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Table of Contents
Year : 2019  |  Volume : 20  |  Issue : 2  |  Page : 131-140

Organophosphate poisoning: Overview, management and nursing care

Department of Medical Nursing, College of Nursing, CMC, Vellore, Tamil Nadu, India

Date of Submission20-Dec-2019
Date of Acceptance30-Dec-2019
Date of Web Publication01-Jun-2020

Correspondence Address:
Mrs. Mary Jancy Joy
College of Nursing, CMC, Vellore, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/IJCN.IJCN_24_20

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Acute poisoning by organophosphates (OPs) for suicidal purpose poses a major problem, leading to high mortality in the developing countries. This occurs as OPs irreversibly bind to acetylcholinesterase, leading to the accumulation of acetylcholine at the neuromuscular junction and subsequent over-activation of cholinergic receptors in various parts of the body. Early identification of the signs and symptoms and prompt management enhance better outcomes reducing mortality. Atropine, oximes, neuroprotection and quality care remain the mainstay of treatment for OP poisoning and can reverse the life-threatening features of acute poisoning. Supportive treatment includes maintaining airway, breathing, circulation and decontamination of the poison. Nurses working in the critical care units play a vital role in monitoring the patient closely, providing quality nursing care and thereby preventing complications.

Keywords: Anticholinergics, decontamination, organophosphate, poisoning

How to cite this article:
Joy MJ, Radhakrishnan B, Sekar M, David S. Organophosphate poisoning: Overview, management and nursing care. Indian J Cont Nsg Edn 2019;20:131-40

How to cite this URL:
Joy MJ, Radhakrishnan B, Sekar M, David S. Organophosphate poisoning: Overview, management and nursing care. Indian J Cont Nsg Edn [serial online] 2019 [cited 2022 Dec 7];20:131-40. Available from: https://www.ijcne.org/text.asp?2019/20/2/131/285590

  Introduction Top

Organophosphates (OPs) have been used as insecticides world over for more than 50 years. OP compounds and carbamates, also known as cholinesterase inhibitors, are widely used pesticides. These agents comprise thousands of structurally related substances, which are responsible for a number of suicidal or accidental poisonings, with an estimated 200,000 deaths per year in rural areas of developing countries.[1]

During the 1930s, German military scientists synthesised numerous OP compounds, including parathion, and several highly potent chemical warfare agents (e.g., GA [tabun], GB [sarin] and GD [soman]).[2] Because these chemicals affect the autonomic nervous system, they are referred to as 'nerve agents'. Terrorist attacks in Japan (1994 and 1995) affected thousands of urban civilians who were exposed to the OP compound sarin.[2] Accidental poisoning with cholinesterase inhibitors can also occur from the contamination of food or beverages. Medical applications of OPs and carbamates include reversal of neuromuscular blockade (neostigmine, pyridostigmine and edrophonium) and treatment of glaucoma, myasthenia gravis and Alzheimer's disease (echothiophate, pyridostigmine, tacrine and donepezil).

  Prevalence Top

Globally, it is reported that 3 million or more people are exposed to OPs every year, accounting for 300,000 mortality. In the United States, there are around 8000 exposures per year, with fewer deaths.[3] Poisoning leads to significant morbidity and mortality each year in India. According to the National Crime Records Bureau of India, there were 27,657 deaths and suicides by poisoning in 2015.[4] A retrospective analysis of data from the National Poisons Centre of India reports that the most common poisonings include the use of household products such as ant and cockroach spray, followed by pharmaceuticals, agricultural pesticides and industrial chemicals.[5],[6] According to the World Health Organization, it is estimated that India's mortality rate from poisonings is 31.3/100,000 individuals.[7]

Toxicity generally results from accidental or intentional ingestion or exposure to agricultural pesticides. Toxic ingestions, both intentional and unintentional, represent a significant public health issue worldwide.


  1. Poison: A foreign chemical that is capable of producing a harmful effect on a biologic system (xenobiotic)
  2. Poisoning: The development of harmful effects on normal body functions following exposure to chemicals after it is swallowed, inhaled, injected or absorbed.

