Microbiology Case Study: A 40 Year Old Man with LVAD Exit Site Pain

Case history

A 40 year old male with a history of cardiomyopathy requiring a left ventricular assist device (LVAD) was seen in clinic with a complaint of pain at the exit site of the LVAD driveline. History is notable for multiple admissions for driveline-associated complications. Despite extensive prior evaluation, cultures and imaging of the driveline exit site had been repeatedly negative with the exception of a methicillin-susceptible Staphylococcus aureus.This was treated with nafcillin, followed by doxycycline for oral suppression. The patient had stopped taking oral antibiotics two months prior to presentation. Imaging revealed a 1.4 cm region around the driveline exit site suggestive of either phlegmon, hematoma, or a developing abscess. Blood cultures and cultures of the driveline exit site were collected and sent to the clinical microbiology laboratory. Upon physical examination, the driveline exit site was tender, but no erythema was noted. The patient endorsed intermittent rust-colored drainage from the site. Blood cultures remained negative for the duration of the patient’s hospital course, and the patient was discharged on nafcillin with plans to transition to doxycycline.

Laboratory identification

The Gram stain of the driveline exit site was unremarkable, with no organisms and few neutrophils seen. Aerobic cultures yielded a light amount of gram positive cocci in addition to mixed skin flora. Colonies were small, and weakly beta hemolytic on blood agar (Image 1A). This organism was catalase- and coagulase-positive, and definitively identified as Staphylococcus aureus by MALDI-TOF MS. Susceptibility testing was performed by broth microdilution, where the organism was determined to be a vancomycin-intermediate Staphylococcus aureus (VISA, MIC=4, Image 1C). Due to the unusual nature of the result, it repeated and confirmed by E-test (Image IB) in our laboratory, and independently verified at our contract reference laboratory. The isolate was also referred to the Texas State Public Health Laboratory where the vancomycin-intermediate phenotype was again confirmed. This isolate was also daptomycin non-susceptible, but remained susceptible to oxacillin, trimethoprim/sulfamethoxazole, linezolid, rifampin, and clindamycin.

Image 1. A. Growth of the weakly beta-hemolytic vancomycin-intermediate S. aureus strain on blood agar. B. Measurement of vancomycin susceptibility by E-test (MIC=4). C. Confirmation of the VISA phenotype by broth microdilution (MIC=4).

Discussion

All models of LVADs require a percutaneous driveline which is a link between the implanted device and the external power source.1In addition to providing power, the driveline also provides controlling and sensing functions for the LVAD.2 The driveline exit site is one of the most common sites of LVAD infection as the driveline creates a conduit for entry of bacteria from the external environment. Additionally, the prosthetic material of the driveline can serve as an ideal substrate for biofilms formation.1 The most common microorganisms associated with LVAD-related infections members of the skin microbiota (i.e. staphylococci), Pseudomonas sp., and enteric bacteria.3

Staphylococcus aureus remains an important human pathogen globally. While antibiotic intervention remains a mainstay of treatment, the emergence of resistance has historically changed the way patients are managed. Mobile genetic elements (including plasmids and transposons) are important mediators of antibiotic resistance in S. aureus, particularly with respect to beta-lactams and glycopeptide antibiotics. Due to the widespread emergence of beta-lactamase conferred penicillin-resistance, semisynthetic penicillinase-resistant penicillins (including methicillin, oxacillin, and nafcillin) were developed for clinical use in the late 1950s. However, resistance to these compounds in S. aureus was reported only a few years following their introduction. Vancomycin became the antibiotic of choice for methicillin-resistant S. aureus (MRSA) therapy in the 1980s, and contemporary management remains largely reliant on this antibiotic despite the recent availability of newer agents from different antibiotic classes.4Thus, vancomycin non-susceptibility among S. aureus isolates is a rare phenomenon with serious clinical implications, with only modest increases in vancomycin MICs resulting in treatment failures.5

The first vancomycin-intermediate S. aureus (VISA) isolate was reported in 1997 in Japan, followed by the first vancomycin-resistant isolate in 2002 in the US.4 It is important to note that the mechanisms driving these two phenotypes are entirely different. The fully vancomycin-resistant phenotype is due to the acquisition of the vanA gene which confers cell wall alterations that prohibit vancomycin from efficiently binding its target. By contrast, the vancomycin-intermediate phenotype remains less well described mechanistically, but VISA strains share similar phenotypic traits. These include: alterations in growth kinetics, increased cell wall thickness, a reduction in peptidoglycan crosslinking, decreased autolysis, altered surface protein profile, and variation of expression levels of global genetic regulators.4,5 These phenotypes are due to mutations and alterations in expression of a number of candidate genes involved in cell wall synthesis, capsule production, and global regulators of virulence.

The emergence of a VISA phenotype is usually found in the setting of MRSA strains that have been treated with prolonged vancomycin therapy.5 However, in this patient’s case, vancomycin had only been utilized infrequently for unrelated infections several years prior. Daptomycin had not previously been used in this patient’s clinical care. This VISA isolate was also oxacillin-susceptible which is a less common finding among reported VISA strains. While exposure of S. aureus to non-glycopeptide antibiotics including beta-lactams can trigger VISA phenotypes in vitro,6 it is currently not possible to elucidate the mechanism underpinning vancomycin non-susceptibility, nor what has driven this resistant phenotype, in this patient’s isolate. The patient currently is doing well on doxycycline suppressive therapy after completing his course of nafcillin, and continues to be monitored through follow-up appointments.

References

  1. Leuck A-M. 2015. Left ventricular assist device driveline infections: recent advances and future goals. Journal of Thoracic Disease 7:2151-2157.
  2. Long B, Robertson J, Koyfman A, Brady W. 2019. Left ventricular assist devices and their complications: A review for emergency clinicians. The American Journal of Emergency Medicine 37:1562-1570.
  3. Zinoviev R, Lippincott CK, Keller SC, Gilotra NA. 2020. In Full Flow: Left Ventricular Assist Device Infections in the Modern Era. Open Forum Infectious Diseases 7.
  4. McGuinness WA, Malachowa N, DeLeo FR. 2017. Vancomycin Resistance in Staphylococcus aureus
The Yale Journal of Biology and Medicine 90:269-281.
  5. Gardete S, Tomasz A. 2014. Mechanisms of vancomycin resistance in Staphylococcus aureus. The Journal of Clinical Investigation 124:2836-2840.
  6. Roch M, Clair P, Renzoni A, Reverdy M-E, Dauwalder O, Bes M, Martra A, Freydière A-M, Laurent F, Reix P, Dumitrescu O, Vandenesch F. 2014. Exposure of Staphylococcus aureus to subinhibitory concentrations of β-lactam antibiotics induces heterogeneous vancomycin-intermediate Staphylococcus aureus. Antimicrobial agents and chemotherapy 58:5306-5314.

