Gastric atresia is a congenital defect with complete occlusion of the pyloric outlet of the stomach. Cause
Gastric atresia is a birth defect. It can be genetic, inherited in an autosomal recessive manner, and associated with conditions like Down syndrome and junctional epidermolysis bullosa (medicine). In about 60% of cases, the outlet of the stomach is covered by a membrane. In around 35% of cases, solid tissue blocks the outlet. In the remaining cases (less than 10%), there is a complete separation of the stomach and the small intestine. Diagnosis
Polyhydramnios is often seen during pregnancy, and prenatal diagnosis is common. Infants with gastric atresia will exhibit forceful vomiting upon the first feeding. Imaging is required for diagnosis. Treatment
Treatment is surgical and involves removing or bypassing the obstruction. Epidemiology
It is seen in approximately 1 in 100,000 live births. == References ==
Treatment
Non-surgical
Early treatment for mild cases of hallux rigidus may include prescription foot orthotics, shoe modifications (such as a pad under the joint, and/or a deeper toe box to take the pressure off the toe and/or facilitate walking), specialized footwear (rocker-sole shoes), medications (anti-inflammatory drugs) or injection therapy (corticosteroids to reduce inflammation and pain). Physical therapy programs may be recommended, although there is very limited evidence that they provide benefit for reducing pain and improving function of the joint. Surgical
The goal of surgery is to eliminate or reduce pain. There are several types of surgery for treatment of hallux rigidus. The type of surgery is based on the stage of hallux rigidus. According to the Coughlin and Shurnas Clinical Radiographic Scale:Stage 1 hallux rigidus involves some loss of range of motion of the big toe joint or first MTP joint and is often treated conservatively with prescription foot orthotics. Stage 2 hallux rigidus involves greater loss of range of motion and cartilage and may be treated via cheilectomy in which the metatarsal head is reshaped and bone spurs reduced. Stage 3 hallux rigidus often involves significant cartilage loss and may be treated by an osteotomy in which cartilage on the first metatarsal head is repositioned, possibly coupled with a hemi-implant in which the base of the proximal phalanx (base of the big toe) is resurfaced. Stage 4 hallux rigidus, also known as end stage hallux rigidus, involves severe loss of range of motion of the big toe joint and cartilage loss.