Acute Encephalopathy

Educational Objectives

The goals of this program are to improve the diagnosis and treatment of encephalopathy. After hearing and assimilating this program, the clinician will be better able to:

1. Determine whether a patient has alterations in the level or content of consciousness and make appropriate differential diagnoses for each.

2. Change medication regimens to treat encephalopathy.

Summary

Case example: how to evaluate “change in mental status” in patient for whom little other information available

Mental status: term used to describe patients whose condition may range from obtunded to confused; important to distinguish content vs level of consciousness

Agitated vs withdrawn delirium: patients with agitated delirium require more time and effort from staff; outcome decrement identical between withdrawn and agitated patients

Anatomy: level of consciousness — maintained in brainstem, ie, reticular activating system (RAS); starts in medulla; ends at end of thalamus (intralaminar nucleus of thalamus on both sides); and projects throughout brain; network throughout cortex also responsible; content of consciousness — maintained in memory circuit, ie, Papez circuit; includes thalamus, amygdala, fornix, hippocampus, and cingulate gyrus (area highly susceptible to many medications); changes in content of consciousness often associated with medications

Delirium: underlying neural basis unclear; associated with poor outcome for unknown reasons; study (Girard et al, 2010) showed number of days of delirium predicted outcome among overall population but not individual patients; treatments alleviate symptoms but do not reverse delirium; another study showed patients with delirium have decreased brain volumes later in life (unknown whether smaller volumes preceded delirium); also unknown whether symptoms attributed to delirium actually caused by medications, eg, benzodiazepines (especially midazolam [Versed]); recent decrease in incidence of delirium appears to correlate with decrease in use of benzodiazepines

Evaluation of delirium: diagnostic gold standard unknown; Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) questionnaire administered once (spot check); Intensive Care Delirium Screening Checklist (ICDSC) filled out at end of shift covering period of shift; study compared metrics with evaluation according to Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition; DSM-IV) criteria and judgment of neurointensivist; 44% of patients considered delirious according to DSM-IV criteria, ≈29% considered delirious according to CAM-ICU and ICDSC, and ≈25% diagnosed as delirious by neurointensivist; delirium represents subset of encephalopathy (“brain failure”)

Encephalopathy: causes include acute metabolic disarray (eg, hypoxia, hypoglycemia, acidosis, thyrotoxicosis), seizures, effects of medication (especially polypharmacy and errors); other underlying causes, eg, N-methyl-D-aspartic acid (NMDA) receptor antibody encephalitis (associated with ovarian teratomas; manifests as psychiatric symptoms and seizures followed by frank encephalopathy and inflammation of brain)

Differential diagnosis: for alterations in level of consciousness, consider ischemia, infection, neoplasia, vasculitis, conversion, and malingering; for alterations in content of consciousness, consider epileptic, metabolic, toxic, and infectious disorders

Treatment: administer oxygen if patient hypoxic; administer naloxone (Narcan) and check glucose if needed; use collar until spinal cord injury ruled out; do not use flumazenil initially because of increased seizures; rule out or treat conditions that could kill patient within 24 hr, eg, meningitis, status epilepticus, infection, bleeding

General recommendations: for difficult-to-manage patients, speaker uses neuroleptics and haloperidol (Haldol); lower doses (eg, 1 mg) not effective; begin treatment at same time as evaluation; perform directed examination specifically for brainstem function, global cortical function, and mental status; treat problems that affect outcome immediately (eg, oxygen, glucose level, electrolytes); review serum bicarbonate levels for acidosis; keep looking until cause found; examine all encephalopathic patients personally to make better physical examinations and diagnoses; assume loss of consciousness usually structural; focus on medical portion of examination in addition to neurologic portion; start eliminating medications as soon as possible; do not treat with antibiotics unless infectious source identified (antibiotics cause much delirium); if dementia or sundowning likely (diagnosis of exclusion), speaker uses antipsychotics; avoid sedating or mind-altering drugs

 

Readings

Albin MS: Pharyngeal cooling, brain temperature, and a neglect of history. Anesthesiology 118:467, 2013; Arrich J et al: Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database Syst Rev 9:CD004128, 2012; Candy B et al: Drug therapy for delirium in terminally ill adult patients. Cochrane Database Syst Rev 11:CD004770, 2012; Clifton GL et al: Early induction of hypothermia for evacuated intracranial hematomas: a post hoc analysis of two clinical trials. J Neurosurg 117:714, 2012; Diringer MN et al: Elevated body temperature independently contributes to increased length of stay in neurologic intensive care unit patients. Crit Care Med 32:1489, 2004; Fernandez A et al: Fever after subarachnoid hemorrhage: risk factors and impact on outcome. Neurology 2007 Mar 27;68(13):1013-9; Fisher M et al: Endovascular cooling and endothelial activation in hemorrhagic stroke patients. Neurocrit Care 17:224, 2012; Girard TD et al: Delirium as a predictor of long-term cognitive impairment in survivors of critical illness. Crit Care Med 38:1513, 2012; Koehn J et al: Head and neck cooling decreases tympanic and skin temperature, but significantly increases blood pressure. Stroke 48:2142, 2012; Kvistad CE et al: Low body temperature associated with severe ischemic stroke within 6 hours of onset: the Bergen NORSTROKE Study. Vasc Health Risk Manag 8:333, 2012; Mrozek S et al: Brain temperature: physiology and pathophysiology after brain injury. Anesthesiol Res Pract 2012:989487, 2012; Park SM et al: Efficacy spectrum of antishivering medications: meta-analysis of randomized controlled trials. Crit Care Med 40:3070, 2012; Poli S et al: Induction of cooling with a passive head and neck cooling device: effects on brain temperature after stroke. Stroke Jan 22, 2013 [Epub ahead of print]; Roberts R et al: Not hysteria: ovarian teratoma-associated anti-N-methyl-D-aspartate receptor encephalitis. Scott Med J 57:183, 2012; Rossi S et al: Brain temperature, body core temperature, and intracranial pressure in acute cerebral damage. J Neurol Neurosurg Psychiatry 71:448, 2001; Scaravilli V et al: Fever management in SAH. Neurocrit Care 15:287, 2011; Springborg JB et al: First clinical experience with intranasal cooling for hyperthermia in brain-injured patients. Neurocrit Care Jan 24, 2013 [Epub ahead of print]; Wang W et al: Haloperidol prophylaxis decreases delirium incidence in elderly patients after noncardiac surgery: a randomized controlled trial. Crit Care Med 40:731, 2012; Whiteley WN et al: Do acute phase markers explain body temperature and brain temperature after ischemic stroke? Neurology 79:152, 2012.

Disclosures

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, Dr. Provencio and the planning committee reported nothing to disclose.

Acknowledgements

Dr. Provencio spoke at Miami Neuro Symposium, held December 7-8, 2012, in Coral Gables, FL, and presented by the Baptist Health Neuroscience Center, Baptist Health South Florida, and Florida International University Herbert Wertheim College of Medicine. To learn more about CME meetings presented by Baptist Health South Florida, please visit baptisthealth.net/en/physicians/Pages/Continuing-Medical-Education.aspx. The Audio-Digest Foundation thanks the speaker and the sponsor for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

NE040703

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.

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