16 09 13

Prof. A. K.
SethisEORCAPS-2013
1
Prof.A. K. SethisEORCAPS-2013
ChronicObstructiveLungDisease
DrKirti NSaxena,
Professor
GOLD
Globalinitiativeforchronic
Obstructive
Lung Lung
Disease
COPD
Preventableandtreatablediseasewithsome
significantextrapulmonary effectsthatmay
contributetotheseverityinindividualpatients
Pulmonary component is characterized by airflow Pulmonarycomponentischaracterizedbyairflow
limitationthatisnotfullyreversible
Theairflowlimitationisusuallyprogressiveand
associatedwithanabnormalinflammatory
response
ofthelungtonoxiousparticlesorgases
RiskfactorsforCOPD
Geneticdefeciency ofalpha1antitrypsin
Exposureto:tobaccosmoke,occupationaldust,
cookinginpoorlyventilateddwellings
Respiratoryinfections
Previoustuberculosis
Socioeconomicstatus
Nutrition
Mechanismsofairflowlimitationin
COPD
Inflammation
SmallAirwaydisease
Airwayinflammation
Airwayremodelling
Parenchymal destruction
Lossofalveolarattachments
Decreaseofelasticrecoil
AirflowLimitation
Chronicbronchitisvs Emphysema
Feature Chronicbronchitis Pulmonaryemphysema
Mechanismofairway
obstruction
Mucus&inflammation Loss ofelasticrecoil
Dyspnea Moderate Severe
FEV1
PaO2
Diffusingcapacity normal
Hematocrit normal
Cor pulmonale Marked mild
Prognosis poor good
Prof. A. K. SethisEORCAPS-2013
2
Stage Severity FEV1/FVC FEV1 Symptoms
0 Atrisk,chronic
symptoms
normal normal cough,sputum
production
1 Mild <0.70 >80%predicted ,,
Spirometric ClassificationofCOPD
SeverityBasedonPostBronchodilatorFEV1
2 Moderate <0.70 >50%predicted ,,
3 Severe <0.70 3050% predicted Chronic respiratory
failure
4 Verysevere <0.70 <30%predicted PaO2<60mmHg,
PCO2>50mmHg
Case1
56years,maleforpyelolithotomy
h/ocoughwithexpectorationoffandon2years
h/odyspnea grade2
h/ ki 30 20 30 i /d h/osmoking30years,2030cigarettes/day
h/oadmissiontohospitallastwinterwithcough
andseveredyspnea.RequiredO2therapy
Noh/oDM,HT,IHD
Examination
Pulse80/min,BP 140/80mmHg
Nopallor,clubbing,koilonychia
ChestBarrelshaped,B/Lreducedairentry,
rhonchi+ rhonchi+
CVS S1,S2 normal,nomurmur
Airway Interincisor gap >3fingers,MPgrade2
Investigations
Hb 12gm%
Bl sugar(random) 112mg%
KFT Bl urea 38mg%,s.creat 1.1mg%
Urine albumin ve sugar ve Urine albuminve,sugarve
Xraychest (pic)
ECG RAD
PFT FEV1/FVC0.55,FEV160%
ABG PaO280mmHg,PaCO2 48mmHg
XRayChest
Lungsarehyperinflated
Diaphragmisflattened
Vascularmarkingsareincreased
Heart size is marginally increased
back
Heartsizeismarginallyincreased
Preoperativeoptimisation
Smokingcessationoptimally6weeksbefore
Optimaldrugtreatmentofobstructiveairflow
1. 2agonists
2. Corticosteroids 2. Corticosteroids
3. ?Anticholinergic agents
4. Theophylline
Treatmentofinfectionwithantibiotics
Physiotherapy lungvolumeexpansion
maneuvres
3
EffectsofPreoperativesmoking
cessation
Cardiac:
1. Preventsfurtheradvancement
2. COO2delivery,myocardialwork
3. Coronaryvasoconstriction
4. Improved exercise capacity 4. Improvedexercisecapacity
Respiratory:
1. Mucociliary activity
2. Hyperreactivityofairways
3. Pulmonaryimmunefunction
Impairedwoundhealing
Improved
Anestheticmanagement
Bronchodilatorstocontinueperioperatively
Premedication Benzodiazepinespreferred
Regionalanesthesiaispreferable notadvisedfor
pyelolithotomy
Ai i LMA ETT Airwaymaintenance LMAvs ETT
Volatileanestheticsfavoured formaintenance
Guardagainstopioid inducedrespiratory
depression
Controlledventilationpreferred RR, TV,
Expiratorytime,noPEEP
Postopcare
Lungexpansionmaneuvres
Goodanalgesia useofRAtechniques
?Postop mechanicalventilation
Oxygenation
COR PULMONALE
Characteristics
Rightventricularenlargement
Causedbymanytypesofrespiratorydiseases
Associatedwithchronichypoxia
Usuallyseenafter50years
Ultimatelyrightventricularfailuresetsin
Diagnosis
ECGPeakedPwavesinL11,L111&aVF
suggestiveofRightventricularandrightatrial
hypertrophy
Partial or complete RBBB PartialorcompleteRBBB
XRay: widthofRpulmonaryartery,
pulmonaryvascularmarkings
ECHO SizeandfunctionofRatrium
4
Management
Supplementaloxygen
Diuretics
Digitalis
Anestheticmanagement
SimilartoCOPD
Hydration
Correctionofelectrolyteimbalances
BRONCHIALASTHMA
Differencesinpulmonaryinflammation
betweenasthmaandCOPD
COPD BronchialAsthma
Cells Neutrophils,macrophages,CD8+ T
cells
Eosinophils,macrophages,CD4+
Tcells
Keymediators IL8,TNF,IL1,IL6,NO Eotaxin,IL4,IL5,IL13,NO
SiteofDisease Peripheral airways,
lungparenchyma,pulmonary
vessels
Proximalairways
Consequences Squamous metaplasia,Mucous
metaplasia,smallairwayfibrosis,
parenchymal destruction
Fragileepithelium,mucous
metaplasia,basement
membrane,bronchoconstriction
Responseto
therapy
Smallbronchodilatorresponse,poor
responsetosteroids
Large bronchodilatorresponse,
goodresponsetosteroids
Case2
26yearsfemale
Diagnosedcaseofbronchialasthma
Hadroadsideaccident2daysago
Scheduled to undergo surgery for trimalleolar Scheduledtoundergosurgeryfortrimalleolar
fractureRankle
Noprevioushistoryofsurgery/anesthesia
O/E GPE NAD
Chest B/Lclear
Historyspecifictobronchialasthma
Ageatonset
Triggersforacuteasthmaticattack
PreviousexposuretoNSAIDSandresponse
Duration of disease Durationofdisease
Severityofattack
Timingoflastattack
Presenttreatmentandresponsetoit
Whethersteroiddependent
5
TreatmentofBronchialAsthma
Antiinflammatory corticosteroids
Inhibitorsofmediatorreleasefrommastcells
cromolyn
Leukotreine synthesisinhibitors zafirlukast, y ,
pranlukast,monteleukast
Bronchodilators:
1. B2receptoragonists
2. Anticholinergics
3. Methylxanthines
ResponsetoBronchodilators
PFTdonepreandpostbronchodilatortherapy
criteriaforreversibility
1. >15%improvementinFEV1&FVC
2 30% i i 2 0 2. >30%improvementinFEF2575or50
Criteriafortakinguppatientfor
surgery
Appropriateseason
Chestauscultationoptimised
Bloodeosinophil countsshouldbenormal
Preop preparation
Chestphysiotherapy lungvolumeexpansion
maneuvres
Premedicationhasspecialsignificancein
bronchial asthma bronchialasthma
Optimizebronchodilatortherapyandcontinue
bronchodilatorstillmorningofsurgery
Stressdoseofcorticosteroids
Choiceofanesthesia
Regionalanesthesa preferredifsurgerypermits
GA IVinductionpreferred
Preventbronchospasm byattainingadequate
depth,IVLignocaine
Musclerelaxants nondepolarising,noreleaseof
histamine
ETorLMA?
Mechanicalventilation
Adequatefluids
Extubation indeepplaneadvocated
Intraoperative bronchospasm
Deepenplaneofanesthesia
B2agonist,corticosteroidadministrationby
nebulisation
h l hi Intravenousmethylxanthines
IVketamine
6
Postop analgesia
AvoidNSAIDS
Judicioususeofopiates
RA
Paracetamol
1
Prof.A. K. SethisEORCAPS-2013 Prof.A. K. SethisEORCAPS-2013
2
Pulmonarychanges Pulmonarychanges
PulmonaryAgenesis
Vesselwallthickening
Pulmonaryhypertension
Pulmonaryelastin expressionisdecreased
anddisorganizedinthenitrofeninduced
rat model of CDH
Mychaliska GB, Officer SM, Heintz CK, Starche BC, Pierce RA.Pulmonaryelastin expressionisdecreasedinthe
nitrofeninducedratmodelofcongenitaldiaphragmatichernia.J.Pediatr Surg.2004;39:666671.
ratmodelofCDH.
Histopathological Histopathological featuresofCDHlungs featuresofCDHlungs
include
Reducednumbersofalveoliarea
Thickenedalveolarwalland
Increased interstitial tissue Increasedinterstitialtissue
leadingto
diminishedpostnatalalveolarairspace
decreasedgasexchangesurfacearea
Persistentpulmonaryhypertension(PPHN) Persistentpulmonaryhypertension(PPHN)
characterizedby
theabnormalvascularstructureandnumber theabnormalvascularstructureandnumber
medialhyperplasia
peripheral extension of the muscle layer peripheralextensionofthemusclelayer
intothesmallintraacinary arterioles
adventitialthickening
leadingto
increasedmuscularization ofthearterioles
increasedvasculartone
3
Preoperativepreparation
Intrauterineperiod
Afterbirth
Trachealocclusion
didnotimprovesurvivalor
morbidityratein
thiscohortofinfantswithCDH
Pathophysiology Pathophysiology
PreoperativeStabilisation p
4
RespiratoryStrategy
Hyperventilation
Gentleventilation
PIP<25,cmH2O,RR<65/min,Insp
time0.35s,PEEP+<2cmH2O
aimofmaintainingpH>7.25
Permissivehypercapnia upto60mmHg
Volumeresus andinotropes
Correctionofelectrolyteandacid
basestatus
Alternateventilatory strategy
Surfa ctant therapyconfersnobenefit
Issurfactanttherapybeneficialinthetreatmentofthetermnewborninfantwith
congenitaldiaphragmatichernia?VanMeurs KandtheCongenitalDiaphragmatic
HerniaStudyGroup. JPediatr 2004;145:312316.
ECMO benefits only when predicted mortality is > 80 % ECMObenefitsonlywhenpredictedmortalityis 80%
Doesextracorporealmembraneoxygenationimprovesurvivalinneonateswith
congenitaldiaphragmatichernia?TheCongenitalDiaphragmaticHerniaStudy
Group.JournalofPediatricSurgery1999;34:720725
costUS$160000//patient(Seminarperinatol 2005;29:129133)
HFO
Respiratorycarestrategy Respiratorycarestrategy
EarlyHFO,NO
Delayedsurgerytillrespiratory
andhaemodynamic
stabilisation
5
Anaesthetic management
Painmanagement
Post op management Postopmanagement
Unquestionedcornerstone Unquestionedcornerstonein
treatmentofCDH
1. 1. Deferredsurgery Deferredsurgery
2. 2. Gentleventilation Gentleventilation
3. 3. Stabilisation Stabilisation
1
POTASSIUM CHLORIDE
ampoule
DrDeepti Agarwal
Learning Objectives
Howtodescribeanampouleinviva
Assessmentofseverityandclinicalpresentations
f h k l i d h k l i ofhypokalemiaandhyperkalemia
Ascertainingthecauseofbothdisorders
Managementandanaestheticimplicationsof
both
Describe this
AmpoulesofPotassiumChlorideareprovidedinthe
followingvarietyofconcentrationsandsizes
Ampoules*
(conc.&size)
K+
mEq/mL
KCl
mg/mL
mOsmol/mL
(calc.)
30mEq/20mL 1.5 112 3
10mEq/5mL 2 149 4
20mEq/10mL 2 149 4
30mEq/15mL 2 149 4
40mEq/20mL 2 149 4
*MaycontainhydrochloricacidforpHadjustment.
Description of ampoule
Volume 10mlampoule
Mainandadditionalcontents(antimicrobial
) agent,buffer,bacteriostatic) Potassium
Chloride
Concentrationofeach eachmlcontains149
mgor2mEq/ml
149mg/mlor14.9%or14.9g/100ml
2
Can you convert mg to mEq ?
Equivalentweight=gramatomicweight/valency
AtomicweightofKCl 39+35.5=74.5g/1
Eq weightofKCl =74.5g
convertingtomEq =74.5g/1000=74.5mg co e t g to q 5 g/ 000 5 g
74.5mg=1mEq ofKCl =1mEq ofK
+
and1
mEq ofCl
149mg=Approx 2mEq K
+
/ml
What about in mmol ?
mmol =mEq forK
+
Description
Route forintravenoususeonlyafterdilution
PhysicalpropertylikepHorosmolality pH
4.6,osmolality 4000mOsm/L
Indicationsforuse
Contraindications
Relevantpharmacology
Dosageandadministration
Indication of Use
TreatmentofHypokalemia
Potassiumreplacementforpatientsonenteral
andparenteralnutrition
For preparing glucose insulin and potassium Forpreparingglucose,insulinandpotassium
solutions
Contraindication
PatientswithHyperkalemia,renalfailureandin
conditionswithpotassiumretention
What is the role of K
+
in body ?
Role of K
+
in body - Clinical pharmacology
K
+
extracellulartointracellularratiomaintains
therestingmembranepotentials,generates
actionpotential,cofactor,fluidbalance,rolein
pathogenesisofessentialhypertension
Totalbodystores 50mEq/kg
98%intracellularand2%extracellular
Extracellular 3.5 5mEq/L
Intracellular 125140mEq/L
8090%excretedbykidneys,restbygut
ArchInternMed.2000;160:24292436
What is Hypokalemia ?
Serumpotassium<3.5mEq/L
Mild 3.1 3.4mEq/L
Moderate 2.5 3mEq/L
S 2 / Severe <2.5mEq/L
How will you assess the K
+
deficits ?
Acuteloss deficit10%oftotalbodyK
+
stores
forevery1mEq/LfallinSerumK
+
Chronicloss deficitsmuchmore
3
Estimateddeficitsfora70kgperson(withtotalbodyK
+
of50
mEq/L)=3500mEq
Sr K
+
(mEq/L)
K
+
deficits
mEq %TotalbodyK
+
3 0 175 5 3.0 175 5
2.5 350 10
2.0 470 15
1.5 700 20
1.0 875 25
Changes in serum K
+
and total body K
+
curvilinear-
assessment difficult
Sr.K
+
(mEq
/L) /L)
K
+
deficit(mEq) K
+
excess(mEq)
What factors regulate serum potassium?
