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PubMed1984

Mucormycosis in patients with multiple-organ failure.

Mucormycosis in two patients with multiple-organ failure appeared as a cutaneous lesion and spread rapidly. In the first case, wet mounts and potassium hydroxide preparations were unhelpful, but a punch biopsy specimen established the diagnosis. Prompt and extensive debridement and amphotericin B administration arrested the infection. In the second case, virulent progression of the lesion occurred despite limited amputation, debridement, transfer factor, and amphotericin B, but finally responded to further amputation. Diagnosis was made by histologic examination of infected tissue. Both patients shared the following predisposing factors: sepsis, low blood flow, acidosis, multiple-organ failure, and multiple-antibiotic therapy. Although the mucormycosis was controlled, as confirmed in the first case at autopsy and in the second case by clear margins following reamputation, the outcome was fatal in both cases due to other features of multiple-organ failure.

Adult↗

PubMed1988

Endotoxaemia in multiple organ failure due to sepsis.

Patients with multiple organ failure secondary to intraabdominal sepsis are often blood culture negative despite exhibiting the features of septic shock. This study examined the possible central role of endotoxin in such patients. In 15 consecutive intensive care patients with the above clinical picture endotoxin was measured by a chromogenic limulus (LAL) assay; on admission and thereafter 4 hourly. Regular blood cultures and cultures of any primary septic focus were also performed and liver function was assessed by measurement of indocyanine-green clearance from plasma (ICGC). All 15 patients had significant endotoxaemia at least intermittently. No significant difference was observed between survivors (n = 5) and non-survivors (n = 10) in either initial or peak endotoxin levels, although the pattern of endotoxaemia differed with non-survivors exhibiting consistently high or steadily increasing levels. Of 5 patients with an intra-abdominal (I/A) septic focus only one had a positive blood culture while 5 of 10 patients with extra-abdominal (E/A) infection had positive cultures. Despite this the I/A group had higher initial and peak endotoxin levels. 3 patients with Gram-positive septicaemia had significant endotoxaemia in the absence of any gram-negative infection. Changes in ICGC appeared to be of useful prognostic significance. ICGC was significantly lower in the I/A group and in both groups there was a significant negative correlation between ICGC and the level of endotoxaemia. These results suggest that endotoxin may play a central role in the syndrome of multiple organ failure and further suggest that the endotoxin is endogenous (gut-derived) secondary to failure of hepatic filtration.

Adult↗

PubMed2001

Cytokines and inflammatory pathways in the pathogenesis of multiple organ failure following abdominal aortic aneurysm repair.

Multiple organ failure is a common mode of death following abdominal aortic aneurysm repair, particularly after rupture. Cytokines are the principal mediators of the inflammatory response to injury and high levels of circulating cytokines have been associated with poor outcome in major trauma and sepsis. Abdominal aortic aneurysm repair results in an ischaemia-reperfusion injury to the tissues distal to the site of aortic clamping. The inflammatory response in these tissues causes the release of cytokines, principally Interleukins 1-beta, 6, and 8, and Tumour Necrosis Factor alpha. If released in large enough concentrations, these cytokines may enter the circulation and gain access to organs distant to the site of initial injury. Circulating cytokines cause dysfunction of the renal, cardiovascular, respiratory, nervous and musculo-skeletal systems. The combination of these individual changes in organ function is the multiple-organ dysfunction syndrome, which may progress to multiple organ failure.

Aortic Aneurysm, Abdominal↗

PubMed2000

[Multiple organ failure in experimental pancreatitis].

BACKGROUND: Multiple organ failure (MOF) is the most severe complication and the most frequent cause of death in acute necrotizing pancreatitis (ANP). OBJECTIVE: To evaluate the components and the time course of MOF in an experimental model of ANP. METHOD: Induction of ANP in rats by a standardised bile-salt infusion into the pancreatic duct and i.v. cerulein hyperstimulation. Six hours after AP-induction animals were randomised into 4 groups to receive (I) no therapy; (II.) 4 ml/kg/h Ringer lactate (R.L) i.v.; (III) 8 ml/kg/h RL i.v.; or (IV) 4 ml/kg/h RL plus an endothelin receptor antagonist. Animals were observed for 24 hours and vital parameters were investigated. RESULTS: After 6 hrs all animals presented with severe haemoconcentration (hematokcrit > 57%) and oliguria (< 0.5 ml/6 hrs). Until 12 hrs following AP-induction in animals without therapy increased hematocrit and oliguria was observed. Animals receiving fluid resuscitation had a significant drop in hematocrit and kept their blood gas values compensated. Between 12 and 24 hrs urine production significantly increased with fluid resuscitation and respiratory parameters stabilised except for animals treated with 8 ml/kg/h RL. These animals developed arterial hypoxia and hypercapnia. CONCLUSIONS: (1) In the early phase of ANP in our model renal failure developed. (2) Massive fluid resuscitation that is necessary to increase urine output may lead to respiratory distress. (3) Reduction of intravascular fluid loss by endothelin receptor blockade is associated with improved renal and respiratory function.

