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DIABETIC KETOACIDOSIS

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					DIABETIC KETOACIDOSIS
        ( DKA)

BY ELHAM SOBHY MD
    ETIOLOGY OF DKA
 IT OCCURS IN 5% OF PATIENTS WITH TYPE 1 DM
  ANNUALLY; IT IS SEEN LESS FREQUENTLY IN
  TYPE 2 DM. IT IS A MANIFESTATION OF SEVERE
  INSULIN DEFICIENCY, OFTEN IN ASSOCIATION
  WITH STRESS & ACTIVATION OF
  COUNTERREGULATORY HORMONES e.g.,
  CATECHOLAMINES, GLUCAGON.
 PPT FACTORS FOR DKA INCLUDE INTERRUPTION
  OF INSULIN THERAPY, SEPSIS, TRAUMA, MI &
  PREGNANCY. DKA MAY BE THE FIRST
  PRESENTATION OF TYPE 1 & RARELY TYPE 2 DM.
        DIAGNOSIS
    CLINICAL FEATURES:

 CLINICAL PRESENTATION MAY BE NON-
  SPECIFIC . THEY INCLUDE:
 * POLYURIA, POLYDIPSIA, WT LOSS, VOMITING &
  VAGUE ABD. PAIN.
 *TACHYCARDIA WITH SMALL PULSE VOL.
 * RAPID DEEP RESPIRATION ( KUSSMAUL
  RESPIRATION).
 * DEHYDRATION IS INVARIABLE, SHOCK & COMA
  MAY OCCUR.
         LABORATORY
         EVALUATION
 LABS WILL SHOW ACIDOSIS WITH RAISED ANION
  GAP METABOLIC ACIDOSIS .
 ANION GAP = [(Na + K)-( Cl + HCO3)=10-18mmol/L]
 PLASMA GLUCOSE USUALLY IS ELEVATED, BUT
  THE DEGREE OF HYPERGLYCEMIA MAY BE
  MODERATE ( < 300mg/Dl) in 10%-15% of
  PATIENTS. PREGNANCY & ALCOHOL ARE
  ASSOCIATED WITH EUGLYCEMIC KETOSIS .
 HYPONATREMIA , HYPERKALEMIA & AZOTEMIA
  ARE OTHER FINDINGS.
 SERUM AMYLASE&TRANSAMINASES MAYBE↑
MANAGEMENT & TTT OF
       DKA
 IV ACCESS & SUPPORTIVE MEASURES SHOULD BE
  INSTITUTED WITHOUT DELAY.
 FLUID DEFICIT: THE AVERAGE DEGREE OF DEHYDRATION
  FOR MOST PATIENTS IS APPROX. 7%-9% OF BODY WT.
 HYPOTENSION INDICATES A LOSS > 10% OF BODY FLUIDS.
 INITIALLY , RESTORATION OF CIRCULATING VOLUME
  USING ISOTONIC SALINE(0.9%) SHOULD BE DONE. THE 1ST
  LITER SHOULD BE INFUSED RAPIDLY & FOLLOWED BY
  ADDITIONAL FLUIDS AT A RATE OF1L / Hr UNTIL THE
  DEFICIT IS CORRECTED.
 HYPOTONIC SALINE CAN BE USED IN PATIENTS WITH
  SEVERE HYPERNATREMIA (> 155 mEq/ L).
MANAGEMENT & TTT OF
       DKA
REPLENISH TOTAL BODY WATER DEFICIT;
  THIS CAN BE ACCOMPLISHED USING SALINE
  INFUSION AT A RATE OF 150-500mL/hr. THE RATE
  OF FLUID REPLACEMENT DEPENDS ON THE
  DEGREE OF DEHYDRATION, CARDIC & RENAL
  FUNCTIONS.
MAINTENANCE FLUID REPLACEMENT: IS
  CONTINUED UNTIL THE FLUID INTAKE/OUTPUT
  RECORDS INDICATE AN OVERALL +VE BALANCE
  SIMILAR TO THE ESTIMATED FLUID DEFICIT.
THE SUCCESS OF FLUID REPLACEMENT IS JUDGED
  BY IMPROVEMENT IN BP, MEASUREMENT OF
  FLUID BALANCE & CLINICAL EXAM.
    INSULIN THERAPY
 SUFFICIENT INSULIN MUST BE TAKEN TO
  TURN OFF KETOGENESIS.
 AN IV BOLUS OF REGULAR INSULIN ;10-15
  UNITS(0.15U/KG) CAN BE ADMINISTERED.
 THIS SHOULD BE FOLLOWED BY CONT.
  INFUSION OF REGULAR INSULIN AT AN
  INITIAL RATE OF 5-10U/H.
 A DECREASE IN BLOOD GLUCOSE OF 50-
  75mg/dl/hr IS AN APPROPRIATE
  RESPONSE.
    INSULIN THERAPY
 LESSER DECREMENTS SUGGEST INSULIN
  RESISTANCE, VOLUME DEPLETION OR A
  PROBLEM WITH INSULIN DELIVERY.
 IF INSULIN RESISTANCE IS SUSPECTED, THE
  HOURLY DOSE SHOULD BE INCREASED
  PROGRESSIVELYBY 50%-100% UNTIL
  APPROPRIATE GLYCEMIC RESPONSE IS
  OBSERVED.
 EXCESSIVELY RAPID CORRECTION OF
  HYPERGLYCEMIA AT RATES > 100mg/dl SHOULD
  BE AVOIDED TO REDUCE THE RISK OF OSMOTIC
  ENCEPHALOPATHY.
    INSULIN THERAPY
 MAINTENANCE INSULIN INFUSION RATE OF 1-2
  U/h ARE APPROPRIATE WHEN HCO3 IS
  15mEq/LOR HIGHER.
 ONCE ORAL INTAKE RESUMES , INSULIN CAN BE
  ADMINISTERED S.C AND THE PARENTRAL ROUTE
  CAN BE STOPPED.
 DEXTROSE 5% SHOULD BE INFUSED ONCE
  PLASMA GLUCOSE DECREASE TO 250mg/dL AND
  THE INSULIN INFUSION RATE SHOULD BE
  DECREASED TO 0.05U/h TO AVOID DANGEROUS
  HYPOGLYCEMIA.
  POTASSIUM DEFICIT
 THIS SHOULD ALWAYS BE ASSUMED OR
  ANTICIPATED REGARDLESS OF PLASMA LEVELS
  ON ADMISSION. INSULIN RESULTS IN RAPID
  SHIFT OF K IN THE INTRACELLULAR
  COMPARTMENT.

