4- 6 cm
3- 7 cm
PP-index (depending on
< 30 years:
< 60 years:
> 60 years
The normal configuration of the kidney (Fig. 37.2) can show several findings that can be traced to its embryologie development. Hyperplastic columns of Bertin can protrude from the parenchyma (29) into the renal pelvis (31) and do not differ in echogenicity from the remaining renal parenchyma. An equally iso-echogenic parenchymal bridge can completely divide the collecting system. A partial or complete parenchymal gap at the same location indicates a renal duplication (Fig. 38.1) with separate ureters and blood supply for each moiety. The prevertebral parenchymal bridge of horseshoe kidneys might even be mistaken at first sight for preaortic lymphadenopathy or a thrombosed aortic aneurysm. A lobulated renal contour can be seen in children and young adults as manifestation of persistent fetal lobulation, characterized by an otherwise smooth renal surface that is indented between the individual medullary pyramids. These changes have to be differentiated from renal infarcts (Fig. 42.3) that can be found in old patients with atherosclerotic stenosis of the renal artery.
Localized parenchymal thickening along the lateral border of the left kidney, usually just below the inferior pole of the spleen, is found in about 10% of patients. This is an anatomic variant, generally referred to as "dromedary hump," and its differentiation from a true renal tumor might occasionally be difficult.
Renal cysts (64) are echo-free and produce, as shown in Figure 38.2, distal acoustic enhancement (70). Additional criteria for the diagnosis of a cyst are the same as for the diagnosis of hepatic cysts (see p. 29). Cysts can be separated into peripheral cysts along the renal surface, parenchymal cysts, or peripelvic cysts, with the latter to be differentiated from an obstructed and dilated renal pelvis (Fig. 41.2). The evaluation of a cyst should include measuring its diameter as well as stating its approximate location (upper, middle, or lower third of the kidney).
Finding a few renal cysts is clinically inconsequential, though re-evaluation at regular intervals is advisable. In contrast, the adult form of polycystic renal disease (Fig. 38.3) presents with innumerable cysts (64) that progressively increase in size. Since the cysts can reach a considerable size, the patients can complain of fullness and pressure in the upper abdomen. Furthermore, polycystic renal disease leads to renal atrophy by displacing and thinning the renal parenchyma, resulting in renal insufficiency in early adulthood and eventually requiring dialysis or a renal transplant. Other causes of renal atrophy will be discussed on the next page.
The kidney reacts to the various inflammatory conditions with similar sonographic changes. It can be entirely normal in early pyelonephritis or glomerulonephritis. Later, edema causes an enlargement and interstitial infiltration an increased parenchymal echogenicity with accentuated demarcation of the parenchyma (29) relative to the hypoechoic pyramids (30) (Fig. 39.3). This is referred to as "punched-out medullary pyramids/' In comparison with the adjacent hepatic or splenic parenchyma (9), the renal parenchyma appears more echogenic (Fig. 39.3) than the parenchyma of the normal kidney (Fig. 38.2). Interstitial nephritis can be caused by chronic glomerulonephritis, diabetic nephropathy, urate nephropathy (hyperuricemia as manifestation of gout or increased nucleic acid turnover), amyloidosis or autoimmune disease, but the etiology cannot be deduced from the increased parenchymal echogenicity.
Another sign indicating an inflammation is the indistinct interface between parenchyma and collecting system.
In addition to causing peripheral infarcts (Fig. 42.3), renal artery stenosis can induce a generalized decrease in renal size (Fig. 39.1), which, however, can also be a manifestation of recurrent or chronic inflammation. The marked thinning of the parenchyma (29) found in end-stage chronic nephritis leads to renal atrophy (Fig. 39.2), which is frequently accompanied by degenerative calcifications (53) or concrements (49) with their corresponding acoustic shadows (45). The atrophic kidney can be so small that it eludes sonographic detection. The associated loss of excretory function can be made up by compensatory hypertrophy of the contralateral kidney. In a unilaterally small kidney, the PP index (see p. 37) should be determined. If this index is normal, a developmen-tally hypoplastic kidney might be present.
