This is an acute terrifying emergency following delivery in which patient suddenly develops dyspnoea, apnoea, cyanosis with or without seizure and shock among other features. It usually occurs secondary to several catastrophic events and may be a tragic experience to the patient and the physician
5. INTRODUCTION
•This is an acute terrifying emergency following delivery in which
patient suddenly develops dyspnoea, apnoea, cyanosis with or
without seizure and shock among other features. It usually occurs
secondary to several catastrophic events and may be a tragic
experience to the patient and the physician
•Maternal Collapse: an acute event involving the cardiorespiratory
systems and/or brain, resulting in a reduced or absent conscious
level (and potentially death), at any stage in pregnancy and p to six
weeks after delivery
6. INTRODUCTION/2
•Incidence is hard to define because of the causes and
nature of the condition
•It will include near misses and many cases of severe
maternal morbidity
•A system of maternal audits may help shed more light on
the incidence of maternal collapse/post partum collapse
•A look at the incidence of the causes could give an idea of
how common this condition could be
7. AETIOLOGY AND INCIDENCE
(1) Eclampsia ----- 1 in 300-1,500 pregnancies
(2) Post partum Haemorrhage --- 3.7-8.6% of deliveries
(3) Pulmonary Embolism---- 1 in 2,500 pregnancies
(4) Amniotic fluid embolism – 1 in 3,360-80,000 pregnancies
(5) Myocardial infarction – 1 in 10,000 – 42000 pregnancies
(6) Regional Anesthetic Toxicity – 1 in 1,000 procedures
(7) Acute uterine inversion – 1 in 2,000 deliveries
(8) Severe sepsis
(9) Ruptured aneurysm (Aorta, liver, spleen)
8. PATIENTS AT RISK
Increasing maternal age
◦ Maternal mortality rises 5-fold between age 20 – 40
Obesity
◦ The modern epidemic
Social Class
◦ Low socioeconomic class
Pre existing Maternal Disease
◦ One of the main reasons for antenatal care
10. CAUSES OF POSTPARTUM COLLAPSE/2
Cerebral
◦Post ictal (epilepsy)*
◦Eclampsia
◦Cerebrovascular accident
Drugs & Metabolism
◦ Prescribed e.g. MgSO4
◦ Illicit drugs and toxins
◦ Hypoglycaemia
11. CAUSES OF POSTPARTUM COLLAPSE/3
Concealed Haemorrhage
◦ Blood in the uterus (APH or PPH)
◦ Or vagina/paravaginal space
◦ Blood in the abdominal cavity
◦ Ruptured liver, spleen or splenic artery
◦ Post Caesarean
◦ Blood in the chest
◦ Aortic dissection
Pulmonary
◦ Thromboembolism
◦ Amniotic fluid embolism
◦ Pneumothorax
◦ Aspiration syndrome
12.
13. TREATABLE CAUSES OF COLLAPSE
4 H’s and 4 T’s plus E
◦ Hypovolaemia
◦ Hypoxia
◦ Hypo or Hyperkalaemia
◦ Hypothermia
◦ Thromboembolism
◦ Toxins
◦ Tension Pneumothorax
◦ Tamponade (cardiac)
Eclampsia/Epilepsy
14. POSTPARTUM HAEMORRHAGE
•Bleeding per vaginam excess of 500mls following vaginal delivery
•Bleeding PV greater than 1% body weight
•Bleeding PV in excess of 1000mls following C/S
•Any amount of blood loss that will compromise the maternal
cardiovascular system
• PPH Primary
• Secondary
•It is the commonest cause of maternal mortality in the developing
world - 30%
15. POSTPARTUM HAEMORRHAGE/2
•Uterine atony
•Genital tract lacerations
•Retained products of conception
•Uterine inversion
•Rupture uterus
•Coagulation defects
•BE WARY OF SLOW STEADY BLEEDING ESPECIALLY IN FIT HEALTHY WOMEN
WHO CAN TOLERATE SIGNIFICANT LOSS PRIOR TO EXHIBITING SIGNS OF
DECOMPENSATION
16. ECLAMPSIA
•Generalized tonic-clonic seizure that occur in a woman during pregnancy, labour or
puerperium in the absence of an underlying neurological disease.
