A sixty nine year old female who underwent right breast reconstruction about 13 years ago due to breast cancer presents to the doctor office with right breast pain and right breast enlargement over the last two months. She has lost some weight and does not recall any trauma to this area. She had a textured saline implant. Examination reveals no definite palpable masses. MRI of right breast showed intact saline implant with moderate amount of fluid surrounding the implant within the intact external capsule. No adenopathy was noted. Right breast implant was removed and complete capsulectomy was performed.
anaplastic large cell lymphoma.
Breast implant associated
anaplastic large cell lymphoma is a provisional entity that is morphologically
and immunophenotypically similar to ALK-negative anaplastic large cell lymphoma.
It arises primarily in association with a breast implant. It is a very rare
entity with an incidence of 1 in 500,000 to 3 million women with implants. Tumor
cells may be localized to the seroma cavity or may involve pericapsular fibrous
tissue. Sometimes it can form a mass lesion. Locoregional lymph node may be
involved. The mean patient age is 50 years. Most patient presents with
stage 1 disease, usually with peri-implant effusion. The mean interval from
implant placement to lymphoma diagnosis is 10.9 years. There is no association
with the type of implant. Histologic examination shows two different types of
proliferations. In patients with seroma, the proliferation is confined to the
fibrous capsule (“in situ” iALCL). However, the distribution of neoplastic
lymphocytes could be heterogeneous with some cellular areas with numerous large
pleomorphic cells of varying size and some fibrotic areas with rare atypical
lymphocytes. It is beneficial to look at the seroma fluid in addition to
capsule sections, because sometimes the neoplastic lymphocytes are
predominantly present in fluid (as in our case). Patients presenting with tumor
mass show more heterogeneous proliferations infiltrating surrounding tissues
(“infiltrative” iALCL). They consists of either sheets are clusters of large
neoplastic cells accompanied by a large number of eosinophils. By immunohistochemistry,
the tumor cells are strongly positive for CD30. CD2 and CD3 are more often
positive than CD5. CD43 is almost always expressed. Most cases are CD4 positive. The
prognosis is very good in patients with disease confined to the capsule.
The median overall survival is 12 years. However, patients with a tumor mass
could have a more aggressive clinical outcome.
1. Swerdlow SH, Campo E, Harris NL, et al. WHO Classification of Tumours of
Haematopoetic and Lymphoid Tissues (Revised 4th edition). IARC: Lyon
2. Jaffe, E , Arber, D, et al. Hematopathology (second edition) 2017.
-Junaid Baqai, MD, was born in Chicago, IL but spent most of his life in Karachi, Pakistan. He graduated from DOW Medical College in Pakistan and did his residency in anatomic and clinical pathology at Danbury Hospital, CT followed by hematopathology fellowship from William Beaumont Hospital, Michigan and oncologic-surgical pathology fellowship from Roswell Park Cancer Institute, New York. He currently serves as Medical Director of hematology, coagulation and flow cytometry at Memorial Medical Center and Medical Director of Laboratory at Taylorville Memorial Hospital.
A 44 year old male with history of cocaine use presented with 1 year history of headache and progressive frontal lobe syndrome, including symptoms like apathy, personality changes, lack of ability to plan, poor working memory for verbal information or spatial information, Broca aphasia, disinhibition, emotional lability, etc. CT scan found extensive destruction of osteocartilaginous structures of the nasal cavity and MRI showed extensive edema of the frontal lobe. Biopsy showed chronic inflammation but negative for granulomatous inflammation. Patient’s CSF laboratory analysis was normal but ANCA was tested positive, in a P-ANCA pattern without MPO detectable. Patient was diagnosed as CIMDL. After stopping cocaine use, patient was doing better but still has mild frontal lobe syndrome.
