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Obstetric Shock Obstetric Shock DR.KOHINOOR BEGUM DR.KOHINOOR BEGUM

Obstetric Shock 21.11.08

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Page 1: Obstetric Shock 21.11.08

Obstetric ShockObstetric Shock

DR.KOHINOOR BEGUMDR.KOHINOOR BEGUM

Page 2: Obstetric Shock 21.11.08

DefinitionDefinition

Shock is a condition resulting from inability of Shock is a condition resulting from inability of the circulatory system to provide the tissues the circulatory system to provide the tissues requirements from oxygen & nutrients to requirements from oxygen & nutrients to remove metabolitesremove metabolites

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IntroductionIntroduction

The circulatory inadequecy is due to a The circulatory inadequecy is due to a disparity between the circulatory blood disparity between the circulatory blood volume & the capacity of the circulatory bed.volume & the capacity of the circulatory bed.

The effect of these disparity is:The effect of these disparity is:

- Inadequate exchange of o2 & co2 - Inadequate exchange of o2 & co2 between intra& extra vascular compartment between intra& extra vascular compartment -leading to metabolic acidosis-cellular -leading to metabolic acidosis-cellular deathdeath

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Types and Causes of ShockTypes and Causes of Shock

A. Hypovolemic ShockA. Hypovolemic Shock Haemorrhagic shock-excessive blood loss Haemorrhagic shock-excessive blood loss

may be due to –bleeding in early pregnancy, may be due to –bleeding in early pregnancy, APH, PPH.APH, PPH.

Exessive fluid loss-vomiting, diarrhoea, Exessive fluid loss-vomiting, diarrhoea, diuresis etc.diuresis etc.

Supine hypotension syndrome.Supine hypotension syndrome. Plasma loss-Intes.obst. ,acute pancreatitisPlasma loss-Intes.obst. ,acute pancreatitis

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B. Neurogenic shockB. Neurogenic shock

Associated with painful conditionsAssociated with painful conditions::

Disturbed ectopic pregnancy.Disturbed ectopic pregnancy.Concealed accidental haemorrhageConcealed accidental haemorrhageForceps or Breech extraction before full dilatation of Forceps or Breech extraction before full dilatation of

the cx.the cx.Rough internal podalic versionRough internal podalic versionRuptured uterusRuptured uterusAcute inversion of the uterusAcute inversion of the uterusRapid evacuation of the uterusRapid evacuation of the uterus

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Causes of shockCauses of shock..

C. Cardiogenic ShockC. Cardiogenic Shock

Myocardial IschemiaMyocardial Ischemia

Heart failure.Heart failure.

D. Endotoxic(Septic/Bacteremic) shockD. Endotoxic(Septic/Bacteremic) shock – –

generalised vascular disturbence due to generalised vascular disturbence due to release of toxin: Most common in septic release of toxin: Most common in septic abortion , pyelonephritis, puerperal sepsis abortion , pyelonephritis, puerperal sepsis etc.etc.

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Causes of shockCauses of shock..

E . Anaphylactic Shock-E . Anaphylactic Shock- by sensitivity to drugs.: by sensitivity to drugs.:

F. EmbolismF. Embolism-amniotic fluid, air or thrombus-amniotic fluid, air or thrombus

G. Anaesthetic complication- asG. Anaesthetic complication- as Mendelson’s Mendelson’s syndrome.syndrome.

HH. Shock due to . Shock due to more than one factormore than one factor like like

-Incomplete abortion -leads to haemorrhagic -Incomplete abortion -leads to haemorrhagic and endotoxic shock and endotoxic shock

-Disturbed ectopic pregnancy & rupture -Disturbed ectopic pregnancy & rupture uterus leads to haemorrhagic & neurogenic shock.uterus leads to haemorrhagic & neurogenic shock.

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Pathophysiology of shockPathophysiology of shock

Primary pathophysiologic mechanism in Primary pathophysiologic mechanism in shock is impaired oxygen utilization by the shock is impaired oxygen utilization by the tissue.tissue.

Impaired utilization encopasses a continuumImpaired utilization encopasses a continuum Impaired utilization may be from:Impaired utilization may be from: -reduced perfusion-reduced perfusion -deficient uptake-deficient uptake -abnormal relative perfusion.-abnormal relative perfusion.