Acute Kidney Injury↗

PubMed1996

Neutrophil priming and activation in the pathogenesis of postinjury multiple organ failure.

The continuing study of multiple organ failure (MOF) has led to the development of inflammatory models of tissue injury in contrast to earlier infectious models. This change of focus is in response to more recent clinical observations suggesting that postinjury MOF frequently occurs in the absence of infection. In the alternative "two-hit" inflammatory model that has been proposed, the initial traumatic insult "primes" the inflammatory response such that a delayed, otherwise innocuous, inflammatory insult triggers an exaggerated response. The neutrophil (PMN), being uniquely equipped to cause oxidative tissue injury via the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system, has been implicated as an early pivotal player in this model of postinjury MOF. Similar to the "two-hit" inflammatory model, circulating PMNs respond to proinflammatory mediators by becoming primed for enhanced superoxide anion (O2.) production and by increasing adherence to endothelium of organs that are susceptible to PMN-mediated injury. Subsequent proinflammatory insults promote further neutrophil sequestration and activate them for enhanced release of O2.-. The resulting tissue injury can be perpetuated and lead to eventual end-organ damage and failure. In terms of the NADPH oxidase system, PMN priming and activation by various agonists have been well documented in vitro and lead to increased endothelial damage. PMN priming and activation are also operable in an in vivo model of gut ischemia/reperfusion, a surrogate of shock and trauma resuscitation, leading to distant organ damage. Finally, in clinical studies of severely injured trauma patients, PMN priming and activation sequences identify patients at risk for developing MOF with its associated high mortality. Further characterization of the mechanisms that regulate PMN priming and activation in the trauma patient is necessary for the development of new therapeutic interventions designed to block deleterious PMN responses which lead to MOF while not compromising beneficial PMN functions of host defense and tissue repair.

Animals↗

PubMed1999

Multiple organ failure: by the time you predict it, it's already there.

OBJECTIVE: Validate an at-risk population to study multiple organ failure and to determine the importance of organ dysfunction 24 hours after injury in determining the ultimate severity of multiple organ failure. METHODS: We evaluated 105 patients admitted to five academic trauma centers during a 1-year period who survived for more than 24 hours with Injury Severity Scores > or = 25 and who received 6 or more units of blood. Organ dysfunction was scored daily with a modified multiple organ failure scoring system made up of individual adult respiratory distress syndrome score, renal dysfunction, hepatic dysfunction, and cardiac dysfunction scores. Multiple organ failure (MOF) severity was quantitated using the maximum daily multiple organ failure score and the cumulative sum of daily multiple organ failure scores for the first 7 days (MOF 7) and 10 days (MOF 10). Independent variables included markers of tissue injury, shock, host factors, physiologic response, therapeutic factors, and organ dysfunction within the first 24 hours after admission. Data were subjected to a conditional stepwise multiple regression analysis, first excluding and then including 24-hour MOF as an independent variable. RESULTS: Of the 105 high-risk patients, 69 (66%) developed a maximum daily multiple organ failure score > or = 1; 50 (72%) did so on day 1 one and 60 (87%) did so by day 2. In multiple regression models, the multiple correlation coefficient increased from 0.537 to 0.720 when maximum MOF was the dependent variable, from 0.449 to 0.719 when maximum daily MOF was the dependent variable, from 0.519 to 0.812 when MOF 7 was the dependent variable, and from 0.514 to 0.759 when MOF 10 was the dependent variable. CONCLUSION: We have confirmed that the population of patients with Injury Severity Scores > or = 25 who received 6 or more units of blood represent a high-risk group for the development of multiple organ failure. Our data also indicate that multiple organ failure after trauma is established within 24 hours of injury in the majority of patients who develop it. It appears that multiple organ failure is already present at the time when most published models are trying to predict whether or not it will occur.

Adult↗

PubMed1997

Rehabilitation results of patients with multiple injuries and multiple organ failure and long-term intensive care.

