FLUID MANAGEMENT AND

OBSTETRIC SHOCK

Dr Surya Pd Rimal, JR 2013

Moderator: Dr Tarun Pradhan, MD

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 fluids CSF,
intraocular fluids, serous membranes, and in
GI, respiratory and urinary tracts
(third space)

 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
6

Balance

Fluid and electrolyte homeostasis is maintained

in the body
Neutral balance: input = output
Positive balance: input > output
Negative balance: input < output

It is the excretion of water that is tightly regulated

10

Solutes dissolved particles

Electrolytes

charged particles

Cations positively charged ions

Na+, K+ , Ca++, H+
Anions negatively charged ions
Cl-, HCO3- , PO43

Non-electrolytes
11

Proteins,

- Uncharged

urea, glucose, O2, CO2

Body fluids are:

Electrically neutral
Osmotically maintained 275 to 290
Specific number of particles per
volume of fluid

12

Homeostasis maintained by:

13

Ion transport
Water movement
Kidney function( Filtration, reabsorption
mainly from TALH, AVP mediated water
pores)

MW (Molecular Weight) = sum of the weights of

atoms in a molecule

mEq (milliequivalents) = MW (in mg)/ valence

mOsm (milliosmoles) = number of particles in a
solution

14

Tonicity
Isotonic
Hypertonic
Hypotonic
15

16

Cell in a
hypertonic
solution

17

Cell in a
hypotonic
solution

18

Movement of body fluids

Where sodium goes, water follows.
Diffusion movement of particles down a
concentration gradient.
Osmosis diffusion of water across a
selectively permeable membrane
Active transport movement of particles up
a
concentration
gradient
;
requires
energy
19

ICF to ECF osmolality changes in ICF not

rapid
IVF ISF IVF happens constantly due
to changes in fluid pressures and osmotic
forces at the arterial and venous ends of
capillaries

20

21

Maintenance requirements

Daily maintenance fluid requirements vary

between individuals.
4/2/1..100/50/20 rule
40 Kg woman = 2.0L water,
70 90 mmol sodium
and 40 mmol potassium

Hypovolemia
1.
2.

Renal
Extra renal
1.
2.

3.

GI
Skin/ respiratory tract(sweating/ Burns)

Hemorrhage

All are NOT the cause of obstetrics shock but may

precipitate or accentuate the gravity of the
problem in a woman with shock
23

Features of volume deficit

1.
2.
3.
4.
5.
6.

Weight loss
Decreased skin turgor
Tachycardia
Hypotension
Collapsed vein
Oliguria

Regulation of body water

ADH antidiuretic hormone + thirst

25

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 thirst

Result:

increased water consumption

increased water conservation

Increased water in body,

increased volume and

decreased Na+ concentration

Volume excess
1. Iatrogenic
2. Renal dysfunction
3. Congestive heart failure
4. Cirrhosis

Features of volume excess

1.
2.
3.
4.
5.
6.

Weight gain
Peripheral edema
Increased central venous pressure
Distended neck veins
Murmur
Pulmonary edema

 Dysfunction or trauma can cause:

Decreased amount of water in body
Increased amount of Na+ in the body
Increased blood osmolality
Decreased circulating blood volume

29

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

 Decreased plasma osmotic pressure:

plasma albumin (liver disease or

protein malnutrition)
Plasma proteins lost in :
glomerular diseases of kidney
hemorrhage, burns, open wounds and
31 cirrhosis of liver

Increased capillary permeability:

Inflammation
immune responses
Lymphatic channels blocked:
surgical removal
32

infection involving lymphatics lymphedema

Fluid accumulation:
increases distance for diffusion
may impair blood flow = slower healing
increased risk of infection

33

pressure sores over bony

prominences

Isotonic fluid excess

Excess IV fluids
Hypersecretion of aldosterone
Effect of drugs cortisone

Get hypervolemia weight gain, decreased hematocrit,

diluted plasma proteins, distended neck veins, B.P.
Can lead to edema ( capillary hydrostatic pressure)
pulmonary edema and heart failure

34

TYPES OF I.V. FLUIDS

1.

Crystalloids vs. Colloids

CRYSTALLOIDS

COLLOIDS

Normal (0.9%) saline

Human Albumin

Ringer's lactate solution

(Hartmann's' solution)
5% Dextrose

Gelatin solutions
(Haemaccel,Gelafundin )
Dextran
Hydroxyethyl starches
(Hetastarch)

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

TYPES OF I.V. FLUIDS

3.

