Tissue necrosis due to norepinephrine

Oglesby, James E.; Baugh, Joseph H.

doi:10.1016/0002-9610(68)90171-2

Cited by 14 publications

(8 citation statements)

References 21 publications

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“…Subsequent increases in the hydrostatic pressure of the venous circulation cause further effusion of the vasopressor into the tissues. 9,16 Ischemia then follows parallel to the infusion site as the vasopressor diffuses into tissue space and the tributary veins constrict. As venous inflammation occurs, backflow commences into the arteriolar capillaries due to hydrostatic pressure.…”

Section: Vasopressorsmentioning

confidence: 99%

“…As venous inflammation occurs, backflow commences into the arteriolar capillaries due to hydrostatic pressure. 9,16 Sloughing has also been reported at the insertion site of longer peripheral catheters despite the maintenance of vein integrity. 16 Risk factors for vasopressor necrosis include presence of vasculopathy, preexisting hypotension, diabetic neuropathy, Raynaud disease, coagulopathy, advanced age, and altered mental status.…”

Section: Vasopressorsmentioning

confidence: 99%

“…9,16 Sloughing has also been reported at the insertion site of longer peripheral catheters despite the maintenance of vein integrity. 16 Risk factors for vasopressor necrosis include presence of vasculopathy, preexisting hypotension, diabetic neuropathy, Raynaud disease, coagulopathy, advanced age, and altered mental status. 10,17,18 Local venous anatomy remains an important variable as well, with higher frequencies of extravasation reported in areas with smaller veins or slower circulation such as the antecubital fossa of the wrist or the saphenous vein of the ankle.…”

Section: Vasopressorsmentioning

confidence: 99%

“…10,17,18 Local venous anatomy remains an important variable as well, with higher frequencies of extravasation reported in areas with smaller veins or slower circulation such as the antecubital fossa of the wrist or the saphenous vein of the ankle. 9,10,16,18 Larger veins provide adequate dilution of the vasopressor and are less likely to spasm. 9 Although the absolute rate of peripheral vasopressor-induced necrosis is unknown, the original rates of ulceration from the peripheral administration of norepinephrine were as high as 46-60%.…”

Section: Vasopressorsmentioning

confidence: 99%

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Management of Extravasation Injuries: A Focused Evaluation of Noncytotoxic Medications

et al. 2014

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Extravasations are common manifestations of iatrogenic injury that occur in patients requiring intravenous delivery of known vesicants. These injuries can contribute substantially to patient morbidity, cost of therapy, and length of stay. Many different mechanisms are behind the tissue damage during extravasation injuries. In general, extravasations consist of four different subtypes of tissue injury: vasoconstriction, osmotic, pH related, and cytotoxic. Recognition of high-risk patients, appropriate cannulation technique, and monitoring of higher risk materials remain the standard of care for the prevention of extravasation injury. Prompt interdisciplinary action is often necessary for the treatment of extravasation injuries. Knowledge of the mechanism of extravasation-induced tissue injury, agents for reversal, and appropriate nonpharmacologic treatment methods is essential. The best therapeutic agent for treatment of vasopressor extravasation is intradermal phentolamine. Topical vasodilators and intradermal terbutaline may provide relief. Intradermal hyaluronidase has been effective for hyperosmotic extravasations, although its use largely depends on the risk of tissue injury and the severity of extravasation. Among the hyperosmotic agents, calcium extravasation is distinctive because it may present as an acute tissue injury or may possess delayed clinical manifestations. Extravasation of acidic or basic materials can produce significant tissue damage. Phenytoin is the prototypical basic drug that causes a clinical manifestation known as purple glove syndrome (PGS). This syndrome is largely managed through preventive and conservative treatment measures. Promethazine is acidic and can cause a devastating extravasation, particularly if administered inadvertently through the arteriolar route. Systemic heparin therapy remains the accepted treatment option for intraarteriolar administration of promethazine. Overall, the evidence for managing extravasations due to noncytotoxic medications is nonexistent or limited to case reports. More research is needed to improve knowledge of patient risk, prompt recognition of the extravasation, and time course for tissue injury, and to develop prevention and treatment strategies for extravasation injuries.

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Section: Vasopressorsmentioning

confidence: 99%

Section: Vasopressorsmentioning

confidence: 99%

Section: Vasopressorsmentioning

confidence: 99%

Section: Vasopressorsmentioning

confidence: 99%

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Management of Extravasation Injuries: A Focused Evaluation of Noncytotoxic Medications

et al. 2014

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“…1–3 Cases of skin necrosis with peripheral infusions continue to be seen despite longstanding awareness that vasopressors need to be administered through a central venous catheter for rapid dilution 2. Treatment of extravasation injuries includes prompt discontinuation of the peripheral intravenous infusion, and the administration of a pharmacological vasodilator such as phentolamine, an ɑ-adrenergic antagonist 3. Should subcutaneous necrosis occur, general wound care measures such as mechanical debridement are recommended.…”

Section: Descriptionmentioning

confidence: 99%

Well recognised but still overlooked: norepinephrine extravasation: Figure 1

2012

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A 46-year-old man was transferred from an outside hospital for evaluation of acute renal failure and non-ST-segment elevation myocardial infarction. During his initial presentation at the outside hospital, the patient was profoundly hypotensive with signs of respiratory failure. Owing to the perceived urgency, he was started on norepinephrine for haemodynamic support through a peripheral intravenous line. Following the resolution of haemodynamic instability, the patient was noted to have a large subcutaneous lesion on his right forearm around his peripheral intravenous site. The lesion consisted of a large serous bullae and exhibited marked pallor, coldness and mottling of the skin. The patient underwent mechanical debridement of the necrotic tissue and was treated with topical silver sulfadiazine.Norepinephrine is an ɑ-adrenergic agonist commonly used for the treatment of shock. A well-known side effect of norepinephrine is the potential for subcutaneous tissue ischaemia in the event of inadvertent extravasation. When extravasation from a peripheral cannula occurs, the relatively high concentration of epinephrine in both the recipient vein and adjacent blood vessels induce subcutaneous tissue ischaemia through marked vasoconstriction and increased vascular permeability (figure 1).1-3 Cases of skin necrosis with peripheral infusions continue to be seen despite longstanding awareness that vasopressors need to be administered through a central venous catheter for rapid dilution.2 Treatment of extravasation injuries includes prompt discontinuation of the peripheral intravenous infusion, and the administration of a pharmacological vasodilator such as phentolamine, an ɑ-adrenergic antagonist.3 Should subcutaneous necrosis occur, general wound care measures such as mechanical debridement are recommended. Learning points▸ Skin necrosis with subcutaneous extravasation of vasopressors continues to occur despite widespread knowledge of need to avoid peripheral venous administration. ▸ The pathophysiology involves the relatively high concentration of norepinephrine in both the recipient vein and adjacent blood vessels leading to vasoconstriction and increased vascular permeability. ▸ Treatment following the extravasation includes discontinuation of the intravenous site, pharmacological vasodilators and wound care.Competing interests None.

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