Transtracheal oxygen therapy for the treatment of obstructive sleep apnea

TRANSTRACHEAL OXYGEN THERAPY FOR THE TREATMENT OF OBSTRUCTIVE SLEEP APNEA ROBERT J. FARNEY, MD, ACP, FCCP, JAMES M. WALKER, PhD, ACP, JEFFREY C. ELMER, MD, ACP, VINCENT A. VISCOMI, MD, ACP, R. JON ORO, MD, FACS

Patients with sleep-disordered breathing, such as obstructive sleep apnea, require individualized therapy based on their unique circumstances. In addition to consideration of various surgical procedures, 1 a comprehensive approach should include attention to all pot~ntial contributing factors such as obesity, alcohol, nasal airway obstruction, therapy of congestive heart failure. Most patients with severe obstructive sleep apnea who were routinely managed in the past with a tracheostomr can now be successfully treated using nasal continuous positive airway pressure (CPAP).3 However, the combined immediate and long-term failure rate with nasal CPAP measures 25% to 40 %,4,5 and other than a tracheostomy, there are few viable alternatives with established value. Z Transtracheal oxygen (IT O~, which was originally developed for patients with chronic pulmonary disease,6,7 may also be an effective treatment for some patients w!th sleep-disordered breathing including severe obstructive sleep apn ea. The advantages of IT 0 2, relate to the smaller size of the catheter compared with a standard tracheostomy (Fig I), which permits insertion on an outoatient basis and fewer complications. We have used IT )2 in sleep apnea patients in whom nasal CPAP therapy .vas either intolerable or unsuccessful. Polysomnograohy was used in all of these cases to document the type 1nd severity of sleep-disordered breathing, to adjust the flow of oxygen, and to verify the adequacy of tr.eatment. In addition, five patients with severe obstructive sleep apnea were systematically studied in order to compare IT O 2 to more traditional therapies, ie, nasal CPAP and O 2 via nasal cannula. Due to the limited number of studies performed to this point,8'10 the precise mechanisms of action and the indications for IT O 2 in this disorder have not been completely elucidated. In this article w.e will dis~uss ~he su~­ gical technique and the hypothetI~al phYS.lOlogiC bas.ls and summarize some of our expenence WIth IT O 2 10 patients with sleep-disordered breathing.

From the Departments of Medicine and Otolaryngology. University of Utah Medical Center, and the Intermountain Sleep Disorders Center, LOS Hospital, Salt Lake City, UT. Supported in part by a grant from the Deseret Foundation, LDS Hospital, Salt Lake City, UT. Address reprint requests to Robert J. Farney, MD, Intermountain Sleep Disorders Center, Latter Day Saints Hospital, 8th Ave and CSt, Salt Lake City, UT 84143. • All necessary materials are provided in disposable trays. Detailed information can be obtained from Transtracheal Systems. 8755 E. Orchard Rd., Suite 607, Englewood, CO 80111Copyr ight © 1991 by W.B. Saunders Company 1043·1810/91/0202·0006$05.00/0

132

TRANSTRACHEAL CATHETER SURGICAL TECHNIQUE Transtracheal catheter placement was accomplished using the Scoop catheter system developed by Christopher and Spofford.P A detailed description of this technique is beyond the scope of this article; however, a brief description of the procedure follows.* The patient is placed in a sitting erect posture and the superficial anatomic landmarks are identified and marked. Local anesthesia is applied subcutaneously, in the pretracheal fascia and in the tracheal lumen. A vertical midline I-cm incision is made through which a 7ern-long 18-gauge·thin-wall needle is passed down to the trachea. The needle is used to palpate the cartilages and is inserted through an intercartilaginous membrane into the trachea (Fig 2A). The cricothyroid membr?ne. is avoided in order to prevent hoarseness. After aspirating air, the syringe is remov ed and the wire guide is passed through the needle (Fig 2B). .. , The needle is removed and a special dilator IS passed over the wire through the tracheal wall and left in place for a few minutes to gain enough opening to allow the catheter to pass through the tracheal wall (Fig 2C): We have discontinued using the stent, which was designed to establish the tract, and instead insert the Scoop-I catheter at this point (Fig 20) . The catheter position is verified by aspiration of air and by radiography. Transtr~­ cheal oxygen can then be initiated. Polysomnography IS performed as soon as feasible in order to document the effectiveness and appropriate dose of 'oxygen . The Scoop-2 catheter can replace the Scoop-l in about 4 to 6 weeks. If oxygen is only required during sleep, the Scoop catheter can be plugged with a plastic cap off a syringe during wakefulness. Patients selected for Tf O 2 therapy must be screened for potential problems such as bleeding diathesis, und:rlying pulmonary disease, cardiac arrhyth~i.as, ~nd history of previous neck surgery. Unusual difficulties ~ave been encountered in patients who have had prevIOUS procedures resulting in distortion of th~ anatomy or excessive scar tissue, or very obese patients who have short, thick necks. Follow-up care is more comI?licated if patients live in remote areas, are not psychologically stable, or are unable to maintain proper hygiene.

