Maternal Collapse

in
labour ward

Dr . J. Edward Johnson. M.D., D.C.H.

Asst. Professor ,
Dept. of Anaesthesiology,
KGMCH.
 Case Summary: 1
2 a.m.
Mrs. Everybody’s Patient
 A 30 year old woman, 37 weeks pregnant with
TWINS arrives at the hospital
 Cervix: 6 cm dilated. Patient is in severe pain. Labor
is progressing rapidly
 Epidural block: 15 ml 0.125% bupivacaine + fentanyl
75 µg
 15 minutes later - patient is still in severe pain
 12 ml 0.25% bupivacaine given in two increments
 Patient is comfortable. You go to bed and fall into a
deep sleep…...
 Case Summary: 1 Cont…….
3 a.m.

 Obstetrician and anesthesiologist called “stat” to labor

room
 Membranes ruptured spontaneously 10 min ago
 3 min ago, the patient complained of difficulty
breathing and lost consciousness
 Fetal heart rate: 90 beats/min
 Vaginal bleeding
 Patient cyanotic
 Maternal BP and Pulse not obtainable
 Case Summary:1 Cont…..
3.03 a.m.

 Patient mask ventilated with Ambu bag and O2

 No improvement…
 You start CPR with the aid of the anesthesiologist

3.07 a.m.

 Patient is intubated - she aspirates gastric

contents!

 ASYSTOLE diagnosed
 Case Summary:1 Cont….
3.10 a.m. • All IV lines displaced during CPR

• Epinephrine given via endotracheal tube

• IVs replaced with difficulty

3.13 a.m. • No maternal Pulse or BP detected

• FHR: 50-60 beats/min

• Cervix 8 cm dilated

3.17 a.m.
• Patient transported to OT while closed chest
massage (CPR) continues

• Cesarean Section started

 Case Summary:1 Cont….
3.23 a.m.

Delivery of male infants:

A: Apgar: 0, 1, 4 (at 1, 5, and 10

minutes)
B: Apgar: 0, 0, 0

Delivery occurred 23 minutes after start of CPR

 Case Summary: 1 Cont….

3.25 a.m.  Maternal heart rate returns

3.30 a.m.  BP 100/70; Pulse 130

 Significant bleeding

22.00 p.m.
• Mother unconscious in ICU

• Coagulopathy (DIC) resolving

Possible Causes of Cardiac
Arrest
• Amniotic fluid embolism

• Pulmonary embolism

• Hemorrhage (including ruptured

uterus)

• Myocardial infarction,
cardiomyopathy

• High spinal (or sub-dural) anesthesia

• Spinal opioid respiratory depression

 Mrs. Everybody’s Patient 2

“Let’s Do an Elective C/Section…”

• Healthy 30 y old primigravida with twins for elective C/S

(breech/Vx)

• 5 ft 4 inches tall, 70 kg

• Pre-operative: BP = 98/60; Pulse 52

• Fluid preload - 1500 ml crystalloid solution

• Uncomplicated spinal at L3/4, patient sitting

• Bupivacaine 12 mg + Fentanyl 10 µg
Continue
d:
• Patient is placed supine, left uterine displacement

• Block T4 bilaterally (3 min after spinal)

• “I don’t feel well… My hands are numb”

• “I can’t breathe.”

• Poor hand strength - patient cannot raise arm

• Patient is anxious, diaphoretic, nauseated

Events after Spinal Block for Cesarean Section
Hands numb Chest Pain
Nausea Dyspnea
180

160 Syst BP
Diast BP
140 Pulse
SPO2 Cardiac
120
Arrest!
100

80

60

40

20
Ephedrine Phenylephrine
0 (mg): 5 5 10 10 10 10 10 10 100 µg
0 2 4 6 8 10 12 14 16
Time after spinal block (min)
 Cardiac Arrest during Spinal for
Cesarean Section Cont……

• CPR / ACLS started

• Immediate Cesarean Section performed

• Delivery: 5 min after arrest occurred

Apgar scores:
A: 5, 6, 7
B: 3, 4, 5

• Babies to Intensive Care; severely

acidotic
Post-Delivery Course Cont……

• Mother responds to epinephrine: 1 mg x 3 after 10

minutes of resuscitation (5 min after delivery)

