Finals Flashcards
How can pain be managed?
Next question
Management of pain
World Health Organisation Analgesic Ladder
Initially peripherally acting drugs such as paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs) are given.
If pain control is not achieved, the second part of the ladder is to introduce weak opioid drugs such as codeine or dextropropoxyphene together with appropriate agents to control and minimise side effects.
The final rung of the ladder is to introduce strong opioid drugs such as morphine. Analgesia from peripherally acting drugs may be additive to that from centrally-acting opioids and thus, the two are given together.
The World Federation of Societies of Anaesthesiologists (WFSA) Analgesic Ladder
For management of acute pain
Initially, the pain can be expected to be severe and may need controlling with strong analgesics in combination with local anaesthetic blocks and peripherally acting drugs.
The second rung on the postoperative pain ladder is the restoration of the use of the oral route to deliver analgesia. Strong opioids may no longer be required and adequate analgesia can be obtained by using combinations of peripherally acting agents and weak opioids.
The final step is when the pain can be controlled by peripherally acting agents alone.
Local anaesthetics
Infiltration of a wound with a long-acting local anaesthetic such as Bupivacaine
Analgesia for several hours
Further pain relief can be obtained with repeat injections or by infusions via a thin catheter
Blockade of plexuses or peripheral nerves will provide selective analgesia in those parts of the body supplied by the plexus or nerves
Can either be used to provide anaesthesia for the surgery or specifically for postoperative pain relief
Especially useful where a sympathetic block is needed to improve postoperative blood supply or where central blockade such as spinal or epidural blockade is contraindicated.
Spinal anaesthesia
rovides excellent analgesia for surgery in the lower half of the body and pain relief can last many hours after completion of the operation if long-acting drugs containing vasoconstrictors are used.
Side effects of spinal anaesthesia include: hypotension, sensory and motor block, nausea and urinary retention.
Epidural anaesthesia
An indwelling epidural catheter inserted. This can then be used to provide a continuous infusion of analgesic agents. It can provide excellent analgesia. They are still the preferred option following major open abdominal procedures and help prevent postoperative respiratory compromise resulting from pain.
Disadvantages of epidurals is that they usually confine patients to bed, especially if a motor block is present. In addition an indwelling urinary catheter is required. Which may not only impair mobility but also serve as a conduit for infection. Epidural haematoma is a recognised complication. They are contraindicated in coagulopathies.
Transversus Abdominal Plane block (TAP)
In this technique an ultrasound is used to identify the correct muscle plane and local anaesthetic (usually bupivicaine) is injected. The agent diffuses in the plane and blocks many of the spinal nerves. It is an attractive technique as it provides a wide field of blockade but does not require the placement of any indwelling devices. There is no post operative motor impairment. For this reason it is the preferred technique when extensive laparoscopic abdominal procedures are performed. They will then provide analgesia immediately following surgery but as they do not confine the patient to bed, the focus on enhanced recovery can begin sooner.
-The main disadvantage is that their duration of action is limited to the half life of the local anaesthetic agent chosen. In addition some anaesthetists do not have the USS skills required to site the injections.
Patient Controlled Analgesia (PCA)
Patients administer their own intravenous analgesia and titrate the dose to their own end-point of pain relief using a small microprocessor - controlled pump. Morphine is the most popular drug used.
Strong Opioids
Severe pain arising from deep or visceral structures requires the use of strong opioids
Morphine
Short half life and poor bioavailability.
Metabolised in the liver and clearance is reduced in patients with liver disease, in the elderly and the debilitated
Side effects include nausea, vomiting, constipation and respiratory depression.
Tolerance may occur with repeated dosage
Pethidine
Synthetic opioid which is structurally different from morphine but which has similar actions. Has 10% potency of morphine.
Short half life and similar bioavailability and clearance to morphine.
Short duration of action and may need to be given hourly.
Pethidine has a toxic metabolite (norpethidine) which is cleared by the kidney, but which accumulates in renal failure or following frequent and prolonged doses and may lead to muscle twitching and convulsions. Extreme caution is advised if pethidine is used over a prolonged period or in patients with renal failure.
Weak opioids
Codeine: markedly less active than morphine, has predictable effects when given orally and is effective against mild to moderate pain.
Non opioid analgesics
- Mild to moderate pain.
Paracetamol
Inhibits prostaglandin synthesis.
