A Case of Diabetic ketoacidosis

Kalaiselvi1, Subadhra Devi2, Maha Lakshmi3

1Nursing Supervisor, Kauvery Hospital, Cantonment

2Nurse Educator, Kauvery Hospital, Cantonment

3Nursing Superintendent, Kauvery Hospital, Cantonment

Abstract

Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus characterized by hyperglycemia, metabolic acidosis, and ketosis. It occurs due to an absolute or relative insulin deficiency, often precipitated by factors such as infection, inadequate insulin therapy, or physiological stress. The pathophysiology involves an increased level of counter-regulatory hormones, leading to enhanced lipolysis and ketogenesis. Clinical presentation typically includes symptoms such as polyuria, polydipsia, nausea, vomiting, and abdominal pain, with laboratory findings revealing hyperglycemia, metabolic acidosis, and elevated serum ketones. Prompt recognition and treatment are crucial to prevent complications, including cerebral edema, respiratory failure, and cardiac arrest. Management involves aggressive fluid replacement, insulin therapy, and electrolyte monitoring to restore fluid balance, reduce ketone production, and normalize blood glucose levels. Understanding the precipitating factors, clinical features, and treatment strategies is essential for healthcare providers to deliver optimal care and prevent adverse outcomes in patients with DKA.

Background:

Diabetic ketoacidosis (DKA) is a complex metabolic disorder that arises from the interplay of insulin deficiency, counter-regulatory hormone excess, deranged glucose metabolism. The underlying pathophysiology involves a lack of insulin, leading to increased glucose production in the liver and impaired glucose uptake in peripheral tissues. Concurrently, the excess of counter-regulatory hormones such as glucagon, cortisol, and catecholamines enhances lipolysis, resulting in the production of ketone bodies. As ketones accumulate in the blood, metabolic acidosis develops, leading to a vicious cycle of worsening acidosis and ketosis. Various factors can precipitate DKA, including infections, inadequate insulin therapy, new-onset diabetes, and physiological stress. Understanding the multifactorial etiology and pathophysiological mechanisms of DKA is crucial for developing effective prevention and treatment strategies.

Case Presentation:

The 45-year-old male patient, with a known history of type 2 diabetes mellitus presented to the emergency department with symptoms of tachypnea, vomiting, and cough. Clinical examination revealed signs of dehydration, which were likely exacerbated by poor oral intake over the preceding 48 hours. The patient’s non-compliance with diabetes medications may have contributed to the development of diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar state (HHS).

Given the patient’s clinical presentation, immediate management should focus on fluid replacement, insulin therapy, and electrolyte monitoring. Intravenous fluids will help correct dehydration, while insulin will address hyperglycemia and ketosis. Close monitoring of vital signs, fluid balance, and blood glucose levels is crucial to prevent complications and ensure optimal care.

Social History

He does not have any history of cigarette smoking or alcohol addiction.

Allergies

No known medicine or environmental allergies

Past Medical History:

➔ Type 2 diabetes mellitus; Systemic hypertension
Chronic kidney disease. The patient was on irregular treatment.

Physical Examination:

Vital signs Temp: 98.6ŸF, .HR:114/min, RR:32/min, BP 150/80 mmHg, Spo2 :98%

A: Patient vocalizing no obstruction in airways

B: Deep and rapid breathing, tachypnea -32/mt

C: All peripheral pulse present.HR 114/min BP 150/80 mm Hg, No pallor, icterus, or pedal edema

D: Neurological Examination – Alert but bit restless, mild confused

Others : odor breath, dry mucous membranes

Investigations:

POCUS:

Mild hepatomegaly.

Bilateral renal parenchymal changes.

Right renal simple cortical cyst and calculus.

Markable investigations

Chloride106 mmol/L
Chloride Blood111 mEq/L
Creatine Phosphokinase (CPK)758 U/L
Creatinine10.2 mg/dL
Glucose750 mg/dL
HbA1c11.1 %
K +7.5 mmol/L
Magnesium2.44 mg/dL
PCO240 mm Hg
Potassium7.4 mmol/L
Procalcitonin4.31 ng/mL
Sodium143 mmol/L
Uric Acid9.55 mg/dL
KetonePositive (+)
Urine ProteinPresent (+++)
Haemoglobin7.7 g/dl
Packed Cell Volume (PCV)31.4 %
Platelet Count503000 cells/µl

Imaging examination – USG

He reported taking high-sugar drinks, and his arterial blood gas (ABG) analysis showed high anion gap metabolic acidosis. The patient was initiated on non-invasive ventilation (NIV) support, intravenous fluids, insulin infusion, and empirical antibiotics, and was admitted to the critical care unit. Basic laboratory investigations revealed elevated total leukocyte count, procalcitonin, and renal parameters, as well as high blood ketone levels. An ultrasound of the abdomen showed mild hepatomegaly, bilateral renal parenchymal changes with cysts, and calculi. A nephrologist was consulted to manage the patient’s renal complications. Further investigations revealed high CPK and HbA1C levels. With serial laboratory monitoring, the patient’s renal function tests and sugar levels showed significant improvement, allowing for optimization of his treatment plan.