Kidney
Excretedbytwoprincipalfactors
Aldosterone
Intrinsicrenalmechanism(rateoftubular
flow, solutedelivery)
AbsorbedagainstH
+
ionsecretion
Muscleandliver Insulin,Catecholamines
H
+
ions acuteriseof0.1pHunitsK
+
by0.8
acutefallof0.1pHunitsK
+
by0.5
Causes of Hypokalemia
Transcellular
shift
insulin,alkalosis,
2
agonist,hypokalemicperiodic
paralysis,hypothermia
Renallosses diuretics,steroids,Mgdepletion
renaltubularacidosis,nephrotoxin(amphotericinB,
aminoglycosides)
primaryhyperaldosteronism,cushingsyndrome,
congenitaladrenalhyperplasia
nonreabsorbableanions(penicillins),DM
polyuria
GIlosses vomiting,gastricsuction,intestinalloss
Other Sweat,inadequateintake
Case 1
A57yearsoldwomanpostedfor
cholecystectomyforsymptomaticgallbladder
(complaintsofpainabdomenandvomiting)
Known hypertensive and controlled on Knownhypertensiveandcontrolledon
HydrochlorothiazidesandAtenololforpast
5years.
Investigation K
+
2.4mEq/L
4
How will you prepare the patient for
anaesthesia and surgery ?
History determineandtreatthecause,stopoffending
drug
Identifycomplications cardiovascular,neuromuscular
Investigations renalfunctions,bloodglucose,SerumNa
+
,
Mg
++
andCa
++
,ABG,plasmaaldosterone,urinaryK
+
g , , p , y
excretion
What is the normal conc. of K
+
in urine ?
5 15mEq/L
>20mEq/L renallosses
<20mEq/L extrarenal causes
What are the Complications of
hypokalemia ?
ChangesinratioofextracellulartointracellularK
+
concentrationalterrestingmembranepotential
hyperpolarizaonaltertheexcitabilityof
tissues slowing of nerve conducon tissuesslowingofnerveconducon
Acuteonset disturbanceofraomoresigns
andsymptoms
Chronicloss ratioofintracellulartoextracellular
relavelystablelesssymtomsdespitehigh
deficit
Neuromuscular
Theeffectsofhypokalaemiadependuponthe
serumlevel
3.03.5mmol/L asymptomatic
3.0mmol/L symptomsofweakness,
lassitude andconstipation
2 5 l/L k l 2.5mmol/L severeweakness,muscle
necrosis
2.0mmol/L paralysisleadingtorespiratory
compromise.
Others
polyuriaduetodefectinrenalconcentratingability,
Ileus,gastroparesis
Cardiovascular-
IHD,CHForleftventriculardysfunction,patient
ondigitalis atriskofarrhythmiaswithonlymild
ormoderatehypokalaemia
What are the ECG changes in hypokalemia ?
fl i Twaveflattening
Uwaveprominent
STsegmentdepression
Prematureventricularcontractions,
Prematureatrialcontractions
Reentrant arrhythmias,VT,VF
Nonspecificandunreliable
ECG changes
5
How will you treat hypokalemia ?
Causetransmembrane shiftsordepletion?
Iftransmembrane shiftsreplacementcanleadsto
overshootandhyperkalemia
Causeacuteorchronic?
Acute urgent treatment if symptomatic or Acute urgenttreatmentifsymptomaticor
arrhythmias
Chronic asymptomatic,slowreplacement
K
+
replacementsalts chloride(best)
bicarbonate(inacidosis)
phosphate(DM)
Mild to moderate hypokalemia
Oralsalts safer,gastricirritant
Dose 13meq/kg/dayin2 4divideddosesper
day
Preparations powder,elixir,controlledrelease
microencapsulatedtablets
Intravenous
Rate 1020mEq KCl/hr
Concentration 40mEq/Lofsaline
Maxallowable 200mEq in24hrs
monitorlevels
Severe hypokalemia
Rate 40mEq/hrwithECG
monitoring orabolusof5 6
mEq
Maxallowable 400mEq/24hrs
MonitorK
+
levels1 3hrly
Refractory lookforhypomagnesemia
Cautiouslyinfusedinmetabolicacidosis,renal
impairement,diabetes,patientonNSAIDs,ACE
inhibitors,ARBsor
2
blockers
What is the route of administration ?
OsmolalityofK
+
solutions4000mOsm/L
largeperipheralline upto 40mEq/L g p p p q
avoidcentralveinifcatheterinatriaor
ventriclewithinfusions>20mEq/hr
ifhigherconcentrationrequired,usetwo
peripherallinesorfemoralvein
What are the Anaesthesia concerns ?
NominimumK
+
levelsatwhichconductofanaesthesiasafe(>2.6
mEq/L)
Mildtomoderatehypokalemia,optimumcondition,causeis
knownneednotpostponed
Acutehypokalemia rapidcorrectionrequiredinpresenceof
i h h i preoperativearrhythmias,pre
existingcardiacdisease,patientsondigoxin
Chronichypokalemia 0.2mEq/kg/hr beneficialifstarted
preoperatively
Other Anaesthesia concerns.
myocardialcontraclity,sensivetocardiac
depressanteffectsofvolatileagents,diuretics
NDMRaconprolonged(doseby2550%)
Adrenaline in LA further K
+
AdrenalineinLA furtherK
+
Hyperventilation,insulin,glucose, agonist,
rylestubesuctioning furtherK
+
Monitoring ECG,serumK
+
,capnography,
neuromuscularmonitor
6
Case 2
Emergencyrequisitionforobstructedhernia
surgeryfora65yearoldmale,presentedwith
painabdomenandpoorlycharacterized
history of generalized chest pain generalized historyofgeneralizedchestpain, generalized
bodypainandgeneralizedweakness.Known
caseofHT(onenalapril),CKD.Missed
yesterdaydialysis.ECGshowspeakedT
wavesandPRintervalincreased.Bloodurea
100mg/dl,creatinine3.5mg/dl.K
+
is7.2
mEq/L.
How will you define hyperkalemia ?
K
+
>5.0mEq/L
Potentiallylifethreatening
Mild 5.1 6.0mEq/Lusuallywelltolerated
Moderate 6.1 7.0mEq/LproduceECGchanges
Severe >7mEq/Ldangerousleadingto
cardiac arrest
What are the causes of hyperkalemia?
RenaldysfunctioncausingimpairedK
+
excretion
ARF,CRF,obstructivediseasesofurinarytract,
glomerulonephris,transplantrejeconGFR<
10ml/min
Diseasesofadrenalglands Addisonsdiseases, g
hypoaldosteronism
Transmembraneshifts metabolicacidosis,
diabeticketoacidosis, blockers,acutedigitalis
toxicity,succinylcholine,hyperkalemicperiodic
paralysis
Causes of hyperkalemia.
EndogenousandExogenousadditionofK
+
massivebloodtransfusions,crushinjury,burns,
upperandlowermotorneurondisease,
rhabdomyolysis,haemorrhages, potassium
supplements,saltsubstitutes pp ,
Medications ACEinhibitors,NSAIDs,ARBs,
Heparin,K
+
sparingdiuretics
Pseudohyperkalemia haemolysed bloodsample,
faultyvenepuncture,severeleucocytosis,
thrombocytosis,erythrocytosis
SerumK
+
measuredinunclotted sample
What is the Clinical presentation ?
Depolarizescellmembraneexcitability
transmissionofelectricalimpulses
Cardiac slowingofelectricalconduction,reentry
arrhythmias fibrillation asystole arrhythmias,fibrillation,asystole
Neuromuscular paresthesias,muscleweakness
sparingdiaphragm,flaccidparalysis,
hypoventilation
Others impairsrenalcompensationfor
metabolicacidosis
Clinical presentation ECG changes
ECG changes K
+
levels
Symmetric peakingofTwaves K
+
>6mEq/L
PRprolongation (K
+
>7mEq/L)
AbsentPwave,wideningof
QRS
(K
+
>89mEq/L)
Atrialactivitylost,ventricular
tachycardia/fibrillation
Sensitivityislow
7
ECG changes
ECG changes
Diagnosing the cause
History renalfailure,trauma,diabetes,drugs
Examination cardiovascular,neurological
examinaon(DTR,cranialnervesandsensory
systemspared)
Investigations serumK
+
,renalfunction,serum
l i l ABG di i l l ti l d calcium,glucose,ABG,digoxinlevels,cortisoland
aldosteronelevels,urineK
+
Urinepotassium
>30mEq/Ltranscellularshi
<30mEq/Limpairedrenalexcreon
How will you treat hyperkalemia ?
When to treat?
>6mEq/Lstepsshouldbetakentoprevent
further increase
If the serum K
+
is 6 5 mEq/L or IftheserumK
+
is6.5mEq/Lor
MildhyperkalaemiaaccompaniedbyECG
changes orsymptoms(muscleweaknessor
flaccid paralysispalpitations,paresthesias)
Goals
Stabilizingthemyocardium
ShiftingK
+
fromextracellularspace
PreventingadditionsofK
+
PromotingrenalandGIlosses
Mild hyperkalemia
Lowerpotassiumintake,K
+
losingdiuretics
(furosemide),Cation exchangeresins,treat
cause
Moderate to severe hyperkalemia-
Stabilizing membranes- Calcium
CalciumGluconate(10%)
Dose 30mg/kgIV,repeatdoseafter5min
Rate givennot>1ml/min,510ml/2minunder
cardiacmonitoring
Onset15min
Duration 30 60min
How much Ca is provided by 1ml of Ca
gluconate? 0.45mEq/ml
8
Stabilizing membranes- Calcium
CalciumChlorideincirculatorycompromise
Dose 10mg/kg,repeatdoseafter5min
Rate notgiven>1ml/min
Onset 15min,Duration 3060min
How is Ca chloride different ?
Provides1.35mEq/ml,moreirritanttoveins
Caution
Calciumcautiouslygiven pt.ondigitalis(diluted
in 100mlsalineinfusedover2030min)
CalciumwillnotlowerK
+
levels,definitiveT/t
must bestarted
Stabilizing membranes- Hypertonic saline
Intravenoushypertonicsodiumchloride
showntoreverseECGchangesinpatientswith
hyponatremia
Role in eunatremic patients not established Roleineunatremicpatientsnotestablished
Userestrictedtohyponatremicpatients
Caution volumeoverload
Insulin with glucose
Dose 1015Uregularinsulinwith50mlof50%
dextrose(25g)
Rate50ml/hrIV,bolusdosealsorecommended
Onset in15min,levelsby0.6mEq/Lin60min
Duration 4 6hrs
Caution Largeorcentralveinchosen,monitorglucose
Would you give glucose with insulin in DM?
Insulincanbeadministeredasasingleagentwithout
glucoseifglucose>15mmol/L
2
Adrenergic agonist
PromotescellularuptakeviaNa
+
/K
+
ATPase,K
+
within3060min,moreeffectivewithinsulin
glucose(1.2)
Dose Albuterol10 20mgnebulization(0.6,1)
0.5mgI/V(1)
( ) MDI(0.4)
subcutaneousTerbutaline7g/kg
Onset 15 30min
Duration 23hrs
Caution Tachycardia cardiovasculardisorders,
hyperthyroidism;dialysisdependentpatientand
Patientsonbetablockersmayberesistant
Cation exchange resin- sodium polystyrene
sulphonate
BindsK
+
inexchangeofNa,promoteexcretion
viagastrointesnaltract,1gram 0.65mEq
Oraldose 30gin50mlsorbitol
Rectal dose 50 g in 200 ml sorbitol, kept for at Rectaldose 50gin200mlsorbitol,keptforat
least3060min
Reducelevelsafter2hrsby0.51mEq/L
Multipledosesrequired,34hrlyupto5
doses/day
Caution intestinalnecrosis,volumeoverload,
poorchoiceforurgenttreatment
Sodium bicarbonate
CounteractsacidosisandmovesK
+
from
extracellularspacetocells
Dose 1mEq/kgIVover5minrepeatedafter
30 min 30min,
totaldoseatonetimenottoexceed100mEq
Onset <30min
Duration 12hrs
Caution canbindcalcium,CHF,hypernatremia
9
Diuretics
Furosemide,K
+
excretioninurinebut
effectis inconsistent,dose20 40mgIV
Dialysis Dialysis
Mosteffectiveanddefinitivebutinvasive,
effectiveinhyperkalemiaunresponsiveto
pharmacologicalmeasureslikeinrenal
failure orinmarkedtissuebreakdown,
lowerbyas muchas1.2to1.5 mEq/h
Agent Onset Duration
Calciumgluconate (10%) Immediate 3060min
Insulin(shortacting) 20min 46hrs
Albuterol 30min 2hrs
Loop diuretics 15 min 23 hrs Loopdiuretics 15min 23hrs
Sodiumbicarbonate Hrs Durationofinfusion
Sodiumpolystyrenesulfonate 2hrs 46hrs
Hemodialysis Immediate 3hrs
CritCareMed2008Vol.36,No.12
A recent Cochrane review of the efficacy of various
potassium lowering therapies showed-
Glucose Insulinandbetaagonistsbothseemto
beeffective,andacombinationseemsmore
effective.Theevidenceforsodiumbicarbonateis
equivocal.
Administrationofcalciumrecommendedasa
means of rapidly reversing the repolarisation meansofrapidlyreversingtherepolarisation
abnormalitiesandissupportedbyexperimental
andanimalstudies.
Cornerstoneoftreatmentistodiagnosethe
underlyingcauseofhyperkalaemiaandtakesteps
toreversethis.
What are the Anaesthetic concerns ?
K
+
shouldbe<5.9mEqbeforegivinganaesthesia
Continuetreatment Keepcalciumandglucose
insulinavailable
Donotadministersuccinylcholine(K
+
by0.30.5
mEq/L)
Titratedoseofnon depolarizingrelaxants
requirementmay
Anaesthesia concerns
MinimizelikelihoodofaddionalinK
+
levels
avoidpotassiumcontainingfluids,avoid
metabolicandrespiratoryacidosis
Careful bloodtransfusions,tourniquetrelease
MonitorK
+
levels,ECG,neuromuscularfunction,
capnography
Continuemonitoringinpostoperativeperiod
To Summarize
Hypokalemiaandhyperkalemiaarefrequently
encounteredandaretheresultofdisturbances
intranscellularshifts,potassiumexcretionor
potassiumintake.
Serum potassium is not a true reflection of Serumpotassiumisnotatruereflectionof
totalbodystores.
Presentingsymptomsgenerallyaffectthe
cardiac,neuromuscularandgastrointestinal
systemsorattimesvague.
Severityshouldbeassessedusingserum
potassiumlevelsandclinicalevaluation.
10
To Summarize
Nourgencytotreatmildhypokalemiaunless
thereiscardiacpathologyorpatienton
digitalis.
Hypokalemia should be treated using Hypokalemiashouldbetreatedusing
potassiumchloridesalts.
HyperkalemiamanagedwithCalcium,
glucose insulinandB
2
agonist.
Sodabicarbonateuseisnoteffectiveand
reserved.
