|TOXICOLOGY SYMPOSIA – REVIEW ARTICLE
|Year : 2015 | Volume
| Issue : 1 | Page : 46-51
Organophosphorus poisoning: A social calamity
Udit Narang1, Purvasha Narang2, OmPrakash Gupta1
1 Department of Medicine, MGIMS, Sewagram, Wardha, Maharashtra, India
2 Department of Ophthalmology, MGIMS, Sewagram, Wardha, Maharashtra, India
|Date of Web Publication||19-Feb-2015|
Dr. Udit Narang
Department of Medicine, MGIMS, Sewagram, Wardha, Maharashtra
Source of Support: None, Conflict of Interest: None
Poisoning with organophosphorus (OP) compounds is a global public health problem. According to World Health Organization (WHO), 3 million cases of pesticide (mainly OP compounds) poisoning occur every year, resulting in an excess of 250,000 deaths. Of these, about 1 million are accidental, and 2 million are suicidal poisonings. The incidence has steadily increased in the recent past and has reached a level in the developing countries, where it can be called a "social calamity." Diagnosis is mainly on clinical grounds. The wellknown antidotes of OP poisonings are atropine and oximes. However, investigations over the recent years have introduced new adjunct therapy and cheap medications such as sodium bicarbonate and magnesium sulfate as well as antioxidants that should be considered for the management of OP poisoning. While efficacy of atropine is clinically proven, clinical experience with pralidoxime has been controversial. A lot of new modalities of management like K-oximes, hemoperfusion, and Fresh frozen plasma are under evaluation. Prevention still appears to be the best modality of management. Appropriate legislations and pesticides control are recommended for the developing countries to prevent occupational, accidental, and intentional poisonings.
Keywords: Acetyl-cholinesterase, carbamate, organophosphorus poisoning
|How to cite this article:|
Narang U, Narang P, Gupta O. Organophosphorus poisoning: A social calamity. J Mahatma Gandhi Inst Med Sci 2015;20:46-51
| Introduction|| |
Poisons are subtle and silent weapons that can be easily used without violence and often, without arousing suspicion. Vast developments in the field of industries, medicine, and agriculture have led to the utilization of various new poisonous compounds. India predominantly being an agrarian country, wide use coupled with easy accessibility, i.e., "over the counter" availability of organophosphorus (OP) compounds, makes it the most common modality of poisoning.  Poisoning with OP compounds is a global public health problem. According to World Health Organization (WHO), 3 million cases of pesticide (mainly OP compounds) poisoning occur every year, resulting in an excess of 250,000 deaths. , Of these, about 1 million are accidental, and 2 million are suicidal poisonings.  As per estimates of National Crime Bureau of India, suicides by consumption of pesticides account for 19.4 and 19.7% of all cases of suicidal poisoning in the year 2006 and 2007, respectively.  The incidence has steadily increased in the recent past and has reached a level in the developing countries, where it can be called a "social calamity."
Common OP compounds used in agriculture are parathion, malathion, chlorpyrifos, and dichlorvos. OP compounds exist in a military setting as well in the form of nerve gas. Common among them are sarin, tabun, soman, and VX. Discussion of these compounds is beyond the scope of this review. OP agents or their metabolites cause toxicity by inhibiting the function of acetyl-cholinesterase  an enzyme responsible for hydrolyzing and inactivating the neurotransmitter acetylcholine. Atropine  is an established specific antidote for organophosphorus poisoning (OPP). WHO recommends that a second type of antidote called pralidoxime (acetyl-cholinesterase reactivator) be given along with atropine. Although the beneficial effects of atropine are clear, controversy surrounds the role of pralidoxime in treating organophosphate poisoning. Recent studies regarding the use of pralidoxime have shown contrasting outcomes resulting in confusion about the management of OPP patients. Study by Pawar et al. showed decreased morbidity and mortality using high-dose pralidoxime regimen, whereas study by Eddleston et al. concluded that use of pralidoxime was associated with increased mortality.
