10/23/18

Case Scenario-1
§ 4-yrs (12 kg) male term child
Anaesthetic Implications of a § Tachypnea, suprasternal retractions, stridor
( respiratory distress )
Syndromic child § Multiple anomalies
§ hydrocele, bilateral TMJ Ankylosis, glaucoma
§ Syndromic look (Retrognathia, micrognathia)
?Pierre robins syndrome? Stickler Syndrome
Dr Manpreet Kaur § Obstructive Sleep Apnoea → Pulm HT
Department of Anaesthesiology, Pain Medicine and § Abdominal distension → Mild Hepatomegaly
Critical Care
§ For emerg tracheostomy
All India Institute of Medical Sciences, New Delhi
§ For TMJ Surgery

Case Scenario-2
§ 2-days (1.86 kg) male term child
§ Delayed cry ,multiple anomalies
§ SFA, TEF, hypospadiasis, UDT
§ Syndromic look (Retrognathia, cleft Palate)?Pierre robins
syndrome
§ Excessive salivation, drooling, coughing
§ Inability to pass a catheter down esophagus
§ Diagnosed Tracheo-osophageal fistula
§ Posted for VATS

DEFINITIONS EMBRYOLOGY

• Possibility of teratogenic insult after gastrulation

• Malformations: Structural anomalies (Absent/Alt Str)
• Dysplasias : Abn of a particular tissue
• Organogenesis: 3-8 wks
• Syndromes: Anomalies linked by common aetiology
• Association: >=2 abn of unknown aetiology
• Teratogenic insult can occur throughout a pregnancy
• Complex: Mix of abn linked due to their close location on
the body
• Exposure to teratogens → gross abnormalities
• Sequence: Series of ordered consequence (single cause)
A→B → C → D
• Abn in one → deficit in organ of embryological origin

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CLINICAL APPROACH
Embryogenesis
If you find one abnormality, actively search for another one
Ectoderm :
CNS,PNS, hair
& nails, glands,
Teeth enamel

Endoderm :
Epithelium of GIT,
respiratory tract,
Mesoderm : bladder, Thyroid,
Muscle,cartilag, parathyroid
bone,heart Liver, pancreas
Urogenital Tympanic cavity
(NOT bladder)
Spleen
Adrenal cortex

Height Head size

Tall or short? Macrocephaly-Mucopolysaccharidosis.
Small child-chronic disease(cardiac, renal or Microcephaly -Foetal Alcohol Syndrome & Angelman Syndrome
respiratory)
Excessively tall child -Marfan’s syndrome Head shape
Beware the airway difficulty in a child
Weight with an abnormally shaped head!
Underweight -Chronic conditions,Turners
Overweight -Beckwith Wiedemann, Prader-Willi Fontanelles
Delayed closure.
Developmental Delay
Facial Symmetry
Other CNS: Hypotonia -myopathies & Facial asymmetry are obvious
dystrophies e.g. Goldenhar Syndrome,
Facial hypoplasia / dysplasia

Eyes: Hypotelorism or Hypertelorism , Neck

epicanthic folds, abn palpebral fissures, short or webbed
colobomata, cataracts, ptosis, blue sclera atlanto-axial subluxation:Trisomy 21,
fusion : Klippel Feil.
Ears: Misshapen, tags or low set ears Hands
Ear abn: linked with airway & renal Polydactyly, syndactyly, short fingers or long thin
abnormalities (shared time of development) fingers (arachnodactyly).

Nose: Large or small , Nares hypoplastic, Feet

Club feet –isolated /complex problem.
Mouth: Macro or microstomia and trismus
Actively search for co- existing abnormalities
Cleft lip & palate : Assoc 66 synd
Actively search for assoc anomalies
Examination of the parents important : merely a normal variant
Jaw
Micrognathia and prognathism: Intubation challenges

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WHY IS THE DYSMORPHIC CHILD Pre-operative cardiac investigation

IMPORTANT TO THE ANAESTHETIST?
• History /CE suggests cardiac disease
• Poor exercise tolerance or feeding difficulty
1) Occult, systemic abnormalities : not identified • Frequent RTI
2) Difficult airway • Signs of valvular disease
• Cardiac failure, arrhythmias etc.
3) Difficult vascular access • Primary myopathies
4) Risk of Malignant Hyperthermia • Diagnosis with frequent cardiac involvement

5) Psychological problems / mental retardation • Investigations :

resulting in extreme anxiety or difficulty with – Baseline room air SpO2
– CXR
induction
– ECG
– Cardiology assessment –echocardiography

Skeletal deformities:
Other Systems
• Contractures → Positioning difficult
• Renal Abnormalities:
• Osteogenesis Imperfecta → injuries / fractures → gentle
handling.
• Kyphosis and scoliosis → Respiratory complications. • Respiratory problems :
• Instability and fusion → Radiology cervical spine. → • Secondary to skeletal deformities or myopathies
difficult airway.

• Metabolic Abn:
• Glycogen storage diseases
• Hypocalcaemia

MALIGNANT HYPERTHERMIA (MH) Potential Airway difficulties

• Dysmorphic features
• Genetic abnormalities (calcium homoeostasis)
– Muscular Dystrophies • Limited neck extension ( klippel– feil syndrome)
– Noonan’s • ↓MO (TMJ mob)
– Larsen Syndrome
• Macroglossia (beckwith – wiedemann
syndrome)
• Limited sub- mandibular space
• Hypotonic child ⇢neuromuscular disease
• Use TIVA • Str abn laryngo-tracheal passage
• Succinylcholine CI • Storage diseases (mucopolysaccharidoses)

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Difficult airway Case Scenario-1

• Difficult Assessment
• Cooperation for airway assessment § 4-yrs (12 kg) male term child
• Mallampati score in paediatric: questioned
§ Tachypnea, suprasternal retractions, stridor
( respiratory distress )
• The lateral profile: more useful for mandibular hypoplasia § Multiple anomalies
• History of apnoea episodes § hydrocele, bilateral TMJ Ankylosis, glaucoma
§ Syndromic look (Retrognathia, micrognathia)
• Daytime somnolence, noisy breathing, stridor, snoring, & ↑work ?Pierre robins syndrome? Stickler Syndrome
of breathing
§ Obstructive Sleep Apnoea → Pulm HT
• Previous Anaesthesia § Abdominal distension → Mild Hepatomegaly
• Colorado Pediatric Airway Score (COPUR): more reliable
§ For emerg tracheostomy
§ For TMJ Surgery

Present history Clinical examination

§ Reduced MO ⇢3 yr(2 FB→no)

§ Drowsy, responsive to stimulation
§ History of snoring, day time somnolence § Pallor+/clubbing+/cyanosis+
§ Tachypnea, suprasternal retractions, stridor § HR: 130 bpm , regular
( respiratory distress ) § NIBP : 98/54 mm of Hg
§ Oxygen & Nebulization → Still worsened symptoms § RR – 30/min
§ Airway Examination:

COPUR Index COPUR Index

16

Raj D. BJA 2015;15: 7–13

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Anticipated problems Anaesthetic plan

• Obstruction during induction and extubation; HDU

• Difficult mask ventilation Parents/care-givers consent (Surgical

airway, HDU)
• Jaw Thrust
• Oral airway Plan (A,B,C) & Equipment prep
• Awake FOB

• Airway blocks
Premedication?

• Inh Induction⇢Tongue fall ⇢Pull Tongue forward Insertion of IV cannula,

SpO2, 5-lead ECG, NIBP attached
• Visceromegaly- Diaph up ,↓FRC,↑Endobronchial Int
Check adequacy of mask ventilation
• Readiness for surgical airway (Inh Induction )

Peri operative concerns and planning

Ventilation Adequate § Positioning

• Preparation for Tracheostomy
• Check ventilation
FOB (sevo in 100% O2) CVCI • Oxygen supplementation

Intubate with 5.0 ETT Tracheostomy

Anaesthetic Management Anaesthetic sequence

Preop Counselingà Operating room FOB guided ETT (#5mm ID)

Confirmed by ETCO2
SpO 2 , 5-lead ECG, NIBP attached

Fentanylà Atracurium

Inhalational induction and FOB Maintainance: O2- air- Sevoflurane

(MAC 0.8 – 1.0)

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Same child for Mandibular distraction Case Scenario-2

Already Tracheosomised (Cuffed 5mm TT)
Parents/care-givers consent (HDU)
Insertion of IV cannula,
SpO2, 5-lead ECG, NIBP attached
Induction: Fentanyl,Prop, § Inability to pass a catheter down esophagus
Atracurium
Maintainance: O2- air- Desflurane
(MAC 0.8 – 1.0)
§ 2-days (1.86 kg) male term child
§ Delayed cry ,multiple anomalies
§ SFA, TEF, hypospadiasis, UDT
§ Syndromic look (Retrognathia, cleft Palate)?
Pierre robins syndrome
§ Excessive salivation, drooling, coughing
§ Diagnosed Tracheo-osophageal fistula
§ Posted for VATS

Problems Anaesthetic plan

Difficult Mask Ventilation
• Neonatal Pierre Robins
Oral Airway may lodge in cleft Parents/care-givers consent (Surgical
Difficult Laryngoscopy
airway, HDU)

Back up Plan

Video laryngoscopy Premedication?

Fibreoptic intubation via LMA.

Smallest Air Q LMA(0.5) :NA IV cannula in situ,

Smallest Fibreoptic :Not working SpO2, 5-lead ECG, NIBP attached
• Gastric inflation through TEF Check adequacy of mask ventilation
(Inh Induction )

Ventilation Adequate

IV Propofol,Atracurium
Low TV,high freq
CVCI Discussion

C –Mac:Cant visualise Tracheostomy

2

Ambu –LMA(#1)

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 10/23/18

Pierre Robin sequence Pierre Robin sequence

• Incidence: 1:8500 live births Small Failure of tongue Cleft
• Often isolated abnormality Mandible to descend
• 1/3 patients : Associated malformation
↓
– Stickler syndrome (40%)
– velocardiofacial syndrome (15%) → ←
– chromosome 22 deletion

• Clinical features: (TRIAD)

– Micrognathia
– Glossoptosis
– Cleft palate

Degree of upper airway obstruction

Type 1 (True Tongue touches the posterior pharynx at the level just
glossoptosis) below the soft palate
Hypotonia
Central Apnea
Type 2 The tongue touches at or just above the level of the
soft palate
Micrognathia True glossoptosis
Cleft Palate
Retrognathia Tongue Retracts Post Type 3 Medial compression by the lateral pharyngeal walls

Medial mov of lat pharyngeal wall
Pharynx constricts in sphincteric
manner
Flexion of basicranium
Cervical instability
Tracheobronchiomalacia
Type 4 The pharynx constricts the airway in a sphincteric
manner
Type 1 and 2 :nasopharyngeal airway or mandibular distraction
Some type 2: tracheostomy.
Most type 3 and 4 :require tracheostomy
Raj D. BJA 2015;15: 7–13

Anticipated airway Problems Difficult Airway

Micrognathia “The clinical situation in which a
Glossoptosis Difficult conventionally trained anesthesiologist
+_Cleft lip/palate Laryngoscopy
Anterior larynx experiences difficulty with face mask ventilation
of the upper airway,
difficulty with tracheal intubation, or both.”
Difficult Mask
Ventillation

Video laryngoscopes & fibreoptic -Suggested definition from 2003

intubation via LMA. ASA Practice Guidelines

Fibreoptic intubation is the gold standard

Raj D. BJA 2015;15: 7–13

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Pawar DK. IJA 2016;15: 906–14

Major references for Syndromic child

• Online Mendelian Inheritance in Man Web site (omim.org)

clinical synopsis”

• Smith’s Recognizable Patterns of Human Mal-

formation(7th edition)

• Bruno Bissonnette’s Syndromes: Rapid Recognition

and Periopera- tive Implications2 and Anesthesia for
Genetic, Metabolic, and Dysmorphic Syndromes of
Childhood

• Anesthesia for Genetic, Metabolic, and Dysmorphic

Syndromes of Childhood -Baum and O’Flaherty’s
Baum VC. Anesthesiology 2015; 123:737-9

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‘Take-home’

• If you find one abnormality, look for another

• Always be prepared for the difficult airway
• No 1 way to manage pediatric difficult airway
• Need meticulous peri operative management:
– Effective preparation
– expertise in difficult paediatric airway
– difficult airway management algorithms
– regular refresher training are essential for success

Case Scenario
SGRH

n 3 year old male child

Adenotonsillectomy in a Child n Weight 14 kg

of Obstructive Sleep Apnoea n Chief complaints

n Mouth breathing and snoring since 6 months

n Throat pain since 2days

n Fever and cough

Dr. Deepanjali Pant
n Posted for adenotonsillectomy due to adenotonsillar hypertrophy
Sr. Consultant
leading to OSA
Deptt. of Anaesthesiology,
How will you approach?
Pain and Perioperative Medicine,
Sir Ganga Ram Hospital, New Delhi

Importance for the Anaesthesiologist

n Paediatric age group

What are the Tonsils and Adenoids?
n Obstructive sleep apnea
n Adenotonsillectomy
What is their Significance?

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Tonsils and Adenoids

n Lymphoid tissue
n Waldeyer’s tonsillar ring
n 1 Pharyngeal tonsil
n 2 Tubal tonsil What is the Difference Between
n 2 Palatine tonsil
n 1 Lingual tensile
n Part of the immune system to protect against infection
n Diseased tonsils function not significant SDB and OSA?
n Important structures deep to inferior pole
n Glossopharyngeal nerve
n Lingual artery
n Internal carotid artery

Sleep Disordered Breathing (SDB) Obstructive Sleep Apnoea (OSA)

n Non obstructive n Periodic episodes of nocturnal airflow restriction (hypopnoea) or obstruction

n Sleep related hypoventilation disorder (apnoea) in association with sleep disruption, arousals from sleep, oxygen
n Central sleep apnea syndrome
desaturation & possible hypercapnea
n Obstructive
n Exceedingly common in children
n Most common etiology : adenotonsillar hypertrophy
n Important cause of morbidity if untreated
n Primary snoring (20%)
n Peak age 2-6 yrs
n Upper airway resistance syndrome (UARS )
n Obstructive hypoventilation (OH)
n Sleep study / polysomnograph (PSG) - definitive diagnosis
n Obstructive sleep apnoea (OSA)- 2%

OSA in Adults versus Children

n Young children mostly not obese
Is there a Difference Between OSA n Severe failure to thrive
n Decreased sleep at night
n Increased WOB at night
in Adults and Children ? n Reduced calorie intake
n Reduced secretion of growth hormone

n Obesity is a common cause of OSA in older children and

adolescents

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Significance of OSA
n Growth failure
n Cognitive level
What are the consequences of untreated n Somnolence, diminished attention, concentration & memory
n Fine skill deficit
n Behavioural
OSA? n Aggressive, hyperactive
n Listless, reduced activity
n Cardiovascular effects
n Cor pulmonale
n Systemic HTN
n Right and left ventricular dysfunction

Polysomnography (PSG)
OSA Severity Scoring
n Gold standard
n Measure
n Nasal airflow (apnea)
Mild OSA Moderate OSA Severe OSA
n Chest and abdominal wall movement
Clinical Mouth breathing, s light Mouth breathing with Mouth breathing,
n Continuous expired CO2
signs inc reas ed res piratory moderate inc reas e in mark edly inc reas ed
n O2 saturation
effort, ± s noring, res piratory effort, ± res piratory effort, loud
n Standard risk children – controversial s leeps quietly at night s noring or ‘s norting’, s noring and ‘s norting’,
n Indicated in high risk children restless s leep disrupted s leep

n Limitation Sleep SpO2 in normal limits , Normal bas eline SpO2 , Frequent prolonged
n Labor intensive, expensive, not validated, not widely available, Lack of study ± minor dips repeated des aturation to epis odes of paradox ic al
uniformity , disparity between measures and symptoms mid 80s breathing, frequent
n Mini-sleep studies- overnight pulse oximetry & HR monitoring prolonged des aturation

Walker I. ATOTW 159, 2009, 1-6

High-risk Population for OSA

n Chromosomal abnormalities - Down syndrome
Which Children are at high-risk n Craniofacial abnormalities - Apert syndrome

n Cerebral palsy Crouzon syndrome

for OSA?
n Sickle cell disease

n Severe obesity

n Neuromuscular disorder

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Contraindications for
Indications for Tonsillectomy Adenotonsillectomy
n Absolute
n Upper airway obstruction, dysphagia, OSA
n Peritonsillar abscess, unresponsive to adequate medical management
and surgical drainage
n Presence of acute infection
n Recurrent tonsillitis with associated febrile convulsion
n Biopsy in suspected neoplasia
n Relative
n Recurrent tonsillitis unresponsive to medical treatment n Abnormal coagulation profile
n > 7 episodes in past year
n > 5 episodes per year x 2 years
n > 3 episodes per year x 3 years
n Severe episodes of sore throat
n Persistent bad breath / taste in mouth
n Uncorrected partial / complete cleft palate
n Persistent tonsillitis in streptococcus carrier, unresponsive to antibiotic

Adenotonsillectomy in OSA
How strong is the indication of
n First line of therapy in mod-to-severe OSA over 2

years of age with adenotonsillar hypertrophy

adenotonsillectomy in treatment
n AAP and AAO – HNS guidelines

n Most appropriate initial therapy for multifactorial OSA

of OSA?
n Should be considered in a child with OSA who does not have

clear adenotonsillar hypertrophy

Preoperative Assessment Relevant History

n Routine anaesthesia history for a pediatric patient

n History n H/o easy bruising, epistaxis, bleeding gums

n Family h/o bleeding disorders

n Clinical Examination n Repeat episodes of fever, throat pain, dysphagia

n Growth failure

n Investigation n Any complaint of ear-ache, discharge or decreased hearing

n Anaesthetic plan

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Contd….

Relevant History Clinical Examination

n Symptoms during sleep n Routine exam of a paediatric patient
n Snoring, apneic episodes, followed by grunting, sweating, restlessness n Loose / missing teeth – for application of mouth gag
n Daytime syndrome n Look for adenoid facies (long face, open mouth, narrow and flattened mid-
n Mouth breathing, excessive somnolence, morning headache, irritability,
face, hyponasal speech)
hyperactivity
n Microgenathia / macroglossia/ craniofacial abnormalities
n Poor school performance
n Secondary enuresis n Evaluation of tonsillar size

n Family h/o OSA n Tonsillar and pharyngeal exudates, visibly inflamed tonsils

n H/o medications like saline/ n Cervical lympadenopathy

anti-allergic sprays & nebulization n Oral and Nasal cavity patency
n H/o use of CPAP n Direct FO transnasal laryngoscopy
n Velopharyngeal insufficiency

Investigation Grading of Enlargement

n CBC – anaemia, polycythemia

n Coagulation profile and platelet count – if h/o bleeding tendency

n X-ray nasopharynx – lateral view for adenoid

n Chest x-ray – signs of cardiomegaly, prominent central pulm artery

n ECG – signs for RVH (RAD, Rt Vent strain)

n ECHO – confirms pulm. HTN, RVH ± dilatation

n PSG / mini- sleep studies – documentation of severity

Grade 1-4 Grade 0 - 4

Severe OSA : PSG Finding Anaesthetic Plan

n Pre-assessment identifies children at risk
n Plan for appropriate peri-operative care
n AHI > 24 events / hour n Children with OSA with URTI – postponed for 2-4 weeks
n Children with severe OSA with cardiac involvement – cardiologist
consultation
n REM AHI > 60
n Options of anaesthesia
n Mostly GA
n And /or O2 sat nadir < 70% n Rarely LA
n GA + LA infiltration
Merits Demerits
n Peak Pa CO2 > 60 mmHg
• Reduc es reflex response • Vas c ular area
• Reduc es bleeding • Liable to obs truc tion and aspiration
• Aids dis s ection
• Reduc es op time and postop dis comfort

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Anaesthetic Considerations Premedication

n Basic principles of paediatric anaesthesia n Goal
n Smooth atraumatic induction n A clam child

n Airway protection during surgery n Easy parental separation

n Maintenance of adequate depth to prevent reflex responses n Avoid sedative anxiolytics

n Smooth & rapid emergence for return of protective airway reflexes n Solution: Non-pharmacological method
n Adequate postoperative analgesia n Distraction technique

n Prevention of PONV n Parental presence during induction of anaesthesia (PPIA)

n Sedative premedication totally avoided if h/o OSA

n Topical EMLA cream for IV cannula placement

Induction Airway Management

n Intravenous or inhalational n Close sharing of airway
n Endotracheal intubation
n Smooth, atraumatic induction desirable n Orotracheal / cuffed / RAE/ reinforced / regular ETT
n Inhalation induction with sevoflurane n Throat should be well packed
n Fixation in mid-line (RAE tube) or at angle of mouth (regular tube)
n IV induction with thiopentone or propofol n Difficult intubation - severe micrognathia, kissing tonsils
n Severe OSA or multiple risk factors – IV induction preferred n Flexible LMA as an alternative
Merits
n Oral airway inserted as soon as deep enough to tolerate n Lighter plane
n Relaxant avoided
n Obstruction on induction – a good indicator of postoperative requirement of n Rapid induction
n Smooth recovery
NP prong airway
Demerit
n Airway may get lost
n Severe OSA with pulmonary HTN – Increased hypoxia on induction further
n Aspiration
exaggerate PVR n Obstruction / accidental extubation / endobronchial intubation

Maintenance Positioning During Surgery

n Adequate depth to prevent reflex response
n Inhaled anaesthetics n Supine position
n Short acting opioids with spontaneous respiration
n Short acting muscle relaxant with controlled ventilation n Neck slightly extended by shoulder rolls
n Analgesia titrated to effect
n Severe OSA – increased opioid sensitivity n Mouth kept open and tongue held out by a Boyle – device
n LA with adrenaline infiltration in tonsillar fossa mouth gag
n Blood loss – difficult to estimate
n Protection of eyes n Ensure ETT position
n At the end, pack removal and suction under vision
n Advantages : direct view of tonsil
n Prone to PONV – antiemetic prior to extubation
ondansetron (0.1mg/kg) : Posterior pharynx - sump for suction
dexamethasone (0.1-0.2 mg/kg)

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 10/23/18

Monitoring Reversal and Extubation

n Extubate only when awake and return of protective
n ECG n IVF airway reflexes

n SPO2 n Blood Loss n Smooth extubation prevents bleeding

n Transport to PACU in tonsillar position
n Temp n Precordial stethoscope

n NIBP

n EtCO2

Postoperative Analgesia Surgical Approach

n Usually mild to moderate pain
n Extracapsular tonsillectomy
n Paracetamol should suffice
n Removal of entire palatine tonsil & surrounding fascia or capsule
n NSAIDs – controversial
n Most common traditional approach
Demerit
n Intracapsular tonsillectomy
n Increased bleeding
n Increasingly used for OSA
n Bronchospasm
n More rapid recovery
Merit n Decrease postoperative bleeding
n Improved analgesia n Less duration of postop pain
n Opioid sparing n Demerits – tonsillar regrowth , revision surgery
n Decrease PONV

Methods Coblation Technology

n Dissection and snare method

n Electrocautery (400ºC) - increased postop pain

n RF ablation – monopolar, only for hypertrophied tonsils

n Harmonic scalpel – ultrasonic vibrations

n CO 2 laser – sig. ¯bleeding / pain

n Microdebrider – less postop pain

n Coblation – RF energy & saline plasma field (40-70°

C)

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Postoperative Complications Post Tonsillectomy Bleed

n Primary haemorrhage (within 24 hrs)
n Secondary haemorrhage (upto 28 days)
nBleeding n 0.5-2% depending upon surgery technique
n More often in older children and chronic tonsillectomy
nRespiratory complications n Direct signs : bright red blood
n Indirect signs: Frequent swallowing, tachycardia
coffee- ground emesis
nPain and sore throat n Challenges
n Intubation
n Hypothermia
nPONV n
n
Smooth extubation
Aspiration

Postoperative
Management Respiratory Complication
nQuick review of previous anaes record OSA is an important risk factor
nPreparation for difficult intubation n Transient laryngospasm
nIV access n Mild desaturation
nVolume resuscitation n Airway obstruction – life threaten
nPreoxygenation (lateral head down)
n Pulmonary Edema
nRSII
Overnight hospitalization + PICU
nAim for rapid & smooth emergence

Take Home Message

Management
n SDB vary from simple snoring to severe OSA

n Adenotonsillar hypertrophy – most common etiology of OSA

n Severe OSA - failure to thrive, behavioral problems, CVS problems and rarely,

of
pulm HTN and RHF

n Children with OSA sensitive to opioids

n Should be awake and pain free postoperatively

n Observation in monitored environment postoperatively

n Concerns – bleeding, respiratory problems TEF

n Knowledge, anticipation, prevention, observation and timely management
key to safety and success

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58 Neonatal Emergency
60
AIIMS : July 2010 - June 2011 Diagnosis
50

40
Inability to pass a suction catheter into the
30 26
25 stomach
20
12
CXR orogastric tube in the cervical pouch
10
4 Air in the stomach and intestine
0
EA/TEF NEC CDH ARM Int Atresia

TEF
Anatomical classification and incidence

failure in mesenchymal separation

of
upper foregut

failure in mesenchymal separation of

upper foregut Neonatal Emergencies
AIIMS July 2010-June 2011
Upper oesophageal pouch
with secretions 178
4.5 3.7 total admissions
17 operated
Trachea age at presentation
period of ventilation 73%
Fistula 204

Age of presentation
for TEF
range from 1 day to 12 days
Stomach

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Anaesthetic Concern

• Sick baby – dehydrated, acidotic, electrolyte

disturbance,hypoglycemic,hypothermia,sepsis
• Risk Factors
• Possible chest infection and possibility of need • Anaesthetic management
for respiratory support • Airway management

Need physiological and biochemical

stabilisation

• Low birth weight

• Prematurity
• Associated cardiac
anomaly

100
94
90

80
No Anomalies Major associated anomalies

70 63.3
60 117(39%)
50 41.6 184(61%)
40

30
18
20

10

0
Survival 104 (89%) Survival 136 (74% )
cardiac ARM duodenal Multiple
anomalies atresia anomalies

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Pre operative preparation

• NPO
• Head up tilt
• Sump tube and slow suction
• Correction of fluid deficit
there is a wide range of
• Correction of electrolyte & acid base anesthetic practice and that no
disturbances standard technique is
• Pre operative ventilatory support in the presence used for the management of
infants for TOF/OA
of chest infection repair
• ECHO

Anaesthetic Technique Anaesthetic Technique

• associated co morbidity
• type of EA/TEF
• anesthetist preference &
• local hospital practice
Induction - Inhalational / intravenous
Bronchoscopy after induction preferred
would detect size, site and numbers of the
fistula & ballon occlusion of large fistula
Intubation - awake / spontaneous Sevo / with paralysis
Maint. - air, oxygen and paralysis
Analgesia - epidural / narcotic / LA infiltration +
paracetamol PR
Post op - elective ventilation with morphine infusion

Intraoperative Issues

7 cases of difficult
ventilation
4 large fistulae
1 needed gastrostomy
• Endobronchial intubation
• Intubation of fistula
• Obstruction of ETT
Intubation and tube • V/Q mismatch
placement lateral decubitus position
• Under FBG nondependent lung retraction
• Right bronchial intubation • Vagal response to tracheal manipulation
gradual withdrawl
• Tube manipulation in tachea • Return to transitional circulation and shunting

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Summery
• Patients present with minimal respiratory distress
and good lung compliance
• Tolerate GA with muscle relaxation and gentle
ventilation
• Pre operative gastrostomy is rare
• Low birth wt. and associated cardiac anomalies
are independent predictors of mortality

Pornswan Ngamprasertwong, Anesthesia for Tracheoesophageal Fistula

Anesthesiology pp 381-386 ( e-book) June 2018

CDH

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Aetiology

Results from
failure of the pleuroperitoneal
canal
to close at ~ 8th wk of gestation

Pulmonary changes

• Pulmonary Agenesis
• Vessel wall thickening
• Pulmonary hypertension

21

Histopathological features of CDH lungs
include
• Reduced numbers of alveoli ⁄ area
• Thickened alveolar wall and
• Increased interstitial tissue
leading to
• diminished postnatal alveolar air
space
• decreased gas-exchange surface area
Preoperative preparation
• Intra uterine period
• After birth
10/23/18
Persistent pulmonary hypertension (PPHN)
characterized by
the abnormal vascular structure and number
• medial hyperplasia
• peripheral extension of the muscle layer
• into the small intra-acinary arterioles
• adventitial thickening
leading to
• increased muscularization of the arterioles
• increased vascular tone
Tracheal occlusion
did not improve survival or
morbidity rate in
this cohort of infants with CDH
22
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Pathophysiology

Pre operative Stabilisation

Management

• Role of protective lung ventilation

• Permissive hypercapnia Infant with CDH require
• HFO • Intensive cardiopulmonry support after birth
• ET Intubation and gentle ventilation
• ECMO • Fluid therapy
• Inotropic support
• NO • Assessment of pulmonary hypertension and may require
pulm. vasodilators ( Prostaglandin E1,Milrinone )or ECMO
• Open surgical repair should be delayed until physiological
stability achieved
• Failure to operate within two weeks discuss with family

Respiratory care strategy

• Early HFO, NO
• Delayed surgery till respiratory
and haemodynamic
stabilisation

23
 10/23/18

Respiratory Strategy
• Hyperventilation
• Gentle ventilation
PIP <25,cm H2O,RR < 65/min,Insp
time 0.35 s, PEEP +<2 cm H2O
aim of maintaining pH >7.25
• Permissive hypercapnia up to 60 mm Hg

• Volume resus and inotropes

• Correction of electrolyte and acid
base status

Intraoperative acidosis and hypercapnia during

thoracoscopic repair of congenital diaphragmatic
hernia and esophageal atresia/tracheoesophageal
fistula
Augusto Zani Ruben Lamas-Pinheiro Irene Paraboschi Sebastian K. King
Justyna Wolinska Elke Zani-Ruttenstock Simon Eaton Agostino Pierro
Pediatric Anesthesia 27;2017:841-848
TEF 62
Th o raco sco p i c

Op en
C DH 96

0 20 40 60 80 100

20
25
15 20
TEF Op en
10 15
TEF Th o raco sco p i c
10
5
5
0
0
Aci d o si s Hyp ercap n i a

Anaesthetic management

24
 10/23/18

• 1 year old boy from Ludhiana

• Fever and productive cough for 1 month
Foreign body bronchus • No difficulty in breathing, no noisy breathing
or bluish discolouration
• Similar symptoms 3 months ago, lasted for a
month
Sandhya Yaddanapudi
Dept. of Anaesthesia and Intensive Care
• Local hospital advised chest drain insertion
PGIMER, Chandigarh.

• 9.8 Kg • Nasal flaring Risk factors

• Conscious • RR 32 /min
• Age <3 y (max. incidence 1-2 y)
• Afebrile • SpO 2 93% room air
– Oral exploration
• Pulse 110 bpm • RS: – Incomplete dentition
L: no air entry – Poor coordination during swallowing
R: normal breath
– Easy distraction while eating
sounds
• Boys > girls
• Small objects

Epidemiology of FB bronchus Prevention

• Seasonal variation • Federally mandated test of object size (US)
– More in winters – Screen toy parts for children <3 yrs.
– Small Parts Test Fixture (SPTF)
• High morbidity and mortality
• Consumer Product Safety Commission (CPSC)
– Delay in recognition
– Warning labels on all packages of balloons, small
– Delay in treatment due to lack of equipment and balls and marbles
expertise • Public awareness and education
– Mortality during procedure (0.42%) – Home safety
– Education of parents and caregivers

25
 10/23/18

Types of foreign bodies Pathophysiology

• Organic (77-86%) • Location : size & shape
– Nuts, seeds, fruits and vegetables, meat – Bronchial tree (85-91%), R>L
• Inorganic – Larynx / trachea: high mortality
– Toys, toy parts, pins, needles, tablet • Degree of obstruction:
– Smooth conforming occlusive objects: balloons, • Hyperinflation or atelectasis
marbles • Nature of FB: organic, inorganic
• Duration of obstruction

Clinical presentation
• Time of presentation • Event of aspiration of FB
– Immediate or late – Choking followed by paroxysmal cough
• Site and amount of obstruction – Sudden onset respiratory distress
– Trachea, main bronchus, distal In absence of infection/trauma/underlying
pathology
– Partial, complete
• Unilateral decreased air entry
• Nature of FB
– Bronchial obstruction
– Organic or inorganic

Chronically lodged airway FB

• Dyspnea, stridor • Recurrent or intractable pneumonia
• Dysphonia / aphonia • Unexplained atelectasis or emphysema
– Laryngeal FB • Massive haemoptysis
• Wheezing • Lung abscess
• Cyanosis • BPF
• Bronchiectasis
• Mediastinitis

26
 10/23/18

X-ray chest
• Radio-opaque FB (8-16%)
• Normal film (< 24 hrs, 13-22%)
• Obstruction
– Partial: hyperinflation, depressed diaphragm,
mediastinal shift
– Complete: atelectasis
• Pneumonia
• Sensitivity 73%, specificity 45%

CT scan
• CT scan
– Radioluscent FB
– Parenchymal changes
• Virtual tracheobronchoscopy
– Multislice CT with 3-D reconstruction
– 100% sensitivity, 67% specificity
– PPV 93%, NPV 100%

Removal of FB Rigid bronchoscope

• Rigid bronchoscopy (gold standard) • Bronchoscope/sheath

– Urgency depends on respiratory distress • Optical telescope
– Successful in 95-98% of cases • Suction channel
• Fiberoptic bronchoscopy • Side arm with a 15 mm
connector
• Repeat bronchoscopy
• Fiberoptic light source
• Tracheostomy • Forceps
• Thoracotomy and bronchotomy • Video camera &
monitor

27
 10/23/18

Preparation for anaesthesia

• Consider the urgency of procedure
• Determine “what, where, when”
• Fasting
• Premedication
• Monitoring
– ECG, SpO2, NIBP, ETCO2
– Chest expansion/auscultation
• IV access

Anaesthesia technique
• Communication between anaesthetist, • Induction of anaesthesia: IV vs. inhalational
bronchoscopist and assistants – Full stomach
• 2 anaesthetists – Airway obstruction
• Maintenance with TIVA
(propofol, dexmed, remifentanil, fentanyl)
– Consistent and adequate depth of anaesthesia
– OT pollution avoided
– N2O decreases FiO2, increases volume of trapped
air

Spontaneous better than controlled

Muscle relaxants ventilation?
• No relaxants • FB in larynx or trachea
• Suxamethonium – Lower risk of complete obstruction
• Atracurium • Distal displacement of FB by IPPV
• Better V/Q matching
• Continued ventilation during removal of FB
• Rapid assessment of airway after FB removal

28
 10/23/18

Problems with spontaneous

ventilation
Advantages of using a relaxant
• Deep plane of anaesthesia required • Immobile patient, removal of FB facilitated
– Depression of circulation • Lesser anaesthetics required, less cardiac
– Hypoventilation depression, early recovery
• Increased resistance to breathing when • Positive pressure ventilation
telescope is being used – Decreases atelectasis
• Patient movement, bucking, breath holding – Overcomes increased resistance
– Better oxygenation

Problems with controlled ventilation Spontaneous vs. controlled ventilation

• Risk of ball-valve hyperinflation • Meta-analysis: 5 trials (Liu 2014)

– Difficult to remove FB – 441 spontaneous ventilation
– Risk of rupture of lung distal to obstruction – 423 controlled ventilation
• No difference in desaturation,
laryngeal edema, breath holding
• Controlled ventilation had
– Less laryngospasm
– Less bucking, coughing, movements
– Shorter operation

Other drugs Inadequate ventilation

• Anticholinergic: atropine or glycopyrrolate • Telescope occupies most of the lumen
– Higher risk of arrhythmias – Increased resistance
• Steroids: dexamethsone – Hyperinflation (decreased CO, barotrauma)
– Decreases airway oedema – Hypoventilation
• Topical anaesthesia: lignocaine 1%, 3-4 mg/kg • Scope inside a bronchus
• System is open: suction, removal of FB
• Primary pathology

29
 10/23/18

Positive pressure ventilation Jet ventilation

• Allow adequate time for expiration • Catheter through nose into trachea, or
• Remove telescope and close open end of Side port of bronchoscope
bronchoscope with a glass ocular piece/finger • Driving pressure
– Age <1 year: 0.6-1 bar
– Age >1 year: 1-2.5 bar
• Advantages: Continuous ventilation, Less
hypoxia
• Disadvantages: Barotrauma, dislodgement

Postoperative respiratory adverse

Intraoperative complications events
• Inadequate ventilation, hypoxia • Incidence 9.5%
• Arrhythmias, cardiac arrest
– Vagal stimulation
• Preoperative respiratory impairment a risk
– Inadequate ventilation factor
– Inadequate anaesthetic depth • Minor: hemorrhage, minor desaturation,
– Anaesthetic drugs
partial laryngospasm
• Tracheal / bronchial laceration, laryngeal edema,
laryngospasm, bronchospasm, pneumothorax, • Major: complete laryngospasm, major
mediastinal emphysema, bronchial rupture desaturation, pneumothorax
• Dislodgement of FB/dropped FB

Postoperative management Fibreoptic bronchoscopy

• Steroids • Used since 1990s, high success rate
– Dexamethasone for 2-3 days • Increased safety, fewer complications
• Humidified oxygen • Extraction instruments include fiberoptic
• Nebulized racemic adrenaline (1:6 to 1:10 forceps, urological instruments, Fogarty’s
dilution) under ECG monitoring catheter
• Antibiotics • Introduction through tracheal tube or LMA
• Bronchodilators • Rigid bronchoscope should be available

30
 10/23/18

Lessons learnt
• Foreign bodies in children’s airways are
common and dangerous
• High index of suspicion needed
• Delay worsens the patient’s condition;
increases risk
• Good communication required between
surgeon and anaesthetist

31
 10/23/18

Learning Objectives....

T
• Pain pathway
• Non pharmacological methods
echniques • Pharmacological methods
• Indications and C/I of various techniques
echnology • Complications

herapeutics • Myths and Controversies

• Conclusions

JY Simpson Sedan Chair Pathology of Labour Pain

Techniques of labor Analgesia..

Complementary or Alternative Treatment
• Mind Body interventions, Hypnosis
• Bioelectromagnetic, Biofeedback
• Physical methods: Massage, Heating pads, water bath
• Alternative medication: Acupuncture
Non neuraxialtechniques…
• TENS
• Sterile water injections

Local anaesthetic blocks

• Paracervical block
• Pudendal nerve block
• Paravertebral Lumbar sympathetic block

1
 10/23/18

Systemic Analgesia.. Comparison of IV regimes

IV Fentanyl IV Remifentanil
IV/ Inhalational Agents
• Fentanyl • PCA bolus 25-50 ug with a • PCA bolus 0.25 ug/kg with a
• Remifentanil lockout interval of three to lockout interval of two
Conclusions Intravenous patient-controlled
six minutes and a four-hour analgesia
minutes, a four-hour limit of
• Entonox/ Nitronox (O2: N2O::50:50) with either remifentanil 3 mg, and a background
limit of 1-1.5 mg. or fentanyl provides a
moderate degree of labour analgesia, whereas
• Isoflurane infusion of 0.025-0.05 ug/
transient maternal oxygen
kg/min desaturation is observed
• Desflurane more commonly with remifentanil. Fentanyl is
associated with a higher need for
• Sevoflurane neonatal resuscitation.
Marwah R et al, Can J Anesth/J Can Anesth (2012) 59:246–254

Remifentanil for LA: an evidence-

based narrative review
Van de Veldeand CarvalhoB; Feb 2016, Int J Obs Anesth

N2O use for LA:

50% Finland, Norway, Australia, New Zealand
70% Sweden
60% UK

Nitronox
Nitronox:
§ Separate sources of O2 and N2O
§ Blender device delivers preset 50:50
§ Scavenger unit
§ Wall suction for exhaled N2O

Neuraxialtechniques…

2
 10/23/18

Spinal
Technique

Neuraxial
DPE Epidural
technique

Drugs
Drug CSE
Delivery

Common Indications for CSE

• Difficult back
• Previous suboptimal analgesia with Labour
epidural
• Rapid analgesia in late I /early II stage
• Severe maternal distress during labour
• Multiparae in established labour

3
 10/23/18

DPE vs LEA

• > rapid onset of analgesia

• < chances of asymmetric
block
• Early bilateral sacral block
• Fewer maternal/neonatal
side effects

Technique Drugs

Local
Low Dose Opioid
anaesthetic
Drugs
Drug
Delivery Bupivacaine Fentanyl
Ropivacaine Sufentanil
Levobupivacaine

Drugs Technique

Local
Low Dose Opioid
anaesthetic
Drugs
Drug
Bupivacaine Fentanyl
0.0625%-0.1%
✚ 2ug/ml
Delivery

CSE: 3 ml LDM (spinal)

Epidural: 15-20 ml LDM

4
 10/23/18

Variable frequency, automated mandatory

boluses, with a basal infusion for PCEA during
Labour (Sia et al, Anaesth 2013;68:267-275)

LORS Vs LORA

• Saline superior to air

• Reduced blood taps
• Reduced patchy blocks
• Inadvertent wet tap
• Pneumo- encephalocele
can be avoided Provides visual confirmation for:
- Mentoring trainees
Prefer Lateral position! - Patients with challenging anatomy
Sitting, if Obese!

5
 10/23/18

Myths and controversies

• Early vs late
• Maternal outcomes: +/- ?
Controversy 1
• Breastfeeding,
• Fever Timing of epidural during labor:
Epidural taken early vs. late

Controversy 2
In summary, the results of this randomized trial suggest that nulliparous women
in spontaneous labor or with spontaneous rupture of membranes who request
Outcomes & Epidurals
pain relief early in labor can receive neuraxial analgesia at that time without
adverse consequences. When compared with systemic opioid analgesia, initiation
of early neuraxial analgesia does not increase the risk of cesarean delivery and
may shorten labor. • Duration of II stage
• Instrumental delivery
• CS rate

Controversy 3
Does the use of Epidural labour analgesia
adversely affect Breast feeding?

6
 10/23/18

Controversy 4
• Are women with LEA more likely to have
fever? YES
• Is it associated with increased rates of
infection in mother or neonate? NO
• Can elevated maternal temperature Proinflammatory
Cytokines: ILβ1, IL-18
cause fetal / newborn complications?
POSSIBLY

Still a hot topic?? Conclusions....

• Non neuraxial techniques

• Can labour epidural analgesia cause
• DPE technique
inflammation? How?
• Bolus doses: 15-20 ml LDMixtures
• Can epidural associated fever cause neonatal
brain injury? • Computer integrated AMB
• Can we safely suppress maternal fever • How to confirm epidural placement
associated with epidural analgesia? • Myths and controversies

7
 10/23/18

Valvular Heart
Disease in
AIIMS PGA 2018

Pregnancy:
Management of
labor and delivery

Rajeshwari Subramaniam
A.I.I.M.S., New Delhi

Overall death rates per million maternities UK, 2003–05;

7th report of the Confidential Enquiries into Maternal
Deaths in the UK

Overview

Thorne et al.Heart 2006;92:1520–1525

Roos-Hesselink JW et al. Heart 2009;95:680–686

Effect of valvular heart disease on maternal

and fetal outcome

Maternal VHD is associated with a significantly high

incidence of:
Congestive failure
Arrhythmias
Initiation of new treatment
Hospitalization
10.39
Adverse neonatal outcome:
Preterm delivery
IUGR
Low birth weight

RHD accounts for >90% maternal cardiac disease worldwide

Hameed A, Karaalp IS et al. J Am Coll Cardiol 2001;37:893–9
Roeder HA, Kuller JA. Et al. Obstet Gynecol Surv 2011;66:561-571

8
 10/23/18

Questions regarding valvularheart

disease in pregnancy
• What are the normal CV changes in pregnancy?
• Why are stenotic lesions worse tolerated?
• What evaluation do they need? Which are the symptoms and
• Drug therapy? Surgical intervention? findings in normal pregnancy that
• Can labor analgesia be given?
• What level of monitoring is needed? mimic significant heart disease?
• What are the indications for Cesarean section?
• Is neuraxial/ GA better?
• For patients on prosthetic valves:
• Management of anticoagulation

Symptoms Case I
• Heart disease:
• Normal pregnancy:
• Easy fatiguability
• Progressive dyspnea • 26 year primigravida, POG 32 weeks
• Progressive orthopnea • Breathlessness on exertion since II trimester
• Dyspnea
• Hemoptysis • Nocturnal dyspnea, cough: 2 weeks
• Edema over feet
• Exertional syncope • On examination:
• Syncope with position
• Persistent neck vein distension
• Prominent neck veins • HR 130/ min, BP 95/60 mm of Hg
• Diastolic murmurs, thrills
• PACs/ PVCs • Edema feet +, JVP é
• Sustained dysrhythmias
• Chest pain • Murmur on auscultation: mid-diastolic; loud S1
• Progreesive edema
• Pseudo-cardiomegaly • Referred for advice on management of delivery
• Findings of pulmonary
• S3
hypertension
• R sided flow murmurs
• Persistent cough

What are the auscultatory findings

How should she be evaluated? in MS?
• Loud S1:
• Physical evaluation • Wide closing excursion of mitral leaflets
² NYHAstatus • Becomes softer and subdued as valve calcifies
• Cardiovascular evaluationà
Mitral stenosis ² Sinus tachycardia • Opening snap:
• Advised: R Ventricular heave LPSB
² Atrial fibrillation/ • Tensing of leaflets after they open in diastole
• EKG Palpable S1, P2
PVCs • Heard after S2
• Greater the LA gradient, closer OS to S2
• Echocardiography ² Elevated JVP
Diastolic thrill
² Pulmonary • Diastolic rumble:
Auscultation:
• Low pitched, best at apex, L lateral position
Diagnosed as Mitral
congestion • é with exercise, ê with rest/ Valsalva
Stenosis
² Pedal edema • Pre-systolic accentuation in NSR

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 10/23/18

Other murmurs?

• Graham-Steell
• High pitched decrescendo diastolic murmur of PR
• Pansystolic murmur of TR
• S3 originating from RV

Ruys TPE et al. Journal of Cardiology 2013;61: 107–112

Sanghavi M, Rutherford JD. Circulation. 2014;130:1003-1008

Hemodynamic changes in MS
Why is MS tolerated poorly?
during pregnancy
Pregnancy
• é in cardiac output by 30-50% • Fixed CO, é blood volumeà Increased trans valvular gradients
• é by end of I trimester, peaks II-III • Increased incidence of pulmonary edema
• é initially due to SV, later by HR • Increased RV failure
• SVR ê in II trimester • Poor tolerance of increase in heart rate, CO
• Resultà é Transvalvar gradient • Poor tolerance of sudden reduction in SVR
Labor
• CO é 30% I stage; up to 80% post partum
• Auto transfusion of 300-500 ml/contraction
• Risk of thrombosis: peaks at 6 weeks post partum

What are the EKG findings in What are the drugs used for rate
MS? control in MS?
• Digoxin
• Beta blockers
• Calcium channel blockers
• What is the indication for digoxin?
• What are the effects of digoxin seen on EKG?
• Sinus bradycardia
• Digoxin effect
• Atrial tachycardia with 2:1 block
• Bi directional ventricular tachycardia

10
 10/23/18

What is the therapeutic digoxin What information does echo give

level in plasma? us?
• MVA
• 0.8-2 nanogr/ml • Pressure half-time
• Toxic:> 2 nanogr/ml • LA gradient
• LA thrombus
• MV calcification
• ‘Spontaneous Echo contrast’
• PA pressures
• Lead to diagnosing severity of MS
Predict success of PTMC
• Other valve function (TR, MR)

Quantification of severity of
MS

Kannan M, Vijayanand J.Indian J Anaesth. 2010 ; 54: 439–444

Weiner MM et al. Anesthesiology 2011; 114: 949–57

Echocardiographic criteria Patient’s findings are as follows

• MVA 0.8 cm 2
• Trans-mitral gradient 15 mm Hg
• PA pressures 55 mm Hg
What is the reason for hemoptysis?
• Valve morphology: No calcification
• What is the ideal management option
Patient started on metoprolol, furosemide
• Not much symptomatic improvement x 2 weeks
at this stage?
• One episode of hemoptysis

11
 10/23/18

Hemoptysis in MS Indications for PTMC

• é in transvalvular gradient
• é in LA pressures • NYHA III / IV
• à back pressure and rupture of bronchial veins • Symptomatic despite medical
treatment
• MVA <1.5 cm2 with suitable
morphology
• Gestation> 20 weeks

Percutaneous Transmitral Mitral Commissurotomy

(PTMC)

Routray SN et al. Int J Gynecol Obstet 2004;85: 18–23

Esteves CA et al. Am J Cardiol 2006;98:812–816

Effects of PMV
Plan for labor and delivery
• Significant increase in MVA (.8 • At 36 weeks, premature ROM
to 1.2 cm2 ) • Timing and mode of
• Obstetricians plan normal
delivery
Joint decision
• êNYHA status to I / II vaginal delivery Multidisciplinary
--Complications
• êTrans mitral gradient • Vaginal delivery
--Blood loss
Planned at 37 weeks
• Increase CO by 20% • Cesarean section ++Obstetric indications
Adequate Analgesia
• Relief of symptoms • Invasive hemodynamic ++Cardiac deterioration
Hemodynamic monitoring
monitoring
+Patient
Shortening preference
of II stage
Symptomatic Parturients
Severe stenotic disease
Left ventricular dysfunction

Hemodynamic targets for labor Labor analgesia II and III

analgesia stage
Do’s Don’ts
• Small fluid aliquots for hydration
• Maintain HR ≤ 90 • Precipitate tachycardia
• Low threshold for invasive • Large fluid boluses, • Adequate segmental, perineal analgesiaà ê tachycardia, urge to
monitoring ‘preloading’, ephedrine push
• Titrated, incremental regional • ‘Single-shot’ spinals
anesthesia: EA/ CSE with EVE/ • Large volume epidurals • Minimize oxytocin use
• Opioid based I stage • Lithotomy position may be avoided in severe MS
• Propped position, oxygen by nasal prongs

• Shorten II stage
• Observe in HDU for 24 hours

12
 10/23/18

In case I stage prolonged/ fetal

Also…. status non-reassuring/ maternal
• ‘Saddle’ SAB, pudendal blocks good alternatives if epidural not fatigueàCS
placed • CS:
• Marked fluid shifts
• Blood loss
• Treat excessive blood loss
• Extra visceral, somatic stimulation
• Minimize oxytocin use
• EA: Incremental volumes of LA (3-4 ml 2% lignocaine + 25-50 μg
• Diuretics, if patient develops symptoms of overload: fentanylàT6
• Coughing • Avoid epinephrine
• Desaturation
• Pulmonary rales
• Hemodynamic monitoring
• Vasopressor boluses

What are the indications for CS in

maternal cardiac disease in GA for CS
general? • Can afford very stable hemodynamics
• Obstetric reasons • Primary CS • Allows use of TEE à real-time preload status, LA pressures
• Placenta previa, abruption • Patient on oral anticoagulation
• Blunt stimuli during: Fentanyl
• Abnormal placentation in labor
• Severe heart failure • Tracheal intubation Remifentanil
• Non-progress Etomidate
• Suction
• Fetal distress • AO dilatation >45 mm
• Extubation
• Cardiac status • Acute on chronic aortic
dissection • Delayed extubation without reversal
• Advanced cardiac disease
severity • Use pharmacological ‘blunting’
Esmolol
• Functional deterioration • Avoid inadequate analgesia
Fentanyl
Remifentanil
Lignocaine

Case II On examination
• 30 year, III gravida at 36 weeks • No obvious dyspnea
• I fetal loss at 14 weeks of gestation • HR 96-110 bpm, irregularly irregular
• During II pregnancy developed DOE, palpitationsà severe MS • BP 110/70 mm Hg
with AFà LSCS • Prosthetic valve sounds heard
• Underwent Mitral valve replacement 2 years ago • Patient expresses desire for normal delivery
• Present pregnancy:
• On warfarin since II trimester
• Has presented for safe confinement

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 10/23/18

What pre-operative investigations What are the concerns of warfarin

are needed? therapy in each trimester?
• Routine blood work up, r/o anemia, infection • First trimester: Warfarin embryopathy
• Coagulation profile (INR) • Interferes with Vit K dependent proteins responsible for bone
• 12-lead EKG and cartilage synthesis
• Echocardiography? • ‘Warfarin window’:
• LA thrombus • 6-12 weeks
• Prosthetic valve function • Half-life of warfarin
• Vegetations • Spontaneous abortions at any stage
• PA pressure, trans-valvular gradient • CNS anomalies (? Hemorrhage)

Guidelines for warfarin At 36 weeks

• If MVR with risk factor (old mechanical valve, AF, •
thromboembolic episodes, multiple valves):
• Continue warfarin throughout pregnancy
• 6-12 weeks BD sc heparin
• If no risk factor, < 5 mg warfarin/day:
• Dose-adjusted sc LMWH BD for I trimesterà warfarin
• If > 5 mg warfarin/day:
• LMWH target anti-Xa activity 1.0 to 1.2 units/mLà warfarin
• Add aspirin up to 36 weeks
Switch to LMWH BD with previous targets
• Last dose 24 hours before induction
• 12 hours after cessation:
• Start UFH 18 U/kg/hour infusion WITHOUT loading
• Stopped 6 hours before neuraxial block
• Or delivery

Epidural analgesia planned Post partum questions

• Heparin stopped 6 hours ago • Monitoring of block
• APTT 35 sec • Re-institution of LMWH
• Catheter inserted uneventfully • Is MVR thrombogenic?
• Bolused with 0.125 % bupivacaine 8 ml with 2μg/ml fentanyl • Diagnosis of epidural hematoma
• Infusion of 0.1 % bupivacaine at 5 ml/hour • Management
• Baby delivered after 6 hours

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 10/23/18

Situations necessitating emergent

LSCS Aortic stenosis
• If mother still on LMWH? • Etiology: congenital bicuspid aortic valve
• Protamine: will partially reverse • AS consequent to RHD occurs late
• If mother on warfarin: • May be associated with coarctation, PDA, VSD
• 4 factor Prothrombin Factor Concentrateà INR 2 • 6-8% risk of AS in fetus
• FFP 15-30 ml/kg • Screening of mother necessary
• Vit K 2 mg IV
• Valve area>1 cm 2 , normal LV functionà pregnancy tolerated
• LSCS mandatory to avoid fetal hemorrhage well
• If on UFH, just stop infusion • In symptomatic patients, percutaneous valvuloplasty may be
• Keep protamine handy done as bridging to AVR

Pregnancy outcome in AS: the

CARPREG I study ZAHARA study
• Ten predictors of maternal cardiac complications • Mild AS: Pregnancy tolerated well
• 5 general:
• Prior cardiac events • Severe AS:
Maternal NYHA deterioration,CHF
• Poor functional class
• No intervention
Obstetric complications (23%):
• 25.7% perinatal complications:
• High risk valves/ LVOT obstruction •
é Blood volume, é CO, ê SVR é
IUGR,
• LV dysfunction •
HRà deterioration of cardiac status
Congenital heart defects
• 4 specific: éincidence of maternal arrhythmias
• Mechanical valves é pulmonary edema
• Aortopathy (Ao dilatation)
étransient ischemic attacks
• PAH
• CAD
Maternal mortality 2%

Silversides J Am Coll Cardiol. 2018

Severity of AS (AHA/ACC) 2014 Evaluation

Mild: AVA > 1.5 cm 2 , LV-AO gradient < 35
• Severity of mmHg
• Functional class
stenosis Moderate: AVA 1-1.5 cm 2 , gradient 36-63
• Regular re evaluation
mmHg
Severe: AVA <1 cm 2 , gradient >63 mm Hg • Echocardiography
• Risk factors for deterioration
• ECG:
• LVH, Strain
• Medical optimization
Poor NYHA status in I trimester
AVA < 0.6 cm 2 , gradient >60 mmHg
Co existing coarctation
Maternal age >30 years
Maternal smoking

15
 10/23/18

Planning for labor and delivery in

severe AS Heart rate, rhythm
• Condition with most stringent anesthetic requirements and • Both tachycardia, bradycardia deleterious
hemodynamic goals
• Normal sinus rhythm essential
• Mandates close monitoring, maintenance of HR, volume,
myocardial contractility • AFà Poor LV filling, é myocardial oxygen demand

• Mandates involvement of experienced multidisciplinary team • Junctional rhythmà loss of atrial contribution to SV

• Low threshold for cardioversion

Fluid management Hemodynamic goals: RA:

therapeutic window
• Pregnancy associated é CO, HR, blood volume
• à precariously é LVEDP, LAP • Maintain heart rate < 90 bpm
• Excess preloadà é LVEDP, myocardial ischemia • Incremental LA • Tachycardia
• Mandatory hemodynamic monitoring: • Maintain SVR: small doses of • Epinephrine in LA
• Arterial phenylephrine • ‘Single shot’ RA
• CVP • Maintain preload with invasive • Large volumes of LA
• ? PA monitoring
• Large fluid boluses
• TEE • Avoid aortocaval compression • Ephedrine, atropine
• Treat hypotension aggressively; phenylephrine
• Avoid aorto-caval compression

Use of RA GA for CS in severe AS

Pittard A, Vucevic M. Anaesthesia 1998; 53: 169-191
Hyuga S. J Anesth 2016 DOI 10.1007/s00540-016-2238-6
• Avoids sympathetic blockade, hypotension, vasopressor use
• Removes anxiety of awake patient
• Allows use of positive pressure ventilation
• Allows institution of TEE
• Avoids excess fluid use
• Avoids problems of inadequate RA
• Eliminates Valsalva and problems

Suntharalingam G et al. Int J Obstet Anesth 2001;10:129–134

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Case reports on use of GA for

AS
• Successful use of GA and Epidural in 12 patients with severe
AS: 5/12 had CS; 2 EA, 3 GA
• EA:
• 0.625-0.5% bupivacaine + fentanylàPCEA ‘E Orme RML et al. Int J Obstet Anesth 2004; 13: 183–187
• GA:
• Etomidate, suxamethonium
• CSE:
• Bupivacaine 3 mg+ sufentanil 5μg
Ghosh S. Obes Surg 2011; 21:264–266

Fanning N et al. Can J Anesth 2011; 58:837–841

Intervention for AS in
pregnancy
Severe AS before pregnancy Treat AS, counsel re pregnancy

Symptomatic AS before Ist MTP/ balloon valvotomy

trimester
Severe AF with CHF, II trimester Valvotomy/AVRà delivery at
term/lifesaving AVR/Valvotomy
AO> 40, CHF, Viable fetus LSCS with AVR

Asymptomatic severe AS with Conservative treatment, delivery

pregnancy and viable fetus with monitoring, AVR after 3
months
AS with high risk of AVR Valvotomy as bridging therapy

CPB during pregnancy: fetal loss 33% Regurgitant lesions

• Pulsatile flowà Preserves placental hemodynamic • AR and MR ‘physiologically suited’ lesions
function
•
• ê SVRà Augmented forward flow
• High flow rates (>2.5 l/min) +
•
• ê Regurgitant flow due to é in HR
• High perfusion pressuresà prevent hypotension and
associated decreased utero-placental flow
• May need fluid restriction/diuretics/ hydralazine/ nitrates to
reduce preload
• Normothermic flowà avoids hypothermia related fetal
heart rate changes, uterine hypertony
• Vaginal delivery generally recommended
• CS: Aortic root> 45 mm, Ehler-Danlos syndrome
• Progesterone-prevents dilution of circulating progesterone
and uterine irritability

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Special considerations in AR Dilated aortic root

• Tendency to have aortic dissection in pregnancy:
• Hemodynamic changesà é forces on aorta
• é Strain on LV due to é volume, regurgitation
• Elastin degeneration due to estrogen effect
• Careful echo every trimester to monitor AO diameter
• If ≤ 40 mm, can have vaginal delivery with invasive monitoring
• If > 45 mm, ELECTIVE CS
• May need emergent CS with valve replacement (Bentall
procedure)

Anesthesia for AR,MR To summarize

• Regional anesthesia: Physiologically beneficial
• Valvular heart disease still prevalent in a significant maternal
population
• May be difficult if AR associated with Marfan syndrome:
• Scoliosis
• Dural ectasia
Hemodynamic goals: • Pre-conception counseling imperative
Avoid bradycardiaà é LV fillingà Pulmonary edema • Important to diagnose, quantify severity early
Avoid vasoconstrictors, pressorsà é SVR, é RF • Important to understand pathophysiology of lesion
• GA:
Careful fluid management • Stenotic lesions fraught with problems
• Only for obstetric indications
Invasive monitoring rarely indicated
• Hypertrophic myocardium sensitive to volatiles
• RA/GA: Choice not so important as meticulous hemodynamic
monitoring and analgesia

Take home: Evaluation and

optimization of parturient with heart
disease
• Functional class Frequency: Stenotic
• ECG 4 weekly for
Outcome related to
Regurgitant
• Echocardiography Diuretic, Digoxin, Ca
mild, fortnightly
NYHA
Sinus tachycardia
• Drug therapy channel blocker,
for severe
Diabetes, pre eclampsia,
Consider valvotomy?
AFà Anticoagulant
• Other pregnancy-related anticoagulant
Valve area,
placenta previa
co-morbidities Symptoms may
considerations, rate Are easier to manage
Least doses required
anatomy,
resemble normal
control ,
Fetal toxicitys
LA thrombus
pregnancy
PHT
LV function
Other valves

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Be prepared!!

Anaemia and Pregnancy

Dr Anju R Bhalotra
Dir. Prof. MAMC

What is Anaemia? Magnitude of the problem?

• Commonest haematological
§ A quantitative or qualitative reduction of Hb or disorder in pregnancy
RBCs or both in circulation • 41.8% of pregnant women
worldwide are anaemic
§ A Hb <2 SD below the mean for a healthy • > 50 % cases have IDA
matched population • India has the highest prevalence
of anaemia ie. 57-96.2% among S.
§ Resulting in ↓ed O2 carrying capacity of blood Asian countries
to organs & tissues • Nearly ½ of global maternal
deaths d/t anemia occur in S. Anemia directly causes ≈20% of
Asian countries, 80% contributed maternal deaths & indirectly accounts
by India for another ≈ 20% ; These figures
(FOGSI 2016) have remained same in last 5 decades

Definitions of anaemia in pregnancy How do you classify severity

WHO- In adult non-pregnant female, a Hb of <12 gm% of anaemia?
§ In pregnancy Hb <11g% WHO CATEGORIES

CDC/ FOGSI* Category Severity Hb (gm%)

§ Hb < 11gm% (or Hct < 0.33) in 1st & 3rd trimesters
§ Hb <10.5 gm% (Hct < 0.32) in 2nd trimester 1 Mild 10 -10.9

2 Moderate 7 - 9.9
ACOG 2008/ BCSH** 2012
§ Hb <11.0 g% in 1st trimester 3 Severe <7.0
§ Hb < 10.5 g % in the 2 nd & 3rd trimesters
* FOGSI (Fe de ra tio n o f Obste tric a l & Gy n a e c o lo g ic a l Soc ie tie s o f In dia )
* * BCSH (British Co mmitte e f o r Sta n da rds in Ha e ma to lo g y )

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 10/23/18

CAUSES OF
ANAEMIA
ICMR CATEGORIES
↓ RBC Loss from
↑ plasma ↑ RBC
Category Severity Hb (gm%) intravascul
volume production destruction
1 Mild 10-10.9
ar space
Physiological Nutritional Acute blood Acquired - malaria,
- ↑ plasma - IDA
2 Moderate 7-9.9 - FA, B12 def
loss CRF
volume in - APH, PPH
pregnancy - Dimorphic Familial Hbpathies
3 Severe 4-6.9 Chronic blood - impaired synthesis
Non-nutritional - loss (thallasaemia)
- Chronic ds ( TB,
4 (decompensated) V. severe <4 HIV, renal
-hookworm - structural (sickle
infestation, cell )
failure) piles - variant of Hb
- BM disorders
( aplastic anaemia,
BM infiltration)

How do you classify anaemia morphologically? Physiological anaemia in pregnancy ?

§ ↑ PLASMA VOLUME (40-50%)
1. Microcytic hypochromic (MCV< 75 fl, MCH <25pg, MCHC <30%) - To meet ↑ demands of blood flow for uterus and foetus
- Fe deficiency, thalassaemia, sideroblastic - To maintain BP in presence of ↓vascular tone
- Protect mother from hypotension in anticipation of blood loss at childbirth
2. Normocytic normochromic (MCV 75-100 fl, MCH 25-33pg, MCHC § ↑ RBC VOLUME (20-40%)
- ↑ O2 carrying capacity
30-36%)
↑ PV >> ↑RBC DILUTIONAL ANAEMIA
- Acute blood loss, haemolytic anemia, bone marrow failure, chronic
↓viscosityà↓res. to blood flow→ enhanced placenta perfusion & exchange
disease, physiological
Lesser net RBC loss at delivery

3. Macrocytic (MCV >90 fl; MCH 33– 40 pg, MCHC 32-38%)

- Vitamin B12 or folic acid deficiency, thyroid disease, reticulocytosis,
↑alcohol intake, liver dysfunction

What are the haematological criteria Pathological/Acquired Anemias

for physiological anaemia ?
§ RBC 3.2million/mm3 Nutritional - Iron deficiency, folate, Vit B12 deficiency
§ Hb 10 gm% Haemorrhagic - acute (APH) & chronic (hookworms) blood loss
§ PCV 30% Infections - malaria, HIV
Bone marrow suppression: aplastic anemia, drugs
§ P/S - normal RBC with central pallor
Renal Diseases
Haemoglobinopathies - sickle cell dis, thalassaemias

However, if the Hb conc

falls < 10 gm/dL, other
causes of anaemia should
be considered

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 10/23/18

Why is anaemia so common in pregnancy?

• Superimposed on the physiological dilutional anaemia …….

• Nutritional anaemia is commonest cause

§ Physiological iron demand in
• Iron deficiency accounts for most cases of anaemia in pregnant pregnancy is 3 times more than in
women
nonpregnant
1. ↑ IRON DEMANDS IN PREGNANCY § Demand ↑s as pregnancy advances
- ↑ in RBC mass (450mg)
- foetal growth (225mg) = 1000mg § Average daily requirement ↑s from 4-6mg/day in 2 nd &
- placental development (80mg) (150 mg saved by 3rd trimester → 10 mg/day during last 6-8 wks of preg
- blood loss in normal vaginal delivery (250mg) amenorrhea)

Net requirement ≈ 850mg

2. DEFICIENT IRON STORES in women

- menorrhagia, rpted pregnancies at short interval, prolonged
lactation, twins, teenage pregnancy, born to anaemic mothers 4. ACUTE AND CHRONIC
BLOOD LOSS
Chronic blood loss - hookworm
3. DEFICIENT INTAKE OF IRON &
infestation, piles
HAEMATOPOIETIC FACTORS
Acute blood loss - APH, PPH
- poor dietary intake of Fe (before and during preg)
- faulty dietary habits & illiteracy
5. INFECTIONS
- reduced absorption (phytates, tannins, fiber rich)
- Vit B12 deficiency - diet deficient in animal protein – chronic/recurrent infections

Regular iron supplementation is

required in pregnancy

Complications of anaemia in pregnant

Folic acid deficiency parturient
§ Co-factor in nucleic acid synthesis DURING PREGNANCY
§ Dietary deficiency -faulty cooking habits, endemic § Maternal transfusion, Pre-eclampsia, Intercurrent
malaria infections, Heart failure, IUGR, Preterm labour
§ Stores are limited (6 -10 gms) & demand increased
DURING LABOUR
• Increased reqt - multigravida, twins, hyperemesis
gravidarum, alcohol consumption, smoking § Uterine inertia, PPH, Cardiac failure, Shock
• Effect on mother - high incidence of abortions
PUERPERIUM
• Effect on fetus - neural tube defect, premature § Puerperal sepsis, Sub involution, Failing lactation,
birth, cleft palate Postpartum depression

21

Complications in the Baby
Moderate to severe anemia may cause
• Low birth weight, prematurity, IUD, stillbirths
• 5 min APGAR < 7, ↑ NICU admission, congenital malformations
• Low fetal store of Fe/ Vit B12/folate → ↑risk of
anemia/nutritional disorders in infancy
• Poorer cognitive development & IDA among children
Hb < 8gm% → 2-3 fold ↑ neonatal deaths/perinatal mortality
Hb < 5gm% → 8 -10 fold↑ in neonatal deaths/perinatal mortality
What are the
pathophysiological changes in
anANAEMIA
IN anaemic
THERE IS patient
A ↓ TISSUE O2?
DELIVERY (DO2)
DO2 is determined by the O2 content of the blood (CaO2) and the
cardiac output (CO)
O2 content of blood = (O2 in RBC )+ ( O2 dissolved in plasma)
CaO2= (Hb ×1.34 × SaO2) + (0.003 × PaO2 mm Hg)
= 19.7 + 0.3 = 20ml O2/dl blood
• Thus a fall in Hb →fractional reduction in the CaO2
What are the compensatory mechanisms in an
anaemic pt?
1. INCREASE IN CO:
Anaemia→ ↓blood viscosity → ↓ SVR →↑ CO
Sympathetic stimulation → ↑ venous return→↑ CO
2. INCREASED O2 EXTRACTION in tissues with a low OER such as
the kidney, skeletal muscle, skin
3. REDISTRIBUTION OF CO: CO is redistributed to organs with
high O2 demands (brain and heart) & ↓in skin, mm, muscles (pallor)
4. RELEASE OF RENAL ERYTHROPOIETIN & stimulation of
erythroid precursors in BM
10/23/18
Oral iron prophylaxis in pregnancy
WHO Recommendations (2012)
In countries where prevalence > 40%
§ 60 mg Fe + 400 mcg folic acid till term in pregnancy followed by
same dose for 3 mths during lactation
Govt of India Recommendations (MoHFW 2013)
§ 100 mg Fe + 500 mcg FA OD for 100 days for 6 months during
pregnancy followed by same dose for 100 days in 6 months
postpartum
All pregnant women at 14-16th week during the 2 nd trimester
should be given one tablet of Albendazole 400mg – single dose
Important equations
• Tissue oxygen delivery = CaO2 x CO
DO2 = 20ml/dl x 5 L/min = 1000 ml/min
• O2 consumption= VO2 = (CaO2 - CvO2) x CO = 250ml/min
• O2 extraction ratio (OER) = (CaO2 - CvO2) x CO = 25%
= VO2/DO2 = 250/1000 = 25%
In an anaemic patient, there is a ↓in DO2 and an ↑ in OER
In order to maintain DO2, certain compensatory mechanisms are
activated in anaemia
5. ALTERED AFFINITY OF Hb FOR
O2:
↑ 2,3-DPG & H+ → rightward shift in
the ODC → ↑ release of O2 to tissues
6. RESPIRATORY ADJUSTMENTS;
↓ physiologic shunt in lung & tachypnea
→ ↑paO2
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Role of the Anaesthesiologist

Which factors affect the
degree of compensation ?
• Magnitude and rate of blood loss • Labour analgesia
• Chronic vs acute anaemia
• Preop status - cardio-pulmonary status, left • Caesarean delivery
ventricular dysfunction, comorbidities etc
- elective / emergency
Thus, while tissue oxygenation may not be impaired in - chronic anemia/ acute anemia (APH)
chronic anaemia d/t compensation, it may be compromised
in patients with ;
- Limited capacity to mount a compensatory response - • Management of complications like heart failure etc
significant cardiac/respiratory ds in ICU
- ↑ O2 demand - infection, pain, fever, exercise
- Further ↓in O2 supply - blood loss, pneumonia

Preoperative assessment- HISTORY

What are the anaesthetic considerations?
§ Cause of the anaemia & its functional significance
§ Severity of anaemia
§ Rate & volume of blood loss
§ Effects on tissue oxygenation
§ Adequacy of compensatory mechanisms
§ Transfusion trigger?
§ s/o poor tissue perfusion
Mild /moderate anemia - tiredness, easy fatigability, lassitude,
weakness, , headache, loss of appetite, nausea, constipation,
indigestion
Severe anemia - breathlessness, confusion, dizziness, irritability,
palpitations, postural hypotension, angina, symptoms of heart failure
§ History related to secondary cause - Bleeding (DUB, melena,
hematuria etc.), renal failure, hepatic ds, endocrine dis, pica/
pagophagia
§ Past h/o anemia, need for blood transfusion, medications
§ Occupation / Diet
§ Family h/o bleeding disorders, splenectomy, anemia, early onset gall
stones etc

EXAMINATION INVESTIGATIONS
§ GPE –pulse rate, RR, JVP, temp, BP • Hb, TLC, DLC, peripheral smear- MCV, MCH, MCHC, Ret. count,
§ Pallor, glossitis, angular cheilitis ESR, Blood grouping
• LFT, serum protein, KFT
§ nail ridging, koilonykia, alopecia
• ECG (ischemia)
§ hepato-splenomeg aly, lymphadenopathy, edema
• Stool, urine analysis
§ Bruises, ecchymosis, petechiae – platelet disorders • IDA - serum ferritin assay, serum Fe, TIBC, % saturation, free
§ Signs of high CO - tachycardia, wide pulse pressure, erythrocyte protoporphrin, soluble transferrin receptor, folate &
functional murmur (ESM), cardiomegaly, heart B12 levels
failure (crepts) • Nestroft test, Hemolysis workup, sickledex test, Hb
electrophoresis, BM
§ Obs examn – gestational growth, fetal wellbeing

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 10/23/18

Diagnosis of iron deficiency anemia

Treatment
§ Plasma iron (↓) < 60 µg/dl • Adequate antenatal care, treatment of infection
§ Transferrin saturation (↓) < 15%
• Protein & Fe rich diet & green leafy vegetables
§ TIBC (↑) > 400 µg/dl
§ Serum ferritin (↓) • Iron, Vit C, FA supplementation
< 12 µg/l (established IDA) • Iron therapy - oral/parenteral
< 30 µg/l (↓iron reserves – tt indicated)
§ MCV (↓) < 80 fl
§ MCH (↓) < 27pg Microcytic
hypochromic
§ MCHC (↓) < 33g% anaemia

What are the indications for

When is parenteral iron therapy indicated?
oral ironIDA-
Mild -moderate therapy
in 1 & early 2 trimester
st nd
Moderate to severe anaemia; from 2 nd tri and in pp when ;
§ Intolerance, noncompliance. malabsorption, failure to respond to
WHO Recommendations oral iron therapy
§ IFA tablets (120 mg Fe + 400µg FA) 1 OD Prophylactic doses § Rapid replenishment of iron stores required
once Hb is restored § Presence of concurrent disease like CRF, infections etc
to normal
MoHFW (2013) ADVANTAGE - Certainty of administration
§ IFA tablets (100 mg Fe + 500µg FA ) 1 BD
CALCULATION OF DOSE OF PARENTERAL IRON
Problems - used <30 wks • Required dose (mg) = [2.4 x (target Hb –actual Hb) x
- GIT upset ( nausea, diarrhea, constipation), unpredictable prepregnacy weight] + 1000 mg for replenishing stores
absorption, non compliance § 200- 250 mg raises Hb by 1g%

Parenteral preparations
What are the indications for
• Iron dextran complex (Imferon) (im , iv)
intramuscular iron ?
MODERATE ANAEMIA, 2nd trimester
• Iron sorbitol citrate (Jactofer) (im) • im iron (iron dextran)
• Iron sucrose complex (Venofer) each ml has 20 mg of • Precede by test dose 25 mg & observe for at least 1 hr
elemental iron. (iv) (6hrs).
• Jectofer plus contains folic acid and vitamin Bl2 along-with • S/E – mild joint pain, discoloration at inj site, severe rns
elemental iron (im , iv) (allergy, itching, fever, lymphadenopathy, arthralgia,
• Iron gluconate is available as sodium ferric gluconate headache, malaise, anaphylaxis)
(ferrlecit) (iv)

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 10/23/18

Response to iron therapy

What are the indications for
intravenous
Moderate & severe anaemia iniron ?
2 & 3 trimester
nd rd
• Subjective – feeling better/ ↑appetite
In small fractionated doses (dextran, iron sucrose) or TDI (total
dose infusion) (dextran) • Improvement in symptoms
Iron sucrose (MOHFW) (in divided doses) • ↑ in Hb – 0.1g % per day irrespective of route of
- Safe, No adverse effects, test dose admn
- Rapidly taken up by BM (erythropoiesis) and RES (storage) • Rise is seen after 2-3 weeks of therapy
• 100 mg. in 100 ml of NS over 20 -30 minutes once a day x 4
days over a period of 2 weeks (with 2-4 days of interval • Early response is reticulocytosis (5-10%) – seen in 5-
between each infusion) 10 days & is accompanied by a steady rise in red cell
• For 5 mins @ 20-30 drops/min : then 80-90 drops/ min count (by day 15)
• Failure of response (ie Hb rise <1.0 or 2.0 g% within 14
or 28 days resp)

Role of Blood Transfusion Indications for BT in pregnancy (FOGSI 2016)

• Rapid improvement, Hb increases by 1gm/unit
ANTEPARTUM
• Supplies natural constituents of blood& ↑es O2 carrying capacity
1. Preg <34 wks – Hb < 5g% OR Hb 5-7 g% in presence of impending
heart failure
• Transfused RBC contains haem iron (200– 250 mg per unit), + small amount of
labile iron immediately available for erythropoiesis 2. Preg >34 wks - Hb <7 g% with/without decompensation
Consider 3. Anaemia not due to haematinic deficiency (haemoglobinopathy / BM
• Severity of anemia/refractory anemia failure syndrome
• Duration of pregnancy 4. Acute haemorrhage - Hb <6 g% or a haemodynamically unstable pt
• Assoc. complicating factors/infections with ongoing haemorrhage
• Emergency surgery /acute bloodloss INTRAPARTUM
• Pt’s signs & symptoms - Hb < 7 g% (in labour) or patient with s/o inadequate oxygenation

POSTPARTUM
For urgent ↑ in O2 carrying capacity of blood, a - Hb <7 g% or patient with s/o inadequate oxygenation
minimum acceptable Hb level does not exist - Anaemia with signs of shock/ acute hge with haemodynamic
instability

Protocol for severe

Blood Transfusion
Guidelines anemia in
Preg <30wks
pregnancyPreg >36wks
Preg 30-36wks
• Prefer packed cells /fresh blood
• Correctly typed and cross matched
• Transfuse slowly under diuretic cover in patient with IDA FA def IDA FA def Blood transfusion
severe anaemia and impending failure
• Watch for signs of transfusion reaction Parenteral Oral FA
• Do not repeat transfusion within 24hrs
Oral iron Oral FA
I/M iv
Problems ;
• Trigger premature labor Intolerance/ Non-compliance
• CHF
• Infectious and noninfectious complications of BT
I/M iron I/V iron

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 10/23/18

Principles of anaesthesia for anaemic pts III. MAINTAIN CV STABILITY

Minimize any changes interfering with O2 delivery to
tissues
I. ENSURE ADEQUATE OXYGENATION/ AVOID
HYPOXIA
- Optimize paO2; preoxygenation during induction ; high FiO2;
O2 supplementation peri- and postoperatively
- Maintenance of airway at all times
II. PREVENT ANY ↑ IN O2 CONSUMPTION
- Prevent & treat any ↑ in O2 demand (fever, shivering, pain,
acute massive blood losses)
- Prevent aortocaval compression
- Avoid drug induced depression of cardiac output
Slow titrated IV induction
Low conc. of volatile agents (High concentration of volatile
agents - depress myocardium & ventilation)
- Careful positioning to minimize position associated volume shifts
- Adequate volume replacement
IV. PREVENT LEFTWARD SHIFT OF ODC
• Avoid hyperventilation; maintain normocapnia
• Prevent hypothermia ; maintain normothermia

Choice of anaesthesia for LSCS?

Labor analgesia

Is beneficial Will depend on

§ Decreases blood loss • Severity & type of anemia
§ Improves uterine blood flow
• Chronic or acute
§ Prevents resp alkalosis & leftward shift of ODC
• Extent of physiological compensation
§ Inhibits sympathetic stimulation → decreased
maternal stress; less chance of CHF • Concomitant medical conditions
§ Allows for a more controlled delivery • Anticipated & ongoing blood loss
C/I -• Uncorrected maternal hypovolemia (e.g.,
hemorrhage)

Regional Anaesthesia RELATIVE C/I to RA

• Hb < 8gm% or 8gm% with cardiac decompensation
Inherent advantages of RA in LSCS • Ongoing haemorrhage
• Mother is aware of child birth ( psychological ) • Major blood loss anticipated
• No risk of aspiration / “failed intubation“ • Parturients with overt Vitamin B12 deficiencies & neurological
• Less blood loss symptoms PRINCIPLES
• Analgesia can be extended à postop period TECHNIQUE - SAB/ EA/ CSE - ensure adequate oxygenation
- O2 by facemask - prevent any ↑ O2
consumption
Disadvantage - low dose LA + opioid - maintain CV stability
PRECAUTIONS - prevent leftward shift of
§ RA induced sympathectomy - ↓BP ODC
Careful pre-load/ co-load:
- Haemodilution →CHF /pulm edema on return of vascular tone
Monitor & replace blood losses
Early use of vasoconstrictors to sustain BP

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 10/23/18

General Anaesthesia
Advantages
INDICATIONS
When RA C/I -Hb < 8gm% or 8gm% with cardiac decompensation /
• Rapid induction ongoing haemorrhage / major blood loss anticipated / parturients with
• Less hypotension & better CVS stability overt Vitamin B12 def
• Control of airway and ventilation PRINCIPLES
- ensure adequate oxygenation
• No anxiety of being awake - prevent any ↑ O2
• Extend to postop. ventilatory support if required GA TECHNIQUE consumption
- maintain CV stability
• Aspiration prophylaxis - prevent leftward shift of
Disadvantages • LUD- Supine with wedge under rt. hip ODC
• Airway related morbidity - failed intubation/aspiration • Preoxygenation →RSII with thiopentone /etomidate
• Awareness (low conc of volatile agents , high FiO2) • N2O used cautiously in pts with folate & Vit B12 def
• Fluids to be titrated carefully - avoid overload and decompensation
• Neonatal effects
• High incidence of uterine atony, PPH

Compensatory mechanisms
in acute anaemia
• ↑Sympathetic stimulation - vasoconstriction,
tachycardia, → ↑ed venous return → maintain CO
Pregnant patient with acute • ↑ed velocity of blood flow
anaemia / acute blood loss • Constriction of capillary beds in skin, splanchnic
• Redistribution of blood flow to vital organs
• Renal water & electrolyte conservation
(vasopressin, renin angiotensin +)
• Anaerobic metabolism→ acidemia→
hyperventilation

Intraoperative management
Preoperative preparation
• Preoperative blood transfusion - actual blood loss, physical status,
compensatory abilities • Preoxgenation→ GA with RSI
• Remember - if anemia develops throughrapid enough bleeding, Hb and Hct may • Induction agent - Etomidate/ketamine, min inhalational agent
be normal (in acute hge, RBCs and plasma are lost in proportion) • Optimize ventilation -high FiO2 & maintain normocarbia
• O2 inhalation • Optimize volume status & cardiopulmonary hemodynamics
• Secure large bore iv access (es) • Consider use of inotropes to maintain preload
• Blood for CBC, BG & CM, other investigations • If massive blood loss – activate massive transfusion protocol
• Maintain Left uterine displacement
• Careful fluid resuscitation
• Acid aspiration prophylaxis
• Difficult airway cart PRINCIPLES
- ensure adequate oxygenation
• Choice of anaesthesia -GA - prevent any ↑ O2consumption
- maintain CV stability
- prevent leftward shift of ODC

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 10/23/18

Intraoperative Monitoring Postoperative Care

To assess adequacy of perfusion & oxygenation of vital organs.
• Routine monitors - ECG, NIBP, SpO2, EtCO2, Temp • Recovery in HDU if normovolemic/ normothermic &
• Urine output, CVP, IBP, ABG, mixed venous PvO2, etc depending haemodynamically stable
on clinical situation
• Blood loss = weight of swabs (1gm=1ml) + (suction volume -
• If excessive intraoperative haemorrhage with
amniotic fluid) + visual assessment (drapes, floor) + status of
hemodynamic instability/ hypothermia – postoperative
vagina, uterus ventilation
• Serial Hb & Hct values to monitor ongoing blood losses • Oxygen supplementation
• Monitor for complications like CHF • Prevent any ↑ in O2 consumption – treat pain , shivering,
• Coagulation testing if massive blood loss fever etc
• Continue monitoring
Blood replacement and conservation • Transfuse blood and blood components as indicated
• Use of techniques to minimize blood loss – positioning/ surgical
hemostasis
• Replace I/o blood loss with packed cells/blood components

Summary

•
•
IDA is very common in pregnancy in India
Leads to increased morbidity in both mother & baby
THANK
•
•
Iron prophylaxis is required during pregnancy
IDA should be detected early and treated with iron
YOU!
therapy, oral or parenteral
• Blood transfusion is indicated if IDA is severe and the
patient is close to term or is in haemorrhagic shock
• Choice of anaesthesia depends on the Hb, degree of
compensation & ongoing haemorrhage

Case
• 22 years primigravida, booked case,31 weeks
gestation
• H/o headache and pain in upper abdomen – 2 days
• Uneventful till last ANC visit 2 weeks back
• Not on any antihypertensives
Preeclampsia and Eclampsia
Medha Mohta • HR- 88/min
• BP - 170/110 mmHg
Director Professor • Chest – clear
University College of Medical Sciences & • Urine protein +
GTB Hospital, Delhi

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 10/23/18

Differential Diagnosis Preeclampsia

Pregnancy specific multisystem disease
• Preeclampsia
New onset of HT and proteinuria after 20 weeks
• Gestational HT gestation; resolves by 12 weeks postpartum

• Chronic HT Classified as
• Preeclampsia without severe features
• Chronic HT with superimposed preeclampsia • Severe preeclampsia

(ACOG Task Force on hypertension in pregnancy, 2013)

Preeclampsia without severe Severe Preeclampsia

features • Sustained BP > 160 mmHg systolic or > 110 mmHg diastolic
(measured twice, at least 4 hrs apart, with patient on bed rest)
• BP > 140/90 mmHg on two or more occasions at • Thrombocytopenia (<100,000/mm 3 )
least 4 hrs apart (measured at rest, with an • Elevated serum creatinine (>1.1 mg/dl or >2 times baseline)
appropriately sized BP cuff) • Pulmonary oedema
• New onset cerebral or visual disturbances
• Proteinuria > 300 mg/ 24 hrs or > 1+ dipstick (30 • Impaired liver function i.e. ↑ liver enzymes (>2 times normal)
and severe persistent epigastric or right upper quadrant pain
mg/dl)
(Fetal growth restriction and severe proteinuria (> 5 g in 24
• Urine protein:creatinine ratio (UPCR) > 0.3 hours) are no longer considered features of severe
(with both measured in mg/dl) preeclampsia)
(ACOG Task Force on hypertension in pregnancy, 2013)

Gestational Hypertension Chronic Hypertension

• Systolic BP > 140 mmHg or diastolic BP > 90 mmHg • Systolic BP > 140 mmHg or diastolic BP > 90 mmHg
for first time after 20 weeks gestation before pregnancy or diagnosed before 20 weeks
gestation not attributable to gestational
• No proteinuria or other systemic findings trophoblastic disease

• HT persistent after 12 weeks postpartum

• HT resolves by 12 weeks postpartum

• Final diagnosis made only postpartum

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Chronic HT with
superimposed preeclampsia
• New onset proteinuria > 300 mg/24 hours after
20 weeks gestation in hypertensive women, or What are the clinical
manifestations in a patient with
• Sudden increase in proteinuria and/or HT or other preeclampsia?
manifestations of preeclampsia after 20 weeks
gestation in women having chronic HT and
proteinuria before 20 weeks

Clinical Manifestations Clinical Manifestations...

CNS
CVS
• Headache, visual changes, hyperexcitability, • Increased vascular tone and sensitivity to
hyperreflexia, coma, convulsions (eclampsia)
vasoconstrictors → HT, vasospasm, end-organ
• Visual disturbances – photophobia, diplopia, blurred ischaemia → ↑ BP and SVR
vision • Intravascular volume depletion
Due to ischaemia caused by vasospasm of posterior
• Majority – hyperdynamic LV function
cerebral arteries or cerebral oedema in occipital regions
• Smaller, high risk group – ↓LV function, markedly
• Headache, hyperreflexia, clonus – warning signs of
↓ SVR, ↓ intravascular volume
increased cerebral irritation

Clinical Manifestations... Clinical Manifestations...

Respiratory system
Renal system
• Pharyngolaryngeal oedema
• ↓GFR, ↑proteinuria, ↑ uric acid
• Increased risk of pulmonary oedema due to lower • ↑ urine protein:creatinine ratio
colloid osmotic pressure, increased hydrostatic
pressure and increased vascular permeability • Oliguria

Hepatic system
Haematologic system
• Periportal hmg, fibrin deposition in hepatic sinusoids
• Thrombocytopenia in severe disease (15-20%) • ↑ serum transaminases
• Hypercoagulability in disease without severe features, • Hepatic oedema/right upper quadrant abdominal
hypocoagulability in severe disease pain; rupture of Glisson’s capsule with hepatic hmg
• DIC

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Clinical Manifestations...
Uteroplacental system
• Persistence of a high-resistance circuit with ↓ blood
flow
• IUGR; oligohydramnios How do you classify these
Endocrine system
patients based on onset of
• Imbalance of prostacyclin relative to thromboxane symptoms?
• Upregulation of systemic renin angiotensin aldosterone
system

Eye
• Retinal arteriolar constriction, retinal detachment,
blindness

Early onset (Type I) Late onset (Type II)

Onset of clinical symptoms < 34 weeks gestation > 34 weeks gestation
Relative frequency 20 80
(% of cases)
Risk for adverse outcome High Negligible
Association with Yes No
intrauterine fetal growth
retardation
Clear familial component
Placental morphology
Yes
Abnormal
No
Normal
Management of Preeclampsia
Etiology Placental Maternal
Risk factors( relative risk) Family history Diabetes, multiple pregnancy,
increased BP at registration,
Increased BMI, Maternal age
> 35 yrs, Cardiovascular
disorders
Haemodynamics at 24 Higher total vascular Lower total vascular
weeks resistance, lower cardiac resistance, higher cardiac
output output

Management
Severe preeclampsia
• Delivery of fetus and placenta is the only cure
• Vaginal delivery preferable • 34 weeks or later - Induction of labour
• CS - maternal/fetal condition mandates • Less than 34 weeks – Expectant management,
immediate delivery OR other indications for CS corticosteroids
• Indications of expedited delivery – eclampsia,
Preeclampsia without severe features pulmonary oedema, DIC, placental abruption,
• Same as any other healthy pregnant woman abnormal fetal surveillance, IUD, refractory
• Careful monitoring needed to detect progression severe HT (on antihypertensives), persistent
to severe preeclampsia cerebral symptoms (on MgSO4)
• Induction of labour beyond 37 weeks

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Management of Severe Preeclampsia... Treatment of hypertension

• SBP>160 mmHg or DBP>110mmHg must be treated -
prevents maternal complications e.g. myocardial ischaemia,
Supportive hypertensive encephalopathy, cerebrovascular hmg, CHF
• Hospital admission
• Avoid precipitous fall in BP to maintain uteroplacental
• Treatment of hypertension perfusion and O2 delivery to fetus
• Seizure prophylaxis
• Optimization of intravascular status • Lower MAP not > 15-25%, with target SBP 120-160 mmHg
and DBP 80-105 mmHg
• Administration of corticosteroids
• Monitoring
• Commonly used drugs – Labetalol, hydralazine, nifedipine
• Second line agents – Nicardipine, SNP, esmolol

Drug Mechanism Dose & route Onset Side-effects/caution

of action of
action
Hydralazine Direct 5 mg IV every 15- 10-20 Hypotension, tachycardia,
vasodilator 20 min, max 20 min palpitations, headache,
mg neonatal thrombocytopenia
Labetalol α1 & β 20 mg IV every 2-5 min Less than hydralazine, avoid
blocker (1:7) 10 min, max 220 in severe asthma, CHF Which is the drug of choice for
mg
Nifedipine Calcium 10 mg oral, 10-20 Interactions with MgSO4 - seizure prophylaxis, what is its
channel
blocker
repeated after 20
min, if needed,
min severe hypotension,
neuromuscular blockade. MOA & how it is administered?
max 50 mg S/L not recommended.
Nicardipine Calcium IV infusion 5 mg/h, 10-15 Headache, hypotension,
channel ↑by 2.5 mg/h min tachycardia,
blocker every 5 min to max nausea/vomiting
15 mg/h
Sodium nitro- Smooth 0.25-5 μg/kg/min 0.5-1 Hypotension, bradycardia.
prusside muscle IV infusion min Risk of fetal cyanide
vasodilator – toxicity. Used for limited
releases NO period only,continuous
intra-art monitoring

Seizure prophylaxis Magnesium sulphate

• Magnesium sulphate – DOC for prevention of • Cerebral vasodilator

recurrent seizures in eclampsia • Mechanism of anticonvulsant action – not well
understood
• Earlier – Eclamptic seizures thought to result from
• Effective (Magpie trial) and superior to diazepam cerebral vasospasm
and phenytoin (Collaborative eclampsia trial)
• Later evidence – Abrupt sustained BP elevation
overwhelms myogenic vasoconstriction – forced
• Use extended to seizure prophylaxis in severe dilation of cerebral vessels, hyperperfusion,
preeclampsia cerebral oedema

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Magnesium sulphate dosage

Magnesium sulphate MOA
schedule
• Mesentric vessels more sensitive to Mg induced Continuous IV infusion
vasodil than cerebral vessels → part of effect • Loading dose – 4-6 g IV in 100 ml fluid over 15-20
mediated through decreasing peripheral vascular min
resistance
• Maintenance infusion 1-2 g/hr
• Monitoring for Mg toxicity
• May protect BBB
- Assess DTR, urine output, RR and O2 saturation
• May decrease cerebral oedema - S. Mg levels at 4-6 hrs or if S. creatinine > 1.0 mg/dl
• Discontinued 24 hrs after delivery
• Action at NMDA receptors to raise seizure threshold

Magnesium sulphate dosage Magnesium toxicity

schedule... S. Mg conc.
Intermittent IM injections • Normal range – 1.7-2.4 mg/dl (1.4-2.2 meq/l or 0.7-1.1
• 4 g IV @ not to exceed 1g/min mmol/l)
• Therapeutic range – 4.8-8.4 mg/dl (4-7 meq/l or 2.0-3.5
• 5 g deep IM in each buttock mmol/l)
• 5 g deep IM every 4 hrs in alternate buttock after • Loss of DTR – 12 mg/dl
ensuring that • Respiratory arrest – 15-20 mg/dl
• Cardiac arrest > 25 mg/dl
- Patellar reflex is present (mg/dl X 0.411 = mmol/l)
- Respiration is not depressed Treatment
- Urine output in previous 4 hrs > 100 ml • Discontinuation of infusion
• IV Ca gluconate 1 g over 10 min
• Discontinued 24 hrs after delivery • O2 , mechanical ventilation, if required

Optimization of intravascular
Monitoring
status
• Careful administration of fluids (high incidence of Regular haemodynamic monitoring required
pulmonary oedema) • Rapid changes in BP due to disease progression,
antihypertensive drugs and IV fluids
• Limit maintenance fluids to 80 ml/hr unless there are • Intravascular volume depletion
other ongoing fluid losses e.g. haemorrhage
(NICE clinical guideline 107, August 2010) Indications for intra-arterial BP
• Poorly controlled BP, need for continuous BP
• If oxytocin is required → used in high concentration & monitoring
volume of fluid included in total input • Use of SNP/NTG
• Need for frequent ABG samples
• Need to monitor cardiac output using minimally-
invasive technique

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Monitoring... Monitoring – Recent advances

Transthoracic echocardiography (TTE)
• Quantifies cardiac function and volume status - can guide
Invasive central monitoring fluid management in patients at risk for pulmonary
oedema and with oliguria
• Indications similar to those in other multisystem
disorders e.g. severe sepsis, MODS, pulmonary • Recommended as a diagnostic and monitoring tool for
oedema, cardiomyopathy acute haemodynamic complications of preeclampsia -
acute pulm. oedema, significant HT, chest pain
• Presence of severe preeclampsia per se not an (Curr Opin Anesthesiol 2015, 28:254–260)
indication for CVP or PA pressure monitoring
• Preferred method of cardiac monitoring in pregnancy
(European Society of Cardiology guidelines, 2011)

Monitoring – Recent
advances…
Lung ultrasonography
• Promising method of predicting pulmonary
oedema in women with severe preeclampsia
What is the role of
anaesthesiologist in
Passive leg-raising test
• May be useful to predict fluid responsiveness in management of preeclamptic
oliguric patients with severe preeclampsia.
(Curr Opin Anesthesiol 2015, 28:247–253) patient ?
Pulse waveform analysis
• Cardiac output measurement
• Minimally invasive

Role of Anaesthesiologist
• To provide labour analgesia
You have been called to provide
• To provide anaesthesia for caesarean section labour analgesia to this patient.
What will be your plan?
• Resuscitation

• Intensive care management

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Labour analgesia
• In absence of C/I, lumbar neuraxial analgesia is
appropriate for women with preeclampsia during • Place early epidural catheter in parturients with
labour preeclampsia, which may even precede onset of
• Continuous lumbar epidural analgesia or CSE labour or the patient’s request for analgesia.

Early administration of epidural analgesia (ASA Task Force on Obstetric Anesthesia. Practice
• Avoids GA in event of emergency CS guidelines for obstetric anesthesia.
• Beneficial effect on uteroplacental perfusion Anesthesiology 2016;124:270-300)
• Good analgesia attenuates hypertensive response to
pain
• Reduces circulating catecholamines, stress-related
hormones

Considerations during
neuraxial analgesia
What are specific considerations • Assessment of coagulation status

during neuraxial analgesia in

• IV hydration prior to LA administration
preeclampsia?
• Treatment of hypotension

• Use of epinephrine-containing LA solutions

Coagulation status
• Platelet count 50,000-80,000/mm3 – weigh risk/benefit
• Platelet count > 100,000/mm3 – further coagulation
testing not required - Skilled anaesthesiologist
- Spinal technique preferred (smaller needle)
• Platelet count < 100,000/mm3 – PT, PTT, fibrinogen - Careful neurologic monitoring
levels - Immediate neurosurgical consultation, if required
• Platelet count > 80,000/mm3 in absence of other
coagulation abnormalities is not expected to increase • Trends in platelet count important
likelihood of neuraxial anaesthetic complications in Serial counts stable and within normal range during
setting of preeclampsia – adequate for catheter antenatal period – measure every 24-48 hours
insertion as well as removal Decision to induce labour – measure every 6 hrs
Falling trend – within 1-3 hrs before neuraxial procedure
• Platelet count < 50,000/mm3 – neuraxial procedure C/I

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Intravenous hydration
• ↑ risk of pulmonary oedema → careful attention to fluid
infusion rate
• IV fluid loading not used in patients with severe
preeclampsia before establishing low dose analgesia
Can epinephrine be used in
Treatment of hypotension patients with preeclampsia?
• Preeclampsia without severe features – routine doses of
vasopressors
• Severe preeclampsia – small doses of vasopressors
initially (e.g. Ephedrine 2.5 mg or phenylephrine 25-50
μg) to assess maternal BP response before giving larger
doses

The patient has been posted for

• No typical tachycardic response in beta blocked
patients
caesarean section at 34 weeks
• Addition to LA →only modest LA sparing effect gestation.
Use of Epinephrine
• Consequences of intravascular administration of What will be the anaesthetic
epinephrine containing test dose in hypertensive
patient considerations?
How will you anaesthetize this
Safer not to use epinephrine in preeclamptic patient?
patients

Anaesthetic considerations Anaesthetic management

in severe preeclampsia
• Hypertension, antihypertensive drugs • Pre-anaesthetic evaluation
• Risk of seizures
• Difficult airway
• Reduced plasma volume • Choice of anaesthetic technique
• Risk of pulmonary oedema
• Coagulopathy
• Renal dysfunction
• Anaesthetic management
• Hypoproteinemia
• Altered liver function • Postoperative management
• Increased sensitivity to NMBA (MgSO4 )

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Pre-anaesthetic evaluation
History T/t History
• Gravida • Medications
• Headache (antihypertensives?)
• Visual blurring, diplopia, Family History
photophobia • 1 st deg relative with
How will you evaluate this patient? • Epigastric /rt upper quadrant preeclamptic pregnancy
pain GPE
• Urine output • Level of consciousness
• Abnormal bleeding • BMI
• Seizures • Icterus
• Pre-existing HT/DM • Oedema
Obstetric History • BP
• Preeclampsia in previous • Airway exam
pregnancy Systemic examination
• DTR important

Choice of anaesthetic
Investigations technique
• Hb, Hct (haemoconcentration, haemolysis) with platelet • Neuraxial anaesthesia is the preferred method
count (thrombocytopenia), P/S (if suspecting HELLP)
• BG & CM (risk of PPH)
• Urine – albumin (proteinuria), sugar (DM) • Avoids disadvantages of GA
• KFT - Urea, creatinine, uric acid (severe preeclampsia) - Hypertensive response to intubation →intracranial
• LFT – bilirubin, transaminases, LDH (severe hmg
preeclampsia, HELLP), proteins (hypoproteinemia) - Airway oedema → possibility of difficult intubation
• PT, PTT, fibrinogen (if coagulopathy suspected)
• S. Magnesium conc. (if on MgSO4 and evidence of
toxicity) • Single shot spinal / epidural / CSE
• Fundus examination (severe cases)

Traditional view Recent Evidence

• Epidural anaesthesia considered the optimal • Patients with severe preeclampsia experience less
technique in severe preeclampsia frequent, less severe hypotension than healthy
• Spinal anaesthesia relatively C/I (rapid onset of parturients
sympathetic block – possibility of marked • Spinal may cause greater degree of hypotension than
hypotension) epidural; however hypotension is easily treated and
short lived; no difference in outcome
Advantages of epidural • Spinal anaesthesia is reasonable anaesthetic option
• Ability to titrate LA and fluids for CS in severe preeclampsia when there is no
• Stable maternal BP without precipitous fall indwelling epidural catheter or C/I to spinal
• Less risk of fluid overload & pulmonary oedema anaesthesia
• Optimization of uteroplacental perfusion • Hypotension – titrated vasopressor doses (greater
vascular sensitivity to vasoconstrictors)
(Anaesthesia and Analgesia 2013; 117: 686-693)

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Administration of GA to
Indications of GA patient with severe
• Coagulopathy/severe thrombocytopenia
preeclampsia
• Preparation to deal with difficult airway (smaller tracheal
tubes, difficult airway equipment)
• Severe ongoing maternal haemorrhage
• Avoid repeated intubation attempts – LMA reasonably
safe alternative (? Risk of aspiration)
• Pulmonary oedema
• Attenuation of hypertensive response to laryngoscopy and
intubation/extubation (risk of cb hmg, pulm oedema)
• Sustained fetal bradycardia
Goal – to reduce BP to approx. 140/90 mmHg before
• Eclampsia with evidence of ↑ ICP induction, to maintain SBP 140-160 mmHg and DBP 90-
100 mmHg during laryngoscopy and intubation

Drugs to attenuate hypertensive

response to
laryngoscopy/intubation
Drug FM ratio Neonatal Maternal Doses
effect side-effects studied What are the interactions of
Esmolol 0.2 None Transient
bradycardia
1-2 mg/kg
Magnesium Sulphate with
Labetalol 0.38 Transient Hypotension, 20 mg upto 1 neuromuscular blockers?
hypotension, bronchospas mg/kg
bradycardia m

Nitroglycerin 0.18 None Transient 1.5-2.5 µg/kg

e tachycardia

Remifentanil 0.88 Respiratory 0.5-1 µg/kg

depression

Use of oxytocic agents in

Non-depolarizing muscle relaxants
• Increased potency & duration → give small severe preeclampsia
doses, monitor with peripheral nerve stimulator • Oxytocin – drug of choice, carefully titrated to
• ↓Ach release, ↓end-plate sensitivity to Ach, haemodynamic responses
↓muscle membrane excitability • Ergometrine – not used (hypertensive crisis)
• Prostaglandins (15 methyl PGF2α/ misoprostol)–
Succinylcholine second-line drugs
• Onset and duration not prolonged Associated with elevations in BP, but to a lesser
degree than ergometrine

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Monitoring
• HR • EtCO2
• ECG • Neuromuscular
• NIBP monitoring How will you manage this patient
• SpO2 in post-operative period?
• Urine output
• Coagulation profile
• Fetal monitoring
• Mg levels

Postoperative care
• NSAIDs considered to contribute to HT
• Oxygen
• Vitals monitoring including NIBP, RR • Can be used in all but the most persistently
hypertensive women
• Analgesics
( Int J Obstet Anesth 2015 Aug;24(3):264-71)
• Prophylaxis for VTE (intermittent pneumatic
compression devices)
• Antihypertensives to be continued • Postpartum hypertension persisting longer than
one day → NSAIDs replaced by alternative
• MgSO4 for 24 hours analgesics
• Careful administration of IV fluids (ACOG Task Force on hypertension in pregnancy, 2013)
• Urine output

HELLP Syndrome
• Variant of severe preeclampsia
• Haemolysis(H), elevated liver enzymes (EL),
low platelets (LP)
What is HELLP
• Right upper quadrant/ epigastric pain
syndrome? • Nausea, vomiting
• Headache
• Hypertension
• Proteinuria

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HELLP - Diagnostic Criteria HELLP - Management

• Haemolysis
• Similar to severe preeclampsia (including
antihypertensives, seizure prophylaxis)
Abnormal P/S – fragmented RBC, schistocytes
Lactic dehydrogenase > 600 IU/L
• Stabilize maternal condition
Bilirubin > 1.2 mg/dl with decreasing Hct
• Correct coagulation abnormalities – platelet
transfusion in cases of significant bleeding, platelet
count < 20,000/mm3 or < 50,000/mm3 undergoing
• Elevated liver enzymes surgery
SGOT > 70 IU/L
• Assess fetal condition
Lactic dehydrogenase > 600 IU/L
• GA- anaesthetic technique of choice for caesarean
delivery if platelet count is <50,000/mm3
• Thrombocytopenia – Platelet count < 100,000/mm3

Pulmonary oedema
• Incidence 3%
• Can occur postpartum (within 2-3 days of delivery)
This patient develops crepts in the • Only 30% cases occur before delivery
• Higher risk in older, multigravid women and in
chest with pink frothy secretions. preeclampsia superimposed on chronic HT or renal
What is the most probable disease
• Causes - low colloid osmotic pressure,
diagnosis and how it should be ↑ intravascular hydrostatic pressure and
managed? ↑ pulmonary capillary permeability
• Treatment – similar principles as in non-obstetric
population

Pulmonary oedema...
• O2 saturation monitoring
• O2 supplementation via non-invasive methods or
intubation and ventilation This patient has convulsions in the
• IV furosemide bolus 20-40 mg over 2 min –
repeated doses of 40-60 mg after 30 min, if
recovery room. What is your
inadequate diuretic response (max dose-120 diagnosis and how will you manage?
mg/hr)
• IV morphine 2-5 mg
• Fluid restriction, strict fluid balance
• Positioning – elevated head, antenatal uterine
displacement
(Anaesthesia 2012;67:646-59)

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Eclampsia Eclampsia
• Occurrence of generalized convulsions or • Antepartum
unexplained coma during pregnancy, labour or • Intrapartum
postpartum period in a woman with signs and
symptoms of preeclampsia in absence of epilepsy • Postpartum
or another condition predisposing to convulsions
• Most common – intrapartum or within first 48
• Onset of convulsions in a woman with hours after delivery
preeclampsia that cannot be attributed to other
causes
Clinical presentation
Until proven otherwise, occurrence of seizures • Any pathophysiologic changes of preeclampsia
during pregnancy should be considered eclampsia • Seizures – abrupt onset, tonic-clonic

Management Management of seizures

Airway Drugs
• Left lateral, jaw thrust
• Stop seizures IV Magnesium sulphate
• Nasopharyngeal airway,
• Establish patent airway if necessary • 4-6 g IV → 1-2 g/hr infusion
• 2 g IV over 10 min for recurrent
• Prevent complications e.g. aspiration, Breathing seizures
hypoxemia • Bag and mask ventilation with
100% O 2 Antihypertensive agents
• Antihypertensives • Monitor O 2 saturation • Labetalol 10-20 mg IV or
hydralazine 5-10 mg IV
• Expeditious delivery (preferably vaginal)
Circulation
• IV access
• Monitor BP
• Monitor ECG

Anaesthetic management
Considerations
If the patient develops eclampsia • Considerations related to severe preeclampsia
• Assessment of seizure control and neurologic function
during antenatal period and CS is • Fluid balance – 80 ml/hr
planned, what will be the • Antihypertensive therapy if BP > 160/110 mmHg
anaesthetic management? • Continuous pulse oximetry monitoring of maternal
oxygenation
• FHR monitoring
• Investigations – coagulation studies required
irrespective of platelet count

