Total Joint Arthroplasty Outcomes in Eligible Patients Versus Patients Who Failed to Meet at Least 1 Eligibility Criterion: A Single-Center Retrospective Analysis.

BACKGROUND: This study looks to investigate how not meeting eligibility criteria affects postoperative outcomes following total joint arthroplasty surgery. METHODS: A retrospective review was conducted of total joint arthroplasty patients at a single academic institution. Demographics, laboratory values, and complications were recorded. Continuous and categorical variables were compared using the Student's T-test and the Chi-Square test, respectively. Multivariable analysis was used to control for confounding variables. RESULTS: Our study included 915 total hip and 1,579 total knee arthroplasty patients. For total hip and total knee arthroplasty, there were no significant differences in complications (P = .11 and .87), readmissions (P = .83 and .2), or revision surgeries (P = .3 and 1) when comparing those who met all criteria to those who did not. Total hip arthroplasty patients who did not meet two criteria had 16.1 higher odds (P = .02) of suffering a complication. There were no differences in complications (P = .34 and .41), readmissions (P = 1 and .55), or revision surgeries (P = 1 and .36) between ineligible patients treated by total joint arthroplasty surgeons and those who were not. Multivariable analysis demonstrated no eligibility factors were associated with outcomes for both total hip and knee arthroplasty. CONCLUSIONS: There was no significant difference in outcomes between those who met all eligibility criteria and those who did not. Not meeting two criteria conferred significantly higher odds of suffering a complication for total hip arthroplasty patients. Total joint arthroplasty surgeons had similar outcomes to non-total joint surgeons, although their patient population was more complex. LEVEL OF EVIDENCE: III.

The traveling intensive care unit patient. Road trips.

Transport of critically ill or injured patients in the hospital is a necessary part of ICU care. Although the overall severity of misadventures occurring during patient transfer is minimal, potential complications risk patient deterioration in settings that may not be equipped to handle cardiovascular, respiratory, or neurologic emergencies safely. The critical care team should provide the same level of monitoring and care to the transported patient outside the ICU as he or she receives the unit. Each hospital should have a system that meets acceptable standards for safe transfer of the ICU patient, which minimizes risk and maximizes diagnostic and treatment yield.

Assessing the need for reintubation: a prospective evaluation of unplanned endotracheal extubation.

OBJECTIVE: Unplanned endotracheal extubation (UEE) is a common complication in medical intensive care units but very little data about UEE in surgical populations are available. Our hypothesis is that the surgical intensive care unit (SICU) population requires reintubation less frequently compared with the medical intensive care unit population. We prospectively gathered data on patients in a SICU in an attempt to identify the incidence of UEE and to study the need for reintubation after UEE. METHODS: During an 18-month period, we prospectively identified SICU patients from a quality improvement database who required ventilatory support. All patients who self-extubated were included in the study. RESULTS: Fifty-eight of 1,178 intubated patients experienced unplanned extubation 61 times during the 18-month period. A total of 22 patients (36%) required reintubation, whereas 39 patients (64%) did not. Thirty-three patients self-extubated while being actively weaned from ventilatory support. Of these, only 5 patients (15%) required reintubation and 28 patients (85%) did not (p < 0.01). CONCLUSION: A total of 85% of patients who self-extubate during the weaning process did not require reintubation in our study. Those who have an FiO2 >50%, a lower PaO2/FiO2 ratio, had UEE occur by accident, or were not being weaned when UEE occurred required reintubation more frequently. These data suggest that some of our SICU patients are intubated longer than necessary, which may translate into more ventilator related complications, longer ICU stays and increased cost.

Parenteral nutrition facilitates activation of coagulation but not of fibrinolysis during human endotoxemia.

Venous thrombosis and bacterial infections are common complications of parenteral nutrition. To test the hypothesis that infection facilitates activation of coagulation during parenteral nutrition, healthy subjects were intravenously injected with endotoxin (2 ng/kg) after they had received either 1 week of standard parenteral nutrition (n = 7) or normal enteral feeding (n = 8). Compared with enteral feeding, parenteral nutrition was associated with a selectively enhanced activation of the coagulation system (plasma levels of thrombin-antithrombin III complexes) during endotoxemia. Activation of the fibrinolytic system (plasminogen activator activity, tissue-type plasminogen activator, plasminogen activator inhibitor type 1) proceeded similarly in both study groups. In patients receiving parenteral nutrition, one common complication (bacterial infection) may facilitate the occurrence of another common complication (venous thrombosis) by synergistic stimulation of the coagulation system.

Epinephrine exerts anticoagulant effects during human endotoxemia.