Timelymanagementcanavertacriticalevent.
Suggested reading
MillerRD.Anaesthesia.6
th
Edition.
MarinoPL.TheICUbook.3
rd
Edition
CivettaJM.CriticalCare.3
rd
Edition
Stoelting RK Dierdorf SF Anaesthesia and Coexisting StoeltingRK,DierdorfSF.AnaesthesiaandCo existing
Diseases.5
th
Edition
Brash,Cullen,Stoelting,Cahalan,Stock.ClinicalAnaesthesia.
6
th
Edition
FarokhErachUdwadia.PrinciplesofCriticalCare.2
nd
Edition
IrwinandRippe'sIntensiveCareMedicine,6thEdition.
Harrison'sPrinciplesofInternalMedicine,18
th
Edition
1
Sodiumbicarbonate
DrNandita
objectives
Tolearnhowtodescribeanampoule
Toknowtheindications,contraindications,
complicationsandmethodofadministrationof
bicarbonate
Tounderstandthebasicsofuseofbicarbonatein
variousclinicalsituations
Tolearnaboutalternativealkalizingagents
Describeit
Itisanampoulecontaining10ml
solutionofsodiumbicarbonatein
a strength of 7.5% w/v astrengthof7.5%w/v
Itissterileaqueous,pyrogen
freepreparationofNaHCO3
Description
Availableas
Concentration Bicarbonate&sodium Osmolarity
4.2% 0.5meq/ml 1000mOsmol/L
7.5% 0.9meq/ml 1800mOsmol/L
8 4% 1 meq/ml 2000 mOsmol/L 8.4% 1meq/ml 2000mOsmol/L
pHadjustedbymeansofaddedCO
2
andisapproximately7.8
(78.5)
Preservativefreesingledoseampoules
Pharmacology
NaHCO
3
H
2
ONa+andHCO
3
Increasesplasmabicarbonate
HCO
3
+H
+
H
2
OandCO
2
Buffers excessive hydrogen ion concentration Buffersexcessivehydrogenionconcentration
IncreaseplasmaNa
Increasesplasmaosmolarity
Normalkidneyfunctionallglomularfiltratebicarbonateis
absorbedlessthan1%excretedinurine
Indicationandusage
Metabolicacidosis
Hyperkalemia
Poisoning and drug intoxications Poisoninganddrugintoxications
Urinaryalkalization drugs,rhabdomyolysis
Addedtolocalanestheticstoenhanceonset
andpotencyofeffects
2
Inconsideringacutebicarbonatereplacementfour
questionsshouldbeconsidered
Whatarethedeleteriouseffectsofacidemiaandwhenare
theymanifest?
Whenisacidemiasevereenoughtowarranttherapy?
How much bicarbonate should be given and how is that Howmuchbicarbonateshouldbegivenandhowisthat
amountcalculated?
Whatarethedeleteriouseffectsofbicarbonatetherapy?
OptimalextracellularpH7.4
OptimalintracellularpH7.1
DeviationsfromnormalpHdecreasestheefficiencyofall
reactions reactions
ExtracellularpHisasurrogateforintracellularpH
Isallacidemiaharmful?
Effectofacidemiaondrugmetabolism
Decreasedbindingofnorepinephrinetoitsreceptors
Drugswhicharesaltsofweakacidsaremoreactiveduring
acidemia
More receptor binding Morereceptorbinding
Moreentrytocells
BestexampleisASA,tolbutamide,methotrexate
Phenobarbitalphenytoin
Whenisacidemiasevereenoughto
warrantalkalitherapy?
BloodpHbelow7.157.20lifethreateningacidemia
WhenHCO
3
fallsbelow10mEq/l.
Treatmentofhyperkalemiawithmetabolicacidosis
AimofHCO
3
therapy
pH>7.2
HCO
3
>10meq/l
3
q
3
HCO
3
bufferpoolisgeneratedbythedissociationofH2CO
3
:
CO
2
+H
2
OH2CO
3
H
+
+HCO
3
Dissociationconstantofcarbonicacidis6.1
Buffersaremosteffectivewithin1pHunitoneitherside
effectiverangeofHCO
3
bufferECFpHbetween5.1and7.1
pHunits
Thevolumeofdistributionofbicarbonateisapproximately
thatoftotalbodywater
In patients with metabolic acidosis it is said to vary from 50% Inpatientswithmetabolicacidosisitissaidtovaryfrom50%
togreaterthan100%,dependingontheseverityofthe
acidemia
Henceestimatedbicarbonatedeficit
HCO
3
deficit(mEq)=0.5 wt(kg) (15measuredHCO
3
)
Bicarbonatetherapyusefulinhyperchloremic (normalAG)
metabolic acidosis metabolicacidosis
ControversialinincreasedAG startedlatediscontinuedearly
Whatarethedeleteriouseffectsof
bicarbonatetherapy?
HypernatremiaandvolumeoverloadespeciallyinCHFor
renalfailure
Hypertonicrapidinfusion(>1mEq/kg/min)intravascular
volumeexpansionintracranialhemorrhage
CNSacidosisandhypercapnia
Hypokalemiaandhypocalcaemia
Overshootorreboundalkalosisinorganicacidosis
Howtoadministerbicarbonate
Administerhalfcorrection over48hours
HighlyirritantsouselargeI.V.lineforinfusion
Desireddilutesolutionspreparedusingdextrose5%,sterile
l waterorNaCl0.9%
AvoidbolusesofNaHCO3exceptinemergency
Correcthypokalemiabeforecorrectingacidosis
Roleinspecificsituations
LacticacidosisOnlysevereacidosispH<7.2
DKAnoroleindicatedonlyifpH<7.1
ARFandCRFhighAGmetabolicacidosistreatment
dialysis
CRFBicarbonatesupplementationtopreventrenalrickets
orosteomalacia
4
GILossofbicarbonatecorrectionwithNaHCO
3
required
DistaltypeIBicarbonatesupplementationnecessary
ProximaltypeIIBicarbonatetherapyonlyinseverecases
Precautions
Donotuseunlesssolutionisclear
Discardunusedportion
CautionincirculatoryoverloadCoexistenthypokalemea,
hypocalcaemia
Pediatric rapidinjectionmayproducehypernatremia,
decreaseinCSFpressure,intracranialhemorrhagedose
8meq/kg/day4.2%solution
Druginteractions
Additivesincompatible
Norepinephrineanddobutamineincompatible
Precipitateswithsolutionscontainingcalcium
Contraindication
PatientsloosingchloridebyvomitingorcontinuousGIsuction
Diuretics hypochloremicmetabolicalkalosis
Overdose
Metabolicalkalosis
Symptoms
Muscletwitching,irritabilityortetany
Treatment
bi b Stopbicarbonate
0.9%NaClinjection
Treathypokalemia
Severealkalosis calciumgluconate
Acidifyingagentlikeammoniumchloride
Hypernatremia
EachmlofNaHCO
3
contains 4.2%=0.5mEqNa+/L
8.4%=1mEqNa+/L
OverdosecanleadtohypernatremiawithincreasedECF
volume
Clinicalfeatures nausea,vomiting,alteredmentalstatus,
irritabilityoccasionallycomaandseizures
5
Treatthecause
Loopdiureticadministeredalongwithwatertofacilitate
sodiumexcretion
Bicarbonatetherapyonlyinseverecases
RoleinACLS
ACLS2010Noevidencetosupportitsuse
Restorationoftissueperfusion,ventilationsupportrapid
ROSC mainstayofrestoringacidbasebalance
Deliritiouseffectsduringarrest
ReducesvascularresistanceCompromisesCPP
MetabolicalkalosisO
2
dissociationcurveshiftstoleft
hamperstissueoxygenation
I t ll l id i Intracellularacidosis
CO2productionexacerbatescentralvenousacidosis
inactivatescatecholamine
Hypernateremiaandhyperosmolarity
Indicationsduringarrest
Preexistingmetabolicacidosis
Hyperkalemia
TriCyclicAntidepressant
DOSE 1mEq/kgguidedbybicarbonateconcentrationand
basedeficit
Roleinhyperkalemia
Severesymptomatichyperkalemia
NaHCO
3
intracellularshiftofK+
Dosage7.5%50100ml(4590mEq)bolusi.v.over1020
minutes followed by I V NaHCO3 drip minutesfollowedbyI.V.NaHCO3drip
Onset510minuteseffectlastsfor12hours
Adverseeffect hypocalcaemia
Contraindication CHF,CRFESRD
Roleintoxicitiesanddrugoverdosage
Toxicologicalindications:
Cardiotoxicitysecondarytofastsodiumchannelblockers:
Tricyclics
Bupropion p p
Dextropropoxyphene
Propranolol
Type1aand1cantiarrhythmics(flecainide,quinidineandquinine)
PreventionofredistributionofdrugtotheCNS
severesalicylatepoisoning
6
Eliminationofpoisons
Immediatecorrectionofprofoundlifethreateningmetabolic
acidosis:
cyanidepoisoning
isoniazidpoisoning
toxicalcoholpoisoning(ethyleneglycol,methanol&othertoxic
alcohols) alcohols)
Enhancedurinarydrugelimination
salicylateintoxication(anysymptomaticpatient)
phenobarbitoneintoxication(anysymptomaticpatient)
increasedurinarysolubility
methotrexatetoxicity
druginducedrhabdomyolysis
Roleinanaesthesia
LAwithpKa closesttophysiologicalpHnonionizedform
readilycrossesplasmamembrane
Commercial preparation pH67
Epinephrine containing local anesthetic solutions pH 45 Epinephrine containing,localanestheticsolutionspH4 5.
Hencethesehavelowconcentrationoffreebaseanda
sloweronset
Additionofsodiumbicarbonate(e.g.1mL 7.5%sodium
bicarbonateper10mL 2%lidocaine)
Speedsonset
Improvesthequalityoftheblock
Prolongs blockade by increasing the amount of free base available Prolongsblockadebyincreasingtheamountoffreebaseavailable
Decreasespainduringsubcutaneousinfiltration
Alternativealkalizingagents
Carbicarb
Commerciallyavailablebuffersolution1:1mixtureofsodium
bicarbonateandsodiumcarbonate
Generates HCO
3
rather than CO
2
while buffering H+ ions GeneratesHCO
3
ratherthanCO
2
whilebufferingH+ions
CO
3
2
+H
+
HCO
3
Increasesbloodandintracellularphwithlittleornorisein
PCO
2
levels
THAM(trometamol ortrishydroxymethyl
aminomethane
Biologicallyinertaminoalcohol
Weakbasepkaof7.8atphysiologicalpH
ProtonacceptorandcanbindbothCO
2
andmetabolicacids
RNH
2
+H
2
O+CO
2
RNH
3
+
+HCO
3
RNH
2
+H
+
RNH
3
Protonated THAMexcretedbykidney
Availableas0.3mol/LsolutionwithpH8.6
D THAM ( l f 0 3 l/L ) L b d i ht b DoseTHAM(mlof0.3mol/L)Leanbodyweight base
deficit
Maximumdailydose=15mmol/kg
7
Advantages sodiumfree,limitsCO2production,increasesPh
Disadvantage Hyperkalemia,hypoglycemia,ventilatory
depression,vasospasmandtissuenecrosis
E l li i l ffi bi b t Equalclinicalefficacyasbicarbonate
Preferredinmixedacidosis,hypothermia,controlled
hypercapnea ,cardioplegic solutions.
Keypoints
Acidosisperseisnotharmfulandcorrectionofcauseisimportant
NaHCO3tobeusedonlyforseverelifethreateningacidosisorif
clearlyindicated
Onlyhalfcorrectiontobegivenover48hours
Alternativealkalizingagentsmayhaveamoreimportantrolein
future
1
FOREIGNBODYBRONCHUS
Dr.Homay Vajifdar
FOREIGNBODYBRONCHUS
Maximumincidence agegroup why?
1 3years
Relatedto
Lackofmolarteeth ediblesbrokenup,notadequately
chewed
Habitofputtingallthingsinmouth
Preponderanceinboys aggressivenature
TYPEOFFOREIGNBODY
Commonlyinhaledobjectsare:
Organicfoods seeds,nuts,chunksofcarrots,bones
Lesscommonlyaspirated:
Coins,toyparts,jewels,batteries,needlesandpins
2
NATUREOFFOREIGNBODY
Organicforeignbodiesswellupandobstructthebronchial
passage.
Swollenorganicforeignbodiesgeteasilyfragmented
whengrasped,fragmentsmayoccludebothmainstem
bronchi inabilitytoventilate.
ORGANICF/B
Irritation
METALLICF/B
Lessinitialinflammation
Inflammation
Oedema
Granulation
Pneumonia
Oxidizes
Roughedges
Penetrateswalls
DIAGNOSIS
ClinicalPresentation
H/oaspiration
choking,coughingwhileeating
audiblewheeze
respiratorydistress(stridor,tachypnoea,
indrawingofchest,cyanosis)
Patientmaypresentlate
cough,sputum,fevernotrespondingtot/t
CXR collapseandconsolidation
syndromeofforgottenforeignbody
contd
Physicalfindings
breathsounds
Wheeze,
Crepts,conductedsounds
Mediastinalshift
DIAGNOSISSUPPORTEDBY
XRaychest APandLatviews
Fluoroscopy
Ultrasonography
CTscan
MRI
V/Qscan
TYPESOFBRONCHIALOBST
1. Checkvalve
2. Ballvalve
3. Stopvalve
4. Bypassvalve
3
CHECKVALVE
Ingressofairininspiration,butnoegressduring
expirationObstructiveemphysema
Mediastinalshifttooppositeside
Depresseddomeofdiaphragm
BALLVALVE
Smoothroundedforeignbody
Dislodgesinexpiration,reimpactsininspiration
earlyatelectasis
Mediastinalshifttosameside
Elevateddomeofdiaphragm
STOPVALVE
Totalocclusionduetolargeorswollenorganicforeign
body in both inspiration and expiration body,inbothinspirationandexpiration
Collapseandconsolidationofaffectedbroncho
pulmonarysegment
BYPASSVALVE
Partialobstructionoflumenduringboth inspirationand
expiration
R d i i il i Reductioninventilation
aerationandopacityininvolvedlungfield
Slightmediastinalshift
RADIOLOGICALFINDINGS
Radio opaque readilyidentified
Radiolucent signsofpartialorcompleteobstruction
Complete obst atelectasis Completeobst atelectasis
Partialobst obstructiveemphysemawithdepressed
diaphragmandmediastinalshifttooppositeside
Pneumonia
Pneumothoraxuncommon,duetoobstemphysemaand
penetrationduetosharpforeignbody
NormalXraywithinfirst24hrs
4
GOALSOFANAESTHESIA
Controlofairway
Suppressionofairwayreflexes
Amnesia
Unobstructed,immobilesurgicalfield
Notimerestrictionforsurgeon
secretionsandpreventaspiration
Smoothemergence
Safeextubation
HOWTOACHIEVEGOALS?
Rushforsurgery/assess?
Inhalationalorintravenousinduction?
