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Renal fracture

Pre- and post-contrast series are combined. Time delay should be adapted to pathology arterial time should be acquired in the context of trauma or tumor. Very delayed acquisition can sometimes be necessary to look for stagnant iodine within the parenchyma in acute pyelonephritis (Ishikawa et al. 1985 Dalla Palma et al. 1995) or a peri-renal leak in cases of renal fracture. Two-dimensional reformatting is especially useful in evaluating renal fractures or retroperitoneal tumors (Fig. 1.1.9). Maximal intensity projection images in the coronal and sagittal planes advantageously replace IVU at any time of the examination. [Pg.13]

Fig.25.8a-c. Left renal fracture in an 11-year-old girl. No associated intra-abdominal or bone lesion was found by CT (a). Delayed scan (b) showed opacification oftheurinomaby the contrast medium. In spite of this severe leak, the urinary excretory system remained patent. Six months later, followup ultrasound showed the fracture between two normalsized segments (c). Excellent function of the left kidney was shown by nuclear medicine studies (not shown)... [Pg.467]

Renal fracture is usually more difficult to characterize by grey scale ultrasound or Doppler (PiETRERA et al. 2001) injection of intravenous contrast medium can help approach that diagnosis (Fig. 25.5). Of course, the ultrasound examination of the abdominal cavity should be complete. For example, in cases of a right kidney lesion, it is common to find an associated liver lesion. [Pg.467]

Fig.25.12a-c. Right renal fracture in a 15-year-old boy. Initial workup showed perirenal leak and two vascularized small fragments (a). Delayed DMSA scan (b) showed severely decreased uptake of the right kidney (b). Delayed MRI provided the same functional results as DMSA scan, plus excellent depiction of renal morphology (c) (Courtesy of S. Hanquinet)... [Pg.469]

Contraindications to percutaneous nephrolithotomy are infrequent, but include a child with an uncorrectable coagulopathy. Children with a small renal pelvis cause technical problems. Renal access maybe difficult, and there maybe insufficient room to maneuver instruments if the collecting system is not large enough. Also, in small children, the size of the kidneys may make dilation to greater than 10-12 French dangerous for fear of a renal fracture. [Pg.483]

A major regulator of bone metabolism and calcium homeostasis, parathyroid hormone (PTH) is stimulated through a decrease in plasma ionised calcium and increases plasma calcium by activating osteoclasts. PTH also increases renal tubular calcium re-absorption as well as intestinal calcium absorption. Synthetic PTH (1-34) has been successfully used for the treatment of osteoporosis, where it leads to substantial increases in bone density and a 60-70% reduction in vertebral fractures. [Pg.934]

Several studies have evaluated dietary supplements such as isoflavones, which are found in soy products and red clover. A well-controlled trial in more than 400 postmenopausal women evaluating a specific isoflavone, ipriflavone, found no benefits on bone mineral density or fracture rates after 3 years.47 Nevertheless, because these therapies are available without prescription and are not regulated by the FDA, patients may choose to self-medicate with isoflavones. Lymphocytopenia appeared in several patients treated with ipriflavone in clinical trials. Additionally, ipriflavone should be used with caution in immunocompromised patients or those with renal disease. It may inhibit CYP1A2 and CYP2C9 and may interact with drugs metabolized by those pathways, such as warfarin. [Pg.864]

Chronic exposure to high levels of cadmium in food has caused bone disorders including osteoporosis and osteomalacia. Long-term ingestion of water, beans, and rice contaminated with cadmium by a Japanese population was associated with a crippling condition, Itai-Itai disease. The affliction is characterized by pain in the back and joints, osteomalacia, bone fractures, and occasional renal failure, and it most often affected women with multiple risk factors such as multiparity and poor nutrition. ... [Pg.109]

Severe renal impairment (Ccr less than 30 mL/min) fondaparinux as prophylactic therapy in patients with body weight less than 50 kg undergoing hip fracture, hip replacement, or knee replacement surgery active major bleeding bacterial endocarditis thrombocytopenia associated with a positive in vitro test for antiplatelet antibody in the presence of fondaparinux known hypersensitivity to fondaparinux. [Pg.166]

Monitoring Closely monitor patients coinfected with HBV and HIV who discontinue tenofovir with both clinical and laboratory follow-up for at least several months. Monitor patients at risk for, or with a history of, renal dysfunction and patients receiving concomitant nephrotoxic agents for changes in serum creatinine and phosphorus. Consider bone monitoring for HIV infected patients who have a history of pathologic bone fracture or are at substantial risk for osteopenia. [Pg.1839]

For the relief of pain arising from spasm of smooth muscle, as in renal or biliary colic, morphine is frequently employed. Other measures including antispasmodics such as atropine, atropine substitutes, theophylline, nitrites, and heat may be employed first however, if they are ineffective, meperidine, methadone, or opiates must be used. Morphine relieves pain only by a central action and may aggravate the condition producing the pain by exaggerating the smooth muscle spasm. Morphine may also be indispensable for the relief of pain due to acute vascular occlusion, whether this be peripheral, pulmonary, or coronary in origin. In painful acute pericarditis, pleurisy, and spontaneous pneumothorax, morphine is likewise indicated. Carefully chosen and properly spaced doses of codeine or morphine may occasionally be necessary in pneumonia to control pain, dyspnea, and restlessness. Traumatic pain arising from fractures, bums, etc., frequently requires morphine. In shock, whether due to trauma, poisons, or other causes, morphine may be required to relieve severe pain. [Pg.457]

