Often, the optic nerve shows an abnormal amount of cupping.If treated early, it is possible to slow or stop the progression of disease with medication, laser treatment, or surgery. The goal of these treatments is to decrease eye pressure. A number of different classes of glaucoma medication are available. Laser treatments may be effective in both open-angle and closed-angle glaucoma. A number of types of glaucoma surgeries may be used in people who do not respond sufficiently to other measures. Treatment of closed-angle glaucoma is a medical emergency.About 70 million people have glaucoma globally, with about two million patients in the United States. It is the leading cause of blindness in African Americans. It occurs more commonly among older people, and closed-angle glaucoma is more common in women. Glaucoma has been called the "silent thief of sight", because the loss of vision usually occurs slowly over a long period of time. Worldwide, glaucoma is the second-leading cause of blindness after cataracts. Cataracts caused 51% of blindness in 2010, while glaucoma caused 8%. The word "glaucoma" is from the Ancient Greek glaukos, which means "shimmering." In English, the word was used as early as 1587 but did not become commonly used until after 1850, when the development of the ophthalmoscope allowed doctors to see the optic nerve damage. Signs and symptoms
As open-angle glaucoma is usually painless with no symptoms early in the disease process, screening through regular eye exams is important.
Pathophysiology
Cold agglutinins, or cold autoantibodies, occur naturally in nearly all individuals. These natural cold autoantibodies occur at low titers, less than 1:64 measured at 4 °C, and have no activity at higher temperatures. Pathologic cold agglutinins occur at titers over 1:1000 and react at 28-31 °C and sometimes at 37 °C. Cold agglutinin disease usually results from the production of a specific IgM antibody directed against the I/i antigens (precursors of the ABH and Lewis blood group substances) on red blood cells (RBCs). Cold agglutinins commonly have variable heavy-chain regions encoded by VH, with a distinct idiotype identified by the 9G4 rat murine monoclonal antibody. Diagnosis
Classification
AIHA can be classified as warm autoimmune hemolytic anemia  or cold autoimmune hemolytic anemia, which includes cold agglutinin disease and paroxysmal cold hemoglobinuria. These classifications are based on the characteristics of the autoantibodies involved in the pathogenesis of the disease. Each has a different underlying cause, management, and prognosis, making classification important when treating a patient with AIHA. Autoimmune hemolytic anemiaWarm-antibody typePrimary
Secondary  (lymphoproliferative disorders, autoimmune disorders) : 259 Cold-antibody type (anemia)Primary cold agglutinin disease
Secondary cold agglutinin syndromeAssociated with malignant disease
Acute, transient, infection-associated  (acute cold antibody mediated AIHA complicating Mycoplasma pneumoniae or viral infections )
Chronic (lymphoproliferative disorders) : 259 Paroxysmal cold hemoglobinuria: 259 Idiopathic
SecondaryAcute, transient (Infections other than syphilis): 259 
Chronic (syphilis): 259 Mixed cold- and warm-antibody typeIdiopathic
Secondary (lymphoproliferative disorders, autoimmune disorders) Drug-induced immune hemolytic anemia : 259 Autoimmune type
Drug absorption type
Neoantigen type

Treatment
Cold agglutinin disease may be managed successfully using protective measures (clothing) alone in most cases. Special protective clothing is sometimes necessary in extreme cases.