Who goes to the ICU postoperatively?

OBJECTIVE: To describe changes in ICU postoperative management strategies utilized for patients undergoing cardiac surgery. The treatment of these patients serves as a useful illustration of the changing patterns of ICU utilization and care associated with contemporary surgery. DESIGN: Evidence-based review of the clinical literature following a MEDLINE search, direct observation of rapid recovery programs following surgery, and informal inquiry of others utilizing similar approaches to postoperative cardiac surgery care. SETTING AND PATIENTS: The reports reviewed are from a diverse set of hospitals providing cardiac surgery services in both Europe and the United States. Most reports focus efforts on patients undergoing coronary artery revascularization. MEASUREMENTS: Outcome measures used to gauge the effectiveness of postoperative ICU care typically include time to extubation, ICU and hospital length of stay, postoperative complications including reintubation and ICU readmission, patient satisfaction, and health resource savings. MAIN RESULTS: The literature regarding current practice for postoperative ICU management in cardiac surgery consists primarily of grade 2 and 3 literature. CONCLUSIONS: Despite the paucity of controlled data, rapid recovery, extubation, and discharge from the ICU following cardiac surgery is an approach to care that is growing in acceptance. The goals include reduction in the utilization of resources and costs associated with cardiac surgery and maintenance of quality of care and patient satisfaction. Assessment of outcomes requires a program to monitor outcomes. Success does not appear to be linked to preoperative risk for most patients but does relate directly to the anesthetic management delivered in the operating room. Few adverse consequences from this approach have been reported. Experience to date suggests that programs designed to truncate ICU admission following cardiac surgery can be implemented with the cooperation between the health delivery team including surgeon, anesthesiologist, intensivist where available, nursing, respiratory care, and patient and family. These programs can serve as useful models for reassessing the utilization and role of the ICU in the postoperative treatment of routine surgical patients.

Reperfusion injury in single-lung transplant recipients with pulmonary hypertension and emphysema.

BACKGROUND: The early postoperative course of single-lung transplant recipients depends on the recipient's underlying lung pathophysiology and the degree of ischemic-reperfusion injury. We examined the effect of pulmonary hemodynamics and preoperative diagnosis on early allograft function and the effects of pulmonary hemodynamics, allograft blood flow, and chest radiographs on length of mechanical ventilation and intensive care unit length of stay. METHODS: We retrospectively collected data on 30 single-lung transplant recipients, 15 each with pretransplantation pulmonary hypertension and emphysema. Blood flow to the allografts was quantitated by perfusion scans obtained on the first postoperative day. Chest radiographs were graded for reperfusion injury. Pulmonary and hemodynamic data, gas exchange parameters, duration of mechanical ventilation, and intensive care unit stay were recorded. RESULTS: Patients with pulmonary hypertension had a prolonged intensive care unit stay compared with emphysema patients, but pulmonary artery pressures were not quantitatively related to duration of ventilation during the intensive care unit stay. There was no difference in the severity of allograft infiltrate between the emphysema and pulmonary hypertensive patients. The day 1 chest radiograph score was highly predictive of an intensive care unit stay of > or = 7 days, although the threshold score of those with pulmonary hypertension was significantly lower than in emphysema patients. Allograft blood flow and pulmonary hypertension were not contributors to early graft dysfunction. Allograft perfusion decreased with increasing radiographically demonstrated infiltrate in those with emphysema but not in those with pulmonary hypertension. CONCLUSIONS: Elevated allograft blood flow and pressures do not exacerbate radiographically confirmed reperfusion injury. Reperfusion injury is the major cause of early respiratory morbidity after single-lung transplantation. Allograft perfusion in emphysema patients decreases in response to reperfusion injury, but pulmonary hypertension patients remain almost entirely dependent on allograft function, even with severe chest radiograph scores. This may be an important mechanism by which single-lung transplant recipients with emphysema, unlike those with pulmonary hypertension, are able to mitigate the degree of respiratory impairment associated with reperfusion injury.

