[Nutrition for the intensive care patient].
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Biomedical subjects
Publications and source records attributed to J M Hackl.
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Patients with hyperdynamic symptoms of a severe sepsis and patients after severe head injury show remarkable metabolic disturbances, which become apparent in a persistent catabolic stage. This was found in 17 septic patients (group I) and in 20 patients after severe head injury (group II), who were studied for a period of 10 days. During this time the urea production rate (UPR) and the catabolic index (CI) were measured. After a preliminary period of 5 days a stimulation test of hGH secretion using arginine was carried out to estimate the secretion of hGH, insulin and blood glucose. After this stimulation test a substitution therapy using 0.05 IU/kg B.W. i.m. hGH (Crescormon, Kabi Vitrum, München) was applied to 11 patients in group I (group Ia) and in 8 patients in group II (group IIa) who were then compared with patients without substitution therapy. The mean values of hGH basic secretion were the same in all groups and were within the normal range. 30 min after stimulation it was possible to identify a distinct response pattern; 90 min after stimulation there was no significant response. All groups showed significantly elevated levels of insulin; no further elevation after stimulation was observed. The blood glucose levels in all groups remained within the normal range at all times. All the groups were similar regarding behavior of the investigated parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
In 12 severely burned patients the input of fluid and sodium, as well as sodium concentration in plasma and urine, was studied. The osmolarity in plasma and 24-h urine was measured. The high initial sodium input is noted. Plasma sodium levels stay within the normal range when the amount of sodium given during the further treatment is reduced. The importance of urea production in affecting plasma osmolarity is demonstrated.
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A prospective randomized double blind investigation was made in 24 multiple injured patients. All patients were treated with a combined parenteral-enteral nutrition during 7 days. A group of 11 patients received as a continuous infusion over 16 h 60 mg/kg BW carnitine daily. Beside carnitine and acetylcarnitine levels in plasma and urine the following parameters were determinated to evaluate the effect of carnitine: for the metabolism of fatty acids: triglycerides, free fatty acids (FFA), alpha-hydroxy-butyrate for the metabolism of carbohydrates: glucose, insulin and lactate in plasma. Finally for amino acid metabolism: urea, creatinine, cholinesterase and kolloid osmotic pressure in plasma as well as ureanitrogen and alpha-aminonitrogen excretion in urine. In the patients receiving carnitine especially acetyl-carnitine in plasma and acetyl-carnitine excretion in urine increased, proving that the administered carnitine can pass through the mitochondrial membrane. In these patients the plasma level of FFA was markedly lower than in the group without carnitine. Simultaneously the level of the alpha-hydroxybutyrate was elevated, equivalent to an increased oxydation of fatty acids. There was no difference between the two groups in the metabolism of carbohydrates. Administration of carnitine caused a slight increase of the production of urea (PU), catabolism could not be reduced. The excretion of alpha-aminonitrogen in urine augmented after carnitine infusion. Carnitine is an AA itself and so the amount of excreted alpha-amino nitrogen will increase; additionally the reabsorption of AA in the proximal renal tubulus may be inhibited by carnitine.
152 patients, who had suffered head and brain injury during the years 1980 to 1982 were interviewed by letter using a standardized questionnaire to assess the individual outcome. There were questions concerning activities of daily life, invalidity, work activities, social relationships with family and other persons, leisure activity and the grade of persisting sequelae. There were 106 replies, 16 patients had died meanwhile. According to their neurological symptoms on admission at the intensive care unit the patients were divided into two groups. Group I included patient, who showed symptoms of midbrain syndrome stage 1 and 2, while group II presented patients had midbrain syndrome stage 3 and 4. Activities of daily life (feeding, dressing, toiletting and ability to get out of bed and move around the room) were restored in the great majority of patients. 15 patients of group II were classified as invalid. Significant changes in social relationships with the family were seen in 50% of the patients. Further, a decrease of contacts with friends, and a significant decrease in leisure activity (sport) was noted. 28.4% of the patients of group I and 36.8% of the patients of group II, who were at work before the trauma, now were out of work. The others generally worked below their previous level. Persisting sequelae included headache, lack of concentration and weakness of extremities. These symptoms were more prominent in the patients of group II; surprisingly little complaints concerned sexual life and somatic problems. It was found, that severe head and brain injury had significantly changed the patient's life in most cases. Work activities were strongly impaired in about 30% of cases.(ABSTRACT TRUNCATED AT 250 WORDS)
The appearance of the syndrome of phosphate depletion (plasma phosphorus level: 0,12 mmol/l) in a patient with uncontrolled diabetes mellitus is reported. The inorganic phosphorus is essential for the resynthesis of 2,3-DPG and ATP, therefore phosphate depletion results in tissue hypoxia and decrease of energy rich phosphate with disturbances of various organ systems. The causes, pathogenetic mechanisms and the clinical signs and symptoms are discussed. Regular controlls of plasma phosphorus levels and a prophylactic substitution of phosphate are recommended.
The effect of intragastric nutrion and its complications, especially the reflux pattern, were studied in 104 patients, who had to be intensively treated for more than 10 days. Patients suffering from polytrauma without abdominal injury (group I) or with abdominal injury (group III) and patients with isolated head/brain injury (group II) were included in this study. Parenteral nutrition was changed to intragastric administration as soon as possible and enteral nutrition was softly increased from 327 calories per day during the first week to 1800 calories or more in the next weeks. The general duration of feeding by nasogastric tube was between 16,1 and 19,8 days. The occurrence of reflux varied from 23,2% in patients of group II to 29,4% in patients of group I. Significant changes of reflux pattern were seen during the different weeks of treatment. The amount of reflux fluid was between 184,8 ml in group II and 355,4 ml in group III. The percentage of reflux fluid, if compared with the total enteral fluid administration revealed the maximum (16,6%) in patients of group III. Patients in group I had the highest frequency of defecation, the highest incidence of diarrhea was in all the groups really the same. Diarrhoea was seen in 6,7% of all patients. The underlying mechanism for these complications were discussed.
30 patients who consecutively underwent cardiac surgery with extracorporeal circulation were investigated with regard to preoperative, intraoperative and postoperative activities of creatine kinase (CK) and CKMB isoenzyme (CK-MB), as well as myoglobin concentrations in the blood. 12 lead electrocardiograms were taken before and after the operation. At subsequent control angiography, of 18 patients with coronary heart disease 10 showed patent bypass grafts, whilst the remaining 8 patients had at least one occluded graft. 12 patients served as a control group, half of them undergoing mitral valve replacement and the other half aortic valve replacement. There was no significant difference in enzyme activity patterns between the groups. Specific determinations together with ECG monitoring can be of diagnostic help in perioperative control of these patients.
Short latency evoked potentials (SEPs) were elicited by stimulation of the median nerve at the wrist and recorded simultaneously from the neck and the contralateral scalp in 44 comatose patients with signs of brain stem impairment due to head injury. Thirty-four patients were studied in acute coma on day 1 or 2 after brain injury. Twenty-three patients were studied in prolonged coma during days 3-12 after trauma. Six patients were examined in brain death. Brain stem involvement was divided clinically and by CT scan into secondary lesions due to supratentorial mass displacement and primary lesions due to direct violence to the brain stem. The central somatosensory conduction time (CCT) was measured by subtracting the peak latency of the major response from the neck (N14) from that of the primary scalp response (N20). The amplitude ratios (ARs) N20/N14 were calculated for each trace. Further asymmetries and absence of SEP over one or both hemispheres were noted. In cases in coma due to supratentorial lesions CCT and AR were close to normal in patients with good outcome. CCT increased and AR decreased with the worsening of outcome both in acute and prolonged coma. Asymmetries of SEPs indicated moderate or severe final disability. Patients with absent SEPs over one or both hemispheres due to supratentorial lesions died or survived severely disabled (1 case). In patients suffering from primary brain stem dysfunction, confirmed by a normal or slightly abnormal CT scan, prolonged CCT, asymmetric but also absent SEPs were also found in patients with good outcome both in acute and prolonged coma. AR was generally low in these cases. Early appearance of SEPs or early recovery of initially distorted SEPs and decrease of CCT in prolonged coma or during recovery was a favourable prognostic sign. Therefore even absent or severely distorted SEPs should be interpreted cautiously in patients who may suffer from primary brain stem involvement. Scalp SEPs were totally absent in patients with brain death.
One hundred and thirty-three EEGs were analysed from 80 comatose patients with signs of brain stem impairment due to head/brain injury. Seventy EEGs were taken in acute coma on day 1 or 2 after brain injury. Sixty-three EEGs were recorded in prolonged coma 3-12 days after brain injury. Brain stem involvement was divided by neurological signs and by CT scan into secondary lesions due to supratentorial mass displacement and primary lesions due do direct violence to the brain stem. Different EEG patterns were observed, but spindle activity was of special interest. Spindles were classified as typical (easily recognizable, well organized, 12-14 c/sec activity) or atypical (hardly recognizable, distorted form, 6-11 c/sec activity). Furthermore, asymmetries of spindles were noted. The spindles and their alterations were related to different stages of outcome. Spindles were seen in 91% of the EEGs in acute coma and in 30% in prolonged coma. In acute coma due to secondary brain stem involvement a good outcome was heralded by the occurrence of typical symmetrical spindles combined with early stages of secondary brain stem impairment at neurological examination. In cases of primary brain stem involvement typical spindles also suggested a good prognosis despite the observation of serious clinical signs (decerebrate posturing). The percentage of spindle activity decreased, and distortion and asymmetry of spindles increased with the worsening of outcome. Severe intracerebral lesions (confirmed by clinical and CT scan examinations) led to distortion, asymmetry and finally disappearance of spindles. In prolonged coma spindle activity was markedly reduced regardless of the final outcome. When spindles were present atypical and asymmetric forms significantly increased in patients with bad outcome. There were no significant differences in spindle activity in the different outcome categories, if primary and secondary brain stem lesions were compared.
