Download - Fluid Management and Obstetric Shock
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Dr Surya Pd Rimal, JR 2013
Moderator: Dr Tarun Pradhan, MD
FLUID MANAGEMENT AND
OBSTETRIC SHOCK
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Body Fluid Compartments
2/3 (65%) of TBW is intracellular (ICF)
1/3 extracellular water 25 % interstitial fluid (ISF)
5- 8 % in plasma (IVF intravascular fluid)
1- 2 % in transcellular fluidsCSF,
intraocular fluids, serous membranes, and i
GI, respiratory and urinary tracts
(third space)3
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Fluid compartments are separated by membranes
that are freely permeable to water.
Movement of fluids due to:
hydrostatic pressure
osmotic pressure\ Capillary filtration (hydrostatic) pressure
Capillary colloid osmotic pressure
Interstitial hydrostatic pressure
Tissue colloid osmotic pressure
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Balance
Fluid and electrolyte homeostasis is maintained
in the body Neutral balance: input = output
Positive balance: input > output
Negative balance: input < output
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It is the excretion of water that is tightly regulated
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Solutes dissolved particles
Electrolytescharged particles
Cationspositively charged ionsNa+, K+, Ca++, H+
Anionsnegatively charged ions
Cl-, HCO3-, PO43-
Non-electrolytes - Uncharged
Proteins, urea, glucose, O2, CO
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Body fluids are:
Electrically neutral
Osmoticallymaintained 275 to 290
Specific number of particles pervolume of fluid
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Homeostasis maintained by:
Ion transport
Water movement Kidney function( Filtration, reabsorption
mainly from TALH, AVP mediated water
pores)
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MW (Molecular Weight) = sum of the weights of
atoms in a moleculemEq (milliequivalents) = MW (in mg)/ valence
mOsm (milliosmoles) = number of particles in a
solution
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TonicityIsotonic
Hypertonic
Hypotonic
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Cell in a
hypertonic
solution
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Cell in a
hypotonic
solution
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Movement of body fluids
Where sodium goes, water follows.
Diffusionmovement of particles down a
concentration gradient.
Osmosisdiffusion of water across a
selectively permeable membrane
Active transportmovement of particles up
a concentration gradient; requires energy
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ICF to ECFosmolality changes in ICF not
rapid
IVF ISF IVF happens constantly due
to changes in fluid pressures and osmoticforces at the arterial and venous ends of
capillaries
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Maintenance requirements
Daily maintenance fluid requirements vary
between individuals.4/2/1..100/50/20 rule
40 Kg woman = 2.0L water,
7090 mmol sodiumand 40 mmol potassium
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Hypovolemia
1. Renal
2.
Extra renal1. GI
2. Skin/ respiratory tract(sweating/ Burns)
3. Hemorrhage
All are NOT the cause of obstetrics shock but may
precipitate or accentuate the gravity of the
problem in a woman with shock23
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Features of volume deficit
1. Weight loss
2. Decreased skin turgor3. Tachycardia
4. Hypotension
5.
Collapsed vein6. Oliguria
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Regulation of body water
ADHantidiuretic hormone + thirst
Decreased amount of water in body Increased amount of Na+ in the body
Increased blood osmolality
Decreased circulating blood volume
Stimulate osmoreceptors in hypothalamus ADH
released from posterior pituitary(synthesized at
supraoptic nucleus)
Increased thirst25
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Result:
increased water consumption
increased water conservation
Increased water in body,
increased volume and
decreased Na+ concentration
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Volume excess
1. Iatrogenic
2. Renal dysfunction3. Congestive heart failure
4. Cirrhosis
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Features of volume excess
1. Weight gain
2. Peripheral edema3. Increased central venous pressure
4. Distended neck veins
5.
Murmur6. Pulmonary edema
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Dysfunction or trauma can cause:
Decreased amount of water in bodyIncreased amount of Na+in the body
Increased blood osmolality
Decreased circulating blood volume
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Hydrostatic pressure
increases due to
Venous obstruction:
thrombophlebitis (inflammation of veins) hepatic obstruction
tight clothing on extremities
prolonged standing Salt or water retention
congestive heart failure
renal failure
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Decreased plasma osmotic pressure:
plasma albumin (liver disease orprotein malnutrition)
Plasma proteins lost in :
glomerular diseases of kidney
hemorrhage, burns, open wounds and
cirrhosis of liver
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Increased capillary permeability:
Inflammation
immune responses
Lymphatic channels blocked:
surgical removal
infection involving lymphatics lymphedema
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Fluid accumulation:
increases distance for diffusion
may impair blood flow = slower healing
increased risk of infection
pressure sores over bony
prominences
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Isotonic fluid excess
Excess IV fluids
Hypersecretion of aldosterone
Effect of drugscortisone
Get hypervolemiaweight gain, decreased hematocrit,diluted plasma proteins, distended neck veins, B.P.
Can lead to edema ( capillary hydrostatic pressure)
pulmonary edema and heart failure
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TYPES OF I.V. FLUIDS
1. Crystalloids vs. Colloids
CRYSTALLOIDS COLLOIDS
Normal (0.9%) saline Human Albumin
Ringer's lactate solution
(Hartmann's' solution)
Gelatin solutions
(Haemaccel,Gelafundin )
5% Dextrose Dextran
Hydroxyethyl starches
(Hetastarch
)
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TYPES OF I.V. FLUIDS
2. Hypotonic, Isotonic and Hypertonic
solutions
HYPOTONIC
SOLUTIONS
ISOTONIC
SOLUTIONS
HYPERTONIC
SOLUTIONS
0.45% (N/2) Saline Normal (0.9%) saline 3% Saline
0.18% (N/5) Saline Hartmann's' solution Mannitol
5% Albumin 20% Albumin
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TYPES OF I.V. FLUIDS
3. Balanced vs. unbalanced intravenous fluids
UNBALANCED SOLUTIONS BALANCED SOLUTIONS
0.9% Saline Hartmann's' solution
Dextrans
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TYPES OF I.V. FLUIDS
4. Natural vs. Synthetic
NATURAL SOLUTIONS SYNTHETIC SOLUTIONS
Human Albumin Gelatin solutions
(Haemaccel,Gelafundin )
Fresh Frozen Plasma Hartmanns solution
Dextran
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CRYSTALLOIDS
saline/sugar based
Consist of inorganic ions and small organic molecules
dissolved in water Either glucose or sodium chloride (saline) based.
May be isotonic, hypotonic or hypertonic
Both water and the electrolytes in the crystalloid solution
can freely cross the semi permeable membranes of the
vessel walls into the interstitial space
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Normal Saline (0.9 NaCl)
Contains sodium and chloride ions in water and it is
isotonic with extracellular fluid
Cell membrane is impermeable to Na+ and Cl-ions
owing to the presence of the energy dependant
Na+/K+- ATPase
Intravenous infusion of an isotonic solution of sodium
chloride will expand only the extracellular compartment
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Normal Saline (0.9 NaCl)
Na+is the main solute in ECF saline is well suited to
replace ECF fluid losses
e.g. dehydration due to nausea/vomiting
Na+ andCl-freely moves across vascular membrane
into the interstitium.
