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A patient with Mediterranean spotted fever presented an initial history of enteritis, pyrexia, and rash. He subsequently developed shock, multiple organ failure, thrombocytopenia, hypocalcemia with hypercalcitoninemia, and a euthyroid sick syndrome.
We measured the level of resting energy expenditure (BEE) and its evolution in patients with multiple organ failure (MOF). We studied 30 patients requiring mechanical ventilation and sedation. REE was measured by means of a closed circuit method on days 1-5, 7, 10 and 14 after initiating the protocol. REE values between 115% and 145% of the REE calculated from the Harris-Benedict's formula were considered as moderate hypermetabolism and values above 145% as severe hypermetabolism. A predictive formula for determining caloric requirements was developed and validated in another 25 MOF patients. In the study group, 25 patients presented moderate hypermetabolism (83%) and two severe hypermetabolism(7%). Mean REE in the whole group was stable but individual patients may have had a large variability in REE. The anthropometric variables, body temperature and reason for admission predicted the REE with a coefficient of determination of 0.73, according to the model: REE= -3295 + 105.5S - 8A + 11.7 W + 7.7 H + 93.2 T + 123.1 Tr - 145.6 Su where: S = sex (male = 1, female = 0); A: age in years; W: weight in Kg; H: height in cm; T: temperature in degrees C; Tr: trauma (Tr = 1); Su: surgical (Su = 1). The reliability of the model, taken from the validation group, showed that the shrinkage was 0.8%. In conclusion, when MOF patients are sedated they present moderate hypermetabolism. Day-to-day variability of REE in the individual patients and the large variability in estimating REE with our formula preclude its clinical utility and we recommend to measure REE in MOF patients.
A new reproducible animal model of sepsis was established to investigate interrelationship between disseminated intravascular coagulation (DIC) and multiple organ failure (MOF). Sepsis was induced by injecting fecal suspension into bile duct of rabbits, in which the amount of endotoxin in circulating blood was gradually increased and manifestations of sepsis were confirmed. During 9 hours' observation period, an occurrence of hypercoagulable state leading to DIC was evidenced by the abnormal hemostaseological parameters. Simultaneously the elevation of plasma bilirubin and creatinine levels was observed, indicating the presence of liver and kidney failure, which was confirmed by the histological examination. Thereby, the present sepsis model complicates DIC and MOF with high reproducibility, which is relevant to sepsis seen in clinical patients.
OBJECTIVE: The evaluation of incidences and relating factors of severe persisting critical illness polyneuropathy (CIP) in survivors of multiple organ failure (MOF). DESIGN: Prospective study with an entry period of 24 months. Electrophysiological studies for the diagnosis of CIP were performed 1 or 2 days before the patients were discharged from the intensive care unit (ICU). Factors which might have been related to the development of CIP were identified by a retrospective chart analysis. SETTING: The interdisciplinary ICU of a university hospital. PATIENTS: Thirty-three patients who survived MOF. Sixteen of these critically ill patients developed severe sepsis due to nosocomial infections with gram-negative bacteria. RESULTS: In seven survivors of MOF and sepsis typical electrophysiological features of CIP, like spontaneous fibrillations and low compound muscle action potentials, were detectable at the time of discharge from the ICU. Seventeen patients with MOF following multiple trauma who developed no sepsis, and nine survivors of MOF with sepsis showed no signs of persisting CIP at the end of their ICU stay. Chart analysis revealed that eight survivors of MOF with sepsis and without the development of CIP had been treated with intravenous immunoglobulin (IVIG) with a dosage of 0.3 g/kg per day for 3 days immediately (within 24 h) after the diagnosis of sepsis. Four out of seven patients with MOF and sepsis who developed CIP were transferred to our ICU after the onset of sepsis and had not received IVIG treatment. The IVIG treatment in three patients was delayed for more than 24 h after the diagnosis of sepsis and was then omitted. Obviously not related to the development of CIP were aminoglycoside antibiotics, steroids, nutritional disturbances and episodes of hypotension or hypoxia. Neuromuscular blocking agents were not used during intensive care treatment. CONCLUSIONS: A high incidence of severe CIP persisting until the day of discharge from the ICU was related to gram-negative sepsis but not to MOF alone. Retrospective chart analysis suggested that early application of IVIG may prevent or mitigate this severe complication. However, these results have to be confirmed in a prospective, placebo-controlled study.
