Arginine-vasopressin attenuates beneficial norepinephrine effect on jejunal mucosal tissue oxygenation during endotoxinaemia.

BACKGROUND: The objective of the present study was to investigate the effects of increasing doses of norepinephrine (NE) with or without arginine-vasopressin (AVP) on intestinal oxygen supply and jejunal mucosal tissue oxygen tension in an acute endotoxic pig model. METHODS: In this prospective, randomized, experimental study on 24 domestic pigs, jejunal mucosal tissue PO2 (PO2muc) was measured using two Clark-type surface oxygen electrodes. Oxygen saturation of jejunal microvascular haemoglobin (HbO2j) was determined by tissue reflectance spectrophotometry. Systemic haemodynamic variables, mesenteric-venous and systemic acid-base and blood gas variables, and lactate measurements were recorded. Measurements were performed at baseline, after Escherichia coli lipopolysaccharide (LPS) administration, and at 20 min intervals during incremental NE infusion (0.05, 0.1, 0.5, 1.0, and 2 microg kg(-1) min(-1), respectively) with 57 mU kg(-1) h(-1) AVP (n=8; NE+AVP group) or without (n=8; NE group); or infusion of an equal amount of normal saline (n=8; CON group). RESULTS: LPS infusion led to a significant (P<0.05) decrease of PO2muc and HbO2j. Both NE and NE+AVP increased arterial pressure, cardiac output, and mesenteric artery blood flow. Concomitant to an increase in systemic oxygen delivery, NE improved PO2muc and HbO2j. NE alone was superior in restoration of PO2muc when compared with NE+AVP. CONCLUSIONS: Both NE and NE+AVP improved global haemodynamics and systemic oxygen transport variables when compared with control animals in an acute endotoxic pig model. NE improved jejunal PO2muc at all dosages. NE effects were significantly blunted by simultaneous administration of AVP.

Effects of phenylephrine on the sublingual microcirculation during cardiopulmonary bypass.

BACKGROUND: The objective of the present study was to investigate sublingual microvascular blood flow and microcirculatory haemoglobin oxygen saturation (Smc(O(2))) during cardiopulmonary bypass (CPB) using constant systemic blood flow but different perfusion pressures achieved by phenylephrine administration. METHODS: Fifteen patients undergoing coronary artery bypass grafting were enrolled in this pilot study. Systemic haemodynamics, oxygen transport variables, arterial and mixed venous blood gas analysis, and microcirculatory variables were determined after initiation of general anaesthesia, during CPB (systemic blood flow=2.4 litre m(-2)), after increasing perfusion pressure by 20 mm Hg with a continuous infusion of phenylephrine, and after termination of phenylephrine infusion. RESULTS: CPB immediately resulted in a significant (P<0.05) decrease in systemic oxygen transport without alterations in sublingual microcirculatory blood flow and Smc(O(2)). Increasing perfusion pressure from 47 (SD 9) to 68 (7) mm Hg using phenylephrine=1.4 (1.0) microg kg(-1) min(-1) resulted in a significant decrease in sublingual small vessel blood flow (from median 2.5 to 1.8 arbitrary units) representing mostly capillary blood flow, but not in medium-sized vessels (median 3 to 2.8 arbitrary units). Concurrently, global tissue blood flow from 110 (54) to 197 (100) perfusion units and Smc(O(2)) increased from 72 (11)% to 84 (7)%, suggesting significant microcirculatory blood flow shunting in vessels with diameters >25 microm. CONCLUSIONS: Our data demonstrate that an increased perfusion pressure produced by phenylephrine at constant CPB flow may decrease microcirculatory blood flow in the sublingual mucosal microcirculation due to microvascular blood flow shunting.

[Microcirculation of intensive care patients. From the physiology to the bedside]. / Mikrozirkulation beim Intensivpatienten. Von der Physiologie zur Klinik.

