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Example research essay topic: W B Saunders Amniotic Fluid - 1,496 words

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... eceleration pattern is indicative of a uterine and / or placental blood flow problem. In the case of PIH, the late deceleration types will most likely be the pattern seen due to the compromised utero placental blood flow. Another risk associated with preeclampsia points to the propensity for decreased maternal renal blood flow due to vasoconstriction.

Vasospasm, with the resulting decrease in blood flow, leads to a decrease in glomerular filtration rate (GFR), decreased clearance of uric acid, and sodium retention. Plasma creatinine levels may be elevated and glomerular damage, which causes increased membrane permeability, results in the diffusion of large protein molecules and the diagnostic finding of proteinuria. Hematological changes can also carry a significant risk to the patient with preeclampsia. As described earlier, vaso spastic activity causes endothelial damage. In response to this damage, platelets aggregate to the site of injury. With the narrowing of the lumen of the vessels, red blood cells (RBCs) and platelets can become damaged as they attempt to traverse through the system.

The resulting damage to the RBCs can reduce the oxygen carrying capacity of the attached hemoglobin molecule as well as causing hemolysis. Damaged and decreased platelet numbers (thrombocytopenia) can have a devastating effect on clotting mechanisms. PIH can result in disseminated intravascular coagulation (DIC) in the most severe of cases. Risks to hepatic function are also associated with vaso spasm. Continued and profound vaso spasm can lead to life-threatening complications such as hepatic hemorrhage, rupture, and necrosis. Clinical signs and symptoms of epigastrium or right-upper-quadrant pain are considered highly suspicious for hepatic involvement and warrant further investigation (Leicht & Harvey, 1999).

Elevated serum liver function tests [bilirubin, serum glutamic-oxaloacetic transaminase / aspartate transaminase (SGOT/AST), lactic acid dehydrogenase (LDH), alkaline phosphatase (alk phos), and blood urea nitrogen (BUN) ] will assist in evaluating the severity and hepatic progression of this disease (Creasy & Resnik, 1999). The neurological sequelae of preeclampsia can also present challenges and risks to the PIH patient. Again, vaso spasm is the culprit in the visual disturbances sometimes noted in the severe preeclampsia patient. Retinal detachment caused by vaso spasm of the retinal artery has been documented in 1 - 3 % of the PIH cases. The progression of preeclampsia to eclampsia (the presence of seizure activity) is associated with the same cascading mechanisms of vaso spasm. Seizure activity is caused by cortical brain spasms that occur in response to the other vaso spastic precipitators.

Pharmacological prevention is key to diverting these types of episodes (Creasy & Resnik, 1999). J. B. and her fetus, the case study subjects, carry other risks besides those of preeclampsia. Her gestation of 25 + weeks as well as her premature ruptured membranes complicated the scenario further. Her abdominal tenderness was suspicious for possible abruption.

This was an emergency situation requiring collaborative medical and nursing action to prevent the potential for further maternal and fetal compromise. The obstetrician responded to the bedside within four minutes (0930), was given report, and performed an ultrasound to rule out placenta previa (bleeding), confirm the FHR, assess cervical dilatation, and verify amniotic fluid volume. Results revealed no previa, decreased amniotic fluid volume, positive fetal cardiac activity, and a closed thick cervix. The perinatologist was consulted and the patient and family discussed options for transfer and treatment.

The decision was made to initiate intravenous Magnesium Sulfate (Mg SO 4) therapy and transport via helicopter to a tertiary Level III facility. Nursing diagnoses for the case at this time were possible alteration in utero placental perfusion related to the PIH, preterm gestation, and uterine contractions. Also, possible alteration in umbilical blood flow related to the decreased amniotic fluid volume, and again PIH and uterine contractions. Interventions were directed toward the goals to enhance utero placental and umbilical blood flow by maintaining left lateral positioning, hydrating the patient, improving oxygenation, reducing uterine activity, reducing maternal anxiety, providing safety measures for seizure precautions, continuous monitoring of the maternal and fetal status, maintaining strict I& O, administering medications as prescribed, and planning for possible emergency surgical intervention. The first readable EFM tracing occurred at 0940. Contractions were palpated every 2 minutes.

The contractions were mild to moderate intensity, and marked on the fetal tracing as UC by the nurse, as the monitor still would not trace contractions. At 0945, Mg SO 4 therapy was initiated per protocol. The FHR was 125 - 130 bpm with decreased long-term variability and late decelerations. At 0950 the obstetrician and perinatologist were again called to the bedside to review the FHR tracing. At this time the decision to abort transfer and prepare the patient for an emergency cesarean was made.

