Chronic hyperglycemia, associated with diabetes, leads to many ocular complications. The effects on the eye of rapidly correcting acute hyperglycemia, however, are less well appreciated.

A 59-year-old man with no prior history of diabetes presented to our hospital with several weeks of polyuria, polydipsia, and blurred vision. He had last seen an ophthalmologist 3 years previously when, in addition to his known hyperopia, he was diagnosed with bilateral cataracts; intraocular pressures (IOPs) were normal at that time, and corrected visual acuity was 20/50 in oculus dexter (OD) and 20/20 in oculus sinister (OS).

Laboratory data on presentation included 118 mmol/l serum sodium, 5.7 mmol/l potassium, 54 mg/dl BUN, 1.6 mg/dl creatinine, and a normal anion gap of 10. The serum glucose was 1,550 mg/dl. Calculated serum osmolality was 340 mosm/kg.

On physical examination, the subject was classified as overweight (BMI 37.4 kg/m2). He appeared dehydrated and was tachycardic with stable blood pressure. Conjunctiva were injected bilaterally without exudates, and extraocular movements were normal. The remainder of the physical examination was unremarkable.

A diagnosis of hyperglycemic hyperosmolar syndrome was made. The patient was hydrated with 3.5 l normal saline i.v. over the first 3 h. He then received 10 units regular human insulin i.v. and 10 units s.c. His plasma glucose levels decreased from 1,520 to 1,050 mg/dl over 5 h with intravenous hydration alone before falling precipitously from 1,050 to 322 mg/dl over the next hour following administration of insulin.

At that point, the patient began to complain of increasing pain OD with a right frontal headache. His right conjunctiva was now markedly injected, and his visual acuity was reduced OD with inability to count fingers. His visual acuity OS was close to the baseline of 20/25. IOPs were 59 mmHg OD and 35 mmHg OS, and a diagnosis of acute angle closure glaucoma was made. He was treated with timolol, brimonidine, dorzolamide, pilocarpine, and prednisolone eye-drops. Within 2 h, his IOP began to decrease to 51 mmHg OD and 21 mmHg OS. Oral Acetazolamide was begun. Two hours later, IOP fell further to 39 mmHg OD and 18 mmHg OS, and the patient’s eye pain improved. By the following morning, his IOP was within normal limits at 21 mmHg OD and 19 mmHg OS.

There are several putative mechanisms as to why hyperglycemia might contribute to angle closure glaucoma. The lens is freely permeable to glucose and does not require insulin for glucose penetration (1). Hyperglycemia leads to an increased level of glucose within the aqueous humor that in turn leads to elevated lens glucose levels. Aldose reductase within the lens converts the glucose to sorbitol, which increases lens hypertonicity, leading to water influx and lens swelling (2).

Although the lens is freely permeable to glucose, once acute hyperglycemia has been corrected, and normoglycemia restored, the osmotic changes within the lens do not immediately correct. Studies with amphibian lenses have not only shown significant changes in lens swelling during hyperglycemia but also further lens swelling when euglycemia is restored (3). This sequence, termed “double osmotic shock, ” is explained by the fact that as blood glucose levels normalize, further water is drawn into the lens by the differential level of glucose in the lens compared with the surrounding aqueous fluid. The enlarged lens can acutely obstruct the canal of Schlemm and lead to increased IOP.

Fortunately, acute angle closure glaucoma following rapid correction of acute hyperglycemia is exceedingly rare in clinical practice (4,5). Our case is remarkable because of the clear temporal relationship between development of acute eye pain and the rapid drop in plasma glucose levels. Clinicians should be aware of the potential to precipitate angle closure glaucoma during rapid correction of hyperglycemia.

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Sorokanich S, Wand M, Nix HR: Angle closure glaucoma and acute hyperglycemia.
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Arch Ophthalmol