DIABETIC KETOACIDOSIS

Precipitating Factors

 Failure to take insulin  Medical Stress

 Failure to increase insulin  Counterregulatory hormones
 Illness/Infection  Oppose insulin
 Pneumonia  Stimulate glucagon release
 MI  Hypovolmemia
 Stroke  Increases glucagon and
 Acute stress catecholamines
 Trauma  Decreased renal blood flow

 Emotional  Decreases glucagon

degradation by the kidney
DKA is defined as the presence of all three of the

following:

(i) Hyperglycemia (glucose >250 mg/dL)

(ii) Ketosis, Urine ketones and serum ketones
(iii) Acidemia (pH <7.3). Anion gap acidosis
(Na + K) – (Cl + Bicarb) >12
Bicarbonate <15 mEq/L
pH <7.3
(iv) Hyperosmolarity
 Signs and Symptoms of DKA

 Polyuria, polydipsia  Fruity breath

 Enuresis  Acetone
 Dehydration  Kussmaul breathing
 Tachycardia
 Mental status changes
 Orthostasis
 Combative
 Abdominal pain  Drunk
 Nausea  Coma
 Vomiting
SYMPTOMS PHYSICAL FINDINGS

PHYSICAL FINDINGS
 Tachycardia

 Dehydration/hypotension

 Tachypnea/kussmaul
respirations/respiratory
distress
 Fruity odour in breath.

Abdominal tenderness(may
resemble acute pancreatitis or
surgical abdomen)
 Lethargy/obtundation/cerebra
l edema/possibly coma.
 ROLE OF INSULIN
 Required for transport of glucose into:
Muscle
Adipose
Liver
 Inhibits lipolysis

 Absence of insulin
Glucose accumulates in the blood.
Uses amino acids for gluconeogenesis
Converts fatty acids into ketone bodies :
Acetone, Acetoacetate, β-hydroxybutyrate.
 LABORATORY VALUES IN DKA AND HHS
DKA HHS

Glucose,mg/dl 250-600 600-1200

Sodium meq/L 125-135 135-145

Potassium Normal to↑ Normal

Osmolality mosm/kg 300-320 330-380

Plasma ketones ++++ +/-

Serum bicarbonate <15meq/L Normal to slightly ↓

Arterial pH 6.8-7.3 >7.3

Arterial pCO2 20-30 Normal

Anion gap ↑ Normal to slightly↑

Hyperosmolar Hyperglycemic Nonketotic Syndrome
Presentation

 Extreme dehydration
 Supine or orthostatic hypotension
 Confusion coma
 Neurological findings
 Seizures
 Transient hemiparesis
 Hyperreflexia
 Generalized areflexia
Hyperosmolar Hyperglycemic Nonketotic
Syndrome Presentation

 Glucose >600 mg/dl

 Sodium
 Normal, elevated or low
 Potassium
 Normal or elevated
 Bicarbonate >15 mEq/L
 Osmolality >320 mOsm/L
Hyperosmolar Hyperglycemic Nonketotic
Syndrome Presentation

 Fluid repletion
 NS 2-3 liters rapidly
 Total deficit = 10 liters
 Replete ½ in first 6 hours

 Insulin
 Make sure perfusion is adequate
 Insulin drip 0.1U/kg/hr
 Treat underlying precipitating illness
TREATMENT OF DKA
Initial hospital management

Replace fluid and electrolytes

IV Insulin therapy
Watch for complications
Treat causes

Once resolved
Convert to home insulin regimen
Prevent recurrence
 DIAGNOSIS LAB INVESTIGATIONS

❑ Complete blood count

❑ Serum ketones/ Urine ketones and sugar

❑ Calculate serum osmolality and anion gap

❑ Urinalysis and urine culture

❑ Consider blood culture

❑ Consider chest radiograph

❑ Acid-base assessment
  GUIDELINES FOR MANAGEMENT OF DKA

 ON ADMISSION-
1. INITIAL TREATMENT- CBC, BLOOD GLUCOSE, ELECTROLYTES, CREATININE, UNINE KETONES, PLASMA
KETONES AND ABG.
2. SECURE 2 IV LINES,
 LINE-1 - GIVE 10 UNITS OF HUMAN REGULAR INSULIN, IV BOLUS.
 50 ML NS + 50 UNITS OF HAI—INFUSE AS PER ICU INSULIN PROTOCOL.
 LINE-2 – IV FLUIDS REPLACEMENT
 USUALLY NS + POTASSIUM REPLACEMENT @ 200ML PER HOUR (RATE OF INFUSION TO BE LESS
IF EF IS LOW)

 0-4 HOURS- MONITOR ABG AND POTASSIUM 2 HOURLY

 LINE 1- CONTINUES INSULIJN INFUSION.