Analgesic and antipyretic properties but little anti-inflammatory effect
It is well absorbed orally and is metabolised almost entirely in the liver
Side effects in normal dosage and is widely used for the treatment of minor pain. It causes hepatotoxicity in over dosage by overloading the normal metabolic pathways with the formation of a toxic metabolite.
NSAIDs
Analgesic and anti-inflammatory actions
Inhibition of prostaglandin synthesis by the enzyme Cyclooxygenase which catalyses the conversion of arachidonic acid to the various prostaglandins that are the chief mediators of inflammation. All NSAIDs work in the same way and thus there is no point in giving more than one at a time. .
NSAIDs are, in general, more useful for superficial pain arising from the skin, buccal mucosa, joint surfaces and bone.
Relative contraindications: history of peptic ulceration, gastrointestinal bleeding or bleeding diathesis; operations associated with high blood loss, asthma, moderate to severe renal impairment, dehydration and any history of hypersensitivity to NSAIDs or aspirin.
Neuropthic pain
National Institute of Clinical Excellence (UK) guidelines:
First line: Amitriptyline (Imipramine if cannot tolerate) or pregabalin
Second line: Amitriptyline AND pregabalin
Third line: refer to pain specialist. Give tramadol in the interim (avoid morphine)
If diabetic neuropathic pain: Duloxetine
References
- http://guidance.nice.org.uk/CG96/Guidance/pdf/English
- Charlton E. The Management of Postoperative Pain . Update in Anaesthesia. Issue 7 (1997)
How does digoxin toxicity present?
Digoxin is a cardiac glycoside now mainly used for rate control in the management of atrial fibrillation. As it has positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure.
Mechanism of action
decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump. Also stimulates vagus nerve
digoxin has a narrow therapeutic index
Monitoring
digoxin level is not monitored routinely, except in suspected toxicity
if toxicity is suspected, digoxin concentrations should be measured within 8 to 12 hours of the last dose
Digoxin toxicity
Plasma concentration alone does not determine whether a patient has developed digoxin toxicity. Toxicity may occur even when the concentration is within the therapeutic range. The BNF advises that the likelihood of toxicity increases progressively from 1.5 to 3 mcg/l.
Features
generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
arrhythmias (e.g. AV block, bradycardia)
gynaecomastia
Precipitating factors
classically: hypokalaemia
digoxin normally binds to the ATPase pump on the same site as potassium. Hypokalaemia → digoxin more easily bind to the ATPase pump → increased inhibitory effects
increasing age
renal failure
myocardial ischaemia
hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
hypoalbuminaemia
hypothermia
hypothyroidism
drugs: amiodarone, quinidine, verapamil, diltiazem, spironolactone (competes for secretion in distal convoluted tubule therefore reduce excretion), ciclosporin. Also drugs which cause hypokalaemia e.g. thiazides and loop diuretics
Management
Digibind
correct arrhythmias
monitor potassium
What is contraindicated with the use go phosphodiesterase inhibitors?
Phosphodiesterase type V (PDE5) inhibitors are used in the treatment of erectile dysfunction. They are also used in the management of pulmonary hypertension. PDE5 inhibitors cause vasodilation through an increase in cGMP leading to smooth muscle relaxation in blood vessels supplying the corpus cavernosum.
Examples
sildenafil (Viagra) - this was the first phosphodiesterase type V inhibitor
tadalafil (Cialis)
vardenafil (Levitra)
Contraindications
patients taking nitrates and related drugs such as nicorandil
hypotension
recent stroke or myocardial infarction (NICE recommend waiting 6 months)
Side-effects visual disturbances e.g. blue discolouration, non-arteritic anterior ischaemic neuropathy nasal congestion flushing gastrointestinal side-effects
What is the king’s college criteria for liver transplantation in acute liver failure?
King’s College Hospital criteria for liver transplantation (paracetamol liver failure)
Arterial pH < 7.3, 24 hours after ingestion
or all of the following:
prothrombin time > 100 seconds
creatinine > 300 µmol/l
grade III or IV encephalopathy
*an overdose is considered staggered if all the tablets were not taken within 1 hour
What are the indications for dialysis in aspirin poisoning?
Indications for haemodialysis in salicylate overdose
serum concentration > 700mg/L
metabolic acidosis resistant to treatment
acute renal failure
pulmonary oedema
seizures
coma
*salicylates cause the uncoupling of oxidative phosphorylation leading to decreased adenosine triphosphate production, increased oxygen consumption and increased carbon dioxide and heat production
