Nursing Case Study On Pregnancy Induced Hypertension

Citation: Luk A, Ma RCW, Lam CW, Tam WH, Lo AWI, Ng EKW, et al. (2009) A 21-Year-Old Pregnant Woman with Hypertension and Proteinuria. PLoS Med 6(2): e1000037. https://doi.org/10.1371/journal.pmed.1000037

Published: February 24, 2009

Copyright: © 2009 Luk et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The authors received no specific funding for this article.

Competing interests: RCWM is Section Editor of the Learning Forum. The remaining authors have declared that no competing interests exist.

Abbreviations: CT, computer tomography; I, iodine; MIBG, metaiodobenzylguanidine; MRI, magnetic resonance imaging; SDH, succinate dehydrogenase; SDHD, succinate dehydrogenase subunit D

Provenance: Commissioned; externally peer reviewed

Description of Case

A 21-year-old pregnant woman, gravida 2 para 1, presented with hypertension and proteinuria at 20 weeks of gestation. She had a history of pre-eclampsia in her first pregnancy one year ago. During that pregnancy, at 39 weeks of gestation, she developed high blood pressure, proteinuria, and deranged liver function. She eventually delivered by emergency caesarean section following failed induction of labour. Blood pressure returned to normal post-partum and she received no further medical follow-up. Family history was remarkable for her mother's diagnosis of hypertension in her fourth decade. Her father and five siblings, including a twin sister, were healthy. She did not smoke nor drink any alcohol. She was not taking any regular medications, health products, or herbs.

At 20 weeks of gestation, blood pressure was found to be elevated at 145/100 mmHg during a routine antenatal clinic visit. Aside from a mild headache, she reported no other symptoms. On physical examination, she was tachycardic with heart rate 100 beats per minute. Body mass index was 16.9 kg/m2 and she had no cushingoid features. Heart sounds were normal, and there were no signs suggestive of congestive heart failure. Radial-femoral pulses were congruent, and there were no audible renal bruits.

Baseline laboratory investigations showed normal renal and liver function with normal serum urate concentration. Random glucose was 3.8 mmol/l. Complete blood count revealed microcytic anaemia with haemoglobin level 8.3 g/dl (normal range 11.5–14.3 g/dl) and a slightly raised platelet count of 446 × 109/l (normal range 140–380 × 109/l). Iron-deficient state was subsequently confirmed. Quantitation of urine protein indicated mild proteinuria with protein:creatinine ratio of 40.6 mg/mmol (normal range <30 mg/mmol in pregnancy).

What Were Our Differential Diagnoses?

An important cause of hypertension that occurs during pregnancy is pre-eclampsia. It is a condition unique to the gravid state and is characterised by the onset of raised blood pressure and proteinuria in late pregnancy, at or after 20 weeks of gestation [1]. Pre-eclampsia may be associated with hyperuricaemia, deranged liver function, and signs of neurologic irritability such as headaches, hyper-reflexia, and seizures. In our patient, hypertension developed at a relatively early stage of pregnancy than is customarily observed in pre-eclampsia. Although she had proteinuria, it should be remembered that this could also reflect underlying renal damage due to chronic untreated hypertension. Additionally, her electrocardiogram showed left ventricular hypertrophy, which was another indicator of chronicity.

While pre-eclampsia might still be a potential cause of hypertension in our case, the possibility of pre-existing hypertension needed to be considered. Box 1 shows the differential diagnoses of chronic hypertension, including essential hypertension, primary hyperaldosteronism related to Conn's adenoma or bilateral adrenal hyperplasia, Cushing's syndrome, phaeochromocytoma, renal artery stenosis, glomerulopathy, and coarctation of the aorta.

Renal causes of hypertension were excluded based on normal serum creatinine and a bland urinalysis. Serology for anti-nuclear antibodies was negative. Doppler ultrasonography of renal arteries showed normal flow and no evidence of stenosis. Cushing's syndrome was unlikely as she had no clinical features indicative of hypercortisolism, such as moon face, buffalo hump, violaceous striae, thin skin, proximal muscle weakness, or hyperglycaemia. Plasma potassium concentration was normal, although normokalaemia does not rule out primary hyperaldosteronism. Progesterone has anti-mineralocorticoid effects, and increased placental production of progesterone may mask hypokalaemia. Besides, measurements of renin activity and aldosterone concentration are difficult to interpret as the renin-angiotensin-aldosterone axis is typically stimulated in pregnancy. Phaeochromocytoma is a rare cause of hypertension in pregnancy that, if unrecognised, is associated with significant maternal and foetal morbidity and mortality. The diagnosis can be established by measuring levels of catecholamines (noradrenaline and adrenaline) and/or their metabolites (normetanephrine and metanephrine) in plasma or urine.

