My elderly nursing home patient is admitted with recent poor oral intake, falls and oral temperatures of 99.1°-99.3° F(37.3°-37.4°C). Is she considered febrile at these temperatures?

Yes! Even though we often think of temperatures of 100.4°F (38° C) or greater as fever, older people often fail to mount an appropriate febrile response despite having a serious infection. 1

Infectious Diseases Society of America (IDSA) guideline on evaluation of fever in older adult residents of long-term care facilities has defined fever in this population as:2

  • Single oral temperature >100° F (>37.8° C) OR
  • Repeated oral temperatures >99° F (>37.2° C) OR
  • Rectal temperatures >99.5° F (>37.5° C) OR
  • Increase in temperature of >2° F (>1.1° C) over the baseline temperature

Even at these lower than traditional thresholds for defining fever, remember that many infected elderly patients may still lack fever. In a study involving bacteremic patients, nearly 40% of those 80 years of age or older did not have fever (defined as maximum temperature over 24 hrs 100° F [37.8°C] or greater).3  

So our patient meets the criteria for fever as suggested by IDSA guidelines and, particularly in light of her recent poor intake and falls, may need evaluation for a systemic source of infection.

Bonus Pearl: Did you know that blunted febrile response of the aged to infections may be related to the inability of cytokines (eg, IL-1) to reach the central nervous system?1

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References 

  1. Norman DC. Fever in the elderly. Clin Infect Dis 2000;31:148-51. https://academic.oup.com/cid/article/31/1/148/318030
  2. High KP, Bradley SF, Gravenstein S, et al. Clinical practice guidelines for the evaluation of fever and infection in older adult residents of long-term care facilities: 2008 update by the Infectious Disease Society of America. Clin Infect Dis 2009;48:149-71. http://www.idsociety.org/uploadedFiles/IDSA/Guidelines-Patient_Care/PDF_Library/Fever%20and%20Long%20Term%20Care.pdf
  3. Manian FA. Fever, abnormal white blood cell count, neutrophilia, and elevated serum C-reactive protein in adult hospitalized patients with bacteremia. South Med J 2012;105;474-78. http://europepmc.org/abstract/med/22948327

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers, Mass General Hospital, Harvard Medical School or its affiliated institutions. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My elderly nursing home patient is admitted with recent poor oral intake, falls and oral temperatures of 99.1°-99.3° F(37.3°-37.4°C). Is she considered febrile at these temperatures?

My patient with COPD has new clubbing of his finger tips. What is the mechanism of clubbing?

The mechanism behind digital clubbing has yet to be fully elucidated, with hypotheses ranging from a circulating vasodilator, tissue hypoxia, a neurocirculatory reflex, and genetic factors. 1 Although hypoxemia is often cited as a cause of clubbing, it is often absent in the presence of clubbing and many patients with hypoxemia do not have clubbing.

A potentially unifying pathophysiologic mechanism of clubbing revolves around platelet clustering and associated growth factor release. 2.3 Platelet clumps/megakaryocytes—either because of circumvention of the lung capillary network (eg, in intracardiac shunts or lung cancer) or increased production (eg, in left-sided endocarditis or chronic inflammatory conditions)—may wedge in the fine vasculature of distal fingertips or toes and cause release of platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF).

Together, PDGF and VEGF promote neovascularization, increase vessel dilation and permeability, and modify connective tissue to create the distinct club-like appearance. Local hypoxic condition from reduced capillary perfusion is thought to further stimulate the release of these growth factors.

