Profound Hypoxemia in a Patient With Hypertriglyceridemia-Induced Pancreatitis

Abstract

Background: Acute lung injury and acute respiratory distress syndrome are potentially fatal complications of severe acute pancreatitis. In some cases, respiratory failure in acute pancreatitis is associated with negative radiographic findings. Hypertriglyceridemia is a known precipitant of acute pancreatitis; however, whether the severity of the hypertriglyceridemia can accurately predict the severity of the hypoxemia in acute pancreatitis remains unclear.

Case presentation: A male with morbid obesity and untreated sleep apnea presented with hypoxemia in the setting of severe hypertriglyceridemia, but with negative chest imaging. The severity of the patient's respiratory dysfunction coincided with elevations in his serum triglycerides.

Conclusions: This case demonstrates the complex relationship between hypertriglyceridemia, inflammation, and pulmonary dysfunction.

FIGURE 1

Chest anteroposterior X-ray (A) and coronal computed tomography (B) taken upon admission did not reveal any evidence of an acute cardiopulmonary process despite reported hypoxemia.

FIGURE 2

Abdomen and pelvis computed tomography without contrast demonstrating severe acute interstitial edematous pancreatitis.

FIGURE 3

Trends in serum triglyceride levels (A) and arterial oxygen pressure (B) from arterial blood gas.

FIGURE 4

Proposed model by which hypertriglyceridemia initiates a feedback loop to exacerbate pancreatitis, ARDS, and hypoxemia. (1) In hypertriglyceridemia-induced pancreatitis, it is proposed that excess triglycerides result in elevated serum chylomicrons which can cause capillary plugging due to increased plasma viscosity as well as damage to platelets and vascular endothelium resulting in pancreatic ischemia, which triggers acute pancreatitis. (2) ARDS may occur secondary to acute pancreatitis. In the initial exudative phase of ARDS, there is endothelial barrier dysfunction and a proinflammatory cascade activation through mediators, activating alveolar macrophages, and recruiting neutrophils resulting in increased permeability into the alveolar space. In the case of pancreatitis associated acute respiratory distress syndrome, effects of pancreatitis enzymes such as phospholipase A2 may be directly involved, damaging pulmonary surfactant and impairing alveolar fluid clearance. (3) Hypoxemia in ARDS occurs due to ventilation-perfusion defects causing gas exchange impairments which may be worsened further by high distending volumes and pressures on mechanical ventilation, dysynchronous breathing, and/or lung derecruitment., (4) Hypoxemia may further impact triglyceride clearance resulting in further elevation in triglyceride levels. This can occur in both acute and chronic hypoxic conditions. Abbreviation: ARDS, acute respiratory distress syndrome. Courtesy Dale Jun and Eileen Nguyen.