BACKGROUND: Multiple organ failure is regarded to be the major complication of trauma victims treated in the intensive care unit. Long-term rehabilitation results of this special group of patients have not been analyzed so far. METHODS: Fifty patients with multiple injuries and multiple organ failure (Injury Severity Score > or = 36.8) were followed-up 4.9 +/- 0.3 years after the trauma. To show any organotopic sequelae, laboratory tests for the function of lungs, liver, kidney, and the hematologic system were performed. Additionally their functional (locomotion and neurologic system) and occupational rehabilitation results were investigated. RESULTS: The laboratory tests showed entirely normal results. The only pathologic values could be found in the lung function tests. Nineteen percent of the patients showed nonphysiologic results in either spirometry, body plethysmography, or diffusion capacity of carbon monoxide. In more than 25% of the patients, permanently decreased range of motion (limitation of more than 30% of the entire range of motion) of the elbow, hip, knee, or ankle joint were found. In 40% of the patients, permanent motoric nerve lesions were identified; in 50% of the patients, permanent sensoric nerve lesions could be verified. The return to work rate was 60%. CONCLUSIONS: Patients with multiple injuries, who survived multiple organ failure during their long-term intensive care treatment, show an excellent functional and occupational rehabilitation result. They show no major sequelae in their organ function even years after the trauma. Although often these patients suffer from permanent central or peripheral paralysis and decreased range of motion, this finding does not correlate with the patients' ability to return to work.

Activities of Daily Living↗

PubMed1989

[Polytrauma as a cause of multiple organ failure].

In recent years progress in anaesthesia and surgery has led to improvements in care for traumatized patients. This progress not only affects emergency treatment, but also critical care. Although today a failure of one organ system can be successfully treated in most cases, the problem of multiple organ failure is still unsolved. Mortality even in young patients remains high (about 30 to 90%). Among the special problems are disturbances of the patients immune system, nosocomial infections with the development of sepsis and its impact on organ functions, hypermetabolism and metabolic failure. The improved insight into the cellular and humoral pathophysiology has led to changes in diagnostic and therapeutic procedures in these patients. Only an aggressive, combined effort of many medical specialties from the beginning and an early recognition and treatment of complications and organ dysfunctions can lead to optimal results.

Critical Care↗

PubMed1989

Development of a bacteria-independent model of the multiple organ failure syndrome.

Criteria that allow definition of the multiple organ failure syndrome include pulmonary, hepatic, renal, and gut barrier dysfunction along with characteristic histopathologic changes. It has been difficult to study multiple organ failure due to lack of a satisfactory experimental model that would reproduce the pathophysiologic and histopathologic characteristics, would be stable enough to allow study over several days, and would be free of exogenous primary bacterial infection. We have studied pathophysiologic and histopathologic alterations in a potential model of multiple organ failure. Wistar rats received one of the following solutions by intraperitoneal injection: 4 mL of saline, 4 mL of mineral oil, or 1 mg per gram of body weight of zymosan A in 4 mL of mineral oil. Animals that received zymosan developed hypoxia, decreased creatinine clearance, and changes in hepatic microsomal cytochrome P450 content and aniline hydroxylase activity. Bacterial translocation occurred in the zymosan group. The lungs, liver, and kidneys of the animals that received zymosan exhibited histopathologic changes. We conclude that this model fulfills our criteria for a model of multiple organ failure.

Animals↗

PubMed2002

Candidemia as a cause of septic shock and multiple organ failure in nonimmunocompromised patients.

OBJECTIVE: To describe outcomes of septic shock and multiple organ failure arising from candidemia. DESIGN: Secondary cohort analysis of data from the placebo arm of the North American Septic Shock Trial (NORASEPT II), the largest prospective, randomized, double-blind, controlled multiple center study of septic shock conducted to date, with predetermined end point analysis of outcomes. SETTING: Adult intensive care units in 105 hospitals in the United States and Canada. SUBJECTS: A cohort of ten purely candidemic patients in septic shock were compared with a cohort of 376 purely bacteremic patients in septic shock. Patients were not immunocompromised, because patients on corticosteroids, with neutropenia, or posttransplantation were excluded from enrollment in NORASEPT II. MEASUREMENTS AND MAIN RESULTS: Demographic variables, baseline characteristics, 28-day mortality rates, and multiple organ failure were compared for the two cohorts. Candidemic patients were more likely to have a history of underlying renal failure at baseline and to require dialysis at onset of septic shock. Both causes of septic shock are associated with an extremely high severity of illness (Acute Physiology and Chronic Health Evaluation II: candidemic septic shock, 32 +/- 10; bacteremic septic shock, 30 +/- 8; p =.44). More than 70% of patients with candidemia and septic shock were in multiple organ failure at days 3, 7, and 14; patients with candidemic septic shock sustained persistent multiple organ failure and showed delayed recovery from multiple organ failure compared with patients with bacteremic septic shock. Mortality rate at 28 days was 60% in candidemic septic shock and 46% in bacteremic septic shock (p =.38). CONCLUSIONS: Candidemia with septic shock is infrequent in nonimmunocompromised patients but has a very high mortality rate, a high likelihood of associated multiple organ failure, and possibly a delayed recovery from multiple organ failure. Patients with candidemic septic shock are more likely to have underlying renal failure at baseline.

