1. Critical care in pregnancy - physiological changes, shock, sepsis, respiratory failure, cardiac disease, and ICU monitoring.
2. Obstetric emergencies - postpartum hemorrhage, eclampsia, sepsis, uterine rupture, embolism, and massive transfusion.
3. Tactical obstetric decision-making - when to stabilize the mother first, timing and mode of delivery, fetal monitoring, multidisciplinary escalation, and transfer to a higher-level center.
4. Special procedures - airway management, ventilation, vasopressors, resuscitation, blood products, anesthesia, and perimortem cesarean delivery.
5. ICU organization - communication between obstetricians, anesthetists, intensivists, neonatologists, blood bank, and operating theatre.

1. Maternal resuscitation
   • Use standard ABCDE assessment.
   • Give high-flow oxygen when indicated, obtain IV/IO access, monitor continuously.
   • In cardiac arrest after about 20 weeks, manually displace the uterus to the left to relieve aortocaval compression.
   • Consider resuscitative cesarean delivery if return of spontaneous circulation is not achieved promptly.
2. Obstetric hemorrhage
   • Recognize and treat postpartum hemorrhage immediately.
   • Uterine massage, uterotonics, tranexamic acid early, blood-product resuscitation, correction of hypothermia/acidosis/coagulopathy.
   • Escalate to balloon tamponade, compression sutures, arterial embolization, or hysterectomy when needed.
3. Hypertensive emergency and eclampsia
   • Stabilize airway and prevent injury during seizures.
   • Magnesium sulfate is used for seizure prevention/treatment.
   • Treat severe hypertension urgently with appropriate antihypertensives.
   • Definitive management is delivery once the mother is stabilized.
4. Sepsis in pregnancy/postpartum
   • Obtain cultures when feasible but do not delay antibiotics.
   • Start broad-spectrum antimicrobials, fluids, source control, and vasopressors if shock persists.
   • Consider obstetric sources such as chorioamnionitis, septic abortion, pyelonephritis, endometritis, and retained products.
5. Respiratory failure
   • Pregnancy increases oxygen consumption and reduces functional residual capacity, so hypoxemia can develop rapidly.
   • Escalate early from oxygen to ventilatory support when needed.
   • In late pregnancy, airway management may be difficult and aspiration risk is increased.
6. Venous thromboembolism and pulmonary embolism
   • Pregnancy and the puerperium are hypercoagulable states.
   • Suspect PE in acute dyspnea, chest pain, syncope, tachycardia, or unexplained hypoxemia.
   • Stabilize first, then investigate and anticoagulate when indicated.
7. Timing and mode of delivery
   • Delivery is not automatically required solely because a patient is in ICU.
   • It may be therapeutic or life-saving in conditions such as uncontrolled hemorrhage, eclampsia/HELLP syndrome, severe maternal deterioration, fetal compromise, or when uterine size interferes with maternal resuscitation or ventilation.
   • Decisions require joint input from obstetrics, anesthesia, ICU, neonatology, and relevant specialists.
8. Team tactics
   • Activate an obstetric emergency/major hemorrhage protocol early.
   • Assign clear roles: airway, circulation, medications, documentation, blood bank liaison, obstetric procedure lead, neonatal team.
   • Use closed-loop communication and frequent reassessment.
   • Arrange early transfer to a higher-level maternal critical-care center if needed.

Intensive Care and Obstetric Tactics

Resuscitate and stabilize the mother first.
Maternal oxygenation, circulation, and treatment of the underlying cause are the best initial treatment for the fetus.

1. Goals of obstetric intensive care

1. Identify life-threatening maternal illness early.
2. Support airway, breathing, circulation, renal function, and neurologic status.
3. Diagnose and treat the underlying cause rapidly.
4. Monitor fetal well-being when the fetus is viable and monitoring will alter management.
5. Decide the safest timing, place, and method of delivery.
6. Prevent complications such as hemorrhage, thromboembolism, aspiration, renal failure, disseminated intravascular coagulation, and multiorgan dysfunction.

2. Why pregnancy changes intensive-care management

Cardiovascular changes

• Blood volume and cardiac output increase.
• Heart rate rises modestly.
• Systemic vascular resistance falls, so blood pressure may be lower than before pregnancy.
• A pregnant woman may lose a substantial blood volume before hypotension becomes obvious.

Respiratory changes

• Oxygen consumption rises.
• Functional residual capacity decreases because the uterus elevates the diaphragm.
• Pregnancy-related progesterone causes mild chronic respiratory alkalosis.

Hematologic changes

• Plasma volume increases more than red-cell mass, causing physiological anemia.
• Pregnancy is a hypercoagulable state.
• Fibrinogen is physiologically elevated.

Aortocaval compression

3. Indications for ICU or high-dependency care

• Respiratory failure, severe hypoxemia, need for noninvasive or invasive ventilation
• Septic shock or persistent hypotension
• Massive obstetric hemorrhage or major transfusion requirement
• Severe pre-eclampsia, eclampsia, HELLP syndrome, pulmonary edema, or stroke
• Acute kidney injury with oliguria, electrolyte disturbance, or need for renal replacement therapy
• Cardiac disease with heart failure, arrhythmia, cardiomyopathy, pulmonary hypertension, or ischemia
• Major trauma, burns, poisoning, or postoperative complications
• Severe diabetic ketoacidosis
• Acute liver failure or acute fatty liver of pregnancy
• Thromboembolism or suspected massive pulmonary embolism
• Altered consciousness, seizures, coma, or intracranial hemorrhage
• Multiorgan dysfunction.

4. Initial approach: ABCDE with obstetric modifications

A. Airway

• Reduced consciousness
• Recurrent seizures
• Severe respiratory distress
• Massive bleeding with aspiration risk
• Severe agitation or inability to cooperate with treatment
• Need for emergency surgery.

Obstetric airway tactics

• Anticipate difficult intubation because of airway edema, weight gain, enlarged breasts, and reduced oxygen reserve.
• Pre-oxygenate thoroughly.
• Use appropriately sized equipment, often a smaller endotracheal tube may be required.
• Have a difficult-airway plan and senior anesthesia support.
• Treat every emergency general anesthetic in pregnancy as an aspiration-risk situation.

B. Breathing

• Supplemental oxygen
• Noninvasive respiratory support in carefully selected patients
• Mechanical ventilation if respiratory failure occurs
• Treatment of pneumonia, asthma, pulmonary edema, pulmonary embolism, aspiration, or acute respiratory distress syndrome.

Ventilation principle

C. Circulation

• Pulse and blood pressure
• Capillary refill and peripheral perfusion
• Urine output
• Mental state
• Lactate and blood gases
• Hemoglobin, coagulation studies, fibrinogen, renal and liver function.

• Establish large-bore IV access or intraosseous access if required.
• Send blood for grouping, cross-matching, full blood count, coagulation tests, fibrinogen, renal/liver tests, and blood gases.
• Give balanced fluid resuscitation when appropriate.
• Use blood products early in major hemorrhage.
• Start vasopressors if shock persists after adequate resuscitation and the cause requires them.
• Use invasive arterial pressure monitoring when instability persists or frequent blood sampling is necessary.

D. Disability

• Consciousness level
• Pupils and focal neurologic signs
• Blood glucose
• Seizures
• Headache, visual symptoms, hyperreflexia, and clonus in possible severe pre-eclampsia/eclampsia.

E. Exposure and examination

• Bleeding
• Rash or infection source
• Leg swelling or signs of thrombosis
• Abdominal tenderness or uterine rigidity
• Wound infection
• Breast, perineal, or operative-site infection
• Trauma signs.

5. Maternal monitoring in ICU

• Continuous ECG
• Oxygen saturation
• Respiratory rate
• Frequent blood pressure measurement, often invasive arterial monitoring
• Temperature
• Strict fluid balance and hourly urine output
• Serial blood gases and lactate in shock or respiratory failure
• Hemoglobin, platelets, coagulation profile, fibrinogen, renal and liver function
• Central venous access if vasoactive drugs, difficult access, or frequent sampling is needed
• Echocardiography when cardiac dysfunction, pulmonary edema, or shock cause is uncertain.

