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DIABETIC KETOACIDOSIS Uremia

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DIABETIC KETOACIDOSIS Uremia Powered By Docstoc
					DIABETIC KETOACIDOSIS


  BY: HOSAM M. TAHLAWI
 K.A.A.U. MADICAL SCHOOL
            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.
           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.
                      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 .
           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.
   Initial lab result in DKA: (series) in mmol/l
       glucose:              26-41
       sodium:               132
       potassium:            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([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:
    – vomiting and excessive water drinking
    – interference by hypertriglyceridemia
 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.
 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.
   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)
   supporting features are volume depletion and
    Kussmaul’s breathing.
    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 <150 mg/dl
   rapidly reversed with IV glucose, but remember to
    give thiamin to avoid Beriberi
   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 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)
   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.
    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)
 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
   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.
   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.

				
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posted:5/17/2011
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