Anorexia Nervosa Complicated by Acute Pericarditis, Spontaneous Pneumomediastinum, and Liver Injury: A Case Report

Introduction

Anorexia nervosa is an eating disorder that is characterized by restrictive food intake, intense fear of gaining weight, distorted perception of weight, and an abnormally low body weight [1]. Anorexia nervosa disproportionately affects females, with lifetime prevalence rates estimated as high as 4% among females, compared with 0.3% among males [2]. Extreme anorexia nervosa, defined as a body mass index (BMI) <15 kg/m2, results in profound malnutrition and predisposes patients to a wide range of life-threatening complications, affecting nearly every organ system. Cardiovascular manifestations are particularly common and include bradycardia, hypotension, decreased cardiac output, reduced left ventricular mass, pericardial effusion, and arrhythmias, such as prolonged QT interval [3,4]. Pulmonary and hepatic complications have also been described but are less frequently recognized, with spontaneous pneumomediastinum and starvation-associated hepatitis being rare clinical entities [5,6].

We present a patient with extreme anorexia nervosa who developed an unusual constellation of pericarditis, pericardial effusion, spontaneous pneumomediastinum, and acute hepatic injury. This case highlights the importance of recognizing rare but reversible complications of severe malnutrition, as timely diagnosis and nutritional rehabilitation can prevent unnecessary invasive interventions and improve clinical outcomes.

Case Report

A 21-year-old woman presented with generalized weakness, chest pain, and palpitations. The patient reported that she had been making significant efforts to lose weight by skipping most of her meals, walking 60 000 steps daily (35.4 km), and consuming only 1 energy drink and a small amount of dinner in a day (approximately 300–350 calories per day). She reported being on severe caloric restriction for around 2 years prior to presentation, along with intermittent episodes of purging. During the 2 consecutive days prior to presentation, she was unable to reach her goal step count and reported feeling too weak to get out of bed on the day of the presentation. She described extreme fear of gaining weight, feeling she was obese and needed to lose more weight, and reported inducing vomiting to achieve weight loss. She also reported sharp “stabbing-like” central pleuritic chest pain of 8/10 in intensity associated with dyspnea on minimal exertion for 2 days prior to presentation. The pain worsened when lying flat and on deep inspiration and improved in the sitting position. She reported not having any menstruation in the past year. Her past medical history was notable for depression, for which she was on escitalopram. She had no prior diagnosis of anorexia.

The initial vital signs were unremarkable, and BMI on presentation was 10.7 kg/m2. Physical examination was notable for pericardial friction rub, extreme muscle wasting, proximal muscle weakness with Medical Research Council (MRC) grade 3/5 strength in the bilateral hip joint and 4/5 strength in the bilateral shoulder joint, and significant lanugo on the face, thorax, and extremities.

Laboratory test results were notable for hypokalemia, hypophosphatemia, transaminitis, and predominantly neutrophilic leukocytosis (Table 1). The initial electrocardiogram (ECG) showed a diffuse ST-segment elevation consistent with acute pericarditis (Figure 1). Transthoracic echocardiogram showed mild- to moderate-sized pericardial effusion (Figure 2). A computed tomography (CT) scan of the chest with intravenous contrast revealed pneumomediastinum, subcutaneous emphysema predominantly in the base of the neck and right chest wall, and no evidence of extravasation from the esophagus on oral contrast (Figure 3). Infectious workup, including blood cultures, upper respiratory viral polymerase chain reaction panel, and testing for HIV, hepatitis C, tuberculosis, and Coxsackie A, virus was negative.

The patient was admitted and given intravenous rehydration for rhabdomyolysis and dehydration, along with electrolyte and nutritional supplementation. She was counseled and was started on olanzapine for appetite stimulation and distorted perception about eating. Ibuprofen 800 mg 3 times daily for 30 days and colchicine 0.6 mg for 90 days were given for pericarditis. After a week of inpatient care, the chest pain resolved. She continued to report low appetite and felt she was forcing herself to feed. She also had thoughts about self-harm during this period. Mirtazapine was added to her medications to stimulate her appetite and help with depression and suicidal ideations. By day 10, the muscle strength improved, and the patient was able to walk. By day 15, the patient felt more positive about herself and denied any thoughts of self-harm; her appetite and muscular strength continued to improve. She was discharged to an inpatient nutritional rehabilitation service. A follow-up CT scan of the chest done 3 months later demonstrated complete resolution of pneumomediastinum and subcutaneous emphysema and did not show any evidence of pericardial effusion.

Discussion

CARDIAC INVOLVEMENT:

Cardiac manifestations represent the most critical and life-threatening complications of anorexia nervosa, with reported prevalence rates reaching 87% [7]. Cardiac complications are estimated to contribute to at least one-third of anorexia nervosa–related mortality [8]. Bradycardia and hypotension are the most frequent cardiac findings [3,7,9]. Although pericarditis has not been widely reported as a complication of anorexia nervosa, pericardial effusion is increasingly recognized; however, its precise etiology remains incompletely understood [9]. A meta-analysis of 960 patients demonstrated pericardial effusions by echocardiography in 25% of individuals with anorexia nervosa [10]. Notably, these effusions were predominantly subclinical, occurring in up to 71% of patients with anorexia nervosa, without associated symptoms or electrocardiographic abnormalities; most were mild to moderate in size and resolved with nutritional rehabilitation [10,11]. In contrast, our patient presented with acute symptoms, including typical pleuritic chest pain, a pericardial friction rub, and a new widespread ST-elevation on ECG, alongside pericardial effusion and leukocytosis, collectively meeting established diagnostic criteria for acute pericarditis [12]. The observed ECG abnormalities were inconsistent with hypokalemia or hypophosphatemia and persisted despite correction of electrolyte derangements. Comprehensive infectious investigations for pericarditis (including HIV, hepatitis C, tuberculosis, and Coxsackie A virus) yielded negative results.

