Pulmonary thrombosis in acute organophosphate poisoning - Case report and literature overview of prothrombotic preconditioning in organophosphate toxicity
Journal
Toxicology Reports
Date Issued
2019-06-15
Author(s)
Niko Bekarovski
Irena Jurukov
DOI
doi.org/10.1016/j.toxrep.2019.06.002
Abstract
Objective: Acute organophosphate (OP) poisonings are presented with acetylcholine-receptor overstimulation.
There have been a few case reports of thrombotic complications in acute OP poisonings, as well as prolonged
thrombosis preconditions in patients who survived this type of intoxications. The paper presents a case with
pulmonary thrombosis (PT) that develops in the subacute phase of intentional acute OP poisoning, treated only
with atropine, as well as a literature overview of OP-induced prothrombotic toxicity.
Case report: A middle aged woman was brought to the hospital after ingestion of unknown insecticide with
suicidal intentions. She had a history of HTA (arterial hypertension), hyperlipidemia and untreated depression.
The clinical features of poisoning were miosis, vomiting, dizziness, abdominal cramps and diarrhea. Soon after
admission, she developed difficulties in breathing with decrease of serum pseudocholinesterase
(2590...1769...1644...800 U/l), bibasal pulmonary crackles, drop of SpO2 to 84%. Antidote treatment included
carbo medicinalis, atropine, and diazepam, without use of oximes. The seventh day pseudocholinesterase, the
levels started to rise but the patient’s hyposaturation (SpO2 86-88%) persisted. Chest ultrasound detected hypoechoic subpleural lesion to the right. Haemostatic tests showed increased D-Dimmer (2312 ng/ml) with hypercoagulability. The CT pulmonary angiography confirmed PT and after the administration of low molecular
heparin, her clinical condition improved.
Conclusion: Acute organophosphate poisoning treated with atropine showed a potential for inducing prothrombotic coagulation abnormalities, presented with PT. This life-threatening complication may additionally
contribute to prolonged morbidity and mortality in OP poisonings, especially in patients with medical history of
comorbidites.
There have been a few case reports of thrombotic complications in acute OP poisonings, as well as prolonged
thrombosis preconditions in patients who survived this type of intoxications. The paper presents a case with
pulmonary thrombosis (PT) that develops in the subacute phase of intentional acute OP poisoning, treated only
with atropine, as well as a literature overview of OP-induced prothrombotic toxicity.
Case report: A middle aged woman was brought to the hospital after ingestion of unknown insecticide with
suicidal intentions. She had a history of HTA (arterial hypertension), hyperlipidemia and untreated depression.
The clinical features of poisoning were miosis, vomiting, dizziness, abdominal cramps and diarrhea. Soon after
admission, she developed difficulties in breathing with decrease of serum pseudocholinesterase
(2590...1769...1644...800 U/l), bibasal pulmonary crackles, drop of SpO2 to 84%. Antidote treatment included
carbo medicinalis, atropine, and diazepam, without use of oximes. The seventh day pseudocholinesterase, the
levels started to rise but the patient’s hyposaturation (SpO2 86-88%) persisted. Chest ultrasound detected hypoechoic subpleural lesion to the right. Haemostatic tests showed increased D-Dimmer (2312 ng/ml) with hypercoagulability. The CT pulmonary angiography confirmed PT and after the administration of low molecular
heparin, her clinical condition improved.
Conclusion: Acute organophosphate poisoning treated with atropine showed a potential for inducing prothrombotic coagulation abnormalities, presented with PT. This life-threatening complication may additionally
contribute to prolonged morbidity and mortality in OP poisonings, especially in patients with medical history of
comorbidites.
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