“Should I consider cardiac CT angiography in my 76-year-old male patient with chest pain of unclear origin?”  

Probably not!1-4 Although the 2021 AHA/ACC Chest Pain Guidelines have generally widened the scope of indications for cardiac CT angiography (CCTA) to patients at low to intermediate risk of coronary artery disease (CAD) presenting with acute coronary syndrome (ACS)1 (with or without known CAD), several caveats should be considered before ordering this test. In general preference is given to patients with the following characteristics: 

  • Age sixty-five years of age or younger.  Elderly are not ideal candidates for CCTA as the calcium burden may be too high, rendering the test non-diagnostic due to the interference with proper coronary artery lumen assessment. Women tend not to accumulate as much calcium and their age threshold may be increased to 70 years. Some studies like the ROMICAT II Trial extended the age up to 74 years.4 
  • BMI <40.2
  • Sinus rhythm. Atrial fibrillation can be circumvented with expanded padding techniques, albeit at higher radiation exposure.2
  • Without coronary stents, unless their stents are > 3.0 mm in diameter (eg, in left main, very proximal left anterior descending, circumflex or right coronary stents).2
  • Without high coronary calcium burden, or without multiple risk factors for CAD (eg, type 2 diabetes, hypertension, hyperlipidemia) in the setting of typical anginal chest pain.1
  • Other technical requirements: must be able to hold breath during procedure, not have contraindications to beta blockers (ideal heart rate <60 bpm), not have an iodinated contrast allergy, and have stable kidney function.2

Despite these caveats, many patients may still be able to undergo CCTA to help exclude coronary causes of their chest pain.  For example, a 49-year-old patient at low to intermediate risk of CAD presenting with atypical chest pain can potentially undergo CCTA and, if negative, be discharged the same day!4  

In our patient, however, given his older age, CCTA is likely to be non-diagnostic and proceeding to an alternative test, such as stress test or invasive coronary angiography (depending on circumstances and pre-test probability), may be a better option.  

Bonus Pearl: Did you know that, as a “bonus”,  CCTA provides a “free” look at the lungs, calcium score (used largely in asymptomatic patients to help weigh pros and cons of starting a statin)3, and other cardiopulmonary structures that may hint at alternative diagnoses for the cause of chest discomfort and/or dyspnea?

Contributed by Eldin Duderija MD, Cardiologist, Mercy Clinic, St. Louis, Missouri

 

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References:

  1. Gulati M, Levy P, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain. J Am Coll Cardiol. 2021;78:e187–e285. https://pubmed.ncbi.nlm.nih.gov/34709879/
  2. Raff GL, Chinnaiyan KM, Cury RC, Garcia MT, Hecht HS, Hollander JE, O’Neil B, Taylor AJ, Hoffmann U; Society of Cardiovascular Computed Tomography Guidelines Committee. SCCT guidelines on the use of coronary computed tomographic angiography for patients presenting with acute chest pain to the emergency department: a report of the Society of Cardiovascular Computed Tomography Guidelines Committee. J Cardiovasc Comput Tomogr 2014;8:254-71. doi: 10.1016/j.jcct.2014.06.002. Epub 2014 Jun 12. PMID: 25151918. https://pubmed.ncbi.nlm.nih.gov/25151918/
  3. Hecht H, Blaha MJ, Berman DS, Nasir K, Budoff M, Leipsic J, Blankstein R, Narula J, Rumberger J, Shaw LJ. Clinical indications for coronary artery calcium scoring in asymptomatic patients: Expert consensus statement from the Society of Cardiovascular Computed Tomography. J Cardiovasc Comput Tomogr 2017;11:157-168. doi: 10.1016/j.jcct.2017.02.010. Epub 2017 Feb 24. PMID: 28283309. https://pubmed.ncbi.nlm.nih.gov/28283309/
  4. Hoffmann, Udo, et al. “Coronary CT angiography versus standard evaluation in acute chest pain.” N Engl J Med 2012;367:299-308. https://www.nejm.org/doi/full/10.1056/nejmoa1201161

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, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their 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 I consider cardiac CT angiography in my 76-year-old male patient with chest pain of unclear origin?”  

How do I assess the left ventricular (LV) systolic function by bedside point-of-care ultrasound (POCUS)?

