SHOCK IN

OBSTETRICS
 Introduction
• Shock is a critical condition and a life
threatening medical emergency.
• Shock results from acute , generalised
inadequate perfusion of tissues; below
that needed to deliver the oxygen and
nutrients for normal function.
• Prompt recognition and management
can improve maternal and fetal
outcome in obstetrical shock.
 DEFINITION
“Shock is defined as a state of
circulatory inadequacy with poor tissue
perfusion resulting in generalized cellular
hypoxia.”
Circulatory inadequacy is due to a
disparity between the circulating
blood volume and the capacity of
the circulatory bed.
The net effect of this diparity is
inadequate exchange of oxygen
and carbon dioxyde between the
intra and extravsacular
compartments.
CLASSIFICATION OF SHOCK

SHOCK

HYPO CARDIO EXTRA

SEPTIC
VOLEMIC GENIC CARDIC
SHOCK
SHOCK SHOCK SHOCK
 HYPOVOLEMIC SHOCK
 Circulating blood volume is inadeuate
resulting from acute depletion.
 It may be-
ii)Non
Hemorrhagic
i)Hemorrhagic Shock
Shock
Hemorrhagic shock
Associated with postpartum or
postabortal hemorrhage, ectopic
pregnancy, placenta previa, abruptio
placenta, rupture of the uterus and
obstetric surgery.
Shock associated with disseminate
intravsacular coagulation, intrauterine
dead fetus syndrome and amniotic fluid
embolism.
Non Hemorrhagic shock
Fluid Shock:-
Associated with excessing vomiting,
diarrhea, diuresis or too rapid removal of
amniotic fluid.
Supine Hypotensive Syndrome:-
Due to compression of inferior vena cava
by the pregnant uterus.
 SEPTIC SHOCK
(Endotoxic Shock)
 Hypotension is due to sepsis resulting
in derangements in cellular and organ
system dysfunction.
 Hypotension persists in spite of
adequate fluid resuscitation.
 Associated typically with septic
abortion, chorioamnionitis and rarely
postpartum endometriosis.
 CARDIAC SHOCK
Characterised by...
Decreased systolic pressure ( <80 mm
Hg)
Decreased Cardiac Index (<1.8 L /min/m2)
Increased left ventricular filling pressure
(> 18 mm Hg)
C
A
R
D Myocardial
I
O
Infraction
G
E
N Cardia Arrest
I
C
S Cardiac
H
O Tamponade
C
K
 EXTRA CARDIAC SHOCK
Massive pulmonary embolism, amniotic
fluid embolism, anaphylaxis, drug
overdose, neurogenic.

Chemical Drug
Injury Induced
Chemical injury:-
Associated with aspiration of
gastrointestinal contents during
general anesthesia (Mendelson's
syndrome)

Drug induced:-
Associated with spinal anesthesia.
PATHOPHYSIOLOGY OF SHOCK
 Pathophysiological changes in obstetric
shock are predominantly associated with..

