Embolism of air and gas in hysteroscopic procedures: pathophysiology and implication for daily practice.

Hysteroscopic surgery has gained in popularity and has become the method of choice for diagnostic and therapeutic interventions of intrauterine pathology. Advantages consist of short operating time, rapid postoperative recovery, and low morbidity. However, there are concerns about the potential serious complications that can occur, such as venous air and gas embolism. These are rare but hazardous complications, which can occur in all surgical procedures. In hysteroscopic surgery, large uterine veins may be exposed and are, therefore, a point of entry for gas or air. A number of fatal and nonfatal cases have been described as case reports. Although awareness for air and gas embolism is raised this way, proper guidelines as to how to reduce the risk of venous gas or air embolism are lacking. The pathophysiologic difference between gas and air embolism is described herein because composition of the gases differs as does their physiologic effects. A gas embolism is likely to be derived from electrosurgical vapors whereas air embolism seems to arise from improper purging of lines or reinsertion of hysteroscopic instruments. Treatment regimens must, therefore, be designed to address the specific gases involved. Signs and symptoms of these different embolisms are described, as early detection and intervention are crucial for survival. Furthermore, we provide guidelines for operating department personnel, surgeons, and anesthesiologists to reduce the risk of venous gas or air embolism during hysteroscopic procedures. Potential complications of these procedures may be prevented this way.

Expression of angiogenesis-related factors in lungs of patients with congenital diaphragmatic hernia and pulmonary hypoplasia of other causes.

Congenital diaphragmatic hernia (CDH) is a congenital disorder, complicated by pulmonary hypoplasia (PH) and pulmonary hypertension. Hypoplastic lungs have fewer and smaller airspaces than normal, with thicker interalveolar septa; the adventitia and media of pulmonary arteries are thickened, and the total size of the pulmonary vascular bed is decreased compared to normal. Although histological abnormalities in PH have been described, less is known about the underlying molecular mechanisms. Therefore, we have investigated a series of proteins, known to be involved in angiogenesis, including von Hippel-Lindau protein (pVHL), hypoxia-inducible factor-1a (HIF-1a), vascular endothelial growth factor (VEGF), fetal liver kinase 1 (Flk-1), and endothelial and inducible nitric oxide synthase (eNOS, iNOS) by immunohistochemistry on paraffin-embedded lung tissue of CDH patients ( n = 13), patients with lung hypoplasia due to other causes ( n = 20), and normal controls ( n = 33). pVHL was expressed more frequently in the arterial smooth muscle cells of CDH lungs compared with both other groups. Furthermore, HIF-1a was expressed less frequently in the endothelium of arteries, veins, and capillaries of CDH lungs as compared with both other groups. No differences were observed in the expression patterns of VEGF, Flk-1, eNOS, and iNOS between the different groups. Our data suggest a role for pVHL and HIF-1a in normal and abnormal pulmonary angiogenesis. The differential expression of these proteins may provide a molecular basis for the histological differences observed in the lung vessels of patients with CDH.