Respiratory muscles paralysis

Botulism. Clinical features include symmetric cranial neuropathies (i.e., drooping eyelids, weakened jaw clench, and difficulty swallowing or speaking), blurred vision or diplopia, symmetric descending weakness in a proximal to distal pattern, and respiratory dysfunction from respiratory muscle paralysis or upper airway obstruction without sensory deficits. Inhalational botulism would have a similar clinical presentation as food-borne botulism however, the gastrointestinal symptoms that accompany foodborne botulism may be absent. 

The first step in treatment of anticholinesterase poisoning should be injection of increasing doses of atropine sulfate to block all adverse effects resulting from stimulation of muscarinic receptors. Since atropine will not alleviate skeletal and respiratory muscle paralysis, mechanical respiratory support may be required. 

One of the most common substances known to interfere with neurotransmission is nicotine. Neurotoxic effects from nicotine have occurred in children who have ingested nicotine, people who have accidentally ingested nicotine-based insecticides, and even workers who have absorbed nicotine through the skin from handling wet tobacco leaves. The first symptoms of nicotine intoxication include accelerated heart rate, perspiration, and nausea. Later, the heart may slow to such an extent that blood pressure becomes too low. The subject may become drowsy and confused and lapse into a coma. Death occurs from respiratory muscle paralysis. 

SUXAMETHONIUM BAMBUTEROL t effect of suxamethonium Bambuterol is an inhibitor of pseudocholinesterase, which hydrolyses suxamethonium Be cautious of prolonged periods of respiratory muscle paralysis and monitor respiration closely until complete recovery... 

Proper supportive care and administration of antitoxin are the mainstays of current therapy. Patients who present with respiratory failure will need full ventilatory support however, there will be a subgroup of patients who present early without obvious signs of respiratory muscle paralysis. The negative inspiratory force, pulse oximetry, and gag reflex of these patients should be evaluated serially to determine the degree of respiratory muscle weakness and likelihood of impending respiratory failure. 

Respiratory dysfunction from respiratory muscle paralysis or upper airway obstruction... 

The initial effects of nerve agents depend on the dose and route of exposure. A small inhalation exposure from nerve agent vapor causes a response in the eyes, nose and airway, such as miosis, conjunctival injection, eye pain, rhinorrhea, bron-choconstriction, excessive bronchial secretions, and mild to moderate dyspnea (9,13,18). Larger exposures cause central nervous system effects within seconds to minutes, including loss of consciousness, seizures, and central apnea. Death can occur within 5-lOmin of a lethal dose, usually due to respiratory failure from the combined effects of respiratory muscle paralysis, loss of airway control and profuse bronchorrhea (13,14). 

Stimulation or paralysis of nicotinic receptors at the neuromuscular junction causes muscle fasciculations, crampmg, weakness, and respiratory muscle paralysis stimulation of... 

GA GB GD GF VX Frequent micturition, urinary incontinence. Apprehension, giddiness, insomnia, headache, drowsiness, difficulty concentrating, poor memory, confusion, slurred speech, ataxia, weakness, coma and areflexia, Cheyne-Stokes respiration, convulsions. Fasciculations, easy fatigue, cramps, weakness (including respiratory muscles), paralysis. 

BAMBUTEROL MUSCLE RELAXANTS -SUXAMETHONIUM t effect of suxamethorrium Bambuterol is arr irrhibitor of pseudocholirresterase, which hydrolyses suxamethorrium Be cautious of prolorrged periods of respiratory muscle paralysis, arrd morritor respiratiorr closely urrtil complete recovery... 

B. Nicotinic effects include muscle fasciculations, tremor, and weakness. Death is usually caused by respiratory muscle paralysis. Blood pressure and pulse rate may be increased because of nicotinic effects or decreased because of muscarinic effects. 

Neuromuscular function Respiratory muscle paralysis leading to hypercapnic respiratory failure requiring mechanical ventilation has been attributed to intravenous and inhaled colistimethate sodium [103 ]. 

Fernandez AB, Perez M, Soto L. Sudden respiratory muscle paralysis and apnea in a patient infected with multidrug-resistant Pseudomonas aeruginosa treated with intravenous colistin. Int J Infect Dis 2013 17(5) e357. 

Well-known symptoms of sarin toxicity include miosis, hypersecretions, bradycardia, and fasciculations. However, the mechanism of organophosphate toxicity seems to involve conflicting actions. For example, mydriasis or miosis, and bradycardia or tachycardia may occur. Acute respiratory insufficiency is the most important cause of immediate death. Early symptoms include (i) tachypnea due to increased airway secretions and bronchospasm (a muscarinic effect), (ii) peripheral respiratory muscle paralysis (a nicotinic effect), and (iii) inhibition of respiratory centers (a CNS effect), all of which lead to severe respiratory deficiency. If left untreated at this stage, death will result. Cardiovascular symptoms may include hypertension or hypotension. Various arrhythmias can also occur, and caution is required when the QT interval is prolonged. In particular, if hypoxemia is present, fatal arrhythmias may occur with intravenous administration of atropine... 

Lethality contributing factors of Toxin-PC were probably the cardiotoxic or neuromuscular blocking activity or a combination of these two factors. Respiratiory distress followed by respiratory failure induced by the R Canius venom (Auddy et al. 1993) indicated respiratory muscle paralysis induced by neuromuscular blocking by the toxin. The cardiotoxic action of Toxin-PC may also contribute lethality in experimental animals. 

---