Obs anaesthesia

Moderator - Dr. Vatsala Aggarwal
Presenter – Dr. Shalini Patidar
*

*
Global Maternal Mortality Rates(MMR)- 400/100,000 live
births
Significant inequality between developed and developing
countries with 99% maternal deaths in developing countries.
MMR in developed country <15/100,000 live births.

*Embolism
*Hypertensive disorders
*Haemorrhage
*Infection
*Cardiomyopathy
*CVA
*Anaesthesia
*21.4%
*19.4%
*13.4%
*12.6%
*9.7%
*5.3%
*1.8%
*

●Although anaesthesia has become the 7th cause of
pregnancy related mortality , the predisposing factors are
similar
Inexperienced anaesthesia personnel
Airway problems
lack of appropriate monitoring
lack of resuscitation equipment
●Maternal mortality can be reduced by
increasing the use of neuraxial anaesthesia
improving airway management skills
Simulation of anaesthesia techniques for education
purpose

*
*Overview of maternal physiology
*Anesthesia concerns in the parturient-recent
changes in clinical practice
*Management of complicated pregnancies
*Regional anesthesia in PIH
*Use of supraglottic airway devices in obstetric
patient.
*CPR in pregnant patients

*
Almost all the changes seen are due to high
levels of progesterone and include:
*35%  Total Blood Volume
* heart rate 15 beats/min
*40%  CO
*30%  SV
*15%  SVR
*500ml/min  blood flow to uterus
* venous return from legs
*AORTOCAVAL COMPRESSION (mechanical)

*
*Patients with pre-existing cardiac disease may
decompensate either during labor or
immediately post delivery. This corresponds to
the time of maximal CO
*Approx. 400 – 600ml blood loss occurs at
delivery
*Supine hypotensive syndrome

*
* oxygen consumption ~ 20% (100% in labor) due
to increased metabolic rate
* minute ventilation ~ 50% (due to increased
tidal volume)
* arterial pCO2
* FRC causing a decrease in oxygen reserves

*
*Uptake of inhalational agents is faster
*Decreased FRC and increased oxygen
consumption increase the risk of hypoxia with
apnea
*Preoxygenation prior to GA less effective

*
*Venous engorgement of airway mucosa
*Edema of airway mucosa
*Worsening of Mallampati score in labor

*
*Trauma to upper airway with suctioning,
intubation
*Increased incidence of difficult/failed intubation
x10
*Require smaller ETT

*
*Decrease in MAC by 25 – 40%
*Decreased dose of Local Anesthetic requirement
for regional techniques
*More rapid onset of neural blockade

*
*Decreased inhalation anesthetic agent
requirements
*Decreased dose of local anesthetic for same effect
*Increased risk of local anesthetic toxicity

*
*Increased gastric fluid volume
*Increased gastric fluid acidity
*Decreased competency of lower
esophageal sphincter

*
*Increased risk of aspiration
*All parturients are “full stomach”
*Aspiration prophylaxis recommended for C/S
i.e.
*0.3M Sodium citrate 30 mls po
*Ranitidine 50mg iv
*Metoclopramide 10mg iv

*
*Where is the pain coming from?
*Is pain bad in labor?
*Analgesic options

*
Nociceptive
pathways
involved
T10 – L1 during
labour
plus
S2-S4 for delivery

*
●Psychological stress can cause:
-increased levels of catecholamines
-hyperventilation
These may result in decreased
uterine blood flow leading to
hypoxia and acidosis in the fetus

*
*Mental preparation
*Family support
*Medical support
*Cultural expectations
*Underlying mental status
*Parity
*Size and presentation of the fetus
*Maternal pelvic anatomy
*Duration of labor
*Medications

*
*Non-medication
*Inhalational
*Parenteral
*Regional

*
*Breathing exercises
*Autohypnosis
*Acupuncture
* Music
*Massage/ walking
*TENS
*Water bath

*
*Nitronox: 50:50 mixture of oxygen and nitrous
oxide
*Low dose desflurane(0.2%),enflurane,
Isoflurane(0.2-0.25%),Sevoflurane(0.8%) in oxygen
Advantages: on demand delivery, relatively safe
Disadvantages: variable efficacy, nausea,
drowsiness, loss of airway reflexes and
unconciousness with volatile analgesics .

