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Peri-operative medicine
Published in Henry J. Woodford, Essential Geriatrics, 2022
Cholinesterase inhibitors can interact with muscle relaxants. The effects of depolarising neuromuscular blocking drugs (e.g. suxamethonium) can be prolonged, and the effects of non-depolarising neuromuscular blocking drugs can be decreased or reversed, thus requiring higher doses.17 Galantamine or rivastigmine can be stopped two days prior to elective surgery, but donepezil has a longer half-life and takes over two weeks to clear from the body, so it is usually continued. Memantine can enhance the central nervous system toxicity of ketamine.
Adult Anaesthesia
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Daphne A. Varveris, Neil G. Smart
Propofol is often used in combination with remifentanil, an ultra short-acting synthetic opioid, as part of a total intravenous anaesthesia (TIVA) technique. Remifentanil is metabolized by non-specific plasma esterases and with a context sensitive half-time of 3 minutes and elimination half-time of 6 minutes, it has minimal active metabolites. Used by infusion including target control with the Minto pharmacokinetic model, remifentanil has a short, predictable duration of action with no accumulating effect. Deep intra-operative analgesia can be achieved quickly and yet reversed rapidly. This can contribute to improved intraoperative cardiovascular stability and may also be used to negate the need for neuromuscular blocking drugs, useful when nerve monitoring is required. At the end of surgery, faster recovery and less respiratory depression are achieved in comparison with other opioids but the short duration of action means that alternative post-operative analgesia is required.2 Remifentanil can also be used to provide sedation during awake fibre-optic intubation. By suppressing airway reflexes, it facilitates excellent intubating conditions (Figure 32.2).3
Anaphylaxis
Published in Daniel Cottle, Shondipon Laha, Peter Nightingale, Anaesthetics for Junior Doctors and Allied Professionals, 2018
Vandana Girotra, Geraint Briggs
Any drug has the potential to cause an anaphylactic reaction. The commonest causes in anaesthesia are as follows. Neuromuscular blocking drugs (60%): › sensitisation is due to quaternary amine groups in toothpaste, detergent, shampoo, cough medicine› the commonest to cause reactions is suxamethonium.Latex (20%): › this is most commonly found in gloves, but also in equipment such as non-invasive blood pressure cuffs› the patient may report reactions prior to admission to hospital (e.g. condoms).Antibiotics (15%): › those with β-lactam ring account for 70%› there is cross-sensitivity between penicillins and first-generation cephalosporins and carbapenems.Colloids (4%): › anaphylaxis is mainly caused by gelatins, but also the starches.Others: › non-steroidal anti-inflammatory drugs› chlorhexidine› local anaesthetics (rare)› opioids› intravenous anaesthetic agents (rare).
Pharmacological management of adult patients with acute respiratory distress syndrome
Published in Expert Opinion on Pharmacotherapy, 2020
Maria Gabriella Matera, Paola Rogliani, Andrea Bianco, Mario Cazzola
Mechanical ventilation does not influence the body’s inflammatory response and stress response although it can improve the respiratory function of patients with ARDS. Therefore it is combined with pharmacologic therapies. The pharmacologic management of ARDS entails at least three aspects: etiologic, pathophysiological, and support. ARDS is primarily managed by identifying the underlying disease and administering appropriate, disease-specific treatment. There is evidence that in patients with sepsis-associated ARDS the use of adequate antibiotics and source control can allow obtaining good outcomes [14], although still an important fraction of patients with pneumonia die. Neuromuscular blocking drugs are critical because they provide optimal ventilator synchrony, reduce peak airway pressures, reduce oxygen consumption, and improve pulmonary compliance [15]. However, also corticosteroids, inhalation of nitric oxide (NO) and vasodilators, β2-adrenoceptor (AR) agonists, surfactant therapy, agents that accelerate lung water resolution and ion transports are suggested as pharmacological treatments [6,9,15] (Table 1). Nevertheless, no pharmacologic therapy has been shown to ensure a reduction in either short-term or long-term mortality [16], although the complex pathophysiology of ARDS provides multiple potential targets for pharmacologic therapy.
The acute respiratory distress syndrome: pathophysiology, current clinical practice, and emerging therapies
Published in Expert Review of Respiratory Medicine, 2018
Matthias Derwall, Lukas Martin, Rolf Rossaint
The routine use of neuromuscular blocking drugs has been discussed controversially. Papazian and colleagues published a multicenter clinical trial in 340 patients with severe ARDS that were matched to receive either 48 h pharmacological paralysis or placebo during the first two days of their ARDS [28]. In this study, the use of neuromuscular drugs was associated with a reduced 90 day mortality with a number needed to treat (NNT) of 11. In a subgroup analysis in patients with a Horowitz index of less than 120, the NNT was even lower with seven patients to prevent one death at 90 days. Remarkably, no higher risk for ICU-acquired weakness was observed for patients in the paralysis group [28]. However, muscle paralysis should be restricted to the most severe forms of ARDS and may only be used in the early phase of the disease.
Impact of CYP2A6 gene polymorphism on the pharmacokinetics of dexmedetomidine for premedication
Published in Expert Review of Clinical Pharmacology, 2018
Ling Wang, Shaoming Wang, Juan Qi, Rongguo Yu, Jie Zhuang, Boyang Zhuang, Yongming Lou, Junshan Ruan, Hong Ye, Fangfang Lin
Dexmedetomidine must be diluted to a concentration of 200 μg/50 mL with 0.9% sodium chloride solution before administration. The prepared dexmedetomidine was pumped intravenously to patients at a dosage of 0.5 μg/kg in about 10 min, and vital signs were closely monitored. The drugs used in the course of anesthesia included nondepolarizing neuromuscular blocking drugs, propofol and opioids, which were intravenously administrated, and if necessary, nondepolarizing neuromuscular blocking drugs and opioids were added to maintain the anesthetic effect. The combined drugs have no definite effects on the pharmacokinetics of dexmedetomidine. The above anesthesia steps are routine steps of anesthesia for patients undergoing surgery.