Palliative care (from Latin palliare, to cloak) is a specialized area of healthcare that focuses on relieving and preventing the suffering of patients. Unlike hospice care, palliative medicine is appropriate for patients in all disease stages, including those undergoing treatment for curable illnesses and those living with chronic diseases, as well as patients who are nearing the end of life. Palliative medicine utilizes a multidisciplinary approach to patient care, relying on input from physicians, nurses, chaplains, social workers, psychologists, and other allied health professionals in formulating a plan of care to relieve suffering in all areas of a patient's life. This multidisciplinary approach allows the palliative care team to address physical, emotional, spiritual, and social concerns that arise with advanced illness.
Medications and treatments are said to have a palliative effect if they relieve symptoms without having a curative effect on the underlying disease or cause. This can include treating nausea related to chemotherapy or something as simple as morphine to treat a broken leg or aching related to an influenza (flu) infection.
Although we make everyday progress in cancer treatment, cancer remains a mortal disease for about half of the patients, depending of the location (from 0% for localized tumour to 100% for rapidly progressive uncontrolled tumours or metastatic tumours).
The history of palliative care for cancer patients is relatively old: during 18th century, Canon Jean-Baptiste Godinot founded in Reims an institute for 'cancerous' after many difficulties. His aim was to bring some dignity to patients, noticeably those with necrotic skin tumours, with strong odours.
In 1842, Jeanne Garnier, a young widow, creates in Lyons the 'Calvary Ladies', a lay congregation gathering lay widows who desire consecrate their life for untreatable patients. They install another house in Paris in 1874 (the future Jeanne Garnier medical house). With her, the word 'hospice' takes the meaning of a place to receive patients at the end of their life.
Most of these patients suffer from cancer.
A physician (or any caregiver) who will be in charge of cancer patient will have to provide palliative care. The continuous progress in palliative care, the more and more precise pain treatments are major progresses for the quality of life of our patient. For so many patients where nothing new happened for cure, we could write that palliative care is the only real progress for them.
The named medications are reflecting my experience (or absence of experience). Names are DCI. Other medications may be useful, and I will be grateful to everyone who helps me correct mistakes or lapses.
Continuous and palliative care :
Pain is more or less present on a permanent basis at a certain point in cancer progression, particularly during palliative care phases (in at least 70% of patients). The aim of this chapter is not to teach everything about pain but rather to define practical attitudes and reasoning. At least 90% of pain can be relieved.
Pain can be defined as an unpleasant personal sensorial and emotional experience associated with real, potential or feared tissue damage.
It is clear from this large definition that all pain, even if perfectly isolated and described, very rapidly involves affective, emotional, cognitive or behavioural components. Physical pain is most often completed by 'moral' pain or total pain.
Neural pathways in pain :
Prostaglandins sensitise receptors to many algogen compounds. Therefore, the use of anti-inflammatory drugs, aspirin or glucocorticosteroids has a positive effect.
There, many peptides are involved in pain transmission: substance P, vasoactive intestinal peptide (VIP), ocytocin, galanine, angiotensin 2, dynorphine, enkephalin.
The classical theory considers that all of these chemical molecules are a gate filtrating pain transmission towards the superior centres. Pain is transmitted:
either if it provokes stimulation that is too important to be inhibited at medullar level,or if the medullar filter is altered.
Thus two different types of pain are considered: nociception pain (too much stimuli) or deafferentation pain (no inhibition), with different therapeutic attitudes.
The presence of such a medullar filter allows local medullary treatment (peridural injection, intrathecal injection), particularly by morphine or its derivatives, in order to reduce the general dosing and diminish side effects.
The lateral thalamus discriminates sensitive information to precisely locate its origin.
The central thalamus has less systematised information responsible for motor reactions and the emotional components of pain.
From the thalamus, the pain information is transmitted to the ascending parietal area (precisely discriminating pain location) as well as towards the limbic system provoking emotional and behavioural reactions and towards the hypothalamus inducing neurovegetative and endocrine manifestations.
Treating pain requires precise knowledge on analgesic medications but, first and foremost, it requires listening to and examining the patient in order to precisely diagnose the origin of pain.
Pain evaluation should be the basis of treatment: it must be performed by both th physician and the patient. This evaluation should be performed:
at regular intervals,for each new painful episode,
after any analgesic action (half an hour after any IV analgesic treatment, one to two hours after oral treatment).
During cancer, some causes are most frequent:
chronic osseous pains from metastases,
osseous pain with mechanical outbursts: for which fracture or vertebral crushing should be feared,
pain through organ compression or nerve infiltration (sciatica, plexalgia),
headache from brain metastases,
digestive pain in relation to transit disturbance,
mucuous pain (mucitis, esophagitis, cystitis, rectitis).
During the palliative phase, cancer pain generally is chronic, persisting, progressively aggravating, disturbing the patient's liberty and sleep. Nocturnal pain is very typical of cancer.
When questioning the patient, the physician should consider:
the words the patient uses to describe pain ('it pinches', 'it burns', 'it twists', and so on)
factors influencing its arrival, its aggravation, its duration, its variation throughout the day,
precise pain location, asking the patient to trace pain on the body or a body diagram,
pain intensity (as evaluated by the patient but also in relation to induced perturbation of normal life),
sometimes, trying to guess when the patient can no longer easily express himself/herself.
The clinical examination should be careful and cautious since the patient is in pain:
pain due to excessive stimulation, generally related to extension of the tumour towards nearby structures with, most often, a precise, permanent topography with pain exacerbation attacks.
pain due to deafferentation, located on neural routes, by the deterioration of peripheral neurones, with fulgurating pains similar to electric shock, but also hypoesthesia or localised hyperesthesia, burning or stinging sensations (for instance post zoster pain, phantom limb pain),
psychogenic pain, with no systematisation but occurring in a major anxiety context,
simple verbal pain scale: no pain, mild pain, moderate pain, intense pain, intolerable pain,
analogic visual pain scale (marked from 1 - no pain to 10 intolerable pain) which necessitates patient cooperation.
pain questionnaires (Mc Gill Pain Questionnaire, QDSA: Questionnaire de Saint-Antoine) which also needs good patient cooperation and allows multifactorial analysis,
behavioural scales: observing the patient permits an evaluation of pain, in particular child pain (DEGR scale: douleur enfant de l'Institut Gustave Roussy) or in elderly patients (Doloplus scale),
precise study of analgesic consumption.
Cancer pain:
Pain during cancer may have three different causes:
Treatment principles :
Pain therapeutic scale :
The World Health Organisation (WHO) published, some time ago, pain scales in order to improve pain management with increasingly potent analgesics. Below, we have reproduced this scale with a few modifications made:
The main analgesic drugs are:
Two drugs are used:
Three drugs are used:
Neuropathic pain :
Neuropathic pain is pain related to the abnormal function of the peripheral or central nervous system which does not correctly control pain influx. Such pain can be very difficult to treat even with opioids.
We can distinguish:
It is characterised by acute transfixing attacks complicating a permanent dull pain. Furthermore local paresthesia can be observed.
Two examples:
neurapathy by inflammatory or toxic lesion of the small nerves of major neurological trunks (nervi nervorum),
or by the formation of a neuroma after axon section.
These neuroma are particularly sensitive to touch or chemical stimuli (such as norepinephrin).
autonomic dysregulation (cold or hot sensations, limb moistness, swelling, redness,..),
motor symptoms (stiffness, muscle weakness, abnormal movement),
trophic symptoms in bone (bone algodystrophy) or skin (reduced dermal thickness, dermoskeleton modification).
Dystrophic pain is most frequent after plexus radiation fibrosis (head and neck cancer with painful stiff shoulder) and constitutes a major therapeutic challenge.
Opioid treatment
Adjuvant medications
Many adjuvant drugs have been tried in order to prevent hyperalgic crises: their number and the diversity of their therapeutic classes demonstrate the difficulty in treating such acute pain phenomena:
Digestive tract disorders in palliative care :
For the patient, gastrointestinal problems are among the most frequent and cumbersome disorders during palliative care.
They can concern all segments of the digestive tract:
During palliative care, patients often suffer from their mouth. This is due to:
Poor hygiene often leads to a very foul-smelling breath or halitosis which may increase family uneasiness, speech difficulty and pain during meals associated with difficulty in swallowing.
Prevention of mucitis and the use of simple therapeutic methods are mandatory and should be repeated every day without provoking pain:
The use of Q-tips and compresses to humidify the oral cavity,
Soft tooth-brushing with a pleasant non-irritating tooth paste,
Frequent gargles (when feasible) with Coca-Cola or antifungal mouth rinsing solutions (many magistral preparations exist),
The use of morphinic mouth rinsing solutions when severe, painful mucitis prevents feeding,
Alcoholic solutions should be avoided, since they induce pain when mucitis or mouth ulcers occur.
Dysphagia :
Dysphagia can be defined as the difficulty in transferring the alimentary bolus (liquid or solid) from the mouth to the stomach.
In a palliative care unit (like St Christopher), dysphagia is observed in approximately 10% of patients (however, the unit also welcomes patients with lateral sclerosis for which dysphagia is an evolutive phase of the disease).
endobuccal preparation of the alimentary bolus (mastication, salivation),
oral swallowing phase, with closed lips and anterior tongue retraction pushing the bolus towards the oropharynx,
pharyngeal phase: partial occlusion of the nasal fossa, complete occlusion of larynx, stopped breathing,
esophageal phase: peristalsis pushes the bolus towards stomach.
Treatment of the tumour also provokes major swallowing side-effects:
surgery,radiotherapy: post-radiotherapy sclerosis, mouth dryness, candidiasis,
chemotherapy, not onlyvia chemotherapy alone, but also through the increased risk of candidiasis complicating dry irradiated mucosa,
other potential mouth infections: herpes zoster, cytomegalovirus.
mouth leakage (the patient slavers): lip sensation disorders, abnormal tongue movement, reduced swallowing reflex,
frequent nasal regurgitations poor palatal function (often after surgery or radiotherapy),
swallowing difficulty: the patients pushes his head backwards in order to swallow,
The following table summarises enteral and parenteral feeding indications:
Some simple advice may help a dysphagic patient to eat normally by mouth:
Dyspepsia :
Dyspepsia can be defined as a postprandial discomfort or upper abdominal pain. It can also be called indigestion (and in France 'mal au foie' - liver problem!). It is a common situation since 40% of the general population may be more or less concerned.
general epigastric discomfort, not always pain as such,
premature satiety (the patient states being hungry but stops eating after only a few bites),
postprandial heaviness, fullness, or bloating,
sensation of incomplete digestion (as if food stayed in the stomach for several hours),
epigastric acidity,
frequent and repeated belching, gulping, hiccups,
nausea, retching, vomiting.
Small stomach dyspepsia: the patient is hungry but rapidly repleted, he/she experiences epigastric fullness or heaviness soon after eating,
Borborygmus dyspepsia: postprandial bloating with frequent belching associated with dry air swallowing, increased by anxiety,
Reflux dyspepsia (gastro-oesophageal reflux): retrosternal burning when the patient bends over, when he/she eats more than usual or lies flat.
Gastric ulcerations or ulcer: precise localised pain wakening the patient at night, relieved by meal or antiacid medication,
Intestinal motility disorder dyspepsia: abdominal distension, premature satiety, gastric 'heaviness' or fullness, multiple alimentary intolerance, diffuse pain, frequent nausea with irritable bowel syndrome.
Cancer-related dyspepsia: gastric tumour, massive ascitis, paraneoplastic neuropathy
dyspepsia related to the poor general health state during cancer (candidiasis, reduced alimentation, anxiety),
treatment-related dyspepsia (abdominal surgery, radiotherapy especially in the abdomen volume, chemotherapy, morphine treatment, other medications),
associated pre-existing dyspeptic syndromes.
Not forgetting auto-medication by the patient at home, which is not always known by the physician (aspirin, gassy water).
A little simple dietary advice can help, such as a more varied diet.
Small stomach dyspepsia can be treated by smaller, more frequent meals.
Drug administration may be reduced (such as anti-inflammatory drugs) but not always stopped.
In the case of gastric acidity, antacid treatment may be prescribed, for example ranitidine, an H2-receptor antagonist avoiding proton pump inhibitors because of their prolonged effect on gastric parietal cells.
Gassy syndromes may be improved by defoaming antiflatulent agents such as simethicone derivatives.
Dyspepsia related to motility syndromes may be treated by prokinetic drugs such as metoclopramide, domperidone, cisapride.
Occlusion syndrome :
During palliative care, occlusion (or obstructive syndrome) generally announces disease progression and the fear of a fatal short-term evolution. It should be totally distinguished from a nascent neoplastic occlusion.
Around 5% of cancer patients suffer from end of life occlusion, mainly those with colon and ovarian carcinoma with a more or less diffuse peritoneal carcinomatosis.
At clinical examination, we can distinguish a ballooned abdomen (by dilatation upstream of the lesion) and a flat abdomen (if occlusion is high or total). Palpation also often reveals tumour masses.
Progression can be long: occlusion is often well tolerated over several days or weeks. However, the psychological consequences are important for patients who do not eat, do not pass stools and who permanently suffer from abdominal pain.
However, most often, occlusion is slow to progress, the abdomen is flat, peritoneal masses are found and, in the case of surgery, the surgeon would find himself/herself in an inextricable surgical situation.
An untimely intervention would only add post-surgical pain and the increased risk of numerous adhesions.
Pain (generally major spasms) should always be treated and small dosages of subcutaneous morphine are not contraindicated when pain is intense.
In colon cancer, an endoprothesis (generally a wired metal endoprothesis) may be installed by colonoscopy providing a more or less regular passage for faecal matter, but with relatively minor colic discomfort.
Sometimes, episodical vomiting in the absence of intestinal cramps is relatively well tolerated.
Terminal occlusion of peritoneal carcinomatosis is a very slow evolutive death process.
Nausea and vomiting:
Unfortunately, in palliative care, nausea may be more or less permanent, therefore very toilsome for the patient and often more unpleasant than vomiting itself.
Vomiting is the rejection of eaten matter: it may be beneficial (for instance after food poisoning). When vomiting is repeated, digestive spasms, muscle contractures and the usual accompanying vagal manifestations (bradycardia, hypersialorrhea) end in patient exhaustion. This phenomena is frequently observed during palliative care
the mouth and the pharynx region (olfactory, gustatory and tactile sensations),
the bronchial tree,
the vestibule (motion sickness),
the digestive tract (numerous receptors),
the meninges,
the brain itself (importance of psychology in triggering vomiting).