The present paper aims at discussing, in brief, the controversies involved in the management of OPP and to provide an update on the recent advances in the management of OPP.
| Mechanism of Action of Organophosphorus Poisoning|| |
Organophosphorus compounds contain carbon and phosphorous acid derivatives that are well absorbed through the skin, lungs, and gastrointestinal tract. They bind to red blood cell (RBC) acetylcholinesterase (AChE) and render this enzyme nonfunctional leading to an overabundance of acetylcholine at the neuronal synapses and the neuromuscular junction. ,, In addition, plasma cholinesterase (butyrylcholinesterase [BuChE] or pseudocholinesterase [PsCE]) and neuropathy target, esterase are also inhibited, but clinical significance of these interactions are uncertain. ,, A conformational change in the compound renders the enzyme irreversibly resistant to reactivation by an antidotal oxime, and this is known as "aging." 
The use of OP compounds has declined in the last 10-20 years, in part due to the development of carbamate insecticides, which are associated with similar toxicities but slightly different mechanism of action.  Carbamate compounds unlike organophosphates are transient cholinesterase inhibitors, which spontaneously hydrolyze from the cholinesterase enzymatic site within 48 h,leading to shorter duration of toxicity, but have similar mortality rates. 
| Clinical Features|| |
Clinical features depend upon organophosphorus agent's route of absorption, enzymatic conversion to active metabolites, rate of AChE inhibition and the lipophilicity of agent. Oral or respiratory exposures generally result in signs or symptoms within 3 h, while symptoms of toxicity from dermal absorption may be delayed up to 12 h. Lipophilic agents such as dichlofenthion, fenthion, and malathion are associated with delayed onset of symptoms (up to 5 days) and prolonged illness (>30 days), which may be related to rapid adipose fat uptake and delayed redistribution from the fat stores. 
Manifestations include: 
- Expression of muscarinic overstimulation: Bradycardia, bronchorrhea, bronchospasm, diarrhea, hypotension, lacrimation, miosis, salivation, urination and vomiting.
- Expression of nicotinic overstimulation in the sympathetic system: Hypertension, mydriasis, sweating, and tachycardia.
- Expression of nicotinic overstimulation in the central nervous system: Agitation, coma, confusion and respiratory failure.
- Expression of nicotinic overstimulation at the neuromuscular junction: Fasciculation, muscle weakness and paralysis.
The muscarinic signs can be remembered using of one of the two mnemonics: 
- SLUDGE/BBB - Salivation, Lacrimation, Urination, Defecation, Gastric Emesis, Bronchorrhea, Bronchospasm, Bradycardia
- DUMBELS - Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/Bradycardia, Emesis, Lacrimation, Salivation
"Intermediate syndrome" (IMS) is a distinct neurological disorder occurring 24-96 h after exposure in 10-40% of poisoning. It is characterized by neurological findings including neck flexion weakness, decreased deep tendon reflexes, cranial nerve abnormalities, proximal muscle weakness, and respiratory insufficiency. , The proposed mechanisms of IMS include varying susceptibilities of various cholinergic receptors, muscle necrosis, prolonged AChE inhibition, inadequate oxime therapy, down regulation or desensitization of postsynaptic acetylcholine receptors, failure of postsynaptic acetylcholine release, and oxidative stress-related myopathy.  Although IMS is well recognized as a disorder of the neuromuscular junction, its exact etiology, incidence, and risk factors are not clearly defined because existing studies are mainly small case series and do not employ a consistent and rigorous definition of IMS. The treatment of IMS is mainly supportive. The IMS has rarely been described following carbamate poisoning.
