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By Dr.Amena Fatima The International Association for the Study of Pain defines pain as an “unpleasant sensory and emotional experience associated with actual or potential tissue damage,or described in terms of such damage”. pain can have deleterious consequences • provoking anxiety • contributing to lack of sleep • worsening delirium • increasing the stress response --Increased circulating catecholamines can cause arteriolar vasoconstriction, impair tissue perfusion, and reduce tissue-oxygen partial pressure . ,Catabolic hypermetabolism resulting in hyperglycemia, lipolysis, and breakdown of muscle ,leading to impair wound healing and increase the risk ofwound infection. • causing respiratory embarrassment due to atelectasis and sputum retention • causing immobility with venous and gut stasis. Pain suppresses natural killer cell activity ,, a critical function in the immune system a caring and supportive ICU team, whom the patient can trust warm and comfortable surroundings attention to pressure areas bowel and bladder care adequate hydration and amelioration of thirst (e.g.moistening the mouth). early tracheostomy where indicated to reduce the discomfort of endotracheal intubation supplemental treatments such as acupuncture, acupressure, massage and transcutaneous electrical nerve stimulation (TENS). Music therapy,relaxation. Pain management relies largely on the use of opioid analgesics, regional anaesthic and other adjuncts. Opioids : morphine and its analogues (e.g. diamorphine,codeine) • semisynthetic and synthetic agents: – phenylpiperidine derivatives (e.g. pethidine, fentanyl, sufentanil, remifentanil) – methadone – thebaine derivatives (e.g. buprenorphine,oxycodone). Local and regional anesthetics (e.g., bupivacaine). Adjuncts:Nonsteroidal anti-inflammatory medications (e.g., ketorolac,ibuprofen), IV acetaminophen, and anticonvulsants, can be used to reduce opioid requirement. Four opioid receptor subtypes; mu,kappa,delta and nociceptin/orphanin FQ. These are Gprotein-coupled receptors that inhibit adenyl cyclase to reduce cAMP. This results analgesia mediated at supraspinal, spinal and peripheral nerve endings. Opioids are titrated to effect by intermittent i.v. injection, or by continuous infusion. 1 mg/mL of morphine,or 20 µg/mL of fentanyl titrated to effect. Can also be administered via the subarachnoid, epidural, transdermal, oral, sublingual and intranasal routes. Side effects: 1. wide inter-individual response. 2. severe hypotension following rapid administration, particularly in hypovolaemic patients. 3. prolonged duration of action, due to accumulation of parent compound and metabolites (e.g. morphine and its major metabolites morphine-3-glucuronide and morphine-6-glucuronide) in the elderly and inpatients with renal and hepatic dysfunction. Use of drugs with shorter half-lives (e.g. fentanyl or sufentanil) or those with organ-independent metabolism (e.g. remifentanil) can reduce this problem. 4. constipation, often requiring concomitant administration of aperients to promote regular evacuation and prokinetics to prevent gastrostasis and allow enteral feeding. 5. the development of tolerance. 6. withdrawal symptoms on cessation or reduction of Treatment is by reinstitution of and then slow withdrawal of the opioid. Alternatively, symptoms may be controlled by substitution for a long-acting opioid (e.g. methadone), BZAs or α2-agonists. The specific opioid antagonist naloxone has little role to play in the ICU, except for the treatment of severe hypotension, unwanted sedation or respiratory depression following opioid usage or overdose. IV opioids be considered as the first-line drug class of choice to treat nonneuropathic pain in critically ill patients. Neuropathic pain, poorly treated with opioids alone, can be treated with enterally administered gabapentin and carbamazepine in ICU patients with sufficient gastrointestinal absorption and motility . This is a synthetic, selective mu receptor agonist. half-time of 4 minutes. it causes sedation, tube tolerance and a slowed respiratory rate. The loading dose is usually 1 µg/kg.Continuous infusion rates of 0.05–0.5 µg/kg/min are usually required and a starting rate of 0.1 µg/kg/min is recommended. Dosage alterations are usually in increments of 0.025–0.1 µg/kg/min. Due to the shorthalf-life, adequacy of response can be assessed within 20 minutes. Weaning should also be done by incremental dose reductions due to the risks of rebound hyperalgesia. Adding ketamine during the weaning process may modulate this risk. Tramadol is a synthetic, racemic preparation. The (+) enantiomer is a mu receptor agonist and serotonin reuptake inhibitor, whereas the (−) enantiomer is a nor epinephrine reuptake inhibitor.In addition to mu receptor action, it also enhances the descending inhibitory pathways involved in pain modulation. It is useful for