6. Fetal assessment in the critically ill mother

• Intermittent fetal heart auscultation
• Cardiotocography
• Ultrasound for fetal heart activity, growth, amniotic fluid, placental location, and Doppler assessment.

Key tactical rule

1. The fetus is potentially viable.
2. The mother consents where possible.
3. Staff and facilities are available to act on an abnormal result.
4. Emergency delivery would be considered if fetal compromise is detected.

7. Obstetric tactics: deciding about delivery

Reasons delivery may be required

Maternal indications

• Uncontrollable postpartum or antepartum hemorrhage
• Severe pre-eclampsia/eclampsia or HELLP syndrome after stabilization
• Acute fatty liver of pregnancy
• Chorioamnionitis or uterine infection requiring source control
• Worsening maternal organ failure where pregnancy is contributing substantially
• Severe cardiopulmonary compromise in which the gravid uterus impedes ventilation or circulation
• Uterine rupture, placental abruption, or other surgical catastrophe.

Fetal indications

• Persistent severe fetal compromise despite maternal optimization
• Cord prolapse
• Placental abruption with a live compromised fetus
• Nonreassuring fetal status where prompt delivery is feasible and appropriate.

Timing

• Pregnancy can safely continue while maternal treatment proceeds
• Delivery should occur after initial stabilization
• Immediate delivery is necessary as part of resuscitation or source control.

Mode of delivery

• Vaginal delivery is often preferred if the mother is stable and delivery is likely to be rapid, because it avoids surgery, anesthesia, and additional blood loss.
• Cesarean delivery is needed for standard obstetric indications, fetal emergency, severe maternal deterioration requiring immediate delivery, uterine rupture, major placental abruption, or when rapid delivery is essential.

• Labor room for a stable patient likely to deliver vaginally
• Operating theater for anticipated cesarean, hemorrhage, or need for anesthesia
• ICU only in exceptional circumstances when transfer is unsafe and resources are available.

8. Major obstetric emergencies in intensive care

A. Obstetric hemorrhage

Causes

• Tone: uterine atony
• Trauma: genital tract laceration, uterine rupture, hematoma
• Tissue: retained placenta, placenta accreta spectrum
• Thrombin: coagulation disorder or DIC.

Tactical management

1. Call for help and activate a major obstetric hemorrhage protocol.
2. Assess ABCDE and quantify blood loss.
3. Massage the uterus and empty the bladder where relevant.
4. Give uterotonic treatment for atony according to local protocol.
5. Give tranexamic acid early in postpartum hemorrhage where indicated.
6. Obtain large-bore IV access and send urgent blood tests.
7. Start balanced transfusion if major bleeding continues.
8. Correct hypothermia, acidosis, hypocalcemia, and coagulopathy.
9. Identify and treat the cause:
   • Repair tears
   • Remove retained tissue
   • Use uterine balloon tamponade
   • Apply compression sutures or vessel ligation
   • Consider radiologic embolization where feasible
   • Perform hysterectomy without dangerous delay if bleeding cannot be controlled.

B. Severe pre-eclampsia, eclampsia, and HELLP syndrome

Warning features

• Severe hypertension
• Severe headache or visual symptoms
• Epigastric or right upper quadrant pain
• Pulmonary edema
• Thrombocytopenia
• Rising liver enzymes
• Acute kidney injury
• Seizures.

ICU management

• Protect the airway during seizures and place the patient laterally if possible.
• Magnesium sulfate is the standard anticonvulsant for eclampsia and seizure prevention in severe pre-eclampsia.
• Treat severe hypertension urgently with appropriate agents.
• Avoid unnecessary large-volume fluid administration because pulmonary edema is a major risk.
• Monitor urine output, reflexes, respiratory rate, platelet count, liver enzymes, renal function, and fetal status.
• Plan delivery after maternal stabilization. Delivery is definitive treatment for pre-eclampsia, but stabilization precedes transfer to theater whenever possible.

C. Sepsis and septic shock

Possible obstetric sources

• Chorioamnionitis
• Postpartum endometritis
• Septic abortion
• Retained products of conception
• Pyelonephritis
• Wound infection after cesarean delivery
• Necrotizing soft-tissue infection
• Mastitis or other non-obstetric infections.

Management tactics

1. Recognize sepsis early. Fever may be absent.
2. Obtain cultures if this does not delay treatment.
3. Give broad-spectrum IV antibiotics rapidly.
4. Measure lactate and assess organ dysfunction.
5. Resuscitate with fluids as clinically appropriate.
6. Start vasopressors if hypotension persists.
7. Achieve source control:
   • Evacuate retained infected tissue
   • Drain abscesses
   • Remove infected devices
   • Perform surgery when necessary.
8. Consider delivery if intrauterine infection or pregnancy itself is the source and maternal condition requires it.

D. Acute respiratory failure and pulmonary edema

• Severe pneumonia or viral infection
• Aspiration
• Asthma
• Pulmonary embolism
• Cardiomyopathy
• Fluid overload
• Severe pre-eclampsia
• ARDS
• Amniotic fluid embolism.

Management

• Provide oxygen and escalate respiratory support early.
• Use imaging and echocardiography as needed to distinguish pulmonary edema, embolism, pneumonia, and cardiac failure.
• Treat the cause: diuresis for cardiogenic pulmonary edema when appropriate, antibiotics for infection, anticoagulation for thromboembolism when indicated, and ventilatory support for ARDS.
• Consider whether delivery could improve ventilation in a late gestation patient, but do not assume it will reverse the underlying lung disease.

E. Venous thromboembolism and pulmonary embolism

• Sudden breathlessness
• Chest pain
• Syncope
• Tachycardia
• Unexplained hypoxemia
• Hemodynamic instability.

• Immediate resuscitation and oxygenation
• Diagnostic imaging when clinically indicated
• Anticoagulation when appropriate
• Specialist input for high-risk or massive PE, especially if shock is present.

F. Maternal cardiac arrest

Modified resuscitation

• Begin high-quality standard CPR immediately.
• Apply manual left uterine displacement after about 20 weeks of gestation.
• Manage the airway early and optimize oxygenation.
• Search for reversible causes, including hemorrhage, thromboembolism, eclampsia, sepsis, anesthetic complications, and amniotic fluid embolism.
• Prepare for resuscitative cesarean delivery if there is no rapid return of spontaneous circulation in a potentially viable pregnancy.

9. Fluid, blood, and coagulation tactics

Fluid strategy

• Give fluids according to the cause of shock and clinical response.
• Be cautious in pre-eclampsia, cardiac disease, renal failure, and pulmonary edema.
• Reassess frequently using clinical examination, blood pressure, urine output, lactate, bedside ultrasound, and echocardiography where available.

Massive transfusion

• Activate the massive hemorrhage protocol early.
• Use red cells, plasma, platelets, and fibrinogen replacement according to local laboratory results and protocol.
• Monitor ionized calcium, temperature, acid-base status, and coagulation continuously.
• Avoid delayed fibrinogen replacement when fibrinogen is low or falling in ongoing obstetric hemorrhage.

10. Practical team tactics

Early escalation

Clear role allocation

• Team leader
• Airway clinician
• Circulation/vascular access clinician
• Obstetric procedural lead
• Medication nurse
• Blood bank liaison
• Documentation nurse
• Neonatal team liaison.

Closed-loop communication

• “Activate major hemorrhage protocol.”
• “Tranexamic acid administered at 14:10.”
• “Four units of red cells are en route.”
• “Theatre is ready for laparotomy.”

Anticipate the next step

• Difficult airway
• Major transfusion
• Transfer to theater
• Emergency hysterectomy
• Neonatal resuscitation
• Renal replacement therapy
• Invasive monitoring
• Interventional radiology.

Debrief and documentation

• Document timeline, blood loss, drugs, transfusions, procedures, and decisions.
• Debrief the team.
• Provide psychological support and follow-up, especially after severe morbidity, stillbirth, hysterectomy, or ICU admission.