*
*Narcotics: meperidine, morphine ,fentanyl
Advantages: relatively good analgesia
Disadvantages: nausea, vomiting, sedation,
neonatal depression (max. 2 hours after
meperidine dose), short duration of action.

*
*Epidural, spinal, combined spinal-epidural
Advantages: excellent pain control, minimal
impact on progress of labor with low doses, less
drug transfer to fetus, improved uterine blood
flow, decrease in birth trauma e.g. use of
forceps, minimal neonatal depression
Disadvantages: invasive technique, side effects
(hypotension, headache, itching, nausea, urinary
retention, limited mobility), nerve damage,
infection

*
*General considerations of the parturient
undergoing surgery
*Obstetric surgery

*
*Altered physiology as mentioned
*Risks to the fetus:
*Effect of the disease process/therapies
*Possible teratogenicity of anesthetic
agents
*Intraoperative effects on uteroplacental
blood flow
*Increased risk of preterm labor/ risk of
abortion

*
*Altered physiology
*Altered response to anesthesia
*Decrease in MAC
*Increased sensitivity to neuraxial agents
*Decreased plasma cholinesterase
*Decreased protein binding (more free drug)
*Limited drug information in parturients

*
*Teratogenicity:
*Limited information due to impracticality of
conducting trials with sufficient power
*Guidelines based on a) effects on reproduction
in animals; b) epidemiological surveys of OR
personnel; c) studies of pregnancy outcomes in
parturient undergoing ante partum surgery

*Nitrous oxide has been shown to have a
teratogenic effect in rats during the first
trimester
*No anesthetic agent is a proven teratogen in
humans
*Anesthetic agents deemed safe include:
thiopental,morphine, meperidine,fentanyl,
succinylcholine, NDMRs
*Limiting nitrous oxide use but only if
hypotension secondary to volatiles can be
avoided

Avoidance of hypoxemia
Avoidance of hypotension
Avoidance of acidosis
Maintain PaCO2 in the normal
range for the parturient
Minimize effects of aortocaval
compression
*

*
*The rate of cesarean delivery has increased(4.5% in
1965 to 31.1% in 2006)
* One of the most common surgical procedure
*As more patients become high risk, anaesthetic
challenges also Increase
Despite increasing complexity including obesity,
congenital heart disease and other chronic
diseases,anaesthesia related maternal mortality has
decreased over the past 50 years from 36 per
100,000 Caesarean deliveries to one per 100,000
cesarean deliveries.

The current level of safety of cesarean delivery
has been achieved
* Dynamic changes in the training and practice of
obstetric anaesthesia
* Use of High-fidelity simulators
*Widespread use of neuraxial anaesthesia

*
* Preparation
*Preventing complications
*Choice of Anesthetic technique
*Effects on the fetus

*
*Premeds: antacid (sodium citrate)
*IV access and fluid bolus within 30 minutes of
operating (avoid glucose containing fluids)
*Left lateral tilt with wedge under right pelvis
*Routine Monitors: ECG, NIBP, pulse oximeter,
fetal monitoring
*Additional monitors for GAs: ETCO2, nerve
stimulator, temp probe

*
*Aspiration prophylaxis
*Detailed airway assessment
*Fluid resuscitation/left lateral tilt to prevent
hypotension
*Safe practice for placement of neuraxial blocks

*
*Local infiltration by surgeon
*Regional anesthesia: spinal,
epidural, combined spinal-epidural
*General anesthesia

*
*Rarely performed
*Patient usually in extremis
*Surgery must be done via midline incision,
gentle retraction, no exteriorization of the
uterus
*Usually done to supplement a regional
technique if local anesthetic toxicity not a
concern

*
These include withdrawal of
*0.75% bupivacaine from obstetrics,
* widespread use of test doses,
* fractionation of epidural injection
*the use of dilute solutions by continuous infusion.

