Diabetic Ketoacidosis

Diabetic Ketoacidosis

Done by:

Mohammed Qazzaz


It is a life threatening but reversible complication of type 1 diabetes due to absolute insulin deficiency.

Ketoacidosis: High anion gap metabolic acidosis due to excessive blood concentration of ketone bodies (Ketoanion).


153,000 Hospital admission.

2.4 billion US $




A-The basic underlying mechanisms are:

-Absolute deficiency of circulating insulin.

-secretion of insulin counterregulatory hormones; glucagon, adrenaline, cortisol and growth hormone.


B-This leads to disturbances in the following physiological processes:

-glucose utilization (hyperglycemia). - proteolysis ( amino acids, glutamine and

alanine). - lipolysis ( glycerol and FFAs). - glycogenolysis (breakdown of muscle glycogen

lactate). - gluconeogensis (glutamine & alanine & glycerol &

lactate are the precursors).


acetone,

acetoacetic acid,

beta-hydroxybutyric acid


C-This results in the following metabolic abnormalities: 1-Hyperglycemia. 2-Hyperketonemia: 2 main mechanisms: a- Production of ketone bodies (ketogenesis): -Increase FFAs hepatic uptake FFAs enter the mitochondria oxidation to form acetoacetic acid. -Large part of acetoacetic acid reduced to -hydroxy butyric acid ( -HBA). -Small part of acetoacetic acid is decarboxylated to acetone. The 3 ketone bodies are released to the blood in a ratio between acetoacetic acid to -HBA of 8 : 1 .

b- Utilization of ketone bodies.


D-The consequences of these metabolic abnormalities are: a-Hyperglycemia: -Osmotic diuresis. -Excessive urinary losses of H2O & Na, K. -Dehydration and hypotension.

b-Hyperketonemia: -Ketonuria. - Blood acidity (acetoacetic acid and -HBA are strong acids). -Acetone is a CNS anaesthetic.


E-Electrolytes and acid base disturbances during DKA:a-Serum K: Usually high (hyperkalemia) secondary to:

1-Shift of K from intracellular to extracellular compartment due to: -Insulin deficiency and hyperglycemia. -Extracellular hyperosmolarity. -Acidosis. - Catabolism and breakdown of cellular protein. 2-Impaired cellular uptake of K.

Diabetic Ketoacidosisb-Serum sodium: Usually low secondary to:

-Hyperglycemia leads to osmotic flux of H2O from intracellular to extracellular space. -Obligate sodium loss with ketonuria.

c-Metabolic acidosis: Secondary to: - Production and utilization of strong acids; acetoacetic acid and -HBA. - Alkaline reserve (sodium and K losses).


Clinical features of DKA A-Symptoms of DKA:1-Classic symptoms of hyperglycemia: short period of time:

Polyuria, polydipsia, wt loss and thirst.

2-Other symptoms: - General weakness, malaise and lethargy. -Nausea, vomiting and abdominal pain. - Perspiration. - Disturbed consciousness and confusion. 3-Symptoms of underlying infections or other conditions; fever,

abdominal pain, dysuria, chest pain…etc.•

Diabetic KetoacidosisPrecipitating Factors:

StressInfections: UTI, Chest, FungalStroke, MI, PEPregnancySteroidsTraumaPancreatitisSurgeryHyperthyroidisim

Diabetic KetoacidosisB- Physical signs of DKA:

a-General signs: Ill appearance and disturbed consciousness. b-Signs of dehydration:

-Skin: Dry, hot, flushed, and loss of skin turgor. -Tongue: Dry (sometimes woody tongue). -Eyes: Sunken eyes and dark circles under the eyes.

c-Vital signs:

-Tachycardia, hypotension and tachypnea. d-Specific signs:

-Ketotic breath: A strong, fruity breath odour (similar to nail polish remover or acetone).

-Acidotic breath (Kussmaul's respiration): deep and rapid. -Abdominal tenderness.


Diagnostic criteria of DKA:

• Blood glucose > 250 mg/dl.• Mild to moderate dehydration.• Ketonuria: (++). • Serum bicarbonate < 15 m Eq/L.• pH is acidic (Metabolic acidosis): Arterial < 7.3. Or Venous < 7.25.

