I am delighted to see a pro-con pair of manuscripts published side by side in Acta Anesthesiologica Scandinavica, and would congratulate the Journal Editors for agreeing to this style of presentation. Earlier criticisms of my work by Professor Hahn’s team did not afford me a right to reply. I also thank Imperial College London for agreeing to make Michel/ Woodcock/ Curry an Open Access document, as we do not currently have access to Grant or Pharmaceutical company funds pay the required fees.
Understanding and extending the Starling Principle is, I would suggest, a state of the art account of Starling forces for clinicians. It is not The Last Word on Starling forces, because many researchers around the world continue to unravel the mysteries.
In “The Extended Starling principle needs clinical validation” Robert Hahn lays out his concerns about the clinical corollaries of Starling physiology for fluid prescribers that I have been proposing since 2012. I will not address here each of his criticisms – it is proper that Fluid Physiologists read his account carefully. But I will offer a Reminder of what my son and I actually wrote:
In conclusion, fluid resuscitation studies require us to ‘re- appraise the basics’. The revised Starling equation and glycocalyx model paradigm appears to be an improvement on the original Starling principle paradigm. Colloids are widely prescribed for resuscitation from hypovolaemia, despite evidence-based protocols and guidelines. An important feature of the revised Starling equation and glycocalyx model paradigm is that it explains why albumin or plasma substitutes have no advantage over ISS when Pc or transendothelial pressure difference is low. The finding that pis has little effect on Jv focuses our attention on the subglycocalyx space. The EGL is a fragile structure and is disrupted by rapid i.v. infusion of fluids, acute hyperglycaemia, surgery, and sepsis. The glycocalyx model describes how psg, pis, and Jv balance one another, and raises concerns about disease processes or plasma substitute therapies that might disturb the protected low psg. In the absence of absorption by capillaries and venules, filtered fluid returns to the circulation mostly by lymphatics, and the importance of preserving lymphatic flow is highlighted. The new paradigm provides an explanation of context sensitivity of colloid and crystalloid volume kinetics in awake, anaesthetized, or hypotensive patients, and the rational prescriber will consider the desired effect on Pc and transendothelial pressure difference. Endothelial dysfunction associated with increased capillary porosity increases Jv at any Pc, and lowers the Pc at which Jv approaches zero. This J point can be taken into account when faced with a patient with systemic inflammation or sepsis. It is likely that the revised Starling equation and glycocalyx model paradigm will be modified and refined in the light of physiology and clinical trial evidence. In its current form, it strengthens the arguments for preferring ISSs over plasma or plasma substitutes for resuscitation, but accepts a rational use of colloids for euvolaemic or hypervolaemic haemodilution. The use of plasma or plasma substitutes to achieve a sustained supranormal plasma volume or to reduce tissue oedema is not rational.doi:10.1093/bja/aer515
I am entirely happy to stand by that as a reasoned contribution to the literature that existed at the time. If the last sentence offends the Hahn Team’s current efforts to promote albumin as a plasma expander and cure for peripheral oedema, let me remind him of the following statement in his own textbook:
Maintenance of normovolaemia by infusion of plasma volume expanders in critically ill patients is always associated with interstitial accumulation of fluid due to the increased TER, the reduced capacity of lymphatic recirculation in these patients and the fluid distribution to the extracellular space.Grand PO and Persson J. In; Clinical Fluid Therapy in the Perioperative Setting. Ed Hahn RG Cambridge University Press 2011 p124.
So who gets The Final Word? In the same edition of Acta Anes we find this intriguing laboratory experiment on human tissues. Commercial albumin increases endotoxin‐induced TNF‐α, IL‐6 and IL‐10 release from monocytes. The effect on arteries was to decrease the median maximum contraction and increase release of IL‐6 and IL‐8. Our friends at Grifols will not be pleased about that.