You can assess the LV systolic function by POCUS by just zeroing in on the following cardiac parameters: 1. Anterior mitral valve leaflet motion in early diastole; 2. Change in LV chamber diameter; and 3. LV wall thickness during systole.1

First assess the anterior mitral valve leaflet motion towards the interventricular septum in early diastole in the parasternal long axis view (Figure). Estimated or measured distance between anterior mitral valve leaflet and the interventricular septum is called E-point septal separation (EPSS). When LV systolic function is normal, anterior mitral valve leaflet opens fully in early diastole, resulting in a small or minimal separation between it and the interventricular septum. Due to the fixed length of the chordae and the enlarged LV chamber size, anterior mitral valve leaflets are unable to fully open as systolic function worsens. This results in increased separation between the anterior mitral valve leaflet and the interventricular septum. An estimated EPSS greater than 10 mm is considered abnormal and suggests LV dysfunction.1,2

You can also estimate the LV ejection fraction (LVEF) quantitatively  by utilizing the following formula:3

LVEF (%)=75.5 – 2.5xEPSS (mm)

Keep in mind that aortic insufficiency and mitral stenosis can affect the accuracy of this formula.1

As for assessing the LV chamber diameter and wall thickness, recall that these parameters are also dynamic throughout the cardiac cycle. In systole, LV diameter should decrease by 30-40% while LV wall thickness should increase by approximately 40%. Using this as a guide, you can perform qualitative assessment by “eyeballing” the LV systolic function in parasternal long axis, parasternal short axis, apical 4-chamber and subcostal 4-chamber views. Beware that in parasternal long axis, apical 4-chamber and subcostal 4-chamber views, off axis of images can foreshorten the chamber size, resulting in overestimation of systolic function. Also be sure to use the midventricular papillary muscle view when assessing systolic function in the parasternal short axis.1   

Once you have obtained all the necessary images, feel free to categorize the systolic function as either “hyperdynamic”, “normal”, “reduced” or “severely reduced” (watch video below).1

Bonus pearl:  Did you know that qualitative assessment of the LV systolic function  following brief training sessions have been shown to significantly correlate with that obtained by formal echocardiography (k = 0.77, p <0.001).1,4,5 

Contributed by Woo Moon, D.O, Director POCUS Training Program, Mercy-St. Louis Hospital, St. Louis, Missouri

Figure: EPSS in normal vs reduced EF 

Note: EPSS (yellow arrows) is narrow in normal but wide in reduced EF

Video: Four categories of systolic function

 

References

  1. Soni MD MS NJ, Arntfield MD FRCPC R, Kory MD MPA P. Point of Care Ultrasound. 2nd ed. St. Louis, MO: Elsevier; 2019. . https://www.elsevier.com/books/point-of-care-ultrasound/soni/978-0-323-54470-2
  2. Kimura BJ, Yogo N, O’Connell CW, Phan JN, Showalter BK, Wolfson T. Cardiopulmonary limited ultrasound examination for “quick-look” bedside application. Am J Cardiol 2011;108(4):586–90. https://linkinghub.elsevier.com/retrieve/pii/S0002-9149(11)01424-X
  3. Silverstein JR, Laffely NH, Rifkin RD. Quantitative estimation of left ventricular ejection fraction from mitral valve E-point to septal separation and comparison to magnetic resonance imaging. Am J Cardiol 2006;97(1):137–40. https://www.ajconline.org/article/S0002-9149(05)01683-8/fulltext
  4. Melamed R, Sprenkle MD, Ulstad VK, Herzog CA, Leatherman JW. Assessment of left ventricular function by intensivists using hand-held echocardiography. Chest 2009;135(6):1416–20. https://journal.chestnet.org/article/S0012-3692(09)60341-X/fulltext 
  5. Johnson BK, Tierney DM, Rosborough TK, Harris KM, Newell MC. Internal medicine point-of-care ultrasound assessment of left ventricular function correlates with formal echocardiography. J Clin Ultrasound 2016;44(2):92–9. https://onlinelibrary.wiley.com/doi/10.1002/jcu.22272

 

 

 

 

 

 

 

How do I assess the left ventricular (LV) systolic function by bedside point-of-care ultrasound (POCUS)?

My patient presents for evaluation of a mole on her arm. What features of the mole should I look for to help me distinguish a benign mole from melanoma?

Great question! Identifying a melanoma is a lot easier than you might think. A good starting point is the ABCDE criteria, which stands for Asymmetry, Border irregularity, Color variation, Diameter > 6 mm/Dark, and Evolution over time (see Fig 1 below). 1 Higher number of these characteristics in a particular lesion increases the probability of it being melanoma. For example, in the presence of just one characteristic, the positive likelihood ratio (LR) is 1.5 with the probability of melanoma of 7.4%. However, if all five characteristics are present, the positive LR rises to 107, while the probability of melanoma increases to 85%. 2,3,4

Another useful trick is looking for the “ugly duckling sign” (UDS), which refers to any pigmented lesion that appears obviously different than others on a patient’s body.5 For example, let’s say you’re seeing a patient with multiple small, circular, equally-sized moles on his forearm. A few inches away, he has a significantly larger mole with an irregular border. This would qualify as a positive UDS.  While the sensitivities of melanoma recognition are similar for the UDS and the ABCDE criteria (100% and 99%, respectively), the UDS has been shown to significantly improve specificity (88.3%) and accuracy (90.9%) when compared to the ABCDE criteria alone (57.4% and 66.7 %, respectively).6 So incorporating both sets of criteria into your approach to melanoma recognition may be prudent.

