Pacific Cataract and Laser Institute optometrists Brooks Alldredge, OD, and Kerri Norris, OD, FAAO, discuss comanagement of cataract, refractive, glaucoma and corneal surgical cases, including surgical concepts and postoperative complications. The authors report no financial disclosures.

BLOG: A guide to postop ocular hypertension

It’s not unusual for us to have more than three dozen patients on our schedules the morning after a typical cataract surgery day. Because the vast majority are doing well 1 day postop, these are usually brief examinations.

The most frequent patient concerns – a swollen eyelid, a dry or swollen cornea, a few flickering lights to the side – can be addressed quickly with a smile and reassurance; they will almost always resolve with time and on their own.

Probably the most common adverse event seen early in the postop period that requires some form of treatment is ocular hypertension. Having a strategy on when and how to treat it can help avoid the rare but real complication of optic nerve damage and vision loss.

On average, IOP is about 3 mm Hg higher the day after surgery. While the incidence of postop ocular hypertension varies depending on the experience of the surgeon as well as the definition of elevated pressure, studies have found around a 12% to 15 % incidence of IOP equal to or above 26 mm Hg 1 day after cataract surgery. The percentage of those with pressures higher than 40 mm Hg at 1 day has been reported at more than 2% (Kim et al.). If you see enough postops at 1 day, you will occasionally encounter a very high pressure.

Cause of increased pressure

So why is the pressure high? Several mechanisms have been proposed, some of which make more sense than others. The catchall term “inflammation” is given as a one explanation, yet high postop IOP frequently doesn’t correlate with the number of anterior chamber cells. Furthermore, IOP is usually lower in anterior uveitis, not higher. so the physical clogging of the trabecular meshwork by inflammatory cells or fibrin leading to a decrease in aqueous outflow isn’t by itself a convincing explanation.

An explanation that does make sense is that phacoemulsification causes trauma to the trabecular endothelium and a subsequent decrease of aqueous outflow. We see a similar dramatic rise in IOP with few anterior chamber cells in patients with trabeculitis from Posner-Schlossman syndrome. If the vibration from phacoemulsification can lead to a temporary shock and inflammation of the corneal endothelium and subsequent transient corneal stromal edema, it makes sense that it could also lead to the same temporary loss of function in the trabecular endothelium as well.