Intensive-care management of snakebite victims in rural sub-Saharan Africa: An experience from Uganda.

Background: Antivenom is rarely available for the management of snakebites in rural sub-Saharan Africa(sSA). Objectives: To report clinical management and outcomes of 174 snakebite victims treated with basic intensive-care interventions in a rural sSA hospital. Methods: This cohort study was designed as a retrospective analysis of a database of patients admitted to the intensive care unit (ICU) of St. Mary's Hospital Lacor in Gulu, Uganda (January 2006 - November 2017). No exclusion criteria were applied. Results: Of the 174 patients admitted to the ICU for snakebite envenomation, 60 (36.5%) developed respiratory failure requiring mechanical ventilation (16.7% mortality). Results suggest that neurotoxic envenomation was likely the most common cause of respiratory failure among patients requiring mechanical ventilation. Antivenom (at probably inadequate doses) was administered to 22 of the 174 patients (12.6%). The median (and associated interquartile range) length of ICU stay was 3 (2 - 5) days, with an overall mortality rate of 8%. Of the total number of patients, 67 (38.5%) were younger than 18 years. Conclusion: Results suggest that basic intensive care, including mechanical ventilation, is a feasible management option for snakebite victims presenting with respiratory failure in a rural sSA hospital, resulting in a low mortality rate, even without adequate antivenom being available. International strategies which include preventive measures as well as the strengthening of context-adapted treatment of critically ill patients at different levels of referral pathways, in order to reduce deaths and disability associated with snakebites in sSA are needed. Provision of efficient antivenoms should be integrated in clinical care of snakebite victims in peripheral healthcare facilities. Snakebite management protocols and preventive measures need to consider specific requirements of children. Contributions of the study: It is estimated that up to 138 000 people die each year following snakebites. Currently, reliable provision of efficient snake-bite antivenom is challenging in many rural health facilities in sub- Saharan Africa (sSA). Our results suggest that basic intensive-care interventions, including mechanical ventilation, is a feasible management option for critically ill snakebite victims in a rural sSA hospital, resulting in a low mortality rate, even without adequate antivenom doses being available.

Videolaryngoscopy versus direct laryngoscopy for emergency orotracheal intubation outside the operating room: a systematic review and meta-analysis.

Videolaryngoscopy (VL) may improve the success of orotracheal intubation compared with direct laryngoscopy (DL). We performed a systematic search of PubMed, Embase, and CENTRAL databases for studies comparing VL and DL for emergency orotracheal intubations outside the operating room. The primary outcome was rate of first-pass intubation, with subgroup analyses by location, device used, clinician experience, and clinical scenario. The secondary outcome was complication rates. Data are presented as [odds ratio (95% confidence intervals); P-values]. We identified 32 studies with 15 064 emergency intubations. There was no difference in first-pass intubation with VL compared with DL [OR=1.28, (0.99-1.65); P=0.06]. First-pass intubations were increased with VL compared with DL in the intensive care unit (ICU) [2.02 (1.43-2.85); P<0.001], and similar in the emergency department or pre-hospital setting. First-pass intubations were similar with GlideScope®, but improved with the CMAC® [1.32 (1.08-1.62); P=0.007] compared with DL. There was greater first-pass intubation with VL compared with DL amongst novice/trainee clinicians [OR=1.95 (1.45-2.64); P<0.001], but not amongst experienced clinicians or paramedics/nurses. There was no difference in first-pass intubation with VL compared with DL during cardiopulmonary resuscitation or trauma. VL compared with DL was associated with fewer oesophageal intubations [OR=0.32 (0.14-0.70); P=0.003], but more arterial hypotension [OR=1.49 (1.00-2.23); P=0.05]. In summary, VL compared with DL is associated with greater first-pass emergency intubation in the ICU and amongst less experienced clinicians, and reduces oesophageal intubations. However, VL is associated with greater incidence of arterial hypotension. Further trials investigating the utility of VL over DL in specific situations are required.

Intensive care medicine in rural sub-Saharan Africa.

We undertook an audit in a rural Ugandan hospital that describes the epidemiology and mortality of 5147 patients admitted to the intensive care unit. The most frequent admission diagnoses were postoperative state (including following trauma) (2014/5147; 39.1%), medical conditions (709; 13.8%) and traumatic brain injury (629; 12.2%). Intensive care unit mortality was 27.8%, differing between age groups (p < 0.001). Intensive care unit mortality was highest for neonatal tetanus (29/37; 78.4%) and lowest for foreign body aspiration (4/204; 2.0%). Intensive care unit admission following surgery (333/1431; 23.3%), medical conditions (327/1431; 22.9%) and traumatic brain injury (233/1431; 16.3%) caused the highest number of deaths. Of all deaths in the hospital, (1431/11,357; 12.6%) occurred in the intensive care unit. Although the proportion of hospitalised patients admitted to the intensive care unit increased over time, from 0.7% in 2005/6 to 2.8% in 2013/4 (p < 0.001), overall hospital mortality decreased (2005/6, 4.8%; 2013/14, 4.0%; p < 0.001). The proportion of intensive care patients whose lungs were mechanically ventilated was 18.7% (961/5147). This subgroup of patients did not change over time (2006, 16%; 2015, 18.4%; p = 0.12), but their mortality decreased (2006, 59.5%; 2015, 44.3%; p < 0.001).

