eMedicine Specialties > Emergency Medicine > Psychosocial

Anxiety

Lemeneh Tefera, MD, FAAEM, Attending Physician, Department of Emergency Medicine, Beth Israel Medical Center
Lauren Claire Tomao, MD, JD, Resident, Department of Emergency Medicine, Albert Einstein College of Medicine, Beth Israel Medical Center

Updated: Nov 20, 2008

Introduction

Background

Anxiety is a complex feeling of apprehension, fear, and worry often accompanied by pulmonary, cardiac, and other physical sensations. It is a common condition that can be a self-limited physiologic response to a stressor, or it can persist and result in debilitating emotions. When pathologic, it can exist as a primary disorder, or it can be associated with a medical illness or other primary psychiatric illnesses (eg, depression, psychosis).

Mental health disorders account for approximately 5.5% of emergency department (ED) visits and, among these mental health visits, 21% are due to anxiety. Because generalized anxiety disorder (GAD) and panic attacks present with a similar constellation of symptoms, a similar approach can be used for both.

The goal of the emergency physician (EP) is to differentiate whether the anxiety is due to an acute medical condition or is the primary diagnosis. This differentiation can be difficult since many anxiety symptoms are indistinguishable from common cardiopulmonary and neurological complaints. Unfortunately, a chaotic emergency department is not the best environment to take a detailed history of the symptoms or to comfort an anxious patient. In addition, because of the high volume of ED’s nationally, EPs are under great pressure to see patients faster. Anxiety, like other psychiatric diagnoses, requires more time to take a history and engage the patient about the underlying cause of the symptoms.

Pathophysiology

Heightened physiologic response and elevated catecholamine levels play an important role in the normal physiologic response of the body to stress and anxiety. Pathologic anxiety has been hypothesized to result from disturbances in the cerebral cortex, specifically the limbic system.

The neurotransmitters primarily associated with anxiety in these regions are norepinephrine, gamma-aminobutyric acid (GABA), and serotonin. The efficacy of benzodiazepines in treating anxiety has implicated GABA in the pathophysiology of anxiety disorders. Drugs that affect norepinephrine (eg, tricyclic antidepressants, monoamine oxidase inhibitors [MAOIs]) are also efficacious in the treatment of several anxiety disorders.

Frequency

United States

The 1-year prevalence of GAD is approximately 3%, with a lifetime prevalence of 5%. Panic disorder has a lifetime prevalence of 1.5-3.5%. One third to one half of these individuals also have agoraphobia. Major depressive disorder occurs frequently (50-65%) in individuals with panic disorder. In contrast, phobic disorders have a lifetime prevalence as high as 10-13%, but they encompass several subcategories of anxiety conditions. Many of these are underreported due to mild subclinical presentations.

Mortality/Morbidity

Approximately 20-30% of individuals with panic disorders have persistent symptoms up to 10 years from the time of initial diagnosis and treatment. Such statistics are startling and reflect the ever-growing concern regarding the appropriate use of current health care resources.

Race

• In some Far East cultures, individuals with social phobia may develop fears of being offensive to others rather than fears of being embarrassed.
• Some cultural groups restrict the participation of women in public life. Treating physicians must distinguish this kind of taboo from agoraphobia.

Sex

• The female-to-male ratio of GAD is 2:1.
• Obsessive-compulsive disorders usually occur earlier in males (6-15 y) than in females (20-29 y).

Age

• Panic disorders have a bimodal distribution; one peak occurs in late adolescence and a second, smaller peak occurs in the mid-fourth decade of life.
• Phobic disorders, obsessive-compulsive disorders, and GAD tend to occur in late adolescence or early in the third decade of life.