-Zoya Khan MS, MLS(ASCP)CM is a medical technologist in the clinical microbiology laboratory at UT Southwestern with almost 10 years’ experience. She received a BS in Medical Technology from Texas Women’s University, and an MS in Clinical Practice Management from Texas Tech Health Science Center. She has an active interest in mycology and laboratory assay verification.

Francesca Lee, MD, is an associate professor in the Departments of Pathology and Internal Medicine (Infectious Diseases) at UT Southwestern Medical Center.

-Andrew Clark, PhD, D(ABMM) is an Assistant Professor at UT Southwestern Medical Center in the Department of Pathology, and Associate Director of the Clements University Hospital microbiology laboratory. He completed a CPEP-accredited postdoctoral fellowship in Medical and Public Health Microbiology at National Institutes of Health, and is interested in antimicrobial susceptibility and anaerobe pathophysiology.

Stable Chimerism Post-Double Cord Transplant

Hello again! The last case study was an example of a patient with a loss of allele at two STR loci on a shared chromosome. Today, I wanted to share an interesting and unusual case that we monitor in our lab. This case explores the use of cord bloods as the source of the donor, and in this case, a double cord blood transplant.

Cord blood (CB) unit transplants can be advantageous over other donor sources, such as bone marrow or peripheral blood. The Leukemia and Lymphoma Society summarizes these advantages well, with some being their availability (CB can be prescreened/tested and then frozen for use when needed – decreasing the risk of disease transmission), less-strict HLA matching requirements, decreased graft versus host disease (GVHD) occurrence and severity, long-term storage (CB over 10 years old has been successfully transplanted), increased diversity of donors, and reduced risk of disease relapse, to name a few.2, 3

CB also has its disadvantages, some include: less stem cells for engraftment which leads to longer engraftment times, these longer engraftment times lead to longer immunological recovery and a higher risk of infection, less available clinical data relative to stem cell and bone marrow transplants (newer procedure comparatively in transplant), and no additional cells for infusions later on in treatment. Further, selecting the best cords for transplant can be challenging due to the static variables of a CB (again, there is no donor to go back and get more cells). Considering all that CB has to offer, haplo-identical transplants are preferred in the U.S. over CB transplants. 2,3,4

Before the University of Minnesota pioneered the strategy of double cord transplants, single cord transplants gave rise to a high incidence of graft failure and transplant related mortality. 2 Double cord transplants have now become standard when utilizing CB as the donor, as a single CB unit contains a small number of required and necessary cells for a successful transplant and double units help overcome the issues that this presents.

Double cord transplants are interesting and complicated for analysis purposes (and in general!). All stem cell transplants involve a dynamic process between the cells of the donor and recipient. Yet, double cords bring in another dynamic process including an additional donor.1,2 Through the chimerism monitoring process, the complexity of the engraftment process can be appreciated as one cord ultimately becomes the “winner” and the other the “loser”. In other words, one engrafts and is detectable, while the other cord fails to engraft and becomes undetectable. Figure 1 demonstrates this process, where both cords are present initially after transplant. Then, at 43 days post-transplant, a single donor cord (D2) engrafts while the other donor cord (D1) does not engraft. D1 is most likely eliminated from the host, potentially explained by multiple theories, and no longer is detectable by chimerism testing.

Figure 1. “D1” (blue) and “D2” (pink) represent donor cord one and two alleles, respectively. “D2R” (green) represent a shared allele among donor cord two and the recipient. Each image is a time lapse of the “D18S51” STR locus post-transplant. Alleles 12, 14, 15, and 19 are present at this locus. At 21 days post-transplant, both donors are present. At 43 days post-transplant and following, only donor 2 is present and alleles 14 and 15 are no longer observed.

In the case study below, the patient was diagnosed with chronic myeloid leukemia and received a double cord transplant in 2014. One would expect, as described above, that one cord would become the “winner” while the other is rejected and becomes the “loser” and becomes undetectable. Interesting enough, this patient never achieved a status of a “winner” or “loser” cord. Rather, both remained persistent within the patient’s chimerism profile and over time have become relatively stable in their percentages.

In the electropherogram below (Figure 2), alleles from both donors can be appreciated from the CD3 (top) and CD33 (bottom) lineages. Each lineage exhibits different constitutions of the donor cord percentages, where CD3 has a greater proportion of cord two than CD33; yet both lineages have a greater overall percentage of cord two than cord one. Looking at the line graph (Figure 3), the differences between the cord percentages can be further appreciated over time. It can even be noted that the cord proportions in the CD33 lineage swapped in 2017, only to swap back to favor cord two and to remain that way since. Changes of donor-recipient relative percentages occur throughout the post-transplant journey and these events are due to complex processes. Some patients become transient mixed chimerisms (who initially are mixed chimerism but later achieve total/complete chimerism), others achieve complete chimerism, and yet others may become stable mixed chimerism. It is important to note that, even in cases where complete chimerism is not achieved, disease remission can still be present.1 In this case, the patient has achieved a stable mixed chimerism status among both donor cords and, to our lab’s knowledge, is doing well clinically.

Figure 2. “D1” (blue) and “D2” (pink) represent donor cord one and two alleles, respectively. Green D1D2R, D2R, and D1D2 represent shared alleles (where “R” represents recipient alleles). Comparing the top (CD3) and bottom (CD33) electropherograms, it can be appreciated that the percentage of each cord is different for each lineage population.
Figure 3. The red line graph on the left depicts the donor percentage of each cord blood unit (CBU) of CD3 lineage over time (11/2016 – 07/2020). It can be appreciated that CBU 2 is the dominant cord for CD3. The blue line graph on the left depicts the donor percentage of each CBU of CD33 lineage over time (11/2016 – 07/2020). It can be appreciated that CBU 2 is also dominant, but the differences between the cord donor percentages are much less compared to that of the CD3 lineage. Also, you can see over time that the two cords are relatively stabilizing in the percentages.

This case brings me back to a memory of my professor, who spoke briefly of this occurrence in a lecture only to quickly admit of its rarity. This is an interesting case because it represents one of those extremely uncommon instances. It is a privilege to be a part of a transplant center, like Northwestern’s, where we can witness rare and unique presentations like this. It opens up opportunities to learn and explore the complexities that transplant medicine and molecular HLA have to offer.

