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Failure to Thrive, Part 1 Oct 16, 2020

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Michelle Thompson, MD, and Solomon Behar, MD discuss the diagnosis of and evaluation of a child with failure to thrive.

Pearls:

Failure to thrive is a weight for age that is less than the third percentile, a weight for height that is below the fifth percentile, or a weight that decreases two or more major percentile lines.
There are generally three reasons kids fail to thrive; they do not take enough calories in, they take enough calories in but they do not properly absorb the calories, or their metabolic needs outweigh the amount of calories that they are taking in.
The majority of the workup is in the history and physical exam.

What is failure to thrive (FTT)? Failure to thrive is the inavailability or unavailability of usable calories. Usually, it is in a child who is less than 2 years of age who meets certain criteria. The three most common criteria used clinically are: 1) a weight for age that is less than the third percentile, 2) a weight for height that is below the fifth percentile, and 3) a weight that decreases two or more major percentile lines.
When babies are first born, they can be large and then at the two or four month visit they are crossing a number of growth percentage lines. How does this type of weight loss play into it? There is wiggle room for adjustment for large babies, preemie babies and babies with intrauterine growth restriction or IUGR. When we talk about an initially large baby in the first months of life 0-3, weight is generally more representative of the placental health and pregnancy factors.
For a premature baby who is really tiny and starts out in the third percentile, how do you make the diagnosis of FTT? We continue to plot preemie infants on a preemie growth chart until about two years of age. You have to look at the velocity of the child’s weight and then take into consideration the height as well. A child who is running below the third percentile consistently, but is tracking along a line below the third percentile, i.e. normal growth velocity, and the weight for height is demonstrating that he is on the normal curve, then genetically the baby may be programmed to be that way. That is not necessarily going to be defined as FTT.
What about a child with a syndrome like Down syndrome who has their own growth curve? Can you do the same thing for them? Plotting along the available growth curves for those special populations when we have growth curves available is very important. To have a diagnosis of failure to thrive, you really do need to see the weight falling off the curve and dropping through percentiles. These days most children who have failure to thrive tend to have some combination of an underlying physical or developmental issue combined with environmental or social factors.
Why do kids fail to thrive? There are generally three reasons kids fail to thrive.
- 1) The children are not getting enough calories
- 2)The children are getting enough calories, but they are not able to absorb the calories
- 3) The children have excess caloric expenditure because their metabolic needs outweigh the amount of calories that they are taking in. This increased metabolic demand can be seen in chronic hypoxemia, chronic lung disease, and congenital heart disease
Let’s say you have a patient who comes to your clinic and he has dropped a few percentiles on his growth chart. Where do we start? Try to identify any patterns to the way the child is growing or not growing. Look at the timing of the concern in the growth. For instance, if a child starts falling off the growth curve at an age when certain foods were introduced, then we might think about some sort of food allergy or intolerance, like celiac disease or a fructose intolerance.
In what situation does the weight start falling off, but the height and head circumference are preserved? That means the child has inadequate nutrition. You can actually reach a point with malnutrition where the height and head circumference suffer as well, but typically you will see the weight drop off first, followed by the length or height and then ultimately if the child is not evaluated and is not treated, then the head circumference can fall as well.
What if the weight and height and head circumference are all falling off together? What is that indicative of? If everything is falling off then typically I am thinking something like a central nervous system (CNS) abnormality or some sort of in utero insult. I go back to the birth parameters. Perhaps this child was IUGR. Maybe there was a in utero congenital infection.
What is the work up for FTT? I want to emphasize that the majority of the workup is in the history and physical exam. There will be some screening labs as well, but these are guided by the history and exam.
- Start off very general with dietary questions. “Tell about meal times in your home”. You really want to ask about what the child is eating and how much the child is eating. Sometimes that means having the family actually do a meal by meal food recall or giving them a chart and having them fill that out at home and bring it back to the next visit.
- I want to know how the meal times are organized and if the meal times are scheduled. Is the child seated at the table with other family members for meals? Are there distractions like TV? Is the child allowed to graze in between meals and play and eat at the same time? What do they drink in between meals? This is where a lot of the over consumption of juice and milk comes in. Are there certain textures or types of foods that the child avoids? For example, some children with autism may avoid certain textures. Or you may have a child who has an inborn error of metabolism that will basically avoid all proteins because every time he eats too much protein, he will start to throw up and feel sick.
What other aspects of the medical history are really important to ask about?
- You definitely you want to go back and get a good prenatal history and a perinatal history.
- - Are there any concerns for in utero substance exposure, drugs or alcohol?
  - Was there any prenatal stress? Was there any perinatal hypoxia or possibility for that?
  - Is there a history of prematurity? What was the baby’s size at birth?
