and Abdominal Disorders

Blunt Trauma to Duodenum

√  retroperitoneal hematoma

√  stranding of retroperitoneal fatty tissue

√  thickening of duodenal wall

1.   Duodenal contusion

√  edema / hematoma of the duodenal wall

√  intramural gas accumulations

√  focal duodenal wall thickening > 4 mm

Rx:   conservative

2.   Hematoma of the duodenal wall

3.   Duodenal perforation and disruption

√  retroperitoneal collection of contrast (infrequent)

√  extraluminal gas

√  lack of continuity of duodenal wall

Blunt Trauma to Spleen (40%)

◊  Most frequently injured intraperitoneal organ in blunt abdominal trauma (40% of abdominal organ injuries)

Associated with:   other solid visceral / bowel injuries (29%); lower rib fractures in 44%, injury to left kidney in 10%, injury to left diaphragm in 2%

◊  20% of left rib fractures have splenic injury!

◊  25% of left renal injury have splenic injury!

Technique:   scanning delay of 60–70 sec to avoid heterogeneous splenic enhancement

CECT (95% accurate):

◊  CT not reliable to determine need for surgical intervention!

√  hemoperitoneum ← disruption of splenic capsule

√  “sentinel clot” (= area of > 60 HU adjacent to spleen) as sensitive predictor of injury = perisplenic hematoma

√  active extravasation:

√  high-attenuation blush (80–370 HU)

√  focal high-attenuation area in / emanating from injured splenic parenchyma

√  growing larger with time (delayed phase imaging!)

N.B.:   active extravasation of contrast material requires emergent surgery in 83–93%

√  mottled parenchymal enhancement = contusion

√  hypoattenuating line connecting opposing visceral surfaces = linear parenchymal defect = splenic laceration:

√  almost always associated with hemoperitoneum

√  crescentic region of low attenuation along splenic margin flattening / indenting / compressing the normal parenchyma = subcapsular hematoma

√  round hypodense inhomogeneous region ± hyperdense clot = intrasplenic hematoma

√  hypoattenuating hematoma with complete separation of splenic fragments = laceration traversing two capsular surfaces = splenic fracture

√  multiple lacerations = “shattered spleen


√  hyperechoic intraparenchymal region (= acute hematoma / laceration)

√  anechoic intralesional collection (= brisk hemorrhage)

√  diffusely heterogeneous parenchymal pattern containing hyper- and hypoechoic areas (= extensive splenic injury)

√  loss of normal organ contour ← perisplenic clot


(1)  scar / fibrosis

(2)  splenic pseudocyst (20–30 HU)

(3)  Vascular injury: pseudoaneurysm, AV fistula

(4)  delayed splenic rupture

=  hemorrhage > 48 hours after trauma

Cause:   subcapsular hematoma

Prevalence:   0.3–20% of blunt splenic injuries

Time of onset:  in 70% within 2 weeks of injury; in 90% within 4 weeks of injury

Prognosis:  splenectomy / splenorrhaphy; 80–90% success in nonoperative management

Rx:     up to 91% of stable patients can be treated conservatively with observation; transcatheter embolization

◊  Preservation of spleen and its immune function = standard of care


(1)   Normal lobulation / splenic cleft (smoothly contoured, medially located)


(2)  Adjacent unopacified jejunum simulating splenic tissue


(3)  Early differential enhancement of red and white pulp (scan obtained within 20–50 seconds)


(4)  Perisplenic fluid from ascites / urine / succus / bile / lavage

Blunt Trauma to Liver (20%)

Prevalence:   2nd most frequently injured abdominal viscus

Associated with:   splenic injury in 45%

•  clinical manifestation often delayed by days / weeks

Location:  right (posterior segment) > left lobe

Site:     perivascular, paralleling right + middle hepatic arteries + posterior branches of right portal vein, avulsion of right hepatic vein from IVC (13%)

◊  Left lobe injuries are more often associated with damage to duodenum, pancreas, transverse colon


√  liver laceration = predominantly irregular linear branching / round regions of low attenuation:
(a) superficial ≤ 3 cm deep; (b) > 3 cm in depth

◊  Most frequently identified injury pattern

Associated with:

›  retroperitoneal hematoma surrounding IVC ← posterosuperior segment VII laceration of bare area

›  hematoma involving adrenal gland

›  biloma ← laceration extending into porta hepatis


(1)  beam-hardening artifact from adjacent ribs / from air-contrast level in stomach


(2)  Focal fatty infiltration

√  liver hematoma:

√  hyperattenuating mass in acute phase of 54 (range, 28–82) HU decreasing over time ← clotted blood:

›  intraparenchymal hematoma: single / multiple

›  subcapsular hematoma: lenticular / elliptical configuration flattening underlying liver margin

Resolution:   usually within 6–8 weeks

√  active (potentially life-threatening) liver hemorrhage:

√  focal hyperattenuating area during early phase of 155 (range, 91–274) HU ← extravasated contrast material

Prognosis:   75% become hemodynamically unstable

Rx:   angiographic embolization

DDx:   focal hyperdense area of 80–350 HU during early phase ← pseudoaneurysm / AV fistula

√  major (life-threatening) hepatic venous injury

=  liver laceration or hematoma extending into major hepatic vein / IVC

◊  3.5 x more frequently associated with arterial bleeding

√  focal / diffuse periportal tracking (in up to 22%)

=  areas of low attenuation paralleling portal vein + its branches 2° to

›  dissecting hemorrhage / bile

›  dilated engorged periportal lymphatics ← ↑ central venous pressure ← vigorous IV fluid administration / tension pneumothorax / pericardial tamponade

√  flat IVC

=  AP diameter < ¼ of IVC width not caused by external compression

Cause:   hypovolemia, poor fluid resuscitation, shock

√  hypodense wedge extending to liver surface = focal hepatic devascularization

√  hemoperitoneum ← violation of liver capsule with inability of liver veins to contract

√  intrahepatic / subcapsular gas, usually ← necrosis


√  localized area of increased intraparenchymal echogenicity (= acute hematoma / laceration)

√  widespread heterogeneous liver echogenicity + absence of normal vascular pattern (= global parenchymal injury)

Cx:     in 5–23%

(1)delayed hemorrhage(2–6%)

(2)abscess (0.6–4%) ← superinfection of hematoma / biloma / devascularized hepatic parenchyma

(3)pseudoaneurysm (1%) → hemobilia, melena, hematemesis (decompression into biliary system)

(4)bile peritonitis

(5)biliary fistula: external (to skin / hollow viscus), internal (to intestine / bronchus), biliovascular (to hepatic artery, portal / hepatic vein)

Rx:     conservative treatment in up to 80% in adults + 97% in children; transcatheter embolization

Prognosis:  healing in 1–6–15 months; 4–12% mortality

Blunt Trauma to Gallbladder (2%)

Associated with:   injury to liver (91%), duodenum (54%), spleen (54%)

√  pericholecystic fluid (extraperitoneal location of GB)

√  free intraperitoneal fluid


√  blurred contour of GB

√  focal thickening / discontinuity of GB wall

√  intraluminal enhancing mucosal flap

√  blood within GB lumen = attenuation > 50 HU

√  mass effect on adjacent duodenum

√  collapsed GB ← GB rupture

√  focal periportal tracking ← GB rupture


√  focal hypoechoic thickening

√  echogenic mass within GB lumen

Blunt Trauma to GI Tract (5%)

◊  3rd most common type of injury from blunt trauma to abdominal organs

Cause in children:   MVA (lap belts), bicycle handle bar, child abuse

May be associated with:   Chance fracture; traumatic hernia (disruption of the rectus abdominis m.)


(1)  crush / compression injury: direct force; near spine

(2)  burst injury: sudden increase in intraluminal pressure

(3)  shear injury: rapid deceleration at points of transition between mobile and fixed bowel portions

Location:  jejunum distal to ligament of Treitz > duodenum > ascending colon at ileocecal valve > descending colon > distal ileum near ileocecal valve

•  Classic triad (in only 33%):

•  abdominal pain + tenderness (100% sensitive)

•  abdominal rigidity; absent / decreased bowel sounds

•  ↑ temperature + heart rate; ↓ urine output over 24 hours

•  lap belt ecchymosis (not highly correlated)

•  Lavage:  90% sensitive for hemoperitoneum → compromises interpretation of CT exam

N.B.:     clinical signs + symptoms may be delayed for 24 hours (increasing mortality to 65%)


√  nonspecific free intraabdominal fluid (86% sensitive, 98% specific)


√  abdominal wall injury: SQ fat stranding (“seat belt” sign) ← hematoma ← tear

√  extraintestinal free air (30–60% sensitive, 95% specific):

√  intraperitoneal air: small gas bubbles anteriorly near liver / trapped within leaves of mesentery (with small bowel perforation) / porta hepatis

√  retroperitoneal air (with disruption of duodenum / rectum / colon)