Once you suspect a melanoma, your should refer your patient to a dermatologist for an excisional biopsy, the gold standard for melanoma diagnosis.  This procedure consists of excising the entire lesion with 1-3 mm margins.7 The resulting sample can then be used to histologically confirm the diagnosis, prognosticate, and guide management.

Primary care providers play a crucial role in the early detection and treatment of melanoma, so keep your eyes open for any “unusual” looking moles, even if you’re seeing a patient for something unrelated!

Bonus Pearl

Did you know that cardiac involvement with melanoma is not uncommon, affecting an estimated 28% to 56% of patients with metastatic melanoma? 8

 

Figure 1: ABCDE criteria to help differentiate benign skin lesions from melanoma

i

 From Pawan Sonawane, Sahel Shardhul, Raju Mendhe, “Cloud based mobile solution for early detection of Skin Cancer using Artificial Intelligence”, International Journal of Scientific Research in Computer Science, Engineering and Information Technology (IJSRCSEIT), ISSN : 2456-3307, Volume 7 Issue 3, pp. 312-324, May-June 2021. Available at doi : https://doi.org/10.32628/CSEIT217327 Journal URL : https://ijsrcseit.com/CSEIT217327 (https://www.researchgate.net/publication/352394140_Cloud_based_mobile_solution_for_early_detection_of_Skin_Cancer_using_Artificial_Intelligence)

Contributed by Aditya Nellore, 4th year Medical Student, St. Louis University Medical School, St. Louis, Missouri

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References:

  1. Goldsmith SM. Why Is Darkness an Essential Feature for Melanoma Recognition? Skinmed. 2021 Oct 1;19(5):334-336. PMID: 34861912. (https://pubmed.ncbi.nlm.nih.gov/34861912/)
  2. Duarte AF, Sousa-Pinto B, Azevedo LF, Barros AM, Puig S, Malvehy J, Haneke E, Correia O. Clinical ABCDE rule for early melanoma detection. Eur J Dermatol. 2021 Dec 1;31(6):771-778. doi: 10.1684/ejd.2021.4171. PMID: 35107069. (https://pubmed.ncbi.nlm.nih.gov/35107069/)
  3. Thomas L, Tranchand P, Berard F, Secchi T, Colin C, Moulin G. Semiological value of ABCDE criteria in the diagnosis of cutaneous pigmented tumors. Dermatology. 1998;197(1):11-7. doi: 10.1159/000017969. PMID: 9693179. (https://pubmed.ncbi.nlm.nih.gov/9693179/)
  4. Ebell M. Clinical diagnosis of melanoma. Am Fam Physician. 2008 Nov 15;78(10):1205, 1208. PMID: 19035070. (https://pubmed.ncbi.nlm.nih.gov/19035070/)
  5. Gaudy-Marqueste C, Wazaefi Y, Bruneu Y, Triller R, Thomas L, Pellacani G, Malvehy J, Avril MF, Monestier S, Richard MA, Fertil B, Grob JJ. Ugly Duckling Sign as a Major Factor of Efficiency in Melanoma Detection. JAMA Dermatol. 2017 Apr 1;153(4):279-284. doi: 10.1001/jamadermatol.2016.5500. PMID: 28196213. (https://pubmed.ncbi.nlm.nih.gov/28196213/)
  6. Ilyas M, Costello CM, Zhang N, Sharma A. The role of the ugly duckling sign in patient education. J Am Acad Dermatol. 2017 Dec;77(6):1088-1095. doi: 10.1016/j.jaad.2017.06.152. Epub 2017 Sep 28. PMID: 28964538. (https://pubmed.ncbi.nlm.nih.gov/28964538/)
  7. Swetter SM, Tsao H, Bichakjian CK, Curiel-Lewandrowski C, Elder DE, Gershenwald JE, Guild V, Grant-Kels JM, Halpern AC, Johnson TM, Sober AJ, Thompson JA, Wisco OJ, Wyatt S, Hu S, Lamina T. Guidelines of care for the management of primary cutaneous melanoma. J Am Acad Dermatol. 2019 Jan;80(1):208-250. doi: 10.1016/j.jaad.2018.08.055. Epub 2018 Nov 1. PMID: 30392755. (https://pubmed.ncbi.nlm.nih.gov/30392755/)
  8. Goldberg AD, Blankstein R, Padera RF. Tumors metastatic to the heart. Circulation. 2013 Oct 15;128(16):1790-4. doi: 10.1161/CIRCULATIONAHA.112.000790. PMID: 24126323. (https://pubmed.ncbi.nlm.nih.gov/24126323/)

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, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their 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!

 

My patient presents for evaluation of a mole on her arm. What features of the mole should I look for to help me distinguish a benign mole from melanoma?

My elderly hospitalized patient with pneumonia has developed hypoglycemia within days of initiating piperacillin/tazobactam (Zosyn). Is there a connection between piperacillin/tazobactam and hypoglycemia?

