Diabetes Complications Dr. Mujeeb Ahmed Shaikh Assistant Professor AlMaarefa College

Learning Objectives Describe the pathology, clinical manifestations, of – diabetic ketoacidosis – hyperosmolar hyperglycemic state, – hypoglycemia (insulin reaction), – the Somogyi effect and the dawn phenomenon. Identify chronic complications of diabetes, and explain their effect on body systems.

Acute Complications The three major acute complications of impaired blood glucose regulation are Diabetic ketoacidosis (DKA) Hyperosmolar hyperglycemic state Hypoglycemia. All are life-threatening conditions that demand immediate traetment

Diabetic Ketoacidosis (DKA) Hyperglycemia Ketosis, Metabolic acidosis DKA primarily affects persons with type 1 diabetes, but may also occur in persons with type 2 diabetes when severe stress such as sepsis or trauma is present.

Diagnosis Metabolic acidosis is caused by the excess ketoacids that require buffering by bicarbonate ions; this leads to a marked decrease in serum bicarbonate levels. Blood glucose levels >250 mg/dL [13.8 mmol/L]), Low serum bicarbonate, Low arterial pH, and positive urine and serum ketones.

Three types of DKA Mild DKA(serum bicarbonate of 15 to 18 mEq/dL [15 to 18 mmol/L], pH 7.25 to 7.30); Moderate DKA(serum bicarbonate 10 to <15 mEq/dL, pH 7.00 to 7.24) and Severe DKA(serumbicarbonate <10 mEq/dL pH <7.00).

Hyperglycemia leads to osmotic diuresis, dehydration, and a critical loss of electrolytes. Hyperosmolality of extracellular fuids from hyperglycemia leads to a shift of water and potassium from the intracellular to the extracellular compartment. Abdominal pain Fruity smell breath Hypotension and tachycardia Rate and depth of respiration increase (i.e., Kussmaul respiration)

Hyperosmolar Hyperglycemic State Characterized by hyperglycemia (blood glucose >600 mg/dL[33.3 mmol/L]), Hyperosmolarity (plasma osmolarity>320 mOsm/L) and Dehydration, the absence of ketoacidosis, and depression of the sensorium. Manifestations are weakness, dehydration, polyuria, neurologic signs and symptoms, and excessive thirst.

HHS contd.. The neurologic signs include hemiparesis, Babinski refexes, aphasia, muscle fasciculations, hyperthermia, hemianopia, nystagmus, visual hallucinations, seizures, and coma.

Hypoglycemia Characterized by below normal blood glucose levels. Most common in patient treated with insulin. C /F – Altered cerebral function and – Activation of the autonomic nervous system. T/t: 15 to 20 g of glucose

The Somogyi effect and Dawn Phenomenon The Somogyi Effect: Hypoglycemia associated with alternate episodes of hyperglycemia. The Dawn phenomenon is characterized by increased levels of fasting blood glucose or insulin requirements, or both, between 5 and 9 AM without antecedent hypoglycemia.

Chronic Complications Microvasculature Neuropathies Nephropathies Retinopathies Macro vasculature Coronary artery Cerebral arteries Peripheral vasculature Foot ulcers

Theories of Pathogenesis Polyol pathway: Intracellular Glucose  sorbitol  fructose Advanced glycation end products (AGEs): formation of glycoproteins in the basement membrane of microcirculation Protein kinase C – vascular damage in vs of kidney, nerves, & retina.

Neuropathies Somatic Neuropathy Glove-stocking Decrease pain, vibration & temp. sensation Sensory motor dysfunction Autonomic neuropathy Vasomotor function Postural hypotension Gastroparesis Paralytic bladder Erectile dysfunction Cranial nerve involvement

Nephropathies Diffuse glomerular sclerosis Nodular glomerular sclerosis Microalbuminuria Hypoalbuminemia Edema Prevention: glycemic control & BP maintenance (<130/80 mm of Hg)

Retinopathies Microanurysm Neovascularization Hemorrhage Scaring Retinal detachment

Macrovascula Complications Atherosclerotic coronary artery disease, cerebrovascular disease, and peripheral vascular disease. Risk factors – Obesity, – Hypertension, – Hyperglycemia, – Hyperinsulinemia, – Hyperlipidemia, – Altered platelet function, – Endothelial dysfunction, – Systemic infammation (as evidenced by increasedCRP), and elevated fbrinogen levels

Diabetic Foot Ulcers Effects of neuropathy and vascular insufficiency. Distal symmetric neuropathy is a major risk factor for foot ulcers. People with sensory neuropathies have impaired pain sensation and often are unaware of the constant trauma to the feet caused by poorly fitting shoes, improper weight bearing, hard objects or pebbles in the shoes, or infections such as athlete’s foot.

Motor neuropathy with weakness of the intrinsic muscles of the foot may result in foot deformities, which lead to focal areas of high pressure. When the abnormal focus of pressure is coupled with loss of sensation, a foot ulcer can occur. Common sites of trauma are the back of the heel, the plantar metatarsal area, or the great toe, where weight is borne during walking.

Infections Soft tissue infections of the extremities, osteomyelitis, urinary tract infections and pyelonephritis, candidal infections of the skin and mucous surfaces, dental caries and periodontal disease, and tuberculosis.

FUNGAL INFECTION BETWEEN TOES J Am Podiatr Med Assoc 98(5): 353–356, 2008

References Essentials of Pathophysiology: Concepts of Altered Health States, Third EditionCarol Mattson Porth Davidson's Principles and Practice of Medicine, 21st Edition