11. Summary algorithm

1. Recognize deterioration early.
2. ABCDE resuscitation with left uterine displacement in later pregnancy.
3. Call obstetric, anesthesia, ICU, neonatal, surgical, and blood-bank support early.
4. Identify the cause: hemorrhage, hypertension/eclampsia, sepsis, respiratory failure, thromboembolism, cardiac disease, or another medical/surgical problem.
5. Treat the cause immediately while supporting organs.
6. Monitor mother continuously and fetus when appropriate.
7. Decide whether delivery is needed for maternal stabilization, source control, fetal rescue, or obstetric indication.
8. Use early escalation and definitive treatment rather than repeated ineffective temporizing measures.

1. Regulation of the menstrual cycle
   • Hypothalamic-pituitary-ovarian axis
   • Follicular, ovulatory, and luteal phases
   • Endometrial changes and hormonal feedback
2. Dysmenorrhea
   • Primary versus secondary
   • Causes, assessment, red flags, and management
3. Amenorrhea
   • Primary versus secondary
   • Pregnancy exclusion, endocrine causes, ovarian and uterine causes, evaluation
4. Other menstrual-cycle disorders
   • Heavy menstrual bleeding
   • Abnormal uterine bleeding
   • Oligomenorrhea, polymenorrhea, irregular cycles
   • Premenstrual syndrome/PMDD and anovulatory bleeding

1. Critical care in pregnancy - physiological changes, shock, sepsis, respiratory failure, cardiac disease, and ICU monitoring.
2. Obstetric emergencies - postpartum hemorrhage, eclampsia, sepsis, uterine rupture, embolism, and massive transfusion.
3. Tactical obstetric decision-making - when to stabilize the mother first, timing and mode of delivery, fetal monitoring, multidisciplinary escalation, and transfer to a higher-level center.
4. Special procedures - airway management, ventilation, vasopressors, resuscitation, blood products, anesthesia, and perimortem cesarean delivery.
5. ICU organization - communication between obstetricians, anesthetists, intensivists, neonatologists, blood bank, and operating theatre.

1. Maternal resuscitation
   • Use standard ABCDE assessment.
   • Give high-flow oxygen when indicated, obtain IV/IO access, monitor continuously.
   • In cardiac arrest after about 20 weeks, manually displace the uterus to the left to relieve aortocaval compression.
   • Consider resuscitative cesarean delivery if return of spontaneous circulation is not achieved promptly.
2. Obstetric hemorrhage
   • Recognize and treat postpartum hemorrhage immediately.
   • Uterine massage, uterotonics, tranexamic acid early, blood-product resuscitation, correction of hypothermia/acidosis/coagulopathy.
   • Escalate to balloon tamponade, compression sutures, arterial embolization, or hysterectomy when needed.
3. Hypertensive emergency and eclampsia
   • Stabilize airway and prevent injury during seizures.
   • Magnesium sulfate is used for seizure prevention/treatment.
   • Treat severe hypertension urgently with appropriate antihypertensives.
   • Definitive management is delivery once the mother is stabilized.
4. Sepsis in pregnancy/postpartum
   • Obtain cultures when feasible but do not delay antibiotics.
   • Start broad-spectrum antimicrobials, fluids, source control, and vasopressors if shock persists.
   • Consider obstetric sources such as chorioamnionitis, septic abortion, pyelonephritis, endometritis, and retained products.
5. Respiratory failure
   • Pregnancy increases oxygen consumption and reduces functional residual capacity, so hypoxemia can develop rapidly.
   • Escalate early from oxygen to ventilatory support when needed.
   • In late pregnancy, airway management may be difficult and aspiration risk is increased.
6. Venous thromboembolism and pulmonary embolism
   • Pregnancy and the puerperium are hypercoagulable states.
   • Suspect PE in acute dyspnea, chest pain, syncope, tachycardia, or unexplained hypoxemia.
   • Stabilize first, then investigate and anticoagulate when indicated.
7. Timing and mode of delivery
   • Delivery is not automatically required solely because a patient is in ICU.
   • It may be therapeutic or life-saving in conditions such as uncontrolled hemorrhage, eclampsia/HELLP syndrome, severe maternal deterioration, fetal compromise, or when uterine size interferes with maternal resuscitation or ventilation.
   • Decisions require joint input from obstetrics, anesthesia, ICU, neonatology, and relevant specialists.
8. Team tactics
   • Activate an obstetric emergency/major hemorrhage protocol early.
   • Assign clear roles: airway, circulation, medications, documentation, blood bank liaison, obstetric procedure lead, neonatal team.
   • Use closed-loop communication and frequent reassessment.
   • Arrange early transfer to a higher-level maternal critical-care center if needed.

Resuscitate and stabilize the mother first.
Maternal oxygenation, circulation, and treatment of the underlying cause are the best initial treatment for the fetus.

1. Goals of obstetric intensive care

1. Identify life-threatening maternal illness early.
2. Support airway, breathing, circulation, renal function, and neurologic status.
3. Diagnose and treat the underlying cause rapidly.
4. Monitor fetal well-being when the fetus is viable and monitoring will alter management.
5. Decide the safest timing, place, and method of delivery.
6. Prevent complications such as hemorrhage, thromboembolism, aspiration, renal failure, disseminated intravascular coagulation, and multiorgan dysfunction.

2. Why pregnancy changes intensive-care management

Cardiovascular changes

• Blood volume and cardiac output increase.
• Heart rate rises modestly.
• Systemic vascular resistance falls, so blood pressure may be lower than before pregnancy.
• A pregnant woman may lose a substantial blood volume before hypotension becomes obvious.

Respiratory changes

• Oxygen consumption rises.
• Functional residual capacity decreases because the uterus elevates the diaphragm.
• Pregnancy-related progesterone causes mild chronic respiratory alkalosis.

Hematologic changes

• Plasma volume increases more than red-cell mass, causing physiological anemia.
• Pregnancy is a hypercoagulable state.
• Fibrinogen is physiologically elevated.

Aortocaval compression

3. Indications for ICU or high-dependency care

• Respiratory failure, severe hypoxemia, need for noninvasive or invasive ventilation
• Septic shock or persistent hypotension
• Massive obstetric hemorrhage or major transfusion requirement
• Severe pre-eclampsia, eclampsia, HELLP syndrome, pulmonary edema, or stroke
• Acute kidney injury with oliguria, electrolyte disturbance, or need for renal replacement therapy
• Cardiac disease with heart failure, arrhythmia, cardiomyopathy, pulmonary hypertension, or ischemia
• Major trauma, burns, poisoning, or postoperative complications
• Severe diabetic ketoacidosis
• Acute liver failure or acute fatty liver of pregnancy
• Thromboembolism or suspected massive pulmonary embolism
• Altered consciousness, seizures, coma, or intracranial hemorrhage
• Multiorgan dysfunction.

4. Initial approach: ABCDE with obstetric modifications

A. Airway

• Reduced consciousness
• Recurrent seizures
• Severe respiratory distress
• Massive bleeding with aspiration risk
• Severe agitation or inability to cooperate with treatment
• Need for emergency surgery.

Obstetric airway tactics

• Anticipate difficult intubation because of airway edema, weight gain, enlarged breasts, and reduced oxygen reserve.
• Pre-oxygenate thoroughly.
• Use appropriately sized equipment, often a smaller endotracheal tube may be required.
• Have a difficult-airway plan and senior anesthesia support.
• Treat every emergency general anesthetic in pregnancy as an aspiration-risk situation.

B. Breathing

• Supplemental oxygen
• Noninvasive respiratory support in carefully selected patients
• Mechanical ventilation if respiratory failure occurs
• Treatment of pneumonia, asthma, pulmonary edema, pulmonary embolism, aspiration, or acute respiratory distress syndrome.

Ventilation principle

C. Circulation

• Pulse and blood pressure
• Capillary refill and peripheral perfusion
• Urine output
• Mental state
• Lactate and blood gases
• Hemoglobin, coagulation studies, fibrinogen, renal and liver function.