Hypoglycemia is a rare (<1%) reported side effect of piperacillin/tazobactam (P/T) [1].  While the exact mechanism is unclear, hypoglycemia in this setting may be related to the adverse impact of P/T on renal function or possibly competitive inhibition of renal organic anion transporter 3 (OAT3).

The association of P/T with acute kidney injury (AKI) is well known. In a retrospective cohort analysis of 11,650 patients, P/T was associated with AKI in 7.8% of patients [2]. Of interest, compared to other antibiotics, P/T has also been shown to delay renal recovery in critically ill patients [3].  Decline in renal function may in turn reduce clearance of insulin and lead to hypoglycemia, particularly in patients who already have risk factors for hypoglycemia, such as malnutrition [4]. This is not surprising because renal clearance accounts for 25% of insulin clearance (rest is hepatic).  

Another plausible mechanism is the impact of P/T on glucose metabolism through competitive inhibition of OAT3 [5]. OAT3 is important in reabsorption of gluconeogenic precursors as well as excretion of uremic metabolites [6], which may further dysregulate hepatic gluconeogenesis and precipitate hypoglycemia. Fascinating!

Bonus pearl: Did you know that elderly patients may be at risk of reactive (post-prandial) hypoglycemia particularly in the setting of pre-diabetes or diabetes due to loss of coordination between glucose load and insulin secretion [7]? 

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Contributed by Michael Nance, MD, PhD, Department of Medicine, Mercy Hospital-St. Louis, St. Louis, Missouri

References:

  1. Wyeth Pharmaceutical Inc. Zosyn (piperacillin/tazobactam) [package insert]. U.S. Food and Drug Administration website. https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/050684s88s89s90_050750s37s38s39lbl.pdf. Revised May 2017. Accessed January 16, 2021.
  2. Rutter WC, Burgess DR, Talbert JC, Burgess DS. Acute kidney injury in patients treated with vancomycin and piperacillin-tazobactam: A retrospective cohort analysis. J Hosp Med. 2017 Feb;12(2):77-82. doi: 10.12788/jhm.2684. PMID: 28182801; PMCID: PMC5573255. https://pubmed.ncbi.nlm.nih.gov/28182801/
  3. Jensen JS, Hein L, Lundgren B, et al. Kidney failure related to broad-spectrum antibiotics in critically ill patients: secondary end point results from a 1200 patient randomised trial. BMJ Open 2012;2:doi: 10.1136/bmjopen-2011-000635  https://bmjopen.bmj.com/content/2/2/e000635
  4. Leibovitz E, Adler H, Giryes S, Ditch M, Burg NF, Boaz M. Malnutrition risk is associated with hypoglycemia among general population admitted to internal medicine units. Results from the MENU study. Eur J Clin Nutr. 2018 Jun;72(6):888-893. doi: 10.1038/s41430-018-0143-9. Epub 2018 Mar 27. PMID: 29588529. https://pubmed.ncbi.nlm.nih.gov/29588529/
  5. Wen S, Wang C, Duan Y, Huo X, Meng Q, Liu Z, Yang S, Zhu Y, Sun H, Ma X, Yang S, Liu K. OAT1 and OAT3 also mediate the drug-drug interaction between piperacillin and tazobactam. Int J Pharm. 2018 Feb 15;537(1-2):172-182. doi: 10.1016/j.ijpharm.2017.12.037. Epub 2017 Dec 23. PMID: 29277663. https://pubmed.ncbi.nlm.nih.gov/29277663/
  6. Wu, W., Bush, K.T. & Nigam, S.K. Key Role for the Organic Anion Transporters, OAT1 and OAT3, in the in vivoHandling of Uremic Toxins and Solutes. Sci Rep 7, 4939 (2017). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5504054/
  7. Tamura Y, Araki A, Chiba Y, Horiuchi T, Mori S, Hosoi T. Postprandial reactive hypoglycemia in an oldest-old patient effectively treated with low-dose acarbose. Endocr J. 2006 Dec;53(6):767-71. doi: 10.1507/endocrj.k05-140. Epub 2006 Sep 12. PMID: 16966825. https://pubmed.ncbi.nlm.nih.gov/16966825/ 

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, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their 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!

My elderly hospitalized patient with pneumonia has developed hypoglycemia within days of initiating piperacillin/tazobactam (Zosyn). Is there a connection between piperacillin/tazobactam and hypoglycemia?

Is there a connection between eosinophils and sickle cell anemia?

Patients with sickle cell anemia (SCA) frequently (~55%) demonstrate absolute eosinophil count (AEC) (>450 cells/uL) during non-crisis steady state without significant change during sickle cell crisis [1-4]. Although the exact mechanism for this finding is not clear, it may be related to elevated plasma levels of circulating factors such as eotaxin, IL-5, and GM-CSF in SCA [2,3].

Cumulative data from 3 independent cross-sectional studies involving 131 SCA patients reported a mean AEC of ~498 cells/u (range 490-504 cells/uL) when not in crisis [2,3,6]. Surprisingly, two additional studies evaluating 200 patients did not observe a significant difference in AEC between steady- and crisis-states [1,4].

