Director of MIU (Major Injuries Unit)

• Single-handedly answered MIU calls for advice or help at any time, day or night until Anne Sutcliffe took up her consultant post in December 1981
• He also read widely. He knew what patient’s needed for survival and as soon as he read about something (usually but not always in US Journals)
• often cobbling together pieces of available equipment using jubilee clips to achieve the desired result. (When we lacked a required piece of equipment, we used our imagination to create a substitute. Such innovative life-saving practice is sadly prevented in the modern NHS due to Health and Safety regulations)
• Ruscoe Clarke pioneered adequate fluid resuscitation after trauma. Colin took this further believing that if after fluid replacement, urine output was still poor, the renal circulation needed dilating. The rest of the world did this by using low dose dopamine, but all acknowledged that this treatment rarely, if ever, worked. Colin’s solution was to use sub toxic doses of sodium nitroprusside that universally dilated blood vessels. Then and now his approach to improving blood flow to tissues was unique.
• Tissue blood flow depends on adequate blood volume and hence the potential for adequate cardiac output, and also the pressure differential between the arterial and venous circulation. Colin’s solution was to reduce the pressure and resistance to flow in the venous circulation. Everywhere else, the solution was to increase arterial blood pressure using noradrenaline, a vasoconstrictor.
• By 1979, there was acceptance that if at the end of a spontaneous breath the intra- alveolar pressure was kept slightly above atmospheric pressure this would prevent alveolar collapse. For spontaneously breathing patients this was called CPAP (continuous positive airway pressure) and for ventilated patients PEEP (positive end expiratory pressure).
• In the UK there was no commercially available equipment so in 1979 Colin taught me how to put commonly available equipment together using the previously mentioned jubilee clips and a large plastic container with water to the required level of pressure. I do not know what was going on in the rest of the UK, but no-one in the West Midlands was making their own equipment.
• By 1979, we were using Manley ventilators that had been developed in Oxford and Cape-Wayne ventilators that were made in Warwick by Cape and had been designed by ‘Curly’ Wayne who was an anaesthetist working in Coventry.
• Another innovation was the orange plastic head bucket suggested by Colin and built by both of us (my contribution was to melt a hole with my lighter through which we could introduce the tubing carrying oxygen) when we had three infants admitted with smoke inhalation. We had only one head box and one oxygen tent and could not find any not in use across Birmingham. The orange bucket was our solution for the third infant and the concentration of oxygen could be increased according to flow of oxygen and also by lowering the handle with was covered with a layer of plastic sheet stuck to the top half of the bucket.
• Colin was an earlier adopter of the Trinkle regime advocated in the US for treating flail chest injuries without ventilation. 
• At the time, traditional treatment was ventilation for three weeks to ‘splint’ the flail and to prevent ‘pendeluft’. Trinkle argued and Colin agreed that hypoxia after chest injury was due to pulmonary contusion and therefore treatment goals should be to reduce lung oedema and promote lung healing and that only in extreme cases was ventilation necessary.
• The regime required crystalloid fluid restriction, maintenance of plasma albumen and adequate pain relief using a thoracic epidural and plenty of physiotherapy to encourage coughing.

• 1980s intensivists began to recognise that an inflammatory response caused by tissue injury or sepsis led to multiple organ failure, later called multiple organ dysfunction syndrome (MODS). 
• At the time, acute respiratory dysfunction syndrome (ARDS) was a major killer and ECMO was not available. In the mid-1980s Colin suggested that we try another US technique to treat ARDS. It was called high PEEP and IMV (intermittent mandatory ventilation). 
• By then ventilators had been developed so that rather than weaning patients by intermittently taking them off the ventilator for increasing periods of time, IMV became available on more advanced ventilators and allowed us to gradually reduce the support the ventilator provided and to combine this with intermittent breaths from the patient while still maintaining CPAP and PEEP depending on the type of breath involved. At the time, excessively high PEEP levels were possible on these ventilators. 
• This technique was only used for patients with ARDS that was so severe that without extreme measures their survival was unlikely. It was scary and required extensive discussion with family members because it was risky.  
• At the start, the patient’s ventilatory rate was reduced to 4 and if they survived this, the level of PEEP (normally set at between 5 and 10) was slowly increased to upwards of 30cm of mercury to expand stiff and rigid alveoli. 
• The improvements in blood oxygen levels were dramatic as the PEEP level got higher and higher. The risk was always that as the PEEP increased, we might cause a pneumothorax but thankfully that never happened. 
• The results were dramatic, and we never lost a patient although once in a while we came close. As pressure induced lung injury was recognised, most newer ventilators limited the amount of PEEP that could be used so our ability to treat ARDS this way was relatively short lived.

• Our ability to treat ARDS, did not ensure the survival of our patients because renal failure became the killer. The problem was that haemodialysis used for patients with chronic renal failure was unsuitable for unstable critically ill patients because they could not tolerate the rapid fluid shifts. Instead we used peritoneal dialysis which involved filling the abdomen with fluid through a catheter that would, if left for 2 hours, draw out toxins. The problem was that the fluid distended the abdomen, splinted the diaphragm, and meant the patient could not breathe adequately for himself and even ventilation was difficult. 
• As a consequence, by the time MIU was decanted to Ward A, Colin and I were having serious discussions about whether it was ethical to prolong a patient’s life using peritoneal dialysis given than in our collective experience not a single patient had survived after the onset of renal failure despite peritoneal dialysis. 
• Then just before Christmas in that year an article appeared in the BMJ describing continuous arterio-venous haemofiltration (CAVH). This involved cannulating the femoral artery and femoral vein and relying on the patient’s blood pressure to drive blood through a filter which acted like an external kidney. 
• I remember with fondness that Christmas Day because Colin was in a playful mood because the filter was working well, and we had high hopes that at last we could treat renal failure in ITU.
• Although our success with CAVH was not as high as we hoped, we did have three survivors amongst the first 17 patients treated and even though they did not survive, renal function returned in four patients.