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PSUN139 Leukemoid Reaction in Severe Diabetic Ketoacidosis: An Indicator of Severity or Predictor of Infection?

BACKGROUND: Acute infectious illness can precipitate episodes of ketoacidosis in patients with diabetes mellitus. For this reason, a diligent search for a focus is essential in the initial evaluation of patients with DKA since patients often appear ill and may have non-specific symptoms. CLINICAL CA...

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Detalles Bibliográficos
Autores principales: Sarigumba, Marion, Gonzales, Cecilia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9624950/
http://dx.doi.org/10.1210/jendso/bvac150.752
Descripción
Sumario:BACKGROUND: Acute infectious illness can precipitate episodes of ketoacidosis in patients with diabetes mellitus. For this reason, a diligent search for a focus is essential in the initial evaluation of patients with DKA since patients often appear ill and may have non-specific symptoms. CLINICAL CASE: An 18-year old Filipino with Type 1 Diabetes Mellitus sought consult due to abdominal pain. He is on premixed NPH/regular insulin twice daily but was lost to follow-up due to the COVID-19 pandemic. He has no other comorbidities but asserted a prior history of poor compliance with both diet and insulin therapy besides an erratic sleep-wake cycle. Prior to consult, he reported 5 episodes of vomiting associated with generalized abdominal pain. Due to poor appetite, he missed due doses of insulin with subsequent worsening of condition. On admission, he was lethargic with Kussmaul's breathing. Initial vital signs were stable. He had dry lips and oral mucosa, sunken eyeballs and generalized abdominal tenderness. COVID-19 PCR was negative. Serum lipase (8.79, n: 8-78) and CT scan of abdomen were likewise unremarkable. Initial CBG was HIGH with elevated ketones (5.4, n: <0.6) and arterial blood gas revealed a pH of 7.0, pCO2 22, HCO3 incalculable, lactate 3.9, with high anion gap. The initial WBC was high (44.3×10(9)/uL, n: 4.4-11) with 84% neutrophils, 10% lymphocytes, 1% metamyelocytes, and 5% monocytes. Hemoglobin (18.5 g/dl), hematocrit (51.7%) and platelet count (614k/uL) were also elevated. Peripheral blood smear revealed normal cell morphology. Urinalysis revealed elevated specific gravity, marked glycosuria and ketonuria, negative nitrites and leukocyte esterases. Blood specimen were obtained for culture. Therapy was instituted with intravenous fluids, insulin drip and broad spectrum antibiotics. The following day, glucose was 218 mg/dl, pH 7.16, bicarbonate 7.8 meq/L, hematocrit 44%, WBC 25.21×10(9)/uL and platelet count was 401k/uL. LAP score was requested but was unavailable. On the fourth hospital day, the patient was well and tolerating diet, with normalization of blood glucose, WBC 9.87 (85% neutrophils, 10% lymphocytes, 5% monocytes) and control of acidosis. Since cultures were negative and patient was afebrile, antibiotics were discontinued. He was discharged stable on with basal-bolus insulin. CONCLUSION: The association between DKA and leukocytosis in the absence of infection is described in literature. Exact mechanism is unknown but may in part be attributed to increased catecholamine release in response to stress and hemoconcentration from marked dehydration. Studies show a statistically significant relationship between pH, bicarbonate and leukocytes which denotes that WBC in DKA can be an indicator of the severity of ketoacidosis rather than a predictor of infection. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.