ADVERTISEMENT

Issue Navigator

Volume 11 No. 06
Earn CME
Accepted Papers
Classifieds





Case Reports

Worsening of Obstructive Sleep Apnea Associated with Catheter-Related Superior Vena Cava Syndrome

Marie Jouvenot, MD1; Serge Willoteaux, MD, PhD2; Nicole Meslier, MD1,3; Frédéric Gagnadoux, MD, PhD1,3
1Université d'Angers, Département de Pneumologie, CHU, Angers, France; 2Université d'Angers, Département de Radiologie, CHU, Angers, France; 3INSERM 1063, Angers, France

ABSTRACT

There is growing evidence that fluid accumulation in the neck contributes to the pathogenesis of obstructive sleep apnea (OSA). We describe a case of catheter-related superior v ena cava (SVC) thrombosis revealed by rapid onset of typical symptoms of OSA. A marked improvement in OSA severity was observed after central venous catheter removal, anticoagulant therapy, and SVC angioplasty

Citation:

Jouvenot M, Willoteaux S, Meslier N, Gagnadoux F. Worsening of obstructive sleep apnea associated with catheter-related superior vena cava syndrome. J Clin Sleep Med 2015;11(6):681–682.


There is growing evidence that fluid accumulation in the neck as a consequence of overnight rostral fluid shift contributes to the pathogenesis of obstructive sleep apnea (OSA).1 Superior vena cava syndrome (SVCS) includes various symptoms due to external compression or intrinsic obstruction of the superior vena cava (SVC), including cyanosis, distension of subcutaneous vessels, and edema of the upper extremities, head, and neck. Fluid accumulation in the neck may compromise the function of the larynx or pharynx, causing dyspnea, stridor, cough, hoarseness, and dysphagia.2 This is a report of a catheter-related SVC thrombosis revealed by worsening of snoring and rapid onset of typical OSA related symptoms.

REPORT OF CASE

A 67-year-old man was referred for clinical suspicion of OSA. His main medical history was multifocal motor neuropathy with conduction block treated with intravenous immunoglobulin every 6 weeks through a subcutaneously implanted port-chamber catheter in the right cephalic vein. Apart from a long history of loud snoring, the patient reported no typical OSA associated symptoms in the past. In recent weeks, his wife noted an increase in snoring intensity and described gasping episodes. The patient had severe excessive daytime sleepiness with an Epworth Sleepiness Scale (ESS) score of 19/24.

His body mass index (BMI) was 26 kg/m2 with no recent history of weight gain. Physical examination revealed typical signs of SVC obstruction with facial and neck edema, jugular venous distension, and dilated superficial thoracic collateral vein. Upper airway exam revealed no evident septal deviation, no dental anomalies, and no adenotonsillar hypertrophy. The patient had a relatively large tongue with a Mallampati II presentation of the palate's velum. Chest computed tomography (CT) revealed a large occlusive thrombus in the SVC, in the brachiocephalic vein and in the right internal jugular vein. Overnight respiratory monitoring with continuous recording of oxygen saturation (SpO2), nasal-oral airflow, and chest and abdominal wall motion showed severe OSA with an apneahypopnea index (AHI) of 64 events/h (Table 1). The patients received low-molecular-weight heparin followed by fluindione oral anticoagulation and the central venous catheter was removed. Continuous positive airway pressure (CPAP) was initiated with self-adjusted pressure support between 4 and 14 cm H2O. At 6 weeks, mean CPAP compliance was 4.5 h/night, the patient was no longer sleepy (ESS = 4/24), and physical examination showed a partial reduction of the signs of SVCS. Overnight respiratory recording after 5 nights of CPAP withdrawal showed a marked decrease in the apnea index but only a slight decrease in the AHI (Table 1). A repeat chest CT showed the disappearance of the brachiocephalic vein thrombosis but persistence of 70% occlusion of the SVC near its junction with the right atrium. A percutaneous transluminal balloon angioplasty was performed, and the patient was maintained on oral anticoagulant therapy. Three months later, BMI was unchanged, mean CPAP compliance was 6.1 h/night, the ESS was 6/24, and physical examination showed a complete resolution of the signs of SVCS. A third overnight respiratory recording after 5 nights of CPAP withdrawal demonstrated a 58% reduction in AHI (Table 1).

Clinical and nocturnal polygraphic evaluation at baseline and during follow-up.

jcsm.11.6.681.t01.jpg

table icon
Table 1

Clinical and nocturnal polygraphic evaluation at baseline and during follow-up.

(more ...)