Anti-neutrophil cytoplasmic antibody (ANCA) are a group of
autoantibodies that directed toward antigens expressed mainly in neutrophil
granulocytes, such as proteinase 3 (RP3) and myeloperoxidase (MPO). The
presence of ANCA is mainly associated with a distinct form of small vessel
vasculitis, known as ANCA-associated vasculitis, but is also detected in other
disease, like autoimmune hepatitis, primary sclerosing cholangitis, ulcerative
colitis, and other chronic inflammatory disease. The gold standard laboratory
method to screen ANCA is indirect immunofluorescence assay (IFA or IIF), which qualitatively
capture antibodies in serum/or plasma bound to fixed human neutrophil
Two form of ANCA-associated vasculitis, granulomatous with
polyangiitis (GPA) and eosinophilic granulomatous with polyangiitis (EGPA), are
systemic diseases that commonly associated with necrotizing granulomatous
vasculitis. GPA has a primary involvement of the upper and lower respiratory
tract and kidney. Autoantibodies to PR3 are found in 90% of active GPA cases,
which generates a cytoplasmic-ANCA (C-ANCA) pattern on ANCA IFA test. EGPA is a
rare form of systemic necrotizing vasculitis characterized by asthma and
eosinophilia. A perinuclear-ANCA (P-ANCA) IFA pattern directing towards MPO
antibody are often seen in EGPA cases.
Both GPA and EGPA may also present with sinonasal
involvement, causing non-infectious inflammatory lesions of the sinonasal
tract. Sinonasal inflammatory disease can also result from bacterial and fungal
infections, or other non-infectious process, such as sarcoidosis,
polychondritis, or obstruction. ANCA is detected in the majority of GPA and
EGPA case, therefore it provides useful information in differential diagnosis
of sinonasal inflammatory disease. Both GPA and EGPA are autoimmune diseases,
corticosteroids and immunosuppressive agents are effective treatment.
Sinonasal inflammation can also been seen in a subset of
patients with cocaine abuse, who normally present with midline destructive
lesions, known as cocaine-induced midline destruction lesions (CIMDL). Long-term
cocaine use has been associated with ischemia of mucosal tissue, cartilage and
bone, and cocaine abuser using intranasal inhalation route can have midline
deformity and septal perforation. Interestingly, ANCA are also found in a large
portion of CIMDL, and in contrast to GPA or EGPA, ANCA in CIMDL are primarily
directed against neutrophil elastase, generate a P-ANCA or atypical P-ANCA
pattern, without detection of MPO. Therefore, ANCA serology testing could help
the differentiation between CIMDL and GPA although these two can overlap
clinically and histopathologically. Also, CIMDL does not respond well to
immunosuppressive therapy and only consistent removal of stimuli (cocaine) can
halt the disease process.
Montone KT. Differential Diagnosis of Necrotizing Sinonasal Lesions. Arch Pathol Lab Med. 2015 Dec;139(12):1508-14. doi: 10.5858/arpa.2015-0165-RA.
Trimarchi M, Bussi M, Sinico RA, Meroni P, Specks U. Cocaine-induced midline destructive lesions – an autoimmune disease? Autoimmun Rev. 2013 Feb;12(4):496-500. doi: 10.1016/j.autrev.2012.08.009. Epub 2012 Aug 24.
Madani G, Beale TJ. Sinonasal inflammatory disease. Semin Ultrasound CT MR. 2009 Feb;30(1):17-24.
Timothy R. Helliwell Non-infectious Inflammatory Lesions of the Sinonasal Tract. Head Neck Pathol. 2016 Mar; 10(1): 32–39.
-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 24 year old male with no past medical history presented with
fevers, myalgia, and cough following return from a 1-week trip to Guatemala
where he spent significant time within caves. The patient described his cough
as persistent, non-productive, and associated with mild shortness of breath at
rest that significantly worsens with activity. In the emergency department, the
patient was afebrile with a WBC of 10.2, Transaminitis, and chest X-ray showed
diffuse reticular pattern. He underwent a bronchoscopy and BAL washout.
Histoplasmosis Urine Antigen test came back positive.
capsulatum is an intracellular, thermally dimorphic fungus (grows as a
yeast at body temperature/37°C in humans or culture media and as mold at 25°C
in the environment/culture media). Histoplasma
is found in soil, particularly in areas containing bird and bat droppings,
such as caves. Within the United States Histoplasma
in found in central and eastern states with a predominance in the Ohio and
Mississippi River Valleys. This fungus is also found in parts of Central and
South America, Africa, Asia, and Australia.
