Ideas About Colic

A treatise….

Constipative Colic: Cause and Cure
David Lyman Sharp, M.D.
Board Certified Family Physician
Grand Rapids, Michigan, 49505, USA

CONTENTS:
Summary
Introduction
Etiology, Distribution and Clinical Expression
Making the Connection: Clinical Application of Embryology
A Brief Physiology of Infant Digestion
Pathophysiology and Clinical Presentation of Colic
Resolution of Colic
Social Considerations and Associated Conditions
Clinical Management of Constipative Colic
Discomfort and Anesthesia
Aftercare
Indicated Studies
A Few More Questions
Final Thoughts

March 12, 2002; minor editing and updating March 5, 2008

To Whom It May Concern: This paper is a semi-formal description of my personal professional experiences with infant colic since 1972, with elaboration of my current insights into embryological origins, pathophysiology and treatment of what we refer to as "infant colic." Given my current understanding, this condition might better be called CONSTIPATIVE COLIC, in order to differentiate it from other conditions that lead to infant distress.

"If you've taken a good history and are still not sure of what is ailing the patient, go back and take another history." Sir William Osler

"Everything important that I know, I learned from my patients." Author unknown

SUMMARY
During the fifth to eighth weeks of gestation, the embryonic gut undergoes several developmental stages that can result in variable rectal stenosis in the newborn infant, and in extreme cases, imperforate anus. This narrowing at the pectinate line (with or without a rectal membrane) can cause greatly-varying degrees of clinical obstipation and constipation that become evident by one to three weeks after birth, resulting in the multiple expressions of abdominal discomfort observed in colicky infants. A digital rectal examination (DRE) can detect this rectal stenosis and by its very performance, dilate the stenosis and offer definitive relief of constipative colic. If the DRE is done soon after birth, constipative colic is extremely unlikely to ever develop.

INTRODUCTION
Colic has been a problem throughout recorded history. It has equally affected infant girls and boys in all civilizations and in all races. In recent times, colic has been variously attributed to milk or formula deficiencies or allergy, to an immature nervous system and to improper parenting techniques. Dr. Morris Wessel has quantitated colic crying, and defined it as: "…paroxysms of irritability, fussing or crying lasting for a total of more than three hours a day and occurring on more than three days in any one week." Investigators have performed spectrographic analyses of crying babies, and have determined that the crying was not identical to pain, but similar. Many other theories have been advanced, including neurologic and intestinal immaturity. The current fad seems to favor "gastroesophageal reflux" with a host of diagnostic and therapeutic suggestions. None of these theories, however, addresses the known embryological origins or the distribution of clinical expression that we see in infantile colic.

ETIOLOGY, DISTRIBUTION AND CLINICAL EXPRESSION
Colic is so universally distributed because it is a developmental variable that has been well described in the embryological literature since at least 1969. Between the fifth and eighth weeks after conception, the developing hindgut (of entodermal origin) migrates toward the proctodeum (of ectodermal origin). The proctodeum becomes the rectal pit, and the urogenital sinus and anus are fully formed from the entoderm by the eighth week following conception. Even earlier, in 1961, E.S. Crelin, Ph.D., D.Sc. wrote: "The lumen of the rectum, during its early stages of development, is occluded by a proliferation of epithelial cells and is later recanalized. Partial or complete failure of the lumen to recanalize results in rectal stenosis or atresia. [In the extreme case - about one in every 5000 births] - if the union fails to take place between the rectum and the proctodeal depression, an imperforate anus is the result." Consider that all infants in all world cultures have traveled this same developmental pathway, and that the degree of recanalization is individualized, perhaps by genetic predisposition or by random chance, or by a combination of these two, or even by other unknown factors. One can now place all babies along a continuum between full recanalization (completely normal) and the opposite extreme of an imperforate anus, and one quickly realizes that there would result many clinical expressions and degrees of rectal "blocking" which will result in a varying degree of outlet obstruction at the rectal/anal level and a variable degree of "constipative colic," a term I would propose to explain infant behavior resulting from a varying degree of outlet obstruction at the rectal/anal level of the gut. Thus, there is no reason to suspect a distribution other than random. This seems to be borne out by epidemiological studies of colic incidence.
My own clinical experience with constipative colic dates back to 1972. I would like to relate this sentinel case in a "story" format:

