Transcript OBSTETRIC ANAESTHETIC EMERGENCIES

Obstetric ‘Anaesthesia’
Emergencies
John Laffey
National University of Ireland,
AND Galway University Hospital,
Galway, IRELAND
IARNA Conference, Galway, October 2nd 2010
Key Points
• 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’ every anaesthetists nightmare!
Obstetric Critical Care at GUH
in 2009
• 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)
Maternal Obstetric Emergencies
• Obstetric Haemorrhage
• Hypertension/ Pre-Eclampsia
• Embolism
• Sepsis e.g. Chorioamnionitis
• Trauma
Physiologic Alterations
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Cardiovascular
– Heart Rate; Blood Pressure
– Blood Volume; Cardiac Output
– Venous Circulation; Vascular Resistance
– Colloid Osmotic Pressure
•
Haematologic
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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
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Drugs
– Decreased serum drug concentration; Serum Albumin
Maternal Obstetric Emergencies
• Obstetric Haemorrhage
• Hypertension/ Pre-Eclampsia
• Embolism
• Sepsis
• Trauma
Size of the Problem
Size of the Problem
• 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
Incidence and Causes
• 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
Disseminated Intravascular
Coagulation
• 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
Management of Massive
Haemorrhage
• Preparation
– Identify patients at risk
– Large bore IV access x 3
– Blood available [Type specific; O neg]
– Avoid caval obstruction; supplemental O2
– Foetal monitoring,
massive bleed
change
indicative
of
• Search for evidence of DIC
- Peripheral blood smear
- PT, PTT, Platelet counts, Fibrinogen level; Ddimer level
- ? Specific factor analyses
- Bedside coagulation testing (TEG)
Volume Replacement
• 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
Specific Therapies
• 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
Maternal Obstetric Emergencies
• Obstetric Haemorrhage
• Hypertension/ Pre-Eclampsia
• Embolism
• Sepsis e.g. Chorioamnionitis
• Trauma
Size of the Problem
• 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
Differential Diagnosis
• 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
Treatment Recommendations
• 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
– Increased maternal mortality and end organ damage
• Treatment recommended if SBP ≥ 160mmHg of DBP ≥ 110mmHg
– Treat lower BP’s if patient symptomatic
• Treatment Options
– PO: -methyldopa and Labetalol
– IV: Labetalol, Hydralazine, Sodium Nitroprusside
Management of a
Hypertensive Crisis
Clinical Features
• SBP generally ≥ 150mmHg; DPB ≥ 110 with
• Hypertensive Encephalopathy
– Confusion; Papilloedema; Retinal Haemorrhages
• Other end-organ dysfunction e.g. Nephropathy, Neuropathy,
Retinopathy
• Uteroplacental
haemorrhage
hyperperfusion,
placental
abruption,
• Maternal Catastrophe e.g. Intracranial Haemorrhage
• Severe Maternal Hypertension
– SBP ≥ 240mmHg; DPB ≥ 140
– ICU management irrespective of presence of clinical sequelae
Investigation and Management
• Investigations
– Bloods incl U+E, Coagulation, CBC, LFT’s
– 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
Therapeutic Strategies – Oral
•
Labetalol PO
– Dose 200-400mg BID
 -methyldopa
– BID/TID to max 4g/d
• ACEI’s and AT II Blockers
– C/I antepartum
• Nifedipine
– Rapid effect; increases CI; Uteroplacental flow
– 10mg capsule PO, repeat every 15 – 30mins to max 30mg
IV Antihypertensives
• Labetalol
– Rapidly decreases BP (5 mins) but not at expense of Uteroplacental blood
flow; 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 0.25-0.5mg/Kg/min; max 4mg/Kg/min
– S/E’s: Headache, dizziness, flushing, ototoxicity, cyanide toxicity
– Foetal Cyanide toxicity not a major issue
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
•
b Blockers
– Atenolol [IUGR]
– Esmolol [Foetal Bradycardia]
Pre-Eclampsia
• Incidence
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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
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Multi-system disease
Endothelial cell injury
Placental toxin release
Genetic and immunologic factors
Generalised vasospasm; ?PG/TX imbalance
Microthrombi
• Classic Clinical Triad
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
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
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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
Preeclampsia
• 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)
Barrileaux et al, Obst Gynecol 2005
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
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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
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
Belfort et al NEJM 2003
Maternal Obstetric Emergencies
• Obstetric Haemorrhage
• Hypertension/ Pre-Eclampsia
• Thrombosis/Embolism
• Sepsis e.g. Chorioamnionitis
• Trauma
Venous Thromboembolism
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Pregnancy and puerperium a hypercoagulable state
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Incidence
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Risk Factors
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Clinical signs
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Investigations
– Clinically symptomatic venous TE in 1-2 per 1000 pregnancies
– 3 times more common in Postpartum period
– Maternal age [>40yrs]
– Ethnic and genetic factors
– Caesarean section [3 – 16 times increased risk]
– ABG, ECG
– D-Dimers less useful
– Radiographic testing [V/Q scan; CT-PA]
• Require less than the 5 rads associated with teratogenesis
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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
Amniotic Fluid Embolism
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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
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Treatment is supportive
– Emergent C/S in unresponsive Cardiac Arrest [5min CPR]
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Outcome
– Mortality 60 to 80%
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Most survivors have permanent neurologic impairment.
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Neonatal survival is 70%.
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No evidence increased AFE risk in future pregnancies.
Maternal Obstetric Emergencies
• Obstetric Haemorrhage
• Hypertension/ Pre-Eclampsia
• Embolism
• Sepsis e.g. Chorioamnionitis
• Trauma
Epidemiology
• Most common non-obstetric cause of Maternal Death
– 46% of deaths among pregnant women in one US series
– 57% homicides; 9% suicides; 21% RTA’s
• 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
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
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
Summary
•
Pregnancy is not a disease state!
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Obstetric emergencies not infrequent
– May be associated with serious morbidity
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Potential for conflict in regard to Mother vs Foetus overstated
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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
Questions