METHODOLOGY Polysomnographic recor~inl?s with standard me~sure­ ments of sleep and respiration 2,13 were conducted 10 the Intermountain Sleep Disorders Center at Latter Day

OPERATIVE TECHNIQUES IN OTOLARYNGOLOGY-HEAD AND NECK SURGERY, VOL 2, NO 2 (JUNE). 1991 : PP 132·136

FIGURE 1 Campa nson ' . of an SF S coop 2 transtra h catheter (11 c eal 36F fenestra~~) and a 1ow-pre tracheo:tsure cuffed (Shiley). omy tube

FIGURE 2 . steps of t . Pnncipal catheter rfnstracheal (A) p acement Insertion of th . needle . e of the .' (8) Insertion . wire guide (C dilation of th' ) (0) insertio e ;ract, and catheter. n 0 Scoop 1 FARNEY ET AL

133

TABLE 1. Anthropometric Data of Five Patients With Severe Obstructive Sleep Apnea PI

Sex

Age (yrs)

HI (em)

WI (kg)

Pa02 (mm Hg)

5a0 2 (%)

Hb (g/dL)

Pac0 2 (mm Hg)

pH

SAHI

PO JW JS JF CM

F M M M M

60 57 48 47 37

157 183 183 167 188

106 135 147 116 206

58 62 71 58

90 93 93 88 82

14 17 15 16 15

37 31 40 43 45

7.47 7.50 7.41 7.43 7.43

36 50 74 78 86

49

Additional Ox CB CB

Abb.reviation~ :. SAHI, sleep apnea plus hypopnea index computed as total apneas and hypopneas per total sleep time in hours' CB chron ic bronchitis. • •

Saints Hospital, Salt Lake City! VT at an elevation of 1,400 meters. Records were scored manually for sleep stages and respiratory events without knowledge of treatment condition. Apneas were defined by an 80% to 100% reduction in airflow signal compared with baseline and hypopneas were defined as a 50% to 80% reduction for per~ods of at least 10 seconds. Obstructive apneas were ~ndlcated by the presence of respiratory effort or paradoxical thoracic-abdominal motion, while central events were defined by the absence of any apparent respiratory effort. If there ,~ere both central and obstructive components to a respiratory event, an event was considered to be obstructive. Hypopneas were not differentiated as obstructive or central. Cheyne-Stokes respiration was defined by the typical smooth crescendo-decrescendo changes in tidal volume with interspersed periods of central apnea. The sleep apnea index was computed as the total of all apneas divided by the total sleep time (TST) in hours. The sleep hypopnea index and the sleep apnea/ hypopnea index were computed similarly .

COMPLICATIONS There were no complications related to the procedure such as hemorrhage, infection, subcutaneous emphysema, or pneumothorax. Subsequent clinical interviews indicated that the patients preferred TI 0z, felt more alert! experienced less daytime sleepiness, and snoring was reportedly diminished. TABLE 2. Experimental Levels of Oxygen and Nasal CPAP in Five Patients With Severe Obstructive Sleep Apnea Patient

CPAP (cm H2O)

NC O2 (Um in)

rr o,

PO JW JS JF CM

10 10 15 15 15

1.0 5.0 6.0 2.5 6.0

1.0 3.0 3.0 2.0 6.0

(Umin)

TABLE 3. Respiratory Measurements (Mean ± SO) in Five Patients With Severe Obstructive Sleep Apnea Across All Experimental Conditions Respiralory Evenls (per hour sleep) Central apnea Obstructive apnea Hypopnea Apneas and hypopneas

Baseline

NC O2

CPAP

n0 2

2=4

2=3

4::':6

0=0

36 = 19··t 27 = 20

39 = 16'"t 18:!: 17

4=4 6 = 11

6=8 20 = 17

65 = 22,·t

59 = 11·-t

14 = 10

26 = 21

• Differs from nasal CPAP P < .01. t Differs from rr O2 P < .or.