Spontaneousorcontrolledventilation?
TouseoravoidN
2
O?
RUSHFORSURGERY
Acutestridorwithairhungerandcyanosis
Severerespiratoryobstruction
100%O
2,
immediatebronchoscopy
INDUCTION
Inhalational or intravenous induction depending on Inhalationalorintravenousinductiondependingon
patientsconditionandsituation
SPONTANEOUSRESPIRATION
Advantage
NoIPPV nodistalmigrationoff/b
Disadvantages
Noprotectionagainstaspiration
Suddenmovementtracheal/laryngealdamage
Deepanaesthesianeededhypoventilation,delayed
recovery
Instrumentationturbulence,resistanceand workof
breathing
5
CONTROLLEDVENTILATION
Advantages
Relaxedglottisallowssmoothpassageofbronchoscope
Minimallaryngospasm,coughing,bucking,unwanted y g p , g g, g,
vocalcordmotion
Rapidrecoverywithintactreflexes
Disadvantage
Distaldislodgementofforeignbody
WHYTOAVOIDN2O
100%oxygennotpossible
Expansionoftrappedairspaces
Furthermediastinalshift
CVScompromise
Pneumothorax
ANAESTHESIA
Induction
Preoxygenation,atropine(0.02mg/kg)orglycopyrrolate
(0.01mg/kg) ( g/ g)
O
2
+N
2
O+Halothane/Sevofluorane
IVthiopentone/ketamine/propofol
Maintenance
O
2
+N
2
O+inhalationalagent+opioid
Intermittentsuxamethonium/NDMR
Contd..
Reversal
Removebronchoscope
Ventilatewith100%O
2
(bag&mask)
Intubateandventilate
Neostigmine0.05mg/kg+atropine0.02mg/kgor
glycopyrrolate0.01mg/kg
MONITORING
SpO
2
ECG
NIBP
Precordialstethoscope
Temperature
Neuromuscularmonitoring
6
TECHNIQUESOFVENTILATION
Apnoeicoxygenation
Jetventilation
HFJV
DISADVANTAGES
Uncertainoxygenconcentration
Hypoxia
CO
2
retention
Barotrauma
COMPLICATIONS
Cardiacarrhythmias
Lightanaesthesia, vagaltone
Hypoventilation,hypoxemia
Managedwith
FiO
2
Hyperventilate normalEtCO
2
Deepenlevelofanaesthesia,
Lidocaine1mg/kg
Contd.
Bronchospasm
Bronchial/carinalstimulation(lightGA)
Deepenlevelofanaesthesia p
Bronchodilators terbutaline510g/kgi/mors/c
(maximumdoseof0.4mg)
Pneumothorax
IPPVinnecrotizingbronchopneumoniaorcheck
valveobstruction
Bleeding
POSTOPERATIVECARE
Closeobservationfor:
stridor
respiratorydistress
Physiotherapyandposturaldrainage
CheckXray
Contd
Humidifiedoxygen
Bronchodilators Bronchodilators
Antibiotics
Misc:
Dexamethasone(0.5 1.5mg/kg)
Racemicepinephrine(2.25%),
nebulizeover10minin1:6 1:10dilution
7
FLEXIBLEBRONCHOSCOPY
Onlyindicatedifpatientisstabletodiagnosethepresenceof
foreignbody performedundersedationandLA
Ifforeignbody isfound,itisremovedwithrigidbronchoscope
Noroleinpresenceofrespiratorydistress
FOREIGNBODYOESOPHAGUS
Endotrachealintubation&airwayprotection:
Accidentaldroppingofforeignbody
intounprotectedlarynx disaster
F/BOESOPHAGUS
Largeforeignbodyinoesophagus pressureontrachea
mimicsfeaturesofrespiratoryobstruction
RETAINEDF/BOESOPHAGUS
Complicationsinclude:
Bronchoesophagealfistula
Aortoesophagealfistula
Mediastinitis
Oesophagealdiverticulum
Lobaratelectasis
requiresthoarcotomyforremoval
1
General Principles Of
Neuro Anaesthesia
Dr Rajiv Chawla
Role of Neuroanaesthetist
Provision of anaesthesia : OT or radiologic
suite
Intensive care unit
Pain clinic
Areas operated upon
Anatomy, physiological control and effect of drugs on
cerebral blood volume and flow, ICP, CMRO2
Preoperative assessment and management of patients
What all you must know ?
Anaesthesia related
with neurological disease
Anaesthesia for imaging relevant to the CNS including
MRI and problems of magnetic fields
Perioperative management of interventional
neuroradiological procedures
Principles of anaesthesia for craniotomy: vascular
disease, cerebral tumours and posterior fossa lesions
Anaesthesia related
Anaesthetic implications of pituitary disease including
endocrine effects (acromegaly) and trans-sphenoidal
surgery
Anaesthesia for spinal column surgery and anaesthetic
implications of spinal cord trauma
Management and assessment of Head Injury
Principles of immediate postoperative management
including pain relief and special considerations with
narcotics
Principles of neurological monitoring : SSEP, AER etc
ICU related
Anaesthetic and critical care implications of
neuromedical diseases:
Guillain-Barr syndrome
Myasthenia gravis - pharmacological management
/ thymectomy,myasthenic syndrome,
Paraplegia and long-term spinal cord damage
Control of convulsions including status epilepticus
Tetanus
Trigeminal neuralgia including thermocoagulation
Dystrophia myotonica,
Muscular dystrophy,
2
How we proceed ??
Lets see some basic issues of importance
to anaesthesiologists ( Theoretical -RAPIDLY !!!!)
Anaesthesia technique for NS procedure
(Discuss the practical aspects) (Discuss the practical aspects)
See some important exam oriented topics
which are marked :
Specific neurosurgical procedures :
(Time permitting !!!)
Cerebral circulation : Anatomy
Cerebral circulation
Consists of anterior circulation ( via internal
carotid arteries) and posterior circulation ( via
vertebral arteries). Anastomosed by anterior and
posterior communicating arteries forming circle
of Willis.
Brain receives ~15-20% of cardiac output
CBF : 50ml/100gm/min ( 80 ml/100gm/min in
grey matter,20 ml/100 gm/min white matter)
Brain sensitive to falls in CBF :
if 20ml/100gm/min EEG slows;
if 10ml/100gms/min : irreversible brain damage.
Measurement of cerebral blood flow
Kety Schmidt technique : subject breathes
nitrous oxide for 10 minutes. Serial samples of
blood are taken from jugular bulb and radial
artery analysed for N
2
O levels.
CBF =uptake / AV difference CBF =uptake / AV difference
Inhalation of Xe
133
and creation of decay curves
under the detector allows regional blood flow
measurement
Positron emitted tomography (PET)
Functional MRI
Control of CBF
Metabolic control
Chemical control:
PaCO2 : CBF rises by 4% for every mmHg rise in CO2. This holds true
between PaCo2 of 80mmHg (max dilation) and 25 mmHg (max
constriction)
PaO2 : little change until PaO2 less than 50 mmHg. Then steep rise in
CBF
Cerebral Autoregulation : constant CBF despite wide variation in
CPP
Normal autoregulation 60-140 mmHg
Curve shifts to right in hypertensives
Failure of autoregulation caused by hypoxemia, hypercarbia, ischaemia,
trauma, volatile anaesthetic agents
Neurogenic control : small contribution. Sympathetic stimulation
causes vasoconstriction; parasympethetic causes vasodilation.
Temperature : CMRO2 falls 5% per degree C fall in temperature.
Because of a fall in metabolic rate, get secondary fall in CBF
The brain has the ability
to control its blood
supply to match its
metabolic requirements
Blood: Cerebral Blood Flow
metabolic requirements
Chemical or metabolic
byproducts of cerebral
metabolism can alter
blood vessel caliber and
behavior
3
Regulation of Cerebral Blood Flow Regulation of Cerebral Blood Flow
120
o
w

(
m
l
/
m
i
n
/
1
0
0
g
)
Autoregulation
of cerebral
blood flow
Hypercapnia
60
60 120 180
Mean Arterial Blood Pressure (mmHg)
C
e
r
e
b
r
a
l

B
l
o
o
d

F
l
o
Sympathetic
nerve stimulation
Remember
Metabolic
Hyperemia!
Normal Hypertensive
Relative
CBF
(Autoregulation)
CBF in the hypertensive : Shift to right
50 100 150
200
MAP
Human Brain: Facts & Figures of relevance
Weight : 2-3% of total body weight
Receives 15% of cardiac output
( ~750ml/min) ( 750ml/min)
Consumes 20% of oxygen required by
body at rest ( 170 umol/100gm/min)
Consumes 25% of glucose used by body
(31 umol/100gm/min)
Is an obligate aerobe; Cannot store oxygen
Energy requirement : Substantial;
Stores : Too small
( At normal rates of ATP production, the available
Human Brain: Facts & Figures of relevance
( At normal rates of ATP production, the available
stores of glycogen exhaust within 3 minutes)
Oxygen consumption : 40-70 ml/min
Oxygen delivery : 150ml/min
% of oxygen consumption by white matter = 6%
% of oxygen consumption by gray matter = 94%
Human Brain: Facts of relevance
Brain as an organ : Brain as an organ : its different its different
Energy converter Energy converter : Glucose & Oxygen to
energy
EE Hi h ti Energy consumer Energy consumer: High consumption
Energy conserver Energy conserver : The Working Brain
Uses More Energy than The Resting
Brain. ( Less Work : Less Pay Policy !!!)
CEREBRAL PERFUSION PRESSURE
MAP-ICP = CPP
4
Values in normal brain
CPP =critical level >50 mmHg
ICP =0-15 mmHg
CBF =MAP ICP/ CVP or CPP/CVP
Average CBF: 50 ml/100 Gm/min
Ischemia CBF: <18 20 ml/100 Gm/min
Tissue death: <8 10 ml/100 Gm/min
Hyperemia (CBF in excess of tissue demand) >55 60
ml/100 Gm/min
Brain auto regulation maintains CBF between 50-
130 mmHg
Values in normal brain
CMRO2* =CBF x OEF x SaO2
OEF is the oxygen extraction fraction. How much oxygen is extracted
can be measured by the Fick principle based on measurements of the
arterial and venous oxygen content
N l b i l 1400 l Normal brain volume : ~1400 ml
Intracranial CSF volume : 75-100 ml
Cerebral vascular volume : 150 ml
(*Cerebral Metabolic Rate of Oxygen )
Monro-Kellie doctrine
As the cranial vault is essentially a closed, fixed bony
box, its volume is constant :
v.intracranial (constant) =
b i CSF bl d l i v.brain + v.CSF + v.blood + v.mass lesion
As an intracranial mass lesion or oedematous brain
expands, some compensation is possible as
cerebrospinal fluid (CSF) and blood move into the
spinal canal and extracranial vasculature respectively.
Beyond this critical point, further compensation is
impossible and ICP rises dramatically
Monro-Kellie doctrine
Thus,
Cerebral Perfusion Pressure Cerebral Perfusion Pressure:
the primary determinant of
oxygen supply
is
influenced by
multiple factors
Anaesthetic agents on cerebral dynamics
No Enflurane
No Halothane
Yes 40% Nitrous oxide
CO2reactivity
preserved
CMR ICP CBV CBF Agent
Ketamine
Yes Propofol
Yes Midazolam
Yes Opioids
Yes Thiopentol
No Isoflurane /
sevoflurane
No Enflurane
5
Anaesthetic agents on cerebral dynamics
No Enflurane
No Halothane
Yes 40% Nitrous oxide
CO2reactivity
preserved
CMR ICP CBV CBF Agent
Ketamine
Yes Propofol
Yes Midazolam
Yes Opioids
Yes Thiopentol
No Isoflurane /
sevoflurane
No Enflurane
Isoflurane
Halothane
ICP CBV CSF abs CSF
prodn
CBF CMR Agent
Anaesthetic agents on cerebral dynamics :
Inhalation Agents
+ + + Nitrous
oxide
_ _ _ Sevoflurane
_ Desflurane
+
Isoflurane
Isoflurane
Halothane
ICP CBV CSF abs CSF
prodn
CBF CMR Agent
Inhalation Agents
+ + + Nitrous
oxide
_ _ _ Sevoflurane
_ Desflurane
+
Isoflurane
+ Barbiturates
ICP CBV CSF abs CSF
prodn
CBF CMR Agent
IV Anaesthetics
+ + Ketamine
+ + Benzodiaze
pines
? ? Propofol
+
Etomidate
+ Barbiturates
ICP CBV CSF abs CSF
prodn
CBF CMR Agent
IV Anaesthetics
+ + Ketamine
+ + Benzodiaze
pines
? ? Propofol
+
Etomidate
Anaesthetic considerations for
neurosurgery
6
Basic aims of anaesthesia
for neurosurgery
Maintenance of cerebral perfusion
pressure (CPP)
Cerebral oxygenation
Brain relaxation
Preservation of neurological functions
Rapid neurological recovery
Types of procedures
Intracranial procedures :
Tumour surgery : meningioma, glioma
Neurovascular surgery : aneurysms clipping
Pituitary surgery : endoscopic (TNTS)
Epilepsy surgery : awake craniotomy
Sterotactic surgery
Spinal surgery : laminectomy, instrumentations
Interventional neuro-radiology: aneurysm coiling
Types of procedures
Intracranial procedures : WE DISCUSS ONLY THIS
Tumour surgery : meningioma, glioma
Neurovascular surgery : aneurysms clipping
Pituitary surgery : endoscopic (TNTS)
Epilepsy surgery : awake craniotomy
Sterotactic surgery
Spinal surgery : laminectomy, instrumentations
Interventional neuro-radiology: aneurysm coiling
Pre-operative visit
Standard anaesthetic history
Neurological status
GCS
Raised ICP
Motor / sensory deficit
Scans :
Size and position of tumour
Cerebral oedema
Drugs :
Dexamethasone
Aspirin/ NSAIDs
Anti epileptics
Meningioma : Vascular tumour
Large bore IV
cannulation
CVP
Arterial monitoring
Sub arachnoid haemorrhage
Risk of vasospasm :
Role of Calcium blockers
Role of HHH therapy Role of HHH therapy
( hypertension, hypervolemia,
hemodilution)
Need for CVP monitoring
7
Investigations and planning
Avoid premedication (unless anxious)
Blood :
CBC
Clotting
G i / C t hi Grouping/ Cross matching
Urea
Electrolytes
ECG
CxR
Destination: Post operative
Principles of induction
Avoid increase in ICP
No coughing
Consider prevention of hypertensive
response
Cardio-stable anaesthetic technique
Key issues :
Most common stimuli leading to rise in
SBP are : laryngoscopy, intubation,
skeletal fixation of the head
Venous pressure : increase in CVP is Venous pressure : increase in CVP is
directly transmitted to intracranial cavity
Coughing and straining on ETT, flexion of
neck / kinking of neck veins, head low can
be harmful.
