All posts by andersodav

Chief Complaints –Gratitude

(a brief preamble: this message might feel like a bit of a throwback since it was originally 10 days prior.  due to some mysterious server snafu, it did not reach you all.  we believe the lines of communication are up and running again, so here you go!  this might explain any of the random praise you’ve received from faculty over the past week…)

 Hello Team,

 Turkey and gravy are quickly followed by navy blue blazers and leather portfolios here at UCSF.   Interview season marks the perfect time to reflect on what makes our program so special.  It is the cumulative impact of your good deeds, big and small, that has created such a rich community.  We wanted to share our appreciation for everything that each one of you does for our program, our patients, and each other, and have included just a sliver of specific examples in this month’s edition of Chief Complaints.  Know that we notice how hard you work, and this generosity of spirit amazes us every day.    

 With gratitude,

Your Loving Chiefs

 VA

#”Shredding” at the VA- If you’ve worked with Dave Anderson, you know that he often uses the verb “to shred” to mean he survived a difficult time and came out victorious (E.g. “Dude, I got shredded during that call night!”). At the VA, we mean it in the old-fashioned sense– we spent a couple weeks piling protected health information in the chiefs’ office after our old shredder bins were removed, but we now have new, beautiful shredders everywhere. Thanks for your patience! #SHREDCITY!

#Wellness Walks- We are SO thankful to Diana Thiara, our fantastic DSARS, who spent an afternoon creating the “Wellness Walks” maps that can found around the VA. There are walks to fit various time and length constraints. We appreciate the reminder of the natural beauty all around us at the VAspa and that self-care can happen even at work!

#New dinner restaurant- Stay tuned for a new restaurant for dinner at the VA in January!!!!! We’re in discussions with several options, and we’ll keep you updated. And don’t give up hope on a new Wednesday lunch option– it’s winding its way through the VA bureaucracy!

#Presents for patriots- Here’s a little secret: did you know the VA has its own convenience store near the cafeteria that is more like a mini Walmart? Also: it has NO sales tax! Here are some of the amazing things they carry– snuggies, sick-nasty train sets for the little ones, Chanel perfume, plasma screen TVs, novelty socks! Hours are extended for the season: 7a-6p Mon-Fri and 8a-4p Saturdays until 1/2018.

SFGH

#Tryptophan From Turkey Got You TiredYou are in luck! Big thanks to Melody and the Dept. of Medicine for supporting the purchase of new couch for the resident’s room. Whether it’s sign-out, post-call rounds, or afternoon teaching, the couch is there to comfort you at all times. Also, thanks for the new white board to make sure this space continues to be used for teaching

 #Gravy on Top-Look up, look up, new cork boards are like a bountiful cornucopia over at ZSFG. Thanks to the Dept of Medicine for getting us some new cork boards to maximize our announcements and make this place feel like home while also helping ensure that all the info you need is but a glance away!

 #Grateful For All of YouShout out to Dawnee Wong for her personal project to make large posters with the facecards of all the IM residents now gracing the halls of ZSFG res room. These photos are awesome and help avoid any confusion about who is who in the res room!

#The Gift of Narcan-The ZSFG Housestaff Incentive Project is UNDERWAY. With the goal of increasing Narcan prescriptions to coincide with any opioid prescription from the discharge pharmacy, we are working to stomp out overdose in the current opioid epidemic.  Thank you to Jessica Wang, Nadine Pardee, Chloe Ciccariello, & intern Shirin Hemmat for leading the charge and to all of the wards teams for their careful attention to the needs of patients with an opiate use disorder and/or pain managed with opioids. 

#Praise from the ChiefSusan Ehrlich, the CEO of ZSFG, shadowed Mike Incze & Timothy Dyster’s wards team on rounds and wrote a hospital-wide memo praising the team’s compassionate approach to patient care. Way to go team!

Moffitt

#Better Recognize:  UCSF Health is pioneering a digitial shout-out platform for the entire organization! Get familiar with recognize.ucsf.edu, which allows you to share praise with any member of your interprofessional care team.