- Going through your systems review, you want to make sure that you are asking about any signs or symptoms that may be related to feeding intolerance.
- - Is there a history of unexplained weight loss in the past?
  - Is the child displaying any vomiting?
  - Is there any evidence of choking with their feeds or difficulty swallowing?
  - Do they have any respiratory symptoms that are chronic or recurrent?
  - Is the child complaining constantly of abdominal pain? Do they have constipation or diarrhea?
- Urinary symptoms are important to ask about as well. You may find a kid producing too little or too much urine, which could be indicative of chronic renal disease or diabetes respectively. Unusual urine odors could be suggestive of an inborn error of metabolism.
- A history of recurrent infections is another important detail to inquire about. Too many episodes of otitis media or pneumonias that aren’t clearing could be suggestive of an immune deficiency.
- A history of rashes could be significant. A persistent rash could go along with any type of atopic history or allergic type history. Some of the immune problems are also associated with rashes.
Moving onto the physical exam what are you looking for that is going to tip you off and give you that diagnosis of FTT?
- Start with growth parameters and get a head circumference, even if you feel the child is older than the age where you normally would check a head circumference.
- Take a good look at dentition and examine the teeth for any evidence of cavities. Actually watch the child eat something. If you cannot, then setting them up to be observed by a feeding specialist or occupational therapist is helpful.
- Examine the neck to see if there is a goiter or any abnormalities of the thyroid gland that we can feel. We want to evaluate for lymphadenopathy that maybe an indication of a chronic condition, oncologic condition or infection.
- Thoroughly examine the heart, looking for any signs of congenital heart problems, listening for murmurs and extra heart sounds, and examining the pulses.
- Listen to the lungs. A child who is constantly wheezing or has adventitious lung sounds may have something like cystic fibrosis or some other chronic respiratory issue.
- A thorough abdominal exam is important to check for masses and organomegaly. Checking for stool retention could indicate constipation or poor motility.
- Look around the anal area, looking for skin tags, fissures, or other signs of constipation may suggest some underlying gastrointestinal pathology.
- The skin exam is important as well. Look for rashes or hypo- or hyperpigmented lesions that may be a sign of a genetic disease.
- On the neurological exam, look for any subtle signs of cerebral palsy or any kind of coordination issue involving mouth movements, chewing, or swallowing.
If the history and the exam do not reveal the cause of FTT, what sort of preliminary lab tests do you do? At that point Thompson does a few preliminary labs with the understanding that sometimes this is going to be very low yield. Some of this testing may clue me into the sequelae of the nutritional issues that the child is having and every once in awhile may lead to the diagnosis.
- Start with a complete blood count (CBC). This can be helpful especially in looking at the hemoglobin and the indices for any indication of a nutritional anemia. We look for a microcytosis for iron deficiency or a macrocytosis indicating a potential vitamin B12 or a folate issue, especially if the child is very restrictive in their diet.
- Order a chemistry panel, specifically looking at the creatinine, and a urinalysis looking at the pH and the specific gravity. Make sure the child can properly concentrate her urine and can screen for renal tubular acidosis.
- Get an erythrocyte sedimentation rate (ESR) which is non-specific, but may help point to an underlying inflammatory condition.
- Consider placement of a PPD skin test if there is concern for tuberculosis exposure or check a lead level if there are any other developmental concerns. Screen for thyroid disease with a thyroid stimulating hormone (TSH) level.
How do you decide to admit a child for failure to thrive? If there is concern for the child’s immediate safety, admit the child to the hospital. For example, if we have uncovered that there is domestic violence or if there are signs of physical abuse, then admit the child. If there is dehydration and we are at the stage where the child clinically does not seem like he will be able to keep up with at least the minimum of his fluid requirements, then admit to the hospital. If there has been a patient that is being followed and we have made interventions that have not resulted in appropriate weight gain, then consider admission to the hospital to expedite further work up. Another reason to admit a child to the hospital for failure to thrive would be a sudden acute weight loss or an excessive amount of weight loss.
What are we doing once the child is in the hospital? As an inpatient, usually the expedited workup is engaging a multidisciplinary team to work together. Sometimes that requires direct feeding observation by speech or occupational therapists. The therapists may suggest additional work up such as a modified barium swallow study. Dieticians can help us ramp up the calories for some of these kids who have really not had adequate nutrition for prolonged period of time.
Is there any imaging that is routinely ordered? No, not really. This is going to be a case by case basis and guided by history and physical.
Is there a definite connection between failure to thrive and parental mental health? Yes, this has been described. The mental health of whoever is responsible for spending time with the child during the day and feeding him will play a role. The caretaker’s own experience with feeding and nutrition even in their childhood can come into play. Addressing issues related to the stressors and the mental health of the caretakers and providing resources for that are really important. One of the examples that Thompson uses is the child who grazes at the breast all day long. That is a source of comfort for the infant and also the mother who maybe tackling her own stressors. Putting the baby to the breast is a way for her to feel more comforted. The baby is basically just grazing all day and fails to thrive because she is not getting any other nutrition.