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Conscious patient, seizures well controlled, no Signs/symptoms of cerebral oedema

evidence of increased intracranial pressure
• GA – intubate & ventilate for at least 24 hours
• Neuraxial anaesthesia acceptable after CS to control haemodynamics and cerebral
perfusion
(Practice Guidelines – Analgesia and Anesthesia for Obstetric • Avoid hyper/hypoventilation
Patient. By: American Association of Nurse Anesthetists;
2017)
• Avoid precipitous fall in BP
• Avoid hypoxia, hyperthermia, hyperglycemia

Obstetric hemorrhage

Sandhya Yaddanapudi
Dept. of Anaesthesia and Intensive Care
PGIMER, Chandigarh

Obstetric hemorrhage
Obstetric hemorrhage in India
worldwide
• Incidence is increasing in developed countries • High MMR: 130 / 100,000 live births
• Grand multiparity, advanced age, previous Cs, fibroids, multiple (2014-16)
gestation, polyhydramnios, placenta previa or abruption, • Higher MMR in rural areas
induction of labour
• 25% of maternal deaths due to hemorrhage (Montgomery
• Haemorrhage accounts for 27% of maternal deaths globally 2014)
• Most deaths in intrapartum period

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Consensus bundles on obstetric

70% fatalities are preventable hemorrhage
• Underestimation of blood loss • Developed by National Partnership for Maternal Safety
• Lack of blood product availability • Require multidisciplinary collaboration
• Insufficient interdisciplinary communication • Organised into 4 domains
• Delayed escalation of invasive interventions • Readiness
• Recognition and prevention
• Response
• Reporting and systems learning

Morbidity due to obstetric

hemorrhage Definition
• Loss of fertility Blood loss >500 ml following vaginal delivery
• Pituitary necrosis Blood loss >1000 ml following cesarean section
• Renal insufficiency
• Coagulopathy Cumulative blood loss of ≥1,000 mL
• Respiratory failure OR
Blood loss accompanied by signs and symptoms of hypovolemia
within 24 hours following the birth process
American College of Obstetricains and Gynecologists

Causes of hemorrhage Uterine atony

• Antepartum hemorrhage • Uterine distension
• Placenta previa • High parity, multiple gestations, polyhydramnios, macrosmia
• Uterine rupture • Oxytocin desensitization
• Placental abruption • Induced / prolonged labour
• Postpartum hemorrhage • Impaired uterine involution
• Uterine atony (80% of PPH) • Retained placenta, placenta accreta
• Genital tract trauma • Decreased myometrial tone
Normal Placenta previa
• Placenta accreta • Anaesthetics, Mg, tocolytic drugs
• Coagulation disorders: hemophilia, vW disease • Chorioamnionitis

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Placenta accreta Placenta accreta

Abnormal attachment of placenta to uterus • Incidence has risen exponentially in last 50 y
• Accreta is direct attachment to myometrium without • Increase in uterine interventions
intervening deciduabasalis • Placenta accreta is asymptomatic
• Increta in infiltration into myometrium • Ultrasound and color Doppler
• Percreta is infilteration upto serosa or beyond. Loss of retroplacental –myometrial hypoechoic zone, increased
vascularity and vascular lacunae (moth eaten or Swiss cheese
appearance)
• Sensitivity 80%, specificity 90%, NPV 98%
• Multidisciplinary management planned

Management Management of uterine atony

• Determine the cause and treat • Early use of uterotonics
• Status of uterus • Uterine massage
• EUA to look for genital tract injury • Manual removal of placenta
• Estimation of blood loss and resuscitation • Bakri balloon
• Visual estimation usually unreliable • B-Lynch compression sutures
• Hemodynamic perturbations are late
• Hysterectomy
• HR and BP near normal till a loss of 1500 ml of blood
• Lab evaluation of Hct and coagulation is slow

Uterotonics Invasive obstetric management

• Oxytocin: 10-40 U/L IV infusion, 10 U IM
• Hypotension, nausea/vomiting
1. Internal uterine tamponade
• Methergine: 0.2 mg IM, 2-4 h
• Hypertension, nausea/vomiting
• PGF2α (carboprost): 0.25 mg IM, 15-90 min
• Bronchoconstriction, diarrhea
• Misoprostol: 400 μg buccal, 1000 μg rectal, once
• Nausea/vomiting, diarrhea
• Foley catheter
• Bakri balloon

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Invasive obstetric management Invasive obstetric management

3. Embolisation of uterine ateries
2. External uterine tamponade 4. Surgical ligation of uterine / internal iliac arteries
5. Hysterectomy

B-Lynch sutures

Resuscitation Intravenous fluids

• Oxygenation; ventilation if required • Crystalloids
• Normovolemic resuscitation • Warm, non-dextrose containing fluids: RL,NS
• Early administration of RBC, FFP, cryoprecipitate and platelets • Traditional 3:1 ratio
• Prohemostatic and antifibrinolytic agents • Large volumes lead to interstitial edema and impairs
microcirculation
• Cell salvage
• Synthetic colloids (not indicated)
• Prevent hypothermia
• Smaller volume, longer intravascular half life
• Inhibit platelet aggregation, impair clot formation
• High cost, risk of anaphylaxis

Red blood cells Fresh frozen plasma

• Increase the blood volume • Contains 20-300 ml
• Increase the oxygen carrying capacity • Increases fibrinogen by 7-10 mg/dl
• Required for interaction between platelets and endothelium • Indications
for coagulation • 4 or more units of PRBC
• Elevated PT, APTT >1.5
• RBC transfusion to target Hb of 8 gm/dl
• 1 unit of RBC increases Hb by about 1 gm/dl

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Fibrinogen concentrate Cryoprecipitate and platelets

Maintain fibrinogen level >2 g/L • Cryoprecipitate
• Small volume • Contains fibrinogen, factor VIII, vW factor, factor XII
• Does not require blood typing, thawing • Platelets
• Safer as devoid of viruses due to pasteurization • Platelet count of >50,000 should be maintained
• One unit (6 donors) increases platelet count by 25,000-30,000
/mm 3

Ratio of FFP and platelets to RBC

during massive blood transfusion PROPPR trial (Holcomb 2015)
• Multicentric RCT in 680 patients with severe trauma
• Guidelines and recommendations till 2008 (1:1:1 vs. 1:1:2)
• 1:1:2 or 1:1:3 • No difference in mortality at 24 h and 30 d
• Practice changed • No differences for the 23 prespecified complications (ARDS,
• 1:1:1 MOF, venous thromboembolism, sepsis, transfusion-related
• Based on retrospective studies with high degree of bias in trauma and
complications)
obstetric patients • Exsanguination was decreased in the 1:1:1 group (9.2% vs
(Holcomb 2008, Lustenberger 2011, 14.6%; difference, −5.4% [95% CI, −10.4% to −0.5%]; P = .03)
Pasquier 2013) • More patients in the 1:1:1 group achieved hemostasis (86% vs
78%, P = .006)

Procoagulants Antifibrinolytic
Recombinant activated factor VII (rFVIIa) Tranexamic acid
• Aids in hemostasis via extrinsic pathway • Inhibits degradation of fibrin clots
• May be used for intractable hemorrhage • Evidence: small RCTs, metaanalysis, found it useful
Low level of evidence • A large RCT (WOMAN) is underway
• Effective only if parameters are normal • Neonatal safety is to be tested
(RBC, platelets, pH, temp, etc.) • 1 g IV, followed by 1 g
• Complications: thrombosis

46
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Cell salvage Monitoring

• Minimizes risk of alloimmunization, viral transmission, and • HR, invasive BP, CVP, dynamic indices, urine output, CO
hemolytic transfusion reactions (Doppler, arterial pulse wave analysis)
• Platelets and coagulation factors removed during processing • Temperature
• Concerns of amniotic fluid embolism, re-injection of fetal RBC • ABG: pH, oxygenation, lactate
• CBC: Hb/hematocrit, platelets
• Electrolytes: Calcium, potassium
• Coagulation : PT, APTT, fibrinogen, D-dimer,
thromboelastography, thromboelastometry
• Fibrinogen levels predictive of severity of PPH

Anaesthesia for obstetric

Indications of anaesthesia hemorrhage: Assessment
• Cesarean: placental abnormalities • History
• EUA and repair of genital tract laceration • Medical, obstetric and anaesthetic
• Manual removal of placenta • Examination
• B-Lynch sutures • HR, BP, capillary refill, temperature (extremities), urine output
• Ligation of vessels • Consciousness
• Airway: status may change during labour
• Hysterectomy
• Correlate hemodynamics with blood loss
• Discuss discrepancy with obstetrician

Anaesthesia for obstetric hemorrhage

/ Anticipated major hemorrhage
• Bedside ABG, Hb, electrolytes, coagulation
• GA vs. RA
• Postoperative ICU care
• 2 large bore (14/16) peripheral IV cannulae
• Cell salvage device
• Central venous large bore (7F) access • Preoperative bilateral femoral sheaths (for embolization)
• Invasive arterial pressure monitoring
• Communication with blood bank and lab
• Rapid infusion pump, pressure bags (Percreta: 20 U RBC and FFP, 12 of platelets)
• In-line fluid warmer
• Vasopressors loaded in infusion pumps

47
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Summary
• Multidisciplinary management: obstetrician, anaesthetist,
blood bank, radiologist
• Anaesthetist to be involved early
• Anticipate blood loss
• Continual assessment of ongoing blood loss
• Measures to control bleeding, to go hand-in-hand with
resuscitation

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Topic Guidelines
Case Discussion: CKD for renal • CRF definition
Transplant and Non transplant • Systemic Manifestations in CRF
• Preoperative Assessment
surgery
• Perioperative management.
Lakshmi Kumar, AIMS, Kochi • Postoperative pain management.
• CKD for Non transplant surgery

16/ 10/ 18 CKD for Trans plant AIIMS PG ass embly 1 16/ 10/ 18 CKD for Trans plant AIIMS PG ass embly 2

Case Scenario
• A 56 y old gentleman, diabetic for 15 y
• Diabetic nephropathy leading to ESRD
• Insulin Mixtard and Actrapid
• On hemodialysis thrice weekly since the last 2
What is meant by End stage
years. Renal Disease?

• Scheduled to have a LD renal transplant

16/ 10/ 18 CKD for Trans plant AIIMS PG ass embly 3 16/ 10/ 18 CKD for Trans plant AIIMS PG ass embly 4

Definition Definition
• Chronic irreversible and progressive
deterioration of renal function .

• The kidneys adapt to the decrease in function.

• Occurrence of renal failure coincides with less

than 25% functioning of the kidneys.

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Is there a bedside assessment?

Cockroft Gault formula
• [140- age] x weight in kg x 0.85[for females]
72 x S. creatinine

This formula tends to underestimate the GFR

and most normal adults may show values
between 65-70 ml/min/1.73 m2 .
16/ 10/ 18 CKD for Trans plant AIIMS PG ass embly 7 16/ 10/ 18 CKD for Trans plant AIIMS PG ass embly 8

Changes in the
Cardiovascular System
Hypertension
Systemic Manifestations of
• Extracellular Fluid volume expansion.
Chronic Renal Failure
• Rennin angiotensin aldosterone axis
activation.
• ACE Inhibitors & ARB slow the progression of
renal disease
• Hyperlipidemias: need concurrent treatment.
16/ 10/ 18 CKD for Trans plant AIIMS PG ass embly 9 16/ 10/ 18 CKD for Trans plant AIIMS PG ass embly 10

CVS CVS
• Uncontrolled hypertension: worsens • Pharmacologic Stress testing: Dobutamine
myocardial ischemia versus dipyridamole.

• Accelerates the progression of renal disease • Role for Angiogram?

• Preoperative Evaluation. • Creatine Kinase Elevations in CKD.

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2
 10/23/18

Cardio- Respiratory System Anemia In CKD

• Volume overload can manifest as pulmonary • Erythropoetin synthesis affected.
edema. • Decreased life span of
• Pleural effusions • RBC due to uremia.
• Orthopnea manifestation • GI losses.
• of fluid overload. • Dietary intake.
• Poor effort tolerance • Anemia of chronic disease.
• Coexistent decrease in Fe and folate.
• Marrow fibrosis hyperparathyroidism

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Ideal value for Hb?

• Target hemoglobin between 11-12 g/dL
What are the target hemoglobin
• CREATE: cardiovascular risk reduction with
levels in ESRD patients? early anemia treatment with epoetin beta.

• CHOIR : correction of hemoglobin and

outcomes in renal disease

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Electrolyte Abnormalities- Na & K Electrolytes

• Sodium and water retention • Magnesium-
• Hyponatremia increase in ECF • Hyperkalemia muscle weakness
• Poor ability to compensate for water losses due • Calcium
to vomiting diarrhea and dehydration.
• Secondary hyperparathyroidism.
• Potassium:
• Ca Po4 deposition
• Hyperkalemia due to failure to secrete the K in
the DCT.
• NSAIDS,ACEI, ARB, aminoglycosides, cyclosporins • Renal Rickets

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Coagulation CNS
• Qualitative dysfunction of platelets. • Glove and stocking sensory loss.
• Decrease in factor VIII and vWF
• Desmopressin • Decrease in mobility leading to atonia
• Cryoprecipitate
• Synthetic estrogens.

• Uremia enhances effects of endothelial NO

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Uremic Syndrome
• Constellation of signs and symptoms ,
anorexia, pruritus, vomiting, malaise.
How would you perform a Preoperative
• Related to severity of BUN concentration. Evaluation for renal transplant surgery?

• Treatment restriction of dietary protein

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What history will you elicit? Immune status

1.What is his treatment history for the CKD? Immune status assessment and modifications:
Cause for CKD? 1. History of vaccinations, Hepatitis B,
2. Duration of initiation of dialysis. Frequency of pneumococcal and varicella.
dialysis and time of last dialysis.
2. Anti Hepatitis B titre is to be done to document
immune status.
3.What are the associated co morbidities:
hypertension, diabetes, CAD, bronchial asthma?
What treatment was he on for these?

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How much fluid can be given safely? Investigations

Does he have a urine output? How much urine does • CBC
he void everyday? Is he on a fluid restriction? How • Blood sugars, Hb A1 C
much water is he allowed?
• Optimisation of Insulin doses and type before
surgery.
Is he on erythropoetin? • RFT
Medications for blood pressure? • Electrolytes
• PT/INR
• aPTT

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Circulation 2012: Guidelines for Renal

Other investigations Transplant
• Chest X ray.

• ECG
• Echocardiogram.

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Indications for Angiogram

• Documented CAD.

• Inability to perform pharmacologic stress Dialysis and vascular access

testing.

• ? Indications for revascularisation

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 10/23/18

Physical Basis of Dialysis Physical Basis of Dialysis

Semipermeable Membrane Diffusion

Start: End:
Different Time Equal
Concentrations Concentrations
Erythrocyte,
Red Blood Cell Bacteria

Albumin, as
Example of a Big
Protein Molecule Medium sized
Molecules, e.g.
β 2-Microglobulin

Electrolytes
Water Flow is
Easily Possible

The semipermeable membrane functions similar to a fine sieve, Diffusion is a consequence of the random movement
only molecules that are small enough can pass. of all molecules (Brownian Movement).

H23/
ealthy Kidney
10/ 18 D is eas ed Kidney Phys ical Bas
RRT in the ICU is
ISACON 2014 Renal Replacement 31 H23/
ealthy Kidney
10/ 18 D is eas ed Kidney Phys ical Bas
RRT in the ICU is
ISACON 2014 Renal Replacement 32

Physical Basis of Dialysis

Renal Replacement Techniques
Ultrafiltration
Time Intermittent Hybrid Continuous
Pressure

IHD SLEDD CVVH

Intermittent Sus tained (or s low) Continuous veno-venous
haemodialys is low efficiency daily haemofiltration
dialys is

CVVHD
Continuous veno-venous
haemodialys is
IUF
Is olated SLEDD-F CVVHDF
Ultrafiltration Sus tained (or s low) Continuous veno-venous
low efficiency daily haemodiafiltration
Exertion of pressure on one side of the membrane produces filtration of
dialys is with
water with solutes, as long as they can pass the membrane.
filtration
SCUF
Slow continuous
H23/
ealthy Kidney
10/ 18 D is eas ed Kidney Phys ical Bas
RRT in the ICU is
ISACON 2014 Renal Replacement 33 23/ 10/ 18 RRT in the ICU ISACON 2014 ultrafiltration 34

Dialysis Preoperative Instructions

• Indications. • Fasting guidelines.
• Clear fluids: gastro paresis/limited fluid intake.
• Vascular access: patency thrill, complications • What clear fluid in a diabetic ESRD???
• Antihypertensive medications.
• ACE Inhibitors/ARB?
• Heparinisation.
• Doses of Insulin?
• Details of pre transplant dialysis
• Intermediate and long acting insulins avoided
night before.

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Preparation/Induction
• IV access non fistula arm.
• NIBP on the same arm.
Anaesthesia for renal transplant • Protection of fistula arm.

• Intraarterial line in the foot..side opposite to

the implant site.

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Possibility of Difficult airway!

METICULOUS ASEPSIS

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Thrombosis from previous central

Lines
Drugs!
• Propofol: Inactivated in liver and excreted
by the kidneys.

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Etomidate Ketamine
• More cardio stable. • Metabolised to nor-ketamine that has one
third of activity as parent compound.
• Metabolised by the liver and then by plasma
esterases. • Nor ketamine can accumulate in renal disease
• Inhibits 11 beta hydroxylase (cortisol and predisposes to convulsions.
synthesis)

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Inhalational Agents
• All are safe with exception of halothane.

• Nitrous Oxide?? • Desflurane superior to sevoflurane superior to

• Expansion of closed air spaces, middle ear halothane.
cavity, risk of postoperative nausea and
vomiting.
• Bone marrow suppression and altered
immunologic responses
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Muscle Relaxants
• Succinylcholine safe to use in the presence of
normal potassium levels.
• Atracurium, cisatracurium are safe… even Fluids during transplant surgery
with compromised functions.

• Azathioprine increases the dose required and

maintain relaxation.
• Cyclosporine prolongs duration of blockade
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Post dialysis and pre-transplant

• What is the actual fluid status?

• Patients dialysed to bone weight: Delayed

graft function.

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Reductions in RBF velocity

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Is Ringer’s lactate superior? Catherine O’Malley

• Anesth Analg. 2005 May;100(5):1518-24, table • 51 patients undergoing renal transplant.
of contents.
• A randomized, double-blind comparison of • 5 patients(19%) vs. 0 hyperkalemia K > 6.0 mEq/L
lactated Ringer's solution and 0.9% NaCl
during renal transplantation. • 8 patients (31%) vs. 0 treated for metabolic
acidosis.
• O'Malley CM 1 , Frumento RJ, Hardy
• Use of RL in renal transplant produces less
MA, Benvenisty AI, Brentjens TE, Mercer hyperkalemia and metabolic acidosis in
JS, Bennett-Guerrero E. comparison with NS

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More acidosis and hyperkalemia with

saline

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Does Ringer lactate result in increased

thrombogencity?

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AIMS practice
• Plasmalyte or Ringer’s Lactate if K <4.0 mEq/L

• ½ NS with 25 cc sodabicarb to 500 ml if K > 4.5 Synthetic colloids and albumin

mEq/L.

Keep CVP 8-10 mm Hg on ventilation with PEEP

before reperfusion and after.
Nor epinehrine used to maintain MAP if < 100 mm
Hg

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Lancet March 2018 What about gelatins?

• United Kingdom liberal on the use of gelatins
even amidst the knowledge that it can cause
anaphylaxis and coagulation abnormalities.

• Surviving sepsis guidelines : inferior to

crystalloids

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Pulse Pressure Variation Stroke Volume Variation

PPmax SVmax

PPmin
SVmin

PP % = PPmax – PPmin SVV = SVmax – SVmin

PPmean SVmean
(PICCO, LiDCO
Flotrac)
(N < 13%) (N < 10%)
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11
 10/23/18

EV 1000 Next best to a TEE

1/ 10/ 18 Fluid in Renal Recipient 67 1/ 10/ 18 Fluid in Renal Recipient 68

Mechanism of action
• Medullary nephrons receive lesser blood flow
in comparison to cortical nephrons.
Role of Mannitol & Furosemide
in Renal recipient
• Damage to the kidney during retrieval and
storage predisposes to ischemic injury with
cell swelling, sludging and debris.

1/ 10/ 18 Fluid in Renal Recipient 69 1/ 10/ 18 Fluid in Renal Recipient 70

Mannitol Management of transplant

• Filtered at the glomerulus not reabsorbed and
excreted with sodium and water. • Maintain MAP > 90 mm Hg.
• Improves renal blood flow by improving pressure
flow responses in the kidney. • CVP 10 mm Hg at the time of reperfusion.
• Reduces endothelial cell swelling post injury. Free
radical scavenger.
• Steroid 7.5 mg/kg methylprednisolone, lasix
and mannitol given prior to reperfusion.
• Reduces the need for post transplantation dialysis
but not related to overall improved graft survival.

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 10/23/18

Furosemide
• Loop diuretic that acts at the thick ascending limb
of the Loop of Henle in the medulla and cortex.
• Combines with the chloride in the Na K Cl carrier
resulting in natriuresis and calciuresis Dopamine and Fenoldepam

• Questionnaire distributed across 18 transplant

centres.Variability in its use. No evident benefit

1/ 10/ 18 Fluid in Renal Recipient 73 1/ 10/ 18 Fluid in Renal Recipient 74

Dopamine Fenoldepam
• Acts on dopaminergic receptors in the kidney. • Selective dopamine receptor agonist (DA1
• At doses of 5mcg/kg/min..increase in RBF, receptors
decrease in resistive index and improvement • Renal vasodilatory effects and natriuretic
in UO.
effects.
• Grafts from brain dead and live donors
showed improvement with dopamine • Comparable doses with dopamine in renal
recipients no differences.
Does not have any beneficial effect in a • Smaller dose versus dopamine in renal donors
transplanted denervated kidney showed nephroprotective effect

1/ 10/ 18 Fluid in Renal Recipient 75 1/ 10/ 18 Fluid in Renal Recipient 76

Pain Management during Renal

Transplant
• Intravenous Opioid.( Fentanyl/Remifentanyl)

• Abdominal wall Blocks. PostOperative pain management

• Epidural Analgesia.

• SAB with opioid

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What are the options? Aneurysm

• Central Neuraxial Block: Epidural, • In surgical repair of abdominal aortic
• SAB/SAB with opiod. aneurysm, an axillary to femoral arterial graft
• TAP block if sometimes indicated to maintain the
perfusion to the graft kidney.
• Erector spinae blocks

• Opioids/multimodal analgesia

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Intra aortic balloon pump

ESRD for Non transplant Surgery

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Get a good surgeon! And a better anesthetist!

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 10/23/18

CKD for Non Tx Key messages

• Elective ? Emergency? • Understand the multi systemic manifestations
• Timing of last HD. of CKD.
• ABG • Assess efficiency of dialysis , electrolytes and
• Electrolytes coagulation preoperatively.
• ECG/Echo • Bleeding from CKD corrected by correction of
vWF and not platelets.
• Rapid Sequence Induction ?
• Regional? GA

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..key messages
• Target hemoglobin/ minimise transfusions.
• Balanced salt solutions superior.
• Care of vascular access/thrombosis of veins
• Pain management strategies.

• Postoperative care

16/ 10/ 18 CKD for Trans plant AIIMS PG ass embly 87

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 10/23/18

Pheochromocytoma

➤Pheochromocytomas are chromaffin cell tumours that

Anesthetic Management-
arise from the adrenal medulla
➤Paragangliomas arise from extra-adrenal sympathetic
Pheochromocytoma tissue of abdomen, pelvis, chest and other organs
➤First diagnosis- 1886 by Felix Fränkel- bilateral tumors
of adrenal gland on autopsy of a patient who had sudden
Rashmi Ramachandran death
Department of Anesthesiology, Pain Medicine and Critical care ➤“Pheochromocytoma” - phaios, which means dusky
All India Institute of Medical Sciences, Delhi (brown), and chroma , which means color (staining that
occurs when tumors are treated with chromium salts)

Pheochromocytoma Epidemiology

➤Catecholamine- ➤10% extra-adrenal

➤Production
➤10% occur in children
➤Effects
➤Metabolism
➤10% familial

➤Clinical Presentation ➤10% bilateral

➤Treatment ➤10% recur

➤Perioperative management ➤10% malignant

➤10% discovered incidentally

Pathophysiology Catecholamine effects

Tyr osine ➤Catecholamines – norepinephri ne, epinephrine, and dopamine

Tyros ine hydroxylas e

➤Norepinephrin e signals through α 1, α 2, and β1 receptors

DOPA

L-D OPA D ecarboxylas e

Nor E pi
P NM T
➤Epinephrine will primarily stimulate only β1 and β2 receptors
Do p amin e b -h yd ro xylase

Dopamine ➤Dopamine does not have much of an effect on any of the

adrenergic receptors; High levels-can stimulate both α and
E pi β receptors

1
 10/23/18

α-adrenergic receptors β-adrenergic receptors

➤α1 -adrenergic receptors ➤β 1 -adrenergic receptors

➤Smooth muscle tissue including peripheral (coronary, cerebral,
renal, etc.) arteries and veins
➤Vasoconstriction upon stimulation- ↑systemic pressure and ↓organ
perfusion
➤+ve inotropic effects in cardiomyocytes
➤α2-adrenergic receptors-
➤Pre-synaptic surface of sympathetic ganglia, acting as a negative
feedback loop for NE release ➤β 2-adrenergic receptors
➤Smooth muscles arterial vasodilation and coronary vasoconstriction
➤Stimulated by NE and Epi.
➤Positive inotropic effect in cardiomyocytes (significantly more
pronounced than α1 stimulation)
➤Positive chronotropic effect through stimulation of the cardiac
pacemaker
➤Release of renin, which will increase mean arterial blood pressure
by converting angiotensinogen to angiotensin I
➤Stimulated mainly by Epi
➤Vasodilation of muscular arteries
➤Increase norepinephrine release from the sympathetic ganglia

Dopamine Effect on Glucose metabolism

➤Epi is more potent than NE in producing hyperglycemia

➤Target D1 and D2 dopaminergic receptors
➤Higher affinity to β-2 receptors
➤D1 receptors- vasodilation of the renal arteries ➤Acts on pancreatic β-cells and liver
➤Pancreas-
➤D2 activation- Inhibits NE secretion from sympathetic
➤Inhibits insulin secretion by stimulating α-2 receptor
nerve terminals and have a mild negative inotropic effect ➤Inducing glucagon secretion via β adrenergic receptor
➤Liver-
➤Lack of hypertension and palpitations in patients with ➤Increases transient glycogenolysis
➤Sustained gluconeogenesis (β-2 receptors)
dopamine-secreti ng pheochromo cyt om as
➤Stimulation of muscle glycolysis and adipose tissue lipolysis
➤Pharmacologically high levels- α and β 1 receptors causing ➤Insulin resistance- reduced peripheral glucose utilisation
vasoconstriction and increased heart rate

Cardiomyopathy Cardiomyopathy

➤Functional hypoxia due to increased contractility and

coronary spasm leading to decreased blood flow,
increased O2 consumption

➤Prolonged exposure produces interstitial fibrosis

➤Myocyte apoptosis, contractile dysfunction due to

structural remodelling- cardiomyopathy

2
 10/23/18

Three clinical scenarios

➤Patients or their physicians note the symptoms or signs of

catecholamine excess

Clinical Presentation ➤Adrenal tumor is noted incidentally on a radiologic study in

an asymptomatic patient or one with minimal symptoms or
signs

➤A Specific evaluation for a PCC is pursued owing to a

significant family history of PCC or endocrine tumor
syndrome (ie, multiple endocrine neoplasia[MEN])

Symptoms Signs

➤Symptoms ➤Abdominal pain

➤Hypertension
➤Headache ➤Constipation
➤Flushing ➤Diarrhea (rare) ➤Tachycardia
➤Diaphoresis ➤Blurred vision
➤Orthostatic hypotension
➤Palpitations ➤Dizziness
➤Anxiety ➤Weakness and fatigue ➤Heart failure
➤Chest pain ➤Anorexia and weight loss
➤Dyspnea ➤Polyuria and polydipsia

Diagnosis-Biochemical testing Biochemical testing

➤NE ➤Catecholamines
➤Neuronal cytosol- after neuronal reuptake or after leakage of the ➤Nor/metanephri ne s
transmitter from storage vesicles- MAO → →VMA
➤Extra-neuronal tissues/ adrenal chromaffin cells- COMT →→ ➤VMA
Normetanephrine
➤Epi
➤Adrenal chromaffin cells- COMT → → metanephrines
➤Plasma
➤24 Urine collection
➤Nor/metanephri ne s- conjugated and secreted in urine

3
 10/23/18

Catecholamine Secretion Imaging

➤Large Pheo: more metabolites-(metab oliz ed within tumor

before release) Sensitivity% Specificity%

➤ Small Pheo: more catecholamines

➤ Sporadic Pheo: Norepi > Epi

➤ Familial Pheo: Epi > Norepi

➤ Paraganglioma: Norepi

➤ Malignant Pheo: Dopamine, HVA

Suppression/Stimulation Testing Goals Treatment

➤Control of hypertension ➤Alpha blockade
➤Clonidine suppression
➤Control of glycemic status ➤Beta blockade
➤May precipitate hypotensive shock!
➤Intravascular volume ➤Calcium channel blockers
➤Pheo- No suppression of plasma NE with clonidine
expansion ➤Metyrosine
➤Control of arrhythmias
➤Second line drugs
➤Glucagon stimulation
➤Optimize cardiac status ➤Fluid and salt
➤May precipitate hypertensive crisis!