The microcirculation is unique in its anatomy and physiology and is a self-contained organ system within the human body. It is the site where gas exchange and nutrient supply takes place, but it is also the site which experiences pathological alterations during various shock states and therefore compromises the oxygen supply to tissues and organs. Systemic inflammation for example leads amongst others to increased heterogeneous blood flow, formation of interstitial edema, altered viscosity, leukocyte activation, disturbances in the coagulation system, and to a breakdown of the endothelial barrier function. These alterations inevitably lead to limitations of the oxygen supply to tissues. Without interruption of these pathomechanisms, the dysfunction of the microcirculation will consequently result in organ dysfunction. In this review article a short description of the microcirculatory physiology, the interaction between the macrocirculation and the microcirculation, as well as microcirculatory alterations generated by a systemic inflammatory response will be given. Finally, various therapy options will be described, which, experimentally, can lead to an improvement in microcirculatory dysfunction.

Oscillation frequency of skin microvascular blood flow is associated with mortality in critically ill patients.

BACKGROUND: Microcirculatory dysfunction has been hypothesized to play a key role in the pathophysiology of multiple organ failure and, consequently, patient outcome. The objective of this study was to investigate the differences in reactive hyperemia response and oscillation frequency in surviving and non-surviving patients with multiple organ dysfunction syndrome. METHODS: Twenty-nine patients (15 survivors; 14 non-survivors) with two or more organ failures were eligible for study entry. All patients were hemodynamically stabilized, and demographic and clinical data were recorded. A laser Doppler flowmeter was used to measure the cutaneous microcirculatory response. Reactive hyperemia and oscillatory changes in the Doppler signal were measured during 3 min before and after a 5-min period of forearm ischemia. RESULTS: Non-survivors demonstrated a significantly higher multiple organ dysfunction score when compared with survivors (P= 0.004). Norepinephrine administration was higher in non-survivors (P= 0.018). Non-survivors had higher arterial lactate levels (P= 0.046), decreased arterial pH levels (P= 0.001) and decreased arterial Po(2) values (P= 0.013) when compared with survivors. A higher oscillation frequency of the skin microvasculature at rest (P= 0.033) and after an ischemic stimulus (P= 0.009) was observed in non-survivors. The flow motion frequency observed in reactive hyperemia was associated with the severity of multiple organ dysfunction (P= 0.009) and, although not statistically significant, with the arterial lactate concentration (P= 0.052). CONCLUSION: Increased skin microvascular oscillation frequency at rest and in the hyperemic state after an ischemic stimulus is associated with increased mortality in patients suffering from multiple organ dysfunction. The underlying mechanism could be a response of the skin microvasculature to an impaired oxygen utilization of the skin tissue.

Comparison of lactated Ringer's, gelatine and blood resuscitation on intestinal oxygen supply and mucosal tissue oxygen tension in haemorrhagic shock.

OBJECTIVES: To evaluate the effects on intestinal oxygen supply, and mucosal tissue oxygen tension during haemorrhage and after fluid resuscitation with either blood (B; n=7), gelatine (G; n=8), or lactated Ringer's solution (R; n=8) in an autoperfused, innervated jejunal segment in anaesthetized pigs. METHODS: To induce haemorrhagic shock, 50% of calculated blood volume was withdrawn. Systemic haemodynamics, mesenteric venous and systemic acid-base and blood gas variables, and lactate measurements were recorded. A flowmeter was used for measuring mesenteric arterial blood flow. Mucosal tissue oxygen tension (PO(2)muc), jejunal microvascular haemoglobin oxygen saturation (HbO(2)) and microvascular blood flow were measured. Measurements were performed at baseline, after haemorrhage and at four 20 min intervals after fluid resuscitation. After haemorrhage, animals were retransfused with blood, gelatine or lactated Ringer's solution until baseline pulmonary capillary wedge pressure was reached. RESULTS: After resuscitation, no significant differences in macrohaemodynamic parameters were observed between groups. Systemic and intestinal lactate concentration was significantly increased in animals receiving lactated Ringer's solution [5.6 (1.1) vs 3.3 (1.1) mmol litre(-1); 5.6 (1.1) vs 3.3 (1.2) mmol litre(-1)]. Oxygen supply to the intestine was impaired in animals receiving lactated Ringer's solution when compared with animals receiving blood. Blood and gelatine resuscitation resulted in higher HbO(2) than with lactated Ringer's resuscitation after haemorrhagic shock [B, 43.8 (10.4)%; G, 34.6 (9.4)%; R, 28.0 (9.3)%]. PO(2)muc was better preserved with gelatine resuscitation when compared with lactated Ringer's or blood resuscitation [20.0 (8.8) vs 13.8 (7.1) mm Hg, 15.2 (7.2) mm Hg, respectively]. CONCLUSION: Blood or gelatine infusion improves mucosal tissue oxygenation of the porcine jejunum after severe haemorrhage when compared with lactated Ringer's solution.