I was in my third year of practice following a Family Practice residency and was serving as a volunteer camp physician at Saranac Village, a Young Life camp in upstate New York. I was asked to make a "cabin-call" on a young mother who was having back pain. I saw her that afternoon, and it was immediately evident why she was having back pain. She was contorted in an overstuffed chair with her infant son nursing in a position essentially behind and below her right breast. She explained that this was the only position in which he would nurse without crying. He was about three weeks old and seemed otherwise healthy. She explained that she had experienced a normal delivery and that early breast-feeding had been uneventful. But her son had become progressively fussier since about one week of age, particularly after feedings. He would draw his legs up onto his abdomen, turn red in the face and cry and grunt, swinging his arms almost angrily. Despite these protestations and efforts on his part, progressively smaller amounts of stool were being passed as the weeks had evolved. He would also fuss more easily with each feeding, and in trial and error fashion, she had found this contorted position to be the one which resulted in the least fussing, though it certainly did not relieve the problem completely. I examined the baby on the dining room table. His lungs were clear and no heart murmurs were appreciated. I did find his abdomen to be somewhat tense and mildly distended. His kidneys were not palpable, as they ordinarily would be. It sounded like he was constipated. I thought a rectal exam might help explain what was going on and left briefly to obtain a glove and some water-soluble lubricant. His rectum was very tight and admitted my pinky finger only with considerable difficulty. Upon removing my finger, the stool, which had obviously been under considerable pressure, erupted (for lack of a better term!) about three to four feet off the end of the table. "Well," I said, shocked by the result of my innocent examination, "I guess he had to go." The mother agreed. The next morning I was greeted in the dining hall with a hug. The mother reported, "He's better, and so's my back." Okay, tuck that one away under the growing file of things I've learned from my patients. I returned home, and shortly thereafter delivered a baby who became fussy at three weeks of age, following a normal two-week checkup. Remembering the first case, I asked the mother to bring him in, and again noted a normal baby - except for the fussiness, mild general irritability and history of decreasing stool frequency and amount. Again I performed a digital rectal examination, and again noted the tightness and resistance to examination. This time the poop only shot out about a foot. But again, the baby was completely relieved and quickly returned to the normal eat-poop-sleep cycle of the newborn. I was slowly becoming experienced in the strange new world of constipative colic.

