Saturday, January 31, 2009

Diabetic ketoacidosis (DKA)

Introduction

Diabetes ketoacidosis is an acute complication of diabetes as hyperglycemic hyperosmolar state (HHS).It was formerly considered a hallmark of type 1 DM, but it also occurs in individuals with type 2 diabetes mellitus as well. This is associated with potentially serious complications if not promptly diagnosed and treated.

Clinical Features

The symptoms and physical signs of DKA are listed below and usually develop over 24 hours. DKA may be the initial presentation of type 1 DM, but more frequently it occurs in individuals with established diabetes. Nausea and vomiting are often prominent,

1. Symptoms

Nausea
Vomiting
Thirst
Polyuria
Abdominal pain
Shortness of breath

2. Physical findings

Tachycardia
Dry mucous membranes
Reduced skin turgor
Dehydration
Hypotension
Tachypnea
Kussmaul respirations
Respiratory distress
Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen)
Lethargy
Obtundation
Cerebral
Edema
Possibly coma

3. Precipitating events

Inadequate insulin administration
Infection (pneumonia/UTI/gastroenteritis/sepsis)
Infarction (cerebral, coronary, mesenteric, peripheral)
Drugs (cocaine)
Pregnancy

Pathophysiology

DKA results from relative or absolute insulin deficiency combined with counterregulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormone). Both insulin deficiency and glucagon excess, in particular, are necessary for DKA to develop. The decreased ratio of insulin to glucagon promotes gluconeogenesis, glycogenolysis, and ketone body formation in the liver, as well as increases in substrate delivery from fat and muscle (free fatty acids, amino acids) to the liver.

Laboratory Abnormalities and Diagnosis

The timely diagnosis of DKA is crucial and allows for prompt initiation of therapy. DKA is characterized by hyperglycemia, ketosis, and metabolic acidosis (increased anion gap) along with a number of secondary metabolic derangements;

Glucose 13.9–33.3 mmol/L (250–600 mg/dL)
Sodium 125–135 meq/L
Potassium Normal to higher
Magnesium Normal to higher
Chloride Normal
Phosphate Normal
Creatinine Slightly high
Osmolality 300–320 mOsm/mL
Plasma ketones ++++
Serum bicarbonate >15 meq/L
Arterial pH 6.8–7.3
Arterial PCO 20–30mmHg
Anion gap [Na-(Cl+HCO3)] higher

Treatment

1) Confirm diagnosis
2) Admit to hospital; intensive-care setting
3) Assess: Serum
4) Replace fluids
5) Administer regular insulin
6) Assess patient: What precipitated the
7) Measure capillary glucose every 1–2 h
8) Monitor blood pressure, pulse, respirations, mental status, fluid intake and output every 1–4 h.
9) Replace potassium
10) Continue above until patient is stable
11) Administer intermediate or long-acting insulin as soon as patient is eating. Allow for overlap in insulin infusion and subcutaneous insulin injection.

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