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Normal Saline (0.9 NaCl)
Remain in the intravascular space for only a short
period before diffusing across the capillary wall into the
interstitial space.
1 liter infusion of normal (0.9%) saline will result in
~ 250 ml expansion of the circulating volume.
Achieve equilibrium in 2-3 hours.
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Normal Saline (0.9 NaCl)
Indications:
1. Replacement of fluids in hypovolaemic ordehydrated patients ( Needs 3 blood loss)
2. A small amount of saline as a special adjunct can
be used to keep the veins open for medication
administration3. As the initial plasma expander in blood loss while
blood is typed and matched
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Normal Saline (0.9 NaCl)
Adverse Effects
1. Fluid overload (peripheral and pulmonaryoedema)
2. With high volume administration,
Dilutional reduction of normal plasma components such
as calcium and potassium
Dilutional coagulopathy
Hyperchloraemic acidosis
3. Diuresis.
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5 Dextrose
Initially behave as an isotonic solution.
Glucose is soon metabolized, leaving behind
water making the solution hypotonic.
Water freely moves between intravascular,
interstitial and intracellular fluid compartments till
the osmolalities become the same.
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5 Dextrose
Indications:
1. To maintain water balance ( In pure water deficit andfor patients on sodium restriction)
2. To supply calories ( ~ 200kcal/l)
An adult require ~2500 kcal/day
Hence, glucose alone cant meet the need.
Would need >10 liters of 5% glucose to supply
all calories !!
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5 Dextrose
Adverse effects:
1.
Causes red cell clumping (cannot be given withblood).
2. May cause water intoxication
3. Can cause hyponatraemia
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Ringers Lactate
A balanced isotonic electrolyte solution.
Similar to 0.9% saline in all aspects except,
Contains sodium, chloride, potassium, calcium and
lactate in water. ( physiological)
Prevents dilutional reduction of normal plasmacomponents such as calcium and potassium
Avoids hyperchloraemic acidosis ( Lactate
converted to bicarbonate in liver.)
Preferred to normal saline when large quantities of
volume infused rapidly
Disadvantage D isomer shows inflammatory
response
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COLLOIDS
Colloids contain large molecules such as proteins that do not readily
pass through the capillary membrane
Remain in the intravascular space for extended periods These large molecules also increase the osmotic pressure in the
intravascular space
Cause fluid to move from the interstitial and intracellular space to the
intravascular space
Often referred to as volume expanders
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Colloids
Disadvantages
Detrimental in severe hemorrhagic shockwhen capillary permeability is high it may
worsen edema
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Composition of colloids
Volume effect (%) Average MW (kDa) Circulatory half life
Gelatins (Haemaccel) 80 35 2-3 hours
4% Albumin 100 69 15 days
Dextran 70 120 41 2-12 hours
6% Hydroxyethyl
Starch100 70 17 days
Monodispersed = All molecules of similar molecular weight
Polydispersed = Molecules have spread of molecular weights
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INDICATIONS
1. When rapid expansion of plasma volume is
desirablee.g. in haemorrhage prior to blood
transfusion
2. For fluid resuscitation in the presence ofhypoalbuminaemia
3. In large protein losses e.g. in burns
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Gelatins
Prepared by hydrolysis of bovine collagen.
a). Gelafusine
- succinylated gelatin in isotonicsaline
b). Haemaccel- urea-linked gelatin and polygeline
in an isotonic solution of sodium chloride with
potassium and calcium.
Theoretical risk of transmitting bovine spongiformencephalopathy. (new-variant Creutzfeldt-Jakobdisease)
Volume expanding effect lasts 2-3 hrs.
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Dextrans
High molecular weight D-glucose polymers prepared
from the juice of sugar beets.
Preparations of different molecular weights
e.g. Dextran 40 (MW 40,000)
Dextran 70 (MW 70,000)
Volume expanding effect lasts 5-6 hrs.
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Dextrans
Causes haemostatic derangements
Factor VIII activity is reduced
plasminogen activation and fibrinolysis is increased
platelet function impaired
Interfere with blood cross matching Alter laboratory tests
e.g. Plasma glucose, plasma proteins
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Human Albumin
Two preparations 5% albumin (isotonic) and 25%
albumin (Hypertonic)
20% albumin expands the plasma volume up to five
times the volume infused.
Heat treated - no risk of transmitting viral infections.
Reduce ionized calcium level.
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Inadequate perfusion (blood flow)
leading to inadequate oxygen delivery to
tissues
OBSTETRIC SHOCK
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critical condition and a life threatening
medical emergency.
Prompt recognition and management can
improve maternal and fetal outcome in
obstetrical shock.
Shock can occur with a normal bloodpressure and hypotension can occur
without shock
OBSTETRIC SHOCK
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Maintaining perfusion
requires:
Volume = blood
Pump = heart Container = Vessels
Failure of one or more of these causes
shock
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Major causes of shock include
1. Hypovoluemic Hemorrhage(occult /overt) , hyperemesis,
diarrhoea, diabetic acidosis, peritonitis, burns.
2. Septicsepsis, endotoxaemia.
3.Cardiogeniccardiomyopathies , obstructive structural ,
obstructive non structural , dysrrhythmias, regurgitant lesions.
4.DistributiveNeurogenic- spinal injury, regional anesthesia,
5.Anaphylaxis.
AETIOLOGY OF SHOCK
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In Obstetric cases shock is most
commonly due to either hemorrhageor sepsis
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.Stage1 Compensated--compensated by adjustment of
homeostatic mechanismit is reversible.
Stage2 Decompensated--Maximal compensatorymechanism are acting but tissue perfusion is reduced. Vital organ(cerebral , renal, myocardial)
function reduced.
Stage3 Irreversible--Vital organ perfusion badly impaired.
Acute tubular necrosis , severe acidosis, decreased
myocardial perfusion and contractility the profound
decrease in perfusion leads to cellular death & Organ failure.
PATHOPHYSIOLOGY
Untreated shock progresses through three stages
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A high index of suspicion and physical signsof
inadequate perfusion and oxygenation are the
basis of initiating prompt treatment. Initial management does not rely on knowledge of
the underlying cause.
There are no laboratory tests for shock. Basic investigations should be sent
e.g.Hb,BT,CT,PCV. Blood for grouping and cross
matching , FB Sugar , routine urine analysis.
