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