diabetic ketoacidosis ( dka ) is an acute complication of diabetes mellitus and is characterized by excessive production of betahydroxybutyric and acetoacetic acids leading to low blood ph .
an arterial ph of less than 7.3 is required in order to diagnose dka . rarely , because of other complicating factors
, blood ph may be in the alkalemic range and the term diabetic ketoalkalosis has been coined to describe this condition . currently , less than 30 such cases have been reported in the literature .
a 34-year - old woman was admitted to the emergency department of nemazee hospital , shiraz university of medical sciences , because of polyuria and polydipsia .
one year prior to admission she had underwent pancreas transplantation with pancreatoduodenal anastomosis because of repeated episodes of hypoglycemia , diabetic ketoacidosis , and poor diabetic control . after transplantation , she was on immunosuppressant drugs such as mycophenolate mofetil ( cellcept ) and tacrolimus ( prograf ) and had normal blood sugar .
she discontinued her immunosuppressant drugs from 2 weeks prior to admission and gradually developed polyuria and polydipsia . at the time of admission to the emergency room
her laboratory data were as follows : blood sugar : 385 mg / dl , blood ph : 7.41 , bicarbonate : 22 meq / l , bun : 28 mg / dl , creatinine : 1.1 ng / ml , k : 3.9 meq / l , na : 138 meq / l , negative urine ketone , and 3 + glucosuria .  
her immunosuppressant drugs were restarted and she received one pulse of 1000 mg methylprednisolone . during the next 72 hours she received an intravenous infusion of 4 units regular insulin per hour .
however , her blood sugar remained high and she had repeated episodes of vomiting and had diffuse abdominal pain and extremity weakness . because of her deteriorating condition , she was transferred to the intensive care unit ( icu ) .   at the time of her icu admission ,
her vital signs were as follows : temp : 36.5c orally , blood pressure : 100/70 mmhg , pr : 110/min , and rr : 34/min .
her initial laboratory data showed : hb:13.5 g / dl , wbc : 18500/ml , 80% pmn , blood sugar : 385 mg / dl , bun : 32 mg / dl , creatinine : 1.3 ng / ml , na : 144 meq / l , k : 2.5 meq / l , blood ph : 7.50 , paco2 : 32 mmhg , bicarbonate : 25 meq / l , chloride : 92 meq / l , serum albumin : 4.2 g / dl , globulin : 2.1 gd / l , calcium : 9.2mg / dl , and magnesium : 1.6mg / dl .
the patient was diagnosed as having dka and mixed metabolic acidosis and metabolic and respiratory alkalosis .
because of her hypokalemia , she received 40 meq potassium chloride and normal saline during the first hour of treatment .
the routine treatment of dka was started with 10 units of regular insulin per hour . during the first 4 hours of treatment , her alkalosis progressed to a ph of 7.64 .
her nausea , vomiting , and abdominal pain subsided after 5 hours of treatment and her serum ketone became negative after 8 hours .
she was able to eat after 14 hrs and 2 days later she was discharged on insulin ( twice daily ) .
because of her undetectable c - peptide level , she was diagnosed as a case of pancreas transplant failure and her immunosuppressant drugs were discontinued .
our patient had strongly positive serum ketone , but at the same time her blood ph was in the alkalemic range of 7.5 .
this alkalemic ph in our patient can be explained by the presence of mixed acid - base disturbance .
if the patient had pure metabolic acidosis , the serum bicarbonate was expected to drop to 11 meq / l . the serum bicarbonate in our patient had failed to decrease which signifies the presence of concomitant metabolic alkalosis . in our patients ,
repeated vomiting and the effect of a high dose of methylprednisolone were two causes for metabolic alkalosis .
moreover , the expected arterial paco2 is 40 mmhg , but our patient had an arterial paco2 of 32 mmhg , reflecting the presence of respiratory alkalosis .
pain and anxiety can be the causes of respiratory alkalosis in this patient . as expected , treatment of dka led to the progression of alkalosis , but with therepletion of water and electrolytes , plasma ph gradually returned normal . in most previously reported cases the main causes of dka were hypovlemia because of vomiting and use of diuretics , and alcohol ingestion .
use of diuretics and repeated vomiting result in electrolyte depletion and hypovolemia , leading to bicarbonate reabsorption and alkalosis .
two cases of endogenous cushing s syndrome because of adrenal adenoma and ectopic adrenocorticotropin ( acth ) production with dka have also been reported .
excess endogenous or exogenous glucocorticoids can promote h excretion from the kidneys by their effect on mineralocorticoid receptor and contribute to alkalosis .
respiratory alkalosis , as in our patient , has also been implicated as a contributing factor .
vomiting and hypercortisolemia caused by steroid pulse therapy were the causes of dka in our patient .
we conclude that a normal or even alkalemic blood ph does not rule out the presence of dka . in order to prevent delayed diagnosis and treat this potentially fatal condition , attention
should be paid to the changes in plasma anion gap and bicarbonate and the presence of ketonemia .
 diabetic ketoacidosis ( dka ) is characterized by excessive production of organic acids leading to a low blood ph . rarely , because of other complicating factors blood ph may be in the alkalemic range and the term diabetic ketoalkalosis has been coined to describe this condition . 
 so far , less than 30 such cases have been reported in the literature . 
 we report a 34-year - old woman who received methylprednisolone pulse therapy for the treatment of pancreas transplant rejection . 
 thereafter , she developed vomiting and abdominal pain . 
 her laboratory data showed high blood sugar , hypokalemia , alkalemic ph , elevated plasma anion gap , and significant ketonemia . 
 she responded well to the treatment of dka . 
 it was concluded that an alkalemic ph does not rule out the presence of ongoing dka . in suspected cases , changes in plasma anion gap and bicarbonate and 
 the presence of ketonemia should be noted . 
Introduction
Case Description
Discussion
Conclusion
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