DIAGNOSIS
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INITIAL MANAGEMENT
Shocked pt requires teamwork--Senior anaesthetist, obstetrician , physician
Obstetrical units should have established protocols
for dealing with shock. Practice FIRE DRILL.
MOET,ALSO, PROMPT trainingcourses for
individuals and team. Active management of shock should start as soon
as it is suspected or expected aiming for promptrestoration of tissue perfusion and oxygenation.
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Resuscitation follows---ABC
A Airway--Patent airway is assured and highpressure oxygen (15 l/min)using mask/intra tracheal
intubation and anaesthesia machine. B Breathing--Ventilation checked and supported if
needed .
C Circulation-- 1 Insert two wide bore cannulas
2 Restore blood volume and
reverse hypotension with
crystalloids/colloids.
3 Initial request for4-6 units of blood
should be sent. O Rh negative
blood may be transfused
INITIAL RX
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Optimizing Circulation
Isotonic crystalloids
Titrated to: CVP 8-12 mm Hg
Urine output 0.5 ml/kg/hr (30 ml/hr)
Improving heart rate
MAP 65 to 90 mmHg
May require 4-6 L of fluids
No outcome benefit from colloids
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Monitor the response to therapy
Pulse , BP , SPO2 /pulse oxymetry, urine output & itspH .
Position of patient - Head down and left lateral tiltto avoid aortocaval compression which mayfurther worsen the hypotension.
Vasoactive drugs (inotropes and vasopressors)are considered if the cause of shock is thought tobe due to myocardial depression or profoundvasodilatation.
These drugs have no part in hypovolemic shock.
RX - CIRCULATION
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Persistent Hypotension
Inadequate volume resuscitation
Hidden bleeding Adrenal insufficiency, CIRCI
Pneumothorax
Cardiac tamponade Medication allergy
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Hypovolemic Shock
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HYPOVOLEMIA
1. Haemorrage
2. Renal3. Extra renal
1. GI
2. Skin/ respiratory tract(sweating/ Burns)
4. Other medical/ surgical causes: RTA, BURN
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AntenatalRuptured ectopic pregnancy,
Incomplete abortion, MTP, Uterine perforation
during evacuation , APH, Uterine rupture,
Abdominal wall hematoma, Non obstetrical intra
abdominal bleeding.
Intra nataluterine rupture. Post natalPPH(primary, secondary) Atonic ,
Traumatic, Retained tissue , Thrombosis, Acute
uterine inversion .
CAUSES OF HEMORRHAGIC SHOCK
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Clinical classification of maternal
hemorrhage
Class Blood loss
(mL)
Volume deficit
(%)
Signs and symptoms
I 1000 15 Orthostatic tachycardia ( 20 bpm)
II 10011500 1525 HR 100 120 bpm
Orthostatic changes ( 15 mmHg)
Cap refi ll > 2 secMental changes
III 15012500 2540 HR (120 160 bpm)
Supine BP
RR (30 50 rpm)Oliguria
IV > 2500 > 40 Obtundation
Oliguria - anuria
CV collapse
PATHOPHYSIOLOGY
OF LOW BP
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Shock
how to estimate quickly
blood pressure by pulse?
60
80
70
90
If you palpate a pulse,
you know SBP is at
least this number
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Oxygenation
Inadequate oxygenation or perfusion causes: Inadequate cellular oxygenation
Shift from aerobic to anaerobic metabolism
Thus, increasing the partial pressure of oxygen acrossthe pulmonary capillary membrane by giving 810 L of
oxygen per minute by tight - fitting mask is a logical first
priority.
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AEROBIC METABOLISM
6 O2
GLUCOSE
METABOLISM
6 CO2
6 H2O
36 ATP
HEAT (417 kcal)
Glycolysis: Inefficient source of energy production; 2 ATP for
every glucose; produces pyruvic acid
Oxidative phosphorylation: Each pyruvic acid is converted
into 34 ATP
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ANAEROBIC METABOLISM
GLUCOSE METABOLISM
2 LACTIC ACID
2 ATP
HEAT (32 kcal)
Glycolysis: Inefficient source of energy production; 2 ATP for
every glucose; produces pyruvic acid
b b l
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Anaerobic Metabolism
Occurs without oxygen
oxydative phosphorylation cant occur without
oxygen
glycolysis can occur without oxygen
cellular death leads to tissue and organ death
can occur even after return of perfusion
organ or organism death
l l
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Volume replacement
Protracted shock appears to cause secondarychanges in the microcirculation; and these
changes affect circulating blood volume.
In early shock, there is a tendency to drawfluid from the interstitial space into the
capillary bed
As the shock state progresses, damage to thecapillary endothelium occurs and is
manifested by an increase in capillary
permeability
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This deficit is reflected clinically by thedisproportionately large volume of fluidnecessary to resuscitate patients in severeshock.
Sometimes, the amount of fluid required forresuscitation is twice the amount indicated bycalculation of blood loss volume.
Prolonged hemorrhagic shock also altersactive transport of ions at the cellular level,and intracellular water decreases.
M t i t f h l i h k i
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Most instances of hypovolemic shock in
obstetrics are hemorrhagic and immediate.
The two most common crystalloid fluids usedfor resuscitation are 0.9% sodium chloride and
lactated Ringer s solution.
Both have equal plasma volume - expandingeffects
I f i R
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Infusion Rates
Access Gravity Pressure
18 g peripheral IV 50 mL/min 150 mL/min
16 g peripheral IV 100 mL/min 225 mL/min
14 g peripheral IV 150 mL/min 275 mL/min8.5 Fr CV cordis 200 mL/min 450 mL/min
Th l l f i d ll id
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The large volumes of required crystalloids can
markedly diminish the colloid osmotic pressure
(COP). Fluid resuscitation in young, previously healthy
patients can be accomplished safely with modest
volumes of crystalloid fluid and with little risk ofpulmonary edema.
The enormous volumes of crystalloids necessary
to adequately resuscitate profound hypovolemic
shock, however, will reduce the gradient between
the COP and PCWP and may contribute to the
pathogenesis of pulmonary edema
Unfortunately only 20% of infused crystalloid
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Unfortunately, only 20% of infused crystalloid
solution remains intravascular after 1 hour in
the critically ill patient. Their use should be limited to immediate
resuscitation and till arrival of blood products.
The most effective replacement therapy for lost
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The most effective replacement therapy for lost
blood volume is its replacement with whole
blood.
Red blood cells are administered to improve
oxygen delivery in patients with decreased redcell mass resulting from hemorrhage
Massive blood replacement is defi ned astransfusion of one total blood volume within
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transfusion of one total blood volume within
24 hours.
Pathologic hemorrhage in the patientreceiving a massive transfusion is caused
more frequently by thrombocytopenia than
by depletion of coagulation factors.
Thus, during massive blood replacement,
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, g p ,correction of specific coagulation defects (fibrinogen levels < 150 mg/ dL) and
thrombocytopenia (platelet count < 30000/mL) will minimize further transfusionrequirements.
