MEDICINE
REVIEW ARTICLE
Nausea and Vomiting in Pregnancy
Ioannis Mylonas, Andrea Gingelmaier, Franz Kainer
SUMMARY
Introduction: About 50–90% of all pregnant women experience nausea and vomiting. Generally,
these symptoms discontinue within the first 20 weeks of pregnancy. However, in up to 20%
symptoms persist for the duration of pregnancy. Methods: Selective literature review. Results:
Symptoms are often nonspecific. Most women suffer from frequent or constant vomiting. Blood
results (for example urea and electrolyte disturbance, hematocrit elevation) and urinalysis (in
particular ketonuria) are helpful diagnostic indicators. First treatment should be dietary advice.
Vitamin B6 (pyridoxine), antihistamines and anticholinergics as well as other low-dose antiemetics
and gastrointestinal agents, may be given. Inpatient treatment is advisable for severe cases with
electrolyte imbalance. Discussion: The etiology of emesis and hyperemesis gravidarum are not
fully understood. It is likely that physiological as well as psychological causes play a part in its
development. If vomiting persists and symptoms are severe alternative differential diagnoses
should be considered.
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Key words: emesis, vomiting, pregnancy, diagnosis, treatment
S
ome 50–90% of pregnant women develop nausea and vomiting during pregnancy (1).
Isolated morning sickness affects only about 2% of pregnant women, whereas over
80% suffer from symptoms throughout the entire day. As a rule, nausea and vomiting cease
in the first 20 weeks of pregnancy; in up to 20% of cases, symptoms may last for the entire
pregnancy (1, 2).
Emesis gravidarum is the term used for nausea as well as pregnancy-related vomiting,
but without feelings of sickness and impairment to wellbeing. An important distinction
needs to be made for the transition to persistent vomiting with a frequency of more than
five times a day, weight loss of more than 5%, and impaired intake of food and fluids;
this is known as hyperemesis gravidarum (synonyms: excessive vomiting during
pregnancy, early gestosis). The condition can be life threatening for the patient and has
to be diagnosed and treated at once. Hyperemesis gravidarum is vomiting with
threatening symptoms during pregnancy, accompanied by dehydration, acidosis due to
lack of nutrition, alkalosis due to loss of hydrochloride, and hypokalemia. Clinically,
hyperemesis gravidarum is differentiated into grade 1, with feelings of sickness without
metabolic imbalance and grade 2 with pronounced feelings of sickness and metabolic
imbalance. The incidence of hyperemesis is 0.5–2% worldwide; regional, social, and
temporal differences exist (5).
This review article presents etiology, pathophysiology, clinical presentation, diagnosis,
and therapy, on the basis of a selective literature review.
Etiology and pathophysiology
The etiology of emesis and hyperemesis gravidarum is not clear. Physiological as well as
psychological factors are likely to be involved.
Likely risk factors for hyperemesis gravidarum to develop include: a background
of migration, obesity, multiple pregnancy, trophoblastic disorders, hyperemesis
gravidarum in previous pregnancy, nulliparity, metabolic causes (e.g., hyperthyroidism,
hyperparathyroidism, hepatic dysfunction, impaired lipid metabolism), and eating disorders
such as bulimia or anorexia (2, 6, 7).
1. Frauenklinik – Klinikum Innenstadt, Ludwig-Maximilian-Universität München, München: Dr. med. Mylonas, Dr. med. Gingelmaier,
Prof. Dr. med. Kainer
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DIAGRAM 1
Algorithm for diagnosis of hyperemesis gravidarum, according to (e20)
GOT, glutamatoxalacetate transaminase; GPT, glutamatpyruvate transaminase
Psychosomatic causes
The often assumed cause of hyperemesis gravidarum during the first trimester is a
psychosomatic disorder, which may be explained with fear of becoming a parent.
Pregnant women with stress and emotional tensions often have this condition. But only
few scientific data confirm this theory. In the best known study, the psychological
Cornell Medical Index was measured in 44 pregnant patients with, and 49 pregnant
women without, hyperemesis gravidarum. The psychological test Minnesota Multiphasic
Personality Inventory (MMPI) was applied only to the pregnant women with hyperemesis
gravidarum.
Both studies with different question scores showed that patients with hyperemesis had an
excessive bond with their mothers and more frequently had hysterical fits and infantile
personalities (8, 9).
