Mystery Quiz #2

January 22, 2007

Posted By Robert Smith, MD Associate Professor of Medicine, Division Pulmonary and Critical Care Medicine

The patient is a 77 year old male whose chief complaint was severe left hip pain of five years duration.  As part of a preoperative evaluation for hip surgery, a routine chest x-ray was obtained as below.  Click on the thumbnails below for full size images:


A prior film done six months previously showed similar but less impressive findings. Upon review, the patient denied any pulmonary symptoms or significant history of smoking. There was no history of pets, occupational exposures, recent travel or illicit drug abuse.   His only medication was oxcodone. Read more »

How Aggressively Should You Treat a Patient with a Pulmonary Embolus?

January 17, 2007

An otherwise healthy 57 year old patient presents with shortness of breath and pleuritic chest pain.  The patient is hemodynamically stable without evidence of shock.  A chest CT reveals a pulmonary embolus.

Questions: 1. When should an echocardiogram to assess for right heart strain be performed in a patient with a pulmonary embolism?  Should stable patients without evidence of shock have a routine echo once a diagnosis of pulmonary embolism is made?

2. If the echo shows signs of right heart strain, but the patient is stable (normal vitals, no evidence of shock), when is it appropriate to administer thrombolytic therapy?

-Tiki Ahuja PGY-3

Commentary by Kevin Felner, M.D.  Division of Pulmonary/Critical Care

1. There is no current data or guideline regarding the routine use of echocardiography in the setting of a pulmonary embolus.  It is clear that if there is evidence of cardiovascular compromise, refractory hypoxemia, or radiographic evidence to suggest a large pulmonary embolus, then an echo would be useful in identifying a patient with right heart dysfunction which does portend a worse outcome and may change therapy.  The echo may also show features that suggest a worsened outcome and may change therapy, such as a free floating RA or PA thrombus, or evidence of a right to left shunt through a patent foramen ovale. A TEE is better for identifying PA thrombus and for patients who are on mechanical ventilation. 

While there is no data or guideline suggesting routine use of echo in stable patients with pulmonary emboli, doing so seems to have little risk and much potential benefit.  Excluding cost, routine use of echocardiography for stable patients with pulmonary emboli can provide important information including underlying pulmonary hypertension (from chronic pulmonary emboli or other causes, the presence of additional cardiopulmonary disease that identifies the patient as someone who might not tolerate a second pulmonary embolus- e.g., significant mitral or aortic valve stenosis, or left ventricular dysfunction.  This information may shape treatment in the hospital and at discharge. Read more »

Morning Report: How Do You Approach a Patient With Bronchiectasis

January 16, 2007

Chief complaint: 85 year old female presents with worsening shortness of breath for one day.

History of present illness:

The patient’s history of present illness begins at the age of 60 when she was diagnosed with asthma, for which she had been treated with inhaled anticholinergics, beta agonists and intermittent oral steroids.  Twelve years prior to admission, the patient was diagnosed with diabetes, which was managed with oral medications.  Two years prior to admission, the patient was diagnosed with Mycobacterium avium complex (MAC) at an outside hospital and received a full course of treatment.  On the day prior to admission, the patient noted a worsening cough productive of green sputum, along with wheezing and shortness of breath.  The patient was evaluated by her primary doctor and started on prednisone 20 mg twice a day.  However, after two doses of prednisone, she reported feeling worse and was instructed by her doctor to come to the ER. Read more »

To Lavage or Not to Lavage?

January 10, 2007

Case and Commentary by Minisha Sood PGY-3 and Ilseung Cho Fellow, Division of Gastroenterology

The patient is a 57 year-old man with a past history of hypetension, hyperlipidemia, hepatitis B/C cirrhosis and coronary artery disease status/post a non-st-elevation mi in August 2006, during which time he was on a heparin drip and developed an upper gastrointestinal bleed. Upper endoscopy at that time revealed non-bleeding esophageal varices and he was discharged on a beta blocker. He again presented to Tisch hospital in December 2006 with complaints of dyspnea and exertional chest pain. Upon further questioning, he revealed that he had been having watery, black bowel movements for several days. He denied any dizziness or palpitations. His vital signs were stable (no orthostatic hypotension) and his hematocrit was at baseline 31%. The evaluating ER physicians elected not to place a nasogastric tube, and he was admitted to the medicine floor where he experienced no further episodes of melena that evening.