Potential causes of clubbing in our patient include lung cancer, interstitial lung disease, bronchiectasis, core pulmonale and secondary polycythemia, among many others. 1

Fun Fact: Did you know that clubbing, also known as “Hippocratic finger”, was first described by Hippocrates in a patient with chronic empyema (don’t ask how chronic empyema was diagnosed in 400 BC!)?1

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References

  1. McPhee SJ. Clubbing. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths;1990. Chapter 44. Available from https://www.ncbi.nlm.nih.gov/books/NBK366/
  2. Dickinson CJ, Martin JF. Megakaryocytes and platelet clumps as the cause of finger clubbing. Lancet 1987;2:1434-4. https://www.ncbi.nlm.nih.gov/pubmed/2891996/ 
  3. Atkinson S, Fox SB. Vascular endothelial growth factor (VEGF)-A and platelet-derived growth factor (PDGF) play a central role in the pathogenesis of digital clubbing. J Pathol 2004;203:721-8. https://www.ncbi.nlm.nih.gov/pubmed/15141388

 

Contributed by George Bugarinovic, Medical Student, Harvard Medical School

My patient with COPD has new clubbing of his finger tips. What is the mechanism of clubbing?

Can I rely on the physical exam to rule out symptomatic urinary tract infection (UTI) in my hospitalized patient?

Suprapubic tenderness, costovertebral angle tenderness (CVAT) and fever seem to be more helpful in ruling in than ruling out infection. And, before you hang your hat on the available data, remember that most of the studies involve women with uncomplicated UTI in primary care or emergency department settings, not our older hospitalized patients at risk of complicated infections.  With these caveats in mind….

Suprapubic tenderness has been reported in only about 15-20% of women with acute cystitis. 1

CVAT has been associated with symptomatic UTI but with only a weakly positive LR (1.7, 1.1-2.5), and an insignificant negative LR. 2  In a single center study involving hospitalized patients (mean age 53 y), CVAT was either absent or “obscure” in about 10% of patients with acute pyelonephritis on CT.3

Fever was associated with a positive likelihood ratio (1.6, 1.0-2.6) by 1 systematic study 2 but not another, 4 with insignificant negative LR in both. Fever was also absent in about 10% of hospitalized patients with pyelonephritis in the single center study above.3

So, when evaluating a patient with possible symptomatic UTI (particularly cystitis), the presence of physical exam findings  may be more helpful than their absence.

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References

  1. Kurowski K. The woman with dysuria. Am Fam Physician 1998, 57:2155-2164. https://www.aafp.org/afp/1998/0501/p2155.html
  2. Bent S, Nallamothu BK, Simel DL, et al. Does this woman have an acute uncomplicated urinary tract infection? JAMA 2002;287:2701-2710. https://www.ncbi.nlm.nih.gov/pubmed/12020306
  3. Lee Y-J, Cho S, Kim SR. Unilateral and bilateral acute pyelonephritis: differences in clinical presentation, progress and outcome. Postgrad Med 2014;90:80-85. https://www.ncbi.nlm.nih.gov/pubmed/24255118
  4. Median-Bombardo D, Jover-Palmer A. Does clinical examination aid in the diagnosis of urinary tract infections in women? A systematic review and meta-analysis. BMC Family Practice 2011;12:111. https://bmcfampract.biomedcentral.com/articles/10.1186/1471-2296-12-111

 

Can I rely on the physical exam to rule out symptomatic urinary tract infection (UTI) in my hospitalized patient?

What should I include in my hospital admission note to meet the criteria for “moderate” or “high-complexity encounter” as defined by the Centers for Medicare & Medicaid Services (CMS)?

Aside from clearly documenting the chief complaint or reason for the encounter to establish medical necessity for your service,  certain history, exam and medical decision making elements in the admission note are required to support your billing.

Level 2 (moderate complexity) and 3 (high complexity) initial hospital care have the same comprehensive history and exam requirements. If a required history or exam element is lacking, the documentation would support a level 1 (low complexity) service. If you are attesting to an admission note by housestaff, make sure these elements are covered in either of your notes. 

A. HISTORY

Comprehensive history requires:
• Chief complaint
• An extended history of present illness 
• Complete (10 or more elements) review of systems
• Past medical, family and social history
Note: Phrases such as ‘family history deferred/unknown’, ‘review of systems as per HPI’ or ‘ROS negative’ are not acceptable substitutes.

