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”

US:

√  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

Sequelae:

(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

Blunt Trauma to Liver (20%)

Prevalence:   2^nd 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

CECT:

√  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

√  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

US:

√  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

CECT:

√  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

US:

√  focal hypoechoic thickening

√  echogenic mass within GB lumen

Blunt Trauma to GI Tract (5%)

◊  3^rd 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.)

Mechanism:

(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%)

US:

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

NECT:

√  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%)

Classification:

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)

(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%)

BOERHAAVE SYNDROME

[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

Pathophysiology:

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

CXR:

√  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)

CT:

√  esophageal wall thickening

√  supradiaphragmatic periesophageal air collection

√  mediastinal fluid collection + pneumomediastinum

BRUNNER GLAND HAMARTOMA

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

Terminology:

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)

MORPHOLOGIC TYPES:

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% 2^nd portion, 4% 3^rd 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

UGI:

√  multiple nodular filling defects (usually limited to 1^st 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

NECT:

√  isoattenuating relative to pancreas

CECT:

√  hypoattenuating relative to pancreas (portal venous phase)

√  peripheral rim enhancement (of duodenal mucosa)

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

BURKITT LYMPHOMA

=  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

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)

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

=  NONENDEMIC FORM OF BURKITT LYMPHOMA

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

Barium:

√  displacement of bowel loops by a large mass

√  abnormally separated bowel loops ← extensive bowel wall thickening

√  narrowing of distal ileum

US:

√  large hypoechoic masses ± engulfing of bowel / mesenteric vessels

√  cystic central areas ← necrosis

√  omental caking (unusual)

CT:

√  bowel wall thickening / mural masses

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

MR:

√  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

PET/CT:

√  highly FDG avid

Cx:   intussusception, aneurysmal dilatation, perforation

◊  Most common cause of intussusception in children ≥ 4 years

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