AM Report Pearls 6/19: diarrhea framework

PEARL: atenolol is mostly cleared by the kidney, so sticks around longer in patients with CKD. Metoprolol is the beta-blocker of choice in CKD patients.

Diarrhea framework (there are many, this is just one)

  • Acute: usually toxic/infectious
    • Inflammatory: campylobacter, Shigella, EHEC, C diff etc.
    • Noninflammatory: Norwalk, Rotavirus, Giardia, drugs etc.
  • Chronic
    • Watery (check stool osm gap)
      • Secretory: chronic infections, non-osmotic laxatives, microscopic colitis, endocrine tumors
      • Osmotic: lactose intolerance, sorbitol, meds
      • Functional: IBS
    • Inflammatory: IBD, ischemic colitis, chronic infasive infections, radiation enteritis
    • Fatty:
      • Malabsorptive: celiac, gastric bypass, bacterial overgrowth
      • Maldigestive: bile acid malabsorption, pancreatic insufficiency

SFVA Morning Report Pearls: Management of the Spinal Epidural Abscess

THE PEARL:   There is a general consensus that for patients with spinal epidural abscesses, acute/progressive neurological deficit, spinal instability, or disease progression despite antibiotics are indications for urgent surgical intervention.

Quick Hits on Spinal Epidural Abscesses:

– bacteria can gain access to epidural space via hematogenous spread from infected contiguous tissue (vertebral body, psoas muscle) or via direct inoculation into spinal canal (e.g. during spinal or epidural procedures/surgery)

– risk factors include epidural catheters, diabetes mellitus, alcoholism, HIV, bacteremia, IVDU

– Staph aureus is responsible for two-thirds of cases caused by pyogenic bacteria (less common causes include GNR, CONS, Strep, Anaerobes)

– MRI is the imaging test of choice for diagnosis; an less sensitive/specific alternative is CT w/ contrast

– clear indications for urgent surgical interventions include acute/progressive neurological deficits, spinal instability, or disease progression despite antibiotics

Operative Management of Spinal Epidural Abscess

Tuchman A, Pham M, Hsieh P.   The indications and timing for operative management of spinal epidural abscess: literature review and treatment algorithm.  Neurosurg Focus 37(2):E8:1-8, 2014


Providing Patients Access To Their Doctors’ Notes

A few weeks ago Carly and I were away on vacation in Bali and on an excursion to visit some of the local artisan shops outside of Ubud. We entered a batik (special Balinese textile) shop with plans to browse and maybe pick up a sarong as a gift for my mother. Upon entering, our plans changed. The shop had been set up to give the visitor an idea of how the batik was made before you could see the final product and make purchases. It turned out that each finished piece went through a careful and artistic process of drawing an image, painting with wax, and dipping in dye that was repeated over and over again to create the beautiful and colorful images decorating the cloth. Actually witnessing and understanding this process made us much more interested in the batik and substantially increased my desire to buy some. Retrospectively, I was surprised at how understanding the production process and the work that goes in to the final piece impacted my appreciation (and willingness to pay) for it overall.

Similarly, when I stumbled across this article from Kaiser Health News, What Patients Gain by Reading Their Doctor’s Notes ( it immediately resonated with me. I recalled an experience on the wards at SFGH a few weeks ago. My Sub-I received a call about a patient who needed an IV for a contrast CT and who was a difficult stick. Several RN’s had tried and our PICC nurse who usually puts in difficult IVs was away. When my Sub-I and I arrived to the bedside with our ultrasound machine the patient was annoyed and upset at all the needle sticks and failed attempts but he begrudgingly agreed to let us try with the ultrasound. I tied off the tourniquet and set up the ultrasound and began explaining what I was doing and seeing on the machine step by step to the Sub-I. As I demonstrated how small the veins were and how they looked different from the arteries on the ultrasound, the patient spoke up and said, “wow, I can see why this is so tough without the machine.” As we got the IV set up and he thanked us for our efforts and his anger about the failed attempts seemed to have evaporated. All in all, it had taken about 15 minutes, but this patient was able to see and appreciate the efforts that his team had gone through for his health.

