management of diabetic ketoacidosis

514 Volume 25, Number 6

Julie Miller, Greater Cincinnati Chapter, is Family Nurse Practition-er, St Luke Pediatric Center, Bellevue, Ky.J Emerg Nurs 1999;25:514-9.Copyright © 1999 by the Emergency Nurses Association.0099-1767/99 $8.00 + 0 18/1/102864

Management of diabetic ketoacidosisAuthor: Julie Miller, RN, MSN, ARNP, Union, Ky

Joe, a 37-year-old white man with a 3-day history ofvomiting and progressive weakness, was brought

to the emergency department by basic life squad. Pre-hospital personnel said he had flulike symptoms. Hedenied having chest pain, shortness of breath, ab-dominal pain, fever, or diarrhea. His medical historywas unremarkable, with no hospitalizations or surg-eries. He was taking no medications and had noknown drug allergies.

A primary survey revealed a thin, ill-appearingman with dry mucous membranes. His vital signswere as follows: blood pressure, 100/60; temperature,98°F; pulse, 120; and respirations, 32. Because the EDnurse caring for him detected a faint odor of ketones,she obtained blood for a serum glucose level whilestarting his intravenous infusion. The glucometerread “HHH.” If the nurse had not recognized the odor,which was quite possible, the patient’s diagnosismight not have been made or might have been de-layed, with worse sequelae. A high index of suspicionfor ketoacidosis is crucial.

Diabetic ketoacidosis (DKA) is a serious, life-threatening metabolic complication of diabetes melli-tus. Although DKA most commonly occurs in personswith type 1 diabetes, persons with type 2 diabetes arealso susceptible to DKA under stressful conditions(Table 1).1,2 This article presents clinical decision-making guidelines for the care of adults with DKA forboth nurses and advanced practice nurses in theemergency department.

DKA is a metabolic disorder consisting of 3 con-current abnormalities: hyperglycemia, hyperketone-mia, and metabolic acidosis. DKA develops in personswith either an absolute deficiency of insulin or a rela-tive deficiency caused by an excess of counterregula-tory hormones (glucagon, catecholamines, cortisol,and growth hormone). Although the counterregulato-ry hormones alone cause an increase in the produc-tion of glucose in the liver, the body with DKA is un-able to use the glucose because of insulin deficiency.As a result, severe alterations occur in the metabolismof carbohydrates, proteins, and lipids.3

PathophysiologyThe pathophysiology of DKA is a direct result of an in-creased glucagon:insulin ratio. Hyperglycemia causescellular dehydration because glucose does not diffuseeasily through cell membrane pores, and the increasedosmotic pressure in the extracellular fluid causes os-motic transfer of water out of the cells. Glycosuria re-sults when the renal threshold for glucose is exceeded.The osmotic effect of glucose in the renal tubulesmarkedly decreases tubular reabsorption of fluid anddraws water, sodium, potassium, magnesium, calci-um, and phosphorus from the circulation into theurine, resulting in marked electrolyte imbalances. Thecombination of large losses of fluid in the urine andvomiting leads to both intracellular and extracellulardehydration and may result in circulatory collapse.4,5

Ketoacidosis is a result of increased ketone pro-duction and decreased ketone use. Both acetoaceticand β-hydroxybutyrate are strong acids that must beneutralized with bicarbonate before being excreted inthe urine. Rapid development of ketonemia occurswhen the ability to excrete and neutralize ketoacidsby the body is surpassed and metabolic acidosis en-sues.6 However, no correlation exists between theseverity of hyperglycemia and the severity of meta-bolic acidosis in patients with DKA.7

Precipitating factorsThe search for a precipitating factor in triggeringDKA is of utmost importance, because hyperglycemiaand acidosis are rarely the sole cause of mortality inpatients with DKA. Rather, serious underlying illness-es, such as myocardial infarction and pneumonia, aremajor causes of mortality, particularly in older diabet-ic patients.8 Myocardial infarction must always beconsidered in older persons who have DKA, even in

Patients with DKA typicallygive a history of polydipsia,polyuria, fatigue, andweakness, which is a resultof the osmotic diuresis.