*
Simple to perform
Rapid onset
Single shot technique
Profound neural block
Technique of choice for uncomplicated
elective caesarean sections and in many
emergency caesarean sections

*
*Potential Complications:
*Hypotension
*Headache (rare ~1:100)
*Backache (temporary ~24hrs)
*Nausea/vomiting (secondary to BP,
narcotics)
*Neurological damage (very rare)
*Anaphylaxis (very rare)

*Incidence of Hypotension after spinal anaesthesia
for Caesarean section - 80% (without prophylactic
management)
*Preventive measures include fluid preload, lateral
tilt, and use of vasopressors.

*
*Ephedrine has been
recommended .
*Potential complications
-supraventricular tachycardia,
-tachyphylaxis
-fetal acidosis.
Equivalent dose of ephedrine and phenylephrine in the
prevention of post-spinal hypotension in Caesarean
section: S. Saravanan1, M. Kocarev2,* R. C. Wilson2, E.
Watkins2, M. O. Columb3 and G. Lyons2 Oxford
Journals, Medicine, BJA, Volume 96, Issue 1, Pp. 95-
99)
*Phenylephrine
- better fetal acid–base
status
-similar efficacy in
blood pressure control
Potential complications
-bradycardia
-serial dilution for i.v.
administration is a
source of error.
phenylephrine is more
potent than ephedrine by
a factor of 80 for
equivalent maternal blood
pressure control

*
*More technically challenging
*Slower onset
*Used when already placed for labor analgesia
*Useful in parturient where a slow, controlled
onset of block is needed
*Allows prolongation of block should surgery be
complicated

*
Potential Complications:
*Hypotension
*Headache (approx1:100)
*Transient backache~24hrs
*Urinary retention
*Unintentional spinal
injection
*Intravascular injection of
local anesthetic
*Neurological damage
*Infection

*
*Used when require the speed and density of a spinal anesthetic
with the flexibility of prolonging the block by supplemental
increments of local anesthesia via the epidural catheter
*Complications: as mentioned for spinals and epidurals
*However, high block with delay in recognizing and treating its
cardiorespiratory consequences, as well as lack of appropriate
resuscitation equipment and drugs continue to result In
maternal injury.

*
*Used when
*Patient refuses regional technique
*Regional technique is contraindicated
*Emergency C/S when there is
inadequate/absent regional analgesia and
to delay will cause undue risk to the fetus /
mother

*
*Complications:
*Failed intubation
*Failed ventilation causing death or
neurological injury
*Awareness
*Aspiration pneumonia

*
*Avoid hypotension, hypoxia, acidosis,
hyperventilation
*Limit time between uterine incision and delivery
to less than 3 minutes
*Infants exposed to GA have lower Apgar at one
minute but no difference at 5 mins
*No significant alteration in neurobehavioral scores
with regional techniques

*
*Supraglottic airway devices - laryngeal mask airway (LMA)
& LMA Proseal-TM have been used successfully in obstetric
patients undergoing GA.
* LMA Proseal-TM incorporates a second tube intended to
permit continuity with the gastrointestinal tract and
isolation from the airway, minimizing gastric insufflations
during positive-pressure ventilation.
*The LMA Proseal-TM has been used successfully as a
rescue device during failed rapid sequence induction in
obstetric patients and has been incorporated in the
obstetric difficult airway algorithm .

*
*A prospective cohort study involving 1,067obstetric patients
concluded that the LMA is effective and probably safe in
most elective caesarean deliveries.
SAFE use of SGD requires
*Proper Patient selection
*Proper airway assessment,
*Adequate fasting
*Non-obese parturients.
*An anaesthetist with proficient regular use of LMA.
Effective airway was obtained in 99% of the parturients and
only seven parturients required intubation.
There were no reported episodes of aspiration, gastric
insufflations, hypoxia, layrngospasm or bronchospasm.