moderate to severe pain in the post operative patient in doses of 50–100 mg i.v., p.o. or i.m. 4-hourly to amaximum of 600 mg/day. Patients are at risk of developing serotonin syndrome Short-term administration of Entonox (50% nitrous oxide in oxygen) is still useful for analgesia during painful procedures (eg:burns dressings) Carried out by adequately trained personnel. time-consuming,require additional staff to properly position the patient and assist the proceduralist. Serious complications (e.g.subarachnoid injection of local anaesthetic or epidural haematoma during placement of epidural catheters) as well as the risk of local anaesthetic toxicity. informed consent,recent normal coagulation profile or correction of abnormal profile, Platelet counts above 75 000/µL antiplatelet agents should be ceased. adequate training of nursing staff to monitor pain often emanating from multiple sources. The requirement for i.v. sedation/analgesia. The need to treat pain over a prolonged period, mandating either repetition of the regional block or the placement of an indwelling catheter (e.g. epidural catheter). Indwelling catheters have a defined duration of insertion (usually 3–4 days) before needing to be removed due to increasing infection risk. Pts with coagulopathy and thrombocytopenia. Ropivacaine 0.2% is used for regional infusions and can be combined with an opioid, such as fentanyl 2 µg/mL or 4 µg/mL, for epidural infusion. Ropivacaine;a single bolus of upto 3 mg/kg - a maximum of 300 mg,while continuous infusion rates should not exceed 400 µg/kg/h midazolam and propofol remain the dominant medications used for ICU sedation, with decreasing lorazepam use, and rare use of barbiturates, diazepam, and ketamine in the ICU a treatment: seizures,raised intracranial pressure, serotonin syndrome and alcohol withdrawal. For tolerating intubation, mechanical ventilation and active cooling. To reduce oxygen consumption by reducing patient arousal, activity and anxiety. To maintain the safety of patient and carers when dealing with the hyperactive delirious patient. palliation. Providing adequate rest. Reducing the distress of unpleasant sensations, invasive treatments and monitoring. Blunting awareness of the environment. • goal-directed sedation • patient-targeted sedation protocols • daily interruption of sedation • intermittent sedation • ‘analgosedation’ or analgesia-based sedation • patient-controlled sedation. sedatives are freely adjusted (usually by the bedside nurse) to attain a prescribed level of sedation a structured approach to the assessment of patient pain and distress, coupled with an algorithm that directs drug escalation and deescalation based on assessment this strategy employs a goal of sedative and analgesic titration to a desired depth of sedation. The risk of excessive sedation is minimised by a daily interruption of both sedative and analgesic infusions until the patient awakens or exhibits distress that mandatesresumed drug administration, usually with an initial bolus followed by a reduced infusion rate. Involves use of longer-acting sedative agents, typically lorazepam,given by intermittent bolus titrated via a sedation scoring system. Here sedation is notrequired as a treatment of their disease process. In these patients, opioid analgesia is instituted first, and once pain is adequately controlled, verbal measures are usedto calm the patient to a targeted sedation level . Major tranquillisers (e.g. haloperidol) are given for delirium and only then are sedative agents (propofol) used for short-term infusion andpromptly ceased. Pros: shorter duration of mechanical ventilation • shorter length of ICU and hospital stay • economic benefit • less need for diagnostic studies (e.g. computed axial tomography (CT) scans) to assess impairedconscious state • less ventilator-associated pneumonia • a possible mortality benefit. Cons: • high self-extubation rates • promotion of myocardial ischaemia • triggering of a withdrawal syndrome. Gamma amino butyric acid (GABA) is a major neurotransmitter involved in the complex process of sedation. It binds to the alpha subunit of the GABA-A receptor and, by activation, causes a conformational change that opens the ligandgated channel, allowing chloride ion influx into the neuron. This hyperpolarises the neuronal membrane and reduces neuronal activity leading to sedation. The GABA-A receptor agonists used in intensive care are benzodiazepines, propofol and barbiturates. They all share amnesic, hypnotic, anxiolytic and anticonvulsant effects, but have no analgesic properties. most widely used sedatives in ICUs. BZAs are good anticonvulsant drugs and also provide some muscle relaxation. commonest agents used are midazolam, lorazepam and diazepam. BZAs (e.g. midazolam) are shortacting, water-soluble agents, there is potential for accumulation of both parent compound and active metabolites in patients with