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Updated: Jul 10, 2026

Optimization of the Retinal Vein Occlusion Mouse Model to Limit Variability
Published on: August 6, 2021
Phenylephrine-induced microvascular occlusion syndrome in a patient with a heterozygous factor V Leiden mutation
Andrew H Kalajian1, Klark B Turpen, Kristin O Donovan
1Division of Dermatology, Department of Medicine, University of Louisville, 310 E Broadway, Floor 2A, Louisville, KY 40202, USA. akalajian@yahoo.com
Background:
Cutaneous microvascular occlusion syndromes (MOS) present with noninflammatory retiform purpura with variable outcomes that are dependent on the severity, duration, and specific underlying cause. Transient cases are often associated with few sequelae, while severe forms such as symmetrical peripheral gangrene may be associated with amputation and death.
Observations:
A middle-aged man developed MOS after exposure to phenylephrine hydrochloride and experienced complete resolution when treatment with the vasopressor was discontinued. Further evaluation detected a previously subclinical heterozygous factor V Leiden mutation.
Conclusions:
We propose that phenylephrine-mediated vasoconstriction superimposed on an underlying thrombotic predisposition precipitated the transient MOS. The role of vasopressors in the development of cutaneous MOS is well documented in the critical care literature; however, it is underrepresented in the dermatologic literature, and, to our knowledge, there are no reports of phenylephrine use inducing MOS. We hope to raise awareness of the potential role of vasopressor medications in causing MOS.
Insights
Phenylephrine-induced vasoconstriction can trigger microvascular occlusion syndromes (MOS) in individuals with a thrombotic predisposition. Discontinuing the vasopressor led to complete resolution of MOS symptoms in a reported case.
Area of Science:
- Dermatology
- Vascular Medicine
- Pharmacology
Background:
- Cutaneous microvascular occlusion syndromes (MOS) manifest as noninflammatory retiform purpura.
- Outcomes vary based on severity, duration, and cause, ranging from minor sequelae to severe conditions like peripheral gangrene.
Observation:
- A middle-aged male patient presented with MOS following exposure to phenylephrine hydrochloride.
- Symptoms resolved completely upon discontinuation of the vasopressor medication.
- Subsequent genetic testing revealed a heterozygous factor V Leiden mutation, indicating a thrombotic predisposition.
Findings:
- Phenylephrine-mediated vasoconstriction, combined with an underlying thrombotic tendency, likely precipitated the transient MOS.
- This case highlights a potential, underreported cause of MOS in dermatologic literature.
Implications:
- Vasopressor medications, particularly phenylephrine, should be considered as potential triggers for MOS.
- Increased awareness among dermatologists regarding vasopressor-induced MOS is crucial for timely diagnosis and management.
- Further research is warranted to explore the link between specific vasopressors and MOS development.
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