Over the next ten years, still doing obstetrics as part of my family practice, I performed DRE's only on the fussing babies, and never had occasion to examine normal children's rectal canals. At that point, I became very curious what the normal baby's rectum was like. With parental consent and foreknowledge of what I was seeking, several newborns were examined, all with the same results: I encountered a slight amount of sphincter tone and then the normal open area of the rectal ampulla.
In 1986 we followed our oldest child and only daughter to Michigan. She had matriculated at Hope College in Holland, Michigan and we were taken with the state and its people, and moved to Grand Rapids, Michigan. At one point I had occasion to discuss my findings with two colo-rectal surgeons from the world-renowned Ferguson Institute [of colo-rectal surgery and digestive problems], who reassured me that the normal newborn anus was capable of considerable dilation and would not be harmed by digital examination. Nonetheless, I continued to use my pinkie (which proved to measure 2.5 cm. in diameter) for DRE. Over time, it appeared that about half of the cases of constipative colic had what felt like a membrane across the rectum at about the level of the pectinate line. I went to the library and did some research. I encountered the work of Dr. Edmund S. Crelin in the Ciba Clinical Symposium series and in the large Ciba volumes that I had purchased a number of years earlier. Dr. Crelin and I corresponded, and he confirmed my suspicion of a "rectal hymen." Dr. Crelin expressed the thought that:
"the constriction [that I had noted on my exams of colicky infants] can be attributed to the developmental formation of the anorectal junction… I theorize that the ring of connective tissue that is normally formed at the junction [of the rectum with the anus] can cause a constriction to a variable degree just as the hymen does at the vulvo-vaginal junction… Even though [this tissue] may not be as anatomically circumscribed as what is known as the hymen, it produces a constriction that causes colic."
Quite often, in examining the colicky infants, the tip of my examining finger could easily detect a small, medium or larger opening more or less centered in the middle of the membrane, which I likened to a "Roman coin defect." The examining finger could then, with a mild to moderate effort, push through this membrane, always revealing a normal rectal ampulla beyond the ruptured membrane. There was usually a small amount of blood on the examining finger to validate the presence and rupture of this membrane. However, in roughly half of the cases, there was no membrane, and this was initially disturbing. If there was no membrane, what was causing the constipative colic? These children presented the same constipative symptom complex, and received the same symptom reduction and improvement as the infants with the membrane finding, following DRE. Could this simply be a muscular stenosis or non-membranous atresia? Returning to the library I encountered the more recent work of Drs. Moore and Larsen. It has been helpful to mentally picture the sphincter muscles of the rectum as a miniature doughnut, positioned perpendicular to the plane of the anal canal, with the "outside" representing the ectodermal origin of the epidermis and the "inside" representing the entodermal origin of the rectal tissue. The "lining of the hole" of the doughnut is the pectinate line where the two tissues meet and fuse. In some cases the membrane is evident, as I have noted in many of my cases. In others, according to embryologist Larsen,
"it may simply be the residual tissue of fusion, following obstruction by endodermal proliferation and incomplete recanalization, resulting in stenosis."
Another noted embryologist and author, Keith Moore, states that,
"In anal stenosis, the anus is in the normal position, but the anus and anal canal are narrow… Sometimes only a small probe can be inserted into the anal canal."
There is thus abundant evidence in past and current embryological literature to explain what I have been finding clinically since 1972 in approximately 100 referred and personal practice cases.

MAKING THE CONNECTION: CLINICAL APPLICATION OF EMBRYOLOGY
Why the "disconnect" with clinical practice? Why are Pediatric and Family Practice clinicians unaware of these findings, which apparently explain at least that portion of "colic" cases, which are in actuality "constipative colic," with a clear anatomical etiology and causality? I can only honestly answer that I too was only following my patients' lead and had no idea what I was actually doing until I got angry at another banal article in a parenting journal in 1991 (I continue to see them periodically) and personally dug into the literature and found Drs. Crelin, Moore and Larsen.
The further paradox is that it is much easier to prevent colic in a three to four week old infant than it is to cure constipation in a two month old baby. On one occasion in the early 1990's, I delivered a bouncing baby boy to a mother who was a nurse. He was over 9 pounds and passed an abundant amount of meconium onto the pad of the scale, so it counted in his birth weight. He seemed fussy and irritable, and I asked the mother if I might do a rectal exam. She consented, and I found, somewhat to my surprise, what I would characterize as no more than a moderate stenosis, with no membrane or rectal hymen. What was even more surprising was the immediate passage of a huge amount of meconium after withdrawal of my examining finger. The change in her son was remarkable! He unclenched his fists, stopped fussing and nursed with vigor - and continued as a model baby. What misery had we prevented? We'll never know.
Yet another paradox is that the same maneuver used to diagnose the condition of constipative colic is also used to cure the condition. Thus it is impossible to do a classical "double-blind" study of the "cure" of digital rectal examination! This presents quite a challenge for the research-minded physician investigating colic. One can hope that in time the DRE will replace the simple notation of "meconium passed" as the only assessment of the status of the rectal canal during the newborn's "complete physical examination."
In theory, if each newborn had a DRE, this would completely prevent all constipative colic. In terms of statistical power, a statistician has explained to me that it would take 10,000 such cases NOT developing colic to prove it was not a statistical "fluke." The other option would be to include the DRE with the routine two-week check-up of newborns. Several problems are evident with this approach. Compliance is automatically down: every baby born in the hospital has an examination, but not every baby returns for the two-week check-up. Secondly the minor discomfort and tiny amount of bleeding associated with the DRE, which dilates the residual ring of fusion tissue, are ideally better confined to the newborn nursery than the physician's office. Until the DRE becomes a routine part of the newborn physical exam, however, we must carry on wherever we encounter the "child in pain," as Dr. Bill Sears likes to call them. And right now that most often is in our medical offices.