Targets of perioperative fluid therapy and their effects on postoperative outcome: a systematic review and meta-analysis.

Perioperative fluid management plays a fundamental role in maintaining organ perfusion, and is considered to affect morbidity and mortality. Targets according to which fluid therapy should be administered are poorly defined. This systematic review aimed to identify specific targets for perioperative fluid therapy. The PubMed database (January 1993-December 2013) and reference lists were searched to identify clinical trials which evaluated specific targets of perioperative fluid therapy and reported clinically relevant perioperative endpoints in adult patients. Only studies in which targeted fluid therapy was the sole intervention were included into the main data analysis. A pooled data analysis was used to compare mortality between goal-directed fluid therapy and control interventions. Thirty-six clinical studies were selected. Sixteen studies including 1224 patients specifically evaluated targeted fluid therapy and were included into the main data analysis. Three specific targets for perioperative fluid therapy were identified: a systolic or pulse pressure variation <10-12%, an increase in stroke volume <10%, and a corrected flow time of 0.35-0.4 s in combination with an increase in stroke volume <10%. Targeting any one of these goals resulted in less postoperative complications (pooled data analysis: OR 0.53; CI95, 0.34-0.83; P=0.005) and a shorter length of intensive care unit/hospital stay, but no difference in postoperative mortality (pooled data analysis: OR 0.61; CI95, 0.33-1.11; P=0.12). This systematic review identified three goals for perioperative fluid administration, targeting of which appeared to be associated with less postoperative complications and shorter intensive care unit/hospital lengths of stay. Perioperative mortality remained unaffected.

The association between early hemodynamic variables and outcome in normothermic comatose patients following cardiac arrest.

BACKGROUND: Currently, few data exist on the association between post-cardiac arrest hemodynamic function and outcome. In this explorative, retrospective analysis, the association between hemodynamic variables during the first 24 h after intensive care unit admission and functional outcome at day 28 was evaluated in 153 normothermic comatose patients following a cardiac arrest. METHODS: Medical records of a multidisciplinary intensive care unit were reviewed for comatose patients (Glasgow Coma Scale < or = 9) admitted to the intensive care unit after successful resuscitation from an in- or an out-of-hospital cardiac arrest. The hourly variable time integral of hemodynamic variables during the first 24 h after admission was calculated. At day 28, outcome was assessed as favorable or adverse based on a Cerebral Performance Category of 1-2 and 3-5, respectively. Bi- and multivariate regression models adjusted for relevant confounding variables were used to evaluate the association between hemodynamic variables and functional outcome. RESULTS: One hundred and fifty-three normothermic comatose patients were admitted after a cardiac arrest, of whom 64 (42%) experienced a favorable outcome. Neither in the adjusted bivariate models (r(2), 0.61-0.78) nor in the adjusted multivariate model (r(2), 0.62-0.73) was the hourly variable time integral of any hemodynamic variable during the first 24 h after intensive care unit admission associated with functional patient outcome at day 28 in all patients as well as in patients after an in- or an out-of-hospital cardiac arrest. CONCLUSION: Commonly measured hemodynamic variables during the first 24 h following intensive care unit admission due to a cardiac arrest do not appear to be associated with the functional outcome at day 28.

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.

[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).

[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.

[How do I write an original article? An introduction for beginners]. / Wie schreibe ich eine Originalarbeit? Eine Anleitung für Einsteiger.

Less than 50% of abstracts presented on scientific conferences get published as full articles. This manuscript is a hands-on instruction on how to collate a scientific investigation into an article. Criteria for authorship should be decided based on the Vancouver statement. The first step is a description of materials and methods including the statistical analysis (approximately 1,000 words), which should already be done during the study itself. The second step is describing the results without interpretation (approximately 350 words); graphs are better than tables. The discussion (approximately 1,000-1,350 words) is initiated with a short description of the most important results, followed by a defence of the model employed. Subsequently, the mechanisms of the results are discussed and put into context with the results of comparable studies; the clinical implication of the most important aspects should be discussed. This is followed by the limitations of the investigation to allow a realistic classification; the conclusions should be low-key rather than exaggerated. The last step is the introduction (approximately 350 words), which has to "hit the nail on the head" in order to attract the reader; this is followed by the abstract and references. Issues that are absolutely to be avoided are insufficient preparation of the study, no answers to the hypothesis of the study, contradictions within the manuscript, superficial discussion, changing terms, reflexive sentences, and a conclusion that is not supported by the data. The first author and mentor should write the first draft of the manuscript; subsequently, the co-authors have to contribute with constructive critique to improve the article until a final draft has been achieved after several rounds of revision and further critique. A journal should be targeted where the manuscript has a realistic chance of publication. If the reviewer's comments can be answered, a careful revision is always warranted and should be performed even if the editor rejected the manuscript. All parties involved should be informed about each step of the project by the first author in order to ensure enduring success.

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.

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.

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.

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.

Cardiac failure and multiple organ dysfunction syndrome in a patient with endocrine adenomatosis.

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 x 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.