Preeclampsia - Nursing Case Study
Pathophysiology
• Primary Mechanism: Impaired Placental Development - In preeclampsia, the placenta doesn't develop properly due to issues with blood vessels that supply it. This is triggered by poor placental implantation, leading to reduced blood flow and inadequate oxygen and nutrients to the fetus.
• Secondary Mechanism: Endothelial Dysfunction - The impaired placental development causes release of anti-angiogenic factors into maternal circulation. These factors cause widespread inflammation and damage to the endothelial cells (lining of blood vessels), resulting in high blood pressure and multi-system organ damage.
• Key Complication: HELLP Syndrome - A severe form of preeclampsia, it involves Hemolysis (destruction of red blood cells), Elevated Liver enzymes (indicating liver damage) and Low Platelet count (increasing risk of bleeding). It's a life-threatening condition requiring immediate medical intervention.
Patient Profile
Demographics:
28-year-old pregnant female, school teacher
History:
• Key past medical history: Hypertension, history of a previous miscarriage
• Current medications: Prenatal vitamins, low-dose aspirin
• Allergies: No known allergies
Current Presentation:
• Chief complaint: Severe headache, blurry vision, upper abdominal pain
• Key symptoms: Swelling in hands and face, rapid weight gain, decreased urine output
• Vital signs: Blood pressure 160/100 mmHg, heart rate 92 bpm, respiratory rate 18 breaths per minute, temperature 98.6°F, oxygen saturation 97% on room air
Section 1
Change in Patient Status:
The patient's condition began to deteriorate the next day. She complained of increased upper abdominal pain, and her blood pressure had increased to 170/110 mmHg. She also reported worsening vision and a severe headache, which suggested potential central nervous system involvement. Her urine output continued to decrease and she had gained an additional two pounds overnight. Her heart rate rose to 105 bpm, and her respiratory rate increased to 22 breaths per minute, indicating her body's increased effort to compensate for the hypertension and potential fluid overload.
Response to Interventions:
Despite administration of antihypertensive medications, the patient's blood pressure remained persistently high. Magnesium sulfate was initiated to prevent seizures, but her symptoms continued to worsen. Fetal monitoring showed signs of distress, with decreased movement and heart rate variability. An emergency cesarean section was decided upon to safeguard both maternal and fetal health. The patient was prepped for surgery and counseled about the risks and benefits. She was overwhelmed but agreed to the procedure, understanding the urgency of the situation.
Section 2
New Diagnostic Results:
Post cesarean section, the patient's blood pressure readings continued to fluctuate and remain high at 175/115 mmHg. The lab results revealed a significant increase in liver enzymes, with AST at 70 U/L and ALT at 90 U/L, indicating possible liver damage. The platelet count had dropped to 90,000 per microliter, suggesting a risk for disseminated intravascular coagulation. Her serum creatinine levels also elevated to 1.5 mg/dL, pointing towards deteriorating kidney function. The patient's urine output remained low at 20 mL/hr, and her weight increased by another pound, suggesting persistent fluid retention.
Change in Patient Status:
Despite successful delivery of the baby, the patient's condition continued to worsen. She was experiencing more frequent bouts of upper abdominal pain and her headache persisted. She also began exhibiting signs of confusion and agitation, suggesting an escalation of the central nervous system involvement. Her vision disturbances worsened, with her reporting blurred vision and seeing spots. Her breaths became more labored, increasing to 24 breaths per minute. The patient's skin appeared pale and her extremities felt cold to touch, indicating compromised perfusion due to the ongoing hypertensive crisis.
Section 3
New Complications:
Over the following hours, the patient began to complain of severe chest pain and shortness of breath. Her respiratory rate increased to 30 breaths per minute and pulse oximetry revealed oxygen saturation levels dropping to 90%. Auscultation of the chest revealed crackles in the lower lobes of both lungs, suggesting the development of pulmonary edema - a serious complication of preeclampsia. Additionally, her urine output continued to decrease further to 15 mL/hr, despite attempts to optimize her fluid status.
On further investigation, her cardiac enzymes - Troponin I levels elevated to 0.3 ng/mL, indicating possible myocardial damage. An emergency ECG showed ST-segment elevation, suggesting the possibility of a myocardial infarction. Her platelet count further dropped to 80,000 per microliter, raising the risk of disseminated intravascular coagulation. Her mental status continued to deteriorate, demonstrating increased confusion and restlessness. These new developments necessitated immediate reassessment of the ongoing treatment plan and a need for critical clinical decision-making to prevent further deterioration of the patient's condition.
Section 4
Change in Patient Status:
Over the next few hours, the patient's condition continued to deteriorate. She became increasingly restless and confused, and her Glasgow Coma Scale (GCS) score dropped to 12 from 15, indicating a significant decrease in the level of consciousness. Her blood pressure remained dangerously high at 170/100 mmHg despite antihypertensive therapy. The patient's respiratory rate further increased to 35 breaths per minute, and her oxygen saturation continued to decline, reaching as low as 88% on 4 L of supplemental oxygen. Her urine output remained low at 15 mL/hr, and she developed abdominal tenderness, particularly in the right upper quadrant.
New Diagnostic Results:
An urgent computed tomography (CT) scan of the head was performed to rule out cerebral edema or intracranial hemorrhage, which could explain her altered mental status. The scan revealed mild cerebral edema without any signs of hemorrhage. Repeat lab work showed a further decrease in platelets to 65,000 per microliter and a significant rise in liver enzymes - AST and ALT levels were elevated to 240 U/L and 200 U/L, respectively. This suggested the development of HELLP syndrome (hemolysis, elevated liver enzymes, low platelets), a severe form of preeclampsia. An echocardiogram was ordered to evaluate her cardiac function and revealed a reduced ejection fraction of 45%, indicative of possible heart failure. These new developments created a need for immediate intervention and alterations to the current treatment strategy.
Section 5
New Complications:
As the patient's condition continued to decline, she began to complain of worsening headache and blurred vision, indicative of impending eclampsia. Furthermore, she developed petechiae - small, red or purple spots on the skin caused by minor bleeding from broken capillaries - suggesting possible DIC (disseminated intravascular coagulation), a potentially life-threatening complication of severe preeclampsia and HELLP syndrome. Her worsening respiratory status, combined with her declining mental status and the development of petechiae, were indicative of a deteriorating condition requiring further aggressive intervention.
Response to Interventions:
The medical team initiated immediate measures to prevent the progression of the patient's condition. Magnesium sulfate was administered for seizure prophylaxis, and the patient was intubated to maintain airway patency and improve oxygenation. The patient's blood pressure was continuously monitored, and further doses of antihypertensive medication were administered to maintain her BP below the target of 160/110 mmHg. Platelets and fresh frozen plasma were transfused to improve the patient's coagulation status. Moreover, preparations were made for immediate delivery of the baby, as it would not only potentially halt the progression of the patient's preeclampsia, but would also prevent further fetal distress.