52 research outputs found

    Diagnosis and management of respiratory adverse events in the operating room

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    Perioperative respiratory adverse events cause more than three-quarters of all perioperative critical incidents in pediatric anesthesia and approximately half of anesthesia-related cardiac arrests. We can define seven main clinical types of perioperative respiratory adverse events: upper airway obstruction, laryngospasm, bronchospasm, severe persistent cough, apnea, stridor, and oxygen desaturation. Depending on the definitions used for preoperative respiratory adverse events and the cohort of children examined, the incidence varies between 8 and 21 %. This review discusses the recognition and treatment of perioperative respiratory adverse events. Furthermore, it provides guidance on how to identify children who are at increased risk for developing perioperative respiratory adverse events and how to tailor the perioperative anesthetic management for the individual child in order to minimize the risk of perioperative respiratory adverse events

    An update on the perioperative management of children with upper respiratory tract infections

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    Purpose of review: This review summarises the current evidence for the management for children with recent upper respiratory tract infections. Furthermore, the review includes management guidelines for children with upper respiratory tract infections. Recent findings: Good history and clinical examination is sufficient in most children presenting with URTI. Testing for immune markers or preoperative NO measurement does not add any additional value. Preoperative bronchodilator administration, iv induction with propofol and non-invasive airway management all reduce the occurrence of respiratory adverse events. Summary: Most children can be safely anaesthetised even in the presence of an upper respiratory tract infection if the perioperative anaesthesia management is optimised. In this review article we have included a management algorithm for children with URTI presenting for elective surgery

    Abdominal compliance: A bench-to-bedside review

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    Abdominal compliance is an important determinant and predictor of available workspace during laparoscopic surgery. Furthermore, critically ill patients with a reduced abdominal compliance are at an increased risk of developing intra-abdominal hypertension and abdominal compartment syndrome both of which are associated with high morbidity and mortality. Despite of this, abdominal compliance is a concept, which has been neglected in the past. Abdominal compliance is defined as a measure of the ease of abdominal expansion, expressed as a change in intra-abdominal volume per change in intra-abdominal pressure: abdominal compliance = delta intra-abdominal volume / delta intra-abdominal pressure. AC is a dynamic variable, dependent on base-line IAV and IAP as well as reshaping and stretching capacity. Whereas abdominal compliance itself can only rarely be measured, it always needs to be considered an important component of intra-abdominal pressure. Patients with decreased abdominal compliance are prone to fulminant development of abdominal compartment syndrome when concomitant risk factors for intra-abdominal hypertension are present. This review aims to clarify the pressure-volume relationship within the abdominal cavity. It highlights how different conditions and pathologies can affect abdominal compliance and which management strategies could be applied to avoid serious consequences of decreased abdominal compliance. We have pooled all available human data to calculate abdominal compliance values in patients acutely and chronically exposed to intra-abdominal hypertension and demonstrated an exponential abdominal pressure-volume relationship. Most importantly, patients with high level of intra-abdominal pressure have a reduced abdominal compliance. In these patients, only small reduction in intra-abdominal volume can significantly increase abdominal compliance and reduce intra-abdominal pressures. A greater knowledge on abdominal compliance may help in selecting a better surgical approach as well as reducing complications related to intra-abdominal hypertension

    The respiratory pressure-abdominal volume curve in a porcine model

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    Background: Increasing intra-abdominal volume (IAV) can lead to intra-abdominal hypertension (IAH) or abdominal compartment syndrome. Both are associated with raised morbidity and mortality. IAH can increase airway pressures and impair ventilation. The relationship between increasing IAV and airway pressures is not known. We therefore assessed the effect of increasing IAV on airway and intra-abdominal pressures (IAP). Methods: Seven pigs (41.4 +/−8.5 kg) received standardized anesthesia and mechanical ventilation. A latex balloon inserted in the peritoneal cavity was inflated in 1-L increments until IAP exceeded 40 cmH2O. Peak airway pressure (pPAW), respiratory compliance, and IAP (bladder pressure) were measured. Abdominal compliance was calculated. Different equations were tested that best described the measured pressure-volume curves. Results: An exponential equation best described the measured pressure-volume curves. Raising IAV increased pPAW and IAP in an exponential manner. Increases in IAP were associated with parallel increases in pPAW with an approximate 40% transmission of IAP to pPAW. The higher the IAP, the greater IAV effected pPAW and IAP. Conclusions: The exponential nature of the effect of IAV on pPAW and IAP implies that, in the presence of high grades of IAH, small reductions in IAV can lead to significant reductions in airway and abdominal pressures. Conversely, in the presence of normal IAP levels, large increases in IAV may not affect airway and abdominal pressures