Anaesthetic Induction Agents
Consider effect on CBF, ICP and CMRO2
Propofol or thiopentone : ideal for induction
Vasoconstriction,
Decrease in CBF, CBV, ICP , ,
Preserve auto-regulation. Caution with myocardial
depression
Fentanyl : negligible effect on cerebral
circulation
Alfentanyl : may cause in ICP( transient)
Muscle Relaxants
Non depolarising MR : no effect on CBF or
CMRO2
Suxamethonium : transient rise in ICP. So
use with caution use with caution
Short acting muscle relaxant beneficial for
rapid wake and extubation
Anaesthetic maintenance
Volatile anaesthetic agents:
Vasodilatation
Rise in CBF
Fall in CMRO2 Fall in CMRO2
Isoflurane and sevoflurane have minimal
cerebrovascular effects
8
Nitrous oxide
Potent vasodilator
Produces rise in ICP
Expands air filledspaces Expands air filled spaces
Avoid in neurosurgery
Remifentanyl
Favourable pharmacological profile
Rapid titration for stimulating periods
T
1/2
: 3-5 mins
Rapid wake up achievable
Infuse at 0.05 0.25 mcg/kg/min
Not available in India
Anaesthesia technique : GBPH
Induction: Thio +Fenatnyl +Norcuron/
Atracurium
Maintainence : O2 +N2O +Propofol
infusion+Norcuron/ Atracuriuminfusion infusion +Norcuron / Atracurium infusion
Reversal : Neostigmine +atropine
Anaesthesia technique : NHNN
Induction: Propofol +Fentanyl +Norcuron/
Atracurium
Maintainence : O2 +air + Remifentanyl
infusion+sevoflurane infusion +sevoflurane
NOTE : No nitrous oxide, no relaxant for maintenance, no reversal
Airway management
Intubation and IPPV for PaCO2 control
Re-inforced tubes to avoid kinking.
Aim : PaO2 >13.5kPa ( ~100 mmHg),
P CO2 4 5 5kP ( 35 40 H ) PaCO2 <4.5-5kPa ( ~35-40 mmHg)
Tape the tube well.
Monitoring
Routine :
ECG
Capnography
SpO2
IBP
Temperature
ICP monitoringg
BIS
SSEP
CVP : (Int jugular can cause impairment of venous drainage.
So better avoid this route)
Patient indications
Large blood loss ( meningioma, spinal surgery, aneurysms)
Urinary catheterization : long procedures, mannitol admn
Nasogastric tube
9
Temperature
Nasal probe for all
No evidence of outcome benefit of
hypothermia
M d t h th i d ICP Moderate hypothermia reduces ICP
Do not wake and extubate until re-
warmed. Otherwise shivering can cause
rise in ICP
Monitoring in critically sick (In ICU)
Transcranial Doppler Sonography (TCD)
J ugular bulb oximetry (SjO2)
Intra cerebral microdialysis
Cerebral tissue oxygen pressure
Near infra red spectoscopy
Brain tissue oxygenation
Position in NS
Problems due to positioning ( Facilitate
Surgical Assess)
Positioning problems due to lesion
Eff t f i l t h t i Effect of pin placement : hypertensive
response
Sitting Position
Mayfield frame
Lateral position
Difficult positioning
10
Prone Position
Positions : 1
Supine:
Allow head up tilt for venous drainage
Beware of neck flexion
Venous drainage
Spinal cord ischemia
Prone:
Eye padding : IOP rise; ischemic ocular
neuropathy. Rarely blindness reported
Pressure points protected
Intra abdominal pressure
Positions : 2
Sitting:
Hypertensive response to pin insertion
Hypotension on sitting
Venous air embolism
Pressure points protected
Park bench / lateral
Head and body support
Brachial plexus injury
Post operative
Wake and extubate at end of surgery :
allows neurological assessment (GBPH)
OR
Extubate deep: avoids coughinghence Extubate deep : avoids coughing hence
rise in ICP. (NHNN)
Analgesia & antiemesis
Opioids ( morphine)
Careful respiratory monitoring
NSAIDS avoided for 24 hours
Regular paracetamol
5HT3 antagonists as anti-emetics
Specific Topics
ICP
Venous Air Embolism
Head injury
Glasgow Coma Scale
Fluid therapy in intracranial procedures
Hyperventilation : Status in NS
11
Case
Pituitary Tumours :
salient features of management
Pituitary tumour :Presentation
Hormonal hypersecretion syndromes
hyperprolactinaemia, acromegaly and Cushings disease
Mass effect
visual disturbance or raised intracranial pressure p
Non-specific
infertility, headache, epilepsyor pituitary hypofunction
Incidental
detectedduring imaging for other conditions
Increasein sizeof skull and supraorbital ridges; enlarged lower
jaw; increasein spacing between teeth/malocclusion
Face
Spade-shaped; carpal tunnel syndrome Hands and feet
Macroglossia; thickened pharyngeal and laryngeal soft tissues;
Mouth/tongue
Clinical features Affected area
Clinical features of acromegaly
obstructivesleep apnoea
Thick skin; doughlikefeel to palm Soft tissue
Vertebral enlargement; osteoporosis; kyphosis Skeleton
Hypertension; cardiomegaly; impaired left ventricular function Cardiovascular
Impaired glucosetolerance; diabetes Endocrine
Arthropathy; proximal myopathy Other
Surgical Approach
The pituitaryfossa can be approached using the transsphenoidal,
transethmoidal or transcranial route
The transsphenoidal route is preferredfor all but the largest of
tumours
Transsphenoidal access to the pituitary fossa is obtained using a Transsphenoidal access to the pituitary fossa is obtained using a
sublabial or endonasal approach
Ensure an oral pack to prevent blood aspiration
Deepen plane of anaesthesia to overcome hemodynamic
disturbances due to manipulations of nasal mucosa, bony tissues
and duramater.
1
LaparoscopicSurgeries
Anaesthetic Implications
Dr Aanchal Kakkar
Laparoscopic Surgeries
Thoracic Surgery
Gastro-Intestinal Surgery
Gynaecological Surgery
Urology
Vascular Procedures
Bariatric Surgery
Laparoscopy Vs Open Surgery
Advantages
Improved & Rapid recovery
Day Care surgery
Decreased Stress response to surgery
Shorter hospital stay
Improved cosmetic appearance
Improved dissection
Advantages
Minimal pain
Decreased requirement of analgesics
Rapid recovery of GI function
Decreased post op i/v fluid infusion
Improved postoperative respiratory function
Less postoperative wound infection
Disadvantage
More expensive
More operative time
Potential for major complications in inexperienced Potential for major complications in inexperienced
hands
Difficult in complicated cases
Technique
Insufflation of a gas into peritoneal cavity under
pressure
Separates the abdominal wall from the visceral
organs organs
Insufflation initially @ 4-6 l/min
Maintained @ 200-400 ml/min
Usual IAP in adults 12-14 mmHg
2
Various Insufflating Gases
Gas B:G
Coefficient
Advantages Disadvantages
Air, Oxygen 0.017 / 0.036 Easily available
Inexpensive
Limited physiological effect
Supports combustion
Nitrous Oxide 0.042 May be beneficial for laproscopic
d d i l
Supports combustion
PONV procedure under regional
anesthesia
PONV
Helium, Argon 0.00098 Poorly absorbed avoids
hypercapnia
Does not support combustion
Not cost effective
Low blood solubility:
dangerous if gas embolism
occurs
Carbon
Dioxide
0.49 Does not support combustion Absorbed in large quantities
from peritoneum
Physiological Changes
Insufflating gas: Carbon dioxide
Pneumoperitoneumi.e. Increased Intra-abdominal
pressure
Patient positioning
Hypercapnia: PaCO
2
Absorption from peritoneal cavity
High diffusibility and solubility.
absorption area
perfusion of wall of the cavity
Respiratory Changes: ventilation-perfusion mismatch
Abdominal distension
Patient positioning
Hypercapnia ( PaCO
2
):
Progressive in PaCO
2
15-30 min, then plateau.
Capnography & Pulse oximetry Reliable monitors
Mean gradient (a-EtCO
2
): normal in healthy
patients BUT in COPD & Cardiac patients.
pressure
Patient positioning
Respiratory system
Cardiovascular system
GI system
Mesentric circulation
ICP & IOP
Deep vein thrombosis GI system
Renal Function
Hepatic circulation
Deep vein thrombosis
Temperature
3
Respiratory Changes: pushed up diaphragm
Thoracopulmonary compliance (47%)
FRC (30-50%) FRC (30-50%)
Atelactasis
Peak Airway Pressure (upto 50%)
Plateau Airway Pressure (upto 80%)
Cardiovascular Changes: IAP >10 mmHg
/ Heart Rate
venous return
Cardiac output (10-30%)
Systemic vascular resistance
Mean arterial pressure
Cardiovascular Changes: Cardiac output
venous return
caval compression
Peripheral pooling of blood Peripheral pooling of blood
venous resistance
Management:
Increased filling pressure by preloading
Tilting the patient slightly head low
Intermittent sequential pneumatic compression device
Cardiovascular Changes: SVR mechanism
Mechanical Causes
Systemic vascular resistance & MAP
Increased Vasopressin Release
Stimulation of peritoneal receptors
Cardiovascular Changes: SVR mechanism
Intrathoracic pressure & vascular resistance of intra abdominal
organs
SVR & MAP
Release of neurohumoral factors(vasopressin, catecholamines etc)
Gastrointestinal System
Intra gastric pressure Increases
Lower esophasgeal sphincter tone > Intra gastric
pressure
Risk of Aspiration
4
Hepatic & Splanchnic Circulation Not Effected
Renal function: IAP causes
Urine output
Renal plasma flow
Glomerular filteration rate
Cerebral blood flow & ICP
venous stasis Thromboembolic phenomenon
Temperature Variation: Hypothermia
Mechanism:
Compressed gas cylinders
Rate of gas flow Rate of gas flow
0.3C fall per 50L CO
2
flow (Joule Thomson Effect)
Leak from port site
Suction of gas and cautery smoke
Lavage with Cold fluid
Insertion and removal of cannula
pressure
Patient positioning
Trendelenburg Position:
Central blood volume
central venous pressure
cardiac output
FRC, TLC
Pulmonary compliance
Atelectasis Hypoxemia
IOP & ICT
Nerve compression
Reverse Trendelenburg Position:
Improved lung function
Cardiac output
Mean arterial pressure
Venous stasis
Deep vein thrombosis
Nerve Compression
A 45 yrs old female, weight 56 kg and
height 53, ASA I, with symptomatic gall
stone disease, is posted for laparoscopic
cholecystectomy.
5
Pre-Operative Evaluation
History
Cardiac reserves
Pulmonary reserves
GERD
DVT
Contra indications for Laparoscopy: relative Contra-indications for Laparoscopy: relative
IncreasedICP
Hypovolemicshock
Impendingrenalshutdown
Advancedpregnancy
SevereCOPD
SevereischemicorValvularheartdisease
Pre Operative Evaluation
Drug Allergy
Previous Anaesthesia record
Airway Examination
Investigations Investigations
Complete blood count
Liver function test
Renal function test
ECG Age> 60yrs or history s/o cardiac dysfunction
Chest X ray History s/o pulmonary disease
Pre-operative Orders
NPO
Anxiolytic
H
2
receptor antagonist
Antiemetic
Monitoring
Heart rate
ECG
NIBP
Pulse Oximetry (SpO
2
)
Capnograph (EtCO
2
)
Temperature
Airway Pressure
Monitoring
Optional
Peripheral Nerve Stimulator
Urine output
CVP CVP
Invasive Arterial blood pressure
Trans-esophageal echocardiography (severe cardiac
disease)
BIS
Arterial Blood Gas
Choice of Anaesthesia
General Anaesthesia
Regional Anaesthesia Regional Anaesthesia
Local Anaesthesia
6
Balanced General Anaesthesia with Endotracheal
intubation and controlled ventilation is the
SAFEST d RECOMMENDED f i ti t d SAFEST and RECOMMENDED for inpatients and
long laparoscopic procedures
General Anaesthesia
Goals:
Maintain hemodynamic stability
M i t i bi d d t ti Maintain normocarbia and adequate oxygenation
Prevent gastric regurgitation
General Anaesthesia
Induction:
Preloading
Clonidine/Dexmedetomidine
Morphine/Fentanyl
Propofol/Thiopentone/Etomidate
Oxygen + Air/N
2
O + Isoflurane
Muscle relaxant, controlled ventilation & Normocarbia
General Anaesthesia
Intra-op :
Continue routine monitoring
Naso gastric tube
Temperature p
Hemodynamic stability
Maintain normocarbia (35-45 mmHg)
Increase minute ventilation by 15-20%
Increase tidal volume in healthy patients
Increase Respiratory rate in COPD
General Anaesthesia
Controversies:
Spontaneous respiration
Nitrous oxide
Supra glottic airway device
General Anaesthesia
Post operative:
Continue hemodynamic monitoring and oxygen
supplementation
Pain
Local infiltration
Intra peritoneal infiltration
NSAIDs
Opioids
Dexamethasone
Careful evacuation of residual CO
2
7
General Anaesthesia
Post operative:
PONV
40-75% patients
Antiemetics
Propofol
Dexamethasone
Adequate Hydration
Gastric content drainage
Oxygen supplementation
Local Vs Regional Anaesthesia
Choice ofAnaesthesia
Local Anaesthesia:
Advantages
Quicker recovery
Decreased PONV
Fewer hemodynamic changes
Early diagnosis of complications
Disadvantage
Increased patient anxiety
Increased pain & discomfort
Shoulder tip pain
Regional Anaesthesia:
Epidural
Spinal p
Combined spinal epidural
Sensory block required: T4-L5
Advantages & Disadvantages: same as local
anaesthesia
Complications
Surgical complications:
Haemorrhage
Injury to bile duct
Injury to other visceral organs
Respiratory complications:
CO
2
Subcutaneous Emphysema
Pneumothorax, Pneumomediastinum, Pneumopericardium
Capnothorax
Gas Embolism
Endobronchial Intubation
Risk of aspiration of gastric content
Trouble Shoot
A 45 yrs old female, weight 56 kg and height
53, ASA I, with symptomatic gall stone
disease, is posted for laparoscopic
cholecystectomy.
Intra-operative:
EtCO
2
SpO
2
Airway pressure
8
Diagnosis ?
Pneumothorax
Trouble Shoot
cholecystectomy cholecystectomy.
Intra-operative:
EtCO
2
SpO
2
Airway pressure
Diagnosis ?
Capnothorax
Complications
Embryonic remnant potential communicating
channels between peritoneum, pleural and
i di l pericardial sacs
IAP gas passes through weak points in aortic
and esophageal hiatus into thorax
Complications
Pneumothorax:
EtCO
2
( capnothorax EtCO
2
)
SpO
2
Airway pressure
cardiac output
Reduced air entry
Hyperresonance
Complications
Pneumothorax: management
Stop N
2
O, Give 100% O
2
Spontaneous resolution (if no pulmonary trauma) Spontaneous resolution (if no pulmonary trauma)
Thoracocentesis
PEEP
COPD patients: No PEEP; Only Thoracocentesis
9
Trouble Shoot
cholecystectomy.