References

  1. Faraci M, Bagnasco F, Leoni M, et al. Evaluation of Chimerism Dynamics after Allogeneic Hematopoietic Stem Cell Transplantation in Children with Nonmalignant Diseases. Biol Blood Marrow Transplant. 2018;24(5):1088-1093. doi:10.1016/j.bbmt.2017.12.801
  2. Gutman JA, Riddell SR, McGoldrick S, Delaney C. Double unit cord blood transplantation: Who wins-and why do we care?. Chimerism. 2010;1(1):21-22. doi:10.4161/chim.1.1.12141
  3. Leukemia & Lymphoma Society. Transplantation Facts.https://www.lls.org/sites/default/files/file_assets/FS2_Cord_Blood_Transplantation_6_16FINAL.pdf. Published May 2016. Accessed December 15, 2020.
  4. Gupta AO, Wagner JE. Umbilical Cord Blood Transplants: Current Status and Evolving Therapies. Front Pediatr. 2020;8:570282. Published 2020 Oct 2. doi:10.3389/fped.2020.570282

-Ben Dahlstrom is a recent graduate of the NorthShore University HealthSystem MLS program. He currently works as a molecular technologist for Northwestern University in their transplant lab, performing HLA typing on bone marrow and solid organ transplants. His interests include microbiology, molecular, immunology, and blood bank.

Microbiology Case Study: A 60 Year Old Male with Dysuria

Case Description

A 60 year old Hispanic male with a past medical history significant for chronic pancreatitis, hypertension and cirrhosis was admitted with decompensated cirrhosis. He underwent paracentesis for ascites and subsequently developed a hematoma as a complication of the procedure which required embolization. During his 12-day long hospital stay, he also developed hypoxia due to volume overload that improved with diuresis. A Foley catheter was placed during his hospital stay which was removed prior to discharge. Weeks later, at a follow up appointment with urology, he complained of dysuria, very little urine during voiding and the sensation of incomplete bladder emptying. A clean catch urine culture was performed and grew >100,000 colonies of Escherichia coli. As shown in Table 1, the isolate was resistant to multiple classes of antibiotics including penicillins, cephalosporins, fluoroquinolones, one aminoglycoside (Tobramycin), Trimethoprim/Sulfamethoxazole, aztreonam and carbapenems (Ertapenem/Meropenem) making this isolate multi-drug resistant (MDR). Because of the resistance profile to the carbapenems, molecular testing for carbapenemase genes was performed and the New Delhi metallo-beta-lactamase (NDM-1) gene was detected. The patient was treated with nitrofurantoin for his symptomatic urinary tract infection (UTI).

Table 1. Antimicrobial susceptibility of this isolate of E. coli.

Discussion

Escherichia coli is a gram negative, motile bacillus that is a normal constituent of the gastrointestinal tract and is one of the most common causes of uncomplicated UTI. Antimicrobial susceptibilities are nearly always performed because the isolates of E. coli can vary in resistance. E. coli do not have any intrinsic resistance to antibiotics other than penicillin; however, they can acquire resistance through numerous mechanisms including structural mutations and plasmid-borne genes that encode enzymes to various classes of antibiotics. One such plasmid-encoded enzyme is the NDM, which was identified in our patient’s isolate. Its resistance is the result of bacterial synthesis of a carbapenemase that deactivates carbapenems by breaking down the beta-lactam ring.1 In the United States, K. pneumoniae carbapenemase (KPC) is the most common, but other types carbapenemase enzymes have also been reported.1,2 NDM is uncommonly isolated in E. coli; it is more often identified in other gram negative bacteria including MDR Pseudomonas aeruginosa or Acinetobacter baumannii complex, which can cause, among other things, devastating nosocomial infections within a healthcare setting. Because these enzymes are on mobile elements, a patient can be colonized with one bacterial strain that carries the plasmid with the carbapenemase on it and transfer a copy of that plasmid to another bacterial strain, thereby conferring new carbapenem resistance to the new bacterium (e.g., P. aeruginosa with the NDM on a plasmid shares that plasmid with an E. coli). Carbapenem resistant Enterobacteriaceae (CRE) are of great importance in healthcare. Carbapenem resistance mediated by enzyme activity (e.g., KPC, NDM, OXA-48, etc), typically confers resistance to all beta lactams. Interestingly, NDM enzymes typically do not destroy aztreonam, a monobactam;3 however, it is common for bacteria to have multiple resistance genes, so NDM carrying strains can be resistant to aztreonam. Although these CRE isolates can cause significant morbidity and mortality when found in clinical samples including sputum or blood, luckily for our patient, he had an uncomplicated UTI and nitrofurantoin was susceptible.

-Limin Yang is a PGY-1 resident in Anatomic and Clinical Pathology at University of Texas Southwestern. She has varied interests including anatomic pathology specialties.

-Dominick Cavuoti is a professor of Anatomic and Clinical Pathology at UT Southwestern and active faculty on both Microbiology and Cytology services.

-Clare McCormick-Baw, MD, PhD is an Assistant Professor of Clinical Microbiology at UT Southwestern in Dallas, Texas. She has a passion for teaching about laboratory medicine in general and the best uses of the microbiology lab in particular.

Will the B.1.1.7 variant evade the Vaccine/Tests?

Will the B.1.1.7 variant evade the vaccine/tests?

This question came up recently and I wanted to share some cutting edge information the addresses this. This was in part adapted from Akiko Iwasaki’s (Yale HHMI immunologist) Twitter discussion of this subject.1

Will B.1.1.7 evade our tests?

The UK variant commonly called lineage B.1.1.7 (officially Variant of Concern 202012/01) has 23 genetic variants that result in 17 protein coding changes.2 Most tests including the ones at our institution (Abbott) are not currently affected (see below). Only the ThermoFisher assay has declared a target that covers the 69-70del variant in the S gene (in green). This conversely makes the TaqPath® assay one way to detect a potential B.1.1.7 variant.

Figure 1. A picture of the SARS-CoV-2 genome with red lines indicating mutation sites and different assays and relative location of their qPCR targets.

Will the vaccine protect against the B.1.1.7 variant?

The Pfizer and Moderna RNA vaccines create an immune response against the spike protein. We don’t know the exact sequences or reactivity of the vaccines’ spike protein. However, a recent study looked at the antibody reactivity to linear epitopes of COVID-19 in 579 patients who were naturally infected with COVID-19. For the antibodies against the spike, the major reactive linear epitopes are indicated in Red at the bottom. None of the B.1.1.7 mutations (Orange) overlap with these major reactive epitopes.3 

Figure taken from Reference 3.

For a closer look, see below.

Figure taken from Reference 3.

A limitation of these analyses is the use of only linear epitopes. Mutations might impact a 3D epitope affecting Ab binding. However, people make multiple antibodies to the spike protein.4 So, broad coverage should arise after exposure to the either the vaccine or natural infection with COVID-19.

The vaccine should induce a polyclonal antibody response that recognizes multiple parts of the spike protein, making it effective, even against novel variants. Also, there should be few to no False Negative COVID-19 tests due to the new variant, but we will continue to monitor and test this experimentally. 

