Pregnancy induced hypertension, also known as gestational hypertension, is a potentially life-threatening disorder that usually develops late in the second trimester or in the third trimester. The non-convulsive form of PIH is termed as preeclampsia ranging from mild to severe. The convulsive form is eclampsia. The cause of this disorder is unknown but geographic, ethnic, racial, nutritional, immunologic, and familial factors and preexisting vascular disease may contribute to its development.
Nursing care for PIH involves providing adequate nutrition, good prenatal care, and control of pre-existing hypertension during pregnancy decrease the incidence and severity of preeclampsia. Early recognition and prompt treatment of preeclampsia can prevent progression to eclampsia.
Deficient Fluid Volume
May be related to
- Osmotic pressure
- Plasma protein loss
- Decreasing plasma colloid
- Allowing fluid shifts out of the vascular compartment
Possibly evidenced by
- Edema formation
- Sudden weight gain
- Decreased urine output
- Epigastric pain
- Visual changes
- Patient engages in therapeutic regimen and monitoring, as indicated.
- Patient verbalizes understanding of need for close monitoring of weight, BP, urine protein, and edema.
- Patient is free of signs of generalized edema (i.e., epigastric pain, cerebral symptoms, dyspnea, nausea/vomiting)
- Patient exhibits Hct WNL and physiological edema with no signs of pitting.
|Weigh patient regularly. Tell patient to record weight at home in between visits.||Abrupt, notable weight gain (e.g., more than 3.3 lb (1.5 kg)/month in the second trimester or more than 1 lb (0.5 kg)/wk in the third trimester) reflects fluid retention. Fluid moves from the vascular to interstitial space, resulting in edema.|
|Differentiate physiological and pathological edema of pregnancy. Locate and determine degree of pitting.||The presence of pitting edema (mild, 1+ to 2+; severe, 3+ to 4+) of face, hands, legs, sacral area, or abdominal wall, or edema that does not disappear after 12hr of bedrest is vital. Note: Significant edema may actually be present in nonpre-eclamptic patient sand absent in patients with mild or moderated PIH.|
|Note signs of progressive or excessive edema i.e., epigastric/RUQ pain, cerebral symptoms, nausea, vomiting). Assess for possible eclampsia.||Edema and intravascular fibrin deposition (in HELLP syndrome) within the encapsulated liver are manifested by RUQ pain; dyspnea, indicating pulmonary involvement; cerebral edema, possibly leading to seizures; and nausea and vomiting, indicating GI edema.|
|Note alteration in Hct/Hb levels.||Identifies degree of hemoconcentration caused by fluid shift. If Hct is less than 3 times Hb level, hemoconcentration exists.|
|Check on dietary intake of proteins and calories. Give information as needed.||Proper nutrition decreases incidence of prenatal hypovolemia and hypoperfusion; insufficient protein/calories increases the risk of edema formation and PIH. Intake of 80–100 g of protein may be required daily to replace losses.|
|Monitor intake and output. Note urine color, and measure specific gravity as indicated.||Urine output is a sensitive indicator of circulatory blood volume. Oliguria and specific gravity of 1.040 indicate severe hypovolemia and kidney involvement. Note: Administration of magnesium sulfate (MgSO4)may cause transient increase in output.|
|Examine clean, voided urine for protein each visit, or daily/hourly as appropriate if hospitalized. Report readings of 2+, or greater.||Aids in identifying degree of severity/progression of condition. A 2+ reading implies glomerular edema or spasm. Proteinuria affects fluid shifts from the vascular tree. Note: Urine contaminated by vaginal secretions may test positive for protein, or dilution may result in a false-negative result. In addition, PIH may be present without significant proteinuria.|