 LINE 2 – CONTINUE IV FLUID REPLACEMENT ( CAN SHIFT TO HALF NS IN CASE OF HYPERNATREMIA)

 POTASSIUM REPLACEMENT :

 CHANGE TO 5 % DEXTROSE WHEN BLOOD GLUCOSE DROPS TO 200 MG/DL.

 START KCl, 40 mEq /L OF IV FLUIDS IF SERUM POTASSIUM IS LESS THAN 3.5 MeQ/ L OR IF URINE OUTPUT IS GOOD AND BLOOD
GLUCOSE IS DROPPING,

 4-24 HOURS
 MONITOR ABG AND POTASSIUM 4 HOURLY

 LINE 1 – ADJUST INSULIN INFUSION RATE AS PER ICU PROTOCOL . TO MAINTAIN BLOOD SUGAR BETWEEN 140-180

 LINE 2- NS/5% DEXTROSE IV TO CORRECT HALF OF CALCULATED FLUID REQUIREMENT- KCL 40 mEq/ L OF IV FLUIDS.

 24-48 HOURS

 REPEAT CBC, ELECTROLYTES, CREATININE ONCE A DAY

 LINE 1 – IV INSULIN INFUSION AT AS PER ICU2 PROTOCOL.

LINE 2-. REDUCE IV FLUIDS WHEN ABLE TO RETAIN FLUIDS ORALLY.
AFTER 48 HOURS SHIFT TO ORAL FEEDS- START MULTIPLE DOSE INSULIN REQIMEN
SUBCUT AS PER SPLIT DOSE GIVEN BY THE DIABETOLOGIST.
POTASSIUM THERAPY IN DKA.
1.DO SERUM POTASSIUM INITIALLY EVERY 2 HOUR FOR 4 HOURS, EVERY 4 HOURS
FOR NEXT 12 HOURS AND 12 HOURLY THEREAFTER.
2.INITIALLY SERUM K IS LOW, NORMAL OR HIGH
3.IF INITIALLY K IS LOW GIVE 40 mEq KCL / L OF FLUIDS. MAKE SURE URINE OUTPUT IS
ADEQUATE MORE THAN 50 ML/HOUR
4.K WILL DROP PRECIPITOUSLY AFTER 2-4 HOURS OF TREATMENT AND SUCESSFUL
LOWERING OF BLOOD GLUCOSE.
5.CONTINUE 40 mEq KCL/L OF IV FLUIDS ADMINISTERED.
BICARBONATE THERAPY IN DKA
1.GIVE BICARBONATE ONLY IF Ph IS LESS THAN 7.2.
2.GIVE HALF OF THE CALCULATED DOSE.
3. GIVE SODIUM BI CARBONATE DILUTED IN NS OR 5% DEXTROSE IN RATIO OF 1:4. (BI-
CARB 1 PART, SALINE 4 PARTS) OVER 1 HOUR.
 KETONE MONITORING

 URINE KETONE TO BE MEASURED 4 HOURLY INITIALLY FOR 12 HOURS FOLLOWED BY 6

HOURLY FOR 12 HOURS FOLLOWED BY 8 HOURLY TILL DISAPPEARANCE.

 OTHER IMPORTANT POINTS TO REMEMBER

1. TREAT THE UNDERLYING CAUSE OF DKA ( ACUTE MI , INFECTION, SEPSIS, STROKE, ETC)
2. URINE KETONES WILL DECREASE INITIALLY BUT REPAPPEAR THERE AFTER, BEFORE FINAL
RESOLUTION ( BECAUSE OF CONVERSION
 OF ACETOACETATE TO BETA HYDROXYBUTYRATE.
 3. AVOID NaHCO3 THERAPY UNTILL PH IS LESS THAN 7.2 ( TO AVOID CEREBRAL
OEDEMA)
Complications of DKA
 Infection  Cerebral Edema
 Precipitates DKA  First 24 hours
 Fever  Mental status changes
 Leukocytosis can be secondary  Tx: Mannitol
to acidosis
 May require intubation with
 Shock hyperventilation
 If not improving with fluids
r/o MI
 Vascular thrombosis
 Severe dehydration
 Cerebral vessels
 Occurs hours to days after DKA

 Pulmonary Edema
 Result of aggressive fluid
resuscitation
Prevention of DKA
 Never omit insulin
 Cut long acting in half
 Prevent dehydration and
hypoglycemia
 Monitor blood sugars
frequently
 Monitor for ketosis
 Provide supplemental
fast acting insulin
 Treat underlying triggers
 Maintain contact with
medical team
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