Shock in Obstetrics
Shock is a condition
resulting from inability of the circulatory system to
provide the tissues requirements from oxygen and
nutrients and to remove metabolites.
Types and Causes:
(I)
Hemorrhagic
shock
excessive blood loss may be due to:
1.
Causes of bleeding early in pregnancy (see bleeding in
early pregnancy. Abortion; Ectopic pregnancy and
Gestational Trophoblastic Disease)).
2.
Causes of Antepartum hemorrhage (see Placenta praevia ad
Abruptio placenta).
3.
Causes of postpartum hemorrhage.
(II)
Neurogenic
shock painful
conditions my be due to :
1- Disturbed Ectopic
pregnancy.
2- Concealed accidental
hemorrhage.
3- Forceps or breech
extraction before full cervical dilatation.
4- Rough internal
version.
5- Crédé’s method.
6- Rupture uterus.
7- Acute inversion of
the uterus.
8- Rapid evacuation of
the uterine contents as in precipitate labor and rupture
of membranes in polyhydramnios. This is accompanied by
rapid accumulation of blood in the splanchnic area due
to sudden relief of pressure (splanchnic shock).
(III)
Cardiogenic shock
: ineffective
contraction of the cardiac muscle due to
1- Myocardial
infarction.
2- Heart failure.
(IV)
Endotoxic
shock:
generalized vascular disturbance due to release of
toxins.
(V)
Anaphylactic shock:
caused by sensitivity to drugs.
(VI)
Other causes:
1.
Embolism:
amniotic fluid , air or thrombus.
2.
Anesthetic complications
: as
Mendelson's syndrome.
The shock may be caused
by more than one factor as:
·
Incomplete abortion : leads to hemorrhagic and Endotoxic
shock.
·
Disturbed Ectopic and rupture uterus: lead to
hemorrhagic and Neurogenic shock.
Classic Clinical Picture of Shock:
1- Low blood pressure.
2- Rapid weak (thready )
pulse.
3- Pallor.
4- Cold clammy sweat.
5- Cyanosis of the
fingers.
6- Air hunger.
7- Dimness of vision.
8- Restlessness.
9- Oliguria or anuria.
HEMORRHAGIC SHOCK
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. |
|
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. |
Tilt test:
·
It is done in patient with considerable bleeding but the
blood pressure and/ or pulse rate are normal.
·
When this patient is in a sitting position, she develops
hypotension and / or tachycardia.
Phases of Hemorrhagic Shock:
The normal pregnant
woman can withstand blood loss of 500 ml and even up to
1000 ml during delivery without obvious danger due to
physiological cardiovascular and hematological
adaptations during pregnancy.
(I) Phase of
compensation:
·
Sympathetic
stimulation:
It is the initial
response to blood loss leading to peripheral
vasoconstriction to maintain blood supply to the vital
organs.
·
Clinical picture:
- Pallor, -
tachycardia, - tachypnea.
(II) Phase of
decompensation:
·
Blood loss exceeds 1000 ml in normal patient or less if
other adverse factors are operating.
·
Clinical picture:
is the classic clinical picture of shock (see before).
·
Adequate treatment at this phase improves the condition
rapidly without residual adverse effects.
(III) Phase of cellular
damage and danger of death:
·
Inadequately treated hemorrhagic shock results in
prolonged tissue hypoxia and damage with the following
effects:
1.
Metabolic acidosis:
due to anaerobic metabolism initiated after lack of
oxygen.
2.
Arteriolar dilatation :
caused by accumulation of metabolites leading to pooling
and stagnation of blood in the capillaries and leakage
of fluid into the tissues.
3.
Disseminated
intravascular coagulation:
caused by release of thromboplastin from the damaged
tissues.
4.
Cardiac failure:
due to diminished coronary blood flow.
·
In this phase death is imminent, transfusion alone is
inadequate and if recovery from acute phase occurs
residual tissue damage as renal and/ or pituitary
necrosis will occur.
Management:
Urgent interference is
indicated as follow:
1.
Detect the cause and
arrest hemorrhage.
2.
Establish an airway and
give oxygen
by mask or endotracheal tube.
3.
Elevate the legs
to encourage
return of blood from the limbs to the central
circulation.
4.
Two or more intravenous
ways are established
for blood, fluids and drugs infusion which should be
given by IV route in shocked patient. If the veins are
difficult to find a venous cut down or intrafemoral
canulation is done.
5.
Restoration of blood
volume by:
a. Whole blood:
cross-matched from the same group if not available group
O-ve may be given as a life -saving.
b. 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 edema.
c. Colloid solutions:
as dextran 40 or 70, plasma protein fraction or fresh
frozen plasma.
