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Carbamate Poisoning

Poisoning by Carbamates

Carbamates are acetylcholinesterase inhibitors abundant in various pesticides and they are also used in medicine. Poisoning with carbamates produces overstimulation of muscarinic and nicotinic receptors, resulting in specific clinical presentations. It is important to identify the cause of poisoning and manage patients accordingly to avoid instances of death.


Presentation

Carbamate poisoning, as well as poisoning with organophosphorus compounds (OP), have indistinguishable clinical presentation. Both are the same class of molecules that inhibit acetylcholinesterase causing accumulation of acetylcholine, consequently overstimulating the neural transmission [1].

Patient history may reveal occupational exposure to pesticides containing carbamates (farming, agriculture etc.). One study confirmed that out of 1100 patients presenting with carbamate poisoning, 93.8% had tried to attempt suicide [2]. Hence, non-occupational exposure can be due to an intent to self-harm. In these cases, observation of the patient and inquiry about negative life situations and overall psychological well-being is advisable to document. Evidence of self-harm or acute occupational exposure may be indicated by the presence of pesticide or solvent smells [3].

Clinical manifestation of carbamate poisoning is highly dependent on the dose, type of carbamate, route of exposure, and concomitant diseases [4].

Excessive stimulation of the sympathetic and parasympathetic system with carbamates is responsible for deleterious effects on the respiratory system ranging from difficulty breathing to respiratory failure [5]. The muscular system is also dependent on acetylcholine (Ach) activation and so signs of fasciculation or brief contractures of muscles, and incoordination of movements can be observed in some cases. Additionally, excessive sweating, headache, miosis, cramping in the abdominal cavity, changes in the cardiovascular system are all signs of possible carbamate poisoning [4]. Cardiovascular system symptoms include palpitations and changes in pulse rate, more commonly demonstrating as tachycardias [3].

Fortunately, spontaneous recovery is possible within 4 hours of poisoning if the patient presents only with nausea, vomiting, headache and excessive salivation [6].