Just after Insufflation: Just after Insufflation:
EtCO
2
SpO
2
Airwaypressure Nochange
Hypotension
Arrythmias
Diagnosis ?
Gas Embolism
Complications
Gas Embolism:
Direct needle or trocar in vessel or gas insufflation into
abdominal organ
R id i ffl i G l k i Rapid gas insufflation Gas lock in vena cava.
cardiac output, circulatory collapse
dead space
V/Q mismatch
Complications
Gas Embolism:
Diagnosis
Hypotension
cardiac output
EtCO EtCO
2
pulse oximetry
Cyanosis
Airway pressure No change
Mill Wheel Murmur
Arrhythmias
Complications
Gas Embolism:
Treatment
Immediate cessation of insufflation
Release of pneumoperitoneum
Stop N
2
O, Ventilate with 100% oxygen
Steep head down & left lateral position
Aspirate through CVP
Cardiopulmonary resuscitation
Cerebral gas embolism Hyperbaric therapy
10
Diagnosis ?
Subcutaneous Emphysema
Complications
CO
2
Subcutaneous Emphysema:
Accidental extraperitoneal insufflation
PaCO
2
EtCO
2
Airway pressure: No change
SpO
2
: No change
Swelling & crepitus
Complications
CO
2
Subcutaneous Emphysema:
Management
I t ti f l Interruption of laparoscopy
Allow CO
2
elimination
Correct hypercapnia
Allow insufflations at lower pressures
Special Case Scenarios
Assess Cardiac reserves
Pre operative Echocardiography
Invasive monitoring (IABP, TEE)
Slow insufflation
Low intra abdominal pressure
Laparoscopy
p
Patient tilt
Hemodynamic optimization before pneumoperitoneum
Remifentanyl, fentanyl, nicardipine, NTG
Experienced surgeon
Gasless Laparoscopy?
Laparoscopy In Pregnancy
Concerns:
Miscarriage
P t l b Preterm labour
Damage to gravid uterus
Fetal acidosis
11
Laparoscopy In Pregnancy
Recommendation:
To be done in 2
nd
trimester, before 23 wk
Left uterine displacement
Pregnancy induced changes
Open Hassons Technique Open Hassons Technique
Rapid sequence induction
Oro gastric tube
Intra operative continuous Fetal monitoring
Maintain maternal alkalosis
Pneumatic compression device
Prophylactic Tocolytics Controversial
Concerns:
High CO
2
absorption
High vagal tone
IAP
Infants 6 mmHg
Laparoscopy
g
Children 8-10 mmHg
Older Children upto 12 mmHg
Volume of gas required is Less
Restoration of EtCO
2
Adjust MV 25-30%
Laparoscopy In COPD
Advantages:
Minimal pain
Better post operative respiratory function
P ti ti i ti Pre-operative optimization
Stop smoking
Bronchodilator therapy
Antibiotics
Hydration
Chest physiotherapy
Laparoscopy In COPD
Anaesthetic Concerns:
Increase in PaCO
2
- EtCO
2
gradient
P i i h i Permissive hypercapnia
Maintain adequate expiratory time
High Airway pressures
Pressure control ventilation
Laparoscopy In Obese
Concerns:
Cardiac reserve
Pulmonary reserves
Difficult Airway Difficult Airway
Better view
post operative complications
Rapid recovery
Quick return of reflexes
Gasless Laparoscopy
Abdominal wall lifted with fan retractor
Avoids hemodynamic and pulmonary changes
Severe cardiac or pulmonary disease
Compromised Surgical exposure
Increased technical difficulty
1
Col(Prof.)Rashmi Datta
CaseHistory
26yoldservingNavaloffr
H/Ogiddinessx1month
CTscanshowedCPangletm
( ) Optd inAH(RR)07Feb2013
Massiveintraop cerebraloedema
Managedwithmannitol,furosemide and
hyperventilation
Pupilsstarteddilatingon08Feb2013at0010
h
CaseHistory
UrgentCTScan:CerebralOedema
Reoptd on08Feb2013at0530h
Postsurgeryat0800h
P i i d i f l i li Patientunresponsivetodeeppainfulstimuli
Pupilsfixedanddilated
DTRmute
Suspectedbraindeath
Whatisit?
Organdonation
Donationofbiologicaltissue/organofthe
humanbody
Fromaliving/deadperson
Optin :Anyonewhohasnotgivenconsentisnota
donor
Spain,Austria,Sweden
Toalivingrecipientinneedofa
transplantation
Optout:Anyonewhohasnotrefusedisadonor
Germany,Greece
RecognizedMechanismsofDeath
DonationafterCirculatoryDeath:
PreviouslyknownasNonHeartBeatingDonation.
Irreversiblecardiopulmonaryarrest
DonationafterNeurologicalDeath:
Total brain death:
Neurological criteria
Study of brainstem
reflexes
Electroencephalographic
criteria
Brainstem death:
Irreversible loss of consciousness
Irreversible loss of capacity to breathe
Irreversible loss of integrated
functioning
Totalbraindeath USA{AmericanPresidents
CommissionfortheStudyofEthical
ProblemsinMedicineandBiologicaland
Behavioural Research(1981)}
TheUniformDeterminationofDeathAct
:irreversiblecessationofallfunctionsof
theentirebrain
Neurologicalcriteria,studyofbrainstem
Death of the brain stem and
death of the whole brain
becomes in-distinct.
As a corollary, the presence or
absence of small groups of
g , y
reflexesandEEGcriteria
BrainstemdeathUK
irreversiblelossofconsciousness,
irreversiblelossofthecapacitytobreathe
andirreversiblelossofintegrated
functioning
Permitscriteriatobederivedthatarenot
onlyexplicitbutalsotestable.
living cells in the cortex is
irrelevant to a diagnosis of
death that relies on irreversible
coma as a diagnostic criterion.
2
EuropeanMaastrichtClassificationof
Donors
Class1patientswhoaredeadonarrivaltomedicalcare
Class2Patientswhoarriveinextremisandhaveunsuccessful
resuscitative attempts
Class5 Patientdonorswhohavedocumentedcardiacarrest.
Class4 Patientsdeclaredbraindeadafterunexpected
cardiacarrest
Class3 Patientswithterminalprognosisawaitingcardiac
arrest
resuscitativeattempts
Whoshoulddiagnosebraindeath?
OriginalRecommendationsofTransplantationofHuman
OrgansAct1994
Aneurologistorneurosurgeon
Asecondspecialistauthorizedbythestate
Treating physician Treatingphysician
Amedicaladministratorinchargeofthehospital
Modification
Neurologistorneurosurgeonmaybesubstitutedby
anotherphysician/surgeonoranasthetist/intensivist
Idealorgandonorcandidate
Indl whohassufferedafatalinjurytothe
brainwithimpendingoractualbraindeath&
intactCVfunction:
Severetraumaticheadinjury
Primarybraintumors
CVAs
Byvirtueofthenatureoftheirinjuries,theseindls aremost
oftencaredforinICUsbutcanalsobeidentifiedinthe
emergencydepartmentorageneralward!
Criteriaforpotentialdonors
Mustmeetageandbraindeathcriteria
Mustbefreeofinfection
Must have no history of carcinoma with the Musthavenohistoryofcarcinomawiththe
exceptionoflowgradeskinorbraintumors
Mustbefreeofseveresystemicdiseaseand
haverelativelynormalorganfunction
Shouldbehaemodynamicallysalvageable
Possibleindicationsofbraindeath
Diabetesinsipidus
Hypotensionrequiringmorethanone
pressor/inotrope
Hypothermia
Nonreactivepupilsshouldnottriggertheprocessofestablishing
braindeath
TESTING TESTING
OF OF
DONOR DONOR
3
TestsforBrainDeath
General
physical
examination
Clinical Clinical
neurological
examination
Confirmative
tests
Shock/hypotension
Severeelectrolytedisturbances hypophosphatemia
Acidbasedisturbances
E d i di b
Confounderstosubsequentexaminationofcorticalor
brainstemfunctionsshouldberuledout
Endocrinedisturbances
Severehypothermia(corebodytemperature32C)
Drugintoxication,poisoning(methaqualone,
barbiturates,benzodiazepines,highdosebretylium,
amitryptiline,meprobamate,trichloroethylene,alcohols)
Brainstemencephalitis
Guillain Barre'syndrome
Generalexamination
Carefuldocumentationof:
Deepcomawithnoresponsetoverbalstimuli/noxious
stimuliadministeredthroughacranialnervepathway
Beingmaintainedonaventilator
foratleastfor6h
Ifcardiacarrest,atleast24hpostROSC
b l d d b d Noabnormaldecorticateordecerebrate posturedpresent
Noepileptiform movementsobserved.
Nospontaneousrespiratorymovements
Noshivering
Physicalexaminationmustbedonecarefullyandconscientiously
Resultsrecordedinordertoallowforserialexaminationbythesame
examiner/confirmatoryexaminationbyanother
Phenomenathatdonotexclude
braindeath Lazarussign
Sweating
Blushing
Normalbloodpressurewithout
vasopressors
Presenceofdeeptendonreflexes
Tripleflexionresponse
Extensorplantarresponse
Spontaneousmovements
Spinalcordfunction&reflexescanpersist/canreturnafterinitial
absenceevenafterirretrievabledamagetothebrainstem
of limbs and trunk
Plan:
No
spontaneous
respiration
Stopms
relaxants
Checkbrain
stem reflexes stemreflexes
after2h
Stop
sedatives/
narcotics
Checkbrain
stemreflexes
after2h
Cerebral&BrainStemFunction
QuickCOWS
4
Apnoea Testbyoxygendiffusion
method
V
T
6mL/kg
PreoxygenationwithFiO2of1.0for10min
BaselineABG
Disconnecttheventilator
Deliver100%O2@6L/minviacatheterthruthe /
ETT.Catheteratlevelofcarina(1cmbeyondend
ofETT)
Observeforabdominaland/orrespiratory
movements
After10minrepeatABG
Reconnectpttoventilator
Apnoea Test:Interpretation
Positivetest:
Apneawithoutrespiratorymovements
despiteadequatestimulation
Patientremainsapneic
PaCO
2
is>55mmHgor>20mmHgfrombaseline
Negativetest:
Apneanotpresentwithrespiratoryefforts
notedatanytimeduringthetest
Apnoea Test:Interpretation
Equivocal:
testeitherrepeated/anotherconfirmatorytest
performed
PaCo2doesnotrise>55mmHgor<15mmHg
increaseoverbaseline
Abort:
Apnoea testshouldbeabortedifthepatientdevelops
Hypotension
Significantcardiacarrhythmias
IfthepatientshowsafallinSpO2<91%
Repeattests
Dependingonthepatient'sage,thetime
intervalsbetweenneurologicexaminations
areasfollows:
48 h for newborn term infant to 2 months 48hfornewbornterminfantto2months
24hfor>2monthsto1year,
12hfor>1yearto<18years
Optionalfor18years.
ConfirmatoryTests
Ifapatientissuspectedofbeingdead.But.
...
Examcannotbedone(e.g.facialinjury)
Apneatestcannotbecompleted
Cause of the injury is unclear Causeoftheinjuryisunclear
Patientisonsedativeagents,paralyticagents
orhypotensive
Aconfirmatorytestdoesnotsupplantthe
physicalexam,itonlyaddstoit.
TimeforConfirmatoryTests
Guidelinesforconfirmatorytestsarealsobasedonthepatient'sage:
2confirmatorytestsnecessaryfornewbornterminfant 2months
1confirmatorytestnecessaryfor>2months 1year
Useofconfirmatorytestsoptionalfor>1year
6hwithaconfirmatoryisoelectric EEGi.e.;"Electrocerebralsilence"
12hwithoutaconfirmatoryEEG.
h f b h f l 24hforanoxicbraininjurywithoutaconfirmatoryisoelectric EEG
Atropine,EEG,cerebralangiography,cerebralbloodflow
measurements,CTscans,isotopescintiscans,echoencephalography
orothersophisticatedtests
arenotnecessary
fordiagnosisofbrainstemdeath.
Howevertheymaybeofuseintheprecisediagnosisofbraindamage
priortoconsiderationofbrainstemdeath
5
CaseHistory
Detailedexamination&clinicalneurological
testingdoneat1100hon08Feb2013
NOKinformedat1130hon08Feb2013
Coordinatorapproachedfamilyforinitial
primingfororgandonation
CaseHistory
RptClinicalneurologicaltestingdoneat1700
hon08Feb2013
Familyagreedfororgandonationfor09Feb
2013
RptClinicalneurologicaltestingdoneat1000
hon09Feb2013
DOD09Feb2013
Goals
Earlydonorrecognition
Rapidandaccuratedeclarationofbraindeath
EarlyICUadmissionandmanagementbya
dedicatedteam
Earlyandaggressivephysiologicalmaintenance
ofpotentialorgandonorsbyresuscitationwith
fluids,vasopressors,andhormonetherapy
EarlyreferraltoOrganProgrammeCoordinator
Approachingfamilyandobtainingconsentfor
organdonation
Continuedcriticalcareunitintensityof
support
Criticalperiod
Focusshiftfromcerebralprotectivestrategies
tooptimizingdonororgansfortransplantation
Maintenanceofphysiologichomeostasis
Treatmentof
Hypotension
Potentialcardiacarrhythmias
Diabetesinsipidus
Metabolicacidosis
ImprovingtheSupplyofDonorOrgans:BeingCarefulWiththeGiftofLifeJAMA
2010304:26432644
6
Protocols
Centraltriplelumenline
Largeboreperipheralline
Intraarterialline
Earlyinvasivehemodynamicmonitoring:
Pressuremonitoring
FrequentABGanalysis
Testing
Total & differential white
blood count
Blood group
Liver function tests
Renal functions tests
HCV HbsAg, HIV
Electrolytes
PT, PTT and platelets
Protocols.
Temperaturemonitoring
Coverpatientwithablanketatalltimes
Convectivemeasuresmaybeused
Itisnotrequiredtogivewarmfluids
Aggressiverewarmingtomaintaintemp>34
o
C
Loss of hypothalamic temperature regulation
Fall in metabolic rate
Core temperature < 32
o
C
Dysrrhythmias
Bradycardia and myocardial depression
Coagulopathy
Pancreatitis
Left shift in ODC
Protocols.
Mechanicalventilation
Vt 6 mL/kg once suspicion of brain death
PEEP+5 cm H
2
O
Static Paw 30 cm H
2
O Static Paw 30 cm H
2
O
Highest PaO
2
with lowest FiO
2
Avoidance of a markedly positive fluid balance
Hypotension&Hemodynamicinstability
Neurogenic shock
Resultofdefectivevasomotorcontrol lossof
SVR
Hypovolemic shock
Therapeuticdehydrationforcerebraledema
Hemorrhage Hemorrhage
DIwithmassivediuresis
Osmoticdiuresisduetohyperglycemia
Cardiogenic shock
Hypothermicdepressionofmyocardial
contractility
LVdysfunction
Protocols.
