Obstetric shock.PDF
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About This Presentation
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 disparity is inadequate exchan...
Slide Content
Obstetric shock
Prepared by
DR.MONEERA ALFAIQ
Obstetric shock
Prepared by
DR.MONEERA ALFAIQ
DEFINITION: Shock is defined as a state of
circulatory inadequacy with poor tissue perfusion
resulting in generalized cellular
hypoxia.
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 disparity is inadequate
exchange of oxygen and carbon dioxide between
the intra and extravascular compartments.
Circulatory inadequacy is due to a disparity
between the circulating blood volume and the
capacity of the circulatory bed.
The net effect of this disparity is inadequate
exchange of oxygen and carbon dioxide between
the intra and extravascular compartments.
The stagnation of carbon dioxide and other
metabolites in the tissue leads to metabolic
acidosis and cellular death.
The stagnation of carbon dioxide and other
metabolites in the tissue leads to metabolic
acidosis and cellular death.
The series of changes observed in shock and their
clinical manifestations, are therefore, dependent on
two sets of changes :
(a) Circulatory inadequacy at the ‘filtration’ level
(microvascular compartment)
(b) Cellular damage and ultimately death.
The series of changes observed in shock and their
clinical manifestations, are therefore, dependent on
two sets of changes :
(a) Circulatory inadequacy at the ‘filtration’ level
(microvascular compartment)
(b) Cellular damage and ultimately death.
Pathophysiological changes in obstetric shock are
predominantly associated with
a) general changes due to hypovolemia
(b) specific changes due to liberation of endotoxin.
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.
PATHOPHYSIOLOGY
OF SHOCK
1) Hypotension stimulates release of
neuroendocrine mediators like
adrenocorticotrophic hormone (ACTH
growth hormone (GH)
, β endorphine,
cortisol and glucagon.
1) Hypotension stimulates release of
neuroendocrine mediators like
adrenocorticotrophic hormone (ACTH
growth hormone (GH)
, β endorphine,
cortisol and glucagon.
2 ) Stimulation of vasomotor center
Chemoreceptor
baroreceptor
2 ) Stimulation of vasomotor center
Chemoreceptor
baroreceptor
TEMPORARY COMPENSATORY MECHANISM
TEMPORARY COMPENSATORY MECHANISM
There are four phases of changes.
The first two phases are reversible;
the third one probably correctable
the fourth is irreversible:
General Changes in
Shock
There are four phases of changes.
The first two phases are reversible;
the third one probably correctable
the fourth is irreversible:
General Changes in
Shock
Sympathetic impulses and the level of circulating
catecholamines 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 center via the
ninth and tenth cranial nerves.
The vasomotor center responds by sending
efferent impulses through the sympathetic
nervous system.
First phase:
Sympathetic impulses and the level of circulating
catecholamines 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 center via the
ninth and tenth cranial nerves.
The vasomotor center responds by sending
efferent impulses through the sympathetic
nervous system.
First phase:
As a result of excessive sympathetic stimulus,
there is constriction of the pre- and postcapillary
sphincters,
resulting in
inadequate venous return leading to diminished
cardiac output, clinical manifestations of which
are hypotension and tachycardia.
Second phase
As a result of excessive sympathetic stimulus,
there is constriction of the pre- and postcapillary
sphincters,
resulting in
inadequate venous return leading to diminished
cardiac output, clinical manifestations of which
are hypotension and tachycardia.
Second phase
Compensatory mechanisms that operate at this
stage, to maintain the blood pressure has been
discussed in the scheme above
Compensatory mechanisms that operate at this
stage, to maintain the blood pressure has been
discussed in the scheme above
These mechanisms attempt to correct
hypovolemia, improve cardiac output and the
perfusion of vital organs.
At this stage, transfusion and control of
hemorrhage are usually effective in restoring the
normal circulatory balance and tissue perfusion.
These mechanisms attempt to correct
hypovolemia, improve cardiac output and the
perfusion of vital organs.
At this stage, transfusion and control of
hemorrhage are usually effective in restoring the
normal circulatory balance and tissue perfusion.
On the other hand, 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.
On the other hand, 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.
Prolonged anoxia of the tissues will lead to
excessive production of lactic acid (acidosis).
Lactic acid and anoxia cause relaxation of the
precapillary sphincters but not the postcapillary
sphincters.
