Clinical diagnosis of brain death: Prerequisites and criteria (UpToDate – login required.)
Clinical or neuroimaging evidence of an acute central nervous system (CNS) catastrophe (eg, traumatic brain injury, subarachnoid hemorrhage) Exclusion of complicating medical conditions that may confound clinical assessment (no severe electrolyte, acid-base, endocrine, or circulatory [ie, shock] disturbance) No drug intoxication or poisoning, including any sedative drug administered in hospital, which may confound the clinical assessment Core temperature >36°C (97°F) Systolic blood pressure >100 mmHg; vasopressors may be required
Coma Absent brain-originating motor response, including response to pain stimulus above the neck or other brain-originating movements (eg, seizures, decerebrate or decorticate posturing) Absent pupillary light reflex; pupils are midposition (3.5 to 4 mm) Absent corneal reflexes Absent oculocephalic (doll’s eyes) and oculovestibular reflexes (caloric responses) Absent jaw jerk Absent gag reflex Absent cough with tracheal suctioning Absent sucking or rooting reflexes (in neonates) Apnea as demonstrated by apnea test
At least 6 hours; longer time periods recommended in children and for certain conditions such as after cardiac arrest
Visceral and somatic hypersensitivity are present in some patients with functional gastrointestinal disorders
Injury to visceral afferents is the most common underlying cause of visceral hypersensitivity that is maintained by either peripheral and/or central nervous system mechanisms
Animal models of hypersensitivity have been used to examine the neural mechanisms of hypersensitivity following inflammatory injury, such as alterations in the N-methyl, D-aspartate receptor, dorsal horn neurons or c-Fos
Increased intestinal permeability might lead to hypersensitivity and abdominal pain in patients with functional gastrointestinal disorders
Functional gastrointestinal disorders are similar to other chronic pain disorders in which persistent nociceptive mechanisms are activated
Results: In total, 206 patients were administered 259 courses of cefepime, with an overall CIN incidence of 6% (16/259 courses). A total of 64 courses had a cefepime trough concentration measured (24.7%). A cefepime trough concentration of 36 mg/L provided the best differentiation between patients who experienced neurotoxicity and those who did not. No other patient covariates were identified to be significantly associated with neurotoxicity occurring.
Conclusions: A cefepime trough plasma concentration ≥36 mg/L appears to be the most sensitive and specific cut-off to predict CIN occurring. No patient factors were associated with the development of CIN when accounting for cefepime trough plasma concentrations.