What are the common things pediatricians should be doing in their offices before referring their patients either to the ER or to the hospital to get admitted for a FTT workup? Frequent follow up visits,, a really thorough history and a good physical exam. Your main goal in that very first visit is to determine if the child is in danger right now. If he is not, then you can do a history and a full physical and bring the child back. It is really over the course of more than one visit that you are going to get to the core of what the issues are and the interplay between those issues.

Bilious Emesis in Neonates Oct 16, 2020

Sol Behar, MD, and Jason Woods, MD discuss the evaluation and management of bilious emesis in a neonate.

Bilious emesis in an infant should be treated as an emergency because this is often a symptom of obstruction due to intestinal atresia or midgut volvulus.
Causes of intestinal obstruction that present during the neonatal period include:
- Malrotation with or without volvulus
- Intestinal atresia
- Hirschsprung disease
- Intussusception (rare in the neonatal period)
- Necrotizing enterocolitis
Malrotation with volvulus. In this condition, the cecum is abnormally positioned in the right upper quadrant and this abnormal positioning predisposes the intestine to twist on its mesentery resulting in volvulus. This causes acute small bowel obstruction and ischemia.
- An upper GI, the gold standard for diagnosing or evaluating malrotation, classically shows a duodenum with a "corkscrew" appearance.
Intestinal atresia. This is a term used to describe a complete blockage or obstruction anywhere in the intestine. Approximately 30% of infants with duodenal atresia have a chromosomal anomaly, most typically Down syndrome.
- The "double bubble" sign is caused by dilation of the stomach and proximal duodenum and strongly suggests duodenal atresia
Hirschsprung disease. This is a disorder of the motor innervation of the distal intestine that leads to a functional obstruction. In Hirschsprung, the nerves that allow the relaxation of the smooth muscle within the intestine wall are missing, so the area that is affected is constricted.

A contrast enema can support the diagnosis of Hirschsprung disease. It will often show the presence of a “transition zone” which represents the change from the normal caliber rectum to the dilated colon proximal to the aganglionic region.

For younger kids who have not had time to develop the “transition zone”, the rectosigmoid index, the ratio between the diameter of the rectum and the sigmoid colon, is typically >1 in normal children

Necrotizing enterocolitis. This is a condition characterized by bowel necrosis with associated severe inflammation, bacterial invasion, and dissection of gas into the bowel wall.
- Pneumatosis intestinalis, a hallmark of NEC, appears as bubbles of gas in the bowel wall.

