Lupus is a high yield topic because there are many risks, but those risks are often hidden.

Renal:
About 1/3 of patients with SLE get renal disease. Lupus nephritis will present with proteinuria, hematuria and increased Cr. For just about any presentation a UA and BMP is reasonable in a lupus patient.

Clotting:
About 50% of people with lupus also have anti-phospholipid syndrome (APS): This makes them a huge risk for clots. DVT with leg pain. PE with chest pain. Dural venous sinus thrombosis with headache. All of these are treated with anti-coagulation. (The three antibodies you may see in their chart are anticardiolipin, anit-B-glycoprotien I and lupus anticoagulant (poorly named, because it is actually extremely pro-coagulant)).

Headaches:
The HA treatment algorithm for a patient with SLE is simple: if there is no meningismus, focal neurologic findings or fever—>treat it like a normal HA. This is based on extensive studies/meta-analysis of the risk of SLE/HA.  If there are any of those red flags, the work-up is extensive as you need to rule out CNS infection (LP), venous sinus thrombosis (CTV of the brain), stroke(MRI) and lupus cerebritis (LP and imaging).  If they are on immunosuppressants add a cryptococcal antigen to the LP tests.

STROKE: huge risk

Chest Pain:
The risk of MI is 52x higher in women with SLE who are 35 to 44 years old compared to the general population—OH SNAP (I have never written that before, but it seems appropriate here). In a study of 22-45 year old women with SLE who presented with CP, dyspnea or decrease exercise capacity—>82% had CAD (and 42% of the asymptomatic controls with SLE also had CAD). THESE ARE NOT LOW RISK CP PATIENTS.

PE—> Huge risk. 20-30x the risk of the average Joe or Jane. D-Dimer is still okay if the pre-test probability is low to start with, but if they are hypoxic with a big swollen leg, just get the CTPE.

Pericarditis, with or without a pericardial effusion: Here is the rub (totally intended), if the EKG has ST-elevation and they have CP, it is hard to chalk it up to pericarditis when the risk of CAD is so huge in SLE—>at least get serial troponins and ensure they get provocative testing soon. Pericardial effusions rarely cause tamponade in SLE. Pericarditis and the pericardial effusions are typically treated with NSAIDS and steroids to control the inflammation.

Pleuritis: can have a pleural effusion and you may be able to hear a pleural rub. Treat with NSAIDs and steroids.

Deep breath—we are almost done.

Pneumonia: high risk, especially if immunocompromised. If the patient takes cyclophosphamide or long term steroids you need to cover for pseudomonas and legionella—>4th gen cephalosporins and fluoroquinolone/macrolide.

Non-infectious heart vegetations can cause mitral valve insufficiency.  This would typically present as new onset dyspnea and possibly a new murmur.

High rate of anemia, which can cause dyspnea.

GI symptoms:
Oral lesions—treat with chlorhexidine and lidocaine.

Lupus enteritis is the most common cause of acute abdominal pain in SLE—>diffuse pain, n/v, +/- bloody diarrhea. CT is the best way to differentiate this from other conditions, and imaging typically shows bowel wall thickening and stranding of the mesenteric fat.  Treatment includes high dose methylprednisolone (1-2 mg/kg/day) and possible cyclophosphamide. Surgery is indicated if there is bowel necrosis, but this doesn’t happen a lot.


Here is the take home: THESE ARE HIGH RISK PATIENTS. It is okay to be careful with them and to take time to figure out what is causing their symptoms. This may be done with a careful history and exam, but most of the time it will take some lab work and possibly imaging to properly risk stratify them.