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PubMed1992

Louis Gdalman, pioneer in hospital pharmacy poison information services.

The role played by hospital pharmacist Louis Gdalman in the development of poisoning information services in the Chicago area is described. In the 1930s, decades before the creation of the Chicago Poisoning Control Program, Louis Gdalman had already established a poison information service at St. Luke's Hospital in Chicago. Pharmacists provided poison information to the physicians and nurses working in the emergency room. By the early 1950s, Gdalman had established an extensive library of information on the management of acute and chronic poisoning and had developed a standard form for the collection of data from poison information calls. He personally provided a 24-hour poison information service and often took calls at home. In 1953, the American Academy of Pediatrics initiated the Chicago Area Poisoning Control Program and established treatment and referral centers at 11 hospitals, including St. Luke's Hospital. Louis Gdalman was the only pharmacist involved in this city-wide program. By 1962, the Master Poison Control Center was established at St. Luke's Hospital, which had merged with Presbyterian Hospital in 1956. Today, this center, known as the Chicago and Northeastern Illinois Regional Poison Control Center, is located at the Rush-Presbyterian-St. Luke's Medical Center in Chicago. Louis Gdalman, a hospital pharmacist, pioneered the area of poison information and established what was perhaps the first hospital-based comprehensive poison control center.

Chicago↗
PubMed1991

[Drug poisoning in children in Vojvodina].

Epidemiological characteristics of acute drug poisoning in children were investigated over a period of two years (1988-1989). The total number of poisonings was 450. Among causes of poisoning psychopharmaca, especially benzodiazepine, came first (33.3%). They were followed by drugs affecting the nervous system (9.1%), usually by analgoantipyretics, and by drugs affecting the cardiovascular system (7.8%). In 10.6% of the cases poisoning was due to two or more drugs. In 12.3% of the poisonings drug was unknown. Sodium fluoride was the most frequent single cause of acute poisoning. The average age of the poisoned children was 5.1 years. Poisoning with drugs was more frequent among girls than among boys (55:45%). In more than half poisoning accidents there was no one present when poisoning occurred. A major number of poisonings were an attention-getting gesture or a suicidal attempt. There were 11 cases of repeated poisoning with the same drug.

Adolescent↗
PubMed1997

Effectiveness of a poison center: impact on medical facility visits.

To estimate the effectiveness of a poison center by determining the number of potential medical facility visits for childhood poisonings which are prevented, and to determine how callers learned about the poison center in order to help guide future public educational efforts, a cross-sectional telephone survey was done. A systematic sample of caretakers of children < 6-y-of-age living in Harris County, TX, and who called the poison center about a poisoning incident between February 1993 and January 1994, was taken. One hundred sixty-six/197 eligible caretakers (84%) completed the survey. Of the 166 caretakers, only 5 (3%) were referred by the poison center to a medical facility for treatment, although 6 (3.6%) actually sought medical attention. The remaining 160 (96.4%) were successfully managed at home. The majority of these (74%) required no intervention and the remaining 26% required only minimal treatment, including ipecac, dilution, irrigation or observation. Of the 160 caretakers managed at home, 69 (43%) would have sought medical attention for the child at a health care facility if the poison center did not exist, and of those 81% would have gone to an emergency center or hospital for evaluation. Callers learned about the poison center most often from family/ friends, doctors, Mr Yuk stickers, television, previous use, or pharmacists. Poison centers decrease health care costs by preventing unnecessary medical facility visits for minor childhood poisonings which can be successfully managed at home. Methods effective in educating the public about poison centers should be continued and other methods explored to increase poison centers' use.

Adolescent↗
PubMed1997

Trends in hospitalizations and mortality due to medicinal or non-medicinal poisonings in Hong Kong.