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Shock-SIRS continuumShock-SIRS continuum

Shock represents one extreme of a continuum of Shock represents one extreme of a continuum of SYSTEMIC INFLMMATORY RESPONSE SYNDROME (SYSTEMIC INFLMMATORY RESPONSE SYNDROME (SIRSSIRS)) SIRS characterised by (any 2):SIRS characterised by (any 2): Fever or hypothermiaFever or hypothermia Pulse > 90/min.Pulse > 90/min. Tachypnea >20min or PaCo2 < 32Tachypnea >20min or PaCo2 < 32 leucocytosis(>12K),leucocytosis(>12K), Relative leukopenia(<4K),Relative leukopenia(<4K), or >10% immature form.or >10% immature form.

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Shock-SIRS continuumShock-SIRS continuum

Hypovolemia / pump failureHypovolemia / pump failure

Impaired perfusion.Impaired perfusion.

Mediator releaseMediator release

Tissue Tissue injury injury

SIRSSIRS

Shock Shock

multi system dysfunction.multi system dysfunction.

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Mediators of injuryMediators of injury

Compliment/Leucocytes/ SuperoxidsCompliment/Leucocytes/ Superoxids Kallikrein-Kinin.Kallikrein-Kinin. Prostaglandins/ Leukotriens/PAFProstaglandins/ Leukotriens/PAF Nitrous OxideNitrous Oxide Cytokines.Cytokines.

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Haemodynamics of shockHaemodynamics of shock

Shock can be classified haemodynamically Shock can be classified haemodynamically as:as:

-Hyperdynamic-Hyperdynamic

-Hypodynamic/Cardiogenic-Hypodynamic/Cardiogenic

-Hypovolemic( normodynamic)-Hypovolemic( normodynamic)

Haemodynamics may change during the Haemodynamics may change during the natural progression of a particular aetiology natural progression of a particular aetiology of shock of shock

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Haemodynamics of shockHaemodynamics of shock

Septic shock is initially Septic shock is initially hyperdynamic hyperdynamic ( normal ( normal filling pressure enhanced contractility) ,BP is filling pressure enhanced contractility) ,BP is related to decrease in SVRrelated to decrease in SVR

Haemorrhagic shock is initially Haemorrhagic shock is initially normodynamic normodynamic (diminished filling pressure & CO: normal LV (diminished filling pressure & CO: normal LV function), BP drop is related to low COfunction), BP drop is related to low CO

Late shock is usually Late shock is usually hypodynamichypodynamic with with increased SVR eventually progressing to total increased SVR eventually progressing to total systemic collapse. systemic collapse.

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Classic clinical picture of ShockClassic clinical picture of Shock

Low blood pressureLow blood pressureRapid weak pulseRapid weak pulsePallorPallorCold clammy sweatCold clammy sweatCyanosis of the fingerCyanosis of the fingerAir hungerAir hungerDimness of visionDimness of visionRestlessnessRestlessnessOliguria or anuria.Oliguria or anuria.

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Common causes of obstetricCommon causes of obstetric haemorrhagehaemorrhage

AntepartumAntepartum --Placeta praeviaPlaceta praevia --Abruptio PlacentaeAbruptio Placentae -Trauma-Trauma

IntrapartumIntrapartum -ruptured uterus-ruptured uterus

Postpartum:Postpartum: --retained placentaretained placenta- - - - Uterine atonyUterine atony -laceration-laceration -coagulopathy-coagulopathy

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Haemorrhagic shockHaemorrhagic shock

Classification Classification

Class1: 10-20% loss(500-1000ml),normal BP ,no Class1: 10-20% loss(500-1000ml),normal BP ,no signssigns

Class2: 15-20% loss(1000-1500ml),BP -100 Class2: 15-20% loss(1000-1500ml),BP -100 mmHg, dizziness, tachycardiammHg, dizziness, tachycardia

Class3: 25-35%loss(1500-2000ml),BP- 70-80 Class3: 25-35%loss(1500-2000ml),BP- 70-80 mmHg, restlessness, pallor, oliguriammHg, restlessness, pallor, oliguria

Class 4: 35-45% loss(2000-3000ml),BP < 70 Class 4: 35-45% loss(2000-3000ml),BP < 70 mmHg, collapse, air hunger, anuria.mmHg, collapse, air hunger, anuria.

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Phases of haemorrhagic shockPhases of haemorrhagic shock

The normal pregnant women can withstand The normal pregnant women can withstand blood loss of 500 ml & even upto 1000ml blood loss of 500 ml & even upto 1000ml during delivery without obvious danger due during delivery without obvious danger due to physiological cardiovascular & to physiological cardiovascular & haematological adaptations during haematological adaptations during pregnancy.pregnancy.

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Phases of compensationPhases of compensation

In response to hypovolemia, cardiogenic or In response to hypovolemia, cardiogenic or neurogenic stimulus, vasomotor centre neurogenic stimulus, vasomotor centre responds by sympathetic stimulation-responds by sympathetic stimulation-causing peripheral vasoconstriction to causing peripheral vasoconstriction to maintain blood supply to the vital organsmaintain blood supply to the vital organs

Clinical pictureClinical picture : :

-pallor, tachycardia, tachypnoea.-pallor, tachycardia, tachypnoea.

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Decompensation or Reversible Decompensation or Reversible phasephase

*Vasoconstriction*Vasoconstriction *Adequate tissue perfusion to vital organs*Adequate tissue perfusion to vital organs *Squeezing of blood from MCU*Squeezing of blood from MCU *Trans-capillary filling from migration of fluids from the *Trans-capillary filling from migration of fluids from the

interstitial spacesinterstitial spaces

Clinical pictureClinical picture: classic picture of shock: classic picture of shock

Adequate treatment at this stage improves the condition Adequate treatment at this stage improves the condition rapidly without residual adverse effectrapidly without residual adverse effect

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Irreversible or phase of cellular Irreversible or phase of cellular damagedamage

Inadequatly treated haemorrhagic shock Inadequatly treated haemorrhagic shock results in prolonged tissue hypoxia & results in prolonged tissue hypoxia & damage with the following effects:damage with the following effects:

Metabolic acidosisMetabolic acidosis -due to anaerobic -due to anaerobic metabolism initiated after lack of oxygen - metabolism initiated after lack of oxygen - lactic acidosislactic acidosis

Arteriolar dilatationArteriolar dilatation: caused by : caused by accumulation of metabolites leading to accumulation of metabolites leading to pooling and stagnation of blood in the pooling and stagnation of blood in the capillaries & leakage of fluid into the tissues.capillaries & leakage of fluid into the tissues.

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Irreversible phase-contdIrreversible phase-contd

DIC:DIC:caused by release of thromboplastin from caused by release of thromboplastin from the damaged tissues.the damaged tissues.

Cardiac failureCardiac failure: due to diminished coronary : due to diminished coronary blood flow.blood flow.

In this phase death is imminent, transfusion In this phase death is imminent, transfusion alone is inadequate & if recovery from acute alone is inadequate & if recovery from acute phase occurs, residual tissue damage as phase occurs, residual tissue damage as renal and/or pituitary necrosis will occur.renal and/or pituitary necrosis will occur.

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Management of haemorrhagic Management of haemorrhagic shockshock

Urgent interference as follows:Urgent interference as follows: Detect the cause & arrest haemorrhageDetect the cause & arrest haemorrhage Establish an airway & give o2 by mask or Establish an airway & give o2 by mask or

endotracheal tubeendotracheal tube Elevate the leg Elevate the leg Two or more IV line established for blood, Two or more IV line established for blood,

fluids & drugs , if needed venesection.fluids & drugs , if needed venesection. Prevent & manage hypothermia.Prevent & manage hypothermia.

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Management of H.shockManagement of H.shock

Restoration of blood volume byRestoration of blood volume by::

Whole blood-same group,if not available Whole blood-same group,if not available group O-ve can be given as life saving.group O-ve can be given as life saving.