B. EXAM

Comprehensive physical exam requires a minimum 8 of 12 organ systems listed below:
o Constitutional
o Eyes
o Ears, nose, mouth and throat
o Cardiovascular
o Respiratory
o Gastrointestinal
o Genitourinary
o Musculoskeletal
o Skin
o Neurological
o Psychological
o Lymphatic/hematologic/immunologic
Note: Body areas such as head, neck or extremities do not qualify as an “organ system”.

C. MEDICAL DECISION MAKING

Requires assessment, clinical impression or diagnosis and the plan for each problem managed.

Reference
https://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNProducts/Downloads/eval-mgmt-serv-guide-ICN006764.pdf 

 

Contributed by Jodie Medeiros CPC, COC, ICDCT-CM, Compliance Analyst & Educator, Mass General Hospital, Boston, MA

 

What should I include in my hospital admission note to meet the criteria for “moderate” or “high-complexity encounter” as defined by the Centers for Medicare & Medicaid Services (CMS)?

My previously healthy 55 year old patient is admitted with a respiratory tract infection and a respiratory rate of 22 breaths/min. Should I be concerned?

Any respiratory rate (RR) greater than 20/min in an adult patient may be cause for concern, particularly in the setting of potentially serious disease and absence of an obvious cause such as pain or fever.

Our patient’s RR is outside the commonly cited normal range of 12-20/min. It indicates increased alveolar ventilation which may in turn be caused by hypoxia, hypercapnea, or metabolic acidosis, all portending possibly poor outcome, if left untreated.It’s no surprise that an abnormal RR is often the first sign of clinical deterioration.2 RR is also the least likely of the vital signs to be affected by polypharmacy (eg, NSAIDs affecting temperature, beta-blockers affecting heart rate and blood pressure). 

Another reason for not dismissing an RR of 22 in our patient is the common practice of guessing rather than measuring the RR by healthcare providers in part likely due to the  more “labor-intensive” nature of measuring RRs compared to other vital signs and lack of appreciation for its importance in assessing severity of disease. 1 Of note, in an experimental study of doctors viewing videos of mock patients, over 50% failed to detect abnormal RR when using the “spot” technique of estimating without a timer.3 Even when presented with a RR of 30/min, over 20% of doctors reported it as normal (12-20/min)!

Final tidbit: Do you want to know what a RR of 20/min really feels like? Take a breath every 3 seconds.  If you are like most, it doesn’t feel “normal”!

References
1. Cretikos MA, Bellomo R, Hillman K. Respiratory rate: the neglected vital sign. MJA 2008;188:657-59. https://www.ncbi.nlm.nih.gov/pubmed/18513176
2. Flenady T, Dwer T, Applegarth J. Accurate respiratory rates count: So should you! Australas Emerg Nurs J 2017; 20:45-47. https://www.ncbi.nlm.nih.gov/pubmed/28073649
3. Philip KEJ, Pack E, Cambiano V et al. The accuracy of respiratory rate assessment by doctors in a London teaching hospital: a cross-sectional study. J Clin Monit Comput2015;29:455-60. https://www.ncbi.nlm.nih.gov/pubmed/25273624

My previously healthy 55 year old patient is admitted with a respiratory tract infection and a respiratory rate of 22 breaths/min. Should I be concerned?

My patient with aortic sclerosis has a loud systolic ejection murmur. What is the exact mechanism of this murmur?

We usually blame cardiac murmurs on the “turbulence” caused by blood flowing past an irregular valve surface but, believe it or not, how the murmur is created has been a matter of controversy. 1-4

For sure, murmurs are generated by disturbance of laminar blood flow (ie, turbulence) but over the years many have argued that turbulence per se fails to produce adequate acoustic force to be audible at the chest wall.2 Although challenged by some,1  the concept of “vortex shedding” borrowed from fluid dynamics is fascinating and has been proposed as a potential explanation.

Per this theory, just as a boulder causes a stream to separate and generate vortices, valves (particularly when abnormal) also create vortices. As the vortices are shed near the valve, they leave in their place relatively calm wakes which are then rapidly filled by flowing blood, creating the sound of a murmur.  

