9%20ECOGRAFIA%20ABDOMINAL%20COMO%20CUANDO%20DONDE

Recommendations

Info

PATHOLOGY OF THE GALLBLADDER AND BILIARY TREE 71 the Far East and South America. The hyperechoic linear structures in the gallbladder lumen should raise the sonographer’s suspicion in patients native to, or who have visited these countries. Impacted worms in the biliary ducts may mimic other ductal masses. 36 They are a rare cause of obstructive biliary dilatation (Fig. 3.43). Patients may present with acute cholangitis or abdominal pain and vomiting. Endoscopic management is frequently highly effective. 37 ECHOGENIC BILE Biliary stasis A Figure 3.43 Ascaris worm in the gallbladder. B Figure 3.44 (A) Inspissated bile in the normal gallbladder of a fasting patient. (B) Gravity-dependent biliary sludge with a small stone. Fine echoes in the bile within the gallbladder are not uncommon on an ultrasound scan. This is commonly due to the inspissation of bile following prolonged starving, for example following surgery (Fig. 3.44). These appearances disappear after a normal diet is resumed and the gallbladder has emptied and refilled. It occurs when the solutes in the bile precipitate, often due to hypomotility of the gallbladder, and can commonly be seen following bone marrow transplantation and in patients who have undergone prolonged periods (4–6 weeks) of total parenteral nutrition. 38 Prolonged biliary stasis may lead to inflammation and/or infection, particularly in postoperative patients and those on immunosuppression (Fig. 3.44B). Its clinical course varies from complete resolution to progression to gallstones. However, following the resumption of oral feeding, the gallbladder may contract and empty the sludge into the biliary tree causing biliary colic, acute pancreatitis and/or acute cholecystitis. 39 For this reason, cholecystectomy may be considered in symptomatic patients with biliary sludge. The fine echoes may form a gravity-dependent layer and may clump together, forming ‘sludge balls’. To avoid misdiagnosing sludge balls as polyps, turn the patient to disperse the echoes or
72 ABDOMINAL ULTRASOUND rescan after the patient has resumed a normal diet. Biliary stasis is associated with an increased risk of stone formation. 40 Biliary crystals Occasionally, echogenic bile persists even with normal gallbladder function (Fig. 3.45). The significance of this is unclear. It has been suggested that there is a spectrum of biliary disease in which gallbladder dysmotility and subsequent saturation of the bile lead to the formation of crystals in the bile and also in the gallbladder wall, leading eventually to stone formation. 41 Pain and biliary colic may be present prior to stone formation and the presence of echogenic bile seems to correlate with the presence of biliary crystals. 42 Biliary crystals, or ‘microlithiasis’ (usually calcium bilirubinate granules) have a strong association with acute pancreatitis 43 and its presence in patients who do not have gallstones is therefore highly significant. Obstructive causes of biliary stasis Figure 3.45 Biliary crystals. Pathological bile stasis in the gallbladder is due to obstruction of the cystic duct (from a stone, for example) and may be demonstrated in a normalsized or dilated gallbladder. The bile becomes viscous and hyperechoic. The biliary ducts remain normal in calibre. Eventually the bile turns watery and appears echo-free on ultrasound; this is known as a mucocoele (see above) (Fig. 3.8). Bile stasis within the ducts occurs either as a result of prolonged and/or repetitive obstruction or as a result of cholestatic disease such as primary biliary cirrhosis (PBC) (Chapter 4) or PSC. This can lead to cholangitis. Haemobilia Blood in the gallbladder can be the result of gastrointestinal bleeding or other damage to the gallbladder or bile duct wall, for example iatrogenic trauma from an endoscopic procedure. The appearances depend upon the stage of evolution of the bleeding. Fresh blood appears as fine, low-level echoes. Blood clots appear as solid, nonshadowing structures and there may be hyperechoic, linear strands. 44 The history of trauma will allow the sonographer to differentiate from other causes of haemobilia and echogenic bile, particularly those associated with gallbladder inflammation, and there may be other evidence of abdominal trauma on ultrasound such as a haemoperitoneum. Pneumobilia Air in the biliary tree is usually iatrogenic and is frequently seen following procedures such as ERCP, sphincterotomy or biliary surgery. Although it does not usually persist, the air can remain in the biliary tree for months or even years and is not significant. It is characterized by highly reflective linear echoes (Fig. 3.46), which follow the course of the biliary ducts. The air usually casts a shadow which is different from that of stones, often having reverberative artefacts and being much less well-defined or clear. This shadowing obscures the lumen of the duct and can make evaluation of the hepatic parenchyma difficult. Pneumobilia may also be present in emphysematous cholecystitis, an uncommon complication of cholecystitis in which gas-forming bacteria are present in the gallbladder (see above), or in cases where a necrotic gallbladder has formed a cholecystoenteric fistula.