To determine the effect of a physiologically relevant elevation in the plasma concentrations of epinephrine on the activation of the hemostatic mechanism during endotoxemia, 17 healthy men were studied after intravenous injection of lipopolysaccharide (LPS, 2 ng/kg), while receiving a continuous infusion of epinephrine (30 ng/kg/min) started either 3 h (n = 5) or 24 h (n = 6) before LPS injection, or an infusion of normal saline (n = 6). Activation of the coagulation system (plasma concentrations of thrombin-antithrombin III complexes and prothrombin fragment F1+2) was significantly attenuated in the groups treated with epinephrine when compared with subjects injected with LPS only (P <0.05). Epinephrine enhanced LPS-induced activation of fibrinolysis (plasma levels of tissue-type plasminogen activator and plasmin-alpha2-antiplasmin complexes; P <0.05), but did not influence inhibition of fibrinolysis (plasminogen activator inhibitor type I). In subjects infused with epinephrine, the ratio of maximal activation of coagulation and maximal activation of fibrinolysis was reduced by >50%. Hence, epinephrine exerts antithrombotic effects during endotoxemia by concurrent inhibition of coagulation, and stimulation of fibrinolysis. Epinephrine, whether endogenously produced or administered as a component of treatment, may limit the development of disseminated intravascular coagulation during systemic infection.

Effects of IL-10 on systemic inflammatory responses during sublethal primate endotoxemia.

IL-10 protects mice from LPS-induced lethality. To determine the effects of IL-10 on LPS-induced inflammatory responses, six Papio anubis baboons were i.v. injected with a sublethal dose of LPS (Salmonella typhimurium; 500 microg/kg) directly preceded by either human rIL-10 (n = 3, 500 microg/kg) or diluent (n = 3). IL-10 strongly inhibited LPS-induced release of TNF, IL-6, IL-8, and IL-12 (all p < 0.05). By contrast, IL-10 did neither influence the activation of the coagulation system (plasma levels of thrombin/antithrombin III complexes), nor the activation of the fibrinolytic system (plasma levels of tissue-type plasminogen activator, plasminogen activator inhibitor type I, and plasmin/alpha 2-antiplasmin complexes). IL-10 modestly attenuated neutrophilic leukocytosis and neutrophil degranulation (plasma concentrations of elastase/alpha1-antitrypsin complexes) (both p < 0.05). Changes in surface TNF receptor expression on circulating granulocytes were not affected by IL-10. These results suggest that during sublethal endotoxemia the predominant anti-inflammatory effect of IL-10 treatment is inhibition of proinflammatory cytokine release.

Epinephrine inhibits tumor necrosis factor-alpha and potentiates interleukin 10 production during human endotoxemia.

Short-term preexposure of mononuclear cells to epinephrine inhibits LPS-induced production of TNF, whereas preexposure for 24 h results in increased TNF production. To assess the effects of epinephrine infusions of varying duration on in vivo responses to LPS, the following experiments were performed: (a) Blood obtained from eight subjects at 4-24 h after the start of a 24-h infusion of epinephrine (30 ng/kg per min) produced less TNF after ex vivo stimulation with LPS compared with blood drawn before the start of the infusion, and (b) 17 healthy men who were receiving a continuous infusion of epinephrine (30 ng/kg per min) started either 3 h (EPI-3; n = 5) or 24 h (EPI-24; n = 6) were studied after intravenous injection of LPS (2 ng/kg, lot EC-5). EPI-3 inhibited LPS-induced in vivo TNF appearance and also increased IL-10 release (both P < 0.005 versus LPS), whereas EPI-24 only attenuated TNF secretion (P = 0.05). In separate in vitro experiments in whole blood, epinephrine increased LPS-induced IL-10 release by a combined effect on alpha and beta adrenergic receptors. Further, in LPS-stimulated blood, the increase on IL-10 levels caused by epinephrine only marginally contributed to concurrent inhibition of TNF production. Epinephrine, either endogenously produced or administered as a component of sepsis treatment, may have a net antiinflammatory effect on the cytokine network early in the course of systemic infection.

Fat emulsion infusion potentiates coagulation activation during human endotoxemia.

