obstetric anaesthetic emergencies laffey

7/30/2019 Obstetric Anaesthetic Emergencies LAFFEY

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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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Embolism

Sepsis

Trauma



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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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Embolism


Trauma



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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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Thrombosis/Embolism


Trauma



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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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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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Embolism


Trauma


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


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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