Adapted from source

 1 .PATHOGENESIS
 2 .CLINICAL FEATURES
 3 .DIAGNOSIS
 4 .TREATMENT
 5. COMPLICATIONS
 1. KETO ACIDOSIS- DKA
 2. DEGREE OF HYPERGLYCEMIA
 3. DEGREE OF HYPOVOLEMIA
 DEFINITIONS:

 1 .HHS
 -LITTLE/NO KETOACID ACCUM.
 S-GLUCOSE > THAN 56MMOL/L
 PLASMA OSMOL. 380MOSMOL/KG
 N=278-305MOSMOL/KG
 NEURO SX=FREQUENT
 PH>7.3
 2:DKA
 -TRIAD: 1. HYPERGLYCEMIA
2.HIGH ANION GAP
METABOLIC ACIDOSIS

3.KETONEMIA
 INFECTION
 INADEQUATE INSULIN THERAPY
 ACUTE MAJOR ILLNESS
 NEW ONSET IDDM
 DRUGS:GLUCOCORTICOIDS,THIAZIDES
SYMPATHOMIMETIC , 2ND GEN
ANTIPSYCHOTICS
 COCAINE
 EATING DISORDERS AND PURPOSEFULL
INSULIN OMISSION
 POOR COMPLIANCE
 DKA AND HHS =EMERGENCIES
 DKA
-USUALLY RAPID EVOLUTION/24H
 HHS
 –INSIDIOUS OVER DAYS-
-NEUROLOGICAL SYMPTOMS MOST COMMON
 1. A/B/C STATUS
 2. MENTAL STATUS
 3. POSSIBLE PRECIPITATING EVENTS
 4. VOLUME STATUS
 1.S-GLUCOSE
 2.S-ELECTROLYTES
 3.FBC +DIFF
 4.URINALYSIS AND URINE KETONES
 5.PLASMA OSMOLALITY
 6. S-KETONES
 7. ABG
 8. ECG
 ONLY A FEW POINTERS:

 1. Sx. OF VOLUME DEPLETION

 2. HHS-NEUROLGIC FINDINGS
 3. DKA-FRUITY ODOR
 -KUSSMAUL BREATHING
 4. FEVER=RARE
 NEUROLOGIC DETERIORATION USUALLY
 OCCURS IF PLASMA OSMOLALITY IS
 >320-330 MOSMOL/KG

 IF STUPOR/COMA IS PRESENTAND
 OSMOLALITY IS < 320 MOSMOL/KG
 = LOOK FOR OTHER CAUSES
 3 KETONE BODIES –
 A: BETA-HYDROXY BUTYRIC ACID
 B: ACETOACETIC ACID
 C: ACETONE

 WHY KETONES IN DKA AND NOT HHS

 DKA= HIGH ANION GAP ACIDOSIS

 SEVERITY OF ACIDOSIS
 1. RATE OF KETOACID PRODUCTION
 2. DURATION OF KETOACID PRODUCTION
 3. RATE OF ACID EXCRETION IN URINE

 S-BICARBONATE IS REDUCED IN
VARIABLE DEGREES IN DKA
 FINAL Na CONCENTRATION REFLECTS
THE BALANCE BETWEEN DILUTION AND
CONCENTRATION OF Na

 PT`s MOSTLY PRESENT WITH A MILD

HYPONATREMIA
 DKA+HHS=DEFECIT 3-5MG/KG

 ON ADMISSION =N OR RAISED

 CONTRIBUTING FACTORS TO DEECIT

 1.OSMOTIC DIURESIS
 2. LOSS OF POTASSIUM TO MAINTAIN
ELECTRONEUTRALITY AS ACIDS ARE
EXCRETED
 1. S-GLUCOSE
 2. ELECTROLYTES/POTASSIUM
 3. UREA
 4. CREATININE
 5. OSMOLALITY
 6. VENOUS PH/BICARBONATE
 1. BETA-HYDROXY BUTYRIC ACID
 2. VENOUS PH
 3. S-BICRBONATE
 4. ANION GAP
 AIM OF FLUID REPLACEMANT
 ADEQUATE REHIDRATION AND
CORRECTION OF HYPEROSMOLAR STATE
 ISOTONIC SALINE
 SUBSEQUENT FLUIDS FOR REPLACEMENT
 _ WHAT ?
 _ WHEN ?
 EFFECT OF INSULIN:
 1. REDUCE HYPERGLYCEMIA
 2. REDUCE ACIDOSIS

 ? DELAY INSULIN TREATMENT

 DOSE= SAME FOR DKA AND HHS

 ?RESPONSE TO INSULIN
 WHEN TO REDUCE /STOP
 S/C INSULIN TO OVERLAP IV INFUSION
 EFFECT OF INSULIN THERAPY
 CAREFULL MONITORING !
 MAINTAIN BETWEEN 4.0- 5.0 meqw/l
 EFFECT OF INSULIN THERAPY

 CORRECTED S-Na+:
 =MEASURED S-Na+ +( S-GLUCOSE ABOVE
NORMAL( mmol/l) divided by 3.2)
 INDICATIONS FOR USE OF BICARBONATE
IN DKA IS CONTROVERSIAL

 CONSIDER IF Ph < 7.0

 DKA: 1. KETOACIDOSIS RESOLVED
 2. NORMAL ANION GAP
 HHS :1. MENTALLY ALERT
 2.PLASMA OSMOLALITY <315
MOSMOL/KG

 WHEN PT CAN EAT .

 IN DKA>HHS = MAINLY A COMPLICATION
SEEN IN CHILDREN
 NEARLY ALL AFFECTED < 20 YEARS OLD

 WHEN?
 CLINICAL: 1. HEADACHE
 2. LETHARGY
 3. REDUCED AROUSAL
 RAPID DETERIORATION
 1. SEIZURES
 2. INCONTINENCE
 3. PUPILARRY CHANGES
 4. BRADYCARDIA
 5. RESPIRATORY ARREST

 THIS RAPID PROGRESSION USUALLY WHEN

THERE IS BRAINSTEM HERNIATION
 MORTALITY OF >70%
 PREVENTATIVE MEASURES

 RECOMMENDED TREATMENT
 1. MANNITOL : ,25-1,0g/Kg
 2. HYPERTONIC SALINE 3%
Protocol for DKA management in adults