    Commonly applied positive end-expiratory pressures do not prevent functional residual capacity decline in the setting of intra-abdominal hypertension: a pig model

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    Introduction Intra-abdominal hypertension is common in critically ill patients and is associated with increased morbidity and mortality. The optimal ventilation strategy remains unclear in these patients. We examined the effect of positive end-expiratory pressures (PEEP) on functional residual capacity (FRC) and oxygen delivery in a pig model of intra-abdominal hypertension. Methods Thirteen adult pigs received standardised anaesthesia and ventilation. We randomised three levels of intra-abdominal pressure (3 mmHg (baseline), 18 mmHg, and 26 mmHg) and four commonly applied levels of PEEP (5, 8, 12 and 15 cmH2O). Intra-abdominal pressures were generated by inflating an intra-abdominal balloon. We measured intra-abdominal (bladder) pressure, functional residual capacity, cardiac output, haemoglobin and oxygen saturation, and calculated oxygen delivery. Results Raised intra-abdominal pressure decreased FRC but did not change cardiac output. PEEP increased FRC at baseline intra-abdominal pressure. The decline in FRC with raised intra-abdominal pressure was partly reversed by PEEP at 18 mmHg intra-abdominal pressure and not at all at 26 mmHg intra-abdominal pressure. PEEP significantly decreased cardiac output and oxygen delivery at baseline and at 26 mmHg intra-abdominal pressure but not at 18 mmHg intra-abdominal pressure. Conclusions In a pig model of intra-abdominal hypertension, PEEP up to 15 cmH2O did not prevent the FRC decline caused by intra-abdominal hypertension and was associated with reduced oxygen delivery as a consequence of reduced cardiac output. This implies that PEEP levels inferior to the corresponding intra-abdominal pressures cannot be recommended to prevent FRC decline in the setting of intra-abdominal hypertension

    Incidence, Risk Factors, and Outcomes of Intra-Abdominal Hypertension in Critically Ill Patients-A Prospective Multicenter Study (IROI Study)

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    To identify the prevalence, risk factors, and outcomes of intra-abdominal hypertension in a mixed multicenter ICU population. Prospective observational study. Fifteen ICUs worldwide. Consecutive adult ICU patients with a bladder catheter. None. Four hundred ninety-one patients were included. Intra-abdominal pressure was measured a minimum of every 8 hours. Subjects with a mean intra-abdominal pressure equal to or greater than 12 mm Hg were defined as having intra-abdominal hypertension. Intra-abdominal hypertension was present in 34.0% of the patients on the day of ICU admission (159/467) and in 48.9% of the patients (240/491) during the observation period. The severity of intra-abdominal hypertension was as follows: grade I, 47.5%; grade II, 36.6%; grade III, 11.7%; and grade IV, 4.2%. The severity of intra-abdominal hypertension during the first 2 weeks of the ICU stay was identified as an independent predictor of 28-and 90-day mortality, whereas the presence of intra-abdominal hypertension on the day of ICU admission did not predict mortality. Body mass index, Acute Physiology and Chronic Health Evaluation II score greater than or equal to 18, presence of abdominal distension, absence of bowel sounds, and positive end-expiratory pressure greater than or equal to 7 cm H2O were independently associated with the development of intra-abdominal hypertension at any time during the observation period. In subjects without intra-abdominal hypertension on day 1, body mass index combined with daily positive fluid balance and positive end-expiratory pressure greater than or equal to 7 cm H2O (as documented on the day before intra-abdominal hypertension occurred) were-associated with the development of intraabdominal hypertension during the first week in the ICU. In our mixed ICU patient cohort, intra-abdominal hypertension occurred in almost half of all subjects and was twice as prevalent in mechanically ventilated patients as in spontaneously breathing patients. Presence and severity of intra-abdominal hypertension during the observation period significantly and independently increased 28-and 90-day mortality. Five admission day variables were independently associated with the presence or development of intra-abdominal hypertension. Positive fluid balance was associated with the development of intra-abdominal hypertension after day 1474535542NIGMS NIH HHSUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of General Medical Sciences (NIGMS) [U54 GM104940

    Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

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    IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570
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