Several neurotransmitters are implied in triggering vomiting:
in the area postrema, dopamine and serotonin (5-hydroxy-tryptamin)
in the vomiting centre, histamine and acetylcholine.
gastrointestinal causes: infiltration or stenosis of the digestive tract, independently of the primitive tumour,
metabolic causes: renal insufficiency, hypercalcaemia, hepatic insufficiency,
treatment causes: vomiting induced by morphine, antibiotics, chemotherapy, radiotherapy,
intracranial hypertension: brain metastase, carcinomatous meningitis.
Care should be taken before diagnosing psychogenic vomiting (anxiety of death, repeated medication intake, fear of suffering), which should only acknowledged after the elimination of other causes.
oesogastric burning which might lead to Mallory-Weiss syndrome (oesophageal hemorrhage),
false passage with deglutition pneumopathies,
metabolic complications: dehydration, alcalosis, renal insufficiency,
impossibility of administrating oral medication (a major hindrance during palliative care),
diet problems: wasting, despair, necessity of parenteral hydration (SC or IV).
Firstly, the physician should eliminate a surgical indication, responsible radiotherapy or medication.
Sometimes, vomiting is not frequent and should be respected in order to avoid over-prescription. Vomiting due to morphine is generally transitory.
The main available drugs act either:
rectal examination: is the rectum empty or is there a fecaloma (potentially provoking pseudo-diarrhoea),
Respiratory disorders:
The main respiratory disorders observed during the palliative phase are:
Infectious pneumopathies require antibiotics that are well adapted to germs.
Effusions may be punctured (except in genuinely terminal phases).
Anaemia may be corrected by blood transfusion or erythropoietin injections.
Coughing:
Bronchial congestion :
Otherwise, treatment is the same as for coughing.
Superior vena cava syndrome :
Other frequently responsible cancers are: lymphoma, breast cancer, mediastinal geminal tumours, thymoma and various others.
Due to the anatomical configuration, superior vena cava syndrome is observed four times more frequently on the right.
Differential diagnoses are rare: idiopathic mediastinal fibrosis, histoplasmosis, venous thrombosis related to a catheter or surgery. In fact, all pathological processes which invade or destroy the lymph structures of the superior mediastinum may provoke an obstruction to the return of venous blood and thrombosis.
Its severity depends on:
The revealing patient complaint is dyspnea, coughing, headache and facial swelling. Then, neck, chest and upper limb swelling is observed. All of these symptoms are worsened when the patient bends forwards. Diagnosis is evident as soon as this is evoked.
In reality, the development of superior vena cava syndrome is rarely acute (most often neglected). Half of the patients reveal their cancer through this syndrome. Chest radiography and thoracic scan are the best imaging procedures before a diagnostic biopsy.
You can view a typical case of superior vena cava with thrombosis and important collateral circulation.
Other palliative measures are semi-seated position, rest, oxygen and short courses of corticosteroids.
A poor response to aetiological and palliative treatment suggests concurrent thrombosis which may require further anticoagulant treatment.
Unfortunately, most superior vena cava syndromes relapse since underlying cancer is not cured by treatment (lung cancer). The use of intravenous stents has been suggested in order to avoid acute complications.
Hemoptysis:
For instance, local treatment by pulmonary artery embolisation or by laser or by endobronchial brachytherapy or by external radiotherapy and if necessary and feasible a simple surgical intervention.
The most frequently concerned cancer is epidermoid lung cancer since it invades blood vessels and is highly necrotic.
Another frequent cause of hemoptysis is pulmonary aspergillosis which often occurs in immunodeprived patients (after prolonged chemotherapy).
More rarely, hemoptysis is related to therapy (laser, endobronchial brachytherapy).
Treatment includes very simple measures such as adopting a semi-seated position, oxygenation, aspiration, and a rapid search for the aetiology (bronchosopy if the patient’s status permits).
In terminal hemoptysis, patient anxiety should be relieved (subcutaneous morphine, midazolam), and a carer/family member should remain at the patient’s bedside until sleeping.
If no efficient aetiological treatment is possible (surgery for instance), various techniques have been proposed such as a Fogarty catheter, arterial embolisation, radiotherapy or laser beam.
Pleural effusion:
The causes are not always related to cancer:
If pleural effusion is massive, the first evacuation should generally be limited to approximately one litre in order to prevent a feared 'a vacuo' pulmonary oedema.
Even during the preterminal phase, an evacuating puncture may offer genuine relief to the patient.
In these cases, talc pleurodesis may be performed:
This therapeutic procedure is well tolerated, and is generally not painful. It is a rapid procedure with a low rate of benign complications (light fever during the first 48 hours).
Efficiency is very high since pleural drainage may last several months for 90 to 95% of patients. This procedure should therefore be proposed when potential survival is above one month.
A few contraindications should be respected: non re-expanding lung (after puncture), lung having lost its elasticity through lymphangitis carcinomatis or severe post-radiotherapy sclerosis or when diffuse pleural metastases are present.The major hindrance to a complete pleurodesis is a multiple partitioned effusion: in order to obtain a large diffusion of talc into the pleural cavity, pleural effusion should be relatively abundant before the procedure.
Proximal airways obstruction :
Main symptoms include: bradypnea, stridor (inspiration with acute noise), crowing noise, wheezing and symptoms of obstructive pneumopathy.
Except in the very last terminal phase, rapid relief should be offered to the patient (even if only for a few months).
Chemotherapy is rarely efficient except on lymphoma and small cell lung carcinoma (at the onset of disease).
Yag laser beam
The procedure is performed through a flexible fibroscope.Its efficiency is immediate.However, obstruction should be symptomatic and no longer than 4 cm along the bronchial tree.
The endoscopist should be able to perceive the bronchial hole and the downstream lung should be functional.
Laser is not indicated for extrinsic compression or in the case of an oesotracheal fistula.
It is efficient on extrinsic compression, however stenosis should not be wide enough to enable its introduction.
Urinary disorders :
Urinary disorders are very frequent during palliative care. They may be related to the patient's progressively altered general state and to certain necessary drugs. They may also be related to genital or urinary cancer.
Incontinence :
There are several forms of incontinence within the palliative setting. A urologic consultation is often advisable.
Treatment usually involves the use of an indwelling Foley catheter in female patients and condom drainage or penile clamp in male patients (and, if required, also a Foley catheter).
The complicated surgical interventions and rehabilitation required for artificial sphincters are most inappropriate in palliative settings.
In palliative cancer setting, the main causes are:
a tumour close to the trigone (bladder, prostate, cervix),
inflammatory reaction of the bladder wall related to irradiation, post-chemotherapy bladder irritation or infection.
In patients with good prognosis, treatment may involve sphincter surgery. In palliative care, parasympathetolytic drugs such as flavoxate, trospium or tolterodine or possibly low doses of tricyclic antidepressants (imipramine) can be used.
Acute urine retention :
Occasionally, diagnosis should be made before the appearance of overflow incontinence: the patient cannot avoid micturition with a full bladder due to retention.
Investigation of the cause should involve:
clinical examination of urethral meatus and urethra to discover any evident mechanical obstruction,
prostate examination,
neurological examination looking for cord compression,
looking for metabolic disorders (such as hypercalcaemia).
hypertonic internal sphincter (organic lesion of paraympathetic nerves).
hypercalcaemia,
use of anticholinergic drugs (such as phenothiazine, haloperidol, antihistaminic, cyclic antidepressants),
constipation may also compress urethra in a bedridden patient.
either by a suprapubic catheter (non-infected urine, acute and short-lasting situation),
or urethral Foley catheter,
modifications in medication (if necessary)
surgical treatment if the patient's general status is good (stent, prostatic resection).
Unilateral ureteral compression :
Unilateral ureteral compression is most often asymptomatic. It is revealed during systematic examinations (ultrasonography or TDM) which are part of the usual post-therapeutic follow-up procedures.
However, major pain may occur in relation to pyelic or renal calyce dilatation.
It is often related to retroperitoneal uni- or bilateral sclerosis due to previous radiotherapy.
Sometimes, pelvic cancer can be discovered by ureteral dilatation.
Symptomatic treatment is ureteral derivation .
If dilatation cannot be satisfactorily reduced, and when major clinical complications are involved (repeated pyelonephritis) with poor unilateral renal function, if the other kidney is functional, and within a palliative setting, it may be possible to propose unilateral nephrectomy which is a simpler surgical act than ureteral reimplantation.
Urinary fistula :
Urinary fistula is one of the most devastating complications of cancer during palliative and terminal phases. The psychological consequences of such total incontinence often lead to complete patient (and family) discouragement.
Urinary diversion (urethral catheter reducing intravesical pression) may lead to healing when the fistula is not a complication of progressing carcinoma.
When no local cancer progression is evidenced, surgical treatment of fistula may be proposed (epiploic flap technique).
In rare cases, bilateral ureteral diversion may be proposed.
When surgery is contraindicated (palliative terminal care) and catheterism is inefficient, a vaginal pack may be a temporary solution.
neurological disorder:
A neurological disorder is a disorder of the body's nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord, or in the nerves leading to or from them, can result in symptoms such as paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be revealed by neurological examination and studied and treated within the specialities of neurology and clinical neuropsychology.
Neurological disorders are very frequent during palliative care.
They can concern all parts of nervous system:
Spinal cord compression:
Spinal cord compression is a genuine therapeutic emergency.
Living the last months of life bedridden, motionless and completely dependent upon carers, is a terrible agony for patients that we should endeavour to avoid through early diagnosis and rigorous treatment.
Spinal cord compressions may be due:
The following symptoms may appear (not necessarily all of them or in the following order):
A unique lesion, in most cases, is a good indication of neurological decompression surgery.
The quicker the surgical intervention, the larger patient's chances of recovering normal function. Even if long term prognosis is unknown, such surgery should be performed.
After 12 to 18 hours of complete palsy, the patient has lost most of his/her chances of function recovery.
Localised radiotherapy associated with corticosteroid therapy may be very efficient in association with surgery, or when surgery is not feasible..
Leptomeningeal metastases:
They are caused by the dissemination of cancer cells into the subarachnoid space. Cancer cells reach the meningeal spaces:
RMI with contrast enhancement may reveal localised menigneal tumours which can be irradiated.
Local intrathecal chemotherapy remains a subject of controversy (particulary due to its meningeal toxicity), but it may provide very impressive remissions.
Radiotherapy of the whole spine has been proposed, however, generally speaking, more localised radiotherapy is prescribed in zones where tumour development is more intense.
Without treatment, patient survival is limited to a few months.
When the aetiological treatment is efficient, impressive remission may be obtained with a mean duration of 20 months.
Skull base lesions :
Lesions of the base of the skull are most often combined with carcinomatous meningitis (particularly metastases from breast or prostate carcinoma).
However, a continuous local head and neck cancer invasion may be observed.
Symptomatology is generally dominated by more or less localised headache and a neurological syndrome in relation to the cranial nerve concerned.
Diagnosis is generally performed by TDM using both bone and brain windows.
Treatment is mainly localised radiotherapy of the tumour lesion.
Cavernous syndromes also provoke ocular disorders, particularly hemianopsia and papilloedema.
Middle crania fossa syndrome associated diffuse headache, facial pain and numbness along the distribution of trigeminal nerves, with paroxysmal episodes of lancinating pain.
Jugular foramen syndrome provokes hoarseness and dysphagia, and various palsies (IXth , Xth, XIth , XIIth nerves) or Horner's syndrome (myosis, palpebral ptosis, enophtalmia, unilateral sweating).
Occipital condyle syndrome with frequent nuchal stiffness and palsy of XI th and XII th nerves.
Glossopharyngeal nerve infiltration (by head and neck cancer) provokes pharyngeal pain, with severe irradiation to ear (aggravated by swallowing and associated with syncopes).
Trigeminal nerve infiltration provokes dull, constant facial pain with paroxysmal episodes of throbbing or lancinating pain.
Patients concerned should request specialised pain consultations since their relief is most often difficult to obtain.
Radiculopathies:
Pain is generally focalised on the compression zone and irradiates according to the neurological distribution. If necessary, an electrophysiological study may be performed in order to better distinguished polyradicular lesions from plexic lesions. TDM and RMI are also useful imaging examinations.
Sometimes, herpes zoster may be considered, particularly in immunodeprived patients after chemotherapy. Looking for typical vesicles is good clinical practice. A good knowledge of clinical history may help to detect post-herpetic neuralgia in elderly patients.
They often complicate severe skin and soft tissue sclerotic disorders related to previous surgery and radiotherapy.
CT and RMI should detect potential local relapse.
Their treatment is difficult (frequent severe and relapsing neuropathic pain).
Pain is typically neuropathic, with anaesthetic zone, paresthaesia and hyperesthaesia.
A precise study of pain or anaesthesia location enables the precise determination of the incriminated root.
Specific serial TDM sections are necessary to study the incriminated zone.
When plexic pain is due to a tumour progression, irradiation (when feasible) brings good relief. However, in post-radiotherapy or post-surgical pain, treatment is difficult and should be entrusted to specialized pain team.
Pain is lancinating with excruriating paroxysms but rarely a burning sensation.
Other neurological disorders are often associated: perineal saddle sensory loss, motor and sphincter disorders, lower limb oedema.
Most often, this pain is related to cancer progression (rarely a complication of the treatment like for cervical or brachial plexopathy).
Precise radiological study with TDM or RMI sometimes enables further irradiation if possible.
If not, these patients need to be entrusted to a specialised pain team.
Skin disorders:
Skin disorders are very frequent during palliative care.
Skin is the most exposed organ of our body. Skin disorders may become major problems for patients during the terminal phase. Specific attention to skin should be paid by caregivers (particularly physicians who often spontaneously delegate this pathology to nurses), in order to avoid major pain (physical and psychological pain), a consequence of skin lesions.
Skin is a natural barrier avoiding the transmission of microbes inside the organism: clean skin and regular body care avoiding maceration are simple ways to avoid many of the general infections observed at the end of life. On the contrary, local irritation may represent the basis of any local and potentially generalised superinfection.
Skin is also the area of thermal exchange between the constant internal temperature (around 37°C) and external thermal variations. Good skin circulation enables the correction of such divergent temperature. Major skin lesions may modify these exchange possibilities (particularly near pressure points).
Skin is a very sensitive organ with several nerve terminations. Skin lesions are often very painful. These nerve terminations are most important for maintaining skin trophicity, thus explaining trophicity modifications observed during herpes or diabetes lesions.
Skin has an excellent power of regeneration (wounding and repairing), requiring a regular well furnished blood supply. Irrigation disorders (for instance through lengthy pressure in more or less conscious patients) will rapidly lead to trophic skin lesions and bedsores.
The following pages deal with:
Pruritus:
Pruritus or itching is a cutaneous sensation leading patients to regularly and severely scratch either because of a skin lesion or in the absence of any skin lesion. Scratch lesions may occur if pruritus is severe. Pruritus can be of moderate intensity and is generally and well tolerated, however it can also be intense involving considerable discomfort for the patient.
