Nasogastric lansoprazole is effective in suppressing gastric acid secretion in critically ill patients.
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AIM: To evaluate the effect of nasogastric lansoprazole on acid suppression in critically ill patients. METHODS: Patients were eligible for the study if they had a nasogastric tube in place and had not received acid-suppressive agents for 3 days prior to enrolment into the study. Patients with active gastrointestinal bleeding or a baseline gastric pH > 4.0 were excluded. Patients served as their own controls during a 24 h lead-in period. Lansoprazole 30 mg was administered once daily with water through a nasogastric tube for 2 days. Intragastric pH was measured by continuous 24 h pH-metry for 3 days. RESULTS: Fifteen patients were enrolled into the study. The baseline median 24 h intragastric pH was 2.25 +/- 1.01, and increased to 6.70 +/- 0.82 (P= 0.001) after 2 days of lansoprazole. Mean percentage of time intragastric pH was > or = 4.0 was 25 +/- 13% at baseline, and increased to 84 +/- 14% (P=0. 001) after 2 days of lansoprazole. CONCLUSIONS: Nasogastric lansoprazole 30 mg daily is effective in suppressing gastric acid secretion in critically ill patients. (+info)
Effects of glutamine supplementation, GH, and IGF-I on glutamine metabolism in critically ill patients.
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During critical illness glutamine deficiency may develop. Glutamine supplementation can restore plasma concentration to normal, but the effect on glutamine metabolism is unknown. The use of growth hormone (GH) and insulin-like growth factor I (IGF-I) to prevent protein catabolism in these patients may exacerbate the glutamine deficiency. We have investigated, in critically ill patients, the effects of 72 h of treatment with standard parenteral nutrition (TPN; n = 6), TPN supplemented with glutamine (TPNGLN; 0.4 g x kg(-1) x day(-1), n = 6), or TPNGLN with combined GH (0.2 IU. kg(-1). day(-1)) and IGF-I (160 microg x kg (-1) x day(-1)) (TPNGLN+GH/IGF-I; n = 5) on glutamine metabolism using [2-(15)N]glutamine. In patients receiving TPNGLN and TPNGLN+GH/IGF-I, plasma glutamine concentration was increased (338 +/- 22 vs. 461 +/- 24 micromol/l, P < 0.001, and 307 +/- 65 vs. 524 +/- 71 micromol/l, P < 0.05, respectively) and glutamine uptake was increased (5.2 +/- 0.5 vs. 7.4 +/- 0.7 micromol x kg(-1) x min(-1), P < 0.05 and 5.2 +/- 1.1 vs. 7.6 +/- 0.8 micromol x kg(-1) x min(-1), P < 0.05). Glutamine production and metabolic clearance rates were not altered by the three treatments. These results suggest that there is an increased requirement for glutamine in critically ill patients. Combined GH/IGF-I treatment with TPNGLN did not have adverse effects on glutamine metabolism. (+info)
Survival and functional outcome after prolonged intensive care unit stay.
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OBJECTIVE: To examine the functional outcome and costs of a prolonged illness requiring a stay in the surgical intensive care unit (SICU) of 7 of more days. SUMMARY BACKGROUND DATA: The long-term benefits and costs after a prolonged SICU stay have not been well studied. METHODS: All patients with an SICU length of stay of 7 or more days from July 1, 1996, to June 30, 1997, were enrolled. One hundred twenty-eight patients met the entry criteria, and mortality status was known in 127. Functional outcome was determined at baseline and at 1, 3, 6, and 12 months using the Sickness Impact Profile score, which ranges from 0 to 100, with a score of 30 being severely disabled. Hospital costs for the index admission and for all readmissions to Johns Hopkins Hospital were obtained. All data are reported as median values. RESULTS: For the index admission, age was 57 and APACHE II score was 23. The initial length of stay in the ICU was 11 days; the hospital length of stay was 31 days. The Sickness Impact Profile score was 20.2 at baseline, 42.9 at 1 month, 36.2 at 3 months, and 20.3 at 6 months, and was lower than baseline at 1 year. The actual 1-year survival rate was 45.3%. The index admission median cost was $85,806, with 65 total subsequent admissions to this facility. The cost for a single 1-year survivor was $282,618 (1996). CONCLUSIONS: An acute surgical illness that results in a prolonged SICU stay has a substantial in-hospital death rate and is costly, but the functional outcome from both a physical and physiologic standpoint is compatible with a good quality of life. (+info)
Contrast echocardiography clarifies uninterpretable wall motion in intensive care unit patients.
