The initial step in the management of children with major or multisystem injuries is the identification of potentially life-threatening injuries, which include (a) acute respiratory failure from airway obstruction, tension pneumothorax, or hemothorax; (b) massive hemorrhage, causing hypovolemic shock; and (c) severe intracranial injuries (1,9,10).

Patients who are hemodynamically unstable often require emergency surgical intervention. CT is usually reserved for hemodynamically stable patients who are at higher risk of a thoracic or abdominal injury. Clinical and laboratory variables associated with a significantly higher risk of injury include substantial respiratory distress, hypoxemia, abdominal tenderness or distention, lap-belt ecchymosis, gross hematuria, dropping or low hematocrit levels, elevated liver transaminase levels, and a trauma score (Glasgow Coma Score) <12 (7,8,9,10,11,12,13,14). Neurologic impairment without signs referable to the chest or abdomen is a low-yield indication for thoracoabdominal CT (15).

The CT technique is similar to that for a conventional examination of the mediastinum and lungs. Posttraumatic thoracic CT examinations are performed following a bolus administration of intravenous contrast material, which is administered with a power injector whenever possible. The contrast volume varies with patient weight. Scanning is initiated after a delay of 25 to 30 seconds. The milliamperage and kilovoltage need to be the lowest possible that maintain image quality (16,17). Typical collimation and pitch are 0.75 to 1.5 mm and 1 to 1.5, respectively, for a 16-row detector, and 0.6 to 1.25 mm and 1 to 1.5, respectively, for a 64-row detector. Images are reviewed with 3- to 5-mm section thickness at lung, soft tissue, and bone windows. Images are reconstructed at 1 to 2 mm if multiplanar and 3D reconstructions are indicated. (See Chapter 1 for more detailed discussion of techniques). Artifacts can be minimized by positioning the patient's arms above the head and by removing overlying
tubes and other opaque objects from the scanning field whenever possible.

CT examinations for evaluation of abdominal trauma should be performed with intravenous contrast medium. Intravenous contrast agent improves differentiation between normal and pathologic parenchyma, and it aids in detection of active arterial bleeding and extravasation of contrast-opacified urine (66,67). Normal parenchyma enhances, whereas hematomas and lacerations do not. Intravenous contrast medium can be administered by a power injector or hand injection. Scanning is usually initiated 55 to 60 seconds after the start of contrast administration (see Chapter 1 for more detail).

The use of oral contrast medium is controversial. Disadvantages of oral contrast use include delay in diagnosis and treatment of injuries, and risks of vomiting and aspiration (68). Recent studies in adults have suggested that bowel and mesenteric injuries requiring surgical intervention are not missed when patients undergo CT with a multirow detector scanner without oral contrast material (69,70,71,72). Experience (personal communication) in pediatric trauma patients also suggests that oral contrast is not necessary for diagnostic accuracy when CT examinations are performed on a multirow detector scanner.

The abdomen should be scanned from the dome of the diaphragm to the pubic symphysis. Delayed scans obtained 3 to 5 minutes after the initial helical acquisition may help to assess the renal collecting system and the urinary bladder. Typical collimation and pitch are 0.75 to 1.5 mm and 1 to 1.5, respectively, for a 16-row detector, and 0.6 to 1.25 mm and 1 to 1.5, respectively, for a 64-row detector. Images are reviewed with 3- to 5-mm section thickness at lung, soft tissue, and bone windows. Lung windows are useful to detect pneumothorax and pneumoperitoneum. Small pneumothoraces identified solely on abdominal CT scans, however, uncommonly require tube thoracostomy (73).

Prior to the initiation of scanning, all extraneous tubes, catheters, and metallic leads should be removed from the scanning field to reduce streak artifacts that otherwise might degrade the image and mimic a traumatic injury. Artifacts also can be minimized by positioning the patient's arms above the head rather than along the sides of the body.