Meconium ileus is caused by the obstruction of the small intestines with inspissated meconium. Approximately 10% of patients with CF present with meconium ileus.

Cephalosporins - Part One Oct 16, 2020

Pediatric ID specialist Michael Neely, MD, and Michael Cosimini, MD discuss how cephalosporins work and which bugs they do and do not kill.

Pearls:

In general, cephalosporins do not cover anaerobes, enterococcus, listeria and MRSA.
Oral cephalosporins are generally not first line in pediatrics. Some exceptions include the treatment of UTIs and some skin and soft tissue infections; group A strep and sinopulmonary infections in penicillin allergic patients are other common indications.
1st generation cephalosporins do have gram positive coverage, but do not work well against strep pneumo, MRSA, enterococcus. They do cover some enteric gram negative bacteria, the “PECK” organisms.

What are cephalosporin antibiotics and how do they compare to penicillins? Chemically, both penicillins and cephalosporins are beta-lactam antibiotics, with the beta-lactam portion responsible for bacterial killing. The chemical portions off the beta-lactam ring make the antibiotics different.
- Beta-lactam antibiotics work by binding to the penicillin-binding protein on the bacterial cell wall. These proteins have structural functions that maintain the integrity of the bacterial cell wall and therefore, when these antibiotics bind, the penicillin-binding protein is disrupted, the cell wall falls apart and the bacterial dies.
How do you keep a straight spectrum of activity for antibiotics? To help with this, think of bacteria into big categories: gram-positive, gram-negative and “other”.
- Gram-positive bacteria include:
- - Staph aureus (MSSA, MRSA), Streptococcus (Group A Strep, Group B Strep, Strep pyogenes, Strep viridans), Enterococcus, Pneumococcus, Listeria
- Gram-negative bacteria are a much bigger group and can be divided into:
- - Respiratory gram-negatives include Moraxella, Haemophilus, Meningococcus
  - Enteric gram-negatives include the “PECK” bacteria: Proteus, E.coli, Klebsiella
What bacteria do cephalosporins not cover? In general, cephalosporins do not cover anaerobic bacteria, enterococcus, listeria and MRSA. There are a few exceptions to this rule.
- Cefoxitin (a second generation cephalosporin), for example, does have anaerobic coverage. It is commonly used in the treatment of PID as it covers enteric anaerobes and Neisseria gonorrhea.
- There is a 5th generation cephalosporin that does cover MRSA (discussed later).
Are cephalosporins well absorbed? Generally speaking, cephalosporins in oral formulations are not as well absorbed as penicillins and are more difficult to get where they need to go outside the urinary tract.
- Also, generally speaking, no beta-lactam really gets into the spinal fluid in very high concentrations; all of them do have better penetration when there is inflammation. Practically, remember that the penetration into the CSF between ampicillin and ceftriaxone is negligible.
What bacteria do first generation cephalosporins cover? Although the classic teaching is that cephalosporins are good for gram-positive coverage (staph and strep), this is not a hard and fast rule. As stated, enterococcus is not covered by any cephalosporin and MRSA is not covered by most cephalosporins. First generation cephalosporins are also good for coverage of the “PECK” enteric gram negative bacteria, but not good for coverage of other gram negative bacteria. These organisms tend to cause UTIs and therefore, first generation cephalosporins (for example, cephalexin) are frequently used for UTI treatment. Of course, resistance can occur.
- Even though strep pneumo is a gram-positive organism, when it comes to first generation cephalosporins, it acts like a gram-negative organism and therefore, first generation cephalosporins do not work well against strep pneumo.
What about bacteria that develop resistance? A patient with an E. Coli UTI, for example, may have a microbiology laboratory report stating that the E. Coli is resistant to a first generation cephalosporin but the patient is still getting better. This may have to do with the type of infection the patient had; for example, a healthy patient with a simple cystitis may have been able to stay well hydrated and the normal immune system was able to clear the E. Coli.
- This question can also be answered in the context of breakpoints, that is when the bacteria become susceptible or resistant to the antibiotic depending on the site of infection. Some labs will actually label a bacteria resistant or susceptible depending on whether the infection is in the urine, spinal fluid or blood.
- - Therefore, if a lab that reports site-specific breakpoints suggests that an E. Coli is resistant to a first generation cephalosporin in the urine, the lab has already taken into account the higher concentration of drug in the urine. Similarly, a pneumococcal isolate that may be resistant to ceftriaxone in the CNS may be susceptible to ceftriaxone as a pneumonia because there are much higher concentrations of ceftriaxone in the lungs than in the spinal fluid.
When should a skin or soft tissue infection be treated with a first-generation cephalosporin? When should MRSA be suspected? This can be a tricky question as an outpatient, but there are some clues to gauge whether or not the infection may be caused by MRSA.
- One, it is helpful to know the community prevalence of MRSA. In some communities, community acquired staph aureus infections are up to 80-90% MRSA. In these communities, MRSA coverage should of course be given. If the prevalence is much lower, using a first generation cephalosporin, such as cephalexin may be reasonable.
- Other clues can be more specific to the patient the their families. Is the patient or family known to be colonized with MRSA? Have they had an MRSA infection in the past?
- - If MRSA coverage is needed, either trimethoprim-sulfa or clindamycin generally is a good approach. A randomized controlled trial published in the NEJM showed no difference in outcomes when treating a known MRSA infection.

