A Case Presentation by Group X

Name: Amy Amniona Semilla Address: Central Casiguran, Sorsogon Age: 42 years old Sex: F Civil Status: M Birthday: February 14, 1969 Date of Admission: December 7, 2011

Religion: Roman Catholic Nationality: Filipino Educational Attainment: College LMP: March 3, 2011 EDD: December 10, 2011 OB Score: G10P3

 Chief complaint : Dyspnea, cough and dizziness Vital Signs: Blood Pressure= 80/60 mmHg Principal Diagnosis: t/c Amniotic Fluid Embolism Past Medical History of illness (-) Hypertension (-) Diabetes Mellitus (-) Allergies (+) Anemia

Lifestyle (-) Smoking (-) Alcohol (-) Exercise: not much, walking (+) Disturbed sleep pattern due to dyspnea (+) Diet: Loves to eat fatty/ cholesterol containing foods Diagnostic exams undergone: Chest X-ray results revealed pulmonary congestion

History of Present Illness: The patient consulted the institution due to dyspnea and dizziness 3 days PTC. The patient has a known history of recurrent miscarriages and each pregnancy had been carried till term assisted with a cervical cerclage. The patient also had abruptio placenta.

 Amniotic fluid embolism (AFE) is a rare obstetric emergency in which it is postulated that amniotic fluid, fetal cells, hair, or other debris enter the maternal circulation causing cardio-respiratory collapse.

 The diagnosis of AFE has traditionally been made at autopsy when fetal squamous cells are found in the maternal pulmonary circulation; however, fetal squamous cells are commonly found in the circulation of laboring patients who do not develop the syndrome.

AFE is also known as anaphylactoid syndrome of pregnancy" instead of AFE. The exact mechanism of this anaphylactoid reaction to amniotic fluid is not clearly understood.

Amniotic fluid and the surrounding sac provide important protective mechanisms for the developing fetus. Throughout gestation, intact fetal membranes isolate amniotic fluid from the maternal circulation. At delivery, uterine vessels on the raw service of the endometrium become exposed following placental separation and can potentially serve as a portal of entry for amniotic fluid.

 However, uterine contractions are very effective in collapsing these veins, thereby minimizing the risk of entry.

 Normally, amniotic fluid does not enter the maternal circulation because it is contained safely within the uterus, sealed off by the amniotic sac. AFE occurs when the barrier between amniotic fluid and maternal circulation is broken and, possibly under a pressure gradient, fluid abnormally enters the maternal venous system via the endocervical veins, the placental site (if placenta is separated), or a uterine trauma site.

 The devastating consequence of circulating fetal debris (carried by amniotic fluid) occurs only rarely, even though during normal labor and delivery, cesarean deliveries, and minor traumatic procedures fetal tissue may pass into maternal circulation and cause no symptoms. That AFE develops in only a minute proportion of these women suggests that either it is an effect of the amount of exposure to fetal debris or the type of fetal debris (containing meconium or not) or that some maternal factors may play significant role.

Amniotic fluid and fetal cells enter the maternal circulation D biochemical mediators D pulmonary artery vasospasm D pulmonary hypertension D elevated right ventricular pressure D hypoxia D myocardial and pulmonary capillary damage, D left heart failure B acute respiratory distress syndrome

placental abruption uterine overdistention fetal death Trauma tumultuous or oxytocin-stimulated labor Multiparity advanced maternal age rupture of membranes.

 However, in numerous documented cases of AFE, none of these conditions or demographic characteristics occurred or were applicable at the time of the event. Furthermore, a recent analysis of 46 verified cases of AFE did not substantiate most of these as associated factors; 12% of the cases occurred in women with intact membranes, 70% during labor, 11% after vaginal delivery, and 19% during cesarean delivery with or without labor.

The classic clinical presentation of the syndrome has been described by five signs that often occur in the following sequence: Respiratory distress Cyanosis Cardiovascular collapse cardiogenic shock Hemorrhage Coma

 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.

 10-15% of patients will develop grand mal seizures. CXR may be normal or show effusions, enlarged heart, or pulmonary edema. ECG may show a right strain pattern with ST-T changes and tachycardia.

Arterial Blood Gas Complete Blood Count with platelets Urinalysis Type and Cross 4-6 units packed Red Blood Cells Coagulation studies

 Prothrombine Time (PT) Partial Thromboplastin Time(PTT) Fibrin split products (Fibrin Degradation Products) Fibrinogen Clot test

Monitoring 1.Check Hemoglobin every 1 hour (keep above 10 mg/dl) 2.Check Hematocrit every 1 hour (keep above 30) 3.Check coagulation studies every 2 hours 4.Fetal scalp electrode 5.Tocometry or intrauterine pressure catheter 6.Monitor strict intake and output 7.Keep urine output > 30 cc per hour

GOALS : 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

 Administer oxygen to maintain normal saturation. Intubate if necessary. In the event of cardiac arrest, the resuscitation team should follow standard Advanced Cardiac Life Support protocols for obstetric patients. Treat hypotension with crystalloid and blood products. Use pressors as necessary. Consider pulmonary artery catheterization in patients who are hemodynamically unstable.

