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Hyperemesis Gravidarum at 12 Weeks with Haematemesis - Complete Clinical Review
BACKGROUND & DEFINITION
Hyperemesis gravidarum (HG) is severe, persistent vomiting that leads to complications - defined by:
- Weight loss >5% of pre-pregnancy body weight
- Ketonuria
- Dehydration and electrolyte imbalance
It occurs in 0.3-3% of pregnancies and is the most common cause of hospitalization in the first half of pregnancy (second only to preterm labor in the US). Peak symptom onset is 8-12 weeks gestation, which is exactly where this patient is.
The presence of haematemesis (2 episodes) marks this as a complicated case, most likely due to Mallory-Weiss tears - a recognized complication of forceful, repeated vomiting.
ETIOLOGY
The etiology is multifactorial:
1. Hormonal Factors
- hCG (beta-HCG): Peak levels correlate with peak HG symptoms. The alpha subunit of hCG shares homology with TSH - this causes thyroid-stimulating activity, transient gestational thyrotoxicosis, and suppressed TSH with mildly elevated free T4, seen in ~two-thirds of HG patients. Conditions with elevated hCG (multiple gestation, gestational trophoblastic disease, trisomy 21, hydrops fetalis) increase HG risk.
- Estrogen: Elevated estrogen (e.g., obesity) is associated with HG; estrogen and progesterone alter gastric motility and slow GI transit time.
- Gut hormones: Ghrelin and leptin are also implicated.
2. GI Dysmotility
Progesterone-mediated slowing of GI transit contributes to nausea and vomiting.
3. Helicobacter pylori Infection
Two meta-analyses have shown increased H. pylori infection rates in HG patients. Some studies report symptomatic improvement after H. pylori eradication.
4. Psychosocial/Sensory Triggers
Vomiting in HG is often triggered by olfactory, auditory, and visual stimuli. Psychosocial stress may contribute.
5. Genetic Predisposition
Familial clusters suggest a genetic component. HG recurs in 15-19% of second pregnancies in women who had HG in their first pregnancy (vs. 0.7% in women with unaffected first pregnancies).
Risk Factors
- Young, nulliparous women; non-Caucasian ethnicity (especially Asian, Middle Eastern)
- Female fetus or multiple gestation
- Personal/family history of HG
- Gestational trophoblastic disease, fetal trisomy 21, hydrops fetalis
- Pre-existing hyperthyroidism, psychiatric disorders, diabetes, GI disorders, asthma
HAEMATEMESIS IN HG - SPECIFIC ETIOLOGY
Two episodes of haematemesis in this context most likely represent:
- Mallory-Weiss tear (most common): Longitudinal mucosal laceration at the gastroesophageal junction from forceful, repeated retching/vomiting. Classic history is initial nonbloody vomiting followed by bloody emesis. Pregnancy, retching, and increased intra-abdominal pressure are direct causative factors.
- Boerhaave syndrome (rare but life-threatening): Full-thickness esophageal rupture from severe vomiting - a rare but serious complication.
- Peptic ulcer disease (less common in pregnancy; use of NSAIDs rare)
- Esophagitis/GERD: Up to 80% of pregnant women experience heartburn; severe retching can cause mucosal trauma.
- Sleisenger and Fordtran's Gastrointestinal and Liver Disease, p. 655 explicitly lists "Mallory-Weiss tears with upper GI bleeding" as a severe maternal complication of HG.
