2023 ANAESTHESIA FOR HIGH RISK PARTURIENT AND OBSTETRIC EMERGENCIES.pdf
Georgechimaobi
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Mar 08, 2025
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About This Presentation
A presentation on Anaesthetic considerations for high risk obstetric patient's. This also covers major perioperative morbidity and post operative complications as well as obstetric surgical emergencies.
Size: 697.75 KB
Language: en
Added: Mar 08, 2025
Slides: 83 pages
Slide Content
ANAESTHESIA FOR HIGH RISK PARTURIENT AND
OBSTETRIC EMERGENCIES
S. Fyneface-Ogan
Faculty of Clinical Sciences
College of Health Sciences
University of Port Harcourt
Port Harcourt
PHYSIOLOGICAL CHANGES -RESPIRATORY
•oxygen consumption ~ 20% (100% in labor) due to
increased metabolic rate
•minute ventilation ~ 50% (due to increased tidal
volume)
•arterial PCO
2
•FRC causing a decrease in oxygen reserves
IMPACT OF RESPIRATORY CHANGES
•Uptakeofinhalationalagentsisfaster
•DecreasedFRCandincreasedoxygenconsumptionincreasetheriskof
hypoxiawithapnoea
•PreoxygenationpriortoGAlesseffective
PHYSIOLOGICAL CHANGES -AIRWAY
•Venous engorgement of airway mucosa
•Oedema of airway mucosa
•Worsening of Mallampati score in labour
IMPACT OF AIRWAY CHANGES
•Trauma to upper airway with suctioning, intubation
•Increased incidence of difficult/failed intubation x10
•Require smaller ETT
PHYSIOLOGICAL CHANGES -CNS
•Decrease in MAC by 25 –40%
•Decreased dose of local anaesthetic requirement for regional techniques
•More rapid onset of neural blockade
IMPACT OF CNS CHANGES
•Decreased inhalation anaesthetic agent requirements
•Decreased dose of local anaesthetic for same effect
•Increased risk of local anaesthetic toxicity
IMPACT OF GIT CHANGES
•Increasedriskofaspiration
•Allparturientsare“fullstomach”
•AspirationprophylaxisrecommendedforC/S
•0.3MSodiumcitrate30mlorally
•Ranitidine50mgiv
•Metoclopramide10mgiv
Maternal
oxygen carrying
capacity
Maternal cardiac
output
Uteroplacental
perfusion
Any interventions that compromise these factors may lead to foetal asphyxia
FOETAL
OXYGENATION
MORBID OBESITY
Obesity
Chest Wall Compliance
O
2and CO
2
Consumption
Lung volumes
Oxygenation from
Trend and supine
positions
CO and blood
volume
Hypertension
Skewed distribution, elimination, and response to
anaesthetic drugs
Difficult airway +
Metabolic rate + FRC
Airway catastrophes
Difficulties in establishing
regional blocks + IV lines
Risk for postop
pulmonary
morbidity
•ThosewithLtoRshunt(ASD,VSDoraPDA)earlyneuraxialanalgesiaiscommenced
topreventincreasedSVRwhichcouldworsentheLtoRshunt→pulmonary
hypertensionandRHF
•Avoid air trappings both in the epidural and intravenous
•Drastic reduction of BP be avoided to prevent a R to L shunt and maternal hypoxaemia
•Neuraxial analgesia should be with opioids
•O
2be monitored. Hypoxaemiacan →R to L shunt
•Will focus on Maternal ‘driven’ emergencies
•Generallymuch more difficult situations!
•Need to consider 2 patients rather than 1
•Role of Physiologic Alterations of Pregnancy
•Impact of pathologic conditions related to Pregnancy
•Deliveryofthefoetusmayabrogatepregnancyinducedconditions
•Outcome
•Generally Good….
•Obstetric ‘disasters’ -the Anaesthetist’snightmare!
KEY POINTSKEY POINTS
•Leadingcause 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
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 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
DISSEMINATED INTRAVASCULAR COAGULATION
•Preparation
–Identifypatientsatrisk
–LargeboreIVaccessx3
–Bloodavailable[Typespecific;O-ve]
–Avoidcavalobstruction;supplementalO
2
–Foetalmonitoring,changeindicativeofmassivebleed
•SearchforevidenceofDIC
-Peripheralbloodsmear
-PT,PTT,Plateletcounts,Fibrinogenlevel;D-dimerlevel
-?Specificfactoranalyses
-Bedsidecoagulationtesting(TEG)
MANAGEMENT OF MASSIVE HAEMORRHAGE
MANAGEMENT OF MASSIVE HAEMORRHAGE
•Immediate aggressive volume replacement
•Crystalloid until blood available[warming+]
•Consider PRBC once blood loss > 2000 ml
•Anticipateneed 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
VOLUME REPLACEMENT
•Uterine atony
•Uterine Massage; Oxytocin, Carbetocin
•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 gelatinsponge
•Consider prophylacticplacement of embolectomy catheters
in internal iliac arteries of patients at high PPH risk.
