Download Clinical Emergencies In Palliative Care The usual time frame of

Clinical Emergencies In Palliative Care
The usual time frame of hospice and palliative care interventions are modulated by the
need for calmness and patient comfort. There are however several emergency
situations which can occur requiring urgent and prompt diagnosis and management.
This may create some dissonance among others who may feel that the patient
should be left in peace. It is vital that all staff appreciate the nature of these
emergencies and the importance of the need, on occasion, to make urgent
decisions.
It is important to have a clear understanding of the management of clinical emergencies in
palliative care. Clear thinking is crucial in handling an emergency and a sense of calm authority
can provide a source of decisiveness to patient and family and can transform a crisis situation.
All health care professionals involved with the care of patients with palliative care needs must
have awareness of the few emergency situations which require a prompt response.
SEPSIS IN THE NEUTROPENIC PATIENT
As more and more patients undergo chemotherapy and radiotherapy from home, we all need to
be aware of the risks of lowered immune response, typically in the second week after
chemotherapy. Manifestation of sepsis in a neutropenic patient who is undergoing
oncological treatment can be minimal, and there should be a high index of suspicion.
The routine signs of infection, a raised temperature, a fast pulse, sweating etc. may be
absent, especially if the patient is taking corticosteroids. Without such vigilance, patients may
deteriorate over a few hours and become septicaemic which, for a significant proportion, will be
fatal.
Management
Awareness of the seriousness of this risk for patients who have recently undergone
oncological treatments
Prompt checking of a white cell count (specifically neutrophil count) to confirm the
risk
Admission to a unit where intravenous antibiotics can be given and appropriate
monitoring carried out
Empirical treatment of an ill neutropenic patient while blood culture results are
awaited
Treatment options should be discussed with the local bacteriologist, as antibiotic
regimes will vary across regions/ countries, and should include antibacterial,
fungal and viral consideration.
MALIGNANT SPINAL CORD COMPRESSION.
Spinal cord compression (SCC) occurs in 3-5% of patients with cancer. 10% of patients
with spinal metastases develop spinal cord compression (Kaye 1999), the frequency
being highest in multiple myeloma and cancers of the prostate, breast and bronchus.
Those looking after such patients should always be vigilant in checking for early
symptoms and signs of spinal cord compression.
The keys to diagnosing Spinal Cord Compression include:
Having a high index of suspicion in patients with spinal metastases
particularly in patients with multiple myeloma, breast, lung and prostate
cancer
Taking complaints seriously e.g. back pain, difficulty in walking and in passing urine
It is important for all health professionals to have a high index of suspicion for
possible spinal cord compression because of the catastrophic consequences of a
delay in diagnosis.
Symptoms and Signs of Spinal Cord Compression
Back pain 90%
Weak legs
Increased reflexes
Sensory level
Urinary hesitancy or retention
Back pain, a sensation of weakness in the legs and often vague sensory symptoms may be
early manifestations
For those presenting with profound weakness, a sensory 'level' and sphincter disturbance,
which are relatively late features, the outcome is poor and the compression is much less likely
to be reversible.
The site of compression is
thoracic 70%
lumbosacral 20%
cervical 10%
80% of cases are caused by extradural deposits due to direct extension from the vertebral body
into the a epidural space.Lesions above L1 (lower end of spinal cord) will
produce upper motor neurone signs and often a sensory level whereas lesions below L1
will produce lower motor neurone signs and peri-anal numbness (cauda equina syndrome).
Management
Spinal cord compression is an EMERGENCY and two questions need to be answered
urgently:
1. Does this patient have a reasonable likelihood of having spinal cord
compression?
Even the most skilled clinician is unable to diagnose early spinal cord compression with
absolute certainty. Often by the time clinical signs are “classical” it is “too late”. Once the
compression has fully developed treatment outcome is very poor. Thus if intervention to
prevent paraplegia is to be meaningful, spinal cord compression needs to be diagnosed
early.
2. Would this patient benefit from instituting emergency investigation and
treatment?
Once the possibility of spinal cord compression has been raised, the patient may now be
committed to a course of management that will include urgent transfer to a specialised
unit where an MRI scan can be carried out and definitive treatment given. This is likely to
be radiotherapy but may be surgery or chemotherapy.
Key Questions in deciding on emergency investigations and management.
Does the patient who is reluctant for further treatment understand why
emergency management is being advised?
Is the patient still walking?
Is the patient suffering from severe back pain?
Has the patient already established cord compression?
Deciding whether this course of treatment is appropriate for a particular patient involves
an overall assessment.
Where suspicion of Spinal Cord Compression is high, it is quickest to involve the
oncological team who has been managing the patient, who will be able to co-ordinate
the necessary scan and appropriate treatment rapidly.
If the patient is still walking, emergency treatment gives a 1 in 3 chance of regaining leg
strength and treatment should be started immediately with dexamethasone 8-16mg
daily orally while arrangements are made for urgent transfer to an oncology centre.