With massive obstetric hemorrhage (the usualreason for hypovolemic shock) coagulationfactors as well as red blood cells are lost.
Specific replacement with PRBC s andcrystalloid solution may lead to dilutionalcoagulopathy and subsequently more bloodloss.
In acute hemorrhagic shock central venous
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In acute hemorrhagic shock, central venous
pressure (CVP) or pulmonary capillary wedge
pressure (PCWP) reflect intravascular volumestatus and may be useful in guiding fluid
therapy.
In the critically ill patient, however, CVP maybe a less reliable indicator of volume status
due to compliance changes in the vein walls
Ph l i t
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Pharmacologic a gents
During the antepartum and intrapartumperiods, only correction of maternal
hypovolemia will maintain placental perfusion
and prevent fetal compromise. Although vasopressors may temporarily
correct hypotension, they do so at the
expense of uteroplacental perfusion. Thus, vasopressors are not used in the
treatment of obstetric hemorrhagic shock.
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E l ti f H l i Sh k
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Evaluation of Hypovolemic Shock
CBC
ABG/lactate
Electrolytes BUN, Creatinine
Coagulation studies
Type and cross-match
As indicated
CXR
Pelvic x-ray
Abd/pelvis CT
Chest CT
GI endoscopy
Bronchoscopy Vascular radiology
Serial evaluation of vital signs urine output
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Serial evaluation of vital signs, urine output,
acidbase status, blood chemistry, and
coagulation status aid in this assessment. In select cases, placement of a pulmonary
artery catheter should be considered to assist
in the assessment of cardiac function andoxygen transport variables.
In general, however, central hemodynamic
monitoring is not necessary in simplehypovolemic shock
Evaluation of the fetal cardiotocograph may
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g p y
indicate fetal distress during an acute
hemorrhagic episode. As a rule, maternal
health trumps fetal health.
This means that delivery, under these
circumstances, should not be considered until
maternal condition has been stabilized.
Once stabilized and the fetus continues to
demonstrate persistent signs of fetal distress,
then consider delivery
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It is important to realize that as the maternalhypoxia, acidosis, and underperfusion of the
uteroplacental unit are being corrected, the
fetus may recover. Serial evaluation of the fetal status and in
utero resuscitation are preferable to
emergency delivery of a depressed infant froma hemodynamically unstable mother.
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Preventable surgical death in obstetrics may,
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on occasion, represent an error in judgment
and a reluctance to proceed with laparotomy
or hysterectomy, rather than deficiencies in
knowledge or surgical technique.
Proper management of serious hemorrhage
requires timely medical and surgical decision -
making as well as meticulous attention to the
aforementioned principles of blood and
volume replacement
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The diagnosis of underlying cause and
definitive treatment is initiated once
resuscitation is under way.
Surgical/ obstetrical--- ectopic pregnancy,
abortion, uterine perforation ,APH, uterine
rupture. PPH, inversion of uterus.
MANAGEMENT
DEVELOPMENTS IN
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A. CELL SALVAGE
Auto transfusion.
Blood is removed from operative sitethrough heparinised suction tubing
The resulting RBC have a haematocrit of 55-80 % and can be returned to patient quickly.
The risk of amniotic fluid is obviously aconcern.
MANAGEMENT OF SHOCK
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B.RECOMBINANT ACTIVATED FACTOR VII
rFVIIa promotes clot formation through its action
at many stages in clotting cascade. It forms acomplex with tissue factor a key initiator inhomeostasis, leading to production of smallamount of thrombin and activating factor V ,VIIand platelet aggregation at the site of injury.
Hence aids inconversion of fibrinogen in to fibrinand formation of clot.
C.PELVIC ARTERIAL EMBOLISATION
MANAGEMENT
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Complications of Hypovolemic
shock
1) Acute renal failure.
2) Pituitary necrosis (Sheehans
syndrome).
3) Disseminated intravascular coagulation
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It remains a significant cause of maternaldeath. Mortality Rate due to it , is 3% inobstetric patients.
SEPTIC SHOCK
Mixed Shock
Overwhelming infection and Inflammatory
response
Blood vessels Dilate (loss of resistance)
Leak (loss of volume)
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SEPSIS SYNDROME
Sepsis is derived from the ancient Greek
sepein, to rot.
The sepsis syndrome is induced by a
systemic inflammatory response to bacteria
or viruses or their by-products such as
endotoxins or exotoxins. The severity of the syndrome is a continuum
or spectrum
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Nomenclatures -1 Systemic inflammatory response syndrome(SIRS)
is recognized by presence of one or two of thefollowing :-
i) temp 38 degree centigrade.
ii) HR >90 per minute.
iii) blood gas PaCO2< 4.3KPa (32mmHg).
iv) WBC >12000/mm3 or with immatureneutrophils.
2 Sepsis SIRS with clinical evidence of infection.
SEPTIC SHOCK
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Nomenclature -3 Septic shockSepsis with hypotension despite
adequate fluid resuscitation.
To diagnose it:-
(i)Evidence of infection.
(ii) +ve blood culture
(iii) refractory hypotension , patient requiring
vasopressors /inotropic drugs.4 Sepsis with multi organ failure(MODS)Hypotension ,hypoxia , oliguria metabolic acidosis , thrombocytopenia ,DIC , depressed level of consciousness
SEPTIC SHOCK
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Sepsis
Two or more of SIRS criteria Temp > 38 or < 36 C
HR > 90 RR > 20
WBC > 12,000 or < 4,000
Plus the presumed existence of infection
Blood pressure can be normal!
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Septic Shock
Sepsis (remember definition?)
Plus refractory hypotension
After bolus of 20-40 mL/Kg patient still has one of
the following:
SBP < 90 mm Hg
MAP < 65 mm Hg Decrease of 40 mm Hg from baseline
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SEPSIS SYNDROME IN
OBSTETRICS
Pyelonephritis
chorioamnionitis puerperal sepsis,
septic abortion, and
necrotizing fasciitis .
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PREDISPOSING FACTORS IN
OBSTETRICS TO SEPTIC SHOCK
Post LSCS Endometritis(15-85%)
PROM
Infected RPOC(1-2%) Post vaginal delivery endometritis (1-4%)
Chorioamnionitis
Water birth delivery - due to faecal contamination.
Pyelonephritis , pneumonia , appendicitis.
Toxic shock syndrome
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BACTERIOLOGY
Pyelonephritis : Escherichiacoliand Klebsiellaspecies
And although pelvic infections are usually
polymicrobial, bacteria that cause severe sepsissyndrome are frequently endotoxin-producing
Enterobacteriaceae, most commonly E coli.
