NLE High-Risk Pregnancy & Obstetric Complications — Hypertensive & Metabolic Disorders of PregnancyDetailed Explanation

Hypertensive disorders in pregnancy are classified into four main categories based on timing, presence of proteinuria, and associated features. Understanding the classification is the foundation for all clinical decisions.

1. Gestational Hypertension: Blood pressure (BP) ≥140/90 mmHg that develops AFTER 20 weeks of gestation WITHOUT proteinuria and WITHOUT signs of end-organ damage. It resolves within 12 weeks postpartum. Think of it as 'high blood pressure only — no other problems yet.'

2. Preeclampsia: BP ≥140/90 mmHg after 20 weeks WITH proteinuria (≥300 mg in 24-hour urine, or urine protein-to-creatinine ratio ≥0.3, or dipstick reading of 2+ if quantitative testing is unavailable). Preeclampsia can also be diagnosed WITHOUT proteinuria if any of the following signs of end-organ involvement are present: thrombocytopenia (platelets <100,000), impaired liver function (elevated liver enzymes to twice normal), new kidney insufficiency (creatinine >1.1 mg/dL), pulmonary edema, or new-onset headache/visual disturbances unresponsive to medication. Remember: proteinuria is the classic finding, but it is no longer required if end-organ damage is present.

3. Eclampsia: Preeclampsia PLUS new-onset tonic-clonic seizures NOT attributable to another neurological cause (e.g., epilepsy, meningitis). This is the most life-threatening stage. The seizures can occur antepartum, intrapartum, or up to 48 hours postpartum.

4. Chronic Hypertension: Hypertension that was present BEFORE pregnancy or diagnosed BEFORE 20 weeks of gestation. It does not resolve postpartum.

5. Chronic Hypertension with Superimposed Preeclampsia: A woman with chronic hypertension who develops NEW proteinuria, worsening end-organ signs, or a sudden rise in BP after 20 weeks. This is the HIGHEST-RISK category for both mother and fetus — it combines the dangers of long-standing vascular disease with the acute pathophysiology of preeclampsia.

Key Diagnostic Threshold to memorize: 140/90 for diagnosis; 160/110 marks SEVERE features.

Understanding the pathophysiology of preeclampsia explains WHY all the clinical signs occur and guides nursing interventions. This is a classic NLE topic because pathophysiology-based questions require you to connect the mechanism to the clinical presentation.

The Root Problem — Abnormal Placentation:
Normally in early pregnancy, trophoblast cells invade the spiral arteries of the uterus and remodel them into wide, low-resistance vessels that supply abundant blood to the placenta. In preeclampsia, this remodeling FAILS. The spiral arteries remain narrow and high-resistance. The poorly perfused placenta becomes ischemic and releases factors (including anti-angiogenic proteins like sFlt-1) that cause GENERALIZED ENDOTHELIAL DYSFUNCTION — meaning the inner lining of blood vessels throughout the whole body is damaged.

Endothelial Dysfunction → Vasospasm:
Damaged endothelium loses its ability to produce vasodilators (nitric oxide, prostacyclin) and instead promotes vasoconstriction (thromboxane A2). The result is widespread VASOSPASM — abnormal constriction of blood vessels throughout the body. This raises blood pressure and reduces perfusion to every organ.

Consequences of Vasospasm (Organ by Organ):

• Placenta: Reduced perfusion → fetal growth restriction (IUGR), placental abruption risk
• Kidneys: Vasospasm → glomerular damage (glomeruloendotheliosis) → reduced GFR → proteinuria, oliguria, rising creatinine
• Liver: Vasospasm + ischemia → periportal hemorrhage → elevated liver enzymes, right-upper-quadrant/epigastric PAIN (this is the hepatic capsule stretching)
• Brain: Vasospasm + cerebral edema → severe headache, visual disturbances (scotomata, blurring), and ultimately seizures (eclampsia)
• Eyes: Retinal vasospasm → visual disturbances
• Platelets: Endothelial damage activates platelets and the coagulation cascade → thrombocytopenia (used up clotting) → risk of DIC

The Fluid Paradox — Why This Matters for Nursing:
Vascular endothelial damage increases PERMEABILITY — fluid leaks OUT of blood vessels into tissues. This causes:

1. EDEMA (visible — face, hands, feet) — fluid in the tissues
2. HEMOCONCENTRATION — the blood becomes more concentrated because plasma volume decreases
3. INTRAVASCULAR VOLUME DEPLETION — the patient is fluid-overloaded in the tissues but VOLUME-DEPLETED in the blood vessels

This is the critical paradox that guides fluid management: these patients appear edematous (swollen) but are actually hypovolemic in the vascular compartment. Therefore:

• Aggressive DIURETICS are dangerous (they worsen intravascular depletion → shock, placental hypoperfusion)
• Aggressive FLUID LOADING is also dangerous (the leaky vessels will dump the fluid into the lungs → pulmonary edema)
• Fluids must be given CAUTIOUSLY with an infusion pump, strict intake/output monitoring, and close auscultation of lung sounds.

Preeclampsia with SEVERE FEATURES is a medical emergency. The nurse must be able to recognize these features instantly, because rapid escalation of care — including magnesium sulfate initiation, antihypertensive therapy, and preparation for delivery — is required.

Diagnostic Criteria for Severe Features (any ONE of the following):

1. BP ≥160/110 mmHg on two occasions at least 4 hours apart (while the patient is at rest)
2. Thrombocytopenia: Platelet count <100,000/microliter
3. Impaired liver function: Liver enzymes elevated to twice normal AND/OR severe, persistent RUQ or epigastric pain unresponsive to medication and not accounted for by other diagnoses
4. Progressive renal insufficiency: Creatinine >1.1 mg/dL OR doubling of serum creatinine in the absence of other causes
5. Pulmonary edema (new onset)
6. New-onset headache unresponsive to medication and not accounted for by other diagnoses
7. Visual disturbances: blurring, scotomata (blind spots), photophobia, diplopia

Clinical Mnemonic for Severe Features: 'H-COVE-RR'

• Headache (severe, persistent)
• Clonus / hyperreflexia
• Oliguria (<500 mL/24h or <30 mL/hr)
• Visual changes
• Epigastric/RUQ pain
• Raised BP (≥160/110)
• Raised labs (platelets <100,000; elevated liver enzymes, creatinine)

Clonus: An abnormal neurological finding indicating CNS irritability. To test: rapidly dorsiflex the ankle and hold — if the foot rhythmically beats (oscillates) 2 or more times, clonus is present. Clonus + hyperreflexia = impending seizure risk.

HELLP Syndrome:
HELLP is a severe variant of preeclampsia (or can occur without classic hypertension/proteinuria in some cases). The acronym stands for:

• H — Hemolysis (destruction of red blood cells — microangiopathic hemolytic anemia)
• EL — Elevated Liver enzymes (AST, ALT)
• LP — Low Platelets (<100,000/microliter)

Clinical presentation: Right-upper-quadrant OR epigastric pain (hallmark), nausea, vomiting, malaise, and jaundice. The woman may not have obvious hypertension, which makes HELLP easy to miss.

Complications of HELLP: Disseminated Intravascular Coagulation (DIC), hepatic rupture (life-threatening), placental abruption, acute renal failure, and pulmonary edema.

Key Nursing Action in HELLP: NEVER palpate the liver — the hepatic capsule is under tension and physical pressure can cause rupture and massive hemorrhage.

Management of Preeclampsia with Severe Features:

1. Administer MAGNESIUM SULFATE (seizure prophylaxis)
2. Administer ANTIHYPERTENSIVES for BP ≥160/110 (to prevent maternal stroke)
3. Prepare for DELIVERY — the definitive treatment (timing depends on gestational age and maternal/fetal condition)
4. Strict monitoring: BP, DTRs, respiratory rate, urine output, fetal heart rate

Magnesium sulfate (MgSO4) is the MOST IMPORTANT DRUG in obstetric nursing pharmacology for the NLE. It is the drug of choice for BOTH seizure PREVENTION (prophylaxis) in severe preeclampsia AND seizure TREATMENT (termination) in eclampsia. It is classified as a HIGH-ALERT MEDICATION because a small dosing error can cause serious harm or death.

