U235> Если он каким-то невероятным чудом, всего лишь на двух кубиках атропина умудрился за 2 дня не умереть от критической тяжести отравления ФОС, то в овощ превратиться должен был однозначно.
С атропином вообще достаточно много непоняток. Как с самим фактом применения, так и с его значением.
Одни утверждают, что атропин в Омске вводили, и быстро. Другие - что то ли да, то ли нет, то ли непонятно когда, и мало, и поздно.
Издание опубликовало описание отравления ингибитором холинэстеразы
// www.kommersant.ru
После экстренной посадки в Омске его госпитализировали в местную больницу; по разным данным, во время транспортировки или уже с реанимационном отделении омские врачи вводили находившемуся в коме господину Навальному атропин.
В The Lancet подробно описывается состояние пациента на момент прибытия в немецкую клинику. Авторы указывают, что «остаются неизвестными сроки начала терапии атропином и ее продолжительность в течение первых двух дней», но заявляют, что токсикологический анализ образцов крови и мочи, взятых при поступлении в реанимацию в Берлине, «выявил несколько препаратов, в том числе атропин»: «Это мы связали с предыдущим лечением, которое пациент проходил в реанимационном отделении в Омске перед транспортировкой».
С другой стороны, в декабре же в "Ланцете" была опубликована еще одна статья про отравления ФОС, в т.ч. упоминавшая, помимо Навального, еще и солсберийских травленых и многочисленные отравления пестицидами. Где упоминается и атропин, но с ним полная путаница - несмотря на то, что, ссылаясь на статью немцев, говорится, что в анализах Навального в Берлине НАШЛИ следы атропины, позднее утверждается, что везли его без атропина, и антидоты вводить начали только в Шарите.
In The Lancet, David Steindl and colleagues describe the case of a 44-year-old man who was poisoned by a novichok organophosphorus nerve agent.1 The man was a passenger on a domestic flight in Russia when he became confused, and vomited and collapsed unconscious; 2 h later, he was hospitalised in Omsk, Russia, and treated for respiratory failure and coma. After transfer by air ambulance to Berlin, Germany, features of the cholinergic toxidrome (ie, small or pinpoint pupils, bradycardia, sweating, and hypersalivation) allowed a diagnosis of organophosphorus poisoning to be made.
// www.thelancet.com
An important theme is the delay in diagnosis of organophosphorus poisoning. The first cases from Salisbury did not intentionally receive atropine or other anticholinergic drugs until later the following day.3
When the individuals were found, they were unconscious with small pupils, similar to opioid poisoning; however, they had other cholinergic features, such as excess sweat, frothing at the mouth, vomitting, and diarrhoea—effectively a wet opioid. In the case reported by Steindl and colleagues,1
despite initially presenting to hospital with hypersalivation, sweating, and respiratory failure, the man was not continuously treated with antidotes for cholinergic poisoning. He was transferred to Berlin without atropine administration, and antidotal therapy was started only on his arrival at Charité.
Atropine has been the pivotal antidote for organophosphorus compound poisoning since 1955,2
, 5
offering balanced peripheral and central antimuscarinic effects.6
A randomised trial done in Chittagong, Bangladesh,7
showed that rapid intravenous dose escalation with atropine, which was titrated to the patient's heart rate, blood pressure, and bronchorrhoea, reduced the time to resuscitation (atropinisation) from 2·5 h to 24 min and case fatality from 22·5% to 8%. Guidelines recommend atropine administration as early as possible, in appropriate and sometimes large doses, to save lives.8
However, the case reported by Steindl and colleagues1
and the two Salisbury cases all survived without early atropine therapy, with only intensive supportive care. This outcome seems surprising because novichok nerve agents are considered the most potent organophosphorus compounds known, reportedly five to ten times more toxic than the organophosphorus nerve agent VX, which rapidly killed a man after dermal exposure.9
Ingestion of less potent organophosphorus insecticides (eg, parathion) can cause severe poisoning and respiratory arrest within 30 min.10
Survival of most of the novichok poisoning cases suggests that the nerve agent is less toxic than feared, doses administered were low, or the administration route modified toxicity.
Oxime antidotes reactivate inhibited acetylcholinesterase;11
however, they are poorly effective in organophosphorus insecticide self-poisoning and are limited by aging—a chemical change in the phosphorylated acetylcholinesterase that prevents oxime-induced reactivation. Obidoxime was administered in the case reported by Steindl and colleagues1
more than 2 days after poisoning, without reactivating acetylcholinesterase or improving neuromuscular function. Preliminary data from Salisbury suggest that pralidoxime also did not reactivate novichok-inhibited acetylcholinesterase.
Every day, thousands of patients are admitted to hospitals worldwide with organophosphorus insecticide self-poisoning, which is almost identical to poisoning with an organophosphorus nerve agent.12
If we are to get better at treating such poisoning, we must improve treatment of organophosphorus insecticide poisoning and put effort into finding cheap, effective, already licensed drugs. All available oximes should be robustly compared to understand relative effectiveness and safety—information that should be highly relevant to poisoning with a nerve agent.
Recognising organophosphorus insecticide poisoning in a hospital admitting three patients per day is easy; recognising organophosphorus nerve agent poisoning as an isolated case, by people with no practical experience of this poisoning, is difficult. Sporadic cases are likely to continue to occur. Being aware of the possibility of organophosphorus poisoning, remembering cholinergic poisoning as a wet opioid overdose, and having easy access to cholinesterase assays will speed up diagnosis, thereby augmenting public safety, reducing poisoning of health-care workers, and improving outcomes for patients.
Oxime antidotes reactivate inhibited acetylcholinesterase;11
however, they are poorly effective in organophosphorus insecticide self-poisoning and are limited by aging—a chemical change in the phosphorylated acetylcholinesterase that prevents oxime-induced reactivation. Obidoxime was administered in the case reported by Steindl and colleagues1
more than 2 days after poisoning, without reactivating acetylcholinesterase or improving neuromuscular function. Preliminary data from Salisbury suggest that pralidoxime also did not reactivate novichok-inhibited acetylcholinesterase.
Every day, thousands of patients are admitted to hospitals worldwide with organophosphorus insecticide self-poisoning, which is almost identical to poisoning with an organophosphorus nerve agent.12
If we are to get better at treating such poisoning, we must improve treatment of organophosphorus insecticide poisoning and put effort into finding cheap, effective, already licensed drugs. All available oximes should be robustly compared to understand relative effectiveness and safety—information that should be highly relevant to poisoning with a nerve agent.
Recognising organophosphorus insecticide poisoning in a hospital admitting three patients per day is easy; recognising organophosphorus nerve agent poisoning as an isolated case, by people with no practical experience of this poisoning, is difficult. Sporadic cases are likely to continue to occur. Being aware of the possibility of organophosphorus poisoning, remembering cholinergic poisoning as a wet opioid overdose, and having easy access to cholinesterase assays will speed up diagnosis, thereby augmenting public safety, reducing poisoning of health-care workers, and improving outcomes for patients.
(отдельную пикантность придаёт место работы одного из авторов - Centre for
Pesticide Suicide Prevention and Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK)