إعداد و تقديم طالب سنة سادسة إعداد و تقديم طالب سنة سادسة

سمهر العلي – معاذ عّي�اد – يزيد سمهر العلي – معاذ عّي�اد – يزيد جبريلجبريل

ObjectivesObjectivesDefinition of DKA and its PathophysiologyCauses and precipitating factorsClinical features by history and physical

examinationInvestigations for DKA (Diagnosis &

Monitoring)Management Complications Prognosis.

IntroductionIntroductionDiabetic ketoacidosis (DKA) is an ACUTE,

MAJOR, LIFE-THREATENING complication of diabetes.

DKA is defined: o Clinically as an acute state of severe

uncontrolled diabetes that requires emergency treatment with insulin and intravenous fluids.

o Biochemically as an increase in the serum concentration of ketones greater than 5 mEq/L, a blood glucose level of greater than 250 mg/dL (although it is usually much higher), blood pH of less than 7.2, and a bicarbonate level of 18 mEq/L or less.

PathophysiologyPathophysiologyDKA is characterized by hyperglycemia, acidosis, and

ketonuria.DKA is consequence of absolute or relative insulin

deficiency with increase in counter-regulatory hormones .

↓Insulin and ↑counter-regulatory hormone→ Gluconeogenesis and glycogenolysis → Hyperglycemia .

Lipolysis → Free Fatty Acids → Ketogenesis →

Ketonemia and ketonuria→ ↓ pH and bicarbonate serum

levels→ Metabolic acidosis → Ketoacidosis.

Pathophysiology Pathophysiology cont.cont.Hyperglycemia→ Glycosuria→ Osmotic diuresis→

dehydration and tissue hypoperfusion.Hyperglycemia, osmotic diuresis, serum

hyperosmolarity, and metabolic acidosis→ concentration disturbance.

Osmotic diuresis→ Potassium Sodium loss in the urine.

High serum osmolarity→ Dilutional hyponatremia.

Causes and Precipitating FactorsCauses and Precipitating FactorsThe most common

precipitants1.Infections (30–50%): pneumonia,

urinary tract infections, sepsis, gastroenteritis

2.Inadequate insulin treatment (20–40%): includes noncompliance, insulin pump failure

3.Myocardial ischemia or infarction (3–6%): often clinically “silent” in diabetic patients

Other precipitants1. CVA2. Intracranial bleeding3. Acute pulmonary embolism 4. Intestinal or mesenteric thrombosis 5. Intestinal obstruction 6. Acute pancreatitis 7. Alcohol intoxication or abuse 8. Severe burns, hyperthermia or

hypothermia 9. Endocrine disorders: Cushing's

syndrome, thyrotoxicosis, acromegaly

10.Total parenteral nutrition 11.Drugs: β-blockers, diuretics,

corticosteroids, antipsychotics

Clinical FeaturesClinical FeaturesSymptoms:1.Polydypsia.2.Polyuria.3.Hyperglycemia.4.Nausea, lethargy,

anorexia, weakness.5.Abdominal pain.6.Reduced motility of GI.7.Vomiting.

Signs:1.Dehydration:

o Dry skin and mucous .o Orthostatic

hypotension. o Tachycardia. o Reduced JVP.o Reduced mental

function2.Ketosis:

o Sweet odor o Kussmaul breathing

DiagnosisDiagnosisTable -1 Diagnostic criteria for diabetic ketoacidosis and the hyperosmolar hyperglycemic state

Mild DKA Moderate DKA Severe DKA

Plasma glucose (mg/dL) >250 >250 >250

Effective serum osmolality (mOsm/kg) Variable Variable Variable

Urine or serum ketones (NP reaction) Positive Positive Positive

Arterial pH 7.25–7.30 7.00–7.24 <7.00

Serum bicarbonate (mEq/L) 15–18 10–15 <10

Anion gap (mEq/L) >10 >12 >12

Typical mental status Alert Drowsy Stupor or coma

InvestigationsInvestigationsGlucose level.Serum Ketones.Acid-base status: pH, Serum bicarbonate and

Anion gap.Electrolytes: Na +K+ Cl - Mg +2

ECGCBC, WBC.Urinalysis.Cardiac markers, Liver enzymes and Amylase.Chest X-Ray.Blood and urine culture.

ManagementManagementConfirm diagnosis and admit to hospital or ICU.Assess:

o Serum electrolytes, Acid-base status and Renal function.

Replace fluids: o 2–3 L of 0.9% saline over first 1–3 h (10–15 mL/kg

per hour); o subsequently, 0.45% saline at 150–300 mL/h; o change to 5% glucose and 0.45% saline at 100–200

mL/h when plasma glucose reaches 250 mg/dL (14 mmol/L).

Management Management cont.cont.Administer short acting insulin: IV (0.1 units/kg)

or IM (0.3 units/kg), then 0.1 units/kg/hour by continuous IV infusion; increase 2- to 3-fold if no

response by 2–4 h. If initial serum K+ is < 3.3 mmol/L ,do not administer insulin until the potassium is corrected to > 3.3 mmol/L.

Assess patient: What precipitated the episode (noncompliance, infection, trauma, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, CXR, ECG).

Measure capillary glucose every 1–2 h; measure electrolytes (especially K+, bicarbonate, phosphate) and anion gap every 4 h for first 24 h.

Monitor vital signs, mental status, fluid intake and output every 1–4 h.

Replace K+: 10 mEq/h when plasma K+ < 5.5 mEq/L, ECG normal, urine flow and normal creatinine documented; administer 40–80 mEq/h when plasma K+ < 3.5 mEq/L or if bicarbonate is given.

Continue above until patient is stable, glucose goal is 150–250 mg/dL, and acidosis

is resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg per hour.

Administer intermediate or long-acting insulin as soon as patient is eating. Allow for overlap in insulin infusion and subcutaneous insulin injection.

Management Management cont.cont.

ComplicationsComplicationsCerebral edemaCardiac dysrhythmiaPulmonary edemaNonspecific myocardial injury may occur in

severe DKA.Microvascular changes consistent with diabetic

retinopathy.

PrognosisPrognosisExcellent: especially in younger patients if

intercurrent infections are absent.The worst prognosis: is usually observed in

patients who are older with severe intercurrent illnesses, eg, myocardial infarction, sepsis, or pneumonia, especially when they are treated outside an ICU.

signs of poor prognosis: deep coma at the time of diagnosis, hypothermia, and oliguria.

ReferencesReferencesCecil Medicine, 23rd EdHarrison's Principles of Internal Medicine,

17th Edition, 2008eMedicine.com Specialties > Endocrinology

> Diabetes Mellitus

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