Case summaryA 6-year-old boy was admitted to the hospital with presumptive diagnosis of acute pyelonephritis. He had a 2-day history of fever and vomiting. On admission he had high fever (39.7 C) and diffuse abdominal tenderness. Renal percussion was negative. Laboratory investigations revealed high erythrocyte sedimentation rate (60 mm/h), C-reactive protein 136 mg/l and leukocytosis of 21.310 9 / l. His urine was cloudy; nitrite and esterase tests were positive and microscopic examination of the sediment revealed many white blood cells. Ultrasound examination of his kidneys, liver, gallbladder, spleen and urinary bladder did not show any abnormal changes. The boy was administered intravenous fluids and ceftriaxone 1.0 g/day (50 mg/kg/day). Within 48 h he became afebrile and his urine cleared. The bacteriology report showed that his pyelonephritis was due to Escherichia coli (10 6 /CFU), which was sensitive to ceftriaxone. The parenteral treatment with ceftriaxone continued at the same dose on outpatient basis. On the fifth post-admission day, the boy's parents reported that he complained of right lumbar pains and macroscopic hematuria. Ultrasound examination was performed the same day and demonstrated a small non-obstructive calculus (5 mm) in the right kidney (Fig. 1). Also, echogenic material with acoustic shadowing was seen in the gallbladder (Fig.2). Additional laboratory investigations were performed afterwards and revealed normal complete blood counts; urinalysis was positive for blood 3+; nitrite and esterase tests were negative and pH was 5. Serum biochemistry showed normal values for calcium (2.33 mmol/l), phosphate (1.55 mmol/l), magnesium (1.0 mmol/l), uric acid (236 mmol/l), bicarbonate (23 mmol/l), alkaline phosphatase (133 U/l), and PTH (22 pg/ml). Examination of the solute/creatinine ratios (mmol/mmol) in the random urine sample were as follows: calcium/creatinine (0.22, normal <70), uric acid/creatinine (0.33, normal <1.0),The answer to this question can be found at http://dx.
AnswerCeftriaxone-induced nephrolithiasis and biliary pseudolithiasis. Infrared spectroscopy revealed that the stone was composed of calcium ceftriaxonate. CommentaryNephrolithiasis in children is principally caused by metabolic factors, obstruction and urinary tract infection. In our case there was no anatomical abnormality of the urinary tract. Urinary tract infection, which was caused by E. coli, had a very favorable clinical course. Appearance of echogenic material in the gallbladder and urinary tract is very suggestive of ceftriaxone (CTX)-induced precipitates. Clinical studies have demonstrated that CTX can induce reversible precipitations in gallbladder with posterior acoustic shadowing, which mimics cholelithiasis [1,2,3,4,5,6]. This complication is termed "biliary pseudolithiasis" or "reversible cholelithiasis". Gallbladder sludge is defined as echogenic material without associated acoustic shadowing. Most patients are asymptomatic, but in a few cases right upper quadrant pain, nausea, vomiting, and even cholecystitis may develop. Clinicians should be aware of these phenomena in order to save patients from unnecessary interventions.Risk factors for CTX-induced gallbladder precipitations are: high-dose CTX therapy (>2 g/day), increased calcium secretion into the bile (hypercalcaemia), decreased bile flow (such fasting or total parenteral nutrition), renal failure and gallbladder stasis after major surgical operations. Although high-dose, long-term CTX therapy is incriminated for this complication, Blais and Duperval reported a case where 48 h of therapy were sufficient for biliary pseudolithiasis to develop [7].There are only a few reports on ceftriaxone-induced nephrolithiasis [1,8,9,10,11]. Among the patients from the original series of Shaad et al, who first reported on CTX-induced biliary pesudolithiasis in 1988 [1], one child was found to have renal colic and obstruction caused by multiple stones. The clinical symptoms were transitory and impairment of renal function resolved after cessation of CTX therapy. Prince and Senac reported a case of both ceftriaxone-induced biliary pseudolithiasis and nephrolithiasis [8]. Their patient presented with acute renal failure due to bilateral ureteral obstruction with calculi, which necessitated placement of ureteral stents. De Moor et al reported a seven-year-old boy who developed biliary pseudolithiasis and nephrolithiasis four days after initiation of treatment with CTX [9]. Avci et al prospectively followed 51 children with various infections who were treated with CTX, and found that 4 (7.8%) developed nephrolithiasis [10]. All stones were small (2 mm) and disappeared spontaneously in three cases. Arcun et al, in their series of 35 children treated with CTX, demonstrated gallbladder precipitation in five children; only one of these had associated urinary bladder sludge [3].Risk factors for CTX-induced urolithiasis are positive familiar history, high CTX dose, rapid infusion rate, dehydration and combination with nephrotoxic drugs [1,8,9,10,11]. Although bilia...
Rhabdomyolysis represents a life-threatening condition, which results in release of cellular contents (myoglobin, enzymes, and electrolytes) into the plasma. We report a pediatric patient with mild rhabdomyolysis who had a favorable outcome. A 3-year-old girl had been ill for 2 days with high fever, anorexia, pain in both thighs, and passage of dark-red urine. Myoglobinuria was demonstrated by a "blood"-positive dipstick in the absence of red blood cells in the urinary sediment. Diagnosis was confirmed by the presence of a high serum creatine kinase activity. The child was treated on an outpatient basis and has shown full clinical and biochemical recovery. There has been no recurrence of myoglobinuria during the 2-year follow-up.Keywords Myoglobinuria · Rhabdomyolysis · Hematuria 12 µmol/l (indirect 5, direct 7). Complement C3 was 1.65 g/l and C4 0.42 g/l. IgG was 6.92 g/l, IgM 0.77 g/l, and IgA 0.55 g/l. Large amounts of myoglobin were detected by polyacrylamide gel electrophoresis of the urine sample. The diagnosis of rhabdomyol-
Portal venous system, apart from the main portal vein, includes its tributaries: superior and inferior mesenteric vein, as well as splenic vein,
Thyroid disorders, especially thyrotoxicosis, are commonly associated with hepatic dysfunction, but cholestasis is rarely reported. Heart failure, infection, weight loss may play role in the pathogenesis of cholestasis. Cholestasis could be worsened by treatment of hyperthyroidism using Thiamazole, but cholestasis in undiagnosed thyrotoxicosis is uncommon. We present 23 year old female with jaundice, goiter, palpitation and confirmed thyrotoxicosis associated with hepatomegaly, hepatocelluar damage and cholestasis. Liver biopsy excluded the suspicion of autoimmune hepatitis. Therapeutic plasma exchange was performed 5 days after starting the treatment with thyroid supressive therapy, and hepatoprotective therapy due to progressive increase of serum levels of bilirubin (conjugated/direct) and liver enzymes. The patient treatment continued with low doses of thyroid suppressive therapy. Patient achieved euthyroid state after 2 months with normalization of the serum levels of liver enzymes and bilirubin. The final treatment option for our patient was surgical total thyroidectomy.
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