Tadrous P.J. Diagnostic criteria handbook in histopathology: a surgical pathology vade mecum
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Cut-Up and Reporting Guidelines 49
or surround in a viscous medium [e.g. Tissue-Tek
R
O.C.T. compound] and snap freeze is isopentane
slush) and the rest for routine LM (formalin).
r
A separate portion for IF may be omitted if the lab uses immunoperoxidase for immuno.
r
Dividing the Bx for IF/EM may be omitted in the early (≤6 months) post Tx period for ?rejection unless
there are unusual findings or ?development of GN in the graft (de novo or recurrent).
r
If EM is considered essential but glomeruli are not identifiable (as is often the case in chronically
diseased kidneys), take a 1mm piece from both ends of the Bx into glutaraldehyde.
r
Other variations on handling depend on the clinical questions asked – CPC is required.
Kidney (Adult Renal Tumours)
r
Dissect and examine the hilar structures – some do this by serial en face slices – prior to slicing to fix
(partial slicing, avoiding transection of the hilum, is acceptable if the specimen is to be fixed first).
r
Specify side and size of kidney – is it a radical or partial (nephron-sparing) nephrectomy?
r
Tumour: size (3D incl. max. ), location, type and grade; blocks ≥ 1 per cm max. , include adjacent
necrosis (is it coagulative tumour necrosis, hyaline necrosis or therapeutic embolisation infarction?)
r
Sample any hilar / other LNs (need ≥ 8–10 nodes for reliable staging of pN0; use TNM6 criteria)
r
State if adrenal is present and serially slice and sample it – identify if tumour invades into it by direct
extension (= pT3a) or as isolated foci (= pM1)
r
Sample vascular resection margins (some take a block through the hilum)
RCC
r
Renal vein involvement must be sought macroscopically (confirm by microscopy) – pT3b includes the
main renal vein, its segmental tributaries with muscular media and the IVC below the diaphragm.
r
Perirenal fat: infiltration = cellular infiltration without a capsule (NOT just bulged into).
r
Renal sinus fat: cellular infiltration (as defined above) = pT3a (microvascular invasion in this fat, as
elsewhere, does not affect the stage – but document it). Tumour blocks should include ≈ all the renal
sinus – tumour interface.
r
Is there invasion of adjacent organs or beyond Gerota’s fascia (the perirenal fatty dissection plane)?
r
Is there invasion of the collecting system? (does not affect TNM but record it).
r
Serially slice the tumour (look for white solid areas – ?sarcomatoid).
r
Serially slice the kidney (look for synchronous tumours) and sample uninvolved kidney.
TCC
r
Take distal resection margin of ureter, examine the pelvis for synchronous tumours and sample for CIS.
r
Seek invasionof renal parenchymaor peripelvic fat (pT3) or perirenal fat via renal parenchymal invasion
(pT4).
r
The size of LN mets are important for TNM staging (not just the n˜o.)
Urinary Bladder
Biopsies
r
Punch Bx (specify how many and sites), TURBT (specify weight and either embed all or ≈4 blocks to
include likely muscle/solid areas – if microscopy shows pT1 or no muscle, embed more +/ do levels).
r
Specify tumour presence, type, grade and level of invasion (pT stage upto ‘at least pT2a’ i.e. tumour
infiltrates thick cohesive muscle bundles – not the thin separated fibres of the muscularis mucosae).
r
Specify whether or not there is flat CIS or invasion of prostatic / urethral tissue.