Gastric Lavage
  • Special Considerations: Special Considerations O rganophosphates are usually dissolved in hydrocarbon bases; thus, the clinician should consider hydrocarbon pneumonitis and not to do gastric lavage. Slide 21: Thanks For Listening[authorstream.com]
  • Once the patient is stable and atropinised, consider careful brief gastric lavage using a NG tube. Never perform lavage until the patient is stable/atropinised.[aic.cuhk.edu.hk]
  • lavage ) Washing of the skin (irrigation), perhaps every few hours for several days Surgery to remove burned skin Breathing support, including tube through the mouth into the lungs and connected to a breathing machine (ventilator) How well someone does[medlineplus.gov]
Pathologist
  • , and forensic pathologists develop accurate, unbiased drug monitoring and toxicology reports.[books.google.com]
Agent Orange
  • Orange Other Military Personal and General Environment 1381 Pentachlorophenol and Tetrachlorophenol 1194 George D Thurston and Lance A Wallace 1400 Trimellitic Anhydride and Other Acid Robert B Devlin and Donald W Graff 1434 Carbon Disulfide 1219 97[books.google.com]
Bronchorrhea
  • Bronchorrhea and bronchospasm are treated with titrated high-dose atropine . Neuromuscular toxicity is treated with IV pralidoxime . Organophosphates and carbamates, although different structurally, both inhibit cholinesterase activity.[merckmanuals.com]
  • Less than 30 min after tracheal extubation, the patient’s respiratory status worsened because of major bronchorrhea and inefficient cough.[link.springer.com]
  • Organophosphates and carbamates are common insecticides that inhibit cholinesterase activity, causing acute muscarinic manifestations (salivation, lacrimation, urination, diarrhea, emesis, bronchorrhea, bronchospasm, bradycardia, miosis) and some nicotinic[gii.co.jp]
Dyspnea
  • Dyspnea and vomiting were the most common symptom and miosis and cyanosis were the most frequently observed signs. Plasma and red cell cholinesterase levels were lowest in the mixed poison group and highest in the carbamate group.[ncbi.nlm.nih.gov]
Vomiting
  • The clinical manifestations of occupational carbofuran poisoning recorded were nausea and vomiting (82.3%), headaches (56.3%) and miosis (19.8%).[ncbi.nlm.nih.gov]
  • Dyspnea and vomiting were the most common symptom and miosis and cyanosis were the most frequently observed signs. Plasma and red cell cholinesterase levels were lowest in the mixed poison group and highest in the carbamate group.[ncbi.nlm.nih.gov]
  • Fortunately, spontaneous recovery is possible within 4 hours of poisoning if the patient presents only with nausea, vomiting, headache and excessive salivation.[symptoma.com]
  • 抄録 A 50-year-old man was admitted to the emergency room complaining oppression on his chest, sweating and vomiting. He had drunk a 30 ml volume nutrition supplement 60 minutes before.[ci.nii.ac.jp]
  • Symptoms of paradichlorobenzene poisoning: STOMACH AND INTESTINES Diarrhea Abdominal pain Nausea and vomiting MUSCLES Muscle spasms Note: Paradichlorobenzene mothballs are not very toxic.[medlineplus.gov]
Nausea
  • The clinical manifestations of occupational carbofuran poisoning recorded were nausea and vomiting (82.3%), headaches (56.3%) and miosis (19.8%).[ncbi.nlm.nih.gov]
  • Fortunately, spontaneous recovery is possible within 4 hours of poisoning if the patient presents only with nausea, vomiting, headache and excessive salivation.[symptoma.com]
  • Symptoms of paradichlorobenzene poisoning: STOMACH AND INTESTINES Diarrhea Abdominal pain Nausea and vomiting MUSCLES Muscle spasms Note: Paradichlorobenzene mothballs are not very toxic.[medlineplus.gov]
  • Adverse effects of pralidoxime: dizziness, headache, nausea, blurred vision, muscle weakness. Patient Disposition: Admit for observation (for 36-72hrs?)[ozemedicine.com]
  • Receptor type Location Effect Muscarinic (stimulation) Pupils Miosis Ciliary body Blurred vision Exocrine glands Increased secretions Heart Decreased heart rate Bronchial smooth muscle Bronchoconstriction GI smooth muscle Nausea, vomiting, abdominal cramps[aic.cuhk.edu.hk]
Abdominal Pain
  • Symptoms of paradichlorobenzene poisoning: STOMACH AND INTESTINES Diarrhea Abdominal pain Nausea and vomiting MUSCLES Muscle spasms Note: Paradichlorobenzene mothballs are not very toxic.[medlineplus.gov]
Hypotension
  • Consider volume resuscitation with normal saline or ringer to treat Bradycardia and hypotension. Use activated charcoal within one hour of an ingestion.[authorstream.com]
  • These insecticides inhibit the enzyme acetylcholinesterase (AChE), producing an 'acute cholinergic crisis' with reduced consciousness, bradycardia, hypotension, and acute respiratory failure.[clinicaltrials.gov]
  • Most patients have bradycardia and, if poisoning is severe, hypotension. CNS toxicity is common, sometimes with seizures and excitability and often with lethargy and coma.[gii.co.jp]
