15.Postpartum hemorrahage. Uterine hypotonia and atonia. Hemorrhagic shock.

Of all the stages of labor, third stage is the most crucial one for the mother. Fatal
complications may appear unexpectedly in an otherwise uneventful first or second
stage. The following are the important complications: (1) Postpartum hemorrhage, (2)
Retention of placenta, (3) Shock—hemorrhagic or nonhemorrhagic, (4) Pulmonary
embolism either by amniotic fluid or by air, (5) Uterine inversion (rare).
POSTPARTUM HEMORRHAGE (PPH) DEFINITION: Quantitative definition is
arbitrary and is related to the amount of blood loss in excess of 500 mL following
birth of the baby (WHO). It may be useful for statistical purposes. As the effect of the
blood loss is important rather than the amount of blood lost, the clinical definition,
which is more practical states, “any amount of bleeding from or into the genital tract
following birth of the baby up to the end of the puerperium, which adversely affects
the general condition of the patient evidenced by rise in pulse rate and falling blood
pressure is called postpartum hemorrhage”. The average blood loss following vaginal
delivery, cesarean delivery and cesarean hysterectomy is 500 mL, 1000 mL and 1500
mL respectively. Depending upon the amount of blood loss, PPH can be ♦ Minor (<
1L), ♦ Major (> 1L) or ♦ Severe (> 2L). CAUSES Four basic pathologies are
expressed as the four Ts’ (RCOG): Tone (atonicity), Tissue (retained bits, blood
clots), Trauma (genital tract injury) and Thrombin (coagulopathy). ♦ Atonic ♦
Traumatic ♦ Atonicity of the uterus is the commonest cause of postpartum
hemorrhage. With the separation of the placenta,

the uterine sinuses, which are torn, cannot be compressed effectively due to imperfect
contraction and retraction of the uterine musculature and bleeding continues. The
following are the conditions, which often interfere with the retraction of the uterus as
a whole and of the placental site in particular. — Grand multipara—Inadequate
retraction and frequent adherent placenta contribute to it. Associated anemia may also
probably play a role. — Overdistension of the uterus as in multiple pregnancy,
hydramnios and big baby (>4 kg). Imperfect retraction and a large placental site are
responsible for excessive bleeding. — Malnutrition and anemia (12 hours): Poor
retraction, infection (amnionitis), dehydration are important factors (Tone). —
Anesthesia: Depth of anesthesia and the anesthetic agents (ether, halothane) may
cause atonicity. — Initiation or augmentation of delivery by oxytocin: Postdelivery
uterine atonicity is likely unless the oxytocin is continued for at least one hour
following delivery. — Malformation of the uterus: Implantation of the placenta in the
uterine septum of a septate uterus or in the cornual region of a bicornuate uterus may
cause excessive bleeding. — Uterine fibroid causes imperfect retraction mechanically.
— Mismanaged third stage of labor: Tis includes—(a) Too rapid delivery of the baby
preventing the uterine wall to adapt to the diminishing contents, (b) Premature attempt
to deliver the placenta before it is separated, (c) Kneading and fiddling the uterus, (d)
Pulling the cord. All these produce irregular uterine contractions leading to partial
separation of placenta and hemorrhage, (e) Manual separation of the placenta
increases blood loss during cesarean delivery. — Placenta: Morbidly adherent
(accreta, percreta), partially or completely separated and/or retained cause PPH. —
Precipitate labor: In rapid delivery, separation of the placenta occurs following the
birth of the baby. Bleeding continues before the onset of uterine retraction. Bleeding
may be due to genital tract trauma also Similarly, blood loss in cesarean section
amounting to 800–1000 mL is most often ignored. Trauma involves usually the
cervix, vagina, perineum (episiotomy wound and lacerations), and paraurethral region
and rarely, rupture of the uterus occurs. Te bleeding is usually revealed but can rarely
be concealed (vulvovaginal or broad ligament hematoma).

