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OBJECTIVE: To give critical care clinicians in Western nations a general overview of intensive care medicine in less developed countries and to stimulate institutional or personal initiatives to improve critical care services in the least developed countries. DATA SOURCE: In-depth PubMed search and personal experience of the authors. DATA SYNTHESIS: In view of the eminent burden of disease, prevalence of critically ill patients in the least developed countries is disproportionately high. Despite fundamental logistic (water, electricity, oxygen supply, medical technical equipment, drugs) and financial limitations, intensive care medicine has become a discipline of its own in most nations. Today, many district and regional hospitals have units where severely ill patients are separately cared for, although major intensive care units are only found in large hospitals of urban or metropolitan areas. High workload, low wages, and a high risk of occupational infections with either the human immunodeficiency virus or a hepatitis virus explain burnout syndromes and low motivation in some health care workers. The four most common admission criteria to intensive care units in least developed countries are postsurgical treatment, infectious diseases, trauma, and peripartum maternal or neonatal complications. Logistic and financial limitations, as well as insufficiencies of supporting disciplines (e.g., laboratories, radiology, surgery), poor general health status of patients, and in many cases delayed presentation of severely sick patients to the intensive care unit, contribute to comparably high mortality rates. CONCLUSION: More studies on the current state of intensive care medicine in least developed countries are needed to provide reasonable aid to improve care of the most severely ill patients in the poorest countries of the world. [ABSTRACT FROM AUTHOR]

Objective: 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.Design: Retrospective study.Patients: A total of 316 patients.Interventions: AVP infusion (4 units/hr).Measurements and Main Results: 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 of >0.5 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.Conclusions: 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. [ABSTRACT FROM AUTHOR]

Objectives: To evaluate the endocrinologic response to a combined arginine vasopressin and norepinephrine (AVP/NE) infusion in advanced vasodilatory shock, and to examine the relationship between baseline plasma AVP concentrations and the hemodynamic response to AVP.Design: Preliminary, prospective, randomized, controlled clinical study.Setting: Twenty-three-bed general and surgical intensive care unit.Patients: Thirty-eight patients with advanced vasodilatory shock. Hemodynamic and laboratory data of 34 patients have already been presented in a recently published prospective, randomized, controlled study.Interventions: Continuous AVP (4 units/hr) and NE infusion in study patients; NE infusion only in control patients.Measurements and Main Results: At baseline, 24 hrs, and 48 hrs after randomization, plasma concentrations of AVP, adrenocorticotropic hormone, cortisol, renin, angiotensin II, aldosterone, prolactin, endothelin I, and atrial natriuretic factor were determined. Hemodynamic variables were recorded at baseline and 1, 12, and 24 hrs after randomization. Linear mixed effects models were used to test for differences between groups. The relationship between AVP plasma concentrations and hemodynamic response to AVP was analyzed using linear regression analyses. AVP/NE patients exhibited significantly higher AVP (p <.001) and prolactin (p <.001) plasma concentrations during the study period; there were no significant differences in plasma concentrations of other hormones. No significant correlation was detected between plasma AVP concentrations and the increase in mean arterial pressure after 1 hr (Pearson's correlation coefficient =.134, p =.584) and after 24 hrs (Pearson's correlation coefficient = -.198, p =.417). There were further no correlations between AVP plasma concentrations and the 24-hr response to AVP therapy in heart rate (Pearson's correlation coefficient = -.065, p =.791), stroke volume index (Pearson's correlation coefficient = -.106, p =.687), and NE requirements (Pearson's correlation coefficient =.04, p =.869).Conclusions: The preliminary results of this study indicate that a combined AVP and NE infusion increases prolactin plasma concentrations in advanced vasodilatory shock. Hemodynamic effects of AVP infusion are independent of baseline plasma AVP concentrations. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To report on the incidence and risk factors associated with the development of ischemic skin lesions (ISL) in critically ill patients with catecholamine-resistant vasodilatory shock treated with a continuous infusion of arginine-vasopressin (AVP). DESIGN: Retrospective analysis. SETTING: Twelve-bed general and surgical intensive care unit in a university hospital. PATIENTS: A total of 63 critically ill patients with catecholamine-resistant vasodilatory shock. INTERVENTIONS: Continuous AVP infusion. MEASUREMENTS AND MAIN RESULTS: Demographic, hemodynamic, laboratory data, and skin status were evaluated 24 hrs before and during AVP therapy (24 and 48 hrs). Patients were grouped according to development of new ISL during AVP therapy. A mixed-effects model was used to compare groups. A multiple logistic regression analysis was used to identify independent risk factors for the development of ISL. ISL developed in 19 of 63 patients (30.2%). Thirteen of 19 patients (68%) developed ISL in distal limbs, two patients (10.5%) developed ISL of the trunk, four patients (21%) developed ISL in distal limbs and in the trunk. Five patients (26%) had additional ischemia of the tongue. Body mass index, preexistent peripheral arterial occlusive disease, presence of septic shock, and norepinephrine requirements were significantly higher in patients developing ISL. ISL patients received significantly more units of fresh frozen plasma and thrombocyte concentrates than patients without ISL. Preexistent peripheral arterial occlusive disease and presence of septic shock were independently associated with the development of ISL during AVP therapy. CONCLUSIONS: ISLs are a common complication during continuous AVP infusion in patients with catecholamine-resistant vasodilatory shock. The presence of septic shock and a history of peripheral arterial occlusive disease are independent risk factors for the development of ISL. [ABSTRACT FROM AUTHOR]

