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SEPTIC SHOCK AND
DISSEMINATED INTRAVASCULAR
COAGULATION IN PREGNANCY
DIC
Consumptive coagulopathy
 a pathological activation of coagulation (blood
clotting) mechanisms that happens in response to
a variety of diseases
 a situation of inappropriate coagulation within
the blood vessels which leads to the consumption
of clotting factors, thus resulting in the failure of
the clotting mechanism at the site of bleeding
 leads to the formation of small blood clots inside
the blood vessels throughout the body

DIC
As the small clots consume coagulation proteins
and platelets, normal coagulation is disrupted
and abnormal bleeding occurs
 The small clots also disrupt normal blood flow to
organs such as the kidneys
 can occur acutely but also on a slower, chronic
basis, depending on the underlying problem
 common in the critically ill, and may participate
in the development of multiple organ failure,
which may lead to death

DIC
Begins with an event that triggers widespread
clotting with the formation of microthrombi
throughout the circulation
 Triggers fibrinolysis, which is the bodies’response
to the abnormal clotting by attempting to break
up the unneeded clots
 Production of FDPs that further reduce the
efficiency of normal clotting process

If DIC occurs during or after delivery, the
reduced level of clotting factors and the presence
of FDPs prevent normal hemostasis at the
placental site
 FDPs inhibit myometrial action and prevent the
uterine muscle from constricting the blood
vessels in a normal way
 Torrential hemorrhage may be the outcome, and
even if clotting does occur, the clot is unstable
 Microthrombi in the bloodstream may cause
circulatory obstruction in the small blood vessels
and lead to cyanosis of fingers and toes to CVAs,
or organ failure

ABRUPTIO PLACENTA
ABRUPTIO PLACENTA
Premature separation
of the normally
implanted placenta
 Occurs in 1 in 200
deliveries
 Can cause concealed
or external
hemorrhage

ABRUPTIO PLACENTA

Concealed hemorrhage
Effusion of blood behind the placenta but with intact
margins
 Completely separated placenta with membranes still
attached to the uterine wall
 Blood gains access to the
amniotic cavity after breaking
through the membranes
 Fetal head closely applied to
the lower uterine segment that
the blood cannot make its way
past it

ABRUPTIO PLACENTA

Symptoms:
Vaginal bleeding
 Hypertonic uterus
that is tender on
palpation
 Fetal heart rate
deceleration

ABRUPTIO PLACENTA

1.
2.
3.
4.
5.
6.
7.
8.
9.
Risk Factors:
Increased age and parity
Preeclampsia/ chronic HPN
PROM
Multifetal gestation
Hydramnios
Cigarette smoking
Prior abruption
External trauma
Leiomyomas
ABRUPTIO PLACENTA

Pathology
Hemorrhage into the decidua basalis
 The decidua splits leaving a thin layer adherent to
the myometrium
 Development of decidual hematoma that leads to
separation, compression, and the ultimate
destruction of the placenta adjacent to it
 Rupture of decidual spiral artery causing a
retroplacental hematoma

ABRUPTIO PLACENTA
Bleeding is almost always maternal
 Significant fetal bleeding occurs in traumatic
abruption which results from a tear or fracture in
the placenta rather than from the placental
separation

ABRUPTIO PLACENTA

Complications:
Shock – occurs in
proportion to blood
loss
 Uteroplacental
apoplexy

Couvelaire uterus
 Widespread
extravasation of blood
into the myometrium
and serosa
 Not an indication for
hysterectomy

ABRUPTIO PLACENTA

Complications:

DIC



Placental abruption causes damaged tissue at placental site
and large quantities of thromboplastins are released into
the circulation, resulting in large scale clotting throughout
the system, not just placental site
Overt hypofibrinoginemia with increase levels of fibrinogenfibrin degradation products
Fibrin may in turn cause small blood vessel occlusion
resulting in tissue necrosis, occuring more often in the
glomerular capillaries causing acute renal failure
ABRUPTIO PLACENTA

Management








Nasal oxygen
IV hydration
Prepare blood for possible transfusion
Evaluate hematologic and clotting studies (CBC, PT,
aPTT, Fibrinogen, platelet count)
Monitor urine output
Continuous fetal heart rate monitoring
Amniotomy
Delivery of the baby
ABRUPTIO PLACENTA

Management

Delivery of the baby


Vaginal delivery – if the fetus is dead and the mother is
hemodynamically stable and with controlled
vaginal bleeding
Cesarean delivery
Evidence of fetal compromise
Severe uterine hypertonus
Life threatening vaginal bleeding
DIC when vaginal delivery is not imminent
INTRAUTERINE FETAL DEATH
INTRAUTERINE FETAL DEATH



