Surgical Pathology Case Study: A 63 Year Old Male with a ~60 Year Recurring Neck Mass

Case History

A 63 year old man presented with a long standing history of a recurring pleomorphic adenoma of the parotid gland. As a child, the patient had radiotherapy to the bilateral parotid glands for parotid swelling. He then developed a left parotid mass ~15 years later and underwent parotidectomy. After another recurrence ~15 years after the initial parotidectomy, he underwent a second resection of multiple masses in the preauricular region. The patient then developed a recurrence ~20 years after the second resection and underwent neutron beam therapy. The patient tolerated the treatment well noting mild dry mouth, which is persistent, and left ear pain, but otherwise has no major long-term sequelae from the treatment. Eighteen years after the neutron beam therapy, the patient developed a left submandibular mass. A subsequent biopsy of the mass revealed a pleomorphic adenoma.  Enlarged left and right submental and submandibular nodes were noted, with biopsies performed at an outside hospital of these nodes demonstrating metastatic poorly differentiated carcinoma within three lymph nodes. It was noted on this pathology report that the histological features, in light of the history, could represent a carcinoma ex pleomorphic adenoma. A CT scan of the head and neck revealed a large multiloculated, cystic, rim-enhancing mass within the left parotid gland, as well as large enhancing lymph nodes within the right anterior and posterior cervical triangle and the right submandibular space, the largest of which measured 2.1 cm. A PET scan showed increased activity within the right neck. Upon meeting with otolaryngology, a 4.0 x 7.0 cm lobular, non-fixed left parotid mass, and two level 1B right sided nodes, were palpated. Based on the patient’s history, physical exam, and prior biopsy results, it was decided to proceed with a parotidectomy and bilateral neck dissection. 

Diagnosis

Received in the Surgical Pathology laboratory is a soft tissue mass resection from the area of the left parotid gland measuring 9.0 x 6.0 x 4.2 cm. The specimen is oriented by a single long stitch designating the superior aspect, and a double long stitch designating the lateral aspect (Figure 1). The specimen is entirely inked black, and then bisected to reveal multiple discrete, white-tan, partially cystic masses ranging in size from 0.2-4.0 cm in greatest dimension and measuring 7.0 x 3.5 x 3.0 cm in aggregate dimension (Figure 2). The largest mass is partially cystic with the cystic component measuring 1.2 cm in greatest dimension. This largest mass abuts the anterior, medial and lateral margins. The remaining tumor deposits are located:

– 1.2 cm from the inferior margin

– 0.4 cm from the superior margin

– 0.9 cm from the posterior margin

No gross salivary gland tissue is identified. The remainder of the specimen consists of unremarkable yellow adipose tissue and red-brown skeletal muscle. The specimen is submitted as follows.

Cassette 1:   superior margin

Cassette 2:   representative sections of anterior margin

Cassette 3:   anterior superior margin

Cassette 4:   anterior inferior margin

Cassette 5:   posterior margin

Cassette 6-9:   representative sections of mass with approach to lateral margin

Cassette 10:   representative sections of mass with approach to medial margin

Cassette 11:   mass in relation to surrounding skeletal muscle

Cassette12-15:   representative sections of mass

On microscopy, the specimen contains nests of tumor cells ranging in size from 0.2 to 4.0 cm within a dense fibrous matrix. Although these deposits may represent lymph node metastases, no residual lymphoid tissue is present. The tumor is represented by residual pleomorphic adenoma and numerous soft tissue deposits of pleomorphic adenoma (Figure 3). Admixed are broad areas of high grade carcinoma with necrosis (Figure 4). Most regions show adenocarcinoma, although a rare focus of squamous differentiation is also present. The lateral margin is positive for carcinoma, and a pleomorphic adenoma component approaches within 0.1 cm of the medial margin. The anterior, posterior, inferior, and superior margins are all free of tumor. No salivary gland tissue is identified.

In addition, eleven frozen sections are submitted from various areas surrounding the mass, with five of the eleven frozen sections demonstrating tumor deposits. A right neck dissection is performed with following results:

Level IB: 2 of 3 positive (largest deposit: 1.8 cm)

Level II and III: 1 of 14 positive, Level II (1.9cm)

Level IV: 1 of 8 positive (2.0 cm)

Based on these results, the specimen was signed out as carcinoma ex-pleomorphic adenoma, and designated as pT4aN2cMx

Figure 3. 2x photomicrograph showing a classic appearing pleomorphic adenoma with satellite nodules along the periphery

Discussion

Carcinoma ex pleomorphic adenoma (CXPA) is a carcinoma that arises in a primary (de novo) or recurrent benign pleomorphic adenoma (PA). While a PA is the most common salivary gland tumor, accounting for approximately 80% of all benign salivary gland tumors, a CXPA is quite uncommon, accounting for only 3.6% of all salivary gland tumors. CXPA is predominantly found in the sixth to eighth decades of life, with a slight predilection for females. CXPA arises most commonly in the salivary glands, in particular the parotid and the submandibular glands. CXPA can also arise in the minor salivary glands in the oral cavity, although these tumors tend to be smaller than their counterparts in the parotid and submandibular gland. There have also been cases of CXPA in the breast, lacrimal gland, trachea, and nasal cavity.

