SHOCK IN

OBSTETRICS
By: Nwokotubo Beulah, 6th
course, Group 28
What is Shock?
Shock is a state of compromised tissue perfusion that causes cellular hypoxia
and is defined as a syndrome initiated by acute hypoperfusion, leading to
tissue hypoxia and vital organ dysfunction.

Perfusion may either be decreased globally or simply distributed poorly, as in

septic shock.
Why talk specifically about shock in
obstetrics?
The treatment of shock in pregnancy differs in two important aspects from
the treatment of shock in other adults.

First, normal physiological changes occur in most organ systems during

pregnancy. Second, the mother AND the fetus are both vulnerable during the
pregnancy.

Therefore, obstetric critical care involves simultaneous assessment and

management of the mother and fetus, who have differing physiological
profiles.
Types of shock that may occur in
pregnancy
❖ Hemorrhagic shock following excessive blood loss
❖ Endotoxic/septic shock as a result of toxemia
❖ Neurogenic shock
❖ Cardiogenic shock due to ineffective cardiac muscle contraction as in
heart failure or MI
❖ Anaphylactic shock following sensitivity reactions
❖ Shock due to amniotic embolism (also other types of embolism such as
air or thromboembolism)
The general clinical presentation of shock
Other than the disparities in clinical presentation that may occur depending of
the type of shock the patient is experiencing, there are classic clinical signs of
shock that can help in putting a preliminary diagnosis right away. They are:

❖ Low blood pressure

❖ Rapid, weak (thready) pulse
❖ Hyperventilation
❖ Cold, clammy skin with pallor
❖ Cyanosis of fingers and lips
❖ Enlarged pupils
❖ Oligo- or anuria
❖ Restlessness,dizziness, nausea and vomiting
HEMORRHAGIC
SHOCK
Background
Hemorrhagic shock occurs due to excessive blood loss. Excessive blood loss
may occur in pregnancy antepartum or postpartum, postpartum being more
common.

Antepartum hemorrhages often occur due to placental disruption or

spontaneous or traumatic uterine rupture. Postpartum hemorrhages occur
due to uterine atony and cervical or vaginal lacerations.
Antepartum causes
❖ Placenta previa: implantation of placenta in the lower uterine segment
(near the cervix), with the classic presentation of painless vaginal bleeding
and a soft, nontender uterus.
❖ Placental abruption: placenta detaches prematurely from the uterus. This
manifests as uterine pain between contractions, hemorrhage, and uterine
tenderness.
❖ Uterine rupture: manifests as vaginal bleeding, lower abdominal pain, and
a nonreassuring fetal tracing. This often occurs following a high dose of
oxytocin or prostaglandins that may be given for induction.
Placenta previa vs Placenta abruptio
The Tilt Test for hemorrhagic shock
This test is done in a patient with considerable bleeding, but whose pulse
and/or blood pressure are normal.

When this patient is in a sitting position, she develops hypotension and/or

tachycardia.
 Classification of hemorrhage
Class Blood loss % Clinical Picture

I 15% Normal pulse & blood pressure. Tilt test +ve.

II 20-25% Tachycardia. Tachypnoea. Pulse pressure

(<30mmHg). Low systolic pressure. Delayed
capillary filling.

III 30-35% Skin: cold, clammy and pale. Severe drop in

blood pressure. Restlessness. Oliguria (<30
ml/hour). Metabolic acidosis (blood pH <7.5).

IV 40-45% Profound hypotension.

The carotid pulse is the only felt one.
Irreversible shock.
Management
Restoration of blood volume by:

Whole blood: cross-matched from the same group if not available group O-ve
may be given as a life -saving.

Crystalloid solutions: as ringer lactate, normal saline or glucose 5%. They have
a short half life in the circulation and excess amount may cause pulmonary
oedema.

Colloid solutions: as dextran 40 or 70, plasma protein fraction or fresh frozen

plasma.
Management
Pharmacologic therapy:

Analgesics: 10-15 mg morphine IV if there is pain, tissue damage or irritability.

Corticosteroids: Hydrocortisone 250 mg or dexamethasone 20 mg slowly IV. Its mode of

action is controversial; it may decrease peripheral resistance and potentiate cardiac response
so it improves tissue perfusion.

Sodium bicarbonate: 100 mEq IV if metabolic acidosis is demonstrated.