Vasopressin as adjunct vasopressor for vasodilatory shock due to non-occlusive mesenteric ischemia.

We present the case of an 83-year-old patient who underwent cardiac surgery and developed postoperative non-occlusive mesenteric ischemia (NOMI), which was treated with a local intra-arterial papaverine and prostaglandin E1 infusion. After successful mesenteric reperfusion, a multiple organ dysfunction syndrome with severe cardiovascular failure developed. High norepinephrine dosages (1.09 microg/kg body weight/min) and catecholamine-related complications (tachycardiac atrial fibrillation) required initiation of supplementary argininevasopressin (AVP) infusion (4 U/h). AVP stabilized vasodilatory shock, ensured adequate gut perfusion pressure and had no adverse clinical or angiographic effects on restitution of gut integrity. In conclusion, after reperfusion of NOMI in this patient, adjunct AVP therapy combined with local vasodilator infusion was beneficial as a potentially life-saving vasopressor.

Craniotomy during ECMO in a severely traumatized patient.

Extracorporeal membrane oxygenation (ECMO) can be a last resort treatment in acute respiratory distress syndrome after thoracic trauma. However, co-existent brain trauma is considered to be a contra-indication for ECMO. This is the first report on successful craniotomy under ECMO treatment in a multiply traumatized patient with severe thoracic and brain injuries. This successful treatment with beneficial neurological outcome suggests that ECMO therapy should not be withheld from severely injured patients with combined brain and thoracic trauma presenting with life-threatening hypoxemia. Moreover, even craniotomy may be performed during ECMO therapy without major bleeding and adverse effects on neurological function.

Arginine vasopressin reduces intestinal oxygen supply and mucosal tissue oxygen tension.

We investigated intestinal oxygen supply and mucosal tissue PO2 during administration of increasing dosages of continuously infused arginine vasopressin (AVP) in an autoperfused, innervated jejunal segments in anesthetized pigs. Mucosal tissue PO2 was measured by employing two Clark-type surface oxygen electrodes. Oxygen saturation of jejunal microvascular hemoglobin was determined by tissue reflectance spectrophotometry. Microvascular blood flow was assessed by laser-Doppler velocimetry. Systemic hemodynamic variables, mesenteric venous and systemic acid-base and blood gas variables, and lactate measurements were recorded. Measurements were performed at baseline and at 20-min intervals during incremental AVP infusion (n = 8; 0.007, 0.014, 0.029, 0.057, 0.114, and 0.229 IU.kg(-1).h(-1), respectively) or infusion of saline (n=8). AVP infusion led to a significant (P < .05), dose-dependent decrease in cardiac index (from 121 +/- 31 to 77 +/- 27 ml.kg(-1).min(-1) at 0.229 IU.kg(-1).h(-1)) and systemic oxygen delivery (from 14 +/- 3 to 9 +/- 3 ml.kg(-1).min(-1) at 0.229 IU.kg(-1).h(-1)) concomitant with an increase in systemic oxygen extraction ratio (from 31 +/- 4 to 48 +/- 10%). AVP decreased microvascular blood flow (from 133 +/- 47 to 82 +/- 35 perfusion units at 0.114 IU.kg(-1).h(-1)), mucosal tissue PO2 (from 26 +/- 7 to 7 +/- 2 mmHg at 0.229 IU.kg(-1).h(-1)), and microvascular hemoglobin oxygen saturation (from 51 +/- 9 to 26 +/- 12% at 0.229 IU.kg(-1).h(-1)) without a significant increase in mesenteric venous lactate concentration (2.3 +/- 0.8 vs. 3.4 +/- 0.7 mmol/l). We conclude that continuously infused AVP decreases intestinal oxygen supply and mucosal tissue PO2 due to a reduction in microvascular blood flow and due to the special vascular supply in the jejunal mucosa in a dose-dependent manner in pigs.

