SHOCK IN OBSTETRICS

SHOCK IN OBSTETRICS
 DEFINITION
A state of circulatory impairment characterized
by defective tissue perfusion resulting in
abnormal cellular function and metabolism. This
leads to a clinical syndrome of signs of
decreased perfusion of vital organs, with
possible alterations in the mental status
(somnolence) and oliguria (urine output <30
ml/Hr.)
Types and etiology of shock

• Hypovolaemic shock: secondary to

– Bleeding (various causes of bleeding in early pregnancy, ante- or
postpartum hemorrhage).
– Other causes of fluid loss (e.g. nasogastric suction or diarrhea).
• Distributive shock: secondary to increased venous pooling
(i.e. early septic shock, peritonitis, anaphylaxis and neurogenic
shock).
• Cardiogenic shock: secondary to decreased myocardial
contractility and function (as in myocardial infarction).
• Obstructive shock: secondary to mechanical obstruction (i.e.
cardiac tamponade, massive pulmonary embolism or
thrombosed prosthetic valve).
CLINICAL PICTURE
 Hypotension ( a BP decrease of 50-60 mmHg or BP
<100 mmHg) & subnormal temperature.
 Tachypnia & tachycardia (weak rapid -thready-
pulse).
 Pallor, cyanosis of fingers and cold clammy sweat.
 Dimness of vision and mental confusion.
 Oliguria.
Remote Complications

 Renal failure (due to cortical necrosis).

 Postpartum anterior pituitary necrosis
(Sheehan syndrome).
HYPOVOLEMIC OR HEMORRHAGIC SHOCK

A healthy pregnant woman can lose 25% of her

blood volume (1500ml) before clinical signs of shock
are evident. However, the conditions that predispose
to the development of shock in obstetrics include: a)
anemia & malnutrition; b) bleeding in early
pregnancy, antepartum or postpartum hemorrhage;
c) prolonged labor with dehydration and acidosis; d)
hypertensive with pregnancy.
Compensatory Mechanisms
 Arterioles: they control capillary blood flow in various organs. They‘re
resistance vessels controlled by the CNS.
 Venules: they contain 70% of the total blood volume. They‘re passive
resistance vessels controlled by humoral factors.
 Catecholamine release during hemorrhage causes increased venular
tone resulting in autotransfusion from this capacitance reservoir.
 There is compensatory increase in heart rate, systemic and pulmonary
vascular resistance, and myocardial contractility.
 There is redistribution of cardiac output & blood volume by selective
centrally mediated arteriolar constriction resulting in decreased blood
flow to kidneys, splanchnic bed, uterus and skin with relative
maintenance of blood flow to the heart, brain & adrenal glands (organs
that autoregulate their own flow).
 Decompensation
 When blood volume deficit exceeds 25%.
 Rapid clinical deterioration results from
maldistribution of blood flow that causes local tissue
hypoxia & metabolic acidosis, producing a vicious
circle of vasoconstriction, organ ischemia and
cellular death.
 Loss of capillary membrane integrity.
 Increased platelet aggregation resulting in small
vessel occlusion.
 Electrolyte shifts: Na+ & H2O enter skeletal muscles
and cellular K+ is lost to the extracelluar space.
 Classification Of Shock Based On
Extent Of Blood Loss

Parameter Class I Class II Class III Class IV

Blood volume lost (%) <15 15-30 30-40 >40

Pulse rate (beats/min) <100 >100 >120 >140

Supine blood pressure Normal Normal Decreased Decreased

Urine output (ml/hr) >30 20-30 5-15 <5

Mental status Anxious Agitated Confused Lethargic

 Pathophysiology
System Effect
CNS Cerebral Confusion, somnolence, coma and
combativeness
Hypothalamus Fever, hypothermia
CVS BP Hypotension (vasodilatation)
Cardiac Increased cardiac output (early), myocardial
depression (late), tachyarrhythmia
Pulmonary Shunting with hypoxemia, diffuse infiltrates
(capillary leak)
Renal Hypoperfusion (oliguria), acute tubular necrosis
Hematological Thrombocytopenia, leukocytosis, DIC
 TREATMENT
 General measures:
 Adequate ventilation providing oxygen by mask, nasal tube or
tracheal intubation if needed.
 Insertion of two wide bore cannulas with blood sample
collection for blood grouping, Rh & cross-matching, CBC,
electrolytes, liver & kidney function tests, blood sugar and
coagulation profile (PT, PTT, fibrinogen & FDPs).
 Warmth, recumbent position with legs slightly elevated.
 Morphine to alleviate pain and apprehension if needed.
 TREATMENT
Fluid, blood and blood component replacement:
 Crystalloid solutions as lactated Ringer’s solution or normal
saline (basic therapy for acute hemorrhage is crystalloid and
blood).
 Colloid therapy (as plasma substitutes) will provide more
volume expansion than crystalloids.
 Whole blood: only used in torrential bleeding.
 Packed RBCs are usually used.
Blood component replacement is rarely necessary with acute
component replacement of 5-10 packed RBCs or less.
Transfusion is needed when Hb concentration falls to <8 g/dL
or Ht <25 %.
7. Red cell substitutes: still under research.
 Blood Components Commonly
Transfused In Obstetrics