Box 1: Causes of Hypertension in Pregnancy

  • Pre-eclampsia
  • Essential hypertension
  • Renal artery stenosis
  • Glomerulopathy
  • Renal parenchyma disease
  • Primary hyperaldosteronism (Conn's adenoma or bilateral adrenal hyperplasia)
  • Cushing's syndrome
  • Phaeochromocytoma
  • Coarctation of aorta
  • Obstructive sleep apnoea

What Was the Diagnosis?

Catecholamine levels in 24-hour urine collections were found to be markedly raised. Urinary noradrenaline excretion was markedly elevated at 5,659 nmol, 8,225 nmol, and 9,601 nmol/day in repeated collections at 21 weeks of gestation (normal range 63–416 nmol/day). Urinary adrenaline excretion was normal. Pregnancy may induce mild elevation of catecholamine levels, but the marked elevation of urinary catecholamine observed was diagnostic of phaeochromocytoma. Conditions that are associated with false positive results, such as acute myocardial infarction, congestive heart failure, acute cerebrovascular event, withdrawal from alcohol, withdrawal from clonidine, and cocaine abuse, were not present in our patient.

The working diagnosis was therefore phaeochromocytoma complicating pregnancy. Magnetic resonance imaging (MRI) of neck to pelvis, without gadolinium enhancement, was performed at 24 weeks of gestation. It showed a 4.2 cm solid lesion in the mid-abdominal aorto-caval region, while both adrenals were unremarkable. There were no ectopic lesions seen in the rest of the examined areas. Based on existing investigation findings, it was concluded that she had extra-adrenal paraganglioma resulting in hypertension.

What Was the Next Step in Management?

At 22 weeks of gestation, the patient was started on phenoxybenzamine titrated to a dose of 30 mg in the morning and 10 mg in the evening. Propranolol was added several days after the commencement of phenoxybenzamine. Apart from mild postural dizziness, the medical therapy was well tolerated during the remainder of the pregnancy. In the third trimester, systolic and diastolic blood pressures were maintained to below 90 mmHg and 60 mmHg, respectively. During this period, she developed mild elevation of alkaline phosphatase ranging from 91 to 188 IU/l (reference 35–85 IU/l). However, liver transaminases were normal and the patient had no seizures. Repeated urinalysis showed resolution of proteinuria. At 38 weeks of gestation, the patient proceeded to elective caesarean section because of previous caesarean section, and a live female baby weighing 3.14 kg was delivered. The delivery was uncomplicated and blood pressure remained stable.

Progress

Following the delivery, computer tomography (CT) scan of neck, abdomen, and pelvis was performed as part of pre-operative planning to better delineate the relationship of the tumour to neighbouring structures. In addition to the previously identified extra-adrenal paraganglioma in the abdomen (Figure 1), the CT revealed a 9 mm hypervascular nodule at the left carotid bifurcation, suggestive of a carotid body tumour (Figure 2). The patient subsequently underwent an iodine (I)131 metaiodobenzylguanidine (MIBG) scan, which demonstrated marked MIBG-avidity of the paraganglioma in the mid-abdomen. The reported left carotid body tumour, however, did not demonstrate any significant uptake. This could indicate either that the MIBG scan had poor sensitivity in detecting a small tumour, or that the carotid body tumour was not functional.

In June 2008, four months after the delivery, the patient had a laparotomy with removal of the abdominal paraganglioma. The operation was uncomplicated. There was no wide fluctuation of blood pressures intra- and postoperatively. Phenoxybenzamine and propranolol were stopped after the operation. Histology of the excised tumour was consistent with paraganglioma with cells staining positive for chromogranin (Figures 3 and 4) and synaptophysin. Adrenal tissues were notably absent.

Figure 4. Histological Section of the Resected Tumour

The tumour cells are polygonal with bland nuclei. The cells are arranged in nests and are immunoreactive to chromogranin (shown here) and synaptophysin.

https://doi.org/10.1371/journal.pmed.1000037.g004

The patient was counselled for genetic testing for hereditary phaeochromocytoma/paraganglioma. She was found to be heterozygous for c.449_453dup mutation of the succinate dehydrogenase subunit D (SDHD) gene (Figure 5). This mutation is a novel frameshift mutation, and leads to SDHD deficiency (GenBank accession number: 1162563). At the latest clinic visit in August 2008, she was asymptomatic and normotensive. Measurements of catecholamine in 24-hour urine collections had normalised. Resection of the left carotid body tumour was planned for a later date. She was to be followed up indefinitely to monitor for recurrences. She was also advised to contact family members for genetic testing. Our patient gave written consent for this case to be published.