The major population at risk for aluminum loading and toxicity consists of individuals with renal failure. In a study by Alfrey (1980), 82% of nondialyzed uremic patients and 100% of dialyzed uremic patients had an increased body burden of aluminum. The decreased renal function and loss of the ability to excrete aluminum, ingestion of aluminum compounds to lessen gastrointestinal absorption of phosphate, the aluminum present in the water used for dialysate, and the possible increase in gastrointestinal absorption of aluminum in uremic patients can result in elevated aluminum body burdens. The increased body burdens in uremic patients has been associated with dialysis encephalopathy (also referred to as dialysis dementia), skeletal toxicity (osteomalacia, bone pain, pathological fractures, and proximal myopathy), and hematopoietic toxicity (microcytic, hypochromic anemia). Pre-term infants may also be particularly sensitive to the toxicity of aluminum due to reduced renal capacity (Tsou et al. 1991)... [Pg.154]

Light chains are filtered readily through the glomeruli and can be detected in urine, when the reabsorption capacity of the proximal tubule is exceeded. In addition to hypercalcemia, the clinical features of multiple myeloma include anemia, renal insufficiency, and osteolytic lesions revealed during radiologic examination. These lesions weaken the bone matrix and are prone to fractures. Patients are subject to recurrent infections. [Pg.327]

Much clinical and experimental experience has been obtained about the manifestation of bone diseases, especially in renal patients. Many patients with Al-induced bone disease remain asymptomatic. There are two distinct forms of Al bone disease. The most severe form is osteomalacia, with recurrent fractures and resistance to vitamin D therapy. This disease is characterized by an increase of osteoid due to a mineralization defect induced by Al that is localized at a critical site in the bone, i.e., the osteoid calcification front [250]. The adynamic bone disease is another form of Al-related bone disease, characterized by a reduced bone turnover [97]. Al can have a direct negative effect on the bone by deposition at the mineralization front, causing a defective calcification. This is due to the influence of Al on calcium-phosphorus precipitation, crystal formation and crystal growth [251]. There might also be a toxic effect on the proliferation of osteoblasts and on mature osteoblasts with a time- and dose-dependent effect on osteoblast growth and function [143]. [Pg.43]

Calcium homeostasis. Renal caldum loss is increased by the loop diuretics in the short term this is not a serious disadvantage and indeed frusemide may be used in the management of hypercalcaemia after rehydration has been achieved. In the long term h3rpocalcaemia may be harmful especially in elderly patients who tend in any case to be in negative calcium balance. Thiazides, by contrast, decrease renal excertion of calcium and this property may influence the choice of diuretic in a potentially calcium deficient or osteoporotic individual, for thiazide use is associated with reduced risk of hip fracture in the elderly. The h5rpocalciuric effect of the thiazides has also been used effectively in patients with idiopathic hypercalduria, the commonest metabolic cause of renal stones. [Pg.538]

Skeleton Renal phosphate diabetes associated with hypercalciuria may lead to osteomalacia or osteoporosis. Likewise, inflammatory or degenerative arthrosis is thought to be a late manifestation of Wilson s disease. (354) Often, these developments are combined with intra-articular calcium deposits and chondromalacia, in particular patellar chondromalacia. Bone fractures are frequently observed even with minor traumas. Calcification may occur in articular cartilage, capsule and tendinous insertions, and deposits of calcium pyrophosphate dihydrate can appear in the intervertebral disks. [Pg.613]

After persistent hypercalciuria, osteopenia can develop, causing metabolic bone disease, pathological fractures, and immobilization. Hypercalciuria can also lead to nephrolithiasis and nephrocalcinosis, factors that can impair renal function. Intravenous chlorothiazide has been successfully used for its hypocalciuric effect, with remarkable effect over a period of 6 months in a 13-year-old child who had received parenteral nutrition for 6 years. Calcium excretion and tubular reabsorption of phosphate returned to normal (48). What is not clear from this study is whether the drug actually has a positive long-term beneficial effect on metabolic bone disease. [Pg.2705]

Bisphoshonates are used for treatment of hypercalcemia, fracture prevention and in patients with metastatic cancer. This class of drugs reduce morbidity from hypercalcemia is increasingly recognized to cause nephrotoxicity [14]. Both pamidronate and zoledronate have been associated with nephrotoxicity that features nephrotic syndrome with a collapsing glomerular sclerosis [47]. The mechanism is unkown and the return of renal function is slow. [Pg.33]


See other pages where Renal fracture is mentioned: [Pg.453]    [Pg.461]    [Pg.466]    [Pg.453]    [Pg.461]    [Pg.466]    [Pg.305]    [Pg.309]    [Pg.342]    [Pg.94]    [Pg.258]    [Pg.276]    [Pg.322]    [Pg.222]    [Pg.204]    [Pg.759]    [Pg.258]    [Pg.276]    [Pg.322]    [Pg.27]    [Pg.583]    [Pg.39]    [Pg.158]    [Pg.766]    [Pg.74]    [Pg.271]    [Pg.37]    [Pg.509]    [Pg.305]    [Pg.248]    [Pg.250]    [Pg.281]    [Pg.462]    [Pg.557]   
See also in sourсe #XX -- [ Pg.453 , Pg.461 , Pg.466 , Pg.467 ]




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