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Miller/JOURNAL OF EMERGENCY NURSING

the absence of symptoms,3 because autonomic dia-betic neuropathy may result in loss of cardiovascularsensation.9

DKA is the initial manifestation of diabetes in ap-proximately 20% of patients. In known diabetics, ap-proximately 75% of episodes of DKA will have anidentifiable precipitating factor, with infection beingthe most common cause.8 Urinary tract infection andpneumonia are the most common causes of infec-tion.3 Other causes include stopping insulin therapy,10

congestive heart failure, gastrointestinal hemorrhage,pancreatitis, cerebrovascular accident, bowel infec-tion, and physical or emotional response to stress.8

Drugs that have been reported to precipitate DKA in-clude dobutamine, terbutaline, and pentamidine.Glucosteroids may also precipitate DKA because theystimulate gluconeogenesis and increase peripheralresistance to insulin.11

Clinical presentationPatients with DKA typically give a history of polydip-sia, polyuria, fatigue, and weakness, which is a resultof the osmotic diuresis created in the presence of hy-perglycemia. Other complaints include abdominalpain and vomiting, which are believed to be the resultof ketoacidosis and gastric stasis.12 Family membersmay report episodes of lethargy and alterations inlevel of consciousness, which may be related to an in-crease in serum osmolality.11

Patients with DKA have variable physical find-ings depending on the severity of illness, degree ofextracellular volume depletion, and presence of a co-existing condition. Although most patients havetachycardia, the mean blood pressure is usually nor-mal. Profound hypotension is associated with a high-er risk of mortality.13 Tachypnea and Kussmaul’srespirations may be present in an attempt to com-pensate for the metabolic acidosis, and the fruity odorof acetone may be present on the breath.14

A mental status examination may be normal orabnormal. Approximately 10% of patients with DKApresent in a coma, and another 70% are lethargic or

obtunded. The remaining 20% will have no mentalstatus changes.14 Signs of dehydration may be pre-sent on physical examination. These signs includedry mucus membranes, dry furrowed tongue, poorskin turgor, and soft sunken eyes. An abdominal ex-amination may reveal tenderness and rebound, whichshould resolve with the treatment of ketoacidosis ifthe pain is caused by acidosis. Persistent pain neces-sitates further evaluation.14 Hepatomegaly is the re-sult of fatty infiltration of the liver and resolves withthe administration of insulin.5 Lastly, the feet mustnot be forgotten in the physical examination, becausediabetic foot disease may be a source of infection.15

Diagnostic criteriaThe diagnosis of DKA is confirmed by the presence ofhyperglycemia, ketosis, and acidosis. However, al-though a consensus on exact criteria has not beenreached, the most frequent diagnostic criteria includethe following: (1) serum glucose level greater than 250mg/dL, (2) pH less than 7.3, (3) serum bicarbonatelevel less than 15 mmol/L, and (4) positive serum ke-tones at a greater than 1:2 dilution using the nitro-prusside reaction.3,12

Laboratory assessmentIn addition to a concise history and physical, immedi-ate laboratory studies performed at the bedside canassist in establishing the diagnosis of DKA and initi-ating appropriate therapy in a timely manner. Aserum glucose level can be measured immediately at

Table 1Type 1 diabetes• Formerly insulin-dependent diabetes mellitus or

juvenile-onset diabetes• Results from a cell-mediated autoimmune destruc-

tion of the B-cells of the pancreas• Approximately 10% of diabetics• Individuals are ketosis prone and dependent on in-

sulin for survival• Peak incidence in childhood and adolescence

Type 2 diabetes• Formerly non-insulin–dependent diabetes or adult-

onset diabetes• Individuals have insulin resistance in combination

with a relative deficiency of insulin secretion• Approximately 90% of diabetics• Eighty percent to 90% of individuals are obese• Ketosis is rare• Mean age of diagnosis 51 years

Data from Report of the Expert Committee on the diagnosisand classification of diabetes mellitus. Diabetes Care 1997;20:1183-98.

Severe total body potassiumdepletion in DKA results fromosmotic diuresis, acidosis,loss of intracellular proteinand water, decreased intake,and frequent vomiting.

the bedside with blood obtained by fingerstick orfrom the intraducer of the intravenous catheter. Urineshould be obtained and assessed for ketones. Arterialblood gas analysis demonstrating pH should be avail-able from the laboratory in a short time. An EKG helpsidentify acute myocardial infarction and provides es-timates of serum potassium16 before the return of lab-oratory determinations.

