Diabetic ketoacidosis

Supervised by : Dr. Rasha Bondok Assistant professor of anesthesia and intensive care Presented by : Lamya Elsayed Resident of anesthesia and intensive care

case scenario :  23 yrs old female, IDDM for 15 yrs.  Presents

with disturbed level of consciousness ,confusion, looks very unwell after having a normal vaginal delivery without anesthesia.  Vital data: BP 90/60 mmHg, Pulse 132 bpm, RR 32 breath/m with deep breaths (Kussmauls)  Examinaton: dry mucous membrane, mild epigastric tenderness, fruity breath odour and no fever.

Case scenario :  Labs: Hb 14gm/dl, WBC 20,000, Plt 312,000  S. glucose 400mg/dl.  Na = 137mEq/L, K = 3.8mEq/L, Cl = 101mEq/L.  ABG: pH = 7.15, pCo2 = 23 mmHg, Hco3 = 8 mmol/L

& pO2 = 100 mmHg.  Blood chemistry shows:

BUN 40, creatinine 2 mg/dl. Urine: Glucose +4, Ketone +3 .

What Does The ABG Tells Us ? ( PH = 7.15, PCO2 = 23, HCO3 = 8 & PO2 = 100) o

pH = 7.15 therefore acidosis (severe).

o

pCO2 = 23 therefore not resp. acidosis.

o

HCO3 = 8 therefore metabolic acidosis

o

Anion gap = Na + K – (Cl + HCO3 ) =137 + 5 – (101+ 8) = 33 (>14)

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High anion gap metabolic acidosis with respiratory compensation

Ketonemia / ketonuria hyperglycemia

DKA

Metabolic acidois

Questions :  Can serum glucose be normal in DKA ?

 What are the cut off values for PH and HCO3 in DKA ?  Is there any other types of acidosis in DKA ?

Who is at risk of DKA ?  More common in IDDM esp. in pts on insulin pump. why ?!  Can still happen in NIDDM. When ?!

 1/5 of cases are 1st time presenters  Most of cases are precipitated by certain factors : stress of

surgery, infection, trauma or a serious underlying medical illness e.g. stroke, MI

 No underlying precipitating factors can be detected in small

percentage of cases.

Pathophysiology of DKA

INSULIN

COUNTERREGULATORY HORMONES

 DKA is considered an extension of the

physiological state desinged to overcome starvation. in this case the relative carbohyrate unavailability caused by lack of insulin mimics a state of starvation.  Both lack of insulin and excess glucagon

contribute to the 2 main processes taking place in DKA : hyperglycemia and ketosis

Mechanism of hyperglycemia 1. Lack of insulin : inhibit glycolysis , stimulate glycogenolyis and gluconeogenesis.

2. Excess glucagon : inhibit glycolysis. How ? It inhibits formation of fructose 2,6 biphosphate which is an extremely potent allosteric regulator of a major rate limitting enzyme in the pathway of glycolysis (phosphofructokinae enzyme)

Effects of hyperglycemia : o Hyperglycemia leads to hyperosmolarity that in turn

cause osmotic diuresis and loss of water and electrolytes in urine and although hyperosmolarity shifts water to ECF, hypervolemia doesn’t occur dt concomitant osmotic diuresis. o severe dehydration, dehydration is augmented by

vomiting and later DCL decreasing fluid intake.

Mechanism of ketosis : 1. Lack of insulin : stimulates lipolysis that deliver FFA used for ketogenesis.

2. Excess glucagon : Citric acid (the product of krebs cycle I.e. glucose metabolism that Is inhibited by glucagon as decribed before) is responsible for regulation of activity of acetyl coA carboxylase. The later synthesize malony coA in the liver which turn off carnitine acyl transferase 1 that is the rate limitting enzyme in ketogenesis. ( so turn off the supply of substrate into krebs cycle and ketogenesis is automatically turned on ).

Effects of ketosis :  Metabolic acidosis increasing anion gap  Draws out intracelluar cations a sodium and potasium  Vomiting that aggravates dehydration

Total body stores of K are depleted due to urinary loss however s.K maybe intially elevated due to acidosis pulling intacellular K out. It markedly decrease with insulin therapy that stimuate the influx of K into the cells and with correction of acidosis.

fat cell

DKA: Pathophysiology Glucose

Insulin

+ PFK

TG

Ketoacids

Insulin

+

HSL FFA

Liver Cell

Pyruvate

Kreb’s Cycle

Acetyl-CoA

+

Fatty Acyl-CoA

Glucagon Insulin

+

VLDL (TG)

Clinical manifestations of DKA  Polyuria, Polydipsia, Polyphagia  Dehydration + orthostasis  Vomiting (50-80%)  Abdominal pain present in at least 30%.  Küssmaul respiration if pH < 7.2  Temperature usually normal or low, if elevated think

infection!  Lethargy, delirium

How to manage a case of DKA ?

Broad lines of treatment : Rehydration

Insulin therapy

DKA Electrolyte repletion

Management of complications and evaluation of therapy

 Priority is given to correction of the state of

hyperosmolarity and dehdration. rehydration should be done gradually to prevent overshooting of s.NA levels.  Insulin therapy is started only after support of

heamodynamics to prevent latent shock of rehydration  Potassium replacement is started even with normal

levels as it is expected to dramatically drop with insulin therapy.  100 % O2 is given to all cases of DKA even if the

saturation is 100 % on RA.

rehydration

Rehydration Volume! Volume! Volume 

Objectives:

 1- Restore intravascular volume.  2- Reduce blood glucose level.  3- Reduce counter regulatory hormones.

(catecholamines, glucagon)

Augment insulin sensitivity.

How much fluid will you give ?  15 – 20 ml/kg . (1-2 L ) in 1st hour  500 ml/h for next 2 hours or 1L /h if in shock  500-250 ml/h according to hydration status ( UOP & renal

functions).

 maintainence fluids should be provided.

How much fluid will you give ?  Subsequent choice for IV fluids depends on:

1-Corrected serum Na (Nac) 2- Effective serum osmolarity (E osm) o If E osm > 320 mOsm/L or Nac is normal/elevated

 0.45% NaCl 4-14 ml/Kg/hr o If E osm