The anesthesia and neonatology crews were notified. J. B. delivered a viable male at 1009 via primary cesarean section under general anesthesia. Upon exam of the placenta a 40 % abruption was noted. Apgars of the male infant were 3 and 7 at 1 and 5 minutes respectively.

Cord gases were drawn. The infant was resuscitated with intubation and positive pressure ventilation and was transported to the NICU. Further stabilization occurred in the Level II NICU and the infant was transferred to a Level III tertiary facility for long-term ventilator therapy. The cord gas results were: arterial pH 6. 902, pCO 2 83. 8, pO 2 17. 6, BE - 19. 3, venous pH 6. 968, pCO 2 68. 5, pO 2 22. 1, BE 17. 3. These values revealed a mixed respiratory and metabolic acidosis.

Postoperatively, J. B. was taken to the Labor and Delivery recovery area where she was intensively monitored for 12 hours. She continued on Mg SO 4 therapy for 24 hours. After becoming hemodynamic ally stable (labs, BP, and output WNL), the medication was discontinued. Due to the ruptured membranes and surgical intervention, J.

B. was also treated with IV Angel 1 gram every 6 hours for three doses. As per protocol, to facilitate uterine involution, she was treated with IV oxytocin. She was discharged stable on her third day post-op to join her infant at the Level III NICU.

Later, the infant progressed and was discharged home at 3 months of age with to date, no known neurologic sequelae. Due to the emergent nature of this scenario, the diagnostic lab values were reviewed retrospectively after delivery. They did serve the purpose of providing a baseline for future comparisons in measuring the resolution of the preeclampsia in J. B. , as delivery is the only cure for this disease of pregnancy. She was negative for all drugs of abuse. Her CBC values were normal with the exception of the MPV and neutrophil counts.

These were slightly elevated but the extent of this elevation was normal for the pregnant client, especially in labor (having uterine contractions) (Creasy & Resnik, 1999). Most liver function markers such as BUN, uric acid, SGOT/AST, and alkaline phosphatase levels were normal, with only LDH demonstrating a slight elevation, ruling out the progression of liver involvement at this time. The LDH returned to normal on the first day post-op. Serum total protein and albumin levels were low as expected due to the GFR and membrane permeability allowing for diffusion of protein into the urine (+ 1 urine protein on admission). Urine was negative for protein 13 hours post-op and remained so up to discharge.

In summary, the expedient and goal directed actions of all healthcare providers in this case study scenario, contributed significantly to the positive outcomes of this client and her fetus. Despite the high-risk nature of this situation, the circumstances of this client coming to a community hospital instead of a Level III tertiary care center, did not affect care. Even more possible, the delay that would have ensued in seeking care at such a facility could have had grave consequences in this case. Consistency in the obstetrical nurses knowledge regarding the pathophysiology basis for disease and complications of pregnancy should be universal, despite the expected level of care for any facility. References Creasy, R. , & Resnik, R. (1999). Maternal-fetal medicine (4 th ed. ).

Philadelphia, PA: W. B. Saunders. Feinstein, N. , & McCartney, P. (Ed. ). (1997). Fetal heart monitoring principles and practices (2 nd ed. , Rev. ). Dubuque, IA: Kendall Hunt Publishing Company.

Leicht, T. , & Harvey, C. (1999). Hypertensive disorders of pregnancy. In Mandeville, L. , Troiano, N. (Ed. ), High-risk and critical care intra partum nursing (2 nd ed. , Rev. , pp. 159 - 170). Philadelphia, PA: J. B. Lippincott Company.

Mattson, S. , & Smith, J. (Ed. ). (2000). Core curriculum for maternal-newborn nursing (2 nd ed. , Rev. ). Philadelphia, PA: W. B. Saunders Company. Morin, K. (1998).

Perinatal outcomes of obese women: A review of the literature. Journal of Obstetric, Gynecologic, and Neonatal Nursing, 27, 434. Murray, M. (1997). Antepartal and intrapartal fetal monitoring. Albuquerque, NM: Learning Resources International, Inc.

Parer, J. T. (1983). Fetal cardio respiratory physiology. Handbook of fetal heart rate monitoring. Philadelphia, PA: W.

B. Saunders Company.


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