RSS

Category Archives: neonates

prenatal care

(pic: http://www.camelliawomenshealth.com/Prenatal-Care)

The importance of prenatal visits can never be underemphasized. It is a must that all pregnant mothers, regardless of social and economic strata, should receive adequate prenatal care for a successful outcome of the pregnancy.

I was once called to attend to a baby who was born premature at 36 weeks via emergency cesarean section due to uncontrolled maternal hypertension. The baby was having uncontrolled seizure despite the fact that the baby was already seen by a neurologist and on anti-convulsant. I requested some laboratory tests and results revealed that he has low sodium levels (hyponatremia) at a level that can trigger seizures.

Going back to the mother’s prenatal course, she didnt know she was pregnant then because of irregular menstrual cycle. There was a certain period when she noticed that she was having bipedal edema (swelling of both lower extremities). She was self-medicating with furosemide, to no avail. She consulted a nephrologist who noted that she too was having elevated blood pressure. Unknown to both of them, she was pregnant and this was not at all investigated. The mother too was a bit plump and she never noted abdominal enlargement until few days prior to delivery when the abdomen was already large enough to disregard. Furosemide was continued. Abdominal ultrasound revealed a singleton pregnancy. Because of the uncontrolled blood pressure, baby had to be delivered thus.

The mother’s prolonged intake of furosemide, a loop diuretic, lead her to have electrolyte imbalance, particularly sodium. This was reflected to the baby who also had low sodium levels at a level that could trigger seizure. Had she known she was pregnant, and had she been receiving prenatal care, this could have not happened to her baby. The effect of the seizure to the baby’s brain is another story.

Advertisements
 
Leave a comment

Posted by on May 22, 2017 in neonates, Pregnancy

 

Giving Birth in the Cordillera Mountains

It has been two years since I started attending the Regional Neonatal and Maternal Death Review in our region, the Cordilleras. I had been invited to be a panelist and as such, it is my duty to critique why such happened, and what should have been the intervention, and what could have been the possible problem that really transpired for such a death. But this forum is not only me and my fellow panelists giving our “expert opinions.” Rather, I in particular had so much learnings and realizations that makes the scenario surrounding each death very painful to accept and embrace as a health care provider. These are some of the few things I came to realize…

GEOGRAPHY

One of the problems identified in our region is the geography. Because of the mountainous terrain of Cordilleras, one pregnant woman would need to hike 45 minutes, some 1 or 2 hours from their house just to reach the road or access a vehicle that will bring them to the nearest barangay health station (BHS), or rural health unit (RHU). Imagine a pregnant woman in labor, walking this distance in between contractions, you would expect a longer time to access the road. Likewise, because of this terrain, some areas are infested with the rebels (New People’s Army) that deters them to go the the nearest health facility, no matter what stage or phase of health emergency they are already in. So if the mother is having post-partum bleeding, they will wait till sunrise before the go to the nearest BHS. And if the midwife at the RHU or BHS would not be able to address the problem, they will have to transfer the patient to the nearest district hospital, which might again take them a while to look for a vehicle that will transport them there.

Another problem that the geography poses is the lack of telecommunication network’s signal. While the nurses, barangay health workers may have mobile phones that would facilitate referral to their superiors for proper advise while patients are being transported to higher centers, the lack of communication signal deters such and thus are only addressed when the midwives or the receiving doctor in the district hospital sees the patient

LACK OF HEALTH CARE PROVIDERS

Another deterrence to full delivery of health care to every household in the rural is the lack of midwives. While there may be barangay health workers (lay people who are not necessarily midwives who can be first line to check on ailing residents), it is the midwives who supervise them and who will ultimately decide whether she can manage the scenario or refer the patient to higher institution. In one municipality alone in Ifugao with 18 barangays, they only have 5 midwives. ONLY 5 midwives. Again, consider the distances of each house, their distance from the BHS or RHU or district hospital. And they usually access these houses on foot. Midwives need to track women who are pregnant, follow them up at the RHU, refer them to higher centers if the pregnancy is high-risk, deliver their babies if unable to reach a birthing facility, follow them up to make sure the mother-baby dyad is in perfect condition, submit monthly report to their municipal health officers.

During the past administration, nurses (nurse deployment program, NDP) and doctors (doctors to the barrios, DTTB) were hired to augment this vacuum of labor force. The nurses were deployed to each barangay or two, to help and facilitate the work of the midwives. Definitely being novice in the community and public health, there are flaws and misgivings, that given more time and experience, these will eventually be addressed. Nevertheless, there was a noted decrease in the number of maternal and neonatal deaths because they were monitored.

