Search

Hintergrund: Die vorliegende Arbeit beschäftigt sich mit der Diagnostik des Adipositas Hypoventilations Syndroms (OHS). Die Diagnostik erfolgt routinegemäß durch eine Blutgasanalyse nach dem Schlaf. Nun stellt sich die Frage ob man mit der Methode einer Blutgasanalyse vor dem Schlaf dieselbe Aussage treffen kann. Ziel: In dieser Arbeit wird der Frage nachgegangen ob die Methode der Blutgasanalyse nach dem Schlaf gleichwertig zu der vor dem Schlaf ist. Somit könnten mögliche Sauerstoffinterventionen bereits früher eingeleitet werden. Aus diesem Grund werden folgende Blutgasparameter miteinander verglichen: partieller O2, partieller CO2, Sauerstoffsättigung, Basenüberschuss/Base Exzess, pH Wert und der Standardbicarbonatwert. Methodik: Hierbei handelt es sich um eine prospektive Studie bei der eine Blutgasanalyse von 26 Patienten*innen mit einem BMI von über 35kg/m2 vor und nach dem Schlaf erfolgte. Bei all diesen Patienten*innen besteht bereits ein Verdacht auf OSAS, weshalb sie eine Überweisung für eine polysomnographische Untersuchung erhalten haben. Vor der Blutabnahme wurde jeder Patient*in über die Studie aufgeklärt und unterschreib eine Einwilligungserklärung. In die Auswertung eingeschlossen wurden Personen im Alter von 18 bis 90 Jahren. Schwangere Frauen und nicht zeichnungsberechtige Personen wurden von der Studie ausgeschlossen. Ergebnisse: Die statistische Auswertung erfolgte mittels Shapiro Wilk Test und einer Korrelationsanalyse, anhand von Pearsons r und Spearmans rho. Des Weiteren wurden Accuracy, Sensitivität und Spezifität für alle abendlichen Parameter berechnet. Die berechneten Hauptzielgrößen wurden mit dem Goldstandard verglichen. Dies ermöglichte eine Aussage über die Gleichwertigkeit der Tests zu treffen. Die Ergebnisse besagen, dass ein Unterschied in den Hauptzielgrößen zwischen abendlicher und morgiger Messung besteht und diese somit nicht gleichwertig sind. Schlussfolgerung: Aufgrund der durchgeführten Korrelationsanalyse kann beobachtet werden, dass eine signifikante Korrelation zwischen den abendlichen und morgigen Werten vorliegt. Da die berechneten Hauptzielgrößen einen deutlichen Unterschied zum Goldstandard (Messung am Morgen) zeigen, kann die Blutgasanalyse vor dem Schlaf nicht als gleichwertig mit der nach dem Schlaf angesehen werden. Dies hat als Grund die unterschiedlichen Cut Off Werte, zwischen Morgen und Abend. Um bessere Werte zu erzielen, müssten die Cut Off Werte mittels einer Regressionsanalyse angepasst werden. Dies hätte zur Folge eine deutlich höhere Sensitivität und Spezifität und somit eine gewisse Vergleichbarkeit mit dem Goldstandard Background: The present work deals with the diagnosis of obesity hypoventilation syndrome (OHS). The diagnosis is made routinely by a blood gas analysis after sleep. Now the question arises whether one can make the same statement with the method of a blood gas analysis before sleep. Objective: In this work the question is investigated whether the method of blood gas analysis after sleep is equivalent to that before sleep. Thus, possible oxygen interventions could be initiated earlier. For this reason the following blood gas parameters are compared: partial O2, partial CO2, oxygen saturation, base excess/base excess, pH value and the standard bicarbonate value. Methods: This is a prospective study in which a blood gas analysis of 26 patients with a BMI of more than 35kg/m2 was performed before and after sleep. All of these patients were suspected of having OSAS and were referred for polysomnography. Before blood sampling, each patient* was informed about the study and signed an informed consent form. Individuals aged 18 to 90 years were included in the analysis. Pregnant women and persons not authorized to sign were excluded from the study. Results: Statistical analysis was performed using Shapiro Wilk test and correlation analysis, using Pearson's r and Spearman's rho. Furthermore, accuracy, sensitivity and specificity were calculated for all evening parameters. The calculated main outcome measures were compared with the gold standard. This allowed to make a statement about the equivalence of the tests. The results indicate that there is a difference in the main target parameters between the evening and morning measurements and that they are therefore not equivalent. Conclusion: Based on the correlation analysis performed, it can be observed that there is a significant correlation between the evening and morning values. Since the calculated main target values show a significant difference to the gold standard (measurement in the morning), the blood gas analysis before sleep cannot be considered equivalent to the one after sleep. This has as reason the different cut off values, between morning and evening. In order to achieve better values, the cut off values would have to be adjusted by means of a regression analysis. This would result in a significantly higher sensitivity and specificity and thus a certain comparability with the gold standard.

