Diabetes/Prediabetes/Hypoglycemia
Abstract E-Poster Presentation
Goonja S. Patel, MD
Resident
Crozer Chester Medical Center
Cherry Hill, New Jersey, United States
Anupam Sharma
Goonja S. Patel, MD
Resident
Crozer Chester Medical Center
Cherry Hill, New Jersey, United States
Devashish Desai
Wei Bin
Diabetic ketoacidosis (DKA) is a known sequela of high levels of circulating glucose with an insulin deficiency. Patients usually present with increased thirst, dyspnea, abdominal pain, and fatigue. Without immediate treatment, the patient may suffer detrimental outcomes from electrolyte abnormalities, acidosis, and other irregularities. We describe the case of a man who suffers from recurrent pulmonary edema as a consequence of DKA.
Case Description :
A 40- year-old male with a history of brittle insulin-dependent diabetes mellitus, COPD, and sarcoidosis, presented to the emergency room with complaints of shortness of breath and dizziness for the past day. He denied vision changes, excessive thirst, chest pain, abdominal pain, nausea, vomiting, fever, and chills. On physical exam he was afebrile, heart rate was 118 beats/min, respiratory rate was 21 breaths/min, blood pressure was 113/73 mmHg and he was saturating at 96% on a non-rebreather. The remainder of the physical exam was normal. On laboratory investigation his blood sugar was found to be 705 mg/dL, bicarbonate of 10 mmol/L, and beta-hydroxybuterate was 7.9 mmol/L. An arterial blood gas resulted as a pH of 7.23, pCO2 of 28 mmHg, pO2 of 38 mmHg and bicarbonate of 13 mEq/L. His EKG did not indicate any signs of ischemia and troponin was undetectable. Therapy was initiated per DKA protocol. A chest x-ray was done which showed diffuse bilateral extensive reticular nodular pulmonary infiltrates. A follow up CTA scan of the chest was negative for pulmonary embolism and positive for severe ground-glass opacities and hilar mediastinal lymphadenopathy consistent with pulmonary edema. His cardiac echocardiogram did not show any systolic or diastolic dysfunction. After a difficult ICU course, the pulmonary edema resolved completely with treatment of DKA. He was discharged with close follow up, however, he continued to have recurrent hospitalizations. Over the span of one year, he had ten episodes of DKA, of which eight were complicated by pulmonary edema. With each admission, his pulmonary edema resolved with control of DKA.
Discussion :
Pulmonary edema is an unusual complication of DKA, and its pathophysiology falls under two categories. Firstly, an increase in hydrostatic pressure causes a shift of fluid from the intracellular to the extracellular compartment due to solute deposition. The resolution of DKA shifts fluid back into the cells and resolves the edema over the course of treatment. The second pathology, non-hydrostatic pulmonary edema, is caused by increased permeability through the walls of the alveoli and pulmonary capillaries. It is similar to ARDS, and is a more frequent complication of DKA than hydrostatic edema. Both forms of pulmonary edema require close monitoring and prompt treatment of DKA.