Non-competitive neuromuscular blocking agents such as succinylcholine (suxamethonium) are rarely used in the ICU setting because they may induce prolonged blockade, circulatory collapse, and hyperkalemia.
Sepsis and multiple organ failure in themselves will not cause a defect in neuromuscular transmission ( Bolton 199.6). However, whenever competitive neuromuscular blocking agents are used to ease mechanical ventilation, there is a risk of muscle weakness as a complication. This may occur through the induction of a pure axonal motor neuropathy.
A second mechanism is a defect in neuromuscular transmission which occurs when neuromuscular blocking agents such as vecuronium or pancuronium bromide are given in the presence of renal failure. The action of these drugs is prolonged beyond hours to a number of days after they have been discontinued. Nerve stimulation studies show a typical postsynaptic defect. There is a decrement of the compound muscle action potential at slow rates of stimulation. The prognosis for recovery of muscle strength is quite good, although an accompanying critical illness (polyneuropathy) is often present and may further prolong recovery.
The third situation results in the induction of a thick-filament myopathy (see below). Myopathies presenting after admission to the ICU
Myopathies presenting in this situation are frequently associated with sepsis and share theoretical pathophysiological mechanisms with neuropathy. Thick-filament myopathy
A distinctive syndrome occurs in children or adults in the setting of sudden severe asthma or at the post-transplant state ( Lacomis ef al 1996). Endotracheal intubation and placement on a ventilator is necessary. High-dose steroids and neuromuscular blocking agents to ease ventilation are given, often for a number of days. On attempted weaning from the ventilator, it will be noted that the patient has severe neuromuscular respiratory insufficiency and limb weakness. Ophthalmoplegia may be present. Creatine kinase levels are often considerably elevated. Repetitive nerve stimulation studies are usually normal. Sensory conduction is normal, as is motor conduction, except for a low-amplitude compound muscle action potential. On needle electromyography, motor unit potentials tend to be polyphasic and of low amplitude and short duration, indicating a primary myopathy. The muscle may be electrically unexcitable on direct stimulation, suggesting inactivation of sodium, chloride, or potassium channels. Muscle biopsy shows a loss of structure centrally in muscle fibers. This has been shown by electron microscopy to be due to destruction of the thick myosin filaments (Dano.D §.D.d...CarpeDter!991). Denervation of muscle, secondary to either critical illness polyneuropathy or the neuromuscular blocking agent, probably predisposes to this distinctive pathological change ( Bolton 1996).
Recovery is quite rapid. The clinical and electrophysiological features of this syndrome are usually so distinctive that muscle biopsy is often unnecessary; this is a worthwhile consideration in children because of the disfiguring scar
Although the subject is still controversial, the author believes that neuromuscular blocking agents should be used to ease ventilation in asthmatics only when there are clear-cut indications, and at as low a dosage and for as short a period as possible. The use of steroids should also be limited as much as possible.
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.