Previous epidemiologic studies of poisonings in Hong Kong are regional hospital-or poison information center-based and have focused on either adults or children. This paper reports on the territory-wide hospitalization and mortality rates, comparing medicinal and non-medicinal poisonings in the general population. Between 1980 and 1995, the figures for hospitalizations and mortality due to medicinal (ICD codes 960-977) or non-medicinal (ICD codes 980-989) poisonings were obtained from the Annual Reports of the Department of Health, Hong Kong Government. Rates of medicinal poisonings increased between 1980/81 (57.3/100,000) and 1987/88 (80.9/100,000), but then declined (59.1/100,000) in 1993/94. Rates of non-medicinal poisonings were rather static (49-53/100,000) between 1980/81 and 1988/89, but then declined (22.0/100,000) in 1994/95. Between 1980/81 and 1988/89, rates of fatal medicinal poisonings (0.73-1.31/100,000) were similar to those of fatal non-medicinal poisonings (0.98-1.70/100,000). However, from 1989/90, there was an increase in the rates of fatal medicinal poisonings (1.94-2.80/100,000), although rates for non-medicinal poisonings remained much the same (0.80-1.38/100,000). Hospitalizations due to poisonings are now less common in Hong Kong than before, due largely to a greater decline in non-medicinal poisonings.

Adult↗
PubMed1997

Telephone toxicological information service on pesticide poisonings.

The problem of pesticide poisonings has been discussed with reference to the records of the toxicological information provided in 1993-1995 by the staff of the National Poison Information Centre and the physicians of the Clinic of Acute Poisonings in Lódź. Based on those data, pesticide poisonings occupy second place among the categories of chemical most frequently responsible for acute poisonings, while the first place is occupied by drugs. In the pesticide category, most of the information related to poisonings with pyrethroids, followed by organophosphorous compounds, coumarine derivatives, carbamates. Pesticide poisonings in children continue to be a serious problem. Coumarine derivatives and zinc phosphide found in rodenticides constitute the most frequent source of pesticide poisoning among children. Considering the circumstances of pesticide poisoning, accidental poisonings are the most frequent. The high incidence of pesticide poisoning shows that it is a serious problem and the steps should be taken to prevent poisonings with pesticides.

Adolescent↗
PubMedDate not supplied

Trends in poisoning in children: experience at a large referral teaching hospital.

BACKGROUND: Poisoning is a major problem in the paediatric population. The offending substances used vary from place to place. Information on poisoning trends in India is meagre and there is an impression among clinicians that there has been a change in the commonly used poisons over the years. This retrospective study aimed to determine the pattern of poisoning in children and to study the nationwide trend over the past five decades. METHODS: Case records of children (age group: 1 month and above) admitted to the Department of Paediatrics, King George's Medical College, Lucknow, Uttar Pradesh in three alternate calendar years, i.e. 1989, 1991 and 1993 were screened. All children were grouped into three categories based on the poison: (i) bites and stings, (ii) medicinal compounds, and (iii) non-medicinal compounds. The Indian literature on poisoning in children was reviewed and decade-wise data from a total of 22 studies (including the present study) were used to determine the changing trend. RESULTS: Childhood poisoning constituted 2.1% of the total paediatric admissions and 1.2% of total deaths. Non-medicinal compounds were the largest contributors (69.2%), of which kerosene alone was responsible for 47% of cases. Medicinal compounds, and bites and stings accounted for 21.6% and 9.2% of these cases, respectively. The case-fatality rate was 9.2%. Comparison of our data, after excluding bites and stings, with a previous study (1977-79) from our institution showed that kerosene poisoning continues to be responsible for a substantial part of the morbidity (51.8% v. 31.5%). Also, poisoning due to insecticides and pesticides has increased (13.7% v. 2.1%) while that due to plant poisons (primarily dhatura) has reduced markedly (4.8% v. 19.2%). CONCLUSION: Mortality due to poisoning in children has remained high over the last five decades (2.9%-4.7%). Kerosene has remained the single largest contributor to childhood poisoning (51.5% in the 1960s v. 52.8% in the 1990s).

