Introduction:

Shock is a life-threatening condition of circulatory

failure that most commonly presents with
hypotension. It can also be heralded by other vital
sign changes or the presence of elevated serum
lactate levels. The effects of shock are initially
reversible but can rapidly become irreversible,
resulting in multi-organ failure (MOF) and death.
 Definition:
Shock is defined as a state of circulatory inadequacy
with poor tissue perfusion resulting in generalized
cellular hypoxia.
The series of changes observed in shock and their clinical
manifestations, are therefore, dependent on two sets of
changes:
 Circulatory inadequacy at the ‘filtration’ level
(microvascular compartment)
 Cellular damage and ultimately death.
 Classification:

1)HYPOVOLEMIC SHOCK-
Associated with post partum or post abortal haemorrhage,
ectopic pregnancy, placenta previa, abruption placentae,
rupture of the uterus and obstetric surgery.
 Fluid loss shock
 Supine hypotension syndrome
 Shock associated with disseminated intravascular
coagulation
 Classification of hemorrhagic shock (based on total
blood volume)
Parameter Class I Class II Class III Class IV
Blood volume loss % (ml) ≤15 15-30 30-40 >40
(750-1500) (1500-2000) (>2000)
Heart Rate No Tachycardia Moderate Marked tachycardia
change tachycardia
Respirations Normal Tachypnea Tachypnea Marked Tachypnea
Mean arterial pressure Normal Mildly <60 mm Hg Decreased
decreased
Cardiac output Normal Mildly reduced Reduced Markedly reduced
Systemic vascular Normal Increased Increased Increased
resistance
Urine output(ml/hr) >30 20-30 5-15 Anuric
Mental status Normal Anxious Confused Obtunded
JOURNAL STUDY 1:
 2) SEPTIC SHOCK (endotoxic shock):
 Associated typically with septic abortion, chorio amnionitis,
pyelonephritis, and rarely postpartum endometriosis.
Causes:
 Septic Abortion
 PROM
 Trauma
 Post operative endomyometritis
 Retained placenta
 Puerperal sepsis
 Pyelonephritis
 Ogranisms: E.Coli /proteus/pseudomonas/ bacteroids
 Cont…..

Signs and symptoms:

 Hypotension
 Tachycardia
 Pyrexia
 Rigors
 Cold skin
 Cyanosis
 3) CARDIOGENIC SHOCK
 Pump failure due to myocardial inefficiency, for example
myocardial infarction and cardiac arrhythmias.
 The basic element here is the failing heart which cannot
cope with the normal venous return and thus the central
venous pressure (CVP) becomes elevated.
 The left ventricle is not able to pump sufficient blood to
meet the metabolic demands of the tissues
 There will be tachycardia, hypervolemia, pulmonary venous
congestion and generalized edema. Inadequate oxygen
delivery leads to cellular damage, multiorgan failure and
death.
 Cont.….
Clinical features:
charecterized by decreased systolic pressure (<80mm of Hg),
decreased cardiac index,(1.8 L/min/m2) and increased left
ventricular filling pressure(>18 mm of Hg).
 Distended neck veins,
 dyspnea,
 tachypnea,
 the presence of a third heart sound,
 systolic or diastolic murmurs
 Generalized edema.
 Cont.….

 Peripartum cardiomyopathy, an idiopathic disorder that occurs

during the last month of pregnancy and upto 6months
postpartum is another cause. In this condition, mortality is up
to 50%, mostly due to congestive cardiac failure.
 Coronary artery disease is uncommon in reproductive aged
women, but Myocardial Infarction has occurred because of the
excessive hemodynamic stress of pregnancy. Management of
coronary artery disease in a pregnant patient is similar to that
in a non-pregnant patient.
89 Cardiogenic shock in pregnancy: Analysis from the national inpatient sample:
Medical complications of pregnancy related to hypertensive syndromes
 4) NEUROGENIC SHOCK:
 Chemical injury: associated with
aspiration of gastric contents
during general anesthesia specially
in LSCS (Mendelson’s syndrome)

 Drug induced: associated with spinal anesthesia.