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 but not the postcapillary
sphincters.
Third phase
In addition, thromboxane A2 and leukotrienes
(endogenous mediators) cause damage to the
endothelial cells of the capillaries of the
microcirculatory bed.
These lead to formation of thrombus within the
capillaries (diffuse intravascular coagulation)
and increased capillary permeability.
In addition, thromboxane A2 and leukotrienes
(endogenous mediators) cause damage to the
endothelial cells of the capillaries of the
microcirculatory bed.
These lead to formation of thrombus within the
capillaries (diffuse intravascular coagulation)
and increased capillary permeability.
Consequent to persistent constriction of the
postcapillary sphincter, blood remains stagnant
within the capillary bed.
from the capillaries leaks into the tissue spaces
due to increased permeability.
All fluids administered intravenously will go
into the tissue spaces and circulatory blood
volume cannot be restored.
Fourth phase
Consequent to persistent constriction of the
postcapillary sphincter, blood remains stagnant
within the capillary bed.
from the capillaries leaks into the tissue spaces
due to increased permeability.
All fluids administered intravenously will go
into the tissue spaces and circulatory blood
volume cannot be restored.
Fourth phase
this is the stage of
irreversible shock.
this is the stage of
irreversible shock.
There is severe loss of systemic vascular
resistance
, severe myocardial depression (↓ cardiac
output),
unresponsive hypotension
and ultimately multiple organ system failure.
There is severe loss of systemic vascular
resistance
, severe myocardial depression (↓ cardiac
output),
unresponsive hypotension
and ultimately multiple organ system failure.
Presence of endotoxin (lipopolysaccharide), in
septic shock activate the leukocytes through
complement system.
There is release of inflammatory mediators such
as proteases, superoxide (O2–), hydroxyl (OH–)
radicals, cytokines, prostaglandins and many
cytotoxic enzymes.
PATHOPHYSIOLOGY
OF SEPTIC SHOCK
Presence of endotoxin (lipopolysaccharide), in
septic shock activate the leukocytes through
complement system.
There is release of inflammatory mediators such
as proteases, superoxide (O2–), hydroxyl (OH–)
radicals, cytokines, prostaglandins and many
cytotoxic enzymes.
PATHOPHYSIOLOGY
OF SEPTIC SHOCK
These interfere with the function of a number of
enzyme systems and increase capillary
permeability.
Cytokines such as interleukines (ILS) and tumor
necrosis factor (TNF) interact by autocrine and
paracrine mechanism to cause cellular or organ
dysfunction.
These interfere with the function of a number of
enzyme systems and increase capillary
permeability.
Cytokines such as interleukines (ILS) and tumor
necrosis factor (TNF) interact by autocrine and
paracrine mechanism to cause cellular or organ
dysfunction.
In presence of hypoxia, sepsis and acidosis,
lysosomal enzymes which are cytotoxic, are
released.
Bacterial endotoxin causes selective vasospasm
at the post capillary, end. Blood is pooled in the
capillary bed.
They can cause myocardial depression and
coronary vasoconstriction.
In presence of hypoxia, sepsis and acidosis,
lysosomal enzymes which are cytotoxic, are
released.
Bacterial endotoxin causes selective vasospasm
at the post capillary, end. Blood is pooled in the
capillary bed.
They can cause myocardial depression and
coronary vasoconstriction.
Prostacyclin is a vasodilator and inhibits platelet
aggregation.
Thromboxane A2 causes pulmonary
vasoconstriction and platelet aggregation.
Leukotrienes cause vasoconstriction, platelet
activation and increased vascular permeability.
Thrombosis is increased due to inhibition of
antithrombin III. Thrombocytopenia is common.
Prostacyclin is a vasodilator and inhibits platelet
aggregation.
Thromboxane A2 causes pulmonary
vasoconstriction and platelet aggregation.
Leukotrienes cause vasoconstriction, platelet
activation and increased vascular permeability.
Thrombosis is increased due to inhibition of
antithrombin III. Thrombocytopenia is common.
The patient in early septic shock, feels warm due
to vasodilatation.
This is called warm shock.
In the late phase, the patient feels cold due to
vasoconstriction (sympathetic squeeze).
This is called cold shock or late shock
The patient in early septic shock, feels warm due
to vasodilatation.
This is called warm shock.
