[Post-obstructive pulmonary edema as a complication of endotracheal tube obstruction]. / Das postobstruktive Lungenödem als Komplikation einer Endotrachealtubusokklusion.

Pulmonary edema following acute or chronic upper airway obstruction is a threatening complication. A case is presented in which a 15 year old boy developed a massive pulmonary edema after a acute endotracheal tube obstruction during emergence from anesthesia. Leading pathophysiologic cause for the formation of the edema is a markedly negative intrapleural pressure due to the forceful inspiration against the obstructed airway. Treatment modalities include the instantaneous solution of the obstruction, a rapid reoxigenation and the ventilation with PEEP or CPAP. Sound knowledge of the disease increases the vigilance of the caring anaesthesiologist and helps to identify patients at risk. Preventing measures may further reduce the risk of occurrence of the postobstructive pulmonary edema.

Posttraumatic movement disorders after moderate or mild head injury.

We examined the occurrence of posttraumatic movement disorders after moderate or mild head injury with a three-level follow-up study including questionnaires, telephone interviews, and personal examinations 4-6 years after the trauma (mean 5.2 years). Sixteen of 158 patients (10.1%) for whom a detailed follow-up was available had developed movement disorders most probably related to craniocerebral trauma. The most frequent finding was a low-amplitude postural/intention tremor that appeared to resemble enhanced physiological or essential tremor. Twelve patients reported transient tremor, two patients had persistent tremor, one patient had transient tremor and persistent hyperekplexia, and another patient had mild persistent cervical myoclonic twitches. Overall, the movement disorder was transient in 12 patients (7.6%) and persisted in only 4 patients (2.6%). These movement disorders were not disabling and did not require medical therapy. Taking into account possible bias by selection of the sample group, the frequency of movement disorders secondary to moderate or mild head trauma might be lower than 10.1%. Posttraumatic movement disorders occurred significantly more often in the group of patients with Glasgow Coma Scores between 9 and 14 than in those with a score of 15. Severe movement disorders such as low-frequency kinetic tremor or hemidystonia were not identified in this survey.

Post-traumatic movement disorders in survivors of severe head injury.

The present study investigates the occurrence of post-traumatic movement disorders in survivors of severe head injury. We studied a series of 398 consecutive patients who were admitted to the hospital with a Glasgow Coma Score of 8 or less after they sustained a head trauma. One hundred thirty-four out of 398 patients (34%) died after they were admitted to the hospital or in the further course. A recent follow-up was obtained in 221 of the 264 remaining patients (84%). Follow-up consisted of a three-level assessment, including questionnaires, telephone interviews, and personal examinations. Fifty out of 221 patients (22.6%) had developed movement disorders secondary to the head trauma, which were transient in 23 patients (10.4%) and persistent in 27 patients (12.2%). Forty-two patients (19%) had tremors, nine (4.1%) had dystonia, and seven (3.2%) had other movement disorders. Twelve patients (5.4%) had disabling low-frequency kinetic tremors (2.5 to 4 Hz) or dystonia, or both. Low-frequency kinetic tremors developed with a latency from 2 weeks to 6 months after trauma, and dystonia with a latency from 2 months to 2 years. When compared with patients without movement disorders, this subgroup was characterized by a different distribution profile of Glasgow Coma Scores with a higher proportion of lower scores on admission (p < 0.05). When we compared the initial CT findings, there were highly significant associations between generalized brain edema and the occurrence of any movement disorders, between generalized brain edema and the occurrence of persistent movement disorders, and between generalized brain edema and the occurrence of kinetic tremors and dystonia. We detected similar associations for focal cerebral lesions, but not for subdural and epidural hematomas. In conclusion, transient or persistent movement disorders are common sequelae in survivors of severe head injury. Disabling movement disorders such as kinetic tremors and dystonia, however, occur only in a small group of patients.

Differences in effects of isoflurane and enflurane on splanchnic oxygenation and hepatic metabolism in the pig.

