| Abstract |
Purpose: There is limited data regarding the sleep quality in survivors of critical illness, while the time
course of the sleep abnormalities observed after ICU discharge is not known. The aim of this study
was to assess sleep quality and the time course of sleep abnormalities in survivors of critical illness.
Methods: Eligible survivors of critical illness without hypercapnia and hypoxemia were evaluated
within 10 days (1st evaluation, n = 36) and at 6 months after hospital discharge (2nd evaluation, n =
29). At each visit, all patients underwent an overnight full polysomnography and completed healthrelated
quality of life questionnaires (HRQL). Lung function and electro-diagnostic tests (ED) were
performed in 24 and 11 patients, respectively.
Results: At 1st evaluation, sleep quality and HRQL were poor. Sleep was characterised by high
percentages of N1, low of N3 and REM stages, and high apnea–hypopnea index (AHI, events/h).
Twenty-two out of 36 patients (61%) exhibited AHI ≥ 15 (21 obstructive, 1 central). None of the
patients’ characteristics, including HRQL and lung function, predicted the occurrence of AHI ≥ 15. At 6
months, although sleep quality remained poor (high percentages of N1 and low of REM), sleep
architecture had improved as indicated by the significant increase in N3 [4.2% (0–12.5) vs. 9.8% (3.0–
20.4)] and decrease in AHI [21.5 (6.5– 29.4) vs. 12.8 (4.7–20.4)]. HRQL improved slightly but
significantly at 6 months. Neither the changes in HRQL nor in lung function tests were related to these
of sleep architecture. Six out of eight patients with abnormal ED at 1st evaluation continued to exhibit
abnormal results at 6 months.
Discussion: Our study resulted in the following findings: (1) in survivors of critical illness without gas
exchange abnormalities, within 10 days of hospital discharge, sleep quality was poor characterised by
severe disruption of sleep architecture and excessive sleep-disordered breathing, mainly of the
obstructive type. (2) at 6 months after hospital discharge sleep quality remained relatively poor, in
comparison to the 1st sleep study, however significant improvement in N3 stage and AHI was
observed, resulting in significantly more patients being classified as normal or with mild SDB. (3)
quality of life improved at 6 months, however continued to be abnormal. (4) the change in quality of
life and that of sleep disturbances had no relationship between each other.
The demonstration of obstructive events could be explained by four pathophysiologic mechanisms
which are the following: (1) increased upper airway collapsibility, (2) high chemical loop gain, (3) low
arousal threshold and (4) poor responsiveness of pharyngeal dilators (mainly the genioglossus
muscle) to negative pharyngeal pressure. Although our study has some limitations, it is to our
knowledge the first one to prospectively collect data regarding the sleep quality of survivors of critical
illness at hospital discharge and 6 months later Conclusions: Survivors of critical illness exhibited a high prevalence of obstructive sleep-disordered
breathing and poor sleep architecture at hospital discharge, which slightly improved 6 months later,
indicating that reversible factors are partly responsible for these abnormalities.
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