Monthly Archives: September 2012

Waging Children

Is poverty alleviation a GAME OF CHANCE? Children are now bet by parents as pawn for poverty alleviation. Just like a raffle draw, the more number of entries you have, the more chances of winning. So your children are your wager to uplift you from poverty?

Listen to what these inconsiderate bastard of fathers say: “pag mas maraming anak, mas malaki ang posibilidad na maiaahon ka sa hirap (the more number of children, the greater chance of having a child that will unburden us from poverty).” Another guy, a farmer said, kung naipasa na ang RHBill, sino ang magiging katulong namin sa pagsasaka (if RH Bill has been passed, how can we have children who will help us tend the farm).” Another absurd statement I hear is “di bale nang hirap sa buhay, basta magkakasama. (it doesn’t matter that we’re hard up in life as long as we are all together).”

If you are poor, and sire a lot of children, there are several things that you deprive your children of.


Being a minimum daily wage earner, it will be lucky if you can bring home 500 pesos for your family, regularly, that is, DAILY. Imagine, with a family of 10 (couple and 8 children), what would a 500 pesos afford them on the table? Rice (carbohydrates) and 2 instant noodles (carbohydrates) for a viand each meal? What about their protein needs – for growth and body tissue repair, and fats, for energy and carriage of vitamins? Nutrients are not only these macronutrients. There are also micronutrients that our body needs. Often than not, these kids are deficient of these too – vitamin A, iron, iodine, leading as well to poor school and academic performance. How many meals/day can 500 pesos afford them? Are these kids well-fed? Often, parents sacrifice, giving their share to their children. But how can a mother, who isn’t eating enough provide a good breastmilk to her nursing child? If the children are going to school, do they bring along snacks? If they are inadequately nourished, how can they learn well at school? How can they be at par with those who eat healthily? How can they cope up if their brain and body are screaming for nutrition? It has been validated by several studies that children who do not eat well during breakfast perform poorly academically. And if so, how can they be educated well, a tool that will help them for their employment in the future?


Will the mother have access to prenatal care every time she gets pregnant? Is she well-nourished every time she gets pregnant? Is her body well rested from the previous pregnancy to carry on another baby? How many of these kids will be delivered in a hospital? Will the parents afford the cost of vaccine that each  of these kids need? The government only subsidizes a few and select vaccines.

The most common causes of mortality among under 5 years old are neonatal death (death within 30 days from birth), pneumonia and diarrhea. The latter are two vaccine-preventable diseases, affecting children worst during the 1st 6 months of life. Children who are unable to receive these vaccines, because of high cost, at this most vulnerable period are at increased risk. Just recently, the government announced it will provide rotavirus vaccines, but only to select indigenous people only; itt would still not cover many of our kids most of our indigenous kids.

A child’s health status and nutritional status have direct relationship. And health does not only encompass one’s physical well-being, it also includes his mental faculty. The better nourished a child is, the less sickly he becomes. Protein helps in the patient’s growth. In relation to diseases, protein brings about formation of antibodies needed to combat infection. It is easily understood therefore that a malnourished child is less-equipped when it comes to combatting diseases, and thus is more vulnerable. Compound this fact again with the child lacking vaccines. He has already nil immune system to begin with, then lump it with malnutrition; this now brings the child at a double jeopardy. And when they need hospital care, will they afford it? Often than not, those who need one are from the poor sector. Will they be always at the mercy of random samaritans to be able to survive?


Will they be able to afford quality education a private school can offer? If not, in the government school, what is the quality of education will they imbibe; wIth congested class rooms, abbreviated class periods, rotating in shifts? Physically, their lack of nutrition impairs their academic performances. Their sickliness aggravates their deficiencies. And then, now, this environment as school, who from my humble opinion, isn’t conducive for learning. Can the poor parents afford to send all children to college, with such income, without resorting to working while studying? Of course, I am not saying it is wrong to be a working student, but ideally, academic years should be solely dedicated to studying, or else, the child will easily burn out if he still has to work, especially with the younger generations.

So what have we here in reality? Many of these kids do not finish elementary, few reach high school education and rarely if not nil achieve college degree. Children are forced to help their parents to augment the family income. But when they reach adult and join the labor force, they are disadvantaged, courtesy of their lack of education and frail health. If it is their time to be parents, how many of them will follow their parents’ example? It usually ends up in a vicious cycle, and its sickening.

