Summary 13

YAC, a 49 years old lorry driver diagnosed with type 2 diabetes mellitus for 10 years, did not take medicine (Mixtard 30 48 units OM and 36 units ON, tablet metformin 1g BD PO, and tablet simvastatin 40 mg ON PO) due to busy working schedule for two days.

Question: What does Mixtard insulin contain? What does "30" in Mixtard-30 mean?

On the first day, he only had red bean buns for lunch and dinner, and two serving of chicken rice at night. Subsequently, he woke up to urinate thrice, and passed urine ten times the next day. The volume of urine was more than usual. On day 2 of illness, there was tiredness, poor appetite, abdominal pain (persistent, non-radiating, localized to epigastric region, pain score: 5/10, without worsening and alleviating factor), nausea, and vomiting. He vomited four time a day. Vomitus contained ingested food.

Question: What does the absence of bile in the vomitus imply?

He did not have fever, loss of consciousness, tremor, profuse sweating, cough, dyspnoea, chest pain, and dysuria. 10 years ago, he was admitted once for hyperosmolar hyperglycaemia state.

Question: Why do some people develop HHS and not DKA?

His compliance had been well, but he did not take medicine two days before admission due to increased workload. The findings of physical examination were normal and stable vital signs, Glasgow coma scale: 15/15, normal capillary refill and skin turgor, and an intravenous cannula connected to intravenous infusion of normal saline on left dorsum of hand.

Question: What is it obvious that there is a narrative gap (that is, the history is at time of presentation but the physical findings are not)?

Cardiovascular, respiratory, abdominal, thyroid, nervous, and eye examination were normal. On admission, the investigation results were: Random capillary blood glucose: 21.2 mmol/L. Urinalysis showed ketone: 15 mmol/L and glucose: 56 mmol/L. Full blood count: white blood cells: 13.52 x109/L (leucocytosis), neutrophil: 12.01 x103/uL (neutrophilia), haematocrit: 49.5% (increased).

Question: What does the increased hematocrit imply here?

Renal profile: urea: 9.0 mmol/l (increased), creatinine: 104 umol/L, and corrected sodium: 135.7 mmol/L.

Question: What is meant by "corrected sodium"?

Arterial blood gases: pH: 7.289 (acidosis), pCO2: 29 mmHg (decreased), pO2: 149.3 mmHg (increased), HCO3: 13.9 mmol/L (decreased). Base excess: -11.0 mmol/L. Anion gap: 37.2 mmol/L.

Question: Why is the PaCO2 reduced? Why is the PaO2 increased? What is the significance of an increased anion gap?

Electrocardiogram: heart rate: 110 beats per minute. Sinus rhythm and regular rhythm were present. QRS complexes were narrow. Normal axis of heart. Diagnosis: diabetic ketoacidosis secondary to non-compliance. He was treated with intravenous infusion of insulin at 0.1 unit/kg/hour, and intravenous crystalloid.

Question: What is the crystalloid solution that is used? At which point is it necessary to change the type of IV fluids in the management of diabetic ketoacidosis? What aspect of treatment has not been mentioned?

Diabetic ketoacidosis resolved after seven hours, and intravenous infusion of insulin was replaced with basal bolus regime of insulin. After counselling, he agreed to switch to basal bolus regime for insulin, and be compliant. He was well during 24 hours of observation. On day 3 of admission, he was discharged with medicine (metformin and insulin), and a referral letter for dietitian. Appointment for follow-up at medical outpatient department was made.

Question: Does he have Type 1 or Type 2 diabetes? What is the difference between his new insulin regimen ("he agreed to switch to basal bolus regime for insulin") and his previous insulin schedule?

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