Balanced vs. unbalanced intravenous fluids

UNBALANCED SOLUTIONS

0.9% Saline
Dextrans

BALANCED SOLUTIONS
Hartmann's' solution

TYPES OF I.V. FLUIDS

4.

Natural vs. Synthetic

NATURAL SOLUTIONS
Human Albumin
Fresh Frozen Plasma

SYNTHETIC SOLUTIONS
Gelatin solutions
(Haemaccel,Gelafundin )
Hartmanns solution
Dextran

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

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

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+ and Cl- freely moves across vascular membrane

into the interstitium.

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.

Normal Saline (0.9% NaCl)

Indications:
1.

2.

3.

Replacement of fluids in hypovolaemic or

dehydrated patients ( Needs 3 blood loss)
A small amount of saline as a special adjunct can
be used to keep the veins open for medication
administration
As the initial plasma expander in blood loss while
blood is typed and matched

Normal Saline (0.9% NaCl)

Adverse Effects
1.

Fluid overload (peripheral and pulmonary

oedema)

2.

With high volume administration,

3.

Dilutional reduction of normal plasma components such

as calcium and potassium

Dilutional coagulopathy

Hyperchloraemic acidosis

Diuresis.

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.

5% Dextrose
Indications:
1.

To maintain water balance ( In pure water deficit and

for 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 !!

5% Dextrose
Adverse effects:
1.

Causes red cell clumping (cannot be given with

blood).

2.

May cause water intoxication

3.

Can cause hyponatraemia

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 plasma
components 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

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

Colloids

Disadvantages
Detrimental in severe hemorrhagic shock
when capillary permeability is high it may
worsen edema

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
Starch

100

70

17 days

Monodispersed = All molecules of similar molecular weight

Polydispersed = Molecules have spread of molecular weights

INDICATIONS
1.

When rapid expansion of plasma volume is

desirable

e.g. in haemorrhage prior to blood

transfusion
2.

For fluid resuscitation in the presence of

hypoalbuminaemia

3.

In large protein losses e.g. in burns

Gelatins

Prepared by hydrolysis of bovine collagen.

a). Gelafusine - succinylated gelatin in isotonic
saline
b). Haemaccel - urea-linked gelatin and polygeline
in an isotonic solution of sodium chloride with
potassium and calcium.

Theoretical risk of transmitting bovine spongiform

encephalopathy. (new-variant Creutzfeldt-Jakob
disease)

Volume expanding effect lasts 2-3 hrs.

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.

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

Hydroxyethyl starches

Synthesized from amylopectin(a D-glucose polymer with

a branching structure) derived from maize or sorghum.

The larger molecular size leads to prolonged

intravascular retention compared to other colloids.
e.g. Hetastarch, Pentastarch

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.

OBSTETRIC SHOCK

Inadequate perfusion
(blood flow)
leading to inadequate oxygen delivery to
tissues

OBSTETRIC SHOCK

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 blood
pressure and hypotension can occur
without shock

Maintaining perfusion
requires:

Volume = blood
Pump = heart
Container = Vessels
Failure of one or more of these causes
shock

60

AETIOLOGY OF SHOCK
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.

In Obstetric cases shock is most

commonly due to either hemorrhage
or sepsis

62

PATHOPHYSIOLOGY
Untreated shock progresses through three stages

.Stage1 Compensated --compensated by adjustment of

homeostatic mechanism it is reversible.
Stage2 Decompensated--Maximal compensatory
mechanism 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.

DIAGNOSIS

A high index of suspicion and physical signs of

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.

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 training courses for
individuals and team.
Active management of shock should start as soon
as it is suspected or expected aiming for prompt
restoration of tissue perfusion and oxygenation.

INITIAL RX

Resuscitation follows---ABC

A Airway--Patent airway is assured and high

pressure 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

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

RX - CIRCULATION

Monitor the response to therapy

Pulse , BP , SPO2 /pulse oxymetry, urine output & its

pH .

Position of patient - Head down and left lateral tilt

to avoid aortocaval compression which may
further worsen the hypotension.
Vasoactive drugs (inotropes and vasopressors)
are considered if the cause of shock is thought to
be due to myocardial depression or profound
vasodilatation.
These drugs have no part in hypovolemic shock.