Clinical

History

• The initial assessment must include a complete history with a focus on the patient's social history and a discussion of possible recent stressors (eg, problems with employment, financial stress, recent family illness/death, spousal conflict/abuse, illicit drug use). In addition, a detailed dietary history is critical. Caffeine, nicotine, chocolate, over-the-counter "exercise" or weight loss pills, and other natural supplements are often implicated as causes of an acute anxiety attack. Patients often do not realize that these agents are stimulants and can cause pronounced palpitations and other signs of anxiety.
• The family is an excellent source of history for a patient with acute anxiety and may be able to provide information that the patient is reluctant to discuss or does not feel is relevant to the presentation.
• The Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV) classifies anxiety disorders as follows¹ :
  • Global anxiety disorder (GAD) requires a clinical duration of at least 6 months. GAD occurs frequently with mood disorders (eg, major depression).
  • Panic disorder with or without agoraphobia: Panic attacks are recurrent episodes of spontaneous, intense periods of anxiety, usually lasting less than 1 hour. Panic attacks accompany complications of agoraphobia within the first year. (Agoraphobia is a condition involving anxiety about being in places or situations where escape might be difficult.). Patients with panic attacks are often in significant distress and seek medical attention in the ED. A patient with a classic panic attack experiences at least 4 of the following symptoms: palpitations, diaphoresis, tremulousness, shortness of breath, chest pain, dizziness, nausea, abdominal discomfort, fear of injury or going crazy, derealization (perception of altered reality), and depersonalization (perception that one's body is surreal).
  • Anxiety disorder due to a general medical condition is itself a unique diagnosis, but the emergency practitioner must thoroughly evaluate the known medical problem before making this diagnosis.
  • Substance-induced anxiety disorder and anxiety disorder not otherwise specified are characterized by symptoms of anxiety that occur as a direct consequence of drug abuse, medications, or toxins.

Physical

• While the physical examination of patients with anxiety is often normal, a great deal can be learned from observing the patient during the ED visit. The general demeanor, appropriateness, insight, hygiene, mood, cognitive capacity, and ability to engage the clinician in a discussion of the symptoms. However, a good physical examination allows the emergency physician to identify any potential life-threatening illnesses. The clinician should focus on the signs and symptoms of anxiety. Examination results may guide laboratory and imaging studies needed to evaluate cardiopulmonary causes of anxiety.
• As can be expected, comorbid diseases have their own characteristic examination findings.
• Mental status examination
  • A mental status examination can be especially helpful in distinguishing functional from organic disorders. Differentiating among the numerous psychiatric illnesses is essential, as many share symptoms similar to those of anxiety disorders.
  • The examination should focus on the following:
    • Affect
    • Behavioral observation
    • Speech pattern
    • Level of attention
    • Language comprehension
    • Memory, calculation, and judgment

Causes

• Comorbid diseases have been known to cause intrinsic anxiety. Many abused drugs (eg, alcohol, amphetamines, narcotics) raise anxiety levels.
• Panic attacks in patients who are susceptible to them can be precipitated by caffeine or iatrogenic agents, such as inhaled beta2-agonists.
• Many anxiety disorders demonstrate a familial pattern. First-degree biological relatives of patients with panic disorders have up to a 7-fold increased probability, as compared to the general population, of presenting with the same illness.

Differential Diagnoses

Other Problems to Be Considered

Neuropathy
Pheochromocytoma
Sinus tachycardia
Brugada syndrome

Workup

Laboratory Studies

The history remains the best tool available to the emergency physician in the evaluation of anxiety. Laboratory tests are rarely needed to affirm the diagnosis.

However, if there is an abnormal physical examination finding, such a goiter or prominent nystagmus, or the clinician suspects a toxic ingestion, laboratory testing can help distinguish anxiety from drug-induced causes and organic illnesses (eg, systemic infection, toxin, electrolyte and endocrine disturbances).

Imaging Studies

• Imaging studies are not useful in diagnosing anxiety but may be needed to exclude other possibilities in the differential diagnosis.

Other Tests

• Electrocardiograms are useful for evaluating possible tachydysrhythmia and screening for adverse medication effects such as QT prolongation.

Treatment

Prehospital Care

Prehospital personnel may provide reassurance and symptomatic relief within the usual protocols of EMS. Early identification of symptoms can facilitate evaluation and therapy by the emergency physician.

Emergency Department Care

• Patients with significant discomfort from their anxiety can benefit from emergency anxiolytic treatment, primarily with a benzodiazepine. In addition to ED treatment, patients in an acute anxious state of such severity that they pose a danger to themselves and or to others should have a psychiatric consultation.
• In addition to anxiolytic treatment, the clinician should be vigilant in addressing any abnormal vital signs. Patients who present with initial elevated blood pressure should have it repeated when they are less anxious. Initial tachycardia that resolves with reassurance is common. However, persistent tachycardia should not only be attributed to anxiety and organic causes (eg, dysrhythmia, pulmonary embolism, thyrotoxicosis, toxin, withdrawal, dehydration) should be considered (See Differentials).
• While remaining vigilant for life-threatening illness, EPs should provide a reassuring encounter to those with anxiety. Place the patient in a calm quiet room where a formal evaluation can begin to identify the functional components of the patient's anxiety. Unfortunately, such a quiet place is scarce and the ED environment often compounds the patient’s stress. Overcrowding and long wait times may also contribute to anxiety.
• In the best of circumstances, a calm environment and social support from family, friends, and the emergency staff is ideal. For patients with more severe anxiety, a short course of a fast-acting anxiolytic agent is recommended. Chronic anxiety requires a comprehensive approach and the best pharmacotherapy varies for each individual and outpatient follow up with a psychiatrist is recommended. However, these patients can be discharged on a short course of benzodiazepines until they see a psychiatrist. Patients who express suicidal or homicidal thoughts should have an emergent psychiatric evaluation in the ED.

