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Obstetric ‘Anaesthesia’ Emergencies

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Presentation on theme: "Obstetric ‘Anaesthesia’ Emergencies"— Presentation transcript:

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

2 Key Points 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! Office of the Dean of Research

3 Obstetric Critical Care at GUH in 2009
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)

4 Maternal Obstetric Emergencies
Obstetric Haemorrhage Hypertension/ Pre-Eclampsia Embolism Sepsis e.g. Chorioamnionitis Trauma Office of the Dean of Research

5 Physiologic Alterations
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 Office of the Dean of Research

6 Maternal Obstetric Emergencies
Obstetric Haemorrhage Hypertension/ Pre-Eclampsia Embolism Sepsis Trauma Office of the Dean of Research

7 Size of the Problem Office of the Dean of Research

8 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 Office of the Dean of Research

9 Incidence and Causes Late Pregnancy Postpartum Placenta Praevia
Placental Abruption Spontaneous uterine rupture DIC e.g. due to Amniotic Fluid Embolism Trauma Postpartum Uterine Atony Surgical Trauma Retained Placenta DIC Office of the Dean of Research

10 Disseminated Intravascular Coagulation
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 Office of the Dean of Research

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 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) Office of the Dean of Research

12 Volume Replacement 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 Office of the Dean of Research

13 Specific Therapies 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 Office of the Dean of Research

14 Office of the Dean of Research

15 Maternal Obstetric Emergencies
Obstetric Haemorrhage Hypertension/ Pre-Eclampsia Embolism Sepsis e.g. Chorioamnionitis Trauma Office of the Dean of Research

16 Size of the Problem 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 Office of the Dean of Research

17 Differential Diagnosis
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 Office of the Dean of Research

18 Treatment Recommendations
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 Office of the Dean of Research

19 Management of a Hypertensive Crisis
Office of the Dean of Research

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 Office of the Dean of Research

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 Office of the Dean of Research

22 Therapeutic Strategies – Oral
Labetalol PO Dose mg BID a-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 Office of the Dean of Research

23 IV Antihypertensives Labetalol Hydralazine Na Nitroprusside
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 mg/Kg/min; max 4mg/Kg/min S/E’s: Headache, dizziness, flushing, ototoxicity, cyanide toxicity Foetal Cyanide toxicity not a major issue Office of the Dean of Research

24 IV Antihypertensives Nicardipine Nitroglycerin b Blockers
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 b Blockers Atenolol [IUGR] Esmolol [Foetal Bradycardia] Office of the Dean of Research

25 Pre-Eclampsia Incidence Pathogenesis Classic Clinical Triad
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 Office of the Dean of Research

26 Severe Pre-Eclampsia Cardiorespiratory Renal Hepatic Neurologic
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 Office of the Dean of Research

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% Office of the Dean of Research

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) Office of the Dean of Research

29 Barrileaux et al, Obst Gynecol 2005
Office of the Dean of Research

30 Office of the Dean of Research

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 Office of the Dean of Research

32 Coma / Seizure 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 Office of the Dean of Research

33 Belfort et al NEJM 2003 Office of the Dean of Research

34 Maternal Obstetric Emergencies
Obstetric Haemorrhage Hypertension/ Pre-Eclampsia Thrombosis/Embolism Sepsis e.g. Chorioamnionitis Trauma Office of the Dean of Research

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 Office of the Dean of Research

36 ‘Right to Life Issues’ Office of the Dean of Research

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. Office of the Dean of Research

38 Maternal Obstetric Emergencies
Obstetric Haemorrhage Hypertension/ Pre-Eclampsia Embolism Sepsis e.g. Chorioamnionitis Trauma Office of the Dean of Research

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 Office of the Dean of Research

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 Office of the Dean of Research

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 Office of the Dean of Research

42 Summary 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 Office of the Dean of Research

43 Questions Office of the Dean of Research

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