  • Stimulation of muscarinic parasymp. receptors: miosis, bronchoconstriction, wheezing, SOB, nausea, vomiting, diarrhoea, tenesmus, fecal incontinence, urinary frequency & incontinence, excessive lacrimation, salivation, broncorrhoea, sweating, bradycardia, hypotension[ozemedicine.com]
  • Some muscarinic causes of cardio-respiratory failure (bronchorrhoea, bronchospasm, bradycardia, hypotension) generally respond well to atropine. Rapid atropinisation of patients on admission should reduce the number of early deaths.[aic.cuhk.edu.hk]
Drooling
  • […] rate LUNGS AND AIRWAYS Breathing difficulty Wheezing NERVOUS SYSTEM Anxiety Coma (decreased level of consciousness and lack of responsiveness) Convulsions Dizziness Headache Weakness BLADDER AND KIDNEYS Increased urination EYES, EARS, NOSE, AND THROAT Drooling[medlineplus.gov]
Trismus
  • Indeed, major trismus rapidly followed succinylcholine administration, and neither the concurrent disease nor the simultaneous drugs could account for the trismus.[link.springer.com]
Muscle Twitch
  • twitching/fasciculations, weakness CNS effects if penetrate BBB: emotional lability, restlessness, tremors, headaches, withdrawal & depression, drowsiness, lethargy If highly toxic exposure, pts can quickly (min-hrs) progress to: ataxia, generalised[ozemedicine.com]
Lacrimation
  • Physician, Department of Emergency Medicine, Einstein Medical Center Click here for Patient Education Organophosphates and carbamates are common insecticides that inhibit cholinesterase activity, causing acute muscarinic manifestations (eg, salivation, lacrimation[merckmanuals.com]
  • She had the following symptoms of severe carbamate poisoning: coma, fasciculations, salivation, lacrimation, myosis, bronchorrhea, and difficult breathing. Her arterial blood pressure was normal and her heart rate was 56 beats · min 1 .[link.springer.com]
  • Clinical effects of anticholinesterase poisoning: Classically, symptoms develop over a few hours (less if massive exposures or up to 2days if lipophilic) and present as the “SLUDGE” syndrome : Salivation, Lacrimation, Urination, Diarrhoea, GIT effects[ozemedicine.com]
  • Organophosphates and carbamates are common insecticides that inhibit cholinesterase activity, causing acute muscarinic manifestations (salivation, lacrimation, urination, diarrhea, emesis, bronchorrhea, bronchospasm, bradycardia, miosis) and some nicotinic[gii.co.jp]
Blurred Vision
  • Adverse effects of pralidoxime: dizziness, headache, nausea, blurred vision, muscle weakness. Patient Disposition: Admit for observation (for 36-72hrs?)[ozemedicine.com]
  • Receptor type Location Effect Muscarinic (stimulation) Pupils Miosis Ciliary body Blurred vision Exocrine glands Increased secretions Heart Decreased heart rate Bronchial smooth muscle Bronchoconstriction GI smooth muscle Nausea, vomiting, abdominal cramps[aic.cuhk.edu.hk]
Seizure
  • Miosis (73%), excessive salivation (70%), muscle weakness (68%), and lethargy (54%) were the most common abnormal signs; 49% and 22% of patients had tachycardia and seizures, respectively, and 38% of children had respiratory insufficiency that required[utexas.influuent.utsystem.edu]
  • Diazepam 0.1-0.2 mg/kg IV, repeat as necessary if seizures occur. phenytoin has no effect on organophosphate agent-induced seizures.[authorstream.com]
  • CNS toxicity is common, sometimes with seizures and excitability and often with lethargy and coma. Pancreatitis is possible, and organophosphates may cause arrhythmias such as heart block and QTc interval prolongation.[gii.co.jp]
  • Symptoms of pyrethrin poisoning: LUNGS AND AIRWAYS Breathing difficulty NERVOUS SYSTEM Coma (decreased level of consciousness and lack of responsiveness) Seizures SKIN Irritation Redness or swelling Symptoms of organophosphate or carbamate poisoning:[medlineplus.gov]
Headache
  • The clinical manifestations of occupational carbofuran poisoning recorded were nausea and vomiting (82.3%), headaches (56.3%) and miosis (19.8%).[ncbi.nlm.nih.gov]
  • Fortunately, spontaneous recovery is possible within 4 hours of poisoning if the patient presents only with nausea, vomiting, headache and excessive salivation.[symptoma.com]
  • Adverse effects of pralidoxime: dizziness, headache, nausea, blurred vision, muscle weakness. Patient Disposition: Admit for observation (for 36-72hrs?)[ozemedicine.com]
  • […] swelling Symptoms of organophosphate or carbamate poisoning: HEART AND BLOOD Slow heart rate LUNGS AND AIRWAYS Breathing difficulty Wheezing NERVOUS SYSTEM Anxiety Coma (decreased level of consciousness and lack of responsiveness) Convulsions Dizziness Headache[medlineplus.gov]
Tremor
  • […] hypotension, ventricular tachycardia; Stimulation of nicotinic motor & sympathetic receptors: tachycardia, palor, hypertension, hyperglycaemia, muscle twitching/fasciculations, weakness CNS effects if penetrate BBB: emotional lability, restlessness, tremors[ozemedicine.com]
Dysmetria
  • We report the case of a 4-year-old boy who was admitted to the Pediatric Department of the Second University of Naples for evaluation of stupor, lethargy, severe hypotonia, generalized weakness of his arms and legs, ataxia, dysmetria, miosis, excessive[ncbi.nlm.nih.gov]

