Pruritic folliculitis of pregnancy is currently classified as atopic eruption of pregnancy (AEP) in a retrospective study done in 2006 that compared this condition to eczema and prurigo of pregnancy, which occurred in 49.7% and 0.8% of cases respectively, with eczema clearly being more frequent. Unlike typical pruritic folliculitis which does not resolve on its own, pruritic folliculitis of pregnancy clears spontaneously on delivery or in postpartum period. Fortunately, pruritic folliculitis of pregnancy has no mortality effects or significant adverse effects on the mother or on the fetus.Currently, there are no treatment guidelines for this condition due to the nature of its unknown etiology but symptom relief is strongly emphasized using non-pharmacological interventions such as warm baths or wearing loose clothing. If itchiness and discomfort persists, benzoyl peroxide, low to mid potency topical steroids, or antihistamines can be tried. Novel treatments have also shown potential in treating case studies of pruritic folliculitis of pregnancy, such as using ultraviolet phototherapy. However, further investigation is still required to study its efficacy and safety in second to third trimester pregnant patients. History
This condition was first observed in six people in 1981 with many different speculations but no real evidence as to a specific cause. These people had papules starting at various times throughout the second to third trimester with varying severity. Biopsies were taken from these people over a 15 month period in order to examine the composition of these papules.
The brain is relatively poorly supplied by oxygen as a result of mild hypoventilation during the sleeping hours, and cerebral edema may worsen during the night due to the lying position. The headache is worse on coughing, sneezing, or bending and progressively worsens over time. There may also be personality or behavioral changes.In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may include pupillary dilatation, abducens palsies, and Cushings triad. Cushings triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern. In children, a low heart rate is especially suggestive of high ICP.Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. Biots respiration, in which breathing is rapid for a period and then absent for a period, occurs because of injury to the cerebral hemispheres or diencephalon. Hyperventilation can occur when the brain stem or tegmentum is damaged.As a rule, patients with normal blood pressure retain normal alertness with ICP of 25–40 mmHg (unless tissue shifts at the same time). Only when ICP exceeds 40–50 mmHg does CPP and cerebral perfusion decrease to a level that results in loss of consciousness. Any further elevations will lead to brain infarction and brain death.In infants and small children, the effects of ICP differ because their cranial sutures have not closed. In infants, the fontanels, or soft spots on the head where the skull bones have not yet fused, bulge when ICP gets too high.