Obstetric Shock

DR.KOHINOOR BEGUM

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

Introduction
The circulatory inadequecy is due to a disparity between the circulatory blood volume & the capacity of the circulatory bed. The effect of these disparity is: - Inadequate exchange of o2 & co2 between intra& extra vascular compartment -leading to metabolic acidosis-cellular death

Types and Causes of Shock

A. Hypovolemic Shock
Haemorrhagic shock-excessive blood loss may be due to bleeding in early pregnancy, APH, PPH. Exessive fluid loss-vomiting, diarrhoea, diuresis etc. Supine hypotension syndrome. Plasma loss-Intes.obst. ,acute pancreatitis

B. Neurogenic shock
Associated with painful conditions: Disturbed ectopic pregnancy. Concealed accidental haemorrhage Forceps or Breech extraction before full dilatation of the cx. Rough internal podalic version Ruptured uterus Acute inversion of the uterus Rapid evacuation of the uterus

Causes of shock.
C. Cardiogenic Shock Myocardial Ischemia Heart failure. D. Endotoxic(Septic/Bacteremic) shock generalised vascular disturbence due to release of toxin: Most common in septic abortion , pyelonephritis, puerperal sepsis etc.

Causes of shock.
E . Anaphylactic Shock- by sensitivity to drugs.: F. Embolism-amniotic fluid, air or thrombus G. Anaesthetic complication- as Mendelsons syndrome. H. Shock due to more than one factor like -Incomplete abortion -leads to haemorrhagic and endotoxic shock -Disturbed ectopic pregnancy & rupture uterus leads to haemorrhagic & neurogenic shock.

Pathophysiology of shock
Primary pathophysiologic mechanism in shock is impaired oxygen utilization by the tissue. Impaired utilization encopasses a continuum Impaired utilization may be from: -reduced perfusion -deficient uptake -abnormal relative perfusion.

Shock-SIRS continuum
Shock represents one extreme of a continuum of
SYSTEMIC INFLMMATORY RESPONSE SYNDROME (SIRS)

SIRS characterised by (any 2): Fever or hypothermia Pulse > 90/min. Tachypnea >20min or PaCo2 < 32 leucocytosis(>12K), Relative leukopenia(<4K), or >10% immature form.

Shock-SIRS continuum
Hypovolemia / pump failure Impaired perfusion. Mediator release Tissue injury SIRS Shock multi system dysfunction.

Mediators of injury
Compliment/Leucocytes/ Superoxids Kallikrein-Kinin. Prostaglandins/ Leukotriens/PAF Nitrous Oxide Cytokines.

Haemodynamics of shock
Shock can be classified haemodynamically as: -Hyperdynamic -Hypodynamic/Cardiogenic -Hypovolemic( normodynamic) Haemodynamics may change during the natural progression of a particular aetiology of shock

Haemodynamics of shock
Septic shock is initially hyperdynamic ( normal filling pressure enhanced contractility) ,BP is related to decrease in SVR Haemorrhagic shock is initially normodynamic (diminished filling pressure & CO: normal LV function), BP drop is related to low CO Late shock is usually hypodynamic with increased SVR eventually progressing to total systemic collapse.

Classic clinical picture of Shock

Low blood pressure Rapid weak pulse Pallor Cold clammy sweat Cyanosis of the finger Air hunger Dimness of vision Restlessness Oliguria or anuria.

Common causes of obstetric haemorrhage

Antepartum
-Placeta praevia -Abruptio Placentae -Trauma

Intrapartum
-ruptured uterus

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

Haemorrhagic shock
Classification Class1: 10-20% loss(500-1000ml),normal BP ,no signs Class2: 15-20% loss(1000-1500ml),BP -100 mmHg, dizziness, tachycardia Class3: 25-35%loss(1500-2000ml),BP- 70-80 mmHg, restlessness, pallor, oliguria Class 4: 35-45% loss(2000-3000ml),BP < 70 mmHg, collapse, air hunger, anuria.

Phases of haemorrhagic shock

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

Phases of compensation
In response to hypovolemia, cardiogenic or neurogenic stimulus, vasomotor centre responds by sympathetic stimulationcausing peripheral vasoconstriction to maintain blood supply to the vital organs Clinical picture : -pallor, tachycardia, tachypnoea.

