Obstetrics Questions 26-30

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26. Vomiting of pregnancy

English translation

Definition

Classification

1. Mild vomiting
   • Up to 5 episodes/day
   • General condition is satisfactory.
   • No major dehydration, weight loss, or metabolic abnormality.
2. Moderate vomiting
   • About 6-10 episodes/day
   • Weakness, reduced appetite, tachycardia, weight loss.
   • May have dehydration and ketonuria.
3. Severe or excessive vomiting / hyperemesis gravidarum
   • More than 10 episodes/day, sometimes continuous.
   • Cannot retain food or fluids.
   • Weight loss, dehydration, hypotension, tachycardia, oliguria.
   • Ketonuria, electrolyte abnormalities, metabolic alkalosis or acidosis.
   • Severe cases can cause hepatic dysfunction, renal impairment, Wernicke encephalopathy, thrombosis, and rarely death.

Etiology and risk factors

• High or rapidly rising hCG levels
• Multiple pregnancy
• Hydatidiform mole
• Previous hyperemesis gravidarum
• Thyroid stimulation by hCG, sometimes transient thyrotoxicosis
• Young age, nulliparity, obesity
• Female fetus
• Gastrointestinal disease, migraine, motion sickness
• Psychological stress may worsen symptoms but is not the primary cause

Clinical features

• Nausea and vomiting, usually in the first trimester
• Ptyalism, anorexia, weakness
• Weight loss
• Dry tongue and skin, reduced skin turgor
• Tachycardia, hypotension, oliguria
• Acetone odor from the mouth
• Ketonuria

Diagnosis

Investigations

• Weight and vital signs
• Urinalysis: ketones, specific gravity, protein, infection
• CBC and hematocrit
• Serum electrolytes, urea, creatinine, glucose
• Liver enzymes and bilirubin if severe
• Thyroid function if clinically indicated
• Ultrasound: confirm intrauterine pregnancy, gestational age, multiple pregnancy, molar pregnancy

Differential diagnosis

• Gastroenteritis
• Appendicitis
• Pyelonephritis
• Hepatitis, pancreatitis, cholecystitis
• Diabetic ketoacidosis
• Thyrotoxicosis
• CNS pathology
• Drug-related vomiting

Treatment and management

Mild disease: outpatient

• Reassurance and dietary advice
• Small, frequent meals
• Avoid fatty, spicy, or trigger foods
• Dry food before rising in the morning
• Adequate oral fluid intake, preferably in small frequent amounts
• Ginger may help some patients
• Vitamin B6 (pyridoxine), usually first-line
• Add doxylamine where available

Persistent symptoms

• Metoclopramide
• Promethazine or other antihistamine/phenothiazine according to local protocol
• Ondansetron when first-line treatment is ineffective, after weighing benefits and risks

Indications for hospital admission

• Inability to maintain oral intake
• Clinical dehydration
• Ketonuria
• Significant weight loss, especially more than 5% of prepregnancy weight
• Electrolyte disturbance
• Failed outpatient treatment
• Suspected alternative diagnosis or serious complication

Inpatient management

1. IV isotonic crystalloid rehydration, usually normal saline.
2. Correct potassium, magnesium, and other electrolyte disturbances.
3. Give thiamine before any dextrose-containing infusion to prevent Wernicke encephalopathy.
4. Antiemetics by oral, IV, IM, rectal, or subcutaneous route as needed.
5. Consider acid suppression if reflux/gastritis is present.
6. Monitor weight, urine output, ketones, electrolytes, renal and liver function.
7. Consider thromboprophylaxis in women admitted with severe hyperemesis, unless contraindicated.
8. Enteral feeding is preferred if prolonged nutritional support is necessary. Parenteral nutrition is a last resort.

Obstetric tactic

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27. Edema, proteinuria, and hypertensive disorders in pregnancy

English translation

Definitions

Hypertension in pregnancy

• Systolic BP ≥140 mmHg and/or diastolic BP ≥90 mmHg
• Confirmed on two readings at least 4 hours apart, except severe hypertension, which requires prompt confirmation and treatment.

Severe hypertension

• BP ≥160/110 mmHg

Proteinuria

• ≥300 mg/24 hours
• Protein/creatinine ratio ≥0.3
• Dipstick ≥2+ if quantitative testing is unavailable

Edema

Risk factors for preeclampsia

• Previous preeclampsia, especially early or severe disease
• First pregnancy
• Multiple pregnancy
• Maternal age >40 years
• Obesity
• Chronic hypertension
• Chronic kidney disease
• Diabetes mellitus
• Systemic lupus erythematosus or antiphospholipid syndrome
• Family history of preeclampsia
• Assisted reproductive technology
• Long interpregnancy interval

ICD-10 classification

Clinical classification

1. Chronic hypertension
   • Present before pregnancy, diagnosed before 20 weeks, or persists beyond 12 weeks postpartum.
2. Gestational hypertension
   • New hypertension after 20 weeks.
   • No proteinuria or maternal organ dysfunction.
   • May progress to preeclampsia.
3. Preeclampsia
   • New hypertension after 20 weeks plus proteinuria, or
   • New hypertension plus maternal organ dysfunction even without proteinuria.
4. Preeclampsia superimposed on chronic hypertension
   • Chronic hypertension with new proteinuria, sudden worsening BP, or new maternal organ dysfunction after 20 weeks.
5. Eclampsia
   • Generalized tonic-clonic seizure in a woman with preeclampsia, with no alternative neurologic cause.

Pathogenesis

1. In early pregnancy, trophoblast invasion of the spiral arteries is inadequate.
2. Spiral arteries remain narrow, high-resistance vessels rather than becoming low-resistance uteroplacental vessels.
3. Placental hypoperfusion and ischemia occur.
4. The ischemic placenta releases antiangiogenic, inflammatory, and vasoactive factors into maternal blood.
5. These cause widespread maternal endothelial dysfunction.
6. Endothelial dysfunction leads to:
   • Vasoconstriction and hypertension
   • Increased capillary permeability and edema
   • Renal glomerular endotheliosis and proteinuria
   • Platelet activation and thrombocytopenia
   • Hepatic ischemia and elevated transaminases
   • Placental insufficiency, fetal growth restriction, placental abruption, and fetal hypoxia

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28. Edema, proteinuria, and hypertensive disorders: clinical features, diagnosis, treatment, and severity assessment

English translation

Clinical features

Gestational hypertension

• BP ≥140/90 after 20 weeks
• Usually asymptomatic
• No proteinuria or end-organ damage

Preeclampsia

• Hypertension
• Proteinuria may be present
• Headache, especially persistent and unresponsive to analgesia
• Visual symptoms: blurred vision, scotomata, flashing lights
• Epigastric or right upper quadrant pain
• Nausea and vomiting in severe disease
• Sudden edema of face/hands, rapid weight gain
• Reduced urine output
• Hyperreflexia or clonus
• Fetal growth restriction or reduced fetal movements

Diagnosis

Maternal evaluation

• Repeated BP measurement with an appropriate cuff
• Urinalysis and urine protein/creatinine ratio or 24-hour urine protein
• CBC and platelet count
• Serum creatinine
• AST, ALT, bilirubin, LDH
• Coagulation studies if HELLP syndrome, bleeding, abruption, or DIC is suspected

Fetal assessment

• Ultrasound for fetal growth and amniotic-fluid volume
• Umbilical artery Doppler when indicated
• Non-stress test / cardiotocography
• Biophysical profile where appropriate

Severe features of preeclampsia

• Persistent BP ≥160 systolic or ≥110 diastolic
• Platelets <100 × 10⁹/L
• AST or ALT at least twice the normal limit
• Persistent severe epigastric or right-upper-quadrant pain
• Serum creatinine >1.1 mg/dL or doubling of baseline level
• Pulmonary edema
• New persistent headache not explained by another cause
• Visual disturbance
• HELLP syndrome: Hemolysis, Elevated Liver enzymes, Low Platelets

Treatment

Gestational hypertension or preeclampsia without severe features

• Outpatient or inpatient surveillance according to reliability and risk
• BP monitoring
• Maternal symptoms and laboratory monitoring
• Serial assessment of fetal growth and wellbeing
• Antihypertensive medication if persistent hypertension requires treatment according to local protocol
• Plan delivery at 37+0 weeks if no severe features develop

Preeclampsia with severe features

• Admit to hospital, ideally a tertiary obstetric center
• Stabilize mother first
• IV access, strict fluid balance, urine output monitoring
• CBC, platelets, renal function, liver enzymes, coagulation assessment
• Magnesium sulfate for seizure prevention
• Treat severe BP promptly with one of:
  • IV labetalol
  • IV hydralazine
  • Oral immediate-release nifedipine
• Avoid fluid overload because pulmonary edema is a major risk.
• Corticosteroids for fetal lung maturation if preterm birth is expected, usually before 34 weeks.
• Continuous or frequent fetal monitoring depending on gestation and maternal stability.

Prevention in high-risk patients

• Low-dose aspirin from early pregnancy, generally started between 12 and 16 weeks according to local guideline.
• Optimize chronic hypertension, diabetes, renal disease, and body weight before pregnancy.

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29. Preeclampsia

English translation

Definition

Diagnosis

• Proteinuria, or
• Thrombocytopenia
• Renal impairment
• Elevated liver enzymes or right-upper-quadrant/epigastric pain
• Pulmonary edema
• Cerebral or visual symptoms

Management principles

1. Maternal stabilization is the first priority.
2. Assess disease severity and fetal condition.
3. Prevent seizures with magnesium sulfate in severe disease.
4. Treat acute severe hypertension urgently.
5. The only definitive cure is delivery of the placenta.

Timing of delivery

Route of delivery

• Induction and vaginal delivery are appropriate if mother and fetus are stable and there is no obstetric contraindication.
• Cesarean delivery is indicated for usual obstetric reasons or when urgent birth is required and vaginal delivery is not feasible.

Magnesium sulfate

• Eclampsia treatment
• Seizure prophylaxis in preeclampsia with severe features
• Often continued for 24 hours postpartum

• Respiratory rate
• Deep tendon reflexes
• Urine output
• Serum magnesium when renal function is impaired

Maternal complications

• Eclampsia
• HELLP syndrome
• Stroke, cerebral hemorrhage
• Pulmonary edema
• Acute kidney injury
• DIC
• Placental abruption
• Maternal death

Fetal complications

• Fetal growth restriction
• Oligohydramnios
• Chronic hypoxia
• Preterm birth
• Stillbirth

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30. Eclampsia

English translation

Definition

Pathogenesis

• Severe hypertension and endothelial dysfunction
• Cerebral vasospasm and impaired autoregulation
• Breakdown of the blood-brain barrier
• Cerebral edema and posterior reversible encephalopathy syndrome
• Cerebral ischemia, hemorrhage, and seizures

Clinical features

Premonitory symptoms

• Severe headache
• Visual impairment, scotomata, blurred vision
• Epigastric or right-upper-quadrant pain
• Nausea/vomiting
• Hyperreflexia and ankle clonus
• Marked hypertension

Seizure phases

1. Preconvulsive phase: facial twitching, fixed gaze.
2. Tonic phase: generalized muscle rigidity, apnea, cyanosis.
3. Clonic phase: rhythmic generalized jerking.
4. Postictal coma/confusion: variable duration.

Diagnosis

• BP, oxygen saturation, respiratory rate
• Urinalysis/proteinuria
• CBC and platelets
• Creatinine, AST/ALT, LDH, bilirubin
• Coagulation profile if HELLP/DIC is suspected
• Fetal monitoring after maternal stabilization

Differential diagnosis of seizure in pregnancy

• Epilepsy
• Cerebral hemorrhage or ischemic stroke
• Cerebral venous sinus thrombosis
• Meningitis/encephalitis
• Brain tumor
• Hypoglycemia
• Drug toxicity
• Metabolic disorders

Emergency management: answer in sequence

1. Call for help

• Obstetrician, anesthetist, senior midwife, neonatal team, critical-care support.

2. Prevent injury and maintain airway

• Place woman in the left lateral position.
• Protect from trauma. Do not restrain violently.
• Clear secretions and administer oxygen.
• Suction only if needed and safe.
• Secure IV access.
• Do not put fingers, spoon, or other objects into the mouth.

3. Stop and prevent recurrent seizures

• Loading dose: 4 g IV over 5-15 minutes
• Maintenance: 1-2 g/hour IV infusion

• Additional 2 g IV magnesium sulfate slowly.

4. Monitor for magnesium toxicity

• Patellar reflexes
• Respiratory rate, usually maintain >12/min
• Urine output, usually maintain >25-30 mL/hour

• Stop magnesium sulfate.
• Give 10 mL of 10% calcium gluconate IV slowly.
• Support ventilation if required.

5. Treat severe hypertension

• IV labetalol, or
• IV hydralazine, or
• Oral immediate-release nifedipine.

6. Delivery

• Stabilize the mother first.
• Eclampsia is an indication for delivery after stabilization.
• The route depends on gestational age, cervical condition, fetal status, and urgency.
• Cesarean is not automatic. If labor is advanced and fetal condition is reassuring, vaginal delivery may be possible.
• Continue magnesium sulfate for 24 hours after delivery or the last seizure, according to protocol.

Complications

Maternal

• Aspiration pneumonia
• Pulmonary edema
• Cerebral hemorrhage, stroke, coma
• DIC
• Acute renal failure
• HELLP syndrome
• Placental abruption
• Liver hematoma/rupture
• Maternal death

Fetal

• Acute fetal hypoxia and bradycardia during maternal seizure
• Placental abruption
• Fetal growth restriction
• Prematurity
• Stillbirth or neonatal death

Short oral-exam summary

Eclampsia is a generalized tonic-clonic seizure caused by preeclampsia. Immediate priorities are left lateral positioning, airway and oxygenation, IV magnesium sulfate, urgent treatment of severe hypertension, assessment for HELLP/DIC and fetal compromise, and delivery after maternal stabilization.

Obstetrics Questions 31-40

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31. Abnormalities of labor

English translation

Definition

Classification

1. Hypotonic uterine dysfunction

• Primary uterine inertia: weak contractions from the onset of labor.
• Secondary uterine inertia: contractions initially adequate but later become weak.

2. Hypertonic uterine dysfunction

• Discoordinated labor
• Uterine tetany
• Pathological contraction ring

3. Excessively strong or rapid labor

• Very frequent, powerful contractions.
• Rapid cervical dilatation and fetal expulsion.
• Classically, delivery within less than 3 hours from onset is termed precipitous labor.

Modern diagnosis

• Clinical evaluation of contraction frequency, duration, strength, uterine relaxation
• Vaginal examination: cervical effacement/dilatation, fetal head descent, position, presenting part
• Labor progress chart or partograph
• Continuous CTG when risk factors or abnormal labor are present
• Ultrasound if fetal position, presentation, estimated weight, placental location, or obstruction is uncertain
• Intrauterine pressure catheter only in selected cases when accurate assessment of contraction strength is necessary
• Exclude:
  • Cephalopelvic disproportion
  • Malpresentation or malposition
  • Full bladder
  • Occiput posterior/transverse position
  • Fetal macrosomia
  • Placental abruption
  • Uterine scar complications

Complications

Maternal

• Exhaustion, dehydration, ketoacidosis
• Chorioamnionitis and postpartum endometritis
• Uterine rupture, especially with obstruction or injudicious oxytocin
• Cervical, vaginal, and perineal tears
• Postpartum hemorrhage due to uterine atony
• Operative delivery and cesarean section

Fetal

• Fetal hypoxia and acidosis
• Birth trauma
• Intracranial hemorrhage
• Infection after prolonged rupture of membranes
• Stillbirth or neonatal depression in severe untreated cases

Risk groups

• Nulliparity
• Previous dysfunctional labor
• Maternal age extremes
• Obesity
• Overdistended uterus: multiple pregnancy, polyhydramnios, macrosomia
• Uterine fibroids or congenital uterine anomalies
• Malpresentation, occiput posterior position
• Contracted pelvis or suspected cephalopelvic disproportion
• Induction/augmentation of labor
• Epidural analgesia, if labor was already abnormal
• Maternal exhaustion, fear, inadequate analgesia
• Uterine scar

Prevention

• Good antenatal identification of pelvic, fetal, and maternal risk factors
• Ultrasound assessment when macrosomia, multiple pregnancy, or malpresentation is suspected
• Timely referral of high-risk women to an appropriate maternity unit
• Continuous labor support, hydration, bladder emptying, effective pain relief
• Proper use of a partograph
• Rational induction and careful oxytocin titration
• Avoid oxytocin where obstruction, malpresentation, uterine hyperstimulation, or scar rupture is suspected

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32. Pathological preliminary period

English translation

Definition

Normal versus pathological preliminary period

Etiology and risk factors

• Increased neuropsychological stress, fear of childbirth
• Maternal fatigue and sleep deprivation
• Autonomic nervous-system dysfunction
• Uterine overdistension: polyhydramnios, multiple pregnancy, large fetus
• Uterine fibroids or uterine malformations
• Cervical rigidity, especially in older nulliparous women
• Fetal malposition, especially occiput posterior
• Inflammatory disease of the genital tract
• Endocrine and metabolic disturbances

Clinical features

• Irregular contractions, usually painful
• Pain in the lower abdomen and sacral area
• Contractions may occur mainly at night
• No progressive cervical dilatation
• High presenting part and absent or poor fetal head engagement may be present
• Maternal anxiety, exhaustion, insomnia
• Possible fetal compromise if the condition is prolonged

Diagnosis

• History of prolonged painful contractions without labor progress
• Abdominal examination: irregular contractions and sometimes increased basal uterine tone
• Vaginal examination: cervix not progressively effacing or dilating
• Repeat vaginal examination after an appropriate interval confirms no progression
• CTG to assess fetal condition and uterine activity
• Ultrasound if malpresentation, macrosomia, placenta previa, or cephalopelvic disproportion is suspected

Management

Main objectives

1. Provide rest and reduce maternal exhaustion.
2. Relieve pain.
3. Correct uterine dysfunction.
4. Exclude obstruction and fetal compromise.

Tactics

• Admit if prolonged, painful, or associated with maternal/fetal risk.
• Psychological support and explanation.
• Empty bladder; ensure hydration and light nutrition if appropriate.
• Sedation and therapeutic rest, according to local protocol.
• Adequate analgesia, often neuraxial analgesia when established labor develops.
• Antispasmodic therapy may be used according to local practice.
• Continuous fetal assessment if contractions are frequent or risk factors are present.
• Do not start oxytocin before excluding cephalopelvic disproportion and confirming true labor with inadequate contractions.
• If labor does not establish, maternal condition deteriorates, fetal compromise occurs, or an obstetric indication exists, delivery may be required, commonly by cesarean section.

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33. Excessively rapid labor

English translation

Definition

Etiology

• Increased uterine excitability and hypercontractility
• History of rapid labor
• Multiparity
• Cervical insufficiency
• Small fetus or preterm fetus
• Wide pelvis
• Fetal growth restriction
• Placental abruption in some cases
• Excessive oxytocin administration or prostaglandin effect
• Severe maternal stress

Clinical features

• Sudden onset of very strong, frequent contractions
• Short or absent intervals between contractions
• Rapid cervical dilatation
• Rapid descent and expulsion of the fetus
• Intense urge to push early in labor
• Possible uterine hypertonus and fetal heart-rate abnormalities

Maternal complications

• Cervical, vaginal, vulvar, and perineal tears
• Uterine rupture, especially if there is a scar or obstruction
• Placental abruption
• Postpartum hemorrhage due to uterine atony or genital-tract trauma
• Retained placenta
• Embolism by amniotic fluid is rare but may occur in catastrophic cases
• Psychological trauma

Fetal complications

• Acute fetal hypoxia from impaired uteroplacental perfusion during hyperstimulation
• Intracranial hemorrhage
• Birth trauma
• Fractures or nerve injury
• Umbilical-cord injury
• Aspiration
• Hypothermia or infection if born outside hospital

Management in hospital

1. Call the obstetric team and assess fetal status immediately.
2. Position the woman laterally, preferably on the side opposite the fetal back if known.
3. Continuous CTG if feasible.
4. Stop oxytocin or prostaglandin infusion immediately.
5. Avoid uncontrolled pushing before full dilatation, if possible.
6. Provide analgesia and consider short-acting uterine relaxation only under senior obstetric/anesthetic supervision if uterine hyperstimulation is causing fetal compromise.
7. Prepare for neonatal resuscitation.
8. After birth, carefully inspect cervix, vagina, and perineum for tears.
9. Actively manage the third stage and observe closely for postpartum hemorrhage.

Delivery outside a medical institution

• Call emergency medical services immediately.
• Do not attempt to delay delivery by force.
• Support the perineum and guide the fetal head gently.
• Do not pull on the fetal head or umbilical cord.
• If the cord is around the neck, gently slip it over the head if loose. If tight and delivery cannot proceed, emergency trained personnel may need to clamp and cut it.
• Dry the newborn, keep warm skin-to-skin, and assess breathing.
• Clamp/cut the cord only with sterile equipment and only when appropriate.
• Do not pull on the placenta.
• Monitor maternal bleeding and uterine tone.
• Transfer mother and newborn urgently to hospital, even if both appear well.

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34. Uterine inertia or weak labor

English translation

Definition

Classification

Primary uterine inertia

• Contractions are weak, short, infrequent, and ineffective from the beginning of established labor.

Secondary uterine inertia

• Labor begins normally, but contractions later become weak and ineffective.
• Commonly occurs after prolonged labor, maternal exhaustion, or obstruction.

Etiology

Maternal factors

• Exhaustion, dehydration, starvation
• Fear, anxiety, inadequate pain relief
• Obesity
• Advanced maternal age
• Endocrine/metabolic disease
• Uterine fibroids, uterine malformations
• Previous uterine surgery

Uterine overdistension

• Multiple pregnancy
• Polyhydramnios
• Fetal macrosomia

Fetal and mechanical factors

• Cephalopelvic disproportion
• Malpresentation or malposition
• Occiput posterior/transverse position
• Large fetal head
• Full urinary bladder

Iatrogenic factors

• Inappropriate sedation
• Excessive analgesics
• Poorly managed induction or augmentation

Clinical features

• Weak, short, infrequent contractions
• Slow cervical dilatation
• Delayed fetal head descent
• Prolonged labor
• Maternal exhaustion
• Increasing risk of fetal hypoxia and infection

Diagnosis

• Partograph shows delayed labor progress.
• Evaluate cervical dilatation, fetal descent, contraction pattern, and fetal position.
• CTG for fetal wellbeing.
• Vaginal examination to exclude malpresentation, cord prolapse, and obstruction.
• Assess bladder filling.
• Ultrasound when needed to clarify fetal position, estimated fetal weight, and placental status.

Treatment

General measures

• Reassure and support the woman.
• IV fluids if dehydrated.
• Encourage bladder emptying or catheterize if needed.
• Provide appropriate analgesia.
• Correct electrolyte/glucose abnormalities.
• Continuous fetal monitoring if augmentation is planned.

Oxytocin augmentation

• Membranes are ruptured or amniotomy is appropriate.
• Cephalopelvic disproportion is excluded.
• There is no fetal distress requiring immediate delivery.
• There is no contraindication to vaginal birth.

Indications for cesarean delivery

• Failure of progress despite adequate contractions
• Suspected or confirmed cephalopelvic disproportion
• Nonreassuring fetal status
• Malpresentation not suitable for vaginal delivery
• Obstructed labor
• Uterine scar with concern for rupture
• Maternal deterioration or infection

Prevention

• Identify women at risk antenatally.
• Correct anemia, malnutrition, and medical disease.
• Plan hospital delivery for high-risk pregnancies.
• Use partograph and CTG appropriately.
• Avoid unnecessary induction.
• Use oxytocin carefully, never in suspected obstruction.

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35. Discoordinated labor

English translation

Definition

Pathophysiology

• The fundal dominance is lost.
• Multiple uterine pacemakers may arise.
• The lower uterine segment may contract excessively.
• Basal uterine tone rises.
• Uterine relaxation between contractions becomes inadequate.
• Uteroplacental perfusion decreases, risking fetal hypoxia.

Causes and risk factors

• Anxiety, fear, severe pain
• Pathological preliminary period
• Cervical dystocia or rigidity
• Nulliparity or older primiparity
• Uterine anomaly or fibroids
• Fetal malposition
• Inappropriate oxytocin use
• Obstetric interventions without adequate analgesia
• Maternal exhaustion

Clinical features

• Very painful, frequent, irregular contractions
• Poor uterine relaxation between contractions
• Increased basal uterine tone
• Slow or absent cervical dilatation despite painful contractions
• High fetal head or poor descent
• Maternal distress and fatigue
• Abnormal CTG due to reduced placental blood flow

Diagnosis

• Clinical assessment of painful irregular contractions with poor labor progress
• Partograph: protracted or arrested dilatation/descent
• CTG: may reveal fetal hypoxia
• Vaginal examination: cervix may be rigid or edematous
• Exclude:
  • Placental abruption
  • Uterine rupture
  • Cephalopelvic disproportion
  • Malpresentation
  • Cord prolapse
  • Excessive oxytocin effect

Management

1. Stop oxytocin/prostaglandins if they are being administered.
2. Assess maternal vital signs and fetal condition.
3. Ensure IV access, hydration, and bladder emptying.
4. Provide effective pain relief, often epidural analgesia if appropriate.
5. Sedation or therapeutic rest may be used under senior supervision.
6. Do not initiate oxytocin until hypertonus/discoordination resolves and obstruction is excluded.
7. If fetal compromise, persistent hypertonus, no cervical progress, or suspected obstruction occurs, proceed to cesarean delivery.