A BRIEF PHYSIOLOGY OF INFANT DIGESTION
According to Dr. Crelin, fetuses swallow approximately 750 ml of amniotic fluid per day and pass urine back into the amniotic sac. In utero, the lower fetal digestive tract is fairly inactive; nonetheless:
"Along with amniotic fluid a lot of other material is brought into the intestinal tract, where it accumulates in the colon, such as sloughed epithelial cells from the skin, sloughed cells from the oral cavity and from the upper intestinal tract and respiratory tubes, lanugo hairs, fatty material from the sebaceous gland secretion of the skin (vernix caseosa), secretions from the gastrointestinal glands and of the liver and pancreas, occult blood, mucoproteins, mucopolysaccharides (including blood group substances), steroids, urea and a sufficient amount of biliverdin to give a green color to the foregoing conglomerate known as meconium… At birth there may be 60-200 gm of viscid, sticky meconium …that dilates the colon to a diameter of 2-3 cm …94% of full-term infants have their first defecation within 24 hours after birth."
Infants are often urged to nurse in the delivery room and begin oral intake of formula soon after birth. Following initial milk ingestion, the infant responds to the presence of coagulated milk-solids in the stomach with an increased peristalsis of the distal ileum and colon. These gastro-ileal and gastro-colic reflexes, mediated through the vagus nerve to the distal ileum and through the pelvic splanchnic nerves to the descending and sigmoid colon regions, are responsible for the urge to defecate in response to food being ingested into the stomach. This response is essential if intestinal distention and obstruction are to be avoided as food enters the upper end of the alimentary tract. The infant gut, as is the case in later life, is responsive to distention (with a sensation of cramping), but not to pinprick, temperature or vibration. What would happen if these perfectly normal responses to food intake were partially or completely blocked? We may make a rather crude analogy with the plumbing in our homes. If something blocks the sewer line exiting the house, sewage backs up in the system and overflows first the lower level toilets and sinks and then (if the blockage is not removed) the upper level toilets and sinks. There may be an analogous situation with constipative colic, backing up in the infant GI tract to the degree that there is esophageal reflux. Maybe we should check the outlet obstruction before suggesting reflux remedies??

