septic shock and disseminated intravascular coagulation in pregnancy
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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 - PowerPoint PPT PresentationTRANSCRIPT
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