|Assess lung sounds and respiratory rate/effort.||Dyspnea and crackles may mean pulmonary edema, which needs immediate treatment.|
|Check BP and pulse.||Rise in BP may happen in response to catecholamines, vasopressin, prostaglandins, and, as recent findings suggest, decreased levels of prostacyclin.|
|Respond to questions and review rationale for avoiding use of diuretics to treat edema.||Diuretics further increase chances of dehydration by decreasing intravascular volume and placental perfusion, and they may cause thrombocytopenia, hyperbilirubinemia, or alteration in carbohydrate metabolism in fetus/newborn. Note: May be useful in treating pulmonary edema.|
|Schedule prenatal visit every 1–2 wk if PIH is mild; weekly if severe.||Important to monitor changes more closely for the well-being of the patient and fetus.|
|Review moderate sodium intake of up to 6 g/day. Tell patient to read food labels and avoid foods high in sodium (e.g., bacon, luncheon meats, hot dogs, canned soups, and potato chips).||Some sodium intake is necessary because levels below 2–4 g/day result in greater dehydration in some patients. However, excess sodium may increase edema formation.|
|Collaborate with dietitian as indicated.||Nutritional consult may be beneficial in determining individual needs/dietary plan.|
|Place patient on strict regimen of bedrest; encourage lateral position.||Lateral recumbent position decreases pressure on the vena cava, increasing venous return and circulatory volume. This enhances placental and renal perfusion, reduces adrenal activity, and may lower BP as well as account for weight loss through diuresis of up to 4 lb in 24-hr period.|
|Educate patient and family members or significant others on home monitoring/day-care program, as appropriate.||Some mildly hypertensive patients without proteinuria may be managed on an outpatient basis if adequate surveillance and support is provided and the patient/family actively participates in the treatment regimen.|
|Substitute fluids either orally or parenterally via infusion pump, as indicated.||Fluid replacement treats hypovolemia, yet must be given cautiously to prevent overload, especially if interstitial fluid is drawn back into circulation when activity is reduced. With renal involvement, fluid intake is restricted; i.e., if output is reduced (less than 700 ml/24 hr), total fluid intake is restricted to approximate output plus insensible loss. Use of infusion pump allows more accurate control delivery of IV fluids.|
|When fluid deficit is severe and patient is hospitalized:|
|Allows more accurate monitoring of output/renal perfusion.|
|Gives a more precise measurement of fluid volume. In normal pregnancy, plasma volume increases by 30%–50%, yet this increase does not occur in the patient with PIH.|
|Elevated levels, especially of uric acid, indicate impaired kidney function, worsening of maternal condition, and poor fetal outcome.|
|Patients with HELLP syndrome awaiting delivery of the fetus may benefit from transfusion of platelets when count is below 20,000.|
Decreased Cardiac Output
Decreased Cardiac Output: Inadequate blood pumped by the heart to meet metabolic demands of the body.
May be related to
- Hypovolemia/decreased venous return
- Increased systemic vascular resistance
Possibly evidenced by
- Change in blood pressure/hemodynamic readings
- Shortness of breath
- Alteration in mental status
- Patient remains normotensive throughout remainder of pregnancy.
- Patient reports absence and/or decreased episodes of dyspnea.
- Patient alters activity level as condition warrants.
