VA Ambulatory report 10.18.17: Chronic diarrhea

Case summary

Thanks to Michelle from presenting a really interesting case of a 26F with chronic diarrhea of unclear etiology despite an extensive evaluation

Top pearls

1. Divide patients with diarrhea into one of four categories: acute inflammatory, acute non-inflammatory, chronic inflammatory and chronic non-inflammatory. This makes a the long DDx of diarrhea easier to approach.

2. Attempting to classify chronic diarrhea as secretory or osmotic by history alone is unreliable.

3. See below for one approach to chronic non-inflammatory diarrhea

4. Factitious diarrhea accounts for up to 15% of chronic, non-inflammatory diarrhea that remains unexplained. Consider a laxative screen and stool osms in these patients.

An approach to diarrhea


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What makes diarrhea inflammatory?

  • Signs/Symptoms
    • Fever
    • Abdominal Pain
      • Pain alone is insufficient, but in the context of other features may add further support to an inflammatory cause
    • Hematochezia
  • Labs
    • Serum tests
      • Leukocytosis
      • Elevated inflammatory markers
    • Stool tests
      • Stool WBC
      • Fecal calprotectin
      • Fecal  Lactoferrin

Chronic non-inflammatory diarrhea

This category is often the hardest of diagnose and in many cases, will need the expertise of GI [and other consultants]

Here’s one approach:



“Factitious” diarrhea

  • Accounts for up to 15% of chronic, non-inflammatory diarrhea that remains unexplained
    • Most patients have a healthcare background
  • Factitious diarrhea develops in two clinical contexts
    • Laxative use
      • Surreptitious  or unintentional [e.g herbal tea with osmotic agent]
      • Dx
        • Laxative screen – stool, urine, blood
        • Stool Mg measurement may be information
    • Addition of fluid
      • Hyopotonic fluid —> serum Osm < 290
        • Consider measuring urine osms (as urine may be accidentally mixed in)
        • Consider measuring osms of colonoscopy sample
      • Hypertonic fluid —> Serum osm > 600

Moffitt Endocrine Pearls 10/18/17 – Thyroiditis

Thank you, Lily, for presenting a case of an older woman reporting several weeks of painful anterior neck and throat, signs of hyperthyroidism on exam, found to have subacute thyroiditis (antibodies still pending)!

Key Pearls:
1)  Thyroiditis refers to inflammation of the thyroid – there are many potential causes to this – see below for a full DDx.
2)  A painful thyroid can considerably narrow your differential – the 4 causes that are associated with spontaneous pain include non-Hashimoto autoimmune thyroiditis, suppurative thyroiditis, trauma-related, post-radiation thyroiditis.  Both Hashimoto and Graves are typically painless.
3)  The pathophysiology Graves thyrotoxicosis and Hashimoto thyroiditis originate with aberrant T-cell activity. One can really think of these disease as a spectrum rather than two distinct conditions given the overlap in pathophys and shared genetic predisposition.

Classification of Thyroiditis (adapted from – linked to a GREAT article by Slatosky, Shipton, and Wahba)



VA report 10.17: Approach to fungal disease and candidemia

Case summary

Thanks to Ashleigh and Katie for presenting a fascinating case of a 55M who p/w flank pain found to have pyelonephritis c/b persistent leukocytosis attributed to candidemia

Top pearls

1. Toxidromes account for the majority of pupillary changes [big and small]. In patients with a dilated pupil consider compression of CN III by [1] elevated ICP or [2] PCOM aneurysm. In patients with pinpoint pupils, consider the possibility of a brainstem stroke.

2. First line therapy for candidemia are the echinocandins [e.g caspofungin or micafungin]. Prompt removal of any indwelling lines reduces mortality.

3. 15% of patients with candidemia develop endophthalmitis mandating an dilated eye exam in all these patients.

Here’s one approach to fungi



Here’s an evernote about candidemia:

Morning Report – 10/17 – How Fahr do you go to work up AMS?

Thank you, Lily, for presenting the case of an older woman with dementia, Fahr disease, and diabetes presenting with AMS.

