Menu
Acetylcholinesterase inhibitors, antidote therapy – nerve-paralytic agents, automatic medical syringe, carbamates, duodot, insecticides, organophosphorus compounds, pesticides, weapons of mass destruction.
The mnemonic DUMBELS is used to describe the signs and symptoms of acetylcholinesterase inhibitor poisoning. Patients of all age groups with existing signs of poisoning by these drugs and whose symptoms correspond to the mnemonic DUMBELS are included.
Absent.
1. Use appropriate personal protective equipment.
2. Remove the patient’s clothing and wash the skin with soap and water:
a) acetylcholinesterase inhibitors can be absorbed through the skin;
b) infected clothing can serve as a source of further spread of the toxin.
3. Quickly assess breathing, consciousness and pupils.
4. Administer the antidote immediately after confirmation or suspicion of acetylcholinesterase inhibitor poisoning.
5. Administer oxygen, target saturation 94-98% and monitor airway.
6. Provide in/out access (if possible).
7. Use a heart monitor (if available).
8. Heart rate can be normal, bradycardia or tachycardia.
9. Clinical improvement should be based on decreased secretions and easier breathing, not on heart rate and pupillary response.
10. Constant and long-term reassessment of the condition is critical.
1. Acetylcholinesterase inhibitors are very toxic and can quickly lead to death.
2. Patients who are constantly in contact with small doses of the toxin may have a slower onset of symptoms.
3. Antidotes (atropine and pralidoxime) are effective if administered before circulatory arrest.
4. The patient may develop:
a) miosis (pupil-dots);
b) bronchospasm;
c) bradycardia;
d) vomiting;
e) excessive secretion in the form:
5. Penetration of acetylcholinesterase inhibitors into the CNS causes:
a) headache;
b) disorientation;
c) general muscle weakness;
d) nausea and vomiting;
e) drowsiness and weakness.
6. Assess the level of intoxication based on signs and symptoms:
a) light:
b) average (in addition to symptoms of mild intoxication):
c) severe (in addition to the previous symptoms):
7. The manifestation of symptoms can be instantaneous in the case of the action of a large concentration of an acetylcholinesterase inhibitor:
a) usually in the first few minutes after poisoning, symptoms do not appear;
b) the effect of poisoning by vapors occurs instantly.
8. Signs and symptoms of poisoning with a large amount of an acetylcholinesterase inhibitor (regardless of the route of administration):
a) sudden loss of consciousness;
b) convulsions;
c) excessive secretion;
d) apnea;
e) death.
9. Collect a detailed history of use (since the patient may pass out before arriving at the reception department):
a) time of administration or exposure;
b) route of exposure;
c) amount of drug or toxin used (carefully collect all remnants of drugs/substances);
d) intake of alcohol or other toxic substances;
e) history of diseases of the cardiovascular system or prescribed medicines that require regular use.
10. The patient may show any or all signs and symptoms of the intoxication syndrome, depending on the route of entry of the agent into the body and its concentration:
a) vapor emissions will have a direct effect on the eyes and cause miosis;
b) patients with isolated skin lesions will have normal pupil size with a normal reaction;
c) certain acetylcholinesterase inhibitors pose a threat in the form of one-time entry into the body through the skin and vapor inhalation.
1. Drugs.
1.1. Atropine:
a) atropine is the main antidote for exposure to organophosphorus compounds, carbamates, or nerve agents, and repeat doses should be given to patients with signs and symptoms of exposure or toxicity;
b) atropine can be in multidose ampoules, pre-filled syringes or automatic injectors.
1.2. Pralidoxime (2-pyridyline aldoxime methyl chloride (2-PAM):
a) pralidoxime is a secondary treatment and must be used simultaneously with other drugs to reactivate acetylcholinesterase;
b) pralidoxime can be in multidose ampoules, prefilled syringes or automatic injectors;
c) auto-injectors contain 600 mg of pralidoxime;
d) for the maximum effect, the drug must be administered immediately after poisoning with a nerve agent or an organophosphorus compound, since in case of delay, the drug has a minimal clinical effect.
1.3. Benzodiazepines:
a) benzodiazepines are administered as anticonvulsants for existing convulsions (see the “Convulsions” guideline for determining doses and routes of administration);
b) lorazepam, diazepam, and midazolam are the most used benzodiazepines at the pre-hospital stage;
c) in conditions of poisoning with acetylcholinesterase inhibitors, preference is given to diazepam and midazolam due to their greater effect;
d) benzodiazepines can be in multidose ampoules, pre-filled syringes or automatic injectors.
