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Codeine is indicated in patients older than 12 years of age for the treatment of acute moderate pain which is not considered to be relieved by other analgesics such as paracetamol or ibuprofen alone. Prior to starting treatment with opioids, a discussion should be held with patients to put in place a strategy for ending treatment with co-codamol in order to minimise the risk of addiction and drug withdrawal syndrome see section 4. One to two tablets every four to six hours when necessary to a maximum of eight tablets per 24 hours.
Codeine should not be used in children below the age of 12 years because of the risk of opioid toxicity due to the variable and unpredictable metabolism of codeine to morphine see sections 4. Dosage should be adjusted accordingly to the severity of the pain and the response of the patient.
However, it should be kept in mind that tolerance to codeine can develop with continued use and that the incidence of untoward effects is dose related. Doses of codeine higher than 60 mg fail to give commensurate relief of pain but merely prolong analgesia and are associated with an appreciable increased incidence of undesirable side effects. Known hypersensitivity to paracetamol or codeine, or other opioid analgesics, or to any of the excipients.
Head injury or raised intracranial pressure in addition to the risk of respiratory depression and increased intracranial pressure, may affect papillary and other responses vital for neurological assessment. In acute diarrhoeal conditions such as acute ulcerative colitis or antibiotic associated colitis e.
It should be avoided or the dose reduced in patients with hepatic or renal impairment. Codeine is metabolised by the liver enzyme CYP2D6 into morphine, its active metabolite. If a patient has a deficiency or is completely lacking this enzyme an adequate analgesic effect will not be obtained. However, if the patient is an extensive or ultra-rapid metaboliser there is an increased risk of developing side effects of opioid toxicity even at commonly prescribed doses.
These patients convert codeine into morphine rapidly resulting in higher than expected serum morphine levels. General symptoms of opioid toxicity include confusion, somnolence, shallow breathing, small pupils, nausea, vomiting, How long does co codamol last and lack of appetite. In severe cases this may include symptoms of circulatory and respiratory depression, which may be life-threatening and very rarely fatal.
Estimates of prevalence of ultra-rapid metabolisers in different populations are summarized below:. All children received doses of codeine that were within the appropriate dose range; however there was evidence that these children were either ultra-rapid or extensive metabolisers in their ability to metabolise codeine to morphine.
How long does co codamol last is not recommended for use in children in whom respiratory function might be compromised including neuromuscular disorders, severe cardiac or respiratory conditions, upper respiratory or lung infections, multiple trauma or extensive surgical procedures.
These factors may worsen symptoms of morphine toxicity. Opioid analgesics should be avoided in patients with biliary tract disorders or used in conjunction with an antispasmodic. Administration of pethidine and possibly other opioid analgesics to patients taking a monoamine oxidase inhibitor MAOI has been associated with very severe and sometimes fatal reactions. If the use of codeine is considered essential then great care should be taken in patients taking MAOIs or within 14 days of stopping MAOIs see section 4.
Caution should be exercised when using paracetamol prior to less than 72 hours or concurrently with intravenous busulfan see section 4. Their concurrent use should be avoided. Patients should be advised that immediate medical advice should be sought in the event of an overdose, because of the risk of delayed, serious liver damage.
They should be advised not to take other paracetamol-containing products concurrently and to keep the product out of the reach of children. For all patients, prolonged use of this product may lead to drug dependence addictioneven at therapeutic doses. The risks are increased in individuals with current or past history of substance misuse disorder including alcohol misuse or mental health disorder e.
Additional support and monitoring may be necessary when prescribing for patients at risk of opioid misuse. A comprehensive patient history should be taken to document concomitant medications, including over-the-counter medicines and medicines obtained on-line, and past and present medical and psychiatric conditions. Patients may find that treatment is less effective with chronic use and express a need to increase the dose to obtain the same level of pain control as initially experienced. Patients may also supplement their treatment with additional pain relievers.
These could be s that the patient is developing tolerance. The risks of developing tolerance should be explained to the patient. It is important that patients only use medicines that are prescribed for them at the dose they have been prescribed and do not give this medicine to anyone else. Prior to starting treatment with any opioids, a discussion should be held with patients to put in place a withdrawal strategy for ending treatment with co-codamol.
