pathology of smoking and smoking related disorders
Smoke carcinogens:
- Initiators: benzopyrenes
- Promoters: phenol derivatives
- Radioactive substances: polonium, C14, K40
Pathogenesis:
- Normal trachea: ciliated pseudostratified simple columnar à smoke injures epithelium à metaplasia to stratified squamous epithelia (protective mechanism to reduce further injury) à mucous dysplasia, loss of cilia and accumulation of mucous à secondary infections à COPD
- Further damage from inhaled carcinogens and continuous cell division à mutations in nucleus (3p/EGFR) à dysplasia à more mutations (KRAS, C-Myc) à infiltration à spread à metastases (p53)
- NOTE: non smokers can get cancer from EGFR deletions ; smokers more commonly have 3p deletion
- Treatment is personalised to specific mutation for patient
pathology of Primary lung cancers
Classification of lung tumours (bronchogenic carcinomas account for 95%):
- SCLC- small cell carcinoma
- NSCLC- non small cell lung cancers
- SCC- squamous cell carcinoma
- Adenocarcinoma
Biology of lung cancer
- Grading: microscopic features – how much does the cell resemble normal tissue for that location
- Low grade: well differentiated cells for its tissue, clear glands (if applicable)
- High grade: no structures resembling tissue, poorly differentiated from more mutations
- Staging: clinical features, degree of growth and spread
- T: tumour size and level of infiltration (T0-T4)
- T1: _<_3cm, no invasion, proximal to lobar bronchus
- T2: >3cm, main bronchus, invasion of visceral pleura
- T3: any size, main bronchus, invasion of chest wall/ diaphragm/ parietal pericardium
- T4: any size, invasion of mediastinum/ trachea/ vertebral body/ carina/ oesophagus
- N: node involvement
- N1- Hilar node: ipsilateral/ peribronchial
- N2- mediastinal node: subcarinal/ ispilateral
- N3- contralateral mediastinal/ scalene / supraclavicular node
- M: metastasis (MO absent M1 present)
- T: tumour size and level of infiltration (T0-T4)
Clinical features and complications of lung cancer:
Local
Systemic
- Obstruction, effusion
- Pneumonia
- Bronchiectasis: yellow purulent sputum, foul smelling
- Atelectasis, haemoptysis
- SVC syndrome (Pemberton’s)
- Pancoast tumour (apical- results in Horner’s)
- Horner’s syndrome- sympathetic nerves (anhydrosis, miosis, ptosis)
- Cachexia
- Paraneoplastic syndrome (ACTH, ADH)
- Clubbing
- Bone pain (METs)
- Epilepsy (METs)
Investigations
- CXR, MRI, CT, PET
- Cytology: sputum and bronchial lavage
- Biopsy: excision/ needle
- Tumour markers: epithelial, neuro, endo
details on major types: Scc, small cell cancer and adenocarcinoma
Small cell carcinoma
Squamous cell carcinoma
Adenocarcinoma
Category
Small cell cancer
Non small cell cancer
Non small cell cancer
At risk
Males
Smokers- 3p deletion
Males
Smokers
Females
Non smokers
imaging
Central, infiltrative (diffuse- spread early along bronchi)
Hilar opacity
Central, expanding (localised)
Clear border, nodular tumour
Peripheral, expanding (localised)
Opacity in periphery
Cytology
‘oat cells’ scanty cytoplasm, no glands or keratin
Dark blue
Pink cells: keratin
Blue nucleus, cytoplasm and vacuoles à mucin (glands)
Pale blue
Microscopy
Irregular dark blue cells in sheets
Pleomorphic cells with irregular nuclei
Necrosis (no gland or keratin pearl)
Neuroendocrine- (ACTH)
Irregular cells forming irregular clusters
Pleomorphic with irregular nuclei
Keratin formation – epithelial pearls
Infiltration, invasion and necrosis
Pleomorphic cells with irregular dark nuclei
Forming irregular glands
Infiltration and invasion into surrounding tissue
Areas of necrosis
Gross specimen
Grey white, diffuse infiltration, hilar
Spread around bronchi
Infiltrative
Early spread
Grey white, nodular infiltrating in hilum