| Diagnosis|| |
Diagnosis is mainly on clinical grounds. In the absence of a known ingestion or exposure, the clinical features of cholinergic excess should indicate the possibility of organophosphate poisoning. In the case of doubt, a trial of 1 mg atropine in adults (or 0.01-0.02 mg/kg in children) may be employed. The absence of signs or symptoms of anticholinergic effects following atropine challenge strongly supports the diagnosis of poisoning with an AChE inhibitor. The duration of toxicity and the therapeutic window during which oxime treatment is likely to be effective are markedly different for dimethyl and diethyl compounds. Dimethyl compounds undergo rapid aging, making early initiation of oxime therapy critical whereas diethyl compounds may exhibit delayed toxicity and may require prolonged treatment.  Direct measurement of RBC AChE activity provides a measure of the degree of toxicity and also helpful in evaluating chronic or occupational exposure. Sequential assays may help in measurement of effectiveness of the therapy. However, most labortaries do not have this facility.
| Role of Pseudocholinesterase|| |
In a study conducted by Rehiman et al.  the severity of poisoning directly correlated with serum cholinesterase level when compared to peradeniya organophosphorus poisoning scale but the initial value failed to predict the mortality. In another study by Johnson  showed the inability of the PsCE to correlate with the severity of poisoning and proposed not to use it as a guide to therapy. Çolak et al. proposed low initial serum cholinesterase and high glucose levels as a useful marker in predicting organophosphate-induced intermediate syndrome. Sun et al. suggested that with the same level of enzymatic activity of cholinesterase, the symptoms of the patients poisoned via gastrointestinal tract are more serious than poisoning through skin. Hence, the levels of cholinesterase are not helpful in judging the severity of poisoning. However, reactivation of the cholinesterase is earlier in patients poisoned by skin route.
| Principles of Management|| |
The management of acute organophosphate poisoning depends on its severity. In mild cases, removing the patient from the area of exposure and low dose of atropine may suffice. However, in severe cases, resuscitation, artificial ventilation and high-doses of antidotes become necessary. The well known antidotes of OPs are atropine and oximes. However, investigations over the recent years have introduced newer adjunct therapy and cheap medications such as sodium bicarbonate, magnesium sulfate as well as antioxidants that should be considered in the management of OP poisoning.  In a recent systematic review,  the authors suggested the following treatment protocol that include removal of contaminated clothes, washing the poisoned person using gloves, administering sodium bicarbonate, & activated charcoal (single or multiple doses), gastric lavage, alpha2 adrenergic agonists, organophosphorus hydrolases, oximes, atropine, benzodiazepines, BuChE replacement, glycopyrronium bromide (glycopyrrolate), magnesium sulfate, N-methyl-D-aspartate receptor antagonists, and neuroprotective agents. It is beyond the scope of this review to establish the efficacy of all these different treatments and also due to the lack of evidence-based data.
| Atropine|| |
Atropine is considered the most acceptable and widely used treatment for OP and carbamate poisoning. It is a competitive inhibitor of the muscarinic Ach receptor; therefore, it diminishes some of the pathological cholinergic effect, but is ineffective on nicotinic receptor-medicated manifestations. Atropine should be administered at a beginning dose of 2-5 mg intravenous (IV) for adults and 0.05 mg/kg IV for children. If no effect is noted, the dose should be doubled every 3-5 min until pulmonary muscarinic signs and symptoms are alleviated. Dosing should be titrated to the therapeutic end point of the clearing of respiratory secretions and the cessation of bronchoconstriction and never by tachycardia and mydriasis.  At least the same amount as the initial atropinization dose should be infused in 500 mL dextrose 5% constantly to sustain the atropinization and may be repeated till patient becomes completely asymptomatic. 