The significance of elevated AEC in patients with SCA is unclear. Of interest, several studies of eosinophils isolated from patients with SCA have demonstrated increased eosinophil adhesion to blood vessels, degranulation, and reactive oxygen species production compared to healthy controls [5,6]. In another study, hydroxyurea was shown to reduce eosinophil adhesion and degranulation [2].

While it is unknown whether eosinophils directly contribute to the development of vaso-occlusive crisis, these studies suggest eosinophils may be an important therapeutic target in SCA. 

Bonus pearl: Did you know that low eosinophil count may help predict infection in SCA patients? A retrospective study of SCA patients with and without infection showed that relative eosinopenia (0.025 compared to 0.2 x 109 cells/L) was highly sensitive (100%) and specific (93.3%) for infection [7].

Contributed by Michael Nance MD, PhD, Department of Medicine, Mercy Hospital-St. Louis, St. Louis, Missouri

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References:

  1. Ekeke GI. Sickle cell disease: some haematological changes in steady state and crisis. Biomed Biochem Acta 1987; 46:S197-S201. https://pubmed.ncbi.nlm.nih.gov/3593298/
  2. Pallis FR, Nicola Conran, Kleber Yotsumoto Fertrin, Sara T. Olalla-Saad, Fernando Ferreira Costa, Carla Fernanda Franco-Penteado; Altered Functional Properties of Eosinophils In Sickle Cell Anemia and Effects of Hydroxyurea Therapy. Blood 2010; 116 (21): 2656. https://doi.org/10.1182/blood.V116.21.2656.2656
  3. Conran N, Saad ST, Costa FF, Ikuta T. Leukocyte numbers correlate with plasma levels of granulocyte-macrophage colony-stimulating factor in sickle cell disease. Ann Hematol. 2007; 86(4):255-261. https://pubmed.ncbi.nlm.nih.gov/17205286/
  4. Klouda T, Raybagkar D, Bernstein B, Apollonsky N, “Changes in Blood Profile from Steady State in Patients with Sickle Cell Anemia Admitted for Vaso-occlusive Crisis and Acute Chest Syndrome”, Advances in Hematology, vol. 2020, Article ID 3656717, 5 pages, 2020. https://doi.org/10.1155/2020/3656717
  5. Canalli AA, Conran N, Fattori A, Saad ST, Costa FF. Increased adhesive properties of eosinophils in sickle cell disease. Exp Hematol. 2004; 32(8):728-734. https://pubmed.ncbi.nlm.nih.gov/15308324/
  6. Pallis FR, Conran N, Fertrin KY, Olalla Saad ST, Costa FF, Franco-Penteado CF. Hydroxycarbamide reduces eosinophil adhesion and degranulation in sickle cell anaemia patients. Br J Haematol. 2014; 164(2):286-295. https://pubmed.ncbi.nlm.nih.gov/24383847/
  7. Ahmed, SG and Uraka, A. Eosinopenia as a marker of infection in patients with sickle cell anemia: A preliminary report. Int. J. Biomed. Health Sci. 2010. 6(1):57-61. http://www.ojs.klobexjournals.com/index.php/ijbhs/article/viewFile/671/741

 

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, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their 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!

Is there a connection between eosinophils and sickle cell anemia?

Can I have some tips on how to improve my PowerPoint presentation?

Effective or “high value” PowerPoint presentations take some planning and work. Here are some tips (by no means comprehensive) on how you can improve your PowerPoint presentation,1-4 divided into 4 stages:

Stage I: Planning for your talk

    • “Know your stuff”
    • Prioritize the main objectives of your talk given time  constraints ie, “What would you like your audience to really take away from your talk?”
    • Accept the fact that you will not be able to cover all that you know about the topic during the allotted time
    • Think about how you might keep your audience engaged throughout your talk as you introduce topics and concepts!

Stage II: Preparing your slides

  1. General rules
    • Keep them simple (“Less is more”)
      • Minimize number of slides eg, average no more than 1 slide/min
      • Minimize number of concepts/slide eg,1/slide
      • Minimize clutter 
    • Avoid “apologetic” slides ie, if not easily readable or visible or “too busy”, don’t use them!
    • Practice, practice, practice and edit as needed
  2.  Text
    • Minimize number of words/slide eg, 6×6 rule, maximum 6 words/line, 6 lines/slide
    • Use easily readable font types and sizes
      1. Minimum 24 for small rooms
      2. Minimum 36 for larger rooms
      3. If not readable 10 feet away from monitor, don’t include
    • Check spelling!
    • Choose high contrast colors between background and text eg, black text on white, yellow on dark blue background, not red on green
  3. Tables
    • Avoid reproduction of large tables with tons of data that cannot be read or can easily overwhelm the audience
    • If you use large tables, zero in on a particular section and display a magnified version of that section so that the audience can follow along with you

Stage III: Presenting your talk

  • Remember, you are the presenter, not PowerPoint
  • Engage the audience from the beginning to the end
    • Beginning: Use a “hook” ie, why should the audience be interested in your talk?
    • During
      • Maintain eye contact with the audience
      • Be dynamic/animate
      • Use speech intonations as if you are having a conversation with the audience
      • Do not read slides word-by-word
    • End: Highlight your take-home points eg, “if you don’t remember anything else…”

Stage IV: Post-Presentation

  • Ask for feedback from colleagues, audience, coordinators, etc… 
  • Self-reflect ie, what went well, what didn’t go so well?
  • Apply lessons learned to your next PowerPoint presentation!