hepatic and/or renal dysfunction. Midazolam, in doses of 0.02–0.2 mg/kg/h. Longer-acting agents, such as diazepam, may be given by intermittent i.v. injection (e.g. diazepam 5–10 mg) as necessary. BZAs are often combined with opioids in a compound ‘sedative’ infusion. This allows lower doses of BZA to be used, while capitalising on the opioid effects of respiratory and cough suppression, to facilitate mechanical ventilation and tube tolerance. Flumazenil (flumazepil), the specific BZA antagonist, may be used to reverse the effect of BZAs to reduce unwanted acute side-effects, such as severe hypotension or respiratory depression, or to allow acute neurological assessment of the sedated patient. i.v. anaesthetic agent propofol (2,6-di-isopropylphenol. It binds to the beta subunit on the receptor and causes a conformational change to the chloride channel. It has a rapid hepatic and extrahepatic conjugation reactions to inactive metabolites,short ½ life. Caution is required in hypovolaemic patients or those with impaired myocardial function as severe hypotension may result. The diluent in which propofol is delivered is lipidrich( indeed cause of hyperlipidaemia). ‘Propofol infusion syndrome’ particularly in paediatric patients,severe heart failure (preceded by metabolic acidaemia, fatty infiltration of the liver and striated muscle damage). Hyperlipidaemia may be a warning sign for development of the syndrome and serum triglyceride monitoring should be considered in patients at risk. Management requires immediate cessation of propofol and cardiovascular supports, which may necessitate ECMO. Thiopentone is reserved for specific indications, such as management of intractable intracranial hypertension,treatment of status epilepticus. It is not commonly used as a general sedative agent due to a long half-time. Volatile agents are useful for short periods of anaesthesia during invasive procedures in the ICU. They have classically been used for longer periods of sedation in acute severe asthma, due to their bronchodilator effect. • lack of a withdrawal syndrome• predictable offset independent of renal or hepaticdysfunction • cardioprotective effects• no tachyphylaxis• lower incidence of delirium• ability to measure and titrate end-tidal volatileconcentration. The use of volatile anaesthetic agents for sedation in the ICU has been limited by: • the cost of prolonged administration • the more complex set-up required for the administration of these agents (vaporiser, scavenging apparatus, etc.) • specific side-effects such as; ‘halothane’ hepatitis; accumulation of fluoride ions and consequent renal dysfunction (sevoflurane (fluoromethyl hexafluoroisopropyl ether) and isofurane. • occupational health and safety concerns (e.g. spontaneous miscarriage) Ketamine acts by blocking NMDA receptors,has the following characteristics: • mild sedation • amnesia • analgesia • reduced motor activity. The lack of respiratory and cardiovascular depression at lower doses makes this a relatively safe drug for use in the ICU. Limitations to its use include hallucinations, and delirium during the recovery/withdrawal phase. These may be ameliorated by BZA administration. Ketamine may be used specifically for sedation in severe asthmatics (for its bronchodilator effect), inpatients following head injury (for its effect at theNMDA receptor) or in patients where analgesia is difficult (e.g. extensive burns). Butyrophenones (e.g. haloperidol) and phenothiazines(e.g. chlorpromazine) are very useful agents for thesedation of delirious patients in the ICU. They act via a range of receptors including dopaminergic (D1 and D2), alpha-adrenergic, histamine, serotonin and cholinergic receptors. Main actions include: • reduced motor activity• apathy and reduced initiative• sedation and drowsiness • reduced aggression• antiemetic. Unwanted effects with these drugs are common and include: • extrapyramidal effects (dystonia, akathisia and parkinsonism) • endocrine effects (e.g. lactation) • anticholinergic effects ( blurred vision,dry mouth,urinaryretention,constipation) • hypotension • neuroleptic malignant syndrome. The advantage is that they can be used to gain control in difficult situations, without major risk of respiratory depression. haloperidol, diluted to a 1 mg/mLsolution. Atypical antipsychotic agents, such as olanzapine and quetiapine Dexmedetomidine is a highly selective α2-agonist with a half-life of 2 hours. It provides safe analgesia and sedation in the ICU. dexmedetomidine results in less delirium and shorter time to extubation. an effective treatment of agitated delirium in critically ill patients. A loading dose of 1 µg/kg over 10 minutes , Infusion rates of 0.2–1.0 µg/kg/h Side-effects may be predicted from the mechanism of action and include hypotension and bradycardia. Clonidine, an established long-acting α2-agonist,. The usual i.v. dose range is 50–150 µg, 4–6 hourly.