Consultations

• Psychiatrist
  • Anxiety disorders are often chronic illnesses and require follow-up psychiatric intervention for successful treatment.
  • Any patient with anxiety who presents with homicidal or suicidal ideation requires urgent psychiatric intervention in the ED.

Medication

Short-acting benzodiazepines are most useful in the ED. 

Barbiturates are not recommended because of their high addictive potential, marked side effects, slow onset of action, and low therapeutic indices. Tricyclic antidepressants and MAOIs should not be prescribed in the acute setting. Beta-blockers do not reduce intrinsic anxiety, although they do reduce anatomic components (eg, tachycardia, diaphoresis). 

Buspirone has a low abuse potential, and a short course can safely be prescribed in the ED. However, peak efficacy may take several weeks and, in patients with concomitant depression, buspirone alone is often not effective. However, because of its excellent safety profile and low risk for abuse, it may be a preferred choice for patients that are at risk for substance abuse.

Benzodiazepines

Benzodiazepines are agents of choice due to their short half-lives and high therapeutic indices. By binding to specific receptor sites, these agents appear to potentiate the effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters.

Lorazepam (Ativan)

Lipophilic inhibitory CNS agent that acts on GABA receptors as well as specific benzodiazepine receptors. CNS effects include sedation, anxiolysis, and striated muscle relaxation. Its IV administration has a rapid onset of action (3-5 min), and the half-life has been reported as 9-19 min.

Dosing

Adult

0.5-2 mg IV q6-8min, with precautions for respiratory depression
In acute settings, 2.5-10 mg IV has been utilized for seizures; may also be given PO and IM; IM absorption has been known to be reliable

Pediatric

0.05 mg/kg/dose PO/IV q4-8h for anxiolytic effects

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

Contraindications

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Respiratory depression can occur, especially when used with other anxiolytics
Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Midazolam (Versed)

Similar to lorazepam but has shorter duration of action, approximately 1-4 h with a half-life of 2.5 h.

Dosing

Adult

1 mg IV q2-3min, up to 5 mg total
0.07 mg/kg IM
May also be given via endotracheal tube at twice usual dose

Pediatric

0.1 mg/kg slow IV; in children, injectable preparation may be given reliably

Interactions

Sedative effects of midazolam may be antagonized by theophyllines; narcotics and erythromycin may accentuate sedative effects of midazolam due to decreased clearance

Contraindications

Documented hypersensitivity; preexisting hypotension; narrow-angle glaucoma; sensitivity to propylene glycol (the diluent)

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause hypotension, bradycardia, and respiratory depression
Caution in congestive heart failure, hypotension, bradycardia, respiratory depression, renal impairment, pulmonary disease, and hepatic failure

Serotonin receptor agonists

These agents stimulate 5-HT1-receptors, producing anxiolytic effects. Buspirone is a nonsedating antipsychotic drug unrelated to benzodiazepines, barbiturates, and other sedative-hypnotics. Has been found to be comparable with benzodiazepines in reducing symptoms of anxiety in double-blind placebo-controlled clinical trials and has fewer sedative or withdrawal adverse effects than benzodiazepines. Also has fewer cognitive and psychomotor adverse effects, which makes its use preferable in elderly patients. Major limitations include lack of antipanic activity and reduced anxiolytic effects in patients recently withdrawn from benzodiazepines. Also has a longer onset of action and, thus, is of fairly limited use as a sole agent in the treatment of acute anxiety in the ED.

Buspirone (BuSpar)

5-HT1A agonist affecting serotonergic neurotransmission in CNS. Has some dopaminergic activity as well. In addition, has demonstrated anxiolytic effect but can take up to 2-3 wk for full efficacy. Also has a low abuse potential and does not mitigate panic attacks. Not useful in benzodiazepine withdrawal but has a low adverse-effect profile.