Clinically, CXPA presents as a firm, asymptomatic mass that can go undetected for years since they are not generally invasive. When the patient does experience any symptoms, with pain being the most common, it is usually due to the mass extending to adjacent structures. If the mass was to involve the facial nerve, paresis or palsy can occur. Other signs and symptoms include skin ulceration, mass enlargement, skin fixation, lymphadenopathy, dental pain, and dysphagia. The onset of symptoms can range anywhere from 1 month up to 60 years (such as with this case), with a mean onset of 9 years. Half of patients will have a painless mass for less than 1 year. Since these symptoms are similar to those of a benign PA, it’s important that the treating physician be aware of the possibility of a CXPA, especially considering the rarity of the cancer.

Grossly, CXPA appears as a firm, ill-defined tumor, and can vary greatly depending on the predominant component. If the PA is the predominant component, the mass may appear gray-blue and translucent, and it could be possible to grossly differentiate between the PA areas and the CXPA areas. If the malignant component predominates, then the mass may contain cystic, hemorrhagic and necrotic areas.

Microscopically, CXPA is defined as having a mixture of a benign PA, admixed with carcinomatous components. Zbaren et al, in an analysis of 19 CXPA cases, found 21% of the tumors were composed of less than 33% carcinoma, 37% of the tumors were composed of 33-66% carcinoma, and 42% of the tumors were composed of greater than 66% carcinoma. Most often, the malignant component is adenocarcinoma, but can also include adenoid cystic carcinoma, mucoepidermoid carcinoma, salivary duct carcinoma, and other less common variations. In cases where the entire tumor is replaced by carcinoma, the diagnosis of CXPA will be based on the presence of a PA on the previous biopsy. Conversely, you could also have a tumor that is predominately composed of a PA, with sparse areas of malignant transformation, such as nuclear pleomorphism, atypical mitotic figures, hemorrhage and necrosis. The likelihood of malignant transformation increases with the length of the PA being present, from 1.5% at 5 years, up to 10% after 15 years.

CXPA can be further sub-divided into four categories based on the extent of invasion of the carcinomatous component outside the capsule: in-situ, non-invasive, minimally invasive, and invasive carcinoma.

#1) In-situ carcinoma occurs when nuclear pleomorphism and atypical mitotic figures are found within the epithelial cells, but do not extend out beyond the border of the myoepithelial cells (Figure 5).

#2) Non-invasive CXPA, which can include in-situ carcinoma, is maintained within the fibrous capsule of the PA, but extends beyond the confines of the myoepithelial cells. Non-invasive CXPA may begin to show malignant transformation, but will overall behave like a benign PA.

#3) Minimally invasive CXPA is defined as <1.5 mm extension into the extracapsular tissue, with a mix of benign PA components and carcinomatous components.

#4) Invasive CXPA is defined as a > 1.5 mm extension into the extracapsular tissue, and will begin to demonstrate more carcinomatous components, such as hemorrhage and necrosis.

As the carcinomatous areas begin to increase in prevalence, the PA nodules will begin to be composed of hyalinized tissue with sparse, scattered ductal structures, and the malignant cells will begin to decrease in size as they move away from the site of origin. Perineural and vascular invasion can be easily identified as the tumor extends into the neighboring tissue (Figure 6).

The development of CXPA has been shown to follow a multi-step model of carcinogenesis with a loss of heterozygosity at chromosomal arms 8q, followed by 12q, and finally 17p. Both PA and CXPA demonstrate the same loss of heterozygosity, however, the carcinomatous components exhibit a slightly higher loss of heterozygosity at 8q, and a significantly higher loss of heterozygosity at 12q and 17q. The early alterations of the chromosomal arm 8q in a PA often involves PLAG1 and MYC, with the malignant transformation of the PA to a CXPA being associated with the 12q genes HMGA2 and MDM2.

Treatment for CXPA involves surgery, radiotherapy and chemotherapy, with a parotidectomy being the most common procedure performed. If a benign PA had originally been resected, but residual remnants of the PA were left behind, then satellite PA nodules will arise in its place (Figure 3). If in-situ, non-invasive or minimally invasive carcinoma is suspected in the superficial lobe of the parotid gland, than a superficial parotidectomy can be performed. Invasive carcinoma will result in a total parotidectomy, with every attempt made to try and preserve the facial nerve. If metastasis is suspected to the cervical lymph nodes, a neck dissection may also be performed. Reconstructive surgery following the removal of the tumor may be necessary, depending on where the tumor was resected from. Other treatment options currently being considered include a combination therapy of trastuzumab and capecitabine, as well as the possibility of a WT1 peptide based immunotherapy.