Two important variables in this theory are velocity and viscosity. When the velocity of blood flow increases substantially as in high cardiac output states (eg, fever, pregnancy), vortex shedding and the intensity of the murmur also increase. Similar phenomenon may be expected when the blood viscosity is lowered (eg, in anemia).

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References

  1. Sabbah HN, Stein PD. Turbulent blood flow in humans: Its primary role in the production of ejection murmurs. Circ Res 1976;38: 513-24. https://www.ncbi.nlm.nih.gov/pubmed/1269101
  2. Alpert MA, Systolic murmurs. In Walker HK, Hall WD, Hurst JW. Clinical methods: The history, physical, and laboratory examinations. 3rd ed. Butterworths, Boston, 1990. https://www.ncbi.nlm.nih.gov/books/NBK345/
  3. Bruns D. A general theory of the causes of murmurs in the cardiovascular system. Am J Med 1959;27:360-74. http://www.amjmed.com/article/0002-9343(59)90002-6/fulltext
  4. Guntheroth WG. Innocent murmurs: A suspect diagnosis in non-pregnant adults. Am J Cardiol 2009;104:735-7. https://www.ncbi.nlm.nih.gov/pubmed/19699354
My patient with aortic sclerosis has a loud systolic ejection murmur. What is the exact mechanism of this murmur?

In my critically ill patient with infection, is capillary refill time greater than 2 seconds indicative of septic shock?

The data on the performance of capillary refill time (CRT) in adults is quite limited and what’s available does not suggest that the commonly cited 2 seconds cutoff is useful in assessing peripheral perfusion in critically ill adults1,2.

For example, a large study involving 1000 healthy adults reported that 45% of participants had a CRT > 2 seconds3.  Age also affects CRT with its 95 percentile upper limits reaching 4.5 seconds among healthy adults >60 y old3

Among patients with septic shock, a baseline median CRT of 5 seconds has been reported.  Values <5.0 seconds within 6 hours of treatment of septic shock has also been highly associated with successful resuscitation even before normalization of lactate levels4.

For these reasons, if CRT is used as a measure of peripheral perfusion in critically ill adults, a cut off of 5 seconds, not 2 seconds, may be more appropriate. But just like many other diagnostic tests, CRT should never be interpreted in isolation from other clinical parameters. 

References

  1. Lima A, Bakker J. Clinical Assessment of peripheral circulation. Critical Care 2015:21: 226-31. https://www.ncbi.nlm.nih.gov/pubmed/25827585  
  2. Lewin J, Maconochie I. Capillary refill time in adults. Emerg Med J 2008;25:325-6. https://www.ncbi.nlm.nih.gov/pubmed/18499809
  3. Anderson B, Kelly AM, Kerr D, et al. Impact of patient and environmental factors on capillary refill time in adults. Am J Emerg Med 2008;26:62-65. https://www.ncbi.nlm.nih.gov/pubmed/18082783
  4. Hernandez G, Pedreros C, Veas E, et al. Evolution of peripheral vs metabolic perfusion parameters during septic shock resuscitation. A clinical-physiologic study. J Crit Care 2012;27:283-288.  https://www.ncbi.nlm.nih.gov/pubmed/21798706
In my critically ill patient with infection, is capillary refill time greater than 2 seconds indicative of septic shock?

Should male patients with suspected urinary tract infection routinely undergo a prostate exam?

Yes! That’s because any urinary tract infection (UTI) in men has the potential for prostatic involvement1 —-as high as 83% by one report. 2  

To make the matters more confusing, patients with acute bacterial prostatitis (ABP) often present with symptoms just like those of UTI,  such as urinary frequency, dysuria, malaise, fever, and myalgias. 3  In the elderly, atypical presentation is not uncommon (eg, confusion, incontinence, fall). 4  Under these circumstances, bacteriuria and pyuria may also be related to ABP and the prostate exam should be an important part of your evaluation.