Persistent Hypotension

Inadequate volume resuscitation

Hidden bleeding
Adrenal insufficiency, CIRCI
Pneumothorax
Cardiac tamponade
Medication allergy

HEMODYNAMIC CONSIDERATION IN
PREGNANCY
Pregnancy produces a hyperdynamic , hypervolaemic ,
maternal circulation.
Saves against haemorrhage to some extent.
Cardiac output increases by 50% , blood volume by 45%
reaching a peak at 32-34 wks.
30% loss of fluid may be tolerated without any
tachycardia.
Aortocaval compression aggravates the unstability seen
in haemorrhage.
In antenatal period , uteroplacental hypoperfusion
may occur before maternal signs are evident .
Adversely affects on fetal well-being , can be detected
FHR abnormalities on cardiotocograph.

Hypovolemic Shock

HYPOVOLEMIA
1.
2.
3.

Haemorrage
Renal
Extra renal
1.
2.

4.

72

GI
Skin/ respiratory tract(sweating/ Burns)

Other medical/ surgical causes: RTA, BURN

CAUSES OF HEMORRHAGIC SHOCK

AntenatalRuptured ectopic pregnancy,

Incomplete abortion, MTP, Uterine perforation
during evacuation , APH, Uterine rupture,
Abdominal wall hematoma, Non obstetrical intra
abdominal bleeding.
Intra natal uterine rupture.
Post natal PPH(primary, secondary) Atonic ,
Traumatic, Retained tissue , Thrombosis, Acute
uterine inversion .

Clinical classification of maternal

PATHOPHYSIOLOGY
hemorrhage
OF LOW BP
Class

Blood loss
(mL)

Volume deficit
(%)

Signs and symptoms

1000

15

Orthostatic tachycardia ( 20 bpm)

II

1001 1500

15 25

HR 100 120 bpm

Orthostatic changes ( 15 mmHg)
Cap refi ll > 2 sec
Mental changes

III

1501 2500

25 40

HR (120 160 bpm)

Supine BP
RR (30 50 rpm)
Oliguria

IV

> 2500

> 40

Obtundation
Oliguria - anuria
CV collapse

Shock
how to estimate quickly
blood pressure by pulse?
If you palpate a pulse,
you know SBP is at
least this number

60

70
80

90

Oxygenation
Inadequate oxygenation or perfusion causes:
Inadequate cellular oxygenation
Shift from aerobic to anaerobic metabolism
Thus, increasing the partial pressure of oxygen across
the pulmonary capillary membrane by giving 8 10 L of
oxygen per minute by tight - fitting mask is a logical first
priority.

AEROBIC METABOLISM
6 CO2

6 O2
METABOLISM

GLUCOSE

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
77

ANAEROBIC METABOLISM

2 LACTIC ACID

GLUCOSE

METABOLISM

2 ATP

HEAT (32 kcal)

Glycolysis: Inefficient source of energy production; 2 ATP for

every glucose; produces pyruvic acid
78

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

79

Volume replacement
Protracted shock appears to cause secondary
changes in the microcirculation; and these
changes affect circulating blood volume.
In early shock, there is a tendency to draw
fluid from the interstitial space into the
capillary bed
As the shock state progresses, damage to the
capillary endothelium occurs and is
manifested by an increase in capillary
permeability

 This deficit is reflected clinically by the

disproportionately large volume of fluid
necessary to resuscitate patients in severe
shock.
Sometimes, the amount of fluid required for
resuscitation is twice the amount indicated by
calculation of blood loss volume.
Prolonged hemorrhagic shock also alters
active transport of ions at the cellular level,
and intracellular water decreases.

 Most instances of hypovolemic shock in

obstetrics are hemorrhagic and immediate.
The two most common crystalloid fluids used
for resuscitation are 0.9% sodium chloride and
lactated Ringer s solution.
Both have equal plasma volume - expanding
effects

Infusion Rates
Access
18 g peripheral IV
16 g peripheral IV
14 g peripheral IV
8.5 Fr CV cordis

Gravity Pressure
50 mL/min 150 mL/min
100 mL/min
225 mL/min
150 mL/min
275 mL/min
200 mL/min
450 mL/min

 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 of
pulmonary 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

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

blood volume is its replacement with whole
blood.
Red blood cells are administered to improve
oxygen delivery in patients with decreased red
cell mass resulting from hemorrhage

 Massive blood replacement is defi ned as

transfusion of one total blood volume within
24 hours.
Pathologic hemorrhage in the patient
receiving a massive transfusion is caused
more frequently by thrombocytopenia than
by depletion of coagulation factors.