References

  1. Prof. Akiko Iwasaki @VirusesImmunity
  2.  Chand, Meera et al. Investigation of novel SARS-COV-2 variant: Variant of Concern 202012/01 Public Health England.
  3. Haynes WA et al. High-resolution mapping and characterization of epitopes in COVID-19 patients. MedRxiv. https://www.medrxiv.org/content/10.1101/2020.11.23.20235002v1#p-5
  4. Shrock E et al. Viral epitope profiling of COVID-19 patients reveals cross-reactivity and correlates of severity. Science 2020 370(6520). https://science.sciencemag.org/content/370/6520/eabd4250

Jeff SoRelle, MD is Assistant Instructor of Pathology at the University of Texas Southwestern Medical Center in Dallas, TX working in the Next Generation Sequencing lab. His clinical research interests include understanding how lab medicine impacts transgender healthcare and improving genetic variant interpretation. Follow him on Twitter @Jeff_SoRelle.

Cervical Cancer Prevention: The Disparate Reality Across the Globe

One of the most effective public health strategies to date is the development of the pap smear test and its use as a screening tool in cervical cancer prevention. Before the emergence of the pap test, cervical cancer used to be the leading cause of cancer-related deaths for women in the United States.1 However, with effective pap tests screening programs and the availability of the HPV vaccine against high-risk serotypes known to be a major cause of cervical cancer, many developed countries have been able to address this disease with its attendant catastrophic consequences including loss of lives, income and long-term disabilities.

Now, cervical cancer doesn’t even make it as one of the top 10 causes of cancer-related deaths for women in the United States.2 Unfortunately, the progress that has been made with this disease is not a universal one. While many developed countries have made giant strides in addressing this disease burden, most developing countries still grapple with significant morbidities and mortalities attributable to cervical cancer. Recent statistics show that cervical cancer is the second most commonly diagnosed cancer after breast cancer and the third leading cause of cancer death after breast and lung cancers in developing countries.3 In fact, almost 90% of cervical deaths in the world occur in developing countries, with India alone accounting for 25% of the total cases.3 Cervical cancer incidence and mortality rates are highest in sub-Saharan Africa, Central and South America, South-eastern Asia, and Central and Eastern Europe.3 A combination of factors may be responsible for these discrepant findings in developing countries.

First is the lack of effective screening programs that detect precancerous lesions before they become invasive diseases. Unfortunately, this factor is linked to lack of awareness through education and sub-optimal laboratory services that still exists in many of these countries. Laboratory services are scarce and there has been a gradual decline in laboratory professionals. Even if the supplies and equipment needed to run a lab were available, where are the laboratory professionals and pathologists that are needed to provide this critical healthcare service? In addition, a lack of regulatory oversight in some of these countries makes the replication and standardization of results increasingly challenging.

Secondly, is the role of HPV vaccinations in preventing cervical cancer. Many of these developing countries are yet to incorporate routine HPV vaccinations into their vaccination programs and access to these services are still very low. In contrast, many developed countries have made HPV vaccinations available and accessible, which is a major defense against cervical cancer.

Thirdly, is the impact of government policies on laboratory medicine. Pathology and laboratory medicine continue to face cuts in services and compensations, even in developed countries including the United States. These practices impact the ability of laboratory services to deliver optimal results, a scenario that could be even more problematic in developing nations.

As January marks cervical cancer awareness month, public health and policy professionals need to take steps to address the root causes of this problem, in order to proffer sustainable solutions, especially in developing countries. In addition to prioritizing health education and public health campaigns on cervical cancer prevention, the role of effective laboratory services in addressing these challenges also need to be emphasized.

A successful healthcare initiative requires a strong and functioning laboratory system, especially in the 21st century. Any health policy program or public health campaign that fails to recognize this fact is most likely headed for failure before it even starts off.

References

  1. https://www.cdc.gov/cancer/cervical/statistics/index.htm
  2. https://www.cancer.org/research/cancer-facts-statistics/all-cancer-facts-figures/cancer-facts-figures-2020.html
  3. Ferlay J, Soerjomataram I, Ervik M, Dikshit R, Eser S, Mathers C, Rebelo M, Parkin DM, Forman D, Bray F. GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11 [Internet]. Lyon, France: International Agency for Research on Cancer. Available from: http://globocan.iarc.fr, 2013.

-Evi Abada, MD, MS is a Resident Physician in anatomic and clinical pathology at the Wayne State University School of Medicine/Detroit Medical Center in Michigan. She earned her Masters of Science in International Health Policy and Management from Brandeis University in Massachusetts, and is a global health advocate. Dr. Abada has been appointed to serve on the ASCP’s Resident’s Council and was named one of ASCP’S 40 under Forty honorees for the year 2020. You can follow her on twitter @EviAbadaMD.

A Case of Amiodarone Induced Thyrotoxicosis

A 69 year old male presented to the hospital due to worsening back pain and lower extremity weakness.  He had a medical history of follicular thyroid cancer and underwent lobectomy back in 2016. After admission, patient was found to have multiple metastasis of follicular thyroid cancer with lesion in the lumber spine, and his serum thyroglobulin level was elevated at 1,500 ng/mL (1.3 – 31.8 ng/mL) without thyroglobulin antibody detected. Patient did not present hyperthyroidism symptoms. TSH and total T4 were normal, and free T4 was slightly decreased. During hospitalization, patient was prescribed with Amiodarone, to control atrial fibrillation. Amiodarone is an antiarrhythmic drug used for severe ventricular arrhythmias, paroxysmal atrial tachycardia, and atrial fibrillation. It has high content of iodine and a direct toxic effect on thyroid gland, resulting in thyroid dysfunction in 3-5% of patients. In this case, severe hyperthyroidism was observed after amiodarone administration.

Patient’s FT4 level significantly elevated to >5.2 ng/dL (0.9-1.7ng/dL), total T4 was increased to 21.8 ug/dL (4.5-11.7 ug/dL), and TSH was suppressed to below the detection limit. The sudden increase of FT4 suggested Amiodarone induced thyrotoxicosis (AIT). High content of iodine in Amiodarone could raise blood iodine concentration up to 40 folds and enhance thyroid hormone biosynthesis in thyroid cells. This is the main cause of type 1 AIT, which is more common in patients with underlying thyroid diseases, such as Graves’ disease, or autonomous nodular goiter. Type 2 AIT typically happens in patients without underlying thyroid diseases and is caused by a direct toxic effect of amiodarone on thyroid follicular cells. Pre-formed T4 and T3 in thyroid cells are released into the circulation due to destructive thyroiditis in type 2 AIT. Differentiating these two types is important because it has therapeutic implications. However, the distinction may be difficult because patients may have a mixture of both mechanisms. Thyroid function tests are usually not helpful in the differentiation, but ultrasonography and thyroid scan with iodine uptake can help differentiate type 1 from type 2 AIT. 