Blunt injury to the gallbladder and biliary tree are rare. CT findings of gallbladder injury include pericholecystic fluid, thickening or interruption of the gallbladder wall, an enhancing mucosal flap within the gallbladder lumen, and high-attenuation intraluminal clot (97,98). Avulsion results in displacement of the gallbladder from its fossa (98). Pericholecystic fluid and a collapsed gallbladder lumen are nonspecific findings but should elicit concern for gallbladder trauma if associated with other CT signs of gallbladder injury.

Blunt injuries to the biliary tract are usually associated with hepatic parenchymal lacerations and take the form of biloma formation and hemobilia. Hemobilia on CT appears as a high-attenuation fluid collection within the gallbladder lumen. A late sequela of bile duct injury is biliary stricture.

The spleen is the second most frequently injured abdominal organ in children with blunt abdominal trauma, accounting for approximately 30% of abdominal injuries (2). An injury severity score based on the extent of anatomic disruption of the spleen on CT has been developed to classify splenic injuries. The scoring system for splenic injuries is scaled from I to V, indicating the least to most severe injury (Table 13.2). However, similar to the scenario in the liver, it cannot
reliably predict the success or failure of nonoperative management versus surgical intervention.

The spectrum of splenic injuries is similar to that seen in the liver and includes subcapsular and parenchymal hematoma, laceration, and vascular pedicle injury (99). Subcapsular hematomas are typically seen as crescentic, low-attenuation fluid collections that flatten the underlying parenchyma on contrast-enhanced CT scans (Fig. 13.26) (99). Intrasplenic hematomas appear as round or oval hypoattenuating lesions with smooth or irregular margins (Fig. 13.27). They may contain high-attenuation regions, reflecting active arterial hemorrhage.

Splenic lacerations appear as linear or branching low-attenuation areas (Fig. 13.28). Similar to the liver, splenic lacerations are classified as superficial (<3 cm depth from the surface) or deep (>3 cm depth). Deep lacerations that traverse the full thickness of the splenic parenchyma often extend into splenic hilum, injuring a branch artery and resulting in segmental or lobar nonperfusion (i.e., infarction) (Fig. 13.29). Multiple lacerations, usually resulting from a compressive force, are termed a shattered spleen (Fig. 13.30).

Vascular pedicle injuries include avulsion and occlusion of the splenic artery. CT findings of main splenic
artery avulsion and occlusion are a normal-sized, nonenhancing spleen. There is minimal hemoperitoneum with arterial thrombosis, whereas avulsion is associated with a large hemoperitoneum (Fig. 13.31). Occlusion of a segmental vessel results in a wedge-shaped, unenhancing area with the base at the splenic capsule and its apex pointing toward the splenic hilum. In both avulsion and occlusion, the upper pole of the spleen can be perfused by short gastric arteries.

Perisplenic hematoma usually resolves within 2 to 4 weeks (99,100). Intrasplenic hematomas and lacerations decrease in attenuation and become more sharply circumscribed as they diminish. Small hematomas and lacerations may resolve within several weeks, whereas larger hematomas and tears may require several months to heal (99). Splenic injuries may resolve with no sequelae, leave a deformed splenic margin, or form a posttraumatic pseudocyst (Fig. 13.32) or pseudoaneurysm. Pseudocyst is seen as a well-defined, low attenuation lesion, whereas the pseudoaneurysm appears as a well-circumscribed area of dense vascular enhancement.

An increase in splenic volume of >10% may be seen on serial CT scans after blunt abdominal trauma and is not a sign of deterioration. The apparent splenic enlargement is thought to represent a return of the spleen to normal size following physiologic contraction in response to adrenergic stimulation and volume depletion at the time of initial injury (101).

Delayed splenic rupture, defined as hemorrhage after an asymptomatic period of 48 hours, has been described in some patients whose initial CT scans were interpreted as normal (102). Poor contrast enhancement of the splenic parenchyma, making injury indistinguishable from normal parenchyma, in part may explain the false-negative diagnoses. In other cases, true delayed rupture of an intrasplenic or subcapsular hematoma may be the cause of late-onset hemorrhage.

