Psoriatic Arthritis (PsA)

The cervical spine is the airway problem - Axial PsA involves the cervical spine more often than the peripheral joint picture suggests, and HLA-B27-negative axial patients have particularly frequent cervical disease. Check neck flexion, extension, and rotation and look for fixed flexion deformity before induction; if range is limited, pull cervical imaging or a prior anesthetic record and plan a video laryngoscope or flexible scope rather than finding out after induction.

Skin decides where lines and blocks go - Psoriatic plaques are the rule in this population, and skin trauma induces new lesions at the injured site (the Koebner phenomenon). Site lines, blocks, and adhesive through clear skin where you can, and avoid needling straight through an active plaque. Nail disease is common — if the plethysmograph is poor, move the probe to another digit or the ear rather than chasing a perfusion problem that is not there.

Dactylitis complicates access - Dactylitis (sausage digit) and DIP disease are characteristic. Swollen digits make hand and wrist cannulation and radial arterial siting harder, so look proximal early instead of working through swollen fingers.

Ask which biologic and when the last dose was - Most of these patients are on a TNF inhibitor, an IL-17 inhibitor (secukinumab, ixekizumab), an IL-23 inhibitor, or a JAK inhibitor such as tofacitinib, often combined with methotrexate or apremilast. Tofacitinib carries serious infection risk — CMV, EBV, BK virus, tuberculosis — plus anemia and leukopenia, and is not given alongside other potent immunosuppressants. The hold-and-restart decision belongs to the rheumatologist, and the National Psoriasis Foundation perioperative guideline in the reading list is the document to hand them.

Chronic NSAID burden - Continuous maximum-dose NSAIDs are first-line for the axial and enthesitis components, so many patients arrive with a heavy NSAID load. Check a creatinine, ask about peptic ulcer disease, and remember NSAIDs exacerbate existing reactive airway disease.

Do not undercall cardiac risk - PsA carries increased metabolic syndrome, obesity, diabetes mellitus, hyperlipidemia, and hypertension, plus increased ischemic cardiovascular disease and increased mortality from coronary disease compared with the general population. Get a baseline ECG and pin down functional capacity from the history rather than reading a 45-year-old as low risk.

Neuraxial in axial disease - Sacroiliitis and spondylitis are present in about 30%. PsA syndesmophytes are non-marginal, bulky, asymmetric, and skip vertebral levels, and the sacroiliitis is asymmetric and often unilateral — irregular anatomy rather than the uniform fusion of ankylosing spondylitis, so landmarks mislead in both directions. Review recent films, use ultrasound for midline and interspace, and have a paramedian approach ready.

The eye - Acute anterior uveitis occurs in this group, is treated with topical corticosteroids, and sometimes with systemic steroid-sparing agents. Ask whether the patient uses eye drops the morning of surgery, and protect the corneas deliberately.

Plan for the arthroplasty case - Joint replacement is a recurring indication in PsA. Approach it as inflammatory-arthritis anatomy: fixed deformity, restricted range, erosive and osteolytic periarticular bone, and a patient whose immunosuppression drives the infection conversation with the surgeon.

Emergence and analgesia - These patients arrive with established inflammatory pain on top of chronic NSAID and DMARD therapy. Build a multimodal plan, use regional where the skin allows it, and set the emergence position around the joints that will not extend.

Psoriatic arthritis (PsA) is a chronic inflammatory arthritis that develops in about 20% of patients with psoriasis, usually with onset in the 30s and 40s and equally in men and women. It is seronegative and belongs with the spondyloarthropathies. The dominant lesion is enthesitis — inflammation where tendon, ligament, and joint capsule insert into bone — rather than the synovitis of rheumatoid arthritis (RA). IL-23 stimulates resident T cells to make IL-17, IL-22, and TNF-alpha, which together drive inflammation, erosion, and new bone formation.

Patterns range from oligoarthritis and polyarthritis to distal interphalangeal disease, sacroiliitis and spondylitis (about 30%), and arthritis mutilans with osteolysis and digital telescoping. Despite DMARD therapy, roughly 47% show radiographic damage within the first two years of disease.