Comparison of postoperative respiratory function after laparoscopy or open laparotomy for cholecystectomy.

Cholecystectomy performed via laparotomy is associated with reduction of lung volumes including functional residual capacity that may lead to postoperative hypoxia and atelectasis. Laparoscopic cholecystectomy is associated with faster recovery compared to open laparotomy and cholecystectomy. To determine whether laparoscopic cholecystectomy was associated with less pulmonary dysfunction, 20 patients (ASA Physical Status I) undergoing elective cholecystectomy were randomly assigned to surgical teams performing either laparoscopy or open laparotomy for cholecystectomy. Patients in whom one or the other surgical technique had to be performed for medical or psychologic indications were excluded from the study. A standardized anesthetic technique and postoperative analgesic regimen were used. Forced vital capacity and forced expiratory volume in 1 s; functional residual capacity determined by a closed-circuit, constant volume helium dilution technique; and arterial O2 and CO2 tensions were measured preoperatively and at 6, 24, and 72 h postcholecystectomy. Forced vital capacity and forced expiratory volume in 1 s were significantly greater (P less than 0.05) in the laparoscopy compared to the laparotomy group at 6, 24, and 72 h postoperatively. Forced vital capacity relative to preoperative values was significantly (P less than 0.05) greater in patients with laparoscopy (24 h, 70 +/- 14%; 72 h, 91 +/- 6%) compared to open laparotomy (24 h, 57 +/- 23%; 72 h, 77 +/- 14%). Similarly, forced expiratory volumes in 1 s relative to preoperative values were significantly (P less than 0.05) greater in patients with laparoscopy (24 h, 85 +/- 13%; 72 h, 92 +/- 9%) compared to open laparotomy (24 h, 54 +/- 22%; 72 h, 77 +/- 11%).(ABSTRACT TRUNCATED AT 250 WORDS)     

The course of extravascular lung water in severely injured patients in intensive care with and without thoracic trauma

In patients with multiple injuries, the development of permeability edema can be assumed. However, no uniform shape of this fluid accumulation can be found even in the presence of severe injuries. Based on the first clinical observations, our aim was to search for correlations between the development of extravascular lung water (EVLW) and the individual injury pattern in severely traumatized ICU patients. PATIENTS and METHODS. Our investigations were performed in 48 artificially ventilated ICU patients. According to the prevailing injury pattern patients were divided into three groups: group A: 18 patients (mean age: 32 years, mean Injury Severity Score (ISS) = 29) with isolated thoracic trauma; group B: 10 patients (mean age: 27 years, mean ISS = 42) with severe multiple trauma but without any thoracic injury; group C: 20 patients (mean age: 33 years, mean ISS = 43) with severe multiple trauma and concomitant thoracic trauma. In all patients (group A, B, C), EVLW was determined by means of a double indicator method on a daily basis from the patient's admission to the ICU (day of trauma) until day 10. Additionally, the hemodynamic parameters (heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary capillary wedge pressure and cardiac index) were determined at the same time. RESULTS. As shown in Fig 1, EVLW was slightly elevated on day 1. However, on day 2 EVLW decreased within normal values and remained in that range until the end of the observation period. On day 3 a slight and fleeting increase of EVLW, but within normal range, can be seen. In group B (Fig.2), EVLW can be observed within normal range within a period of 4 days. Starting from day 5 until day 7 a marked increase (p greater than 0.01) in EVLW can be seen. From that maximum point EVLW development reverses slightly until day 10--however, without returning to the normal range. In group C, a marked biphasic pattern can be seen due to EVLW maximum values on post-traumatic days 3 and 7. However, in this group the EVLW was in the pathological range during the whole observation period. No statistically significant differences could be seen, when looking at hemodynamic variables. CONCLUSION. Isolated thoracic trauma will not lead to a marked pathological elevation of EVLW within the lungs. Moreover, EVLW decreases rapidly within a short time period. Based on our results, it seems that severe extrathoracic injuries will intensify microvascular injury in the initial period, as shown in our patients in group C. Increase of EVLW at a later time (day 7), as observed in groups B and C, is possibly the expression of a mediator and activator-induced "septiformal" injury of the microvascular endothelium. This may be caused by the underlying massive peripheral soft-tissue trauma. Specific elevations of EVLW subsequent to the individual injury pattern can indicate that that process has begun and is responsible for the origin of the microvascular injuries.     

Cardiorespiratory effects of automatic tube compensation during airway pressure release ventilation in patients with acute lung injury