Arising from major bronchus or trachea
Infiltrating into surrounding region
Spread to lymph nodes or extrapulmonary
Grey white, nodular- peripheral/hilar
Hx of Central scar, women, non smokers
Expanding tumour
Spread to lymph nodes or extrapulmonary
Markers
Neuroendocrine cells
ACTH, ADH, calcitonin
Epithelial cells
PTH-rp
EGFR
ALK
KRAS
Extra information
Paraneoplastic:
- Cushing’s (ACTH)
- ADH (low Na+, SIADH, diabetes insipidus
- Calcitonin: hypocalcemia
- Gastrin releasing peptide: peptic ulcer
- Myasthenic syndrome
- Hypercalcaemia
Haematologic syndromes:
- Migratory thrombophlebitis
- Non bacterial endocarditis
Prognosis/ treatment
Poor- early spread
Surgery not an option (chemotherapy and radiotherapy)
Rb mutations >90%
KRAS, EGFR, ALK negative
Better prognosis
Late spread
Early surgical resection
Rb mutations 20%
KRAS EGFR ALK often +
Better prognosis
Late spread
Early surgical resection
Rb mutations 20%
KRAS EGFR ALK often +
Other types of lung cancers:
Other types of lung cancers:
- Bronchiolo-alveolar carcinoma (adenocarcinoma in situ):
- Involves peripheral parts of the lung, as a single nodule
- Diameter of 3 cm or less; columnar cells grow along pre-existing structures (bronchioles and alveoli) with no destruction of alveolar architecture or stromal invasion
- May present with pneumonia-like consolidation on imaging; excellent prognosis
- Carcinoid tumour:
- Bronchial carcinoids occur at an early age (mean 40 years); represent 5% of all pulmonary neoplasms; no relation to smoking
- Malignant tumours composed of cells that contain neurosecretory granules in their cytoplasm
- Most originate in main bronchi and grow in one of two patterns: (1) an obstructing polypoid, spherical, intraluminal mass or (2) a mucosal plaque penetrating the bronchial wall to fan out in the peri-bronchial tissue
- Well demarcated; distant metastasis is rare
- Most manifest with signs and symptoms related to their intraluminal growth (cough, haemoptysis)
- Rarely may secrete hormonally active polypeptides, inducing the carcinoid syndrome (intermittent attacks of diarrhoea, flushing and cyanosis)
- Often resectable and curable
- Pleural tumours – mesothelioma:
- Rare cancer of mesothelial cells, usually arising in the parietal or visceral pleura
- Related to occupational exposure to asbestos in the air (approximately 50% of patients with this cancer have a history of asbestos exposure
- Latent period for developing malignant mesothelioma is long, often 25-40 years after initial asbestos exposure (suggests that multiple somatic genetic events are required for neoplastic conversion of a mesothelial cell)
- Often preceded by extensive pleural fibrosis and plaque formation; tumours begin in a localised area and over time spread widely
- The affected lung typically is ensheathed by a yellow-white, firm, sometimes gelatinous layer of tumour that obliterates the pleural space
- Distant metastases are rare
- Other tumours:
- Metastasis to lung:
- Most common sources are breast and colon carcinoma
- Multiple ‘cannon-ball’ nodules on imaging
- More common than primary tumours
- Lung hamartoma:
- Benign lung tumour; due to embryonic disorganisation
- Approximately 80% are found in the lung periphery
- Rounded or nodular
- Composed of normal tissue like cartilage, connective tissue, fat and muscle but in a haphazard arrangement
- Pancoast tumours:
- Apical neoplasm – may invade the brachial or cervical sympathetic plexus to cause severe pain in the distribution of the ulnar nerve or to produce Horner syndrome (ipsilateral enophthalmos, ptosis, miosis and anhidrosis)
- Accompanied by destruction of the first and second ribs and sometimes thoracic vertebrae
Anatomy of the lung and pleura – including blood supply & lymphatic drainage.
