Palliative Care Flashcards

1
Q

What is breathlessness?

A

-A subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity’
-The experience of dyspnoea derives from interactions among multiple physiological, psychological, social and environmental factors, and may induce secondary physiological and behavioural responses’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the breathing thinking functioning model

A

-Breathing
=Inefficient breathing, increased work of breathing
=Increased respiratory rate, use of accessory muscles, dynamic hyperinflation

-Thinking
=Thoughts about dying, misconceptions, attention to the sensation, memories, past experiences
=Anxiety, distress, feelings of panic

-Functioning
=Deconditioning of limb, chest wall and accessory muscles
=Reduced activity, tendency to self-isolate, more help from others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Assessment of breathlessness

A

/

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Non-pharmacological management of breathlessness

A

-Breathing:
=Recovery breathing, Square breathing
=Fan
=Positioning
-Thinking:
=Relaxation, distraction
-Functioning
=Pacing

-Setting expectations – management rather than cure
-Self management plan
-Sources of support – local palliative care team, helpful information for patients (Marie Curie, Macmillan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pharmacological management of breathlessness

A

-Disease modifying treatments – where appropriate
-Opioids
-Steroids
-Oxygen
-Benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe cough in palliative care

A

-Impact on QoL – sleep, continence, social functioning, anxiety &depression
-May be under-reported in presence of other symptoms
-Holistic assessment and management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of cough unrelated to cancer

A

-Neuromuscular disease
-HF
-Respiratory failure
-Renal failure
-Asthma
-COPD
-GORD
-ACEi
-Autoimmune disease
-Infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of cough directly related to cancer

A

-Pulmonary parenchymal disease
-Lymphangitis
-Pleural effusion
-Superior vena cava obstruction
-Tumour microemboli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of cough indirectly related to cancer

A

-Immunotherapy induced pneumonitis
-Aspiration
-PE
-Paraneoplastic syndrome
-Radiotherapy sequelae
-Chemotherapy-induced fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Management of cough

A

-Non-pharmacological
=Simple advice for dry cough, smoking cessation, improved ventilation
=Special Mechanical aids for neuromuscular disease (cough assist machine)

-Pharmacological – evidence is poor
=DRY COUGH - Antitussive therapy for dry cough – simple linctus, morphine 2mg PRN 4-6 hourly in opioid naïve. methadone linctus (specialist advice only)
=WET COUGH - Protussive therapy to aid expectoration of wet cough –saline nebs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe respiratory secretions at End of Life, and causes

A

-Retained respiratory secretions can develop towards EoL
-Onset generally occurs 60-70 hours before death
-How common - Noted in 23-92% of dying patients in PCUs
-Potential risk factors – artificial hydration, cerebral malignancies, lung pathology, Neuromuscular disorders
-Causes
=Inability to cough or swallow
=Partial airway obstruction
=Further production of respiratory secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Assessment of respiratory secretions at EoL

A

-Carefully consider likely prognosis
-Are there signs of global deterioration – reduced consciousness, reduced mobility, reduced oral intake?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Management of respiratory secretions at EoL

A

-Careful explanation to family – very important, likely not troubled by secretions
-Non-pharmacological
=Positioning
=Suctioning
=Consider stopping parenteral fluids: avoid fluid overload, stop IV or subcutaneous fluids
-Pharmacological
=1st line: Hyoscine Butylbromide s/c 20mg hourly (max120mg/24hours)PRN
=2nd line: Glycopyrronium s/c 200micrograms, 6-8 hourly PRN
=Opioids and midazolam for associated respiratory distress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why is N&V important in cancer patients?

A

-Prevalence …. in cancer patients
=Up to 68% of cancer patients suffer from nausea/vomiting
=80% of those receiving cancer chemotherapy

-Prevalence … in other advanced disease
=17-48% patients with heart failure had nausea
=33% patients with end stage renal failure had nausea/vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Complications of N&V

A

-Dehydration
-Electrolyte imbalance
-Hypoglycaemia
-Malnutrition
-Aspiration risk
-Mallory Weiss tears
-Anticipatory and refractory N/V
-Depression
-Poor symptom control
-Poor quality of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does N&V occur?

