Preeclampsia - Nursing Case Study

Pathophysiology

• Primary mechanism: Aberrant placental development leads to shallow trophoblastic invasion, resulting in impaired spiral artery remodeling. This causes reduced placental perfusion and placental ischemia, triggering systemic endothelial dysfunction.

• Secondary mechanism: Endothelial dysfunction elevates circulating anti-angiogenic factors (e.g., sFlt-1), disrupting vascular homeostasis. This imbalance leads to widespread vasoconstriction, hypertension, and organ hypoperfusion.

• Key complication: Endothelial damage and reduced organ perfusion can result in severe complications such as HELLP syndrome, characterized by hemolysis, elevated liver enzymes, and low platelet count, posing significant maternal and fetal risks.

Patient Profile

Demographics:

32, female, high-stress corporate executive

History:

• Key past medical history: Chronic hypertension, Type 2 diabetes, previous preeclampsia in first pregnancy

• Current medications: Labetalol, Metformin, Prenatal vitamins

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe headaches and visual disturbances

• Key symptoms: Shortness of breath, upper abdominal pain, swelling in hands and face, confusion

• Vital signs: Blood pressure 190/120 mmHg, heart rate 110 bpm, respiratory rate 28 breaths per minute, temperature 37.8°C, oxygen saturation 91% on room air

Section 1

As the healthcare team conducts an initial assessment of the patient, they immediately recognize the severity of her condition. Her severe headaches and visual disturbances, coupled with her elevated blood pressure of 190/120 mmHg, signal a critical need for intervention. The patient's respiratory rate is elevated at 28 breaths per minute, and her oxygen saturation is concerning at 91% on room air, indicating potential respiratory compromise. The upper abdominal pain and swelling in her hands and face further suggest the possibility of developing HELLP syndrome, a life-threatening complication of preeclampsia. Neurological assessment reveals confusion and disorientation, raising concerns about cerebral edema or impending eclampsia.

Laboratory tests are expedited to confirm the suspicion of HELLP syndrome. Results reveal a hemolytic anemia with a hemoglobin level of 9.5 g/dL, elevated liver enzymes with an AST of 178 U/L and ALT of 165 U/L, and a critically low platelet count of 85,000/mm^3. These findings confirm the presence of HELLP syndrome and necessitate immediate management strategies. Renal function tests show a rising creatinine level of 1.8 mg/dL, indicating kidney involvement and further emphasizing the need for urgent intervention.

Given the patient's deteriorating condition, the medical team initiates magnesium sulfate to prevent seizures, administers intravenous antihypertensives to manage severe hypertension, and provides supplemental oxygen to improve her oxygen saturation. Despite these measures, her condition remains precarious, and the decision is made to expedite delivery to mitigate worsening maternal and fetal outcomes. The healthcare team prepares for an emergency cesarean section, recognizing that timely delivery is the definitive treatment for preeclampsia and its associated complications.

Section 2

As the medical team prepares for the emergency cesarean section, the patient experiences a sudden change in status. Her respiratory rate escalates to 34 breaths per minute, and her oxygen saturation drops further to 87% despite supplemental oxygen, indicating worsening respiratory distress. Auscultation of the lungs reveals diffuse crackles, suggesting the development of pulmonary edema, a serious complication of preeclampsia that necessitates immediate attention. The patient's heart rate rises to 130 beats per minute, and her blood pressure remains dangerously high at 198/122 mmHg, despite intravenous antihypertensive therapy. Neurologically, her confusion intensifies, and she becomes increasingly lethargic, raising concerns about possible intracranial hemorrhage or progression to eclampsia.

In response to these alarming developments, the healthcare team conducts a rapid point-of-care ultrasound, which confirms bilateral pleural effusions and a congested inferior vena cava, indicative of fluid overload. A stat chest X-ray corroborates the findings of pulmonary edema, showing bilateral infiltrates. Laboratory results reveal further deterioration: her creatinine has risen to 2.3 mg/dL, her platelet count has dropped to 68,000/mm^3, and her liver enzymes continue to climb, with an AST of 210 U/L and ALT of 192 U/L. These findings underscore the urgency of the situation and the need for swift action to prevent further maternal and fetal compromise.

The team intensifies their interventions, initiating diuretics to manage the pulmonary edema and increasing the dosage of magnesium sulfate to control the risk of seizures. Despite these efforts, the patient's declining status and the risk of multi-organ failure necessitate an immediate decision to proceed with the cesarean section under general anesthesia. The team collaborates to stabilize the patient as much as possible before surgery, understanding that the balance of time and intervention is critical in averting catastrophic outcomes for both mother and child.

Section 3

As the team prepares for the cesarean section, the patient's condition continues to evolve, presenting new diagnostic challenges. While transitioning to the operating room, the patient's confusion deepens, and she becomes unresponsive to verbal stimuli, although she still responds to painful stimuli. A repeat neurological assessment reveals brisk reflexes with clonus, and the team is now increasingly concerned about the progression to eclampsia or the development of cerebral edema. Her blood pressure, despite aggressive management, spikes further to 210/130 mmHg, compounding the risk of cerebral complications.