Influence of working conditions on job satisfaction in anaesthetists.

BACKGROUND: We studied job satisfaction, physical health, emotional well-being and working conditions in 125 Austrian and Swiss anaesthetists. METHODS: Responses to self-reporting questionnaires were evaluated. Dependent variables included job satisfaction, emotional well-being and physical health. Independent variables included age, sex, marital status, position and working conditions as assessed by the Instrument for Stress-related Job Analysis. RESULTS: Control over work shows a strong effect on job satisfaction in anaesthetists, for example influence on handling tasks (P=0.001), time control (P=0.002) and participation (P=0.001), whereas task demands and task-related problems did not have any effect. Anaesthetists in leading positions and specialists reported lower job satisfaction (P=0.012) than did anaesthetists in non-leading positions. Job satisfaction was associated with better physical health (P=0.001) and better emotional well-being (P=0.005). CONCLUSIONS: Our results suggest that a high level of job satisfaction in anaesthetists correlates with interesting work demands and the opportunity to contribute skills and ideas. To improve job satisfaction, more attention should be paid to improving working conditions, including control over decision-making, and allowing anaesthetists to have more influence on their own work pace and work schedule.

Oxygen distribution in microcirculation after arginine vasopressin-induced arteriolar vasoconstriction.

The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle contraction to oxygen consumption of the microvascular wall during arginine vasopressin (AVP)-induced vasoconstriction. AVP was infused intravenously at the clinical dosage (0.0001 IU.kg(-1).min(-1)) and caused a significant arteriolar constriction, decreased microvascular flow and functional capillary density, and a substantial rise in arteriolar vessel wall transmural Po(2) difference. AVP caused tissue Po(2) to be significantly lowered from 25.4 +/- 7.4 to 7.2 +/- 5.8 mmHg; however, total oxygen extraction by the microcirculation increased by 25%. The increased extraction, lowered tissue Po(2), and increased wall oxygen concentration gradient are compatible with the hypothesis that vasoconstriction significantly increases vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. This conclusion was supported by the finding that the small percentage of the vessels that dilated in these experiments had a vessel wall oxygen gradient that was smaller than control and which was not determined by changes in tissue Po(2). These findings show that AVP administration, which reduces oxygen supply by vasoconstriction, may further impair tissue oxygenation by the additional oxygen consumption of the microcirculation.

Cardiac performance during vasopressin infusion in postcardiotomy shock.

OBJECTIVE: Arginine-vasopressin (AVP) might be a potent vasopressor agent in catecholamine-resistant postcardiotomy shock. However, its use remains experimental because of considerations about deleterious effects on the heart. We report on the effects of continuous AVP-infusion on cardiac performance, biomarkers of myocardial ischemia, and systemic hemodynamics in catecholamine-resistant postcardiotomy shock. DESIGN: Retrospective study. SETTING: Twenty-one-bed general and surgical intensive care unit. PATIENTS: Forty-one patients with catecholamine-resistant postcardiotomy shock. INTERVENTIONS: Continuous infusion of AVP. MEASUREMENTS AND RESULTS: Heart rate (HR), heart rhythm, mean arterial pressure (MAP), central venous pressure, mean pulmonary arterial pressure, cardiac index (CI), stroke volume index (SVI), left ventricular stroke work index (LVSWI), systemic vascular resistance (SVR) as well as milrinone and norepinephrine requirements were collected before and 1, 4, 12, 24, and 48 h after start of AVP infusion. Creatine kinase MB and troponin-I serum concentrations were measured daily. During AVP administration we observed a significant decrease in HR (-14.8%), milrinone (-17.5%), and norepinephrine requirements (-54.9%) as well as biomarkers of cardiac ischemia and a significant increase in LVSWI (+46.2%), MAP (+41.8%) and SVR (+60%). CI and SVI remained unchanged. Forty-five percent of postoperative new-onset tachyarrhythmias (TA) converted into sinus rhythm during AVP infusion. CONCLUSIONS: AVP was devoid of adverse effects on the heart in these patients with catecholamine-resistant postcardiotomy shock. The significant reduction in HR, vasopressor, and inotropic support suggest a substantial improvement in myocardial performance. These findings are supported by a significant decrease of cardiac enzymes and cardioversion of TA into sinus rhythm in 45.5% of patients with new-onset TA.

