abdominal radiology congress... scottsdale 2012
TRANSCRIPT
Unusual CT Manifestations of CommonAbdominal Diseases
Rosa Bouzas-Sierra, MD--- [email protected]
Milagros Otero-Garcia, MD----- [email protected]
Spain
NO DISCLOSURES
Rectosigmoidoscopy:
Solitary linear ulcer in Sigma
CASE 1 : 55 y-old male with rectal bleeding
Solitary rectal ulcer Syndrome:
• occurring mainly in young patients who experience rectal bleeding
Giant ulcers in ileum and colon by citomegalovirus :
• in AIDS patients
• Feczko PJ et al. AJR 1980• Balthazar EJ. AJR 1996
- Carcinoma
CTC
A- GIST
B- Colon Cancer
C- Submucosal Lipoma
D- Intramural Hematoma
Bowel laceration?
* Pickhardt PJ. RadioGraphics 2007
Woman 45 y, IUD
Acute pelvic pain, fever
Bimanual uterine and adnexal tenderness
WCC: 15,000/μL [reference value, <10,000/μL]
US: No possible (very painful)---- CT
A- Pelvic Inflammatory disease (TOA)
B- Ovarian torsion
C- Hemorrhagic ovarian cyst
D- Ovarian mass
At surgery and pathologic analysis, the ovary was hemorrhagic and necrotic
- Ovarian torsion is the twisting of an ovary on its ligamentous supports - Concomitant ovarian and tubal torsion (adnexal torsion) occur in up to 67% of
cases- It is generally considered an acute condition (subacute…)
- All ages- Reproductive years (pregnancy: 5-fold – first trim.)- highest prevalence
Predisposing Conditions- Large (>5 cm) cysts and cystic neoplasms (benign mature cystic teratomas….)- Ovarian hyper- stimulation syndrome - Normal ovaries (usually right ovary) in adolescent or teenagers
- Non-specific symptoms and laboratory tests. DD: PID, appendicitis…..- Imaging plays a central diagnostic role (ovary-sparing)
Ovarian torsion
. Chang HC et al. RadioGraphics 2008
. Appelbaum HL et al. AJR 2007
. Rha SE et al. RadioGraphics 2002
Ovarian torsion Imaging findings
US
Color Doppler
- Complex adnexal mass- Unilateral enlarged ovary (>4 cm)- String of pearls sign: Multiple peripheral cysts- Free pelvic fluid (8%)
- Decrease or absence of venous flow (93%)- Absence of arterial flow (60-73%)- Ovaries without flow in the vascular pedicle
- Twisted vascular pedicle: (circular vessels: “whirlpool sign“)
Ovarian torsion Imaging findings
CT- Adnexal mass in the midline, rotated towards the contralateral side of the pelvis - Deviation of the uterus to the side of the affected ovary- Free fluid
- Necrosis seems to be the cause of a cystic appearance on CT
T2 FSTIRT2
Ovarian torsion Imaging findings
MR - Pregnant women, young girl- MR imaging is recommended to help detect the twisted vascular pedicle
(“whirlpool sign“) or in patients with a suspected ovarian mass.
Take home message: Ovarian torsion in a “women in their reproductive years”, without an underlying mass
49 y-old woman, breast cancer
Liver and bone metastasis (IV)
CHT induction and consolidation
No hepatic massesChemotherapy-induced pseudocirrhosis
Control: 20 weeks later
A- Carcinomatosis
B- Hepatic failure
C-Fluid retention
D- Peritoneal tuberculosis
42 radiology.rsna.org n Radiology: Volume 258: Number 1—January 2011
REVIEW: CT Findings of Chemotherapy-induced Toxicity Torrisi et al
the toxicities of the molecularly targeted
agents are less predictable.
Targeted therapies can be classifi ed
according to their mechanism of action
( Table 4 ). Monoclonal antibodies are
designed to bind to antigenic determi-
nants of specifi c molecules, the expres-
sion of which is sometimes upregulated
in malignancy, but the action of such
antibodies does not necessarily rely on
the activation of immune effector cells.
