Hyperemesis Gravidarum

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9 أقسام

Summary

Hyperemesis gravidarum is a serious pregnancy complication characterized by severe, persistent vomiting with weight loss, dehydration, and metabolic disturbances. It is strongly associated with elevated β-hCG and high-risk pregnancies such as multiple gestation and trophoblastic disease. Diagnosis is clinical, supported by laboratory and imaging investigations to exclude other causes. Management is stepwise, involving antiemetics, IV fluids, thiamine supplementation, and nutritional support, with care tailored to disease severity. Prompt recognition and treatment are essential to reduce maternal morbidity and adverse fetal outcomes

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Definition

Hyperemesis gravidarum (HG) is a severe form of nausea and vomiting in pregnancy, leading to significant maternal morbidity. Unlike the common nausea and vomiting of pregnancy (NVP), HG is characterized by persistent vomiting, >5% pre-pregnancy weight loss, dehydration, and electrolyte disturbances, often necessitating hospital care. It affects 0.3–3.6% of pregnancies and represents one of the most frequent indications for admission in early gestation.

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Etiology and Pathophysiology

NVP usually begins between 4–7 weeks’ gestation, peaks around week 9, and resolves by 20 weeks in most women. HG develops when symptoms are prolonged and severe.

  • Hormonal factors: Rapidly rising levels of β-hCG are implicated, stimulating the chemoreceptor trigger zone and vomiting center.

  • Other contributors: Genetic predisposition, immunological mechanisms, psychosocial factors, and associations with high hCG states (multiple gestation, molar pregnancy, Down syndrome).

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Risk Factors

  • Primigravidity

  • Previous history of HG

  • Multiple pregnancy

  • Hydatidiform mole

  • High maternal BMI

  • Migraine and gastroesophageal reflux disease (GERD)

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Clinical Features

HG typically presents in the first trimester with:

  • Severe nausea and vomiting

  • Weight loss >5% pre-pregnancy weight

  • Dehydration (dry mucous membranes, reduced skin turgor, oliguria)

  • Orthostatic hypotension, tachycardia

  • Hypersalivation, fatigue, constipation

  • Rarely, jaundice or neurological complications (e.g., Wernicke’s encephalopathy from thiamine deficiency)

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Investigations

Bedside

  • Weight monitoring

  • Urine dipstick: ketonuria (>1+)

Laboratory

  • Urea & electrolytes (hypokalemia, hyponatremia, dehydration)

  • Full blood count (infection, hemoconcentration)

  • LFTs, amylase (exclude hepatitis, gallstones, pancreatitis)

  • Thyroid function tests

  • Blood glucose (exclude DKA if diabetic)

  • Arterial blood gas in severe cases

Imaging

  • Obstetric ultrasound: confirm viability, gestational age, exclude multiple pregnancy or trophoblastic disease.

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Differential Diagnosis

Alternative causes of vomiting in pregnancy should be excluded, especially if onset is after 10 weeks:

  • Gastroenteritis, peptic ulcer disease, pancreatitis, hepatitis, cholecystitis

  • Urinary tract infection or pyelonephritis

  • Thyroid dysfunction, metabolic disorders

  • Neurological or drug-induced causes

  • Pregnancy complications (e.g., ectopic pregnancy, preeclampsia, acute fatty liver, hydatidiform mole)

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Complications

  • Maternal: electrolyte imbalance, hypokalemia, hyponatremia, metabolic alkalosis or acidosis, renal impairment, Wernicke’s encephalopathy.
  • Fetal: intrauterine growth restriction, low birth weight, preterm delivery.
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Management

Treatment is guided by severity:

  • Mild cases (community): oral antiemetics (first-line: cyclizine, prochlorperazine, promethazine, chlorpromazine), oral hydration, dietary advice, reassurance.

  • Moderate cases (ambulatory daycare): IV fluids (0.9% saline + potassium as indicated), parenteral antiemetics, thiamine supplementation, monitoring until ketonuria resolves.

  • Severe cases (inpatient): intensive IV rehydration, electrolyte correction, stepwise antiemetic therapy, proton pump inhibitors/H2 blockers if reflux present, thromboprophylaxis.

    • Second-line antiemetics: metoclopramide (≤5 days), domperidone, ondansetron.

    • Third-line: corticosteroids (IV hydrocortisone, then tapering oral prednisolone).

    • Refractory HG: enteral feeding or parenteral nutrition may be required.

Supportive Measures

  • Thiamine supplementation for all women with prolonged vomiting to prevent Wernicke’s encephalopathy.

  • VTE prophylaxis during admission.

  • Nutritional support and psychological reassurance.

Rare Indications for Pregnancy Termination

Considered only when HG is refractory to treatment and complicated by progressive renal impairment, hepatic dysfunction, or Wernicke’s encephalopathy.

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