What is post-vasopressor (vasopressor) induced tissue necrosis?

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From the FDA Drug Label

ADVERSE REACTIONS The following reactions can occur: Body As A Whole: Ischemic injury due to potent vasoconstrictor action and tissue hypoxia. Prolonged administration of any potent vasopressor may result in plasma volume depletion which should be continuously corrected by appropriate fluid and electrolyte replacement therapy If plasma volumes are not corrected, hypotension may recur when LEVOPHED is discontinued, or blood pressure may be maintained at the risk of severe peripheral and visceral vasoconstriction (e.g., decreased renal perfusion) with diminution in blood flow and tissue perfusion with subsequent tissue hypoxia and lactic acidosis and possible ischemic injury. Gangrene of extremities has been rarely reported. 5. 4 Extravasation and Tissue Necrosis with Intravenous Infusion Avoid extravasation of epinephrine into the tissues, to prevent local necrosis.

Post-vasopressor (vasopressor) induced tissue necrosis refers to ischemic injury due to the potent vasoconstrictor action of vasopressors, leading to tissue hypoxia. This can result in:

  • Gangrene of extremities (rarely reported)
  • Extravasation necrosis at the injection site
  • Ischemic injury due to decreased blood flow and tissue perfusion Key factors contributing to this condition include:
  • Prolonged administration of potent vasopressors
  • Plasma volume depletion if not corrected with fluid and electrolyte replacement therapy
  • Severe peripheral and visceral vasoconstriction 1, 2

From the Research

Post-vasopressor induced tissue necrosis refers to the tissue death that occurs following the use of vasopressor medications, which are commonly administered to critically ill patients to maintain blood pressure during shock states, and is associated with high morbidity and mortality as seen in a study published in 2022 3. This complication typically manifests as skin and tissue necrosis in peripheral areas such as fingers, toes, and occasionally the nose or ears.

Key Points

  • Management involves prompt discontinuation of the vasopressor if possible, switching to alternative agents with less peripheral vasoconstriction effects, and providing supportive wound care.
  • For established necrosis, treatment includes debridement of necrotic tissue, appropriate wound care with regular dressing changes, infection prevention with topical or systemic antibiotics if indicated, and pain management.
  • Prevention strategies include using the lowest effective dose of vasopressors, considering early addition of vasodilators like nitroglycerin when peripheral perfusion is compromised, regular monitoring of extremities for early signs of ischemia, and maintaining adequate hydration.
  • The mechanism involves intense vasoconstriction of peripheral blood vessels by vasopressors like norepinephrine, epinephrine, and vasopressin, leading to reduced blood flow to extremities, resulting in tissue ischemia and eventual necrosis, as reported in a study published in 2021 4.

Recent Evidence

A recent study published in 2022 3 highlights the importance of early recognition and prompt treatment of vasopressor-induced acute limb ischemia (VIALI) in minimizing tissue necrosis and preventing amputations. Another study published in 2020 5 recommends a tiered approach to manage vasopressor-induced limb ischemia, which includes phase 1 to phase 4 care, and emphasizes the importance of early recognition and treatment in minimizing morbidity.

Clinical Implications

The use of vasopressors should be carefully considered and monitored, as it can increase the risk of mortality in traumatic hemorrhagic shock patients, as seen in a nationwide cohort study in Japan published in 2018 6. In addition, the use of vasopressors can lead to digital ischemia and necrosis, as reported in a case study published in 2021 4, highlighting the need for careful monitoring and management of patients receiving vasopressors. Overall, post-vasopressor induced tissue necrosis is a serious complication that requires prompt recognition and treatment to minimize morbidity and mortality, and prevention strategies should be implemented to reduce the risk of this complication, as supported by the evidence from recent studies 3, 4, 5.

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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