PATHOPHYSIOLOGY AND CLINICAL PRESENTATION OF COLIC
The clinical presentation of "constipative colic" is a dramatic example of the "irresistible force" meeting the "immovable object!" It is a battle between the colon trying to empty itself and the variably stenotic ano-rectal opening resisting passage of stool. Most infants without frank imperforate anus are fine during the first two weeks of life, and thus pass their two-week check-up with flying colors. Digestive complaints, if present, are minimal and transient and can be passed off to feeding-adjustment problems between the parent and newborn infant. The early meconium-dominated stools pass relatively freely through the intestine, despite whatever mild, moderate or severe exit restriction may exist at the ano-rectal juncture. Formed stools are just beginning to be encountered by the lower intestinal tract at age two weeks. Those few infants with more severe stenosis (and more severe crying) may have already been "cured" by a digital rectal exam performed by the surgical resident at the emergency room, and are unlikely to have any further problems. Most colic as we know it involves infants with a mild to moderate stenosis, who begin to have problems with stooling during the second to third week after birth. Shortly after a feeding, the infant will experience his/her gastro-ileal and gastro-colic reflexes beginning to trigger increased peristalsis. Stool is propelled toward the rectum and enters the rectal ampulla. The natural response is to grimace a bit because of the perceived distention in the colon [note, again, that the colon records "pain" only from distension, not from touch, hot, cold or vibration], hold the breath and exert increased diaphragmatic and abdominal muscle pressure in an effort to empty the rectal ampulla, which is now uncomfortable with a bolus of stool. Facial reddening may indicate the degree of attempted Valsalva maneuver. The more liquid portion of the stool and any gas present may be expelled with these efforts. More formed stool cannot be passed because of the partial obstruction.
Paradoxically, this passage of liquid stool often prompts the baby's clinician to prescribe anti-spasmodic medications, which leads to bowel relaxation, temporary relief and then increased symptoms in response to the further bowel dilatation. The firmer stool and dilated colon can certainly elicit an uncomfortable feeling on the infant's part, and lead to the clenched fists so often seen in colicky infants. As time goes on and greater amounts of firm stool collect in the distal sigmoid colon and rectum, the magnitude of discomfort increases for the infant. The grunting, facial grimacing and increased redness are testament to the degree of discomfort and Valsalva effort being made by the infant. Adults have a degree of cerebral control over canceling the "urge to go" that is caused by gastro-ileal and gastro-colic reflexes, but the infant has not yet learned this response.
Eventually the discomfort persists between feedings and attempted defecations. At this point some of the milder expressions of stenosis may be cured by desperate parental insertion of a lubricated rectal thermometer or infant glycerin suppository. This insertion causes a brainstem/spinal cord reflex response of squirming, vocalizing (cry) or wincing, but is not perceived as pain because of the under-developed cerebral cortex. Quite often, the parent or caregiver is or becomes fearful of doing harm to the infant because of this reflex response. Nonetheless, if this partial dilatation can allow the formed stool to pass through the partially dilated rectal opening, the passage of the stool itself may complete the dilatation, and the problem is at least partially resolved. Ever-larger bowel movements continue the dilatation process and feedings with higher residue content are well tolerated and are passed with only transient discomfort. In the infants with a more pronounced degree of rectal stenosis, greater intra-luminal pressures are generated by the infant's more strenuous Valsalva maneuvers. They will grunt longer and louder, stay red in the face longer and be more distressed in general. Their crying is no longer confined to the immediate post-prandial periods. Their cry is not one of pain per se, but they are obviously quite uncomfortable and increasingly inconsolable, and complex interventions (such as being placed atop the moving clothes dryer and rides in the car), massages and auditory distractions may be required to achieve any degree of quietude and peace for their families. They may be sleeping fitfully and up much of the night. They may never adapt to any particular cycle of awakening and sleeping.

RESOLUTION OF COLIC
Spontaneous resolution at three to four months of age has long been observed and documented. How is this explained? While the definitive answer to this question is elusive, one can speculate that by that age, the infant with even severe stenosis can generate enough intra-abdominal pressure to force the obstipated stool past the stenotic ano-rectal opening and effect a self-cure. Indeed, a number of parents that I have interviewed tell of the colic disappearing "overnight," not infrequently accompanied by an extra-large bowel movement in the morning diaper, sometimes with a small amount of blood staining noted, which gives testimony to the rupture of the stenotic membrane. It may also simply be a matter of growth and development, with the larger-diameter perineum and anal canal granting the infant a rectal canal that will finally pass the stools presented to it by the digestive tract. This would explain the more gradual improvement in colicky behavior noted by other parents.

SOCIAL CONSIDERATIONS AND ASSOCIATED CONDITIONS
The response of the parents, family and caregivers to the infant screaming with colicky discomfort is initially understanding and pity. "What can we do to help this poor baby?" would be a typical response. As time wears on, and the infant's discomfort increases, despite all efforts to assuage it, the attitude of parent, siblings, grandparents, neighbors, respite helpers, babysitters and neighbors changes. The pity is replaced by and overwhelming sense of helplessness and even resentment against "this noisy baby… can't you DO SOMETHING?!" Guilt accompanies these negative feelings toward the infant, and everyone re-doubles their efforts, reads the pediatric reference manuals, consults the pertinent websites - and come up with swaddling techniques, formula changes and advice on infant comforting techniques which do not seem to help much. The crying continues, and if anything, intensifies. The parents (now fairly well isolated, because, after all, it is their child) begin to go for car rides, leave the vacuum cleaner running, place the baby atop the running clothes dryer, spend longer times away from the squalling infant, take longer showers, etc. Some of the young first fathers simply leave, never to return. ("They never told it was going to be like this!") Sometimes, in their desperation, perhaps angry and at their wits end, the parents or babysitter will shake the infant, hoping that somehow the cause of this visitation from hell will fall out of the child, like a coin falls out of a shaken piggy bank. This may well account for the greatest majority of "shaken-baby syndrome" cases, an all-too-common form of child abuse. The parental anger and frustration cause rifts between the parents, between the nuclear family and their extended families, neighbors and friends, and between the colicky infant and his or her siblings. It is a time of poorly understood isolation on the part of the baby, and happens when the baby most needs consolation and parental/familial bonding. Failure to love and comfort and infant can certainly have later consequences in the relationships between a child and their family, and negatively impacts the infant's self-image and sense of self-worth. The parents experience hostility, guilt and anguish. What did they do to conceive such a child in pain? Why are their parenting skills so deficient that they cannot even comfort their crying infant?

