PubMed · 13045434
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1953-05-02. MITRAL valvotomy.. https://pubmed.ncbi.nlm.nih.gov/13045434/
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OBJECTIVES: Umbilical venous pulsation is an important sign of hemodynamic compromise, but is also found under normal physiological conditions. Mathematical modeling suggests that vascular compliance is a determinant for pulsation, and we tested this by studying velocity pulsation at three sites on the umbilical vein. METHODS: In a cross-sectional study of 279 low-risk pregnancies (20-40 weeks' gestational age) blood flow velocity in the umbilical vein was determined before, within and after the umbilical ring in the fetal abdominal wall, and the incidence and magnitude of pulsation (the difference between the maximum and minimum velocity during a pulse, and pulsatility index) were noted. Based on the fact that the vessel cross-sectional area is an important determinant of compliance, we measured the diameter and time-averaged maximum velocity to reflect variation in diameter and compliance at the three sites. RESULTS: The incidence of umbilical venous pulsation was higher at the umbilical ring in the abdominal wall (242/279, 87%, 95% CI 82-90) than in the cord (43/198, 22%, 95%CI 16-27) or intra-abdominally (84/277, 30%, 95% CI 25-36) (P < 0.001). When pulsation was observed intra-abdominally, the pulsatility was not different from that at the umbilical ring (P = 0.16). However, the lowest pulsatility was found in the cord vein (P < 0.0001), where the largest vein diameter was found. CONCLUSION: The high incidence of venous pulsation at the umbilical ring where diameter and compliance are low supports the suggestion that local compliance is an important factor influencing pulsation in fetal veins.
We describe a case of the posterior interosseous nerve (PIN) syndrome in a patient with gout. Exploration of the PIN revealed multiple hourglass-like constriction of the PIN, which did not correspond to any extrinsic compressing structures. Hourglass-like constrictions of the PIN is one of the causes of the painful PIN syndrome.
Pulmonary hypertension associated with increased pulmonary vascular resistance occurring in the setting of portal hypertension, referred to as "portopulmonary hypertension", is a complication of chronic liver disease, and occurs in 2% to 3% of patients with portal hypertension. Portal hypertension is a relatively common finding in patients with chronic myeloproliferative disorder (CMPD). Pulmonary hypertension is also an occasional finding in CMPD patients. Latent myeloproliferative disorder, on the other hand does not fulfill the diagnostic criteria of classical CMPD and is characterized by younger age of onset, slow disease progression, a high risk of thrombosis, platelet dysfunction, and normal or increased platelet count in spite of the presence of splenomegaly. We report findings in a 50-year-old woman with portal hypertension for which there were three major etiological findings-increased splenic blood flow, infiltration of hematopoietic cells in the liver, and thrombosis in the portal or hepatic vein-over a 25-year clinical course, during which there was also reversible stenosis of the portal vein. Twenty-three years after her first admission, her condition was diagnosed as latent myeloproliferative disorder, and she developed pulmonary hypertension. Her clinical history and data indicated that the portopulmonary hypertension was due to the latent myeloproliferative disorder.