Unfortunately, starting next year, these contractual employees will no longer have their contracts renewed, making again the workload of our midwives double, maybe triple or quadruple when the NDPs are gone. Thus a rise again in the number of maternal and neonatal deaths will not be a surprise.

LACK OF SKILLS

We the panelists are specialists and subspecialists. We talk of interventions appropriate to our settings, which is way far up compared to the birthing facilities that the NDPs, midwives and MHOs work at. For one our NDPs, who are mostly first time on the job, still lack clinical acumen to detect subtle signs of disorder in the newborn, or signs of high risk pregnancy. Thus they only become alerted when the severe complications have set in, and thus intervention would be late already. Recognition of these subtle signs and early referral would definitely make a significant difference in these conditions.

Not all midwives are skilled in performing episiotomy. Not a single midwife in the region is even skilled in performing full course of neonatal resuscitation. Even doctors at district hospitals are not specialists to correctly treat these problematic parturients and/or their babies.

CULTURE

One thing that I commonly noticed is the influence of the matriarch of the family or clan. Usually, especially in a place where the house of the parturient is far from the nearest birthing facility, a birth plan is laid out. They assign which (of the limited vehicle) will be used to transport in case she goes on labor. And after birth, how soon they will be visited by the midwive or NDP. In other instances however, the matriarch interferes and alter already the planned contingency. A first-time mother ought not to contradict what their “experienced” seniors dictate upon them. While our health workers are campaigning and encouraging health facility deliveries, some “experienced” matrons insists that their daughters deliver at home, with them helping out. Only then will they call for help when they encounter a major problem. One classic example was when a woman on her third pregnancy delivered at home, assisted by the family members. It took them several minutes attempting to deliver the placenta. And because the placenta was adherent to the uterine wall, as they were tagging the former, the uterus inverted. Only then was the midwife called. And because there was no “birth plan” it took them several hours before the parturient was brought to the hospital. There was massive hemorrhage, with the source not identified, that eventually lead to hemorrhagic shock and her death. Such useless loss of lives would have been prevented had it not been for the “usual practice” that these elder people enforced.

 

Many of these problems presented are often preventable but it takes interplay of so many factors to prevent one maternal or newborn death. Our region as a long long way to go…

 
Leave a comment

Posted by on November 29, 2016 in Deliveries, neonates, Pregnancy

 

Tags: , , , , , , , , , , , , ,

My First Case of Congenital Cytomegalovirus Infection

I have this opportunity to demystify an infant’s case of long standing jaundice…

The mother’s prenatal course was apparently unremarkable, save for gestational diabetes that was controlled. The mother cannot remember any other symptoms such as flu-like illness, skin rashes, nor was she hypertensive during the prenatal period. Baby was delivered via repeat cesarean section, small for gestational age. He stayed quite long in the hospital because of infection. He was purely breastfeeding. His newborn metabolic screening result was normal. I was not the attending then.

At home, baby was quite fuzzy and irritable. Baby has been being attended to by the original neonatologist. He was jaundiced. In cases of purely breastfed babies, sometimes jaundice can be expected to last for about 3 months but the intensity is not that much compared to that during the first week of life. His stool color was still yellow. He developed umbilical hernia. The skin texture was fine; tongue was normal in size; hair was not coarse; there was no hypotonia; nor was there any constipation (something that is a remarkable findings among babies with hypothyroidism). Baby was worked up for possible hypothyroidism. Thyroid function test was normal. They were advised to go to a pediatric endocrinologist for evaluation.

Mother brought baby to my clinic for second opinion. I saw the laboratory result, it was normal. But what is puzzling is the jaundice that was quite intense. I could not evaluate baby well, especially the abdomen, because he is irritable. I advised mother that baby needs further test and treatment thus they agreed to be confined in the hospital.

I repeated the thyroid function test, it was normal. That reassured me baby has no congenital hypothyroidism which is one dreaded condition a baby can have because of life dependency on thyroid hormones for better quality of life and to attenuate whatever cognitive impairment it has already caused. I still called up an endocrinologist friend to confirm my understanding of baby’s thyroid function test result and she agreed baby is not a case of metabolic disorder.