Cystectomy
r
Type of operation: partial / radical, simple or with prostate, urethra, uterus or cervix.
r
Inflate with formalin then bivalve coronally via urethral probe.
r
Measure dimensions of all organs and N˜o., size, position and depth of any tumours.
r
Is there macroscopic invasion of perivesical tissues (extravesical mass = pT3b) ?
r
Blocks: tumour(s) – to see the factors described above [for biopsies] and completeness of excision;
stage multiple tumours according to the most advanced and use the ‘m’ suffixe.g. pT2b(m)
urethral and ureteric margins – to check for flat CIS
bladder walls: dome, trigone, left, right, anterior, posterior
any LN (defined according to TNM6 criteria) / accompanying organs (sample prostate
well for synchronous prostate
CA)
JWBK208-04 December 8, 2007 15:59 Char Count= 0
Cut-Up and Reporting Guidelines 50
Prostate
Resections (radical prostatectomy)
r
Weigh and ink left vs. right (NB: seminal vesicle on posterosuperior aspect helps orientation – see
Figure 4.11).
r
Shave (or cone) urethral margins from apex (inferior) and base (superior)
r
Slice into transverse serial sections ± photo; use large blocks to embed whole sections (some local
guidelines prefer to use standard-sized blocks concentrating on tumour and prostate capsule as these
are easier to use for immuno, quicker to process and easier to get good thin diagnostic sections).
r
Embed first slice above the apex and EITHER representative (if tumour can be seen going close to
margins) and random blocks of peripheral margins OR embed the whole gland.
r
Representative blocks of seminal vesicles (esp. proximally i.e. near the prostate)
r
Accompanying lymphadenectomy specimens should be all embedded.
r
Report: Gleason score
is tumour organ-confined? (see criteria for extraprostatic extension in Chapter 16:
Urological)
circumferential margin, seminal vesicle and LN status .
T1 Prostate cancers (i.e. those diagnosed on TURP or core Bx)
NB: the term ‘minimal adenocarcinoma’ is defined
as
CA involving <5% of the whole specimen (usu.
applied to core Bx) and some ‘experts’ diagnose
this on as few as 2–3 acini
r
T1a involves ≤5% of the sample (by volume or area)
r
T1b involves >5% of the sample (by volume or area)
r
T1c if tumour is diagnosed on core Bx
r
NB: these are clinical T stages that depend on
histology – there is no pT1 category
TURP chips
r
Protocol depends on attitude of local surgeons to T1 cancers re further management.
r
In the following points ‘AGE’ is the age below which the patient will be considered for radical prosta-
tectomy upon diagnosis of carcinoma (the UK National Dataset for 2000 suggests a value for AGE of
70 years. Some local practices use other values e.g. 65 years. However other factors may also contribute
to the question of operability such as fitness, patient choice, etc.)
r
In the following points, a filled cassette will contain about 2g of tissue.
r
If known carcinoma, only process a small sample of 6g (3 cassettes) to compare grade.
r
If not known carcinoma and:
<AGE → embed all tissue
>AGE and <12g total sample → embed all tissue
>AGE and >12g → embed first 12g (6 cassettes) then 1 cassette per additional 5g
(Some say embed the first 12g then the rest if no tumour detected in this first sample.)
r
If high grade PIN is seen then more tissue should be embedded to detect carcinoma.
r
Some local guidelines advise that:
◦
1
if initial sample shows high grade carcinoma → no further tissue embedded
◦
2
if initial sample shows low grade carcinoma → embed more tissue
r
Needle core Bx: (cut multiple levels and spares for immuno)
◦
1
Bx from single nodule: confirm malignancy / grade
◦
2
sextant biopsies for ↑ PSA: detect carcinoma, grade and estimate extent of disease
N˜o., site and size of cores and % involved by carcinoma (for each core).
Whether carcinoma infiltrates adipose tissue, skeletal muscle or seminal vesicle.
Report high grade PIN (if carcinoma is not present).
Any other pathology that might account for ↑ PSA (e.g. active / chronic prostatitis).
Testicular Tumours
Aims: Distinguish spermatocytic seminoma vs. pure seminoma vs. tumours with NSGCT elements.
Identify vascular invasion and invasion of any part of the cord or the tunica vaginalis testis.
Macro Note cysts / haemorrhage / necrosis and whether the tunica vaginalis slides freely on the testis.
Blocks: cord (margin, mid, root); measure tumour(s) and take multiple blocks (≥1 per cm
),
adjacent testis, uninvolved testis.
