Meconium Impaction

Jon Palmer, VMD, Associate Professor, New Bolton Center, University of Pennsylvania

Meconium is formed from swallowed amniotic fluid, intestinal secretions (e.g. bile), cellular debris, and other debris. It first appears during the 1st trimester and accumulates throughout fetal development. Bile acids are excreted by the beginning of the second trimester. At full term fetal meconium consists of water, mucopolysaccharides, cholesterol, sterol precursors, proteins, lipids, bile acids, bile salts, enzymes, blood group substances, squamous cells, and vernix caseosa (sebum and desquamated cells from fetal skin).

In utero meconium passage is often associated with fetal distress. But it can occur as early as the second trimester and is not associated with fetal compromise at this early stage. Late term meconium passage appears to occur as the fetal GI nervous innervation matures and responds to stimuli. This is one reason that it is more often seen in post-term gestations. Defecation is primarily under the control of parasympathetic pathway stimulation. It may be secondary to vagal stimulation with cord or head compression. Although it is commonly believed to be a response to stress, this has not been confirmed experimentally.

In human medicine the finding at birth of "thin meconium" in the fetal fluids is not associated with fetal asphyxia or low Apgar scores. Many believe it is a result of passage of meconium from earlier fetal distress (not at birth). Finding "thick meconium" at birth is thought to represent more recent passage, and is associated with meconium aspiration syndrome (MAS) and fetal asphyxia. Fetal diarrhea may also occur with the neonate being born passing profuse, liquid meconium. This diarrhea usually resolves within 48 hours of birth. I have associated fetal diarrhea in the foal with hypoxic insults, but others have wondered if it is a manifestation of fetal enteritis as may be caused by Ehrlichia risticii.

Meconium Impaction

There is an increase incidence of meconium impactions in colts. This is often blamed on their narrow pelvic canal. It may also be caused by excessive meconium formation in utero or impaired gastrointestinal motility associated with asphyxia (hypoxic-ischemic GI disease), sepsis, or dysmaturity/prematurely. It may also the secondary to prolong recumbency, dehydration, or changes in motility caused by drugs such as dopamine.

Foals with meconium impactions will strain to defecate with an arched back, nurse frequently as a source of comfort, and shows signs of persistent abdominal pain (colic) including rolling on their back, kicking at their abdomen and frantically swishing their tail. Although they nurse frequently they don't nurse effectively because of the distraction of pain. They often have dried milk on their head from standing under the mare’s streaming udder. They develop significant abdominal distension if the meconium occludes the lumen sufficiently to prevent gas passage. During periods of tenesmus or colic the umbilicus may reopen and either bleed or drip urine. These foals are predisposed to umbilical infections. On rare occasions rectal prolapse occurs.

Diagnosis is usually easily made by reviewing the history and performing a physical examination. At times attendants place much emphasis on whether the foal " past his meconium". However, since there is a variable amount of meconium in the colon of each foal, seeing some being passed cannot rule out impaction. The absence of observation also should not be weighted too highly. Despite careful observations, passage of meconium is easily missed. Searching the stall looking for the meconium often is futile unless it ends up on the bottom of your shoe. However the general observation that little or no meconium has been passed coupled with the onset of straining and colic should lead you to suspect meconium impaction. Usually a definitive diagnosis can be made by performing a digital rectal examination. Often a meconium fecal ball can be palpated in the pelvic canal. An enema can also be diagnostic if it produces meconium and temporarily relieves signs. When digital examination is negative, the value of deep abdominal palpation should not be overlooked. If the foal is quiet (sleeping or sedated) and is not overly distended with gas, deep abdominal palpation may reveal large amounts of retain meconium. Meconium is readily identified because it is firm and distinct. There are no other structures in the neonate's abdomen which can be confused with it. Usually the most rewarding areas to palpate are in the caudal abdomen above the bladder, or in the anterior abdomen under the ribs (in the sternal and diaphragmatic flexures of the colon). At times the meconium can be palpated coursing from the anterior abdomen to the caudal abdomen. When abdominal palpation is unrewarding or impossible because of the resistance of the foal to manipulations, abdominal ultrasound can be helpful, especially when several differential diagnoses remain possible.

