiac arrhythmia
  • sudden cardiac death
  • seizure
65
Q

Discuss the preventative management of TLS

A

Pts are categorised as low, intermediated & high risk; prophylaxis depends on risk level:

Low risk

  • Stop nephrotoxic drugs
  • Stop drugs that increase electrolytes/metabolites e.g. K+, uric acid etc…

Intermediate risk

  • Stop nephrotoxic drugs
  • Stop drugs that increase electrolytes/metabolites e.g. K+, uric acid etc…
  • At least 24hrs of prehydration (ensuring good urine output. ~2-3L IV fluids/24hrs) +/- loop diuretic
  • PO allopurinol (start 1-2 days before chemotherapy and continue for 3-7 days)
  • If allopurinol fails → rasburicase

High risk

  • Stop nephrotoxic drugs
  • Stop drugs that increase electrolytes/metabolites e.g. K+, uric acid etc…
  • At least 24hrs of prehydration (ensuring good urine output. ~2-3L IV fluids/24hrs) +/- loop diuretic
  • IV rasburicase single dose (can also give for longer with once daily dose for 5-7 days)
66
Q

Discuss the management of TLS (not including preventative management)

A
  • IV fluids (for aggressive hydration) +/- loop diuretic
  • Allopurinol (xanthine oxidase inhibitor that prevents formation of uric acid) ** generally only used in prophylaxis; use Rasburicase if have TLS. Doesn’t do anything to existing uric acid
  • Rasburicase (synthetic uricase that degrades uric acid to allantoin which is water soluble and can be excreted)
  • Dialysis if above fails
  • Appropriate management of electrolyte abnormalities e.g. hyperkalaemia
67
Q

Discuss the prognosis of TLS

A
  • In most cases should be predictable and preventable
  • If TLS does occur, if prompt treatment is given it’s usually successful and usually resolves within 5-7 days
68
Q

Cancer patients are at increased risk of VTE; discuss whether cancer pts are prophylactically given anticoagulants

A

No as risk of bleeding still seen to outweigh risk of clot

Give if they have a clot for at least 6 months

69
Q

Discuss the management of VTE in cancer pts (excluding massive PE)

A

*Signs & symptoms would be same. Investigations also same (although don’t do d-dimer in cancer pt as it would be raised anyway)

VTE (excluding massive PE)

NICE guidance regarding VTEs changed in 2020; main change was use of DOACs. If the patient has active cancer

  • previously LMWH was recommended
  • the new guidelines now recommend using a DOAC (e.g. apixaban or rivaroxaban), unless this is contraindicated
  • Continue for 3-6 months?? CHECK

Massive PE

  • Thrombolysis using alteplase (give UFH prior to thrombolysis and stop within 24hrs of thrombolysis)
70
Q

How is high dose dexamethasone given?

A
  • PO if possible
  • High dose is 16mg (which is 8 2mg tablets); often have 8mg at breakfast (8:00am) then 8mg at lunchtime (12:00pm)
  • Want to give in morning as can cause sleep disturbance
71
Q

Why check TFTs (specifically TSH) if you have a pt presenting with SIADH?

A

Hypothyroidism can cause SIADH

Yr4: Cancer Care (19 decks)

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