Category Archives: Morning Report

VA ICU Report 5.26.17

Morning, some good neuro critical care action at the VA this week, thought we’d cover something today not yet covered on the blog: non-invasive estimations of elevated ICP, namely fundoscopy and ocular ultrasound

Dan Reiss correctly pointed out the acute finding in elevated ICP on an ocular ultrasound is the optic nerve sheath diameter, a handful of smaller studies (n in each about 40-60) have evaluated the correlation between nerve sheath diameter and MRI/CT findings of elevated CT, Sensitivity and Specificy depends on the cutoff chosen, in adults typically a ONSD of >4.5mm is considered too high, which yields a sens and spec of around 70-80% for the detection of elevated ICP. The challenge here, as with fundoscopy, is inter-observer variability presumably due to operator characteristics. Here is a review paper on non-invasive determination of ICP.

Other quick pearls

#generally opt for beta blockers and ccb in the acute treatment of hypertensive emergency due to the theoretical concern for cerebral vasodilation with nitro/hydral, nicardipine and esmolol are good options

#PRES, covered elswhere, stands for posterior reversible encephalopathy syndrome, though not always posterior or reversible. Remember, MRI is the diagnostic test for PRES.


VA Intern Report 5.25.17-Last one of the GJ/CVG era!

Big thanks to all the interns who survived intern report out at the VA, what a year. It was a fitting end to the year as we ranged from heat stroke, to cobalt-beer cardiomyopathy, and that was before we even got to the cases! (JK) Anyway here are the top pearls, and thanks again we will miss you guys.

#Cobalt beer cardiomyopathy: We got here by talking about cobalt toxicity in the s/o hip prostheses, not the metallosis associated w/ the hip resurfacing (see here) but acute heart failure! Seems some hearty Quebecois and midwesterners who liked to drink a case of cheap beer after a hard day of work were turning up in acute cardiogenic shock and LV failure. In a case review from 1972 28 patients were profiled, seems that cobalt improves the foamy head of a glass of beer and so was added for aesthetic reasons. It was an old treatment for aplastic anemia because it boosts red cell counts, unfortunately cobalt is toxic to hemoglobin and causes it to tightly bind oxygen, resulting in hypoxia and ischemic injury, it also disrupts the conversion of pyruvate to acetyl-coA (krebs cycle shenanigans) leading to a disruption in oxidative metabolism similar to thiamine deficiency. Needless to say, no more adding cobalt to cheap beer.

#Heat stroke/Heat illness: Something we don’t often cover in inpatient medicine in San Francisco but those of us who will practice in warmer climes (ahem yours truly) should know the basics of the spectrum of heat-related illness. Basics, remember when you are exercising you generate heat. A lot of heat. Heat can be dissipated through evaporation, i.e. sweat evaporates on contact with cooler air which helps cool the skin, conduction direct transfer of heat from a hotter to cooler object, like your fancy “sweat wicking” workout clothes, radiation, heat just flowing as energy from hotter to colder areas of space, and convection, or cold air flowing across a surface absorbing heat continuously. You’ll notice all these processes require that the surrounding temperature is lower than that of the bodies surface and core temperature, when that’s not the case, the potential for ineffective heat removal arises and can progress to the most dangerous stage of heat illness: heat stroke.

Generally to distinguish when the weather is more predisposing to heat illness, we use the wet-bulb globe temperature, which takes into account both ambient air temperature as well as radiant heat (from the sun duh) and humidity. This technique provides a heat index which is more useful than just temperature in determining the safety of participating in outdoor activities. Note that older patients are at risk of developing heat illness at baseline regardless of activity level. The main culprit in the progression of heat related illness is inadequate fluid intake, so staying hydrated is key. You can lose up to 2L of sweat in an hour in a hot enough environment.

Heat exhaustion vs. Heat stroke: The distinguishing factor is a breakdown in thermoregulatory mechanisms, in heat exhaustion you can feel crummy: GI upset, dizziness, maybe even some headache or vertigo, but once you become altered you worry more about heat stroke. Patients with heat stroke actually stop sweating due to volume depletion and peripheral vasoconstriction, a compensatory response to the lowered MAP, unfortunately this eliminates radiation and evaporation as heat removal strategies, and also causes a subsequent spike in core temp, in fact temp > 40.5 plus encephalopathy should raise the suspicion for heat stroke to the top of your list. Early and aggressive fluid resuscitation is key, as well as active cooling.

Interestingly, some younger patients can present diphoretic even though they meet the above criteria for eat stroke, can also present with rhabdo and acute kidney injury, and can even see thermal injury to the myocardium resulting in ST changes and trop elevation!

