Transcript DIC
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