134

OBSTRUCTIVE SLEEP APNEA PATIENTS Five patients were selected because they were either noncompliant with nasal CPAP or also required cont inuous supplemental oxygen 24 hours a day (Table 1). All were previously diagnosed as having severe obstructive sleep apnea that could be corrected with nasal CPAP. Subjects were restudied with polysomnography on four nonconsecutive nights using four experimental conditions: room air (RA)! nasal CPAP, oxygen via nasal cannula (NC 02), and oxygen via transtracheal catheter (Tl' Oz)' Oxygen or nasal CPAP was titrated as quickly as possible! usually within the first hour following "lights out," to a target Sa0 2 of 90% or to a maximum level of 15 em HzO or 6 Umin and then remained constant (Table 2). In these systematic comparisons, data obtained during the initial oxygen or nasal CPAP titration periods were excluded from the analysis.

Respiratory Parameters The effect of TI Oz on apnea and hypopnea frequency was variable (Table 3). In some cases! both apneas and hypopneas were markedly reduced (Fig 3), while in others moderately frequent hypopneas remained. Despite persistent respiratory disturbances, however, the Sa02 was always maintained at about 90% except during some REM sleep periods when mild de saturations were cecasionallyobserved. There was no significant effect on duration of apnea or hypopnea compared with baseline room air measurements. Although there was a trend, NC Oz therapy did not result in a significant reduction in apnea or hypopnea frequency, but the degree of oxygen desaturation was ameliorated. As expected, nasal CPAP was very effective at eliminating both apneas and hypopneas. The Sao, with nasal CPAP was also generally maintained about 9.0% (except when there was baseline hypoxia). In addition, nasal CPAP was not completely effective during some portions of REM sleep.

Sleep Variables Sleep parameters are presented in Table 4. The administration of TI O 2 reduced the number of arousals and stage 1 NREM sleep as compared with the baseline cond i~ion . However, there were no differences in sleep architecture when the effects ofTI O 2 were compared with NC Oz. Sleep tended to be more normal in the nasal CPAP condition. Nasal CPAP reduced stage 2 NREM sleep, but increased stages 3 and 4 and REM sleep as compared to all other conditions.

CHEYNE-STOKES APNEA Two patients who presented with clinical features of obstructive sleep apnea complicated by congestive heart TRANSTRACHEAL O 2 FOR SLEEP APNEA

FIGURE 3. Oximetric recordings from a 37-year-old man (patient CM) with severe obstructive sleep apnea. Transtracheal oxygen therapy was recommended in this case because of the need for combined oxygen and nasal CPAP. The Sa0 2 levels recorded from the second to fourth hour after "lights out" of each experimental condition are shown. The more severe desaturations in each panel are related to REM sleep. Abbreviations: SAl, sleep apnea index; SAHI, sleep apnea plus hypopnea index.

100j~L1m)

~

60

4.3

8.9

40

failure were found to have a Cheyne-Stokes respiratory pattern. Unlike the other patients with typical obstructive sleep apnea, these subjects did not respond as favorably to nasal CPAP. Transtracheal oxygen therapy markedly reduced sleep apnea, stabilized the Sa02 at 90%, and improved the sleep architecture.

DISCUSSION The most significant observation from our experience is that IT O2 corrects hypoxemia related to sleep-disordered breathing even if some types of respiratory events are not completely eliminated (ie, hypopnea). Improvement in arterial oxygen content results from the combination of a more stable alveolar oxygen fraction (FA02) and a reduction in the frequency of apneas and hypopneas. Because IT O2 is effective and well-tolerated, the need for tracheostomy in our patients has been essentially eliminated. Our results are consistent with other limited studies of obstructive sleep apnea. Spofford et al8 reported a reduction in the median sleep apnea plus hypopnea index of 118 to 46 using IT O2 in four patients with sleep apnea syndrome. Chauncey and Aldrich'? have recently reported on transtracheal oxygen in four patients with obstructive sleep apnea and have reached very similar conclusions to ours. The mean apnea/hypopnea index in their group decreased from 54 per hour sleep to 11 per hour sleep. Considering the elevation at which our study