DISCUSSION

Complex anatomic and physiologic factors are involved in upper airway (UA) collapse in patients with OSA. Recent advances in the understanding of the pathogenesis of OSA has provided strong evidence that fluid accumulation in the neck as a consequence of overnight rostral fluid shift contributes to increase UA collapsibility.1 In humans with obstruction of the SVC, the cervical venous pressure is usually increased to 20 to 40 mm Hg (normal range, 2 to 8 mm Hg).3 The increased hydrostatic pressure in the cervical veins is likely to cause transudation of fluid into the interstitial space surrounding the UA.1 Intrathoracic malignancies are responsible for 60% to 85% of SVCS cases.2 A few cases of OSA associated with SVCS due to malignant or non-malignant mediastinal compression of the SVC have been previously described,49 with some cases reporting relief of OSA after radiation, chemotherapy, and/or stent insertion into the stenotic SVC.59 A case of OSA associated with SVC thrombosis has also been previously described in a patient with familial Mediterranean fever.10 The modern practice of medicine has seen increased use of intravascular catheters. Although accounting for a substantial proportion of non-malignant SVCS, the incidence of catheter-related SVC thrombosis appears to be low.11 A recent report described severe OSA requiring continuous positive airway therapy as a complication of catheter-related SVC thrombosis in a 15-year-old girl with infantile nephrotic syndrome.12

In the present report we describe a case of catheter-related SVC thrombosis revealed by worsening of snoring and rapid onset of typical symptoms of OSA. Although our patient did not report typical OSA related symptoms in the past, the persistence of moderate sleep disordered breathing (SDB) with an AHI of 27 events/h after resolution of SVCS indicates that he had at least moderate OSA prior to presentation. However, the contribution of SVC thrombosis to the worsening of OSA was supported by a marked decrease in SDB severity and related symptoms after central venous catheter removal, anticoagulant therapy, and SVC angioplasty. It seems highly unlikely that any confounding factor contributed to the improvement of SDB, as the patient had no weight loss and took no drug except oral anticoagulation during the follow-up period.

Clinicians should be aware that SVC obstruction might be revealed by symptoms of OSA.

DISCLOSURE STATEMENT

This was not an industry supported study. The authors have indicated no financial conflicts of interest.

REFERENCES

1 

White LH, Bradley TD, authors. Role of nocturnal rostral fluid shift in the pathogenesis of obstructive and central sleep apnoea. J Physiol. 591:1179–93. [PubMed Central][PubMed]

2 

Lepper PM, Ott SR, Hoppe H, Schumann C, et al., authors. Superior vena cava syndrome in thoracic malignancies. Respir Care. 56:653–66. [PubMed]

3 

Wilson LD, Detterbeck FC, Yahalom J, authors. Clinical practice. Superior vena cava syndrome with malignant causes. N Engl J Med. 2007;356:1862–9. [PubMed]

4 

Stradling JR, Huddart S, Arnold AG, authors. Sleep apnoea syndrome caused by neurofibromatosis and superior vena caval obstruction. Thorax. 1981;36:634–5. [PubMed Central][PubMed]

5 

Fuyuno G, Kobayashi R, Iga R, Nomori H, Kodera K, Morinaga S, authors. Obstructive sleep apnea syndrome associated with superior vena cava syndrome. Nihon Kyobu Shikkan Gakkai Zasshi. 1995;33:322–6. [PubMed]

6 

Fernandez B Jr.; Smolley LA, Swirsky SM, Kaye MD, authors. Relief of sleep apnea after intravascular stenting for superior vena cava syndrome. Vasc Med. 1999;4:33–6. [PubMed]

7 

Ito M, Tanaka J, Kubota K, et al., authors. Obstructive sleep apnea syndrome in a patient with superior vena cava syndrome caused by lung cancer. Nihon Kokyuki Gakkai Zasshi. 2000;38:471–5. [PubMed]

8 

Amemiya M, Takise A, Kaira K, Endou K, Horie T, Inazawa M, authors. Obstructive sleep apnea syndrome in a patient with superior vena cava syndrome caused by malignant lymphoma. Nihon Kokyuki Gakkai Zasshi. 2006;44:197–201. [PubMed]

9 

Ursavasş A, Karadag M, Burgazlioglu B, et al., authors. Relief from sleep apnea after radiation and chemotherapy. Clinical Lung Cancer. 2007;8:502–3. [PubMed]

10 

Ustündag Y, Bayraktar Y, Emri S, authors. Superior vena cava thrombosis and obstructive sleep apnea in a patient with familial Mediterranean fever. Am J Med Sci. 1998;316:53–5. [PubMed]

11 

Otten TR, Stein PD, Patel KC, Mustafa S, Silbergleit A, authors. Thromboembolic disease involving the superior vena cava and brachiocephalic veins. Chest. 2003;123:809–12. [PubMed]

12 

Rinat C, Ben-Shalom E, Becker-Cohen R, Feinstein S, Frishberg Y, authors. Complications of central venous stenosis due to permanent central venous catheters in children on hemodialysis. Pediatr Nephrol. 2014;29:2235–9. [PubMed]