Executive Summary Introduction Methodology Used to Prepare the Guideline Epidemiology Incidence Etiology Major Epidemiologic Points Pathogenesis Major Points for Pathogenesis Modifiable Risk Factors Intubation and Mechanical Ventilation Aspiration, Body Position, and Enteral Feeding Modulation of Colonization: Oral Antiseptics and Antibiotics Stress Bleeding Prophylaxis, Transfusion, and Glucose Control Major Points and Recommendations for Modifiable Risk Factors Diagnostic Testing Major Points and Recommendations for Diagnosis Diagnostic Strategies and Approaches Clinical Strategy Bacteriologic Strategy Recommended Diagnostic Strategy Major Points and Recommendations for Comparing Diagnostic Strategies Antibiotic Treatment of Hospital-acquired Pneumonia General Approach Initial Empiric Antibiotic Therapy Appropriate Antibiotic Selection and Adequate Dosing Local Instillation and Aerosolized Antibiotics Combination versus Monotherapy Duration of Therapy Major Points and Recommendations for Optimal Antibiotic Therapy Specific Antibiotic Regimens Antibiotic Heterogeneity and Antibiotic Cycling Response to Therapy Modification of Empiric Antibiotic Regimens Defining the Normal Pattern of Resolution Reasons for Deterioration or Nonresolution Evaluation of the Nonresponding Patient Major Points and Recommendations for Assessing Response to Therapy Suggested Performance Indicators

Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia the official statement of the American Thoracic Society and the Infectious Disease Society of America (特集 救急診療ガイドライン) -- (海外のガイドライン)

Areas of general agreement: Total creatine kinase (CK) levels depend on age, gender, race, muscle mass, physical activity and climatic condition. High levels of serum CK in apparently healthy subjects may be correlated with physical training status, as they depend on sarcomeric damage: strenuous exercise that damages skeletal muscle cells results in increased total serum CK. The highest postexercise serum enzyme activities are found after prolonged exercise such as ultradistance marathon running or weight-bearing exercises and downhill running, which include eccentric muscular contractions. Total serum CK activity is markedly elevated for 24 h after the exercise bout and, when patients rest, it gradually returns to basal levels. Persistently increased serum CK levels are occasionally encountered in healthy individuals and are also markedly increased in the pre-clinical stages of muscle diseases. Areas that are controversial: Some authors, studying subjects with high levels of CK at rest, observed that, years later, subjects developed muscle weakness and suggested that early myopathy may be asymptomatic. Others demonstrated that, in most of these patients, hyperCKemia probably does not imply disease. In many instances, the diagnosis is not formulated following routine examination with the patients at rest, as symptoms become manifest only after exercise. Some authors think that strength training seems to be safe for patients with myopathy, even though the evidence for routine exercise prescription is still insufficient. Others believe that, in these conditions, intense prolonged exercise may produce negative effects, as it does not induce the physiological muscle adaptations to physical training given the continuous loss of muscle proteins. Growing points: High CK serum levels in athletes following absolute rest and without any further predisposing factors should prompt a full diagnostic workup with special regards to signs of muscle weakness or other simple signs that, in both athletes and sedentary subjects, are not always promptly evident. These signs may indicate subclinical muscle disease, which training loads may evidence through the onset of profound fatigue. It is probably safe to counsel athletes with suspected myopathy to continue to undertake physical activity at a lower intensity, so as to prevent muscle damage from high intensity exercise and allow ample recovery to favour adequate recovery.

Creatine kinase monitoring in sport medicine

Muscle tissue may be damaged following intense prolonged training as a consequence of both metabolic and mechanical factors. Serum levels of skeletal muscle enzymes or proteins are markers of the functional status of muscle tissue, and vary widely in both pathological and physiological conditions. Creatine kinase, lactate dehydrogenase, aldolase, myoglobin, troponin, aspartate aminotransferase, and carbonic anhydrase CAIII are the most useful serum markers of muscle injury, but apoptosis in muscle tissues subsequent to strenuous exercise may be also triggered by increased oxidative stress. Therefore, total antioxidant status can be used to evaluate the level of stress in muscle by other markers, such as thiobarbituric acid-reactive substances, malondialdehyde, sulfhydril groups, reduced glutathione, oxidized glutathione, superoxide dismutase, catalase and others. As the various markers provide a composite picture of muscle status, we recommend using more than one to provide a better estimation of muscle stress.

Biochemical markers of muscular damage.

Tracheobronchial foreign bodies: presentation and management in children and adults.

This article emphasizes significant recent advances regarding heat stress and its impact on exercise performance, adaptations, fluid electrolyte imbalances, and pathophysiology. During exercise-heat stress, the physiological burden of supporting high skin blood flow and high sweating rates can impose considerable cardiovascular strain and initiate a cascade of pathophysiological events leading to heat stroke. We examine the association between heat stress, particularly high skin temperature, on diminishing cardiovascular/aerobic reserves as well as increasing relative intensity and perceptual cues that degrade aerobic exercise performance. We discuss novel systemic (heat acclimation) and cellular (acquired thermal tolerance) adaptations that improve performance in hot and temperate environments and protect organs from heat stroke as well as other dissimilar stresses. We delineate how heat stroke evolves from gut underperfusion/ischemia causing endotoxin release or the release of mitochondrial DNA fragments in response to cell necrosis, to mediate a systemic inflammatory syndrome inducing coagulopathies, immune dysfunction, cytokine modulation, and multiorgan damage and failure. We discuss how an inflammatory response that induces simultaneous fever and/or prior exposure to a pathogen (e.g., viral infection) that deactivates molecular protective mechanisms interacts synergistically with the hyperthermia of exercise to perhaps explain heat stroke cases reported in low-risk populations performing routine activities. Importantly, we question the "traditional" notion that high core temperature is the critical mediator of exercise performance degradation and heat stroke. Published 2011. This article is a U.S. Government work and is in the public domain in the USA.

