Hepatobiliary system, pancreas, spleen

The presence of hepatic portal venous gas (HPVG) as a manifestation of pyelophlebitis (suppurative thrombophlebitis of the PV) may indicate a surgical emergency in ICU patients who are in shock (Figure 41-2). Gastrointestinal mucosal damage (e.g., ischemic bowel, arterial and venous mesenteric occlusion, perforated peptic ulcer), intraabdominal sepsis (e.g., cholecystitis, abscesses, diverticulitis), and ileus are possible causes. B-mode allows early diagnosis of HPVG by identifying hyperechoic foci moving with blood flow in the PV, whereas Doppler depicts sharp bidirectional spikes (an artifact appreciated audibly as a crackle). In smaller intraparenchymal portal branches, punctiform hyperechoic foci disseminated within the liver parenchyma may be depicted. If sufficient, these foci may display a linear branching pattern in either lobe. In supine ICU patients, gas bubbles accumulate in the rather anteriorly positioned left PV. HPVG should be distinguished from gas in the biliary tree and from other causes of hyperechoic foci, which are usually located randomly in the liver parenchyma (see Figure 41-2).¹

Aerobilia, or pneumobilia, is commonly iatrogenic (e.g., after endoscopic retrograde cholangiopancreatography) or physiologic (incompetent sphincter of Oddi secondary to advanced age or drugs, bilioenteric bypass), but it could reflect pathologies such as a spontaneous biliary-enteric fistula secondary to gallstone ileus, perforating duodenal ulcer, neoplasia, trauma, or infections such as cholangitis or emphysematous cholecystitis. In contrast to HPVG, which usually extends peripherally, aerobilia is often located centrally in larger bile ducts (see Figure 41-2).

In the case of hepatomegaly, additional sonographic findings suggestive of the cause may be present. Hepatomegaly with dilated hepatic veins, IVC, and right heart chambers might indicate right-sided heart failure. A “starry-sky” liver appearance (hypoechoic parenchyma accentuating the portal venule walls) has been identified in patients with acute hepatitis, toxic shock syndrome, and fasting liver (Figure 41 E-7).² Cirrhosis initially causes hepatomegaly, but over time the liver becomes shrunken with an irregular surface and echogenic coarse or nodular parenchymal appearance (Figure 41-3). Evidence of portal hypertension (PH) includes a PV diameter greater than 13 mm, splenic and superior mesenteric vein diameter greater than 10 mm, and variation in PV diameter of less than 20% with respiration. PV blood flow gradually becomes monophasic (without respiratory variation), biphasic (to and fro), and ultimately hepatofugal (away from the liver). The HAs become enlarged and tortuous with increased flow. Portosystemic venous collaterals are highly diagnostic of PH (e.g., hepatofugal flow in a paraumbilical vein dilated >2 mm is 100% specific). Secondary signs of PH are splenomegaly and ascites (see Figure 41-3). A transjugular intrahepatic portosystemic shunt is used to treat complications of PH. Its function is monitored with Doppler ultrasound since stent stenosis or relapse of PV flow toward the liver indicate shunt malfunction.

Focal hepatic lesions (occasionally associated with hepatomegaly) are easily detected, and hepatic abscesses should be kept in mind in the ICU (Figure 41-4). An ill-defined, heterogeneous lesion, typically showing no central perfusion on Doppler, is usually encountered. Echogenic gas bubbles may be present. Travel history, serologic tests, and physical examination help in diagnosing an amebic abscess or other specific infections. Metastatic and intrinsic hepatic tumors may be incidental findings; however, since variable echo patterns are encountered depending on lesion histology, patients should be referred to imaging specialists (see Figure 41-4). Hepatic vein thrombosis (Budd-Chiari syndrome) is manifested as an acute onset of abdominal pain, ascites, and hepatomegaly. In the acute phase the liver is enlarged and tender with a heterogeneous mottled echo pattern. The hepatic veins may appear isoechoic to adjacent parenchyma as a result of an intraluminal echogenic thrombus, and Doppler demonstrates abnormal (absent) flow. Acute PV thrombosis is associated with sepsis, trauma, hypercoagulable states, neoplasms, and acute dehydration. The PV appears dilated, but an acute thrombus may be relatively anechoic and therefore be overlooked unless Doppler is used. Finally, liver transplant scanning can detect abnormalities in the HA or PV (e.g., thrombosis, stenosis) and CBD complications (e.g., leaks, strictures, necrosis, stones).³

