The vomited material does not contain bile because the pyloric obstruction prevents entry of duodenal contents (containing bile) into the stomach. The chloride loss results in a low blood chloride level which impairs the kidneys ability to excrete bicarbonate. This is the factor that prevents correction of the alkalosis leading to metabolic alkalosis.A secondary hyperaldosteronism develops due to the decreased blood volume. The high aldosterone levels causes the kidneys to avidly retain Na+ (to correct the intravascular volume depletion), and excrete increased amounts of K+ into the urine (resulting in a low blood level of potassium).The bodys compensatory response to the metabolic alkalosis is hypoventilation resulting in an elevated arterial pCO2. Diagnosis
Diagnosis is via a careful history and physical examination, often supplemented by radiographic imaging studies. Pyloric stenosis should be suspected in any young infant with severe vomiting. On physical exam, palpation of the abdomen may reveal a mass in the epigastrium. This mass, which consists of the enlarged pylorus, is referred to as the olive, and is sometimes evident after the infant is given formula to drink. Rarely, there are peristaltic waves that may be felt or seen (video on NEJM) due to the stomach trying to force its contents past the narrowed pyloric outlet.Most cases of pyloric stenosis are diagnosed/confirmed with ultrasound, if available, showing the thickened pylorus and non-passage of gastric contents into the proximal duodenum. Muscle wall thickness 3 millimeters (mm) or greater and pyloric channel length of 15 mm or greater are considered abnormal in infants younger than 30 days.
A two-month course of antibiotics such as ciprofloxacin, levofloxacin and doxycycline after exposure can also prevent infection. If infection occurs, treatment is with antibiotics and possibly antitoxin. The type and number of antibiotics used depend on the type of infection. Antitoxin is recommended for those with widespread infection.A rare disease, human anthrax is most common in Africa and central and southern Asia. It also occurs more regularly in Southern Europe than elsewhere on the continent and is uncommon in Northern Europe and North America. Globally, at least 2,000 cases occur a year, with about two cases a year in the United States. Skin infections represent more than 95% of cases. Without treatment the risk of death from skin anthrax is 23.7%. For intestinal infection the risk of death is 25 to 75%, while respiratory anthrax has a mortality of 50 to 80%, even with treatment. Until the 20th century anthrax infections killed hundreds of thousands of people and animals each year. Anthrax has been developed as a weapon by a number of countries. In herbivorous animals infection occurs when they eat or breathe in the spores while grazing. Animals may become infected by killing and/or eating infected animals. Etymology
The English name comes from anthrax (ἄνθραξ), the Greek word for coal, possibly having Egyptian etymology, because of the characteristic black skin lesions developed by people with a cutaneous anthrax infection. The central black eschar surrounded by vivid red skin has long been recognised as typical of the disease.