 Thus, during massive blood replacement,

correction of specific coagulation defects (fi
brinogen levels < 150 mg/ dL) and
thrombocytopenia (platelet count < 30
000/mL) will minimize further transfusion
requirements.
With massive obstetric hemorrhage (the usual
reason for hypovolemic shock) coagulation
factors as well as red blood cells are lost.
Specific replacement with PRBC s and
crystalloid solution may lead to dilutional
coagulopathy and subsequently more blood
loss.

 In acute hemorrhagic shock, central venous

pressure (CVP) or pulmonary capillary wedge
pressure (PCWP) reflect intravascular volume
status and may be useful in guiding fluid
therapy.
In the critically ill patient, however, CVP may
be a less reliable indicator of volume status
due to compliance changes in the vein walls

Pharmacologic a gents
During the antepartum and intrapartum
periods, 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.

Further evaluation
After stabilization, it is to evaluate the patients
response to therapy, to diagnose the basic
condition that resulted in circulatory shock, and
to consider the fetal condition

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,

acid base 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 and
oxygen transport variables.
In general, however, central hemodynamic
monitoring is not necessary in simple
hypovolemic shock

 Evaluation of the fetal cardiotocograph may

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

 It is important to realize that as the maternal

hypoxia, 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 from
a hemodynamically unstable mother.

 Preventable surgical death in obstetrics may,

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

MANAGEMENT

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.

DEVELOPMENTS IN
MANAGEMENT OF SHOCK

A. CELL SALVAGE
Auto transfusion.
Blood is removed from operative site
through heparinised suction tubing
The resulting RBC have a haematocrit of 5580 % and can be returned to patient quickly.
The risk of amniotic fluid is obviously a
concern.

MANAGEMENT

Disadvantages of salvaged cell transfusion1 capital and maintenance cost.

2 Staff require training and regular
CME/workshops to update itself.
3 Technique is of no use in PPH as faecal and
urine contamination with blood.

MANAGEMENT

B.RECOMBINANT ACTIVATED FACTOR VII

rFVIIa promotes clot formation through its action
at many stages in clotting cascade. It forms a
complex with tissue factor a key initiator in
homeostasis, leading to production of small
amount of thrombin and activating factor V ,VII
and platelet aggregation at the site of injury.
Hence aids inconversion of fibrinogen in to fibrin
and formation of clot.
C.PELVIC ARTERIAL EMBOLISATION

Complications of Hypovolemic
shock
1) Acute renal failure.

2) Pituitary necrosis (Sheehans

syndrome).
3) Disseminated intravascular coagulation

SEPTIC SHOCK

Mixed Shock
Overwhelming infection and Inflammatory
response
Blood vessels

Dilate (loss of resistance)

Leak (loss of volume)

It remains a significant cause of maternal

death. Mortality Rate due to it , is 3% in
obstetric patients.

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

SEPTIC SHOCK
Nomenclatures

1 Systemic inflammatory response syndrome (SIRS)

is recognized by presence of one or two of the
following :i) temp <36 , or >38 degree centigrade.
ii) HR >90 per minute.
iii) blood gas PaCO2< 4.3KPa (32mmHg).
iv) WBC >12000/mm3 or with immature
neutrophils.
2 Sepsis SIRS with clinical evidence of infection.

SEPTIC SHOCK

Nomenclature -

3 Septic shock Sepsis 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

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!

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

Sepsis

SEPSIS SYNDROME IN
OBSTETRICS

Pyelonephritis
chorioamnionitis
puerperal sepsis,
septic abortion, and
necrotizing fasciitis .

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 <1%
Septic abortion RPOC , Uterine perforation peritonitis.
Pregnancy with retained IUCD.
Cx cerclage in PROM cases.
Intra amniotic infection.