 Cont…..
Pathophysiology:
Disruption of sympathetic nervous system
Loss of sympathetic tone para sympathetic system response
Venous and arteriolar vasodialation
Decreased in BP
Decreased venous return decreased heart rate
Decreased stroke volume
Decreased cardiac output
Decreased cellular O2 supply
Decreased tissue perfusion
Impaired cellular metabolism
 Common causes of obstetric
shock:

 Blood loss associated with antepartum and postpartum bleeding

(hypovolemic)
 Trauma and operative delivery
 Uterine rupture
 . Uterine inversion, hypovolemic and neurogenic
In all these cases, when a patient is dehydrated and exhausted from
prolonged labor, she withstands blood loss and trauma poorly.
Also, when anaesthetized, the compensatory mechanisms are
depressed and the shock may appear to worsen quite suddenly.
 Cont…..
 General anesthetic accidents-
 Cardiac arrest or arrhythmias (cardiogenic)
 Acid aspiration(neurogenic and hypovolemic)
 Drug anaphylaxis
 Bacteremic shock
 Septic abortion
 Prolonged rupture of membranes
Embolism
 Air embolism
 Amniotic fluid(anaphylactic)
 Cont.…..
Cardiac failure
 Rheumatic heart disease
 Cerebrovascular accident(CVA) and eclampsia
Others:
 Spinal anaesthesia
 Drug anaphylaxis (especially local anesthetics)
 Adrenal insufficiency
 Postoperative vomiting or ileus
 Stages of Shock:
1) COMPENSATED NONPROGRESSIVE SHOCK:
 Lowering of BP leads to an increase in the sympathetic responses.
 Vasoconstriction in the periphery.
 Vasoconstriction to the kidneys leading to decreased urinary
output.
 Release of epinephrine and norepinephrine
 Increased heart rate and increase in cardiac output.
 Release of aldosterone to reabsorb Na+ and water
 Release of antidiuretic hormone (ADH) to reabsorb water
 Hypoxia leads to an increase of blood flow to the tissue
 Cont.….

2) DECOMPENSATED PROGRESSIVE SHOCK:

 Loss of more than 15-20% of blood volume and the
detoriation of the cardiovascular system.
 Decreased of BP below 60mm Hg leads to myocardial
ischemia and a decreased cardiac output
 Decreased of BP below 50mm Hg leads to general
vasodilatation causing further lowering of BP.
 Increased hypoxia leads to the increased permeability of
the capillaries causing the loss of blood plasma into the
tissue decreasing blood volume.
 Cont.….

 Intravascular clotting- Decrease in blood volume leads

to lowering of velocity of the blood and increase
viscosity. The platelets tend to aggregate in the vessel
leading to clot formation
 Lactic acid build up leads to acidosis with pH dropping to
7.30 or below
IRREVERSIBLE SHOCK:
 Heart deteriorates until it can no longer pump and
possibly a terminal.
 Clinical Manifestations:

Features that are highly suspicious of shock

include:
 Hypotension
 Tachycardia
 Oliguria
 Abnormal mental status
 Tachypnea
 Cool, clammy, cyanotic skin
 Metabolic acidosis
 Assessment in Shock:

 The clinical picture of the pale, cold and clammy, shivering, and
confused patient is of value in hypovolaemic shock.
 The blood pressure is often unreliable because of the wide individual
variation and also considerable blood may be lost insidiously without
a marked fall in blood pressure.
 The pulse may be a better indicator at times than the BP.
 CVP, the most valuable information is obtained from the CVP
readings. It is also a good guide to the volume and rate of
transfusion, especially in cases with occult (concealed) bleeding, for
example accidental hemorrhage
 Cont….

 Urinary output: If the circulation to the kidneys is adequate then

there will be minimum urinary output of 25ml/hr. Catheterization
in shocked patients to monitor this output accurately is of great
value.
 Clinical estimation of blood loss is notoriously inaccurate but may
be helped by swab weighing.
 Acid-base studies to provide accurate correction of acidosis.
 Blood coagulation studies may be helpful in suspected cases.
 Electrolytes and urea in those where fluid and electrolyte loss is
predominant.
 Practical management of obstetric shock:

DIAGNOSIS:
Antenatal-
 Blood loss-Antepartum hemorrhage, Abortion, Concealed
accidental hemorrhage
 Bacteraemia, any evidence of unsafe abortion
 Pulmonary embolism, any predisposing factors such as
prolonged bed rest
 Nonobstretic cause, cardiac failure and diabetic coma.
 Cont.….
Labor and immediate postpartum period-
 Blood loss+ trauma-PPH, difficult operative delivery
 Occult-Uterine rupture, Uterine inversion, Hematoma, broad
ligament & paravaginal
 Any drug that could cause anaphylaxis
 Embolism, air, blood thrombus or amniotic fluid
 CVA and look for localizing signs in the central nervous system.
 Bacteraemia, prolonged rupture of membranes
 Bleeding disorders
 Cardiac
 Spinal or epidural
 Cont…..

