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Diverticulosis of the sigmoid colon is a common condition and occurs more often in elderly patients. A well-known complication is infection or even perforation which often requires surgery. Necrotizing fasciitis as a complication of perforated diverticulitis is very rare. Here, we present a case of a covered perforated diverticulitis in an immunosuppressed patient leading to life-threatening necrotizing fasciitis requiring extracorporeal membrane oxygenation. Either hematogenous or local dissemination via the inguinal canal seemed the most probable mechanism of leg infection leading to hip articulation.

Multidisziplinare Arbeitsgruppe (ARGE) Ethik in Anasthesie und Intensivmedizin der Osterreichischen Gesellschaft fur Anasthesiologie, Reanimation, Intensivmedizin (OGARI) Die vorliegende Arbeit soll Arzten Hilfestellung bei Entscheidungen in intensivmedizinischen Grenzbereichen geben. Anhand einer strukturierten Checkliste werden die zwei Saulen jeder medizinischen Entscheidung, die Indikation und der Patientenwille in systematischer Weise abgefragt. Vier Stufen moglicher Therapiezielanderungen werden erlautert und Empfehlungen fur die korrekte Dokumentation von Therapiezielanderungen vorgestellt.

Das Wort ,Anamie’ kommt aus dem Altgriechischen ἄναiμoς (anaimos) und bedeutet „blutlos“. Das heist, beim anamen Patienten ist die Anzahl der roten Blutkorperchen (Erythrozyten, RBC) reduziert. Da die Erythrozyten als zellulare Hauptbestandteile des Blutes fur den Hamatokrit (Hkt) und damit die Viskositat (Vis) des stromenden Blutes verantwortlich sind, hat der aname Patient einen erniedrigten Hkt und als Folge davon eine deutlich reduzierte Blutviskositat, die wiederum eine der bestimmenden Determinanten fur die mikrovaskulare Perfusion ist. Insbesondere fur Patienten mit koronarem Risikoprofil (KHK) ist das Mortalitatsrisiko durch eine Anamie aufgrund der schlechten koronaren Reserve und der begrenzten Fahigkeit Herzzeitvolumen (HZV) zu steigern, deutlich erhoht, weswegen diese Patientengruppe einen gewissen „kritischen“ Hkt nicht unterschreiten sollte. Da man aber andererseits aus verschiedenen klinischen Studien weis, dass die Gabe von Erythrozytenkonzentraten (EK) die Mortalitat signifikant erhoht, ist fur jeden Patienten individuell abzuwagen, wo sein kritischer Toleranzwert fur die Anamie liegt, um einerseits eine optimale mikrovaskulare Rheologie zu erreichen und andererseits unnotige Bluttransfusionen zu vermeiden. Ein wenig Klarheit in diesen „Konflikt“ zu bringen, ist die Absicht des folgenden Artikels.

The microvascular wall is metabolically active and plays a key role in maintaining homeostasis. Additionally, it regulates the delivery of nutrients to the tissue and removal of its byproducts. Large oxygen gradients have been found to occur across the vessel wall. By using pharmacologic challenges, studies have demonstrated that the vascular wall regulates oxygen release from the blood to the tissue. Thus, these findings lead to the hypothesis that vasoactive substances used clinically may inadvertently partition proportionately more oxygen to the vascular wall and reduce the amount received by the tissue, leaving it potentially at risk.

The patients who do not respond even to very high dosages of heparin are assumed to suffer from heparin resistance. The aim of this study was to investigate whether critically ill patients suffering from heparin resistance generally have low antithrombin III (AT) levels, and if the direct thrombin inhibitor argatroban in that case can be an effective option to achieve prophylactic anticoagulation. The study was conducted at the Department for General and Surgical Intensive Care Medicine at the University Hospital Innsbruck. We retrospectively included all patients between 2008 and 2012, who received argatroban because of poor response to high-dosage heparin prophylaxis. The period under observation lasted in total for 9 days, 2 days of anticoagulation with unfractionated heparin (UFH) and 7 days with argatroban. The primary objective was to investigate if after 7 (± 1) hours of switching to argatroban the activated partial thromboplastin time (aPTT) levels were in a prophylactic range of 45 to 55 seconds. Further objectives were to assess the AT level, side effects such as bleeding or thromboembolism, platelet count, correlation between organ function and argatroban dose as well as any need for allogeneic blood products. The study population, consisting of 5 women and 15 men with a mean (± standard deviation, SD) age of 54.6 ± 16.3 years, differed in many clinical aspects. A median (interquartile range) heparin dose of 1,000, 819 to 1,125 IU/h was administered for 2 days and failed in providing a prophylactic anticoagulation measured by the aPTT. The mean aPTT level with heparin treatment was 38.5 seconds (± 4.7) its change within that period was not significant. After switching to argatroban, the mean increase of the aPTT levels in all study patients amounted from 38.5 to 48.3 seconds (p

Context: Determination of arginine vasopressin (AVP) concentrations may be helpful to guide therapy in critically ill patients. A new assay analyzing copeptin, a stable peptide derived from the AVP precursor, has been introduced. Objective: Our objective was to determine plasma copeptin concentrations. Design: We conducted a post hoc analysis of plasma samples and data from a prospective study. Setting: The setting was a 12-bed general and surgical intensive care unit (ICU) in a tertiary university teaching hospital. Patients: Our subjects were 70 healthy volunteers and 157 ICU patients with sepsis, with systemic inflammatory response syndrome (SIRS), and after cardiac surgery. Interventions: There were no interventions. Main Outcome Measures: Copeptin plasma concentrations, demographic data, AVP plasma concentrations, and a multiple organ dysfunction syndrome score were documented 24 h after ICU admission. Results: AVP (P < 0.001) and copeptin (P < 0.001) concentrations were significantly higher in ICU patients than in controls. Patients after cardiac surgery had higher AVP (P = 0.003) and copeptin (P = 0.003) concentrations than patients with sepsis or SIRS. Independent of critical illness, copeptin and AVP correlated highly significantly with each other. Critically ill patients with sepsis and SIRS exhibited a significantly higher ratio of copeptin/AVP plasma concentrations than patients after cardiac surgery (P = 0.012). The American Society of Anesthesiologists’ classification (P = 0.046) and C-reactive protein concentrations (P = 0.006) were significantly correlated with the copeptin/AVP ratio. Conclusions: Plasma concentrations of copeptin and AVP in healthy volunteers and critically ill patients correlate significantly with each other. The ratio of copeptin/AVP plasma concentrations is increased in patients with sepsis and SIRS, suggesting that copeptin may overestimate AVP plasma concentrations in these patients.

