Obstetric Collapse
Transcript of 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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AMNIOTIC FLUID EMBOLISM
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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AMNIOTIC FLUID EMBOLISM
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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Clinical presentation
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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Clinical presentation
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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