The effects of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock: a retrospective analysis.

UNLABELLED: We retrospectively investigated the effects of continuous arginine vasopressin (AVP) infusion on systemic hemodynamics, acid/base status, and laboratory variables in patients (mean age [mean +/- SD]= 66.3 +/- 10.1 yr) with catecholamine-resistant septic (n = 35) or postcardiotomy shock (n = 25). Hemodynamic and acid/base data were obtained before; 30 min after; and 1, 4, 12, 24, 48, and 72 h after the start of AVP infusion. Laboratory examinations were recorded before and 24, 48, and 72 h after the start of AVP infusion. For statistical analysis, a mixed-effects model was used. The overall intensive care unit mortality was 66.7%. AVP administration caused a significant increase in mean arterial pressure (+29%) and systemic vascular resistance (+56%), accompanied by a significant decrease in heart rate (-24%) and mean pulmonary arterial pressure (-11%) without any change in stroke volume index. Norepinephrine requirements could be reduced by 72% within 72 h. During AVP infusion, a significant increase in liver enzymes and total bilirubin concentration and a significant decrease in platelet count occurred. Arginine vasopressin was effective in reversing systemic hypotension. However, adverse effects on gastrointestinal perfusion and coagulation cannot be excluded. IMPLICATIONS: In this retrospective analysis, the influence of a continuous infusion of an endogenous hormone (arginine vasopressin) on systemic hemodynamics and laboratory variables was assessed in patients with vasodilatory shock unresponsive to conventional therapy. Arginine vasopressin was effective in reversing systemic hypotension. However, adverse effects on gastrointestinal perfusion and coagulation cannot be excluded.

Effects of norepinephrine and phenylephrine on intestinal oxygen supply and mucosal tissue oxygen tension.

OBJECTIVES: To investigate effects of intravenous norepinephrine (NE) and phenylephrine (PE) on intestinal oxygen supply in an autoperfused, innervated jejunal segment. DESIGN AND SETTING: Prospective, randomized animal study in an animal research laboratory. MATERIALS AND METHODS: In 24 anesthetized and normoventilated pigs a segment of the jejunal mucosa was exposed by midline laparotomy and antimesenteric incision. Mucosal oxygen tension (PO2muc; Clark-type surface oxygen electrodes), microvascular hemoglobin oxygen saturation (HbO2, tissue reflectance spectrophotometry), and microvascular blood flow (perfusion units, PU; laser Doppler velocimetry), systemic hemodynamics, mesenteric-venous acid base and blood gas variables, and systemic acid base and blood gas variables were recorded after a resting period and at 20-min intervals during infusion of NE (0.01, 0.05, 0.1, 0.5, 1, 2 micrograms x kg-1 x min-1; n = 8) or PE (0.1, 0.5, 1, 2, 5, 10 micrograms x kg-1 x min-1; n = 8) and in controls (n = 8) without treatment. RESULTS: NE infusion led to significant tachycardia, an increase in cardiac output, and systemic oxygen delivery and consumption while PE progressively increased mean arterial pressure with only small effects on systemic blood flow. NE or PE infusion did not affect mesenteric venous oxygen tension (baseline: PE 53 +/- 5, NE, 52 +/- 4.2 mmHg), mesenteric oxygen extraction ratio (baseline: PE 0.29 +/- 0.08, NE 0.3 +/- 0.06), jejunal microvascular blood flow (baseline: PE 254 +/- 127, NE 282 +/- 72 PU), PO2muc (baseline: PE 31 +/- 9.1, NE 33 +/- 11 mmHg), and HbO2 (baseline: PE 52 +/- 9.6%, NE 58 +/- 11.6%). CONCLUSION: Despite major differences in systemic hemodynamics jejunal tissue oxygen supply is not affected by progressively increasing intravenous infusion of norepinephrine and phenylephrine.

Risk factors associated with new onset tachyarrhythmias after cardiac surgery--a retrospective analysis.

