Reactive arthritis and post-infectious inflammatory syndromes: SAQ

This child has the textbook presentation of the classic reactive arthritis, and the task is to outline the diagnosis and the differential, then to discuss the stepwise management with the sepsis exclusion as the first priority. [4][9]

Question 1 (10 marks)

Outline the diagnosis of the reactive arthritis, the mechanism, and the differential from the septic arthritis, the post-streptococcal reactive arthritis and the acute rheumatic fever. [4]

A full-mark answer covers the definition with the latency, the trigger organisms, the HLA-B27 association, the mechanism of the molecular mimicry, and the four-way differential with the discriminating features. [4][5]

The definition and the latency (2 marks). Reactive arthritis is the sterile inflammatory arthritis that erupts one to four weeks after a distant gastrointestinal or genitourinary infection, in a joint that contains no cultivable organism. The latency is the single most discriminating feature, and the one-to-four-week window separates it from the septic arthritis, which has no latency, and from the post-streptococcal reactive arthritis, which has the latency under ten days. This child has the three-week latency after the diarrhoea, which anchors the diagnosis. [4]

The trigger organisms and the HLA-B27 (2 marks). The classic triggers are the enteric bacteria Salmonella, Shigella, Campylobacter and Yersinia, and the genitourinary Chlamydia trachomatis. The HLA-B27 allele is present in roughly half to three-quarters of the patients, and it is a susceptibility marker that modifies the severity and the risk of the chronicity, the sacroiliitis and the uveitis, but it is not diagnostic on its own because it is present in a substantial fraction of the healthy population. This child has the positive HLA-B27 and the enthesitis at the Achilles tendon, which are the spondyloarthritis hallmarks. [5][4]

The mechanism (2 marks). The central mechanism is the molecular mimicry. The HLA-B27 molecule on the antigen-presenting cell picks up the bacterial peptide, and it presents it to the CD8-positive T cell. The activated T cell cross-reacts with the self-antigens in the synovium because the bacterial peptide and the self-peptide share a similar shape, and the interleukin-23 and interleukin-17 axis sustains the sterile synovitis. The joint remains sterile because the live organisms do not seed it, though the bacterial antigens persist in the synovial macrophages. [5]

The differential from the septic arthritis (1 mark). The febrile, unwell child with a single hot joint and a refusal to bear weight is the septic arthritis, which is excluded by the Kocher criteria, the blood cultures and the joint aspirate. This child is afebrile and well, and the aspirate is sterile, which excludes the septic arthritis. [9]

The differential from the post-streptococcal reactive arthritis and the acute rheumatic fever (3 marks). The post-streptococcal reactive arthritis follows the group A streptococcal pharyngitis with the latency under ten days, the additive and persistent pattern, the prominent enthesitis and the absent carditis, and it is distinguished from this child by the streptococcal trigger and the shorter latency. The acute rheumatic fever follows the streptococcal pharyngitis with the latency of two to three weeks, the migratory polyarthritis, the dramatic response to the non-steroidal anti-inflammatory drugs, and the carditis as the hallmark, and the 2015 revised Jones criteria require the two major or the one major and two minor criteria with the evidence of the preceding streptococcal infection. This child has the enteric trigger and the enthesitis, and the streptococcal serology is normal, which excludes both the streptococcal syndromes. [3][1]

Question 2 (10 marks)

Discuss the stepwise management of this child, from the exclusion of the septic arthritis through the non-steroidal anti-inflammatory drugs to the escalation for the persistent disease, with the treatment of the trigger and the safety-net. [9]

A full-mark answer covers the sepsis exclusion, the non-steroidal anti-inflammatory drug doses, the intra-articular corticosteroid, the disease-modifying and the biologic escalation, the trigger treatment, and the safety-net for the uveitis and the chronicity. [9]

The exclusion of the septic arthritis (2 marks). The immediate priority is the exclusion of the septic arthritis, because a missed septic joint scars the cartilage within hours. The joint aspirate is sent for the cell count, the gram stain and the culture, the blood cultures are drawn, and the empiric intravenous antibiotics are commenced if the septic arthritis is suspected. This child has the sterile aspirate, which confirms the reactive arthritis and allows the stepwise management to proceed. [9]

The first-line non-steroidal anti-inflammatory drugs (3 marks). The first-line treatment is the non-steroidal anti-inflammatory drugs, given regularly rather than as needed. The naproxen is given at ten milligrams per kilogram per day in two divided doses, and the ibuprofen is given at thirty milligrams per kilogram per day in three divided doses. The full anti-inflammatory dose is continued for the duration of the active arthritis and is tapered as the symptoms resolve. The regular dosing controls the inflammation and the morning stiffness, and the child is reviewed at the two-to-four-week interval. [9][4]

The intra-articular corticosteroid (2 marks). The persistent monoarthritis or oligoarthritis that does not respond to the non-steroidal anti-inflammatory drugs is the indication for the intra-articular corticosteroid injection. The triamcinolone hexacetonide is the preferred agent because its insolubility gives it the longest intra-articular duration and the lowest systemic absorption, and it is injected under the aseptic technique, often under the sedation or the general anaesthetic in the young child. [9]

The escalation for the persistent disease (2 marks). The disease-modifying drugs are the third step for the persistent disease beyond the three to six months. The sulfasalazine is started at thirty to fifty milligrams per kilogram per day in divided doses and is the preferred agent for the spondyloarthritis pattern, and the methotrexate at ten to fifteen milligrams per square metre once weekly is reserved for the disease that does not respond to the sulfasalazine. The anti-tumour-necrosis-factor biologic, the adalimumab at twenty-four milligrams per square metre every two weeks or the etanercept at zero point eight milligrams per kilogram once weekly, is the fourth step for the refractory disease under the specialist supervision. The child on the biologic with the fever has the serious infection until proven otherwise. [9]

The trigger treatment and the safety-net (1 mark). The triggering infection is treated in parallel, though the antibiotics do not shorten the sterile arthritis once the trigger has been cleared. The safety-net is explicit: the family is told to return immediately for the fever, the visual change, the increasing pain or the spreading redness, and the slit-lamp surveillance is organised for the HLA-B27-positive child because the uveitis is silent until it scars the sight. [4][10]