Several monoclonal antibodies are in
clinical use. Rituximab (Rituxan; Biogen
Idec), a chimeric monoclonal antibody
that is used to treat B-cell non-Hodgkin
lymphoma, binds to the CD20 protein
on the surface of both normal and ma-
lignant B cells ( 2 ). Binding the CD20
receptor init iates apoptosis, down-
regulat ion of CD20 expression, and
antibody-dependent cell phagocytosis
or complement-mediated lysis of the
tumor cell. The drug is also licensed for
use in the treatment of rheumatoid ar-
thritis, and effi cacy has been reported
in other autoimmune disorders. More
recently, cetuximab (Erbitux; Bristol
Myers Squibb, ImClone, Merck) was li-
censed to treat colon adenocarcinoma
and squamous head and neck cancers.
It binds to the EGFR and prevents
the interaction of its ligand ( epidermal
growth factor) with its receptor (EGFR),
thereby blocking the activation of intra-
cellular signaling pathways that would
normally instruct the cell to grow and
divide. Hence, it acts as a tyrosine kinase
inhibitor. Important to notice is a recent
discovery that cetuximab is active only
in tumors that are wild type for KRAS
( 3 ). The exact mechanism of action is
unclear, as cetuximab recently demon-
strated antitumor activity in patients
with colorectal cancer whose disease
Paradigm Shift in the Systemic
Treatment of Cancer
Cytotoxic chemotherapy agents usually
interfere with RNA and DNA synthesis
or cell division and, therefore, affect cell
growth by various mechanisms of ac-
tion. Some of the most commonly used
drugs include classic agents such as cy-
clophosphamide (an alkylating agent),
cisplatin (a DNA intercalating agent),
fl uorouracil (5-FU; an antimetabolite),
doxorubicin (an anthracycline), vincris-
tine (a mitotic spindle inhibitor), and
bleomycin. Some of the more recently
developed cytotoxic agents include gem-
citabine (another antimetabolite), ox-
aliplatin (a cisplatin analog), paclitaxel
and docetaxel (the ―taxanes,‖ which are
mitotic spindle poisons), and ir inotecan
(a topoisomerase inhibitor) ( Table 1 ).
Common trade names are provided for
reference ( Table 2 ). If the drug’s damage
to the cell is too severe to be repaired,
cell death or apoptosis will occur. The
goal is a preferential effect on tumor over
normal tissues. Drugs that interfere with
nucleic acid synthesis and cell division have
the greatest effect on rapidly dividing cells.
Therefore, these drugs will also affect
the rapidly dividing cells of the intestine
and bone marrow, leading to common and
sometimes dose-limiting gastrointestinal
toxicity and myelosuppression. Nearly any
organ can be affected, however, de-
pending on the drug. Peripheral nerves
(eg, vinca alkaloids, cisplatin, taxanes),
lungs (eg, bleomycin and gemcitabine),
kidneys (eg, cisplatin), heart (eg, anthra-
cyclines), and central nervous system
(eg, high-dose methotrexate, 5-FU) are
only a few examples ( Table 3 ).
Molecular therapies have developed
as a result of an improved knowledge of
cancer biology. They target cell surface
antigens (as in the case of monoclonal
antibodies) or various signaling mole-
cules (as in the case of kinase inhibitors).
Many of these agents affect multiple
targets and, therefore, have the poten-
tial to inhibit molecules that are critical
to unsuspected pathways, causing toxic-
ity that has not been previously observed
( 1 ). While some of the toxicities of the
cytotoxic agents and molecularly targeted
therapies overlap, there is concern that
Classic chemotherapy agents inhibit
cell division and target rapidly
proliferating cells. In contrast, the
newer molecular targeted therapies are
directed at specifi c molecules respon-
sible for regulating cell activities, and the
onset and presentation of their toxicities
may therefore differ. Understanding
the mechanisms of action of the newer
molecular agents may aid recognition
of their associated toxicities, though
the mechanisms of the toxicities are
not completely understood. Several of
the monoclonal antibodies and tyrosine
kinase inhibitors bind known membrane
cell receptors. Others bind intracellular
molecules and are multitargeted, and
their toxicities may be more ubiquitous.