Discussion

Phaeochromocytoma in Pregnancy

Hypertension during pregnancy is a frequently encountered obstetric complication that occurs in 6%–8% of pregnancies [2]. Phaeochromocytoma presenting for the first time in pregnancy is rare, and only several hundred cases have been reported in the English literature. In a recent review of 41 cases that presented during 1988 to 1997, maternal mortality was 4% while the rate of foetal loss was 11% [3]. Antenatal diagnosis was associated with substantial reduction in maternal mortality but had little impact on foetal mortality. Further, chronic hypertension, regardless of aetiology, increases the risk of pre-eclampsia by 10-fold [1].

Classically, patients with phaeochromocytoma present with spells of palpitation, headaches, and diaphoresis [4]. Hypertension may be sustained or sporadic, and is associated with orthostatic blood pressure drop because of hypovolaemia and impaired vasoconstricting response to posture change. During pregnancy, catecholamine surge may be triggered by pressure from the enlarging uterus and foetal movements. In the majority of cases, catecholamine-secreting tumours develop in the adrenal medulla and are termed phaeochromocytoma. Ten percent of tumours arise from extra-adrenal chromaffin tissues located in the abdomen, pelvis, or thorax to form paraganglioma that may or may not be biochemically active. The malignant potential of phaeochromocytoma or paraganglioma cannot be determined from histology and is inferred by finding tumours in areas of the body not known to contain chromaffin tissues. The risk of malignancy is higher in extra-adrenal tumours and in tumours that secrete dopamine.

Making the Correct Diagnosis

The diagnosis of phaeochromocytoma requires a combination of biochemical and anatomical confirmation. Catecholamines and their metabolites, metanephrines, can be easily measured in urine or plasma samples. Day collection of urinary fractionated metanephrine is considered the most sensitive in detecting phaeochromocytoma [5]. In contrast to sporadic release of catecholamine, secretion of metanephrine is continuous and is less subjective to momentary stress. Localisation of tumour can be accomplished by either CT or MRI of the abdomen [6]. Sensitivities are comparable, although MRI is preferable in pregnancy because of minimal radiation exposure. Once a tumour is identified, nuclear medicine imaging should be performed to determine its activity, as well as to search for extra-adrenal diseases. I131 or I123 MIBG scan is the imaging modality of choice. Metaiodobenzylguanidine structurally resembles noradrenaline and is concentrated in chromaffin cells of phaeochromocytoma or paraganglioma that express noradrenaline transporters. Radionucleotide imaging is contraindicated in pregnancy and should be deferred until after the delivery.

Treatment Approach

Upon confirming the diagnosis, medical therapy should be initiated promptly to block the cardiovascular effects of catecholamine release. Phenoxybenzamine is a long-acting non-selective alpha-blocker commonly used in phaeochromocytoma to control blood pressure and prevent cardiovascular complications [7]. The main side-effects of phenoxybenzamine are postural hypotension and reflex tachycardia. The latter can be circumvented by the addition of a beta-blocker. It is important to note that beta-blockers should not be used in isolation, since blockade of ß2-adrenoceptors, which have a vasodilatory effect, can cause unopposed vasoconstriction by a1-adrenoceptor stimulation and precipitate severe hypertension. There is little data on the safety of use of phenoxybenzamine in pregnancy, although its use is deemed necessary and probably life-saving in this precarious situation.

The definitive treatment of phaeochromocytoma or paraganglioma is surgical excision. The timing of surgery is critical, and the decision must take into consideration risks to the foetus, technical difficulty regarding access to the tumour in the presence of a gravid uterus, and whether the patient's symptoms can be satisfactorily controlled with medical therapy [8,9]. It has been suggested that surgical resection is reasonable if the diagnosis is confirmed and the tumour identified before 24 weeks of gestation. Otherwise, it may be preferable to allow the pregnancy to progress under adequate alpha- and beta-blockade until foetal maturity is reached. Unprepared delivery is associated with a high risk of phaeochromocytoma crisis, characterised by labile blood pressure, tachycardia, fever, myocardial ischaemia, congestive heart failure, and intracerebral bleeding.

Patients with phaeochromocytoma or paraganglioma should be followed up for life. The rate of recurrence is estimated to be 2%–4% at five years [10]. Assessment for recurrent disease can be accomplished by periodic blood pressure monitoring and 24-hour urine catecholamine and/or metanephrine measurements.