Predicting ICU length of stay following single lung transplantation.

STUDY OBJECTIVE: The aim was to identify potential predictors of ICU length of stay (LOS) for single lung transplant patients. DESIGN: Retrospective chart review. SETTING: University medical center. PATIENTS: All single lung transplant recipients for 1992 and 1993 at our institution. RESULTS: Data were collected from 69 patients. The median ICU LOS was 5 days, and this was highly correlated with the duration of mechanical ventilation. The mean acute physiology and chronic health evaluation (APACHE II) score was 10. Patients with pulmonary hypertension had the longest ICU LOS. Similarly, patients with a measured transpulmonary gradient of 20 mm Hg or less had a significantly shorter ICU LOS. Patients with an immediate postoperative PaO2/fraction of inspired oxygen (FIo2) ratio greater than 200 mm Hg and a flow mismatch between the two lungs of 30% or less also had a significantly shorter ICU LOS. Positive and negative predictive values for the immediate postoperative PaO2/FIo2 ratio of 200 mm Hg or less were 77% for an ICU LOS greater than 5 days, and the calculated receiver operating characteristic (ROC) curve area was 0.74. CONCLUSION: Overall, the immediate postoperative PaO2/FIo2 ratio of 200 mm Hg or less had the best positive and negative predictive values as well as the highest ROC curve area for predicting an ICU LOS greater than 5 days.

Mechanical circulatory assist devices.

A ventricular assist device (VAD) is a heterotopic mechanical pump that augments or replaces the output of a failing ventricle. In the past decade, investigation and use of these devices has greatly improved our understanding of their potential roles and limitations. Successful univentricular and biventricular support has allowed for myocardial recovery and survival in several settings of intractable cardiogenic shock. The development of long-term VADs has allowed for successful bridging of patients to heart transplantation, and it has laid the groundwork for a permanent implantable replacement ventricle. In this review, we address indications, complications, management, and results of mechanical support in postcardiotomy, bridge to recovery, and bridge to transplantation settings. The tools to achieve ventricular support in the United States, and the VADs themselves, are described, with emphasis on unique features, indications, and limitations.

Transesophageal echocardiographic identification of a malpositioned extracorporeal membrane oxygenation cannula.

Transesophageal echocardiography identified malposition of an extracorporeal membrane oxygenation venous cannula across the interatrial septum into the left atrium and the presence of a clot within the cannula's lumen. Transesophageal echocardiography also guided the withdrawal of the cannula into the inferior vena cava.

Neutrophil attractant protein-1 and monocyte chemoattractant protein-1 in human serum. Effects of intravenous lipopolysaccharide on free attractants, specific IgG autoantibodies and immune complexes.

We recently found that normal human sera contain IgG antibodies against two chemoattractants, neutrophil attractant protein-1 (NAP-1/IL-8) and monocyte chemoattractant protein-1 (MCP-1), as well as immune complexes of these proteins. Intravenously administered LPS was reported to cause a sharp rise in serum NAP-1 concentration. Our study was designed to determine if LPS also caused an increase in MCP-1 and to measure associated changes in concentrations of antibody and immune complex. LPS caused a rise to peak within 2 to 3 h in serum concentrations of free NAP-1 and MCP-1, followed by an almost equally rapid fall toward base-line levels by about 5 h postinjection. MCP-1 concentration in sera from the 11 subjects rose to a peak of 330 +/- 52 pM. The peak value for NAP-1 was 80 +/- 11 pM. In 10 of the 11 subjects, free IgG autoantibody to MCP-1 decreased from a mean pre-LPS value of 1820 +/- 660 pM to a mean low of 53% of the respective initial values. Corresponding data for IgG anti-NAP-1 were a pre-LPS concentration of 216 +/- 7 pM, which decreased to a mean low of 44% of the respective initial values. The finding in some subjects of a rapid rise in free antibody after the nadir suggests the possibility of acute regulation of autoantibody secretion rates. Although the results suggested that LPS-induced chemoattractant combined with free antibody, serum concentrations of MCP-1-IgG or NAP-1-IgG did not increase, which points to an as yet unknown mechanism for trapping and elimination of the immune complexes.

