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Biomedical subjects

J M Hackl

Publications and source records attributed to J M Hackl.

At least 55 records · Page 3Linked to original sources

[Serum lactates in the reconstruction of the aortic bifurcation].

The change in serum lactate level was investigated in 20 patients undergoing reconstruction of the aortic bifurcation. This group of patients was compared with 16 patients undergoing abdominal surgery. There was a remarkable increase of serum lactate in course of the operation in both groups. After the aortic graft serum lactate level was specially elevated (24,96 mg/100 ml +/- 9,71) due to aortic gross-clamping. Simultaneously occurred a decrease in pH and base excess from 7,43 (+/- 0,03) to 7,34 (+/- 0,05) and from -2,2 mmol/1 (+/- 2,5) to -5,7 mmol/l (+/- 1,6). We mentioned the risk of lactic acidosis in vascular surgery caused by fluid therapy with fructose, sorbitol, xylitol and with electrolyte solutions containing lactate.

Aged↗

[Periodic paresis due to hypokalaemia (author's transl)].

A case of periodic paralysis is reported that had to be treated by mechanical ventilation. Symptoms and course of this attack are demonstrated and it is shown how diagnosis was reached. Provocative factors of periodic hypokaliemic paralysis are discussed and their importance in anaesthesia is emphasised.

Adult↗

[Plasma catecholamines in accidental hypothermia (author's transl)].

The plasma levels of adrenaline and noradrenaline were measured by a radioenzymatic method in 3 patients with accidental hypothermia and followed up until normal body temperature was achieved. In all 3 patients the hypothermia was accompanied by markedly elevated levels of noradrenaline, whereas adrenaline increased considerably only in one of the 3 patients. During normalization of body temperature the elevated catecholamine levels started to decrease. In 2 of the 3 patients nearly normal catecholamine levels were measured, when body temperature had normalized. In spite of the high levels of catecholamines in plasma the heart rate was strikingly low at the lowest temperature. During the increase of the lowered body temperature the heart rate increased in contrast to the decreasing catecholamine levels. The increase of the catecholamine levels in plasma in patients with accidental hypothermia can be explained either by an augmented stimulation of the sympathetic nervous system or by a decreased metabolism. On the basis of the high endogeneous catecholamine levels the use of beta-sympathomimetics appears contraindicated in case a haemodynamic insufficiency develops during the course of accidental hypothermia.

Adult↗

The activity of the sympathetic nervous system following severe head injury.

The activity of the sympathetic nervous system during the course of severe closed head injury has been evaluated in 15 patients by measuring plasma levels of epinephrine and norepinephrine. With the onset of the transition stage from midbrain syndrome to the apallic syndrome the plasma levels mainly of norepinephrine started to increase and remained high during the further course of the disease. During the remission from the apallic syndrome the elevated norepinephrine levels started to decline. The data indicate that a longlasting overactivity of the sympathetic nervous system is a characteristic feature in the course of severe head injury. As a rational therapy to protect the peripheral tissues against the consequences of a longlasting sympathetic overactivity we suggest the use of beta-adrenergic blocking agents and adrenergic neuron blocking drugs.

Adolescent↗

[Hypermetabolism in head injury and tetanus: patho-physiological and new therapeutic conceptions].

Longlasting overactivity of the sympathetic nervous system can be considered as one of the causes of the hypermetabolism developing in patients with head injury or tetanus. In tetanus elevated plasma levels of catecholamines can be demonstrated as long as disturbances of the motor nervous system are present. In patients with head injury the plasma catecholamines, mainly noradrenaline, start to increase with the onset of the transition stage from midbrain syndrome to the apallic syndrome. The activity of the sympathetic nervous system remains elevated also in the full stage of the apallic syndrome and during the remission. The influence of such a longlasting sympathetic overactivity on the metabolism is discussed. For the suppression of hypermetabolism caused by sympathetic overactivity the use of the adrenergic neuron blocking drug debrisoquine combined with a nonselective beta-adrenergic blocking drug is suggested. This treatment enables a normocaloric nutrition in patients with head injury or tetanus. Additionally such a treatment protects the cardiovascular system against the consequences of a longlasting sympathetic overactivity. The influence of debrisoquine on the plasma levels of noradrenaline is demonstrated in a patient with head injury.

