Acidosis is not a sine qua non for DKA

Göktuğ Sarıbeyliler; Caner Kapar; Ayșenur Yılmaz; Alpay Alibeyoğlu; Cemile İdiz; Ümmü Mutlu; Vefa Nasifova; Caklili Ozge Telci; Çelik Ayșe Merve; Ramazan Çakmak; Nurdan Gül; Kubilay Karșıdağ; Nevin Dinççağ

doi:10.1530/endoabs.70.AEP455

Although Diabetic ketoalkalosis (DKAlk) has beendescribed as a mixed acid-base disorder over half a century ago, there is unawareness among physicians. Here, we present two cases to emphasize DKAlk which is more common than it’s thought.

Case-1: A thirty-year-old female patient with type-1 diabetes and ten weeks of pregnancy presented with several weeks of vomiting. She also reported that she had hyperthyroidism for 2 weeks and that she used propylthiouracil 50 mg/day in addition to insulin. Physical examination revealed volume depletion findings such as dehydration andtachycardia. Laboratory findings are shown in the table. These findings suggested metabolic acidosis masked by alkalosis. Fluid replacement and insulin infusion therapy was applied rapidly. Propylthiouracil was increased to 150 mg/day, in addition to iodine restriction. After 3 days, ketonuria disappeared and pH and delta gap were found as 7,44 and 13,5, respectively. In this case, the acid-base disorders were DKA, metabolic alkalosis due to hyperemesis gravidarum and respiratory alkalosis due to pregnancy and gestational thyrotoxicosis.

Case-2: A thirty-two-year-old female patient with type-1 diabetes and sixteen weeks of pregnancy was admitted to emergency department with vomiting, dysuria and sore throat. She had hypotension andtachycardia as results of severe dehydration. Laboratory findings are shown in the table. She also had pyuria and high levels of CRP (42.99 mg/l) and ESR (85 mm/h). These results were compatible with combined alkalosis and acidosis. After 24-hour fluid replacement, insulin infusion and ceftriaxone therapy, hypovolemia improved, ketonuria disappeared, glucose levels returned to normal range. While clinical situation improved within days, all other laboratory results ameliorated. Thyroid disorder was interpreted as subacute thyroiditis and followed without treatment; fT4 and fT3 levels decreased spontaneously at the end of the second week (fT4:11.29 pmol/l, fT3:3.88 pmol/l). In this case DKA, metabolic alkalosis due to vomiting caused by acute pyelonephritis and respiratory alkalosis due to pregnancy and thyroiditis were observed. As conclusion, acidosis is not a sine qua non for DKA. Awareness should be raised about DKAlk. It should always be kept in mind that mixed acid-base disorders can mask DKA and DKAlk may be in the foreground of the picture.


	pH	HCO3 (mEq/l)	PCO2 (mmHg)	ketonuria	Glucose (mg/dl)	WBC/neu	Crea (mg/dl)	Na/K/Cl (mmol/l)	Anion gap	Delta gap	TSH (mIU/l)	fT4/fT3 (pmol/l)
Case-1	7.55	27.3	29.7	+++	413	14 600/mcl/84,4%	1.53	134/4.84/88.1	16.2	20.9	0.005	81.9/15.08
Case-2	7.50	28.3	35	+++	682	15 900/mcl/85,8%	2.1	132/3.87/72.4	31.3	34.6	0.026	26.94/7.72

Endocrine Abstracts

AEP455