Other pelvic pathogens are aerobic and anaerobic
streptococci, Bacteroidesspecies, and
Clostridiumspecies
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Some strains of group A -hemolytic
streptococci and Staphylococcus aureus
including community-acquired methicillin-resistant strains (CA-MRSA)produce a
superantigenthat activates T cells to rapidly
cause all features of the sepsis syndrome toxic shock syndrome
Potent bacterial exotoxins that can cause
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Potent bacterial exotoxins that can cause
severe sepsis syndrome.
exotoxins from Clostridium perfringens,
toxic-shock-syndrome toxin-1 (TSST-1) from S
aureus, and
toxic shock-like exotoxin from group A -hemolyticstreptococci
These last exotoxins cause rapid and extensive
tissue necrosis and gangrene, especially of thepostpartum uterus, and may cause profound
cardiovascular collapse and maternal death
ETIOPATHOGENESIS
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ETIOPATHOGENESIS
LPS or endotoxin
The lipid A moiety is bound by mononuclearblood cells,becomes internalized, and
stimulates release of mediators
Clinical aspects of the sepsis syndrome aremanifest when cytokines are released that
have endocrine, paracrine, and autocrine
effects
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1. The pathophysiological response to thiscascade is selective vasodilation with
maldistribution of blood flow.
2. Leukocyte and platelet aggregation causecapillary plugging.
3. Worsening endothelial injury causes
profound permeability capillary leakage andinterstitial fluid accumulation
SEPTIC SHOCK PATHOPHYSILOGY OF
SEPSIS
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SEPSIS
4. Cytokininsdisturb body modulators of coagulation/inflammation -- protien C & S , Anti thrombin III andtissue factor inhibitorthus worsen Coagulopathy bydecreasing fibrinolysis.
5. Imbalance between Inflammation , Coagulation &
Fibrinolysis Massive wide spread intravascular microthrombi formation.
6. Massive production of cytokinins , Protiens C & SInterleukinsdecreased peripheral resistance
vasodilatation
hypotension
hypovolemia
decreased Pco2decreased tissue perfusionincreasedcell wall permeabilitytransfer of fluid intravascular &intracellular to extracellular compartmenttissue edemageneralized tissue anoxia .
SEPTIC SHOCK PATHOPHYSILOGY OF
SEPSIS
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SEPSIS
7. Decreased myocardial , renal , cerebral pulmonary andliver perfusion occurs.
8. Various cytokinins , nitric oxide , B receptor downregulation , prostacyclins, endothelin -- massivevasodilatation micro thrombi , decreased oxygenation ,
anoxia - lipid acidosis .9. Decreased placental perfusion -- fetal anoxia -- fetal death
in utero.
10. Pulmonary edemaARDs
11. Decreased renal perfusionacute tubular necrosisoliguriarenal failure .
12. Cerebral dysfunctiondecreased level of consciousnesscoma.
13 DICMODS Death
Pathogenesis of Sepsis
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Pathogenesis of Sepsis
Nguyen H et al. Severe Sepsis and Septic-Shock: Review of the Literature and Emergency Department Management Guidelines. Ann Emerg Med. 2006;42:28-54.
SEPTIC SHOCK - SYMPTOMS
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Abdominal pain.
Vomiting.
Diarrhea.
Fever later on hypothermia
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Tachycardia
Tachypnoea
Pallor Temperature >38/
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Abnormal TLC , DLC Low platelet , CoagulopathyLow Fibrinogen
Fibrinogen degradation products , d-Dimer ,
abnormal BT, CT, PT, Clot retraction , ATPT, INR Raised blood urea , Serum creatinine
Abnormal liver function tests
INVESTIGATIONS
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Clinical Manifestations
Central nervous system: confusion,
somnolence, coma, combativeness, fever, or
hypoxemia Cardiovascular: tachycardia, hypotension
Pulmonary: tachypnea, arteriovenous
shunting with dysoxia and hypoxemia,exudative infiltrates from endothelial-alveolar
damage, pulmonary hypertension
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Gastrointestinal: gastroenteritisnausea,
vomiting, and diarrhea; hepatocellular
necrosisjaundice, hyperglycemia Renal: prerenal oliguria, acute kidney injury
Hematological: leukocytosis or leukopenia,
thrombocytopenia, activation of coagulation withdisseminated intravascular coagulation
Cutaneous: acrocyanosis, erythroderma, bullae,
digital gangrene
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Initially a high cardiac output, low systemic
vascular resistancecondition
Concomitantly, pulmonaryhypertension
develops, and despite the high cardiac output,
severe sepsis likely also causes myocardial
depression referred to as the warm phase of septic shock.
These findings are the most common
cardiovascular manifestations of early sepsis.
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The response to initial intravenous hydration
may be prognostic.
Most pregnant women who have early sepsisshow a salutary response with crystalloidand
antimicrobialtherapy, and if indicated,
debridement of infected tissue.
Conversely, if hypotension is not corrected
following vigorous fluid infusion, then the
prognosisis more guarded.
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Another poor prognostic sign is continued
renal, pulmonary, and cerebraldysfunction
once hypotension has been corrected The average risk of death increases by 15 to
20 percent with failure of each organ system.
With three systems, mortality rates are 70percent
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Management
Surviving Sepsis Campaign
(Dellinger, 2008).The cornerstone of management is
early goal-directed management,
Institution of this protocol hasimproved survival rates
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The threebasic steps include
evaluationof the sepsis sourceand its
sequelae,
cardiopulmonary function assessment,
and immediate management.
The most important step in sepsismanagement is rapidinfusionof 2 L and
sometimes as many as 4 to 6 L of crystalloid
fluids to restore renal perfusion in severely
affected women
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Simultaneously, appropriately chosen broad-
spectrum antimicrobials are begun.
There is hemoconcentrationbecause of the
capillary leak.
Thus, if anemiacoexists with severe sepsis,
then bloodis given along with crystalloid The use of colloid solution such as hetastarch is
controversial,
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Treatment of Sepsis
Antibiotics- Survival correlates with how quicklythe correct drug was given
Cover gram positive and gram negative bacteria Zosyn 3.375 grams IV and ceftriaxone 1 gram IV o r Imipenem 1 gram IV
Add additional coverage as indicated Pseudomonas- Gentamicin or Cefepime
MRSA- Vancomycin
Intra-abdominal or head/neck anaerobic infections-Clindamycin or Metronidazole
Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae
NeutropenicCefepime or Imipenem
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In vasopressor-dependent shock, some
recommend albumin infusions
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Aggressive volume replacement ideally is
promptly followed by urinary output of at
least 30 and preferably 50 mL/hr, as well asother indicators of improved perfusion.
If not, then consideration is given for vasoactive
drug therapy.
Mortality rates are high when sepsis is further
complicated by respiratory or renal failure.
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With severe sepsis, damage to pulmonary
capillary endothelium and alveolar epitheliumcauses alveolar flooding and pulmonary
edema.