In this case, thyroid scan with technetium showed reduced thyroid uptake in thyroid lobe, and mild uptake within metastatic lesions, suggesting possible thyroiditis due to amiodarone. Type 2 AIT develops as an inflammatory process and anti-inflammatory glucocorticoids are used in the treatment. Amiodarone was discontinued in this patient and his thyroid function tests indicated improvement of thyroid dysfunction. Amiodarone and its metabolites have a long half-life and accumulate in adipose tissues due to its lipophilic property. Therefore, in some cases, amiodarone toxicity effect can last for months, even after drug withdrawal. To be noted, amiodarone can also induce hypothyroidism, especially in patients with underlying Hashimoto’s thyroiditis or positive antithyroid antibodies.

Xin-small

-Xin Yi, PhD, DABCC, FACB, is a board-certified clinical chemist, currently serving as the Co-director of Clinical Chemistry at Houston Methodist Hospital in Houston, TX and an Assistant Professor of Clinical Pathology and Laboratory Medicine at Weill Cornell Medical College.

A Roller Coaster called 2020

2020 has come to an end. I think we can all agree that it’s been a year like no other! It would be an understatement to say that 2020 has been merely “different.” In the lab, we have seen new things, had new challenges, and, despite the craziness of it all, have learned a few things along the way.

I think the word of the year in our lab and many others for 2020 would be “adaption.” We’ve had to adapt, change our thoughts and processes and be more creative. In the spring, in the first wave of COVID, many labs were struggling with procuring, validating, and performing new COVID tests. With the influx of cases and patients, particularly in some hard hit areas, lab staff were overwhelmed with an unprecedented increase in workload. In the hospital where I work, early on we had very few cases and the lab was impacted in the opposite extreme. With canceled elective surgeries and a huge drop in outpatient work, we found ourselves being asked to take flex time. Workload was down and techs were taking time off to help the lab and hospital adjust to the decreased revenue and to say within budget. Things were pretty slow and calm.

When surgeries resumed and physician offices opened back up, things were busier than ever. Everyone seemed to be coming in for lab work that had been pushed aside for months. In addition to an increased volume in our existing tests, we were bringing on new COVID tests. Procedures had to be written and signed off, validations had to be done and everyone needed to be trained on the new tests. We found ourselves faced with supply issues for the new tests and had to do some juggling acts to get new testing onboard. At the same time, we also had to deal with a lot of other “supply” issues. While the hospital as a whole has done very well to manage PPE distribution, the lab has had to get creative, reaching out to new suppliers for cleaning supplies, lab coats and gloves. Lab coats became and still are very difficult to keep in supply. We’ve gone colorful! We used to have blue gloves and purple lab coats, but now have multi colored gloves and lab coats all over the lab from multiple vendors.

Possibly the worst of our supply issues has been the lack of trained technologists. In a profession that is graduating fewer and fewer new techs, and as our work force is getting older, we have been experiencing a shortage of qualified Medical laboratory Scientists and Technicians across the country for a number of years. This past year, with the current pandemic, we have seen techs who were working way past retirement age decide to finally retire, and others taking early retirement. In the past 5 years I have worked in 2 hospitals that have continuously had revolving open positions. In 2020, om a large number of COVID cases amongst lab staff, but have had a few. We have had many more staff out on quarantine for 2 weeks at a time for exposures, sometimes several at a time. And, after waiting for months with elective surgeries on hold, the minute these were again allowed, we have had several staff on simultaneous leaves of absence for surgeries.

How have we compensated and adapted for these shortages and changes? At a time when visitors have been restricted in the hospital, we have found ourselves with a severe shortage of staff. We are also competing with other hospitals in the area in the same situations so are having a hard time hiring and keeping new employees. We have adapted by conducting Zoom interviews for hiring. We are in the middle of a big chemistry project bringing on new instruments and some of this training has also moved to virtual venues. ASCP and other organizations have held totally virtual conferences and symposiums. But, having been forced to implement these new technologies, we have learned new skills that can be used in the future to broaden our outreach and educational opportunities.

It has been a challenge to train new techs and to simply get the daily work done with ongoing staff shortages. Staffing has been at critical levels. We’ve been resilient. We’ve been creative. We have had to implement an On Call list to help fill critical holes in the schedule. This is not popular, and is still a work in progress, but has helped us to think of other ways to solve the problem at hand. Bonuses for working extra shifts have helped. We have relied on our great technologists to fill in extra shifts. I’m very proud of everyone working together. Team work is helping hold us together and get through this very difficult year!

I think If I had to find any “good” about this pandemic, I’d have to say it’s been the lack of commuter traffic, and the fact that all this talk about COVID testing has shone a little light on our profession. Yet, with all the talk of “testing,” even though the general public has some concept of lab testing, they still know very little about the profession and the people doing these tests. They may recognize the terms PCR, and antigen and antibody but we’re still a hidden profession. What can we all do? Talk about the profession in your community. Community groups, high schools and community colleges often welcome speakers, and now you can even do it online! You’ve all heard people talking about antigens and antibodies and PCR, but you can tell them about the profession and the people who work with these tests every day. It would be very hopeful to say that this pandemic could highlight the Medical Laboratory profession to the point where students would be filling our programs and we’d see a new interest in the field.

Did we ever think this would last this long? in the spring, making hundreds of masks, I thought making holiday masks would be fun. But then I thought to myself, “ I won’t need to make Halloween masks or Christmas masks.” I never thought we’d still be wearing masks at New Year’s! But masks have become so normal that we have even gotten used to them. I took a cold walk a couple days ago and thanked the mask for keeping my face warm!

2020 has had many ups and downs, many challenges. I am proud to say that Medical laboratory professionals have lived up to those challenges and we can and should feel good about our accomplishments and contributions to fighting this pandemic. We’ve been resilient, we’ve adapted and we’ve grown. We’re on a roller coaster ride but we’re still holding on. Hold on tight and wear that mask!

-Becky Socha, MS, MLS(ASCP)CM BB CM graduated from Merrimack College in N. Andover, Massachusetts with a BS in Medical Technology and completed her MS in Clinical Laboratory Sciences at the University of Massachusetts, Lowell. She has worked as a Medical Technologist for over 30 years. She’s worked in all areas of the clinical laboratory, but has a special interest in Hematology and Blood Banking. When she’s not busy being a mad scientist, she can be found outside riding her bicycle.

The Pathology Value Chain and Global Health

In part 1, we reviewed Michael Porter’s Value Chain and looked at inbound logistics for pathology. Now we will turn to operations, or the production of diagnostic results.

