Audio-Digest Foundation: emergency-medicine

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Audio-Digest FoundationEmergency Medicine


Volume 26, Issue 09
May 7, 2009

The following is an abstracted summary, not a verbatim transcript, of the lectures/discussions on this audio program. If, after reviewing this written summary, you would like to hear the contents and/or earn CME/CE credit:

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Head Emergencies

Educational Objectives

The goal of this program is to understand causes and risks associated with syncope and intensive care unit (ICU) de­lirium. After hearing and assimilating this program, the clinician will be better able to:

Define true syncope and differentiate it from seizure.

Identify pathophysiologic causes of syncope.

Explain features of history and physical examinations that help risk-stratify patients with syncope.

Interpret electrocardiograms for signs of Brugada syndrome, hypertrophic cardiomyopathy, and prolonged QT in­terval.

Implement nonpharmacologic and pharmacologic interventions for ICU delirium.

Faculty Disclosure

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, the faculty and planning committee reported nothing to disclose.

Acknowledgments

Dr. Mattu was recorded at High Risk Emergency Medicine, presented May 21-23, 2008, in San Francisco, CA, and spon­sored by the Division of Emergency Services, San Francisco General Hospital, and the Department of Medicine, University of California, San Francisco, School of Medicine. Dr. Lam was recorded at the 15th Annual USC Trauma/Critical Care Symposium, presented May 12-13, 2008, in Pasadena, CA, and sponsored by the Division of Trauma/Critical Care and the Office of Continuing Medical Education of the Keck School of Medicine of the University of Southern California, and the Institute of Continuing Education for Nurses, Department of Nursing, Los Angeles County/USC Medical Center. The Au­dio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.

Syncope

Amal Mattu, MD, Associate Professor, Department of Emergency Medicine, and Program Director, Emergency Medicine Residency, University of Maryland School of Medicine, Baltimore

Definition: brief loss of consciousness (associated with inability to maintain postural tone) that resolves spontane­ously; brief loss of consciousness    not syncope if loss lasts for hours (eg, overuse of alcohol, metabolic abnormal­ity); no prolonged postictal period; if confused or “out cold” for longer than 5 to 10 min, then not syncope (eg, seizures, metabolic problems); spontaneous recovery    no intervention needed; rules out hypoglycemia (rare cause); complete neurologic recovery    patient returns to baseline (state before episode occurred); if residual neu­rologic deficit present, consider structural lesion or metabolic abnormality

Background: terms    “passed out,” “blacked out,” or “fell out”; syncope work-up can be applied to presyncope (along continuum, with sudden death at end); self-terminating arrhythmias often present as syncopal episodes (ie, carefully scrutinize electrocardiograms [ECGs]); responsible for 1% to 3% of all emergency department (ED) visits and 1% to 6% of all hospital admissions

Pathophysiology: bilateral cerebral hemisphere dysfunction or acute dysfunction of midbrain’s reticular activating system (RAS) required for loss of consciousness

Transient ischemic attacks (TIAs): cannot transiently knock out bilateral hemispheres to produce syncope; poste­rior circulation TIA can cause brief loss of consciousness, but with other signs or symptoms (eg, dysarthria, dip­lopia, dysphasia); computed tomography not necessary; history and physical examination will rule out TIA

Systemic hypoxia or hypoglycemia: cause loss of consciousness, but not transiently

Take-home message: syncopal episodes related to hypoperfusion of brain (caused by, eg, dehydration, arrhythmias, myocardial infarction [MI]); can result in transient hypoxia or hypoglycemia in brain

ED evaluation: goals    avoid litigation; admit patients who would benefit from inpatient evaluation; anticipate short- and long-term negative outcomes (for long term, discharge patient and arrange primary care visit); diagnose reversible or deadly causes of syncope in ED; history    ask about events leading up to syncope;  witnesses; new prescription drugs; recreational drug and alcohol use; symptoms, eg, chest pain, shortness of breath, abdominal pain; physical examination    focus on cardiac and neurologic examinations

Distinguishing seizure from syncope: seizures commonly misdiagnosed as syncope: factors favoring syncope    preceding nausea or diaphoresis; brief episode of confusion (<5-10 min); age >45 yr; prolonged sitting or standing before episode; history of congestive heart failure (CHF) or coronary artery disease; factors favoring seizure    history of seizure disorder; noncompliance with medication; tongue biting; confusion (>5-10 min) after awaken­ing; loss of consciousness for >5 min; preceding aura; unusual posturing or head jerking (myoclonic jerks can oc­cur in syncope for 10-20 sec but not longer)