Drug withdrawal syndrome may occur upon abrupt cessation of therapy or dose reduction. When a patient no longer requires therapy, it is advisable to taper the dose gradually to minimise symptoms of How long does co codamol last.
Tapering from a high dose may take weeks to months. The opioid drug withdrawal syndrome is characterised by some or all of the following: restlessness, lacrimation, rhinorrhoea, yawning, perspiration, chills, myalgia, mydriasis and palpitations. Other symptoms may also develop including irritability, agitation, anxiety, hyperkinesia, tremor, weakness, insomnia, anorexia, abdominal cramps, nausea, vomiting, diarrhoea, increased blood pressure, increased respiratory rate or heart rate.
If women take this drug during pregnancy, there is a risk that their newborn infants will experience neonatal withdrawal syndrome. Hyperalgesia may be diagnosed if the patient on long-term opioid therapy presents with increased pain. This might be qualitatively and anatomically distinct from pain related to disease progression or to breakthrough pain resulting from development of opioid tolerance. Pain associated with hyperalgesia tends to be more diffuse than the pre-existing pain and less defined in quality.
Symptoms of hyperalgesia may resolve with a reduction of opioid dose. In high doses or with regular treatment, paracetamol may potentiate the effects of warfarin. The absorption of paracetamol is reduced by cholestyramine and accelerated by domperidone and metoclopramide.
Cytotoxic drugs: Paracetamol possibly inhibits metabolism of intravenous busulfan manufacturer of intravenous busulfan advises caution within 72 hours of paracetamol. Codeine antagonises the effect of metoclopramide and cisapride on gastrointestinal activity. It delays the absorption of flecainide and mexiletine and potentiates the effect of hypnotics and anxiolytics. The analgesic activity of codeine is likely to be ificantly impaired by quinidine which impairs codeine metabolism. Antidepressants: The depressant effects of opioid analgesics may be enhanced by tricyclic antidepressants.
MAOIs taken with pethidine have been associated with severe CNS excitation or depression including hypertension or hypotension. Although this has not been documented with codeine, it is possible that a similar interaction may occur and therefore the use of codeine should be avoided while the patient is taking MAOIs and for 2 weeks after MAOI discontinuation. Alcohol: the hypotensive, sedative and respiratory depressive effects of alcohol may be enhanced.
Concurrent use of codeine with antidiarrhoeal and antiperistaltic agents such as loperamide and kaolin may increase the risk of severe constipation. Ulcer-healing drugs: Cimetidine may inhibit the metabolism of dihydrocodeine resulting in increased plasma concentrations. Interference with laboratory tests: Opioids may interfere with gastric emptying studies as they delay gastric emptying and with hepatobiliary imaging using technetium Tc 99m disofenin as opioid treatment may cause constriction of the sphincter of Oddi and increase biliary tract pressure.
As with all medication, caution should be exercised during pregnancy, especially in the first trimester. Regular use during pregnancy may cause drug dependence in the foetus, leading to withdrawal symptoms in the neonate. If opioid use is required for a prolonged period in a pregnant woman, advise the patient of the risk of neonatal opioid withdrawal syndrome and ensure that appropriate treatment will be available. Administration during labour may depress respiration in the neonate and an antidote for the child should be readily available.
A possible association with respiratory and cardiac malformations has been reported following first trimester exposure to codeine. Opioid analgesics may cause gastric stasis during labour, increasing the risk of inhalation pneumonia in the mother. There is epidemiological evidence of safety in human pregnancy when paracetamol is used in normal stated dosages. Epidemiological studies on neurodevelopment in children exposed to paracetamol in utero show inconclusive. If clinically needed, paracetamol can be used during pregnancy however it should be used at the lowest effective dose for the shortest possible time and at the lowest possible frequency.
Administration to nursing women is not recommended as codeine may be secreted in breast milk and may cause respiratory depression in the infant. Codeine should not be used during breastfeeding see section 4. At normal therapeutic doses, codeine and its active metabolite may be present in breast milk at very low doses and is unlikely to adversely affect the breast fed infant. However, if the patient is an ultra-rapid metaboliser of CYP2D6, higher levels of the active metabolite, morphine, may be present in breast milk and on very rare occasions may result in symptoms of opioid toxicity in the infant, which may be fatal.
