Maternal Collapse
in
labour ward
Dr . J. Edward Johnson. M.D., D.C.H.
Asst. Professor ,
Dept. of Anaesthesiology,
KGMCH.
DISCUSSION
CAUSES OF MATERNAL
COLLAPSE
•
•
•
•
•
•
•
•
Haemorrhage (APH, PPH)
Pul.Embolism
Amniotic Fluid Embolism
Pre-eclampsia/eclampsia
Cardiac (Valvular HD)
Syncope
Sepsis
Respiratory
Causes of Collapse
•
4 H’s:
Hypoxia
Hypovolaemia (bleeding/block)
Hypothermia
Hypo/hyperkalaemia (metabolic)
•
4 T’s:
Thromboembolic (PE or AFE)
Toxic/therapeutic (local anaesthetic)
Tension pneumothorax
Tamponnade
•
Eclampsia
Leading causes of Direct Deaths
(Mortality rates/Million Maternities)
Postpartum
Hemorrhage
“Obstetrics is
Bloody Business”*
*Cunningham, et. al: Williams Obstetrics, 21st ed., 2001
DIAGNOSIS
OF
ETIOLOGY
Postpartum
Hemorrhage
Diagnosis of Causes
Postpartum Hemorrhage
Retained placenta
 Placenta Accreta
 Uterine atony
 Vaginal and cervical laceration
 DIC, AFE
 Factor disorder
 Uterine rupture / Uterine inversion

MANAGEMENT
RESUSITATION
OF
Haemorrhagic Shock &
Cardiac Arrest -(CPR)
RESUSITATION
Haemorrhagic
Shock
Classification of
Haemorrhage
Class
Acute Blood
Loss
% Lost
1
900cc
15
2
1200-1500cc
20-25
3
1800-2100cc
30-35
4
2400cc
40
Baker R, Obstet Gynecol Annu, 1997
ASSESSMENT OF BLOOD LOSS
AFTER DELIVERY
•
•
•
•
•
Difficult
Mostly Visual estimation (So, Subjective &
Inaccurate)
Underestimation is likely
Clinical picture -Misleading
Our Mothers-Malnourished, Anaemic,
Small built, Less blood volume
SYMPTOMS & SIGNS
Blood loss Systolic BP Signs & Symptoms
(% B Vol)
( mm of Hg)
10-15
Normal
postural hypotension
15-30
slight fall
PR, thirst, weakness
30-40
60-80
40+
40-60
pallor,oliguria,
confusion
anuria, air hunger,
coma, death
Recognition is late - >30% B Vol loss
Modified Early Warning Scoring System
(MEWS)
MEWS calculated from 5 physiological
variables
•
•
•
•
•
Mental response
Pulse rate
Systolic BP
Respiratory rate
Temperature
Modified Early Warning Scoring System
(MEWS)
The senior nurse would call the doctor for three or more of
the following criteria:
• Respiratory rate of ≥25 or <10 breaths per minute.
• Arterial systolic blood pressure of <90mmHg.
• Heart rate of ≥110 or <55 beats per minute.
• Not fully alert and orientated.
• Oxygen saturation of <90 per cent.
• Urine output over the last four hours of <100ml.
• Respiratory rate ≥35 breaths per minute or a heart rate ≥140 beats per
minute.
Vigilance is great, but you have
to remember that studies show
the half-life of vigilance is
about 15 minutes.
Author unknown
DO NOT UNDERESTIMATE BLOOD LOSS
Clinical Features of Shock
System
Early Shock
Late Shock
CNS
Altered mental states
Obtunded
Cardiac
Tachycardia
Cardiac failure
Orthostatic hypotension
Arrhythmias
Hypotension
Renal
Oliguria
Anuria
Respiratory
Tachypnea
Tachypnea
Respiratory failure
Hepatic
No change
Liver failure
Gastrointestinal
No change
Mucosal bleeding
Hematological
Anemia
Coagulopathy
Metabolic
None
Acidosis
Hypocalcemia
Hypomagnesemia
Goals of Therapy
•
Maintain the following:
Systolic pressure >90mm Hg
Urine output >0.5 mL/kg/hr
Normal mental status
•
Eliminate the source of hemorrhage
•
Avoid overzealous volume replacement that may
contribute to pulmonary edema
Management of Obstetrical Hemorrhage
Oxygen by mask 10 liter/min.
– to keep O2 saturation > 94%
 1st IV Line: Ringer Lactate with Pitocin 20-40 units at 1000 ml/
30 minutes
 2nd IV Line: 18 G IV: warm RL - administer wide open
 Sample blood; CBC, fibrinogen, PT/PTT, platelets, T&C and
order 4u PRBCs
 Monitor I&O, urinary Foley catheter
 Get help
Senior Obstetrician, Anesthesiologist,
Interventional Radiology, Intensivist,
Haemotologist etc.