Although the sensitivity of prostate tenderness on digital rectal exam varies widely for ABP (9%-100%), a painful exam should raise suspicion for ABP, and by itself may be an independent predictor for clinical and bacteriologic failure of therapy. 1 Along with tenderness, fluctuance of prostate, particularly in the setting of voiding difficulties and longer duration of symptoms, may also suggest the presence of prostatic abscess. 5,6 

But be gentle when performing a prostate exam and don’t massage it because you could potentially cause bacteremia and worsening of sepsis! 1,7

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References

  1. Etienne M, Chavanet P, Sibert L, et al. Acute bacterial prostatitis: heterogeneity in diagnostic criteria and management. Retrospective multicentric analysis of 371 patients diagnosed with acute prostatitis. BMC Infectious Diseases 2008;8:12. https://bmcinfectdis.biomedcentral.com/track/pdf/10.1186/1471-2334-8-12?site=bmcinfectdis.biomedcentral.com
  2. Ulleryd P, Zackrisson B, Aus G, et al. Prostatic involvement in men with febrile urinary tract infection as measured by serum prostate-specific antigen and transrectal ultrasonography. BJU Int 1999;84:470-4. http://onlinelibrary.wiley.com/doi/10.1046/j.1464-410x.1999.00164.x/pdf
  3. Krieger JN, Nyberg L, Nickel JC. NIH consensus definition and classification. JAMA 1999;282:236-37. http://jamanetwork.com/journals/jama/article-abstract/1030245
  4. Harper M, Fowlis. Management of urinary tract infections in men. Trends in Urology Gynaecology & Sexual Health. January/February 2007. http://onlinelibrary.wiley.com/doi/10.1002/tre.8/pdf
  5. Lee DS, Choe HS, Kim HY, et al. Acute bacterial prostatitis and abscess formation. BMC Urology 2016;16:38. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936164/
  6. Oliveira P, Andrade JA, Porto HC, et al. Diagnosis and treatment of prostatic abscess. International Braz J Urol 2003;29: 30-34. http://www.scielo.br/pdf/ibju/v29n1/v29n1a06.pdf
  7. Lipsky BA, Byren I, Hoey CT. Treatment of bacterial prostatitis. Clin Infect Dis 2010; 50:1641-52. https://academic.oup.com/cid/article/50/12/1641/305217

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Should male patients with suspected urinary tract infection routinely undergo a prostate exam?

Can I assess the severity of aortic stenosis by physical exam alone?

Even in this age of high-tech medicine, physical exam is still a great starting point for assessing the severity of aortic stenosis (AS) even if you are not a skilled cardiologist like most.

Start out by listening over the right clavicle. If you don’t hear a systolic murmur, you can be pretty confident that your patient doesn’t have moderate to severe AS (>98% sensitivity, LR 0.10)1.

After you hear a systolic murmur,  look for combination of findings that may increase the likelihood of moderate to severe AS: slow carotid artery upstroke, reduced carotid artery volume, maximal murmur intensity at the second right intercostal space, and reduced intensity of the second heart sound.  The presence of 3 or 4 of these signs increases the likelihood of moderate to severe AS (LR 40), with less than 3 not helping much1.

When considered individually, many of the signs we often attribute to significant AS2 may not be as helpful in part because most of us are not skilled cardiologists and over the years the cause of AS has changed from primarily rheumatic heart disease-related to that advancing age and valve degeneration3.  

