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Biomedical subjects

E Pfenninger

Publications and source records attributed to E Pfenninger.

At least 55 records · Page 3Linked to original sources
PubMed1989

[An infusion of THAM (trishydroxymethylaminomethane) as therapy to lower increased intracranial pressure in acute craniocerebral injuries].

Despite of the use of all the current intensive care measures, some patients develop dangerously high intracranial pressures (ICP) after head injury. We have studied the use of THAM for the rapid control of dangerously high ICP in these patients. PATIENT AND METHODS. After all conventional methods of lowering ICP had been applied without sufficient effect, 1 mmol/kg body wt. THAM was given i.v. over a period of 10 min to ten patients with head injury. All patients were hyperventilated, sedated with thiopental (3-6 g/day), and the upper body was elevated to 30 degrees. The intracranial pressure and mean arterial pressure were monitored, arterial blood gas levels measured, and cerebral perfusion pressure (CPP) calculated. RESULTS. Our patients had a mean ICP of 37.4 Torr, which fell to 27.2 Torr within 10 min after the administration of THAM. The CPP rose from 46.5 to 56.3 Torr, no rebound was observed. There was no change in arterial blood gas values. DISCUSSION. Our study indicates that THAM not only decreases an elevated ICP, but also improves CPP. These results are of note because only patients with otherwise unresponsive increases in ICP were included.

Adult↗
PubMed1989

[The effect of adrenaline and noradrenaline on the oxygen supply of the myocardium during cardiopulmonary resuscitation].

The effect of epinephrine and norepinephrine on myocardial oxygen delivery and consumption during cardiopulmonary resuscitation using open cardiac massage after a 5-min period of electrically induced ventricular fibrillation was studied in 21 pigs with a mean body weight of 21 kg. Norepinephrine, like epinephrine, is a sympathomimetic agent with marked alpha- and beta-1-sympathomimetic activity, but the degree of beta-2-stimulation is less marked than that obtained with epinephrine. After mechanical measurements over 3 min (compression rate = 60/min), 7 animals received 10 ml physiological saline, 7 further animals, 45 micrograms/kg epinephrine, and the remaining 7 animals, 45 micrograms/kg norepinephrine. At 90 s and again at 5 min after the administration of epinephrine or norepinephrine, the mean arterial blood pressure was significantly higher than in the control group, while mean pulmonary artery pressure, central venous pressure and cardiac index were not significantly different. Total myocardial blood flow was only measured before the induction of cardiac arrest in the control group, where it was found be 193 +/- 30 ml/min/100 g. During the open cardiac massage but before the injection of catecholamines we found a myocardial blood flow of 51 +/- 23 in the control group, 71 +/- 10 in the epinephrine group, and 74 +/- 11 ml/min/100 g in the norepinephrine group. At 90 s after the injection, blood flow increased by 78% to 126 +/- 18, with epinephrine and by 45%, to 107 +/- 30 ml/min/100 g tissue with norepinephrine. At 5 min after administration of these catecholamines significant differences from the control group were present.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

[Arteriovenous pH- and carbon dioxide gradients during cardiopulmonary resuscitation].

During external cardiac massage and after restoration of spontaneous circulation, the arterial and central venous blood gas status of ten patients was determined. During cardiopulmonary resuscitation the median arterial pH value was 7.29 and the median central-venous pH value was 7.16. The low central-venous pH during resuscitation was probably caused by the high partial pressure of carbon dioxide, because no significant difference between arterial and central-venous base deficit was found. The arteriovenous pH and carbon dioxide gradients were significantly lower after spontaneous circulation had been restored. The arterial pH does not parallel the marked fall in central venous pH, and therefore only partly indicates acid-base changes during resuscitation. On the other hand, a central-venous blood gas status not only indicates the degree of metabolic acidosis present, but also the "respiratory" acidosis that in turn is a measure of the severity of intracellular acidosis.

Adult↗
PubMed1987

The respiratory aspect of the treatment of brain injury associated with acute alcohol intoxication--results of an animal experiment.

The effects of spontaneous respiration and mechanical ventilation were examined by investigating the interaction between elevated intracranial pressure and alcohol intoxication. Ethanol (200 ml 48%) was infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (group 1), 7 young pigs with elevated cerebral pressure during spontaneous respiration (group 2), and 4 young pigs without elevated cerebral pressure during spontaneous respiration (group 3). While the behavior of intracranial pressure during mechanical ventilation in the animals from group 1 was inhomogeneous with a tendency to rise (29-34 mmHg), cerebral pressure (28-55 mmHg) increased drastically in the animals from group 2. This increase was associated with a sharp rise of Pa,CO2 (37.6-73.3 mmHg) and a decrease of Pa,O2 (74 mmHg to 13 mmHg). None of the animals in group 2 survived. Pa,CO2 also rose in alcoholized animals without elevated cerebral pressure (group 3) (41.9-63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory center. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure generally avoided.

Alcoholic Intoxication↗
PubMed1987

[Behavior of blood gases in patients with craniocerebral trauma at the accident site and at the time of admission to the clinic].