• Establish large-bore IV access or intraosseous access if required.
• Send blood for grouping, cross-matching, full blood count, coagulation tests, fibrinogen, renal/liver tests, and blood gases.
• Give balanced fluid resuscitation when appropriate.
• Use blood products early in major hemorrhage.
• Start vasopressors if shock persists after adequate resuscitation and the cause requires them.
• Use invasive arterial pressure monitoring when instability persists or frequent blood sampling is necessary.

D. Disability

• Consciousness level
• Pupils and focal neurologic signs
• Blood glucose
• Seizures
• Headache, visual symptoms, hyperreflexia, and clonus in possible severe pre-eclampsia/eclampsia.

E. Exposure and examination

• Bleeding
• Rash or infection source
• Leg swelling or signs of thrombosis
• Abdominal tenderness or uterine rigidity
• Wound infection
• Breast, perineal, or operative-site infection
• Trauma signs.

5. Maternal monitoring in ICU

• Continuous ECG
• Oxygen saturation
• Respiratory rate
• Frequent blood pressure measurement, often invasive arterial monitoring
• Temperature
• Strict fluid balance and hourly urine output
• Serial blood gases and lactate in shock or respiratory failure
• Hemoglobin, platelets, coagulation profile, fibrinogen, renal and liver function
• Central venous access if vasoactive drugs, difficult access, or frequent sampling is needed
• Echocardiography when cardiac dysfunction, pulmonary edema, or shock cause is uncertain.

6. Fetal assessment in the critically ill mother

• Intermittent fetal heart auscultation
• Cardiotocography
• Ultrasound for fetal heart activity, growth, amniotic fluid, placental location, and Doppler assessment.

Key tactical rule

1. The fetus is potentially viable.
2. The mother consents where possible.
3. Staff and facilities are available to act on an abnormal result.
4. Emergency delivery would be considered if fetal compromise is detected.

7. Obstetric tactics: deciding about delivery

Reasons delivery may be required

Maternal indications

• Uncontrollable postpartum or antepartum hemorrhage
• Severe pre-eclampsia/eclampsia or HELLP syndrome after stabilization
• Acute fatty liver of pregnancy
• Chorioamnionitis or uterine infection requiring source control
• Worsening maternal organ failure where pregnancy is contributing substantially
• Severe cardiopulmonary compromise in which the gravid uterus impedes ventilation or circulation
• Uterine rupture, placental abruption, or other surgical catastrophe.

Fetal indications

• Persistent severe fetal compromise despite maternal optimization
• Cord prolapse
• Placental abruption with a live compromised fetus
• Nonreassuring fetal status where prompt delivery is feasible and appropriate.

Timing

• Pregnancy can safely continue while maternal treatment proceeds
• Delivery should occur after initial stabilization
• Immediate delivery is necessary as part of resuscitation or source control.

Mode of delivery

• Vaginal delivery is often preferred if the mother is stable and delivery is likely to be rapid, because it avoids surgery, anesthesia, and additional blood loss.
• Cesarean delivery is needed for standard obstetric indications, fetal emergency, severe maternal deterioration requiring immediate delivery, uterine rupture, major placental abruption, or when rapid delivery is essential.

• Labor room for a stable patient likely to deliver vaginally
• Operating theater for anticipated cesarean, hemorrhage, or need for anesthesia
• ICU only in exceptional circumstances when transfer is unsafe and resources are available.

8. Major obstetric emergencies in intensive care

A. Obstetric hemorrhage

Causes

• Tone: uterine atony
• Trauma: genital tract laceration, uterine rupture, hematoma
• Tissue: retained placenta, placenta accreta spectrum
• Thrombin: coagulation disorder or DIC.

Tactical management

1. Call for help and activate a major obstetric hemorrhage protocol.
2. Assess ABCDE and quantify blood loss.
3. Massage the uterus and empty the bladder where relevant.
4. Give uterotonic treatment for atony according to local protocol.
5. Give tranexamic acid early in postpartum hemorrhage where indicated.
6. Obtain large-bore IV access and send urgent blood tests.
7. Start balanced transfusion if major bleeding continues.
8. Correct hypothermia, acidosis, hypocalcemia, and coagulopathy.
9. Identify and treat the cause:
   • Repair tears
   • Remove retained tissue
   • Use uterine balloon tamponade
   • Apply compression sutures or vessel ligation
   • Consider radiologic embolization where feasible
   • Perform hysterectomy without dangerous delay if bleeding cannot be controlled.

B. Severe pre-eclampsia, eclampsia, and HELLP syndrome

Warning features

• Severe hypertension
• Severe headache or visual symptoms
• Epigastric or right upper quadrant pain
• Pulmonary edema
• Thrombocytopenia
• Rising liver enzymes
• Acute kidney injury
• Seizures.

ICU management

• Protect the airway during seizures and place the patient laterally if possible.
• Magnesium sulfate is the standard anticonvulsant for eclampsia and seizure prevention in severe pre-eclampsia.
• Treat severe hypertension urgently with appropriate agents.
• Avoid unnecessary large-volume fluid administration because pulmonary edema is a major risk.
• Monitor urine output, reflexes, respiratory rate, platelet count, liver enzymes, renal function, and fetal status.
• Plan delivery after maternal stabilization. Delivery is definitive treatment for pre-eclampsia, but stabilization precedes transfer to theater whenever possible.

C. Sepsis and septic shock

Possible obstetric sources

• Chorioamnionitis
• Postpartum endometritis
• Septic abortion
• Retained products of conception
• Pyelonephritis
• Wound infection after cesarean delivery
• Necrotizing soft-tissue infection
• Mastitis or other non-obstetric infections.

Management tactics

1. Recognize sepsis early. Fever may be absent.
2. Obtain cultures if this does not delay treatment.
3. Give broad-spectrum IV antibiotics rapidly.
4. Measure lactate and assess organ dysfunction.
5. Resuscitate with fluids as clinically appropriate.
6. Start vasopressors if hypotension persists.
7. Achieve source control:
   • Evacuate retained infected tissue
   • Drain abscesses
   • Remove infected devices
   • Perform surgery when necessary.
8. Consider delivery if intrauterine infection or pregnancy itself is the source and maternal condition requires it.

D. Acute respiratory failure and pulmonary edema

• Severe pneumonia or viral infection
• Aspiration
• Asthma
• Pulmonary embolism
• Cardiomyopathy
• Fluid overload
• Severe pre-eclampsia
• ARDS
• Amniotic fluid embolism.

Management

• Provide oxygen and escalate respiratory support early.
• Use imaging and echocardiography as needed to distinguish pulmonary edema, embolism, pneumonia, and cardiac failure.
• Treat the cause: diuresis for cardiogenic pulmonary edema when appropriate, antibiotics for infection, anticoagulation for thromboembolism when indicated, and ventilatory support for ARDS.
• Consider whether delivery could improve ventilation in a late gestation patient, but do not assume it will reverse the underlying lung disease.

E. Venous thromboembolism and pulmonary embolism

• Sudden breathlessness
• Chest pain
• Syncope
• Tachycardia
• Unexplained hypoxemia
• Hemodynamic instability.

• Immediate resuscitation and oxygenation
• Diagnostic imaging when clinically indicated
• Anticoagulation when appropriate
• Specialist input for high-risk or massive PE, especially if shock is present.

F. Maternal cardiac arrest

Modified resuscitation

• Begin high-quality standard CPR immediately.
• Apply manual left uterine displacement after about 20 weeks of gestation.
• Manage the airway early and optimize oxygenation.
• Search for reversible causes, including hemorrhage, thromboembolism, eclampsia, sepsis, anesthetic complications, and amniotic fluid embolism.
• Prepare for resuscitative cesarean delivery if there is no rapid return of spontaneous circulation in a potentially viable pregnancy.

9. Fluid, blood, and coagulation tactics

Fluid strategy

• Give fluids according to the cause of shock and clinical response.
• Be cautious in pre-eclampsia, cardiac disease, renal failure, and pulmonary edema.
• Reassess frequently using clinical examination, blood pressure, urine output, lactate, bedside ultrasound, and echocardiography where available.