So what happens now to the wager of their parents? Who among them can indeed uplift their family from poverty, given their disadvantaged background?

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Posted by on September 27, 2012 in Personal, RHBill


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Why Single Women, And Yes, Nuns, Ought To Take Contraceptive Hormones


Birth Control Pills (Image courtesy of © iStockPhoto / Ceneri)

When I once said that nuns and single women who do not intend to get pregnant would benefit from taking contraceptive pills, one anti-RH Bill reacted saying “that is hysterical!” I didn’t think HYSTERICAL was even the appropriate word to say, even if she wanted to express disgust based on her knackered beliefs.

Let us put it that a woman has her first menstruation (called menarche) at age 15 years of age, and menopauses at 45 years of age. Granting she has a regular monthly menstrual cycle, that would make her mens 12 times a year. If she will have 30 years of reproductive age, then that would mean, she will have 360 menses in her lifetime. (Although realistically, nowadays, some girls already start menstruating at 9 years of age. To give you an idea when to expect the girl will mens for the first time, note at how old she is when her breasts start to enlarge — termed medically as thelarche. Approximately two years after that, she will now start her menstruation.)

During a woman’s menstruation, there is interplay between estrogen and progesterone. During the first day until day 14 of a woman’s menstrual cycle, ESTROGEN predominates especially on the day just before ovulation. The latter is responsible to prepare the uterus for an incoming pregnancy as well as ovulation in concert with other hormones; it’s level declines once the ovary has released an ovum. Once ovulation occurs, the corpus luteum (the cells surrounding the ovum in the ovary) release PROGESTERONE. The latter on the other hand ensures that the reproductive organs are optimum for a pregnancy to proceed.


I have emphasized in my other blogs the role of progesterone as the hormone responsible for keeping the pregnancy intact. While estrogen may still be produced during pregnancy (as estriol), its potency is a lot weaker than the estrogen produced during non-pregnancy state (estradiol).

If woman gets pregnant for 9 months, the effect of progesterone is greater than the effect of estrogen. Even if estrogen is also produced during pregnancy as estriol, its effect to other organs such as ovary and uterus is dampened to nil. Thus, in cases where the woman is able to carry her pregnancy to full term, that would save her 9 months from the potent effects of estradiol to her body. If she will exclusively breastfeed (no breastmilk substitute whatsoever is given to the baby) after giving birth as well, this will have the effect of LACTATION-INDUCED AMENORRHEA (woman’s menstrual cycle remain arrested as effect of exclusively breastfeeding her baby) for about 6 months. Thus, one pregnancy will save the woman at least 15 months free from effects of elevated estrogen (estradiol) level. If in her lifetime, a woman will bear 4 children, all of which were term pregnancies, then she will have a total of (15 x 4) 60 menstruation free months in her lifetime. This means, she is on the advantage of 300 months exposure only, compared to women who never got pregnant, who are exposed to the potent effects of estradiol for 360 months.


What effect does estrogen have to a woman? Most commonly discussed effects of unopposed estrogen elevation would range from benign (leiomyoma, or myoma of the uterus) to malignant such as cancer of the uterus, ovary, and breast, among other else.


It has been established that most cancers are mainly genetic (meaning, inheritance of cancer genes from either side of the parents). But aside from the genes for expression of cancers, there are also genes for cancer suppression that comes along with its inheritance. Whichever of these genes predominates, that is  what is manifested clinically or physically or biochemically or physiologically by the person involved. If a person has breast cancer gene, and the gene for its suppression is muted or ineffective, then the person will have breast cancer manifestations. On the other hand, if the person has breast cancer genes, but his cancer suppression genes are enhanced and working effectively, then the person will not show signs of breast cancer, but still at risk and will readily convert once those cancer suppression genes are skewed. (Confused? hahaha). These cancer suppression/expression genes are regulated by the environmental factors to which the person is exposed to. In the case of breast cancer, one environmental factor is elevated estrogen (estradiol) level.

Estrogen naturally exists in 3 forms in women. The ovary produces (1) estradiol, the most potent form of estrogen, and this is the form usually seen elevated among nonpregnant women during the reproductive age group. This is believed to be the most potent of the three forms. Another form of estrogen is produced during pregnancy is (2) estriol; this has been noted to be the a lot weaker in comparison to potency of estradiol. Another form of estrogen is found among menopausal women, (3) estrone. During the reproductive age group, estrogen is produced by complex enzymatic process at the ovary. Postmenopausally, estrone is converted peripherally at the liver, adrenal glands, breast and fat tissues.