Workup

Carbamate poisoning can be diagnosed if there is a suspicion of exposure and a typical clinical presentation.

Objective evidence of acetylcholinesterase (AchE) inhibition can be sought with butyrylcholinesterase (BChE) assay. This assay reveals information about the amount and activity of butyrylcholinesterase (a cholinesterase molecule related to acetylcholinesterase) in the blood. The activity of BChE correlates with the severity of poisoning and is a good tool to elucidate a prognosis [7]. This type of blood analysis is inexpensive [8] but inconvenient in terms of time taken to obtain the results. This delay can interfere with the management of patients if prompt intervention is necessary [7].

Cardiovascular effects of AchE inhibitors can lead to death. Thus, it is important to document the electrical potentials of the heart on electrocardiogram (ECG). ECG may reveal tachycardia or rarely bradycardia. Arrhythmias such as ventricular extrasystoles, atrial fibrillation, and ventricular fibrillation are evidence of abnormal cardiac rhythm. A presence of prolonged QT interval should be investigated as it is pathognomic for carbamate poisoning [3].

A study analyzed 115 patients exposed to organophosphate poisoning and compared their clinical presentation and findings on ECG. About 50% of the patients developed sinus tachycardia and only 3 of the subjects had sinus bradycardia. More serious findings included prolonged QT interval, polymorphic ventricular tachycardia (VT) which manifested in five patients and ventricular fibrillation (VF) that was found in 3 patients. Those who developed ventricular tachycardia died regardless of appropriate medical management. This study emphasizes the importance of rapid diagnosis and significance of monitoring in the patients throughout their inpatient stay [3].

Glycosuria
  • There were 13 men and 10 women. 10 subjects had euglycemia associated with glycosuria; 6 subjects had transient glycosuria with hyperglycemia (defined as random glucose over 160 mg%).[ncbi.nlm.nih.gov]
Prolonged QT Interval
  • More serious findings included prolonged QT interval, polymorphic ventricular tachycardia (VT) which manifested in five patients and ventricular fibrillation (VF) that was found in 3 patients.[symptoma.com]
QTc Interval Prolonged
  • Pancreatitis is possible, and organophosphates may cause arrhythmias such as heart block and QTc interval prolongation.[gii.co.jp]

Treatment

  • The toxic agent was determined to be a carbamate insecticide, for which treatment with pralidoxime is considered controversial.[ncbi.nlm.nih.gov]
  • The golden time for treatment of acute organophosphate or carbamate poisoning was the initial 96 hours. No RF occurred after this time.[ncbi.nlm.nih.gov]
  • Oximes, which were found useful in some cases of OP poisoning and useless in some cases of CRB poisoning, are absolutely safe as empiric treatment, which is often needed since the major differential diagnosis of OP poisoning is CRB poisoning, which is[ncbi.nlm.nih.gov]
  • Administering atropine treatment for respiratory poisoning and pralidoxime treatment for skin inflammations are widely implemented for curing organophosphates and carbamates poisoning.[transparencymarketresearch.com]
  • INTERVENTION: Treatment with atropine and pralidoxime and mechanical ventilation for patients with respiratory failure.[ncbi.nlm.nih.gov]