Renal injuries account for 15% to 40% of incidents of children with blunt abdominal trauma (2,5). The presence of hematuria and hypotension are two clinical signs associated with an increased likelihood of renal
trauma (105,106,107,108). Most children with renal injuries have gross or microscopic hematuria (>50 red blood cells per high-power field), but 30% can have normal urinalyses, particularly those with vascular pedicle injuries (105,106,107).

The mechanisms of renal injury are a direct impact, laceration by the lower ribs, or disruption by a rapid acceleration–deceleration event (108). An abnormal kidney is more susceptible to injury than a normal one. Common pre-existing abnormalities include hydronephrosis, Wilms tumor, horseshoe kidney, and renal cystic disease.

Renal injuries are classified into five broad categories based on the renal injury scale of the American Association of Surgeons in Trauma (109,110,111) (Table 13.3). The extent of the renal injury and its relationship to renal artery and vein may serve as a guide for potential surgical or angiographic intervention.

The principal types of renal injury include hematoma, laceration, and vascular injuries. Subcapsular hematomas appear crescentic and flatten the lateral contour of the kidney. They can extend into the perinephric (Gerota) fascia when the renal capsule is lacerated. Large perinephric hematomas may displace the kidney anteriorly, medially, and superiorly. On contrast-enhanced CT scans, subcapsular hematomas have lower attenuation values relative to enhancing parenchyma. On delayed scans, the attenuation value of the fluid may increase if opacified urine leaks into the subcapsular or perinephric spaces. Subacute and
chronic hematomas may demonstrate peripheral rim enhancement. Parenchymal contusions, also know as hematomas, appear as ill-defined areas of slightly increased attenuation on unenhanced CT scans. Areas of decreased enhancement or a striated nephrogram, caused by delayed tubular transit time secondary to edema, can be seen on contrast-enhanced scans (Fig. 13.35).

Renal lacerations are recognized as linear or branching low-attenuation areas within the enhancing renal parenchyma (Fig. 13.36). They may be superficial (<1 cm deep) or deep (>1 cm in depth) (Figs. 13.37 and 13.38). Deep lacerations may involve the collecting system resulting in contrast extravasation; they also can transect the kidney into two parts (i.e., fractures) (Fig. 13.38). Lacerations usually
occur in an axial plane and parallel segmental arteries and veins, so that parenchymal enhancement is preserved. Multiple lacerations resulting from a compressive force are termed a shattered kidney. Some of the multiple lacerations may cross vascular structures, producing renal infarction (109,110,111,112,113).

Vascular injuries can involve the artery or vein. CT signs of main renal artery occlusion and avulsion are a normal-sized nonenhancing kidney (i.e., absent nephrogram), abrupt termination of the contrast-filled renal artery at the point of injury, and retrograde filling of the renal vein (Fig. 13.39) (109,110,111,114,115,116). Cortical rim enhancement, as a result of perfusion by capsular collateral vessels, may be seen, although usually not in the first few hours after infarction (109,110). The cortical rim sign is more typical of subacute infarction. Renal artery avulsion is associated with massive hemorrhage, involving the perirenal space and several other retroperitoneal compartments. Because arterial flow is completely disrupted, renal artery occlusion is not associated with a significant perinephric hematoma. Occlusion or laceration of a segmental or branch artery produces a peripherally based, wedge-shaped area of nonperfusion that extends to the renal capsule. CT findings of traumatic renal vein thrombosis are an enlarged rather than normal-sized kidney, persistent nephrogram, absent or decreased enhancement of the renal vein, and clot in the renal vein.

Myoglobinuria secondary to rhabdomyolysis is a rare cause of a prolonged nephrogram on CT (117). Iodinated contrast agents should be administered with caution if myoglobinuria is suspected clinically because of their potential to initiate or worsen actual renal failure. It is the discrepancy between the dark color of the urine, the positive Hematest, and the absence of significant hematuria on microscopic examination that should suggest the diagnosis of myoglobinuria.

