High-risk anaemic Jehovah's Witness patients should be managed in the intensive care unit.

Abstract

Severely anaemic Jehovah’s Witness (JW) patients who refuse blood transfusion on religious grounds have high mortality and morbidity1,2. Carson et al. have shown that the odds of death increase 2.5 times for every 10 g/L postoperative haemoglobin (Hb) decrease below 70 g/L3. The latest study4 demonstrated that an unadjusted nadir Hb concentration is a poor predictor of mortality of anaemic JW patients (Figure 1). Early risk factors including age ≥45 years of age, weight ≥90 kg, hypertension, cardiac arrhythmia, angina, previous myocardial infarction, valvular heart disease, heart failure, being on haemodialysis, acute admission and Hb ≤80 g/L on admission to hospital are associated with mortality of anaemic JW patients5. It was shown that an Auckland Anaemia Mortality Risk Score (Auckland AMRS), which is a composite score of the number of early risk factors each anaemic JW patient had, was associated with mortality. JW patients with Auckland AMRS of 0 to 3 had 4% mortality, Auckland AMRS 4 to 5, 32%, Auckland AMRS 6 to 7, 50% and Auckland AMRS ≥8, 83%5. During their hospital stay JW patients can develop anaemia-related (late) mortality risk factors including shock, acute gastro-intestinal bleeding, pneumonia, nadir Hb concentration ≤70 g/L, septicaemia, worsened congestive heart failure and neurologic complications4. Among these late risk factors, shock was the strongest predictor of mortality followed by acute gastro-intestinal bleeding and pneumonia. Figure 1 ROC curve: Nadir haemoglobin concentration as a predictor of Jehovah’s Witness patients mortality. When weights of individual statistically significant anaemia-related risk factors of mortality were combined and a composite mortality risk score, the Hamilton Anaemia Mortality Risk Score (Hamilton AMRS), was calculated, it was shown that JW patients with Hamilton AMRS of 0 to 2 had 4% mortality, Hamilton AMRS of 3 to 4, 29%, Hamilton AMRS of 5, 40%, and Hamilton AMRS of ≥6, 67%. On admission to hospital the trauma patient described by Lorentzen et al.6 had an Auckland AMRS of 3 (age, acute admission and Hb ≤80 g/L on admission to hospital) and a Hamilton AMRS of 6 (shock, ischaemic bowel perforation and the nadir Hb concentration ≤70 g/L) that estimated the patient’s mortality risk exceeding 70%. The patient underwent an open bowel resection and was managed in an intensive care unit (ICU) with physiologic parameters monitoring, ventilatory support, fluid resuscitation and an administration of vasopressors. The patient’s infective complications were treated with broad spectrum intravenous antibiotics, collection drainage, and wounds debridement and washout. Also the patient was treated with intravenous iron, B12 supplementation and subcutaneous administration of erythropoetin (EPO) in the dose of 10,000 units every second day. JW patients accept EPO, which is an erythropoiesis stimulating agent, as an alternative to blood transfusion. EPO is a 165 amino-acid glycoprotein, which is mainly produced by renal peritubular capillary endothelial cells in response to hypoxia7. As a haematopoietic cytokine, EPO promotes proliferation, differentiation and survival of erythroid progenitor cells8. In addition, EPO exerts a potent protective effect against hypoxia through its anti-apoptotic action9. After binding to its receptor on the cell surface, EPO initiates a JAK2 signalling cascade leading to NF-kB- and STAT5-dependent transcription of anti-apoptotic genes, including Bcl-xL, Bcl-210. Furthermore, EPO exerts a potent vascular protection and induces neoangiogenesis11–13.