Case Presentation: A 46-year-old Caucasian male with a past medical history of spastic quadriplegia secondary to MVC, Seizure disorder, CVA, Diabetes Mellitus type II on insulin, Neurogenic Bladder s/p suprapubic catheter, Chronic G-J Tube, Chronic Tracheostomy on Trach Collar, Severe protein calorie malnutrition and all extremities contractures who was admitted for dislodged G-J tube from his nursing facility. At baseline he was nonverbal and could not communicate.Interventional Radiology was consulted, and G-J tube was replaced on the day of admission. Next morning RN could not flush the tubeand Interventional Radiology was re consulted. Of note he was feeding tube dependent for more than 10 years and had prior complications including multiple exploratory laparotomies, chronic gastrocutaneous fistula and chronic skin excoriations around feeding tube site.Interventional Radiology recommended surgical consult as they had exhausted all other options. General surgery reviewed his case and deemed that he was not a surgical candidate and will not survive this procedure. His only option was feeding tube placement by Interventional Radiology or life long Total Parenteral Nutrition. By then he had been NPO on MIVF Ringer Lactate with strict glucose monitoring. On fourth day of admission, he was found to be hypoglycemic with blood glucose 48 mg/dl. Serum bicarbonate was 13 mm/L and Anion Gap had increased to 17 mm/L. Venous Blood gas was checked with pH 7.39, pCO2 35 mmHg, pO2 27 mmHg. Serum Ketones were elevated to 4.50 mm/L and lactic Acid 9.0 mm/L. He was started on D5 and 0.45 NS infusion, insulin sliding scale and IV Thiamine. Repeat labs at 6 hours showed Anion Gap had resolved, bicarbonate improved to 20 MM/L and rapid clearance of Lactic Acid. Given the complexity of this case Palliative care was consulted and his guardian opted for hospice care.

Discussion: Acute Starvation Ketosis can occur in diabetic patients without Diabetic Ketoacidosis. Very high lactic acidosis cannot be explained by ketone formation alone and points to severe metabolic derangements. Patients with inadequate nutrition, increased excretion (diuretic therapy), stress (surgery, infection) and hypermetabolic states are at high risk of thiamine deficiency. Typically, body stores are depleted in 1-2 weeks. Thiamine is an important co-factor in Krebs cycle. In its absence cellular metabolism shifts to anaerobic respiration and pyruvate shifts to lactate. Krebscycle disruption can lead to significantly high amount of Type B Lactic acidosis. Since it is used in aerobic metabolism, prolonged deficiency canresult in cardiac, central nervous system and GI dysfunction. It has been linked with delirium and critical neuropathy as well.

Conclusions: Malnourished patients, patients who are tube feed dependent or critically ill are at very high risk of thiamine deficiency. Although it is easily available and inexpensive, knowledge about this condition is low. Internist and intensivists should have awareness and a low threshold to treat it.