Pain and pruritus do pass through the same neurological networks. At medullar level, opioids generally provoke a pruritus sensation whereas naloxone (opioid antagonist) has an anti-pruritic effect. Pruritus related to cholostasis is well controlled with anti-5HT3 treatment.
Sweating :
Sweating is a physiological function of the human skin regulating body temperature by aqueous evaporation. Except in the rare hereditary disease 'anhidrosis' (absence of development of sweat glands), infants and the sedentary elderly may have thermal regulation disorders in relation to inefficient sweating.
Regulation of sweating depends on the autonomic neurological system and is coordinated by vasodilatation (or vasoconstriction for intensely cold temperatures). Palms and soles have a basic sweat pattern which is increased by psychological stress. Other body regions (axillary, forehead) may also sweat without any increase of external temperature.
Excessive sweating or hyperhidrosis may be either localised (in neurological disorders) or generalised (pheochromocytoma, hyperthyroidism, diabetes, acromegaly, menopause, tuberculosis, lymphoma, endocarditis). Most often, sweating is related to a chronic infection which can be treated.
Discovering the cause of important sweating can help to determine efficient treatment.
Hot flushes may be a major problem for women treated for breast carcinoma with early menopause as well as for men with prostate cancer treated by hormonal therapy. Non hormonal treatment of these forms of sweating is not always efficient.
During the terminal phase, abundant sweating may appear in patients constituting major discomfort. Symptomatic treatment with cimetidine may be useful.
Skin lesions treatment :
In the terminal phase (and unfortunately sometimes far earlier), major skin lesions can be observed, either in the form of deep craters, scars or fungating tumours. These lesions are most often painful, foul smelling and exudating. They require repeated treatment which can be difficult for the caregiver to perform and may give rise to a barrier between the patient and his/her family.
The wound should first be cleansed (if necessary an infectious lesion should be treated by systemic medication) and excessive exudates should be evacuated.
The dressing should not adhere to the wound (numerous 'fat' or 'humid' dressings) but should allow high humidity to be maintained to obtain cicatrisation and should allow correct oxygenation of tissues whilst simultaneously being impermeable to bacteria.
Other treatment modalities are dressings with carbon powder.
Sugar (honey and icing sugar) is another treatment for foul wounds.
You may consult the specific page on urinary and digestive fistula.
Bedsore problems :
Bedsore can be defined as an excavating wound resulting from skin hypoxia provoked by excessive prolonged pressure. Our skin needs a constant regular circulation in order to maintain its normal trophicity.
Bedsores will therefore develop at usual pressure zones when the patient lies or sits fro long periods, particularly on the buttocks and heel.
During excessive prolonged skin pressure, the progressive stages of skin lesions may be observed
Many scales have been proposed to evaluate bedsore risk: they generally consider the patient's weight (the risk is greater among slim patients), urinary or anal incontinence, general nutritional state, complete or incomplete immobilisation, possibility to move (even passively) the patient.
The most important treatment is prevention of the constitution of bedsores by:
There are two major points to consider:
Nutrition and metabolic disorders:
Nutrition and metabolic disorders are very frequent and are of great concern for the patient's family. Seeing a patient eating nothing is, for the family, a great source of suffering, synonymous to imminent death.
Severe under nourishment may be observed during complicated treatment (such as radiotherapy for head and neck cancers or poorly tolerated chemotherapy). These therapies may have to be temporarily stopped in order to take corrective measures (such as hyperalimentation by nutritive components or IV feeding).
Severe cachexia is frequently observed at the end of life. Major emaciation is due to the disappearance of all muscular and fat masses. The skin becomes very fragile like parchment, dentures become too big for the mouth, the patient becomes skeletal. In such a state of under nourishment, complications arise very quickly: a dry mouth further reduces feeding, the body support zones are the target of necrosis process (decubitus bedsore).
Biologically, such cachexia induces an increased metabolism of lipids and proteins, anaemia (without any clear aetiology), hypo-albuminemia (further inducing oedema), hyponatremia.
Treatment of anorexia :
The main goal of palliative care is to improve the patient's comfort.
Anorexia is an almost constant symptom during the terminal phase of cancer: it is a concern for family members who generally wish to see their patient eating correctly.
Many metabolic factors may promote anorexia during the terminal phase: among which, TNF secretion (Tumour Necrosis Factor) and various Interleukin factors. Moreover, anorexia is a sign of the chronic depression which is observed in most patients at the end of life. Finally, local organic causes will increase this anorexia: chronic constipation, mouth dryness, intracranial hypertension, chronic nausea (in relation to morphine treatment, metabolic abnormalities, analgesic radiotherapy, etc..).
Whereas the patient should be encouraged to eat some food, he/she should not be force-fed against his/her personal will and comfort. Certain carers are tempted to use parenteral nutrition very early on in disease progression: if such nutrition may be useful during acute treatment phases (during radiotherapy or intense chemotherapy, to prepare surgery), it has no place in the terminal phase, since it totally disregards the patient's liberty for only minimal benefit. Randomised studies have shown that parenteral nutrition does not increase patient survival and this aspect should be explained to families in order to calm their anxiety.
A few drugs may be useful. Progesterone derivatives such as megestrol at relatively high dosages (800 to 1,600 mg per day) may have a stimulatory effect on appetite.
Corticosteroids are to be largely employed for their numerous beneficial effects during terminal phase (particularly on appetite).
Practically, very simple therapeutic means may often be sufficient: fractionation of feeding into smaller, more frequent meals, taking care to respect patient taste (meat is not necessary!), treatment of permanent nausea, mouth care.
Anorexia is one symptom of terminal cancer: it should therefore be respected and explained to the patient's family. Giving precise information to family members on the futility of parenteral infusions may reassure them: a French by-word says that 'when appetite is OK everything is OK'. For families, a patient who does not eat, is never going to be cured. Unfortunately, this is the precise truth and one should learn to respect patient anorexia if it is well supported by the patient him/herself (the absence of ravenous hunger crises due to hypoglycaemia). Such respect will facilitate dialogue between the dying person and his/her family.
Hypercalcemia :
Hypercalcaemia is a common manifestation among cancer sufferers: 20 – 40 % of multiple myeloma, 35% of lung cancers, 24% of kidney cancers, 8-10% of breast cancer. Hypercalcaemia generally underlines the poor prognosis of cancer, although new therapies may offer longer patient survival.
If osteolytic lesions are present, then hypercalcaemia is generally a late phenomenon underlining poor prognosis. Hypercalcaemia induces symptoms that should be corrected with efficient palliative care.
Many hypercalcaemia appear without any osteolytic lesions and are therefore true paraneoplastic syndromes possibly due to several mechanisms:
Untreated hypercalcaemia leads to severe dehydration and possibly to patient death by cardiac rhythm disorders.
However, diphosphonates (in particular intravenous forms) have totally modified such modalities allowing ambulatory treatment over several weeks, with prolonged survival and good quality of life.
The only major point to ensure is correct patient rehydration, if necessary intravenously. Corticosteroids are still useful if hypercalcaemia is very high.
Hyponatremia:
Cancer patients frequently suffer from hyponatraemia, the physiopathology of which is not always clearly understood. Generally, it is fortuitously discovered on a systematic ionogram. However, hyponatraemia increases patient fatigue and can possibly be complicated by somnolence or seizures.
Hyponatraemia is often observed in preterminal stages of severe disease. Patients excrete the sodium excesses administered in order to correct hyponatraemia and liquid restriction leads to more severe dehydration than that already observed. Surprisingly, if patients are able to resume normal eating, a spontaneous correction of hyponatraemia is observed.
Thus, this preterminal hyponatraemia should be distinguished from an inappropriate secretion of ADH which is a genuine paraneoplastic syndrome (occurring in lung cancer for instance). Hyponatraemia leads to severe neurological disorders and to an exaggerated water excretion by the kidney (excessive urinary osmolality). In such cases, fluid restriction is useful, but more particularly the treatment of cancer, where possible, will improve the clinical situation.
Another frequent cause of hyponatraemia in cancer patients is the presence of oedema leading to a dilution syndrome. Such a clinical situation can be observed when ascitis or major pleural effusion occur. Whereas symptomatic treatment (ascitic puncture, diuretics) may be useful, only aetiological treatment will actually correct hyponatraemia for a reasonably long time.
Medications and treatments are said to have a palliative effect if they relieve symptoms without having a curative effect on the underlying disease or cause. This can include treating nausea related to chemotherapy or something as simple as morphine to treat a broken leg or aching related to an influenza (flu) infection.
Although we make everyday progress in cancer treatment, cancer remains a mortal disease for about half of the patients, depending of the location (from 0% for localized tumour to 100% for rapidly progressive uncontrolled tumours or metastatic tumours).
Historical remarks
(I muss confess that these are French historical remarks! Any comment from abroad is welcomed)The history of palliative care for cancer patients is relatively old: during 18th century, Canon Jean-Baptiste Godinot founded in Reims an institute for 'cancerous' after many difficulties. His aim was to bring some dignity to patients, noticeably those with necrotic skin tumours, with strong odours.
In 1842, Jeanne Garnier, a young widow, creates in Lyons the 'Calvary Ladies', a lay congregation gathering lay widows who desire consecrate their life for untreatable patients. They install another house in Paris in 1874 (the future Jeanne Garnier medical house). With her, the word 'hospice' takes the meaning of a place to receive patients at the end of their life.
 | In fact, most of the modern concepts of palliative care come from the works of Cicely Saunders at St Luke's Home for the Dying Poor (1946) then at St Christopher's Hospice. "I became conscious through listening to patients, that I perceived something of their capacity to transform this part of their life into a success". Since that time, her team used morphine preventively, invented the famous 'morphine elixir' and demonstrated the absence of habit in painful patients. Lady Cicely Saunders also originally expresses the concept of total suffering. Another important point was to explain why many caregivers were abandoning their patients at the end of life: it is the non acceptance of mortal characteristic of their patient (or of themselves). |
Another pioneer in palliative care was Elisabeth Kübler-Ross, a Swiss physician living in Chicago. Her experience of dialoguing with patients was clearly demonstrated during a famous conference of 1961, when she let young medical students dialog with a young patient with leukaemia at the end of her life (something they had never done). She specifically studied the usual death denial among patients in terminal phase, but also in our society. She described the steps of the dying process. Also, like La Palisse's expression, she underlines the concept that a dying person lives until death. We should therefore help them up to this date. |  |
 | The English model of hospices has spread around the world. The concepts of mobile team for palliative care and home care teams have then completed the original model. In France, after the revelation of the English experience by Father Patrick Verspieren, conferences from Dr Thérèse Vannier (Quebec), the experimentally work of Pr.Maurice Abiven (photo), many new teams are created and palliative care is progressively integrated in the University teaching. |
A physician (or any caregiver) who will be in charge of cancer patient will have to provide palliative care. The continuous progress in palliative care, the more and more precise pain treatments are major progresses for the quality of life of our patient. For so many patients where nothing new happened for cure, we could write that palliative care is the only real progress for them.
General note about this chapter
They are only principles for treatments.The named medications are reflecting my experience (or absence of experience). Names are DCI. Other medications may be useful, and I will be grateful to everyone who helps me correct mistakes or lapses.
Continuous and palliative care :
Frequent cancer evolution
We are unable to cure around 60% of cancer patients. However, caregivers (physician, nurse, technician) should endeavour to offer the best possible care to patients who have faith in them , up to the very end.
In reality, relatively soon before the patient's situation becomes tragic leading to what is known as the 'terminal' stage, caregivers know that treatment will not offer cure, but may lengthen the patient's life, improve quality of life and prepare him/her for a dignified death. Remission periods, that can last years, may be observed.
Such apparent failure requires personal psychological preparation for each caregiver: it is easier and far more comfortable to treat with a curative intent than to be faced with an incurable person to care for.
Continuous care principle
Most oncologists and caregivers prefer not to entrust their patient to any specialised palliative team. They believe that patients feel better if they remain in the care network within which they were actively treated.
Many patients, however, express their desire to end their life at home. For this reason, many home care teams, mobile units and various external care groups have been set up, with specifically designed systems, which may slightly differ from one location to another.
In fact, the desire to return home is not always quite as clear as it often appears: many patients express this wish when they are still in relatively good health. In acute or preterminal phases (dyspnea, hemorrhage, anxiety, death proximity) or because they are aware of their family's disarray, they often ask to be brought back to hospital and then feel more secure within a professional team. Families should always be comforted since they often feel they have failed in their duty of keeping their patient at home: the most important thing to bear in mind is that they tried and that they should respect, every day and as best they can, the patient's personal comfort and wishes.
Therefore, more and more, genuine care networks (associating hospital and home care) are the most appropriate structures to assume care continuity.
Palliative care at home
Nevertheless, for those patients desiring to stay or to return home, the main actor will be the general practitioner who will ensure terminal care together with the district nursing team.
The general practitioner completely fulfils the duty of human medicine towards the sick person by offering adapted palliative care, taking into account not only the medical but also the social, psychological and spiritual aspects.
When able to bear the burden, the patient's family will turn out even stronger and more united when dignified death at home is made possible. There are many discussions with the dying person that can only be broached within the context of usual daily life. The assumed difficulties lead to a more serene bereavement.
Good home care organisation is mandatory to help the family to assume and fully invest in the care of the beloved person. Caregivers often experience intense care periods and good personal self-confidence is necessary for providing the best care every day. Work within a team and participation in discussion groups (even in private city practice) are essential in the prevention of caregiver burn-out (cf. chapter on psychological aspects).
Palliative care technicality
Wherever palliative care is to be provided, it constitutes complete and genuinely satisfactory medicine.
Precise diagnosis (requiring excellent knowledge on the symptoms or syndromes generally encountered during the palliative care phase) is mandatory for instituting appropriate treatment.
Cooperation is generally necessary with a number of other specialists (radiotherapist, nutritionist, pain specialist but sometimes also surgeon, medical oncologist and other carers). Failing to call upon such specialists can place patients in dead-end situations, every added delay bringing new iatrogenic events.
Precise use of analgesic medications but also of other palliative drugs can transform the patient's life from a lengthy and painful "cul-de-sac", with a vision limited to pain and symptoms, into an enlightened appeased end of life, allowing intense dialogue, rich affective life and a profound spiritual (potentially religious) experience.
Offering a 'beautiful death' requires a genuine dialogue with the patient but also, for the caregiver, profound self knowledge on one's own reactions. Prior personal and team work can help each caregiver in this specific context.
Therefore, palliative medicine is an intellectually, technically and spiritually rich medical practice.
