Chapter 53 Nausea and vomiting
Nausea is the feeling of impending vomiting, while vomiting consists of retching and expulsion (Pleuvry 2006). The physiology of both reflexes is integrative and multifaceted, involving autonomic and somatic neural pathways (Palmer et al 2002). It has been postulated that they occur when the vomiting centres in the brain, situated in the lateral reticular formation of the medulla, are stimulated by the chemoreceptor trigger zones in the floor of the fourth ventricle and vagal afferents from the gut (Kumar & Clark 2001). This is despite there being no distinct anatomical vomiting centre to be located in this region of the brain (Pleuvry 2006).
There have been several theories that have been used to elucidate the function of nausea and vomiting in pregnancy. One of these suggests that through the consequential lessening of energy intake, there is a reduction of insulin and insulin growth hormone-1, which facilitates diversion of nutrients, for example, glucose from the maternal cells to the placenta and fetus in early pregnancy (Huxley 2000). Flaxman & Sherman (2008) highlight another hypothesis regarding the prophylactic benefit of nausea and vomiting to enable expulsion of foods which may contain harmful toxins and micro-organisms that trigger aversions to such foods throughout pregnancy. The specific role of nausea and vomiting remains unknown. However, Flaxman & Sherman (2008) suggest the prophylaxis hypothesis is more consistent with patterns of cravings and aversions observed in some women and societies.
The aetiology of the conditions in pregnancy is also poorly understood and the literature suggests a multiplicity of probable origins. Reviews by Davis (2004) and Verberg et al (2005) highlight factors that are predominantly promulgated as causes. These include rising levels of hormones, including oestrogen, progesterone, human chorionic gonadotrophin (hCG), thyroxine (T4) and thyroid stimulating hormone (TSH). This may be compounded by physiological adaptations to pregnancy, such as reduced gastric motility or reflux oesophagitis, and metabolic alterations, such as carbohydrate and vitamin B deficiency. A presumed anatomical positioning of a right-sided corpus luteum is also thought to cause high concentrations of sex steroids in the hepatic portal system, which induce nausea and vomiting. Female fetal sex has also been shown to be associated with the symptoms (Tan et al 2006).
While there are limited data to support the psychogenic origins of nausea and vomiting, 21st-century medical texts continue to suggest a link (Davis 2004). Prejudice towards women appears to have guided such concepts, which are currently being replaced by biological (Sostre et al 2008) and sociocultural theories (Munch 2002). Midwives need to be aware of the debate to ensure that they do not stereotype women and impede adequate treatment of the conditions. It is premature to advocate that there is no psychological basis for nausea and vomiting, as there appears to be an integration of various elements incorporating psychogenic, sociocultural and biological causes (Buckwalter & Simpson 2002).
Mild and Moderate Vomiting in Pregnancy
Mild vomiting is an unpleasant but transient and self-limiting condition that commonly appears in the fifth week of pregnancy and peaks in severity at around 11–13 weeks. It usually resolves by 16–20 weeks (NCC-WCH 2008). The typical manifestation is that women feel nauseated on waking, and may vomit on rising from bed. Women may complain of an increased sense of smell, which initiates feelings of nausea that leads to aversion of some foods (Davis 2004). Actual vomiting recedes during the day, but nausea may persist.
Moderate vomiting is more serious, as the woman will vomit several times during the day, often after meals, and this may be accompanied by some weight loss and ketonuria. The fetus appears to fare well with mild and moderate vomiting (Davis 2004).
Hyperemesis Gravidarum
Hyperemesis gravidarum is a pathological condition characterized by unremitting, severe vomiting in pregnancy. It occurs in 0.3–2.0% of pregnancies and is more common in women who are younger, non-smokers and non-Caucasian (Ismail & Kenny 2007). It is diagnosed by exclusion (Kametas & Nelson-Piercy 2008) and is a leading cause of hospital admission during pregnancy (Cedergren et al 2008).
Studies have shown that a gastric infection caused by the Helicobacter pylori bacterium may also be linked to hyperemesis gravidarum (Golberg et al 2007). The infection responds well to antibiotic therapy, such as erythromycin or clarithromycin.
Hyperemesis gravidarum is associated with significant weight loss, ketonaemia, electrolyte imbalance and dehydration, together with hepatic, central nervous system and renal damage (Holmgren et al 2008). On examination, the woman may have sunken eyes, loss of skin elasticity, parched mouth and lips, ketonuria and/or oliguria. The woman may appear jaundiced as the condition worsens. Oesophageal tears (Mallory–Weiss syndrome) and haematemesis may occur because of the trauma produced by the persistent vomiting.
Wernicke’s encephalopathy is a rare but serious complication that has been reported in women with severe hyperemesis gravidarum (Indraccolo et al 2005). It is a neuropsychiatric syndrome that is caused by severe thiamine (vitamin B1) deficiency because of the persistent vomiting (Sechi & Serra 2007). It is manifest by signs of confusion, ocular abnormalities and ataxia (Chiossi et al 2006). Diagnosis may be confirmed through low red cell transketolase or an enhanced magnetic resonance imaging (MRI) scan (Kametas & Nelson-Piercy 2008). The condition responds well to thiamine (Welsh 2005).
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