Pupillendilatation

Pupillendilatation, or pupil dilation, is the enlargement of the pupil due to widening of the iris’ radial dilator muscle. It occurs primarily through sympathetic stimulation but can also be produced pharmacologically or by certain disease processes.

The size of the pupil is controlled by two antagonistic muscles: the sphincter pupillae, which constricts the pupil under parasympathetic control, and the dilator pupillae, which enlarges it under sympathetic control. The sympathetic pathway originates in the hypothalamus, travels down the spinal cord, exits at the superior cervical ganglion, and reaches the iris by the long ciliary nerves. In low light or during arousal, this pathway promotes dilation to allow more light entry and enhance vision.

Causes of pupillary dilation can be classified as physiologic, pharmacologic, or pathologic. Physiologic dilation occurs in dim environments or with heightened arousal. Pharmacologic dilation results from topical mydriatic agents (for example, tropicamide, phenylephrine) used during eye examinations or from systemic anticholinergic or sympathomimetic drugs. Pathologic dilation may arise from disorders affecting the autonomic or ocular nervous system, such as Adie’s tonic pupil, oculosympathetic palsy, third nerve palsy, or intracranial processes that impair pupillary reflexes.

Clinical evaluation focuses on pupil size, symmetry, and reactivity to light. A new, unilateral fixed dilated pupil with poor light response is a red flag that may indicate critical intracranial pathology and requires urgent assessment. Bilateral persistent dilation often reflects pharmacologic effects or systemic autonomic dysfunction.

Management targets the underlying cause. In ophthalmology, dilation is deliberately induced for examinations, while in acute care, rapid diagnosis and treatment of potential neurological or systemic etiologies are essential.