APACHE↗

PubMed2003

Multiple organ failure in trauma patients.

SUMMARY: BACKGROUND As care of the critically ill patient has improved and definitions of organ failure have changed, it has been observed that the incidence of organ failure and the mortality associated with organ failure appear to be decreasing. In addition, many early studies included large heterogeneous populations of both medical and surgical patients that may have influenced the incidence and outcome of organ failure. The purpose of this study is to establish the current incidence and mortality of organ failure in a homogenous population of critically ill trauma patients. METHODS All trauma patients admitted to the intensive care unit (ICU) at an urban Level I trauma center were prospectively studied. Patients were evaluated for the presence of organ failure using definitions proposed by Knaus and by Fry. Newer definitions of organ failure incorporating organ dysfunction and severity-of-illness scores were also obtained in all patients in an attempt to predict outcome. These included lung injury scores (acute respiratory distress syndrome scores), Acute Physiology and Chronic Health Evaluation (APACHE) II and III scores, Injury Severity Score (ISS), and multiple organ dysfunction scores. Primary outcomes assessed were death and the occurrence of organ failure by the various definitions. RESULTS Eight hundred sixty-nine trauma patients were admitted to the ICU and survived longer than 48 hours. Mean APACHE II and APACHE III scores at admission to the ICU and ISS were 12.2 +/- 22, 30.5 +/- 22.7, and 19 +/- 10, respectively. Single organ failure (SOF) occurred in 163 patients (18.7%) and multiple organ failure occurred in 44 patients (5.1%). All SOF was caused by respiratory failure. Respiratory failure occurred first in the majority of patients with multiple organ failure. Mortality was 4.3% with one organ system failure, 32% with two, 67% with three, and 90% when four organ systems failed. None of the patients with SOF died secondary to respiratory failure. Multiple stepwise regression analysis was performed to determine which of the following risk factors are associated with the occurrence of organ failure: mechanism of injury, lactate at 24 hours, ISS, APACHE II, APACHE III, acute respiratory distress syndrome score at admission, multiple organ dysfunction score at admission and total blood products transfused in 24 hours. Of these factors, APACHE III, lactate at 24 hours, and total blood products transfused in 24 hours were associated with the occurrence of organ failure. CONCLUSION The overall incidence of organ failure in a homogeneous trauma population appears to be lower than that reported in studies performed in heterogeneous patient populations in the 1980s. Mortality for SOF is low and appears to be related primarily to the patient's underlying injuries and not to organ failure. Mortality for two or three organ system failures is lower than reported 15 to 20 years ago. Mortality for patients with four or more organ system failures remains high, approaching 100%.

APACHE↗

PubMed1998

[The intestine as the central organ in the development of multiple organ failure after severe trauma--pathophysiology and therapeutic approaches].

Multiple organ failure is with an incidence of 10-25% and a mortality of 50-70% the most severe complication after severe trauma. Intestinal ischemia and a corresponding impaired gut barrier function is thought to have a high impact on the development of multiple organ failure after severe trauma. Under normal conditions the intestinal wall is a sufficient barrier against bacteria and their products. Gut ischemia is followed by mucosal lesions, the intestinal permeability is increased. Translocating bacteria and bacterial products (endotoxin, peptidoglykan) can lead to a local and/or systemic immun-inflammatory response, which is made responsible for the development of multiple organ failure. Tonometry as a possibility of monitoring intestinal ischemia as well as a tool to estimate the prognosis of multiple trauma patients is still discussed controversially. Dopexamin, which directly influences intestinal ischemia (goal directed therapy) might be a successful treatment option, however until now no clinical study about beneficial effects of dopexamine in severely injured patients is available. Selective gut decontamination showed no clinical benefits in multiple trauma patients. Early enteral nutrition especially with immunomodulating ingredients ("immunonutrition") decreases posttraumatic complications as well as the incidence of MOF. However a reduction of mortality could not be described in severely injured patients so far.

