Diabetic ketoacidosis with High anion gap metabolic acidosis

Prasanna Venkatesh

1st Year CCT – EM, Kauvery Hospital Cantonment, Trichy

Case presentation

A 32-year-old male, previously nil comorbid state, presented in ER on 27/11/23 with

  1. C/O increased urination for past 5 days,
  2. H/O dribbling of urine/urinary incontinence(+),
  3. Vomiting (+),
  4. Epigastric pain for 2days,
  5. Polydipsia, marked weight loss prior to admission.

Past Medical History

  1. No h/o abdominal pain, headache, and altered sensorium,
  2. No h/o dysuria and no other relevant history.
  3. Patient was initially evaluated in nearby clinic, where his blood sugars found to be high (HbA1c – 9), urine acetone was positive
  4. Patient referred here for further management.

Primary Assessment

Airway – Patent vocalizing, No secretions.

Breathing – Spontaneous, Tachypneic not in distress, B/L air entry equal, RR – 22/min, spo2 – 99% RA.

Circulation – All four peripheral pulse felt, Heart rate – 108/min, BP – 130/80 mmhg, crt<3sec.

Disability – GRBS – 484 mg, Temp-98.6℉, GCS – E4 V5 M6, pupil B/L RTL, Moving all 4 limbs.

Exposure – No other notable findings, no bedsores.

Pocus Investigation

  1. Adequate LV function.
  2. IVC completely collapsing.
  3. B/L sliding present, no B lines.
  4. No free fluid abdomen.
  5. Bowel and bladder normal.
Diabetic1

Secondary Assessment

  1. Patient was conscious, oriented, afebrile, dehydration (+)
  2. Not pale, no icterus, no cyanosis, no clubbing, no pedal edema, and no lymphadenopathy.

Vitals

  1. CVS – S1,S2 no murmur,
  2. RS – NVBS both side, tachypnea, no added sounds,
  3. ABD – soft, no tenderness, no organomegaly,
  4. CNS – No focal neurological deficit.

Lab Investigations (ABG)

Initially ABG was taken on 27/11/23

  1. pH – 7.06
  2. PCO2 – 19
  3. PO2 – 133
  4. HCO3 – 6.8
  5. Lactate – 1.8
  6. Glucose – 438mg
  7. AG – 29 mmol/l
  8. BE (B) – 23.2 mmol/l.

Impression

  • ABG shows High anion gap metabolic acidosis (HAGMA)

Hematology Reports on 27/11/23

  1. Total count – 9900 cells/cumm,
  2. PCV – 45%,
  3. Platelet – 3,50,000,
  4. Urea – 47 mg/dl,
  5. Creatinine – 1.3 mg/dl,
  6. Plasma acetone – Positive ++,
  7. Sodium – 135 mEq/l,
  8. Potassium – 5.0 mEq/l,
  9. GAD 65 antibody – 9.34,

Urine Analysis

  1. Sugar – 3+,
  2. Blood – Negative,
  3. Pus cells – 1-2,
  4. leucocyte – negative,

ECG Report

Diabetic22024-01-06-02:26:07pm

Provisional Diagnosis

  1. Diabetic ketoacidosis with HAGMA
  2. Newly diagnosed T2DM

Treatment in ER

  1. Secured two 18 G venflon.
  2. Given 1.liter 0.9% Nacl over 30 min.
  3. Additional 2.liters infused till hydration status and output improved.
  4. Total body water deficit calculated according to that 0.9% changed to 0.45% Nacl infused at 100-125 ml/hr.
  5. Since serum potassium level is 5.0 mEq/l, Inj. H. Actrapid infusion started at 0.1 unit/kg/hr infusion was started.
  6. Hourly blood sugar monitor done and insulin titrated according to blood sugar.
  7. The 4th hourly k+ monitoring was done.

Discussion

  1. A 30-year-old male, with nil comorbids presented with above said complaints. Initial resuscitation done in ER, necessary labs sent shifted to ICU for further care. In ICU, Blood sugars closely monitored, insulin tapered accordingly. Patient clinical condition gradually improved and plasma acetone negative. Infusion insulin switched to subcutaneous route and shifted to ward. Work up done for young adult diabetes. glutamic acid decarboxylase 65-kilodalton isoform (GAD) 65 antibody was sent, which was negative. Dosage optimised and discharged patient in a stable status.
  2. A patient with Ketone positive Diabetes has severe hyperglycemia with associated ketosis that can be managed without insulin after a few months; and can maintain acceptable glycemic control with diet or oral agents. Ketoacidosis is not rare inT2DM but occurs in settings of acute illness and infections.
  3. Our patient had a phenotype compatible with T2DM but was diagnosed with DM after an episode of DKA which is a presentation more commonly seen among those with T1DM.
  4. Assessment of autoimmunity and β-cell secretory reserve of newly diagnosed DM patients after 1-3 weeks of resolution of the index DKA episode was reported to predict the ability of the newly diagnosed ketone positive diabetes patient to discontinue insulin and remain in near-normoglycemic remission. They are divided into four groups based on autoimmunity and β-cell function (Aβ) classification scheme: those patients with autoimmune disease with absent (A+β-) or preserved (A+β+) β-cell function and those without autoimmune diabetes with absent (A-β-) or preserved (A-β+) β-cell function.
  5. Patients with negative β-cell function, with or without autoimmune markers, have clinical and biochemical characteristics of T1DM implying lifelong insulin dependency. These groups are comparable to the American Diabetes Association (ADA) classification of autoimmune and idiopathic T1DM respectively. Adequate β-cell function after an episode of DKA, regardless of autoimmunity is compatible with T2DM. Types A+β+ and A-β+ are termed as ‘ketosis prone type 2 DM’. β- cell reserve determines the definitive management of diabetes and is the best predictor of remission in KPD. Insulinopenia will require lifelong insulin (T1D), while those with adequate β-cell function benefit from lifestyle modification and OHA.

ABG on 30/11/23

  1. pH – 7.42,
  2. PCO2 – 41,
  3. PO2 – 96,
  4. HCO3 – 26,
  5. Lactate – 1.4,
  6. Glucose – 80mg,
  7. AG – 12mmol/l,
  8. BE (B) – 2mmol/l.

Discharge Advice

  1. Home monitoring of GRBS.
  2. Inj. Insulatard 25 units – 0-16 units s/c half an hour before food.
  3. Inj. Actrapid 16 units – 16-12 units s/c half an hour before food.
  4. Tab. Pantoprazole 40mg 1-0-0 p/o.
Diabetic3

Dr. Prasanna Venkatesh

1st Year CCT – EM

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