Intravenous fat emulsions are frequently given to malnourished patients who are prone to suffer from infectious complications. As injection of low dose endotoxin represents a model to study the human response to acute infection, we sought to determine the effect of lipid emulsion infusion on endotoxin-induced activation of the hemostatic mechanism in man. Ten healthy men received a bolus intravenous injection of endotoxin (lot EC-5; 20 U/kg) midway through a 4-h infusion (125 ml/h) of either dextrose 5% (n = 5) or Intralipid 20% (n = 5). Lipid infusion potentiated endotoxin-induced coagulation activation, as indicated by higher plasma levels of the prothrombin fragment F1 + 2 and of thrombin-antithrombin III complexes (both p < 0.05 for the difference between groups). However, lipid infusion did not influence the fibrinolytic response to intravenous endotoxin, as reflected by similar increases in the levels of tissue-type plasminogen activator and plasmin-alpha 2-antiplasmin complexes in both groups. Endotoxin-induced appearance of plasminogen activator inhibitor type I was enhanced by lipid infusion (p < 0.05). These data suggest that fat emulsion infusion may enhance the tendency towards thrombotic complications in patients with infections.

Endotoxin induces downregulation of tumor necrosis factor receptors on circulating monocytes and granulocytes in humans.

Leukocytes rapidly lose their surface receptors for tumor necrosis factor (TNF) after exposure to various stimuli in vitro. To assess the effect of endotoxin on cellular TNF receptors in humans in vivo, binding of biotinylated TNF to circulating monocytes and granulocytes was determined by fluorescence-activated cell sorter analysis in six healthy subjects after intravenous injection of endotoxin (lot EC-5, 20 U/kg). Endotoxin administration was associated with a transient decrease in monocyte TNF receptors, reaching a nadir after 2 hours (P < .0001), and a more sustained decrease in granulocyte TNF receptors (P < .001). Although the decrease in cellular TNF receptors coincided with increases in soluble TNF receptors types I and II, no correlations were observed between trough monocyte or granulocyte TNF receptors and peak plasma concentrations of soluble TNF receptors. Stimulation of human whole blood with endotoxin resulted in reduced expression of both type I and type II TNF receptors on monocytes and granulocytes. Endotoxin induces downmodulation of monocyte and granulocyte TNF surface receptors in humans in vivo, which may represent a mechanism to reduce excessive activity of TNF during systemic infection.

Effect of hypertriglyceridemia on endotoxin responsiveness in humans.

Triglyceride-rich lipoproteins can inhibit endotoxin activity in vitro and in rodents. We sought to determine whether Intralipid, a triglyceride-rich fat emulsion which in contact with plasma functions similarly to endogenous lipoproteins, can alter the human response to endotoxin. Intralipid inhibited endotoxin-induced cytokine production in human whole blood in vitro in a dose-dependent manner, with maximal inhibition (up to 70%) being achieved at a concentration of 10 g/liter. In healthy men, a bolus intravenous injection of endotoxin (lot EC-5; 20 U/kg of body weight) was given midway through a 4-h infusion (125 ml/h) of either 5% glucose (n = 5) or 20% Intralipid (n = 5). The infusion of Intralipid led to an increase in triglyceride levels in serum from 95 +/- 16 to 818 +/- 135 mg/dl prior to endotoxin administration, i.e., levels that importantly reduced cytokine production in endotoxin-stimulated whole blood. However, in vivo hypertriglyceridemia did not influence inflammatory responses to endotoxin (fever, release of tumor necrosis factor and soluble tumor necrosis factor receptors, and leukocytosis) or even potentiated endotoxin responses (release of interleukins 6 and 8 and neutrophil degranulation). Hypertriglyceridemia does not inhibit the in vivo responses to endotoxin in humans.

Parenteral nutrition alters monocyte TNF receptor activity.

The route of nutrient provision has been reported to influence some aspects of the host inflammatory response in both patient populations and normal subjects. The tumor necrosis factor receptor system is a complex regulatory mechanism that modulates the bioavailability of tumor necrosis factor (TNF). We sought to determine whether maintenance on total parenteral nutrition (TPN) can alter host response to endotoxin challenge, specifically as it relates to the TNF receptor system. Seventeen healthy men were randomized to receive either TPN (n = 8) or a defined formula enteral diet (ENT, n = 9) prior to intravenous infusion of endotoxin (Lot EC-5, 20 U/kg). The subjects that received 1 week of antecedent TPN exhibited an increased heart rate and temperature and decreased mean arterial pressure post-LPS compared to those subjects maintained on enteral nutritional support. The TPN subjects also exhibited comparatively higher TNF and interleukin-6 levels in response to endotoxin. Monocyte TNF receptor levels decreased in both groups post-LPS, but TPN subjects exhibited consistently greater expression of this functional membrane-associated TNF receptor. After LPS, soluble tumor necrosis factor receptor II (sTNFr II, p75) peaked three times higher in TPN subjects than in ENT subjects. Conversely, sTNFr I (p55) was higher in the enterally fed group. From these studies it appears that antecedent TPN not only influences clinical manifestations of endotoxin but also modulates the regulation of all associated TNF receptors and shedding of soluble receptors.