In contrast, I recalled a recent experience on the wards when after hours of calling various consultants to get final recs, doing an MD to MD call to get a patient placement at a SNF, and communicating with our case manager to set up transport, I entered a patient’s room only to find them irate and upset that they were still waiting. They felt like our team had done nothing that day and they were stuck in the hospital waiting for someone to pay attention to them and just call a cab.

Unlike many of our procedural colleagues, on the medicine wards much of our time and energy is spent thinking, reading, and communicating with other members of the health care team- all of which is largely invisible to the patient sitting in bed on the ward. In the article, Luthra argues that opening up doctor’s notes to patients can help increase patient engagement in their own health and make for improved physician-patient communication, with which I agree. However, when applied to the inpatient setting I see an opportunity to improve patient satisfaction and the patient experience as well. If patients had the chance to get a glimpse of the dedicated time spent developing differentials and treatment plans, working with consultants, and organizing follow up care their impression of their hospital care and their relationship with their team would improve. Knowing that what at first glance appear to be delays are really effects of the complexity of speaking to experts and that the people in charge of their care are working tireless on their behalf throughout the day even if they are not at the bedside would serve to provide reassurance and a sense of value to patients. Despite some of the very real worries (patients misinterpreting information, or doctors sugar-coating diagnoses) opening up doctors’ notes offers a real opportunity for us to enrich the patient experience while in the hospital and improve their understanding of an increasingly complex care system.

Moffitt AM Report Pearls 6/16: complications of STEMI, management of afib

Complications of STEMI

  • Much less common nowadays with thrombolytic and antiplatelet therapy
  • Time to presentation (and intervention) is key; complications in first 24h is rare, complications 3-4 days out is much more common
  • Think about the vessel that is occluded!
    • LAD: worry more about free wall rupture, papillary muscle rupture, LV aneurysms
    • RCA: worry more about heart blocks
  • PEARL: to r/o a new MI, get CK-MB and CK, and look at the ratio (not just the absolute #s): CK-MB/CK <2.5% = negative for new MI, CK-MB/CK > 5% = positive for new MI
  • See attached handout of post-MI complications (from my favorite chiefs cover sheets website), and an article by YY on etiologies and management of post-MI shock!! Overall, portends significant M&M

Management of afib with RVR: advanced edition

  • Remember: always first consider if the patient is unstable: if so, cardiovert!
  • Think about and correct the underlying cause (examples: new heart failure/volume overload, arrhymogenic drugs like dobutamine, thyrotoxicosis (which can be unmasked with iodinated contrast – Jod-Bosedow syndrome)
  • **Think about contraindications to certain pharmacologic agents. For example, don’t give an AV nodal blocker to a patient with recent complete heart block!
  • Think about indications/contraindications to anticoagulation early!
    • Remember that CHADS2 scoring is applicable only to non-valvular afib and that the risk of stroke is higher in those with valvular/structural afib
    • Patients with new afib <48h: ok to cardiovert even if not on anticoagulation. If afib >48h, ideally, would delay cardioversion until >3 weeks if stable
    • At least 4 weeks of oral anticoagulation after cardioversion



Post-MI shock J Intensive Care Med-2013-Ng-151-65

Moffitt AM Report Pearls 6/15: Lead poisoning, peripheral eosinophilia, and adrenal insufficiency!

Lead poisoning

  • Acute (days to weeks) vs chronic (months)
    • Sxs are nonspecific: abd pain (“lead colic”), neuropsychiatric sxs, peripheral neuropathies, sxs of anemia
  • See microcytic anemia with basophilic stippling on smear. In adults, can also see hemolysis.
  • If Pb>100 à admit for IV chelation with EDTA. Can improve sxs (such as lead colic)
    • Watch for side effects! hypoglycemia, hypocalcemia –> arrhythmias
    • When sxs improve, can discharge with po chelation
  • If Pb<100 à po chelation with succimer, removal from exposure
    • Pt will need to be on chelation therapy for a long time, as it takes months for lead levels to come down (half life of lead is decades in the bones!)
  • R/o other heavy metal toxicities! Work with local poison control/environmental health