Conservative management is appropriate for patients with grades I and II injuries and even for most patients
with grades III and IV injuries with assurance of close monitoring and the ability to intervene quickly in the event of hemodynamic instability. Contrast extravasation alone is not an indication for surgery (109,110). Traumatic thrombosis or occlusion need to be treated with prompt surgical revascularization to minimize the risk of loss of renal function. Penetrating injuries are also often an indication for surgical intervention. Category IV and V injuries often result in parenchymal atrophy. Hypertension can develop years after the renal injury (118).

Injuries of the ureteropelvic junction are usually caused by deceleration that creates tension on the renal pedicle (119). Although the kidney is relatively mobile, the ureter is fixed in the retroperitoneum, and thus, it may be lacerated or avulsed at its junction with the renal pelvis in a deceleration injury. The diagnosis may be delayed because hematuria can be absent.

CT findings of ureteropelvic junction injuries are prompt renal excretion of contrast material, an intact collecting system, absent opacification of the ipsilateral ureter distal to the disruption, and contrast medium leakage, which may be confined to the medial perirenal space or extend into the periureteral and anterior pararenal spaces (119,120,121,122,123). Ureteropelvic junction disruption is best seen on delayed CT scans.

Bladder injuries may occur as a result of blunt, penetrating, or iatrogenic trauma. The likelihood of bladder injury varies directly with the degree of bladder distention. A distended urinary bladder is more susceptible to injury than a decompressed one. The signs and symptoms of bladder injury are nonspecific. Patients with bladder rupture usually present with suprapubic pain or tenderness. However, in patients with concomitant pelvic fractures, the pain associated with the fractured pelvis can overshadow the pain associated with the bladder injury. Nearly all patients with bladder injuries have gross hematuria.

CT has replaced conventional cystography as the imaging method of choice for evaluating suspected bladder injury, and it can be done in conjunction with CT of the abdomen to assess potential associated injuries. CT cystography performed with adequate bladder distention is as sensitive as conventional cystography for detecting bladder injury (124,125,126,127). Causes for false-negative CT cystography include inadequate bladder distention, associated hematoma preventing contrast leakage, and extremely dilute contrast material. To optimize the sensitivity of CT cystography for diagnosis of bladder rupture, the urinary bladder should be fully distended, either by retrograde filling or antegrade filling using intravenous contrast material administration and clamping the urinary catheter (128).

The spectrum of bladder injuries includes rupture and contusion (127). Bladder rupture is further subdivided into intraperitoneal and extraperitoneal types, depending on the relationship of the tear to the peritoneal reflections. Intraperitoneal bladder rupture usually results from a direct impact to a distended bladder and necessitates operative repair. Extraperitoneal bladder rupture may result from a shearing injury at the bladder base, a direct blow, or penetration of the bladder wall by a bony spicule from a fractured pelvis. A nonpenetrating extraperitoneal bladder injury is treated with suprapubic cystostomy or transurethral catheter drainage. Penetrating bladder rupture requires surgical repair.

Intraperitoneal bladder rupture results in leakage of opacified urine into the peritoneal spaces and recesses, outlining the bladder and bowel and pooling in the paracolic gutters (Fig. 13.40) (129). Extraperitoneal rupture results in leakage of contrast and urine pooling in the prevesical (space of Retzius) and perivesical space. Extravasation may also extend into the inguinal canal, thigh, scrotum, penis, and perineum or into the anterior abdominal wall (Fig. 13.41) (124,130).

Bladder contusion is defined as an incomplete tear of the bladder mucosa or wall, resulting in hemorrhage into a localized segment of the bladder wall (126). CT findings are focal wall thickening without contrast medium leakage (125,126). Bladder contusion is self-limiting and is treated conservatively.

Adrenal hemorrhage occurs in approximately 3% of children who sustain blunt abdominal trauma. Clinical signs and symptoms are nonspecific and include abdominal tenderness and hematuria (131). Adrenal hemorrhage is usually unilateral, commonly on the right side, and often associated with ipsilateral intra-abdominal and intrathoracic injuries. CT findings are an enlarged oval or triangular gland that is hypoattenuating relative to liver and spleen on contrast-enhanced CT scans (Fig. 13.42). Associated findings include increased attenuation of the periadrenal fat, intraperitoneal and retroperitoneal blood, and ipsilateral diaphragmatic crural thickening (131).