BACTERIOLOGY
Pyelonephritis : Escherichia coli and Klebsiella
species
And although pelvic infections are usually
polymicrobial, bacteria that cause severe sepsis
syndrome are frequently endotoxin-producing
Enterobacteriaceae, most commonly E coli.
Other pelvic pathogens are aerobic and anaerobic
streptococci, Bacteroides species, and
Clostridium species

Some strains of group A -hemolytic

streptococci and Staphylococcus aureus
including community-acquired methicillinresistant strains (CA-MRSA)produce a
superantigen that activates T cells to rapidly
cause all features of the sepsis syndrome
toxic shock syndrome

 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 -hemolytic
streptococci

These last exotoxins cause rapid and extensive

tissue necrosis and gangrene, especially of the
postpartum uterus, and may cause profound
cardiovascular collapse and maternal death

ETIOPATHOGENESIS
LPS or endotoxin
The lipid A moiety is bound by mononuclear
blood cells,becomes internalized, and
stimulates release of mediators
Clinical aspects of the sepsis syndrome are
manifest when cytokines are released that
have endocrine, paracrine, and autocrine
effects

1. The pathophysiological response to this

cascade is selective vasodilation with
maldistribution of blood flow.
2. Leukocyte and platelet aggregation cause
capillary plugging.
3. Worsening endothelial injury causes
profound permeability capillary leakage and
interstitial fluid accumulation

SEPTIC SHOCK PATHOPHYSILOGY OF

SEPSIS
4. Cytokinins disturb body modulators of coagulation
/inflammation -- protien C & S , Anti thrombin III and
tissue factor inhibitor thus worsen Coagulopathy by
decreasing fibrinolysis.
5. Imbalance between Inflammation , Coagulation &
Fibrinolysis Massive wide spread intravascular micro
thrombi formation.
6. Massive production of cytokinins , Protiens C & S
Interleukins decreased peripheral resistance
vasodilatation hypotension hypovolemia
decreased Pco2 decreased tissue perfusion increased
cell wall permeability transfer of fluid intravascular &
intracellular to extracellular compartment tissue edema
generalized tissue anoxia .

SEPTIC SHOCK PATHOPHYSILOGY OF

SEPSIS
7. Decreased myocardial , renal , cerebral pulmonary and
liver perfusion occurs.
8. Various cytokinins , nitric oxide , B receptor down
regulation , prostacyclins, endothelin -- massive
vasodilatation micro thrombi , decreased oxygenation ,
anoxia - lipid acidosis .
9. Decreased placental perfusion -- fetal anoxia -- fetal death
in utero.
10. Pulmonary edema ARDs
11. Decreased renal perfusion acute tubular necrosis
oliguria renal failure .
12. Cerebral dysfunction decreased level of consciousness
coma.
13. DIC MODS Death

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

Abdominal pain.
Vomiting.
Diarrhea.
Fever later on hypothermia

SEPTIC SHOCK - SIGNS OF SEPSIS

Tachycardia
Tachypnoea
Pallor
Temperature >38/<36 degree centigrade
Hypertension --later Hypotension
Cold peripheries , Clamminess
Peripheral shut down
Systemic inflammation
Organ Hypoperfusion , Confusion , Oliguria , Blleeding diathesis ,
Altered mental state

SEPTIC SHOCK
LABORATORY
INVESTIGATIONS
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

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

Gastrointestinal: gastroenteritisnausea,
vomiting, and diarrhea; hepatocellular
necrosisjaundice, hyperglycemia
Renal: prerenal oliguria, acute kidney injury
Hematological: leukocytosis or leukopenia,
thrombocytopenia, activation of coagulation with
disseminated intravascular coagulation
Cutaneous: acrocyanosis, erythroderma, bullae,
digital gangrene

Initially a high cardiac output, low systemic

vascular resistance condition
Concomitantly, pulmonary hypertension
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.

The response to initial intravenous hydration

may be prognostic.
Most pregnant women who have early sepsis
show a salutary response with crystalloid and
antimicrobial therapy, and if indicated,
debridement of infected tissue.
Conversely, if hypotension is not corrected
following vigorous fluid infusion, then the
prognosis is more guarded.

Another poor prognostic sign is continued

renal, pulmonary, and cerebral dysfunction
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 70
percent

Management
Surviving

Sepsis Campaign
(Dellinger, 2008).
The cornerstone of management is
early goal-directed management,
Institution of this protocol has
improved survival rates

The three basic steps include

evaluation of the sepsis source and its
sequelae,

cardiopulmonary function assessment,

and immediate management.

The most important step in sepsis

management is rapid infusion of 2 L and
sometimes as many as 4 to 6 L of crystalloid
fluids to restore renal perfusion in severely
affected women

Simultaneously, appropriately chosen broadspectrum antimicrobials are begun.

