Altered Mental Status and Hypothermia

Guidelines of the Polish Society of Anaesthesiology and Intensive Therapy regarding prevention of inadvertent intraoperative hypothermia

“…The body heat reserves in the initial stage of anaesthesia, in the phase of blood (and heat) redistribution, do not change; therefore, the higher the amount of heat in the body (together in the core compartment and the peripheral compartment which is usually cooler by 2-3°C), the more difficult the lowering of core temperature is, so patients with initially low core temperatures develop hypothermia more easily, and the pre-induction temperatures below 36°C are a relevant risk factor of anaesthesia-related hypothermia. Moreover, there is convincing evidence for increased incidence of this complication in patients with concomitant systemic diseases, such as hypo thyroidism, diabetic polyneuropathy, and those undergoing treatment with drugs causing thermoregulation disorders, such as anxio lytics and antiepileptic drugs [28].…”

Metabolic Abnormalities of Erythrocytes as a Risk Factor for Alzheimer's Disease

“…During the past decades, a lot of work has proved Quastel's theory to be prescient and showed that the cause-effect relation is nonspecific as impairing cerebral energy metabolism can induce mental disorders to varying degrees (confusion, mental fatigue, agnosia, or dementia) in different pathological situations. Thus, impaired mental function has been reported in association with hypoglycemia (Bruce et al, 2009 ), inadequate transportation of glucose across the blood-brain barrier (Klepper and Voit, 2002 ; Pascual et al, 2004 ), defective astroglial glutamate transportation (Rönnbäck and Hansson, 2004 ), hypoxia (Gibson et al, 1981 ), diabetes (Richardson, 1990 ), heart failure (Riegel et al, 2002 ), reduced glucose tolerance (Vanhanen et al, 1997 ), bradycardia, hypotension (Ackerman, 1974 ), high intracranial pressure (Yoshida et al, 1996 ), stroke (van der Zwaluw et al, 2011 ), hypothermia, alcohol intoxication, thiamine and vitamin C deficiency, sedative-hypnotic drugs, opioids consumption (Martindale et al, 2010 ), general anesthesia (Parikh and Chung, 1995 ; Xie et al, 2006b ), hypocapnia (Dodds and Allison, 1998 ), chronic stress (Conrad et al, 1996 ; Conrad, 2006 ), chronic noise stress (Arnsten and Goldman-Rakic, 1998 ; Manikandan et al, 2006 ), mixed brain pathologies (Schneider et al, 2007 ), hepatic encephalopathy (Butterworth, 2003 ), hyperammonemia (Llansola et al, 2007 ), trauma (Brooks et al, 2000 ), and so forth. Interestingly, after trauma, a large number of Aβ positive neurons appeared in human (Chen et al, 2004 ; Uryu et al, 2007 ) and animal brain (Kamal et al, 2001 ; Kasa et al, 2001 ; Papp et al, 2002 ; Hamberger et al, 2003 ).…”