Category: Diabetes/Prediabetes/Hypoglycemia


Monday, Apr 8
1:00 AM – 2:00 AM

Objective :

It is well known that patients with Type 2 Diabetes (T2DM) may present with Hyperosmolar Hyperglycemic State (HHS) as well as with diabetic ketoacidosis (DKA). We present herein a patient with T2DM who presented the first time with DKA and a second time with HHS within a 2-year period.

Methods :


Results :

A 47 year old African American male, with medical history of T2DM, hidradenitis suppurativa, protein calorie malnutrition, chronic hyponatremia, chronic pancreatitis secondary to alcohol abuse, presented for evaluation of worsening foot pain. In the emergency department, physical exam showed an ill-appearing man with chronic lower extremity wounds productive of purulent drainage. Vital signs were within normal limits but BMI was very low at 13.7kg/m2. Lab data revealed sodium 117 mmol/L, potassium 5.7 mmol/L, bicarbonate 26 mmol/L, chloride 83 mmol/L and venous pH 7.29 with a normal anion gap. Serum glucose was 1054 mg/dL and serum osmolality was 326 mOsm/kg. The patient was admitted for HHS and treated with IV insulin with gradual return of euglycemia. This same patient had previously been admitted for DKA 2 years prior. At that time he presented with leukocytosis (15.1 thousand/mcl), C-reactive protein of 21.8 mg/dL and acute osteomyelitis of left foot with MRSA infection of sacral wounds. Anti- glutamic acid decarboxylase (GAD65) and anti-islet cell antibodies were negative. His HbA1Cs had ranged between 14.8% and 18.9%.

Discussion :

Patients with T2DM may be prone to developing DKA and HHS in different settings. This case is unique because of the two different presentations of diabetic emergencies on two different occasions within a period of 2 years. It is even more fascinating that the first presentation was in DKA suggesting very much decreased or dysfunctional beta cell reserve while the subsequent presentation was HHS, suggesting that the patient has a higher or more functional insulin reserve. Preserved beta cell function may explain alternating presentations between HHS and DKA in our patient. Due to non-humoral beta-cell dysfunction in T2DM, patients may have an adequate beta cell reserve to suppress lipolysis. However in the setting of severe stress or infection (such as acute osteomyelitis), the insulin-glucagon ratio is affected which shifts the patient into lipolysis, ketogenesis and thus DKA. Patients with HHS usually have enough preserved beta cell reserve to abate lipolysis and prevent ketogenesis, but not adequate to prevent hyperglycemia.

Conclusion :

DKA prone diabetics, with adequate beta cell reserve, can present in DKA and HHS depending on the clinical scenario.


Michael Sorrenti

Internal Medicine Resident (PGY-1)
University of Illinois at Chicago/ Advocate Christ Medical Center
Oak Lawn, Illinois

I am a PGY-1 internal medicine resident at UIC/ACMC. I am originally from Ottawa, Ontario, Canada. I have a professional interest in the field of endocrinology - I have been drawn to the field ever since I was diagnosed with type 1 diabetes. I aspire to be a clinical endocrinologist when I am done with residency in addition to practicing as a locum hospitalist in some capacity. Some personal interests of mine include hockey, hiking, movies and running.

Fatima M. Kazi

Internal Medicine Resident
Advocate Christ Medical Center
Oak Lawn, Illinois

I am currently a PGY-2 Internal Medicine resident. I am deeply interested in pursuing a career in Endocrinology.

Joumana T. Chaiban

Associate Professor of Clinical Medicine; Internal Medicine Residency Program Research Director
University of Illinois at Chicago; Advocate Christ Medical Center, Department of Internal Medicine, Endocrinology Division

Dr. Chaiban is an attending endocrinologist at UIC/Advocate Christ Medical Center. She teaches UIC/ACMC internal medicine residents as well as UIC endocrinology & metabolism fellows from UIC. She also serves as the research director for the internal medicine residency at UIC/ACMC.