 K SHOULD BE ADDED ROUTINELY TO THE IV
  FLUID AT A RATE 10-20MEq/hr EXCEPT IN
  PATIENTS WITH HYPERKALEMIA (> 6mmol/L AND
  /OR ECG CHANGES) , RENAL FAILURE, OR
  OLIGURIA CONFIRMED BY BLADDER
  CATHETERIZATION
   POTASSIUM DEFICIT
 PATIENTS WHO PRESENT WITH HYPOKALEMIA
  SHOULD RECEIVE HIGHER DOSES OF K .
  40mEq/hr OR GREATER DEPENDING ON
  SEVERITY.
KCL IS AN APPROPRIATE INITIAL CHOISE, BUT CAN
  BE LATER BE CHANGED TO KP TO DECREASE
  CHLORIDE LOAD.
K STATUS SHOULD BE DOCUMENTED FROM THE
  START; THIS INCLUDES ECG TO RULE OUT RARE
  LIFE THREATENING HYPERKALEMIA
BICARBONATE THERAPY
 THIS IS NOT ROUTINLY NECESSARY & MAY BE
  DELETERIOUS IN CERTAIN SITUATIONS.
 BICARBONATE THERAPY MAY BE APPROPRIATE
  IN :
 1- PATIENTS WITH SHOCK & COMA.
 2- IN SEVERE ACIDOSIS (PH 6.9-7.1).
 3- SEVERE DEPLETION OF BUFFERING RESERVE
  (HCO3 < 5mEq/L).
 4- ACIDOSIS- INDUCED CARDIAC OR
  RESPIRATORYDYSFUNCTION.
 5- SEVERE HYPERKALEMIA.
BICARBONATE THERAPY
 SODIUM BICARBONATE50-100mEq IN 1 LITER OF
  45% NACL INFUSED OVER 30-60 MINUTES , CAN
  BE GIVEN IN THESE SITUATIONS. HCO3 TTT
  SHOULD BE GUIDED BY BLOOD GASES &
  CONTINUED UNTIL THE INDICATION IS NO
  LONGER PRESENT..

 CARE SHOULD BE TAKEN TO AVOIDE
  HYPOKALEMIA; AN ADDITIONAL DOSE OF K
  10mEq, SHOULD BE INCLUDED WITH EACH
  INFUSION OF HCO3 UNLESS HYPERKALEMIA IS
  PRESENT.
COMPLICATIONS OF DKA
  LACTIC ACIDOSIS: MAY RESULT FROM
  PROLONGED DEHYDRATION, SHOCK
  INFECTION& TISSUE HYPOXIA IN DKA. IT SHOULD
  BE SUSPECTED IN PATIENTS WITH REFRACTORY
  METABOLIC ACIDOSISAND PERSISTENT ANION
  GAP INSPITE OF OPTIMAL THERAPY OF DKA.

  ADEQUATE VOLUME REPLACEMENT, CONTROL
   OF SEPSIS AND JUDIJIOUS USE OF
   BICARBONATE CONSTITUTE THE APPROACH TO
   MANAGEMENT.
COMPLICATIONS OF DKA