Above temps of 42 direct cellular injury occurs and multi-organ failure ensues, often resulting in death.

Evaporative cooling is most useful in these settings, constantly changing cool wet blankets or spraying the skin with cool water and placing fans at the bedside is another strategy, cold IV fluids are less effective due to the changes described above. ECMO can be used but is often not practical.


Poaching from Moffitt at VA report. Mini case of a young patient presenting with palpitations with the 1st EKG above.

Several things: Notice the extremely fast rate (>200 BPM!), wide complex, irregularly irregular rhythm, and variable QRS amplitudes and morphologies.

AFIB w/ BBB is certainly on the differential, as is VT (more commonly regular, but can look irregular with fusion/capture beats making their way down the AVN). However, notice how the QRS morphology changes. This makes AFIB w/ BBB less likely. Polymorphic VT is also less likely given that the axis of the QRS complexes does not change with this different beats!

This is a case of AFIB w/ a WPW bypass tract! Treatment of choice? Procainamide which preferentially slows the fast conduction down the bypass tract.

In this case, procainamide failed and cardioversion resulted in the second EKG. Notice the clear delta-waves  in the precordial leads! (Also RBBB morphology that may have been leading to some of the QRS morphology variability in the 1st EKG).

AFIB w/ WPW is a dangerous rhythm that may degenerate into VF.

It is important to recognize as nodal blocking agents should be avoided since it would result in conduction only down the fast bypass pathway and an unstable rhythm!


VA AM Report 5.23.17: Bag o’ Pearls

Credit GJ for the catchy blog title. Today one of our sub-I’s Christina presented a fascinating case of long standing leukopenia/thrombocytopenia along with some neuropathy. We had at least 7 killer pearls so I’m just gonna list them.

#From goop: his own case series of patients admitted for the hated “failure to thrive” diagnosis with gait instability, his most common cause of the dwindles regarding gait and ADL/IADL is painless cervical stenosis(!!!) Other dx that pop up more rarely: early Parkinson dz, ALS, myasthenia gravis

#From LT: In the days prior to . . . NSAIDS? just kidding, patients with ankylosing spondylitis used to get radiation therapy to the spine/pelvis! It worked really well for the pain and progression, but unfortunately the bone marrow in the pelvis took a hit and there are some case series of weird hematologic malignancies arising in these patients 20-30 years after treatment. Worth asking about in your older adults w/ unexplained cytopenias.

#The two-minute hyperthyroidism exam: Credit Dr. Elizabeth Murphy, master clinician at ZSFG for this one. The diagnosis of Graves dz can be made with the exam and positive antibodies, precluding the need for radiouptake of Iodine in the dx workup. The presence of exophthalmos, a thyroid bruit and enlarged thyroid, are specific to the dx of Graves disease. Other things to look for in general, an enlarged painful thyroid argues for an acute thyroiditis, tremor, warm sweaty skin, and overly brisk reflexes.

#All comers, most common cause of elevated MCV and anemia is underlying myelodysplastic syndrome. however MCV > 110 are less likely to be MDS and point more toward megaloblastic anemias aka B12/folate.

#Sometimes patients with reported gait instability can correct their deficit when completely focussed on the task, such as when we ask patients to walk while we watch. Always helpful to watch your patient walk to/from the waiting room, or have them do a task while walking or standing. This attentional instability can point to progressive loss of proprioception or a progressive sensory neuropathy.

#Elevated B12: Rule out exogenous B12, but can also see in acute hepatocellular destruction such as ALI or acute viral hepatitis, long standing think of hematologic malignancy namely the myeloproliferative disorders. LT points out the mechanism, increased expression of and production of transcobalamin which then binds more B12, the assay picks up all B12 not just free B12.

#Greg mentioned POEMS toward the end: Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal gammopathy, and Skin findings. File this under your plasma cell dyscrasia heading. Rare, but in our patient w/ long standing undetectable TSH, polyneuropathy, it came up. Dx criteria (don’t memorize you nerds, keep it on file) are attached below. Thanks gang!


MOFFITT CARDIOLOGY REPORT PEARLS 5/23/17: Digoxin Toxicity and DigiFab!

Hey Everyone! Thanks to Jesse and YY for discussing the case of an elderly man with bradycardia due to possible digoxin toxicity! We also discussed a second case of possible Heyde syndrome and looked at an echo with aortic valve endocarditis. Pearls below focusing on digoxin toxicity:


Top Pearls:

  1. In a patient with a-fib, regularization of a-fib is a sign of digoxin toxicity!
  2. An elevated digoxin level is helpful, but a normal level does not rule out digoxin toxicity!
  3. Digoxin-specific Fab fragments (DigiFab) indicated for unstable arrhythmias, among other indications (see below). Digibind was discontinued in the U.S.