OBJECTIVE: : Early treatment in sepsis may improve outcome. The aim of this study was to evaluate how the delay in starting resuscitation influences the severity of sepsis and the treatment needed to achieve hemodynamic stability. DESIGN: : Prospective, randomized, controlled experimental study. SETTING: : Experimental laboratory in a university hospital. SUBJECTS: : Thirty-two anesthetized and mechanically ventilated pigs. INTERVENTIONS: : Pigs were randomly assigned (n = 8 per group) to a nonseptic control group or one of three groups in which fecal peritonitis (peritoneal instillation of 2 g/kg autologous feces) was induced, and a 48-hr period of protocolized resuscitation started 6 ([Delta]T-6 hrs), 12 ([Delta]T-12 hrs), or 24 ([Delta]T-24 hrs) hrs later. The aim of this study was to evaluate the impact of delays in resuscitation on disease severity, need for resuscitation, and the development of sepsis-associated organ and mitochondrial dysfunction. MEASUREMENTS AND MAIN RESULTS: : Any delay in starting resuscitation was associated with progressive signs of hypovolemia and increased plasma levels of interleukin-6 and tumor necrosis factor-[alpha] prior to resuscitation. Delaying resuscitation increased cumulative net fluid balances (2.1 ± 0.5 mL/kg/hr, 2.8 ± 0.7 mL/kg/hr, and 3.2 ± 1.5 mL/kg/hr, respectively, for groups [Delta]T-6 hrs, [Delta]T-12 hrs, and [Delta]T-24 hrs; p < .01) and norepinephrine requirements during the 48-hr resuscitation protocol (0.02 ± 0.04 [mu]g/kg/min, 0.06 ± 0.09 [mu]g/kg/min, and 0.13 ± 0.15 ug/kg/min; p = .059), decreased maximal brain mitochondrial complex II respiration (p = .048), and tended to increase mortality (p = .08). Muscle tissue adenosine triphosphate decreased in all groups (p < .01), with lowest values at the end in groups [Delta]T-12 hrs and [Delta]T-24 hrs. CONCLUSIONS: : Increasing the delay between sepsis initiation and resuscitation increases disease severity, need for resuscitation, and sepsis-associated brain mitochondrial dysfunction. Our results support the concept of a critical window of opportunity in sepsis resuscitation. [ABSTRACT FROM AUTHOR]

BACKGROUND: Current knowledge of the situation of anaesthesia in developing countries is limited. A survey of the status of education and research based on hospital records, records of the anaesthesia section, nursing records, personal observations as well as personal communication with staff, patients and hospital managers was carried out in a 1863-bed university teaching hospital located in the capital of a least developed Sub-Saharan African Country. METHODS: Classification and evaluation of the data was based on the three aspects of the role of university teaching hospitals in Western countries: (I) patient care, (II) university teaching and post-graduation training, as well as (III) research activities. The section 'patient care' was sub-divided into anaesthesia, intensive care medicine, emergency medicine, and pain therapy. The Department of Anaesthesia at the University Teaching Hospital of Lusaka, Zambia, is organized as a subdivision of the surgical department and is not involved in emergency medicine or pain therapy. Thirteen out of seventeen operating theatres, one recovery room, and a ten bed intensive care unit are serviced by the Department of Anaesthesia. RESULTS: Anaesthetic equipment, medical supplies, drugs, and consumables are all in limited supply. There are limited statistics on perioperative complications and mortality. Anaesthesia at the university teaching hospital of a least developed Sub-Saharan African Country is severely short of both a workforce and resources. CONCLUSION: We have described strategies which may help to reverse this trend, the most important of which is to promote anaesthesia as an essential specialty within hospitals in developing countries. [ABSTRACT FROM AUTHOR]

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). [ABSTRACT FROM AUTHOR]

Objective: To evaluate the effects of two arginine vasopressin (AVP) dose regimens (0.033 vs. 0.067 IU/min) on treatment efficacy, hemodynamic response, prevalence of adverse events, and changes in laboratory variables.Design: Retrospective, controlled study.Patients: A total of 78 patients with vasodilatory shock (mean norepinephrine dosage, 1.07 microg.kg-1.min-1; 95% confidence interval, 0.82-1.56 microg.kg-1.min-1).Interventions: Supplementary infusion of AVP at 0.033 (n = 39) and 0.067 IU/min (n = 39).Measurements and Main Results: Cardiocirculatory, laboratory, and clinical variables were evaluated and compared between groups before and at 0.5, 1, 4, 12, 24, 48, and 72 hrs after initiation of AVP. Treatment efficacy was assessed by the increase in mean arterial blood pressure and the extent of norepinephrine reduction during the first 24 hrs of AVP therapy. Standard tests and a mixed-effects model were used for statistical analysis. Although the relative increase in mean arterial pressure was comparable between groups (0.033 vs. 0.067 IU/min: 16.8 +/- 18.4 vs. 21.4 +/- 14.9 mm Hg, p = .24), norepinephrine could be reduced significantly more often in patients receiving 0.067 IU/min. AVP at 0.067 IU/min resulted in a higher mean arterial pressure (p < .001), lower central venous pressure (p = .001), lower mean pulmonary arterial pressure (p = .04), and lower norepinephrine requirements (p < .001) during the 72-hr observation period. Increases in liver enzymes occurred more often in patients treated with 0.033 IU/min (71.8% vs. 28.2%, p < .001). The prevalence of a decrease in cardiac index (69.2% vs. 53.8%, p = .24), decrease in platelet count (94.8% vs. 84.6%, p = .26), and increase in total bilirubin (48.7% vs. 71.8%, p = .06) was not significantly different between groups. Bilirubin levels (3.1 +/- 3.4 vs. 5.2 +/- 5.5 mg/dL, p = .04) and base deficit (-7.2 +/- 4.3 vs. -3.9 +/- 5.9 mmol/L, p = .005) were lower and arterial lactate concentrations higher (76 +/- 67 vs. 46 +/- 38 mg/dL, p < .001) in patients receiving 0.033 IU/min.Conclusions: AVP dosages of 0.067 IU/min seem to be more effective to reverse cardiovascular failure in vasodilatory shock requiring high norepinephrine dosages than 0.033 IU/min. [ABSTRACT FROM AUTHOR]

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, <0.83 pg/mL), and 32 (13.4%) met criteria for a relative AVP deficiency (AVP, <10 pg/mL, and mean arterial pressure, <70 mm Hg). In shock patients, relative AVP deficiency occurred in 22.2% (septic shock), 15.4% (postcardiotomy shock), and 10% (shock due to a severe systemic inflammatory response syndrome) (p = .316).Conclusions: AVP serum concentrations 24 hrs after intensive care unit admission were significantly increased in this mixed critically ill patient population. The lack of a correlation between AVP serum concentrations and hemodynamic parameters suggests complex dysfunction of the vasopressinergic system in critical illness. Relative and absolute AVP deficiency may be infrequent entities during acute surgical critical illness, mostly remaining without significant effects on cardiovascular function. [ABSTRACT FROM AUTHOR]