Abnormal liver function tests associated with severe rhabdomyolysis

Rhabdomyolysis is a syndrome of skeletal muscle injury with release of cellular constituents such as potassium,phosphate,urate and intracellular proteins such as myoglobin into the circulation,which may cause complications including acute kidney injury,electrolyte disturbance and cardiac instability.Abnormal liver function tests are frequently observed in cases of severe rhabdomyolysis.Typically,there is an increase in serum aminotransferases,namely aspartate aminotransferase and alanine aminotransferase.This raises the question of liver injury and often triggers a pathway of investigation which may lead to a liver biopsy.However,muscle can also be a source of the increased aminotransferase activity.This review discusses the dilemma of finding abnormal liver function tests in the setting of muscle injury and the potential implications of such an association.It delves into some of the clinical and experimental evidence for correlating muscle injury to raised aminotransferases,and discusses pathophysiological mechanisms such as oxidative stress which may cause actual liver injury.Serum aminotransferases lack tissue specificity to allow clinicians to distinguish primary liver injury from muscle injury.This review also explores potential approaches to improve the accuracy of our diagnostic tools,so that excessive or unnecessary liver investigations can be avoided.     

Behandlung des Morbus Sudeck

Complex regional pain syndrome (CRPS) was formerly known as “Sudeck’s atrophy”. The disease belongs to the group of neuropathic pain syndromes and is differentiated into three types. Type I is characterized by a lack of nerve lesions, type II by the presence of nerve lesions, and type III by the presence of other entities such as fibromyalgia. The exact pathogenic factors leading to the disease are still unknown and are currently the subject of investigation in various studies. These studies suggest a contribution of the central nervous system to the development and maintenance of CRPS. However, the clinical symptoms are well documented and include pain, autonomic changes and impaired motor function of the affected extremity. Diagnosis is based clinically on signs and symptoms. However, in a few cases radiography and scintiscanning may be useful to finalize the diagnosis. The treatment options are centred on the symptoms of pain, autonomic changes and functional impairment. A multidisciplinary treatment strategy is recommended, with surgeons, anaesthesiologists, physiotherapists and psychotherapists working together. Surgical intervention in this disease is only required in rare cases of neurological and bone pain, and the indications for such intervention are narrow and should be strictly observed.     

Free flap monitoring with continuous tissue oxygen tension measurement

Intraoperative and postoperative free flap monitoring by means of oxygen tension measurement was carried out in 11 patients. We used an invasive flexible microcatheter that allowed for measurement of oxygen tension in all types of free flaps. Two cases of the measured flaps were buried free flaps which do not allow monitoring by clinical assessment. All flaps monitored in this study survived. One case of displacement of the microcatheter occurred. In one patient, the tissue pO₂ monitor successfully detected early vascular thrombosis with subsequent reoperation and salvage of the free flap.     

Responses of CDKs and p53 in Delayed Ischemic Neuronal Death

Stroke is a debilitating disease that affects millions each year.While in many cases cerebral ischemic in jury can be limited by effectivw resuscitation or thrombolytic treatment,the injured neurons wither in a process known as delayed neuronal death(DND).Mounting evidence indicates that DND is not simply necrosis played out in slow motion but apoptosis is triggered.Of particular interest are two groups of signal proteins that participate in apoptosis-cyclin dependent kinases(CDKs) and p53-among a myriad of signaling events after an ischemic insult.Recent investigations have shown that CDKs,a family of enzymes initially known for their role in cell cycle regulation,are activated in injured neurons in DND.As for p53,new reports suggest that its up-regulation may represent a failed attempt to rescue in jured neurons,although its up-regulation was previously considered an indication of apoptosis.These observations thus rekindle an old quest to identify new neuroprotective targets to minimize the stroke damage.In this review,the author will examine the evidence that indicates the participation of CDKs and p53 in DND and then introduce pre-clinical data to explore CDK inhibition as a potential neuroprotective target.Finally,using CDK inhibition as an example,this paper will discuss the pertinent criteria for a viable neuroprotective strategy for ischemic in jury.     

Chronic occupational exposure to organic solvents

Summary Twenty-two persons (20 men and 2 women) were examined for their external and internal exposure to the glycol ether 1-methoxypropan-2-ol (PGME) during the production, leak testing and mounting of brake-hoses. For the measurement of external exposure, personal air monitoring was the method of choice. Average concentrations of PGME of 82.2 mg/m³ (22.3 ppm), 68.6 mg/m³ (18.6 ppm) and 11.3 mg/m³ (3.1 ppm) were found in the air of the brakehose production, leak test and mounting areas, respectively. For the estimation of internal exposure to PGME, this glycol ether was measured in both urine and blood. The biological samples were taken post-shift. The highest internal exposure levels were found in the brakehose production section and in the leak test area. The average post-shift concentrations for PGME in workers in the brakehose production section were 4.6 mg/l in urine and 13.5 mg/l in blood; the corresponding figures for workers in the leak test area were 4.2 mg/l in urine and 11.0 mg/l in blood. In blood and urine samples of workers engaged in the mounting area, PGME levels were below the detection limits. The elimination kinetics of PGME were also studied in three highly exposed persons, and mean excretion half-lives of PGME of approximately 4.4 h were found. On the basis of our results we made a rough calculation of a future biological tolerance value: we would except that concentrations of 38-109 mg per litre of blood and 10–31 mg per litre of urine would correspond to the German MAK value for PGME (375 mg/m³).     

Relation of elevated ST segment in the electrocardiogram to echocardiography determined wall kinetics in patients after myocardial infarct

The connection of ECG findings and disturbances of the kinetics after myocardial infarction was controlled on 104 patients in correlation to the echocardiography. The investigations were performed at discharge from hospital and in the 3rd month after infarction by means of ECG at rest and exercise electrocardiogramme as well as echocardiography. In this case was shown that the elevation of the ST-segment after anterior-wall infarction was above all the expression of an ischaemia and was in most cases accompanied by an akinesia of the anterior wall. Only patients with a precordial ST-elevation over 2 mm at rest with increase to more than 4 mm under exercise or patients with a smaller ST-elevation, but a symptom-limited performance to 50 Watt, connected with ST-elevation, ventricular extrasystoles or pathological diastolic pressure of the pulmonary arteries as withdrawal criterion belonged to the group with dyskinesias and aneurysms, respectively.     

Longitudinal study on potential neurotoxic effects of aluminium: II. Assessment of exposure and neurobehavioral performance of Al welders in the automobile industry over 4 years

Objectives  

This is the second of two parallel longitudinal studies investigating Al exposure and neurobehavioral health of Al welders over 4 years. While the first published study in the trail and truck construction industry examined the neurobehavioral development of Al welders from age 41–45 in the group mean (Kiesswetter et al. in Int Arch Occup Environ Health 81:41–67, 2007), the present study in the automobile industry followed the development from 35 to 39. Although no conspicuous neurobehavioral developments were detected in the first study, which furthermore exhibited the higher exposure, it cannot be excluded that exposure effects appear in earlier life and exposure stages.