Peripheral eosinophilia ddx

  1. Parasitic infections
  2. Endocrine – adrenal insufficiency!
  3. Malignancy (esp leukemias and lymphomas)
  4. Drugs
  5. Allergic diseases (atopy)


Adrenal insufficiency

  • Clinical manifestations – nonspecific, including fatigue, anorexia, n/v. On labs, can see peripheral eosinophilia!
  • Think about primary vs secondary.
    • Primary: see electrolyte abnormalities (hypoNa, hyperK, hyperCa – from mineralocorticoid effects), hyperpigmentation.
    • Secondary: no electrolyte abnormalities or hyperpigmentation
  • Workup: beautiful diagram from!
  • Adrenal insufficiency
    • Primary AI: Addison’s disease (most common in US), TB, bilateral adrenal hemorrhage, drugs
    • Secondary AI: withdrawal of steroids is most common! Others include pituitary lesions/surgery, drugs
    • Tertiary AI: from inadequate secretion of CRH
  • Advanced learning: Nonclassic (late onset) 21-hydroxylase deficiency (CAH) = often confused with PCOS!
    • Often see acne, hirsutism, oligo/amenorrhea! To dx this, check an AM 17-hydroxyprogesterone level.
    • Super advanced pathophys: low 21-hydroxylase enzyme activity à decreased cortisol production à increased ACTH secretion à increased androgen secretion, such as DHEA and 17ohydroxyprogesterone


Evernote link:

Moffitt AM report PEARLS 6/12: Enteric fever; Fever in a returning traveler

Enteric Fever (both typhoid and paratyphoid)

  • Transmitted by contaminated food and water
  • Presentation: variable, but generally fever, chills, abdominal pain +/- rash (classically, “rose spots”). Do NOT have to have diarrhea.
  • Chronic carriage: occurs in 1-6%, less common these days with modern antibiotics per HH
  • Diagnosis: culture
  • Complications to consider: splenic rupture, bowel perforation, chronic carriage
  • Treatment: increasing fluoroquinolone resistance in S and SE Asia. Must check test with nalidixic acid. Otherwise CTX and azithromycin are acceptable alternatives depending on clinical situation
  • Vaccinations: not very good
    • Efficacy at year 1 (35% oral; 69% IM) and efficacy at year 2 (58% oral; 59% IM)
    • Typhoid vaccinates against S. typhi but does NOT vaccinate against S. paratyphi

Fever in a returning traveler

  • Think about geography and incubation period to narrow the ddx. Here is a super helpful table of incubation periods and geography from the CDC Yellow Book chapter on fever in returned travelers

Fever in returning traveler

Evernote link:

Moffitt AM report PEARLS: strep anginosus, brain abscesses

**FIRST, A PEARL FROM YESTERDAY’S AM REPORT: A clue to diagnosing lymphoma is new alcohol intolerance (alcohol-related pain at lymph node sites)! A one-page case is attached.

Intern report PEARLS: strep anginosus, brain abscesses

**PEARL: when you uncover strep anginosus (a strep viridans spp), look for abscesses!! Treatment is abscess drainage and prolonged abx.


Approach to brain abscesses:

  • Causes: 1. direct spread (from oral cavity, sinuses), 2. hematogenous seeding (eg from endocarditis or bacteremia), or 3. trauma (including recent surgery)
    • Subacute/chronic otitis media and mastoiditis à inferior temporal lobe, cerebellum
    • Frontal/ethmoid sinuses, dental infections à frontal lobes
    • Hematogenous: often multiple abscesses
  • Micro: Usually will give a clue to the primary source of infection. Can think of it as monomicrobial or polymicrobial, depending on the cause.
    • Think about immune status: immunocompromised hosts (HIV/AIDs, neutropenic, on immunosuppression) are also at risk of TB, fungal, parasitic infections
  • Dx: suggestive MRI/CT findings, CT-guided aspiration or surgery.
    • **If focal s/sx, or imaging c/f mass effect, LP is contraindicated!
  • Check out the attached NEJM review article on brain abscesses for more!

Evernote link: