DIABETIC KETOACIDOSIS

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DIABETIC KETOACIDOSIS

• BY HOSAM M. TAHLAWI
• K.A.A.U. MADICAL SCHOOL

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Diabetic Ketoacidosis

• 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.

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Gluconeogenesis

• Maximal gluconeogenesis occurs as glucagon lowers
  the concentration of F2,6-bisphosphate 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

• 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)
• this results in high levels of acetone,
  acetoacetate and ?-hydroxybutyrate .

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Clinical Presentation

• 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 26-41 sodium 132 potass
  ium 4.8-6.0 bicarbonate 6.0-
  10 BUN 9.0-15
• acetoacetate 4.8 ?-hydroxybutyrate
  13.7 free fatty acid 2.1-2.3 lactate
  4.6 osmolality 310-331
• osmolality 2(NaK) Glu BUN

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• 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
• vomiting and excessive water drinking
• interference by hypertriglyceridemia

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• Initial potassium could be normal or high but
  this is misleading since there is a huge
  total-body 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 (gt250 mg/dl)
• ketosis (ketonemia or ketonuria)
• acidosis (pHlt7.3, HCO3lt15mEq/L)
• supporting features are volume depletion and
  Kussmauls breathing.

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Diabetic Vs. Alcoholic Ketoacidosis

• by definition AKA occurs in chronic alcoholism
  especially after a binge drinking!?
• always occurs with starvation.
• sever abdominal pain and tenderness and
  pancreatitis occur in 75.
• 90 presents with glucose level lt150 mg/dl
• 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
• IVF the usual fluid deficit is 3-5L
• on arrival the patient is given 1-2L of isotonic
  saline or ringers 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 40-50 mmol of K are given
• 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.

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THERAPUTIC CONSIDERATIONS

• 1) Plasma glucose will invariably fall more
  rapidly than ketones. So, dont 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 (NaK) - (ClHCO3)

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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.

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Complications of DKA and clues to their
development

• 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.