Massive transfusion

• Activate the massive hemorrhage protocol early.
• Use red cells, plasma, platelets, and fibrinogen replacement according to local laboratory results and protocol.
• Monitor ionized calcium, temperature, acid-base status, and coagulation continuously.
• Avoid delayed fibrinogen replacement when fibrinogen is low or falling in ongoing obstetric hemorrhage.

10. Practical team tactics

Early escalation

Clear role allocation

• Team leader
• Airway clinician
• Circulation/vascular access clinician
• Obstetric procedural lead
• Medication nurse
• Blood bank liaison
• Documentation nurse
• Neonatal team liaison.

Closed-loop communication

• “Activate major hemorrhage protocol.”
• “Tranexamic acid administered at 14:10.”
• “Four units of red cells are en route.”
• “Theatre is ready for laparotomy.”

Anticipate the next step

• Difficult airway
• Major transfusion
• Transfer to theater
• Emergency hysterectomy
• Neonatal resuscitation
• Renal replacement therapy
• Invasive monitoring
• Interventional radiology.

Debrief and documentation

• Document timeline, blood loss, drugs, transfusions, procedures, and decisions.
• Debrief the team.
• Provide psychological support and follow-up, especially after severe morbidity, stillbirth, hysterectomy, or ICU admission.

11. Summary algorithm

1. Recognize deterioration early.
2. ABCDE resuscitation with left uterine displacement in later pregnancy.
3. Call obstetric, anesthesia, ICU, neonatal, surgical, and blood-bank support early.
4. Identify the cause: hemorrhage, hypertension/eclampsia, sepsis, respiratory failure, thromboembolism, cardiac disease, or another medical/surgical problem.
5. Treat the cause immediately while supporting organs.
6. Monitor mother continuously and fetus when appropriate.
7. Decide whether delivery is needed for maternal stabilization, source control, fetal rescue, or obstetric indication.
8. Use early escalation and definitive treatment rather than repeated ineffective temporizing measures.

1. Regulation of the menstrual cycle
   • Hypothalamic-pituitary-ovarian axis
   • Follicular, ovulatory, and luteal phases
   • Endometrial changes and hormonal feedback
2. Dysmenorrhea
   • Primary versus secondary
   • Causes, assessment, red flags, and management
3. Amenorrhea
   • Primary versus secondary
   • Pregnancy exclusion, endocrine causes, ovarian and uterine causes, evaluation
4. Other menstrual-cycle disorders
   • Heavy menstrual bleeding
   • Abnormal uterine bleeding
   • Oligomenorrhea, polymenorrhea, irregular cycles
   • Premenstrual syndrome/PMDD and anovulatory bleeding

1. Regulation of the menstrual cycle
2. Dysmenorrhea
3. Amenorrhea
4. Other menstrual disorders, including abnormal uterine bleeding, oligomenorrhea, polymenorrhea, PMS/PMDD, and anovulatory cycles

Regulation of Menstrual Cycle and Menstrual Disorders

1. Normal menstrual cycle

• Typical cycle interval in adults: about 24-38 days
• Menstrual bleeding duration: usually up to 8 days
• Normal blood loss is variable, but bleeding should not impair daily life or cause anemia.
• Day 1 is the first day of menstrual bleeding.

2. Hormonal regulation: hypothalamic-pituitary-ovarian axis

A. Hypothalamus

• Pulsatile GnRH is necessary for normal secretion of FSH and LH.
• Stress, severe weight loss, excessive exercise, chronic illness, and some endocrine disorders can suppress GnRH pulsatility and cause amenorrhea.

B. Anterior pituitary

• Follicle-stimulating hormone (FSH): promotes recruitment and growth of ovarian follicles and estrogen production.
• Luteinizing hormone (LH): triggers ovulation and supports the corpus luteum.

C. Ovary

• Estrogen, mainly estradiol: causes proliferation of endometrium.
• Progesterone: converts the estrogen-primed endometrium into a secretory, implantation-ready endometrium.
• Inhibin: suppresses FSH secretion.

3. Phases of the ovarian and uterine cycles

A. Follicular phase

Ovarian events

1. At the end of the preceding cycle, estrogen and progesterone fall.
2. The fall removes negative feedback on pituitary FSH.
3. FSH rises and recruits several ovarian follicles.
4. One follicle becomes dominant.
5. The dominant follicle secretes increasing estradiol and inhibin B.
6. Rising estrogen suppresses FSH, causing non-dominant follicles to undergo atresia.

Uterine event: proliferative phase

• Regeneration of endometrium after menstruation
• Proliferation of endometrial glands and stroma
• Thickening of endometrium
• Elongation of spiral arteries
• Thin, watery, stretchable cervical mucus near ovulation.

B. Ovulation

• A large LH surge
• A smaller FSH surge
• Rupture of the mature follicle
• Release of the oocyte, usually about 24-36 hours after the beginning of the LH surge.

C. Luteal phase

• Progesterone
• Estrogen
• Inhibin A.

Effects of progesterone

• Converts proliferative endometrium into secretory endometrium
• Produces coiled glands containing glycogen-rich secretions
• Makes cervical mucus thick and less permeable to sperm
• Slightly raises basal body temperature
• Suppresses further LH and FSH secretion through negative feedback.

D. Menstruation

• Vasoconstriction of spiral arterioles
• Ischemia and breakdown of the functional layer of endometrium
• Prostaglandin release
• Endometrial shedding and menstrual bleeding.

4. Dysmenorrhea

A. Primary dysmenorrhea

Mechanism

• Uterine ischemia
• Increased uterine tone
• Cramp-like pain.

Typical features

• Begins shortly before or at onset of menstrual bleeding
• Most severe during the first 24-72 hours
• Improves after the first few days of bleeding
• Often occurs in adolescents and young adults
• Pelvic examination is usually normal.

Management

1. NSAIDs are first-line treatment because they inhibit prostaglandin synthesis. They work best when started shortly before expected menses or at the onset of pain and taken regularly for the first 2-3 days.
2. Hormonal contraception can reduce ovulation, endometrial proliferation, and prostaglandin production. Options include combined hormonal contraceptives and progestogen-based methods.
3. Exercise, heat therapy, adequate sleep, and lifestyle measures may help some patients.
4. Persistent severe pain despite treatment requires reassessment for secondary dysmenorrhea.

B. Secondary dysmenorrhea

Important causes

• Endometriosis
• Adenomyosis
• Uterine fibroids
• Pelvic inflammatory disease
• Ovarian cysts
• Cervical stenosis
• Pelvic adhesions
• Congenital obstructive genital tract anomalies
• Intrauterine device-associated symptoms in some users.

Red flags suggesting secondary dysmenorrhea

• New pain after years of painless periods
• Progressively worsening pain
• Pain beginning several days before bleeding and continuing after menses
• Deep dyspareunia
• Chronic pelvic pain
• Painful bowel movements or urination during menses
• Heavy menstrual bleeding or intermenstrual bleeding
• Infertility
• Abnormal pelvic examination
• Poor response to NSAIDs or hormonal treatment.

Evaluation

• Pregnancy test when relevant
• Menstrual, sexual, contraceptive, and pain history
• Pelvic examination when appropriate
• Pelvic ultrasound for fibroids, adenomyosis, ovarian pathology, or structural abnormalities
• Further gynecologic evaluation for suspected endometriosis or other pathology.

5. Amenorrhea

A. Primary amenorrhea

• Menstruation has not occurred by age 15 years in a girl with normal secondary sexual characteristics, or
• Menstruation has not occurred by age 13 years with absent secondary sexual characteristics.

B. Secondary amenorrhea

• 3 months in a person with previously regular cycles, or
• 6 months in a person with previously irregular cycles.

Pregnancy

C. Causes of amenorrhea

1. Physiological causes

• Pregnancy
• Lactation
• Menopause
• Prepubertal state.

2. Hypothalamic causes

• Psychological stress
• Marked weight loss
• Eating disorders
• Excessive exercise
• Chronic systemic illness
• Functional hypothalamic amenorrhea.