  Types of Organophosphate Poisoning Top

Organophosphate poisoning

E.g., parathion, fenthion, malathion, diazinon, dursban, quinalphos and prothoate.

OPs are a group of chemicals that have many domestic and industrial uses. They are most commonly used as insecticides. Although the use of the organophosphorus compounds cannot be denied in daily life, they are commonly used as agents for ingestions by those who attempt suicide because of its easy availability and its potency to kill a person if immediate treatment is not provided. There is a high incidence of aspiration pneumonia as the most common OPs have a petroleum base.[8]

Routes of absorption [3],[8]

  • Ingestion - Gastrointestinal (GI) tract (accidental, deliberate)
  • Cutaneous - Skin
  • Inhalation - Lungs.

  Pathophysiology Top

OPs exert their acute effects by causing overstimulation at cholinergic nerve terminals. Acetylcholine (Ach) is found in the central and peripheral nervous systems, neuromuscular junctions and red blood cells (RBCs).[9] Normally, acetylcholinesterase (AChE) catalyses the degradation of the neurotransmitter Ach into choline and acetic acid in the synapse. OP pesticides act by binding irreversibly to the AChE, thereby reducing the ability of the enzyme to break down the neurotransmitter. This produces an accumulation of Ach in the central and peripheral nervous systems, resulting in an acute cholinergic syndrome via continuous neurotransmission.[9] The clinical onset of cholinergic overstimulation can vary from almost instantaneous to several hours after exposure. Although most patients rapidly become symptomatic, the onset and severity of symptoms depend on the specific compound, amount, route of exposure and rate of metabolic degradation.[3]

[TAG:2]Clinical Manifestations [1][/TAG:2]

Signs and symptoms of OP poisoning can be divided under the following categories:[Table 1]
Table 1: Clinical manifestations in Organphosphorus poisoning

Click here to view

  1. Muscarinic effects (cholinergic excess)
  2. Nicotinic effects (cholinergic excess)
  3. Central nervous system effects
  4. Cardiovascular effects
  5. Other symptoms.

Other symptoms

Neuropsychiatric effects

  • Impaired memory
  • Confusion
  • Irritability
  • Lethargy
  • Psychosis
  • Chronic OP-induced neuropsychiatric disorders.

Neurological manifestations

  1. Type I paralysis or acute paralysis [10]
  2. Type II paralysis or intermediate syndrome occurs due to fat solubility of the compound, resulting in long-lasting cholinesterase inhibition and muscle necrosis. It results in paralysis of various muscle groups – respiratory predominantly proximal limb muscles and neck flexors. It commences 1–4 days after acute poisoning. It lasts for approximately 3 weeks.[10] It is unresponsive to atropine and oximes [11]
  3. Type III paralysis or OP-induced delayed polyneuropathy starts 2 weeks or more after exposure, resulting in the degeneration of large myelinated motor and sensory fibres, and affects distal muscles. It is characterised by flaccid weakness and atrophy of distal limb muscles or spasticity and ataxia.[12],[13] It does not respond to atropine or oximes. This sensory–motor neuropathy lasts for 6–12 months [12]
  4. Delayed organophosphate encephalopathy: Patient presents with normal sensorium and progresses to coma in 5 days and persists for 4 days
  5. During this period, examination reveals miosed unreactive pupils, with no clinically detectable brainstem/cortical activity – brain is suppressed due to toxin. Electroencephalography shows bihemispheric slow waves. Computed tomography brain and cerebrospinal fluid analysis are normal. No treatment is needed. Excellent prognosis is noted with supportive care.[12],[11]

  Diagnosis of Organophosphate Poisoning Top

  1. History
  2. Physical examination

    • Vital signs: Depressed respirations, bradycardia and hypotension are possible findings.

  3. Laboratory investigations [14]

    • Plasma pseudocholinesterase levels: Normal 3000–8000 U/L. Serum levels may be < 1000 U/L
    • RBC AChE level:
    • White blood cells (WBC) – Leucocytosis is seen
    • ABG values to rule out acidosis – Metabolic and/or respiratory acidosis
    • Potassium and magnesium levels are decreased.

  4. Imaging studies

    • Chest X-ray for pneumonitis.