Crystalloid solusion -as Ringer lactate, Crystalloid solusion -as Ringer lactate, normal saline or 5% DNSnormal saline or 5% DNS

Colloid solusions :as dextran 40 or 70, Colloid solusions :as dextran 40 or 70, plasma protein fractionplasma protein fraction

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Blood component therapyBlood component therapy

Fresh frozen plasma is not indicated for Fresh frozen plasma is not indicated for volume replacement.volume replacement.

Consider platelet transfusion with platelet Consider platelet transfusion with platelet count less than 50,000/M2.count less than 50,000/M2.

Each unit donor platelets will raise platelet Each unit donor platelets will raise platelet count 5-10000 cm3/M3.count 5-10000 cm3/M3.

FFP—replaces all clotting factors FFP—replaces all clotting factors Cryoprecipitets - best choice for Cryoprecipitets - best choice for

hypofibrinogenemiahypofibrinogenemia

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Drug therapyDrug therapy

AnalgesicsAnalgesics Corticosteroids-seems to improve tissue Corticosteroids-seems to improve tissue

perfusionperfusion Sodium bicarbonate-if metabolic acidosis.Sodium bicarbonate-if metabolic acidosis. Vasopressors -to increase B.P. so maintain Vasopressors -to increase B.P. so maintain

renal perfusion:renal perfusion:

DopamineDopamine

Beta-adrenergic stimulant.Beta-adrenergic stimulant.

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Monitoring of the patientsMonitoring of the patients

By: By: CPV-:normal 10-12 cm waterCPV-:normal 10-12 cm water Pulse rate & Blood pressurePulse rate & Blood pressure Urine output: 60 ml / hr.Urine output: 60 ml / hr. Pulmonary capillary wedge pressure:Pulmonary capillary wedge pressure:

normal 6-18 torr.normal 6-18 torr. Clinical improvement in the pallor, Clinical improvement in the pallor,

cyanosis, air hunger , sweating & cyanosis, air hunger , sweating & conciousness.conciousness.

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Complications of severe bleedingComplications of severe bleeding

Acute renal failureAcute renal failure Pituitary necrosis(Sheehan’s syndrome)Pituitary necrosis(Sheehan’s syndrome) DIC.DIC.

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Septicemic shockSepticemic shockObstetric causes:Obstetric causes: -Septic abortion-Septic abortion -Prolonged rupture of the membrane-Prolonged rupture of the membrane -Manipulations & Instrumentation-Manipulations & Instrumentation -Trauma-Trauma -Retained placental tissue-Retained placental tissue -Puerperal sepsis-Puerperal sepsis -Severe acute pyelonephritis.-Severe acute pyelonephritis.

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Causative organismsCausative organisms

Gram negetive bacilli(70-80%)Gram negetive bacilli(70-80%) – –E.coli,proteus,pseudomonas& bacterioids -E.coli,proteus,pseudomonas& bacterioids -

release release endotoxinendotoxin ,a lipopolysaccaride ,a lipopolysaccaride Gram positive organism(20-30%)-Gram positive organism(20-30%)-

Beta haemolytic streptococci , anaerobic Beta haemolytic streptococci , anaerobic stretococci & clostridia-stretococci & clostridia-

release release exotoxin exotoxin ,a Lipoteichoic acid,a Lipoteichoic acid

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Pathogenetic steps of endotoxic Pathogenetic steps of endotoxic shockshock

InfectionInfection Organisms (gram positive & negetive, Organisms (gram positive & negetive,

aerobic & anaerobic).aerobic & anaerobic). Exogenous toxins -organisms,structural Exogenous toxins -organisms,structural

component,exotoxin& endo toxins.component,exotoxin& endo toxins. Systemic inflammatory response(SIRS)Systemic inflammatory response(SIRS) Release of endogenous mediators-Release of endogenous mediators-

cytokines, platelet activating actors(PAF) cytokines, platelet activating actors(PAF) prostaglandins,complements etc.prostaglandins,complements etc.

