20 09 13

Prof. A. K.
SethisEORCAPS-2013
1
Prof.A. K. SethisEORCAPS-2013
ASPIRATION OF GASTRIC ASPIRATION OF GASTRIC
CONTENTS CONTENTS
Dr. RachnaWadhwa
Learning objectives Learning objectives
Define
Identify population at risk
Prevention
Diagnosis
Management
Case scenario Case scenario
43 year old male, obese, agitated, gunshot
wound in abdomen plan exploratory
laparotomy
Does not allow airway examination
RSI, laryngoscopy difficult senior called for
help, ventilation continued
Neuromuscular function returns
Vomits massive quantity of semi digested food
Definition Definition
Aspiration can be defined as the inhalation of
material into the airway below the level of the true
vocal cords.
Or/Inhalation of gastric contents into larynx and
lower respiratory tracts
Pneumonitis
Chemical injury of
sterile contents
Pneumonia
Infectious process
from colonized
contents
Background Background
Curtis Lester Mendelson (1946)
Observed 44016 obstetric pts. under anesthesia from
1932-1945
66 aspirated (1:667)
Complete recovery in 24 36 hrs except 2 pts died Complete recovery in 24-36 hrs, except 2 pts died
(1:22008)
Mendelson two syndromes involving the
aspiration of gastric contents.
First, an obstructive picture, .aspiration of
solid gastric material.
S/S cyanosis, wheezing, coughing, tachypnoea,
hypotension CXR- mediastinal shift and consolidation.
Second, classical Mendelsons syndrome
from acid aspiration >25ml of pH <2.5
S/S-bronchospasm, tachypnoea, wheezing, cyanosis
and fever
Prof. A. K. SethisEORCAPS-2013
2
Incidence Incidence
1 in 3000 to 1 in 6000 anaesthetics
1 in 600 for emergency anaesthesia in adults
1 per 2600 paediatric anaesthetics
1 per 400 emergency paediatric anaesthetics
1 per 430900 for caesarean section and 1 per 1 per 430900 for caesarean section and 1 per
6000 for vaginal assisted anaesthesia
Survey in New Zealand over 71% of all
respondents had at least one case of aspiration in
their careers
The phase of anaesthesia at which aspiration occurs
most frequently is on induction and laryngoscopy
(Kluger MT, Short TG. Anaesthesia 1999;54:1926)
High Risk Group High Risk Group
Full stomach
Obstetrics
Diabetes
Obesity
Emergency
Gastro-intestinal obstruction
Trauma
GERD/PUD/ Hiatal Hernia
Ascites
Head Injury
Difficult Airway
Drugs - opioids
Pathophysiology Pathophysiology
Barrier pressure is the difference between LOS
pressure (normally 20-30 mmHg) and
intragastric pressure (normally 5-10 mmHg)
Intragastric pressure when
the gastric volume exceeds 1000 ml the gastric volume exceeds 1000 ml
with raised intra-abdominal pressure, e.g.
pneumoperitoneum during laparoscopy
Complications arising:
Particle related
Acid related
Bacterial
Particle Related Particle Related
Thick particles/ large foreign bodies
Acute upper airway obstruction
Prompt removal
Maintain oxygenation and ventilation yg
Small particles may trickle down atelectasis of
dependent distal small airways
Acid related changes Acid related changes
Two phases
1. Immediate direct tissue injury
Desquamation of superficial cell layer
with complete loss of ciliated & non-
ciliated cells within 6hours.
Rapid in lysophosphatidyl choline
within 4 hrs after acid exposure
alveolar permeability and lung water
Pulmonary oedema
compliance
V/Q mismatch
alveolar arterial oxygen gradient
2. Subsequent inflammatory response
Release of pro-inflammatory cytokines like- TNF , IL-8
Promote a neutrophilic inflammatory response
Trigger expression of L-selectin and beta 2 integrins on
neutrophils and ICAM (intercellular adh) on lung endothelium
3
Prof.A. K. SethisEORCAPS-2013 Prof.A. K. SethisEORCAPS-2013
Gastric aspiration + particulate injury focal
inflammatory changes and foreign body reaction
Particle and acid aspiration synergize to
increase alveolar capillary leak
Blood - relatively innocuous
Bacteria Related Complications Bacteria Related Complications
Pseudomonas aeruginosa and Klebsiella and
Escherichia Coli account for most gram
negative nosocomial pneumonias and
Staphylococcus aureus is the main gram p y g
positive pathogen
Feculent material severe infectious pneumonia
Prevention Prevention
Fasting
H2 receptor blockers
Pro-kinetic drugs
Positioning in ICU Positioning in ICU
Residual volume determination
Ryle Tube Aspiration
RSI
SPECIAL ARTICLE
Practice Guidelines for Preoperative
Fasting and the Use of Pharmacologic
Agents to Reduce the Risk of Pulmonary
A i ti A li ti t H lth Aspiration: Application to Healthy
Patients Undergoing Elective Procedures
An Updated Report by the American Society of
Anesthesiologists: Committee on Standards and
Practice Parameters
Anesthesiology 2011; 114: 495511
Fasting Guidelines Fasting Guidelines
Ingested material Minimum fasting period (h)
Clear liquid 2
Breast Milk 4
Infant Formula 6
Volume of liquid ingested is not as important as
the type of liquid ingested
Infant Formula 6
Non human milk 6
Light Meal 6
AANA Journal 2003;71:301
4
Gastric emptying of orange-flavoured glucose
(group I), low-fat milk (group II) and breast milk
(group III) was evaluated in children <= 5yrs
3% fat milk or 17.5% glucose in a volume of 10 3% fat milk or 17.5% glucose in a volume of 10
ml.kg-1 (maximum volume of 100 ml) can be given
in children safely 3 h and 2 h, but 13.3% required
Sethi AK, Chatterji C, Bhargava SK, Narang P,Tyagi A. Safe
pre-operative fasting times after milk or clear fluid in
children. A preliminary study using real-time
ultrasound.Anaesthesia. 1999 ;54(1):51-9.
H2 H2--receptor blockers receptor blockers
Threshold values for increased risk of aspiration
are gastric volume 0.4 mL/kg with a pH 2.5
H2-receptor antagonists bind competitively to
receptors on the basal parietal cell membrane. receptors on the basal parietal cell membrane.
increase gastric pH, although they do not affect
the pH of fluid already in the stomach
e.g. Ranitidine, Cimetidine and Famotidine
Ranitidine Ranitidine
Oral IM IV
Dose (mg) 150 50 50
Peak 2-3 hrs 15-60 min 15-60 min
D rati n 8 12 hrs 8 12 hrs 8 12 hrs Duration 8-12 hrs 8-12 hrs 8-12 hrs
Absorption 30-60 min - -
Excretion
Kidneys:30-50%,
Liver: 30%
Proton Pump Inhibitors ( Proton Pump Inhibitors (PPIs PPIs) )
PPIs bind to the cysteine residue of H+/K+
ATPase pump on the gastric luminal surface
acidity of gastric contents and lower gastric
volume
Omeprazole, Lansoprazole, Rabeprazole,
Pantoprazole, Esomeprazole
Unlike H2s- PPIs affect all three known
stimulators of acid production: Gastrin,
Acetylcholine, Histamine
routine administration of these drugs ---not routine administration of these drugs ---not
recommended by the ASA
Tolerance to H2-receptor antagonists occur ----
- consider use of a proton pump inhibitor
Prokinetic Prokinetic drugs drugs
Metoclopramide decrease the risk of aspiration
by decreasing the volume of gastric contents.
Greatest antagonistic affinity for dopamine-2
(DA2) and serotonin-2 (5HT2) receptor
b b i l DA1 A 2 d 5HT3 subtypes, but is also a DA1, A-2 and 5HT3
antagonist and 5HT1 and 5 HT4 partial agonist.
The anti-emetic effects .attributed to
5HT3 antagonism and prokinetic effects to
5HT4 agonism.
5
Extrapyrimidal side-effects are mediated via the
DA1 receptor
The prokinetic properties of metoclopramide
are limited to the proximal part of the gut,
ti l ti h l t i d ll b l stimulating oesophageal, gastric and small bowel
activity
The prokinetic effects are blocked with atropine
(10 g/kg)
Antacids Antacids
Bases that interact with gastric acid to form salt
and H2O
Used to neutralize the acids in gastric contents
Raise stomach pH
Particulate
Non particulate
Particulate antacids
Colloid suspension ---- contain aluminum or
magnesium hydroxide as their base substance
Combination of Al and Mg achieve rapid and
sustained neutralization of acid and to balance their sustained neutralization of acid and to balance their
effects on bowel function
Aluminum: Slow and constipating
Magnesium: Fast and laxative
Advantage: Most effective in increasing pH
Disadvantage: Harmful if aspirated
Non-particulate antacids
Usually NaHCO3 preparations
Sodium Citrate (Bicitra)
30ml of .3M sodium citrate
Not harmful if aspirated
Single dose given 15-30 minutes prior to induction
is almost 100% effective in increasing pH >2.5
No lag time-starts working immediately
Effective on fluid already present in stomach
Reduced gastric acidity or volume ~
decreased morbidity or mortality in patients
given preoperative antacids ???
Preoperative antacids s/n/b routinely
administered before elective procedures
requiring GA / RA / MAC in patients who have
i d i k f l no apparent increased risk for pulmonary
aspiration
Only nonparticulate antacids - when antacids
are indicated for selected patients
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Prevention of aspiration in ICU Prevention of aspiration in ICU
Maintain head-of-bed elevation at angle of 30-
45deg
Sedatives as sparingly as feasible
Tube-fed patients, assess placement of the
feeding tube at 4-hour intervals feeding tube at 4 hour intervals
Assess for g.i.intolerance to the feed at 4-hr
intervals
Avoid bolus feedings in high risk group
Maintain endotracheal cuff pressures at an
appropriate level, and clear secretions from
above the cuff
Residual volume determination Residual volume determination
No consistent relationship between aspiration and
GRVs, aspiration occurred relatively often when GRVs
were consistently low.
High GRVs have an independent effect on risk for
aspiration when entwined with other known risk
factors.
Additional risk factors (a mean GCS score <9 and a
mean head-of-bed elevation <30) were significant in
some of the analyses
Metheny NA et al. Clouse. Am J Crit Care 2008; 17(6): 512520.
Ryle tube aspiration Ryle tube aspiration
Drain gastric contents
Decompress the stomach
Treat gastric immobility, and bowel obstruction.
In trauma prevention of vomiting and
aspiration, as well as for assessment of GI
bleeding
LES cannot close when RT is in situ
Remove the nasogastric tube before anesthesia
induction to hopefully prevent aspiration
Rapid sequence induction ( Rapid sequence induction (RSI) RSI)
Performed to prevent aspiration of gastric
contents in patients
- who are not fasting, full stomach
- have impaired gastric emptying or
- are known to have a h/o gastric reflux.
Aim --intubate the trachea as quickly and as
safely as possible
Employed essentially during emergency surgery
Essential features of RSI Essential features of RSI
Pre oxygenation 3-5 min
IV induction using a predetermined induction
dose
Cricoid pressure p
Insertion of a tracheal tube
Air entry check and cuff inflated
Release cricoid
Now initiate IPPV
Modified RSI Modified RSI
Three defining features of a modified RSII:
(1) oxygen administration before induction
(2) the use of cricoid pressure ( ) p
(3) an attempt to ventilate the patient's lungs
before securing the airway.
Ehrenfeld JM et al. Anesthesia- Analgesia2012;115:95-101
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Cricoid Cricoid pressure pressure
Brian A Sellick (1918-1996) London
Anaesthetist
The esophagus is compressed between the
posterior aspect of the cricoid and the
t b b hi d vertebrae behind
The cricoid is used because it forms the only
complete ring of the larynx and trachea
How pressure on the cricoid cartlilage can occlude the
esophagus
Technical limitations to success
The frequency with which the technique is applied incorrectly
Timing of its application
Reproduction of the effective force
Earlier recommendations: 44 N (4.45 kg) modified to
10 N (1 kg) in the awake patient, to be increased to 30
N (3 kg) upon LOC
Sellick described the application of CP with the head
and neck in extreme extension for the esophagus to be
tethered against the cervical vertebrae.
CP . also found to decrease the lower
esophageal sphincter (LES) tone from 24 to 15
mm Hg when a force of 20 N was applied, and
the LES tone further decreased to 12 mm Hg
when the force was increased to 40 N when the force was increased to 40 N.
Prophylactic administration of metoclopramide
could not prevent CP-induced decrease in LES
tone.
Diagnosis Diagnosis
Witnessed aspiration
History of aspiration
Positive signs and symptoms
Any obvious non-respiratory secretions y p y
suctioned via a tracheal tube
Chest X-ray evidence of new pathology after an
incident
Signs of new wheeze or crackles after an
episode of regurgitation or vomiting
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Signs and symptoms Signs and symptoms
Abrupt onset of dyspnoea
Coughing & wheezing
Tachycardia & tachypnoea
Hypotension
Fever
Cyanosis
Hypoxemia and increased inspiratory pressure
Diffuse crackles or decreased breath sounds on
auscultation
Differential diagnosis Differential diagnosis
Bronchospasm
Laryngospasm
Endotracheal tube obstruction
Pulmonary oedema
ARDS
Pulmonary embolism
XX--ray findings after aspiration ray findings after aspiration
Management Management
Inform the surgeon
Head down 30 degrees
Clear and suction the airway
100% oxygen
Apply cricoid pressure and ventilate
RSI
Tracheal suction
Consider bronchoscopy
Bronchodilators if necessary
Steroids ineffective rather increase
mortality
Antibiotics not per se for pulmonary
aspiration pneumonitis, but required if infection
ensues.
Summary Summary
Consider intubation with RSI in the following:
delayed gastric emptying (3rd trimester pregnancy, opioids,
diabetes, renal failure)
increased intra-abdominal pressure (obesity, ascites,
masses)
Shift the focus from GV and pH to patient Shift the focus from GV and pH to patient
characteristics, conditions and anaesthetic practice
Cricoid pressure- right technique, no airway
distortion
No pharmacotherapy if no high risk
Ensure fasting appropriately
Extubate high-risk cases awake and on their side
1
Laryngospasm&Bronchospasm
DrPoonam Motiani
Introduction
Laryngospasm can be defined as prolonged
glottic closure due to reflex constriction of the
laryngeal muscles.
Prolongedhypoxiaandhypercapnea reflex
maybeabolishedandtheproblemmaybe
selflimited.
If sustained, morbidity (Arrhythmia,
pulmonary edema, bronchospasm, gastric
aspiration or Cardiac arrest) and mortality
ensue.
Epidemiology
Olsson and Hallen*(1984);11 yr period (1967
1978); 136,929 patients
Incidence =8.7/1000
Infants(Birthto3mnths)=28.2/1000
In Children(0 9 yrs) 17 4/1000 InChildren(09yrs)=17.4/1000
AdolescenceMales>Females
Males12.1/1000;Females7.2/1000
* Laryngospasm during anaesthesia. A computer-aided incidence
study in 136,929 patients. Olsson GL,Hallen B.
Acta Anaesthesiol Scand. 1984 Oct;28(5):567-75.
Incidenceoflaryngospasm
Calculated in subgroups by age, gender,
preanaesthetic conditions,
premedication, anaesthetic technique,
type of surgery and concomitant type of surgery and concomitant
complication.
Anatomy
Physiology
A multitude of mechanoreceptors, chemoreceptors and
thermoreceptors present throughout the larynx
Densitygreatestaroundthelaryngealopening
(Posterior>Anterior)
Stimulation of these receptors induce shortlived glottic Stimulation of these receptors induce short lived glottic
adduction to protect from aspiration (Glottic Closure
Reflex)
Laryngospasm: A prolonged form of vocal cord adduction
(Occurs if laryngeal closure reflex becomes overtly
sensitive)
2
Physiology
AfferentImpulses
Stimulationofthenasalmucosa,softpalateand
pharynx
Stimulation of the epiglottis and larynx Stimulationoftheepiglottisandlarynx
Stimulationofthetracheobronchialtree
Stimulationoftheabdominalvisceraand
diaphragm
Mechanism
Laryngeal reflexes
By stimulation of afferent
fibers in the Internal
b h f th S i branch of the Superior
laryngeal nerve ( Sensory
N innervation : the area
above the true vocal cord)
Anatomy
Laryngospasm involves three
structures the Aryepiglottic
folds, false vocal cords (FVC)
and the true vocal cords(TVC).
The muscles involved are the
lateral cricoarytenoid and the lateral cricoarytenoid and the
thyroarytenoids (adductors of
the glottis) and the cricothyroid.