Retained tissues: Bits of placenta, blood clots cause PPH due to imperfect uterine
retraction. t Combination of atonic and traumatic causes. Thrombin: Blood
coagulation disorders, acquired or congenital, are less common causes of postpartum
hemorrhage. The blood coagulopathy may be due to diminished procoagulants
(washout phenomenon) or increased fbrinolytic activity. The firmly retracted uterus
can usually prevent bleeding. Te conditions where such disorders may occur are
abruptio placentae, jaundice in pregnancy, thrombocytopenic purpura, severe
preeclampsia, HELLP syndrome or in IUD . Specifc therapy following coagulation
screen including recombinant activated factor VII (rF VIIa) may be given.
DIAGNOSIS AND CLINICAL EFFECTS: In the majority, the

vaginal bleeding is visible outside, as a slow trickle. Rarely, the bleeding is totally
concealed as either vulvovaginal or broad ligament hematoma. The effect of blood
loss depends on—(a) Predelivery hemoglobin level, (b) degree of pregnancy induced
hypervolemia and (c) speed at which blood loss occurs. Alteration of pulse, blood
pressure and pulse pressure appears only after class 2 hemorrhage (20–25% loss of
blood volume). On occasion, blood loss is so rapid and brisk that death may occur
within a few minutes. State of uterus, as felt per abdomen, gives a reliable clue as
regards the cause of bleeding. In traumatic hemorrhage, the uterus is found well
contracted. In atonic hemorrhage,the uterus is found flabby and becomes hard on
massaging. However, both the atonic and traumatic cause may coexist. Even
following massive blood loss from the injured area, a state of low general condition
can make the uterus atonic.

MANAGEMENT Immediate measures are to be taken by the attending house officer

(doctor/midwife). „ Call for extra help—involve the obstetric registrar (senior staff)
on call. „ Put in two large bore (14-gauge) intravenous cannulas. „ Keep patient fat
and warm. „ Send blood for full blood count, group, cross matching, diagnostic tests
(RFT, LFT), coagulation screen including fbrinogen and ask for 2 units (at least) of
blood. „ Infuse rapidly 2 liters of normal saline (crystalloids) or plasma substitutes
like Haemaccel (colloids), an urea-linked gelatin, to reexpand the vascular bed. It does
not interfere with cross matching. „ Give oxygen by mask 10–15 L/min. „ Start 20
units of oxytocin in 1 L of normal saline IV at the rate of 60 drops per minute.
Transfuse blood as soon as possible. „ One midwife/rotating houseman should be
assigned to monitor the following—(i) Pulse (ii) Blood pressure (iii) Temperature (iv)
Respiratory rate and oximeter (v) Type and amount of fluids (blood, blood products)
the patient has received (vi) Urine output (continuous catheterization) (vii) Drugs-
type, dose and time (viii) Central venous pressure (when sited). ACTUAL
MANAGEMENT: Atonic Traumatic Retained tissues Coagulopathy . The first step is
to control the fundus and to note the feel of the uterus. If the uterus is flabby, the
bleeding is likely to be from the atonic uterus. If the uterus is firm and contracted, the
bleeding is likely of traumatic origin. Atonic uterus: Step—I: (a) Massage the uterus
to make it hard and express the blood clot, (b) Methergine 0.2 mg is given
intravenously, (c) Injection oxytocin drip is started (10 units in 500 mL of normal
saline) at the rate of 40–60 drops per minute, (d) Foley catheter to keep bladder empty
and to monitor urine output, (e) To examine the expelled placenta and membranes, for
evidence of missing cotyledon or piece of membranes. If the uterus fails to contract,
proceed to the next step. Step—II: The uterus is to be explored under general
anesthesia. Simultaneous inspection of the cervix, vagina especially the paraurethral
region is to be done to exclude coexistent bleeding sites from the injured area. In
refractory cases: „ Injection 15 methyl PGF2α 250 µg IM in the

deltoid muscle every 15 minutes (up to maximum of 2 mg). OR „ Misoprostol (PGE1

) 1000 µg per rectum is ef ective. „ When uterine atony is due to tocolytic drugs,
calcium gluconate (1 g IV slowly) should be given to neutralize the calcium blocking
ef ect of these drugs