Atropine should not be given IV to a hypoxic patient. If the patient is hypotensive, atropine can be given through an endotracheal tube or intratracheally for rapid absorption through the peribronchial vessels.  Aerosolized atropine can also be administered quickly by inhalation. Studies suggest that in addition to the local effects in the lungs, it is also absorbed systemically. 
| Oxime|| |
Discovered in 1956, pralidoxime has been used in the management of OPP in addition to atropine. While efficacy of atropine is clinically proven, clinical experience with pralidoxime has been controversial. In the early nineties, clinicians started questioning the efficacy of pralidoxime in OP poisoning. The early research in this field was led by Duval et al. and de Silva et al.,  which was followed by trials by many other researchers using a variety of dosing regimens of pralidoxime. All these studies revealed that either add-on pralidoxime therapy did not offer any added benefit or was associated with worse outcomes when compared to treatment with atropine. ,, In a recently published trial by Syed et al.,  administration of the WHO-recommended regimen of pralidoxime to patients with symptomatic OPP showed no change in the mortality rates in patients treated with pralidoxime compared to patients who were treated with atropine only (28% vs. 26%). Banerjee et al. further showed that use of pralidoxime neither had any beneficial effect on mortality nor on the duration of hospital stay. In their study the mean duration of stay in the hospital (in days) was 5.68 ± 1.87 (mean ± standard deviation [SD]) in atropine only group as compared to 7.02 ± 1.12 (mean ± SD) in the group receiving both atropine and pralidoxime (P < 0.001). Conversely, in one large prospective study, patients poisoned with diethyl compounds (e.g., chlorpyrifos) had significantly lower mortality and intubation rates following treatment with pralidoxime than those poisoned with dimethyl agents (e.g., dimethoate, fenthion).  Johnson et al. have argued that the failure of oxime therapy does not indicate ineffectiveness of the drug nor does it necessarily indicate delay in administration; indeed, failure of treatment is usually a function of inadequate dosing. They emphasized that dosage should be maintained continuously until clear, irreversible, clinical improvement is achieved. Although more and more studies are discouraging the use of oxime in the management of OP poisoning, a final verdict is yet to be made. Until this variability is better understood, and other treatments become available, we believe that all patients poisoned with OPs should be treated with an oxime also.
| Benzodiazepines|| |
Benzodiazepines have favorable effects on anxiety, restlessness, muscle fasciculation, seizures, apprehension and agitation and decrease morbidity and mortality when used together with atropine and an oxime in nerve agent's poisoning.  The recommended dose of diazepam by WHO is 5-10 mg intravenously over a period of 3 min that can be repeated every 10-15 min in adult patients (up to a maximum of 30 mg). For children, the dose is 0.2-0.3 mg/kg given intravenously over 3 min. The maximum dose for children up to 5 years old is 5 mg, while up to 10 mg can be used for children who are older than 5 years. 
| Sodium Bicarbonate|| |
Intravenous infusion of sodium bicarbonate (5 mEq/kg in 60 min followed by 5-6 mEq/kg/day) helps in moderate alkalinization (blood pH between 7.45 and 7.55) in OP pesticide poisoning, which has been shown to have beneficial effects.  However, further studies are required to validate these findings in these studies.
| Magnesium Sulfate|| |
Magnesium sulfate blocks calcium channels and thus reduces acetylcholine release. Given in a dose of 4 g on 1 st day of admission, it has been shown to decrease hospitalization period and improve outcomes in patients with OP poisoning. 
| Other Agents|| |
Various other agents have been tried in animal models in the management of OPP. The alpha2-adrenergic receptor agonists such as clonidine can reduce acetylcholine synthesis and release in presynaptic junctions.  However, efficacy in humans is still not well established. Antioxidants have also been proposed to have a therapeutic effect in OPP by increased thiobarbituric reactive substances and lipid peroxidation either as acute, subchronic or chronic exposure.  An animal study on rats reported beneficial effect of Vitamin E in dimethoate and malathion-induced oxidative stress in rat erythrocytes. 
| Newer Therapies in Management of Organophosphorus Poisoning|| |
In recent years, efforts have been made to develop efficacious broad-spectrum AChE reactivators. Hundreds of compounds have been prepared; of which K-oximes appear to be among the most promising ones. Several in vivo and in vitro studies on paraoxon, malaoxon and diisopropylfluorophosphate, showed that K-27, K-48 and K-75 reactivation ability was significantly higher than that of pralidoxime.  As the therapeutic efficacy of pralidoxime is more and more debated, these newer oximes might constitute an interesting therapeutic strategy in OPP treatment.