There is hemoconcentration because of the
capillary leak.
Thus, if anemia coexists with severe sepsis,
then blood is given along with crystalloid
The use of colloid solution such as hetastarch is
controversial,

Treatment of Sepsis
Antibiotics- Survival correlates with how quickly
the correct drug was given
Cover gram positive and gram negative bacteria
Zosyn 3.375 grams IV and ceftriaxone 1 gram IV or
Imipenem 1 gram IV

Add additional coverage as indicated

Pseudomonas- Gentamicin or Cefepime
MRSA- Vancomycin
Intra-abdominal or head/neck anaerobic infectionsClindamycin or Metronidazole
Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae
Neutropenic Cefepime or Imipenem

In vasopressor-dependent shock, some

recommend albumin infusions

Aggressive volume replacement ideally is

promptly followed by urinary output of at
least 30 and preferably 50 mL/hr, as well as
other 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.

With severe sepsis, damage to pulmonary

capillary endothelium and alveolar epithelium
causes alveolar flooding and pulmonary
edema.
This may occur even with low or normal
pulmonary capillary wedge pressures

Broad-spectrum antimicrobials are chosen

empirically based on the source of infection.
They are given promptly in maximal doses after
appropriate cultures are taken of blood, urine,
or exudates not contaminated by normal flora.

 For pelvic infections, empirical coverage with

regimens such as
ampicillin plus
gentamicin plus
clindamycin generally suffices
soft-tissue infections are increasingly likely to be

caused by methicillin-resistant S aureus, thus

vancomycin therapy is needed
With a septic abortion, a Gram-stained smear
may be helpful in identifying Clostridium
perfringens or group A streptococcal organisms.
This is also true for deep fascial infections

Surgical Treatment

debridement of necrotic tissue or

drainage of purulent material is crucial
In obstetrics, the major causes of sepsis are
infected abortion, pyelonephritis, and
puerperal pelvic infections that include infection

of perineal lacerations or of hysterotomy or

laparotomy incisions.
With an infected abortion, uterine contents
must be removed promptly by curettage
Hysterectomy is seldom indicated unless
gangrene has resulted

For women with pyelonephritis, continuing sepsis

should prompt a search for obstruction caused by
calculi or by a perinephric or intrarenal phlegmon or
abscess.
Renal sonography or one-shot pyelography may
be used to diagnose obstruction and calculi.
Computed tomography (CT) may be helpful to
identify a phlegmon or abscess.
With obstruction, ureteral catheterization,
percutaneous nephrostomy, or flank exploration may
be lifesaving

Most cases of puerperal pelvic sepsis are

clinically manifested in the first several days
postpartum, and intravenous antimicrobial
therapy without tissue debridement is
generally curative.
There are several exceptions. First is massive
uterine myonecrosis caused by group A hemolytic streptococcal or clostridial
infections

The mortality rate 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 toxicshock syndrome-like toxin or clostridial
exotoxin that evolved from S aureus

A second exception is necrotizing fasciitis of

the episiotomy site or abdominal surgical
incision.
These infections are a surgical emergency and
are aggressively managed

Third, persistent or aggressive uterine infection

with necrosis, uterine incision dehiscence, and
severe peritonitis may lead to sepsis
These infections tend to be less aggressive than
necrotizing group A streptococcal infections and
develop later postpartum.

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

Adjunctive Therapy

Vasoactive Drugs and

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 vasopressors are norepinephrine,
epinephrine, dopamine, dobutamine, or
phenylephrine

The use of corticosteroids remains

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.

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

Other Therapies

There are several other therapies that have

proven ineffective.
Some of these include antiendotoxin
antibody 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 antibiotics
Immediate source control
Ventilation support (ETT, NIPPV

Hemodynamic
Management
Start with fluid therapy
(crystalloids 30 mL/kg initially)
Target CVP > 8 mmHg

Patient on ventilator, not triggering,

sinus rhythm, TV of 810 mL/kg

Electronic fetal monitoring

if > 24 weeks
Early enteral nutrition
DVT prophylaxis

Patient spontaneously breathing, or on ventilator,

but no sinus rhythm (cannot use pulse pressure
variation)

Continue fluids until MAP>65 mmHg Continue fluids until MAP> 65 mmHg or as long as
or as long as pulse pressure variation non invasive cardiac output increase > 10% with
is > 13% if hypotension remains
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 therapy

MAP remains < 65 mmHg despite fluid

therapy

MAP> 65 mmHg achieved,

UO > 0.5 cc/kg/hr, normal pulse

Start norepinephrine (0.053.3 g/kg/min)