Key Pearls:

  1. Fahr disease is a rare neurodegenerative condition characterized by accumulation of calcium deposits in the basal ganglia that results in movement disorder and cognitive impairment. See below for more!
  2. The most common cause of hypercalcemia in the hospitalized patient is underlying malignancy.
  3. Remember the Cl:Ph ratio can help suggest if hypercalcemia is PTH dependent or independent. A ratio <35 suggests PTH independent, but AKI can make this a bit difficult to interpret – if fluids resolve your AKI, recheck the ratio!

What the heck is Fahr disease?

  • Fahr disease AKA idiopathic basal ganglia calcification (IBGC) AKA bilateral striopallidodentrate calcinosis
  • Rare neurodegenerative condition characterized by accumulation of calcium deposits in the basal ganglia.
  • Clinical signs and symptoms vary, but include parkinsonism, chorea, dystonia, cognitive impairment, and ataxia.
  • In addition to the idiopathic variant, there is an autosomal dominant inherited form, known as primary familial brain calcification (PFBC).
  • Interestingly, IBGC and PFBC are not associated with disorders of calcium or PTH metabolism.
  • If you want to learn more, here is a description of sporadic and familial cases in a registry of patients. The authors note that the amount of calcification seen on brain CT seems to correlate with the severity of symptoms.  Movement disorders were the most common manifestations of the disease, and among movement disorders, parkinsonism in particular.

Hypercalcemia Review – here’s an approach based on the PTH:


Moffitt Pearls 10.16.17 – JIA and RA

Thank you to Faren for presenting a mini-case of a young woman presenting with subacute oligoarticular arthritis found to have severe erosive arthritis of the R wrist, elevated CCP and RF factor, consistent with oligoarticular JIA vs. RA, given unclear timeline of symptom onset.

Key Pearls

  1. The ddx for Oligoarticular arthirits is broad. Major categories include infection, crystalline disease, and Rheumatic disease. Check out this previous post for more details.
  2. The ddx of oligoarticular JIA includes Lyme disease, psoriatic arthritis, enthesitis-related arthritis (ERA), inflammatory bowel disease (IBD), pigmented villonodular synovitis, and malignancy, all of which may initially involve four or fewer joints.
  3. One should have a low threshold to treat STIs in high risk patients, especially when unsure if a patient will return to clinic for results. In this study to evaluate treatment compliance among asymptomatic adolescents (ages 14-21) with positive STI results, 27% of patients never filled their prescriptions for STI treatment! Consider single dose regimens for GC, Chlamydia, and trichomonas when concerned.

Think of Juvenile Idiopathic Arthritis as an umbrella term for several different categories of disease.

Oligoarticular JIA is the most common JIA category. It is more common in females than males, and the peak incidence is two to three years of age. The typical presentation is limping without complaint. The large joints (particularly knees and ankles) are most commonly affected, but the hips are virtually never the first involved joint. Systemic manifestations other than uveitis are characteristically absent.

Juvenile Idiopathic Arthritis (JIA) Sub-types:

  • Systemic JRA (formerly called Still’s disease) (10-15% of JIA cases): patients have rash and intermittent fever, in addition to arthritis of any number of joints.
  • Oligoarticular JRA (~50% cases): involvement of < 5 joints after 6 months of illness. This disease is now also broken down into several distinct subgroups with varying prognosis!
  • Polyarticular JRA (30-40% cases): involvement of >4 joints after six months of illness. As with oligoarticular JRA, it is now recognized to contain many distinct subgroups with varying prognosis.

Interestingly, annual optho screening is required for those with oligoarticular JIA given uveitis or iridocyclitis occurs in up to 25% of patients, often initially without symptoms.


VA morning report 10.16.17: Another legionella case???

Case summary

Thanks to Hengameh and Max for presenting a very interesting case of a 66M with CLL, cutaneous eosinophilic syndrome who presented with dyspnea, cough and diarrhea found to have hyponatremia, hypophosphatemia and an elevated CK concerning for legionella!

Top pearls

1. Gerald Hsu taught use a lot about CLL. It is a disorder of  mature lymphocytes [CD 5 positive, smudge cells] and has a wide clinical spectrum ranging from an asymptomatic benign disease to an aggressive lymphoma with potential for transformation to a diffuse large B cell lymphoma.

