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Clinical examination
Published in Nicholas Summerton, Primary Care Diagnostics, 2018
Thus the most useful signs for making a diagnosis of ascites are a positive fluid wave, shifting dullness and peripheral oedema. To rule out ascites a negative history of ankle swelling, no increase in abdominal girth and an inability to demonstrate bulging flanks, flank dullness, shifting dullness or peripheral oedema are most helpful.
A lawyer with a drink problem
Published in Tim French, Terry Wardle, The Problem-Based Learning Workbook, 2022
There may be few signs in acute-onset liver disease or in advanced cirrhosis. However, the following signs should be sought: jaundice: when serum bilirubin exceeds 35 µmol/l, the skin and the sclerae may become yellow; this is especially obvious in fair-skinned peoplespider naevi: these are superficial, tortuous arterioles, and typically fill from the centre outwards. They are usually restricted to the arms, face, and upper torso (usually in the distribution of the superior vena cava). They can be pulsatile and difficult to detect in dark-skinned individualspalmar erythema: this is reddening of the palms, and to a lesser extent the fingertips, indicating a hyperdynamic circulationgynaecomastia: the altered catabolism of oestrogen in a damaged liver can produce breast enlargement in men. In women this may be more difficult to detectperipheral oedema: this is due to salt and water retention and lowered plasma oncotic pressureascites: fluid accumulation in the abdomen produces abdominal distention and bulging flanks. This often indicates severe liver disease, usually cirrhosis. Fluid accumulates in the abdomen because of portal hypertension and lowered plasma oncotic pressurecaput medusae: caput medusae consists of dilated collateral veins seen radiating from the umbilicus. This sign results from recanalisation of the umbilical vein due to portal hypertensionsplenomegaly: this is present clinically whenever the spleen can be felt protruding beneath the left rib cage. The spleen enlarges secondary to portal hypertension, since the splenic vein drains into the portal vein. If suspected, splenomegaly should be confirmed by ultrasound.
Early diagnosis and successful treatment of cytomegalovirus peritonitis in children with primary nephrotic syndrome: case series and literature review
Published in Renal Failure, 2020
Haiting Lin, Lizhi Chen, Songyang Wen, Zhihui Yue, Ying Mo, Xiaoyun Jiang, Liuyi Huang
A 13-year-old girl was transferred to our institution on 26 April 2018, with a history of NS lasting for 1-month. She was initially treated with intravenous methylprednisolone 60 mg qd (1.5 mg/kg). Initial laboratories of peripheral blood included ALB 14.0 g/L, CHOL 9.8 mmol/L, CREA 95 μmol/L (CCr was 64.28 mL/min/1.73 m2). 24-h urine protein was 13.470 g. CMV DNA was detected in blood (7550 copies/mL) but negative in urine. Because of a large amount of ascites and poor diuretic effect, abdominal puncture was performed on 28 April 2018. The routine biochemical screening tests of ascites are shown in Table 1. Cultures of the specimen produced no growth of fungi, mycobacteria, or bacteria and EBV DNA was negative in ascites. CMV DNA was detected in ascites (769 copies/mL). Therefore, the girl was treated with intravenous GCV (the dose was adjusted for renal function: 2.5 mg/kg, q12h). On 4 May 2018, the child had abdominal pain, cough, and expectoration without fever, vomiting or diarrhea. Physical examination revealed normal vital signs, severe facial and lower limbs edema. There were rales at auscultation of both lungs. Abdominal examination showed bulging flanks, generalized tenderness and rebound tenderness, shifting dullness. Laboratories of peripheral blood included WBC 10.70 × 109/L (NEUT 63.2%; LY 30.4%), normal hemoglobin and platelets, CRP 0.80 mg/L, PCT 0.42 ng/mL, ALT 5.0 U/L, mycoplasma pneumoniae IgM 1:160. The child was treated with oral azithromycin and other intravenous antibiotic treatment. Also, she received intravenous fluids, albumin and diuretics. After 3 days, cough and expectoration mitigated significantly and the rales of lungs disappeared. Urinary output increased gradually. However, there was still abdominal pain and the abdominal circumference increased gradually. Imaging showed that no gas under the diaphragm (Figure 4). Abdominal paracentesis was performed again on 8 May 2018. The copy number of CMV DNA in ascites increased (455 000 copies/mL) and the renal function improved (CREA 69 μmol/L, CCr 116.78 mL/min/1.73 m2). Considering the improvement of renal function, the dosage of GCV was adjusted (5 mg/kg q12h for 2 weeks; 5 mg/kg qd for 1 week). One week later, the patient’s clinical symptoms were completely relieved, CMV DNA was negative in ascites and the routine biochemical screening tests of ascites were normal. After 3 weeks, she was transferred to the local hospital for further treatment and lost to follow up.