- Left lung has 2 lobes (upper and lower) divided by oblique fissure, smaller vs right due to heart
- Right lung is larger and has 3 lobes: upper and middle divided by horizontal fissure and middle and lower divided by the oblique fissure
- Pleura: parietal and visceral layers but continuous with each other – tiny amount of serous fluid separating the layers (prevent friction) – pleura allows for creation of negative pressure – allows for inspiration of air into lungs
- Hilum: major bronchi, pulmonary vessels, hilar LN
- Normal = left hilum higher than right
- Blood supply:
- Pulmonary trunk from RV (carrying deoxygenated blood) à bifurcates early into L + R pulmonary arteries à passes through each hilum and branches to supply L + R lung eventually terminating in pulmonary capillaries à O2 diffuses into pulmonary capillaries and CO2 diffuses out into alveolar space à blood travels back to heart oxygenated via 4x pulmonary veins
- pulmonary system is low pressure system (much lower vs systemic circuit)
- in response to low PaO2 blood vessels undergo hypoxic pulmonary vasoconstriction to promote blood flow to areas of the lung that are better ventilated (automatic mechanism for matching ventilation and perfusion)
- V/Q ratio highest at apex (high PO2, low PCO2), base of lung has lowest V/Q ratio (lower PaO2, higher PCO2) – regardless of this both ventilation and perfusion are better at the base of the lung
- Note: bronchial arteries carry oxygenated blood and branch from systemic circulation
- Left bronchial from thoracic aorta
- Right bronchial from posterior intercostal artery
- These bronchial arteries supply the pulmonary tissue and then empty into pulmonary veins and enter LA
- There are bronchial veins too but only a small proportion of blood supplied by bronchial arteries is returned by bronchial veins (mostly via pulmonary veins)
- Lymphatic drainage:
- Segmental and interlobar nodes of bronchiole and bronchi drain toward the hilus (there is a superficial and deep lymphatic plexus)* à drain to the pulmonary (intrapulmonary) nodes à bronchopulmonary nodes àinferior (carinal) and superior tracheobronchial nodes à the tracheal (paratracheal) nodes à bronchomediastinal nodes and trunks àeventually to the thoracic duct on the left and right lymphatic duct on the right.
- Superficial lymphatic plexus = subpleural
- Deep lymphatic plexus à accompanies bronchovascular structures with associated intrapulmonary LN
Number
Name
superior mediastinal
paratracheal
paratracheal/retrotracheal
lower paratracheal/azygous/tracheobronchial
subaortic
para-aortic
carinal/sub-carinal
paraoesophageal
pulmonary ligament (not a LN = parietal pleura folded)
hilar
intrapulmonic/interlobar
peribronchial
segmental
Note: in terms of “N” staging (TNM) of lung cancer
Note: in terms of “N” staging (TNM) of lung cancer
Pulmonary LN = 12, 11, 10, 13 = N1
Superior mediastinal LN = 1,2,3,4 = N2-3
Aortic LN = 5,6 = N2-3
Inferior mediastinal
- 7 = N2
- 8,9 = N2-3
Physiology of respiration, blood gases and lung function tests.
- Inspiration: use diaphragm and external intercostal muscles (active process)
- Diaphragm contracts down, external intercostals contract (ribs move out and up) à creates negative intrapulmonary pressure à air flows in to increase lung volume
- Expiration: passive, elastic recoil of lungs causes decreases lung volume, positive intrapulmonary pressure and air flows out
- Blood gases:
- Measure: PaO2, PaCO2, anion gap, bicarb, pH, H+, base excess
- PaO2 below 60mmHg (non-COPD patient) = respiratory failure (point at which O2 dissociation curve takes sharp decline – rapid unloading of oxygen)
- Type I vs type II resp failure
- Type I: PaO2 dec but PaCO2 normal or decreased
- Type II: PaO2 dec, PaCO2 increased
- Metabolic acidosis/alkalosis? Respiratory alkalosis/acidosis?