For those who want more info:

Check out Myung’s previous pearls on bradycardia and digoxin toxicity:

A few additional pearls from today’s discussion:

  • In a patient with a-fib, regularization of a-fib is a sign of digoxin toxicity!
  • An elevated digoxin level is helpful, but a normal level does not rule out digoxin toxicity!

Management of digoxin toxicity:

  • CABs, tele, IV access, ECG, finger stick glucose if AMS
  • Digoxin-specific antibody (Fab) fragments (Digibind was discontinued in the U.S. The newer model is called DigiFab! LOVE that name.)
    • See below for recommended indications
  • Atropine can temporize bradyarrhythmias
  • IV fluid can temporize hypotension (caution heart failure)
  • ACLS for life-threatening ventricular arrhythmias

Indications for DigiFab:

  • Life-threatening or hemodynamically unstable arrhythmia
    • VT, VF, asystole, complete heart block, Mobitz II heart block, symptomatic bradycardia
  • Hypotension
  • Hyperkalemia (K>5)
  • End-organ dysfunction (renal failure, AMS)
  • Some advocate treating based on dig level or amount ingested, controversial

More info on DigiFab:

  • Each vial (40 mg) of Fab binds approximately 0.5 mg of digoxin. Dosing is complicated- look it up or discuss with pharmacy! 10 vials initially for ingestion of unknown amount.
  • Side effects = hypotension, phlebitis, hypokalemia, hypersensitivity reaction, serum sickness, and digoxin withdrawal effect can lead to VT or decompensated heart failure.




Have a great day everyone!


ZSFG can’t be MIF’d by penile lesion ddx & indications for sgy in endocarditis

At the General, we give you a little bit of this and a little bit of that in report. And same thing goes for the chiefs’ blog. This is a quick run-through of a few recent legendary reports!


In Neuro Report today, we crushed, I mean discussed, hypercarbic respiratory failure and the role of neuromuscular causes for it. We were joined by neurology guru, Andy Romeo, and here are a few of his pearls:

-Whenever you come across someone reporting dysphagia, make sure to ask about other bulbar sx’s
-In a patient with increased work of breathing in whom you’re considering if diaphragmatic weakness is playing a role, check neck flexor strength to assess if a new neuromuscular weakness is present
MIF & VC are the confrontational tests for the diaphragm. To remind ourselves about those two entities:

  • For Vital capacity (VC) and Mean inspiratory force (MIF), there is the 20-30 rule
  • VC: deep breath and exhalation maximally into spirometer; goal is at least 20cc/kg
  • MIF: inhalation against a closed valve with negative force recorded; goal is “more negative” than -30 cmH20. -60cmH20 is expected or what is associated with weak cough in NL person


In a recent ID report, we discussed the well-known penile lesion ddx and added in a lesser known branch point of the *PRURITIC* penile lesion. The following is a non-exhaustive (and likely with much overlap) summary of what we came up with:

PAINFUL penile lesion

  • Chancroid/H. ducreyi
  • SJS/TEN drug lesion
  • SCC
  • Traumatic lesion/entrapment injury
  • Ulcers in s/o foley
  • HSV
  • Paraphimosis

 PAINLESS penile lesion

  • Syphilis
  • LGV (Of note, the lymphadenopathy *IS* painful in Lymphogranuloma venereum; LGV caused by L1, L2, L3 serovars of Chlamydia trachomatis)
  • Granuloma Inguinale (uncommon infection caused by K. granulomatis)
  • HIV
  • HPV
  • Pearly penile papule

*PRURITIC* penile lesion

  • Fixed drug reaction, DRESS/DHR
  • Yeast
  • Infestation-scabies/pubic lice
  • HSV
  • Behcet’s

 So how do we diagnosis LGV? Does our usual urine test work??????
Lisa Winston teaches us:

Turns out the usual Chalmydia culture or the more commonly ordered/sensitive NAAT test will be positive in LGV as the serovars will be picked up—it just won’t specify that it detected the L1-3 serovars. Usually when the sx’s are classic, empiric tx (longer course) is initiated. If you want a definitive dx, you can talk to colleagues at communicable dz and public health to see if need to send serology or special PCR to the SF public health lab (and then potentially to state’s public health lab or CDC).


