It is best described as a downward cycle, where a child punished for bedwetting feels shame and a loss of self-confidence. This can cause increased bedwetting incidents, leading to more punishment and shaming.In the United States, about 25% of enuretic children are punished for wetting the bed. In Hong Kong, 57% of enuretic children are punished for wetting. Parents with only a grade-school level education punish bedwetting children at twice the rate of high-school- and college-educated parents. Families
Parents and family members are frequently stressed by a childs bedwetting. Soiled linens and clothing cause additional laundry. Wetting episodes can cause lost sleep if the child wakes and/or cries, waking the parents. A European study estimated that a family with a child who wets nightly will pay about $1,000 a year for additional laundry, extra sheets, diapers, and mattress replacement.Despite these stressful effects, doctors emphasize that parents should react patiently and supportively. Sociopathy
Bedwetting does not indicate a greater possibility of being a sociopath, as long as caregivers do not cause trauma by shaming or punishing a bedwetting child. Bedwetting was part of the Macdonald triad, a set of three behavioral characteristics described by John Macdonald in 1963. The other two characteristics were firestarting and animal abuse. Macdonald suggested that there was an association between a person displaying all three characteristics, then later displaying sociopathic criminal behavior.Up to 60% of multiple-murderers, according to some estimates, wet their beds post-adolescence.Enuresis is an "unconscious, involuntary [..] act".Bedwetting can be connected to past emotions and identity.
In medicine, hepatopulmonary syndrome is a syndrome of shortness of breath and hypoxemia (low oxygen levels in the blood of the arteries) caused by vasodilation (broadening of the blood vessels) in the lungs of patients with liver disease. Dyspnea and hypoxemia are worse in the upright position (which is called platypnea and orthodeoxia, respectively). Pathophysiology
The hepatopulmonary syndrome results from the formation of microscopic intrapulmonary arteriovenous dilatations in patients with both chronic and far less common, acute liver failure. The mechanism is unknown but is thought to be due to increased liver production or decreased liver clearance of vasodilators, possibly involving nitric oxide.The dilation of these blood vessels causes overperfusion relative to ventilation, leading to ventilation-perfusion mismatch and hypoxemia. There is an increased gradient between the partial pressure of oxygen in the alveoli of the lung and adjacent arteries (alveolar-arterial [A-a] gradient) while breathing room air. Patients with HPS have platypnea-orthodeoxia syndrome (POS); that is, because intrapulmonary vascular dilations (IPVDs) predominate in the bases of the lungs, standing worsens hypoxemia (orthodeoxia)/dyspnea (platypnea) and the supine position improves oxygenation as blood is redistributed from the bases to the apices. Additionally, late in cirrhosis, it is common to develop high output failure, which would lead to less time in capillaries per red blood cell, exacerbating the hypoxemia. Diagnosis
The hepatopulmonary syndrome is suspected in any patient with known liver disease who reports dyspnea (particularly platypnea). Patients with clinically significant symptoms should undergo pulse oximetry. If the syndrome is advanced, arterial blood gasses should be measured on air.