Pyloric Stenosis
- Pyloric stenosis is a thickened, overgrown pylorus — the muscular valve at the stomach's exit — that slowly clamps the door shut.
- The classic patient is a young infant (often a few weeks old) with forceful, projectile, non-bile-stained vomiting who is hungry again right afterward.
- Ultrasound is the test. You're measuring a muscle: a thick wall and a long, narrow channel are the diagnosis.
- The two numbers people quote are a single-wall muscle thickness of roughly ≥3 mm and a channel length of roughly ≥15–17 mm — but treat these as soft thresholds, not magic.
- It's a fixable plumbing problem, not an emergency of the bowel itself — but the dehydration and electrolyte mess it causes are real and must be corrected first.
Imagine the exit from your stomach is a doorway, and the doorframe is a ring of muscle called the pylorus. In pyloric stenosis, that doorframe quietly hypertrophies — it bulks up like it's been doing curls — until the doorway it surrounds is squeezed down to a slit. Food goes in, food can't get out, and eventually it comes back the way it arrived. At speed.
Who gets it and why you'd suspect it
The textbook patient is an infant in the first weeks to couple of months of life, classically a firstborn boy, brought in because the milk keeps coming back up — and not in a gentle spit-up way. The hallmark is projectile vomiting: the kind that clears the changing table. Crucially, the vomit is non-bilious (no green), because the blockage sits above where bile enters the gut. The baby vomits, then immediately roots around looking for more, because the problem is mechanical, not a lack of appetite.
Bile is the tell. Bile is green-yellow and joins the party downstream of the stomach exit. Non-bilious vomiting points at a blockage at or above the pylorus, like this. Bilious (green) vomiting in a baby is a different, scarier conversation — it raises the specter of a downstream obstruction, which is a surgical emergency until proven otherwise.
On a good day a clinician can feel the thickened muscle as a firm "olive" in the upper abdomen, but bellies are squirmy and olives are shy, so we usually reach for imaging.
Why ultrasound owns this diagnosis
This is a muscle measurement problem, and ultrasound is perfect for it: no radiation, real-time, and it lets you literally watch the pylorus refuse to open while you measure its dimensions. You put the probe on the upper abdomen, find the pylorus, and ask two questions: how thick is the muscle wall, and how long is the channel it's squeezing?
The two numbers radiologists chase:
| What you measure | Roughly abnormal when | Plain-English version |
|---|---|---|
| Single muscle-wall thickness | ≥ 3 mm | The doorframe is too beefy. |
| Pyloric channel length | ≥ 15–17 mm | The squeezed tunnel is too long. |
Treat those as soft cutoffs, not commandments. Borderline measurements happen, premature and very young infants run a little smaller, and a single still image can lie. The real confidence comes from watching: in pyloric stenosis the channel stays clamped and almost nothing passes through, even when the stomach is contracting hard and clearly wants to empty.
A couple of word-pictures get thrown around for the appearance: a thick muscular ring with a thin central mucosal line can look like a target or doughnut in cross-section, and the elongated channel poking toward the duodenum gets called the cervix sign because it resembles a cervix. You don't need the nicknames to make the call — they're just memory hooks.
The detail that saves the baby
Here's the part that's easy to forget when you're excited about your beautiful pylorus measurement: the dangerous thing isn't the muscle, it's the chemistry.
Days of vomiting stomach contents strips out acid and chloride and dries the baby out. The classic derangement is a hypochloremic, hypokalemic metabolic alkalosis. Surgery is the cure for the pylorus, but you do not rush a dehydrated, alkalotic infant to the operating room. Fluids and electrolytes are fixed first; the operation can wait a few hours for the labs to look human again.
The fix itself is mechanical and satisfying: a surgeon splits the overgrown muscle (a pyloromyotomy), which releases the squeeze without cutting all the way through the lining. Doorframe relaxed, doorway reopened.
The traps and the lookalikes
The biggest trap is gastroesophageal reflux / overfeeding, which also produces a vomiting, fussy infant — but the muscle measurements are normal and you'll see stomach contents happily passing through the pylorus. Don't diagnose pyloric stenosis off the history alone. Also beware a stomach so distended with fluid that it shoves the pylorus backward out of view; decompress or reposition and try again rather than calling the study negative.
It's worth separating this clearly from the other classic pediatric "won't stop vomiting" entity: intussusception, where one segment of bowel telescopes into the next. Different age skew, different ultrasound look, different story — but both are reminders that in a vomiting infant, ultrasound is usually your fastest, kindest first move.
A young, hungry infant with forceful non-bilious projectile vomiting needs a pyloric ultrasound. You're measuring a muscle — thick wall, long channel, nothing passing through — and once you've made the call, the first priority is correcting the dehydration and the hypochloremic, hypokalemic metabolic alkalosis before anyone goes to surgery.