Mechanism of Action:
Magnesium acts as a CNS DEPRESSANT and MEMBRANE STABILIZER. It competes with calcium at the neuromuscular junction, reducing neuromuscular excitability. It raises the seizure threshold in the brain by stabilizing neuronal membranes. It also causes some vasodilation (lowering BP slightly) and relaxes smooth muscle. NOTE: It is NOT primarily an antihypertensive — it is an ANTICONVULSANT.

DOSING — These Numbers Are Heavily Tested on the NLE:

• Loading Dose: 4 to 6 grams IV, administered over 15 to 30 minutes (via infusion pump or controlled drip)
• Maintenance Dose: 1 to 2 grams per hour as a continuous IV infusion (always via infusion pump)

Therapeutic Serum Level: 4 to 7 mEq/L (approximately 4.8 to 8.4 mg/dL)

• Below 4 mEq/L: Sub-therapeutic — seizures are not adequately prevented
• 4 to 7 mEq/L: THERAPEUTIC RANGE — optimal seizure prophylaxis
• Above 7 mEq/L: TOXIC RANGE — danger signs appear

Signs of Magnesium Toxicity — IN ORDER OF APPEARANCE (Critical to Memorize):

The 'Rule of Safety' — Three Parameters to Check BEFORE and DURING Every Magnesium Dose:

1. Deep Tendon Reflexes (Patellar Reflex): Must be PRESENT. Absent patellar reflex = HOLD the infusion.
2. Respiratory Rate: Must be ≥12 breaths per minute. RR <12 = HOLD the infusion.
3. Urine Output: Must be ≥30 mL/hour. Why? Magnesium is cleared by the KIDNEYS. Oliguria → drug accumulates → toxicity.

Additional Monitoring During Magnesium Therapy:

• Blood pressure (magnesium causes some vasodilation)
• Level of consciousness (increasing drowsiness = early toxicity)
• Fetal heart rate (magnesium crosses the placenta; neonatal hypotonia and respiratory depression are possible)
• Serum magnesium levels as ordered
• Lung sounds (pulmonary edema risk)

ANTIDOTE for Magnesium Toxicity:
CALCIUM GLUCONATE — 1 gram (10 mL of a 10% solution) IV, given SLOWLY over 3 minutes.

Calcium gluconate MUST be kept at the bedside at all times during ANY magnesium sulfate infusion. It competitively antagonizes magnesium at the neuromuscular junction, reversing respiratory depression and restoring neuromuscular function.

Important Distinction: Calcium GLUCONATE vs. Calcium CHLORIDE

• Calcium GLUCONATE 1g IV: Used for magnesium toxicity in obstetric settings
• Calcium CHLORIDE: Used in cardiac arrest — more concentrated, more irritating to veins; NOT the first choice for MgSO4 reversal in obstetric care

Route and Administration Safety:

• Always use an INFUSION PUMP — never free-flow magnesium
• Monitor at least every 30 minutes to 1 hour during infusion
• Label the IV line clearly as 'MAGNESIUM SULFATE — HIGH ALERT'
• Neonatal team should be notified if delivery is imminent and mother received magnesium (newborn may need calcium gluconate too)

Nursing management integrates assessment, priority interventions, drug administration, and patient education. This section organizes care using the nursing process framework.

ASSESSMENT (Data Collection):

• Vital Signs: BP every 15–30 minutes during acute phase; note pulse rate and quality
• Neurological: Level of consciousness, severe headache (PQRST), DTRs (patellar reflex — 1+ to 4+ scale; absent = 0), clonus
• Visual: Ask about blurring, scotomata, photophobia, diplopia
• Respiratory: Rate (must be ≥12 for MgSO4), lung sounds (pulmonary edema)
• Renal: Strict intake and output (Foley catheter for accurate measurement), urine protein (dipstick or 24-hour collection)
• Fetal: Continuous or frequent fetal heart rate monitoring (FHR baseline, variability, decelerations — late decelerations indicate placental insufficiency)
• Edema: Weight daily (sudden weight gain from fluid retention), pitting edema of face/hands/dependent areas
• Labs: CBC (platelets, hematocrit), liver enzymes (AST, ALT), serum creatinine, serum magnesium level, uric acid, coagulation studies (in HELLP)

