Transcranial Doppler: preventing stroke during carotid endarterectomy.
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Carotid endarterectomy (CEA) is more effective at preventing strokes than medical therapy alone in those patients with severe symptomatic stenosis of the internal carotid artery and this benefit persists despite a perioperative stroke/death rate of approximately 5%. Thromboembolism has been established as the underlying cause of the majority of perioperative strokes, but this could not be detected using the existing methods of monitoring or quality control. Early studies demonstrated that transcranial Doppler monitoring (TCD) could detect intraoperative embolism, but the clinical significance of this finding was questioned as the incidence of these emboli far exceeded the incidence of perioperative strokes. This study aimed to establish the clinical relevance of TCD-detected emboli during CEA by differentiating emboli into two broad categories; air and particulate, and comparing the quantity of each with a variety of clinical outcomes including neurological and cognitive function, retinal fundoscopy, automated visual fields and CT/MRI brain scans. This prospective study was performed on 100 consecutive patients undergoing CEA with all assessments performed pre- and postoperatively by independent specialists in the relevant fields. Embolisation was detected in 92% of successfully monitored operations. Most emboli were characteristic of air microbubbles and not associated with the development of adverse clinical events. However, emboli characteristic of particulate material were detected during the initial dissection phase and in the recovery phase after final restoration of flow. These particulate emboli were associated with the development of both neurological and cognitive deficits. In particular, persistent embolisation after final restoration of flow heralded incipient carotid artery thrombosis and the development of stroke. Early intervention based on the TCD evidence of continuing embolisation can prevent the stroke from occurring. (+info)
Death due to air embolism during sexual intercourse in the puerperium.
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We describe the cases of two young women who died due to air embolism during sexual intercourse early in the puerperium. (+info)
Brain injury after cerebral arterial air embolism in the rabbit as determined by triphenyltetrazolium staining.
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BACKGROUND: Microscopic cerebral arterial air embolism (CAAE) occurs commonly during cardiac surgery and causes acute and chronic nonfocal neurologic dysfunction. Nevertheless, most neuroimaging studies do not detect brain injury after cardiac surgery. Using a rabbit model, the authors hypothesized they could detect and quantitate severe brain injury and infarction 24 h after microscopic CAAE using the vital stain triphenyltetrazolium chloride. METHODS: Experiments were conducted in methohexital anesthetized New Zealand white rabbits. Surgical shams (n = 5) underwent surgery but had no neurologic insult. Positive controls (n = 3) received 200 microl/kg of intracarotid air. Other animals were randomized to receive either 50 microl/kg intracarotid air, which produces microscopic CAAE (n = 18), or 300 microl intracarotid saline (control, n = 18). Outcomes included somatosensory evoked potential amplitude at 90 min, neurologic impairment score at 4 and 24 h (0 [normal] to 99 [coma]), and percentage of nonstaining brain at 24 h using color-discrimination image analysis. Severely injured or infarcted brain does not stain with triphenyltetrazolium chloride. RESULTS: Surgical shams had little neurologic impairment and a small amount of nonstaining brain at 24 h (5.2 +/- 2.4%; mean +/- SD). Positive controls had profound neurologic impairment and large amounts of nonstaining brain (40-97%). Ninety-minute somatosensory evoked potential amplitude was less in animals receiving 50 microl/kg air versus saline: 38 +/- 28% versus 102 +/- 32%, respectively, P < 1 x 10(-7). Neurologic impairment scores were greater in animals receiving 50 microl/kg air versus saline: at 4 h, 43 +/- 16 versus 23 +/- 9, P < 1 x 10(-7); at 24 h, 24 +/- 12 versus 15 +/- 8, P = 0.013. Nevertheless, there was no difference between 50 microl/kg air and saline in nonstaining brain: 5.5 +/- 2.9% versus 6.8 +/- 5.4%, P = 0.83. CONCLUSIONS: Neurologic injury after CAAE is dose-dependent. Although microscopic CAAE causes somatosensory evoked potential abnormalities and neurologic dysfunction, severe cerebral injury or infarction is not present at 24 h. The author's findings are consistent with clinical imaging studies that suggest microscopic CAAE causes neurologic dysfunction even though overt infarction is absent. (+info)
Carbon dioxide embolism during laparoscopy: effect of insufflation pressure in pigs.