We will review the most common
toxicities of the classic and newer cyto-
toxic chemotherapy agents and discuss
what is known about the toxicities of
the molecularly targeted agents accord-
ing to the available clinical and radio-
logic literature. Our discussion is limited
to toxicities that may be seen on com-
puted tomographic (CT) studies of the
chest, abdomen, and pelvis, because
these are the imaging examinations most
commonly used in the follow-up of can-
cer patients. Also noted are the clinical
contexts in which these toxicities occur
and details that radiologists should look
for, not only on images but in the clini-
cal history.
Essentials
Classic chemotherapy agents n
target rapidly proliferating cells;
molecularly targeted therapies
target specifi c key cell membrane
and intracellular molecules.
Radiologists may more easily rec- n
ognize the manifestations of che-
motherapy toxicities by under-
standing the mechanisms of
action of the chemother apeutic
agents.
The radiologist should be aware n
that toxicities can be asymptom-
atic and that radiologists are
instrumental in reporting early
manifestations of toxicities to
referr ing physicians.
Published online
10.1148/radiol.10092129 Content Code:
Radiology 2011; 258:41–56
Abbreviations:
EGFR = epidermal growth factor receptor
5-FU = fl uorouracil
TKI = tyrosine kinase inhibitor
VEGF = vascular endothelial growth factor
L.H.S. has disclosed fi nancial relationships with
AstraZeneca and Novartis.
Peripheral edemaWeight increase
Pleural and PericardialeffusionsAscites
Capillary protein leak syndrome
Ascites alone, should not be mistaken for disease progression
Peritoneal carcinomatosis from ovarian tumor
Failed available standard CHT
“Double blind” Trial : Placebo / Antiangiogenic
CT, basal CT, 9 weeks
A- Intestinal obstruction and perforation
B- Partial response with gastric metastases
C-Partial response with peritoneal carcinomatosis
D- Partial response and GI perforation
Oral contrast media extravasation
GI perforation secondary tothe Antiangiogenic agent
160 patients
The pathogenesis of bowel perforation is unknown, but suggested mechanisms include ischemia with thrombosis of intestinal mesenteric vessels
Acute B-L Leukemia
CHT: Since day +35 coincident with medullary recovery:
Fever and facial rash and oedema . Cultures: (-)
Fever and facial rash and oedema disappeared withhigh doses of steroids
• Pneumatosis Coli• Pneumoperitoneum
Rutinary follow-up
• Minimal abdominal pain anddistension • No peritoneal signs, fever, orleukocytosis
A- Linear Pneumatosis Coli
B- Subclinical bowel perforation
C- Typhlitis
D- Cystic Pneumatosis Coli ( NSP)
“ Pneumoperitoneum usually denotes a perforation of an intra-abdominal viscus, but in about 10% of patients, a nonsurgical source is responsible for free air in the peritoneum”.
• Mularski RA. et al. Crit Care Med 2000• Mularski RA. et al. West JMed 1999
• Heng Y et al. Am J Gastro 1995• Liu DM. Can J Emerg Med 2003
PneumatosisType
Characterization Asociation Surgicaltreatment
Microvesicularpneumatosis
Small collections of air within the lamina propria
Associated with invasive procedures
-
CysticPneumatosis
Macroscopic submucosalcysts(mm-cm)- Pneumoperitoneum. 10% of patients with small bowel pneumatosis. 2% of those with large bowel pneumatosis
• COPD• Immunosupression
therapy (haematologic)• Bevacizumab• Immunocompromise• Steroid usage• Inflammatory bowel
disease• Post bone marrow
transplantation
-
LinearPneumatosis
Represent the tracking of gas through compromised submucosa
. Bowel ischemia or infarction +
20 days without steroids
• Take home message
• To be aware of possibleCHT toxicity manifestations
We should look for, not onlyon images but in the clinicalhistory to help distinguishnew-onset toxicity fromdisease progression.