If a person has inherited the breast cancer genes, and keeps on being exposed to elevated estradiol, then she can develop breast cancer, especially if her breast tissue also has the hormone receptors for estrogen. These receptors will bind with the circulating estrogen and thus bring about the genesis of cancer. Between non-pregnant woman (who has 360 times of exposure) and a woman who got pregnant for four times (who only has 300 times of exposure), it is the former who is more susceptible. This only goes to show that even if the woman never took exogenous sources of estrogen (such as oral contraceptive pills), they can still have breast cancer. (I previously blogged a colleague who was single and died at the age of 42 from breast cancer. She too was not taking contraceptive pills — The Pain She Should Never Have.


Contraceptive pills contain synthetic progesterone alone or in combination with estrogen. Among its many benefits, the effect in focus is its role in suppressing ovulation. With a sustained elevated level of progesterone from religious intake of contraceptive pills or injectable hormones, this suppresses elevation of estradiol (which leads to ovulation). With lesser if not complete non-exposure of the reproductive organs to estradiol, nothing will stimulate the cancer expression genes and therefore no cancer formation. Of course this is NOT always absolute and there are always exceptions, but these exceptions are often minimal compared to those who will benefit from the treatment.

A meta-analysis on the effect of oral contraceptive pills among women who had genetic mutations (BRCA1/2) for expression of ovarian cancers have shown that oral contraceptives reduce the risk for ovarian cancers, proportional to the length of use. The same meta-analysis also stated that OC formulations used before 1975 were associated with a significant increased risk of breast cancer (SRR: 1.47; 95% 1.06, 2.04), but no evidence of a significant association was found with use of more recent formulations (SRR: 1.17; 95% 0.74, 1.86). (highlights were mine). (Reference: Oral contraceptive use and breast or ovarian cancer risk in BRCA1/2 carriers: A meta-analysis.S. Iodice, M. Barile, N. Rotmensz, I. Feroce, B. Bonanni, P. Radice, L. Bernard, P. Maisonneuve, S. Gandini. European Journal of CancerVolume 46, Issue 12August 2010Pages 2275-2284).

Do women ought to take contraceptive pills, even if they are not married? 

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Posted by on September 22, 2012 in Breast Cancer, RHBill


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The Myths of Breakthrough Ovulation & It’s Purported Abortion

A woman posted a meme on twitter talking about “breakthrough ovulation” and how these eggs fertilized after breakthrough ovulation gets killed by contraceptive pills. I asked her to explain scientifically how does the killing happen, but I never got a reply. My guess was she really did not know what she was talking about and thus the answer (because she just want to instill fear among her readers). How responsible tweet that was huh?

Breakthrough ovulation can happen, especially when the female taking pills is not compliant and does not follow instructions well. According to Dr. Dennis Higginbotham, “failure rates for pregnancy with BCP’s (birth control pills) can be 1% to 5% depending on the particular pill and on the patient compliance. Skipping pills is the usual cause for failure, but ovulation (and pregnancy) can occur even when the pill is taken properly.” (highlight is mine; Reference: Following his statement, it would show that the pills are 95-99% effective in suppressing ovulation.

Pill are composed of synthetic estrogen and/or synthetic progesterone. Some pills are plain progesterone, while some are combined estrogen and progesterone. The hormonal contents of birth control pills are minute as compared to the volume released by the ovary. It mimics the hormone’s action by causing ovary to stop ovulating, thins out the uterine wall, thickens the cervical secretions, all for the purpose of preventing pregnancy.