While sonography does not contribute to the differential diagnosis of inflammatory renal disease, it is of value in monitoring any renal inflammation during therapy, in excluding any complications (e.g., acute obstruction) and in guiding any percutaneous needle biopsy.
The collecting system is seen as a central complex of strong echoes that are only traversed by small thin vascular structures (Fig. 37.2). With increased diuresis after fluid intake, the renal pelvis (31) can distend and be visualized as a more echo-free structure (87) (Fig. 40.1). The same finding can represent the developmental variant of an extrarenal pelvis. In both conditions, the dilation does not involve the calices and infundibula.
It can be difficult to separate this finding from a first degree (mild) obstructive dilatation (Fig. 40.2), which also causes a dilated renal pelvis but without infundibular extension and detectable parenchymal thinning. A second degree (moderate) obstructive dilatation causes increasing fullness of the infundibula and calices as well as the onset of parenchymal thinning (Fig. 40.3). The bright central echo complex (31) becomes rarefied and eventually disappears. The third degree (severe) obstructive dilatation is characterized by severe pressure atrophy of the parenchyma (no case illustrated).
Sonography cannot reveal all the causes of an obstructive uropathy. Since the midureter is obscured by overlying air in the majority of cases, a ureteral stone is generally not visualized unless it is lodged at the ureteropelvic junction or in the prevesical ureter. Less frequent causes of ureteral obstruction are a tumor of the bladder or uterus and aggregated lymph nodes as well as retroperitoneal fibrosis after radiation, or idiopathic as a manifestation of Ormond disease. A latent obstruction can develop during pregnancy, caused by ureteral atony, and during infection. Furthermore, an over-distended bladder as manifestation of a neurogenic bladder or secondary to prostatic hypertrophy can cause ureteral obstruction, and the sonographic evaluation must include the bladder and a search for an enlarged prostate gland in men (compare Figs. 56.1,56.2). For assessing the postvoid residual see page 54.
The obstruction causing the dilatation of the collecting system can be relieved by cystoscopically placed ureteral stents (compare Figs. 45.3, 45.4) or by sonographically guided percutaneous nephrostomy.
Not every dilated renal pelvis (31) is indicative of obstructive uropathy. The developmental variant of an extrarenal pelvis was already mentioned on the preceding page. Furthermore, the renal hilum can show prominent vessels (25) (Fig. 41.1) that can be followed to the hypoechoic medullary pyramids (30) and might be mistaken for structures of the collecting system. These vessels generally appear rather delicate and lack the characteristic fullness found with an obstructed and dilated collecting system (compare Fig. 40.2).
If the findings are inconclusive, color Doppler sonography can easily determine whether these structures represent blood vessels containing rapidly flowing blood or the collecting system filled with essentially stationary urine. Blood vessels are seen as color-coded structures with the color depending on the direction and velocity of blood How, while the barely moving urine in the collecting system remains black. The same principle of difference in relative flow can be employed to differentiate pelvic or peripelvic cysts (64), which do not require any therapy, from an obstructively dilated renal pelvis (87), which has to be expectantly observed or treated. Both conditions can, of course, concur (Fig. 41.2).
Detecting concrements in the kidney (nephrolithiasis) is more difficult than detecting stones in the gallbladder since the echogenic renal stones (49) are often located within the equally echogenic collecting system (31) (Fig. 42.1) and might not elicit any echogenicity that is discernible from its surrounding structures. Concrements in a dilated collecting system are a notable exception since they are easily revealed as echogenic structures within the echo-free urine. In the absence of any dilatation, it is of utmost importance to look for acoustic shadowing (45) caused by concrements or calcifications, such as is found in hyperparathyroidism.
Depending on its composition, a renal stone (49) can be either completely sound transmitting (as seen in Fig. 42.1) or so reflective that only its near surface is seen as echogenic cap (Fig. 42.2). The differential diagnosis includes the arcuate arteries between the renal cortex and medullary pyramids (bright echoes without shadowing), vascular calcifications in diabetic patients, and calcified fibrotic residues following renal tuberculosis. Finally, papillary calcifications can occur after phenacetin abuse. Large staghorn calculi are difficult to diagnose if the distal acoustic shadowing is weak and its echogenicity mistaken for the central echogenic complex.
