Nicotinic signs

Nicotinic signs of intoxication include muscle weakness, tremor and fasciculations, and involuntary twitching. Muscle weakness that affects the respiratory muscles may contribute to dyspnea and cyanosis. Tachycardia may result from stimulation of sympathetic ganglia in cardiac tissue and may mask the bradycardia due to the muscarinic action on the heart. Nicotinic action at the sympathetic ganglion may also result in pallor, high blood pressure, and hyperglycemia. 

Nicotinic signs and symptoms result from the accumulation of acetylcholine at motor nerve endings in skeletal muscle and autonomic ganglia. Thus, there is fatigue, involuntary twitching, and muscular weakness, which may affect the muscles of respiration. Hypertension and hyperglycemia may also reflect the action of acetylcholine at sympathetic ganglia. 

In another letter to Lancet, doctors from Kelo University Hospital confirmed the somewhat unexpected domination of nicotinic signs and symptoms over the muscarinic ones (only one patient had mild bradycardia, 50 beats per minute) and questioned usefulness of treatment of mild cases of sarin intoxication with atropine sulphate eye drops, because of atropine-induced photophobia and poor focusing [25]. 

Acute intoxication by anti-ChE agents causes muscarinic and nicotinic signs and symptoms, and, except for compounds of extremely low lipid solubility, affects the CNS. Systemic effects appear within minutes after inhalation of vapors or aerosols. The onset of symptoms is delayed after GI and percutaneous absorption. Duration of effects is determined largely by the properties of the compound lipid solubility, whether it must be activated to the oxon, stability of the organophos-phorus-AChE bond, and whether aging of phosphorylated enzyme has occurred. 

In a case report, continuous PAM infusion (with atropine sulfate) was successful in treating chlorpyrifos poisoning, and the nicotinic signs and symptoms were controlled (Tush and Anstead, 1997). In a case series, Tbiermann ef al. (1997) reported that in parathion poisoning, obidoxime... 

Yokoyama et al. (1998) have evaluated the chronic neurobehavioral effects related to post-traumatic stress disorder induced by exposure to sarin in male and female patients in the Tokyo subway incident in 1995. Naka-jima et al. (1998) conducted an epidemiological stndy and discussed the muscarinic and nicotinic signs in the victims of sarin poisoning in Matsumoto City, Japan, in 1994. 

Dipherhydramine (4 mg/kg orally, 3 times daily) may help to cortrol refractory nicotinic signs. It should not be u in combination vritfi atropine. 

Sevin), a common caifoamate insecticide. Thus, most authorities have continued stress the lack of efficacy or need for oximes a insl carbamates and the potential, although largely undocumented, adverse effects they may cause when us with specific carbamates. Diphenhydramine may help control refractory nicotinic signs, but it is not the agent of first choice for the treatment of carbamate toxicosis and it should never be administered with atropine. 

Clinical signs are indistinguishable from organophosphate poisoning. Muscarinic signs include salivation, lacrimation, urinary incontinence, and defecation. Nicotinic signs include muscle tremors and fascicula-tions, convulsions, and respiratory failure (Mahmood and Carmichael, 1986). The muscarinic effects of ana-toxin-a(s) can be suppressed by atropine (Cook et al., 1990), but it is relatively resistant to oxime reactivation, compared with typical organophosphate insecticides, because of the formation of an enzyme-adduct (Hyde and Carmichael, 1991). 

Clinically, nicotinic signs often predominate early in the course of cholinesterase inhibitor poisoning. However, concurrent nicotinic and muscarinic signs and symptoms are often present in both the PNS and CNS. Later in the course of cholinesterase inhibitor poisoning, muscarinic signs and symptoms predominate. 

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