  5. Electrocardiogram for ventricular arrhythmias.

Medical management

Step I: Identify the nature of poison

OP, carbamate, chloride, pyrethroid.

Step II: Decontamination

Staff must have on protective equipment before commencing treatment including mask, gloves, gowns and eye protection.[15] Staff involved in direct contact with patient's bodily secretions should immediately and thoroughly wash the affected area with soap and water.[8]

Gastric lavage should be done only after stabilising the patient.[2] Forced emesis if patient is awake. Gastric lavage is given within 1 h of ingestion of OP.[16] Activated charcoal 0.5–1 g/kg can be given within 1 h of ingestion, but studies have shown no benefit.[1]

Step III: Maintaining airway, breathing and circulation

a. Airway

Maintain clear airway and ensure adequate oxygenation. Check gag reflex. If absent, intubate before stomach wash.[16]

b. Breathing

Administer oxygen 6 L/min by mask. Intubate if breathing is inadequate, oximetry is <90%, or Glasgow coma scale (GCS) <8. Administer injection atropine 0.05 mg/kg (2 mg in adults) every 5 min to reduce bronchial and oral secretions until adequately atropinised.[16]

c. Circulation

Administer adequate intravenous (IV) fluids through a wide bore cannula to replace volume loss.

Step IV: Cardiac monitoring

Monitor for arrhythmias.

Step V: Specific therapy

a. Antidotes

Atropine is given in intermittent boluses 2 mg every 5 min or as an infusion. The aim is to keep patient airway dry. Atropinisation is to be initiated as soon as diagnosis is suspected.

  • Signs of atropinisation: Heart rate about 100/min, pupils mid position, bowel sounds just heard, clear lung sounds, dry skin [12]
  • Protocol for atropinisation: Injection atropine 2 mg IV bolus is administered, and then the dose is doubled every 5 min till atropinisation is achieved [8]
  • Signs of atropine toxicity (anticholinergic toxidrome):[12] Dry mucus membranes (dry as a bone), mental status changes (mad as a hatter), flushed skin (red as a beet), mydriasis (blind as a bat), fever (hot as hell), tachycardia, hypertension, decreased bowel sounds/GI motility and urinary retention
  • Treatment

    1. Atropine toxicity is treated with injection haloperidol 5 mg intramuscular or IV and by reducing the dose of atropine [12]
    2. Glycopyrrolate is used as a substitute for atropine when the dose of atropine used to prevent bradycardia causes psychosis since it does not cross blood–brain barrier.[9] It is considered if patient is agitated with atropine and is not reaching target heart rate. Ensure other causes for agitation is ruled out, viz. hypoxemia, distended bladder, pain
    3. Pralidoxime (2PAM) is administered within 48 h of ingestion. Although oximes are part of several guidelines for OP poisoning, several studies fail to show benefits.[1] Patients who may benefit are those who present early (<2.5 h) with diethyl poisoning.[1] If prescribed, it can be given at a loading dose of 2 g over 30 min, followed by 0.5–1 g/h for 48 h. 2PAM is not commonly preferred due to respiratory complications and high mortality.[12]

b. Antibiotics

Antibiotics are not usually indicated for OP poisoning. Gastric lavage with an unprotected airway and/or a low GCS in the setting of poisoning are the risk factors for aspiration pneumonia. If aspiration pneumonia is suspected (fever, leucocytosis, pulmonary infiltrates with worsening oxygenation), antibiotics such as penicillin (ceftriaxone, amoxycillin or clauvulenic acid, piperacillin tazobacterium [Piptaz]) may be considered.

c. Sedation

Agitation in the setting of OP poisoning may indicate over atropinisation, hypoxaemia, or distress due to pain/discomfort. Intubated patients need a combination of an analgesic and a sedative such as morphine + lorazepam as an infusion. Haloperidol may increase seizure threshold and is not recommended unless patients are unresponsive to other drugs.

d. Lasix is the drug of choice if pulmonary oedema persists even after full atropinisation

e. Seizure control – Diazepam 5–10 mg.[16]

[TAG:2]Complications [16][/TAG:2]

  • Respiratory failure – Due to respiratory muscle paralysis, bronchial constriction, and copious respiratory secretions
  • Aspiration pneumonitis
  • Complete heart block
  • Ventricular arrhythmias occurs in severely poisoned patients
  • Convulsions
  • Atropine psychosis.