The effects of end-tidal concentrations of 1.45% isoflurane and 2.12% enflurane on splanchnic blood flow (electromagnetic flow probes), oxygen (O2) extraction and surface PO2 (Clark-type electrode), and hepatic metabolism (organic acids) were compared in an animal model relevant to humans. Eighteen laparotomized, ventilated pigs, anesthetized and paralyzed with ketamine/flunitrazepam and pancuronium, were studied. Enflurane caused significantly (P less than 0.05) greater decreases in mean arterial pressure, cardiac output, and superior mesenteric arterial, portal, and total hepatic blood flows. In addition, hepatic arterial blood flow decreased during enflurane administration but increased markedly (40%) during isoflurane administration. However, mean surface PO2 of liver and small intestine decreased to similar degrees (20%) during isoflurane and enflurane. Summary histograms of surface PO2 values were leftward shifted but did not show O2 values in the hypoxic range (0-5 mm Hg). Except for a decrease in hepatic lactate uptake during enflurane, there were no changes in either hepatic uptake or release of organic acids during anesthesia with either agent. These data show that splanchnic O2 supply is better maintained during isoflurane than during enflurane. Although this was not reflected in differences in tissue oxygenation and metabolism, decreased portal and hepatic venous O2 contents during enflurane indicate that an increase in preportal and hepatic oxygen extraction was necessary to preserve tissue oxygenation.

Adenosine and diltiazem. A new therapeutic concept in the treatment of intestinal ischemia.

To determine the therapeutic effect of two vasodilators, adenosine and diltiazem, in mesenteric ischemia, 13 dogs were treated with an intra-arterial perfusion of the drugs after digitalis intoxication. Blood flow was restored to the control value after a dose of 2 micrograms/kg/minute adenosine or 5 micrograms/kg/minute diltiazem. The advantage of adenosine is that its effect begins and ends very rapidly, but because doses of more than 2 micrograms/kg/minute may cause a drop in blood pressure, strict pressure control is mandatory when the drug is applied clinically. Its limited use is appropriate, for example, when operative measures cannot be excluded. Diltiazem can be used for long-term therapy with a reduced risk of a drop in blood pressure.

Oxygen supply of skeletal muscle in experimental endotoxic shock.

In our model of hypodynamic endotoxic shock systemic pulmonary and metabolic alterations such as -hypotension, tachycardia, low output syndrome -pulmonary hypertension -pulmonary failure with arterial hypoxemia and - lactacidosis developed earlier than disturbances in oxygen supply of skeletal muscle. This points to the different responses of the organ systems in endotoxic shock.

Human endothelial cell proliferation inhibiting activity in the sera of patients suffering from 'shock' or 'sepsis'.

The response of DNA-synthesis of human endothelial cells to sera derived from twenty-five patients suffering from 'sepsis' or 'shock' was measured by autoradiographic methods. In eight cases a constant decrease in proliferative response was found compared to that of sera from healthy donors. These proliferation values were shown to lie below the '60%-of-control-line'. The difference between the means of control and of corresponding 'low-response' values was significant (P less than 0.05). In three cases a diminished response was caused only by some of several serum samples taken at different times. These results correlated well with the clinical state and outcome of patients but not with any of the over sixty clinical, therapeutic, laboratory and post-mortem parameters of investigation. Evidence is presented for a proliferation inhibiting activity in sera of patients in clinically poor states, and some physico-chemical properties of this 'factor' are described. Lethal injury to the cells or an impairment of cellular migration could not be observed within the observation periods used in this study.

[The effect of low-molecular hydroxyethyl starch and dextran 60 on the muscle oxygen supply in intensive care patients]. / Der Einfluss von niedermolekularer Hydroxyaethylstärke und Dextran 60 auf die Muskelsauerstoffversorgung bei Intensivpatienten.