Organophosphorus pesticides are fat-soluble macromolecular substances that can bind to the proteins easily. As hemoperfusion therapy is highly effective in clearing lipid soluble or plasma protein-bound poisons, it has been proposed that repeated hemoperfusion would rapidly attenuate the poisoning symptoms and minimize complications. In a recent study in China, Bo  found that early & repeated hemoperfusion was more efficient than single hemoperfusion in treating organophosphate poisoning.
Fresh frozen plasma
Bio-scavengers such as fresh frozen plasma (FFP) or albumin have been recently suggested as a useful therapy through clearing of free organophosphates. In a nonrandomized controlled study of 12 patients and 21 control, authors found that FFP therapy increased the levels of 2-BuChE in OP poisoned patients and suggested that it may prevent the development of intermediate syndrome and mortality rate.  In another study, despite significant increase in BuChE concentrations with FFP, authors did not find considerable benefit following treatment with FFP or albumin. 
ICU-based clinical scoring systems like the Acute Physiology and Chronic Health Evaluation II (APACHE-II), Simplified Acute Physiology Score II, and the Mortality Prediction Model II have been found to be a better predictor of mortality than the poisoning severity scale.  In the only prospective study, to examine prognostic factors for patients acutely poisoned with OP or carbamate (n = 1365), the authors found that a Glasgow coma score (GCS) of less than 13 was associated with a poor prognosis, and using the GCS was as good as using the International Program on Chemical Safety Poison Severity Score.  However, the OP agent involved must also be taken into account.
| Conclusions and Recommendations|| |
A lot of development has occurred in the field of management of OPP. Recent investigations have revealed more understanding on the basic principles of treatment, and newer medications are now available for the management of OP poisonings. However, further studies are required to find out more effective treatments for the severe OP poisonings. Prevention still appears to be the best modality of management. Appropriate legislations and pesticide control are recommended for the developing countries to prevent occupational, accidental, and intentional poisonings.
| References|| |
Malik GM, Mubarik M, Romshoo GJ. Organophosphorus poisoning in the Kashmir Valley, 1994-1997. N Engl J Med. 1998;338:1078.
Banerjee I, Tripathi S K, Roy A S. Efficacy of pralidoxime in organophosphorus poisoning: Revisiting the controversy in Indian setting. J Postgrad Med. 2014;60:27-30.
Joshi S, Biswas B, Malla G. Management of organophosphorus poisoning. Indian J Pharmacol. 2006;41:69-70.
Bairy KL, Vidyasagar S, Sharma A, Sammad V. Controversies in the management of organophosphate pesticide poisoning. Indian J Pharmacol. 2007;39:71-4.
Chugh SN, Agarwal N, Dabla S. Comparative evaluation of "atropine alone" and atropine with pralidoxime in the management of organophosphorus poisoning. J Indian Acad Clin Med. 2006;6:33-7.
du Toit PW, Müller FO, van Tonder WM, Ungerer MJ. Experience with the intensive care management of organophosphate insecticide poisoning. S Afr Med J. 1981;60:227-9.
Pawar KS, Bhoite RR, Pillay CP, Chavan SC, Malshikare DS, Garad SG. Continuous pralidoxime infusion versus repeated bolus injection to treat organophosphorus pesticide poisoning: A randomised controlled trial. Lancet. 2006;368:2136-41.
Eddleston M, Eyer P, Worek F, Juszczak E, Alder N, Mohamed F, et al
. Pralidoxime in acute organophosphorus insecticide poisoning: A randomised controlled trial. PLoS Med. 2009;6:e1000104.
Rotenberg M, Shefi M, Dany S, et al
. Differentiation between organophosphate and carbamate poisoning. Clin Chim Acta. 1995;234:11.
