Introduction

Cardiopulmonary resuscitation, while a critically important life-saving technique, has been well documented to be a potential cause of thoracic wall damage and in some instances pericardial rupture. Rarely, however, the violent forces required to perform cardiopulmonary resuscitation, can prove to be therapeutic in an unintended fashion.1–5 In this unique case study, we describe a patient who, scheduled to undergo pericardial window for a pericardial effusion, experiences spontaneous resolution of his condition following cardiopulmonary resuscitation.

Patient Information

An 84 year-old white male presented to the emergency department with a chief complaint of non-radiating chest pain experienced at rest. The patient admitted to inadvertently taking apixaban and clopidogrel earlier that morning rather than his usual regiment of just apixaban prescribed for his atrial fibrillation. Past medical history was positive for coronary artery disease, which had been addressed via percutaneous coronary intervention years prior. Comorbidities included type 2 diabetes mellitus, essential hypertension, chronic kidney disease stage 3, and hypercholesterolemia. The patient was unaware of any family medical history and he denied use of alcohol, tobacco, and illicit drugs. Review of systems during initial evaluation revealed several weeks of diffuse weakness. He denied dyspnea as well as gastrointestinal symptoms.

Clinical Findings

During transport to the emergency department, the patient received 300 mL of IV normal saline in attempts to correct his initial blood pressure of 68/40 mmHg. EMS reported an EKG revealing borderline ST elevations in the inferior leads. Upon arrival, his blood pressure had improved to 100/48 mmHg, heart rate was recorded at 100 bpm, with an oxygen saturation of 98%, and a respiratory rate of 18 bpm. On physical exam, the patient appeared chronically-ill and had global pallor. His head exam was largely unremarkable. Eyes were without scleral icterus or corneal arcus. Poor inspiratory effort was noted with decreased bilateral breath sounds on auscultation. He was without wheezing, rhonchi, or rales. Cardiac exam revealed an irregularly irregular rhythm without murmurs. First and second heart sounds were normal. The patient was alert and oriented and no focal neurological deficits were noted. Extremities were non-edematous and bilateral upper and lower peripheral pulses were normal. A repeat EKG showed no ST elevations and troponin levels were found to be non-elevated, ruling out myocardial infarction.

Diagnostic Assessment

Patient’s initial labs were significant for leukocytosis, metabolic acidosis, lactic acidosis, acute on chronic kidney injury, markedly elevated transaminases, and normocytic anemia. Abdominal ultrasound revealed heterogeneous liver parenchyma consistent with chronic liver disease. CT of the chest revealed bilateral lower lobe infiltrates with minimal bilateral pleural fluid, confirming the diagnosis of community-acquired pneumonia. CT also showed high density pericardial fluid and hemopericardium to a moderate degree. Transthoracic echocardiogram confirmed the diagnosis of a moderate to large pericardial effusion with no compromise of the right ventricle and right atrium. Cardiothoracic surgeon was consulted, and a pericardial window was scheduled for the following day.

Therapeutic Intervention

The patient was admitted to the intensive care unit for treatment of sepsis secondary to community acquired pneumonia, acute hepatitis, kidney injury, and management of pericardial effusion. The patient was treated with vancomycin, received dialysis, and was well hydrated with lactated ringers and sodium bicarbonate. A nurse noticed the patient become progressively bradycardic and he subsequently developed pulseless electrical activity. The patient was intubated, and CPR was begun with return of spontaneous circulation within 18 minutes. The patient’s post-resuscitation vitals were significant for mild hypotension at 95/72. A new bedside transthoracic echocardiogram taken after resuscitation measures displayed a resolved pericardial effusion compared to the previous echocardiogram. It also revealed a new left pleural effusion.

Follow-up and Outcomes

While both the transthoracic echocardiogram and CT of the chest revealed a significantly reduced pericardial effusion, there were other findings unfavorable for the patient. CT of the chest also revealed new nondisplaced sternal fracture, new mildly displaced right anterior rib fractures of ribs 3-7, and new displaced left anterior rib fractures of ribs 7 and 8. There were no signs of pneumothorax. CT of the chest and abdomen also revealed left sided pleural effusion and new mild ascites and anasarca. Additionally, post-resuscitation labs demonstrated worsening leukocytosis and significantly increased LFTs indicating shock liver. The patient continued to require more vasopressors and was unable to recover from multisystem organ failure.

Discussion

The case was limited in that we were unable to obtain patient-assessed outcomes as the patient was deceased a few days following the resuscitation. There have only been a handful of reported cases of resolved pericardial effusion following CPR. Three of these cases have described the resolution of pericardial effusion/tamponade from pericardial damage without rib fractures.1–3 Only 2 case reports were found in which CPR resulted in the resolution of pericardial tamponade with associated rib fractures and pericardial damage as in our case.4,5 Both of these cases report the presence of new pleural effusion following chest compressions. Our case is unique in that, while the patient in our report also presented with a new left sided pleural effusion following CPR, he developed a case of mild ascites as well. This phenomenon could potentially be explained by the newly displaced rib fractures over the diaphragm. These fractures likely injured the diaphragm and pleural cavity, allowing fluid to travel from the pleural space into the peritoneal cavity. This proposed mechanism is not believed to have been previously described in the literature. Alternatively, the suspected shock liver may have resulted in reduced osmotic vasculature pressure, leading to extravasation of fluid.

Conclusion: This case is an excellent example of how the different organ systems are impacted by one another and how correction of one primary issue does not necessarily result in patient improvement. With pericardial effusion fluid, here, likely entering the pleural space and then possibly the peritoneal cavity, we can trace how the spontaneous resolution of pericardial effusion ultimately led to a new problem. However, by reflecting on this study, we can understand the value of expedited action; if the patient had not developed cardiopulmonary arrest and required chest compressions, a pericardial window could have facilitated resolution of the pericardial effusion without resulting changes to the pleural space or the abdomen. While watchful waiting is sometimes important, it is through these cases that we realize why quick surgical correction is, at other times, worthwhile.

Patient Perspective

The patient expired prior to sharing treatment perspectives.

Patient deceased. At the time of CPR, the patient was designated as “Full-Code”. At a time point later on after CPR, the patient’s status was changed to “DNR”. All personally identifying information has been removed from the case.