  Case Report Top

The nursing management of a patient with OP poisoning is discussed using nursing process approach based on a case report of a patient who deliberately self-harmed with OP poisoning and developed intermediate syndrome.

Mr M, 47-year-old, married, electrician from a middle class family consumed 100 ml of pesticide (chlorpyriphos and cypermethrin). He had two episodes of non-bilious vomiting. He was immediately taken to a local hospital where gastric lavage was given and referred to higher centre for further treatment where he was intubated and treated with atropine and antibiotics. After 48 h, he was extubated and reintubated as he had bradycardia and hypoxia. He also had jaundice and dark-coloured urine. The relatives got him discharged against medical advice and brought him to CMC for further management.

On examination, at Accident and Emergency Department, he had GCS of 14/15, drowsy, pupils dilated and fixed, heart rate of 86/min, blood pressure (BP) of 120/90 mmHg and respiratory rate of 20/min. His neck holding power was poor, power 4/5 in all four limbs, with no sensory or cerebellar abnormality. He was diagnosed to have intermediate syndrome and alcohol withdrawal symptoms. He was admitted in intensive care unit (ICU). During his stay in the ICU, he developed episodes of fluctuating sensorium. He was treated with high dose of thiamine, folate and lactulose. Liver function test was deranged due to toxicity. Laboratory investigations showed psuedocholinesterase level 110 U/L, magnesium - 2.38 mg/dl, potassium - 2.2 mmol/L, pH - 7.43, PaO2-68 mmHg PaCO240 mmHg, HCO326.3 mmol/L, sodium 137 mmol/L, chlorine 104 - mmol/L, BE ecf 2.2 mmol/L, FiO221%.

He was stabilised and psychiatry opinion was sought for adjustment disorder and previous history of self-harm with OP poisoning, high intentionality and lethality. His mental state examination had no active suicidal ideas but had depressive ideas related to financial crisis for which psychosocial intervention was suggested at a later stage. He was discharged to follow-up as outpatient.

1. Nursing diagnosis

Ineffective airway clearance related to excessive secretions, presence of artificial airway

Expected outcome

He maintains patent airway as evidenced by saturation within normal range and normal respiratory rate and breath sounds


  • Assessed the airway for bilateral equal air entry, respiratory rate and breath sounds
  • Assessed for cough and gag reflex and for bronchospasm
  • Changed position every 2 hourly to mobilise secretions
  • Positioned him in semi-fowlers at 45° to promote lung expansion and to prevent aspiration
  • Performed suctioning whenever required
  • Maintained adequate hydration by administering IV fluids
  • Provided humidification to airways to thin secretions.


He maintained patent airway as evidenced by saturation above 95%, normal respiratory rate, bilateral equal air entry and normal breath sounds on auscultation.

2. Nursing diagnosis

Ineffective breathing pattern related to neuromuscular impairment

Expected outcome

He maintains effective breathing pattern as evidenced by a normal rate and depth of respirations


  • Checked for neck muscle weakness, use of accessory muscles for breathing
  • Assessed single breath count
  • Assisted for intubation
  • Checked the ventilator settings of the patient
  • Positioned patient in semi-fowler's position to promote diaphragmatic descent and maximal inhalation
  • Performed suctioning whenever needed.

Expected outcome

He maintained effective breathing pattern as evidenced by gradually weaned off the ventilator settings and was extubated. He maintained normal respiratory rate and breath sounds.

3. Nursing diagnosis

Decreased cardiac output related to the cholinergic effects of OP poisoning (arrhythmia, bradycardia and hypokalaemia)

Expected outcome

He achieves maintenance of optimal cardiac output as evidenced by BP within normal range, absence of signs of poor organ perfusion, normal urine output


  • Assessed heart rate, rhythm for arrhythmias, BP, capillary refill time, skin turgor, vital signs every hour
  • Assessed peripheral sites for perfusion
  • Administered IV fluids as per order
  • Monitored urine output every hour
  • Administered atropine infusion to maintain the heart rate above 90/min.


