Neonatal Arytenoid Dislocation

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580

PEDIATRICS Vol. 81 No. 4 April 1988

EXPERIENCE

AND

REASON-Briefly

Recorded

.‘In Medicine one must pay attention not to plausible theorizing but to experience and reason

together. . . . I agree that theorizing is to be approved, provided that it is based on facts, and systematically makes its deductions from what is observed. . . . But conclusions drawn from

unaided reason can hardly be serviceable; only those drawn from observed fact. “ Hippocrates:

Precepts. (Short communications of factual material are published here. Comments and criticisms appear as Letters to the Editor.)

Neonatal

Arytenoid

Dislocation

Arytenoid dislocation is a well-described injury

in adults.’6 We report here what we believe is

the first neonatal case and contrast the findings

and course to those previously described.

CASE REPORT

A 2,640-g girl was born at 38 weeks’ gestation by

spontaneous delivery after labor complicated by the

passage of meconium-stained amniotic fluid. She was

intubated with a 3.0-mm oral endotracheal tube

with-out a stylet. No meconium was found below the vocal

cords. Apgar scores at 1, 5, and 10 minutes were 5, 7,

and 9, respectively. When the baby was admitted to the

nursery, she was described as having pink color, a

strong cry, no retractions, a cardiac rate of 136 beats

per minute, and a respiratory rate of 48 breaths per minute.

At some unnoted time, the infant’s cry became weak,

and the nurse observed frequent cessations of feeding

to breathe. Additionally, 26 hours after birth, “coarse”

breath sounds, occasional sternal retractions, and faint

duskiness of the oral mucosa were noted. A chest

ra-diograph obtained at 28 hours of age was interpreted as normal, and at 38 hours of age, the baby was

dis-charged from the hospital. The mother, however, was

aware of chest retractions and a weak cry from the time

of discharge. The infant took formula for 2* hours but refused feedings thereafter. She returned to the

hos-pital two days after the initial discharge.

The baby’s neck was hyperextended and she had

in-spiratory stridor, labored gasping inspiration with in-tercostal, sternal, and suprasternal retractions. A chest radiograph including the neck appeared normal except

for distention of the hypopharynx with air. Arterial

Received for publication April 23, 1987; accepted June 5, 1987. Reprint requests to (D.R.) 4001 Dale St, Suite 210, Anchorage,

AK 99508.

American Academy of Pediatrics.

blood values were pH 7.22, Pco2 Si mm Hg, Po2 59 mm

Hg, bicarbonate 21 mEq/L while the infant was

breath-ing room air. Direct laryngoscopy without anesthesia,

done in preparation for tracheal intubation revealed

anterior and caudad displacement of the right

aryten-oid cartilage (Figure). The cartilage along with its

ar-yepiglottic fold descended below the glottis with each

inspiration. Laryngeal edema was present with intact

position and movement of the left vocal cord.

Orotra-cheal intubation, which was accomplished with consid-erable difficulty because of the obstruction, was fol-lowed by complete relief of respiratory symptoms.

Four days after admission, a rigid bronchoscopy and

repeat laryngoscopy were performed under general

anesthesia and intact vocal cords, with marked edema

of the right arytenoid, were seen. Because the degree

of edema was sufficient to obstruct respiration and to

obscure the presence or absence of continued arytenoid dislocation, a tracheostomy tube was placed.

When the baby was 4 weeks of age, fiberoptic

lar-yngoscopy with topical anesthesia showed minimal

edema with no dislocation. One month later a rigid

bronchoscopy revealed no residual injury and the infant

was decannulated without symptoms of upper airway

obstruction recurring.

DISCUSSION

The arytenoid cartilages are paired, small,

ap-proximately pyramidal, paramedian structures of

the larynx perched atop and connected to the

pos-tenor superior cricoid cartilage via shallow

syn-ovial joints. Two processes extend from the base

ofeach cartilage: anteriorly, the vocal process

pro-vides attachment to the vocal ligament, and

pos-terolaterally the muscular process provides

in-sertion for the lateral and posterior cricoarytenoid muscles. These muscles together create lateral

and medial movements of the attached vocal

hg-aments which open and close the glottis. The

pos-tenor cricoarytenoid functions also as a vocal cord

tensor.

