A51-01 Unilateral Whiteout Triggered by Fluid Resuscitation in a Patient With DKA and Occult Pneumonia

Abstract Case Presentation A 48-year-old male with a history of alcohol use disorder, chronic hepatitis C, and type 1 diabetes mellitus presented with altered mental status. Initial evaluation revealed hypotension, tachycardia, and diabetic ketoacidosis (DKA) with a glucose of 1067 mg/dL and an anion gap of 41, alongside significant alcohol intoxication and lactic acidosis. On admission, his initial chest X-ray was deceptively benign, showing only minimal opacification in the right lung base. He was admitted to the ICU for DKA management. Following aggressive fluid resuscitation, he developed progressive hypoxemia. His condition rapidly deteriorated, with chest imaging progressing to a complete ‘whiteout’ of the right lung, necessitating intubation, paralytic therapy, and prone positioning for refractory hypoxemia. A bedside echocardiogram showed a preserved ejection fraction, ruling out acute cardiogenic failure. A chest CT confirmed near-total atelectasis of the right lung with superimposed consolidation. Bronchoalveolar lavage was positive for Staphylococcus aureus and Enterobacter cloacae. With targeted antibiotics and diuresis, his pulmonary status improved. After a two-week ICU stay, he was stabilized and transferred to a long-term acute care facility. Discussion The unilateral lung whiteout was not attributable to a single cause but was the result of a pathophysiological cascade. An underlying polymicrobial pneumonia was likely masked by the profound dehydration from DKA. Aggressive fluid resuscitation restored perfusion to the infected lung and “unmasked” the pneumonia, causing it to appear radiologically. Concurrently, the severe metabolic acidosis of DKA induced a systemic inflammatory response, increasing pulmonary capillary permeability. This pre-existing hyperpermeability, combined with the hydrostatic pressure from large-volume fluid administration, resulted in severe, asymmetric pulmonary edema. The massive accumulation of both exudate from the pneumonia and transudative fluid from the edema led to secondary obstructive and compressive atelectasis, culminating in the complete opacification of the hemithorax. Conclusion This case demonstrates a synergistic interplay between infection, metabolic derangement, and iatrogenic fluid overload. The patient’s successful recovery with a dual strategy of antibiotics and diuresis confirms this multifactorial etiology. It underscores the critical need for vigilant respiratory monitoring and judicious fluid management, particularly the timely de-escalation of fluid therapy, in high-risk patients undergoing treatment for DKA. This abstract is funded by: None