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• A potentially life-threatening complication in patients with
diabetes mellitus
• Predominantly in those with type 1 diabetes……. but it can
also occur in those with type 2 diabetes also
• Results from a shortage of insulin; in response the body
switches to burning fatty acids and producing acidic ketone
bodies that cause most of the symptoms and complications
• Mortality of less than 1% with adequate and timely treatment
HISTORY:
• 1886 – Royal College of Physicians, London – Lecture by Julius
Dreschfeld
• 100% mortality till 1920, discovery of Insulin
• 1930 - Mortality came down to 29%
• 1950 – Less than 10%
• 1936 – Cerebral oedema described by doctors at Philadelphia
• 1987 – ketosis prone type 2 DM, aka. "idiopathic type 1 diabetes",
"Flatbush diabetes", "atypical diabetes" and "type 1.5 diabetes"
EPIDEMIOLOGY:
Diabetic ketoacidosis occurs in 4.6–8.0 per 1000 people
with type 1 diabetes annually
About 30% of children with type 1 diabetes receive their
diagnosis after an episode of DKA.
• Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA (December 2006).
"Hyperglycemic crises in adult patients with diabetes: a consensus statement from
the American Diabetes Association“
• Silverstein J, Klingensmith G, Copeland K, et al. (January 2005)."Care of children and
adolescents with type 1 diabetes: a statement of the American Diabetes Association"
CAUSES:
• Intercurrent illness (pneumonia, influenza, gastroenteritis, a urinary
tract infection)
• Pregnancy
• Inadequate insulin administration (e.g. defective insulin pen device)
• Myocardial infarction
• Stroke
• Use of cocaine
PRECIPITATING
FACTOR
DKA in type 2 DM – The “Ketosis-prone type 2 DM”
A study evaluating 138 consecutive admissions for DKA at
a large academic center observed that 21.7% had type 2
diabetes
(Newton CA, Raskin P: Diabetic ketoacidosis in type 1 and type 2 diabetes: clinical and
biochemical differences. Arch Intern Med)
“When DKA occurs in patients with type 2 diabetes, the presumed mechanism of
ketoacidosis is the combination of relative insulin deficiency and increased secretion of
glucagon (as well as other counteregulatory hormones such as cortisol, catecholamines,
and growth hormone) in response to stress from 1) overwhelming infection, 2) infarction
of tissue, or 3) other severe illness. The elevated catecholamines further suppress insulin
secretion to perpetuate a downward spiral. The increased glucagon-to-insulin ratio
causes a mismatch that promotes unregulated lipolysis and proteolysis with subsequent
uninterrupted formation of ketoacidosis”.
More common in African, African-American and Hispanic people. Their
condition is then labeled "ketosis-prone type 2 diabetes"
SIGNS & SYMPTOMS: usually evolve over the period of about 24 hours
• Nausea and vomiting, pronounced thirst, excessive urine production and
abdominal pain, high blood sugar levels
• In severe DKA, breathing becomes labored and of a deep, gasping character, a
state referred to as "Kussmaul respiration” - respiratory compensation for a
metabolic acidosis
• Ketotic/fruity odor in breath
• “Coffee ground vomiting” (vomiting of altered blood) occurs in a minority of
patients, d/t esophageal erosion
• Marked decrease in the level of consciousness
• Clinical evidence of dehydration, such as a dry mouth and decreased skin turgor,
the average adult DKA patient has a total body water shortage of about 6 liters (or
100 mL/kg)
• Severe dehydration can lead to tachycardia and hypotension
• Small children with DKA are relatively prone to cerebral edema, 0.3–1.0% of
children, 20–50% mortality
INVESTIGATIONS & DIAGNOSIS:
• May be diagnosed when the combination of hyperglycemia (high blood sugars), ketones
in the blood(negative: < 1 mg/dl) or in urine and acidosis are demonstrated
• In addition to the above, blood samples are usually taken to measure urea and creatinine
(measures of kidney function, which may be impaired in DKA as a result of dehydration)
and electrolytes
• High anion gap; due to consumption of bicarbonate and CO2 loss in hyperventilation
• Markers of infection (complete blood count, C-reactive protein) and acute pancreatitis
(amylase and lipase) may be measured
• Chest radiography and urinalysis are usually performed
• If cerebral edema is suspected because of confusion, recurrent vomiting or other
symptoms, computed tomography may be performed to assess its severity and to
exclude other causes such as stroke
The American Diabetes Association categorizes DKA in adults into one
of three stages of severity:
A 2004 statement by the European Society for Paediatric
Endocrinology and the Lawson Wilkins Pediatric Endocrine Society (for
children) uses slightly different cutoffs, where:
• mild DKA is defined by pH 7.20–7.30 (bicarbonate 10–15 mmol/l)
• moderate DKA by pH 7.1–7.2 (bicarbonate 5–10)
• severe DKA by pH<7.1 (bicarbonate below 5).
Grade pH Bicarbonate
(mmol/L)
Mental
State
Mild 7.25-7.30 15-18 Alert
Moderate 7.00-7.24 10-14.9 Drowsy
Severe <7.00 <10 Stupor to
coma
RESOLUTION:
Resolution of DKA is defined as general improvement in
the symptoms, such as the ability to tolerate oral nutrition
and fluids, normalization of blood acidity (pH>7.3), and
absence of ketones in blood (<1 mmol/l) or urine. Once this
has been achieved, insulin may be switched to the usual
subcutaneously administered regimen.
COMPLICATIONS:
• Cerebral Oedema – Most dangerous
• Pulmonary Oedema
• ARDS
• Electrolyte imbalance
• CCF
• Acute MI
• Acidosis & Cardiac arrest
• Acute Kidney Failure
• Sepsis syndrome and shock
PROGNOSIS
The overall mortality rate for DKA is 2% or less. The
presence of deep coma at the time of diagnosis,
hypothermia, and oliguria are signs of poor prognosis.
The prognosis of properly treated patients with diabetic
ketoacidosis is excellent, especially in younger patients if
intercurrent infections are absent. The worst prognosis
usually is observed in older patients with severe
intercurrent illnesses (e.g. myocardial infarction, sepsis, or
pneumonia), especially when these patients are treated
outside an intensive care unit.