BACKGROUND: Tachyarrhythmias (TA) represent a frequent and serious problem after cardiac surgery. We retrospectively analyzed 987 cardiac surgery patients admitted to a surgical intensive care unit between 1996 and 1999 to assess incidence and risk factors associated with development of postoperative TA in the intensive care unit. METHODS: TA (n=149) were defined as non-sinus rhythm with a heart rate (HR) > or =100 bpm in patients with preoperative sinus rhythm or as heart rate > or =130 bpm in patients with preoperative atrial fibrillation. A total of 787 patients served as controls (C). Demographic, premorbidity and perioperative data, admission SAPS and MODS-score, presence of clinical syndromes systemic inflammatory response syndrome (SIRS) and sepsis were univariately compared between groups. For prediction of independent risk factors for TA-development two multiple logistic regression models were finally established. RESULTS: Concerning TA, atrial fibrillation and flutter (76%) were observed most frequently, followed by paroxysmal supraventricular tachycardia (15%) and ventricular tachycardia/fibrillation (11%). Age, a history or presence of congestive heart failure, development of SIRS and sepsis, severity of multiple organ dysfunction syndrome and in particular severity of cardiovascular failure proved to be independent risk factors for development of TA. CONCLUSION: In cardiac surgery patients, age, a history or presence of congestive heart failure, postoperative development of a systemic inflammatory response syndrome or sepsis and the severity of multiple organ function syndrome were independent predictors for development of TA in the intensive care unit. The association of severity of cardiovascular dysfunction with TA strongly suggests a causal relationship between catecholamine therapy and TA-development.

Effects of epinephrine on intestinal oxygen supply and mucosal tissue oxygen tension in pigs.

OBJECTIVE: To study the effects of increasing dosages of epinephrine given intravenously on intestinal oxygen supply and, in particular, mucosal tissue oxygen tension in an autoperfused, innervated jejunal segment. DESIGN: Prospective, randomized experimental study. SETTING: Animal research laboratory. SUBJECTS: Domestic pigs. INTERVENTIONS: Sixteen pigs were anesthetized, paralyzed, and normoventilated. A small segment of the jejunal mucosa was exposed by midline laparotomy and antimesenteric incision. Mucosal oxygen tension was measured by using Clark-type surface oxygen electrodes. Microvascular hemoglobin oxygen saturation and microvascular blood flow (perfusion units) were determined by tissue reflectance spectrophotometry and laser-Doppler velocimetry. Systemic hemodynamics, mesenteric-venous acid-base and blood gas variables, and systemic acid-base and blood gas variables were recorded. Measurements were performed after a resting period and at 20-min intervals during infusion of increasing dosages of epinephrine (n = 8; 0.01, 0.05, 0.1, 0.5, 1, and 2 microg x kg(-1) x min(-1)) or without treatment (n = 8). In addition, arterial and mesenteric-venous lactate concentrations were measured at baseline and at 60 and 120 mins. MEASUREMENTS AND MAIN RESULTS: Epinephrine infusion led to significant tachycardia; an increase in cardiac output, systemic oxygen delivery, and oxygen consumption; and development of lactic acidosis. Epinephrine significantly increased jejunal microvascular blood flow (baseline, 267 +/- 39 perfusion units; maximum value, 443 +/- 35 perfusion units) and mucosal oxygen tension (baseline, 36 +/- 2.0 torr [4.79 +/- 0.27 kPa]; maximum value, 48 +/- 2.8 torr [6.39 +/- 0.37 kPa]) and increased hemoglobin oxygen saturation above baseline. Epinephrine increased mesenteric venous lactate concentration (baseline, 2.9 +/- 0.6 mmol x L(-1); maximum value, 5.5 +/- 0.2 mmol x L(-1)) without development of an arterial-mesenteric venous lactate concentration gradient. CONCLUSIONS: Epinephrine increased jejunal microvascular blood flow and mucosal tissue oxygen supply at moderate to high dosages. Lactic acidosis that develops during infusion of increasing dosages of epinephrine is not related to development of gastrointestinal hypoxia.

Tachyarrhythmias in a surgical intensive care unit: a case-controlled epidemiologic study.