Unfortunately, such medicine is not always taught by universities (neither from a theoretical point of view nor in daily patient practice). Therefore, many physicians and nurses train themselves within post-graduate teaching programmes
Pain :Pain is more or less present on a permanent basis at a certain point in cancer progression, particularly during palliative care phases (in at least 70% of patients). The aim of this chapter is not to teach everything about pain but rather to define practical attitudes and reasoning. At least 90% of pain can be relieved.
Pain can be defined as an unpleasant personal sensorial and emotional experience associated with real, potential or feared tissue damage.
It is clear from this large definition that all pain, even if perfectly isolated and described, very rapidly involves affective, emotional, cognitive or behavioural components. Physical pain is most often completed by 'moral' pain or total pain.
Neural pathways in pain
Assessment of a painful patient
Cancer pain
Treatment principles
Therapeutic scales
Opioid rotation
Neuropathic pain
Neural pathways in pain :
Pain origin
Following tissue aggression, independently of its type, nociceptive messages are transmitted from various nociceptors towards spinal cord roots through small sensitive calibrated nervous fibres. Many algogen products are implicated in pain genesis: bradykinin, H+ or K+ ions, histamine, serotonin, various derivatives of arachidonic acid (prostaglandins, prostacyclins, leucotriens).Prostaglandins sensitise receptors to many algogen compounds. Therefore, the use of anti-inflammatory drugs, aspirin or glucocorticosteroids has a positive effect.
Transmission within the spinal cord
The dorsal horn of the spinal cord is the first step for the transmission and modulation of pain. Nociceptive afferent neuronal fibres transmit information to converging neurons, then to the ascending spinothalamic tract.There, many peptides are involved in pain transmission: substance P, vasoactive intestinal peptide (VIP), ocytocin, galanine, angiotensin 2, dynorphine, enkephalin.
The classical theory considers that all of these chemical molecules are a gate filtrating pain transmission towards the superior centres. Pain is transmitted:
either if it provokes stimulation that is too important to be inhibited at medullar level,or if the medullar filter is altered.
Thus two different types of pain are considered: nociception pain (too much stimuli) or deafferentation pain (no inhibition), with different therapeutic attitudes.
The presence of such a medullar filter allows local medullary treatment (peridural injection, intrathecal injection), particularly by morphine or its derivatives, in order to reduce the general dosing and diminish side effects.
Transmission towards the brain
Pain is then transmitted through spinothalamic tracts (anterolateral medullar chord) towards brainstem reticular formations and ventral thalamic nuclei.The lateral thalamus discriminates sensitive information to precisely locate its origin.
The central thalamus has less systematised information responsible for motor reactions and the emotional components of pain.
From the thalamus, the pain information is transmitted to the ascending parietal area (precisely discriminating pain location) as well as towards the limbic system provoking emotional and behavioural reactions and towards the hypothalamus inducing neurovegetative and endocrine manifestations.
| Assessment of a painful patien: |
Treating pain requires precise knowledge on analgesic medications but, first and foremost, it requires listening to and examining the patient in order to precisely diagnose the origin of pain.
Assessment of patient pain
The first principle is to always believe the patient (and his/her family) when complaining about pain. Pain is a purely subjective phenomenon, the quality and the intensity of pain and the way it is described will vary from one patient to another. The physician should therefore precisely analyse the symptoms described by the patient.Pain evaluation should be the basis of treatment: it must be performed by both th physician and the patient. This evaluation should be performed:
at regular intervals,for each new painful episode,
after any analgesic action (half an hour after any IV analgesic treatment, one to two hours after oral treatment).
During cancer, some causes are most frequent:
chronic osseous pains from metastases,
osseous pain with mechanical outbursts: for which fracture or vertebral crushing should be feared,
pain through organ compression or nerve infiltration (sciatica, plexalgia),
headache from brain metastases,
digestive pain in relation to transit disturbance,
mucuous pain (mucitis, esophagitis, cystitis, rectitis).
During the palliative phase, cancer pain generally is chronic, persisting, progressively aggravating, disturbing the patient's liberty and sleep. Nocturnal pain is very typical of cancer.
When questioning the patient, the physician should consider:
the words the patient uses to describe pain ('it pinches', 'it burns', 'it twists', and so on)
factors influencing its arrival, its aggravation, its duration, its variation throughout the day,
precise pain location, asking the patient to trace pain on the body or a body diagram,
pain intensity (as evaluated by the patient but also in relation to induced perturbation of normal life),
sometimes, trying to guess when the patient can no longer easily express himself/herself.
The clinical examination should be careful and cautious since the patient is in pain:
mucuous examination,
mild limb mobilisation,
soft pressure on painful zones (provoking pain!)
pelvic examination in case of sciatica.
Diagnosing pain type
Classically, two types of pain are observed:pain due to excessive stimulation, generally related to extension of the tumour towards nearby structures with, most often, a precise, permanent topography with pain exacerbation attacks.
pain due to deafferentation, located on neural routes, by the deterioration of peripheral neurones, with fulgurating pains similar to electric shock, but also hypoesthesia or localised hyperesthesia, burning or stinging sensations (for instance post zoster pain, phantom limb pain),
psychogenic pain, with no systematisation but occurring in a major anxiety context,
Pain scales
Many 'scales' have been developed in order to objectify pain intensity. Among them:simple verbal pain scale: no pain, mild pain, moderate pain, intense pain, intolerable pain,
analogic visual pain scale (marked from 1 - no pain to 10 intolerable pain) which necessitates patient cooperation.
pain questionnaires (Mc Gill Pain Questionnaire, QDSA: Questionnaire de Saint-Antoine) which also needs good patient cooperation and allows multifactorial analysis,
behavioural scales: observing the patient permits an evaluation of pain, in particular child pain (DEGR scale: douleur enfant de l'Institut Gustave Roussy) or in elderly patients (Doloplus scale),
precise study of analgesic consumption.
Cancer pain:
Pain during cancer may have three different causes:
Pain in relation with tumour progression
In approximately 70% of cases, pain is related to tumour progression:bone pain (most frequent):
in relation to metastatic bone tumours,
unique or multiple locations,
without or with fracture (specific problem of prefracture syndrome),
potentially concerning all bones (skull, spine, limb bones, ribs, pelvis).compression or infiltration of neural structures:
peripheral or central nerves,
with or without associated motor deficiency,
with or without associated sensitive deficiency,
potentially concerning various nerves (vertebral nerves, brachial plexus, cervical plexus, lumbosacral plexus, medullary compression, cranial nerves).visceral or muscular infiltration
intestinal occlusion through infiltration,
inflammation and serous effusion,
compressive muscle pain.mucinous lesions
mouth, oesophagus, vagina, rectum, bladder, and so on
Iatrogenic pain
Treating cancer is difficult and treatment generally agresses the patient. Approximately 20% of pain are due to treatment.in relation to surgical or diagnostic procedures:
abnormal wound healing,
neuropathy in relation to neural section, phantom limb syndromes,
stomy complications.in relation to chemotherapy:
mucitis,
sensitive neuropathies,
muscle pain (taxane, interferon),
osseous pain (growth factors),
drug extravasation (cf. chemotherapy chapter).in relation to radiotherapy
mucitis, cystitis, rectitis, ..
radionecrosis,
radiotherapy induced plexalgias,
visceral post radiotherapy alterations.
Pain from other origins
In about 10% of cases, pain is not related to cancer or its treatment and the patient may have previously taken analgesics for its treatment.
Treatment principles :
False dilemma
Faced with a cancer patient, the clinician has two objectives:There is no contradiction between these two aims: what is the use in asking for analgesic radiotherapy if the patient cannot lie five minutes on the table without suffering major pain? On the contrary, what is the use in prescribing high doses of morphine to a patient suffering from a mobile fracture? In the former situation, the administration of a strong initial analgesic allows efficient radiotherapy; in the latter, rapid immobilisation (involving surgery if necessary) offers quick relief to the patient.To treat the patient's pain as soon as possible, to make it disappear, if possible totally and indefinitely,
To treat (if feasible) the cause of pain in order to adjust the drug prescription.
The clinician should propose realistic and demonstrable aims:
The patient should:not suffer at night thus allowing sleep repair,
not suffer during meals,
not suffer during movement,
be able to eat, urinate without pain,
whilst remaining as clear-headed as possible.
Principle: pain should not appear
Pain is not a fatality for patients with cancer. Cancer does not have be be a 'prolonged and painful disease'. Good palliative management should transform the last months of our patients' lives.
Pain should be anticipated and should not be left to overwhelm the patient. Pain provokes patient anxiety. The patient, as his/her family, believes that disease progression is quicker when pain is present. Such anxiety increases
the pain sensation. Even benign procedures should not provoke pain: for instance, more or less powerful analgesics could be prescribed before body care in order to restore the pleasure of feeling clean and fresh.
Treatment is preferably prescribed by oral or transdermal routes rather than via intramuscular or intravenous injections. The two former routes give more regular pain relief and promote patient autonomy.
The patient (and his/her family) should be taught the benefits of regular intake. Patients may try to be less of an 'addict' and may try to space out analgesic intake until pain resumes. In such situations, analgesic dosage should be increased to be efficient: however, this also provokes unnecessary side-effects. Regular analgesic intake may lead to complete and permanent pain control without side-effects or drug dependency.
Medication associations
Following the precise analysis of pain, performed together by both the patient and his/her physician, the treatment of pain will then associate several therapeutic resources:pure analgesic drugs,
other adjuvant drugs depending on the type of cancer and the cause of pain,
non medicinal therapies (such as surgery, radiotherapy, dressing) depending on pain
Without going into detail, we will describe analgesic treatment principles (only for cancer pain).psychotropic medications, when a major psychological component increases the pain sensation.
Pain therapeutic scale :
The World Health Organisation (WHO) published, some time ago, pain scales in order to improve pain management with increasingly potent analgesics. Below, we have reproduced this scale with a few modifications made:
The WHO scale mainly concerns nociception pain.
- after the emergence of new opioid non morphine analgesics (Scale II B)
- considering poorly relieved morphine treated pain necessitating specific administration techniques.
WHO Level I
Pain is generally moderate (1 to 4 on the visual analogic pain scale).The main analgesic drugs are:
Acetaminophen
Nonsteroidal anti-inflammatory drugs
Aspirin
Noramidopyrin
WHO level II (A)
Pain is more intense (between 4 to 8 on the visual analogic pain scale).Two drugs are used:
Codeine and dihydrocodeine
Dextropropoxyphen
WHO level II (B)
Same pain intensity, but inefficiency of previous drugs.Three drugs are used:
Tramadol
Nalbuphine
Buprenorphine
WHO level III
Intense sustained pain resistant to previous medicationsIn level II or III, other adjuvant drugs can be administered, such as anti-inflammatory drugs.Injectable morphine
Oral morphine
Fentanyl
Hydromorphone chlorhydrate
Oxycodone chlorhydrate.
WHO level III B
This pain requires specific pain consultation for various techniques:specific morphine administration,
stimulation,
pain surgery.
Neuropathic pain :
Neuropathic pain is pain related to the abnormal function of the peripheral or central nervous system which does not correctly control pain influx. Such pain can be very difficult to treat even with opioids.
We can distinguish:
Neuropathic peripheral pain
Pain is related to the destruction mechanism of peripheral nerves: this pain can therefore concern one or several nerves.It is characterised by acute transfixing attacks complicating a permanent dull pain. Furthermore local paresthesia can be observed.
Two examples:
neurapathy by inflammatory or toxic lesion of the small nerves of major neurological trunks (nervi nervorum),
or by the formation of a neuroma after axon section.
These neuroma are particularly sensitive to touch or chemical stimuli (such as norepinephrin).
Central neuropathic pain
Two different types of central neuropathic pain are observed:Deafferentation pain
Many syndromes illustrate this deafferentation: pain from phantom limb pain, post-zoster burning sensations, painful anaesthesia, central pain.Dystrophic pain
This sympathetic or dystrophic pain (also called causalgia or burning pain) is accompanied by:autonomic dysregulation (cold or hot sensations, limb moistness, swelling, redness,..),
motor symptoms (stiffness, muscle weakness, abnormal movement),
trophic symptoms in bone (bone algodystrophy) or skin (reduced dermal thickness, dermoskeleton modification).
Dystrophic pain is most frequent after plexus radiation fibrosis (head and neck cancer with painful stiff shoulder) and constitutes a major therapeutic challenge.
Therapy of neuropathic pain
This type of pain requires the competence of a specialised multidisciplinary medical team.Opioid treatment
Opioid treatment should always be attempted: dosages are slowly and progressively increased up to major (if not complete) clinical pain remission or to major morphine intolerance symptoms.In fact, most often, neuropathic pain requires a very high dosage but is not truly insensitive to morphine drugs.
Adjuvant medications
Many adjuvant drugs have been tried in order to prevent hyperalgic crises: their number and the diversity of their therapeutic classes demonstrate the difficulty in treating such acute pain phenomena:
tricyclic antidepressive drugs: amitriptyline, imipramine, desipramineAnesthetic approach
other antidepressive drugs: paroxetine, maprotiline, gabapentin,
local anesthetic drugs: mexiletine , flecainide,
anticonvulsivant : carbamazepine, phenytoin, valproate,
alpha-2 adrenergic antagonist: clonidine,
anesthetic drug: ketamine,
other sympathic drugs: prazosin , propranolol , nifedipine.
This approach concerns the testing of typathetic blockade, for instance for brachial plexus pain or peripheral nerve blockade or opioid intrathecal injections.
These techniques should be performed by a specialised anaethesiologist.Neurostimulatory approach
Transcutaneous electrical nerve stimulation may be of benefit among patients with untreatable and intolerable pain. Since many adaptations are necessary in order to maintain, for as long as possible, the obtained benefit, a perfect technique is mandatory to ensure success.Surgical approach
The surgical approach concerns the resection of neuroma, or the denervation of a painful zone (cordotomy). Since this surgery leads to permanent lesions, a multidisciplinary discussion should be organised in order to specify appropriate indications.
Digestive tract disorders in palliative care :
For the patient, gastrointestinal problems are among the most frequent and cumbersome disorders during palliative care.
They can concern all segments of the digestive tract:
Mouth care :Mouth care,
Dysphagia ,
Dyspepsia,
Hiccups,
Occlusion,
Nausea and vomiting,
Constipation
During palliative care, patients often suffer from their mouth. This is due to:
Some very difficult situations are observed in head and neck cancer during the terminal phase.mouth dryness or xerostomia,
Treatment related stomatitis (radiotherapy, chemotherapy, antibiotherapy),
very frequent fungal infection,
open mouth breathing,
nutritional imbalance,
loss of autonomy and general weakness (difficult mouth rinsing).