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36. Anatomically contracted pelvis and clinically contracted pelvis

English translation

Anatomically contracted pelvis

Definition

Causes

• Constitutional small stature
• Rickets, osteomalacia
• Childhood malnutrition
• Pelvic fractures or pelvic tumors
• Congenital pelvic deformity
• Spinal deformity: scoliosis, kyphosis
• Hip disease or lower-limb deformity
• Previous pelvic surgery
• Skeletal dysplasia

Classification

By shape

• Generally uniformly contracted pelvis
• Flat pelvis
• Generally flat pelvis
• Transversely contracted pelvis
• Obliquely contracted pelvis
• Funnel-shaped pelvis
• Osteomalacic pelvis
• Spondylolisthetic pelvis
• Pelvis deformed by fractures or tumors

By degree of contraction

Pelvic assessment

External pelvimetry

• Distantia spinarum: about 25-26 cm
• Distantia cristarum: about 28-29 cm
• Distantia trochanterica: about 31-32 cm
• External conjugate: about 20-21 cm

Internal pelvic assessment

• Diagonal conjugate
• Sacral promontory reachability
• Sacral curvature
• Ischial spines
• Side walls
• Interspinous diameter
• Subpubic angle
• Pelvic outlet
• Mobility and engagement of the fetal head

Important point

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Clinically contracted pelvis

Definition

Causes

• Anatomically narrow pelvis
• Fetal macrosomia
• Hydrocephalus
• Persistent occiput posterior or transverse position
• Deflexed head presentation
• Brow presentation
• Pelvic soft-tissue obstruction: tumor, full bladder, cervical edema
• Inadequate molding capacity of the fetal head

Clinical features

• Fetal head remains high or does not descend
• Lack of progress despite adequate contractions
• Increasing caput succedaneum and molding
• Cervical edema
• Maternal exhaustion and dehydration
• Distended bladder
• Signs of threatened uterine rupture:
  • Severe constant pain
  • Pathological retraction ring
  • Tender lower uterine segment
  • Maternal tachycardia
  • Fetal distress

Diagnosis

• Labor progress assessment by partograph
• Repeated, careful vaginal examination
• Assessment of fetal head position and station
• CTG monitoring
• Ultrasound if position/weight is uncertain
• Clinical evidence of obstruction despite adequate uterine activity

Management

• Do not augment labor with oxytocin when obstruction or cephalopelvic disproportion is suspected.
• Stop oxytocin if already running.
• Establish IV access, resuscitate, catheterize the bladder.
• Continuous fetal monitoring.
• Perform cesarean delivery in living fetus with clinically significant disproportion.
• If fetal death is confirmed and vaginal delivery is considered, management must be individualized by an experienced obstetrician, following local law and protocol.

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37. Maternal mortality

English translation

Definition

Maternal mortality ratio

Classification of causes

Direct obstetric deaths

• Obstetric hemorrhage
• Hypertensive disorders: preeclampsia/eclampsia
• Sepsis
• Unsafe abortion and complications
• Thromboembolism and amniotic-fluid embolism
• Ectopic pregnancy
• Uterine rupture
• Complications of anesthesia or operative delivery

Indirect obstetric deaths

• Cardiac disease
• Severe anemia
• Diabetes
• Renal disease
• HIV and other severe infections
• Malaria in endemic regions
• Neurological disease
• Cancer
• Mental-health-related causes, including suicide, in some settings

The “three delays” model

1. Delay in deciding to seek medical care.
2. Delay in reaching an appropriate facility.
3. Delay in receiving adequate care after reaching the facility.

Risk groups

• Previous severe obstetric hemorrhage or preeclampsia
• Multiple pregnancy
• Maternal age <18 years or >35-40 years
• Grand multiparity
• Previous cesarean section or uterine surgery
• Placenta previa or placenta accreta spectrum risk
• Chronic hypertension, heart disease, renal disease, diabetes
• Severe anemia
• Obesity
• Thrombophilia or history of thromboembolism
• Substance use
• Poor access to antenatal care
• Social deprivation, domestic violence, poor nutrition
• Delayed referral or delivery outside an equipped facility

Prevention

• Early registration for antenatal care
• Identification and referral of high-risk pregnancies
• Skilled attendance at birth
• Blood products, emergency surgery, anesthesia, and intensive care availability
• Prevention and prompt treatment of hemorrhage, sepsis, and hypertensive emergencies
• Safe abortion and post-abortion care where legally available
• Postpartum follow-up, including mental-health assessment

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38. Assessment at the first antenatal visit

English translation

Importance of early attendance

• Accurate dating of pregnancy
• Identification of high-risk conditions
• Early detection of ectopic pregnancy, multiple pregnancy, or miscarriage risk
• Screening for anemia, infection, diabetes, and hypertension
• Prevention of neural tube defects with folic acid
• Timely screening for fetal chromosomal and structural abnormalities
• Early treatment of chronic maternal disease
• Planning the appropriate level and place of delivery

History

General history

• Age, occupation, social situation
• Smoking, alcohol, drugs
• Allergies and medications
• Family history: hypertension, diabetes, thrombosis, congenital anomalies, genetic disorders
• Medical history: hypertension, renal disease, diabetes, thyroid disease, epilepsy, heart disease, infections, thrombosis

Obstetric and gynecological history

• Gravidity and parity
• Previous miscarriage, ectopic pregnancy, preterm birth, stillbirth, neonatal death
• Previous cesarean delivery or uterine surgery
• Previous postpartum hemorrhage, preeclampsia, gestational diabetes, fetal growth restriction
• Last menstrual period and menstrual regularity
• Contraception and fertility treatment
• Gynecological infections and cervical screening history

Physical examination

• Height, weight, BMI
• Blood pressure in both arms when indicated
• Pulse, respiratory rate, temperature when needed
• General examination: edema, thyroid, heart, lungs, abdomen
• Breast examination if indicated
• Pelvic examination when clinically indicated:
  • External genitalia
  • Speculum examination
  • Cervix
  • Bimanual assessment of uterine size and adnexa

Laboratory investigations

• Complete blood count
• Blood group and Rh(D) type
• Red-cell antibody screen
• Urinalysis and urine culture where indicated
• Blood glucose assessment according to local protocol
• HIV testing with consent
• Syphilis serology
• Hepatitis B screening; hepatitis C screening according to national policy/risk
• Rubella immunity assessment where part of local protocol
• Cervical cytology if screening is due and clinically appropriate
• Screening for sexually transmitted infections in at-risk women

Ultrasound

• Confirming intrauterine pregnancy and viability
• Accurate dating
• Detecting multiple pregnancy
• Determining chorionicity in twins
• Nuchal translucency and first-trimester aneuploidy screening where available
• Detecting major early anomalies

Counseling at the first visit

• Folic acid and nutrition
• Avoid alcohol, tobacco, and recreational drugs
• Review medication safety
• Vaccination advice
• Warning signs: vaginal bleeding, severe vomiting, abdominal pain, fever, headache/visual symptoms, reduced fetal movement later in pregnancy
• Birth preparedness and emergency contact plan
• Screening options and consent

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39. Multiple pregnancy

English translation

Definition

Frequency

• Assisted reproductive technologies
• Ovulation induction
• Increasing maternal age
• Family history of dizygotic twins
• Higher parity

Types by zygosity

Dizygotic twins

• Result from fertilization of two ova by two sperm.
• Genetically similar to ordinary siblings.
• Always dichorionic diamniotic.

Monozygotic twins

• Result from division of one fertilized ovum.
• Chorionicity depends on the timing of embryonic division.

Types by chorionicity and amnionicity

Diagnosis

• Uterus larger than expected for gestational age
• Excessive weight gain or symptoms of pregnancy
• Palpation of multiple fetal poles
• Two distinct fetal heart rates
• Ultrasound confirms fetal number, viability, chorionicity, amnionicity, growth, anatomy, and placental location

Maternal complications

• Hyperemesis gravidarum
• Iron-deficiency anemia
• Gestational hypertension and preeclampsia
• Gestational diabetes
• Polyhydramnios
• Preterm labor and preterm birth
• Placental abruption
• Postpartum hemorrhage due to uterine overdistension
• Cesarean delivery and operative complications

Fetal complications

• Preterm birth, the leading complication
• Growth restriction
• Discordant growth
• Congenital anomalies, more frequent in monozygotic twins
• Twin-to-twin transfusion syndrome in monochorionic twins
• Twin anemia-polycythemia sequence
• Selective fetal growth restriction
• Cord entanglement in monoamniotic twins
• Intrauterine death of one twin
• Malpresentation
• Perinatal mortality

Antenatal management

• Early ultrasound: establish chorionicity/amnionicity.
• Care by a specialist obstetric or maternal-fetal medicine team.
• More frequent ultrasound surveillance, especially for monochorionic pregnancies.
• Monitor maternal BP, anemia, symptoms of preterm labor, and fetal growth.
• Counsel regarding symptoms of preterm labor and preeclampsia.
• Assess cervical length in appropriate settings.
• Low-dose aspirin may be indicated for preeclampsia prevention in women with qualifying risk factors.
• Avoid routine bed rest because it has not shown benefit and increases thromboembolic risk.
• Corticosteroids if preterm birth is likely within the recommended time period.

Delivery planning

Mode of delivery

• First twin is cephalic
• No major obstetric contraindication
• Estimated fetal sizes are suitable
• Skilled obstetrician and immediate cesarean capability are available

• First twin is non-cephalic
• Monoamniotic twins
• Major fetal compromise
• Placenta previa, prior classical cesarean, or other standard contraindication
• Certain triplet or higher-order pregnancies

Timing

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40. Miscarriage and recurrent pregnancy loss

English translation

Definition

Classification

By clinical form

1. Threatened miscarriage
2. Inevitable miscarriage
3. Incomplete miscarriage
4. Complete miscarriage
5. Missed miscarriage
6. Septic miscarriage
7. Recurrent pregnancy loss

By timing

• Early miscarriage: usually before 12-13 weeks
• Late miscarriage: approximately 13-22 weeks

Recurrent pregnancy loss

• Many authorities use two or more failed clinical pregnancies.
• Some older exam systems use three or more consecutive losses.

Etiology

1. Genetic causes

• Fetal chromosomal abnormalities, especially aneuploidy
• Parental balanced translocation in a minority of recurrent cases

2. Anatomical causes

• Congenital uterine malformations: septate uterus, bicornuate uterus
• Intrauterine adhesions
• Submucosal fibroids
• Cervical insufficiency, especially in recurrent painless second-trimester loss

3. Endocrine/metabolic causes

• Uncontrolled diabetes mellitus
• Thyroid disease
• Hyperprolactinemia
• Severe obesity
• Polycystic ovary syndrome may be associated through metabolic factors
• Luteal-phase insufficiency is historically described, but diagnosis and treatment remain debated

4. Immunological and thrombotic causes

• Antiphospholipid syndrome is an established treatable cause.
• Inherited thrombophilia testing is not routinely indicated in all cases.

5. Infection

6. Lifestyle and environmental factors

• Smoking
• Alcohol and drugs
• Excess caffeine intake
• Obesity or severe underweight
• Toxic occupational exposure

Assessment of women with recurrent pregnancy loss

• Detailed obstetric, medical, family, and medication history
• Ultrasound assessment of uterine anatomy
• Consider hysteroscopy, saline infusion sonography, or MRI where indicated
• Antiphospholipid antibody testing:
  • Lupus anticoagulant
  • Anticardiolipin antibodies
  • Anti-beta-2 glycoprotein I antibodies
• Thyroid function, diabetes screening when indicated
• Genetic testing of pregnancy tissue when available
• Parental karyotyping in selected cases, especially with abnormal fetal genetic result or repeated losses
• Evaluate cervical insufficiency after recurrent second-trimester painless losses

Prevention

• Preconception counseling
• Folic acid supplementation
• Stop smoking, alcohol, and recreational drugs
• Optimize body weight
• Control diabetes, thyroid disease, hypertension, and other chronic disease
• Review potentially teratogenic medication
• Treat antiphospholipid syndrome appropriately
• Provide psychological support and early pregnancy surveillance

Management of a woman at risk

Threatened miscarriage

• Confirm intrauterine viable pregnancy by ultrasound.
• Assess bleeding severity and rule out ectopic pregnancy.
• Avoid unnecessary vaginal examinations when bleeding is heavy.
• Provide anti-D immunoglobulin to Rh-negative unsensitized women when indicated by gestation and local protocol.
• Progesterone may be considered in women with early-pregnancy bleeding and a history of previous miscarriage, according to local guidance.
• Bed rest is not routinely effective.

Cervical insufficiency

• Serial cervical-length surveillance.
• Vaginal progesterone in selected patients.
• Cervical cerclage in women with a clear history or ultrasound indication, after excluding infection and active labor.

Antiphospholipid syndrome

• Low-dose aspirin plus prophylactic heparin during pregnancy is standard management under specialist care.

Unexplained recurrent pregnancy loss

• Supportive care and early ultrasound monitoring are important.
• Do not prescribe empiric anticoagulation, corticosteroids, antibiotics, or immunotherapy without a specific indication.

Obstetrics Questions 51-57

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51. Bleeding during pregnancy

English translation

Definition

Classification by gestational age

A. First half of pregnancy

1. Threatened, inevitable, incomplete, complete, or missed miscarriage
2. Ectopic pregnancy
3. Gestational trophoblastic disease, especially hydatidiform mole
4. Cervical/vaginal causes
   • Cervical ectropion
   • Cervical polyp
   • Cervicitis
   • Cervical cancer
   • Vaginal trauma, including after intercourse or examination
5. Implantation bleeding, which is mild and self-limiting

B. Second half of pregnancy: antepartum hemorrhage

1. Placenta previa
2. Premature placental abruption, also called abruptio placentae
3. Vasa previa with rupture of fetal vessels
4. Uterine rupture, particularly in a scarred uterus
5. Labor-related cervical dilatation, “bloody show”
6. Cervical, vaginal, or vulvar lesions

Etiology and differential diagnosis

General emergency approach to any significant bleeding in pregnancy

1. Immediate maternal assessment

• Call senior obstetric, anesthesia, neonatal, and blood-bank teams.
• ABCDE approach.
• Assess conscious level, pulse, BP, respiratory rate, oxygen saturation, temperature.
• Put the woman in left lateral tilt to reduce aortocaval compression.
• Give oxygen if hypoxemic or clinically unstable.
• Insert two wide-bore IV cannulas.
• Take blood for:
  • CBC and platelet count
  • Blood group, antibody screen, and crossmatch
  • Coagulation screen
  • Fibrinogen
  • Renal and liver function tests
  • Blood gas/lactate in major hemorrhage
• Begin warmed crystalloid only while arranging blood products. Do not delay transfusion in shock.
• Quantify blood loss objectively where possible.
• Insert urinary catheter and monitor hourly urine output.

2. Fetal assessment

• Continuous CTG if fetus is viable and maternal condition permits.
• Ultrasound for fetal viability, placental location, fetal growth, and amniotic-fluid volume.
• Remember: a normal ultrasound does not exclude placental abruption.

3. Examination rule

• Speculum examination may be performed carefully to look for lower genital tract bleeding if clinically needed.
• Never perform a digital vaginal examination in unexplained late-pregnancy bleeding until placenta previa has been excluded by ultrasound.

4. Rh prophylaxis

Risk groups

Risk factors for placenta previa

• Previous cesarean birth
• Previous uterine curettage, abortion, or uterine surgery
• Previous placenta previa
• Multiparity
• Multiple pregnancy
• Assisted reproductive technology
• Smoking
• Advanced maternal age
• Placenta accreta spectrum risk, especially previa over a uterine scar

Risk factors for placental abruption

• Chronic hypertension or preeclampsia
• Previous abruption
• Smoking, cocaine or stimulant use
• Abdominal trauma
• Premature rupture of membranes
• Chorioamnionitis
• Polyhydramnios with sudden uterine decompression
• Thrombophilia in selected cases
• Multiparity and advanced maternal age

Prevention

• Early and regular antenatal care
• Control hypertension and diabetes
• Smoking and substance-use cessation
• Prevention of abdominal trauma and domestic violence
• Early ultrasound to locate the placenta
• Referral of women with placenta previa, prior cesarean, or suspected placenta accreta spectrum to a tertiary maternity center
• Correction of antenatal anemia and preparation of blood products for high-risk births

In late pregnancy, placenta previa and placental abruption must be differentiated urgently. The first priority is maternal resuscitation and blood preparation. Digital vaginal examination is prohibited until placenta previa is excluded.

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52. Premature placental abruption

English translation

Definition

Classification

By site and type of bleeding

1. Revealed abruption
   • Blood escapes through the cervix.
   • Vaginal bleeding is present.
2. Concealed abruption
   • Blood collects behind the placenta.
   • Vaginal bleeding may be absent or minimal.
   • This may be more dangerous because actual blood loss is underestimated.
3. Mixed abruption
   • Part of the blood is concealed and part is external.

By severity

• Mild
• Moderate
• Severe

Etiology and pathogenesis

Main mechanism

Important causes/risk factors

• Hypertension and preeclampsia
• Previous abruption
• Trauma to abdomen
• Smoking and cocaine use
• Premature rupture of membranes
• Chorioamnionitis
• Multiple pregnancy
• Polyhydramnios, especially after sudden loss of amniotic fluid
• Thrombophilia in selected women
• Advanced maternal age and multiparity

Clinical features

1. Vaginal bleeding
2. Abdominal or back pain
3. Uterine tenderness and hypertonus

• Sudden, severe abdominal pain
• Uterus hard, tense, tender, often described as “board-like”
• Frequent contractions or uterine tetany
• Fetal movement reduction
• Fetal tachycardia, bradycardia, late decelerations, or absent fetal heart activity
• Maternal pallor, tachycardia, hypotension, shock
• Blood loss may be much greater than visible bleeding
• DIC: bleeding from injection sites, petechiae, oozing wounds

Diagnosis

Investigations

• Continuous CTG if fetal heart activity is present
• CBC, platelets
• Group and crossmatch
• PT/INR, aPTT, fibrinogen
• Renal function, liver function, lactate, blood gas
• Ultrasound:
  • May demonstrate retroplacental clot
  • Excludes placenta previa
  • Has limited sensitivity, so a normal ultrasound does not rule out abruption

Differential diagnosis

• Placenta previa
• Uterine rupture
• Labor with bloody show
• Ruptured vasa previa
• Acute abdomen: appendicitis, renal colic, ovarian torsion

Emergency management

Initial resuscitation

1. Call obstetric, anesthesia, neonatal, blood-bank, and operating-theater teams.
2. ABCDE approach and left lateral tilt.
3. Two large-bore IV lines.
4. Crossmatch blood and activate massive hemorrhage protocol when needed.
5. Warm the patient and give warmed fluids/blood products.
6. Insert Foley catheter. Target urine output is generally at least 30 mL/hour.
7. Monitor BP, pulse, oxygen saturation, urine output, and serial coagulation studies.
8. Correct coagulopathy promptly:
   • Packed red cells for significant blood loss
   • Fresh frozen plasma for factor deficiency
   • Platelets if thrombocytopenia with bleeding/procedure
   • Cryoprecipitate or fibrinogen concentrate for low fibrinogen

Obstetric tactic

Urgent cesarean delivery

• Live fetus with severe fetal distress
• Severe abruption with maternal deterioration
• Delivery is not imminent vaginally
• Persistent hemorrhage
• Inability to correct maternal instability while awaiting vaginal birth

Vaginal delivery

• Fetus has died in utero
• Mother is stable or can be stabilized
• Labor is established or vaginal birth is likely soon
• There is no obstetric contraindication

Complications

Maternal

• Hemorrhagic shock
• DIC
• Acute renal failure due to hypoperfusion
• Couvelaire uterus: blood infiltrates myometrium and possibly serosa
• Postpartum hemorrhage from uterine atony
• Sheehan syndrome after massive blood loss
• Maternal death

Fetal

• Acute hypoxia/asphyxia
• Prematurity
• Fetal growth restriction in chronic abruption
• Stillbirth
• Neonatal death

In placental abruption, the amount of visible vaginal blood does not reflect the true blood loss because hemorrhage may be concealed behind the placenta.

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53. Placenta previa

English translation

Definition

Classification

1. Placenta previa
   • Placental tissue covers the internal cervical os, partially or completely.
2. Low-lying placenta
   • Placental edge is close to but does not cover the internal os, commonly within 20 mm.

• Complete/central placenta previa
• Partial placenta previa
• Marginal placenta previa
• Low-lying placenta

Etiology and risk factors

• Previous placenta previa
• Previous cesarean birth, especially multiple cesareans
• Previous curettage, abortion, or intrauterine surgery
• Endometritis or endometrial damage
• Multiparity
• Multiple pregnancy
• Assisted reproductive technology
• Smoking
• Advanced maternal age
• Uterine scar or fibroids

Clinical features

Sudden, painless, recurrent, bright-red vaginal bleeding in the second half of pregnancy.

• Bleeding often begins after 28 weeks.
• It may follow intercourse, an examination, or uterine contractions, but can occur spontaneously.
• Uterus is soft and non-tender.
• Fetal parts are easy to palpate.
• Presenting part may remain high and mobile.
• Malpresentation is more common: breech, transverse lie, unstable lie.
• Maternal shock is proportional to visible blood loss unless another diagnosis is present.

Diagnosis

Ultrasound

• Transabdominal ultrasound can identify a low placenta.
• Transvaginal ultrasound is safe and more accurate for determining the relationship between the placental edge and the internal os.

Examination precautions

• Do not perform a digital vaginal examination when placenta previa is suspected.
• If examination is necessary to identify a vaginal/cervical source, a careful speculum examination may be performed in a facility prepared for hemorrhage.

Additional assessment

• CBC, blood group, antibody screen, crossmatch
• CTG if fetus is viable
• Ultrasound evaluation for placenta accreta spectrum if prior cesarean plus anterior previa/low placenta

Management

General principles

• Hospital assessment for any active bleeding.
• ABCDE, IV access, blood tests, crossmatch.
• Fetal monitoring if viable.
• Anti-D immunoglobulin for Rh(D)-negative unsensitized women according to local protocol.
• Correct anemia.
• Administer antenatal corticosteroids if preterm delivery is likely.
• Consider magnesium sulfate for fetal neuroprotection at very preterm gestations according to local protocol.

Expectant management

• Bleeding stops or is minor
• Mother is stable
• Fetus is reassuring
• Pregnancy is preterm
• No evidence of labor requiring birth

• Close observation, sometimes inpatient depending on recurrence, distance from hospital, and social circumstances
• No intercourse and no vaginal insertion unless medically necessary
• Return urgently for recurrent bleeding, contractions, pain, or reduced fetal movements
• Planned delivery in a center with blood products, senior obstetricians, anesthesia, and neonatal support

Delivery

• Placenta previa covering the os: cesarean delivery is indicated.
• Low-lying placenta: delivery route depends on ultrasound distance from the os, bleeding, fetal position, and obstetric circumstances.
• Major placenta previa is commonly delivered by planned cesarean before labor begins, with exact timing based on bleeding history, placenta accreta risk, and local guideline.

Complications

Maternal

• Massive hemorrhage and hemorrhagic shock
• Placenta accreta spectrum
• Need for transfusion, interventional radiology, hysterectomy
• Postpartum hemorrhage
• Infection and thromboembolism after emergency surgery

Fetal

• Prematurity from indicated early delivery
• Fetal growth restriction in some cases
• Malpresentation
• Fetal hypoxia with severe hemorrhage
• Perinatal mortality, chiefly related to prematurity

Placenta previa is typically painless bleeding with a soft uterus. Placental abruption is typically painful bleeding with uterine tenderness and hypertonus.

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54. Bleeding in the early postpartum period

English translation

Definition

• More than 500 mL after vaginal birth
• More than 1000 mL after cesarean delivery

Causes: the “4 Ts”

Uterine hypotony and atony

Definitions

• Hypotony: reduced uterine contraction and tone.
• Atony: failure of the uterus to contract adequately after placental delivery.

Risk factors

• Overdistended uterus: twins, polyhydramnios, fetal macrosomia
• Prolonged labor or precipitate labor
• Oxytocin augmentation/prolonged induction
• Chorioamnionitis
• Retained placenta
• Uterine fibroids
• Magnesium sulfate
• General anesthesia
• Previous postpartum hemorrhage
• Placenta previa/accreta spectrum
• Grand multiparity

Clinical diagnosis

• Excessive vaginal bleeding
• Boggy, enlarged uterus on abdominal palpation
• Tachycardia, hypotension, pallor, dizziness, altered mental status
• Reduced urine output
• If uterus is firm but bleeding continues, strongly suspect trauma, retained tissue, or coagulopathy.

Sequence of management for hypotonic postpartum hemorrhage

Simultaneously: call for help and resuscitate

1. Activate postpartum hemorrhage protocol.
2. Call obstetric senior, anesthetist, operating theater, blood bank, and neonatal team.
3. ABCDE approach.
4. Left lateral tilt if necessary.
5. Two large-bore IV lines.
6. CBC, coagulation tests, fibrinogen, blood group/crossmatch, blood gas/lactate.
7. Warm fluids and early blood-product replacement as indicated.
8. Insert Foley catheter and monitor urine output.
9. Quantify ongoing blood loss.

First-line uterine measures

1. Uterine fundal massage and bimanual uterine compression.
2. Empty the bladder.
3. Ensure the placenta and membranes are complete.
4. Give oxytocin as first-line uterotonic, using the local protocol.

Additional uterotonics if bleeding persists

• Ergometrine or methylergometrine
  • Avoid in hypertension, preeclampsia, and significant heart disease.
• Carboprost
  • Avoid in asthma and use cautiously in cardiac, pulmonary, renal, or hepatic disease.
• Misoprostol
  • Useful where injectable uterotonics are unavailable or as an adjunct.
• Tranexamic acid
  • Give as early as possible, ideally within 3 hours of birth, in clinically diagnosed postpartum hemorrhage, unless contraindicated.

Exclude the other “Ts”

1. Inspect cervix, vagina, perineum, and surgical wounds for tears.
2. Check for retained placenta or retained products. Perform manual exploration/evacuation when indicated, with adequate analgesia/anesthesia and asepsis.
3. Check coagulation results and replace deficient components.

Mechanical measures

1. Intrauterine balloon tamponade if atony continues and retained tissue/rupture is excluded.
2. Continue bimanual compression while preparing definitive treatment.

Surgical and radiological treatment

1. Compression sutures, for example B-Lynch-type sutures.
2. Uterine artery ligation, stepwise devascularization, or internal iliac artery ligation in selected cases.
3. Uterine artery embolization if the woman is stable and interventional radiology is immediately available.
4. Peripartum hysterectomy if bleeding is uncontrollable or placenta accreta spectrum is present with life-threatening hemorrhage.

Prevention

• Identify women at risk antenatally.
• Treat anemia.
• Active management of the third stage of labor with prophylactic uterotonic.
• Ensure access to blood products and a hemorrhage protocol in high-risk cases.
• Deliver suspected placenta accreta spectrum in a tertiary center.