PULMONARY COMPLICATIONS:

Spontaneous pneumomediastinum, although rare, is a recognized complication of anorexia nervosa [5,13,14]. Typically, its development is attributed to respiratory maneuvers generating high intrathoracic pressures, such as the Valsalva maneuver, severe paroxysmal coughing, intense crying, or forceful emesis leading to alveolar wall rupture [15]. Forceful vomiting frequently precipitates pneumomediastinum via esophageal or alveolar rupture. Notably, the present case lacked any antecedent history of vomiting, and comprehensive diagnostic evaluation revealed no evidence of esophageal or upper airway laceration. The pathophysiological mechanism underlying pneumomediastinum in this patient is believed to have involved alveolar wall rupture. Chronic starvation is believed to impair alveolar development, leading to structural compromise characterized by enlarged, thin-walled alveoli [14,16]. Subsequent air leakage tracks into the mediastinum during the respiratory cycle, facilitated by the relative pressure gradient between the pulmonary parenchyma and mediastinum. This escaped air can subsequently dissect into cervical subcutaneous tissues, the epidural space, pericardium, and/or peritoneal cavity, consistent with the Macklin effect [17].

HEPATIC COMPLICATIONS:

Hepatic manifestations in anorexia nervosa frequently include asymptomatic elevations in serum aminotransferases, predominantly alanine aminotransferase (ALT) and aspartate aminotransferase (AST), indicative of underlying hepatic dysfunction [6]. According to the American Psychiatric Association, these biochemical abnormalities occur more commonly in severe or chronic anorexia nervosa and are typically reversible with nutritional rehabilitation and weight restoration [18]. Consistent with this pattern, our patient with chronic malnourishment (BMI 10.7 kg/m2) presented with significant transaminitis (ALT 308 U/L, AST 191 U/L), which demonstrated progressive improvement to ALT 132 U/L and AST 29 U/L by hospital day 10, ultimately normalizing at discharge. Aminotransferase elevations can arise from starvation-induced hepatocellular injury or, during refeeding, from hepatic steatosis secondary to increased lipid deposition [18]. Recent clinical evidence further clarifies that marked transaminitis correlates strongly with an extremely low BMI, of less than 13 kg/m2, and primarily reflects hepatocellular injury mediated by starvation-induced autophagy and glycogen depletion, rather than classical necrosis or apoptosis [19,20]. Histopathologic analyses consistently demonstrate preserved hepatic architecture despite significant transaminase elevation, with prominent autophagosomes providing morphological evidence for autophagy as the principal injury mechanism [20,21]. Although acute liver failure with coagulopathy and encephalopathy represents a rare complication in profoundly malnourished individuals, most cases of starvation-related hepatitis resolve rapidly under supervised nutritional rehabilitation [22].

ENDOCRINE AND METABOLIC DERANGEMENTS:

Endocrine abnormalities in anorexia nervosa reflect adaptive responses to chronic energy deficiency but contribute to significant clinical complications. Hypothalamic suppression reduces gonadotropin-releasing hormone secretion, leading to hypogonadotropic hypogonadism with amenorrhea and low sex hormone levels, as seen in our patient [23]. The hypothalamic–pituitary–thyroid axis demonstrates a “sick euthyroid” pattern, characterized by low T3, increased reverse T3, normal to low T4, and inappropriately normal or low TSH, reflecting metabolic downregulation rather than primary thyroid disease, which was also evident in our patient. The hypothalamic–pituitary–adrenal axis is typically hyperactive, with elevated cortisol that exacerbates bone loss, while reduced insulin-like growth factor 1 (IGF-1) levels despite normal or elevated growth hormone reflect peripheral resistance; our patient likewise demonstrated low IGF-1. Together, these neuroendocrine adaptations conserve energy during starvation but predispose to infertility, osteoporosis, altered metabolism, and increased cardiovascular risk. In addition to this, electrolyte derangements are frequently observed in anorexia nervosa. Our patient had hypokalemia and hypophosphatemia. Hypokalemia is the most frequently observed abnormality, particularly in patients with the binge-purge subtype [24]. Hypophosphatemia is less common at presentation but can become pronounced during refeeding, increasing the risk for refeeding syndrome and associated complications, such as cardiac arrhythmias and neuromuscular dysfunction [24]. In addition, rhabdomyolysis from starvation and excessive compulsive exercising has been described in the literature [25].

Conclusions

This case highlights the severe multi-system complications of extreme anorexia nervosa, including acute pericarditis with pericardial effusion, spontaneous pneumomediastinum, hepatic injury, endocrine dysfunction, electrolyte disturbances, and rhabdomyolysis. Despite the breadth of organ involvement, these complications proved reversible with careful nutritional rehabilitation, electrolyte correction, and targeted medical therapy. Awareness of such rare but clinically significant manifestations is essential to ensure timely diagnosis, appropriate management, and avoidance of unnecessary invasive procedures in patients with profound malnutrition.