Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Case Reports
. 2015 Jan 3:16:1-3.
doi: 10.12659/AJCR.892324.

Prolonged bilateral reactive miosis as a symptom of severe insulin intoxication

Ilse Gradwohl-Matis  1 , Jakob Pann  1 , Christian A Schmittinger  2 , Andreas Brunauer  1 , Daniel Dankl  1 , Martin W Duenser  1
Affiliations
Case Reports

Prolonged bilateral reactive miosis as a symptom of severe insulin intoxication

Ilse Gradwohl-Matis et al. Am J Case Rep. .

Abstract

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.

PubMed Disclaimer

References

    1. Kosnoski EM, Yolton RL, Citek K, et al. The Drug Evaluation Classification Program: using ocular and other signs to detect drug intoxication. J Am Optom Assoc. 1998;69:211–27. - PubMed
    1. Hon KL, Ho JK, Hung EC, et al. Poisoning necessitating pediatric ICU admissions: size of pupils does matter. J Natl Med Assoc. 2008;100:952–56. - PubMed
    1. Hoffman RS, Nelson LS, Howland MA, editors. Ophthalmic principles. Goldfrank’s manual of toxicologic emergencies. 8th ed. New York: McGraw Hill Medical; 2007. pp. 177–87.
    1. Beckmann U, Gillies DM, Berenholtz SM, et al. Incidents relating to the intra-hospital transfer of critically ill patients. An analysis of the reports submitted to the Australian Incident Monitoring Study in Intensive Care. Intensive Care Med. 2004;30:1579–85. - PubMed
    1. Mitchell AA, Lovejoy FH, Goldman P. Drug ingestions associated with miosis in comatose children. J Pediatr. 1976;89:303–5. - PubMed

Publication types