For atonic postpartum hemorrhage, management is simultaneous resuscitation plus uterine massage, oxytocin and other uterotonics, tranexamic acid, exclusion of trauma/tissue/thrombin causes, balloon tamponade, surgical hemostasis, and hysterectomy if life-saving.

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55. Obstetric disseminated intravascular coagulation syndrome

English translation

Definition

Major obstetric causes

• Massive postpartum hemorrhage
• Placental abruption, especially with retained dead fetus or concealed hemorrhage
• Amniotic fluid embolism
• Severe preeclampsia/HELLP syndrome
• Sepsis and septic abortion
• Retained dead fetus for a prolonged period
• Acute fatty liver of pregnancy
• Massive tissue trauma, uterine rupture
• Incompatible blood transfusion
• Placenta accreta spectrum with severe hemorrhage

Pathogenesis

1. A trigger releases tissue factor/thromboplastin or causes severe endothelial injury.
2. The coagulation cascade is activated throughout the circulation.
3. Fibrin microthrombi form in small vessels.
4. Platelets and clotting factors are consumed.
5. Fibrinolysis is activated.
6. The patient develops simultaneous:
   • Microvascular thrombosis and organ ischemia
   • Severe hypocoagulable bleeding

Clinical stages

Stage 1: Hypercoagulable phase

• Often short and clinically subtle.
• Microthrombi form.
• Peripheral ischemia and early organ dysfunction may occur.
• Laboratory abnormalities may be minimal initially.

Stage 2: Consumption coagulopathy

• Platelet count falls.
• Fibrinogen decreases.
• PT/aPTT become prolonged.
• Bleeding starts from injection sites, wounds, genital tract, and mucosa.

Stage 3: Secondary fibrinolysis

• Marked bleeding and oozing.
• Petechiae, ecchymoses, hematomas.
• Massive uterine/wound bleeding.
• Fibrin degradation products/D-dimer markedly increased.
• Severe hypofibrinogenemia.

Stage 4: Recovery or irreversible multiorgan failure

• If the cause is removed and replacement is adequate, coagulation may recover.
• If untreated: shock, acute kidney injury, ARDS, hepatic failure, cerebral injury, and death.

Diagnosis

Clinical signs

• Diffuse bleeding from multiple sites
• Persistent postpartum/operative bleeding despite suturing and uterotonics
• Oozing from IV sites, surgical wounds, gums
• Petechiae, bruising
• Hypotension/shock
• Oliguria/anuria
• Respiratory distress or altered consciousness

Laboratory features

• Thrombocytopenia
• Low fibrinogen, particularly important in obstetric hemorrhage
• Prolonged PT/INR and aPTT
• High D-dimer/fibrin degradation products
• Falling hemoglobin
• Evidence of hemolysis in certain conditions
• Abnormal thromboelastography/rotational thromboelastometry when available

Principles of treatment

1. Treat the cause immediately

• Deliver in severe placental abruption when indicated.
• Evacuate infected retained products in septic abortion after antibiotics/resuscitation.
• Control uterine hemorrhage.
• Treat sepsis with source control and broad-spectrum antibiotics.
• Manage amniotic fluid embolism with intensive resuscitation.

2. Resuscitate

• Activate massive obstetric hemorrhage protocol.
• Secure airway/oxygenation and circulation.
• Two wide-bore IV lines or rapid infuser.
• Warm patient, fluids, and blood products.
• Monitor urine output, lactate, blood gas, temperature, and serial coagulation tests.

3. Replace blood components rationally

• Packed red cells for significant blood loss/anemia.
• Fresh frozen plasma for prolonged clotting times with bleeding.
• Platelets for severe thrombocytopenia with active bleeding/procedure.
• Cryoprecipitate or fibrinogen concentrate for low fibrinogen.
• Repeat testing frequently and guide replacement by clinical loss and results.

4. Avoid unhelpful delay

5. Heparin

Prevention

• Timely management of abruption, hemorrhage, sepsis, and severe preeclampsia
• Safe blood transfusion practice
• Early correction of hypofibrinogenemia and thrombocytopenia in active bleeding
• Management in a tertiary institution for high-risk obstetric emergencies

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56. Hemorrhagic shock in obstetrics

English translation

Definition

Causes in obstetrics

• Placental abruption
• Placenta previa and placenta accreta spectrum
• Uterine rupture
• Ectopic pregnancy rupture
• Miscarriage with severe hemorrhage
• Atonic/hypotonic postpartum hemorrhage
• Retained placenta
• Cervical, vaginal, or perineal tears
• Surgical bleeding after cesarean section
• Coagulopathy/DIC
• Hemorrhage after unsafe abortion

Pathogenesis

1. Blood loss decreases venous return.
2. Cardiac output falls.
3. Compensatory tachycardia and peripheral vasoconstriction occur.
4. Tissue perfusion declines.
5. Anaerobic metabolism produces lactate and metabolic acidosis.
6. Hypothermia, acidosis, and coagulopathy reinforce one another: the “lethal triad.”
7. Untreated shock progresses to renal failure, DIC, ARDS, multiorgan failure, and death.

Clinical classification

Shock index

Management

Immediate actions

1. Call for help and activate the massive hemorrhage protocol.
2. ABCDE approach.
3. Lay the patient flat with left uterine displacement if still pregnant.
4. High-flow oxygen if hypoxemic/unstable.
5. Two large-bore IV cannulas or rapid vascular access.
6. Collect blood immediately: CBC, coagulation tests, fibrinogen, electrolytes, blood gas/lactate, group and crossmatch.
7. Keep patient warm.
8. Insert Foley catheter and monitor hourly urine output.
9. Quantify blood loss continuously.

Fluid and blood replacement

• Begin warmed crystalloid only as an initial bridge.
• Do not give excessive crystalloid because it dilutes coagulation factors and worsens hypothermia/coagulopathy.
• Initiate early transfusion of blood products when bleeding is major.
• Use packed red cells, plasma, platelets, and fibrinogen replacement according to local major hemorrhage protocol and lab/viscoelastic test results.
• Give tranexamic acid early in postpartum hemorrhage and in other appropriate obstetric hemorrhage settings, unless contraindicated.

Stop the bleeding

• Atony: massage, uterotonics, balloon, surgery.
• Retained tissue: manual removal/evacuation.
• Trauma: surgical repair.
• Abruption with instability/fetal distress: urgent delivery.
• Uterine rupture: emergency laparotomy.
• Placenta accreta spectrum: planned or emergency surgical management, often hysterectomy.

Monitoring goals

• Improving pulse and BP
• Normalizing mental status
• Warm extremities and adequate perfusion
• Urine output usually ≥30 mL/hour
• Falling lactate
• Correction of acidosis, hypothermia, and coagulopathy

Hemorrhagic shock is managed by simultaneous resuscitation, early balanced blood-component therapy, active warming, correction of coagulopathy, and immediate surgical or obstetric control of the bleeding source.

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57. Uterine rupture

English translation

Definition

Classification

By completeness

1. Complete rupture
   • Full-thickness tear through endometrium, myometrium, and serosa.
   • The fetus, placenta, or both may enter the abdominal cavity.
   • Severe intraperitoneal bleeding is common.
2. Incomplete rupture/dehiscence
   • Myometrium separates but serosa remains intact.
   • Often occurs in a previous cesarean scar.
   • May be clinically silent and found at surgery.

By cause

1. Spontaneous rupture
   • Scarred uterus or obstructed labor.
2. Traumatic rupture
   • External trauma, difficult instrumental manipulation, internal version, destructive operation, injudicious fundal pressure.
3. Iatrogenic rupture
   • Excessive oxytocin/prostaglandins, inappropriate induction, uterine instrumentation.

By timing

• During pregnancy
• During labor
• Rarely postpartum

By location

• Lower uterine segment
• Previous cesarean scar
• Lateral uterine wall
• Fundus
• Extension into cervix, vagina, broad ligament, bladder, or uterine vessels

Etiology and risk factors

Scarred uterus

• Previous cesarean, especially classical/high vertical incision
• Previous uterine rupture
• Myomectomy entering the uterine cavity
• Previous hysterotomy or fetal surgery

Obstructed labor

• Cephalopelvic disproportion
• Contracted pelvis
• Fetal macrosomia
• Malpresentation: transverse lie, brow, neglected shoulder presentation
• Pelvic tumor

Hyperstimulation

• Excess oxytocin
• Prostaglandin induction in an inappropriate setting
• Inadequate monitoring during induction/augmentation

Other risk factors

• Grand multiparity
• Trauma
• Placenta percreta invading the uterine wall
• Congenital uterine anomaly
• Previous curettage/perforation
• Instrumental or operative obstetric maneuvers

Etiopathogenesis

1. Mechanical rupture due to obstruction
   • Upper uterine segment contracts and retracts strongly.
   • Lower uterine segment becomes thin and overstretched.
   • A pathological retraction ring, Bandl ring, may appear.
   • Continued force results in rupture.
2. Scar rupture
   • A previous uterine scar fails under mechanical stress, sometimes with few warning symptoms.

Threatened uterine rupture

Clinical features

• Painful, frequent, ineffective contractions
• Maternal anxiety and agitation
• Lower uterine segment tenderness
• Rising pathological retraction ring
• Bandl ring may be visible or palpable
• Round ligaments tense and painful
• Fetal head remains high despite good contractions
• Fetal distress
• Vaginal edema, cervical edema
• Maternal tachycardia

Management of threatened rupture

• Stop oxytocin/prostaglandins immediately.
• Call senior obstetric and anesthesia teams.
• ABC resuscitation and two IV lines.
• Continuous fetal monitoring.
• Urgent cesarean delivery/laparotomy before actual rupture occurs.
• Do not attempt continued labor or instrumental vaginal delivery in obstructed labor.

Completed uterine rupture

Clinical features

• Sudden severe “tearing” abdominal pain, though pain may be less obvious with epidural or scar dehiscence
• Contractions may suddenly stop
• Fetal parts become easily palpable abdominally
• Loss of fetal presenting part from the pelvis
• Change in fetal station
• Abnormal CTG, especially sudden fetal bradycardia, often the earliest sign
• Vaginal bleeding may be present or absent
• Maternal tachycardia, hypotension, shock
• Hematuria if bladder is injured
• Intra-abdominal bleeding and peritoneal signs

Diagnosis

• CTG abnormalities
• Maternal shock
• Abdominal tenderness and altered fetal station
• Ultrasound may show free intraperitoneal fluid, but should not delay laparotomy in an unstable woman

Emergency management

1. Activate emergency response: senior obstetrician, anesthetist, neonatal team, blood bank, operating theater.
2. ABCDE resuscitation, oxygen if required.
3. Left uterine displacement if pregnant.
4. Two large-bore IV cannulas.
5. Crossmatch blood and activate massive transfusion protocol.
6. Stop oxytocin/prostaglandins.
7. Insert Foley catheter and assess for hematuria.
8. Immediate laparotomy and delivery. This is the definitive treatment.
9. Resuscitate newborn as required.
10. Repair associated bladder, ureteric, cervical, vaginal, or vascular injury with appropriate specialist involvement.

Surgical management: repair versus hysterectomy

Uterine repair may be possible when

• Tear is limited and accessible
• Bleeding is controllable
• Tissue is viable
• No extensive lateral extension
• No major vascular, cervical, or bladder involvement
• Woman desires future fertility
• Hemodynamic state permits repair

Hysterectomy is indicated when

• Rupture is extensive or multiple
• Tissue is devitalized
• Bleeding cannot be controlled rapidly
• Tear extends into uterine vessels/cervix/broad ligament
• Placenta accreta spectrum is present
• Severe infection is present
• The woman is unstable and fertility-preserving repair would dangerously delay hemostasis

Complications

Maternal

• Massive hemorrhage and shock
• DIC
• Bladder/ureteric injury
• Hysterectomy and loss of fertility
• Sepsis
• Acute renal failure
• Maternal death

Fetal

• Acute profound hypoxia
• Fetal hemorrhage
• Stillbirth
• Severe neonatal encephalopathy or death

Uterine rupture is a clinical diagnosis and an indication for immediate laparotomy. Maternal resuscitation and hemorrhage control occur simultaneously. The operation is either uterine repair or hysterectomy, chosen according to the extent of rupture, bleeding, tissue condition, associated injury, and maternal stability.

Obstetrics Questions 58-64

Important for treatment: doses below are commonly used adult regimens for examination purposes. In practice, antibiotic choice and dosing must follow local resistance patterns, microbiological results, renal function, allergy history, severity of illness, and hospital protocol.

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58. Postpartum purulent-septic diseases. Postpartum ulcer

English translation

Definition

Etiology

Common microorganisms

• Anaerobes:
  • Bacteroides spp.
  • Peptostreptococcus
  • Prevotella
  • Clostridium spp.
• Gram-negative aerobic bacteria:
  • Escherichia coli
  • Klebsiella
  • Proteus
• Gram-positive bacteria:
  • Group A, B, and D streptococci
  • Staphylococcus aureus
  • Enterococci
• Occasionally:
  • Chlamydia trachomatis
  • Mycoplasma
  • hospital-acquired multidrug-resistant flora

Routes of infection

1. Ascending infection from vagina/cervix to uterus.
2. Direct inoculation into tears, episiotomy wound, cesarean wound, or uterine cavity.
3. Lymphogenous spread to parametrial tissue.
4. Hematogenous spread in severe infection or sepsis.

Predisposing factors

• Cesarean delivery, especially emergency cesarean after prolonged labor
• Prolonged rupture of membranes, usually more than 18 hours
• Prolonged labor, multiple vaginal examinations
• Chorioamnionitis
• Manual removal of placenta, intrauterine procedures
• Retained placental tissue or membranes
• Postpartum hemorrhage and anemia
• Birth canal trauma, hematoma, episiotomy
• Diabetes mellitus, obesity, immunosuppression
• Poor asepsis/antisepsis
• Untreated vaginal infection or bacterial vaginosis

Classification

By localization and spread

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Postpartum ulcer

Definition

Etiology

• Infection of a perineal tear or episiotomy
• Contamination with mixed vaginal and bowel flora
• Poor wound care or poor hygiene
• Hematoma or tissue ischemia
• Inadequate suturing, wound tension, devitalized tissue
• Diabetes, anemia, immune compromise

Clinical features

• Local pain, burning, throbbing pain in the perineum
• Fever, sometimes chills
• Edema, erythema, induration around the wound
• Separation of wound edges
• Gray-yellow or dirty necrotic coating
• Purulent or foul-smelling discharge
• Tender inguinal lymph nodes may occur
• Severe pain out of proportion to examination, rapidly spreading edema, crepitus, or systemic toxicity suggests necrotizing infection and is an emergency.

Diagnosis

• Clinical inspection of external genitalia, perineum, episiotomy, vagina, and cervix
• Assess vital signs and sepsis signs
• Wound swab/pus culture before antibiotics if this does not delay treatment
• CBC, CRP, renal function in moderate/severe disease
• Blood cultures if temperature ≥38°C, chills, tachycardia, hypotension, or suspected systemic infection
• Ultrasound/CT only if deep abscess, hematoma, foreign body, retained material, or extension into pelvis is suspected

Treatment: sequential approach

1. Assess severity

• Mild localized infection with no fever/systemic toxicity: local management plus oral antibiotics if cellulitis is present.
• Fever, spreading cellulitis, severe pain, wound separation, abscess, or systemic signs: admit and give IV therapy.

2. Wound treatment

• Remove contaminated dressings.
• Inspect wound under adequate analgesia.
• Open part or all of the wound if there is pus, hematoma, infected collection, or wound-edge necrosis.
• Drain pus and evacuate hematoma.
• Debride devitalized/necrotic tissue.
• Irrigate with sterile saline.
• Leave infected wounds open initially for drainage.
• Daily wound review, irrigation, and dressing changes.
• Secondary closure is considered only after infection is controlled and healthy granulation tissue is present.

3. Antibiotics

• Oral amoxicillin-clavulanate, if appropriate locally and no allergy.
• If severe penicillin allergy, choose an alternative according to local microbiological guidance.

• Clindamycin 900 mg IV every 8 hours plus gentamicin 5 mg/kg IV once daily, or
• Ampicillin-sulbactam 3 g IV every 6 hours, or
• Piperacillin-tazobactam 4.5 g IV every 6-8 hours in severe hospital-acquired/polymicrobial infection.

4. Supportive treatment

• Antipyretics and adequate analgesia
• Fluid replacement if dehydrated
• Correct anemia, diabetes, malnutrition, and immunosuppressive factors
• Tetanus prophylaxis if relevant and wound care was nonsterile

Prevention

• Strict asepsis during delivery and suturing
• Proper repair of tears and hemostasis
• Avoid unnecessary episiotomy
• Prophylactic antibiotic before cesarean delivery
• Perineal hygiene and regular wound inspection
• Early treatment of hematoma, urinary retention, and wound pain

A postpartum ulcer is treated by drainage and debridement of infected or necrotic tissue, culture sampling, broad antimicrobial therapy when indicated, daily wound care, and delayed secondary suturing only after infection is controlled.

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59. Postpartum endometritis, metroendometritis, metrothrombophlebitis, and parametritis

English translation

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A. Postpartum endometritis

Definition

Etiology

• E. coli
• Group B streptococci
• Enterococci
• Anaerobic streptococci
• Bacteroides spp.
• Peptostreptococcus
• Gardnerella vaginalis
• Occasionally Chlamydia trachomatis

Risk factors

• Cesarean section
• Prolonged labor or rupture of membranes
• Repeated vaginal examinations
• Chorioamnionitis
• Internal fetal monitoring
• Retained products of conception
• Manual removal of placenta
• Postpartum hemorrhage
• Anemia, diabetes, obesity

Clinical features

• Fever ≥38°C
• Chills, weakness, malaise
• Suprapubic/lower abdominal pain
• Uterine tenderness
• Delayed uterine involution or subinvolution
• Enlarged, soft uterus
• Foul-smelling, cloudy, purulent, or bloody lochia
• Tachycardia
• Leukocytosis, elevated CRP

Diagnosis

• Full history and examination
• Palpate uterine fundus: tender, enlarged, poorly involuted
• Inspect lochia
• CBC, CRP, renal/liver function in severe disease
• Urinalysis/urine culture to exclude pyelonephritis or UTI
• Blood cultures before antibiotics if fever with systemic illness, hypotension, rigors, or suspected sepsis
• Pelvic ultrasound if:
  • retained products are suspected
  • bleeding is excessive
  • fever persists despite treatment
  • subinvolution is marked
  • pelvic abscess is suspected

Differential diagnosis

• UTI/pyelonephritis
• Breast engorgement or mastitis
• Wound infection
• Septic pelvic thrombophlebitis
• Retained placental tissue
• Pneumonia, COVID/influenza, drug fever
• Appendicitis or other surgical abdomen

Treatment

First-line IV regimen

• Clindamycin 900 mg IV every 8 hours plus
• Gentamicin 5 mg/kg IV once daily

Add ampicillin

• Ampicillin 2 g IV every 6 hours

• Enterococcus is suspected,
• group B streptococcal infection is suspected,
• there is no clinical improvement after 24-48 hours,
• culture results indicate need.

• Ampicillin-sulbactam 3 g IV every 6 hours
• Piperacillin-tazobactam 4.5 g IV every 6-8 hours
• A carbapenem in severe resistant infection or septic shock

Duration

• Continue IV antibiotics until the patient is clinically improved and afebrile for at least 24-48 hours.
• For uncomplicated endometritis, oral antibiotics after successful IV treatment are often unnecessary, unless there is another infection source or incomplete response.
• Modify therapy based on culture results and clinical response.

Source control

• Stabilize first.
• Start IV broad-spectrum antibiotics.
• Perform careful uterine evacuation under senior supervision if retained infected tissue is present.
• Avoid blind curettage if placenta accreta spectrum or uterine perforation is possible.

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B. Postpartum metroendometritis

Definition

Clinical features

• High fever, often 39-40°C
• Recurrent chills
• Severe lower abdominal pain
• Marked uterine tenderness
• Enlarged, poorly involuted, soft uterus
• Foul purulent lochia, sometimes reduced lochia because of outflow obstruction
• Tachycardia, leukocytosis
• Possible bacteremia, sepsis, and DIC

Diagnosis

• Clinical picture is more severe than simple endometritis.
• CBC, CRP/procalcitonin, renal/liver function, lactate
• Blood cultures before antimicrobials, if possible without delay
• Pelvic ultrasound to assess retained tissue, hematometra, intrauterine gas, abscess, and fluid collection
• CT/MRI if abscess, parametritis, thrombophlebitis, or peritonitis is suspected

Treatment

• Admit to high-dependency/ICU setting if unstable.
• Begin IV broad-spectrum antibiotics immediately.
• Resuscitate with IV fluids, oxygen as needed, blood products if hemorrhage/DIC.
• Evaluate for retained products and drain/evacuate if present.
• Treat as sepsis if hypotension, elevated lactate, altered mental status, oliguria, or organ dysfunction occurs.

• Piperacillin-tazobactam 4.5 g IV every 6 hours, or
• Clindamycin 900 mg IV every 8 hours plus gentamicin 5 mg/kg daily, with ampicillin 2 g IV every 6 hours if Enterococcus coverage is required.

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C. Postpartum metrothrombophlebitis / septic pelvic thrombophlebitis

Definition

• Uterine venous thrombophlebitis
• Ovarian vein thrombosis
• Pelvic septic thrombophlebitis

Risk factors

• Cesarean delivery
• Severe endometritis
• Pelvic surgery
• Postpartum hemorrhage
• Sepsis
• Thrombophilia
• Prolonged labor, dehydration, immobility

Clinical features

• Persistent or recurrent spiking fever despite 48-72 hours of adequate broad-spectrum antibiotics
• Tachycardia
• Lower abdominal/pelvic pain, often unilateral with ovarian vein thrombosis
• Uterine tenderness may improve while fever continues
• Sometimes minimal local findings
• Pulmonary embolism may occur: chest pain, dyspnea, hypoxemia

Diagnosis

• Suspect it when postpartum fever persists despite apparently appropriate endometritis treatment and no retained tissue/abscess is found.
• CBC, CRP, blood cultures
• Pelvic CT with contrast or MRI/MR venography may visualize thrombosed ovarian/pelvic veins.
• Doppler ultrasound may help but may miss deep pelvic veins.
• Exclude abscess, retained products, pyelonephritis, wound infection, and pulmonary embolism.

Treatment

1. Broad-spectrum IV antibiotics as for severe endometritis.
2. Therapeutic anticoagulation, usually low-molecular-weight heparin:
   • Example: enoxaparin 1 mg/kg subcutaneously every 12 hours, adjusted for renal impairment and body weight.
3. Continue anticoagulation duration according to thrombus extent, clinical course, and specialist advice. Proven ovarian vein thrombosis often requires several weeks to about 3 months of anticoagulation.
4. CT pulmonary angiography or specialist evaluation if pulmonary embolism is suspected.
5. Consult hematology/vascular medicine and infectious diseases where available.

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D. Postpartum parametritis

Definition

Clinical features

• Fever and chills
• Unilateral lower abdominal or pelvic pain
• Pain radiating to groin, thigh, or sacrum
• Tenderness beside uterus on bimanual examination
• Uterus may be displaced toward the healthy side
• Dense, painful infiltration in the parametrium
• Constipation, dysuria, or painful defecation if adjacent organs are affected

Diagnosis

• Bimanual pelvic examination
• CBC, CRP, cultures where indicated
• Ultrasound may show parametrial collection
• CT/MRI is more useful for deep pelvic abscess, spread to retroperitoneum, ureteral compression, or uncertain diagnosis

Treatment

• IV broad-spectrum antibiotics with anaerobic coverage.
• Analgesia, IV fluids, antipyretics.
• Monitor urine output and renal function if ureteric involvement is suspected.
• If abscess forms: image-guided drainage or surgical drainage is needed.
• Persistent sepsis despite antibiotics means assume undrained pus, retained tissue, thrombophlebitis, or resistant organism until proven otherwise.

Persistent fever after 48-72 hours of correct endometritis therapy should prompt active search for retained tissue, pelvic abscess, infected hematoma, septic pelvic thrombophlebitis, or another non-genital source of infection.

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60. Postpartum pelvioperitonitis and obstetric peritonitis after cesarean section

English translation

Definition

Postpartum pelvioperitonitis

Obstetric peritonitis after cesarean section

Routes and mechanisms of infection

1. Ascending infection from vagina/cervix to the endometrium and through the uterine incision.
2. Direct extension from endometritis, metroendometritis, parametritis, infected hematoma, or pelvic abscess.
3. Contamination during cesarean delivery, especially after prolonged rupture of membranes or chorioamnionitis.
4. Uterine wound dehiscence, necrosis, or leakage of infected lochia into the peritoneal cavity.
5. Bowel, bladder, or urinary tract injury during surgery.
6. Hematogenous spread in severe sepsis.

Risk group

• Emergency cesarean section
• Cesarean after prolonged labor or prolonged rupture of membranes
• Chorioamnionitis
• Repeated vaginal examinations
• Intraoperative blood loss/hematoma
• Postpartum hemorrhage and anemia
• Obesity, diabetes, immunosuppression
• Poor aseptic conditions
• Retained products of conception
• Unrecognized bowel injury or uterine incision dehiscence

Clinical features

Pelvioperitonitis

• Fever and chills
• Lower abdominal pain
• Pelvic tenderness
• Guarding mainly in lower abdomen
• Nausea and vomiting
• Pain on vaginal/rectal examination
• Bowel sounds may be reduced
• Leukocytosis and raised inflammatory markers

Generalized peritonitis after cesarean

• Severe diffuse abdominal pain
• Fever, tachycardia, hypotension
• Marked abdominal distension
• Guarding, rebound tenderness, rigidity
• Nausea/vomiting
• Paralytic ileus: absent or markedly reduced bowel sounds, no flatus/stool
• Offensive lochia or wound discharge may occur
• Oliguria, confusion, elevated lactate, sepsis/septic shock
• Wound erythema, pus, or fascial disruption may coexist

Diagnosis

• Urgent clinical assessment, do not delay treatment.
• CBC, CRP/procalcitonin, electrolytes, renal/liver function.
• Serum lactate and arterial/venous blood gas.
• Blood cultures before antibiotics if possible, but antibiotics must not be delayed.
• Urine culture and wound/lochia cultures.
• Pelvic/abdominal ultrasound for fluid collection, hematoma, retained tissue, or abscess.
• Contrast CT abdomen/pelvis in a hemodynamically stable patient to identify abscess, bowel injury, uterine dehiscence, free air, or intra-abdominal fluid.
• If generalized peritonitis or unstable shock is present, do not wait for CT: proceed to surgical exploration after immediate resuscitation.

