This month’s question concerns fluid administration in patients with septic shock. Are the surviving sepsis guidelines suggestion of an initial “rapid bolus of 30ml/kg crystalloid” in those patients with hypotension and lactate>4mmol/L more harmful than useful?
A – I always think the proposal to limit fluid resus is pragmatically difficult, but it may well be a valid improvement in care.
A ‘rapid’ bolus could well be harmful, as quickly filling the central compartment leads to an increase in Pc and Jv, causing more tissue oedema, and increasing the need for further fluid. Maybe the medics have got it right all along with their 8 hourly bags of fluid?
In terms of optimal treatment, the NHS is not adequately staffed to provide ED/ crit care discussion and review at a senior level for all the hypotensive ‘septic’ patients who come through the door. We certainly do not have the staff and bed resource to provide timely review and vasopressor therapy to all these patients, as may happen in a trial setting. I think a large cohort of patients avoid crit care admission with probably a bit too much fluid and a slightly inadequate blood pressure. What that does to their length of stay, nephron numbers and mortality is uncertain.
Does small volume tissue oedema cause harm? I think it does in post operative patients where the majority of oedema is focused around the injured area, for example the anastomosis, and increased oedema increases oxygen diffusion distance. I wonder who the surgeons blame when an anastomosis breaks down- the equipment, the epidural, the patient, (themselves??), or do they look at the fluid prescription? However, in patients with sepsis, I think the harm is smaller, and to some extent acceptable.
C – I think sensible fluid administration in the initial presentation of sepsis is probably ok. However there are lots of reasons why ongoing high volume IV fluids in this patient group are a bad thing. What I find a bit of an issue in the initial fluid resuscitation is that fluids are generally prescribed in litres with probably little regard for the patient’s weight. There is usually also little consideration of the other sources of fluid that are administered to the patient e.g. antibiotics. What is probably being given to the majority of patients is actually well over 30ml/kg. This may be something worthwhile auditing in order to direct people towards more tailored fluid therapy.
I agree that the current critical care capacity in the UK won’t be able to support an increase in numbers of patients having early vasopressor support in sepsis, however this may be something that could be solved by the current discussion of the level 1.5 patient. There are programs at the moment trialling nurse-led ward-based care in postoperative patients (e.g. York) so there is no reason why it couldn’t be extrapolated to this patient group as well.
D – The prevalence of responsiveness to initial fluid challenge among hypotensive sepsis patients is unclear. To avoid fluid overload, and unnecessary treatment, it is important to differentiate these phenotypes
Most evidence against the efficacy of fluids for sepsis patients addresses harms from long-term positive fluid balance , an outcome probably distinct from rapid initial fluid resuscitation. Evidence suggests the latter is protective.
There is a lack of any randomized investigations for either intervention in defined sepsis populations. In fact patients in the three recent goal-directed therapy trials received comparable initial fluid volumes in similar times.What is still needed is to refine and validate the baseline predictors of the initially fluid refractory phenotype until then we have to guess for each patient
Not helped by the fact that in the current framework defining sepsis as “dysregulated host response to infection,” any broad modulation of this system could logically predispose or exacerbate a state of dysregulation. Endothelial activation and damage are pivotally implicated in sepsis, which could explain connection between coagulopathy and initial blood pressure responsiveness.
The size of the bolus and the duration for resuscitation is to tailor made for each patient as it is both beneficial and potentially harmful
E – Do any of you FICE competent folks ever scan the IVC in A&E etc…? Is it a tool used routinely as part of your assessment pre and post fluid bolus if you have the skills?
F – I write this in simplistic words as it makes sense in my head…
I feel that I would open myself up to criticism if sepsis was suspected and I did not resuscitate with fluid.
G – I do feel that that the rapid 30ml/kg advice is potentially harmful (looking at up to 3L in a significant proportion of our population given the 70kg man and 60kg woman were left back in 1981) if only because it perpetuates the notion that sepsis is primarily a hypovolaemic rather than a vasoplegic state. Obviously this is a spectrum when you consider those who have significantly reduced PO intake and losses (pyrexia, D&V etc.) associated with an infection.Kumar makes a valid point about separating this from persistent and aggressive fluid resuscitation where there does seem to be accumulating evidence that it is associated with worse outcomes (obviously the more extreme examples of this are the FEAST trial NEJM 2011 and more recently SSSP2 in JAMA end of last year).
I do worry that we focus on arterial pressure and extrapolate that to stroke volume and cardiac output when fluid resuscitating (a jump in itself), completely ignoring the venous portion of the system and the inevitable venous hypertension and reduction in organ perfusion (particularly of capsular organs) even though the systolic BP reads higher. However I’m not entirely sure how to combat this except by advising aliquots of fluid depending on size and co-morbidities and frequent assessment with a view to stopping the administration of fluid boluses when this response is blunted or absent, although this later part is a contentious issue in itself…….
Regarding the IVC collapsability/distensibility I do remain to be convinced of it’s use outside of extremes in much the same way we use CVP to be honest!
A – Agree with G on IVC assessment.
I don’t think anybody could be criticised for resuscitating with any particular volume as long as their approach is rational and based on repeated assessment of response.
I do think the bigger problem for us on the unit is the perception that repeated boluses of fluid are entirely benign and the repeated dosing whenever the urine output drops below some arbitrary threshold is without harm.
I had optimism about the use of sequential measurements of the velocity time integral (VTI) across the left ventricle outflow tract (LVOT) on trans thoracic echo. When I tried to do this, it became apparent in my eyes, this would not be a realistic technique for regular practice.
Then I got interested by Marik paper (see below) My interest shifted to the carotids. Dynamic assessment of the carotid flow/ velocity/ flow time to a straight leg rise is interesting and makes sense to me. (I accept the evidence base is sparse)
I had a go at measuring carotid blood flow but I found that unlike the LVOT area which is fixed, the carotids require 2 diameter measurements. This adds hassle, and potential error in the diameter measurement and can give misleading results. There can also be faff with getting the doppler insonation angle correct.
Now I have become more interested in carotid corrected flow time for fluid responsiveness, mainly because it is really quick and easy. (I accept the evidence base is sparse) It is quite interesting to put the USS doppler over the carotids, just before your central line, then I ask the nurse to do a straight leg raise, and look at the dynamic change in carotid flow time.
I do think this is an interesting method at helping guide fluid but as you say unproven. I know that other POCUS (point of care ultrasound) advocates are looking at this from a different angle, using US to determine when a patient has had too much fluid searching for sonographic evidence of increased extravascular lung water and changes in portal vein flow. I wonder if a combination of these will be protocolised and trialled in the near future.
Interestingly I met Prof Andrew Rhodes (talking through Surviving Sepsis Guidelines 2016/17) at critical care reviews and asked him why despite the general reduction in how aggressively SSG suggest we resuscitate people (from Rivers supraphysiology circa 2004) the initial fluid bolus has increased from 20ml/kg to 30ml/kg and he seemed to suggest that this was in view of the initial resuscitation volume that patients tended to get in the relatively recent RCTs e.g ARISE, PROMISE (prior to randomisation) rather than any specific evidence to show a larger volume was better. Make of that what you will…………………………
The current trials remain confusing as it is such a heterogeneous patient group. I remain convinced however that both under resuscitation (too little too slow) and over resuscitation are harmful (too much OR too fast through different mechanisms including endothelial sheer and accelerated value also damage). Do you central problem as we have not yet defined of the goal of resuscitations is to target the central circulation and major organs, or the wider microvasculature, with the risk of increased tissue oedema. The aims of resuscitations of the two strike me as fundamentally incompatible.
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