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Carbon dioxide embolism is a rare but potentially devastating complication of laparoscopy. To determine the effects of insufflation pressure on the mortality from carbon dioxide embolism, six swine had intravascular insufflation with carbon dioxide for 30 seconds using a Karl Storz insufflator at a flow rate of 35 mL/kg/min. The initial insufflation pressure was 15 mm Hg. Following recovery from the first embolism, intravascular insufflation using a pressure of 20 mm Hg at the same flow rate was performed in the surviving animals. Significantly less carbon dioxide (8.3 +/- 2.7 versus 16.7 +/- 3.9 mL/kg; p < 0.02) was insufflated intravascularly at 15 mm Hg than at 20 mm Hg pressure. All of the pigs insufflated at 15 mm Hg pressure with a flow rate of 35 mL/kg/min survived. In contrast, 4 of the 5 pigs insufflated at 20 mm Hg pressure died. The surviving pig died when insufflated with 25 mm Hg pressure following an embolism of 15.7 mL/kg. Intravascular injection was often associated with an initial rise in end-tidal carbon dioxide tension, followed by a rapid fall in all cases where the embolism proved fatal. Insufflation should be begun with a low pressure and a slow flow rate to limit the volume of gas embolized in the event of inadvertent venous cannulation. Insufflation should immediately be stopped if a sudden change in end-tidal carbon dioxide tension occurs. (+info)
Theoretical and experimental intravascular gas embolism absorption dynamics.
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Multifocal cerebrovascular gas embolism occurs frequently during cardiopulmonary bypass and is thought to cause postoperative neurological dysfunction in large numbers of patients. We developed a mathematical model to predict the absorption time of intravascular gas embolism, accounting for the bubble geometry observed in vivo. We modeled bubbles as cylinders with hemispherical end caps and solved the resulting governing gas transport equations numerically. We validated the model using data obtained from video-microscopy measurements of bubbles in the intact cremaster microcirculation of anesthetized male Wistar rats. The theoretical model with the use of in vivo geometry closely predicted actual absorption times for experimental intravascular gas embolisms and was more accurate than a model based on spherical shape. We computed absorption times for cerebrovascular gas embolism assuming a range of bubble geometries, initial volumes, and parameters relevant to brain blood flow. Results of the simulations demonstrated absorption time maxima and minima based on initial geometry, with several configurations taking as much as 50% longer to be absorbed than would a comparable spherical bubble. (+info)
Spatial distribution of venous gas emboli in the lungs.
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The distribution of gaseous pulmonary emboli is presumed to be determined by their buoyancy. We hypothesized that regional pulmonary blood flow may also influence their distribution. Therefore, pulmonary blood flow was measured in supine, anesthetized dogs with use of 15-microm fluorescent microspheres at baseline and during N(2) embolism. The animals were killed, and the lungs were excised, air-dried, and diced into approximately 2-cm(3) pieces with weights and spatial coordinates recorded. Embolism was defined as a >10% flow decrease relative to baseline. Vertically, the incidence of embolism increased substantially by 6 +/- 1% per additional centimeter in height compared with baseline (P = 0.0003). Embolism also increased radially by 3 +/- 1%/cm from the hilum (P = 0.002). There was a weaker but statistically significant increase in embolism to pieces with greater baseline flow, 9 +/- 2% for every 1. 0 increase in relative baseline flow (P = 0.008). We conclude that the distribution of gaseous emboli is influenced by buoyancy and flow dynamics within the pulmonary vasculature. (+info)
Hemodilution during venous gas embolization improves gas exchange, without altering V(A)/Q or pulmonary blood flow distributions.