Treatment

1. Immediate resuscitation

• Call obstetrician, anesthetist, general surgeon, ICU, blood bank, and microbiology.
• ABCDE assessment.
• Oxygen if hypoxemic or in shock.
• Two large-bore IV cannulas.
• Balanced crystalloid resuscitation while preparing vasopressors/blood products if needed.
• Insert urinary catheter and monitor hourly urine output.
• Measure lactate and repeat to assess response.
• Start sepsis pathway.

2. Broad-spectrum IV antibiotics

• Piperacillin-tazobactam 4.5 g IV every 6 hours, or
• Meropenem 1 g IV every 8 hours in severe hospital-acquired infection, prior resistant organisms, or septic shock, or
• Clindamycin 900 mg IV every 8 hours plus gentamicin 5 mg/kg daily plus ampicillin 2 g IV every 6 hours.

3. Source control

• Drainage of pelvic/intra-abdominal abscess
• Evacuation of infected hematoma
• Repair of uterine incision dehiscence if feasible
• Removal of retained infected products
• Repair of bowel injury
• Peritoneal lavage and drainage
• Hysterectomy if uncontrolled uterine infection, uterine necrosis, extensive wound dehiscence, uncontrolled bleeding, or non-salvageable infected uterus causes life-threatening sepsis

4. ICU care where indicated

• Norepinephrine is first-line vasopressor if hypotension persists after fluid resuscitation.
• Target mean arterial pressure generally ≥65 mmHg.
• Mechanical ventilation for respiratory failure.
• Renal replacement therapy if severe renal failure.
• Correct DIC and provide blood-component therapy if required.

Prevention

• Timely prophylactic antibiotics before cesarean incision.
• Strict asepsis and gentle surgical technique.
• Proper hemostasis and treatment of hematomas.
• Timely management of prolonged labor and rupture of membranes.
• Early diagnosis and treatment of postpartum endometritis.
• Careful postoperative monitoring of temperature, pulse, abdominal pain, lochia, uterine involution, and wound.

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61. Infectious-toxic shock

English translation

Definition

Importance in maternal mortality

Obstetric causes

• Septic abortion, especially unsafe or incomplete abortion
• Retained infected products of conception
• Postpartum endometritis or metroendometritis
• Cesarean wound infection, uterine dehiscence, peritonitis
• Chorioamnionitis
• Pyelonephritis
• Necrotizing fasciitis of perineum/cesarean wound
• Mastitis with bacteremia, rarely
• Group A streptococcal or clostridial infection

Pathogenesis

1. Pathogen and toxins activate innate immune response.
2. Cytokines cause systemic vasodilation and increased capillary permeability.
3. Intravascular volume falls relative to vascular capacity.
4. Myocardial depression and impaired microcirculation develop.
5. Tissue oxygen delivery falls.
6. Lactate rises, metabolic acidosis develops.
7. DIC, acute kidney injury, ARDS, hepatic failure, and encephalopathy can follow.

Clinical features

Early/warm phase

• Fever or hypothermia
• Tachycardia
• Tachypnea
• Anxiety/agitation
• Flushed warm skin
• Uterine/pelvic pain, foul lochia, wound pus, or another infection focus
• Decreased urine output

Late/cold phase

• Hypotension
• Cold mottled extremities
• Confusion/drowsiness
• Oliguria/anuria
• Cyanosis
• Severe metabolic acidosis
• DIC with bleeding
• Multiorgan failure

Red flags

• Systolic BP <90 mmHg or rapidly falling BP
• MAP <65 mmHg
• Lactate ≥2 mmol/L, especially if rising
• New confusion
• Urine output <0.5 mL/kg/hour
• Respiratory distress/hypoxemia
• Platelet fall, coagulopathy, rising creatinine or bilirubin

Diagnosis

Investigations

• CBC with differential and platelets
• CRP/procalcitonin
• Serum lactate, blood gas
• Electrolytes, glucose, renal/liver function
• Coagulation profile and fibrinogen
• Two sets of blood cultures before antibiotics if this causes no meaningful delay
• Urine, lochia, wound, cervical, or operative-site cultures
• Ultrasound/CT as appropriate to locate retained products, abscess, hematoma, peritonitis, or obstruction

Treatment: first hour bundle

1. Call for help and transfer to critical care

• Obstetrician, anesthetist/ICU, surgeon if source control required, microbiology/infectious diseases, and blood bank.

2. ABCDE and monitoring

• Oxygen to maintain adequate saturation.
• Airway protection/intubation if reduced consciousness or respiratory failure.
• Two large IV lines or central access.
• Continuous monitoring: BP, ECG, SpO₂, temperature, urine output.
• Urinary catheter.
• Measure lactate and repeat within hours.

3. Cultures

4. Antibiotics within one hour

• Piperacillin-tazobactam 4.5 g IV every 6 hours, or
• Meropenem 1 g IV every 8 hours for severe resistant/nosocomial infection, or
• Clindamycin 900 mg IV every 8 hours + gentamicin 5 mg/kg once daily + ampicillin 2 g IV every 6 hours.

5. Fluids

• Give balanced crystalloids initially.
• A commonly used target is up to 30 mL/kg in hypotension or lactate elevation, but obstetric patients must be reassessed frequently because excess fluids can cause pulmonary edema.
• Reassess BP, capillary refill, lung examination, urine output, ultrasound where available, and lactate response.

6. Vasopressors

• Norepinephrine is first-line.
• Aim for MAP ≥65 mmHg.
• Add vasopressin or epinephrine in ICU if refractory shock.

7. Source control

• Evacuate retained infected tissue
• Drain pelvic/intra-abdominal abscess
• Drain infected hematoma
• Debride necrotic wound
• Repair/remove infected uterine incision pathology
• Laparotomy for generalized peritonitis
• Hysterectomy when the uterus is the uncontrollable source of infection and conservative control is unsafe

8. Correct complications

• DIC: blood products and fibrinogen replacement guided by bleeding/labs
• Acute kidney injury: optimize perfusion, avoid nephrotoxins, dialysis if necessary
• Respiratory failure/ARDS: ventilation in ICU
• Severe anemia/hemorrhage: transfuse blood products
• Hypoglycemia/electrolyte imbalance: correct promptly

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62. Obstetric sepsis

English translation

Definition

Importance

Etiopathogenesis

• Microbial invasion from uterus, placenta, genital tract, urinary tract, wound, breast, or abdominal cavity
• Bacterial toxins and inflammatory mediators trigger widespread endothelial injury
• Vasodilation, capillary leak, microcirculatory failure, coagulopathy, myocardial dysfunction
• Tissue hypoxia and organ dysfunction
• Progression to septic shock, DIC, ARDS, renal failure, and death if untreated

Clinical features

• Fever, foul lochia, uterine tenderness, pelvic pain
• Dysuria/flank pain from pyelonephritis
• Wound erythema or purulent discharge
• Breast pain with mastitis/abscess
• Abdominal guarding/distension in peritonitis
• Retained products after abortion/miscarriage

• Fever or hypothermia
• Tachycardia, tachypnea
• Hypotension
• Altered mental status
• Oliguria
• Elevated lactate
• Thrombocytopenia
• Jaundice, elevated creatinine, acidosis
• Bleeding due to DIC

Diagnosis

Core investigations

• CBC, platelets
• CRP/procalcitonin
• Lactate and blood gas
• Creatinine, urea, electrolytes, liver function
• Coagulation profile, fibrinogen
• Blood cultures ×2 before antibiotics if feasible
• Urine culture
• Culture of lochia/wound/pus/placental tissue
• Ultrasound for retained products or pelvic collection
• CT/MRI for abscess, peritonitis, necrotizing infection, or deep thrombophlebitis in stable women

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Treatment

A. Antibacterial therapy

Principles

1. Start IV antibiotics within one hour of recognizing probable sepsis/septic shock.
2. Cover gram-positive, gram-negative, and anaerobic organisms.
3. Obtain cultures first only if this does not delay therapy.
4. Review at 24-48 hours and narrow treatment according to culture and sensitivity.
5. Adjust all doses for kidney function, liver function, body weight, and critical illness.
6. Continue therapy according to source control, organism, and clinical response. Many uncomplicated controlled infections require roughly 5-7 days, whereas abscess, bacteremia, thrombophlebitis, or necrotizing infection needs longer specialist-guided treatment.

Example empiric regimens for severe obstetric/pelvic sepsis

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B. Infusion program and hemodynamic support

Immediate measures

• Two large-bore IV lines.
• Insert Foley catheter.
• Monitor BP, heart rate, oxygen saturation, respiratory rate, consciousness, temperature, and hourly urine output.
• Measure initial lactate and repeat serially.
• Keep the woman warm.
• Give oxygen if hypoxemic or in shock.

Fluid resuscitation

• Use balanced crystalloids, such as Ringer’s lactate or another buffered crystalloid, as initial fluid.
• In hypotension or hypoperfusion, a commonly used initial amount is up to 30 mL/kg during the first 3 hours, but give in reassessed boluses in postpartum patients to avoid pulmonary edema.
• Reassess after each bolus:
  • BP/MAP
  • pulse
  • capillary refill
  • lung auscultation and oxygenation
  • urine output
  • lactate
  • bedside ultrasound if available

Targets

• MAP ≥65 mmHg
• Urine output ≥0.5 mL/kg/hour, usually at least 30 mL/hour
• Improving mental state and peripheral perfusion
• Decreasing lactate
• Avoid positive fluid balance and pulmonary edema

Vasopressors

• Start norepinephrine through a central line if possible, but do not delay in life-threatening shock if temporary peripheral infusion is required under strict monitoring.
• Add vasopressin or epinephrine under ICU supervision if shock is refractory.

C. Source control

• Evacuation of infected retained products
• Drainage of abscess/infected hematoma
• Debridement of necrotic tissue
• Repair/debridement of cesarean wound
• Laparotomy and peritoneal lavage for generalized peritonitis
• Hysterectomy if uterine infection is uncontrolled and life-saving removal is required

In obstetric sepsis, treatment must begin before culture results: take cultures rapidly, give broad-spectrum IV antibiotics within one hour, resuscitate with carefully reassessed balanced crystalloid, use norepinephrine for persistent hypotension, and eliminate the source of infection urgently.

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63. Lactational mastitis

English translation

Definition

Pathogenesis

1. Ineffective milk removal or oversupply
2. Milk stasis and ductal narrowing
3. Local inflammation, edema, pain, and impaired milk flow
4. Dysbiosis or bacterial infection in some cases
5. Phlegmon or abscess if untreated or severe

Common organisms

• Methicillin-sensitive Staphylococcus aureus
• MRSA in some regions/settings
• Streptococci
• Less commonly gram-negative organisms

Classification

By stage

1. Lactostasis/milk stasis
2. Serous/inflammatory mastitis
3. Infiltrative mastitis
4. Suppurative mastitis:
   • Abscess
   • Phlegmon
   • Gangrenous mastitis, rare

By location

• Subareolar
• Intramammary
• Retromammary
• Diffuse

Clinical features

Lactostasis

• Breast fullness, tenderness, firmness
• Local lump/engorgement
• No severe systemic symptoms
• Temperature may be mildly elevated but usually settles after effective feeding/milk removal

Mastitis

• Wedge-shaped erythema, warmth, swelling, tenderness
• Fever, usually >38.5°C
• Chills, malaise, myalgia, headache
• Pain during feeding
• Cracked/damaged nipple may be visible
• Axillary lymphadenopathy can occur

Breast abscess

• Persistent fever/pain after 24-48 hours of appropriate treatment
• Fluctuant mass or localized collection
• Marked tenderness
• Ultrasound shows fluid collection

Diagnosis

• Mainly clinical.
• Ultrasound if:
  • abscess is suspected
  • discrete persistent mass exists
  • failure to improve in 24-48 hours
  • recurrent mastitis in the same region
• Milk culture is not routine but should be considered if:
  • severe infection
  • recurrent mastitis
  • hospital-acquired infection
  • no response to first-line antibiotics
  • MRSA is suspected
• CBC/CRP if systemic illness, admission, abscess, or sepsis is suspected.

Treatment

A. Lactostasis or mild inflammatory mastitis

Continue physiological milk removal

• Continue direct breastfeeding from both breasts.
• Begin feeding on the affected breast if tolerable, because effective feeding improves drainage.
• Ensure correct latch and positioning with lactation support.
• Feed responsively. Avoid forced excessive pumping because this may worsen oversupply and inflammation.
• If the infant cannot feed effectively, express only enough milk for comfort and to maintain supply.

Symptomatic treatment

• Ibuprofen, if no contraindication, because it treats pain and inflammation.
• Paracetamol for pain/fever.
• Cold packs after feeds for edema and pain.
• Rest, hydration, adequate nutrition.
• Avoid deep painful breast massage, vigorous squeezing, and prolonged heat, because these can worsen tissue edema and trauma.

B. Bacterial mastitis

• Fever/systemic illness is significant
• Symptoms persist or worsen after 12-24 hours of optimal milk removal and anti-inflammatory treatment
• There is clear cellulitis
• Infection is severe or woman is immunocompromised

Common oral regimens

• Dicloxacillin or flucloxacillin 500 mg orally every 6 hours, usually for 10-14 days
• Cephalexin 500 mg orally every 6 hours, usually for 10-14 days

• Clindamycin 300 mg orally every 6-8 hours
• Trimethoprim-sulfamethoxazole may be considered in appropriate settings, but avoid or seek specialist advice if the infant is premature, jaundiced, has G6PD deficiency, or is very young.

Severe mastitis requiring admission

• IV anti-staphylococcal therapy, such as flucloxacillin/cefazolin depending on local policy.
• Add MRSA coverage, such as vancomycin, if risk is high or culture confirms MRSA.
• IV fluids if dehydrated and sepsis assessment if hypotensive/tachycardic/confused.

C. Breast abscess

• Confirm by ultrasound.
• Drainage is essential.
• Ultrasound-guided needle aspiration, often repeated, is preferred when feasible.
• Catheter drainage may be needed for larger collections.
• Surgical incision and drainage is used if the abscess is large, multiloculated, recurrent, skin is compromised, or aspiration fails.
• Send aspirated pus for culture/sensitivity.
• Continue targeted antibiotics.
• Breastfeeding can usually continue, including from the affected breast, provided the infant’s mouth does not contact purulent drainage or an open wound.

Breastfeeding decision

Breastfeeding should usually continue

• Lactostasis
• Uncomplicated mastitis
• Mastitis treated with antibiotics compatible with breastfeeding
• Drained abscess, if the infant does not contact pus or the drain/wound directly

Temporary interruption of direct feeding may be needed

• Direct contact between infant mouth and open infected wound/purulent drainage cannot be avoided
• Maternal medications are incompatible with breastfeeding
• Mother is critically ill and unable to feed safely

Indications for lactation suppression

• Intrauterine fetal death or neonatal death and woman requests/needs suppression
• Contraindication to breastfeeding because of a medication or maternal condition
• HIV where safe replacement feeding is acceptable and recommended by national policy
• Severe maternal disease preventing breastfeeding
• Breastfeeding must be permanently avoided for another medical reason

Prevention

• Antenatal breastfeeding education
• Correct attachment and positioning from the first feed
• Avoid long intervals between feeds
• Avoid nipple trauma and treat cracks promptly
• Avoid tight bras and pressure on the breast
• Hand hygiene
• Avoid abrupt weaning
• Prompt lactation consultation for oversupply, poor infant latch, nipple pain, or recurrent blocked ducts
• Treat maternal anemia, diabetes, and other immune-risk conditions

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64. Rh isoimmunization between mother and fetus

English translation

Definition

Etiopathogenesis

Basic mechanism

1. Mother is RhD-negative.
2. Fetus inherits RhD-positive blood from the father.
3. Fetal red cells enter maternal circulation.
4. Mother forms anti-D antibodies.
5. In a later RhD-positive pregnancy, maternal anti-D IgG crosses placenta.
6. Fetal hemolysis leads to anemia.
7. Severe anemia causes high-output cardiac failure, hydrops fetalis, stillbirth, or severe neonatal jaundice/kernicterus.

Routes of sensitization

• Delivery, especially manual placental removal or cesarean birth
• Miscarriage, ectopic pregnancy, abortion
• Antepartum hemorrhage
• Placental abruption
• Abdominal trauma
• External cephalic version
• Amniocentesis, chorionic villus sampling, cordocentesis
• Intrauterine fetal procedures
• Stillbirth
• Transfusion of RhD-positive blood to an RhD-negative woman
• Occasionally, spontaneous small fetomaternal hemorrhages during normal pregnancy

Risk assessment at booking

• Determine maternal ABO and RhD group.
• Perform an antibody screen, often called an indirect antiglobulin test.
• If RhD-negative and no anti-D antibody is present: she is unsensitized and eligible for prophylaxis.
• If anti-D or another clinically significant red-cell antibody is present: she is already sensitized and anti-D prophylaxis will not treat established alloimmunization.

Prevention

A. Routine antenatal anti-D prophylaxis

• A single 300 microgram dose at about 28 weeks, or
• Two smaller doses at around 28 and 34 weeks.

B. Anti-D after sensitizing events

• Vaginal bleeding
• Miscarriage/abortion
• Ectopic pregnancy
• Amniocentesis/CVS
• Abdominal trauma
• External cephalic version
• Fetal reduction
• Stillbirth
• Delivery of an RhD-positive infant

C. Postpartum prophylaxis

• Test cord blood for newborn RhD status.
• If the infant is RhD-positive, give anti-D immunoglobulin to the unsensitized RhD-negative mother within 72 hours postpartum.
• Quantify fetomaternal hemorrhage after birth if indicated and give additional doses if the bleed exceeds the protection of the standard dose.

Management of a sensitized pregnancy

Step 1. Confirm antibody type and level

• Identify the antibody and serially measure titer/quantitation.
• Anti-D, anti-c, and anti-Kell are particularly important.
• Remember: anti-Kell can suppress fetal erythropoiesis, so even a low titer may be clinically significant.

Step 2. Determine fetal risk

• Test paternal RhD genotype/zygosity where appropriate.
• Use noninvasive fetal RhD genotyping from maternal blood where available.
• If fetus is RhD-negative, it is not at risk from anti-D antibodies.
• If fetal antigen status is positive or unknown, continue fetal surveillance.

Step 3. Fetal surveillance

• Middle cerebral artery peak systolic velocity (MCA-PSV) Doppler.

• Serial ultrasound for hydrops:
  • Skin edema
  • Ascites
  • Pleural/pericardial effusion
  • Placental thickening
  • Polyhydramnios
• Fetal growth and wellbeing assessment
• CTG later in pregnancy, as appropriate

Step 4. Intrauterine transfusion

• Evidence of significant fetal anemia, commonly MCA-PSV >1.5 MoM
• Hydrops fetalis
• Confirmed severe anemia by fetal blood sampling

• Cordocentesis with transfusion of appropriately prepared antigen-negative, irradiated, leukocyte-reduced packed red cells into the umbilical vein.
• This is performed only in a specialized fetal medicine center.
• Repeat transfusions may be required until fetal maturity.

Step 5. Timing and mode of delivery

• Plan delivery in a tertiary center with neonatal intensive care and blood-bank support.
• Timing depends on fetal anemia, number/timing of intrauterine transfusions, fetal wellbeing, and gestational age.
• Vaginal delivery is possible if there is no obstetric contraindication and fetal condition is reassuring.
• Deliver earlier if hydrops, worsening anemia, fetal compromise, or inability to safely continue intrauterine management.

Neonatal management

• Cord blood group/Rh type
• Direct antiglobulin test, hemoglobin, bilirubin
• Monitor bilirubin and anemia closely
• Phototherapy for hyperbilirubinemia
• IV immunoglobulin in selected cases under neonatal guidance
• Exchange transfusion if severe hyperbilirubinemia or rapidly rising bilirubin
• Top-up transfusion for significant anemia
• Monitor for late anemia after discharge

Complications

Fetal

• Progressive anemia
• Cardiomegaly and heart failure
• Hydrops fetalis
• Intrauterine death

Neonatal

• Severe jaundice
• Kernicterus
• Anemia
• Hepatosplenomegaly
• Heart failure
• Death

Prevention of Rh disease depends on identifying unsensitized RhD-negative mothers, routine antenatal anti-D prophylaxis, anti-D after sensitizing events and after delivery of an RhD-positive infant. In sensitized pregnancies, fetal anemia is monitored mainly by MCA-PSV Doppler, and severe anemia is treated by intrauterine transfusion in a specialist center.

Gynecology Questions 1-8

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1. Endometrial cancer

English translation

Definition

Classification

A. Histological types

1. Endometrioid carcinoma

• Most common type.
• Usually estrogen-dependent.
• Often develops from endometrial hyperplasia with atypia.
• Often associated with obesity, anovulation, diabetes, hypertension, and unopposed estrogen.
• Usually lower grade and relatively favorable prognosis.

2. Non-endometrioid high-grade carcinoma

• Serous carcinoma
• Clear-cell carcinoma
• Carcinosarcoma
• Undifferentiated carcinoma
• Mixed carcinoma

B. Molecular classification

• POLE-mutated
• Mismatch-repair deficient
• p53-abnormal
• No specific molecular profile

Risk factors

Risk factors related to prolonged unopposed estrogen

• Obesity, because adipose tissue converts androgens to estrogens
• Chronic anovulation and polycystic ovary syndrome
• Nulliparity and infertility
• Early menarche and late menopause
• Estrogen-only hormone therapy in a woman with a uterus
• Estrogen-producing ovarian tumors, for example granulosa cell tumor
• Tamoxifen use

Other risk factors

• Increasing age, especially postmenopausal age
• Diabetes mellitus
• Hypertension
• Family history of endometrial or colorectal cancer
• Lynch syndrome
• Previous endometrial hyperplasia with atypia

Protective factors

• Combined oral contraceptives
• Pregnancy and breastfeeding
• Physical activity and normal body weight
• Progestin exposure, including levonorgestrel intrauterine system in appropriate women

Clinical features

Main symptom

Postmenopausal bleeding is endometrial cancer until proven otherwise.

• Postmenopausal vaginal bleeding, spotting, or watery/blood-stained discharge
• Abnormal uterine bleeding in perimenopausal women
• Intermenstrual bleeding
• Heavy irregular bleeding in women with risk factors
• Watery, offensive, or serosanguineous discharge, sometimes called “meat-wash” discharge
• Pelvic pain, pressure, pyometra, weight loss, anemia, or enlarged uterus in advanced disease

Diagnosis

1. History and examination

• Bleeding pattern and duration
• Menopausal status
• Obesity, diabetes, hypertension, PCOS
• Tamoxifen or hormone therapy
• Family history of Lynch syndrome-associated cancers
• Prior endometrial hyperplasia

• General examination, BMI, lymph nodes
• Speculum examination to exclude cervical/vaginal bleeding
• Bimanual examination for uterine size, mobility, parametrial involvement, adnexal mass

2. Transvaginal ultrasound

• Assess endometrial thickness, regularity, focal lesion, uterine cavity fluid, myometrium, and adnexa.
• In a woman with postmenopausal bleeding, an endometrial thickness of 4 mm or less makes endometrial carcinoma less likely.
• Thickened, heterogeneous, irregular endometrium or intracavitary mass requires tissue diagnosis.

3. Endometrial sampling

• Office endometrial biopsy using a Pipelle device
• Hysteroscopy-directed biopsy
• Fractional diagnostic curettage where indicated

4. Histological confirmation

5. Staging evaluation

• Pelvic MRI: best for depth of myometrial invasion and cervical stromal involvement.
• CT chest/abdomen/pelvis: assess nodal or distant disease in high-risk/advanced cancer.
• Chest imaging, CBC, renal and liver tests.
• Molecular testing, especially mismatch repair status and p53 status where available.

FIGO staging: simplified

Treatment

A. Primary treatment: surgery

Total hysterectomy + bilateral salpingo-oophorectomy + surgical staging.

• Sentinel lymph-node mapping and biopsy
• Pelvic ± para-aortic lymph-node assessment in selected high-risk disease
• Peritoneal washings in some protocols
• Omental assessment/biopsy in serous carcinoma or other high-risk histology

B. Adjuvant treatment

Low-risk stage I disease

• Surgery alone is often sufficient.

Intermediate/high-intermediate risk

• Vaginal brachytherapy may reduce vaginal recurrence.
• Some patients require external beam pelvic radiotherapy.

High-risk disease, stage III, or aggressive histology

• Chemotherapy, usually carboplatin plus paclitaxel.
• Radiotherapy may be added, either before, after, or in combination with chemotherapy according to multidisciplinary planning.

Advanced or recurrent disease

• Cytoreductive surgery if complete/near-complete resection is feasible.
• Systemic chemotherapy.
• Immunotherapy in selected mismatch-repair deficient tumors.
• Hormonal treatment for low-grade, hormone receptor-positive endometrioid tumors, especially indolent recurrence:
  • Progestins
  • Aromatase inhibitor in selected cases
  • Other endocrine approaches under oncology care
• Palliative radiotherapy for bleeding, pain, or local recurrence.

C. Fertility-sparing treatment

• Grade 1 endometrioid carcinoma
• Disease confined to the endometrium
• No myometrial invasion on imaging
• No metastatic disease
• Strong wish to preserve fertility
• Ability to comply with strict surveillance

• High-dose oral progestin
• Levonorgestrel intrauterine system, sometimes combined with oral therapy

Prognosis

• FIGO stage
• Histological type
• Tumor grade
• Depth of myometrial invasion
• Lymphovascular space invasion
• Lymph-node involvement
• Molecular subtype
• Patient age and comorbidities

The cardinal symptom of endometrial carcinoma is postmenopausal bleeding. Diagnosis requires endometrial histology. Standard treatment is total hysterectomy with bilateral salpingo-oophorectomy and appropriate staging, followed by risk-adapted radiotherapy and/or chemotherapy.

