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

Recommendations

Info

PATHOLOGY OF THE LIVER AND PORTAL VENOUS SYSTEM 105 Management of portal hypertension This depends on the cause and on whether the PV is still patent or not. The most pressing problem is likely to be bleeding from varices, especially oesophageal varices, and patients may present with melaena or haematemasis. Management may involve medical means, endoscopic techniques (either injection sclerotherapy of oesophageal varices or banding, in which a ring is placed around the base of the varix causing thrombosis), compression using a Sengstaken tube with an inflated balloon, surgical or percutaneous transjugular intrahepatic portosystemic shunt (TIPS). All these methods are relatively temporary, and can relieve pressure in the portal venous system, controlling portal hypertensive complications in order to plan further management. TIPS is a percutaneous method used to relieve the symptoms of portal hypertension in cirrhotic patients. It connects the portal vein directly to the right hepatic vein with an expandable metal shunt. A catheter and guide wire are passed, under X-ray control, through the jugular vein to the inferior vena cava (IVC) and into the hepatic vein. A pathway is then forged with a needle through the liver parenchyma to join the PV with the insertion of a shunt to keep the channel open. Portal venous blood then effectively bypasses the liver, flowing straight into the hepatic vein. This usually results in the speedy decompression of varices and improvement of other symptoms of portal hypertension. Ultrasound may be used to monitor stent patency (Fig. 4.24). Shunt stenosis or occlusion is a common problem, particularly in long-term shunts; this can be detected with routine postprocedure ultrasound screening and treated with reintervention. The most common site for a stenosis is at the junction of the stent with the PV. The velocity of blood flow in the shunt should be between 1 and 2 m/s and this should be consistent throughout the stent. A variety of Doppler parameters can be used to detect the malfunction of the shunt. A shunt velocity of less than 50 cm/s is a sign of stenosis 25 RHV IVC LPV RPV MPV STENT HA PV A B Figure 4.24 (A) Transjugular intrahepatic portosystemic shunt (TIPS). (B) TIPS shunt in a patient with severe portal hypertension. The higher-velocity MHA is seen anterior to the shunt, which demonstrates flow from right to left of the image. (Continued)
106 ABDOMINAL ULTRASOUND but this has not been reproducible in all institutions, and other factors such as a change of 50 cm/s or more from the baseline scan, a localized elevation of velocity at the stenotic site (with an upper limit of normal of up to 220 cm/s) or an increase in the velocity gradient (as the stenotic stent exhibits an increased maximum velocity and a decreased minimum velocity) are also poor prognostic signs. 26 TIPS is regarded as a temporary measure but can considerably improve the patient’s condition pending treatment of chronic liver disease, relieving haemorrhage from varices, relieving intractable ascites and stabilizing liver function. It is increasingly used as a bridge to liver transplant. It is also used as an alternative to surgery in patients who are poor surgical risks, although the diversion of blood away from the liver can result in adversely affected liver function and eventual encephalopathy. 27 Hepatitis Viral hepatitis HA C Figure 4.24 cont’d (C) Thrombosed TIPS shunt. A recanalized left portal vein (LPV) (arrow) can be seen anterior to this. Acute viral hepatitis may be caused by one of several viruses: A, B, C, D or E. The viruses which cause hepatitis B, C and D may also go on to chronic disease and predispose the liver to HCC in the later stages. Vaccines exist for A and B, but not yet for the others. Hepatitis A and E are transmitted via contaminated food or drink and are particularly prevalent in third-world countries. Hepatitis B, C and D are likely to be transmitted through transfusion or sexual contact. Fulminant hepatitis, in which there is complete liver failure, is a rare complication of acute hepatitis B. Most patients with acute hepatitis recover completely, but hepatitis B, C and D may go on to develop chronic hepatitis. This has two forms: ● Chronic persistent hepatitis is a mild form of inflammation limited to the portal tracts. It is usually of comparatively little clinical significance and does not show ultrasound changes. ● Chronic active hepatitis is a more serious and aggressive form of the disease which causes diffuse, persistent inflammation. This may eventually lead to cirrhosis, which can be associated with HCC. Other causes of acute hepatitis Acute hepatitis may also occur with many other conditions. The most common of these are alcoholic hepatitis (see alcoholic cirrhosis, above), infectious mononucleosis, herpesvirus and cytomegalovirus. Patients with AIDS and those who are immunosuppressed are also particularly prone to hepatitis. Clinical features of hepatitis It may be asymptomatic (patients who have antibodies present, but who deny having had the disease, must have had subclinical disease at one time). Other signs include lethargy, nausea, vomiting and jaundice. The liver is enlarged and tender in the acute phase. The diagnosis and classification of hepatitis must be made histologically, ideally with an ultrasoundguided biopsy. Ultrasound appearances of hepatitis The liver frequently appears normal on ultrasound. In the acute stage, if ultrasound changes are pres-
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: 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 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

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

Delete template?

Save as template?