What are the circumstances surrounding ovulation? When a woman ovulates, there is a high estrogen level in her blood, there is the surge of luteinizing hormone. These two events are important to trigger the eruption of the ovum from the ovary. What are the sequela of elevated levels of estrogen? In the uterus per se, it causes thickening of the walls, increase in blood vessels, as if preparing for a possible pregnancy. That’s what estrogen does to the uterine lining. So, what will happen in cases of breakthrough ovulation, and this egg becomes fertilized? It has a rich uterine lining for implantation. This is contrary to the claim of misinformed anti-reproductive health bill measure that because the woman is taking pills, the uterus is thin and cervical mucus is thick disallowing pregnancy to happen. This is false! Estrogen and progesterone are endocrine hormones. This means that it is secreted by a certain organ, but its effect is transmitted to other organs sensitive to it via the bloodstream. In contrast, paracrine hormones/substances are substances which exert effect to nearby organs by diffusion but not via bloodstream. So in breakthrough ovulation, where the egg gets fertilized, PREGNANCY will take place, NOT ABORTION. As Dr. Higginbotham mentioned, there is 1-5% failure rate.

During the woman’s menstrual cycle, estrogen hormone predominate during the 1st 2 weeks (day 0-14). This hormone prepares the uterus and other reproductive organs for the forthcoming “pregnancy,” assuming that the egg gets fertilized upon its release – uterine lining thickens, there is increase in blood vessels, glycogen, etc. Everything happens in a concerted fashion for the anticipated pregnancy. By around day 14 of the menstrual cycle, the luteinizing hormone surges (released by the pituitary gland) and then triggers the release of the ovum.


Beautiful series of pictures taken by accident by the team of Jacquez Donnez as they were preparing the woman for partial hysterectomy. (source:


Image courtesy of


Image courtesy of

When the ovum is released, the follicle is converted into corpus luteum. Estrogen level now declines dramatically. The corpus luteum now releases progesterone to sustain the ovum. If the ovum gets fertilized, there is rapid proliferation of cells until the fertilized ovum will transform into blastocyst. This happens until about 13 days from fertilization. Up to this point, the corpus luteum provides progesterone for this developing embryo.

By around 13th day post-fertilization, the blastocyst implants. It may cause a minor bleeding in some women (post-implantation bleeding) while others may not. The outer layer of the blastocyst now imbeds itself into the rich vascular uterine wall and forms the placenta. Once implanted, the placenta now assumes the role of producing progesterone for nine months until the baby’s birth, as the corpus luteum has already involuted. This predominance of progesterone over estrogen during the period of pregnancy inhibits the ovary to release ovum for nine months as well.

This effect of progesterone predominance during pregnancy is mimicked by intake of contraceptive pills.  When the woman takes in hormonal pills, the progesterone becomes elevated thereby inhibiting the ovary to release an ovum, the uterine lining not prepared for pregnancy and the cervical mucus viscid, unfriendly to sperm that might swim up to the fallopian tube. Hence pregnancy will become unlikely.

Now it makes me wonder why these anti-rh bill supporters keep on saying that contraceptive pills are abortifacient. How can abortion happen when no ovum is released? And when there is no ovum released, what is there to fertilize? As of now, majority are in acceptance of the fact that fertilization is when human life begins. In cases of breakthrough ovulation which they repeatedly claim, again, if there is ovulation, then the uterus and the cervix is also prepared for a pending pregnancy because the effect of estrogen that lead to ovulation is also echoed in other parts of the female reproductive organ and not on the ovary alone. It does not happen that estrogen causes ovulation, but uterus remains thin and cervical mucus remains viscid. Estrogen and progesterone effects contradicting at the same time? No, dear anti-rh bill supporters, estrogen effect is endocrine. Again, read the meaning of endocrine as I have mentioned above. And if you insist on this premise that an ovum is released but the uterus and cervix is unprepared for a pregnancy, leading to the abortion of that fertilized ovum, then you should be one who is menstruating while pregnant because you think that estrogen and progesterone effects can happen at the same time. I wonder what subspecies of homo sapiens you are, perhaps Homo sapiens mutatis?


Posted by on September 19, 2012 in Pregnancy, RHBill


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When Intestines Go Out Of The Abdominal Cavity (Gastroschisis)


(Image courtesy of:

GASTROSCHISIS is a condition where there is a defect at the anterior abdominal wall (usually towards the right of the umbilical cord insertion), leading to the evisceration of the intestinal segments or abdominal contents as seen in the picture above. Because of this, the intestines is now exposed to the amniotic fluid where the baby floats. (Amniotic fluid is made up mostly of the fetus’ urine, thus may contain chemicals that can be irritating to the intestines but not to the baby’s skin). This exposure triggers the intestines to react to the amniotic fluid, causing inflammatory response, thickening of the intestinal walls than their regular diameter when not exposed to amniotic fluid. If an operation is attempted immediately at birth, it would be impossible to put back all those intestines into the abdominal cavity at once hence a silo bag is placed to contain the intestines outside of the abdominal cavity. Slowly the intestinal contents in the silo bag is pushed (in days or weekly basis) until the abdominal cavity is able to contain everything, thus the wound is now closed.


