Extracorporeal therapy in sepsis

Abstract

Acute renal injury (AKI) occurs in 19% of patients with sepsis, 23% of those with severe sepsis and up to 50% of patients with septic shock. AKI represents an independent prognostic factor of mortality (about 45%); epidemiological studies have pointed out that the onset of AKI in sepsis (S-AKI) correlates with an unfavourable outcome, reaching a mortality of 75%.

Over the years, efforts have been made to prevent and treat “low flow” hemodynamic damage resulting from shock by increasing renal blood flow, improving cardiac output and perfusion pressure. New experimental studies in S-AKI have shown that renal blood flow is maintained, and indeed increases, in the course of septic shock. Recently, a “single theory” has been proposed that defines acute renal injury as the final result of the interaction between inflammation, oxidative stress, apoptosis, microcirculatory dysfunction and the adaptive response of tubular epithelial cells to the septic insult.

The type of treatment, the dose and the starting time of RRT are of strategic importance in the recovery of AKI in septic patients.

The use of new anticoagulation strategies in critically ill patients with S-AKI has allowed treatments to be carried out for enough time to reach the correct dose of purification prescribed, minimizing down-time and bleeding risk.

The availability of new technologies allows to customize treatments more and more; the collaboration between nephrologists and intensivists must always increase in order to implement modern precision medicine in critical care.

Keywords: S-AKI, septic shock, CRRT, citrate, CPFA, adsorption

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Introduzione

La sepsi è una disfunzione d’organo pericolosa per la vita causata da una risposta dell’ospite abnorme e deregolata all’infezione, associata alla comparsa di manifestazioni sistemiche del processo infettivo.

La massiva risposta dell’ospite al quadro settico può evolvere verso un quadro di shock settico, definito come la comparsa di disfunzione d’organo o di segni di ipoperfusione tissutali secondari all’infezione, con ipotensione non responsiva all’espansione volemica che richiede l’utilizzo di terapia con vasopressori al fine di incrementare la pressione arteriosa media (MAP) ≥65 mmHg [1]. 

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Bilirubin removal with Coupled Plasma Filtration and Adsorption in patients affected by hilar cholangiocarcinoma

Abstract

Background: Patients affected by hilar cholangiocarcinoma are eligible for surgery only in the 20-30% of the cases and postoperative mortality is 40-50%. Many specialists are involved in the treatment of this disease, like surgeons, gastroenterologists, oncologists and radiotherapists. Recent studies have shown that preoperative bilirubinaemia is a predictor of morbidity and mortality after surgery.
Coupled Plasma Filtration and Adsorption (CPFA) is a blood purification extracorporeal therapy recommended for sepsis and able to reduce bilirubinaemia.
Methods: We treated 10 patients referred to our centre affected by hilar cholangiocarcinoma complicated by obstructive jaundice with 34 CPFA sessions to test its ability to reduce preoperative bilirubin levels and we checked for mortality at 90 days.
Results: CPFA reduced preoperative bilirubin of 30% for session; it also improved others inflammation and coagulation tests. Mortality at 90 days was 40%.
Conclusion: CPFA is an effective therapy for hyperbilirubinaemia. Lowering preoperative bilirubinaemia and improvement of coagulation tests subsidized the management of the patients but in our study did not affect postoperative mortality. Further studies to evaluate the indications for treatments that remove bilirubin in this setting are needed.

KEYWORDS: bilirubinaemia, cholangiocarcinoma, Coupled Plasma Filtration and Adsorption, CPFA

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INTRODUZIONE

La bilirubina è responsabile di tossicità acuta per valori molto elevati, ma anche di tossicità cronica per valori moderati se persistenti. Oltre i 15-20 mg/dl la bilirubina crea danno alle cellule alterando il sistema mitocondriale e la produzione di energia. Il danno neurologico è il più noto, ma anche altri organi ed apparati sono coinvolti (1).

Relativamente al sistema nervoso centrale (SNC) valori elevati di bilirubina nel neonato causano ittero nucleare con danno motorio severo, ipotonia o spasticità e sordità. Anche l’esposizione persistente a livelli moderati di bilirubina può causare danno allo sviluppo del SNC con manifestazioni neurologiche minori che sono identificate dalla “syndrome of bilirubin-induced neurologic dysfunction (BIND)” (2, 3).

La bilirubina esercita i suoi effetti tossici sul sistema nervoso con meccanismi di danno noti (4), ai quali se ne sono aggiunti altri recentemente scoperti come il blocco dell’ubiquitina nelle cellule dell’ippocampo con inibizione del proteasoma e danno cellulare (5). 

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