Unusual CT Manifestations of CommonAbdominal Diseases

Rosa Bouzas-Sierra, MD--- Rosa.bouzas.sierra@sergas.es

Milagros Otero-Garcia, MD----- Milagros.otero.garcia@sergas.es

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