Paralysis, neuromuscular blocking

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. 

For the purposes of the present discussion the term curariform neuromuscular block will be taken to refer to a post-neural membrane effect, resulting in paralysis of striated muscle, having the following characteristics ... 

WARNING Systemic absorption of oral route may cause neuro/oto/nephrotox may result resp paralysis possible w/ any route of administration Uses Hepatic coma, bowel prq) Action Aminoglycoside, poorly absorbed PO -1- GI bacterial flora Dose Adults. 3-12 g/24- h PO in 3-4 doses Peds. 50-1 (X) mg/kg/24 h PO in 3-4 doses Caution [C, /-] Renal failure, neuromuscular disorders, hearing impair Contra Intestinal obst Disp Tabs, PO soln SE Hearing loss w/ long-term use rash, NA EMS Use neuromuscular blockers w/ caution, reduced dose may be necessary t bleeding risk w/ concurrent anticoagulant use OD May cause neuromuscular block and kidney failure calcium salts can be used to revise neuromuscular block... 

E. Succinylcholine is the only depolarizing neuromuscular blocking in widespread clinical use, particularly as an aid for intubation. Its administration may produce muscle fasciculation and postoperative muscle pain. It can produce hyperkalemia in patients with muscle damage or prolonged paralysis in patients with atypical plasma cholinesterase. 

Neuromuscular blocking activity. Decoction of the seed oil, administered orally to adults of both sexes at a dose of 4.6 g/per-son, was active. A mixture of Piper longum, Zingiber officinale, Piper cubeba, Curcuma zedoaria, Juniperus communis, Cichorium intybus, Mentha arvensis. Commiphora mukul, and Sesamum indicum was given. Twenty five patients with laquwa (spastic facial paralysis) were treated with this mixture in divided doses of 4.6 g in 24 hours. Six grams of a decoction of Lavendula stoechas was also given in some cases. Sev-... 

Mechanism of Action A depolarizing neuromuscular blocking agent that causes the release of acetylcholine and inhibits cholinesterase. Therapeutic Effect Results in a spastic paralysis of the worm and consequent expulsion from the host s intestinal tract. 

Vecuronium has an elimination half-life of about one hour (Table 6.4) and is metabolised to 3-, 17-, and 3,17-hydroxy metabolites, the main route of elimination being via the liver. The metabolites have potent neuromuscular blocking action and are eliminated by the kidneys. As a result, the effects of vecuronium are prolonged in hepatic and renal disease. The metabolites may be responsible for cases of prolonged paralysis seen after long-term administration of vecuronium to patients in intensive care units. The effects of vecuronium are also prolonged in the elderly and in hypothermia due to the kinetic factors. 

Following the administration of succinylcholine, 0.75-1.5 mg/kg IV, transient muscle fasciculations occur over the chest and abdomen within 30 seconds, although general anesthesia and the prior administration of a small dose of a nondepolarizing muscle relaxant tends to attenuate them. As paralysis develops rapidly (< 90 seconds), the arm, neck, and leg muscles are initially relaxed followed by the respiratory muscles. As a result of succinylcholine s rapid hydrolysis by cholinesterase in the plasma (and liver), the duration of neuromuscular block typically lasts less than 10 minutes (Table 27-1). 

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