So it may not be surprising that murmur intensity (eg grade 3/6 or above) may have a poor sensitivity and is an unreliable predictor of the severity of AS when patients with left ventricular failure are also studied3.  Remember also that the absence of the 2nd sound may not distinguish between moderate and severe AS4

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References

  1. Etchells E, Glenns V, Shadowitz S, et al. A bedside clinical prediction rule for detecting moderate or severe aortic stenosis. J Gen Intern Med 1998;13:699-704. https://link.springer.com/article/10.1046/j.1525-1497.1998.00207.x
  2. Etchells EE, Bell C. Robb KV. Does this patient have an abnormal systolic murmur? JAMA 1997;277:564-71. https://www.ncbi.nlm.nih.gov/pubmed/10376577
  3. Das P, Pocock C, Chambers J. The patient with a systolic murmur: severe aortic stenosis may be missed during cardiovascular examination. Q J Med 2000;93:685-8. https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/qjmed/93/10/10.1093_qjmed_93.10.685/1/930685.pdf?Expires=1500852139&Signature=TwyO6Z4fUfbPc1yiA~2xZC7jOjed0juH604DshdvRYy~VqeNQ57Sv1yE-LNsImthgQogkawMruBPdXn6PvVCVmdvXxE9QsMzQYhZ13JqXDTQhRiPBcsIBKDdROr~xbz0gp0nv-zEmjCp1M8-CXjrlVnjVtwJ6q2nIPTRW5h-CUOnDAmf8vCeJHRi2M9Dt3a4vGALDJQPaETvxKDfoADamBDtZHzzoCIH3OyXT3–jHRtv9AJI2uHlzN79Vzkh~oIrR-rI5mkHle3Yz0R3qIBY0l4P3PssMng~v-IXMNKS~Ghjav8YFTigHN23aEA5yUYllsC7hR25L6h9PA0SZP3QA__&Key-Pair-Id=APKAIUCZBIA4LVPAVW3Q
  4. Aronow WS, Kronzon I. Prevalence and severity of valvular aortic stenosis determined by Doppler echocardiography and its association with echocardiographic and electrocardiographic left  ventricular hypertrophy and physical signs of aortic stenosis in elderly patients. Am J Cardiol 1991;67:776-7. https://www.ncbi.nlm.nih.gov/pubmed/1826070
Can I assess the severity of aortic stenosis by physical exam alone?

Where should I expect to hear radiation of mitral regurgitation in my patient with endocarditis?

 

Mitral regurgitation (MR) murmur can radiate to several places on the chest wall as well as the spine and….ready for this…. the top of the head!

Classically, MR is thought to have 4 patterns of radiation1,2

  1. Axilla and the inferior angle of the left scapula (typical)
  2. Left sternal border, base of the heart and into the neck
  3. Cervical and lumbar spine (down to sacrum)
  4. Right of the sternum (associated with a “giant left atrium”)

Less well-known and perhaps most intriguing is the radiation of MR to the top of the head. Original reports involved patients who often had ruptured chordae tendineae due to subacute bacterial endocarditis and/or rheumatic heart disease2.

It was posited that “the flail portion of the mitral valve folds back into the left atrial cavity forming a hood which deflects the regurgitant stream against the atrial wall”.  In the setting of a flail anterior leaflet, if the jet stream is sufficiently high energy and comes in contact with the spine, the murmur may be transmitted by bone conduction to the top of the skull2

I suggest you explain to your patient what you are doing before you auscultate the top of their heads!

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References

  1. Chatterjee K. Physical examination. In Topol EJ, ed. Textbook of cardiovascular medicine, 2007, pp 193-224. Lippincott, Williams &Wilkins. Philadelphia. https://books.google.com/books?id=35zSLWyEWbcC&pg=PA219&lpg=PA219&dq=top+of+the+head+mitral+regurgitation+murmur&source=bl&ots=56Erim4eNM&sig=82TrOiU52ojmhVBMG7G2jMULxVo&hl=en&sa=X&ved=0ahUKEwit8_WnmorVAhVGyj4KHcwUC_8Q6AEIRzAF#v=onepage&q=top%20of%20the%20head%20mitral%20regurgitation%20murmur&f=false
  2. Merendino KA, Hessel EA. The “murmur on top of the head” in acquired mitral insufficiency: Pathological and clinical significance. JAMA 1967;199:892-896. http://jamanetwork.com/journals/jama/article-abstract/663746

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Where should I expect to hear radiation of mitral regurgitation in my patient with endocarditis?