A

-Vomiting centre

-Emotions, fear, pain, memory
-Vestibular and raised ICP
-Chemoreceptor trigger zone outside BBB: drugs, metabolic, toxins
-GI tract/ viscera (vagus nerve): gastric paresis, visceral stretch, bowel obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Assessment of N&V

A

-History
=Pattern recognition – emesis pathways
-Consider nausea and vomiting separately
-Explore timing, appearance, what’s helped
-Consequences
=Dehydration
=pain relief
=diabetic Rx
=Meds eg cardiac, anti-epileptics
-Reversible factors
=Medication, Infection, Biochemical
-Contributing factors
=Constipation, Anxiety, Pain
-Examination
=Obs, fluid status
-Investigations (as appropriate)
=Blood tests incl FBC, U&E, LFTs, Ca, Mg
=Imaging
=Microbiology-stool, MSU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of N&V

A

-Vestibular
-Obstruction
-Motility
-Infection
-Toxins
-Stress

-Reduced gastric motility
=May be opioid related
=Related to serotonin (5HT4) and dopamine (D2) receptors

-Chemically mediated
=Secondary to hypercalcaemia, opioids, or chemotherapy

-Visceral/serosal
=Due to constipation
=Oral candidiasis

-Raised intra-cranial pressure
=Usually in context of cerebral metastases

-Vestibular
=Related to activation of acetylcholine and histamine (H1) receptors
=Most frequently in palliative care is opioid related
=Can be motion related, or due to base of skull tumours

-Cortical
=May be due to anxiety, pain, fear and/or anticipatory nausea
=Related to GABA and histamine (H1) receptors in the cerebral cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Approach to reduced gastric motility

A

-Pro-kinetic agents are useful in these scenarios as the nausea and vomiting is usually resulting from gastric dysmotility and stasis
-According to NICE CKS and BMJ best practice, first-line medications include metoclopramide and domperidone
-However, NICE CKS indicate that metoclopramide should not be used when pro-kinesis may negatively affect the gastrointestinal tract, particularly in complete bowel obstruction, gastrointestinal perforation, or immediately following gastric surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Approach to chemically mediated N&V

A

-If possible, the chemical disturbance should be corrected first
-In the context of other chemically mediated syndromes, for example due to opioid medications, there are a number of suggested medications
-Key treatment options include ondansetron, haloperidol and levomepromazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Approach to visceral/ serosal causes

A

-Cyclizine and levomepromazine are first-line
-Anti-cholinergics such as hyoscine can be useful

22
Q

Approach to raised intra-cranial pressure

A

-The NICE CKS guidelines recommend using cyclizine for nausea and vomiting due to intracranial disease
-Dexamethasone can also be used
-Radiotherapy can be considered if there is likely raised intra-cranial pressure due to cranial tumours

23
Q

Approach to vestibular N&V

A

-NICE CKS and BMJ best practice recommends use of cyclizine as a first-line treatment in disorders due to the vestibular system
-Refractory vestibular causes of nausea and vomiting can be treated alternatively with metoclopramide or prochlorperazine
-Atypical antipsychotics such as olanzapine or risperidone can be used in refractory cases according to UptoDate

24
Q

Approach to cortical N&V

A

-If anticipatory nausea is the clear cause, a short acting benzodiazepine such as lorazepam can be useful
-If benzodiazepines are not ideal, BMJ best practice recommends use of cyclizine
-Ondansetron and metoclopramide can also be trialled

25
Q

Approach to management of N&V

A

-Treat reversible causes
-Non-pharmacological strategies
=Oral care
=Small portions
=Avoid food prep
=Environment
=Acupuncture
-Anti-emetic

26
Q

Overview of metoclopramide

A

-Pro-kinetic class
-SE
=Colic, oesophageal spasm, EPSE’s (extra-pyramidal side-effects)

10mg oral TDS or 30mg-80mg over 24h via syringe driver (CSCI)

27
Q

Overview of Domperidone

A

-Pro-kinetic
-SE
=Colic, oesophageal spasm, EPSE’s (rare)

10mg oral TDS

28
Q

Overview of Cyclizine

A

-Anti-histamine, anti-cholinergic
-SE: sedation, dry mouth, blurred vision, constipation

50mg oral TDS or 150mg over 24h via CSCI

29
Q

Overview of Haloperidol

A

-Anti-psychotic (strong D2 antagonist)
-ESPE SE

Oral 0.5mg-1mg s/cut or oral BD (starting doses)