Five take-home points for this pearl

  • Less is more, keep your presentation clear and simple
  • Time is limited; prioritize your message
  • Keep your audience engaged throughout the talk
  • Conclude with take-home points
  • Practice, practice, practice

Bonus Pearl: Did you know that people generally remember 20% of what they hear, 30% of what they see, and 50% of what they see and hear? 2

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References

  1. Collins J, et al. Evaluation of speakers at a national radiology continuing medical education course. Med Educ Online 2002;7:17 https://pubmed.ncbi.nlm.nih.gov/28253766/ 
  2. Collins J. Education techniques for lifelong learning. RadioGraphics 2004;24:1177-83. https://pubmed.ncbi.nlm.nih.gov/15256637/ 
  3. Harolds JA. Tips for giving a memorable presentation, Part IV. Using and composing PowerPoint slides. Current Nuclear Medicine 2012;37:977-80. https://pubmed.ncbi.nlm.nih.gov/22899205/ 
  4. Grech V. WASP (write a scientific paper):Optimization of PowerPoint presentations and skills. Early Human Development 2018;125:53-56.https://pubmed.ncbi.nlm.nih.gov/29929910/ 

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, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their 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!

Can I have some tips on how to improve my PowerPoint presentation?

Why doesn’t my patient with lactic acidosis have hyperkalemia?

Although hyperkalemia may be observed in a variety of conditions associated with metabolic acidosis, it is less likely to be seen in conditions associated with excess organic acids (eg, in lactic acidosis or diabetic ketoacidosis). A likely explanation for this finding revolves around the amazing organic anion transporter (OAT) and its attendant role in counteracting hyperkalemia by bringing potassium (K+) back into the cells.1-5 See details of impact of extracellular and intracellular pH on K+ homeostasis in Figure.1 

Recall that in metabolic acidosis the increased concentration of hydrogen ion (H+) outside the cell reduces sodium (Na+) influx into cells through the Na+-H+ exchange channel resulting in a drop in the intracellular Na+.  Since the Na+K+ATPase ion channel depends on the intracellular Na+ for bringing K+ into the cells, the end-result is higher K+ concentrations in the extracellular space, potentially resulting in hyperkalemia.  This is what is often seen in conditions of mineral (non-organic) acid excess (eg, in respiratory acidosis or poor renal function).

In the case of organic acidosis, however, the OAT also plays an important factor in K+ homeostasis (Figure)1.  As the name suggests, this transporter allows  organic acids such as lactic acid or ketones to enter the cell. As the H+ concentration increases intracellularly, there is more Na+-H+ exchange and more influx of Na+ into the cell.  More available Na+ intracellularly means more Na+ is pumped out by Na+K+ATPase, and more K+ is brought into the cell,1-5 mitigating the impact of metabolic acidosis on K+ efflux into the  extracellular space and potentially even causing hypokalemia! 

Concurrent hyperkalemia and lactic acidosis or diabetic ketoacidosis may of course still occur.  However, in such cases, hyperkalemia is often due to an epiphenomenon related to complicating factors.  In the case of lactic acidosis, this may be related to concurrent renal dysfunction,3 while in diabetic ketoacidosis it may be related to hyperosmolarity or insulin deficiency.1

So next time you see a patient who has hyperkalemia and lactic acidosis, ask yourself  “What else am I missing that can explain the hyperkalemia?“.

Bonus Pearl

Did you know that lactic acid in human blood was first discovered by the German physician–chemist, Johann Joseph Sherer, who sampled post-mortem blood from 2 women who died of puerperal fever in 1843? 6

Contributed by Nabi Chaudhri-Martinez MD, Mercy Hospital-St. Louis, St. Louis, Missouri

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References:

  1. Aronson PS, Giebisch G. Effects of pH on potassium: new explanations for old observations. J Am Soc Nephrol. 2011 Nov;22(11):1981-9. doi: 10.1681/ASN.2011040414. Epub 2011 Oct 6. PMID: 21980112; PMCID: PMC3231780. https://jasn.asnjournals.org/content/22/11/1981.long
  2. Orringer CE, Eustace JC, Wunsch CD, Gardner LB. Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated with hyperkalemia. N Engl J Med. 1977 Oct 13;297(15):796-9. doi: 10.1056/NEJM197710132971502. PMID: 19702. https://www.nejm.org/doi/10.1056/NEJM197710132971502?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
  3. Fulop M. Serum potassium in lactic acidosis and ketoacidosis. N Engl J Med. 1979 May 10;300(19):1087-9. doi: 10.1056/NEJM197905103001905. PMID: 34793. https://www.nejm.org/doi/10.1056/NEJM197905103001905?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub 0pubmed
  4. Adrogué HJ, Madias NE. Changes in plasma potassium concentration during acute acid-base disturbances. Am J Med. 1981 Sep;71(3):456-67. doi: 10.1016/0002-9343(81)90182-0. PMID: 7025622. https://www.amjmed.com/article/0002-9343(81)90182-0/pdf
  5. Nigam SK, Bush KT, Martovetsky G, et al. The organic anion transporter (OAT) family: A systems biology perspective. Physiol Rev 2015;95:83:123. The Organic Anion Transporter (OAT) Family: A Systems Biology Perspective (physiology.org)
  6. Kompanje EJ, Jansen TC, van der Hoven B, Bakker J. The first demonstration of lactic acid in human blood in shock by Johann Joseph Scherer (1814-1869) in January 1843. Intensive Care Med. 2007;33(11):1967-1971. doi:10.1007/s00134-007-0788-7 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040486/

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, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their 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!

Why doesn’t my patient with lactic acidosis have hyperkalemia?

Does my patient testing positive for hepatitis A IgM really have acute hepatitis A infection even though he is completely asymptomatic?

Not necessarily! A positive hepatitis A (HA) IgM in a patient without any symptoms could indicate a few different things: 1. Asymptomatic infection; 2. Prior HA infection with prolonged IgM presence; 3. False positive results due to cross-reacting antibodies; and 4. Commercial kits with a falsely low cutoff value.1

A 2013 retrospective study found that of patients testing positive for HA IgM antibody, only 11% could be confirmed to have acute HA infection; 57% had recent and/or resolved hepatitis and 29% had reasons to have elevated hepatic enzymes other than HA infection, at least some likely to be false-positive.1

Other viral illnesses and autoimmune conditions have been associated with false positive HA-IgM.1-3  One case report described a patient with malaise, fever, jaundice, and elevated liver enzymes who tested positive for HA-IgM but ultimately was found to be infected with Epstein-Barr virus (EBV)2. In another case report, a patient was described as having a drug-induced liver injury in the setting of infliximab usage. False positive Hep A IgM was suspected to be due to a polyclonal B-cell autoimmune-mediated response stimulated by the infliximab.3

So, even a positive HA-IgM should always be interpreted in the context of the patient’s history and likelihood of active HA infection based on epidemiological factors.1

Bonus Pearl: Did you know that modes of transmission of HA include person-to-person via saliva or sex, consuming raw/undercooked shellfish, or drinking contaminated drinking water?4

Contributed by Joseph Kinsella, Medical Student, A.T. Still Osteopathic Medical School,  Kirksville, Missouri

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References

  1. Alatoom A., Ansari M. Q, Cuthbert J. (2013). Multiple factors contribute to positive results for hepatitis a virus immunoglobulin M antibody. Arch Pathol Lab Med 2013;137:90–95. https://doi.org/10.5858/arpa.2011-0693-oa
  2. Valota M, Thienemann F, Misselwitz B. False-positive serologies for acute hepatitis A and autoimmune hepatitis in a patient with acute Epstein–Barr virus infection. BMJ Case Reports CP 2019;12: e228356.
  3. Tennant E, Post JJ. Production of false-positive immunoglobulin m antibodies to hepatitis a virus in autoimmune events. J Infect Dis 2016;213: 324–325. https://doi.org/10.1093/infdis/jiv417
  4. Mayo Foundation for Medical Education and Research. (2020, August 28). Hepatitis A. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/hepatitis-a/symptoms-causes/syc-20367007.

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!

Does my patient testing positive for hepatitis A IgM really have acute hepatitis A infection even though he is completely asymptomatic?

What’s the evidence that immunocompromised patients need a 3rd booster mRNA Covid vaccine shot?

At this time, the Centers for Disease Control and Prevention (CDC) recommendation for a booster shot of an mRNA vaccine in patients with moderate to severe immunocompromised state (1,2) is based primarily on the concern for waning immunity following the initial series—including a decline in neutralizing antibodies— in this patient population, and the finding that at least some immunocompromised patients may have a significant improvement in certain laboratory measurements of immunity following their booster shot. 

Although there are no randomized-controlled trials of the efficacy of the 3rd shot in protecting against Covid-19 in immunocompromised patients, the recent surge in the highly transmissible SARS-CoV-2 variants in many parts of the world (including the U.S.)  as well as immunocompromised patient population accounting for nearly one-half of all breakthrough Covid-19 cases requiring hospitalization (1) make it urgent to adopt these recommendations. 