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2. Topographic anatomy of the female genital organs

English translation

Division of female genital organs

External genitalia

• Mons pubis
• Labia majora
• Labia minora
• Clitoris
• Vestibule of vagina
• External urethral opening
• Openings of Bartholin glands
• Perineum

Internal genital organs

• Vagina
• Uterus
• Fallopian tubes
• Ovaries

Supporting structures

• Pelvic floor muscles
• Endopelvic fascia
• Uterosacral ligaments
• Cardinal or transverse cervical ligaments
• Pubocervical fascia
• Round ligaments
• Broad ligaments

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Vagina

Position and relations

• Anterior wall: related to urethra and urinary bladder
• Posterior wall:
  • Upper vagina: rectouterine pouch, also called pouch of Douglas
  • Lower vagina: rectum
• Lateral walls: levator ani muscles and pelvic fascia

• Anterior vaginal fornix
• Posterior fornix
• Two lateral fornices

Blood supply

• Vaginal artery, a branch of internal iliac artery
• Contributions from uterine, internal pudendal, and middle rectal arteries

Lymphatic drainage

• Upper vagina: internal and external iliac lymph nodes
• Lower vagina/vulva: superficial inguinal lymph nodes

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Uterus

Normal position

• Anteverted: uterine body tilted forward relative to vagina
• Anteflexed: uterine body bent forward relative to cervix

• Urinary bladder anteriorly
• Rectum posteriorly

Parts of the uterus

1. Fundus
2. Body
3. Isthmus
4. Cervix

Relations

• Anterior surface: bladder and vesicouterine pouch
• Posterior surface: rectouterine pouch, loops of bowel, rectum
• Lateral borders: broad ligaments, uterine vessels, ureters

Important surgical relation

The ureter passes below the uterine artery, approximately 1-2 cm lateral to the cervix.

“Water passes under the bridge.”

• Water = ureter
• Bridge = uterine artery

Blood supply

• Main supply: uterine artery, a branch of internal iliac artery
• Anastomoses with ovarian artery
• Venous drainage: uterine venous plexus to internal iliac veins

Lymphatic drainage

• Fundus: along ovarian vessels to para-aortic nodes
• Cornua: along round ligament to superficial inguinal nodes
• Body: external iliac nodes
• Cervix: internal iliac, external iliac, obturator, and sacral nodes

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Fallopian tubes

Anatomy

1. Interstitial/intramural part
2. Isthmus
3. Ampulla
4. Infundibulum with fimbriae

Clinical importance

• Ampulla is the most common site of fertilization.
• Ampulla is also the most common site of ectopic tubal pregnancy.
• The fimbriae collect the ovulated oocyte from the ovarian surface.

Blood supply

• Tubal branches of uterine and ovarian arteries

Lymphatic drainage

• Mainly para-aortic and pelvic lymph nodes.

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Ovaries

Position

• Anterior: external iliac vessels
• Posterior: ureter and internal iliac vessels
• Floor: obturator nerve and vessels

Attachments

1. Mesovarium: attaches ovary to broad ligament.
2. Ovarian ligament: connects ovary to uterus.
3. Suspensory ligament of ovary, also called infundibulopelvic ligament:
   • Connects ovary to lateral pelvic wall.
   • Contains ovarian artery, vein, lymphatics, and nerves.

Blood supply

• Ovarian artery from abdominal aorta
• Anastomosis with uterine artery

Lymphatic drainage

• Along ovarian vessels to para-aortic lymph nodes.

Surgical importance

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Broad ligament

• Mesometrium: adjacent to uterus
• Mesosalpinx: adjacent to fallopian tube
• Mesovarium: adjacent to ovary

• Uterine tube
• Round ligament
• Ovarian ligament
• Uterine and ovarian vessels
• Lymphatics and nerves
• Mesonephric remnants

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Uterine support apparatus

Active support

• Levator ani muscles, especially pubococcygeus
• Perineal body
• Urogenital diaphragm

Passive support

• Cardinal ligaments
• Uterosacral ligaments
• Pubocervical fascia
• Round ligaments, which help maintain anteversion
• Broad ligaments, limited supporting function

The most important topographic relation in gynecologic surgery is that the ureter runs beneath the uterine artery near the cervix. The ovaries drain to para-aortic lymph nodes, whereas the cervix drains mainly to pelvic lymph nodes.

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3. Prevention of HIV infection in obstetric and gynecologic practice

English translation

Routes of HIV transmission

• Unprotected vaginal or anal sexual intercourse
• Blood exposure, contaminated needles, sharps injuries
• Vertical transmission from mother to child:
  • During pregnancy
  • During labor and delivery
  • Through breastfeeding

Main principles of prevention

1. Prevent HIV acquisition in women and their partners.
2. Diagnose infection early.
3. Treat all HIV-positive women with effective antiretroviral therapy.
4. Achieve and maintain undetectable viral load.
5. Prevent vertical transmission.
6. Protect health-care workers using standard precautions.
7. Prevent and treat sexually transmitted infections.

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A. Primary prevention in gynecology

Sexual prevention

• Sexual education and safer-sex counseling
• Correct and consistent use of male or female condoms
• Reduction of multiple/concurrent sexual partners
• Prompt diagnosis and treatment of STIs
• Partner notification and testing
• Screening for sexual violence and provision of post-exposure care

HIV testing

• At first gynecologic or antenatal contact
• During pregnancy
• In women with STIs, tuberculosis, hepatitis, substance use, sexual violence, or high-risk exposure
• To sexual partners of HIV-positive individuals
• Repeatedly during pregnancy if ongoing risk exists

Pre-exposure prophylaxis, PrEP

Post-exposure prophylaxis, PEP

• Start PEP as soon as possible, ideally within hours.
• It should not be started later than 72 hours after exposure.
• Continue for 28 days.
• Test for HIV, hepatitis B/C, pregnancy, and other STIs.
• Arrange follow-up HIV testing and psychological support.

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B. Prevention of mother-to-child transmission

Antenatal period

1. Offer HIV testing early in pregnancy.
2. Start or continue combination antiretroviral therapy immediately in every pregnant woman with HIV, regardless of CD4 count or clinical stage.
3. Monitor viral load regularly.
4. Screen and treat coinfections:
   • Syphilis
   • Hepatitis B and C
   • Tuberculosis
   • STIs
5. Counsel about adherence and avoidance of breastfeeding decisions that do not follow local recommendations.

Intrapartum period

• Continue maternal ART.
• Avoid procedures that increase fetal exposure to maternal blood where possible:
  • Avoid fetal scalp electrode
  • Avoid fetal scalp blood sampling
  • Avoid artificial rupture of membranes unless necessary
  • Avoid prolonged rupture of membranes
  • Avoid routine episiotomy and traumatic instrumental delivery when avoidable

Delivery route

• If maternal viral load is suppressed near delivery, vaginal birth is generally appropriate.
• Planned cesarean delivery may reduce transmission when viral load is high or unknown near term, according to national HIV guideline.
• Delivery planning must be individualized by HIV and obstetric teams.

Neonatal prophylaxis

• Begin antiretroviral prophylaxis for the newborn as soon as possible after birth.
• Regimen intensity depends on maternal viral load, treatment history, and transmission risk.
• Higher-risk infants may need multi-drug prophylaxis.
• Test the infant using virological testing according to pediatric HIV protocol.

Infant feeding

• Where safe replacement feeding is feasible, affordable, sustainable, and safe, formula feeding may be recommended.
• In settings where breastfeeding is recommended for women living with HIV, maternal ART and adherence are essential, and exclusive breastfeeding for the recommended period is preferred over mixed feeding.

C. Prevention in health-care workers

Standard precautions

• Hand hygiene
• Gloves for exposure to blood/body fluids
• Mask, eye protection, gown for anticipated splashes
• Sterile single-use needles and syringes
• Safe disposal of sharps
• Never recap needles manually
• Safe surgical technique and proper instrument handling
• Adequate sterilization/disinfection of instruments

Management of occupational exposure

1. Wash skin with soap and water immediately.
2. Flush mucous membranes with water.
3. Do not squeeze a needlestick wound aggressively.
4. Report the exposure urgently.
5. Assess source-patient HIV risk.
6. Start PEP immediately if indicated, without waiting for test results.
7. Complete a 28-day regimen and follow-up testing.

D. Special gynecological issues in women living with HIV

• Higher incidence and persistence of HPV infection
• Higher risk of cervical intraepithelial neoplasia and cervical cancer
• More frequent vulvovaginal candidiasis and STIs
• Need for regular cervical screening and prompt treatment of precancerous lesions

Prevention of perinatal HIV transmission is based on universal testing, maternal combination ART with viral suppression, safe obstetric practice, appropriate delivery planning, neonatal prophylaxis, and feeding advice according to national policy.

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4. Posthysterectomy syndrome

English translation

Definition

Types

1. After hysterectomy with bilateral oophorectomy

2. After hysterectomy with ovarian conservation

3. After subtotal hysterectomy

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Clinical manifestations

A. Vasomotor/endocrine symptoms

• Hot flushes
• Night sweats
• Palpitations
• Sleep disturbance
• Fatigue
• Vaginal dryness
• Reduced libido
• Dyspareunia
• Osteoporosis risk in premature estrogen deficiency

B. Psychological symptoms

• Anxiety
• Depressive symptoms
• Irritability
• Reduced self-esteem
• Fear about sexual function or femininity
• Grief concerning infertility or loss of reproductive function

C. Genitourinary symptoms

• Vaginal dryness and recurrent irritation
• Dyspareunia
• Urinary urgency/frequency
• Stress urinary incontinence
• Recurrent urinary tract infections
• Pelvic organ prolapse, particularly in women with pre-existing support defects

D. Pelvic symptoms

• Chronic pelvic pain
• Adhesive disease
• Vaginal cuff pain/granulation tissue
• Persistent endometriosis if ovaries were retained
• Pelvic floor muscle spasm

E. Sexual problems

• Reduced desire or arousal
• Dyspareunia
• Fear of intercourse
• Altered body image
• Vaginal shortening or reduced elasticity, especially after radical surgery

Diagnosis

Clinical approach

• Type and reason for hysterectomy
• Were ovaries and cervix removed?
• Timing of symptoms in relation to surgery
• Menopausal symptoms
• Pelvic pain, bleeding, discharge, dyspareunia
• Urinary/bowel symptoms
• Mood, sleep, sexual function
• Past endometriosis, fibroids, cancer, prolapse, or pelvic inflammatory disease

Examination

• General examination, BP, BMI
• Abdominal scar and tenderness
• Speculum examination:
  • vaginal cuff healing
  • granulation tissue
  • discharge, infection, bleeding, dehiscence
• Bimanual examination:
  • pelvic mass
  • tenderness
  • adhesions
  • pelvic-floor dysfunction/prolapse

Investigations as indicated

• CBC, CRP, urinalysis/culture if infection suspected
• FSH/estradiol only if menopausal status is unclear in a younger woman
• Pelvic ultrasound for pelvic mass, retained ovary pathology, hematoma, or fluid collection
• MRI/CT for complex pelvic pain or suspected malignancy
• Cystoscopy/urology referral for persistent urinary symptoms
• Bone-density assessment in premature surgical menopause or high fracture risk
• Psychological/psychiatric assessment for major depression or significant sexual dysfunction

Treatment

A. Treat the identified cause

B. Menopausal hormone therapy

• Systemic estrogen therapy is usually indicated until the average age of natural menopause.
• Because the uterus is absent, estrogen-only therapy is usually sufficient.
• However, if severe endometriosis was present, a progestogen may be considered with estrogen under specialist advice because residual disease could be stimulated.

• Estrogen-sensitive malignancy
• Active/history of venous thromboembolism in some situations
• Severe liver disease
• Unexplained vaginal bleeding
• Selected cardiovascular risks

C. Genitourinary syndrome of menopause

• Vaginal moisturizers and lubricants
• Local vaginal estrogen if not contraindicated
• Pelvic-floor physiotherapy
• Treatment of recurrent UTI or vulvovaginal conditions as indicated

D. Pelvic pain

• Exclude infection, endometriosis recurrence, ovarian cyst, adhesions, and malignancy.
• NSAIDs or other analgesia as appropriate
• Pelvic-floor physiotherapy
• Hormonal suppression if residual endometriosis is suspected and ovaries are present
• Laparoscopy only for selected persistent cases when diagnosis/treatment is likely to change management

E. Vaginal cuff complications

• Granulation tissue: may be treated with silver nitrate application in clinic.
• Cuff infection: antibiotics, drainage if abscess.
• Cuff dehiscence/evisceration: surgical emergency requiring immediate assessment, broad-spectrum antibiotics, and repair.

F. Psychological and sexual support

• Clear preoperative and postoperative counseling
• Cognitive behavioral therapy or psychotherapy where indicated
• Couple/sexual counseling
• Treatment of depression/anxiety when diagnosed

Prevention

• Correct indication for hysterectomy
• Preoperative counseling about fertility, ovarian conservation, sexual function, menopause, and complications
• Ovarian conservation in premenopausal women when oncologically safe
• Meticulous surgery to protect nerves, ureter, bladder, and pelvic support
• Early mobilization, DVT prophylaxis, infection prevention
• Postoperative pelvic-floor rehabilitation and mental-health support

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5. Colposcopy: simple and extended

English translation

Definition

Indications

• Positive high-risk HPV test with abnormal triage result
• Abnormal cervical cytology, such as ASC-H, HSIL, AGC, or persistent abnormal results
• Visible suspicious cervical lesion
• Persistent postcoital bleeding when cervical pathology is suspected
• Unexplained abnormal bleeding with suspicious cervix
• Follow-up after treatment of CIN
• Suspected vaginal/vulvar intraepithelial lesion
• Women living with HIV who have abnormal cervical screening results

Contraindications

• Heavy active bleeding, which prevents visualization
• Severe acute cervicitis/vaginitis, treat first when possible
• Inability to tolerate speculum examination
• Pregnancy is not a contraindication, but endocervical curettage is contraindicated in pregnancy.

Simple colposcopy

Meaning

Technique

1. Explain procedure and obtain consent.
2. Confirm pregnancy status if relevant.
3. Position the woman in lithotomy position.
4. Insert an appropriate sterile speculum without lubricant or using minimal water-based lubricant.
5. Inspect vagina and cervix with naked eye.
6. Remove mucus/blood gently using saline-soaked swabs.
7. Examine cervix under low and then higher magnification.
8. Identify:
   • Squamocolumnar junction
   • Transformation zone
   • Ectropion
   • Polyps
   • Leukoplakia
   • Ulceration
   • Exophytic growth
   • Abnormal vessels
9. Document findings with a diagram, lesion size, location by clock face, transformation-zone type, and adequacy of examination.

Extended colposcopy

Meaning

Step 1: 3-5% acetic acid test

• Apply 3-5% acetic acid to cervix.
• Wait about 1 minute.
• Acetic acid causes abnormal cells with increased nuclear protein to appear white, called acetowhitening.

• Onset and intensity of acetowhitening
• Borders of lesion
• Surface contour
• Punctation
• Mosaic pattern
• Atypical vessels
• Lesion location and size

Colposcopic interpretation

• Thin acetowhite epithelium
• Indistinct borders
• Fine punctation or fine mosaic
• Often associated with CIN 1/low-grade squamous intraepithelial lesion

• Dense, opaque acetowhite epithelium
• Sharp borders
• Coarse punctation
• Coarse mosaic
• Inner border sign/ridge sign
• More likely CIN 2/3

• Atypical irregular vessels
• Fragile exophytic lesion
• Ulceration or necrosis
• Irregular mass
• Contact bleeding

Step 2: Lugol iodine test, Schiller test

• Apply Lugol iodine.
• Mature glycogen-rich squamous epithelium stains dark brown/black.
• Abnormal, immature, metaplastic, dysplastic, columnar, or atrophic epithelium remains yellow, mustard-colored, or unstained.

Step 3: Directed biopsy

• Biopsy the worst lesion, usually at the most abnormal acetowhite area.
• If lesion is not visible but screening is high risk, endocervical sampling may be indicated in nonpregnant women.
• Send specimen for histopathology.

Complications

• Mild discomfort or vasovagal reaction
• Spotting after biopsy
• Rare infection
• Rare significant bleeding
• Anxiety

Post-biopsy instructions

• Mild spotting/discharge is expected.
• Avoid intercourse, tampons, and vaginal douching for several days according to local advice.
• Seek medical review for heavy bleeding, fever, increasing pelvic pain, or foul discharge.

Extended colposcopy consists of inspection under magnification after 3-5% acetic acid and Lugol iodine. Its main role is to identify the transformation zone, characterize abnormal epithelium, and perform a targeted biopsy of the most suspicious area.

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6. Juvenile abnormal uterine bleeding

English translation

Definition

Etiology

1. Anovulatory dysfunction

• Hypothalamic-pituitary-ovarian axis is immature.
• Ovulation is irregular or absent.
• Progesterone is not produced adequately.
• Estrogen stimulates continuous endometrial proliferation.
• The unstable endometrium breaks down irregularly, causing prolonged heavy bleeding.

2. Pregnancy-related causes

• Miscarriage
• Ectopic pregnancy
• Pregnancy complications

3. Coagulopathies

• von Willebrand disease
• Platelet function disorders
• Thrombocytopenia
• Leukemia

• Heavy bleeding starts at menarche
• Easy bruising, epistaxis, gum bleeding
• Family history of bleeding
• Excessive bleeding after dental extraction or surgery

4. Endocrine disorders

• Thyroid disease
• Hyperprolactinemia
• PCOS
• Obesity and insulin resistance
• Severe weight loss/eating disorder
• Chronic systemic disease

5. Structural causes

• Endometrial polyp
• Fibroid
• Infection
• Rare genital tract malignancy

Clinical features

• Irregular menstrual cycles
• Delayed periods followed by prolonged heavy bleeding
• Bleeding lasting more than 7 days
• Passage of clots
• Soaking pads very frequently
• Fatigue, dizziness, palpitations, syncope
• Iron-deficiency anemia
• Severe bleeding may cause hemodynamic instability

Assessment of severity

Mild

• No significant anemia
• Hemodynamically stable
• Minimal effect on daily activity

Moderate

• Prolonged/heavy bleeding
• Mild to moderate anemia
• Weakness, tachycardia may be present

Severe

• Active heavy bleeding
• Hemodynamic instability, syncope, hypotension
• Severe anemia
• Need for hospital admission and urgent treatment

Diagnosis

History

• Age at menarche and menstrual pattern
• Amount/duration of bleeding
• Pregnancy possibility and sexual history confidentially
• Medication, including anticoagulants
• Symptoms of anemia
• Bleeding tendency/family history
• Weight change, acne/hirsutism, thyroid symptoms
• Chronic illness, eating disorder, stress

Examination

• Assess hemodynamic stability: pulse, BP, orthostatic signs, pallor
• BMI, signs of androgen excess or thyroid disease
• Abdominal examination for mass
• External genital examination only if indicated
• Speculum/bimanual examination is usually not required in a non-sexually active adolescent unless severe bleeding, trauma, foreign body, infection, or mass is suspected

Investigations

• Pregnancy test: mandatory in postmenarchal adolescent with bleeding
• CBC, ferritin
• Blood group and crossmatch if bleeding severe
• PT/INR, aPTT, fibrinogen
• von Willebrand testing if history suggests coagulopathy
• TSH if thyroid symptoms or unexplained bleeding
• Prolactin/androgen profile when PCOS/endocrine cause is suspected
• Pelvic ultrasound if structural lesion, pelvic mass, pain, or failure to respond to therapy
• STI testing if sexually active and indicated

Treatment

A. First step: stabilize the patient

1. Admit to hospital.
2. Monitor pulse, BP, oxygen saturation, and urine output.
3. IV access.
4. CBC, crossmatch, coagulation tests.
5. IV crystalloid if unstable.
6. Transfuse packed red cells if hemodynamic instability, severe symptomatic anemia, or ongoing major hemorrhage.
7. Consult gynecology, hematology, and pediatrics/adolescent medicine if needed.

B. Hormonal hemostasis

High-dose combined oral contraceptive

• One tablet every 6-8 hours until bleeding substantially decreases, then
• Gradual taper to daily dosing

High-dose progestin

• Medroxyprogesterone acetate, for example 10-20 mg orally every 6-8 hours initially, or
• Norethisterone, according to local protocol

Intravenous estrogen

C. Nonhormonal treatment

Tranexamic acid

• Common oral regimen: 1 g three times daily during heavy bleeding, adjusted to local guidance.
• Avoid in active thromboembolism and use carefully with significant thrombotic risk.

NSAIDs

• Ibuprofen, naproxen, or mefenamic acid can reduce menstrual blood loss and pain.
• Avoid if a platelet dysfunction, significant renal impairment, peptic ulcer disease, or certain bleeding disorders are present.

Iron therapy

• Oral elemental iron, commonly 40-65 mg once daily or on alternate days, depending on tolerance and protocol.
• IV iron when severe deficiency, malabsorption, intolerance, or need for rapid repletion.
• Continue until hemoglobin normalizes and iron stores are replenished.

D. Procedural treatment

• Hemorrhage is uncontrolled despite medical treatment
• Retained products of conception are suspected
• Structural lesion is suspected
• Severe bleeding creates an immediate life-threatening emergency

Prevention

• Menstrual education and early medical consultation for heavy bleeding
• Treat iron deficiency
• Identify bleeding disorders early
• Treat PCOS, obesity, thyroid disease, and eating disorders
• Regular follow-up after an acute episode
• Use cyclic hormonal treatment where recurrent anovulatory bleeding persists

The most common cause of juvenile uterine bleeding is anovulation due to immaturity of the hypothalamic-pituitary-ovarian axis. First exclude pregnancy and coagulopathy, assess hemodynamic stability, stop acute bleeding with hormonal and/or antifibrinolytic therapy, and correct anemia with iron and transfusion when indicated.

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7. Endometriosis

English translation

Definition

• Ovaries: endometriomas
• Pelvic peritoneum
• Uterosacral ligaments
• Pouch of Douglas
• Rectovaginal septum
• Fallopian tubes
• Bladder and ureters
• Bowel
• Surgical scars, umbilicus, rarely distant organs

Classification

By site

1. Peritoneal superficial endometriosis
2. Ovarian endometrioma
3. Deep infiltrating endometriosis
4. Extrapelvic endometriosis

By extent

Pathogenesis

• Retrograde menstruation through fallopian tubes
• Implantation and survival of endometrial cells in pelvis
• Immune dysfunction and chronic inflammation
• Estrogen dependence
• Genetic predisposition
• Coelomic metaplasia
• Lymphatic or hematogenous dissemination, especially for distant lesions

Clinical features

Pain symptoms

• Progressive secondary dysmenorrhea
• Chronic pelvic pain
• Deep dyspareunia
• Dyschezia, painful defecation, cyclical rectal bleeding if bowel involvement
• Dysuria, cyclical hematuria if bladder involvement
• Low back pain

Reproductive symptoms

• Infertility or subfertility
• Recurrent ovarian endometriomas
• Possible impaired tubal transport/adhesions

Other findings

• Tender nodules in uterosacral ligaments
• Fixed retroverted uterus
• Adnexal mass
• Painful pelvic examination
• Cyclical scar pain/swelling after cesarean or other pelvic surgery

Diagnosis

Clinical suspicion

• Severe dysmenorrhea not responding to simple therapy
• Chronic pelvic pain
• Deep dyspareunia
• Infertility
• Cyclical bowel or urinary symptoms

Pelvic examination

• Fixed retroverted uterus
• Tenderness in posterior fornix
• Uterosacral ligament nodularity
• Adnexal mass
• Reduced uterine mobility

Ultrasound

• Detects ovarian endometriomas
• Can identify some deep infiltrating lesions
• Helps exclude other pathology

• Homogeneous low-level internal echoes, described as “ground-glass” appearance.

MRI

• Deep infiltrating disease
• Bowel, bladder, ureteral, or rectovaginal involvement
• Preoperative mapping

Laparoscopy

Treatment goals

• Relieve pain
• Improve quality of life
• Preserve fertility where desired
• Prevent progression/recurrence where possible
• Treat endometriomas/deep lesions safely
• Avoid unnecessary repeated surgery

A. Non-drug treatment

• Detailed education about chronic disease and recurrence
• Regular physical activity as tolerated
• Sleep and stress management
• Pelvic-floor physiotherapy for pelvic-floor overactivity
• Psychological support, cognitive behavioral therapy where needed
• Multidisciplinary pain management in chronic pain

B. Medical treatment for pain

1. NSAIDs

• Ibuprofen
• Naproxen
• Mefenamic acid

2. Combined hormonal contraceptives

• Combined oral pills
• Vaginal ring
• Transdermal patch

3. Progestins

• Dienogest 2 mg orally daily
• Norethisterone acetate
• Medroxyprogesterone acetate
• Depot medroxyprogesterone acetate
• Levonorgestrel intrauterine system

4. GnRH agonists

• Leuprolide
• Goserelin

• Hot flushes
• Bone-density loss
• Vaginal dryness
• Mood symptoms

5. GnRH antagonists

6. Aromatase inhibitors

Important principle

C. Surgical treatment

Indications

• Persistent severe pain despite adequate medical therapy
• Endometrioma with suspicious features or significant symptoms
• Infertility with anatomic distortion
• Deep endometriosis involving bowel, ureter, or bladder
• Hydronephrosis/ureteric obstruction
• Diagnostic uncertainty or suspicion of malignancy

Procedures

• Laparoscopic excision or ablation of superficial lesions
• Adhesiolysis
• Ovarian cystectomy for endometrioma where indicated
• Excision of deep infiltrating lesions by an experienced multidisciplinary team
• Hysterectomy with or without oophorectomy only for selected women with refractory symptoms who have completed childbearing

Important surgical point

D. Treatment of infertility

• Do not give hormonal suppression solely to improve natural fertility.
• Consider laparoscopic treatment of minimal/mild disease in selected infertile women.
• Refer for assisted reproductive technology when tubal disease, severe endometriosis, reduced ovarian reserve, male factor, or persistent infertility exists.

