Chapter 7, Day 5
Hypercoagulability in pregnancy is the propensity of pregnant women to develop thrombosis (blood clots). Pregnancy itself is a factor of hypercoagulability (pregnancy induced hypercoagulability) as a physiologically adaptive mechanism to prevent postpartum bleeding.
Describe hypercoagulability during pregnancy?
Magnesium sulfate 4 gram loading dose with 1-3gram an hour infusion rate Antihypertensive therapy Induction or cesarean delivery (fetal pulmonary maturity depending on gestational age should be considered if less than or at 34 weeks)
Describe management for severe preeclampsia?
If immature fetus, bed rest mainly in laterla decubitis position Hypertension therapy if needed
Describe management of mild eclampsia?
There is a decreased intervillous space for blood to flow from the spiral arteries of the maternal side to the placenta (thus a reduction in blood flow) There are three stages: Stage 1, Primary: Abnormal development/poor placentation Stage 2, Secondary: Oxidative stress/placental injury Stage 3, Tertiary: Fetal growth restriction and/or preeclampsia Leading to possible complications such as: HELLP syndrome, elcampsia, stillbirth, placental abruption, prematurity, still birth
Describe normal placwentation vs abnormal placentation at 15-16 weeks of pregnancy?
AMniotic fluid enters the venous criculation, leading to dyspnea Persisten neurologic deficits can result, leading to cardiogeneic and noncardiogenic pulmonary edema, intrapulmonary shunting, bronchonstriction and desaturation leading to dyspnea, bronchospasm, cyanosis and pulmonary edema Decreased coronary blood flow can also occur leading to decreased intropism leading to decreased cardiac output and pulmonary congestion leading to hypotension shock (the amniotic fluid can enter the maternal body circulation by intrapulmonary shunts?) The amniotic fluid enters the maternal body circulation by intrapulmonary shunts Thromboplastic release occurs leading to DIC lading to bleeding. A patient can bleed out of the uterus, have decreased uterine perfusion and hypoxia, leading to fetal hypoxia, bradycardia, and fetal death.
Describe the pathway for amniotic fluid embolisM/
Exposure to amniotic fluid or fetal antigens leads to Immunological release of medicators, mechanical obstruction, and complement system activation, leading to cardiopulmonary effects and acute pulmonary hypertension, hypoxia and right ventricular failure, leading to left ventricular failure, neurological problems such as coma, seizures, residual deficits, acute respiratory dstress syndrome, leading other organ dysfunction such as acute kidney injury Can also lead to coagulation system activation leading to consumption coagulatphy leading to caripulmonary collapse and death
Describe the resulting effects of an amniotic fluid embolism?
Coagulation process is abnormally stimulated Excessive amounts of thrombin are generated Fibrinolytic mechanisms are activated and cause exgensive destruction of clotting factors
Descrieb the pathophysiology of DIC?
Proteinuria Edema Hemoconcetration
Increased permeability and capillary leakage due to endothelial cell dysfunction for preeclampsia can lead to?
Hemolysis of RBC (getting stuck in the clot?) Platelet adhesion Increased factor VIII antigen Decreased platelets
Intravascular cogulation during preeclampsia leads to?
Hypertension Decreased uteroplacental perfusion causing IUGR Glomerular damage leading to a decreased GFR and oliguria Cortical brain spasm leading to headache, hyperreflexia, and seizure Retinal arteriolar spasm leading to blurred vision and scotoma Liver ischemia leading to nausea, vomiting, epigastric and right upoer quadrant pain
Vasospasm from preeclamspai can lead to?
DIC is a disorder of the clotting cascade. It results in depletion of clotting factors in the blood.
WHat are some basic consideratiosn regarding DIC?
Epigastric pain CNS Bleeding Nausea/vomiting
What are general symptoms of preeclampsia?
4-7: A required level for prevention of eclampsia 8-10: Uterine relaxation 10: Patellar reflex disappears 10-12: Respiratory depression Greater than 12: Respiratory paralysis
What are plasma levels to consider with preeclampsia?
Excessive bleeding from orficies Petechaie, purpura, and hypotension Multi-organ failure Extensive purpurua, shock, prostration, cyanosis Circulatory collapse, marked hypotension Hemorrhagic destrction of adrenal gland Presence of a fluctuating fever
What are some S&S of DIC?
Headaches Changes in vision Nausea/vomiting Pain in the abdomen and back
What are some S&S of severe preeclampsia?
