Article Text


Upper airways sarcoidosis presenting as obstructive sleep apnoea
  1. R N H Shah,
  2. P R Mills,
  3. P J M George,
  4. J A Wedzicha
  1. Department of Respiratory Medicine, The London Chest Hospital, Bonner Road, London E2 9JX, UK
  1. Dr J A Wedzicha.


Sarcoidosis may present in a number of different ways, affecting many organ systems. The case history is presented of a 32 year old woman who presented with symptoms of severe obstructive sleep apnoea (OSA) due to infiltration of the upper airway by sarcoidosis. To our knowledge this presentation of sarcoidosis has not previously been described.

  • obstructive sleep apnoea
  • sarcoidosis
  • continuous positive airway pressure ventilation
  • sleep study

Statistics from

A 32 year old woman of West Indian descent was referred to our hospital with a three month history of worsening hypersomnolence and loud snoring. She was repeatedly falling asleep during the daytime and, as a result, was having difficulty looking after her children. It had also been noted that she snored loudly and had prolonged apnoeic episodes throughout the night. During the week prior to admission the patient had developed a sore throat and hoarse voice.

She had been diagnosed as having cutaneous sarcoidosis four years previously which was treated successfully with a six month course of oral steroids. One year prior to referral to our hospital she was diagnosed as having diabetes insipidus secondary to cranial sarcoid involvement. She had been on intranasal desmopressin since then.

On admission a coherent history was difficult to obtain from the patient as she was unable to stay awake for longer than a few minutes. On examination the patient had marked lupus pernio as well as erythema nodosum on her shins. A hoarse voice and mild stridor were noted. There were no other abnormalities detected on physical examination. Notably her chest was clear on auscultation with good air entry throughout both lung fields. The patient’s weight was 132 kg.

Full blood count, urea, and electrolytes were normal. The corrected calcium level was 2.77 mmol/l and the serum angiotensin converting enzyme (ACE) level was 181 u/l (normal range 10–70 u/l). Arterial blood gas analysis on air showed a pH of 7.44, Paco 2 of 6.65 kPa, Pao 2 of 8.43 kPa, and oxygen saturation (Sao 2) of 92%. Respiratory function tests showed a peak expiratory flow rate (PEFR) of 254 l/min (65% of predicted). Forced expiratory volume in one second (FEV1) was 2.35 l (77% of predicted), forced vital capacity (FVC) 3.17 l (91% of predicted) with an FEV1/FVC ratio of 74%. The chest radiograph was normal, the lung fields were clear, and there was no hilar lymphadenopathy. Radiography of the neck soft tissue showed no tracheal obstruction.

Multichannel monitoring of chest wall motion, airflow, Sao 2, and heart rate (EdenTrace, Nellcor Puritan Bennet, Minnesota, USA) was recorded directly on admission, which was during the daytime, with 2 l/min supplemental oxygen (fig1).

Figure 1

Recording from EdenTrace showing variations in heart rate, airflow, impedance and pulse oximetry with time.

Nasendoscopic examination showed severe swelling of the nasal mucosa with mucoid discharge. There was disrupted architecture of the left glottis, with a narrowed and irregular subglottis to approximately 50% of the normal diameter. Tissue biopsy specimens confirmed the presence of non-caseating granulomas.

The patient was started on high dose oral corticosteroids and nasal continuous positive pressure ventilation (CPAP) at a pressure of 7.5 cm H2O. Within 24 hours the patient was noticeably more alert and was discharged home with a nasal CPAP machine for nocturnal use six days after admission. Optimum CPAP pressure was titrated by a repeat sleep study while on treatment.

One month after discharge she was not experiencing any apnoeas or complaining of hypersomnolence. She admitted to not using the CPAP and had not altered in weight. Arterial blood gas tensions on air showed a pH of 7.41, Paco 2 of 5.39 kPa, Pao 2 of 10.20 kPa, and an Sao 2 of 95%. Respiratory function tests showed an FEV1 of 3.1 l (102% of predicted), FVC of 3.7 l (106% of predicted), with an FEV1/FVC ratio of 84%. The serum ACE concentration was 52 u/l. Six months after initial presentation a sleep study on air without nasal CPAP produced normal results.


Laryngeal involvement in sarcoidosis is rare (0.5–1.4% of cases).1 It classically causes supraglottic swelling and erythema which is thought to be pathognomonic. It usually presents with stridor but has also been reported to present with dysphagia2 as well as being in the differential diagnosis of childhood epiglottic enlargement.3 Laryngeal sarcoidosis may be treated with systemic corticosteroids, intralesional steroid injections, microendoscopic surgery, as well as tracheostomy if needed.4

Sleep apnoea has been associated with a wide range of metabolic and structural disorders; however, to our knowledge, there is no previous report of sleep apnoea being caused by infiltration of the upper airway with sarcoidosis. This patient had laryngeal sleep apnoea due to sarcoidosis infiltration as opposed to the more common pharyngeal sleep apnoea seen in clinical practice. Upper airway obstruction is notoriously difficult to diagnose clinically, particularly when the chest radiograph is normal. The diagnosis was aided in this patient by the combination of a low PEFR, hoarse voice, and the presence of stridor.5

Our case report describes a patient with the rapid onset of symptoms of life threatening obstructive sleep apnoea. Her initial sleep study, which was performed during the daytime due to the severity of her initial presenting symptoms, showed marked sleep apnoea. Nasendoscopic examination and biopsy specimens confirmed the presence of laryngeal sarcoidosis infiltration. CPAP provided effective and rapid resolution of her symptoms before definitive treatment with systemic corticosteroids had an effect. Infiltration of the upper airway with sarcoidosis should be considered as a reversible cause of obstructive sleep apnoea in the appropriate clinical setting.


We would like to acknowledge the assistance of Mrs Rubina Ishtiaq in the preparation of this manuscript.


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