Severe external trauma to the neck may

pro-duce arytenoid dislocation as an element of

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Left

Right

EXPERIENCE

AND REASON 581

Normal

Displaced

Figure. Paramedian views of affected and unaffected

sides of the larynx. VC, vocal cord; E, epiglottis; A,

ar-ytenoid cartilage; C, cricoid cartilage; AE, aryepiglottic

fold.

eralized injury. Isolated arytenoid dislocation has

been described almost exclusively in adults and

is most often associated with medical

instrumen-tation of the larynx and/or esophagus such as

tra-cheal intubation,’8 laryngoscopy,6 gastroscopy,6 and nasogastric tube insertion.2’6 Typically, these

injuries involve only one cartilage, although

bi-lateral dislocation has been described.8 Symptoms

of hoarseness, aphonia, weak cough, dysphagia,

odynophagia, and constant pain in the laryngeal

region are reported.’7 Anterior, posterior, and

re-current dislocations are described.24’7

The incidence ofthis injury may be greater than

is generally appreciated. Kambi and Radel7

identified it in one of 1,000 patients (1.5% of

sig-nificant injuries) examined prospectively by

lar-yngoscopy following short-term tracheal

intuba-tion. Rudert6 reported an incidence of more than

30% in 19 patients referred to him with laryngeal

dysfunction after laryngeal or pharyngeal

instru-mentation. He speculated that some suspected

cases of vocal cord paralysis may represent

un-recognized arytenoid dislocations.

Diagnosis depends on the appropriate index of

suspicion followed by laryngoscopy, although one

recent report describes the value of computed

to-mography.4 Local inflammation and edema may

make repeated laryngoscopy necessary.2

In the adult, closed reduction of the dislocated

joint is often sufficient treatment2’4’5; some

au-thors additionally advocate steroid injections into

the joint capsule at the time of reduction.6

Long-term dislocation results in a fibrotic ankylotic

joint.6 Acute dislocations occasionally reduce

spontaneously.6’8

The case reported here differs from previously

recorded ones. We believe that it is the first

re-ported case that has occurred secondary to a

com-mon event, ie, neonatal tracheal intubation. More

important, it demonstrates that a unilateral

dis-location may progress to respiratory failure

be-cause of the high resistive work of breathing

as-sociated with even mild or moderate degrees of

upper airway obstruction in infant airways. The

infant’s refusal to suck for the 24 hours prior to

arrival in the emergency room may have

repre-sented odynophagia or dyspnea, either of which

may be associated with this injury. Marked

hy-popharyngeal dilation detected radiographically was initially thought to be retropharyngeal air.

However, direct observation of the hypopharynx

and disappearance of the radiographic finding

after intubation suggested, instead, proximal

compensatory dilation secondary to laryngeal

obstruction.

Respiratory distress may not develop in adults

with arytenoid dislocation and, indeed, the

in-fant’s first hours seemed uneventful. The

pro-gressive respiratory embarrassment thereafter

was likely due to development of progressive

edema surrounding the dislocation.

It appears that in the present case reduction of

the dislocation either occurred spontaneously or

was effected by the splinting action of the

endo-tracheal tube. Placement of an endotracheal tube

must either force a dislocated arytenoid further

caudally or displace it posteriorly into a near

nor-mal anatomic position. Continued presence of the

tube would act as a splint to maintain anatomic

position. Upon removal of the endotracheal tube,

the tracheostomy functioned to prevent recurrent

dislocation by diverting airflow from the glottis.

The apparent rarity of this complication of

in-tubation during the newborn period deserves

some speculation. In contrast with adults,

new-borns may have greater flexibility of laryngeal

structures and thus some protection against

ar-ytenoid dislocation. Additionally, the more

su-perior and anterior position of the neonate’s

la-ryngeal structures may alter the stresses acting

on the arytenoid articulation during

instrumen-tation. Some cases may be misdiagnosed as

lar-yngomalacia or vocal cord paralysis because of the

edema that can develop with this injury; further

cases may be subtler than that reported here, with

transient dislocations reducing spontaneously.

Finally, laryngomalacia may have played a role

in our patient.

Arytenoid dislocation, although uncommon,

should be added to the list ofcomplications of

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582 PEDIATRICS Vol. 81 No. 4 April 1988 natal intubations and differential diagnosis of res-piratory distress.

ACKNOWLEDGMENT

This work was supported, in part, by grant MCT 952 from the Public Health Service of the US Department

of Health and Human Services.