Decompensation or Reversible phase

*Vasoconstriction *Adequate tissue perfusion to vital organs *Squeezing of blood from MCU *Trans-capillary filling from migration of fluids from the interstitial spaces Clinical picture: classic picture of shock Adequate treatment at this stage improves the condition rapidly without residual adverse effect

Irreversible or phase of cellular damage

Inadequatly treated haemorrhagic shock results in prolonged tissue hypoxia & damage with the following effects: Metabolic acidosis -due to anaerobic metabolism initiated after lack of oxygen lactic acidosis Arteriolar dilatation: caused by accumulation of metabolites leading to pooling and stagnation of blood in the capillaries & leakage of fluid into the tissues.

Irreversible phase-contd
DIC:caused by release of thromboplastin from the damaged tissues. Cardiac failure: due to diminished coronary blood flow. In this phase death is imminent, transfusion alone is inadequate & if recovery from acute phase occurs, residual tissue damage as renal and/or pituitary necrosis will occur.

Management of haemorrhagic shock

Urgent interference as follows: Detect the cause & arrest haemorrhage Establish an airway & give o2 by mask or endotracheal tube Elevate the leg Two or more IV line established for blood, fluids & drugs , if needed venesection. Prevent & manage hypothermia.

Management of H.shock
Restoration of blood volume by:
Whole blood-same group,if not available group O-ve can be given as life saving. Crystalloid solusion -as Ringer lactate, normal saline or 5% DNS Colloid solusions :as dextran 40 or 70, plasma protein fraction

Blood component therapy

Fresh frozen plasma is not indicated for volume replacement. Consider platelet transfusion with platelet count less than 50,000/M2. Each unit donor platelets will raise platelet count 5-10000 cm3/M3. FFPreplaces all clotting factors Cryoprecipitets - best choice for hypofibrinogenemia

Drug therapy
Analgesics Corticosteroids-seems to improve tissue perfusion Sodium bicarbonate-if metabolic acidosis. Vasopressors -to increase B.P. so maintain renal perfusion: Dopamine Beta-adrenergic stimulant.

Monitoring of the patients

By: CPV-:normal 10-12 cm water Pulse rate & Blood pressure Urine output: 60 ml / hr. Pulmonary capillary wedge pressure: normal 6-18 torr. Clinical improvement in the pallor, cyanosis, air hunger , sweating & conciousness.

Complications of severe bleeding

Acute renal failure Pituitary necrosis(Sheehans syndrome) DIC.

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

Causative organisms
Gram negetive bacilli(70-80%) E.coli,proteus,pseudomonas& bacterioids release endotoxin ,a lipopolysaccaride Gram positive organism(20-30%)Beta haemolytic streptococci , anaerobic stretococci & clostridia-

release exotoxin ,a Lipoteichoic acid

Pathogenetic steps of endotoxic shock

Infection Organisms (gram positive & negetive, aerobic & anaerobic). Exogenous toxins -organisms,structural component,exotoxin& endo toxins. Systemic inflammatory response(SIRS) Release of endogenous mediatorscytokines, platelet activating actors(PAF) prostaglandins,complements etc.

Pathogenesis- contd
Clinical mediators have:: Myocardial effectdepression & dilatation Vascular effect- vasodilatation, asoconstriction,Maldistribution of blood flow,Endothelial destruction,ARDS,tissue hypoperfution Cardiovascular insufficiency if does not properly managed may lead to : severe decreased SVR, depressed CO & persistent hypotension, multiple organ system failure - death.

Pathogenesis

contd

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

Clinical presentation of septic shock

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

C/F of late (cold) of septic shock

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

C/F of irreversible stage

Irreversible stage-prolonged cellular hypoxia -Metabolic acidosis -acute renal failure -cardiac failure -pulmonary oedema -DIC -adrenal failure & ultimately death.

Differential diagnosis of septic shock

Amniotic fluid embolism Pulmonary embolism Pulmonary aspiration syndrome Myocardial infarction Incompatible blood transfusion.

