Transcript Palliative care emergencies

Palliative care emergencies
Dr Claire Curtis
Consultant in Palliative Medicine
September 2010
Content
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Spinal cord compression
Hypercalcaemia
Bowel obstruction
Haemorrhage
Seizures
Spinal cord compression
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NICE guidelines
Early detection
At risk patients:
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Cancer and back pain – review frequently
for progressive symptoms
Known bone mets
High risk of bone mets
Give them information about possible
symptoms and what to do
Spinal cord compression: early
detection
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Symptoms suggestive of spinal mets:
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pain in the thoracic or cervical spine
progressive lumbar spinal pain
severe unremitting lumbar spinal pain
spinal pain aggravated by straining
localised spinal tenderness
nocturnal spinal pain preventing sleep.
Any of the above – contact oncologist
within 24 hours
Spinal cord compression: early
detection
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Neurological symptoms or signs
suggestive of cord compression
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radicular pain
limb weakness
difficulty walking
sensory loss
bladder or bowel dysfunction
signs of spinal cord or cauda equina compression.
Emergency – immediate discussion with
oncologists
Imaging
MRI
 Within 1 week if
symptoms suggestive
of spinal mets
 Within 24 hours
if SCC
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Treatment - SCC
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Nurse flat until spinal and neurological
stability known
Dexamethasone 16mg od immediately
Continue until surgery or start of RT
Then gradually reduce over 5-7 days
If neurological function deteriorates –
temporarily increase dose again
If not for surgery or RT – gradually
reduce dose,
Treatment
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Take into account:
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patient preferences
neurological ability
functional status
general health and fitness
previous treatments
Do not deny surgery or radiotherapy
on the basis of age alone.
Hypercalcaemia of malignancy
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Common (10%)
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Squamous cell (esp lung)
Breast
Prostate
Myeloma
Treatable
Untreated – distressing and fatal
Poor prognosis – 3-4 months
Hypercalcaemia of malignancy
Mechanisms:
 Humoral hypercalcaemia of malignancy:
release of factors acting on skeleton to
increase bone resorption and renal
conservation of calcium eg PTHrP
parathyroid hormone related protein.
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Osteolysis due to bone mets
Hypercalcaemia
General
Pain
Weakness
Dehydration
Polydypsia
Pruritus
Hypercalcaemia
General
Pain
Weakness
Dehydration
Polydypsia
Pruritus
CVS
Arrhythmias
Hypercalcaemia
General
Pain
Weakness
Dehydration
Polydypsia
Pruritus
CVS
Arrhythmias
Neurological
Fatigue
Lethargy
Confusion
Seizures
Psychosis
Hypercalcaemia
General
Pain
Weakness
Dehydration
Polydypsia
Pruritus
CVS
Arrhythmias
Neurological
Fatigue
Lethargy
Confusion
Seizures
Psychosis
GI
Anorexia
Nausea
Vomiting
Constipation
Ileus
Hypercalcaemia: treatment
Correct dehydration with N saline.
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Leads to a small reduction in calcium due to dilutional
effect and an improvement in symptoms.
Rate of admin depends on severity of
hypercalcaemia, degree of dehydration, ability of CV
system to tolerate volume expansion.
Clinical improvement over 24-48hours, but Ca rarely
normalises and other treatment is needed.
Hypercalcaemia: treatment
Bisphosphonates
 Potent inhibitors of bone resorption. Not
metabolised, renal clearance.
SE’s:
 Nephrotoxicity – precipitation of complexes in
the kidney
 Transient febrile reaction
 Osteonecrosis of the jaw - rare
Bisphosphonates
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Pamidronate
 2-4 hour infusion
 Variable dose often recommended (30-90mg)
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in practice most patients will need 90mg
Zoledronic acid
 More potent – more effective
 4mg over 15 min infusion – more convenient
Reduce dose if renal impairment
 Guidance in BNF
Bisphosphonates
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Delay of 24-48 hours before begin to
act
Max effect 6 days
Likely to recur in the future – need
monitoring
Bowel obstruction
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Establish diagnosis:
History
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Predisposition – abdominal malignancy/adhesions
Symptoms – acute or more chronic
Depends on level of obstruction
Consider:
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Constipation – bowel history, AXR, pr
motility disorder – exclude peritonitis, sepsis, SCC,
anti-peristaltic drugs
Symptoms
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High proximal obstruction
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Small bowel obstruction
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Severe, large volume vomits, quickly dehydrate,
sucussion splash?, often no pain and no distension
Vomiting and distension, usually hyperactive
bowel sounds with borborygmi, upper to central
abdominal colic
Large bowel obstruction
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Distension++, borborygmi, central to lower
abdominal colic, vomiting a late feature
Terms
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Complete obstruction
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Partial/subacute obstruction
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More chronic onset of symptoms – may gradually
worsen, be intermittent and obstructive episodes
may resolve spontaneously
Ileus/dysmotility
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May be acute, complete onset of symptoms
Absent/reduced bowel sounds
Faeculent vomiting
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Not faeces (unless gastro-colic fistula) – small
bowel contents colonised by colonic bacteria in
obstructions lasting >1 week
Bowel obstruction
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Surgery
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Possible of patient agrees and reasonable
medical and nutritional condition
Poor prognosis from surgery if
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Poor medical condition
Previous abdominal RT
Multiple blockages
Abdominal masses or diffuse peritoneal disease
Small bowel obstruction
Rapidly recurring ascites
Manage at home?
