Jack Tinker

Jack Tinker's influence upon the evolution of intensive care in the
UK and Europe was large, and his work highly acclaimed, but how will
history judge it? Might it prove to be a supreme example of the power of
one individual to put medical care back decades?

It was, in retrospect, very appropriate that it was on April Fool's
day in 1989 (1) that a group of leading "intensivists" were gathered in
Bermuda to address the adequacy of tissue oxygenation in shock and
critical illness. These leaders, which did not include Tinker but did
include one from Manchester where he had worked as a cardiothoracic
surgeon, came from the UK, Brussels, Holland, Germany and the US. The
consensus was that our aim should be to improve or optimize the adequacy
of tissue oxygenation. Tinker did just that by using the latest
ventilators and RBC transfusions to improve arterial oxygenation and the
oxygen carrying capacity of blood, and pulmonary artery catheters as an
aid to optimizing intravenous infusions of fluids and blood and intotropes
to increase cardiac output.

We now know that a lack of oxygen aids cell survival in the face of
cellular stress by inducing, either directly or indirectly, the expression
of the hypoxia inducible factor(2). This can partly explain why RBC
transfusions and even recombinant erythropoietin can have adverse effects
upon outcomes. We also know that oxygen can be harmful especially during
reperfusion seemingly because it promotes the release of toxic free
radicals. What is more we have known for a long time that beta agonists
increase oxygen utilization by promoting the metabolism of fatty acids and
that beta blockers inhibit it and the associated generation of ATP by
oxidative phosphorylation.

The inference is that we should have been doing exactly the opposite,
exploiting permissive hypoxaemia, avoiding RBC transfusions, and improving
the efficiency of ATP resynthesis, which in theory appears to reduce
myocardial work load by reducing the need for global oxygen delivery, by
promoting the metabolism of fatty acids and avoiding beta blockers. Indeed
it was the Canadian Russell, I believe, who showed that in dying patients
supply-dependent oxygen consumption, as determined by the development of a
gastric intramucosal acidosis, did not occur until global oxygen delivery
had fallen to extremely low levels equivalent to those seen on climbing
Everest without supplementary oxygen. In which case current therapeutic
meme complexes in the acutely ill are completely and utterly false, in the
absence of hypovolaemia or airway obstruction.

These false meme complexes need to be erradicated before new ones
can evolve to replace them for they contaminate management protocols
selected for study. That will be a daunting task for these false meme
complexes are so deeply imbedded in our pathophysiological thinking and
therapeutic interventions. Compare, for example, the prospective
randomized studies that have examined the possibility that using the
gastric intramucosal pH as the primary end-point in management might
improve outcome. The first study, conducted in Argentina with US
oversight, showed improved outcome (3). When reproduced other countries no
such difference was found (4) but in trauma patients (5) might well have
shown a difference had the group of patients studied been larger.

The difference between these studies is that the one conducted in
Argentina was done in a time of financial austerity and clinicans there
used and reused pulmonary artery catheters very sparingly. The same
applied to dobutamine. More importantly the clinicans had little or no
familiarity in using pulmonary artery catheters and dobutamine in managing
their patients. The net effect is that whilst few of the patients in
Argentina received the supposed benefits of these advances in care all
patients in the other two studies did. The inference is that the routine
use of the pulmonary artery catheters and dobutamine may have an adverse
effect upon some supportive evidence.

One of the biggest change in patients I have observed since the vogue
of optimizing oxygen delivery with fluids, RBCs and inotropes is the
frequency with which one sees grossly oedematous patients, unequivocal
evidence of fluid overload. Pari passu has been the evolution the intra-
abdominal compartment syndrome. The inference is that practices espoused
by the intensive care gurus, such as Jack Tinkler, may have lead to fluid
overload, increased metabolic work and poorer outcomes. If so might there
have been some contributary practices such as being involved in the
management of patients having open heart surgery in whom the goal of
optimizing myocardial tissue energetics and function has eclipsed the goal
of optimizing the adequacy of tissue oxygenation, to energy metabolism, in
all organs. That inadequacies of tissue oxygenation in peripheral tissues
can have an adverse effect upon cardiac and indeed hepatic tissue
energetics and functioning is a compounding factor.

What of Jack Tinker's associations with those companies marketing the
ventilators, pulmonary artery catheters and pharmaceuticals he used? Might
they have influenced his practices and indirectly all those professionals
with whom he came in contact? What of him having trained first as a
cardiothoracic surgeon and then as a cardiologist? Might this have made
him focus to much upon the heart and tend to ignore peripheral tissues?
More importantly how should one go about repairing the damage if one
acknowledges that serious damage has been done? Surely that will take more
than one influencial person such as Jack Tinker. There would seem to be
much to learn about clincial behaviour from Jack Tinker's career.

1. Haglund, RG Fiddian-Green. Assessment of adequate tissue
oxygenation in shock and critical illness: oxygen transport in sepsis,
Bermuda, April 1+ 2, 1989 - Intensive Care Medicine, 1989.

2. Jo Anne Powell-Coffman & Clark R. Coffman. Apoptosis: Lack of
oxygen aids cell survival. Nature,
465:554-555 (3 June 2010) | doi:10.1038/465554a

3. GG Gutierrez, F Palizas, G Doglio, J Pusajo, N et al. Gastric
intramucosal pH as a therapeutic index of tissue oxygenation in critically
ill patients
The Lancet, Volume 339, Issue 8787, Pages 195-199.

4. Gomersall, Charles D, EDIC; Joynt, Gavin M; Freebairn, Ross C;
Hung, Veronica; Buckley, Thomas A; Oh, Teik E. Resuscitation of critically
ill patients based on the results of gastric tonometry: A prospective,
randomized, controlled trial. Critical Care Medicine. March 2000 - Volume
28 - Issue 3 - pp 607-614.

5. Ivatury, Rao R. MD, FACS; Simon, Ronald J. MD, FACS; Havriliak,
Damien MD; Garcia, Carlos MD; Greenbarg, James MD; Stahl, William M. MD,
FACS. Gastric Mucosal pH and Oxygen Delivery and Oxygen Consumption
Indices in the Assessment of Adequacy of Resuscitation after Trauma: A
Prospective, Randomized Study. The Journal of Trauma: Injury, Infection,
and Critical Care: July 1995 - Volume 39 - Issue 1 - pp 128-136

Competing interests:
Tonometric patents issued in my name