Paralysis, neuromuscular blocking drugs causing

When kaolin or aluminum is administered widi die lincosamides, die absorption of the lincosamide is decreased. When the lincosamides are administered with the neuromuscular blocking drag (drag diat are used as adjuncts to anesthetic drag diat cause paralysis of the respiratory system) die action of die neuromuscular blocking drug is enhanced, possibly leading to severe and profound respiratory depression. 

In critically ill patients who have ventilatory failure from various causes (eg, severe bronchospasm, pneumonia, chronic obstructive airway disease), it may be necessary to control ventilation to provide adequate gas exchange and to prevent atelectasis. Muscle paralysis is produced by administration of neuromuscular blocking drugs to eliminate chest wall resistance and ineffective spontaneous ventilation. 

Suxamethonium is a neuromuscular blocking drug frequently used as an adjunct to anaesthesia it causes muscle paralysis (see Chapter 12). Normally it is metabolized by an enzyme, plasma pseudocholinesterase. One in 2500 of the population has a less active form of the enzyme. The effect of this is that the duration of action of suxamethonium is extended from about 6 minutes to 2 hours. 

Muscle relaxants with a depolarizing type of action suffer from several disadvantages, for, as with acetylcholine, their initial response before paralysis sets in may be to stimulate muscle contraction, and this can cause severe postoperative muscle-pain and cramp. It also means that there is a prolonged period during which the muscle is unable to respond to stimulation. Intraocular pressure may be raised and in burned patients they may cause hyper-kalaemia. In addition, the neuromuscular-blocking effects of such drugs cannot be readily reversed by anticholinesterases such as neostigmine (152, 485, 501). 

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