Rule of 15s: 15% of cases of subarachnoid hemorrhage, acute coronary syndrome (ACS), thoracic aortic dissection, pulmonary embolism, abdominal aortic aneurysms that rupture or leak, and ruptured ectopic pregnancies present with syncope; always ask about severe headache, chest pain, back pain, lower back pain, lower abdominal pain, re­cent menses, and breathing problems immediately before syncope; 50% of patients admitted to hospital receive di­agnosis before discharge; 80% of diagnoses made during hospitalization occur in ED

Risk stratification: perform if unable to diagnose; high risk for early complications    admit to hospital; low risk    discharge for outpatient follow-up

Clinical policy (Annals of Emergency Medicine): addresses 3 clinical questions for risk stratification in syncope pa­tients

What history and physical examination data helpful in risk stratification? high-risk historical features    older age; history of coronary artery disease; structural heart disease; young patients with exertional syncope; signs and symptoms of ACS; family history of sudden death; murmurs  consider hypertrophic cardiomyopathy (HCM) in young patients with systolic murmur (especially one that radiates to axilla); consider aortic stenosis for patient with systolic murmur radiating up to carotids; orthostatic examination  overused; often done incorrectly; not relevant to older patients with syncope; low sensitivity and specificity; results can vary with time of day (due to diurnal variations in cortisol levels) and medications (including antihypertensives and antipsychotics); 20% of patients with positive orthostatic changes return for significant cardiac problems; reliable  orthostatic test    patient passes out or becomes lightheaded upon standing; tongue biting and loss of continence  point strongly to seizure; abdominal and rectal examination  consider guaiac test (if positive, check hematocrit); detailed neu­rologic examination    will indicate abnormalities associated with structural brain lesions

Do particular diagnostic tests have positive yield not predicted based on history and physical examination? no, ex­cept for ECGs; do not “shotgun” tests; ECG    perform on nearly everyone presenting with syncope; other tests (including complete blood cell count [CBC], C-reactive protein, urinalysis, and pregnancy test) rarely useful un­less indicated by history and physical examination; other unnecessary tests (with exceptions)  chemistry panels, head CT, echocardiography, and outpatient Holter monitoring (unless high risk for arrhythmia)

Who should be admitted after syncope of unclear cause? patient should be admitted if physician suspects patient at risk for significant dysrhythmia or sudden death, and observation may enable intervention; arrange outpatient follow-up; observation units   t heoretically useful but not common; admission decisions    initially based on predictors of long-term (6-12 mo) mortality; should include syncope patient with abnormal ECG, ventricular dysrhythmia, CHF, and age >45 yr; syncope itself does not necessarily cause increased 1-yr mortality; 6- to 12- mo mortality of limited usefulness to ED physician

Predicting short-term mortality: San Francisco syncope rules (CHESS)    syncope with CHF, hematocrit <30%, ECG abnormalities, shortness of breath, or systolic blood pressure <90 mm Hg on arrival predict higher risk for negative outcome at 7 days; use as risk stratification guidelines to support admission and discharge decisions; Bos­ton syncope rules    evaluates patients at 30 days; 25 criteria; too inclusive to help with selective admissions; study (Journal of American College of Cardiology)    evaluates patients at 10 days; 4 independent predictors, including concomitant trauma, absence of prodrome, and male sex; problems    many older rules do not evaluate short-term risk; newer rules too inclusive; rules should not alter clinical decision making by experienced ED physicians

Interpreting ECGs: common to look for abnormal rhythms (eg, nonsinus rhythms, bundle branch block, and acute MI); look for Wolff-Parkinson-White (WPW) syndrome, delta waves, and short PR and wide QRS waves; Bru­gada syndrome

