obstetric collapse

8/18/2019 Obstetric Collapse

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Maternal Mortality Conference, Hotel BayviewPenang, 30-31 Oct 2007

POST PARTUM COLLAPSE

PROF. DR. MA JAMIL

FACULTY OF MEDICINE

UNIVERSITI KEBANGSAANMALAYSIA


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Introduction

Fortunately a rare condition

May be life threatening

Aim is to institute immediate and effectiveresuscitation to maintain adequate

oxygenation and effective cardiac output

Find out the cause and treat Important to have guidelines and training


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Definition of Collapse

Non specific term that imply loss of

consciousness

Can be a primary cerebral event or a

secondary to a cardiac event leading to

cerebral hypo perfusion


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Pathophysiology

Cerebral Event that leads to loss of

Consciousness

1. Epileptic fits

2. Hypoglycemia

3. Profound hypoxia

4. Intracerebral bleeding

5. Cerebral infarction

6. Anesthetic or analgesic drugs


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Cardiovascular Events

Primary cardiac like arrhythmias, MI

A blockage in circulation as in Pulmonary.

Embolism

A reduction in circulating volume eg

massive PPH

A relative decrease of effective circulatingvolume as in anaphylaxis


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A clinical approach to obstetrics

collapse


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Think of the causes

1.Inversion of Uterus: usually thirdstage, profound hypotension

2. Drugs : If opiates give Naloxone

3. Sepsis : Clinically vasodilated,

tachycardia,Cyanosis and PYREXIA

4. CVA : h/o intracranial problems,nausea, vomitting, headache or

presence of PE

5. Embolism : Amniotic fluid embolism:

Multip, Precipitate labour,uterine

stimulation, CS, Sudden

dyspnoea,fetal distress,

hypotension,And cardiovascular

collapse Lungs shows pleuritic

chest pain, sudden Dyspnoea,

cough, hemoptysis, and collapse


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Still thinking……

6.Anaphylaxis:Cyanosis, hypotension,wheezing

Pallor, prostration, tachycardia and uticaria

7. MI : history of heart disease, chest pain

8. Bleeding : APH or PPH. Usually bleeding is

underestimated esp in abruptio. Can be due

to uterine rupture : Shock, loss of contractionsLoss of fetal heart and presenting part

9. Eclampsia : seizures, tonic clonic contractions

Have to differentiate from epilepsy and

AF Embolism

10.Hypoglycaemia : h/o DM, pale and clammy.Treat with IV glucose or Glucagon.

11.Abruption : abdo pain, antepartum bleeding,

Coagulopathy, fetal distress


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Management of Post Partum Collapse

Check responsiveness

Open Airway

Assess

Check breathing

Breathe

Circulation present,

Continue rescue

breathing ( Check every

minute)

No Circulation

Compress chest,(100/min

15:2 Ratio

Shake and shout

Head tilt / Chin Lift

Look, Listen and feel

Two effective breath

Signs of Circulation


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Reversible Causes for Collapse

Four “H”

1. Hypoxia

2. Hypovolaemia3. Hypo or hyperkalaemia and metabolic

disorders

4. Hypothermia


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Reversible Causes for Collapse

Four “T’s”

1. Thromboembolic (pulmonary or amniotic

embolism )

2. Toxic and therapeutic (local anesthetic)

3. Tension Pnemothorax

4. Tamponade


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1. Post Partum Haemorrhage

Cause and management is obvious and

covered in other lectures

Bleeding may be concealed due to

paravaginal or broad ligament hematoma

Other rare causes of bleeding includes

hepatic rupture, rupture of aneurysm of

splenic artery, Bleeding from AV

malformation


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2. Uterine Rupture

Symptoms and signs as previously

described

Highest in second stage

Associated with instrumental deliveries or

rupture in a previous CS

May collapse soon after the deliveryResuscitation - repair or hysterectomy


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3. Uterine Inversion

Rare but dramatic event

All labor ward MUST have a guideline tomanage this complication

Causes include traction prior toseparation, fundal compression, morbidlyadherent placenta

Clinically as describedManagement is to rapidly try to replace the

inverted uterus after resuscitation.


