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Obstetric AnaesthesiaObstetric Anaesthesia
EmergenciesEmergencies
John LaffeyNational University of Ireland,
AND Galway University Hospital,
Galway, IRELAND
IARNA Conference, Galway, October 2nd 2010
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Will focus on Maternal driven emergencies
Generally much more difficult situations!
Need to consider 2 patients rather than 1
A pregnant patient should not be penalised
Role of Physiologic Alterations of Pregnancy
Impact of pathologic conditions related to Pregnancy
Delivery of the Foetus may abrogate pregnancy induced conditions
Outcome
Generally Good.
Obstetric disasters ever anaesthetists ni htmare!
Key PointsKey Points
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30 admissions to ICU/HDU in 2009
14 Obstetric Admissions 4 PPH
3 PET/HELLP
7 other
16 Major Gynaecologic Surgery
Average LOS 2.2 days
2 ICU deaths (both Gynaecologic)
Obstetric Critical Care at GUHObstetric Critical Care at GUH
in 2009in 2009
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Obstetric Haemorrhage
Hypertension/ Pre-Eclampsia
Embolism
Sepsis e.g. Chorioamnionitis
Trauma
Maternal Obstetric Emergencies
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Cardiovascular
Heart Rate; Blood Pressure
Blood Volume; Cardiac Output
Venous Circulation; Vascular Resistance
Colloid Osmotic Pressure
Haematologic Hb - Decreased by max 2 g/dL
Relative Leukocytosis
Gestational Thrombocytopaenia
Procoagulant State [Fibrinogen; Protein S
Pulmonary
Reduced residual lung volume and FRC
Supine Hypoxia
Urinary System
Increased GFR [approaches 150%]; Protein Excretion
Drugs
Decreased serum drug concentration; Serum Albumin
Physiologic AlterationsPhysiologic Alterations
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Obstetric Haemorrhage
Hypertension/ Pre-Eclampsia
Embolism
Sepsis
Trauma
Maternal Obstetric Emergencies
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Size of the Problem
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Leading cause of maternal death worldwide
2 55% of deliveries complicated by PPH
Regional variation marked
Characteristically massive and swift
Blood flow to uterus late pregnancy 10% of CO
Haemorrhage may be concealed
Usual signs of hypovolaemia late or disguised
Size of the Problem
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Late Pregnancy Placenta Praevia
Placental Abruption
Spontaneous uterine rupture
DIC e.g. due to Amniotic Fluid Embolism Trauma
Postpartum
Uterine Atony
Surgical Trauma
Retained Placenta
DIC
Incidence and Causes
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Incidence 0.1% of Pregnancies
Causes
Placental Abruption
HELLP syndrome Intra-uterine Foetal Death
Acute fatty Liver of Pregnancy
Amniotic Fluid Embolism
Clinical Features
Oozing from IV or skin puncture sites, mucosal surfaces, surgical
site
Dramatic decrease in Fibrinogen level
Disseminated IntravascularCoagulation
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Management of MassiveHaemorrhage
Preparation
Identify patients at risk
Large bore IV access x 3
Blood available [Type specific; O neg]
Avoid caval obstruction; supplemental O2
Foetal monitoring, change indicative of
massive bleed
Search for evidence of DIC
- Peripheral blood smear
- PT, PTT, Platelet counts, Fibrinogen level; D-
dimer level
- ? Specific factor analyses-
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Immediate aggressive volume replacement
Crystalloid until blood available [warming+]
Consider PRBC once blood loss > 2,000mL
Anticipate need early
Unmatched type specific or Type O blood available if required
Dilutional coagulopathy once >80% of blood volume replaced
Platelets - if < 20,000/mm3 or higher if bleeding persisting
FFP only to correct measured clotting abnormalities
Cryoprecipitate
Volume Replacement
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Uterine atony
Uterine Massage; Oxytocin
Ergometrine [post delivery]; Prostaglandins [Intra-Endometrial]
U/S to detect retained products
Surgical exploration to repair lacerations, ligate arteries, perform
hysterectomy
Angiography
Selective embolization of Uterine, internal iliac or internal pudendal artery
with slowly absorbable gelatin sponge
Consider prophylactic placement of embolectomy catheters in internal
iliac arteries of patients at high PPH risk.