|Record and graph vital signs especially BP and pulse.||The patient with PIH does not display the normal cardiovascular response to pregnancy (left ventricular hypertrophy, increase in plasma volume, vascular relaxation with decreased peripheral resistance). Hypertension (the second manifestation of PIH after edema) occurs owing to increased sensitization to angiotensin II, which increases BP, promotes aldosterone release to increase sodium/water reabsorption from the renal tubules, and constricts blood vessels.|
|Assess MAP at 22 weeks’ gestation. A pressure of 90 mm Hg is considered predictive of PIH. Assess for crackles, wheezes, and dyspnea; note respiratory rate/effort.||Pulmonary edema may transpire, with modification in peripheral vascular resistance and drop in plasma colloid osmotic pressure.|
|Institute bedrest with patient in lateral position.||Improves venous return, cardiac output, and renal/placental perfusion.|
|Check for invasive hemodynamic parameters.||Provides precise picture of vascular changes and fluid volume. Prolonged vascular constriction, increased hemoconcentration, and fluid shifts decrease cardiac output.|
|Give antihypertensive drug such as hydralazine (Apresoline) PO/IV, so that diastolic readings are between 90 and 105 mm Hg. Begin maintenance therapy as needed, e.g., methyldopa (Aldomet) or nifedipine (Procardia).||If BP does not respond to conservative measures, short-term medication may be needed in conjunction with other therapies, e.g., fluid replacement and MgSO4. Antihypertensive drugs work directly on arterioles to promote relaxation of cardiovascular smooth muscle and help increase blood supply to cerebrum, kidneys, uterus, and placenta. Hydralazine is the drug of choice because it does not produce effects on the fetus. Sodium nitroprusside is being used with some success to lower BP (especially in HELLP syndrome).|
|Check on BP and side effects of antihypertensive drugs. Administer propranolol (Inderal), as appropriate.||Side effects such as tachycardia, headache, nausea, and vomiting, and palpitations may be treated with propranolol.|
|Prepare for birth of fetus by cesarean delivery, labor when severe PIH/eclamptic condition is stabilised, but vaginal delivery is not feasible.||If conservative treatment is ineffective and labor induction is ruled out, then surgical procedure is the only means of halting the hypertensive problems.|
Altered Tissue Perfusion (Uteroplacental)
Impaired Tissue Perfusion: Decreased in the oxygen resulting in the failure to nourish the tissues at the capillary level.
May be related to
- Maternal hypovolemia
- Interruption of blood flow (progressive vasospasm of spiral arteries)
Possibly evidenced by
- Intrauterine growth retardation
- Changes in fetal activity/heart rate
- Premature delivery
- Fetal demise
- Patient demonstrates normal CNS reactivity on nonstress test (NST)
- Patient is free of late decelerations;
- Patient has no decrease in FHR on contraction stress test/oxytocin challenge test (CST/OCT).
- Patient is full-term, AGA.
|Present information to patient/couple concerning home assessment or noting daily fetal movements and when to seek immediate medical attention.||Decrease in placental blood flow results in reduced gas exchange and impaired nutritional functioning of the placenta. Potential outcomes of poor placental perfusion include a malnourished, LBW infant, and prematurity associated with early delivery, abruptio placentae, and fetal death. Reduced fetal activity means fetal compromise (occurs before detectable alteration in FHR and indicates demand for immediate evaluation/intervention.|
|Name factors affecting fetal activity.||Cigarette smoking, medication/drug use, serum glucose levels, environmental sounds, time of day,and sleep-wake cycle of the fetus can increase or decrease fetal movement.|
|Report signs of abruptio placentae (i.e., vaginal the bleeding, uterine tenderness, abdominal pain, and decreased fetal activity).||Immediate attention and intervention increases the likelihood of a positive outcome.|
|Present contact number for patient to direct questions, address changes in daily fetal movements, and so forth.||Provides chance to address concerns/misconceptions and intervene in a timely manner, as indicated.|
|Evaluate fetal growth; measure progressive fundal accompany growth at each office visit or periodically during stress home visits, as appropriate.||Reduced placental functioning may accompany PIH, resulting in IUGR. Chronic intrauterine stress and uteroplacental insufficiency decrease amount of fetal contribution to amniotic fluid pool.|
|Note fetal response to medications such as MgSO4, phenobarbital, and diazepam.||Depressant effects of medication reduce fetal respiratory and cardiac function and fetal activity level, even though placental circulation may be adequate.|
|Check FHR manually or electronically, as indicated.||Helps evaluate fetal well-being. An elevated FHR may show a compensatory response to hypoxia, prematurity, or abruptio placentae.|
|Assess fetal response to BPP criteria or CST, as maternal status indicates.||BPP helps evaluate fetus and fetal environment on five specific parameters to assess CNS function and fetal contribution to amniotic fluid volume. CST assesses placental functioning and reserves.|
|Assist with assessment of fetal maturity and well-being using L/S ratio, presence of PG, estriol levels, FBM, and sequential sonography beginning at 20–26 weeks’ gestation.||In the event of declining maternal/fetal condition, risks of delivering a preterm infant are weighed against the risks of continuing the pregnancy, using results from evaluative studies of lung and kidney maturity, fetal growth, and placental functioning. IUGR is associated with reduced maternal volume and vascular changes.|
|Assist with assessment of maternal plasma volume at 24–26 weeks’ gestation using Evans’ blue dye when indicated.||Identifies fetus at risk for IUGR or intrauterine fetal demise associated with reduced plasma volume and reduced placental perfusion.|
|Utilizing an ultrasonography, assist with assessment of placental size.||Reduced placental function and size are associated with PIH.|
|Give corticosteroid (dexamethasone, betamethasone) IM for at least 24–48 hr, but not more than 7 days before delivery, when severe PIH necessitates premature delivery between 28 and 34 weeks’ gestation.||Corticosteroids are thought to induce fetal pulmonary maturity (surfactant production) and prevent respiratory distress syndrome, at least in a fetus delivered prematurely because of condition or inadequate placental functioning. Best results are obtained when fetus is less than 34 weeks’ gestation and delivery occurs within a week of corticosteroid administration|
Risk for Maternal Injury
Risk for Injury: Vulnerable for injury as a result of environmental conditions interacting with the individual’s adaptive and defensive resources, which may compromise health.
