The longitudinal muscle is both the leading character of this book and the
villain of the piece. It would seem that, on the whole, we might be better off
without it. There are no maladies (other than livestock bloat) that can be blamed
on a non-functional LM. It is, however, necessary for belching, vomiting and
gagging and provides an assist in swallowing, particularly with solid food.
Vector resolution of its force by the PEL opens the sphincter. A solitary hiccup
is the mechanical equivalent of a sharp contraction of the LM and has the same
sphincter-opening effect. Taking the LM into consideration doubles the number
of esophageal muscle states, vastly increasing its repertory of sequential operations.
On the debit side, LM hyper function leads to reflux and hiatal transtraction
of the fundus. The latter can lead to chronic blood loss, anaemia and achlorhydria
as well as rupture of the phrenoesophageal ligament. Reflux of acid/pepsin damages
the mucosa of the esophagus, hypopharynx and tongue. It can destroy the teeth
and cause angular stomatitis. Together these mechanisms produce all the features
of Plummer-Vinson syndrome.
An incarcerated transtraction causes obstruction and leads to "achalasia,"
EMDs and "idiopathic diffuse muscular hypertrophy." At a minimum LM tension
produces the "gas/bloat" symptom in adults - colic in babies.
Longitudinal muscle tension stresses its proximal attachments as much as those
to the diaphragm. This results in Zenker's diverticula and/or the hypopharyngeal
disruption that masquerades as "cricopharyngeal spasm."
There are serious doubts about the validity of the postulated metaplasia
of Barrett's esophagus. The appearances can be better explained by esophageal
Two questions remain to be pursued: (1.) What makes the LM hyper-function and (2.) What can be done about it.
On the first question I have some clues. One of them is the dramatic postpartum
relief of the heartburn, nausea and vomiting of pregnancy - not due to pressure
of the gravid uterus on the diaphragm as is usually supposed. Progesterone is
surely the cause as it also produces pyrosis in patients on birth control pills.
A search of the literature, unfortunately, reveals no studies of the effect
of progesterone on the LM.
There are also hormones of intestinal origin that could affect the LM, particularly
CCK and secretin. Fats entering the duodenum trigger CCK secretion triggering
smooth muscle contraction in the GB to inject emulsifying bile into the duodenum.
The systemic release of CCK may have the side effect of stimulating the LM.
This would explain the paradox of soothing oils causing esophageal irritation;
why the third helping of turkey dressing causes heartburn.
Patients with pyrosis are often greatly improved by cholecystectomy. The connection
warrants looking into. The gallbladder requires CCK to contract. How does make
its requirements known to the duodenum? Does it have a neuronal path or does
it produce a duodenum stimulating hormone (DSH)? If so a diseased GB could stimulate
overproduction of CCK or another intestinal hormone thus overstimulating the
LM, opening the sphincter, and so on. Removal of the GB might break this chain.
A related clue is the fact that nearly everyone with reflux has duodenitis.
My subjective statistic is 80-90%. We know that the duodenum is the source of
intestinal hormones. Are duodenal hormones produced in excess when the duodenal
mucosa is inflamed - in the same way that H. pylori infections of the
antrum cause hypergastrinemia? If so, then H. pylori may be a culprit.
Its treatment is becoming well known and better drugs are around the corner.
The problem of treatment, therefore, seems more endocrinological than surgical. Unfortunately nothing is known about the effects of these hormones on the LM. Investigators have been concentrating their effects on the sphincter.
I believe the rationale of most operations on either end of the esophagus is
wrong. It's not the mythical angle of His or a subphrenic esophagus that inhibits
reflux. It is the sphincter. The mechanics of vector resolution are such that
anything that destroys the PEL destroys one of the two things involved in opening
the sphincter. Many operations succeed because they fail, inadvertently destroying
the PEL in the process. A direct attack on the PEL might be indicated. There
are worse things than a type III "hernia."
The treatment of "achalasia," EMDs and "idiopathic diffuse hypertrophy" should
be reduction of the incarcerated fundus and enlargement of the hiatus. This
might even be done endoscopically by incising the hiatal ring. Stretching the
hiatus helps but the effect may not be permanent. Muscle splitting is irrational
and can cause epiphrenic diverticula.
The technical aspects of reconstructing the proximal attachments of the esophagus would be formidable but would make more sense than doing further damage by resecting a "bar."
Last Updated July 31 2007 by David PJ Stiennon