Poor hygiene often leads to a very foul-smelling breath or halitosis which may increase family uneasiness, speech difficulty and pain during meals associated with difficulty in swallowing.
Prevention of mucitis and the use of simple therapeutic methods are mandatory and should be repeated every day without provoking pain:
The use of Q-tips and compresses to humidify the oral cavity,
Soft tooth-brushing with a pleasant non-irritating tooth paste,
Frequent gargles (when feasible) with Coca-Cola or antifungal mouth rinsing solutions (many magistral preparations exist),
The use of morphinic mouth rinsing solutions when severe, painful mucitis prevents feeding,
Alcoholic solutions should be avoided, since they induce pain when mucitis or mouth ulcers occur.
Good air hydration (use of misty water spray or a nebuliser) also offers improved preservation of oral comfort.
Dysphagia :
Dysphagia can be defined as the difficulty in transferring the alimentary bolus (liquid or solid) from the mouth to the stomach.
In a palliative care unit (like St Christopher), dysphagia is observed in approximately 10% of patients (however, the unit also welcomes patients with lateral sclerosis for which dysphagia is an evolutive phase of the disease).
Deglutition physiology
Four steps are necessary for correct swallowing:endobuccal preparation of the alimentary bolus (mastication, salivation),
oral swallowing phase, with closed lips and anterior tongue retraction pushing the bolus towards the oropharynx,
pharyngeal phase: partial occlusion of the nasal fossa, complete occlusion of larynx, stopped breathing,
esophageal phase: peristalsis pushes the bolus towards stomach.
The first two phases are voluntary; the latter two are reflexive.
Pathophysiology of deglutition disorders
A tumour mass in the mouth or the superior pharynx will rapidly lead to swallowing difficulties, whereas a low pharynx tumour or an oesophageal tumour will be troublesome only when voluminous.Treatment of the tumour also provokes major swallowing side-effects:
surgery,radiotherapy: post-radiotherapy sclerosis, mouth dryness, candidiasis,
chemotherapy, not onlyvia chemotherapy alone, but also through the increased risk of candidiasis complicating dry irradiated mucosa,
other potential mouth infections: herpes zoster, cytomegalovirus.
Major problems
Depending of the location, patients may suffer from:mouth leakage (the patient slavers): lip sensation disorders, abnormal tongue movement, reduced swallowing reflex,
frequent nasal regurgitations poor palatal function (often after surgery or radiotherapy),
swallowing difficulty: the patients pushes his head backwards in order to swallow,
coughing when swallowing may occur
- before deglutition (poor deglutition reflex),
- during deglutition (poor laryngeal occlusion),
- after deglution (difficulty in emptying the pharynx, poor functionning of cricco-pharyngeal muscles, tracheo-esophageal fistula).
Therapeutic attitude
Should enteral alimentation (feeding) or parenteral alimentation (hydration) be proposed to the patient?The following table summarises enteral and parenteral feeding indications:
General indications | Parenteral route | Nasogastric tube, gastrostomy |
| Indications Swallowing time greater than 10 seconds No improvement after rehabilitation or nutritional support Radical treatment proposed (surgery, radiotherapy) | Indications Complete pharyngeal or oesophageal obstruction Short use (a few weeks), Other intestinal or gastric problems | Indications Prolonged use (more than two weeks) |
| Contraindications Rapid terminal deterioration Other major difficulties | Contraindications Presence of sepsis Difficulties at home No access to biochemical monitoring No access to nutritional team Superior vena cava compression | Contraindications For the tube: oesophageal obstruction, fistula For gastrostomy: gastric tumour, occlusion |
Some simple advice may help a dysphagic patient to eat normally by mouth:
- (if possible) always eat while comfortably seated, head upright, relaxed,
- do not talk while eating or drinking, largely yawn before eating to ease any constriction,
- eat small amounts, with closed lips, and try to slowly chew and volontarily swallow small quantities,
- take a break between each deglutition, eat slowly, do not mix solid and liquid food,
- drink a small amount of water after each meal to rinse your mouth and clear your throat,
- remain seated a good while after eating or drinking.
Dyspepsia :
Dyspepsia can be defined as a postprandial discomfort or upper abdominal pain. It can also be called indigestion (and in France 'mal au foie' - liver problem!). It is a common situation since 40% of the general population may be more or less concerned.
Main symptoms
Patients have various complaints:general epigastric discomfort, not always pain as such,
premature satiety (the patient states being hungry but stops eating after only a few bites),
postprandial heaviness, fullness, or bloating,
sensation of incomplete digestion (as if food stayed in the stomach for several hours),
epigastric acidity,
frequent and repeated belching, gulping, hiccups,
nausea, retching, vomiting.
Simple classification
In a simple classification, five types of dyspepsia can be described:Small stomach dyspepsia: the patient is hungry but rapidly repleted, he/she experiences epigastric fullness or heaviness soon after eating,
Borborygmus dyspepsia: postprandial bloating with frequent belching associated with dry air swallowing, increased by anxiety,
Reflux dyspepsia (gastro-oesophageal reflux): retrosternal burning when the patient bends over, when he/she eats more than usual or lies flat.
Gastric ulcerations or ulcer: precise localised pain wakening the patient at night, relieved by meal or antiacid medication,
Intestinal motility disorder dyspepsia: abdominal distension, premature satiety, gastric 'heaviness' or fullness, multiple alimentary intolerance, diffuse pain, frequent nausea with irritable bowel syndrome.
Causes of dyspepsia in palliative care
To simplify, causes can be divided into:Cancer-related dyspepsia: gastric tumour, massive ascitis, paraneoplastic neuropathy
dyspepsia related to the poor general health state during cancer (candidiasis, reduced alimentation, anxiety),
treatment-related dyspepsia (abdominal surgery, radiotherapy especially in the abdomen volume, chemotherapy, morphine treatment, other medications),
associated pre-existing dyspeptic syndromes.
Dyspepsia treatment
Depending on the cause:Not forgetting auto-medication by the patient at home, which is not always known by the physician (aspirin, gassy water).
A little simple dietary advice can help, such as a more varied diet.
Small stomach dyspepsia can be treated by smaller, more frequent meals.
Drug administration may be reduced (such as anti-inflammatory drugs) but not always stopped.
In the case of gastric acidity, antacid treatment may be prescribed, for example ranitidine, an H2-receptor antagonist avoiding proton pump inhibitors because of their prolonged effect on gastric parietal cells.
Gassy syndromes may be improved by defoaming antiflatulent agents such as simethicone derivatives.
Dyspepsia related to motility syndromes may be treated by prokinetic drugs such as metoclopramide, domperidone, cisapride.
Occlusion syndrome :
During palliative care, occlusion (or obstructive syndrome) generally announces disease progression and the fear of a fatal short-term evolution. It should be totally distinguished from a nascent neoplastic occlusion.
Around 5% of cancer patients suffer from end of life occlusion, mainly those with colon and ovarian carcinoma with a more or less diffuse peritoneal carcinomatosis.
Clinical presentation
Contrary to usual surgical occlusions, palliative care occlusion generally begins slowly and progressively and its site is imprecise. In relation to peritoneal carcinomatosis, it is accompanied by a inflammatory phenomena. The specific date of gas and matter blockage is unclear in these constipated patients. Pain may be due to the tumour itself (compression of nerve plexi) or to intestinal spasms induced by occlusion. Rare cases of vomiting are observed.At clinical examination, we can distinguish a ballooned abdomen (by dilatation upstream of the lesion) and a flat abdomen (if occlusion is high or total). Palpation also often reveals tumour masses.
Progression can be long: occlusion is often well tolerated over several days or weeks. However, the psychological consequences are important for patients who do not eat, do not pass stools and who permanently suffer from abdominal pain.
Discussing surgery
At the onset of occlusion, the clinical examination should eliminate any surgical indication: an acute onset and noisy symptoms may be due to an acute obstacle which could be solved by a simple surgical act.However, most often, occlusion is slow to progress, the abdomen is flat, peritoneal masses are found and, in the case of surgery, the surgeon would find himself/herself in an inextricable surgical situation.
An untimely intervention would only add post-surgical pain and the increased risk of numerous adhesions.
Medical treatment
Medical treatment of occlusion is often efficient (mainly corticosteroids at a dosage of 2 - 3 mg/kg of prednisone. When necessary, a nasogastric tube may reduce pain and vomiting. Intravenous infusion is not always necessary.Pain (generally major spasms) should always be treated and small dosages of subcutaneous morphine are not contraindicated when pain is intense.
In colon cancer, an endoprothesis (generally a wired metal endoprothesis) may be installed by colonoscopy providing a more or less regular passage for faecal matter, but with relatively minor colic discomfort.
Preventing vomiting
When occlusion cannot be stopped, a strong analgesic and antispasmodic treatment should be instituted (pethidine may be interesting), avoiding stimulating drugs (such as metoclopramide). When profuse vomiting occurs, octreotide (synthetic somatostatine unfortunately a very costly drug) may be attempted to reduce intestinal secretions. An intermittent nasogastric tube may solve this problem, avoiding a pseudo angina syndrome. In very profuse vomiting, certain physicians would try a per-endoscopic gastrostomy .Sometimes, episodical vomiting in the absence of intestinal cramps is relatively well tolerated.
Terminal occlusion of peritoneal carcinomatosis is a very slow evolutive death process.
Nausea and vomiting:
Definitions
Nausea is a multiple sensation: the need to vomit, epigastric pain, distaste for food and general malaise. Nausea is generally relieved by vomiting.Unfortunately, in palliative care, nausea may be more or less permanent, therefore very toilsome for the patient and often more unpleasant than vomiting itself.
Vomiting is the rejection of eaten matter: it may be beneficial (for instance after food poisoning). When vomiting is repeated, digestive spasms, muscle contractures and the usual accompanying vagal manifestations (bradycardia, hypersialorrhea) end in patient exhaustion. This phenomena is frequently observed during palliative care
Physiopathology
Vomiting occurs in response to the stimulation of the vomiting centre situated in the mid brain. Several brain zones may stimulate this centre in response to stimuli coming from:the mouth and the pharynx region (olfactory, gustatory and tactile sensations),
the bronchial tree,
the vestibule (motion sickness),
the digestive tract (numerous receptors),
the meninges,
the brain itself (importance of psychology in triggering vomiting).
By studying induced vomiting in animal chemotherapy, a trigger zone has been discovered in the area postrema, i.e. on the floor of the fourth ventricle. These studies showed the importance of serotonin. Stimulating this area stimulates the vomiting centre.
Several neurotransmitters are implied in triggering vomiting:
in the area postrema, dopamine and serotonin (5-hydroxy-tryptamin)
in the vomiting centre, histamine and acetylcholine.
The main causes of vomiting in a palliative setting
Four major causes should be looked for:gastrointestinal causes: infiltration or stenosis of the digestive tract, independently of the primitive tumour,
metabolic causes: renal insufficiency, hypercalcaemia, hepatic insufficiency,
treatment causes: vomiting induced by morphine, antibiotics, chemotherapy, radiotherapy,
intracranial hypertension: brain metastase, carcinomatous meningitis.
Other causes are either not so frequent or easy to recognize (persisting coughing leading to vomiting, vertigo).
Care should be taken before diagnosing psychogenic vomiting (anxiety of death, repeated medication intake, fear of suffering), which should only acknowledged after the elimination of other causes.
Vomiting complications
They only occur with repeated vomiting:oesogastric burning which might lead to Mallory-Weiss syndrome (oesophageal hemorrhage),
false passage with deglutition pneumopathies,
metabolic complications: dehydration, alcalosis, renal insufficiency,
impossibility of administrating oral medication (a major hindrance during palliative care),
diet problems: wasting, despair, necessity of parenteral hydration (SC or IV).
Treatment
Treatment depends on the cause.Firstly, the physician should eliminate a surgical indication, responsible radiotherapy or medication.
Sometimes, vomiting is not frequent and should be respected in order to avoid over-prescription. Vomiting due to morphine is generally transitory.
The main available drugs act either:
on the trigger zone:
antidopaminergic: phenothiazine, haloperidol, metoclopramide, domperidone,Constipation:
antiserotonin from the setron family.on the vomiting centre (and vestibular centres)
antihistaminic: diphenhydramine, promethazine,on the digestive tract itself
anticholinergic: scopolamine
antiserotonin, antidopamin and anticholinergic medications may be useful (see above),
prokinetic medications may also be used: metoclopramide, domperidone, alizapride.
Definition
Although invalidating and apparently evident to everyone, it is difficult to scientifically define constipation:it may be reduced defecation frequency (but 5% of healthy persons only pass stools three times per week),
Whatever the definition, constipation is an obsession for bedridden patients, particularly during the terminal phase, involving constant abdominal discomfort. More than 65% of patients suffer from constipation.it may also involve difficult defecation (long and strenuous defecation)
Causes
During palliative phases, many causes are encountered:low motility (little walking),
frequent bedridden periods,
opioid intake (and other constipating medication such as anticholinergic drugs),
poor feeding: frequent dehydration and poorly hydrated diet,
pain provoked by defecation of hard stools (patients fearing to pass stools) provoking intracranial hypertension, muscular pain, anal fissure, haemorrhoid.
Diagnosis
Precise diagnosis is necessary before treatment. It is based on:rectal examination: is the rectum empty or is there a fecaloma (potentially provoking pseudo-diarrhoea),
abdominal examination: presence of peritoneal carcinomatosis or of a ballooned abdomen.
Treatment
Preventive treatment
Prevention of constipation is essential as soon as a patient is bedridden. It is done through:
quality hydration (per os if possible),
patient mobilisation as often as possible,
adding fibres to diet,
regular intake of fruits, prunes,
systematic laxative prescription with morphine like analgesics.Curative treatment
A simple diagram based on the stool consistency may be proposed:
hard stools
They should be treated by a stool softener (stimulating peristalsis on an obstruction can only increase pain):
soft stoolsliquid paraffin (with various taste enhancers),
docusate,
lactulose.
They can be treated with peristaltic drugs:
Use of rectal laxatives (like bisacodyl) may be interesting for fecaloma but these products rapidly provoke irritation.anthracenes (senna),
polyphenolics (bisacodyl).
If necessary, manual evacuation of a fecaloma can be performed under light sedation.
Respiratory disorders:
The main respiratory disorders observed during the palliative phase are:
Other respiratory disorders are mainly observed during lung cancer:Dyspnoea,
Coughing,
Bronchial congestion.
Dyspnoea:Superior vena cava syndrome
Haemoptysis,
Pleural effusion,
Proximal airway obstruction.
Definition
Dyspnoea or shortness of breath is a subjective, toilsome and agonising sensation of suffocation. It induces major modifications in respiratory rhythm and respiratory time ratio.