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Pathogenesis- contdPathogenesis- contd

Clinical mediators haveClinical mediators have::::– Myocardial effect-Myocardial effect-

depression & dilatationdepression & dilatation– Vascular effect-Vascular effect- vasodilatation, vasodilatation,

asoconstriction,Maldistributioasoconstriction,Maldistribution of n of blood blood flow,Endothelial destruction,ARDS,tissue flow,Endothelial destruction,ARDS,tissue hypoperfutionhypoperfution

– Cardiovascular insufficiency if does not properly Cardiovascular insufficiency if does not properly managed may lead to : severe decreased SVR, managed may lead to : severe decreased SVR, depressed CO & persistent hypotension, multiple depressed CO & persistent hypotension, multiple organ system failure - death.organ system failure - death.

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PathogenesisPathogenesis contd contd

Cardiovascular insufficiency if does not Cardiovascular insufficiency if does not

properly managed may lead to : properly managed may lead to : – severe decreased SVRsevere decreased SVR– depressed CO & depressed CO & – persistent hypotension,persistent hypotension,– multiple organ system failure ------- death.multiple organ system failure ------- death.

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Clinical presentation of septic Clinical presentation of septic shockshock

Posseses 2 main stages- Posseses 2 main stages- Reversible stageReversible stage & & Irreversible stageIrreversible stage..Reversible stage has 2 phases:Reversible stage has 2 phases: Early (warm) phase: Early (warm) phase: --hypotensionhypotension-tachycardia , pyrexia , rigors-tachycardia , pyrexia , rigors-flushed skin , low SVR , patient is alert-flushed skin , low SVR , patient is alert-leucocytosis develops within hours-leucocytosis develops within hours

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C/F of late (cold) of septic shockC/F of late (cold) of septic shock

-cold & clammy skin-decreased CO-cold & clammy skin-decreased CO -mottled cyanosis-mottled cyanosis -purpura-purpura -jaundice-jaundice -oliguria & acidemia-oliguria & acidemia -acute lung injury-acute lung injury -progressive mental confusion-progressive mental confusion -coma.-coma.

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C/F of irreversible stageC/F of irreversible stage

Irreversible stage-prolonged cellular Irreversible stage-prolonged cellular hypoxiahypoxia

-Metabolic acidosis-Metabolic acidosis-acute renal failure-acute renal failure-cardiac failure-cardiac failure-pulmonary oedema-pulmonary oedema-DIC-DIC-adrenal failure & ultimately death.-adrenal failure & ultimately death.

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Differential diagnosis of septic shockDifferential diagnosis of septic shock

Amniotic fluid embolismAmniotic fluid embolism Pulmonary embolismPulmonary embolism Pulmonary aspiration syndromePulmonary aspiration syndrome Myocardial infarctionMyocardial infarction Incompatible blood transfusion.Incompatible blood transfusion.

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Management of septic shockManagement of septic shock

3 major lines of treatment3 major lines of treatment:: Restoration of circulatory function & Restoration of circulatory function &

oxygenationoxygenation Eradication of infection-antibiotic therapy Eradication of infection-antibiotic therapy

& surgical treatment& surgical treatment Correction fluid & electrolyte deficitsCorrection fluid & electrolyte deficits

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Treat. ContdTreat. Contd..

Restoration of circulatory function& oxigenationRestoration of circulatory function& oxigenation -replacement of blood volume by whole blood ,if-replacement of blood volume by whole blood ,if not available start with crystalloids or colloidsnot available start with crystalloids or colloids -Corticosteroids-Corticosteroids -beta- adrenergic stimulants- causes -beta- adrenergic stimulants- causes -arteriolar dilatation-arteriolar dilatation - increase heart rate & stroke volume- increase heart rate & stroke volume -Oxygen-if respiratory function is impaired-Oxygen-if respiratory function is impaired -Aminophylline -improves respiratory functions by -Aminophylline -improves respiratory functions by

alleviating bronchospasm alleviating bronchospasm

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Treat. contdTreat. contd..