3. Pituitary causes

• Hyperprolactinemia
• Pituitary adenoma
• Postpartum pituitary necrosis
• Pituitary surgery or irradiation.

4. Ovarian causes

• Polycystic ovary syndrome
• Primary ovarian insufficiency
• Turner syndrome or other gonadal dysgenesis
• Ovarian damage after chemotherapy, radiotherapy, surgery, or autoimmune disease.

5. Uterine or outflow tract causes

• Asherman syndrome, in which intrauterine adhesions occur after uterine trauma or infection
• Congenital absence of uterus
• Transverse vaginal septum
• Imperforate hymen
• Cervical stenosis.

6. Endocrine and systemic causes

• Thyroid disease
• Poorly controlled diabetes
• Cushing syndrome
• Congenital adrenal hyperplasia
• Androgen-secreting tumors
• Chronic renal or liver disease
• Some medicines, including antipsychotics that elevate prolactin.

6. Evaluation of amenorrhea

History

• Pregnancy possibility and contraception
• Age at menarche and previous cycle pattern
• Weight changes, diet, exercise, stress, and eating behaviors
• Galactorrhea, headaches, visual symptoms
• Acne, hirsutism, hair loss, or voice deepening
• Hot flushes, vaginal dryness, low libido
• Pelvic pain or cyclic pain without visible bleeding
• Past uterine procedures, curettage, infections, chemotherapy, or radiotherapy
• Drug history and chronic illness
• Family history of delayed puberty, early menopause, or genetic disorders.

Examination

• Height, weight, BMI
• Pubertal development and breast development
• Signs of androgen excess
• Thyroid signs
• Galactorrhea
• Visual fields if pituitary disease is suspected
• Pelvic anatomy, when appropriate.

Investigations

1. Pregnancy test
2. Serum TSH
3. Serum prolactin
4. FSH, LH, and estradiol
5. Androgen testing if hirsutism or virilization is present
6. Pelvic ultrasound
7. MRI of pituitary if markedly elevated prolactin or symptoms suggest pituitary lesion
8. Karyotyping in selected cases of primary amenorrhea or suspected gonadal dysgenesis.

Interpretation in broad terms

• High FSH with low estrogen suggests primary ovarian insufficiency or gonadal failure.
• Low or normal FSH/LH with low estrogen suggests hypothalamic or pituitary dysfunction.
• High prolactin suggests hyperprolactinemia, medication effect, hypothyroidism, or prolactinoma.
• Normal estrogen with irregular or absent ovulation plus androgen excess may suggest PCOS.

7. Other disorders of the menstrual cycle

A. Oligomenorrhea

Causes

• PCOS
• Pregnancy
• Hypothalamic dysfunction
• Hyperprolactinemia
• Thyroid disease
• Primary ovarian insufficiency
• Perimenopause
• Chronic illness.

B. Polymenorrhea

• Anovulatory cycles
• Thyroid dysfunction
• Endometrial or structural pathology
• Perimenopausal hormonal changes
• Hormonal contraception effects.

C. Abnormal uterine bleeding

• Heavy menstrual bleeding
• Intermenstrual bleeding
• Irregular bleeding
• Prolonged bleeding
• Frequent bleeding
• Infrequent bleeding.

Causes: PALM-COEIN classification

• P: Polyp
• A: Adenomyosis
• L: Leiomyoma, or fibroid
• M: Malignancy and hyperplasia.

• C: Coagulopathy
• O: Ovulatory dysfunction
• E: Endometrial causes
• I: Iatrogenic causes, including hormonal drugs or anticoagulants
• N: Not otherwise classified.

D. Heavy menstrual bleeding

Possible clues

• Changing sanitary products very frequently
• Flooding or bleeding through clothing/bedding
• Passing large clots
• Tiredness, breathlessness, dizziness, or iron-deficiency anemia.

Causes

• Fibroids
• Adenomyosis
• Endometrial polyps
• Anovulatory bleeding, including PCOS
• Bleeding disorders
• Thyroid disease
• Anticoagulant use
• Endometrial hyperplasia or cancer, particularly with risk factors or increasing age.

Assessment and management principles

• Exclude pregnancy.
• Check for anemia and consider iron studies.
• Pelvic examination and ultrasound are used when indicated.
• Medical treatments may include tranexamic acid, NSAIDs, hormonal methods, progestogens, or a levonorgestrel-releasing intrauterine system.
• Structural causes may need hysteroscopic treatment, myomectomy, endometrial ablation in selected patients who do not desire future fertility, or hysterectomy.

E. Anovulatory bleeding

• Adolescence, when cycles are often initially anovulatory
• PCOS
• Perimenopause
• Obesity
• Thyroid disease
• Hyperprolactinemia
• Hypothalamic disorders.

F. Premenstrual syndrome and PMDD

Premenstrual syndrome

• Irritability
• Mood changes
• Anxiety
• Breast tenderness
• Bloating
• Headache
• Fatigue
• Food cravings.

Premenstrual dysphoric disorder

• Symptom diary for at least two cycles
• Exercise, sleep measures, stress reduction
• Combined hormonal contraception in selected patients
• Selective serotonin reuptake inhibitors for significant PMS/PMDD
• Referral where severe symptoms, suicidality, or diagnostic uncertainty is present.

8. Polycystic ovary syndrome and menstrual irregularity

• Oligomenorrhea or amenorrhea
• Acne, hirsutism, or androgenic hair loss
• Polycystic ovarian morphology on ultrasound in some, but not all, cases
• Increased risk of insulin resistance, type 2 diabetes, and endometrial hyperplasia.

• Lifestyle measures where appropriate
• Cycle regulation and endometrial protection
• Treatment of acne/hirsutism
• Fertility treatment when pregnancy is desired
• Metabolic screening and risk reduction.

9. When urgent medical assessment is needed

• Possible pregnancy with abdominal pain, fainting, shoulder-tip pain, or vaginal bleeding, because ectopic pregnancy must be excluded
• Very heavy bleeding with dizziness, collapse, chest pain, shortness of breath, or rapidly soaking pads
• Severe new pelvic pain, fever, vomiting, or foul-smelling discharge
• New severe menstrual pain that is worsening
• Amenorrhea with headache, visual disturbance, or milky nipple discharge
• Signs of severe anemia, such as marked fatigue, palpitations, breathlessness, or syncope
• Virilization, such as rapidly progressing facial hair, deep voice, or increased muscle mass.

Key summary

• The menstrual cycle depends on coordinated pulsatile GnRH, FSH/LH, estrogen, progesterone, ovarian activity, and endometrial response.
• Primary dysmenorrhea is usually prostaglandin-mediated and responds to NSAIDs and hormonal suppression.
• Secondary dysmenorrhea suggests pathology such as endometriosis, adenomyosis, or fibroids.
• Pregnancy must be excluded first in secondary amenorrhea.
• Amenorrhea may arise from hypothalamic, pituitary, ovarian, uterine, endocrine, or systemic causes.
• Heavy, irregular, or prolonged bleeding should be assessed using the PALM-COEIN framework and with attention to anemia, pregnancy, structural disease, and endometrial risk.

Regulation of Normal Menstrual Cycle, Dysmenorrhea, and Other Menstrual Disorders

1. Normal menstrual cycle

• Day 1 is the first day of menstrual bleeding.
• A typical adult cycle is about 24 to 38 days long.
• Menstrual bleeding usually lasts up to 8 days.
• Cycle length may be irregular in the first few years after menarche and near menopause because ovulation is less consistent.