According to the literature, hypoxemia is considered to be severe when oxygen saturation (Sa O(2)) falls below 90 %. Frequently one can discover lower values without impairment of the patient. Especially patients with the obesity hypoventilation syndrome (OHS) will have frequent night time desaturations of significant duration below 50 % Sa O(2), but do still cope with their daytime jobs. This discrepancy can only be explained by the fact, that hypoxemia is not equivalent to tissue hypoxia. The latter is mainly being determined by oxygen delivery (DO2) which is being calculated by multiplying cardiac output (CO) and oxygen content (CaO2). Ca O(2) is determined by the product of Sa O(2) and haemoglobin (Hb) times 1.35. From this context it becomes evident, that assessing hypoxemia without considering oxygen content will frequently be misleading. The human organism has several possible ways of compensation in order to avoid tissue hypoxia. In case of acute hypoxemia that evolves within minutes the organism can shift the oxygen binding curve by changing 2 - 3-DGP erythrocytic activity. Additionally non vital organ systems might reduce their oxygen uptake. During sustained hypoxia (lasting 2 - 3 days) the Krebs cycle and the respiratory chain will express hypoxia-resistant iso-enzymes. Long lasting hypoxia can be compensated by polycythemia. Indirect data suggest, that the critical number for the oxygen content is rather low and is estimated to be somewhere around 33 % of the normal value. These mechanism of hypoxia-resistance are hardly ever maxed out in patients on critical care units.Lack of knowledge of the above described mechanisms does frequently result in diseases like ARDS which frequently develops due to excessive ventilatory pressures and excessive inspired O(2) concentrations.

The obesity hypoventilation syndrome (OHS) is defined by extreme overweight (BMI 30 kg/m2), daytime hypoventilation (PaCO245 mm Hg, the absence of other known causes of hypoventilation) and sleep-related breathing disorders. Obesity impairs breathing due to a restrictive ventilatory disorder, reduction of the capacity of respiratory muscles and diminishment of the ventilatory response. The restriction cannot serve as the only explanation of OHS because body weight or compliance on the one hand and hypoventilation on the other hand only correlate weakly. Obesity increases the work of breathing by greater body mass with its increased oxygen demand, impaired diaphragmatic mobility, upper airway obstruction, and oxygen desaturation which result in an inadequacy of oxygen demand and supply. The adjustment of the chemoreceptors can avoid the overload on the capacity of the respiratory muscles, at least in a number of patients or in the course of the disease. This disproportion results in hypercapnia. Furthermore, the level of leptin is an important factor in the pathophysiology of OHS. The blood level of leptin correlates with the body fat mass in humans. However, there seems to be a relative leptin deficiency in the brain in overweight humans. Therefore, in contrast to animals, leptin cannot sufficiently increase ventilation in man to avoid hypercapnia.

Regular and unobstructed breathing during the night is the prerequisite for an undisturbed and restful sleep. The most prevalent nocturnal breathing disturbance with morbid consequences is the obstructive sleep apnea syndrome. Forms severe enough to need therapy and, therefore, a thorough work-up, can be usually detected by a detailed history. Pathophysiology, clinical findings, differential diagnosis as well as work-up and therapy of the sleep apnea syndrome are discussed.

Nocturnal intrinsic disorders of sleep are much more common than hitherto assumed. In middle-aged men, a prevalence of 0.3 to 3% of severe obstructive sleep apnea syndromes necessitating treatment is expected. The international classification of sleep disorders (ICSD 1990) contains the definitions and descriptions of the different entities. A patient with combined obstructive sleep apnea and a hypoventilation syndrome due to obesity serves to illustrate problems with diagnosis and particularly treatment of this respiratory disorder during sleep. The most frequent sleep disorders are briefly presented and placed in the context of other concomitant somatic diseases. Because of the possible serious course of nocturnal hypoxemias, the conclusion is justified that a timely and accurate diagnosis is essential for the patient. Transcutaneous oximetry during the night is sufficient as screening procedure. It can be applied to outpatients. In depth, evaluation should be carried out at a specialized center with polysomnography.

A simple technique for time-encoded recording of snoring sounds is presented. An electronic circuit connected to a stereo cassette recorder via cord remote control will start the recorder when the sound pressure of the snoring sound surpasses a preset level. The snoring sound is recorded on one track of the cassette recorder. The other track is used for the time code. Every 120 seconds the tape recorder is switched on by the electronic circuit and a short high level signal is recorded. The time interval between two time coding signals equals the snoring time. Analysis of the time coding signals is performed by an A/D converter installed in a Personal Computer. The converter amd accompanying software are used to calculate the duration of the intervals between the coding signals. The results are displayed graphically where sleeping time is plotted against snoring time (Fig.2). The length of each bar equals the snoring time in seconds for each 120 second interval. Snoring periods can be recognised at a glance and the snoring pattern can be evaluated. Three cases studies are presented demonstrating the performance of the technique. A 39-year-old female with nonpathological snoring (Fig.2), a 45-year-old male with heavy and regular snoring (Fig. 3) and a 36-year-old male with a full-blown Pickwickian Syndrome (Fig. 4). This patient's response to nasal cPAP is demonstrated in Fig. 5.

