Candida peritonitis.

BACKGROUND: Fungal infections including Candida peritonitis (CP) are being observed with increasing frequency in the ICU. We summarize current knowledge on epidemiology, risk factors, diagnostic tests and treatment options in the previously immunocompetent patient suffering from CP. METHODS: An electronic medical database search using "Candida" and "Peritonitis" as main search terms in conjunction with specific key words relevant to the topic. RESULTS: CP is associated with high mortality particularly after complicated abdominal surgery and in the presence of severe sepsis or septic shock. Risk factors for developing CP include upper gastrointestinal tract perforation, Candida colonization, tertiary peritonitis, the severity of disease, premorbid conditions, cardiovascular failure, total parenteral nutrition, any drain/line breaching normally sterile barriers, development of peritonitis in the hospital, abdominal surgery and previous antibiotic therapy. Laboratory diagnosis primarily relies on histopathological diagnosis and culture-based methods. The usefulness of new diagnostic tests designed to identify immunogenic structures of fungal components or polymerase chain reaction for the detection of nucleic acids is still under investigation. Concerning treatment of invasive Candida infections echinocandins are recommended as first-line agents in most critically ill patients while fluconazole is still appropriate to prevent invasive fungal infections in peritonitis patients. Definitive antifungal therapy should be chosen based on susceptibility analyses. CONCLUSION: Besides skilled surgical management, the decision for empirical antifungal treatment in any patient with suspected CP has to be based on the exact knowledge regarding origin, type of peritonitis, severity of disease, knowledge of patient specific risk factors and previous exposure to antibiotics or azole antifungals.

Plasma copeptin levels before and during exogenous arginine vasopressin infusion in patients with advanced vasodilatory shock.

BACKGROUND: Plasma copeptin levels before and during exogenous arginine vasopressin infusion (AVP) were evaluated, and the value of copeptin levels before AVP therapy to predict complications during AVP therapy and outcome in vasodilatory shock patients was determined. METHODS: This prospective, observational study was nested in a randomized, controlled trial investigating the effects of two AVP doses (0.033 vs. 0.067 IU/min) on the hemodynamic response in patients with advanced vasodilatory shock due to sepsis, systemic inflammatory response syndrome or after cardiac surgery. Clinical data, plasma copeptin levels and adverse events were recorded before, 24 hours after and 48 hours after randomization. RESULTS: Plasma copeptin levels were elevated before AVP therapy. During AVP, copeptin levels decreased (P<0.001) in both groups (P=0.73). Copeptin levels at randomization predicted the occurrence of ischemic skin lesions (AUC ROC, 0.73; P=0.04), a fall in platelet count (AUC ROC, 0.75; P=0.01) during AVP and intensive care unit mortality (AUC ROC, 0.67; P=0.04). Twenty-five patients (64.1%) exhibited a decrease in copeptin levels. Patients experiencing a decrease in copeptin levels were older (P=0.04), had a higher Sequential Organ Failure Assessment score count before (P=0.03) and during AVP therapy (P=0.04), had a longer intensive care unit stay (P<0.001) and required AVP therapy longer (P=0.008) than patients without a decrease in copeptin levels during AVP. CONCLUSION: Plasma copeptin levels are elevated in patients with advanced vasodilatory shock. During exogenous AVP therapy, copeptin levels decrease, suggesting suppression of the endogenous AVP system.

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.

Critical care of the patient with acute pancreatitis.

Acute pancreatitis is an inflammatory process of the pancreas with variable involvement of regional tissues and remote organs. This review gives a comprehensive overview of the aetiology, pathophysiology, diagnosis and therapy of acute pancreatitis relevant to the intensivist. Recent international guidelines on the management of acute pancreatitis are summarised. Eighty percent of acute pancreatitis episodes are related either to gallstones or to alcohol abuse. Independent of its aetiology, the pathophysiologic hallmark of acute pancreatitis is the premature activation of trypsin, which leads to massive pancreas inflammation, systemic overproduction of pro-inflammatory mediators and ultimately remote organ dysfunction. All guidelines agree that the diagnosis of acute pancreatitis should include clinical symptoms, increased serum amylase or lipase levels and/or characteristic findings on computed tomography. Endoscopic retrograde cholangiopancreatography is recommended as a causative therapy in patients with acute cholangitis or a strong suspicion of gallstones. All guidelines underline the importance of vigorous fluid resuscitation and supplemental oxygen therapy and prefer enteral over parenteral nutrition, with the majority favouring the nasojejunal route. In view of lacking scientific evidence, antibiotic prophylaxis to prevent infection of pancreatic necroses is discouraged by most guidelines. Computed tomography-guided fine needle aspiration is the technique of choice to differentiate between sterile and infected pancreas necrosis. While sterile pancreatic necrosis should be managed conservatively, infected pancreatic necrosis requires debridement and drainage supplemented by antibiotic therapy. Surgical necrosectomy is the traditional approach, but less invasive techniques (retroperitoneal or laparoscopic necrosectomy, computed tomography-guided percutaneous catheter drainage) may be equally effective.

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.

[Advanced vasodilatory shock. One-year survival after arginine vasopressin therapy]. / Fortgeschrittene vasodilatatorische Schockzustände. Einjahresüberleben nach Argininvasopressintherapie.

BACKGROUND: Arginine vasopressin (AVP) is increasingly being used to treat advanced vasodilatory shock states due to sepsis, systemic inflammatory response syndrome (SIRS) or after cardiac surgery. There are currently no data available on long-term survival. PATIENTS AND METHODS: Demographic and clinical data, length of intensive care unit (ICU) stay, 1-year survival and causes of death after ICU discharge of 201 patients who received AVP because of advanced vasodilatory shock were collected retrospectively. RESULTS: The intensive care unit (ICU) survival rate was 39.8% (80 out of 201 patients). After ICU discharge 13 out of the 80 patients died within 1 year resulting in a 1-year survival rate of 33.3% (67 out of 201 patients). In nine patients, the cause of death was attributed to the same disease that led to ICU admission. One-year survival of patients with shock following cardiac surgery (42.1%) was higher than in patients suffering from SIRS (22.6%, p=0.005) or sepsis (28.3%, p=0.06). CONCLUSIONS: If advanced vasodilatory shock can be reversed with AVP and patients can be discharged alive from the ICU, 1-year survival rates appear to be reasonable despite severe multi-organ dysfunction syndrome (MODS).

[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.

[Vasopressin as a rescue vasopressor agent. Treatment of selected cardiogenic shock states]. / Vasopressin als Reservevasopressor. Behandlung ausgewählter kardiogener Schockzustände.

Vasodilatory shock is the most common form of shock in the critically ill patient. As a consequence of overwhelming and prolonged mediator production, vasodilatory shock can be the common final pathway of primary non-vasodilatory shock (e.g. cardiogenic or hypovolemic shock). A supplementary infusion of arginine vasopressin (AVP) showed beneficial effects on hemodynamics and potentially on the outcome in patients with vasodilatory shock due to sepsis or after major surgery. In this case series, successful administration of AVP in three surgical patients with primary cardiogenic shock forms is reported. The hemodynamic effects of AVP were comparable to those AVP-induced alterations described in septic shock and seem to be predominantly mediated by potent vasoconstriction and the facilitated reduction of higher, potentially toxic catecholamine doses. Thus, an AVP-induced decrease in heart rate and pulmonary arterial pressures may be particularly beneficial in patients with impaired cardiac function.

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.

[Vasopressin for therapy of persistent traumatic hemorrhagic shock: The VITRIS.at study]. / Vasopressin zur Therapie eines therapierefraktären traumatisch-hämorrhagischen Schocks: Die VITRIS.at-Studie.

While fluid management is established in controlled hemorrhagic shock, its use in uncontrolled hemorrhagic shock is being controversially discussed, because it may worsen bleeding. In the irreversible phase of hemorrhagic shock that was unresponsive to volume replacement, airway management and catecholamines, vasopressin was beneficial due to an increase in arterial blood pressure, shift of blood away from a subdiaphragmatic bleeding site towards the heart and brain and decrease of fluid resuscitation requirements. The purpose of this multicenter, randomized, controlled, international trial is to assess the effects of vasopressin (10 IU IV) vs. saline placebo IV (up to 3 injections at least 5 min apart) in patients with prehospital traumatic hemorrhagic shock that persists despite standard shock treatment. The study will be carried out by helicopter emergency medical service teams in Austria, Germany, Czech Republic, Portugal, the Netherlands and Switzerland. Inclusion criteria are adult trauma patients with presumed traumatic hemorrhagic shock (systolic arterial blood pressure <90 mmHg) that does not respond to the first 10 min of standard shock treatment (endotracheal intubation, fluid resuscitation and use of vasopressors) after arrival of the first emergency physician at the scene. The time window for randomization will close after 30 min of shock treatment. Exclusion criteria are terminal illness, no intravenous access, age <18 years, injury >60 min before randomization, cardiac arrest before randomization, presence of a do-not-resuscitate order, untreated tension pneumothorax, untreated cardiac tamponade, or known pregnancy. Primary study end-point is the hospital admission rate, secondary end-points are hemodynamic variables, fluid resuscitation requirements and hospital discharge rate.

Lowered microvascular vessel wall oxygen consumption augments tissue pO2 during PgE1-induced vasodilation.

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.

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.

Course of vasopressin and copeptin plasma concentrations in a patient with severe septic shock.

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.

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.

Arginine vasopressin and serum nitrite/nitrate concentrations in advanced vasodilatory shock.

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 < 0.001). The magnitude of pressure response to AVP was not correlated with NOx concentrations before start of AVP infusion (Pearson's correlation coefficient, -.009; P = 0.971). CONCLUSION: Cardiovascular effects of AVP infusion in advanced vasodilatory shock are not mediated by a clinically relevant reduction in serum NOx concentrations. Therefore, hemodynamic improvement of patients in advanced vasodilatory shock during continuous infusion of AVP has to be attributed to other mechanisms than inhibition of nitric oxide synthase. In addition, the magnitude of pressure response to AVP is not correlated with baseline concentrations of NOx.

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.

[Near drowning: epidemiology--pathophysiology--therapy]. / Beinaheertrinken: Epidemiologie--Pathophysiologie--Therapie.

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.