Adenotonsillar hypertrophy as a cause of failure to thrive

Two infant aged 11 and 15 months presented to the Gastroenterology 
Clinic at Alberta Children's Hospital because of failure to thrive. 
Clinical and laboratory investigations excluded any underlying abnormality of 
1he gastrointestinal tract. Because of a history of obstructive upper respiratory 
symptoms, both were referred for ear, nose and throat evaluation, and both were 
found to have partial upper airway obstruction secondary to adenotonsillar 
hypertrophy. Subsequent adenotonsillectomy led to resolution of obstructive 
upper respiratory symptoms and dramatic increases in weight gain and growth. 
Adenotonsillar hypertrophy should be included among the potential causes of 
failure to thrive in infancy, especially if the child has a history of obstructive 
upper respiratory symptoms.

T ONSILLH'TOMY AND ADFNOl[)F(' tomy rc1m11n the most common maior operations c.imed tlUl in childlwod ( I ).S urgical md1cat1111v, vary from recurren t or chronic tons1 l1 1t1s and otitis media to rhe more extreme alvl'• nlnr hypovenulation wnh cm ru lmnnale ( l ).Recently, 11 was rccngnizcd that adcnotonsillar hypenwphy may abo present as failure co thrive wh ich resolves wi t h tons ill ecwmy and aden-rndcctrnn~ (2)(3)(4)(5)(6)(7)(8)(9).Two similar cases arc rcpt)rted m which children riged 11 and 15 months, respectively presented with fa il ure to thrive due 1n pa rual upper airway ohstructio n from tonsdlar and adenoida l hypertrophy.In hmh children, tonsillectomy and adcnrndcctomy resul ted in d ramatic weight gain and catch-up growl h.These rnses arc reported to increase awareness of this recently recognized clinKal entity, ,mJ ro emphaMze the importance of an ear, nose and throat evaluation in an infant who presents with horh failure ro rhnve and ohstructivc upper resp1rnrory symptoms.Figure 1) \~ eight and height before and after adenownsill.eccomy in case ( left) and case 2 ( right) illustrating the weight gain which followed adenoronsillecwm'I H ospita l.U niversit y of Calgary, because of fai lure to thri ve.

CASE ONE
She haJ been the product of a normal pregnancy with a birth weight of 3 41 0 g (75th percentile).Sh e was breastfed fro m birth.Pablum and cerea ls were introduced at five months, with progression to pureed cable food shortly thereafter.Who le milk was started at nine months.The patient's history was unremarkable apart from very frequent upper respiratory tract infections: eight in the previous six months.There was also a history of la boured mo uth breathing and ma rkeJ snoring du ring sleep.Detailed dietary history revealed a caloric intake equa l to 66% of recomme nded dietary allowances.The fall-off in the patient's height and wei ght is illustrated in Figure I.The patient's parents, her 10-yearold brother and four-year-old sister were well.The younger sibling had had a fund o plication fo r gasrroesophagea l reflu x.A paternal cousin had t hree children wi th cystic fibrosis.
Ph ys ical examinatio n revealed a thin wasted infant whose weight of 5.82 kg was below the fifth percentile, and whose he ight of 69 cm was greate r than the 25th percenti le.S he h ad nasal congest io n and rhino rrhea, and was mo uth breathing.Her to nsils were enlarged but nor inflamed and met in the midline.Examinatio n was o therwise unremarkable.
Laboratory investiga tio ns including complete blood count, prothrombin time, partia l thrombo plast in tim e, calcium, phosphorus, alkaline phospha-case, total protein, a lbumin, clecmilytes, urea, creatinine, li ver function tests, serum immunoglobulins, cholesterol, urine metabo lic screen including amino ac ids and o rganic acids, thyroxine and thyroid stimulating hormone levels were a ll no rma l.Urinalysis and c ul ture were negative.A three-day quantitat ive feca l fat collection was no rma l with a n excretion of 3% of intake.The sweat chlo ride was normal at 7 mmol/L.Two subseq uent o utpatient visits revealed pe rsiste nt anorexia with failu re to ga in weight.Beca use of c hronic post nasa l airway obstruction, lo ud s noring a t nig h t a n d mouth breathing, an ear, n ose and throat cons ult was req ues t e d.Ex a minat ion revealed no se rvicea ble nasal airway due to enlarged adenoids a n<l oral examination again demonstrated grossly enlarged but no ninflame <l tons ib couching at the mic.lline.As it was thought th at severe adenotonsi llar h ypertrophy was contributing significa ntly to the infant's anorexia and poor weight ga in , to n s illeCLo my and adenoi<leccomy were performe<l at the age of one year.
One week priorto surgery, the infant was admitted for supplementa l nigh ttime nasogastric feedi ngs to improve nutritional status.These feeds were discontinued postoperatively as oral intake impro ved.Two mo nth~ afte r adenoronsillectomy she had gained 1. 2 kg.At 19 months, her weight was 9. 5 kg {10th percentile), and her height was 710 cm (25th percentile ).Her we ight as a pe rcentage of ideal we ight for height before surgery was 72.5% and after surgery at 19 momhs it was 96%.

CASE TWO
A I 5-month-ol<l male was referred to the outpatient Gastroe nterology Clinic because of failure to thrive.
History revealed a no rmal delive ry at term wit11 a birth weight of 3380 g.He was breastfed for seven weeks a nd then sw itch ed to S imilac (R oss La boratories).At three and four months of age, he had acute gastroenteritis and dehydration requiring hospitalization.After the second adm ission, he was switch ed LO Nutramigen (M ead Johnson).In addition, for the first seven months of his life, the patient had upper respiratory infections with a ch ronic cough, nasal congestion and rh inorrhea.During this time he was given at least iO courses of an tibiotics.
At eight mo nths he was started on whole cow's milk.From eight co 29 months, inte r val examinatio n s revealed a thin wasted child whose weight was consistently below the fifth percentile and whose height was between the 25th and 50th percentiles (Figure l ).He was a mouth breather with nasal speech and his consils were enlarged but not inflamed .At 20 months, asthma was diagnosed and he was started on th eophylline (Somophytlin; Fisons) and sa lbutamo l (Ventolin; Glaxo).
Both parents we re welt, buL his mother had bee n on a gluten-free JieL since infancy because of a clinical d iagnosis (not biopsy prove n) of celiac disease.A two-an<l -a-half-year-old sibling was healthy.
S ubseque nt laboratory investigations inclu<ling a complete blood count, prothrombin time, partial rh romboplastin time, calcium , phosphorus, alkaline phosphatase, total protein, a lbumin , elec trolytes, urea , creatininc, urine m etabolic screen including amin1) and organic ac ids, li ve r function tesLs and c ho leste ro l were normal.A three-Jay quantitati ve fecal fat collection showed an excretion of 0.8% of intake, anJ a ca lo ric intake that met the recommended daily allowa nce for age.A jejuna! biopsy showed norma l vil lo us architecture.S weaL c hl o ride was 9 mmot/L.At 29 momhs the child continued to have intermittent upper respiratory infections.A blocked nasal airway an<l c hronic mouth breathing made eating difficult.At night he snored lo udly and awakened imermittently with respiratory diffic ulty Jue to partia l upper airway obst ru ctio n wh ic h was not asthma.His weight of 10 kg remained al less than the fifth percentile.O n exa mination, he ha J a co mplete ly obstructed upper a irway a nd was drooling because of constant mouth breathing.Post n asa l space x-ray showed adenoida l hypertrophy and posterior ton s illar enlargement.Maxillary s inuses were opaque.A ronsillecwmy and adenoidectomy were performed.
O n e mo nch laLe r the child was eating well, breathing through his nose and sleeping throughout the night.H e had gained 1.6 kg.Three months later and still well, his we ight ha<l increased to 12.2 kg (between the fifth and 10th percentiles ) and his he igh t o f90cm was on the fifth to 10th pe rcentile.His weight as a percentage of ideal weight for height before surgery was 89% and two m o nths pos top e rati ve ly it was 100%.
Seven months poscoperatively, he was again symptoma tic with anorexia, inc reased m outh breathing a nd snoring.His weight of 15.5 kg remained in the 10th to 25th percentile.S inus x-rays Adenotonsillor hypertrophy and high kilovo lLage views of Lhe neck showed e nlargement of the re~idual ad enoidal tissue and hi lateral opacificarion of the maxillary sinuses.Ear, nose and throat exa minati o n revea le d prominent inferior turbinates obstructin g the nasal airway.A repeat adc noidectomy was performed with submucosal diathermy o f inferior turbinates.The p,1tient d iJ wcl I postopera-Li ve l y and had n ormal s ubseque nt growth ve lociLy.