•Up to 35% of cases occur in early puerperium
•Often with Pre-existing preeclampsia
*Absent in 20% of cases (Sibai 1981)
•*Seizure preceded by:
-Headaches -Vomiting
-Epigastric pain -Restlessness
-Visual disturbance
Epilepsy should always be considered in cases of maternal collapse associated
with seizure activity
17. THROMBOEMBOLISM
•In the UK CEMACH 2007 report there were 41 deaths from
thromboembolism (33 pulmonary embolism and eight cerebral vein
thrombosis), making it the most common cause of direct maternal
death
•Usually occurs in the immediate post partum period
•Up to 6 fold increase in susceptibility to PE in pregnancy compared
to non-pregnant state.
• Appropriate use of thromboprophylaxis has improved maternal
morbidity and mortality, but improvements in clinical risk
assessment and prophylaxis are still required
19. THROMBOEMBOLISM/3
Preceding history of DVT
Signs include:
Tachycardia
Anxiety Cyanosis
Dyspnoea Pleural friction
Retrosternal pain Pleural friction rub
Restlessness Splitting of S2 with
Haemoptysis Accentuation of P2
Apnea S3 gallop rhythm
Loss of consciousness Coma
20. AMNIOTIC FLUID EMBLOISM
•Amniotic fluid entering maternal circulation
•Termed one of the most dangerous conditions in obstetrics
•Difficult to diagnose in life and typically confirmed at postmortem
•Incidence in the UK 2/100,000
•Fatality rate 85% (Duff 1987)
•Survival rates have improved significantly over time from 14% in
1979 to 30% in 2005 and 80% in 2010
•However neurological morbidity in survivors is common
22. AMNIOTIC FLUID EMBOLISM/3
Presentation: Dramatic without warning signs:
◦Dyspnoea
◦Cough
◦Pink, frothy sputum
◦Cyanosis
◦Apnea
◦Shock
◦Convulsion (10-20%)
◦Coma
◦DIC & LVF are common in survivors of the acute hypoxic
episode.
23. ACUTE UTERINE INVERSION
•Typically occurs with cord traction and the uterus disappears from
the abdomen
•Because it is inside out & in the vagina
•Degree of shock is out of proportion to blood loss
•1 in 2000 deliveries
•Predisposition:
•Crede’s manoeuvre during delivery
•Fundal insertion of placenta
•Vigorous cord traction
24. ACUTE UTERINE INVERSION/2
•Presentation
• Haemorrhage – 90%
• Shock – 40% usually out of proportion to blood loss
• Uterus as a pelvic mass or protruding from the vagina
•Resuscitate with IV Fluids
•Analgesia if necessary
•Attempt manual replacement of the uterus followed by manual
removal placenta
•O’Sullivans hydrostatic replacement
25. CARDIAC DISEASE
•Common overall cause of death in CEMACH 2007 report
•Majority of deaths occurred in women with no previous history of
cardiac disease
•Causes include myocardial infarction, aortic dissection, cardiomyopathy
•Majority occur in 3rd trimester and puerperium
•Predisposing Factors:
Preexisting atherosclerotic heart disease Age>35years
Hyperlipidemia Diabetes mellitus
Hypertension Obesity
Smoking Sedentary life style
26. SEPSIS
•May present without fever or a raised white cell count (WCC)
• Beware the patient with low WCC
•Can progress very rapidly
•Principal obstetric organisms...
• Streptococci A, B and D
• Pneumococci
• E Coli
27. TOXICITY TO REGIONAL ANAESTHESIA
Usually due to:
◦Inadvertent intravascular injection of LA
◦Administration of excessive dose
◦Incorrect use of long acting agent e.g. Bupivacaine,
Ethidocaine
◦High spinal block
28. TOXICITY TO REGIONAL ANAESTHESIA/2
Pathophysiology:
•Pregnant women are more susceptible to toxicity because
•Increase in blood flow to the vessels surrounding the spinal cord and
meninges therefore greater surface area for systemic absorption
•Decrease in epidural space capacity due to distended vessels
•Increase pressures in the subarachnoid and epidural space during
contraction and voluntary expulsive effort. This increase the
possibility of agents being widely disseminated
29. TOXICITY TO REGIONAL ANAESTHESIA/3
Presentation:
•Symptoms usually occur within 20mins of administration
•Metallic taste
•Ringing in the ears
•Ptosis & Miosis due to blockade of sympathetic B fibres present in upper
thoraxic spinal nerves.
