Does the Direct Bilirubin/Total Bilirubin Ratio Reflect Prognosis in Acute Hepatic Failure?

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The direct bilirubin/total bilirubin (D/T) ratio, which is not affected by such therapy as plasma exchange (PE), has been need for the determination of severity of acute hepatic failure. We studied 20 patients with acute hepatic failure who had received PE to examine whether the D/T ratio reflects prognosis, in association with tumor necrosis factor-alpha (TNF-a). Total bilirubin before the final PE was significantly higher than that before the initial PE (p=0.0064). No significant difference was observed between the D/T ratios before the initial PE and at the end of PE. No significant difference was observed between TNF-a before the initial PE and before the final PE. No significant correlation was observed among total bilirubin, D/T ratio, and TNF-a. No significant difference was observed between the survivor group and the nonsurvivor group in any factor. In the nonsurvivor group, total bilirubin before the final PE was significantly higher than that before the initial PE (p=0.0217). However, no significant difference was observed between the D/T ratios before the initial PE and before the final PE in the nonsurvivor group. In this study, the rise in total bilirubin reflected ineffectiveness of treatment. However, the D/T ratio failed to become an index of prognosis.

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Clinical Profile and Management of Heart Failure in a Cardiac Center.

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Heart failure is a progressive and serious disease. In the future this syndrome is likely to become a major public health problem in a developing country like Indonesia because of an aging population and increasing frequency of some major coronary heart disease risk factors. At the moment there is no systematically collected information on the clinical profile and the pattern of management of heart failure in Indonesia. The present study sought to examine some important demographics and clinical characteristics of patients hospitalized for heart failure and the pattern of anti failure treatment as performed by cardiologist in a National Cardiac Center. All consequtive patients who were admitted because of heart failure in 2000 were included in this survey. Information was abstracted from medical records by trained personel using standardized froms. There were 397 patients (male 68%, mean age 58.14 ± 13.57 years) included in the present study. Heart failure was due to coronary artery disease in 47% of patients, hypertensive heart disease 27%, valvular heart disease 15%, cardiomyopathy 8% and others 3%. During hospitalization (mean length of stay 8.69 ± 6.61 days) 5% of the patients died, 8% complicated by stroke, and 2% developed thromboembolism. Recurrent admission rate was 39%. The results of this study showed that standard treatment for heart failure were not given equally well to all patients: ACE inhibitors 62%, beta blockers 31%, angiotensin II receptor blockers 10%, and digitalis 66%. Symptomatic treatment were given as follow: furosemid 80% HCT 6%, spirolactone 44% and nirate 66%. In summary, the present survey highlighted some important clinical characteristics patients of hospitalized for heart failure. Despite advances in the management of heart failure, patients currently hospitalized for this syndrome still have high mortality and morbidity and high readmission rate. There is still room for improvement of evidence-based therapy.

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Non-Equilibrium Method for the Non-Invasive Estimation of Arterial PCO2

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Background: Under conditions of pulmonary ventilation/perfusion mismatch, end-tidal PCO2 (ETPCO2) may severely underestimate arterial PCO2 (PaCO2). Objective: We aimed to develop a method for the accurate non-invasive estimation of PaCO2 from ETPCO2. Methods/Patients: The fact that ETPCO2 is a mixture of PCO2 from both the ventilated and perfused alveoli, and the ventilated but unperfused ones (‘alveolar deadspace’), was brought into mathematical terms. Using the model, by inspiring two gases with different CO2 content and determining the corresponding ETPCO2 values, the PCO2 of the ventilated and perfused alveoli (truePCO2) may be calculated as an estimate of PaCO2. The model was applied on 12 ventilated patients aged 53 to 78 yrs. Estimates of PaCO2 were compared to the results of invasive determination. Results: Conventional ETPCO2 and PaCO2 differed on average by 22 percent (95% confidence interval, 18 to 26). Depending on the difference between the two inspiratory PCO2 levels used, the unsigned error of the model-based estimate typically was 5 percent (95% confidence interval, 3.5 to 7) or better. Conclusion: We provide a non-invasive method for the accurate estimation of PaCO2 and suggest its implementation into ventilators for the close monitoring of pulmonary treatment response.