May be related to
- Tissue edema/hypoxia
- Tonic-clonic convulsions
- Abnormal blood profile and/or clotting factors
Possibly evidenced by
- [Not applicable: Presence of signs/symptoms establishes an actual diagnosis]
- Patient participates in treatment and/or environmental modifications to protect self and enhance safety.
- Patient is free of signs of cerebral ischemia (visual disturbances, headache, changes in mentation).
- Patient displays normal levels of clotting factors and liver enzymes
|Check for CNS involvement (i.e., headache, irritability, visual disturbances or changes on funduscopic examination).||Cerebral edema and vasoconstriction can be evaluated in terms of symptoms, behaviors, or retinal changes.|
|Emphasize importance of patient promptly reporting signs/symptoms of CNS involvement.||Delayed treatment or progressive onset of symptoms may result in tonic-clonic convulsions or eclampsia.|
|Check for alterations in level of consciousness.||In progressive PIH, vasoconstriction and vasospasms of cerebral blood vessels reduce oxygen consumption by 20% and result in cerebral ischemia.|
|Assess for signs of impending eclampsia: hyperactivity of deep tendon reflexes (3+ to 4+), ankle clonus, decreased pulse and respirations, epigastric pain, and oliguria (less than 50 ml/hr).||Generalized edema/vasoconstriction, manifested by severe CNS, kidney, liver, cardiovascular, and respiratory involvement, precede convulsive state.|
|Establish measures to lessen likelihood of seizures; i.e., keep room quiet and dimly lit, limit visitors, plan and coordinate care, and promote rest.||Lessens environmental factors that may stimulate irritable cerebrum and cause a convulsive state.|
|Enforce seizure precautions per protocol.||If seizure does occur, reduces risk of injury.|
|In the event of a seizure:||Maintains airway by reducing risk of aspiration and preventing tongue from occluding airway. Maximizes oxygenation. Note: Be cautious with use of airway/bite block, because attempts to insert when jaws are set may result in injury.|
|These signs may indicate abruptio placentae, especially if there is a preexisting medical problem, such as diabetes mellitus, or a renal or cardiac disorder causing vascular involvement.|
|Convulsions increase uterine irritability; labor may ensue.|
|During seizure activity, fetal bradycardia may occur.|
|Monitor for signs of DIC easy/spontaneous bruising, prolonged bleeding, epistaxis, GI bleeding.||Abruptio placentae with release of thromboplastin predisposes patient to DIC.|
|Hospitalize if CNS involvement is present.||Immediate introduction of therapy helps to ensure safety and limit complications.|
|Give MgSO 4 IM or IV using infusion pump.||MgSO4 a CNS depressant, decreases acetylcholine release, blocks neuromuscular transmission, and prevents seizures. It has a transient effect of lowering BP and increasing urine output by altering vascular response to pressor substances. Although IV administration of MgSO4 is easier to regulate and reduces the risk of a toxic reaction, some facilities may still use the IM route if continuous surveillance is not possible and/or if appropriate infusion apparatus is not available. Note: Adding 1 ml of 2% lidocaine to the IM injection may reduce associated discomfort. (Current research suggests the use of phenytoin infusion may be effective in the treatment of PIH without the adverse side effects, such as respiratory depression, and tocolytic effect on uterine smooth muscle, which can impede labor during intrapartum therapy.)|
|Monitor BP before, during, and after MgSO4 administration. Note serum magnesium levels in conjunction with respiratory rate, patellar/deep tendon reflex (DTRs), and urine output.||A therapeutic level of MgSO4is achieved with serum levels of 4.0–7.5 mEq/L or 6–8 mg/dL. Adverse/toxic reactions develop above 10–12 mg/dL, with loss of DTRs occurring first, respiratory paralysis between 15–17 mg/dL, or heart block occurring at 30–35 mg/dL.|