Hyperemesis gravidarum occurs more often in personality disorders and depressive
disorders, but the association has not been studied to a sufficient extent (10).
Human chorionic gonadotropin
An association between nausea, vomiting, and an increased production of human chorionic
gonadotropin (hCG) is assumed because hyperemesis is often associated with multiple
pregnancies and trophoblastic disorders, with hCG concentrations being elevated in both
(11, e1–e5). However, this has not been proven conclusively up to now. Many women with
elevated hCG do not suffer from nausea and vomiting. And patients with chorionic
carcinoma, who also have raised hCG measurements, have not nausea either.
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Hormones
Estrogen, progesterone, adrenal, and pituitary hormones may also trigger hyperemesis. The
data situation is not straightforward, however (12). In patients with hyperemesis,
progesterone levels are lower (13) or elevated (14). Other researchers found no association
between hyperemesis and progesterone concentrations (e5, 15). Progesterone treatment
does not improve the complaints (8, 9). The fact that nausea is known to occur during
estrogen treatment suggests that estrogen may play a role in hyperemesis. Several
prospective studies found raised estrogen concentrations in association with hyperemesis
(14, 16), whereas others found no association (9, e6). Interestingly, hyperemesis
gravidarum is more often associated with a female fetus and might thus hint at a higher
concentration of estrogen in utero (17). Patients with hyperemesis probably react more
sensitively to estrogen effects than asymptomatic pregnant women (13).
TABLE 1
Differential diagnosis in sustained nausea and vomiting in pregnancy
Causes
Pregnancy associated
Gastrointestinal
Urogenital
Metabolic
Neurological
Other causes
Differential diagnosis
Diagnostic pointers
Emesis gravidarum (< 5 x/d)
Mostly in the morning, watchful waiting
Hyperemesis gravidarum (> 5 x/d)
Ketonuria, ketonemia
Pre-eclampsia
Prodromal stage of eclampsia in 2nd and 3rd trimester
Acute fatty liver
Clinical symptoms, serology, ultrasonography
Gastroenteritis
Clinical symptoms, watchful waiting, stool culture
Hepatitis
Raised transaminases
Appendicitis
Early pregnancy: typical points for pain on pressure
Late pregnancy: no typical leading symptoms (caution!)
Pancreatitis
Clinical symptoms, serology, amylases, lipases
Ileus and subileus
Clinical symptoms, plain abdominal radiography
(even in pregnancy)
Hepatic or
cholecystic disorders
Serology, ultrasonography of upper abdomen
Stomach ulcer or duodenal ulcer
Gastroscopy
Stomach cancer
Gastroscopy
Diaphragmatic hernia
Gastroscopy
Pyelonephritis
Clinical symptoms, urinary status, creatinine
Nephrolithiasis
Ultrasonography
Degenerative uterine fibroids
Ultrasonography
Uremia
Urinary status, creatinine
Diabetic ketoacidosis
Clinical symptoms, urinary status
Porphyria
Serology
Addison's disease
Clinical symptoms, serology
Hyperthyroidism
fT3, fT4, TSH
Thyrotoxicosis
Clinical symptoms, serology
Wernicke’s encephalopathy
Medical history, clinical course, if required magnetic
resonance imaging
Vestibular disorders
Nystagmus, impaired hearing
Korsakoff's psychosis
Medical history, clinical course
Migraine
Medical history
Food poisoning
Medical history
Iron medication
Medical history
Drug poisoning
Medical history
fT3, free triiodothyronine; fT4, free tretraiodothyronine; TSH, thyreoid stimulating hormone
Adapted from e20, in: Facharzt Geburtsmedizin, Urban und Fischer Verlag, with kind permission of Elsevier GmbH
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Helicobacter pylori
Chronic infection with Helicobacter pylori is also a possible cause of hyperemesis
gravidarum (18). Histological evaluation of the stomach mucosa showed that this causative
agent was present in almost 95% of patients with hyperemesis and in 50% of controls (19).
Another study found the H pylori genome in the saliva of 61.8% of patients with
hyperemesis gravidarum (21 of 34 patients), compared with 27.6% of pregnant women
without symptoms (20). This association seems confirmed by the fact that in two
observational studies with a total of five patients, no improvement in symptoms occurred
after standard drug treatment, whereas antibiotic treatment for H pylori resulted in a clear
improvement of symptoms (21, e7).