Here are some of our recent medicine residency shoutouts at Moffitt…

 “…to Kenny, who during the very first day of the new interns acted as the senior for all post-call interns – even went beyond by writing notes, doing sign-outs, and being “practice” for ppd placement!  He prophylactically read all notes to learn the patients. He stabilized my sick ICU pt who started bleeding.”

 “To Dr. Huat Lim for helping me today in the ICU with a very sick patient transitioning to comfort care. He helped me lead a family meeting and helped me prepare for the transition to comfort care. He was very supportive and really took the time to educate me and walk me through the process. He is an AWESOME doctor and teacher!”

 “To Muazzum and Salman for coming in on back to back nights to save the CCU team from super-capping!!”

 “Ngheim was pulled off of his procedure service month onto our service right before starting LTU, which is I’m sure not what he was planning on, but he came onto the team with such a great attitude and willingness to work and to teach the medical students.”

 #HIP-HIP-Hooray-AWOL has taken on a whole new meaning for the #DeleteDelirium brigade.  An enormous shout out to Leslie Suen, Carine Davila, Lev Malevanchik, Connie Wang, Cary Kraft, Serge Gajic, Sharmin Shekarchian, Janet Chu, and Karen Antsey for advocating for APeX upgrades, working to improve interprofessional communication at UBLT meetings, and for providing “gentle nudges” to our wards teams. 

Ambulatory

#GratefulForMyHardWorkingPCP-Shout out to every resident for all the hard work you put into caring for your primary care patients.  You all provide care for >10,000 primary care patients!

 Residency-Wide

#Covered for CAP: A tremendous shoutout to the 38 residents who provided coverage during the first half of the year (not to mention the 33 others who volunteered for the pool)!  Many of you served several times over the course of the month, and we are blown away by your generosity.  We look forward to celebrating the first wave of accomplishments next Wednesday (shoutout-within-a-shoutout to Annsa for organizing)!  

 #Social Kitchen Takeover: Carine Davila & Tyler Mains, thank you for all of the time you’ve poured into recruitment efforts for the Residency Diversity Committee, and to Amanda Wright, Alicia Morehead-Gee, and Sarah Schaeffer for their leadership!  You’ll find many residents, faculty, and applicants hanging out in the window seats at Social Kitchen before the Nopalito dinners—do join!

 

Advertisements

Moffitt Cardiology Pearls 12.5.17 – Sinus Exit Block and Endocarditis

Thank you Nadia (my co-fellow to be next year!!) for presenting an amazing cardiology case with Anne Thorson. She presented the case of a man w/ hx of crack cocaine use and recent strep pneumo meningitis p/w acute SOB found to have a diastolic murmur, PR prolongation, sinus exit block and an perivalvular abscess!! The patient was found to have severe chronic AI and was being evaluated by CT surgery for definitive management while on IV abx. Keep us updated!!

Key Pearls

  1. ECG conduction changes, from first degree AV block to complete heart block, are associated with increased mortality in patients with known endocarditis (Am Heart J 2001;142:280-5.)
  2. See this study in the American Heart Journal for more information about conduction abnormalities and endocarditis (remember that these will occur at the level of AV node).
  3. See Figure below for more information on sinus exit block.

For more information see – https://lifeinthefastlane.com/ecg-library/sa-exit-block/

 

Cardiology Pearls 11.28.17

Thank you to Arvind for presenting one of the most fascinating cards cases all year! We discussed the case of a young man who had a family history of SCD presenting after collapsing while exercising. The patient received immediate BLS in the field and was found to be in monomorphic VT. He was brought into the hospital and after extensive w/u was found with the help of molecular medicine to have monomorphic VT from a LV foci 2/2 to a Filamin C mutation!!  He is s/p ICD placement and EP study w/ ablation of a LV apex foci (location diagnosed based on the ECG!) WHATTTTT!!!