- Can be used to assess whether mechanical ventilation is necessary
Clinical assessment of lung function, arterial blood gas analysis.
Metabolic Alkalosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
pH
↓
↑
↓
↑
PaCO2
N (uncompensated)
↓ (compensated)
N (uncompensated)
↑ (compensated)
↑
↓
HCO3ˉ
↓
↑
N (uncompensated)
↑ (compensated)
N (uncompensated)
↓ (compensated)
Base excess
↓
↑
N/↑
N/↓
Clinical features
Kussmaul-type breathing (deeper, faster respiration), shock, coma
Paraesthesia, tetany, weakness
Acute: air hunger, disorientation
Chronic: hypoventilation, hypoxia, cyanosis
Acute: hyperventilation, paraesthesia, light-headedness
Chronic: hyperventilation, latent tetany
Common causes
With raised anion gap: diabetic ketoacidosis, lactic acidosis, poisons (e.g. ethylene glycol), drug overdoses (paracetamol, aspirin, isoniazid, alcohol)
With normal anion gap: diarrhoea, secretory adenomas, ammonium chloride poisoning, interstitial nephritis
Vomiting, prolonged therapy with potassium-wasting diuretics or steroids, Cushing’s disease, ingestion/overdose of sodium bicarbonate (e.g. antacids)
Hypoventilation
chronic lung disease with CO2retention, e.g. chronic obstructive pulmonary disease, respiratory depression from drugs (e.g. opioids, sedatives), severe asthma, pulmonary oedema
Hyperventilation anxiety, pain, febrile illness, hypoxia, pulmonary embolism, pregnancy, sepsis
Clinical examination for lung disorders
- spirometry
- physical examination
- Flow volume tests
- Assessing acute response to bronchodilators
- Confirm or exclude asthma
- Specialist referral
- Exercising testing
- Sleep studies
- Chest x-ray
- High resolution CT
- Ventilation and perfusion scans
- Transcutaneous oxygen saturation
- Arterial blood gad measurements
- Sputum examination
- Haematology and biochemistry
- ECG and Echo
- Trials of therapy
- Optimise function
- Prevent deterioration
- Develop a care plan
- Manage exacerbations
Diagnosis of malignant hypertension.
A diagnosis of malignant hypertension is based on blood pressure readings and signs of acute organ damage. Order blood and urine tests that may include: Blood urea nitrogen (BUN) and creatinine levels, which increase if you have kidney damage.
Diagnosis of paraneoplastic syndromes – especially those associated with lung cancer.
PNS are detected before cancer is diagnosed in 80% of cases. … Depending on the affected nervous system compartment, PNS symptoms may include cognitive and personality changes, ataxia, cranial nerve deficits, weakness, or numbness. A full neurological examination is performed.
Imaging
Solitary pulmonary nodules:
- A solitary pulmonary nodule is radiologically defined as a nodule <3cm in diameter with no associated atelectasis or lymphadenopathy
- The lesion is likely to be benign if there has been no change in the size of the nodule after two years.
- Lesions that have the potential for malignancy require evaluation and follow-up
Image 2: There is a circumscribed mass arising from the right hilum with spotty calcification. Biopsy confirmed bronchial carcinoid tumour
Non small cell cancer (staging)
- Staging of NSCLC is important as stages I-III are potentially resectable and sometimes curable.