Choiceoffluidsusedforvolumeexpansion
basedon
Hb levels
Typeoffluidlost
Serumelectrolytes
Aggressivefluidresuscitativetherapy
Urine output, 1.0 ml/kg/hr
MAP > 60 &< 100 mm Hg
CVP 10-12 mmHg / PCWP 8-12
Hb > 10 mg/dl
CVP 10-12 mmHg / PCWP 8-12
mm Hg
LV EF >45%
CI >2.4 liters/min
LV stroke work index >15
gmeters/cm5/beat
Na+ <150 mEq/L
K+>3 mEq/L
Glucose > <150 mg/dL
Protocols.
ExpansionofIVSvolume
Initialbybalancedcrystalloidsolution(RL/NS)
Subsequentbyhypotonicsolutions(5%D)
Avoid HES
Aggressivefluidresuscitativetherapy.
AvoidHES
Earlyuseofcolloidstopreventpulmonary
edema
AlbuminifPTandPTTarenormal
FFPifPTandPTTabnormal(value>1.5X
control)
PRBC
7
Protocols.
Vasopressors iftheMAPremains<70mmHg
Ifneedofeithernorepi ordopaminealone,or
incombination>10mcg/kg/min
Addlevothyroxine bolusof20mcg infusionof
Aggressivefluidresuscitativetherapy.
10mcg/h
Vasopressin1unitbolus,0.54units/hr (titrate SVR
800 1200)
??? First line agent
Independently improves SVR
Reduces need for exogenous inotropic support
Treatment of diabetes insipidus
EndocrineDisturbances
Braindeathmayinterrupt
hypothalamicpituitaryaxis
Hypothyroidism& adrenal Hypothyroidism&adrenal
insufficiencymayleadto
depletionofthemitochondrial
abilitytoregenerateATPresulting
infunctionalorganinstability
RoleofT3
RapiddeclineinfreeT3:
ImpairedTSHsecretion
Decreasedperipheral
conversionofT4
Resultsinanaerobic
metabolism&acidosis
Progressivelossofcardiac
contractilityassociatedwith
depletionofhighenergy
phosphates
Salim A,etal.,Clin Transpl 2007;21:405409
EarlydepletionofADH
Characterizedbyinappropriatediuresisleadingto
Severehypovolemia
Hemodynamicinstability
Electrolytedisturbances
DiabetesInsipidus
LowlevelsofCortisol
Effects of extraneous steroids:
Improves donor organ function and graft survival
Increases tissue oxygenation and donor lung recovery
Improves cardiac function following transplantation
Attenuate the effects of proinflammatory cytokines
Protocols
Methylprednisolone 15mg/kgbolus
T34mcgbolus,3mcg/hr
T420mcgbolus,10mcg/hr
Arginine vasopressin
HormonalResuscitationGuidelines:
T4protocol
1 ampule 50% Dextrose
2 g solumedrol
20 U regular insulin
200mcg of levothyroxine in 500cc NS at 25 cc/hr and titrate
up to 40 mcg/hr
Argininevasopressin
1unitbolus,0.54units/hr (titrate SVR800 1200)
0.50.6units/hrreducesUOP
SeverecasesUOP>1000ml/hrmayrespondto
DDAVP0.3mcg/kg
Insulininfusion1unit/hrtitratebloodglucoseto120
180mg/dl)
RosendaleJD,KauffmanHM,etal.AggressivepharmacologicDonorManagement
ResultsinMoreTransplantedOrgans.TRANSPLANTATION2003:75:482
Protocols.
Organdonorstypicallywithnutritionaldepletion
HepaticglycogenandATPenergysourceduring
warm/coldischemia
Animalexperimentssupportnutritional
NutritionalSupport
supplementationtorestoreliverglycogen better
outcome
Moderateamountsofcarbohydrates
Lipids,longchaintriacylglycerols/fishoil
Aminoacids
8
Protocols.
Miscellaneous
Surveillance for infection:
Routine blood cultures/chest X-ray
Routine administration of non-nephrotoxic
antibiotics to prevent transmission of infection to antibiotics to prevent transmission of infection to
immunosuppressed recipient
DIC
Necrotic brain tissue
DIC may persist despite factor replacement
necessitating early organ retrieval
ClinicalVariablesAffectingShort
termGraftFunction
Age
Sex
ABO Blood Type
Hypernatremia Donor
Sodium > 155
Cold Ischemia Time > 12
hours
ABOBloodType
CauseofDeath
ICULOS
Warm Ischemia Time > 45
minutes
Nutrition and Liver
Glycogen
Hypotension/Vasoactive
Drugs
Totsukaetal:Transpl Proc,2004;36:22152218
MOTIVATION MOTIVATION
Ramachandra Protocol
Request for EYES
FIRST - See How
Family Reacts
Family Willing Family Unwilling Family Willing
Ask For Solid Organs
Inform Transplant Co-coordinator
Family Unwilling
Abandon Efforts
Relativesfindtheconceptdifficultto
understandandhavetroubleinaccepting
thattheirrelativeisactuallydead
Familymembersderivetremendous,lasting
comfortfromtheknowledgethat
somethingpositivehasresultedfromtheir
loss
EarlymeetingwithCoordinator
Buildupconfidence
Avoid:
Givingfalsehope
Usinghighlytechnicalmedicalterms
Approachingtooearly,notallowingthedeathto
beaccepted
Beingstonecold,uncaring,abruptorpompous
After2
nd
apnoea test,allowrelativestosee
patientinbatches
Ensurenoproceduraldelayinreleasingbody
Somesortofrecognition???
9
Bioethicalissues
Mostreligionssupportdonationasacharitableact
ofgreatbenefittothecommunity
Probleminclinicalbioethics:
Shouldabraindeadpatientbekeptartificiallyin
ordertopreserveorgansforprocurement?
Involuntaryorgandonationissues patient
autonomy,livingwills,guardianshipmakeit
nearlyimpossiblefortooccur
Cloning BioethicsinOrganHarvesting
CaseHistory..
Organsharvestedandsuccessfully
transplanted:
Liver
Twokidneys
Twocorneas
Heartleftinsidethebody
.Attherequestofthewife,
marriedfor2years,engagedfor8years!!!
1
MassiveTransfusion
DrVinod Kalla
MassiveHemorrhage
>30%lossoftotalbloodvolume
MassiveHemorrhage
>150mls./minbloodloss
Causes
Trauma
GIhaemorrhage
Vascularsurgery
Livertransplant
Majorobstetrichaemorrhage
Trauma
Leadingcauseofdeathin<45yearsold
Deathwithin6hoursoftraumainvariably
b f h h becauseofhaemorrhage
Massivehaemorrhage ismajorcauseof
potentiallypreventabledeath
MassiveHaemorrhage
Australia:
>50unitsperepisodeassociatedwithtrauma
Denmark:
>50unitsperepisodeassociatedwithGI
bleeding
(SurveyconductedinUSA,UK,AUSTRALIA&
DENMARK 2007)
2
MassiveHaemorrhage
Leadsto:
Decreasedcirculatoryvolume
Decreasedcardiacoutput
Decreasedoxygendelivery
Aggressive
FluidResuscitation(Crystalloids)
Increasesbloodpressure
Reversesvasoconstriction
Dislodgesearlythrombus
Increasesbloodloss
Haemodilution Haemodilution
Causes:
Dilutional coagulopathy
Metabolicacidosis
Hypothermia
Depletes:
Fibrinogen
AggressiveFluidResuscitation
(Colloids)
Prothrombin
FactorVIII&vonWillebrand
Inhibitionofplateletfunction
FactorXIIIa(reducedinteractionwithfibrin)
AggressiveBloodTransfusion
Trauma
Increasestissueinjury
Causeshypoperfusion
Causesdilutional &consumptioncoagulopathy
AggressiveFluidTherapy
LethalTriad
Coagulopathy
Hypothermia Hypothermia
Metabolicacidosis
(BloodyViciousCycle)
Taskforceonperioperative blood
transfusionandadjuvanttherapies
Earlyadministrationoffluidsinconjunction
withPRBC
FFPandplatelates tobeadminstered
according to conventional caugulation accordingtoconventionalcaugulation
analysisafterwholebloodvolumehadbeen
adminstered
Thisstrategyledtocaugulopathy anddeath
3
DamageControlResuscitation
OriginatedfromUSNavyconceptforship
boarddamage
(Toapplyminimumrepairnecessarytorestore
operations) operations)
IntroducedintoUKDefence MedicalServices
in2007
Nowadaptedforciviliantrauma
Aim:
Minimizebloodloss
Maximizetissueoxygenation
Optimize outcome Optimizeoutcome
Normalize:
INR
Bodytemperature
Basedeficit
Consistsofthreeparts:
Permissivehypotension
Hemostatic volumeresuscitation
Damagecontrolsurgery
Permissivehypotension
EasternAssociationfortheSurgeryofTrauma
practicemanagement(EAST)guidelines2009
IVfluidstobewithheldinperipheralsettings
in patients with penetrating torso injuries inpatientswithpenetratingtorsoinjuries
IVfluidstobewitheld untilactivebleedingis
addressed
IVfluidstobetitratedforpalpableradial
pulseusingto250mls.boluses
Hemostatic volumeResuscitation
SupplementinglargetransfusionsofPRBC
withFFPandplateletsinanimmediateand
sustainedmanner
PRBC:FFP:Platelets 1:1:1
MassiveTransfusion
WHOdefinition(2002):
Replenishmentoflostbloodequivalenttoor
greaterthanpatientsbloodvolumeinless
than24hours
4
MassiveTransfusion
Pediatrics:
1unitPRBCXAgein24hours
Adults:
4 PRBC i 1 h >4PRBCsin1hour
Halftotalbloodvolumereplacedover3hours
Totalbloodvolumereplacedover24hours
>20PRBCstransfusedduringhospitalstay
Transfusionof>10unitsPRBCsin24hours
HistoryofBloodTransfusion
1829 JamesBlundell
1
st
documentedbloodtransfusioninPPH
1901 Karl Landsteiner (A B O blood groups) 1901 KarlLandsteiner(A,B,Obloodgroups)
1902 Struli &Descastrello (ABbloodgroup)
1939 KarlLandsteiner(Rh antibody)
TypesofTransfusion
Direct
Autologous
Homologous
Xenologous
Exchangetransfusion
Risks&SideEffectsofTransfusion
Infections:
Viruses(HBV,HCV,HIV,CMV)
Bacteria
Parasites
Prions (CreutzfeldJakob disease)
Risks&SideEffectsofTransfusion
Mildreactions:
Fever,chills,rigors,urticaria,itching
Severereactions:
Acuteintravascularhaemolysis y
Anaphylaxis
Immunologicalreactions:
Alloimmunization
Immunosupression
TRALI
Hypothermia
Exposure
Infusionofcoldfluidsandbloodproducts
Openbodycavities
Decreasedheatproduction
Impairedthermoregulatorymechanism
5
Hypothermia
Morbidity&mortalityincreased
Cardiacarrhythmias
Myocardialdepression
Decreasedcardiacoutput
Hypotension
ODCshiftedtoleft
Reducedplatelet&coagulationfunctions
Reducedcitratemetabolism
InductionofFibrinolysis
WarmingDevices
(AmericanAssociationofBloodBank)
Surfacecontactwarming
Countercurrentwarmers
Heatedsalineadmixture
Inlinemicrowavewarmers
Additivesinstoredblood
CPDA&SAGM
BufferpH
Preventcoagulation
Delaybiochemical,metabolical &molecular
changes(RBCstoragelesion)
ProvideshighdegreeofRBCsurvival
Preserveoxygencarryingcapacity
StoredBlood
RBCstoragelesion
Decreased2,3DPG
RBCschangefromadeformablebiconcave
di d f d hi d h disctodeformedechinocytes andthento
irreversiblydeformedspherechinocytes
Resultingininabilitytoflowthrough
microcirculation
Decreasedoxygentransport
StoredBlood
LowerspHto7.0
Accumulationoflactic&pyruvic acid
Moreafter21days
Alongwithcitratemetabolised tobicarbonate
Maycauseprofoundalkalosis
Acidosis
Storedblood
Hypoperfusion
Salineadminstration
Plateletdysfunction
ImpairedThrombingeneration
Increasedfibrinogendegradation
Coagulopathy
6
Coagulopathy
ISS>25
Bloodloss
Thrombocytopenia
Dilutional coagulopathy
Consumptioncoagulopathy
Hyperfibrinolysis
Hypothermia
Hypocalcimia
Acidosis
Patientsbiologicresponsetoinjuryandtreatment
(Dilutionandconsumption)
(ActivationofAnticoagulantpathway)
(ActivationofFibrinolytic pathway)
ConsumptionCoagulopathy
Bloodlossactivates
hemostatic mech. anticoagulationmech.
ProteinCpathway
IrreversiblyinactivatesFVa &FVIIIa
Limitsthrombinproduction,enhancesfibrinolysis
InhibitsFVII&reducesfibrinogenuse
Coagulopathy (Mechanism)
TraumaHaemorrhage Resuscitation
Dilutional Coagulopathy
ResuscitationHypothermia Coagulopathy yp g p y
TraumaShock Acidosis
TraumaandshockACoTS Factor
consumptionandfibrinolysis
Implications(Mechanism)
Currentmanagementisdirectedataugmenting
thrombingeneration(componentorrVIIa)
Augmentationofthrombingenerationinthe
presence of hypoperfusion can cause further presenceofhypoperfusioncancausefurther
activationofanticoagulant&fibrinolytic
pathways
OnceproteinCisexhausted.increasedthrombin
generationwillresultinmicrovascular thrombosis
andsubsequentlyMOF
ReversalofCoaugulopathy
Normalizationofbodytemperature
Haemorrhage control
TransfusionofPlatelets,FFPand
Cryoprecipitate
CitrateToxicity
Eachunitcontains3gmcitrate
Bindsionizedcalcium
Healthylivermetabolises in5minutes
T f i @ 1 i / 5 i h l i Transfusion@1unit/5min hypocalcemia
Mayproducetetany &hypotension
Inpresenceofhypothermia&acidosiscancause
CO,HR&dysrrhythmia
Calciumifbiochemical,clinicalorECGevidence
7
Hypocalcemia
Muscletremors/tetany
DecreasedPVR hypotension
Decreasedventricularcontractility
ProlongedQTinterval
PEAorVF
Hyperkalemia
Rarelyaproblem(Noclinicalsequelae)
OnePRBCgivesabout7meq.ofK
Extendedstoragebeyond21daysmay
i i 30 / ( /l ) increaseitto>30meq./L(777meq./l.)