Pancreatic injuries account for <5% of all abdominal injuries from blunt trauma in children (2,5,132). They are
most often associated with motor vehicle accidents, followed by bicycle handlebar injuries, and child abuse. The common mechanism of injury is compression of the pancreas between the vertebral column and the anterior abdominal wall. Injuries of the pancreatic head are more likely to occur when the vector of force is to the right of the spine, whereas the neck, body, and tail of the pancreas are injured more often when the force of impact is midline or left sided (133). Most injuries occur in the pancreatic neck and body as the result of compression of the pancreas against the spine.

The early diagnosis of pancreatic injury is often difficult because clinical and laboratory findings are not specific. The typical signs of abdominal pain, leukocytosis, and elevated serum amylase levels may not be present for one or more days after the trauma. In addition, an increase in the serum amylase level may occur with salivary gland contusion or bowel injury. Moreover, serum amylase levels do not vary in proportion to the severity of pancreatic injury and may be higher in patients with pancreatic contusions than in those with pancreatic fractures.

Pancreatic injuries include contusion or hematoma, laceration, transection (i.e., fracture), ductal disruption, and pancreatitis (133). On contrast-enhanced CT, hematoma appears as a poorly marginated, hypoattenuating area within the normal enhancing parenchyma. Laceration (less than full-thickness injury) and transection (full-thickness injury) appear as a low-attenuation linear cleft coursing perpendicular to the long axis of the gland (133,134,135,136) (Fig. 13.43). Pancreatic duct disruption cannot be directly seen on CT. However, ductal injury can be suggested based on the degree of parenchymal injury (137). Deep lacerations (>50% pancreatic thickness) and transections are commonly associated with ductal disruption (137) (Fig. 13.43). The duct is usually intact when there is a superficial laceration (<50% pancreatic thickness).

Unexplained fluid in the anterior pararenal space or lesser sac should strongly suggest the possibility of pancreatic injury (132,133,135,138,139). However, fluid in the anterior pararenal space is not de facto evidence of
pancreatic injury. Other causes of peripancreatic fluid include third spacing of intravascular fluid in children with hypovolemic shock (81,82), blood extending from a splenic injury or bare area of the liver, blood or bowel contents extending from a duodenal injury, and blood or urine dissecting from a renal injury following disruption of the renal fascia (122).

CT findings of pancreatitis include focal or diffuse enlargement of the gland, increased attenuation of the peripancreatic fat, thickening of the renal fascia, and intrapancreatic or extrapancreatic fluid collections (132,133,135). Posttraumatic pancreatitis is the result of autodigestion by pancreatic enzymes liberated after the injury. In general, pancreatic inflammatory changes evolve over time and usually will not be present immediately following the injury.

The severity of pancreatic injury is graded based on the modified Moore organ injury scale (140) (Table 13.4). Disruption of the pancreatic duct is treated surgically or by endoscopy with stent placement, whereas injuries without duct involvement are treated conservatively (137,140). Endoscopic retrograde cholangiopancreatography (ERCP) or MR pancreatography may be necessary for further evaluation of ductal anatomy when CT findings are equivocal (133,137).

Damage to the ductal system is the principal determinant of the development of significant complications,
such as pseudocyst, abscess formation, pancreatic fistula, and sepsis (137,140). The CT appearance of pseudocyst and abscess is that of a low-attenuation fluid collection with well-defined, enhancing walls (Fig. 13.44). A specific diagnosis of abscess can be made if the mass contains air or an air–fluid level. Otherwise percutaneous or surgical aspiration will be required for differentiation.