In the United States, almost all cancer diagnosis and care are in the private sector. There are very few examples of diagnostic services that are provided for free. Because laboratories derive revenue from every specimen for the most part, there is a natural desire to increase the volume in the laboratory from management because volume equals revenue. Pathology also has inherent economy of scope and scale such that a basic system that could process 1 case per day for an operating cost of $500,000 per year, could process 200 cases per day for a cost of $4,000,000 per year (a 200-fold increase in volume with only a 8-fold increase in cost). It is important to note in this comparison that in the former, the cost per case is $2000 while in the latter it is $80 (a 25-fold difference). When we consider an allocated or operating budget to run a pathology diagnostic laboratory where revenue is not reflected to laboratory management, this desire to increase volume is lacking directly by laboratory staff (more work but no additional funding) but still may be desired by higher level administration for revenues that pay for other aspects of the system (cross-subsidization). Consider a laboratory that is asked to process 25,000 samples per year, has 6 support staff and 3 pathologists. This would equate to each pathologist signing out ~50 cases per day on average, Monday – Friday, with four weeks of vacation annually. If those pathologists are the direct recipients of the profits of the laboratory, such a high case sign-out rate may be acceptable. If they only receive their allotted salary with no potential for profit sharing, they are unlikely to maintain such a high rate of production. Moreover, they will likely demand higher salary and/or additional staff and will do so much more quickly as volumes increase than would pathologists who share in profits. When we transfer this concept to a public low-resourced laboratory setting in a low- and/or middle-income country where government salaries are lower, there are far fewer skilled personnel, and budgets are smaller, there is essentially no incentive for public/government-funded laboratories to increase volume because it results in more work for the existing staff with no benefit. Yet, with the small volumes we see in LMICs currently, their costs per case are much higher than in HICs. When we turn our lens to the patient and that patient’s maximum value, the profit-sharing model is likely to yield the shortest turnaround time for a given patient. There is a trade-off in this scenario between speed of results and amount of communication/coordination between the clinician and the pathologist. Allocated budgets and public laboratories may produce slower results that are of the same technical quality and, in academic settings, may include additional communication/coordination with clinical teams. Standards exist for a maximum turnaround time goal (i.e., for the College of American Pathologists, it is 3 days). Without external regulation and accreditation, laboratories may fail to provide value to the patient by delaying diagnoses until they essentially are useless. Turnaround times in LMICs may be considered “very good” at 2-weeks, a timepoint that would not be sustainable for HICs laboratories.

Operations – This activity “includes procedures for converting raw materials into a finished product or service”. For the lens of maximum value to the patient, from the moment a biopsy is received in the laboratory to the moment a final report is generated should be minimized and the report itself should adhere to quality standards internally and externally. Once all reagents and supplies are obtained and specimens are received, the operations process can be engaged which includes grossing, processing, embedding, microtomy, staining, special stains, immunohistochemistry, case professional review, and report production. In each step of this stepwise process, specific skilled personnel are needed, matched with specific reagents and supplies to complete the step. Laboratory efficiency and product quality can be dually achieved with highly trained personnel, functioning, well-maintained equipment, optimized workflow, continuous communication and data collection, and highly skilled management to control the process wholly and in parts. One of the challenges for HIC pathology laboratories or health systems are large resections (i.e., mastectomies, colectomies, etc.) and autopsies. The former is integral to cancer care for mid-stage cancers to inform margins and guide treatment; however, they require more personnel time to gross, process, and read, more physical resources to dissect and sample, and may have a series of challenges related to “what’s left in the bucket?” that do not occur when a small biopsy is entirely submitted (although standardization of grossing and reporting can often ameliorate this issue). For the latter (i.e., autopsies), the costs of these procedures are extremely high across the board and there is, to date, no reimbursement or payment for this final procedure in a patient’s medical journey. The value of the autopsy has been explained elsewhere but such value to healthcare systems and to individual and groups of patients is often not delineated enough to make these services a priority, unfortunately. Stepping back from operations, what is commonplace in HICs is that large academic center pathology laboratories most often associated with comprehensive cancer centers are evaluating major cancer surgery specimens as well as autopsies while their private practice and community hospitals focus on small biopsies. There are certainly private practice and community hospitals that evaluate large specimens, but they do so in the context of large biopsy volumes (i.e., cross-subsidization). Tertiary care center pathology laboratories receive referrals (secondary review of biopsies) and surgical samples without the large volumes of primary biopsies to provide off setting revenue. Without high volumes of biopsies to subsidize the costs of large resections, value chain for laboratories becomes quickly degraded and laboratories may even become cost centers, especially if complex immunohistochemical works ups are considered. For patients, care at academic centers and comprehensive cancer centers is viewed as superior with access to clinical trials, multidisciplinary teams, advanced technology, and highly complex diagnosis of rare entities; however, the bulk of pathology services provided, being standardized, are essentially task-shifted from for-profit high volume laboratories that could subsidize the costs to large health systems that cost more to run often without the benefit of the primary diagnostic biopsy material revenue flow.

It is quite easy to see how this part of the value chain can fail in an LMIC because pathology operations are large, complex, and interlocking. For example, if the single embedding center goes offline, manual processes, which are slower and produce poorer quality blocks must be used and efficiency is lost. If the tissue processor goes offline, the entire process is stopped until it is restarted. If there is one pathologist and they go on vacation or immigrate to another country offering better salary, the process is stopped indefinitely. As mentioned above, for a laboratory with a low volume and limited staff, increases in volume are a considered negative because incentivization is lacking. Because these laboratories are often the “only game in town”, they must deal with small biopsies, large resections, and autopsies but without the revenue streams seen in HICs to offset costs or create cross-subsidization (i.e., reimbursement, private pay, etc). This is due to limited access for patients and biopsy rates for the population that may be less than 20% (i.e., of all people that NEED a biopsy, less than 20% receive a biopsy due to access issues). There is a great need to achieve balance in this problem between the minimal volume a lab should process and adequate compensation for laboratory staff to achieve this volume. Modelling and projections expected for a given population can be used to inform governments and market makers about what number of services are needed and, subsequently, public-private partnerships become a primary tool to achieve the balance. For individual gaps such as lack of staff, the value of the operations can be improved with training, telepathology support, visiting pathologists, and management training and improve the overall value improved for the patient.

To summarize this piece, operations for diagnostic pathology has an inherent economy of scope and scale such that an optimal case mix exists which creates maximum value for the patient—shortest turnaround time with most accurate results—and creates a sustainable revenue stream for the laboratory operations (mix of biopsies and resections). Competitive advantage is complex in this space because speed and volume are contrasted with specimen complexity, all of which should be performed through a standard of care.