I treated the baby as a case of sepsis pending work up results. Ultrasound of the abdomen showed the liver is enlarged, the biliary tree is intact. I am not afraid that this baby has biliary atresia which is another “lethal” condition that usually leads to baby’s death in a slow fashion.

Liver enzyme, alkaline phosphate and bilirubin were all elevated (it was a direct hyperbilirubinemia). I started the baby on ursodeoxycholic acid to help eliminate the bilirubin that could also cause inflammation of the liver cells.

After a week in the hospital, baby’s jaundice has significantly decreased and yet the direct hyperbilirubinemia (50%) was still persistent, and alkaline phosphatase level was still significantly elevated. I have discharged baby with instruction to undergo karyotyping and TORCH screening as I haven’t ascertained yet what was causing the baby’s jaundice.

A week later, mother brought back the results of baby’s tests. Karyotyping was NORMAL (thank God). On the other hand, TORCH panel revealed (+) IgM and IgG for cytomegalovirus. I referred the baby immediately to an ophthalmologist for chorioretinitis screening, and to a pediatric infectious disease specialist for further management. CT Scan of the head showed that there were periventricular calcifications near the parietal areas of the brain.

Baby is still jaundiced although the intensity is no longer that dark. He is on supportive treatment.

He will undergo repeat head CT scan as well as chorioretinitis screening one month after the first.

 
 

Tags: , , , , , ,

OF BLOOD SUGAR AND CLUELESSNESS

Neonatal emergencies really make pediatricians and neonatologists high-strung as this event in the baby’s life significantly affects his future. One of those emergencies is a problem with baby’s blood sugar, whether it is elevation or depletion. Either way will produce a grave sequela if not immediately corrected.

The cut off value whether to consider the blood sugar low or high is quite controversial. Hyperglycemia (elevation of blood sugar) may be considered when the reading is above 120 mg/dL; but others may use higher cut off value. In one study, the ceiling value was 140 mg/dL. That study mentioned that any blood sugar elevation above 140mg/dL within the first week of the baby’s life is highly associated with infant mortality. (Of course, this elevation is not a product of medical and nursing error). But the study does not state whether higher value means greater risk of dying and vice versa. In my limited practice, I have noticed that this study finding is true in almost all cases, except for one. Elevation of blood sugar may mean hormonal imbalance, but most commonly an infectious process.

Hypoglycemia (low blood sugar) also has controversial cut off value. Some use 50 mg/dL, others use 40 mg/dL and another article uses operational cut off value at 36mg/dL.  As with hyperglycemia, hypoglycemia as well has unwanted sequela. Baby can either be asymptomatic or have life-threatening nervous system or cardiopulmonary disturbances. Some of the symptoms include lethargy, cyanosis (bluish discoloration), apnea (cessation of breathing), jitteriness/seizures, congestive heart failure, or hypothermia. Clinical manifestations of hypoglycemia with the activation of autonomic nervous system include anxiety and tremulousness, diaphoresis (sweating), tachycardia, palor, hunger, nausea and vomiting. When the central nervous system is depleted of blood sugar (hypoglycorrhachia) it may manifest with the following

  • Headache
  • Mental confusion, staring, behavioral changes, difficulty concentrating
  • Visual disturbances (eg, decreased acuity, diplopia)
  • Dysarthria
  • Seizures
  • Ataxia, somnolence, coma
  • Stroke (hemiplegia, aphasia), paresthesias, dizziness, amnesia, decerebrate or decorticate posturing

(reference: http://emedicine.medscape.com/article/802334-clinical#a0256)

During fetal life, glucose is a very significant fuel for development, especially that of the brain. If glucose level is maintained adequate, it brings about normal levels of the substance insulin-like growth II (IGF-2). The latter, IGF-2, promotes increase in the number of neurons, also increase in dendritic-axonal arborizations, which thus means faster transfer of neuronic impulse. Depletion then of the brain of blood sugar brings about the opposite, and may thus lead to a patient with cognitive-impairment. Babies who had intrauterine growth restrictions (IUGR) during pregnancy are often the victims of this.

Hypoglycemia may be caused by a lot of factors. It may be due to lack of supply and storage in the liver (eg, prematures, IUGRs); may be caused by excessive consumption during stressful conditions (eg, sepsis, asphyxia) or maybe due to excessive insulin production (infants of diabetic mothers, large for gestational age).

Once my patient, your baby, is detected to have a low blood sugar reading, you now understand why I get so hyped to have it corrected at once. I do not only want your baby not to have seizures… I don’t want your baby to grow up CLUELESS.