Differential diagnosis include: colonic atresia (is ruled out if any feces has been passed or the enema fluid comes back colored), rectal perforation (usually caused by over zealous enema administration ), ruptured bladder, NEC, intestinal volvulus, intussusception, and unusual conditions such as a pendulous ovary wrapping around colon causing an obstruction (much like a lipoma does in aged horses).

Mild meconium impactions respond readily to soapy water gravity enemas. A soft enema tube should be use with care, since it is possible to perforate the rectum. Three to 500 mls of warm soapy water (a mild soap such as Ivory is usually used) should be given gently. The soapy water solution can the replaced by a solution of lubricants (e.g. J-lube ). Soapy water enemas can the repeated frequently however even with mild soap a certain degree of rectal irritation occurs. This rectal irritation may result in persistent tenesmus interpreted as continued impaction, resulting in the perceived need for more enemas. Also, even before the first enema is given, often the rectum is very irritated and edematous secondary to the impaction. Great care should be taken not to exacerbate this condition. Rectal perforations are more likely with a damaged rectum.

When solutions such as dioctyl sodium sulfasuccinate (DSS) are used, great care should be taken. DSS is irritating and results in sloughing of epithelial cells. Even though this solution is being given as an enema, care should be taken not to use too high a dose. Glycerin is another irritant which is sometimes used as an enema solution. The mild irritating properties of all of these solutions (including soapy water) enhances their action. Irritation results in active colonic secretion helping loosens the impaction. However, too much irritation can not only increase the likelihood of traumatic perforation, it also can act as a portal for sepsis.

An alternative to a gravity enema in meconium impactions is the so-called "retention enema". To give a retention enema, a large bulb (50-75 mls) Foley catheter is placed in the rectum. The bulb is inflated so that a moderate seal is produced between the catheter's bulb and the rectum (it is vital that the catheter's bulb is in the pelvic inlet and not pushed further into the abdomen when it is inflated - this helps confine the bulb an prevent rectal perforation). The enema solution is introduced through the Foley catheter ( a volume of 100 to 150 mls), the catheter is clamped and allowed to remain for up to 20 minutes. The foals often strain against the catheter and may push it out prematurely. The most common solution to use in a retention enema for meconium impactions is 4% acetylcysteine (six grams acetylcysteine powder in 150 mls of water). Acetylcysteine is expected to dissolve disulfide bonds which are commonly found in meconium. This solution will not dissolve the meconium but will make the outer surface slippery because of its action and may allow the meconium to pass. Much of the effect of a retention enema may be in the rectal distension resulting in secondary stimulus of motility. In man, often barium is mixed with the acetylcysteine to result in an osmotic effect. I have used milk of magnesia for an osmotic effect in foals, but have not seen a dramatic effect. Others occasionally add sodium bicarbonate, however in my opinion, the large amount of sodium introduced to the rectum could be dangerous as well as irritating. Retention enemas can be repeated several times without a problem. If they are not retained for the desired time period, they can be repeated.

If the impaction persists despite the use of enemas, oral laxatives may be considered. Mineral oil ( 2 to 4 ounces), milk of magnesia (2 to 4 ounces) or DSS(10 to 15 mls) can be used. DSS presents more of a risk of secondary sepsis set resulting from translocation of bacteria due to damaged epithelium. Some practitioners like to use Castor oil. I feel this is a bad idea because, although it is effective, it is also extremely irritating and many foals become leukopenic and show of signs sepsis after its use. Since neonates are so susceptible to sepsis and the Castor oil mediated damage can result in bacterial translocation, I feel it is contraindicated.

If the impaction is present for a long period of time and if the impaction prevents adequate nursing on part of the foal, intravenous fluids are indicated and supplementing the patient with dextrose may be required. The foal can be fed although large quantities of luminal fluids may result in reflex motility and more colic. This problem occurs during the period when colostrum is absorbed. Close attention should be paid to adequate passive transfer. Plasma transfusions may be required. As noted above these foals are at a higher risk for generalized sepsis with translocation of bacteria through damaged colonic epithelium and through the umbilical structures.

Meconium impactions almost never require surgical intervention. Patience is the key to success in most cases. When surgery is required, a poor outcome is more likely. Meconium impactions are very rare in other farm animals, but do occasionally occur in small ruminants.

Copyright 1997 Dr. jon Palmer, Neonatal Intensive Care Unit