During a laryngospasmeither
TVC
TVC and FVC
become apposed in the midline
and close the glottis.
Diagnosis
Complete laryngospasm
Absence of Breath Sound(silent chest),
no bag movement,
no ventilation
Tracheal tug,
Paradoxical respiratory movements of the thorax and Paradoxical respiratory movements of the thorax and
abdomen(ineffective chest wall movement).
Incomplete/Partial laryngospasm
Breath Sounds+
Tracheal tug, Paradoxical respiratory movements of the
thorax and abdomen(ineffective chest wall movement).
Diagnosis
154/189(77%):Clinicallyobviousandeasily
diagnosed
23%:Notclinicallyobvious
27/189(14%) (P t d i b t ti ) 27/189(14%)(Presentedasairwayobstruction)
9/189(5%):Vomitinganddesaturation
7/189(4%):Desaturation
AustralianIncidentMonitoringStudy(AIMS):189/4000,2005Feb
Theincidenceofresultantmorbidity
OxygenDesaturation61%
Bradycardia6% (commonerinyoungerpatient)
lessthan1yearofage(23%),
114years(8%),
over14years(2%).
Pulmonaryaspiration3%
PostobstructivePulmonaryEdema4%
Cardiacarrest0.5%
Crisis management during anaesthesia: laryngospasm .T
Vishvanathan
1
,MT Kluger
2
, RK Webb
3
et al.
Qual Saf Health Care 2005;14
AustralianIncidentMonitoringStudy(AIMS):189/4000,2005Feb
3
AustralianIncidentMonitoringStudy(AIMS):189/4000
Precipitating causes of
laryngospasm
No of incidents %
Airway manipulation 83 44
Blood/secretions in the pharynx 22 12
Regurgitation/vomiting 17 9
Surgical stimulus 9 5
Moving patient 8 4
Irritant volatile agent 4 2
Failure of anaesthetic delivery
system
3 2
Unable to determine 43 22
Total 189 100
Crisis management during anaesthesia: laryngospasm
T Visvanathan, M T Kluger, R K Webb, R N Westhorpe.
Qual Saf Health Care 2005;14
Prevention
IdentifyingtheRiskfactors
Patientrelatedfactors
Anaesthesiarelatedfactors
Surgeryrelatedfactors
Patientrelatedfactors
MostimportantYoungage
Upperrespiratorytractinfection(URI)theriskfrom
2.3tovefold.
Passive smokers and children with hyperactive
airway 10 times more prone
Upperairwayanomalies
Expremature under 1 year old, whooping cough
ASA IV, Obstructive sleep apnea, obesity,
Gastroesophageal reflux, patients with elongated
uvula and with h/o choking during sleep.
Electrolyte disturbances: low magnesium and low
calcium level.
Anaesthesiarelatedfactors
Induction28%,Maintenance24%,Emergence48%
1. InsufficientDepthof anaesthesiaduringinduction
2. Intravenousinductionagents
Barbiturates>Ketamine >Propofol
3. LMA* >ETT>facemask
4. Airwayirritation
Volatileanesthetics:Desflurane >Isoflurane >
Enflurane>Halothane>Sevoflurane
Mucus, secretions, blood, laryngoscope, suction catheter or any other
foreign body in the laryngopharynx (specially in light plane of anaesthesia)
5. A relatively less experienced anaesthesia provider also
encounters more number of laryngospasms
*Riskfactorsforlaryngospasm inchildrenduringgeneralanesthesia.FlickRP,WilderRT,
PieperSFetal.Paediatr Anaesth.2008Apr;18(4).
Surgeryrelatedfactors
Upper airway surgeries (tonsillectomy & adenoidectomy)
have a higher incidence (2126%)
Other surgeries like appendicectomy, dilatation of anal
sphincter or cervix, mediastinoscopy, hypospadias
surgery and skin transplant in children also highly
associated.
Thyroid surgery
Damage to the SLN
Hypoparathyroidism (iatrogenic removal of the parathyroid
glands causing hypocalcemia)
Esophageal procedures(due to stimulation of the distal
afferent nerves)
Analgorithm* forthepreventionoflaryngospasm
*Pediatric laryngospasm: prevention and treatment. Achir Ahmad et al.
Current Opinion in Anaesthesiology 2009, 22:388395
4
Analgorithm* forthepreventionoflaryngospasm
Artificial cough: Positive Pr inflation of the lungs just before
extubation to expel the remaining secretions.
Treatment
Treatment with airway management
Open the mouth, tight seal with facemask, extend the neck
with jaw lift and apply CPAP ventilation with 100% oxygen .
Can be enhanced by Guadagni Technique( two maneuvers) :
1. Place the middle nger of each hand in the laryngospasm
notch located between the mastoid process and the ear
lobule and press inward on the styloid process. This
induces periosteal pain resulting in autonomic nervous
system reex and vocal cords relaxation .
2. Vigorous forward pull of the mandible causing a painful
stimulus; stretches the geniohyoid muscle to partially open
the larynx .
Guadagni Technique
TheLaryngospasmNotch
Treatmentcontd..
Treatmentusingdrugs:
Recent studies laryngospasm is always complete thus
anaesthesia with inhalational agents alone is not therapeutic;
Rather, airway management and i.v.; therapy is indicated.
Propofol (0.250.8 mg/kg i.v. ) can treat laryngospasm in
76.9% of cases. However, No study in children < 3 yr .
Succinylcholine is still considered the gold standard( 0.13
mg/kg i.v.) Give with atropine (0.02 mg/kg) to avoid
succinylcholineinduced bradycardia and cardiac arrest .
Laryngospasm may recur after succinylcholine metabolism
and a second dose may be given following atropine .
Analgorithmfortreatmentoflaryngospasm*
Analgorithmfortreatmentoflaryngospasm*
5
FollowUp
Assessforthepossibilityofdeveloping
Pulmonaryaspiration
Postobstructivenegativepressurepulmonary
edema
BRONCHOSPASM
BronchospasmduringGA
Canpresent:
inisolationor
asacomponentofamoreseriousunderlying
h l h h l i pathologysuchasanaphylaxis.
Untreateditcancausehypoxia,hypotensionand
increasedmorbidityandmortality.
Theoverallincidenceofbronchospasm during
GAisapprox.0.2%1
Reactive Airways Disease:
Common features : Bronchospasm and wheeze
Hyperreactive airway responses to mechanical
and chemical irritants.
Combination of constriction of bronchial
smooth muscle mucosal oedema and mucous smooth muscle, mucosal oedema and mucous
hypersecretion with plugging.
Perioperative bronchospasm is however
relatively uncommon.
In patients with wellcontrolled disease, the
incidence of bronchospasm is approx. 2%.
FeaturesofBronchospasm Anaesthesia
Prolongedexpiration
Expiratory wheeze auscultated in Chest/Breathing circuit; In
Severe bronchospasm wheeze may be absent.
ReducedorabsentBreathsounds
Narrowed airways and prolonged expiration result in a
delayed rise in ETCO2( sharkfin appearance)
peakairwaypressureswithIPPV
dalvolumes
OxygenSaturaon
Hypotension
VentilationPerfusion(V/Q)mismatch& pulmonaryvascular
resistance(PVR)
OthercausesofwheezingduringGA
Partialobstructionoftrachealtube(including
ETTabuttingthecarinaorendobronchial
intubation)
Pulmonaryoedema
Aspiration of gastric contents Aspirationofgastriccontents
Pulmonaryembolism
Tensionpneumothorax
Foreignbodyinthetracheobronchial tree
Bronchospasm
6
AcuteBronchospasm
Commonerduringinductionand
maintenancethanduringemergence
andrecoverystages.
Causes duringinduction
Airway Manipulation or surgical stimulation under
light anaesthesia.
Airway irritation
Relatedtointubation; Vagalsympathetictone
i b l URTI S ti imbalance;URTI;Secretions
Airway soiling
Secretions, regurgitation or aspiration particularly
with the use of LMA ,uncuffed ETT or an
inadequately inflated/punctured cuff.
Causes DuringMaintenance
Inadequate depth of anaesthesia
Exacerbation of asthma
Allergic or Anaphylactic reaction
Drugs (antibiotics, neuromuscular blockers)
Blood products (red blood cells, fresh frozen plasma)
Other allergens(Latex etc)
Certainsurgicalprocedures
Analorcervicaldilatation
Strippingofthelongsaphenousveinduringvaricoseveinsurgery
Tractionontheperitoneum.
Nonspecific Bronchial Hyperesponsiveness
Stimulation of parasympathetic fibres
DuringtheMaintenancestageofanaesthesia:
Pharmacological:
Certain volatile anaesthetic agents (isoflurane, desflurane).
IV agents including betablockers, prostaglandin inhibitors
(NSAIDs) and cholinesterase inhibitors (neostigmine).
Histamine release (thiopentone atracurium mivacurium Histamine release (thiopentone, atracurium, mivacurium,
morphine, dtubocurarine)
Others: Protamine ,Nonsynthetic opioids, Drug
preservatives, Ester local anaesthetics.
Careshouldbetakenwiththesedrugsinhigherriskpatients.
Independentriskfactors*foradverse
respiratoryeventsinchildrenwithactiveURIs
UseofanETT(<5yrofage)
H/oprematurity
H/oReactiveairwaydisease
paternalsmoking
AirwaySurgery
Copioussecretions
Nasalcongestion.
* Risk factors for perioperative adverse respiratory events in children
with upper respiratory tract infections.
Tait AR, Malviya S et al.Anesthesiology 2001 Aug;95(2):299-306
PreventionofBronchospasm
Thoroughly assess and optimize patients with asthma and
COPD. Wheezing, cough, sputum production, shortness of
breath and diurnal variability in PEFR indicate poor control.
Recent, frequent exacerbations or hospital admission
t ti l postpone nonessential surgery.
Continue bronchodilators, inhaled or oral corticosteroids
perioperatively. Chest physiotherapy and referral to a
respiratory physician if required.
Counsel and encourage patients to stop smoking
preoperatively(6 to 8 wks )
7
PreventionofBronchospasm
Careful medication history ; drug sensitivities( NSAID
induced bronchospasm)
In children URTI the risk. Complete resolution of
symptoms (approx. 2 wks) ses incidence of
airway hyperreactivity.
Pretreatment with an inhaled/nebulised beta
agonist, 30 mins preoperatively.
Induction of anaesthesia with propofol and adequate
depth of anaesthesia before airway instrumentation .
Prefer LMA (in suitable patients) to ETT.
Regional techniques avoid GA and intubation.
Algorithmtoguidemanagementofintraoperative
bronchospasm.
Onsuspectingbronchospasm:
Switchto100%oxygen
Ventilatebyhand
Stopstimulation/surgery
Considerallergy/anaphylaxis;stop
administrationofsuspecteddrugs/colloid/
bloodproducts
Difficulty with Ventilation/falling SpO2
CALL FOR HELP
Management of bronchospasm during general
anaesthesia .Alex Looseley.Update in Anesthesia 2011.
Immediatemanagement;preventhypoxia&reverse
bronchoconstriction
Deepenanaesthesia
IfventilationthroughETTdifficult/impossible,check
DifficultywithVentilation/fallingSpO2
CALLFORHELP
DifficultywithVentilation/fallingSpO2
CALLFORHELP
g / p ,
tubepositionandexcludeblocked/misplacedtube
Ifnecessaryeliminatebreathingcircuitocclusionby
usingselfinflatingbag
Innonintubatedpatientsexcludelaryngospasmand
consideraspiration
Secondary management, provide ongoing therapy and
address underlying cause
1. Optimise mechanical Ventilation (incorporate a long expiratory time
to allowcomplete exhalation and reduce breath-stacking and intrinsic
PEEP)
2. Reconsider allergy/anaphylaxis - expose and examine the patient,
Consider shifting to ICU/HDU
reviewmedications
3. If no improvement consider pulmonary oedema/ pneumothorax/
pulmonaryembolus/ foreign body
4. Consider abandoning / aborting surgery
5. Request &reviewchest X-ray
6. Consider transfer to a critical care area .
Algorithmtoguidemanagementofintraoperative
bronchospasm.
1st Line Drug Therapy
Salbutamol
Metered Dose Inhaler: 68 puffs
repeated as necessary (using in
line adaptor/barrel of 60ml
2ndLineDrugTherapy
Ipratropium bromide:0.5mg
nebulised6hourly
Magnesiumsulphate:50mg.kg1
IVover20min(max2g)
Hydrocortisone:200mgIV6
line adaptor/barrel of 60ml
syringe with tubing or down ETT
directly)
Nebulised: 5mg (1ml 0.5%)
repeated as necessary
Intravenous: 250mcg slow IV then
5mcg.min1 up to 20mcg.min1
hourly
Ketamine:Bolus1020mg.
infusion13mg/kg/hr
INEXTREMIS:Epinephrine
(Adrenaline)
Nebulised:5mls1:1000
Intravenous:10mcg(0.1ml
1:10,000)to100mcg(1ml
1:10,000)titratedtoresponse
An MDI canister is placed in the
A t d d i h l (MDI)
An MDI canister is placed in the
barrel of a 60ml syringe; A 15cm
length of IV tubing is attached via
the Luer lock. Feed the tubing
down the ETT and press the
plunger to administer the drug,
then reconnect the breathing
circuit and ventilate
A metered dose inhaler (MDI)
adaptor fitted in the breathing
circuit, on the patient side of the
HME.Depress the canister by
hand during inspiration to
administer the drug.
8
TakeHomeMessage:
EasilyDetectedandManaged
IfPoorlymanaged PotentialMorbidityand
Mortality
i i h k h Preventionisthekeytotherapy.
AStructuredapproach,correctlyappliedmay
resultinaquickerand/orbetterresolutionof
thesecomplications.
References
Van der Walt J. Laryngospasm. In: Bissonnette B, Dalens B, editors.Pediatric
anesthesia: principles and practice. New York: McGrawHill;2002. p. 644.
Fink BR. The etiology and treatment of laryngeal spasm. Anesthesiology1956;
17:569577.
Suzuki M, Sasaki CT. Laryngospasm: a neurophysiologic redenition. Anesthesia for
eye, ear, nose and throat surgery. In: Miller RD, editor.Millers Anesthesia, 6th ed.
Philadelphia: Elsevier Churchill Livingstone;2005. p. 2538.
Olsson GL, Hallen B. Laryngospasm during anesthesia. A computeraided incidence
study in 136 929 patients Acta Anaesthesiol Scand 1984; 28:567575 study in 136,929 patients. Acta Anaesthesiol Scand 1984; 28:567 575.
Tait AR, Pandit UA, VoepelLewis T, et al.Use of the laryngeal mask airway in
children with upper respiratory tract infections: a comparison with endotracheal
intubation. Anesth Analg 1998; 86:706711.
Olsson GL. Bronchospasm during anaesthesia. A computeraided incidence study
of 136,929 patients. Acta Anaesthesiol Scand 1987; 31: 24452.
Pepe PE, Marini JJ. Occult positive endexpiratory pressure in mechanically
ventilated patients with airflow obstruction: the auto PEEP effect. Rev Respir Dis
1982; 126: 16670.
Westhorpe RN, Ludbrook GL, Helps SC. Crisis management during anaesthesia:
bronchospasm. Qual Saf Health Care 2005; 14: e7.
ToSucceedinlife,youneedtwo
things:ignoranceandconfidence
MarkTwain
1
LOCAL ANAESTHESIA OF THE
AIRWAY FOR AWAKE
PROCEDURES Laryngoscopy,
SGD Insertion, Endotracheal
Intubation ..
Prof. Anju R. Bhalotra
LA OF THE DIFFICULT AIRWAY
2 main indications
To perform an awake intubation
To topicalise the airway even if GA is
required - to obtund cardiovascular & airway
responses and maintain the patient in a
li ht l f th i
lighter plane of anaesthesia
Others ..
Fibreoptic Bronchoscopy
Transesophageal Echocardiography
ICU Patients to tolerate ETT
PATIENT PREPARATION
PSYCHOLOGICAL PREPARATION
PHARMACOLOGICAL PREPARATION
- Antisialogogues
- Nasal decongestion
- Sedation
PREOPERATIVE VISIT- develop rapport and explain
reasons & procedure; Reassure
Patient cooperation is vital to the success of the
procedure
DRY THE AIRWAY Antisialogogues
Wellintime
Secretions in the airway
* prevent LAs reaching intended areas
* dilute/wash away LAs
* induce repeated swallowing of LA
induce repeated swallowing of LA
* obscure view
Present with cotton dry mouth
Inj. Glycopyrrolate 0,2-0.4 mg iv/im
Inj. Atropine 0.5-1 mg iv/im
NASAL DECONGESTION
Imperative if contemplating using the nasal
route
To cause mucosal vasoconstriction to;
- limit bleeding
- improve visualisation
p
- prolong duration of action of LAs
Various drugs used
- cocaine
- epinephrine with lignocaine
- phenylephrine (0.25%)
- oxymetazoline (0.05%-0.1%)
Basic Preparation for Difficult
Airway Management*
(1) Availability of equipment for management of a
difficult airway
(2) Informing the patient
(3) Assigning an individual to provide assistance
( ) h k
(4) Preanesthetic preoxygenation by mask
(5) Administration of supplemental oxygen
throughout the process of difficult airway
management
*Practice Guidelines for Management of the Difficult Airway. An Updated
Report by the American Society of Anesthesiologists Task Force on Management
of the Difficult Airway. Anesthesiology, V 118 No 2. February 2013
2
Once in the OT
Monitoring
Intravenous access
O l t ti
Oxygen supplementation
SEDATION
Degree of sedation should be inversely proportional to the
difficulty of the airway
- Benzodiazepenes, narcotics, dexmedetomidine
Titrate to end point of asleep if unstimulated but
responsive to commands
Minimise respiratory depression
p y p
Maintain spontaneous respiration
Lessen likelihood of aspiration
Maintain lower oesophageal sphincter tone
Allow early detection of LA toxicity
Ensure patient cooperation
Maintain ability to take deep breaths on command which
helps align the vocal cords, larynx and fiberscope.
- ORAL ROUTE
- NASAL ROUTE
Each route has a
well-defined
MAKE A PLAN
III
IX
well defined
pattern of
innervation that
needs to be
specifically
blocked
X
- Spraying or swishing of
LA directly onto the
mucosa
- Inhalation;nebulization/
atomizer
- LA Reservoirs ; LA-
soaked cotton pledgets /
swabs
Glossopharyngeal
Superior laryngeal
Transtracheal
TOPICALISATION NERVE BLOCKS
swabs
- Spraying via working
channel of FOB
Nerve blocks - technically difficult; painful;
misplacement of needle - intravascular injection of
LA; bleeding, haematoma; nerve damage, C/I if
local infection, distorted anatomy, coagulopathy
etc
Topical Anaesthesia
Inhalation techniques
- Nebulisation of LA
- Use of atomisers
Topicalisation of ; p
- Nasal mucosa nasopharynx
- Oropharynx
- Supraglottic area
- Infraglottic area
NEBULISATION
Can topicalise entire respiratory tract
Particles rain out depending on size
Particle size Site of deposition
> 100 mouth/pharynx
> 60 trachea/mainstem bronchi
30-60 larger bronchi
10-30 smaller bronchi
< 3 alveoli
3
INHALATION TECHNIQUES
Atomisers
Nebulisation
Delivers particles
about 5 size
Atomisers-oral
Atomisers
Mucosal Atomisation Device MAD deliver
medication in a fine mist ; Typical
particle size: 30-100
Nasal
The MADgic laryngo-tracheal MAD device consists
of a small atomizing tip at the end of an 8.5 long
flexible applicator used for dispensing topical
medications to the nose, mouth, throat,
hypopharynx, larynx and trachea in a fine, gentle
mist.
Typical particle size: 30-100 microns
NEBULISATION DOSES*
Patient weight vol/conc. of lignocaine
< 10 kg Upto 3 ml 1%
10-20 kg Upto 3 ml 2%
g p 3
20-30 kg Upto 3 ml 3%
> 30 kg Upto 5 ml 4%
* Steve M Anden. Flexible fibreoptic laryngoscopy in the paediatric
patient. Anaesthesiology Clinics of N America , 16; 763-793; 1998
TOPICAL ANAESTHESIA
Further topical anaesthesia can be
supplemented along the air passages as
and where required
Nasal mucosa
Nasal mucosa
Tongue & Oropharynx
Supraglottic
Infraglottic
ANAESTHESIA - NASAL MUCOSA
Suppliedbybranchesoftrigeminalnerve
Topical
Prior vasoconstriction in all
Several techniques described
Nasal packing
Nasal instillation
Nasal spray/ atomiser
Nasal gel
Nasal applicators
Nasal dilatation
NASAL PACKING
A special ENT packing
forceps is used to pack the
nasal cavity with LA solution
soaked ribbon gauze
The pack should be left in
situ for at least 10-15
minutes for an optimum minutes for an optimum
effect
Can gauge the size of the
nostrils
NASAL INSTILLTION of LA solution
NASAL JELLY
NASAL SPRAY 2 -3 metered doses/nostril
4
COTTON TIPPED APPLICATORS
Soaked in LA can be inserted into the nostrils
One is inserted along the floor of the nose to reach
the nasopharynx.
Second is inserted parallel to the line of the external
nose to reach the superior extent of the nasal cavity
Third is inserted at an angle of 20 to the floor of the
nose to reach the sphenopalatine foramen
the angle of ET insertion can be predicted
- the angle of ET insertion can be predicted
- Dilation of the nasal cavity achieved
The passage of these 3 applicators held tightly
together indicates that a 7.5 mm ETT should pass
through that nostril easily
NASAL DILATATION using
progressively larger NPAs or a lubricated
gloved finger
Gargling
Spray
ANAESTHESIA OF TONGUE/OROPHARYNX
(Supplied by branches of IX nerve)
p y
Ointment /Gel / EMLA cream/ lidocaine
Lollipop/ Toothpaste method
Glossopharyngeal nerve block- rarely required,
to block deep pressure receptors at tongue
base
GARGLING
4-6 ml of 2 or 4% xylocaine viscous
This is done 2-3 times and any excess should be
spat out
The posterior pharyngeal wall may not be reached
as the isthmus of the oropharynx closes during
gargling
ORAL SPRAY
A lignocaine metered spray may be sprayed in the
oropharynx
For adequate topicalisation of the oropharynx, 10-15
metered doses may be required
OINTMENT/GEL/EMLA/
LIDOCAINE LOLLIPOP
Paste onto lingual surface of oropharyngeal
airway / tongue depressoranaesthetizes, melts & trickles
and is aspirated
TOOTHPASTE METHOD
Ointment is squeezed in 1 or 2 lines along the length of
tongue; melts at body temp. trickles down
Oropharyngeal anaesthesia is followed by
anaesthesia of supraglottic structures and
maybe glottis
DrummondJC.Airwayanesthesia:thetoothpastemethod.CanJAnaesth 2000;47:
94.
ANAESTHESIA-SUPRAGLOTTIC
& INFRAGLOTTIC
Sup laryngeal N
Rec Laryngeal N
SUPRAGLOTTIC
ANAESTHESIA (SLN)
INFRAGLOTTIC
ANAESTHESIA ( RLN)
10 % spray
10 % spray through NPA
Spray LTA kit/SAYGO
Aspiration techniques,
Spray-LTA kit/SAYGO
Aspiration techniques, p q
Toothpaste method
I/ L Instillation method
p q
Toothpaste method
I/ L-Instillation method
SLNB - External/ internal Translaryngeal
anaesthesia
5
Direct spraying using ..
LTA (Laryngotracheal Anaesthesia ) kit
Consists of a curved plastic
cannula with multiple perforatons
attached to a prefilled syringe
Laryngotracheal MAD
Indirect laryngoscopy-Instillation technique
described by Fry. Visualize glottis with light and mirror and apply
LA to glottis with a curved cannula under indirect visualization
via mirror
(Fry WA. Techniques of topical anesthesia for bronchoscopy. Chest 1978; 73(Suppl):
694-6)
ASPIRATION METHOD
After oral topicalisation,
tongue is pulled forward
Lidocaine (20cc max) slowly
trickled onto posterior
tongue g
Once swallowing subsides,
lidocaine flows past
arytenoids and into
trachea
Chung DC, et. al. Canadian Journal of Anesthesia, 1999;46:215-219
SPRAY AS YOU GO (SAYGO)
Instill LA through working
channel of FOB
Use 1cc of LA and 9cc of
air
Triple stopcock; Oxygen
set to flow at 2 to 4 L/min.
Spray with aliquots of 0 2 Spray with aliquots of 0.2
to 1.0 mL of 2% to 4%
lidocaine
Can use long angiographic /
epidural catheters for
accuracy
Once vocal cords are
judged anaesthetised -go
beyond and inject
additional aliquots
Clamp or kink suction tubing during
injection
Avoid suctioning immediately after
injection
Accurate delivery of LA possible
Nerve Blocks of the Airway
1. Glossopharyngeal nerve block
2. Superior Laryngeal Nerve block
3. Transtracheal anaesthesia
Glossopharyngeal Nerve Block
Anaesthesia of the mucosa of the pharynx and soft
palate
To eliminate the gag reflex when pressure is applied
to the posterior 1/3 of the tongue.
The gag reflex arises from the stimulation of
s b s l d ss t s t th b s f
submucosal deep pressure receptors at the base of
the tongue which are not easily reached by diffusion
of LAs through the mucosa
Indications - if topicalisation is inadequate
- where direct laryngoscopy is required
External or peristyloid and internal approach
In both there is proximity to ICA ASPIRATE!
Internal approach
Patient should be able to open mouth wide
After anaesthesia of the tongue,
the patient sits up and faces anaesthetist
He opens his mouth as wide as possible &
the tongue is retracted medially
The base of the palatopharyngeal arch is
identified and a 25G spinal needle with the distal shaft bent at an
angle of 45 is used to inject 3-5 ml of 1-2% lignocaine at the base
of the posterior tonsillar pillar
Repeated on the opposite side
Alternatively, a LA soaked gauze may be firmly applied in the same
area using a right angled forceps
6
External approach
The patient lies supine with the
head in the neutral position
The angle of the mandible and the tip of the
mastoid process are identified and a line is drawn
between them
At the midpoint of that line, a needle is inserted
perpendicular to the skin to contact the styloid
process
The needle is then withdrawn and redirected
posteriorly. As soon as bony contact is lost, 5-7
ml of LA is injected following negative aspiration
This is repeated on the opposite side
a
Superior Laryngeal Nerve Block
Landmarks for SLN block;
a. Cornu of the Hyoid
b. Cornu of the Thyroid
c. Thyroid Notch
Successful block is indicated by the development of a hoarse
voice.
SLNB Internal Approach
Pledgets soaked in LA solution are
placed in the pyriform fossa using a
curved forceps such as a Krause forcep or even a Magill
forcep f p
They must be kept there for 3-5 minutes on each side
The position can be checked by palpating the neck
lateral to the thyroid cartilage for a bulge
Successful block is indicated by the development of a hoarse
voice.
TRANSLARYNGEAL ANAESTHESIA
Patient lies supine with neck extended
The cricothyroid membrane is
identified
A small intradermal wheal is raised
while the trachea is stabilized by
h ldi th th id til holding the thyroid cartilage.
A 20 G catheter over needle assembly
is introduced into the cricothyroid
membrane in the midline while aspirating
for air.
Once air is aspirated, the cannula is advanced into the
trachea & 2 ml of 2-4 % lignocaine is injected at the end
of a normal expiration.
Direct Laryngoscopy And Intubation
LA of oropharyngeal mucosa-
Gargling, Spray, Ointment /Gel /
EMLA cream/ lidocaine Lollipop/
Toothpaste method
Glossopharyngeal nerve block may be
I
N
H
A
L
Glossopharyngeal nerve block- may be
required to block deep pressure receptors
LA supraglottic & infraglottic
10 % spray, LTA kit, MAD,
Aspiration techniques, SLNB,
Translaryngeal anaesthesia
L
A
T
I
O
N
Videolaryngoscopy
Use of a Glidescope video laryngoscope with an
anatomically shaped blade creates less pressure on
the tongue when compared with the Macintosh blade*
Topicalisation usually adequate
Glossopharyngeal nerve may be required in those
patients who have a strong gag reflex**
Supra & infraglottic anaesthesia can be supplemented Supra & infraglottic anaesthesia can be supplemented
under direct view
After topicalisation a quick view can be taken using a
VL to decide further course of action
*Russell T, et al : A comparison of the forces applied to a manikin during laryngoscopy with the
GlideScope and Macintosh laryngoscopes. Anaesth Intensive Care 2011; 39:1098102
*Carassiti M, et al : Force and pressure distribution using Macintosh and GlideScope
laryngoscopes in normal and difficult airways: A manikin study. Br J Anaesth 2012; 108:14651
**Moore et al. Awake videolaryngoscopy-assisted tracheal intubation of the morbidly obese.
Anaesthesia 2012, 67, 232235
7
SGD placement
LA of oropharyngeal mucosa-
Gargling, Spray, Ointment /Gel / EMLA cream/
lidocaine Lollipop/ Toothpaste method
LA of supraglottic structures
10 % spray, LTA kit, MAD, Aspiration techniques,
SLNB
I
N
H
A
L
A
T
SLNB
If planning intubation through the SGD SAYGO
for infraglottic anaesthesia
I
O
N
Fibreoptic Intubation
ORAL NASAL
LA of oropharynx LA nasal mucosa
Gargling, Spray, Ointment / Nasal packing, instillation,
Gel / EMLA cream/ lidocaine spray/ atomizer, gel,
Lollipop/ Toothpaste method applicators, dilatation
I
N
H
A
L
A
LA supraglottic/infraglottic
SAYGO
10 % spray, LTA kit, MAD, Aspiration techniques,
SLNB, Translaryngeal anaesthesia
A
T
I
O
N
COMPLICATIONS
1. LA toxicity
2. Aspiration of GI contents
3. Complete airway obstruction
4 C hi t sl l
4. Coughing -- translaryngeal
5. Haematoma Associated with
6. Infection nerve blocks
7. Trauma
LOCAL ANAESTHETIC TOXICITY
National Center for Patient Safety ***A reasonable
dose that is safe for topical lidocaine is 4 mg/kg.
(Doses as high as 7 mg/kg may be considered safe if a
topical vasoconstrictor (oxymetazoline) is applied prior
or simultaneously to lidocaine.)
*** A guidance on the Use of Topical Anesthetic for Naso/oropharyngeal and Laryngotracheal
procedures. National Center for Patient Safety 2006
B iti h Th i S i t G id li ** t t l d
British Thoracic Society Guidelines ** - total dose
should be limited to 8.2 mg/kg with extra care in elderly
or liver/ cardiac impairment
**Honeybourne D. British Thoracic Society Guidelines on diagnostic flexible bronchoscopy.
Thorax 2001; 56;i1-i21
Use of 9.3 mg/kg lignocaine*- No toxicity
*Efthimiou J, Higenboltan T, Holt D, Cichrane GM. Plasma concentrations of lignocaine during
fibreoptic bronchoscopy. Thorax, 37:68-71,1982
ASPIRATION OF GI CONTENTS
After topical anaesthesia larynx is no longer awake
No translaryngeal anaesthesia ? SLNB?
Ovassapian* 1989 - 129 patients, no aspiration. Apply LA
through fiberscope
SAYGO- especially useful in patients at risk for
p y p
aspirating gastric contents because the topical
anesthetic is applied only seconds before the intubation
is accomplished and allows the patient to maintain his or
her airway reflexes as long as possible.
*Ovassapian A, Krejcie TC, Yelich SJ, Dykes MHM. Awake
fibreoptic intubation in the patients at high risk of aspiration.
BJA, 62:13-16,1989.
UPPER AIRWAY OBSTRUCTION
Decrease in upper airway caliber
Depression of laryngeal ms and normal laryngeal
function
Interference with activity of specific receptors
in upper airway loss of the normally in upper airway loss of the normally
coordinated opposition to the tendency of the
upper airway mucosa to collapse on inspiration
8
Administration of LA should be performed with
accuracy to ensure that a predetermined amount of
drug is administered to allow for the intended effect
while minimizing the risk of toxicity
Topical anesthesia of nasal or oral mucosa along with a
method to anesthetize the laryngeal/ tracheal
structures is the most effective and commonly chosen
CONCLUSION
y
plan
Nebulisation, SAYGO
Nerve blocks limited by anatomy, require practice
Individualize plan based on patient variables
Back-up plans
1
In August 1898,a German surgeon, injected
cocaine 1015 mg into the subarachnoid space of
seven patients, himself and his assistant.
Six out of nine of them described the symptoms
associated with postdural puncture headache.
The surgeon surmised that the headache was
attributable to loss of CSF.
Who was the Surgeon?
