From a review of 48 reports of nonpregnant adults, Turcotte and associates (2006) concluded that peripherally placed catheters provided no advantages compared with centrally placed ones. Still, for short-term nutrition lasting a few weeks, it seems reasonable that PICC placement has a greater beneit-versusrisk ratio (Bistrian, 2012).
Mild to moderate nausea and vomiting are especially common in pregnant women until approximatel) 16 weeks' gestation (Chap. 9, p. 174). In a small but significant proportion of these, however, it is severe and unresponsive to simple dietary modiication and antiemetics. Severe unrelenting nausea and vomiting-hyperemesis gravidarum-is deined variably as being suiciently severe to produce weight loss, dehydration, ketosis, alkalosis from loss of hydrochloric acid, and hypokalemia. Acidosis develops from partial starvation. In some women, transient hepatic dysfunction develops, and biliary sludge accumulates (Matsubara, 2012). Other causes should be considered because ultimately hyperemesis gravidarum is a diagnosis of exclusion (Benson, 2013).
Study criteria have not been homogeneous, thus reports of population incidences vary. here does, however, appear to be an ethnic or familial predilection (Grjibovski, 2008). In population-based studies from California, Nova Scotia, and Norway, the hospitalization rate for hyperemesis gravidarum was 0.5 to 1 percent (Bailit, 2005; Fell, 2006; Vikanes, 2013). Up to 20 percent of those hospitalized in a previous pregnancy for hyperemesis will again require hospitalization (Dodds, 2006; Trogstad, 2005). In general, obese women are less likely to be hospitalized for this (Cedergren, 2008).
The etiopathogenesis of hyperemesis gravidarum is unknown and is likely multifactorial. It apparently is related to high or rapidly rising serum levels of pregnancy-related hormones. Putative culprits include human chorionic gonadotropin (hCG), estrogen, progesterone, leptin, placental growth hormone, prolactin, thyroxine, and adrenocortical hormones (Verberg, 2005). More recently implicated are other hormones that include ghrelins, leptin, nesfatin-1, and peptide Y (3-36) (Albayrak, 2013; Gungor, 2013).
Superimposed on this hormonal cornucopia are an imposing number of biological and environmental factors. Moreover, in some but not all severe cases, interrelated psychological components playaa major role (Christodoulou-Smith, 20a11a; McCarthy, 2011). Other factors that increase the risk for admission include hyperthyroidism, previous molar pregnancy, diabetes, gastrointestinal illnesses, some restrictive diets, and asthma and other allergic disorders (Fell, 2006; Mullin, 2012). n association of Helicobacter pylori infection has been proposed, but evidence is not conclusive (Goldberg, 2007). Chronic marijuana use may cause the similar cannabinoid hyperemesis syndrome (Alaniz, 2015; Andrews, 2015). And for unknown reasons-perhaps estrogenrelated-a female fetus increases the risk by 1.5-fold (Schif, 2004; Tan, 2006; Veenendaal, 2011). Finally, some but not all studies have reported an association between hyperemesis gravidarum and preterm labor, placental abruption, and preeclampsia (Bolin, 2013; Vandraas, 2013; Vikanes, 20l3).