➤Pheo- > 3x increase in plasma NE with glucagon

Treatment- Alpha blockade Treatment- Alpha blockade

Nonselective, irreversible, alpha-recept or antagonists- Selective alpha-1 receptor antagonists- Prazosin, doxazosin,
Phenoxybenzami ne terazosin

➤Irreversible inactivation of α1 and α2-rec by covalent

➤Preferentially act on α1 rec and cause vasodilatation
bonding
➤New receptors- for reversal of effect of ➤Alpha-2 receptors are spared- presynaptic release of NE is
phenoxybenza min e- 24–48 h after stopping the drug not enhanced- less severe tachycardia
➤Increased incidence and duration of postoperative ➤Antagonism reversible
hypotension ➤Postural hypotension
➤Crosses BBB- inactivation of centrally located α1 and α2-rec-
➤Vertigo, dizziness, malaise, mild headache
side effects such as headache, drowsiness
➤Gastrointestinal symptoms
➤Orthostatic hypotension, tachycardia, dizziness, and
syncope

4
 10/23/18

Treatment- Beta blockade Treatment-Calcium channel blockers

➤Tachycardia ➤Vasodilation Amlodipine (5–20 mg/day)

➤Alpha-blockade ➤Inhibit NE-mediated transmembrane calcium influx
➤Vasodilatation
Nicardipine (60–90 mg/day)
➤Decrease coronary spasm
Nifedipine (30–90 mg/day)
➤Epi secreting tumors
➤Primary therapy or as adjunct to alpha-antago nists
Verapamil (180–540 mg/day)
➤Arrhythmias, features of myocardial ischemia
➤Should never be used before α1 blockade in patients with ➤Especially useful in normotensive patients/with paroxysmal
Diltiazem (90–240 mg/day)
hypertension with no elevation in baseline blood pressure
functional tumors
➤Unopposed α1 effect- acute cardiac insufficiency and
pulmonary edema
➤After α1 blockade- Pulmonary edema- -ve inotropy
➤ Cardioselective beta-antagonist s

Treatment- Second line drugs Vascular expansion

➤Fluid-
➤Metyrosine ➤Oral
➤IV-crystalloids/colloids
➤Clonidine
➤Salt-5-10 gm

➤Ace-inhibitors
➤May unmask covert hypertension
➤Urapidil ➤Fall in hematocrit

Case Description History

➤28 year old male ➤Duration

➤History of headache, sweating and palpitations- ➤Chest pain

Paroxysmal X 6months ➤Weight loss
➤Local GP ➤Family history
➤Hypertension ➤Duration of medications
➤Referred ➤Orthostatic hypotension
➤Diagnosed Left Adrenal Pheochromocytoma ➤Syncopal attacks

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Examination Investigations

➤Essentially normal except ➤Pertaining to diagnosis

hypertension!
➤Hemogram- Serial Hct
➤Familial association (Syndromes)
➤Biochemistry
➤Heart failure
➤End organ effects-
➤Anesthetic concerns- Airway, IV
access, Allen’s, Spine ➤Renal
➤Ophthalmic
➤BP/ HR – Trends more important
➤Cardiac (LVH, cardiomyopathy)
➤Orthostatic hypotension

Goals of Preoperative optimization Anesthesia Plan

➤Anxiolysis
➤Pre-induction-
➤Standard monitoring
➤Invasive blood pressure
➤Epidural
➤SNP/NTG ready to go!
➤Anesthetic drugs
➤Post-intubation-
➤Central venous catheter
➤Guiding fluid infusion
➤Use of vasoactive drugs

Anesthesia Remember…..

➤Induction agent ➤Inhalational Agent ➤Diligent and prompt management of hypertensive episodes
➤Thiopentone ➤Isoflurane associated with a good plane of anaesthesia
➤Propofol ➤Sevoflurane
➤Etomidate ➤Desflurane The choice of anaesthetic drugs, however,
➤Ketamine
➤Halothane
plays a smaller role in the overall
perioperative haemodynamic stability, which
➤Muscle relaxation ➤Analgesia depends more on the tumour properties and
➤Vecuronium ➤Fentanyl the surgical handling rather than the
➤Cis-atracurium ➤Remifentanyl
➤Atracurium ➤Morphine individual anaesthetic drugs
➤Succinylcholine ➤NSAIDs

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Intraoperative antihypertensive drugs Nitroglycerin

➤ Nitroglycerine and Nitroprusside

➤Systemic and coronary venodilator

➤Release nitric oxide (NO) ➤Onset, 2-5 minutes, t ½ 4 minutes

➤NO activates guanylyl cyclase, increasing cGMP ➤Duration, 5-10 minutes

➤cGMP activates myosin light chain phosphatase (MLCP) ➤Dose: Start at 20-30 mg/min

➤MLCP dephosphorylates myosin light chains ➤Titrate by 10 mg/min every 3-5 minute

➤Leads to relaxation ➤Methemoglobin emia

Nitroprusside Nitroprusside versus Nitroglycerin

➤Arterial and venodilator Drug Nitroprusside Nitroglycerin

Rapid onset of peak effect ++++ +++
➤Decreases preload and afterload (more potent) Afterload reduction ++++ +
Preload reduction ++ ++++
➤No chronotropic effect, but HR ­(baroreceptors )
Coronary steal reported + 0

➤Onset 1-2 minutes, t ½ 3-4 minutes Coronary dilation – large vessel + ++++
Coronary dilation – small vessel +/- +/-
➤Start at 20 mg/min, then titrate
Tachycardia ++ ++

➤Average effective dose is 3 mg/kg/min (0.5-10 mg/kg/min) Ease of administration ++ +++

Cyanide toxicity ++++ 0
➤Cyanide toxicity

Other drugs Postoperative Management

➤ Hypotension
➤Esmolol
➤incidence 20–70%
➤Fluid loading
➤Labetalol
➤Vasopressor infusion
➤May somewhat be dependent on preoperative and intraoperative
➤Diltiazem
hypotensive agents
➤Urapidil
➤Rebound hyperinsulinemia
➤Phentolamine ➤Already depleted glycogen stores
➤Severe hypoglycemia
➤Magnesium Sulphate ➤Hourly blood sugar monitoring

➤Dexmedetomidine

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Perioperative Management of
Hypothyroidism
Thank You Dr Babita Gupta
Professor
Department of Anaesthesiology, Pain Medicine and Critical Care, AIIMS,
New Delhi

Anatomy Physiology

➤Endocrine gland: Consist of two lobes Hormones:

➤Located: Anteriorly in neck extending from C5 to T1 ➤Thyroxine (T4)
➤Size: 5 cm long, 3cm wide and 2 cm thick ➤Tri iodothyronine (T3)
➤Weight: 20 -25 gm in adult ➤Calcitonin

Thyroid Follicular Cell ➤T4:T3 ratio of secreted hormones is 10:1

➤ Upon entering blood, T4 & T3 bind reversibly to 3 major
proteins: thyroxine-binding globulin (80% of binding),
prealbumin (10%–15%), & albumin (5%–10%)
➤ Only small amount of free fraction of hormone, however, is
biologically active
➤10% of thyroid hormone secretion is T3, T3 is 3-4 X more
active than T4 per unit of weight

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Thyroid Hormone Regulation

Hypothyroidism

Impaired secretion of thyroid hormones or under activity of

the thyroid glands leading to hypometabolic state

➤TSH assay -single best test of thyroid hormone action at
cellular level
➤Normal TSH level: 0.4–5.0 milliunits/L
➤TSH level of 5.0–10 milliunits/L with normal levels of FT3 &
FT4 - diagnostic of subclinical hypothyroidism
➤ TSH level >20 milliunits/L (may be as high as 200 or even 400
milliunits/L) with reduced levels of T3 &T4 - diagnostic of
overt hypothyroidism
Severity of Hypothyroidism
➤Severe hypothyroidism –Patients with myxedema coma; with
severe clinical symptoms of chronic hypothyroidism or with
very low levels of total T4 (<1.0 mcg/dL) or free T4 (<0.5
ng/dL) 

➤Moderate hypothyroidism – Includes all other patients with
overt hypothyroidism without features of severe
hypothyroidism

➤Mild hypothyroidism –Patients with subclinical hypothyroidism,
defined biochemically as normal serum free T4 concentration in
the presence of an elevated serum TSH levels


Thyroid gland essential for body to –

Cause of Hypothyroidism ➤Regulation of gene expression
➤Regulation of growth & development
➤Primary hypothyroidism ➤Regulation of general metabolism
➤Autoimmune (Hashimoto’s thyroiditis) ➤Regulation of tissue differentiation
➤ Post thyroidectomy
➤Post radioactive iodine
➤Over dosage of antithyroid medication
➤ Iodine deficiency
➤ Secondary hypothyroidism (failure of the hypothalamic -
pituitary axis)

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Cardiovascular Manifestations of
Pulmonary effects of Hypothyroidism
Hypothyroidism

Effect on Renal Function and Plasma

Hematologic effect of Hypothyroidism
volume

Effect on GIT Clinical features

Slow, insidious progressive growth
➤Patients with hypothyroidism -chronic constipation
➤Atony and hypomotility of the GI tract -develop paralytic or General Cardio-respiratory
‘‘myxedema ileus.’’ ➤Tiredness, ➤ Bradycardia
➤Stomach may be another important target for thyroid Somnolence ➤Angina
hormone. eg., hypergastrinemia has been described in cases
of hyperthyroidism & hypogastrinemia in cases of ➤Weight gain ➤Cardiac Failure
hypothyroidism ➤Cold intolerance ➤Pericardial & Pleural effusion
➤Malabsorption & worsening intestinal motility seen in postop ➤Hoarseness, slow speech
period (especially after intestinal resection) could be ➤Goitre
exacerbated in the presence of hypothyroidism

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Treatment
Neuromuscular Others
➤Full replacement dose of levothyroxine -1.6 µg/kg/day
➤ Delayed relaxation of tendon ➤ Constipation ➤ In elderly or those with known CAD, the initial dose is usually
25 µg daily, with a planned increase every 2 to 6 weeks until
reflexes ➤ Pretibial swelling euthyroid state is attained
➤Muscle fatigue
➤Dry, flaky skin ➤Once TSH values normalize, surgery can be performed
➤Lethargy and hair
➤Depression
➤Deafness

Timing of Surgery Preoperative Assessment

Elective Surgery: Postpone elective surgery until euthyroid Airway evaluation

status is restored ➤Edematous VC
Emergency Surgery:
➤Patients tend to be obese
➤Moderate, overt hypothyroidism: Surgery without delay. ➤Large tongue
Initiate thyroid hormone replacement as soon as diagnosis
made ➤Short neck

➤Severe Hypothyroidism: Start treatment. IV T3 and T4 ➤Goitre

• T4- Loading dose of 200-300 mcg IV followed by 50 mcg ➤Swelling of upper airway
daily 

• T3 - 5 to 20 mcg IV followed by 2.5-10 mcg every 8 hours
depending upon the patient's age and coexistent cardiac risk
factors

Investigations ➤Serum sodium

➤S. Creatinine
➤Serum cholesterol and triglyceride
Thyroid function tests ➤E.C.G
Free & total T4 ➤Platelet count, Coagulation profile
Free & total T3 Endocrinology Consultation
Serum TSH
Radioactive iodine uptake test

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Anaesthetic Considerations Intraoperative

➤Continue thyroid replacement medication on morning of
surgery. Patient may miss the dose of levothyroxine that day - Patients are more sensitive to hypotensive effects of anaesthetic
long half-life of approximately 7 days agents because –
➤Aspiration prophylaxis-due to delayed gastric emptying time ➤Decreased cardiac output
➤Sedative & narcotic administered more cautiously – ➤Blunted baroreceptor reflexes &
more prone to drug induced respiratory depression
➤Decreased intravascular volume
So, Invasive monitoring on a per patient basis
Pharmacologic support best provided with ephedrine,
dopamine or epinephrine
Unresponsive hypotension – Supplemental steroids

➤ Ketamine or Etomidate may be induction agents of choice

➤ Increased sensitivity to volatile anaesthetics – probably due
➤Decreased neuromuscular excitability exacerbated by to decreased CO, decreased blood volume & decreased
anaesthetic drugs excretion
➤Succinylcholine and non-depolarizing muscle relaxants like ➤Controlled ventilation is recommended as patients tend to
atracurium are generally safe for use hypoventilate
➤ Use peripheral nerve stimulator for monitoring muscle ➤ Hypothermia occurs quickly
relaxant
➤Hematological (anaemia, platelet, coagulation dysfunction)
disorder - Close monitoring required

➤Electrolyte imbalances Postoperative

➤Hypoglycemia is common
➤Extubation/ Emergence may be delayed secondary to
➤Try to maintain normothermia
hypothermia, respiratory depression, or slowed drug
metabolism ➤Cautiously administer Opioids
➤Consider regional techniques or Ketorolac for pain control

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Myxedema Coma Characterized by

- Stupor or coma
- Hypoventilation
➤Rare form of decompensated Hypothyroidism
- Hypothermia
➤Medical emergency with mortality rate of 15-20%
- Bradycardia
➤Infection, trauma, cold- predispose hypothyroid patients to
myxedema coma - Hypotension,
- Severe dilutional hyponatremia (SIADH)
- CHF

Treatment Take home message

➤ IV thyroxine is indicated (L-thyroxine loading dose 300-
500ug, followed by 50ug/day for 24-48hrs)
➤IV hydration with dextrose containing crystalloid
➤Correction of electrolyte abnormalities
➤Temperature regulation
➤Support cardiovascular and pulmonary systems as necessary
➤Hydrocortisone 100-300 mg/day
➤Patient should be Euthyroid state in case of elective
surgery
➤If emergency surgery consultation may be taken from
Endocrinologist to get highest benefit from minimum period
➤Our small effort can get maximum result- so perioperative
period must be monitored cautiously

Perioperative management of
Thyrotoxicosis

THANK YOU Devalina Goswami

Associate Professor
Anaesthesia, Pain Medicine and Critical
Care
AIIMS, New Delhi

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

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Definition of Thyrotoxicosis

➤Hyperthyroidism is characterized by increased thyroid Hyperthyroidism is of two types:

hormone synthesis and secretion from the thyroid gland. ➤Overt hyperthyroidism is characterised by low serum TSH
➤Thyrotoxicosis refers to the clinical syndrome of excess concentrations and raised serum concentrations of thyroid
circulating thyroid hormones, irrespective of the source. hormones: thyroxine (T4), tri-iodothyronine (T3), or both.

(Lancet 2016 Aug 27;388(10047):906-918. ➤Subclinical hyperthyroidism is characterised by low serum

TSH, but normal serum T4 and T3 concentrations .
Harrison’s textbook on Internal
medicine,19thEd)

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

Causes of thyrotoxicosis Signs and symptoms

➤Primary Hyperthyroidism SYMPTOMS SIGNS
-Graves disease, Toxic multinodular goitre, toxic adenoma,
Hyperactivity, irritability Tachycardia, AF in elderly
struma ovarii, drugs:iodine excess
➤Thyrotoxicosis without Hyperthyroidism Heat intolerance, sweating Tremor
- Subacute thyroiditis, ingestion of excess thyroid hormone Palpitations, Goiter
➤Secondary Hyperthyroidism
Fatigue, Weakness Warm, moist skin
-TSH secreting pit. adenoma, gestational thyrotoxicosis
(Harrison’s textbook on Internal medicine, Weight loss and increased appetite Muscle weakness, proximal myopathy

19thEd) Diarrhea Lid retraction or lag

Polyuria Gynecomastia

Oligomenorrhea, loss of libido

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

Assessment of Thyrotoxicosis (Lancet 2016)

Assessment of Thyrotoxicosis

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

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Medical management of
Management
thyrotoxicosis
➤Treatment of thyrotoxicosis:
1) Treatment directed against the thyroid gland:
A) Medical
- Inhibition of new hormone synthesis
B) Radio-ablation
(thionamide drugs)
C) Surgical
- Inhibition of hormone release
Preoperative thyrotoxicosis is a potentially life-threatenin g
condition that requires medical intervention before surgery ( Lugol’s iodine, lithium carbonate,
(thyroid or non-thyroid). potassium iodine, iopanoic acid)

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

Medical management of Medical management of

thyrotoxicosis thyrotoxicosis
2) Treatment directed against peripheral effects 3) Treatment of systemic decompensation:
of thyroid hormone: - Treatment of hyperthermia
- Inhibition of T4 - T3 conversion (acetaminophe n, cooling)
(PTU, Corticosteroids, Propanolol etc) - Correction of dehydration and nutritional
- Anti adrenergic drugs deficit (fluid and electrolytes, glucose)
(Reserpine, Guanethidine) - Supportive therapy (corticosteroids,
- Removal of excess hormone from circulation vasopressor, digoxin ± diuretics for CCF)
(Plasmapheresis, charcoal plasmaperfusion)

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

Overview of the drugs used in

Pharmacological agents
thyrotoxicosis
Thionamides: (Propylthiouracil (PTU), Methimazole (MMI), Iodine: Earliest effective agent in preoperative preparation
Carbimazole)
- Preferred for long term treatment and for
The Wolff-Chaikov effect: In supraphysiological doses, iodine
preoperative preparation acts to decrease the synthesis of new thyroid hormone and
decreases release of preformed hormone from the thyroid.
- Takes several weeks to be euthyroid (3-8weeks)
Patients with normal thyroid reserve escapes this phenomenon
- MMI is preferred over PTU as it has longer half life (4-6hrs within 24hours.
Vs 90mins)

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

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Pharmacological agents Pharmacological agents

Jod-Basedow effect: In hyperthyroid patients the excess ➤Radioactive iodine: first line of treatment for Grave’s
iodine is utilized for even more thyroid hormone production disease, toxic adenoma, MNG. Absolute contraindications
resulting in worsening of thyrotoxicosis. are pregnancy, lactation, inability to comply with radiation
safety recommendations, severe ophthalmopat hy .

Inorganic iodine is generally not given in the absence of

pretreatment with ATD to prevent the iodine induced
thyrotoxicosis.

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

Additional pharmacological agents Indications for thyroidectomy

Absolute Indications Relative Indications
➤Iopanoic acid (Oral cholecystogra p hic agent): severe
thyrotoxicosis requiring rapid control where thionamides
alone have failed. Failed medical therapy Symptomatic goitre

Intolerance to anti- Pregnancy

thyroid drug
➤When conventional therapies fail: Lithium, Guanethidine, Severe Grave’s ophthalmopathy
Reserpine, Glucocorticoids, Charcoal treatment, Persistent thyrotoxicosis
plasmapheresis Refractory thyroiditis (amiodarone
Suspected thyroid cancer induced)

Toxic adenoma

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

American Thyroid Association (ATA)

Preparation of thyrotoxic patient
➤Elective surgery should always be postponed until the
patient has become clinically and biochemically euthyroid
➤Rapid preoperative preparation is occasionally needed for
patients requiring urgent or emergent surgery
recommendations
Those undergoing thyroidectomy for the Grave’s disease
should be rendered euthyroid prior to the procedure with
ATD pretreatment, with or without β adrenergic blockade,
and potassium iodide should be given in the immediate
preoperative period.

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

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American Thyroid Association (ATA) Rapid preparation for surgery

recommendations Drug class Recommended Dosage Post op
drug continuation?
When it is not possible to render the patient euthyroid prior Β blocker Propanolol / 40-80mg tid-qid po Yes
to thyroidectomy or when the patient is allergic to ATDs, the
patient should be treated with β blockade, potassium iodide, Esmolol 50- Convert to oral
glucocorticoids, and “potentially cholestyramine” in the 100mcg/kg/min Propanolol
immediate preoperative period
Thionamide Propylthiouracil/ 200mg po 4h Continue in non
thyroidal surgery,
Methimazole 20mg po 4h stop immediately
if thyroid surgery
Oral cholecysto- Iopanoic acid 500mg po bd Stop
graphic agent
Corticosteroid Hydrocortisone/ 100mg po or IV 6h Taper over 72h

Dexamethasone/ 2mg po or IV 6h
1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly
Betamethasone 0.5mg po 6h, IM,IV

Preparation for surgery Preparation for surgery

➤Close cardiac monitoring is required in overt thyrotoxicosis
➤Invasive arterial line and central venous pressure monitoring
whenever needed
➤ATD like PTU or MMI can be used. Takes about 3-8 weeks
➤Combined use of B blocker and thionamides prepares the
patient within few weeks
➤Inorganic iodide in adjunct to thionamides is used in the
immediate preoperative period (Wolff-Chaikov effect), as
the treatment effect wears off within 10 days.
➤Calcium channel blockers if B blocker contraindicated
➤Reserpine and Guanethidine if the above two
contraindicated

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

Preparation for surgery Preparation for surgery

➤In toxic thyroid nodules, thionamides should precede Iodide
for prevention of Jod-Basedow effect.
➤Glucocorticoids : prevents conversion of T4-T3
➤Cholestyramine: binds thyroid hormone in the intestine and
prevents reabsorption and leads to rapid lowering of the
active hormones.
In patients undergoing thyroidectomy:
➤Continue B blockers for a week as the half life of T4 is 7-8
days.
➤Supplementation of oral calcium, vitamin D, or both is
recommended preoperatively to reduce the risk of
postoperative hypocalcemia due to parathyroid injury or
increased bone turnover.

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17

Conduct of Anesthesia
➤Evaluation of the upper airway for tracheal compression or
deviation is important.
➤Chest X Ray or CT scan may also be helpful
➤Adequate anesthetic depth is important to prevent
exaggerated sympathetic stimulation.
➤Drugs stimulating the sympathetic nervous system should
be avoided (ketamine, atropine, ephedrine epinephrine)
1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly
Conduct of Anaesthesia
➤Intra operative hypotension: direct acting
vasopressor(P he nyl ep hrin e )
➤Ephedrine, epinephrine, norepinephrine and dopamine should
be avoided or administered in extremely low doses to
prevent exaggerated hemodynamic responses.
➤Regional anesthesia is safe, epinephrine containing LA
should be avoided.
1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly
Post operative management
➤Bilateral recurrent laryngeal nerve injury necessitates
reintubation. Unilateral recurrent laryngeal nerve damage is
characterized by hoarseness and a paralyzed vocal cord
➤Collapse of the tracheal rings due to preexisting damage
requires emergency reintubation.
1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly
10/23/18
Conduct of Anaesthesia
➤Inhalation agents are required for maintenance of
anaesthetic depth. Organ toxicity secondary to increased
drug metabolism is to be borne in mind.
➤N 2O and fentanyl are safe
➤Coexisting muscle disease (myasthenia gravis) requires less
non depolarizing muscle relaxant.
1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly
Post operative management
➤Hypocalcemia may develop within the first
24-96 hrs of surgery. Laryngeal stridor/
laryngospasm is an early indication of
hypocalcemic tetany.
➤Treatment is IV calcium chloride/gluconat e.
Magnesium levels should also be monitored
and corrected if low.
1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly
Thyroid storm
➤It is a life threatening exacerbation of hyperthyroidism,
most commonly in patients with underlying Grave’s disease,
precipitated by trauma, infection, medical illness or surgery
➤Signs and symptoms are similar to malignant hyperthermia
viz, hyperpyrexia, tachycardia , hypermetabolism, CVS
instability, altered consciousness and liver dysfunction.
1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly
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Thyroid storm Diagnostic Criteria

➤Commonly seen in post op period of emergency surgery in Burch and Wartofsky diagnostic criteria for
inadequately treated hyperthyroid patients thyroid storm is based on the following:
➤Thermoregulato ry dysfynction
➤The diagnosis of thyroid storm must be made on the basis ➤CVS dysfunction
of suspicious and nonspecific clinical findings.
➤CNS dysfunction
➤GI-Hepatic System dysfunction
➤Presence of Previous episode of thyroid
storm.

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

Management of thyroid storm Management of thyroid storm

➤Treatment: General supportive care and rapid alleviation of ➤Circulatory shock - IV administration of a direct
thyrotoxicosis vasopressor(p he nyl ep hri ne )
➤Consider ICU or HDU management ➤Atrial fibrillatioan - β-adrenergic blocker/digitalis
➤Manage ABCDE ➤Tachycardia- β Blockers titrated to decrease heart rate to
< 90/minute
➤Dehydration - IV administration of glucose-contai nin g
crystalloid solutions. ➤Dexamethason e 2 mg every 6 hours or cortisol 100–200 mg
➤Nutritional support-electr olyt es, vitamins every 8 hours.
➤ATD (PTU 200–400 mg every 8 hours).

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

Management of thyroid storm Thyroid specific management

➤Fever- Cooling measures (e.g., cooling blanket, ice packs, ➤Five ‘B s’: Block synthesis (antithyroid drugs);
cool humidified oxygen, avoid salicylates) Block release (iodine);
➤Serum thyroid hormone levels generally return to normal
Block T4 into T3 conversion (high
within 24–48 hours, and recovery occurs within 1 week.
dose PTU, propranolol,
➤The mortality rate for thyroid storm is very high at
approximately 20%. corticosteroid and amiodarone);
Betablocker;
Block enterohepatic circulation
(cholestyramine) .

