Warfarin-induced skin necrosis in a patient with protein S deficiency

Fraga, Ruana; Diniz, Lúcia Martins; Lucas, Elton Almeida; Emerich, Paulo Sergio

doi:10.1590/abd1806-4841.20187310

Cited by 12 publications

(4 citation statements)

References 5 publications

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“…There are two distinct, although overlapping, warfarin-induced microthrombosis syndromes: (a) "classic" warfarin-induced skin necrosis, and (b) warfarin-induced venous limb gangrene [64][65][66]. Whereas the former ("classic") syndrome usually involves predominantly non-acral tissue sites and is frequently associated with hereditary abnormalities in the protein C natural anticoagulant pathways (protein C deficiency [81][82][83][84], protein S deficiency [85,86], factor V Leiden [87,88], prothrombin gene mutation [89]), the latter disorder ("venous limb gangrene") usually features a severe underlying DIC state such as HIT or metastatic adenocarcinoma [64,[68][69][70][71][72][73][74]. A common misconception is that the microthrombosis reflects severe failure of the natural anticoagulant system per se; however, the key concept is that there is profoundly disturbed procoagulant-anticoagulant balance, as the depletion in vitamin K-dependent anticoagulants results in failure to control the greatly increased thrombin generation reflecting the underlying DIC state [64,[68][69][70][71].…”

Section: Natural Anticoagulant Depletion and Disturbed Procoagulantanmentioning

confidence: 99%

Symmetrical peripheral gangrene in critical illness

Warkentin

Ning

2021

Transfusion and Apheresis Science

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Symmetrical peripheral gangrene (SPG) is a disabling complication that affects a small proportion of patients who survive critical illness. Its pathogenesis reflects profoundly disturbed procoagulant-anticoagulant balance in susceptible tissue beds secondary to circulatory shock (cardiogenic, septic). There is a characteristic SPG triad: (a) shock (hypotension, lactic acidemia, normoblastemia, multiple organ dysfunction), (b) disseminated intravascular coagulation (DIC), and (c) natural anticoagulant depletion (protein C, antithrombin). In recent years, risk factors for natural anticoagulant depletion have been identified, most notably acute ischemic hepatitis ("shock liver"), which is seen in at least 90% of patients who develop SPG. Moreover, there is a characteristic time interval (2-5 days, median 3 days) between the onset of shock/shock liver and the beginning of ischemic injury secondary to peripheral microthrombosis ("limb ischemia with pulses"), reflecting the time required to develop severe depletion in hepatically-synthesized natural anticoagulants. Other risk factors for natural anticoagulant depletion include chronic liver disease (e.g., cirrhosis) and, possibly, transfusion of colloids (albumin, high-dose immunoglobulin) lacking coagulation factors. A causal role for vasopressor therapy is unproven and is unlikely; this is because critically ill patients who develop SPG do so usually after at least 36-48 hours of vasopressor therapy, implicating a time-dependent pathophysiological mechanism. The most plausible explanation is a progressive time-dependent decline in key natural anticoagulant factors, reflecting ongoing DIC ("consumption"), proximate liver disease whether acute or chronic ("impaired production"), and colloid administration ("hemodilution"). Given these evolving concepts of pathogenesis, a rationale approach to prevention/treatment of SPG can be developed.

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Section: Natural Anticoagulant Depletion and Disturbed Procoagulantanmentioning

confidence: 99%

Symmetrical peripheral gangrene in critical illness

Warkentin

Ning

2021

Transfusion and Apheresis Science

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“…Indeed, there are reported cases of WISN developing upon recommencement of warfarin in non-warfarin naïve patients. 9 , 10 Certain conditions such as Protein C deficiency are believed to play a contributory role.…”

Section: Discussionmentioning

confidence: 99%

Warfarin-induced skin necrosis: a rare condition

Nsaful

Adjei

Dedey

et al. 2020

gmj

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Warfarin induced skin necrosis is a rare debilitating and, in some cases, life-threatening complication. A 47-year-old male on life-long anticoagulation omits his medication and develops extensive skin necrosis of the left leg complicated by acute renal failure three days after restarting warfarin. Investigations reveal possible Protein S deficiency which is known to be a predisposing condition. Various mechanisms have been proposed as the underlying cause. He was managed on heparin, wound debridement and skin grafting. Warfarin was restarted concurrently with heparin. Knowledge of this complication will enable timely diagnosis and treatment.

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“…There are reports that warfarin directly causes toxic vasculitis at the junction of the precapillary and arterial capillary of the dermovascular loop. The damaged capillaries dilate and rupture leading to petechial rash whereas, veins distal to the damaged capillaries thrombose culminating into tissue necrosis [10].…”

Section: Discussionmentioning

confidence: 99%

A Case Report on Warfarin Induced Skin Necrosis: Drug-drug Interaction or Inappropriate Therapy

Dutta

Sharma

Misra

et al. 2018

JPT

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Introduction: Warfarin is one of the most frequently prescribed oral anticoagulant. Necrosis and/or gangrene ofskin and other tissues is an uncommon but serious risk associated with warfarin. The incidence of warfarin inducedtissue necrosis is about 0.01 % to 0.1%.Case description: A 62-year-old male presented to emergency with a complaint of skin discoloration and edema onleft lower limb diagnosed as warfarin induced skin necrosis. He had an episode of hemiparesis 20 days back for whichhe was started on oral warfarin along with other medications. On diagnosis warfarin was stopped and fresh frozenplasma (FFP) was given along with vitamin K. Due to progressing tissue necrosis, above knee limb amputation wasdone. We assume that an interaction between rosuvastatin and warfarin or possibly lack of adequate bridge therapywith heparin resulted in this complication.Conclusion: Warfarin induced skin necrosis is a known early complication of the therapy. Though late onsetappearance of this event is rare but not unknown. Bridging therapy with heparin and avoiding use of interactingdrugs concomitantly could prevent many such reactions.

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Warfarin-induced skin necrosis in a patient with protein S deficiency

Cited by 12 publications

References 5 publications

Symmetrical peripheral gangrene in critical illness

Symmetrical peripheral gangrene in critical illness

Warfarin-induced skin necrosis: a rare condition

A Case Report on Warfarin Induced Skin Necrosis: Drug-drug Interaction or Inappropriate Therapy

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