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.

Colloids and crystalloids are usually administered as treatment for hypovolemia in severely injured patients. However, dilution of clotting factors and platelets together with impaired fibrinogen polymerization are associated with fluid therapy and may aggravate hemorrhage, thus worsening final outcome of these patients. We investigated, in an in vitro model, whether the addition of fibrinogen to diluted blood samples can reverse dilutional coagulopathy. Blood from 5 healthy male volunteers was diluted by 60% using lactated Ringer's solution, 4% modified gelatin solution, or 6% hydroxyethyl starch 130/0.4, as well as the combination of lactated Ringer's solution with either of the 2 colloid solutions. Thereafter, aliquots of diluted blood samples were incubated with 3 different concentrations of fibrinogen (0.75, 1.5, and 3.0 mg/mL). Measurements were performed by modified thrombelastography (ROTEM; Pentapharm, Munich, Germany). After 60% dilution, clotting times increased, whereas clot firmness and fibrin polymerization decreased significantly. After administration of fibrinogen, clotting times decreased and clot firmness, as well as fibrin polymerization, increased in all diluted blood samples. The effect of in vitro fibrinogen substitution on ROTEM variables was dependent on the fibrinogen dosage and the type of solution used to dilute the blood samples.

Purpose of review The development of the phosphorescence quenching oxygen measurement technique has allowed for a simultaneous measurement of intra and perivascular partial pressure oxygen along arteriolar vessels in vivo. Mapping the microvascular distribution and oxygen gradients across the vascular walls using this high-resolution technique reveals the existence of large radial gradients between the vasculature and the tissue, with concomitant longitudinal oxygen loss. Mass balance analysis along vessel segments indicates that the vascular wall has a high rate of oxygen consumption. This review presents the current status of in-vivo studies on the partitioning of oxygen between blood, the vascular wall and the surrounding tissue, thereby positioning an oxygen sink between blood and tissue regulating oxygen release. Recent findings Induced vasoactivity (vasoconstriction and vasodilation) has been shown to modulate oxygen consumption of the vascular wall and directly affect the portion of oxygen available to the tissue. Inhibition of the endothelial layer of the vessel wall resulted in a decrease in the oxygen gradient across the vessel. Summary The vascular wall is a sink for oxygen. The modulation of vessel wall oxygen consumption can substantially impact the amount of oxygen released to the tissue.

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 relaxation to oxygen consumption of the microvascular wall during verapamil-induced vasodilatation. Verapamil HCl delivered in a 0.1 mg/kg bolus injection followed by a continuous infusion of 0.01 mg·kg−1·min−1caused significant arteriolar dilatation, increased microvascular flow and functional capillary density, and decreased arteriolar vessel wall transmural Po2difference. Verapamil caused tissue Po2to increase from 25.5 ± 4.1 mmHg under control condition to 32.0 ± 3.7 mmHg during verapamil treatment. Total oxygen released by the microcirculation to the tissue remained the same as at baseline. Maintenance of the same level of oxygen release to the tissue, increased tissue Po2, and decreased wall oxygen concentration gradient are compatible if vasodilatation significantly lowers vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. These findings show that treatment with verapamil, which increases oxygen supply through vasodilatation, may further improve tissue oxygenation by lowering oxygen consumption of the microcirculation.

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.

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 Po2 difference. AVP caused tissue Po2 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 Po2, 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 Po2. 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.

Background: Arginine-vasopressin (AVP) can successfully stabilize hemodynamics in patients with advanced vasodilatory shock. It has been suggested that inhibition of cytokine-induced nitric oxide production may be an important mechanism underlying AVP-induced vasoconstriction. Therefore, serum concentrations of nitrite/nitrate (NOx), the stable metabolite of nitric oxide, were measured in patients suffering from advanced vasodilatory shock treated with either AVP in combination with norepinephrine (NE) or NE alone. Methods: This trial was a separate study arm of a previously published prospective, randomized, controlled study on the effects of AVP in advanced vasodilatory shock. Thirty-eight patients were prospectively randomized to receive a combined infusion of AVP (4 U h−1) and NE, or NE infusion alone. Serum NOx concentrations were measured at baseline, 24, and 48 h after randomization. The increase in mean arterial pressure during the first hour after study enrollment was documented in all patients. Results: No difference in NOx concentrations was found between groups throughout the study period. AVP patients demonstrated a significantly greater increase in mean arterial pressure than NE patients (22 ± 10 vs. 5 ± 9 mmHg; P

Martin W. Dunser a, Markus Ohlbauer b, Josef Rieder a, Isabella Zimmermann a, Helmut Ruatti a, Anton H. Schwabegger b, Florian Bodrogi a, Georg M. Huemer b, Barbara E. Friesenecker a, Andreas J. Mayr a,∗, Philipp Lirk a a Department of Anaesthesiology and Critical Care Medicine, Division of General and Surgical Intensive Care Medicine, Leopold-Franzens-University, Anichstrasse 35, Innsbruck, Ti 6020, Austria b Department of Plastic Surgery, Leopold-Franzens-University Innsbruck, Innsbruck, Austria

Near-drowning is a frequent preventable accident with a significant morbidity and mortality in a previous healthy population. In most patients the primary injury is pulmonary failure due to fluid aspiration, resulting in severe arterial hypoxemia and secondary damage to other organs. Immediate interruption of hypoxia is of utmost importance in the emergency situation. Accurate neurologic prognosis cannot be predicted from initial clinical presentation, laboratory, radiological or electrophysiological examinations. Prompt resuscitation and aggressive respiratory and cardiovascular treatment are crucial for optimal survival. This review provides the reader with detailed information on epidemiology, pathophysiology, emergency decision making and general treatment in near drowning accidents.

