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At least 577 records · Page 32Linked to original sources
PubMed1994

Multiple organ failure syndrome in the 1990s. Systemic inflammatory response and organ dysfunction.

OBJECTIVE--This review of the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) provides an overview of a common but complex problem found in critically ill patients. It emphasizes definitions, common clinical patterns, metabolic responses, and pathophysiological changes. A brief discussion of treatment concepts is also included. DATA SOURCES--Data for this review were gathered from peer-reviewed journals, review articles by experts in SIRS/MODS, and selections from reference volumes written on SIRS/MODS. STUDY SELECTION--Reference selections were chosen on the basis of quality of research. Peer-reviewed journals were given primary consideration. Those review articles cited were felt to be essential to any discussion of SIRS/MODS. DATA EXTRACTION--Where possible, randomized, controlled, prospective studies were reviewed and conclusions used in this overview of SIRS/MODS. CONCLUSION--Our ability to care for critically ill patients has led to a new problem, SIRS and eventually MODS, which may become progressive organ failure and death. Unfortunately, these conditions are extremely frequent and carry high mortality rates. Increased oxygen consumption demands highlight the physiological response. The typical metabolic responses are characterized by hyperglycemia and accelerated protein catabolism. Unrecognized perfusion deficits, an uncontrolled septic focus, a persistent source of inflammation, or injured tissue is commonly present with SIRS/MODS and should be corrected. Restoration of oxygen transport and metabolic support are also important components of treatment. The cause of SIRS/MODS is complex and not fully understood, but multiple mediators and stimulated macrophages likely are important components and areas where treatment may well be focused.

Critical Illness↗
PubMed1996

Multiple organ failure after ingestion of pennyroyal oil from herbal tea in two infants.

BACKGROUND: Hepatic and neurologic injury developed in two infants after ingestion of mint tea. Examination of the mint plants, from which the teas were brewed, indicated that they contained the toxic agent pennyroyal oil. METHODS: Sera from each infant were analyzed for the toxic constituents of pennyroyal oil, including pulegone and its metabolite menthofuran. RESULTS: Fulminant liver failure with cerebral edema and necrosis developed in the first infant, who died. This infant was positive only for menthofuran (10 ng/mL). In the other infant, who was positive for both pulegone (25 ng/mL) and menthofuran (41 ng/mL), hepatic dysfunction and a severe epileptic encephalopathy developed. CONCLUSION: Pennyroyal oil is a highly toxic agent that may cause both hepatic and neurologic injury if ingested. A potential source of pennyroyal oil is certain mint teas mistakenly used as home remedies to treat minor ailments and colic in infants. Physicians should consider pennyroyal oil poisoning as a possible cause of hepatic and neurologic injury in infants, particularly if the infants may have been given home-brewed mint teas.

Beverages↗
PubMed2002

[Use of midazolam in postoperative sedation of patients with multiple organ failure treated with hemodiafiltration. Clinical study and pharmacokinetics].

OBJECTIVES: Evaluate the risk of accumulation of midazolam and conjugated 1-hydroxy-midazolam in high-risk ICU patients treated by continuous veno-venous haemofiltration. STUDY DESIGN: A prospective pharmocokinetic and clinical evaluation in 11 patients, with hepatic and renal failure. METHODS: Midazolam and metabolites were dosed in plasma and ultratiltration liquid by chromatography. Sedation was assessed by a simplified Ramsay score (EDS) with 4 levels. RESULTS: The mean duration of continuous infusion was 11 +/- 6 days. Peak plasma levels were over 150 ng ml-1 during the first 3 days, but normalized after that, only by drug adjustment based on scoring and clinical observation. There was no progressive accumulation of OH-midazolam, in spite of high levels (> 1000 ng ml-1). The Sieving coefficient (S) was 0.11 +/- 0.10 and 0.44 +/- 0.15 for midazolam and conjugated OH-midazolam respectively. A significant clearance (9.6 +/- 1.9 ml min-1) was observed for the conjugated products. T 1/2 beta was 11 h and was correlated with the mean time of recovery. A significant correlation was found between sedation score and both midazolam (r = 0.47) and OH-midazolam (r = 0.32). CONCLUSION: OH-midazolam risk of accumulation and significant clearance by haemodiafiltration should be taken into account in the drug adjustment in patients treated by continuous veno-venous haemofiltration.

Adjuvants, Anesthesia↗