Child, Preschool↗
PubMed2005

Soman poisoning increases neural progenitor proliferation and induces long-term glial activation in mouse brain.

To date, only short-term glial reaction has been extensively studied following soman or other warfare neurotoxicant poisoning. In a context of cell therapy by neural progenitor engraftment to repair brain damage, the long-term effect of soman on glial reaction and neural progenitor division was analyzed in the present study. The effect of soman poisoning was estimated in mouse brains at various times ranging from 1 to 90 days post-poisoning. Using immunochemistry and dye staining techniques (hemalun-eosin staining), the number of degenerating neurons, the number of dividing neural progenitors, and microglial, astroglial or oligodendroglial cell activation were studied. Soman poisoning led to rapid and massive (post-soman day 1) death of mature neurons as assessed by hemalun-eosin staining. Following this acute poisoning phase, a weak toxicity effect on mature neurons was still observed for a period of 1 month after poisoning. A massive short-termed microgliosis peaked on day 3 post-poisoning. Delayed astrogliosis was observed from 3 to 90 days after soman poisoning, contributing to glial scar formation. On the other hand, oligodendroglial cells or their precursors were practically unaffected by soman poisoning. Interestingly, neural progenitors located in the subgranular zone of the dentate gyrus (SGZ) or in the subventricular zone (SVZ) of the brain survived soman poisoning. Furthermore, soman poisoning significantly increased neural progenitor proliferation in both SGZ and SVZ brain areas on post-soman day 3 or day 8, respectively. This increased proliferation rate was detected up to 1 month after poisoning.

Animals↗
PubMed2000

Human topoisomerase I poisoning by protoberberines: potential roles for both drug-DNA and drug-enzyme interactions.

Protoberberines represent a structural class of organic cations that induce topoisomerase I-mediated DNA cleavage, a behavior termed topoisomerase I poisoning. We have employed a broad range of biophysical, biochemical, and computer modeling techniques to characterize and cross-correlate the DNA-binding and topoisomerase poisoning properties of four protoberberine analogues that differ with respect to the substituents on their A- and/or D-rings. Our data reveal the following significant features: (i) The binding of the four protoberberines unwinds duplex DNA by approximately 11 degrees, an observation consistent with an intercalative mode of interaction. (ii) Enthalpically favorable interactions, such as stacking interactions between the intercalated ligand and the neighboring base pairs, provide <50% of the thermodynamic driving force for the complexation of the protoberberines to duplex DNA. Computer modeling studies on protoberberine-DNA complexes suggest that only rings C and D intercalate into the host DNA helix, while rings A and B protrude out of the helix interior into the minor groove. (iii) All four protoberberine analogues are topoisomerase I-specific poisons, exhibiting little or no topoisomerase II poisoning activity. (iv) Modifications of the D-ring influence both DNA binding and topoisomerase I poisoning properties. Specifically, transference of a methoxy substituent from the 11- to the 9-position diminishes both DNA binding affinity and topoisomerase I poisoning activity, an observation suggesting that DNA binding is important in the poisoning of topoisomerase I by protoberberines. (v) Modifications of the A-ring have a negligible impact on DNA binding affinity, while exerting a profound influence on topoisomerase I poisoning activity. Specifically, protoberberine analogues containing either 2,3-dimethoxy; 3,4-dimethoxy; or 3, 4-methylenedioxy substituents all bind DNA with a similar affinity. By contrast, these analogues exhibit markedly different topoisomerase I poisoning activities, with these activities following the hierarchy: 3,4-methylenedioxy > 2,3-dimethoxy >> 3, 4-dimethoxy. These differences in topoisomerase I poisoning activity may reflect the differing abilities of the analogues to interact with specific functionalities on the enzyme, thereby stabilizing the enzyme in its cleavable state. In the aggregate, our results are consistent with a mechanistic model in which both ligand-DNA and ligand-enzyme interactions are important for the poisoning of topoisomerase I by protoberberines, with the DNA-directed interactions involving ring D and the enzyme-directed interactions involving ring A. It is reasonable to suggest that the poisoning of topoisomerase I by a broad range of other naturally occurring and synthetic ligands may entail a similar mechanism.