It is difficult to quantify but is generally a poor prognostic factor.
Physiopathology
Several effectors are involved during dyspnoea modifying respiration:
- central chemoreceptors (acidosis),
- peripheral carotid and aortic chemoreceptors sensitive to hypoxia,
- thermoreceptors of the superior airways,
- bronchial and pulmonary mecanoreceptors (which may be sensitive to opioids),
- muscle mecanoreceptors (diaphragm and thoracic muscles)..
Etiology
Several causes are easy to diagnose (and sometimes to treat):
- pneumopathy (decubitus pneumopathy, superrinfection pneumopathy or due to oesotracheal fistula),
- pleural or pericardial effusion,
- airway obstruction through adenopathy, metastasis or primitive lung tumour,
- lymphangitis carcinomatosous (particularly during breast cancer progression
- anaemia,
- cardiac or vascular disease (acute or subacute pulmonary oedema, pulmonary embolism),
- ascitis,
- phrenic paralysis.
Aetiological treatments
Tumour obstruction justifies (when feasible) chemotherapy or decompressive radiotherapy. When an isolated bronchial or tracheal obstruction exists, laser treatment may clear the airway for at least a period of time. Another efficient method may be the insertion of an endoprosthesis.Infectious pneumopathies require antibiotics that are well adapted to germs.
Effusions may be punctured (except in genuinely terminal phases).
Anaemia may be corrected by blood transfusion or erythropoietin injections.
Symptomatic treatments
Several treatment modalities are useful:Morphine is a good treatment for dyspnoea. The following effects are described:
reduced receptor sensitivity (implied in the dyspnoea sensation): the signal is cut if the clinical situation cannot be improved,
reduced respiratory rhythm (reduced dead space),
reduced muscle fatigue generating dyspnoea anxiety,
reduced cardiac rhythm with reduced reactional hypertension on the peripheral and pulmonary circuit.
Precise monitoring of respiratory function is mandatory (to avoid overdosage).
Corticosteroids are major adjuvant drugs..
Scopolamine helps to reduce bronchial hypersecretion.
Anxiolytic drugs reduce anxiety and respiratory frequency.
The use of oxygen is highly debatable: many caregivers prefer using fresh air, sitting the patient in front of a window, for fear of a paradoxal effect of oxygen (stopping the respiratory stimulus),
No precise study has ever demonstrated the interest of oxygen but patients and their families often request it.other caregivers use it at low concentration.
Coughing:
Principle
Coughing is a reflex mechanism that protects airways: it should therefore theoretically be respected.
However, when it becomes chronic and when no aetiological treatment is available, coughing can lead to dyspnoea, muscle pain, insomnia, vomiting or even conjunctival or nasal haemorrhage or headache.
It is exhausting for the patient.
Physiopathology
Many sensitive zones provoke coughing and any lesion of these structures may result in severe coughing:larynx and cavum,
trachea,
bronchi,
pleura and pericardium.
Aetiology
During palliative care, coughing may result from:The initial pathology
bronchopulmonary carcinoma, mesothelioma, neoplastic pleural effusion, lymphangitis carcinomatosisA complication of the initial pathology
(coughing may be the revealing symptom)
superinfectious pneumopathy,
pulmonary embolism,
atypical acute oedema,
iatrognic (chemotherapy induced) or spontaneous cardiac insufficiency.
Aetiological treatments
Same reasoning as for dyspnoea: all feasible treatment is administered.
Symptomatic treatments
Two different situations:Cough producing sputum (see next page on bronchial effusion)
When the patient is able to cooperate:Dry cough
If patient can no more cooperate::physiotherapy,
fluidifying nebulisation (or hydration with a nebuliser): acetylcysteine, dornase alpha,
fluidifying agents by general route: bromhexine,
regular aspiration
use of drying agent to reduce mucus production:
opioid, (see below),
antihistaminic and anticholinergic: alimemazin, dexchlorpheniramine or sodium cromoglicate
use of β-2 mimetic bronchodilator agents:
opioid cough suppressanteither by general route or by inhalation: terbutaline, salbutamol,
non opioid cough suppressantmainly codeine,
if the patient is already receiving opioids for pain, the dose could be increased (up to 50%) then decreased when coughing is under control.
high dosage corticosteroids (for treating the irritation of pleura or diaphragm by the tumour),dextromethorphane bromhydrate , clobutinol,
local anesthetic: lidocaine or bupivacaine, with all the required care to avoid false passages (the effect on coughing lasts longer than the anaesthetic effect on deglutition).
Bronchial congestion :
Definition
Bronchial congestion is in relation with abnormal production of bronchial mucus with or without coughing.Clinical aspects
The circumstances of bronchial congestion together with the aspect of sputum enable us to distinguish the origin of bronchial congestion:simple chronic bronchitis (non-puriform expectoration),
infectious bronchopneunomathies (puriform expectoration),
vomica of pulmonary abcess with or without blood
Treatment
Strong antibiotherapy should be instituted in the case of pulmonary infection.Otherwise, treatment is the same as for coughing.
If the patient is able to expectorate
Coughing should be respectedIf the patient is unable to expectorate
If the patient can cooperate: regular suctions should be performed, either with a tube or during fibroscopy,
If the patient is exhausted (or in terminal phase): mucosa must be dried:
scopolamin butylbromure or bromhydrate used in patch form, offering rapid sedation for around 4 hours,
atropine (in nebulisation).
Superior vena cava syndrome :
Aetiology
Superior vena cava syndrome is related to cancer in almost 90% of cases and especially to lung cancers (among them small cell carcinoma).Other frequently responsible cancers are: lymphoma, breast cancer, mediastinal geminal tumours, thymoma and various others.
Due to the anatomical configuration, superior vena cava syndrome is observed four times more frequently on the right.
Differential diagnoses are rare: idiopathic mediastinal fibrosis, histoplasmosis, venous thrombosis related to a catheter or surgery. In fact, all pathological processes which invade or destroy the lymph structures of the superior mediastinum may provoke an obstruction to the return of venous blood and thrombosis.
Clinical presentation
Its onset is generally insidious.Its severity depends on:
- rapidity of the obstructive process,
- thrombosis syndrome,
- precise location of the obstruction,
- possibility and rapidity of the constitution of collateral circulation.
The revealing patient complaint is dyspnea, coughing, headache and facial swelling. Then, neck, chest and upper limb swelling is observed. All of these symptoms are worsened when the patient bends forwards. Diagnosis is evident as soon as this is evoked.
In reality, the development of superior vena cava syndrome is rarely acute (most often neglected). Half of the patients reveal their cancer through this syndrome. Chest radiography and thoracic scan are the best imaging procedures before a diagnostic biopsy.
You can view a typical case of superior vena cava with thrombosis and important collateral circulation.
Treatment
Most cancers, which are discovered via this syndrome, are more and less chemosensitive (small cell lung cancer, lymphoma, germ tumours). Chemotherapy is therefore the choice treatment. In less chemosensitive tumours, radiotherapy may be a good palliative option.Other palliative measures are semi-seated position, rest, oxygen and short courses of corticosteroids.
A poor response to aetiological and palliative treatment suggests concurrent thrombosis which may require further anticoagulant treatment.
Unfortunately, most superior vena cava syndromes relapse since underlying cancer is not cured by treatment (lung cancer). The use of intravenous stents has been suggested in order to avoid acute complications.
Hemoptysis:
Small and moderatly abundant hemoptysis
They generally do not necessitate specific emergency measures. Bronchofibroscopy may permit finding the origin of hemoptysis and potentially propose a specific treatment (even in palliative non terminal phase).For instance, local treatment by pulmonary artery embolisation or by laser or by endobronchial brachytherapy or by external radiotherapy and if necessary and feasible a simple surgical intervention.
Massive hemoptysis
Massive bronchial haemorrhage (hemoptysis) is rarely involved in patient death in lung cancer. The flooding of the bronchial tubes is far more life-threatening than the actual quantity of blood lost.The most frequently concerned cancer is epidermoid lung cancer since it invades blood vessels and is highly necrotic.
Another frequent cause of hemoptysis is pulmonary aspergillosis which often occurs in immunodeprived patients (after prolonged chemotherapy).
More rarely, hemoptysis is related to therapy (laser, endobronchial brachytherapy).
Treatment includes very simple measures such as adopting a semi-seated position, oxygenation, aspiration, and a rapid search for the aetiology (bronchosopy if the patient’s status permits).
In terminal hemoptysis, patient anxiety should be relieved (subcutaneous morphine, midazolam), and a carer/family member should remain at the patient’s bedside until sleeping.
If no efficient aetiological treatment is possible (surgery for instance), various techniques have been proposed such as a Fogarty catheter, arterial embolisation, radiotherapy or laser beam.
Pleural effusion:
Clinical aspects
The main clinical symptoms of pleural effusion are dyspnoea, coughing and thoracic pain. Diagnosis is established on clinical examination by percussing and sounding the patient's thorax (X-ray chest radiography corroborating the clinical diagnosis).The causes are not always related to cancer:
All cancer types may provoke pleural effusion, which generally relapses after puncture. The most frequent localisations are:left ventricular insufficiency,
atelectasis,
pulmonary embolism.
bronchopulmonary cancer,
breast carcinoma,
lovarian carcinoma,
mesothelioma.
Puncture
Evacuating pleural effusion by puncture allows confirmation of diagnosis and offers information for determining aetiology.
It is a very interesting therapeutic procedure since it generally relieves patient dyspnoea very rapidly.If pleural effusion is massive, the first evacuation should generally be limited to approximately one litre in order to prevent a feared 'a vacuo' pulmonary oedema.
Even during the preterminal phase, an evacuating puncture may offer genuine relief to the patient.
Talc pleurodesis
Long before the terminal phase, the patient will be profoundly affected by the often rapid relapse of pleural effusion, involving pain but, more importantly, increasing dyspnoea. The patient's quality of live and relative well being are therefore considerably altered.In these cases, talc pleurodesis may be performed:
The major hindrance to complete pleurodesis is a multiple partitioned effusion: in order to obtain a large diffusion of talc into the pleural cavity, pleural effusion should be relatively abundant before the procedure.either by the thoracic drain (blind pleurodesis)
or during pleuroscopy.
This therapeutic procedure is well tolerated, and is generally not painful. It is a rapid procedure with a low rate of benign complications (light fever during the first 48 hours).
Efficiency is very high since pleural drainage may last several months for 90 to 95% of patients. This procedure should therefore be proposed when potential survival is above one month.
A few contraindications should be respected: non re-expanding lung (after puncture), lung having lost its elasticity through lymphangitis carcinomatis or severe post-radiotherapy sclerosis or when diffuse pleural metastases are present.The major hindrance to a complete pleurodesis is a multiple partitioned effusion: in order to obtain a large diffusion of talc into the pleural cavity, pleural effusion should be relatively abundant before the procedure.
Proximal airways obstruction :
Clinical aspects
Proximal airway obstruction is most often a respiratory emergency: there are no obstructive symptoms until the tracheal or main bronchial calibre is reduced by more than 80%.Main symptoms include: bradypnea, stridor (inspiration with acute noise), crowing noise, wheezing and symptoms of obstructive pneumopathy.
Except in the very last terminal phase, rapid relief should be offered to the patient (even if only for a few months).
Therapeutic modalities
Surgery should remain exceptional (at the very onset of disease).Chemotherapy is rarely efficient except on lymphoma and small cell lung carcinoma (at the onset of disease).
Yag laser beam
The procedure is performed through a flexible fibroscope.Its efficiency is immediate.However, obstruction should be symptomatic and no longer than 4 cm along the bronchial tree.
The endoscopist should be able to perceive the bronchial hole and the downstream lung should be functional.
Laser is not indicated for extrinsic compression or in the case of an oesotracheal fistula.
Endoprosthesis
Here again, efficiency is immediate.
The endoprosthesis is installed through endoscopy.It is efficient on extrinsic compression, however stenosis should not be wide enough to enable its introduction.
Endobronchial brachytherapy.
Its effect is not immediate.
It can complete the laser action and avoid relapse for patients with longer survival prognosis (a few months) and can be performed even after external irradiation.Other local techniques may be used (such as phototherapy, cryotherapy, thermocoagulation) which are very useful in the experienced hands of physicians working with a palliative intent.
Urinary disorders :
Urinary disorders are very frequent during palliative care. They may be related to the patient's progressively altered general state and to certain necessary drugs. They may also be related to genital or urinary cancer.
Physiology of micturition
Notre vessie comporte deux sphincters : Our bladder has two sphincters:internal sphincter, intimely related to bladder muscles (detrusor), with an innervation which is:
sympathetic (through hypogastric and lumbar nerves, and whose neurotransmitter is adrenalin),
parasympathetic (through pelvis nerves originating from S2-S3).
Bladder distension stimulates mechanical receptors inside the bladder wall and provokes a motor parasympathetic response with the contraction of bladder muscles and the opening of the internal sphincter.
external sphincter
constituted by striated muscle fibres originating from pelvic floor (distal region of prostate in men and median third of urethra in women).
The external sphincter is controlled of nerves originating from the sacrum (pudental nerve).
For a normal micturition, three elements are necessary:
a free passage from the bladder to the urethral meatus, tonic bladder wall muscles (muscle contraction for micturition),
a good neurological coordination.CONTENTS:
Incontinence,
Acute urine retention,
Ureteral bilateral compression and urinary stoppage,
Ureteral unilateral compression,
Urinary fistula.
Incontinence :
There are several forms of incontinence within the palliative setting. A urologic consultation is often advisable.
Total incontinence
Total incontinence is related to complete sphincteric incompetence. Three main pathologies may be responsible:Endoscopic examination or urodynamic evaluation are rarely necessary in a palliative setting.tumour invasion,
previous surgical procedure,
neurological damage of spinal or nerve root
Treatment usually involves the use of an indwelling Foley catheter in female patients and condom drainage or penile clamp in male patients (and, if required, also a Foley catheter).
The complicated surgical interventions and rehabilitation required for artificial sphincters are most inappropriate in palliative settings.
Overflow incontinence
Strictly speaking, this is not incontinence but an acute urine retention . The bladder is full as demonstrated by percussion or palpation .Urgency incontinence
The bladder musculature in this type of incontinence is normal: the detrusor muscle is too active for a too weak urethral sphincter tonicity. The urge to urinate is so pressing that the patient cannot control it and urinary loss may be abundant. Bedridden patients are often incapacitated to such an extent that they cannot reach the toilet in time.In palliative cancer setting, the main causes are:
a tumour close to the trigone (bladder, prostate, cervix),
inflammatory reaction of the bladder wall related to irradiation, post-chemotherapy bladder irritation or infection.