It is known that early mortality after acute craniocerebral trauma (CCT) depends heavily on the extent of any hypoxia and, even more, hypercapnia in the early phase after the trauma. Hypoxia and hypercapnia are very difficult to appraise at the scene of an accident without measuring instruments. It is now generally recognized that appraisal in accordance with the Glasgow coma scale (GCS) is a suitable way of estimating the depth of impairment of consciousness (eye opening in response to stimuli, verbal response to stimuli, motor response to stimuli). The maximum number points is 15, and the minimum, 3. We therefore decided to investigate whether there is a correlation between the degree of impairment of consciousness measured with the GCS and onset of hypercapnia or hypoxia soon after. In 33 patients with acute CCT, arterial blood was taken for analysis of blood gases at the scene of the accident before therapy was started. At the same time, we evaluated the level of consciousness on the basis of the GCS. The blood samples were taken within 6-21 min after the trauma in all patients. It was shown that there is a very close correlation between the severity of trauma (measured with the GCS) and the degree of hypercapnia (r = -0.88). This was true of all CCT patients with multiple trauma without exception. The PaO2 correlates with the severity of trauma (r = 0.60) far less closely, and above all much less consistently.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Injuries↗
PubMed1987

[Intravenous analgesia with ketamine for emergency patients].

Twenty traumatized patients suffering from fractures and soft tissue injury were given either 0.25 mg/kg or 0.5 mg/kg ketamine intravenously for analgesia. Within 5 min effective analgesia was present in both groups and lasted for 10-15 min. The higher dose of ketamine led to an impairment in the level of consciousness. These findings were in agreement with plasma levels of ketamine: in the 0.25 mg/kg group the plasma levels (median) were 167 ng/ml after 5 min, 92 ng/ml after 10 min, 82,5 ng/ml after 15 min, and 46 ng/ml after 30 min (n = 4). In the 0.5 mg/kg group the plasma levels (median) were 238 ng/ml after 5 min, 189 ng/ml after 10 min, 135 ng/ml after 15 min, and 118 ng/ml after 30 min. Considering the influence on consciousness, we recommend the administration of 0.25 mg/kg ketamine intravenously for analgesia in traumatized patients without head injury. It may be necessary to repeat the same dose if pain re appears.

Adolescent↗
PubMed1986

[Early measurement of intracranial pressure in polytrauma with associated craniocerebral trauma. II: Clinical and therapeutic aspects].

During the time from 1982/83 the intracranial pressure was continuously measured from patients who were polytraumatized and also had severe head injuries. In 53% of these cases the first readings could be obtained within 6 hours after the injury and in 33% first after 12 hours. During the time of evaluation this relationship shifted to earlier implantation. From 27% of these patients the intracranial pressure values fell into a range that instigated immediate therapeutical measures. This proves how important it is to have a direct reading from the intracranial pressure as soon as possible after injury. The aspects of therapy by increased intracranial pressure were discussed.

Accidents, Traffic↗
PubMed1986

[Clinical study of the bacterial contamination of 2 differently prepared enteral feeding solutions].

The incidence of bacterial contamination under ICU-conditions of two solutions designed for enteral feeding; the oligopeptide mixture Peptisorb and the nutrient defined diet Biosorb, were investigated. 54% of the specimens taken prior to use from the oligopeptide mixture, which is marketed as a powder and brought into solution before application, were found to be bacterially contaminated. At the end of the 6-12 h application period this percentage has risen to 79%. Prior to use the sterile packed prepared nutrient defined diet was found to be free of bacterial contamination in 97% of cases, while at the end of the period of application 21% of the samples taken contained bacteria. In most instances the solutions prepared on ICU were contaminated with gram positive spore forming bacteria and typical gram negative hospital flora. Based on the results of this investigation, only those enteral feeds which are marketed as sterile solutions should be used, in order to protect ICU patients from potential sources of contamination.

Bacteria↗
PubMed1986

[Effect of various types of artificial respiration on raised intracranial pressure, associated with acute alcoholic intoxication].

The effects of spontaneous respiration and mechanical ventilation on ICP were examined by investigating the interaction between elevated pressure and alcohol intoxication. 200 ml ethanol 48% were infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (Group 1), 7 young pigs with elevated intracranial pressure during spontaneous respiration (Group 2), and 4 young pigs without elevated intracranial pressure during spontaneous respiration (Group 3). While the behaviour of intracranial pressure during mechanical ventilation in the animals from Group 1 was inhomogeneous with a tendency to rise (29 mmHg to 34 mmHg), intracranial pressure (28 mmHg to 55 mmHg) increased dramatically in Group 2. This increase was associated with a sharp rise of paCO2 (37.6 mmHg to 73.3 mmHg) and a decline of paO2 (74 mmHg to 13 mmHg). None of the animals in Group 2 survived. paCO2 also rose in alcoholized animals without elevated ICP (Group 3) (41.9 mmHg to 63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in Group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory centre. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure can be generally avoided.

