Obstetric ‘Anaesthesia’ Emergencies John Laffey National University of Ireland, AND Galway...

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