Genetics of Phaeochromocytoma

Approximately one quarter of patients presenting with phaeochromocytoma may carry germline mutations, even in the absence of apparent family history [11]. The common syndromes of hereditary phaeochromocytoma/paraganglioma are listed in Box 2. These include Von Hippel-Lindau syndrome, multiple endocrine neoplasia type 2, neurofibromatosis type 1, and succinate dehydrogenase (SDH) gene mutations. Our patient has a novel frameshift mutation in the SDHD gene located at Chromosome 11q. SDH is a mitochondrial enzyme that is involved in oxidative phosphorylation. Characteristically, SDHD mutation is associated with head or neck non-functional paraganglioma, and infrequently, sympathetic paraganglioma or phaeochromocytoma [12]. Tumours associated with SDHD mutation are rarely malignant, in contrast to those arisen from mutation of the SDHB gene. Like all other syndromes of hereditary phaeochromocytoma, SDHD mutation is transmitted in an autosomal dominant fashion. However, not all carriers of the SDHD mutation develop tumours, and inheritance is further complicated by maternal imprinting in gene expression. While it may not be practical to screen for genetic alterations in all cases of phaeochromocytoma, most authorities advocate genetic screening for patients with positive family history, young age of tumour onset, co-existence with other neoplasms, bilateral phaeochromocytoma, and extra-adrenal paraganglioma. The confirmation of genetic mutation should prompt evaluation of other family members.

Box 2: Hereditary Phaeochromocytoma/Paraganglioma Syndromes

  • Von Hippel-Lindau syndrome
  • Multiple endocrine neoplasia type 2A and type 2B
  • Neurofibromatosis type 1
  • Mutation of SDHB, SDHC, SDHD
  • Ataxia-telangiectasia
  • Tuberous sclerosis
  • Sturge-Weber syndrome

Key Learning Points

  • Hypertension complicating pregnancy is a commonly encountered medical condition.
  • Pre-existing chronic hypertension must be considered in patients with hypertension presenting in pregnancy, particularly if elevation of blood pressure is detected early during pregnancy or if persists post-partum.
  • Secondary causes of chronic hypertension include renal artery stenosis, renal parenchyma disease, primary hyperaldosteronism, phaeochromocytoma, Cushing's syndrome, coarctation of the aorta, and obstructive sleep apnoea.
  • Phaeochromocytoma presenting during pregnancy is rare but carries high rates of maternal and foetal morbidity and mortality if unrecognised.
  • Successful outcomes depend on early disease identification, prompt initiation of alpha- and beta-blockers, carefully planned delivery, and timely resection of the tumour.

Conclusion

Phaeochromocytoma complicating pregnancy is uncommon. Nonetheless, in view of the potential for catastrophic consequences if unrecognised, a high index of suspicion and careful evaluation for secondary causes of hypertension is of utmost importance. Blood pressure should be monitored in the post-partum period and persistence of hypertension must be thoroughly investigated.

Author Contributions

All authors participated in the management of the patient or writing of the article. AL and RCWM wrote the article, with contributions from all the authors.