6-Drug
therapy:
a. Analgesics:
10-15 mg morphine IV if there is pain, tissue damage or
irritability.
b. Corticosteroids:
Hydrocortisone 1gm or dexamethazone 20 mg slowly
IV. Its mode of action is controversial; it may decrease
peripheral resistance and potentiate cardiac response so
it improves tissue perfusion.
c. Sodium
bicarbonate: 100 mEq IV if metabolic acidosis is
demonstrated.
d. 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 1mg in 500 ml 5%
glucose slowly
IV infusion.
7-
Monitoring:
a- Central venous
pressure (CVP) : normal 10-12 cm water.
b- Pulse rate.
c- Blood pressure.
d- Urine output: normal
60 ml/hour.
e- pulmonary capillary
wedge pressure: Normal 6-18 Torr.
f- Clinical improvement
in the : pallor, cyanosis, air hunger, sweating and
consciousness.
Complications:
1.
Acute renal failure.
2.
Pituitary necrosis (Sheehan’s syndrome).
3.
Disseminated intravascular coagulation.
ENDOTOXIC (SEPTIC OR BACTERAEMIC ) SHOCK
Obstetric Causes:
1- Septic abortion.
2- Prolonged rupture of
membranes.
3- Manipulations and
instrumentations.
4- Trauma.
5- Retained placental
tissues.
6- Puerperal sepsis.
7- Severe acute
pyelonephritis.
Causative Organisms:
- Gram-negative bacilli:
E.coli, proteus, pseudomonas and bacteroids. The
endotoxin is a phospho-lipo-polysacharide released by
lysis of its cell envelope.
- A similar picture is
produced from exotoxin of ß - haemolytic
streptococci, anaerobic streptococci and clostridia.
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
®
hemorrhagic 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 Features:
Endotoxic shock passes
with 2 main stages:
(I) Reversible stage:
which has 2 phases:
(A) Early (warm) phase :
there are;
- hypotension,
- tachycardia,
- pyrexia,
- rigors,
- flushed skin,
- patient is alert,
- leucocytosis develops
within hours.
(B) Late (cold) phase:
there are;
- cold and clammy skin,
- mottled cyanosis,
- purpura,
- jaundice,
- progressive mental
confusion,
- coma.
(II) Irreversible
stage:
Prolonged cellular
hypoxia leads to :
- metabolic acidosis,
- acute renal
failure,
- cardiac failure,
- pulmonary edema,
- adrenal failure and
ultimately death.
Differential Diagnosis:
1- Amniotic fluid
embolism.
2- Pulmonary embolism.
3- Pulmonary aspiration
syndrome.
4- Myocardial
infarction.
5- Incompatible blood
transfusion.
Management:
It includes 3 major
lines of treatment:
(I) Restoration of
circulatory function and oxygenation:
1. Replacement of blood
loss: by
whole blood, if not available start with colloids or
crystalloids. The CVP measurement is essential to guard
against circulatory overload.
2. Corticosteroids:
as;
- Hydrocortisone 1gm IV
/ 6 hours or,
- Dexamethasone 20 mg
initially followed by 200 mg/day by IV infusion.
3.
b -adrenergric
stimulants:
as isoprenaline cause arteriolar dilatation,
increase heart rate and stroke volume improving tissue
perfusion. Blood volume must be normal prior to its
administration.
4. Oxygen
: if respiratory function is impaired.
5. Aminophylline:
improves respiratory function by alleviating
bronchospasm.
(II) Eradication of
infection:
(1) Antibiotic therapy:
- Swabs for culture and
sensitivity are taken first.
- Antibiotic therapy is
starting immediately till the result of culture and
given by IV route. The therapy should cover the wide
range of organisms:
|
Antibiotic
|
Actions/ upon
|
Dose
|
Regimen 1 |
Ampicillin or Cephalosporines |
Aerobic gram +ve organisms and gram
-ve cocci. |
500-1000 mg/6 hours. |
|
Gentamycin |
Aerobic gram -ve bacilli. |
80 mg/ 8 hours.
(not to be given in the
solutions). |
|
Metronidazole |
Anaerobic. |
500 mg/ 8 hours. |
Regimen 2 |
Clindamycin |
Aerobic gram +ve organisms + gram -ve
cocci + Anaerobic organisms. |
600 mg/ 6 hours. |
|
Gentamycin |
Aerobic gram-ve bacilli. |
80 mg/ 8 hours. |
(2) 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 traumatized uterus.
