Anand Rose

Sleep disordered breathing and chronic respiratory failure in patients with chronic pain on long term opioid therapy.

STUDY OBJECTIVES The use of opioid medication for chronic pain has been increasing. The main aim of this study was to assess how many patients on opioids for chronic pain had sleep disordered breathing (SDB) and the type of SDB. The impact of these medications on daytime arterial blood gas (ABG) measurements and psychomotor vigilance was also studied. METHODS Twenty-four patients (aged 18-75 years) on long-term opioids were prospectively recruited. Patients underwent home polysomnogram (PSG), psychomotor vigilance testing (PVT), and awake daytime ABG. Overnight PSG findings were compared to those of patients matched for age, sex, and BMI referred to our sleep service for evaluation of SDB. PVT results in the patient cohort were compared to PVT in healthy controls. RESULTS Forty-six percent of opioid patients had severe SDB as defined by an apnea hypopnea index (AHI) > 30/h. The severity of SDB was similar in opioid-treated pain clinic patients and sleep clinic patients (mean ± SD AHI: Opioid-treated patients 32.7 ± 25.6; Sleep Study comparator group 28.9 ± 24.6, p = 0.6). Opioid patients had a higher frequency of central apneas and a lower arousal index (CAI: 3.9 ± 8.3 vs. 0.3 ± 0.5 events/h; p = 0.004, AI 8.0 ± 4.1 vs. 20.1 ± 13.8, p < 0.001). Pain clinic patients had impaired gas exchange during sleep and wakefulness. Nine of 20 (45%) had daytime hypercapnia, indicating a surprising number were in chronic respiratory failure. Morphine equivalent doses correlated with the severity of SDB. PVT was impaired when compared to a healthy PVT comparator group (RT: Opioid-treated patients 0.43 ± 0.27: Healthy PVT comparator group 0.28 ± 0.03 sec; p < 0.001). CONCLUSIONS Patients on long-term opioids frequently have severe SDB, which in part is central in origin. PVT was markedly impaired. Half of the patients studied have evidence of chronic ventilatory failure. COMMENTARY A commentary on this article appears in this issue on page 853

Restless leg syndrome, dopamine agonists and sleep attacks

Episodes of sudden sleep onset, which occur without warning, have been termed sleep attacks. Sleep attacks have been described in patients with Parkinson’s disease on treatment with dopaminergic agents – L-DOPA and DOPA agonists (DA). These attacks are said to be more commonly associated with non-ergoline DOPA agonists (Pramipexole and Ropinirole). Restless leg syndrome (RLS) is a known cause of sleep fragmentation. DOPA agonists have been used to treat RLS as well. We report an 86-year-old woman who lived alone and was independent with all her activities. She had a long-standing history of restless legs, which was not of concern to her. Associated with recent stresses in the family, her restless leg symptoms intensified over a period of 3 months. They began to occur on a daily basis, disruptedher sleep and caused daytime somnolence. Thiswas a significant change from her normal sleep pattern. She was screened for secondary causes of RLS. Her iron studies and renal function were normal. She was treated with the ergoline DA cabergoline for 6 weeks at a dose of 0.5 mgonce daily followed by another 4 weeks at 1 mg once daily. This resulted in complete resolution of her restless leg symptoms. Her sleep quality and her daytime somnolence improved. However, during this period (of taking cabergoline 1 mg once daily) she had five episodes of sleep attacks. They were episodes of sudden onset of sleepiness, which occurred without warning when she was awake, in the middle of anactivity. The family described a typical attack – in which the patient fell asleep while drinking tea at a restaurant and dropped her cup. Another was a sudden inappropriate cessation of a conversationmid-sentence, at which time the patient was found to be asleep. In both these instances she had to be roused. The patient was amnesic to these events. There was no suggestion of generalized tonic clonic seizure activity or cerebrovascular events associated with these attacks. Drug-related side-effects were considered possible and cabergoline was stopped. The sleep attacks ceased within 72 h of stopping the drug. The temporal relationship of this phenomenon to the use of cabergoline strongly suggested that sleep attacks were a drug-related side-effect. Following cessation of cabergoline, her restless legs, sleep fragmentation and daytime somnolence returned incapacitating her. A 4-week trial of L-DOPA was ineffective. Subsequently she was treated with the non-ergoline DA – Ropinirole. She was commenced on Ropinirole 0.25 mg nocte (4 weeks) increasing to 0.5 mg per day nocte (4 weeks). This resulted in excellent control of her restless leg symptoms. Her sleep quality and her daytime somnolence improved markedly. No sleep attacks were noted. The patient returned to her previous functional state and was independent within 2 weeks. She has been well and not having excessive daytime sleepiness for the last 4 months on Ropinirole at 0.5 mg once daily. Sleep attacks were first described in 1999 in eight patients who were on treatment for Parkinson’s disease with the non-ergoline DOPA agonist – Pramipexole. It was

Partial anomalous pulmonary venous return in patients with pulmonary hypertension

Anomalous pulmonary venous return is an uncommon congenital malformation, and may be partial or total. Partial anomalous pulmonary venous return (PAPVR) is more common than total anomalous pulmonary venous return, and is often associated with other congenital cardiac anomalies. Whilst many patients with PAPVR remain asymptomatic, some may present in later age with symptoms related to left‐to‐right shunt, right heart failure and pulmonary hypertension. We report two cases of PAPVR detected on Computed Tomography Pulmonary Angiogram (CTPA) for the work up of pulmonary hypertension. The cases demonstrate that, although uncommon, partial anomalous pulmonary venous return can be a contributing factor to pulmonary hypertension and pulmonary veins should be carefully examined when reading a CTPA study.

Endobronchial Diagnosis of a Malignant Mesothelioma.

deficiency virus infection.1,2 In these patients, the prognosis is clearly worse than in patients with MALT and require an aggressive treatment. Solomonov and colleagues, in 2008, reviewed 441 patients with NHL diagnosis over a period of 7 years. In this report, 8 patients (1.8%) had localized lung disease, 5 of them in the form of mediastinal masses and in 3 cases exclusively with isolated endobronchial involvement. The main symptom was dyspnea. Even though the literature describes that the main histological type of PPL is MALT, only one of the patients in this series exhibited the condition, whereas in the remaining patients, the histologic findings were that of DLBCL.3 According to published data, DLBCL with a primary pulmonary location represents 11% to 19% of all PPL, although its incidence is probably higher. The underdiagnosis could be due to the slower growth and the infrequent involvement of the mediastinum and extratoracic locations, the latter of course associated with a worse prognosis. In summary, the lung is a common site for a secondary involvement of malignant lymphomas, with an incidence of 25% to 40%; primary NHLs involving the endobronchial tree are extremely rare.4,5 Yet, they should be included in the differential diagnosis of uncharacteristic endobronchial lesions.