Micro List elements present and if there is ITGCNU; is there evidence of regression (scar +ITGCNU)
Tumour size and invasion (vascular, rete, epididymal, cord, tunica vaginalis testis) – rete inva-
sion includes invasion of the rete stroma i.e. tumour does not have to be seen in the rete tubule
lumens
Immuno: PLAP, AFP, hCG (also c-kit, CD30, NSE, EMA, CK).
JWBK208-04 December 8, 2007 15:59 Char Count= 0
Cut-Up and Reporting Guidelines 51
Retroperitoneal LN
Assess:
◦
1
Margins
◦
2
Surviving tumour and types (esp. transformation to somatic malignancies)
◦
3
Whether there is recognisable residual LN architecture. For detail, see p. 228.
Penis (Amputation)
r
Insert a catheter (or Pasteur pipette) into urethra, fix (24 hours) and ink proximal margin of shaft and
skin.
r
Specify type (partial/full amputation or glansectomy), length of specimen and whether circumcised
r
Describe tumour location, extent and type (exophytic or ulcerated)
r
Bisect in sagittal plane (may use scissors to cut ventral urethra to skin first, then knife to complete)
r
Sample to assess tumour depth (esp. if extending to urethra / corpora), ulceration, extent of shaft
invasion, laterality and margins (skin and proximal shaft) – big blocks may be helpful.
Endometrial Cancer / Atypical Hyperplasia
Curettings:
r
Presence of atypical hyperplasia or carcinoma (type, grade, background hyperplasia)
Hysterectomy
r
Tumour type: endometrioid (FIGO grade) / others
r
Invasion: myometrium, cervical stroma,
7
adnexa serosa, vessels, LN
r
Peritoneal washings cytology (result alters FIGO and TNM sub-stage)
r
Distinguish solid adenocarcinoma from squamous differentiation. Grade only on adeno part (For FIGO
criteria for squamous differentiation, see p. 241)
Cervical Neoplasia
Biopsies
r
Presence of CIN, CGIN, HPV and invasion
r
If Bx large enough to include whole lesion: type, size and FIGO stage
r
Completeness of excision (not if punch Bx)
Wertheim’s Hysterectomy
r
Tumour: size (max. dimension may be across blocks), type, grade, site, depth of invasion
r
Margins: vaginal, soft tissue (anterior and posterior) and parametrial
r
Sample full circumference of vaginal margin (because there may be microscopic lymphatic spread)
r
Type: SCC (keratinising / non-keratinising), SmCC, basaloid, verrucous, glassy cell, adenosquamous
Vulval Bx and Vulvectomy
r
Distinguish FIGO stage IA disease: ≤2cm max. and ≤1mm stromal invasion (depth measured from
the level of the tip of an adjacent uninvolved dermal papilla)
r
Background changes (VIN, HPV, dystrophies) – see p. 232 for the two types of SCC
r
Type and differentiation of tumour (? no agreed guidance for Paget’s disease)
r
Minimum tumour-free margins (mm): skin, vaginal ( urethral), anal, deep
r
Vascular invasion
r
LN status incl. extracapsular spread
Ovaries
Macro
r
Measure of intact cyst (otherwise state it was collapsed).
r
Sample ≥1 block per cm of solid (and non-smooth cystic) tumour. Upped to 2 blocks/cm for tumours
>10cm in max.
. [These guidelines are to ensure that a borderline diagnosis is accurate – fewer blocks
may be taken if the tumour is obviously malignant and homogeneous].
r
Differentiate surgical puncture from tumoural perforation from tumour growing on the surface.
r
State the size of the largest extra-ovarian tumour nodule (e.g. omental).