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4.Septic shock

Described in other lectures

Key is collapse with pyrexia

Look for risk factors like chorioamnionitis

Treatment is to restore tissue perfusion, treatunderlying infection which is invariably

bacterial

Fluid, invasive monitoring of cardiac function,Inotropes invariably,

Appropriate antibiotics


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5. Eclampsia

Usually associated with PE

38 % may occur in normotensive women

44 % occurs post delivery

Initial fist usually self limiting and may notneed diazepam. Sufficient to preventinjuries to the patient

Diazepam may cause respiratorydepression and use only in uncontrolledfits


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Complications of Treatment for

eclampsia

Mg Toxicity :

Monitor patella reflex and respiratory rate

Stop infusion if loss of patella reflex anddo se.Magnesium

Resp arrest accurs when se Mg is at 6.3-

7.0,cardiac arrest at 12 mmol/l10ml of 10% Ca Gluconate over 10 mins

IV


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6. Anaphylaxis

Hypersensitivity reaction causing severebrochospasm, profound hypotension andcardiac arrest

Clinically exposure to allergens, developtachycardia, hypotension with uticarial rash orwheezing

Treatment includes O2, adrenalin 500µg im and

may be repeated.(0.5 ml in 1:1000)Other treatment include antihistamines, and

hydrocortisone in severe cases


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8. Puerperal Cardiomyopathy

Usually the last month of pregnancy up to 5months after delivery

Mortality is high up to 50 %

LV heart failure may be diagnosed antenatallybut may be difficult.

Do echo in suspected cases

Resuscitate, treat heart failure with diuretics,inotropes, ACE inhibitors and

thromboprophylaxis If not responding, cardiac transplantation is an

option


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9.Heart Disease : Congenital

and Acquired

An increasing cause of maternal death

Leading indirect cause of maternal death inMalaysia

Highest risk at the end of labour and postdelivery

Delivery should be planned with appropriatediscussion with cardiologist and anesthetist

Patient with primary pulmonary stenosis and

Eisenmengers Syndrome runs the greatest riskof deterioration due to RV failure and atrialtachyarrythmias. Should be appropriatelycouncelled


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Amniotic Fluid Embolism CEMD 97-00

Year 97 98 99 2000

No of

Cases

18 20 30 23

No of Cases of Cases of Maternal Deaths due to obstetric embolism


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Causes of Obstetric Embolism 1997-2000

Causes 97 n=19 98 n=20 99 n=30 00 n=23

AF

Embolism15 (80%) 16(80%) 19(63.3%) 10(43.5%)

Obstetricblood clot

embolism

3 4 11 13

NB:a big number have no post mortem done


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AMNIOTIC FLUID EMBOLISM

AFE is thought to occur when amniotic fluid , fetal cells,hair, or other debris enter the maternal circulation.

Ricardo Meyer (1926); reported the presence of fetal cellulardebris in the maternal circulation.

Steiner and Luschbaugh (1941) described the autopsyfindings of eight cases of AFE.

Until 1950, only 17 cases had been reported.

AFE was not listed as a distinct heading in causes ofmaternal mortality until 1957 when it was labeled asobstetric shock.

Since then more than 400 cases have been documented,probably as a result of an increased awareness.


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Overall incidence ranges from 1 in 8,000 to 1 in 80,000pregnancies.

10% of maternal deaths in USA &16% in U.K.

The first well-documented case with ultimate survival was

published in 1976(Resnik R, et al. Obstet Gynecol 1976;47:295-8).

75 % of survivors are expected to have long-term neurologic

deficits.

If the fetus is alive at the time of the event, nearly 70 % willsurvive the delivery but 50% of the survived neonates will incur

neurologic damage.


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Time of event:

- During labor.

- During C/S.- After normal vaginal delivery.

- During second trimester TOP.

AFE syndrome has been reported to occur as lateas 48 hours following delivery.


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Risk factors of AFE

Advanced maternal age Multiparity

Meconium

Cervical laceration

Intrauterine foetal death Very strong frequent or uterine

tetanic contractions

Sudden foetal expulsion (short

labour)

Placenta accreta Polyhydramnios

Uterine rupture

Maternal history of allergy or

atopy

Chorioamnionitis

Macrosomia

Male fetal sex

Oxytocin (controversial)

Nevertheless, these and other frequently cited risk factors

are not consistently observed and at the present time

Experts agree that this condition is not preventable.


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Pathophysiology

- Poorly understood.- Cotton (1996), has proposed a biphasic model.Phase 1:

Amniotic fluid and fetal cells enter the maternalcirculation biochemical mediators pulmonary artery

vasospasm pulmonary hypertension elevated rightventricular pressure hypoxia myocardial and pulmonarycapillary damage, left heart failure acute respiratorydistress syndrome

Phase 2:

biochemical mediators DIC Hemorrhagic phasecharacterized by massive hemorrhage and uterineatony.


