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

Recommendations

Info

THE PAEDIATRIC ABDOMEN 217 A B SPLEEN C D Figure 9.1 Cystic fibrosis (CF). (A) Coarse, hyperechoic liver with a lobulated outline. At least two discrete nodules can be seen at the inferior margin. (B) Hyperechoic, coarse pancreas, typical of CF. (C) Massively enlarged spleen caused by portal hypertension in CF. (D) Varices around the lower margin of the spleen in a 12-year-old CF sufferer. (Continued) intrahepatic bile lakes may be seen close to the porta hepatis in infants with biliary atresia. Approximately 10–20% of infants with biliary atresia have associated congenital abnormalities, including choledochal cyst, situs inversus, polysplenia, preduodenal portal vein and interruption of the inferior vena cava (IVC) with azygous continuation, all of which may be detected on sonography. The main role of sonography is to exclude other less frequent causes of neonatal cholestasis such as a congenital choledochal cyst and obstruction to the common bile duct due to bile inspissation where
218 ABDOMINAL ULTRASOUND E Figure 9.1 cont’d (E) Microgallbladder. The gallbladder is thick-walled and small, despite fasting. biliary tract dilatation will be noted. The diameter of the normal common bile duct should not be greater than 2 mm in the infant up to 1 year old (or 4 mm in children up to 10 years of age). 6 Liver biopsy and radioisotope studies are used to differentiate biliary atresia from neonatal hepatitis. Excretion of radionuclide from the liver into the duodenum excludes biliary atresia although a lack of excretion into the duodenum may be seen in both atresia and severe neonatal hepatitis. In these cases laparotomy with intraoperative cholangiogram will be necessary to reach a final diagnosis, although in a few centres MR cholangiography and/or endoscopic retrograde cholangiopancreatography (ERCP) have been used to identify a patent biliary tree and thus exclude the diagnosis of biliary atresia. Biliary atresia is usually treatable by early surgery, provided the diagnosis is made before the age of 8 weeks, at which time irreversible biliary cirrhosis may have developed. Liver transplant may eventually be required, particularly in those presenting late with established biliary cirrhosis. Choledochal cyst Choledochal cysts are congenital dilations of the biliary tree that may present at any age, and can be diagnosed in the fetus during routine obstetric scanning. In the neonate the main presenting feature will be cholestatic jaundice but the classic triad of pain, jaundice and a palpable mass is more likely to be seen in the young adult. A number of types of choledochal cysts have been recognized and in many cases there is an anomalous insertion of the bile duct into the pancreatic duct of Wirsung. On sonography a well-defined cyst will be identified close to the porta hepatis and in about 50% of patients there will be dilatation of the proximal bile ducts which may be seen to communicate directly with cyst (Fig. 9.2A). Sludge or calculi may be seen within the cyst. Small choledochal cysts may be seen in association with biliary atresia but in these cases there will be no associated biliary tract dilatation (Fig. 9.2B). Definitive diagnosis is made by MR cholangiography, although scintigraphy and ERCP may be useful in difficult cases. 7 Other causes of cholestasis in children and neonates include bile duct stones (more common in girls), sclerosing cholangitis, CF, infections and Alagille’s syndrome (a congenital paucity of the bile ducts). Acute cholestasis may also be caused by viral hepatitis, drugs, toxins, metabolic diseases or hypoxaemia. Hepatoblastoma and hepatocellular carcinoma (HCC) Primary malignant tumours of the liver are comparatively rare in children and frequently present as a large abdominal mass. Large hepatic tumours may present acutely as a result of haemorrhage. Hepatoblastoma is the commonest primary liver malignancy in childhood, generally occurring in children under 3 years of age, and may be associated with predisposing conditions such as Beckwith–Wiedemann syndrome and children infected with HIV 8 (Fig. 9.3A). HCC is more usually associated with chronic liver disease and tends to develop during the later stage of disease with peak incidences of 4–5 years and 12–14 years. Both tumours are associated with increased levels of serum alpha-fetoprotein. On ultrasound, these tumours appear solid, heterogeneous and are often large and poorly demarcated from the adjacent liver parenchyma. Areas of necrosis or haemorrhage may be identified in the mass. Occasionally they may be multifocal. Although
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:
Page 36 and 37:
Page 38 and 39:
Page 40 and 41:
Page 42 and 43:
Page 44 and 45:
Page 46 and 47:
Page 48 and 49:
Page 50 and 51:
Page 52 and 53:
Page 54 and 55:
Chapter 3 41 Pathology of the gallb
Page 56 and 57:
PATHOLOGY OF THE GALLBLADDER AND BI
Page 58 and 59:
Page 60 and 61:
Page 62 and 63:
Page 64 and 65:
Page 66 and 67:
Page 68 and 69:
Page 70 and 71:
Page 72 and 73:
Page 74 and 75:
Page 76 and 77:
Page 78 and 79:
Page 80 and 81:
Page 82 and 83:
Page 84 and 85:
Page 86 and 87:
Page 88 and 89:
Page 90 and 91:
Page 92 and 93:
Chapter 4 79 Pathology of the liver
Page 94 and 95:
PATHOLOGY OF THE LIVER AND PORTAL V
Page 96 and 97:
Page 98 and 99:
Page 100 and 101:
Page 102 and 103:
Page 104 and 105:
Page 106 and 107:
Page 108 and 109:
Page 110 and 111:
Page 112 and 113:
Page 114 and 115:
Page 116 and 117:
Page 118 and 119:
Page 120 and 121:
Page 122 and 123:
Page 124 and 125:
Page 126 and 127:
Page 128 and 129:
Page 130 and 131:
Page 132 and 133:
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 228 and 229: Chapter 9 215 The paediatric abdome
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 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 280 and 281:
INTERVENTIONAL AND OTHER TECHNIQUES
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

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?