Alcoholic Intoxication↗
PubMed1986

[The behavior of intracranial pressure under spontaneous respiration or artificial respiration in hemorrhagic shock during volume substitution].

Haemorrhagic shock and cranial injury frequently present together in the polytraumatised patient. The effect of different forms of ventilation--spontaneous respiration, controlled normoventilation, and intubation followed by hyperventilation--on the raised intracranial pressure of young pigs given volume replacement subsequent to haemorrhagic shock, was therefore investigated. During volume substitution, the intracranial pressure (initially 30 mmHg) both of those animals breathing spontaneously and of those being ventilated rose significantly (44.6 and 49.2 mmHg respectively). In contrast, intubation and hyperventilation resulted in an initial fall in intracranial pressure to 18.6 mmHg, and a rise to just below initial values (27.4 mmHg) after volume replacement. A similar blood pressure rise was noted in all three groups but arterial PCO2 changes were analogous to those of intracranial pressure. In the presence of both haemorrhagic shock and cranial injury, volume replacement alone is not sufficient treatment, and can in some circumstances be dangerous. Early intubation and controlled hyperventilation course a fall in intracranial pressure secondary to decreasing the PCO2.

Animals↗
PubMed1985

The effect of ketamine on intracranial pressure during haemorrhagic shock under the conditions of both spontaneous breathing and controlled ventilation.

Seventeen piglets of both sexes, seven with O2/air-buprenorphine anaesthesia and controlled ventilation, and ten unanaesthetized animals with normal, spontaneous respiration, were used for the study. The intracranial pressure of both groups of animals was raised by insufflation of an epidural balloon and the arterial blood pressure was reduced to approximately 70% of the original value by controlled haemorrhage. 0.5 mg/kg body weight of ketamine was given intravenously, followed by a further dose of 2.0 mg/kg body weight of ketamine five minutes later. Both ketamine doses led to a significant rise in the intracranial pressure of those animals breathing spontaneously (31.8 mm Hg to 39.1 mm Hg). In contrast, the ventilated animals showed a significant reduction in intracranial pressure. No changes in arterial PCO2 were observed in this group, while those piglets breathing spontaneously had dangerous PCO2 rises. At both ketamine doses a significant correlation could be found between the PCO2 and the intracranial pressure.

Animals↗
PubMed1985

[Early measurement of intracranial pressure in polytrauma with associated craniocerebral trauma. I: Principles].

In West Germany, head injury is the major cause both of death following trauma and of irreversible cerebral damage. The successful management of these cases largely depends on the prevention and treatment of secondary rises in intracranial pressure. The only certain way of detecting such increases is with the invasive technique of intracranial pressure monitoring. The pressure module should be implanted as soon as possible, ideally, before extensive definitive surgical treatment is carried out. Ease of usage has led us to prefer epidural pressure monitoring systems. Being relatively easy to learn and apply, this form of monitoring should be used in all hospitals involved in the treatment of severe head injury.

Brain Edema↗
PubMed1985

[Intracranial pressure during ketamine administration with spontaneous respiration. An animal experimental model].

A sequence of i.v. ketamine injections, 0.5, 2.0, and 5.0 mg/kg body weight, was given to thirty piglets. At the beginning of the investigation, 10 of these animals had a normal intracranial pressure and stable circulation. The intracranial pressure of the remaining 20 piglets was raised to 30 mm Hg, and an additional haemorrhagic shock was induced in 10 of these animals. Those animals with a normal intracranial pressure showed no alteration there of at any of the three doses given, and the arterial pCO2 remained practically unchanged. In contrast, all animals with a raised intracranial pressure, both with and without superimposed haemorrhagic shock, had a significant rise in intracranial pressure and pCO2. These two parameters were found to correlate well with each other. We conclude that in the model used, where the animals were breathing spontaneously, the intracranial pressure rise seen following ketamine application is secondary to the increase in pCO2.

Animals↗
PubMed1985

The influence of ketamine on both normal and raised intracranial pressure of artificially ventilated animals.

The effect of two different doses of ketamine, 0.5 mg kg-1 body weight, and 2.0 mg kg-1 body weight, on intracranial pressure and cerebral perfusion pressure were investigated in 21 young pigs (26-34 kg) under controlled artificial ventilation. Three groups each containing seven animals were studied: Group 1. Initially normal blood pressure and an intracranial pressure within the normal range (10.7 mmHg). Group 2. Normal blood pressure and increased intracranial pressure caused by inflating an epidural balloon (29.2 mmHg). Group 3. Increased intracranial pressure (32.7 mmHg) and mean arterial pressure reduced by approximately 30% through controlled haemorrhage. There was no increase in intracranial pressure from either normal or initially increased values. This applied to animals with normal blood pressure values and also to those in haemorrhagic shock. This observation can be explained by the lack of an increase in PCO2 under controlled ventilation. During haemorrhagic shock cerebral perfusion pressure fell significantly as a result of the fall in mean arterial pressure. This particularly applied to the 2.0 mg kg-1 dose of ketamine. We therefore consider volume substitution to be essential in this situation.

Animals↗