Antioxidants↗
PubMedDate not supplied

Long-term neurobehavioral effects of mild poisonings with organophosphate and n-methyl carbamate pesticides among banana workers.

Organophosphate poisoning has been associated with chronic neurobehavioral dysfunction, but no epidemiologic data exist with regard to long-term consequences from carbamate poisoning. This cross-sectional study evaluated the neurobehavioral performances of 81 banana workers who, on average 27 months earlier, had received medical attention not requiring hospitalization for mild occupational poisoning by either an organophosphate or a carbamate pesticide. These performances were compared with those of 130 banana workers who had never sought medical attention for pesticide poisoning. Poisoned subjects did less well than controls on tests measuring psychomotor and visuomotor skills, language function, and affect, the differences being significant for coding skills on the Digit-Symbol test and two tests of neuropsychiatric symptoms. These deficits, in particular a marked increase of neuropsychiatric symptoms, occurred among the organophosphate-poisoned subjects, but small deficits in performance were also seen in the carbamate-poisoned subjects. The performances of the previously poisoned subjects who had had contact with cholinesterase inhibitors within three months before testing were particularly poor. These findings in workers with mild poisoning are consistent with previous findings of persistent damage to the central nervous system from organophosphate poisoning. The possibility of persistent neurobehavioral effects associated with poisonings by nmethyl carbamate insecticides cannot be excluded. Workers with histories of poisoning may be more susceptible to neurobehavioral effects with subsequent exposures.

Adult↗
PubMed2003

Antidotal treatment of cyanide poisoning.

Cyanide poisoning may result from different exposures: residential fires, industrial accidents, drug and plant intoxication. Clinical features include coma, respiratory arrest and cardiovascular collapse. The biological hallmark is lactic acidosis. A plasma lactate concentration > or = 10 mmol/L in fire victims without severe burns and > or = 8 mmol/L in pure cyanide poisoned patients is a sensitive and specific indicator of cyanide intoxication. Many antidotes are available and efficient. However, therapeutic strategies are still debated. Our objective was to compare conventional treatments to hydroxocobalamin. This article reviews the literature on cyanide poisoning treatment. Conventional treatment of cyanide poisoning includes decontamination, supportive and specific treatment. Decontamination should be adapted to the route of poisoning and never postpone supportive treatment. Basic life support includes immediate administration of high flow of oxygen, airway protection and cardiopulmonary resuscitation. Advanced life support includes mechanical ventilation, catecholamine and sodium bicarbonate infusion. Supportive treatment is efficient but does not modify the time course or the body burden of cyanide. Numerous antidotes are available. Oxygen counteracts efficiently cyanide action at the mitochondrial level. Sodium thiosulfate, methemoglobin forming agents and cobalt compounds act efficiently by complexing or transforming cyanide into non-toxic stable derivatives. However, regarding the main clinical condition of cyanide poisoning, i.e. smoke inhalation, we should take into account not only the efficiency of antidotes but also their safety. Sodium thiosulfate is both efficient and safe, but acts with delay. Methemoglobin-forming agents are potent, but due to the transformation of hemoglobin into methemoglobin, they impair tissue delivery of oxygen. Experimental data showed increased mortality in carbon monoxide- and cyanide-poisoned rats treated with these agents. Cobalt EDTA and hydroxocobalamin are efficient and act immediately. Cobalt EDTA is more potent on a molar basis; however, numerous side effects limit its use to evidenced cyanide poisoning. In a prospective study, hydroxocobalamin appeared safe in fire victims with or without cyanide poisoning. The only reported side effect was a red coloration of skin and urine. In conclusion, antidotes are beneficial in cyanide poisoning. In suspected cyanide-poisoned patients, we recommend the use of hydroxocobalamin as first-line antidote, owing to its safety. In massive cyanide poisoning, due to the limited potency of hydroxocobalamin, continuous infusion of sodium thiosulfate should be associated.

