CGM Precision Monitoring : Facilitating Stable Outcome of Sepsis Complicated with Diabetic Ketoacidosis

Release time : 2025-12-25
View count : 17

Medical History and Basic Information

Chief Complaint:

A 60-year-old male patient was admitted to our hospital due to "high fever for 6 days and low back pain for 3 days".

Present History:

Six days ago, the patient developed high fever with a maximum body temperature of 39.5℃, accompanied by anorexia, occasional periumbilical pain, and loose stools. In the past 3 days, he has felt low back pain. His temperature could decrease after taking antipyretic drugs by himself, but the fever recurred. During the course of the disease, there was no gross hematuria, no obvious cough or expectoration, no sore throat, no nausea or vomiting, no acid regurgitation, no skin rash, petechiae or ecchymoses, oral ulcers, or other discomfort.

Physical Examination:

Mild periumbilical tenderness (related to intestinal infection); right costovertebral angle tenderness (perirenal effusion suggests possible pyelonephritis); weakened or normal bowel sounds (slightly rough ascending colon wall suggests local inflammation, but no signs of intestinal obstruction); mild pitting edema of both lower extremities (sodium and water retention caused by hypoalbuminemia or acute kidney injury).

Auxiliary Examinations:

March 1, 2025: White Blood Cell (WBC) count: 18.59x10⁹/L, Neutrophil %: 74.50%, Platelet (PLT): 47x10⁹/L, C-Reactive Protein (CRP): 106.34 mg/L, Glucose (Glu): 24.39 mmol/L, Creatinine (Cr): 149 μmol/L, Sodium (Na): 124 mmol/L, Alanine Aminotransferase (ALT): 155 U/L, Aspartate Aminotransferase (AST): 340 U/L, Prothrombin Time (PT): 15.8 seconds, Activated Partial Thromboplastin Time (APTT): 53.1 seconds, D-Dimer: 7.57 mg/L; Urinalysis: Glucose: +++, Ketone Bodies: +; Abdominal Plain CT: Fatty liver; bilateral perirenal effusion, slightly rough wall of ascending colon with inflammatory changes. The patient received hypoglycemic, anti-infective, fluid replacement and volume expansion, hepatoprotective, acid-suppressing and gastric mucosal protection treatments in the emergency resuscitation room. For further diagnosis and treatment, he was admitted to the hospital as an outpatient with the diagnosis of "sepsis and diabetic ketoacidosis".

March 3, 2025: Glucose: 16.5 mmol/L, Glycated Serum Albumin (GSA): 22.9%, Glycated Hemoglobin (HbA₁c): 8.40%; Urinalysis: Protein: +++, White Blood Cells (WBC): 2.14 p/HPF, Red Blood Cells (RBC): 10.56 p/HPF, Urine Microalbumin-Creatinine Ratio (UACR): 789.65 mg/g, 24-hour Urinary Protein Quantification: 0.89 g/24h; Biochemistry: Urea: 12.8 mmol/L, Creatinine: 192 μmol/L, Uric Acid (UA): 405 μmol/L, Estimated Glomerular Filtration Rate (eGFR-EPI): 31.92 mL/min, Alanine Aminotransferase (ALT): 66 U/L, Aspartate Aminotransferase (AST): 61 U/L.

Admission Diagnosis:

1. Sepsis; 2. Type 2 Diabetic Ketoacidosis; 3. Acute Kidney Injury; 4. Hepatic Insufficiency; 5. Type 2 Diabetes Mellitus.

Treatment Regimen Based on Continuous Glucose Monitoring (CGM) Interpretation

The application of CGM provided a precise blood glucose management tool for this patient with sepsis complicated with metabolic crisis. The physical examination findings (such as fever, dehydration, deep and rapid breathing, costovertebral angle tenderness, etc.) were highly consistent with the pathophysiological mechanisms of septic shock, diabetic ketoacidosis, and multiple organ injury. The combination of the two provided a key basis for early identification of disease changes and formulation of individualized treatment plans.

The patient had a history of diabetes mellitus for more than 15 years, and had been taking sitagliptin-metformin and repaglinide orally for hypoglycemia. The usual blood glucose control was unknown, and islet function was not regularly evaluated. This time, due to sepsis complicated with diabetic ketoacidosis and hepatorenal insufficiency, oral hypoglycemic drugs were discontinued after admission. Low-dose insulin combined with fluid replacement was adopted, followed by intensive insulin therapy.