30
Q

Overview of Levomepromazine

A

-Anti-psychotic (broad-spectrum)
-SE: ESPE’s sedation, hypotension

2.5mg-5mg s/c BD

31
Q

Overview of Ondansetron

A

-5HT3 antagonist
-SE: constipation, dizziness, headache

32
Q

Overview of Prochlorperazine

A

-Anti-psychotic
-ESPEs, sedation

3mg BD buccal or 5-10mg oral TDS

33
Q

Management of N&V when caused by higher neurological centres (raised intracranial pressure due to cancer)

A

-Clinical picture
=Worse in the morning
=Headache
=Neurology

-Treatment
=Cyclizine
=?? Trial Dexamethasone 8mg to reduce oedema
=Second line Levomepromazine, Prochlorperazine

34
Q

Management of N&V when caused by vestibular dysfunction (movement related nausea)

A

-Clinical picture
=Vertigo – dizziness with nausea
=Movement related nausea

-Treatment
=Cyclizine
=Cinnarizine
=Prochlorperazine

35
Q

Chemical/ metabolic causes of N&V

A

-Causes:
=Drugs
=Extensive cancer
=Sepsis
=Renal/liver failure
=Biochemical causes
=Chemotherapy/radiotherapy induced

-Clinical history: persistent often severe vomiting, little relief from vomiting

-Causes: chemical stimulation via CTZ

-Treatment
=Treat metabolic imbalance / Address cause
=Metoclopramide or domperidone OR
=Haloperidol OR
=levomepromazine s/c
=For cytotoxic/chemo related – check local policy

36
Q

Describe N&V caused by motility disorder

A

-Clinical history
=Intermittent vomits.
=Nausea often relieved by vomiting
=Early satiety, reflux, hiccups
=Often little nausea until immed prior to vomit

-Causes
=Gastric stasis
=Gastric outlet obstruction - pseudo obstruction - intestinal
By
=Autonomic neuropathy (paraneoplastic)
=Drugs
=Mechanical obstruction, tumour, nodes, enlarged liver leading to squashed stomach
=Metabolic (hypercalcaemia)

37
Q

Treatment of motility disorder

A

-Metoclopramide
-Domperidone (if elderly/higher risk of EPSEs)
-Consider trial of dex if external compression (trial 3/7, aim to reduce/stop)
+/- stent if appropriate

NB prokinetics may cause oesopheal spasm

38
Q

Treatment of multifactorial/ unknown/ refractory

A

-Consider route
-Metoclopramide
-Levomepromazine
-Trial of dexamethasone
-Consider higher centres eg pain, anxiety – offer psychological input/medication

39
Q

Describe bowel obstruction history/ exam

A

Due to mechanical obstruction (partial/ complete) and/or peristalsis failure

-Constipation / faecal incontinence
-Complete bowel obstruction – no flatus PR
-Intermittent nausea , often relieved by vomiting
-Worsening nausea / faeculent vomiting as obstruction progresses(small bowel contents become colonised by colonic bacteria)
-Continuous pain / colic
-Altered bowels sounds
-Abdo distension

40
Q

Management of bowel obstruction

A

-Multidisciplinary approach (surgical, oncological, palliative care)
-Assess on clinical condition, likely benefits/risks, patient preference
-Exclude faecal impaction (can complicate/mimic BO)
-Consider surgery if localised obstruction
-Other interventional palliative treatments:
=Stenting (gastric outlet, proximal small bowel, colon) or laser Rx
=Venting gastrostomy (Gastro-duodenal or jejunal obstrn)

-Medical management
=Frequent mouth care
=In acute phase (2-3 days) – conservative management may be appropriate (rest bowel, NBM +/- NG tube)
=Low fibre diet,
=Consider additional hydration
=Exclude / treat constipation
=Most will need SC infusion of medication

-Peristalsis failure
=N&V: prokinetic metoclopramide (stop if colic)
=Pain: opioid

-Mechanical obstruction
=Nausea: Cyclizine or buscopan +/ Haloperidol, or levomep
-Dexamethasone: 8mg subcut 4-7 days may relieve partial obstruction, reduce gut wall oedema
=Pain: opioid
=Colic: Buscopan
=Vomiting: Buscopan or Octreotide (reduces volume of vomit)