Brugada syndrome: first described (early 1990s)    in Southeast Asian boys; first patients at autopsy had structur­ally normal hearts; electrical phenomenon; propensity to later develop polymorphic ventricular tachycardia car­diac arrest (patients pass out, wake up, and present with syncopal episode); if episode did not end, sudden death occurred; current prevalence    worldwide, across ethnic groups; in both sexes;  electrophysiologists say syn­drome likely responsible for 1 in 20 to 25 cardiac arrests; diagnosis    many patients show signs 1 to 2 wk before terminal event; ECG abnormalities give initial clues; send patients to and consult with electrophysiologist; treatment    implantable cardioverter defibrillator (ICD); high survival rate for patients with ICD (without, mor­tality 10% per year from symptom onset); researchers trying to determine reason for late onset of symptoms (30-40 yr of age); ECG pattern    “sodium channelopathy”; look for right bundle or incomplete right bundle pattern in V1 and V2, with ST segment elevation (normal right bundle patient has ST depression in V1 or V2); types of ST elevations    saddle-type (resembles cup holding water) and cove-type (convex outward; more sensitive and more specific); ECG machines not programmed to detect Brugada syndrome

Hypertrophic cardiomyopathy: focus attention on high voltage, deep and narrow Q waves in lateral leads (I, aVL, V5, V6), and do not mistake for old lateral MI; send patient for Doppler echocardiography to confirm

Prolonged QT: with syncope, might be torsades de points; ECG will read prolonged QT when QTc 460 to 480; most studies indicate patients at higher risk when QTc ³500 (worry about torsades); always check ECG on new seizure patients and look for prolonged QT (might be syncope with episodes of torsades); electrolyte abnormali­ties can cause prolonged QT; take medications into account

Conclusion: ED physicians responsible for 80% of diagnoses; important to perform thorough history and physical examination; ECGs    remember WPW syndrome; look for Brugada syndrome, HCM, and prolonged QT

Prevention and Management of Intensive Care Unit (ICU) Psychosis and Depression

Lydia Lam, MD, Critical Care Fellow, Division of Trauma and Critical Care, Keck School of Medicine of the University of Southern California, Los Angeles

Definition of delirium: acute confusional state; fluctuating mental status, inattention, and either disorganized think­ing or altered level of consciousness; usually due to general medical condition (rather than organic brain disor­der)

Intensive care unit (ICU) delirium subtypes: hyperactive   »1.6% of patients diagnosed with ICU delirium; hypoactive    more common; more deleterious because it goes unrecognized; symptoms include apathy and flat affect (drug withdrawal); mixed    fluctuating symptoms from hypoactive to hyperactive

Effects of delirium: can accelerate permanent dementia; cumulative risks    days spent in delirium add to length of stay; 10% increased mortality risk each day; susceptibility  children, older patients; £50% of patients not on mechanical ventilation;  £80% of mechanically ventilated patients; study (JAMA 2004)    275 ICU patients; found delirium serves as independent predictor of 6-mo mortality and longer ICU stay, with resultant increased cost; degree of delirium predicts costs

Long-term cognitive impairment: mild to moderate dementia; in patients who develop delirium, present £6 yr after ICU stay; effects include inattention and problems with executive thinking and memory (can affect daily activi­ties); seen in £33% of ICU survivors; study (Journal of Trauma; 2007)  trauma ICU patients with injury sever­ity score >25 (without intracranial hemorrhage); functional problems and poor quality of life during £2-yr follow-up

Risk factors: hundreds, including advanced age, hypertension, alcoholism, hypoxia, medications, liver problems, and kidney problems; modifiable risks    sedatives; analgesics; treating sepsis and metabolic derangements; modifica­tion of environment

Sedation: important consideration in ICU patients on mechanical ventilation; agitated patient may develop    hypoxia or hypercarbia (from fighting ventilators); increased oxygen consumption and inadvertent removal of airway catheters; adequate sedation    reduces stress response and improves tolerance of routine ICU proce­dures; maintains safety of patient and staff

Current guidelines of Society of Critical Care Medicine (SCCM): recommend validated sedation scale (clinician sets goals for individual patients); daily sedation holiday (NEJM 2000)    decreased ventilator days and shorter ICU stay

Therapies: lorazepam (eg, Ativan) recommended; guidelines recommend intermittent boluses first, then continuous administration if sedation goals not achieved

Assessment using Richmond Agitation Sedation Scale (RASS): scale of +4 to -5; +4 to +1    patient moving; +4 patient combative, +1 patient restless; zero    patient alert and calm; -1 to -3    verbal stimulation (call patient’s name and note duration of eye contact); -4 to -5    -5 comatose state; -4 and below, confusion assessment method (CAM) cannot be used