BACKGROUND: Early classification of severity of peritonitis by scoring systems, including the Mannheim peritonitis index (MPI) and the multiple organ failure (MOF) score, modulates surgical and medical management. AIM: To predict outcome of patients with peritonitis using the MPI and MOF scoring systems. METHODS: Prospective evaluation of the MPI and MOF score was performed in 80 consecutive patients with peritonitis who underwent uniform surgical treatment. Risk ratios were calculated for the MPI and other patient characteristics. Risk ratio was not calculable for the MOF score. RESULTS: Overall in-hospital mortality rate was 17.5%, including 80% of patients with MPI>29. In non-survivors the mean score was 4.8 (SD 1.46) and 33.07 (4.81) for the MOF score and MPI, respectively. Survivors had mean MOF score of 0.28 (0.20) and mean MPI of 19.39 (6.68). CONCLUSION: The MPI and MOF score provide simple and objective means to predict the outcome of patients with peritonitis.
We report two cases of axonal sensori-motor polyneuropathies complicating sepsis and multiple organ failure (MOF) among severely burned patients (total burned surface area of 35 to 40 per cent) in which no other cause of neuropathy was retrospectively identified. No steroids or neuromuscular blocking agents had been given. The date of onset was not established but the diagnosis was late, between the 30th and 45th day, at the recovery of consciousness. Regression was incomplete, with severe sequellae especially in one patient who was unable to walk 10 months after the injury. Burned patients can present with many kinds of peripheral neuropathies. Postburn polyneuropathies with nerve conduction slowing were described by Henderson. Mononeuropathies can result from nerve compression complicating unfavorable postures in comatose patients or from nerve entrapment in ischemic limbs. Polyneuropathy in postburn sepsis with MOF does not appear to have been previously reported. Postburn sepsis usually occurs in young patients, without other cause of MOF; and therefore represents a relatively "pure" sepsis syndrome.
Energy intake and energy expenditure, nitrogen intake, and urinary nitrogen excretion (or urea production rates) were measured in 35 intravenously fed patients with multiple organ failure over the course of their illness to determine to what extent nutrient requirements were met despite fluid retention. Energy and nitrogen balance were related to serial measurements of midupper-arm circumference (MAC). The target feeding regimen of 176 kJ (42 kcal)/kg fat-free mass (FFM) was achieved in only three patients and the target of 0.24 g N/kg FFM in only four. Two patterns of change in MAC were noted: a steady decrease with time and no change with time. Serial muscle biopsy data indicated that all the patients were wasting away; the maintenance of MAC in the group with no change over time was due to fluid retention. Abnormal losses were not measured, but energy and nitrogen balance in the group in which arm circumference decreased had no apparent effect on the rate of wasting.
A possible role of platelet-activating factor (PAF) in the occurrence of the two septic complications, i.e., disseminated intravascular coagulation (DIC) and multiple organ failure (MOF) was investigated, employing a rabbit model and a novel PAF antagonist E5880. By an instillation of fecal suspension into the common bile duct of the rabbit, manifestations of DIC and MOF were observed with high reproducibility by 9 hours after the septic insult. E5880 was intravenously administered to 12 rabbits for 1 hour after the septic insult at dose of 1 mg/kg (n = 6) or 3mg/kg (n = 6). All the rabbits were subjected to observation of vital signs and serial determination of laboratory tests for 9 hours and then lung, liver and kidney were removed for histological examination. Blood endotoxin level increased significantly by 9 hours after the septic insult. Although administration of E5880 did not affect the endotoxemia, the antagonist attenuated in a dose related manner laboratory manifestation of DIC such as thrombocytopenia and prolonged prothrombin time as well as that of MOF such as increase in serum bilirubin and creatinine level. The beneficial effect of E5880 on MOF was also confirmed by the histological evaluation. These observations indicated that PAF is deeply involved in the occurrence of DIC and MOF due to sepsis and E5880 may be one of the modalities to treat or prevent these two major septic complications.