CLINICAL MANAGEMENT OF CONSTIPATIVE COLIC
Now that we have established a definitive cause and demonstrated an effective remedy for constipative colic, wishful thinking ("There is no such thing as colic.") and banal reassurances ("Oh, it's just colic. It will go away in a few months.") are no longer appropriate response to parents' concerns about their colicky infant. We have long known in medicine that "Prevention is the best cure." And since the digital rectal examination is both diagnostic and curative, the following approaches, in descending order, would be the preferred method of handling the major problem of constipative colic:
1. The complete newborn physical examination would include a digital rectal examination (DRE), which - again - is both diagnostic and curative.
2. A DRE at age two weeks in all infants.
3. A DRE at age two weeks in all symptomatic infants.
4. A DRE examination when the diagnosis of "Wessel's Colic" is made (three hours or more of crying on three days in a week) .
During my years of obstetrical service as part of my Family Practice (1969-1995) I would estimate that approximately 20% of the approximately 350 deliveries I performed later developed constipative colic symptoms. All symptomatic infants were treated after obtaining informed consent from the parents or guardians. About half of the infants required a second examination a week later, and approximately 10% of the total group required a third DRE because of continuing symptoms. None of the treated infants developed full-blown constipative colic during follow-up ranging up to 17 years. As luck would have it, I have never personally encountered Hirschsprung's disease, toxic megacolon or imperforate anus.
As with many complaints, the history and physical examination are of utmost importance. Typically this history will reveal a normal pregnancy, delivery and early infancy, regardless of feeding method. Symptoms of red face, grunting with bowel movements, pulling up of the legs and arms onto the trunk, sleeping fitfully and with clenched fists and increased time of crying and fussiness and decreased frequency and amount of stool will have begun between one and three weeks of age. The general examination typically reveals a normal infant, except for the subtle findings of impalpable renal outlines, a mildly or moderately distended abdomen and sometimes the palpable presence of stool in the transverse and descending colon. Pressure over the distended abdomen elicits an uncomfortable response. It is notoriously difficult to measure the abdominal circumference, since this is a tapered cylinder, and varies in diameter in response to feedings, intestinal gas formation and defecation. If this could be reliably measured, it would inevitably show marked decrease as backed-up stool was released following definitive treatment of constipative colic.
Digital rectal examination is carried out with the infant lying prone on a suitably large, covered and protected surface, such as an examination table with a plastic padding with an absorbent surface. The buttocks will be up in the air, with the thighs at least partially flexed onto the abdomen. The right-handed examiner will have the infant's head to her/his left and will be standing alongside the table, using the left hand to support the abdomen and provide (if needed) mild counter-pressure to the digital rectal examination. The digital rectal examination is performed with the gloved finger that is closest to 25 mm. in diameter. Water-soluble lubricant is used. In order to assure proper alignment with the anal canal and prevent injury, the examining finger is directed toward the fingertip of the examiner's other hand, which is placed against the umbilical dimple. If a transverse rectal membrane is present at the pectinate line, it will be encountered about 1.5-2.0 cm. into the rectal canal. A central opening will be noted, varying from a few millimeters (severe) to more than a centimeter (moderate to mild). If non-membranous rectal stenosis is present, it will be immediately evident as a "tight fit" for the examiner's finger, but no membrane will be noted. Further insertion is required if full benefit is to be obtained. As the examining finger is inserted past the second knuckle (the proximal inter-phalangeal joint, or PIP), the tip of the examining finger will have completed rupture of the rectal hymen and will have entered the rectal ampulla and may encounter the smaller diameter of the sigmoid colon. Depending on the length of time the infant has been symptomatic, findings will range from a relatively empty ampulla (exam at age 1-3 weeks) to abundant, dense, putty-like stool (very common beyond 6 weeks of age). The PIP joint at this point is performing a secondary dilatation to the membrane or stenosis. The examining finger is then withdrawn at roughly twice the speed that was used in insertion. The total time to perform the DRE is approximately 20-60 seconds.
I have always felt that the examining finger was important to use because of the "tissue feedback" received during the examination. MECHANICAL DILITATION DEVICES WOULD NOT PROVIDE THIS TYPE OF ESSENTIAL FEEDBACK. One develops a sense of timing, speed of insertion and any necessary hesitation between insertion and withdrawal with increasing experience with the procedure. Upon withdrawal of the examining finger, a variety of results have been encountered. My first two cases were the most dramatic, with stool-under-pressure being expelled three to four feet and two feet, respectively. In some cases, a large amount of gas was released. Examinations performed after 6 weeks of age often are followed by a more or less continuous stream of putty-like stool being expelled in a continuous ribbon. Other cases fall between these extremes.
It is extremely helpful to maintain a "running dialogue" with the parents as to findings and process during the digital rectal exam. I very much encourage the parents to be present, since there is a certain amount of reflexic pain response involved, and it is helpful to have them present to comfort the baby following the procedure. This is typically accomplished with cuddling, nursing or a bottle feeding.