Product Indication content Effect

Whole blood (450 ml) Symptomatic anemia All components Increases Ht 3-4 % per
with large volume unit
deficits
Packed RBCs (250 ml) Symptomatic anemia Erythrocytes Increases Ht 3-4 % per
unit
Fresh frozen plasma Deficit of labile and All clotting factors Supplies fibrinogen 150
(FFP 250 ml) stable coagulation mg per unit and other
factors factors

Cryoprecipitate (50 ml) Hypofibrinogenaemia Factors VIII, VWF, Supplies selected

XIII, fibronectin, clotting factors
and fibrinogen

Platelets (50 ml) Bleeding from Platelets Increases platelet count

thrombocytopenia by 5000-8000/μl per unit
 TREATMENT
 Monitoring: Vital signs, urine output, central venous
pressure (CVP), pulmonary artery pressure (by
Swan-Ganz catheter in selected patients) & repeat
lab investigations.
 Vasoactive and inotropic agents:
– Dopamine.
– Dobutamine.
– Epinephrine.
– Norepinephrine.
 SEPTICEMIC SHOCK
Etiology:
As pelvic infection is polymicrobial, septic shock may
be caused most commonly by endo-toxin producing
enterobacteriaceae family especially E. coli, less
often by aerobic and anaerobic streptococci,
Bacteroides and Clostridium species. Virulent
exotoxin producing Group A ß-hemolytic streptococci
and also Staphylococcus aureus may also be the
cause.
 Pathophysiology
Bacterial toxins result in mediator release with:
 Activation of complement, kinins and the coagulation system
causing DIC & induction of fibrinolytic state with bleeding.
 Selective vasodilatation with maldistribution of blood flow.
 Leukocyte & platelet aggregation causing capillary plugging.
 Vascular endothelial injury causing profound capillary leakage.
 Early septic shock is a form of distributive shock while in late
stages it is both distributive and cardiogenic. The end result of
this cascade is septic shock syndrome with multiple organ
failure.
CLINICAL PICTURE

Passes into 3 stages of increasing severity:

systemic inflammatory response syndrome
(SIRS), severe sepsis then septic shock.
TREATMENT
 Aggressive fluid replacement. Oxygenation
and ventilation.
 Administration of vasopressor and inotropic
agents.
 Broad spectrum antibiotics.
 Removal of the infectious source.
 Steroids and NSAID: are not beneficial.
 Immunotherapy is still under research.
CARDIOGENIC SHOCK

Can also occur in the setting of septic shock

or hemorrhagic shock, especially in patients
who have baseline cardiovascular disease.
Treatment requires invasive monitoring and
dealing with the underlying disorder.
NEUROGENIC SHOCK
Etiology: trauma and tissue damage as in cases of:
 Disturbed extrauterine pregnancy.
 Concealed accidental hemorrhage.
 Difficult forceps delivery or breech extraction (especially if the cervix
isn’t fully dilated).
 Difficult internal version.
 Repeat rough attempts at Crede’s method.
 Rupture of the uterus or cervical tears extending into the lower uterine
segment.
 Acute inversion of the uterus.
 Rapid evacuation of the uterus as in precipitate labor and
polyhydramnios
 Retained placenta especially for more than 2 hours.
Differences between Neurogenic and
Hemorrhagic Shock

Neurogenic shock Hemorrhagic shock

The patient is quiet and apathetic The patient is restless and anxious
with air hunger

No external or internal bleeding External or internal bleeding

Superficial veins are full of blood Superficial veins are collapsed

Hemoconcentration Hemodilution

Slow pulse Weak and rapid pulse

Slow and shallow respiration Rapid and shallow respiration

TREATMENT

 General measure: mentioned earlier.

 Fluid replacement.
 Vasopressor and inotropic agents.
 Dealing with the cause.