In the next part, we will look at outbound logistics or the outgoing report to the clinical team.

References

  1. Porter, M. (1985). The value chain and competitive advantage, Chapter 2 in Competitive Advantage: Creating and Sustaining Superior Performance. Free Press, New York, 33-61.
  2. Histology. Wikipedia. https://en.wikipedia.org/wiki/Histology#:~:text=In%20the%2019th%20century%20histology,by%20Karl%20Meyer%20in%201819.
  3. Thorpe A et al. The healthcare diagnostics value game. KPMG International. Global Strategy Group. https://assets.kpmg/content/dam/kpmg/xx/pdf/2018/07/the-healthcare-diagnostics-value-game.pdf
  4. Digital Pathology Market CAGR, Value Chain Study, PESTEL Analysis and SWOT Study|Omnyx LLC, 3DHISTECH Ltd, Definiens AG. https://www.pharmiweb.com/press-release/2020-06-30/digital-pathology-market-cagr-value-chain-study-pestel-analysis-and-swot-study-omnyx-llc-3dhistec
  5. Friedman B. The Three Key Components of the Diagnostic Value Chain. Lab Soft News. January 2007. https://labsoftnews.typepad.com/lab_soft_news/2007/01/the_three_eleme.html
  6. XIFIN. The Evolution of Diagnostics: Climbing the Value Chain. January 2020. https://www.xifin.com/resources/blog/202001/evolution-diagnostics-climbing-value-chain
  7. Sommer R. Profiting from Diagnostic Laboratories. November 2011. Seeking alpha. https://seekingalpha.com/article/305931-profiting-from-diagnostic-laboratories#:~:text=The%20three%20year%20average%20operating,current%20operating%20margin%20of%2012.9%25.
milner-small


-Dan Milner, MD, MSc, spent 10 years at Harvard where he taught pathology, microbiology, and infectious disease. He began working in Africa in 1997 as a medical student and has built an international reputation as an expert in cerebral malaria. In his current role as Chief Medical officer of ASCP, he leads all PEPFAR activities as well as the Partners for Cancer Diagnosis and Treatment in Africa Initiative.

Set the World on Fire, but Don’t Burnout

Hello everyone and welcome back!

So here I am: a med school matriculant, top-choice program matched, doing exactly the training and work I’ve wanted to since before medical school. Totally made it! But before I go all “Fresh Prince of Maywood” on you, there’s a lot to unpack within the word “residency.” I’ve discussed this before, comparing pathology subspecialties with my primary care friend Dr. Raja’s rotation schedule, but you probably already know a little about what pathology residents do. I want to talk about what most folks might not know, why most residents absolutely disappear from their families or loved ones, and why going in with already greying hair isn’t going to make this any better, ha-ha…

Image 1. Me, and me. Look what 6 months of residency can do. Wow. Kidding. It’s an Instagram filter. Or is it…? It is. But what if it isn’t….?

I’m a resident at Loyola Medicine in Maywood, IL; I also went to undergrad (over a decade ago) at Loyola Chicago. So, for me, this is a very cool full-circle experience. I bring this symmetry up because a lot of people talk about the “culture” of an institution when they’re looking for a perfect match. I’ve talked about my experiences with hospitals’ institutional cultures before, at Bronx Care, Staten Island, Mayo Clinic, Danbury, Brooklyn, and more before medical school. I choose to highlight Loyola for you both because it’s already home to me, and also because it has a unique disposition.  When you walk across the stage at graduation, Loyolans are instructed to “Set the world on fire”—a quote from the university’s namesake and patron St. Ignacious Loyola. It follows a Jesuit tradition of valuing education as one of the most powerful tools to address social inequality, injustice, poverty, and whatever ails our society. By being bold and passionate (like a fire, get it…?) true leadership can manifest in graduates’ futures.

Image 2. Me again. Imbued with Jesuit mantras, ready to set the world “aflame.” Notice me in the bottom right, however, not really seeming to pay attention to the stage. Thinking about my poor future colleagues perhaps…

But all graduations are decorated with pomp and circumstance. As graduates sit and wait for their name, they are pontificated at about the importance, poignancy, and grand scale of opportunity that awaits them. But what happens after graduating, college, or graduate school, or medical school? The answer varies widely for many, but I can speak to those who end up with the long white coats. I’ll be honest, allegorically, college is a lesson in walking, graduate school is a lesson in running, medical school is a lesson in cartwheels—after you’ve somewhat mastered this, the world that awaits you demands powerful cartwheels (with tricks) up multiple Mt. Everests, and you might be able to use the bathroom…you might. Haha, a little hyperbole. I mean I am SO glad pathology training isn’t like some other specialties (looking at you surgery…) but the demand is there, nonetheless. I would say ours might be more cerebral because, what we trade in for not having an intern year, we are “gifted” with having to lean 4+ years of material presented as an iceberg tip in medical school.

In a recent Inside the Lab podcast, the topic of burnout was discussed. (Check it out here!) Labratorians—and healthcare staff in every role—have been feeling the COVID push all year. More is expected of us, more is demanded of our system and its output, and there is no relief or break in sight. That prolonged demand on our expertise (and time) puts a significant strain on all our collective psyche’s. Nowhere is that more apparent than in healthcare. Paramedics run long uninterrupted shifts seeing tragic emergency one after another. Nurses do 12hr shifts back to back for days, especially when there isn’t enough staff to support days off (while patient census climbs higher and higher). But in medicine, poor medical school post-graduates are expected to literally “reside” in the hospital, ergo resident. The term came from the training model coined at Johns Hopkins in the early 1900s. And, up until a few years ago, the powers that be decided that residents should log no more than a maximum of 80 hours a week with the longest shift you can work 24 hours. Fun fact: the IRS, yes those guys, defines full-time work as 30-40 hours per week or 130 hours per month. If you work a “full time” job, you probably work 40 hours a week/160 hours a month. So, for young resident physicians: that two full time jobs, coming in hot at just about the average US salary of 55-60k. Outstanding. However, while I find myself lucky and would anecdotally say that I don’t think I’ll be getting any notifications or flags on logging too many hours at the hospital, the reality is that many physician trainees work right up to the maximum (and more). The old guard cites that 80 hours isn’t enough time to train a functioning physician, as they leave patient care at a sensitive time where they effectively abandon their learning. But …burnout. The “reduction” to 80 hours one would think reduces stress and burnout, but lo and behold a paper (from FIFTEEN years ago) says nu-uh. “Changes in parameters of resident and faculty emotional exhaustion, depersonalization, and personal accomplishment did not show statistical significance…Despite successful reductions in resident work hours, measures of burnout were not significantly affected.” (JAMA, 2004)

Image 3. I’m not here to cite stuffy papers and the voluminous research on physician and resident burnout. Instead, I’m here to highlight the motivations those of us in healthcare cite as our driving force to keep at it, especially in a pandemic.