Other Treatments: Anti-infection (meropenem), immune enhancement (intravenous immunoglobulin), hepatoprotection (monoammonium glycyrrhizinate and cysteine), anticoagulation (enoxaparin) and other symptomatic and supportive treatments; next-generation sequencing (NGS) showed Epstein-Barr virus infection, so ganciclovir was used for antiviral treatment.

Time Hypoglycemic Regimen Blood Glucose Profile Average Blood Glucose (mmol/L) TIR (%) TAR(%) TBR(%) Blood Ketone Bodies (mmol/L)
March 2 0.9% NS + RI and 5% GS + RI for fluid replacement; Insulin Glargine 10U   10.3 30.0% 70.0% 0.0% 2.3
March 3 5% GS + RI for fluid replacement; Insulin Glargine 16U   9.7 65.4% 34.6% 0.0% 0.7
March 4 Insulin Lispro Injection 8U-8U-8U; Insulin Glargine 16U   7.1 100% 0.0% 0.0% 0.3
March 5 Insulin Lispro Injection 8U-8U-8U; Insulin Glargine 16U   7.7 100% 0.0% 0.0% 0.1
March 6 Insulin Lispro Injection 8U-8U-10U; Insulin Glargine 16U   7.3 89.6% 10.4% 0.0% 0.1
March 7 Insulin Lispro Injection 12U-6U-8U; Insulin Glargine 12U   6.5 100% 0.0% 0.0% 0.1

Note: TIR: Time in Range (3.9~10.0 mmol/L); TAR: Time Above Range (>10.0 mmol/L); TBR: Time Below Range (<3.9 mmol/L)

March 7, 2025: Biochemistry: Urea: 10.2 mmol/L, Creatinine: 106 μmol/L, Uric Acid: 571 μmol/L, Estimated Glomerular Filtration Rate (eGFR-EPI): 65.32 mL/min, Alanine Aminotransferase (ALT): 34 U/L, Aspartate Aminotransferase (AST): 28 U/L, C-Peptide: 0.270 nmol/L.

After active treatment, the rechecked inflammatory indicators improved, ketoacidosis was alleviated, and liver and kidney functions were improved. The patient was gradually switched to oral hypoglycemic drugs.

Time Hypoglycemic Regimen Blood Glucose Profile Average Blood Glucose (mmol/L) TIR (%) TAR(%) TBR(%) Blood Ketone Bodies (mmol/L)
March 8 Miglitol 50mg tid; Sitagliptin-Metformin 50mg/850mg qd; Insulin Glargine 10U   8.1 78.8% 21.2% 0.0% /
March 9 Miglitol 50mg tid; Sitagliptin-Metformin 50mg/850mg qd; Insulin Glargine 10U   8.0 83.8% 16.2% 0.0% /
March 10 Miglitol 75mg-50mg-75mg; Sitagliptin-Metformin 50mg/850mg qd; Insulin Glargine 8U   7.5 98.1% 1.9% 0.0% /

Note: TIR: Time in Range (3.9~10.0 mmol/L); TAR: Time Above Range (>10.0 mmol/L); TBR: Time Below Range (<3.9 mmol/L)

  • March 11, 2025 Biochemistry: Urea: 5.9 mmol/L, Creatinine: 84 μmol/L, Uric Acid: 304 μmol/L, Urinary Creatinine: 1778 μmol/L, Urine Microalbumin-Creatinine Ratio (UACR): 107.51 mg/g, eGFR-EPI: 86.64 mL/min, Alanine Aminotransferase (ALT): 44 U/L, Aspartate Aminotransferase (AST): 43 U/L, C-Peptide: 0.540 nmol/L.
  • Insulin was discontinued, and hypoglycemic treatment was adjusted to Miglitol 50mg bid combined with Sitagliptin-Metformin 50mg/850mg bid.
  • Renal function was further improved, urinary protein decreased compared with before, and Urine Microalbumin-Creatinine Ratio was 107.5 mg/g, so Finerenone was added to improve urinary protein.
  • The patient was followed up in the outpatient clinic after discharge.

Case Summary

According to the recommendations of the Guidelines for the Prevention and Treatment of Diabetes Mellitus in China (2024 Edition) and the 2025 ADA Standards of Care in Diabetes[1-2], TIR can be used as an effective indicator to evaluate blood glucose control. CGM can significantly improve TIR, reduce the risk of hyperglycemia and hypoglycemia, and improve clinical outcomes. At present, CGM has become the core tool for refined blood glucose management, especially suitable for critically ill patients, perioperative patients, and patients with metabolic crisis.