Histoplasma capsulatum causes
significant morbidity and mortality worldwide. Upon inhalation of conidia, H. capsulatum transforms into the
pathogenic yeast phase. This form replicates within macrophages that carry the
yeast from the lungs to other organs. Histoplasmosis has three main forms:
primary histoplasmosis which presents as a pneumonia with fever, cough,
cavitary histoplasmosis which is characterized by pulmonary lesions that often
resemble cavitary tuberculosis.
disseminated histoplamosis that spreads to infect many organs in
In the laboratory, culture of blood, tissue and respiratory
specimens may be completed. In addition, a test for H. capsulatum
antigen is sensitive and specific when simultaneous serum and urine specimens
are tested. It is important to note that cross-reactivity with other fungi (Coccidioides
immitis, Blastomyces dermatitidis, Paracoccidioides brasiliensis,
Penicillium marneffei) has been identified.
Growth on fungal culture shows white/tan, fluffy mold
that turns to brown to buff with age. The organism may also produce wrinkled,
moist, or heaped yeast-like colonies that are soft and cream when grown at 37°C
on certain media. Scotch tape preparation of the mold form shows tuberculate
macroconidia, a diagnostic structure of Histoplasma
capsulatum. The mycelia are septate and produce microconidia and
macroconidia. Yeast forms of Histoplasma
capsulatum are small (2 to 4 μm) and reproduce by budding. These budding
forms may be seen on histology specimens. A commercially available DNA probe
can be performed on culture material to confirm identification.
Patients with mild-moderate histoplasmosis can often have
resolution of their symptoms without treatment. Those with more moderate-severe
disease require antifungal agents including amphotericin B or itraconazole.
-Nicole Mendelson, MD
is a 1st year Anatomic and Clinical Pathology resident at the
University of Vermont Medical Center.
-Christi Wojewoda, MD, is the Director of Clinical Microbiology at the University of Vermont Medical Center and an Associate Professor at the University of Vermont.
Nichole Baker, PA, works at Mercy Regional Medical Center in
Durango, Colorado as a Pathologists Assistant. Nichole started working as a
volunteer with Mbarara University of Science Technology (MUST) in 2017 through
the existing partnership with Massachusetts General Hospital Pathology
department– she responded to an advertisement looking for pathology volunteers
Drucilla Roberts had placed in a pathology journal. She decided to visit
the laboratory and see in what ways she could help. In total, she has visited
three times, and in that time, has accomplished incredible things! What was
particularly impressive to me is that Nichole single-handedly solved a very
complex problem in the MUST laboratory. In fact, it was this same problem that
many people (including myself!), had attempted to solve and could not find the
means to do so! Not only did she implement a solution to the problem, but she
did it in just two weeks!
Read on to hear from Nichole about her experience making
positive changes in her global community. I guarantee you will be inspired by
her work, her enthusiasm, and her can-do attitude!
Q: Nichole, I know that you recently returned from
Uganda, and you were able to team up with the pathology staff at MUST to make
some major changes and implemented a solution to a major problem. Can you tell
me about your project?
A: It started with realizing from my two prior visits
to the anatomic pathology lab at MUST that the laboratory had a faulty internal
tracking system for cases. This had two consequences: The first is that the
case turn-around time has been very difficult to track. This even results in
occasional cases being lost entirely. The second is that there is no repository
of cases to be able to easily conduct research.
What I decided to do was build a free computer program that
could accession the cases, track them, generate a pathology report, and give a
report of turn-around-time. Not having a computer science background myself, I
contacted a friend who connected me with a software engineer in Denver,
Colorado. He helped guide me in what would be feasible to accomplish and helped
me find a pro-bono programmer based in Belize named Maurice, who had some
background in healthcare IT. We started building the system less than a month
away from my departure to Uganda.
My goal was to work with the laboratory staff to build a
program based around their needs, for which I needed to be there in person to
clearly identify – I set out on my third trip in March 2019, this time for two
weeks. Maurice and I built a cloud-based tracking program and every day, we
would try it out in the laboratory. Day by day, issues would arise, such as the
need to add a sign-out function, general localization changes, or adding a
timestamp for a particular function. Fortunately for me, Maurice and I had a
substantial time difference which really worked to our advantage. I would try
the system out during the day and then email Maurice a report that he would
just be waking up to. He was able to work in Belize while we were asleep in
Uganda, and when I returned to the lab the next day, the program had been
updated with the changes. This allowed for rapid progress and the pathology
staff grew more and more excited to use the system as it improved. So, day by
day, we made the program better and better.