In this case report, we present the successful therapy of severe cardiac failure in pituitary adrenal insufficiency. A previously healthy 56-year-old-man in pituitary coma due to an atypical variant of multiple endocrine adenomatosis (pituitary adenoma and pheochromocytoma) suffered from cardiac failure resistant to catecholamine and standard hydrocortisone therapy. After two bolus injections of dexamethasone (2 × 24 mg) mean arterial pressure and cardiac function dramatically improved, probably due to restoration of permissive effects on catecholamine action and reversal of pathophysiological mechanisms of cardiac failure. We conclude that in patients with severe cardiovascular failure in pituitary coma the administration of potent glucocorticoids may be more effective in reversing cardiovascular failure than standard dosages of hydrocortisone.

Effect of increasing blood viscosity during extreme hemodilution on capillary perfusion and tissue oxygenation was investigated in the awake hamster skinfold model. Two isovolemic hemodilution steps were performed with 6% Dextran 70 [molecular weight (MW) = 70,000] until systemic hematocrit (Hct) was reduced by 65%. A third step reduced Hct by 75% and was performed with the same solution [low viscosity (LV)] or a high-molecular-weight 6% Dextran 500 solution [MW = 500,000, high viscosity (HV)]. Final plasma viscosities were 1.4 and 2.2 cP (baseline of 1.2 cP). Hct was reduced to 11.2 ± 1.1% from 46.2 ± 1.5% for LV and to 11.9 ± 0.7% from 47.3 ± 2.1% for HV. HV produced a greater mean arterial blood pressure than LV. Functional capillary density (FCD) was substantially higher after HV (85 ± 12%) vs. LV (38 ± 30%) vs. baseline (100%).[Formula: see text] levels measured with Pd-porphyrin phosphorescence microscopy were not statistically changed from baseline until after the third hemodilution step. Wall shear rate (WSR) decreased in arterioles and venules after LV and only in arterioles after HV. Wall shear stress (WSR × plasma viscosity) was substantially higher after HV vs. LV. Increased mean arterial pressure and shear stress-dependent release of endothelium-derived relaxing factor are possible mechanisms that improved arteriolar and venular blood flow and FCD after HV vs. LV exchange protocols.

One of the most important functions of the blood circulation is O 2 delivery to the tissue. This process occurs primarily in microvessels that also regulate blood flow and are the site of many metabolic processes that require O 2 . We measured the intraluminal and perivascular pO 2 in rat mesenteric arterioles in vivo by using noninvasive phosphorescence quenching microscopy. From these measurements, we calculated the rate at which O 2 diffuses out of microvessels from the blood. The rate of O 2 efflux and the O 2 gradients found in the immediate vicinity of arterioles indicate the presence of a large O 2 sink at the interface between blood and tissue, a region that includes smooth muscle and endothelium. Mass balance analyses show that the loss of O 2 from the arterioles in this vascular bed primarily is caused by O 2 consumption in the microvascular wall. The high metabolic rate of the vessel wall relative to parenchymal tissue in the rat mesentery suggests that in addition to serving as a conduit for the delivery of O 2 the microvasculature has other functions that require a significant amount of O 2 .

Anemia may promote intestinal hypoxia. We studied the effects of progressive isovolemic hemodilution on jejunal mucosal (Po 2 muc), and serosal tissue oxygen tension (Po 2 ser, Clark-type surface electrodes), mucosal microvascular hemoglobin oxygen saturation (Hbo 2 muc), and hematocrit (Hctmuc; tissue reflectance spectophotometry) in a jejunal segment. Twelve domestic pigs were anesthetized, paralyzed, and mechanically ventilated. Laparatomy was performed, arterial supply of a jejunal segment isolated, and constant pressure pump perfused. Seven animals were progressively hemodiluted to systemic hematocrits (Hctsys) of 20%, 15%, 10%, and 6%. Baseline for Po 2 muc, Po 2 ser and Hbo 2 muc was 23.5 ± 2.1 mm Hg, 57.5 ± 4 mm Hg, and 47.0% ± 6.4% which were not different from the five controls. Despite a significant increase in jejunal blood flow, jejunal oxygen delivery decreased and oxygen extraction ratio increased significantly at Hctsys 10% and 6%. Po 2 ser decreased significantly below or at Hctsys of 15%, whereas Po 2 muc and Hbo 2 muc were maintained to Hctsys of 10%, but less than 10% Hbo 2 muc and mesenteric venous pH decreased significantly, implying that physiological limits of jejunal microvascular adaptation to severe anemia were reached. Decrease of Hctmuc was less pronounced than Hctsys. In conclusion, redistribution of jejunal blood flow and an increase in the ratio of mucosal to systemic hematocrit are the main mechanisms maintaining mucosal oxygen supply during progressive anemia.

The present work provides assistance for physicians concerning decision making in clinical borderline situations in the ICU. Based on a structured checklist the two fundamental aspects of any medical decision, the medical indication and the patient's preference are queried in a systematic way. Four possible steps of withholding and/or withdrawing therapy are discussed. Finally, recommendations regarding appropriate documentation of end of life decisions are provided.

Effects of Escherichia coli lipopolysaccharide (2 micrograms.kg-1.20 min-1; LPS), given systemically (S) or via superior mesenteric artery (M), and consecutive dopamine infusion (16 micrograms.kg-1.20 min-1) on jejunal mucosal tissue O2 tension (PO2muc) and serosal tissue O2 tension (PO2ser; Clark-type surface electrodes) and jejunal mucosal microvascular hemoglobin O2 saturation (HbO2muc; tissue reflectance spectrophotometry) were investigated in a hemodynamically stable pig model. Twenty-one pigs were anesthetized, paralyzed, and mechanically ventilated. After laparotomy, a mesenteric venous catheter was inserted and a jejunal antimesenteric enterotomy performed. LPS-infused animals developed similar degrees of pulmonary hypertension. No differences in cardiac output and mean arterial blood pressure between groups were found. PO2muc and HbO2muc were significantly lower in M animals compared with control (C) [210 min; PO2muc: 7.12 +/- 1.81 (M), 19.01 +/- 3.12 mmHg (C); HbO2muc: 28.78 +/- 3.36 (M), 49.09 +/- 3.84% (C)], whereas S animals ranged in between (PO2muc: 13.36 +/- 2.2 mmHg; HbO2muc: 40.68 +/- 4.43%). Of measured PO2muc values, 12.6 (C), 20.6 (S), and 46.3% (M) ranged from 0 to 5 mmHg. PO2ser was lower in LPS animals compared with control [59.43 +/- 5.4 (C), 45.00 +/- 6.12 (S), 47.33 +/- 4.34 (M) mmHg]. Dopamine increased PO2muc and HbO2muc to similar absolute values and significantly decreased frequency of PO2muc (0-5 mmHg) in M animals. We conclude that LPS impairs mucosal tissue oxygenation independently of systemic hemodynamics. Mucosal microvascular dysfunction depends on regional LPS concentrations. Under conditions of compromised tissue oxygenation, dopamine significantly improves PO2muc and HbO2muc.

