Mood disorders are divided into depressive and bipolar disorders. Worldwide, depressive disorder affects approximately 10% of the population,¹ whereas bipolar disorder has a lifetime prevalence of 2.4%.² In the United States, there is a 21% lifetime prevalence of any mood disorder.³ One urban study showed that 32% of ED patients screened positive for depressive disorder, and 7% screened positive for bipolar disorder.^4,5 Depressive disorder affects women twice as often as men, whereas bipolar disorder affects men and women equally. Bipolar disorder is characterized by mania cycling with periods of depression. The depressive periods tend to last longer that the manic periods.

Although mood disorders may occur at any age, the average onset of depressive disorder is about 40 years of age, and that of bipolar disorder is about 30 years of age. There are no differences in prevalence regarding race.⁶

Depressive disorder is often unrecognized, as the investigation of somatic complaints usually takes priority during patient evaluation.^7,8 Adolescents⁹ and the elderly (especially nursing home patients)¹⁰ appear to be particularly vulnerable populations for depression. Increased rates of depressive disorder are seen in many chronic illnesses including CNS diseases,^11,12 cardiovascular disorders,¹³ and cancer.¹⁴ Also, patients with depressive disorder have increased risk of certain medical diseases, such as diabetes and coronary artery disease.¹⁵

The most common type of depressive disorder is major depressive disorder (also called unipolar or major depression). Diagnosis requires at least 5 of the 10 following symptoms: depressed mood, anhedonia (loss of pleasure in things that used to give pleasure), suicidal ideation with or without a specific plan, significant weight loss or gain, insomnia or hypersomnia, feelings of restlessness, agitation or psychomotor retardation, feelings of worthlessness or inappropriate guilt, fatigue or loss of energy, and difficulty with concentration. At least one of the symptoms must be depressed mood or anhedonia. Symptoms must be present for at least 2 weeks, cannot be due to substance abuse or a medical condition, and must cause significant impairment in normal functioning.¹⁶

PATHOPHYSIOLOGY

The pathophysiology of depressive disorder is likely multifactorial including genetic, biological, and psychosocial factors. A genetic predisposition, as evidenced by a 37% concordance rate in twin studies,¹⁷ heightens susceptibility. Malfunctioning monoamine neurotransmitters (especially serotonin, norepinephrine, and dopamine)^18,19,20 are implicated and may explain the effectiveness of some current medical therapies. Abnormal γ-aminobutyric acid and glutamate levels in various areas of the brain have been noted.²¹ Early childhood stress may alter corticotropin-releasing hormone cells in the hypothalamus to heighten future stress responses.^22,23 Four areas of the brain involved in normal emotional responses (the prefrontal cortex, anterior cingulate cortex, hippocampus, and amygdala) appear to be altered in patients with depressive disorder. Finally, psychosocial factors including isolation, lack of family support, stressful life events,^24,25 and substance abuse are risk factors for development of depression.

CLINICAL FEATURES

The most important part of evaluation is the assessment of suicide risk. The acronyms SAD PERSONS²⁶ (Table 289-1) and SIG-E-CAPS (Table 289-2) are helpful tools to assess suicide risk and identify depressive disorder, respectively. The easiest method is using straightforward, nonthreatening questions regarding the patient’s suicide or homicide thoughts or intent, but seek corroborative information from family members, friends, law enforcement, EMS, or outside providers.

If the patient is at potential risk for harm to self or others, perform a thorough search for weapons, medicines, and potentially harmful items, and place the patient in a safe environment with monitoring. Follow with appropriate history taking, physical examination, and laboratory studies. Detailed evaluation of patients with mental health disorders is provided in chapter 286, “Mental Health Disorders: ED Evaluation and Disposition” and Table 286-1 of that chapter.

Consider depressive disorder in a patient with vague, general complaints with unclear medical etiologies and multiple ED visits.²⁷ Two simple questions that have only been validated for depressive disorder assessment in primary care²⁸ but may prove useful in the ED setting are as follows:

1. 
   

   During the past month, have you been bothered by feeling down, depressed, or hopeless?

   
   
2. 
   

   During the past month, have you been bothered by little interest or pleasure in doing things?

Ask about substance abuse, because alcohol and drug abuse are important comorbidities.²⁹ Alcohol abuse is associated with an increased risk of suicide, and many of those with completed suicide demonstrate positive alcohol levels at autopsy. Patients cannot be adequately evaluated for depression or suicidal intent until they are no longer intoxicated. This does not necessarily mean an alcohol level of 0, but rather a return to normal (or baseline) cognition.

