Z
Dorkova, A Somos, M Orolin, J Farah, P Joppa, R Tkacova
Department of Respiratory Medicine and Tuberculosis, Faculty of Medicine, P.J. Safarik University and L. Pasteur Teaching Hospital, Kosice, Slovakia
Correspondence:
Ruzena Tkacova, MD, PhD, Professor of Medicine, Department of Tuberculosis and
Respiratory Medicine, L. Pasteur Teaching Hospital, Rastislavova 43, SK-041 90
Kosice, Slovakia
E-mail: rtkacova@central.medic.upjs.sk
SMJ 2008 53(2): 65
This
work was supported by operating grant VEGA 1/2312/05 of the Ministry of
Education, Slovakia, and VVGS 22/2006 of PJ
Safarik University, Kosice, Slovakia
Abstract.
Acute
hypercapnic respiratory failure is a rare but life-threatening complication
in grossly obese patients with severe obstructive sleep apnoea (OSA). Facial
trauma or upper airway surgery, respiratory tract infections, bronchospasm, use
of pain medication and concomitant obstructive or restrictive pulmonary
impairment predispose to the development of respiratory failure in such
patients. We present a case of a morbidly obese male patient in whom
moderately severe OSA (the apnoea-hypoponea index, AHI of 37/hour) was treated
with uvulapalatopharyngoplasty (UPPP) because
he declined treatment with non-invasive
ventilation. The early postoperative period was complicated by severe
hypercapnic respiratory failure in association with worsening of OSA: arterial
PO2 was 4.14 kPa, PCO2 9.7 kPa, AHI increased to
93.8/hour, minimal nocturnal arterial oxygen saturation was 46%. Therapy with
non-invasive ventilation using bi-level positive airway pressure (BiPAP) was
initiated immediately, and resulted in marked improvements in the patient’s
clinical condition, in association with the improvements in arterial blood
gases. Before the discharge, nocturnal continuous positive airway pressure (CPAP)
therapy to treat OSA on the long-term basis was initiated. Two months after the
release, the patient’s
blood gases were within the
normal range, and he reported marked improvements in his clinical condition
including alleviation of daytime sleepiness and increased physical endurance.
Our case demonstrates that in the presence of severe OSA, life-threatening
hypoxaemia and hypercapnia were successfully alleviated using BiPAP in the
postoperative period after UPPP.
Key
words: Obstructive sleep apnoea, uvulopalatopharyngoplasty, respiratory failure,
non-invasive ventilation
Introduction
Obstructive
sleep
apnoea (OSA)
is a common
disease that affects about 4% of the male and 2% of the female population in
industrialized countries1. OSA is characterized by intermittent
episodes of partial or complete obstruction of the upper airway during sleep
that disrupts normal ventilation, impairs sleep structure, and results in
nocturnal chocking episodes, excessive daytime sleepiness, impaired cognition
and reduced quality of life. In addition, OSA has recently been identified as an
independent cardiovascular risk factor2.
Early
reports indicated high in-hospital mortality in patients with severe OSA and
features of Pickwickian syndrome3. The association between sudden
death and OSA may result from the increased risk of cardiovascular complications
on one hand4, and/or progression of respiratory failure on the other5.
Postoperative period and recovery from general anaesthesia pose a significant
risk for worsening of OSA, and subsequent development of acute respiratory
failure in such patients6. Respiratory failure and presumably death
from this acute complication can be reversed with effective treatment of OSA7.
We report a case of acute respiratory failure that developed during the
postoperative period following uvulopalatopharyngoplasty (UPPP) in a patient
with OSA who has successfully responded to treatment with non-invasive
ventilation using bi-level positive airway pressure (BiPAP).
Case
report
A
50-year old Caucasian man was admitted to the Clinic for Respiratory Medicine
and Tuberculosis in a University
hospital setting for
progressive worsening of acute respiratory failure. The patient was morbidly
obese and suffered from arterial hypertension. In November 2004 he was diagnosed
with moderately severe OSA (apnoea-hypopnoea index - AHI: 37 episodes per hour
of sleep, mean nocturnal SaO2 68%, in association with excessive
daytime sleepiness including drop-outs in the standing position). The
patient was advised to start the treatment with continuous positive airway
pressure (CPAP) for his moderately severe OSA, however, he was not willing to
give a try to this therapy mode. Consequently, UPPP was suggested as a therapeutic
option, and he agreed to that.
In December 2005, the patient underwent UPPP and bilateral tonsillectomy to
alleviate his OSA. The postoperative period was complicated by hypercapnic
respiratory failure, acute upper gastrointestinal bleeding due to gastric ulcer
diagnosed by gastroscopy, and lower airway infection. The hemorrhage stopped
while he was treated conservatively. However, his clinical condition worsened as
the result of the progression of hypercapnic respiratory failure.