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OBJECTIVES: The study examined the value of contrast echocardiography in the assessment of left ventricular (LV) wall motion in intensive care unit (ICU) patients. BACKGROUND: Echocardiograms done in the ICU are often suboptimal. The most common indication is the evaluation of LV wall motion and ejection fraction (EF). METHODS: Transthoracic echocardiograms were done in 70 unselected ICU patients. Wall motion was evaluated on standard echocardiography (SE), harmonic echocardiography (HE), and after intravenous (IV) contrast echocardiography (CE) using a score for each of 16 segments. A confidence score was also given for each segment with each technique (unable to judge; not sure; sure). The EF was estimated visually for each technique, and a confidence score was applied to the EF. RESULTS: Uninterpretable wall motion was present in 5.4 segments/patient on SE, 4.4 on HE (p = 0.2), and 1.1 on CE (p < 0.0001). An average of 7.8 segments were read with surety on SE, 9.2 on HE (p = 0.1), and 13.7 on CE (p < 0.0001). Ejection fraction was uninterpretable in 23% on SE, 13% on HE (p = 0.14), and 0% on CE (p = 0.002 vs. HE; p < 0.0001 vs. SE). The EF was read with surety in 56% of patients on SE, 62% on HE (p = 0.47), and 91% on CE (p < 0.0001). Thus, wall motion was seen with more confidence on CE. More importantly, the actual readings of segmental wall motion and EF significantly differed using CE. CONCLUSIONS: CE should be used in all ICU patients with suboptimal transthoracic echocardiograms. (+info)
Redox imbalance in the critically ill.
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The majority of deaths amongst critically ill patients requiring intensive care are attributable to sepsis and its sequelae: septic shock, the systemic inflammatory response syndrome (SIRS) and the acute respiratory distress syndrome (ARDS). Clinically, sepsis/SIRS and ARDS are characterised by disordered vascular control, manifest as systemic hypotension and peripheral vasodilation refractory to intravascular volume resuscitation and vasopressor therapy; and pulmonary hypertension. Experimental and clinical evidence demonstrates that these patients suffer from severe oxidative stress. Thus, our own and other groups have shown that the vascular pathology of sepsis/SIRS and ARDS is initiated through the uncontrolled production of reactive oxygen (ROS) and reactive nitrogen species (RNS) which modulate inflammatory cell adhesion and cause direct injury to endothelium (Fig. 1). (+info)
Sedation and analgesia.
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Sedation is a process of soothing. The concept of the ideal level of sedation is controversial and has changed over the last decade. A shift from deep sedation, often enhanced by muscle relaxants that completely detaches the patient from their environment, to light sedation rendering the patient sleepy but easily arousable has been widely accepted. This change in attitude has been brought about by sophisticated modes of ventilation allowing the ventilator to synchronize with the patient's own breathing pattern. In addition, the increasingly recognised adverse effects of over-sedation have contributed to the reduction in the depth of sedation. (+info)
The oxygen trail: measurement.
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Tissue hypoxia may be defined as abnormal oxygen utilization such that cells are experiencing anaerobic metabolism. Tissue hypoxia can be defined biochemically by low levels of ATP, high levels of NADH, or decreased oxidized cytochrome aa3. It is possible to measure these biochemical markers in the laboratory setting with, for example, nuclear magnetic resonance spectroscopy. However, this is not as yet a clinical option. There is no 'gold standard' for the diagnosis of clinical hypoxia. We can detect the gross consequences of tissue hypoxia, such as organ dysfunction and metabolic markers of anaerobic metabolism (e.g. lactic acidosis). We have also become familiar with the measurement of both global and regional oxygen dispatch and consumption. However, organ dysfunction and metabolic acidosis consistent with established tissue hypoxia commonly exists in the presence of normal and even supra normal global measures of oxygen dispatch and consumption. Therefore, we should ideally make measurements at the end of the oxygen trail, i.e. cellular oxygen delivery and effective utilization. (+info)
The oxygen trail: the goal.
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Over the last 10 years, there have been great advances in knowledge concerning changes in tissue perfusion and its prognostic implications. Has this translated into improved patient management? We review the clinical trials that have deliberately increased tissue oxygen delivery by increasing cardiac output. We have divided the studies into those that intervene early or those that intervene late in the course of a patient's illness. Although there are methodological problems limiting interpretation of the results, we show a combined odds ratio of a reduction in mortality for the early studies but not for the late studies. We conclude that a treatment policy whereby oxygen delivery is deliberately increased improves patient outcome if it is initiated early, prior to the onset of organ failure. (+info)