Diagnostic ultrasound ( PDFDrive )

CHAPTER 52 The Pediatric Urinary Tract and Adrenal Glands 1805
low is caused by edema and obstruction to outlow of arterial
blood entering the kidney. In babies, these signs are much less
reliable because low is rapidly reestablished in the main renal
vein, as well as within intrarenal veins. he pathophysiologic
response of the kidney to renal vein thrombosis depends on the
acuity of the occlusion, extent of thrombosis, and the development
of venous collateral circulation. his reestablishment of venous
low occurs not only in native kidneys but also in renal transplants,
although the process takes much longer, up to 3 weeks in the
transplanted kidney. he degree of recovery of the afected kidney
ater acute renal vein thrombosis ranges over a wide spectrum,
from full recovery to a variety of abnormalities, including complete
absence of function, to tubular disorders and renovascular
hypertension. 89
Renal Artery Stenosis
Approximately 1% to 3% of children have hypertension, with
an increasing prevalence caused by the childhood obesity epidemic.
Most hypertensive children are at low risk for renovascular
hypertension, which accounts for approximately 5% to 10% of
all childhood hypertension. 109 he most common underlying
cause of renovascular hypertension in infants is thromboembolism
related to umbilical artery catheterization, 110 whereas renal arterial
ibromuscular dysplasia and Takayasu arteritis are the most
common causes in older children. 111 here are many other
developmental and acquired causes of renovascular hypertension
in the pediatric population (Table 52.9).
he precise role of noninvasive imaging in children with
suspected renovascular hypertension is unclear. here is no
imaging technique currently available that can reliably exclude
every potentially treatable cause of renovascular hypertension. 113
Ultrasound of the abdominal aorta and depiction of renal size
and architecture are useful to exclude global nephropathy, focal
scarring, or tumor. Doppler ultrasound can be used to demonstrate
an increase in blood velocity as it passes through a stenotic
arterial lumen. he presence of a proximal stenosis can also be
inferred from the depiction of a tardus (late) and/or parvus (lat)
arterial waveform in vessels distal to a stenosis. 114,115 However,
even in experienced hands, localization of an accessory renal
artery stenosis or branch vessel stenosis can be time-consuming
and challenging.
he classic signs of stenosis described in adults and also applied
to children include increased resistance to low proximally
(decreased or absent diastolic or even systolic low), high velocity
at the site of narrowing (>180 cm/sec), turbulence immediately
distally, and low possibly returning to normal at some
distance from the stenosis (Fig. 52.45). he following renal arterial
Doppler criteria have been found to suggest signiicant
stenosis 114 :
1. Flow velocity measurements exceeding 180 cm/sec
2. Velocity ratio between renal artery and abdominal aorta greater
than 3.5 : 1
Doppler ultrasound waveforms return to normal immediately
ater repair of stenosis. It must be remembered that the parvustardus
waveforms identiied in the downstream circulation will
relect any stenosis occurring upstream, including Takayasu
aortitis and aortic coarctation.
TABLE 52.9 Causes of Renovascular
Hypertension 112
Category
Fibromuscular
dysplasia
Inlammatory
disease
Genetic disorders
Atherosclerosis
Vascular anomaly
Thromboembolism
Renal
transplantation
Other
Examples
Takayasu arteritis
Kawasaki disease
Moyamoya disease
Irradiation
Williams syndrome
Neuroibromatosis
Klippel-Trénaunay-Weber syndrome
Feuerstein-Mims syndrome
Rett syndrome
Degos-Kohlmeier disease
Marfan syndrome
Hyperlipidemias
Renal arteriovenous malformation
Renal artery aneurysm
Renal artery hypoplasia
Renal arteriovenous malformation
Umbilical artery catheterization
Neonate of diabetic mother
Sepsis, dehydration
Rejection
Arterial narrowing
Congenital rubella
Compression by mass
Congenital ibrous band
Posttraumatic cause
Retroperitoneal ibrosis
Intrarenal Arterial Disease
Hemolytic-uremic syndrome is one of the most common causes
of AKI in nonhospitalized infants and children. It is characterized
by endothelial cell injury, intravascular platelet-ibrin thrombi,
and vascular damage. It may occur sporadically, in epidemic
outbreaks, or as a genetic or familial disorder. Patients with typical
HUS will experience bloody diarrhea associated with Shiga
toxin–producing bacteria, predominately Escherichia coli
O157:H7. 116 Atypical HUS occurs without bloody diarrhea
and is due to defective complement system activation and
regulation. 117
he lesions of HUS cause increased resistance to renal arterial
inlow. At sonography, the renal cortex is uniformly hyperechoic,
and the pyramids are sharply demarcated (Fig. 52.46). he kidneys
may greatly enlarge. A study of 20 children with HUS found
that during the phase of anuria there was no diastolic low. 118
As the acute vascular lesions healed, diastolic low returned,
followed by diuresis within 24 to 48 hours. Because the Doppler
examinations predicted the onset of diuresis, the duration of
peritoneal dialysis was kept to a minimum, thereby reducing
the risk of complications.