Q: What were some of the unique challenges that you faced
when implementing the program?
A: Originally, we had planned to use a laptop with
boosted RAM to act as a local server, but the network in the hospital wasn’t
functioning as needed. On-site we realized we’d need to shift to an internet
server and to do so we had to improve the internet access in the laboratory in
order to run the program –this was difficult because IT progress can be slow
Another example that is unique to this setting is the difficulty we had in generating unique patient identifiers in the registration system. In the US, two patient identifiers are required for each sample, and that is easy to obtain because everyone knows their date of birth. In Uganda, things are not as clear and straightforward. We might only have the village they live in, or a phone number. We had to look to see what items were most consistently reported and use those.
Q:How are you financing the data storage and
A: All fees and
costs associated with the program were raised by a small charity organization I
started in 2017 called “Path of Logic”
which has 501c3 status, making any donations tax deductible. With the funds raised,
a shared laboratory laptop was purchased. We are using a cloud-based system
that charges based on storage space. Right now, the storage need is low because
reports are stored as PDFs, but we may need to expand in the future. The
internet connection is also a low expense, as it’s simply a backup modem that’s
used when the university internet is not functioning.
Q: It’s now been two months since you rolled out the
program in the lab. What results have you seen from that?
A: Once we got going, we have been able to identify
where the delays were in processing the cases. After I returned back to the US,
Maurice and I continued to work on small issues remotely, such as single vs.
double click preferences and those sorts of things.
So far, 421 cases have been
registered in the system. The average turnaround time is 12.5 days. We still have a lot of work to go, but this is
the first we’ve been able to track this number. Many of the cases that were
started in the weeks following my departure were not signed out, but as the
team sees the value in the system, the more accurate that average will be,
allowing adjustments to be made accordingly.
We also added in the ability to assign ICD codes to the
final diagnosis to allow for a way to categorize the cases to make the
diagnosis searchable. Now we are going to be able to generate epidemiological
data. This feature is not yet in use by the pathology team, but we are hopeful
that as the system becomes more routine, this will be the next step to incorporate.
Q: What future impact do you think this program might
A: In addition to being able to easily track cases, build pathology reports, generate icd codes for researching cases more easily, we also hope that this will eventually result in increased funding for pathology services in Uganda. Right now, the money allocated from the Ugandan Ministry of Health is going towards HIV, malaria, and cancer treatment – but not for diagnostics. The Department of Education allows some funds for Pathology, but only about 30% of what is needed. Part of the reason why is that until now, there has been no way to quantify the number of cancer cases. With our program, we will be able to generate that data to show real numbers when lobbying for increased funds.
-Dana Razzano, MD is a Chief Resident in her third year in
anatomic and clinical pathology at New York Medical College at
Westchester Medical Center and will be starting her fellowship in
Cytopathology at Yale University in 2020. She was a top 5 honoree in
ASCP’s Forty Under 40 2018 and was named to The Pathologist’s Power List
of 2018. Follow Dr. Razzano on twitter @Dr_DR_Cells.
76 year old man with a history of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) with new anterior mediastinal mass and increasing lymphadenopathy.
Lymph Node Biopsy
Tissue sections show a diffuse atypical lymphoid infiltrate
that completely effaces the normal nodal architecture. The infiltrate is
composed of numerous small lymphocytes with round to mildly irregular nuclei,
clumped chromatin, inconspicuous nucleoli and scant cytoplasm. There are also
expanded pale areas that contain intermediate sized cells with more open
chromatin and distinct single to multiple nucleoli. These cells are most
consistent with prolymphocytes/paraimmunoblasts and form the proliferation
centers characteristic of CLL/SLL. Occasional centroblastic-type B-cells are
noted within these proliferation centers. In addition, there are scattered single
to multinucleated cells that have irregular nuclear membranes with pale,
vesicular chromatin and prominent inclusion-like, eosinophilic nucleoli. These
cells morphologically resemble Hodgkin cells, Reed-Sternberg cells, mummified
forms and other variants. These large cells are more evident in areas with a
histiocyte rich background and around foci of necrosis. Occasionally, apoptotic
bodies and mitotic figures are seen.
show that the vast majority of the small-intermediate lymphocytes express B-cell
markers CD20 (dim) and PAX5 and co-express CD5 and CD23 (subset). This is
consistent with a background of CLL/SLL. The large atypical cells are positive
for CD30, PAX5 and CD20 (variable). CD3 highlights numerous scattered
background small T-cells, which are increased in the areas with the large cells.