Prognosis
Overall, 30% of patients may survive for one year. Function will be retained in 70% of
patients who were ambulant prior to treatment but will return in only 5% of those who
were paraplegic at the outset. Return of motor function is better in those with an
incomplete block and particularly with partial lesions of the cauda equina. Loss of
sphincter function is a bad prognostic sign.
In practice, most patients with an established diagnosis are relatively unwell and have
multiple metastases, and will be referred for radiotherapy.
Care of patients with malignant spinal cord compression
Such patients provide great challenges to the MDT. These challenges include:
Therapeutic interventions:
The patient in cord compression is invariably left with either a paraparesis or paraplegia
from the point of the infiltrated cord downwards. Either of these symptoms can
significantly impact on functional performance and hence affect the patient’s quality of
life. Therapy input is vital to assess the patient’s potential for rehabilitation and enable
the patient to maintain a measure of independence. There can be overlap of roles within
the therapy team and co-ordination of care is essential.
Physiotherapy interventions:
These should take place as soon as the cord compression has been diagnosed.
During the treatment phase, treatments include:
Chest physiotherapy
Passive movements
Positioning
Static quads (if able)
Post treatment, assessment will include:
Muscle power testing
Testing of sitting balance, sit to stand and transfer capabilities
Assessment of mobility
Treatment will depend on the findings of the assessment and the degree of disability but
will mainly focus on:
Maintenance of joint range and muscle power by passive and active exercises
Stimulation of sitting and standing balance
Re-education of gait and adaptation of transfers
Provision of walking aids
Occupational Therapy interventions:
Assessment is comprehensive and focuses primarily on the following areas:
functional mobility
transfers
personal hygiene
toileting
posture, seating and pressure care
home management and environmental set up
Treatment may involve:
Exploration of options with the patient and family for returning to live at home which
may include an access visit
Graded activity to facilitate independent participation in valued tasks
The teaching of alternative techniques for mobility, transfers, personal care and
continence
Timely provision of adaptive equipment such as sliding boards, standing or mobile
hoists, commodes and wheelchairs
Advice on environmental changes to facilitate independence e.g. use of portable
ramping, stair lifts etc
Education of relatives and carers on handling issues and the use of equipment
Skin care in a patient confined to bed
Bowel interventions
Urinary system management
Psychosocial support
SUPERIOR VENA CAVA OBSTRUCTION
Superior vena cava obstruction (SVCO) is due to compression or invasion of the SVC by
mediastinal lymph nodes or tumour in the region of the right main bronchus. It is caused
most commonly by carcinoma of the bronchus (75%) and lymphomas (15%). Cancers of
the breast, colon, oesophagus and testis account for the remaining 10%. Symptoms are
those of venous hypertension and include breathlessness (laryngeal oedema),
headache (cerebral oedema), visual changes, dizziness and swelling of the face, neck
and arms. Signs include engorged conjunctivae, peri-orbital oedema, non-pulsatile
dilated neck veins and dilated collateral veins (chest and arms). Without treatment,
SVCO can progress over several days leading to death. Prognosis is poor in a patient
presenting with advanced SVCO unless the primary tumour is responsive to
radiotherapy or chemotherapy.
Management For advanced, acute SVCO:
Sit patient upright and give 60% oxygen if safe to do so
Maintain calmness and consider oral anxiolytic or low dose midazolam to reduce
anxiety
Dexamethasone 8-16mg p.o. or i/v
Furosemide 40mg p.o. or i/v
Emergency radiotherapy (or chemotherapy for chemosensitive tumours such as
small cell carcinoma of bronchus, lymphoma or testicular cancer), can be given
with steroid cover. Survival may be prolonged for several months by treatment
but a recurrence may be more difficult to control. Intraluminal stents, inserted via
the femoral vein, can also be considered (and may be the treatment of choice) in
consultation with the local oncologist and radiologist.
HAEMORRHAGE
Haemorrhage may be directly related to the underlying tumour or caused by treatments
such as non-steroidal anti-inflammatory drugs which may result in gastric/duodenal
erosion. A generalised clotting deficiency, thrombocytopaenia, hepatic insufficiency or
anti-coagulation with warfarin, are contributory factors in patients with cancer. The need
for investigation will depend on the clinical situation
Treatments for NON-ACUTE haemorrhage include oncological, systemic and local
measures. Palliative radiotherapy is useful for superficial tumours and those of the
bronchus and genito-urinary tract. If radiotherapy is not appropriate, coagulation should
be enhanced with oral tranexamic acid 1g t.d.s., but caution is necessary with
haematuria since clots may form in the bladder resulting in further problems. The risks of
encouraging hypercoagulation need to be considered carefully in patients with a history
of a stroke or ischaemic heart disease. Local measures where appropriate such as
topical tranexamic acid or adrenalin (1:1000) soaks may be useful. Sucralfate may stop
stomach mucosal bleeding although it will inhibit the absorption of a proton pump inhibitor such
as lansoprazole.
Erosion of a major artery such as the carotid artery from locally invading tumour can
cause ACUTE haemorrhage which may be a rapidly terminal event. It may be possible
to anticipate such an occurrence and appropriate medication and a red blanket to reduce
the visual impact should be readily available. Relatives or others who witness such an
event will need a great deal of support. If the haemorrhage is not immediately fatal such
as with a large haematemesis or bleed from the rectum, vagina or superficially ulcerated
wound, the aim of treatment is local control if possible and sedation of a shocked,
frightened patient.