•Generalised convulsion may accompany anoxia
•Confusion
•Disorientation
•Cardiac arrest
• - Anoxia
• - Direct myocardial depressant effect
30. INTRACRANIAL HAEMORRHAGE
•Usually a complication of uncontrolled systolic hypertension
•Can also result from ruptured aneurysms and arteriovenous
malformations
•Often preceded by severe headaches
31. ANAPHYLAXIS
•Severe life threatening generalized or systemic hypersensitivity
reaction
•Results in respiratory, cutaneous and circulatory changes and
possibly gastrointestinal disturbances and collapse
•Significant intravascular volume redistribution, reduced cardiac
output, ventricular failure and cardiac ischaemia
•Upper airway obstruction contributes to hypoxia
•Incidence is 3-10/1000 with mortality rate of 1%
•Triggers are variety of drugs, latex, animal allergens and food
34. GENERAL CLINICAL FEATURES
Symptoms Signs
Dizziness Pallor
Feeling of illness Tachycardia
Vomiting Hypotension
Chest pain Loss of
Dyspnoea consciousness
36. INVESTIGATIONS: Specific
•Tailored to -making a diagnosis
• -managing the patient
•Arterial blood gas analysis
•ECG
•Evaluation of haemodynamic monitoring data
•Examination of blood from central circulation
•Radiological studies
39. MYOCARDIAL INFARCTION
ECG
◦ Elevation of ST segments
◦ Q waves in leads II, III and aVf
◦ Poor R wave progression-precordial leads
Cardiac iso-enzymes
◦ ↑ALT, ↑AST,↑LDH
Radionuclide scan
◦ Technitium-99 (99mTc) -- affinity for damaged myocardium
◦ Thallium-201 (201Tl)-- normal myocardium
41. MANAGEMENT
Resuscitative
•ABC of resuscitation:
• Secure an airway
• Provide effective ventilation & oxygenation
• This may require endotracheal intubation & mechanical ventilation
• Maintain circulation
•Both basic and advanced life support may be required
•Early warning systems have been developed although none has been
deemed optimal
42. OBSTETRIC PHYSIOLOGY IMPACTS ON RESUSCITATION
Aortocaval compression
◦ Also known as supine hypotension
◦ Progressively increases from 20wks
◦ May reduce cardiac output by up to 40%
◦ CPR thus less likely to be effective in an uterus >20wks size
◦ Always use a 15 degree tilt position when resuscitating
Pregnant uterus compromises external cardiac massage (ECM)
◦ By up to 90%
◦ Also compromises chest ventilation
◦ So hypoxaemia occurs more rapidly
43. OBSTETRIC PHYSIOLOGY IMPACTS ON RESUSCITATION/2
Respiratory changes
◦ Diaphragmatic splinting reduces functional residual capacity
◦ Weight gain, large breasts and laryngeal oedema can restrict intubation
◦ Increased risk of regurgitation and aspiration due to sphincter relaxation
Blood volume is increased
◦ By up to 50%
◦ Increased cardiac output and hyperdynamic circulation mean large volumes
of blood can be lost in bleeding
◦ But mother may tolerate blood volume loss up to 30%
44. OBSTETRIC PHYSIOLOGY IMPACTS ON RESUSCITATION/3
•Always use a 15 degree tilt (Cardiff wedge)
•Airway should be protected ASAP by intubation with a cuffed tube
•Supplemental oxygen should be administered ASAP
•Chest compressions should be started early
•Two wide bore cannulas should be inserted ASAP with an aggressive
approach to volume replacement
•Same defibrillation energy levels can be used
•No alterations in drugs doses
45. EMERGENCY MANAGEMENT - 1
Does the mother respond?
◦ To verbal commands
◦ To stimulation
Is she breathing?
◦ Is she cyanosed
Is there a heartbeat?
◦ Capillary filling
Clear the airway
Coma position or prepare for CPR
◦ Always with left lateral tilt
Attempt diagnosis
◦ But proceed with basic life support
Always check that the environment is safe
46. EMERGENCY MANAGEMENT - 2
If the mother is not breathing (but a pulse is present)...
◦ Provide oxygen
◦ Assess over 10 sec
◦ Artificially ventilate with a face mask/airway
◦ Early intubation is desirable
If there is no carotid pulse...
◦ Proceed immediately with ECM
◦ 30 compressions, mid chest and vertical
◦ With >4 cm chest movement
◦ At 100 per minute
◦ Then give 2 “breaths” (the 30:2 rhythm)
◦ When intubated 100 ECM/min and 10 breaths/min
◦ Get an ECG connected ASAP
◦ Is it arrhythmia or asystole?