BACKGROUND: Spontaneous breaths during airway pressure release ventilation (APRV) have to overcome the resistance of the artificial airway. Automatic tube compensation provides ventilatory assistance by increasing airway pressure during inspiration and lowering airway pressure during expiration, thereby compensating for resistance of the artificial airway. The authors studied if APRV with automatic tube compensation reduces the inspiratory effort without compromising cardiovascular function, end-expiratory lung volume, and gas exchange in patients with acute lung injury. METHODS: Fourteen patients with acute lung injury were breathing spontaneously during APRV with or without automatic tube compensation in random order. Airway pressure, esophageal and abdominal pressure, and gas flow were continuously measured, and tracheal pressure was estimated. Transdiaphragmatic pressure time product was calculated. End-expiratory lung volume was determined by nitrogen washout. The validity of the tracheal pressure calculation was investigated in seven healthy ventilated pigs. RESULTS: Automatic tube compensation during APRV increased airway pressure amplitude from 7.7+/-1.9 to 11.3+/-3.1 cm H2O (mean +/- SD; P < 0.05) while decreasing trans-diaphragmatic pressure time product from 45+/-27 to 27+/-15 cm H2O x s(-1) x min(-1) (P < 0.05), whereas tracheal pressure amplitude remained essentially unchanged (10.3+/-3.5 vs. 10.1+/-3.5 cm H2O). Minute ventilation increased from 10.4+/-1.6 to 11.4+/-1.5 l/min (P < 0.001), decreasing arterial carbon dioxide tension from 52+/-9 to 47+/-6 mmHg (P < 0.05) without affecting arterial blood oxygenation or cardiovascular function. End-expiratory lung volume increased from 2,806+/-991 to 3,009+/-994 ml (P < 0.05). Analysis of tracheal pressure-time curves indicated nonideal regulation of the dynamic pressure support during automatic tube compensation as provided by a standard ventilator. CONCLUSION: In the studied patients with acute lung injury, automatic tube compensation markedly unloaded the inspiratory muscles and increased alveolar ventilation without compromising cardiorespiratory function and end-expiratory lung volume.     

Drotrecogin alfa (activated) treatment in severe sepsis from the global open-label trial ENHANCE: further evidence for survival and safety and implications for early treatment

OBJECTIVE: To provide further evidence for the efficacy and safety of drotrecogin alfa (activated) treatment in severe sepsis. DESIGN: Single-arm, open-label, trial of drotrecogin alfa (activated) treatment in severe sepsis patients. Enrollment began in March 2001 and day-28 follow-up completed in January 2003. SETTING: ENHANCE took place in 25 countries at 361 sites. PATIENTS: Patients with known or suspected infection, three or four systemic inflammatory response syndrome criteria, and one or more sepsis-induced organ dysfunctions. Of 2,434 adults entered, 2,378 received drotrecogin alfa (activated), and of these, 2,375 completed the protocol. INTERVENTIONS: Drotrecogin alfa (activated) was infused at a dose of 24 mug/kg/hr for 96 hrs. MEASUREMENTS AND MAIN RESULTS: The 28-day all-cause mortality approximated that observed in PROWESS (25.3% vs. 24.7%). Although patients in ENHANCE had increased serious bleeding rates compared with patients in the drotrecogin alfa (activated) arm of PROWESS (during infusion, 3.6% vs. 2.4%; postinfusion, 3.2% vs. 1.2%; 28-day, 6.5% vs. 3.5%), increased postinfusion bleeding suggested a higher background bleeding rate. Intracranial hemorrhage was more common in ENHANCE than PROWESS (during infusion, 0.6% vs. 0.2%; 28-day, 1.5% vs. 0.2%). The incidence of fatal intracranial hemorrhage was the same during infusion (0.2%) and higher at 28 days (0.5% vs. 0.2%). ENHANCE patients treated within 0-24 hrs from their first sepsis-induced organ dysfunction had lower observed mortality rate than those treated after 24 hrs (22.9% vs. 27.4%, p = .01). CONCLUSIONS: ENHANCE provides supportive evidence for the favorable benefit/risk ratio observed in PROWESS and suggests that more effective use of drotrecogin alfa (activated) might be obtained by initiating therapy earlier.     

Hemodynamic monitoring in shock and implications for management

Objective

Shock is a severe syndrome resulting in multiple organ dysfunction and a high mortality rate. The goal of this consensus statement is to provide recommendations regarding the monitoring and management of the critically ill patient with shock.

Methods

An international consensus conference was held in April 2006 to develop recommendations for hemodynamic monitoring and implications for management of patients with shock. Evidence-based recommendations were developed, after conferring with experts and reviewing the pertinent literature, by a jury of 11 persons representing five critical care societies.

Data synthesis

A total of 17 recommendations were developed to provide guidance to intensive care physicians monitoring and caring for the patient with shock. Topics addressed were as follows: (1) What are the epidemiologic and pathophysiologic features of shock in the ICU? (2) Should we monitor preload and fluid responsiveness in shock? (3) How and when should we monitor stroke volume or cardiac output in shock? (4) What markers of the regional and micro-circulation can be monitored, and how can cellular function be assessed in shock? (5) What is the evidence for using hemodynamic monitoring to direct therapy in shock? One of the most important recommendations was that hypotension is not required to define shock, and as a result, importance is assigned to the presence of inadequate tissue perfusion on physical examination. Given the current evidence, the only bio-marker recommended for diagnosis or staging of shock is blood lactate. The jury also recommended against the routine use of (1) the pulmonary artery catheter in shock and (2) static preload measurements used alone to predict fluid responsiveness.

Conclusions

This consensus statement provides 17 different recommendations pertaining to the monitoring and caring of patients with shock. There were some important questions that could not be fully addressed using an evidence-based approach, and areas needing further research were identified.