* Focus on Maternal ‘driven’ emergencies
*Need to consider 2 patients rather than 1
*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

*
*Maternal Age < 15 & > 35.
*Parity Factors - 5 or more - great risk.
PP hemorrhage if new pregnancy
within 3 months
*Medical-Surgical Hx - hx of previous uterine
surgery &/or uterine rupture, DM, cardiac dis,
lupus, HTN, PIH, HELLP, DIC etc.

*Obstetric Haemorrhage
*Hypertension/ Pre-Eclampsia
*Embolism
*Sepsis e.g. Chorioamnionitis
*Trauma
Common complicated Obstetric
Emergencies

*Embolism
*Sepsis
*Trauma
Common complicated Obstetric
Emergencies

*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
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 VIIa
* Rescue therapy in severe haemorrhage
Specific Therapies

*Embolism
*Trauma
Maternal Obstetric Emergencies

*
•Most common medical problem encountered
during pregnancy
•8% of pregnancies
•4 categories:
*Chronic Hypertension
*Pregnancy Induced hypertension
*Preeclampsia-eclampsia
*Preeclampsia superimposed on chronic HTN
*Hypertensive disorder in pregnancy may cause an increase in
maternal and fetal morbidity and remains a leading source of
maternal mortality*

* 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
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 0.25-0.5mg/Kg/min; max 4mg/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
* b 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

*
•New onset HTN
•After 20 weeks of gestation, or
•Early post-partum, previously normotensive
•Resolves within 48 hrs postpartum
•With the following (Renal or other systemic)
• Proteinuria > 300 mg/24hr
• Oliguria or Serum-plasma creatinine ratio > 0.09 mmol/L
• Headaches with hyperreflexia, eclampsia, clonus or visual disturbances
• ↑ LFTs, glutathione-S-Transferase alpha 1-1, alanine aminotransferase or right
abdominal pain
• Thrombocytopenia, ↑ LDH, hemolysis, DIC
•10% in primigravida
•20-25% with history of chronic HTN

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

*
Mild Severe
Systolic arterial pressure 140 mm Hg – 160 mm Hg ≥160 mm Hg
Diastolic arterial pressure 90 mm Hg – 110 mm Hg ≥110 mm Hg
Urinary protein <5 g/24 hr
Dipstick +or 2 +
≥5 g/24 hr
Dipstick 3+or 4+
Urine output >500 mL/24 hr ≤500 mL/24 hr
Headache No Yes
Visual disturbances No Yes
Epigastric pain No Yes

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)

*
*One of the most important advantages of labor
epidural analgesia is that it provides a route for rapid
initiation of anesthesia for emergency C/S.
*In the past there were concerns re: use of regional
anesthesia for C/S in preeclamptics
*possibility of severe  BP secondary to
sympathectomy in patient with volume contraction
*risk of pulmonary edema due to excessive fluid
administration with regional block
*risk with use of pressor agents to treat  BP

*
*Epidural anesthesia would probably be preferred
by many anesthesiologists in a severely
preeclamptic pt in a non-urgent setting
*For urgent cases it is reassuring to know that
spinal is also safe
*This allows us to avoid general anesthesia with
the potential for encountering a swollen, difficult
airway and/or labile hypertension

*
*Prior to placing regional block in a preeclamptic it is
recommended to check the platelet count.
*No concrete evidence at to the lowest safe platelet count
for regional anesthesia in preeclampsia
*Any clinical evidence of DIC would contraindicate regional
*In the absence of such signs, most anesthesiologists would
proceed at plt count >100K, many would proceed at 80-
100K, <80K some would proceed (esp. spinal)

*
*When placing a regional block in a patient with a platelet
count < 100K, the most important thing is to monitor
resolution of block closely
*Bleeding time has been discredited as an indicator of
epidural bleeding risk and is not indicated.
Channing-Rogers, Semin Thromb Hemost 1990;16:;1-30
*Low-dose aspirin is not a contraindication to regional
anesthesia in preeclampsia
* CLASP study: 1422 women on aspirin received epidurals without any bleeding complications