Rehabilitation and follow-up

• Long-term hormonal suppression after conservative surgery if pregnancy is not immediately desired
• Pelvic-floor physiotherapy
• Pain management
• Fertility counseling and reproductive planning
• Management of sexual dysfunction
• Follow-up for recurrence, endometrioma growth, bowel/urinary symptoms

Prevention

• Early recognition of severe dysmenorrhea
• Avoid delayed diagnosis
• Continuous hormonal suppression in women not trying to conceive, if appropriate
• Avoid unnecessary repeated surgery
• Long-term follow-up for endometrioma and deep disease

Endometriosis should be suspected in women with progressive dysmenorrhea, deep dyspareunia, chronic pelvic pain, and infertility. Ultrasound is first-line imaging; MRI maps deep disease. Treatment is individualized and includes NSAIDs, continuous combined hormonal contraception or progestins, GnRH therapy for refractory pain, and conservative laparoscopy when indicated.

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8. Dysmenorrhea

English translation

Definition

Classification

1. Primary dysmenorrhea

• Begins within 6-12 months after menarche, after ovulatory cycles develop
• Usually occurs in adolescents and young women
• Pain begins just before or at onset of menstruation
• Pain lasts 8-72 hours

2. Secondary dysmenorrhea

• Endometriosis
• Adenomyosis
• Pelvic inflammatory disease
• Uterine fibroids
• Endometrial polyps
• Ovarian cysts
• Cervical stenosis
• Congenital outflow obstruction
• Intrauterine device-related pain in selected cases

Pathogenesis of primary dysmenorrhea

1. Endometrial breakdown causes increased prostaglandin production, especially prostaglandin F2-alpha.
2. Prostaglandins cause strong uterine contractions and vasoconstriction.
3. Uterine ischemia occurs.
4. Ischemia and contractions cause cramp-like pain.

• Nausea
• Vomiting
• Diarrhea
• Headache
• Dizziness
• Sweating

Clinical features

Primary dysmenorrhea

• Cramping colicky suprapubic pain
• Pain radiating to lower back and medial thighs
• Starts shortly before or at onset of menses
• Maximum in first 24 hours
• Improves within 2-3 days
• Associated nausea, diarrhea, fatigue, headache, dizziness
• Normal pelvic examination

Secondary dysmenorrhea

• Pain begins years after menarche
• Progressive worsening of pain
• Pain begins well before menses and continues after bleeding
• Dyspareunia
• Infertility
• Heavy menstrual bleeding or irregular bleeding
• Pelvic mass
• Abnormal pelvic examination
• Poor response to NSAIDs/combined hormonal contraceptives

Diagnosis

History

• Age at onset
• Timing/duration/severity of pain
• Relation to bleeding
• Cycle regularity and bleeding amount
• Dyspareunia, bowel/urinary symptoms
• Pregnancy possibility
• STI risk
• Family history of endometriosis
• Previous operations or IUD use
• Response to previous treatment

Examination

• General and abdominal examination
• Pelvic examination if sexually active, if symptoms are severe, or if secondary cause is suspected
• In adolescents with classic primary dysmenorrhea and no red flags, pelvic examination may be deferred

Investigations

• Pregnancy test
• STI testing where indicated
• Transvaginal/pelvic ultrasound
• MRI for suspected adenomyosis or deep endometriosis
• Diagnostic laparoscopy if pain persists despite adequate empirical treatment and endometriosis/other pathology is suspected

Treatment

A. Primary dysmenorrhea

1. NSAIDs: first-line therapy

• Ibuprofen 400 mg orally every 6-8 hours with food
• Naproxen 500 mg initially, then 250 mg every 6-8 hours or 500 mg twice daily, depending on formulation/local protocol
• Mefenamic acid 500 mg initially, then 250-500 mg every 6-8 hours

• Start 1 day before anticipated menstruation, or at the first sign of pain/bleeding.
• Continue regularly for the first 2-3 days of menstruation.

• Peptic ulcer disease
• Significant renal disease
• NSAID allergy/asthma sensitive to NSAIDs
• Anticoagulant use
• Certain bleeding disorders

2. Hormonal contraception: first-line or second-line

• Combined oral contraceptive
• Vaginal ring
• Transdermal patch
• Progestin-only pill
• Depot medroxyprogesterone acetate
• Levonorgestrel intrauterine system

3. Non-pharmacological measures

• Local heat pad
• Regular aerobic exercise
• Adequate sleep
• Smoking cessation
• Psychological stress reduction
• TENS may help selected patients
• Nutrition/alternative treatments have variable evidence and should not replace proven therapy

B. Secondary dysmenorrhea

• Endometriosis: hormonal suppression and/or surgery
• Adenomyosis: levonorgestrel IUS, hormonal therapy, or surgery in selected women
• PID: antibiotics according to STI/PID regimen
• Fibroids: medical therapy, myomectomy, embolization, or hysterectomy depending on age and fertility wishes
• Cervical stenosis: cervical dilatation where appropriate
• Obstructive congenital anomaly: corrective surgery

When to refer urgently

• Sudden severe unilateral pelvic pain: consider torsion or ectopic pregnancy
• Fever, purulent discharge, cervical motion tenderness: consider PID
• Positive pregnancy test with pain/bleeding: exclude ectopic pregnancy
• Severe anemia or hemodynamic instability
• Pelvic mass
• New severe pain in a woman after menopause

Primary dysmenorrhea is due to excess endometrial prostaglandins causing uterine hypercontractility and ischemia. NSAIDs are first-line therapy, ideally started before or at menstrual onset. Hormonal contraception is used when NSAIDs fail or contraception is needed. Secondary dysmenorrhea requires investigation and treatment of its cause, especially endometriosis.

Gynecology Questions 9-16

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9. Ectopic pregnancy

English translation

Definition

Frequency

• Occurs in approximately 1-2% of reported pregnancies.
• Tubal implantation accounts for about 95-98% of ectopic pregnancies.
• It remains an important cause of maternal morbidity and early-pregnancy maternal death.

Classification by location

1. Tubal ectopic pregnancy

2. Non-tubal ectopic pregnancy

• Ovarian pregnancy
• Cervical pregnancy
• Cesarean-scar pregnancy
• Interstitial pregnancy
• Abdominal pregnancy
• Intramural pregnancy
• Heterotopic pregnancy: simultaneous intrauterine and ectopic pregnancy, more likely after assisted reproductive technology

Etiology and risk factors

A. Tubal damage or impaired tubal transport

• Previous pelvic inflammatory disease, especially chlamydial infection
• Previous ectopic pregnancy
• Previous tubal surgery, sterilization, salpingostomy, or reconstructive tubal surgery
• Peritubal adhesions due to endometriosis
• Previous appendicitis or pelvic surgery
• Genital tuberculosis in endemic settings
• Congenital tubal anomaly

B. Factors affecting tubal motility

• Smoking, which impairs tubal ciliary function
• Progestin effects on tubal motility
• Endometriosis
• Hormonal stimulation/ovulation induction

C. Assisted reproduction

• In vitro fertilization and embryo transfer
• Multiple embryo transfer
• Previous infertility treatment

D. Contraceptive-related factors

• An intrauterine device in situ
• Progestin-only pill
• Implant
• Previous sterilization

Pathogenesis

• Tubal cilia
• Tubal smooth-muscle contractions
• Tubal secretions
• Normal hormonal environment

1. Fertilization usually occurs in the ampulla.
2. The embryo is delayed in its passage to the uterine cavity because of damaged cilia, spasm, narrowing, adhesions, or reduced peristalsis.
3. The blastocyst reaches the implantation stage while still in the tube or another ectopic site.
4. Trophoblast invades the local wall.
5. The tube cannot expand sufficiently as the pregnancy grows.
6. This leads to:
   • Tubal abortion through the fimbrial end, or
   • Tubal rupture with hemoperitoneum.

Clinical forms by course

1. Progressive unruptured ectopic pregnancy
2. Tubal abortion
3. Ruptured ectopic pregnancy
4. Chronic ectopic pregnancy, with repeated small bleeding and inflammatory mass formation

Clinical presentation: high-yield triad

• Amenorrhea
• Lower abdominal pain
• Vaginal bleeding/spotting

• Unilateral pelvic pain
• Shoulder-tip pain from diaphragmatic irritation by intraperitoneal blood
• Dizziness, syncope, collapse
• Cervical motion tenderness
• Adnexal tenderness or mass
• Signs of shock in rupture

Diagnosis

• Urine/serum pregnancy test
• Quantitative serum beta-hCG, repeated after 48 hours if needed
• Transvaginal ultrasound
• CBC, blood group, Rh status, crossmatch in suspected bleeding
• Diagnostic laparoscopy if diagnosis remains uncertain or the woman is unstable

Basic treatment principles

Immediate surgery

• Hemodynamic instability
• Suspected/confirmed rupture
• Significant hemoperitoneum
• Persistent severe pain
• Fetal cardiac activity in ectopic pregnancy in many settings
• Contraindication to methotrexate
• Inability to comply with follow-up

Medical therapy

• Methotrexate 50 mg/m² intramuscularly on day 1.
• Measure beta-hCG on days 4 and 7.
• A fall of at least 15% between day 4 and day 7 is expected.
• Continue weekly beta-hCG until undetectable.

Surgical options

• Salpingectomy: removal of the affected tube. Preferred if tube is ruptured, severely damaged, bleeding is uncontrolled, or the other tube is healthy.
• Salpingostomy: incision and removal of ectopic tissue while preserving the tube. May be considered when fertility preservation is important and the opposite tube is damaged. Requires follow-up beta-hCG because persistent trophoblast can occur.

The commonest ectopic pregnancy is ampullary tubal implantation. The main pathogenetic factor is disturbed tubal transport. A ruptured ectopic pregnancy is an emergency requiring immediate resuscitation and surgical treatment.

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10. Amenorrhea of peripheral origin

English translation

Definition

• Ovarian failure or ovarian hormone dysfunction
• Müllerian anomalies
• Uterine/endometrial damage
• Outflow tract obstruction

Classification

A. Ovarian cause: hypergonadotropic hypogonadism

• Primary ovarian insufficiency
• Gonadal dysgenesis
• Resistant ovary syndrome
• Iatrogenic ovarian failure after chemotherapy, radiotherapy, or bilateral oophorectomy
• Autoimmune oophoritis

B. Uterine/endometrial cause

• Asherman syndrome: intrauterine adhesions
• Endometrial destruction after curettage, infection, tuberculosis, or radiation
• Endometrial fibrosis

C. Outflow tract obstruction

• Imperforate hymen
• Transverse vaginal septum
• Cervical agenesis/atresia
• Cervical stenosis
• Vaginal agenesis or vaginal atresia

Etiology

Primary ovarian insufficiency

• Genetic: Turner syndrome, fragile-X premutation
• Autoimmune disease
• Chemotherapy/radiotherapy
• Oophorectomy
• Severe infection, rarely
• Idiopathic, common

Asherman syndrome

• Curettage after pregnancy, especially postpartum curettage
• Septic abortion
• Genital tuberculosis
• Intrauterine surgery
• Severe endometritis

Congenital outflow anomalies

Pathogenesis

Ovarian insufficiency

1. Follicles are depleted or dysfunctional.
2. Estrogen production falls.
3. Negative feedback to hypothalamus/pituitary decreases.
4. FSH and LH rise.
5. Ovulation and menstruation cease.

Asherman syndrome

1. Endometrial basal layer is damaged.
2. Adhesions form and partly or completely obliterate the uterine cavity.
3. Functional endometrium cannot proliferate or shed normally.
4. Menstrual blood flow becomes scant or absent.

Outflow obstruction

1. Ovarian cycles and endometrial shedding may be normal.
2. Menstrual blood cannot exit.
3. Blood accumulates as:
   • Hematocolpos: blood in vagina
   • Hematometra: blood in uterus
   • Hematosalpinx: blood in fallopian tubes
4. Cyclic pain occurs despite amenorrhea.

Clinical features

Diagnosis

Step 1. Exclude pregnancy

Step 2. Basic hormonal assessment

• FSH, LH
• Estradiol
• TSH
• Prolactin
• Androgens if hyperandrogenism is present

Interpretation

• High FSH with low estradiol: ovarian failure/peripheral ovarian cause
• Normal/low FSH with low estradiol: hypothalamic-pituitary cause
• Normal hormones with no menstruation: suspect uterine/outflow problem

Step 3. Imaging

• Pelvic ultrasound: uterus, ovaries, endometrial thickness, hematometra, hematocolpos
• MRI: congenital uterine/vaginal anomaly, complex obstruction, pituitary pathology if indicated

Step 4. Tests for uterine cavity/outflow tract

• Hysteroscopy: gold standard for intrauterine adhesions
• Hysterosalpingography: may demonstrate adhesions or cavity distortion
• Saline infusion sonography in selected women
• Vaginoscopy or examination under anesthesia for obstructive anomalies

Step 5. Genetic assessment

• Karyotype in primary amenorrhea, suspected gonadal dysgenesis, or unexplained ovarian insufficiency in young women
• FMR1 premutation testing in selected women with primary ovarian insufficiency

Treatment

Primary ovarian insufficiency

• Estrogen replacement plus progestogen if uterus is present, usually until the normal age of menopause.
• Calcium, vitamin D, weight-bearing exercise, and bone-density assessment.
• Cardiovascular risk assessment.
• Fertility counseling:
  • Spontaneous ovulation may rarely occur.
  • IVF with donor oocytes is the most effective fertility option for many women.
• Treat autoimmune/endocrine comorbidities if present.

Asherman syndrome

• Hysteroscopic adhesiolysis.
• Use of mechanical measures such as a balloon catheter or intrauterine device may be considered to reduce re-adhesion.
• Postoperative estrogen therapy may promote endometrial recovery.
• Follow-up hysteroscopy/ultrasound assessment.
• Treat genital tuberculosis if present.

Imperforate hymen

• Cruciate or circumferential hymenotomy/hymenectomy with drainage of hematocolpos.
• Avoid excessive pressure on the uterus because retrograde flow can increase endometriosis risk.

Vaginal/cervical obstruction

• Surgical reconstruction by a specialized gynecologic team.
• Cervical stenosis may require cervical dilation and treatment of the cause.

Peripheral amenorrhea may be ovarian, uterine, or obstructive. High FSH with low estradiol indicates ovarian failure; normal ovarian hormones with amenorrhea requires exclusion of intrauterine adhesions and genital outflow obstruction.

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11. Gonadal dysgenesis

English translation

Definition

Classification

1. Turner syndrome

• Karyotype: 45,X or mosaic variants, such as 45,X/46,XX.
• Most common cause of gonadal dysgenesis in phenotypic females.

2. Pure gonadal dysgenesis, 46,XX

• Female phenotype.
• Normal Müllerian structures.
• Streak ovaries.
• Primary amenorrhea and failure of puberty.

3. Swyer syndrome, 46,XY complete gonadal dysgenesis

• Female external genitalia.
• Uterus and fallopian tubes present because Müllerian inhibiting substance is absent.
• Streak gonads.
• Important risk of gonadoblastoma and dysgerminoma.

4. Mixed gonadal dysgenesis

• Often mosaic karyotype, for example 45,X/46,XY.
• Variable genital development.
• May have asymmetric gonads and ambiguous genitalia.

Etiology

• Chromosomal abnormalities
• Failure of migration or differentiation of primordial germ cells
• Mutations in genes involved in gonadal differentiation, such as SRY and others
• Mosaicism
• Structural X-chromosome abnormality

Pathogenesis

1. Gonads fail to develop normally.
2. Follicles are absent or rapidly lost.
3. Estrogen production is inadequate.
4. Puberty does not occur normally.
5. Lack of negative feedback causes elevated FSH and LH.
6. The uterus remains small because estrogen stimulation is absent or reduced.

Clinical features

Turner syndrome

• Short stature
• Webbed neck
• Broad chest with widely spaced nipples
• Cubitus valgus
• Low posterior hairline
• Lymphedema of hands/feet at birth
• Congenital heart disease, especially coarctation of aorta and bicuspid aortic valve
• Renal anomalies
• Primary amenorrhea
• Delayed/absent puberty
• Infertility

Pure 46,XX gonadal dysgenesis

• Normal female external genitalia
• Usually normal stature
• Primary amenorrhea
• Poor breast development
• Sparse or normal pubic/axillary hair
• Small uterus, streak gonads

46,XY gonadal dysgenesis

• Female phenotype
• Primary amenorrhea
• Absent/incomplete secondary sexual development
• Uterus present
• Streak gonads
• High risk of gonadal malignancy

Diagnosis

Clinical assessment

• History of absent menarche by age 15 with secondary sexual characteristics, or by age 13 without breast development
• Family history
• Assessment of height, body proportions, dysmorphic features, hearing, cardiovascular and renal signs

Laboratory tests

• High FSH and LH
• Low estradiol
• TSH, prolactin, adrenal function as indicated
• Anti-Müllerian hormone may be very low/undetectable

Imaging

• Pelvic ultrasound: small uterus, streak/absent ovaries
• MRI if gonads cannot be visualized
• Echocardiography and renal ultrasound for Turner syndrome

Genetic tests

• Karyotyping is essential.
• Y-chromosome material testing if indicated.
• Targeted genetic testing in specialist care.

Treatment

1. Induction of puberty and hormone replacement

• Start low-dose estrogen, then increase over approximately 2-3 years to an adult replacement dose.
• Add cyclic progestogen after breakthrough bleeding occurs, after about 12-24 months of estrogen, or when adequate endometrial development occurs.

• Develop secondary sexual characteristics
• Maintain uterine health
• Protect bone density
• Support cardiovascular and psychological wellbeing

2. Management of Y-chromosome material

Prophylactic gonadectomy is indicated because dysgenetic gonads have a significant malignancy risk.

3. Turner syndrome multidisciplinary care

• Growth hormone in childhood when indicated
• Cardiology follow-up
• Blood-pressure monitoring
• Renal assessment
• Thyroid screening
• Diabetes/metabolic screening
• Hearing assessment
• Bone-density surveillance
• Psychological support

4. Fertility options

• Donor-oocyte IVF may be possible if uterus is present and medically safe.
• Pregnancy in Turner syndrome requires strict cardiovascular evaluation because of increased aortic dissection risk.
• Gestational carrier or adoption may be safer for women with significant cardiovascular disease.

Gonadal dysgenesis produces hypergonadotropic hypogonadism: high FSH/LH and low estrogen. Diagnosis requires karyotyping. Treatment is pubertal induction and long-term hormone replacement; dysgenetic gonads containing Y-chromosome material require removal because of malignancy risk.

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12. Endocrine infertility

English translation

Definition

Main causes

World Health Organization ovulatory disorder groups

• Hyperprolactinemia
• Thyroid disease
• Non-classic congenital adrenal hyperplasia
• Cushing syndrome
• Diabetes/insulin resistance
• Obesity
• Severe underweight
• Androgen-secreting ovarian/adrenal tumor
• Luteal dysfunction, historically described but difficult to diagnose reliably

Pathogenesis

• Failure of follicle recruitment
• Failure of dominant follicle selection
• Absence of LH surge
• Anovulation
• Short/inadequate luteal phase
• Abnormal endometrial development
• Hyperandrogenism and insulin resistance, particularly in PCOS

Clinical features

• Infertility, defined as no pregnancy after 12 months of regular unprotected intercourse, or after 6 months if age 35 years or older
• Oligomenorrhea or amenorrhea
• Irregular bleeding
• Hirsutism, acne, alopecia in hyperandrogenism
• Galactorrhea in hyperprolactinemia
• Weight change
• Hot flushes in ovarian insufficiency
• Signs of thyroid/adrenal disease
• Obesity, acanthosis nigricans, metabolic syndrome in PCOS

Diagnosis

First principle

• Male factor: semen analysis
• Tubal disease: HSG or other tubal assessment where indicated
• Uterine pathology

History

• Menstrual pattern
• Previous pregnancy and miscarriage
• Weight changes, eating disorder, exercise
• Galactorrhea, headache, visual symptoms
• Acne, hirsutism, virilization
• Thyroid symptoms
• Drugs: antipsychotics, metoclopramide, opioids
• Pelvic infection, surgery, STI history

Examination

• BMI, waist circumference
• Signs of hyperandrogenism
• Thyroid examination
• Breast examination for galactorrhea
• Pelvic examination and ultrasound

Investigations

Ovulation assessment

• Mid-luteal serum progesterone, timed to approximately 7 days before expected menstruation
• Serial ultrasound folliculometry, if needed
• Ovulation-prediction kits can be supportive but not definitive in PCOS

Hormones

• FSH, LH, estradiol
• Prolactin
• TSH
• Total/free testosterone, DHEAS, 17-hydroxyprogesterone if hyperandrogenism
• HbA1c/glucose testing and lipid profile in PCOS/obesity
• AMH may help estimate ovarian reserve, but does not independently diagnose infertility

Imaging

• Pelvic ultrasound for polycystic ovarian morphology, ovarian reserve, uterine pathology
• Pituitary MRI if significant hyperprolactinemia, headache, visual symptoms, or suspected pituitary lesion

Treatment

A. General measures for all causes

• Optimize BMI:
  • Weight loss may restore ovulation in overweight women with PCOS.
  • Nutritional rehabilitation is essential in underweight women.
• Stop smoking, alcohol excess, recreational drugs.
• Treat diabetes, thyroid disease, anemia, and chronic disease.
• Folic acid supplementation before conception.
• Timed intercourse during fertile window.
• Assess semen and tubal patency before prolonged ovulation induction.

B. PCOS-related anovulatory infertility

First-line

• Lifestyle intervention if overweight.
• Letrozole is commonly first-line ovulation induction where available.

• Letrozole 2.5-5 mg orally daily for 5 days early in the cycle, with escalation if no ovulation, following specialist protocol.

Alternative

• Clomiphene citrate, with or without metformin in selected insulin-resistant women.
• Metformin is mainly useful for metabolic indications and selected women with PCOS, rather than universally as sole fertility therapy.

Second-line

• Gonadotropin stimulation with ultrasound monitoring.
• Laparoscopic ovarian drilling in selected resistant cases.
• IVF if other treatments fail or there are additional infertility factors.

C. Hyperprolactinemia

• Exclude pregnancy, hypothyroidism, and drug causes.
• Treat hypothyroidism with levothyroxine.
• Review and change prolactin-raising medication if possible.
• Dopamine agonist:
  • Cabergoline is commonly preferred due to good efficacy and tolerability.
  • Bromocriptine is an alternative.
• Refer for pituitary assessment if macroadenoma or visual symptoms.

D. Hypothyroidism

• Treat with levothyroxine and optimize TSH before conception.
• Ovulation may resume after correction.

E. Functional hypothalamic amenorrhea

• Restore adequate calorie intake.
• Reduce excessive exercise.
• Treat stress and eating disorders.
• Psychological support.
• Pulsatile GnRH therapy or gonadotropins may be used by fertility specialists if lifestyle recovery is insufficient.

F. Primary ovarian insufficiency

• Spontaneous ovulation is possible but uncommon.
• Hormone replacement for health, not reliably for fertility.
• Donor-oocyte IVF is generally the most effective fertility treatment.

G. Congenital adrenal hyperplasia/non-classic CAH

• Specialist glucocorticoid therapy to suppress adrenal androgen excess.
• Genetic counseling where appropriate.

Endocrine infertility is mainly anovulatory infertility. The commonest cause is PCOS. The investigation includes confirmation of ovulation, FSH/LH/estradiol, prolactin, TSH, androgen profile, pelvic ultrasound, and simultaneous male/tubal assessment. Treatment targets the cause, with letrozole commonly first-line for PCOS-related anovulation.

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13. Pelvic organ prolapse

English translation

Definition

• Uterus and cervix
• Vaginal vault after hysterectomy
• Bladder and anterior vaginal wall
• Rectum and posterior vaginal wall
• Small bowel/peritoneum into upper vagina

Classification

By compartment

1. Anterior compartment prolapse
   • Cystocele: bladder bulges into anterior vaginal wall
   • Urethrocele: urethra descends
2. Apical compartment prolapse
   • Uterine prolapse
   • Cervical elongation
   • Vaginal vault prolapse after hysterectomy
   • Enterocele
3. Posterior compartment prolapse
   • Rectocele
   • Perineocele

By degree of uterine descent

• First degree: cervix descends but remains within vagina
• Second degree: cervix reaches the introitus
• Third degree: cervix/uterus protrudes beyond introitus
• Complete prolapse/procidentia: whole uterus lies outside the vagina

Etiology and risk factors

• Vaginal childbirth, especially prolonged second stage, forceps delivery, large fetus, multiple births, severe perineal tears
• Aging and menopause, due to estrogen deficiency and connective-tissue change
• Obesity
• Chronic increased intra-abdominal pressure:
  • Chronic cough
  • Constipation/straining
  • Heavy physical labor
• Connective tissue disorders
• Prior pelvic surgery, especially hysterectomy
• Pelvic-floor trauma
• Family history/genetic predisposition
• Neurologic disease

Pathogenesis

• Levator ani muscles
• Perineal body
• Endopelvic fascia
• Uterosacral and cardinal ligaments
• Pubocervical and rectovaginal fascia

1. Vaginal walls lose support.
2. Pelvic organs descend.
3. Apical support failure permits uterine/vault prolapse.
4. Secondary bladder, bowel, and sexual dysfunction may develop.

Clinical features

• Sensation of vaginal bulge or “something coming down”
• Seeing or feeling tissue at the introitus
• Pelvic pressure, dragging pain, low back discomfort
• Difficulty walking or sitting in advanced prolapse
• Urinary frequency, urgency, stress incontinence, incomplete emptying, recurrent UTI
• Constipation, incomplete defecation, need to press on vagina/perineum to defecate
• Dyspareunia or reduced sexual satisfaction
• Vaginal dryness, discharge, bleeding, ulceration of exposed tissue
• In complete prolapse: cervical/vaginal ulceration, infection, urinary retention, hydronephrosis in severe cases

Diagnosis

• History of urinary, bowel, and sexual symptoms
• Examination in lithotomy position, and ideally standing/straining if prolapse is not seen supine
• Speculum examination of anterior, apical, and posterior compartments
• POP-Q staging where available
• Assess for ulceration, discharge, cervical pathology
• Cough stress test for stress urinary incontinence
• Post-void residual urine if incomplete emptying
• Urinalysis/culture if urinary symptoms
• Urodynamic study only in selected complex cases
• Cervical screening must be up to date before uterine-preserving surgery

Treatment

A. Conservative treatment

1. Pelvic-floor muscle training
   • Supervised physiotherapy for at least several months.
   • Most useful in mild to moderate prolapse.
2. Lifestyle measures
   • Weight reduction if overweight
   • Treat chronic cough
   • Treat constipation and avoid straining
   • Avoid repeated heavy lifting
   • Smoking cessation
3. Vaginal estrogen
   • In postmenopausal women with atrophic tissues.
   • Improves comfort and reduces pessary-related erosion risk.
   • Does not independently correct major prolapse.
4. Pessary
   • Vaginal device providing mechanical support.
   • Ring pessary is common for cystocele/mild prolapse.
   • Gellhorn pessary is often used for more advanced uterine prolapse.
   • Needs fitting, education, regular removal/cleaning/follow-up.
   • Complications: discharge, odor, erosion, bleeding, rarely fistula if neglected.

