Clostridium difficile Infection

The following table summarizes the current Infectious Diseases Society of America (IDSA) Guidelines on the management of Clostridium difficile infections (Hint: click on the table to make it bigger):

It is borrowed from the recent succinct article by some of our own colleagues in Internal Medicine in Toronto, which you can find at this link!

For the full set of guidelines, click on this link.

If you are concerned about toxic megacolon, always remember to order a flat plate of abdomen. Even though a maximum colonic diameter greater than 6 cm is consistent with the diagnosis of megacolon, the overall clinical condition of the patient is more important than the absolute width of the dilated segment. Early surgical consultation is of utmost importance.

Cryptogenic Organizing Pneumonia

Cryptogenic organizing pneumonia (COP), previously known as Bronchilitis Obliterans Organizing Pneumonia (BOOP), is a distinct clinical entity with predominant features of pneumonia.

To summarize:

- It usually occurs in fifth or sixth decades of life.
- Men and women are affected equally.
- Most patients are symptomatic for less than two months, with a clinical presentation that mimics community-acquired pneumonia.
- Multiple ground-glass opacities and/or consolidations (with air bronchograms) are commonly noted on imaging.
- An open or thoracoscopic lung biopsy is suggested to confirm the diagnosis.
- Histopathology typically demonstrates excessive proliferation of granulation tissue within small airways (proliferative bronchiolitis) and alveolar ducts, associated with chronic inflammation in the surrounding alveoli.
- The diagnosis of COP requires positive histopathology AND the exclusion of any other possible cause of pneumonia (in particular, infectious causes).
 - Glucocorticoid therapy typically induces rapid clinical improvement and clearing of the opacities on chest imaging, usually without significant sequelae.
- Relapses are common upon tapering or discontinuation of glucocorticoids.
- It can be idiopathic, but also associated with connective tissue diseases, a variety of drugs, malignancy, and other interstitial pneumonias.

Please click on this link to read an excellent 2011 review from Chest on this topic.

Respirology Pearls

Here are a few respirology (and non-respirology) pearls for you to mull over today:

1) Correlation between arterial and venous blood gases

Much of the literature surrounding this concept is found in the Emergency Medicine literature. A prospective study involving 95 patients in Emergency Medicine Journal  from 2007 comparing ABG and VBG samples drawn as close in time as possible concluded that VBG analysis for pH, bicarbonate, and pCO2 (but not paO2, not surprisingly) may be a reliable substitute for ABG analysis in the initial evaluation of an adult patient population presenting to the ED. Click on this link to read the full article.

2) Hypertrophic pulmonary osteoarthropathy

Hypertrophic pulmonary osteoarthropathy, also known as Bamberger-Marie disease, is periostitis of the long bones of the upper and lower extremities. It is thought to be a paraneoplastic manifestation of lung carcinoma. These patients often get clubbing and increased bone deposition on long bones. Their presenting symptoms are sometimes only clubbing and painful ankles. Check out this link for an interesting "Images in Clinical Medicine" in NEJM illustrating the paraneoplastic phenomena of hypertrophic pulmonary osteoarthropathy and tripe palms (or acanthosis palmaris).

3) Batson venous plexus

The Batson venous plexus is a network of valveless veins that connect the deep pelvic and thoracic veins draining the inferior end of the bladder, breast, and prostate to the internal vertebral venous plexuses. They are thought to to provide a hematogenous route for metastatic spread of rectal and prostate cancer to the vertebral column or brain. The plexus is named after anatomist Oscar Vivian Batson, who first described it in 1940.

Right Heart Failure

Yesterday's Rapid Fire Morning Report was a testament to the breadth of clinical presentations that Internal Medicine has to offer.

We heard about the smörgåsbord of cases that were seen the evening prior, including cases of:

- transient hypoxia of unclear etiology
- paraspinal absess
- management of cancer-related pain
- right-heart failure

I thought I was take a moment to review the diagnosis and management of right heart failure, which are gleaned from guidelines published by the Canadian Cardiovascular Society in 2009. You can find the full set of guidelines by clicking on this link.

Right heart failure (RHF) can be due to systolic and/or diastolic dysfunction, and can be an isolated occurrence, though it is more commonly associated with left heart failure.

To make the diagnosis, at least two features should be present:

1) Signs and symptoms consistent with RHF. These typically fall into three categories:

- Fluid retention (eg, ascites, peripheral edema, anasarca)
- Exercise intolerance and fatigue (eg, low cardiac output, diastolic and systolic dysfunction)
- Hypotension (especially with atrial and ventricular arrhythmias, and low cardiac output)

2) Objective evidence of abnormal right-sided cardiac structure or function or elevated intracardiac pressures

The etiology of RHF can often be broken down into the following categories:


- Increased afterload, including left-sided heart failure and pulmonary arterial hypertension
- Right ventricular (RV) myopathic process, RV infarction and restrictive heart disease
- Right-sided valvular heart disease (triscuspid and pulmonary)
- Congenital heart disease
- Pericardial disease (a mimic of RHF)

On physical examination, one may find one or more of the following:

- Elevated JVP (with CV waves possibly present with tricuspid regurgitation)
- Hepatomegaly (from passive hepatic regurgitation)
- Ascites
- Peripheral edema
- RV heave
- Palpable P2
- Systolic murmur at left lower sternal border consistent with tricuspid regurgiation
- Right-sided S3

The diagnosis is typically made using:
- Echocardiography
- Consider cardiac MRI and MUGA scan, as indicated
- If the diagnosis of pulmonary arterial hypertension is felt to be the cause, then right-heart catheterization should be considered, as it is the gold standard for the diagnosis of pulmonary hypertension.

