Fluid Management and Obstetric Shock

8/10/2019 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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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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3. Balanced vs. unbalanced intravenous fluids

UNBALANCED SOLUTIONS BALANCED SOLUTIONS

0.9% Saline Hartmann's' solution

Dextrans


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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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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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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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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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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



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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



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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



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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

Documents

Fluid Management and Obstetric Shock