Key Pearls

  1. Unlike the European guidelines, the AHA does NOT recommend routine ECG in the screening of athletes prior to exercise. Instead focus on personal and family history in addition to exam (see table below).
  2. The most common arrhythmia in HCOM is atrial in etiology!
  3. See below for approach to SCD in the young patient and current understanding of incidence. These are likely to change with new postmortem data coming out of UCSF.
  4. For patient with refractory VT storm (already on 2 agents – lidocaine, amiodarone or procainamide) it is important to maximize sedation to limit the adrenergic drive that may be contributing to recurrent arrthymias.
  5. The autosomal dominate early stop mutation in the protein Filamin C (FLNC gene) can casue an overlapping phenotype of dilated and left-dominant arrhythmogenic cardiomyopathies complicated by frequent premature sudden death (more details via Vaibhav and attachment below)

A high yield summary of Filamin C (see attachment for more details):

-Filamin C is a large and major structural protein essential for sarcomere attachment and has been associated with myofibrillar myopathies and cardiac involvement has been reported

– Filamin C has an N terminal with an Actin-binding domain and a C-terminus that binds to integrins and potentially other cellular signaling proteins

– In this case, although there is not definitive loss of cardiac function or evidence of skeletal muscle dysfunction, this is more often the finding and and example of mutations in filamin c leading to cardiomyopathy is in the family case review (Valdez-Mas). It is important to note that this type of dysfunction could occur in the future though.

– Finally, the mechanism of cellular dysfunction could be linked to protein aggregation (Schroder et al) leading to overall myocyte dysfunction (Dalkilic et al)

 

APPROACH TO SCD



Figure. Distribution of cardiovascular causes of sudden death in 1435 young competitive athletes. From the Minneapolis Heart Institute Foundation Registry, 1980 to 2005. ARVC indicates arrhythmogenic right ventricular cardiomyopathy; AS, aortic stenosis; CAD, coronary artery disease; C-M, cardiomyopathy; HD, heart disease; LAD, left anterior descending; LVH, left ventricular hypertrophy; and MVP, mitral valve prolapse.

From AHA Guidelines – A positive response or finding in any one of the following categories should prompt further cardiac evaluation by a cardiologist (in this patient the family history should have prompted evaluation for example, however may not have changed the outcome given normal ECG and TTE).

https://www.evernote.com/shard/s307/sh/a6c959bf-08b9-415c-8363-c3b2ebba7bd8/31b9cb4cb1230c43627982833a81db37

Moffitt Renal Report Pearls– 11.17.17

Thank you to HH and Katie for co-presenting a case of a young woman with T1DM, CKD presenting with a severe non-anion gap metabolic acidosis with a pH of 7 and a Bicarb of 6! Overall, it was felt that her initial presentation was 2/2 to a mix of GI losses given her profound diarrhea and renal losses of bicarb in early renal dysfunction.

Key Pearls:

  1. When calculating the serum anion gap, there’s no need to correct serum sodium for hyperglycemia. The osmotic pull of water would dilute all of the electrolytes in an equal manner, so the sodium, potassium, and chloride are all relatively dilute, and the anion gap calculation would not change.
  2. When trying to determine where a patient is losing bicarbonate – you can calculate a urine anion gap UAG – see more below.
  3. In a patient with normally functioning kidneys, they will secrete ketones in their urine. In patients with DKA, this can eventually result in a non-anion gap acidosis.
  1. Remember risk factors for central pontine demyelination with rapid correction > 10 in 24 hours include: very low sodium levels < 110 (in most cases), premenopausal females and severe malnutrition.

Urine Anion Gap (UAG)

Na +  K  –  Cl = Ur Anion Gap (this is calculating unmeasured anions NH4+ primarily)

Interpretation:

  • Assumes that the patient is volume replete (Una > 20) and is without an anion gap acidosis
  • If UAG + in setting of non-gap metabolic acidosis this suggests the kidneys are FAILING to excrete ammonia à renal tubular acidosis
    • DDx: RTAs (see below)
  • If UAG zero or negative, suggests bicarbonate losses from GI tract (this means the kidneys are appropriately getting rid of NH4+ to compensate for acidosis).
    • DDx: GI losses (diarrhea or fistulas), early renal failure& ingestions
  • These labs must be interpreted in the context of patient’s presentation and there are not strict cut-offs.
  • Depending on the severity of the metabolic acidosis, if you have normal kidneys, the urine anion gap should be even more negative (kidney is responding appropriately to excrete NH4+).
  • If you have severe metabolic acidosis, and the urine anion gap is zero or only slightly negative, this suggests a mixed picture – in that there are GI losses, but the kidney’s are not responding as robustly as they should to get rid of NH4+. With excretion of NH4+ the CL- amount increases and this should drive the equation above more and more negative.