In the late phase, the patient feels cold due to
vasoconstriction (sympathetic squeeze).
This is called cold shock or late shock
Metabolic changes:
Hepatic glycogenolysis due to increased level of
glucagon, catecholamine and cortisol leads to
hyperglycemia
Metabolic changes:
Hepatic glycogenolysis due to increased level of
glucagon, catecholamine and cortisol leads to
hyperglycemia
is manifested by two or more of the following
conditions:
(i) Temperature > 38°C or < 36°C
(ii) HR > 90 bpm
(iii) Respiratory rate > 20/min or
(iv) PaCO2 < 32 mm Hg or
(v) WBC > 12000/µl or < 4000/µl or more than
10% immature forms
Systemic inflammatory
response syndrome (SIRS)
is manifested by two or more of the following
conditions:
(i) Temperature > 38°C or < 36°C
(ii) HR > 90 bpm
(iii) Respiratory rate > 20/min or
(iv) PaCO2 < 32 mm Hg or
(v) WBC > 12000/µl or < 4000/µl or more than
10% immature forms
Systemic inflammatory
response syndrome (SIRS)
Clinical features of shock depend on the basic
etiological factors and consequently the sequence
of pathological changes occurring within the
microvascular unit.
In early stages, the features of hypovolemic and
septic shock are different. In the irreversible
(late) phase, the clinical features are the same as
the final pathology is multiple organ failure. It
carries mortality of 30%–100%.
CLINICAL FEATURES OF
SHOCK
Clinical features of shock depend on the basic
etiological factors and consequently the sequence
of pathological changes occurring within the
microvascular unit.
In early stages, the features of hypovolemic and
septic shock are different. In the irreversible
(late) phase, the clinical features are the same as
the final pathology is multiple organ failure. It
carries mortality of 30%–100%.
CLINICAL FEATURES OF
SHOCK
If the shock condition dose not improve, the
patient passes clinically to the stage of
‘irreversible shock’. She remains cold and
clammy with ashen gray cyanotic appearance.
If the shock condition dose not improve, the
patient passes clinically to the stage of
‘irreversible shock’. She remains cold and
clammy with ashen gray cyanotic appearance.
Severe sepsis is associated with hypotension (< 90
mm Hg systolic) → organ hypo perfusion and
dysfunction → lactic acidosis → oliguria, renal
failure, ARDS, cardiac failure → multiple organ
dysfunction syndrome.
Severe sepsis is associated with hypotension (< 90
mm Hg systolic) → organ hypo perfusion and
dysfunction → lactic acidosis → oliguria, renal
failure, ARDS, cardiac failure → multiple organ
dysfunction syndrome.
HEMORRHAGIC SHOCK:
ABC
Airway
Breathing
Circulation
One or two large bore (14 or 16 gauge) cannula are
inserted for volume replacement.
MANAGEMENT OF SHOCK
HEMORRHAGIC SHOCK:
ABC
Airway
Breathing
Circulation
One or two large bore (14 or 16 gauge) cannula are
inserted for volume replacement.
MANAGEMENT OF SHOCK
Administration of oxygen to avoid metabolic
acidosis
: In the initial phase, administration of oxygen by
nasal cannula at a rate of 6-8 liters per minute is
enough
but in the later phases, ventilation by
endotracheal intubation may be necessary.
Administration of oxygen to avoid metabolic
acidosis
: In the initial phase, administration of oxygen by
nasal cannula at a rate of 6-8 liters per minute is
enough
but in the later phases, ventilation by
endotracheal intubation may be necessary.
Oxygen delivery should be continued to maintain
O2 saturation > 92%,
PaO2 80-100 mm Hg,
PaCO2 30-35 mm Hg
and pH > 7.35.
Oxygen delivery should be continued to maintain
O2 saturation > 92%,
PaO2 80-100 mm Hg,
PaCO2 30-35 mm Hg
and pH > 7.35.
Endotracheal intubation and mechanical
ventilation may be needed for patients with
septic shock.
Indications of mechanical ventilation are :
severe tachypnea (RR > 40/min),
altered mental status,
severe hypoxemia, despite O2 supplementation.
Endotracheal intubation and mechanical
ventilation may be needed for patients with
septic shock.
Indications of mechanical ventilation are :
severe tachypnea (RR > 40/min),
altered mental status,
severe hypoxemia, despite O2 supplementation.
