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Obstetric ‘Anaesthesia’ Obstetric ‘Anaesthesia’ Emergencies Emergencies
John LaffeyNational University of Ireland,
AND Galway University Hospital, Galway, IRELAND
IARNA Conference, Galway, October 2nd 2010
• 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!
Key PointsKey Points
• 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 GUH Obstetric Critical Care at GUH in 2009in 2009
• Obstetric Haemorrhage
• Hypertension/ Pre-Eclampsia
• Embolism
• Sepsis e.g. Chorioamnionitis
• Trauma
Maternal Obstetric Emergencies
• 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
• Obstetric Haemorrhage
• Hypertension/ Pre-Eclampsia
• Embolism
• Sepsis
• Trauma
Maternal Obstetric Emergencies
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
Size of the Problem
• 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
• 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 Intravascular Coagulation
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, 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
- Bedside coagulation testing (TEG)
• 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
• 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
• Obstetric Haemorrhage
• Hypertension/ Pre-Eclampsia
• Embolism
• Sepsis e.g. Chorioamnionitis
• Trauma
Maternal Obstetric Emergencies
• 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
• 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
• 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
Treatment Recommendations
Management of a Management of a Hypertensive Crisis 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 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
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 0.25-0.5g/Kg/min; max 4g/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
• Blockers
– Atenolol [IUGR]
– Esmolol [Foetal Bradycardia]
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
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– 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– 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
• Obstetric Haemorrhage
• Hypertension/ Pre-Eclampsia
• Thrombosis/Embolism
• Sepsis e.g. Chorioamnionitis
• Trauma
Maternal Obstetric Emergencies
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
‘Right to Life Issues’
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.
• Obstetric Haemorrhage
• Hypertension/ Pre-Eclampsia
• Embolism
• Sepsis e.g. Chorioamnionitis
• Trauma
Maternal Obstetric Emergencies
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
• 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
QuestionsQuestions