Changes in gastrointestinal motility
During pregnancy, a woman's gastrointestinal motility is limited owing to progesterone
(22). Gastric dysrythmias may also occur (23). The impaired motility may therefore contribute
to hyperemesis gravidarum.
Hyperthyroidism
Hyperthyroidism has also been linked to hyperemesis gravidarum (24). While fT3 and fT4
were in the normal range, the expression of thyroid stimulating hormone (TSH) was
decreased. The assumption is that a self limiting, transient hyperthyroidism of hyperemesis
gravidarum (THHG) exists. THHG may prevail up to the 18th week of gestation and does
not require treatment. The conditions for the diagnosis of THHG are:
> That pathological serology results are confirmed during hyperemesis,
> That no hyperthyroidism existed before the pregnancy,
> That no clinical signs of hyperthyroidism exist, and
> That a negative antibody is present.
Clinical presentation and diagnosis
The clinical symptoms are mostly unspecific and uncharacteristic. The main symptom is
excessive, frequent vomiting that lasts all day. Clinical signs of desiccation with a loss in
volume, weight loss, and metabolic ketoacidosis and ketonemia (fruity smell on the breath)
may also be present. This may be associated with pyrexia and hepatic symptoms such as
jaundice. Rare symptoms include drowsiness and intellectual slowness, which may result
in delirium. Further to the clinical symptoms, chemical laboratory tests (hematocrit,
electrolytes, transaminases, bilirubin, thyroid function) and urinary status (positive ketone
bodies, specific weight, aciduria) are pointers (diagram 1). Ultrasonography to confirm an
TABLE 2
Antiemetics and dosages in hyperemesis
gravidarum
FDA
Effective substance Dosage
category
A
Pyridoxone (vitamin B6) 20 mg p.o.; 3 x daily
B
Dimenhydrinate
62 mg IV; 2 x daily
50 mg p.o.; 3–4 x daily
Supp.: 1–3 x daily
Diphenhydramine
25–50 mg IV/p.o.;
Every 6–8 hours
Meclozine
25–100 mg p.o.; 2–4 x
daily; Supp.: 1 x daily
C
Metoclopramide
10 mg p.o.; 4 x daily
Ondansetron
2–4 mg IV every 6–8 hours
Promethazine
12.5–25 mg p.o./IV
up to 6 x daily
Adapted from e20: Facharzt Geburtsmedizin, Urban und Fischer Verlag, with
kind permission of Elsevier GmbH
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intact, intrauterine pregnancy and to rule out a multiple pregnancy, trophoblastic disorders,
and neoplasia should also be conducted (diagram 1). If the vomiting is sustained and the
symptoms are striking, differential diagnostic causes should be considered (table 1).
Treatment
Nausea and vomiting in early pregnancy are mostly self limiting and often need merely
symptomatic treatment. The therapy depends on the respective symptoms, and the range
of treatments includes dietary changes, e.g., with several, small meals and avoidance of
acidic fruit or fruit juices, to inpatient admission with parenteral feeding. Primarily,
dietary changes on an outpatient basis seem advisable; if necessary, antiemetics may be
added in small dosages. In hyperemesis gravidarum grade 2, the woman should be admitted
as an inpatient.
DIAGRAM 2
Inpatient procedure in hyperemesis gravidarum, adapted from e20
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Outpatient treatment
The first therapeutic step should be extensive dietary advice. The desirable foods should be
rich in carbohydrates and low in fat and should be consumed in many small meals.
Disagreeable smells that might trigger nausea and vomiting should be avoided (e.g., the
smell of meat). Emotional support and, if needed, psychosomatic care administered by a
psychologist or a doctor with additional psychosomatic training is also important.
Depending on the severity of the patient's illness, supportive counselling, crisis interventions,
or psychosomatic or psychiatric care might be required. A more extensive explanation of
the therapeutic options would lead too far in this context. Drug treatments include vitamin
B6 (pyridoxine), antihistamines, anticholinergics, further low-dosage antiemetics, and
gastrointestinally effective substances. An analysis of 28 randomized trials into the
treatment of hyperemesis gravidarum showed that antiemetics reduce the frequency of
nausea in early pregnancy and are more effective than placebo. But some drugs had side
effects, especially fatigue. Vitamin B6 (pyridoxine) was more effective than placebo on
treating nausea and vomiting in pregnant women (25). At a dosage of 10–25 mg, thrice
daily, pyridoxine reduces symptoms; treatment should be started using a low dose (e8).