*
*Airway edema is common
*Mandatory to reexamine the airway soon before
induction
*Edema may appear or worsen at any time during the
course of disease
*tongue & facial, as well as laryngeal
*Laryngoscopy and intubation may  severe BP
*Labetolol & NTG are commonly used acutely
*Fentanyl (2.5 mcg/kg), alfentanil (10 mcg/kg), lidocaine
may be given to blunt response

*
*Magnesium sulfate potentiates depolarizing &
non-depolarizing muscle relaxants
*Pre-curarization is not indicated.
*Initial dose of succinylcholine is not reduced.
*Neuromuscular blockade should be monitored &
reversal confirmed.

*
*Usually reserved for patients with complications
*oliguria unresponsive to modest fluid challenge (500 cc
LR X 2)
*pulmonary edema
*refractory hypertension
*may have increased CO or increased SVR
*Poor correlation between CVP and PCWP in PIH
*However, at most centers anesthesiologists would begin
with CVP & follow trend
*not arbitrarily hydrate to a certain number
*If poor response, change to PA catheter

HELLP(can progress to DIC)
* 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%

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

*
*Preeclampsia is a serious multi-organ system disorder of
pregnancy that continues to defy our complete understanding.
*It is characterized by global endothelial cell dysfunction.
*The cause remains unknown.
*There is no effective prophylaxis.

*Thrombosis/Embolism
*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

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.

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(Focussed assessment with sonography with trauma); DPL(Diagnostic
peritoneal lavage)
*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 during
trauma
* 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

GOALS
1. To understand and perform basic and advance
life support in pregnant patients
2. Understand the adaptations of CPR
3. Understand the importance of early
defibrillation when appropriate
4. Understand the need to perform perimortem
cesarean section

*ANATOMICALAND
PHYSIOLOGICAL CHANGES
IN PREGNANCY
CARDIOVASCULAR SYSTEM
Uteroplacental
blood flow
Maternal blood volume
Arterial
pressure
Cardiac output Increases 30 –
45%
20th week of
gestation
Maternal heart
rate
increases 10- 15 beats/min
SBP and DBP First two trimesters –
decreases by 10 – 15 mm hg
Returns to
baseline by term

Supine pregnant patient
Gravid uterine pressure
Compression of IVC
Decreased venous return
Decreased cardiac output – 10 – 30%

Poor venous flow
Compromises
infradiaphragmatic
i.v sites
Femoral / saphenous routes
Not recommended for
i.v access
During resuscitation

*RESPIRATORY SYSTEM
Increased Tidal
Volume
Progesterone
stimulated
hyperventilation
Increased minute
ventilation
Chronic
respiratory
alkalosis
Decreased
Functional
Residual
Capacity – 20%
Rapid decrease
in arterial
oxygen content
during arrest
Right side shift of
oxyhemoglobin
curve during
arrest state
Maintain maternal
PO2 of >60 mm hg
in arrest state

Delayed Gastric emptying
in pregnancy
(progesterone like effects
of placental hormones)
Increased acidity of
stomach contents
cardiac sphincter
relaxation causes
regurgitation of stomach
contents
Increased chance of
aspiration and vomiting
*GASTO-INTESTINAL
SYSTEM

*AIRWAY AND
VENTILATION
CONSIDERATION IN
PREGNANCY
Decreased tolerance for hypoxia and apnoea
Tongue, mucosa, supraglottic edema & friability
Difficult mask ventilation
• Low FRC
• Elevated diaphragm
• Raised intra-abdominal pressure
Mallampatti class 3 airway
Weight gain & obesity
• Increased neck folds
• Foreshortened neck
Increased risk of aspiration
• Increased gastric emptying time
• Decreased lower esophageal sphincter tone

*
Key Interventions to Prevent Arrest
* Place the patient in the full left-lateral position to
relieve possible compression of the inferior vena cava.
Uterine obstruction of venous return can produce
hypotension and may precipitate arrest in the critically
ill patient.
* Give 100% oxygen.
* Establish intravenous (IV) access above the
diaphragm.

