DIABETIC KETOACIDOSIS GUIDELINES

DIABETIC KETOACIDOSIS–
MANAGEMENT EMERGENCY
MEDICINE
.
BY DR DARAYUS P. GADER

Diabetes Ketoacidosis (DKA)Definition
All the major definitions by various authorities are rather subjective but
emphasize on the following points :
 1 Acute life threatening metabolic complication of diabetes
 2 Characterized by absolute insulin deficiency and hyperglycemia
A Life-threatening medical emergency with a Mortality rate:
 Under 5% in individuals under 40 years of age
 With a serious prognosis in older adults, who have mortality rates over
20%.
Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JA, Courtney CH, Hilton L, Dyer
PH, Hamersley MS, Joint British Diabetes Societies. Joint British Diabetes Societies
guideline for the management of diabetic ketoacidosis. Diabetic Medicine. 2011

Diabetic Ketoacidosis: Pathophysiology
Unchecked gluconeogenesis → Hyperglycemia
Osmotic diuresis → Dehydration
Unchecked ketogenesis → Ketosis
Dissociation of ketone bodies into
hydrogen ion and anions
→
Anion-gap metabolic
acidosis
Often a precipitating event is identified
(infection, lack of insulin administration)

Symptoms and Signs
 DKA is usually preceded by a day or more of polyuria
and polydipsia associated with marked nausea, vomiting's
 If untreated, mental stupor ensues that can progress to coma.
(Frank coma only occurs in about 10% of patients).
 On physical examination:
1) Evidence of dehydration with rapid deep breathing and a “fruity” breath odor
of acetone strongly suggests the diagnosis.
2) Hypotension with tachycardia indicates profound fluid and electrolyte
depletion, and mild hypothermia is usually present.
3) Abdominal pain and even tenderness may be present in the absence of
abdominal disease. Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JA, Courtney CH, Hilton L, Dyer

Clinical Presentation of
Diabetic Ketoacidosis
History
• Thirst
• Polyuria
• Abdominal pain
• Nausea and/or vomiting
• Profound weakness
Physical Exam
• Kussmaul respirations
• Fruity breath
• Relative hypothermia
• Tachycardia
• Supine hypotension, orthostatic drop
of blood pressure
• Dry mucous membranes
• Poor skin turgor
Handelsman Y, et al. Endocr Pract. 2016;22:753-762.
Patients with any form of diabetes
who present with abdominal pain,
nausea, fatigue, and/or dyspnea
should be evaluated for DKA.

Essentials of Diagnosis
 RBS > 250 mg/dl
 Serum ketone positive
 Acidosis with Ph less than 7.3
 Serum bicarbonate less than 15 mEq/L

Clinical Classification of DKA
(Kitabchi et al – Diabetes care )
Mild DKA Moderate DKA Severe DKA
Plasma glucose More than 250 mg /dl in all grades
ph 7.25 to 7.3 7 to 7.24 Less than 7
Bicarbonate 15 -18 10 to 15 Less than 10
Anion Gap > 10 >12 >12
Mental Status Alert Altert & or drowsy Stuper & or coma

Management
Essential therapy (in all patients of DKA )
 IV fluids
 Supportive Care +/- ICU admission
 K treatment
 IV Insulin once K is more than / equal to 3.3 mEq/l
Adjuvant Treatment (in select cases )
 Vasopressors
 Bicarbonate
 Phosphate

Initial Laboratory Evaluation of Hyperglycemic
Emergencies
• Comprehensive metabolic profile
• Serum osmolality
• Serum and urine ketones
• Arterial blood gases
• CBC
• Urinalysis
• ECG

Sodium Correction in Hyperglycemia
“Classic” 1.6 mEq/L Na⁺ decrease for every 100 mg/dL
Glucose
Hillier Method 2.4 mEq/L Na⁺ decrease for every 100 mg/dL
Glucose when sugars >400mg/dl
Serum sodium is generally reduced due to loss of sodium ions (7–
10 mEq/kg) by polyuria and vomiting and because severe
hyperglycemia shifts intracellular water into the interstitial
compartment.
Hypertriglyceridemia should be considered if the corrected
sodium is very low.
Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JA, Courtney CH, Hilton L, Dyer PH, Hamersley MS, Joint British Diabetes Societies. Joint British
Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabetic Medicine. 2011 May;28(5):508-15.