Peurperium-
 Hemorrhage
 Pulmonary embolism, remembers that this can occur in
the early days of the peurperium
 Bacteraemic, puerperal infection
 CVA
 Postoperative intestinal obstruction, acute dilation of
the stomach
 Management of shock:

1)HEMORRHAGIC SHOCK:
a) Infusion and transfusion: Colloids:
Polygelatin solutions ( Haemaccel, gelofusion) are iso osmotic with plasma. They
donot interfere with the coagulation system. Large volumes can be administered.
They promote osmotic dieresis. Dextrans: they are polymolecular poly
saccharides. They interfere with cross matching, so they are avoided.
b) Maintenance of cardiac activity: to maintain systolic BP>90 mm of Hg, mean
arterial pressure more than or equal to 60 mm of Hg, CVP 12-15 cm of water and
pulmonary capillary wedge pressure 14-18 mm of Hg.
c) Administration of oxygen to avoid metabolic acidosis: To maintain the
oxygen saturation >92%, Pa O280-100 mm of Hg, Pa CO2 30-35 mm of Hg and
PH>7.35
 Cont.…..

d) Pharmacological agents: use of vasopressor drugs should be kept to a

minimum, since peripheral vasoconstriction is already present.
e) Control of hemorrhage: specific surgical and medical treatment for control
of hemorrhage should start along with the general management of shock.

f) Monitoring
 Visible peripheral veins can be helpful to assess the degree of tissue
perfusion. Urine flow of atleast 30ml/hr preferably 60ml/hr should be
maintained.
 In critically ill patients, measurement of CVP is needed. Pulse oximeter and
blood gas analysis are useful to assess tissue perfusion. Measurement of PAWP
can be done by using a Swan-ganz catheter.
JOURNAL ARTICLES 3: Obstetric hemorrhage and shock management: using the low technology Non-
pneumatic Anti Shock Garment in Nigerian and Egyptian tertiary care facilitie s
Non-pneumatic anti-shock garment
 Cont….

2) ENDOTOXIC SHOCK:
a)Antibiotics: endotoxic shock is most commonly due to gram
negative organisms, so proper antibiotics should be administered in
adequate doses.
Ampicillin IV every 6 hours. Gentamycin 2mg/kg IV loading dose
followed by 1.5 mg/kg IV every 8 hourly) and metronidazole 500mg
IV every 8hours is a good combination to start with.
Alternative regimen is to give ceftazidime IV every 8hours combined
with Gentamycin. Clindamycin 600mg IV infusion is an alternative to
metronidazole.
 Cont.….
b) Intravenous fluids and electrolytes:
c) Correction of acidosis:
Bicarbonate can be administered to correct persistent metabolic
acidosis.(PH<7.2)A reasonable first dose should be 50-100mEq(60-
100ml of 7.5%) of sodium bicarbonate solution. Further doses will
depend on the clinical state and ABG analysis.
d) Maintenance of BP:
e) Inotropic agents: when MAP< 60mm of Hg and impaired perfusion
of vital organs
e.g Adrenaline, Noradrenaline, Dopamine, Dobutamine etc. Dopamine
is the drug of choice (1-3micro gram/kg body weight).
 Cont.…

f) Vasodilator therapy: if MAP>70mm of Hg afterload reduction may

improve stroke volume and reduce ventricular wall tension. Drugs used are
sodium nitro prusside and nitroglycerine.
g) Diuretic therapy: to reduce fluid overload and pulmonary edema. Drug
is frusemide.
h) Corticosteroids: in specific conditions the dose recommended in septic
shock is 50mg/kg body weight.
i) Treatment of myocarditis: sometimes this occurs in septic shock.
Digitalis can be administered when there is no signs of congestive cardiac
failure.
 