7
Determines sub-stage of stage II disease: IIA = cx glandular involvement, IIB = cx stromal involvement
JWBK208-04 December 8, 2007 15:59 Char Count= 0
Cut-Up and Reporting Guidelines 52
Micro
r
Tumour type (or types if mixed – defined as minor component(s) comprising >10% of the tumour)
r
Grade epithelial tumours and immature teratomas (grade 1
◦
separately from deposits)
r
State additional prognostic factors for non-epithelial tumours: mitotic count per 10 hpf (for sex
cord / stromal tumours, dysgerminoma and FATWO); vasc. invasion (for dysgerminoma, FATWO
and SCTAT); state if there is marked nuclear pleom. (for dysgerminoma, steroid cell tumour NOS and
FATWO) and some tumour-specific features (heterologous elements in Sertoli/Leydig, sparse lympho-
cytic infiltrate in dysgerminoma and stromal invasion in SCTAT)
r
The result of any peritoneal washing cytology is included in the UK National Dataset report
r
If the appendix is sent, embed it all and state the extent/site of any tumour (serosal, mucosal, intramural,
etc.)
Breast Carcinoma
r
Specify side, weight (except mastectomies) and type (core Bx, localisation Bx, segmental excision)
r
Have you seen the specimen X-ray (one should be done for X-ray detected/localised lesions)? Is the
radiographic abnormality present in the specimen? Sample such as to include it in the blocks [may need
to X-ray your slices / blocks to confirm this and identify which blocks contain the lesion(s)].
r
In axillary dissections aim to find ≥16 LN for accurate staging; identify the apical LN if possible
r
Size of invasive tumour (max. dimension; combine macro and micro information as necessary):
this is the measurement used for TNM staging (not ‘whole size’ vide infra)
in multifocal tumours use the size of the largest focus (if they are discrete and separate)
if a single tumour mass is composed of ill-defined separate parts (i.e. not a well-defined main
tumour with a well-defined small satellite) use the aggregate size of all the parts
r
Whole size (= size of invasive tumour + overhanging DCIS) if there is an extensive DCIS component
(defined as DCIS extending >1mm beyond the edge of the invasive tumour)
r
Distance to nearest margin – for invasive tumour and separately for any extensive DCIS component
r
Other factors: tumour type, grade and multifocality, peritumoural vasc. invasion, presence of Ca
2+
(and
whether assoc
d
with benign or malignant structures); any background disease.
Placenta
Indications
r
Fetal abnormalities or neonatal diseases with possible intrauterine origin (incl. neurological signs)
r
Premature rupture of membranes >36 hours
r
Multiple gestation (to establish chorionicity ± other anomalies)
r
Maternal illnesses that may affect the neonate (pyrexia / group B Strep., HT/PET, CTD, DM (and other
metabolic disease), thrombotic disorders, neoplasia, etc.)
r
No examination is indicated for normal births of normal singleton infants regardless of whether there
is placenta praevia, PPH or other maternal conditions such as HIV/ viral hepatitis, etc.)
Macro
r
Clin.: maternal age, gestational age, birth weight, fetal presentation and mode of delivery, time of
rupture of membranes, time of delivery, maternal PMHx, any complications
r
Cord: length (<32cm is too short, >100cm is too long), insertion, knots (true and false), vessels, n˜o.
of twists (normally 1 per 5cm of length; sig. more – hypercoiling – may accompany hypoxia)
r
Placental shape and if any succenturiate lobes
r
Membranes: insertion, completeness, colour
r
Maternal surface: completeness, thickness (average <2cm = abnormally thin), clots/craters/focal le-
sions (give position and % involvement)
r
Twins/multiple: amount of placenta serving each fetus (keep cords and placental zones identifiable for
each infant), vascular anastomoses (arteries lie superficial to the veins, veno-venous anastomoses are
a worse prognostic than arterio-venous or arterio-arterial anastomoses). May need injection studies in
the fresh placenta if ?twin-twin transfusion. Take ‘T’-junction block to confirm chorionicity
r
Measure the trimmed weight (membranes and cord removed) and state if fixed/fresh
r
Blocks: cord (×2 ± funix), membrane roll, full-thickness placenta away from edge (×3).