- Chest radiography is indicated in all patients but has a low sensitivity for detecting lesion spread
- CT is most useful in staging of NSCLC and is often combined with PET
Image 1a: Left hilar mass causing collapse of the left upper lobe and elevation of the left main bronchus
Image 1b, 1c and 1d: CT of the same patient reveals a large, relatively homogenous mass within the left upper lobe measuring 95mm and extending from the apex to the hilum. Central areas of low attenuation are compatible with tissue necrosis. There is also encasement of the left upper lobe bronchus and pulmonary artery with extensive background emphysema
Image 2a: Lobectomy showing large non-small cell lung carcinoma arising from the proximal bronchus and invading into the surrounding parenchyma. Note the patchy central necrosis and punctate areas of haemorrhage
Images 2b and 2c: Post-mortem specimens showing infiltration of lung parenchyma by bronchoalveolar carcinoma.
Staging of lung cancer and the likely prognosis.
Stage using CT. Common site such as liver, adrenal bone and brain need to be included. PET-CT has got a low PPV.
Outlining the likely course of events and interventions once the diagnosis has been made.
Who should investigate and manage this patient? How urgently? How is this arranged?
Assess fitness before radical treatment. Full lung function testing, if CVD is present, stress echo need to be done.
this arranged?
Surgery is performed at early stage of NSCLC (I, II, IIIa) with a curative intention. Patients with stage III can undergo intensive chemoradiation to downstage rendering it amenable to surgical resection.
Radiation therapy provide a comparable outcome to surgery and is the treatment of choice for patient not qualify for surgery due to other comorbidities.
The importance of providing continuity of primary care throughout this process.
Patients with lung cancer are often independent and pain free in comparison to other form of cancer but they die rapidly at terminal stage. Patient and family require emotional and psychological support. The palliative care team include the respiratory team, social workers, hospital chaplains, and the nurses.
Side effects of chemotherapy drugs.
Most common: Nausea, hairloss, tiredness, mucositis and myelosuppression. Side effects are much more dose dependent than the anti-cancer effect so it has been practice to give the highest dose patients can tolerate.
· All chemotherapy need to be administered by trained staff because leakage outside the vein will cause tissue necrosis so immediate local measure such as aspiration has to be instigated.
· Nausea and vomiting: A stepped wise antiemetics approach. Such as metoclopramide and domperidone followed by 5-HT3 antagonists with dexamethasone.
· Hairloss: Beau’s line – white line on nails reflecting the periods of cessation of growth. Skin toxicity pronounced with 5-FU.
· Fatigue: continue beyond completion of therapy. Compound with anemia or depression.
· Myelosuppressive: platelet, WBC and RBC. Can be managed by transfusion and prophylactic antimicrobials/G-CSF.
· Mucositis: mucosa is very sensitive. Can cause severe pain at oropharynx and life threatening diarrhea. Palifermin is a recombinant keratinocyte-derived growth factor.
Epidemiology of smoking – Australian statistics (greater in rural, Indigenous, certain migrant groups and growing in women).
15 000 deaths per year
- 5% of adults over 18 were daily smokers. Has been decreasing over the last two decades.
- 9% of males and 12.1% of females smoke daily – in 1995 was 27.3% M, 20.3% F so M is decreasing more than F but is still higher
Daily Smokers: Regional/Remote 20.9%, Inner Regional 16.7%, Major Cities 13%
ATSI: 42% are daily smokers
As far as I can tell females smoking is still decreasing, just in proportion to males looks like more
Revision of Year 3 Health promotion in preventing smoking.
Tobacco Use WHO ‘best buys’ – most effective and cost-effective interventions
- Tax increases
- Smoke free indoor workplaces and public spaces
- Health information and warnings
- Bans on tobacco advertising, promotion and sponsorship
Revision of successful interventions for encouraging smoking cessation.
