Metabolic encephalopathies

Abstract

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.

Sedation, Sucralfate, and Antibiotic Use Are Potential Means for Protection against Early-Onset Ventilator-Associated Pneumonia

“…Neurological impairment, as measured by the GCS, may indicate both coma related to a neurological condition (e.g., encephalitis, meningitis, drug overuse, and suicide attempt) or altered consciousness associated with sepsis or critical conditions mimicking sepsis (e.g., pancreatitis, severe burns, and trauma without neurological impairment) [19][20][21]. Posttraumatic coma is associated with early VAP [22] but was too rare in our population to explain the association between coma and EOP.…”

Assessment of the prognosis of cirrhosis: Child–Pugh versus MELD

“…Decreased prothrombin index may be related to the activation of coagulation, the major cause of which is sepsis [11]. Metabolic encephalopathy can be precipitated by sepsis or renal insufficiency [12]. As a result, albumin, bilirubin, prothrombin and encephalopathy represent prognostic markers coming from a broader source than the pure assessment of liver 'functions'.…”

Neonatal neurological disorders involving the brainstem: neurosonographic approaches through the squamous suture and the foramen magnum

“…Many of the inborn errors of metabolism, including urea cycle defects, organic acidaemias, certain disorders of ami- no acid and fatty acid metabolism, can present with symptoms of acute metabolic encephalopathy in the neonatal period [15]. The patients with metabolic encephalopathy secondary to inborn errors of metabolism usually had an extensive hyperechoic change over the cerebral and midbrain parenchyma, suggesting diffusely edematous changes.…”