Hyperemesis Gravidarum

Hyperemesis Gravidarum: Intro & Risks - Beyond Morning Sickness

• Severe, intractable nausea & vomiting of pregnancy (NVP).
• Diagnostic pointers:
  • Persistent vomiting unrelated to other causes
  • Weight loss >5% of pre-pregnancy body weight
  • Ketonuria, dehydration
  • Electrolyte imbalances (e.g., hypokalemia)
• Onset usually <9 weeks gestation; often resolves by 20 weeks.
• Risk Factors:
  • Multiple gestation (e.g., twins)
  • Molar pregnancy (hydatidiform mole)
  • History of HG in prior pregnancy
  • Female fetus
  • Hyperthyroidism
  • Nulliparity

⭐ HG is strongly associated with elevated levels of human chorionic gonadotropin (hCG) and estradiol, often seen in molar or multiple pregnancies.

HG Pathophysiology - Hormonal Havoc

• hCG Overdrive: ↑↑ Human Chorionic Gonadotropin (hCG) is a key culprit.
  • Specific hCG isoforms are more emetogenic.
  • hCG structurally similar to TSH, can stimulate thyroid → gestational transient thyrotoxicosis.
• Estrogen & Progesterone: ↑ Estrogen may sensitize vomiting centers. ↑ Progesterone relaxes GI smooth muscle, delaying gastric emptying.
• GDF15: Placental Growth Differentiation Factor 15 (GDF15) acts directly on brainstem chemoreceptor trigger zone.

⭐ hCG levels often peak around 9-10 weeks gestation, coinciding with the typical peak of HG symptoms.

HG Clinical Features & Diagnosis - Unmasking the Misery

• Key Manifestations:
  • Severe, intractable Nausea & Vomiting (NVP).
  • Significant weight loss: >5% of pre-pregnancy body weight.
  • Ketonuria (marker of starvation).
  • Dehydration signs: Tachycardia, hypotension, dry mucous membranes, oliguria.
  • Electrolyte imbalances: Hypokalemia, hyponatremia, hypochloremic alkalosis.
  • Ptyalism (excessive salivation).
  • Rare: Wernicke's encephalopathy (thiamine deficiency).
• Diagnostic Process:
  • Primarily a clinical diagnosis of exclusion.
  • Rule out other causes (e.g., UTI, gastroenteritis, molar pregnancy, thyroid disease).

  • ⭐ Gestational transient thyrotoxicosis (↓TSH, ↑free T4) is common (50-60%), typically resolving by 20 weeks without specific antithyroid treatment.

HG Complications & Workup - Danger Signs

• Maternal:
  • Weight loss >5%
  • Dehydration, electrolyte imbalance (↓K⁺, ↓Na⁺, alkalosis)
  • Ketonuria
  • Wernicke's encephalopathy (thiamine deficiency) 📌 (B1)
  • Mallory-Weiss tear, liver/renal issues
• Fetal: IUGR, low birth weight, preterm birth.
• Workup:
  • Urine ketones, electrolytes, LFTs, RFTs, TSH.
  • USG: Exclude molar/multiple pregnancy.
• Danger Signs: Persistent vomiting, weight loss >5%, dehydration (↓urine, tachycardia), neurological symptoms (confusion, ataxia), jaundice.

  ⭐ Prophylactic thiamine (B1) is crucial in severe HG to prevent Wernicke's encephalopathy.

HG Management - Stemming the Storm

• Initial: Small, frequent, bland meals; avoid triggers. Hydration (ORS).
• Pharmacotherapy (Stepwise):
  • 1st Line: Pyridoxine (Vit B6) ± Doxylamine.
  • 2nd Line: Antihistamines (Promethazine), Dopamine antagonists (Metoclopramide).
  • 3rd Line: Ondansetron (⚠️ QTc prolongation; caution in 1st trimester).
  • Refractory: Corticosteroids (e.g., Prednisolone 10-20mg TDS, after 10 weeks gestation, taper slowly).
• Severe HG (Inpatient):
  • IV fluids: Normal Saline + KCl. Correct dehydration & electrolytes.
  • Thiamine 100mg IV/IM daily (prevent Wernicke's).
  • Nutritional support: Enteral/Parenteral if oral intake fails.

⭐ In severe HG, always administer thiamine before glucose-containing IV fluids to prevent precipitating Wernicke's encephalopathy.

High‑Yield Points - ⚡ Biggest Takeaways

• Severe NVP causing >5% weight loss, dehydration, ketonuria, and electrolyte imbalance (hypokalemia).
• Onset usually <9 weeks, peaks 10-12 weeks, typically resolves by 20 weeks.
• Strongly linked to high hCG levels (e.g., molar pregnancy, multiple gestations).
• Diagnosis of exclusion: rule out UTI, gastroenteritis, thyrotoxicosis.
• Management: IV hydration, antiemetics (e.g., ondansetron), thiamine to prevent Wernicke's encephalopathy.
• Ptyalism can occur; risk factors include nulliparity and prior HG history.