IOO

~80 SAl SAHI

80

60

40

was performed and the mean apnea/hypopnea index, our subjects may have been somewhat more severe as a group. The clinical and polysomnographic features of patients with Cheyne-Stokes respiration (CSR) presenting as obstructive sleep- apnea have been recently reviewed by Dowdell et aI. 14 The effectiveness of IT O 2 is especially interesting in our patients with CSR since we have not had invariable success using nasal CPAP in this condition as reported by Takasaki et al. 15 Our data suggest that IT O2 stabilizes chemoreceptor activity and eliminates the central component of this respiratory pattern. If upper airway obstruction is present, IT O2 seems to provide a more reliable means of delivery than NC 02' Administration of oxygen by means of nasal cannula above the site of airway closure is partially effective by raising the baseline FA02. Transtracheal oxygen, on the other hand, is more effective because it supplies oxygen to the alveolar gas compartment even during obstructive apnea. An intratracheal oxygen flow rate of 1 Llmin or more easily offsets the oxygen consumed (typically 0.25 to 0.50 Llmin), but probably does not completely compensate for the effects of ventilation/perfusion mismatching. In addition, the continuous flow of oxygen below an obstructed airway may increase mean airway pressure, which would increase functional residual capacity (FRC) and reduce upper airway resistance similar to the effects of nasal CPAP. Hypoxemia is perhaps not only the most important

TABLE 4. Sleep Measurements (Means:!: SO) In Five Patients With Severe Obstructive Sleep Apnea Across All Experimental Conditions

Sleep Parameters

Baseline

Total sleep time (h) Stage 1 NREM (%) Stage 2 NREM (%) Stage 3 and 4 NREM

6.7 20.4 64.0 0.5 15.1 88.6 74.0

(%)

REM (%)

Sleep efficiency (%) Arousal index (events/h)

=: 0.8 =: 12.3 =: 7.2 =: 0.6 =: 6.0 =: 6.2 =: 46.0

CPAP 6.8 =: 11.0 =: 74.2 =: 0.3 =: 14.5 ± 90.7 =: 53.5 =:

0.1 6.0' 8.0 0.5 4.8 5.8 29.8

5.6 =: 13.6 ± 48.3 =: 8.9 =: 29.2 =: 84.9 =: 22.9 =:

0.8 5.0' 19.6,·t-:t: 10S·t·; 10.8''f'; 11.7 9.3'of

6.8 =: 11.1 =: 72 .3 =: 1.7 =: 14.9 =: 90.4 =: 41.5 =:

0.9 3.9' 3.3 2.6 4.7 7.4 28.1'

• Differs from baseline P < .05.

t Differs from NC O 2 P < .05.

; Differs from TT O2 P < .05. FARNEY ET AL

135

physiologic consequence of sleep-disordered breathing, but has also been imp-licated as a factor in the genesis of periodic breathing. 16 -18 Various mechanisms have been proposed for the salutary effect of oxygen on sleep apnea frequency: (1) direct stimulation of the central nervous system, (2) reduction in upper airway resistance, and (3) stabilization of chemical feedback by reduction of chemoreceptor activity. Hypoxemia associated with sleep apnea arises from multiple processes: alveolar hypoventilation, ventilation/perfusion mismatch, and increased venous admixture. The rate and magnitude of oxygen desaturation will be affected by aRnea frequency, baseline Pa02, and venous O2 content. 9 The alveolar fraction of oxygen (FA0 2) and FRC are critically important because these determine a major reservoir from which oxygen is available during apnea. Upper airway resistance and potential for collapse are also directly influenced by FRC.20 In conclusion, we have found transtracheal oxygen therapy to be especially useful in the following subsets of patients with severe sleep apnea: (1) patients intolerant of nasal CPAP for whom a tracheostomy might otherwise be performed; (2) patients who also have significant hypoxemia during wakefulness that is often related to underlying pulmonary disease; and (3) patients with obstructive sleep apnea and Cheyne-Stokes respiratory pattern. An additional potential subset might include morbidly obese patients with severe apnea undergoing upper abdominal surgery in whom nasal CPAP might be hazardous postoperatively. In each case, we feel that the underlying sleep disorder should be carefully documented with all-night polysomnography and that a second examination should be performed to adjust and determine the correct amount of transtracheal oxygen. Additional studies are needed to establish the long-term efficacy and to define the mechanisms of TT O 2 on various types of sleep-disordered breathing.

