6 Pregnancy Induced Hypertension Nursing Care Plans

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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 Plans

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.

Here are six (6) nursing diagnosis for your nursing care plans on Gestational Hypertension or Pregnancy Induced Hypertension

  1. Deficient Fluid Volume
  2. Decreased Cardiac Output
  3. Altered Tissue Perfusion (Uteroplacental)
  4. Risk for Maternal Injury
  5. Risk for Imbalanced Nutrition: Less Than Body Requirements
  6. Deficient Knowledge
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Risk for Maternal Injury

Nursing Diagnosis

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  • Risk for Injury

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]

Desired Outcomes

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  • 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
Nursing Interventions Rationale
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:

  • Position patient on side; insert airway/bite block only if mouth is relaxed; suction nasopharynx, as indicated; administer oxygen; avoid restrictive clothing; do not restrict movement. Document motor involvement, duration of seizure, and postseizure behavior.
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.
  • Palpate for uterine tenderness or rigidity; check for vaginal bleeding. Review history of other medical problems.
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.
  • Observe for signs and symptoms of labor or uterine contractions.
Convulsions increase uterine irritability; labor may ensue.
  • Assess fetal well-being, noting FHR.
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.
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