Figure 5. 40x microphotograph demonstrating an in-situ carcinoma confined within the myoepithelial cells
Figure 6. 10x photomicrograph of carcinoma at the lateral margin with areas of perineural invasion

References

  1. Antony J, Gopalan V, Smith RA, Lam AK. Carcinoma ex pleomorphic adenoma: a comprehensive review of clinical, pathological and molecular data. Head Neck Pathol. 2011;6(1):1–9. doi:10.1007/s12105-011-0281-z
  2. Chooback N, Shen Y, Jones M, et al. Carcinoma ex pleomorphic adenoma: case report and options for systemic therapy. Curr Oncol. 2017;24(3):e251–e254. doi:10.3747/co.24.3588
  3. Di Palma S. Carcinoma ex pleomorphic adenoma, with particular emphasis on early lesions. Head Neck Pathol. 2013;7 Suppl 1(Suppl 1):S68–S76. doi:10.1007/s12105-013-0454-z
  4. Handra-Luca A. Malignant mixed tumor. Pathology Outlines. http://www.pathologyoutlines.com/topic/salivaryglandsmalignantmixedtumor.html. Revised March 21, 2019. Accessed April 5, 2019.

-Cory Nash is a board certified Pathologists’ Assistant, specializing in surgical and gross pathology. He currently works as a Pathologists’ Assistant at the University of Chicago Medical Center. His job involves the macroscopic examination, dissection and tissue submission of surgical specimens, ranging from biopsies to multi-organ resections. Cory has a special interest in head and neck pathology, as well as bone and soft tissue pathology. Cory can be followed on twitter at @iplaywithorgans.

Surgical Pathology Case Study: A 42 Year Old Woman with an Enlarging Mass of the Forearm

Case History

A 42 year old female with a history of neurofibromatosis, hypertension and Hashimoto’s thyroiditis had noted a mass on her forearm approximately 15 years ago. According to the patient, the mass did not change in size and did not cause her any discomfort during that time. Approximately 6 months prior to presenting to her primary physician, the mass began to increase in size and caused discomfort and pain. Upon examination with the Orthopedic Surgery department, a 20 x 20 cm firm, smooth mass on her forearm with mild pain on palpation was noted (Image 1). On MRI, the mass appeared to partially surround the radius and ulna, and encased the median, radial and ulnar nerves. A needle core biopsy was subsequently performed on the mass revealing a high grade malignant peripheral nerve sheath tumor (MPNST). A CT scan of the chest showed no evidence of metastatic disease. During her clinical visit, the use of neoadjuvant chemotherapy and chemoradiotherapy were discussed, but based on the large size of the mass, tumor response would have to be significant in order to allow for limb conserving surgery. At the time that the patient was seen, MPNSTs were not known to be chemosensitive and the chances of significant tumor response was very low (clinical drug trials have since shown some improvements in this area). In light of the poor response to systemic therapy of these tumors and the potentially toxic side effects of chemotherapy, the decision was made to proceed with amputation of the arm through the humerus.

Diagnosis

Frozen sections were sent from all the major peripheral nerves, including the ulnar, radial and median nerves. There was no evidence of any tumor consistent with a high-grade MPNST, although there was evidence of neurofibromas. There were atypical cells with hyperchromasia in the ulnar nerve margin, however, this was not considered to be consistent with a high grade MPNST. Received in the surgical pathology lab was an above elbow amputation consisting of a 30.0 cm long distal arm, an attached hand measuring 17.0 cm in maximum length., and a 4.5 cm long exposed humerus. The specimen is covered by grossly unremarkable skin, with a palpable mass in the mid-portion of the forearm. Sectioning reveals an 18.0 x 12.0 x 11.0 cm well-circumscribed mass composed of bulging, myxoid, white-tan tissue with central areas of hemorrhagic degeneration and yellow-tan friable tissue (Image 2). The bulging white-tan tissue is mainly found peripherally and encompasses approximately two-thirds of the mass. The mass is confined to a thin translucent lining and does not grossly invade neighboring soft tissue or overlying skin. The radial, median and ulnar nerves are adjacent to but not invaded by the mass, although the distal aspect of the mass shares a translucent, myxoid-like tissue with the peripheral nerve sheath of the ulnar and median nerves.

In addition to the standard bone and soft tissue margins that are taken, representative sections of the mass with the closest approach to the overlying skin are submitted. Sections demonstrating the relationship of the distal mass to the radial, median and ulnar nerves are submitted in separate cassettes. Lastly, representative sections sampled from various areas of the mass are submitted in an additional 15 blocks.

Histologically, the tumor consisted of spindle cells arranged in a fascicular pattern with intermittent whorled areas. The cells contained pleomorphic, hyperchromatic nuclei and intervening myxoid hypocellular areas. Mitotic figures were observed with sparse areas of necrosis and hemorrhage. S-100 was ordered on the prior biopsy of the mass, which was weakly positive. Based on these findings, the specimen was signed out as a malignant peripheral nerve sheath tumor.

Image 1. Above elbow amputation with a large forearm mass.
Image 2. Longitudinal cross section of arm demonstrating a bulging, white-tan mass with areas of hemorrhage and necrosis.

Discussion

Malignant peripheral nerve sheath tumors (MPNST) are locally invasive tumors that are associated with medium to large nerves (as opposed to cranial or distal small verves) and commonly recur with eventual metastatic spread. Common sites for metastatic spread include lung, liver, brain, bones and adrenals. They are usually found in adults between the second and fifth decades of life, and account for only 5% of malignant soft tissue tumors. Approximately half of MPNSTs will occur sporadically, with the other half generally arising in the setting of neurofibromatosis type 1 (such as in this case). There is a high clinical suspicion for MPNST if the patient has a history of neurofibromatosis type 1 or if the tumor arises within a major nerve component.