At
the time of admission to our clinic, the patient was somnolent, dyspneic at
rest, his body temperature was 37.8oC, and he was expectorating
massive yellow sputum. His bodyweight was 125.0 kg and height 183.0 cm (Body
Mass Index of 37.3 kg/m2), with neck circumference of 58 cm, and
abdominal circumference of 162 cm. He suffered from severe bilateral ankle edema.
His daytime arterial
blood gases revealed severe hypoxaemia, hypercapnia and respiratory acidosis:
PaCO2 9.7 kPa; PaO2,
4.14 kPa; SaO2,
49.7%; pH, 7.27. Laboratory tests indicated increases in white blood cell count:
11.1x109/l with neutrophilia of 73.5% and increases in plasma
inflammatory proteins: C-reactive protein, 113,1 mg/l; mucoproteins 0,078 g/l.
Chest x-ray revealed nodular
pattern with nonhomogenous consolidation of the right middle lobe. Bodyplethysmography
(Jaeger,
Germany) revealed a restrictive respiratory pattern with forced exspiratory
volume in 1 second of 2.68 l, forced vital capacity of 3.1 l, and total lung
capacity of 5.2 l (69.8%, 64.4%, and 69.0% of predicted values, respectively). Echocardiographic
examination indicated preserved left ventricular function, right ventricular
dilation and hypertrophy (6.5 mm), and pulmonary hypertension with systolic
pulmonary artery pressure of 50 mm Hg. An overnight polysomnography (Alice-4
diagnostic equipment, Respironics, Inc, Murrysville, Pennsylvania, USA) revealed
severe OSA with an AHI of 93.8 obstructive apnoeas and hypopnoeas per hour of
sleep. Mean sleep SaO2 was 63%, lowest SaO2 was 46%.
In
addition to oxygen, antibiotics (cefotaxim) and diuretics (furosemide and
spironolactone), therapy with non-invasive ventilation using bi-level positive
airway pressure (BiPAP, Respironics Inc.) was initiated immediately. The
inspiratory positive airway pressure was set at 12
cm H2O, and expiratory positive airway pressure at 3 cm H2O.
After 4 days, the clinical condition markedly improved, as evidenced by
alleviation of dyspnea and fatigue. Improvements in clinical condition were
associated with improvements in arterial blood gases: PaCO2, 7.5 kPa;
PaO2, 7.0 kPa; SaO2, 88.8%; pH, 7.47; reductions in white
blood cell count: 6x109/l, without neutrophilia (57.4% neutrophils);
and reductions in plasma inflammatory proteins: C-reactive protein, 22.7 mg/l;
mucoproteins, 0,065 g/l.
Upon
the resolution of hypercapnic respiratory failure, nocturnal CPAP therapy to
treat OSA on the long-term basis was introduced to the patient. While on 8
cm H2O CPAP pressure, obstructive apnoeas and hypopnoeas were
effectively alleviated; the AHI was 5.6 obstructive episodes per hour of sleep.
The patient was released from the hospital in a stable clinical condition.
He returned to the out-patient clinic 2 months post-discharge. He was compliant
with the CPAP therapy, and, in addition, he lost 10 kg in the meanwhile. His
blood gases were within the normal range, and he
reported marked improvements in clinical status including alleviation of daytime
sleepiness and increased physical endurance.
Discussion
Acute
respiratory failure necessitating non-invasive and/or invasive ventilation is a rare
complication of OSA. However, once developed, it poses a life-threatening
situation requiring intensive care management5. In our patient with
OSA, acute hypercapnic respiratory failure developed
in the postoperative period after UPPP.
OSA
results from a partial or complete collapse of narrowed upper airways
during sleep, followed by inefficient respiratory efforts. Although the site of
obstruction is most frequently pharyngeal, other upper respiratory tract
segments may also be involved8.
There is general agreement that
patients with OSA should have treatment to reduce the frequency of apnoeas and
hypopnoeas and thus alleviate the symptoms of the disease9. The
cornerstone of treatment in adult patients with OSA utilizes positive airway
pressure ventilation. However, despite the effectiveness of CPAP in the
management of OSA, the tolerance and acceptance can be occasionally a significant
problem. As a result, surgery remains an option for some patients. Surgery
for OSA involves treatment directed toward the anatomic site(s) of obstruction:
the nose, the palate (oropharynx), and the tongue base. A variety of
surgical approaches have been utilized for OSA. These include UPPP,
tonsillectomy with or without adenoidotomy, septoplasty, oral maxillofacial
surgery, and multilevel reconstruction of the upper airway10.
