Perinatal/Neonatal Casebook - Nature

8 downloads 0 Views 4MB Size Report
drome, treated with beractant (Survanta; Ross Pharmaceuticals,. Columbus, OH) 2 and high frequency oscillatory ventilation;. (2) right pneumothorax; (3) ...
Perinatal/Neonatal Casebook n

n

n

n

n

n

n

n

n

n

n

n

n

n

Neonatal Apnea Casebook Bruce D. Sindel, MD, Section Editor Contributed by: Bruce D. Sindel, MD Bettye Winkubourne, RN CASE REPORT Baby girl “R” was born by breech vaginal delivery at 26 weeks’ gestation. Birth weight was 1200 gm. The baby was floppy at birth and required cardiopulmonary resuscitation. Apgars were 1, 4, 5, and 7 at 1, 5, 10, and 15 minutes, respectively. The baby was transferred to the neonatal intensive care unit (NICU) where umbilical catheters were placed. She was placed on mechanical ventilation. Problems in the NICU included: (1) respiratory distress syndrome, treated with beractant (Survanta; Ross Pharmaceuticals, Columbus, OH) 3 2 and high frequency oscillatory ventilation; (2) right pneumothorax; (3) hypoglycemia; (4) metabolic acidosis; (5) nosocomial infection with Staphylococcal aureus; (6) anemia, treated with transfusion and Epogen; (7) apnea and bradycardia, treated with Aminophylline, which was discontinued after 56 days of age as the apnea and bradycardia seem to improve; (8) persisting oxygen requirement; and (9) retinopathy of prematurity, grade II in zone II, which subsequently resolved spontaneously. An auditory brainstem response (ABR) was performed at 73 days of age and was normal. Due to chronic lung disease, persisting oxygen requirement with occasional desaturation episodes and a previous history of apnea, a polysomnographic evaluation was performed at 74 days of age. DENOUEMENT AND DISCUSSION Gastroesophageal Reflux (GER)-Associated Apnea The polysomnography performed on this baby clearly demonstrates GER-associated apnea as demonstrated in Figures 1 and 2. Figure 1 clearly shows a reflux episode, shown on line 16 (labeled pH), followed by a central apnea of 7 seconds, shown on lines 8, Pediatric Polysomnography Laboratory, Citrus Valley Medical Center, Queen of the Valley Campus, West Covina, CA, and University of California, Irvine School of Medicine, Orange, CA. Address correspondence and reprint requests to Bruce D. Sindel, MD, Citris Valley Medical Center, Queen of the Valley Campus, 1115 S. Sunset Avenue, West Covina, CA 91790.

10, and 12 (labeled NAF, CRE, and ARE), with a mild desaturation to 92%, shown on line 14 (labeled O2 SAT) and a heart rate deceleration, shown on line 7 (labeled EKG). Figure 2 shows a reflux episode, shown on line 16 (labeled pH), simultaneous with a prolonged apnea, shown on lines 8, 10, and 12 (labeled NAF, CRE, and ARE) also associated with desaturation, shown on line 14 (labeled O2 SAT) and a heart rate deceleration, shown on line 7 (labeled EKG). The baby was subsequently treated with aggressive medical management consisting of prone positioning, feedings thickened with rice cereal, and Reglan 0.2 mg/dose given four times daily. She showed a marked improvement in her desaturation episodes allowing her to be weaned off oxygen. DISCUSSION GER-associated Apnea is a relatively uncommon event, occurring in about 10% of infants with apnea.1 With the advent of continuous pH monitoring, which is now the gold standard for the diagnosis of GER, especially GER-associated respiratory disease,2,3 there has been a flurry of research activity investigating GER and its relationship to apnea and respiratory disease. Many of these are trying to elucidate the mechanism by which GER exerts respiratory effects. Most of the research currently centers around the laryngeal chemoreflex (stimulation of the laryngeal chemoreceptors causing laryngeal spasm [apnea], bradycardia, and alterations in blood pressure),4 –7 or vagal reflexes (either by acid infusion in the lower esophagus or by esophageal distension causing apnea, bronchospasm, and/or bradycardia).8,9 Infants are likely more susceptible to these problems due to possible disturbances of both esophageal function and respiratory regulation at this stage of life.10 The “diving seal reflex,” is a well known reflex involving the laryngeal chemoreceptors in aquatic mammals. Some of these pathways may still be present in human infants as well. Two recent reviews of GER in children devoted large sections to GER-associated respiratory disease.2,11 Both spoke to the difficulty of correlating the reflux seen on pH studies to the patients symptoms. In older children and adults, a “symptoms-sensitivity index” can be helpful.2 This is obviously not useful in infants, since they can not communicate. Therefore, more extensive monitoring may be helpful. We have found that using polysomnography we can correlate the episodes of GER with apnea and other respiratory diseases in infants. The case presented demonstrates clearly how effective polysomnography can be at correlating the apnea with the GER. The determination of whether the Apnea is associated with the GER is critical to developing a proper plan of treatment for each individual infant.