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BACKGROUND: Isovolemic anemia results in improved gas exchange in rabbits with normal lungs but in relatively poorer gas exchange in rabbits with whole-lung atelectasis. In the current study, the authors characterized the effects of hemodilution on gas exchange in a distinct model of diffuse lung injury: venous gas embolization. METHODS: Twelve anesthetized rabbits were mechanically ventilated at a fixed rate and volume. Gas embolization was induced by continuous infusion of nitrogen via an internal jugular venous catheter. Serial hemodilution was performed in six rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; six rabbits were followed as controls over time. Measurements included hemodynamic parameters and blood gases, ventilation-perfusion (V(A)/Q) distribution (multiple inert gas elimination technique), pulmonary blood flow distribution (fluorescent microspheres), and expired nitric oxide (NO; chemoluminescence). RESULTS: Venous gas embolization resulted in a decrease in partial pressure of arterial oxygen (PaO2) and an increase in partial pressure of arterial carbon dioxide (PaCO2), with markedly abnormal overall V(A)/Q distribution and a predominance of high V(A)/Q areas. Pulmonary blood flow distribution was markedly left-skewed, with low-flow areas predominating. Hematocrit decreased from 30+/-1% to 11+/-1% (mean +/- SE) with hemodilution. The alveolar-arterial PO2 (A-aPO2) difference decreased from 375+/-61 mmHg at 30% hematocrit to 218+/-12.8 mmHg at 15% hematocrit, but increased again (301+/-33 mmHg) at 11% hematocrit. In contrast, the A-aPO2 difference increased over time in the control group (P < 0.05 between groups over time). Changes in PaO2 in both groups could be explained in large part by variations in intrapulmonary shunt and mixed venous oxygen saturation (SvO2); however, the improvement in gas exchange with hemodilution was not fully explained by significant changes in V(A)/Q or pulmonary blood flow distributions, as quantitated by the coefficient of variation (CV), fractal dimension, and spatial correlation of blood flow. Expired NO increased with with gas embolization but did not change significantly with time or hemodilution. CONCLUSIONS: Isovolemic hemodilution results in improved oxygen exchange in rabbits with lung injury induced by gas embolization. The mechanism for this improvement is not clear. (+info)
Incidence of venous air embolism during craniectomy for craniosynostosis repair.
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BACKGROUND: Investigations to determine the incidence of venous air embolism in children undergoing craniectomy for craniosynostosis repair have been limited, although venous air embolism has been suspected as the cause of hemodynamic instability and sometimes death. A precordial Doppler ultrasonic probe is an accepted method for detection of venous air embolism and is readily available at most institutions. METHODS: A prospective study was conducted using a precordial Doppler ultrasonic probe in children undergoing craniectomy for craniosynostosis repair. The Doppler signal was continuously monitored intraoperatively for characteristic changes of venous air embolism. A recording was made of the precordial Doppler probe pulses, which was later reviewed by a neuroanesthesiologist, blinded to the intraoperative events. This information was correlated with the intraoperative events and episodes of venous air embolism were graded. RESULTS: Twenty-three patients were enrolled in the study during the 2-yr study period. Nineteen patients (82.6%) demonstrated 64 episodes of venous air embolism; six patients (31.6%) had hypotension associated with venous air embolism. Thirty-two episodes of hypotension were demonstrated in eight patients (34.7%). None of the patients developed cardiovascular collapse. CONCLUSION: The incidence of venous air embolism in our study of 23 children undergoing craniectomy for craniosynostosis was 82.6%. Though most episodes of venous air embolism during craniosynostosis repair are without hemodynamic consequences, the preemptive placement of a precordial Doppler ultrasonic probe is a noninvasive, economic, and safe method for the detection of venous air embolism. Prompt recognition may allow for the early initiation of therapy, thereby decreasing morbidity and mortality rates related to venous air embolism. (+info)