INTRODUCTION
Peripartum cardiomyopathy (PPCM) is a rare but serious condition that affects women worldwide and is characterized by the onset of heart failure during the peripartum period. It is defined as idiopathic cardiomyopathy with left ventricular dysfunction (left ventricular ejection fraction [LVEF] <45%, with or without ventricular dilatation) occurring in the last month of pregnancy or within five months postpartum in the absence of pre-existing cardiac disease [1]. The diagnostic challenge arises from the overlap of PPCM symptoms, such as dyspnea, fatigue, and edema, with normal physiological changes in late pregnancy and the postpartum period, often leading to a delayed diagnosis [2]. While some patients experience mild disease with the potential for full recovery, others face significant morbidity and mortality due to severe cardiac impairment.
The acute clinical presentation of PPCM typically includes signs of congestion and poor organ perfusion, necessitating urgent therapeutic intervention [3]. Acute decompensated heart failure (ADHF) secondary to PPCM may range from moderate volume overload to cardiogenic shock. Acute pulmonary edema, a critical complication, frequently results from left heart failure and is a primary reason for intensive care unit (ICU) admission, often requiring mechanical ventilation in critical cases [4]. Management of heart failure in this context demands tailored strategies, considering fetal safety during pregnancy or breastfeeding postpartum, with a focus on controlling volume status, mitigating maladaptive neurohormonal responses, and preventing thromboembolism and arrhythmias [5].Diagnostic complexity increases with concurrent conditions, such as community-acquired pneumonia (CAP), diagnosed by the presence of new pulmonary infiltrates with clinical evidence of infection [6]. CAP can precipitate acute decompensation of underlying chronic diseases, including congestive heart failure, potentially obscuring the initial diagnostic clarity and delaying treatment. Thus, maintaining vigilance for alternative diagnoses throughout a patient’s clinical course is essential. This case report aimed to illustrate the intricate management of a postpartum patient with PPCM complicated by ADHF, acute pulmonary edema, and CAP, emphasizing the need for a multidisciplinary approach in the ICU setting.
CASE DESCRIPTION
A 36-year-old female (gravida 4, para 0, weight 60 kg) presented to the emergency department with a 1-day history of progressive dyspnea that was unrelieved by rest, accompanied by intermittent fever and productive cough for 2 days. She had undergone an uncomplicated vaginal delivery 6 days prior assisted by a midwife. On admission, the patient was somnolent, with vital signs indicating a blood pressure of 140/90 mmHg, heart rate of 170 beats/min, respiratory rate of 45 breaths/min, oxygen saturation of 90-92% on a 15 L/min non-rebreather mask, and temperature of 37.4°C. Physical examination revealed jugular venous pressure of 5+4 cmH₂O, bilateral coarse wet rhonchi, regular heart sounds without murmurs, and no peripheral edema. Her medical history was unremarkable for hypertension, cardiac disease, and diabetes, although she reported a childhood history of asthma that had been quiescent for years without regular medication. Initial management in the emergency department included ceftriaxone 1 g IV every 12 h, levofloxacin 750 mg IV daily, paracetamol 1 g orally three times daily, N-acetylcysteine 400 mg orally three times daily, nebulized combivent plus fluticasone every 8 h, furosemide 40 mg IV twice daily, calcium gluconate 2 g IV, and 40% dextrose 2 flasks. Owing to deteriorating respiratory status, she was intubated and transferred to the intensive care unit (ICU) for advanced care.