Management of Obstetrical
Hemorrhage





LR or NS replaces blood loss at 3:1
Volume expander 1:1 (albumin, hetastarch, dextran)
Anticipate Disseminated Intravascular Coagulapathy (DIC)
Verify complete removal of placenta, may need ultrasound
Inspect for bleeding
-episiotomy, laceration, hematomas, inversion, rupture

Emperic transfusion
-2 u PRBC; FFP 1-2 u/4-5 u PRBC
-Cryo 10 u,
-Uncrossed (O neg.) PRBC – For emergency

Warm all blood products and I.V.infusions
-prevent hypothermia, coagulopathy, arrhythmias
Platelets
Random Donor
Apheresis
Pooled 4-8 units, ABO
+ Rh compatible
Expire 4 h after pooling
Single donor
Expire 4 h after released
3-5 day survival in vivo
(in DIC)
FFP
(contains all coag factors)
PT, PTT > 50% increase or INR > 1.5
Warm
Spin
Cryoprecipitate
(VIII, XIII, Fibrinogen, VW)
Fibrinogen 5 mgldL
Blood Component Therapy

Fresh Frozen Plasma
– INR > 1.5 - 2u FFP
– INR 2-2.5 - 4u FFP
– INR > 2.5 - 6u FFP
 Cryoprecipitate ( 1u/ 10Kg )
– Fibrinogen < 100 mg/dl – 10u cryo
– Fibrinogen < 50 mg/dl – 20u cryo
 Platelets
– Platelet. count. < 100,000 – 1u plateletpheresis
– Platelet. count. < 50,000 – 2u plateletpheresis
Blood Component Therapy
Blood Comp
Contents
Volume
(ml)
Effect
Packed RBCs
RBC, Plasma
300
Inc. Hgb by 1 g/dl
Platelets
Platelets, Plasma
250
Inc. count by 25,000
FFP
Fibrinogen, antithrombin III,
clotting factors, plasma
250
Inc. Fibrinogen 10
mg/dl
Cryoprecipita
te
Fibrinogen, VonWillebrand F,
Factor V111, X111,
Fibronectin
40
Inc. Fibrinogen 10
mg/dl
Target Values
•
•
•
•
•
•
•
Maintain systolic BP>90 mmHg
Maintain urine output > 0.5 ml per kg per hour
Hct > 21%
Platelets > 50,000/ul
Fibrinogen > 100 mg/dl
PT/PTT < 1.5 times control
Repeat labs as needed – every 30 minutes
Management of Major Obstetric
Haemorrhage
Recombinant factor VIIa
(rFVIIa)
1.
rFVIIa works at the site of
vascular injury, where
tissue factor (TF) is
expressed and activated
platelets aggregate.
rFVIIa
The fibrin clots formed in
the presence of of a high
thrombin concentration
have a different architecture
that is stronger and more
resistant to degradation by
fibrinolytic enzymes.
Fibrin
Fibrinogen
Thrombin
Va
rFVIIa
In pharmacological doses
rFVIIa binds directly to
the activated platelet
surface.
Xa
X
Prothrombin
Here it enhances localized
thrombin generation and
the formation of a stable
fibrin-based clot.
Recombinant factor VIIa
• It is not licensed for use in obstetric haemorrhage and
there have been no randomised contolled trials for its
use in this situation
• The dose is approximately 90μg/kg.
• Its efficiacy is dependent on
-normothermia,
-non-acidotic milieu
-adequate levels of fibrinogen (> 1.0-1.5gr)
-platelets (> 50,000)
• A relatively early itervention to control PPH
appears to be crucial for the success of rVIIa
Management of Major Obstetric
Haemorrhage - rFVIIa
1. rFVIIa will not replace ligatures in controlling bleeding
from damaged or torn vessels.
2. To be effective there must be adequate circulation
delivering platelets and fibrinogen to the site of
bleeding.
3. You should make your best efforts to correct acidosis
and hypothermia.
TREAT
THE
ETIOLOGY
OF PPH
MANAGEMENT OF PPH

TEAM
- Obstetrician,
- Anesthesiologist,
- Haematologist and
- Blood Bank





Correction of hypovolaemia
Ascertain origin of bleeding
Ensure uterine contraction
Surgical management
Management of special situation
Massive Obstetric
Haemorrhage Treatment
 Medical
 Surgical
 Blood Component
Therapy
 Post Treatment Care
Massive Obstetric Haemorrhage
Medical