Tafuri J, Roberts J. Organophosphate poisoning. Ann Emerg Med. 1987;16:193.
Khurana D, Prabhakar S. Organophosphorus intoxication. Arch Neurol. 2000;57:600.
Morgan JP. The Jamaica ginger paralysis. JAMA. 1982;248:1864.
Mutch E, Blain PG, Williams FM. Interindividual variations in enzymes controlling organophosphate toxicity in man. Hum Exp Toxicol. 1992;11:109.
Balali-Mood M, Saber H. Recent advances in the treatment of organophosphorous poisonings. Iran J Med Sci. 2012;37:74-91.
Eddleston M, Szinicz L, Eyer P, Buckley N. Oximes in acute organophosphorus pesticide poisoning: A systematic review of clinical trials. QJM. 2002;95:275.
Eddleston M, Eyer P, Worek F, et al
. Differences between organophosphorus insecticides in human self-poisoning: A prospective cohort study. Lancet. 2005;366:1452.
Bird S, Traub SJ, Grayzel J. Organophosphate and carbamate poisoning. Uptodate Version 15.0. 2014;339.
Sidell FR. Clinical effects of organophosphorus cholinesterase inhibitors. J Appl Toxicol. 1994;14:111.
Indira M, Andrews MA, Rakesh TP. Incidence, predictors, and outcome of intermediate syndrome in cholinergic insecticide poisoning: A prospective observational cohort study. Clin Toxicol (Phila). 2013;51:838.
Karalliedde L, Baker D, Marrs TC. Organophosphate-induced intermediate syndrome: Aetiology and relationships with myopathy. Toxicol Rev. 2006;25:1.
Yang CC, Deng JF. Intermediate syndrome following organophosphate insecticide poisoning. J Chin Med Assoc. 2007;70:467-72.
Eyer P. The role of oximes in the management of organophosphorus pesticide poisoning. Toxicol Rev. 2003;22:165.
Rehiman S, Lohani SP, Bhattarai MC. Correlation of serum cholinesterase level, clinical score at presentation and severity of organophosphorous poisoning. J Nepal Med Assoc. 2008;47:47-52.
Johnson MK. Mechanisms of and biomarkers for acute and delayed neuropathic effects of organophosphorus esters. In: Use of Biomarkers in Assessing Health and Environmental Impact of Chemical Pollutants. NATO Advanced Study Workshop. 1992;169.
Çolak Þ, Erdoðan MÖ, Baydin A, Afacan MA, Kati C, Duran L. Epidemiology of organophosphate intoxication and predictors of intermediate syndrome. Turk J Med Sci. 2014;44:279-82.
Sun ZJ, Zhang JM, Wang H, Liu JP. Cholinesterase activity is not parallel to symptoms in patients suffering from organophosphorous pesticide poisoning through skin or by gastrointestinal tract. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2007;19:485-7.
Blain PG. Organophosphorus poisoning (acute) Clin Evid. 2011;17:2102.
Sevim S, Aktekin M, Dogu O, et al
. Late onset polyneuropathy due to organophosphate (DDVP) intoxication. Can J Neurol Sci. 2003;30:75.
Balali-Mood M, Balali-Mood K. Neurotoxic disorders of organophosphorus compounds and their managements. Arch Iran Med. 2008;11:65-89.
Ohbu S, Yamashina A, Takasu N. Sarin poisoning on Tokyo subway. Southern Med J. 1997; 90: 587-593.
Kassa J, Fusek J. The positive influence of a cholinergic-anticholinergic pretreatment and antidotal treatment on rats poisoned with supralethal doses of soman. Toxicology. 1998;128:1-7.
Duval G, Rakouer JM, Tillant D, Auffray JC, Nigond J, Deluvallee G. Acute poisoning by insecticides with anticholinesterase activity. Evaluation of the efficacy of a cholinesterase reactivator, pralidoxime. J Toxicol Clin Exp. 1991;11:51-8.
de Silva HJ, Wijewikrema R, Senanayake N. Does pralidoxime affect outcome of management in acute organophosphate poisoning? Lancet. 1992;339:1136-8.