 ATERIAL THROMBOSIS: MANIFESTING AS STROKE , MI, OR
  AN ISCHEMIC LIMB. HOWEVER ROUTINE ANTICOAGULANT
  IS NOT A PART OF DKA THERAPY.
 CERBRAL OEDEMA: IS OBSERVED MORE FREQUENTLY IN
  CHILDREN MORE THAN ADULTS..
 SYMPTOMS OF INCREASED INTRACRANIAL TENSION OR A
  SUDDEN DETERIORATION OF LEVEL OF CONCIOUSNESS
  AFTER INITIAL IMPROVEMENTIN A PATIENT WITH DKA
  SHOULD RAISE SUSPICION OF CEREBRAL OEDEMA.
 ↓ IN Na OR FAILUR TO RISE DURING TTT IS A CLUE TO
  IMMENET OR ESTABLISHED OVERHYDRATION WITH FREE
  H2O.
 CT CAN ESTABLISH DIAGNOSIS. PROMPT THERAPY WITH
  IV MANNITOL IS ESSENTIAL & MAY PREVENT
  NEUROLOGICAL SEQUELAE.
  THYROID
EMERGENCIES
      THYROID STORM
 IT IS RARE, LIFE THREATENING COMPLICATION
  OF THYROITOXICOSIS IN WHICH A SEVERE
  FORM OF THE DISEASE IS PPT BY
  INTERCURRENT MEDICAL PROBLEM.
 PPT FACTORS MAY BE INFECTION, STRESS,
  TRAUMA, THROIDAL & NON THYROIDAL
  SURGERY,DKA, LABOR, IODINATED CONTRAST
  STUDIES, THYROID HORMONE OVERDOSE,
  RADIOIODINE TTT ESP IF THERE WERE NO PRE
  TTT WITH ANTITHYROID DRUGS.
 THE CAUSE IS THOUGHT TO BE A SUDDEN
  INHIBITION OF THYOID H. BINDING TO PLASMA
  PROTEINS BY PPT FACTOR, CAUSING A RISE IN
  THE ALREADY ELEVATED FREE HORMONE
  POOL.
CLINICAL PRESENTATION

 SYMPTOMS:
*FEVER : USUALLY >38.5C , TACHYCARDIA OUT OF
  PROPORTION TO THE
  FEVER.TACHYARRYTHMIAS ESP AF IN THE
  ELDERLY ARE COMMON.
*MENTAL STATUS CHANGES, AGITATION &
  DELERIUM.
*NAUSEA, VOMITING & DIARRHEA.
*COMA & DEATH MAY ENSUE IN 20% OF CASES ,
  DUE TO CARDIACARRYTHMIA, CONG. HF.,
  HYPERTHERMIA OR PPT FACTOR.
CLINICAL PRESENTATION

 SIGNS:
*CLASSIC SIGNS OF GRAVES INCLUDING
   OPHTHALMOPATHY & DIFFUSE GOITRE (MAY
   OCCUR WITH NODULAR GOITRE);
*IN THE ELDERLY, SVERE MYOPATHY& PROFOUND
   WT LOSS & MINIMAL THYROID ENLARGEMENT
   MAY BE OBSERVED.
*NO DISTNICT LAB ABNORMALITY . THYROID H
   LEVELS ARE SIMILAR TO UNCOMPLICATED
   CASES. LITTLE CORRELATION BETWEEN THE
   CRISIS & THE HORMONAL LEVEL.
TREATMENT OF THYROID
       STORM
 SUPPORTIVE TTT:
 TREATMENT OF UNDERLYING ILLNESS.
 INTRAVENOUS FLUIDS.
 COOLING BLANKETS &/OR ANTIPYRETICS.
 β ADRENERGIC BLOCKING DRUGS:
 PROPRANOLOL:1mg IV/MIN TO A TOTAL DOSE OF 10mg
  THEN 40 TO 80 mg PO q 6h,OR
 METOPROLOL: 100 TO 400mg PO /12h OR
 ATENOLOL 50-100mg/DAY.
TREATMENT OF THYROID
       STORM
               ANTITHYROID DRUGS
 INHIBITION OF THYROID HORMONE SYNTHESIS:
 PROPYLTHIOURACIL: 800mg PO 1ST DOSE THEN 200 TO 300
  Mg PO q8h, IT IS PREFFERED BE CAUSE IT IMPAIRS
  PERIPHERAL CONVERSION OF T4 TO T3 ,or
 METHIMAZOLE: 80mg PO 1ST DOSE THEN 40-80mg PO
  q\12h.
 BLOCK RELEASE OF THYROID HORMONES FROM THE
  GLAND:
 IODIDES, ORALLY OR INTRAVENOUSLYMAY BE USED ONLY
  AFTER ANTITHYROID DRUGS HAVE BEEN ADMINSTERED.
TREATMENT OF THYROID
       STORM
           BLOCK T4 TO T3 CONVERSION
 HIGH -DOSE DEXAMETHASONE 1-2mg PO/6h. IT IS NEEDED
  AS SUPPORTIVE TTT , AS INHIBITOR OF T4 TO T3 & AS A
  POSSIBLE TTT OF INTERCURRENT ADRENAL
  INSUFFICIENCY.
 PROPYLTHIOURACIL
 MOST β BLOCKERS

      REMOVE THYROID HORMONE FROM THE
                 CIRCULATION:
 PLASMAPHARESIS,OR
 PERITONEAL DIALYSIS,OR
 ION EXCHANGE RESINS (COLISTEPOL OR
  CHOLESTYRAMINE) CAN TRAP THE HORMONE IN THE
  INTESTINE & PREVENT RECIRCULATION.

				
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