PRIORITY NURSING DIAGNOSES (NANDA-Based, Maslow-Prioritized):

1. Risk for Maternal Injury (Seizures) — highest priority (safety, physiologic)
2. Risk for Decreased Cardiac Output related to vasospasm
3. Excess Fluid Volume (tissue) with Deficient Fluid Volume (intravascular)
4. Risk for Impaired Fetal Gas Exchange related to uteroplacental insufficiency
5. Anxiety related to high-risk diagnosis

KEY NURSING INTERVENTIONS — PREECLAMPSIA:

1. Reduce Sensory Stimulation:
Keep the room QUIET and DIM (low lighting, limit visitors, speak softly, minimize procedures). Sensory stimulation (bright lights, loud noise, painful stimuli) can precipitate a seizure in a woman with CNS irritability from preeclampsia.

2. Positioning:
Place the woman in the LEFT LATERAL RECUMBENT (left side-lying) position. This:

• Relieves compression of the inferior vena cava (IVC) and aorta by the gravid uterus
• Improves venous return to the heart
• Maximizes uteroplacental blood flow
• Promotes renal perfusion (often improves urine output)

3. Seizure Precautions:

• Padded side rails UP at all times
• Suction equipment at the bedside (to clear airway after seizure)
• Oxygen and mask/bag-valve-mask at the bedside
• Emergency airway equipment available
• Call bell within reach
• Magnesium sulfate infusing as ordered
• Calcium gluconate at the bedside

4. Medication Administration:

• Magnesium sulfate as ordered (seizure prophylaxis)
• Antihypertensives as ordered for BP ≥160/110 (hydralazine IV, labetalol IV, or nifedipine oral)
• Do NOT give diuretics unless specifically ordered for pulmonary edema

5. Monitoring:

• Vital signs (especially BP and RR)
• DTRs and clonus
• Intake and output (Foley catheter; output ≥30 mL/hr)
• Fetal heart rate and activity
• Serum magnesium levels

MANAGING AN ECLAMPTIC SEIZURE — Priority Actions in Order:

During the seizure:

1. Ensure AIRWAY PATENCY — turn the woman to her LEFT SIDE (prevents aspiration, maintains uteroplacental flow)
2. Do NOT restrain — restraint causes fractures and worsens injury
3. Do NOT force anything into the mouth — this is an outdated and harmful practice; airway adjuncts (nasopharyngeal airway) are used by trained personnel
4. Protect from injury — pad the side rails, clear the area
5. Note the time, duration, and characteristics of the seizure

After the seizure (postictal phase):

1. Maintain the airway — suction secretions, apply oxygen
2. Assess maternal status — vital signs, LOC, fetal heart rate
3. Administer magnesium sulfate if not already running (loading dose) or increase the rate as ordered
4. Prepare for delivery — eclampsia = delivery is imminent, regardless of gestational age
5. Document the event completely

POSTPARTUM MONITORING:
Preeclampsia can WORSEN after delivery. The risk of eclampsia is highest in the first 24–48 hours postpartum. Continue magnesium sulfate for 24–48 hours after delivery. Monitor BP, DTRs, and urinary output throughout this period.

Antihypertensive drugs in pregnancy are used when BP reaches SEVERE levels (≥160/110 mmHg) to prevent MATERNAL STROKE — NOT to prevent preeclampsia progression. For mild-to-moderate hypertension (140–159/90–109), the evidence for treatment is less clear and management is individualized.

Why Treat Severe Hypertension?
When systolic BP reaches ≥160 mmHg, the risk of hemorrhagic stroke (cerebral hemorrhage) becomes significant. A stroke at 160+ mmHg can cause permanent maternal disability or death within minutes. Therefore, immediate antihypertensive treatment is required.