Adrenergic beta-Antagonists↗

[Behavior of the growth hormone in severe cerebral trauma with secondary injuries of the brain stem. New viewpoints for therapy I].

19 patients developing signs os secondary brain stem involvement after severe head-brain injury underwent human growth hormone (HGH) provocation tests with arginine to determine the significance of HGH during the course of catabolism due to vegetative dysfunction. The results of provocation suggest a normal release of HGH to arginine stimulus during the postagression syndrome. The release decreases in the further course dependent on duration of intensive therapy and degree of brain injury. During recovery the HGH-release slowly became normalized. There was no correlation between blood glucose levels before as well as after stimulation and the percentage increase of HGH. A negative correlation was found between urea-nitrogen-excretion and HGH increase. This finding suggests the retention of nitrogen due to an elevated release of HGH after arginine-stimulation. The therapeutic aspects of these results were discussed, especially the effect of HGH and beta-blocking agents on the traumatically disturbed metabolism and also the value of a higher supply of insulin and amino acids.

Amino Acids↗

The involvement of the sympathetic nervous system in tetanus.

Besides the characteristic disturbances of the motor nervous system symptoms indicating an overactivity of the sympathetic nervous system can complicate the course of severe cases of tetanus. These symptoms include fluctuating tachycardia and hypertension, electrocardiographic changes, sweating, constipation with development of paralytic ileus and metabolic disorders. These symptoms are comparable to these developing in patients with phaeochromocytoma. Elevated catecholamine levels in plasma and urine have been found in several patients with tetanus who developed these symptoms. The prolonged over-activity of the sympathetic nervous system is thought to contribute to the still considerably high mortality rate. Myocardial lesions observed at necropsy are comparable to those found in patients dying of phaeochromocytoma. These lesions are suggested to be associated with sudden death from arrhythmias or cardiac failure in patients with tetanus. For the protection of the organism against the overactivity of the sympathetic nervous system a treatment using the combination of beta-adrenergic receptor blocking agents and adrenergic neuron blocking agents has been introduced. A reduction of the mortality rate was achievable by this treatment. Experimental evidence is accumulating that the tetanus toxin affects not only the motor, but also the sympathetic and sensory neurons.

Adrenergic beta-Antagonists↗

Dysfunction of the sympathetic nervous system in tetanus. A study of 3 cases.

In severe cases of tetanus an overactivity of the sympathetic nervous system has been postulated because of the clinical symptoms including hypertension, fluctuating blood pressure, tachycardia, tachyarrhythmia and peripheral vasoconstriction. In the present study the involvement of the sympathetic nervous system in tetanus was investigated by serial determinations of plasma adrenaline (A) and noradrenaline (NA) in 2 patients who developed severe symptoms of tetanus and the characteristic cardiovascular disturbances. Sustained high circulating levels of NA and A could be observed indicating a prolonged overactivity of the sympathetic nervous system. In one case, the elevation of the NA level in plasma persisted until the disturbances of the motor nervous system ceased. In a third case of tetanus without cardiovascular abnormalities, the plasma NA and A only increased slightly on a few occasions. The results demonstrate that an overactivity of the sympathetic nervous system can complicate the course of severe tetanus.

Adult↗

The EEG at different stages of acute secondary traumatic midbrain and bulbar brain syndromes.

One hundred and thirty EEGs were analysed from 113 patients with acute secondary traumatic midbrain and bulbar brain syndromes. The EEG pattern was related to the stage of the midbrain syndrome caused by supratentorial brain shift. A decrease in the number of different EEG patterns was associated with increasing intracranial pressure. Unfavourable prognosis was indicated by the disappearance of sleep or sleep-like activities alternating pattern and loss of reactivity. Lateralization by the EEG proved to be superior to clinical findings in full stages of the midbrain syndrome. EEG abnormalities due to the herniation itself interfered with EEG changes due to secondary circulatory, respiratory and metabolic encephalopathies. In such cases, the above mentioned regularities were blurred.

Adolescent↗

[Electroencephalographic changes in coma due to hepatic insufficiency with porto-caval shunt (author's transl)].