Karl August Bier
Develops within 5 days after dural puncture
Worsens within 15 minutes after sitting or standing
and improves within 15 minutes after lying, with
Atleast one of the following
Neck stiffness photophobia tinnitus Neck stiffness photophobia tinnitus
Hypoacusia nausea
Resolves either
1. spontaneously within 1 week
2. within 48 hours after effective treatment of the
spinal fluid leak(usually by epidural blood patch)
Dura Mater:
Foramen Magnum to S2
Collagen and elastic fibers
probably not in a longitudinal
orientation- laminar Reina MA orientation- laminar. Reina MA,
et al. (2000)
CSF:
500ml/day or 20 ml/hr
150 ml total in space: 20-75 ml
in Lumbar-sacral sac
10% loss=> orthostatic HA
Puncture of the dura excessive
leakage of CSF intracranial
hypotension reduction in CSF
volume
Rate of CSF loss - 0.084
1
4.5 ml s
1
rate of CSF
production - 0.35 ml min
1
,
(particularly with needle sizes larger
than 25G.)
Adult subarachnoid pressure of
515 cm H
2
0 is reduced to
4.0 cm H
2
0 or less.
2
TRACTION on pain sensitive intracranial
structures and cranial nerves in the upright
position.
Cervical: C1-3 stretch: neck & shoulder
pain p
Cranial: especially CN III VII
REFLEX VASODILATION- the loss of CSF
produces a compensatory venodilatation
visvis the MonroKellie doctrine.
Monroe-Kellie Doctrine?
ONSET
< 48 hrs - 66%
< 3 days - 90%
5 and 14 days Rarely
CHARACTER: severe, throbbing and
distributed over frontal and occipital
areas radiating to the neck and
shoulders.
Postural nature of the pain is hallmark.
RESOLUTION
72% of headaches resolve within 7 days
87% resolve in 6 months.
In a minority of patients the headache can
persist as long as 18 yr after dural puncture
Cranial Nerve Palsy
Diplopia and other visual disturbances : abducens and
oculomotor.
Tinnitus/ Vertigo: vestibulocochlear dysfunction
Paraesthesia
Hearing loss
Seizures
Subdural hematoma due to downward stretching
on dura.
H/O accidental or deliberate dural puncture
symptoms of a postural headache, neckache.
spinal source of the CSF leak
CT myelography,
retrograde radionuclide myelography retrograde radionuclide myelography,
cisternography,
thin section MRI
MRI Brain - Meningeal enhancement,subdural fluid
collection,engorgement of cerebral venous
sinuses,prominence of spinal epidural venous
plexus,enlargement of pituitary gland
3
Intracranial tumours
Intracranial haematoma
Pituitary apoplexy
Cerebral venous thrombosis Cerebral venous thrombosis
Migraine
Chemical or infective meningitis,
Nonspecific headache
MILD PDPH ( VAS Score1-3):
little interference with daily activity , not confined to bed,
no associated symptoms
MODERATE PDPH ( VAS Score 4-7):
i t f ith d il ti it fi d t b d f some interference with daily activity, confined to bed for
part of day, associated symptoms present.
SEVERE PDPH (VAS Score 8-10):
Bedridden, unable or unwilling to stand, associated
symptoms always present.
PATIENT RELATED NEEDLE RELATED
Age ( younger>
older)
Sex (female > male)
Diameter
(larger>smaller)
Needletip(cutting>nonc
utting)
Obstetric patients
utting)
Direction of bevel
insertion(perpendicular
>parallel)
Angle of insertion
(midline>paramedian)
LOR technique with
air> saline
Older subjects have less incidence of PDPH.
Decreased A delta and c- fibre function.
Attenuated central sensitization.
Elevated pain threshold.
sensitivity to low intensity noxious stimuli
? Decreased elasticity of dural fibers
? Decreased reactivity of cerebral vessels
Uncommon in children
? Low CSF pressure
? Low reporting rate
High risk of dural puncture and the subsequent
headache because
sex,
young age,
widespread application of epidural anaesthesia
Incidence of dural puncture is between 0 and
2.6%.
Consider differential diagnosis, as intracranial
haematoma or tumour presenting with similar
symptoms
Large diameter needle produce larger hole.
Balance between the risks of dural puncture
headache and technical failure.
25G 26G d 27G dl b bl 25G, 26G and 27G needles probably
represent the optimum needle size for spinal
anaesthesia.
For the purposes of diagnostic CSF tap, 22G
needles are the smallest practical needles.
4
1900s Quincke
1951 Whitacre -diamond tip PENCIL TIP
1987 Sprotte - conical tip
Less incidence of PDPH with pencil point
needles.
Initial studies proposed pencil tip
needles separate dural fibres. Greene
HM JAMA(1926)
Reduction in PDPH incidence not
attributed to hole size nor shape attributed to hole size nor shape.
Pencil Point causes more traumatic
dural rent than Quincke resulting in
inflammatory reaction. Reina MA, et.al.
(2000)
Postulated that the tear causes an
edematous plug preventing CSF leak.
PDPH from Pencil Point needles require less
Epidural Blood Patches than those associated
with Quincke needles.
Needle Type Gauge Incidence of PDPH
Quincke 20 16%
Quincke 22 10%
Quincke 24 6%
Quincke 25 6%
Quincke 27 1.5%
Pencil Point 22 1.6%
Incidence of PDPH (based on Review of literature
and data from Choi)
Tuohy 18 52.5%
PARALLEL PERPENDICULAR
Quincke needle produces clean cut U shaped
lesions
Electron microscopy shows no difference in
size/type of lesions Ready LB, et.al. (2004)
5
Median vs. Paramedian
Midline insertion produces tin lid
flap unimpeded CSF flow.
Paramedian approach produces a
more lateral lesion with overlapping
dural flap than a posterior midline
lesion upon lumbar
flexion/extension Ready (1989)
Presence of air in subarachnoid space/
pneumocephalus is an independent risk factor.
L f R i t t h i ith i li Loss of Resistance technique with air vs saline
has shown increased incidence of PDPH in air
group.
Aida S, et al (1998)
CONSERVATIVE INVASIVE
Analgesics ( NSAIDs,
Opioids)
Epidural Blood Patch
( 15-30 ml of
Hydration
Bed Rest
Methylxanthine ( e.g.
caffeine)
ACTH analogues
(
autologus blood)
Other Epidural
injection (e.g. saline,
dextran, fibrin glue)
ANALGESICS
Paracetamol, non-steroidal anti-inflammatory drugs,
opioids, and antiemetics may control the symptoms
POSITION
Bedrest ?
Prone preferable as abdominal compression
increases epidural venous pressure thus decreasing
CSF leak.
Any position which is comfortable.
HYDRATION
Increasing oral fluid intake has not shown to
decrease the incidence of PDPH.
CAFFEINE
ROUTE
Oral
Tablet
peak levels - 30 min.
T1/2 3 7 5h T1/2 3-7.5hrs
Beverages
One cup coffee 50-100mg
Cold drink 35-50mg
Intravenous - caffeine sodium benzoate.
DOSE - 300-500mg once or twice daily
6
MECHANISM
cerebral vasoconstriction
Blocking central adenosine receptors
ADVERSE EFFECTS
CNS toxicity
t i l fib ill ti atrial fibrillation
AMINOPHYLLINE
5-6 mg/kg intravenous over 20 min.
THEOPHYLLINE
300 mg orally every 6-8 h.
Cosyntropin is an ACTH analog that is less
antigenic
MECHANISM
increases CSF production through a sodium active
transport mechanism.
increasing beta-endorphins in the CNS -increase in the
pain threshold.
Stimulates adrenal cortex
activates adenyl cyclase with increase in intracellular
cAMP.
DOSE
The dose is 0.25-0.75 mg IV.
SIDE EFFECTS
mood elevation and
anti-inflammatory effects
5HT
1D
receptor agonist that promotes cerebral
vasoconstriction
only a few case reports where sumatriptan was
used successfully used successfully
a recent RCT found no evidence of benefit from
Sumatriptan for the conservative management
of postdural puncture headache.
GABAPENTIN AND PREGABALIN
Recent RCT shows better results when
compared with placebo
HYDROCORTISONE
H d ti ith ti l t t t Hydrocortisone with conventional treatment
more effective than conventional treatment
alone
HISTORY:
1960 Gormley observed that bloody taps were
associated with a reduced headache rate
TECHNIQUE:
Lateral position
Tuohy needle at same or lower intervertertebral space
2-30 ml of autologus blood is aspirated and injected
until backache or leg pain
the patient asked to lie still for one or 2h and then
allowed to walk
7
MECHANISM:
Immediate Relief within 30-60min
Mass effect increased lumbar intrathecal
pressure shifting of CSF cephalad to
decrease tension on pain producing structure
Reactive cerebral vasoconstriction
Long term relief
sealant effect due to fibroblastic activity and
collagen deposition
No conclusive evidence for preventive effect of
EBP
SIDE EFFECTS
low back pain
aseptic meningitis
lumbovertebral syndrome
radicular pain
bradycardia
f
CONTRAINDICATIONS
presence of fever
infection on back
coagulopathy
patient refusal are
fever
seizures
Success rates have been reported as 90%
after first EBP and 96% after second EBP.
MECHANISM:
Thecal compression raising the CSF pressure
Regimens :
1.01.5 litre of epidural Hartmanns solution over 24 h
35 l h
1
f id l li H t l ti f 24 35 ml h
1
of epidural saline or Hartmanns solution for 24
48 h;
a single 30 ml bolus of epidural saline
10120 ml of saline injected as a bolus via the caudal
epidural space
ADVERSE EFFECT
intraocular haemorrhages through a precipitous
rise in intracranial pressure.
Epidural Blood Patch Vs Epidural Saline: Epidural Blood Patch Vs Epidural Saline:
no studies demonstrate sustained rise in CSF
pressure or accelerated closure of the dural
perforation with epidural saline
No longterm efficacy of epidural saline
placement
Used when medical therapy and multiple EBPs
have failed.
Preparation of pooled human plasma obtained
from plasmapheresis from plasmapheresis.
Mixture forms a gel with high tensile strength
that tolerates moist environments.
Risks include a potential for viral transmission.
A 25 yr old primigravida in
labor at 38 wk gestation
requested for labor
analgesia. Continuous
epidural analgesia was
planned A second yr planned. A second yr
anaesthesia resident
performed the epidural
technique which resulted in
a situation like this.
EPIDURAL WET TAP
8
Injection of CSF from the epidural syringe back
into the subarachnoid space
Insertion of an epidural catheter into the
subarachnoid space
Administration of continuous intrathecal labor
analgesia
Leaving the intrathecal catheter in situ for a total of
12 to 20 hours
Injection of preservative-free normal saline
through the intrathecal catheter before its removal
Epidural morphine decreases incidence of PDPH
Intravenous cosyntropin and aminophylline can be
used for prophylaxis used for prophylaxis.
Prophylactic EBP is controversial.
Epidural and spinal morphine proved to be
effective.
Intravenous aminophylline and intravenous Intravenous aminophylline and intravenous
cosyntropin also prevent PDPH
The other interventions spinal fentanyl, oral
caffeine, and intravenous dexamethasone did not
show conclusive evidence of effectiveness.
Caffeine has shown effectiveness for treating
PDPH
Gabapentin theophylline and hydrocortisone have Gabapentin, theophylline and hydrocortisone have
also shown a decrease in pain severity scores
There is a lack of conclusive evidence for the
other drugs assessed (sumatriptan and ACTH)
OB Epidural Wet tap PDPH incidence ~76%
115 Unintentional epidural wet tap obstetric
patients at Cleveland Clinic divided into 3
groups: n=115
A Epidural catheter reinserted different level
B Epidural catheter inserted subarachnoid &
removed immediately after delivery
C Epidural catheter inserted subarachnoid &
removed 24 hours after delivery
Ayad S, et.al. (2003)
A 30-year-old primigravida woman.
spinal anaesthesia for an elective caesarean
section.
uneventful surgery and had a healthy baby boy.
day 2 post delivery she developed a fronto-
occipital headache with postural characteristics.
associated nausea, vomiting and photophobia.
9
Bilateral headaches that develop within 5 days
after a lumbar puncture and disappear within 1
week spontaneously or 48 hrs after effective week spontaneously or 48 hrs after effective
treatment of spinal fluid leak. The headache
worsens within 15 min of resuming the upright
position, disappears or improves within 15 min of
resuming the recumbent position.
1
Peri PerioperativeFluid operativeFluid
Management Management
Prof. Prof.Mridula Mridula Pawar Pawar
Case1
25yrsyoungmaleforfixationoffracturebothbones
rightarm
Case2
65yrsoldmaleforhasCAsigmoidcolonpostedfor
APR,HasIHD ,
Case3
1yroldbaby,hasinguinalhernia,postedfor
herniotomy
Case4
35yrsfemale,diagnosedasAPH,foremergencyLSCS
FluidTherapyisEmpirical
ClinicalexperienceisMakingsamemistakes
withincreasingconfidenceoveranimpressive
numberofyears. MichaelODonnell
Tachycardia hypotention Rush fluids Tachycardia,hypotention Rushfluids
Controversies
Colloidarebetter/notbetterthanISS
LiberalVsRestrictedfluids.
Peri Peri operativeFluids operativeFluids
WhyNeedoffluids&Whatisthepurpose
Revisethephysiologyoffluiddistribution
Factorsinfluencingfluidtherapy
Howmuchfluid
Whattypeoffluid
Whentoinfuse
WhydoweneedFluids WhydoweneedFluids? ?
Toexcrete thesolutesand
endproductofmetabolism
Tomaintaincellularfunction and
energyproduction
Distribution of Body Fluid
Total Body Water, 60% of B W
Intracellural 40% Extracellular 20% Extracellular 20%
Interstitial 15% Interstitial 15% Plasma Vol 5%
2
Interstitial comp Interstitial comp
15% 15%
Intracellular Comp 40 % Intracellular Comp 40 %
I V 5% I V 5%
volume volume
capacity capacity
osmotic properties osmotic properties
GoalsofFluidAdministration
O2delivery/bloodflow perfusion
O2utilization
Metabolism,excretionofwaste
Maintaindistribution,composition
offluid&Electrolytes
ElectrolyteCompositionofBodyFluids ElectrolyteCompositionofBodyFluids
Plasma
(mEq/L)
Intracellular
Fluid
(mEq/L)
Extracellular
Fluid
(mEq/L)
Sodium 142 10 140 Sodium 142 10 140
Potassium 4 150 4.5
Magnesium 2 40 2
Chloride 103 103 117
Bicarbonate 25 7 28
calcium 5 1 5
Oxygen Oxygen
RBC RBC
Intravascular Intravascular
volume volume
Intracellular Intracellular
fl id fl id
Capillary Capillary
fluid fluid
Interstitial Interstitial
Fluid Fluid
Criticaloxygendelivery(DO
2
):abovethisvalue,VO
2
isindependentofDO
2
.Belowthis
value,VO
2
becomesDO
2
dependentandextractioncapacitiesarenolongersufficient.
Theanaerobicpathwayisactivatedresultinginlacticacidproduction.
vigorous fluid loading and inotropic
agents by increasing DO
2
to
supraphysiologic levels, cellular
metabolism could be maintained in an
aerobic state
ShoemakerWC, Appel PL, Kram HB, etal: Chest 1988; 94:1176. , pp , , ;
Two large, randomized trials showed
this therapy to be ineffective and
potentially dangerous
HayesMA, TimminsAC, Yau E, etal: NEngl JMed 1994; 330:1712.
Gattinoni L, Brazzi L, PelosiP, etal: NEngl JMed 1995; 333:1025.
Early and late shock
3
O2Delivery
DO2~QxCaO2
CaO2~SaO2, CO,Hgb
CO~SVxHR
SV~preload, afterload,contractility
FINDtheCAUSEandTREAT
MaximizingCO
SlopeofcurveisEF
Goodventriclesare
preload dependent
Poor ventricles are
Frank Starling Curves
Poor ventriclesare
afterload dependent
(notpreload
dependent)
ForLowSV/CO
GoodLVfunction>givefluid
PoorLVfunction>Inotropes
d l Vasodilators
Diuretics
Distribution of fluid throughout the body Distribution of fluid throughout the body
compartments is represented by the Starling compartments is represented by the Starling- -
Landis equation: Landis equation:
JJ
vv
= = K K
hh
A ([P A ([P
CC
P P
IF IF
] [COP ] [COP
CC
COP COP
IF IF
]) ])
The hydrostatic and colloid pressure e yd ostat c a d co o d p essu e
differences across capillary walls (i.e., Starling
forces) cause movement of water and dissolved
solutes into the interstitial spaces
The endothelium The endothelium
is is
a a highly dynamic cell layer highly dynamic cell layer
that is involved in that is involved in
A multitude of physiological functions A multitude of physiological functions
including including including including
control of vascular tone control of vascular tone
movement of cells and nutrients movement of cells and nutrients
maintenance of blood fluidity and maintenance of blood fluidity and
growth of new vessels growth of new vessels
4
Electron microscopic view of the endothelial Electron microscopic view of the endothelial glycocalyx glycocalyx
StarlingEquation
IVvolconsistsofplasma
andcellularelements
Fluidisfilteredfromtheart
endofcap.andabsorbed
fromtheven.end.