OBJECTIVE: To determine whether translocation of bacteria or endotoxin occurred into the thoracic duct in patients with multiple organ failure (MOF). SUMMARY BACKGROUND DATA: Translocation of bacteria or endotoxin has been proposed as a causative factor for MOF in patients without an infectious focus, although it has rarely been demonstrated in patients at risk for MOF. Most studies have investigated the hematogenic route of translocation, but it has been argued that lymphatic translocation of bacteria or endotoxin by the thoracic duct is the major route of translocation. METHODS: The thoracic duct was drained for 5 days in patients with MOF caused either by generalized fecal peritonitis (n = 4) or by an event without clinical and microbiologic evidence of infection (n = 4). Patients without MOF who were undergoing a transthoracic esophageal resection served as controls. In lymph and blood, concentrations of endotoxin, proinflammatory cytokines, and antiinflammatory cytokines were measured. RESULTS: Endotoxin concentrations in lymph and blood of patients with MOF ranged from 39 to 63 units per liter and were not significantly different from concentrations in patients without MOF. The quantity of endotoxin transported by the thoracic duct in the study group was small. In patients with MOF, low levels of proinflammatory cytokines and high levels of antagonists of these cytokines were found. CONCLUSION: This study provides evidence that translocation (especially of endotoxin) occurs into the thoracic duct. However, these data do not support the concept that the thoracic duct is a major route of bacterial translocation in patients with MOF.
BACKGROUND AND METHODS: We investigated the effects of tempol, a membrane-permeable radical scavenger, on the multiple organ failure (MOF) caused by zymosan in the rat. Zymosan (500 mg/kg, suspended in saline solution, ip) enhances formation of reactive oxygen species, which contribute to the pathophysiology of MOF. After zymosan or saline administration, animals were monitored for 12 days. RESULTS: Treatment of rats with tempol (10, 30, or 100 mg/kg ip, 1 and 6 hrs after zymosan) attenuated the peritoneal exudation and the migration of polymorphonuclear cells caused by zymosan in a dose-dependent fashion. Tempol also attenuated the lung, liver, and intestinal injury (histology) as well as the increase in the concentrations of myeloperoxidase and malondialdehyde caused by zymosan in the lung, liver, and intestine. Immunohistochemical analysis for nitrotyrosine and for poly(adenosine 5'-diphosphate-ribose)synthetase demonstrated a positive staining in lung, liver, and intestine from zymosan-treated rats. The degree of staining for nitrotyrosine and for poly(adenosine 5'-diphosphate-ribose) synthetase was markedly reduced in tissue sections obtained from zymosan-treated rats that had received tempol (100 mg/kg ip). Furthermore, treatment of rats with tempol significantly reduced the following: a) the formation of peroxynitrite, b) the DNA damage, c) the impairment in mitochondrial respiration, and d) the decrease in the cellular concentration of oxidized nicotinamide adenine dinucleotide observed in macrophages harvested from the peritoneal cavity of rats treated with zymosan. CONCLUSION: This study provides the first evidence that tempol, a small molecule that permeates biological membranes and scavenges reactive oxygen species, attenuates the degree of MOF associated with zymosan-induced peritonitis in the rat.