Blink reflex studies were carried out on 51 comatose patients with signs of brain stem impairment due to head injury. Twenty-five patients were studied in acute coma on day 1 or 2 after trauma. Twenty-six patients were studied in prolonged coma during days 3-12 after brain injury. Brain stem involvement was divided clinically and by CT scan into secondary lesions due to supratentorial mass displacement and primary lesions due to direct violence to the brain stem. Further, the comatose states were separated by behavioural and EEG signs of sleep into "sleep' and more "alert' states. The blink reflexes were recorded after mechanical and electrical stimulation. Mechanical stimulation appeared to be more effective in evoking late responses than the electrical stimulus. The elicitability of the late responses was also dependent on the time of stimulation. During "sleep', usually accompanied by a spindle-EEG, the late responses were totally absent after both mechanical and electrical stimulation in acute coma. In more "alert' states, usually accompanied by high voltage delta waves in the EEG, the late responses, especially direct R2, could be frequently elicited by mechanical stimulation. These differences decreased during prolonged coma. All patients with signs of secondary brain stem involvement who had at least one late component in the acute stage of coma recovered well. So did all patients, with one exception, with primary brain stem injuries. Early recovery of the blink reflexes in cases of primary brain stem injury was a further favourable sign. Consistent absence of R2 (and R1) in prolonged coma indicated a bad outcome. The presence of all components in prolonged coma was of less prognostic significance than in the acute stage.
This case report describes the occurrence of multiple atypical milker's nodules in scalded skin. This hitherto unknown manifestation of paravaccinia virus infection is transmitted indirectly by virus contaminated water.
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We have studied some central and peripheral hormones in patients suffering from severe head injury. There exists a significant increase in plasma noradrenaline at the beginning of the apallic syndrome and the values remained raised until the reintegration of the neurological symptomatic set in. Besides there exists a decreased stimulation of growth hormone (HGH) excretion after arginine infusion at different stages of the treatment. Testosterone, triiodothyronine (T3) and thyroxine (T4) show lowered values, even though they can be stimulated. The cause of these restrictions in hormonal function may be a direct disturbance of diencephalic-hypophyseal regulation. The influence of the hormones on metabolism and symptomatic therapy of these central dysregulations is also discussed.
A 51-year-old male patient with no history of musculo-skeletal or myopathic abnormalities, but suffering from manic-depressive psychosis, attempted suicide with an overdose of dolpersin hydrochloride (Mydocalm), dipenzepine hydrochloride (Noveril), meprobamate (Mepronox) and nitrazepam (Mogadon). He developed high fever, muscle rigidity, tachycardia, arrhythmias, hypotension and mottled cyanosis, symptoms well-known in persons with malignant hyperthermia, an autosomally inherited disease of skeletal muscle. There is also discussed the manifestation and the symptoms of an acute rhabdomyolysis. The diagnosis was confirmed by chemical pathological laboratory findings, including respiratory and metabolic acidosis, myoglobinaemia accompanied by myoglobin diuresis, and elevated creatine phosphokinase (CPK values up to 2790 U/l). Electron microscopic examination of muscle tissue revealed signs of myolysis and mitochondrial reactions with pleoconic hyperplasia. No inhalation anaesthetics or skeletal muscle relaxants, such as succinyl choline, were used in this case. Therefore, malignant hyperthermia might have been induced by a combination of drugs which were not known to induce this abnormal muscular reaction. However, the muscle relaxant effect of dolpersin hydrochloride may have acted as a possible inducer of the attack.
Plasma exchange has been used for therapy in eight patients with the Guillain-Barré syndrome. All patients were severely ill. They became tetraplegic and showed cranial nerve involvement. Five patients received assisted respiration, but the others were also at risk of ventilatory insufficiency. Recovery was abrupt in all cases after the first plasma exchanges. Improvement was more marked when plasmapheresis was done on three successive days with plasma exchanges of 2.0-3.01 each in the initial progressive stage of the disease. A considerable advantage of this therapy is the avoidance of continued artificial respiration and nutrition, which both carry the risk of further complications.
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