Factor 7a Rescue therapy in severe haemorrhage
Specific Therapies
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Obstetric Haemorrhage
Hypertension/ Pre-Eclampsia
Embolism
Sepsis e.g. Chorioamnionitis
Trauma
Maternal Obstetric Emergencies
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Hypertensive disorders are seen in 12% of pregnancies
18% of maternal deaths in the US
Predate / Unmasked / Precipitated
Predisposing Factors
Prenatal DM, renal disease, vascular disease
FHx of Hypertension
Primigravid State
Multiple gestational pregnancies
Definition of Hypertension in Pregnancy Degree of increase in SBP and DBP versus absolute value
30mmHg increase in SPB
15mmHg increase in DPB
Sustained elevated BP key risk factor
Size of the Problem
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Pregnancy Induced Hypertension
(Gestational Hypertension without Proteinuria)
After 20th gestational week; Longterm risk
Essential Hypertension
Before 20/40; Persists after delivery
Secondary Hypertension
consider if SPB consistently > 200mmHg
Primary Hyperaldosteronism
Cushings Syndrome
Phaeochromocytoma Renal Artery Stenosis
Coarctation of Aorta
Pre-Eclampsia
Gestational Hypertension with Proteinuria
Differential Diagnosis
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Perinatal mortality increased if severe sustained Maternal BP elevation
Outcome effect in less severe hypertension less clear
Intra-Uterine Growth Retardation
Caution: Effects on uteroplacental perfusion
Increasedmaternal mortality and end organ damage
Treatment recommended if SBP 160mmHg of DBP 110mmHg
Treat lower BPs if patient symptomatic
Treatment Options
PO: -methyldopa and Labetalol
IV: Labetalol, Hydralazine, Sodium Nitroprusside
Treatment Recommendations
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Management of aManagement of a
Hypertensive CrisisHypertensive Crisis
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Clinical Features
SBP generally 150mmHg; DPB 110 with
Hypertensive Encephalopathy
Confusion; Papilloedema; Retinal Haemorrhages
Other end-organ dysfunction e.g. Nephropathy, Neuropathy,
Retinopathy
Uteroplacental hyperperfusion, placental abruption,haemorrhage
Maternal Catastrophe e.g. Intracranial Haemorrhage
Severe Maternal Hypertension
SBP 240mmHg; DPB 140
ICU management irrespective of presence of clinical sequelae
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Investigation and Management
Investigations
Bloods incl U+E, Coagulation, CBC, LFTs Toxicology
Urinalysis
ECG, CXR;CT Brain
Monitoring
Maternal non-invasive monitoring
Foetal telemetry post viability threshold
Arterial Line + CVC
Treatment Goal
To reduce DBP to just below 100mmHg
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Therapeutic Strategies Oral
Labetalol PO
Dose 200-400mg BID
-methyldopa
BID/TID to max 4g/d
ACEIs and AT II Blockers
C/I antepartum
Nifedipine
Rapid effect; increases CI; Uteroplacental flow
10mg capsule PO, repeat every 15 30mins to max 30mg
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IV Antihypertensives
Labetalol
Rapidly decreases BP (5 mins) but not at expense of Uteroplacental bloodflow; no effect foetal HR
Decreases SVR and slows maternal HR
Hydralazine
Direct arterial vasodilator (preferred by Obstetricians) Care as onset action 10-20 mins; lasts approx 8 hrs
5 10mg boluses every 15-30mins until BP controlled
Na Nitroprusside
Potent, rapid, arterial and venous vasodilator
IV infusion 0.25-0.5g/Kg/min; max 4g/Kg/min
S/Es: Headache, dizziness, flushing, ototoxicity, cyanide toxicity
Foetal Cyanide toxicity not a major issue
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IV Antihypertensives
Nicardipine Onset action 10mins; duration 4 6hrs
Initial infusion 5mg/hr; increase by 2.5mg/hr every 5min; max 10mg/hr