Basic management of hemorrhagic shock is to
stop the bleeding and replace the volume which
has been lost
Packed red blood cells (specific blood
component), combined with normal saline, are
used for hemorrhagic shock.
Basic management of hemorrhagic shock is to
stop the bleeding and replace the volume which
has been lost
Packed red blood cells (specific blood
component), combined with normal saline, are
used for hemorrhagic shock.
. Crystalloids :
Normal saline has to be infused initially for
immediate volume replacement.
But
they are rapidly lost from circulation.
. Crystalloids :
Normal saline has to be infused initially for
immediate volume replacement.
But
they are rapidly lost from circulation.
Colloids:
Polygelatin solutions (Hemaccel, Gelofusion) are
iso-osmotic with plasma.
They do not interfere with the coagulation
system. Large volumes can be administered.
They promote osmotic diuresis
Colloids:
Polygelatin solutions (Hemaccel, Gelofusion) are
iso-osmotic with plasma.
They do not interfere with the coagulation
system. Large volumes can be administered.
They promote osmotic diuresis
. Dextrans:
are polymolecular polysaccharides.
They interfere with cross matching and they are
avoided.
. Dextrans:
are polymolecular polysaccharides.
They interfere with cross matching and they are
avoided.
. Hemodynamic monitoring is aimed to
maintain systolic BP > 90 and MAP > 60 mm Hg,
CVP 12-15 cm H2O
and pulmonary capillary wedge pressure 14-18
mm Hg.
. Hemodynamic monitoring is aimed to
maintain systolic BP > 90 and MAP > 60 mm Hg,
CVP 12-15 cm H2O
and pulmonary capillary wedge pressure 14-18
mm Hg.
Pharmacological agents:
Use of vasopressor drugs should be kept to a
minimum,
Pharmacological agents:
Use of vasopressor drugs should be kept to a
minimum,
Monitoring:
Clinical parameters like skin temperature, visible
peripheral veins can be helpful to assess the degree
of tissue perfusion.
Urine output (> 30 mL/hr) is a useful guide.
Monitoring:
Clinical parameters like skin temperature, visible
peripheral veins can be helpful to assess the degree
of tissue perfusion.
Urine output (> 30 mL/hr) is a useful guide.
This includes administration of antibiotics,
intravenous fluids, adjustment of acid base
balance, steroids, inotropes, prevention and
treatment of intravascular coagulation and toxic
myocarditis, administration of oxygen and
elimination of the source of infection.
ENDOTOXIC SHOCK
This includes administration of antibiotics,
intravenous fluids, adjustment of acid base
balance, steroids, inotropes, prevention and
treatment of intravascular coagulation and toxic
myocarditis, administration of oxygen and
elimination of the source of infection.
ENDOTOXIC SHOCK
Endotoxic shock is most commonly due to Gram-
negative organisms, so proper antibiotics should
be administered in adequate doses
broad spectrum antibiotics covering Gram-
positive, Gram-negative and anaerobic
organisms should be started
Antibiotics:
Endotoxic shock is most commonly due to Gram-
negative organisms, so proper antibiotics should
be administered in adequate doses
broad spectrum antibiotics covering Gram-
positive, Gram-negative and anaerobic
organisms should be started
Antibiotics:
Ampicillin (IG IV every 6 hours),
gentamicin (2 mg/kg IV loading dose followed by
1.5 mg/kg IV every 8 hours)
and metronidazole (400 mg IV every 8 hours) is a
good combination to start with
Ampicillin (IG IV every 6 hours),
gentamicin (2 mg/kg IV loading dose followed by
1.5 mg/kg IV every 8 hours)
and metronidazole (400 mg IV every 8 hours) is a
good combination to start with
Septic shock associated with hemorrhagic
hypotension should be treated by liberal infusion
and blood transfusion.
The amount of fluid to be administered can be
precisely assessed by recording the central
venous pressure.
Intravenous fluids and
electrolytes
Septic shock associated with hemorrhagic
hypotension should be treated by liberal infusion
and blood transfusion.
The amount of fluid to be administered can be
precisely assessed by recording the central
venous pressure.
Intravenous fluids and
electrolytes
Acidosis and hypoxemia depress myocardial
contractility.
Bicarbonate should be administered to correct
persistent metabolic acidosis (pH < 7.2) only.
