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Diabetic Ketoacidosis
Diabetic Ketoacidosis
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An anion gap acidosis due to severe insulin
deficiency and excess of counterregulatory
hormones
Insulin Deficiency
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Insulin is required for efficient transport of glucose into muscle,
adipose, and liver cells
Proper utilization of glucose within liver cells is also dependent
on insulin
In the absence of insulin glucose cannot be effectively
transported into cells and it accumulates in the blood
The liver begins to manufacture glucose from amino acids
(gluconeogenesis)
Additional glucose is thus secreted into the bloodstream
Insulin Deficiency: Effects on the
Kidney
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When the degree of hyperglycemia exceeds the
kidney’s capacity for tubular reabsorption glucose
appears in the urine
Osmotic diuresis ensues and the patient develops
polyuria
Severe dehydration may result
Insulin Deficiency: Effects on
Lipolysis
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Under normal circumstances insulin inhibits lipolysis
In the absense of insulin adipose cells degrade their
stores of triglycerides into fatty acids
Fatty acids are converted by the liver into ketone
bodies (acetoacetate and b-hydroxybutyrate)
A metabolic acidosis develops
Actions of Glucagon
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Glucagon when unopposed by normal insulin is
responsible for the hepatic components of diabetic
decompensation
Increased glycogenolysis
Increased gluconeogenesis
Increased ketogenesis
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Insulin deficiency causes augmented delivery to the
liver of substrates for glucose and ketone
production
Glucagon is the switch that activates the hepatic
production machinery for glucose and ketones
Precipitating Factors in DKA
 Failure to take insulin
 Failure to increase insulin during acute illness, infection
 Other intercurrent illness such as myocardial infarction,
pancreatitis, stroke, trauma or severe emotional stress
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The counterregulatory hormones released during medical
stress oppose insulin and stimulate glucagon release
Hypovolemia increases the secretion of glucagon,
catecholamines by decreasing renal blood flow and this further
reduces glucagon degradation by the kidney
Signs and Symptoms of DKA
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Polyuria and polydipsia
Kussmaul hyperventiation
Vomiting and abdominal pain
An acetone odor to breath
Dehydration
Stupor and coma
Initial Lab Findings
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Hyperglycemia
Anion gap acidosis
Positive urine and serum ketones
Hyperosmolarity
Differential Diagnosis
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Anion gap acidosis: (Na + K) - (Cl +Bicarb) >16
Alcoholic ketoacidosis
Lactic acidosis
Renal failure
Ethylene glycol or methyl alcohol poisoning
Starvation in late pregnancy or lactation (rare)
Initial Lab Findings in DKA
Glucose
475
Sodium
132
Potassium
4.8
Bicarbonate
<10
BUN
25
Acetoacetate
4.8
B-hydroxybutyrate
13.7
Free Fatty acids
2.1
Lactate
4.6
Osmolarity
310
Treatment of DKA
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Replacement of fluid and electrolytes
Insulin therapy
Glucose administration
Replacement of Fluid and Electrolytes
 Restores perfusion of tissues to normal and lowers levels of
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counterregulatory hormones
Average fluid deficit is 3-5 liters
1-2 liters of normal saline administered rapidly in the first 2
hours
If hypernatremia develops 1/2 NS can be substituted
Hyperkalemia usually present on admission recedes when
insulin action begins; potassium replacement is then required
Phosphate deficit becomes apparent after insulin administration
but is usually clinically silent
Bicarbonate is usually not given unless pH is below 7 or bicarb
less than 5 mmol/l
Insulin Therapy
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IV bolus of 10-20 units regular insulin
Follow by hourly insulin infusion
Insulin should be given intravenously until the urine
is free of ketones
Glucose Administration
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Once insulin has restored glucose uptake and
suppressed hyperglucagonemia, hypoglycemia will
occur unless exogenous glucose is provided
Glucose levels always fall before ketone levels
decrease therefore exogenous glucose must be
provided to cover the insulin needed to reverse
ketosis
Glucose is usually started when plasma glucose
reaches 250-300 mg/dl
Insulin-Glucose Infusion for DKA
Blood glucose
Insulin infusion
D5W infusion
<70
0.5 units per hour
150 cc/hour
70-100
1.0
125
101-150
2.0
100
151-200
3.0
100
201-250
4.0
75
251-300
6.0
50
301-350
8.0
0
351-400
10.0
0
401-450
12.0
0
451-500
15.0
0
>500
20.0
0
Following Resolution of DKA
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Most patients require 0.5-0.6 units of insulin per kg body
weight
1/2 - 2/3 requirement is given as long-acting insulin - NPH,
Lente, Ultralente or Lantus
1/3-1/2 is given as short-acting meal time insulin - regular,
Humalog or Novolog
Give both long and short acting insulin subcutaneously about
2 hours prior to tapering insulin infusion
Patient education key to avoiding future episodes
Clinical Errors
 Administration of hypertonic glucose solutions at the outset
 Giving insulin in patients with severe volume deficit without
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sufficient fluids can cause fluid shift into cells can precipitate
shock
Premature administration of potassium before insulin has
begun to act can cause fatal hyperkalemia
Failure to administer potassium after insulin has begun to act
can lead to fatal hypokalemia
Recurrent ketoacidosis caused by failure to maintain IV insulin
and glucose until ketones have cleared or by failure to
administer subcutaneous insulin before stopping IV infusion
Hypoglycemia caused by insufficient glucose administration
DKA and Pregnancy
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Pregnancy is a state of relative insulin resistance marked by
enhanced lipolysis and ketogenesis
High serum ketones may be teratogenic
DKA represents a substantial risk for the fetal compromise
Complications of DKA
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Death is usually due to precipitating or complicating
illness such as MI, pancreatitis or sepsis
Infection
Vascular thrombosis
Cerebral edema
Respiratory distress syndrome
Hyperosmolar Nonketotic Coma
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Extreme hyperglycemia and dehydration which results when
the ability to excrete glucose as rapidly as it enters the
extracellular space
Maximum hepatic glucose output results in a plateau of plasma
glucose no higher than 300-500 mg/dl
When sum of glucose excretion plus metabolism is less than
the rate at which glucose enters extracellular space
Hyperosmolar Nonketotic Coma
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Older patients with intercurrent illness with impaired ability to
ingest fluids
When urine volume falls the ability to excrete glucose falls
As glucose rises CNS dysfunction occurs and water intake is
additionally impaired
The result is extreme hyperglycemia and hyperosmolarity with
high mortality
Either enough insulin is present to prevent ketosis or the
extreme hyperglycemia inhibits lipolysis
Admission Findings: Hyperosmolar
Nonketotic Coma
 Extreme dehydration
 Supine or orthostatic hypotension
 Confusion to coma
 Seizures or other neurological findings
Admission Findings: Hyperosmolar
Nonketotic Coma
 Average glucose 1200
 Na 144
K5
 Bicarb 17
 Osm 384
Treatment of HONK
 Fluid repletion: give first 2-3 liters rapidly
 Total deficit may be 10 liters: replete 1/2 the
deficit in the first 6 hours
 Insulin 10 unit bolus followed by sliding scale
hourly
 Treat underlying precipitating illness