10th July 2014  Transfusion complications in SAH

Presented By Dr Chiara Pieretti

Transplantation of red blood cells into our patients should be a decision we agonise over every time we do it. Clearly, there are times when packed red cells are life saving but even during massive haemorrhage we possibly need to give less, however we don’t have effective tools to work out transfusion requirements in emergencies.

For the vast majority of the time, giving stable patients someone else’s blood is fraught with complications barely mitigated by limited evidence of benefit.

The landmark Canadian study, TRICC, established the baseline transfusion trigger for critically ill patients at a haemoglobin of 7.0g/dl, reviewed here, and a good, broad perspective on the literature on LITFL. Since then lower transfusion thresholds have been employed in a wide range of critical (and non-critical) illnesses and we will discuss some of these in forthcoming journal clubs. The complications arising from transfusion are widespread and include infection and lung injury, although the evidence does not reach unanimity.

Guidelines on the management of critically ill patients tend to identify a restrictive transfusion strategy as being optimal. For example, The Australian National Blood Authority has recently produced guidance on the use of blood products in critically ill patients and their documents cover much of the up to date literature in this field. They summarise the evidence nicely, see examples in the figures below (click the arrows to scroll through figures and click the image for the original document).

Despite consensus settling on a restrictive transfusion strategy uncertainty remains about some subgroups, such as patients with ischemic heart disease, and acute brain syndromes. This uncertainty arises because many of the studies looking at transfusion thresholds have used a wide heterogeneous group of critically ill patients, and those which have tried to tease out the signal in neurocritical care patients have been inconclusive.

In the face of such uncertainty consensus guidance on the management of anaemia in SAH patients is difficult to establish. Those which have been published report that the landscape is unclear but that SAH patients probably benefit from Hb levels above 7g/dl however they express reservations about transfusion. For example, the 2011 Neurocritical Care Society’s guidelines recommend transfusing SAH patients to a Hb of 8-10 g/dl, advice supported by brain imaging studies.

The paper we will discuss this week has examined the association between transfusion and thromboembolic events in patients with acute, aneurysmal subarachnoid haemorrhage. As we have seen there are problems interpreting retrospective analyses of prospectively collected data but, even so, this study is interesting because of the well defined patient group and because embolic disease is probably not the first thing which comes in to our mind when managing this group.

Discussing transfusion in critically ill patients is very hard. The debate is perhaps disproportionally informed by a single trial which, arguably, represents practise in another era. That notwithstanding, no subsequent study has show an unequivocal benefit from higher Hb targets. Furthermore, there is perhaps a lack of clarity about the question being answered – many of the studies examine the relationship between anaemia and outcome or between transfusion and outcome but very few, and none in neurocritical care, have combined both of these questions in a robust prospective randomised trial. The issue is further clouded by the  current debate about the age of blood and, in the case of SAH, it is contaminated by the now redundant triple-H strategy which has such a profound effect on Hb.

The real, persistent, dilemma at the centre of this is that we may think that higher Hb levels are associated with better outcomes but that does not necessarily mean that transfusion is justified. Even so, assuming that we need higher haemoglobin concentrations in our SAH patients and that transfusion is the wrong way to achieve it, what else can we do? The first thing must be to do everything we can to eliminate iatrogenic anemia of critical illness – some ideas.