Objective : To evaluate the effects of dopamine- 1-receptor stimulation on intestinal mucosal tissue oxygenation. Design : Prospective, experimental, controlled trial. Setting : Animal research laboratory. Subjects : Anesthetized domestic pigs (30 to 45 kg). Interventions : A small segment of the jejunal mucosa and serosa was exposed by midline laparotomy and antimesenteric incision. Fenoldopam, a selective dopamine-1-receptor agonist, was infused in steps, exponentially increasing from 0.6 to 9.6 μg/kg/min via a central venous catheter (n = 8, fenoldopam group), whereas a second group (n = 6, saline group) was only given the solvent. Measurements and Main Results : Systemic hemodynamics as well as systemic and jejunal acid base and blood gas variables were measured using an arterial catheter, a thermodilution pulmonary artery catheter, and a jejunal venous catheter. Jejunal mucosal and serosal tissue Po 2 were measured by means of Clark-type surface oxygen electrodes. Oxygen saturation and relative concentration of mucosal microvascular hemoglobin were measured by means of tissue reflectance spectrophotometry. In the fenoldopam group, systemic oxygen delivery (12.5 ± 0.8 mL/kg/min at baseline) increased by 56% (p

Functional capillary density is variable in both normal and diseased tissue. When this parameter is defined as the number of capillaries that possess red blood cell transit, changes in functional capillary density reflect mechanisms that modulate the entrance of red blood cells into the capillaries. These mechanisms have anatomical origin, whereby the capillary diameter changes, and may also be hydrodynamic, when flow conditions prevent red blood cells from entering a capillary branch. An intrinsic feature of both processes is that capillaries undergo lumenal changes. Capillary lumen is determined by a composite of mechanical and cellular factors, where intravascular pressure is one of the principal determinants affecting diameter as a consequence of the elastic properties of the capillary/tissue system. The hydration of the surrounding tissue and the cellular volume regulation of the endothelium are additional factors. There is increasing evidence that capillaries possess contractility and that this phenomenon has spontaneous components. Consequently, functional capillary density is the resultant of both passive and active processes present at the level of individual vessels.

Ischemia-reperfusion injury was investigated in terms of functional capillary density (FCD), capillary red blood cell velocity (cRBCv), and arteriolar and venular diameter after 4-h ischemia in the unanesthetized hamster skin-fold preparation. Animals in group 1 were studied by transillumination. Group 2 received a bolus injection of fluorescein isothiocyanate (FITC)-dextran (mol wt 150,000) and was studied by transillumination (zone 1) and epi-illumination (zone 2). In group 1, FCD decreased after ischemia (92% of baseline, 30 min), returning to control up to 24 h. cRBCv increased after reperfusion, being 175% of baseline at 24 h. Arterioles and venules dilated for 24 h after reperfusion. In group 2/zone 2, FCD progressively decreased to 11% of control, arteriolar dilation was inhibited, and cRBCv increased 30 min and 2 h after reperfusion. Tissue perfusion index (FCD x cRBCv) increased 158% in group 1 at 24 h, did not change in group 2/zone 1, and was 9% of control at 24 h in group 2/zone 2 (P < or = 0.05). We conclude that increased perfusion is a normal reaction to ischemia-reperfusion injury in this model, and previously observed capillary no reflow is due to FITC-dextran phototoxicity.

The mucosa of the small intestine has some unique microcirculatory features that may result in significant tissue oxygenation changes even under physiological conditions. To prove this hypothesis we investigated mucosal and serosal oxygenation in an autoperfused, innervated jejunal segment in pigs. Eight animals (30-40 kg) were anesthetized, paralyzed, and normoventilated. A small segment of the jejunal mucosa and serosa was exposed by a midline laparotomy and an antimesenteric incision. Mucosal and serosal oxygen tensions were measured using Clark-type surface oxygen electrodes. Mucosal hemoglobin saturation and concentration were determined by tissue reflectance spectrophotometry. Systemic hemodynamics, mesenteric-venous acid base, and blood gas variables, as well as systemic acid-base and blood gas variables and jejunal electromyogenic potentials, were recorded. Measurements were performed after a rest period at 0, 30, 60, and 90 min. All animals remained hemodynamically stable. At time 0 the jejunal oxygen extraction ratio was 0.33 +/- 0.05, the mean serosal PO2 was 60.25 +/- 7.69, the mean mucosal PO2 was 25.47 +/- 4.41 mmHg, and the mean mucosal hemoglobin saturation was 46.36 +/- 6.22%. Mean values did not change with time. In contrast to serosal PO2, mucosal PO2, mucosal hemoglobin oxygen saturation, and hemoglobin concentration showed rhythmic oscillations with a frequency of 3.4-5 cycles/min that were unrelated to systemic hemodynamic parameters, respiratory frequency, and intestinal peristalsis. From this we concluded that the jejunal mucosa demonstrates significant, regular changes in oxygenation parameters that are locally mediated. We speculate that the physiological basis for this phenomenon is the countercurrent arrangement of microvessels in conjunction with vasomotion.(ABSTRACT TRUNCATED AT 250 WORDS)

Recombinant activated factor VII has been used successfully in many cases of traumatic and surgical bleeding complications that were unresponsive to standard treatment. However, because disseminated intravascular coagulation can develop from a thrombin burst as a side effect of recombinant activated factor VII, it is not yet established for bleeding complications induced by disseminated intravascular coagulation. This article presents 3 patients with severe sepsis and fulminant disseminated intravascular coagulation. Excessive microvascular bleeding persisted despite conventional therapy, and surgical intervention and radiologic embolization did not control bleeding. After administration of recombinant activated factor VII, bleeding ceased in all patients, and no overt thromboembolic events occurred. One patient survived to be discharged from the hospital. The other 2 patients died from refractory multiorgan failure and overall poor prognosis. Recombinant factor VIIa might be an option for the treatment of severe bleeding complications in the case of DIC refractory to the conventional therapy.