A randomized trial involving 120 solid organ transplant patients (median age 67 y) found higher neutralizing antibody levels and SARS CoV-2 specific T-cell counts after the mRNA-1273 (Moderna) vaccine booster dose compared to placebo (3).

In another study involving 101 solid organ transplant patients, of 59 subjects who were seronegative before the 3rd dose, 44% became seropositive 4 weeks after the 3rd vaccine dose ( BNT162b2-Pfizer vaccine administered 2 months after the second dose). Patients who did not have an antibody response were older, had higher degree of immunosuppression and had a lower estimated glomerular filtration rate than those with antibody response (4).

A “spectacular increase” in anti-spike antibodies with levels close to the general population has also been reported among hemodialysis patients receiving a third dose of Pfizer mRNA vaccine (5). 

Until further data from larger studies become available,  these studies support administration of a 3rd dose booster mRNA vaccine in moderate to severely immunosuppressed individuals.

Bonus Pearl: Did you know that although immunocompromised patients have significantly worse influenza outcome, the data on the impact of immunocompromised status on the outcome of Covid-19 is less clear with published evidence that both supports and refutes this association (6)?  

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References

  1. CDC. Data and clinical considerations for additional doses in immunocompromised people: ACIP Meeting, July 22, 2021. ACIP Data and Clinical Considerations for Additional Doses in Immunocompromised People (cdc.gov)
  2. CDC. Interim clinical considerations for use of Covid-19 vaccines currently authorized in the United States. August 13, 2021. Interim Clinical Considerations for Use of COVID-19 Vaccines | CDC
  3. Hall VG, Ferreira VH, Ku T, et al. Randomized trial of a third dose of mRNA-1273 vaccine recipients. N Engl J Med 2021, Aug 11. Randomized Trial of a Third Dose of mRNA-1273 Vaccine in Transplant Recipients | NEJM
  4. Kamar N, Abravanel F, Marion O. Three doses of an mRNA Covid-19 vaccine in solid-organ transplant recipient. N Engl J Med 2021, Aug 12.Three Doses of an mRNA Covid-19 Vaccine in Solid-Organ Transplant Recipients | NEJM
  5. Frantzen L, Thibeaut S, Moussi-Frances J, et al. Covid-19 vaccination in haemodialysis patients: Good things come in threes… Neph Dial Transplant, 20 July 2023. COVID-19 Vaccination in Haemodialysis Patients: Good things come in threes… – PubMed (nih.gov)
  6. Parisi C. An opportunity to better understand the impact of coronavirus on immunocompromised patients. J Infect Dis 2021;224:372-3. Opportunity to Better Understand the Impact of Coronaviruses on Immunocompromised Patients | The Journal of Infectious Diseases | Oxford Academic (oup.com)

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate 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!

What’s the evidence that immunocompromised patients need a 3rd booster mRNA Covid vaccine shot?

What’s the connection between severe hypoglycemia and hypothermia?

The association of severe hypoglycemia and low body temperatures has been well documented at least since 1960s.  Hypothermia is thought to be caused by low blood glucose in the brain (neuroglucopenia) which may serve as a protective mechanism for decreasing energy demand during glucose deprivation.1-2

A 2012 retrospective study involving mostly patients with diabetes mellitus with severe hypoglycemia (majority with serum glucose 18-54 mg/dl) found that 23% of patients had hypothermia (defined as body temperature < 95◦F or 35◦C). The incidence of hypothermia was not affected by age, diabetes, season or time of day.  Two patients had extremely low temperatures (<90◦F).  There was an association between hypothermia and severity of hypoglycemia.1

An older experimental study (1974) involving 36 recumbent nude men in thermoneutral environment found that that insulin-induced hypoglycemia was associated with rectal temperatures below 96.2◦F (36◦C) in 33%.  Cooling was attributed to reduction in heat production and to secretion of sweat, peripheral vasodilatation and hyperventilation.2

But before you attribute hypothermia to hypoglycemia, make sure other causes of hypothermia such as sepsis, hypoadrenalism, hypothyroidism, alcohol and stroke are ruled out.3  

Bonus Pearl: Did you know that heat production is accomplished by shivering, which can increase the normal basal metabolic rate by 2-5 times as well as via non-shivering thermogenesis through increased levels of thyroxine and epinephrine?3

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References

  1. Tran C, Gariani K, Hermann FR, et al. Hypothermia is a frequent sign of severe hypoglycaemia in patients with diabetes. Diab Metab 2012;38:370-72. https://www.sciencedirect.com/science/article/abs/pii/S1262363612000535?via%3Dihub
  2. Strauch BS, Felig P, Baxter JD, et al. Hypothermia in hypoglycemia. JAMA 1969;210:345-46. https://jamanetwork.com/journals/jama/article-abstract/349081
  3. McCullough L, Arora S. Diagnosis and treatment of hypothermia. Am Fam Physician 2004;70:2325-2332. https://www.aafp.org/afp/2004/1215/p2325.html

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!

What’s the connection between severe hypoglycemia and hypothermia?