47. EMERGENCY MANAGEMENT - 3
The treatment for ventricular fibrillation is...
◦ External Defibrillation
◦ Establish IV lines
◦ Repeat if necessary
The treatment for asystole is...
◦ IV adrenaline 1 mg
◦ Correct reversible causes i.e.
◦ Hypoxia
◦ Hypvolaemia
◦ Hypo or hyperkalaemia
◦ Hypothermia
◦ Repeat adrenaline every 5 min if necessary
Empty the uterus if not responding after 4 min
48. EMERGENCY UTERINE EVACUATION
The aim is to facilitate maternal resuscitation
◦ Not to save a baby
◦ To be done even if the baby is already dead
This is the responsibility of the most obstetrically competent person present
◦ Who may be anyone
Should be done “on the spot”
◦ Anaesthesia not required
◦ Only a scalpel and two clamps for the cord required
Incise the abdomen and uterus in any way you like
Can facilitate cardiac compression
◦ Through the diaphragm and against the sternum
If the mother responds to resuscitation then transfer to theatre for anaesthesia and haemostasis
49. FURTHER AND SPECIFIC MANAGEMENT
Manage according to predisposing cause after initial ABCD
resuscitation
Standard protocols for the management of
◦ postpartum hemorrhage
◦ eclampsia
◦ Sepsis
◦ thromboembolism
Multidisciplinary approach where necessary
Anesthetist very crucial to management
50. UTERINE INVERSION
Manual replacement of uterus
◦ Without anaesthesia
◦ With GA (preferably halogenated agent)
◦ IV nitroglycerin to relax uterus & avoid ETT
Hydrostatic replacement
Surgical replacement:
◦ Abdominally: Huntington’s procedure
◦ Vaginally: Haultin’s procedure
Placenta then removed by controlled cord traction
Blood replacement, antibiotics, oxytocics & careful monitoring necessary for
successful peri-operative management
51. REGIONAL ANAESTHESIA TOXICITY
Prevention:
◦ Anaesthetic technique
◦ Altered dose requirements in pregnancy
◦ Extended observation
Support of airway & oxygenation till effects dissipate
Lipid rescue with 20% intralipid should be given if cardiac arrest
ensues
IV diazepam, if seizures occur
Excellent prognosis if complications recognized fast
53. AMNIOTIC FLUID EMBOLISM/2
•Final goal of therapy is to provide optimal support until dysfunction
is corrected
•Minimise thermal instability
•Correct metabolic & electrolyte abnormalities
•Maintain careful infection surveillance
54. PULMONARY EMBOLISM
Anticoagulation
◦ IV Heparin 5000-10000 iu, then infusion (PTT- 1.5 to 2 times the
control / serum heparin concentration 0.2-0.7 iu/ml)
◦ Continue for 7-10 days, then oral anticoagulants for 3 mths
◦ Fibrinolytic agents: risk of bleeding
◦ Recombinant tissue-plasminogen activators
◦ Streptokinase, Urokinase
55. PULMONARY EMBOLISM/2
Surgery
◦Pulmonary embolectomy
◦Plication of IVC
◦Insertion of an IVC umbrella filter
◦Acute DVT with absolute contra-indication to anti-
coagulant therapy
◦Massive PE in which recurrence would be fatal
◦Objectively demonstrated recurrent DVT, despite
adequate anti-coagulant therapy
56. IMPROVING OUTCOMES AFTER MATERNAL COLLAPSE
Be Ready
◦ Trained staff (senior midwife, senior registrar in obstetrics and in anaesthesia)
◦ Have emergency equipment assembled & quarantined for emergency use
◦ Have systems that assemble more staff
◦ Practice drills
Be Forewarned
◦ Needs an obstetric early warning system to identify...
◦ The patient at risk
◦ When she is on the slippery slope
Review and Revise
◦ After each event
◦ And each “near miss”
57. CONCLUSION
•Sudden postpartum collapse is an obstetric emergency where
prompt intervention is critical
•A deep understanding of the possible causes and management
protocols is essential
•Early warning systems can be used to prevent postpartum collapse
•All obstetricians must have certification in basic life support
•A multidisciplinary approach is often necessary especially in the
follow up period and immediate resuscitation is not conclusive
•Mortality and significant morbidity can be prevented