B. Surgical treatment

• Bothersome symptomatic prolapse
• Failure/intolerance of pessary
• Ulceration, obstruction, recurrent urinary retention, hydronephrosis
• Patient preference after informed counseling

Reconstructive surgery

• Anterior colporrhaphy, with native tissue repair.

• Posterior colporrhaphy/perineorrhaphy.

• Vaginal hysterectomy with apical suspension
• Uterosacral ligament suspension
• Sacrospinous fixation
• Abdominal/laparoscopic sacrocolpopexy for vaginal vault prolapse
• Sacrohysteropexy or other hysteropexy if uterus is preserved

Obliterative surgery

• Colpocleisis narrows/closes the vagina.
• Suitable only for women who do not desire vaginal intercourse.

Mesh

• Vaginal mesh has important risks: erosion, infection, pain, dyspareunia, bladder/bowel injury.
• Mesh use depends on national regulation and specialized practice.
• Abdominal sacrocolpopexy mesh has a different risk-benefit profile and is used selectively.

Prevention

• Prevention and good repair of obstetric perineal trauma
• Pelvic-floor exercises during and after pregnancy
• Weight management
• Treat constipation and chronic cough
• Avoid chronic heavy physical strain
• Postmenopausal vaginal estrogen when indicated for atrophy
• Early assessment of postpartum pelvic-floor symptoms

Pelvic organ prolapse is caused by failure of pelvic-floor and fascial support. Management ranges from pelvic-floor rehabilitation and pessary to reconstructive or obliterative surgery, selected according to compartment involved, severity, sexual function, age, comorbidities, and fertility wishes.

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14. Background diseases of the cervix

English translation

Definition

Main background conditions

• Cervical ectropion, often historically called “erosion”
• True cervical erosion, rare
• Cervicitis
• Nabothian cysts
• Endocervical polyps
• Cervical endometriosis
• Cervical ectropion after childbirth/trauma
• Cervical leukoplakia requires special attention because it can be associated with dysplasia and should not simply be considered benign
• Condyloma acuminata, HPV-related

A. Cervical ectropion

Definition

Causes

• Puberty
• Pregnancy
• Combined hormonal contraception
• Postpartum cervical trauma
• Hormonal changes

Clinical features

• Often asymptomatic
• Increased mucus discharge
• Postcoital spotting
• Contact bleeding during examination
• Red area around external os on speculum examination

Management

• Exclude pregnancy, infection, cervical cancer, and cervical precancer if symptoms are persistent.
• No treatment is needed if asymptomatic and screening is normal.
• Treat cervicitis/STIs if present.
• Persistent troublesome bleeding/discharge after exclusion of malignancy may be treated by:
  • Cryotherapy
  • Thermal coagulation
  • Electrocautery
  • Laser ablation in selected settings

B. Cervicitis

Etiology

• Chlamydia trachomatis
• Neisseria gonorrhoeae
• Trichomonas vaginalis
• Herpes simplex virus
• Bacterial vaginosis-associated flora
• Mechanical or chemical irritation

Clinical features

• Mucopurulent cervical discharge
• Friable cervix, contact bleeding
• Postcoital bleeding
• Pelvic discomfort
• Dysuria
• Often asymptomatic

Diagnosis

• Speculum examination
• Nucleic acid amplification test for chlamydia/gonorrhea
• Tests for trichomoniasis, bacterial vaginosis, HIV, syphilis according to risk
• Cytology/HPV screening as appropriate
• Colposcopy/biopsy if suspicious lesion or unexplained persistent bleeding

Treatment

• Chlamydia: doxycycline 100 mg orally twice daily for 7 days, unless pregnancy, where an appropriate alternative such as azithromycin is used according to local guidelines.
• Gonorrhea: ceftriaxone-based treatment according to current local guideline.
• Trichomoniasis: metronidazole-based treatment, and treat sexual partners.
• Counsel abstinence or condom use until patient and partner treatment is completed.

C. Nabothian cysts

Definition

Clinical significance and treatment

• Usually small, benign, incidental findings.
• No treatment is needed.
• Large, atypical, or symptomatic lesions require colposcopy/imaging to exclude other pathology and may be drained/excised if needed.

D. Endocervical polyp

Clinical features

• Often asymptomatic
• Intermenstrual bleeding
• Postcoital bleeding
• Excessive discharge
• Red/purple polyp protruding through external os

Diagnosis

• Speculum examination
• Cytology/HPV testing according to screening schedule
• Colposcopy if atypical/suspicious
• Histology is required after removal

Treatment

• Polypectomy by twisting/removing the polyp at its base using forceps.
• Cauterize the base if bleeding.
• Send every removed polyp for histopathology.
• Hysteroscopy/endometrial assessment may be indicated in postmenopausal bleeding, recurrent polyps, or suspected intrauterine lesion.

E. Cervical endometriosis

• Cyclical postcoital/contact bleeding
• Blue-red nodules on cervix
• Pain, especially with prior cervical trauma/procedures

• Observation if asymptomatic and diagnosis is certain
• Biopsy to exclude malignancy if lesion is atypical
• Excision/ablation if symptomatic

Prevention

• HPV vaccination
• Condom use and STI prevention
• Prompt diagnosis and treatment of cervical infection
• Regular cervical screening according to national protocol
• Avoid unnecessary destructive cervical procedures
• Smoking cessation
• Timely colposcopy for abnormal HPV/cytology or suspicious cervical lesion

The commonest background cervical condition is ectropion. It is frequently physiological and requires no treatment unless symptoms persist after infection and precancer have been excluded. Every suspicious cervical lesion requires colposcopy and biopsy.

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15. Abnormal positions of female genital organs

English translation

Definition

Classification

A. Abnormal uterine version and flexion

• Retroversion: uterus tilted posteriorly relative to vagina
• Retroflexion: uterine body bent posteriorly relative to cervix
• Excessive anteversion/anteflexion
• Lateral deviation: dextrorotation or sinistrorotation

B. Vertical displacement

• Uterine descent
• Partial/complete uterine prolapse
• Vaginal vault prolapse after hysterectomy

C. Fixation of the uterus

• Fixed retroverted uterus due to adhesions
• Uterine fixation after pelvic inflammatory disease, endometriosis, surgery, or tumor

D. Displacement due to adjacent organs/masses

• Fibroids
• Ovarian tumors
• Pelvic adhesions
• Bladder/rectal distension
• Pregnancy-related displacement

Etiology

• Congenital variation
• Weakness of pelvic floor or ligaments
• Childbirth trauma
• Menopause/estrogen deficiency
• Pelvic inflammatory disease
• Endometriosis
• Pelvic adhesions after surgery
• Uterine fibroids or ovarian masses
• Chronic constipation, bladder overdistension
• Connective-tissue disorders

Pathogenesis

• Pelvic-floor muscles
• Uterosacral and cardinal ligaments
• Endopelvic fascia
• Round ligaments, supporting anteversion
• Normal relationships with bladder and rectum

Clinical features

• Pelvic pressure or pain
• Deep dyspareunia
• Dysmenorrhea
• Low back pain
• Urinary frequency, retention, or incomplete emptying
• Constipation
• Infertility is usually due to associated disease, for example endometriosis/PID, rather than retroversion itself
• Recurrent miscarriage is not usually caused by simple mobile retroversion
• Fixed retroversion suggests endometriosis, adhesions, or pelvic inflammatory disease

Diagnosis

• Bimanual examination:
  • Cervix may be directed anteriorly.
  • Fundus palpated posteriorly through posterior fornix or rectovaginal examination.
• Ultrasound confirms uterine position and detects fibroids/adnexal mass.
• MRI/diagnostic laparoscopy when endometriosis, adhesions, or deep pelvic pathology is suspected.
• Evaluate urinary, bowel, and sexual symptoms.

Treatment

Asymptomatic mobile retroversion

• Reassurance only.
• No treatment is needed.

Treat the cause

• PID: appropriate antibiotics.
• Endometriosis: hormonal treatment and/or surgery.
• Fibroids/ovarian mass: disease-specific medical or surgical treatment.
• Constipation/bladder dysfunction: bowel/bladder management.

Symptomatic retroversion without major pathology

• Pelvic-floor physiotherapy.
• Analgesia/NSAIDs for pain.
• Pessary may be considered in selected cases.
• Uterine suspension procedures are rarely indicated and only after exclusion/treatment of underlying pathology.

Uterine prolapse

Simple mobile retroversion is usually a normal anatomical variant and does not need treatment. A fixed, painful retroverted uterus requires investigation for endometriosis, pelvic inflammatory disease, adhesions, or pelvic mass.

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16. Uterine fibroids. Prolapsing submucosal fibroid

English translation

Definition

Classification by location

Risk factors

• Reproductive age
• Family history
• Black ethnicity
• Obesity
• Early menarche
• Nulliparity
• Hypertension
• Increasing age until menopause

Clinical features

Bleeding symptoms

• Heavy menstrual bleeding
• Prolonged menses
• Intermenstrual bleeding, especially submucosal lesion
• Iron-deficiency anemia

Bulk symptoms

• Pelvic pressure/heaviness
• Increased abdominal girth
• Urinary frequency, urgency, retention
• Constipation, rectal pressure
• Hydronephrosis in very large fibroids

Reproductive symptoms

• Infertility, especially submucosal fibroids or cavity-distorting intramural lesions
• Recurrent miscarriage
• Pregnancy complications:
  • Miscarriage
  • Malpresentation
  • Preterm labor
  • Placental abruption
  • Labor dystocia
  • Postpartum hemorrhage

Pain

• Degeneration, especially red degeneration in pregnancy
• Torsion of pedunculated subserosal fibroid
• Ischemia/necrosis

Diagnosis

Clinical examination

• Enlarged, firm, irregularly contoured uterus
• Usually mobile and non-tender
• Large mass may rise out of pelvis

Imaging

1. Transvaginal and transabdominal ultrasound: first-line.
2. Saline infusion sonography: useful to identify submucosal fibroids and cavity distortion.
3. Hysteroscopy: diagnostic and therapeutic for submucosal intracavitary fibroids.
4. MRI: best for mapping multiple fibroids, assessing degeneration, planning myomectomy, UAE, or high-intensity focused ultrasound.
5. CBC/ferritin: assess anemia.
6. Pregnancy test in reproductive-age bleeding.
7. Endometrial sampling if abnormal bleeding with age/risk factors suggesting endometrial hyperplasia or cancer.

Differential diagnosis

• Adenomyosis
• Ovarian tumor
• Pregnancy
• Uterine sarcoma, rare
• Endometrial polyp
• Endometrial hyperplasia/cancer
• Pelvic inflammatory mass

Possible complications

Degeneration

• Hyaline degeneration, most common
• Cystic degeneration
• Red degeneration: acute painful hemorrhagic infarction, often in pregnancy
• Calcification, especially after menopause
• Rare infection/suppuration

Torsion

Effects on reproductive function

• Infertility
• Implantation failure
• Recurrent miscarriage
• Obstetric complications

Anemia

Compression complications

• Hydroureter/hydronephrosis
• Urinary retention
• Constipation
• Venous compression and edema

Malignancy

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Prolapsing submucosal fibroid

Definition

Clinical features

• Severe cramping, labor-like lower abdominal pain caused by uterine contractions
• Heavy bleeding, sometimes acute hemorrhage
• Foul-smelling discharge if ulcerated/infected
• Sensation of a mass in the vagina
• Anemia, weakness, dizziness
• On speculum examination: round red-purple/gray mass in vagina, often protruding through external os
• Cervix is dilated around the stalk
• The uterus may be enlarged and tender
• Necrosis, ulceration, and infection can occur

Differential diagnosis

• Cervical polyp
• Cervical cancer
• Prolapsed endometrial polyp
• Inverted uterus, especially postpartum
• Vaginal tumor
• Products of conception

Diagnosis

• Speculum examination: vaginal mass arising from cervical canal
• Bimanual examination: uterine size, tenderness, cervical dilatation
• Transvaginal ultrasound: confirms uterine origin, stalk, residual intracavitary component
• Hysteroscopy if stable and diagnosis uncertain
• CBC, ferritin, blood group/crossmatch if bleeding is heavy
• Histology of removed mass is mandatory

Treatment

Emergency priorities

1. Assess ABCDE and hemodynamic state.
2. Obtain IV access.
3. CBC, coagulation profile, blood group and crossmatch.
4. IV fluids and blood transfusion if indicated.
5. Analgesia.
6. Broad-spectrum antibiotics if necrosis, foul discharge, fever, or suspected infection.
7. Urgent gynecologic surgery.

Definitive treatment: vaginal myomectomy

1. Examination under anesthesia.
2. Grasp the fibroid with forceps.
3. Identify and clamp/twist/ligate the pedicle as high as possible.
4. Remove the fibroid by vaginal myomectomy.
5. Secure hemostasis.
6. Inspect uterine cavity, often by hysteroscopy where feasible.
7. Send tissue for histopathology.

If vaginal removal is not feasible

• Hysteroscopic resection for suitable intracavitary lesion, or
• Laparoscopic/laparotomy myomectomy, depending on size, location, and access, or
• Hysterectomy if woman has completed childbearing, bleeding is uncontrollable, malignancy is suspected, or there are multiple symptomatic fibroids.

Medical treatment before planned surgery

• Iron therapy, oral or IV
• Tranexamic acid during heavy bleeding if no contraindication
• GnRH agonist or antagonist may be used temporarily to reduce bleeding/volume and optimize hemoglobin before surgery
• This is not definitive treatment for a prolapsing necrotic fibroid

A prolapsing submucosal fibroid presents with cramping pain, bleeding, a dilated cervix, and a mass in the vagina. After stabilization and treatment of anemia/infection, the standard treatment is vaginal myomectomy with control of the pedicle and mandatory histological examination.

Gynecology Questions 17-24

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17. Acute inflammatory diseases of the external genital organs

English translation

Definition

• Acute vulvitis
• Vulvovaginitis
• Bartholinitis
• Bartholin gland cyst and abscess
• Skene gland infection
• Vulvar cellulitis, furuncle, or abscess
• Necrotizing soft-tissue infection, rare but life-threatening

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A. Acute vulvitis

Definition

Etiology

Infectious

• Candida species: intense itching, thick curd-like discharge
• Trichomonas vaginalis: frothy yellow-green discharge, vulvar irritation
• Bacterial vaginosis-associated irritation
• Herpes simplex virus: painful vesicles and ulcers
• Human papillomavirus: condylomata
• Gonorrhea/chlamydia, usually cause cervicitis but may be associated with vulvovaginal inflammation
• Staphylococcal or streptococcal skin infection

Non-infectious

• Soap, perfume, vaginal sprays, pads, detergents, lubricants, latex
• Tight synthetic underwear
• Poor hygiene or excessive washing/douching
• Diabetes mellitus
• Obesity and skin-fold maceration
• Atrophic vulvovaginitis in menopause
• Dermatoses: lichen sclerosus, lichen planus, eczema, psoriasis
• Foreign body, particularly in children

Clinical features

• Vulvar itching, burning, soreness
• Pain during urination due to contact with inflamed skin
• Dyspareunia
• Erythema, edema, excoriations
• Fissures, ulcers, vesicles, pustules, or discharge depending on cause
• Enlarged inguinal nodes in severe infection

Diagnosis

1. History:
   • Onset, discharge, sexual exposure, hygiene products, diabetes, antibiotic use.
2. Inspection of vulva and perineum.
3. Speculum examination if appropriate and tolerated.
4. Vaginal pH, microscopy/wet mount where available.
5. NAAT for chlamydia/gonorrhea/trichomonas when indicated.
6. Fungal microscopy/culture in recurrent or treatment-resistant candidiasis.
7. HSV PCR/culture from vesicle/ulcer if herpes is suspected.
8. Biopsy any persistent, ulcerated, pigmented, thickened, or treatment-resistant lesion to exclude VIN or vulvar carcinoma.

Treatment

General measures

• Avoid irritants: scented soap, douches, perfumes, pads, tight underwear.
• Use water or a gentle unperfumed emollient for washing.
• Keep the area dry.
• Cotton underwear and loose clothing.
• Avoid intercourse until acute infection is resolved.
• Give analgesia: paracetamol or an NSAID if suitable.

Vulvovaginal candidiasis

• Fluconazole 150 mg orally once, if not pregnant and no contraindication, or
• Topical azole, for example clotrimazole vaginal cream/pessary for 1-7 days depending on preparation.

Trichomoniasis

• Metronidazole, commonly 500 mg orally twice daily for 7 days.
• Treat sexual partners simultaneously.
• Avoid sexual intercourse until patient and partners complete treatment.

Genital herpes

• Start antiviral therapy promptly:
  • Acyclovir 400 mg orally three times daily for 7-10 days for a first episode, according to local guideline.
• Give analgesia, local saline bathing, and counsel about recurrence and transmission.

Bacterial cellulitis/furuncle

• Drain fluctuant abscess.
• Oral anti-staphylococcal antibiotics for cellulitis, selected by local resistance patterns.
• Severe infection requires admission and IV antibiotics.

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B. Acute bartholinitis and Bartholin abscess

Anatomy

Etiology

• Anaerobic vaginal flora
• Enteric gram-negative organisms including E. coli
• Staphylococci/streptococci
• Occasionally gonorrhea or chlamydia

Clinical features

Bartholin cyst

• Usually painless unilateral fluctuant mass at posterolateral introitus.
• May cause dyspareunia or discomfort if large.

Bartholin abscess

• Severe unilateral vulvar pain
• Fever and malaise may occur
• Painful swelling at introitus
• Erythema, edema, fluctuance
• Difficulty walking, sitting, or having intercourse

Diagnosis

• Mainly clinical.
• Test for gonorrhea/chlamydia when STI risk is present.
• Culture pus in severe, recurrent, or nonresponsive infection.
• Biopsy or excise a new Bartholin mass in women aged over 40 years or when the mass is irregular/fixed, to exclude malignancy.

Treatment

Cyst

• Small asymptomatic cyst: observation.
• Symptomatic cyst: drainage with Word catheter or marsupialization.

Abscess

1. Analgesia and assessment for fever/systemic illness.
2. Drainage is the main treatment:
   • Incision and drainage with Word catheter placement, or
   • Marsupialization, especially for recurrent cyst/abscess.
3. Antibiotics are not always necessary after adequate drainage, but give them if:
   • Cellulitis
   • Fever/systemic illness
   • Pregnancy/immunosuppression
   • High-risk STI
   • Recurrent/severe infection
4. Antibiotic selection should cover likely polymicrobial flora and be adapted to cultures/local policy.
5. Treat confirmed STI and partners.

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C. Vulvar abscess and necrotizing infection

Vulvar abscess

• A fluctuant painful mass, often due to infected follicle, hidradenitis, trauma, or diabetes.
• Management: incision and drainage, culture, antibiotics if cellulitis/systemic illness, and glycemic control.

Necrotizing fasciitis/Fournier gangrene

• Severe pain disproportionate to findings
• Rapidly spreading edema/erythema
• Skin discoloration, bullae, necrosis, crepitus
• Fever, hypotension, confusion, high lactate

Emergency treatment

• Immediate admission to ICU/surgical team.
• Broad IV antibiotics, for example piperacillin-tazobactam plus clindamycin, with MRSA cover when indicated.
• Urgent radical surgical debridement.
• Repeated debridement may be necessary.
• Hemodynamic resuscitation and management of sepsis.

Prevention

• Vulvar hygiene without irritants
• Condom use and STI screening/treatment
• Good diabetes control
• Avoid self-treatment of persistent lesions
• Prompt treatment of vulvar trauma, skin infection, and Bartholin cyst infection

Acute vulvar inflammation is treated according to cause. Bartholin abscess requires drainage, usually by Word catheter or marsupialization. A painful rapidly progressive vulvar infection with systemic toxicity requires immediate broad-spectrum IV antibiotics and surgical debridement.

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18. Congenital malformations of the external genital organs

English translation

Definition

Classification

A. Hymenal anomalies

• Imperforate hymen
• Microperforate hymen
• Septate hymen
• Cribriform hymen
• Rigid/fibrous hymen

B. Vulvar anomalies

• Labial agenesis, hypoplasia, or asymmetry
• Labial fusion/adhesion
• Hypertrophy of labia minora
• Congenital clitoral hypertrophy
• Bifid clitoris
• Accessory labioscrotal folds

C. Vaginal-introital anomalies

• Vaginal agenesis/hypoplasia
• Vaginal atresia
• Low transverse vaginal septum
• Persistent urogenital sinus

D. Disorders of sex development

• Congenital adrenal hyperplasia causing virilization
• 46,XY disorders of sex development
• Mixed gonadal dysgenesis
• Androgen-insensitivity syndrome

A. Imperforate hymen

Clinical features

• Primary amenorrhea
• Normal secondary sexual characteristics
• Cyclic lower abdominal/pelvic pain
• Bulging, tense, bluish hymenal membrane
• Hematocolpos: retained blood in vagina
• Hematometra: retained blood in uterus
• Urinary retention, constipation, back pain

Diagnosis

• Inspection of vulva reveals bulging bluish hymen.
• Transabdominal/transperineal pelvic ultrasound confirms hematocolpos/hematometra and excludes more proximal obstruction.
• MRI is useful if transverse vaginal septum or complex Müllerian anomaly is suspected.

Treatment

• Definitive treatment is hymenotomy or hymenectomy under anesthesia.
• A cruciate incision or circumferential excision is made, with careful controlled drainage of retained blood.
• Edges are sutured if needed to prevent re-adhesion.
• Avoid forceful uterine compression, which may promote retrograde flow.
• Follow up to assess normal vaginal patency and menstrual function.

B. Labial adhesions

Definition

Clinical features

• Often asymptomatic
• Thin midline membrane
• Deflected urinary stream, post-void dribbling
• Recurrent vulvovaginitis/UTI in some children

Treatment

• Reassurance and hygiene if asymptomatic.
• Treat irritation/vulvovaginitis.
• Topical estrogen cream or topical steroid in selected symptomatic cases, following pediatric gynecology guidance.
• Manual/surgical separation only if severe obstruction, recurrent UTI, or failed conservative therapy.

C. Vaginal agenesis or Mayer-Rokitansky-Küster-Hauser syndrome

Clinical features

• Primary amenorrhea
• Normal breast development and pubic hair
• Normal 46,XX karyotype
• Normal ovarian function
• Short blind vagina or absent upper vagina
• Uterus may be absent or rudimentary

Diagnosis

• Pelvic examination, ultrasound, and MRI.
• Karyotype where diagnosis is uncertain.
• Renal imaging, because urinary tract anomalies may coexist.

Treatment

• Psychological support and specialist counseling.
• First-line treatment is progressive vaginal dilation if the woman wishes to achieve vaginal length.
• Surgical vaginoplasty is reserved for selected women after careful counseling.
• Fertility depends on uterine anatomy. If uterus is absent, genetic motherhood may be possible through oocyte retrieval and gestational carrier where legally permitted.

D. Virilized external genitalia

Causes

• Congenital adrenal hyperplasia, especially 21-hydroxylase deficiency
• Maternal androgen exposure
• Fetal androgen-producing tumor
• 46,XY disorder of sex development

Diagnosis

• Pediatric endocrinology
• Pediatric gynecology/urology
• Genetics
• Psychology

• Electrolytes, glucose
• 17-hydroxyprogesterone
• Karyotype/genetic testing
• Pelvic ultrasound for uterus/gonads
• Hormonal assessment

Treatment

Prevention

• Genetic counseling for known inherited disorders
• Antenatal detection of major associated urinary/genital anomalies
• Avoid maternal exposure to androgenic drugs during pregnancy
• Early neonatal examination and prompt specialist referral if genital ambiguity is present

Imperforate hymen presents with primary amenorrhea, cyclic pain, and hematocolpos despite normal puberty. Diagnosis is clinical and ultrasonographic, and treatment is controlled hymenotomy/hymenectomy. Ambiguous genitalia requires urgent multidisciplinary endocrine and genetic evaluation.

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19. Adenomyosis

English translation

Definition

Classification

• Diffuse adenomyosis: widespread involvement of myometrium.
• Focal adenomyosis/adenomyoma: localized nodular lesion.
• Superficial or deep adenomyosis, based on depth of myometrial invasion.

Etiology and pathogenesis

1. Invagination theory
   • Basal endometrium penetrates into the myometrium through a disrupted endometrial-myometrial junction.
2. Tissue injury and repair
   • Repeated uterine injury, inflammation, hyperperistalsis, pregnancy-related trauma, curettage, or cesarean scar can disrupt the junctional zone.
   • Estrogen-driven repair promotes abnormal gland invasion.
3. De novo metaplasia
   • Müllerian remnants or stem cells within myometrium transform into endometrial tissue.
4. Inflammatory and hormonal mechanisms
   • Local estrogen production, prostaglandins, neuroangiogenesis, and chronic inflammation produce pain, bleeding, fibrosis, and uterine enlargement.

Risk factors

• Age 35-50 years
• Multiparity
• Prior uterine surgery or curettage
• Cesarean delivery
• Endometriosis
• Tamoxifen exposure
• High lifetime estrogen exposure

Clinical features

• Heavy menstrual bleeding
• Progressive secondary dysmenorrhea
• Globular enlarged tender uterus

• Chronic pelvic pain
• Deep dyspareunia
• Intermenstrual bleeding
• Infertility or recurrent pregnancy loss in some women
• Anemia due to heavy bleeding

Examination

• Enlarged, symmetrically globular uterus
• Soft/boggy or firm but tender uterus
• Usually mobile unless coexisting endometriosis/adhesions is present

Diagnosis

1. Transvaginal ultrasound

• Globular enlarged uterus
• Asymmetric myometrial thickening
• Heterogeneous myometrium
• Myometrial cysts
• Fan-shaped shadowing
• Irregular or interrupted junctional zone
• Linear striations

2. MRI

• Thickened junctional zone, often greater than 12 mm
• High-signal myometrial foci on T2 images
• Diffuse or focal adenomyoma

3. Histology

Differential diagnosis

• Uterine fibroids
• Endometriosis
• Endometrial hyperplasia/cancer
• Pregnancy-related uterine enlargement
• Chronic endometritis

Treatment

A. Medical treatment

1. NSAIDs

• Ibuprofen, naproxen, or mefenamic acid during menses.
• They reduce pain but do not remove disease.