• Reporting CHT toxicityfindings to the oncologist isimportant, in order to chooseto discontinue therapy
A- Well-differenciated liposarcoma
B- Exophytic renal angiomyolipoma
C- Lipoma
D- Myelolipoma
E- N-differenciated liposarcoma
Benign Malignant
Angiomyolipoma
LipomaHibernomaMyelolipoma
Liposarcoma: 35% of all malignant retroperitoneal soft-tissue tumors(a) well-differentiated (most common)(b) myxoid and round cell(c) pleomorphic
Retroperitoneal fatty masses in adult
• CraigWC. et al RadioGraphics 2009
Exophytic angiomyolipoma
WD liposarcoma
Myxoid liposarcoma
CT characteristics Exophytic renal angiomyolipoma
Well-differentiated liposarcoma
Defect in the Renal Parenchyma + -
Vessels in the Lesion + (enlarged internal vessels with aneurysm formation)
-
Additional Angiomyolipomas + +/-
Size Usually larger
• Careful evaluation enables accuratedifferentiation of large exophyticangiomyolipomas and well-differentiatedretroperitoneal liposarcomas
Take home message:
Arthrosis for several years treated with NSIDs
Neutropenia. Medulary biopsy: normal
Hepatomegaly, abnormal liver function test and jaundice(total bilirrubin: 14 mg)
GP: requested an abdominal CT
A- HCC
B- Hipervascular Metastasis
C- Vasculitis
D- A-V shunt
We recomended a hepatic biopsy and antibodies determination in order to diagnose any reumatoid disease.
Cronic hepatitis with severeinflammatory activity
Necrotic Arteritis in mediumsize hepatic artery
Autoimmune Hepatitis, Aneurism
Outcome: normalization of allparameters after appropriate treatment
Liver Aneurysm
ANA(+)/ ENA(+)/ antiSSA(+)
LES
—58-year-old man with polyarteritis nodosa.
Tarhan N C et al. AJR 2003;180:1617-1619
HEPATIC INVOLVEMENT
- Hepatomegaly is seen in 39% to 40% - Steatosis due to glucocorticoid therapy or to SLE itself - Arteritis (21%) of SLE- Nodular regenerative hyperplasia of the liver, is a rare but important
complication of SLE associated with noncirrhotic portal hypertension.
- Autoinmune hepatitis. The most common one, is the classic “lupoid hepatitis” with chronic active hepatitis
• Up to 4,7% of patients with SLE have chronic active hepatitis• Up to 10% of patients with Autoinmune hepatitis have SLE
INTESTINAL VASCULITIS
GASTRIC INVOLVEMENT
COLON AND SMALL BOWEL INVOLVEMENT
INTESTINAL PSEUDOOBSTRUCTION
PANCREATIC AND GALLBLADDER INVOLVEMENT
PERITONITIS AND ASCITES
MALABSORPTION AND PROTEIN-LOSING ENTEROPATHY
- In 53% in those with active SLE and abdominal pain. Involves small arteries- CT: shows ischemic bowel disease- Opportunistic infections (eg. Mucormycosis) may mimic GI vasculitis and should
be suspected in these immunocompromised patients with not active LES
- Perforation from peptic ulcer disease ( 6% to 8%)- Pernicious anemia
- Pneumatosis cystoides intestinalis (benign pneumoperitoneum)- Necrotizing enterocolitis- CMV enteritis, prone to salmonella infection
- Intestinal obstruction without a mechanical cause. Initial manifestation of lupus ( 41% to 50% .
- Associated urinary tract involvement with ureterohydronephrosis, suggesting a smooth muscle dysmotilityand secondary vesiculoureteric reflux or to fibrosis of the ureterovesicular junction. One- third of patients have interstitial cystitis
- Recurrent pancreatitis occurs in 43% of patients. Chronic pancreatitis in 14% - Primary sclerosing cholangitis and autoimmune cholangiopathy. - Acute pancreatitis is a rare. Associated with thrombosis and cutaneous vasculitis.
- Ascites from infection, bowel infarction, perforation, pancreatitis, mesenteric vasculitis, or serositis.
- Chronic ascites lupus can be due to nephrotic syndrome, heart failure, protein-losing enteropathy, constrictive pericarditis, lupus peritonitis, or indolent infections such as tuberculosis.