Grossly, MPNST will present as a large, poorly defined, fleshy tumor that runs along a nerve and involves adjacent soft tissue. Often, these tumors will have areas of hemorrhage or necrosis and can track along the length of a nerve. Histologically, the tumors are composed of monomorphic spindle cells arranged in fascicles, palisades and whorls, with compact comma-shaped, wavy or buckled hyperchromatic nuclei with alternating hypocellular foci. (Image 3 and 4). Mitotic figures and necrosis are common, and although S-100 is considered the best marker for MPNST, there is a lack of specificity and sensitivity for immunohistochemical markers. Due to the lack of immunohistochemical markers and molecular findings, as well as the variability associated with the cells, it has traditionally been difficult to diagnose MPNST. The differential diagnosis includes fibrosarcoma, monophasic synovial sarcoma, desmoplastic melanoma, and pleomorphic liposarcoma. Goldblum et al put forth the idea that a diagnosis of MPNST can be made if the tumor falls into any one of the following three categories:

  1. The tumor arises along a peripheral nerve
  2. The tumor arises from a pre-existing benign nerve sheath tumor, such as a neurofibroma
  3. The histologic features are consistent with a malignant Schwann cell tumor

Unfortunately, due to the aggressiveness of the tumor and high recurrence rate, MPNST has a poor prognosis with a 2 year overall survival rate of around 57% and a 5 year survival rate around 39%.

Image 3. Low power photomicrograph showing a spindle cell neoplasm arranged in a fascicular pattern.
Image 4. High power photomicrograph demonstrating spindle cells with hypercellular nuclei in a whorled arrangement and adjacent myxoid hypocellular areas.

References

  1. Case of the week #443. Pathology Outlines. http://www.pathologyoutlines.com/caseofweek/case443.htm. Published November 15, 2017. Accessed March 10, 2019.
  2. Frosch MP, Anthony DC, De Girolami U. Malignant Peripheral Nerve Sheath Tumor. In: Kumar V, Abbas AK, Fausto N, Aster JC. Robbins and Cotran Pathologic Basis of Disease, 8th edition. Philadelphia, PA: Elsevier, Inc. 2010: 1341-1342
  3. Guo A, Liu A, Wei L, Song X. Malignant Peripheral Nerve Sheath Tumors: Differentiation Patterns and Immunohistochemical Features – A Mini-Review and Our New Findings. J Cancer. 2012; 3:303-309. http://www.jcancer.org/v03p0303.html. Accessed March 9, 2019.
  4. Hirbe AC, Cosper PF, Dahiya S, Van Tine BA. Neoadjuvant Ifosfamide and Epirubicin in the Treatment of Malignant Peripheral Nerve Sheath Tumors. Sarcoma. https://www.hindawi.com/journals/sarcoma/2017/3761292/cta/. Accessed March 10, 2019.
  5. Ramnani, DM. Malignant Peripheral Nerve Sheath Tumor. WebPathology. https://www.webpathology.com/case.asp?case=499. Accessed March 9, 2019.
  6. Shankar V. Malignant peripheral nerve sheath tumor (MPNST). Pathology Outlines. http://www.pathologyoutlines.com/topic/softtissuempnst.html. Revised September 12, 2018. Accessed March 9, 2019.

-Cory Nash is a board certified Pathologists’ Assistant, specializing in surgical and gross pathology. He currently works as a Pathologists’ Assistant at the University of Chicago Medical Center. His job involves the macroscopic examination, dissection and tissue submission of surgical specimens, ranging from biopsies to multi-organ resections. Cory has a special interest in head and neck pathology, as well as bone and soft tissue pathology. Cory can be followed on twitter at @iplaywithorgans.

Surgical Pathology Case Study: A 64 Year Old Man with History of Loose Stools and Abdominal Pain

Case History

A 64 year old male presented with a one year history of loose stools, lower abdominal crampy/gassy pain that improved with defection, and an unclear history of melena. A colonoscopy revealed a circumferential, villous, carpet-like lesion extending from 15 cm to the anal verge, with biopsies demonstrating fragments of a villous adenoma. A follow-up CT scan was negative for metastatic disease. The decision was then made to proceed with a low anterior resection with hand-sewn colo-anal anastomosis and diverting loop ileostomy.

Diagnosis

Upon opening the rectum, a 13.8 cm long circumferential, carpet-like lesion is identified, extending to the distal margin (Image 1). Sectioning demonstrated a lesion with a maximum thickness of 1.0 cm, which grossly appears to be confined to the mucosa. Due to the prior biopsy history of a villous adenoma, the entire lesion was completely submitted. This required 116 blocks to be submitted, which were then mapped out to show where each block would have been taken from (Image 2). Although there were many foci of intramucosal carcinoma present, clear cut submucosal invasion was not identified, and the specimen was signed out as a villous adenoma (Image 3).

Image 1. Opened rectum demonstrating the 13.8 cm-long carpet-like lesion.
Image 2. Mapping the lesion to show from where each block is taken.
Image 3. Photomicrograph showing the transition from normal mucosa (black arrow) to villous adenomatous tissue (red arrow).