a) General changes due to hypovolemia

b) Specific changes due to liberation of
endotoxin
 Hypotension stimulates release of
neuroendocrine mediators like
adrenocorticotropic hormone (ACTH),
Growth hormone (GH), β endorphin,
cortisol and glucagon.
 There is also sympathoadrenal
response.
 Presence of endotoxin
(lipopolysaccharide), in septic shock
activates the luecocytes through
complement system.
There is release of inflammatory
mediators such as protease,
superoxide (o2-), hydroxy (OH-)
radicals, cytokines, prostaglandins
and many cytotoxic enzymes.
These interfere with the function of
a number of enzyme systems and
increase capillary permiability.
 Cytiokines such as interleukines (ILS)
and tumor nacrosis factor ( INF)
interact by autocrine and paracrine
mechanism to cause cellular or organ
dysfunction.
 In presense of hypoxia, sepsis and
acidosis, lysosomal emzymes which
are cytotoxic, are released.
 They can cause myocardial depression
and coronary vasoconstriction.
 Prostacycline is a vasodilator and
inhibits platelet aggregation.
 Thromboxane A2 causes pulmonary
vasoconstriction and platelet
aggregation.
 Leukotrines cause vasoconstriction,
platelet activation and increased
vascular parmiability.
 Endothelium derived relaxing factor
( EDRF) which is identified as an nitric
oxide (NO) is found to produce
sustained vasodilation and
 Thrombosis is increased due to inhibition
of antithrombin III.
 Thrombocytopenia is common.
 METABOLIC CHANGES
 Hepatic glycogenolysis due to
increased level of glucagon,
catecholamine and cortisol leads to
hyperglycemia.
 There is diminished peripheral
utilization of glucose due to incearsed
level of insulin antagonist like cortisol
and growth hormone.
 Inadquate oxygen supply to issue
initiates anaerobic metabolism.
 Consequently there is metbolic
acidosis, production of lactic acid and
H+ irons.
 Sodium pump fails to operate.
 Finally the lysosomal enzymes are
released.
 These lead to cell death.
GENERAL CHANGES IN SHOCK
(Hypovolemic Shock)
 There are four phases of changes.
 The first two phases are reversible, the
third one probably correctable and
fourth is irreversible.
 FIRST PHASE
 Sympathetic impuses and the level of
cicrculating catacholamines increase in
response to hypovolemia, cardiogenic or
neurogenic stimulus.
 Stretch receptors monitoring blood pressure in
the carotid sinus and aortic arch supply
information to the vasomotor centre via the
ninght and tenth cranial nerves.
 The vasomotor centre responds by sending
efferent impulses through the sympathetic
nervous sytem.
 SECOND PHASE
 As a result of excessive sympathetic
stimulus, there is constriction of the pre
and post capillary sphincters, resulting in
inadequate venous return leading to
diminished cardiac output, clinical
manifestations of which are hypotension
and tachycardia.
 The mechanisms attempt to correct
hypovolemia, improve cardiac output
and the perfusion of vital organs.
 At this stage, transfusion and control of
haemorrhage are usually effective in
restoring the normal circultory balance
and tissue perfussion.
 On the otherhand, if bleeding continues
or treatment is delayed, the changes at
microcirculatory unit will continue to
persist and will pass into the third and
fourth phases of shock.
 THIRD PHASE
 Prolonged anoxia of the tissues will lead to
excessive production of lactic acid (acidosis).
 Lactic acid and anoxia cause relaxation of the
precapillary sphincters.
 In addition, thromboxane A2 and leukotrines
(endogenous mediators) cause damage to the
endothelial cells of the capillaries of the
microcirculatory beds.
 These lead to formation of thrombus within the
capillaries (diffuse intravascular coagulation
and increaded capillary permiability.
 FOURTH PHASE
 Consequent to persistant constriction of
the postcapillary sphincter, blood remains
stagnant within the capillary bed.
 Fuid from the capillaries leaks in to the
tissue spaces due to increased
permiability.
 All fluids administered intravenously will
go into the tissue spaces and circulatory
blood volume cannot be restored.
 Clinically, this is the stage of
irreversible shock.
 There is severe loss of systemic
vascular resistence, severe myocardial
depression, (decreased cardiac output),
unresponsive hypotension and
ultimately multiple organ system
failure.
 CHANGES IN ENDOTOXIC
SHOCK
 Endotoxic shock usually follows infection
with Gram-negative organism (75-80 %).
 The most common organism involved is
Escherichia coli (50 %).
 Other organism occasionally responsible
for endotoxic shock are, Pseudomonas
aeruginosa, klebsiella, proteus,
bacteroides and aerobacter aerogenes.
 Gram positive organisms, anaerobes,
clostridium group are less common
(20%).
 Bacterial endotoxin causes selective
vasospasm at the postcapillary end.
 Blood is pooled in the capillary bed.
 There is inhibition of myocardial
function and cellular damage through
complex biochemical changes.
 The patient in early septic shock feels
warm due to vasoconstriction.
 This is called Warm shock.
 In the late phase, the patient feels cold
due vasoconstriction.
 This is called cold shock or late shock.
 Patient's skin becomes cold, clammy
and ashen gray.
VARIOUS BIOCHEMICAL AND PATHOLOGICAL
CHANGES IN ENDOTOXIC SHOCK
Diffuse intravsacular coagulation
Increased capillary permiability
Metabolic acidosis
Release of superoxide and hydroxyl
radicals
Failure of sodium pump operation
Water and electrolyte imbalance
Excessive and uncontrolled systemic
inflammatory response (SIR) - leads to
organ changes
 Organ changes depends on the degree
of hypoperfusion and extent of the
underlying pathology:
Kidney: Patchy and massive chortical
necrosis leading to oliguria, anuria and
azotemia. Persistant hypotension
leads to acute tubular necrosis and
ultimately renal failure.
Liver: Hepatocellular necrosis and
degeneration ultimately leading to
hepatic failure.
GI Tract: Hypoxic mucosal injury increases
systemic sepsis by translocation of
intraluminal microbes. Congestion,
hemorrhage and ulceration are responsible
for hematemesis.
Lungs: Congestion or atelectasis leads to
tachypnea, progressive hypoxemia and
reduced pulmonary compliance.
ARDS results from increased capillary
permiability and thickening of the alveolar
capillary membranes. Arterial PaO2 is low.
Mechanical ventilation is needed.
Heart: Cardiac output decreases
depending on the degree of hypotension,
hypoperfusion and vasoconstriction.
Myocardial Cardiac
Dysrrhythmia
Ischemia Dysfunction

Pulmonary Increased Cardiac

Edema LVEDP Failure

Tissue LVEDP: Left Ventricular End

Hypoxia Diastolic Pressure
 Ultimately multiple organ failure
develops.
 Endotoxins have got special affinity for
kidneys and lungs for reasons which
are not very clear.
CLINICAL FEATURES OF SHOCK
 Clinical features of shock depend on
the basic etlogical factors and
consequently the sequence of
pathological changes occuring within
the microvascular unit.
 In early, the features of hypovolemic
and septic shock are different.
 In the irreversal phase, the clinical
features are the same as the final
pathology is multiple organ failure.
 It carries mortality of 30%-100%.
 MANAGEMENT OF SHOCK
HEMORRHAGIC SHOCK:
 Basic management of hemorrhagic shock
is to stop the bleeding and replace the
volume which has been lost.
 Restoring circulatory volume
 Maintenance of cardiac efficiency
 Administration of oxygen to avoid
metabolic acidosis
 Pharmacological agents- corticosteroids
 Control of hemorrhage
 ENDOTOXIC SHOCK
INVESTIGATIONS:
CBC
Hematocrit
Coagulation Profile
Liver and Renal function test
Chest radiography
 USG, CT, MRI
ECG monitoring
PRINCIPLE OF MANAGEMENT:
 To correct the hemodynamic unstability
due to sepsis
 Appropriate supportive care
 To remove the source of sepsis

Two wide bore cannulas sited.

Foly's catheter.
Oxygenation with face mask is to be
given.
Mechanical ventilation may be needed in
severe cases.
 Antibiotics
 IV fluids and electroytes
 Correction of acidosis
 Maintenance of blood pressure
 Vasodilator therapy
 Diuretic therapy
 Corticosteroids
 Treatment of diffuse intravsacular
coagulopathy
 Treatment of myocarditis
 Elimination of source of infection
 Intensive insulin therapy