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Hyperemesis gravidarum - definition, epidemiology, pathophysiology, complications, management

Definition:
Mild to moderate nausea and vomiting are seen commonly until approximately 16 weeks in most pregnant ladies. Although nausea and vomiting tend to be worse in the morning, thus erroneously termed morning sickness, they frequently continue throughout the day. In some cases, however, it is severe and unresponsive to simple dietary modification and antiemetics.
Hyperemesis gravidarum is defined as vomiting sufficiently severe to produce weight loss, dehydration, alkalosis from loss of hydrochloric acid and hypokalemia. Rarely, acidosis from partial starvation and transient hepatic dysfunction develop.
Modified PUQE scoring index (Pregnancy-Unique Quantification of Emesis and Nausea) can be used to quantify the severity of nausea and vomiting. 

Epidemiology:
There appears to be an ethnic or familial predilection. The hospitalization rate for hyperemesis is around 0.5 to 0.8%. Hospitalization is less common in obese women. In women hospitalized in a previous pregnancy for hyperemesis, up to 20 percent require hospitalization in a subsequent pregnancy.

Pathophysiology:
Hyperemesis appears to be related to high or rapidly rising serum levels of pregnancy-related hormones. The presumed culprits include human chorionic gonadotropin (hCG), estrogens, progesterone, leptin, placental growth hormone, prolactin, thyroxine and adreno-cortical hormones. Some studies have implicated the vestibular system while others have showed some involvement of psychological components.
Other factors that increase the risk for admission include
1) hyperthyroidism, 
2) previous molar pregnancy, 
3) diabetes, 
4) gastrointestinal illnesses and 
5) asthma. 
For unknown reasons, a female fetus increases the risk by 1.5-fold.

Complications:
Vomiting may be prolonged, frequent and severe.
1) Various degrees of acute renal failure from dehydration are encountered.
2) Life-threatening complications of continuous retching include Mallory-Weiss tears shown in the figure below. Others are esophageal rupture, pneumothorax and pneumomediastinum.
3) At least two serious vitamin deficiencies have been reported with hyperemesis in pregnancy. Wernicke encephalopathy from thiamine (vitamin B1) deficiency is not uncommon. Vitamin K deficiency has been reported causing maternal coagulopathy and fetal intracranial hemorrhage.


The photo shows a Mallory Weiss tear with the endoscope in retroflexion.

Management:
1) Eating small meals at more frequent intervals but stopping short of satiation is valuable. The herbal remedy, ginger, was effective as showed by this meta-analysis published in 2014. Ginger capsules 250 mg 4 times daily.
2) A number of antiemetics given orally or by rectal suppository as first-line agents. When simple measures fail, intravenous crystalloid solutions are given to correct dehydration, ketonemia, electrolyte deficits, and acid-base imbalances. Thiamine, 100 mg, is given to prevent Wernicke encephalopathy. Diclegis (Doxylamine and Pyridoxine (Vitamin B6) ) is the only FDA approved medication for nausea and vomiting in pregnancy. 
3) If vomiting persists after rehydration and failed outpatient management, hospitalization is recommended. Antiemetics such as 
- Promethazine 12.5-25 mg 4 hourly, 
- Prochlorperazine 5-10 mg 6 hourly, 
- Metoclopramide 5-10 mg 8 hourly are given parenterally.
With persistent vomiting after hospitalization, appropriate steps should be taken to exclude possible underlying diseases as a cause of hyperemesis (gastroenteritis, cholecystitis, pancreatitis, hepatitis, peptic ulcer and pyelonephritis).

Further readings:
- Hyperemesis gravidarum: current perspectives
- The clinical management of hyperemesis gravidarum
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