Complications of Diabetes Mellitus

Diabetic ketoacidosis (DKA) is an acute complication characterized by hyperglycemia, ketonemia, and metabolic acidosis. It occurs primarily in type 1 diabetes due to severe insulin deficiency but can develop in type 2 diabetes during metabolic stress such as infection or missed insulin doses. DKA requires immediate medical attention.

Hyperosmolar hyperglycemic state (HHS) primarily affects type 2 diabetes and features extreme hyperglycemia with high plasma osmolality but minimal or absent ketosis. Unlike DKA, HHS develops more gradually and is often triggered by infections or poor glucose control during acute illness. Both are serious acute complications requiring urgent treatment.

Hypoglycemia (blood glucose below 70 mg/dL) is a treatment complication occurring primarily with insulin or insulin secretagogues. Symptoms include shakiness, confusion, and diaphoresis; severe cases may cause seizures or coma. It is more common in type 1 diabetes but can develop in type 2 diabetes, requiring immediate glucose administration.

Macrovascular complications affect large blood vessels, increasing risk of coronary artery disease, stroke, and peripheral arterial disease. Contributing factors include hypertension, dyslipidemia, obesity, smoking, and inactivity. These complications can lead to amputations and are among the most serious long-term consequences of sustained hyperglycemia.

Prolonged hyperglycemia causes microvascular complications affecting small blood vessels, resulting in diabetic retinopathy (vision loss), diabetic nephropathy (albuminuria and kidney failure), and diabetic neuropathy (sensory loss). Neuropathy increases ulcer and infection risk. These complications develop gradually but significantly impact quality of life and organ function.

Hyperglycemia impairs immune function, increasing susceptibility to infections including urinary tract infections and candidiasis. Elevated glucose also delays wound healing by disrupting normal inflammatory and tissue repair processes. Combined with neuropathy and vascular disease, these effects predispose diabetic patients to diabetic foot ulcer formation and serious complications.

Sustained hyperglycemia disrupts metabolic homeostasis, leading to both acute complications like DKA and chronic vascular damage. It increases infection risk, impairs wound healing, and damages both large and small blood vessels. Skin changes including diabetic dermopathy and acanthosis nigricans also occur. These effects collectively increase morbidity and mortality across multiple organ systems.