Cataract

Place of cataract in the structure of complications

Opacification of the lens (cataract) is classified as a late, or delayed, complication of diabetes mellitus. Such delayed consequences of the disease are always based on systemic damage to blood vessels — diabetic angiopathies. It is important to note that angiopathies are precisely the direct cause of death in 65–85% of cases in this category of patients. Pathology of the visual analyzer develops in parallel with damage to retinal vessels (diabetic retinopathy), which collectively leads to a significant decrease in vision and complete blindness.

Pathogenesis of vascular changes (Microangiopathy)

The morphological basis for the development of cataract and retinopathy is microangiopathy — damage to small blood vessels, capillaries, and arterioles. This is the most specific manifestation of diabetes mellitus.

The essence of the pathological process lies in the non-enzymatic glycosylation of proteins forming basement membranes. Herein, pronounced biochemical shifts occur:

• The synthesis of type IV collagen increases significantly.
• In parallel, the level of heparan sulfate drops.

As a result of these changes, thickening of basement membranes occurs, along with their plasmatic imbibition and subsequent hyalinosis. In terminal stages, this process reaches up to complete obliteration (closure of the lumen) of the affected vessel.

Associated organ lesions

The development of cataract occurs against the background of a severe comorbid condition caused by systemic angiopathy:

1. Diabetic nephropathy: Specific intracapillary glomerulosclerosis develops (known as Kimmelstiel–Wilson syndrome). It is accompanied by proteinuria, uremia, nephrogenic edema, and arterial hypertension. In 30% of patients with type 1 diabetes mellitus, the terminal stage of kidney damage sets in.
2. Diabetic neuropathy: Arises due to microangiopathy of vessels nourishing the nerves (vasa nervorum), as well as due to activation of the polyol pathway of glucose metabolism. Sorbitol accumulates in Schwann cells, leading to edema and demyelination of fibers. Sensory nerves of the lower extremities are most frequently affected, and the consequence of autonomic neuropathy is dangerous painless myocardial infarctions.
3. Macroangiopathy: Damage to large and medium-sized arteries. Atherosclerosis develops significantly earlier and proceeds more severely. Diffuse intimal fibrosis and Mönckeberg's mediacalcinosis (calcification of the tunica media) are observed, leading to coronary artery disease and strokes. Hypertension is aggravated due to the destruction of baroreceptors in rigid vascular walls.

Early complications and systemic background

Lens damage forms over years; however, this is frequently preceded or accompanied by early (acute) complications associated with sharp decompensation of carbohydrate metabolism. These include hypoglycemic and hyperglycemic comas.

The most specific is diabetic ketoacidotic coma. Its pathogenesis is strictly built upon a triad: hyperglycemia, metabolic acidosis, and electrolyte disorders. Severe dehydration and a critical increase in intracellular osmotic pressure develop. In the prodromal period, the patient experiences severe thirst, gastrointestinal syndrome with abdominal pain, and neurological disorders. A specific marker of an already developed coma is the characteristic acetone odor from the mouth, described as the «smell of rotting apples».

Specific secondary syndromes

In addition to cataract and angiopathies, patients encounter specific secondary lesions:

• Diabetic foot syndrome: Can be ischemic (gangrene due to angiopathy), neuropathic (formation of trophic ulcers), and mixed. Due to neuropathy, pain syndrome during the development of gangrene is often mildly expressed.
• Infectious complications: Arise against the background of pronounced secondary immunodeficiency (pyelonephritis, sepsis, furunculosis, tuberculosis develop).
• Cognitive impairment: Type 2 diabetes mellitus doubles the risk of developing dementia. In type 1 and a glycated hemoglobin (HbA1c) level above 7%, the risk of mild cognitive impairment increases instantly by 4 times. This is directly associated with cerebral microangiopathy and lacunar strokes.
• Complications of gestational diabetes: Gestosis, arterial hypertension, and polyhydramnios occur in the mother. Diabetic macrosomia (large fetus due to maternal hyperglycemia), high postnatal mortality, and diabetic embryopathy (risk of malformations increases 2-fold) are characteristic of the fetus.
• Mauriac syndrome: Specific for children with decompensated type 1 diabetes mellitus. It manifests as growth and sexual development retardation, moon face, fat deposition on the thighs, and hepatomegaly (due to secondary glycogenosis).

Class and exam questions

What else to study on this topic

• Morphological changes in diabetic retinopathy
• Pathogenesis of Kimmelstiel–Wilson syndrome
• Biochemistry of the polyol pathway of glucose metabolism
• Mönckeberg's mediacalcinosis and macroangiopathies
• Pathological anatomy of the diabetic foot
• Morphology of Mauriac syndrome in children

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.