RaisingplasmaCOP
RevisedStarlingEquation
IVvolconsistsofglycocalyx
vol,plasmavol,andRBC
distributionvol.
Jvis<thanpredictedby
Starlingsprinciple,andthe
majorrouteforreturntothe
i l ti i l h
enhancesabsorptionand
shiftsfluidfromISFto
plasma
circulationisaslymph
RaisingplasmaCOPreduces
Jvbutdoesnotcause
absorption
RevisedstarlingEquation
Atsupranormalcapillarypressure,infusionof
colloidsolutionpreservesplasmaCOP,raises
capillarypressure,andincreasesJv
Atsupranormalcapillarypressure,infusionofISS
also raises capillary pressure but it lowers COP alsoraisescapillarypressure,butitlowersCOP
andsoincreasesJvmorethanthesamecolloid
solutionvolume
Atsubnormalcapillarypressure,infusionof
colloidsolutionincreasesplasmavolumeand
infusionofISSincreasesintravascularvolume,but
Jvremainsclosetozeroinbothcases
RevisedStarlingEquation
Initscurrentform,itstrengthenstheargumentsfor
preferringISSsoverplasmaorplasmasubstitutesfor
resuscitation,butacceptsarationaluseofcolloids
foreuvolaemicorhypervolaemichaemodilution.
Theuseofplasmaorplasmasubstitutestoachievea
sustainedsupranormalplasmavolumeortoreduce
tissueoedemaisnotrational.
Starlingequationandglycocalyxmodelparadigm
needtoberefinedinthelightofphysiologyand
clinicaltrialevidence
Factorsaffectingtheendothelial
glycocalyx
Degradation
Ischaemia/reperfusion
Protection
Sevoflurane
Hypoxia/reoxygenation
Inflammatorycytokines
proteases
Atrialnatriureticpeptide
Hydrocortisone
Antithrombin
5
TissueOxygenationParameterstoGuideFluidTherapy
BenoitVallet,MD,PhD;EmmanuelFutier,MD;EmmanuelRobin,MD,PhD
TransfusionAlterTransfusionMed. 2010;11(3):
Goal Goal--directed therapy with ScvO2 directed therapy with ScvO2- -P(cv P(cv--a)CO2 a)CO2--SVV guided treatment protocol SVV guided treatment protocol
(SVV is stroke volume variation, an index of preload (SVV is stroke volume variation, an index of preload--dependency and fluid dependency and fluid
responsiveness when larger than 12%). responsiveness when larger than 12%).
UseofCentralVenous UseofCentralVenousto toarterialCarbonDioxide arterialCarbonDioxide
DifferencetoAddressAdequacyofOxygenUtilization DifferencetoAddressAdequacyofOxygenUtilization
Asasurrogatefortissueperfusionassessment
PresenceofaP(cva)CO
2
>6mmHgwasassociated
with the largest lactate value and might have been a withthelargestlactatevalueandmighthavebeena
usefultooltoidentifypatientswhoremained
inadequatelyresuscitateddespitea70%ScvO
2
goal
beingreached
'Static'MeasuresofIntravascularVolume
Clinicalparameters
TheCentralVenousPressure
PulmonaryArteryOcclusionPressure
LeftVentricularEnddiastolicArea
InferiorVenaCavalDiameter
DynamicIndicesofIntravascularVolume DynamicIndicesofIntravascularVolume
Pulsepressurevariation(PPV)derivedfrom Pulsepressurevariation(PPV)derivedfrom
analysisofthearterialwaveform, analysisofthearterialwaveform,
Strokevolumevariation(SVV)derivedfrom Strokevolumevariation(SVV)derivedfrom
pulse contour analysis pulse contour analysis pulsecontouranalysis pulsecontouranalysis
DynamicChangesinAorticFlow DynamicChangesinAorticFlow
Velocity/StokeVolumeAssessedby Velocity/StokeVolumeAssessedby
Echocardiography Echocardiography
PositivePressureVentilationInducedChanges PositivePressureVentilationInducedChanges
inVena inVenaCaval Caval Diameter Diameter
Ananalysisofmorethan12000patients
showedthatdynamicparametersareusable
in39%ofallsurgicalpatients,andin53%of
patientswithanarterialline.
NationalInstituteforClinicalExcellence
(NICE)recommendstoguidefluidtherapyin
highrisksurgicalpatientsusingDynamicP
Itmaybepossibletoprevent3million
postoperativecomplications&
Tosave>800000lives/yr
MeasuresofVolumeOverload MeasuresofVolumeOverload
Interstitialfluid(Edema) Interstitialfluid(Edema)
Extravascularlungwater(EVLW)asdeterminedby
transpulmonarythermodilution.
The 'normal' value 57 mL/kg The normal value5 7mL/kg
30mL/kgduringseverepulmonaryedema
IAPMonitoringIAHisdefinedasanIAP12mmHg
Abdominalcompartmentsyndrome(IAPabove20
mmHg)withevidenceoforgandysfunction/failure
6
Abdperfusionpressureisamoreaccuratepredictor
ofvisceralperfusion(MAPIAP)
MajorriskfactorsforIAHincludeabdominal
surgery/trauma,fluid>3500mL/24hours,blood
transfusion(>10units/24hours),largeburns,ileus,
Abdominal Perfusion Pressure Abdominal Perfusion Pressure
laparotomy,liverfailurewithascites,severe
pancreatitisandlivertransplantation
InpatientswithanincreasingIAP,volume
resuscitationshouldbelimitedwithattemptsto
achieveanegativefluidbalance.
WhyNotenoughfluid?
Lessoralintakepriortofasting
Prolongedpreopfasting
Fluidandbloodlossintraop
Direct bl loss Directblloss
Exposureoflargeinternalsurfaces
DryGaseswhileintubated
Postopileuswiththirdspacelossesinto
thebowel(intraabdominalsurgery)
Kidneysuffers
Manyofthefactorsthatcontroltubular
sodiumreabsorptionareaffectedduringthe
perioperativeperiod,
includinghemodynamic
physicalfactors(e.g.,increasedintra
abdominalpressureduringlaparoscopic
procedures),
hormonalfactors
Renalsympatheticnerveactivity
Howmuchtogiveandwhentogiveit
ITDEPENDS
Typeofpatient
Type of surgery Typeofsurgery
Amountoftrauma
Acuteinjuryvs.elective
Anesthetic,positioning
Case1
25yrsyoungmaleforfixationoffracturebothbones
rightarm
Case2
65yrsoldmaleforhasCAsigmoidcolonpostedfor
APR,HasIHD ,
Case3
2yroldbaby,hasinguinalhernia,postedfor
herniotomy
Case4
35yrsfemale,diagnosedasAPH,foremergencyLSCS
Classic fluid
management
Deficits
Maintenance Maintenance
3
rd
Space
Blood loss
7
Deficits
Estimate
Preop NPO (hourly maintenance x duration)
Preop blood loss (trauma) or fluid loss (burns) Preop blood loss (trauma) or fluid loss (burns)
Typically replaced over first 2-4 hours
Maintenance
(421rule)
4ml/kg/hr forfirst10kgofbodyweight
2ml/kg/hr for2nd10kgofbodyweight
1ml/kg/hr foreachkgofbodyweightabove
20kg
Basedonwaterlossfromburningcalories
fromHollidayandSegar
Replacefluidlosses
Thirdspace210ml/kg/hr
Bloodloss:
3to1ratioofcrystalloiduptoEBL
1to1forcolloidorblood
SurgicalTrauma:ThirdSpacing
CapillaryandEndothelialinjury;leak
Sequestrationoffluidintotissues
i e TRAUMA causes FLUID Retention i.e.TRAUMAcausesFLUIDRetention
Creationofnonfunctional component
Returnoffluidfromthisthirdspace14daysaftersurgery
Healthyoutpatients minorprocedure
RisksofExcessFluids
Interstitialedema
Impairedcellularmetabolism
Poorwoundhealing
Decreasedpulmonarycompliance
Heartfailure overload
Delayedreturnofbowelfunction
Hemodilution
8
RiskofExcessFluids
Dependsontheamountoftraumatothe
tissue
THUSTHEAMOUNTOF3RDSPACELoss
Thepatientsabilitytohandlethefluidload
SpecificScenarios
Postoperativeweightgain
Pulmonarysurgery
Hepaticsurgery
Vascularsurgery g y
Hipsurgery
Trauma
Neurotrauma
Outcomestudiesshowingilleffectsofexcess
fluidadministration
EffectsofAnesthesia
transient
Regional
Vasodilation venouspooling
General
Myocardialdepressants
Vasodilation
Reductions in natriuretic hormone Reductionsinnatriuretichormone
IncreaseinAntidiuretichormone
MechanicalVentilation
Decreaseinvenousreturn
FLUIDELIMINATIONISGREATERPOSTOP
BUTTHERATEOFELIMINATIONISNOTRELATEDTOAMTOF
FLUIDADMINISTERED
Isoflurane
Promotesextravascularfluidaccumulation
duringcrystalloidloading(i.e.3
rd
spaceloss)
Notrelatedtomechanicalventilation
Is this due to increased ADH ANP? IsthisduetoincreasedADH,ANP?
ReducesGFRby3050%
Renalbloodflowby4060%
Urineoutputby65%
Fluids?Drugs?Both?
Volumestatus
Whatishypovolemia?
Checkneckveins,urinevolumeandcolor
Labile blood pressure suggests hypovolemia Labilebloodpressuresuggestshypovolemia
TheRotenbergRule whentheHRishigher
thanthesystolicBP>givefluid
RespiratoryvariationinBPorpulseoxpleth
Thequestionishowdoyoudealwiththe
hypotensiveandpotentiallyhypovolemicpt?
Firstmakeapresumptivediagnosis
Isithypovolemia
vasodilation
anemia anemia
myocardialdysfunction.
Usuallyyoufirstaddressvolumestatus.Basedon
thesecriteria,ifyoususpecthypovolemia in
generalyoudoboth i.e.temporize withdrugs
givefluidbasedonSVgoals.
9
Monitors
Skincolor,reperfusion,mucousmembranes,
HR,BP(systolicpressurevariation)
Is/Os;FluidAdministration,Urineoutput,
l d l Bloodloss
ETCO2;PaCO2ETCO2
CVP,PAP,PCWP,CO,SvO2
TEE DopplerCOmeasurements
Respiratory variation in art BP
ArterialvsPlethysmographicDynamic
IndicesforTestingFluidAdministrationin
HypotensivePatients
Onlyofhypotensivepts increaseCOs/pfluid
challenge
BPandplethysmographic variationw/PPV
predictsresponsivenesstofluids
Anes Anal103:1478(Dec06)
ART BP
SaO2
PLETH
3 points need to be noted
Filling pressures may not be predictive of
increase in CO in response to fluid
Nor is the increase in filling pressures
following fluid challenge, but
variation in art BP or pulse oximetry pleth may
be predictive
Predictingresponsetofluids
?BaselineBP X
?BaselineHR X
?BaselineFillingpressures XX
BaselineCI!
RespiratoryvariationofBPorSaO2pleth!
Responsetofluidloadingoftheabove!
10
Timingoffluids
Choiceoffluids
Crystalloids
Colloids
Bloodproducts
Whole blood Wholeblood
PRBC
FFP
Platelets
Fluid Na(mEq/L) K(mEq/L) Glucose(g/L) Osm pH Other
5%Albumin 145 15 <2.5 0 330 7.4 COP=3235
mmHg
Haemaccel 145 5.1 0 310 7.30.3 Chloride=145
Calcium=6.25
Hetastarch 154 0 0 310 5.9 Starch60
100g
Gelofusine 154 <0.4 0 274 7.4 Gelatin=40g
Chloride=125
0.9%NaCl 154 0 0 308 6.0
RL 131 5.0 0 280 6.5
Lactate=28
Cl
=111,Ca=2
5%Dextrose 0 0 50 252 4.5
D
5
LR 130 4.0 50 525 5.0
D
5
0.9%NS 154 0 50 585 4.5
IsolyteP 25 20 50 360 6.0
Mg=3,Cl=22
acetate=23
phosphate=3
Colloids donotimproveoutcome
Metaanalysisshoweda12.3%
worsened mortality withcolloids
in multiple trauma inmultipletrauma
Salinesolutionsmayproduce
hyperchloremicacidosis
ColloidsandRenalDysfunction
Thedehydratedpt whoreceives
considerableamountsofcolloidsis
especiallyatriskfordevelopingARF.
b d bl d ll d b d bl d ll d Itmaybeadvisabletoadministercolloid Itmaybeadvisabletoadministercolloidin in
additionto additionto,ratherthaninlieuof ,ratherthaninlieuof
crystalloids crystalloids.
Boldt &Priebe,AandA2003
MyRecipe
Ifyouneedfluid
ISStill10%loss
Then,considercolloid/Bl
Products>1020%loss
MoreorSick,give
bloodproducts
11
FluidtherapyinChildren
Maintenancefluid
in24hour in24hour (Holiday&Segar) (Holiday&Segar)
Newborn(FT)day 1 70ml/kg
280ml/kg.
390ml/kg. / g
Day4toupto10kg 100ml/kg.
1120kg 1000+50ml/kgover10kg.
>20kg. 1500+20ml/kgover20kg.
Guides?
*heartrate *skinturgor
*bloodpressure *fontanelle
* temperature * urine output temperature urineoutput
*capillaryfill *baseexcess
Maintenance fluid Maintenance fluid
4 ml/k /h 4 ml/k /h 4 ml/kg/hr 4 ml/kg/hr
FA Berry FA Berry
1stHour
FABerry
<15kg 25ml/kg
>15kg 15ml/kg
2ndHouronwards
Maintenance 4ml/kg/hr.
3rdspaceloss
mildtrauma4ml/kg
moderate trauma 6 ml/kg moderatetrauma6ml/kg
severetrauma 8ml/kg
Replacement
accordingtobloodvolumeloss
crystalloid 1x3timesBL
colloids 1x1timeBL
12
Peri Peri--operative fluid therapy operative fluid therapy
continues to be continues to be
an exercise in an exercise in empiricism empiricism,, an exercise in an exercise in empiricism empiricism, ,
with with
nagging questions nagging questions
about about efficacy and complications efficacy and complications
PostoperativeWeightGain
LowelletalCCM1990
48patientsadmittedtoSICU
40%ofpatientshad>10%weightgain
Whenmatchedtocontrols,fluidadministration was f
significantvariable
Sickpts havingbigoperations
RestrictedfluidsinIntraabdominalSurgery
Restricted=4ml/kg/hr (e.g.850ml)vs.
Liberal=10ml/kgbolus+12ml/kg/hr (e.g.
3200)
li b l f i d h i l di h Earlierbowelfunctionandhospitaldischarge,
lessweightgainwithrestriction
Nodiffinmortality
Nisanevich etal.Anesth 2005
PulmonarySurgery
115pneumonectomies
PPEoccurredin15%withMortalityof43%
MortalityrelatedtoFluidadministration
Milleretal:AnnalsThoracicSurg 2002
Hemodilution:WorsensCardiac
activity
Mangano NEJM1991,JACC1991:
83/474cardiacevents(17%)noncardiac surgery
30/84CHF(35%)
13dayspostop;vascularpatientsmorefrequent
Speculation:relatedtogreaterfluidadministrationtopatientsatrisk
NelsonCCM1993:vascularsurgicalpatients
WorseoutcomewithHct <28%
Speculation:Duetohemodilution
Spahn JTCVS1993:19dogswithacuteLADocclusion
Ischemiawithhemodilution toHgb 7.5gm/dl
BaronAnesth 1987
Epiduraldosingandfluidloading(500cc)inpatientswithWMA
Mangano Circ 1980andDehert Anesth 1999
Impairedcontractileresponsetofluidbolus(5001500)orlegelevationwhen
comparedtoPhenylephrineINNONCARDIACSURGERYPT
HepaticResection
LowCVPTechnique
LowCVPtechnique:496resections
IVF1cc/kg/hr andbolusesasneeded
NTG,dopamine,mannitol asneeded
Urineoutput>25cc/hr
SBP>90mmHg
CVP < 5 mmHg CVP<5mmHg
Results
ReductioninEBLandtransfusion
Onepatientwithrenalfailureduetoaminoglycoside
Improvedvisualizationofsurgicalfield
Reducespressureinhepatictissues
MelendezetalJAmColl Surg 1998
13
HipReplacement
987surgeries
Spinal/Epiduralhypotension(mBP 5055mmHg)
FluidrestrictiontominimizeperioperativeCHF
EpinephrineasneededtomaintainBPandCO
ImprovedOutcome
2myocardialinfarction
ReductioninEBLandtransfusionscomparedto
controls
0renalfailures
3deaths(0.4%)
Sharrock:BrJAnaesth;Reg Anesth
Trauma ScoopandRun
Bickell:NEJM1994
598penetratingtorsoinjuries:preSBP<90mmHg
Immediate(309)vsDelayed(298)fluidresuscitation
Outcome
PreopFluid:2500ccvs350cc
Lessperiopbloodtransfused:2070ccvs1720cc
d l f i Improvedpulmonaryfunction
Decreasedmortality
Survival Survival
Complications Complications
Hospital stay (d) Hospital stay (d)
Immediate Immediate
193 (62%) 193 (62%)
69/227 69/227
(30%) (30%)
14 14
Delayed Delayed
203 (70%) 203 (70%)
55/238 55/238
(24%) (24%)
11 11
1
ACUTEPULMONARYEDEMA
Dr. S. Dam
1
ClinicalCase1.
