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Two Palliative Care Giants. Dr Jennifer Vidrine ST4 Palliative Medicine. Overview. A broad overview of palliative care in relation to general practice Pain Case 1 BREAK Nausea and Vomiting Case 2 Round Up. Palliative Care. Recognised as distinct entity since 1980s
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Two Palliative Care Giants Dr Jennifer Vidrine ST4 Palliative Medicine
Overview • A broad overview of palliative care in relation to general practice • Pain • Case 1 • BREAK • Nausea and Vomiting • Case 2 • Round Up
Palliative Care • Recognised as distinct entity since 1980s • First modern hospice opened 1967 • Based on concept of ‘Holistic’ care • Palliative care teams • Not just for patients with cancer
“GPs found looking after palliative care patients satisfactory and varied but burdensome” • Found barriers on three levels: • Personal • Relational • Organisational
Challenges faced… • Personal • Knowledge symptom and symptom control • Technical procedures in pts who want to stay at home (ie Catheter) • Small numbers of palliative care patients in a year • Emotional • Time constraints • Lack of psychological support in an autonomous worker
Relational • Communication • Between pts, carers, other HCPs • ‘Territory’ (GP? SPCT? Hospital team?)
Organisational • Bureaucracy • Obtaining medications (Controlled drugs, CSCI etc) • Need to organise care/social work review etc
They conclude • Barriers exist • It is imperative to support GPs as the frontline of service provision • Role of specialist palliative care teams in this (both specialist knowledge and emotional support)
Common Symptoms • Pain • Nausea and Vomiting • Shortness of Breath • Anxiety/Psychological Distress
Common Symptoms • Pain • Nausea and Vomiting • Shortness of Breath • Anxiety/Psychological Distress
Neuropathic pain • Disproportionate to stimulation of the nociceptor • Leads to: • Hyperalgesia (exaggerated and prolonged pain response to a mildly painful stimulus) • Allodynia (Pain produced by a stimulus that is not normally painful, such as light touch) • Spontaneous pain • No protective function • Pathological pain
Distinguishing the two… • History History History • Thinking abut possible/likely aetiologies • What has the pain responded to thus far?
Very often in palliative care it is a combination of both • Requires combination treatments (Often one won’t cut it) • Often requires some lateral thinking
An approach… • Patient specific • Tend to start with low dose strong opiate (egOramorph 2.5-5mg PRN) • If possible also give regular paracetamol • Ask patient/relative to write down the following:
Review in a couple of days. • Establish if opioid making ANY difference • Establish any side effects • Calculate what has been taken in last 24 hours (ie 4 doses of 5mg=20mg) • Start BD preparation of long acting opiate • Explain need to continue with Breakthroughs and ongoing monitoring. • Breakthrough is 1/6 total daily opioid dose (except Alfentanil which is 1/10th)
Established on Morphine but still in pain? • Would an adjunct help? Steroids (Dexamethasone) TCA (Amitriptyline) Anti-epileptics (Gabapentin/Pregabalin) • Very often end up on combination
Evidence Base • Amitriptiline-OD dosing, syrup available. • Gabapentin- syrup available, TDS • Pregabablin- ?more tolerable, BD, only tablets • Valporate- OD, syrup available, RCT conflicting • Clonazepam- Concurrent anxiolytic and muscle relaxant properties, SC
Other things to consider • NSAIDs • If no contra-indications • Esp if inflamm element of pain • Useful in bone pain • Ibuprofen used most frequently • Ketorolac useful as can be used subcut (Generally only for short spells/at end of life) • Bisphosphonates
Particular Challenges • Episodic Pain • High anxiety element (Total pain) • Non-concordance Consider referral/involvement SPCT
What might be offered… Methadone Ketamine Spinal Lines (epidural/intrathecal line) Nerve Blocks Cordotomy (Division of lateral spinothalamic tracts in the spine) Involvement of clinical psychology
Case 1 • Break up into groups of 3-5 • Look at the case and start to think about the issues involved for 20 mins • Try to approach as holistically as possible • Feed back to group.
Nausea & Vomiting
Nausea & Vomiting-Background • Extremely common in cancer patients • Deeply distressing • Vomiting generally tolerated better than nausea “Last night we went to a Chinese dinner at six and a French dinner at nine, and I can feel the shark’s fins navigating unhappily in the Burgundy” Peter Flemming, Letter from Yunnanfu, March 1938
Reality of the situation • Often as/more challenging to treat than pain • Many patients have multifactorial N&V • Absorption of the very stuff we are giving them to make them better • May well require more than one anti-emetic • Systematic/logical approach….