Intestines contained in a silo bag. (Image courtesy of


The abdominal wall is sterilized. Then under ultrasound guidance, a needle is poked into the amniotic cavity. Amniotic fluid is then aspirated, and then an equal amount of normal saline solution is replaced back. This is then repeated until the return flow becomes clear in color. This is being done in order to refreshen the amniotic fluid that might irritate and cause inflammation of the intestines that has eviscerated outside the abdominal cavity (as you recall that the amniotic fluid is mainly composed of the fetus’s urine). If the intestines become inflamed, the abdominal cavity might not be able to contain everything when replaced all at once during a corrective operation.


I was lucky again to have witnessed a case of a baby with gastroschisis, diagnosed prenatally via an ultrasound, and who underwent the above procedure. The perinatologist did serial amnio-infusion treatment on the baby (of course, while mom still pregnant with him) until the time that delivery was already inevitable. During one of the amnio-infusion treatment, I was a witness and assisting the perinatologist. The postnatal outcome was marvelous!

During delivery, we did a double set-up at the operating room. At one room was the cesarean section for the delivery of the baby. At the other room was the team of the pediatric surgeon waiting. We, the neonatology team was in between. A sterile plastic container was readily available. When the baby was out of the mother’s uterus, we the neonatology team attended to the baby immediately. We were so lucky that baby was vigorous upon delivery so there was no need to help him breath. Immediately while my colleague was wiping baby dry off the amniotic fluid, I was inserting a line and my other colleague was putting the baby’s legs, intestines and his lower trunk into the sterile plastic. This is to avoid losing much fluid from the abdominal cavity and contaminating the intestines and abdominal cavity. Then we immediately brought baby to the other operating room where the pediatric surgeon was waiting.

Primary closure (all intestines brought inside the abdominal cavity at once) was done on baby. This was easily possible because the intestines weren’t that much inflamed, thanks to the amnio-infusion, thus the abdominal cavity was able to accommodate them all. I wasn’t sure though if all layers of the abdomen were co-aptated and sutured all together, or just the skin and the subcutaneous layer, my bad not to have remembered.

The baby was able to tolerate feeding immediately. Because of this, the baby did not stay long in the hospital, went home in less than two weeks if I was not mistaken. I guess this is another benefit of amnio-infusion – avoid prolonged hospitalization and thus hospital acquired infections. I wish to do this again, now that I am in private practice.


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(Image courtesy of

During my training, I was lucky to witness a case of hydrops fetalis undergo a rare form of management done in our institution.

During the prenatal course, the obstetrician noted the baby to have hydrops fetalis. Serial ultrasound established the diagnosis and at the time the baby was nearing birth, the condition persisted.

As in my previous articles, hydrops means the generalized swelling of a fetus. The skin becomes edematous and very taut, disabling a good expansion of the chest when breathing. The pleural space, where the lungs float is also filled with fluids, compressing the lungs. So once the lungs becomes occupied by air after birth, there will be difficulty of the lungs to expand. The pericardial cavity, which the heart occupies, may also be fluid filled. Abdominal cavity may also contain fluid, termed ascites. At least 2 of these 3rd spaces must be involved before diagnosis could be entertained in an individual.

On the baby’s latest ultrasound, it was noted that the right lung has pleural effusion, the left lung was spared. In order to manage the baby optimally at birth, a pre-natal conference among all parties involved in the delivery of the baby was called – the perinatologist, neonatologist, and pediatric surgeon, to discuss how the delivery process will take place. At that time that this was done, the unang yakap was still in conception so it was not employed in this particular delivery.

The perinatologist wanted to employ EXITextrauterine intrapartum treatment. This means that the treatment will happen when the baby is out of the uterus but is still within the confines of the delivery procedure (umbilical cord remains uncut).

1.The baby was delivered via emergency section. He was brought out of the uterus, the umbilical cord still connected to the placenta.

2. The pediatric surgeon inserted a needled through the right pleural space, drained fluid as much. (The purpose of doing this is to allow maximum expansion of the lungs when it gets aerated; the fluid, if not evacuated, will limit the expansion of the lungs leading to poor tidal volume, lesser oxygenation of the blood, which will aggravate the already compromised baby).

3. Umbilical cord was then cut and baby was handed to the neonatology team.

4. Neonatologist then intubated the baby.

5. Chest x-ray was done to document the level of the tip of the endotracheal tube, check how much of the fluid was drained, and check how expanded the lung after the procedure.

In short, the procedure was successful. We were able to ventilate the baby afterwards. Baby however had other pressing problems, and as expected he when through persistent pulmonary hypertension, or persistent fetal circulation. PPHN or PFC usually results from a thickening of the walls of the arterioles/capillaries that surround the lung alveoli. Because of this thickness, oxygen travels slowly from the alveolar space into the bloodstream, thus leading to lesser oxygenation of the blood. PPHN can be primary (no identifiable cause) or secondary (a result or effect of another primary disorder). In this case, if the baby, who has hydrops fetalis, also has PPHN, it would only mean than the hydrops was a chronic disorder that it has affected the development of the lung tissue and vessels. If the PPHN was primary, then the arterioles and capillaries are thick to begin with, and there’s no way to reverse this anymore. If it is secondary, it means that the arterioles or capillaries have thinned out for postnatal life but then became thicker as a response to/result of an insult/injury. Despite proper ventilation and support given to the baby, he succumbed to PPHN after several days.



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I was again given the opportunity to deal with a very interesting, intriguing, puzzling case in my career as a neonatologist.

I was called for the delivery of a baby presenting with hydrops as seen during prenatal ultrasound. (Hydrops refer to the generalized swelling of the baby, and is defined as the presence of fluid accumulation in third spaces including pleural, peritoneal, pericardial spaces, edema of the skin, as well as swelling/thickening of the placenta). Accordingly, the ultrasound detected fluid in the abdominal cavity and testicular sacs, but none wheresoever. The consideration of hydrops is dubious but still it was highly considered. I called on the different personnel who will be involved in the baby’s care later on. Meanwhile, the obstetrician has already spoken to the mother (the husband is overseas) and explained the possible outcome of the baby’s birth. (Hydrops usually is dreadful, some expire within an hour). They were preparing that the baby might indeed expire immediately after birth.

Upon baby’s birth, we noted that the abdomen was distended, scrotum was bulging, as big as an apple. The skin was not edematous however. It seems that baby did not satisfy the criteria for hydrops. Baby had a weak breath, thus I had to intubate him. In less than an hour, I took an x-ray to confirm presence of fluid in other body cavities. Liver was palpable on examination (though it may be normally appreciated about 2 finger-breadth below the right subcostal margin, baby’s liver was about 4 finger-breadth palpable); there was also a soft mass I palpated at the right side, seemingly an enlarged spleen. Pleural space (where lungs are) is free of fluid. This at least ensures that baby’s breathing would not be difficult, unlike when there’s pleural effusion (fluid in the pleural space), the fluid will prevent full expansion of the lungs with every breath, letting to less oxgenation of the blood, which will make the heart work double time. There was a single bubble (signifying air entry into the stomach), but none for the rest. This is understandable as the x-ray was obtained just minutes after birth. It will takes hours before the air swallowed will pass into intestines, then about 24 hours until the air passes out of the anus.

I requested for ultrasound to see what in the abdomen is causing this disorder in him. But to my and the sonologist’s surprise, we saw nothing but a large liver. There was no tumor, the intestines were being pushed down though, ebbing and bobbing into the scrotal sac. The mass I palpated indeed was the spleen. But these don’t seem explain why there is fluid in the abdomen, and the scrotal sac enlarged, as seen in the prenatal ultrasound. With a liver enlarged, I tried to work up the baby along that line. I tested for blood samples reflecting liver functions, decided to repeat the x-ray of the chest and abdomen 6 hours after birth, this will give ample time for air to pass through to the rest of the intestines distal to the stomach.

Repeat chest and abdominal x-ray showed passage of gas into the distal intestine. This can eliminate pyloric stenosis (part of the stomach before duodenum) as a possible entity. Albumin was low, so I corrected.