In situ hybridization for Epstein Barr viral RNA (EBER ISH) is mainly staining
the large atypical cells. By Ki-67, the proliferation fraction is overall
increased (40%) with increased uptake by the large atypical cells.
The morphologic and immunophenotypic findings are consistent
with involvement by the patient’s known small lymphocytic lymphoma/chronic
lymphocytic leukemia (SLL/CLL) with aggressive morphological features. The
aggressive features include expanded proliferation centers and an elevated
Ki-67 proliferative index (40%). Additionally there are histiocyte/T-cell rich
areas composed of multiple EBV positive large atypical cells with morphologic
and immunophenotypic features compatible with Hodgkin/ Reed-Sternberg cells.
These areas are most in keeping with evolving classic Hodgkin lymphoma. Sheets
of large cells indicative of large cell transformation are not seen, although
increased scattered large centroblastic-type B cells are present.
Lymph node involvement by CLL/SLL will typically show a
diffuse proliferation of small lymphocytes with effacement of the normal nodal
architecture. The small lymphocytes have
round nuclei, clumped chromatin and scant cytoplasm. Scattered paler areas
known as proliferation centers are characteristic of this entity. The
proliferation centers are composed of a mixture of cell types including small
lymphocytes, prolymphocytes and paraimmunoblasts. Prolymphocytes are small to
medium in size with relatively clumped chromatin, whereas paraimmunoblasts are
larger cells with round to oval nuclei, dispersed chromatin, eosinophilic
nucleoli and slightly basophilic cytoplasm. Some cases show increased and
enlarged proliferation centers with a higher proliferation rate. This must be
distinguished from large cell transformation.1
Aggressive features of CLL/SLL include proliferation centers
that are broader than a 20x field or becoming confluent. An increased Ki-67
proliferation >40% or >2.4 mitoses in the proliferation centers can also
portend a more aggressive course. These cases tend to have worse outcomes than
typical CLL/SLL and better outcomes than cases that have undergone Richter
transformation to diffuse large B-cell lymphoma (DLBCL). Transformation to
DLBCL occurs in 2-8% of patients with CLL/SLL. Less than 1% of patients with
CLL/SLL develop classic Hodgkin lymphoma (CHL). In order to diagnose CHL in the
setting of CLL/SLL, classic Reed-Sternberg cells need to be found in a
background appropriate for CHL, which includes a mixed inflammatory background.
The majority of these CHL cases will be positive for EBV.1
Richter’s transformation is defined as an aggressive
evolution of CLL. While the most common type of transformation is to a
high-grade B-cell Non-Hodgkin lymphoma, other histological transformations have
been described. This includes CHL, lymphoblastic lymphoma, hairy cell leukemia
and high-grade T-cell lymphomas. The prognosis for patients who present with
transformation to CHL is poor compared to de novo CHL.2
A large study from the M.D. Anderson Cancer Center described 4121 patients with
CLL/SLL and found that only 18 patients or 0.4% developed CHL. The median time
from CLL to CHL diagnosis was 4.6 years. Fourteen of the patients received
chemotherapy. The overall response rate was 44% with a complete response rate
of 19%. The median overall survival was 0.8 years and all patients eventually
died from disease recurrence or progressive disease.3 This dismal
prognosis is similar to patients with Richter transformation to DLBCL and much
worse than patients with de novo CHL, which is curable in >85% of cases.1
Swerdlow SH, Campo E, Harris NL, et al. WHO
Classification of Tumours of Haematopoetic and Lymphoid Tissues (Revised 4th
edition). IARC: Lyon 2017.
Janjetovic S, Bernd HW, Bokemeyer C, Fiedler W. Hodgkin’s
lymphoma as a rare variant of Richter’s transformation in chronic lymphocytic
leukemia: A case report and review of the literature. Mol Clin Oncol.
Tsimberidou, AM, O’Brien, S and Kantarjian, HM,
et. al. Hodgkin transformation of chronic lymphocytic leukemia. Cancer. 2006;107(6).doi.org/10.1002/cncr.22121.