Journal of Perinatology (1999) 19(1) 77–79 © 1999 Stockton Press. All rights reserved. 0743– 8346/99 $12 http://www.stockton-press.co.uk

77

Sindel

Neonatal Apnea Casebook

Figure 1 An example of the 13-channel study performed. The electroencephalogram (EEG) is on channels 1 through 3, electro-oculogram (EOG) on channels 4 and 5, electromyogram (EMG) on channel 6, electrocardiogram (ECG) on channel 7, nasal air flow on channel 8, chest wall and abdominal on channels 10 and 12, pulse oximetry on channel 14, and lower esophageal pH on channel 16. See text for full explanation.

Figure 2 A second example of the 13-channel study performed. Each channel is the same as in Figure 1. See text for full explanation.

78

Journal of Perinatology (1999) 19(1) 77–79

Neonatal Apnea Casebook

References 1. Martin GI. Infantile Apnea, Neonatology for the Clinician. Norwalk, CT: Appleton & Lange; 1992. p. 267–77. 2. Glassman M, George D, Grill B. Gastroesophageal reflux in children: clinical manifestations, diagnosis, and therapy. Gastroenterol Clin North Am 1995;24:1; 71–98. 3. Andze GO, Brandt ML, St Vil D, Bensoussan AL, Blanchard H. Diagnosis and treatment of gastroesophageal reflux in 500 children: the value of pH monitoring. J Pediatr Surg 1991;26:295–300.

Sindel

6. Rimell F, Goding GS Jr, Johnson K. Cholinergic agents in the laryngeal chemoreflex model of sudden infant death syndrome. Laryngoscope 1993;103:623–30. 7. Loughlin CJ, Koufman JA, Averill DB, et al. Acid-induced laryngospasm in a canine model. Laryngoscope 1996;106:1506 –9. 8. Bauman NM, Sandler AD, Schmidt C, Maher JW, Smith RJ. Reflex laryngospasm induced by stimulation of the distal esophageal afferents. Laryngoscope 1994; 104:209 –14. 9. Ramet J. Cardiac, and respiratory reactivity to gastroesophageal reflux: experimental data in infants. Biol Neonate 1994;65:240 – 6.

4. Wetmore RF. Effects of acid on the larynx of the maturing rabbit and their possible significance to the sudden infant death syndrome. Laryngoscope 1993;103: 1242–54.

10. Kurz R, Hollwarth M, Fasching M, Haidmayer R, Pfeiffer KP, Kenner T. Combined disturbance of respiratory regulation and esophageal function in early infancy. Prog Pediatr Surg 1985;18:52– 61.

5. Rex MAE. Studies on the nerve pathways involved in the laryngeal reflex (laryngospasm) in the cat. Br J Anaesth 1970;42:1067–71.

11. Sutphen JL. Pediatric gastroesophageal reflux disease. Gastroenterol Clin North Am 1990;19:3;617–29.

Journal of Perinatology (1999) 19(1) 77–79

79