DDx of free air:

◊  Most bowel perforations have no free gas due to:

(a)  spontaneous seal of perforation

(b)  developing ileus → no passage of gas

(c)  rapid reabsorption of small gas collections

√  intramural air

√  hypodense free fluid (90–100% sensitive, 15–25% specific), particularly in interloop location ← perforation

DDx:   parenchymal organ injury / osseous injury / large vessel injury / bladder perforation

√  “sentinel clot” sign adjacent to bowel

CECT (84–94% sensitive, 84–99% accurate):

@    bowel injury (CT 94% sensitive, 88% accurate)

Location:  small bowel (proximal jejunum, distal ileum) > colon > stomach

√  extravasation of oral contrast material (8–15% sensitive, 100% specific), densest near perforation

DDx:   hyperattenuating blood, extravasating vascular contrast material, leak of contrast material ← ruptured urinary tract

√  focal discontinuity of bowel wall = direct evidence (5–10% sensitive, 100% specific)

√  focal bowel wall thickening > 3 mm (= intramural hematoma [55–75% sensitive, 90% specific] / vascular compromise and inflammation ← spilling of bowel contents):

√  ± intestinal obstruction / ileus

DDx:   lack of bowel distension

√  abnormal bowel wall enhancement (10–15% sensitive, 90% specific):

√  hyperdense contrast enhancement of injured bowel wall ← delayed venous transit time (20%)

√  lack of bowel wall enhancement (13%) ← bowel infarct, highly SPECIFIC

√  duodenal submucosal / subserosal hematoma → gastric outlet obstruction

@    mesenteric injury (CT 96% sensitive, 96% accurate)

√  mesenteric contrast extravasation (17%)

√  mesenteric vascular beading (39%) = change in caliber

√  abrupt termination of mesenteric artery / vein (35%)

√  mesenteric infiltration (70–77% sensitive, 40–90% specific) = haziness + fat stranding = streaky hyperattenuating infiltration / fluid at mesenteric root ← hemorrhage + inflammatory response

DDx:   retractile mesenteritis

√  mesenteric rent → internal hernia

√  mesenteric hematoma (39%)

√  mesenteric pseudoaneurysm

Cx:     peritonitis, sepsis, hemorrhage

Prognosis:  delay in diagnosis by 8–12 hours increases morbidity + mortality from peritonitis + sepsis

Rx:     surgery based on clinical assessment alone has a 40% negative laparotomy rate

Blunt Trauma to Pancreas (3%)

Mechanism:   compression against vertebral column with shear across pancreatic neck

Frequency:   < 10% of childhood trauma

Cause:  motor vehicle accident (→ compression by seat belt /steering wheel), fall onto handle bars of a bicycle, child abuse

Associated with:   injury to liver (47%, typically left lobe), spleen (28%), stomach (42%), duodenum (19%, typically in younger patients), major vessel (41%), kidney (23%)


I  minor contusion / hematoma, capsule + major duct intact

II  parenchymal injury without major duct injury

III  major ductal injury

IV  severe crush injury

•  epigastric/ diffuse abdominal pain, vomiting

•  leukocytosis, ↑ serum amylase activity

Location:  pancreatic body (65%) > tail / head

CT (70–95% sensitive):

√  within first 12 hours normal CT findings in 20–40% → repeat CT at 24–48 hours

√  posttraumatic pancreatitis:

√  edema / fluid in peripancreatic fat

√  focal / diffuse pancreatic enlargement

√  irregularity of pancreatic contour

√  focal area of low-attenuation / enlargement

(1)  contusion = diffuse / localized hypoattenuating area within normally enhancing parenchyma

(2)  laceration (actual site of laceration difficult to visualize)

N.B.:   pancreatic laceration of > 50% of pancreatic diameter suggests ductal injury. Evaluation of the integrity of the main pancreatic duct remains the critical role of MRCP!

