PubMed · 6656415
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M Ballester Rodés. 1983-11-12. [Functional mitral insufficiency].. https://pubmed.ncbi.nlm.nih.gov/6656415/
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OBJECTIVE: To review current knowledge about the hepatopulmonary syndrome, including definition and clinical features, methods for diagnosing it, pathophysiologic mechanisms of the associated vascular dilatations, and considerations in treatment, with emphasis on potential reversibility of the syndrome after liver transplantation. DATA SOURCES: The MEDLINE database from January 1986 to December 1993 and bibliographies of selected articles. STUDY SELECTION: Case studies and series reporting results from patients with the hepatopulmonary syndrome were reviewed. Clinical reviews and animal studies relevant to the hepatopulmonary syndrome were examined. DATA EXTRACTION: Outcomes, including survival and the frequency of reversibility of the hepatopulmonary syndrome, were extracted from available clinical reports. DATA SYNTHESIS: Mild hypoxemia is multifactorial and occurs in approximately one third of all patients with chronic liver disease. The hepatopulmonary syndrome is one cause of hypoxemia that may also cause dyspnea, platypnea, and orthopnea. Intrapulmonary vascular dilatations and the resulting right-to-left intrapulmonary shunt are characteristic of the syndrome. Pharmacologic treatment with almitrine bismesylate, somatostatin analog, and indomethacin and treatment with plasmapheresis have been disappointing. The underlying cause and the predictors of reversibility of the hepatopulmonary syndrome remain unknown, but it has recently been shown that such reversibility is possible and that contrast-enhanced echocardiography appears to be the most sensitive diagnostic test for detecting intrapulmonary vascular dilatations. CONCLUSIONS: In the context of persisting uncertainty about the cause and treatment of the hepatopulmonary syndrome, future studies must focus on better understanding the pathophysiology of the hepatopulmonary syndrome, predicting reversibility after liver transplantation, and identifying other treatment options.
OBJECTIVE: Our purpose was to determine the degree of fetal pyelectasis predictive of neonatal renal pathologic processes. STUDY DESIGN: Eighty-four cases of pyelectasis were identified during the study period (1989 through 1993). Fetuses with anteroposterior diameter of the renal pelvis > or = 4 mm before 33 weeks or > or = 7 mm after 33 weeks without caliectasis were included. Fetuses with an anteroposterior diameter of > 10 mm were excluded. Postnatal evaluation included renal sonogram, voiding cystourethrogram, and renal flow and function studies. RESULTS: Sixteen cases were excluded because of incomplete postnatal workup. Renal pathologic processes were found in 30 of 68 (44%) at birth; the most common were ureteropelvic junction obstruction (37%) and vesicoureteral reflux (33%). Only four cases required surgical intervention (13%), and the remaining 87% were managed conservatively. A normal urinary tract was found in 25% of the infants and the remaining 21 of 68 (31%) had regression of pyelectasis before birth. Fetuses with a dilated anteroposterior diameter > or = 8 mm after 28 weeks' gestation were found to have renal pathologic features in two of three of the cases, with sensitivity, specificity, and positive and negative predictive values of 87%, 41%, 66.7% and 70%, respectively. CONCLUSION: Fetuses with an anteroposterior diameter of the renal pelvis > or = 8 mm after 28 weeks' gestation require appropriate urologic evaluation after birth.
Interventional radiology (pulmonary angiography, coil embolotherapy, and TIPS) in patients with HPS seems to provide both diagnostic data and therapeutic results of clinical importance. The case report by Riegler et al. is instructive and emphasizes the need for further prospective study to analyze the successes and failures in terms of measurable clinical variable in a procedure such as TIPS. The resolution of hypoxemia following liver transplantation and careful patient selection offers hope to patients with severe, debilitating oxygenation abnormalities caused by HPS.