Discussion

Polyps are an abnormal tissue growth that is a common occurrence within the colon, although they can also be found throughout the small intestine, stomach and esophagus. Polyps can be further classified as being neoplastic or non-neoplastic based on the histological pattern of the cells. The most common types of neoplastic polyps found within the GI tract are colonic adenomas, which are benign polyps that serve as precursors to the majority of colorectal cancers. Nearly half of adults in the Western world will develop adenomas by the age of 50, and there is no gender predilection. It is because of this that it is recommended that all adults get a colonoscopy by the age of 50 (even earlier when there is a family history of developing colorectal cancer).

Most polyps are small, measuring 0.5 cm or less, but can grow to be over 10 cm in size (as seen in this case). When a colonoscopy is performed, these polyps can appear as sessile, meaning flat, or pedunculated, meaning on a stalk. Due to the abnormal epithelial growth of the mucosa, the surface of an adenoma can have a velvety appearance, resembling that of a raspberry. Most patients will not demonstrate any symptoms from their polyps, with the exception of occult bleeding and anemia which are associated with larger polyps.

Dysplasia, which literally means “disordered growth”, occurs when the individual cells lose their uniformity and architecture, often resulting in cells with a hyperchromatic nuclei and a high nuclear to cytoplasmic ratio. The presence of dysplasia contained within the epithelium of a polyp is what classifies the polyp as an adenoma (Image 4). Based on their epithelial growth pattern, adenomas can be classified as either tubular adenomas or villous adenomas. Tubular adenomas tend to be smaller polyps, with a smoother surface and rounded glands on histologic examination. Villous adenomas, in contrast, tend to be larger polyps with long, slender villi noted on histology (Image 5). If an adenoma contains a mixture of tubular and villous elements, they are classified as tubulovillous adenomas. When a dysplastic cell is no longer contained within the epithelium, and instead breaches the basement membrane which separates the epithelium from the underlying tissue, it is termed invasive.

Image 4. Photomicrograph of the villous adenoma, demonstrating the dysplasia that is confined to the mucosa and not extending to the deeper tissue.
Image 5. Photomicrograph of the long, slender villi that are commonly seen in villous adenomas.

What makes this case so interesting is that there is a direct correlation between the size of an adenoma, and the risk of developing colorectal cancer. This is not true with most other cancers, however, as size plays no part in determining whether the tumor is cancerous or not. With colon polyps, the larger the polyp, the greater the chance of developing invasive carcinoma (i.e. cancer). This is why screening colonoscopies are so important. Studies have shown that regular colonoscopies, combined with the removal of the polyps found on the exam, reduce the incidence of colorectal cancer. Why this case is so interesting is that you could assume based on the size of this polypoid lesion, you would find some invasive component. However, after reviewing 116 blocks, not a single focus of invasion could be identified.

It should be stated that although there is a correlation between an adenomas size and the risk of developing cancer, the majority of adenomas will not progress to cancer, and in fact, there are no tools currently available that help to determine why one patient’s adenoma will progress to cancer, while another patient’s adenoma will not.

References

  1. Association of Directors of Anatomic and Surgical Pathology, adapted with permission by the American Cancer Society. Understanding Your Pathology Report: Colon Polyps (Sessile or Traditional Serrated Adenomas). cancer.org. https://www.cancer.org/treatment/understanding-your-diagnosis/tests/understanding-your-pathology-report/colon-pathology/colon-polyps-sessile-or-traditional-serrated-adenomas.html. Accessed February 14, 2019.
  2. Colon Polyps. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/colon-polyps/symptoms-causes/syc-20352875. Accessed February 14, 2019.
  3. Turner JR. Polyps. In: Kumar V, Abbas AK, Fausto N, Aster JC. Robbins and Cotran Pathologic Basis of Disease, 8th edition. Philadelphia, PA: Elsevier, Inc; 2010: 815-820

-Cory Nash is a board certified Pathologists’ Assistant, specializing in surgical and gross pathology. He currently works as a Pathologists’ Assistant at the University of Chicago Medical Center. His job involves the macroscopic examination, dissection and tissue submission of surgical specimens, ranging from biopsies to multi-organ resections. Cory has a special interest in head and neck pathology, as well as bone and soft tissue pathology. Cory can be followed on twitter at @iplaywithorgans.


Cut it Out … No, Really, I Need Margins

Hello everyone! Back again with another post about that interesting space between my experiences working in laboratory medicine as an MLS and my current path through medical school toward a career in pathology. Last month, I discussed how the new 5th generation cardiac enzyme assays are evolving and reaffirming the relationships between lab data and clinical decision making. This month, as I adjust to a very different circadian rhythm, I’d like to talk about some topics in my surgery rotation as they relate to surgical pathology and the lab.

