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Obstetric ‘Anaesthesia’ Emergencies John Laffey National University of Ireland, AND Galway University Hospital, Galway, IRELAND IARNA Conference, Galway,

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Presentation on theme: "Obstetric ‘Anaesthesia’ Emergencies John Laffey National University of Ireland, AND Galway University Hospital, Galway, IRELAND IARNA Conference, Galway,"— Presentation transcript:

1 Obstetric ‘Anaesthesia’ Emergencies John Laffey National University of Ireland, AND Galway University Hospital, Galway, IRELAND IARNA Conference, Galway, October 2nd 2010

2 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 Points

3 30 admissions to ICU/HDU in 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 in 2009

4 Obstetric Haemorrhage Hypertension/ Pre-Eclampsia Embolism Sepsis e.g. Chorioamnionitis Trauma Maternal Obstetric Emergencies

5 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 Alterations

6 Obstetric Haemorrhage Hypertension/ Pre-Eclampsia Embolism Sepsis Trauma Maternal Obstetric Emergencies

7 Size of the Problem

8 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

9 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

10 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

11 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 O 2 –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)

12 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/mm 3 or higher if bleeding persisting –FFP only to correct measured clotting abnormalities –Cryoprecipitate Volume Replacement

13 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


15 Obstetric Haemorrhage Hypertension/ Pre-Eclampsia Embolism Sepsis e.g. Chorioamnionitis Trauma Maternal Obstetric Emergencies

16 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

17 Pregnancy Induced Hypertension –(Gestational Hypertension without Proteinuria) –After 20 th 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

18 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

19 Management of a Hypertensive Crisis

20 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

21 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

22 Therapeutic Strategies – Oral Labetalol PO –Dose mg 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

23 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 mins; lasts approx 8 hrs –5 – 10mg boluses every 15-30mins until BP controlled Na Nitroprusside –Potent, rapid, arterial and venous vasodilator –IV infusion g/Kg/min; max 4g/Kg/min –S/E’s: Headache, dizziness, flushing, ototoxicity, cyanide toxicity –Foetal Cyanide toxicity not a major issue

24 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]

25 Pre-Eclampsia Incidence –7% of pregnancies in the US –Generally after 32 nd 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

26 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

27 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%

28 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)

29 Barrileaux et al, Obst Gynecol 2005


31 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

32 Coma / Seizure Management Management –A, B, C –Left lateral position Increase uterine blood flow Minimize aspiration risk Initial Seizure control –Lorazepam / Diazepam –IV MgSO 4 Prevention of recurrent seizures –MgSO 4 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

33 Belfort et al NEJM 2003

34 Obstetric Haemorrhage Hypertension/ Pre-Eclampsia Thrombosis/Embolism Sepsis e.g. Chorioamnionitis Trauma Maternal Obstetric Emergencies

35 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

36 ‘Right to Life Issues’

37 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.

38 Obstetric Haemorrhage Hypertension/ Pre-Eclampsia Embolism Sepsis e.g. Chorioamnionitis Trauma Maternal Obstetric Emergencies

39 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

40 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

41 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

42 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 appropriatelySummary

43 Questions

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