Respiratory arrest

Hydraziae is toxic and readily absorbed by oral, dermal, or inhalation routes of exposure. Contact with hydraziae irritates the skin, eyes, and respiratory tract. Liquid splashed iato the eyes may cause permanent damage to the cornea. At high doses it can cause convulsions, but even low doses may result ia ceatral aervous system depressioa. Death from acute exposure results from coavulsioas, respiratory arrest, and cardiovascular coUapse. Repeated exposure may affect the lungs, Hver, and kidneys. Of the hydraziae derivatives studied, 1,1-dimethylhydrazine (UDMH) appears to be the least hepatotoxic monomethyl-hydrazine (MMH) seems to be more toxic to the kidneys. Evidence is limited as to the effect of hydraziae oa reproductioa and/or development however, animal studies demonstrate that only doses that produce toxicity ia pregaant rats result ia embryotoxicity (164). 

Stage IV is the stage of respiratory paralysis and is a rare and dangerous stage of anesthesia. At this stage, respiratory arrest and cessation of all vital signs may occur. 

Inexperienced users or individuals who are exposed to the drug unexpectedly (e.g., who unknowingly consume PCP-adulterated cannabis) may develop severe anxiety and panic because of the intensity and variety of symptoms. Perceptual distortions have sometimes led to extremely violent behavior, accidents, or self-damaging acts. An especially high risk of violent behavior has been reported in acutely intoxicated PCP users who have a history of psychiatric problems. Intoxication with doses in excess of 150 mg may lead to convulsions, coma, and death from respiratory arrest. Other complications include hypertensive crisis, intracerebral hemorrhage, and renal failure (Table 6-5). 

Neurological effects related to cholinesterase depression occurred in seven children acutely exposed to methyl parathion by inhalation as well as orally and dermally (Dean et al. 1984). The children were admitted to a local hospital with signs and symptoms of lethargy, increased salivation, increased respiratory secretions, and miosis. Two of the children were in respiratory arrest. Two children died within several days of each other. All of the children had depressed plasma and erythrocyte cholinesterase levels (Table 3-2). These effects are similar to those occurring in methyl parathion intoxication by other routes (see Sections 3.2.2.4 and 3.2.3.4). Three adults exposed in the same incident had normal plasma (apart from one female) and red blood cell cholinesterase, and urinary levels of 4-nitrophenol (0.46-12.7 ppm) as high as some of the ill children. 

IV pruritus flush urticaria angioedema (not mandatory) vomiting defecation diarrhea respiratory arrest cardiac arrest... 

Vital Signs. Although hypertension is common and may be severe, hypotension can also occur. Tachycardia occurs in about 30 percent of cases. Severe tachypnea with respiratory rates as high as 88/min or respiratory depression with rates of 10/min or less may be seen. Respiratory arrest and cardiac arrest may occur. Hyperthermia with temperatures as high as 108.0 °F is a life-threatening event and may be associated with submassive liver necrosis (Armen et al. 1984). 

At blood levels from 0.4g%-0.6g% (86.8 to 130.2 mmol/L) alcoholic coma often occurs, accompanied by decreased respiration, blood pressure, and body temperature Blood levels between 0.6 g% and 0.8 g% (130.2 to 173.6 mmol/L) are often fatal resulting from respiratory arrest, aspiration of gastric contents, or airway obstruction due to flaccid tongue... 

Pinpoint pupils (miosis), bronchoconstrict ion, respiratory arrest, hypersalivation, increased secretions, diarrhea, decreased memory, concentration, loss of consciousness, and seizures... 

The precise mechanism of dimethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute effects of dimethylhydrazine exposure may involve the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Back and Thomas (1963) noted that the deaths probably involve respiratory arrest and cardiovascular collapse. The central nervous system as a target is consistent with the delayed latency in response reported for dimethylhydrazine (Back and Thomas 1963). There is some evidence that 1,1-dimethylhydrazine may act as an inhibitor of glutamic acid decarboxylase, thereby adversely affecting the aminobutyric acid shunt, and could explain the latency of central-nervous-system effects (Back and Thomas 1963). Furthermore, vitamin B6 analogues that act as coenzymes in the aminobutyric acid shunt have been shown to be effective antagonists to 1,1-dimethylhydrazine toxicity (reviewed in Back and Thomas 1963). 

Compared with other tested species, hamsters appear to be resistant to the lethal effects of acute exposure to monomethylhydrazine. Within similar exposure durations, the cumulative exposure data (exposure concentration time) suggest similar sensitivities in response among dogs, rats, and mice. As noted by Back and Thomas (1963), death in monkeys, dogs, rats, and mice was preceded by tonicoclonic convulsions and respiratory arrest. 

Lethal. At time of respiratory arrest, blood plasma concentration was 1.0 mg total CN/L or about 0.4 mg free cyanide/L No measurable effect on food consumption, blood chemistry, behavior, or organ histology... 

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