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‫إعداد و تقدي طلب سنة سادسة‬

‫سهر العلي – معاذ عيّاد – يزيد جبيل‬


Objectives
Definition of DKA and its Pathophysiology
Causes and precipitating factors
Clinical features by history and physical
examination
Investigations for DKA (Diagnosis &
Monitoring)
Management
Complications
Prognosis.
Introduction
Diabetic 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.
Pathophysiology
DKA 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→
1. Gluconeogenesis and glycogenolysis → Hyperglycemia .
2. Lipolysis → Free Fatty Acids → Ketogenesis →
Ketonemia and ketonuria→ ↓ pH and bicarbonate serum
levels→ Metabolic acidosis → Ketoacidosis.
Pathophysiology 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
Factors
The most common Other precipitants
precipitants 2.CVA
3.Intracranial bleeding
2.Infections (30–50%): 4.Acute pulmonary embolism
pneumonia, urinary tract 5.Intestinal or mesenteric thrombosis
6.Intestinal obstruction
infections, sepsis,
7.Acute pancreatitis
gastroenteritis 8.Alcohol intoxication or abuse
3.Inadequate insulin treatment 9.Severe burns, hyperthermia or
hypothermia
(20–40%): includes 10.Endocrine disorders: Cushing's
noncompliance, insulin pump syndrome, thyrotoxicosis,
failure acromegaly
11.Total parenteral nutrition
4.Myocardial ischemia or 12.Drugs: β-blockers, diuretics,
infarction (3–6%): often corticosteroids, antipsychotics
Clinical Features
Symptoms: Signs:
2.Polydypsia. 2.Dehydration:
3.Polyuria. o Dry skin and mucous .
4.Hyperglycemia. o Orthostatic
5.Nausea, lethargy, hypotension.
anorexia, weakness. o Tachycardia.
6.Abdominal pain. o Reduced JVP.
7.Reduced motility of GI. o Reduced mental
8.Vomiting. function
3.Ketosis:
Diagnosis
Table -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
Investigations
Glucose level.
Serum Ketones.
Acid-base status: pH, Serum bicarbonate and
Anion gap.
Electrolytes: Na +K+ Cl - Mg +2
ECG
CBC, WBC.
Urinalysis.
Cardiac markers, Liver enzymes and Amylase.
Chest X-Ray.
Blood and urine culture.
Management
Confirm 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–
Management 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,
Management cont.
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
Complications
Cerebral edema
Cardiac dysrhythmia
Pulmonary edema
Nonspecific myocardial injury may occur in
severe DKA.
Microvascular changes consistent with diabetic
retinopathy.
Prognosis
Excellent: 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.
References
Cecil Medicine, 23rd Ed
Harrison's Principles of Internal Medicine, 17th
Edition, 2008
eMedicine.com Specialties > Endocrinology >
Diabetes Mellitus
Thank You
Any Questions ?

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