Remain with the patient. Midazolam 5-10 mg SC or buccally acts quickly.
Should the patient stabilise following a significant bleed the benefits or futility of
transfusion need to be considered carefully.
It may be appropriate to have emergency medication in the home to sedate the acutely
bleeding patient, but such a strategy can only be arrived at after discussion with the
family, carers, and the patient’s local GP, and needs to be documented clearly.
QUIET WARNING
The health care team need to balance the anxiety of alerting the family to the
possibility of an acute bleed, with the likelihood of such an event occurring and the
need for the family to be prepared.
If the patient chooses to be looked after at home the issues of managing acute
haemorrhage usually need to be discussed with the family and the home care team and
a clear plan worked out.
It is questionable however, how well prepared anybody can be for a massive
haemorrhage of a family member.
CONVULSIONS
Convulsions are usually associated with patients with primary or secondary brain
tumours and present with generalised (grand mal) or focal epilepsy.
Emergency management includes the correct positioning of the patient, if possible, and
the administration of diazepam rectally or sublingually or Midazolam buccally or
subcutaneously. Intravenous or subcutaneous midazolam or intramuscular
phenobarbital may be necessary. Relatives will need support since it is very frightening
to witness a convulsion. If seizures persistant consider commencing regular
anticonvulsant medication. When a dying patient is no longer able to take oral
anticonvulsants subcutaneous medication should be given to prevent further cerebral
irritability.
Useful drugs in syringe driver:
midazolam 20 - 100mg/24 CSCI
clonazepam 1 - 4 mg/24 CSCI
phenobarbital 200 - 600mg/24 CSCI
If a patient is already taking anticonvulsants regularly and needs continuous
subcutaneous medication, midazolam at the dose of 20-30mg/24h CSCI will probably be
needed.
Avoid using drugs that may increase cerebral irritability such as phenothiazines (e.g.
levomepromazine) if possible.
Cerebral Tumours
In a dying, unconscious or semiconscious patient, it should not be necessary to
replace oral steroids for raised intracranial pressure provided headache and
vomiting are adequately controlled and sedation is available. Usually by this stage
the cerebral oedema is not well controlled by steroids which at best may only serve
to prolong the dying period. As ever, decisions should be`made on an individual
basis and in discussion with the family.
HYPERCALCAEMIA
Hypercalcaemia occurs as a result of increased osteoclastic activity, which releases
calcium from bone, in addition to a decrease in excretion of urinary calcium. This is
attributed to locally active substances produced by bone metastases or by factors such
as ectopic parathyroid hormone related protein (PTHrP) or cytokines, and occurs in 10%
of the cancer population. The tumours most commonly associated with hypercalcaemia
include squamous cell carcinoma of the bronchus, carcinomas of the breast and
prostate, multiple myeloma and other squamous cell tumours. Patients do not have to
have bone metastases to develop hypercalcaemia.
Corrected calcium (mmol/L) = measured total Ca (mmol/L) + 0.02 x (40 serum albumin [g/L]), where 40 represents the average albumin level in g/L.
A corrected plasma calcium concentration above 2.6 mmol defines hypercalcaemia. It is
often mild and asymptomatic and significant symptoms usually only develop with levels
above 3.0 mmol. However patients differ and some will become symptomatic at lower
levels. Levels of 4.0 mmol and above will cause death in a few days if left untreated.
Eighty percent of patients with cancer-related hypercalcaemia survive less than one
year. Symptoms include drowsiness, confusion, nausea and vomiting, thirst, polyuria,
weakness and constipation.
Management
Treatment is only necessary if there are symptoms, or a high likelihood of symptoms
developing, and may be unnecessary if the patient is very near to death. Symptoms
associated with hypercalcaemia which are experienced by the patient should be
assessed and managed appropriately.

Fluid Replacement
Intravenous hydration is the mainstay of acute therapy for severe or symptomatic
hypercalcaemia (Bower & Cox 2004).
Bisphosphonates
Bisphosphonates inhibit osteoclast activity and thereby inhibit bone resorption. Because
of poor alimentary absorption, they are usually given intravenously initially. Disodium
pamidronate or zoledronic acid are effective in 70-80% of patients for an average of two
to three weeks.
GIVE:
- e.g. disodium pamidronate 60-90mg in sodium chloride 0.9%, 500ml over 2-4 hrs
- zoledronic acid 4mg in 100ml over 15 minutes to 1 hour
- Sodium clodronate has been used SC but is not as efficient as i/v.
Doses may need to be reduced in the presence of moderate and severe renal failure.
Plasma calcium levels should start to fall after 48 hours and fall progressively for up to 6
days. Oral ibandronate or sodium clodronate have been reported to delay the recurrence
of hypercalcaemia and may be important for maintenance, although due to dietary
restrictions are not always well tolerated.
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Kaye P (1999) Decision Making in Palliative Care. Northampton: EPL Publications:p183
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