Antidotes↗
PubMed2005

Progression of type I to type II paralysis in acute organophosphorous poisoning: is oxidative stress significant?

Organophosphorous poisoning is a common method of deliberate self-harm in countries where the pesticides are readily available and can result in type I, II and/or III paralysis. The in-hospital morbidity and mortality of the poisoning are mostly associated with type II paralysis (intermediate syndrome). The aim of this study was to determine the role of oxidative stress in relation to the severity of poisoning and development of type II paralysis in patients suffering from acute organophosphate poisoning. This prospective study was carried out at the Christian Medical College Hospital. Thirty-two patients with acute organophosphorous poisoning, admitted in one medical unit over 17 months, were included in the study. They were clinically assessed for severity of poisoning and paralysis during the first 10 days of their hospitalisation. Temporal profiles of butyrylcholinesterase (BuChE) and oxidative stress parameters, for 4, 7 and 10 days of hospitalisation, were established in 25 of these patients. Type I and II paralysis were associated with severe poisoning. The majority of patients with type II paralysis had prior evidence of type I paralysis. The pattern of muscles that were paralysed in type I paralysis occurring alone and in type I paralysis proceeding to type II paralysis were similar. BuChE was significantly inhibited in all patients. Oxidative stress occurred in acute organophosphate poisoned patients and was greater in severe poisoning. The results suggest that type I paralysis may progress to type II paralysis in severely poisoned patients. They demonstrate early occurrence of oxidative stress in severe acute organophosphate poisoning. However, the development of type II paralysis is not associated with the level of oxidative stress. They suggest that mechanisms other than acetylcholine induced oxidative stress may be involved in the progression of type I to type II paralysis.

Acute Disease↗
PubMed2004

The experience of starting a poison control centre in Africa--the Ghana experience.

The need for a poison centre in Ghana has been well demonstrated over the years as evidenced by the occurrence of a variety of cases of poisoning. Important causes are accidental poisoning from mishandling of pesticides, accidental poisoning among children from kerosene and pesticide' ingestion due to unsafe storage methods in the home, use of herbal potions of unknown composition, overdoses of certain pharmaceuticals for illegal abortion, and accidental food poisonings. Bites from venomous animals particularly snakes are also common. Though preparations toward the establishment of a poison control centre started in mid 1999, it was not until early 2002 that the operations of a modest information centre commenced. Major roles the centre are currently performing include providing: an information service for health professionals on management advice in cases of poisoning; training for primary health personnel in the management of common poisonings; training for agricultural personnel in prevention and first aid management of pesticide poisoning; public awareness education and information programmes for prevention of poisoning. Some of the important challenges being faced include ensuring adequate sensitization on the need for centers particularly among health professionals, difficulties in acquiring adequate numbers of and appropriate training for staff of the centre, dedicated phone lines, literature and timely acquisition of toxicological data-bases. Others are poor networking among centers in the region and the absence of clinical and laboratory toxicology services dedicated to managing poisonings. The key lessons learned include the need for multi-sectoral involvement and support from the onset, the need to learn from experiences of established centers and the need to model requirements to suit local conditions without compromising the effectiveness of services.

Allied Health Personnel↗
PubMed2005

[Caseload of poisoning among children treated by the Rio Grande do Sul State Toxicology Information Center (CIT/RS), Brazil].