- Nicotine Replacement Therapy – gum, patch, inhaler, tablet
- Match starting dose to level of dependency then taper
- Effectiveness: moderate in motivated people
- Pharmacotherapy: 10% placebo, 15% bupropion, 23% verenicline (champix)
- Psychosocial intervention in conjunction with the above is most effective
- Antidepressant
- 5 As:
- Ask
- Assess
- Advise
- Assist
- Arrange (follow-up appointment)
Revision of screening programmes: the criteria for a screening programme (Wilson + Junger’s criteria). Should smokers/ex smokers be screened for lung cancer?
- Risk of being diagnosed with cancer before 85 is 1 in 2 for males, 1 in 3 for females
- Males: Lung Cancer is 4th most common, but No. 1 mortality
- Females: Lung Cancer is 4th most common, but No. 1 mortality
- Cancer is the second most common cause of death in Australia
- Screening for Cancer:
- The target disease should be a common form of caner with high associated morbidity or mortality
- Effective treatment capable of reducing morbidity and mortality should be available
- Test procedures should be acceptable, safe and relatively inexpensive
- Smoking accounts for 20-30% of cancer
Box 1. Wilson and Jungner classic screening criteria
- The condition sought should be an important health problem.
2. There should be an accepted treatment for patients with recognized disease.
3. Facilities for diagnosis and treatment should be available.
4. There should be a recognizable latent or early symptomatic stage.
5. There should be a suitable test or examination.
6. The test should be acceptable to the population.
7. The natural history of the condition, including development from latent to declared disease, should be adequately understood.
8. There should be an agreed policy on whom to treat as patients.
9. The cost of case-finding (including diagnosis and treatment of patients diagnosed) should be economically balanced in relation to possible expenditure on medical care as a whole.
10. Case-finding should be a continuing process and not a “once and for all” project.
- The condition sought should be an important health problem.
So we should not screen smokers/ex-smokers for lung cancer because you would need to do a CT which is expensive and puts them at risk from contrast (nephrotoxicity) and increases cancer risk (causes cancer in 1 in 20 000) plus you would have to do CTs regularly – can’t just be a once off, hence risk would be increased even more. So cost of case finding would be super high.
Investigation of cancer in rural areas.
- People with cancer in rural areas have poorer survival rates than in major cities- 35% more likely to die within 5 years
- For Prostate and Cervical cancers 3 times more likely to die within 5 years of diagnosis – because less access to screening so late diagnosis.
- Contributing Factors:
- Low socioeconomic status, low physical activity, poor diet, higher rates of smoking (lifestyle)
- PLUS: less access to screening, diagnostic and treatment services
- What is cancer investigation/treatment like rurally:
- Chemotherapy orders often not written by medical oncologist – might not be best care
- Only 7% of rural hospitals that administer chemo also have radiation unit – so patient can’t get radiation therapy unless they travel (and if it’s weekly unlikely to want to travel every week)
Rising Indigenous rates of lung cancer. What interventions should be put in place?
- Due to risk factors – living rurally so less access to services, lower socioeconomic status, less physical activity, higher smoking and alcohol consumption than other Australians
- Same interventions as everyone else but targeted at those of ATSI origin – decrease smoking and alcohol campaigns/interventions, close the gap programs to increase education and raise socioeconomic status
- Use of aboriginal community controlled health centres so that indigenous patients are more likely to approach care and utilise screening
- Cultural sensitivity so that western medicine can be used along-side as traditional medicine (so more likely to keep using western if don’t feel alienated)
communicating bad news: how do you tell a person that he/she has cancer
Communicating bad news is very difficult to do – many professionals don’t have formal training and feel unprepared to deliver bad news to a patient.
- Ensure ample time and a private, quiet setting without risk of interruption
- Consider who should be present for discussion, consider if the family/loved ones will be able to interpret the information (cognitive problems, disabilities, language barriers, too stressed/emotional for serious discussion)
- Spiritual adviser, interpreter required to be present?
- Ensure legal decision maker or power of attorney is present
- Always take into account:
- Cultural, spiritual, and religious beliefs of the patient and their family
- Checking for understanding
- Empathy
Steps to take for delivering bad news:
- Assess the patient’s understanding – How much do you know about this condition/type of cancer? What have other doctors told you? How much do you want to know?
