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 Risk Factors:1. Increased age and parity2. Preeclampsia/ chronic HPN3. PROM4. Multifetal gestation5. Hydramnios6. Cigarette smoking7. Prior abruption8. External trauma9. 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 fibrinogen-fibrin 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 compromiseSevere uterine hypertonusLife threatening vaginal bleedingDIC 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 pyelonephritis2. Chorioamnionitis3. Puerperal infection4. Necrotizing fasciitis

ACUTE PYELONEPHRITIS

ACUTE PYELONEPHRITIS1. shaking chills2. fever (T>38oC)3. flank pain4. nausea and vomiting5. with or without signs and symptoms of

lower urinary tract infections6. 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 signs1. Maternal fever – oral temp >37.8oC

- hallmark for the diagnosis2. Uterine tenderness3. Persistent fetal tachycardia

CHORIOAMNIONITIS Treatment1. 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 Treatment2. 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 Diagnosis of postpartum endometritis is

highly considered when the fever is associated with one or more of the following:

1. Uterine tenderness2. Foul smelling lochia3. 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

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:

1. Septic pelvic thrombophlebitis2. Infected mass i.e. abscess or hematoma3. Resistant organisms4. Suspicion of hospital acquired infection5. 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 Risk Factors:1. Diabetes2. Hypertension3. Obesity4. Anemia5. 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 4 Main Areas in the Pathophysiology of

Sepsis Syndrome:1. The individual host response2. The role of the endothelium3. The disequilibrium of the pro-inflammatory

and antiinflammatory mechanisms4. 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

PATHOPHYSIOLOGYInfection

Activation of immunological systemRelease of inflammatory chemical mediators

Systemic vasodilationCapillary leakage

Intravascular volume depletionMaldistribution of intravascular volume

Impaired myocardial function

SEPSIS SYNDROME

Infection Sepsis Severe Septic MODS Sepsis Shock

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 Severe sepsis with cardiovascular organ

dysfunction i.e. hypotension, despite adequate fluid resuscitation

1. Warm Phase - Compensated warm phase of shock; CO, SVR- Prompt response to fluids and

pharmacologic treatment2. 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