In the ICU, cholestasis is attributed mainly to sepsis, impairment of venous return, trauma, ischemic hepatitis (shock liver), or drugs. Ultrasound is used to screen for both size and continuity of the intrahepatic and extrahepatic bile ducts to exclude obstruction (e.g., choledocholithiasis, blocked biliary stent). A dilated CBD appears as an enlarged, anechoic tubular structure in the main portal triad, anterior to and following the course of the main PV. A CBD larger than 1.1 cm in diameter is suggestive of obstruction. Dilated intrahepatic bile ducts with associated PV branches are shown as anechoic “tramlines” coursing through the hepatic parenchyma (Figure 41 E-8). Acute cholangitis, a complication of choledocholithiasis, is a possible cause of fever in the ICU. However, given the low sensitivity of ultrasound for depicting stones in bile ducts (approximately 50%), normal findings on examination should not exclude it from the differential diagnosis.

Acute acalculous cholecystitis (AAC) is not rare in the ICU (Figure 41-5). Prolonged fasting, total parenteral nutrition, mechanical ventilation, trauma, burns, sepsis, drugs (opiates, sedatives, vasopressors), multiple transfusions, and shock are probable contributing factors leading to bile stasis, GB ischemia, and ultimately acute inflammation in the absence of gallstones. Left untreated, AAC may progress rapidly to GB gangrene, perforation, and empyema (incidence of approximately 40%), which are associated with high mortality. Prompt diagnosis and intervention are crucial. Although high clinical suspicion remains important in diagnosing AAC, the comorbid conditions and status of patients do not facilitate evaluation based solely on clinical criteria. Imaging tests used are ultrasound, CT, and hepatobiliary iminodiacetic acid cholescintigraphy. Ultrasound findings include the sonographic Murphy sign (maximal tenderness elicited by transducer pressure over the GB), thickened GB wall (>3.5 mm), distended GB or sometimes hydrops (which refers to distention with clear fluid), sludge (slightly hyperechoic material, echogenic dots—microlithiasis), intramural striations, and pericholecystic fluid (halo) or subserosal edema. However, GB wall thickening becomes illusory when contiguous to isoechoic hepatic parenchyma with superimposed edema, whereas “GB hepatization” (the GB looks isoechoic to liver because of massive sludge) makes recognition of the GB difficult (see Figure 41-5). Furthermore, the Murphy sign, which is crucial for sonographic diagnosis, may be absent in patients in the ICU as a result of analgesia and sedation. A thickened GB wall may be also encountered in patients with hypoproteinemia, hepatitis, heart failure, and ascites, whereas sludge and hydrops may simply indicate a prolonged lack of bile turnover. Repeated ultrasound monitoring may be of value, whereas guided percutaneous cholecystostomy establishes the diagnosis and results in stabilization of septic patients (thus cholecystectomy can be performed electively).^4–11

GB stones are identified sonographically as mobile hyperechoic structures with posterior acoustic shadowing (see Figure 41-5). Stones may cause acute cholecystitis, which has an appearance similar to that of ACC. Complications of acute cholecystitis, such as GB empyema, result in increased morbidity and mortality and thus necessitate prompt intervention. However, GB empyema cannot be reliably differentiated from uncomplicated AAC because echogenic material consistent with pus within the distended GB is indistinguishable from sludge. Sonographic findings suggestive of gangrenous cholecystitis include floating intraluminal membranes (representing sloughed mucosa) and echogenic foci within the GB wall or lumen secondary to gas. Acute GB perforation with free intraperitoneal bile leading to peritonitis is rare. Usually, subacute perforation occurs and results in pericholecystic abscess formation within the GB fossa, liver, or peritoneal cavity that appears as a complex fluid collection with inflammatory changes in adjacent fat (Figure 41 E-9). Emphysematous cholecystitis is a rare complication associated mainly with gas-forming bacteria in elderly patients with diabetes. The diagnosis is suggested by bright air reflections in the GB wall with ring-down artifacts and moving gas echoes within the GB lumen.¹¹