In this case report, the course of arginine vasopressin and copeptin, the stable C-terminal part of the arginine vasopressin precursor, is described during the period of critical illness in a septic shock patient. Arginine vasopressin and copeptin concentrations were substantially increased during the initial 36 hours of shock. Subsequently, both hormones continuously decreased, but exhibited another peak in response to stress during extubation. During restoration of cardiovascular stability, endogenous arginine vasopressin levels further decreased and obviously did not contribute to haemodynamic improvement. In contrast, the decrease in arginine vasopressin and copeptin can be at least partly explained by an improvement of cardiovascular function.

Arginine vasopressin (AVP) has been employed successfully during cardiopulmonary resuscitation, but there exist only few data about the effects of AVP infusion for cardiovascular failure during the post-cardiac arrest period. Cardiovascular failure is one of the main causes of death after successful resuscitation from cardiac arrest. Although the "post-resuscitation syndrome" has been described as a "sepsis-like" syndrome, there is little information about the haemodynamic response to AVP in advanced cardiovascular failure after cardiac arrest. In this retrospective study, haemodynamic and laboratory variables in 23 patients with cardiovascular failure unresponsive to standard haemodynamic therapy during the post-cardiac arrest period were obtained before, and 30 min, 1, 4, 12, 24, 48, and 72 h after initiation of a supplementary AVP infusion (4 IU/h). During the observation period, AVP significantly increased mean arterial blood pressure (58+/-14 to 75+/-19 mmHg, p0.001), and decreased noradrenaline (norepinephrine) (1.31+/-2.14 to 0.23+/-0.3 microg/kg/min, p = 0.03), adrenaline (epinephrine) (0.58+/-0.23 to 0.04+/-0.03 microg/kg/min, p = 0.001), and milrinone requirements (0.46+/-0.15 to 0.33+/-0.22 microg/kg/min, p0.001). Pulmonary capillary wedge pressure changed significantly (p0.001); an initial increase being followed by a decrease below baseline values. While arterial lactate concentrations (95+/-64 to 21+/-18 mg/dL, p0.001) and pH (7.27+/-0.14 to 7.4+/-0.14, p0.001) improved significantly, total bilirubin concentrations (1.12+/-0.95 to 3.04+/-3.79 mg/dL, p = 0.001) increased after AVP. There were no differences in the haemodynamic or laboratory response to AVP between survivors and non-survivors. In this study, advanced cardiovascular failure that was unresponsive to standard therapy could be reversed successfully with supplementary AVP infusion in90% of patients surviving cardiac arrest.

The pathophysiology of multiple organ dysfunction syndrome (MODS) is believed to be related to that of microcirculatory dysfunction. We hypothesized that the severity of MODS is determined by measuring regional variables of microvascular function and vascular reactivity in critically ill patients. Therefore, we compared (a) reactive hyperemia response in the forearm using transcutaneous Po2/Pco2 electrodes and laser Doppler velocimetry, (b) microvascular permeability assessed by strain-gauge plethysmography in legs, and (c) variables derived from gastric tonometry in hemodynamically stable patients with moderate (n = 15) and severe (n = 15) MODS. There were no differences in systemic oxygen delivery, consumption, and oxygen extraction ratio between the groups. Mortality was 20% in patients with moderate MODS and 60% in patients with severe MODS (P = 0.025). Patients with a high MODS score had significantly larger arterial lactate concentrations (3.81 +/- 2.7 mmol/L) than patients with moderate MODS (1.66 +/- 0.82 mmol/L; P = 0.006). No significant differences in gastric pHi, gastric regional-to-arterial Pco2 difference, capillary filtration coefficient, isovolumetric venous pressure, and skin reactive hyperemia response were observed between patients with moderate and severe MODS. Once MODS is established, regional variables of microvascular function and vascular reactivity measured in this study do not reflect severity of organ dysfunction.

Correction of blood losses with blood substitutes alter the pO2 distribution in the microcirculation, with outcomes depending on the final viscosity of the circulating blood and the vasoactivity induced to the restore normal distribution of pO2. Vasoactivity has an oxygen cost shown by the oxygen consumption of the arteriolar microcirculation. Vasodilators lower arteriolar oxygen consumption delivering more oxygen to the tissues, and vice versa. Increased oxygen delivery to the arterioles by right shifted oxygen dissociation causes autoregulatory vasoconstriction, a problem aggravated by low blood and plasma viscosity that lowers NO endothelial NO production. Restoration of tissue function is achieved when no portion of the tissue falls below the threshold of anaerobic metabolism. This goal is attained by using high affinity modified hemoglobins that act as a reservoir of oxygen only deployed when the circulating blood arrives at tissue regions where pO2 is very low. Given these premises, restoration of tissue function after severe blood losses requires the re-establishment of oxygen delivery capacity and pO2 distribution. This is attained by tailoring blood and plasma viscosity and oxygen dissociation properties to insure that no portion of the tissue lacks oxygen delivery, even though overall tissue pO2 may be abnormally low.

OBJECTIVE To measure arginine vasopressin (AVP) serum concentrations in critically ill patients. DESIGN Prospective study. SETTING Twelve-bed general and surgical intensive care unit in a tertiary, university teaching hospital. PATIENTS Two-hundred-thirty-nine mixed critically ill patients and 70 healthy volunteers. INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS Demographic data, hemodynamic variables, vasopressor drug requirements, blood gases, AVP serum concentrations within 24 hrs after admission, multiple organ dysfunction score, and outcome were recorded. Twenty-four hours after admission, study patients had significantly higher AVP concentrations (11.9 +/- 20.6 pg/mL) than healthy controls (0.92 +/- 0.38 pg/mL; p < .001). Males had lower AVP concentrations than females (9.7 +/- 19.5 vs. 15.1 +/- 20.6 pg/mL; p = .014). Patients with hemodynamic dysfunction had higher AVP concentrations than patients without hemodynamic dysfunction (14.1 +/- 27.1 vs. 8.7 +/- 10.8 pg/mL; p = .042). Patients after cardiac surgery (n = 96) had significantly higher AVP concentrations when compared to patients admitted for other diagnoses (n = 143; p < .001). AVP concentrations were inversely correlated with length of stay in the intensive care unit (correlation coefficient, -0.222; p = .002). There was no correlation between serum AVP concentrations and the incidence of shock or specific hemodynamic parameters. Four (1.7%) of the 239 study patients met criteria for an absolute AVP deficiency (AVP