2. Hormonal regulation: the HPO axis

A. Hypothalamus

• Follicle-stimulating hormone (FSH)
• Luteinizing hormone (LH)

B. Anterior pituitary

FSH

• Stimulates growth and maturation of ovarian follicles
• Promotes estrogen synthesis by granulosa cells
• Helps select a dominant follicle

LH

• Stimulates androgen production by theca cells
• Produces the mid-cycle LH surge
• Triggers ovulation
• Converts the ruptured follicle into the corpus luteum

C. Ovary

• Estrogen, mainly estradiol
• Progesterone
• Inhibin A and inhibin B
• Small quantities of androgens

3. Phases of the menstrual cycle

A. Menstrual phase

Hormonal changes

• Progesterone falls
• Estrogen falls
• Support to the endometrium is withdrawn

Endometrial changes

B. Follicular phase

Events

1. Estrogen and progesterone levels fall at the end of the previous cycle.
2. Reduced negative feedback permits a rise in FSH.
3. FSH recruits a group of ovarian follicles.
4. Developing follicles produce increasing estradiol.
5. One follicle becomes dominant.
6. Increasing estrogen and inhibin B suppress FSH.
7. The remaining non-dominant follicles undergo atresia.

Uterine counterpart: proliferative phase

• Regrowth of the endometrium after menstruation
• Proliferation of endometrial glands and stroma
• Elongation of spiral arteries
• Thick, vascular endometrium
• Production of thin, watery, stretchable cervical mucus near ovulation

C. Ovulation

• A large LH surge
• A smaller FSH surge
• Final maturation and rupture of the follicle
• Release of the oocyte

• Mild unilateral pelvic pain, called mittelschmerz
• Increased clear cervical mucus
• Slight rise in basal body temperature after ovulation

D. Luteal phase

• Progesterone
• Estrogen
• Inhibin A

Effects of progesterone

• Converts the proliferative endometrium into a secretory endometrium
• Causes glands to become coiled and secretory
• Produces glycogen-rich glandular secretions
• Makes cervical mucus thick and less penetrable to sperm
• Reduces uterine contractility
• Causes a small rise in basal body temperature
• Suppresses further LH and FSH secretion

If pregnancy occurs

If pregnancy does not occur

4. Feedback regulation

5. Dysmenorrhea

• Nausea and vomiting
• Diarrhea
• Headache
• Fatigue
• Dizziness
• Sweating

A. Primary dysmenorrhea

Mechanism

• Increased uterine contractions
• Increased uterine tone
• Vasoconstriction
• Reduced uterine blood flow
• Uterine ischemia and pain

Typical features

• Begins just before or at the beginning of menstruation
• Peaks during the first 24 to 72 hours
• Improves as menstrual flow continues
• Usually occurs in adolescents and young adults
• Pelvic examination is normal

Management

• NSAIDs are first-line therapy because they reduce prostaglandin production. They are most effective when started at the onset of pain or shortly before expected menstruation.
• Hormonal contraception can reduce ovulation and endometrial prostaglandin production. Combined hormonal pills, progestogen-only methods, implants, injections, and hormonal intrauterine systems may help, depending on individual suitability.
• Heat application, exercise, adequate sleep, and stress management may provide additional benefit.

B. Secondary dysmenorrhea

Causes

• Endometriosis
• Adenomyosis
• Uterine fibroids
• Pelvic inflammatory disease
• Pelvic adhesions
• Ovarian cysts
• Cervical stenosis
• Congenital obstructive anomalies
• Intrauterine device-related pain in some patients

Features suggesting secondary dysmenorrhea

• Pain begins after years of painless periods
• Increasing severity over time
• Pain before, during, and after menstruation
• Deep dyspareunia
• Chronic pelvic pain
• Infertility
• Painful defecation or urination during menses
• Heavy menstrual bleeding or intermenstrual bleeding
• Poor response to NSAIDs or hormonal treatment
• Pelvic mass, tenderness, or abnormal examination

6. Other disorders of the menstrual cycle

A. Amenorrhea

Primary amenorrhea

• Menstruation has not occurred by age 15 despite normal secondary sexual development, or
• There is no menstruation by age 13 with no secondary sexual development.

Secondary amenorrhea

• Absence of menses for 3 months in someone with previously regular cycles, or
• Absence for 6 months in someone with previously irregular cycles.

First step

Exclude pregnancy first.

Causes

• Pregnancy, lactation, menopause
• Polycystic ovary syndrome, or PCOS
• Functional hypothalamic amenorrhea due to stress, undernutrition, excessive exercise, or chronic illness
• Hyperprolactinemia
• Thyroid disease
• Primary ovarian insufficiency
• Pituitary disease
• Uterine adhesions, such as Asherman syndrome
• Congenital absence or obstruction of the uterus, cervix, vagina, or hymen
• Medicines that affect prolactin or reproductive hormones

B. Oligomenorrhea

• PCOS
• Hypothalamic dysfunction
• Hyperprolactinemia
• Thyroid disorders
• Primary ovarian insufficiency
• Perimenopause
• Chronic illness
• Pregnancy

C. Frequent menstrual cycles

• Anovulatory cycles
• Thyroid disease
• Perimenopause
• Endometrial disorders
• Hormonal medication effects
• Structural uterine lesions

D. Abnormal uterine bleeding

• Heavy menstrual bleeding
• Prolonged bleeding
• Irregular bleeding
• Bleeding between periods
• Frequent bleeding
• Infrequent bleeding
• Bleeding after sex

Structural causes: PALM

• P: Polyp
• A: Adenomyosis
• L: Leiomyoma, also called fibroid
• M: Malignancy and endometrial hyperplasia

Non-structural causes: COEIN

• C: Coagulopathy
• O: Ovulatory dysfunction
• E: Endometrial cause
• I: Iatrogenic, including medicines and contraception
• N: Not otherwise classified

E. Heavy menstrual bleeding

Features

• Soaking pads or tampons very frequently
• Bleeding through clothing or bedding
• Passing large clots
• Prolonged bleeding
• Tiredness, dizziness, palpitations, or shortness of breath due to anemia

Causes

• Fibroids
• Adenomyosis
• Endometrial polyps
• Ovulatory dysfunction, including PCOS
• Bleeding disorders
• Thyroid disease
• Anticoagulants
• Endometrial hyperplasia or cancer, especially with increasing age or risk factors

General management

• Iron replacement where iron deficiency is present
• Tranexamic acid during bleeding
• NSAIDs
• Hormonal contraception
• Progestogen treatment
• Levonorgestrel-releasing intrauterine system
• Hysteroscopic removal of polyps or submucosal fibroids
• Myomectomy, endometrial ablation, or hysterectomy in selected cases

F. Anovulatory bleeding

• Estrogen may continue to stimulate endometrial growth
• The endometrium becomes unstable
• Irregular, prolonged, or heavy bleeding may occur

• Adolescence
• PCOS
• Perimenopause
• Obesity
• Thyroid dysfunction
• Hyperprolactinemia
• Severe stress, illness, weight change, or excessive exercise

G. Premenstrual syndrome and PMDD

Premenstrual syndrome, PMS

• Irritability
• Mood changes
• Anxiety
• Bloating
• Breast tenderness
• Headache
• Fatigue
• Food cravings

Premenstrual dysphoric disorder, PMDD

• Symptom diary for at least two cycles
• Regular exercise, sleep, and stress reduction
• Cognitive behavioral therapy
• Hormonal treatment in selected patients
• Selective serotonin reuptake inhibitors for significant PMS or PMDD

7. When to seek urgent assessment

• Possible pregnancy with bleeding plus abdominal pain, fainting, shoulder-tip pain, or dizziness, because ectopic pregnancy must be excluded
• Very heavy vaginal bleeding with weakness, collapse, chest pain, breathlessness, or rapid soaking of pads
• Severe new pelvic pain, fever, vomiting, or foul-smelling discharge
• Severe dysmenorrhea that is worsening or does not respond to initial treatment
• Amenorrhea with severe headache, visual symptoms, or nipple discharge
• Signs of marked anemia
• Rapid onset of hirsutism, deepening voice, or other virilizing changes

Key points

• The normal menstrual cycle depends on coordinated pulsatile GnRH, FSH, LH, estrogen, progesterone, ovarian follicle development, ovulation, and endometrial response.
• The LH surge triggers ovulation after sustained high estrogen concentrations.
• Progesterone dominates after ovulation and transforms the endometrium into its secretory form.
• Primary dysmenorrhea is usually caused by prostaglandin-mediated uterine contractions and responds to NSAIDs and hormonal suppression.
• Secondary dysmenorrhea should prompt assessment for endometriosis, adenomyosis, fibroids, infection, or other pelvic pathology.
• Menstrual irregularity may result from pregnancy, anovulation, PCOS, endocrine disorders, pituitary disease, ovarian insufficiency, uterine disease, or medications.

