HAEMATOLOGY
patients with the virus, presenting on ICU, demonstrated a degree of anaemia (on average, 100g per litre). “The nature of this anaemia is that it appears to be normocytic and normochromic, but what we don’t know is whether it is COVID itself that causes the anaemia or whether patients with anaemia are more likely to be hospitalised with COVID. It may well be a bit of both,” Dr. Robinson commented.
He added that data from Singapore ICU admissions, did not reflect the same trend and patients did not appear to have been diagnosed with the same degree of anaemia. The median haemoglobin reported in the Singapore ICU population was 132g per litre. However, the data reported by Addenbrooke’s appears to be comparable to the levels of anaemia reported in Wuhan, China. The reasons for anaemia are likely to be multifactorial, according to Dr. Robinson. In serious cases, COVID-19 causes significant damage to the lungs. However, the virus – or the body’s response to it – can injure many other organs and scientists are investigating the scope and nature of that harm. “The lungs are the biggest site of disease and there is a well associated haemophagocytic reaction – a hyper- inflammatory state – and it is partly this that may be one of the reasons for anaemia developing,” he explained. “We also know there is a high risk of thrombogenicity… Kidney damage is also well reported – whether that is due to sepsis, poor perfusion in shock, or alternative reasons. The kidneys are key in regulating production of erythropoietin, so we are almost certainly going to see a degree of anaemia as a result. It is also possible that iron or folate will not be absorbed due to GI inflammation.” He highlighted a paper by Ganz (2019)
It is illogical to manage thrombosis secondary to inflammation with anticoagulation; better to manage upstream with antivirals and anti-inflammatory agents.
which states that responding to infection or injury by favouring host defence processes over housekeeping processes such as erythropoiesis is “a beneficial evolutionary strategy that provides a useful framework for understanding anaemia of inflammation. Hypoferremia and increased production and activation of leukocytes serve host defence at the expense of erythrocyte production and erythrocyte survival.”
“During times of stress, our bodies seem to want to conserve iron, but it certainly isn’t helpful during these kinds of diseased states,” Dr. Robinson commented. Ganz gives a detailed insight into the role of systemic inflammation in anaemia and the complex mechanisms involved, in the paper. But the question now arises, how should we treat anaemic patients with COVID-19 in the ICU?
Dr. Robinson pointed out that normal treatment strategies for anaemia of chronic disease (ACD) are most likely to be inappropriate. COVID-19 patients appear to have a significant thrombotic tendency, so erythropoietin (EPO) is not advised, while many patients are likely to present with hyperferritinaemia, so IV iron will not be an appropriate treatment in this cohort. He went on to point out that patients with specific disorders of haemoglobin are at higher risk for complications. Patients with sickle cell anaemia, for example, are at increased risk of hyposplenism, pulmonary
hypertension, chronic inflammatory state and haemolysis and high thrombotic risk. Patients with thalassaemia also have a higher risk of infection if on iron chelation. This raises some important questions around patient management in the wake of COVID-19.
A recent paper submitted to the British Journal of Haematology (Daniel, Y and Hunt B.J. et al, 2020) provides an insight into oxygen affinity in patients with COVID-19, which points to towards the appropriate strategy for managing anaemia. The authors state: “During critical care, at least until the late stage of the disease, severely ill COVID-19 patients may have relatively well-preserved lung compliance but remain severely hypoxaemic. A recent theoretical study suggested a direct interaction between COVID-19 viral proteins and haemoglobin (Hb) that could lead to a loss of oxygen carrying capacity. “As national guidelines strongly support a restrictive transfusion strategy in the critically ill, any right-shift in the Hb O2
affinity curve could contribute to the hypoxaemia and be potentially harmful. We have measured Hb O2
affinity curves
from severely ill COVID-19 patients and, in comparison to age- and sex-matched controls, find no evidence for a shift in O2
affinity that would support any change in clinical management.” Therefore, Dr. Robinson concluded that a restrictive transfusion strategy is “probably appropriate” in this cohort of patients. He summarised that normochromic, normocytic anaemia is a common finding in patients with a COVID-19 diagnosis. The pathology for anaemia will be variable, but hyperinflammation and anaemia of chronic disease is highly likely to be the underlying mechanism. Treatment is of the underlying disorder and reducing the hyperinflammation, which is best done in clinical trials, and current case series data suggest that transfusion is not appropriate unless required for another indication.
Thrombosis and COVID-19 Professor Beverley Hunt OBE, Professor of Thrombosis & Haemostasis at Kings Healthcare partners and a consultant at the St Thomas’ Thrombosis & Haemophilia centre, provided an insight into thrombosis and thromboprophylaxis in patients with COVID-19. Prof. Hunt explained that the
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