Antibiotic therapy-Antibiotic therapy- should cover wide range of should cover wide range of organisms(gram positive & negetive, aerobic & organisms(gram positive & negetive, aerobic & anaerobic)anaerobic)

Mediator therapyMediator therapy -presently disappointing -presently disappointing Correction of fluids & electrolytes :Correction of fluids & electrolytes :

byby measuring CVP or simply by measuring urine measuring CVP or simply by measuring urine output & sp. gravity of urineoutput & sp. gravity of urine

Correction of acidosisCorrection of acidosis -sodium bicarbonate -sodium bicarbonate -Surgical treatment:-Surgical treatment:

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Cortocosteroids –septic shockCortocosteroids –septic shock

Corticosteroids causes vasodilatation & Corticosteroids causes vasodilatation & improves tissue perfusionimproves tissue perfusion

Can be given as:Can be given as: Hydrocortisne-1 gm IV/6 hours orHydrocortisne-1 gm IV/6 hours or Dexamethasone -20 mg initially followed byDexamethasone -20 mg initially followed by 200mg/day by IV infusion200mg/day by IV infusion High dose treat. 30mg/kg.( attenuate High dose treat. 30mg/kg.( attenuate

inflammation) –is popularized in 1980sinflammation) –is popularized in 1980s Recent data showed –lower dose of 300-450 Recent data showed –lower dose of 300-450

mg/day (adrenal replacing dosing) may be of mg/day (adrenal replacing dosing) may be of benefit for some pts.benefit for some pts.

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Treat. ContdTreat. Contd..Surgical treatment-Surgical treatment- - indicated when there is retained infected - indicated when there is retained infected

tissues as in septic abortiontissues as in septic abortion -should start as soon as antibiotic therapy & -should start as soon as antibiotic therapy &

resuscitative measures started by:resuscitative measures started by: 1.sucktion evacuation1.sucktion evacuation 2.digital evacuation 2.digital evacuation 3.hysterectomy-unresponsive endotoxic 3.hysterectomy-unresponsive endotoxic

shock, gangrenous(clostridium welchii) or shock, gangrenous(clostridium welchii) or traumatised uterus.traumatised uterus.

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Neurogenic shockNeurogenic shock Initially normovolemic but later on becomes Initially normovolemic but later on becomes

hypovolemic due to pooling of blood in the hypovolemic due to pooling of blood in the microvascular capillariesmicrovascular capillaries

-compensatory phase is very transient-compensatory phase is very transient -does not show expected response to volume -does not show expected response to volume

replacementreplacement--Treatment:Treatment: fluid replacement,fluid replacement, vasoactive drugs& cortiocosteroids,,vasoactive drugs& cortiocosteroids,, correction of acidosis & ventilation,correction of acidosis & ventilation, elimination & correction of source of neurogenic elimination & correction of source of neurogenic

stimulusstimulus

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Cardiogenic shockCardiogenic shock

Sudden circulatory collapse caused by sudden Sudden circulatory collapse caused by sudden failure of the heart to pump the blood adequately.failure of the heart to pump the blood adequately.

Types:Types: -complete cessation of mechanical & electrical -complete cessation of mechanical & electrical

activity: activity: asystoleasystole -rapid ineffective activity : -rapid ineffective activity : ventricular ventricular

tachycardiatachycardia & & fibrillationfibrillation -slow ineffective activity : -slow ineffective activity : sinus bradycardia & sinus bradycardia &

complete heart block.complete heart block.

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Cardiogenic shock contdCardiogenic shock contd..

CausesCauses::

Any obstetric shock can end by cardiac arrest, Any obstetric shock can end by cardiac arrest, commonest of which are:- commonest of which are:-

-severe haemorrhage-severe haemorrhage -hypoxia due to eclampsia or anaesthesia-hypoxia due to eclampsia or anaesthesia -Mendelson’s syndrome-Mendelson’s syndrome -Embolism of whatever the nature.-Embolism of whatever the nature.

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Cardiogenic shock contd.Cardiogenic shock contd.

DiagnosisDiagnosis -Sudden collapse-Sudden collapse -loss of conciousness-loss of conciousness -absence of pulse including carotid & -absence of pulse including carotid &

femoral femoral -Apnoea & cyanosis of variable degree-Apnoea & cyanosis of variable degree - fixed dilatation of pupil.- fixed dilatation of pupil.