Table 1: Laboratory Results Before ICU Admission
| Parameter | Result |
|---|---|
| Hematology | Hb 13.6 g/dL, Ht 42.1%, Leukocytes 19,250/µL, Platelets 466,000/µL |
| Renal Function | Urea 41.3 mg/dL, Creatinine 0.64 mg/dL |
| Electrolytes | Na 141 mmol/L, K 3.5 mmol/L, Ca 3.94 mmol/L |
| Glucose | 48 → 112 mg/dL (post-correction) |
| Arterial Blood Gas | pH 7.36, pCO₂ 24.4 mmHg, pO₂ 78.1 mmHg, HCO₃ 14.1 mmol/L, BE -8.6 mmol/L, SaO₂ 95% |
| Procalcitonin | 0.43 ng/mL |
| CRP (Quantitative) | 2.88 mg/L |
| NL Ratio | 8.85 |
The diagnostic evaluation confirmed a complex clinical picture. Chest radiography demonstrated cardiomegaly with pulmonary edema (Figure 1), while electrocardiogram showed sinus tachycardia (Figure 2). Laboratory results prior to ICU admission are shown in Table 1. Echocardiography revealed a dilated left ventricle, reduced left ventricular ejection fraction (estimated 30-35%, possibly underestimated due to tachycardia), left ventricular diastolic dysfunction, mild mitral and pulmonary regurgitation, trivial tricuspid regurgitation, low probability of pulmonary hypertension, and normal right ventricular systolic function (TAPSE, 18 mm). Hemodynamic assessment indicated a cardiac output of 4.82 L/min, cardiac index of 3.03 L/min/m², and lung ultrasound B profile, consistent with peripartum cardiomyopathy (PPCM) complicated by acute decompensated heart failure (ADHF), respiratory failure due to acute pulmonary edema, and community-acquired pneumonia (CAP) confirmed by Streptococcus pneumoniae on sputum culture. In the ICU, the initial ventilation was set to pressure-support synchronized intermittent mandatory ventilation (P-SIMV) at a rate of 12 breaths/min, pressure control of 14 cmH₂O, pressure support of 12 cmH₂O, PEEP of 8 cmH₂O, and FiO₂ of 60%, achieving tidal volumes of 430-470 mL and SpO₂ of 97-98%. Therapy was escalated to include midazolam 5 mg/hour IV for sedation, ceftriaxone, levofloxacin, paracetamol 1 g IV every 6 hours, omeprazole 40 mg IV every 12 hours, digoxin 0.5 mg IV, nebulized combivent every 8 hours, furosemide 20 mg/hour IV, and fluid restriction. A central venous catheter was placed and cardiology consultation with hemodynamic and structural echocardiography was performed.
Table 2: ICU Daily Management Overview
| Day | Oxygen Therapy | Urine Output / Balance | Therapy and Interventions | Key Laboratory Results |
|---|---|---|---|---|
| 1 | P-SIMV: R 12, PC 14, PS 12, PEEP 8, FiO₂: 60%, TV: 430-470 mL | Urine: 2-5 mL/kg/h, -2333 mL/13h | Ceftriaxone, Levofloxacin, Paracetamol, Omeprazole, Digoxin, Furosemide, Nebulized Combivent, CVC, Echo consult | See Table 1 for lab results |
| 2 | P-SIMV: R 12, PC 12, PS 10, PEEP 6, FiO₂: 50%, TV: 380-450 mL | Urine: 1.5-3 mL/kg/h, -1300 mL/24h | Dexmedetomidine, Furosemide ↓, Ca gluconate, Digoxin, Nutrition 1000 kcal | Troponin I: 0.48 ng/mL, Glucose: 136 mg/dL |
| 3 | Spontaneous: PS 10, PEEP 5, FiO₂: 50% | Urine: 0.5-1.5 mL/kg/h, -147 mL/24h | Norepinephrine, Fluid loading, Enoxaparin, Nutrition 1500 kcal | Troponin I: 0.20 ng/mL, Urea: 120 mg/dL |
| 4 | Spontaneous: PS 8, PEEP 5, FiO₂: 40%, Extubation | Urine: 0.5-1.5 mL/kg/h, +545 mL/24h | Norepinephrine/Dexmedetomidine stopped, Bromocriptine, Repeat X-ray | Glucose: 157 mg/dL |
| 5 | Nasal cannula 3 L/min | Urine: 0.3-1.5 mL/kg/h, +585 mL/24h | Transfer to HCU | Glucose: 138 mg/dL |
Over the subsequent days, the patient’s condition improved with tailored interventions. On day 2, persistent fever and tachycardia prompted a switch to dexmedetomidine 0.4 µg/kg/hour for sedation, with ventilator settings adjusted to P-SIMV (rate 12, pressure control 12 cmH₂O, pressure support 10 cmH₂O, PEEP 6 cmH₂O, FiO₂ 50%) and weaning initiated. Fluid balance was closely monitored, and enteral nutrition at 1000 kcal/24 h was started. By day 3, despite reduced rhonchi, hypotension necessitated norepinephrine 0.05 µg/kg/min to maintain mean arterial pressure >65 mmHg, with fluid loading of 4-6 mL/kg and enoxaparin 60 mg SC daily.