EVALUATION
Clinical Assessment
- Detailed history: onset, frequency, severity of vomiting; quantify using PUQE score (Pregnancy-Unique Quantification of Emesis and Nausea - assesses hours of nausea and episodes of emesis/retching per day)
- Assess for haematemesis: volume, color (bright red vs. coffee-ground), associated melaena
- Weight (compare to pre-pregnancy weight), vital signs (hypotension, tachycardia), mucous membranes, skin turgor, urine output
Laboratory Workup
| Test | What to Look For |
|---|
| CBC | Anemia (blood loss from Mallory-Weiss), hemoconcentration |
| Comprehensive metabolic panel | Hypokalemia, hyponatremia, contraction alkalosis, elevated anion gap, elevated transaminases (25-40% of HG), elevated bilirubin |
| Serum lipase | Pancreatitis (differential) |
| Thyroid function (TSH, free T4) | Transient gestational thyrotoxicosis (TSH suppressed, mildly elevated T4 in ~2/3 of HG) |
| Urinalysis | Ketonuria (diagnostic criterion), elevated specific gravity (dehydration), infection |
| Serum beta-hCG | Molar pregnancy, multiple gestation |
| Serum electrolytes | Hypokalemia, hypomagnesemia |
| Renal function | AKI from dehydration |
| H. pylori testing | Stool antigen or serology |
Imaging / Endoscopy
- Obstetric ultrasound: Rule out molar pregnancy, multiple gestation, confirm fetal viability and gestational age
- Upper GI endoscopy (EGD): Indicated in this case given haematemesis - to identify the source (Mallory-Weiss tear, peptic ulcer, esophagitis). EGD is safe in pregnancy when clinically indicated. Defer non-urgent endoscopy to second trimester if possible, but active significant bleeding warrants prompt evaluation.
Differential Diagnosis for Vomiting in Pregnancy (must exclude before diagnosing HG)
- Peptic ulcer disease
- Cholecystitis / biliary colic
- Acute pancreatitis
- Appendicitis
- Pyelonephritis / UTI
- Gastroparesis
- Hepatitis
- Hyperthyroidism (primary, not gestational)
- Central nervous system pathology
- Addison's disease
MANAGEMENT
Management should be stepwise, from conservative to escalating interventions. Goals: adequate hydration, nutrition, symptom control, correction of electrolyte abnormalities, and maternal-fetal wellbeing.
Step 1: Non-Pharmacologic (Outpatient, mild cases)
- Frequent, small meals; avoid empty stomach (triggers nausea)
- High-carbohydrate, dry starchy foods
- Avoid offensive odors; separate solid and liquid intake
- Ginger (extract): RCT evidence shows benefit vs. placebo regardless of dose/preparation
- Pyridoxine (Vitamin B6) + doxylamine (Diclegis/Bonjesta): First-line pharmacologic therapy per guidelines
- Acupressure (P6 pressure point): modest evidence for symptom benefit
Step 2: Pharmacologic Antiemetics
| Drug | Class | Notes |
|---|
| Pyridoxine + doxylamine | B6 + antihistamine | First-line (Diclegis) |
| Promethazine | Phenothiazine | Effective, sedation common |
| Prochlorperazine / Chlorpromazine | Phenothiazines | Dopamine antagonists; good efficacy |
| Metoclopramide | Dopamine antagonist | Effective; higher adverse effect profile |
| Ondansetron | 5-HT3 antagonist | Use when first-line fails; supported by controlled trial and widespread clinical use; some first-trimester cleft concerns (monitor) |
Step 3: IV Fluid Resuscitation (Hospital admission indicated when: hypotension, tachycardia, ketosis, weight loss, muscle wasting, inability to tolerate oral intake)
- Lactated Ringer's solution 2 L over 3-5 hours (500 mL/hr); then adjust to maintain urine output >100 mL/hr
- Thiamine 100 mg IV BEFORE any dextrose infusion - mandatory to prevent Wernicke encephalopathy
- Follow with D5/0.45% NaCl until ketones clear or oral intake resumes
- Correct hypokalemia (add K+ to IV fluids as needed)
- Correct hypomagnesemia, hypocalcemia - monitor ionized calcium