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Lady in 50s, recurrent ovarian cancer, intraabdominal disease, ascites. Previous admission to
WRH 2 months ago with small bowel obstruction, not
operable, resolved with medical management.
Symptoms recur. Discussion with her and family.
Decided not for admission.
84 year old man, IHD. Cancer of descending colon,
liver mets at diagnosis, Increasingly jaundiced and
frail. Symptoms of bowel obstruction. Discussed with
him and family, decided not for hospital admission,
managed at home.
Medical management
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All drugs via non-oral route – ensure
absorption
Encourage resolution
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Trial of prokinetic
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May resolve partial upper GI obstruction
Metoclopramide 80-160mg/24 hours
Dexamethasone
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May help resolve peri-tumour oedema and
open bowel
8mg sc daily – trial for 5 days
Bowel obstruction: nausea
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If obstruction not resolving, or colic
develops control symptoms
Nausea
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Cyclizine 150mg/24hrs
+/- haloperidol 2.5-5mg/24 hours
If persisting nausea replace with
levomepromazine 12.5-25mg/24hrs
Bowel obstruction: vomiting
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Vomiting
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May continue to vomit throughout,
particularly if continue oral intake
(although will absorb from proximal GI
tract)
If troublesome, frequent, large volume try
hyoscine butylbromide 80-160mg/24 hrs
(will also help if colic)
If persistent, add (or replace with)
octroetide 250-750mcg/24hrs
Bowel obstruction
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NG tube – may be helpful in patients
with high obstruction who continue to
vomit profusely despite medication
Outcome
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90% pain free
Small proportion will continue to vomit
once a day
Mean survival from first onset of
obstructive symptoms = 3.7 months but
may survive 12 months or more
Catastrophic haemorrhage
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Very rare
Death is pain free and often no time for fear
Distressing to watch – HC proff and relatives
PATIENTS POTENTIALLY AT RISK
INCLUDE:
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Head and neck cancer
Haematological malignancies
Any cancer around a major artery
Bone marrow failure where platelets < 15
Disseminated intravascular coagulation
Catastrophic haemorrhage
Think:
 Might this patient be at risk?
 Robust Multi Disciplinary Team (MDT)
assessment is recommended liaising closely
with the diagnostic team to assess risk.
 Stop any therapy predisposing to
haemorrhage eg aspirin, heparin or warfarin.
 If patient is assessed as HIGH RISK of
haemorrhage PLAN AHEAD.
Catastrophic haemorrhage
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Who needs to be informed
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Patient/family/primary care team/ OOH
provider/hospice/hospital
Agreed care plan across boundaries
Telephone numbers available for
emergency assistance
Plan for who will clean up afterwards
and how to get hold of them
Catastrophic haemorrhage
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Equipment Needed (as close as is
practical to the patient)
Dark sheets.
Dark towels (green, blue or multicoloured).
Gloves, aprons, wipes
Plastic sheet or inco pad.
Clinical waste disposal system
(including clinical waste bags).
Catastrophic haemorrhage
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Stay calm, encourage carer to stay calm
Priority is to stay with the patient and stem or
disguise the bleeding with dark towels
Crisis medication – in practice difficult to
achieve at home (rarely time to prepare an
injection or calmly measure a sublingual
dose)
If felt appropriate needs to be:
Rapid in onset (2-5 mins).
Kept close to the patient.
Catastrophic haemorrhage
Midazolam 10mg im (deltoid quicker than
gluteal)
 Buccal midazolam 10-15mg (depending on
source of bleeding)
 Opioid – no evidence to suggest pain, but
often given with midazolam – use 10mg im if
opioid naïve or 2 x usual breakthrough dose
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Debriefing – all staff involved
Support carers/relatives
Seizure
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Uncommon even in advanced malignancy and
known cerebral mets
Risk higher if:
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Recent decrease/cessation of steroid
Signs of increased ICP
Myoclonus or other twitching present
History of poor control or recent seizures
Previously needing >1 anticonvulsant to control
seizure
Tonic-clonic usually resolve < 1min
Major Seizure (tonic-clonic
type)
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Put the patient into the standard recovery position.
If the seizure does not resolve spontaneously after
1min, give:
diazepam 5-10mg PR, or midazolam 5-10mg im or
2.5-5mg buccally.
If the seizure is persisting, may need to repeat
above
Unless in terminal phase, if persisting, will need iv
treatment with benzodiazepine and appropriate
monitoring.
Review the anticonvulsant medication.
Seizure in terminal phase
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Unable to manage oral anti-convulsants
Half life of oral anticonvulsants >24 hrs so
parenteral treatment can be started any time
within 24hrs after last dose
Syringe driver – midazolam usual dose 3060mg/24 hrs
If seizures despite increased dose of
midazolam – consider second syringe driver
with phenobarbital 200-400mg /24 hrs
Summary
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Spinal cord compression
Hypercalcaemia
Bowel obstruction
Haemorrhage
Seizures