 
Leave a comment

Posted by on July 3, 2013 in neonates

 

Tags: , , , , ,

Aside

I got an interesting referral from one hospital. It is not really that difficult of a case but it is quite puzzling for the untrained ones, nevertheless interesting.

The mothers’s history is generally unremarkable. She only had some flu-like symptoms during the last trimester of the pregnancy. There was no history of hypertension nor diabetes. Mother’s prenatal visits were timely and regular as this is very much wanted pregnancy. Generally, she never had symptoms. She came to the hospital in labor. She had an ultrasound which stated that the baby is in fine condition, there was adequate fluid. About 12 hours into delivery the bag of waters ruptured. The mom recalled that she noted the fluid to be yellow-stained (normally it should be clear). There was no foul odor.

She gave birth by normal vaginal delivery. The baby was not that big, weighing only 2.6 kgs. There was no difficulty during baby’s delivery. There was no cord loop around the neck (that may have strangulated the baby). The fluid was viscid, thickly saturated with meconium (baby’s first stool). Few minutes thereafter, the baby began to have respiratory distress requiring oxygen support.

Baby had an xray of the chest revealing pneumonia. He was then started on empiric broad spectrum antibiotics. Baby was nursing well from the mother while on oxygen supplementation. There was no progression of the respiratory distress. Despite requirement for oxygen, baby remained comfortable. On the 5th day of life, baby still cant be weaned off from oxygen, breathing was still fast although comfortable. Repeat xray of the chest revealed significant clearing of the pulmonary infiltrates initially seen on the previous xray. An arterial blood gas analysis was done but it was unremarkable. So why then is the baby requiring oxygen despite the comfortable breathing, normal blood gas analysis and clearing of xray picture?

The baby was then referred to me at this time. At first I went with the line of unresolved infection so I suggested shifting of antibiotics as well as determination of c-reactive protein (an indicator of inflammation – often due to infection, that may as well be used to monitor response to treatment).

The CRP was reactive, meaning it indicated presence of an ongoing inflammation/infection, but the value was not congruent with the distress of the baby. So I tried to play along with some of the facts that the baby presented. First, baby was born throught thickly meconium stained amniotic fluid. Second, the baby’s initial xray findings highly suggested pneumonia. Third, the baby remained oxygen dependent despite ample time for antibiotics to have worked, granting this was supposed to be an isolated pneumonia. Fourth, despite improvement of x-ray picture, the baby remained, clinically, unimproved; was still dependent on oxygen support.

With these, I came to rationalize that baby might be having meconium aspiration pneumonia (MAP). (While meconium is supposed to be sterile , meaning it is free of bacteria, antibiotics was a rational modality of treatment as CRP was reactive). But on top of the MAP, I considered that baby might be experiencing as well a complication.

I then requested to obtain blood gas analysis from the right and the left arms, with emphasis on the pulmonary oxygen between the two sites.

pda1

The aorta, the main vessel that arises from the left ventricle (red vessel creating a loop on the above illustration) gives rise to three large vessels that supply the upper part of the human body. The first branch immediately divides into two, one serving as right subclavian artery (that which supplies our right arm) and right carotid artery (that branch supplying to the blood). The second main branch becomes the left carotid artery which also supply our head on the left side whereas the third main branch is the left subclavian artery which supplies our left arm.

There usually is a ductus arteriosus that exists in the fetus and closes permanently about 10 days after the baby is born. It usually arises after the right subclavian and carotid arteries, and before the left subclavian artery. Thus, by origin, the right subclavian artery is usually termed preductal while the left subclavian artery may be, most often, post-ductal. Since preductal vessels include those vessels that send blood supply to the brain, it is also then safe to assume that preductal blood picture also reflects the same blood picture that goes to the brain.

In cases of pathology when the pressure in the right side of the heart is higher than that of the left, and the ductus artery is still patent/open, the unoxygenated blood in the right side may dilute the already oxygenated blood in the left through the ductus arteriosus. In cases therefore involving increased right-sided pressure, the baby tends to be cyanotic from this explanation.

One way of determining whether there is a significant shunting from the right side to the left side via the patent ductus arteriosus is performing a 2-D echocardiography, which exactly measures the pressures between the two sides of the heart. Just compare your obtained pressure from the right side of the heart with the normal values for age and you can immediately say there is elevation of pressure, or simply put pulmonary hypertension. Another way of determination is to obtain blood gas from preductal (right arm) and post ductal (left arm, right foot, left foot) extremities. Then, compare the partial oxygen tension/pressure (pO2). A gradient between right and left of more than 20 mmHg is highly suggestive of right sided pressure, in this case, persistent pulmonary hypertension, of the newborn (also known as persistent fetal circulation).