Continuous infusion of intravenous prostaglandin E1 (PgE1, 2.5 mug/kg/min) was used to determine how vasodilation affects oxygen consumption of the microvascular wall and tissue pO(2) in the hamster window chamber model. While systemic measurements (mean arterial pressure and heart rate) and central blood gas measurements were not affected, PgE1 treatment caused arteriolar (64.6 +/- 25.1 microm) and venular diameter (71.9 +/- 29.5 microm) to rise to 1.15 +/- 0.21 and 1.06 +/- 0.19, respectively, relative to baseline. Arteriolar (3.2 x 10(-2) +/- 4.3 x 10(-2) nl/s) and venular flow (7.8 x 10(-3) +/- 1.1 x 10(-2)/s) increased to 1.65 +/- 0.93 and 1.32 +/- 0.72 relative to baseline. Interstitial tissue pO(2) was increased significantly from baseline (21 +/- 8 to 28 +/- 7 mmHg; P < 0.001). The arteriolar vessel wall gradient, a measure of oxygen consumption by the microvascular wall decreased from 20 +/- 6 to 16 +/- 3 mmHg (P < 0.001). The arteriolar vessel wall gradient, a measure of oxygen consumption by the vascular wall, decreased from 20 +/- 6 to 16 +/- 3 mmHg (P < 0.001). This reduction reflects a 20% decrease in oxygen consumption by the vessel wall and up to 50% when cylindrical geometry is considered. The venular vessel wall gradient decreased from 12 +/- 4 to 9 +/- 4 mmHg (P < 0.001). Thus PgE1-mediated vasodilation has a positive microvascular effect: enhancement of tissue perfusion by increasing flow and then augmentation of tissue oxygenation by reducing oxygen consumption by the microvascular wall.

In this prospective, randomized, controlled, unblinded study, we compared colonization rates of a standard, unimpregnated central venous catheter (CVC) with rates for silver-coated and chlorhexidine-silversulfadiazine (CH-SS)-impregnated CVC. Patient characteristics, CVC insertion site, indwelling time, and colonization detected by semiquantitative and quantitative microbiologic techniques were documented. Two-hundred-seventy-five critically ill patients were included into the study protocol. One-hundred-sixty standard, 160 silver (S)-coated, and 165 externally impregnated CH-SS CVC were inserted. There was a significant difference in CVC colonization rates among study groups (P = 0.029). There was no difference in the colonization rate and the colonization per 1000 catheter days between standard and S-coated (P = 0.564; P = 0.24) or CH-SS-coated CVC (P - 0.795; P = 0.639). When comparing antiseptic CVC with each other, colonization rates were significantly less with CH-SS-impregnated than with S-coated CVC (16.9% versus 7.3%; P = 0.01; 18.2 versus 7.5 of 1000 catheter days; P = 0.003; relative risk, 0.43; 95% confidence interval, 0.21-0.85). Whereas standard and S-coated CVC were first colonized 2 and 3 days after insertion, respectively, CH-SS CVC were first colonized only after 7 days. In conclusion, antiseptic-impregnated CVC could not prevent catheter colonization when compared with standard polyurethane catheters in a critical care setting with infrequent catheter colonization rates and CVC left in place for >10 days.

To assess the effects of arginine vasopressin (AVP) on hemodynamic, clinical, and laboratory variables and to determine its adverse side effects in advanced vasodilatory shock.Retrospective study.A total of 316 patients.AVP infusion (4 units/hr).Cardiocirculatory, laboratory, and clinical variables were evaluated before, 0.5, 1, 4, 12, 24, 48, and 72 hrs after administration of AVP. AVP increased mean arterial pressure, systemic vascular resistance, and stroke volume index. Heart rate, central venous pressure, mean pulmonary arterial pressure, norepinephrine, milrinone, and epinephrine requirements decreased. There was no difference in the hemodynamic response between patients with septic shock, postcardiotomy shock, or systemic inflammatory response syndrome. Cardiac index decreased in 41.1% of patients during AVP treatment. In patients with hyperdynamic circulation before AVP, cardiac index decreased, whereas it remained uncharged or tended to increase in patients with normodynamic or hypodynamic circulation. During the course of AVP treatment, liver enzymes (28.5% of patients) and total bilirubin concentrations (69.3% of patients) increased, whereas platelet count decreased (73.4% of patients). Simultaneous hemofiltration significantly contributed to the decrease in platelet count (p.001) and increase in bilirubin (p.001). Whereas patients with an increase in bilirubin were more likely to die, a decrease in cardiac index or platelet count and an increase in liver enzymes did not affect mortality. Systemic inflammatory response syndrome as admission diagnosis, a high degree of multiple organ dysfunction, and norepinephrine requirements of0.5 microg x kg x min before AVP treatment were independent risk factors for death from advanced vasodilatory shock treated with AVP. If norepinephrine dosages exceeded 0.6 microg x kg x min before AVP treatment, a substantial increase in mortality occurred.Supplementary AVP infusion improved cardiocirculatory function in advanced vasodilatory shock, but an increase in liver enzymes and bilirubin, and a decrease in platelet count occurred during AVP therapy, particularly during simultaneous hemofiltration. Initiation of AVP infusion before norepinephrine requirements exceeding 0.6 microg x kg x min may improve outcome.