Anti-angiosin from placent leading to fibrin deposits and vasospasm leading to renal damage and liver damage RAS gets activated due to renal damage leading to hypertension leading to headache which we treat with antihypertensives, and glomerular damage, which we assess via 24 hour urine renal labors. For liver damage, there is an increase in liver enzymes, decrease in platelets, and possible DIC, thus we must monitor the patient for S&S of bleeding Patient can present with proteinuria due to increase capillary permeability leading to a decrease in osmotic pressure leading to a decrease in intravascular volume, leading to edema and oliguria (there is also a general increase in hematocrit because losing plasma from the blood). A decrase in intravascular volume leads to cerebral edema, and edema, blurred vision, and hyperrelxfiexa, which warants the treatment with mag sulfate. A decrease in intravascular volume can also lead to oliguria, in which we monitor the patient via strict I&O.
What are some concept map considerations regarding preeclampsia?
Assess DTR's, BP, RR, lung sounds, urine output, level of consciousness. Stop infusion if symptoms of toxicity occur. Patient teaching, normal side effects with mag sulfate: warmth over body/flushing, burning at the IV site, mild SOB, mild chest pain, congestion, headache, dizziness
What are some considerations for mag sulfate use for preeclampsia?
Complication of preeclampsia (4-12% of women with preeclampsia) S/S: Nausea, epigastric pain, general malaise, RUQ tenderness, visual changes LAB: Hemolysis of RBC's, platelets lower than 100,000 elevated liver enzymes such as ALT/AST Treatment involves delivery of the baby and placenta (Monitor for hemorrhage and DIC, steroids to increase renal function, platelet transfusion)? HELLP syndrome is a life-threatening pregnancy complication usually considered to be a variant of preeclampsia. Both conditions usually occur during the later stages of pregnancy, or sometimes after childbirth.
What are some considerations regarding HELLP syndrome (Hemolysis, Elevated Liver Enzymes, and Low platelets)
Life threatening pregnancy complication caused by eclampsia Treatment is transfusion of platelets and child birth 15% of the women withj eclampsia develop this complication Reported in the third trimester or after child birth Complication are liver tupture, stroke, brain hemorrhage and death Affects 48,00 women in the US Symtpoms are headache, vomiting, abdominal pain, bleeding and vision changes Death rate is 25% Hallmark signs are blood cell breakdown, liver dysfunction and low platelets Diagnosis is clinical Fetal mortality rate is 8% to 60% due to prematurity
What are some considerations regarding HELLP syndrome?
Eclampsia: Seizure, tonic clonic type Maintain airway, position to the side, O2, pulse ox, suction as needed Continuous fetal monitoring, monitor for possible abruption (vaginal bleeding, non-reassuring FHT) Delivery after stabilization Seizure may cause precipitous birth
What are some considerations regarding eclampsia?
Insufficient extravillous trophoblast invasion of uterine spiral arteries starting in early pregnancy has been posited as a causal factor in the development of preeclampsia, but little attention has been given to the uterine niche invaded by the trophoblasts Impaired or defective decidualization before and during early pregnancy is associated with the development of severe preeclampsia Current results suggest that it may be the soil rather than or in addition to the the seed which is a prime mover.
What are some current research findings for preeclampsia?
Endothelial cell dysfunction (this can lead to increased permeability and capillary leakage, intravascular cogulation and vasospasm)
What is the principal problem in preeclampsia other than an inadequate intervillous space in the placenta?
IDentify the underlying cause Monitor for signs of hemorrhage, bleeding, petechiae, cutaneous oozing, dyspnea, lethargy, pallor, increased heart rate, decreased blood pressure, headache, dizziness, muscle weakness, restless and internal bleeding Do not disturb clots, use pressure and ice to control bleeding Obtain lab tests and admnister blood nad factor products Inform family about plan of care and course of treatment
What are some further considerations for disseminated intravascular coagulation (in regards to nursing care)?
If DIC occurs during or after delivery, the reduced level of clotting factors and fibrin degradation products prevent normal hemostasis (arrest of bleeding) at the placental site. Fibrin degradation products inhibit myometrial action and prevent the uterine muscle from constricting the blood vessls in a normal way? Torrential hemorrhage may be the outcome, and even if clotting does occur, the clot is unstable (due to fibrinolysis and fibrin degradation products). Microthrombi in the bloodstream may cause circulatoru obstriction in the small blood vessels and lead to cyanosis of the fingers and toes to CVAs, or organ failure.
What are some further considerations regarding DIC?