Additional laboratory studies are initiated to de-termine severity of dehydration and acidosis, degreeof electrolyte imbalance, and precipitating factor.Blood should be sent for a complete blood cell count;levels of electrolytes, glucose, blood urea nitrogen,creatinine, serum osmolality, phosphate, calcium, andmagnesium; urinalysis with culture and sensitivity;blood cultures; β-human chorionic gonadotropin forwomen of childbearing age; and creatinine kinase MBbands. Radiologic examinations include chest radiog-raphy, although the presence of pneumonia or pleuraleffusion may not be apparent until the patient isrehydrated.

All laboratory data must be interpreted within thecontext of the individual patient. The degree of hy-perglycemia can vary considerably from 141 mg/dL to1140 mg/dL, with a median value of 416 mg/dL.8 Highglucose values are a reflection of marked dehydrationand subsequent low urinary output.12,14 Althoughpositive serum ketones are used as diagnostic criteriafor DKA, results should be interpreted with caution.Serum ketones are measured by nitroprusside agentsthat react to acetoacetate, not β-hydroxybutyrate. Atlow pH levels, β-hydroxybutyrate is the predominateketone. However, as treatment progresses, the level of

serum ketones will become elevated as the pH risesand acetoacetate becomes the predominate ketone.3

The anion gap is the key in determining the degree ofketoacidosis. Therefore, initial serum ketone valuesmay underestimate the level of ketosis and as suchare considered to be an optional indicator of DKA bysome persons.14,17 Because of the presence of ketones,DKA is associated with an increase in the anion gap(Figure 1). Subsequently, a reduction in the anion gapis a better indicator of treatment success than is a de-crease in serum ketones measured with the nitro-prusside reaction.3,5,14

Marked electrolyte abnormalities are present inpersons with DKA at initial presentation and through-out treatment. Serum sodium levels may be low, normal, or high despite dehydration. Sodium concen-tration is influenced greatly by the degree of hyper-glycemia, because glucose induces water movementfrom the intracellular to extracellular space and di-lutes the sodium concentration.12 The effect of the de-gree of hyperglycemia on the serum sodium value canbe corrected to assist in evaluating the water deficit(Figure 1).18 Alterations in mental status in a diabeticpatient are best evaluated by measurement of serumosmolality (Figure 1). A strong correlation exists be-tween increased serum osmolality and altered level ofconsciousness.19

Persons with DKA can have potassium levelsalong the continuum of dangerously low to danger-ously high. Severe total body potassium depletion inDKA results from osmotic diuresis, acidosis, loss of in-tracellular protein and water, decreased intake, andfrequent vomiting.13,20 The initial elevation of serumpotassium in persons with DKA results from (1) theshift of potassium out of the cells in exchange for


JOURNAL OF EMERGENCY NURSING/Miller

A. Calculation of effective serum osmolality

2 [Na+ + K+] +[glucose in mg/dL]

18The normal range of serum osmolality is 280 to 295 mOsm/kg.

B. Correction of serum sodium

Corrected Na+ = [Na+] + 1.6 × [glucose in mg/dL] – 100100

Assists in estimation of free water deficits.

C. Anion gap calculation[Na+] – [Cl– + HCO3

–]Normal anion gap 8 to 16 mEq/L.Falling anion gap indicates success of therapy.

Figure 1Calculations in the treatment of diabetic ketoacido-sis for advanced practice nurses. (Data from Fleck-man AM. Diabetic ketoacidosis. Endocrinol MetabClin North Am 1993;22:181-207.)

The initial elevation of serumpotassium in persons withDKA results from (1) the shiftof potassium out of the cellsin exchange for hydrogenions moving intracellularly,(2) insulin deficit and the lackof potassium movementintracellularly, and (3)diminished renal function.