Miller LG et al. Clindamycin versus trimethoprim-sulfamethoxazole for uncomplicated skin infections. N Engl J Med. 2015 Mar 19;372(12): 1093-103. https://www.ncbi.nlm.nih.gov/pubmed/25785967

In general, the quality of the infection does not help point to MRSA or not. There is some suggestion that if there is a soft-tissue abscess this is more likely staph aureus and if there is just pure erythema, tenderness and warmth without abscess, this is more likely to be Group A strep.
- Remember, no matter what antibiotic is started for cellulitis (or any infection, for that matter), follow up is essential. If you are on the right antibiotics, cellulitis should be improving within 24 hours.

Herpes Simplex - Part One Oct 16, 2020

Andi Marmor, MD, and Lisa Patel, MD review the cutaneous and systemic manifestations of HSV1, when testing is indicated, potential co-infections, and discuss management strategies depending on presentation.

Transmission of HSV-1 occurs when someone with no prior infection comes in contact with herpetic lesions, mucosal secretions, or skin lesions that contain HSV-1. Transmission can occur when infected body secretions come into contact with a break in the skin.
In the acute phase of the infection, the herpes virus replicates at the site of contact. From there, the virus enters the sensory nerve and travels to the ganglion. Typically it establishes latency in the trigeminal nerve ganglion (or sacral ganglion depending on the initial site of infection) and it can then reactivate in any of the branches of that nerve throughout life.
HSV PCR and viral culture are the two tests used to confirm the diagnosis of HSV.
- A viral culture can distinguish between HSV-1 and HSV-2.
- HSV PCR is typically faster and more sensitive than a viral culture.
- Serologic testing has a limited role in acute infection but can be helpful in establishing prior infection in someone who is, for example, undergoing an organ transplant where antiviral prophylaxis might be needed.
Primary HSV-1 oral infection usually presents as gingivostomatitis in children. High fevers and malaise are the typical prodromal symptoms which are then followed by the development of painful vesicular lesions. Lesions can affect the entire gingiva and also often involves the buccal mucosa, tongue, and the floor of the mouth. There may also be some sores on the outside of the mouth and around the lips.
- In coxsackievirus, the majority of the lesions are in the posterior oropharynx whereas with HSV gingivostomatitis, the majority are in the anterior mouth. The distribution of the lesions can help distinguish between the two viruses.
Children with gingivostomatitis may require hospitalization for pain control and/or dehydration.
For pain management, Andi advises using around the clock NSAIDs and does not recommend using Magic mouthwash.
- Magic mouthwash is typically a 1:1:1: ratio combination of viscous lidocaine, diphenhydramine, magnesium hydroxide (or aluminum hydroxide) mixed with a flavored syrup. Andi does not recommend because 1) viscous lidocaine is well absorbed through the oral mucosa and can quickly reach a toxic level in young kids and 2) there is not much evidence showing that improves pain control or that helps kids hydrate.
- Honey was shown in a recent randomized control trial to both improve pain control and less than the time to healing.
Acyclovir, in addition to supportive care measures, is recommended in children with severe symptoms and who present within 72-96 hours of disease onset. A Cochrane review from 2008 showed that it decreased the time to healing and lessened the amount of pain medicine needed. The typical dosing is 15 mg/kg by mouth (maximum single dose 200 mg) five times per day.