A62yearoldmanpresentswithathreeday
historyofprogressivedyspnea,
nonproductivecough,andlowgradefever.
KnownHTont/twithh/oanginainthepast.
h/ / h/oCHFont/t.
B.P. 95/55mmHg.
H.R. 110/minute.
Temperature 37.9degreesC.
SpO2breathingambientair 76%.
2
ClinicalCase1.
Auscultation B/LRalesandrhonchi.
CXR B/Lpulmonaryinfiltratesand
borderlineenlargementofcardiacsilhouette.
WHATISTHEOBVIOUSDIAGNOSISINTHIS
PATIENT&HOWSHOULDHEBEEVALUATED
&MANAGED?
3
PULMONARYEDEMA.
HowdoesPEdevelop?
Whatarethemajorsubtypeseffecting
management?
h h di i hi h Whatarethecommonconditionswhich
causeit?
Howwouldyoudiagnoseit?
Whatarethetypicalradiologicalfindings?
Howwouldyoumanagethisproblem?
4
Thelungsaredryorgans.
5
Lungsareneverdry.
Fluidandsoluteconstantlyfilteredfromextensive
networkofpulmonarycapillaries.
Rateequalsorexceedsthatinmanyotherorgans.
TheCapillaryendotheliumislooseallowing
passage of water & electrolyte as part of a normal passageofwater&electrolyteaspartofanormal
physiologicalprocess.
Formationoffluidsintheinterstitiumisaconstant
process.
6
2
MicrovascularFluidExchangeinLung
Fluid&solutesfilteredfromcirculationintoalveolar
interstitialspace.
Donotenteralveoliasalveolarepitheliumcomposed
oftightjunctions.
Movesproximallyintoperibronchovascularspace.
Lymphaticsremovemostofthisfluid&returnitto
circulation.
7
ErnestStarlingsequation.
Rateoffiltrationoffluid=Kf([Pcap Pis] [cap
is]).
Kf(hydraulicconductivityandfiltrationsurfacearea),
measurementofpermeabilityofendothelialbarrierto
t t watermovement.
PcapandPis hydrostaticpressures.
capandisprotein/colloidoroncoticpressures.
endothelialpermeabilitytoproteins.
8
Starlingforces.
Filtrationgovernedbynet
balancebetween
prevailinghydrostatic
pressure(Pcap Pis).
Transcapillaryprotein
ti ( osmoticpressure(cap
is),whichretainsfluid.
9
Pathophysiolgy.
Increaseinvascularhydrostaticpressure.
Decreaseininterstitialhydrostaticpressure.
DecreaseinVascularoncoticpressure.
Increaseininterstitialoncoticpressure.
Diffusealveolardamage.
10
IncreasedhydrostaticpressurePE.
Absolutehypervolaemia.
Overtransfusion/overperfusionpulmonary
edema
d O l fl id l d i DecreasedH
2
Oclearancefluidoverloadin
renalfailurept.
Manymixedconditions.
11
IncreasedhydrostaticpressurePE
Cardiogenic.
Increasedhydrostaticpressureinpulmonary
capillaries
ElevatedPVP.
IncreasedLVEDP&LAP.
AsLAPrisesfurther(>25mmHg)
Edemafluidbreaksthroughlungepithelium
floodingalveoliwithproteinpoorfluid.
12
3
ViciouscycleinCardiogenicPE.
IncreasedLVpressuresleadingtoIncreased
pulmonaryvenouspressure.
ReducedLVcontractility&increasedafterload.
SignificantneurohumoralresponseduetoDecreased
LV contractility: LVcontractility:
1. Sympathetic.
2. Activationofreninangiotensin.
3. Endothelin.
4. Inflammatorymediators.
TheseleadtoincreaseinSVR&furtherdecreasein
LVcontractility.
13
IncreasedhydrostaticpressurePE.
Increasedpulmonaryvenouspressure.
LVfailure:
Dysarthythmias.
Valvular disease e g : MS AS AR papillary rupture Valvulardiseasee.g.:MS,AS.AR,papillaryrupture.
SevereacuteMIwithhypokinesia.
Cardiomyopathies.
Myocarditis.
Hypertensivecrisis.
14
Progression.
Interstitialedema.
Alveolarflooding.
Similarprogressioninfluidoverload&LV
failure.
I i i l d f i i Intensityproportionaltodegreeofrisein
pressure.
Radiologicalappearancelagbehindrisein
PAWP.
Similarlyduringrecoveryitlagsbehindclinical
improvement.
15
PAWP&Radiologicalpicture.
PAWP Radiology
512 Normal.
1217. Cephalizationofpulmonaryvessels
9 only in chronic ) 9onlyinchronic.)
17 25. KerleyBlines,Subpleural
effusions.
25. Frankpulmonaryedema.
16
Radiologicalprogression.
Earlylossofdefinitionofsegmental&sub
segmentalvessels.
Enlargementofperibronchovascularspaces.
AppearanceofKerleyBlines.
S b l l ff i Subpleuraleffusion.
Progressivedecreaseinlungradiolucency.
Peribronchialcuffingmoreinhilarareas.
Asalveolaredemadevelopstinynodularareas
ofopacitiesappearwhichmaythencoalesceto
formfrankconsolidation.
17
Cardiomegaly
Cardiacwidth
largerthan
transthoracic
diameter.
CTratio>0.5. 5
18
4
Cephalization.
Occursdueto
increasedflowto
apicesasaresultof
increasedPVP.
Standoutbecause
ofmoreblood,
pressureishigher&
theremaybesome
d di edemasurrounding
them.
Thepatientmust
beuprightwhen
thefilmis
obtained.
19
KerleyBLines
Shortparallellinesat
lungperiphery.
Representinterlobular
septa,usuallylessthan
1cmandparalleltoone
anotheratrightangles
topleuralsurface. p
Maybeseeninany
zonebutmostfrequent
atlungbases.
Costophrenicangleson
thePAradiograph,and
inthesubsternalregion
onlateralradiographs.
20
PeriBronchialCuffing
Occurswhenexcess
fluidormucusbuild
upinsmallairway
passagescausing
localizedpatchesof
atelectasis.
Causesareaaround
bronchustoappear
moreprominent.
21
PulmonaryEffusions.
Fluid
accumulationin
pleuralspace.
22
Pulmonary InterstitialEdema
Classicalbatwing
appearancevisible
asbilateralhilar
haze.
23
AlveolarEdema.
Alveolaredema
manifestsasnodular
opacities.
24
5
Previously undiagnosed MS who developed pulmonary edema following a gynae.
Multiple confluent acinar shadows due to hydrostatic pulmonary edema.
Cardiac silhouette shows enlarged, convex main pulmonary artery segment and a
convex left atrial appendage
25
Batwingedema.
Centralnongravitationaldistributionofedema.
Seenin10%ofpatients.
Seeninrapidlydevelopingcardiacfailureasin
severe MR in papillary rupture massive MI Valve severeMRinpapillaryrupture,massiveMI,Valve
dysfunctionduetoBE.
Rapidprogressionofalveolaredemaincentral
regions.
Previouschangesduetointerstitialedemanot
observed.
26
AsymmetricdistributionPEdueto
Increasedhydrostaticpressure.
Morphologicdestructionoflungparenchyma
inCOPD.
Extensiveemphysema.
fib i i id i b i LungfibrosisinT.B.,sarcoidosis,asbestosis.
InMRedemapredominatesinrupperlobe.
Positionalinventilatedpatients.
27
AsymmetricdistributionPE.
28
Postobstructivepulmonaryedema.
Occursafterrelieffromupperairwayobstruction.
Purehydrostaticedema.
Obstructionwithhighnegativeintrapleural
pressure.
Increasedvenousreturn.
Asobstructionisrelievedsuddendecreasein
negativeintrapleuralpressure.
Largehydrostaticgradientbetweenintravascular&
interstitialpressureleadingtoPE.
29
Postobstructivepulmonaryedema.
Septallines.
Peribronchialcuffing.
Centralalveolaredemaseenasnodular
i i opacities.
Resolvesin24 48hrs.
30
6
Neardrowning.
TYPE1 Acutelaryngospasmwhenwater
reachesthelarynx.Ifprolongedthereisno
floodingoflungsleadingtoDRYDROWNING.
KerleyBlines,peribronchialcuffing&central
alveolaredema.
Resolvecompletelyifproperlytreated.
TYPE2 Laryngospasmfollowedbyinhalation
ofwater.Water&hypoxiawithsubsequent
cytokinemediationcausesevereDADsimilarto
ALI/ARDS.
31
DRYDROWNING.
32
Permeabilityedemawithdiffuse
alveolardamage DAD.
Causedbyconditionsofdiverseetiology.
HeartisnormalsonoincreaseinPAWPor
venoushydrostaticpressure.
l i i i f i Localprecipitatingfactorsorsystemic
disorders Pulmonaryorextrapulmonary
causes.
Primarypathologyisdamagetoalveolar
epitheliumleadingtolossoftightjunctions
33
Directinjury(ARDS).
1. Infection:bacteriaorvirus.
2. Aspirationofgastriccontent.
3. Lungcontusion.
4. Neardrowning.
34
Indirectlunginjury.
1. Sepsissyndrome.
2. Extensiveburns.
3. Drugoverdose
4. Pancreatitis.
5. TRALI.
6. Polytrauma.
35
ARDS permeabilityedemawithDAD.
36
7
37
HAPO.
Occursinpreviouslyhealthyindividuals.
Rapidascenttoheights.
Prolongedexposuretolowatmosphericpressure
oxygen.
Usually preceded by acute mountain sickness Usuallyprecededbyacutemountainsickness.
Pathophysiolgyduetoacutepersistentnon
homogenoushypoxialeadingtopulmonary
vasoconstriction.
Interstitial&alveolarproteinrichedemawithout
DAD.
Resolvesifpatientisbroughtdown.
38
HAPO radiology.
Centralinterstitialedema.
Peribronchialcuffing.
Illdefinedvessels.
FewKerleyblinesmaybepresent.
Patchy&asymmetricconsolidation.
Consolidationmaybecomeconfluent&
ultimatelyinvolvethewholelung.
39
Neurogenicpulmonaryedema.
Followingseverebraindamage.
Combinationofhydrostaticedema&permeability
edemawithoutDAD.
MediatorreleasebutPathophysiolgynotclearly
d t d understood.
Bilateralsymmetrical&homogenousairspace
consolidations.
Predominantapicalinvolvement.
Radiologicalfeaturesgenerallydisappearin23
days.
40
OthercausesofPE.
PostembolismPE.
PulmonaryVenoocclusivedisease.
Postperfusion.
Postpneumonectomy.
PEafterairembolism.
HeroininducedPE.
41
Decreasedoncoticpressure.
Lowalbuminstates:
1. Nephroticsyndrome.
2. Burns.
3. Otherhypolbuminicstates.
42
8
Clinicalderangements.
Interstitialedemacausesdyspnea&tachypnea.
Alveolarfloodingleadstoarterialhypoxemiaand
initiallyhypocapnia.
In severe cases may lead to Hypercapnia InseverecasesmayleadtoHypercapnia.
Coughandexpectorationofbloodstainedfrothy
fluid.
Ifprogressivecancausetissuehypoxemia&
gradualfailureofmajororgansystems.
43
Labsupport.
Electrocardiography.
Elevatedtroponinlevels.
Measurementofelectrolytes,theserum
l i d i l osmolarity,andatoxicologyscreen.
Serumamylaseandlipase.
44
LaboratoryTesting.
BNPissecretedpredominantlybycardiacventricles
inresponsetowallstretchorincreasedintracardiac
pressures.
BNP100pg/mmindicatesheartfailureisunlikely
(negativepredictivevalue,>90%)
BNP500pg/mmindicatesheartfailurelikely
(positivepredictivevalue,>90%).
45
ChestRadiography
46
LaboratoryTesting
BNPlbetween100&500pg/mmprovide
inadequatediagnosticdiscrimination.
BNPcanalsobesecretedbyrightventricle,and
moderateelevationshavebeenreportedinpatients
withacutepulmonaryembolism,corpulmonale,
andpulmonaryhypertension.
47
Echocardiography.
Firstapproachtoassessleftventricularand
valvularfunctioninpatientsinwhomhistory,
physicalandlaboratoryexaminations,andchest
radiographdonotestablishcauseofpulmonary
d edema.
Lesssensitiveinidentifyingdiastolicdysfunction.
Doesnotruleoutcardiogenicpulmonaryedema.
48
9
PulmonaryArteryCatheterization.
AssessPAWP.
Consideredthegoldstandardfordeterminingcause
ofacutepulmonaryedema.
Monitoringofcardiacfillingpressures,cardiacoutput,
andsystemicvascularresistance.
49
CVPnotconsideredavalidsubstitutefor
PAWP.
Datasuggestapoorcorrelationbetweenthetwo.
Acute or chronic pulmonary arterial hypertension Acuteorchronicpulmonaryarterialhypertension
andrightventricularoverload.
Intheabsenceofanyincreaseinleftatrial
pressure.
50
StepwiseApproach
Noninvasiveapproachesfordiagnosiswill
inevitablyleadtomisclassificationofsome
patients.
Repeated and ongoing assessment is necessary Repeatedandongoingassessmentisnecessary.
Requiringsimultaneousdiagnosisandtreatment.
10percentofpatientswithacutepulmonary
edemahavemultiplecausesofedema.
51
52
MANAGEMENTPRINCIPLES.
53
Untreated rapidlyfatal.
ViciouscycleofDecreasedLVcontractility&
IncreasedSVRcanleadto:
1. Decreasedorganperfusion.
2 P i h f il 2. Progressiveheartfailure.
3. PoorOxygenationoftissues.
4. Progressiveacidemia.
5. MOSF.
6. Respiratoryfailure.
7. Braindeath.
54
10
Improvingoxygenation.
Supplementaloxygen.
Uprightposition.
Noninvasiveventilatorysupport.
55
Diuretics.
Furosemideorotherloopdiuretics.
Dosageatleast40 80mg(0.51.0mg/kg.)
IVbutoftenhigherdosesneeded,ifpatientis
already on diuretics alreadyondiuretics.
Higherdosescanleadtointravascular
depletion,prerenalazotemia&
neurohormonalactivation.
56
Morphine.
25mgover3minutesandrepeatin15
minutesifnecessary.
Decreasespatientanxietyandworkof
breathing thereby limiting sympathetic breathing,therebylimitingsympathetic
outflowandaidinginarteriolarandvenous
dilatation.
57
Vasodilators:
Predominantlyvenodilator.
Sublingual0.4mgevery5mts.
IVNTGinallpatientswithSBP120.
Canreducemortality&needforMV.
NitroprussideespeciallyhelpfulforHTN
emergency,acuteaorticormitral
regurgitation,acuteventricularSeptalwall
defect.
58
Afterloadreduction.
BreakstheviciouscyclebetweenLV&
afterload.
Improvesrenalperfusion.
G/S NTG/SNP.
ACEinhibitors ReduceSVR,improveCO,
reducePAWP,
AvoidACEIinhypotensivestates&in
patientswithAS.
59
Dobutamine.
Indicatedifabovemeasuresfailtocontrol
pulmonaryedemainthepresenceofmild
hypotensionandsevereLVsystolicdysfunction.