Titrate to MAP > 65 mmHg

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)

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

Neurogenic shock

Hemorrhagic shock

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

General--It includes initial management of shock and

circulatory management which requires rapid blood
volume expansion to correct the absolute and relative
hypovolaemia and maintain end organ perfusion.
Improvement in maternal haemodynamic stability has
direct 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 SHOCK
SPECIAL ASPECTS MANAGEMENT

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
MANAGEMENT

Early goal directed therapy - modifying the initial

Rx 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 effort
to reduce end organ damage and tissue death . It
improves outcome in septic patients.
Insulin therapy - aggressive control of blood sugar
has been demonstrated to improve outcome in
septic patients.
Activated protein C (APC) - Patient with sepsis has
decreased APC levels. Its administration decreases
mortality and reduces organ dysfunction.

ADVANCES IN SEPSIS
MANAGEMENT

Corticosteroid therapy ?-- In un selected septic

paient it may worsen outcome because of
secondary infection.
In critically ill patient there may be relative
adrenal insufficiency. In septic shock /the
affected adrenals may not respond to increased
demand of adrenocorticosteroids. Studies on
Cortisone therapy in septic shock , have
different results. Its beneficial effects in
obstetrical sepsis is unknown.

CARDIOGENIC SHOCK

The failure of heart to provide adequate output leads

to tissue under perfusion.
Back pressure on lungs leads to Pulmonary edema.
Pregnancy puts progressive strain on cardiac
function as pregnancy progresses , the peak being
between 32-34 wks.
Pre existing cardiac disease further increases the
risk.
Cardiac related death are 2nd most common causes
of death in pregnancy and commoner than the direct
leading cause , thromboembolism.

RX CARDIODGENIC SHOCK

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 lesionBy the team present in cardiac ICU

ANAPHYLACTIC SHOCK
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

Pathophysiology

An exaggerated immunological response to antigen

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 mucous
membranes secretions , increased capillary
permeability and leakage , marked vasodilatation
and bronchospasm.

ANAPHYLACTIC SHOCK
Symptoms and signs 1 .Cutaneous -- (80%) flushing , pruritis , urticaria ,
rhinitis , conjunctival erythema, lacrymation
2.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
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 .

MANAGEMENT OF ANAPHYLACTIC
SHOCK
1. Basic shock management ABC
2. Circulatory management
3. Primary (Special aspect)
- Stop administration of suspected substance
and 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

MANAGEMENT OF
ANAPHYLACTIC SHOCK
4. Secondary
- Atropine may be given if significant
bradycardia.
- If bronchospasm nebulise /I V
Amino/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.

INVESTIGATIONS IN
ANAPHYLACTIC SHOCK

Immediate - Elevated serum Tryptase ,

indicates Mast cell degradation . 3 samples
of blood are taken at 1st,2nd,3rd hr following
suspected reaction.
Late - The aim is to identify causative agent.
Refer to immunologist/allergist for
investigation.

AMNIOTIC FLUID EMBOLISM

Amniotic fluid embolism is a rare , devastating

condition .
It is responsible for (8%) of the direct maternal
deaths .
Its incidence is 1 in 80,000 - 120,000 .
It is characterized by an abrupt cardiovascular
collapse and coagulopathy during labor or in the
immediate post partum period.

AMNIOTIC FLUID EMBOLISM

PATHO - PHYSIOLOGY

Exact mechanism of AFE not clear.

The process is more similar to anaphylactic shock.
Amniotic fluid found in the pulmonary circulation produces
intense pulmonary vasospasm and pulmonary hypertension.
When ventilation perfusion mismatch occurs , profound hypoxia
ensues.
Hypoxia may account for 50% maternal deaths in 1st hr of its
onset.
Following initial phase there is a phase of hemodynamic
compromise caused by left ventricular failure . Right heart
parameters return to normal . This mechanism is yet not clear
(animal model studies).

AMNIOTIC FLUID EMBOLISM

CLINICAL FEATURES

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 which
does not clot DIC .
Pulmonary oedema typical X- Ray changes
present.
Cardiac arrest.

AMNIOTIC FLUID EMBOLISM

MANAGEMENT
Initial management ABC
Circulatory management
1. Treat hypotension with vasopressors crystalloids
and Colloids I V transfusions .
2. Women who survive the initial phase require ICU
admission 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 ?