Regulation of Normal Menstrual Cycle, Dysmenorrhea, and Other Menstrual Disorders

1. Normal menstrual cycle

2. Hypothalamic-pituitary-ovarian axis

1. Hypothalamus releases gonadotropin-releasing hormone, or GnRH, in pulses.
2. Anterior pituitary responds by releasing:
   • Follicle-stimulating hormone, or FSH
   • Luteinizing hormone, or LH
3. Ovary produces estradiol, progesterone, inhibin, and small amounts of androgens.
4. Uterus and endometrium respond to estrogen and progesterone.

• For most of the cycle, estradiol and progesterone inhibit GnRH, FSH, and LH release by negative feedback.
• Near mid-cycle, sustained high estradiol changes to positive feedback, causing the LH surge that triggers ovulation.

3. Ovarian and uterine phases

A. Follicular phase

Hormonal events

• Recruits a group of ovarian follicles
• Stimulates granulosa-cell growth
• Promotes estradiol synthesis

Endometrial effects of estrogen

• Regrowth of endometrium after menstruation
• Proliferation of glands and stroma
• Lengthening of spiral arteries
• Progressive thickening of endometrium

B. Ovulation

• A large LH surge
• A smaller FSH surge
• Completion of oocyte maturation
• Rupture of the dominant follicle
• Release of the oocyte

• Mid-cycle pelvic discomfort, called mittelschmerz
• Clear, slippery cervical mucus
• Slight rise in basal body temperature after ovulation.

C. Luteal phase

• Progesterone
• Estrogen
• Inhibin A

Effects of progesterone

• Endometrial glands become tortuous and secretory.
• Glands contain glycogen-rich material.
• Stroma becomes edematous.
• Spiral arteries become longer and more coiled.
• Cervical mucus becomes thick, scanty, and less permeable to sperm.
• Basal body temperature rises slightly.
• Further FSH and LH release is suppressed.

D. Menstruation

• Spiral-arteriole vasoconstriction
• Ischemia of the functional endometrium
• Prostaglandin production
• Tissue breakdown and shedding of the functional layer

4. Dysmenorrhea

A. Primary dysmenorrhea

Typical pattern

• Begins 6-24 months after menarche, after ovulatory cycles are established
• Starts just before or within hours of menstrual flow
• Peaks during the first day of heaviest bleeding
• Usually lasts 2-3 days
• Pelvic examination is normal when it is appropriate to perform one

Pathophysiology

• Strong and frequent uterine contractions
• Increased uterine tone
• Uterine vasoconstriction
• Reduced uterine blood flow and ischemic pain

Management

1. NSAIDs are first-line treatment.
   They inhibit cyclooxygenase and reduce prostaglandin synthesis. They are most effective when started just before expected menses or at onset of pain and taken regularly through the first 2-3 days of flow. They may be unsuitable in people with certain gastrointestinal, renal, bleeding, allergy, or cardiovascular risks.
2. Hormonal suppression or contraception.
   Combined hormonal contraceptives or progestogen-based methods can reduce ovulation, endometrial growth, and prostaglandin production. They are useful when contraception is also desired.
3. Non-drug measures.
   • Local heat
   • Exercise
   • Sleep and stress management
   • Symptom and cycle diary
4. Reassess non-response.
   Persistent or worsening pain despite adequate NSAID and hormonal treatment should prompt assessment for secondary dysmenorrhea, particularly endometriosis.

B. Secondary dysmenorrhea

Common causes

• Endometriosis
• Adenomyosis
• Uterine fibroids
• Pelvic inflammatory disease
• Endometrial polyps
• Ovarian cysts or pelvic adhesions
• Cervical stenosis
• Congenital obstructive anomalies
• Copper intrauterine device-related symptoms in some people

Features suggesting secondary dysmenorrhea

• New onset after years of painless periods
• Progressively worsening pain
• Pain beginning days before menstruation and continuing after it
• Heavy menstrual bleeding or intermenstrual bleeding
• Deep dyspareunia
• Infertility
• Chronic pelvic pain
• Dyschezia or painful defecation during periods
• Poor response to first-line treatment
• Abnormal pelvic examination

Assessment

• Pregnancy test when applicable
• Detailed pain, bleeding, sexual, contraceptive, and fertility history
• Examination when appropriate
• Pelvic ultrasound for fibroids, adenomyosis, ovarian masses, or endometrioma
• Specialist gynecology assessment if endometriosis or another significant pathology is suspected

5. Other menstrual-cycle disorders

A. Anovulatory cycles

Consequences

• Irregular bleeding
• Prolonged bleeding
• Heavy bleeding
• Infrequent menses
• Unpredictable timing of periods

• During the first 12-18 months after menarche
• During the perimenopausal transition

• Polycystic ovary syndrome, or PCOS
• Thyroid disease
• Hyperprolactinemia
• Obesity
• Stress, eating disorders, low body weight, or excessive exercise
• Chronic systemic illness

B. Abnormal uterine bleeding

• Heavy menstrual bleeding
• Bleeding lasting longer than expected
• Frequent periods
• Infrequent periods
• Irregular periods
• Intermenstrual bleeding
• Postcoital bleeding

Causes: PALM-COEIN classification

Heavy menstrual bleeding

• Fibroids
• Adenomyosis
• Endometrial polyps
• Anovulation and PCOS
• Bleeding disorders, including von Willebrand disease
• Thyroid disease
• Anticoagulant medicines
• Endometrial hyperplasia or malignancy, depending on age and risk factors

C. Oligomenorrhea and infrequent cycles

• PCOS
• Pregnancy
• Hypothalamic dysfunction
• Hyperprolactinemia
• Thyroid disorder
• Primary ovarian insufficiency
• Perimenopause

D. Amenorrhea

• Primary amenorrhea: no menstruation by age 15 years with normal secondary sexual development, or by age 13 years without secondary sexual development.
• Secondary amenorrhea: no period for 3 months in someone with previously regular cycles, or 6 months in someone with previously irregular cycles.

• Hypothalamic: stress, weight loss, eating disorder, intensive exercise
• Pituitary: hyperprolactinemia, pituitary tumor
• Ovarian: PCOS, primary ovarian insufficiency
• Thyroid or other endocrine disorders
• Uterine/outflow tract: intrauterine adhesions, congenital genital tract anomalies, cervical stenosis

E. Premenstrual syndrome and PMDD

Premenstrual syndrome

• Irritability and mood change
• Breast tenderness
• Bloating
• Headache
• Fatigue
• Food cravings
• Poor concentration

Premenstrual dysphoric disorder

6. Important warning signs

• Very heavy bleeding, especially soaking a pad or tampon hourly for more than 2 hours
• Dizziness, fainting, shortness of breath, chest pain, or features of severe anemia
• Possible pregnancy with pain or bleeding, because ectopic pregnancy must be excluded
• Severe new or worsening pelvic pain
• Fever, foul-smelling discharge, vomiting, or severe tenderness
• Intermenstrual, postcoital, postmenopausal bleeding
• Amenorrhea with severe headache, visual change, or nipple discharge
• Rapid onset of hirsutism, voice deepening, or other virilization features

Key points for revision

• GnRH pulses stimulate FSH and LH.
• FSH promotes follicle growth and estradiol synthesis.
• Sustained high estradiol causes positive feedback and the LH surge.
• LH causes ovulation and corpus-luteum formation.
• Estrogen causes the proliferative endometrium.
• Progesterone causes the secretory endometrium.
• Withdrawal of estrogen and progesterone causes menstruation.
• Primary dysmenorrhea is prostaglandin-mediated and usually responds to NSAIDs.
• Secondary dysmenorrhea suggests pelvic pathology, especially endometriosis.
• AUB should be assessed using PALM-COEIN.
• Persistent irregular anovulatory cycles require evaluation and endometrial protection.