Antihistamines and anticholinergics such as meclozine, dimenhydrinate, and
diphenhydramine are used primarily to treat nausea and vomiting in pregnancy (table 2).
These substances are more effective than placebo in treating emesis and hyperemesis (e9).
If needed, ondansetron and promethazine can also be used in severe cases of hyperemesis
gravidarum (table 2). To improve gastrointestinal motility, metoclopramide may also be
used without problems. Additional alternatives include acupressure and ginger extracts.
Acupressure, especially on the P6 point (Neiguan) on the wrist, has also been suggested for
the treatment of pregnancy related nausea (e10). But sufficient scientific proof is absent,
which confirms the efficacy of this method. A popular therapeutic alternative is ginger (e11),
which may be administered in several ways (e.g., as tea). Powdered ginger (1 g/d) has been
found to be more effective than placebo in hyperemesis gravidarum (e12). Although ginger
is apparently not teratogenic, possible side effects and the optimal dosage are unknown
(e8, e13).
Inpatient treatment
Pregnant women with severe hyperemesis gravidarum and electrolyte imbalances should
be admitted as inpatients. The primary treatment is total food withdrawal, accompanied by
substitution of volume and electrolytes (at least 3 000 ml/d), correction of the electrolyte
imbalance, administration of vitamins and antiemetics, and parenteral administration of
carbohydrate and amino acid solutions (about 8 400 to 10 500 kJ/d). Treatment should be
continued until the vomiting ceases or occurs less than three times daily. Subsequently,
food should be slowly reintroduced (diagram 2). Diazepam is also positive in hyperemesis
(e14), probably because of its sedative component. If this is used, however, possible
dependency problems should be taken into consideration. Diazepam should be used with
caution in pregnancy due to possible fetal side effects. Corticoids (e.g., hydrocortisone) may
also be used in hyperemesis that is refractory to treatment (e15). Although corticosteroids
during pregnancy are classed as safe, a meta-analysis showed a slightly increased risk of
fetal malformations, especially during the first trimester (e16). If symptoms persist,
relevant disorders should be excluded by differential diagnosis. Continuing psychosomatic
care and emotional support are also desirable (10). Often, symptoms are improved merely
by inpatient admission. This confirms the therapeutic approach used by Thure von Uexküll,
who demanded primarily supportive, embracing attention for such pregnant women (e17).
If a psychotic component to the disorder is suspected, however, a psychiatrist needs to be
consulted.
Maternal and fetal prognosis
Women with uncomplicated emesis gravidarum have a better fetal prognosis than the
normal cohort, including a lower tendency to miscarry, to retarded intrauterine growth, and
premature birth (2, 4, e18). Hyperemesis gravidarum, however, is associated with increased
esophageal rupture (severe vomiting), Mallory-Weiss syndrome (acute pressure increase
owing to vomiting), pneumothorax, neuropathy, pre-eclampsia, and fetal growth retardation
(2, 4, e19).
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Conclusion
Although hyperemesis gravidarum is very rare compared with frequent mild vomiting
during pregnancy, its clinical and socioeconomic aspects are important. The disorder is
accompanied by a severely impaired quality of life for the patient and with high costs to the
healthcare system. Since the pathogenesis of hyperemesis gravidarum is thus far unknown,
treatment is mostly symptomatic and often suboptimal.
Conflict of Interest Statement
The authors declare that no conflict of interest exists according to the Guidelines of the International Committee of Medical
Journal Editors.
Manuscript received on 28 August 2006, final version accepted on 17 January 2007.
Translated from the original German by Dr Birte Twisselmann.
REFERENCES
For e-references please refer to the additional references listed below.
1. Gadsby R, Barnie-Adshead AM, Jagger C: A prospective study of nausea and vomiting during pregnancy. Br J Gen
Pract 1993; 43: 245–8.
2. Broussard CN, Richter JE: Nausea and vomiting of pregnancy. Gastroenterol Clin North Am 1998; 27: 123–51.
3. Kallen B: Hyperemesis during pregnancy and delivery outcome: a registry study. Eur J Obstet Gynecol Reprod Biol
1987; 26: 291–302.
