Management of Diabetic Keto Acidosis

PLAN• Definition• Etiology• PATHOGENESIS• Clinical manifestation• Physical examination• Differential Diagnosis• Laboratory findings• MANAGEMENT• PROGNOSIS, COMPLICATIONS• REFFERENCES

DIFINITION

• DKA is an acute life- threatening Sd caused by lack Insulin and,

• it represents a derangement of the body`s normal response to starvation, in IDDM(Type 1).

• DKA= glycemia+Ketonemia +Acidosis

ETIOLOGY

DKA Noncompliance with insulin Infection process, Stress, Pregnancy, Trauma, Alcohol abuse in DM-type I, MI, CVA, GIB, New-onset diabetic.

PATHOGENESIS 1.Lack Insulin Peripheral use of glucose and

subsequently blood sugar. Glucose is unavailable for

cellular metabolism2. Body responses by counter-regulatory

hormones(glucagons,cathecolamines,cortisol and GH).

Stimulate the production of glucose and blood sugar.

3.In addition, hepatic gluconeogenesis is stimulated blood sugar.

PATHOGENESIS ( CON`T)

• Source of energy is needed, thus liver begins to break down free fatty acids i.e. LYPOLYSIS Ketoacids used by the Brain and other tissues as substrates energy

Ketonemia + Metabolic acidosis.The acidosis Intracellular K+ to shift to extra cellular

space relative Hyperkalemia (despite a total body potassium ).

PATHOGENESIS( CON`T)

• Hyperglycemia with Ketonemia Hyperosmolar state

osmotic diuresis volume depletion, electrolytes loss and the sequela of DKA.

Clinical manifestation

• HISTORY is very important A.Hyperglycemia symptom`s:

- Blurred vision - Polyuria - Polydipsia DM= D’se of 3P’s

-PolyphagiaB.DKA symptoms at beginning: Nausea, Vomiting, abd

pain, fruity breath odor. at progress DKA: Dehydration,

dizziness, weakness, altered mental status/ shock.

Clinical manifestation(con`t)

• Physical Examination= Dehydration(dry mucous membranes, poor skin turgor), hypotension, tachycardia, abd tenderness, stretching of liver capsule, tachypnea or Kusmaul breathing=a rapid, deep,and labored breathing as compensatory response to MA=> Air hunger, smell of acetone

DIFFERENTIAL DIAGNOSIS• HHNKS( hyperosmolar hyperglycemic nonketotic

syndrome).• Alcohol ketoacidosis• Sepsis• Gastroenteritis,UTI, Pancreatitis• Uremia• Methanol,ethylene glycol or paraldehyde

ingestion• Starvation ketoacidosis• Lactic acidosis

INVESTIGATIONS• DKA= Glucose greater than 250mg /dl = HCO-3 less than 15 meq / l =pH less than 7.3 = hydroxybutyric acid and

acetoacetic acid HAGMAK = Na+ by urinary loss = Total body K+ by renal loss, but because

of the intracellular shifts of K+ because of the acidosis, K+ serum level is normal or .

ABG MA with AG. ECG Hyperkalemia / Hypokalemia, MI CXR Pneumonia (precipitating factor cause

of DKA), Abd. U/S

INVESTIGATIONS

• Urea, creatinine, • URINALYSIS for MCS & KETONES PROTEIN,PROTEIN• ELECTROLYTES,• B/CULTURES• CARDIAC ENZYMES (PRN)

MANAGEMENT OF DKA

I.ABC evaluation II.TWO LARGE VEINS ACCESES III.Fluid replacement III.Fluid replacement

IV.IV.INSULIN V.Potassium

VI.BICARBONATE VII.ADDITIONAL PROCEDURES

MANAGEMENT OF DKA1.ABC evaluation2.Fluid replacement2.Fluid replacement. N. saline 0.9% (NaCl)1litre/30 mins1L / 2 hrs1l over next 2-4hrsWhen blood glucose

15mmoll(250mg/dl) switch to 5% dextrose 1 litre 8- hourly.

If dehydration is still +, continue 0.9% saline and add 5%dextrose 1 litre /12hrs

Fluid requirement=6-8 L/24hrs except in elderly people where a fluid overload is avoided.

∆ Fluid requirement should be based on clinical response including urinary output

MANAGEMENT OF DKA

3.INSULINa. STANDARD PROTOCOL . 50u soluble insulin in 50ml 0.9%

saline iv via infusion pump: 6u/hr initially 3u/hr if BG 250mg/dl(12mmol\

l) 2u / hr if BG180mg

/dl(10mmol\l)

• Check B/Sugar hourly initially, if no Insulin infusion .

• Aim= to fall 55-110mg (3-6mmol / l) / hr

B.If IV INFUSION OF INSULIN IS NOT POSSIBLE

1.A loading dose of 10-20 units of soluble insulin in IM injection, immediately thereafter 5 U/hr.

2. Alternatively, a fast acting insulin 10 -20 u/h in subcutneous injection ( initially 0.3 u/kg body

weight, then 0.1u/kg/hr.The concentration of BG should ↓ 55-110mg/hr.If BG does not ↓ after 2 hrs of the commencing TTT, the dose

of insulin can be doubled, still a good response is obtained .When BG has follen to 180-270mg/dl, the dose of insulin

should be reduced to 1-4 units/hr ,then consider iv Glucose

NB: AVOID S/C INSULIN IN Pts WITH LOW BP (SBP<90mmHg).

CONT

Restoration of the usual insulin regimen, by SC injection, should not be instituted untill the patient is not able to eat , drink normally.

MANAGEMENT OF DKA

4.Potassium.None in first litre of iv fluid

unless 3.0 mmol / L. If plasma K+ 3.5mmol give

40 mmol added potassium in 1L fluid

.Avoid infusion rate 20mmol / hr

.If plasma K+ is 3.5-5.0 mmol, give 20 added K+

. If 5.0mmol/L or anuric patient, no added K+

Avoid K+ within the first 6hrs if no K+ monitoring

5.BICARBONATE

Severely acidotic where pH <7.0TTT =300ml of 1.26% of NaHCO3- infusion /

30min into elarge vein.∆ but its use is nowdays contreversial.

6.ADDITIONAL PROCEDURES IN MGMNT OF D KA

. Catheterisation if anuric status in 3hrs

.NGT to keep stomach empty if sub / or coma state, vomiting+++

. CV line if CVS is compromised for allowing fluid replacement to be adjusted accuretely

. Plasma expander (macromolecular fluid) if SBP<90mmHg or not rise with IV saline

. ATB if infection or suspected.

. ECG monitoring in severe case

. TTT according to the complications.

PROGNOSIS

↑ Mortality = 5 -10% ↑ in elderly ↑ complications

COMPLICATION OF DKA1 CO due to ↑ blood glucose or use hypertonic fluid

and / or Bicarbonate =↑mortality.2. ARDS.3. Thromboembolism4. DIC.(DISSEMINATED INTRAVASC COAG.)5.ACF. (ACUTE CARDIAC FAILURE)6.ACUTE GASTRIC DILATATION7.REBOUND KETO ACIDOSIS_

REFFERENCES

• HARRISSON’S 16th edition-2006• DAVIDSON’s 20th edition-2006• EMERGENCY MEDICINE 31th edition