Volume Replacement (Crystalloid,Colloid)

Blood (O –tive, Group Specific, X Matched)

Coagulation Support (FFP, Cryoprecipitate, Platelets)

Inotropic Support
Uterine Massage / Compression
Uterotonic Agents (Syntocinon ,Ergotamine, Carboprost
Misoprostol )



Temperature Active Warming
Massive Obstetric Haemorrhage
Surgical
• EUA Repair
• Uterine Tamponade (78%)
• B-Lynch Suture (81%)
• Arterial Ligation
• Radiological Arterial Embolisation
• Hysterectomy ( 12%)
Treatment of PPH: Hysterectomy

A conservative option should be quickly efficacious
 The addition of successive conservative approaches is
hazardous
- Risk of delaying radical treatment
Early Decision
 Placenta accreta is a frequent cause of failure of
conservative Treatments
 Hysterectomy may be a life-saving procedure in case of
- Failure of conservative approach
- Uterine rupture
- Placenta accreta
Selective Angiographic Embolization
(SAE)
Strategically difficult in many
centers
Pulmonary
Embolism
Pulmonary Embolism
Pulmonary embolism, along with amniotic fluid
embolism, accounts for the leading cause of maternal
mortality in the United States
(Koonin, et al; MMWR)
DVT: Key Facts
•
40% of asymptomatic patients with DVT have
radiographically documented pulmonary embolism
• DVT of pelvic venous system is often an asymptomatic
condition until clinical pulmonary embolism develops
• Untreated pulmonary embolism mortality is up to
30%. Treated mortality is 3%
(Moser et al, 1994; Cunningham et al, 1997; Toglia & Weg, 1996)
The Wells score







clinically suspected DVT
- 3.0 points
alternative diagnosis is less likely than PE
- 3.0 points
Tachycardia
- 1.5 points
immobilization/surgery in previous four weeks
- 1.5 points
history of DVT or PE
- 1.5 points
hemoptysis
- 1.0 points
malignancy (treatment for within 6 months, palliative) - 1.0 points
Traditional interpretation
 Score >6.0 - High
 Score 2.0 to 6.0 - Moderate
 Score <2.0 - Low
Alternate interpretation
 Score > 4 - PE likely. Consider diagnostic imaging.
 Score 4 or less - PE unlikely. Consider D-dimer to rule out PE.
Diagnosis of Pulmonary
Embolism
•
•
•
•
•
•
•
•
D-dimer (0-300 ng/ml as normal)
Chest X-ray
ECG
Arterial blood gas
Ventilation-perfusion scintography
Angiography
Thoracic enhanced CT (64 slices MDCT)
Extremity Doppler
Chest X-Ray Findings in
PE:
• Hampton’s Hump:
pleural based density at CPJ
• Westermark’s Sign:
peripheral aligemia with
proximal vessel dilatation
• Most common finding is
normal X-Ray (30%)!
ECG Changes in PE:
•
p-pulmonale, RBBB, RAD
• S1 Q3 T3 classic signs
-large S wave in lead I
-a large Q wave in lead III and
-an inverted T wave in lead III
• New Onset A-Fib
• Most common finding is normal (or sinus tach) ECG
Radiographic Diagnosis of
Pulmonary Embolism During
Pregnancy:
• Ventilation/Perfusion (V/Q) Scanning
• Pulmonary Angiography
• Spiral/Helical CT
Treatment- Pulmonary
Embolism in Pregnancy
• Anticoagulation is mainstay of
pharmacotherapy
• Supportive care should not be
forgotten during the rush to diagnose
and treat
Venous Air Embolism
 During
the repair of hysterotomy wound
 Exteriorization of the uterus and traction on
the wound edges increases the risk
 Trendelenburg position to be avoided
 Abdominal and Uterine incision always below
heart
 CVP, High Uterine wound
Air Embolism
Amniotic Fluid
Embolism
“Anaphylactoid syndrome of
pregnancy"
Amniotic Fluid Embolism
AFE is an
- unpredictable
- unpreventable and
-an untreatable
(for the most part)
obstetric emergency
Amniotic Fluid Embolism
• Frequency- 1/15,000 - 1/20,000
Pregnancies
• Catastrophic Consequences
• Multisystem Collapse
• Mortality Quoted as High as 80%
(Probably Lower Now)
First Victim of AFE
1817 an obstetrician named
Sir Richard Croft
 The patient was Princess Charlotte
of Wales
 She died, presumably from an
undetected post-partum haemorrhage
 Condemnation and grief Croft
experienced led him to
commit suicide
 Charlotte's pregnancy is known
in medical history as