Lastly, Mike and Carine presented a patient in intern report with MV endocarditis 2/2 MSSA where we discussed the role of early surgical intervention in infective endocarditis.

There is a fantastic 2013 NEJM Infective Endocarditis review article by Hoen and Duval that breaks down the indications for surgery into three big categories: heart failure, uncontrolled infection, and prevention of embolic events. Or in image form:

indications for sgy

For those of you who want more…

Punag, one of the cardiology fellows, passes on the following for the ACC/AHA class indications for surgical intervention:

Early surgery is recommended for patients with complicated infective endocarditis (IE), but data from randomized trials are scarce. The following are points to remember about the timing of surgery among patients with IE:

  1. The main indications for early surgery in IE are heart failure, uncontrolled infection, and prevention of embolization. The reduction in mortality with surgery is greatest among patients with IE and moderate to severe heart failure.
  2. Heart failure. The European Society of Cardiology (ESC) guideline (2009) recommends emergent surgery for heart failure with refractory pulmonary edema or cardiogenic shock (Class I), or urgent surgery for persistent heart failure with signs of poor hemodynamic tolerance (Class IIa). The American Heart Association (AHA)/American College of Cardiology (ACC) guideline (2014) recommends early surgery for valve dysfunction causing heart failure (Class I).
  3. Uncontrolled infection. The ESC guideline recommends urgent surgery (Class I) for evidence of uncontrolled infection defined as either abscess, fistula, or pseudoaneurysm; or for an enlarging vegetation, persistent fever, or positive blood cultures after 7-10 days of appropriate therapy. The AHA/ACC guideline recommends early surgery (Class I) for evidence of persistent infection, heart block or abscess, or a resistant organism ( aureus, fungi).
  4. Prevention of embolization. The ESC guideline recommends urgent surgery for a vegetation >10 mm with previous embolization or other surgical indication (Class I), or for isolated vegetation >15 mm and feasible valve repair (Class IIb). The AHA/ACC guideline recommends early surgery for recurrent emboli and persistent vegetations despite appropriate antibiotic therapy (Class IIa); or a large mobile vegetation on a native valve (Class IIb).
  5. Neurological complications. Patients with a neurological complication may have other indications for early surgery. However, early surgery may pose a significant risk for perioperative neurological deterioration (related to anticoagulation potentiating the risk of intracerebral bleeding, and to hypotension during cardiopulmonary bypass aggravating neurological ischemia and edema).
  6. Prosthetic valve IE. Prosthetic valve endocarditis is the most serious form of IE, and more difficult to treat using antibiotics alone. In general, current guidelines support consideration of a surgical strategy for high-risk subgroups with prosthetic valve IE, including patients with heart failure, abscess, or persistent fever.
  7. Definitions of early surgery. There is no consensus as to the optimal timing of early surgery. The ESC guideline classifies surgical indications in IE as emergent (within 24 hours), urgent (within a few days), and elective (after 1-2 weeks of antibiotic therapy). The AHA/ACC guideline defines early surgery as occurring during the initial hospitalization and before completion of a full therapeutic course of antibiotics.


Evernote link:


Hoen B, Duval X. Infective Endocarditis. N Engl J Med 2013; 368:1425-1433April 11, 2013DOI: 10.1056/NEJMcp1206782

Ambulatory Report – 5.17.17 – Shin Nodules…Erythema Nodosum!

Thanks to Grant Smith for presenting a case of a 62 yo M h/o questionable SLE presenting with subcutaneous nodules on the shins thought to be Erythema Nodosum with unclear etiology!
  • Turns out this isn’t LT’s first deep dive into EN!  He was already ahead of the curve in 1984.
    • DDC6576B-C1A7-4A62-AE17-199E0C7D8E72
  • As promised, here’s the document to get a FREE version of Visual Dx!  (It’s great for dermatology and more!)
    • Note: you have to be physically present at the VA when doing this, or on the VA VPN.
    • Getting VisualDx
  • We talked a bunch about the Common etiologies of EN vs. the More Uncommon.  Here’s a list of a bunch of those dx’s (Missing from the list below – Pregnancy!)
    • 173C44D6-960C-4DA6-A6C5-0F8FC74233DF
  • When you find a diagnosis of EN, you should send an initial work up (per UpToDate)
    • CBC (to assess for infxn & malig)
    • ESR +/- CRP (elevation sign of systemic dz & widespread inflam)
    • Antistreptolysin O (ASO) titers (repeated 2-4 wks later)
    • CXR (assess for sarcoid, TB, pulm infxn, lymphoma)
    • PPD or Quantiferon

Evernote Link: