Skip to content
Home » Cause

Cause

Quite simply, colicky crying is an infant’s expression of distress caused by abdominal pain, which in turn is caused by distention of the baby’s intestine. What went in is having trouble getting out. The crying is often accompanied by grunting, turning blue or red in the face and flailing movements of the arms and legs.

So, why the pain? The large and small intestine are supplied by autonomic nerve fibers which do not register pain from pinprick, temperature change or vibration. These structures only register pain from stretching or distention. A baby’s colicky pain, crying and inconsolable behavior are caused by stretching of the baby’s large intestine by the contents from eating, and that baby poop not being able to get out freely. Mothers typically note decreased amounts of stool being passed in colicky babies, despite continued good feeding. Why? There can be a functional blockage at the lowest end of the gastrointestinal tract – the ano-rectal canal. We’ve noted that more-liquid stool material may be able to get past the partial obstruction, causing the false impression of diarrhea, and leading to prescription of an anti-spasmodic medications, which may provide partial and temporary relief, but do nothing to relieve the actual cause. The grunting and face turning red or blue in colicky infants signals their discomfort, as the intended full bowel movement cannot happen.

At the end of Dr. Morris Wessel’s original article on colicky infants’ crying behavior, he suggested that there must be a physiological cause for their pain. I had the pleasure of a phone conversation with Dr. Wessel in the early 1990’s and told him of my findings and proposed causes of blockage of the ano-rectal canal. His response: “I was that close…” I agreed. He replied, “I’ll be doing more rectals from now on.”

Embryology textbooks have been detailing this story since the 1960’s. A new human being has formed from two cells (the mother’s egg and the father’s sperm) and grown to the size of a raspberry by the 6th week after conception. At this point, a tubular primitive intestinal structure called the hindgut has developed. This hindgut – the primitive rectum – moves downward toward the bottom of the torso. Simultaneously, an anal pit forms in the skin of the baby’s butt, pushing inward and upward. These two tubular structures then meet and fuse together at a point called the dentate or pectinate line. To picture this, imagine having two index fingers in separate balloons, then bringing the finger tips together, touching each other. No matter how hard you push your two fingers together, the two layers of rubber are still there. Similarly, after fusion, the ano-rectal canal is completely blocked by skin cells. By the 9th week after conception, enough skin cells have normally been reabsorbed to establish an opening, allowing eventual outward passage of stool, liquid and gas from the products of digestion. BUT – the amount of skin cell reabsorption is variable and can leave a residual membrane that varies in thickness and size of opening. This helps to explain the wide range of symptoms in colicky babies, and the lack of “a typical case” of colic.

That’s one cause: the residual membrane. In my correspondence with Anatomist and Embryologist Edmund S. Crelin, D.Sc. from Yale’s medical school faculty, he likened it to a “rectal hymen,” similar to the vaginal hymen, which is formed in parallel fashion in the neighboring vaginal canal in females. Dr. Bouisson (1851) made similar deductions from post-mortem (autopsy) examinations of infants who had not survived, long before formal embryological research was possible. The colo-rectal surgeons refer to this as “Grade I-a Rectal Stenosis” and consider it a curable form of “defect” – if detected in a timely fashion, shortly after birth.

Let’s discuss the second cause. I was puzzled for a number of years. Not all colicky infants I examined had a membrane. Yet the rectal examination was difficult because of the narrowed and tight ano-rectal canal. As I learned through further reading in colo-rectal surgery textbooks, this second type of blockage can be caused by an overly-constricted or enlarged (“hypertrophied” in medical terminology) internal anal sphincter muscle. This muscle is a downward growth extension of the middle muscular layer of the newly-developed rectum. It normally grows down to a level just below the skin of the butt and forms a protective ring around the ano-rectal canal, preventing leakage of stool, liquid or gas between bowel movements. The internal anal sphincter muscle is under continuous stimulation by the autonomic (“automatic”) nervous system and normally serves as a barrier to the unintentional exit of rectal contents. Normal infants have normal amounts of sphincter muscle tone and mass, but colicky babies have distinctly more tone or muscle mass, and present notably more resistance pressure to digital rectal examination (DRE). Our colleagues in colo-rectal surgery use the Krickenbeck Classification (2005) to label this “Type I-b Anal Stenosis,” the mildest form of ARM (ano-rectal malformation). Barbara has a knack for analogies; she has likened this problem to the neck of a brand-new balloon that hasn’t been blown up and stretched yet. Each successive inflation becomes easier. We’ve found this to be true in colicky infants as well – when they are properly treated.

So, to re-state the two most common causes of ano-rectal partial obstruction: 1) a variable, partial blockage by a variably-thick membrane with a variably-sized opening that is formed from skin cells at the juncture where the end of the colon on the inside meets the skin from the outside of the embryo, or 2) functional tightness of the ano-rectal canal from an overly-constricted or enlarged internal anal sphincter muscle.

The newborn physical examination checks every other opening (ears, mouth, nose), but if meconium has passed, the anal canal is typically not examined. Yet when a digital rectal exam (DRE) is carefully performed with a gloved and lubricated pinky finger, this tightness or partial blockage can easily be felt. During my examination of infants’ ano-rectal canals, beginning in 1973, I have noted a vast difference between normal ano-rectal canals and those of babies with constipative colic. I have come to characterize abnormal infant ano-rectal canals as mild, moderate or severe in tightness or stricture. Given the two types of partial blockage (membrane or muscular tension/mass), and three grades of severity, this would provide at least six general degrees of blockage, again adding to the variable nature of constipative colic behavior in the affected infant.

Another common question is, why does colicky behavior start around the third week of life? Most observers believe it is because by that age enough baby’s stool (poop) has accumulated to begin to be obstructed by the “dam” at the bottom of the colon, causing that painful stretching of the large intestine. If the partial blockage is not relieved, the backup can extend upward in the intestines, ultimately causing the stomach to vomit (commonly referred to as “GERD” or gastro-esophageal reflux disorder).

And why does the fussiness get worse through the day, peaking in late afternoon or early evening? That’s harder to answer, but Dr. Morris Wessel found that colicky babies cry almost all day and night by the time they’re a month old! We call it constipative colic simply because the infant has trouble pushing the early stool through the narrow or partially occluded ano-rectal anal. The baby looks and acts “constipated,” and in most cases, is constipated. Again, our colleagues in color-rectal surgery advise early detection and correction of even mild cases of rectal stenosis to prevent major problems developing as the baby grows.

Additional documentation and stories relating to CAUSE are available in the two books below. Clicking on them will take you to Amazon/Kindle for review or purchase.