Figure 1. ICU Vitals Overview (BP, HR, SpO₂, Temperature)
The ventilator mode was shifted to spontaneous breathing with a pressure support of 10 cmH₂O, PEEP 5 cmH₂O, and FiO₂ 50%, and nutrition increased to 1500 kcal/24 h. On day 4, clinical improvement allowed discontinuation of norepinephrine and dexmedetomidine, with extubation following weaning to spontaneous mode (pressure support 8 cmH₂O, PEEP 5 cmH₂O, FiO₂ 40%). Daily oral bromocriptine (2.5 mg) was initiated, and a repeat chest radiograph was performed (Figure 3). By day 5, the patient was hemodynamically stable post-extubation, with SpO₂ of 97-99% on a nasal cannula at 3 L/min, and was transferred to the semi-intensive care unit. The overview details of the ICU Vitals are summarized in Fig. 1.
DISCUSSION
Peripartum Cardiomyopathy (PPCM) is a form of heart failure with reduced left ventricular ejection fraction (LVEF) occurring during the last month of pregnancy or within six months postpartum, without prior heart disease. Diagnosis requires an LVEF <45%, with or without ventricular dilation. The symptoms of PPCM can mimic normal physiological changes during pregnancy, leading to delayed diagnosis. Risk factors include advanced age (>30 years), multiparity, hypertension, and family history of heart disease [4,7].
The etiology of PPCM remains multifactorial. One key mechanism involves immune response and hemodynamic stress during pregnancy, which may cause myocardial apoptosis. Prolactin, in its 16 kDa form, has been implicated in pathophysiology, as it induces vasoconstriction and endothelial damage. Genetic mutations, particularly in STAT3, further predispose individuals to PPCM. Studies have suggested that an imbalance between proangiogenic and antiangiogenic factors plays a role in endothelial dysfunction, increasing the risk of PPCM in genetically predisposed individuals [8,9].
The clinical presentations of PPCM include dyspnea, fatigue, peripheral edema, and orthopnea. These symptoms overlap with other conditions, making the differential diagnosis crucial. Echocardiography revealed left ventricular dilation and systolic dysfunction, which are the hallmarks of PPCM. Elevated BNP levels and signs of pulmonary edema on chest radiography help to confirm the diagnosis [10].
A significant complication of PPCM is thromboembolism, due to left ventricular dilation, poor contractility, and endothelial injury. Hypercoagulability during pregnancy increases this risk. Management includes volume control with diuretics and neurohormonal modulation with beta-blockers, and in severe cases, bromocriptine inhibits prolactin-induced endothelial damage. For patients with low LVEF, anticoagulation therapy is recommended, particularly during the postpartum period [6].
Acute decompensated heart failure (ADHF), often precipitated by infections, such as community-acquired pneumonia (CAP), complicates PPCM. Early administration of broad-spectrum antibiotics such as ceftriaxone and levofloxacin, followed by de-escalation based on culture results, is essential. Additionally, careful fluid management and supportive care, including sedation and analgesia, are vital for ensuring patient comfort and recovery. PPCM is a serious condition requiring early diagnosis and comprehensive management. Understanding its multifactorial etiology and addressing complications, such as thromboembolic events and infections, is crucial for improving maternal outcomes [4,11].
CONCLUSION
Acute decompensated heart failure (ADHF) with acute pulmonary edema complicated by community-acquired pneumonia (CAP) in a patient with peripartum cardiomyopathy (PPCM) represents a critical medical emergency that requires aggressive, coordinated management in a specialized unit. Although rare, PPCM is a potentially fatal condition that is challenging to diagnose, predict, and treat. Delays in diagnosis and treatment, along with worsening LVEF and ventricular dilation, significantly worsen the prognosis. The management of heart failure in PPCM and CAP must be tailored to the unique considerations of pregnancy and breastfeeding to ensure optimal outcomes.
DECLARATIONS
None
CONSENT FOR PUBLICATION
The Authors agree to be published in the Journal of Society Medicine.
FUNDING
None
COMPETING INTERESTS
The authors declare no conflicts of interest in this case report.
AUTHORS’ CONTRIBUTIONS
All authors made substantial contributions to the case report. DFN was responsible for patient management, data collection, and the initial drafting of the manuscript. All authors reviewed and approved the final version of the manuscript, ensuring its accuracy and integrity and being accountable for all aspects of the work.
ACKNOWLEDGMENTS
None
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