 Continuously monitor the fetus. Specific to pregnant women is the importance of positioning. In order to ensure optimal uterine perfusion throughout the management of AFE Drugs are used in amniotic fluid embolism (AFE) to stabilize the patient. Pressors are used to maintain blood pressure, and inotropes are used to improve contractility. Use of steroids has been suggested because the process may be immune mediated. Uterotonics may be used to limit postpartum bleeding.

 Sympathomimetic/vasopressor agents Used in AFE to maintain blood pressure. Dopamine (Inopin) One of several drugs that can be used to maintain perfusion. Dopamine increases myocardial contractility and systolic BP with little increase in diastolic BP. Also dilates the renal vasculature, increasing renal blood flow and GFR.

 Inotropes/ Inotropic agents Used to improve myocardial contractility in patients with amniotic-fluid embolism. Digoxin (Lanoxin) Cardiac glycoside that acts directly on the cardiac muscle and conduction system. Digoxin causes an increase in force and velocity of systolic contraction, a slowing of the heart rate, and decreased conduction velocity through the AV node.

 Corticosteroids Some authorities suggest steroid use may be helpful in AFE because the process may be immune mediated. (Hydrocortisone) Because AFE is more similar to an anaphylactic reaction, steroids that mediate the immune responses are recommended. Uterotonics Cause the uterus to contract. Uterine atony (failure of the uterus to contract and involute, thus closing off the bleeding spiral arteries after delivery of the placenta) may be a source of significant postpartum bleeding.

 Oxytocin (Pitocin) Most commonly used uterotonic. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Methergine Acts directly on uterine smooth muscle, causing a sustained tetanic uterotonic effect that reduces uterine bleeding. Hemabate Prostaglandin similar to F2-alpha (dinoprost), but has longer duration and produces myometrial contractions that induce hemostasis at placentation site, which reduces postpartum bleeding.

 The treatment has traditionally been aggressive supportive care. An emergency Cesarean section is performed as a free-floating interatrial clot is discovered in the patent foramen ovale. Clients are successfully treated with immediate cardiopulmonary bypass, thromboembolectomy, and closure of the patent foramen ovale.

 Upon complete assessment: Subjective: Dizziness as verbalized by the client Objective: Decreased blood pressure of 80/60 mmHg

 DECREASED CARDIAC OUTPUT R/T IMPAIRED CONTRACTILITY

After 8 hours of nursing interventions: Patient maintains: BP within normal limits, regular cardiac rhythm and strong bilateral, equal peripheral pulses.

NI: Assess physical status closely, document changes, report significant changes in parameters RATIONALE: Baseline assessment guides the health team on further intervention NI: Monitor diagnostic and laboratory studies RATIONALE: Continuous monitoring allows the health team updated on the client s current status

NI: Monitor oxygen saturation RATIONALE: Change in oxygen saturation is one of the earliest indicators of reduced cardiac output NI: Monitor ECG reading RATIONALE: Tachycardia, bradycardia and abnormal beats can compromise cardiac output

NI: Administer the medication as prescribed noting response and watching for side effects RATIONALE: Medication therapeutic effect NI: Maintain optimal fluid balance RATIONALE: Maintenance of hemodynamic parameters NI: Position client in supine position RATIONALE: To increase venous return

NI: Administer O2 as ordered RATIONALE: Supplementary O2 for maintenance of adequate supply NI: Maintain physical and emotional rest RATIONALE: Restrict activity to reduce O2 demands NI: Have antiarrythmic drugs readily available RATIONALE: For faster intervention

NI: Health teaching RATIONALE: To decrease the client s anxiety and make them co-managers in health

 Client s vital signs within the normal range Client verbalized relief of symptoms Client verbalized understanding on the teachings given

Subjective: Napapagal akong maghangos ,as verbalized by the client Objective: Tachypnea (+)Cough Use of accessory muscles Cyanosis

 Ineffective breathing pattern r/t amniotic fluid embolus

After 2 hours of nursing interventions: Patient will have improved breathing as manifested by: a. Normalization or decrease in Respiration Rate b. Decrease difficulty of breathing

NI: Assess the vital signs specifically the RR of the mother and the FHT of the baby RATIONALE: RR and rhythm changes are early warning signs of impending respiratory difficulty NI: Assess in any increase in breathing in work RATIONALE: -Serves as baseline data in providing appropriate management

NI: Position in high fowler s RATIONALE: For good lung excursion and chest expansion NI: Promote Complete bed rest RATIONALE: to decrease oxygen demand and to conserve energy NI: monitoring equipment such as pulse oximeter RATIONALE: to know the oxygen saturation and assess respiratory status

NI: Monitor ABG and note for changes RATIONALE: to evaluate the progress of the condition NI: Anticipate the need for intubation and mechanical ventilation RATIONALE: to provide partial or total ventilatory support to patients with respiratory failure NI: Administer oxygen as prescribed by the physician RATIONALE: to promote oxygen circulation and distribution to other parts of the body to increase perfusion

After 2 hours of nursing interventions: Patient will have improved breathing as manifested by: a. Normalization or decrease in Respiration Rate b. Decrease difficulty of breathing