In pregnancy, is due to enchanced platelet turnover, coagulation and fibrinolysis. FUrther enchanced during parturition (Choldbirth) Increase in concentration of coagulation factors particularly 1,5,7,8,10, and 12. Thrombin generation increases. Pregnancy repesants a state of accelerate but compensated intravascular cogulation and the coagulation activity is increased releative to the fibrinoltic activity.
What are some further considerations regarding hypercoagulability in pregnancy?
Micro blood clots form throughout the body, and eventually using up the blood clotting factors. These are then not available to form clots at the local sites of real tissue injury (microthrmobi) Clot dissolving mechanisms are also incrased in fibrinolysis
What are some further considerations regarding the pathophys of DIC?
Proteinuria Facial edema Pulmonary edema Ascites Pleural efusions
What are some maternal manifestations of preeclampsia that are secondary to capillary leaK?
Primiparity Previous preeclamptic pregnacny Chronic hypertension, chronic renal disease or both History of thrombophiliua Multifetal pregnancy In vitro fertilization Family history of preeclampsia Type I DM or TIPE II DM Obesity Systemic lupius erythematosus Advanced maternal age (older than 40 years old)
What are some other additional clinical risk factors for preeclampsia?
Hemorrhagic shock Transfusion reaction Sepsis Severe Pre-eclampsia or HELLP sundrome Retained fetal demise Premature separation of hte placenta (placental abruption) Retained placenta AMniotic fluid embolism (usually not able to be determined until autopsy)
What are some possible precursors to DIC?
First pregnancy Women older than 40 eyars of age History of high blood pressure before pregnnacy Diabetes Obesity Pre-eclampsia in a previous pregnancy (their may a paternal genetic compoenent?) Other medical problems such as kidney disease
What are some risk factors for pre-eclampsia?
Elevated blood pressure Elevated protein in urine Weight gain exceeding 2 pounds a week Water retention and swelling
What are some signs and symptoms of mild preeclampsia?
Systolic bllod pressure is between 140-160 Diastolic blood pressure is between 90-110 Proteinuria between 3 and 5 grams on a 24 hour sample
What are some things that charatcerize mild preelcmpaisa?
Systolic blood pressure greater than 160 mm Hg Diastolic blood pressure greater than 110 mm Hg Proteinuria is greater than 5 grams on a 24 hour sample
What are some values that characterize severe preeclampsia?
HELLP Renal failure DIC Low platelets and increased liver enzymes
What are the maternal manifestations of preeclampsia due to fibrinolysis/hemolysis?
Mild, Severe
What are two ways to categorize blood pressure for preeclampsia?
Placental hypoperfusion leading to defective spiral artery remodeling, leading to a lack of adeequate oxygenation to the baby. A diseased placenta also releases proinflammatory proteins into the maternal circulation leading to systemic vasoconsctrictin and endothelial dysfunction, producing hypertension and end organ damage (damage to the kidneys AEB proteinuria, and HELLP syndrome in the liver which is hemolysis elevated liver enzymes and low platelets) Curative treatment for preeclampsia is delivery of the placenta
What is a consideration/the pathophysiology related to preeclampsia?
A central scotoma is a blind spot that occurs in the center of one's vision. It can appear in several different ways. It may look like a black or gray spot for some and for others it may be a blurred smudge or a distorted view in one's straight ahead vision.
What is a scotoma?
Decidualization involves the transformation of the endometrial stromal fibroblasts into secretory epithelioid decidual cells that is accompanied by the abundance of the uNK cells and angiogenesis
What is decidualization?
Precipitous labor is extremely rapid labor and delivery. It is defined as expulsion of the fetus within less than 3 h of commencement of regular contractions
What is precipitous delivery?
BP decrease Urine output decrease Respiratory rate decrease Patellar reflex absent (Magnesium sulfate MgSO4, is the agent most commonly used for treatment of eclampsia and prophylaxis of eclampsia in patients with severe pre-exlampsia. It is usually given by either the intramuscular or intravenous routes. If magnesium toxicity occurs, stop MgSO4 infusion and admnister antidote of calciul gluconate, which is 10 mL of 10% solution slowly intravenously over approximately 10 minutes)
What is the BURP acronym for magnesium sulfate toxicity?
10% calcium gluconate, 10 mL, IVP over 2-3 minutes
What is the antidote for mag sulfate toxicity?
Tissue factor (clotting factors 7a, 9a, 11a, and 12a) Leading to factor 10a (TM, proteim C amd protein S lead to APC) and there is factor 5a present Prothrombin becomes thrombin and fibrinogen becomes fibrin leading to a thrombus formation
What is the physiology related to clotting?