Delayed post-operative cardiac tamponade manifesting as cardiogenic shock

Abstract

We describe the case of a 32-year-old woman with a history of cardiac surgery two weeks previously who presented with an upper gastrointestinal bleed. She also had symptoms of syncope and abdominal pain, as well as elevated liver enzymes. She had cool, clammy extremities, bilateral lower extremity edema, and oliguria. An echocardiogram was obtained, which revealed a large posterior pericardial effusion with evidence of tamponade physiology, and an emergent pericardiocentesis was performed with insertion of a drainage catheter, which drained bloody fluid, with subsequent hemodynamic improvement.

<Learning objective: Cardiac tamponade symptomatology may vary tremendously from patient to patient, and therefore requires a high clinical suspicion in those presenting with evidence of cardiogenic shock. Understanding signs, symptoms, and physiology of cardiac tamponade is essential for diagnosis of delayed post-operative cardiac tamponade, occurring >7 days after open-heart surgery, a challenging diagnosis given its vague symptoms and signs not classically associated with the condition.>

Introduction

Cardiac tamponade is the accumulation of fluid, blood, pus, or gas within the pericardial sac, leading to life-threatening compression of the heart. As the pericardium becomes more distended, its elastic limit is eventually reached, forcing the heart to compete with the pericardial material for the fixed intrapericardial volume. Increased pericardial pressure leads to decreased myocardial diastolic compliance and smaller chamber size, restricting cardiac inflow and ultimately giving rise to the telltale characteristic of tamponade, equilibration of mean diastolic chamber and pericardial pressures 1, 2, 3.

Case report

A 32-year-old woman with a history of pulmonary embolism and right atrial mass status post right atrial thrombectomy and left pulmonary artery embolectomy presented with epigastric pain, fatigue, and coffee-ground emesis. One month previously, she had shortness of breath and was found to have a left main pulmonary artery embolism thought to be secondary to oral contraceptive use, treated with heparin and discharged on warfarin. Bilateral lower extremity Doppler examinations were performed during the first hospitalization, which were negative for deep venous thrombosis. Three days later, despite an International Normalized Ratio (INR) of 4.9, she had recurrence of her dyspnea and was found to have a right atrial thrombus with elevated pulmonary artery pressures on a transthoracic echocardiogram. She was treated with thrombectomy and embolectomy and discharged on warfarin. The morning of the most recent hospitalization, 2 weeks after her cardiac surgery, she fainted in the bathroom. Given her supratherapeutic INR of 4.2 along with her complaints of abdominal pain and coffee-ground emesis, there was concern of a gastrointestinal bleed.

She was found to have a white blood cell count of 15 and elevated liver function tests, with her aspartate transaminase (AST) and alanine transaminase (ALT) being 1457 and 1025 respectively. Her gamma-glutamyl transpeptidase (GGT) and alkaline phosphatase were also elevated to 423 and 431 respectively. Her acetaminophen level and hepatitis B and C tests were negative. Abdominal ultrasound revealed no acute thrombus, but did show abnormal blood flow in the splenic, portal, and hepatic veins with periodic cessation of forward flow, correlating with respiration.

Her cardiac auscultation was unremarkable, but she was noted to have cool, clammy extremities, bilateral lower extremity edema, and oliguria. At that time, an echocardiogram was obtained, which revealed a large posterior pericardial effusion with evidence of tamponade physiology (Fig. 1). Given the location of the effusion, a pericardiocentesis was deferred. Overnight, the patient developed hypotension to blood pressures of 50/40 mmHg. An emergent pericardiocentesis was performed with insertion of a drainage catheter, which drained bloody fluid. Her hemodynamic status subsequently improved and the patient was transferred in stable condition to the medical floor.

Fig. 1.

Large posterior pericardial effusion with tamponade physiology on parasternal short-axis view of trans-thoracic echocardiogram.

Discussion

This case demonstrates a rare complication of cardiac surgery, the development of cardiac tamponade two weeks after surgery. Furthermore, the presenting symptoms of upper gastrointestinal bleeding are atypical for cardiac tamponade. However, given the patient's respiratory symptoms, as well as supratherapeutic anticoagulation status, there was enough concern for pericardial hemorrhage that ultimately led to the correct diagnosis via echocardiographic findings.

Although we are all taught “Beck's triad” of hypotension, jugular venous distension, and muffled heart sounds as the classic presentation of cardiac tamponade, all three of these signs are present only in a minority of patients with this condition [4]. The clinical manifestations of cardiac tamponade vary greatly, depending on how quickly fluid accumulates within the pericardium and the effectiveness of compensatory mechanisms. Associated symptoms and signs may include chest pain, tachypnea, dyspnea, the classic “Beck's triad,” cool extremities, peripheral cyanosis, and decreased urine output. Sinus tachycardia is quite common as the heart attempts to compensate for decreased cardiac output.