December 1999 517


hydrogen ions moving intracellularly, (2) insulindeficit and the lack of potassium movement intracel-lularly, and (3) diminished renal function.21 An initiallow serum potassium level indicates profound totalbody depletion and requires aggressive manage-ment.22 Insulin will further lower extracellular potassi-um as it facilitates the movement of potassium intra-cellularly and may cause fatal hypokalemia.14

Likewise, an initial elevation in serum phosphoruslevels and normal or elevated serum magnesium levelsin DKA are caused by a transcellular shift because ofthe osmotic effect of hyperglycemia. The incidence ofhyperphosphatemia is common in patients with DKAprior to the initiation of therapy and can be anticipatedin almost all patients with DKA. However, serum phos-phate levels and serum magnesium levels will equili-brate with the initiation of fluids and insulin.23

Patients with DKA can often have a markedleukocytosis of up to 25,000/mm.3 This finding isbelieved to be more of a reflection of the degree ofketosis than the presence of infection.24 However, an

elevation of bands and a white blood cell countgreater than 25,000/mm3 suggests the presence of in-fection.3 Serum amylase is commonly elevated in pa-tients with DKA; in patients with suspected pancre-atitis, obtaining a serum lipase level is indicated.Blood urea nitrogen and creatinine levels are fre-quently elevated and suggest dehydration.14

TreatmentThroughout the literature, the therapeutic goals in thetreatment of DKA are similar. The goals are to (1) re-place fluid losses and improve tissue perfusion, (2) de-crease serum glucose, (3) reverse acidosis and keto-sis, (4) correct electrolyte imbalances, and (5) identifythe underlying precipitating factor.3,11

Initial treatment consists of conducting a prima-ry survey. A patent airway, adequate ventilations, andhemodynamic stability must be ensured before insti-tuting further treatment. Intubation is necessary for avomiting, comatose patient. Hypotension neces-sitates rapid fluid resuscitation with 0.9% saline

Table 2Sample protocol for management of diabetic ketoacidosis*

A. Initial diagnostic dataAt bedside: glucose, urine for glucose and ketonesLaboratory analysis: stat potassium, complete blood cell

count, serum acetone, electrolytes, glucose, blood ureanitrogen, creatinine, serum osmolality, phosphate, calci-um, magnesium, urinalysis, serum pregnancy (womenof childbearing age), cardiac enzymes

Blood cultures, urine for culture and sensitivity (possibleinfectious precipitating factor)

Amylase, lipase (abdominal pain)ElectrocardiogramChest radiograph

B. Fluids1. Normal saline solution at 500 to 1000 mL per hour for

4 hours in presence of renal patency2. One-half normal saline solution at 250 to 500 mL per

hour for 4 hours3. Dextrose 5% one-half normal saline solution when

serum glucose level is less than 250 mg/dL at 100 mLper hour

C. Insulin1. Regular insulin, 100 units in 100 mL normal saline solu-

tion; prime tubing with 50 mL of solution2. Start insulin drip at 0.1 units/kg/h3. If no improvement is seen in 2 to 4 hours, increase rate

to 0.2 to 0.3 units/kg/h4. Once serum glucose level is less than 250 mg/dL, de-

crease rate to 0.05 units/kg/h or half the actual insulinrate

*Sample protocol developed by author based on a review of research-based literature.

5. The insulin and dextrose infusions should be contin-ued for another 12 to 24 hours until ketones arecleared and blood pH is normalized

D. PotassiumIntravenous potassium

Serum potassium infusion rate (mEq/h)<3 403-4 304-5 20>5 0

Do not treat hyperkalemia in the absence of electrocar-diogram changes.

E. PhosphorusIf less than 1.0, give 0.25 mmol/L over 6 hours

F. BicarbonatepH 6.9 to 7.0 1 ampule in 250 mL normal saline

solution over 1 hourpH <6.9 2 ampules in 500 mL normal saline

solution over 1 hour

G. Monitoring1. When stable, vital signs and neurologic checks every

2 hours2. Intake and output every 2 hours3. Sodium, potassium, glucose, bicarbonate, chloride, pH

every 2 hours (may be venous)4. Consider pulmonary artery catheter in patients with

heart failure or renal failure and in elderly patients

solution. The use of a flow sheet allows for laboratoryvalues, intravenous infusion rates, and the patient’sstatus to be recorded in a logical sequence.3,5

Most important in the treatment of patients withDKA is fluid replacement, with normal saline solutionbeing the fluid of choice. Fluid resuscitation alone re-duces hyperglycemia and acidosis. Increased perfu-sion may transport insulin to previously unreached re-ceptor sites and also improves tissue oxygenation.5 Ina recent study of patients with moderate DKA (pH7.10) and no extreme fluid deficits, patients receivingfluids at 500 mL/h as opposed to 1000 mL/h for 4hours experienced a more rapid correction of serumbicarbonate levels.25