A reasonable first dose would be 50-100 mEq
(60–110 mL of 7.5%) of sodium bicarbonate
solution.
Correction of acidosis
Acidosis and hypoxemia depress myocardial
contractility.
Bicarbonate should be administered to correct
persistent metabolic acidosis (pH < 7.2) only.
A reasonable first dose would be 50-100 mEq
(60–110 mL of 7.5%) of sodium bicarbonate
solution.
Correction of acidosis
Inotropic agents—in a critically ill patient when
there is hypotension (MAP < 60 mm Hg) and
impaired perfusion of vital organs despite
adequate volume replacement, inotropes should
be used.
Adrenaline, noradrenaline, dopamine and
dobutamine
Maintenance of blood
pressure
Inotropic agents—in a critically ill patient when
there is hypotension (MAP < 60 mm Hg) and
impaired perfusion of vital organs despite
adequate volume replacement, inotropes should
be used.
Adrenaline, noradrenaline, dopamine and
dobutamine
Maintenance of blood
pressure
Diuretic therapy:
To reduce fluid over load (pre load) and
pulmonary edema, diuretics should be used.
Frusemide is the drug of choice.
Diuretic therapy:
To reduce fluid over load (pre load) and
pulmonary edema, diuretics should be used.
Frusemide is the drug of choice.
Patients with severe sepsis develop systemic
inflammatory response syndrome or relative
adrenal insufficiency. Corticosteroids could be
used as anti-inflammatory agents to improve
mortality.
The dose recommended in septic shock is 50 mg
of hydrocortisone per kg body weight.
Corticosteroids
Patients with severe sepsis develop systemic
inflammatory response syndrome or relative
adrenal insufficiency. Corticosteroids could be
used as anti-inflammatory agents to improve
mortality.
The dose recommended in septic shock is 50 mg
of hydrocortisone per kg body weight.
Corticosteroids
When there is low fibrinogen level, reduced
platelet count and increased fibrin degradation
products, heparin therapy should be considered.
As a prophylactic measure, heparin 5000 IU
subcutaneous or intravenous route at 8 hourly
interval can be given safely.
Alternatively fresh frozen plasma or whole blood
transfusion could be done.
Treatment of diffuse
intravascular coagulation
When there is low fibrinogen level, reduced
platelet count and increased fibrin degradation
products, heparin therapy should be considered.
As a prophylactic measure, heparin 5000 IU
subcutaneous or intravenous route at 8 hourly
interval can be given safely.
Alternatively fresh frozen plasma or whole blood
transfusion could be done.
Treatment of diffuse
intravascular coagulation
Though controversial, but in intractable cases
where simple conservative measures fail to
improve the shock, active treatment in selected
case is sometimes rewarding.
Hysterectomy has been advocated in
unresponsive endotoxic shock following septic
abortion or puerperal sepsis.
Elimination of source of
infection:
Though controversial, but in intractable cases
where simple conservative measures fail to
improve the shock, active treatment in selected
case is sometimes rewarding.
Hysterectomy has been advocated in
unresponsive endotoxic shock following septic
abortion or puerperal sepsis.
Elimination of source of
infection:
is done in patients with severe sepsis and septic
shock to maintain normal blood glucose level.
These patients often develop hyperglycemia
which further increases the risk of septicemia
and death.
Intensive insulin therapy
is done in patients with severe sepsis and septic
shock to maintain normal blood glucose level.
These patients often develop hyperglycemia
which further increases the risk of septicemia
and death.
Intensive insulin therapy
H2–blockers: Antacids to reduce the stress ulcer
of gastric mucosa either by oral or H2-blocking
agents (IV) are used.
Nutritional support is maintained as total
parenteral nutrition (TPN). Usually 20-30
Kcal/kg/day is equally distributed between fat
and carbohydrate. Serum electrolytes, BUN,
glucose, creatinine should be monitored on a
regular basis.
H2–blockers: Antacids to reduce the stress ulcer
of gastric mucosa either by oral or H2-blocking
agents (IV) are used.
Nutritional support is maintained as total
parenteral nutrition (TPN). Usually 20-30
Kcal/kg/day is equally distributed between fat
and carbohydrate. Serum electrolytes, BUN,
glucose, creatinine should be monitored on a
regular basis.
THANKS
THANKS
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