May be secondary to abortion, abruptio placenta
or other pregnancy-related complications
Consumptive coagulopathy usually occurs when
the dead fetus is retained in utero for 4weeks or
more
Hypofibrinogenimia with increase serum fibrin
degradation products with or without decrease
platelet count
INTRAUTERINE FETAL DEATH


retained fetus of more than 3 or 4 weeks causes
thromboplastins to be released from the fetal
tissue, into the maternal circulation, causing the
onset of clotting problems
widespread clotting with the formation of
microthrombi throughout the circulation

triggers fibrinolysis and FDP production

The FDPs reduce the efficiency of normal clotting
INTRAUTERINE FETAL DEATH

Management
Delivery of the dead fetus
 Correction of hematologic and clotting problems
 Blood transfusion
 Antibiotics

PREECLAMPSIA
PREECLAMPSIA


Pregnancy-specific syndrome of reduced organ
perfusion secondary to vasospasm and
endothelial activation
Minimum criteria:
BP>/= 140/90 after 20 weeks AOG
 Proteinuria >/= 300mg/24hrs or >/= +1 dipstick

PREECLAMPSIA

Increase severity of preeclampsia






DBP >/= 110 mmHg
Proteinuria >/= +2 dipstick
+ headache, visual disturbances, upper abdominal
pain
Elevated liver enzymes and serum creatinine
Thrombocytopenia < 100,000/mm3
Pulmonary edema
PREECLAMPSIA

Epigastric or RUQ pain
Hepatocellular necrosis, ischemia, and edema that
stretches the Glisson’s capsule
 Hepatic infarction and hemorrhage or catastrophic
rupture of a subcapsular hematoma
 Accompanied by elevated serum liver enzymes
 A sign to terminate pregnancy


Thrombocytopenia

Caused by platelet activation and aggregation as well
as microangiopathic hemolysis induced by severe
vasospasm
PREECLAMPSIA

DIC and preeclampsia
unknown, and unclear precursor to DIC
 patients have higher amounts of FDPs in the blood
and urine than others
 Thrombocytopenia, increase intravascular
coagulation and erythrocyte destruction can
contribute to the development of DIC
 increase fibrinolysis and increase production of
FDPs

AMNIOTIC FLUID EMBOLISM
AMNIOTIC FLUID EMBOLISM
Characterized by the abrupt onset of
hypotension, hypoxia, and consumptive
coagulopathy
 thought to occur when amniotic fluid , fetal cells,
hair, or other debris enter the maternal
circulation
 Overall incidence ranges from 1 in 8,000 to 1 in
80,000 pregnancies

AMNIOTIC FLUID EMBOLISM
75 % of survivors are expected to have long-term
neurologic deficits.
 If the fetus is alive at the time of the event,
nearly 70 % will survive the delivery but 50% of
the survived neonates will incur neurologic
damage.

RISK FACTORS
Advanced maternal
age
 Multiparity
 Meconium
 Cervical laceration
 Intrauterine fetal
death
 Uterine tetanic
contractions
 Precipitate labor

Placenta accreta
 Polyhydramnios
 Uterine rupture
 Maternal history of
allergy or atopy
 Chorioamnionitis
 Macrosomia
 Male fetal sex
 Oxytocin
(controversial)

AMNIOTIC FLUID EMBOLISM

Pathophysiology

Phase 1: Pulmonary and systemic HPN
Amniotic fluid and fetal cells enter the maternal
circulation  biochemical mediators 
pulmonary artery vasospasm 
pulmonary hypertension

elevated right ventricular pressure 
hypoxia  myocardial and pulmonary
capillary damage
 left heart failure 
acute respiratory distress syndrome
AMNIOTIC FLUID EMBOLISM

Pathophysiology

Phase 2
 biochemical mediators 
DIC 
Hemorrhagic phase characterized by massive
hemorrhage and uterine atony.
AMNIOTIC FLUID EMBOLISM

Clinical Presentation
(1) Respiratory distress
(2) Cyanosis
(3) Cardiovascular collapse (cardiogenic shock)
(4) Hemorrhage
(5) Coma.
CLINICAL PRESENTATION
A sudden drop in O2 saturation can be the initial
indication of AFE during c/s.
 More than 1/2 of patients die within the first
hour.
 Of the survivors 50 % will develop DIC which
may manifest as persistent bleeding from incision
or venipuncture sites.
The coagulopathy typically occurs 0.5 to 4 hours
after phase 1.

