The differential diagnosis list includes glycogenoses types III and VI, fructose 1,6-bisphosphatase deficiency, and a few other conditions (page 5), but none are likely to produce all of the features of GSD I. The next step is usually a carefully monitored fast. Hypoglycemia often occurs within six hours. A critical blood specimen obtained at the time of hypoglycemia typically reveals a mild metabolic acidosis, high free fatty acids and  beta-hydroxybutyrate, very low insulin levels, and high levels of glucagon, cortisol, and growth hormone. Administration of intramuscular or intravenous glucagon (0.25 to 1 mg, depending on age) or epinephrine produces little rise of blood sugar. The diagnosis is definitively confirmed by liver biopsy with electron microscopy and assay of glucose-6-phosphatase activity in the tissue and/or specific gene testing, available in recent years. Treatment
The primary treatment goal is prevention of hypoglycemia and the secondary metabolic derangements by frequent feedings of foods high in glucose or starch (which is readily digested to glucose). To compensate for the inability of the liver to provide sugar, the total amount of dietary carbohydrate should approximate the 24-hour glucose production rate. The diet should contain approximately 65–70% carbohydrate, 10–15% protein, and 20–25% fat. At least a third of the carbohydrates should be supplied through the night, so that a young child goes no more than 3–4 hours without carbohydrate intake. Once a diagnosis is made, the priority in GSD I treatment is to maintain an adequate blood glucose.
In the case of macropsia, the greater density of photoreceptor cells leads to greater stimulation making the object seem larger. In some cases, the effects of macropsia have been shown to be field dependent, in that the degree of visual distortion is related to the visual field angle. Non-uniform stretching or compression of the receptor distribution could explain the field dependency of the macropsia. If the compression forces were closer to the fovea the resulting compression would cause a greater amount of macropsia at lower field angles with little effect at higher field angles where the receptor distribution is not as compressed. Alterations in receptor distribution can be the result of epiretinal membrane, neuroretina detachment and/or re-attachment, or retinoschisis. Macropsia caused by surgical re-attachment of macula-off rhegmatogenous retinal detachment is not symmetrical around the fovea, resulting in differences size changes in the horizontal and vertical meridians. Asymmetry has also been observed with retinoschisis, in which macropsia generally results in the vertical direction while micropsia presents in the horizontal direction. Diagnosis
Macropsia is generally diagnosed once a patient complains of the characteristic symptoms, such as disproportionally large objects in their visual field. The Amsler Grid test can be used to diagnose macropsia, along with other visual maladies depending on the subjective disturbance reported by the patient after looking at the Amsler Grid. Outward bulging of the lines on an Amsler Grid is consistent with patients experiencing macropsisa. The New Aniseikonia Test (NAT) can quantify the degree of macropsia or micropsia independently in the vertical and horizontal meridians.