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Impact of intra-abdominal insufflation pressure on gas leakage occurring during laparoscopy.

ABSTRACT: The advent of the COVID-19 pandemic led to recommendations aimed at minimizing the risk of gas leaks at laparoscopy. As this has continuing relevance including regarding operating room pollution, we empirically quantified carbon dioxide (CO2) leak jet velocity (important for particle propulsion) occurring with different instruments inserted into differing trocars repeated across a range of intra-abdominal pressures (IAPs) and modern insufflators in an experimental model. Laparoscopic gas plume leak velocity (metres/second) was computationally enumerated from schlieren optical flow videography on a porcine cadaveric laparoscopic model with IAPs of 4-5, 7-8, 12-15 and 24-25 mmHg (repeated with 5 different insufflators) during simulated operative use of laparoscopic clip appliers, scissors, energy device, camera and staplers as well as Veres needle (positive control) and trocar obturator (negative control) in fresh 5 mm and 12 mm ports. Close-fitting solid instruments (i.e. cameras and obturators) demonstrated slower gas leak velocities in both the 5 mm and 12 mm ports (p = 0.02 and less than 0.001) when compared to slimmer instruments, however, hollow instrument designs were seen to defy this pattern with the endoscopic linear stapler visibly inducing multiple rapid jests even when compared to similarly sized clip appliers (p = 0.03). However, on a per device basis the operating instrumentation displayed plume speeds which did not vary significantly when challenged with varying post size, IAP and a range of insufflators. In general, surgeon's selection of instrument, port or pressure does not usefully mitigate trocar CO2 leak velocity. Instead better trocar design is needed, helped by a fuller understanding of trocar valve mechanics via computational fluid dynamics informed by relevant surgical modelling.

SUBMITTER: Dalli J

PROVIDER: S-EPMC9063625 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundThe intra-abdominal pressure (IAP) is an important clinical parameter that can significantly change during respiration. Currently, IAP is recorded at end-expiration (IAPee), while continuous IAP changes during respiration (?IAP) are ignored. Herein, a novel concept of considering continuous IAP changes during respiration is presented.MethodsBased on the geometric mean of the IAP waveform (MIAP), a mathematical model was developed for calculating respiratory-integrated MIAP (i.e. MIAPri=IAPee+i??IAP), where 'i' is the decimal fraction of the inspiratory time, and where ?IAP can be calculated as the difference between the IAP at end-inspiration (IAPei) minus IAPee. The effect of various parameters on IAPee and MIAPri was evaluated with a mathematical model and validated afterwards in six mechanically ventilated patients. The MIAP of the patients was also calculated using a CiMON monitor (Pulsion Medical Systems, Munich, Germany). Several other parameters were recorded and used for comparison.ResultsThe human study confirmed the mathematical modelling, showing that MIAPri correlates well with MIAP (R2 = 0.99); MIAPri was significantly higher than IAPee under all conditions that were used to examine the effects of changes in IAPee, the inspiratory/expiratory (I:E) ratio, and ?IAP (P <0.001). Univariate Pearson regression analysis showed significant correlations between MIAPri and IAPei (R = 0.99), IAPee (R = 0.99), and ?IAP (R = 0.78) (P <0.001); multivariate regression analysis confirmed that IAPee (mainly affected by the level of positive end-expiratory pressure, PEEP), ?IAP, and the I:E ratio are independent variables (P <0.001) determining MIAP. According to the results of a regression analysis, MIAP can also be calculated asMIAP=-0.3+IAPee+0.4??IAP+0.5?IE.ConclusionsWe believe that the novel concept of MIAP is a better representation of IAP (especially in mechanically ventilated patients) because MIAP takes into account the IAP changes during respiration. The MIAP can be estimated by the MIAPri equation. Since MIAPri is almost always greater than the classic IAP, this may have implications on end-organ function during intra-abdominal hypertension. Further clinical studies are necessary to evaluate the physiological effects of MIAP.

Project description:IntroductionIntra-abdominal hypertension (IAH) causes atelectasis, reduces lung volumes and increases respiratory system elastance. Positive end-expiratory pressure (PEEP) in the setting of IAH and healthy lungs improves lung volumes but not oxygenation. However, critically ill patients with IAH often suffer from acute lung injury (ALI). This study, therefore, examined the respiratory and cardiac effects of positive end-expiratory pressure in an animal model of IAH, with sick lungs.MethodsNine pigs were anesthetized and ventilated (48 +/- 6 kg). Lung injury was induced with oleic acid. Three levels of intra-abdominal pressure (baseline, 18, and 22 mmHg) were randomly generated. At each level of intra-abdominal pressure, three levels of PEEP were randomly applied: baseline (5 cmH2O), moderate (0.5 × intra-abdominal pressure), and high (1.0 × intra-abdominal pressure). We measured end-expiratory lung volumes, arterial oxygen levels, respiratory mechanics, and cardiac output 10 minutes after each new IAP and PEEP setting.ResultsAt baseline PEEP, IAH (22 mmHg) decreased oxygen levels (-55%, P <0.001) and end-expiratory lung volumes (-45%, P = 0.007). At IAP of 22 mmHg, moderate and high PEEP increased oxygen levels (+60%, P = 0.04 and +162%, P <0.001) and end-expiratory lung volume (+44%, P = 0.02 and +279%, P <0.001) and high PEEP reduced cardiac output (-30%, P = 0.04). Shunt and dead-space fraction inversely correlated with oxygen levels and end-expiratory lung volumes. In the presence of IAH, lung, chest wall and respiratory system elastance increased. Subsequently, PEEP decreased respiratory system elastance by decreasing chest wall elastance.ConclusionsIn a porcine sick lung model of IAH, PEEP matched to intra-abdominal pressure led to increased lung volumes and oxygenation and decreased chest wall elastance shunt and dead-space fraction. High PEEP decreased cardiac output. The study shows that lung injury influences the effects of IAH and PEEP on oxygenation and respiratory mechanics. Our findings support the application of PEEP in the setting of acute lung injury and IAH.

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Impact of intra-abdominal insufflation pressure on gas leakage occurring during laparoscopy.

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