41
Q

Pain assessment

A

-If the pain is severe and overwhelming immediate treatment may be required before further assessment (adjust dose according to current analgesic use and seek specialist advice)
-Breakthrough and incident pain: a transient exacerbation of pain which occurs either spontaneously (breakthrough) or in relation to a trigger (incident pain) in someone who has mainly stable or adequately relieved background pain

-History
-Structured pain assessment tool, pain intensity scores
-Examination: tender hepatomegaly, abnormal sensation
-Impact of pain on: function, sleep, mood, patient, family
-Consider reversible causes

42
Q

Causes of pain in palliative care

A

-Disease related - direct invasion by cancer, distension of an organ, pressure on surrounding structures:
=bone pain: worse on pressure or stressing bone or weight bearing
=nerve pain: burning, shooting, tingling, jagging, altered sensation, dermatomal distribution - consider spinal cord compression
=liver pain: hepatomegaly, right upper quadrant tenderness, referred pain shoulder tip
=raised intracranial pressure: headache, nausea or both, often worse in the morning or with lying down
=colic: intermittent cramping pain. Consider bowel obstruction, bladder spasm. Consider adjuvant therapies (refer to Pain management guideline).
-Treatment-related pain: chemotherapy neuropathy, constipation due to opioids, radiation-induced mucositis.
-Debility: pressure sores, severe cachexia, oral candidiasis.
-Other unrelated illnesses: arthritis, osteoporosis, vascular disease, gastritis

43
Q

Palliative pain management steps

A

-Agree a pain management plan, including goals of treatment, in conjunction with the patient and family.
-Agree arrangements for regular review

  1. Mild intensity:
    =Paracetamol 1g x4 a day
    =NSAID
    =+/- Other adjuvant
  2. Mild to moderate
    =Weak opioid (codeine 30mg to 60mg x4 daily or dihydrocodeine 30mg to 60mg x4)
    =Alternatively: combined paracetamol codeine prep like co-codamol 30/500, 2 tablets x4 daily
    =Laxative and consider anti-emetic
  3. Mod to severe
    =Strong opioid: If titrating with immediate release oral morphine prescribe 5mg, 4 hourly and as required for breakthrough pain/ If starting with modified release oral morphine prescribe 10mg to 15mg,
    12 hourly and immediate release morphine 5mg as required for breakthrough pain
    =Stop any step 2 opioid (Codeine or dihydrocodeine 60mg 4 times daily≈24mg oral morphine in 24 hours)
    =Seek advice if severe pain not responding to treatment (unacceptable side effects or toxicity)
    =Use lower doses and increase dose more slowly if patient is frail, elderly or has renal impairment. In severe renal impairment, an alternative opioid may be needed
44
Q

Caution with paracetamol

A

Consider reducing paracetamol dose to 500mg four times daily when poor nutritional status, low body weight (<50kg), hepatic impairment and/or chronic alcohol abuse (check local policy for paracetamol and NSAIDs if patient receiving chemotherapy)

45
Q

Dose titration for step 3

A

-Increase regular oral morphine dose each day in steps of about 30% (or according to breakthrough doses used) until pain is controlled or side effects develop.
-Increase laxative dose as needed.
-Convert to modified release morphine when stable.
=Divide 24 hour dose of immediate release morphine by 2.
=Prescribe as modified release morphine, 12 hourly.
=Prescribe breakthrough analgesia at correct dose (1/6th to 1/10th of 24 hour morphine dose up to a maximum of 6 doses in 24 hours)

46
Q

Starting pain treatment

A

-when starting treatment, offer patients with advanced and progressive disease regular oral modified-release (MR) or oral immediate-release morphine (depending on patient preference), with oral immediate-release morphine for breakthrough pain
-if no comorbidities use 20-30mg of MR a day with 5mg morphine for breakthrough pain. For example, 15mg modified-release morphine tablets twice a day with 5mg of -oral morphine solution as required
-oral modified-release morphine should be used in preference to transdermal patches
-laxatives should be prescribed for all patients initiating strong opioids
-patients should be advised that nausea is often transient. If it persists then an antiemetic should be offered
-drowsiness is usually transient - if it does not settle then adjustment of the dose should be considered

47
Q

Types of anti-emetics and laxatives

A

-QT Metoclopramide 10mg up to three times a day
-QT Haloperidol 500 micrograms to 1.5mg daily (prescribe as required for 5-10 days)