“the triple obstetrical tragedy”.
Pathophysiology- Animal
Data:
•
Amniotic fluid thought to be composed of some
abnormal factor or mediator
• Factor is heat stable
• Factor is soluble?
• Possible relationship with anaphylactoid
phenomenon
• Abnormal components such as meconium may play
a role
(Hankins, 1995; Hankins, et al, 1993; Clark, 1995)
Situations Related or NOT
Related to AFE:
• Uterine Hyperstimulation- AFE registry suggests
that hyperstimulation is EFFECT rather than
cause of AFE
• Oxytocin use- NOT RELATED
• Drug Allergy and/or Atopy- RELATED, with
41% of patients in AFE registry with allergies
• Normal labor!!??
(Clark, 1997)
Amniotic Fluid Embolism
Mechanism
Clinical presentation
The classic clinical presentation of the syndrome
has been described by five signs that often occur
in the following sequence:
(1) Respiratory distress
(2) Cyanosis
(3) Cardiovascular collapse cardiogenic shock
(4) Hemorrhage
(5) Seizure & Coma.
Diagnosis

The presence of squamous cells in the pulmonary
arterial blood obtained from a Swan-Ganz catheter
once considered pathognomonic for AFE is
neither sensitive nor specific

The monoclonal antibody TKAH-2 may eventually
prove more useful in the rapid diagnosis of AFE.
National registry’s criteria for
diagnosis of amniotic fluid
embolism
AFE- Differential Diagnosis
•
•
•
•
•
•
Pulmonary Embolism
Venous Air Embolism
Myocardial Infarction
Eclampsia
Anaphylaxis
Local Anesthetic Toxicity
Management of AFE
RECOGNITION
FIRST STEP
IMMEDIATE MEASURES :
- Set up IV Infusion,
-O2 administration.
- Airway control  endotracheal intubation
maximal ventilation and oxygenation.
 LABS : CBC,ABG,PT,PTT,fibrinogen,FDP.

Management of AFE
Treat hypotension, increase the circulating volume and
cardiac output with crystalloids.
 After correction of hypotension, restrict fluid therapy to
maintenance levels since ARDS follows in up to 40% to 70%
of cases.
 Steroids may be indicated (recommended but no evidence
as to their value)
 Dopamine infusion if patient remains hypotensive
(myocardial support).
 Other investigators have used vasopressor therapy such as
ephedrine or levarterenol with success (reduced systemic
vascular resistance)
 Treat Coagulopathy

RESUSITATION
OF
CARDIAC ARREST
Cardiopulmonary
Resuscitation in Pregnancy
 If you think that this will never happen to you,
you are wrong!
 Being an Obstetrics provider is no excuse not to be
CPR literate.
 Non-Obstetrics providers may know more than you
do about CPR, but they may know little or nothing
about pregnancy, fetal evaluation, etc.
Possible Outcomes
• Mother and babies die or brain-damaged
• Mother and babies intact
• Mother intact, babies die or impaired
• Mother brain damaged, babies intact
• Family takes legal action against hospital,
anesthesiologist, obstetrician
Cardiac Arrest in Pregnancy
What happens next depends on:

Maternal diagnosis

Fetal condition and maturity

How rapidly and appropriately medical and
nursing personnel respond

Resources available in hospital
Cardiac Arrest in Pregnancy:
Complicated by Physiologic
Changes

Rapid development of hypoxia,
hypercapnia, acidosis

Risk of pulmonary aspiration

Difficult intubation

AORTO-CAVAL COMPRESSION by
pregnant uterus when mother supine

Changes greater in multiple pregnancy,
obesity
Cardiac Arrest in Pregnancy:
Special Problems
•
Cardiac output during closed chest massage
in CPR is only ~ 30% normal
•
Cardiac output in the supine pregnant
woman is decreased 30-50% due to
aortocaval compression
•
Combined effect of above: There may be
NO cardiac output!
MRI Scan
• NORMAL
•
Aortocaval Compression- occurs
during second 1/2 of pregnancy
Cardiff Resusitation Wedge
Guidelines 2000 for Cardiopulmonary
Resuscitation and Emergency Cardiac Care
An international evidence and science-based consensus:
What’s new or different?

Anticipatory treatment of cardiac arrest

Emphasis on Automatic External Defibrillators (AEDs)

Competent bag-mask ventilation - may be better than
intubation attempts

Use of amiodarone 300 mg IV (in place of lidocaine*)

Vasopressin 40 mg x 1 (alternative to repeated doses
epinephrine 1 mg IV every 3-5 min*)

Family presence during resuscitation
*Insufficient evidence to support efficacy
American Heart Association, 2000
Why is Urgent Delivery
Indicated?

