Observe, record, tabulate, communicate…

Observe, record, tabulate, communicate.
© CEphoto, Uwe Aranas / , via Wikimedia Commons

When I was knee high to a grasshopper, I had a teacher that used to be incredibly irritating.  Instead of getting away with a lucky guess, or a grasp at a faded memory, we had to be able to ‘show our workings.’  This meant we had to understand where our answers came from, from first principles, and learning by rote wasn’t going to cut it.  At the time this was infuriating, and led to a whole load of extra work. However, now I realise that she had started me on a learning journey that continues on a daily basis.

This insistence on understanding the basis for an argument or fact has been a common feature amongst a number of my most inspiring tutors over the years since.

One particular tutor was Dr Alan Stevens. He was a pathologist at my medical school and was assigned to me in my first year as my tutor. Pathology made up quite a significant portion of the syllabus in our first years, and what a bore – hundreds of blobs of pink, blue, and occasionally fluorescent green or yellow. And all of these colours were swimming before my eyes in a lab that seemed a million miles from the wards where the ‘real’ work of a hospital was under way.

So when Dr Stevens took us out for a meal in the week before our yearly finals (another insistence that good wine and good company made for better performance than late nights cramming in an airless library – I still nearly believe this one) and he started to explain how pathology is the basis of knowledge of all disease, I was a little upset.  As with most medical students I was sure I knew best and knew what I wanted to learn so pathology remained one of those subjects that was somewhat neglected in my revision schedules.

However, once I hit the wards, I rued the day I forgot to ‘show my workings’.  As I encountered diseases I knew the names, and symptoms of, but had a sketchy understanding of the pathology or pathophysiology, I struggled from time to time with working out why a specific treatment might help, and how treatment decisions were being made.

A paper in this month’s PMJ may appear to be one of those that a casual reader would skip entirely owing to the title, or the description. A clinicopathological paper on fulminant amoebic colitis may not have immediate relevance to my work, but the paper is an example of how medical knowledge has expanded over the years;  a clinical question, borne out of experience is subjected to scientific examination and analysis, in an effort to move beyond the empirical approach to disease.

The paper looks at the clinical featues, pathological findings and outcomes of patients admitted to an 1800 bed tertiary care centre in Western India who underwent colectomy, and were diagnosed with amoebic colitis.  30 patients were included in the study, and the mortality rate was 57%.

Various features are explored – with some information flying in the face of traditional teaching.  For example, the the form of necrosis encountered in the study was not that traditionally associated with the disease – and could lead to a change in practice in the path lab – potentially allowing a more rapid diagnosis.(In the study the authors found basophilic dirty necrosis with neutrophil rich inflammatory exudate in the study population vs eosinophilic necrosis with little inflammation usually reported in textbooks)

The authors also pose some interesting questions in their conclusion regarding their observed increase in disease incidence – relating to many of the current woes in clinical medicine.

Overuse of medication is suggested as a contributing factor to the increased incidence of amoebic colitis. The authors postulate that indiscriminate use of antacid medications may be promoting the increased incidence of amoebic colitis by allowing ameobic cysts to survive transit through the stomach.  This mirrors some of the concerns about the (over)use of PPIs promoting c. diff infections in the UK.  In addition, lifestyle factors are suggested as contributory – a reduction in dietary fibre can increase colonic transit time, increasing opportunities for the amoebae to adhere to the bowel wall – and the organism itself may be changing in virulence.

So whilst I may not have learned a great deal that I will employ next time I am in clinic, this paper is a great example of the value of close observation over time of the population one serves, maintaining an enquiring mind about the pattern of disease encountered, and then subjecting such notions to scientific scrutiny – eliciting new knowledge, new questions for research, and returning this information to the clinical field to improve practice, and hopefully change outcomes for patients of the future. Osler would be proud.