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Pathophysiology

The similar homodynamic derangements seen with AFE

syndrome , anaphylactic, and septic shock have led

investigators to postulate a substance in amniotic fluid resulting

in the release of primary and secondary endogenous mediators

(i.e. arachidonic acid metabolites) which might also beresponsible for the associated coagulopathy in AFE.

The prevention of fatal homodynamic collapse in experimental

AFE with inhibitors of leukotriene synthesis would support an

anaphylactic mechanism for AFE.


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Pathophysiology

Measurement of tryptase ( a degranulation product

of mast cells released with histamine during

anaphylactic reactions) levels to further investigate

the anaphylactic nature of AFE.

The syndrome does not appear to be dependent on

the amount of fluid or particulate matter that

enters the vasculature.


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Pathophysiology

To emphasize that the

clinical findings are

secondary to biochemical

mediators rather than

pulmonary embolicphenomenon; Clark et al

have suggested renaming

this clinical syndrome the

"anaphylactoid syndrome of pregnancy"


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Clinical presentation

The classic clinical presentation of the syndrome has

been described by five signs that often occur in thefollowing sequence:

(1) Respiratory distress(2) Cyanosis

(3) Cardiovascular collapse cardiogenic shock

(4) Hemorrhage(5) Coma.


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A sudden drop in O2 saturation can be the initialindication of AFE during c/s.

More than 1/2 of patients die within the first hour.

Of the survivors 50 % will develop DIC whichmay manifest as persistent bleeding from incision orvenipuncture sites.

The coagulopathy typically occurs 0.5 to 4 hoursafter phase 1.


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10-15% of patients will develop grand mal seizures.

CXR may be normal or show effusions, enlarged

heart, or pulmonary edema.

ECG may show a right strain pattern with ST-T

changes and tachycardia.


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Diagnosis

In 1941, Steiner and Luschbaugh described histopathologicfindings in the pulmonary vasculature in 8 multiparous

women dying of sudden shock during labor.

Findings included mucin, amorphous eosinophilic material ,

and in some cases squamous cells. The presence of squamous cells in the pulmonary

vasculature once considered pathognomonic for AFE is

neither sensitive nor specific (only 73% of patients dying from

AFE had this finding).

The monoclonal antibody TKAH-2 may eventually prove more

useful in the rapid diagnosis of AFE.


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epithelial squames in a peripheral pulmonary artery.


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Laboratory investigations

in suspected AFENon specific

• complete blood count

• coagulation parametersincluding FDP, fibrinogen

• arterial blood gases

• chest x-ray

• electrocardiogram

• V/Q scan

• echocardiogram

Specific

cervical histology

serum tryptase serum sialyl Tn antigen

zinc coproporphyrin

PMV analysis (if PA

catheter in situ )


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Differential diagnosis Obviously depends upon presentation

Anaphylaxis (Collapse)

Pulmonary embolus

(Collapse)

Aspiration (Hypoxaemia)

Pre-eclampsia or

eclampsia (Fits,

Coagulopathy)

Haemorrhage (APH ; PPH)

Septic shock

Drug toxicity (MgSO4, total

spinal, LA toxicity)

Aortic dissection


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Management of AFE

GOALS OF MANAGEMENT: Restoration of cardiovascular and pulmonary

equilibrium

- Maintain systolic blood pressure

>90 mm Hg.

- Urine output > 25 ml/hr

- Arterial pO2 > 60 mm Hg.

Re-establishing uterine tone Correct coagulation abnormalities


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Management of AFE

As intubation and CPR may be required it is necessary

to have easy access to the patient, experienced help,

and a resuscitation tray with intubation equipment, DC

shock, and emergency medications. IMMEDIATE MEASURES :

- Set up IV Infusion, O2 administration.

- Airway control endotracheal intubationmaximal ventilation and oxygenation.

LABS : CBC,ABG,PT,PTT,fibrinogen,FDP.


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Management of AFE

Treat hypotension, increase the circulating volume andcardiac output with crystalloids.

After correction of hypotension, restrict fluid therapy tomaintenance levels since ARDS follows in up to 40% to 70%of cases.

Steroids may be indicated (recommended but no evidenceas to their value) Some suggest as high as 1 gm IV followedby infusion

Dopamine infusion if patient remains hypotensive(myocardial support).