Potential for NM blockade interaction with Magnesium
Nitroglycerin
Titrate to MAP
Less effective in severe Hypertension
Blockers
Atenolol [IUGR]
Esmolol [Foetal Bradycardia]
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Pre-Eclampsia
Incidence
7% of pregnancies in the US
Generally after 32nd week of gestation
May initially present after delivery as the HELLP syndrome
Primigravida versus older multiparous
Pathogenesis
Multi-system disease
Endothelial cell injury
Placental toxin release Genetic and immunologic factors
Generalised vasospasm; ?PG/TX imbalance
Microthrombi
Classic Clinical Triad
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Severe Pre-Eclampsia
Cardiorespiratory
Diastolic dysfunction; LV Failure; Pulmonary Oedema Increased alveolar-capillary permeability; ALI/ARDS
SBP generally 150mmHg; DPB 110
Renal Glomeruloendotheliosis [Proteinuria >5g/d];
Oliguria; Renal Impairment
Hepatic Epigastric Pain; Bilirubin; Transaminases
Subcapsular Haematomas; Hepatic Lacerations
Neurologic Headaches; Visual Disturbances; Focal neurologic deficits
Hyperreflexia Clonus; Cerebral Oedema; CNS irritability Seizures
Haematologic
Thrombocytopenia; DIC; Haemolysis
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HELLP
A severe variant of the preeclamptic spectrum of diseases 0.3% of deliveries
30% post partum Syndrome may develop without substantial BP changes
Clinical Features and Diagnosis Microangiopathic Haemolytic anaemia (H) Consumptive coagulopathy
Elevated Liver enzymes (EL); Low Platelets (LP)
Presenting Symptoms Usually non-specific 20% present with epigastric/RUQ pain, nausea + vomiting
Complications Acute renal failure; nephrogenic DI ALI/ARDS Haemorrhage incl Liver lacerations, subcapsular haematoma Hypoglycaemia; Hyponatremia
Outcome
Maternal mortality up to 24% in some series Perinatal mortality 8 60%
Management of severe
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Management of severePreeclampsia
Early diagnosis; close monitoring; aggressive BP control
Indication for immediate delivery [curative in most cases]
Evidence of cerebral irritability may herald imminent onset of Seizures
Magnesium
Questionable value in mild Preeclampsia
Associated with improved maternal outcome in severe Preeclampsia
Steroids
? Role for high-dose steroid regimen (dexamethasone 10 mg 12-hourly)
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Barrileaux et al, Obst Gynecol 2005
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Coma / Seizures
Neurologic involvement in 50% of critically ill obstetric patients
Coma GCS score independent predictor of maternal mortality Diverse aetiology including Vascular, Infective, Metabolic, Intracranial Mass
lesions, Toxic, Preeclampia
Seizures Commonest cause pre-existing Epilepsy Presence of hypertension increases likelihood of Preeclampsia Fulminant Hepatic Failure due to acute fatty liver of Pregnancy
Eclampsia Seizures or coma in presence of Preeclampsia or gestational hypertension
Potentially lethal phase 50 75% have occipital/frontal headaches 20-30% visual symptoms Cerebral oedema
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Coma / Seizure Management
Management
A, B, C
Left lateral position
Increase uterine blood flow
Minimize aspiration risk
Initial Seizure control
Lorazepam / Diazepam
IV MgSO4
Prevention of recurrent seizures
MgSO4 superior to Phenytoin or diazepam
Initial dose 4 6g, plus infusion of 2g/hr
Mg levels after 6hrs (therapeutic level 4 8mEq/L)
Check for patellar reflexes; muscle weakness; arrythmias (Ca gluconate)
BP Control
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Belfort et al NEJM 2003
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Obstetric Haemorrhage
Hypertension/ Pre-Eclampsia
