301 CASE Study, 2021 PDF

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PARA301 Case study on obstetric/postpartum emergency, preecmplampsia....

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PARA301 CASE STUDY MANAGEMENT PLAN ASSESSMENT TASK ONE

The patient in the depicted scenario is likely experiencing preeclampsia, a gestational hypertensive disorder that afflicts 5-8% of pregnancies worldwide (Jim & Karumanchi, 2017). Clinically, preeclampsia is characterised by new-onset hypertension in a typically normotensive patient, and proteinuria. Given the diagnostic limitations of the prehospital setting, the provisional diagnosis can be ascertained from key red flags that suggest a

preeclamptic patient. Characteristically, a definitive diagnosis requires the acquisition of 2 separate blood pressure readings, with a systolic >140mmHg and diastolic >90mmHg at a minimum of 6 hours apart (Portelli & Baron, 2018). Despite a lack of consistent pre-natal care, an isolated BP reading of 190/115mmHg suggests the patient is severely hypertensive and illustrates a change in cardiovascular function over the last 17 weeks of gestation. Additionally, as a multisystem disorder, symptomatic features of preeclampsia often include oedema, oliguria and visual or cerebral disturbances (Portelli & Baron, 2018). Hypertension, coupled with patient complaints of a severe headache and flickering vision thus, suggest a likely provisional diagnosis of preeclampsia in late-stage pregnancy (Rana, Lemoine, Granger & Karumanchi, 2019). Differential diagnoses could include an array of hypertensive disorders that present both during and outside of gestation such as chronic hypertension and gestational hypertension (Shobo et al., 2020). Though these disorders are plausible given the patient’s notable hypertensive status, they offer no explanation for the patient’s additional neurological symptoms.

The clinical presentation of preeclampsia in the pre-hospital setting remains relatively heterogenous. In light of this, the patient in the depicted scenario presents with numerous clinical characteristics consistent with a preeclamptic presentation. The most prominent symptoms being the BP reading of 190/115mmHG indicative of severe hypertension, the complaints of visual disturbances and a severe headache, and the presence of peripheral oedema. Though the precise aetiology of preeclampsia remains marginally unknown, key pathophysiological dysfunctions do appear to explain the clinical symptoms as experienced by the patient in this scenario. Prominent literature largely recognises the role of the maternal inflammatory response and abnormal placentation in the development of the disorder (Rana, Lemoine, Granger & Karumanchi, 2019). During normal gestation, the invasion and remodelling of the maternal uterine spinal arteries occurs by foetus derived cytotrophoblast cells (Jim & Karumanchi, 2017). These vessels convert into mean diameter and low resistance vessels, optimising the supply of nutrient and oxygen rich maternal blood to the developing “…uteroplacental unit,” (Chaiworapongsa, Chaemsaithong, Yeo & Romero, 2014). In preeclampsia, this process of trophoblastic invasion is compromised, and a considerable reduction of remodelled vessels occurs, leading to decreased placental perfusion (Han et al., 2019). The intermittent supply of maternal blood flow generates local placental hypoxia and results in oxidative stress. “Inflammation, apoptosis, and the release of cellular debris into maternal circulation,” are a direct consequence of placental oxidative damage

(Aouache, Biquard, Vaiman & Miralles, 2018). Additionally, the subsequent release of placental-derived debris and anti-angiogenic factors stimulate the secretion of proinflammatory cytokines and vasoactive compounds from the maternal endothelium (Mayrink, Costa & Cecatti, 2018). Vascular inflammation and vasoconstriction are direct consequences of systemic endothelial dysfunction, contributing to the movement of fluid from the vascular compartment to the interstitium (Portelli & Baron, 2018). This is likely to have a multi-system effect, with oedema resulting in cerebrovascular dysfunction and neurological symptoms as reported by the patient (Rana, Lemoine, Granger & Karumanchi, 2019). Furthermore, vasoconstriction results in hypertension, a key clinical symptom of preeclampsia as seen in the patient depicted. This clinical presentation could be described as a pre-natal hypertensive emergency, and is thus, especially time critical. Significant preeclampsia, and unmanaged in this case, has the potential to progress into eclamptic seizures, leaving both mother and child at risk (Thilaganathan & Kalafat, 2019).