DIFFERENTIAL DIAGNOSIS

A large number of medical disorders, as well as many medications and substances of abuse, may cause symptoms of depression. Important medical mimickers include neurologic (CNS infection, cerebrovascular accident), endocrine (hypo- and hyperthyroid, hypoglycemia), and infectious disorders (especially in the elderly). Opiates, barbiturates, benzodiazepines, alcohol abuse, and corticosteroids may all cause depressive symptoms. A thorough history, examination, and appropriate laboratory studies will help differentiate the disorders. Consider medical causes of depression in patients with new symptoms of depression, in the elderly, and in those with complex medical problems.

TREATMENT OF DEPRESSIVE DISORDERS

Antidepressants are usually prescribed by primary care physicians or psychiatrists for conditions such as depression, neurogenic pain, or smoking cessation. The side effect profiles, potential serious adverse effects, and toxicities of common antidepressants are reviewed in Table 289-3 and in the Toxicology section of this text. Antidepressant therapy is typically not initiated in the ED, although resumption of a well-tolerated, recently stopped medication may be considered. Antidepressants take about 2 to 3 weeks to have clinical effects. Ideally, any antidepressant prescribed from the ED should be done in conjunction with the follow-up practitioner, and the patient should be seen in follow-up within a week. Antidepressants may pose fetal risk, so the risks and benefits during pregnancy must be weighed carefully under the guidance of a psychiatrist and obstetrician. Sertraline and paroxetine are safe to use while breastfeeding (see Table 289-3).

The major categories of antidepressants in use today are the heterocyclic antidepressants (HCAs), monoamine oxidase inhibitors (MAOIs), selective serotonin reuptake inhibitors (SSRIs), the selective serotonin norepinephrine reuptake inhibitors (SNRIs), and the atypical antidepressants.

Heterocyclic Antidepressants

HCAs, once commonly used for depression, are prescribed less often now due to low therapeutic index, many possible side effects at prescribed doses, and dangerous overdose potential. The side effects are mainly anticholinergic related and cardiotoxic, including prolonged QT_c interval and atrioventricular block. One agent in this category, amitriptyline, is commonly prescribed for chronic or neurogenic pain.

Monoamine Oxidase Inhibitors

MAOIs are rarely used first line in treating depression because of potentially lethal drug–drug and dietary interactions. MAOIs block oxidative deamination of tyramine and may precipitate a sometimes fatal hypertensive crisis when certain drugs (sympathomimetic amines, levodopa [l-dopa], narcotics, and heterocyclic antidepressants) or tyramine-containing foods or beverages (aged cheese, beer, and wine) are co-ingested.

Selective Serotonin Reuptake Inhibitors and Selective Serotonin Norepinephrine Reuptake Inhibitors

The mainstays of current antidepressant therapy are the SSRIs and SNRIs, which increase the amount of intrasynaptic serotonin or serotonin and norepinephrine, respectively. A significant advantage of SSRIs and SNRIs over other classes of antidepressants is their high therapeutic index and favorable side effect profile.

Common side effects for the SSRIs include nausea and vomiting, drowsiness, headache, changes in sleep patterns, sexual dysfunction, cognitive dysfunction, and precipitation of mania in bipolar patients. SSRIs may increase suicidal ideation, and the U.S. Food and Drug Administration currently requires that all antidepressants carry a black box warning that antidepressants may increase suicide risk in patients <25 years old. When SSRIs are abruptly stopped, a withdrawal syndrome may occur, characterized by a flulike symptoms, including nausea, vomiting, fatigue, myalgias, vertigo, headache, insomnia, and paresthesias. Although these symptoms are not life threatening, they may be very uncomfortable.

Serotonin syndrome, a potentially life-threatening adverse drug reaction, may occur in patients taking SSRIs (or any other antidepressant) when used in combination with another agent that has serotonergic activity such as MAOIs, opiates (including tramadol), CNS stimulants, serotonin agonists, St. John’s wort, lithium, dextromethorphan, risperidone, olanzapine, ondansetron, and metoclopramide. The syndrome is manifest by neuromuscular hyperactivity (tremor, myoclonus, clonus, hyperreflexia, seizures), altered mental status (restlessness, agitation, excitement, confusion), autonomic hyperactivity (tachycardia, tachypnea, fever, diaphoresis), and GI irritability (nausea, vomiting, diarrhea). Treatment consists of discontinuation of the affecting agents, administering benzodiazepines, and supportive care.

SNRIs

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