If symptoms of opioid toxicity develop in either the mother or the infant, then all codeine containing medicines should be stopped and alternative non-opioid analgesics prescribed. In severe cases consideration should be given to prescribing naloxone to reverse these effects. Codeine produces sedation and may also cause changes in vision, including blurred or double vision.
If affected, patients should not drive or operate machinery. The effects of alcohol are enhanced by opioid analgesics. This medicine can impair cognitive function and can affect a patient's ability to drive safely. This class of medicine is in the list of drugs included in regulations under 5a of the Road of Traffic Act When prescribing this medicine, patients should be told:. Haematological: There have been reports of blood dyscrasias including thrombocytopenia and agranulocytosis, but these were not necessarily causally related to paracetamol.
Leucopenia, neutropenia and pancytopenia have been reported in association with paracetamol. Immune system: Hypersensitivity including skin rash, urticaria or angioedema may occur. A small percentage of aspirin-sensitive asthmatics are also sensitive to paracetamol. In such cases, the deterioration in respiratory function induced by paracetamol is milder and shorter than with aspirin see also 4.
Skin and subcutaneous tissue disorders: Very rare cases of serious skin reactions have been reported. Very rare cases of serious skin reactions have been reported. Renal damage may occur rarely with long term use. Haematological side-effects including thrombocytopenia, neutropenia, pancytopenia and leucopenia have occurred in isolated cases. Regular prolonged use of codeine is known to lead to addiction and tolerance. Symptoms of restlessness and irritability may result when treatment is then stopped. Tolerance and some of the most common side effects — drowsiness, nausea, and vomiting, and confusion — generally develops with long term use.
Immune system disorders: maculopapular rash has been seen as part of a hypersensitivity syndrome associated with oral codeine phosphate; fever, splenomegaly and lymphadenopathy also occurred. Psychiatric disorders: mental depression, hallucinations and nightmares, restlessness, confusion, mood changes, euphoria, dysphoria, drug dependence see section 4.
Nervous system disorders: dizziness, drowsiness, headache prolonged use of a painkiller for headaches can make them worseconvulsions especially in infants and children. Raised intracranial pressure may occur in some patients. Vascular disorders: postural hypotension, facial flushing. Large doses produce hypotension. Respiratory, thoracic and mediastinal disorders: larger doses produce respiratory depression and dyspnoea.
Gastrointestinal disorders: nausea, vomiting, constipation, dry mouth, stomach cramps, pancreatitis. Skin and subcutaneous tissue disorders: allergic reactions such as urticaria, pruritis, skin rashes, sweating and facial oedema. Musculoskeletal and connective tissue disorders: Uncontrolled muscle movements. Muscle rigidity may occur after high doses. Renal and urinary disorders: difficulty with micturation, urinary retention, dysuria, ureteric spasm.
An antidiuretic effect may also occur with codeine. Reproductive system and breast disorders: sexual dysfunction, erectile dysfunction, decreased libido or decreased potency. General disorders and administration site conditions : malaise, tiredness, hypothermia, drug withdrawal syndrome. Reporting suspected adverse reactions after authorisation of the medicinal product is important.
Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www. Patients should be informed of the s and symptoms of overdose and to ensure that family and friends are also aware of these s and to seek immediate medical help if they occur.
Liver damage is possible in adults who have taken 10g or more of paracetamol.
Ingestion of 5g or more of paracetamol may lead to liver damage if the patient has risk factors see below. Is on long term treatment with carbamazepine, phenobarbitone, phenytoin, primidone, rifampicin, St John's Wort or other drugs that induce liver enzymes. Is likely to be glutathione deplete e.
Symptoms of paracetamol overdose in the first 24 hours are sweating, pallor, nausea, vomiting, anorexia and abdominal pain. Liver damage may become apparent 12 to 48 hours after ingestion. Abnormalities of glucose metabolism and metabolic acidosis may occur. In severe poisoning, hepatic failure may progress to encephalopathy, haemorrhage, hypoglycaemia, hypotension, cerebral oedema, coma and death. Prothrombin time may increase with deteriorating liver function.How long does co codamol last
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Codeine for pain relief