Transcript DIABETIC KETOACIDOSIS

DIABETIC KETOACIDOSIS
Chatlert Pongchaiiyakul.
Division of Endocrinology
Department of Medicine
Khon Kaen University.
Diabetic Ketoacidosis
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an acute, life threatening metabolic acidosis
complicating IDDM and some cases of NIDDM with
intercurrent illness (infection or surgery)
usually coupled with an increase in glucagon
concentration with two metabolic consequences:
– 1) Maximal gluconeogenesis with impaired peripheral
utilization of glucose
– 2) activation of the ketogenic process and development
of metabolic acidosis.
Gluconeogenesis
Maximal gluconeogenesis occurs as glucagon
lowers the concentration of F2,6bisphosphate which is the intermediate that
activate glycolysis and inhibit
gluconeogenesis.
 This results in hyperglycemia and osmotic
diuresis with a resultant dehydration
characteristic of DKA.
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Ketogenesis
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KETOGENESIS occurs as a results of high
glucagon/insulin ratio:
– 1) increased liberation of free fatty acids due to the loss
of the inhibitory action of insulin on the hormone
sensitive lipase.
– 2) activation of the transport system (or reestrification to
VLDL will occur and nothing will happen)
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this results in high levels of acetone,
acetoacetate and -hydroxybutyrate .
Clinical Presentation
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anorexia, N/V, along with polydepsia and polyuria for about
24 hrs. followed by stupor (or coma).
Abdominal pain and tenderness could be present (remember
DDx of acute abdomen).
Kussmaul breathing with fruity odor “acetone”
Sings of dehydration ( HR, postural BP, etc.)
normal or low temperature:
NB.: if
fever is present it suggests infection while leukocytosis alone
is not because DKA per se can cause fever.
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Initial lab result in DKA: (series) in mmol/l
glucose:
sodium:
potassium:
bicarbonate:
BUN:
acetoacetate:
-hydroxybutyrate:
free fatty acid:
lactate:
osmolality:
26-41
132
4.8-6.0
6.0- 10
9.0-15
4.8
13.7
2.1-2.3
4.6
310-331
osmolality= 2([Na]+[K])+ [Glu]+ BUN
Sources of acid include acetoacetate and BHB
along with lactate, FFA, & PO4
 Sodium is low due to dilutional effect of
shifting of fluid to the ECF.
 Sodium leveld below 110 mmol/L suggest
either:
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– vomiting and excessive water drinking
– interference by hypertriglyceridemia
Initial potassium could be normal or high but
this is misleading since there is a huge totalbody potassium deficit.
 Prerenal azotemia is a reflection of the volume
depletion.
 Serum amylase might be elevated and frank
pancreatitis can occur.
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Diagnosis of DKA in IDDM patient is not that
difficult.
 The problem is pointing towards the cause of
acidosis with anion gap in a person who is
not known diabetic.
 Causes to consider:
1) lactic acidosis.
2) uremia.
3) alcoholic ketoaciosis (see later)
4) certain poisonings.
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The initial step in diagnostic approach is
testing urine for glucose and ketones.
Diagnostic criteria for DKA:
– hyperglycemia (>250 mg/dl)
– ketosis (ketonemia or ketonuria)
– acidosis (pH<7.3, HCO3<15mEq/L)
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supporting features are volume depletion and
Kussmaul’s breathing.
Diabetic Vs. Alcoholic Ketoacidosis
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by definition AKA occurs in chronic alcoholism
especially after a binge drinking!?
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always occurs with starvation.
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sever abdominal pain and tenderness and
pancreatitis occur in 75%.
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90% presents with glucose level <150 mg/dl
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rapidly reversed with IV glucose, but remember to
give thiamin to avoid Beriberi
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Insulin: is a prerequisite for recovery
– preferable way is to give 25-50U as an initial IV
bolus (or IM) followed by infusion of 15-25U/hour
till ketosis is reversed.
– IGF-1 is used in insulin resistance
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IVF: the usual fluid deficit is 3-5L
– on arrival the patient is given 1-2L of isotonic
saline or ringer’s lactate followed by infusion rates
dependent on fluid status and urine output.
– when glucose reaches 300mg/dl add 5% glucose
solution (? cerebral Edema)
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Potassium: replacement is always necessary
– if value on arrival is high: delay replacement till reversal
of ketosis
– if values are low: give K early
– if values are very low: hold insulin for 60-90 min. till 4050 mmol of K are given
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bicarbonate:
– indicated in sever acidosis (pH 7.0 or below) or with
hypotension (that can be caused by acidosis alone)
– stop the infusion at pH 7.2 to avoid alkalosis upon
reversal of ketosis.
THERAPUTIC CONSIDERATIONS
1) Plasma glucose will invariably fall more
rapidly than ketones. So, don’t stop insulin
unless reversal of ketosis occur.
 2) plasma ketones are not very helpful in
assessing clinical response. So use the pH and
anion gap instead.
AG = (Na+K) - (Cl+HCO3)
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 ALL patients should be followed with a flow
sheet outlining amounts and timing of insulin and
fluids together with record of vital signs, urine
volume, and blood chemistries. Without such a
record therapy tends to be chaotic.
 Patients are not doctors so we have to make sure
that each patient receives intensive detailed
instructions about how to avoid this potentially
disastrous complication of diabetes mellitus.
Complications of DKA
and clues to their development
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Acute gastric dilatation or erosive gastritis
– by vomiting blood or coffee-ground material
Cerebral edema
– obtundation or coma with or without neuro. Signs,
especially if occurring with initial improvement.
Hyperkalemia
cardiac arrest
hypokalemia
cardiac arrythmias.
Infection is known by fever
hypoglycemia is considered when there is adrenergic or
neuorologic signs or rebound ketosis.
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Insulin resistance:
unremitting acidosis after 4-6 hrs of Rx
MI:
chest pain, appearance of HF, hypotension despite adequate
fluids.
Mucormycosis:
facial pain, bloody nasal discharge, blurred vision, proptosis.
ARDS:
hypoxemia in absence of pneumonia, COPD, or HF
Vascular thrombosis:
stroke-like picture or signs of ischemia in nonnervous tissue.