Clinical meaning
Hyperemesis gravidarum involves a complex interplay of hormonal, immunological, and gastrointestinal factors. The primary trigger is rapidly rising hCG, which peaks at 8-12 weeks and stimulates the CTZ via vagal afferents. hCG structural homology with TSH activates thyroid receptors, causing gestational thyrotoxicosis in up to 60% of cases. Estrogen slows gastric motility and relaxes the lower esophageal sphincter. Progesterone reduces smooth muscle tone throughout the GI tract. Severe, prolonged emesis causes dehydration, leading to hemoconcentration, reduced GFR, and prerenal azotemia. Metabolic consequences include hypochloremic hypokalemic metabolic alkalosis from gastric HCl loss, thiamine depletion from impaired intake and increased metabolic demand, and ketosis from fat catabolism. The clinician must prescribe evidence-based stepwise antiemetic therapy, manage fluid and electrolyte replacement, prevent Wernicke encephalopathy, and determine when parenteral or enteral nutrition is required.
Diagnosis & workup
Diagnostics & workup: - Order CMP: assess sodium, potassium, chloride, bicarbonate, BUN, creatinine, glucose, calcium, magnesium, phosphorus - Order urinalysis with specific gravity and ketones: specific gravity >1.030 and ketonuria confirm dehydration - Order TSH and free T4: expect suppressed TSH and mildly elevated free T4 in hCG-mediated thyrotoxicosis - Order liver function tests: mild transaminase elevation (<300 U/L) occurs in severe cases - Order amylase and lipase to rule out pancreatitis if persistent epigastric pain - Order thiamine level if prolonged course (>3 weeks) or neurological symptoms present - Consider abdominal ultrasound if biliary disease or molar pregnancy is suspected - Order quantitative hCG if gestational trophoblastic disease is a concern