This may occur even with low or normalpulmonary capillary wedge pressures
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Broad-spectrum antimicrobialsare chosen
empirically based on the source of infection.
They are given promptly in maximal doses afterappropriate cultures are taken of blood, urine,
or exudatesnot contaminated by normal flora.
For pelvic infections, empirical coverage with
regimens such as
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regimens such as
ampicillinplus
gentamicinplus
clindamycingenerally suffices
soft-tissue infections are increasingly likely to be
caused by methicillin-resistant S aureus, thus
vancomycintherapy is needed
With a septic abortion, a Gram-stained smear
may be helpful in identifying Clostridium
perfringensor group A streptococcal organisms.
This is also true for deep fascial infections
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Surgical Treatment
debridementof necrotic tissue or
drainageof purulent material is crucial
In obstetrics, the majorcauses of sepsis areinfected abortion, pyelonephritis, andpuerperalpelvic infections that include infectionof perineal lacerations or of hysterotomy orlaparotomy incisions.
With an infected abortion, uterine contentsmust be removed promptly by curettage
Hysterectomy is seldom indicated unlessgangrene has resulted
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For women with pyelonephritis, continuingsepsisshould prompt a search for obstructioncaused bycalculi or by a perinephric or intrarenal phlegmon or
abscess.
Renal sonographyor one-shot pyelography maybe used to diagnose obstruction and calculi.
Computed tomography (CT) may be helpful toidentify a phlegmon or abscess.
With obstruction, ureteral catheterization,percutaneous nephrostomy, or flank exploration may
be lifesaving
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Most cases of puerperal pelvic sepsis are
clinically manifested in the first several days
postpartum, and intravenous antimicrobialtherapy without tissue debridement is
generally curative.
There are several exceptions. Firstis massive
uterine myonecrosiscaused by group A -
hemolytic streptococcalor clostridial
infections
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The mortalityrate in these women with
gangrene is high, and prompt hysterectomy
may be lifesaving Group A -hemolytic streptococci and clostridial
colonization or infection also cause toxic-shock
syndrome without obvious gangrene
These are due to either streptococcal toxic-
shock syndrome-like toxin or clostridial
exotoxin that evolved from S aureus
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A secondexceptionis necrotizing fasciitis of
the episiotomysite or abdominal surgical
incision.
These infections are a surgical emergency and
are aggressively managed
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Third, persistent or aggressiveuterine infection
with necrosis, uterine incisiondehiscence, and
severe peritonitismay lead to sepsis These infections tend to be less aggressive than
necrotizing group A streptococcal infections and
develop later postpartum.
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CT imaging of the abdomen and pelvis can
frequently determine
If either is suspected, then prompt surgical
exploration is indicated.
Last, peritonitis and sepsis much less commonly
may result from a ruptured parametrial,intraabdominal, or ovarian abscess
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Adjunctive Therapy
Vasoactive Drugs and
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Corticosteroids
septic woman is supported with continuing
crystalloid infusion, blood transfusions, and
ventilation. vasoactive drugs are not given unless
aggressive fluid treatment fails to correct
hypotension and perfusion abnormalities.
First-line vasopressorsare norepinephrine,
epinephrine, dopamine, dobutamine, or
phenylephrine
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The use of corticosteroidsremains
controversial.
Some but not all studies show a salutary
effect of corticosteroid administration.
It is thought that critical illnessrelated
corticosteroid insufficiencyCIRCImay
play a role in recalcitrant hypotension.
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Coagulopathy
Endotoxin stimulates endothelial cells to
upregulate tissue factor and thus procoagulant
production At the same time, it decreases the anticoagulant
action of activated protein C.
Several agents developed to block coagulation,however, did not improve outcomessome
include antithrombin III, platelet-activating factor
antagonist, and tissue factor pathway inhibitor
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Other Therapies
There are several other therapies that have
proven ineffective.
Some of these include antiendotoxinantibody and E5 murine monoclonal IgM
antiendotoxin antibody; anticytokine
antibodies to IL-1, TNF-, and bradykinin;
and a nitric oxide synthase inhibitor
Sepsis suspected Obtain cultures Start broad-spectrum antibiotic Immediate source control
Ventilation support (ETT, NIPP
Hemodynamic
Management
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Electronic fetal monitoring
if > 24 weeks Early enteral nutrition
DVT prophylaxis
Start with fluid therapy
(crystalloids 30 mL/kg initially)
Target CVP > 8 mmHg
Patient on ventilator, not triggering,
sinus rhythm, TV of 810 mL/kgPatient spontaneously breathing, or on ventilator,
but no sinus rhythm (cannot use pulse pressure
variation)
Continue fluids until MAP>65 mmHg
or as long as pulse pressure variation
is > 13% if hypotension remains
Continue fluids until MAP> 65 mmHg or as long a
non invasive cardiac output increase > 10% with
passive leg raising maneuver if hypotension
remains
Patient with MAP > 65 mmHg
with fluid therapy
MAP remains < 65 mmHg despite fluid therapy
Patient with MAP > 65 mmHg
with fluid therapyMAP remains < 65 mmHg despite fluid
therapy
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Start norepinephrine (0.053.3 g/kg/min) Titrate to MAP > 65 mmHg
Patient on norepinephrine and s/p initial
fluid resuscitation
Persistent hypotension
Start hydrocortisone 200 mg/day
Start second-line pressors like
epinephrine
Consider vasopressin at 0.030.04 U/min
MAP> 65 mmHg achieved,UO > 0.5 cc/kg/hr, normal pulse
Serum lactic acid and ScVO2
If lactic acid > 2 mmol/L and/or
ScVO2 < 70%
Increase O2 delivery with PRBCs
(target hematocrit 30%) and/or
dobutamine (2.520 g/kg/min)
Neurogenic shock Hemorrhagic shock
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Pt is quiet &apatheic Irritable ,anxious,air hunger
No hemorrhage External or internal hemorrhage
Superficial veins are fill Periferal collapse
Hemoconcentration Hemodiluation
154
SEPTIC SHOCK MANAGEMENT
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General--It includes initial management of shock andcirculatory management which requires rapid blood
volume expansion to correct the absolute and relativehypovolaemia and maintain end organ perfusion.
Improvement in maternal haemodynamic stability hasdirect effect on fetal viability.
LSCS for fetal distress in unstable mother will drive last
nail in her coffin. If fetal component is source of sepsis , then delivery
becomes the essential part of active management.
SEPTIC SHOCKSPECIAL ASPECTS MANAGEMENT
Quickly transfer to tertiary medical institution
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Quickly transfer to tertiary medical institution.
Direct arterial and central venous monitoring. Take samples for culture - blood ,wound , higher
swab from vagina and uterus , amniotic fluid ,
peritoneum , pouch of Douglas . Intra venous broad spectrum antibiotics against
gram +ve & gram -ve and anaerobes.