UPPP
was the first operation introduced as a surgical procedure to improve
airway obstruction in the oropharynx. UPPP enlarges
the retropalatal airway, and involves
the removal of a portion of the soft palate and uvula as well as a limited
amount of the lateral pharyngeal wall and if present, the tonsilar tissues. In general,
the overall long-term success rate of UPPP is 52% 10, 11. However,
removal of an excessive amount of tissue can increase the risk of complications
such as palatal breakdown, postoperative bleeding, nasopharyngeal stenosis,
transient neuralgias, tongue base abscess formation, and voice change12.
Velopharyngeal incompetence is a frequent and sometimes severe problem
associated with radical resections10. In addition, in the
postoperative period, the upper airway patency is further compromised by low
tonic pharyngeal support due to general anaesthesia6. Low tonic
pharyngeal support with the post-surgical local oedema may increase the
propensity of the upper airway to collapse resulting in partial or complete
obstruction of the upper airway and worsening of OSA. Consequently, hypercapnic
respiratory failure is a rare but not exceptional complication in such
patients13. At the time when the diagnosis of OSA was established in
our patient, no local guidelines were available that would specify the role of
UPPP as a treatment option for OSA. However, Scottish Intercollegiate Guidelines
Network published in June 2003 a national clinical guideline that clearly
states that the use of UPPP is not recommended for the treatment of OSA14.
Our case report further illustrates the need to adhere to these
guidelines.
Few
papers in the literature addressed the issue of acute respiratory failure in
patients with sleep disordered breathing5, 7, 13. In general,
predisposing factors for the development of hypercapnic respiratory failure in
patients with OSA include facial trauma, respiratory
tract infections or bronchospasm, use of pain medication, and/or concommitant
obstructive or restrictive lung impairment7. In our patient with OSA,
several risk factors for worsening of hypoxaemia and hypercarbia coincided:
respiratory tract infection, use of pain medication in the postoperative period
following UPPP, and restrictive pulmonary function impairment due to morbid
obesity. On the basis of a national survey in the United States, Fairbanks15
reported 16 fatalities and 7 near fatalities from UPPP in the early
postoperative period. Respiratory obstruction, secondary to pharmacologic
sedation and surgical oedema were the most frequent causes of severe
postoperative complications. In addition, hypercapnia persisting after surgical
treatment for OSA might reflect an adaptation process of chemosensitivity and
respiratory control16.
In
general, in obese patients with OSA and hypercapnic respiratory failure,
ventilation using non-invasive positive pressure ventilation is a safe and very
effective treatment modality5. Therapy of OSA with CPAP abolishes OSA
in most patients, in association with the alleviation of nocturnal and daytime
symptoms of sleep disordered breathing. Importantly, CPAP therapy was shown to
be associated with reductions in systemic blood pressure in patients with OSA
and refractory hypertension17, and reductions of several risk factors
of cardiovascular diseases such as platelet aggregability, fibrinogen level,
superoxide release, and cell adhesion molecule expression4.
Therefore, therapy of OSA has a potential role in reducing cardiovascular
disease risk, and there are reasons to believe that effective treatment will
have positive influence on the prognosis2. However, in some
hypercapnic patients with OSA, CPAP has proved to be ineffective in correcting
hypercapnia and hypoxaemia both during sleep and wakefulness. In these cases,
using bi-level positive airway pressure was found to be superior in terms of
correction of nocturnal and daytime blood gases18.
In agreement, our case demonstrates that severe life-threatening hypoxaemia and
hypercapnia were successfully alleviated using bi-level positive airway pressure
therapy with the inspiratory and expiratory pressures of 8 and 3 cm H2O,
respectively. This observation is in accordance with the recent report of
BaHammam5 who used BiPAP with similar set-up pressures in obese
patients presenting with acute respiratory failure in the intensive care unit.
Importantly, our case also indicates that once the triggers of respiratory
failure in the presence of severe OSA such as postsurgical upper airway oedema
and respiratory tract infection were eliminated, CPAP therapy alone proved to be
sufficient to alleviate OSA.
Conclusion
Acute
hypercapnic respiratory failure is a rare but life-threatening complication
in patients with Pickwickian syndrome and OSA. In our patient, factors that
might have contributed to the progression of respiratory failure in the
postoperative period after UPPP were upper airway oedema following the surgery,
analgesia, respiratory infection and concommitant restrictive lung impairment
due to morbid obesity. Our case report demonstrates that early therapy with
non-invasive positive pressure ventilation is an efficient treatment of acute
hypercapnic respiratory failure in the postoperative period in patients with
severe OSA. In addition, adherence to the national
guidelines on the management of OSA14 is warranted.
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