 Assess for hypotension : maternal hypotension that
warrants therapy has been defined as a systolic blood
pressure 100 mm Hg or 80% of baseline.
 Maternal hypotension can result in reduced placental
perfusion.
 In the patient who is not in arrest, both crystalloid and
colloid solutions have been shown to increase preload.
 Consider reversible causes of critical illness and treat
conditions that may contribute to clinical deterioration as
early as possible.

*Resuscitation of the Pregnant
Patient in Cardiac Arrest
MODIFICATIONS OF CARDIOPULMONARY
RESUSCITATION
Patient Positioning
 Important strategy to improve the quality of CPR and resultant
compression force and output.
 The pregnant uterus especially of >20 weeks gestation or gravid
uterus palpated above the umbilicus, compresses the inferior vena
cava, impeding venous return and thereby reducing stroke volume
and cardiac output.
 In non cardiac arrest parturients left-lateral tilt results in improved
maternal hemodynamics of blood pressure, cardiac output, and
stroke volume and improved fetal parameters of oxygenation,
nonstress test, and fetal heart rate.

Left lateral tilt - 30
degrees using wedge
(hard) of predetermined
angle. Eg. Cardiff wedge
Manual left uterine
displacement, with the
patient in supine, also
relieves aortocaval
compression .

 Left uterine displacement -
patient’s left side with the 2-
handed technique
 The patient’s right side with
the 1-handed technique ,
depending on the
positioning of the
resuscitation team.
 If chest compressions
remain inadequate after
lateral uterine displacement
or left-lateral tilt, immediate
emergency cesarean section
should be considered.

*AIRWAY and BREATHING
 Active airway management is the initial consideration.
 Airway management is more difficult during pregnancy
 Secure airway early in resuscitation
 OPTIMAL use of bag-mask ventilation and suctioning, while
preparing for advanced airway placement should be done
 Use small endotracheal tubes, short laryngoscope handles
 Use an ETT 0.5 to 1 mm smaller in internal diameter than
that used for a nonpregnant woman of similar size because
the airway may be narrowed from edema
 Give 100 % oxygen and mainatain good saturation

*CIRCULATION
 Chest compressions should
be performed slightly higher
on the sternum than
normally recommended to
adjust for the elevation of
the diaphragm and
abdominal contents caused
by the gravid uterus.
 Position is slightly above the
centre of the sternum
 Current recommended drug
dosages for use in
resuscitation of adults can
also be used in resuscitation
of the pregnant patient in
cardiac arrest.

*DEFIBRILLATION
*Management of ventricular arrhythmias require
defibrillation during maternal resuscitation.
*There should be no delay if use of defibrillation is indicated
*Energy levels are same as ACLS protocol
*Before delivering the shock, REMOVE FETAL
MONITORING EQUIPMENTS to prevent electrocution
injury to patient or rescuer

*Pregnancy-Related Causes of Maternal
Cardiopulmonary Arrest
B- Bleeding(haemorrhage)/ DIC
E- Embolism/coronary/pulmonary/amniotic fluid embolism
A- anesthetic complications
U- Uterine atony
C- Cardiac diseases/MI/Ischemia/aortic dissection/cardiomyopathy
H- Hypertension / Preclampsia/ Eclampsia
O- Others / Diff. Diag of standard ACLS guidelines i.e 5H’s and 5T’s
P- Placenta previa/ Abruptio placenta
S- Sepsis

*Reversible Causes
Electrolyte
abnormalities
Tamponade Hypothermia
Hypovolemia Hypoxia Hypomagnesemia
Myocardial
infarction
Pulmonary
embolism
Tension
pneumothorax

*Haemorrage
*Case of placenta previa/ abruptio placenta,
where bleeding is significant
*Fluid resuscitation with RL/ NS
*Vasopressor agent - Inj. Ephedrine (5mg every 5
mins till response is seen) , if fluids fail to restore
adequate blood pressure.