Especially in the state of severe infection such as sepsis, the body is in a state of high inflammation, high metabolism, and insulin resistance, with severe blood glucose fluctuations. Traditional fingertip blood glucose monitoring is difficult to capture the whole picture of blood glucose changes. By reflecting blood glucose trends in real time and dynamically, CGM helps to early identify blood glucose abnormalities, guide insulin dose adjustment, and prevent severe hyperglycemia or hypoglycemia events.

This case is a 60-year-old male with a previous history of type 2 diabetes mellitus for 15 years, who has been taking sitagliptin-metformin and repaglinide orally for a long time. This time, sepsis induced diabetic ketoacidosis, combined with acute hepatorenal insufficiency, and the condition was critical. At admission, the blood glucose was as high as 24.39 mmol/L, and ketone bodies were 2.3 mmol/L, indicating severe metabolic decompensation.

In the initial treatment, CGM showed that TIR was only 30% and TAR was as high as 70%, indicating extremely poor blood glucose control. Low-dose intravenous insulin infusion combined with fluid replacement was adopted. After ketoacidosis correction, the insulin regimen was adjusted to the "basal + prandial" mode (Insulin Glargine + Insulin Lispro). According to the data monitored by CGM, the insulin dose was adjusted. The CGM profile showed that blood glucose gradually stabilized, TIR increased from 65.4% to 100%, blood ketone bodies decreased from 2.3 mmol/L to 0.1 mmol/L, and no hypoglycemia occurred during this period.

The advantages of Sinocare iCan CGM at this stage are reflected in:

  • Timely identification of nocturnal hyperglycemia and dawn phenomenon to guide the adjustment of basal insulin dose;
  • Real-time monitoring of postprandial blood glucose peaks to optimize prandial insulin dose and administration time;
  • During the stage of renal insufficiency, insulin clearance rate decreases, and CGM provides early warning to avoid the risk of hypoglycemia.

With the improvement of liver and kidney functions and the recovery of insulin function, the patient was gradually transitioned to the "Insulin Glargine + oral drugs" regimen. CGM data showed that TIR was maintained between 78.8% and 98.1%, the average blood glucose was stable between 7.5 and 8.1 mmol/L, and no hypoglycemia events were observed.

The role of Sinocare iCan CGM at this stage is:

  • Evaluate the efficacy and safety of oral drugs (such as Miglitol, Sitagliptin);
  • Guide insulin reduction or even withdrawal to avoid overtreatment;
  • Provide data support for long-term management after discharge to achieve seamless blood glucose management from hospital to home.

Clinicians often face the dual challenges of blood glucose control and organ function protection when dealing with sepsis complicated with diabetic ketoacidosis (DK) or diabetic ketoacidosis (DKA). The introduction of CGM can real-time evaluate changes in insulin sensitivity, especially in the stage of hepatorenal insufficiency; identify blood glucose fluctuation patterns such as dawn phenomenon and Somogyi effect; combined with blood ketone monitoring, evaluate the trend of metabolic control, and guide fluid replacement and insulin infusion strategies. According to the guidelines[1-2], TIR is used as the core indicator of blood glucose control quality (target TIR >70%), and TAR and TBR are strictly controlled to reduce the risk of infection deterioration and organ injury.

In this case, through the whole-course, dynamic and visualized monitoring of Sinocare iCan CGM, combined with blood ketone and organ function indicators, precise blood glucose regulation from the critical period to the recovery period was achieved, and finally a stable transition to oral drug treatment was realized. It reflects the closed-loop management concept of “monitoring-evaluation-intervention-reassessment" and is a model of the successful application of CGM in critical illness metabolic management. In the future, with the integration of CGM technology and artificial intelligence algorithms, it is expected to establish a standardized CGM path for critically ill patients with glucose metabolism disorders, expand the application of CGM in communities and families, build a full-cycle blood glucose management ecosystem, drive diagnosis and treatment with data, and improve the overall medical quality.

References:

[1] Chinese Medical Association Diabetes Society. Guidelines for the Prevention and Treatment of Diabetes Mellitus in China (2024 Edition). Chinese Journal of Diabetes Mellitus, 2024, 17(00):16-139.

[2] American Diabetes Association Professional Practice Committee. Introduction and Methodology: Standards of Care in Diabetes—2025. Diabetes Care, December 2024, Vol.48, S1-S336.