Just to summarize, besides epidemiological research and public health initiatives I’ve written about here on this blog, I had several years of lab work before medical school. In my experience, I have seen the gamut of required steps for pathology specimens peri/post-operatively. Everything from placenta, bone, blood, marrow, skin, brain, lung, GI, to any other organ system’s tissue is processed, blocked, stained and examined on glass by pathologists who write reports for their clinical colleagues.  Often, we in the lab receive phone calls from providers inquiring about turn-around times and results as they  follow-up on their patients and cases. In Chicago, I was able to see and train in a great trauma center at Northwestern, community hospitals like Swedish Covenant and Weiss Memorial, and an academic hospital centers like Rush and UIC. What I learned there is just how much really depends on those pathology reports. Cytology, diagnostic immunohistochemistry, morphology, margins, and gross analysis all contribute to a final diagnosis. After an extended observership at UAB Medical Center, I was fortunate to see first-hand the critical process involved in signing out dermatology consults, examining gross pathology, and even frozen neuropathology specimens. Sitting with attendings in the OR and frozen rooms deciding between glioblastoma multiforme, lymphoma, or something benign (read: defer to permanent slide diagnosis later) was fascinating. Meanwhile, I’m now a month into formal surgical rotations at Bronx-Care Hospital in NY and I get to see the other side of the pathology report.

The Relationships Between Surgeons and Pathologists are Critical

Many surgical interventions and procedures require resection of known or suspected pathologic tissue. Whether it’s malignancy, benign growth, obstruction, adhesion, or otherwise mechanically compromising tissue, many patients require a surgeon to remove the entity in question. And, while the difficulty of these excisions and resections may vary depending on location, cases rely heavily on the pathologist-surgeon collaboration. Virtually all neoplasms are diagnosed through anatomic pathology assessment under a microscope. Fine needle aspirates, pap smears, bone marrow biopsies, and countless other tissues must go through pathology before being finalized. This interdisciplinary collaboration between the surgical team and the pathology team is, of course, by nature acutely critical. In proper circumstances, open cases in the operating room are consulted to a pathologist STAT. The effective communication between the pathologist and surgeon awaiting the intraoperative consultation is key to effectively treating their shared patient. Sometimes operating rooms will have live microscopic image-casting, sometimes there is an intercom system, sometimes its solely based on electronic forms in the EHR, and sometimes pathologists need to go into the surgical field to examine the resection intraoperatively in person. However it happens, this is a very important relationship that patients might not be aware of.

The Point of View Between Surgical Pathology and Clinical Surgeons Are Different

So this sounds like a perfect match, right? Surgeons and pathologists living in harmony? Unfortunately, harmony isn’t part of regular onboarding at many institutions so, as with any staff, there are different scopes and sometimes this can be a challenge. Getting a frozen notification as a pathologist is a serious task. They are emergent and must be addressed immediately and diagnoses are made with serious gravity, often consulting with other pathologists. This is also, however, a singular teaching moment as every frozen section is different and pathologists use these learning opportunities to teach their residents and medical students. In the interests of accurate diagnoses, educational value, and appropriate response to the OR, pathologists take measures to ensure success. For example, frozen specimens will be received, a history and presentation of the patient is discussed, the specimen is partitioned for frozen section (STAT), permanent section, and further studies (routine). So, for the pathologist it’s all about accuracy, reliability, and what they can confidently report. The surgeon has a different point of view: they are operating with a specific physical goal in mind by either resecting a tumor, or isolating good margins from a known malignancy, or ensuring the tissue being removed is correct/adequate for its therapeutic purpose. Fun fact: surgical pathology was a field originally developed by surgeons! There are things a pathologist only knows, and there are things a surgeon only knows—but when working together, the overlap of medical knowledge increases the coverage of care for their shared patients’ outcomes.

surgpath1
Image 1. A pathologist processes a frozen specimen on a cryostat machine. A summary of frozen sections from JAMA, 2005;294(24):3200. doi:10.1001/jama.294.24.3200

The Cold Truth About Frozen Sections

Frozen specimens aren’t perfect. In these specimens, tissue gets stiffened by freezing instead of routine paraffin embedding, and because of that a frozen section could be distorted by folds, tears, and other artifacts that might appear because of mechanical manipulation during processing. Frozen samples also leave artifacts where water would crystallize and freeze, but one of the caveats regarding artifacts in frozen sections is that FAT DOES NOT FREEZE. Instead, specimens that have large fat content (i.e. brain tissue) have to be examined carefully to not confuse findings with inflammation or other pathologic processes. Ultimately, it takes numerous cases to properly hone the skills required to confidently diagnose from frozen section. While they might not be perfect, it is a critical tool used between the surgical and pathology teams. Challenges in this handoff process relate to proper use of this surgical tool. For instance, if a frozen is called for and the surgery is closed by the time a pathology report is filed, then (assuming there were no serious delays) this may have been an inappropriate specimen decision. Furthermore, specimens must be discussed prior to receipt for appropriateness and clinical relevance. Fatty lipomas aren’t going to go to frozen section, they shouldn’t be ordered. A thyroid lobectomy? That’s a better utilization of resources and tools.

surgpath2
Image 2. A demonstration of water-related crystal formation causing distortion and artifact (LEFT) on frozen section of muscle tissue, compared to normal (RIGHT). From Northwestern, source: http://www.feinberg.northwestern.edu/research/docs/cores/mhpl/tissuefreezing.pdf

Ultimately, with proper training and experience a pathologist can effectively use the frozen section as a useful clinical tool to improve patient outcomes. Surgeons operating in the best interests of their patients, should strive to create a functional and successful communication between both services. My experiences in NY with surgeons of various kinds reveals a common truth among them: pathology is a critical player in surgical interventions, and without margins, diagnostic stains, and other work-ups, those interventions would be much more difficult and risky.