If renal concrements dislodge and migrate from the in-trarenal collecting system into the ureter, they can, depending on their size, pass into the bladder without symptoms or with colics, or become lodged and cause ureteral obstruction. In addition to detecting obstructive uropathy, sonography can exclude other causes of abdominal pain, such as pancreatitis, colitis, and free fluid in the cul-de-sac.
Renal emboli or renal arterial stenosis can cause localized renal infarcts (71), which, conforming to the vascular distribution, are broad-based at the renal surface and tapered toward the renal hilus. Sonographically, they are seen as triangular defects (Fig. 42.3) in the renal parenchyma (29). The resultant scars are as echogenic as renal calculi but should not be mistaken for concrements on the basis of their form and localization.
In contrast to fluid-filled cysts, solid renal tumors exhibit internal echoes and have only weak or no distal acoustic enhancement. Benign renal tumors (fibromas, adenomas, hemangiomas) are altogether rare with no uniform sonomorphology. Only the angiomyolipoma, a benign mixed tumor comprising vessels, muscular tissue, and fat, has in its early stage a characteristic sonographic presentation that separates it from a malignant process. A small angiomyolipoma (72) is as echogenic as the central echo complex and clearly demarcated (Fig. 43.1). With increasing size, angiomyo-lipomas become heterogeneous, rendering their differentiation from malignant tumors more difficult.
Small renal cell carcinomas (hypernephromas) are often iso-echoic with the remaining renal parenchyma (29). Only with further growth do the hypernephromas (54) become heterogeneous and space-occupying with bulging of the renal contour (Fig. 43.2). If a hypernephroma has been detected, the renal vein, related lymph-node-bearing sites, and contralateral kidney have to be carefully scrutinized for neoplastic changes. About 5% of renal cell carcinomas are bilateral, and advanced carcinomas can have vascular invasion with intravenous tumorous extension. If the tumor extends beyond the renal capsule and infiltrates the adjacent psoas muscle, the kidney loses its respiratory mobility.
The left adrenal gland lies anteromedial (not cranial) to the upper renal pole. The right adrenal gland extends posteriorly to the inferior vena cava. In adults, neither of the adrenal glands is visible, or only barely visible, in the perirenal fat. Hormone-producing adrenal tumors, such as an adenoma in Conn syndrome or hyperplasia in Cushing syndrome, are generally too small to be detectable sonographically. Only clinically manifest pheochromocytomas are often already several centimeters in size and can be sonographically detected in 90% of cases.
Sonography plays a more important role in the detection of adrenal metastases (54) (Fig. 43.3). Metastases are usually seen as hypoechoic lesions between the upper renal pole and spleen (37) or inferior hepatic surface, respectively, and must be differentiated from atypical renal cysts (Fig. 43.3). The hematogenous spread of metastases is attributed to the exquisite vascularity of the adrenal glands and can be found with bronchogenic carcinomas as well as with carcinomas of the breast and kidney. Whether or not a suprarenal space-occupying lesion is malignant cannot be deduced from the lesion's echogenicity. Before proceeding to a needle biopsy, a pheochromocytoma must be excluded to avoid precipitating a hypertensive crisis.
Renal transplants can be in either of the iliac fossa and are connected to the iliac vessels. Like the orthotopic kidneys, they are sonographically examined in two projections (Fig. 44.1), but the transducer is placed over the lateral aspect of the lower abdomen. No interfering intestinal air is present because of the superficial position of the transplanted kidney just beneath the anterior abdominal wall.
It is crucial to detect a rejection or other complications early (compare p. 45). It is normal for a renal transplant to show an often permanent increase in size by up to 20% after surgery. In comparison with the native kidneys, its cortex (29) appears wider (Fig. 44.2) and the parenchymal echogenicity can increase so that the medullary pyramids (30) become better demarcated. Progressive inflammatory infiltration must be excluded by serial sonographic studies, which should be obtained at short intervals during the immediate postoperative period. A prominent renal pelvis or a slightly distended (first degree) collecting system (compare Figs. 40.1, 40.2) might be observed without requiring intervention because of functional impairment of the renal transplant. The urinary distention should be documented and measured in cross sec tion (Fig. 44.3) to avoid missing on subsequent studies any progression that might require therapeutic intervention.