Pancreatic pathology is usually evaluated with CT. In the case of acute pancreatitis, contrast-enhanced CT (CECT) is indicated for diagnosis, initial staging, and follow-up. Ultrasound is an alternative monitoring tool for identifying complications (e.g., fluid collection, abscess, pseudocyst, pseudoaneurysm, portal or splenic venous thrombosis, development of abdominal compartment syndrome) or for guiding interventional procedures (Figure 41 E-10, Video 41-1). A pseudocyst appears as a well-defined, smooth-walled anechoic mass often with multiple loculations and internal septations. Internal debris and fluid-fluid levels indicate hemorrhage or infection. Dilated biliary and pancreatic ducts suddenly terminating in a hypoechoic mass at the head of the pancreas are characteristic of a tumor (Figure 41 E-11). The diaphragmatic splenic surface is commonly detected sonographically in the ICU before a left thoracentesis is performed. In the case of splenomegaly, interrogation of the parenchymal echotexture does not usually indicate an underlying cause. A splenic abscess displays variable ultrasound appearances depending on the stage of infection (similar to all abdominal abscesses). Ultrasound may guide percutaneous aspiration for diagnosis and catheter placement. In an ICU patient with shock, “delayed” splenic rupture following blunt abdominal trauma (Figure 41 E-12), spontaneous splenic rupture (e.g., metastasis, hematologic disorders, infarction, infections), and rupture of a splenic artery pseudoaneurysm are possible causes of hemoperitoneum. The spleen may regenerate after splenectomy (Figure 41 E-13).

Solid organ injury is best visualized with CECT. Ultrasound may be used for diagnosis and follow-up examinations, especially in unstable patients who cannot be transferred. Acute liver or spleen lacerations appear as fragmented hyperechoic or hypoechoic areas. A diffuse hyperechoic pattern with hypoechoic areas may be observed in patients with liver contusion (Figure 41 E-14). Contained intraparenchymal hemorrhage, initially isoechoic or slightly hyperechoic with indistinct margins, may form a well-defined, hypoechoic hematoma or dissolve over time. Subcapsular hematoma appears as a crescent-shaped, hypoechoic (occasionally isoechoic) stripe surrounding the organ. Recently, contrast-enhanced sonography was found to enhance visualization of liver and spleen injuries.

Gastrointestinal tract and peritoneum

In the ICU, a key feature in interpreting GI tract pathophysiology is gut failure, which represents a syndrome of temporary or permanent intestinal malabsorption. It may be due to various causes such as iatrogenic disorders (short bowel syndrome), blunt or penetrating trauma, ischemia (arterial, venous embolism/thrombosis, shock), obstruction (adhesions, hernias), infiltrative disorders (neoplasia, carcinoid, amyloidosis), and functional disorders (pseudoobstruction, paralysis, bacterial overgrowth, inflammatory bowel disorders).

Ultrasound can be used to assess correct positioning of a feeding tube by visualizing a tubular structure with strong acoustic shadow. Acute gastric dilatation (e.g., acute abdomen) or gastric stasis (e.g., peptic ulcer) appears as a large fluid collection with multiple echoic particles and sometimes air or fluid levels (Figure 41-6). Ultrasound facilitates dynamic evaluation of the intestinal wall and surrounding environment by demonstrating peristalsis, which when suggestive of an acute abdomen is a strong argument against emergency surgery, and wall thickening, which often involves a large portion of the intestine even with focal disorders.

Acute mesenteric ischemia is caused by arterial or venous occlusion (or both) or low-outflow states. Mesenteric embolism or thrombosis is best appreciated with CECT. Doppler and contrast-enhanced ultrasound contribute greatly by detecting stenosis or occlusion of the celiac trunk and superior and inferior mesenteric arteries (e.g., significant stenosis of the celiac trunk is present with a peak Doppler systolic velocity >1.5 m/sec) and microperfusion intestinal wall defects. The role of endoscopy in identifying early signs of ischemic colitis cannot be overstated (see Figure 41-6). Ultrasound findings of bowel ischemia (right side involvement more common with several causes) include massively distended bowel loops, abolition of peristalsis, wall thickening (thickened hypoechoic wall of 5 to 7 mm as a result of venous causes but a thin wall of 1 to 2 mm as a result of arterial causes), no bowel wall perfusion, disappearance of wall stratification, and in late stages, intramural gas (hyperechoic foci within the bowel wall), portal venous gas, and peritoneal effusion.^12,13