Bacterial Translocation↗

PubMed1996

Aprotinin prevents the development of the trauma-induced multiple organ failure in a chronic sheep model.

Trauma-induced multiple organ failure in sheep was prevented by aprotinin therapy. Multiple organ failure was induced in 16 female merino sheep by initial haemorrhagic shock and intramedullary femoral nailing (day 0), and 12 hourly injections of 0.75 micrograms/kg Escherichia coli endotoxin +0.7 ml/kg zymosan-activated plasma (days 1-5). In addition, the aprotinin group (n = 6) received simultaneous injections of 5 mg/kg (35 695 KIU/kg) aprotinin, whereas ten animals did not receive aprotinin and served as the control group (n = 10). Organ functions were monitored for a total of 11 days by measuring haemodynamic, cardio-respiratory and biochemical quantities of blood, urine and epithelial lining fluid. During the subsequent eleven day period, aprotinin induced a significant (p < 0.05) reduction of the pathological changes (development of multiple organ failure) seen in the control group. Thus, aprotinin prevented an alteration of cardiac function (cardiac index for control/aprotinin groups at day 1: 6.5/6.2, and at day 10: 10.47/7.0 1/min x m2), an impairment of lung function (mean pulmonary arterial pressure at day 1: 2.26/1.86, and at day 10: 3.83/2.13 kPa; epithelial lining fluid/plasma ratio of albumin concentrations as a direct marker of lung capillary permeability damage at day 0: 0.18/0.16, and at day 10: 0.45/0.15), a deterioration of liver function (plasma sorbitol dehydrogenase at day 0: 7.9/7.6, and at day 10: 29.6/7.4 U/1), but not of renal function (creatinine clearance at day 1: 91.4/66.1, and at day 10: 53.1/59.2 ml/min). Urinary aprotinin excretion increased up to day 3, then decreased rapidly despite further aprotinin administration. As a non-specific marker of cell damage, plasma lactate dehydrogenase indicated an aprotinin-induced organ protection (day 0: 501/409, and at day 10: 719/329 U/1). The neutrophil count and the measured chemiluminescence of neutrophils from the blood and epithelial lining fluid showed that aprotinin reduced the in vivo neutrophil activation, the alveolar neutrophil invasion, the production of inflammatory mediators, and the production of reactive oxygen metabolites during the passage of the capillary-interstitial-alveolar space by neutrophils.

Animals↗

PubMed2000

Impact of acute renal failure on antioxidant status in multiple organ failure.

BACKGROUND: Acute renal failure (ARF) can be triggered or aggravated by reactive oxygen species (ROS) but established ARF per se might also affect the antioxidant defence mechanisms of the organism. We evaluated a broad pattern of antioxidants in critically ill patients with multiple organ failure with (MOF-ARF) and without acute renal failure (MOF) to identify any potential involvement of renal dysfunction in the depletion of the antioxidant system. METHODS: Observational study; 13 patients with MOF were investigated (9 with and 4 without ARF), and 17 healthy subjects served as controls. Blood samples were drawn after establishment of MOF. Plasma levels of ascorbate, alpha-tocopherol, retinol, beta-carotene, selenium and lipid peroxidation products (MDA) were determined and the activities of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione-peroxidase (GSH-PX) in erythrocytes were measured. In addition, ROS production (superoxide anion and hydrogen peroxide) in activated neutrophils was assessed. RESULTS: Plasma levels of ascorbate, beta-carotene and selenium were reduced in both patient groups, when compared to controls. Decrease in selenium was more pronounced in the MOF-ARF group. MDA levels were increased in both groups, again being more pronounced in MOF-ARF patients compared to MOF patients. Hydrogen peroxide production by neutrophils from both patient groups was lower than from controls. CONCLUSION: A depression of the antioxidative system is present in critically ill patients with MOF. In patients with associated ARF this was even more pronounced and plasma MDA levels were higher, suggesting an additional effect on the antioxidative potential in the presence of renal dysfunction and/or renal replacement therapy.

Acute Kidney Injury↗

PubMed1987

[Acute lung failure within the scope of multiple organ failure].