Vasopressors: to increase the blood pressure so maintain renal perfusion.

Dopamine: 2.5m g/ kg/ minute IV is the drug of choice.

ß -adrenergic stimulant: isoprenaline 1 mg in 500 ml 5% glucose slowly IV infusion.

Management
In postpartum hemorrhage, uterine atony can be treated with uterine
massage, intramuscular administration of methylergonovine (0.2 mg), and
intravenous oxytocin infusion.

If medical management fails, therapeutic embolization of the internal iliac or

uterine artery has been used to control obstetric hemorrhage. Surgical
exploration to repair lacerations and decrease blood loss by arterial ligation
or hysterectomy may be required as a life-saving measure.
ENDOTOXIC/SEPTIC
SHOCK
Background
Septic shock may occur during pregnancy because of
overwhelming infection caused by gram-positive bacteria,
viruses, or fungi. Gram-negative bacteria such as
Escherichia coli, Klebsiella species, Pseudomonas
aeruginosa, and Serratia species cause most cases of
septic shock.
Obstetric causes
❖ Septic abortion.
❖ Prolonged rupture of membranes
❖ Manipulations and instrumentations
❖ Trauma
❖ Retained placental tissues
❖ Puerperal sepsis
❖ Severe acute pyelonephritis
Pathology
Release of endotoxin results in increased lysosomal permeability and
cytotoxicity. The sequence of events thereafter may occur in few minutes and
include:

Stimulation of the adrenal medulla and sympathetic nervous system →

constriction of arterioles and venules → local acidosis → arteriolar dilatation
but with continuing constriction of the venules → capillary pooling of blood →
haemorrhagic engorgement of bowel, liver, kidneys and lungs.

There is associated extensive disseminated intravascular coagulation due to

sudden massive plasmin generation with which the antiplasmins cannot cope.
Clinical presentation of septic shock
During sepsis, injury to type II pneumocytes impairs surfactant production,
causing alveolar collapse, lowering lung compliance, and producing severe
hypoxemia. This constellation of clinical and physiologic features is described
as acute respiratory distress syndrome (ARDS).

Patients with septic shock present with chills, fever, hypotension, mental
confusion, tachycardia, tachypnea, and flushed skin. As the septic shock
progresses, the patient develops cool clammy skin, bradycardia, and cyanosis.
Management
Treatment of septic shock requires immediate
resuscitation, identification of the underlying cause
of septic shock, and treatment with antimicrobial
therapy.
Principles of management
❖ Early recognition
❖ Early and adequate antibiotic therapy: A combination used often is penicillin,
aminoglycoside, and clindamycin or metronidazole. An alternative combination is a
second- or third-generation cephalosporin combined with metronidazole. Piperacillin-
tazobactam provides fairly comprehensive coverage for an intra-abdominal source of
sepsis.
❖ Source control
❖ Early hemodynamic resuscitation and continued support with vasoactive drugs,
crystalloids and colloids, norepinephrine for increased perfusion. Ephedrine, an alpha
and beta agonist, is a better vasopressor for acutely hypotensive women
❖ Corticosteroids (refractory vasopressor-dependent shock): Hydrocortisone 250 mg IV / 6
hours or, Dexamethasone 20 mg initially followed by 200 mg/day by IV infusion.
❖ Glycemic control
❖ Proper ventilator management with low tidal volume in patients with ARDS
Surgical treatment:
is indicated when there is retained infected tissues as in septic abortion. It
should be removed as soon as antibiotic therapy and resuscitative measures
have been started by:

❖ suction evacuation,
❖ digital evacuation, or
❖ hysterectomy in advanced infection with a gangrenous (clostridium
welchii) or traumatised uterus.
CARDIOGENIC
SHOCK
Background
In cardiogenic shock, the left ventricle is not able to pump sufficient blood to
meet the metabolic demands of the tissues. The compensatory response is
tachycardia, but eventually, hypervolemia, pulmonary venous congestion, and
generalized edema occur. Inadequate oxygen delivery leads to cellular
damage, multiorgan failure, and death.
Clinical presentation
The clinical signs of cardiogenic shock are distended neck veins, dyspnea,
tachypnea, the presence of a third heart sound, systolic or diastolic murmurs,
and generalized edema.