Thanks again! See you next time!

Bonus: for more content specifically detailing some of the cellular morphologies and cytology I discussed above, please check out I Heart Pathology, a compendium website my friend and colleague at UAB, Dr. Tiffany Graham, manages. It’s meant for other pathology residents to review and refresh on material and it’s updated as often as possible. Check out the link here: https://www.iheartpathology.net/

 

 

ckanakisheadshot_small

–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.

Moving Forward One (Baby) Step at a Time

As this summer passes quickly by, I find myself, once again, anticipating the fall Annual Meeting of ASCP. Deadlines are fast approaching as I pull together my own power point presentation, review the schedule for sessions to moderate as well as those I wish to attend on my own time.

Many of you are involved in the planning process for the Annual Meeting and understand the deliberation and organization that this entails. The plethora of educational proposals is vast, submitted by numerous respected individuals and teams. Given the back-drop of this immense undertaking, I must say that I was thrilled this year to be a part of the discussion for the newly -created Hot Topics in Clinical Pathology. This has been a long-awaited moment for me and many of my cronies who have felt for quite a long time that the focus on Surgical Pathology at the Annual Meeting has essentially pushed aside the importance of Clinical Pathology and Laboratory Medicine as a vital part of everyday pathology practice.

With the creation of the “Hot Topics” track, we at least begin to see a small, but significant move forward. Clinical Laboratory Scientists clearly identify their work and the laboratory as primary contributors to patient care. Pathologists should begin to embrace this concept more fervently. The fields of Microbiology, Coagulation, Hematology, Transfusion Medicine, Serology, Chemistry (and a multitude of other areas) are expanding rapidly and are the KEY to understanding, diagnosing, monitoring and treatment of disease. Our clinical laboratories support and enhance our Surgical Pathology practices as well and the sooner pathologists regain the interest and care for these areas within our expertise, the better off our patients will be (and yes…they are OUR patients too!)

Hats off to the Annual Meeting Planning Committee for taking this bold step (although a “baby” one) toward bringing Clinical Pathology back into the fold. I hope to see this agenda pushed forward and expanded, not just at the Annual Meeting, but also in our other educational offerings. We are, by the way, the American Society for Clinical Pathology!

Our clinical laboratories and clinical pathologists are not the departments or doctors of the lesser god! Hope to see you in Tampa, in attendance at the Hot Topics sessions!

 

Burns

-Dr. Burns was a private practice pathologist, and Medical Director for the Jewish Hospital Healthcare System in Louisville, KY. for 20 years. She has practiced both surgical and clinical pathology and has been an Assistant Clinical Professor at the University of Louisville. She is currently available for consulting in Patient Blood Management and Transfusion Medicine. You can reach her at cburnspbm@gmail.com.

PGY-1: First Month

So, as another July 1st has come and passed, neophyte first years have begun their training in pathology residency training programs across the country. Many will begin with either a bootcamp-style orientation and/or an introduction to surgical pathology. Although I do have a PGY-1 friend who started with a CP rotation (and not an intro one at that).

I was fortunate to have a creative surgpath director who has an interest in different styles of medical education during my PGY-1. During the last two weeks of June, in addition to the general administrative orientation requirements, we had what we affectionately refer to as our “bootcamp.” First, we were taught proper blade/cutting technique with various food products (eg – potatoes, bratwurst) to get a feel for how to adjust our cutting technique for various specimen consistencies.

She was truly dedicated and personally went to a butcher in Chicago and picked up pig organ blocks three times for us during those two weeks. Then she and one of our two surgical fellows instructed us in the Rokitansky en bloc method of autopsy dissection after we had watched a narrated DVD that she had created from the previous year PGY-1 training sessions. We then would have to complete a fourth unsupervised pig block dissection and need to score at least a 75% in order to pass our autopsy competency exam. Those who did not pass, had to repeat the exam.

We also learned how to cut mock uteri and prostates since these are common specimens. She had molded and frozen ground turkey to simulate these organs and even added surprises like chick peas to represent leiomyomas. We practiced how to bivalve and cut the uteri for both endometrial and cervical cancers as well as how to gross prostates…although I did go through the whole year and never get one until I rotated in the fall of my second year at the VA where I got them almost daily.

Additionally, in order to learn how to cut frozen sections, we took ten sections from various organs from our pig blocks and embedded, cut, and stained frozen sections. This way we could understand how certain sections cut better than others (eg – fatty tissue is more difficult to cut), how to orient them, and how to cut them well without folding and unevenness. We were then graded on our sections for frozen section competency exam. For those who did not pass, they got some personal remediation at the cryostat with our assistant director of surgical pathology.

In the gross room, we had PAs who were good at teaching. We practiced dictating biopsies and placentas, grossing placentas, and grossing “smalls” like an appendix or gallbladder. Twice a week, we had multi-scope subspecialty sessions in dermpath, liver, renal, and neuropath since most of these types of specimens go to either our fellows or the subspecialty pathologists and our first years rarely saw them.