• BP 160/110, P 140

• To ICU, intubated

• Mother has residual neurologic deficit;

memory and concentration significantly
impaired

• Unable to work or care for babies

• Babies appear normal at 2 years of age

“This wILL never
happen to
my

patient !” Your attitude

Dec 2004
ore Dec 2004 we were not aware of Tsunami
thought it will never happen to us
were not prepared
death toll stood at 169,752 with 127,294 people listed as missing.
This wILL never
happen to
my
patient !
So denial won’t help us
Be prepared for any catastrophes
Maternal Collapse
in
labour ward
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.,

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
 Lab Diagnosis
The Decrease of Fibrinogen is an Early Predictor of the
Severity of Postpartum Haemorrhage

Severe group Nonsevere group

n=50 n=78

Platelets(10² L-1) 173 181

PT (%) 81 88 .02
INR 1.16 1.10 .02
APTT ratio 1.0 1.0 .05
Fibrinogen (g L-1) 3.3 4.4 <.0001
Factor II (%) 83 93 .005
Factor V (%) 72 90 .004
D-Dimer (μg mL-1) 9 6 .007
Antithrombin activity (%) 72 79 .005
Protein C antigen (%) 69 75 .038
Euglobulin lysis time (% <180 min) 26 19
MANAGEMENT

RESUSITATION
OF
Haemorrhagic Shock

Cardiac Arrest
RESUSITATION

Haemorrhagic
Shock
 Classification of
Haemorrhage
Class Acute Blood % Lost
Loss
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 pallor,oliguria,
confusion
40+ 40-60 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 minut
• 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 hea
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
System Shock
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

Gastrointestin No change Mucosal bleeding
al
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,
 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

Red Cells
Leucocyte-Reduced Red Cells
Irradiated Blood
Washed Blood
Frozen Cellular Components
Blood
Component
Therapy
Random Donor Platelets
Single Donor Platelets
Cryoprecipitated AHF
Fresh Frozen Plasma
Fibrinogen Concentrate
Liquid Plasma
Plasma Derivatives
 Platelets

Random Donor Apheresis

Pooled 4-8 units, ABO Single donor

+ Rh compatible

Expire 4 h after released

Expire 4 h after pooling

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 Effect
(ml)

Packed RBCs RBC, Plasma 300 Inc. Hgb by 1 g/dl

Platelets Platelets, Plasma 250 Inc. count by 25,000

Fibrinogen, antithrombin III, Inc. Fibrinogen 10

FFP 250
clotting factors, plasma mg/dl

Fibrinogen, VonWillebrand
Cryoprecipita Inc. Fibrinogen 10
F, Factor V111, X111, 40
te mg/dl
Fibronectin
 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
 Blood Component Replacement
Cost
COSTS UNIT Time to get

Whole Blood Rs 850 1Hr

RBC Rs 850 1Hr

Platelets Rs 900 2 Hrs
FFP Rs 850 1Hr
Cryoprecipitate Not
available
Management of Major Obstetric 
Haemorrhage 
Recombinant factor VIIa 
(rFVIIa)
 the site of
vascular injury, The fibrin clots formed
where tissue in the presence of of a
factor (TF) is
expressed and
rFVII high thrombin
concentration have a
activated
platelets
a different architecture
that is stronger and
aggregate. more resistant to
degradation by
fibrinolytic enzymes.
Fibrin

Fibrinogen

Thromb
in Here it enhances
localized
Va
thrombin
Xa generation and
rFVIIa the formation of a
In
pharmacological X Prothrombin stable fibrin-
doses rFVIIa based clot.
binds directly to
the activated
platelet surface.
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
• rFVIIa will not replace ligatures in
controlling bleeding from damaged or torn
vessels.

• To be effective there must be adequate

circulation delivering platelets and
fibrinogen to the site of bleeding.

• 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
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%
 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
Exteriorization of Uterus
 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
Mechanis m
 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.
 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
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
AIRWAY
AIRWAY CORRECTION
 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
                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
Multidisciplinary Team Approach
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 Early
Recognition intervention
Hypotentio
n

Prevent shock

Shock
Late
Resusitation
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 thera
can prevent
disastrous consequences .