Diabetic Ketoacidosis

Nursakinah Bohari Click to edit Master subtitle style 2008402306

5/2/12

What is Diabetic Ketoacidosis?

A state of absolute or relative insulin deficiency and counterregulatory excess resulting in hyperglycemia, dehydration, acidosis and ketosis. acute, life threatening, complication of DM commonly type 1. 5/2/12

An

Diagnostic criteria
1.

Hyperglycemia with blood glucose > 11 mmol/l Acidemia with arterial pH <7.3, bicarbonate (HCO3-) <15 mmol/l Ketonaemia (>3mmol/l) or ketonuria (>+2)
5/2/12

1.

1.

Epidemiology
Accounts

for 50% of diabetesrelated admissions in young persons and1-2% of all 1 diabetes-related admissions.

Among

type 1 DM, DKA is much more common in young children and adolescents (<19 y/o) than 5/2/12 it is in adults.

Etiology
In type 1 DM
Infection

(40%) : UTI, URTI, sepsis illness (20%) :

Intercurrent Interruption

myocardial infarction, stroke, trauma

insulin therapy (25%) / new-onset DM (15%)

5/2/12

Pathophysiology
Glucose

uptake

by cells
Breakdown

of muscle cell lactic acids FFA ketone 5/2/12 bodies (acetone,

Lipolysis

Pathophysiology
Compensation for the osmotic diuresis
Initially,

glucose levels cause osmolality (a shift

of water from intracellular to
5/2/12

extracellular space)

Signs & symptoms

5/2/12

Coma & osmolality

In DKA, coma occurs (10%). Hyperosmolality (not acidosis) is the cause of coma. in plasma osmolality cellular dehydration. severe loss of intracellular fluid in the brain leads to coma. occurs when the effective plasma osmolality reaches 340 mOsm/L (normal: Plasma osmolality 280295 mOsm/L). 2 ( Na+ + K+) + urea + glucose ( all in mmo/l)
5/2/12

Increase A

Coma

Differential diagnosis
Alcoholic

Ketoacidosis acidosis

Metabolic Shock Urinary

tract infection (UTI)

5/2/12

Laboratory findings Blood glucose level hourly measures Arterial blood gas (ABG)
5/2/12 - measure degree of

 Serum electrolytes: K+ (N~ 3.5-5.0mmol/L) - Serum K+ elevated due to extracellular shift caused by insulin deficiency and acidosis. Later, low K+ reflects the total body K+ depletion. Na+ (N~136-145mmol/L) can be high due to osmotic diuresis and excessive water loss. It can be low due to increased amount of 5/2/12 extracellular water in hyperosmolar

Other Investigations 12-lead ECG to detect ischaemia and changes due to hyper or hypoK+. Chest x-ray to detect pneumonia CT scan to detect neurological changes (eg if stroke is suspected)

5/2/12

Management
Goals of therapy
Correct Correct

dehydration acidosis and reverse blood glucose to near

ketosis
Restore

normal

Avoid complications of therapy

Identify

and treat any 5/2/12 precipitating event

Management
NHS, March 2010)

(Joint British Diabetes Societies Inpatient Care Group,

Action 1 Rapid ABC 2 large bore IV cannulae and start IV fluid replacement Clinical assessment (vital signs, GCS, full exam) Initial lab Ix Urinary catheter to monitor urine output Continuous cardiac monitoring Continuous pulse oximetry

Action 2 (restore the circulating vol.)

Assess the severity of dehydration Pulse and Blood pressures. Total fluid loss in DKA average 4-6 litres. Systolic BP on admission <90 mmHg

5/2/12

500 ml of 0.9% NaCl solution over 10-15 mins. If BP remains low, may be repeated.

Action 3 (K+ replacement) Hypo & hyperK+ are life-threatening.

Serum K+ high on admission (although total body is low) but falls tremendously upon tx with insulin. Regular monitoring is needed.

5/2/12

Action 4 ( restoration of acid base balance)

NaHCO3 is only given if severe hyperK+ or the arterial pH is <7.0 since IV vol. replacement is done. pH 6.9-7.0, give IV 8.4 % NaHCO3 50ml dilute in 200 ml NS in 1 hr. pH <6.9 , give 100 ml 8.4% NaHCO3 dilute in 400 ml NS in 2 hr.