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Management of cardiac arrestManagement of cardiac arrest

Urgent pairs of hands are neededUrgent pairs of hands are needed -Put the pt. in dorsal position onto a firm surface, -Put the pt. in dorsal position onto a firm surface,

even on the flooreven on the floor -A single firm thump over the lower sternum is -A single firm thump over the lower sternum is

sufficient ,if notsufficient ,if notABC steps;ABC steps; -1.-1.AAirway- clear & maintain itirway- clear & maintain it -2.-2.BBreathing -mouth to mouth, mask & umbu reathing -mouth to mouth, mask & umbu

bag with 100% o2, endotracheal tube & IPPVbag with 100% o2, endotracheal tube & IPPV -3.-3.CCardiac messageardiac message

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contdcontd..Drip & drugsDrip & drugs -sodium bicarbonate for metabolic acidosis-sodium bicarbonate for metabolic acidosis -cardiac stimulants (ianotropic drugs)-I.V.or -cardiac stimulants (ianotropic drugs)-I.V.or

intracardiacintracardiac -adrenalin-0.5-1mg.-adrenalin-0.5-1mg. -atropin-0.6mg-atropin-0.6mg -Isoprenalin 4 mg in 500 ml solution-Isoprenalin 4 mg in 500 ml solution -Dopamine1-3mg/kg/min.-Dopamine1-3mg/kg/min. -calcium chloride 10% solution.-calcium chloride 10% solution.ECGECG-to assess the condition& response to the -to assess the condition& response to the

therapytherapyFibrillationFibrillation therapy-direct current defibrillator(DC) therapy-direct current defibrillator(DC)

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Amniotic fluid embolismAmniotic fluid embolism

Rare disorder , totally unpredictable,occuring in Rare disorder , totally unpredictable,occuring in 1:20000-30000 pregnancies.1:20000-30000 pregnancies.

Can occur at any point of pregnancy ,labour or Can occur at any point of pregnancy ,labour or deliverydelivery

A recent analysis of 46 varified cases of AFE A recent analysis of 46 varified cases of AFE showed:showed:

12% occurred in women with intact membrane12% occurred in women with intact membrane 70% during labour70% during labour 11% after vaginal delivery11% after vaginal delivery 19% during caesarean delivery19% during caesarean delivery

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Amniotic fluid embolismAmniotic fluid embolism

Passage of amniotic fluid into the circulation Passage of amniotic fluid into the circulation leads to sudden collapse during labour but leads to sudden collapse during labour but can only be confirmed at necropsy.can only be confirmed at necropsy.

Emboli passes to pulmonary vessels leads Emboli passes to pulmonary vessels leads to:to:

sudden death, shock or later death due to sudden death, shock or later death due to DIC & PPH.DIC & PPH.

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Amniotic Fluid Embolism

Clinical picture-onset is acute with sudden collapse,cyanosis, severe dyspnoea - followed by-twitching, convulsions & right sided heart failure with tachycardia, pulmonary oedema & blood stained frothy sputum- If not death,DIC with in 1 hr.leading to generalized bleeding

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Contd.Contd.

InvestigationsInvestigations -ECG-evidence of right sided heart failure-ECG-evidence of right sided heart failure -X-ray-non-specific mottling-X-ray-non-specific mottling -Lung scan-shows perfusion defect-Lung scan-shows perfusion defect -Lab. test- evidence of DIC.-Lab. test- evidence of DIC.D/D:D/D: -Acute pulmonary oedema-Acute pulmonary oedema -pulmonary aspiration syndrome-pulmonary aspiration syndrome -other coagulation defects.-other coagulation defects.

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Treatment of AFETreatment of AFE Oxygen: intubation & IPPVOxygen: intubation & IPPV Amonophylline -to reduce bronchospasmAmonophylline -to reduce bronchospasm Isoprenalin -to improve Pul. Blood flow & cardiac Isoprenalin -to improve Pul. Blood flow & cardiac

activityactivity Digoxin & atropine- if raised CVP & Pul. Digoxin & atropine- if raised CVP & Pul.

SecretionSecretion HydrocortisoneHydrocortisone Bicarbonate solution- if respiratory acidosisBicarbonate solution- if respiratory acidosis Low molecular weight dextran- to reduce platelet Low molecular weight dextran- to reduce platelet

agrregation in vital organsagrregation in vital organs Heparine –for DIC if no active bleedingHeparine –for DIC if no active bleeding Vaginal delivery is safer than C.SVaginal delivery is safer than C.S

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