Children and adolescents hospitalized for the treatment of physical illness often have feelings of sadness, frustration, or irritability that represent a normal response to their experience. Common factors impacting a child’s ability to cope include disruption of routine, separation from family and peers, uncertainty regarding diagnosis and prognosis, pain related to the illness or its treatment, and fear of the illness or its sequelae. When the sadness becomes pervasive and is associated with cognitive or physiologic symptoms, however, a depressive disorder must be considered. It is incumbent on the hospitalist to distinguish normal feelings of sadness from a depressive disorder and to implement treatment when necessary.
Chronically ill children are at increased risk for developing depressive, anxiety, and eating disorders.1-5 Clinical depression has been reported to increase the risk of poor physical health in the future6 and has been associated with poor adherence to treatment regimens,7 reduced immune function,8 increased disease severity, and death due to nonadherence.9 Emerging data suggest that depression in patients with human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS) is associated with declining CD4 counts, accelerated disease progression, and increased mortality.10 In addition, suicidal ideation and suicide attempts are tragic consequences of depression that increases with the onset of puberty.11 Depressive disorders cause significant suffering on the part of the child and family and are generally highly treatable once they are recognized. The purpose of this chapter is to provide the pediatric hospitalist with a framework for understanding the diagnosis and treatment of depressive disorders in children and adolescents with physical illness.
While multiple theories exist regarding the pathophysiology of depression (Table 135-1), conclusive evidence of its etiology is still uncertain. The Diagnostic and Statistical Manual (DSM) bases the diagnosis of depression on a cluster of symptoms. As the DSM is atheoretical by design, it is important to note that patients who may look similar phenotypically for depression may indeed have different etiological mechanisms for their depression. As such, simply making a diagnosis of depression does not indicate the pathophysiological mechanism or the optimal treatment regimen.
TABLE 135-1 Pathophysiological Hypotheses of Depression12 ||Download (.pdf) TABLE 135-1 Pathophysiological Hypotheses of Depression12
|Mechanism ||Comments |
|Genetic vulnerability ||Based upon evidence from twin studies |
|Altered HPA axis activity ||Based upon effects of stress as a risk factor |
|Monoamine deficiency ||Based upon mechanism of action of medication treatments |
|Brain region dysfunction ||Based upon stimulation of specific brain regions reproducing antidepressant effects |
|Neurotoxic and neurotrophic processes ||Based upon concept of “kindling” and brain volume loss over course of depressive illness |
|Reduced GABAergic activity ||Based upon evidence from magnetic resonance spectroscopy and postmortem studies |
|Glutamate dysregulation ||Based upon mechanism of action of medication treatments |
|Circadian rhythm impairment ||Based upon circadian rhythm changes having antidepressant effects |