Serum Osmolality
2Na⁺ + Glucose + BUN
18 2.8
Normal 285-
295
Serum osmolality can be directly measured by standard tests
of freezing point depression or can be estimated by calculating
the molarity:
Central nervous system depression or coma occurs when the
effective serum osmolality exceeds 320– 330 mOsm/L.
Coma in a diabetic patient with a lower osmolality should prompt a
search for cause of coma other than hyperosmolality

Potassium Balance in DKA
• Potassium is dominantly intracellular
• Urinary losses occur during evolution of DKA (due to glycosuria)
• Total body potassium stores are greatly reduced in any patient
with DKA
• Potassium moves from inside the cell to the extracellular space
(plasma)
– During insulin deficiency
– In presence of high blood glucose
– As cells buffer hydrogen ions
• Blood levels of potassium prior to treatment are usually high but
may drop precipitously during therapy

ABG vs VBG
 The difference between venous and arterial
pH is 0.02 to 0.15 pH units and venous and
arterial bicarbonate is 1.88 mEq/L. These
small differences will not affect either the
diagnosis or the management of DKA, and
there is no need to collect arterial blood for
measuring the acid-base status.

IV fluids
(Initial fluid & maintenance fluid)
 Initial Fluid (first one Hour )
Isotonic saline (0.9 NaCl ) is the initial fluid of choice in all
cases irrespective of volume status and sodium status
Goal : Restoration of Tissue Perfusion
Dose 15 to 20 ml / Kg in 1 hour
This translates to 1 - 1.5 l in first one hour in normal
adults .

IV fluid- Maintenance fluid(after first 1 hour)
 If Severely volume Depleted :
Signs
Orthostatic/ Supine hypotension
Dry mucus membrane
Poor skin turgor
Recommendation is to continue fluid resuscitation
with frequent monitoring and rate adjustments as
required until the patient becomes stable
Fluid of choice : 0.9 % NS

Maintenance fluid(after 1 hour)- if not severely
volume depleted.
 For Moderate to mildly hypovolumic patients :After first 1 hour fluid
resuscitation with NS measure Corrected Serum sodium
 Recommended Rate of infusion : 250 to 500 ml /hr
 Goal :To replenish half of fluid deficit gradually in 12 to 24hrs
 Once RBS is below 250mg /dl shift to
Fluids should be changed to a 5% glucose-containing solution to maintain
serum glucose in the range of 250–300 mg/dL. Preventing hypoglycemia
and reduce the chance of cerebral edema,due to rapid correction
Corrected Na = Measured Na + 0.016 x
(glucose -100)
If Hyponatremic If Normo/Hyperntremic
0.9 % NS 0.45 NaCl

ICU admission /Maintenance
 ICU admission criteria:
Hemodynamic instability
Respiratory Insufficiency
Altered mental status
Severe Acidosis
Maintenance
 Regular NG suction (Frequent Ileus and aspiration)
 CVP catheter should be inserted to evaluate the degree of hypovolemia and to monitor fluid
administration in patients with heart or kidney failure.
 Hourly Plasma Glucose
 2 to 3 hourly : Electrolytes and pH
 Bedside glucose meters should be used to titrate the insulin therapy.
Till all criteria of resolution is met :
RBS <200 , Venus Ph>7.3, HCO3 >18, Anion Gap <10
Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JA, Courtney CH, Hilton L, Dyer PH, Hamersley MS, Joint British Diabetes Societies. Joint British
Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabetic Medicine. 2011 May;28(5):508-15.

Potassium Therapy
 Serum K may be high, low or normal at various stages of DKA but
DKA is always a state of Total K depletion irrespective of serum K
levels (due to osmotic Diuresis)
 If the patient is not uremic or has an adequate urinary output, Start
K therapy @ 10-30 mEq /hr infused in IV FLUID as soon as
initial K levels are available (hold if K >5.3) to maintain K between
3.3 and 5.3
 Insulin should be stopped if K falls below 3.3
 ECG can be of help in monitoring the patient’s potassium status

