Thanks to Connie for presenting a case of a young man with chronic bloody diarrhea, abdominal pain, and fever, found to have a new diagnosis of severe Ulcerative Colitis.
- Acute diarrhea requires work up in anyone >65, immunocompromised, blood in stools, fever, severe abdominal pain, recent antibiotics, known or suspected IBD, risky jobs like food handler, or recent travel.
- Fecal calprotectin can help distinguish inflammatory from non-inflammatory diarrhea and is a more sensitive and specific marker than fecal leukocytes.
- 5-ASA based drugs are generally more effective in the colon so their primary role is in the treatment of Ulcerative Colitis or Crohn’s Colitis.
Disease severity in IBD:
- Mild: <4 stools/day, no systemic toxicity
- Moderate: 4-6 stools/day, no systemic toxicity
- Severe: >6 stools per day, systemic toxicity
- Fulminant: >10 BMs per day, continuous bleed, systemic toxicity
Key distinctions between UC and CD:
Items in red in the table above correlate with disease activity.
Before initiating immunosuppression:
- Check PPD/quantiferon
- Hepatitis serologies
- Administer routine live vaccines
- Check TPMT level (to assess phenotype for bone marrow suppression secondary to 6MP). If TPMT level low, do not give 6MP!
Emily presented a patient with disseminated TB and Pott’s disease presenting with worsening rash, hepatitis, and fever, ultimately diagnosed with DRESS secondary to her TB medications!
Thanks to Naina for presenting an interesting case of a young woman presenting with fever, nausea/vomiting, and R flank pain found to have pyelonephritis and lupus nephritis!
- Renal involvement is noted in ~50% of patients with SLE and can present as nephrotic or nephritic syndromes.
- The most common and severe form is diffuse proliferative lupus nephritis (class IV)
- It is important to distinguish SLE flare from an infection. When infection is present, it must be treated first before starting immunosuppression.
- SLE flare is associated with a normal WBC, low CRP (because CRP production by hepatocytes is down-regulated by type 1 IFN release in lupus flare), and absence of fever
- Lab findings suggestive of flare include elevated anti-dsDNA (correlates with disease activity), low complement levels (predominantly C3 decline), worsening proteinuria, and elevated creatinine.
* Membranoproliferative GN can present with mixed nephrotic/nephritic picture.
SLE and renal disease:
Carriann presented the case of a young woman with HIV (CD4 250 off ARVs) and prior syphilis s/p treatment five years ago who presented with constitutional symptoms and diffuse rash involving the palms and soles, found to have RPR 1:256 consistent with secondary syphilis!
- Lues maligna or malignant syphilis is a rare manifestation of secondary syphilis in immunocompromised individuals and presents as an ulceronodular rash.
- Syphilitic hepatitis is seen in ~10% of patients with secondary syphilis and presents as predominantly elevated alkaline phosphatase with normal or mildly elevated transaminases.
- Neurosyphilis can occur at any point after infection with syphilis!
- Treatment success is defined as a four-fold drop in nontreponemal titers (ie RPR).
Keep in mind the following principles:
- Treponemal tests remain positive long-term
- Non-treponemal tests can become negative after treatment. They are useful for treatment monitoring because they can be quantitative
- Both tests can be falsely negative early in disease course so repeat tests if clinical suspicion remains
- Screening algorithm
- Jarisch-Herxheimer reaction is a self-limited condition that can occur in ~10-35% of patients within 24 hours of treatment with antibiotics.
- A four-fold decline in titers (2 dilutions) is considered treatment success.
- Monitor titers q 6-12 months post treatment. Increasing titer is concerning for treatment failure, neurosyphilis, or reinfection!
Today Eric presented an interesting case of a young Filipino man with no medical history, presenting with chronic intermittent proximal > distal muscle weakness affecting mainly his lower extremities, with associated tremors, weight loss, sweats. He was found to be profoundly hypokalemic on presentation.
Thank you Naina for presenting the case of an elderly man with 20 packyear smoking history presenting with acute onset of dyspnea and scant hemoptysis, found to have new onset A fib and L heart failure secondary to severe mitral regurgitation resulting from papillary muscle rupture!
- In patients with severe mitral regurgitation (MR) and a normal L atrium size, think about acute causes of MR. TEE is often indicated to better visualize the valve structure and determine need for operative intervention.
- MR can be caused by papillary muscle rupture, especially 3-7 days post MI. Other etiologies of rupture include endocarditis and myxomatous valve degeneration.
- Patients with rupture present with acute onset hypotension, pulmonary edema, and a hyperactive precordium. A systolic murmur is not always present!
- Aggressive afterload reduction AND
- Surgery (high mortality rate 20-25%)
- Paroxysmal (terminates within 7 days)
- Persistent (>7 days)
- Long-standing persistent (>1 year)
Differential for new onset A fib: (PIRATES!)
- Pulmonary (OSA, PE, COPD, PNA)
- Rheumatic heart disease/mitral regurgitation
- Alcohol/anemia (high output failure
- Thyrotoxicosis/toxins (stimulants)
- Sepsis/sick sinus syndrome
- Other: HTN*, congenital heart disease, previous cardiac surgery, viral infections
* Most common causes in the US.
- Rate control (preferred method based on AFFIRM and RACE trials)
- Beta blockers
- Calcium channel blockers ⇒ contraindicated in decompensated heart failure
- Digoxin ⇒ avoid use in renal failure, hypokalemia, hypomagnesemia, or hypercalcemia
- Rhythm control
- Chemical (~30% success rate)
- Class III (amiodarone, sotalol, ibutilide)
- Electrical (synchronized to QRS, ~80% success rate)
- Preferred modality in
- Hemodynamically unstable
- Young patient (age <65) or good functional status
- Early in natural history of disease
- Failure of rate control agents
- Heart failure
Complications post MI:
Figure from article by Reed et al. Lancet. 2017.
Papillary muscle rupture:
- Posteromedial muscle is 6-12x more likely because blood supply is through PDA only. Anterolateral muscle receives dual supply from LAD and LCx.
- Clinical presentation
- Acute onset hypotension, pulmonary edema
- Hyperactive precordium
- Mid, late, or holosystolic murmur with widespread radiation (though many have no murmur!)
- Diagnosis requires TTE/TEE
- Aggressive afterload reduction
- Urgent/emergent surgical intervention (20-25% mortality)