Initial management of the patient in the pre-hospital setting should place emphasis on developing rapport, especially due to her intellectual impairment and ongoing distrust of medical professionals. As preeclampsia is a progressive disorder, the patient should be advised to attend hospital with the paramedics for a holistic assessment and observation (Shobo et al., 2020). Additionally, as she presented severely hypertensive, paramedics should identify the increased risk of developing eclamptic seizures. Extrication of the patient from their residence to the stretcher should limit excessive movement and ambulation to avoid additional stress on the heart. To manage cardiac output and maintain maternal preload, the patient should be placed into left lateral recumbent position for transportation (Thilaganathan & Kalafat, 2019). Paramedics should consider the acquisition of intravenous access in the event the patient deteriorates rapidly, and acquire a 12-Lead electrocardiogram. The primary goal of the pre-hospital management of the preeclamptic patient is clinical surveillance. Paramedics should ensure a vital signs survey, particularly a BP reading, is obtained every 5 minutes during transportation (Thilaganathan & Kalafat, 2019). Pharmacological interventions should be applied only when indicated as per relevant guidelines. In-hospital management is far more extensive and effective at navigating hypertensive emergencies such as severe preeclampsia. While delivery is the only conclusive treatment, clinical management of the disorder is utilised to prevent maternal morbidity (Han et al., 2019). This is achieved by addressing the patients presenting symptoms of hypertension, oedema, and the prevention of seizures. As Sarah is 27 weeks’ gestation, the primary focus of practice management

would be to prolong preterm delivery where possible (Han et al., 2019). Initial interventions upon arrival at hospital would involve antihypertensive treatment, achieved by the administration of IV vasodilators and beta blockers. A combination of first-line and secondline anti-hypertensives may be used to manage Sarah’s condition both initially and moving forward, though ACE inhibitors are contraindicated during gestation (Mayrink, Costa & Cecatti, 2018). The administration of oral calcium channel blockers can also be considered as an initial treatment for the management of severe hypertension in preeclamptic patients (Portelli & Baron, 2018). Reductions in BP via pharmacological therapy should be done gradually, with an initial change of 15-25% to avoid decreased placental diffusion (Rana, Lemoine, Granger & Karumanchi, 2019). Increasing literature supports the utilisation of magnesium sulphate in lowering maternal BP, and as a prophylactic measure to prevent eclamptic seizures (Han et al., 2019). Should magnesium sulphate be unsuitable for the patient, anticonvulsants are not contraindicated in gestation and may be utilised. Foetal assessments should additionally be performed, to ensure the management is appropriate for both mother and child. The possibility of intrauterine hypoxia in preeclamptic patients cannot be overlooked, and thus this is an imperative intervention. Should foetal assessment signify distress, time-critical delivery may be necessary.

REFERENCES: Aouache, R., Biquard, L., Vaiman, D., & Miralles, F. (2018). Oxidative Stress in Preeclampsia and Placental Diseases. International Journal Of Molecular Sciences, 19(5), 1496. doi: 10.3390/ijms19051496

Chaiworapongsa, T., Chaemsaithong, P., Yeo, L., & Romero, R. (2014). Pre-eclampsia part 1: current understanding of its pathophysiology. Nature Reviews Nephrology, 10(8), 466-480. doi: 10.1038/nrneph.2014.102 Han, C., Han, L., Huang, P., Chen, Y., Wang, Y., & Xue, F. (2019). SyncytiotrophoblastDerived Extracellular Vesicles in Pathophysiology of Preeclampsia. Frontiers In Physiology, 10. doi: 10.3389/fphys.2019.01236 Jim, B., & Karumanchi, S. (2017). Preeclampsia: Pathogenesis, Prevention, and Long-Term Complications. Seminars In Nephrology, 37(4), 386-397. doi: 10.1016/j.semnephrol.2017.05.011 Mayrink, J., Costa, M., & Cecatti, J. (2018). Preeclampsia in 2018: Revisiting Concepts, Physiopathology, and Prediction. The Scientific World Journal, 2018, 1-9. doi: 10.1155/2018/6268276 Portelli, M., & Baron, B. (2018). Clinical Presentation of Preeclampsia and the Diagnostic Value of Proteins and Their Methylation Products as Biomarkers in Pregnant Women with Preeclampsia and Their Newborns. Journal Of Pregnancy, 2018, 1-23. doi: 10.1155/2018/2632637 Rana, S., Lemoine, E., Granger, J., & Karumanchi, S. (2019). Preeclampsia. Circulation Research, 124(7), 1094-1112. doi: 10.1161/circresaha.118.313276 Shobo, O., Okoro, A., Okolo, M., Longtoe, P., Omale, I., Ofiemu, E., & Anyanti, J. (2020). Implementing a community-level intervention to control hypertensive disorders in pregnancy using village health workers: lessons learned. Implementation Science Communications, 1(1). doi: 10.1186/s43058-020-00076-8 Thilaganathan, B., & Kalafat, E. (2019). Cardiovascular System in Preeclampsia and Beyond. Hypertension, 73(3), 522-531. doi: 10.1161/hypertensionaha.118.11191...