(3)  transection (fracture) = hypoattenuating linear findings with separated parenchyma

√  pancreatic hematoma = mixed / slightly hyperattenuating lesion within margins / in contact with parenchyma

√  fluid / blood accumulation:

(a)  alongside superior mesenteric artery

(b)  in transverse mesocolon / lesser sac

(c)  fluid between pancreas and splenic vein (in up to 90%)

√  thickening of anterior pararenal fascia

Morbidity:  11–62%

Mortality:  5%

Rx:   I + II  conservative management

III + IV   need for surgery within 24 hours

endoscopic stent placement for duct injury

Cx:     pancreatic fistula (23%), posttraumatic pancreatitis (10%), pseudocyst (5%), pseudoaneurysm, pneumonia, abscess (increases mortality to 20%)


[Herman Boerhaave (1668–1738), professor of clinical medicine, botany and chemistry at the University of Leiden, Netherlands]

=  spontaneous emetogenic injury resulting in rupture of esophagus → extrusion of gastric content into mediastinum / pleural space

Frequency:   1÷6,000 persons

Age:   middle-aged men (in 50% with history of alcoholism / heavy drinking)

Cause:   violent retching ← food bolus impaction


incomplete cricopharyngeal relaxation during sudden increase in intraabdominal pressure while vomiting → abrupt increase in intraluminal esophageal pressure (barotrauma) in the presence of a moderate to large amount of gastric contents → complete transmural disruption of esophageal wall

•  Mackler triad:

•  episode of severe retching + forceful vomiting

•  sudden excruciating chest pain (substernal, left chest, neck, pleuritic, epigastric); subcutaneous emphysema

•  odynophagia, tachypnea, cyanosis, fever, shock

•  NO hematemesis (blood escapes outside esophageal lumen)

√  rent of 2–5 cm in length

Location:  3–6 cm above diaphragm (= 2–3 cm above GE junction), predominantly in left posterolateral wall


√  mediastinal widening

√  air-fluid level within mediastinum

√  extravasation of contrast into mediastinum / pleura

√  pneumomediastinum (single most important plain-film finding), pneumopericardium, subcutaneous air:

√  “V” sign of Naclerio = localized mediastinal emphysema with air between lower thoracic aorta + diaphragm

[Emil A. Naclerio (1915–1985), thoracic surgeon at Harlem and Columbus Hospitals in New York City]

√  pleural effusion on left >> right side / hydropneumothorax

√  subcutaneous emphysema

√  patchy pulmonary infiltrate

Esophagography(modality of choice):

Technique:   initially hydrosoluble contrast medium (in 10% falsely negative) followed by barium if negative

√  submucosal collection

√  extravasation of contrast material

√  esophagopleural fistula (most commonly on left)

The use of hydrosoluble contrast material is preferred over barium in suspected esophageal rupture → risk for mediastinitis as a result of irritation caused by barium.


√  esophageal wall thickening

√  supradiaphragmatic periesophageal air collection

√  mediastinal fluid collection + pneumomediastinum


[Johann Conrad Brunner (1653–1727), Swiss professor of anatomy and physiology at the University of Heidelberg, Germany]


Brunner gland hamartoma ≤ 5 mm in diameter

Brunner gland hyperplasia > 5 mm in diameter

Prevalence:   1.2% of all gastric polyps; 5% of all duodenal masses

Etiology:   response to gastric acid in duodenum → glands protect duodenal epithelium + optimize pH for pancreatic enzyme activity

Histo:   diffusely enlarged hyperplastic glands of Swiss cheese appearance and variable amounts of adipose + smooth muscle + lymphoid tissue + sclerosis

Physiology:   mucosal + submucosal Brunner glands contain mucous + serous cells → secrete a clear viscous alkaline mucus into crypts of Lieberkühn

Age:   manifest in middle age; M÷F = 1÷1

•  incidental / symptomatic (abdominal pain)


1.   Diffuse nodular hyperplasia: throughout duodenum

2.   Circumscribed nodular hyperplasia: in suprapapillary portion

3.   Single glandular adenoma with polypoid tumorlike dimensions

Location:   duodenum (70% bulb, 26% 2nd portion, 4% 3rd portion); prepyloric region (distribution of duodenal glands from vicinity of pylorus to proximal ²/³ of duodenum)

Mean size:   2.0 (range, 0.5–6.0) cm; rarely up to 11 cm


√  multiple nodular filling defects (usually limited to 1st portion of duodenum) with “cobblestone appearance” (most common finding)

DDx:  polyposis syndromes, lymphoid hyperplasia, heterotopic gastric mucosa, nodular duodenitis

√  smooth single mass ± central ulceration

DDx:  adenomatous polyp, lipoma, leiomyoma, leiomyosarcoma, lymphoma, ectopic pancreatic tissue, GIST, carcinoid tumor, adenocarcinoma, pancreatic neoplasm, ampullary neoplasm

Endoscopic US:

◊  Guides appropriate depth of endoscopic biopsy!