Postpartum patients may have a localized abscess, resistant organism, or

septic pelvic thrombophlebitis. Patients with septic pelvic thrombophlebitis
usually develop persistent fever.
Management
The following ABC steps are carried out:

❖ Airway:

Clear it: from vomitus, blood, teeth, foreign body ...etc.

Maintain it: Pull mandible and tongue forward.

Insert an airway.

Endotracheal intubation as soon as possible.

❖ Breathing:

Mouth-to-mouth artificial respiration.

Mask and ambu bag with 100 % oxygen.

Cuffed endotracheal tube with intermittent positive pressure of 100% oxygen.

Management (contd.)
❖ Cardiac massage:

Using the heel of one hand, with the other on top, and with the arms extended,
apply pressure to the lower sternum using the full body weight.

This should provide a palpable femoral or carotid pulse.

The optimal compressions is 60 / minute in a ratio of 4:1 to ventilation.

Management (contd.)
❖ Drip and Drugs:

Sodium bicarbonate 8.4% solution: to counteract metabolic acidosis. Give 100 ml initially and a further 10 ml
for each subsequent minute of inadequate circulation.

Cardiac stimulants (inotropic drugs): can be given IV or intracardiac e.g.

Adrenaline 0.5-1.0 mg.

Atropine 0.6 mg.

Isoprenaline 4 mg in 500 ml solution.

Dopamine 500 mg in 500 ml solution (1-3 m g/ kg/ min).

Calcium chloride 10% solution.

Management (contd.)
❖ Electrocardiogram:

to assess the condition and response to the therapy.

❖ Fibrillation treatment

Direct current (DC) defibrillator is used.

AMNIOTIC FLUID
EMBOLISM
Background
Amniotic fluid embolism (AFE) is a catastrophic peripartum syndrome that
manifests as a sudden onset of severe dyspnea, hypoxemia, hemodynamic
collapse, coagulopathy, and seizures.

AFE may occur at any point during pregnancy, labor, or delivery. Uterine
manipulation or trauma may often precede AFE.

The triad of hypotension, hypoxemia, and coagulopathy should make one

consider the diagnosis of AFE.
Pathology of amniotic fluid embolism
The fetal substance, when introduced into maternal circulation, may initiate
an anaphylactoid reaction, resulting in endogenous mediator release and
causing hypotension, tachycardia, hypoxemia, and seizures. This may lead to
pulmonary arterial vasospasm and transient pulmonary hypertension,
followed by left ventricular failure, decreased cardiac output, and hydrostatic
pulmonary edema.

The acute left ventricular dysfunction may be caused by humoral mediators or

cytokines contained in amniotic fluid released during the anaphylactoid
reaction.
Clinical picture
❖ The onset is acute with sudden collapse, cyanosis and severe dyspnoea.
❖ This is soon followed by twitching, convulsions and right side heart
failure, with tachycardia, pulmonary oedema and blood stained frothy
sputum.
❖ If death does not occur in this stage, DIC develops within 1 hour leading
to generalised bleeding.
Diagnostic investigations
❖ ECG: evidence of right side heart failure.

❖ X-ray: non-specific mottled chest appearance.

❖ Lung scan: with technetium-99m albumin shows perfusion defect.

❖ Laboratory tests: evidence of DIC.

Management
The 3 main goals of treatment are:

(1) oxygenation,

(2) maintaining cardiac output and blood pressure, and

(3) correcting coagulopathy.

The fetus should be monitored continuously for signs of compromise. To

ensure optimal uterine perfusion, the mother should be placed in the left
lateral position.
Management
❖ Oxygen: endotracheal intubation and positive pressure respiration is usually
indicated as the patient is often unconscious.
❖ Euphylline: 2.4% - 10 mL slowly IV to reduce bronchospasm.
❖ Isoprenaline: 0.1gm IV to improve pulmonary blood flow and cardiac activity.
❖ Digoxin and atropine: if central venous pressure is raised and pulmonary
secretions are excessive.
❖ Hydrocortisone: 250 mg IV followed by slow IV infusion causes vasodilatation
and improves tissue perfusion.
❖ Bicarbonate solution: if there is respiratory acidosis.
❖ Low molecular weight dextran: reduces platelets aggregation in vital organs.
❖ Heparin: for treatment of DIC if there is no active bleeding.
❖ Immediate delivery