Step—III: Uterine massage and bimanual compression. Step—IV: Uterine

tamponade— It is considered the first line surgical intervention for most women with
atonic PPH. Other Measures: t A non-pneumatic antishock garment may be used
when patient is being transferred to a referral center. t Compression of the abdominal
aorta may be a temporary but effective measure. This allows time for resuscitation
and volume replacement before any surgical intervention is done. Step V: Surgical
methods to control PPH are many. An outline of stepwise uterine devascu larization
procedures are given below: (a) B-Lynch compression suture (1997) and multiple
square sutures: Both these surgical methods work by tamponade (like bimanual
compression) of the uterus . Success rate is about 80% and it can avoid hysterectomy.
(b) Ligation of uterine arteries—the ascending branch of the uterine artery is ligated at
the lateral border between upper and lower uterine segment. In atonic hemorrhage,
bilateral ligation is effective in about 75% of cases.(c) Ligation of the ovarian and
uterine artery anastomosis,(d) Ligation of anterior division of internal iliac artery
(unilateral or bilateral)(e) Angiographic selective arterial embolization (bleeding
vessel. Step VI: Hysterectomy—

SHOCK IN OBSTETRICS DEFINITION: Shock is defined as a state of circulatory

inadequacy with poor tissue perfusion resulting in generalized cellular hypoxia.
PATHOPHYSIOLOGY OF SHOCK: Pathophysiological changes in obstetric shock
are predominantly associated with (a) general changes due to hypovolemia and (b)
specific changes due to liberation of endotoxin. Hypotension stimulates release of
neuroendocrine mediators like adrenocorticotropic hormone (ACTH), growth
hormone (GH), β endorphin, cortisol and glucagon. There is also sympathoadrenal
response. Presence of endotoxin (lipopolysaccharide), in septic shock activates the
leukocytes through complement system. There is release of inflammatory mediators
such as proteases, superoxide (O2 – ), hydroxyl (OH– ) radicals, cytokines,
prostaglandins and many cytotoxic enzymes. These interfere with the function of a
number of enzyme systems and increase capillary permeability. Cytokines such as
interleukines (ILS) and tumor necrosis factor (TNF) interact by autocrine and
paracrine mechanism to cause cellular or organ dysfunction. In presence of hypoxia,
sepsis and acidosis, lysosomal enzymes which are cytotoxic, are released. They can
cause myocardial depression and coronary vasoconstriction. Prostacyclin is a
vasodilator and inhibits platelet aggregation. Thromboxane A2 causes pulmonary
vasoconstriction and platelet aggregation.

Leukotrienes cause vasoconstriction, platelet activation and increased vascular

permeability. Endothelium-derived relaxing factor (EDRF) which is identified as
nitric oxide (NO) is found to produce sustained vasodilatation and hypotension.
Thrombosis is increased due to inhibition of antithrombin III. Thrombocytopenia is
common. Metabolic changes: Hepatic glycogenolysis due to increased level of
glucagon, catecholamine and cortisol leads to hyperglycemia. There is diminished
peripheral utilization of glucose due to increased level of insulin antagonists like
cortisol and growth hormone. Inadequate oxygen supply to tissue initiates anaerobic
metabolism. Consequently there is metabolic acidosis, production of lactic acid and
H+ ions. Sodium pump fails to operate. Finally the lysosomal enzymes are released.
These lead to cell death.