To determine the effects of increasing dosages of continuously infused arginine-vasopressin (AVP) on mucosal tissue oxygen tension and oxygen supply in an auto-perfused, innervated jejunal segment in an acute endotoxic porcine model.Prospective, randomized, experimental study.University hospital animal research laboratory.Jejunal mucosal tissue PO2 was measured employing two Clark-type surface oxygen electrodes. Oxygen saturation of jejunal microvascular hemoglobin was determined by tissue reflectance spectrophotometry. Systemic hemodynamic variables, mesenteric-venous and systemic acid base and blood gas variables and lactate measurements were recorded. Measurements were performed at baseline, after E. coli lipopolysaccharide (LPS) administration and at 20 min intervals during incremental AVP infusion (n=8; 0.014, 0.029, 0.057, 0.114 and 0.229 IU kg(-1) h(-1), respectively) or infusion of saline (n =8).LPS infusion leads to a significant (P0.05) decrease of mucosal tissue oxygen tension (PO2muc, 24+/-3 to 12+/-2 mmHg) and microvascular hemoglobin oxygen saturation (HbO2, 38+/-4 to 21+/-4%). Mesenteric venous lactate level increased (2.4+/-0.3 to 4.7+/-1.7 mmol l(-1)), while mesenteric venous pH decreased (7.38+/-0.02 to 7.26+/-0.12), indicating tissue hypoxia. AVP significantly increased mean arterial pressure (MAP, 81+/-15 to 97+/-17 at 0.057 IU kg(-1) h(-1)). No differences in jejunal mucosal oxygenation occurred between study groups at any dosage during the experimental protocol.AVP administration did not further compromise mucosal tissue oxygen tension and oxygen supply in the acute phase of endotoxic pigs.

Arginine vasopressin (AVP) is a potent supplementary vasopressor in advanced vasodilatory shock, but decreases in platelet count have been reported during AVP therapy. In this study we evaluated the effects of AVP infusion on the coagulation system in advanced vasodilatory shock when compared to norepinephrine (NE) infusion alone. Forty-two patients with advanced vasodilatory shock (NE requirements >0.5 microg x kg(-1) x min(-1), mean arterial blood pressure

Background— Vasodilatory shock is a potentially lethal complication of severe disease in critically ill patients. Currently, catecholamines are the most widely used vasopressor agents to support blood pressure, but loss of catecholamine pressor effects is a well-known clinical dilemma. Arginine vasopressin (AVP) has recently been shown to be a potent vasopressor agent to stabilize cardiocirculatory function even in patients with catecholamine-resistant vasodilatory shock. Methods and Results— Forty-eight patients with catecholamine-resistant vasodilatory shock were prospectively randomized to receive a combined infusion of AVP and norepinephrine (NE) or NE infusion alone. In AVP patients, AVP was infused at a constant rate of 4 U/h. Hemodynamic, acid/base, single-organ, and tonometrically derived gastric variables were reported before the study and 1, 12, 24, and 48 hours after study entry. For statistical analysis, a mixed-effects model was used. AVP patients had significantly lower heart rate, NE requirements, and incidence of new-onset tachyarrhythmias than NE patients. Mean arterial pressure, cardiac index, stroke volume index, and left ventricular stroke work index were significantly higher in AVP patients. NE patients developed significantly more new-onset tachyarrhythmias than AVP patients (54.3% versus 8.3%). Gastrointestinal perfusion as assessed by gastric tonometry was better preserved in AVP-treated patients. Total bilirubin concentrations were significantly higher in AVP patients. Conclusions— The combined infusion of AVP and NE proved to be superior to infusion of NE alone in the treatment of cardiocirculatory failure in catecholamine-resistant vasodilatory shock.

The relationship between flow motion and tissue oxygenation was investigated during hemorrhage/retransfusion with and without dopamine in 14 pigs. During 45% bleed, jejunal microvascular hemoglobin O2saturation (HBjO2) and mucosal tissue Po2(Po2muc) were recorded in seven control and seven dopamine-treated animals. Mean arterial pressure and systemic O2delivery decreased during hemorrhage and returned to baseline after retransfusion. Hemorrhage decreased Po2mucfrom 33 ± 2.8 to 13 ± 1.6 mmHg and HBjO2from 53 ± 4.9% to 32 ± 3.9%, respectively, in control animals. During reperfusion, Po2mucand HBjO2remained low. Dopamine increased Po2mucfrom 28 ± 4.3 to 45 ± 4.6 mmHg and HBjO2from 54 ± 5.7% to 69 ± 1.5% and attenuated the decrease in Po2mucand HBjO2during hemorrhage. After retransfusion, dopamine restored Po2mucand HBjO2to baseline. Control animals developed rhythmic HBjO2oscillations with increasing amplitude (frequency, 4.5 to 7.6 cycles/min) and showed an inverse relationship between Po2mucand HBjO2oscillation amplitude. Dopamine prevented regular flow motion. The association between decreased Po2mucand increased oscillations in HBjO2after normalization of systemic hemodynamics and O2transport in control animals suggests a cause-and-effect relationship between low tissue Po2and flow motion activity within the jejunal microcirculation.

Inflammation activates leukocytes causing the release of agents that disrupt the endothelial barrier to such an extent that retention of plasma protein is impaired. This phenomenon can be observed using microvascular methods in which ischemia-reperfusion-induced inflammation-like condition are analyzed in terms of the increased adherence of leukocytes to the venular endothelium. Pretreatment with Daflon 500 mg, a purified, micronized, flavonoid fraction consisting of 90% diosmin and 10% hesperidin, prior to the induction of 4 h of tourniquet ischemia significantly lowers the number of adherent leukocytes. This observation is linked to the protective effect of flavonoids in the treatment of edema, as decreased activation is also associated with a decreased platelet and complement system activation, leading to a lowered release of histamine and decreased leukocyte-dependent endothelial damage. It is proposed that attenuation of leukocyte adherence during ischemia-reperfusion is evidence of the protective endothelial effect of Daflon 500 mg and its ability to control edema in clinical situation.

The effect of a clinically used purified micronized flavonoid fraction (90% diosmin and 10% hesperidin) on leukocyte-endothelial cell interaction during ischemia-reperfusion injury was studied in the microcirculation of unanesthetized hamsters fitted with a skin fold window chamber. The drug was given orally in suspension with arabic gum (30 mg/kg) 8 h prior to induction of 4-hour tourniquet ischemia in the chamber window. Leukocyte-endothelial cell interaction was observed using fluorescence intravital microscopy in postcapillary venules (15-70 microns in diameter) at control and during reperfusion at 30 min and 2 and 24 h. Leukocytes were classified according to their flow pattern as (1) 'passers', including 'free flowing' leukocytes and those which were 'flowing with endothelial contact', and (2) 'immobilized' leukocytes. Untreated animals exhibited a significant increase of 'immobilized' leukocytes and of those 'flowing with endothelial contact' during reperfusion. Flavonoid-treated animals displayed a statistically significant lower number of 'immobilized' leukocytes at all time points during reperfusion. There was no change in the number of leukocytes 'flowing with endothelial contact' relative to the untreated animals. Since firm leukocyte attachment to the endothelial wall and subsequent emigration of leukocytes into the interstitium is a mechanism for tissue damage during inflammation, attenuation of this phenomenon during conditions of ischemia-reperfusion can in part explain previous observations that this purified micronized flavonoid fraction decreases edema formation.