Thrombosis/Embolism
Sepsis e.g. Chorioamnionitis
Trauma
Maternal Obstetric Emergencies
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Venous Thromboembolism
Pregnancy and puerperium a hypercoagulable state
Incidence Clinically symptomatic venous TE in 1-2 per 1000 pregnancies 3 times more common in Postpartum period
Risk Factors Maternal age [>40yrs]
Ethnic and genetic factors Caesarean section [3 16 times increased risk]
Clinical signs
Investigations ABG, ECG
D-Dimers less useful Radiographic testing [V/Q scan; CT-PA]
Require less than the 5 rads associated with teratogenesis
Begin therapy immediately if high index of suspicion
Heparin [Fractionated or Unfractionated] versus Warfarin
APTT 2 2.5; Anti-Factor Xa 0.6 1.1; INR 2.5 3 Continue therapy for 6 8 weeks post delivery
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Rightt
oLifeIssues
i i l id b li
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Amniotic Fluid Embolism
Catastrophic complication
1 case per 8,000-30,000 pregnancies in US amniotic fluid, fetal cells, hair, or other debris enter maternal circulation
Usually occurs in Labour; Trauma; Abortion
possible anaphylactic reaction to fetal antigens
Clinical Features
Severe respiratory distress; ALI/ARDS Cardivascular collapse
DIC may be major clinical manifestation
Treatment is supportive
Emergent C/S in unresponsive Cardiac Arrest [5min CPR]
Outcome
Mortality 60 to 80%
Most survivors have permanent neurologic impairment.
Neonatal survival is 70%.
No evidence increased AFE risk in future pregnancies.
l Ob i i
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Obstetric Haemorrhage
Hypertension/ Pre-Eclampsia
Embolism
Sepsis e.g. Chorioamnionitis
Trauma
Maternal Obstetric Emergencies
E id i l
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Epidemiology
Most common non-obstetric cause of Maternal Death
46% of deaths among pregnant women in one US series
57% homicides; 9% suicides; 21% RTAs
Patterns and mechanisms of injury same as in nongravid patients
Causes of Maternal Death from Trauma
Head Injury
Haemorrhage
Causes of Foetal death from Trauma
Placental abruption [shear forces]
Head injury [Pelvic fracture]
Compromised Uteroplacental Circulation
M t P i i l I
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Management Principles - I
Optimal management of Mother is best for Foetus
Initial assessment and resuscitation should follow standard protocols
U/S; FAST; DPL
Targeted Radiographic studies
Uterine shielding where possible
Highest foetal risk at 8 15/40
Exposure less than 1RAD low risk
Plain x-ray 0.2 RAD; CT 0.5RAD per slice
Avoid supine Hypotension Syndrome [Left Lateral tilt]
Foetal monitoring and Obstetric consultation once foetus potentially
viable
S ifi P C li ti
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Specific Pregnancy Complications
Foetomaternal Haemorrhage
1 in 4 gravid Trauma pts Kleihauer test
Abruptio Placentae
Amniotic Fluid Embolism
Premature Labour
Uterine rupture
Foetal Demise
Cardiac Arrest Standard algorithms initially+ CPR
Consider open cardiac massage
Caesarean section
SS
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Pregnancy is not a disease state!
Obstetric emergencies not infrequent
May be associated with serious morbidity
Potential for conflict in regard to Mother vs Foetus overstated
Physiologic Alterations of Pregnancy may play role
Early recognition and decisive intervention Paramount
Need for close cooperation with Obstetric Team
Multi-disciplinary Effort required, incorporating
Anaesthesia Team Obstetric team
Nurses and Doctors
Outcome
Depends on specific Problem
Generally good when recognised early and managed appropriately
SummarySummary
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QuestionsQuestions