Management of septic shock

3 major lines of treatment: Restoration of circulatory function & oxygenation Eradication of infection-antibiotic therapy & surgical treatment Correction fluid & electrolyte deficits

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

Treat. contd.
Antibiotic therapy- should cover wide range of organisms(gram positive & negetive, aerobic & anaerobic) Mediator therapy -presently disappointing Correction of fluids & electrolytes : by measuring CVP or simply by measuring urine output & sp. gravity of urine Correction of acidosis -sodium bicarbonate -Surgical treatment:

Cortocosteroids septic shock

Corticosteroids causes vasodilatation & improves tissue perfusion Can be given as: Hydrocortisne-1 gm IV/6 hours or Dexamethasone -20 mg initially followed by 200mg/day by IV infusion High dose treat. 30mg/kg.( attenuate inflammation) is popularized in 1980s Recent data showed lower dose of 300-450 mg/day (adrenal replacing dosing) may be of benefit for some pts.

Treat. Contd.
Surgical treatment - indicated when there is retained infected tissues as in septic abortion -should start as soon as antibiotic therapy & resuscitative measures started by: 1.sucktion evacuation 2.digital evacuation 3.hysterectomy-unresponsive endotoxic shock, gangrenous(clostridium welchii) or traumatised uterus.

Neurogenic shock
Initially normovolemic but later on becomes hypovolemic due to pooling of blood in the microvascular capillaries -compensatory phase is very transient -does not show expected response to volume replacement -Treatment: fluid replacement, vasoactive drugs& cortiocosteroids,, correction of acidosis & ventilation, elimination & correction of source of neurogenic stimulus

Cardiogenic shock
Sudden circulatory collapse caused by sudden failure of the heart to pump the blood adequately. Types: -complete cessation of mechanical & electrical activity: asystole -rapid ineffective activity : ventricular tachycardia & fibrillation

-slow ineffective activity : sinus bradycardia &

complete heart block.

Cardiogenic shock

contd.

Causes: Any obstetric shock can end by cardiac arrest, commonest of which are:-severe haemorrhage -hypoxia due to eclampsia or anaesthesia -Mendelsons syndrome -Embolism of whatever the nature.

Cardiogenic shock

contd.

Diagnosis -Sudden collapse -loss of conciousness -absence of pulse including carotid & femoral -Apnoea & cyanosis of variable degree - fixed dilatation of pupil.

Management of cardiac arrest

Urgent pairs of hands are needed -Put the pt. in dorsal position onto a firm surface, even on the floor -A single firm thump over the lower sternum is sufficient ,if not ABC steps; -1.Airway- clear & maintain it -2.Breathing -mouth to mouth, mask & umbu bag with 100% o2, endotracheal tube & IPPV -3.Cardiac message

contd.
Drip & drugs -sodium bicarbonate for metabolic acidosis -cardiac stimulants (ianotropic drugs)-I.V.or intracardiac -adrenalin-0.5-1mg. -atropin-0.6mg -Isoprenalin 4 mg in 500 ml solution -Dopamine1-3mg/kg/min. -calcium chloride 10% solution. ECG-to assess the condition& response to the therapy Fibrillation therapy-direct current defibrillator(DC)

Amniotic fluid embolism

Rare disorder , totally unpredictable,occuring in 1:20000-30000 pregnancies. Can occur at any point of pregnancy ,labour or delivery A recent analysis of 46 varified cases of AFE showed: 12% occurred in women with intact membrane 70% during labour 11% after vaginal delivery 19% during caesarean delivery

Amniotic fluid embolism

Passage of amniotic fluid into the circulation leads to sudden collapse during labour but can only be confirmed at necropsy. Emboli passes to pulmonary vessels leads to: sudden death, shock or later death due to DIC & PPH.

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

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

Treatment of AFE
Oxygen: intubation & IPPV Amonophylline -to reduce bronchospasm Isoprenalin -to improve Pul. Blood flow & cardiac activity Digoxin & atropine- if raised CVP & Pul. Secretion Hydrocortisone Bicarbonate solution- if respiratory acidosis Low molecular weight dextran- to reduce platelet agrregation in vital organs Heparine for DIC if no active bleeding Vaginal delivery is safer than C.S