Page created on February 3, 2019. Last updated on May 15, 2020 at 17:04
Pyloric stenosis is a condition that is mostly seen in paediatrics. It occurs secondarily to hypertrophy and hyperplasia of the muscular layers of the pylorus, the most distal part of the stomach. This impairs emptying of the stomach contents into the duodenum. In advanced cases can the stomach become dilated due to the obstruction.
Symptoms include colicky pain and projectile vomiting, which may cause exsiccosis in severe cases. The vomit will not contain any bile, which can give suspicion of pyloric stenosis. Starvation is also a possibility.
A small side note: Vomiting is, by definition, the forceful throwing up of stomach contents due to increased intraabdominal and intragastric pressure. If it occurs forcibly can the vomiting be classified as “projectile” vomiting. Babies usually don’t vomit this way – they simply spit up some milk without any significant increase in pressure. Projectile vomiting in babies should always give suspicion that something is wrong.
The cause of pyloric stenosis in infants is multifactorial. There are some genetic factors involving abnormal innervation and other things, and some environmental factors like exposure to macrolide antibiotics like erythromycin.
In adults can it occur due to tumors, scar-forming peptic ulcers, or due to drugs or alcohol effects. Drugs and alcohol may give transient pyloric spasms.
The treatment for infantile pyloric stenosis is surgery in severe cases, however many cases are self-limiting.
Gastric atonia, more commonly known as gastroparesis, occurs when the muscles in the stomach are paralyzed. It occurs most frequently due to autonomic neuropathy, often due to diabetes or uraemia, but it can also occur after abdominal surgery. It corresponds to a very proximal type of paralytic ileus.
The atony impairs mixing and peristaltic movements and because of this the stomach can neither empty its content toward the gut or backwards through vomiting. The passive stretch of the wall therefore increases, which stimulates secretion of gastric juices. The stomach volume increases rapidly causing more stretching and secretion. Since the plasma is the only source of the secreted gastric juices rapid exsiccosis and/or hypovolemic shock develops.
Dumping syndrome is a condition where gastric emptying occurs too early. The most common cause is surgical gastroenteric anastomosis (gastric bypass). There are two types: early dumping syndrome and late dumping syndrome, depending on how long after eating the symptoms occur. Some people have both forms.
Most people with dumping syndrome have symptoms 30 – 60 minutes after eating, meaning that early dumping syndrome is the most common type. 30 – 60 minutes after eating is all the ingested food emptied into the duodenum, which causes the duodenum to stretch significantly. This causes large secretions into the lumen. Osmotically active particles in the food can’t be absorbed, meaning that they remain in the lumen and pull even more fluid from the intestines. The extreme secretion leads to hypovolaemia and light-headedness. The large amount of fluid and osmotically active particles often leads to watery diarrhoea, but in some cases the fluid may be absorbed in more distal portion of the gut causing symptoms to dissapear spontaneously.
People with late dumping syndrome don’t experience the early symptoms, but rather have a different set of symptoms that occur after 1 – 3 hours after eating. Excessive gastric emptying causes a rapid absorption of sugar in the intestines. This stimulates β-cells which causes a peak in insulin levels. The sugar absorption doesn’t last long so the high insulin levels lead to hypoglycaemia with symptoms like sweating, fatigue and palpitations.