Regardless, those of us in postgraduate medical training are here for a reason. I identify as one of the few who finds himself in a lucky spot, where my institution—and my profession of choice—don’t demand that kind of hourly expectation of me. But many of my other colleges aren’t as lucky. Surgeons, internists, family doctors, and more are working themselves to the limit. And that doesn’t include anything about the COVID pandemic. Whether you’re a graduate of Loyola or not, we’re all expected to “set the world on fire,” I just hope we don’t burn out in the process. Stay in tune with your needs and your support system, learn to recognize signs of burnout as much more than fatigue, and remember to extend compassion to everyone—you never know what load they might be carrying. Remember those things and you can navigate a packed work-week…or a pandemic!

Thanks for reading!

See you next time!

Constantine E. Kanakis MD, MSc, MLS(ASCP)CM is a first-year resident physician in the Pathology and Laboratory Medicine Department at Loyola University Medical Center in Chicago with interests in hematopathology, transfusion medicine, bioethics, public health, and graphic medicine. He is a certified CAP inspector, holds an ASCP LMU certificate, and xxx. He was named on the 2017 ASCP Forty Under 40 list, The Pathologist magazine’s 2020 Power List and serves on ASCP’s Commission for Continuing Professional Development, Social Media Committee, and Patient Champions Advisory Board. He was featured in several online forums during the peak of the COVID pandemic discussing laboratory-related testing considerations, delivered a TEDx talk called “Unrecognizable Medicine,” and sits on 
the Auxiliary Board of the American Red Cross in Illinois. Dr. Kanakis is active on social media; follow him at @CEKanakisMD.

Lead Like No One is Watching

Even though I readily share and celebrate my accolades with family and friends, I have generally been quiet with my coworkers regarding career moves. When I passed the ASCP Specialist in Cytotechnology BOC exam three years into my career as a cytotechnologist, I only shared the news with my supervisor, cytopathology director, and a few other pathologists. After dabbling in budget and supply purchasing and compiling monthly and annual QA statistics, I completed ASCP’s certificate program from Lab Management University in 2018. The following year, I traveled to Puerto Rico for the American Society for Cytotechnology (ASCT) conference and sat for the International Academy of Cytology (IAC) Comprehensive Examination. Six weeks after the exam, I received word that I passed, and again, I immediately shared the exciting news with my supervisor and cytopathology director. No one else at work had a clue until a year later when they noticed extra initials behind my sign-out signature. Then, the ASCP 40 Under Forty application and eight weeks of waiting came and went this past summer and once again, I elatedly celebrated with my superiors. I have always moved in silence amongst my peers to maintain an inclusive and docile/same-level environment. While some might be supportive, not everyone actively encourages growth. Furthermore, not everyone wants an all-you-can-eat buffet on their work plate, and many lab professionals are happy with a less stressful, entry-level competency kind of routine. And that is perfectly A-OK too! Regardless, I am who I am, and for the lab professional who loves continuing education and learning new techniques and advancements across the field of health care, I wondered what career moves I would make in 2021. What goals should I set out to achieve? What is my next step?

There it is. A doctoral program. 100% Online and meant for the full-time working professional. I have officially embarked on my eight-semester-long journey to earning a Doctorate of Health Science (DHSc) with a concentration of Organizational Excellence in Healthcare. Rather than a traditional PhD which prepares scholars for research-based careers in a very focused area, the DHSc is an applied doctorate focusing on healthcare leadership in various disciplines. Now that I am halfway through my first semester, I can honestly say this is one of the best decisions I have ever made. Learning about applied leadership theory in healthcare and how to effectively, efficiently, and efficaciously lead in a complex healthcare landscape has been so intellectually stimulating thus far. Most recently, my classmates and I engaged in a discussion emphasizing how today’s leaders must stay relevant in their dynamic fields, and we shared our required competencies (i.e., the knowledge, skills, and abilities) for leading people and managing resources for both today and tomorrow (Ledlow & Stephens, 2018). A recurrent theme we uncovered is the necessity for continuing education – whether it be formal or informal. Staying relevant requires healthcare leaders to read, research, and teach. As cytotechnologists, we have existing continuing education programs in place, such as ASCP’s Credential Maintenance Program, recommending certificants to participate in and record credits to renew their certifications. We have Interlaboratory Comparison Programs through the College of American Pathologists (CAP) that feature ancillary studies as a diagnostic companion to cytology slides. We watch cytoteleconferences provided by the American Society of Cytopathology (ASC). We are encouraged to attend our affiliated societies’ national conferences to collaborate interprofessionally. With all that is available, however, we still need to do more than just claim continuing education credits.

We need to stay abreast on how our field of laboratory medicine is changing and how we can accommodate those changes and adapt to those changes. We need inspiration and motivation throughout the organizational hierarchy. We need passion and commitment from all levels and all disciplines. We need transformational, flexible, and culturally competent leaders to serve as mentors for the next generation of leaders. We need leaders who continuously self-reflect and improve as they build diverse, yet cohesive teams that thrive on generating positive outcomes for the organization. To the current leaders, leaders-in-training, and the followers with potential – we must get better, we must take more initiative, we must aspire to learn more than just the “what” or the “how,” but most importantly the “why.” For the upcoming year and beyond, I challenge you to continuously learn more about your field of laboratory medicine and its impact on society. Ask why the pap guidelines have changed. Ask about the advantages of robotic bronchoscopy. Ask what molecular tests are available and which are currently in development. Ask what we can do to reduce the burden of disease in our community! Refrain from saying, “I don’t know” and respond with, “I’ll find out.” Become an expert in your field by understanding the interdependency of laboratory disciplines and beyond, and strive to actively network with each other. For those who want more, please do more! Pursue more! There is no ceiling on your potential, and there are no limits to your growth.

So sayonara to 2020, and hello to 2021! New year, new me? No. New year, improved me. And hopefully an improved you!

Image 1. “Be a Star!” (Thyroid, FNA – DQ-stained smear. Dx: Papillary Thyroid Carcinoma)

References

1. Ledlow, G.R. & Stephens, J.H. (2018). Leadership for health professionals: Theory, skills, and applications (3rd ed.) Jones & Bartlett Learning.

-Taryn Waraksa, MS, SCT(ASCP)CM, CT(IAC), has worked as a cytotechnologist at Fox Chase Cancer Center, in Philadelphia, Pennsylvania, since earning her master’s degree from Thomas Jefferson University in 2014. She is an ASCP board-certified Specialist in Cytotechnology with an additional certification by the International Academy of Cytology (IAC). She is also a 2020 ASCP 40 Under Forty Honoree.