 Question: Should we perform NG lavage in patients with a suspected upper GI bleeding?

Let’s look a bit more closely at this case. The patient is known to have cirrhosis and had been noted to have had varices in the past. Though it is not mentioned in the case presentation, we assume he is also on aspirin, given his cardiac history. His complaint of black watery bowel movements is certainly consistent with an upper gastrointestinal source of bleeding, but this could also be consistent with a distal small bowel or right-sided colonic source of bleeding. The bleeding does not appear to be variceal in nature, based on his hemodynamic stability and unchanged hematocrit. But we may be easily fooled. So at initial evaluation, we are unsure of the site of bleeding and its severity. NG lavage at this time would be a quick and easy way to better determine the site and severity of such a bleed. Is there any evidence to support this? A short literature review reveals the following: Read more »

Why Are Breast Cancer Rates Trending Down?

January 9, 2007

The recent finding of decreasing breast cancer rates made headlines throughout the media; including a NY Times article entitled, Reversing Trend, Big Drop is seen in Breast Cancer on December 15, 2006.

Striking epidemiological facts tells us that breast cancer is the most common cancer in women in the U.S., and only second to lung cancer as the most common cause of cancer deaths. It is estimated that approximately 212,920 American women will be diagnosed with breast cancer in the year 2006, and 40,970 women will die from this disease. (1)  The unfortunate truth is that during a woman’s life, she has a one in six chance of developing breast cancer.  Between 1940 and 1980 breast cancer rates rose 1.2% per year.  The more pronounced increase in early stage breast cancers during the 1980s was probably due to the use of screening mammography. Since 1987, there have been no significant changes.  Over recent years, we’ve seen that there has been a trend towards increased estrogen receptor/progesterone receptor (er/pr) positive disease and a decrease towards ER/PR negative disease. Read more »

A Bad Break for the Purple Pill…

January 8, 2007

Commentary By Josh Remick, PGY-2

In the December 27th 2006 issue of JAMA, Yang et al. reported the results of a nested case-control study of United Kingdom patients entitled “Long-term Proton Pump Inhibitor Therapy and Risk of Hip Fracture.” Using the General Practice Research Database (GPRD), a computerized medical record system used by several of the general medical practices in the UK, new hip fracture cases were found in patients at least 50 years old (n=13,556) and matched them with up to 10 age and sex matched controls (n=135,386). The primary exposure of interest was proton pump inhibitor (PPI) therapy of more than 1 year prior to their hip fracture. Read more »

Links: Online Dermatology Atlas

January 5, 2007

The best online dermatology atlas I have come across is  The site originates from Germany and includes an excellent, easily searchable database with terrific pictures and clinical information. The most useful feature of the site however is the differential diagnosis list which appears next to the pictures that are displayed.  So if you have an educated guess what the rash you're looking at is, then you can easily review similar rashes and quickly compare and contrast them to your original diagnosis. Then you can make the fancy diagnosis, sound smart to your patient and colleagues, and then give your patient the usual topical steroid cream…

Click on the thumbnail to view a sample page.

Do Statins Get Along With Hepatitis C?

January 4, 2007

A 53 year old male with chronic hepatitis C and type 2 diabetes is found to have a moderately elevated cholesterol.

1. Is it safe to start a statin?

2. Do statins have any effect on viral replication?

Comentary By Ed Bini, M.D. Associate Professor/Director Gastroenterology and Hepatology Research

The many benefits of statins far outweigh the risks associated with this class of medications. However, statins are known to have the potential to cause hepatotoxicity. The most common form of statin-induced hepatotoxicity is elevations in transaminases levels (AST and ALT). Statin-induced hepatoxicity occurs in 1% – 2% of patients treated and is reversible upon discontinuation of the treatment. It is currently recommended that a liver profile be performed at baseline, 6 weeks and 12 weeks after starting treatment, and then every 6 months.