Ifrespiratoryfailurecomplicatespulmonary
edema,dopamineshouldbeavoidedbecause
thisagentmaycauseconstrictionof
pulmonaryveinwillincreasedinpulmonary
capillaryhydrostaticpressureandlung
accumulation.
60
11
Othermodalities.
Milrinone50migmbolusfollowedby0.250.75
migm/kg/mtinCardiogenicshockimprove
contractilitywhilecausingdecreaseinSVR.
IABpp can be life saving. IABppcanbelifesaving.
Levosemindanisanewdrugcalciumsensitizer
asanalternativetoDobutamineinacutely
decompensatedstates.
Appropriatetreatmentofarrhythmias&
precipitatingcause.
61
CPAP
IfarterialPaO2remainlowaftertreatmentwitho2
andappropriatediureticsandcardiacdrugs,mask
CPAPshouldbeinitiated.
Itreducesworkofbreathingandworkofthe
myocardium.
AlsoincreasesPao2,decreasesPaCO2&reduces
needforintubation.
62
CPAP.
Generally,CPAPismostusefulinawake,
orientedandcooperativept.
InvasivemechanicalventilationwithPEEP
should be applied if arterial PaO2 remains shouldbeappliedifarterialPaO2remains
below60mmhgandincreasedPCO2above
7080mmhgwhentheptisbreathing
approximately50%O2thrumaskCPAP.
63
Invasiveventilation.
Inleftventriculardysfunction,preloadis
elevated.
PEEPelevatesintrathoracicpressure,reduces
venousreturnanddecreasespreload,somay p , y
improveleftventricularfunction.
PEEPalsoimproveleftventricularafterload.
64
Ventilatorsettings.
CMVselected,eitherpreesureorvolumeventilation
isacceptable.
Tidalvolumes8to10mL/kg.
RR>10toachieveeucapnia.
k l l h ld b 30 O Peakalveolarpressureshouldbe<30cmH
2
O.
Inspiratorytimeshouldbeshort(1to1.5s).
Fio2shouldinitiallysetat1,titratedperPaO2.
PEEPof5to10H
2
0shouldbeappliedtosupport
failingheart.
65
WEANING.
Relativelyeasy,providednounderlyingCOPDor2
0
pulmonaryproblemsdevelopandtheleftheart
failureisappropriatelymanaged.
InCOPD,itgeneratelargeintrathoracicpressure
swingsduringspontaneousbreathing,thus
eliminationofmechanicalventilator increaseinleft
ventricularpreloadandpulmonaryedemea.
66
12
NonCardiogenicPE.
Lungprotectiveventilation.
67
1
RecentAdvancesinAnaesthesia
Dr.Surendra Kumar
Recent Advances in
Drugs
Equipments q p
Techniques
Concepts
Drugs
Intravenous AnaestheticAgents:
BZD Receptor agonists Remimazolam
Etomidate derivatives Methoxycarbonyl (MOC) etomidate
Carboetomidate
Propofol analogue Fospropofol
NMB reversing agents: Sugammadex
Inodilator: Levosimendan
Benzodiazepine Receptor Agonists
Remimazolam
Incorporation of ester linkage- esterase hydrolysis
Rapid onset, short duration of action
Dose dependent depression of BIS (0 75mg/kg) Dose dependent depression of BIS (0.75mg/kg)
Fast recovery (10 min vs 40 min midazolam)
Recovery to MOA A/S score 5 to 16 mins for 89%.
RCT: UGI endoscopy: less requirement of assisted vent/
supplementary sedation than midazolam.
AE: Mild desaturation of Hb.
Propofol analogue
Fospropofol: Phosphate prodrug of Propofol
Sedation/Hypnosis with minimal excitation
Reduces IOP, SVR,CO, Resp. drive
Slower onset and recovery than Propofol
Water soluble
No pain on injection
MAC Sedation
Safe in Renal disease/ caution in hepatic impairment.
Perineal pain / paraesthesia
Etomidatederivatives
Etomidate
GABA
A
receptor activation, inhibits 11-Hydroxylase at
subhypnotic doses.
Nitrogen atom in etomidates imidazole ring binds to haem Nitrogen atom in etomidate s imidazole ring binds to haem
within 11- Hydroxylase and suppresses steroidogenesis.
2
Pharmacokinetic change
Methoxycarbonyl(MOC) etomidate
MOC-etomidate
Rapid metabolism by esterases.
Less potent than etomidate.
Very brief depression of adrenocortical function after single
bolus administration.
Metabolised to carboxylic acid & methanol- safety unclear.
Pharmacodynamicchange
Carboetomidate
Binding nitrogen atom removed Adrenal suppression.
Maintains anaesthetic property
Suitable for maintenance of anaesthesia/ sedation.
No/minimal hemodynamic effects.
Etomidate induced myoclonus and nausea & vomiting?
NMReversal Agents: Sugammadex
A modified -cyclodextrin:
First selective relaxant binding agent.
Tight complexes in 1:1 ratio with steroidal NMBA.
(Rocuronium> vecuronium >>Pancuronium)
High association, low dissociation (1:25,000,000)
Sugammadex..
Dose of sugammadex depends on
Dose of rocuronium, and
Depth of the neuro-muscular block
Sh ll Bl k 2 0 4 0 /k ithi 3 i Shallow Block: 2.0 4.0 mg/kg reverses within 3 min
Intermediate block: 8.0 mg/kg (after 0.6 mg/kg rocuronium)
Deep (rescue)block: 16 mg/kg (after 1.2 mg/kg rocuronium)
Rocuronium- Sugammadex complex is eliminated in urine
3
Is it faster than Succinylcholine?
Rocuronium 1.0 mg/kg with sugammadex 16mg/kg
Vs
Succinylcholine 1mg/kg
Spont. Respiration 406 sec (for sux) Vs 216 sec.
T
1
90% - 518 sec (for sux) Vs 168 sec (BJ A2012;108:6829).
Re-establishment of block needed
Use BenzylisoquinoliniumNMBA
Use in special populations
Renal impairment
No consistent results in severe renal failure or needing dialysis avoid
Hepatic impairment
Safe to use
Elderly
Safe if no renal impairment
Paeadiatric
Analogous to adults, no info on <2 years
Do not affect clearance
Gender, race
Do not affect clearance
Drug interactions
Toremifene, estrogen receptor modulator can delay reversal
Fusidic acid and flucloxacillin can displace rocuronium bound
to sugammadex
Can bind to contraceptive steroids (clinically insignificant)
Side effects
Hypotension
Coughing
Nausea/ vomiting
Dry mouth
Parosmia
Sensation of changed temperature
Prolongation of Qt interval
Levosimendan
Active isomer (levo rotatory) of Simendan.
Pyridazinone-dinitrile derivative.
Myocardial Ca
2+
sensitiser
Enhances myocardial contractility Enhances myocardial contractility
Causes vasodilation coronary, pulmonary, renal, splanchnic, cerebral &
systemic arteries and veins.
4
Levosimendan
Mechanismof action
Inotropic effect-
Binds to Tn C and stabilises Ca
2+
bound conformation
(dependent on cytosolic Ca
2+
conc.) (dependent on cytosolic Ca conc.)
Inhibits cardiac PDE at higher conc. (>0.3M)
Vasodilation-
Opens K
+
channels
PDE inhibition
Cardiovascular effects
Heart Rate
Neutral on HR, higher conc. rise in HR.
Cardiac performance
Raised CO, reduced PCWP
Raised LVSV & CI
Preserved or positive lusitropy
Vasodilation
Reduced filling pressures of heart.
LevosimendanVs conventional inotropes
No rise in Ca
2+
conc.
No energy/ O
2
consumption.
Good diastolic function
Vasodilation
No arrhythmia potential
Ischemia-reperfusion injury protection
Long term survival better than dobutamine (LIDO)
Dose &metabolism
Bolus 6-24 g/kg over 10 min f/b 24-hr infusion 0.05-0.2 g/kg/min
Response: 5 mins
Therapeutic conc. 0.035-0.35 M (10-100 ng/ml)
97-98% bound to plasma proteins (Vd 0.2 l/kg)
No dose adjustments in mild-mod renal or hepatic impairment
Metabolism
I- Glutathione conjugation to inactive derivatives
II- Reduced to inactive metabolite OR-1855 in lower GIT-
reabsorbed and acetylated to active OR-1896.
OR-1896 similar profile to levosimendan, long half life (81+ 37 hrs)-
prolonged effect- once a week dosing
Clinical applications
Acute decompensation of CHF
Inotropic support during and after myocardial ischemia
Myocardial stunning- PTCA/ cardiac surgery y g g y
Cardiogenic shock
Right ventricular dysfunction
Septic myocardial dysfunction
5
Adverse events
Hypotension
Headache
Dizziness, nausea
Mild reduction in RBC count
Mild fall in serum K
+
Mild prolongation of QTc (high doses)
Pre-requisites-avoid adverse events
Correct hypovolemia
Correct serum electrolyte
IBP & CO monitoring
Exclude loading dose in hypotensive pts.
Concomitant vasopressors may be reqd.
Equipments:
Video laryngoscope: Glidescope, McGrath, C-Mac, AirTraq
Epidural space locating device: Acoustic puncture assist device Epidural space locating device: Acoustic puncture assist device
Video Laryngoscopes
Can be used for direct & indirect laryngoscopy
Reduced learning curve
Helpful in difficult intubations
Less chances of trauma to teeth
Good education tool
Channel for preloadingETT Channel-less
Pentax AWS C-MAC
King vision laryngoscope Glidescope
AirTraq, Res-q-scope McGrath
Pentax AWS Kings Vision Laryngoscope
Airtraq Res-q-scope
6
C-Mac
Glidescope McGrath
Epidural space locating device
Acoustic puncture assist device (APAD)
Pressure generated in an extension tube between epidural
needle and a syringe placed in an infusion pump is translated
into corresponding acoustic & visible signal and is displayed on
the monitor.
APAD
Sense of hearing detects small changes better than sense of touch.
Higher pressure gives higher tone and upward deflection of
pressure curve and vice versa.
Distinguishes between real and pseudo LOR (hole or cyst in Distinguishes between real and pseudo LOR (hole or cyst in
interspinous ligament)
Educational tool
Registration of entering epidural space
Helpful in medicolegal situations
Technique
Sedasys
Ultrasound in Anaesthesia
Patient state index
Sedasys: IV Drug Delivery System
Older concept: TCI
Automated sedation with propofol in conjunction with
comprehensive patient monitoring and sophisticated software.
Computer- assisted personalized sedation (CAPS).
Monitors- ECG, SpO
2
, EtCO
2
& response to auditory commands.
Monitoring values & safety interlocks- propofol sedation in
accordance with prescribing information- titration
7
SedasysCont.
Patient responsiveness and apnoea/ desaturation.
Sedasys may stop or decrease rate of administration, not increase.
Not a closed loop anaesthesia system Not a closed loop anaesthesia system.
Provided satisfactory sedation without AEs attributable to the
device.
Future ..!!!
Patient State Index
PSI is an index of depth of anaesthesia.
EEG based, proprietary algorithm Physiometrix inc.
Uses time, frequency, phase and spatial information as EEG
dominance changes.
Five lead bilateral frontotemporal montage.
Depth as numerical value ranging from 100 to 0 (awake- deep
anaesthesia).
Anaesthetic range index value 25-50.
Displays current number and color coded trend (anaesthetic range,
too light, too deep)
Averages index value over 25 secs.
Ultrasound in Anaesthesia
Useof ultrasound in anaesthetic practiceis well established for:
Regional anaesthesia
Vascular access
Trans-oesophageal echocardiography (TEE) Trans-oesophageal echocardiography (TEE)
Roledeveloping in:
Airway assessment
Central neuraxial blockade
Ultrasound in anaesthesia.. Cont.
Airway assessment
Signs of difficult intubation
Assessment of vocal cord swelling (post extubation stridor)
Assessment of s bglottic diameter (si e of ETT in pediatric pts ) Assessment of subglottic diameter (size of ETT in pediatric pts.)
Ultrasound in Anaesthesia.. Cont.
Central neuraxial block: traditionally administered by landmark
identification.
Landmarks not well defined !!!
Obesity
Previous surgery on spine
Scoliosis
Elderly with degenerative changes
Ultrasound in CNB
Technical difficulties with CNB
Number of needle manipulations required for success; time taken to
perform the block; inadvertant dural puncture, vascular puncture,
paraesthesia (persistent ne rological deficit) paraesthesia (persistent neurological deficit)
Preprocedural USG of spine
Location of interlaminar spaces
Depth of structures
In spinal scoliosis least rotated vertebral body can be identified
8
Ultrasound in CNB
Preprocedural ultrasound scan has resulted in higher success
rate at first needle insertion (Chin. Anesth2011;115:94-101)
Increased time for identification of landmark.
Visualize CSF leak in post dural puncture headache and
application of autologous blood patch
Concepts
Anaesthetists non-technical skills (ANTS)
AnaesthetistsNon-Technical Skills (ANTS)
The cognitive, social, and personal resource skills that
complement technical skills, and contribute to safe and efficient
task performance.
Cognitiveor mental skills
Decision making
Social or interpersonal skills
Team working
AnaesthetistsNon-Technical Skills (ANTS)
Planning
Situation awareness
Communication
Leadership
Deficiencies increase chances of error, of an adverse event.
Upto 80% of cases non technical issues like:
Drug swaps,
Failure in communication
Why ANTS?
Failure in communication,
Failure to recognize developing problem,
Flawed decision making
Good NTS e.g. vigilance, anticipation, clear communication, team
coordination reduce chances of error
Development of ANTS system
Based on task analyses (literature review, Observations,
Interviews, Surveys, and Incident analyses).
Team of anaesthetists and psychologists designed ANTS System
www.abdn.ac.uk/iprc/ants
9
Category Element
Task management Planning & preparing
Prioritizing
Providing and maintaining standards
ANTS Hierarchical System
Identifying and utilising resources
Team working Coordinating activities with team members
Exchanging information
Utilising authority and assertiveness
Assesing capabilities
Supporting others
Category Element
Situation awareness Gathering information
Recognising & understanding
ANTS Hierarchical System
Anticipating
Decision making Identifying options
Balancing risks & selecting options
Re-evaluating
Behaviour markers: Co-ordinatingactivities with teammembers
Goodpractice
Confirms roles and responsibilities of
team members
Poor practice
Does not co-ordinate with surgeons and
other groups
R li t h f ili it f t Discusses care with surgeons or
colleagues
Considers requirements of others
before acting
Co-operates with others to achieve
goals
Relies too much on familiarity of team
for getting things done
Intervenes without informing/ involving
others
Does not involve team in tasks
Can we assess ANTS?
How?
ANTS systemrating options
Ratinglabel Description
4= Good Consistently high standard of performance
(enhancing pt. safety, used as positive example).
3= Acceptable Performance of satisfactory standard, (improvable)
2= Marginal Performance indicated cause for concern,
(considerable improvement needed)
1= Poor Performance endangered or potentially
(endangered pt. safety, serious remediation required)
Not observed Skill could not be observed in this scenario
Where to assess?
NTS can be assessed both in theatre setting and during sessions at a
simulation centre.
Advantages Advantages
Specific feedback to trainee on the observed behaviour.
Video debriefing of NTS.
Performance of NTS can improve with repeated training.
10
Do ANTS have correlation with TS?
Yes
Generic and Transferrable ? Generic and Transferrable ?
Further suggestions
Surviving Sepsis Campaign: International guidelines for
management of severe sepsis and septic shock: 2012
Ulinastatin: Trypsin inhibitor reduces pro- infammatory
response in sepsis.
1
Prof. S Moied Ahmed
CaseSummary
A14yroldmale,hasahistoryoffacialtrauma3
yrsback y
Presentedwithrestrictedmouthopening
DiagnosedasTemporomandibularJointAnkylosis
Postedforb/lcondylectomy
What do you mean by TM joint ankylosis?
Ankylosis of the Temporomandibular joint, an
arthrogenic disorder of the TMJ , refers to
restricted mandibular movements (hypomobility)
with deviation to the affected side on opening of
the mouth.
What is so peculiar about TM joint?
2
Diarthrodial synovial joint with three different
features
Both the joint functions as a single unit that is
the craniomandibular articulation. the craniomandibular articulation.
Articular surfaces are lined by fibrocartilage
instead of hyaline
Articular discs biconcave separates into
two compartments
How much mouth opening does each joint
contribute? contribute?
Hinge joint: 2 3 cm
Sliding joint: 2 3 cm
Atotal of 6 cmwhen the mouth opens fully A total of 6 cm when the mouth opens fully
What are the clinical features of TMJ ankylosis?