- Correct hyponatremia slowly (risk of central pontine myelinolysis with rapid correction)
Step 4: Management of Haematemesis (specific to this case)
- Assess hemodynamic stability
- Active resuscitation if unstable (IV access x2, type and crossmatch, hemodynamic monitoring)
- EGD when stable to identify and potentially treat the source
- Mallory-Weiss tears: most stop bleeding spontaneously; endoscopic therapy (injection, clips, thermal) if active bleeding
- PPI therapy (omeprazole or pantoprazole) - note omeprazole has animal fetal toxicity data; pantoprazole often preferred in pregnancy
- Maintain NPO if active bleeding; nasogastric tube if needed
Step 5: Refractory Hyperemesis
- Corticosteroids: Methylprednisolone 16 mg PO/IV q8h for 3 days (with 2-week taper) - reduces hospital readmission vs. promethazine; last-line agent; avoid in first trimester if possible (weak association with oral clefts - ~1-2 per 1000 treated women); use with caution before 10 weeks
- IV hydrocortisone 300 mg/day for 3 days followed by taper is an alternative
- H. pylori eradication if infection confirmed (use non-teratogenic regimen)
Step 6: Nutritional Support
- Enteral nutrition via nasogastric or nasoenteric tube: Preferred over TPN when oral intake fails
- Total parenteral nutrition (TPN): Last resort; significant complications - catheter sepsis (25%), venous thrombosis (3%); peripherally inserted central catheters have 50% overall complication rate; use only when enteral route has failed
- Thiamine, folate, multivitamins supplementation
COMPLICATIONS TO WATCH FOR
| Complication | Notes |
|---|
| Mallory-Weiss tear / haematemesis | Present in this case - commonest UGI bleed in HG |
| Boerhaave syndrome | Esophageal rupture - rare, life-threatening |
| Wernicke encephalopathy | Vitamin B1 (thiamine) deficiency from prolonged vomiting; triad: confusion, ophthalmoplegia, ataxia |
| Korsakoff psychosis | Follows untreated Wernicke |
| Central pontine myelinolysis | Rapid correction of hyponatremia |
| Retinal hemorrhage | From forceful vomiting/Valsalva |
| Spontaneous pneumomediastinum | Rare |
| Fetal effects | Low birth weight, prematurity, small for gestational age, low Apgar scores (especially if weight gain <7 kg) |
| Maternal psychological | Depression, PTSD during pregnancy and postpartum |
ADMISSION CRITERIA (for this patient)
This patient should be admitted given:
- Haematemesis (2 episodes) - requires evaluation and monitoring
- 12 weeks gestational age (peak HG period)
- Risk of significant dehydration and electrolyte disturbance
- Need for IV fluids, IV antiemetics, electrolyte correction
- Need for EGD to evaluate haematemesis source
SUMMARY FLOWCHART
12-week antenatal with HG + haematemesis
↓
Stabilize: IV access, vitals, fluid resuscitation
↓
Labs: CBC, CMP, TFT, urinalysis, beta-hCG, lipase, H. pylori
Ultrasound: confirm fetal viability, rule out molar/multiple gestation
↓
Thiamine 100mg IV → LR 2L → D5/0.45NS → correct electrolytes
IV antiemetics: metoclopramide / promethazine / ondansetron
↓
EGD (when stable): evaluate haematemesis source
→ Likely Mallory-Weiss tear → PPI therapy, endoscopic Rx if active bleed
↓
If refractory: methylprednisolone (after 10 weeks if possible)
↓
If unable to maintain nutrition: NG tube enteral feeds
↓
TPN: last resort only
Sources:
- Sleisenger and Fordtran's Gastrointestinal and Liver Disease, p. 654-655 (Hyperemesis Gravidarum complications) and p. 3888-3948 (Nausea, Vomiting, and Hyperemesis Gravidarum chapter)
- Creasy & Resnik's Maternal-Fetal Medicine: Principles and Practice, p. 1563-1564 (Management)
- Rosen's Emergency Medicine: Concepts and Clinical Practice, p. 3363-3364 (Diagnostic testing and management)
- Yamada's Textbook of Gastroenterology 7e (Mallory-Weiss tear in pregnancy)