 Cont.…

Elimination of source of infection: Hysterectomy can be

done in unresponsive endotoxic shock following septic
abortion and puerperal sepsis.
j) H2 blockers: Ranitidine can be given to prevent stress
induced bleeding and ulceration of gastric mucosa.
h) Nutritional support: Oral or parenteral nutrition to
provide a calorie of 20-30Kcal/kg/day with fat and
carbohydrate is optimum.
 Nursing
management:
1)Decreased cardiac output related to actual or
potential hypovolemia secondary to shock
2)Ineffective Uteroplacental tissue perfusion
related to hypovolemia.
3)Risk for maternal injury related to blood loss.
4)Fear regarding self, fetus and outcome of
pregnancy
 VASA PREVIA
Definition — Vasa previa refers to a condition in which the
umbilical vessels course through the fetal membranes of the lower
uterine segment and lie over the internal os of the cervix in front of
the presenting part.
It is a rarely reported condition in which fetal blood vessels from
the placenta or the umbilical cord cross the entrance to the birth
canal, beneath the baby.
 Cont…
Prevalence — The prevalence of vasa previa is
approximately 1 in 2500 deliveries, but is much higher in
pregnancies conceived following use of assisted
reproductive technologies (prevalence as high as 1 in 202).
The prevalence is also increased in second-trimester low-
lying placentas or placenta
previa (even if resolved),bilobed or
succenturiate lobe placentas in the lower
uterine segment, and multiple gestations.
 Cont.…

Pathogenesis — Pathogenesis is unknown, but is likely similar to

that for velamentous cord insertion. Resolution of placenta previa or
low-lying placenta may result in type I vasa previa.
 Cont.….

Risk factors — 
Risk factors for vasa previa are not independent and include
velamentous cord insertion, umbilical cord insertion in the
lower part of the uterus at first-trimester ultrasound,
placenta previa or low-lying placenta on second-trimester
ultrasound scan, succenturiate placental lobe or bilobed
placenta .
The placental location and the relationship between the
placenta and internal cervical os should be evaluated carefully
in these patients.
 Cont.….

Etiology-
 The succenturate lobe of placenta
 Low lying placenta
 A velamentous insertion of the cord
 Multiple pregnancy
 IVF pregnancies
 History of uterine surgeries or
D& C bleeding
 Cont.…..
Clinical picture:
 Fetal bradycardia when the vessels are compressed
 Vaginal hemorrhage when the vessels are torn
Imaging — 
On ultrasound examination, vasa previa appears as a linear
sonolucent area that passes over the internal os. Color
Doppler flow mapping showing umbilical artery or vein
waveforms confirms that the sonolucency is a blood vessel.
 Cont.….

Physical examination — 
Rarely, pulsating vessels in the membranes overlying the cervical os
are palpable on digital examination.
Pathology — 
Pathological examination may reveal membranous vessels, but
otherwise is not useful since the pathologist cannot determine the
location of the placenta and cord in the uterus.
 Cont.….

Diagnosis:

Real-time transvaginal ultrasound examination with color

Doppler
Close proximity has been defined as within 2 cm of the
internal os; however, only limited data are available to support
this specific measurement.
Magnetic resonance imaging can be used to clarify the
ultrasound diagnosis if there is diagnostic uncertainty and
confirmation will affect pregnancy management.
 Cont.…..

In the absence of prenatal sonographic diagnosis, a clinical

diagnosis of vasa previa should be suspected in the setting of
vaginal bleeding that occurs upon rupture of the membranes
and is accompanied by fetal heart rate abnormalities,
particularly a sinusoidal pattern or bradycardia.
Confirmation that the blood is fetal via APT, Kleihauer- Betke
tests, or other tests (Ogita ) supports the diagnosis ; however,
there is usually no time to wait for test results before
performing an emergency cesarean delivery for fetal distress.
 Cont.…..

Screening — 
Women with placenta previa (even if resolved) or a low lying
placenta on Midtrimester ultrasound examination should
undergo transvaginal ultrasound with color and pulsed
Doppler at 32 weeks of gestation to screen for vasa previa.
 Cont.….