-Senna 2 tablets at night or Bisacodyl 5mg to 10mg at night plus docusate 100mg twice daily
-Macrogol 1 to 3 sachets per day

48
Q

Advice for Subcutaneous analgesia

A

-Usually given via a CME T34 syringe pump over 24 hours.
-Calculate the 24 hour dose of oral morphine.
-Convert this to SC morphine.
-Oral morphine 30mg≈SC morphine 15mg.
-When large doses of breakthrough SC analgesia are required consider SC diamorphine.
-Prescribe 1/6th to 1/10th of the 24 hour SC opioid dose as required, via SC route for breakthrough pain

49
Q

Advice for breakthrough pain

A

-Defined as a transient exacerbation of pain which occurs either spontaneously or in relation to a specific trigger (incident pain) in someone who has mainly stable or adequately relieved background pain.

-Prescribe immediate release morphine at 1/6th to 1/10th of the regular 24 hour dose, as required up to a maximum of 6 doses in 24 hours. If 3 or more doses have been given within 4 hours with little or no benefit seek urgent advice or review. If more than 6 doses are required in 24 hours seek advice or review.
-Assess 30 to 60 minutes after a breakthrough dose.
-If pain persists give a second dose as required.
-If pain is still not controlled seek advice.
-Change breakthrough dose if regular dose altered

50
Q

Management or incident related predictable pain

A

Can be difficult to manage; a dose of short-acting opioid before moving or when pain occurs may help. If pain is short-lived and the patient develops excessive drowsiness seek specialist advice

51
Q

Advice for opioid toxicity

A

-Can be precipitated by several factors including rapid dose escalation, renal impairment, sepsis, electrolyte abnormalities, drug interactions.
-Wide variation in the dose of opioid can cause symptoms of toxicity.
-Prompt recognition and treatment are needed. Symptoms include:
=persistent sedation (exclude other causes)
=vivid dreams, hallucinations, shadows at the edge of visual field
=delirium
=muscle twitching/myoclonus/jerking
=abnormal skin sensitivity to touch.
-If the pain is controlled reduce the opioid dose by a third. Ensure the patient is well hydrated. Seek advice.
-If patient still in pain consider reducing opioid dose by a third. Consider adjuvant analgesics, alternative opioids or both (refer to Choosing and changing opioids guideline). Seek advice.
-Naloxone (in small titrated doses) is only needed for life-threatening respiratory depression (refer to Naloxone guideline).

52
Q

Adjuvant therapies for pain management

A

-NSAID: for bone pain, liver pain, soft tissue infiltration, or inflammatory pain (side effects: gastrointestinal ulceration or bleeding [consider proton pump inhibitor (PPI)], renal impairment, fluid retention, adverse cardiac events).
-Other analgesics: Nefopam is a non-opioid, non-NSAID analgesic occasionally preferred where alternatives are contraindicated or ineffective, or used as add-on therapy when pain is inadequately controlled. There is limited evidence regarding dose conversions. Seek specialist advice if considering prescribing.
-Antidepressant or anticonvulsant: for nerve pain. Start at low dose: titrate slowly (refer to Neuropathic pain guideline). No clear difference in efficacy between the two types of medicine for this indication.
=amitriptyline (side effects: confusion, hypotension caution in cardiovascular disease).
=gabapentin (side effects: sedation, tremor, confusion; reduce dose if renal impairment).
=amitriptyline (side effects: confusion, hypotension caution in cardiovascular disease).
=gabapentin (side effects: sedation, tremor, confusion; reduce dose if renal impairment).

-Corticosteroids: †dexamethasone
=8mg to 16mg daily for raised intracranial pressure.
=4mg to 8mg daily for neuropathic pain; 4mg to 8mg daily for liver capsule pain.
=Give in the morning; reduce to lowest effective dose. Consider PPI. Monitor blood glucose.
=8mg to 16mg daily for raised intracranial pressure.
=4mg to 8mg daily for neuropathic pain; 4mg to 8mg daily for liver capsule pain.
=Give in the morning; reduce to lowest effective dose. Consider PPI. Monitor blood glucose.

-TENS, nerve block, radiotherapy, surgery, bisphosphonates, ketamine (specialist use) and skeletal or smooth muscle relaxants