Tongue necrosis after intraarterial vasopressin therapy

Zelch, MG; Geisinger, MA; Risius, Barbara

doi:10.2214/ajr.144.6.1283

Cited by 7 publications

(4 citation statements)

References 5 publications

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“…One patient developed gastrointestinal bleeding caused by an ischemic colitis, confirmed by colonoscopy and colon biopsy, together with burning sensation, swelling, and ulcers of the tongue, all latter findings are compatible with tongue ischemia. 14 Reasons for discontinuation of therapy in the remaining three patients were asymptomatic ventricular extrasystoles in one, tongue ischemia in one, and bacteremia secondary to urinary tract infection in the last patient. All compli cations resolved after ornipressin suppression in the first three cases and after ornipressin suppression and antibiotic therapy in the latter.…”

Section: Resultsmentioning

confidence: 96%

“…Some of these side effects were because of the powerful vasoconstrictor action of ornipressin, and were similar to the complications observed in therapeutic trials of vasopressin in cirrhotic patients with gastrointestinal hemorrhage. 14,[44][45][46] These complications should be weighed against the severity of HRS, and the absence of an effective treatment for this complication of cirrhosis. Nevertheless, prospective controlled studies in large series of patients are clearly needed, to evaluate the efficacy and incidence of side effects, before this treatment can be advocated for use in general practice.…”

Section: Discussionmentioning

confidence: 99%

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Reversibility of hepatorenal syndrome by prolonged administration of ornipressin and plasma volume expansion

et al. 1998

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Hepatorenal syndrome is caused by a marked vasoconstriction of the renal circulation. It is suggested that the renal vasoconstriction is related to an overactivity of vasoconstrictor systems secondary to a vasodilation of the arterial circulation that causes a reduction in effective arterial blood volume. To test this hypothesis, 16 cirrhotic patients with hepatorenal syndrome were treated with a combination of ornipressin, a potent vasoconstrictor agent, and plasma volume expansion with albumin to improve effective arterial blood volume. The combined treatment was administered either for 3 or 15 days (8 patients each), and the effects on renal function, vasoactive systems, and systemic hemodynamics were assessed. The 3-day treatment with ornipressin and albumin was associated with a normalization of the overactivity of renin-angiotensin and sympathetic nervous systems, a marked increase in atrialnatriuretic peptide levels, and only a slight improvement in renal function. However, when ornipressin and albumin were administered for 15 days, a remarkable improvement in renal function was observed, with normalization of serum-creatinine concentration, a marked increase in renal plasma flow and glomerular filtration rate, and a persistent suppression in the activity of vasoconstrictor systems. However, 3 of 8 patients on 15-day therapy treatment had to be discontinued because of ischemic complications. In conclusion, the decrease in effective arterial blood volume and the activation of vasoconstrictor systems play a crucial role in the pathogenesis of hepatorenal syndrome. Although the prolonged administration of ornipressin combined with plasma volume expansion reverses hepatorenal syndrome, this treatment should be used with great caution in clinical practice because of the risk of ischemic complications. (HEPATOLOGY 1998;27:35-41.)Hepatorenal syndrome (HRS) is a common and severe complication of patients with advanced cirrhosis, which is characterized by impaired renal function, marked abnormalities in the arterial circulation, and activity of endogenous vasoactive systems. [1][2][3][4][5] In the kidney, marked renal vasoconstriction results in reduced renal perfusion and low-glomerular filtration rate, whereas the extrarenal hemodynamics are characterized by low-systemic vascular resistance, and arterial hypotension. Although HRS is of functional origin and is theoretically reversible, no medical therapy has so far been shown to reverse renal hypoperfusion in these patients. 1,[4][5][6] The pathogenesis of HRS is not completely understood. It has been proposed that HRS represents the extreme expression of the underfilling of the arterial circulation, secondary to a vasodilation located mainly in the splanchnic vascular bed. 2,7 This vasodilation would cause a reduction in effective arterial blood volume with subsequent activation of vasoconstrictor systems, mainly the renin-angiotensin-aldosterone system and the sympathetic nervous system, that would promote renal vasoconstriction. If this is the case, the impro...

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Section: Resultsmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Reversibility of hepatorenal syndrome by prolonged administration of ornipressin and plasma volume expansion

et al. 1998

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“…In another unusual case, tongue necrosis in a 64-year-old woman was attributed to vasopressin treatment [10]. It is unknown if that patient had any underlying vascular pathology, which may have also contributed to the tongue necrosis.…”

Section: Discussionmentioning

confidence: 98%

Tongue necrosis and systemic vascular amyloidosis

et al. 2011

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“…Other causes of tongue ischemia include hyperviscosity syndrome, radiation effects, carotid dissection, and disseminated intravascular coagulation. [6][7][8][9] Although symptoms such as jaw pain with chewing may become manifest with ligation of one or both external carotid arteries, circulation to the face is well preserved because of abundant collateral flow. In our case, however, severe stenosis in the contralateral external carotid artery and embolization to the ipsilateral lingual artery abruptly compromised the limited collateral flow to the tongue, resulting in tissue necrosis.…”

Section: Discussionmentioning

confidence: 99%

Tongue necrosis as an unusual presentation of carotid artery stenosis

Bjordahl

Ammar

2011

Journal of Vascular Surgery

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A 57-year-old man with premature coronary artery disease presented to the emergency department with left facial pain, numbness, and tongue swelling. The patient was found to have significant tongue necrosis, and subsequent arteriography demonstrated carotid bifurcation stenosis with embolization to the left lingual artery. The patient was successfully treated with debridement of his tongue and left carotid endarterectomy.

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Tongue necrosis after intraarterial vasopressin therapy

Cited by 7 publications

References 5 publications

Reversibility of hepatorenal syndrome by prolonged administration of ornipressin and plasma volume expansion

Reversibility of hepatorenal syndrome by prolonged administration of ornipressin and plasma volume expansion

Tongue necrosis and systemic vascular amyloidosis

Tongue necrosis as an unusual presentation of carotid artery stenosis

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