AMNIOTIC FLUID EMBOLISM

Pathogenesis:

Amniotic fluid enters the maternal circulation as a
result of a breach in the physiological barrier that
normally exists between maternal and fetal
compartments

Amniotic fluid abnormally enters the maternal
venous system via the endocervical veins, the
placental site (if placenta is separated), or a uterine
trauma site
AMNIOTIC FLUID EMBOLISM

Diagnosis:

Detection of squamous
cells or other debris of
fetal origin in the
central pulmonary
circulation

Clinical by identifying
characteristic signs
and symptoms
AMNIOTIC FLUID EMBOLISM

Management:

Restoration of cardiovascular and pulmonary
equilibrium
- Maintain systolic blood pressure
>90 mm Hg.
- Urine output > 25 ml/hr
- Arterial pO2 > 60 mm Hg.
Re-establishing uterine tone
 Correct coagulation abnormalities

There are no data that supports that any type of
intervention improves maternal prognosis with
amniotic fluid embolism
AMNIOTIC FLUID EMBOLISM

DIC and AFE

Release of thromboplastins from the amniotic fluid
into the maternal circulation

Increase fibrinoloysis

Increase FDPs that further impairs the clotting
mechanism
SEPSIS SYNDROME
Induced by a systemic inflammatory response to
bacteria or their by-products such as endotoxins
or exotoxins
 Most commonly due to:
1. Acute pyelonephritis
2. Chorioamnionitis
3. Puerperal infection
4. Necrotizing fasciitis

ACUTE PYELONEPHRITIS
ACUTE PYELONEPHRITIS
1.
2.
3.
4.
5.
6.
shaking chills
fever (T>38oC)
flank pain
nausea and vomiting
with or without signs and symptoms of lower
urinary tract infections
Costovertebral angle tenderness
ACUTE PYELONEPHRITIS

Diagnosis:
Urinalysis: pyuria >/= 5 wbc/hpf of centrifuged urine
 Urine culture and sensitivity

Bacteriuria >/= 10,000 cfu of a uropathogen/ml of urine
 Escherichia coli – most common isolate (75-80%)
 Klebsiella pneumoniae (10%)
 Enterobacter or Proteus (10%)

ACUTE PYELONEPHRITIS

Management:





Hospitalization
Urine culture and sensitivity
CBC, serum creatinine
Empiric treatment with IV antibiotic
Post treatment urine culture
CHORIOAMNIONITIS
CHORIOAMNIONITIS
Denotes histologic infection wherein
microorganisms and PMNs reside in the layers
between the chorion and the amnion
 Applies only to pregnancies in which the fetus
has achieved viability, to differentiate it from
septic abortion

CHORIOAMNIONITIS

Diagnosis: Clinical History – Risk Factors






First pregnancy
Young age
Preterm labor (10x increase risk)
Prelabor rupture of membranes (10x increase risk)
Ruptured membranes >12 hours
Prolonged active phase of labor
Primigravid >12 hours
 Multigravid >8 hours


Use of intrauterine monitors
CHORIOAMNIONITIS

Diagnosis: Clinical History – Risk Factors
Frequent and numerous vaginal examinations (>6
times)
 Presence of meconium in the AF (4x increase risk)
 History of untreated or inadequately treated
abnormal vaginal flora

CHORIOAMNIONITIS

Diagnosis: Physical Examination
Presence of 2 out of 3 clinical signs
1. Maternal fever – oral temp >37.8oC

- hallmark for the diagnosis
2.
3.
Uterine tenderness
Persistent fetal tachycardia
CHORIOAMNIONITIS

1.
Treatment
Antimicrobial therapy




Should be given at the time of diagnosis
Ampicillin is the drug of choice for fetal therapy
Aminoglycoside is given as maternal therapy to prevent
development of septic shock from Enterobacteriaceae
If foul smelling amniotic fluid is present, give
Metronidazole for anaerobic coverage
CHORIOAMNIONITIS

2.
Treatment
Delivery


Chorioamnionitis is an indication for delivery but is
not an indication for cesarean birth
CS is indicated if there is fetomaternal
complications or in the presence of obstetric
indications
PUERPERAL INFECTION
PUERPERAL INFECTION
Any infection occurring within 6 weeks after
delivery
 Fever is the cardinal manifestation
 Temp of >/=38oC occurring in any 2 of the first 10
days postpartum, exclusive of the first 24 hours

PUERPERAL INFECTION

Postpartum Endometritis





Manner of delivery – most common with cesarean
delivery
Prolonged active phase of labor
Prolonged rupture of membranes >12 hours
Multiple vaginal examinations >6 hours
Others: Obesity, anemia, DM, low socioeconomic
status
PUERPERAL INFECTION

1.
2.
3.
Diagnosis of postpartum endometritis is highly
considered when the fever is associated with one
or more of the following:
Uterine tenderness
Foul smelling lochia
Uterine subinvolution
PUERPERAL INFECTION

MILD
ENDOMETRITIS
Previous vaginal
delivery
 No signs of sepsis
 No signs of peritonitis


SEVERE
ENDOMETRITIS





Previous CS
With sepsis
With signs of
peritonitis
Suspicion of pelvic
abscess or a probable
failed medical mgt
Suspicion of
exogenous pathogens
i.e. N. gonorrhea or
Chlamydia
PUERPERAL INFECTION