Ifinfusionrateis>100ml/minor>7units
transfused,hyperkalemia mayoccur
RedcellmembraneATPase pumpinactivation
ECGmonitoringmandatory
TRALI
Definition:
Acutelunginjurywhichoccurswithin6hof
transfusion&isnotrelatedtootherfactorsofALI
&ARDS
ALI&ARDSdefinedashypoxemia(PaO2/FiO2
<300&<200),B/Lpulmonaryinfiltrates,no
evidenceofatrial hypertension
DelayedTRALIoccurs672haftertransfusionwith
additionalriskfactorsforALI/ARDS(sepsis,
trauma,burns)
TRALI(Incidence)
RBC 1:5000
FFP 1:2000
Platelets 1:400
8% ifRBCistransfused
24% ifFFPorplateletsareused
TRALI
Syndromecomprisesof:
Acuterespiratorydistress
Hypoxemia
Hypotension
Fever
Pulmonaryedema(Noncardiac)
TransfusionRelatedAdverseOutcome
(Mechanisms)
IncreasedStoragetime:
RBCdeformabilityresultsinmicrocirculatory
perfusion
Profoundinflammatoryresponse y p
Cytokines&lipidsaccumulate
Neutrophil priming&activation
Immunosuppresion
Microchimerism
BindingofFreehaemoglobin withNitricOxide
8
FreeHb withNObinding
FreeHb increaseswithincreasedstoragetime
inhistamineaecngintegrityofRBC
membrane
id f h l i
TransfusionRelatedAdverseOutcome
(Mechanisms)
evidenceofhaemolysis
FreeHb withNOcausesvasoconstriction
(RBCscontainmajorityofintravascularnitrites,
ondeoxygenation reducedtoNO,providinga
mechanismformatchinglocalbloodflowto
oxygendemand)
MechanismofTransfusionRelated
AdverseOutcome(TRALI)
DonorantibodiesreactwithhostWBCviaanti
HLAI&II&antigranulocyte antibodies
Antibodiesactivatecomplement,leadingto
l i i i f Pulmonarysequestration,activationof
neutrophils
Endothelialcelldamage
Capillaryleakinlungs
MechanismofTransfusionRelated
AdverseOutcome(TRALI)
Pulmonaryepitheliumisactivated
Localsequestrationofpolymorphs
Biologicresponsemodifiersintransfused
bl d i h l l i i bloodactivatesthesepolys resultingin:
Endothelialdamage
Capillaryleak
ClinicalmanifestationofALI
Microaggregates
Degenerationofplatelets&functional
Granulocytes
Maycausepulmonaryembolism
MaypromotedevelopmentofARDS
PulmonaryEdema
IfCVScompromised
Children
MonitorCVP
BloodTransfusion&Mortality
Strongpredictorofmortality(OR2.83,CI95%
&OR4.75,CI95%)
RiskincreaseswitheachunitofRBC
transfused (OR/unit 1 16 CI 95%) transfused(OR/unit1.16,CI95%)
Age,ISS,GCS&PRBCindependentpredictors
ofmortality
PRBC>12units&age>75yrsurvival0
9
MassiveTransfusionProtocol(MTP)
OKeefeetal(Prospective,1yrprior&2yrs
afterMTP)
i ki l ( i 2 i & 2 Riskin etal(Prospective2yrsprior&2yrs
postMTP)
Holocomb etal(Retrospective,466patients)
Obtainlabdata(CBC,Serumelectrolytes,Xmatching)
IVaccess(Largeborecannulae)
Maintainnormothermia(Increaseroomtemperature,
warmblankets,fluidwarmer)
Monitorsystemic&regionalperfusion(Standard
monitoring,CVP,arterialline,urineoutput)
Permissivehypotensionwithfluids
Arrestofbleeding(Surgical)
Transfuse 6 packs (PRBC : FFP : Platelets 1:1:1) Transfuse6packs(PRBC:FFP:Platelets1:1:1)
Repeatlabtests
Revaluate(transfuseifrequired)
ConsiderrFVIIa,Tranexemic acid
Tranexemic Acid
Hyperfibrinolysis commonincoagulopathy
Antifibrinolytics preventplasmin frombindingto
itssubstratefibrin
Preventsplasmin degradationofplatelet
glycoprotein Ib receptors glycoproteinIb receptors
Preservesplateletfunction
MonitorTEG/ROTEMtoidentify
hyperfibrinolytic states
Dose:1gmover10minfollowedby1gminfusion
in8h
rFVIIa,
Enhancesthrombingenerationonactivatedplatelets
IndependentofFVIII&IX
Approvedinpatientswithcong.FVIIdeficiency,
hemophilia A or B hemophiliaAorB
Ensurenormalplatelets&fibrinogen
Expensive,hasnoeffecton48hor30daymortality
Isassociatedwithreducedtransfusionrequirement
200mcg/Kg.followedby100mcg/Kg.1&3hrs.
Fibrinogen
Conversionofsufficientamountoffibrinogen
tofibrinprerequisiteforclotformation
Reductionoffibrinogenduetoconsumption
&/or dilution &/ordilution
If<1.52.0gm/L
Dose:34gmfibrinogenor50mg/kgof
cryoprecipitate
10
Prothrombin ComplexConcentrate
ContainsFII,VII,IX,X&ProteinC&S
Amount25timesthatinFFP
Indicatedforcongcoagulationdisorders&to
l i l reverseoralanticoagulants
Dose:35units/kg
Monitoring
CBC(Hb)
Temperature
ABG(pH)
Serumelectrolytes(IonizedCalcium)
Coagulation(platelets,PTINR,aPTT,
fibrinogen)
TEG/ROTEM
WhatIsNew
ArtificialOxygencarriers
HBOC
PFCemulsions
WhatIsNew
Freshwholeblood
USAArmyconcept(Walkingbloodbanks)
Associatedwithimproved30daysurvival
Seriouslogisticchallenges
Spinella PCetal.JTrauma2009
WhatIsNew
Freezedriedplasma
Lyophilizedplasmatopreventbreakageof
frozenplasmaunits&wastageintransport
UsedbyFrenchArmysince1994.
Daban JLetal.Crit Care2010
WhatIsNew
StemCellderivedRBCs
OngoingresearchtoproduceOve RBCsfrom
ll f i l C h stemcellsforuniversalRBCtypewhere
massivetransfusionmayberequired.
11
InaNutShell
DCR
Normothermia
Addresscauseofbleeding
MTP 1:1:1
Monitoring: TEG/ROTEM
Pharmacologicalintervention
1
CASEDISCUSSION
PROF.(DR)M.SHARMA
TracheoesophagealFistula
Incidence:1:4000livebirths
M>F(25:3)
1040%arepreterm
Antenatal history : polyhydramnios (60%) or Antenatalhistory:polyhydramnios (60%)or
characteristicultrasoundfindings(smallorabsent
gastricbubble,littleintestinalfluid).
Etiology:failureinmesenchymal separationofupper
foregut
Embryology
Imperfectdivisionofforegutintoanteriorly
placedLarynxandposeriorlyplaced
oesphagus
TracheoEsophageal Fistula
5Types(GrossandVogt)
7.7% 0.8% 86% 0.7% 4.2%
GregoryGA, GregoryGA, ed ed,PediatricAnesthesia,3 ,PediatricAnesthesia,3
rd rd
edition,1996 edition,1996
2
Diagnosis:
Antenatal maternalpolyhdroaminos
Afterbirth:InabilitytopassNGTafterbirth
Regurgitationof1
st
feedwithcyanosisandchoking g g y g
Excessiveoralsecretions
Diagnosis
Inabilitytopasscatheterbeyond10cms
Xraychestandabdomen
Coiledradioopaquecatheterinproximal
pouch
Air in stomach distal fistula Airinstomachdistalfistula
Instillationofradioopaquedyeavoided
Dangerofchemicalpneumonitis
Htypefistulaspresentlate recurrent
ventilatory distressorchestinfection
TracheosphagealFistula
3565%haveassociatedanomaliesVATERAND
VACTERL
V vertebralanomaliesorVSD
A anorectalmalformation
C cardiacanomalies
(Common)
T TEF
E esophagealatresia
R renalabnormalities
L limb/radialmalformation
WatersonClassification
Category Weight/Comorbidities SurgicalTiming
CategoryA >2500grams undergosurgery
CategoryB 18002500gramsor
congenital anomaly
shorttermdelay,
stabilizing prior to congenitalanomaly stabilizingpriorto
surgery
CategoryC <1800gramsorsevere
pneumoniaorcongenital
anomaly
stagedrepair
PreoperativeEvaluation
Presence&severityofpulmonarydisease
aspirationpneumonia
respiratorydiseaseassociatedwithpre
maturity
Associatedcongenitalanomalies
Problems:
Aspirationpneumonitis
Dehydrationandelectrolyteimbalance
feedingproblems
i d i l li Associatedcongenitalanomalies
cardiac ASD/VSD/TOF/ASD1520%
Vertebralandlimbabnormalities
3
Duetoprematurity4050%
Immatureorgansystems
Incriskofrespdistress
risk of cons Abnormalies riskofcons.Abnormalies
Hypothermia,hypoglycemia,acidosis
Difficultyinventilation
largefistula
overdistensionofstomach
Investigations:
Hb/Hctanemia
TLCinfection/pneumonia
Na/KElectrolyteImbalance
Renal Ultrasound Renal Anomalies RenalUltrasound RenalAnomalies
ECG?ECHO(must) CardiacDisease
ChestXraypneumonitis/medicalconditions
CT/MRI tolocatethefistula
ABGifsignificantpulmonarydysfunction
Preoperativestabilization
Minimizingaspirationby
withholdingoralfeeds
catheterintheupperpouchsuctionto
avoid contamination of lungs avoidcontaminationoflungs
Nursinginuprightposition
Correctionoffluidandelectrolyteimbalances
appropriateI/Vaccess
Ifpneumonits optimizepulmonarystatus
PreoperativePreparation
Optimizepulmonarystatus
Chestphysiotherapy,trachealsuction,
antibiotics.
Improve oxygenation Improveoxygenation
Humidifiedoxygen
Intubation&IPPR respiratory failure
Temp thermallyneutralenvironment
PreoperativePreparation
Ampicillin&gentamicin coexisting
significantcardiacdisease prophylaxis
Optimizevolumeandmetabolicand
biochemical status biochemicalstatus.
Secureappropriatearterialandvenousaccess
Arrangeblood
SurgicalRepair
Primaryrepairwithin2448hoursgood
condition,normallungs.
Stagedsurgicalrepair
Gastrostomy followed by repair when the Gastrostomyfollowedbyrepairwhenthe
neonateisstablized
inprematurebabies,thosewithsignificant
cong.anamoliesandpneumonites
4
Preoperativegastrostomy(LA)
Severegastricreflux aspirationpneumonitis
Preandpostopnutrition
Difficultventilation largefistula
Distensionofstomach
Monitoring
ECG
SPO2fordetectingacutechangesinarterial
oxygenationwhichisverycommonintraop.
problem.
Precordial steth in left axilla indicate accidental Precordialstethinleftaxilla indicateaccidental
rightendobronchialintubation.
Temperature increasedriskofhypothermia
Core&pheripheral
Arterialcannulation continuousmonitoringofBP,
ABG&pH.
Anaestheticconsiderations:
Secureairwaywithoutgastricdistensionand
pulmonaryaspiration
Gastrostomytubeifpresent opentoair
f i i i il i Ifnotmaintainspontorassistventilation
gentlytillfistulaisligated.
Induction
Inhalationalinduction intubationin
spontaneousbreathingpatient.
I/Vorinhalationalinduction intubationwith
muscle relaxants & gentle IPPR musclerelaxants&gentleIPPR.
Awakeintubationinsickandthosewith
difficultairway.
Intubation
Properplacementoftubeiscritical
Tipofthetubebeyondthefistulaandnottoo
fartocauseendobronchialintubation.
l f i i l i Bevalfacinganteriotytopreventcannulation
offistulaopening.
Placementconfirmedbybronchoscopy
Techniques:
Endobronchialintubationwithdrawntill
bilateralbreathsoundsheard.
Intubationwiththehelpofbronchoscope
after the guide wire is placed into the fistula aftertheguidewireisplacedintothefistula
withdrawnafterplacementoftubeHtype
fistula.
Fistulablockedbyfogartycatheterincaseof
repeatedintubationoffistula.
5
Ifgtubepresent,placeend
ofgtubeunderwaterseal:
ETTabovefistula
(+)bubbles
Connectcapnographtog
tube:(+)ETCO2ifETTabove
thefistula
?rigidbronchoscopy
notproven
Maintenance
Spontorassistedventilation(PaW<1015cms
ofH20)tillligationoffistula.
N
2
Odebatablegastricdistension
O
2
withvolatileagents(halothaneor
sevoflurane)withorwithoutmuscle
relaxant
Narcoticsforanalgesia
Intraoperativeproblems
Inadequateoxygenationandventilation
Leakagethroughfistula
ETTmisplacement,compression,blockade,kinking,
V/Qmismatch lateraldecubitusposition,retraction
ofnondependentlungofipsilateraland
contralaterallung
HighF1O2,intermittentinflationofthelungs.
Intraoperativeproblems
Vagalresponse trachealmanipulation
Atropine(Prior)
Hypothermia operatingroomtemp>25
O
C
h i d i i f i fl id heatingdevices,warminfusionfluids.
acidosis
GastricDistensionpreventedby
Preoperativegastrostomy
Intraoperativegastrostomy respiratory
embarrassment/difficultPPV
Occlusion of fistulous opening with fogarty Occlusionoffistulousopeningwithfogarty
ballooncatheterthroughbronchoscopeor
retrogradeviagastrostomy
Applicationofsnugabdominalbinder
PostopConsiderations
* Extubation:Ifthechildisingoodcondition
preoperatively
* Electiveventilation
Aspiration pneumonitis Aspirationpneumonitis
Congenitalheartdisease
Respdistresssyndrome
Monitoringarterialbloodgases,Pao2
temperature
6
Postopanalgesia
EpiduralAnalgesia:Caudal/Lumbar:
Bupivacaine0.1%&fentanyl0.5mcg/ml
IVOpoids fentanyl10 20ug/kgm
l S S l/ i l f RectalNSAIDS Paracetamol/Diclofenac
PostopNutrition
Orgastrictube.Oralfeeds6dayspost
operativelyifnoleakonBariumstudies
Parenteralnutritioniforalfeedingisdelayed
Gastrostomy tube if already placed Gastrostomytubeifalreadyplaced
Aggressivechestphysiotherapy,suctioning
avoidpostoperativecomplications
PrognosisandlongtermSequlae
Healthyneonatesprognosisisgood
Spitzclassificationpredictsoutcomebasedonweight&
cardiacanomalies
SpitzClassification
Group Features Survival(%)
I Birthweight>1500gm,nomajor
cardiacanomaly
98.5
II Birthweight<1500gramsormajor
cardiacanomaly
82
III Birthweight<1500gramsand
majorcardiacanomaly
50
p
Respiratory&GIcomplications maybe
lifelong
RespiratoryComplications
Tracheomalacia
Recurrentpneumonia
Obstructive&restrictiveventilatory defects y
Hyperreactiveairways
GastrointestinalComplications
Intrinsicoesophageal dysfunction GIreflux35% 85%
AbnormalPerstalsis
ImpairedLowerOesophageal tone
PoorOesophageal emptying
Dysphagia

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