Diabetic ketoacidosis
Mosul Medical CollegeDepartment of Medicine
Presented by:
Dr. Salam Fareed8/21/2016
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INTRODUCTIONDiabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes.
This condition is a complex disordered metabolic
state characterized by:
hyperglycemia: blood glucose level > 200 mg/ dl
Ketoacidosis: ketonuria > ++ on standard urine sample.
Metabolic acidosis: PH < 7.3, s. bicarbonate < 15
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Pathophysiology
DKA typically occurs in the setting of hyperglycemia with relative or absolute insulin deficiency and an increase in counterregulatory hormones.
Sufficient amounts of insulin are not present to suppress lipolysis and oxidation of free fatty acids, which results in ketone body production and subsequent metabolic acidosis.
DKA occurs more frequently with type 1 diabetes, although 10% to 30% of cases occur in patients with type 2 diabetes.
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Predisposing FactorsSeveral risk factors can precipitate the development of extreme hyperglycemia:
infection.
intentional or inadvertent insulin therapy.
myocardial infarction.
Stress.
trauma.
confounding medications, such as glucocorticoids or atypical antipsychotic agents.
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Clinical PresentationThe most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA:
Malaise, generalized weakness, and fatigability
Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia
Rapid weight loss in patients newly diagnosed with type 1 diabetes
History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump
Decreased perspiration
Altered consciousness (eg, mild disorientation, confusion)
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Signs and symptoms of DKA associated with possible intercurrent infection are as follows:
Fever
CoughingChills
Chest pain
Dyspnea
Arthralgia
Urinary symptoms
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On examinationIll appearance
Dry skin
Labored respiration
Dry mucous membranes
Decreased skin turgor
Decreased reflexes
Characteristic acetone (ketotic) breath odor
Tachycardia
Hypotension
Tachypnea
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Investigations:
Serum glucose levels
Serum electrolyte levelsAmylase and lipase levels
Urine dipstick
Ketone levels
ABG measurements
CBC count
BUN and creatinine levels
C-RP
Urine and blood cultures if intercurrent infection is suspected
ECG
Chest radiography: to rule out pulmonary infection
Head CT scanning: to detect early cerebral edema.
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Management:Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable.
Plan for therapy:
When treating patients with DKA, the following points must be considered and closely monitored:
Correction of fluid loss with intravenous fluids
Correction of hyperglycemia with insulin
Correction of electrolyte disturbances, particularly potassium loss
Correction of acid-base balance
Treatment of concurrent infection, if present
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Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows:
Blood tests for glucose every 1-2 h until patient is stable, then every 4-6 h
Serum electrolyte determinations every 1-2 h until patient is stable, then every 4-6 hInitial blood urea
Initial arterial blood gas (ABG) measurements, followed with bicarbonate as necessary
Example how to arrange a chart to follow a DKA patient
S. kRBS
Output
Input fluid
Insulin
BP
Time
6.2
410
Nil
2 L/NS
20 units IM
80/50
3:00 PM
4:00 PM
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Insulin Therapy:Using soluble (Short acting) insulin administered either:
I.V infusion(prefered method):
Bolus: 0.1 unit/ kg. I.V direct
then maintain contiueous iv infusion of 0.1 unit/ kg./ hr. using syringe pump.
I.M:
Bolus: 10-20 units
Followed by 5 units hourly.
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Target blood sugar:
Falling 55-110 mg/ dl per hr.
(3-6 mmol/l)
Rapid decline → cerebral edema
Failure to reach the target → require reassessment of insulin therapy.
Shift to subcutaneous insulin regimen when the patient vomiting stopped and become biochemically stable.
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Fluid Replacement:
Average of 6 litres fluid deficit exist
3 L are extracellular replaced by 0.9% isotonic saline.
3 L are intracellular replaced by dextrose
Timing and amount as following:
1st hr: using normal (isotonic) salinesystolic BP > 90 mmHg → 1 L
systolic BP < 90 mmHg → 2 L
Set 2 wide bore IV line initially
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Then as :1 L OVER 2 hrs
1 L OVER 2 hrs
1 L EVERY 6 hrs
Shift to 10% dextrose fluid whenever blood sugar level become < 250 mg/dl (14mmol/l).
Note: be cautious with elderly, pregnant, those with heart or renal failure.
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Potassium Replacememt
According to serum potassium level as:
> 5.5 mmol/l → non to be given
3.5 – 5.5 (mmol/l) → 40 meq/l
be cautious in replacing K usually hyperkalemia occurs initially due to prerenal failure secondary to dehydration for that reason K is not recommended to be given in the first hour of therapy.
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OtherAcidosis: is usually corrected with the time by adequate fluid and insulin replacement. Bicarbonate therapy is not recommended as it can induce cerebral edema
Infection: should be treated by antibiotcs accordingly
Brain edema: is the leading cause of death in DKA, it can exist in spite of metabolic stablisation. It should be treated by mannitol solution 20%
(7 ml/ kg.)
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Case ScenarioA 20-year-old woman is evaluated in the emergency department for polyuria, polydipsia, polyphagia, and an unintentional 5.4-kg (11.9-lb) weight loss over the past month. She has had increasing lethargy over the last 24 hours. Her medical history and family history are unremarkable. She takes no medications.
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On physical examination,
temperature is 37.5 °C , blood pressure is 98/52 mm Hg, pulse rate is 120/min, and respiration rate is 30/min. BMI is 17.
She is lethargic with dry mucous membranes, tachypnea, and tachycardia. Chest auscultation is clear. Abdominal examination shows diffuse mild tenderness and normal bowel sounds. There is no rebound tenderness or guarding with palpation.
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Laboratory studies:
Hemoglobin= 17 g/dL (170 g/L)Leukocyte count= 14,200/µL (14.2 × 109/L)
Blood gases, arterial::
pH= 7.25
PCO2= 21 mm Hg
Creatinine= 1.3 mg/dL
Electrolytes
Sodium= 130 mEq/L
Potassium= 3.0 mEq/L
Chloride= 99 mEq/L
Bicarbonate= 9 mEq/L
Glucose= 620 mg/dL (34.4 mmol/L)
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An electrocardiogram shows sinus tachycardia 120/min.Chest radiograph is normal.
What is the most appropriate management?