Herpetic whitlow is an infection of the soft tissue of the finger caused by HSV. It is usually localized to the nailfold. These lesions are initially clear-yellow vesicles that then coalesce into a larger blister. Herpetic whitlow is often confused with a bacterial infection like paronychia or a pulp abscess.
- Unlike a paronychia, the area filled with pus is not tense in the setting of herpetic whitlow.
- Treatment in most cases is doing nothing. The time that this takes to resolve is two to three weeks. Consider treatment with acyclovir if it is on multiple digits, if the child is systemically ill, or if there is concern for a more widespread infection.
Herpes gladiatorum is a skin infection that classically occurs on the face, neck, and arms of wrestlers.
Eczema herpeticum is a widespread HSV infection of the skin in a patient with pre-existing atopic dermatitis. Vesicles and characteristic "punched-out" lesions with hemorrhagic crust appear on areas of pre-existing skin disease.
Complications of eczema herpeticum include a superimposed bacterial infection, particularly with Staph. Because of the potential seriousness of this condition, treatment with systemic acyclovir is recommended oftentimes with an anti-staphylococcus medication in addition.
- The continued use of topical corticosteroid for the treatment of the underlying eczema is somewhat controversial but a recent paper in Pediatric Dermatology showed that receipt of topical steroids did not prolong hospitalization.
The most common secondary reactivation is recurrent herpes labialis or cold sores of the lip - that is a recurrence of HSV that has been lying dormant in the trigeminal ganglion.
- Triggers for recurrence include immunodeficiency, stress, exposure to sunlight, and fevers.
- The lesions are typically present along the vermilion border but they can also be present on the oral mucosa. Most patients have prodromal symptoms including pain, burning, or tingling,
- Topical treatments, such as Penciclovir, have shown some benefits. However, given the need for frequent application, some people advocate for the use of oral acyclovir. Oral therapy has been shown to shorten the course of infection when taken during the prodromal period.
- Chronic suppressive therapy is recommended if recurrences are happening four or more times a year and there is no predictable prodrome.
Herpes keratitis is a corneal infection that is caused by reactivation of herpes virus that has been latent in the trigeminal ganglion. It tends to present as a unilateral, uncomfortable tearing eye with redness and irritation.
- On fluorescein exam, you will see dendritic lesions.
- Patients should be referred to Ophthalmology for a slit lamp exam and for monitoring the integrity of the cornea.
Herpes virus can cause peripheral facial nerve palsy. In a peripheral seventh nerve palsy, there is weakness affecting the mouth, eye and forehead. It is the involvement of the forehead musculature that distinguishes it from a central lesion. Patients with a peripheral facial nerve palsy will have weakness raising the eyebrow and wrinkling the forehead.
Neonatal HSV is classified into three categories: localized skin, eye and mouth (SEM); CNS and disseminated disease.
- SEM disease is associated with typical herpes ulcers on the face or on the mucous membranes seizures and encephalopathy.
- Manifestations of neonatal HSV CNS disease include seizures and encephalopathy
- Disseminated HSV has a sepsis-like presentation, involving multiple organs. These neonates are critically ill.
- Women with a primary genital HSV infection acquired near the time of delivery have the highest risk for transmission.
HSV encephalitis is mainly caused by HSV-1, whereas meningitis is more often caused by HSV-2

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