2. In patients who truly have sudden onset of symptoms, consider [1] rupture of blood vessel/hollow viscus [2] Perforation of blood vessel/hollow viscus or [3] electrical [arrhythmia/seizure]

3. Legionella is a mutlisystem disorder that frequently causes pneumonia. High fever, relative bradycardia, CNS sx, GI sx, hyponatremia, hypophosphatemia and an elevated CK are also clues to the presence of legionella.

4. In a febrile patient, for each degree fahrenheit increase in temperature an increase of 10 beats/min in the HR is expected. Relative bradycardia refers to a less than expected pulse in a febrile patient. Beta-blockers are the most common cause. In the absence of these medications, infection by intracellular organisms [including Legionella!] or non-infectious fever are possible.


Here’s a short evernote about CLL.


Evernote about legionella:

Sudden onset of Symptoms

Sudden onset as reported by a patient does not always equal sudden in the way physician usually mean [e.g seconds]
Here is a great example of this phenomenon from a recent case report:
“A distinction must be made between sudden onset of visual loss and sudden discovery of preexisting visual loss. If the normal eye is inadvertently covered, a longstanding or gradual loss of vision in the other eye may be mistaken for acute loss”

Relative Bradycardia


  • Physiologically, for each degree fahrenheit increase in temperature, there should be a 10 beat/min increase in HR.
  • However, this only applies for temperatures >102F
  • Patients with conduction system disease or AV block blockade are excluded.

Official criteria + expected values




Note the propensity for intracellular organisms.



VA Ambulatory Report – Polyarthritis and Drug Induced Lupus

Case Summary: Thank you Alicia for presenting your clinic patient a 20 yo F with refractory epilepsy presenting with subacute migratory polyarthritis after starting Oxcarbazepine concerning for Drug-Induced Lupus on top of SLE.


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  • Patients with drug-resistant epilepsy should be seen at a specialized epilepsy center
  • Thanks Chris Sha for teaching us the top three causes of infectious polyarthritis: Disseminated Gonococcal disease, spirochetes, and viral (HIV, HBV)
  • Approach to arthritis: Consider basing it on number of joints and inflammatory vs. non-inflammatory
  • Differentiating drug-induced lupus from SLE is based on clinical picture and  laboratory findings.
  • Anti-TNF drugs are increasing in use and can cause an atypical presentation of drug induced lupus.


Drug-resistant epilepsy

  • No set definition, but has been proposed that drug-resistant epilepsy may be defined as failure of adequate trials of two antiseizure drug schedules (whether as monotherapies or in combination) to achieve sustained seizure freedom
  • Other forms of treatment may be considered; vagal nerve stimulation, surgery
  • If seizures are not controlled after 12 months, the patient should be referred to a specialized epilepsy center
  • Ambulatory EEG monitoring?
    • More cost effective than in-hospital EEG. Can increase the yield of detecting a seizure due to longer time on monitors and patient’s are less sleep deprived when sleeping in their normal environment.
    • Gold standard for differentiating non-epilieptic seizures from epileptic seizures is still in-patient EEG.


Flashback to Katie Auriemma’s post on an approach to polyarthritis from the Moffitt Pearls earlier this week.

Drug-induced lupus (DIL)

  • Common meds: procanamide, hydralazine, penicillamine, INH
    • Also seen with TNF-alpha inibitors
      • Can be more atypically presentation of DIL including negative anti-histone antibodies, hypocomplementemia positive dsDNA antibodies
  • More often causes superficial lupus symptoms (joint pain, rash) over visceral involvement (anemia, nephritis, serositis, etc)
  • Diagnosis
    • History of taking a known offending medication
    • Development of one feature of lupus
    • Serology: Positive ANA.
      • Positive anti-histone antibody is strongly suggestive.
        • Can be seen in idiopathic SLE but those patients will also have positive subserologies
      • You can also see a positive ANCA
    • Resolution of symptoms within weeks of stopping the offending agent


How do I differentiate between SLE and DIL? 

Clinical presentation Average age of onset 20 -30 y

More likely to affect African Americans than Caucasians

Female: Male 9:1

Average age of onset 50 -70 y

More likely to affect Caucasians than African Americans

Female: Male 1:1

Lab Findings ANA positive > 95%

Anti-histone antibodies in 50%

Anti-dsDNA in 80%

Low C3/ C4


ANA positive in > 95%

Anti-histone antibodies in > 95%

Anti-dsDNA can be present

Normal C3/C4