• This patient was complaining of unquenchable thirst and repeated need to urinate so that in retrospect, given the blood sugar that was eventually obtained, he was having osmotic diuresis (caused by passage of glucose into the urine when blood sugar levels were above the threshold levels of 200 mg/dl) and eventual dehydration.
•  Elevation of blood sugar is a poor stimulus of thirst in normal individuals, because its contribution to serum osmodality is relatively limited; only 5 mOsm per 100 mg/dl. On the other hand, in diabetic patients, elevation of blood sugar is associated with increase in thirst, since thirst centers in the hypothalamus are insulin-dependent for glucose utilization.
•  Contraction of extracellular fluid contributed to thirst, and also to weakness and dizziness (often these patients also have orthostatic hypotension). 
• Intravenous saline temporarily expanded the extracellular fluid and restored effective blood volume, allowing this patient to return to duty temporarily.
  
  

2. Why was dyspnea his presenting symptom?

• The admission laboratory results indicated acid pH and low bicarbonate, characteristics of metabolic acidosis. 
• The respiratory center is exquisitely sensitive to changes in pH. 
• Increase in the concentration of hydrogen ion in the blood in this case, is due to hepatic overproduction of the keto acids, betahydroxybutyric and acetoacetic acid, strong organic acids that completely disassociate at body pH (providing 1 mM of hydrogen ion per each mM of betahydroxybutyric acid). 
• When the body buffers are reduced due to loss of cathions and bicarbonate in the urine and respiratory compensation is unable to maintain a normal pH, diabetic acidosis ensues. 
• As long as severe metabolic acidosis is present, dypsnea, characterized by deep inspirations and expirations in a rhythmic pattern, called Kussmaul respiration, will appear.
•  By blowing off CO2, the body is attempting to restore the balance between CO2 and bicarbonate, which are the main regulators of plasma pH (Henderson, Hasselbach equation).
  
  

3. He was hyperkalemic on admission, and yet, why was potassium later added to the IV infusion?

• The initial hyperkalemia is attributed to pH-induced shifts of potassium from the intracellular to the extracellular compartments. 
• In addition, insulin has an independent potassium transport effect, which is defective when there is insulin lack.
• In the course of therapy with fluids and insulin, the electrolyte deficits of diabetic ketoacidosis quickly become apparent, and hypokalemia ensues. 
• As long as the patient is urinating properly, most patients need potassium replacement as part of early treatment of DKA to avoid hypokalemia, which might cause cardiac arrest or fatal arrhythmias.
  
  

4. What is the possible reason why a single injection of insulin in the morning failed to control his diabetes without causing hypoglycemia? 

• The duration of intermediate insulin, that is, Lente or NPH, is about 18 to 24 hours. 
• However, the peak action after subcutaneous injection, is between 6 and 12 hours. 
• In order to obtain a fasting blood sugar within therapeutic range, there would be excessive relative hyperinsulinemia toward the middle of the day, which is not always compensated by food ingestion. 
• Frequently, undetected hypoglycemia occurs in the early hours of sleep. 
• A more physiological regime in type I diabetics (who do not have endogenous insulin), is to correct the hyperglycemic waves after meals with regular insulin injected 1/2 to 1 hour before each meal, and a low-dose bedtime intermediate duration insulin targeted to normalization of fasting sugar. 
• Bedtime insulin injection normally does not raise insulin levels in the early period of sleep enough to cause hypoglycemia, but is effective in achieving peaks on or around breakfast time, when insulin needs are the highest.