As crackles are not specific for IPF, they must prompt a thorough diagnostic process. Causes
The cause of IPF is unknown but certain environmental factors and exposures have been shown to increase the risk of getting IPF. Cigarette smoking is the best recognized and most accepted risk factor for IPF, and increases the risk of IPF by about twofold. Other environmental and occupation exposures such as exposure to metal dust, wood dust, coal dust, silica, stone dust, biologic dusts coming from hay dust or mold spores or other agricultural products, and occupations related to farming/livestock have also been shown to increase the risk for IPF. There is some evidence that viral infections may be associated with idiopathic pulmonary fibrosis and other fibrotic lung diseases. Pathogenesis
Despite extensive investigation, the cause of IPF remains unknown. The fibrosis in IPF has been linked to cigarette smoking, environmental factors (e.g. occupational exposure to gases, smoke, chemicals or dusts), other medical conditions including gastroesophageal reflux disease (GERD), or to genetic predisposition (familial IPF). However, none of these is present in all people with IPF and therefore do not provide a completely satisfactory explanation for the disease.IPF is believed to be the result of an aberrant wound healing process including/involving abnormal and excessive deposition of collagen (fibrosis) in the pulmonary interstitium with minimal associated inflammation.
Obstructive apnea can be detected when the level of oxygen has declined in the blood and/or results in slowing of the heart rate. Home apnea monitors (which must be distinguished from infant monitors that are designed only to allow parents to listen to the infant remotely) most frequently measure only respiratory movements and/or heart rate. They are generally used with premature infants who are otherwise ready for discharge, but who continue to require supplemental oxygen or medication for mild residual AOP. Home apnea monitoring is typically required for 6–12 weeks after discharge. Outcome
Since AOP is fundamentally a problem of the immaturity of the physiological systems of the premature infant, it is a self-limited condition that will resolve when these systems mature. It is unusual for an infant to continue to have significant problems with AOP beyond 43 weeks post-conceptual age. Infants who have had AOP are at increased risk of recurrence of apnea in response to exposure to anesthetic agents, at least until around 52 weeks post-conceptual age. There is no evidence that a history of AOP places an infant at increased risk for SIDS. However, any premature infant (regardless of whether they have had AOP) is at increased risk of SIDS. It is important that other factors related to SIDS risk be avoided (exposure to smoking, prone sleeping, excess bedding materials, etc.) Epidemiology
Apnea of prematurity occurs in at least 85 percent of infants who are born at less than 34 weeks of gestation.