The administration of insulin should be initiatedas soon as the diagnosis of DKA is established. Theuse of constant intravenous infusion is the preferredmode of delivery, because erratic absorption of sub-cutaneous or intramuscular insulin may occur in vol-ume-depleted patients.26 For a continuous low-doseinsulin infusion, regular insulin is mixed with normalsaline solution to give the desired concentration. Aconcentration of solution that yields a 1:1 ratio hasbeen advocated because the rate on the infusionpump will equal the exact number of units of insulinper hour.27 Before administration of the infusion, 50 to100 mL of this solution should be run through the tub-ing because insulin absorbs to polyvinylchloride inboth the intravenous tubing and fluid bag.28

The current recommended initial dose of insulinis 0.1 units regular insulin per kilogram per hour.26 Ifthe glucose does not fall by 50 to 100 mg/dL, the ratecan be doubled. Once the glucose falls to 250 mg/dL,the insulin infusion should be halved and the intra-venous fluid changed to half normal saline solutionwith 5% glucose because the patient now requires

the carbohydrate.3 The insulin infusion should not bediscontinued until the anion gap has normalized, theserum bicarbonate level is greater than 15, and thepatient is ready to eat.14

The usual body deficit of potassium in a patientin DKA at the time of admission is usually 3 to 5 mEq/kg, but it may reach up to 10 mEq/kg.16 Potassiumreplacement should only be given after the results oflaboratory analysis are known. If the initial potassiumlevel is low or normal, replacement must begin imme-diately. Potassium is added to the second liter of 0.9%saline solution and after adequate urinary output isestablished. Table 2 summarizes a common guidelinefor potassium replacement. Potassium replacementshould be guided by hourly serum potassium analysisuntil it has stabilized.3

The use of bicarbonate in patients with DKA hasbeen controversial in the past. Present studies indi-cate that bicarbonate therapy is unnecessary whenthe blood pH is above 7.1.29 The most current recom-mendation is to administer bicarbonate for an arterialpH of less than 7.0. Guidelines are as follows: 44 mEq(1 ampule) of sodium bicarbonate if pH is 6.9 to 7.0 or88 mEq (2 ampules) of sodium bicarbonate if pH isless than 6.9. Bicarbonate should not be given intra-venous push except in patients with life-threateninghyperkalemia; it should be added to a hypotonic solu-tion and administered as an intravenous infusion.30

Similar to potassium depletion, phosphate deple-tion in DKA is severe. However, in patients with DKA,usually no clinical indication of phosphate depletionexists other than in laboratory analysis. If the phos-phate level before treatment is normal or low, it hasbeen recommended that the hypophosphatemia betreated.3,12 Phosphate replacement can be admin-istered as one third or one quarter of the potassiumreplacement.17

ComplicationsThe most frequent complications of therapy are hypo-glycemia, hypokalemia, and hypophosphatemia.12

The use of a flow sheet is the best way to avoid thesecomplications. Cerebral edema is a rare and fatal ia-trogenic complication of DKA.31 Other complicationsinclude adult respiratory distress syndrome, hyper-lipidemia, pancreatitis,3 hyperchloremic acidosis, andvascular thrombosis.12

SummaryED nurses should suspect DKA when patients haveflulike illnesses, dehydration, and confusion. If any de-gree of suspicion exists, a blood sugar level should beobtained, and one should proceed with intravenoushydration and insulin therapy.


JOURNAL OF EMERGENCY NURSING/Miller

An initial low serumpotassium level indicatesprofound total bodydepletion and requiresaggressive management.Insulin will further lowerextracellular potassium as itfacilitates the movement ofpotassium intracellularly andmay cause fatal hypokalemia.