Removal of infective tissue P: evacuation of uterus ,colpotomy , laparotomy and if required caesarean
hysterectomy.
Goal related therapy
ADVANCES IN SEPSIS
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Early goaldirected therapy - modifying the initialRx to achieve mean arterial pressure >65 mmHg ,urine out put >0.5 ml/Kg/hr , CVP 8-12 mm Hg and
normal mixed venous oxygen saturation . An effortto reduce end organ damage and tissue death . Itimproves outcome in septic patients.
Insulin therapy - aggressive control of blood sugarhas been demonstrated to improve outcome inseptic patients.
Activated protein C (APC) - Patient with sepsis hasdecreased APC levels. Its administration decreasesmortality and reduces organ dysfunction.
MANAGEMENT
ADVANCES IN SEPSIS
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Corticosteroid therapy ?-- In un selected septicpaient it may worsen outcome because ofsecondary infection.
In critically ill patient there may be relativeadrenal insufficiency. In septic shock /theaffected adrenals may not respond to increaseddemand of adrenocorticosteroids. Studies onCortisone therapy in septic shock , havedifferent results. Its beneficial effects inobstetrical sepsis is unknown.
MANAGEMENT
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The failure of heart to provide adequate output leadsto tissue under perfusion.
Back pressure on lungs leads to Pulmonary edema.
Pregnancy puts progressive strain on cardiacfunction as pregnancy progresses , the peak beingbetween 32-34 wks.
Pre existing cardiac disease further increases therisk.
Cardiac related death are 2ndmost common causesof death in pregnancy and commoner than the directleading cause , thromboembolism.
CARDIOGENIC SHOCK
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Early diagnosis of cardiac lesion.
Surgical correction of operable cardiac lesion ,
before pregnancy is planned. Medical control of decompensated cardiac lesion by
cardiac correction before pregnancy is planned.
Avoiding Pregnancy/MTP at 6-8 wks if cardiac
condition is not under control. Management of pregnancy in such patients by the
expert team of cardiologist and obstetrician .
Initial Rx of shock is similar , further Rx depends on
cardiac lesion
By the team present in cardiac ICU
RX CARDIODGENIC SHOCK
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Definition- A serious allergic reaction that is rapid
in onset and may result in death.
Aetiology - Pharmacological agents ,insect
stings, foods , latex may trigger ANAPHYLAXIS
ANAPHYLACTIC SHOCK
Pathophysiology An exaggerated immunological response to antigen
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to which an individual has been previously
sensitized.
It is a type 1 hypersensitivity (IgE mediated)
response causing breakdown and degradation of
mast cells and basophils releasing mediators(Histamine , Serotonin, Bradikynin , Thromboxane ,
tryptase and leukotrienes) into plasma .
These substances cause increased mucousmembranes secretions , increased capillary
permeability and leakage , marked vasodilatation
and bronchospasm
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Symptoms and signs -
1 .Cutaneous -- (80%) flushing , pruritis , urticaria ,
rhinitis , conjunctival erythema, lacrymation2.Cardiovascular -- cardiovascular collapse ,
hypotension, vasodilatation, pale , cold clammy
skin , nausea , vomiting.
3.Respiratoryairway oedema , stridor , wheezing
, dyspnoea , cough , chest/throat tightness ,
hypoxiaconfusion , increased airway
resistance
ANAPHYLACTIC SHOCK
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Symptoms and signs -
4. Gastrointestinal -
nausea , vomiting , abdominal pain .
5. C N S -
Hypotension causes collapse
with/without unconsciousness , dizziness ,incontinence , confusion and throbbing
headache .
ANAPHYLACTIC SHOCK
MANAGEMENT OF ANAPHYLACTIC
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1. Basic shock management ABC
2. Circulatory management
3. Primary (Special aspect)
- Stop administration of suspected substanceand call for help.
- Subcutaneous 1ml injection of diluted
Adrenaline (1:1000)
- Early intra tracheal intubation-airway edema
will make it problematic later.
- Supine/trendelenberg position with raised
legs increases venous return.
- Start vasopressor drugs and monitor BP.
Rapid infusion for plasma volume expansion ,
with crystalloids
SHOCK
MANAGEMENT OF
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4. Secondary
- Atropine may be given if significant
bradycardia.
- If bronchospasmnebulise /I VAmino/Derriphyllin or Beta 2 agonist such as
Salbutamol , Inhaled Ipravent may be
particularly useful for treatment of
bronchospasm in patients on B-blockers.- Antihistamines - IV Chlorpheniramine.
- Corticosteroids - Effcorlin in I V drip .
Dexamthesone.
Referral to critical care unit.
ANAPHYLACTIC SHOCK
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Amniotic fluid embolism is a rare , devastating
condition .
It is responsible for (8%) of the direct maternaldeaths .
Its incidence is 1 in 80,000 - 120,000 .
It is characterized by an abrupt cardiovascular
collapse and coagulopathy during labor or in theimmediate post partum period.
AMNIOTIC FLUID EMBOLISM
AMNIOTIC FLUID EMBOLISM
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Exact mechanism of AFE not clear.
The process is more similar to anaphylactic shock.
Amniotic fluid found in the pulmonary circulation producesintense pulmonary vasospasm and pulmonary hypertension.
When ventilation perfusion mismatch occurs , profound hypoxiaensues.
Hypoxia may account for 50% maternal deaths in 1sthr of itsonset.
Following initial phase there is a phase of hemodynamiccompromise caused by left ventricular failure . Right heartparameters return to normal . This mechanism is yet not clear(animal model studies).
PATHO - PHYSIOLOGY
AMNIOTIC FLUID EMBOLISM
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Delivering woman develops acute dyspnoea ,hypotension ,seizures.
Tachycardia , tachypnoea .
cough - blood tinged frothy sputum .
Cyanosis - circum oral and peripheral .
Fetal bradycardia as a result of hypoxic insult.
Uterine atony - PPH . Dark colored blood whichdoes not clotDIC .
Pulmonary oedematypical X- Ray changespresent.
Cardiac arrest
CLINICAL FEATURES
AMNIOTIC FLUID EMBOLISM
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Initial managementABC
Circulatory management
1. Treat hypotension with vasopressors crystalloids
and Colloids I V transfusions .
2. Women who survive the initial phase require ICUadmission and prompt management of DIC and left heart
failure.
3. Coagulopathy is treated with fresh frozen plasma,
cryoprecipitate and platelets as directed by coagulation
studies .
4. Activated recombinant factor VIIa has also being used.5. Plenty of fresh heparinized blood .
6. Surgery - Perform emergency caesarean surgery in arrested
mother who are un responsive ?
MANAGEMENT
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There is no loss in intra vascular volume orcardiac function.