References

  1. 1. Podymow T, August P (2007) Hypertension in pregnancy. Adv Chronic Kidney Dis 14: 178–190.T. PodymowP. August2007Hypertension in pregnancy.Adv Chronic Kidney Dis14178190
  2. 2. Paller MS (1998) Hypertension in pregnancy. J Am Soc Nephrol 9: 314–321.MS Paller1998Hypertension in pregnancy.J Am Soc Nephrol9314321
  3. 3. Ahlawat SK, Jain S, Kumari S, Varma S, Sharma BK (1999) Pheochromocytoma associated with pregnancy: Case report and review of the literature. Obstet Gynecol Surv 54: 728–737.SK AhlawatS. JainS. KumariS. VarmaBK Sharma1999Pheochromocytoma associated with pregnancy: Case report and review of the literature.Obstet Gynecol Surv54728737
  4. 4. Lenders JW, Eisenhofer G, Mannelli N, Pacak K (2005) Phaeochromocytoma. Lancet 366: 665–675.JW LendersG. EisenhoferN. MannelliK. Pacak2005Phaeochromocytoma.Lancet366665675
  5. 5. Lenders JW, Pacak K, Walther MM, Linehan WM, Mannelli M, et al. (2002) Biochemical diagnosos of pheochromocytoma: Which test is best. JAMA 287: 1427–1434.JW LendersK. PacakMM WaltherWM LinehanM. Mannelli2002Biochemical diagnosos of pheochromocytoma: Which test is best.JAMA28714271434
  6. 6. Ilias I, Pacak K (2004) Current approaches and recommended algorithm for the diagnostic localization of pheochromocytoma. J Clin Endocrinol Metab 89: 479–491.I. IliasK. Pacak2004Current approaches and recommended algorithm for the diagnostic localization of pheochromocytoma.J Clin Endocrinol Metab89479491
  7. 7. Pacak K (2007) Preoperative management of the pheochromocytoma patient. J Clin Endocrinol Metab 92: 4069–4079.K. Pacak2007Preoperative management of the pheochromocytoma patient.J Clin Endocrinol Metab9240694079
  8. 8. Harper MA, Murnaghan GA, Kennedy L, Hadden DR, Atkinson AB (1989) Phaeochromocytoma in pregnancy. Five cases and a review of the literature. Br J Obstet Gynaecol 96: 594–606.MA HarperGA MurnaghanL. KennedyDR HaddenAB Atkinson1989Phaeochromocytoma in pregnancy. Five cases and a review of the literature.Br J Obstet Gynaecol96594606
  9. 9. Mannelli M, Bemporad D (2002) Diagnosis and management of pheochromocytoma during pregnancy. J Endocrinol Invest 25: 567–571.M. MannelliD. Bemporad2002Diagnosis and management of pheochromocytoma during pregnancy.J Endocrinol Invest25567571
  10. 10. Amar L, Servais A, Gimenez-Roqueplo AP, Zinzindohoue GC, Plouin PF (2005) Year of diagnosis, features at presentation, and risk of recurrence in patients with pheochromocytoma or secreting paraganglioma. J Clin Endo Met 90: 2110–2116.L. AmarA. ServaisAP Gimenez-RoqueploGC ZinzindohouePF Plouin2005Year of diagnosis, features at presentation, and risk of recurrence in patients with pheochromocytoma or secreting paraganglioma.J Clin Endo Met9021102116
  11. 11. Pacak K, Eisenhofer G, Ahlman H, Bornstein SR, Gimenez-Roqueplo A-P, et al. (2007) Pheochromocytoma: Recommendations for clinical practice from the First International Symposium. Nat Clin Pract Endocrinol Metab 3: 92–102.K. PacakG. EisenhoferH. AhlmanSR BornsteinA-P Gimenez-Roqueplo2007Pheochromocytoma: Recommendations for clinical practice from the First International Symposium.Nat Clin Pract Endocrinol Metab392102
  12. 12. Benn DE, Gimenez-Roqueplo AP, Reilly JR, Bertherat J, Burgess J, et al. (2006) Clinical presentation and penetrance of pheochromocytoma/paraganglioma syndromes. J Clin Endocrin Metab 91: 827–836.DE BennAP Gimenez-RoqueploJR ReillyJ. BertheratJ. Burgess2006Clinical presentation and penetrance of pheochromocytoma/paraganglioma syndromes.J Clin Endocrin Metab91827836

Introduction:

Pregnancy Induced Hypertension (PIH) is a condition in which vasospasms occur during pregnancy in both small and large arteries. Signs of hypertension, proteinuria, and edema develop. It is unique to pregnancy and occurs in 5% to 7% of pregnancies in the united states. Despite years of research, the cause of the disorder is still unknown. Originally it was called toxemia because researchers pictured a toxin of some kind being produced by a women in response to foreign protein of the growing fetus, the toxin leading to the topical symptoms. No such toxins have ever been identified.

A condition separate from chronic hypertension, PIH tends to occur most frequently in women of color or with a multiple pregnancy; primiparas are younger than 20 years of age or older than 40 years, women from low socio economic backgrounds, those who have an underlying disease such as heart disease, diabetes with vessel or renal involvement and essential hypertension.

PIH is classified as gestational hypertension, mild preeclampsia, severe preeclampsia and eclampsia, depending on how far development advances. Gestational hypertension when develops an elevated blood pressure but has no proteinuria or edema. Perinatal mortality is not increased with simple gestational hypertension, so no drug therapy is necessary; and blood pressure returns to normal after birth. Mild preeclampsia when blood pressure rises to 140/90 mmHg or systolic pressure elevated 15 mmHg above pregnancy level; mild edema in upper extremities or face. Severe preeclampsia when blood pressure has risen to 160 mmHg systolic and 110 mmHg diastolic; proteinuria; pulmonary or cardiac involvement; extensive peripheral edema; hepatic dysfunction; theombocytopenia. Eclampsia is the most severe classification of PIH and seizure or coma Accompanied by s/s of preeclampsia. Any woman who falls into one of the high-risk categories for PIH should be observed carefully for symptoms at prenatal visits. She needs instructions about what symptoms to watch for so she can alert her clinician if additional symptoms occur between visits.