EEG studies were done in 19 patients comatose due to severe hepatic insufficiency associated with porto-caval shunting. The neurological deficits were graded in 5 stages and related to the abnormal EEG-pattern observed in 38 records. With deepening of coma, alpha-frequencies were gradually replaced by theta- and delta-activities. The frequency of theta- and delta-runs decreased with neurological deterioration. Triphasic waves (typical and/or atypical) were seen in 26% of the records. Typical triphasic waves were found to be limited to stage 3 of coma, whereas atypical forms appeared in earlier and later stages. After infusions of L-Valin, a transient improvement and disappearance of triphasic waves was observed, but no significant effect could be established on the final course of the disease. Sleep-like potentials and the reactivity to external stimuli decreased in deep stages of coma. Severe EEG abnormalities were correlated to low cholinesterase and high lactid acid blood level, but no correlation was found to the level of ammonia.

Alpha Rhythm↗

[Estimation of myocardial damage after open-heart surgery by CK isoencymes (author's transl)].

After 12 cases of open-heart surgery serum activities of CK and CKMB have been registrated. To make a more exact statement about myocardial damage the portion of CKMB out of the CK-activity has been evaluated by the way of a mathematic programm. The results verify the statement that after aortic valve replacement the CKMB portion is higher than the average, and that after intraoperative complications the highest CKMB portions have been reached. No myocardial infarction occurred.

Aortic Valve↗

[Five cases of lactic acidosis (author's transl)].

Five cases of non-biguanide-induced lactic acidoses are reported. The key role of the liver and kidneys in lactate metabolism is stressed. The patients at risk are enumerated and the particular stress in connexion with surgical procedures and the dangers of fructose infusions are pointed out. The coagulation disturbances due to lactic acidosis are discussed. The different operative procedures and their effectiveness are discussed.

Acidosis↗

[Differential diagnosis between skeletal muscle lesions and myocardial damage in multiple injury by determination of myocardial-specific creatine phosphokinase (CK-MB) (author's transl)].

The serum level of the myocardial-specific isoenzyme of creatine phosphokinase, CK-MB was determined in 50 patients with severe multiple injuries or following extensive surgery. It is concluded that whenever the proportion of CK-MB exceeds 10% of the total creatine phosphokinase activity myocardial damage has occurred, especially since equivalent ECG changes were registered in this group of patients.

Contusions↗

[Postoperative fructose infusion in a case of presumed hereditary fructose intolerance (author's transl)].

Hereditary fructose intolerance (HFI) was diagnosed in a 61 year-old male patient on account of liver dysfunction followed by prolonged shock immediately after the administration of a fructose and lactose infusion postoperatively. The diagnosis of HFI was based on an increased value of fructose, hypoglycaemia, lactic acidosis and diminution of the phosphate level in combination with the typical family history. The patient's children showed a normal reaction to fructose administration. The therapy included glucose, insulin and heparin administration, balance of acidosis and partial exchange of blood, which resulted in improvement in the glucose level, coagulation factors and acidosis, but could not prevent further liver damage and uraemia with a fatal outcome.

Acidosis↗

[The value of CKMB in multiple trauma and high voltage injuries].

The paper deals with a new aspect in patients with polytrauma using a method to distinguish between myocardial or skeletal muscle damage. The isoenzyme CKMB of kreatine kinase is found to be characteristic for myocardial damage when increasing to more than 10% of the whole enzyme activity. It should be mentioned that this elevation is also seen in other disorders. Therefore the correlation to ECG changes is important in considering the diagnosis.

Adolescent↗

[Transitory burst-suppression pattern in endogenous-exogenous encephalopathy (author's transl)].

A status epilepticus was observed in a 22 year old female patient during endotoxinshock. The status epilepticus was treated with a high dosage of diazepame. The EEG showed a burst suppression pattern, in our case mixed by anoxia and diazepame. The burst-suppression pattern and the clinical suspicion of delayed degradation of diazepame caused by toxic hepatic failure suggested the therapy of forced diuresis. This therapy was followed by decreasing suppression periods, indicating the dominante influence of the hypnotic drug. This result shows the diagnostic as well as the therapeutic value of forced diuresis in this case.

Adult↗