Chapter 53 Nausea and vomiting
Nausea and vomiting are common symptoms in pregnancy, occurring in up to 90% of normal pregnancies. The dyad is often regarded as normal and a presumptive sign of pregnancy. However, the conditions may range from mild to severe, which in the latter is pathological where it can become debilitating and life-threatening to women and their fetuses. Severe vomiting is strongly associated with multiple pregnancy, hydatidiform mole and pre-eclampsia.
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 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 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).
In mild, moderate or severe cases, there appears to be a decreased risk of miscarriage, stillbirth and preterm delivery (Welsh 2005), though in very severe cases, fetal growth restriction and fetal death may also be a consequence (Turner 2007).
The care and management of nausea and vomiting in pregnancy depends on the intensity of the symptoms (Davis 2004), requiring a multidisciplinary approach. The initial assessment of severity by the midwife is pivotal.
The midwife should explain to women with mild nausea and vomiting that in most cases the condition will improve spontaneously within 16 to 20 weeks of gestation, with good pregnancy outcome (NCC-WCH 2008). Medication is not usually required and the woman should be advised to rest as much as possible, as tiredness and stress may exacerbate the vomiting. Frequent, small, light meals with a reduction in fatty, spicy or strong-smelling foods; a milky drink at bedtime and dry toast or a biscuit before rising; carbonated drinks, such as soda or non-alcoholic dry ginger ale, if required during the day, have been reported to alleviate the symptoms.
Reflective activity 53.1
Contact your local hospital dietician. What dietary modifications does he/she recommend to reduce nausea and vomiting in pregnancy?
Complementary remedies (see Ch. 18) and supplements such as vitamin B6 and ginger are often useful; however, the midwife may not use any complementary therapy for her clients unless she is properly qualified in that field (NMC 2008). Concerns about the possible toxicity of high doses of vitamin B6 have not yet been resolved. Therefore, in the UK the recommended upper limit of 10 mg should not be exceeded (NCC-WCH 2008). Alternatively, ginger can be useful. It accelerates gastric emptying (Wu et al 2008) and has been found to be as effective as vitamin B6 (Ensiyeh & Sakineh 2009) with no evidence of teratogenicity (Jewell & Young 2003).
Acupuncture and acupressure using the P6 point may also relieve vomiting in pregnancy. The evidence regarding its effectiveness is mixed but it appears to be more efficient than changes in diet or lifestyle (Jewell & Young 2003).
Although not clinically ill, the woman often feels miserable and her symptoms should not be regarded as trivial. Therefore, empathic support is paramount. Her partner and family will also need reassurance and guidance on how to provide assistance during this time.
If the woman is experiencing moderate vomiting or suspected hyperemesis gravidarum, the midwife should arrange for her to be admitted to hospital without delay. She should be cared for in a single room if possible, to avoid undue disturbance. A urinalysis is conducted for ketones, bilirubin, protein and glucose, and a midstream specimen of urine is sent for culture to exclude pyelonephritis.
Antihistamines such as promethazine hydrochloride, prochlorperazine (Stemetil) metoclopramide (Maxolon, Primperan) (Jewell & Young 2003) or corticosteroids such as methylprednisolone (Ismail & Kenny 2007) are considered safe to use in pregnancy and may be utilized to control the nausea and vomiting.
Blood tests, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea and electrolytes, are required to assess renal and liver function. An ultrasound scan may also be useful to eliminate hydatidiform mole and multiple pregnancy as probable causes. A frequent record of the woman’s weight, temperature, pulse and blood pressure is essential to monitor her wellbeing. In addition, the fetal heart rate should be appropriately auscultated (depending on the gestation) to monitor the health of the fetus.
Reflective activity 53.2
Locate and read your local policy for management of severe vomiting in pregnancy.
With moderate vomiting, dietary advice may help, but often the woman continues to vomit and will begin to show signs of dehydration. In cases of severe vomiting, nothing is given by mouth. Intravenous fluids with careful record of fluid balance may be essential to correct dehydration, particularly with hyperemesis gravidarum. Normal saline or Ringer’s lactate (Hartmann’s) solution with added potassium is commonly administered to restore the electrolyte balance. As carbohydrate increases the demand for thiamine (Sechi & Serra 2007), fluids containing dextrose should be avoided to prevent the development of Wernicke’s encephalopathy (Kametas & Nelson-Piercy 2008).
In life-threatening cases of hyperemesis gravidarum, slow-drip enteral feeding may follow and total parenteral nutrition (TPN), supplemented by thiamine 100 mg daily, may be necessary (Ismail & Kenny 2007). However, such aggressive management should be a last option as both methods carry maternal risks such as life-threatening sepsis and thrombosis (Holmgren et al 2008).
Moderate vomiting usually ceases quickly and once the woman is tolerating a normal diet she may be discharged home. Most women with hyperemesis gravidarum will experience relief within 2–3 days and the vomiting is less likely to recur than when conventional antiemetics are used. Once the vomiting ceases, oral fluids and food may be gradually reintroduced and the woman may be discharged when she is taking and tolerating a normal diet and gaining weight.
In rare cases, termination of the pregnancy is considered if the vomiting is intractable and there are signs of major organ failure, such as persistent pyrexia or hypothermia, persistent tachycardia, jaundice, persistent proteinuria, polyneuritis or encephalopathy.
Nausea and vomiting together with amenorrhoea are features of eating disorders such as anorexia nervosa and bulimia nervosa. One recent study found nausea and vomiting in pregnancy to be increased in women with anorexia nervosa and bulimia nervosa (Torgersen et al 2008). A pregnancy may go undetected for some time in a woman who is affected by the above. Alternatively, an existing eating disorder accompanied by such features may not become apparent as it may be mistaken for a normal aspect of a pregnancy. Fear for the health of the child may lead those affected to control and hide their symptoms. Some studies have reported that in most cases there is an apparent improvement in the eating disorder but there is regression to the pre-pregnancy state or even deterioration in the condition after giving birth (Rocco et al 2005).
Women with active eating disorders are at risk of delivering babies who are small for gestational age or with low birthweight (Koubaa et al 2005). Midwives need to be aware of suggestive signs of the eating disorders and discuss the risks of undernutrition in pregnancy (Franko & Spurrell 2000). The midwife and obstetrician need to closely monitor the pregnancy and there should be adequate support for the woman and her family to address the conditions in the postnatal period.
Conclusion
Nausea and vomiting in pregnancy are common and unpleasant but the more serious and potentially life-threatening condition of hyperemesis gravidarum is fortunately rare. Some cases may be avoided if the vomiting is treated promptly and effectively. The midwife should invest time in initial assessment and identification of women who may be at risk, and ensure that support with information is available to them. The midwife should be able to differentiate between physiological and pathological vomiting and manage or refer according to severity.
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