Anatomy and Physiology:

When most people hear the term cardiovascular system, they immediately think of the heart. We have all felt our own heart "pound" from time to time, and we tend to get a bit nervous when this happens. The crucial importance of the heart has been recognized for a long time. However, the cardiovascular system is much more than just the heart, and from a scientific and medical standpoint, it is important to understand why this system is so vital to life.

Most simply stated, the major function of the cardiovascular system is transportation. Using blood as the transport vehicle, the system carries oxygen, nutrients, cell wastes, hormones, and many other substances vital for body homeostasis to and from the cells. The force to move the blood around the body is provided by the beating heart. The cardiovascular system can be compared to a muscular pump equipped with one-way valves and a system of large and small plumbing tubes within which the blood travels.

HEART:

The heart is a muscular organ found in all vertebrates that is responsible for pumping blood throughout the blood vessels by repeated, rhythmic contractions.
The heart is enclosed in a double-walled sac called the pericardium. The superficial part of this sac is called the fibrous pericardium. This sac protects the heart, anchors its surrounding structures, and prevents overfilling of the heart with blood. It is located anterior to the vertebral column and posterior to the sternum. The size of the heart is about the size of a fist and has a mass of between 250 grams and 350 grams. The heart is composed of three layers, all of which are rich with blood vessels. The superficial layer, called the visceral layer, the middle layer, called the myocardium, and the third layer which is called the endocardium. The heart has four chambers, two superior atria and two inferior ventricles. The atria are the receiving chambers and the ventricles are the discharging chambers. The pathway of blood through the heart consists of a pulmonary circuit and a systemic circuit. Blood flows through the heart in one direction, from the atrias to the ventricles, and out of the great arteries, or the aorta for example. This is done by four valves which are the tricuspid atrioventicular valve, the mitral atrioventicular valve, the aortic semilunar valve, and the pulmonary semilunar valve.
Systemic circulation is the portion of the cardiovascular system which carries oxygenated blood away from the heart, to the body, and returns deoxygenated blood back to the heart. The term is contrasted with pulmonary circulation.

Pulmonary circulation is the portion of the cardiovascular system which carries oxygen-depleted blood away from the heart, to the lungs, and returns oxygenated blood back to the heart. The term is contrasted with systemic circulation. A separate system known as the bronchial circulation supplies blood to the tissue of the larger airways of the lung.

Arteries are blood vessels that carry blood away from the heart. All arteries, with the exception of the pulmonary and umbilical arteries, carry oxygenated blood.

Pulmonary arteries
The pulmonary arteries carry deoxygenated blood that has just returned from the body to the heart towards the lungs, where carbon dioxide is exchanged for oxygen.

Systemic arteries
Systemic arteries can be subdivided into two types – muscular and elastic – according to the relative compositions of elastic and muscle tissue in their tunica media as well as their size and the makeup of the internal and external elastic lamina. The larger arteries (>10mm diameter) are generally elastic and the smaller ones (0.1-10mm) tend to be muscular. Systemic arteries deliver blood to the arterioles, and then to the capillaries, where nutrients and gasses are exchanged.

The Aorta
The aorta is the root systemic artery. It receives blood directly from the left ventricle of the heart via the aortic valve. As the aorta branches, and these arteries branch in turn, they become successively smaller in diameter, down to the arteriole. The arterioles supply capillaries which in turn empty into venules. The very first branches off of the aorta are the coronary arteries, which supply blood to the heart muscle itself. These are followed by the branches off the aortic arch, namely the brachiocephalic artery, the left common carotid and the left subclavian arteries.

Aorta the largest artery in the body, originating from the left ventricle of the heart and extends down to the abdomen, where it branches off into two smaller arteries (the common iliacs). The aorta brings oxygenated blood to all parts of the body in the systemic circulation.

The aorta is usually divided into five segments/sections:

  • Ascending aorta—the section between the heart and the arch of aorta
  • Arch of aorta—the peak part that looks somewhat like an inverted "U"
  • Descending aorta—the section from the arch of aorta to the point where it divides into the common iliac arteries
    o    Thoracic aorta—the half of the descending aorta above the diaphragm
    o    Abdominal aorta—the half of the descending aorta below the diaphragm

Arterioles
Arterioles, the smallest of the true arteries, help regulate blood pressure by the variable contraction of the smooth muscle of their walls, and deliver blood to the capillaries.
Veins are blood vessels that carry blood towards the heart. Most veins carry deoxygenated blood from the tissues back to the lungs; exceptions are the pulmonary and umbilical veins, both of which carry oxygenated blood. Veins differ from arteries in structure and function; for example, arteries are more muscular than veins and they carry blood away from the heart.
Veins are classified in a number of ways, including superficial vs. deep, pulmonary vs. systemic, and large vs. small.