Patients with underlying chronic hepatitis C virus (HCV) infection may be at increased risk of statin-induced hepatotoxicity. To date, however, the precise incidence has not been extensively studied. One recent study (Clin Gastroenterol Hepatol 2006;4:838-839) evaluated statin-induced hepatoxicity in 166 hyperlipidemic HCV-infected patients who were treated with a statin (cohort I), 332 HCV-infected patients who did not receive a statin (cohort II), and 332 HCV negative patients who were treated with a statin (cohort III). In patients with HCV, statin therapy (cohort I) was associated with a higher incidence of mild-moderate liver biochemistry value increases compared with those not on statin therapy (cohort II) (22.9% vs 13.3%, respectively, P = .009), but a lower incidence of severe increases (1.2% vs 6.6%, respectively, P = .015). Among patients started on statin therapy (cohorts I and III), the incidence of mild-moderate liver biochemistry value increases (22.9% vs 16.3%, respectively, P = .094), severe increases (1.2% vs 1%, respectively, P = .874), or discontinuation of statin therapy as a result of hepatotoxicity (21.6% vs 9.2%, respectively, P = .147) were similar in HCV positive and HCV negative patients. Although the authors concluded that statin therapy was not associated with a significantly higher risk of hepatotoxicity, it was associated with a non-significant increase in the incidence of mild to moderate hepatotoxicity and higher discontinuation rates and, therefore, we cannot exclude a type II error because of the small sample size.

Nonetheless, treatment should not be withheld in those with underlying chronic HCV infection who have compensated liver disease (no ascites, hepatic encephalopathy, or history of variceal hemorrhage). Instead, these patients should be treated and monitored closely. For patients with chronic HCV and compensated liver disease who are started on a statin, I suggest obtaining a liver profile at baseline, week 4, week 8 and then every 12 weeks during treatment. The use of statins in patients with decompensated liver disease should be used with extreme caution if at all.

Additional benefits of statin therapy in patients with chronic HCV infection include the potential for reduction in hepatic steatosis (which is present in approximately 50% of patients with HCV and is associated with more rapid fibrosis progression) and possible beneficial effects on HCV viral loads. One recent exciting and provocative study showed that statins (especially fluvastatin) in combination with interferon exerted a strong synergistic effect on HCV replication in vivo (Hepatology 2006;44:117-125).

Although the exact mechanism by which HCV enters hepatocytes is a controversial issue, it should be noted that there are data to suggest that HCV may enter hepatocytes via the LDL receptor. Since statins upregulate LDL receptor expression, there is the potential for statins to facilitate HCV entry into hepatocytes (Article in press J Hepatol). The risks and benefits of statin use in patients with HCV, as well as the impact of statin use on the natural history of HCV infection in humans, remain to be determined.

Does the Existence of Community Acquired MRSA Change Empiric Therapy for Skin and Soft Tissue Infections?

January 3, 2007

A 58 year old man with type 2 diabetes and chronic venous insufficiency/recurrent lower extremity cellulitis presents with fever and a left lower extrmity ulcer with purulent drainage. He’s been successfully treated in the past with both Unasyn/Augmentin or Levaquin.  In the face of community acquired methicillin resistant staph aureus (CA-MRSA),  have guidelines for skin and soft tissue infections changed?

Commentary By Howard Leaf, M.D. Assistant Professor, Division of Infectious Diseases and Immunology


1. What would your first line treatment be in a patient with a diabetic ulcer?

Although New York City was not in the vanguard of regions reporting very high rates of CA-MRSA (Bellevue’s rate for S. aureus isolates from purulent skin and soft tissue infections in August 2004 was 15%; NEJM 2006; 355:666), we’re no doubt catching up.  A study from hospitals in Brooklyn (Ann Clin Microbiol Antimicrob 2006; 5:29) reported 22% of all S. aureus isolates from 12/05 to 2/06 were positive for SCCmec type IV (the genetic element encoding resistance in most CA-MRSA), with many of these the most common USA-300 strain.

How does this impact your management of the diabetic foot ulcer?  Given the above rates and the fact that S. aureus remains the most common pathogen isolated from diabetic associated ulcers, coverage of this pathogen would seem reasonable for moderate to severe ulcers as empiric therapy, pending cultures.  This approach was reflected in the 2004 Infectious Diseases Society of America (IDSA) guidelines (Clin Infect Dis 2004;39:885-910).  However, although some smaller series report diabetics as a risk for CA-MRSA acquisition, and perhaps poorer outcomes with disease, the usual scenario for this pathogen is epidemic furunculosis or other purulent complicated skin and soft tissue infections, not the typical diabetes associated ulcer.