Inflammatory "one hit" and "two hit" models have recently been proposed to account for the development of multiple organ failure (MOF) in trauma and critically ill surgical patients when no source of infection can be found. In the "one hit" model, the initial insult is so massive that a systemic inflammatory response syndrome is triggered and leads rapidly to MOF. In the "two hit" scenario, initially less severely injured patients eventually develop MOF as a result of a reactivation of their inflammatory response caused by an adverse and often minor intercurrent event. At first sight, the theory is attractive because it seems to fit commonly observed clinical patterns. Indeed, injured patients often respond to initial resuscitation but, after an insult of some sort, develop organ dysfunction and die. The "two hit" model is furthermore mirrored at the cellular level. Inflammatory cells are indeed susceptible of being primed by an initial stimulus and reactivated subsequently by a relatively innocuous insult. However, in the absence of clinical and biological corroboration based on cytokine secretion patterns, these models should not be accepted uncritically.
UNLABELLED: Acute lung injury is characterized by hypoxemia due to pulmonary ventilation/perfusion-mismatching. I.v. administered prostaglandin E1 (PGE1), a vasodilator with a high pulmonary clearance, has been studied in acute lung injury. Inhalation of the vasodilators nitric oxide and prostacyclin improved oxygenation by selective dilation of the pulmonary vasculature in ventilated lung areas. In the present study, PGE1 inhalation was used for treatment of acute lung injury. Fifteen patients with acute lung injury defined as PaO2/fraction of inspired oxygen (FIO2) <160 mm Hg were treated with PGE1 inhalation in addition to standard intensive care. The drug was continuously delivered via a pneumatic nebulizer. Acute physiology and chronic health evaluation system II and multiple organ failure scores were (mean +/- SEM) 33 +/- 2 and 10 +/- 0.3, respectively. Inhaled PGE1 was administered for 103 +/- 17 h at a dose of 41 +/- 2 microg/h. The PaO2/FIO2 ratio increased from 105 +/- 9 to 160 +/- 17 mm Hg (P < 0.05) and to 189 +/- 25 mm Hg (P < 0.05) after 4 h and 24 h, respectively. PGE1 inhalation decreases in mean pulmonary artery pressure and central venous pressure were not statistically significant. Mean arterial pressure, pulmonary capillary wedge pressure, cardiac output, and heart rate remained unchanged. Intensive care unit mortality was 40%. The present data suggest that inhaled PGE1 is an effective therapeutic option for improving oxygenation in patients with acute lung injury. Whether inhaled PGE1 will increase survival in acute lung injury should be investigated in a controlled prospective trial. IMPLICATIONS: In patients with severe acute lung injury and multiple organ failure, inhaled prostaglandin E1 improved oxygenation and decreased venous admixture without affecting systemic hemodynamic variables. Controlled clinical trials are warranted.
An injury or operation with tissue injury, ischemia, and sepsis provokes a neuroendocrine, immune, and inflammatory response to promote survival and heal the wound. If the injury is massive or complicated by infection, the inflammatory response may become generalized and excessive, producing organ and tissue damage and multiple-organ failure, a modern "horror autotoxicus." Many inflammatory mediators have been identified. In isolated organs, the use of blocking mediators to prevent combined ischemia-reperfusion injury is feasible. With regional ischemia, activator attenuation may be possible. It is unclear whether blockade or modulation of all or part of an excessive inflammatory response will be possible, helpful, and without hazard in patients with multisystem injuries or sepsis. Feedback loops and control mechanisms of these systems will better define such possibilities. Employment of growth factors and other protective agents to stimulate wound healing, infection control, and host resistance may be more helpful. Ultimately, prevention of multiple-organ failure requires sound surgical judgment, techniques, and organ support.