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

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Pregnancy Pregnancy

➤The most common cause of hyperthyroidism during ➤Endocrine society recommends measurement of T3 and THS
pregnancy is Graves’ disease. receptor antibody (TRAb)
➤Risk is high in 1 trimester, low in 3
st rd
trimester and highest ➤TRAb is useful to detect the risk for fetal or neonatal
at 7-9 months post partum hyperthyroidism because thyroid antibodies cross the
➤The ATA guidelines for the diagnosis and management of placenta
thyroid disease during pregnancy and post partum ➤TRAb concentrations should be assessed at 20–24
recommend obtaining serum freeT4 concentrations in all weeks’gestatio n.
women with serum TSH concentrations of less than 0·1
mIU/L.

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

Pregnancy
➤Assessment of serum thyroid hormone concentrations is
important for distinguishing overt from subclinical
hyperthyroidism, (subclinical hyperthyroidism usually does not
need to be treated during pregnancy).
➤Overt hyperthyroidism should be differentiated from
Gestational thyrotoxicosis( transient and benign condition in 1 st
trimester, due to HCG)
Pregnancy
➤First trimester: Propylthiouracil (the associated risk of
first trimester methimazole induced embryopathy - aplasia
cutis, choanal atresia, oesophageal atresia, and omphalocele)
➤Second trimester: Methimazole (PTU has a greater risk of
hepatotoxicity)

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

Pregnancy Suggested reading

➤Radioactive iodine therapy is contraindicated in pregnancy ➤Langley RW, Burch HB. Perioperative management of
the thyrotoxic patient.
because it crosses the placenta and can cause severe Endocrinol Metab Clin North Am. 2003 Jun;32(2):519-3 4. Review.
hypothyroidism in the fetus.

➤Ross DS, Burch HB, Cooper DS et al. 2016 American Thyroid

Association Guidelines for Diagnosis and Management
of Hyperthyroidismand Other Causes of Thyrotoxicosis. Thyroid. 2016
Oct;26(10):134 3-1 42 1.

➤De Leo S, Lee SY, Braverman LE. Hyperthyroidism.Lancet. 2016 Aug

27;388(10047): 90 6-9 18 .

➤Palace MR. Perioperative Management of Thyroid Dysfunction.

Health Serv Insights. 2017 Feb 20;10:11786 32 916 68 967 7.

1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly 1 9 /1 0 /1 8 AIIMS Anaes thesiolo gy PG Ass embly

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Diabetes Mellitus

Perioperative Management ➤Heterogenous group of disorders

➤Characterized by hyperglycemia due to
of Diabetes Mellitus absolute or relative lack of insulin
➤Normal FBG ≤ 100 mg %
Prof R Sehgal

Diagnostic Criteria for DM ADA Categories of DM

➤Any one of following criteria
➤Type I: β cell destruction & insulin deficiency
- HbA1c ≥ 6.5% or
- Symptoms of DM + RBG ≥ 200 mg % or Respond to minimal dose of insulin
- FBG ≥ 126 mg % (8h fasting) or ➤Type II: Insulin resistance & relative insulin deficiency
- 2h OGTT BG ≥ 200 mg % (after oral glucose Require higher dose of insulin
75 gm) ➤Gestational Diabetes mellitus
➤Prediabetic:
➤Secondary: Genetic defects, disease of pancreas,
- FBS 100 - 125 mg% endocrinopathie s,
- HbA1c 5.7-6.4
drug induced
- 2h OGTT BS 140 - 190 mg%

Perioperative Management of DM
Effects of Hyperglycemia
Objectives:
➤Acute:
➤Adverse effects of hyperglycemia - Dehydration (osmotic diuresis)
➤Factors affecting perioperative glucose metabolism - Acidemia (lactic / ketoacidosis)
➤Perioperative glycemic management - DKA / HHS or HONK
➤Management of complications due to DM ➤Chronic:
- Microvascular (retinopathy, nephropathy)
➤Glycemic management of special surgical situations
- Macrovascular (atherosclerosis, CAD, CVA,
peripheral vascular disease)
- Neuropathic (autonomic, peripheral)
Vascular complications responsible for 75%
deaths

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 10/23/18

Perioperative Hyperglycemia
Implications of Effects on Organ Systems
Adverse outcomes due to poor glycemic control
➤Musculoskeletal: Nonenzymatic glycosylation of protein, abnormal cross linkage ➤Postoperative respiratory infection 2.4 times
(Stiff joints, diabetic scleroderma, difficult airway)
➤Surgical site infection 2 times
➤Renal: Diabetic nephropathy
(↑ Risk of ARF with NSAIDS, hypovolemia) ➤Postoperative UTI 3 times
➤Neurologic: Risk of CVA, ↑ susceptibility of nerves to ischemic injury ➤Incidence of MI 2 times
(LA may be toxic, ↓ vasodilatory response to hypercapnia) ➤Acute kidney injury 2 times
➤ANS: Orthostatic hypotension, delayed gastric emptying, loss of autonomic
response to hypoglycemia ➤Mortality > 50%
➤CVS: ↑ Risk of HT, CAD, silent MI, Heart failure, impaired vasodilation,
increase
➤Pulmonary: ↓lung volume, diffusion capacity in poorly controlled Type-1

Increased Perioperative Mortality

Perioperative Hyperglycemia
➤Undiagnosed DM
➤Multiple comorbidities
➤Insulin prescription errors
➤Increased perioperative infections
➤Associated hyper/hypo gly cemi a
➤Lack of Institutional guidelines
➤Inadequate knowledge amongst caregivers

Surgical Stress Response PAC History

➤Magnitude relates to: ➤Type of DM

➤Severity, duration of surgery ➤Glycemic control
➤Anatomical location ➤Chronic complications, organ damage
➤Invasiveness of procedure (open VS laparoscopy)
➤Drug therapy (oral, non-insulin/insulin injectables) dose &
➤Type of anesthesia (GA VS RA)
dosing time
➤Intraoperative fluids, nutritional support
➤Occurrence, frequency of hypoglycemia
➤Relative insulin resistance maximum on 1 st PO day, lasts 9-21
➤Hospitalization for acute decompensation due to DM
days
➤Patient’s ability to manage his disease, measure BS
➤Glucose drink 2h preop recommended to counteract insulin
resistance & avoid catabolic state due to starvation for ➤Other risk factors for atherosclerosis (HT, smoking,
dyslipidemia, sedentary life)
enhanced recovery
➤Recent infection
➤Drugs for comorbidities

22
 10/23/18

Physical Examination
Investigations
➤Blood pressure, orthostatic hypotension ➤Assess diabetic, metabolic status:
➤Stiff joints (prayer sign), airway - Plasma glucose, fasting & PP
➤Fundus examination (status of cerebral vessels, risk of - HbA1c if not done in last 4-6 weeks
POVL, POCD) - S Creatinine, BUN
- S Electrolytes
➤Size of thyroid gland (associated Hashimoto’s, Graves
disease) - ABG
➤Any infection - Urine sugar, ketones, albumin
➤Cardiac Status:
➤Document neurologic function (RA)
- Resting ECG, Stress test if CAD & time permits
➤Others:
- As dictated by comorbidities, surgical indication

Surgical Planning Perioperative Management Goals

➤Post as 1 st case
➤Minimize fasting period
➤Minimize disruption to patient’s usual routine medication
➤Ensure normoglycemia
➤Ensure plan to manage hypo/hyp ergl yc emia
➤Provide written instructions for management
possible hypo/hyper glyc emia
➤Reduction of overall morbidity & mortality
➤Optimize cardiovascular function
➤Optimize renal perfusion
➤Maintenance of physiological fluid and electrolyte balance
➤Maintenance of glycemic targets
of medication, ➤Avoidance of hypo/hyperglycemia
➤Prevention of ketoacidosis and hyperosmolar hyperglycemic syndrome
➤Use multimodal analgesia & PONV prophylaxis to enable early
return to normal diet

Intraoperative Glycemic Targets Management of Existing Therapy

➤Beyond preventing hypo/hyperglycemia optimal perioperative BG ➤Aim:

targets unclear
➤1 st Leuven study (2001): BG 80-110 VS 180-200 mg% had less Avoid perioperative hypo/hyperglycemia till eating & drinking
morbidity normally
➤Allow patient to retain control of self administration
➤2 nd Leuven study (2006): No benefit, risk of hypoglycemia
➤Different targets given by various organizations ➤If missing only 1 meal manipulate normal medication
➤Oral drugs lowering BG: Stop or modify dose
➤Most recommend perioperative BG between 108-180 mg% ➤Oral drugs preventing BG rise: Can be continued
➤BG 72-216mg% acceptable if poorly controlled without VRIII ➤Subcutaneous insulin infusion: Maintain BG 108-180 mg/dL
➤Strict control (90-150 mg/dL) for critical patients, neurosurgery, ➤Start variable rate intravenous insulin infusion (VRIII) if:
cardiac surgery, pregnancy ➤Longer starvation, missing > 2 meals
➤Variety of regimens proposed (Vellore regime, Alberti regime) ➤Type 1 DM without basal insulin
➤Poorly controlled DM
➤All schemes acceptable as long as BG & K + levels are closely ➤Requiring emergency surgery
monitored and treated

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 10/23/18

Existing Therapy: Oral Hypoglycemics

Existing Therapy: Insulin Regimen

Managing Intraoperative Hyperglycemia Correctional Subcutaneous Insulin Scale

➤Exclude diabetic ketoacidosis, HHS

➤Administer subcutaneous rapid acting insulin using insulin syringe for:
➤Ambulatory surgery
➤Short surgical procedures < 4h
➤M inimally invasive surgery with expected hemodynamic stability, early oral intake
➤Check BG 2 hourly, consider 2n d SC dose after 2h to prevent stacking
➤Start VRIII if 2 SC doses do not work
➤Administer variable rate IV insulin infusion (VRIII) for:
➤Procedures > 4h, > 2 missed meals
➤Anticipated hemodynamic changes, fluid shifts
➤Expected hypo / hyperthermia
➤Use of inotropes
➤Critically ill
➤Cardiac surgery
➤Poorly controlled DM type1
➤Check BG hourly, alter rate to adjust BG 108-180 mg%

Variable Rate Intravenous Insulin Infusion Perioperative Insulin Therapy

Consider bolus dose as Cor r ectional insulin = (BG – 100 / Insulin sensitivity factor = 40)
S tar t IV infusion at BG/100 = U/h
Check BG hour ly and cor r ect per table
Points to remember:
➤Dosing guidelines assume patient fasting & not in DKA
➤Insulin binds to sites in PVC bag, set & syringe
Flush with initial 50 ml of dilute solution
Binding not significant if concentration > 10 U/L
➤After initial lag time, onset is immediate
➤Duration is approx. 1-1.5 h, prolonged in renal insufficiency
➤Dosing must be individually titrated based on frequent BG
monitoring
➤20-50% glucose should be readily available to treat
hypoglycemia
➤Monitor BG hrly (108-180 mg%) & K+ 2-4 hrly (4 -
4.5mmol/L)

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 10/23/18

Postoperative Glycemic Management Postoperative Glycemic Management

➤Depends upon: ➤Transition from IV to SC insulin only when tolerating solid

➤Level of consciousness food
➤Recovery conditions
➤Ability to swallow ➤Start SC when next meal related insulin is due
➤Allowed oral feeds or not ➤Calculate TDD over last 8h, administer 70% as basal, 30%
➤Oral antidiabetics generally not recommended for hospitalized as prandial
patients
➤Withhold or reduce sulfonylureas if food intake reduced ➤Continue IV insulin for 2-3 h after long acting & 1-2 h after
➤Assure adequate urine output / GFR before starting metformin regular/rapid acting SC insulin
➤DPP-4 inhibitors (sitagliptin) with basal insulin safe ➤Start SC infusion at normal basal rate & VRIII continued
➤Non-critical patients: Subcutaneous insulin till next meal bolus
➤Critical, ICU patients: IV insulin
➤Adjust dose if infection or decreased food intake
➤Restart preoperative antidiabetics once patient is ready to eat
& drink without nausea or vomiting

Glycemic Management in Ward

Postoperative Care
➤Sliding scale is not recommended
➤Provide good postoperative analgesia to
➤Basal bolus regimen for patients with good oral intake decrease stress response
➤Basal: Long acting insulin (glargine/detemir 0.2-0.25 U/kg/day)
once/twice daily ➤Use NSAIDs with caution due to possible
➤Prandial: Rapid acting (lispro, aspart) before meals renal dysfunction
➤Correctional: If BG > 180 mg% ➤Give PONV prophylaxis and treat vigorously to
➤Basal Plus for patients with poor or no oral intake enable oral intake
➤Basal: Long acting insulin (glargine, detemir) once/twice daily
➤Correctional: Rapid acting

Implanted Insulin Pump Intraoperative Hypoglycemia

➤Delivers basal + self administered bolus via subcutaneous
catheter
➤Rapid acting insulin better than regular
Less incidence of hypoglycemia
➤Technical failure may lead to DKA
➤Metabolic demand may be altered by fasting, stress
➤Absorption may be erroneous in shock states, hypoperfusion
➤Continue only if patient motivated, stable, under RA
➤For major surgery under GA pump should be stopped, insulin
given by VRIII
➤Restart when patient conscious, able to operate pump
➤Determine IV insulin infusion rate by dividing basal dose by
24
➤Monitor BG and K + closely
➤BG ≤ 70 mg %, Severe ≤ 40 mg%
➤Effect exacerbated by alcohol, liver disease, fasting, sepsis
➤Identification of ‘at risk’ patients
➤Labile glycemic control
➤Aggressive glycemic therapy, tight control
➤h/o frequent hypoglycemia
➤Oral + insulin regimen
➤Symptoms masked under sedation, anesthesia
➤Treat with
- Oral sugary drinks in awake patient
- intravenous 20-50 % glucose 50-100 ml
- ‘Rule of 15’ : 15gm, check after 15’, repeat if <70
➤Effect of glucagon 1 mg IV/IM/SC slow (15-30 minutes)

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Diabetic Ketoacidosis
Diabetic Ketoacidosis
➤Seen in Type 1 DM or ‘ketosis prone Type 2 ➤Acidosis:
DM’ ➤Myocardial function depressed at pH < 7
➤Precipitating causes: ➤Plasma acetone may remain elevated for 24-48 h with continuing ketonuria
➤Persistent ketosis with S bicarb < 20 mEq/L & normal BG represents
- Infection, sepsis continued need for glucose & insulin
- Non-compliance with insulin, DM medication ➤Hyperkalemia, hyponatremia
- Dehydration ➤Total body potassium depleted
➤Deficit 3-10 mEq/kg body weight
- Severe illness, MI ➤Declines further 2-4 hrs after insulin therapy
- Impaired renal function ➤Sodium deficit 6-8 mEq/kg (1.6 meq/L for every 100 mg% increase in blood
sugar
- Medication: βblockers, diuretics, steroids, ➤Hypomagnesemia
salicylates, sympathomimetics ➤Phosphorus deficiency
➤Causes muscle weakness, organ dysfunction
➤Replace if falls below 1.0mg%

Diabetic Ketoacidosis -Treatment Diabetic Ketoacidosis

➤ Restore volume with NS 5-10 ml/kg/hr ➤DKA not contraindication for potentially life
May bring down BG levels dramatically (20-40%) saving emergencies
Add 5/D when BG 250 mg% @ 100 ml/hr ➤Futile to try and correct ketoacidosis completely
➤ Regular insulin bolus 5-10 units, followed by 5-10 U/hr ➤Rapid correction produces dangerous swings in
Maximum rate of BG decline averages 75-100mg%/hr serum osmolality , causes cerebral edema
regardless of insulin dose as number of binding sites ➤Sufficient to correct hypovolemeia & produce
limited falling BG
Consider insulin adsorption on plastic bag, tubing ➤Likelihood of intraoperative cardiac arrhythmias
➤ Restore potassium 0.3-0.5 mEq /kg/hr (check KFT) & hypotension reduced if ABG, volume & potassium
➤ Na bicarb only if pH<7.00, hemodynamic instability, deficit partially corrected
cardiac arrhythmia
➤ Monitor BG, serum potassium, ABG, urinary ketones

Hyperosmotic Hyperglycemic Syndrome General Anesthesia

➤Hyperglycemia BG > 600 mg%
➤Hyperosmolarity > 350 mOsm/L ➤Stress response to laryngoscopy & intubation
➤Normal pH / mild acidosis ➤Etomidate blocks cortisol synthesis & decreases hyperglycemic
response by 1 mmol/L
➤Hypokalemia due to osmotic diuresis ➤Benzodiazepines in high doses decreases ACTH secretion &
➤Hypovolemia (deficit 10-12 L) cortisol synthesis
➤Hemoconcentration ➤Effect of Propofol on insulin secretion not known, but diabetics
show reduced ability to clear lipids from circulation
➤CNS depression
➤High dose opiates produce hemodynamic, hormonal & metabolic
➤Treatment: stability
- IV fluids (NS), colloids if CAD ➤Halothane, enflurane & isoflurane inhibit insulin response to
- Vasopressors glucose in a dose-dependent manner
➤Clonidine decreases sympathetic tone, noradrenaline release at
- Heparin nerve terminals
➤NMB have prolonged effect due to muscle wasting, neuropathy

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Regional Anesthesia Regional Anesthesia

➤But
PNB / CNB popular option for diabetics - Increases cardiovascular instability due to autonomic neuropathy
➤Patient is awake - increased risk of infection (epidural abscess)
➤Surgical stress is obtunded - Increased chance of injury during nerve location
- ? Exacerbation of peripheral neuropathy
➤Decreased insulin resistance in early postop
- Increased sensitivity to LA, ? Toxicity
➤Provide better postoperative analgesia - ASRA recommendations:
➤Tracheal intubation avoided Limit concentration & dose of LA
➤Less PONV Avoid adrenaline as adjuvant
Use USG for blocks
➤Decreased blood loss
➤Decreased risk of thromboembolism At present no evidence that regional alone or in
combination with GA confers any benefit in the diabetic
surgical patient in terms of mortality & major
complications

Intraoperative Fluid Management

Monitoring Blood Glucose
➤Aim:
➤Optimize intravascular volume status ➤Reliability of glucose measurement during dynamic
perioperative period is questionable
➤Provide glucose as substrate to prevent proteolysis, lipolysis & ➤Pitfalls related to:
ketogenesis
- Sample site, source (arterial, venous, capillary, plasma)
➤Maintain serum electrolytes in normal range
- Technique of monitoring (Lab, ABG, Glucometer)
➤Avoid iatrogenic hyponatremia (Dextrose 5%)
hyperchloremic metabolic acidosis (NS) - Impact of current pathophysiologic state
- Presence of interfering substances (nonglucose sugars,
➤Ringers lactate/ balanced isotonic crystalloid solutions of choice medications)
if no VRIII - Peripheral hypoperfusion
- Anemia (error upto 30%)
➤Glucose 5% in saline 0.45% if on VRIII
- Elevated bilirubin
Add KCl 20-40 mEq if hypokalemia - Elevated uric acid
➤Administer at rate appropriate for usual maintenance
requirement
➤Blood contains glucose & lactate, may affect glycemic control

When to Postpone Surgery

Monitoring Blood Glucose
➤Glucose values differ between plasma & whole blood ➤Complications of hyperglycemia
FBG: Plasma 126 mg% Whole blood 110 mg% ➤Dehydration
➤Ketoacidosis
➤POC Glucometers use capillary blood, have correction factor 1.12 to report plasma
adjusted value ➤HHS
➤FDA recommendation: 99% reading >70 mg% be within 10% of lab value
<70 mg% be within 7 mg% of lab value ➤HbA1c 8.5% (British Guidelines)
➤Agreement of POC techniques with lab value low (<80%) 9% (Australian Guidelines)
Tend to overestimate during hypoglycemia
Kanji et al Crit Care M ed 2005;33:2778-85 Not practical as HbA1c cannot be corrected within
days
➤Subcutaneous glucose monitoring sensors available for continuous monitoring
➤Infection will not allow good control

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Special Situations Enhanced Recovery

➤ERAS protocols good for diabetics, promotes early feeding,

➤Use of Corticosteroid s drinking
➤Worsen preexisting DM, precipitate hyperglycemia
➤Antiemetic dose may be safe ➤Reduces iatrogenic risk from VRIII
➤2-3 fold increase in insulin needed for high dose steroids ➤Glucose drink 2h preop recommended to
➤Basal- bolus or VRIII is indicated
➤Counteract insulin resistance
➤Hyperalimentation
➤TPN increases serum BG ➤Avoid catabolic state due to starvation
➤VRIII should be started to assess TDD ➤Decrease risk of postop hyperglycemia
➤If TPN rate is stable, insulin can be added to the fluid ➤May cause hyperglycemia
➤If TPN is interrupted for > 1h, start dextrose and recalibrate insulin dose
➤Avoid if fasting period is short
➤Continuous Nasogastric feed
➤VRIII or Basal- Bolus regimen ➤May be safe in Type 2 DM and if VRIII planned
➤Changes in insulin regimen must precede any change in N-G feeding regimen
➤For interruption > 1h start dextrose and recalibrate insulin dose

Emergency Surgery Ambulatory Surgery

➤Delay surgery if possible till metabolic and volume status

➤Assess reliability of patient to self monitor & treat
optimized at home
➤Maximize glucose, electrolyte and acid-base status ➤Keep as 1 st case
➤Instruct to bring medicines, sweet juice for journey
➤Ascertain timing, amount of last dose of antidiabetic
➤Assure preoperative hydration
medication
➤NPO 2h clear fluids
➤VRIII should be the default glycemic technique ➤Aggressive PONV therapy
➤Use IV dextrose 5% with 0.45% saline with KCl 20 or 40 ➤Monitor BG on arrival, before surgery, 1-2 hrly
intraop, before discharge
meq ➤Before discharge observe for hypoglycemia:
➤Check BS hourly 5hrs after rapid acting, 3hrs after regular insulin
➤Give clear instructions to monitor BG, oral intake

Pregnancy
➤Type I DM risk of stillbirth (x5), congenital
abnormality (x10)
➤GDM: onset during pregnancy
➤Associated with adverse neonatal outcome
(macrosomia)
➤Risk of fetal hyperglycemia, neonatal hypoglycemia
➤BG > 90 mg% during delivery significantly increases
the frequency of neonatal hypoglycemia (BG< 40 mg%)
➤Requires tight control with insulin / metformin
➤Increased frequency of monitoring for good control
➤AOGD recommends BG <110mg% during labor &
delivery
Conclusions
➤Perioperative hyperglycemia is associated with adverse
outcome
➤Diabetes per se not harmful as end-organ effects
➤Ideal perioperative BG level or regimen has not been
determined
➤Tighter the control, more frequent the monitoring
➤Maintain intraoperative BG 108-180 mg%
➤Strict control for pregnant women, diabetic undergoing
CABG, neurovascular procedure, ICU management
➤Delay surgery as far as possible to optimize metabolic,
fluid and electrolyte status deranged due to DKA & HHS
➤LA requirements are lower & risk of nerve injury higher
specially with adrenaline

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References

➤Duggan EW et al
Perioperative hyperglycemia management
Anesthesiology 2017;126(3): 547

Thank You
➤Barker P, et al AAGBI Guidelines: Perioperative management of
the surgical patients with DM 2015
Anaesthesia 2015;70:1427-40
➤Jordao Pontes JP et al.
Evaluation & perioperative management of patients with DM.
A challenge for anesthesiologist
Rev Bras Anestesiol 2018;68(1): 75-86
➤Khan NA et al
Perioperative management of blood glucose in adults with
diabetes mellitus
UpToDate.com Aug2018

DKA Vs HHS Perioperative Hyperglycemia

DKA HHS ➤Proinflammatory, prothrombotic
S Glucose (mg%) >300 >600 ➤↑ Production of reactive oxygen species, free fatty acids, inflammatory
mediators (TNF alpha, IL6) → direct cell damage
S Bicarb (mEq/L) <15 ≥15
➤Vascular & immune dysfunction
S Osmolarity (mOsm/L) ≤320 ➤Disrupts autoregulation, vasodilation, cannot compensate for ↑BP
>320 ➤↓NO causes endothelial dysfunction, impaired wound healing
pH <7.3 ≥7.3 ➤Increased ischemic episodes, brain acidosis, worse neurologic outcome
➤Affects host response to infection by impairing
Urinary ketones >3+ Trace
- neutrophil adherence
Serum ketones + Trace - chemotaxis
- phagocytosis

Acid Base Imbalance Electrolyte Imbalance

➤Acidosis in DM is caused by ketones, lactic acid &/or ➤Hyperkalemia, hyponatremia
increased organic acids from renal insufficiency ➤Total body potassium depleted
➤Myocardial function depressed at pH < 7 ➤Deficit 3-10 mEq/kg body weight
➤Rapid correction with bicarbonate produces ➤Declines further 2-4 hrs after insulin therapy
- CSF & CNS acidosis by converting to CO 2 ➤Sodium deficit 6-8 mEq/kg (1.6 meq/L for every
100 mg% increase in blood sugar
- Alters CNS oxygenation
➤Hypomagnesemia
- Decreases cerebral blood flow
➤Phosphorus deficiency
- Produces unfavorable osmotic gradient
➤Plasma acetone may remain elevated for 24-42 hrs ➤1 mmol/kg BW (tissue catabolism. Impaired
with continuing ketonuria cellular uptake, increased urinary losses)
➤Persistent ketosis with S bicarb < 20 mEq/L & normal ➤Causes muscle weakness, organ dysfunction
BG represents continued need for glucose & insulin
➤Replace if falls below 1.0mg%

29
 10/23/18

+ +
Topics

USG Regional n Basic principles of ultrasound

Anaesthesia n How to optimize the US image
n Sonoanatomy of commonly
performed blocks
n Current evidence on use of USG
regional anaesthesia
Dr. Anjolie Chhabra

+ +
Principles
n An ultrasound wave is a form of acoustic energy
n Alternating currentà multiple piezoelectric crystals
inside the transducer vibrate at high frequency
n Longitudinal propagation into the body à short, brief
series of compressions (high pressure) & rarefactions
(low pressure)
n The propagation velocity of a sound wave in the
human body ~1,540 m/sec
n c =λx f
n c= velocity,λ= wavelength, f = frequency
Principles
n Image generated ~ US waves bounces off tissues & returns to
the probe (switched to a receiving mode)
n Piezoelectric crystals vibrate
n Transforming sound energy à electrical energy
n Process of transmission & reception is repeated ~ >7,000
times/ second
n Generation of a real-time 2-dimensional, seamless image
n Degree to which the ultrasound waves reflect off structure &
return to the probe - determines signal intensity on gray
scale

+ +
Image Hyper vs Hypoechoic Nerves
Hyperechoic Hypoechoic

• Amount of US reflected~ acoustic impedance or tendency to resist the

• Bone reflects 43% of ultrasound waves ~hyperechoic passage of ultrasound between adjacent tissues
• Muscle /blood interface reflects 0.1% of the ultrasound waves ~ • Results in forming 2 distinct images on the ultrasound screen
hypoechoic

1
 10/23/18

+ + Attenuation & Resolution

Angle of incidence of US beam

• High frequency transducer probes (5-13 MHz) afford high axial

• Angle of incidence between US beam & needle perpendicular à
good quality image
• Needle inserted deep & at an acute angle à refraction &
reflection of US beam away from the probe à tip less visible
resolution of superficial structures (axillary, ISB, peripheral
nerve block
• Low frequency probes (2-5 MHz) allow for deeper tissue
penetration (sub gluteal, PVB) at the expense of fine axial
resolution Sites et al. Regional Anesthesia and Pain Medicine 2007

+ + Transducer Probes
Frequency

n The frequency used for peripheral nerve blockade is

between 3 and 15 MHz.