Such incontinence may be treated by anticholinergic drugs such as oxybutynin to reduce detrusor activity.
Stress incontinence
This type of incontinence is rarely of concern in a palliative setting. It involves minor involuntary urethral loss when coughing, sneezing, jumping, laughing, standing or walking.In patients with good prognosis, treatment may involve sphincter surgery. In palliative care, parasympathetolytic drugs such as flavoxate, trospium or tolterodine or possibly low doses of tricyclic antidepressants (imipramine) can be used.
Acute urine retention :
Diagnosis
Diagnosing acute urine retention is simple when faced with an agitated patient (particularly a semi-comatose patient). It simply requires percussing and palpating the suprapubic abdominal wall.Occasionally, diagnosis should be made before the appearance of overflow incontinence: the patient cannot avoid micturition with a full bladder due to retention.
Investigation of the cause should involve:
clinical examination of urethral meatus and urethra to discover any evident mechanical obstruction,
prostate examination,
neurological examination looking for cord compression,
looking for metabolic disorders (such as hypercalcaemia).
Causes of major urinary retention in a palliative setting
prostate hypertrophy (benign or malignant),
neurological lesion (paraplegia) related to bone or meningeal metastases, with atony of bladder muscles,hypertonic internal sphincter (organic lesion of paraympathetic nerves).
hypercalcaemia,
use of anticholinergic drugs (such as phenothiazine, haloperidol, antihistaminic, cyclic antidepressants),
constipation may also compress urethra in a bedridden patient.
Treatment
Treatment should bring the return of a normal urinary flow:either by a suprapubic catheter (non-infected urine, acute and short-lasting situation),
or urethral Foley catheter,
modifications in medication (if necessary)
surgical treatment if the patient's general status is good (stent, prostatic resection).
Unilateral ureteral compression :
Unilateral ureteral compression is most often asymptomatic. It is revealed during systematic examinations (ultrasonography or TDM) which are part of the usual post-therapeutic follow-up procedures.
However, major pain may occur in relation to pyelic or renal calyce dilatation.
It is often related to retroperitoneal uni- or bilateral sclerosis due to previous radiotherapy.
Sometimes, pelvic cancer can be discovered by ureteral dilatation.
Symptomatic treatment is ureteral derivation .
If dilatation cannot be satisfactorily reduced, and when major clinical complications are involved (repeated pyelonephritis) with poor unilateral renal function, if the other kidney is functional, and within a palliative setting, it may be possible to propose unilateral nephrectomy which is a simpler surgical act than ureteral reimplantation.
Urinary fistula :
Urinary fistula is one of the most devastating complications of cancer during palliative and terminal phases. The psychological consequences of such total incontinence often lead to complete patient (and family) discouragement.
Vesicoenteric fistula
Vesicoenteric fistula is generally in association with a colic pathology.Symptoms are emitting of foul smelling urine, passage in urine of gas or froth or even feces.
Most often, repetitive severe urinary infections are observed.
Cystoscopy reveals an oedematous zone with gas or feces emission at the fistula mouth. This opening is generally very small and difficult to find.
The best treatment (when feasible) is surgery (intestinal or colic resection) and should be attempted.
In a purely palliative setting, colic diversion (colostomie) may be proposed to dry the fistula.
Vesicovaginal fistula
Generally occurs during gynaecological cancers, either as a complication of local disease progression or after radiotherapy or salvage surgery (non standard conditions).
Clinical diagnosis is simple, with urine in the vagina, and is confirmed by cystoscopy. Pyelography enables the elimination of a ureterovaginal fistula.Urinary diversion (urethral catheter reducing intravesical pression) may lead to healing when the fistula is not a complication of progressing carcinoma.
When no local cancer progression is evidenced, surgical treatment of fistula may be proposed (epiploic flap technique).
In rare cases, bilateral ureteral diversion may be proposed.
When surgery is contraindicated (palliative terminal care) and catheterism is inefficient, a vaginal pack may be a temporary solution.
neurological disorder:
A neurological disorder is a disorder of the body's nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord, or in the nerves leading to or from them, can result in symptoms such as paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be revealed by neurological examination and studied and treated within the specialities of neurology and clinical neuropsychology.
Neurological disorders are very frequent during palliative care.
They can concern all parts of nervous system:
Spinal cord compression,
Leptomeningeal metastases,
Skull base invasion,
Radiculopathies, Brain metastases.
Spinal cord compression:
Spinal cord compression is a genuine therapeutic emergency.
Living the last months of life bedridden, motionless and completely dependent upon carers, is a terrible agony for patients that we should endeavour to avoid through early diagnosis and rigorous treatment.
Spinal cord compressions may be due:
The differential diagnoses are other compressive cord lesions: abcess, haemorrhage, discal lesion, lipomatosis, narrow lumbar spinal canal, all of them also representing emergencies.
- either to an extrinsic compression of epidural space (by a bone metastasis or invasion of adjacent soft tissues),
- or less often by intradural invasion (tumour-like carcinomatous meningitis),
- or even less often by intramedullary invasion.
Clinical diagnosis
Clinical diagnosis requires expertise and alertness on the part of caregivers (particularly home caregivers and general practitioners): most often, the revealing symptoms of this neurological catastrophe are present a few weeks before it occurs.The following symptoms may appear (not necessarily all of them or in the following order):
A rigourous neurological clinical examination should be regularly performed in order to diagnose cord compression:
- onset of vertebral pain or its modification (in location and/or occurrence circumstances),
- appearance of Lhermitte's sign (lightning pain in limbs provoked when the neck is bent forward),
- onset of belt-like pain,
- onset of sensitive deficiency below the pain with an evocative level,
- onset of sphincter modifications (urine retention, recently appeared constipation),
- appearance of minor (then increasing) motor palsies typical of cord lesion.
This is a genuine emergency for which the best paraclinical examination is RMI (probably THE rare emergency indication which should be performed before all others).
- more or less important motor weakness,
- hypertonicity,
- positive Babinski's sign,
- sensitive deficiency (research of a precise level).
Treatment
It should be administered as quickly as possible.A unique lesion, in most cases, is a good indication of neurological decompression surgery.
The quicker the surgical intervention, the larger patient's chances of recovering normal function. Even if long term prognosis is unknown, such surgery should be performed.
After 12 to 18 hours of complete palsy, the patient has lost most of his/her chances of function recovery.
Localised radiotherapy associated with corticosteroid therapy may be very efficient in association with surgery, or when surgery is not feasible..
Leptomeningeal metastases:
They are caused by the dissemination of cancer cells into the subarachnoid space. Cancer cells reach the meningeal spaces:
- via the general circulation,
- by infiltrating perineural spaces along nerve roots,
- by direct invasion of epidural spaces,
- by diffusion from brain metastases.
Clinical symptomes
They are very diverse:Diagnosis is generally made by lumbar puncture: cytology reveals cancer cells in cerebrospinal fluid (with frequent increased fluid protein and decreased glucose concentration).
- various neurological disorders,
- radicular-type pain,
- headache and hydrocephalus (in relation to spinal fluid circulation disorders).
RMI with contrast enhancement may reveal localised menigneal tumours which can be irradiated.
Treatment
Treatment involves high dose general corticotherapy and, if feasible, general chemotherapy.Local intrathecal chemotherapy remains a subject of controversy (particulary due to its meningeal toxicity), but it may provide very impressive remissions.
Radiotherapy of the whole spine has been proposed, however, generally speaking, more localised radiotherapy is prescribed in zones where tumour development is more intense.
Prognosis
Prognosis remains severe.Without treatment, patient survival is limited to a few months.
When the aetiological treatment is efficient, impressive remission may be obtained with a mean duration of 20 months.
Skull base lesions :
Lesions of the base of the skull are most often combined with carcinomatous meningitis (particularly metastases from breast or prostate carcinoma).
However, a continuous local head and neck cancer invasion may be observed.
Symptomatology is generally dominated by more or less localised headache and a neurological syndrome in relation to the cranial nerve concerned.
Diagnosis is generally performed by TDM using both bone and brain windows.
Treatment is mainly localised radiotherapy of the tumour lesion.
Most frequent syndromes
Orbital syndromes are characterised by retro-orbital pain, blurred vision, diplopia, ocular palsy, exophtamos.Cavernous syndromes also provoke ocular disorders, particularly hemianopsia and papilloedema.
Middle crania fossa syndrome associated diffuse headache, facial pain and numbness along the distribution of trigeminal nerves, with paroxysmal episodes of lancinating pain.
Jugular foramen syndrome provokes hoarseness and dysphagia, and various palsies (IXth , Xth, XIth , XIIth nerves) or Horner's syndrome (myosis, palpebral ptosis, enophtalmia, unilateral sweating).
Occipital condyle syndrome with frequent nuchal stiffness and palsy of XI th and XII th nerves.
Glossopharyngeal nerve infiltration (by head and neck cancer) provokes pharyngeal pain, with severe irradiation to ear (aggravated by swallowing and associated with syncopes).
Trigeminal nerve infiltration provokes dull, constant facial pain with paroxysmal episodes of throbbing or lancinating pain.
Treatment
When feasible, radiotherapy may bring relief, although, in most cases, it has already been adminstered and repeated doses may become dangerous.Patients concerned should request specialised pain consultations since their relief is most often difficult to obtain.
Radiculopathies:
General remarks
Radiculopathies are generally provoked by a leptomeningeal invasion or by a metastatic bone compression of nerve roots (or other paravertebral lesions).Pain is generally focalised on the compression zone and irradiates according to the neurological distribution. If necessary, an electrophysiological study may be performed in order to better distinguished polyradicular lesions from plexic lesions. TDM and RMI are also useful imaging examinations.
Sometimes, herpes zoster may be considered, particularly in immunodeprived patients after chemotherapy. Looking for typical vesicles is good clinical practice. A good knowledge of clinical history may help to detect post-herpetic neuralgia in elderly patients.
Cervical plexopathy
Frequent in head and neck cancer or in relation with metastatic nodes,
They provoke intense local pain, with very severe irradiations in the retroaurical region, the back of the neck, the shoulder or the jaw.They often complicate severe skin and soft tissue sclerotic disorders related to previous surgery and radiotherapy.
CT and RMI should detect potential local relapse.
Their treatment is difficult (frequent severe and relapsing neuropathic pain).
Brachial plexopathy
Frequent, brachial plexopathy is often related to breast carcinoma, lung cancer or lymphoma.
The nerve may be compressed either in the axilla or in the supraclavicular region.Pain is typically neuropathic, with anaesthetic zone, paresthaesia and hyperesthaesia.
A precise study of pain or anaesthesia location enables the precise determination of the incriminated root.
Specific serial TDM sections are necessary to study the incriminated zone.
When plexic pain is due to a tumour progression, irradiation (when feasible) brings good relief. However, in post-radiotherapy or post-surgical pain, treatment is difficult and should be entrusted to specialized pain team.
Lumbosacral plexopathy
Frequent during rectum carcinoma, cervix uteri cancer, bladder or prostatic cancer.
It provokes pain located in the back, buttock, perineum and lower limbs.Pain is lancinating with excruriating paroxysms but rarely a burning sensation.
Other neurological disorders are often associated: perineal saddle sensory loss, motor and sphincter disorders, lower limb oedema.
Most often, this pain is related to cancer progression (rarely a complication of the treatment like for cervical or brachial plexopathy).
Precise radiological study with TDM or RMI sometimes enables further irradiation if possible.
If not, these patients need to be entrusted to a specialised pain team.
Skin disorders:
Skin disorders are very frequent during palliative care.
Skin is the most exposed organ of our body. Skin disorders may become major problems for patients during the terminal phase. Specific attention to skin should be paid by caregivers (particularly physicians who often spontaneously delegate this pathology to nurses), in order to avoid major pain (physical and psychological pain), a consequence of skin lesions.
Skin is a natural barrier avoiding the transmission of microbes inside the organism: clean skin and regular body care avoiding maceration are simple ways to avoid many of the general infections observed at the end of life. On the contrary, local irritation may represent the basis of any local and potentially generalised superinfection.
Skin is also the area of thermal exchange between the constant internal temperature (around 37°C) and external thermal variations. Good skin circulation enables the correction of such divergent temperature. Major skin lesions may modify these exchange possibilities (particularly near pressure points).
Skin is a very sensitive organ with several nerve terminations. Skin lesions are often very painful. These nerve terminations are most important for maintaining skin trophicity, thus explaining trophicity modifications observed during herpes or diabetes lesions.
Skin has an excellent power of regeneration (wounding and repairing), requiring a regular well furnished blood supply. Irrigation disorders (for instance through lengthy pressure in more or less conscious patients) will rapidly lead to trophic skin lesions and bedsores.
The following pages deal with:
Paraneoplastic skin syndromes,
Pruritus,
Sweating,
Treatment of skin lesions,
Bedsores,
Skin tumours.
| Paraneoplastic skin syndromes: |
The most frequently observed cancer-related lesions are skin metastases (breast, permeation nodules, tumour fistula). Other skin manifestations are known as paraneoplastic syndromes:
Dermatomyositis
which can complicate many other cancer localisations,
with its typical lilac-coloured (heliotrope) erythema over the bridge of the nose, the orbital regions, cheeks, forehead, with lilac-coloured lines on the hands and fingers (particularly around the nails). The muscular syndrome is more or less severe, and more pronounced on proximal muscles. Treatment involves treating the tumour and is completed by corticosteroids.
Other paraneoplastic syndroms
Breast Paget's disease : eczema of the nipple,
Acquired ichtyosis during Hodgkin’s disease,
Acanthosis nigricans (hyperpigmentation seen on the axilla and hyperkeratosis of skin folds) during digestive cancers,
Erythema gyratum repens,
Acquired hypertrichosis lanuginosa (face hair during pulmonary and digestive cancers).
Pruritus:
Pruritus or itching is a cutaneous sensation leading patients to regularly and severely scratch either because of a skin lesion or in the absence of any skin lesion. Scratch lesions may occur if pruritus is severe. Pruritus can be of moderate intensity and is generally and well tolerated, however it can also be intense involving considerable discomfort for the patient.
Pathophysiology
Many external stimuli (physical or chemical) can provoke pruritus but also endogen stimuli (such as histamine, proteases, prostaglandins or neuropeptides). On the skin, pruritus is sensed by nociceptive unmyelinated fibres C (free endings) quite different from myelinated A fibres which transmit pain sensation. The influx conduction is relatively slow. Endogeneous pruritus is less characterised for its nervous conduction system.Pain and pruritus do pass through the same neurological networks. At medullar level, opioids generally provoke a pruritus sensation whereas naloxone (opioid antagonist) has an anti-pruritic effect. Pruritus related to cholostasis is well controlled with anti-5HT3 treatment.