Inability to open the jaws
In unilateral ankylosis, the lower jaws shifts towards the
affected side on opening of the mouth
In severe cases, there is complete immobilization
There may be abnormal forward protrusion of the mandible
as the excess tissues occupies the space as the excess tissues occupies the space
Facial deformity
Others are related to the underlying cause of the ankylosis
Fever
Pain
Other bones and joints deformities
What is the classical triad of TMJ ankylosis?
3
Pain in the preauricular area
Noises from the region of TMJ
Limited mandibular movement
What physical clinical features are of your
concern? concern?
J oint movement in all directions (max inter incisor gap 4-
6 cm, lateral excursion 1 cm)
Facial asymmetry, hypoplastic and retrognathic
mandible, bird-face deformity
Dentition problems caries, abscess
TMJ clicks
OSA
What are the etiology of TMJ ankylosis
trauma
Infection
Rheumatoid arthritis
Congenital deformity
Howwouldyouinvestigate?
4
Biochemical : ESR, autoantibodies, uric acid levels
Radiography : orthopantomogram , lateral cephalogram
CT scanning ith mo th in open and closed positions CT scanning with mouth in open and closed positions
Arthrography using contrast media into joint spaces
MRI : INVESTIGATION OF CHOICE
What are your ANAESTHETIC considerations?
Difficult airway
Associated OSA
Sensitive to central depressant drugs / sedatives
Poor nutrition
Poor dental hygiene / abscess
Post operative maintenance of airway
Paediatric age group
Difficultairway
Difficultmaskventilation BONES
Difficultlaryngoscopy andintubation LEMON
Difficultsupraglottic airwa yinsertion RODS
/DROPS
Why should there be difficult mask ventilation ?
Difficult mask seal : small and receding mandible
Tongue fall jaw thrust not possible
5
Why should there be difficult laryngoscopy and
intubation?
1. Inter incisor gap : reduced
2. Three finger test : negative
3. Two finger test : negative / positive
4 One finger test : negative 4. One finger test : negative
5. Mallampati grade : cannot be assessed
6. Palate configuration : cannot be assessed
7. Upper lip bite test : negative
Why difficult supraglottic device insertion?
No mouth opening / <1 cm
What if there is partial restriction?
Restriction of movement of tongue away from
airway preventing tongue displacement
Hinders insertion of rigid laryngoscopy Hinders insertion of rigid laryngoscopy
Minimum mouth opening required for insertion of
supraglottics is approx 2 cm
6
Would you like to use sedatives?
Sedatives best avoided in premedication :
- reduce arousal and ventilatory responses to hypoxia
and hypercapnia
- worsen OSA by reducing pharyngeal muscle tone,
thereby increasing the likelihood of upper airway
collapse.
If associated with OSA, risk is increased :
- increased sensitivity to central depressants
- perioperative risk of apnoea and desaturation
How will you deliver anaesthesia to this patient?
Awake Nasal Fibre-optic guided intubation
gold standard
Followed by general anaesthesia
Whatareyourotherairwaymanagement
options? p
Trachlight nasal intubation
Seeing optic stylet (SOS) aided intubation
Flexible airway scope tool (FAST) aided
intubation
Blind awake nasal intubation
Tracheostomy /tracheotomy
Retrograde nasotracheal intubation
7
How would you prepare him for awake nasal
fibreoptic?
Psychological preparation by explaining the
technique,
Anxiolytics Anxiolytics
Antisialogogues
Antiemetics
Nasal decongestants
How would you obtain local anaesthesia?
Spray as you go
Different blocks
Sprays nebulisation gargles Sprays, nebulisation, gargles
What problem do you anticipate while intubating
ith fib ti ? with fibreoptic?
Fixed jaw deformity
Distorted soft tissue anatomy
Position of the larynx may be altered
No mouth opening
Inability to protrude the tongue and lift
epiglottis
Inability to negotiate the tip of fiberoptic
8
How would you solve your problem?
Ask the patient to phonate
What will you do if you encounter bleeding in the
passage? p g
Suction through other nostril
Withd th fib d i t Withdraw the fiberscope and reinsert
Use light wand
Whatwouldbeyourtechnique ifthispatientis
uncooperative?
Under inhalational anaesthesia
Li ht d ti li i f l Light sedation +lignocaine +propofol
9
What other technique would you keep ready
before starting ? before starting ?
Cricothyrotomy with transtracheal jet ventilation
would be safest
Fastest would be needle cricothyrotomy
Surgical tracheostomy should be the last option.
How will you extubate this patient?
Awake
Complete reversal of NMD
Extubate over ventialting stylet
Summarize
TMJ ankylosis patients have limited mouth opening and
facial deformity
Usually associated with OSA
This leads to DMV DL &I DSI This leads to DMV, DL & I, DSI
Awake fiberoptic is the technique of choice
Fiberoptic technique could be difficult because of limited
mouth opening and relatively large tongue
Alternative technique could be inhalational +sedation
Extubation should be awake
MAXILLOFACIALINJURY MAXILLOFACIALINJURY
10
CaseScenario
A28yearoldmalepatientwasinvolvedina
motorvehicleaccidentandsustained
maxillaryandmandibular #postedfordental
wiring wiring
1. Anticipationofdifficultairway/assessmentofdifficult
airway
2. Difficultiesexpectedwhileproceedingwiththetechnique
3. Preparationofthepatient
4. Whichdifficultairwayalgorithmwouldyoufollow
h i f h i 5. Techniqueofchoice
6. Howwouldyouovercomethosetroubleshooting/
difficulties
7. Alternativetechniquesavailable/couldbeundertaken
8. HowwouldyoufixtheETtube
9. Whatprecautionswouldyoutakewhileextubation.
10. Whatmethodsarecontraindicated?
11. Whatotherprecautionswillyoutake?
Maxillofacialtrauma
Fractures of the facial skeleton are commonly
seen after assault, road traffic accidents, falls,
and sporting injuries in a ratio of p g j
mandibular : zygoma : maxillary
6 : 2 : 1.1
58
FRACTURES OF THE FACIAL SKELETON
Divided into:
Upper third( above the eyebrow)
Middle third( above the mouth)
Lower third( the mandible)
59
The middle third
Much of the understanding of patterns of fracture propagation
in midface trauma originates from the work of Ren Le Fort.
Three predominant types were described.
Le Fort I :usually involves the inferior nasal aperture
Le Fort I I :usually involve the inferior orbital rim
Le Fort I I I: along the floor of the orbit along the inferior
orbital fissure
60
11
61
Isthepatientconscious?
Ishe/shebreathingspontaneously?
Whatistheextent,compositionandtheanatomyofthe
airway?
Howextensiveisthedamagetothebonystructuresof
theface?
Istherealimitationinmouthopening?Isthat
limitationtheresultofpain&aftersedationthemouth
couldbeopenedwider?
Istheresofttissueedema&pressureontheairway?
LEMON:
Lookexternally
Evaluate332rule
Mallampati classification Mallampaticlassification
Obstruction
Neckmobility
airway
5. Techniqueofchoice
difficulties
1. Posteroinferiordisplacementofafracturedmaxilla
paralleltotheinclinedplaneoftheskullbase.
2. Abilateralfractureoftheanteriormandible.
3. Haemorrhage.
f ll d d 4. Softtissueswellingandedema.
5. Traumatothelarynxandtrachea.
6. Foreignbodies dentures,debris,shrapnel,exfoliated
teeth,bonefragments.
7. Cspineinjury
8. Fullstomach
airway
h i f h i 5. Techniqueofchoice
difficulties
12
Monitoringequipments
Oxygenationequipments
WideboreSuctioncatheter(Yankauer)
I.V.access&premedication
Intubation equipments Intubationequipments
Gumelasticbougie
Surgicalorneedlecricothyrodotomy kit
Equipmentsforcheckingtubeposition
Preventionofgastricaspiration
Patientpositioning
airway
5. Techniqueofchoice q
difficulties
As with every difficult airway situation, the staff and
equipment for difficult intubation should be prepared and
ready to use.
The approach should be chosen according to the
patients injuries, airway status and the care providers
experience with such equipment & procedures.
1. Anticipationofdifficultairway/assessmentofdifficultairway
6 How would you overcome those trouble shooting / difficulties 6. Howwouldyouovercomethosetroubleshooting/difficulties
There is no single universal technique of intubation
which may be favorable in all circumstances.
Initial decision making based upon A,B,C,; later must be
practical with the need for future jaw wiring.
13
Whatarethekeyquestions?
Life threatening obstruction?
If yes: surgical airway
Not life threatening (i e able to clear airway)? Not life threatening (i.e. able to clear airway)?
Consider difficult airway issues
Regardless of the associated injuries, the
primary means of securing the airway in the vast
majorityof acutelydesaturating patients with majority of acutely desaturating patients with
maxillofacial trauma is awake orotracheal
intubation via direct laryngoscopy.
What are the problems associated?
Uncooperative patient.
Local anaesthetic preparation is time consuming, may
increase the risk of aspiration and constant bleeding in to
the airway is likely to prevent effective local anaesthesia.
During routine laryngoscopy and intubation, presence of
blood would interfere with the visibility of glottis.
What next?
Intubation attempts under induction of General
anesthesia is the next step.
Induce with inhalational anaesthetic Induce with inhalational anaesthetic.
Do not give muscle relaxant.
Now, attempt with Routine laryngoscopy.
14
Patients with bilateral mandibular body fractures
are especially at risk for tongue base prolapse;
tongue retraction with a heavy suture or towel
clamp will allow oxygenation until a definitive
airway is secured.
Suctionisoftennecessarytoclearpharyngeal
secretionsandbleeding.
i li i f h l b i d Visualizationofthelarynxmaybeimproved
withcricoid pressure byanassistant.
Inpatientswherevisualizationofthetrue
vocalcordsisstilldifficult,somehave
describedtheuseofagumelasticbougie.
Manylevel1traumacentersimmobilizetheentirespineinall
blunttraumapatientsuntilspinalinjurycanbedisproved
clinicallyand/orradiographically.
RSI forfullstomach.
Magillsforceps toremoveforeignbodies.
15
Blindairwaydevices
LMA
Combitube
LMA Fastrach LMAFastrach
Others
Submentalintubation
Retrogradeintubation
Lighted stylet Lightedstylet
Bullardlaryngoscope
SurgicalAirway
Cricothyrotomy
T h Tracheostomy
Trachlight assisted intubation
16
SUBMENTALINTUBATION:
Whenbothnasalandoralintubationaredeemed
unsuitable,controloftheairwaycanbeachieved
withsubmentalintubation.
Afterinductionofgeneralanaesthesiaorotracheal
intubationisachievedwithanarmouredtracheal
tube(withadetachableconnector).
Underallsterileconditions,a1.5cmskinincisionis
madeinthesubmentalregionjustmedialtothe
lowerborderofmandible.
Anarteryforcep isintroducedthroughthesubmental incision
towardsthefloorofthemouth.Anincisionisgiveninthefloorof
themouth,andthedeflatedpilottubecuffalongwiththetubeis
pulledoutthroughthesubmental incision.Theconnectoris
reattachedandventilationachieved.
Attheendofthesurgery,thetubeispulledbackintotheoral
cavityandtracheaextubated whenthepatientisawake.
Sincesubmental intubationrequiresadequate
mouthopeningfortheinitialorotracheal intubation,this
techniquemaynotbepossibleinmaxillofacialtraumawith
restrictedmouthopening.Retrogradesubmental intubationwith
thehelpofapharyngealloopassemblyhasbeenperformed
successfullyinsuchsituations.
RETROMOLAR INTUBATION:
Retromolar positioning of the tracheal
tube in the retromolar trigone during
intermaxillary fixation provides an
optimal intraoperative control of dental
occlusion.
The tube is fixed at the angle of the The tube is fixed at the angle of the
mouth.
At the end of the procedure, extubation
can be achieved from the retromolar
space, when the patient is awake.
A wire cutter should always be kept
beside the patient in case of emergency.
Incertaincasesflexiblefiberoptic
bronchoscopyisnotpossibleeither
becauseofdistortedanatomyorblood.
RETROGRADE INTUBATION
Retrogradewirepassedthroughthe
suctionportofthefiberoptic
bronchoscopemayguidethescopeinto
thetrachea.
Requires considerable
experience and expertise.
airway
6 How would you overcome those trouble shooting / 6. Howwouldyouovercomethosetroubleshooting/
difficulties
Extubation should be deferred until normal
anatomy is restored or at least until the edema
subsides.
Close and continuous monitoring.
Preparation for re-intubation.
Steroids.
Wire cutters.
17
airway
difficulties
9. Whichmethodsarecontraindicated?
Opticaldevices:
FOB
Glidescope.
Nasotracheal intubation:
InLeFortfractures.
18
airway
difficulties
EquipmentsforBLS:
Defibrillator
Manual/AED
EquipmentsforACLS: q p f
Drugs
Adrenaline
Vasopressin
Lidocaine
Amiodarone
Sodabicarb
Summarize
Couldberoutineoremergencypresentation
Anticipateddifficultairway
Nodefinitetechniqueofchoice
Ifnotbleedingorallyfiberoptic
Varietyofalternativetechniques
ScopeofSubmental/Retromolarintubation
Fixationoftubecouldbedifficult
Planforextubation/keepwirecutterready
Space occupying lesion in the oral cavity
What are the anatomical considerations one
should enquire
Size
Location Location
Extension
19
What specific history you would like to elicit?
Change in voice
H/O of sleep apnea
Positionone is comfortable during sleep Position one is comfortable during sleep
What specific examinations are important for
you?
Size, location of growth
Mouth opening
Distortionof the lower jaw Distortion of the lower jaw
Indirect larygoscopy
Pliability of submandibular space
Specific investigations you would advice p g y
preoperatively?
X-Ray Neck AP, lateral
CT neck
Indirect laryngoscopy Indirect laryngoscopy
20
What are the challenges faced by an
anaesthetist
Optimisation of disease (malnutrition, infection
Previous surgery distorting the airway anatomy
Radiotherapy and chemo therapy can lead to fibrosis of
oral tissues and restricting movements /reduce
compliance
Friable growth leading to sudden uncontrolled bleeding
Aspiration of blood / tumor debris
What are the difficulties you anticipate while
i t i i i ? maintaining airway?
Difficult mask ventilation
P l dl ti Prolonged laryngoscopy time
Difficulty in placement of ETT
Does previous uneventful airway management
guarantee subsequent smooth airway
management?
No
Why?
21
Anatomymaybechangedduegrowthor
surgery
Postsurgicalhealingwithfibrosis
i di i i d d fib i Postoperativeradiationinducedfibrosis
What are the implications of non-compliant sub-
mandibular space?
Non-compliant sub-mandibular space will not
allow the base of the tongue to be depressed
during laryngoscopy. g y g py
Patient will present anterior / superior larynx
Whatwillbeyourintubationtechnique?
Awake fiberoptic technique of choice
Trachlight aided intubation
Retrograde intubation Retrograde intubation
Direct laryngoscopy intubation
Howwillyoupreparethispatientforawake
intubation?
22
Psychological preparation
Premedication with mild sedation +analgesic +
anti-sialogogue g g
Instillation of vasoconstrictor
Topical administration of local anaesthetic to the
airway using 4% xylocaine, 4% xylocaine gargle
Spray-as-you-go with local anaesthetic?
Willyouperformnerveblocks?
Best to avoid because -
Could cause direct extension of the tumor
secondaryto trauma fromneedle passing secondary to trauma from needle passing
through the tumor
Normal anatomy could be distorted
Whatwillyoudoifyoulosecontrolofairway
inthiscase?
Emergencytranstrachealjetventilation
Needle cricothyrotomy and oxygenation Needlecricothyrotomyandoxygenation
Doyouanticipateanyproblemduring
extubationofthetrachea
23
Yes,becauseofthefollowingreasons
surgicalmanipulationcanleadtoedemaofthe
airway causing post extubation obstruction airwaycausingpostextubationobstruction
Damageofrecurrentlaryngealnerve/vocalcord
paralysisifneckdissection
Whatprecautionwillyoutakepriortoand
after extubation afterextubation
Use of intraoperative dexamethasone to reduce edema
formation
Awaken the patient prior to extubation
Wait for complete reversal of NMB
Extubate over jet stylet
Nurse the patient postoperative in head-up position for
12 24 hours
Keep a tracheostomy kit ready
Summarize
Assessmentofthegrowth
Previoushistoryisimportant
Investigationsbeforedecidingfortechnique
Techniquetobedecidedonthebasisofthe
growth
Avoidnerveblocks
Nosupraglotics
Extubationshouldbewithcaution
Bubbling with questions?
?
?
? ?
?
?
Thank you for asking
You were awake

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