Management — 
There are no high-quality data on which to base recommendations
for optimal timing of antenatal corticosteroid administration,
antenatal fetal monitoring, hospitalization, and scheduled delivery.
 Strict bed rest
 Hospitalization(3rd trimester)
 Steroids to promote lung maturity
 Elective cesarean section at 35 weeks of gestation
 Cont.…..

Antepartum — 
If vasa previa is identified on prenatal ultrasound
examination, treatment begin with weekly Nonstress testing
on outpatients at 32 weeks of gestation to look for any
evidence of cord compression.
Because of the increased risk of emergency preterm
delivery in the third trimester, betamethasone between 28
and 32 weeks of gestation and hospital admission between
30 and 34 weeks of gestation. Hospitalization allows for
close surveillance for signs of cord compression
 Cont.…..

Delivery —Deliver the fetus by emergency cesarean

delivery if any of the following occur:
●Labor
●Premature rupture of membranes
●Repetitive variable decelerations refractory to tocolysis
●Vaginal bleeding accompanied by fetal tachycardia, a
sinusoidal heart rate pattern, or evidence of pure fetal
blood by Apt test or Kleihauer-Betke assessment
 Cont.….
 There is no clear evidence to recommend a different approach in
twin pregnancies with vasa previa. Earlier scheduled delivery at
32 or 33 weeks is reasonable if imminent delivery seems likely
because of a short cervix or threatened preterm labor. In two
series, the median gestational age at delivery for twin
pregnancies with vasa previa was 32 to 33 weeks of gestation.
 Ideally, the hysterotomy should avoid aberrant blood vessels. If
a fetal vessel is lacerated inadvertently during delivery, the cord
should be clamped immediately to prevent fetal/neonatal blood
loss.
 NURSING CARE PLAN

1) Ineffective tissue perfusion related to excessive

blood loss secondary to decreased placental
circulation
2) Anxiety related to unexpected occurrences
3) Risk for injury (fetal) related to reduced placental
perfusion secondary to vasospasm
4) Risk for injury (maternal) related to operative
procedures
Journal Article 4
 Journal article 5:Vasa previa: diagnosis and management 

OBJECTIVE: The purpose of this study was to investigate the diagnostic and management strategies for this potentially
catastrophic entity and to describe further maternal and placental risk factors that may aid in the establishment of a
screening protocol for vasa previa.
STUDY DESIGN: This was a retrospective multicenter descriptive study that included all pregnancies that were
complicated by vasa previa that delivered between January 1, 2000, and December 31, 2012. Nine maternal fetal medicine
practices and the hospitals in which they practice participated in data collection of diagnosis, treatment, and maternal-
neonatal outcomes.
RESULTS: Sixty-eight pregnancies were identified that included the diagnosis of vasa previa or "possible vasa previa"
either in the ultrasound record or in the hospital record at the time of delivery. Four cases (5.8%) appeared to resolve on
repeat ultrasound examination. Fifteen of the 64 cases that were suspected of having vasa previa could not be verified or
were not documented at delivery. Of the remaining 49 cases, where vasa previa was documented, 47 cases (96%) were
diagnosed by ultrasound scanning antenatally. Known risk factors for vasa previa were present in 41 of 47 cases (87%). Of
the 49 cases, 41 were delivered by planned cesarean delivery at a mean gestational age of 34.7 weeks, and 8 cases
required emergent cesarean delivery at a mean gestational age of 34.6 weeks (range, 32.4-36.0 weeks gestation) . Seven of
these emergent cesarean deliveries had been diagnosed previously; 1 case had not. All of the emergent cesarean deliveries
were for vaginal bleeding; 1 case was also for a concerning fetal heart rate, but only 1 of the known cases had a
documented ruptured fetal vessel. None of these cases were found to have cervical shortening before the onset of
bleeding. One of the undiagnosed cases resulted in a ruptured fetal vessel and a baby with no heart beat at birth who
survived but had periventricular leukomalacia at 1 month of age with mild white-matter atrophy. Of the remaining
neonates in this group, there were no deaths and no major complications beyond mild respiratory distress syndrome in 9
cases. There were no other major neonatal complications, which included no cases of periventricular leukomalacia, neonatal
sepsis, necrotizing enterocolitis, or any grade of intraventricular hemorrhage in the confirmed cases of vasa previa.