Prognosis

  • The activity of BChE correlates with the severity of poisoning and is a good tool to elucidate a prognosis. This type of blood analysis is inexpensive but inconvenient in terms of time taken to obtain the results.[symptoma.com]
  • There is little evidence of risk to healthcare workers from managing OP poisoned patients as long as universal precautions are followed see refs 5, 6 below Prognosis Varies markedly. Above all, it will depend on the specific OP and amount ingested.[aic.cuhk.edu.hk]

Etiology

  • The exact etiology of this is unclear but in the light of recent literature, it is likely that oxidative stress at the renal tubular level leading to renal tubular damage may be the most likely explanation.[ncbi.nlm.nih.gov]

Pathophysiology

  • […] odacheis Acetylcholinesterase inhibitor poisoning Organophosphate & Carbamate Insecticide Poisoning: Pathophysiology: Both organophosphate & carbamate insecticides are acetylcholinesterase inhibitors which are readily absorbed through intact skin or mucosa[ozemedicine.com]

Prevention

  • Aggressive treatment and prevention of the above three factors will reduce the incidence of RF, or in other words, reduce the mortality.[ncbi.nlm.nih.gov]
  • An indispensable handbook to the entire suite of toxicology lab tests, as well as all the possible sources of testing error, Resolving Erroneous Reports in Toxicology and Therapeutic Drug Monitoring offers clear remedies for eliminating and preventing[books.google.com]
  • Within seconds, a strong trismus, or spasm of the masseter muscles, was observed, preventing mouth opening and orotracheal intubation.[link.springer.com]
  • You should call if you have any questions about poisoning or poison prevention. It does NOT need to be an emergency. You can call for any reason, 24 hours a day, 7 days a week. Take the container with you to the hospital, if possible.[medlineplus.gov]
  • ABC's, Oxygen if needed Decontaminate skin, eyes to prevent ongoing absorption: remove clothes thoroughly cleanse skin - at least 2 separate water & detergent washes will remove up to 94% of residual organoP, even if done up to 6hrs after exposure; consider[ozemedicine.com]

References

Article

  1. Čolović MB, Krstić DZ, Lazarević-Pašti TD, Bondžić AM, Vasić VM. Acetylcholinesterase Inhibitors: Pharmacology and Toxicology. Curr Neuropharmacol. 2013;11(3):315-335.
  2. Eddleston M, Juszczak E, Buckley NA, et al. Multiple-dose activated charcoal in acute self-poisoning: a randomised controlled trial. Lancet. 2008;371:579–586.
  3. Laudari S, Patowary BS, Sharma SK, Dhungel S, Subedi K, Bhattacharya R, et al. Cardiovascular Effects of Acute Organophosphate Poisoning. Asia Pac J Med Toxicol 2014;3:64-7.
  4. Rosman Y, Makarovsky I, Bentur Y, Shrot S, Dushnistky T, Krivoy A. Carbamate poisoning: treatment recommendations in the setting of a mass casualties event. Am J Emerg Med. 2009; 27: 1117-1124.
  5. Eddleston M, Sudarshan K, Senthilkumaran M, et al. Patterns of hospital transfer for self-poisoned patients in rural SriLanka: implications for estimating the incidence of self-poisoning in the developing world. Bull World Health Organ. 2006;84:276–282.
  6. Morais S, Dias E, de Lourdes Pereira M. Carbamates: Human Exposure and Health Effects. In: The Impact of Pesticides. 1st ed. AcademyPublish.org. January 2012;21-38.
  7. Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet. 2008;371(9612):597-607.
  8. Dhananjayan V, Ravichandran B, Anitha N, Rajmohan HR. Assessment of acetylcholinesterase and butyrylcholinesterase activities in blood plasma of agriculture workers. Indian J Occup Environ Med. 2012;16(3):127-130.

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Last updated: 2019-07-11 21:13