The renal transplant should be further evaluated for the distinctness of its outline and its interface between the parenchyma (29) and collecting system (31). An indistinct PP-interface or a slight increase in volume can be warning signs of the onset of rejection. To allow a valid comparison, reproducible longitudinal and transverse diameters should be selected for measurements and documentation (compare p. 45). After transplantation, the immunosuppressive medications can gradually be reduced and the intervals between the sonographic studies extended.
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Fig. 44.2 a r«MMHMMMMMMMMMH
For an accurate assessment of its size, the renal transplant has to be visualized longitudinally first (Fig. 45.1b) and the position of the transducer then adjusted until the maximal length comes into view. The diagram (Fig. 45.1 a) illustrates a line too far lateral (dotted line) that would measure a spuriously short distance. To get to the "true" longitudinal dimension (d|) the transducer has to be tilted along the straight arrows.
Thereafter, the transducer is slightly turned (Fig. 45.1c) until there is no longer angulation along the curved arrow (Fig. 45.1a). This two-step approach to guiding the transducer should assure that the length documented is not too short, which could lead to a spurious increase in the calcu lated volume (simplified volume formula: vol = AxBxCx 0.5) on follow-up examinations.
A lymphocele (73) can develop as a complication after renal transplant surgery (Fig. 45.2) and is usually found between the lower pole of the renal transplant and the urinary bladder (38), but can be anywhere adjacent to the transplant. Urinary obstruction (87) is an equally frequent complication and, depending on its severity, might require temporary stent drainage (59) (Figs. 45.3, 45.4) to prevent damage of the renal parenchyma (29). Measuring the RI of the supplying renal vessel by Doppler sonography provides additional information concerning the condition of the renal transplant.
It is the goal of this workbook to provide factual knowledge and to facilitate memorization by means of most effective teaching strategies. This should facilitate immediate and rapid recall from memory whenever necessary at a later time. Empirically, it has been shown that beginners in sonography become faster and better oriented with the three-dimen-sional abdominal space if they are able to sketch the few standard orientations from memory. Do not get annoyed at the following questions: there are no better teaching methods that relate new material in a shorter period of time.
From memory, draw a typical transverse section of the right kidney at the level of its hilum, including its position relative to the liver and inferior vena cava. How would the corresponding body marker look? Compare your drawing with the diagram shown on page 37 (the body marker has been left out intentionally).
Try, by means of a sketch, to characterize the different shapes of the normal kidney, the kidney with prominent vessels, and the kidney with mild to severe (grade I to grade III) dilatation. Discuss with a fellow trainee the criteria that differentiate these five possibilities. It is not the other trainee's lack of comprehension but your fault if your he or she cannot reconstruct the findings you describe. Compare your sketches afterwards with Figures 37.2 c, 41.1 b, 40.2 b, and 40.3 b
£1 How would you recognize a nephrolithiasis? What possible underlying conditions are there? By consulting a textbook, try to list the possible causes of hematuria (blood in the urine).
Q List the sonographic criteria of a renal angiomyolipoma. Why can it be difficult to differentiate its findings from other renal tumors?
Write down the normal values for the longitudinal and transverse diameters of the kidneys, for the width of the renal parenchyma, and for the respiratory mobility. Compare your values with those listed on page 37.
Review carefully the sonographic images provided and write down next to each image all visualized organs and muscles as well as your diagnosis, including your reasons for arriving at this diagnosis. After you are done, compare your results with the answers given on page 77.
The spleen is visualized in the right lateral decubitus position with the patient taking a deep breath (Fig. 47.2a). The transducer is placed parallel to the intercostal space to avoid interfering acoustic shadows (45) that arise from the ribs. The spleen is carefully scrutinized from the diaphragmatic dome (13) to the level of its hilar vessels (20) (Fig. 47.1).
Frequently, visualization of the spleen is compromised by air in the left lung (47) or in an adjacent intestinal loop (43). Normal splenic measurements ^ are 4 x 7 x 11 cm ("4711" rule), whereby the maximum diameter measured in this visualized plane between hilum and diaphragmatic surface of the spleen should be 4 cm.
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