OBJECTIVES: To investigate the relationship between fibrinolytic enhancement and the development of multiple organ failure (MOF) in disseminated intravascular coagulation (DIC). To detect the useful prognostic index for outcome in DIC. DESIGN: Case-control study. SETTING: A department of internal medicine in a university hospital, a clinical division for diagnosis and treatment, mainly of respiratory diseases, hematologic diseases, DIC, and other diseases requiring critical care medicine. PATIENTS: A total of 69 DIC patients, 31 with MOF. INTERVENTIONS: None. MEASUREMENT AND MAIN RESULTS: The DIC patients with MOF had more elevated levels of tissue plasminogen activator antigen (t-PA) and plasminogen activator inhibitor antigen (PAI), and more depressed levels of plasmin-alpha2 plasmin inhibitor complex (PIC) and fibrin/fibrinogen degradation products than those without MOF, although no significant difference in thrombin-antithrombin complex (TAT) levels was observed. A fibrinolytic enhancement (shown by PIC) was parallel to an activation of blood coagulation (shown by TAT) in DIC patients without MOF, although no such fibrinolytic enhancement was provoked even by much activation of blood coagulation in DIC patients with MOF. Whereas all the patients without MOF were restored from DIC, 14 of 31 patients with MOF were unable to be restored from DIC and died. A significant increase in plasma levels of t-PA and PAI under the condition of sustained hemostatic activation was observed in the patients who died. CONCLUSION: Enhanced fibrinolysis was considered to be the important defense mechanism in preventing the development of MOF in DIC. The increases in plasma levels of t-PA and PAI were poor prognostic markers in DIC. Further careful study may be useful to clarify whether the fibrinolytic therapy is beneficial in clinical DIC patients with MOF.
Diagnostic criteria for individual organ system failure are imprecise, a factor that adds a considerable amount of ambiguity to this area of clinical research. Nonetheless, multiple organ failure is a common sequela of ARDS and other catastrophic medical and surgical illnesses that continues to limit patient survival. The cumulative weight of investigative evidence currently supports the premise that concepts of acute respiratory failure must encompass the abnormal gas exchange in the systemic as well as the pulmonary microvasculature. In this context, we need not dispense with the term ARDS, as respiratory distress applies equally to the nonpulmonary organs as well as the lungs.
PURPOSE: To review multiple organ dysfunction syndrome with respect to: 1) clinical measurement systems; 2) molecular mechanisms; and 3) therapeutic directions based upon molecular mechanisms. METHODS: The Medline, Cochrane, and Best Evidence databases (1996 to 2000), conference proceedings, bibliographies of review articles were searched for relevant articles. Key index words were multiple organ failure, multiple system organ dysfunction, sepsis, septic shock, shock, systemic inflammatory response syndrome. Outcomes prospectively defined were death and physiological reversal of end organ failure. RESULTS: Multiple organ dysfunction/failure (MODS) is the most common cause for death in intensive care units. The recognition of this syndrome in the last 30 yr may be due to advances in early resuscitation unmasking these delayed sequelae in those that would have died previously. Multiple organ dysfunction occurs after shock of varied etiologies and may be the result of unbridled systemic inflammation. As yet, therapy directed to prevent or improve MODS has not dramatically altered outcomes. CONCLUSION: Multiple organ dysfunction may serve as useful measure of disease severity for risk adjustment and outcome marker for quality of care and therapy provided. Anesthesiologists treating shock patients will note the subsequent development of MODS in the critical care unit and may be required to provide anesthetic support to these patients.
This study tries to identify Nursing Diagnoses and Interventions. It was done with a patient who was in critical health condition: multiple organs failure, in an Intensive Care Unit of a general hospital in Porto Alegre. The Case Study was the methodology used. Nursing Diagnoses is described mostly using NANDA Taxonomy. They are: Risk for Aspiration, Disuse Syndrome, Diarrhea, Risk for Infection, Impaired Tissue Integrity; and a Collaborative Problem was identified: Hypoglicemia. We have elaborated 34 Nursing Interventions for those diagnoses.
The appearance of primary HIV infection ranges from an asymptomatic presentation to a symptomatic illness resembling infectious mononucleosis. Severe unusual presentations include acute myopericarditis, renal failure, and opportunistic infections such as esophageal candidiasis, cytomegalovirus infection, and Pneumocystis jirovecii pneumonia. We report a case of multiple organ failure during primary HIV infection.