Approved Antihypertensives in Pregnancy:

1. HYDRALAZINE (IV) — a classic first-line option

• Dose: 5–10 mg IV; may repeat every 20–30 minutes as needed
• Mechanism: Direct arterial vasodilator
• Side effects: REFLEX TACHYCARDIA (the sudden drop in BP triggers the heart to beat faster), MATERNAL HYPOTENSION (most dangerous — can cause placental hypoperfusion and fetal distress), headache, and flushing
• Monitor: BP every 5 minutes after each dose; assess FHR

2. LABETALOL (IV) — combined alpha and beta blocker

• Dose: 20 mg IV initially; then 40 mg, 80 mg every 10–20 minutes as needed (escalating doses); maximum cumulative dose 300 mg
• Mechanism: Blocks both alpha (vasodilation) and beta (reduces heart rate and contractility) receptors
• Contraindications: ASTHMA (beta-blockade causes bronchoconstriction), heart failure, bradycardia (<60 bpm), heart block
• Monitor: BP, heart rate, respiratory status

3. NIFEDIPINE (Oral) — calcium channel blocker

• Use: Oral short-acting formulation for acute severe hypertension; long-acting for chronic management
• Mechanism: Blocks calcium entry into vascular smooth muscle → vasodilation
• Caution: Can potentiate the effects of magnesium sulfate (both cause vasodilation and neuromuscular relaxation) — monitor for excessive hypotension and neuromuscular blockade when used together
• Monitor: BP, heart rate; check for headache (reflex vasodilation)

4. METHYLDOPA (Oral) — alpha-2 agonist

• Use: CHRONIC hypertension management in pregnancy (long-term oral use)
• Long-established safety record in pregnancy
• NOT for acute severe hypertension (onset is too slow)
• Side effects: Sedation, dry mouth, orthostatic hypotension

DRUGS TO AVOID IN PREGNANCY — CRITICAL:

• ACE Inhibitors (e.g., captopril, enalapril): TERATOGENIC — cause fetal renal tubular dysplasia, oligohydramnios, skull hypoplasia (Potter sequence), and fetal death. CONTRAINDICATED in all trimesters.
• Angiotensin Receptor Blockers (ARBs) (e.g., losartan, valsartan): Same teratogenic effects as ACE inhibitors. ABSOLUTELY CONTRAINDICATED.
• Atenolol: Associated with fetal growth restriction when used throughout pregnancy

Clinical Priority in Antihypertensive Selection:

• Acute severe HTN (intrapartum/emergent): Hydralazine IV or Labetalol IV
• Oral acute management: Nifedipine (short-acting)
• Chronic hypertension maintenance: Methyldopa or long-acting nifedipine or labetalol
• AVOID: ACE inhibitors and ARBs (ALL trimesters)

Gestational Diabetes Mellitus (GDM) is defined as glucose intolerance that is FIRST RECOGNIZED OR DIAGNOSED DURING PREGNANCY. It is distinct from pre-gestational (pre-existing) diabetes, though both carry maternal and fetal risks.

Pathophysiology:
The placenta produces DIABETOGENIC HORMONES, primarily human placental lactogen (hPL), along with progesterone, cortisol, and estrogen. These hormones create progressive INSULIN RESISTANCE as pregnancy advances (peaks at 24–28 weeks). Normally, the pancreatic beta cells compensate by producing more insulin. In women predisposed to GDM, the pancreas CANNOT adequately compensate, resulting in HYPERGLYCEMIA.

Risk Factors for GDM:

• Obesity (BMI >30)
• Family history of type 2 diabetes
• Previous history of GDM
• Previous macrosomic infant (birth weight >4,000 g)
• Age over 25 years
• Polycystic ovary syndrome (PCOS)
• Glycosuria on routine urinalysis
• Multiple gestation
• Ethnicity (higher risk in Filipinos, other Asians, Hispanics — clinically relevant for Philippine practice!)

Screening and Diagnosis:

Step 1 — 50-Gram Glucose Challenge Test (GCT) at 24–28 weeks AOG:

• No fasting required
• Give 50 g oral glucose solution
• Measure plasma glucose at 1 HOUR
• Cut-off: ≥140 mg/dL = ABNORMAL → proceed to diagnostic test
• (Some institutions use ≥130 mg/dL as the cut-off for higher sensitivity)

Step 2 — 100-Gram 3-Hour Oral Glucose Tolerance Test (OGTT): (Confirmatory)

• Patient must be FASTING for 8–14 hours
• Give 100 g oral glucose
• Measure plasma glucose at fasting, 1 hour, 2 hours, 3 hours

• GDM is diagnosed if 2 or more values meet or exceed:

  • Fasting: ≥95 mg/dL
  • 1 hour: ≥180 mg/dL
  • 2 hours: ≥155 mg/dL
  • 3 hours: ≥140 mg/dL

GLYCEMIC TARGETS DURING PREGNANCY (Critical Numbers):

• Fasting blood glucose: <95 mg/dL
• 1-hour postprandial: <140 mg/dL
• 2-hour postprandial: <120 mg/dL

Maternal Complications of GDM:

• Preeclampsia (2–4× higher risk)
• Polyhydramnios (excess amniotic fluid from fetal polyuria)
• Increased risk of cesarean birth (macrosomia)
• Urinary tract infections and candidal infections (hyperglycemia promotes bacterial/fungal growth)
• Progression to type 2 diabetes postpartum (35–70% lifetime risk)

Fetal and Neonatal Complications of GDM:

• MACROSOMIA (birth weight >4,000 g): The most important fetal complication. Maternal hyperglycemia → fetal hyperglycemia → fetal pancreatic hypertrophy → fetal HYPERINSULINEMIA → stimulates fat and protein synthesis → large baby
• NEONATAL HYPOGLYCEMIA (most critical neonatal emergency): After birth, the maternal glucose supply is cut off, but the neonate's pancreas continues producing excess insulin → blood glucose drops rapidly. Must initiate early feedings (breastmilk or formula) within 30–60 minutes of birth
• Shoulder Dystocia: Macrosomic infant's shoulders become impacted at the pelvic outlet during delivery
• Respiratory Distress Syndrome: Insulin antagonizes cortisol, which delays surfactant production
• Hyperbilirubinemia (polycythemia → excess RBC breakdown)
• Hypocalcemia, hypomagnesemia
• Congenital anomalies (primarily with PRE-GESTATIONAL diabetes — especially cardiac and skeletal defects, caudal regression syndrome)

Management of GDM:

1. Medical Nutrition Therapy (MNT) — First Line:

• Consistent carbohydrate-controlled diet
• 3 meals + 2–3 snacks per day (prevents postprandial spikes and fasting ketosis)
• Caloric distribution: ~40–50% carbohydrates (complex, high-fiber), 20–25% protein, 30–35% fat
• Avoid simple sugars and refined carbohydrates

2. Physical Activity:

• Moderate exercise (e.g., walking 30 minutes after meals) improves insulin sensitivity
• Avoid supine position exercises in the third trimester

3. Pharmacological Therapy — Insulin:

• Indicated when diet and exercise FAIL to achieve glycemic targets
• INSULIN is the drug of choice because it does NOT cross the placenta — therefore it does not directly affect the fetus
• Types used: intermediate-acting (NPH), rapid-acting (regular insulin, lispro, aspart)
• Oral agents: Metformin and glyburide are sometimes used but insulin remains the GOLD STANDARD
• Glyburide does cross the placenta to some degree; metformin crosses the placenta significantly

4. Self-Monitoring of Blood Glucose (SMBG):

• Teach the patient to check fasting and postprandial glucose
• Record values in a log and bring to prenatal visits

5. Postpartum Follow-Up:

• GDM usually RESOLVES after delivery
• Perform a 2-hour 75-g OGTT at 6–12 weeks postpartum to check for persistent type 2 diabetes or prediabetes
• Annual blood glucose screening for life (high lifetime risk of type 2 DM)
• Encourage breastfeeding (reduces maternal glucose intolerance and infant obesity risk)

Hyperemesis gravidarum (HEG) is SEVERE, PERSISTENT nausea and vomiting during pregnancy that goes far beyond the normal 'morning sickness' experienced by most pregnant women. It causes significant dehydration, electrolyte imbalances, nutritional deficiency, and weight loss.

