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THE RENAL TRACT 179 As with acute tubular necrosis, the ultrasound appearances are non-specific. In the acute stages the kidneys may be slightly enlarged; changes in the echogenicity of the cortex may be observed. In the chronic stages the kidneys shrink, become hyperechoic, lose cortical thickness and have increased corticomedullary differentiation. 19 Medullary sponge kidney In medullary sponge kidney the distal tubules, which lie in the medullary pyramids, dilate. This may be due to a developmental anomaly but this is not certain. In itself it is usually asymptomatic and therefore rarely seen on ultrasound. However, the condition is prone to nephrocalcinosis, particularly at the outer edges of the pyramids, and stone formation (see above), which may cause pain and haematuria. Amyloid In amyloid disease, excess protein is deposited in the renal parenchyma, predominantly the cortex. This causes proteinuria and may progress to nephrotic syndrome (oedema, proteinuria and hypoalbuminaemia). Amyloidosis can cause acute renal failure and is particularly associated with long-standing rheumatoid arthritis. As with other diffuse renal diseases, the acute stage may cause renal enlargement and the parenchyma tends to be diffusely hyperechoic. By the time the chronic stage of disease has been reached, the kidneys become shrunken and hyperechoic, in keeping with all end-stage appearances. The renal biopsy (See Chapter 11.) Biopsy is rarely merited in endstage renal failure, as the only treatment is dialysis or renal transplantation. Small kidneys, below 8 cm in length therefore, are almost never subjected to biopsy. Histology is required when the kidney is potentially curable, such as in cases of acute disease, or when a specific knowledge of aetiology is paramount. RENAL VASCULAR PATHOLOGY Renal artery stenosis (RAS) Stenosis of the renal artery is due to atrerosclerotic disease in the vast majority of patients, or to fibromuscular dysplasia of the arterial wall in the younger, generally female patient. RAS may cause hypertension and may eventually cause renal failure. It is frequently bilateral, and is responsible for up to 15% of patients who require long-term dialysis. It is associated with aortic aneurysm, neurofibromatosis or can be traumatic in origin. Stenosis generally affects the main vessel at its origin and involves the aorta (ostial) or occurs within 1 cm of its origin (non-ostial). It can occur in both native and transplanted organs. It is frequently bilateral. Ultrasound appearances of RAS If the stenosis is long-standing and/or severe, the kidney is likely to be small. Loss of renal mass is associated with a stenosis of 60% or greater. 20 However, the ultrasound appearances are often normal with milder grades of RAS. Ultrasound has traditionally had a limited role to play in the diagnosis of RAS and digital subtraction angiography is still considered the gold standard, although magnetic resonance angiography (MRA) is now regarded as the first-line imaging modality of choice. However, colour and spectral Doppler techniques have greatly enhanced the usefulness of ultrasound, particularly in experienced hands. 21 At the site of a stenosis, an increase in peak systolic velocity may be found (greater than 1.5–1.8 m/s) with poststenotic turbulence. Although, it is often not technically possible confidently to examine and sample the whole main renal artery and thus make a definitive diagnosis, it nevertheless remains the best Doppler technique for diagnosis. In addition, the intrarenal vessels may show changes on colour or power Doppler which are indicative of a downstream stenosis. Within the kidney, the perfusion may appear subjectively reduced in the number of vessels and velocity of flow and it may be necessary for the operator to use a low PRF value to detect blood flow. This is
180 ABDOMINAL ULTRASOUND very subjective and variable. The spectral waveforms of arteries distal to the stenosis also reflect changes which suggest a proximal stenosis; the normally fast systolic upstroke is replaced by a delayed parvus tardus pattern (Fig. 7.22), making the waveform less pulsatile with a rounded envelope. 22 This type of waveform can be appreciated subjectively, but quantitative measurements may be used to support the diagnosis. The acceleration time (AT) or acceleration index (AI) is the most common; a normal AT is < 0.07s, and a normal AI > 3 m/s. The actual value of these indices, however, does not reflect the severity of stenosis; unfortunately stenoses of < 70–80% narrowing do not normally demonstrate the parvus tardus effect (although these tend to be less clinically significant) and these spectral phenomena may be obscured altogether if the vessels are rigid and severely diseased 23 or if a good collateral circulation has developed. In such cases the Doppler result is falsely negative and the operator should bear this in mind when attempting to exclude RAS. Renal artery occlusion may occur as a result of further progression of the same disease process which causes stenosis. Doppler will confirm the lack of renal perfusion. The kidney is likely to be small as a result of gradually deteriorating arterial perfusion. Management of RAS Stenosis of the main renal artery is amenable to percutaneous angioplasty and/or stenting, which can effect a cure or more realistically stabilize or slow disease progression. A postangioplasty ultrasound scan can confirm vessel patency, and may play a role in monitoring the patient for disease recurrence. For those with deteriorating function, for whom percutaneous techniques have failed, renal failure will ultimately necessitate dialysis. Renal transplant is a viable option, particularly for those who have been treated in the long term. Renal vein thrombosis This can occur when chronic renal disease is already present or in cases of a coagulation disor- A m/s B x z y NORMAL +24.1 MM 51.6 CM/S Acceleration time = y−x (normal = < 0.07 s) Acceleration index = z−x (normal = > 3 m/s) y−x C Figure 7.22 (A) Renal artery stenosis. The kidney is small, with subjectively reduced perfusion on colour Doppler. The spectrum displays the parvus tardus pattern. (B) Measurement of the acceleration time. (C) The arteriogram in case (A) confirms a stenosis (arrow). s
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Abdominal Ultrasound
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Abdominal Ultrasound How, Why and W
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v Contents Contributors Preface ix
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vii Contributors Rosemary Arthur FR
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ix Preface Ultrasound continues to
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ABBREVIATIONS xi MHA MHV MI MPV MRA
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Chapter 1 1 Optimizing the diagnost
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OPTIMIZING THE DIAGNOSTIC INFORMATI
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Chapter 2 17 The normal hepatobilia
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THE NORMAL HEPATOBILIARY SYSTEM 19
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Chapter 3 41 Pathology of the gallb
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PATHOLOGY OF THE GALLBLADDER AND BI
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Chapter 4 79 Pathology of the liver
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PATHOLOGY OF THE LIVER AND PORTAL V
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Chapter 5 121 The pancreas CHAPTER
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THE PANCREAS 123 the patient’s le
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THE PANCREAS 125 Acute pancreatitis
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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 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
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THE PAEDIATRIC ABDOMEN 229 Table 9.
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THE PAEDIATRIC ABDOMEN 231 A LT B C
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THE PAEDIATRIC ABDOMEN 233 A B C D
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THE PAEDIATRIC ABDOMEN 235 A B C D
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THE PAEDIATRIC ABDOMEN 237 mesenter
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THE PAEDIATRIC ABDOMEN 239 E F G Fi
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THE PAEDIATRIC ABDOMEN 241 system i
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Chapter 10 The acute abdomen 243 CH
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THE ACUTE ABDOMEN 245 scan of the p
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THE ACUTE ABDOMEN 247 LIVER LS GB S
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THE ACUTE ABDOMEN 249 D A RT B C E
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THE ACUTE ABDOMEN 251 17. Patlas M,
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Chapter 11 253 Interventional and o
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INTERVENTIONAL AND OTHER TECHNIQUES
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275 Bibliography and further readin
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277 Index A Abdomen, acute gastroin
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INDEX 279 Continuous ambulatory per
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INDEX 281 Intravenous urography (IV
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INDEX 283 Phrygian cap, 29 Pneumobi
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