DISCUSSION
Among Lhe more commo nly encounr ered prohle ms seen in ,1 pediatric gastroenterology clinic is thaL of the infant or child who is fa iling to thrive.The d ifferential diagnosis includes v ir-LUally every chro nic disease of c hildhood.Fortunately, a probable diagnosis can generall y he reached hy a thorough history and physical cxaminaLion (1 0).
There was a delay in diagnosis in both of these cases (o nly o ne month in the firsL case, but a lmost I 4 months in the second) .The delay is partly amiburable to the fact that fi ve LO e ight uppe r respi ratory tract infecLions per year are within normal limits for Lhis age group and can result in temporary adenotonsillar hypertrophy.In retrospect, in case 2, Lhe significant contribution of persistent respiratory symptoms to the fa ilure to thrive was not appreciated.As a result, ex Lensive invest igations were carried o ut which did not idemify th e unde rlying prohlem.Ir is only in recent years that adenotonsillar hypertrophy ca us ing obs tructi ve s leep ap nea has been recognized as a ca use of gro wth fai lure, which can be Lreated with removal of tonsils and adeno ids (2-9 ).Previous reports ha ve a lso highlighted this delay in diagnos is (9).Brouillette e t a l (9) felt that there were two possible contributing facto rs: first, a lack of awa reness of the entity, and second, the fact that most children look surprisingly normal when awake, despite sno ring retracti o ns and inte rmittent complete obstruction when asleep.Delay in d iagnosis may have serious consequences, as ch ronic proble ms can result in fail ure to thri ve, <levelopmental delay and cor pu lmo na le (9-12).
O bst ruc t ive sleep apnea was de-scribed in adu lts in 1966.However, the entity was first reported in children by Guilleminault in 1976 ( 11 ).The most common cause of this type of partial upper a irway obstruction in c hildren was adenotonsillar hypertrophy.A variety of symptoms and signs are described.During the day, there is often excessive sleep iness, mo uth breathing, beh avioura l changes an<l respiratory congestion.A more recent report suggests that vomiting may be a feature of obstructive While poor growth is well documented in patients with obstructive sleep apnea (2-9), there is controversy as to whether recurrent tonsillitis in the absence of obstructive symptoms has an adverse effect on growth (13)(14)(15).Grace et al (13) and Mills and Hibben (14) fo und no significant we ight gain in a group of c hildren post tonsillectomy compared co controls.I lowever, Barr and Osborne ( 15) found a 20% increase in weight in a group of children post tonsillectomy.It wo uld appear that the presence of obstructive symptoms is the principal factor affecting growth ( 13 ).
A review of the literalUre (2-9) suggests that with relief of ohstruction, rapid catch -up growth occ urs within three to 12 months of surgery.The present data arc consistent with these reporrs: case 1 took nine months co ach ieve Lhe 10th percentile fo r weight; case 2 regained his previous weight percentile within two months.Case 2 did nm regain his initia l height percentile within chis period of time, possibly beca use symptoms recurred and a second operation was needed for relief of obstruction , and partly because of asthma.
The mechanism of fai lure to thrive in c hildren with obstructive sleep apn ea remains speculative.Consistent with previous reports, the fir:;t of the present patients had an inadequate caloric intake for age, and demonstrated an increase in appetite and weight gain after 1,urgery.
Another theory is that tissue acidosis occurring <luring periods of apnea m;iy impair end o rgan response to growth factors (8).The reduction of REM sleep in association with obstructive sleep apnea may also impair growth hormone release and further contribute to poor growth.The reversibility of decreased growth hormone secretion in a patient with obstructive sleep apnea following trac heoscomy has been demonstrated ( 16).
These two case reports emphasize the importance of considering upper airway obstruction secondary to adenotonsillar hypertrophy as a potential cause of fa ilure to thrive in infants.An increased clinical awareness of this entity should lead to ea rlier recognition and surgical intervention in affected children.When one suspects adenoronsillar h ypertrophy as a ca use of failure to thrive, one must specifically ask about symptoms a t night, eg, sno rin g, labou red breaching, agitated arousal and sleep apnea.Excessive daytime sleepiness b a lso a signific;int clue to the syndrome, reflecting a disturbed sleep pattern.Polygraphic mo nitoring during sleep can he used to confirm the diagnosis if there is any doubt.