This was an analytical, descriptive, cross-sectional study to establish the profile of poisonings among children 0 to 4 years of age reported to the Rio Grande do Sul State Toxicology Information Center (CIT/RS) in Porto Alegre, Brazil, 2003. A total of 1,311 cases were selected and data were extracted on children who had suffered individual accidental poisoning inside the home. From a systematic random sample of 286 patients, 21 interviews were held with the children's parents or guardians, using a structured instrument. The typical profile of poisoning featured: < or=1 year age bracket; male gender; oral exposure; poisonous agent located on living room or bedroom floor; furniture height < 30cm; time of poisoning from 18:01 to 22:00; time between poisoning and search for emergency medical care less than 30 minutes; analgesics as poisonous agent; medical assessment of purported poisoning as non-toxic, evolving to cure. The data indicate relevant characteristics as to the time of poisoning and place where poisonous agents were located. Definition of a profile helps promote and expand childhood poisoning prevention campaigns by public health agencies.

Accidents, Home↗
PubMed1995

Drug poisoning in older patients. Preventative and management strategies.

Children under 6 years of age are involved in the majority of poisonings. However, the elderly are more likely to require hospitalisation and to die from poisonings compared with younger individuals. Drugs play an important role in the poisoning exposures of older patients. Analgesics, cardiovascular medications, theophylline preparations and antidepressants and other psychotropic medications are most commonly implicated in drug poisoning fatalities in elderly Americans. Careful review of information which characterises drug poisonings in the elderly is essential to the development of effective preventative strategies. Most poison centre calls for elderly patients involve accidental exposures. The ingestion of extra doses of medications because of forgetfulness, mistaken identity of medications, incorrect route of administration, and improper storage of medications are among the the primary reasons for unintentional drug poisonings in older patients. A model for injury control composed of 3 phases can be applied to poison exposures in the elderly: activities in the pre-event phase focus on prevention; it should occur; the post-event phase is directed at appropriate management to reduce the consequence of injury from poison exposure once it occurs. The general management of drug poisonings is similar in older and younger patients. However, management in the elderly is complicated by difficulties in the diagnosis of drug poisoning, pharmacokinetic and pharmacodynamic changes associated with aging, increased incidence of chronic illness, and increased medication with the potential for clinically significant drug interactions. Aggressive initial treatment is imperative because the elderly are generally more susceptible to the toxic effects of drugs.

Aged↗
PubMed1996

Taiwan National Poison Center: epidemiologic data 1985-1993.

UNLABELLED: The Taiwan National Poison Center has received more than 30,000 telephone calls since its establishment in July 1985. OBJECTIVE: To obtain more information about poisoning exposures in Taiwan, a retrospective analysis was conducted of all telephone calls to the center concerning human poisoning exposures July 1985 through December 1993. METHODS: The following data were tabulated: age, sex, intent of exposure, route of exposure, substances ingested and clinical severity. RESULTS: During the eight years (1985-1993), 23,436 telephone calls concerning human poisoning exposure were recorded. Adults accounted for most cases (75.2%) and exposures involving males (54.2%) were somewhat more prevalent than female poisoning exposures (44.7%). Intentional poisonings (54.6%) were more common than unintentional poisonings (40.1%), with an inverse relationship in pediatric poisoning exposures. After amphetamines, the most frequently ingested poisons were pesticides, benzodiazepines, and cleaning products. Fatalities occurred most frequently following ingestion of pesticides. The mortality rate was 5.7% for all exposures. CONCLUSIONS: Human poisoning is a serious problem in Taiwan. The reduction of suicide attempts is a major objective. Childhood poisonings are underreported and of high mortality.

Adolescent↗
PubMed1995

Underreporting of fatal cases to a regional poison control center.