Maternal brain damage may start at ~ 4-6 min

What is good for mother is usually good for baby

Most intact newborns delivered within 5 min

Closed chest massage is less effective with time

CPR may be totally ineffective before delivery:
Many reports of mother “coming back to life”
after delivery
Advantages of Early
Delivery

Aortocaval compression relieved:
Venous return , Cardiac output 

Ventilation improved:
-Functional Residual Capacity 
-Oxygenation improved

Oxygen consumption , CO2 production 

Improved maternal and newborn survival
The Cesarean Delivery
Decision - Not an Easy One!
• Has 3-4 min passed since cardiac arrest?
• Has the mother responded to
resuscitation?
• Was resuscitation optimal - can it be
improved?
“Perimortem” Cesarean
Section

Start by 4 minutes, deliver by 5
minutes (From the time of Arrest)

Perform operation in patient’s room:
Can move to OT after delivery

Don’t worry about sterility

Vertical abdominal incision quickest

Prepare for uterine hypotonia and
bleeding
Optimal Outcome
Immediate CPR 
ACLS
IS THIS REALISTIC
OUTSIDE THE OR?
Early intubation
Left Uterine displacement
Start Cesarean by 4 min
Delivery by 5 min
Essential Equipment (Should be
available in Labour ward)

Pulse oximeter

Cardiac arrest cart; defibrillator

Automatic Electric Defibrillator (AED)?

Cesarean section instruments

Difficult intubation equipment (including LMA, jet
ventilator, fiberoptic laryngoscope)

Thoracotomy instruments

Blood warmer and rapid fluid infuser

Central venous and arterial line equipment
Common Problems in
Obstetrics

Denial of problem  delay in response

Communication errors

Obstetric staff not prepared for catastrophes

Inadequate response from transfusion or labs

No specialty in-house surgeons (e.g., for airway,
vascular, cardiac problems)

No OB-ICU facilities
Family Support
 When
the mother and infant are gravely ill,
keep their family members well informed.
 Be cool and calm while communicating with the
family members
 Allow as much access to the loved ones as
possible.
 Get informed consent at each stage.
WORK FORCE & PROTOCALS
• In such emergency situation
It appears important to:
– Streamline the workflow
– Co-ordinate the efforts
of different specialities
ІObstetrician
ІІAnaesthetist
• Assessment of patient condition
• Resuscitation
– General condition, BP, pulse, revealed blood –Maintenance of haemodynaemic status of patient
loss
– Fluid & blood product replacement
• Assessment of blood loss
• Estimation of blood loss
– Estimation of blood loss is notoriously
–More experienced in blood loss estimation
difficult & inaccurate
• Anaesthesia
• Control bleeding
– Induction a & maintenance of anaesthesia
–Manual pressure, oxytocic, operative
• Drug administration
procedures
5 Elements in
management
ІІІOperating Theatre
• Preparation for emergency operation
• Assistance in operative procedures
– Scrub nurse to conduct operation
– Assist in administration of anaesthesia
– Assist in fluid, blood product and drug
administration
ІV Radiologist
• Control of haemorrhage
– Cannulisation of pelvic vessels
– Embolization of pelvic vessels to control
bleeding
VPaediatrican
• Resuscitation of newborn
– Stand by delivery
– Immediate resuscitation of newborn
– Escort newborn to NICU
Multidisciplinary Team Approach
Obstetrician
Hospital
Administration
Neonatology
Risk
Management
Anesthesiology
PATIENT
Blood Bank
Social Work
Nursing
Radiology
Hemorrhage protocol Logistics
• Protocal should be specific for your hospital
(Hospital specific)
• Protocal depends upon your hospital infra- structure
and the availability of Resource persons
•Determine the hemorrhage response team
•Determine team member responsibilities
• Update and modify your Protocal periodically
• Conduct periodic Emrgency drill
Early Haemorrhage
Early Recognition
Early intervention
Hypotention
Prevent shock
Shock
Resusitation
Late intervention
CPR
Cardiac Arrest
Deliver the baby < 5mts
Summary
Successful treatment requires:
 Communication
 Preparedness
 Multidisciplinary Team Approach
 Hospital Hemorrhage Protocol
A Good
understanding
between
MULTIDISCIPLINARY
TEAM
IS A MUST
FOR THE SUCCESS
Intelligent anticipation,
skilled supervision,
prompt detection and
effective institution of therapy
can prevent
disastrous consequences .