Insulin Therapy
 Immediately after initiation of fluid replacement:
INSULIN CAN BE GIVEN INTRAVENOUSLY
Regular insulin is gien in a loading dose of 0.1 unit/kg as a bolus to prime the tissue insulin
receptor
 Dose IV Regular Insulin @ 0.1 unit /kg/hr >>if RBS doesn’t fall by 10% in first hour a repeat
loading dose (0.1 or 0.14 unit/kg) is recommended. Once RBS falls below 250 half the
current dose and continue IV insulin till all the criteria of resolution are met :
RBS <200 , Venus Ph>7.3, HCO3 >18, Anion Gap <10
INSULIN CAN BE GIVEN INTRAMUSCULARLY.
An initial 0.15 unit/kg of regular insulin is given intravenously, and same dose is given IM.
THEN, regular insulin is given IM hourly at a dose of 0.1 unit/kg until the blood glucose falls to around 250
mg/dL, when the insulin can be given subcutaneously.
NOTE: Patients who normally take insulin glargine or insulin detemir can be given their usual maintenance
doses during initial treatment of their DKA. The continuation of their subcutaneous basal insulins means that
lower doses of intravenous insulin will be needed, and there will be a smoother transition from intravenous
insulin infusion to the subcutaneous regimen.

Subcutaneous Insulin is Recommended over IV Insulin in DKA by some authorities if :
 Once the DKA is controlled, patient is awake and able to eat, subcutaneous insulin therapy can be initiated.
 Patients with type 1 DM may have persistent significant tissue insulin resistance
and may require a total daily insulin dose of approximately 0.6 unit/kg.
 Amount of insulin required in 8 hours can also be helpful in estimating the initial
insulin doses. Half the total daily dose can be given as a long-acting basal insulin
and the other half as short-acting insulin premeals.
 Patients should receive subcutaneous basal insulin and rapid-acting insulin analog
with the first meal and the insulin infusion discontinued an hour later.
 The overlap of the subcutaneous insulin action and insulin infusion is necessary to
prevent relapse of the DKA. In patients with preexisting diabetes, giving their basal
insulin by subcutaneous injection at initiation of treatment simplifies the transition
from intravenous to subcutaneous regimen.

Adjuvant therapy (0nly in Special cases) As per ADA guidelines
2013
Therapy Indication and Dose
Bicarbona
te
(bicarbonate
decreases K)
ph < 7or Bicarbonate < 5
Dose
ph 6.9 to 7 : 50 mmol NaHO3( (1 amp) in 200 ml sterile water with
10mEq KCL Hourly till ph is more than 7
Ph<6.9 : 100mmol NaHO3(2 amp) in 400 ml sterile water with 20
mEq KCL @ 200ml/hr till ph is more than 7
Phosphate
(decreases with
Insulin therapy)
ONLY if Serum phosphate < 1mg/dl
Dose
Potassium Phosphate 20 -30 mEq /L in IV fluid
Vasopress
ors
In hemodynamic instability (hypotension)
First stat Dopamine 5-10 mcg/kg/min adjust with BP
If not effective in moderate does then start Noradrenalin
Start with 0.5 mcg/kg/min titrate to maintain MAP 60

• Hypoglycemia
• HypokalemiaCommon
• Thromboembolic
events Standard lowdose
Heparin prophylaxys
resonable .No evidance to
support full anticoagulation
Sometimes
• Nonaniongap Hyperchloremic
Acidosis
Common in pregnant women
• Cerebral edema
In children ,prevention : careful fluids
and maintain RBS 150-200
• ARDS
Rar
e
Complications

Be Aware of Conditions that may
make DKA Diagnosis Difficult
2018 Diabetes Canada CPG – Chapter 15. Hyperglycemic Emergencies in Adults
Conditions that 
bicarbonate (eg.
vomiting)
Pregnancy SGLT2
inhibitor
Significant
osmotic
diuresis
β-hydroxy
butyrate
Mixed acid-
base so pH not
as low
Normal or mildly 
glucose (euglycemic
DKA)
Loss of keto
anions
Normal
anion gap
Negative
serum
ketones
Order serum
β-hydroxy
butyrate
DKA, diabetic ketoacidosis
. Individuals treated with SGLT2
inhibitors with symptoms of
DKA should be assessed for
this condition even if BG is
not elevated

DIABETIC KETOACIDOSIS GUIDELINES

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