–Chelsea Marcus, MD is a Hematopathology Fellow at Beth Israel
Deaconess Medical Center in Boston, MA. She has a particular interest in
High-grade B-Cell lymphomas and the genetic alterations of these
Last month, I wrote about some
projects I did while rotating through the pathology program at Danbury
Hospital in Connecticut. This month I’m in a more clinical setting with a
hematology/oncology clerkship at Northwell’s Staten Island University Hospital.
But, over the past few months of rotations (and arguably a lot longer before
medical school) I’ve been noticing a part of laboratory medicine which often
intersects with our clinical colleagues at the bedside. I’ve told you about the
pitfalls and successes in the relationships
between surgeons and anatomic pathologists before, where frozen sections
are critical and time is of the essence. And we’ve all seen collaboration
between the bench and bedside before—think microbiology and infectious disease,
blood bank and literally everyone, etc. Still, one collaborative effort sort of
happens behind the shadows, behind phone calls and lab reports, and sometimes
with no communication at all! So, what kind of vigilante medicine am I talking
about? Who is this Batman of medicine? It’s just our friends in hematology.
When you’re working the hematology bench in the lab, it’s
pretty commonplace for a physician on a hematology service to call and ask for
a peripheral smear to review. Many times, it’s for the purpose of teaching
residents, fellows, or medical students but more often than not it’s a
confirmatory exercise. See, when that hematologist asks to review a slide,
she’s probably coming down to the lab to look at the morphology of red cells
and white cells to help in their differential diagnosis. They might have a
patient with a suspected thalassemia or hemoglobinopathy and, before starting
the full work up of lab tests, just want to see if there are any RBC morphology
traits or target cells that stand out. Thrombocytopenia? Let’s make sure
there’s no platelet clumping. Maybe they’ve got a patient with some kind of
liver or kidney pathology and are on the hunt for acantho- or echinocytes. Or
better yet, someone went hiking, there’s an infectious etiology on their
differential—let’s go hunting for babesia, malaria, oh or even erlichia!
I know what you’re thinking. Wait—that’s our job as
medical laboratory scientists; our literal job. Our instruments, that we
validate, and correlate, and make sure work fantastically give us flags. We
investigate those flags and look at smears ourselves! We collaborate with other
lab techs, and with our pathologist colleagues and send out final lab results
with all kinds of helpful information: including platelet clumping,
microorganisms, RBC and WBC morphology, and loads more. What gives?
Hold on to your lab coats. I’ll get there in a minute.
Slide review and differential training in medical school
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A Differential, Differential
So let me address the issue I brought up: why do
hematologists come down to the lab to look at the slides themselves, when
perfectly capable BOC certified, degree-holding medical laboratory scientists
and pathologists sign out validated differentials? It might not happen this way
at all hospitals, but I think the answer is a simple two-part problem.
First, as with the many things I’ve learned in medical
school, one of the lab-centric pieces of information that is well understood is
that, well, no one really knows what the lab does and how it operates.
Virtually nobody knows the depth and breadth of the testing that pathologists
manage, let alone the scientific precision and accuracy that instrument
validation requires. Learning that MLS techs are certified, can hold graduate
degrees, and even do their own research is often surprising to most of our
clinical colleagues. And—I will tell you for a fact—that pathology and
laboratory testing methodology is not covered in medical school the way you
might think. Pathology is more of a class of distinguishing the identifying
details of a disease, not understanding the interdisciplinary diagnostic
teamwork that goes into those CBC index results on a computer screen on the
Second, hematologists are specialists just like any other
practicing clinician. They know their stuff! They manage patient diagnosis,
treatment, and follow-up with the most up to date literature, national cancer
guidelines, and anything else available to better their patients’ outcomes. Despite
the notes in the CBC results that there are numerous macrocytes with
hypersegmented neutrophils, or 3+ schistocytes reported in a manual
differential—seeing is believing. It helps to see the slide yourself and get a
feel for the disease “state” with your own eyes. Moreso, it could be a learning
opportunity. It’s well within a clinicians’ scope to come down and look at a
peripheral smear, I actually encourage it. But it should come with a few
caveats…I’ll get to those too…
One of the places I was proud to hang my lab coat was
actually my first job as an assistant lab technician in the blood bank at Rush
University Medical Center in Chicago. Before I got my MLS and way before grad
school or med school, I was a blood bank “expediter.” Super fancy title, but
all I did was make sure specimens were logged in and blood products were up to
par with labels on their way out. Clerical but critical! (Let me have this,
please…haha) Anyway, part of the culture at that hospital has stayed with me
all these years. I’ve talked before about culture and the
way it permeates an institution’s practice like at the Mayo Clinic, but for
my first foray into clinical work their acronym was clutch: I CARE.