Page 2 and 3:
Abdominal Ultrasound
Page 4 and 5:
Abdominal Ultrasound How, Why and W
Page 6 and 7:
v Contents Contributors Preface ix
Page 8 and 9:
vii Contributors Rosemary Arthur FR
Page 10 and 11:
ix Preface Ultrasound continues to
Page 12 and 13:
ABBREVIATIONS xi MHA MHV MI MPV MRA
Page 14 and 15:
Chapter 1 1 Optimizing the diagnost
Page 16 and 17:
OPTIMIZING THE DIAGNOSTIC INFORMATI
Page 18 and 19:
Page 20 and 21:
Page 22 and 23:
Page 24 and 25:
Page 26 and 27:
Page 28 and 29:
Page 30 and 31:
Chapter 2 17 The normal hepatobilia
Page 32 and 33:
THE NORMAL HEPATOBILIARY SYSTEM 19
Page 34 and 35: THE NORMAL HEPATOBILIARY SYSTEM 21
Page 54 and 55: Chapter 3 41 Pathology of the gallb
Page 56 and 57: PATHOLOGY OF THE GALLBLADDER AND BI
Page 92 and 93: Chapter 4 79 Pathology of the liver
Page 94 and 95: PATHOLOGY OF THE LIVER AND PORTAL V
Page 134 and 135:
Chapter 5 121 The pancreas CHAPTER
Page 136 and 137:
THE PANCREAS 123 the patient’s le
Page 138 and 139:
THE PANCREAS 125 Acute pancreatitis
Page 140 and 141:
THE PANCREAS 127 E F G Figure 5.3 c
Page 142 and 143:
A C DISTANCE = 3.43 CM 5%. 13 Over
Page 144 and 145:
THE PANCREAS 131 G H I Figure 5.5 c
Page 146 and 147:
THE PANCREAS 133 head of pancreas.
Page 148 and 149:
THE PANCREAS 135 pancreatic juice i
Page 150 and 151:
Chapter 6 137 The spleen and lympha
Page 152 and 153:
THE SPLEEN AND LYMPHATIC SYSTEM 139
Page 154 and 155:
Page 156 and 157:
Page 158 and 159:
Page 160 and 161:
Page 162 and 163:
Page 164 and 165:
Page 166 and 167:
Chapter 7 153 The renal tract CHAPT
Page 168 and 169:
THE RENAL TRACT 155 As with any oth
Page 170 and 171:
THE RENAL TRACT 157 A B q 0 LRA AO
Page 172 and 173:
THE RENAL TRACT 159 junctions of or
Page 174 and 175:
THE RENAL TRACT 161 A B Figure 7.5
Page 176 and 177:
THE RENAL TRACT 163 carcinomas, the
Page 178 and 179:
THE RENAL TRACT 165 the vesicourete
Page 180 and 181:
THE RENAL TRACT 167 Table 7.1 Sourc
Page 182 and 183:
THE RENAL TRACT 169 A B Figure 7.13
Page 184 and 185:
THE RENAL TRACT 171 Table 7.2 Diffe
Page 186 and 187:
THE RENAL TRACT 173 Ultrasound stil
Page 188 and 189:
THE RENAL TRACT 175 CT is useful fo
Page 190 and 191:
THE RENAL TRACT 177 Xanthogranuloma
Page 192 and 193:
THE RENAL TRACT 179 As with acute t
Page 194 and 195:
THE RENAL TRACT 181 der with increa
Page 196 and 197:
THE RENAL TRACT 183 ● ● Morphol
Page 198 and 199:
THE RENAL TRACT 185 ● ● hydrone
Page 200 and 201:
THE RENAL TRACT 187 A Figure 7.27 A
Page 202 and 203:
THE RENAL TRACT 189 vascular reject
Page 204 and 205:
THE RENAL TRACT 191 B A C Figure 7.
Page 206 and 207:
THE RENAL TRACT 193 computerised ul
Page 208 and 209:
Chapter 8 195 The retroperitoneum a
Page 210 and 211:
THE RETROPERITONEUM AND GASTROINTES
Page 212 and 213:
Page 214 and 215:
Page 216 and 217:
Page 218 and 219:
Page 220 and 221:
Page 222 and 223:
Page 224 and 225:
Page 226 and 227:
Page 228 and 229:
Chapter 9 215 The paediatric abdome
Page 230 and 231:
THE PAEDIATRIC ABDOMEN 217 A B SPLE
Page 232 and 233:
THE PAEDIATRIC ABDOMEN 219 B A B Fi
Page 234 and 235:
THE PAEDIATRIC ABDOMEN 221 probe de
Page 236 and 237:
THE PAEDIATRIC ABDOMEN 223 When the
Page 238 and 239:
THE PAEDIATRIC ABDOMEN 225 + 78 A 2
Page 240 and 241:
THE PAEDIATRIC ABDOMEN 227 A B C D
Page 242 and 243:
THE PAEDIATRIC ABDOMEN 229 Table 9.
Page 244 and 245:
THE PAEDIATRIC ABDOMEN 231 A LT B C
Page 246 and 247:
Page 248 and 249:
Page 250 and 251:
THE PAEDIATRIC ABDOMEN 237 mesenter
Page 252 and 253:
THE PAEDIATRIC ABDOMEN 239 E F G Fi
Page 254 and 255:
THE PAEDIATRIC ABDOMEN 241 system i
Page 256 and 257:
Chapter 10 The acute abdomen 243 CH
Page 258 and 259:
THE ACUTE ABDOMEN 245 scan of the p
Page 260 and 261:
THE ACUTE ABDOMEN 247 LIVER LS GB S
Page 262 and 263:
THE ACUTE ABDOMEN 249 D A RT B C E
Page 264 and 265:
THE ACUTE ABDOMEN 251 17. Patlas M,
Page 266 and 267:
Chapter 11 253 Interventional and o
Page 268 and 269:
INTERVENTIONAL AND OTHER TECHNIQUES
Page 270 and 271:
Page 272 and 273:
Page 274 and 275:
Page 276 and 277:
Page 278 and 279:
Page 280 and 281:
Page 282 and 283:
Page 284 and 285:
Page 286 and 287:
Page 288 and 289:
275 Bibliography and further readin
Page 290 and 291:
277 Index A Abdomen, acute gastroin
Page 292 and 293:
INDEX 279 Continuous ambulatory per
Page 294 and 295:
INDEX 281 Intravenous urography (IV
Page 296 and 297:
INDEX 283 Phrygian cap, 29 Pneumobi
show all

9%20ECOGRAFIA%20ABDOMINAL%20COMO%20CUANDO%20DONDE

Create successful ePaper yourself

Delete template?

Save as template?