We assessed fatal drug overdose and poisoning case surveillance by a regional poison control center, comparing it with medical examiner determinations of death by poisoning over the same 2-year period and from the same catchment area. We studied 358 fatal cases of poisoning or drug overdose reported by a medical examiner and 10 fatal cases of poisoning or drug overdose reported by a poison control center, analyzing demographics and other case-associated factors with with possible successful poison control center case surveillance. Of the medical examiner cases, 245 (68%) were prehospital deaths. Of the remaining 113 emergency department or hospital cases, only 5 (4.4%) were also reported to the poison control center. Compared with cases involving illicit drugs, other narcotics, and sedative drugs, those that involved other prescription drugs (relative odds, 30.6; 95% confidence interval, 2.7 to 351) and over-the-counter products and other substances (odds ratio, 18.9; 95% confidence interval, 1.4 to 257) were significantly more likely to be reported to the poison control center. Most fatal cases of poisoning and drug overdose are not detected through poison control center surveillance. For prevention and treatment, health planners and policy makers should recognize the implications of case underreporting.

Adult↗
PubMedDate not supplied

Retrospective evaluation of emergency service patients with poisoning: a 3-year study.

The purpose of this retrospective study was to evaluate the characteristics of cases of acute poisoning in adults who were admitted to emergency service over a 3-year period. Clinical charts were analyzed retrospectively for etiologic and demographic patient characteristics. A total of 810 adults were admitted to the emergency center with acute poisoning. The female-to-male ratio was 2:1. Mean ages of female and male patients were 28.8+/-12.9 years and 35.1+/-15.4 years, respectively, and many patients (46.9%) were between the ages of 16 and 25 years. Medicinal drugs were found to be the primary cause (60.5%) of poisoning, and tricyclic antidepressants were the most frequent causative agents (36.3%). Seasonal distribution of poisoning cases suggested a peak in the summer months (35.4%). Overall, 68.6% of acute poisonings were suicide attempts, and of these patients, 84.9%, 14%, and 1.1% were attempting suicide for the first, second, and third times, respectively. Among 810 cases of acute poisoning, 15 were fatal. The following conclusions were reached by investigators: (1) in the test region, younger females, especially single females, were at greater risk for poisoning than other patient groups, (2) self-poisoning cases constituted the majority of all poisonings, and (3) the main agents of self-poisoning were medicinal drugs, with antidepressants used most frequently. It was also found that unintentional poisoning commonly resulted from intake of foods, especially mushrooms.

Adolescent↗
PubMed2003

Muscle injury in organophosphorous poisoning and its role in the development of intermediate syndrome.

Muscle injury and its role in the development of Type II paralysis was studied in 25 patients with acute organophosphate poisoning. All patients were assessed for severity of poisoning at admission and through the course of poisoning for the development and duration of intermediate syndrome (IS) (Type II paralysis). Blood levels of acetylcholinesterase, creatine kinase, creatine kinase MM, LDH and LDH5 were estimated through the course of the poisoning. Of the 25 patients, 22 were severely poisoned and 3 had mild to moderate poisoning. Severely poisoned patients had a significantly greater rate of developing intermediate syndrome (17/22) (P = 0.026). Type I paralysis and fasciculations occurred in 76 and 70.5% of patients who developed intermediate syndrome, in comparison to 38 and 50%, respectively, of those who did not develop intermediate syndrome. Weakness developed in the same groups of muscles in both Types I and II paralysis but was of longer duration in patients who developed Type II paralysis. Acetylcholinesterase was inhibited > 90% throughout the course of poisoning with greater inhibition in patients with longer duration intermediate syndrome. Muscle injury was seen in all patients beginning at admission, peaking over the first 5 days and then declining over the next 5 days. Temporal profiles of blood muscle isoenzymes showed significantly greater muscle injury in those patients with greater severity of poisoning at admission, those who developed intermediate syndrome and in patients with longer duration intermediate syndrome. The findings of this study suggest that Types I and II paralysis in organophosphate poisoning are not separate syndromes but a clinical continuum determined by the severity of poisoning. The magnitude of organophosphate exposure and of muscle injury during the cholinergic crises appears to determine the occurrence and severity of intermediate syndrome.

Acetylcholinesterase↗