*EMBOLISM
Pulmonary embolism
• Thromboembolic disease risk
increased
• Hypoxic/ hemodynamic unstable
• Anticoagulation with heparin –
currently the treatment of choice
• Also , adequate oxygenation and
treating hypotension
• Elevated D-dimer not a helpful
screen in pregnancy
• CT scan or VP scan to confirm
diagnosis on treatment is stated.
• Use of thrombolytics reserved when
potential benefits outweighs the risks,
emergencies beyond 20 wks
gestation, postpartum period
Amniotic fluid embolism
• Dyspnoea, hypotension associated
with pt. is labour/ abortion
• Sudden onset breathlessness, air
hunger, decreased oxygen saturtion
• Develop cardiac arrest within
minutes
• DIC
• Multi- organ failure
• Treatment tried : cardiopulmonary
bypass, open pulmonary artery
thromboembolectomy.

*Anesthetic complication
*Bupivacaine induced arrythmia – amiodarone is the primary drugin
the ACLS arrythmia algorithm.
*Early administration of lipid emulsification (20% intralipid) – used
in resuscitation of bupivacaine- induced cardiotoxicity. ( lipid rescue
therapy : picard J . Anesthesia 2009)

*Cardiac Disease
 The most common causes of maternal death from cardiac disease are
myocardial infarction, followed by aortic dissection.
 Women deferring pregnancy to older ages, increases the chance of
having atherosclerotic heart disease.
 Fibrinolytics is relative contraindication in pregnancy
 PCI(percutaneous coronary intervention)/coronary angioplasty is
the reperfusion strategy of choice for ST-elevation myocardial
infarction.
 illnesses related to congenital heart disease and pulmonary
hypertension are the third most common cause of maternal cardiac
deaths.

*Preeclampsia/Eclampsia
Preeclampsia/eclampsia develops after the 20th
week of gestation and can produce severe
hypertension and ultimately diffuse organ-system
failure.
Magnesium sulphate
If untreated, maternal and fetal morbidity and
mortality results.

*Magnesium Sulfate Toxicity
 Magnesium toxicity present with ECG interval changes: (prolonged PR,
QRS and QT intervals) at magnesium levels of 2.5–5 mmol/L
 AV nodal conduction block, bradycardia, hypotension and cardiac arrest at
levels of 6–10 mmol/L.
 Neurological effects : loss of tendon reflexes, sedation, severe muscular
weakness, and respiratory depression are seen at levels of 4–5 mmol/L.

 Others include: gastrointestinal symptoms (nausea and
vomiting), skin changes (flushing), and electrolyte/ fluid
abnormalities (hypophosphatemia, hyperosmolar
dehydration).
 Patients with renal failure and metabolic derangements can
develop toxicity after relatively lower magnesium doses.
 Iatrogenic overdose is possible in the pregnant woman who
receives magnesium sulfate, particularly if the woman
becomes oliguric.
 Administration of calcium gluconate (10 ml of a 10%
solution) is the treatment of choice
 Empiric calcium administration may be lifesaving

Trauma and drug overdose
*Pregnant women are not exempt from the
accidents & mental illnesses
*Domestic violence also increases during
pregnancy; homicide & suicide are one of the
causes of mortality during pregnancy

*Emergency Cesarean Section
in Cardiac Arrest
*Delivery of the foetus is a part of resuscitation process when
applicable.
*Despite appropriate modifications – mechanical effect of gravid
uterus – decreases venous return from IVC – obstructs blood
flow through abd. aorta – decreases thoracic compliance –
unsuccessful CPR – increased risk of hypoxia going in for
anoxia to mother and foetus BEYOND 4 MINUTES OF
ARREST.