|Ready calcium gluconate. Give 10 ml (1 g/10 ml) over 3 min as indicated.||Serves as antidote to counteract adverse/toxic effects of MgSO4.|
|Administer amobarbital (Amytal) or diazepem (Valium), as indicated.||Depresses cerebral activity; has sedative effect when convulsions are not controlled by MgSO4. Not recommended as first-line therapy because sedative effect also extends to the fetus.|
|Perform funduscopic examination regulary.||Helps to evaluate changes or severity of retinal involvement.|
|Review test results of clotting time, PT, PTT, fibrinogen levels, and FPS/FDP.||Such tests can indicate depletion of coagulation factors and fibrinolysis, which suggests DIC.|
|Scan sequential platelet count. Avoid amniocentesis if platelet count is less than 50,000/mm3. If thrombocytopenia is present during operative procedure, use general anesthesia. Transfuse with platelets, packed red blood cells, fresh frozen plasma, or whole blood, as indicated. Rule out HELLP syndrome.||Thrombocytopenia may arise because of platelet adherence to disrupted endothelium or reduced prostacyclin levels (a potent inhibitor of platelet aggregation). Invasive procedures or anesthesia requiring needle puncture (such as spinal/epidural) could result in excessive bleeding.|
|Monitor liver enzymes and bilirubin; note hemolysis and presence of Burr cells on peripheral smear.||Elevated liver enzyme (AST, ALT) and bilirubin levels, microangiopathic hemolytic anemia, and thrombocytopenia may indicate presence of HELLP syndrome, signifying a need for immediate cesarean delivery if condition of cervix is unfavorable for induction of labor.|
|Prepare for cesarean birth if PIH is severe, placental functioning is compromised, and cervix is not ripe or is not responsive to induction.||When fetal oxygenation is severely reduced owing to vasoconstriction within malfunctioning placenta, immediate delivery may be necessary to save the fetus.|
Risk for Imbalanced Nutrition: Less Than Body Requirements
Imbalanced Nutrition: Less Than Body Requirements: Intake of nutrients insufficient to meet metabolic needs.
May be related to
- Intake insufficient to meet metabolic demands and replace losses
Possibly evidenced by
- [Not applicable; presence of signs/symptoms establishes an
- Patient verbalizes understanding of individual dietary needs.
- Patient demonstrates knowledge of proper diet as evidenced by developing a dietary plan within own financial resources.
- Patient displays appropriate weight gain.
|Determine patient’s nutritional status, condition of hair and nails, and height and pregravid weight.||Establishes guidelines for determining dietary needs and educating patient. Malnutrition may be a contributing factor to the onset of PIH, specifically when client follows a low-protein diet, has insufficient caloric intake, and is overweight or underweight by 20% or more before conception.|
|Provide information about normal weight gain in pregnancy, modifying it to meet client’s needs.||The underweight patient may need a diet higher in calories; the obese patient should avoid dieting because it places the fetus at risk for ketosis.|
|Present oral/written information about action and uses of protein and its role in development of PIH.||Regular intake of 80–100 g/day (1.5 g/kg) is sufficient to replace proteins lost in urine and allow for normal serum oncotic pressure.|
|Provide information regarding effect of bedrest and reduced activity on protein requirements.||Decreasing metabolic rate through bedrest and limited activity reduces protein needs.|
|Collaborate with dietitian, as indicated.||Helpful in creating individual dietary plan incorporating specific needs/restrictions.|
Deficient Knowledge: Absence or deficiency of cognitive information related to specific topic.