GENERAL CHANGES IN SHOCK (WITH SPECIAL REFERENCE TO

HYPOVOLEMIC SHOCK) There are four phases of changes. The first two phases
are reversible; the third one probably correctable and the fourth is irreversible: First
phase: Sympathetic impulses and the level of circulating catecholamines increase in
response to hypovolemia, cardiogenic or neurogenic stimulus. Stretch receptors
monitoring blood pressure in the carotid sinus and aortic arch supply information to
the vasomotor center via the ninth and tenth cranial nerves. Te vasomotor center
responds by sending eferent impulses through the sympathetic nervous system.
Second phase: As a result of excessive sympathetic stimulus, there is constriction of
the pre- and postcapillary sphincters, resulting in inadequate venous return leading to
diminished cardiac output, clinical manifestations of which are hypotension and
tachycardia. Compensatory mechanisms that operate at this stage, to maintain the
blood pressure has been discussed in the scheme above. These mechanisms attempt to
correct hypovolemia, improve cardiac output and the perfusion of vital organs. At this
stage, transfusion and control of hemorrhage are usually effective in restoring the
normal circulatory balance and tissue perfusion. On the other hand, if bleeding
continues or treatment is delayed, the changes at microcirculatory unit will continue to
persist and will pass onto the third and fourth phases of shock. Third phase: Prolonged
anoxia of the tissues will lead to excessive production of lactic acid (acidosis). Lactic
acid and anoxia cause relaxation of the precapillary sphincters but not the
postcapillary sphincters. In addition, thromboxane A2 and leukotrienes (endogenous
mediators) cause damage to the endothelial cells of the capillaries of the
microcirculatory bed. These lead to formation of thrombus within the capillaries
(diffuse intravascular coagulation) and increased capillary permeability. Fourth phase:
Consequent to persistent constriction of the postcapillary sphincter, blood remains
stagnant within the capillary bed. Fluid from the capillaries leaks into the tissue
spaces due to increased permeability. All fluids administered intravenously will go
into the tissue spaces and circulatory blood volume cannot be restored. Clinically, this
is the stage
of irreversible shock. There is severe loss of systemic vascular resistance, severe
myocardial depression (↓ cardiac output), unresponsive hypotension and ultimately
multiple organ system failure. Systemic inflammatory response syndrome (SIRS) is
manifested by two or more of the following conditions: (i) Temperature > 38°C or <
36°C (ii) HR > 90 bpm (iii) Respiratory rate > 24/min or (iv) PaCO2 < 32 mm Hg or
(v) WBC > 12000/µl or leukopenia: < 4000/µl or more than 10% immature forms.

HEMORRHAGIC SHOCK „ Early phase (Compensatory phase): In the early phase

there is mild vasoconstriction and with the compensatory mechanism operating, the
patient has relatively normal blood pressure but tachycardia. This phase can be easily
managed by volume replacement. „ Intermediate phase (Reversible phase): If the
early phase remains untreated, the patient passes into the state of hypotension. Patient
progressively becomes pale; tachycardia persists and due to intense vasoconstriction,
the periphery becomes cold and there may be sweating. Due to diversion of blood to
vital organs, the patient remains conscious and the urine output is within normal
limits. Still with adequate management, the shock state can be reversed.„ Late stage
(Irreversible): Hypotension continues and cannot be reversed by fluid replacement
(CIRCI). Extremities become cold and clammy because of vasoconstriction due to
sympathetic stimulation. Metabolic acidosis, coagulopathy and thrombocytopenia are
associated. Practically imperceptible low volume pulse, oliguria, mental confusion is
observed. Treatment of any kind is practically useless in this phase and mortality
varies between 3% and 100%.

MANAGEMENT OF SHOCK HEMORRHAGIC SHOCK: Basic management of

hemorrhagic shock is to stop the bleeding and replace the volume which has been lost
. Prompt diagnosis and immediate resuscitation is essential failing which multiple
organ failure develops. „ Restore circulating volume (Infusion and transfusion): Blood
should be transfused especially in hemorrhagic shock as soon as it is available.
Crystalloids , Colloids: Polygelatin solutions (Hemaccel, Gelofusion) are iso-osmotic
with plasma, Dextrans. Hemodynamic monitoring is aimed to maintain systolic BP >
90 and MAP > 60 mm Hg, CVP 12-15 cm H2 O and pulmonary capillary wedge
pressure 14-18 mm Hg. „ Administration of oxygen to avoid metabolic acidosis: In
the initial phase, administration of oxygen by nasal cannula at a rate of 6-8 liters per
minute is enough but in the later phases, ventilation by endotracheal intubation may
be necessary. Oxygen delivery should be continued to maintain O2 saturation > 92%,
PaO2 80-100 mm Hg, PaCO2 30-35 mm Hg and pH > 7.35. Endotracheal intubation
and mechanical ventilation may be needed for patients with septic shock. Indications
of mechanical ventilation are : severe tachypnea (RR > 40/min), altered mental status,
severe hypoxemia, despite O2 supplementation. Hemorrhage: Specific surgical and
medical treatment for

control of hemorrhage should start along with the general management of shock..
Monitoring: Clinical parameters like skin temperature, visible peripheral veins can be
helpful to assess the degree of tissue perfusion. Urine output (> 30 mL/hr) is a useful
guide. Arterial blood pressure is a poor indicator to assess tissue perfusion.