Patient 90/1951 was initially transferred from the Newcastle Royal Victoria Infirmary (RVI), having been treated for a lesion on the left os-calcis (heel bone). The pus taken from the lesion was tested and returned positive for tubercle bacilli, tuberculosis infection. The patient was admitted to Stannington in June 1951. Later, in July 1951, a cold abscess formed in the right cuboid. According to the patient’s medical notes both sinus lesions were healed by January 1952, following a course of dihydrostreptomycin which, as a result of the healing, was discontinued.
In March 1952, radiographic imaging revealed the patient had developed tuberculosis osteomyelitis.
Osteomyelitis is an infection of the bone marrow, whereby the bone undergoes inflammatory destruction to create lesions. These lesions, or sinuses, can allow pus formation and ultimately new bone begins to form in repair. Osteomyelitis is caused by non-specific bacterial infection and as such is not a specific indicator of tuberculosis. In cases of tuberculosis, osteomyelitis is likely to be caused by haematogenous spread, also known as miliary tuberculosis.
Patient 90/1951, shown below, developed tuberculosis osteomyelitis affecting the tibiae. The radiograph shows the left leg, both laterally (left) and anteroposteriorly (right). Extensive bone destruction can be seen, as well as swelling with some new bone growth to the proximal tibia. The patient notes indicate that the patient was admitted to the RVI for an operation to incise the abscesses on their left leg in August 1952.
This is but one example of osteomyelitis in connection with tuberculosis. Further examples are evident within the patient files and will be discussed as the project continues.
Henry Mulrea Johnston was born in County Down, Ireland in 1877 and studied medicine at Queen’s College, Belfast graduating in 1903. He went on to study and work at Trinity College, Dublin before moving to London in 1910 where he worked at St Bartholomew’s and Great Ormond Street Hospitals and became a fellow of The Royal College of Surgeons in 1911. In 1912 he was appointed Resident Medical Officer at The Royal Victoria Infirmary in Newcastle.
During WWI he joined the RAMC and was posted to a hospital in Sidcup where he concentrated his efforts on deformities of the face. Prior to joining the army he had been committed to research using the latest radiological techniques for diagnostic purposes, something that was evident in his research for many years. An image in an article from the British Dental Journal demonstrates some of the pioneering work that Johnston was involved in whilst at Sidcup and it is also possible that it is Johnston who is pictured on the right of the picture. http://www.nature.com/bdj/journal/v217/n6/full/sj.bdj.2014.820.html
Following the war he was also appointed Visiting Surgeon to Stannington Children’s Sanatorium, a role which he carried on until 1945. In his obituary from the British Medical Journal it is remarked that “In general surgery he loved to demonstrate bone tumours and cysts and to illustrate his cases with beautiful radiographs of his own taking.” Amongst the records of Stannington Sanatorium we have a selection of photographic copes of some of Mr Johnston’s x-rays reflecting some of his interests outside of the Sanatorium. The collection of images shows patients of varying ages with different skeletal deformities, most of which appear to be unrelated to tuberculosis.
Click on images to enlarge
Sources: ‘Henry M. Johnston, F.R.C.S’, British Medical Journal, Vol. 2, No. 4724, 21 Jul 1951, pp. 181-182
Abdominal tuberculosis was a common diagnosis amongst the patients of Stannington Sanatorium and the patient case notes and radiographs give some indication as to the progression and manifestation of this form of TB. As was seen in the post from 19 November detailing the different types of TB, abdominal tuberculosis was a common extra-pulmonary form of the disease in which patients had often contracted the bovine strain of tuberculosis (mycobacterium-bovis) through the ingestion of unpasteurised or contaminated milk. We will explore the problems that arose from contaminated milk in a later post.
Abdominal TB most commonly affects the intestinal tract, mesenteric lymph nodes, and peritoneum and presents with symptoms such as abdominal pain, diarrhoea, rectal bleeding, and weight loss. The diagnosis of suspected extra-pulmonary forms of TB can often be assisted by chest x-rays where either active or healed tuberculous lesions can be seen. However in the case of abdominal TB where the primary point of infection is often not through the lungs but through the digestive system there may not be any evidence of any associated pulmonary infection. (Lambrianides et al, p.888) We don’t see as many radiographs within the Stannington records relating to abdominal tuberculosis in comparison to other manifestations of the disease such as pulmonary or bones and joints but there are nevertheless some good examples throughout the collection.
Case Study 1
The above radiographs are some of the earliest examples of abdominal TB from amongst the Stannington collection. They both relate to patient 80/21, a 9-year old female admitted in 1939 who presented with “vague abdominal signs and pain and traces of albumin in urine,” and a report on an x-ray taken prior to admission states that “calcified glands visible in abdomen above sacrum.” The reports given on the above two x-rays in the patient’s medical notes are very brief, with the first, figure one, being taken on 20 April 1939 and the report simply stating “gland to right of spine.” The second, figure two, was taken on 12 October 1939 and the report stated “calcification better seen in abdominal glands.”
Case Study 2
Figure 3 relates to a patient who was originally admitted in June 1940 as patient 86/46 and discharged in May 1941 only to be re-admitted some years later in September 1947 as patient 118/1947. On his first admission he was 5 years old and it was reported that during the past year he had had several attacks of vomiting and abdominal pain but an initial examination found no resistance in the abdomen and no mass was felt. No glands were seen in the x-rays of his abdomen taken at this time. The above radiograph was taken in October of 1947 following his second admission and the radiographic images from this slightly later period tend to be much clearer and better defined than those from the early 1940s, such as in figures 1 & 2. When he was admitted the second time he presented with “listlessness, poor appetite, vague abdominal pain & night sweats” but during his stay no evidence of any active disease was actually found, with the above x-ray showing calcified abdominal glands, presumably as a result of his previous, now quiescent, case of abdominal TB from 7 years earlier. He was discharged less than three months later once his symptoms had settled down.
There is little evidence of surgical treatments being employed in Stannington to treat abdominal tuberculosis, particularly in the earlier files. This is corroborated by early literature on abdominal TB in children where rest and sunshine are cited as the main methods of treatment alongside the prevention of the putrefaction of bowel contents by reducing the intake of meat and eggs and the administration of charcoal and the occasional dose of mercurial aperient. (Sundell, 1926) Later studies however recommend the use of surgical treatments to deal with intestinal lesions in order to prevent healing by fibrosis which could lead to obstructions causing later problems. (Kapoor & Sharma, 1988) This healing process is evident in the radiographs of patient 118/1947 showing the calcified glands, with the possibility of problems occurring later on in life being something to consider with many of the Stannington patients.
Sources
KAPOOR, V.K. & SHARMA, L.K. (1988) Abdominal Tuberculosis, British Journal of Surgery, 75 (1), pp.2-3
LAMBRIANIDES, A.L., ACKROYD, N. & SHOREY, B.A. (1980) Abdominal Tuberculosis, British Journal of Surgery, 67 (12), pp.887-889
SUNDELL, C.E. (1926) Abdominal Tuberculosis in Children, Postgraduate Medical Journal, 2 (14), pp.24-26