But this wasn’t of a significant help. It won’t still explain why there was herniation of intestines into the scrotal sac, nor the large liver. It may explain the fluid accumulation, but that’s just it. I was at a loss. I was at a loss what next step to take. There were no other organ systems showing abnormalities, which might suggest a syndrome. It was a clear cut gastrointestinal system derangement. I didn’t shame to call on a gastroenterologist to help me solve this puzzle. I didn’t want to miss a thing for the sake of the baby, who I am being asked to do everything possible to make him survive. (A herculean request).

The gastroenterolist also seemed puzzled by the baby’s case. A toss between malignancy and… it was hard to come up with differential diagnoses… On baby’s second day of life, his abdominal girth dramatically increased, but remained soft. There was feces meconium coming out of the baby’s anus, though the color was like that of a caramel; there was no vomiting. This tells you that there seems no obstruction of the intestinal tract. But we wanted to sieve and scan through and don’t want to miss anything. Even if it was initially mentioned that CT scan might not be of help, we still did it. Surprisingly, the CT scan of the abdomen revealed only a large pneumoperitoneum (air inside abdominal cavity, but outside the intestines – which should never happen in a normal individual), fluid accumulation, but nothing more. This then puzzled me all the more; air can only escape into the abdominal cavity if there is a perforation along the intestinal tract. I then referred the baby to a pediatric surgeon, who scheduled baby for an emergency explore laparotomy.

At the operating room, the stomach, duodenum and jejunum were intact. At the middle of ileum however, there was a perforation, and an atresia (obstruction due to non-recanalization of the intestinal cavity during the development). The atretic portion, together with the perforated segment was then excised, washing and evacuation of the spilled fluid and meconium into the abdominal cavity and creation of ileostomy were done. We marveled at the actual operative findings in this baby because we never expected it to be so. Gladly, it wasn’t a cancer or a tumor. So, in retrospect, the perforation occured even before the baby was born. The reason and when it happened, we dont know. This lead to leakage of fluid and meconium into the abdominal cavity that incited reaction from nearby organs, including the liver which became enlarged. There were adhesions also of the intestines due to inflammatory reaction to the meconium that was spilled. The liver then produced low albumin as well that lead to the edema formation.

Baby did well during the operation. No untoward complications took place. We will have to play close attention to the function of the intestines as we have yet to commence feeding.


One week after the discharge, he came back for his return visit to the office. I was surprised upon seeing him. He was so malnourished, his skin was wrinkled and he looked severely dehydrated. In the medical parlance, that is a condition we refer to as “failure to thrive.” Painful as it may be, I had to admit baby again, to “rehabilitate” him from his dreadful status. It seemed that while on ileostomy, most of the milk he has been taking was not absorbed. Instead, he was dumping them and thus the resultant situation. (This is a condition known as short bowel syndrome).

I referred him back to the surgeon for further management. Finally, we agreed to have baby operated on again, to reunite the intestinal segments that were disconnected before to create an ileostomy. After preparing baby for the said procedure, the operation was finally carried out. It took about 72 hours when we noted that baby has patent intestinal segments, he was having regular passage of stools, hence we started feeding baby, initially minimally, then gradually increasing. After he was able to achieve his full enteral feeds, the venous line was discontinued. We even documented this by doing a fluoroscopy, to really check if the intestines are patent. And yes, the dye passed through without impediment through the intestines, no retention whatsoever. This made us then confident that baby’s problem has been resolved. So, for the remaining days of baby in the hospital, he was being fed, he was moving his bowels regularly, his weight noted to be increasing daily. And we were happy to send him home.

He was asked again for follow-up return after a week. And again, baby surprised me. His abdomen was now bloated like a balloon. Again, this puzzled us once more. He seemed to be having Hirschsprung’s disease and this just contradicts how he behaved during the last hospital stay. Well, we had to abide by the baby’s presentation. The surgeon again created an ileostomy, repeated fluoroscopy and obtained biopsy specimen. Then baby was back to his problem of short bowel syndrome. It was not a challenge how to resolve this but with the help of gastroenterologist, we were able to minimize him dumping watery stool. Baby was discharged once more with confidence that his problem has been resolved. Our aim then is to nutritionally build baby and then when bigger enough, will do the corrective surgery.

For now, baby is stable, with a slow weight gain… I really hope it works this time so baby will recover fully before his next surgery.

A Puzzling Abdomen


Posted by on September 7, 2012 in Congenital Anomalies, neonates


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