•Factor 7a
•Rescue therapy in severe haemorrhage
SPECIFIC THERAPIES
HYPERTENSION AND PRE -ECLAMPSIA
•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
•Family Hx of Hypertension
•Primigravid state
•Multiple gestational pregnancies
•Definition of Hypertension in Pregnancy
•Degree of increase in SBP and DBP versusabsolute 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 20
th
gestational week; Long term risk
•Essential Hypertension
•Before 20/52; Persists after delivery
•Secondary Hypertension
•consider if SPB consistently > 200 mmHg
•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 utero-placental perfusion
•Increasedmaternal mortality and end organ damage
•Treatment recommended if SBP ≥ 160mmHg of DBP ≥ 110mmHg
•Treat lower BP if patient symptomatic
•Treatment Options
•PO: -methyldopa and Labetalol
•IV: Labetalol, Hydralazine, Sodium nitroprusside
TREATMENT/RECOMMENDATIONS
MANAGEMENT OF HYPERTENSIVE CRISIS
•SBP generally ≥ 150mmHg; DPB ≥ 110 with
•Hypertensive Encephalopathy
•Confusion; Papilloedema;Retinal Haemorrhages
•Other end-organ dysfunction e.g. Nephropathy,
Neuropathy, Retinopathy
•Uteroplacentalhyperperfusion, placental abruption,
haemorrhage
•Maternal Catastrophe e.g. Intracranial Haemorrhage
•Severe Maternal Hypertension
•SBP ≥ 240 mmHg; DPB ≥ 140 mmHg
•ICU management irrespective of presence of clinical sequelae
CLINICAL FEATURES
•Investigations
•Bloods including 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 100 mmHg
INVESTIGATION AND MANAGEMENT
•Labetalol PO
•Dose 200-400 mg bid
•α-Methyldopa
•bid/tidto max 4g per day
•Angiotensin converting enzyme inhibitors and
Angiotensin II Blockers
•C/I antepartum
•Nifedipine
•Rapid effect; increases cardiac index; Uteroplacentalflow
•10mg capsule PO, repeat every 15 –30mins to max 30mg
THERAPEUTIC STRATEGIES -ORAL
•Labetalol
•Rapidly decreases BP (5 mins) but not at expense of Uteroplacentalblood 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 approx8 hrs
•5 –10mg boluses every 15-30mins until BP controlled
•Na Nitroprusside
•Potent, rapid,arterial and venous vasodilator
•IV infusion 0.25-0.5mg/Kg/min; max 4mg/Kg/min
•S/E’s: Headache, dizziness, flushing, ototoxicity, cyanidetoxicity
•Foetal Cyanide toxicity not a major issue
IV ANTIHYPERTENSVIES
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
•β-Blockers
•Atenolol[IUGR]
•Esmolol[Foetal Bradycardia]
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
•Primigravidaversus older multiparous
•Pathogenesis
•Multi-system disease
•Endothelial cell injury
•Placental toxin release
•Genetic and immunologic factors
•Generalised vasospasm; ?PG/TX imbalance
•Microthrombi
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)
COMA/SEIZURES
•Neurologic involvement in 50% of critically ill parturients
•Coma
•GCS score independent predictor of maternal mortality
•Diverse aetiology including Vascular, Infective, Metabolic, Intracranial Mass lesions,
Toxin, 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 cont’d
•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 toPhenytoin 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
THROMBOSIS/EMBOLISM
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]
•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
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
•Cardiovascular 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.
MATERNAL TRAUMA
EPIDEMIOLOGY OF MATERNAL TRAUMA
•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 non-gravid
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 Utero-placental Circulation
•Thepatientandrelativesshouldbeproperlycounselledandinformed
•Removalofmyomaispossible,andafinaldecisioncanbetakenatthe
timeofCaesareanbaseduponthesize,number,andlocationofthefibroid
•Availabilityofuterotonicssuchasoxytocin,carbetocinetc.andblood
products
•Modeofanaesthesiaeitherepiduralorcombinedspinalepidural
PREPARATION FOR ANAESTHESIA
•Pregnancy is not a disease!
•Obstetric emergencies not infrequent
•May be associated with serious morbidity
•Potentialforconflictinregardtomothervsfoetusoverstated
•Physiologic Alterations of Pregnancy may play role
SUMMARY
Early recognition and decisive intervention is key
Paramount is:
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 recognized early and managed
appropriately
SUMMARY Cont’d
TAKE HOME MESSAGE I
•Obstetric emergencies require emergent response as life of
mother and child are at risk
•Require in-depth knowledge of the shift in physiology
•Most times blood could be needed and so arrangements be put in
motion
•A clear case of full stomach and the airway be protected at all
times
•Airway management is key
•Life of the mother depends on ANAESTHESIA, BLOODand
ANTIBIOTICS!
TAKE HOME MESSAGE II
•Thereareanumberofanaestheticissuesthatshouldbeconsideredwhenproviding
anaestheticcaretotheparturientwithchronicdisease.
•Inaddition,appropriatelabouranalgesiaandsurgicalanaesthesiamayhelpmitigatesomeof
theadverseaffectsoflabouranddeliveryonchronicdisease.
•Amultidisciplinaryteamapproachinvolvingtheobstetrician,anaesthesiologist,disease
specialist,andotherhealthcareprovidersislikelytoprovidethebestoutcome.
•Antepartumconsultationallowsallmembersoftheteam,andthepatient,tounderstandthe
issuesinvolvedandplanforasafelabouranddelivery.
THANK YOU FOR LISTENING
Please visit: www.soan.org.ng
OFFICIAL WEBSITE FOR THE SOCIETY OF OBSTETRIC ANAESTHETISTS OF NIGERIA
An Affiliate of the Nigerian Society of Anaesthetists
Intending Members are welcome!