Questions to ask • Nausea/vomiting predominant? • Timing? • What is vomited? (Consistency, volume, colour) • Feel better after vomiting? • Associated features? • Exacerbating/relieving factors • Are there are any probable causes? (eg Constipation)
Identify specifically treated causes • Constipation-Laxatives/PR intervention (Prevention) • Gastritis-Would PPI help? • Oropharyngeal Candida-Often difficult to treat • Hypercalcaemia-IV hydration +/- Bisphosphonate • Pain-Optimise analgesia • If drug induced how essential is drug? • Treat infection
Think about non-drug measures • Select anti-emetic based on most likely cause • Basic principals: • Give regular antiemetics • Need to carefully assess risk of non-absorption and consider alt routes (CSCI) early • If you are relatively sure about cause consider maximising dose rather than switching (espMetoclopramide)
Two ‘broad’ avenues.. 1.Gastric-stasis 2.Chemically mediated (central)
1. Gastric Stasis-presentation • Early Satiety • Large volume vomits • Undigested food • Relief after vomiting • Hiccoughs/belching • Exacerbated by eating/medcations
1.Gastric stasis-causes • Slowed gastric emptying • ‘Squashed stomach’ due to Hepatomegally • Ascites • Subacute obstruction (consider specialist input)
1.Gastric Stasis-management • ProkineticegMetoclopramide • Targets peripheral (and central) Dopamine (D2) receptors. • Caution in young females • CAUTION IN PARKINSON’S DISEASE/SYNDROMES • Dose: 10-20mg tds/qds • CSCI 30-120mg/24 hours • Domperidone (less side effects but limited routes) • OBSERVE FOR INTESTINAL COLIC
GI tract Obstruction Gastric stasis Irritation/ hepatic Vestibular Motion sickness Local tumour Medication Central Anxiety Pain Cerebral mets Raised ICP Chemical Medication Biochemical Toxins Dopamine Seretonin 4 Acetylcholine Histamine Metoclopramide CTZ Histamine Dopamine Seretonin 3 Vomiting Centre
Two ‘broad’ avenues.. 1.Gastric-stasis 2.Chemically mediated (central)
2.Central Causes-presentation • Constant nausea • No/little relief after vomiting • May be able to identify cause • Other signs drug toxicity
Central-Causes Drugs: Opiates Antidepressants AEDs Electrolyte Imbalance Renal Failure Hypercalcaemia Sepsis Anxiety Pain Raised Intracranial Pressure Ischemic Bowel
2. Central Causes-Management Cyclizine • Antihistaminic/Anticholinergic antiemetic acting at AChM and H1 receptors • Acts centrally to help with vagally mediated nausea. • Can give anticholinergic side effects • Dose: 25-50mg tds • CSCI: 150mg/24 hour • Particularly useful if raised intracerebral pressure
GI tract Obstruction Gastric stasis Irritation/ hepatic Vestibular Motion sickness Local tumour Medication Central Anxiety Pain Cerebral mets Raised ICP Chemical Medication Biochemical Toxins Dopamine Seretonin 4 Acetylcholine Histamine CTZ Histamine Dopamine Seretonin 3 Vomiting Centre Cyclizine
2. Central Causes-Management Haloperidol • Useful for chemical induced nausea (inc Drug induced) • Centrally acting anti-emetic acting at D2 receptor at the CTZ • Contraindications • Dose: 1.5mg Nocte (0.5-1.5mg bd) • CSCI: 2.5-5mg/24 hours
Haloperidol GI tract Obstruction Gastric stasis Irritation/ hepatic Vestibular Motion sickness Local tumour Medication Central Anxiety Pain Cerebral mets Raised ICP Chemical Medication Biochemical Toxins Dopamine Seretonin 4 Acetylcholine Histamine CTZ Histamine Dopamine Seretonin 3 Vomiting Centre
If at first you don’t succeed • Remember often multifactorial • Consider increasing dose • Consider combinations (that target diff receptors) • Dex 4mg will often enhance affect anti-emetic (unknown mech) • Levomepromazine
GI tract Obstruction Gastric stasis Irritation/ hepatic Vestibular Motion sickness Local tumour Medication Central Anxiety Pain Cerebral mets Raised ICP Chemical Medication Biochemical Toxins Dopamine Seretonin 4 Acetylcholine Histamine CTZ Histamine Dopamine Seretonin 3 Vomiting Centre Levomepromazine
Chemotherapy Induced N&V • Ondansetron often used • Best to time limit it’s use • Headaches • Constipation • Has a very specific role • Consider anticipatory n&v • Levomepromazine • Lorazapam