We initially started with a six-person, six-day schedule of frozens, grossing biopsies/smalls/bigs preview, grossing bigs, autopsy, peds path, and neuropath for 1.5 months. Our PAs usually gross our biopsies and benign smaller specimens. Then we were whittled down to a four-person, four-day schedule of frozens, preview, bigs, and autopsy with two of us taking “mandatory” vacations. The two residents that remained on SP after our five months of intro to SP were incorporate into our standard three-person, three-day schedule of frozen/grossing bigs, biopsy/smalls signout/bigs preview, and bigs signout.

At my new program, it is different because we don’t have surgpath fellows. Since we are a small program, each senior resident serves as a co-chief and one of their responsibilities is the training of the PGY-1 residents in surgpath during an initial one-month intro to SP rotation. Other senior residents on the surgpath rotation also help out with the teaching. They also give AM lectures on grossing topics in Lester’s Manual of Surgical Pathology and the specific nuances of the grossing preferences of our attendings.

As for me, I start off with a comprehensive CP rotation that combines working in both the chemistry and microbiology sections. As a PGY-1 here, they have 2 months of ‘Wet Lab’ or an intro to CP rotation. But since I am a PGY-3 transfer, I am a cross between a PGY-1 in terms of knowing how things are exactly done here and a senior resident. So this month for me combines intro to SP, Wet Lab, and the subsequent comp CP rotation that would come after Wet Lab. So, I get to gross a little (since things may be done differently here), learn about where and how things are done in the labs, and study more specialized CP topics. Since I came from a program where we rotate at four different hospitals for surgpath and can be self-directed in terms of CP, this works fine for me but still can be initially daunting in terms of trying to fit in do things the way they would like them done here.

So what do you think are the best ways to train PGY-1 residents most effectively? Should they start off with an intro to SP rotation and how should that be structured in terms of time, topic areas, and teaching of those topic areas? Or does it matter if they don’t do an intro to SP rotation and go straight into a CP rotation? And who should teach them how to gross? Let us know how things are done at your institution.

 

Chung

-Betty Chung, DO, MPH, MA is a third year resident physician at Rutgers – Robert Wood Johnson University Hospital in New Brunswick, NJ.

General Versus Subspecialty Surgical Pathology Sign-Out

I’m currently on a month of neuropathology/autopsy at our main academic center. After 2 months at a busy surgpath site with a 1-1.5 hour drive each way, it’s finally nice to be able to take a breather. Here, I’m responsible for any neuro frozen and grossing that doesn’t go to the SP resident, helping with the cutting of autopsy brains, and sign-out of neuropath cases. Since we don’t have a heavy neurosurgery service, this allows me more time to learn at my own pace and I feel that I’m able to retain more.

Not including CP rotations, I’ve always learned more, retained knowledge, and performed better on the subspecialty rotations that I’ve had – hematopathology, pediatric pathology, and now neuropathology. While I acknowledge that part of this is my own fault because when I’m on surgical pathology (we do general SP sign-outs), I read up pretty much only on my cases. I know that I need to preview them for sign-out so I read up on the SP diagnoses and differentials. But I often am not motivated to read up on general systems, so I can be real hot mess (and as one senior resident called me recently, “stupid”) during unknown conferences. In CP topics and those subspecialty areas I’ve had rotations in, I’m quite the opposite and tend to excel.

Yesterday, was the first time I’ve been at consensus conference since my first year. At the community and VA hospitals where I’ve spent most of my SP rotations during my second year, we didn’t have group consensus conferences. I remember last year thinking during consensus, “please don’t pick on me to answer a question” during the inevitable pimp sessions that evolved. But yesterday, besides the fellow, I was the only senior resident present. But I was less apprehensive and intimidated than I had been when I sat in the same place the year before. So even though I don’t consider myself a person who is good at SP, I was adequate enough and I must have learned something over the past year without realizing it.

Obviously, how we teach surgical pathology is restricted by the type of sign-out practiced at the institution we are at and this often is dictated by specimen volumes, faculty expertise, and the cultural philosophy dominant there. Even though I thought that I had taken this question into consideration when interviewing and ranking programs, I realize now that I didn’t have a complete grasp on how training styles and cultures really would affect me. Probably since I’m graduate school trained first and naturally think more like a scientist that focuses on one area and learning everything about that area, subspecialty sign-out works best for me.

Before starting residency, I had an intuition that this was true but thought that I would eventually adapt to a general sign-out format since that is how my institution practices. And I’ve adjusted, albeit maybe not progressed as quickly as my peers. It’s difficult to maintain all surgical pathology as subspecialty unless the volume is high enough and this usually means a large, well-known academic center if that’s what you need during your training. The majority of residents will end up in private practice and many often train at places where the sign-out is a more generalized one. So how do we match our learning needs with practice requirements at our training institutions with our eventual responsibilities as a pathologist in terms of sign-out? I can’t say that I have a solution for this conundrum but would welcome opinions on the topic. What works best to train our residents in surgical pathology?

 

Chung

Betty Chung, DO, MPH, MA is a second year resident physician at the University of Illinois Hospital and Health Sciences System in Chicago, IL.