Soft Tissue Sarcomas
r
Type of operation, nature of specimen, anatomical landmarks
r
Consider taking fresh tissue for cytogenetics esp. if young (e.g. <40) or a deep / large fatty tumour
JWBK208-04 December 8, 2007 15:59 Char Count= 0
Cut-Up and Reporting Guidelines 53
r
Tumour size and consistency (fleshy, gritty, and presence of bone, cartilage, haemorrhage, etc.)
r
Presence and amount of necrosis (as a %): take 1 block per 2cm of tumour for this
r
Margins
Bone Sarcomas
r
Biopsies: make imprints (air-dried) for ALP-staining as an adjunct to histology; fix and decalcify the
remainder
r
Resections: description of whole specimen (operation, anatomy, attachments, etc.)
prepare a 5mm thick longitudinal slab in a plane through the max.
of the tumour
X-ray the slab to see soft tissue extension and serve as block guide
many blocks (≥40) to assess % non-viable tumour (= chemoRx response), state of
the excision margins and to confirm / exclude soft-tissue extension
Thyroid Tumours
Macro
r
Weigh, ink, measure and specify left/right; lobectomy/thyroidectomy; total/‘near-total’.
r
Measure max. of main lesion (and search for others); sample any intrathyroid margins, parathyroids.
r
Sample any LN and note site (contralateral / ipsilateral / central / level IV / other).
r
MTC: block all specimen; PTC: sample tumour(s) +≥2 blocks from uninvolved tissue of each lobe;
follicular: sample capsule widely (≥10 blocks if not embedding the whole lesion).
r
All tumours: samples to assess presence and extent of any extrathyroidal spread.
Micro
r
Confirm max. if ≤20mm (NB: the UK RCPath Dataset advocates TNM5 i.e. pT1 is ≤10mm).
r
In multifocal tumours, the largest tumour is used for the T part of the TNM classification.
r
For mixed follicular adenoma/PTC the used for staging is that of the whole tumour (if there are
multiple PTC foci in it) or the
of the focus with recognisable PTC features (if it is the sole focus).
r
Tumour: distance to margins, type(s) and differentiation by predominant area. If well-diff, state if minor
foci of poorly diff carcinoma are present but if an undiff focus is seen, however small, the tumour is
classified as anaplastic carcinoma.
r
Distinguish follicular tumours with capsular invasion (only) from cases with vasc. invasion and state if
the latter is extensive (e.g. >5 intracapsular or extratumoural vessels involved).
Parathyroid Carcinoma
r
Macro: site, weight of gland(s), size, ?intact capsule (?breached during surgery); clin.: ?1
◦
/recurence
r
Micro: diagnosis, completeness of excision, state of LNs and any accompanying thyroid / parathyroids
Adrenal Tumours
Macro
r
Site, weight, size, ?intact capsule, ?necrosis, ?invades surrounding tissues; clin: ?laparoscopic resect
n
r
Blocks: tumour (if <3cm block it all, else take 1 per cm ) + LN + uninvolved cortex (if cortical
tumour) or medullary tail (if phaeochromocytoma) + any needed to give the micro information
Micro
r
Tumour type, max. , distance to margins, capsular/local invasion (?involves adjacent organs), mitotic
count, vasc. invasion, background hyperplasia. [For features of ↑ risk of malignancy, see pp.275–276]
r
A note on staging: There is no pTNM for phaeochromocytomas. A pathological staging’ TNM for ACC
in given in the 2006 RCPath National Dataset but this was designed as a per-operative clinical staging
(done by the dissecting surgeon without microscopy). This explains the lack of any histological (micro)
definition of local invasion in the literature:
T1 is defined by MacFarlane (1958) and Henley et al. (1983) as tumour ≤5cm
and T2 as
tumour >5cm
T3 is defined by MacFarlane (1958) as ‘infiltration locally reaching neighbouring organs’ and
refined by Henley et al. (1983) to ‘tumour any size, locally invading to but not involving
adjacent organs’
T4 is defined by MacFarlane (1958) as ‘infiltration of neighbouring organs – kidney, veins,
etc.’ and by Henley et al. (1983) as ‘tumour any size, locally invading adjacent organs’
JWBK208-04 December 8, 2007 15:59 Char Count= 0
Cut-Up and Reporting Guidelines 54
Many sources speak of T3 as merely ‘local invasion’ but the originators of this staging system imply that
the local invasion should reach upto (but not into) neighbouring organs. In the absence of a well-defined
and standardised pTNM system, the application of this surgical TNM system by histopathologists is thus
questionable.
