Note: DC Dutta's Textbook of Obstetrics is not directly available in the library, but the content below covers all the standard topics DC Dutta addresses on hyperemesis gravidarum, drawn from equivalent authoritative obstetric and clinical references.

Hyperemesis Gravidarum

Definition

• Intractable vomiting in pregnancy
• Weight loss >5% of pre-pregnancy body weight
• Dehydration and ketonuria
• Electrolyte and metabolic disturbances
• Inability to maintain adequate oral intake

Incidence

• Occurs in approximately 0.3% to 3% of all pregnancies (estimates vary by criteria used)
• It is the most common cause of hospitalization during the first half of pregnancy, second only to preterm labor overall
• About 10% of patients are affected throughout the entire pregnancy
• Leads to elective termination in approximately 2% of affected pregnancies

Risk Factors / Predisposing Factors

• Young age and nulliparity
• Non-Caucasian ethnicity (higher in Asian and Middle Eastern women)
• Multiple gestation (twins, triplets)
• Singleton female fetus
• Gestational trophoblastic disease (molar pregnancy - very high hCG)
• Hydrops fetalis
• Fetal karyotypic abnormalities (triploidy, trisomy 21)
• H. pylori infection - several studies show increased prevalence in HG patients
• Comorbidities: hyperthyroidism, psychiatric disorders, diabetes, GI disorders, asthma
• Previous HG (15-19% recurrence in subsequent pregnancies)

Etiology and Pathophysiology

1. Hormonal Theory (most accepted)

• hCG (human chorionic gonadotropin): Peak levels at 8-12 weeks correlate with peak symptoms. Conditions with very high hCG (molar pregnancy, multiple gestation) have more severe vomiting. hCG shares the alpha subunit with TSH and can stimulate TSH receptors.
• Estradiol (estrogen): Rising estrogen levels also correlate with severity of vomiting.

2. Helicobacter pylori

• Studies suggest higher infection rates with H. pylori in HG patients. A non-teratogenic H. pylori eradication regimen has been shown to reduce vomiting.

3. Maternal Cytokines

• Altered cytokine profiles may contribute to the pathogenesis.

4. Gastric Motility

• Gastric dysrhythmias and delayed emptying have been implicated.

5. Psychological Factors

• Psychosocial stress and anxiety are associated, though not causative.

Clinical Features

Symptoms:

• Persistent, intractable nausea and vomiting (often from 4-6 weeks gestation, peaking at 8-12 weeks)
• Dry mouth and altered taste (dysgeusia)
• Sialorrhea (excessive salivation/ptyalism)
• Hyperolfaction (hypersensitivity to smells)
• Inability to tolerate food or fluids
• Significant weight loss

Signs:

• Dehydration: dry mucous membranes, poor skin turgor, sunken eyes
• Hypotension (may be postural)
• Tachycardia
• Jaundice (rare - if liver involvement)
• Features of Wernicke encephalopathy in severe cases (confusion, ophthalmoplegia, ataxia)

Investigations / Laboratory Findings

Differential Diagnosis

• Peptic ulcer disease / gastritis
• Cholecystitis / cholelithiasis
• Appendicitis
• Pyelonephritis / UTI
• Pancreatitis
• Hepatitis
• Thyrotoxicosis (primary)
• Diabetic ketoacidosis
• Central nervous system pathology (raised ICP)
• Addison's disease

Complications

Maternal:

• Wernicke encephalopathy (thiamine/B1 deficiency) - confusion, nystagmus, ophthalmoplegia, ataxia
• Mallory-Weiss tears (esophageal mucosal tears from retching)
• Esophageal rupture (Boerhaave's syndrome - rare)
• Pneumomediastinum (rare)
• Severe hypokalemia causing cardiac arrhythmias
• Hyponatremia causing central pontine myelinolysis (if corrected too rapidly)
• Nutritional deficiencies: B vitamins, fat-soluble vitamins, Vitamin K (bleeding diathesis)
• Psychological: depression, fear of future pregnancy
• Deep vein thrombosis (dehydration + immobility)

Fetal:

• Low birth weight (poor maternal weight gain)
• Small for gestational age (SGA)
• Prematurity
• Low 5-minute Apgar scores
• Vitamin K deficiency leading to bleeding diathesis (fetal)

Management

General Principles:

• Reassurance and psychological support
• Avoid triggers (strong smells, fatty/spicy food)
• Frequent small, bland meals (dry carbohydrates, crackers)
• Rest

Step 1 - Outpatient (Mild Cases):

• Dietary modification: small frequent meals, avoid triggers
• Ginger (extract or supplements) - randomized trials show benefit over placebo
• Pyridoxine (Vitamin B6) - effective, safe first-line agent
• Acupressure at the P6 point (wrist) - some benefit
• Doxylamine + Pyridoxine (Diclegis/Bonjesta) - first-line antiemetic combination (safe in pregnancy)

Step 2 - Pharmacological (Moderate Cases):

Step 3 - Inpatient Management (Severe / Refractory Cases):

• Ringer's lactate or Normal Saline: Up to 2 L over 3-5 hours, then titrate to maintain urine output >100 mL/hour
• Thiamine 100 mg IV must be given before any dextrose-containing fluid to prevent Wernicke encephalopathy
• Dextrose-containing fluids (D5/0.45% NS) continued until ketonuria clears
• Correct hypokalemia (add potassium to fluids)
• Correct hyponatremia slowly (risk of central pontine myelinolysis if corrected too rapidly)
• Monitor magnesium and ionized calcium

• Used for refractory hyperemesis
• Methylprednisolone 16 mg PO/IV 3x/day for 3 days, then taper
• Hydrocortisone 300 mg/day IV for 3 days then taper
• Caution: Avoid in the first trimester if possible - weak association with fetal orofacial clefts (1-2/1000 exposed)

• If H. pylori infection confirmed, a non-teratogenic eradication regimen may reduce vomiting

Step 4 - Nutritional Support:

• Enteral nutrition (nasogastric tube): Preferred over TPN in women who cannot maintain weight despite medical therapy
• Total Parenteral Nutrition (TPN): Last resort
  • Complications include catheter sepsis (~25%), venous thrombosis (~3%)
  • PICC lines preferred over central venous catheters (lower morbidity)

Transient Gestational Hyperthyroidism

• Is transient and self-limiting
• Resolves as vomiting improves
• Usually does not require antithyroid medication
• Treatment is supportive (rehydration and antiemetics)

Prognosis

• Most cases resolve by 20 weeks gestation; 10% persist throughout pregnancy
• Maternal and fetal outcomes are generally good with adequate treatment
• Recurrence risk in subsequent pregnancies: 15-19% (vs. 0.7% in those without prior HG)
• Women with poor weight gain have higher rates of SGA babies, preterm delivery, and low birth weight