He maintained normal vital signs as evidenced by heart rate more than 90/min BP of 130/84 mmHg and warm peripheries.

4. Nursing diagnosis

Deficient fluid volume related to fluid loss due to vomiting, loose stools, diaphoresis and excessive secretions

Expected outcome

He maintains adequate fluid volume as evidenced by normal urine output, normal pulse and BP


  • Assessed his pulse, BP, skin turgor and electrolyte levels
  • Assessed the urine output
  • Administered IV fluids as per the order
  • Administered atropine infusion to maintain the target heart rate.


Optimal fluid volume was maintained as evidenced by normal BP, heart rate of more than 90/min and urine output more than 30 ml/h.

5. Nursing diagnosis

Actual infection related to aspiration, invasive lines

Expected outcome

Infection is treated as evidenced by absence of further infection, culture reports, WBC and erythrocyte sedimentation rate counts


  • Monitored vital signs
  • Followed strict aseptic technique while handling invasive lines and while performing suctioning
  • Positioned in semi-fowlers to prevent aspiration
  • Provided oral care with chlorhexidine solution
  • Subglottic suctioning was done every for hourly
  • Checked for the colour, consistency and volume of secretions
  • Monitored ABG values, WBC counts, culture and sensitivity results, chest X-ray
  • Administer injection Piptaz 4.5 g IV q 8 hourly as per the order.


Infection was treated with antibiotics as evidenced by normal vital signs and WBC counts.

6. Nursing diagnosis

Risk for injury related to seizure activity secondary to OP poisoning

Expected outcome

Injury from self and environment is prevented


  • Assessed GCS every 2 hourly
  • Administered antiepileptic drug - injection midazolam 5 mg IV stat
  • Ensured provision of side rails
  • Positioned him in semi-fowlers position
  • Patient was closely observed.


He did not sustain any injury as he received antiepileptic drugs which kept his seizures under control.

7. Nursing diagnosis

Powerlessness related to lack of control over current situation

Expected outcome

He verbalises increased control over the situation by wanting to do things his way, requests for needed information and support services


  • Evaluated his feelings and perception of the reasons for lack of power and sense of helplessness
  • Involved him in care
  • Identified his usual belief/locus of control that influences his life
  • Increased sensitivity of the health team members to his sense of powerlessness.


He verbalised increased control over the situation by wanting to do things his way, requests for needed information and support services.

8. Nursing diagnosis

Ineffective individual coping related to situational crisis and personal vulnerability

Expected outcome

He verbalised beginning ability to cope up with the crisis. Uses behavioural strategies to manage stress, demonstrates significant reduction in impulsive, angry or agitated outbursts


  • Encouraged him to verbalise his concerns
  • Actively listened and responded to the patients' verbal and behavioural expressions
  • Assisted and encouraged him to use coping strategies effectively to better manage his stress
  • Counselling was offered to him
  • He was sent for psychiatric opinion for psychosocial intervention.


He verbalised that his impulsive behaviour was the cause of a lot of problems for family and was willing to go for follow-up in the psychiatry outpatient department.

9. Nursing diagnosis

Compromised family coping related to the critically ill family member

Expected outcome

Effective family coping is achieved as evidenced by family members identifying and use of effective coping strategies, resolve conflicts and involve in decision-making


  • Encouraged family to verbalise feelings
  • Identified family's perception of crisis situation
  • Identified the strengths of the family
  • Provided honest and accurate information in language persons can understand
  • Family counselling was conducted periodically
  • Encouraged the family members to visit him
  • Instructed family in simple care giving techniques and encouraged participation in care.


Family participated in the treatment decisions and care of the patient. Wife verbalised that they will seek counselling and psychiatric help for their marital discord and financial problems.