Superficial veins
Superficial veins are those whose course is close to the surface of the body, and have no corresponding arteries.

Deep veins
Deep veins are deeper in the body and have corresponding arteries.

Pulmonary veins
The pulmonary veins are a set of veins that deliver oxygenated blood from the lungs to the heart.

Systemic veins
Systemic veins drain the tissues of the body and deliver deoxygenated blood to the heart.
Atrium sometimes called auricle, refers to a chamber or space. It may be the atrium of the lateral ventricle in the brain or the blood collection chamber of a heart. It has a thin-walled structure that allows blood to return to the heart. There is at least one atrium in animals with a closed circulatory system.

Right atrium is one of four chambers (two atria and two ventricles) in the human heart. It receives deoxygenated blood from the superior and inferior vena cava and the coronary sinus, and pumps it into the right ventricle through the tricuspid valve. Attached to the right atrium is the right auricular appendix.

Left atrium is one of the four chambers in the human heart. It receives oxygenated blood from the pulmonary veins, and pumps it into the left ventricle, via the atrioventricular valve.
Ventricle is a chamber which collects blood from an atrium (another heart chamber that is smaller than a ventricle) and pumps it out of the heart.
Right ventricle is one of four chambers (two atria and two ventricles) in the human heart. It receives deoxygenated blood from the right atrium via the tricuspid valve, and pumps it into the pulmonary artery via the pulmonary valve and pulmonary trunk.

Left ventricle is one of four chambers (two atria and two ventricles) in the human heart. It receives oxygenated blood from the left atrium via the mitral valve, and pumps it into the aorta via the aortic valve.

Pathophysiology of Pregnancy Induced Hypertension (PIH):

Clinical Manifestations:

A.  Mild Preeclampsia

  • BP of 140/90
  • 1+ to 2+ proteinuria on random
  • weight gain of 2 lbs per week on the 2nd trimester and 1 lb per week on the 3rd trimester
  • Slight edema in upper extremities and face

B. Severe Preeclampsia

  • BP of 160/110
  • 3-4+ protenuria on random
  • Oliguria (less than 500 ml/24 hrs)
  • Cerebral or visual disturbances
  • Epigastric pain
  • Pulmonary edema
  • Peripheral edema
  • Hepatic dysfunction

C. Eclampsia is an extension of preeclampsia and is characterized by the client experiencing seizures.

 

Diagnostic Evaluation:

  1. Based on the presenting symptoms. Often the disease process has been developing and affecting the renal and vascular system
  2. Frequently a sudden weight gain will occur, of 2 lb. or more in 1 week, or 6 lb. or more within 1 month. This often occurs before the edema is present.

Medical Treatment and Evaluation:

  1. Magnesium Sulfate (Pregnancy risk category B)
      muscle relaxant, prevent seizures
      loading dose 4-6g, maintenance dose 1-2g/h IV
      infuse IV dose slowly over 15-30 min.
       •Always administer as a piggy back infusion.
       •Assess PR, urine output, DTR, and clonus every hour.
       •Observe for CNS depression and hypotonia in infant at birth.
  2. Hydrazaline (Apresoline) Pregnancy risk category C
      anti hypertensive (peripheral vasodilator) use to decrease hypertension
      5-10mg/IV
      Administer slowly to avoid sudden fall of BP
       •Maintain diastolic pressure over 90 mmHg to ensure adequate placental filling.
  3. Diazepam (Valium) Pregnancy risk category D
      halt seizures
      5-10mg/IV
      administer slowly. Dose may be repeated every 10-15 min. (up to 30mg/hr)
       •Observe for respiratory depression for both mother and infant at birth.
  4. Calcium Gluconate (Pregnancy risk category C)
      antidote for Magnesium Sulfate
      1g/IV (10 mL of a 10% solution)
      have prepared at bed side when administering Magnesium Sulfate
      administer at 5mL/min.

