Maternal Collapse In Labour Ward

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.

3.13 a.m.

3.17 a.m.

•

All IV lines displaced during CPR

•

Epinephrine given via endotracheal tube

•

IVs replaced with difficulty

•

No maternal Pulse or BP detected

•

FHR: 50-60 beats/min

•

Cervix 8 cm dilated

•

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 Nausea

180

Chest Pain Dyspnea

Syst BP Diast BP Pulse SPO2

160 140 120

Cardiac Arrest!

100 80 60 40 20 0

Phenylephrine Ephedrine (mg): 5 5 10 10 10 10 10 10 100 µg 0

2

4

6

8

10

Time after spinal block (min)

12

14

16

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 n=50 Platelets(10² L-1) PT (%) INR APTT ratio Fibrinogen (g L-1) Factor II (%) Factor V (%) D-Dimer (μg mL-1) Antithrombin activity (%) Protein C antigen (%) Euglobulin lysis time (% <180 min)

173 81 1.16 1.0 3.3 83 72 9 72 69 26

Nonsevere group n=78 181 88 1.10 1.0 4.4 93 90 6 79 75 19

.02 .02 .05 <.0001 .005 .004 .007 .005 .038

MANAGEMENT

RESUSITATION OF Haemorrhagic Shock Cardiac Arrest

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 following criteria:

the

• 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 al Hematological

No change

Mucosal bleeding

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 2040 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

Blood Component Therapy Random Donor Platelets Single Donor Platelets

Red Cells Leucocyte-Reduced Red Cells Irradiated Blood Washed Blood Frozen Cellular Components

Cryoprecipitated AHF Fresh Frozen Plasma Fibrinogen Concentrate Liquid Plasma Plasma Derivatives

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)

(contains all coag factors)

FFP

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

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, where tissue factor (TF) is expressed and activated platelets aggregate.

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.

rFVII a Fibrin

Fibrinogen

Thromb in Va

In pharmacological doses rFVIIa binds directly to the activated platelet surface.

rFVIIa

Xa

X

Here it enhances localized thrombin generation and the formation of a Prothrombin stable fibrinbased 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 • 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 Compressionoccurs 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 Early intubation

IS THIS REALISTIC   OUTSIDE THE OR?

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 Recognition

Early intervention Hypotentio n

Prevent shock Shock Late intervention

Resusitation 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 .