Reactive arthritis and post-infectious inflammatory syndromes: Viva

Opening question

Examiner: A nine-year-old boy limps into your emergency department with a swollen right knee and a swollen left ankle. He had a bout of bloody diarrhoea on a camping trip three weeks ago. Walk me through how you frame this problem. [4]

Candidate: My first frame is the safety frame. The acute swollen joint in a child is septic arthritis until proven otherwise, so I assess the fever, the systemic wellness, the ability to bear weight and the Kocher criteria, and I aspirate any hot joint that raises the suspicion. Once the sepsis is excluded, the second frame is the post-infectious frame. The one-to-four-week latency after the gastrointestinal infection, the asymmetric lower-limb oligoarthritis, the enthesitis at the Achilles tendon and the dactylitis of the great toe point to the reactive arthritis on the spondyloarthritis spectrum. The three-week latency after the bloody diarrhoea is the anchor. [4][9]

Probe one — the septic arthritis

Examiner: How do you actually exclude the septic arthritis in this child? What does the joint aspirate show in each? [9]

Candidate: I apply the Kocher criteria for the septic hip, and for the knee I use the clinical picture and the aspirate. The septic joint yields the pus with the white cell count above fifty thousand per microlitre and the positive gram stain and culture, while the reactive arthritis yields the sterile fluid with the lower cell count and the negative culture. This child is afebrile and well, which lowers the probability, and the sterile aspirate with the lower cell count confirms the reactive arthritis and excludes the sepsis. I send the blood cultures and the inflammatory markers to complete the screen. [9]

Probe two — the streptococcal syndromes

Examiner: The mother asks whether this could be the rheumatic fever, because her niece had it last year. How do you reassure her, and what would change your mind? [3][1]

Candidate: I reassure her that the acute rheumatic fever follows the streptococcal pharyngitis, not the enteric diarrhoea, with the latency of two to three weeks, and the arthritis is migratory and moves from joint to joint, resolving dramatically with the non-steroidal anti-inflammatory drugs. The carditis is the hallmark, and I examine for the murmur and arrange the echocardiogram if the streptococcal serology is positive. The post-streptococcal reactive arthritis is the other streptococcal syndrome, and it is distinguished by the latency under ten days, the additive pattern, the prominent enthesitis and the absent carditis. This child has the enteric trigger, the enthesitis and the normal streptococcal serology, so the streptococcal syndromes are excluded, though I send the antistreptolysin-O and the anti-DNase B to be certain. [3][1]

Probe three — the mechanism

Examiner: Tell me about the mechanism. Why does the joint inflame when the gut is the site of the infection? [5]

Candidate: The central mechanism is the molecular mimicry. The HLA-B27 molecule on the antigen-presenting cell picks up the bacterial peptide from the Salmonella or the Campylobacter, 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 inflammation. The joint remains sterile because the live organisms do not seed it, though the bacterial antigens persist in the synovial macrophages and sustain the response. This is why the antibiotics treat the infection but do not shorten the arthritis. [5][4]

Probe four — the management

Examiner: So how do you treat him? Give me the doses. [9]

Candidate: The first-line is the non-steroidal anti-inflammatory drugs, given regularly. I use the naproxen at ten milligrams per kilogram per day in two divided doses, or the ibuprofen at thirty milligrams per kilogram per day in three divided doses, and I continue the full anti-inflammatory dose for the duration of the active arthritis. If the monoarthritis persists despite the two weeks of the non-steroidal anti-inflammatory drug, I inject the intra-articular triamcinolone hexacetonide, which is the preferred agent for its long duration and its low systemic absorption. For the persistent disease beyond the three to six months, I escalate to the sulfasalazine at thirty to fifty milligrams per kilogram per day, and then to the methotrexate or the anti-tumour-necrosis-factor biologic under the rheumatology. I also treat the trigger and arrange the stool culture to confirm the organism, though the antibiotics do not shorten the arthritis once the trigger has cleared. [9][4]

Probe five — the safety-net

Examiner: What do you tell the family before they go home? [4][10]

Candidate: I tell them the good news first, that the majority of the reactive arthritis resolves within the three to six months, and that the self-limiting course is the expected outcome. Then I give the safety-net. The child is HLA-B27 positive, so I organise the slit-lamp for the uveitis, because the uveitis is silent until it scars the sight, and I tell the family to return immediately for the red eye, the pain, the photophobia or the visual change. I also tell them to return for the fever, the increasing pain or the spreading redness, because the child on the non-steroidal anti-inflammatory drug may develop the gastrointestinal or the renal effects, and the rare progression to the chronic spondyloarthritis is monitored at the follow-up. I arrange the paediatric rheumatology referral for the ongoing care. [10][4]