I for innovation
C for collaboration
A for accountability
R for respect and
E for excellence
Why am I telling you this? No, there are no royalties. I
just think it’s an easy way to remind ourselves about the meaning of
interdisciplinary medicine and they way we should work together across
specialties, and from bench to bedside. When we incorporate those values into
our work for the purpose of improving patient care and outcomes, everyone wins.
In this case, effective utilization of resources tells us that peripheral slide
review means different things to different people. In the setting of
hematologic work-ups, flags and review at the bench can signal something to the
clinician which could spark a conversation with the pathologist. All parts
contributing to a whole of patient care. Vigilante medicine is bad news.
Collaboration is key.
One place I was lucky enough to be a part of this
interdisciplinary collaboration was Swedish Covenant Hospital. One of the
hematology physicians would routinely call me and ask to look as peripheral
smears down in the lab, often as a group with med students, residents, and
fellows. I’d throw the image of his patients’ slides on a large flat screen and
go over what certain traits meant with regard to morphology and identification
from the lab setting. Dr. Cilley would add what this all meant clinically and
discuss treatment algorithms and next steps. That was collaboration at it’s
finest: lab tech working with pathologists, clinicians working with the lab,
and patient’s benefiting from all of it.
Teamwork makes the dream work
About those caveats for collaboration I mentioned earlier…
Let me put it briefly: it’s well within the scope of a clinician to come over
to the laboratory and get some information on their patient’s lab
results/testing. But why not consider the following:
If a physician calls to review a smear, offer
to go over it with them. Likewise, to our clinical friends: if you go to the
lab for a slide don’t be batman—ask the tech what they think!
Experienced techs are one of the hospital’s most valuable resources. Some
folks I’ve worked with have been looking at slides longer than I’ve been using
my eyes at all! They’ll save you and your residents the time when those
terrifying intracellular microorganisms are really just overlying platelets. I
mean, they’ve got a cute halo.
If you need help, just ask. This applies to
Talking with the tech about the slide is great start, but there’s more
resources in the lab than most people know what to do with! Clinical
physicians: check the shelves around the hematology microscope. Stuck on
something? Find a CAP atlas or a proficiency survey booklet guide. Easy to
read. Techs and pathologists: have someone who constantly comes down for slide
review despite your immaculate and detailed SOPs on CBC results reporting? Have
a quick chat about the work that goes into resulting those diffs—you might even
improve your heme TAT, who knows?
If it’s well within the right of a physician
to leave the unit and see a patient’s slide, logic says that maybe, just maybe,
it should be okay for a pathologist to leave the lab and see a patient at the
are full of never-ending rounding white coats, all asking patients questions,
and all contributing specialty notes to their charts. But its not only
to prevent patients from getting a decent nap. We’re all parts of a large
interdisciplinary patient team. A recent Medscape survey found that somewhere
around 3% of pathologists see patients, routinely! Got an interesting case in
the lab, someone who’s part of lots of tumor boards, someone with an
interesting case to write up, or even someone who nobody knows exactly what’s
going on with? Try walking over to 4 south and have a conversation with Mr.
Jones; it might help. At least he’ll know how many people are working on his
The bottom line: we’re in this together, and like the flag
on the ASCP ship says, we’re Stronger Together. Innovation,
collaboration, accountability, respect, and excellence are—and should be—simple
cornerstones of clinical medicine that translate across every discipline. When
we share information and expertise, everyone gets better at what they do.
Thanks for reading!
See you next time!
–Constantine E. Kanakis MSc, MLS (ASCP)CM graduated from Loyola
University Chicago with a BS in Molecular Biology and Bioethics and then
Rush University with an MS in Medical Laboratory Science. He is
currently a medical student actively involved in public health and
laboratory medicine, conducting clinicals at Bronx-Care Hospital Center
in New York City.