Diabetic KetoacidosisComplications of DKA

1-Complications of associated illnesses e.g. sepsis or MI.

2-Adult respiratory distress syndrome. 3-Thromboembolism (elderly). 4-Complications of treatment:

a-Hypokalemia: Which may lead to: -Cardiac arrhythmias. -Cardiac arrest.

-Respiratory muscle weakness.


b-Hypoglycemia.

c-Overhydration and acute pulmonary edema: particularly in:

-Treating children with DKA. -Adults with compromised renal or cardiac

function. -Elderly with incipient CHF.

Diabetic Ketoacidosisd-Neurological complications: Cerebral Edema.

-It occurs only in children with DKA. -Very dangerous and increases mortality. -The risk is related to the severity, duration and rapid

correction of DKA. Mechanism: The brain adapts by producing intracellular osmoles

(idiogenic osmoles) which stabilize the brain cells from shrinking while the DKA was developing. When the hyperosmolarity is rapidly corrected, the brain becomes hypertonic towards the extracellular fluids water flows into the cells cerebral edema

Diabetic KetoacidosisER EvaluationABCV/SCardiac monitoringPhysical examinationIV access : 2 large bore lines (16-18gauge )CVP may be neededBlood sugarFoley catheter


Baseline 1 hr 2 hr 3 hr 6 hr 12 hr 24 hrGlucose2 √ √ √ √ √ √ √

Urea, electrolytes √ √ √ √ √ √

Creatinine √ √ √ √

Bicarbonate √ √ √ √ √ √ √

Blood gases ) (√ √3 √3

Lab??!!

• Urinalysis for ketones• ECG• Infection screen: full blood count, blood and urine culture, C-reactive

protein, chest X-ray. Although leucocytosis invariably occurs, this represents a stress response and does not necessarily indicate infection

Diabetic KetoacidosisManagement of DKA

• The main lines of management include:

1. Fluid replacement2. Insulin 3. Potassium

Diabetic KetoacidosisFluid replacement

•0.9% saline (NaCl) i.v. • 1 L over 30 mins • 1 L over 1 hr • 1 L over 2 hrs • 1 L over next 2-4 hrs

•When blood glucose < 15 mmol/L (270 mg/dL) • Switch to 5% dextrose, 1 L 8-hourly • If still dehydrated, continue 0.9% saline and add 5% dextrose,

1 L per 12 hrs •Typical requirement is 6 L in first 24 hrs but avoid fluid overload in elderly patients •Subsequent fluid requirement should be based on clinical response including urine output


Insulin

IV bolus of 0.10 units/kg (~ 6 units) regular insulin

6 U/hr 3 U/hr when blood glucose < 15 mmol/L (270

mg/dL) 2 U/hr if blood glucose < 10 mmol/L (180 mg/dL)

•Check blood glucose hourly initially; if no reduction in first hour, rate of insulin infusion should be increased •Aim for fall in blood glucose of 3-6 mmol/L (approximately 55-110 mg/dL) per hour


Potassium

•None in first L of i.v fluid unless plasma potassium < 3.0 mmol/L •When < 3.5 mmol/L, give 20 mmol/hr •When plasma potassium is 3.5-5.0 mmol/L, give 10 mmol/hr


Additional procedures:

•Catheterisation if no urine passed after 3 hrs((do it from the start)) •Nasogastric tube to keep stomach empty in unconscious or semiconscious patients, or if vomiting is protracted •Central venous line if cardiovascular system compromised, to allow fluid replacement to be adjusted accurately •Plasma expander if systolic BP is < 90 mmHg or does not rise with i.v. saline •Antibiotic if infection demonstrated or suspected •ECG monitoring in severe cases


Aim of treatment a-Fluids: 1- Correct volume deficit and hypotension. 2- Improve tissue perfusion. 3-Improve insulin sensitivity (insulin counterregulatory

hormones). 4-Improve glomerular filtration rate: i-↑ excretion of large amount of glucose in urine. ii-Clears hyperketonemia. 5- Correct metabolic acidosis.


b-Insulin: Reversal of metabolic abnormalities : i-Corrects hyperglycemia. ii-Inhibits ketogenesis. c-Potassium: Prevents complications associated

with hypokalemia.


Health & Medicine

Diabetic Ketoacidosis