Dosing

Adult

5 mg PO tid or 7.5 mg PO bid; not to exceed 60 mg/d

Pediatric

Not established

Interactions

Toxicity is increased with MAOIs, phenothiazines, and CNS depressants; increases toxicity of digoxin and haloperidol

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include dizziness and light-headedness; avoid using this medication in patients with hepatic or renal impairment

Duloxetine (Cymbalta)

Potent inhibitor of neuronal serotonin and norepinephrine reuptake. Indicated for generalized anxiety disorder.

Dosing

Adult

30-60 mg PO qd

Pediatric

Not established

Interactions

Metabolized by CYP1A2 and CYP2D6; coadministration with drugs that inhibit CYP1A2 (eg, fluvoxamine, cimetidine, ciprofloxacin, enoxacin) may increase duloxetine blood levels and toxicity; coadministration with drugs that inhibit CYP2D6 (eg, paroxetine, fluoxetine, quinidine) may increase duloxetine blood levels and toxicity; duloxetine moderately inhibits CYP2D6 and may decrease elimination of CYP2D6 substrates (eg, tricyclic antidepressants, phenothiazines [eg, thioridazine], type 1C antiarrhythmics [eg, propafenone, flecainide]); coadministration with MAO inhibitors or triptans may cause serotonin syndrome consisting of serious, sometimes fatal reactions that include hyperthermia, rigidity, myoclonus, autonomic instability, mental status changes including extreme agitation, delirium, and coma (see contraindications)

Contraindications

Documented hypersensitivity; uncontrolled narrow-angle glaucoma; within 14 d of stopping MAO inhibitor use (do not initiate MAO inhibitors within 5 d of stopping duloxetine)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Observe closely for clinical worsening and suicidality when initiating treatment or following dosage change; gradually decrease dose when discontinuing, do not abruptly discontinue; caution with hepatic impairment or end-stage renal disease; recommended not to prescribe to patients with substantial alcohol use or evidence of chronic liver disease; may cause slight blood pressure increase; may activate mania or hypomania; common adverse effects include nausea, dry mouth, constipation, decreased appetite, fatigue, somnolence, and increased sweating; may cause serotonin syndrome (ie, changes in mental status [agitation, hallucinations, coma], autonomic instability [tachycardia, labile blood pressure, hyperthermia], neuromuscular abnormalities [hyperreflexia, incoordination], and/or gastrointestinal tract symptoms

Follow-up

Further Inpatient Care

• All anxious patients with suicidal ideation, homicidal ideation, or acute psychosis require emergent psychiatric consultation.
  

Complications

• Some studies report the failure rate of diagnosing anxiety disorders at as high as 50%. This can result in overuse of health care resources and increased morbidity and mortality rates for anxiety disorders and comorbid medical conditions.

Patient Education

• For excellent patient education resources, visit eMedicine's Anxiety Center. Also, see eMedicine's patient education articles, Anxiety, Panic Attacks, and Hyperventilation.

Miscellaneous

Medicolegal Pitfalls

• Anxiety states may be associated with increased prevalence of other physical illnesses.
• Avoid falsely attributing the somatic symptoms of anxiety to other medical conditions.
• Understand that anxiety can provoke or maintain other medical disorders. For example, the prevalence of hypertension has been found to be 13.6% in patients diagnosed with panic attacks compared to 4.4% in controls without panic attacks.

References

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Keywords

anxiety, anxiety disorder, panic attack, panic disorder, generalized anxiety disorder, GAD, phobic disorder, obsessive-compulsive disorder, apprehension, fear, worry, agoraphobia, tension, tremulousness, shaking, insomnia, irritability, restlessness, cold clammy hands, dry mouth, socialphobia, post-traumatic stress disorder, PTSD

Contributor Information and Disclosures

Author

Lemeneh Tefera, MD, FAAEM, Attending Physician, Department of Emergency Medicine, Beth Israel Medical Center
Lemeneh Tefera, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Lauren Claire Tomao, MD, JD, Resident, Department of Emergency Medicine, Albert Einstein College of Medicine, Beth Israel Medical Center
Lauren Claire Tomao, MD, JD is a member of the following medical societies: American Bar Association
Disclosure: Nothing to disclose.

Medical Editor

Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University
Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Robert Harwood, MD, MPH, FACEP, FAAEM, Program Director, Department of Emergency Medicine, Advocate Christ Medical Center; Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago College of Medicine
Robert Harwood, MD, MPH, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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