Clindamycin has excellent antistaphylococcal activity, but there is the potential for emergence of resistance with strains inducibly resistant to erythromycin. Linezolid, daptomycin, and vancomycin have good efficacy in skin and soft-tissue infections and are choices as empiric therapy in the more severe infections in hospitalized patients. Over 95% of CA-MRSA isolates retain susceptibility to trimethoprim-sulfamethoxazole, and this has been used successfully. A fluoroquinolone (FQ) such as levofloxacin or moxifloxacin may also be chosen, but beware the possibility of emergence of resistance with prolonged therapy.  The bottom line: for outpatient therapy, TMP-SMX plus either a fluoroquinolone or amoxicillin-clavulanate, or in more severe ulcers, linezolid plus a FQ.  In the hospitalized patient, our old standby of vancomycin plus piperacillin-tazobactam is excellent coverage, with substitutions for either of those available.

2. What would your first line rx be in a diabetic patient with a routine cellulitis who you are treating as an inpatient?

Non-purulent cellulitis without an open wound in DM is usually due to β-hemolytic streptococci (A, B, C, and G) and less commonly S. aureus.  Always consider necrotizing cellulitis requiring surgical debridement.  Again, vancomycin or linezolid plus piperacillin-tazobactam or a carbapenem are appropriate for a patient with severe disease.  For more mild infections, oral TMP-SMX plus linezolid or rifampin should do.

3. What would your first line rx be in a non-diabetic patient with a routine cellulitis who you are treating as outpatient? Should it include CA-MRSA coverage in the VA population? at Bellevue?

If “routine” is meant to connote lack of purulence or evidence of deep infection in a patient without some stronger epidemiologic link to CA-MRSA, such as a child, a prisoner, an MSM, a younger non-white patient, or the “classic” patient involved in team contact sports, amoxicillin-clavulanate or dicloxacillin may still be adequate.  Otherwise, the addition of TMP-SMX is prudent, no matter the hospital at which you’re seeing your patient.

How Frequently Should You Perform a Follow-Up Colonoscopy-A multiple choice quiz

January 2, 2007

Commentary By Michael Poles, M.D. Gastroenterologist, Assistant Professor of Medicine, Mircrobiology and Pathology.

Every once in a while I will be feeding this new blorganism (or is it bloganism?) with content from the world of gastroenterology. Today I would like to review an article of importance to both gastroenterologists and internists. There is likely no topic in gastroenterology more important than that of colorectal cancer screening. Colorectal cancer is the second most common cause of cancer death in the U.S., and it takes up an enormous of gastroenterologists’ work effort. The most accepted form of screening for colorectal cancer is by colonoscopy. The most commonly accepted guidelines for colorectal cancer screening and surveillance were proposed by the U.S. Multisociety Task Force (USMSTF) on colorectal cancer, but it is widely held that these guidelines are not correctly followed. The biggest problem regarding CRC screening is that we underscreen; the majority of patients, nationwide, who are eligible, do not undergo appropriate screening. The flipside is likely also true; patients may be over-screened, leading to increased patient-care costs and increased demands on the medical system. With this in mind, I turn to an article in the Annals of Internal Medicine by Dr. Boolchand from University of Arizona (Ann Intern Med. 2006;145:654-659). For this study, the investigators sent out a survey to a random sample of 500 physicians from the American College of Physicians and 500 physicians from the American Academy of Family Physicians. The physicians were asked about when they would reschedule colonoscopy in a fictional 55 year old patient with a variety of findings on an initial colonoscopy.

Now for the fun part, see how you would answer each of the following scenarios.  For each question, the patient is a 55-year-old man in good health who underwent a screening colonoscopy. The colonoscopy was completed to the cecum, the quality of the colon cleansing was excellent, and the patient had no family history of colon cancer.  

Patient 1) On colonoscopy, they found and removed a 6mm polyp that was a tubular adenoma on histology. Would you repeat the procedure in:

A) 6 months

B) 1 year

C) 3 years

D) 5 years

E) 10 years

F) Repeat is not indicated

Patient 2) On colonoscopy, they found and removed a 6mm polyp that was a hyperplastic polyp on histology. Would you repeat the procedure in: 

A) 6 months

B) 1 year

C) 3 years

D) 5 years

E) 10 years

F) Repeat is not indicated

Patient 3) On colonoscopy, they found and removed a 12mm pedunculated polyp that was a tubular adenoma with a focus of high-grade dysplasia away from the biopsy margin on histology. Would you repeat the procedure in:

A) 6 months

B) 1 year

C) 3 years

D) 5 years

E) 10 years

F) Repeat is not indicated

Patient 4) On colonoscopy, they found and removed a 12mm pedunculated polyp that was a tubulvilllous adenoma on histology. Would you repeat the procedure in:

A) 6 months

B) 1 year

C) 3 years

D) 5 years

E) 10 years

F) Repeat is not indicated

Patient 5) On colonoscopy, they found and removed two 6mm polyps that were both tubular adenomas on histology. Would you repeat the procedure in:

A) 6 months

B) 1 year

C) 3 years

D) 5 years

E) 10 years

F) Repeat is not indicated


So, now you can see how you did: Read more »

Morning Report-A Frequently Overlooked Diagnosis

December 28, 2006

A 57 year old female  with a past medical history of hypertension, obesity, remote intravenous drug use and several years of chronic low back pain, with both intermittent radiation to her lower extremities  and decreased sensation in her lower extremities  presented with an acute worsening of the pain in her lower back.  The patient reported that she was awakened from sleep and "had to crawl to the bathroom," because of the pain.  She was febrile on admission with moderate lower spine tenderness.  She was also noted to have a RLE cellulitis.  Hip flexion was limited by pain.  The motor exam was difficult to perform because of pain and there were no sensory deficits.  The patient was treated for cellulitis with amoxicillin/clavulanate for one day.  On hospital day two the patient continued to complain of low back pain, remained febrile despite her cellulitis appearing to improve.  On hospital day 3 the patient's blood cultures from admission grew staph aureus.  She had an echocardiogram and was sent for an MRI of the spine. MRI revealed a lumbar spinal epidural collection, likely inflammatory without well defined borders (phlegmon). Antibiotics were changed to Vancomycin, ceftriaxone and metronidazole.  The following day sensitivities on blood cultures drawn on admission revealed methicillin sensitive staph aureus.  The antibiotic regimen was changed to nafcillin and the patient continued to improve. 

Teaching points:

1. Spinal epidural abscesses are frequently missed and the delay in diagnosis has serious morbidity.

2. The classic triad of fever, back pain, and neurologic symptoms is present only 13% of the time.  Motor symptoms come late in the course of the infection and earlier treatment leads to significantly fewer neurologic sequelae.

 3. Therapy for spinal epidural abscesses requires a multidisciplinary approach between surgery, interventional radiology, neurology and medicine.  The literature regarding surgical/IR intervention is scarce.  Most patients with evidence of mass effect should undergo some type of decompression.  Some cases may be treated with antibiotic therapy alone.  Antibiotic therapy should be directed at the organism (staph in 60% of cases) 

Short Epidural Abscess Powerpoint Presentation

Breaking News: FDA Advises Caution with Gadolinium Based Contrast

December 27, 2006

Commentary By: Minisha Sood PGY-3

The FDA has received reports of 90 patients with moderate to end-stage kidney disease who have undergone MRI or MRA with a gadolinium-based contrast agent and subsequently developed a new disease known as Nephrogenic Systemic Fibrosis (NSF).

Scientists first identified NSF, also known as Nephrogenic Fibrosing Dermopathy (NFD), in 1997 and its cause has not yet been identified.  There have been approximately 200 reports of NSF/NFD only in people with kidney disease.  Neither the duration of kidney disease nor its underlying cause is related to the development of NSF.

Patients with NSF report swelling and tightening of the skin, which usually affects the extremities and leads to an inhibition of flexion and extension.  Muscle weakness is a common symptom as well.  Approximately 5% of patients experience a rapidly progressive course, which may result in death due to widespread fibrosis.  The pathogenesis of NSF is thought to be linked to the circulating fibrocyte (CF), a recently characterized cell that is distinct from a fibroblast.  The CF leaves the circulation, the mechanism of which is still being investigated, and differentiates in the dermis where it resembles normal fibroblasts and leads to a systemic disorder.

Many approaches to treatment are currently under investigation including oral steroids, physical therapy, plasmapheresis, high-dose IVIG therapy, and renal transplantation.

Here is some important information for health care providers:

  • When a patient with moderate to end-stage kidney disease requires an imaging study, a modality other than MRI or MRA with a gadolinium-based contrast agent should be chosen whenever feasible.
  • If MRI or MRA with a gadolinium-based contrast agent is necessary, it may be prudent to arrange prompt dialysis for patients with advanced kidney dysfunction.
  • The FDA requests that health care providers and patients report adverse event information to the FDA online at, by phone (1-800-FDA-1088) or by fax (1-800-FDA-0178).