Pruritus classification
Primary pruritus
Primary pruritus is pruritus for which dermatological disease has been excluded. The main causes are:
biliary hepatic or pancreatic disease (in association with cholostasis) renal insufficiency and uraemia, various drugs (opioids, amphetamine, cocaine, aspirin, etc..),
endocrine disease (diabetes, hyperparathyroidism, thyroid disease),
haematopoietic diseases (Hodgkin's lymphoma, non Hodgkin's lymphoma, fungoid mycosis, mastocytosis, multiple myeloma, polycythaemia vera),
malignant tumours (breast, stomach, lung, carcinoid syndrom),
infectious diseases (syphilis, parasitic infection, HIV, candidiasis),
neurological disorders (distal small fibre neuropathy, tabes dorsalis, multiple sclerosis, psychosis, etc..).
In theses diseases, a liberation of mediators (such as proteases or histamine) leads to generalised and intense itching.
Secondary pruritus
Is associated with dermatological diseases
Treatment
Topical treatment
Topical treatments should be applied in case of localised pruritus or a localised region with accentuated itching. A number of preparations are active although generally for a short period of time (phenol, menthol, camphor, diphenhydramine, lidocaine, isothipendyl, local anti-inflammatory drugs).
Daily skin care is important in order to avoid scratch lesions: nails should be cut short, cool baths should be taken, soothing milky ointments should be applied, light clothes (no wool or synthetic) should be worn, including possibly humid cotton clothes which can be changed several times per day.
General medications
Among the various drugs proposed:
non-sedative antihistaminic (non anticholinergic) or sedative drug,
opioid antagonists (naloxone),
serotonin antagonists (ondansetron, granisetron),
thalidomide,
anaesthetic agents (propofol),
rifampicine is used during severe cholostasis.
Icteric pruritus (for example in pancreas cancer) is rapidly relieved by internal biliary diversion.
Sweating :
Sweating is a physiological function of the human skin regulating body temperature by aqueous evaporation. Except in the rare hereditary disease 'anhidrosis' (absence of development of sweat glands), infants and the sedentary elderly may have thermal regulation disorders in relation to inefficient sweating.
Regulation of sweating depends on the autonomic neurological system and is coordinated by vasodilatation (or vasoconstriction for intensely cold temperatures). Palms and soles have a basic sweat pattern which is increased by psychological stress. Other body regions (axillary, forehead) may also sweat without any increase of external temperature.
Excessive sweating or hyperhidrosis may be either localised (in neurological disorders) or generalised (pheochromocytoma, hyperthyroidism, diabetes, acromegaly, menopause, tuberculosis, lymphoma, endocarditis). Most often, sweating is related to a chronic infection which can be treated.
Discovering the cause of important sweating can help to determine efficient treatment.
Hot flushes may be a major problem for women treated for breast carcinoma with early menopause as well as for men with prostate cancer treated by hormonal therapy. Non hormonal treatment of these forms of sweating is not always efficient.
During the terminal phase, abundant sweating may appear in patients constituting major discomfort. Symptomatic treatment with cimetidine may be useful.
Skin lesions treatment :
In the terminal phase (and unfortunately sometimes far earlier), major skin lesions can be observed, either in the form of deep craters, scars or fungating tumours. These lesions are most often painful, foul smelling and exudating. They require repeated treatment which can be difficult for the caregiver to perform and may give rise to a barrier between the patient and his/her family.
Dressings
Dressings are the major part of treatment. They are often very painful for the patient: light sedation (for instance subcutaneous morphine) should therefore be administered before placing dressings.
The wound should first be cleansed (if necessary an infectious lesion should be treated by systemic medication) and excessive exudates should be evacuated.
The dressing should not adhere to the wound (numerous 'fat' or 'humid' dressings) but should allow high humidity to be maintained to obtain cicatrisation and should allow correct oxygenation of tissues whilst simultaneously being impermeable to bacteria.
Finally, a good dressing should be as comfortable as possible.
Fighting wound foul odors
Foul odours lead to a profound feeling of dishonour and to social withdrawal. Occasionally, odours are so intense that caregivers have great difficulty in hiding their distaste. The psychological consequences for patients are immense.
Most often foul odours are due to necrosis and superinfection. Treatment using metronidazole gel may be indicated.Other treatment modalities are dressings with carbon powder.
Sugar (honey and icing sugar) is another treatment for foul wounds.
Treating fistula
Fistula also constitutes a major embarrassment and self denigration for the patient (foul odour).
The opening of fistula and surrounding skin alteration are most often painful.You may consult the specific page on urinary and digestive fistula.
Bedsore problems :
Bedsore can be defined as an excavating wound resulting from skin hypoxia provoked by excessive prolonged pressure. Our skin needs a constant regular circulation in order to maintain its normal trophicity.
Bedsores will therefore develop at usual pressure zones when the patient lies or sits fro long periods, particularly on the buttocks and heel.
During excessive prolonged skin pressure, the progressive stages of skin lesions may be observed
 | Epidermis |
| Dermis | |
| Hypodermis | |
| Fascia and Muscle Bone with articulation. |
- Diagram of normal skin stage 1: erythematosous stage: redness does not disappear when pressed with the finger,
- serous phlycten,
- bleeding phlycten.
stage 3 : necrosis stage: necrosis covering all underlying tissues ,
stage 4 : ulcer stage: the necrosis shield disappears, profound dermis, muscle and bone are denuded.
Many scales have been proposed to evaluate bedsore risk: they generally consider the patient's weight (the risk is greater among slim patients), urinary or anal incontinence, general nutritional state, complete or incomplete immobilisation, possibility to move (even passively) the patient.
The most important treatment is prevention of the constitution of bedsores by:
Once the bedsore has formed, active treatment should be initiated:
- the use of an adapted support allowing a balanced distribution of the patient's weight,
- the use of regular movements,
- the avoidance of dangerous positions promoting skin shearing, particularly on the buttock skin.
Reading of the website recommended above shows the variety and the complexity of available treatments.
- wound cleansing,
- if necessary surgical cleansing,
- adequate dressing,
- fighting denutrition,
- fighting associated diseases like diabetes, infections or incontinence.
There are two major points to consider:
Pain is most often intense in relation to the wound and to inflammatory and infectious phenomena, and requires systematical treatment. Preventing bedsores is a major analgesic measure in palliative care. Pain may be exacerbated during dressing or when moving the patient to reduce permanent pressure. It therefore justifies preventive prescription (subcutaneous morphine).
The patient's psychological suffering is major, in relation to a degrading self-image, foul odours, movement difficulties, constant fatigue, dependence upon carers and shame before family members. The patient feels excluded by his bedsores. This shame is supplemented by the caregivers' shame in not having been able to prevent the bedsore. However, whereas most bedsores can be prevented, even the best preventive measures do not always succeed. The regular evaluation of clinical practice is necessary to ensure progress.
Nutrition and metabolic disorders:
Nutrition and metabolic disorders are very frequent and are of great concern for the patient's family. Seeing a patient eating nothing is, for the family, a great source of suffering, synonymous to imminent death.
Cancer cachexia
Treatment of cachexia
Hypercalcaemia
Hyponatremia
Cachexia or general state alteration including major weight loss is the consequence of both anorexia and evolution of the cancer process. Various factors have been incriminated:Cancer cachexia:
The easiest way to measure cachexia is to weigh the patient although the weight loss may be masked by oedema or effusion (like ascites). A loss of 10% to 20% of normal weight can be observed in cancers of the stomach or the oesophagus. There is a clear correlation between the weight loss observed before treatment and poor cancer prognosis.
- diversion of the normal metabolism by the growing tumour,
- mass effect of the tumour itself as well as secretion of cytokines with a necrotic effect (see above),
- direct effect on the digestive tract (sub-occlusions, absorption disorders),
- previous poor alimentation or under nourishment due to alcoholism and smoking,
- liver metastases (poor metabolism of normal nutriments).
Severe under nourishment may be observed during complicated treatment (such as radiotherapy for head and neck cancers or poorly tolerated chemotherapy). These therapies may have to be temporarily stopped in order to take corrective measures (such as hyperalimentation by nutritive components or IV feeding).
Severe cachexia is frequently observed at the end of life. Major emaciation is due to the disappearance of all muscular and fat masses. The skin becomes very fragile like parchment, dentures become too big for the mouth, the patient becomes skeletal. In such a state of under nourishment, complications arise very quickly: a dry mouth further reduces feeding, the body support zones are the target of necrosis process (decubitus bedsore).
Biologically, such cachexia induces an increased metabolism of lipids and proteins, anaemia (without any clear aetiology), hypo-albuminemia (further inducing oedema), hyponatremia.
Treatment of anorexia :
The main goal of palliative care is to improve the patient's comfort.
Anorexia is an almost constant symptom during the terminal phase of cancer: it is a concern for family members who generally wish to see their patient eating correctly.
Many metabolic factors may promote anorexia during the terminal phase: among which, TNF secretion (Tumour Necrosis Factor) and various Interleukin factors. Moreover, anorexia is a sign of the chronic depression which is observed in most patients at the end of life. Finally, local organic causes will increase this anorexia: chronic constipation, mouth dryness, intracranial hypertension, chronic nausea (in relation to morphine treatment, metabolic abnormalities, analgesic radiotherapy, etc..).
Whereas the patient should be encouraged to eat some food, he/she should not be force-fed against his/her personal will and comfort. Certain carers are tempted to use parenteral nutrition very early on in disease progression: if such nutrition may be useful during acute treatment phases (during radiotherapy or intense chemotherapy, to prepare surgery), it has no place in the terminal phase, since it totally disregards the patient's liberty for only minimal benefit. Randomised studies have shown that parenteral nutrition does not increase patient survival and this aspect should be explained to families in order to calm their anxiety.
A few drugs may be useful. Progesterone derivatives such as megestrol at relatively high dosages (800 to 1,600 mg per day) may have a stimulatory effect on appetite.
Corticosteroids are to be largely employed for their numerous beneficial effects during terminal phase (particularly on appetite).
Practically, very simple therapeutic means may often be sufficient: fractionation of feeding into smaller, more frequent meals, taking care to respect patient taste (meat is not necessary!), treatment of permanent nausea, mouth care.
Anorexia is one symptom of terminal cancer: it should therefore be respected and explained to the patient's family. Giving precise information to family members on the futility of parenteral infusions may reassure them: a French by-word says that 'when appetite is OK everything is OK'. For families, a patient who does not eat, is never going to be cured. Unfortunately, this is the precise truth and one should learn to respect patient anorexia if it is well supported by the patient him/herself (the absence of ravenous hunger crises due to hypoglycaemia). Such respect will facilitate dialogue between the dying person and his/her family.
Hypercalcemia :
Hypercalcaemia is a common manifestation among cancer sufferers: 20 – 40 % of multiple myeloma, 35% of lung cancers, 24% of kidney cancers, 8-10% of breast cancer. Hypercalcaemia generally underlines the poor prognosis of cancer, although new therapies may offer longer patient survival.
Physiopathological mechanisms
There are two different circumstances, whether osteolytic lesions are present or not.If osteolytic lesions are present, then hypercalcaemia is generally a late phenomenon underlining poor prognosis. Hypercalcaemia induces symptoms that should be corrected with efficient palliative care.
Many hypercalcaemia appear without any osteolytic lesions and are therefore true paraneoplastic syndromes possibly due to several mechanisms:
There is no clear relationship between the presence of bone metastases and the elevation of serum calcium: some diffuse metastases, with major mechanical complications, never produce hypercalcaemia, whereas some very evolutive hypercalcaemia, difficult to reduce, have normal imaging even with gammagraphy and RMI.
- Production of proteins which bind to the parathormone receptor (PTH-like): in the tumour DNA, a gene expresses a polypeptide (PTH-RP or parathormone related protein) with 70% homology with normal parathormone. This gene is normally expressed in mammary tissue during lactation.
- Myeloma tumour cells produce a factor that stimulates osteoclasts (or OAF: Osteoclast Activating factor) which can be produced by in vitro stimulated normal leukocytes. OAF is one member of a larger family of factors called lymphokines, with lymphotoxine (produced by activated lymphocytes) and TNF (tumor necrosis factor or cachectine) produced by normal monocytes. Both factors stimulate osteoclasts.
- Several lymphoma, bone tumours or sarcoma can induce hypercalcaemia by transforming normal 25-hydroxy-vitamine D into 1,25 – dydroxy- vitamine D (the final active metabolite of vitamine D).
Symptoms
The main symptoms of hypercalcaemia are:Diagnosis is made by calcaemic dosage which should systematically be requested in the case of doubt.
- Anorexia, thirst, constipation or even occlusion,
- Consciousness disorders: fatigue, somnolence, lethargy, coma
- More or less intense dehydration, initially extra-cellular then intra-cellular.
Untreated hypercalcaemia leads to severe dehydration and possibly to patient death by cardiac rhythm disorders.
Biological diagnosis
Malignant hypercalcaemia is easy to distinguish from other forms of hypercalcaemia: generally blood phosphorus is normal or elevated (as opposed to hyperparathyroidism).Treatment
Several treatment modalities have been proposed depending on the clinical severity of hypercalcaemia.However, diphosphonates (in particular intravenous forms) have totally modified such modalities allowing ambulatory treatment over several weeks, with prolonged survival and good quality of life.
The only major point to ensure is correct patient rehydration, if necessary intravenously. Corticosteroids are still useful if hypercalcaemia is very high.
Hyponatremia:
Cancer patients frequently suffer from hyponatraemia, the physiopathology of which is not always clearly understood. Generally, it is fortuitously discovered on a systematic ionogram. However, hyponatraemia increases patient fatigue and can possibly be complicated by somnolence or seizures.
Hyponatraemia is often observed in preterminal stages of severe disease. Patients excrete the sodium excesses administered in order to correct hyponatraemia and liquid restriction leads to more severe dehydration than that already observed. Surprisingly, if patients are able to resume normal eating, a spontaneous correction of hyponatraemia is observed.
Thus, this preterminal hyponatraemia should be distinguished from an inappropriate secretion of ADH which is a genuine paraneoplastic syndrome (occurring in lung cancer for instance). Hyponatraemia leads to severe neurological disorders and to an exaggerated water excretion by the kidney (excessive urinary osmolality). In such cases, fluid restriction is useful, but more particularly the treatment of cancer, where possible, will improve the clinical situation.
Another frequent cause of hyponatraemia in cancer patients is the presence of oedema leading to a dilution syndrome. Such a clinical situation can be observed when ascitis or major pleural effusion occur. Whereas symptomatic treatment (ascitic puncture, diuretics) may be useful, only aetiological treatment will actually correct hyponatraemia for a reasonably long time.
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