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Effects of Permissive Hypercapnia on Pulmonary Mechanics and Hemodynamics during Mechanical Ventilation in Severe Acute Respirat

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Objectives: To evaluate effects of permissive hypercapnia (PHC) on pulmonary mechanics and hemodynamics in patients with severe acute respiratory distress syndrome (ARDS). Methods: We observed the influence of different tidal volume (VT) on pulmonary mechanics and hemodynamics in 10 patients with severe ARDS. Results: PHC was induced by decreasing VT from 10 - 12 ml/kg (routine VT) to 6 - 8 ml/kg (small VT). Arterial oxygen pressure and saturation remained unchanged, but pulmonary venous admixture was increased (p < 0.05). Airway plateau pressure and mean pressure were also decreased markedly. C20/C, which reflects lung overdistention, was increased significantly. Mean arterial pressure, central venous pressure, pulmonary arterial pressure were not changed, while systemic vascular resistance index was decreased markedly (p < 0.05). Cardiac index (CI) and oxygen delivery (DO2) were increased (p < 0.05), while oxygen consumption remained unchanged. Conclusions: PHC, which was induced by small VT, might prevent lung overdistention and led to an increase in CI and DO2.

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The Management of Cardiogenic Shock in Acute Myocardial Infarction: Conservative vs Aggressive Approach

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Cardiogenic shock is a cardiac emergency condition defined as the inability of the heart to supply sufficient blood in order to meet the needs of tissue basal metabolism, even though the intravascular volume is sufficient. This condition occurs mainly in acute myocardial infarction. The incidence of cardiogenic shock in acute myocardial infarction remains relatively unchanged over the last 23 years despite significant advances in the management of patients have been achieved. A dilemma on what the best strategy is in managing patients still persists: should it be conservative or aggressive? The criteria of cardiogenic shock according to SHOCK trial include clinical and hemodynamic parameters such as systolic blood pressures of < 90 mmHg for 30 minutes prior to inotropic or vasopressor administration; a condition where intraaortic balloon pump (IABP) is required to maintain the systolic blood pressure of ³ 90 mmHg; evidence of decreased organ perfusion; and heart rate of ³ 60 bpm. The hemodynamic criteria include a pulmonary capillary wedge pressure of ³15 mmHg and an index cardiac output of £ 2.2/ min/ m2. Cardiogenic shock usually occurs as aresult of left ventricular failure associated with acute myocardial infarction with only < 40% of left ventricle mass involved in contraction. The main principle in the management of cardiogenic shock is to open the obstructed coronary vessels as soon as possible. It could be done either through thrombolysis or through invasive revascularization with percutaneous or surgical coronary intervention, popularly known as coronary artery bypass graft surgery (CABG). Various studies, both randomized and non-randomized, have supported more aggressive approach with early revascularization in the effort to increase patient life expectancy.

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Colloid Osmotic Pressure

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Colloid osmotic pressure measurement is easy and cannot be derived by reference to protein measurements Its measurement may have a role in predicting prognosis although this is disputed. A low colloid osmotic pressure may influence the choice of resuscitation fluid since crystalloids would depress colloid osmotic pressure further. However, colloids tend to maintain rather than raise colloid osmotic pressure. One of the most important reasons to measure colloid osmotic pressure in critically ill patients is to prevent an excessive rise in patients on renal replacement therapy. Such a rise will prolong the recovery of renal failure.

