Sepsis-induced digital ischaemia in a professional pianist, in the absence of vasopressors

Kurup, Vishnu; Simpson, Racquel

doi:10.1136/bcr-2019-229659

Cited by 3 publications

(4 citation statements)

References 15 publications

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“…2 summarizes the typical clinical, laboratory, and temporal clinical picture of patients who develop SPG in the setting of critical illness. Since the recognition of a role of proximate shock liver in helping to explain subsequent SPG [1,2,8,40], recent SPG papers by others [90,91] have commented on the occurrence of prodromal shock liver.…”

Section: Prodromal Shock Livermentioning

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: Prodromal Shock Livermentioning

confidence: 99%

Symmetrical peripheral gangrene in critical illness

Warkentin

Ning

2021

Transfusion and Apheresis Science

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“…29 That said, limb ischemia has certainly been seen in septic patients without pressor requirement. 36 Others have suggested that microvasculature thrombosis from protein C and antithrombin deficiency associated with hepatic dysfunction (often 2-5 days before evident ischemia) are prominent factors in the pathogenesis of SPG. 27 This may align with the timeline of "shock liver" that our patient encountered.…”

Section: Discussionmentioning

confidence: 99%

“…Another study of adult septic patients who developed SPG requiring amputation attribute vasopressor, not thrombosis, as the primary instigator, which they do defend is dose and duration‐dependent 29 . That said, limb ischemia has certainly been seen in septic patients without pressor requirement 36 . Others have suggested that microvasculature thrombosis from protein C and anti‐thrombin deficiency associated with hepatic dysfunction (often 2–5 days before evident ischemia) are prominent factors in the pathogenesis of SPG 27 .…”

Section: Discussionmentioning

confidence: 99%

Hirudotherapy for neonatal limb ischemia during ECMO support: A word of caution

Resch

Said

Steiner

et al. 2021

Journal of Cardiac Surgery

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Introduction: Disordered coagulation, clot formation and distal limb ischemia are complications of extracorporeal membrane oxygenation (ECMO) with significant morbidity and mortality. Medicinal leech therapy (hirudotherapy) has been attempted in plastic and orthopedic surgeries to improve venous congestion and salvage ischemic flaps. To our knowledge this has not been reported in pediatric cardiac surgery or during ECMO support. We present a complex neonate whose ECMO course was complicated by distal limb ischemia for whom leech therapy was attempted.Patient and Intervention: A 2-week-old 2.7 kg infant required ECMO support secondary to perioperative multiorgan system dysfunction following repair of critical coarctation and ventricular septal defect. Despite systemic anticoagulation, his clinical course was complicated by arterial thrombus, vasopressor-induced vascular spasm and bilateral distal limb ischemia. Medicinal leech therapy was tried after initially failing conventional measures.Result: Following the third leech application, this patient developed significant hemorrhage from the web space adjacent to the left great toe. An estimated 450 ml of blood loss occurred and more than 300 ml of blood product transfusions were required. He ultimately progressed to irreversible systemic end organ dysfunction and comfort care was provided. Conclusion:The use of medicinal leech therapy in pediatric cardiac surgery may be considered to minimize the consequences of advanced limb ischemia and venous congestion. However, this should be used with caution while patients are systemically anticoagulated during ECMO support. A directed review is presented here to assist in determining optimal application and potential course of therapy.

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“…Um estudo retrospectivo casocontrole sobre uso de DVA e GSP demonstrou que a duração do uso de DVA não influencia o aparecimento de gangrena, mas o pico da dose pode ter papel de relevância no surgimento de gangrena, principalmente para dopamina e noradrenalina 14 . Em trabalhos descritivos de casos de GSP na literatura, os pacientes nem chegaram a fazer uso de DVA para estabelecer correlação entre causa e efeito 16,17 . Uma revisão sobre o assunto não encontrou diferença das doses e a duração de uso de DVA entre pacientes sem e com GSP 18 .…”

Section: Discussionunclassified

Gangrena Simétrica Periférica (Gsp): Relato De Caso E Revisão Narrativa Da Literatura

Siqueira¹,

Borba²,

Vieira³

et al. 2021

Relatos Casos Cir.

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Introdução: A gangrena simétrica periférica (GSP) é uma desordem microvascular caracterizada por isquemia e gangrena majoritariamente nos membros inferiores, sendo intimamente relacionada com quadros de coagulação intravascular disseminada (CIVD) e choque. Consiste numa síndrome rara, porém comumente confundida na prática médica com a má perfusão pelo uso de drogas vasoativas (DVA). Relato do caso: É feito o relato do caso de um paciente de 1 ano e 11 meses, sem antecedentes patológicos relevantes, acometido por metapneumovirose que evoluiu com choque séptico e CIVD. No segundo dia de internação, foi realizado o diagnóstico de GSP em membros inferiores e superiores. Conclusão: Discute-se o papel dos vasopressores na síndrome, sua fisiopatologia e as principais opções terapêuticas para esses casos.

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Sepsis-induced digital ischaemia in a professional pianist, in the absence of vasopressors

Cited by 3 publications

References 15 publications

Symmetrical peripheral gangrene in critical illness

Symmetrical peripheral gangrene in critical illness

Hirudotherapy for neonatal limb ischemia during ECMO support: A word of caution

Gangrena Simétrica Periférica (Gsp): Relato De Caso E Revisão Narrativa Da Literatura

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