Non-Gap Acidosis Ddx

  • GI losses of HCO3- Diarrhea, fistulas/drainage
    • Proximal (Type II): decreased reabsorption & then loss of HCO3-
    • Distal (Type I): defect in H+ excretion (hence profound acidosis)
    • Hypoaldo (Type IV): acidosis 2/2 to inability to excrete acid
  • Early renal failure – impaired generation of NH4+ (this is the KEY to understanding the physiology per above)!
  • Ingestions – acetazolamine, sevelamer, toluene
  • Dilution – rapid infusion of bicarb free IVFs
  • Post-hypocapnia – Rapid correction of respiratory alkalosis -> renal wasting og HCO3 needs to be regenerated
  • RTAs
Location Type Acidosis UAG U pH FeHco3 Serum K
Proximal II Moderate +/- <5.3 > 15% LOW
Distal I Severe + > 5.3 < 3% Variable
Hypoaldo IV Mild + > 5.3 < 3% HIGH

 

 

 

Moffitt Pearls – 11/15/17 – VZV Encephalitis

Thank you to Andrew for presenting the case of an elderly man with recent CVA presenting with progressive encephalopathy 2/2 to VZV encephalitis.

Key Pearls

  • Acute toxic-metabolic encephalopathy (TME) is an acute condition of global cerebral dysfunction in the absence of primary structural brain disease
  • Acyclovir neurotoxicity should be considered with new neurological symptoms or encephalopathy 24 hours initiation of treatment, particularly in the presence of renal impairment.
  • Herpes zoster encephalitis (HZE) is an uncommon complication of herpes zoster with immunosuppression (HIV, immunosuppressive medications, increasing age) being the principal risk factor for the development of HZE.
  • Localized zoster can cause CSF pleocytosis and positive VZV PCR despite lack of active CNS infection -> this is b/c neurons are the primary site of latent virus
  • In suspected cases of zoster encephalitis send BOTH VZV PCR and Viral anti-body. The presence of one or both is evidence of small-vessel encephalitis due to VZV.
  • VZV encephalitis is rare and life-threatening-> Empirical treatment with IV Acyclovir 10-30 mg/kg per day for 10 days is currently recommended, however no RTCs have been performed.

The figure below outlines the disease pathology of VZV infection from primary infection to reactivation. See Dr. Gilden’s (a leader in the study of VZV) for an excellent review of VZV in the NEJM – “Neurologic Complications of the Reactivation of Varicella-Zoster Virus.”

VZV Encephalitis

Moffitt Pearls – 11.14.17 – Complete Heart Block and Cardiac Sarcoid

Thanks you, Arvind, for presenting a case of an older man with exercise-induced bradycardia found to have complete heart block 2/2 to cardiac sarcoidosis.

KEY PEARLS:

  1. In the consideration of bradycardia, one must first rule out MI. 15% of patients with an MI will present with complete heart block.
  2. Bradycardia in an inferior or posterior MI is driven by 1) ischemia AND 2) the Bezold-Jarisch Reflex. This is a cardiovascular decompressor reflex involving a marked increase in vagal (parasympathetic) efferent discharge to the heart, elicited by stimulation of chemoreceptors, primarily in the left ventricle.
  3. Complete AV dissociation with Ps faster than SLOW QRSs suggests complete heart block.

Etiology of Bradycardia

Normal:

  • Healthy children/adults during sleep (HRs in 30s, pauses up to 2 seconds may occur)
  • Well-conditioned athletes
  • Some elderly patients

Abnormal:

An easy way to break down bradycardia is into extrinsic vs intrinsic causes.