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Critical Care↗

PubMed2005

The effects of selective nitric oxide synthase blocker on survival, mesenteric blood flow and multiple organ failure induced by zymosan.

BACKGROUND: Circulatory failure in multiple organ dysfunction syndromes (MODS) is characterized with systemic vasodilation, diminished blood flow to various vascular beds. The aim of this study was to investigate the effects of selective inhibition of nitric oxide on the mesenteric arterial blood flow (MABF), survival and organ injury of the liver, kidney, lung and spleen in zymosan-induced MODS. MATERIALS AND METHODS: Forty Swiss albino mice (20-40 g), 7 to 9 weeks old, were obtained. Animals were randomly divided into four groups. The first group were treated intraperitoneally (i.p) with vehicle (saline) and served as a sham group for aminoguanidine (AG) (n=10). The second group was treated with zymosan (500 mg/kg, suspended in saline solution, i.p). The mice in the third and fourth group received AG (15 mg/kg) 1 h and 6 h after zymosan or saline administration, respectively. Eighteen hours after the administration of zymosan, animals were assessed for MODS described subsequently. The signals from the flowmeter were also recorded on mesenteric arterial blood flow values. RESULTS: In zymosan-treated animals, the MABF was significantly lower than that of solvent (saline)-treated controls (ml min(-1), controls: 4.6 +/- 0.6; zymosan: 1.6 +/- 0.9, P <0.05). When animals were treated with AG, there were no significant differences in MABF values between AG group and solvent (saline)-treated control group. However AG prevented zymosan-induced mesenteric MABF decrease. Treatment with aminoguanidine also decreased mortality. CONCLUSION: AG is capable of inhibiting both the induction and the activity of the already iNOS; it remains a potential therapeutic agent in patients with MODS.

Animals↗

PubMed1992

[Multiple organ failure after severe burns].

36 cases with multiple organ failure (MOF) in a group of 178 severe burn injury patients during 1969-1989 were observed in our department. The rate of occurrence of MOF in this group was 20.2% (36/178). 25 cases out of these 36 patients died, and the mortality rate was 69.5% (25/36). In 10 cases 2 organs were involved, and two patients died; 3 organs were involved in 13 cases and nine of them died; more than 4 organs were affected in 13 cases and all of them died. The relationship between MOF and shock, inhalation injury as well as septicemia was discussed. Although there were many factors which could induce postburn multiple organ failure (PBMOF), the severity of the injury was the most fundamental inducing factor. The severer the burn injury, the higher the morbidity and mortality of PBMOF. Both shock and inhalation injury were important inducing factors in early PBMOF. Wound sepsis and septicemia were major inducing factors in delayed PBMOF. Majority of the delayed PBMOF took place during septicemia. In consideration of the high mortality of PBMOF and lack of effective treatment at present, it is extremely important to prevent severe burn injury patients from developing PBMOF. The measures to prevent PBMOF included: to correct shock adequately as soon as possible, to select the optimal time and appropriate extent of escharotomy and skin grafting, to try our best to ensure complete or near complete take of skin grafts, and to strengthen systemic metabolic support.

Adolescent↗

PubMed1997

Emergency aortic valve replacement for critical aortic stenosis. A lifesaving treatment for patients with cardiogenic shock and multiple organ failure.

OBJECTIVE: To demonstrate that emergency aortic valve replacement can be successfully performed in patients with critical aortic stenosis and reduced left ventricular function even in cardiogenic shock with associated severe multiple organ failure. DESIGN: Retrospective, consecutive case series. SETTING: Multidisciplinary intensive care unit of a tertiary care university hospital. PATIENTS: Five patients admitted to the intensive care unit with critical aortic stenosis (aortic valve area 0.56 +/- 0.13 cm2) and greatly reduced left ventricular ejection fraction (20 +/- 3%) in prolonged cardiogenic shock and associated multiple organ failure (Multiple organ failure score 6.8 +/- 0.5; Acute Physiology, Age, and Chronic Health Evaluation III score 91 +/- 27). INTERVENTION: Emergency aortic valve replacement. RESULTS: All patients survived with full recovery of organ function. At follow-up (18 +/- 10 months) all patients were in New York Heart Association functional class I or II with improvement of left ventricular ejection fraction to 48 +/- 25%. CONCLUSIONS: This excellent outcome suggests that emergency aortic valve replacement should be strongly considered in patients with critical aortic stenosis even in cardiogenic shock and multiple organ failure.

Adult↗