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Prolonged Bilateral Reactive Miosis as a Symptom of Severe Insulin Intoxication

Patient: Female, 64 Final Diagnosis: Insulin self poisoning Symptoms: Coma Medication: — Clinical Procedure: Supportive care Specialty: Critical Care Medicine OBJECTIVE: Unusual clinical course BACKGROUND: Miosis occurs following exposure to toxins that decrease the sympathomimetic tone, increase th...

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Autores principales: Gradwohl-Matis, Ilse, Pann, Jakob, Schmittinger, Christian A., Brunauer, Andreas, Dankl, Daniel, Dünser, Martin W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284992/
https://www.ncbi.nlm.nih.gov/pubmed/25556593
http://dx.doi.org/10.12659/AJCR.892324
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author Gradwohl-Matis, Ilse
Pann, Jakob
Schmittinger, Christian A.
Brunauer, Andreas
Dankl, Daniel
Dünser, Martin W.
author_facet Gradwohl-Matis, Ilse
Pann, Jakob
Schmittinger, Christian A.
Brunauer, Andreas
Dankl, Daniel
Dünser, Martin W.
author_sort Gradwohl-Matis, Ilse
collection PubMed
description Patient: Female, 64 Final Diagnosis: Insulin self poisoning Symptoms: Coma Medication: — Clinical Procedure: Supportive care Specialty: Critical Care Medicine OBJECTIVE: Unusual clinical course BACKGROUND: Miosis occurs following exposure to toxins that decrease the sympathomimetic tone, increase the cholinergic tone, or exert sedative-hypnotic effects, but has not been reported in insulin poisoning. CASE REPORT: A 64-year- old woman without co-morbidities was found unconscious next to an empty insulin pen. Her Glasgow Coma Scale was 3 with absent reflexes, bilateral reactive miosis, and injection marks across the abdominal wall. The patient was endotracheally intubated, mechanically ventilated, and transferred to this hospital. At admission, the blood glucose level was 34 mg/dL. Glasgow Coma Scale remained at 3, with persistent bilateral reactive miosis. The toxicology screening was negative for ethanol, barbiturates, tricyclic antidepressants, phenothiazines, amphetamines, cannabinoids, salicylates, acetaminophen, and cocaine. Cranial computed tomography with angiography and magnetic resonance imaging (MRI) did not show any structural brain lesions. Intravenous glucose was continued at 6–14 g/h for 3 days. On repeated neurological examinations, the patient remained deeply comatose, with partial loss of cranial nerve function. Bilateral reactive miosis persisted for 4 days. From day 5 on, the patient awoke progressively. At discharge, the patient was fully alert and orientated, without a focal neurological deficit. CONCLUSIONS: Prolonged bilateral reactive miosis can be a clinical symptom accompanying metabolic encephalopathy in severe insulin poisoning. Functional impairment of the pons due to relative hypoperfusion during hypoglycemia may serve as a reasonable pathophysiologic explanation for this phenomenon.
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spelling pubmed-42849922015-01-08 Prolonged Bilateral Reactive Miosis as a Symptom of Severe Insulin Intoxication Gradwohl-Matis, Ilse Pann, Jakob Schmittinger, Christian A. Brunauer, Andreas Dankl, Daniel Dünser, Martin W. Am J Case Rep Articles Patient: Female, 64 Final Diagnosis: Insulin self poisoning Symptoms: Coma Medication: — Clinical Procedure: Supportive care Specialty: Critical Care Medicine OBJECTIVE: Unusual clinical course BACKGROUND: Miosis occurs following exposure to toxins that decrease the sympathomimetic tone, increase the cholinergic tone, or exert sedative-hypnotic effects, but has not been reported in insulin poisoning. CASE REPORT: A 64-year- old woman without co-morbidities was found unconscious next to an empty insulin pen. Her Glasgow Coma Scale was 3 with absent reflexes, bilateral reactive miosis, and injection marks across the abdominal wall. The patient was endotracheally intubated, mechanically ventilated, and transferred to this hospital. At admission, the blood glucose level was 34 mg/dL. Glasgow Coma Scale remained at 3, with persistent bilateral reactive miosis. The toxicology screening was negative for ethanol, barbiturates, tricyclic antidepressants, phenothiazines, amphetamines, cannabinoids, salicylates, acetaminophen, and cocaine. Cranial computed tomography with angiography and magnetic resonance imaging (MRI) did not show any structural brain lesions. Intravenous glucose was continued at 6–14 g/h for 3 days. On repeated neurological examinations, the patient remained deeply comatose, with partial loss of cranial nerve function. Bilateral reactive miosis persisted for 4 days. From day 5 on, the patient awoke progressively. At discharge, the patient was fully alert and orientated, without a focal neurological deficit. CONCLUSIONS: Prolonged bilateral reactive miosis can be a clinical symptom accompanying metabolic encephalopathy in severe insulin poisoning. Functional impairment of the pons due to relative hypoperfusion during hypoglycemia may serve as a reasonable pathophysiologic explanation for this phenomenon. International Scientific Literature, Inc. 2015-01-03 /pmc/articles/PMC4284992/ /pubmed/25556593 http://dx.doi.org/10.12659/AJCR.892324 Text en © Am J Case Rep, 2015 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License
spellingShingle Articles
Gradwohl-Matis, Ilse
Pann, Jakob
Schmittinger, Christian A.
Brunauer, Andreas
Dankl, Daniel
Dünser, Martin W.
Prolonged Bilateral Reactive Miosis as a Symptom of Severe Insulin Intoxication
title Prolonged Bilateral Reactive Miosis as a Symptom of Severe Insulin Intoxication
title_full Prolonged Bilateral Reactive Miosis as a Symptom of Severe Insulin Intoxication
title_fullStr Prolonged Bilateral Reactive Miosis as a Symptom of Severe Insulin Intoxication
title_full_unstemmed Prolonged Bilateral Reactive Miosis as a Symptom of Severe Insulin Intoxication
title_short Prolonged Bilateral Reactive Miosis as a Symptom of Severe Insulin Intoxication
title_sort prolonged bilateral reactive miosis as a symptom of severe insulin intoxication
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284992/
https://www.ncbi.nlm.nih.gov/pubmed/25556593
http://dx.doi.org/10.12659/AJCR.892324
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