The primary defect is a massivevasodilatation leading to relativehypovolaemia , reduced perfusion pressure.
Poor blood flow to tissuetissue anoxia
clinical features of shock . ABC of initial management.
DISTRIBUTIVE SHOCK
NEUROGENIC SHOCK
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Spinal cord injury may produce hypotension andshock as a result of sympathetic nervous system
dysfunction . Loss of sympathetic tone causes widespread vasodilatation.
Initial management requires ABC , fluidresuscitation and vasopressor drugs to counteractvasodilatation .
Atropine may be necessary in high lesions asbradycardia may occur due to unopposed vagalactivity.
SPINAL INJURIES
NEUROGENIC SHOCK
ANAESTHESIA
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1. Shock may occur during any type of anaesthesia or analgesia for labour or
delivery.2. Shock caused by general anaesthesia is usually due to adverse drug reaction
(anaphylactic type).
3. High spinal block ---it occurs when over dose of local anaesthetic drug is
administered into epidural or subarachnoid spaces .
Factors include
i . Drug dose is reduced in pregnancy.
ii . High spinal block may follow excessive spread of drug
iii . Accidental intrathecal injection of LA intended for
epidural space. Unrecognised dural puncture, migrationof epidural catheter in to intrathecal space.
iv . Hypotension may be aggravated by incorrect positioning ,
absence of lateral tilt -- aortocaval compression.
NEUROGENIC SHOCK
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All regional anesthesia techniques producesympathetic and motor blockade. This only becomesproblem when it is high and extensive
1. Hypotensionpreceded by nausea or not
feeling well.
2. Bradycardiaunopposed vagal tone due to
blockage of cardio acceleratory fibers(T1-T4)
3. Difficulty in breathing due to paralysis of
intercostal muscles and diaphragm.4. Upper limb neurological signs (C5-T1) tingling of
fingers and weakness.
CLINICAL FEATURES
NEUROGENIC SHOCK
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Basic shock managementABC
Support of cardiovascular system by
Vasopressors , Inotropes. Intra tracheal intubation and ventilation
support with ventilator.
Sedatives can be used to reduce theawareness once initial resuscitation is
achieved.
MANAGEMENT OF HIGH BLOCK
NEUROGENIC SHOCK
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It is related to high plasma concentration due tohigh dose givenI V route , rapid absorption
It may occur during subcutaneous infiltration orepidural top up.
Intravenous injection of LA while giving regionalblocks pudendal , paracervical /episiotomy andcaudal .
Increased and generous blood supply inpregnancy aids rapid absorption.
LOCAL ANAESTHETIC TOXICITY
NEUROGENIC SHOCK
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CNS - light headedness , tinnitus , dizziness ,
circumoral numbness metallic taste , anxiety ,
confusion , feeling of impending doom ,generalized tonic-clonic seizures leading to loss
of consciousness and coma , respiratory
depression
CVStachycardia , hypotension , dysrrhythmiaand refractory cardiorespiratory arrest.
Bupivacaine exhibit signs of toxicity in obstetrical
cases
CLINICAL FEATURES LOCAL
ANAESTHETIC TOXICITY
NEUROGENIC SHOCK
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Basic shock managementABC
Special aspects
1. Circulation - Advanced life support with external cardiacmassage and defibrillation . Arrhythmias may be resistant to
conventional therapy.2.Maintain BPVasopressors and inotropic drugs
3.Seizure managementdiazepam 5-10 mg I V slowly.
4.Lipid rescue recent work on animals now seems to beimportant tool of successful therapy (lipid rescue TM website).
5. LSCS to salvage baby.6.Use of sedatives - to reduce the risk of awareness.
MANAGEMENT OF LA TOXICITY
Key Notes1 Shock results from acute generalized inadequate perfusion of the tissue
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1 .Shock results from acute , generalized , inadequate perfusion of the tissue.
2.Substandard care is still common in its managementpatients death.
3.Sepsis/ haemorrhage are common in obstetrics.
4.Signs of hypovolaemia develop very late because of physiological changes in
pregnancy.
5.Teamwork is required for successful treatment.
6.Obstetrical unitsFire drills regularly.
7.Resusctation to maintain tissue perfusion by ABC should be initiated as soon asshock is diagnosed.
8.Management of underlying cause is secondary task.
9.All therapy Is directed at optimising maternal condition and fetal wellbeing.
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Cardiogenic shock
This type of shock is caused by failure of the
heart as an effective pump.
In the obstetric patient this most often occurs inthe patient with pre - existing myocardial
disease, peripartum cardiomyopathy, congenital
or acquired valvular heart disease, and certain
cardiac arrhythmias. It is important to remember that ischemic
changes in the heart may be induced in the
settling of hypovolemic and septic shock
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Common causes of cardiogenic pulmonary edemain pregnancy are diastolic heart failure due tochronic hypertension and obesity, leading to left
ventricular hypertrophy .
Cyanotic congenital heart disease leads toischemic changes with increasing right to leftshunting due to normal decreases in systemicvascular resistance in pregnancy .
Patients with Eisenmenger syndrome can developright heart failure and cardiogenic shock aspulmonary hypertension worsens temporarily
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Pathogenesis
Cardiogenic shock is characterized by systemic
hypoperfusion in the setting of an adequate
intravascular volume.
Hemodynamic criteria include sustained
hypertension (i.e. systolic blood pressure < 90
mmHg), reduced cardiac index ( < 2.2 L/min/m 2
), and an elevated filling pressure (pulmonarycapillary wedge pressure > 18 mmHg).
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Cardiogenic shock is characterized by a
vicious cycle in which decreased myocardial
contractility, usually due to ischemia, resultsin reduced cardiac output and arterial
pressure.
The cycle continues with hypoperfusion of
the myocardium and further depression ofmaternal cardiac output
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Systolic myocardial dysfunction reduces stroke
volume and, together with diastolic dysfunction,
leads to elevated LV end - diastolic pressure andPCWP as well as to pulmonary congestion.
Reduced coronary perfusion leads to worsening
ischemic and progressive myocardial
dysfunction and a rapid downward spiral, which,if uninterrupted, is often fatal
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Due to the unstable condition of these
patients, supportive therapy must be initiated
simultaneously with diagnostic evaluation. In this circumstance, clinical evaluation of the
patient is important in helping to establish a
diagnosis and to guide patient management
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Blood work including baseline ABG, cardiactroponin, metabolic profi le, hematocrit, and liveenzymes should be sent to the lab. ECG, chest
X - ray, and echocardiogram should be obtained. There is a split of opinion with respect to the use
of pulmonary artery catheterization in patientswith suspected cardiogenic shock.
However, many clinicians believe that the use ofthe pulmonary artery catheter providesdiagnostic clarity and guidance for clinicalmanagement
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Thank you