Bowel and mesentery injuries account for 5% to 15% of blunt abdominal injuries in children (2,142). They are most often caused by bicycle handlebars, child abuse, and the use of lap-type seat belt restraints (12). The diagnosis of intestinal or mesenteric injury is often difficult because clinical findings such as abdominal pain, tenderness, and vomiting are nonspecific. Peritoneal signs, such as rigidity, rebound tenderness, and absent bowel sounds, may not be apparent for several hours or days. Massive bleeding is uncommon, although minimal hematemesis or melena is not unusual. Linear ecchymosis or the seat belt sign should increase concern for bowel and mesenteric injury (12,143).

The mechanisms of injury include (a) direct compression of bowel between the anterior abdominal wall and the spine; (b) a shearing injury near sites of relatively fixed ligaments and mesenteric attachments, such as the ligament of Treitz and ileocecal junction; and (c) an abrupt marked increase in intraluminal pressure. Injuries to bowel usually involve the second and third portions of the duodenum and the proximal jejunum. The duodenum is retroperitoneal and relatively immobile anterior to the spine, whereas the proximal jejunum is fixed by the ligament of Treitz. Ileal, colonic, and gastric injuries occur, but they are less common than proximal bowel injuries. Bowel and mesenteric injuries include contusion/ hematoma, laceration, and complete transection.

CT signs of bowel laceration and transection include free intraperitoneal or retroperitoneal air, extraluminal contrast material, bowel wall disruption, thickened bowel wall, abnormal bowel wall enhancement, and infiltration of the mesentery (143,144,145,146,147,148,149,150,151). Free air in the peritoneal cavity or retroperitoneum is present on CT in 33% to 65% of children with bowel perforations (143,146). Pneumoperitoneum is most often seen in the subdiaphragmatic area, anterior to the liver (Fig. 13.45).
Extraluminal air may also accumulate in the leaves of the mesentery or in the retroperitoneum, commonly in the right paraduodenal and anterior pararenal spaces. Although extraluminal air is highly suggestive of bowel perforation, it is not pathognomonic. Other causes of extraluminal air include dissection of air from a pneumothorax or pneumomediastinum, peritoneal lavage prior to CT, and intraperitoneal bladder rupture (143,145,146). Extraluminal contrast material and bowel wall disruption are specific signs of bowel perforation, but unfortunately these signs occur in a minority of patients (7% and <1%, respectively) (143).

CT signs of bowel contusion/hematoma include thickened bowel wall, intraluminal hematoma, and abnormal wall enhancement (Figs. 13.46 and 13.47) (145). The wall thickening can be eccentric or circumferential and is commonly associated with luminal narrowing (Fig. 13.47). The attenuation of the hematoma is relatively high initially, but it decreases as the blood matures. Wall thickening is not a specific indicator of bowel injury, and it can be seen with insufficient bowel distention or bowel edema secondary to systemic volume overload or the hypoperfusion complex (145,151,152). Wall enhancement also can be seen with hypovolemic shock.

CT findings specific to mesenteric injury include active mesenteric bleeding, mesenteric vasculature beading, and abrupt termination of the mesenteric vessels (145). Although these findings are relatively specific for mesenteric injury, they have low sensitivity. Mesenteric stranding, fluid in the mesenteric root, and focal hematoma are less specific findings of mesenteric injury (Fig. 13.48).

Intraperitoneal and retroperitoneal fluid is a common finding in both bowel and mesenteric injuries (143,145). The specificity of this sign is low if there are other concomitant injuries. If no associated injury is noted, bowel or mesenteric injury should be suspected, particularly if there are moderate or large amounts of fluid (143,145,153). Free intraperitoneal fluid from bowel perforation commonly accumulates between bowel loops (i.e., the interloop compartment) and typically has a triangular appearance. By comparison, free intraperitoneal fluid related to solid organ injuries (e.g., liver or spleen) is
most commonly seen in the paracolic gutters and the pelvis, sparing the interloop spaces.

Free extraluminal air and focal bowel wall thickening are associated with a strong likelihood of a bowel injury that requires surgical repair (143). Complications of blunt trauma to the bowel or mesentery include ischemia, infarction, and stricture of the bowel lumen (154).