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Paediatric and Placental 56
5. Paediatric and Placental
Paediatric
Congenital / Malformative Anomalies
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Of the lung (see pp.82–83, p. 393 and vide infra)
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Of the heart (see p. 385, p. 386, p. 389 and p. 78)
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Of the urinary tract / testis (see pp. 212–213, incl. Potter’s triad)
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Of skeletal muscle (see p. 191 and p. 184)
Alveolar capillary dysplasia
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Incompatible with recovery–!sodiagnosis results in termination of ventilatory support
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Alveolar walls are thickened, cellular and contain ↑numbers of prominent capillaries
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Capillaries not closely apposed to alveolar lining
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Misalignment of pulmonary veins: the small pulm. veins accompany the bronchi and pulm. arteries
(cf. running separately in the interlobular septa) resulting in reduced septal vascularity
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d/dg peripheral lung injury due to ventilation, infection, etc. – look for the venous anomalies
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d/dg do not confuse pulmonary lymphangiectasia or interstitial emphysema for pulm. veins
Hirschprung’s Disease (HD)
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Ultrashort segment (aganglionosis of distal rectum only)
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Short segment (upto the rectosigmoid junction)
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Long segment (beyond the rectosigmoid but not reaching the small bowel)
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Total colonic (includes variable amounts of small bowel)
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Easy to exclude HD (in a particular segment) by seeing the presence of ganglion cells
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Diagnosis based on neural morphology including acetylcholinesterase (AChE) staining:
absence of ganglion cells in the submucosa
hypertrophied nerve trunks and ↑ nerve fibres in the submucosa
↑ density of AChE fibres in the lamina muscularis mucosae (all ages, pathognomonic)
↑ density of AChE fibres in the lamina propria mucosae in older patients which are
1. coarse
2. extend to surface
3. run parallel to surface
4. not present in neonates with HD (! false −ve diagnosis if unaware of this)
! false +ve if unaware of normal appearances, esp. close to the pectinate line i.e.
↑ density of vessels (vessels are normally surrounded by AChE +ve fibres)
hypoganglionosis is normal 1–2 cm proximal to the pectinate line
occ. nerve trunks and fibres are normal in submucosa of right colon and rectum
d/dg ganglion cells vs. CMV inclusions of endothelium
! false −ve if unaware that ganglion cells look different in neonates (small cells without
prominent nucleoli – d/dg stromal cells)
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.
.
. Must know age of patient, distance of Bx and examine ≥50 levels
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Some cases of total colonic HD may not show ↑ fibres in the muscularis mucosae → ! false −ve
Necrotising Enterocolitis
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Radiological pneumatosis in a premature baby ± pneumatosis macroscopically at cut-up
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Mural haemorrhage ± necrosis
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Pneumatosis (may show multinucleated GC around the spaces)
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± signs of healing: granulation tissue, epithelial regenerative atypia, fibrosis (± stenosis)
CIBD in Children
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In UC, 1
st
presentation may be patchy with subtle/absent signs of chronicity and with rectal sparing
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In CD, upper GI involvement (usu. asymptomatic) is more common cf. adults
Infantile Respiratory Distress Syndrome (Hyaline Membrane Disease)
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Alveolar collapse
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Hyaline membranes in terminal and resp. bronchioles (cf. alveoli in adults)
Diagnostic Criteria Handbook in Histopathology: A Surgical Pathology Vade Mecum. Paul J. Tadrous
Copyright
C
2007 by John Wiley & Sons, Ltd. ISBN: 978-0-470-51903-5
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Paediatric and Placental 57
Cutaneous vascular lesions (according to the ISSVA Classification)
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Diagnosis depends on CPC: present at birth? progression/involution? results of flow studies, etc.