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Integrated Physiological Mechanisms of Exercise Performance, Adaptation, and Maladaptation to Heat Stress

Respiratory tract infection during Hajj (pilgrimage to Mecca) is a common illness, and it is responsible for most of the hospital admissions. Influenza virus is the leading cause of upper respiratory tract infection during Hajj, and pneumonia can be serious. Taking into account the close contacts among the pilgrims, as well as the crowding, the potential for transmission of M. tuberculosis is expected to be high. These pilgrims can be a source for spreading infection on their return home. Although vaccination program for influenza is implemented, its efficacy is uncertain in this religious season. Future studies should concentrate on prevention and mitigation of these infections.

Respiratory tract infection during Hajj

Overlooked inhaled foreign bodies: late sequelae and the likelihood of recovery

Pulmonary artery diameter (PAD), the ratio of PAD to the ascending aorta diameter, right pulmonary artery diameter, and left pulmonary artery diameter, measured by using CT, were of limited utility in the prediction of pulmonary hypertension in patients with interstitial lung disease (ILD) compared with those without ILD.

Prediction of Pulmonary Hypertension in Patients with or without Interstitial Lung Disease: Reliability of CT Findings

We measured serum creatine kinase (CK), lactate dehydrogenase (LD), aspartate aminotransferase (AST), and serum alanine aminotransferase (ALT) in 26 heat stroke (HS) victims and 10 control (non-heat-exhausted) subjects during annual Hajj in Makkah, Saudi Arabia. On admission to the HS treatment unit, serum CK, AST, ALT, and LD were higher in HS victims than controls (P < 0.05), and at 6, 12, and 24 h were higher than baseline concentration. The patient group was divided into three groups, (a) those who had a quick recovery, (b) those who were critically ill until the end of the Hajj period (7 days), and (c) those who died. Serum enzymes at the time of admission were significantly higher (P < 0.05) in the nonsurviving group (n = 6) and the severely ill (n = 9) than in those who had a quick recovery (n = 11). ROC curves were plotted for each enzyme. The most useful indicator was LD, as it could distinguish significantly between the groups who died and those who had a quick recovery (area under the curve = 0.991 +/- 0.0286). It was followed by CK and AST as useful prognostic factors. When compared with ROC curves for body temperature, anion gap, and serum potassium, the enzyme results were superior prognostic indicators.

Serum enzymes in heat stroke: prognostic implication

Objective: The aim of this study was to investigate, for the first time, the factors associated with resistance to antituberculous drugs in Saudi Arabia, and to follow the long-term trends in drug resistance.



Methodology: A retrospective study of patients with positive Mycobacterium tuberculosis recorded at the Riyadh Tuberculosis Center in 1990 was undertaken. The resistance figures from the same centre for the period July 1996 to June 1997 were reviewed for comparison.



Results: Resistance was significantly higher in those previously treated (71%) than in those who denied previous treatment (34%). There was a trend towards association of resistance with cavitatory, multilobar, and acid fast bacilli-positive cases. Nationality (Saudis, Yemenis, others) had no significant effect on resistance. The Riyadh Region now has the same high prevalence of rifampicin resistance as previously reported in the Western Region of the Kingdom. The figures on resistance for the years 1986-88, 1990, and 1996-97 were: isoniazid 19.5/13.8/11.1%, rifampicin 10/20.7/24.6%, streptomycin 5/22/27.4%, ethambutol 3.7/3.9/1.8%, respectively. The reduction in isoniazid and ethambutol resistance coincided with a rise in resistance to rifampicin and streptomycin. We speculate that this resulted from the fact that isoniazid and ethambutol are restricted only to the treatment of tuberculosis and cannot, by law, be dispensed by general practitioners or private pharmacies. Rifampicin and streptomycin, however, are widely used for brucellosis; an endemic disease in Saudi Arabia where up to 12 weeks of rifampicin therapy is recommended.



Conclusions: There has been a significant increase in rifampicin and streptomycin resistance in Saudi Arabia over the last 10 years. Possible causes include poor compliance and wide use of these two drugs for non-tuberculosis conditions. These findings could jeopardize the benefits of the directly observed therapy short course policy which is being implemented in Saudi Arabia. Consideration should be given to prohibiting the routine use of rifampicin for the treatment of brucellosis.

Abdulaziz H. Alzeer

Papers

Respiratory tract infection during Hajj

Overlooked inhaled foreign bodies: late sequelae and the likelihood of recovery

Prediction of Pulmonary Hypertension in Patients with or without Interstitial Lung Disease: Reliability of CT Findings

Serum enzymes in heat stroke: prognostic implication

Progressive rise of Mycobacterium tuberculosis resistance to rifampicin and streptomycin in Riyadh, Saudi Arabia.