REFERENCES 1. Op Tech Otolaryngol Head Neck Surg, 2:55-147, 1991 2. Hill MW, Simmons FB, Guilleminault C: Tracheostomy and sleep apnea, in Guilleminault C, Dement W (eds): Sleep Apnea Syndrome. New York, NY, Alan R. Liss Inc., 1978, pp 347-352 3. Sullivan CE, Grunstein RR:Continuous positive airways pressure in sleep-disordered breathing, in Kryger MH, Roth T, Dement WC

136

(eds): Principles and Practice of Sleep Medicine. Philadelphia, PA, Saunders, 1989, pp 559-570 4. Sanders MH, Gruendl CA, Rogers RM: Patient compliance with nasal CPAP therapy for sleep apnea. Chest 90:330-337, 1986 5. Waldorn RE, Herrick TW, Nguyen MC, et al: Long-term compliance with nasal continuous positive airway pressure therapy of obstructive sleep apnea. Chest 97:33-38, 1990 6. Heimlich H, Carr G: Transtracheal catheter technique for pulmonary rehabilitation. Ann Otol Rhinol Laryngol 94:502-504, 1985 7. Heimlich H: Respiratory rehabilitation with transtracheal oxygen system. Ann Otol Rhinol Laryngol 91:643-647, 1982 8. Spofford BT, Christopher KL, Hoddes ES: Transtracheal oxygen therapy for obstructive sleep apnea. Chest 89:484S, 1986 (abstr) 9. Elmer [C, Farney RJ, Walker JM, et al: The comparison of transtracheal oxygen with other therapies for obstructive sleep apnea. Am Rev Respir Dis 137:311A, 1988 10. Chauncey JB, Aldrich MS: Preliminary findings in the treatment of obstructive sleep apnea with transtracheal oxygen. Sleep 13:167174, 1990 11. Christopher KL, Spofford BT, Petrun MD, et al: A program for transtracheal oxygen delivery: Assessment of safety and efficacy. Ann Intern Med 107:802-808, 1987 12. Rechtschaffen A, Kales A: A Manual of Standardized Terminology, Techniques, and Scoring System for Sleep Stages of Human Subjects. Brain Information Service/Brain Research Institute. University of California, Los Angeles, CA, 1968 13. Bornstein SK: Respiratory monitoring during sleep: Polysornnography, in Guilleminault C (ed): Sleeping and Waking Disorders: Indications and Techniques. Menlo Park, CA, Addison-Wesley Publishing Co, 1982, pp 183-212 14. Dowdell WT, Javaheri S, McGinnis W: Cheyne-Stokes respiration presenting as sleep apnea syndrome: Clinical and polysornnographic features. Am Rev Respir Dis 141:871-879, 1990 15. Takasaki Y, Orr D, Popkin J, et al: Effect of nasal continuous positive airway pressure on sleep apnea in congestive heart failure. Am Rev Respir Dis 140:1578-1584, 1989 16. Berssenbrugge A, Dempsey J, Iber C, et al: Mechanisms of hypoxiainduced periodic breathing during sleep in humans. J Physiol 343: 507-524, 1983 17. Phillipson EA: Control of breathing during sleep. Am Rev Respir Dis 118:909-939, 1978 18. Khoo MCK, Kronauer RE, Strohl KP, et al: Factors inducing periodic breathing in humans: A general model. J Appl Physiol Respir Environ Exercise PhysioI53:644-659, 1982 19. Fletcher Ee, Costarangos C, Miller T: The rate of fall of arterial oxyhemoglobin saturation in obstructive sleep apnea. Chest 96:717722,1989 20. Hoffstein V, Zamel N, Phillipson E: Lung volume dependence of pharyngeal cross-sectional area in patients with obstructive sleep apnea. Am Rev Respir Dis 130:175-178, 1984

TRANSTRACHEAL O2 FOR SLEEP APNEA