DISCOMFORT AND ANESTHESIA
In seeking an analogous circumstance to the digital rectal examination for rectal stenosis causing constipative colic, I am reminded of the discomfort noted when a fractured arm is being anesthetized and reduced. While it is true that a certain amount of discomfort is encountered on the way to healing that fracture, it is an accepted part of the total experience. More good than harm is being done. Similarly, in the case of DRE for constipative colic, it is important for the physician and any staff present to understand the pathophysiology and anatomy of constipative colic and to fully anticipate the reflexic discomfort and small amount of potential bleeding associated with the procedure, and to fully explain the situation to the parent(s) about it, and handle the whole matter professionally and sympathetically, rather than empathetically. The parents always have the option to refuse the examination/procedure, and to continue with usual or no care, as they desire. As mentioned above, the infant's reflexic discomfort is momentary, unless he or she is a persistent reactor to stimuli. The parent, the mother being most commonly present, usually easily comforts the baby. The baby can be given a breast- or bottle-feeding.
It is important that we keep a total perspective in this matter. We are (taking a worst-case scenario, for argument's sake) inflicting MOMENTARY REFLEXIC DISCOMFORT upon an infant in order to avoid MONTHS OF DISCOMFORT from the constipative colic which we know is in store for the infant and his/her family if the situation is left undiagnosed and untreated. Since the discomfort is momentary (seconds to minutes), any attempt at local anesthesia would be futile and counter-productive. Topical anesthetics do not readily penetrate intact epithelium and would be of minimal value. Injectable analgesia would produce more discomfort than the DRE itself and is to be avoided. The peri-rectal area is inherently non-sterile. A pressured spray anesthetic would propel bacteria into the subcutaneous tissue and cause a secondary infection that could be disastrous, and certainly would add certain morbidity to an otherwise benign process. Again, it is very important to realize that this discomfort is temporary and will not be "remembered" by the infant.