In regards to management, generally, diuretics are the mainstay of therapy. However, diuretics should be given judiciously, as patient's LV filling pressures are often low, and overdiuresis may lead to intravascular volume contraction, precipitating hypotension, pre-renal acute kidney injury, etc.

Always be mindful of the patient's electrolyte status (in particular, their potassium and magnesium), as diuretics can lead to hypokalemia and hypomagnesemia - a recipe for arrythmias (and thus, further exacerbation of their heart failure).

Acute Tubular Necrosis

Yesterday, in Nephrology Morning Report, we reviewed the tried and true approach to acute kidney injury (AKI). All together now: pre-renal, intra-renal, and post-renal.

Moreover, we learned about the spectrum of injury caused by intravascular volume depletion (which can be either due to true hypovolemia or low effective circulating volume), namely:

- pre-renal AKI (the cardiac equivalent would be "stable angina")
- all the way to intra-renal AKI, in the form of ischemic acute tubular necrosis (ATN) (the cardiac equivalent would be "myocardial infarction")

ATN is largely caused by two broad categories of injury:

1) ischemic ATN (as described above)
2) nephrotoxic ATN (classic causes include aminoglycosides, CT contrast, and hemepigments, such as in rhabdomyolysis)

In order to distinguish pre-renal AKI from ischemic ATN, one can look at the urine sediment looking for heme granular casts, which are often described as "muddy brown" in appearance.

If a patient has sustained AKI in the form of ATN, then it is prudent to monitor for acute indications of dialysis. These include:

1) Hyperkalemia (refractory to medical management)
2) Volume overload (refractory to medical management)
3) Uremia, typically resulting in pericarditis (refractory to medical management)
4) Acidosis (refractory to medical management)
5) Removal of toxins, such as lithium or salicylates (refractory to medical management)

Let's end off today's post by paying homage to one of the greatest puppeteers of all time, Jim Henson, who we learned died from a Group A Streptococcus infection. Thank goodness for the Muppets.

Autoimmune Polyendocrine Syndrome

Although Final Jeopardy! was a stumper this morning, that doesn't mean you still do not have an opportunity to learn more about Autoimmune Polyendocrine Syndrome, which is a heterogeneous diagnosis classified into three distinct types based upon the putative genetic mechanism, and nicely summarized in the table below (hint: click on the table to enlarge it). It is borrowed from a nice review article from NEJM in 2004, which you can find by clicking on this link.

Interesting historical fact: John F. Kennedy was thought to have Autoimmune Polyendocrine Syndrome type II. 

Click on this link for an absolutely fascinating article from the Annals of Internal Medicine that builds the case for this hypothesis based upon historical events and conversations with his personal physicians.

N.B. Alex Trebek sends his apologies and regards for not being able to attend Jeopardy! Morning Report today.

Rapid Fire Morning Report

And now, a smörgåsbord of learning points from today's wonderful Rapid Fire Morning Report:

1) Does This Adult Patient With Suspected Bacteremia Require Blood Cultures?

A recent addition to the JAMA Rational Clinical Examination Series by several members of the Department of Medicine here at Mount Sinai has helped us to better answer the aforementioned age old question.

- The pretest probability of bacteremia varies considerably and is determined largely by the clinical context (including the presence or absence of an identifiable focus of infection).

- Blood cultures should not be ordered simply because isolated fever or leukocytosis is present in patients for whom the pretest probability of bacteremia is low.

- The SIRS criteria and Shapiro decision rule show promise in further defining low-risk patients but require prospective validation.

- The existing data do not allow generalization of these conclusions to immunocompromised patients or those under consideration for endocarditis.

2) HIV-associated Diarrhea

Today's discussion regarding HIV-associated diarrhea reminded me of a previous Rapid Fire Morning Report in which this exact diagnosis and its differential diagnosis was discussed. Clicking on this link will lead you to a previous post discussing this exact entity.

3) Heyde's Syndrome

Bleeding from angiodysplasia in the GI tract in patients with aortic stenosis has been called Heyde's syndrome. This is a well-known association, first reported by Dr. Edward Heyde in the NEJM in 1958, although the hypothesis of causality remains controversial.

The purported mechanism by which aortic stenosis may lead to the development of angiodysplasia is through the development of an acquired form of von Willebrand disease from mechanical disruption of von Willebrand multimers as they pass through a tight aortic valve, as well as from a vWF interaction with platelets that triggers platelet clearance.