OBJECTIVE To study the influence of experimentally induced acute necrotizing pancreatitis on jejunal oxygen transport, jejunal oxygen consumption, and mucosal PO2. DESIGN Prospective, randomized trial. SETTING Animal laboratory. SUBJECTS Domestic pigs aged 7 to 8 wks. INTERVENTIONS Two groups of pigs were anesthetized with midazolam and sufentanyl, mechanically ventilated, and hemodynamically monitored. In controls (n = 9) and in animals with acute necrotizing pancreatitis (n = 9), a segment of the jejunum was isolated and autoperfused in situ. Through an antimesenteric enterotomy, an area of jejunal mucosa was exposed for mucosal PO2 measurements. Acute necrotizing pancreatitis was induced by the injection of 10 mL of 10% sodium-taurocholate into the main pancreatic duct. Both groups received normal saline solution to keep pulmonary artery occlusion pressure constant. MEASUREMENTS Mucosal PO2 was assessed with a modified Clark-type multiwire surface electrode. After two baseline measurements, systemic and regional oxygen transport variables and mucosal PO2 were determined at designated intervals (20, 40, 60, 100, 120, 160, 200, 240, 280 mins). MAIN RESULTS Systemic hemodynamics and oxygen transport were maintained in both groups. In contrast to controls, all animals with pancreatitis showed gross macroscopic and histologic evidence of severe acute necrotizing pancreatitis at autopsy. There were no significant differences between groups in jejunal blood flow, oxygen transport, oxygen consumption, oxygen extraction ratio, or mucosal PO2. CONCLUSIONS Our results demonstrate that, under conditions of sustained systemic hemodynamics, jejunal oxygen transport and mucosal oxygenation are well maintained during the early course of sodium-taurocholate-induced acute necrotizing pancreatitis.

Disturbances in microcirculatory homeostasis have been hypothesized to play a key role in the pathophysiology of multiple organ dysfunction syndrome and vasopressor-associated ischemic skin lesions. The effects of a supplementary arginine vasopressin (AVP) infusion on microcirculation in vasodilatory shock and postoperative multiple organ dysfunction syndrome are unknown. Included in the study were 18 patients who had undergone cardiac or major surgery and had a mean arterial blood pressure below 65 mmHg, despite infusion of more than 0.5 μg/kg per min norepinephrine. Patients were randomly assigned to receive a combined infusion of AVP/norepinephrine or norepinephrine alone. Demographic and clinical data were recorded at study entry and after 1 hour. A laser Doppler flowmeter was used to measure the cutaneous microcirculatory response at randomization and after 1 hour. Reactive hyperaemia and oscillatory changes in the Doppler signal were measured during the 3 minutes before and after a 5-minute period of forearm ischaemia. Patients receiving AVP/norepinephrine had a significantly higher mean arterial pressure (P = 0.047) and higher milrinone requirements (P = 0.025) than did the patients who received norepinephrine only at baseline. Mean arterial blood pressure significantly increased (P < 0.001) and norepinephrine requirements significantly decreased (P < 0.001) in the AVP/norepinephrine group. Patients in the AVP/norepinephrine group exhibited a significantly higher oscillation frequency of the Doppler signal before ischaemia and during reperfusion at randomization. During the study period, there were no differences in either cutaneous reactive hyperaemia or the oscillatory pattern of vascular tone between groups. Supplementary AVP infusion in patients with advanced vasodilatory shock and severe postoperative multiple organ dysfunction syndrome did not compromise cutaneous reactive hyperaemia and flowmotion when compared with norepinephrine infusion alone.

Whereas most studies focus on laboratory and clinical research, little is known about the causes of death and risk factors for death in critically ill patients. Three thousand seven hundred patients admitted to an adult intensive care unit (ICU) were prospectively evaluated. Study endpoints were to evaluate causes of death and risk factors for death in the ICU, in the hospital after discharge from ICU, and within one year after ICU admission. Causes of death in the ICU were defined according to standard ICU practice, whereas deaths in the hospital and at one year were defined and grouped according to the ICD-10 (International Statistical Classification of Diseases and Related Health Problems) score. Stepwise logistic regression analyses were separately calculated to identify independent risk factors for death during the given time periods. Acute, refractory multiple organ dysfunction syndrome was the most frequent cause of death in the ICU (47%), and central nervous system failure (relative risk [RR] 16.07, 95% confidence interval [CI] 8.3 to 31.4, p < 0.001) and cardiovascular failure (RR 11.83, 95% CI 5.2 to 27.1, p < 0.001) were the two most important risk factors for death in the ICU. Malignant tumour disease and exacerbation of chronic cardiovascular disease were the most frequent causes of death in the hospital (31.3% and 19.4%, respectively) and at one year (33.2% and 16.1%, respectively). In this primarily surgical critically ill patient population, acute or chronic multiple organ dysfunction syndrome prevailed over single-organ failure or unexpected cardiac arrest as a cause of death in the ICU. Malignant tumour disease and chronic cardiovascular disease were the most important causes of death after ICU discharge.

Introduction This study was designed to examine differences in the arteriolar vasoconstrictive response between arginine vasopressin (AVP) and norepinephrine (NE) on the microcirculatory level in the hamster window chamber model in unanesthetized, normotonic hamsters using intravital microscopy. It is known from patients with advanced vasodilatory shock that AVP exerts strong additional vasoconstriction when incremental dosage increases of NE have no further effect on mean arterial blood pressure (MAP). Methods In a prospective controlled experimental study, eleven awake, male golden Syrian hamsters were instrumented with a viewing window inserted into the dorsal skinfold. NE (2 μg/kg/ minute) and AVP (0.0001 IU/kg/minute, equivalent to 4 IU/h in a 70 kg patient) were continuously infused to achieve a similar increase in MAP. According to their position within the arteriolar network, arterioles were grouped into five types: A0 (branch off small artery) to A4 (branch off A3 arteriole).