The baby’s right arm blood pO2 was 81.7mmHg, whereas the left arm pO2 was 42.16mmHg. There was a gradient between right and left arm of 39.1mmHg, way higher than 20mmHg cut off, clearly suggesting that the baby has a pulmonary hypertension. Pulmonary hypertension usually arises when the small supposedly thin capillaries in the lungs that carry blood for oxygenation thickens. With thick pulmonary vessels, the transit of oxygen from lung alveoli to the blood vessels is rendered more difficult and hence the slow or lack of oxygenation of the blood that returns to the heart, making the baby a little bluish. And if the pulmonary hypertension is severe, this “resists” the incoming blood from the heart and is shunted directly into the aorta via the ductus arteriosus, unoxygenated, already diluting the blood that may have successfully went into the lungs for oxygenation (but not sufficiently). This can turn into vicious cycle until the baby’s demise.

In cases however of pulmonary hypertension, where the wall between the right and left atrium has a large communication known as patent foramen ovale, since at the level of atrium there is already mixing of blood between right (unoxygenated) and left (oxgenated) sides of the heart, there may not be an appreciable gradient of pO2 between preductal and postductal blood gas analyses.

Respiratory Distress?

 

Tags: , , , , , , , , , ,

Ooops!

I was once called for a referral. A few days old preterm baby having seizures that occurred within the first few hours of life. Baby was having seizures despite the anti-convulsant that was already given. The baby was already referred to a neurologist before I stepped into the picture. Baby was worked up and his electrolytes showed low sodium (112). (The normal level is 135 – 145; if the value is lower than 135, that’s considered hyponatremia. If value is less than 125, baby can have seizure that will not be controlled by anticonvulsant until the problem is corrected). In this case, it seems the most likely cause of seizure was identified. Thus, the immediate thing for me to do was to correct this abnormality and hope that it will eventually stop the seizures.

So after 48 hours, the sodium level was already raised to near normal. The good thing was, seizure already stopped. So I guess the baby’s urgent problem was resolved.

The question that bothered us was, why did the baby have severe hyponatremia? It is a rule of thumb that the electrolyte picture of a baby within 48hrs from birth generally reflects that of the mother. Unless that baby also has a congenital abnormality such as in cases of congenital adrenal hyperplasia (CAH). The baby in this case did not have physical signs highly suggestive of CAH, and the newborn screening eventually was normal, so this as the cause was easily ruled out. So, this made me then thought of the mother’s electrolyte status.

I interviewed the mother when she visited her baby at the NICU. I asked her if she was on prolonged intravenous fluid administration, if she was taking medications. She revealed she was on prolonged furosemide “maintenance.” This was given by an internist she consulted. BINGO! Seems I nailed the culprit with mere few questions. So I went on further with my interview. I asked why was she on prolonged furosemide intake. She said, she consulted the internist because she had edema (swelling) of both her lower legs. I further asked, “at what months of pregnancy did she notice the onset of edema, of hypertension. She did not know she was pregnant then when she had that consultation. Then my next question was, “is your menstrual cycle irregular?” And she replied YES! I was then flabbergasted and felt sorry for the mother, most especially for the baby. Why?

Let me reconstruct the story for a clearer understanding. Here was a woman with irregular menstrual cycle. She became pregnant but was not able to realize it because of her irregular schedule. Then later in the pregnancy, she developed edema of both lower extremities. She consulted an internist because of the latter, who also incidentally discovered she was hypertensive. The internist did not know the patient was pregnant; he did not do pregnancy test nor abdominal ultrasound. Pregnancy was remote from his consideration, thus he did not do these tesst… even if the woman was already showing signs of PREECLAMPSIA. So he gave furosemide. But since the edema was unresolving, she kept on taking the drugs. Few days ago, she was having abdominal pain. She saw another doctor, an OB-Gyn, who requested for an ultrasound. HALLELUJAH of all hallelujahs, she was indeed PREGNANT. And since her blood pressure remained uncontrolled, she was scheduled for emergency CS delivery. Since she was on prolonged furosemide intake, aside from it removing water from the body, furosemide also eliminates electrolytes like sodium and potassium. Since she was already hyponatremic, so was also the baby whose blood supply comes from the mother via the placenta.