*Why Perform an Emergency Cesarean
Section in Cardiac Arrest?
 Emergency cesarean section in maternal cardiac arrest indicate a return
of spontaneous circulation or improvement in maternal hemodynamic
status only after the uterus has been emptied.
 Recent studies indicates ROSC(return of spontaneous circulation) and
maternal hemodynamic stability of the mother and normal neurological
outcome of the neonate post perimortem casarean.
 The critical point to remember is that both mother and infant may die if
the provider cannot restore blood flow to the mother’s heart.

*Decision Making for Emergency
Cesarean Delivery
Gestational age less than 20 weeks
 Need not be considered because this size gravid uterus is
unlikely to significantly compromise maternal cardiac output
Gestational age approximately 20 to 23 weeks
 Perform to enable successful resuscitation of the mother, not
the survival of the delivered infant, which is unlikely at this
gestational age
Gestational age greater than 24 weeks
 Perform to save the life of both the mother & infant

*The Importance of Timing With
Emergency
Cesarean Section
 When the maternal prognosis is grave and resuscitative
efforts appear futile, moving straight to an emergency
cesarean section may be appropriate, especially if the
fetus is viable.
 If emergency cesarean section cannot be performed by the
5-minute mark, it may be advisable to prepare to evacuate
the uterus while the resuscitation continues.

The following can increase the infant’s survival:
 Short interval between the mother’s arrest & the infant’s
delivery
 Perimortem caesarean section to be performed within 4 mins
of cardiac arrest and delivery of the foetus within 5 mins.
 No sustained pre arrest hypoxia in the mother
 Minimal or no signs of fetal distress before the mother’s
cardiac arrest
 Aggressive & effective resuscitative efforts for the mother
 Delivery to be performed in a medical center with easy access
to NICU.

*Post–Cardiac Arrest Care
 Post–cardiac arrest hypothermia can be used safely and
effectively in early pregnancy without emergency cesarean
section (with fetal heart monitoring), with favorable maternal
and fetal outcome after a term delivery.
 No cases in the literature have reported the use of therapeutic
hypothermia with perimortem cesarean section.
 Therapeutic hypothermia may be considered on an individual
basis after cardiac arrest in a comatose pregnant patient based
on current recommendations for the nonpregnant patient
 During therapeutic hypothermia of the pregnant patient, it is
recommended that the fetus be continuously monitored for
bradycardia as a potential complication, and obstetric and
neonatal consultation should be sought

*
*Despite recommendations in the two most recent
Confidential Enquiries into Maternal and Child Health
(CEMACH) reports, and improvements in patient care
using early warning scoring systems (EWS) in the
general adult population, no validated system currently
exists for the obstetric population. The survey results
support CEMACH recommendations for a nationally
agreed obstetric EWS.
International Journal of Obstetric Anesthesia
Volume 18, Issue 3, July 2009, Pages 253–257A national survey of obstetric early warning
systems in the United Kingdom
R.D.J. Swantona, S. Al-Rawib,M.Y.K. Weea

*
*Assessment and optimisation of the patient during pre-
anaesthetic evaluation,robust referral systems,allowing
senior staff to refer high risk parturients to senior on call
anaesthetists are pre-emptive strategies to avoid
requirement of a HDU/ICU admission.
*MEWS includes measurement of urine output,deviation of
blood pressure,heart rate,oxygen saturation,respiratory
rate,temperature and level of consciousness.If threshold
score exceeds,it triggers an immediate call for senior
consultant and other measures.

*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
Summary

*REFERENCES
*MILLERS ANAESTHESIA 7th EDITION
*CURRENT STATUS OF OBSTETRIC ANAESTHESIA: IMPROVING
SATISFACTION AND SAFETY-IJA 2009
*ANAESTHESIA FOR LSCS:CHANGING PERSPECTIVES-IJA 2010
*OBSTETRICS ANAESTHESIA:WIDENING HORIZONS-IJA 2010
*COURTESY : UPDATE JUNE 2012 LITERATURE REVIEW
*AHA : CIRCULATION 2010 – CARDIAC ARREST IN PREGNANCY
*TINTINALLI 7TH EDITION

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