Action 5 (fixed rate IV insulin infusion)

If weight not available, estimate in kg Insulin drip: Bolus: 0.15 units/kg, then infuse at 0.1 mg/kg/hr Ideally should decrease glucose 3-4 mmol/l per hour In DKA: Change to subcutaneous regimen once anion gap has closed and patient is ready to eat. Need to give long-acting insulin dose several hours prior to stopping insulin drip.

Treat the precipitating factors

5/2/12 Establish usual medication for DM

Complications

Cerebral edema

Rare, but life threatening Usually in pediatric, adolescent patients Symptoms: Headache, altered mental status Treat with mannitol, hyperventilation

Hyperkalemia Hypokalemia Aspiration

cardiac arrest cardiac arrythmias. picture

pneumonia

Thromboembolism - stroke-like 5/2/12

References

DKA guidelines, Joint British Diabetes Societies Inpatient Care group Emedicine Kumar & Clark Clinical Medicine, 7th edition ISPAD Clinical Practice Consensus Guidelines 2009 Compendium Emergency Medicine, Shirley Ooi, Peter Manning

5/2/12

Treatment of DKA

HYDRATION!!!

Normal Saline 500-1000 cc/hr for 4 hours, then 250 500 cc/hr for 4 hours, then 125-250 cc/hr Once glucose is < 200, should change fluids to D5 NS until insulin drip is stopped Insulin drip: Bolus: 0.15 units/kg, then infuse at 0.1 mg/kg/hr Ideally should decrease glucose 50-100 mg/dL per hour In DKA: Change to subcutaneous regimen once anion gap has closed and patient is ready to eat. Need to give long-acting insulin dose several hours prior to stopping insulin drip. Every 1 hour initially, then every 2 hours, and so on. 5/2/12

Insulin

Accuchecks

Diabetic Ketoacidosis A profound loss of insulin activity leads not only to increased serum glucose levels because of increased hepatic glucose output and decreased glucose uptake by insulin-sensitive tissues but also to ketogenesis. In the absence of insulin, lipolysis is stimulated, providing fatty acids that are preferentially converted to ketone bodies in the liver by unopposed glucagon action. Typically, profound hyperglycemia and ketosis (diabetic ketoacidosis) occur in Type 1 diabetics, individuals who lack endogenous insulin. However, diabetic ketoacidosis can also occur in Type 2 DM, particularly during infections, severe trauma, or other causes of stress that increase levels of counterregulatory hormones, thus producing a state of profound inhibition of insulin action. Severe hyperglycemia with glucose levels reaching an average of 500 mg/dL can occur if compensation for the osmotic diuresis associated with hyperglycemia fails. Initially, when elevated glucose levels cause an increase in osmolality, a shift of water from the intracellular to the extracellular space and increased water intake stimulated by thirst help to maintain intravascular volume. If polyuria continues and these compensatory mechanisms cannot keep pace with fluid lossesparticularly decreased intake as a result of the nausea and increased losses resulting from the vomiting that accompany ketoacidosisthe depletion of intravascular volume leads to decreased renal blood flow. The kidney's ability to excrete glucose is, therefore, reduced. Hypovolemia also stimulates counter-regulatory hormones. Therefore, glucose levels rise acutely owing to increased glucose production stimulated by these hormones and decreased clearance by the kidney, an important source of glucose clearance in the absence of insulin-mediated glucose uptake. In diabetic ketoacidosis, coma occurs in a minority of patients (10%). Hyperosmolality (not acidosis) is the cause of coma. Profound cellular dehydration occurs in response to the marked increase in plasma osmolality. A severe loss of intracellular fluid in the brain leads to coma. Coma occurs when the effective plasma osmolality reaches 340 mOsm/L (normal: 280295 mOsm/L). Because urea is freely diffusible across cell membranes, blood urea nitrogen is not used to calculate the effective plasma osmolality: The increase in ketogenesis caused by a severe lack of insulin action results in increased serum levels of ketones and ketonuria. Insulinopenia is also thought to decrease the ability of tissues to use ketones, thus contributing to the maintenance of ketosis. Acetoacetate and -hydroxybutyrate, the chief5/2/12 ketone bodies produced by the liver, are organic acids and, therefore, cause metabolic acidosis, decreasing blood pH and serum bicarbonate (Figure 188).