May be related to
- Lack of exposure
- Unfamiliarity with information resources
Possibly evidenced by
- Request for information
- Statement of misconceptions
- Inaccurate follow-through of instructions
- Development of preventable complications
- Patient identifies signs/symptoms requiring medical evaluation.
- Patient performs necessary procedures correctly.
- Patient verbalizes understanding of disease process and appropriate treatment plan.
- Patient initiate lifestyle/behavior changes as indicated.
|Assess patient’s/couple’s knowledge of the disease process. Provide information about pathophysiology of PIH, implications for mother and fetus; and the rationale for interventions, procedures, and tests, as needed.||Establishes data base and provides information. Provide information about areas in which learning is needed. Taking information can improve understanding and reduce fear, helping to facilitate the treatment plan for the client. Note: Current research in progress may provide additional treatment options, such as using low-dose (60 mg/day) aspirin to reduce thromboxane generation by platelets, limiting the severity/incidence of PIH.|
|Provide information about signs/symptoms indicating worsening of condition, and instruct patient when to notify healthcare provider.||Helps ensure that patient seeks timely treatment and may prevent worsening of preeclamptic state or additional complications.|
|Have patient informed of health status, results of when tests, and fetal well-being.||Fears and anxieties can be compounded when patient/couple does not have adequate information about the state of the disease process or its impact on patient and fetus.|
|Educate patient on how to monitor her own weight at home, and to notify healthcare provider if gain is in excess of 2 lb/wk, or 0.5 lb/day.||Gain of 3.3 lb or greater per month in second trimester or 1 lb or greater per week in third trimester is suggestive of PIH.|
|Educate and assist family members in learning the procedure for home monitoring of BP, as indicated.||Encourages cooperation in treatment regimen, allows immediate intervention as needed, and may provide reassurance that efforts are beneficial.|
|Review techniques for stress management and diet restriction.||Strengthens importance of patient’s responsibility in treatment.|
|Provide information about ensuring enough protein in diet for patient with possible or mild preeclampsia.||Protein is essential for intravascular and extravascular fluid regulation.|
|Review self-testing of urine for protein. Reinforce rationale for and implications of testing.||A test result of 2+ or greater is vital and needs to be reported to healthcare provider. Urine specimen contaminated by vaginal discharge or RBCs may produce positive test result for protein.|
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Maternal and Newborn Care Plans
Nursing care plans related to the care of the pregnant mother and her infant. See care plans for maternity and obstetric nursing:
- Abruptio Placenta| 3 Care Plan
- Cesarean Birth | 10 Care Plans
- Cleft Palate and Cleft Lip | 6 Care Plans
- Dysfunctional Labor (Dystocia) | 4 Care Plans
- Elective Termination | 6 Care Plans
- Gestational Diabetes Mellitus | 4 Care Plans
- Hyperbilirubinemia | 4 Care Plans
- Labor Stages, Induced and Augmented Labor | 36 Care Plans
- Neonatal Sepsis | 5 Care Plans
- Perinatal Loss | 5 Care Plans
- Placenta Previa | 3 Care Plans
- Postpartum Hemorrhage | 8 Care Plans
- Postpartum Thrombophlebitis | 4 Care Plans
- Prenatal Hemorrhage | 7 Care Plans
- Prenatal Substance Dependence/Abuse | 6 Care Plans
- Precipitous Labor | 3 Care Plans
- Pregnancy Induced Hypertension | 6 Care Plans
- Premature Dilation of the Cervix | 3 Care Plans
- Prenatal Infection | 3 Care Plans
- Preterm Labor | 6 Care Plans
- Puerperal Infection | 4 Care Plans