1.4. A nerve agent/organophosphorus antidote autoinjector commonly supplied to the military:
a) federal stockpiles of nerve agent antidotes managed by the Centers for Disease Control and Prevention and offered to states that voluntarily agree to maintain CHEMPACK storage and security;
b) they deployed at sites designated by states that are part of the program, such as hospitals and EMD centers;
c) deployment of CHEMPACKs is reserved for events where exposure to a nerve agent/organophosphorus compound depletes local or regional antidote supplies;
br />d) there are two types of CHEMPACK containers:
2. Administration of drugs:
a) atropine in large, often multiple doses, is an antidote to acetylcholinesterase inhibitors;
b) atropine should be administered immediately, in several doses, until the problem of excessive secretion in the patient is resolved ;
c) pralidoxime is a secondary treatment and must be used simultaneously with other drugs;
d) usually the stocks of pralidoxime and atropine in EMD carriages are not enough for full treatment in case of poisoning with acetylcholinesterase inhibitors; nevertheless, rescuers should start early therapy using atropine and, if available, pralidoxime;
e) convulsions should be treated with benzodiazepines. Currently, there is increasing evidence of the effectiveness of intranasal administration of midazolam compared to the intravenous route. However, intramuscular suction may be more clinically effective compared to intranasal administration in situations of severe rhinorrhea;
e) the patient should be quickly transported to the nearest appropriate receiving department (according to the instructions of the medical management).
3. Recommended doses (see table below).
The doses below are based on the severity of clinical signs and symptoms. There are several imperative (required) factors that should be taken into account.
3.1. In severe intoxication with organophosphorus compounds or acetylcholinesterase inhibitors, the necessary dose of atropine to solve the problem of secretion and improve the respiratory status will often exceed 20 mg. Atropine should be administered immediately with a certain frequency until the clinical symptoms are completely relieved. Atropine should be used until complete dissolution of acetylcholinesterase inhibitors. This may require more than 2000 mg of atropine over several days or weeks.
3.2. All of the drugs listed below can be administered IV in the same doses as indicated for IV injections. However, due to the rapid onset of signs and symptoms and the potential for death from ACE inhibitor poisoning, the use of intramuscular injection is recommended to save the time required to obtain IV access and start the infusion.
3.3. Antidotes can also be administered intranasally. However, due to the rapid onset of signs and symptoms and potential death from ACE inhibitor poisoning, the use of intramuscular injections still remains the more accessible route of administration because of the lack of delay for IV or IV access and the limited use nasal administration of other drugs.
Table adapted from: Department of Health and Human Services, ASPR, National Library of Medicine, Chemical Hazards Emergency Medical Management: Nerve AgentsPrehospital Management, www.chemm.nlm.nih.gov
1. Continuous review is critical.
2. The clinical response to treatment is manifested by a decrease in secretion and relief of respiratory efforts.
3. Initiation and subsequent treatment should not be based on heart rate or pupillary response.
4. Cautions when working with pralidoxime.
Although the kits contain atropine – the main antidote for acetylcholinesterase inhibitor poisoning, the inclusion of pralidoxime in an autoinjector can cause problems if additional doses of atropine are required due to the patient’s condition and other forms of atropine are not available:
a) children: an overdose of pralidoxime causes severe neuromuscular weakness and subsequent respiratory depression;
b) adults: especially in the elderly, excessive doses of pralidoxime can cause severe arterial hypertension, neuromuscular weakness, headache, tachycardia, visual disturbances;
c) the elderly: patients who, in addition to poisoning, have impaired renal function or hypertension, should receive a reduced dose recommended for adults intravenous dose of pralidoxime.
5. Precautions when working with autoinjectors:
a) in the case of using an auto-injector, preliminary determination of the dose is not necessary;
b) when using atropine, repeated doses with the use of an auto-injector should be administered until the secretion completely disappears;
c) the kits have not been approved for use in children by the Food and Drug Administrationments, however, they can be used for primary therapy in children of any age with severe symptoms of acetylcholinesterase inhibitor poisoning, especially in the absence of atropine in any form;
d) pediatric autoinjectors are commercially available in a dosage of 0.25 mg (yellow container) and 0.5 mg (red container);
g) pralidoxime 600 mg auto-injector can be used in babies weighing more than 12 kg.
1. Clinical effects of acetylcholinesterase inhibitor agents:
a) clinical effects are manifested due to silencing of the enzyme acetylcholinesterase, thereby ensuring the accumulation of acetylcholine in the nervous system;
b) an excessive amount of acetylcholine causes hyperactivity of muscles, glands and nerves .
2. Organophosphorus compounds (certain insecticides):
a) can be easily purchased in open access;
b) organophosphorus compounds (pesticides) penetrate the skin and combine with the fat cells of the human body, which causes prolonged intoxication and disease even under conditions of aggressive therapy.
3. Nerve-paralytic agents:
a) usually fall under the category of weapons of mass destruction;
b) are not freely available;
c) are extremely toxic and instantly lead to fatal consequences, regardless from the route of exposure;
d) tabun, sarin, zoman, cyclosarin, gas fiber and gas are weapons of mass destruction;
g) nerve agents can settle in the environment and remain toxic for a long period of time.< /p>
Signs and symptoms characteristic of DUMBELS intoxication syndrome (see Inclusion criteria above in this section).