√  heterogeneous echogenicity with various amounts of solid + cystic components


√  isoattenuating relative to pancreas


√  hypoattenuating relative to pancreas (portal venous phase)

√  peripheral rim enhancement (of duodenal mucosa)

Cx:   GI bleeding (chronic melena, hematemesis), intestinal obstruction, intussusception


=  highly aggressive B-cell lymphoma usually found in children or immunocompromised adults

[initially described in a 7-year old Ugandan child in 1958 by Denis Parsons Burkitt (1911–1993), Irish surgeon on Medical Research Council in London]

Prevalence:   1–2% of all NHLs; 1–5% of primary gastrointestinal NHLs in adults

◊  Most common (30–50%) type of pediatric NHL in children < 15 years in USA and western Europe.

Origin:   undifferentiated small noncleaved B-cell–derived lymphocyte

Histo:   uniform deeply basophilic medium-sized cells containing round nuclei with distinct chromatin and multiple nucleoli; characteristic “starry sky” pattern (= scattered macrophages containing apoptotic cellular debris on a basophilic background) at light microscopy; 99% proliferation index

Genetics:   translocation of c-Myc oncogene with one of immuno- globulin genes, most frequently t(8;14)(q24;q32)

Growth rate:   fastest growing of all human tumors with a doubling time of about 24 hours

Rx:   dramatic response to chemotherapy

Prognosis:   90–98% 5-year survival rate in children with localized disease: 75–89% 2-year disease-free survival rate in children with advanced disease; 50–70% survival in adults

Endemic / African Form of Burkitt Lymphoma

Endemic in areas with malaria:

sub-Saharan Africa, New Guinea (exposure to Plasmodium falciparum has a synergistic effect causing a marked decrease in T-cell surveillance)

Incidence in central Africa:

50–80% of all childhood neoplasms

Associated with:   Epstein-Barr virus infection in 95% (implicated as B-cell mitogen in oncogenesis); malaria

Age:     3–10 years

@   Mandible > maxilla / facial bones

•  jaw mass; exophthalmos (orbital extension)

√  grossly destructive lesion, spicules of bone growing at right angles

√  large soft-tissue mass

@   Other skeleton (multifocal in 10%)

√  reminiscent of Ewing tumor / reticulum cell sarcoma

√  lamellated periosteal reaction around major long bones

Sporadic / American Form of Burkitt Lymphoma


=  typically manifests with bulky disease because of its rapid doubling time

Incidence in Europe + North America:

35–45% of all pediatric NHL; 3% of all childhood tumors

Median age:   8 (range, 6–15) years; ⅓ between 5 and 9 years; unusual in children < 5 years; most frequently in white boys

•  paraplegia; NO peripheral leukemia

•  Epstein-Barr virus genome found in only a minority

◊  Widespread extraintestinal disease at presentation (mesenteric ± retroperitoneal lymphadenopathy) in 70%!

@   Gastrointestinal tract (22–69%)

•  abdominal mass, intestinal obstruction

•  acute abdominal complaints (30–40%)

Location:   terminal ileum, ileocecal region (Peyer patches), mesentery >> stomach, colon

√  well-defined sharply marginated homogeneous large abdominal and pelvic masses (31–64%):

√  encasement of bowel and mesenteric vessels

√  invading bowel wall → obstruction

√  central necrosis in large tumor

√  ± enlarged abdominal lymph nodes

√  malignant ascites (25%–63%)

√  peritoneal thickening / nodularity (42%) along liver capsule and peritoneal reflections ← intraperitoneal seeding

√  usually intraabdominal extranodal involvement with sparing of spleen


√  displacement of bowel loops by a large mass

√  abnormally separated bowel loops ← extensive bowel wall thickening

√  narrowing of distal ileum


√  large hypoechoic masses ± engulfing of bowel / mesenteric vessels

√  cystic central areas ← necrosis

√  omental caking (unusual)


√  bowel wall thickening / mural masses

√  “sandwich” sign = enhancing vessels surrounded by mildly enhancing confluent mesenteric mass


√  isointense to muscle on T1WI + T2WI:

√  homogeneous T1 hypointensity

√  heterogeneous intermediate-to-high SI on T2WI

√  intense homogeneous enhancement

√  bright round-to-ovoid lesions > 10 mm in size with restricted diffusion ← lymph node involvement


√  highly FDG avid

Cx:   intussusception, aneurysmal dilatation, perforation

◊  Most common cause of intussusception in children ≥ 4 years

◊  Intussusception and aneurysmal dilatation of bowel suggest lymphoma.

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Jun 29, 2017 | Posted by in GENERAL RADIOLOGY | Comments Off on and Abdominal Disorders
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