Syed S, Gurcoo SA, Farooqui AK, Nisa W, Sofi K, Wani TM. Is the World Health Organization-recommended dose of pralidoxime effective in the treatment of organophosphorus poisoning? A randomized, double-blinded and placebo-controlled trial. Saudi J Anaesth. 2015;9:49-54.
Johnson MK, Vale JA, Marrs TC, Meredith TJ. Pralidoxime for organophosphorus poisoning. Lancet. 1992;340:64.
Cannard K. The acute treatment of nerve agent exposure. J Neurol Sci. 2006;249:86-94.
Balali-Mood M, Ayati MH, Ali-Akbarian H. Effect of high doses of sodium bicarbonate in acute organophosphorous pesticide poisoning. Clin Toxicol (Phila). 2005;43:571-4.
Pajoumand A, Shadnia S, Rezaie A, Abdi M, Abdollahi M. Benefits of magnesium sulfate in the management of acute human poisoning by organophosphorus insecticides. Hum Exp Toxicol. 2004;23:565-9.
Liu WF. A symptomatological assessment of organophosphate-induced lethality in mice: Comparison of atropine and clonidine protection. Toxicol Lett. 1991;56:19-32.
Ranjbar A, Solhi H, Mashayekhi FJ, Susanabdi A, Rezaie A et al
. Oxidative stress in acute human poisoning with organophosphorus insecticides; a case control study. Environ Toxicol Pharmacol. 2005;20:88-91.
Barelli A, Soave PM, Del Vicario M, Barelli R. New experimental Oximes in the management of organophosphorus pesticides poisoning. Minerva Anestesiol. 2011;77:1197-203.
Bo L. Therapeutic efficacies of different hemoperfusion frequencies inpatients with organophosphate poisoning. Eur Rev Med Pharmacol Sci. 2014;18:3521-3.
Güven M, Sungur M, Eser B, Sari I, Altuntaº F. The effects of fresh frozen plasma on cholinesterase levels and outcomes in patients with organophosphate poisoning. J Toxicol Clin Toxicol. 2004;42:617-23.
Peter JV, Thomas L, Graham PL, et al
. Performance of clinical scoring systems in acute organophosphate poisoning. Clin Toxicol (Phila). 2013;51:850.
Davies JO, Eddleston M, Buckley NA. Predicting outcome in acute organophosphorus poisoning with a poison severity score or the Glasgow coma scale. QJM. 2008;101:371.
|This article has been cited by|
||Analyzing organophosphate pesticide-serum albumin binding interaction: a combined STD NMR and molecular docking study
| ||Vandana Dahiya,Bibin G. Anand,Karunakar Kar,Samanwita Pal |
| ||Journal of Biomolecular Structure and Dynamics. 2020; : 1 |
|[Pubmed] | [DOI]|
||In vitro interaction of organophosphate metabolites with bovine serum albumin: A comparative 1H NMR, fluorescence and molecular docking analysis
| ||Vandana Dahiya,Bibin G. Anand,Karunakar Kar,Samanwita Pal |
| ||Pesticide Biochemistry and Physiology. 2019; |
|[Pubmed] | [DOI]|
||Poisoned to paralysed: A case of organophosphate induced delayed neuropathy
| ||Mahadevaiah Mahesh,SindhuRao Malla,ChilkundaRaviprakash Venkatesh,Varsha Tandure |
| ||Journal of Dr. NTR University of Health Sciences. 2019; 8(4): 281 |
|[Pubmed] | [DOI]|
||Recent advances in management of organophosphate & carbamate poisoning
| ||Ashok Kumar,Shubha Laxmi Margekar,Purnima Margekar,Venugopal Margekar |
| ||Indian Journal of Medical Specialities. 2018; 9(3): 154 |
|[Pubmed] | [DOI]|