Paralysis nerve agents

Muscle Fascicu lotion Paralysis Nerve agent Botulinum toxin/nerve agent... 

Differential Diagnosis With single cases, rather than clearly epidemic cases, the illness could be confused with Guillain-Barre syndrome, myasthenia gravis, or tick paralysis. Other possible considerations may include enteroviral infections, as well as nerve agent and atropine poisoning. 

Symptoms Nerve agents exposures results in rhinorrhea, chest tightness, pinpoint pupils, shortness of breath, excessive salivation and sweating, nausea, vomiting, abdominal cramps, involuntary defecation and urination, muscle twitching, confusion, seizures, flaccid paralysis, coma, respiratory failure, and death. 

Muscle fasciculations and eventual paralysis may occur. Symptoms usually occur within seconds of exposure to a nerve agent hut may take several hours when exposure is only transdermal (see Figure 25.1). Effects and time of onset of a nerve agent are dependent on the concentration of the agent and the amount of time exposed, as well as the route of exposure. 

Victims of certain chemical exposures will experience seizure activity. Patients must be protected from harm. Benzodiazepines are the mainstays in seizure treatment. Liberal doses are required titrate to effect. Termination of seizure activity may reflect onset of flaccid paralysis from the nerve agent rather than adequacy of anticonvulsant therapy. A bedside electroencephalograph (EEG) may be required to assess ongoing seizure activity. 

Exposure to acutely toxic concentrations of nerve agents can result in excessive bronchial, salivary, ocular and intestinal secretions, sweating, miosis, bronchospasm, intestinal hypermotility, bradycardia, muscle fasciculations, twitching, weakness, paralysis, loss of consciousness, convulsions, depression of the central respiratory drive, and death (Grob and Harvey, 1953 Grob, 1956 Marrs, 2007 Sidell, 1997 Yanagisawa et al, 2006 many others). Minimal effects observed at low vapor concentrations... 

OPIDN is defined as a delayed onset central and peripheral distal sensorimotor polyneuropathy caused by exposure to nerve agents (Brown and Brix, 1998), typically within 1 to 2 weeks, and less than 4 weeks, after exposure (Johnson, 1980). Symptoms attributable to effects on sensory (numbness, tingling, pain) and motor (fatigue, weakness, and paralysis) targets are present and display a typical axonal length-associated pattern (e.g. predominantly lower extremities, with upper extremities affected at higher agent exposure). No treatment exists, and recovery is slow and rarely complete. 

Nerve agents can be absorbed by any route (ocular, oral, inhalation, dermal) (RTECS, 2008 HSDB, 2008). Onset of signs and duration of effects depend on the form of nerve gas (vapor, hquid) and the route of exposure. With a vapor exposure and inhalation, local signs of nasal discharge and respiratory noise begin within one to several minutes and signs can last for a few hours (mild exposure) up to 1 to 2 days (severe exposure) (Pfaff, 1998). Inhalation of a large amount of the vapor will result in sudden loss of consciousness, apnea, flaccid paralysis, and seizures within seconds to 2 to 3 min (Sidell et al, 1997). Peak effects are seen within 20 to 30 min and death is usually due to respiratory failure (Berkenstadt et al, 1991). 

Nerve agents are organophosphorus (OP) compounds that inhibit acetylcholinesterase (AChE) extremely rapidly, which results in an accumulation of acetylcholine (ACh), leads to muscle fasciculations and paralysis, and finally results in death (Dacre, 1984). There are several strategies available to verify an exposure to nerve agents. It is not... 

FIGURE 62.1. OPs bind to and inhibit acetylcholinesterase (AChE), the enzyme responsible for degrading the neurotrans-mitter, acetycholine (ACh), into choline and acetate. When AChE is inhibited by an organophosphate nerve agent, the subsequent reduced hydrolysis of ACh results in an accumulation of ACh within the synaptic cleft and overstimulation of the post-synaptic nerve. Seizures and possibly paralysis and/or death may occur. 

Toxic effects occur within seconds to 5 min of nerve agent vapor or aerosol inhalation. The muscarinic effects include ocular (miosis, conjunctival congestion, ciliary spasm), nasal discharge, respiratory (bronchoconstriction and increased bronchial secretion), gastrointestinal (anorexia, vomiting, abdominal cramps, and diarrhea), sweating, salivation, and cardiovascular (bradycardia and hypotension) effects. The nicotinic effects include muscular fa-sciculation and paralysis. CNS effects can include ataxia, confusion, loss of reflexes, slurred speech, coma, and paralysis. 

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). 

Atropine administered repeatedly as necessary and pralidoxime (2-PAM Cl) are antidotes for nerve agent toxicity. Although atropine has no effect on nicotinic receptors, and therefore will not reverse muscle weakness or paralysis, it can reduce morbidity and mortahty by reversing some of the muscarinic effects such as bron-chospasm, bradycardia, sahvation, diaphoresis, diarrhea, and vomiting (2). These antidotes may not be available in the field, especially in or near the site of attack. If mihtary Mark 1 kits are available, they provide autoinjectors that automatically dehver 2mg of atropine and 600mg pralidoxime (9). 

Given that early responders may not know for certainty which nerve agent was responsible, patients suffering from nerve agent symptoms should receive pralidoxime immediately, in conjunction with atropine. The adult dose of pralidoxime (see Tables 3.3 and 3.4) is l-2g (15-25mg kg ) intramuscularly (18) or 1 g (15mg kg ) intravenously in lOOmL of saline over 15-30min. Intravenous administration, if possible, is preferable (3). After an hour, if paralysis persists, patients should receive a second dose (21). Severely iU adult patients may benefit from an intravenous 2g pralidoxime bolus followed by a maintenance infusion of 7.5mg kg h ... 

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