Other investigators have used vasopressor therapy such asephedrine or levarterenol with success (reduced systemicvascular resistance)


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Management of AFE

In the ICU

To assess the effectiveness of treatment and resuscitation, it

is prudent to continuously monitor ECG, pO2, CO2, and urine

output.

There is support in literature for early placement of arterial,

central venous, and pulmonary artery catheters to provide

critical information and guide specific therapy.


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Management of AFE

In the ICU Central venous pressure monitoring is important to diagnose

right ventricular overload and guide fluid infusion and

vasopressor therapy. Blood can also be sampled from the right

heart for diagnostic purposes.

Pulmonary artery and capillary wedge pressures andechocardiography are useful to guide therapy and evaluate left

ventricular function and compliance.

An arterial line is useful for repeated blood sampling and blood

gases to evaluate the efficacy of resuscitation.


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Management of AFE

Coagulopathy

• DIC results in the depletion of fibrinogen, platelets,and coagulation factors, especially factors V, VIII,

and XIII. The fibrinolytic system is activated as well.

• Most patients will have hypofibrinogenemia,

abnormal PT and aPTT and low Platelet counts

• Treat coagulopathy with FFP for a prolonged aPTT,

cryoprecipitate for a fibrinogen level less than 100

mg/dL, and transfuse platelets for platelet countsless than 20,000/mm3


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Restoration of uterine tone

Uterine atony is best treated with massage, uterinepacking, and oxytocin or prostaglandin analogues.

Improvement in cardiac output and uterine

perfusion helps restore uterine tone.Extreme care should be exercised when using

prostaglandin analogues in hypoxic patients, as

bronchospasm may worsen the situation.


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Sympathomimetic Vasopressor agentDopamine

• Dopamine increases myocardial contractility and systolic

BP with little increase in diastolic BP. Also dilates the renal

vasculature, increasing renal blood flow and GFR.

• DOSE: 2-5 mcg/kg/min IV; titrate to BP and cardiac output.

• Contraindications: ventricular fibrillation, hypovolemia,

pheochromocytoma.

• Precautions: Monitor urine flow, cardiac output, pulmonary

wedge pressure, and BP during infusion; prior to infusion,

correct hypovolemia with either whole blood or plasma, as

indicated; monitoring central venous pressure or left

ventricular filling pressure may be helpful


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Maternal Mortal i ty in AFE

• Maternal death usually occurs in one of three ways:• (1) sudden cardiac arrest,

• (2) hemorrhage due to coagulopathy,

• (3) initial survival with death due to acute respiratory

distress syndrome (ARDS) and multiple organ failure

• For women diagnosed as having AFE, mortality rates

ranging from 26% to as high as 86% have been reported.

• The variance in these numbers is explained by dissimilar

case definitions and possibly improvements in intensivecare management of affected patients.


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Further issues in the Management

Transfer: Transfer to a level 3 hospital may be required once thepatient is stable.

Deterrence/Prevention: Amniotic fluid embolism is an unpredictable event.

Risk of recurrence is unknown. The recommendation forelective cesarean delivery during future pregnancies in anattempt to avoid labor is controversial.

Perimortem cesarean delivery: After 5 minutes of unsuccessful CPR in arrested mothers,

abdominal delivery is recommended.


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Medical / Legal Pitfal ls

• Failure to respond urgently is a pitfall.

• AFE is a clinical diagnosis. Steps must be taken to stabilizethe patient as soon as symptoms manifest.

•

Failure to perform perimortem cesarean delivery in a timelyfashion is a pitfall.

• Failure to consider the diagnosis during legal abortion is apitfall. A review of the literature indicates that most casereports of AFE have occurred during late second-trimester

abortions.


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SUMMARY

• AFE is a sudden and unexpected rare but lifethreatining complication of pregnancy.

• It has a complex pathogenesis and seriousimplications for both mother and infant

• Associated with high rates of mortality and

morbidity.• Diagnosis of exclusion.

• Suspect AFE when confronted with any pregnantpatient who has sudden onset of respiratory

distress, cardiac collapse, seizures, unexplainedfetal distress, and abnormal bleeding

• Obstetricians should be alert to the symptoms ofAFE and strive for prompt and aggressive treatment.


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10. Uncommon Causes of Collapse

Aortic dissection

Neurological abnormalities

Myocardial infarction

Hypoglycaemia

Drug reactions


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