2. Tranexamic acid

• Common regimen: 1 g orally three times daily during heavy bleeding days, according to local protocol.
• Avoid in active thromboembolism and assess thrombotic risk.

3. Levonorgestrel intrauterine system

• Reduces heavy menstrual bleeding
• Improves dysmenorrhea
• May reduce uterine volume
• Provides contraception

4. Combined hormonal contraceptives

• Cyclic or continuous use.
• Continuous use may better control dysmenorrhea and bleeding.

5. Progestins

• Dienogest 2 mg orally daily
• Norethisterone acetate
• Medroxyprogesterone acetate

6. GnRH agonists or antagonists

• GnRH agonists cause hypoestrogenism and can reduce uterine volume/pain.
• Add-back therapy is needed if treatment is prolonged because of hot flushes and bone loss.
• Symptoms may recur after discontinuation.

B. Fertility-preserving procedures

• Adenomyomectomy, technically difficult and associated with uterine scar risk in a future pregnancy.
• Uterine artery embolization, high-intensity focused ultrasound, and radiofrequency ablation may relieve symptoms in selected women, but their impact on future fertility/pregnancy requires specialist counseling.

C. Definitive treatment

Total hysterectomy is the definitive treatment for severe symptomatic adenomyosis in women who have completed childbearing and fail or decline conservative therapy.

Management of infertility

• Refer early to reproductive medicine.
• Control symptoms while preserving ovarian reserve.
• IVF may be needed in coexisting infertility factors.
• Evidence on prolonged GnRH agonist pretreatment before IVF is mixed, so treatment should be individualized.

Adenomyosis causes heavy menstrual bleeding, progressive dysmenorrhea, and a tender globular uterus. Transvaginal ultrasound is first-line, MRI clarifies uncertain cases, levonorgestrel IUS and progestins are important medical treatments, and hysterectomy is definitive treatment when fertility is no longer desired.

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20. Infertile marriage: evaluation of the infertile couple

English translation

Definition

• 12 months of regular unprotected intercourse, or
• 6 months if the female partner is aged 35 years or older.

Main principle

Infertility is a problem of the couple. Evaluate both partners simultaneously.

Major causes

• Male factor: about 30-40%
• Female factor: about 30-40%
• Combined male and female factors
• Unexplained infertility

• Ovulatory/endocrine disorders
• Tubal/peritoneal disease
• Endometriosis
• Uterine abnormalities
• Diminished ovarian reserve
• Cervical factors, less commonly isolated
• Age-related reduction in oocyte quality

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Stepwise evaluation scheme

A. Initial consultation of both partners

History in the female partner

• Duration of infertility and prior treatment
• Menstrual pattern, dysmenorrhea, dyspareunia
• Previous pregnancies, miscarriages, ectopic pregnancy
• Previous STI/PID, tuberculosis, pelvic surgery, appendicitis
• Contraceptive history
• Symptoms of PCOS, thyroid disease, hyperprolactinemia
• Medical disease and medication
• Smoking, alcohol, weight, exercise
• Family history of early menopause/genetic disease

History in the male partner

• Previous paternity
• Puberty, mumps orchitis, testicular trauma, varicocele
• STI, genital surgery, hernia repair
• Erectile/ejaculatory dysfunction
• Testosterone/anabolic steroid use
• Smoking, alcohol, recreational drugs
• Heat exposure, toxins, chemotherapy/radiation
• Medication and systemic disease

Sexual history

• Frequency of intercourse: ideally every 1-2 days during fertile window.
• Pain, vaginismus, erectile dysfunction.
• Lubricants, because some can impair sperm motility.

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B. Examination

Female

• Height, weight, BMI
• Thyroid signs
• Galactorrhea
• Acne, hirsutism, acanthosis nigricans
• Pelvic examination for uterine size, fibroids, adnexal mass, cervical disease, tenderness, fixed retroverted uterus/endometriosis signs

Male

• Secondary sexual characteristics
• Testicular volume and consistency
• Epididymis and vas deferens
• Varicocele
• Penile abnormalities
• Prostate examination when indicated

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C. Male-factor assessment

Semen analysis

• Obtain after 2-7 days of abstinence.
• Repeat if abnormal because semen quality varies.
• Assess volume, sperm concentration, total sperm number, motility, morphology, vitality, and leukocytes.

• Repeat analysis.
• Refer to andrologist/urologist.
• Hormonal testing: FSH, LH, testosterone, prolactin when severe oligospermia/azoospermia or hypogonadism is suspected.
• Scrotal ultrasound for varicocele/mass if indicated.
• Genetic testing in azoospermia or severe oligospermia where appropriate.

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D. Female assessment

1. Confirmation of ovulation

• Menstrual history: regular 21-35-day cycles often suggest ovulation.
• Mid-luteal progesterone approximately 7 days before expected menstruation.
• Follicular monitoring by transvaginal ultrasound if needed.
• Ovulation-prediction kits may be supportive.
• Basal body temperature is not routinely recommended as a diagnostic test.

2. Ovarian reserve assessment

• Anti-Müllerian hormone
• Antral follicle count on transvaginal ultrasound
• FSH and estradiol early in cycle, usually day 2-5

3. Endocrine testing

• TSH
• Prolactin
• FSH/LH/estradiol in amenorrhea/oligomenorrhea
• Testosterone, DHEAS, 17-hydroxyprogesterone if hyperandrogenism
• HbA1c/glucose and lipids in PCOS or obesity

4. Uterine and ovarian assessment

• Uterine fibroids, especially cavity-distorting lesions
• Endometrial polyps
• Adenomyosis
• Ovarian reserve/antral follicles
• Endometrioma
• Hydrosalpinx
• Adnexal mass

5. Tubal patency assessment

• Hysterosalpingography: common first-line test for tubal patency and uterine cavity outline.
• HyCoSy/hysterosalpingo-contrast sonography where available.
• Laparoscopy with chromopertubation:
  • Indicated when endometriosis, pelvic adhesions, previous PID/ectopic pregnancy, or pelvic pathology is suspected.
  • It is not mandatory for every infertile woman.

6. Uterine cavity assessment

• Saline infusion sonography
• Hysteroscopy if polyp, submucosal fibroid, intrauterine adhesions, abnormal HSG, or recurrent implantation failure is suspected.

E. Additional tests only when indicated

• Genetic testing
• Antiphospholipid antibody testing for recurrent pregnancy loss, not routine infertility
• Infection screening according to risk/ART requirements
• Laparoscopy for suspected endometriosis or adhesions
• Endometrial biopsy is not routine for “luteal phase defect”

Unexplained infertility

• Semen analysis is normal
• Ovulation is confirmed
• Tubes are patent
• Uterine cavity is normal
• No clear female or male cause is identified

Counseling and initial management

• Folic acid for the female partner
• Healthy BMI, smoking cessation, avoid recreational drugs
• Limit alcohol
• Optimize diabetes, thyroid disease, and chronic illness
• Timed intercourse
• Discuss age-related fertility decline
• Psychological support

The basic infertility workup includes simultaneous semen analysis, confirmation of ovulation, assessment of ovarian reserve where appropriate, transvaginal ultrasound, evaluation of tubal patency, and assessment of the uterine cavity. Unexplained infertility is a diagnosis of exclusion.

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21. Cancer of the vulva and vagina

English translation

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A. Vulvar cancer

Definition and frequency

Classification

Histological types

• Squamous cell carcinoma, most common
• Melanoma
• Basal cell carcinoma
• Bartholin gland carcinoma
• Adenocarcinoma
• Sarcoma
• Extramammary Paget disease

Pathogenetic pathways of vulvar squamous carcinoma

1. HPV-associated pathway
   • Usually younger women.
   • Associated with vulvar high-grade squamous intraepithelial lesion.
   • Often HPV 16-related.
2. HPV-independent pathway
   • Usually older women.
   • Often associated with lichen sclerosus and differentiated vulvar intraepithelial neoplasia.
   • Often more aggressive.

Clinical features

• Persistent vulvar pruritus is a key warning sign.
• Vulvar lump, thickened plaque, ulcer, wart-like lesion, pigmentation change, or non-healing sore
• Pain, burning, bleeding, discharge
• Dyspareunia
• Dysuria if lesion near urethra
• Enlarged inguinal nodes in advanced disease

Diagnosis

1. Careful inspection of entire vulva, perineum, clitoris, and perianal area.
2. Palpation of inguinal-femoral lymph nodes.
3. Biopsy any suspicious lesion.
   • Punch biopsy or incisional biopsy.
   • Do not excise a large lesion before diagnosis/staging planning.
4. Colposcopic/vulvoscopic assessment where available.
5. Imaging, CT/MRI/PET-CT, for large lesions, suspicious nodes, or advanced disease.
6. Examination under anesthesia, cystoscopy/proctoscopy when bladder/rectal involvement is suspected.

Treatment

Early localized disease

• Wide local excision with histologically clear margins.
• Radical local excision is preferred over radical vulvectomy where possible, to preserve anatomy and function.
• Sentinel lymph-node biopsy is used for selected unifocal early tumors with clinically negative groin nodes.

Clinically positive groin nodes or larger lesions

• Inguinofemoral lymph-node dissection and/or radiotherapy.
• Chemoradiotherapy may be used for advanced disease or unresectable lesions.

Advanced disease

• Primary chemoradiation, often cisplatin-based, may reduce the need for exenterative surgery.
• Pelvic exenteration is reserved for selected central recurrence or extensive disease.

Prevention

• HPV vaccination
• Smoking cessation
• Diagnosis and treatment of VIN
• Long-term monitoring/treatment of lichen sclerosus
• Prompt biopsy of any persistent vulvar lesion or pruritus

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B. Vaginal cancer

Definition

Risk factors

• Persistent high-risk HPV
• Previous cervical intraepithelial neoplasia or cervical cancer
• Smoking
• Immunosuppression/HIV
• Prior pelvic radiation
• In utero diethylstilbestrol exposure, associated with clear-cell adenocarcinoma

Clinical features

• Postcoital bleeding
• Postmenopausal bleeding
• Watery or blood-stained discharge
• Vaginal mass/ulcer
• Pelvic pain, dyspareunia
• Urinary or rectal symptoms in advanced disease

Diagnosis

• Speculum examination of the entire vagina.
• Colposcopy/vaginoscopy.
• Directed biopsy.
• Examination of cervix to exclude cervical primary.
• MRI/CT/PET-CT for local and distant staging.
• Cystoscopy/proctoscopy if organ invasion is suspected.

Treatment

• External beam radiotherapy plus brachytherapy
• Chemoradiotherapy for selected advanced disease, often cisplatin-based

• Small upper-vaginal lesions
• Selected early tumors
• Recurrence after radiotherapy in highly selected patients

Prognosis

• Stage
• Tumor size
• Histological type
• Nodal involvement
• Age and comorbidity

Any persistent vulvar ulcer, pigmented lesion, mass, or pruritus requires biopsy. Vulvar cancer is usually treated with radical local excision and appropriate groin-node assessment. Primary vaginal cancer is rare and is treated mainly with radiotherapy.

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22. Delayed puberty

English translation

Definition

• No breast development by age 13 years, or
• No menarche by age 15 years, or
• More than 3 years between the onset of breast development and menarche.

Classification

1. Constitutional delay of growth and puberty

• Normal variant.
• Often family history of late puberty.
• Delayed bone age.
• Usually normal eventual sexual development.

2. Hypergonadotropic hypogonadism

• Turner syndrome
• Gonadal dysgenesis
• Primary ovarian insufficiency
• Chemotherapy/radiation-related ovarian failure
• Autoimmune oophoritis

3. Hypogonadotropic hypogonadism

• Functional hypothalamic amenorrhea: malnutrition, eating disorder, excessive exercise, chronic stress
• Chronic systemic disease
• Kallmann syndrome
• Pituitary tumor or pituitary injury
• Hyperprolactinemia
• Hypothyroidism

4. Anatomical disorders with normal hormonal development

• Müllerian agenesis
• Imperforate hymen
• Transverse vaginal septum
• Androgen-insensitivity syndrome

Clinical features

• No breast development or incomplete secondary sexual characteristics
• Primary amenorrhea
• Short stature or dysmorphic features in Turner syndrome
• Low body weight, excessive exercise, eating disorder signs
• Headache/visual symptoms in pituitary lesion
• Absent sense of smell in Kallmann syndrome
• Cyclic pelvic pain in outflow obstruction
• Normal breast development with absent/short vagina in Müllerian agenesis

Diagnosis

History

• Growth pattern and onset of puberty in family
• Nutritional status, exercise, stress, eating disorder
• Chronic illness, chemotherapy/radiotherapy
• Headache, visual symptoms, galactorrhea
• Sense of smell
• Medications
• Cyclic pain
• Family history of genetic disease/early menopause

Examination

• Height, weight, BMI, growth chart
• Tanner staging of breasts and pubic hair
• Signs of Turner syndrome
• Thyroid examination
• Visual fields if pituitary lesion suspected
• External genital examination
• Pelvic ultrasound if uterus/vagina cannot be clinically assessed

Investigations

• Pregnancy test in any postmenarchal possibility
• FSH, LH, estradiol
• TSH and free T4
• Prolactin
• CBC, ESR/CRP, renal/liver function if chronic disease suspected
• Androgen profile/17-hydroxyprogesterone if virilization
• Bone age X-ray
• Pelvic ultrasound
• Karyotype if high FSH, short stature, primary amenorrhea, dysmorphism, or suspected gonadal dysgenesis
• MRI pituitary/brain if low gonadotropins, hyperprolactinemia, headache, visual symptoms, or suspected central lesion

Treatment

Constitutional delay

• Reassurance and regular follow-up.
• Optimize nutrition and treat chronic illness.
• In selected distressed adolescents, short-course low-dose estrogen may be used under pediatric endocrine supervision.

Hypergonadotropic hypogonadism

• Gradual estrogen replacement to induce puberty.
• Start low dose, then increase over 2-3 years.
• Add cyclic progesterone after adequate estrogenization/endometrial development or breakthrough bleeding.
• Continue hormone replacement for bone and cardiovascular health.
• Treat associated disease, for example Turner syndrome multidisciplinary care.

Hypogonadotropic hypogonadism

• Correct nutrition and reduce excessive exercise.
• Treat eating disorder and psychological stress.
• Treat hypothyroidism with levothyroxine.
• Treat hyperprolactinemia, often with a dopamine agonist after cause assessment.
• Treat pituitary tumor as indicated.
• Pubertal induction with estrogen if endogenous recovery does not occur.

Outflow obstruction

• Imperforate hymen: hymenotomy/hymenectomy.
• Vaginal septum/atresia: reconstructive surgery in specialist center.
• Müllerian agenesis: progressive dilation first-line; surgery only in selected cases.

Prevention

• Early recognition of eating disorders and chronic illness
• Adequate adolescent nutrition
• Avoid excessive training without nutritional support
• Genetic counseling where appropriate
• Timely specialist referral for absent puberty or primary amenorrhea

Delayed puberty is classified into constitutional delay, hypergonadotropic hypogonadism, hypogonadotropic hypogonadism, and anatomical outflow anomalies. FSH/LH/estradiol, pelvic ultrasound, bone age, and karyotyping are central to diagnosis. Treatment is directed at the cause and includes gradual estrogen induction when ovarian or central estrogen deficiency is present.

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23. Uterine fibroids: operative treatment

English translation

Indications for intervention

• Heavy menstrual bleeding causing anemia despite medical therapy
• Large symptomatic fibroids causing pressure, pain, urinary or bowel symptoms
• Submucosal fibroid causing heavy bleeding or infertility
• Infertility/recurrent miscarriage with cavity-distorting submucosal or selected intramural fibroid
• Rapid enlargement after menopause or uncertain diagnosis
• Degeneration/torsion of pedunculated fibroid causing acute symptoms
• Suspicion of sarcoma, although this is uncommon
• Patient preference after informed counseling

• Age
• Fertility desire
• Number, size, and location of fibroids
• Uterine size
• Severity of bleeding/anemia
• Coexisting adenomyosis/endometriosis
• Risk of malignancy
• Previous surgery and surgical expertise

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A. Fertility-preserving surgery: myomectomy

Types of myomectomy

1. Hysteroscopic myomectomy

• Performed transcervically with hysteroscopic resectoscope or mechanical morcellator.
• Resects FIGO type 0, 1, and selected type 2 submucosal fibroids.
• Particularly useful for heavy bleeding and infertility caused by cavity distortion.

• Uterine perforation
• Fluid overload/hyponatremia with hypotonic distension media
• Bleeding
• Infection
• Intrauterine adhesions
• Incomplete resection for deep/large type 2 fibroid

2. Laparoscopic or robotic myomectomy

• Less pain
• Faster recovery
• Shorter hospital stay
• Less adhesion formation than open surgery in suitable cases

• Technically demanding
• Large, numerous, deeply intramural fibroids may require open surgery
• Requires careful multilayer myometrial closure to reduce future rupture risk

3. Open abdominal myomectomy

• Very large uterus
• Multiple fibroids
• Deep intramural/cervical fibroids
• Need for extensive reconstruction
• Concern for significant bleeding or technical difficulty

Preoperative preparation

• CBC, ferritin, correction of anemia using oral/IV iron.
• Blood group and crossmatch where major blood loss is possible.
• Ultrasound or MRI mapping.
• Consider temporary preoperative GnRH agonist/antagonist in selected women to reduce bleeding and improve anemia, recognizing that it may obscure tissue planes.
• Counsel on recurrence, adhesions, future cesarean possibility depending on depth/cavity entry, and small risk of hysterectomy for uncontrollable bleeding.

Hemorrhage reduction during myomectomy

• Vasopressin infiltration into myometrium where institutionally approved and safely monitored
• Uterine artery occlusion/tourniquet in selected procedures
• Tranexamic acid where appropriate
• Meticulous layered closure and hemostasis
• Cell salvage in selected high-risk surgery

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B. Definitive surgery: hysterectomy

Indications

• Completed childbearing
• Severe symptoms refractory to conservative treatment
• Large/multiple recurrent fibroids
• Patient chooses definitive treatment
• Suspicion of malignancy
• Coexisting uterine pathology requiring hysterectomy

Surgical routes

1. Vaginal hysterectomy
   • Best when uterus is not excessively enlarged and vaginal access is adequate.
2. Laparoscopic hysterectomy
   • Total laparoscopic, laparoscopic-assisted vaginal, or robotic approaches.
   • Useful for moderate-sized uterus when expertise is available.
3. Abdominal hysterectomy
   • For very large uterus, extensive adhesions, suspected cancer, or when minimally invasive route is unsafe.

Extent of surgery

• Total hysterectomy: removal of uterine body and cervix. Usually preferred over subtotal hysterectomy for benign fibroids unless there is a specific reason otherwise.
• Subtotal/supracervical hysterectomy: cervix remains. Cervical screening must continue and cyclic bleeding can rarely persist.
• Bilateral salpingectomy may be performed opportunistically to reduce future epithelial ovarian cancer risk while preserving ovaries.
• Ovaries should generally be conserved in younger premenopausal women unless diseased, high-risk genetic status exists, or another indication is present.

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C. Uterine-sparing interventional alternatives

Uterine artery embolization

• Catheter-based occlusion of uterine arteries causing fibroid ischemia and shrinkage.
• Effective for bleeding and bulk symptoms.
• Not ideal for women strongly desiring future fertility because reproductive outcomes are less certain than after myomectomy.

MR-guided focused ultrasound or radiofrequency ablation

• Selected women with suitable fibroid location.
• May reduce symptoms with less invasive treatment.
• Need counseling regarding future fertility and access to expertise.

Important postoperative issues

• Histopathology of removed tissue.
• Monitor hemorrhage, infection, DVT, urinary tract/bowel injury.
• After myomectomy: counsel about recurrence and pregnancy planning.
• After hysteroscopic myomectomy: assess for adhesions if infertility persists.

Hysteroscopic myomectomy is the operation of choice for symptomatic submucosal fibroids. Laparoscopic or open myomectomy preserves fertility for intramural/subserosal disease. Hysterectomy is definitive treatment for women with severe symptoms who have completed childbearing.

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24. Ovarian cancer

English translation

Definition

Classification

A. Epithelial ovarian tumors

• High-grade serous carcinoma, most common and aggressive
• Low-grade serous carcinoma
• Endometrioid carcinoma
• Clear-cell carcinoma
• Mucinous carcinoma
• Brenner tumor, rare

B. Germ-cell tumors

• Dysgerminoma
• Yolk sac tumor
• Immature teratoma
• Embryonal carcinoma
• Choriocarcinoma
• Mixed germ-cell tumor

C. Sex cord-stromal tumors

• Granulosa cell tumor
• Thecoma/fibroma
• Sertoli-Leydig cell tumor

D. Metastatic tumors

• Krukenberg tumor, typically metastatic gastrointestinal adenocarcinoma
• Breast, colorectal, gastric, pancreatic cancers

Risk factors

• Increasing age
• Family history of ovarian/breast cancer
• BRCA1/BRCA2 pathogenic variant
• Lynch syndrome
• Nulliparity/infertility in some cases
• Endometriosis, associated with clear-cell and endometrioid carcinoma
• Postmenopausal state

• Combined oral contraceptives
• Pregnancy and breastfeeding
• Tubal ligation/salpingectomy
• Risk-reducing salpingo-oophorectomy in high-risk genetic patients after counseling

Clinical features

• Abdominal bloating or increased abdominal size
• Pelvic or abdominal pain
• Early satiety/loss of appetite
• Urinary urgency/frequency
• Change in bowel habit, constipation
• Fatigue and weight loss
• Ascites, dyspnea from pleural effusion
• Palpable pelvic/abdominal mass

Examination

• Adnexal or fixed pelvic mass
• Ascites
• Nodularity in pouch of Douglas
• Umbilical nodule, enlarged supraclavicular node, or pleural effusion in advanced disease

Diagnosis

1. Pelvic ultrasound

• Solid component/papillary projections
• Thick septa
• Irregular surface
• Bilateral complex mass
• Ascites
• Increased vascularity
• Peritoneal nodules

2. Tumor markers

• CA-125 is useful in postmenopausal women and for treatment monitoring, but is not a screening test.
• It can rise in benign conditions: endometriosis, fibroids, menstruation, pregnancy, liver disease, and PID.
• HE4 and risk algorithms may assist selected cases.
• In young women with suspected germ-cell tumor: AFP, beta-hCG, LDH.
• In suspected sex-cord stromal tumor: inhibin and other markers may be useful.

3. Imaging for staging

• CT chest, abdomen, and pelvis for suspected advanced epithelial cancer.
• MRI for characterization of indeterminate adnexal mass.
• PET-CT is used selectively.

4. Histological diagnosis and staging

FIGO staging: simplified

Treatment

A. Epithelial ovarian cancer

1. Primary cytoreductive surgery

• Total hysterectomy
• Bilateral salpingo-oophorectomy
• Omentectomy
• Peritoneal washings
• Peritoneal biopsies and resection of visible disease
• Pelvic/para-aortic nodal assessment when indicated
• Bowel, diaphragm, spleen, or other organ resection when required to achieve no gross residual disease

The goal is complete cytoreduction: no visible residual tumor whenever possible.

2. Adjuvant chemotherapy

• Carboplatin plus paclitaxel, commonly every 3 weeks for about 6 cycles.

3. Neoadjuvant chemotherapy and interval debulking surgery

• Disease is too extensive for complete primary cytoreduction
• Patient is medically unfit for major initial surgery
• Diagnostic biopsy confirms epithelial ovarian cancer

1. Tissue diagnosis
2. Platinum-taxane chemotherapy, usually 3 cycles
3. Interval cytoreductive surgery if response/stability
4. Additional chemotherapy

4. Maintenance therapy

• PARP inhibitor maintenance, especially with BRCA mutation or homologous recombination deficiency
• Bevacizumab in selected high-risk advanced disease, sometimes continued as maintenance
• Choice depends on molecular testing, stage, response, toxicity, and access

5. Recurrent disease

• Interval from previous platinum therapy
• BRCA/HRD and prior treatment
• Disease distribution
• Performance status
• Symptoms and patient goals

• Platinum-based chemotherapy for platinum-sensitive recurrence
• Non-platinum chemotherapy for platinum-resistant recurrence
• Targeted agents, antiangiogenic therapy, selected immunotherapy approaches
• Secondary cytoreductive surgery only in highly selected cases
• Early palliative care, symptom control, ascites management, nutritional and psychological support

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B. Fertility-sparing treatment

• Stage IA, low-grade epithelial tumor
• Selected germ-cell tumors
• Selected sex cord-stromal tumors

• Unilateral salpingo-oophorectomy
• Full surgical staging
• Preservation of uterus and opposite ovary if safe

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C. Germ-cell tumors

• Fertility-sparing unilateral salpingo-oophorectomy and staging
• Chemotherapy for malignant/high-risk tumors, commonly BEP:
  • Bleomycin
  • Etoposide
  • Cisplatin

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Prevention

Average-risk women

• Combined hormonal contraception for eligible women
• Avoid smoking
• Consider opportunistic salpingectomy during pelvic surgery after informed consent

High-risk women

• Genetic counseling/testing for those with strong family history or known familial BRCA/Lynch syndrome.
• Risk-reducing bilateral salpingo-oophorectomy after completion of childbearing in women with pathogenic BRCA variants, timed according to the gene and family history.
• Screening may be considered temporarily in selected high-risk women who defer surgery, but it does not replace risk-reducing surgery.

Ovarian cancer often presents late with persistent bloating, pelvic pain, early satiety, and an adnexal mass or ascites. Diagnosis relies on ultrasound, CA-125 as an adjunct, staging imaging, and histology. Main treatment for epithelial ovarian cancer is complete cytoreductive surgery by a gynecologic oncologist followed by platinum-taxane chemotherapy, with targeted maintenance therapy selected by molecular profile.