In one year among 16 male patients and 24 female patients who were admitted on account of a considerable obesity and the connected with complaints in order to reduce the weight in the hospital, thrice the diagnosis abortive Pickwick-syndrome was made. Apart from the characteristic symptoms of obesity, hypersomnia, periodical breathing in sleep in all three patients smaller anatomical changes in the nasopharyngeal space were found. Secondary cardiopulmonary or cerebral sequels, as they are described in full pictures and late forms of the Pickwick-syndrome, could not be registered. The diagnosis of abortive Pickwick-syndrome, which we made ex juvantibus (reduction of weight), is perhaps more frequent than up to now assumed. Since the pathological disposition for sleep among others is of great importance in the field of transport and occupational medicine and may be prevented only by reduction of weight, which could be confirmed also in our three cases, it is referred to the necessity of an early recognition and treatment.

The Pickwick syndrome as an independent disease is clearly separated from other respiratory disturbances with adiposity. The diagnostic valency of the symptoms in the Pickwick syndrome is explained. A report on a patient with a Pickwick syndrome is given.

In 11 patients clinically diagnosed as Pickwickian syndrome the results of daytime and night polysomnogramm were compared. The daytime recording was very efficient in identifying apnoea and correlating various types of apnoea to different sleep stages. In polysomnogramms of night sleep we found, as did Lugaresi, a reduction of sleep stages III and IV, and a slight increase of sleep stages I and II. Patients without apnea in daytime sleep also showed a normal apnea index in night sleep. The BAEP's especially the pontomesencephalic components were pathological in six patients (55%). This might be due to a primary lesion or to hypoxic damage of the brainstem.

The case report of a male patient with the Pickwickian syndrome is presented. The results of the relevant neurophysiological examinations (polygraphic registration of EEG, electrocardiogram, respiration, thorax excursions, submental and intercostal electromyogram, electrooculogram) give an insight into the pathomechanisms and enable the differential diagnosis to be made between this condition and narcolepsy and also the Kleine-Levin syndrome; respiratory investigations (spirometry, hypercapnic ventilatory response: mouth occlusion pressure) make it possible to differentiate between the Pickwickian and Ondine's curse syndrome. The therapeutic management is discussed.

Two patients with obstructive sleep apnoea are described and the value of computer tomography in the diagnosis and follow-up is stressed. Narrowing of the oro-pharynx is a major feature in the diagnosis of this condition and is best demonstrated by CT.

Patients suffering from Pickwickian syndrome or primary hypoventilation syndrome present apneas of a predominantly obstructive type which follow one another without interruptions throughout the duration of sleep. It is not possible to ascribe the somnolence of these patients to carbonarcosis, because in most cases Pa CO2, though high during sleep, presents normal values or slightly higher than normal values during wakefulness. Obstructive apneas are the cause of this syndrome: the elimination of obstructive apneas by means of tracheostomy leads to a complete clinical recovery. Before they began to suffer from hypersomnia, all these patients had been snoring heavily for many years. Snoring is therefore a fixed stage in the evolution of this disease. The fact that the overall clinical and polygraphic characteristics of these syndromes are identical suggests that they all constitute a single nosographic entity, which we have called "hypersomnia with periodic apneas".

Disorders of sleep belong to the most frequent troubles. A lot of different factors may contribute to the pathogenesis of sleep disorders. Modern sleep research has opened important views into the structure of sleep and the pathophysiology of sleep disorders. In a narrower sense sleep disorders mean a deficiency of sleep (hyposomnia). This may concern the induction of sleep or its maintenance. Sleep disorders without underlying disease may be differentiated from those caused by different diseases. Hypersomnia may occur as a symptom of various cerebral dysfunctions and processes, as an episodic disorder (Kleine-Levin-syndrome) or as a part of the Pickwick-syndrome. In narcolepsy characteristic symptoms are sleep attacks, kataplexy (emotionally induced loss of muscle tone) and transient pareses during awakening. Disturbances linked with sleep are snoring, somnambulism, speaking and grinding of the teeth during sleep and nocturnal enuresis. They may constitute idiopathic disorders. On the other hand, there may be similarities between epileptic phenomena and these disorders. Some epilepsies demonstrate relations to the rhythm of sleep and wakefulness which become evident in the manifestation of seizures and epileptiform EEG activity at certain stages of vigilance.

This paper reviews the literature on anaesthetic problems in extremely obese patients. The main concerns of the anaesthetist in these patients is pulmonary function, especially hypoxaemia. The pathogenesis of hypoxia is explained by an increased tendency to airway closure by the weight of fat, which compresses the thorax. The significance of the patient's position during and after operation is stressed. The Pickwick-Syndrome is extremely rare, even in large series of obese patients, but its diagnosis is important for therapeutic consequences. For anaesthesia in these patients neuroleptanaesthesia as well as classical inhalational procedures can be used.