Neoplasms
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Congenital haemangioma (M=F, present at birth, subdivided by involution history into RICH/NICH)
RICH involutes from the centre with capillary lobules replaced by fibrosis, haemosiderin
and thromboses ± Ca
2+
leaving dilated abnormal channels with thick or thin walls; other
features may overlap with infantile haemangioma but GLUT1 is −ve and capillaries may be
thin-walled
NICH grows at the same rate as the child, features may overlap with RICH and infantile
haemangioma but GLUT1 is −ve
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Infantile haemangioma (= ‘juvenile / cellular haemangioma’, do not use ‘infantile haemangioendothe-
lioma’)
FM, may be present at birth, grows faster than the infant for a few months then involutes
proliferative phase: abundant lobules of small capillaries with diffusely GLUT1 +ve endothe-
lium
endothelium is plump: lumena may not be evident (but you see packeted and tubular retic
patterns)
involutional phase shows few capillary foci (GLUT1 +ve) with more stroma and prominent
larger feeder vessels (have GLUT1 −ve endothelium by immuno) – see p. 318 for more
d/dg ! do not mis-diagnose involutional phase as AVM (which do not have GLUT1 +ve
capillaries)
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Other (GLUT1 −ve): pyogenic granuloma, KS, HPC, Kaposiform haemangioendothelioma, tufted
angioma (angioblastoma of Nakagawa), etc. For more information, see Chapter 21: Soft Tissues
Malformations
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Simple: one type of vessel (use D2-40 for lymph) It is important to identify if there is an arterial
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Combined: >1 type e.g. lymphovenous or AVM
component (high flow malformations require
different Rx).
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d/dg involutional phase infantile haemangioma: malformations (esp. AVM) may show foci of prolifer-
ative immature vessels (+ve for Ki-67, SMA and CD31 and may ‘infiltrate’ normal tissues) but these
are GLUT-1 −ve
Spindle Cell Lesions of Childhood / Infancy
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Fibrous hamartoma of infancy
◦
1
spindle cell fascicles (CD34 −ve) For mesenchymal hamartoma
◦
2
fat as part of the lesion
and other bone tumours, see
◦
3
primitive mesenchymal cells Chapter 22: Osteoarticular.
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Digital fibroma of infancy affects fingers
spindle cells with eosinophil inclusions (see p. 286)
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Inflammatory myofibroblastic tumour: systemic Sx, inflam
y
cells, spindle cells, ALK1 +ve
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Infantile fibromatosis: single or multiple, 10% recur, Rx is local excision
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Desmoid fibromatosis: never regress, 80% recur, Rx is WLE (± chemo/radioRx)
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Infantile fibrosarcoma: single lesion, may metastasise, 30% recur, Rx: chemoRx and WLE (good prog)
See also Chapter 21: Soft Tissues, for more on some of these entities and specialised textbooks.
Thymic Cyst
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A lymphoepithelial cyst usu. in the lateral neck. and present in <10 year olds
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d/dg branchial cyst:
thymic cysts present in young child, branchial in adults
thymic cyst contains thymic lymphoid tissue in the wall ± Hassall’s corpuscles
Langerhans Cell Histiocytosis / Histiocytosis X (HX)
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Proliferation of Langerhans dendritic cell histiocytes:
abundant cytoplasm
elongated vesicular nucleus, may have a transverse ‘fold’ / ‘belt’
immuno: +ve for CD1a, S100, HLA-DR (MHC class II). CD68 is weakly +ve
EM: ‘tennis racket’ Birbeck granules
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Usu. eosinophils also present, may be numerous
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Paediatric and Placental 58
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Localised form (‘eosinophil granuloma’) has better prog. cf. systemic (Hand-Sch¨uller-Christian and,
worst of all, Letterrer-Siwe)
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d/dg ALCL (see p. 116 and p. 302); non-X histiocytoses (see p. 286); Gaucher’s disease (see p. 123);
Rosai-Dorfman (CD1a −ve, lymphocyte emperipolesis) and epithelioid granulomatous / eosinophilic
inflam
n
Ewing’s, Peripheral Neuroectodermal Tumour (PNET) and Askin Tumour (of chest wall)
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Sheets of small glycogenated cells with scant, ill-defined cytoplasm Askin tumour has features
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PNET (cf. Ewing’s) it is more lobulated, more vascular ± occ. rosettes
intermediate between
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No fibrillar stroma or other neuroblastoma features Ewing and PNET
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Cytogenetics: t(11;22)(q24;p12)(FLI1;EWS) – the same in Ewing’s, PNET and Askin
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PNET and Ewing’s immuno: vimentin +ve (dot-like), CD99 +ve (strong membranous
1
), CK −ve
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PNET selective immuno/stains: NSE, S100, Synaptophysin +ve (also, tends to be −ve for glycogen)
See pp.335–336 for more on Ewing’s incl. EM, d/dg and prognostic factors.