4. Tsang IS, Katz VL, Wells SD: Maternal and fetal outcomes in hyperemesis gravidarum. Int J Gynaecol Obstet 1996; 55:
231–5.
5. Jordan V, MacDonald J, Crichton S, Stone P, Ford H: The incidence of hyperemesis gravidarum is increased among
Pacific Islanders living in Wellington. N Z Med J 1995; 108: 342–4.
6. Abell TL. Nausea and vomiting of pregnancy and the electrogastrogram: old disease, new technology. Am J
Gastroenterol 1992; 87: 689–91.
7. Abell TL, Riely CA: Hyperemesis gravidarum. Gastroenterol Clin North Am 1992; 21: 835–49.
8. Fairweather DV: Nausea and vomiting during pregnancy. Obstet Gynecol Annu 1978; 7: 91–105.
9. Fairweather D: Nausea and vomiting in pregnancy. Am J Obstet Gynecol 1968; 102: 135–75.
10. Munch S: Chicken or the egg? The biological-psychological controversy surrounding hyperemesis gravidarum.
Soc Sci Med 2002; 55: 1267–78.
11. James WH: The associated offspring sex ratios and cause(s) of hyperemesis gravidarum. Acta Obstet Gynecol
Scand 2001; 80: 378–9.
12. Borgeat A, Fathi M, Valiton A: Hyperemesis gravidarum: is serotonin implicated? Am J Obstet Gynecol 1997; 176:
476–7.
13. Jarnfelt-Samsioe A: Nausea and vomiting in pregnancy: a review. Obstet Gynecol Surv 1987; 42: 422–7.
14. Yoneyama Y, Suzuki S, Sawa R, Yoneyama K, Doi D, Otsubo Y, Araki T: The T-helper 1/T-helper 2 balance in
peripheral blood of women with hyperemesis gravidarum. Am J Obstet Gynecol 2002; 187: 1631–5.
15. Lagiou P, Tamimi R, Mucci LA, Trichopoulos D, Adami HO, Hsieh CC: Nausea and vomiting in pregnancy in relation
to prolactin, estrogens, and progesterone: a prospective study. Obstet Gynecol 2003; 101: 639–44.
16. Depue RH, Bernstein L, Ross RK, Judd HL, Henderson BE: Hyperemesis gravidarum in relation to estradiol levels,
pregnancy outcome, and other maternal factors: a seroepidemiologic study. Am J Obstet Gynecol 1987; 156:
1137–41.
17. Schiff MA, Reed SD, Daling JR: The sex ratio of pregnancies complicated by hospitalisation for hyperemesis
gravidarum. BJOG 2004; 111: 27–30.
18. Kazerooni T, Taallom M, Ghaderi AA: Helicobacter pylori seropositivity in patients with hyperemesis gravidarum. Int J
Gynaecol Obstet 2002; 79: 217–20.
19. Bagis T, Gumurdulu Y, Kayaselcuk F, Yilmaz ES, Killicadag E, Tarim E: Endoscopy in hyperemesis gravidarum and
Helicobacter pylori infection. Int J Gynaecol Obstet 2002; 79: 105–9.
20. Hayakawa S, Nakajima N, Karasaki-Suzuki M et al.: Frequent presence of Helicobacter pylori genome in the saliva of
patients with hyperemesis gravidarum. Am J Perinatol 2000; 17: 243–7.
21. El Younis CM, Abulafia O, Sherer DM: Rapid marked response of severe hyperemesis gravidarum to oral erythromycin.
Am J Perinatol 1998; 15: 533–4.
22. Koch KL, Frissora CL: Nausea and vomiting during pregnancy. Gastroenterol Clin North Am 2003; 32: 201–34, vi.
23. Walsh JW, Hasler WL, Nugent CE, Owyang C: Progesterone and estrogen are potential mediators of gastric slow-wave
dysrhythmias in nausea of pregnancy. Am J Physiol 1996; 270: G506–14.
24. Chan NN: Thyroid function in hyperemesis gravidarum. Lancet 1999; 353: 2243.
25. Sahakian V, Rouse D, Sipes S, Rose N, Niebyl J: Vitamin B6 is effective therapy for nausea and vomiting of pregnancy:
a randomized, double-blind placebo-controlled study. Obstet Gynecol 1991; 78: 33–6.
