Complications of diabetes mellitus can be classified into acute and chronic.

Diabetic ketoacidosis is the typical acute complication of DM1. It may represent the clinical onset manifestation, especially in children. Hyperosmolar hyperglycemic coma is the acute DM2 complication.

Diabetic ketoacidosis is due to insulin deficiency and excess counterregulatory hormones (catecholamines, glucagon, growth hormone, cortisol).

In particular, ketosis results from an increased hepatic synthesis of ketone bodies, which, in turn, results from the increased hepatic influx of fatty acids from the adipose tis sue, in which the lack of inhibition by insulin of hormone- sensitive lipase determines the hydrolysis of triglycerides into glycerol and fatty acids, which are released into the circulation and reach the liver, where the fatty acids undergo β-oxidation leading to acetyl-CoA synthesis. The ketone bodies synthesis is favored when the acetyl-CoA concentration the Krebs cycle’s oxidative capacity. At physiological pH, ketone bodies are present as ketoacids and are neutralized by bicarbonates; however, metabolic acidosis appears when the bicarbonate reserves are exhausted. The main symptoms are nausea, vomiting, abdominal pain, polyuria, polydipsia, asthenia, anorexia, mental status alterations, and dyspnea. The most frequent signs are tachycardia, dry skin, and mucous membranes, Kussmaul breathing, tachypnea, respiratory distress, dehydration, hypotension, fever, lethargy, sensory obnubilation, cerebral edema up to coma.

Hyperosmolar coma is a metabolic complication of type 2 diabetes mellitus that mainly occurs in elderly; the precipitating event is an inadequate water intake that, in subjects already at risk of dehydration due to polyuria, leads to hypovolemia, with a reduction in glomerular filtration that aggravates hyperglycemia. The main signs and symptoms are nausea, vomiting, dehydration, dry skin and mucous mem branes, hypotonia of the eyeballs, hypotension, drowsiness, lethargy, and convulsions up to coma. It can be precipitated by infections, stroke, acute myocardial infarction, pancreatitis, uremia, parenteral nutrition, diuretics, peritoneal dialysis, or drugs (e.g., phenytoin, steroids). The diagnosis is based on:

– Severe hyperglycemia  (>600 mg/dL)

– Hyperosmolarity ( >320 mOsm/L)

– Marked dehydration

– Absent or trace ketones

– Absence of acidosis (pH >7.3 ; HCO3  > 15 mEq/L)

Chronic complications can be divided into nonvascular and vascular. The latter, in turn, is classified into microangiopathies, affecting the small vessels, mainly in the retina and renal glomerulus, and macroangiopathies, affecting the peripheral and coronary circulation, with early atherosclerotic lesions formation (Table 1). Nonvascular complications include gastroparesis, infections, and skin lesions; in addition, long-term diabetes may be associated with hearing loss.

Table1. Chronic complications of diabetes mellitus

The risk of complications increases according to the hyperglycemia duration; since type 2 diabetes is often pre ceded by a long period of asymptomatic hyperglycemia, many patients already have almost a complication at the time of diagnosis. Chronic hyperglycemia determines chronic complications through various mechanisms, including nonenzymatic glycation with the formation of advanced glycation end products (AGEs), activation of protein kinase C (PKC), and defects in the polyol pathway leading to increased oxidative stress.

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مواضيع ذات صلة

Therapy of diabetes mellitus

Monitoring of diabetes mellitus

Damage to DNA and Proteins

Morphologic and Biochemical Changes in Apoptosis

Causes of Apoptosis

surgical site Infection

Ventilator-associated pneumonia

Catheter-related Bloodstream Infection (CRBSI)

Etiopathogenesis of Diabetes Mellitus

Classification of Diabetes Mellitus

Defects in Membrane Permeability

Accumulation of Oxygen-Derived Free Radicals(Oxidative Stress)