The immediate initiation of supportive measures, including non-invasive ventilation, insulin therapy, intravenous fluids, and empirical antibiotics, was critical in stabilizing the patient. The identification of renal parenchymal changes and bilateral renal calculi necessitated multidisciplinary management with nephrology input, ensuring comprehensive care of both metabolic and renal complications.

Management:

The patient was immediately started on

1)    IV fluids— isotonic saline for dehydration

2)    Insulin therapy— IV regular insulin infusion

3)    Electrolyte monitoring & correction—Especially potassium

4)    Monitoring—Hourly glucose, electrolytes& vitals

5)   Identification and management of triggers—CXR,blood CSare done  to rule out infection , no evident was found likely precipitated by poor glycemic cause control

6)NIV started–FIO2-40%,

Follow up treatment.

During discharge time he was on

Tab. Pan40 mg
Tab. Nodosis GST500 mg
Tab. Felypo
Tab. Actvie D
Tab. Arkamin0.1 mg
Tab. Nicardia 20 ml
Inj. Wepox1000 U
Inj. InsulatardS/C
Inj. ActrapidS/C

Skilled Nursing Care:

Respiratory Support

  • Monitor Respiratory Status:
    • Assess rate, rhythm, depth, and oxygen saturation every 1–2 hours.
    • Monitor effectiveness of non-invasive ventilation (NIV) support.
  • Airway Management:
    • Ensure NIV mask fit and prevent pressure injuries.
    • Perform chest physiotherapy and suction if needed to manage secretions.
  • ABG Monitoring:
    • Assist with arterial blood gas sampling; report abnormalities (e.g., worsening acidosis).

Metabolic Management (DKA Focus)

  • Blood Glucose Monitoring:
    • Check capillary blood glucose hourly during insulin infusion.
    • Titrate insulin infusion as per protocol.
  • Fluid and Electrolyte Balance:
    • Monitor input/output strictly (urine output, IV fluids).
    • Watch for signs of dehydration or fluid overload.
    • Replace electrolytes (e.g., potassium) as per medical orders and monitor serum levels.
  • Ketonemia Monitoring:
    • Monitor blood/urine ketone levels and report changes.

Renal Support and Monitoring

  • Vital Renal Assessments:
    • Monitor renal function (creatinine, urea) as per schedule.
    • Record urine color, amount, and consistency.
  • Consult Coordination:
    • Collaborate closely with nephrology for renal management plans.
    • Administer prescribed medications (e.g., diuretics, renal-protective drugs).
  • Ultrasound Follow-Up Care:
    • Monitor for symptoms related to cysts or renal stones (e.g., pain, hematuria).

Infection Prevention and Antibiotic Stewardship

  • Empirical Antibiotics Administration:
    • Administer on time; check for adverse reactions.
    • Monitor for fever, chills, or signs of systemic infection.
  • Sepsis Surveillance:
    • Observe tachycardia, hypotension, altered mental status.

Nutritional and GI Care

  • Nutritional Assessment:
    • Collaborate with a dietitian for a renal- and diabetic-friendly nutrition plan.
    • Initiate gradual oral intake when clinically stable.
  • Vomiting Management:
    • Monitor for nausea, vomiting; administer antiemetics as doctors advised.

Education and Psychosocial Support

  • Patient & Family Education:
    • Explained DKA causes, signs, and prevention (e.g., avoiding high-sugar drinks).
    • Educated on the importance of glycemic control and regular follow-ups.
  • Emotional Support:
    • Provide reassurance and reduce anxiety through open communication.

Documentation and Evaluation

  • Ongoing Evaluation:
    • Reassessed the condition and updated the care plan based on clinical progress.

Conclusion

Serial monitoring of laboratory parameters, including renal function, inflammatory markers, and glucose control, allowed for the effective titration of therapy. The patient’s favorable response, evidenced by improvement in biochemical markers and clinical stability, underscores the importance of early recognition, aggressive intervention, and coordinated critical care in managing complex metabolic emergencies.

This case emphasizes the need for ongoing patient education, strict glycemic control, regular follow-ups, and lifestyle modifications to prevent recurrence and ensure long-term health outcomes.

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