Physical examination was generally unremarkable except for a weight loss of 2.2 kg in the last 6 months. He was admitted to the General Hospital for further evaluation and treatment. The preliminary diagnosis was dehydration, with possible acute appendicitis.   

Upon admission, a panel of laboratory tests was ordered, an intravenous drip was started and surgery was also considered for the patient.   

Laboratory results were:  

Chemistry  
  

Na	143mmol/L	(136-145)
K	5.0mmol/L	(3.8-5.1)
Cl	102mmol/L	(98-108)
CO2	14mmol/L	(23-29)
Urea	6.4mmol/L	(2.4-6.4)
Crea	71umol/L	(27-62)
Glu	16.1mmol/L	(6.1-11.1)
Anion Gap	32	(9-17)

Full blood count   
  

WBC	16-10 6 /L	(4.5-11.0)
Hb	8.69	(6.83-9.93))

Urine dipstix   
SG 1.025   
Glu +++   
Ketone bodies Moderate   
Protein, hb, leucocytes, nitrite were negative   

Differential diagnosis  
1. Appendicitis (­ wbc and lower quadrant abdominal pain).   

2. Diabetic ketoacidosis (DKA) due to symptoms of polyuria, polydipsia and weight loss coupled with laboratory evidence of hyperglycaemia, acidosis, glycosuria and ketonuria.   

An arterial blood gas (ABG) profile was obtained to further evaluate the metabolic derangement (about 20% DKA patients can have glu <16.7mmol/L).  
  

pH	7.31	(7.35-7.45)
pCO2	32mmHg	(35-48)
pO2	108mmHg	(83-108)

ABG results confirmed the diagnosis of DKA (pH 6.8-7.3). In DKA, lipids are mobilised and increased amounts of fatty acids (FFA) is produced. FFA are further metabolised to ketone bodies as shown:  
  

FFA ---> acetoacetate (20%) ---> acetone (2%)

--->b-hydroxybutyrate (78%)

- Note that the dipstix test for ketones using nitroprusside is only sensitive to acetoacetate and may be misleading as in this case where it does not reflect the full extent of the ketosis.   

Insulin therapy was initiated. Electrolytes and glucose were monitored hourly for 4 hours. As the patient's metabolic acidosis improved, his abdominal pain was resolved. An endocrinology consultation was obtained and the consultant pointed out that severe abdominal pain as a result of gastric stasis and distension may be a presenting symptom in DKA which often resolves with treatment of the DKA. The possibility of acute appendicitis was therefore dismissed, and attention was focused on diabetes mellitus.