Diagnostics:
CBC
 Cervical culture
 Pelvic ultrasound


Antibiotics

Coverage for polymicrobial organisms which are part
of the normal vaginal flora
PUERPERAL INFECTION

Response to Treatment



1.
2.
3.
4.
5.
Evaluate clinical response within 24-48 hours after
initiation of treatment
Patient must be completely afebrile and
asymptomatic
Patients who did not respond to initial therapy,
consider the following:
Septic pelvic thrombophlebitis
Infected mass i.e. abscess or hematoma
Resistant organisms
Suspicion of hospital acquired infection
Other missed conditions i.e. acute appendicitis
NECROTIZING FASCIITIS
NECROTIZING FASCIITIS
Most serious of wound infections
 Associated with high mortality
 May involve abdominal incisions following CS or
may complicate episiotomy or perineal
lacerations
 Deep soft tissue infection involving muscle and
fascia

NECROTIZING FASCIITIS

1.
2.
3.
4.
5.
Risk Factors:
Diabetes
Hypertension
Obesity
Anemia
Decrease immune system
NECROTIZING FASCIITIS

Pathophysiology

Bacteria proliferate within the superficial
fascia and elaborate enzymes and toxins which
enable the organisms to spread through the fascia
 Angiothrombotic microbial invasion and liquefactive
necrosis of the superficial fascia
 occlusion of perforating nutrient vessels to the skin
causes progressive skin ischemia
 ischemic necrosis of the skin ensues with gangrene
of the subcutaneous fat, dermis and epidermis,
manifesting progressively as bullae formation,
ulceration and skin necrosis
NECROTIZING FASCIITIS

Causes:
Group A beta hemolytic Strep
 Polymicrobial


Diagnosis:

Clinical, based upon the rapid and severe progression
of an infection
NECROTIZING FASCIITIS

Treatment:
Medical – broad spectrum antibiotics
 Surgical – prompt wound debridement with wide
margins of fascial incision

SEPSIS SYNDROME

1.
2.
3.
4.
4 Main Areas in the Pathophysiology of Sepsis
Syndrome:
The individual host response
The role of the endothelium
The disequilibrium of the pro-inflammatory and
antiinflammatory mechanisms
Activation of the coagulation pathways
SEPSIS SYNDROME

Pathophysiology

Invasion of bacteria causes the endothelial cells to
release inflammatory mediators and activate the
clotting cascade

In sepsis, the endothelial response is dysfunctional,
causing an excessive, sustained and generalized
activation of the endothelium

This causes generalized tissue injury, vascular
permeability, shock and multi-organ failure
SEPSIS SYNDROME

Pathophysiology
Selective vasodilatation with maldistribution of blood
flow and volume
 Increase leukocyte and platelet aggregation causing
capillary plugging
 Vascular endothelial injury causes profound capillary
leakage and interstitial fluid accumulation causing
hypovolemia
 Hypoperfusion results in lactic acidosis, decreased
tissue oxygen extraction, and end-organ dysfunction

PATHOPHYSIOLOGY
Infection
Activation of immunological system
Release of inflammatory chemical mediators
Systemic vasodilation
Capillary leakage
Intravascular volume depletion
Maldistribution of intravascular volume
Impaired myocardial function
SEPSIS SYNDROME
Infection
Sepsis
Severe
Sepsis
Septic
Shock
MODS
SIRS
Death
SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME (SIRS)
non-specific systemic inflammatory response to
infection,trauma, burns, surgery etc.
 Characterized by abnormalities in 2 or more of
the following [one of which must be abnormal
temperature or leukocyte count]:
• body temperature
• heart rate
• respiratory function
• peripheral leucocyte count

SEPSIS


SIRS in the presence of or as a result of
suspected or proven infection.
Severe Sepsis

Sepsis plus one of the following:
• cardiovascular organ dysfunction
• acute respiratory distress syndrome
• two or more other organ dysfunction
SEPTIC SHOCK

1.
2.
Severe sepsis with cardiovascular organ
dysfunction i.e. hypotension, despite adequate
fluid resuscitation
Warm Phase - Compensated warm phase of
shock; CO,
SVR
- Prompt response to fluids and
pharmacologic treatment
Cold Phase - Late decompensated phase.
- CO, SVR
- Shock lasting more than 1 hour
despite vigorous therapy necessitating
vasopressor support
MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

Multiple Organ Failure
Presence of severe dysfunction of at least 2 organ
system lasting for more than 24 hours
 Four or more systems involved – mortality is almost
100%

COMPLICATIONS
ARDS
 DIC
 Acute renal failure
 Intestinal bleeding
 Liver failure
 CNS dysfunction
 Heart failure
 Death

TREATMENT
Aggressive volume replacement
 Respiratory support
 Broad spectrum antibiotics
 Septic work up
 Surgical treatment, if necessary