The rest of the baby’s course in the neonatal ICU was unremarkable thus I signed out from the service after making sure baby was ready for discharge.

 

Tags: , , , , ,

Resourcefulness in Saving Babies’ Lives

In rural places where sophisticated technology, medicine are scarce if not available, how do physicians like me deal with a baby with a life threatening medical condition — congenital adrenal hyperplasia?

In my place of practice, with about 250 thousand population as of the latest, there is 1 government tertiary (pediatric residency training) hospital and 3 private hospitals (but one pediatric residency training hospital) that could possibly admit cases such as CAH. We do not have pediatric endocrinologist, and the nearest one is in Manila. There are 3 adult endocrinologists though.

At time that we see babies with the above condition, our training as neonatologist is our first armamentarium especially when our babies are in crisis/es, then a proper communication with our pediatric endocrinologists in Manila for further evaluation and management. It would be best if our patients have all the resources to have all necessary tests done, the medications bought. Unfortunately, not all Filipinos are in the same social stratum.

A baby who is already a month old came to my office for second opinion. Baby has ambiguous genitalia,  small for age and showed wrinkling of the skin (sign of failure to thrive), with a serum electrolyte test result (done weeks ago) and a confirmatory result for congenital adrenal hyperplasia. Mother wanted to know what are her options, and if this condition can be reversed. (It is so hard to tell a very definitive answer for these type of questions as sometimes, patients tend to misquote you when they go to another doctor if they are unsatisfied with your answers, or answer them satisfactorily but those weren’t the answers they were wanting to hear.)

One of the problem of congenital adrenal hyperplasia, aside from low circulating cortisol in the body system, is the loss of sodium. (They usually go together). If the sodium goes below critical level, it can trigger seizures that cannot be controlled by anti-epileptic drugs, until the sodium deficit has been corrected. This was my immediate concern. So I had to check first the sodium level of the baby and true enough, it was very low, near the critical level for seizures.

So what will a “probinsiyano” or rural physician do in this scenario? The best and ideal approach was to admit the baby and do necessary correction of the sodium deficit. But the mother refuses. Even if I strongly disagree with the mother bringing the baby home, I cannot force her. Thus, I had to be resourceful and creative on how to treat baby at home.

With regards the sodium deficit, this is usually computed (based on a formula that we, especially neonatologists should bear in mind). Next, derive the maintenance dose of sodium in 24 hours, which is often between 2 to 4 mEqs/kg/day. (If you are dealing with a baby who has deficit, then better use the maximum, which is 4mEqs/kg). Sodium correction however should not be done rapidly, it should be done in 48 hours, at a steady rate (and hence the requisite for a hospital admission).

I was able to compute baby’s sodium deficit and maintenance. Baby is on formula feeding to begin with. I asked the mother what is the average milk consumption for a day and that is where I based my computation. I was able to derive how much sodium is provided by the milk to the baby and it is just the same as the maintenance requirement. So now, my problem is how to deliver/administer the deficit.

There are sodium tablets that could be divided into papertabs and then you can incorporate that to the milk intake of the baby. (Of course, the taste of the milk will be altered — and that might again cause refusal of baby to feed, but then there’s no other way that I can administer the medication as mother refuses baby’s hospitalization). Unfortunately, there are no sodium tablets available locally. So the next alternative for me is to use the ampules or vials of NaCl solution available in the pharmacy (2.5mEqs/mL). With my computation, I got how many mL of the solution is needed per day, divide it into number of feedings per day. After 48 hours, I asked the mother to have the serum electrolyte repeated. Lo and behold, it went normal… So am I done with the baby’s problem? No… because the salt-losing part of the disorder is permanent, unless corrected by medications… which they cant afford yet as of the moment.

I had to maintain the baby on the available steroid and continue the sodium supplementation until the day when parents are able to save for the expenses baby will incur. A month has passed by already, and the baby’s sodium level has been maintained within acceptable level, and baby has been gaining weight as well. Mom checks baby’s sodium on a weekly basis… for now.. I really wish they will be able to raise funds for this…

(Disclaimer: this method of correcting sodium deficit has not been documented by a randomized controlled trial. But for now, it is the only available option I had for this patient. I credit my mentor Dr. Emilio A. Hernandez for teaching me this technique while I was under his tutelage as a neonatology fellow).

 

Tags: , , ,