OBJECTIVE: Incidence, types, and factors associated with new onset tachyarrhythmias (TA) in surgical intensive care patients. DESIGN: Pairwise-matched case-controlled study. SETTING: Surgical intensive care unit (ICU) with nine intensive care beds. PATIENTS: During a 1-year period, all TA patients (n = 89) were included in the study. Control patients (n = 82) without TA were matched according to age, sex, and surgical region. METHODS: TA workup included: 12-lead ECG, arterial blood gas, serum electrolyte (K+, Mg2+), and serum CK/CKMB isoenzyme analysis. Pre-existing cardiovascular and pulmonary disease, cardiovascular risk factors, preoperative regular medication, and admission SAPS were recorded in all patients. A multiple organ dysfunction syndrome (MODS) score, the presence or absence of SIRS or sepsis, and hemodynamics (MAP and CVP) before onset of TA were evaluated in TA patients, while in control patients highest MODS-score, the presence or absence of SIRS or sepsis, mean hemodynamic and laboratory values calculated from highest and lowest readings during ICU stay were used for statistical comparison. Logistic regression analysis was performed to identify variables multivariately associated with TA. RESULTS: Eighty-nine (14.8%) of 596 patients developed TA. Atrial fibrillation was most frequent (60.7%). Presence of SIRS or sepsis (adj. OR = 36.45; 95% CI: 11.5-115.5), high admission SAPS (adj. OR = 1.25/point; 95% CI: 1.08-1.44), high CVP (adj. OR = 1.27/mmHg; 95% CI: 1.09-1.48), and low arterial oxygen tension (adj. OR = 0.97/mmHg); 95% CI: 0.95-0.99) were found to be significant predictors for development of TA. CONCLUSIONS: In surgical patients hypoxia, high cardiac filling pressures, a greater degree of physiologic derangement at admission, and the presence of SIRS and sepsis are independent risk factors for the development of TA.

Acute respiratory failure associated with catastrophic antiphospholipid syndrome.

We present a case of multiple organ dysfunction syndrome with acute respiratory failure due to alveolar haemorrhage associated with antiphospholipid antibodies in a 42-year-old woman with a medical history of antinuclear antibody-negative systemic lupus erythematosus and antiphospholipid syndrome. Severe respiratory failure, circulatory shock and acute renal failure necessitated artificial ventilation, inotropic and vasopressor therapy, and continuous venovenous haemofiltration. A tentative diagnosis of haemorrhagic lupus pneumonitis or pulmonary manifestation of antiphospholipid syndrome was made. Lupus anticoagulant, IgG anticardiolipin and anti-beta2-glycoprotein I antibodies were positive. High-dose glucocorticoid, anticoagulation with heparin, plasmapheresis and cyclophosphamide improved her clinical condition. Despite this, the patient died several days later of spontaneous intracranial haemorrhage. This case illustrates the uncommon manifestation of acute respiratory failure associated with antiphospholipid syndrome.

[Intestinal ischemic reperfusion syndrome: pathophysiology, clinical significance, therapy]. / Das Ischämie-Reperfusionssyndrom des Darmes: Pathophysiologie--klinische Relevanz--Therapie.

Gut ischemia-reperfusion injury is a serious condition in intensive care patients. Activation of immune cells within the huge endothelial surface area of gut microcirculation may initiate a systemic inflammatory response with secondary injury to distant organs. Translocation of bacteria and toxins through a leaky gut mucosa may amplify or perpetuate systemic inflammation, leading to multiple organ dysfunction syndrome and death in critically ill patients. Gut ischemia promotes regional production of inflammatory mediators, expression of cell adhesion molecules on endothelial and immune cell surfaces and increases the procoagulatory properties of vascular endothelial cells. During reperfusion, gut injury may be amplified by increased production of oxygen radicals and exhaustion of endogenous antioxidant defence mechanisms. Although several therapeutic strategies to interrupt the pathophysiology of ischemia-reperfusion have been shown to be beneficial in animal experiments, none of these interventions has gained clinical relevance. After initial hemodynamic and respiratory stabilisation of critically ill patients, strategies to prevent secondary gut injury by increasing splanchnic oxygen delivery or augment mucosal cell regeneration may be the only therapeutic options for intensive medical specialists at the present time. Early enteral nutrition and treatment with specific vasoactive drugs may reduce morbidity and costs of treatment in certain critically ill patients. However definitive evidence of a reduction in mortality with these therapies has still not be provided.