  Conclusion Top

A clear understanding about organophosphorus poisoning will equip nurses in the critical care to render appropriate care that can directly impact positive patient outcomes in the acute phase of hospitalisation. Counselling and family support play an important role in the rehabilitation of a patient who has attempted suicide using these compounds. Stringent country laws regarding acquisition and handling of these poisons should be enforced to prevent misuse.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  CE Questions- Organophosphate Poisoning Top

  1. The basic compound in most organophosphates is

    1. Petroleum
    2. Paraffin
    3. Asbestos
    4. Benzylconium

  2. Common routes of exposure to OP poisons include

    1. Dermal contact, inhalation, ingestion
    2. Inhalation, inoculation, ingestion
    3. Injection, ingestion, dermal contact
    4. Ingestion, inoculation, ocular exposure

  3. Organophosphates exert their acute effects by causing overstimulation at

    1. Anticholinergic nerve terminals
    2. Cholinergic nerve terminals
    3. Anticholinergic muscle terminals
    4. Cholinergic muscle terminals

  4. Beside in central and autonomic nervous system, Acetylcholine is also found in

    1. Neuromuscular junctions, and red blood cells
    2. Neuromuscular junctions, and white blood cells
    3. Neurovascular junctions, and red blood cells
    4. Neurovascular junctions, and white blood cells

  5. The enzyme that catalyzes the degradation of Acetylcholine into choline and acetic acid in the synapse is

    1. Lipase
    2. Protease
    3. Acetylcholinesterase
    4. Cholinesterase

  6. Onset and severity of symptoms depend on the specific

    1. Enzyme, amount, route of exposure, and rate of metabolic degradation
    2. Hormone, amount, route of exposure, and rate of metabolic degradation
    3. Chemical, amount, time and rate of metabolic degradation
    4. Compound, amount, route of exposure, and rate of metabolic degradation

  7. Signs and symptoms of organophosphate poisoning can be divided into following categories

    1. Muscarinic, Nicotinic, Peripheral nervous system & Cardio Vascular effects
    2. Muscarinic, Nicotinic, Central nervous system & Cardio Vascular effects
    3. Muscarinic, Nicotinic, Central nervous system & Peripheral nervous system effects
    4. Muscarinic, Cardio Vascular effects, Peripheral & Central nervous system effects

  8. Intermediate syndrome is caused due to

    1. Cholinesterase inhibition and muscle necrosis
    2. Cholinesterase stimulation and muscle necrosis
    3. Acetylcholine inhibition and muscle necrosis
    4. Acetylcholine stimulation and muscle necrosis

  9. Organophosphate-induced neuropsychiatric effects include

    1. Impaired memory, confusion, irritability, lethargy
    2. Drowsiness, irritability, lethargy, coma
    3. Impaired memory, confusion, lethargy, coma
    4. Impaired memory, confusion, irritability, drowsiness

  10. The following are included in SLUDGE (Muscarinic symptoms) EXCEPT

    1. Salivation,
    2. Loss of consciousness
    3. Urination
    4. Defecation

  11. Organophosphate induced delayed polyneuropathy lasts for------- months

    1. 0-5
    2. 6-12
    3. 13- 18
    4. 19- 24

  12. Following are the signs of adequate atropinisation EXCEPT

    1. Heart rate about 100/min
    2. Pupils at mid position
    3. Clear lung sounds
    4. Diaphoresis

  13. Plasma pseudo cholinesterase levels in OP poisoning will be in the range of

    1. Less than 1000 U/L
    2. More than 8000 U/L
    3. Between 1000-8000 U/L
    4. Above 8000 U/L

  14. A decrease in the following enzyme level indicates excessive absorption of OP poison

    1. RBC Acetyl cholinesterase
    2. Plasma Acetyl cholinesterase
    3. RBC pseudo cholinesterase
    4. Plasma pseudo cholinesterase

  15. Indication for starting antibiotic in OP poisoning is

    1. Ventilator associated pneumonia
    2. Chemical pneumonitis
    3. Blood stream infection
    4. Aspiration pneumonia

  16. 2PAM is not commonly administered due to its

    1. Delayed action
    2. High mortality rate due to respiratory complications
    3. Rapid lethal action
    4. High mortality rate due to cardiovascular complications

  17. Miosed unreactive pupils are seen in patients with

    1. Intermediate syndrome
    2. Organophosphate induced delayed polyneuropathy
    3. Delayed organophosphate encephalopathy
    4. Immediate syndrome