‘‘Hepatic disease may be more common in SLE than is usually thoughtand we should be aware of it ”
* Abraham S. Ann Rheum Dis 2004** Ebert EC. J Clin Gastroenterol 2011
Patients with liver disease should be treated as soon as possible, especially those patients with jaundice or persistent increase of liver enzymes values”
Take home message:
CASE 8: 65 year-old woman
Left lumbar pain, fever, leukocyturia and WCC rise, … suggesting acute Pyelonephritis
Fecaluria and pneumaturia
• History: pelvic surgery, radiotherapy and chemotherapy
Dec-2007
CT 6 months before, Post-surgery, RT and CHT April-2007
First CT. Post-surgery Dec- 2006
A- Bladder tumor and ureteral infiltration
B- Colon cancer
C- Ovarian cancer
D- Ureteral tumor and colonic invasion
The patient has an acute pyelonephritis secundary to an ureteral fistula
Nov- 2006
Nov- 2006
Ovarian cancer (Transitional Type. GIII, PT1c. FIGO I)
----------- Partial response
Colonic-ureteral fistulae
Fistulas in Malignant Gynecologic Disease
- As a result of a primary or recurrent tumor - As a consequence of:
Surgery (particularly if the surgical procedure is radical and complex or if the surgical field includes previously irradiated tissue)
Radiation therapy (eg, cervical, colorectal, endometrial cancer)
Types:
- Vesicovaginal and enterovaginal fistulas (more frequent)
- Ureterovaginal, enterovesical, enterocutaneous, and uretero-alimentary tract
. Narayanan P et al. RadioGraphics 2009
. Yu NC et al. RadioGraphics 2004
Cervical cancer. Radiotherapy
Nephrectomy. Entero-cutaneous fistulae
- Ureterocolic fistulas are most common and can be caused by urinary calculi, iatrogenic trauma, diverticulitis, radiation therapy, transitional cell carcinoma, and tuberculosis
• Symptoms: flank pain, hematuria, recurrent urinary tract infections, pneumaturia, fecaluria, and diarrhea
• Diagnosis: Retrograde pyelography, and contrast-enhanced CT: Gas in theureter
Barium studies of the intestinal tract often will not reveal the fistula
Uretero–Alimentary Tract Fistula
- Right ureter: terminal ileum, cecum, appendix, and ascending colon and their mesenteries
- Left ureter: descending colon and sigmoid colon and their mesenteries
- Either ureter may be injured during surgery, or radiation performed on these structures, or engulfed in an adjacent mass
. Avritscher R et al. RadioGraphics 2004
I would add: The ovary
Take home message:
CASE 9 : 24 year-old man. Down Syndrome
No abdominal complaints
Abdominal mass (at manual exploration)
Right mass effect that displaces rightabdominal structures
A- Teratoma
B- Sarcoma
C- Germ cell neoplasm
D- Leukemia
Blood test: normal
AFT: 0.9 (0.0-12)
Beta HCG: 440.9 (0.0-6.0)
T1 T2
FS T2
DWI, b:600
CE Cor LAVA
Pathology: Classical seminoma TIIIB (T1N3MOS2)
Metastatic disease from a testicular germ cell neoplasm
Down Syndrome Cancer Incidence in DS
Leukemia
Testicular cancer
Other cancers
- Acute lymphocytic - Acute non-lymphocytic - 19-fold higher
- Seminomatous (gonadal and extragonadal)- 50-fold higher (0.5% compared with an expected incidence of 0.087%
in the general population)
- Non-Hodgkin lymphoma, stomach, colon, small intestine, breast, endometrial, brain, kidney, liver cancers…
* Hill DA et al. Arch Intern Med. 2003 … N: 4872 (DS)** Goldacre MJ et al. Arch Dis Child 2004 ....N: 1453 (DS)--- 460 000(NDS)*** Rima d et al. European Journal of Medical Genetics 2006**** Cools M et al. Human Pathology 2006
• Because of improvement in medical care, a higher proportion of children with DS are now surviving beyond adolescence
• Therefore, more patients reach the predisposition age range when testicular cancer is most prevalent (35 years)
• Testicular palpation in this population should be considered a component of routine physical examination
Take home message:
Happy Spring
Everybody !!!!!
Thank you very much for your attention