Biomedical subjects

Klaus Kunze

Publications and source records attributed to Klaus Kunze.

2 recordsLinked to original sources

PubMed2002

Metabolic encephalopathies.

Metabolic encephalopathies, usually multifactorial in origin, may be important complications of many diseases of patients treated in a critical care unit. In many cases these complications arise from more than one cause. Neurological signs of metabolic encephalopathies, ancillary tests and differential diagnosis, etiology and pathophysiology are discussed. In this context major single causes for metabolic encephalopathies are referred to. Metabolic encephalopathies as diseases per se (e. g. Wernicke's encephalopathy) and encephalopathies as consequences of deteriorating known diseases (e. g. renal or hepatic diseases) and encephalopathies as complications in patients treated with other diseases in the ICU have to be differentiated. Encephalopathies are known to be the most common complication of a large group of diseases treated in the ICU; on the other hand, manifestation of metabolic encephalopathy can be taken as a warning of deterioration or beginning organ dysfunction. So it would be misleading so far to reduce the clinical concept of metabolic encephalopathies in ICH to septic encephalopathy only.

Animals↗

PubMed2002

Decreased plasma and cerebrospinal fluid ascorbate levels in patients with septic encephalopathy.

Septic encephalopathies rapidly affect brain function without the involvement of a specific area causing a broad range of reversible neurologic symptoms. Capillary leakage including dysfunction of the blood-brain barrier has been proposed as a potential pathogenic mechanism in this entity. We tested the hypothesis that oxidative stress measured in plasma and cerebrospinal fluid (CSF) of patients suffering from septic encephalopathy could be linked to the neurologic symptoms of the disease. The neurologic symptoms of eleven patients with septic encephalopathy were described semiquantitatively through a score system. The ascorbate levels were significantly lower in both plasma and CSF from patients with septic encephalopathy than controls, and in CSF but not plasma this decrease correlated with the severity of neurologic symptoms. No significant changes were found for alpha-tocopherol. Our findings suggest that the short-term oxidative stress may be an important factor in the development of septic encephalopathy, possibly through dysregulation of the blood-brain barrier.

Antioxidants↗