Desmoplastic Small Round Cell Tumour (DSRCT)
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Multiple intra-abdominal masses in adolescent (M>F). Also reported in pleura, CNS and lymph node
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Low power: sharply outlined trabeculae of blue cells separated by desmoplastic stroma
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Central necrosis ± Ca
2+
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Uniform cells, scant cytoplasm, indistinct nucleoli, mitoses ++ (a variant has eosinophilic cytoplasm
++)
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t(11;22)(p13;q21) – said to be unique to DSRCT
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Immuno: co-expression of epithelial (CAM5.2, AE1/AE3), neural (vimentin, NSE) and muscle (dot-
like desmin). CD99 +ve in 30%. C-terminal WT1 +ve (C19 Ab), MyoD1, myogenin and myoglobulin
are −ve
Rhabdomyosarcoma (RMS)
FIGURE 5.1
Sites of RMS
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Occurs at sites of embryonic tissue fusion (head, neck and midline – the
grey zone in the Figure 5.1)
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Classification by prognosis: best: botryoid and spindle cell
intermediate: embryonal NOS
poor: alveolar and pleomorphic
unknown: RMS with rhabdoid features.
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Features of striated muscle differentiation: bright cytoplasmic eosinophilia ± cross striations
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Immuno: MyoD1 (nuclear), polyclonal desmin, MSA, myoglobulin, myogenin +ve; CD99 +ve in 15%
(usu. weak granular cytoplasmic)
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d/dg: muscle infiltrative small blue round cells of regenerating muscle, see also Chapter 21: Soft tissues
Embryonal
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Variable cellularity with cambium layer (cellular condensation beneath mucosa) and pericellular retic
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Cells range from primitive stellate to elongated forms with bright eosinophilia ± cross striations
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Anaplastic cells may be present singly or as clonal clusters
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± Myotube-like formations, ± ‘smooth muscle-like’ spindle forms with blunt nuclei, ± myxoid areas
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Variant: Botryoid – has polypoid nodules (usu. occurs in bladder and vagina)
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Variant: Spindle Cell – fascicles ± storiform, not anaplastic (usu. occurs in the paratesticular region)
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Cytogenetics: +8, +2, +11, rea.(12)(q13)
Alveolar
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Fibrous septa delineate cell aggregates with central dyscohesion. Reticulin is peri-aggregate
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Cells are rounded (! d/dg lymphoma) + focal striated muscle differentiation ± clear cells; myxoid is
usu. absent
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Variant: solid – lacks the dyscohesion and fibrous septa but retic is not pericellular cf. embryonal RMS
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Variant: mixed alveolar / embryonal – consider this if there are spindle and myxoid areas
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Cytogenetics: t(2;13)(q35;q14) in 70% or t(1;13)(q36;q14)
Pleomorphic
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Whole tumour must be pleom. without foci of embryonal or alveolar variants; striations are rare
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Diagnosis requires at ≥ 1 striated muscle immuno plus H&E evidence of polygonal rhabdomyoblasts
1
useful pattern to distinguish Ewing’s/PNET from blastematous Wilms’