Compartmentalization of the acute cytokine response in humans after intravenous endotoxin administration.

Lung cytokine production was examined after the intravenous administration of endotoxin to 23 normal human subjects. Bronchoalveolar lavage (BAL) was performed 7 days before and 1.5 or 5 h after endotoxin (4 ng/kg). Cytokine mRNA was evaluated in cell pellets (> 98% macrophages) by use of reverse transcription and the polymerase chain reaction. Immunoreactivity was measured by enzyme-linked immunosorbent assay of 20- to 40-fold concentrated BAL. Interleukin- (IL) 8 was detected in BAL (4-130 pg/ml) but not in the serum at baseline. Few neutrophils were found in BAL (< 1%) despite this IL-8 gradient. Peak serum IL-8 levels occurred 2 h after endotoxin (3,930 +/- 241 pg/ml), but BAL neutrophils and IL-8 did not increase. Peak serum tumor necrosis factor (TNF) levels occurred 1.5 h after endotoxin (1,844 +/- 210 pg/ml), but TNF was detected in only 1 of 20 BAL samples. TNF and IL-8 mRNA were detected by polymerase chain reaction in > 70% of the BAL samples before endotoxin, whereas IL-1 alpha, IL-1 beta, and IL-6 were detected in < 25% of the BAL samples. After endotoxin, no change was detected in cytokine mRNA expression. Actinomycin D treatment of the BAL did not alter the pattern of cytokine mRNA expression. These data suggest that mechanisms exist to insulate the alveolar space from the stimulatory effects of endotoxin and high circulating levels of cytokines. Additional factors appear to control the chemotactic effects of IL-8 on neutrophils in the air spaces during acute systemic inflammation.

Response of man to endotoxin.

Endotoxin, a cell wall component of Gram-negative bacteria, plays a central role in the pathogenesis of septic shock. By administering small doses of intravenous endotoxin to humans, a variety of acute inflammatory responses are induced which are qualitatively similar to those that occur during the early stages of septic shock. Within hours of the administration of intravenous endotoxin to human volunteers, changes occur in systemic hemodynamics, ventricular function, pulmonary gas exchange and permeability. In conjunction with these changes in organ function, a wide variety of inflammatory mediators are released which appear to contribute to these responses. These include the release of proinflammatory cytokines (e.g. tumor necrosis factor-alpha, IL-1 beta, IL-6, IL-8), activation of the fibrinolytic system, kallikrein-kinin generation and phospholipase A2 release. Phagocytic leukocytes are primed for enhanced inflammatory responses following endotoxin administration. Counter-regulatory responses are initiated in parallel and may serve to limit some of the end-organ responses by the inflammatory mediators. This human model provides a unique opportunity to extend previous concepts of acute inflammation and to evaluate the earliest responses activated after exposure to an important bacterial component. Defining the pathways and responses initiated during acute human endotoxemia may allow a better understanding of host responses that are critical to the development of organ dysfunction and shock due to severe infections.

Hyperphospholipasemia A2 in human volunteers challenged with intravenous endotoxin.

Phospholipase A2 (PLA2) activity was measured in the serum of 23 individuals infused intravenously with endotoxin (EN) at a dose of 4 ng/kg body weight. A marked increase in PLA2 was noted 3 h after EN challenge (mean 828 +/- 513 units/ml), reached its maximum at 24 h after the challenge (mean 2667 +/- 2442 units/ml), and was still evident at 48 h (mean 763 +/- 366 units/ml). In contrast, TNF levels were maximal (mean 712 +/- 375 pg/ml) 90 min after the EN challenge and subsided to very low values (5 +/- 5 pg/ml) 5 h after the challenge. There was a positive correlation between the maximum response of TNF and that of PLA2 (r = 0.82, P < 0.01). Administration of ibuprofen or pentoxifylline did not alter the PLA2 response. EN challenge did not affect serum pancreatic PLA2 concentration or that of the lysosomal cationic enzyme, lysozyme. Neutralizing antibody against human recombinant (synovial type) PLA2 completely abolished PLA2 activity in the sera tested. We conclude that EN infusions cause marked intravascular release of nonpancreatic secretory PLA2 and that the magnitude of this response seems to be related to the prior generation of TNF.