Distinguishing Normal Morning Sickness from Hyperemesis Gravidarum:

• Normal nausea/vomiting: Usually resolves by 12–14 weeks, no significant weight loss, patient can maintain hydration orally
• Hyperemesis gravidarum: Persists beyond 14–16 weeks, weight loss >5% of pre-pregnancy body weight, dehydration, ketonuria, electrolyte abnormalities, often requires hospitalization

Etiology and Risk Factors:

• High levels of HUMAN CHORIONIC GONADOTROPIN (hCG): Peaks at 8–12 weeks — timing correlates with HEG severity. This explains why HEG is MORE COMMON WITH:

  • MOLAR PREGNANCY (very high hCG levels)
  • MULTIPLE GESTATION (twins, triplets — more placental tissue → higher hCG)
• Thyroid dysfunction (hCG cross-reacts with TSH receptors)
• Psychological factors (anxiety can worsen symptoms)
• Prior history of HEG
• Female fetus (slightly higher risk)

Clinical Presentation and Assessment:

• Vomiting: Persistent (often >3 times/day), may contain bile, unable to tolerate oral intake
• Weight loss: >5% of pre-pregnancy body weight — this is the quantitative threshold
• Dehydration signs: dry mucous membranes, poor skin turgor, concentrated urine, tachycardia, postural hypotension, sunken eyes
• Ketonuria: The body breaks down fat for energy when carbohydrate intake is insufficient → ketones in urine

• Electrolyte imbalances:

  • HYPOKALEMIA — loss of potassium in vomitus (most common)
  • METABOLIC ALKALOSIS — loss of gastric acid (HCl) = loss of H+ and Cl- ions → alkaline blood pH
  • In severe cases with starvation ketosis: METABOLIC ACIDOSIS
• Wernicke Encephalopathy Risk: Severe HEG depletes THIAMINE (Vitamin B1). Without thiamine, glucose metabolism in the brain fails → ophthalmoplegia (abnormal eye movements), ataxia, confusion. THIAMINE must be given BEFORE glucose administration in prolonged HEG
• Ptyalism: Excessive salivation (common complaint)
• Psychological impact: Fear, anxiety, depression, social isolation

Management of Hyperemesis Gravidarum:

1. NPO and Rest (Initial Acute Phase):
Give the GI tract a rest. NPO initially — this alone often reduces vomiting frequency as there is nothing to vomit.

2. IV Fluid and Electrolyte Replacement:

• Isotonic solutions (normal saline or lactated Ringer's) as primary fluid replacement
• Add POTASSIUM (KCl) to IV fluids to correct hypokalemia
• THIAMINE 100 mg IV or IM BEFORE glucose administration — to prevent Wernicke encephalopathy (glucose metabolism requires thiamine; giving glucose first without thiamine in a thiamine-depleted patient precipitates Wernicke's)

3. Antiemetic Therapy (Step-Up Approach):

• First line: PYRIDOXINE (Vitamin B6) 10–25 mg every 8 hours ± DOXYLAMINE 12.5 mg (antihistamine) — this combination is the first-line pharmacological treatment for nausea/vomiting of pregnancy
• Second line: Metoclopramide (dopamine antagonist — also promotes gastric emptying) or Promethazine (antihistamine/phenothiazine)
• Third line: Ondansetron (5-HT3 antagonist) — effective but use with caution (some concerns about cardiac effects and cleft palate association in first trimester)
• Diclegis (pyridoxine + doxylamine extended-release) is a commonly prescribed combination formulation

4. Diet Advancement:
Once vomiting is controlled, advance slowly:

• Start with dry, bland, carbohydrate-rich foods (plain crackers, toast, plain rice)
• Small, FREQUENT meals (6–8 small meals per day rather than 3 large ones)
• SEPARATE solids from fluids — drink fluids between meals, not with meals
• Avoid fatty, spicy, strongly aromatic foods
• Cold foods are often better tolerated than hot foods (hot food releases more odor)
• Ginger (ginger tea, ginger candies) has evidence for mild antiemetic effect

5. Monitoring:

• Daily weight
• Strict intake and output
• Urine for ketones and specific gravity
• Electrolytes (K+, Na+, Cl-)
• In severe cases: liver function tests (can be mildly elevated in HEG)

6. Supportive Care:

• Calm, odor-free environment
• Avoid olfactory triggers (strong perfumes, cooking odors)
• Emotional support and psychological counseling
• Oral care after each vomiting episode (prevents dental erosion from gastric acid)
• Family support and education

In severe refractory cases: Total parenteral nutrition (TPN) or enteral tube feeding (nasogastric or nasojejunal) may be necessary to maintain nutrition.