  18. Atropine toxicity is commonly treated with

    1. Haloperidol 5mg IM or IV
    2. Haloperidol 15mg IM or IV
    3. Resperidone 5mg IM or IV
    4. Resperidone 15mg IM or IV

  19. Respiratory failure seen in OP poisoning is due to

    1. Diaphragmatic irritation, bronchial constriction and copious respiratory secretions
    2. Respiratory muscle paralysis, bronchial dilatation and copious respiratory secretions
    3. Respiratory muscle paralysis, bronchial constriction and copious gastric secretions
    4. Diaphragmatic irritation, bronchial irritation and reduced respiratory secretions

  20. Neck muscle weakness indicates

    1. Intermediate syndrome
    2. Organophosphate induced delayed polyneuropathy
    3. Delayed organophosphate encephalopathy
    4. Impending respiratory failure

Answers for CE Test No. 36

1. C

2. B

3. D

4. D

5. D

6. D

7. C

8. B

9. A

10. C

11. C

12. A

13 D

14. B

15. B

16. A

17. B

18. C

19. B

20. D

  References Top

Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet 2008;371:597-607.  Back to cited text no. 1
Jokanović M. Medical treatment of acute poisoning with organophosphorus and carbamate pesticides. Toxicol Lett 2009;190:107-15.  Back to cited text no. 2
Robb EL, Baker MB. Organophosphate toxicity. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2020. Available from: http://www.ncbi.nlm.nih.gov/books/NBK470430/. [Last accessed on 2019 Feb 17].  Back to cited text no. 3
Accidental Deaths and Suicides in India; 2015. Available from: http://ncrb.gov.in/StatPublications/ADSI/ADSI2015/adsi-2015-full-report.pdf. [Last accessed on 2019 Mar 09].  Back to cited text no. 4
Srivastava A, Peshin SS, Kaleekal T, Gupta SK. An epidemiological study of poisoning cases reported to the National Poisons Information Centre, All India Institute of Medical Sciences, New Delhi. Hum Exp Toxicol 2005;24:279-85.  Back to cited text no. 5
Peshin SS, Gupta YK. Poisoning due to household products: A ten years retrospective analysis of telephone calls to the National Poisons Information Centre, All India Institute of Medical Sciences, New Delhi, India. J Forensic Leg Med 2018;58:205-11.  Back to cited text no. 6
Blanchard J, Feltes M, Kim JY, Pousson A, Douglass K. Experience of Indian emergency physicians in management of acute poisonings. Toxicol Commun 2019;3:54-60.  Back to cited text no. 7
Pillay VV, editor. Textbook of Forensic Medicine and Toxicology. New Delhi: Paras Medical Publisher; 2007.  Back to cited text no. 8
Hulse EJ, Haslam JD, Emmett SR, Woolley T. Organophosphorus nerve agent poisoning: Managing the poisoned patient. Br J Anaesth 2019;123:457-63.  Back to cited text no. 9
Abhilash KP. Emergency Medicine: Best Practices at CMC (EMAC). JP Medical Ltd; 2018. p. 542.  Back to cited text no. 10
John G, Subramaninan K. Essentials of Critical Care. Vellore: JP publishers. 2006.  Back to cited text no. 11
John G, Subramaninan K. Essentials of Critical Care. 8th ed. Vellore, Tamil Nadu, India: Division of Critical Care, CMC; 2011. p. 33-1, 33-12. [Last accessed on 2019 Feb 18].  Back to cited text no. 12
Peter JV, Sudarsan TI, Moran JL. Clinical features of organophosphate poisoning: A review of different classification systems and approaches. Indian J Crit Care Med 2014;18:735 45.  Back to cited text no. 13
Organophosphate Toxicity Workup: Laboratory Studies, Imaging Studies, Electrocardiography. Available from: https://emedicine. medscape.com/article/167726 workup. [Last accessed on 2019 Mar 07].  Back to cited text no. 14
Sungur M, Güven M. Intensive care management of organophosphate insecticide poisoning. Crit Care Lond Engl 2001;5:211-5.  Back to cited text no. 15
David SS. Handbook of Emergency Medicine, 8th ed. India: Elsevier; 2012. p. 20.  Back to cited text no. 16


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