Effects of ibuprofen and pentoxifylline on the cardiovascular response of normal humans to endotoxin.

Endotoxin is a major mediator of the life-threatening cardiovascular dysfunction that characterizes Gram-negative sepsis. In animal models of endotoxemia, pretreatment with ibuprofen or pentoxifylline attenuates some of these cardiovascular changes. To evaluate the effects of these agents on the human cardiovascular response to endotoxemia, hemodynamic variables were measured serially in 24 normal subjects who were given intravenous endotoxin. The subjects were randomized to receive oral ibuprofen (n = 9), pentoxifylline (n = 10), or no medication before endotoxin administration (n = 5). The subjects were volume loaded 3-5 h after endotoxin administration, and hemodynamic measurements were reassessed. Core temperature after endotoxin alone or endotoxin-pentoxifylline approached a maximum at 3 h (greater than or equal to 38.6 degrees C), while the endotoxin-ibuprofen group remained afebrile. At 3 and 5 h, all three groups had significant increases in heart rate, cardiac index, oxygen delivery, and oxygen consumption, while systemic vascular resistance index decreased significantly from baseline. The oxygen extraction ratio remained unchanged. After volume loading, the left ventricular ejection fraction and left ventricular end-diastolic and end-systolic volume indexes did not differ among the groups. The hyperdynamic cardiovascular response to endotoxin in humans occurs in the absence of fever and is not significantly ameliorated by oral cyclooxygenase or phosphodiesterase inhibition.

Detection of interleukin 8 and tumor necrosis factor in normal humans after intravenous endotoxin: the effect of antiinflammatory agents.

Interleukin 8 (IL-8), a potent activator of neutrophils, may be important in the early host response to serious Gram-negative infections. IL-8 was measured with other acute phase cytokines (tumor necrosis factor alpha [TNF-alpha], IL-6 and IL-1 beta) in 25 normal humans randomized to receive either intravenous endotoxin alone or endotoxin after oral administration of ibuprofen or pentoxifylline, agents that alter some of the inflammatory responses induced by endotoxin in vitro. TNF immunoreactivity was maximum at 1.5 h, and total TNF (area under the curve) was 4.2- and 4.5-fold greater in subjects given endotoxin/ibuprofen compared to subjects given endotoxin alone (p = 0.026) or endotoxin/pentoxifylline (p = 0.004), respectively. IL-6 levels were maximum at 2-3 h and did not differ among the three groups. No IL-1 beta was detected in any subject. IL-8 levels peaked at 2 h in subjects given either endotoxin alone or endotoxin/pentoxifylline, falling towards baseline by 5 h. Subjects given endotoxin/ibuprofen had a more sustained rise in IL-8 with peak levels 2.8- and 2.5-fold higher at 3 h compared to endotoxin alone (p = 0.048) or endotoxin/pentoxifylline (p = 0.023), respectively. Differences in total IL-8 release among groups approached statistical significance (ANOVA, p = 0.07). This trend reflected the increased release of IL-8 by the subjects receiving ibuprofen compared to pentoxifylline (1.9-fold higher; p = 0.024). This suggests that cyclooxygenase products may provide important negative feedback loops for cytokine production in vivo. Increases in circulating IL-8 are part of the acute inflammatory response of humans to endotoxin. Altered cytokine responses caused by antiinflammatory therapy may have important implications for both host defense and injury during septicemia.