ADDITIONAL REFERENCES
e1. Basso O, Olsen J: Sex ratio and twinning in women with hyperemesis or pre-eclampsia. Epidemiology 2001;
12: 747–9.
Dtsch Arztebl 2007; 104(25): A 1821–6 ⏐ www.aerzteblatt.de
7
MEDICINE
e2. Goodwin TM, Hershman JM, Cole L: Increased concentration of the free beta-subunit of human chorionic
gonadotropin in hyperemesis gravidarum. Acta Obstet Gynecol Scand 1994; 73: 770–2.
e3. Askling J, Erlandsson G, Kaijser M, Akre O, Ekbom A: Sickness in pregnancy and sex of child. Lancet 1999;
354: 2053.
e4. del Mar Melero-Montes M, Jick H: Hyperemesis gravidarum and the sex of the offspring. Epidemiology 2001;
12: 123–4.
e5. Masson GM, Anthony F, Chau E: Serum chorionic gonadotropin (hCG), schwangerschaftsprotein 1 (SP1),
progesterone and oestradiol levels in patients with nausea and vomiting in early pregnancy. Br J Obstet Gynaecol
1985; 92: 211–5.
e6. Jordan V, Grebe SK, Cooke RR, Ford HC, Larsen PD, Stone PR, Salmond CE: Acidic isoforms of chorionic
gonadotrophin in European and Samoan women are associated with hyperemesis gravidarum and may be
thyrotrophic. Clin Endocrinol (Oxf) 1999; 50: 619–27.
e7. Jacoby EB, Porter KB: Helicobacter pylori infection and persistent hyperemesis gravidarum. Am J Perinatol
1999; 16: 85–8.
e8. Jewell D, Young G: Interventions for nausea and vomiting in early pregnancy. Cochrane Database Syst Rev 2003:
CD000145.
e9. Leathem AM: Safety and efficacy of antiemetics used to treat nausea and vomiting in pregnancy. Clin Pharm
1986; 5: 660–8.
e10. de Aloysio D, Penacchioni P: Morning sickness control in early pregnancy by Neiguan point acupressure. Obstet
Gynecol 1992; 80: 852–4.
e11. Vutyavanich T, Kraisarin T, Ruangsri R: Ginger for nausea and vomiting in pregnancy: randomized, double-masked,
placebo-controlled trial. Obstet Gynecol 2001; 97: 577–82.
e12. Fischer-Rasmussen W, Kjaer SK, Dahl C, Asping U: Ginger treatment of hyperemesis gravidarum. Eur J Obstet
Gynecol Reprod Biol 1991; 38: 19–24.
e13. Jewell D: Nausea and vomiting in early pregnancy. Clin Evid 2003: 1561–70.
e14. Ditto A, Morgante G, la Marca A, De Leo V: Evaluation of treatment of hyperemesis gravidarum using parenteral
fluid with or without diazepam. A randomized study. Gynecol Obstet Invest 1999; 48: 232–6.
e15. Nelson-Piercy C, Fayers P, de Swiet M: Randomised, double-blind, placebo-controlled trial of corticosteroids for
the treatment of hyperemesis gravidarum. BJOG 2001; 108: 9–15.
e16. Park-Wyllie L, Mazzotta P, Pastuszak A et al.: Birth defects after maternal exposure to corticosteroids: prospective
cohort study and meta-analysis of epidemiological studies. Teratology 2000; 62: 385–92.
e17. Uexküll T et al.: Psychosomatische Medizin. Modelle ärztlichen Denkens und Handelns. München: Urban &
Schwarzenberg Verlag 2002.
e19. Brandes JM: First-trimester nausea and vomiting as related to outcome of pregnancy. Obstet Gynecol 1967;
30: 427–31.
e19. Zhang J, Cai WW: Severe vomiting during pregnancy: antenatal correlates and fetal outcomes. Epidemiology
1991; 2: 454–7.
e20. Mylonas I: Hyperemesis gravidarum. In: Kainer F (Hrsg.), Facharzt Geburtsmedizin: Elsevier München, Jena:
Urban & Fischer Verlag; 2006.
Corresponding author
Dr. med. Ioannis Mylonas
1. Frauenklinik – Klinikum Innenstadt
Ludwig-Maximilian-Universität München
Maistr. 11
80337 München, Germany
[email protected]
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