REFERENCES

DI0N ROBERTS, MD TIM MCQUINN, MD

ROBERT C. BECKERMAN, MD Department of Pediatrics

Section of Pulmonary Diseases

Constance Kaufman Center for the

Study of Breathing Disorders in

In-fants and Children

Tulane University School of Medicine

New Orleans

1. Schultz-Coulon HJ: Luxation des arytaenoidknorpels als intubationsschaden. HNO 1974;22:242-245

2. Quick CA, Merwin GE: Arytenoid dislocation. Arch

Oto-laryngol 1978;104:267-270

3. Prasertwanitch Y, Schwarz JH, Vandam LD: Arytenoid

cartilage dislocation following prolonged endotracheal in-tubation. Anesthesiology 1974;41:516-517

4. Dudley JP, Mancuso AA, Fonkalsrud EW: Arytenoid dis-location and computed tomography. Arch Otolaryngol

1984;110:483-484

5. Kormon RM, Smith CP, Erwin JR: Acute laryngeal injury

with short-term endotracheal anesthesia. Laryngoscope

1973;83:683-690

6. Rudert H: Uber seltene intubationsbedingte innere

kehlk-opftraumen. HNO 1984;32:393-398

7. Kambi V, Radel Z: Intubation lesions of the larynx. Br J Anesth 1978;50:587-590

8. Chatteiji S, Gupta NR, Mishra TR: Valvular glottic ob-struction following extubation. Anaesthesia

1984;39:246-247

Postprandial

Hypoglycemia

Resulting

From Nasogastric

Tube

Malposition

Recurrent, severe hypoglycemia in infants and

children usually reflects an immature or defective

Received for publication April 24, 1987; accepted June 2, 1987. Reprint requests to (D.B.A.) Department of Pediatrics, Uni-versity of Wisconsin Hospital, 600 Highland Aye, H4/442, Madison, WI 53792.

adaptation to fasting (postabsorptive

hypoglyce-mia). Rarely, however, symptoms of

hypoglyce-mia occur predominantly in the postprandial

pe-nod (less than four hours after a meal). Recent

studies have focused attention on postprandial

hypoglycemia as a manifestation of the late

post-prandial dumping syndrome in children following

gastric surgery.”2 In this setting, hypoglycemia

is attributed to reactive hyperinsuhinemia

follow-ing a rapid initial increase in blood glucose

con-centration.3 We report the finding of severe,

re-current hypoglycemia in a nonsurgical patient

receiving nasogastric feedings. In this patient,

in-advertent intubation of the proximal small bowel

simulated the altered gastrointestinal dynamics

associated with the late postprandial dumping

syndrome.

CASE REPORT

An 18-month-old Laotian girl was hospitalized for

ventilatory care and nutrition. She weighed 930 g at

birth after a 28-week gestation. She had a twin. At

birth the patient experienced severe respiratory

dis-tress syndrome with subsequent bronchopulmonary

dysplasia and subglottic stenosis. A tracheostomy was

created at 3 months ofage. Neonatal hypoglycemia was not noted. Prolonged hospitalization was necessitated

by a persistent need for intermittent ventilatory

as-sistance. Height and weight (corrected for gestational age) had increased consistently along the 25th and fifth

to tenth percentiles, respectively. Her feeding regimen

included oral intake as tolerated supplemented by 250

mL of Osmolite (Ross)/SMA (Wyeth) formula (1 : 1

mix-ture), given via nasogastric tube, four times per day. One afternoon, two hours following oral ingestion of applejuice, the patient had a “staring spell” and rapidly

became obtunded. Serum glucose measured 29 mg/dL.

Administration of 10% dextrose led to rapid resolution

of her symptoms and an increase in serum glucose to

156 mg/dL. The frequency ofher supplemental feedings was increased. Within two days, however, hypoglyce-mia (serum glucose 27 mg/dL) associated with lethargy

and weakness reoccurred two and one-half hours

fol-lowing a nasogastric feeding. A urine specimen

ob-tamed at that time revealed glycosuria but no ketones. An IV catheter was inserted and a fasting study was

begun. Throughout a 24-hour period of fasting, the

child remained euglycemic (serum glucose 60 to 90 mgI

dL). A challenge with 220 mL of OsmolytelSMA (1:1)

via nasogastric tube was then performed. At one hour postfeeding, the serum glucose concentration was 294

mgldL. At two hours postfeeding, the child rapidly

be-came unresponsive; serum glucose concentration was

13 mgldL. Concurrent laboratory values included:

serum insulin 96 1iU/mL (normal less than 20 pU/mL

during hypoglycemia), growth hormone 6.2 nglmL,

cor-tisol 18.8 p.gIdL, no serum ketones, lactate 1.2 mmoh/

L.

An abdominal radiograph revealed the nasogastric

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1988;81;580

Pediatrics

DION ROBERTS, TIM MCQUINN and ROBERT C. BECKERMAN