Simultaneously, the anesthesiology team monitors the patient's respiratory status closely. Her oxygen saturation remains critically low at 85% despite high-flow oxygen, and her respiratory rate has slowed to 28 breaths per minute, suggesting fatigue and impending respiratory failure. The decision is made to intubate the patient to protect her airway and stabilize her oxygenation before proceeding with surgery. Arterial blood gases are obtained post-intubation, revealing profound metabolic acidosis with a pH of 7.22, PaCO2 of 48 mmHg, and HCO3- of 18 mmol/L, indicating a mixed respiratory and metabolic acidosis likely exacerbated by poor perfusion and tissue hypoxia.

The laboratory team provides an urgent update on the latest blood work, which shows a further decrease in platelet count to 54,000/mm^3 and a rise in creatinine to 3.1 mg/dL. These indicate worsening renal function and potential disseminated intravascular coagulation (DIC), complicating the clinical picture. Despite the dire circumstances, the multidisciplinary team, fueled by the urgency and gravity of the situation, proceeds with the cesarean section under general anesthesia, fully aware that this is the best course of action to minimize maternal and fetal risk. The team prepares for the possibility of massive transfusion protocols and continued intensive monitoring post-delivery, anticipating the need for advanced critical care interventions.

Section 4

As the cesarean section progresses, the surgical team swiftly delivers the infant, who is immediately assessed by the neonatal team. The newborn, although initially requiring resuscitation, begins to stabilize with Apgar scores improving from 4 to 7 within the first five minutes. Meanwhile, attention shifts back to the mother as the team encounters unexpected intraoperative challenges. During the procedure, the obstetrician notes significant uterine atony, contributing to excessive hemorrhage. Despite uterotonics and manual compression, the bleeding persists, necessitating the activation of the massive transfusion protocol. Blood loss is estimated at over 1500 mL within the first 15 minutes post-delivery, exacerbating the already critical situation.

The patient's hemodynamic status deteriorates rapidly with blood pressure dropping to 80/45 mmHg, and heart rate increasing to 130 beats per minute, indicating hypovolemic shock. The anesthesiology team administers a combination of crystalloids and blood products, including packed red blood cells, fresh frozen plasma, and platelets, in an effort to stabilize her condition. Concurrently, the laboratory results confirm the suspicion of disseminated intravascular coagulation (DIC), showing prolonged prothrombin time (PT) of 22 seconds and activated partial thromboplastin time (aPTT) of 45 seconds, alongside fibrinogen levels plummeting to 120 mg/dL.

Despite these interventions, the patient’s condition remains precarious. Her hemodynamic instability, coupled with the severe coagulopathy, presents a formidable challenge to the clinical team. The multidisciplinary team, including critical care specialists, is now focused on optimizing perfusion and managing the bleeding while preparing for potential further interventions, such as uterine artery embolization or hysterectomy, should conservative measures fail. This complex interplay of complications requires vigilant monitoring and rapid decision-making to navigate the evolving clinical landscape and prevent further deterioration of the patient’s status.

Section 5

As the surgical team grapples with the persistent hemorrhage and hemodynamic instability, they are joined by a vascular interventional radiologist who is prepared to perform uterine artery embolization as a potential next step. However, before proceeding, the patient's condition takes a sudden turn when she develops acute respiratory distress, characterized by a rapid onset of tachypnea with a respiratory rate of 35 breaths per minute and an alarming drop in oxygen saturation to 85%. The critical care team suspects acute pulmonary edema, likely exacerbated by the aggressive fluid resuscitation, and immediately initiates high-flow oxygen therapy and diuretics to address the fluid overload.

In parallel, a new set of laboratory results reveals further deteriorations in the patient’s coagulation profile. The fibrinogen level continues to fall, now at 90 mg/dL, and the D-dimer is markedly elevated at 12,000 ng/mL, confirming ongoing severe coagulopathy. Additionally, the metabolic panel indicates a significant metabolic acidosis with a pH of 7.25 and a base deficit of -10 mmol/L, pointing to inadequate tissue perfusion and oxygenation. These findings necessitate a reevaluation of the current management strategy, as the risk of multi-organ failure looms.

Faced with these compounding complications, the clinical team deliberates on the necessity of proceeding with uterine artery embolization versus emergent surgical intervention, such as a hysterectomy, to definitively control the source of bleeding. The patient's critical status demands swift yet calculated decision-making, balancing the need to manage the immediate life-threatening conditions while preparing for potential long-term implications of these life-saving interventions. As they proceed, the team remains vigilant for any signs of additional complications, such as acute kidney injury or cardiac compromise, which could further complicate the patient's fragile recovery trajectory.