n High-frequency transducers are usually best for target Low

depths of up to 3 to 4 cm frequency -
Echo
n For deeper targets, a lower-frequency transducer is often 2 MHz
necessary

High frequency Low frequency High frequency

Linear array Curvilinear Low frequency 5-13MHz
5-13MHz 2-5 MHz 2-5 MHz

+ +
Fine tuning frequency

n After appropriate transducer selected à fine tune frequency

of the US wave emitted from the transducer

n By actively selecting actual MHz value on some US machines

(Philips Healthcare)

n Or toggling buttons (Sonosite)

n RES (resolution) - upper (8-12 MHz)

n GEN (general) - mid (6-10 MHz)

n PEN (penetration) - lower frequencies (2-5 MHz) of the
transducer’s range
RES (resolution) - upper (8-13 MHz)
GEN (general) - mid (6-10 MHz)
PEN (penetration) - lower frequencies (2-5 MHz)

2
 10/23/18

+ + ? Absent Blood Flow with Doppler

Doppler
418 Regional Anesthesia and Pain Medicine Vol. 32 No. 5 September–October 2007

and artifacts, a solid understanding of the physics of

ultrasound is extremely helpful. A 3-dimensional
ultrasound beam is generated when many multi-
ple tiny piezoelectric crystals rapidly vibrate in
response to an electrical current. This ultrasound
energy is transmitted through tissue where it is
transmitted, reflected, scattered, refracted, and
attenuated. Fortunately, some of the reflected ul-
• Doppler is used to measure velocity and directionality
Fig 12. The Doppler effect. Doppler is used to measure of
trasound returns to the probe to be converted RAPM 2007: 32 (5)
objects
velocity and directionality of objects. In the human body back to electrical energy. This electrical informa-
• Doppler shift ~ decrease frequency of reflected sound
Doppler is most commonly used to measure velocity of tion is processed by the system’s computer to
• Analysis of directionality ~blood flow should be parallel to US beam
blood flow. (A) The signal from fluid moving away from ultimately generate the 2-dimensional
energy • Frequency shift (2 image.
· V · F1 )(cosine )Φ/c
the probe will return at a lower frequency than the The anesthesiologist has the ability anaesthesia
to control image
• Doppler technology in regional anaesthesia à confirms • Regional - blood flow is perpendicular to the US beam
original emitted signal. (B) The signal contacting fluid quality and appearance by interfacing with the system
absence
movingof towards
blood flow ratherwill
the probe than quantification
return of velocity
at a higher fre- • Angle of incidence of beam ~ 90 °; Cosine of 90° = 0 à artifact of no
or direction of flow to change the characteristics of
flow the ultrasound that is
quency than the original emitted signal. It is also impor-
being sent out such as •the frequency,
Tilting focus,handle
the probe wave- toward the patient’s headà flow visualized
tant to note
Brullthat
et al.the cosine
Regional of 0 degrees
Anesthesia is Medicine
and Pain 1 and the2010 length, and frame rate. In
cosine of 90 degrees is 0. Therefore, as the angle ap- a similar fashion, the anes-
proaches 90 degrees large errors are introduced into the thesiologist has the ability to control how the return-
Doppler equation (see Doppler formula). ing image is processed by adjusting such variables as
the gain and various proprietary post processing tech-
have a frequency that is different from the original nologies.
emitted frequency (Fig 12). This change in fre-
quency is known as the Doppler shift.6 It is this References
frequency change that can be used in cardiac and
vascular applications to calculate both blood flow 1. Gray AT. Ultrasound-guided regional anesthesia. Cur-
rent state of the art. Anesthesiology 2006;104:368-
+ velocity and blood flow direction.7 The Doppler
373. +
Image optimization
equation states that:
Depth
2. Sites BD, Brull R, Chan VWS, Spence BC, Gallagher J,
(2) Frequency shift ! (2 · V · F1)(cosine") ⁄ c Beach ML, Sites VR, Abbas S, Hartman GS. Artifacts
and pitfall errors associated with ultrasound-guided
Where V is the velocity of the moving object, Ft is Correct Depth
regional anesthesia. Part II: A pictorial approach to
n Frequency
the transmitted frequency, ! is the angle of inci- understanding and avoidance. Reg Anesth Pain Med
n The objective of depth adjustment is to set the depth to just
dence of the ultrasound beam and the direction of 2007;32:419-433. below the structure of interest
n Depth
blood flow, and c is speed of ultrasound in the 3. Weyman A. Physical principles of ultrasound. In: Prin-
media. ciples and Practice of Echocardiography. 2nd ed. Philadel-
n Focusing
Clinical pearls: The most important application of Dopp- phia: Lippincott Williams & Wilkins; 1994:3-25.
ler technology for the regional anesthesiologist is to confirm 4. Sutton M, Oldershaw P, Kotler M. Textbook of Echocar-
the absence of blood flow in anticipated trajectory of the diography and Doppler in Adults and Children. 2nd ed.
n Gain Cambridge: Blackwell Science; 1996:4-18.
needle, rather than the quantification of the actual velocity
or direction of this flow. Doppler information is complicated 5. Fiegenbaum H. Echocardiography. 5th ed. Philadelphia:
n Doppler
by the frequent occurrence of artifact generation.2 Lea & Febiger; 1994:1.
6. Nanda N. Doppler Echocardiography. 2nd ed. Philadel-
Summary phia: Lea & Febiger, 1993:7.
7. Perinno A, Reeves S, eds. A Practical Approach to Trans-
In summary, in order to optimize clinical imaging esophageal Echocardiography. Philadelphia: Lippincott
and to appreciate ultrasound-related pitfall errors Williams & Wilkins; 2003:77-92.
Too Deep Too shallow

+ +
Gain

n The gain dial allows the operator to change how bright

(hyperechoic) or dark (hypoechoic) the image appears

n Increasing the gain amplifies the electrical signal produced

by mechanical energy of the returning sound waves (echoes)

n Increases brightness, including background noise, and the

potential for artifact generation (Fig. 3, right).

3
 10/23/18

+ +
Time gain compensation Time gain compensation

n The usual pattern ~ a gradual increase in signal intensity

n Less near field gain & progressively increased far field gain

+ + Artifacts
Focus
n Acoustic Shadowing ~ seen most notably when seeking
target that lies deep to bone
n Focal zone is the point where the beam is narrowest

n Lateral resolution or ability of the US machine to correctly

display 2 objects lying at the same depth as separate
structures ~ optimal in this zone

+ +
Acoustic Enhancement Reverberation artifact

Acoustic enhancement occurs when a region behind a weakly

attenuating structure produces stronger echoes than
those observed from adjacent tissues
Sites et al. Regional Anesthesia and Pain Medicine 2010

4
 10/23/18

+ +
Tissue Reverberation Mirror image

Streaks (‘‘comets’’) the arrows represent Image artifact results from an object located on the other
convergence of multiple reverberations side of a very reflective interface –changing scanning
Sites et al. Reg ional Anesthesia and Pain M ed icine 2010
direction may help

+
Bayonet effect

+ How to hold the probe

-Tips

Artifact generated by subtle differences in the velocity of

ultrasound in adipose and muscle tissue

+ +
Holding probe Keep probe firmly in contact

n Ascertain side to be blocked

n Keep probe firmly in contact

n Use coupling medium

n Know Orientation marker

n Know anatomy

n Change angulation

5
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+ +
Orientation marker Know anatomy
To know lateral and medial orientation of US image

M urata et al Anesthesia-analg esia 2012

+ Change angulation

+
USG Brachial plexus block

Nerves visualized best when angle of beam incidence 90°

+ +
Level blocked ~ area of surgery Gross Anatomy
Anesthesia for Arthroscopic Shoulder Surgery 51

Interscalene
Supraclavicular
SCM
Infraclavicular Axilary Clavicle

First rib
Subclavian artery & trunks & divisions of brachial
Fig. 1. Schematic representation of the structures of the left brachial plexus. plexus
Situated at the upper surface of the spinous process of the cervical vertebra. From here they
run out and down between the anterior and middle scalene muscles to reach the lateral base
of the neck, close to the subclavian artery hat is above the pleural dome. They then appear
within the costoclavicular axillary canal, closely associated with the vascular bundle.
In the interscalene space, the middle and upper primary trunks are more superficial than the
lower trunk. The supraclavicular part of the plexus undergoes its first division in the
costoclavicular space, forming a group of clustered secondary trunks lateral and superficial to
the subclavian artery, and above the first rib and pleural dome. At the infraclavicular level, the
plexus forms a series of bundles or cords (lateral, medial and posterior) around the axillary
artery. Distally the terminal branches are individualized, forming the median, ulnar and
brachial cutaneous nerves, the medial forearm and the intercostobrachial nerve in the humeral
canal. The musculocutaneous nerve and the radial nerve run outside the humeral canal. 6
3. Preoperative study
Anesthesia visit should be used to carry out both a global study of the surgical-anesthetic
risk, and to reduce the patient’s anxiety before surgery. Indeed, the treatment of post-
operative pain begins in this pre-operative period, with apprehension and anxiety
increasing when patients are poorly informed as to the upcoming procedures. In examining
the personal background of the patient, it is important to note any previous surgical
 10/23/18

+ +
Interscalene brachial plexus ISB with LA spread on either side

SCM
C5

ASM
MSM

+ +
Supraclavicular Brachial plexus Sonoanatomy – left brachial plexus

Trunks
/Divisions
Brachial plexus
Medial Lateral

Subclavian artery
Rib

Pleura

• Corresponds to area of the trunks and divisions of plexus

• Lateral to subclavian artery going over first rib

+ +
Patient position Probe covering

7
 10/23/18

+ +
Ergonomical positioning Probe position

Clavicle
Head

Shoulder

+ +
Needle & Probe position Supraclavicular Brachial plexus

Brachial plexus

Shoulder Head
Subclavian artery
Rib
Pleura

+ +
Supraclavicular Brachial plexus Supraclavicular block
block
n Indications: upper extremity surgery (arm, elbow, forearm,
Brachial plexus wrist, hand)

n Possible to apply tourniquet for these surgeries

n ‘Spinal anesthesia’ of arm~ rapid onset, reliable block

Subclavian artery
Rib n Compactly packed ~ smallest surface area of plexus here

Pleura n Contraindication
n Bilateral due to fear of BL phrenic nerve block
n Transverse cervical or Dorsal scapular artery passing through the
plexusà change to infraclavicular block
n Avoid injection under pressure

8
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+ +
Tips

n Position patient comfortably to expose supraclavicular area

n Ergonomic position of operator & monitor

n Transducer probe kept parallel to clavicle & tilted to look inside

thorax rather than perpendicular to skin

n Artery should appear round rather than oval

n Vascular area - Doppler to rule out blood vessels (TCA, DSA)

n Look out for the pleura

n Inject above first rib

n Multiple injections under vision

+ +
Axillary Brachial plexus block Axillary Brachial plexus block

+
Anatomy

n Arise from L2,3,4 posterior divisions of ventral rami

n Femoral nerve is the largest branch of the lumbar plexus

+ n Descends into the abdomen between psoas & iliacus muscles

n Passes deep to inguinal ligament to enter femoral triangle

USG Femoral Nerve block

9
 10/23/18

+
Cross section at inguinal crease

+ +
Sonoanatomy Sonoanatomy

Fascia lata Fascia lata

Medial Medial
Femoral sheath Fascia iliaca Femoral sheath Fascia iliaca
Lateral Lateral

Femoral nerve Femoral nerve

Femoral Femoral
vein vein
Femoral artery Femoral artery

+ +
Sonoanatomy Patient & US position

Ergonomic positioning
Compressible femoral
vein
Head
Femoral nerve

Non compressible femoral

artery Inguinal crease

Thigh

10
 10/23/18

+ +
USG Femoral block USG Femoral Nerve block

+ +
Indications & Equipment Tips

n Indications: anterior thigh, femur, and knee n Patient supine with leg abducted & externally
surgery, medial part of leg & foot rotated if possible

n Equipment : n May need to pull overhanging abdomen away

n Linear transducer (8-14 MHz)
n Keep probe in inguinal crease & move up or
n Standard nerve block tray
down- locate femoral artery
n Local anesthetic: 10-20 mL n Ideal- one femoral artery adjacent to nerve
n 50- to 100-mm, 22G short-bevel stimulating
n Move probe upwards- if 2 arteries visible
needle
n Move probe distally- if femoral artery & nerve
n Sterile sleeve, gel & gloves too deep

n Identify & deposit drug below fascia iliaca

+
Essentials

n Indications
n saphenous vein stripping or harvesting
n medial foot/ankle surgery with sciatic nerve
block
+ n Transducer position: transverse on antero-
medial mid thigh 10cms above knee
USG Saphenous nerve block
n Goal: local anesthetic spread lateral to the
femoral artery and deep to the sartorius muscle

n Local anesthetic: 5-10 mL

11
 10/23/18

+ + Sonoanatomy mid-thigh Adductor

USG Saphenous nerve block
canal

n With transducer in transverse position follow

femoral artery down

n Artery in mid-thigh in adductor canal~ sartorius Sartorius

(roof) & vastus medialis (lateral)& adductor magnus
(medial) FA
Vastus medialis
n Follow it till it disappears Adductor magnus

n Move slightly proximally – Femur

n saphenous nerve seen lying lateral to artery

+ +
Sonoanatomy Above knee ~ 10 cm

SN Sartorius
Vastus medialis
FA

Femur

+ +
Popliteal- Sciatic Nerve Popliteal- Sciatic Nerve
block block

CPN
BFM SM
ST TN
Lateral Medial
Lateral Nerve Medial V

Art
V

Art

12
 10/23/18

+ +
Abdominal blocks Quadratus Lumborum block

IO
QL

Post Ant
ESM b owel
Psoas
TP

VB

+ +
Transmuscular QLB Evidence on use of USG RA

+
Evidence on use of USG RA +
n Improves time to do block

n Faster onset time

n Quality of block ~ insufficient data

n Adverse events per 1000 blocks for all peripheral

regional anesthetics was 1.8 (95% CI: 1.1-2.7)

n Incidence of nerve injury

n > 5days ~ 0.9
n > 6months ~ 0.08

n Systemic toxicity due to LA ~ extremely uncommon

13
 10/23/18

USE OF ULTRASOUND IN
CRITICAL CARE

Dr Shrikanth Srinivasan
MD,DNB,F NB,EDIC,F ICCM
Consultant and Head, Critical Care Medicine
Manipal Hospitals, Dwarka, New Delhi

+
CHANGING PARADIGM

n Ultrasound is being increasing used by intensivists for

management of their patients

n The modern USG machines are compact, cheap, better

resolution, portable

n The point-of-care USG is reproducible, repeatable, rapidly

interpretable, bedside and small learning curve

+ +

CLINICAL APPLICATIONS OF
vModifies US IN CRITICAL CARE
admitting n Diag nostic

diagnosis in 26% Airway p atency & d eviation

patients
vChanges in Pleural effusion, p neumothorax, consolid ation
medical therapy:
Pulmonary emb olism
18%
vPrompted LV failure, p ulmonary ed ema
invasive
Fluid resp onsiveness
procedures 22%
DVT

Intrap eritoneal b leed

14
 10/23/18

+ +
USG utilities in Critical Care
n Thera peu tic

Centra l v enou s a cc ess, Arteria l lin e insertion

ICD insertion n Airway with prediction for intubation difficulty

Thora c oc entesis a nd abdom ina l para c entesis
n Breathing with lung pathology detection
Positioning of IABP a nd PA c atheter

Cric othy roidotom y , PCT n Circulation with echocardiography

n FAST
n Assessm ent

F lu id sta tu s
n DVT
L u ng rec riu tm ent
n Pupils and Optic Nerve
Resolu tion of pneu m othora x

n Procedure assistance

+ +

AIRWAY ASSESSMENT

Ne ri L, Storti E, Lic hte ns tein D, Towa rds a n Ultras ound Curric ulum in Critica l Ca re Me dic ine , Crit Care Me d 20 0 7

+ + Predicting Difficult Intubation

AIRWAY ASSESSMENT BY US
n Pre-intubation assessment of a patient using US can predict difficult
intubation
Estimate patency by detecting …
n Hui et al: inability to visualize the hyoid bone predict difficult
> Trachea position, shape, adjacent mass/lesions intubation
… and under spontaneous or mechanical ventilation n Ezri et al. : mean pretracheal tissue of 28 mm (±2.7 mm) at the level of
the vocal cords in obese patients indicate difficult laryngoscopy
> Bilateral and symmetric lung movements
n Adhikari et al: anterior neck thickness at the level of the hyoid bone
and thyrohyoid membrane (more than 2.8 cm) is a better predictor
for difficult laryngoscopy

15
 10/23/18

+ +
VERIFICATION OF ET TUBE
ET INTUBATION Esophageal
n Apart from clinical judgement and ETCO2 technique, US can accurately confirm
Intubation
the position of ET tube

n With an intercostal ultrasonographic view, it is easy to identify the so-called

lung-sliding sign at the lung– chest wall interface, a kind of “to-and-fro”
movement of the pleura synchronized with ventilation

n If the patient is paralyzed or apneic, the esophageal intubation will result in an

immobile or paradoxic state of the diaphragm

+
PRANDIAL STATUS

n Aspiration of gastric contents can be a serious

complication associated with significant morbidity and
mortality

n In particular, aspiration of solid particulate matter, large

volumes, or fluid with low pH carries high morbidity

+ +

FASTING

BREATHING

AFTER 500ML FLUID INGESTION

16
 10/23/18

+ +

BACKGROUND

n Lung ultrasound is based on the principle that

n Acute disease reduces lung aeration
n Generates distinct, predictable patterns
n Thus allowing the diagnosis of conditions and the monitoring of
therapeutic interventions

+ +
Comparative Diagnostic Performances of Auscultation, Chest
Radiography, and Lung Ultrasonography in ARDS

An esth esi o l o gy, V 1 0 0 , No 1, Jan 2 0 04

+
USES OF LUNG ULTRASOUND
A SURFACE IMAGING TECHNIQUE
n Diagnostic:
n Pathology: Pneumonia, ARDS, Pulmonary edema, atelectasis, Pleural effusion
n Endobronchial intubation, Pneumothorax, Pulmonary embolism, d/d of actute
dyspnea

n Monitoring
AI
n Follow-up of resolvingpneumonia, pneumothorax, pulmonary edema and atelectasis, R
aeration/deaeration, lung recruitment, diaphragmatic function, Lung contusions, fine
tuning mechanical ventilatory settings WATER

n Therapeutic
n Safe Thoracocentesis, drainageof pneumothorax

17
 10/23/18

+ +
REQUIREMENTS

Lateral stern al
margi n
n Ultrasound M achine
An teri o r
n Prob es: Any p rob e can b e used for axi l l ary l i n e
artefact assessment

n Have flexib le ap p roach

n S ta rt with c u rv ilinea r probe(3 -5 m hz) for
ra pid a ssessm ent
n L inea r high resolu tion probe (5 -1 0 m hz) P o steri o r axi l l ary l i n e
n F or rela tiv ely su perfic ia l stru c tu res
LUNG
n Training , p ractice and p ractice.. ULTRASOUND
TOPOGRAPHY

+ +
IMAGE GENERATION Assess For

Skin n Lung movement:

SC n Lung slid ing ( to-fro movement of the air-tissue interface artefact ( p leural line) ( confirm on M
tis s ue Real Time M od e: Sea shore sig n)

Rib Images n Cond ition of Lung :

Pleura n Aerated ( A lines+ slid ing )

n Atelectasis

n Deaerated : B Lines ( +/- slid ing ) Consolid ation ( True imag e of d eaerated solid ified lung
Artefacts tissue)

n Collections:

n E ffusions

+ +
LUNG SLIDING ARTIFACTS: A LINES

n Reverberation artifacts

n Horizontal lines parallel to pleural line

n Separated by regular intervals which are equal to

the distance between the skin and the pleural line

SKIN AN D SC TISSU ES n Seen in normal aerated Lung

To and fro n Predominant A lines with lung sliding: A Lines

movement Asthma/COAD
with each
breath PLEU RA AN D LU N G
n Predominant A lines without sliding: Pneumothorax

18
 10/23/18

+ +
SUBCUTANEOUS EMPHYSEMA
B LINES
n Emerge from Pleural line or consolidations

n Well-defined- laser-ray like

n Spreading to the edge of the screen without

fading

n Moving with the Pleural line

n Erasing normal horizontal A lines

n Hyperechoic

n Denote deaeration

+ +
LUNG PULSE ENDOBRONCHIAL INTUBATION

n Sign of ‘Immobile Lung’ with a RIGHT CHEST LEFT CHEST

characteristic transmitted pulsation
of the Heart.

n Present in
n Apnea
n Bronchial Obstruction
n Endobronchial Intubation

MOBILE LUNG IMMOBILE LUNG

SLIDIN G PRESEN T SLIDIN G ABSEN T
PU LSATION S
LU N G PU LSE ABSEN T LU N G PU LSE PRESEN T

+ +
PNEUMOTHORAX PNEUMOTHORAX

n Lung sliding ABSENT

Stratosphere sign onM-mode

n Lung pulse ABSENT

n B line ABSENT

n The A-line PRESENT No

Slid in
n Lung point: may be PRESENT g
Lung
A Lines
n Transition point between mobile and immobile lungspecificto Pneumothorax Point

One B-line is enough for ruling out Pneumothorax, where probe is applied

19
 10/23/18

+ +
Alveolar Interstitial Syndrome B LINES

n Multiple B-lines 7mm apart are caused

by thickened interlobular septa
representing interstitial edema

n B-lines 3mm or less apart are caused

by ground glass areas characterizing
alveolar edema

n Number and intensity of B-lines

increases with the degree of loss of
aeration.
IN CREASE IN W ETN ESS

+ +
ARDS
CONSOLIDATION
Irregular Fragmented
DYN AMIC AIR pleural line
BRON CHOG RAM

LIVER

Subpleural
Cons olidation
s

N on homogenous
B lines

+ +
PLEURAL EFFUSION
The
BLUE
protocol

FREE
FLOATIN G
LU N G

EFFU SIO
N
DIAPHRAG
M

LIVER
Th i s d eci si o n tree d o es n o t ai m at
Sinus oid Sign on M- p ro vi d i n g d i agn o si s. It i n d i cates a
Mode way o f reach i n g 9 0 .5 % accu racy
wh en u si n g l u n g u l traso u n d

Ches t 2008; 134: 117-135

20
 10/23/18

+ US guided management of the +

mechanically ventilated patient

A. Lung aeration/ recruitment assessment

B. PEEP setting
CIRCULATION
C. To decide/optimize ventilator strategy

D. MV related complications

E. Weaning from mechanical ventilation

+ +
FROM the ORG AN-BASED TO the PROBLEM-BASED
ASSESSMENT ASSESSMENT LV
(heart as s es s ment) (s hock as s es s ment)
dilated?
ACU TE, U N EXPLAIN ED, COMPLEX STATES
hypokinetic?
require timely diagnos is , treatment and follow-up CAVA hypertrophic? RV
big or small? dilated?
fixed? hypokinetic?
Trans vers e, D ynamic, Bas ic, Focus ed, Multi-goal
hypertrophic?
Problem-centered Scanning
[1ST: EM ER GENC Y U LTR ASOUND & F OC USED EC HOC AR DIOGR AP HY]

AORTA PERICARDIUM
dilated? effusion?
dissection? tamponade?
Vertical, Specific, Advanced,
Organ/D is trict-centered Scanning VALVES
[2ND : COM P R EHENSIV E EC HOC AR DIOGR AP HY]
hyperechoic?
hypomobile?

Ejection Fraction (EF %) (EDV – ESV) / EDV

Heart Chambers Morphology
THE ONLY 3-D
“Is it a (SIGNIFICANTLY)
ACUTELY DILATABLE
morphologically CHAMBER
normal heart?”
RV
LV

N ORMAL (> 50%) HYPERKIN ETIC

APICAL 4 Chamber View

RV Dilation = ACUTE or CHRONIC

LV Dilation = almost always CHRONIC
Biventricular Dilation = CHRONIC FAILURE
Atrial Dilation = CHRONIC PRESSURE or VOLUME OVERLOAD
LV or RV Hypertrophy= CHRONIC PRESSURE OVERLOAD SEVERE
MILD Dys function MODERATE

21
 10/23/18

C. Inferior Vena Cava Respiratory Variations PERICARDIAL EFFUSION

(H eart-Lung Interactions in Mechanical Ventilation)

ΔIVC = 100 x (IVCinsp – IVCexp) > 18%

IVCinsp

B arb i er C . INTENSIV E C AR E M ED 2 0 0 4

NON
RESPONSIVE

mid SYSTOLE mid DIASTOLE

+
PERICARDIOCENTASIS

Hypovolemia
Hypoxia
Hydrogen ions(acidosis)
Hypo-/Hyperkalemia
Hypothermia

Tension Pneumothorax
Tamponade, Cardiac
Thrombosis, pulmonary
Thrombosis, coronoary
Toxins

+ +
End points of Fluid resuscitation Role of USG in sepsis

n 1. Achieve target CVP (?), MAP n 1. Identify source

or n 2. Guide fluid therapy

n 2. Signs of intolerance to fluid therapy: n 3. End points of fluid therapy-vasopressors

n Desaturation Delayed
manifestation n 4. Identify new organ dysfunction
n Crepitations , after
Worsening chest x ray alveolar
n
flooding n 5. Source control

n 6. Monitor pathology over time

n 7. Identify iatrogenic complications

22
 10/23/18

+ +
Focused USG assessment

Assessment of Disability

W et Lungs Hypokinetic heart Dis tended IVC

NO MORE FLUIDS

+ +
Utility of USG Optic Ultrasound

n Assessment of disability

Ø Optic USG

Ø Trans cranial Doppler

n Therapeutic

Ø Lumbar puncture

+ +
PUPIL ANALYSIS Optic Nerve Sheath

23
 10/23/18

+ + Focussed Assessment with Sonography

HOW TO INTERPRET?
in Trauma

n Fluid pools in predicable locations

n Several studies have finalised the cut-off
value for n Subhepatic
normal ONSD, measured 3 mm posterior to the globe, to n Perinephric

be between from 5.2 to 5.9 mm n Perisplenic

n Pelvic

n Sensitivity is 74–95% and specificity is 74–100% to n Subpleural

identify ICP >20 mmHg n Position patient to best locate fluid

n Head end low for upper quadrants
n With ONSD less than 5.7mm, the chances of ICP>20 n Reverse head low for pelvis
mmHg is less than 5% : Good negative predictive value

+ +
FAST COMPONENTS

n Right Upper Quadrant

n Left Upper Quadrant

n Cardiac
n Subxiphoid

n Parasternal long axis

n Suprapubic

n Extended FAST
n Lung fields
FAST E FAST

+ +
Advantages

• Safer
ULTRASOUND GUIDED • Markedly decreased pneumothorax rate
VASCULAR ACCESS
• Real-time visualization of target

• See needle enter target vein, avoiding adjacent arteries,

nerves

• Standard of care

24
 10/23/18

+ +
Probe Selection Various Approaches

n Linear
n 7.5 Mhz, Vascular, Soft Tissue, Ocular

FINALLYY
• Limited Examination: Extension to knowledge of clinical state and physical
examination

• Mainly Qualitative, Semi-Quantitative Assessment

• It may appear complex at first sight but simply requires a change in thinking
THANKS
• Once the process has been learned, a step- by step use will make it a routine

• Sometimes it is obvious, sometimes it’s not….

• Knowledge of when to call higher competence

25