AFTERCARE
Having thoroughly prepared the parent(s) for the DRE, it is often helpful to review in some detail the findings of the examination and the prognosis for colic relief. If a completely normal examination has been experienced, then the infant's crying is not from constipative colic, and additional consultation, testing or therapeutic trials will be needed. In the infants where the rectal membrane has been ruptured or rectal stenosis encountered, I have found that it helpful to schedule a repeat DRE in one week, to be sure that the dilatation has succeeded in increasing the potential opening of the rectal canal. About half of my colicky patients have shown improved but continued tightness at this second examination, and about 10% will display enough tightness at the second examination to warrant a third exam. I cannot recall any infant requiring more than three examinations.
In order to minimize "losing ground," which I would attribute to "normal shrinkage of healing" following dilatation and/or membrane rupture, I instruct the parents to insert an adult glycerin suppository into the baby's rectal canal, using the same technique of gradual insertion in a line aiming toward the umbilicus, on a daily basis, for 7-10 days, or until it no longer seems to be doing any good, or until the infant's fussiness is resolved and stooling patterns have returned to normal. Timing should follow the guideline of "just before his or her fussiest time of the day," since the main idea is to facilitate passage of the stool that is causing the constipative colic behavior. Occasionally, an infant will require more than one suppository per day to counter multiple, severe fussy times. The frequency of use is then decreased, commensurate with the response to the suppositories. Some parents may wish to simply try the adult glycerin suppositories on their own. This is certainly an option, but they will never know the extent or type of stenosis their baby has if the diagnostic DRE is not performed.

INDICATED STUDIES
Much work needs to be done before this matter can be scientifically "laid to rest." The following studies have occurred to me; other studies may come to the mind of additional clinicians or investigators considering these matters:
1. DRE on 100 consecutively born infants to establish the natural incidence of rectal membrane/stenosis.
2. The definitive double blind study with sham rectal exam determined by random numbers, with follow-up of treated and sham-treated groups.
3. Collection of 10,000 cases of "no colic" following DRE at birth or two weeks of age. This would allow statistical significance without the difficult-to-perform double-blind study.
4. Comparison of results with various-sized examining digits. My 25-millimeter pinky has worked well for 35 years, but is this the optimum size for DRE?
5. Pathological study of infants with colic who die from unrelated traumatic causes: what is the status of their GI tract? Can we verify the small anal canal and dilated/full GI tract with back up of a sufficient degree to cause gastroesophageal reflux? We need to have our Pathology colleagues in large urban areas (where there are sufficient numbers of traumatic deaths to make statistical sense of the observations) verify our suspicions about colic.
6. Post-mortem examination of "shaken-baby" deaths would benefit from examination for presence or absence of rectal membrane, as fully discussed above. While muscular tension would be difficult to assess post-mortem, the membrane (if present) will survive anatomically.
7. Correlation studies with colic and:
a. oppositional-defiant behavior in later childhood
b. "vulnerable child" syndrome
c. attention-deficit, hyperactivity disorder (AD-HD)
d. pediatric allergy due to retained proteins with prolonged stool transit times
e. anal-retentive behavior in the teen and adult years
f. adult attention deficit disorder (adult ADD)
8. Exacting research into WHY and HOW Constipative Colic seems to improve at about four months of age.

A FEW MORE QUESTIONS
Many larger issues remain unanswered:
1. For example, how does the failure to comfort the colicky infant affect parenting in confrontive situations later in toddler-hood?
2. How much over-punishing of misbehavior is an expression of repressed anger generated during those first few months of colic?
3. Does pediatric allergy result from over-exposure of the gut to retained stool (with its protein content) in constipative colic?
4. Is esophageal reflux simply the end-result of stool backing all the way up the GI tract in a colicky infant?
5. Does infant constipation predispose to childhood stooling difficulties and adult anal-retentive problems?
6. Can the constant distraction of prolonged discomfort lead to attention-deficit/hyperactivity disorder later in childhood?
7. Can constipative colic have a later-life expression in problems such as volvulus, diverticulosis/diverticulitis, appendicitis and colon cancer?
8. How does the once-colicky infant respond to pain and frustration later in life?

FINAL THOUGHTS
It takes courage to fly against the wind or row against the current. It took Dr. Barry Marshall more than 15 years to convince the medical world that the Helicobacter pylori organisms discovered by Dr. J. Robin Warren in 1979 could survive and actually cause gastric ulcers in the barren and acidic gastric medium. In any case, the task of putting these ideas about constipative colic into practice will take fortitude and persistence. It may fall to a few brave souls to lead the way and to perform digital rectal exams for the more timid and unbelieving practitioners. But I must believe that the usual progression from "heresy" to "unorthodoxy" to "standard of care" will occur in due time.
The parents of the world will demand our attention and action in the light of these new/old ideas.