In the case of intestinal dilatation, ultrasound contributes to distinguishing obstructive from paralytic ileus. Findings suggestive of intestinal obstruction include dilated fluid-filled loops (“3, 6, 9 rule”), increased peristalsis of distended segments (ineffective contractions may cause to-and-fro fluid movements), and collapsed loops distal to the obstruction (see Figure 41-6). A small amount of intraperitoneal fluid is frequently present. Analysis of the dilated loops may help in determining the level of obstruction, and sometimes the cause is also identified (e.g., neoplasm, hernia, Crohn disease, intussusception, bezoar, or gallstone; see Figure 41-6). Prolonged obstruction causes intestinal paralysis, although loops distal to the obstruction appear contracted. In contrast, in paralytic ileus the entire intestine is congested, no empty bowel segments are visualized, fluid-filled levels may be present within dilated loops, and decreased or absent peristalsis is evident during real-time scanning.¹⁴ In pseudomembranous colitis, a potentially life-threatening complication of antibiotic therapy, marked thickening of the colonic wall (frequently manifested as pancolitis), lumen collapse, pericolic fat changes, and hemorrhagic ascites may be observed. Neutropenic enterocolitis in immunosuppressed patients is characterized by ileal and to a variable extent right-sided colonic involvement. Bowel wall thickening, alteration of adjacent mesenteric fat, and ascites may be present.

Primary GI tract lesions (e.g., colon or gastric cancer, acute colonic diverticulitis) and surgical emergencies (e.g., appendicitis) can be identified with ultrasound. Further analysis is beyond the scope of this chapter; however, it should be emphasized that the role of endoscopy in diagnosing GI tract lesions is invaluable (see Figure 41-6). In shock states, sonographic detection of fluid sequestration within the bowel, which can reach several liters, may indicate hypovolemic mechanisms secondary to digestive disorders. The presence, amount, and rate of accumulation (through serial examinations) of intraperitoneal fluid can be detected sonographically. Free fluid flows, under the effect of gravity, to the most dependent peritoneal recesses (e.g., in supine patients to the hepatorenal recess and pelvic cul-de-sac) and outlines them as anechoic stripes with sharp edges. Loculated fluid collections resemble space-occupying lesions that displace bowel and adjacent organs. Transudative ascites, urine, and bile are anechoic, whereas hemorrhage, pus, malignant ascites, and spilled GI contents may include echogenic particles, layering debris, or septations. Ultrasound-guided paracentesis may facilitate the diagnosis (especially by ruling out bacterial peritonitis and distinguishing a pus collection from postoperative sterile blood) or provide symptomatic relief of tense ascites. Perforation of the GI tract may occur suddenly and be severe enough to produce shock; moreover, physical examination in sedated ICU patients is often unrevealing. Ultrasound may detect pneumoperitoneum (free intraperitoneal air) during scanning of the right intercostal area as hyperechoic foci or echogenic lines on the ventral surface of the liver with posterior reverberations that should be discriminated from gas echoes in the lumen of the GI tract (e.g., hepatodiaphragmatic interposition of the colon) or lung. Because intraperitoneal abscesses are usually formed in dependent recesses, pelvic scanning is crucial. Abscesses containing gas may be mistaken for gas-filled bowel and be overlooked.¹⁴

Metastatic implants (originating from the ovaries, pancreas, or GI tract) are the most common peritoneal tumors and appear as hypoechoic solid masses of varying size on the peritoneal surfaces (see Figure 41-6). Ascites is usually present, often with echogenic debris and septations. Retroperitoneal adenopathy is associated with lymphoma or metastatic cancer (testicular, renal, pelvic, GI tract, melanoma) or infection (e.g., human immunodeficiency virus–positive patients). Retroperitoneal fluid collections include hemorrhage (e.g., rupture of an abdominal aneurysm), infection, urinoma, and pancreatic fluid. Retroperitoneal masses or adenopathy and hypercoagulable states may cause abdominal venous (iliac veins, IVC) thrombosis (Videos 41-2 and 41-3). However, IVC thrombosis usually appears as a sequela of deep venous thrombosis of the lower limbs. Under certain circumstances, IVC thrombi, especially in patients in whom anticoagulation is contraindicated, may be treated by placing IVC filters.

• Depiction of blurred images because of various factors may disappoint new users of abdominal ultrasound in the ICU; however, image quality could be improved by making scanning adjustments. Because a single examination may be inconclusive, performance of serial examinations (monitoring) is usually warranted.

• The presence of HPVG or aerobilia should not be interpreted lightly because they may correspond to serious underlying pathology.

• Ultrasound is valuable in detecting GB abnormalities; however, diagnosis of GB disorders such as AAC requires a high level of clinical suspicion and presumably additional testing.

• Solid organ injury is best visualized with CECT, although ultrasound is still useful for diagnosis and monitoring purposes in the ICU.

• Ultrasound depicts gastric dilatation, bowel obstruction (paralytic vs. obstructive ileus) and ischemia, intraperitoneal fluid, or pneumoperitoneum, thereby aiding in the interpretation of gut failure syndrome.

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