Pulsus paradoxus, a fall in systolic blood pressure by 10 mmHg or more during inspiration, occurs when ventricular filling pressures are equilibrated with the elevated pericardial pressure coupled with decreased intrathoracic pressures, resulting in a decreased pressure gradient from the pulmonary veins to the left ventricle [3]. An electrocardiogram for a patient with a large tamponade may demonstrate electrical alternans, a fluctuation in the amplitude of the QRS complex from beat to beat, due to the heart swinging in the pericardial fluid. It should be noted that a chest X-ray often does not demonstrate cardiomegaly, as the determining factor in clinical manifestations is not the absolute amount of pericardial fluid, but the rate at which such fluid accumulates.

With slower filling of the pericardial space, as in malignancy, inflammation, or uremia, pericardial compliance gradually increases, leading to a slower rise in pericardial pressure. In contrast to acute tamponade where small volumes of fluid lead to rapid hemodynamic compromise, subacute pericardial effusions usually contain much higher volumes, up to 2 l or more, due to this increased compliance. Symptomatology is usually more nonspecific in these circumstances and may include fatigue, dyspnea, chest fullness or discomfort, and peripheral edema.

Cardiac tamponade can be caused by anything that causes pericardial hemorrhage or effusion. The incidences of various etiologies of pericardial effusions differ among different populations [5], but one of the largest series of patients with moderate to severe pericardial effusions with tamponade reported the most common causes to be idiopathic pericarditis (23%), malignancy (22%), iatrogenic effusion (18%), acute myocardial infarction (8%), bacterial infection including tuberculosis (8%), chronic idiopathic effusion (6%), and end-stage renal disease (3%). The last 12% of patients with tamponade were grouped into a miscellaneous category with a mixture of etiologies including aortic dissection, trauma, and other non-specified causes [6]. Other reported causes of pericardial effusions with the potential for tamponade include collagen-vascular diseases and hypothyroidism. Iatrogenic tamponade may occur as a result of several inciting agents or events including radiation, drugs, cardiopulmonary resuscitation, invasive procedures, or cardiac surgery [7].

The diagnosis of cardiac tamponade in the patient described above initially did not cross the mind of anyone on her healthcare team. Her vague complaints of epigastric pain and fatigue did not point toward any particular diagnosis and her episode of coffee-ground emesis raised concern for an upper GI bleed. Her elevated liver enzymes, along with her history of blood clots, was concerning for Budd-Chiari syndrome until abdominal ultrasound showed no thrombus.

The clues that she was at increased risk for pericardial effusion and tamponade included her cardiac surgery 2 weeks prior to presentation and her elevated INR. The signs that she did, in fact, have tamponade physiology included her cool, clammy extremities, respiratory variation in ventricular filling velocities (Fig. 2), and the abnormal blood flow within her splenic, hepatic, and portal vasculature varying with respiration on ultrasound (Fig. 3). Although not classic for all-cause tamponade, this patient's symptoms were actually quite characteristic of how post-operative cardiac tamponade presents when it occurs more than 7 days after open-heart surgery. Although a relatively rare occurrence with incidences ranging from 0.5 to 2.6% of patients undergoing cardiac surgery in the 1970s, delayed post-operative cardiac tamponade is life-threatening if not recognized and treated promptly [8]. With its low incidence, many physicians are not even aware that it exists, and its vague symptomatology makes it particularly difficult to diagnose unless the clinician has a high index of suspicion.

Fig. 2.

Doppler echocardiographic image demonstrating ventricular filling velocity variation with respiration, consistent with tamponade physiology.

Fig. 3.

Abdominal ultrasound demonstrating periodic cessation of forward flow in splenic, portal, and hepatic veins, consistent with tamponade physiology.

In a case series of 28 patients with delayed post-operative pericardial effusions, 8 of whom also developed tamponade, symptoms paralleled those of our patient. Vague complaints of fatigue, malaise, mild dyspnea on exertion, and weight gain were common. In the 8 patients with tamponade, the diagnosis was made, on average, 13 days after surgery. Interestingly, 6 of these patients experienced epigastric or sternal pain, half had excessive prolongation of the prothrombin time, and all had at least moderately abnormal liver function tests. Other common manifestations included fever, leukocytosis, oliguria, and prerenal azotemia. Echocardiography revealed posterior pericardial effusions in all of these patients and pericardiocentesis was successful in decompressing the pericardium in 7 out of the 8 patients with tamponade [9].

The pathophysiology of delayed post-operative cardiac tamponade is not fully elucidated, but is believed to be multifactorial in etiology. The well-documented relationship between post-operative anticoagulation and the development of tamponade makes intrapericardial hemorrhage a likely contributor 8, 9.

As shown by this clinical vignette, the principal tool for diagnosing tamponade, regardless of the etiology, is Doppler echocardiography. Classically, this shows a moderate to large effusion compressing the heart with marked respiratory variation in transvalvular flow. Collapse of any cardiac chamber may also occur when intrapericardial pressure exceeds intracardiac pressure 1, 10.

Whatever the cause, definitive treatment of cardiac tamponade is removal of the intrapericardial fluid. Needle pericardiocentesis with echocardiographic guidance is the preferred method, but surgical drainage may be utilized if the heart cannot be reached with a needle. Surgery is also indicated in patients with loculated effusions, clotted hemopericardium, or hemorrhagic tamponade from cardiac rupture [1]. For our patient, pericardiocentesis was life-saving.

Conflict of interest

Authors declare no conflict of interest.