Confusion assessment method for ICU patients (CAM ICU): helps diagnose delirium; recommended if RASS score >-4; sensitivity and specificity >90%; easy to use and takes <1 min to complete; 4 steps    1) make sure pa­tient had acute onset of mental status change or fluctuating course, and if true, proceed to step 2; 2) examiner tests patient’s attention by saying string of letters and asking patient to squeeze examiner’s hand when letter “A” heard (if incorrect, patient  becoming delirious); 3) lack of organized thinking; 4) check consciousness level and ask diffi­cult questions; patient delirious    if patient fails 1,2, and 3 or 4

Delirium vs alcohol or drug withdrawal: possibly withdrawal if patient improves on alcohol drip; talk with family and understand alcohol/drug abuse history; escalating symptoms seen in patients in withdrawal (in delirium, symp­toms fluctuate)

Nonpharmacologic prevention: studies    performed in non-ICU patients; treat underlying condition and check medications; ICU    environmental interventions (include reorienting and reassuring patient frequently and main­taining sleep-wake cycle)

Pharmacologic prevention: optimize quantity and type of sedation and analgesia; g-aminobutyric acid (GABA)-sparing sedative agents (eg, antipsychotic agents, dexmedetomidine); GABA neurotransmitters increase in delir­ium, and this manifests as decreased cognition; therefore, recommended that benzodiazepines be avoided in acutely delirious patients; norepinephrine decrease    leads to decreased attention; acetylcholine decrease  leads to  de­creased cognition; avoid anticholinergics (including diphenhydramine [eg, Benadryl]); 5-HT decrease    leads to anxiety; use atypical antipsychotics (eg, olanzapine,  quetiapine); dopamine increase  leads to confusion and hal­lucination; use antipsychotics; haloperidol (eg, Haldol)    neuroleptic agent which stabilizes cerebral function; an­tagonizes dopamine neurotransmitters; minimal side effects and hemodynamic effects; side effects include extrapyramidal symptoms, neuroleptic malignant syndrome, and polymorphic ventricular tachycardia, which can progress to torsades

Dexametomidine (eg, Precedex): a2-blocking sedative given intravenously (IV); commonly used for anesthesia; spares GABA receptors; does not exacerbate or trigger delirium; however, indicated for £24 hr, and ICU patients need longer treatment

Dexmedetomidine vs lorazepam (JAMA 2007): in mechanically ventilated patients; 1.5 µg/kg per hour for 120 hr; result    patients taking dexmedetomidine spent more days without delirium or coma; more common to be within 1 RASS score of goal; no increased risk for self-extubation, hypotension, hypertension, or arrhythmia

Suggested Reading

Chen LY et al: Management of syncope in adults: an update. Mayo Clin Proc 83:1280, 2008; Cole MG et al: Persistent delirium in older hospital patients: a systematic review of frequency and prognosis. Age Ageing 38:19, 2009; Cooke J et al: Sitting and standing blood pressure measurements are not accurate for the diagnosis of orthostatic hypotension. QJM 2009 Mar 9. [Epub ahead of print]; Costantino G et al: Short-and Long-Term Prognosis of Syncope, Risk Factors, and Role of Hospital Admission: Results From the STePS (Short-Term Prognosis of Syncope) Study. J Am Coll Cardiol 51:276, 2008; Dovgalyuk J et al: The electrocardiogram in the patient with syncope. Am J Emerg Med 25:688, 2007; Goksu E et al: Seizure or syncope: the diagnostic value of serum creatine ki­nase and myoglobin levels. Eur J Emerg Med 16:84, 2009; Grossman SA et al: Predicting adverse outcomes in syncope. J Emerg Med 33:233, 2007; Han JH et al: Delirium in older emergency department patients: recognition, risk factors, and psychomotor sub­types. Acad Emerg Med Jan 20, 2009 [Epub ahead of print]; Kelly BS et al: Hypertrophic cardiomyopathy: electrocardiographic manifestations and other important considerations for the emergency physician. Am J Emerg Med 25:72, 2007; McDermott D et al: Acute myocardial infarction in patients with syncope. CJEM 11:156, 2009; Meagher DJ et al: Defining delirium for the Interna­tional Classification of Diseases, 11th Revision. J Psychosom Res 65:207, 2008; Schladenhaufen R et al: Application of San Fran­cisco Syncope Rule in elderly ED patients. Am J Emerg Med 26:773, 2008; Schuur JD et al: Measuring quality of care in syncope: case definition affects reported electrocardiogram use but does not bias reporting. Acad Emerg Med 2009 16:40, 2009.

 


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