(III) Correction of
fluid and electrolyte deficits.
(IV) Disseminated
intravascular coagulation:
Heparin therapy (see DIC)
except if there is active bleeding where the condition
is best treated by fresh blood transfusion.
AMNIOTIC FLUID EMBOLISM
Definition:
Passage of amniotic
fluid into the maternal circulation leads to sudden
collapse during labor but can only be confirmed at
necropsy.
Pathology:
·
The condition is more common with strong uterine
contraction, whether spontaneous or induced , occurs
after rupture of membranes particularly when there are
open maternal blood vessels in the placental site or in
cervical lacerations.
·
The embolism passes to the pulmonary vessels leads to :
- sudden death,
- shock, or
- Later death
due to DIC and postpartum hemorrhage.
Clinical Picture:
- The onset is acute
with sudden collapse, cyanosis and severe dyspnea.
- This is soon followed
by twitching, convulsions and right side heart failure,
with tachycardia, pulmonary edema and blood stained
frothy sputum.
- If death does not
occur in this stage, DIC develops within 1 hour leading
to generalized bleeding.
Investigations:
1.
ECG:
evidence of right side heart failure.
2.
X-ray:
non - specific mottled chest appearance.
3.
Lung scan
: with technetium- 99m albumin shows perfusion defect.
4.
Laboratory tests:
evidence of DIC.
Differential Diagnosis:
1.
Acute pulmonary edema.
2.
Pulmonary aspiration (Mendelson’s) syndrome.
3.
Other coagulation defects.
Treatment:
Urgent treatment
includes:
1.
Oxygen:
endotracheal intubations and positive pressure
respiration is usually indicated as the patient is often
unconscious.
2.
Aminophylline:
0.5 gm slowly IV to reduce bronchospasm.
3.
Isoprenaline :0.1gm
IV to improve pulmonary blood flow and cardiac activity.
4.
Digoxin and atropine:
if central venous pressure is raised and pulmonary
secretions are excessive.
5.
Hydrocortisone :
1 gm IV followed by slow IV infusion causes
vasodilatation and improves tissue perfusion.
6.
Bicarbonate solution:
if there is respiratory acidosis.
7.
Low molecular weight
dextran:
reduces platelets aggregation in vital organs.
8.
Heparin:
for treatment of DIC if there is no active bleeding.
9.
Vaginal delivery:
is safer than C.S if the baby is not yet delivered.
CARDIAC ARREST
Definition:
Sudden circulatory
collapse caused by sudden failure of the heart to pump
the blood adequately.
Types:
1.
Complete cessation of
mechanical and electrical activity:
asystole.
2.
Rapid ineffective
activity:
ventricular tachycardia and ventricular fibrillation.
3.
Slow ineffective
activity:
sinus bradycardia and complete heart block.
In practice, asystole
and ventricular fibrillation account for almost all
cases of cardiac arrest.
Causes:
Any cause of obstetric
shock can end by cardiac arrest, the commonest of which
are:
1.
Severe hemorrhage.
2.
Hypoxia due to eclampsia or anaesthesia.
3.
Mendelson’s syndrome: gastric aspiration with
pneumonitis.
4.
Embolism of
whatever the nature.
Diagnosis:
1- Sudden collapse.
2- Loss of
consciousness.
3- Absence of pulse
including the carotid and femoral pulse.
4- Apnea and cyanosis of
variable degree.
5- Fixed dilatation of
the pupils.
N.B. Attempts to
auscultate the heart, to record blood pressure or ECG
are only time wasting procedures unless the patient is
already being monitored during surgery.
Management :
- Urgent pairs of hands
are needed to save the patient’s life.
- Put the patient in the
dorsal position onto a firm surface, even the floor.
- A single firm thump
with the closed fist over the lower sternum may be
sufficient to correct the condition otherwise,
- The following ABC
steps are carried out:
A- Airway:
1.
Clear it :
from vomitus, blood, teeth, foreign body ...etc.
2.
Maintain it :
- Pull mandible and tongue forward.
- Insert an
airway.
-
Endotracheal intubations as soon as possible.
B- Breathing:
One of the following is
used:
1.
Mouth-to- mouth artificial respiration.
2.
Mask and ambubag with 100 % oxygen.
3.
Cuffed endotracheal tube with intermittent positive
pressure of 100% oxygen.
C- 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.
D- Drip and Drugs:
1.
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.
2.
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.
E- Electrocardiogram:
to assess the condition
and response to the therapy.
F- Fibrillation
treatment
Direct current (DC)
defibrillator is used.
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