Respiratory paralysis, neuromuscular

Neuromuscular blockade or respiratory paralysis may occur after administration of the aminoglycosides Therefore, it is extremely important that any symptoms of respiratory difficulty be reported immediately. If neuromuscular blockade occurs, it may be reversed by the administration of calcium salts but mechanical ventilation may be required. 

The neurotoxicity of streptomycin can result in respiratory paralysis from neuromuscular blockage, especially when the drug is given soon after the use of anesthesia or muscle relaxants. Reserve the administration of streptomycin in parenteral form for patients where adequate laboratory and audiometric testing facilities are available during therapy. 

Ticks have a bad reputation for good reasons. Not only are they carriers of a number of diseases, the saliva of some can cause paralysis. North American natives were aware of tick paralysis, but the condition was officially noted as a disease of both animals and humans in 1912. The bites of at least 60 species of ticks can cause paralysis, which often does not appear until several days after the bite. The first indication is redness and swelling around the site of the bite. This is followed by neuromuscular weakness and difficulty in walking. If the tick is not removed, speech and breathing are affected, with eventual respiratory paralysis and death. Fortunately, removal of the tick results in a quick recovery of function. The exact mechanism of paralysis is not known but it appears to come from a substance that affects the neuromuscular junction. While not related to the venom of the tick saliva, the tick can also transmit diseases such as Lyme disease, Rocky Mountain spotted fever, Q fever, typhus, and others. Table 13.1 lists some venomous arachnids. 

In very high doses, aminoglycosides can produce a curare-like effect with neuromuscular blockade that results in respiratory paralysis. This paralysis is usually reversible by calcium gluconate (given promptly) or neostigmine. Hypersensitivity occurs infrequently. 

Clinically, mamba bites may not provoke a major local reaction. If neurotoxins are injected by the bite, clinical symptoms appear within minutes to hours. Clinical signs of impairment of neuromuscular transmission (ptosis, ophthalmoplegia, bulbar symptoms, or generalized weakness) dictate administration of antivenom (Ludolfph, 2000). For Elapidae (coral snakes) venom is known that is a potential neurotoxin and may cause paresthesias, weakness, cranial nerve dysfunction, confusion, fasciculations, and lethargy. Often mild local findings, diplopia, ptosis, and dysarthria are common early symptoms. Patients die because of respiratory paralysis. In these cases, early and aggressive... 

Toxic action is complex, involving both stimulation and blockade of autonomic ganglia and skeletal muscle neuromuscular junctions, as well as direct effects on the central nervous system. Paralysis and vascular collapse are prominent features of acute poisoning, but death is usually due to respiratory paralysis, which may ensue promptly after the first symptoms of poisoning. Nicotine is not an inhibitor of cholinesterase enzyme. 

In severe overdosage, CNS depression, circulatory collapse, and hypotension may occur. Coma and skeletal muscle paralysis may also occur followed by death due to respiratory failure. Acute overdosage with quaternary ammonium antimuscarinics may produce a curariform neuromuscular block and ganglionic blockade manifested as respiratory paralysis. 

Curare mimics acetylcholine by binding to receptor at muscle synapses, preventing nerves from stimulating muscular contraction and causing death by respiratory paralysis. It is a neuromuscular nondepolarizing agent and a nicotinic antagonist. 

Hypersensitivity reactions, primarily skin rashes, occur in 6 to 8% of patients when neomycin is applied topically. Individuals sensitive to this agent may develop cross-reactions when exposed to other aminoglycosides. The most important toxic effects of neomycin are renal damage and nerve deafness this is why the drug is no longer available for parenteral administration. Toxicity has been reported in patients with normal renal function after topical application or irrigation of wounds with 0.5% neomycin solution. Neuromuscular blockade with respiratory paralysis also has occurred after irrigation of wounds or serosal cavities. 

RESPIRATORY PARALYSIS Treatment of respiratory paralysis arising from an adverse reaction or overdose of a neuromuscular blocking agent includes positive-pressure artificial respiration with oxygen and maintenance of a patent airway until recovery of normal respiration is ensured. With the competitive blocking agents, this may be hastened by the administration of neostigmine methylsulfate (0.5-2 mg intravenously) or edrophonium (10 mg intravenously, repeated as required). 

Respiratory paralysis The action of full doses of neuromuscular blockers leads directly to respiratory paralysis. If mechanical ventilation is not provided, the patient will asphyxiate. 

Neuromuscular blockade Though rare, a curare-like block may occur at high doses of aminoglycosides and may result in respiratory paralysis. It is usually reversible by treatment with calcium and neostigmine, but ventilatory support may be required. 

A good example for clinical reality of pharmacogenetic methods is the very frequently performed test for pseudocholinesterase. Inherited deficiency in pseudocholinesterase activity results in prolonged respiratory paralysis when deficient patients receive standard doses of the neuromuscular blockers suxamethonium or mivacurium [41]. 

Complete saponification of aconitine produces an alkan-olamine, aconine (36), that lacks the cardiac effects of aconitine but has antiarrhythmic properties. The compound has curare-like effects on neuromuscular transmission, often resulting in death from respiratory paralysis (Benn and Jacyno, 1983). 

Snake neurotoxins are the main toxic proteins of cobra, krait, tiger snake and sea snake venoms which block neuromuscular transmission and cause animals death of respiratory paralysis. Snake neurotoxins are classified into two distinct types, postsynaptic and presynaptic neurotoxins, in relation to the neuromuscular junction. Postsynaptic neurotoxins bind specifically to nicotinic acetylcholine receptor (AChR) at the motor endplate and produce a nondepolarizing block of neuromuscular transmission. Presynaptic neurotoxins block the release of acetylcholine from the presynaptic motor nerve terminals. 

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. 

Administration of the aminoglycosides with the cephalosporins may increase the risks of nephrotoxicity. When the aminoglycosides are administered with loop diuretics there is an increased risk of ototoxicity (irreversible hearing loss). There is an increased risk of neuromuscular blockage (paralysis of the respiratory muscles) if the aminoglycosides are given shortly after general anesthetics (neuromuscular junction blockers). 

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