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Thyroid Storm: A Forgotten Cause of Arrhythmias with Septic Feature

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Hyperthyroidism is the condition resulting from the effect of excessive amounts of thyroid hormones on body tissues. A dramatic extreme expression of thyrotoxicosis known as thyroid strom occurs rarely but requires prompt recognition and intervention to avoid the 90 percent mortality of untreated disease. Characteristically the patient present with fever, rapid tachyarrhythmias and atrial fibrillation. High output congestive heart failure can result from the tachycardia and severe hypermetabolic state. Frequently the clinical picture is clouded by a secondary infection such as pneumonia, a viral infection, or infection of the upper respiratory tract. Because of its variable presentation and because thyroid storm is rare condition, the correct diagnosis may be missed. We report two interesting cases of thyroid storm. The first was a lady who presented with a supraventricular tachycardia and atrial fibrillation initially misdiagnosed as septicemia with arrhythmias. The second case was a man with longstanding undiagnosed hyperthyroidism who presented with threatening thyroid storm and atrial fibrillation associated with cardiomyopathy. Both patients were subsequently managed successfully at our hospital. We hope misdiagnosis and late treatment of the similar cases will be avoided in the future.

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PMN and Lymphocyte Apoptosis in the Critically Ill: Different Means, Similar Outcome

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Accidental traumatic injury remains the fifth leading cause of death in America Behind heart disease, cancer, stroke and lung disease. Frequently, patients that survive the initial injury and do not succumb to major central nervous system or internal organ damage during the first day develop inflammatory complications, which result in morbidity and mortality due to multiple organ failure/dysfunction. These complications include non-septic inflammation of damaged tissue/organs, the adult respiratory distress syndrome (ARDS), and sepsis. While apoptosis, or programmed cell death, was initially understood as a mechanism by which cells of the immune system are cleared as a means of natural cell turnover or resolution of an inflammatory response, dysregulated apoptosis can be detrimental to the organism. Here we will briefly summarize data from both experimental animal models and critically ill patients that address (1) the suppression of neutrophil apoptosis in the critically ill, (2) the increase of lymphocyte (B and T cell) apoptosis, which leads to immunosuppression, (3) inflammatory mediators, such as cytokines, which appear to play predominant roles in neutrophil and lymphocyte apoptosis, and (4) the importance of the Bcl-2 familty in the regulation of apoptosis in the critically ill. These data clearly demonstrate the complexity of the apoptotic response and, thus, justify the need to increase our understanding of apoptosis in the critically ill. Such information will provide us with new insights, and possibly offer better therapeutic targets for the management of these devastating conditions.

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Cytopathic Dysoxia Revisited

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Most patients in septic shock die from the ensuing multi-organ dysfunction syndrome (MODS) rather than the acute inflammatory process per se. How systemic inflammation produces MODS remains unknown and many conundrums exist. It has been traditionally ascribed to tissue hypoxia secondary to microvascular shunting of blood away from nutrient capillaries. However, cell death, the expected corollary, is surprisingly absent in these failed organs despite gross biochemical and functional abnormality. With increasing severity of sepsis, tissue oxygen extraction falls with a decrease (relative or absolute) in tissue oxygen consumption. Nevertheless, tissue oxygen tensions rise, suggesting cellular availability but decreased utilisation, i.e. dysoxia. As mitochondrial oxygen consumption accounts for around 90% of total body oxygen utilisation, mitochondrial dysfunction leading to bioenergetic failure is a reasonable postulate to account for the biochemical and physiological perturbations witnessed in the septic patient. Importantly, nitric oxide and other reactive species, released in vast excess in sepsis, are potent inhibitors of mitochondrial oxidative phosphorylation. We review the increasing body of evidence derived from cell, animal and patient studies that implicate dysoxia as an important mechanism underlying the pathophysiology of multi-organ dysfunction.

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The Management of Head Trauma in Children

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In the United States, head trauma is a major cause of death and disability in children. There are significant epidemiological, anatomical and physiological differences in pediatric patients, which make them susceptible to additional complications and permanent brain injury. This article presents an over view of the initial assessment and management of pediatric head trauma in the acute care setting.

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