- Prepare the family/loved ones/patient for the upcoming bad news – I’m sorry. Things have taken a turn for the worse. I have bad news.
- Communicate the information/bad news in a way that the patient/family understand based on step 1.
- Avoid medical jargon!
- Express empathy
- Be quiet and listen to what the patient/family has to say.
- Let them make the next move, and expect a myriad of emotions.
- Allow the patient and family to process the information.
- The patient/family will ask questions – this will allow the health professional to give additional information.
- Give the patient realistic hope and not false hope.
- Follow-up with the patient and ensure the patient feels that they are understood and supported.
- Make firm plans and provide interim details
NOTE: as health professionals under huge amounts of stress and pressure, it is important that we take care of ourselves also, through formal or informal debriefing.
People with cancer are usually concerned about facing severe pain – how do you approach this?
do you approach this?
- After the delivery of bad news, often multitude of questions and one of these might be ‘how much pain will I be in?’
- One way to help is to ensure that the patient knows that as a doctor, you will not let them suffer needlessly
Step 1: non-opioids (aspirin/paracetamol)
Step 2: mild opioids (codeine)
Step 3: strong opioids (morphine)
- Until patient is free of pain; adjuvants can be used to calm fears and anxieties
- Should be given by the clock e.g. 3-hourly or 6-hourly rather than as required
- 80-90% effective
- Don’t underestimate how powerful relief from pain can be for a patient – essentially can dictate quality of life which is extremely important, particularly in patients who are terminally ill
Other resources:
http://www.cancernetwork.com/cancer-management/management-pain
Many people with cancer also seek ‘natural’ or alternative therapies. Often there are cultural perspectives at play. Should you bring up the subject? What’s your response if people want to seek advice outside the ‘western medicine’ paradigm?
- Many different cultural aspects to views of death/dying/medical care
- As healthcare professionals, we should never assume that all patients subscribe to western medicine or hold the same views in terms of death and dying
- Important to:
- Demonstrate interest in culture
- Never challenge or change patient’s cultural viewpoint – this creates distance between doctor and patient and makes situation worse
Complementary and alternative medicines (CAM)
- Complementary therapies – used together WITH conventional medical treatments to enhance QoL and well-being
- Not aimed to cure
- Help control symptoms e.g. pain/fatigue
- Some evidence to support effectiveness of some therapies
- Include: relaxation, meditation, reflexology, music therapy, massage, talking therapies for emotional support, acupuncture
- Considerations:
- Side effects
- Cost
- Who will be delivering therapy
- Aim of therapy
- Will it affect conventional medical treatment?
- Alternative therapies – used INSTEAD of conventional medical treatments and are unproven and not scientifically-tested
- May cause harm and/or suffering
- Include: naturopathy, homeopathy, Chinese herbs and megavitamins
When discussing with clinician:
- 40% patients did not discuss alternative medicine w/ clinician but they should
- Issues of effectiveness, safety and cost need to be explored with the clinician
- Important for clinican to be aware of all medications patient is taking to avoid adverse interactions
Justifiable concerns around the use of complementary and alternative medicines (CAM) amongst cancer patients are becoming increasingly prominent. The aim was to develop evidence-based guidelines to assist oncology health professionals (HP) to have respectful, balanced and useful discussions with patients about CAM.
(1) Elicit the person’s understanding of their situation; (2) Respect cultural and linguistic diversity and different epistemological frameworks; (3) Ask questions about CAM use at critical points in the illness trajectory; (4) Explore details and actively listen; (5) Respond to the person’s emotional state; (6) Discuss relevant concerns while respecting the person’s beliefs; (7) Provide balanced, evidence-based advice; (8) Summarize discussions; (9) Document the discussion; (10) Monitor and follow-up.