Complicationsof PIH:

  1. Intrauterine growth restriction (IUGR) – an abnormally restricted symmetric or asymmetric growth of fetus
  2. Oligohydramnios – abnormally low volume of amniotic fluid
  3. Risk of placental abruption – premature separation of a normally situated placenta from the wall of uterus
  4. Risk of preterm delivery (often iatrogenic) – delivery before 37 weeks of gestation
  5. Coagulopathy
  6. Stillbirth
  7. Seizures
  8. Coma
  9. Renal failure
  10. Maternal hepatic damage
  11. Hemolysis
  12. Elevated liver enzymes levels
  13. Low platelet count (HELLP syndrome)

Nursing Interventions:

Intervention for mild PIH:

Rationale:

1. Assess maternal VS and fetal heart rate.

-to detect any increase which is warning that a women’s condition is worsening.

2. Encourage elevation of edematous arms and legs.

-to increase venous blood return.

3. Encourage compliance with bed rest in a lateral recumbent position.

-to increase evacuation of sodium and encouraging diuresis and lateral recumbent position can avoid uterine pressure on the vena cava and prevent supine hypotension syndrome.

4. Provide emotional support.

-this can make a women underestimate the severity of the situation.

5. Support patient with bed rest and darken the room if possible.

-because a bright light can trigger seizures.

6. Obtain daily hematocrit levels as ordered.

-to monitor blood concentration and help to the extent of plasma loss to interstitial space or extent of the edema.

7. Obtain blood studies (CBC, platelets count, liver function, BUN and creatinine, and fibrin degregation).

-to assess for renal and liver function and the development of disseminated intravascular coagulation which often accompanies severe vasospasms.

8. Obtain daily weights at the same time each day.

-to evaluate tissue fluid retention.

9. Raise side rails.

-to help prevent injury if seizure should occur.

10. Support nutritious diet of moderate to high in protein and moderate in sodium.

-to compensate for protein she is losing in her urine.

11. An indwelling catheter may be inserted as ordered.

-to allow accurate recording of output and comparison with intake.

12. Oxygen administration to the mother may be given as ordered.

-to maintain adequate fetal oxygenation and prevent fetal bradycardia.

13. Administer medication for seizures and hypertension episodes as ordered.

-to prevent seizures and hypertension.

 

Intervention for severe PIH:

Rationale:

1. Maintain patient’s airway by not putting a tongue blade between a women’s teeth during seizures.

-to prevent broken of teeth which could then be aspirated.

2. Turn a woman on her side.

-to allow secretions to drain from her mouth.

 

Discharge Plan:

Exercise

  1. encourage patient’s on deep breathing exercises.
  2. move extremities when lying.
  3. elevate the head part when sleeping, to promote increase peripheral circulation
  4. encourage overall passive and active exercises program during pregnancy to prevent need for cesarean birth.
  5. exercises like tailor sitting, squatting, kegel exercise, pelvic rocking, and abdominal muscle contraction will promote easy delivery. 

Treatment:

  1. use of drugs
  2. catheterization
  3. obtaining labs. (CBC, platelets count, liver function, BUN and creatinine, and fibrin degregation)

Health Teaching:

  1. Encourage patient foe sodium restriction.
  2. Encourage to avoid foods rich in oil and fats.
  3. Encourage patient to limit her daily activities and exercises.

Ongoing Assessment:

  1. Observe carefully for symptoms at prenatal visit.
  2. Give instruction about what symptoms to watch for so she can alert her clinician if additional symptoms occur between visits.

Diet:

  1. low fats and sodium diet, restriction if possible.
  2. high in protein, calcium and iron.
  3. Adequate fluid intake

Sex:

  1. limit sexual activity
  2. sexual intercourse at 2nd trimester should be avoided.

 

View Nursing Care Plan – Pregnancy Induced Hypertension (PIH)

References:

  • Maternal and child health nursing by Adele Pillitteri 5th edition;volume 1 page 426-433;page 329-332
  • All-in-one care planning resource page 748; by Pamela L. Swearlngen, RN
  • Maternal neonatal nursing;page 30 by Lippincott Williams and Wilkins
  • Luckman and Sorensen’s Medical-Surgical Nursing a Physiologic Approach 4th edition Volume 1 page 734
  • http://wikipedia.org
  • http://nursingcrib.com

Daisy Jane Antipuesto RN MN

Currently a Nursing Local Board Examination Reviewer. Subjects handled are Pediatric, Obstetric and Psychiatric Nursing. Previous work experiences include: Clinical instructor/lecturer, clinical coordinator (Level II), caregiver instructor/lecturer, NC2 examination reviewer and staff/clinic nurse. Areas of specialization: Emergency room, Orthopedic Ward and Delivery Room. Also an IELTS passer.

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