DISTRIBUTIVE SHOCK

There is no loss in intra vascular volume or

cardiac function.
The primary defect is a massive
vasodilatation leading to relative
hypovolaemia , reduced perfusion pressure.
Poor blood flow to tissue tissue anoxia
clinical features of shock .
ABC of initial management.

NEUROGENIC SHOCK
SPINAL INJURIES

Spinal cord injury may produce hypotension and

shock as a result of sympathetic nervous system
dysfunction . Loss of sympathetic tone causes wide
spread vasodilatation.
Initial management requires ABC , fluid
resuscitation and vasopressor drugs to counteract
vasodilatation .
Atropine may be necessary in high lesions as
bradycardia may occur due to unopposed vagal
activity.

NEUROGENIC SHOCK
ANAESTHESIA
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, migration
of epidural catheter in to intrathecal space.
iv . Hypotension may be aggravated by incorrect positioning ,
absence of lateral tilt -- aortocaval compression.

NEUROGENIC SHOCK
CLINICAL FEATURES

All regional anesthesia techniques produce

sympathetic and motor blockade. This only becomes
problem when it is high and extensive
1. Hypotension preceded by nausea or not
feeling well.
2. Bradycardia unopposed 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.

NEUROGENIC SHOCK
MANAGEMENT OF HIGH BLOCK

Basic shock managementABC

Support of cardiovascular system by
Vasopressors , Inotropes.
Intra tracheal intubation and ventilation
support with ventilator.
Sedatives can be used to reduce the
awareness once initial resuscitation is
achieved.

NEUROGENIC SHOCK
LOCAL ANAESTHETIC TOXICITY

It is related to high plasma concentration due to

high dose given I V route , rapid absorption
It may occur during subcutaneous infiltration or
epidural top up.
Intravenous injection of LA while giving regional
blocks pudendal , paracervical /episiotomy and
caudal .
Increased and generous blood supply in
pregnancy aids rapid absorption.

NEUROGENIC SHOCK
CLINICAL FEATURES LOCAL
ANAESTHETIC TOXICITY

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
CVS tachycardia , hypotension , dysrrhythmia
and refractory cardiorespiratory arrest.
Bupivacaine exhibit signs of toxicity in obstetrical
cases.

NEUROGENIC SHOCK
MANAGEMENT OF LA TOXICITY

Basic shock management ABC

Special aspects
1. Circulation - Advanced life support with external cardiac
massage and defibrillation . Arrhythmias may be resistant to
conventional therapy.
2.Maintain BP Vasopressors and inotropic drugs
3.Seizure management diazepam 5-10 mg I V slowly.
4.Lipid rescue recent work on animals now seems to be
important tool of successful therapy (lipid rescue TM website).
5. LSCS to salvage baby.
6.Use of sedatives - to reduce the risk of awareness.

Key Notes
1 .Shock results from acute , generalized , inadequate perfusion of the tissue.

2.Substandard care is still common in its management patients 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 units Fire drills regularly.
7.Resusctation to maintain tissue perfusion by ABC should be initiated as soon as
shock is diagnosed.
8.Management of underlying cause is secondary task.

9.All therapy Is directed at optimising maternal condition and fetal wellbeing.

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 in
the 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

Common causes of cardiogenic pulmonary edema

in pregnancy are diastolic heart failure due to
chronic hypertension and obesity, leading to left
ventricular hypertrophy .
Cyanotic congenital heart disease leads to
ischemic changes with increasing right to left
shunting due to normal decreases in systemic
vascular resistance in pregnancy .
Patients with Eisenmenger syndrome can develop
right heart failure and cardiogenic shock as
pulmonary hypertension worsens temporarily

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 (pulmonary
capillary wedge pressure > 18 mmHg).

Cardiogenic shock is characterized by a

vicious cycle in which decreased myocardial
contractility, usually due to ischemia, results
in reduced cardiac output and arterial
pressure.
The cycle continues with hypoperfusion of
the myocardium and further depression of
maternal cardiac output

Systolic myocardial dysfunction reduces stroke

volume and, together with diastolic dysfunction,
leads to elevated LV end - diastolic pressure and
PCWP 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

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

Blood work including baseline ABG, cardiac

troponin, metabolic profi le, hematocrit, and live
enzymes 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 patients
with suspected cardiogenic shock.
However, many clinicians believe that the use of
the pulmonary artery catheter provides
diagnostic clarity and guidance for clinical
management

Thank you
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