Skeletal muscle pO2 measurements were performed in two groups of critically ill patients (total n = 19) using the multiwire surface electrode (MDO) by Kessler and Lübbers to evaluate oxygen supply of the measured time. Muscle pO2 in the first group (n = 9) was recorded before and after i.v. application of 250 ml low molecular 6% hydroxyäthylstarch, Mw 40,000, in the second group (n = 10) before and after 250 ml 6% dextran 60. Both groups were tested under normoxemia and hyperoxemia respectively. It was the aim of the study, to examine if these colloidale substances may improve oxygen supply in skeletal muscle. Even the small amount of 250 ml l. m. HAS or dextran 60 respectively was able to raise the mean muscle pO2 of the measured patients significantly. The effect was similar in both groups. Since oxygen transport capacity remained uneffected, the improved oxygen supply after administration of l. m. HAS and dextran 60 must be considered as a beneficial effect of these drugs on the blood flow properties in the capillary bed.

[Nitrous oxide induced intraluminal tube obstruction during endotracheal intubation with armored tubes (author's transl)]. / Tubusverlegung von Silkolatex-Trachealtuben bei der Verwendung von Lachgas.

As demonstrated by a case report, dangerous obstruction of armoured endotracheal tubes may occur when using nitrous oxide during anaesthesia. This is based on N2O diffusion into preexisting air bubbles of the inner part of the tube wall with consequent enhancement of the bubble volume. The bubbles in the tube wall arise during production as well as during resterilisation. Avoidance of resterilisation and meticulous examination of endotracheal armoured tubes should prevent the described complication.

[Laryngoscopy of laryngeal damage in long-term intubated intensive care patients]. / Laryngoskopische Untersuchungen zur Frage der Kehlkopfschädigung bei langzeit-intubierten Intensivpatienten.

67 long intubated, critically ill patients were examined by direct laryngoscopy between the 3rd and 14th day of intubation. It was found that even after 5 days most of the patients investigated had severe laryngeal damage. Damage occurs preferentially on the vocal cord (laryngeal granuloma), on the arytenoid vocal process and on the cricoidal plates (ulcerations). It is concluded that laryngoscopy should be performed after 5 days of intubation at the latest to determine the extent of laryngeal damage. If necessary, secondary tracheotomy should be considered.

[Intensive care in chest trauma (author's transl)]. / Die Intensivtherapie bei Thoraxtraumen.

A statistical analysis of the case material at the Intensive Care Unit, Freiburg, for the years 1975 and 1976 established that 40% and 39% respectively of patients with multiple injuries had also suffered a chest trauma and that the latter was the direct cause of respiratory insufficiency in 61% (1975) and 57% (1976) of patients in need of controlled respiration, i.e. respiratory insufficiency dominated the clinical and pathophysiological picture. The causes were: restricted respiratory movements due to pain, compression of the lungs or pathological changes in the injured lung, and they affected the normal gaseous exchange in a variety of ways. Alveolar hypoventilation with disturbance of ventilation-perfusion, increase in the functional shunt volume, rise in the functional dead space combined with reduced functional residual capacity and compliance result, if left uncorrected, in a drastic increase of resistance on the part of the pulmonary vessels and finally in, often fatal, hyoxaemia and hypercapnia. Regular estimations of the arterial blood gases in air and pure oxygen, of the arterio-alveolar difference in oxygen pressure, shunt volume, dead space and effective compliance of the chest wall and lungs are, therefore, essential. Treatment in an intensive care unit comprises the relief of any acute condition, such as tension pneumothorax, haemothorax, and general measures. Means to relieve pain in patients whose chest injuries are not sufficiently severe to require artificial ventilation are: intercostal blocking, acupuncture or peridural analgesia; efficient breathing exercises are important. The indications for artificial ventilation should be interpreted generously and the decision to perform it should be made at an early stage. The technique is determined by the type of pathological changes in the gaseous exchange and should aim at restoring normal conditions as far as possible.