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References

1. Report of the Expert Committee on the diagnosis andclassification of diabetes mellitus. Diabetes Care 1997;20:1183-98.2. Irwin J, Cohle SD. Sudden death due to diabetic ketoaci-dosis. Am J Forensic Med Pathol 1988;9:119-21.3. Fleckman A. Diabetic ketoacidosis. Endocrinol MetabClin North Am 1993;22:181-207.4. Guyton AC, Hall JE. Textbook of medical physiology. 9thed. Philadelphia: Saunders; 1996.5. Felts PW. Ketoacidosis. Med Clin North Am 1983;67:831-43.6. Rumbak MJ, Kitabchi AE. Diabetic ketoacidosis: etiology,pathophysiology, and treatment. Compr Ther 1991;17:46-9.7. Brandt KR, Miles JM. Relationship between severity ofhyperglycemia and metabolic acidosis in diabetic acidosis.Mayo Clin Proc 1988;63:1071-4.8. National Diabetes Data Group. Diabetes in America. 2nded. Bethesda (MD): National Institutes of Health; 1995.9. American Diabetes Association. Standards of medicalcare for patients with diabetes mellitus. Diabetes Care1995;18(Suppl 1):8-15.10. Mosey VC, Lee JK, Crawford R, Klatka MA, McAdams D,Phillips LS. Diabetes in urban African Americans: cessationof insulin therapy is the major precipitating cause of dia-betic ketoacidosis. Diabetes Care 1995;18:483-9.11. Schneyer CR, Kerkvliet GJ. The critically ill diabetic. In:Ayers SM, Genvik A, Holbrook PR, Shoemaker WC, editors.Textbook of critical care. Philadelphia: Saunders; 1995. p.1081-92.12. Foster DW, McGarry JD. The metabolic derangementsand treatment of diabetic ketoacidosis. N Engl J Med1983;309:159-69.13. Beielman PM. Severe diabetic ketoacidosis: 482 episodesin 257 patients; experience of three years. Diabetes 1971;20:490-500.14. Cefalu WT. Diabetic ketoacidosis. Crit Care Clin 1991;7:89-108.15. Harley JR. Preventing diabetic foot disease. Nurse Pract1993;18:37-42.16. Chava R. ECG in diabetic ketoacidosis. Arch Int Med1984;144:2379-80.

17. Brody GM. Diabetic ketoacidosis and hyperosmolar hyper-glycemic nonketotic coma. Top Emerg Med 1992;14:12-22.18. Katz MA. Hyperglycemia-induced hyponatremia-calcu-lation of expected serum sodium depression. N Engl J Med1973;289:843-6.19. Carroll P, Matz R. Uncontrolled diabetes mellitus inadults: experience in treating diabetic ketoacidosis and hy-perosmolar nonketotic coma with low-dose insulin and uni-form treatment regimen. Diabetes Care 1983;6:579-85.20. Van Gaal LF, De Leeuw IH, Bekaert JL. Diabetic keto-acidosis-induced hyperkalemia. Intensive Care Med 1985;12:416-8.21. Adrogue HJ, Lederer ED, Suki WN, Eknoyan. Determi-nants of plasma potassium in diabetic ketoacidosis. Medi-cine 1986;65:163-71.22. Beigelman PM. Potassium in severe diabetic ketoacido-sis. Am J Med 1973;54:419-20.23. Kebler R, McDonald FD, Cadnapaphornchai P. Dynamicchanges in serum phosphorus levels in diabetic ketoacido-sis. Am J Med 1985;79:571-6.24. Alberti KGM, Hockaday TDR. Diabetic coma: a reap-praisal after five years. Clin Endocrinol Metab 1977;6:421-8.25. Adogue HJ, Barrero J, Eknoyan G. Salutary effects ofmodest fluid replacement in the treatment of adults with di-abetic ketoacidosis. JAMA 1989;262:2108-13.26. Fain JA. Insulin administration in diabetic ketoacidosis.Focus Crit Care 1986;13:47-9.27. Jones TL. From diabetic ketoacidosis to hyperglycemichyperosmolar nonketotic syndrome. Crit Care Nurs ClinNorth Am 1994;6:703-21.28. Petty C, Cunningham NL. Insulin absorption by glass in-fusion bottles, polyvinylchloride infusion containers, and in-travenous tubing. Anesthesiology 1974;40:400-4.29. Okuda Y, Adrogue HJ, Field JB, Nohara H, Yamashita K.Counterproductive effects of sodium bicarbonate in diabet-ic ketoacidosis. J Clin Endocrinol Metab 1996;81:314-20.30. Androgue HJ, Madias NE. Medical progress: manage-ment of life-threatening acid-base disorders. N Engl J Med1998;338:26-34.31. Rosenbloom AL. Intracerebral crisis during treatment ofdiabetic ketoacidosis. Diabetes Care 1990;13:22-33.

management of diabetic ketoacidosis

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