  • Intrinsic
    1. Idiopathic degenerative d/o
    2. Ischemia (ACS or chronic)
    3. Lyme disease
    4. Viral myocarditis
  • Extrinsic
    1. Drugs – antiarrhythmics, b-blocker, calcium channel blocker
    2. Hypothyroid
    3. Hypothermia
    4. Hypoxia
    5. Vagal tone

 

Evaluation of Patient with Complete Heart Block

  1. Rule out Ischemia – ~15% of patient with an acute MI will have complete heart block (usually RCA)
  2. Check for systemic, reversible causes of heart block:
  • Meds: Digoxin, beta-blockers, calcium channel blockers, or anti-arrhythmics
  • Hypothermia
  • Electrolyte abnormalities – hypokalemia
  • Hypothyroid

3. Look for the primary cardiac causes in 3 broad categories:

  • Infiltrative: Amyloidosis, hemochromatosis, sarcoidosis
  • Inflammatory: SLE, scleroderma
  • Infectious: Rheumatic fever, Chagas, endocarditis, viral myocarditis,i syphilis, Lyme disease

Diagnostic Criteria for Cardiac Sarcoid

cardiac sarcoid

Here is a great JACC review on cardiac Sarcoidosis – http://www.onlinejacc.org/content/68/4/411

https://www.evernote.com/shard/s307/sh/6e60d9c4-b324-47bb-a162-03a79c64cb19/bde254d93bdd9f603bd4e3be123b31f2

Moffitt Pearls – 11.13.17 – Pulmonary Report

Thank you to Dr. Wolters for joining us today and to Tyler for presenting the case of a man w/ hx of SCC on pembrolizumab p/w 2 months of DOE & 1 wk of cough not responsive to levofloxacin. We discussed the role of ABGs > VBGs and the ddx for organizing PNA. The patient ended up having pneumonitis 2/2 to his PD-1 inhibitor which was discontinued and he was then started on steroids.

Key Pearls

  1. There are several toxicities associated with PD-1 inhibitors. See here for prior pearls on these check point inhibitors!
  2. One needs to lose ~ 50% of their lung function to have SOB @ rest!!
  3. Try to obtain an ABG in a patient who is hypercarbic given the variability of a VBG and its estimation of pCO2. Per Dr. Wolter’s the pCO2 from a VBG can be wrong ~ 20% of the time.
  4. Reverse Halo Sign (RHS) on a CT Chest is a patch of normal lung surrounded by abnormal densities . There is a ddx and figure for RHS below!

ABG vs. VBG – Thank you Kenny for sharing!!

Pathophysiology:

  • Arterial: accurate O2 content; nl pH = 7.4 (7.35-7.45), CO2 = 40 (35-45)
  • Venous: carries excess CO2 to be ventilated off in the long. ~3-5 mmHg higher than arterial blood

EvidenceSystemic review and meta analysis

  • Arterial pH ~ 0.03 higher than venous
  • Venous and arterial pCO2 do NOT correlate that well (off in ~ 20% of gases)
  • Good negative predictive value of CO2 if low, but not as helpful if high

Practical application:

  • If you want O2 status, you can use SpO2 as a surrogate marker, but ABG is more accurate
  • If concerned for pH or CO2 status and ABG isn’t easy (ie painful and technically challenging); VBG as 1st pass -> understand limitations
  • If the VBG doesn’t make sense or you want to be totally sure, get an ABG

Organizing PNA

Defined as the lung’s response and subsequent repair to any insult. Often associated with the reverse halo sign (RHS) characterized by a central clearing surrounded by denser air-space consolidation (often ground glass) in the shape of ring/crescent. This happens because in the following situations the lung heals from the center outwards. Was initially described in cryptogenic organizing PNA, however is now part of a wider DDX that includes the following:

  • Autoimmune (Sarcoid, Wegener’s granulomatosis)
  • GVHD
  • Aspiration
  • Malignancy
  • Drug effect – PD-1 Inhibitors à 5% of patient’s will develop pneumonitis @ a mean of 7 months; 85% will respond to discontinuation & steroids.
  • Infectious – endemic fungal infections, PCP PNA,
  • Idiopathic – cryptogenic

Here is a great article and figure on the evaluation of Revere Halo Sign (RHS)RHS--g013

https://www.evernote.com/shard/s307/sh/553ffa9d-b57c-4946-a6ec-8d88fac245ad/9cf66d454abb647c86ed5696e6ee1a42