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Nominal diameter Prior to starting treatment with opioids, a discussion should be held with patients to put in place a strategy for ending treatment with Co-Dydramol Tablets 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 up to a maximum of eight tablets in 24 hours. 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-Dydramol Tablets. 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 withdrawal. 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.
The hazards of overdose are greater in those with alcoholic liver disease. Prolonged use may cause hepatic necrosis. Patients should be advised not to exceed the recommended dose and not to take other paracetamol-containing products concurrently. Dosage should be reduced. Opioids should not be administered during an asthma attack and it should be administered with due care to persons liable to such attack.
Headache induced by overuse of analgesics MOH medication-overuse headache should not be treated by dose increase. In such cases, the use of analgesics should be discontinued in consultation with the doctor. Risk from concomitant use of sedative medicines such as benzodiazepines or related drugs. Concomitant use of co-dydramol and sedative medicines such as benzodiazepines or related drugs may result in sedation, respiratory depression, coma and death.
Because of these risks, concomitant prescribing with these sedative medicines should be reserved for patients for whom alternative treatment options are not possible. If a decision is made to prescribe co-dydramol concomitantly with sedative medicines, the lowest effective dose should be used, and the duration of treatment should be as short as possible. The patients should be followed closely for s and symptoms of respiratory depression and sedation. In this respect, it is strongly recommended to inform patients and their caregivers to be aware of these symptoms see section 4.
Alcohol should be avoided. When dihydrocodeine is prescribed for chronic use, care should be taken to avoid unnecessary increase in dosage. Do not take more medicine than the label tells you to. If you do not get better talk to your doctor. Contains paracetamol. Do not take anything else containing paracetamol while taking this medicine. Talk to a doctor at once if you take too much of this medicine even if you feel well. Do not take for longer than directed by your prescriber as taking dihydrocodeine regularly for a long time can lead to addiction.
This is because too much paracetamol can cause delayed serious liver damage. These drugs reduce or delay peak paracetamol blood levels. A poor diet low protein may also have a similar effect on the risk of serious paracetamol toxicity to hepatic enzyme inducers. Patients who have taken barbiturates, tricyclic antidepressants and alcohol may show diminished ability to metabolise large doses of paracetamol, the plasma half-life of which may be prolonged. This risk is greater with pethidine but with other opioids the risk is uncertain.
The concomitant use of opioids with sedative medicines such as benzodiazepines or related drugs increases the risk of sedation, respiratory depression, coma and death because of additive CNS depressant effect. The dose and duration of concomitant use should be limited see section 4. 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.
Administration to nursing women is not recommended as dyhydrdrocodeine may be secreted in breast milk and may cause respiratory depression in the infant. Opioid analgesics can impair mental function and can cause blurred vision and dizziness. Patients should make sure they are not affected before driving or operating machinery. 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 Traffic Act When prescribing this medicine, patients should be told:.
System Organ Class. Methaemoglobinaemia, neutropenia, pancytopenia, leukopenia, haemolytic anaemia, agranulocytosis, thrombocytopenia. Chronic hepatic necrosis has been reported in a patient who took daily therapeutic doses of paracetamol for about a year, and liver damage has been reported after daily ingestion of excessive amounts for shorter periods.
A review of a group of patients with chronic active hepatitis failed to reveal differences in the abnormalities of liver function in those who were long-term users of paracetamol, nor was the control of their disease improved after paracetamol withdrawal. Allergic reactions may be caused by histamine release rash, urticaria, difficulty breathing, increased sweating, redness or flushed faceanaphylactic shock, angioedema.
Constipation 1GI irritation, biliary spasm, nausea, vomiting, loss of appetite, dry mouth, paralytic ileus or toxic megacolon.
Abrupt withdrawal precipitates a withdrawal syndrome. Symptoms may include tremor, insomnia, nausea, vomiting, sweating and increase in heart rate, respiratory rate and blood pressure. Tolerance diminishes rapidly after withdrawal so a ly tolerated dose may prove fatal. Regularly prolonged use of dihydrocodeine is known to lead to addiction and tolerance. Symptoms of restlessness and irritability may result when treatment is then stopped.
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: website: 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. John's Wort or other drugs that induce liver enzymes, or. Symptoms of paracetamol overdosage in the first 24 hours are 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, cerebral oedema, gastrointestinal bleeding and death.
Acute renal failure with acute tubular necrosis, strongly suggested by loin pain, haematuria and proteinuria may develop even in the absence of severe liver damage. Immediate treatment is essential in the management of paracetamol overdose. Despite a lack of ificant early symptoms, patients should be referred to hospital urgently for immediate medical attention. Symptoms may be limited to nausea or vomiting and may not reflect the severity of overdose or the risk of organ damage.
Management should be in accordance with established treatment guidelines see BNF overdose section. Treatment with activated charcoal should be considered if the overdose has been taken within 1 hour. Plasma paracetamol concentration should be measured at 4 hours or later after ingestion earlier concentrations are unreliable. Treatment with N-acetylcysteine may be used up to 24 hours after ingestion of paracetamol, however, the maximum protective effect is obtained up to 8 hours post-ingestion. The effectiveness of the antidote declines sharply after this time.
If required the patient should be given intravenous N-acetylcysteine, in line with the established dosage schedule. If vomiting is not a problem, oral methionine may be a suitable alternative for remote areas, outside hospital. Management of patients who present serious hepatic dysfunction beyond 24h from ingestion should be discussed with the NPIS or a liver unit. Acute overdosage with dihydrocodeine can be manifested by somnolence progressing to stupor or coma, miotic pupils, rhabdomyolysis, non-cardiac pulmonary oedema, bradycardia, hypotension and respiratory depression or apnoea.
Primary attention should be given to the establishment of a patent airway and institution of assisted or controlled ventilation. In the case of massive overdosage, administer naloxone intravenously 0. Repeat the dose at 2 minute intervals if there is no response, or by an infusion. Infusions are not a substitute for frequent review of the patient's clinical state.
Intramuscular naloxone is an alternative in the event that IV access is not possible. As the duration of action of naloxone is relatively short, the patient must be carefully monitored until spontaneous respiration is reliably re-established. Naloxone is a competitive antagonist and large doses 4 mg may be required in seriously poisoned patients. For less severe overdosage, administer naloxone 0. Naloxone should not be administered in the absence of clinically ificant respiratory or circulatory depression secondary to dihydrocodeine overdosage.
Naloxone should be administered cautiously to persons who are known, or suspected, to be physically dependent on dihydrocodeine. In such cases, an abrupt or complete reversal of opioid effects may precipitate pain and an acute withdrawal syndrome. Paracetamol has analgesic and antipyretic effects. It is only a weak inhibitor of prostaglandin biosynthesis, although there is some evidence to suggest that it may be more effective against enzymes in the CNS than those in the periphery.
This fact may partly for its ability to reduce fever a central action and to induce analgesia. Dihydrocodeine tartrate is an opioid analgesic. Dihydrocodeine is a centrally acting analgesic which produces its effects by its action at opioid binding sites within the CNS. Dihydrocodeine is absorbed from the gastrointestinal tract. Dihydrocodeine is metabolised in the liver and excreted almost entirely by the kidney, mainly as conjugates with glucoric acid. Paracetamol is readily absorbed from the gastrointestinal tract with peak plasma concentrations occurring about 0.
Paracetamol is distributed into most body tissues. It crosses the placenta and is present in breast milk. Plasma-protein binding is negligible at usual therapeutic concentrations but increases with increasing concentrations. Paracetamol is metabolised predominantly in the liver and excreted in the urine mainly as the glucoronide and sulfate conjugates. A minor hydroxylated metabolite which is usually produced in very small amounts by mixed-function oxidases in the liver and which is usually detoxified by conjugation with liver glutathione may accumulate following paracetamol overdosage and cause tissue damage.
The elimination half-life varies from about hours. Non-clinical data reveal no special hazard for humans based on conventional studies of safety pharmacology, repeated dose toxicity, genotoxicity, carcinogenic potential, toxicity to reproduction and development. Also contains: pregelatinised maize starch, maize starch, colloidal silicon dioxide, stearic acid, water. Compliant with BS PP tablet container with or without polyfoam wad or polyethylene ullage filler and a PE closure for supply to nursing homes. Name or style and permanent address of registered place of business of the holder of the Marketing Authorisation:.
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