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Biomedical subjects

M Stäubli

Publications and source records attributed to M Stäubli.

At least 19 recordsLinked to original sources
PubMed1998

[Esophageal surgery in the regional hospital].

In a small series of surgically treated patients with esophageal cancer (n = 22) modern trends are observed, namely--the frequent occurrence of adenocarcinoma (50% of cases) and of early stage (pT1) (36% of cases),--a low operative mortality (5%),--favorable oncological results for tumors not penetrating the esophageal wall (pT1, 2)(64% of patients at life without recurrence 2-7 1/2 years after surgery). For curative or palliative resection of distal tumors the abdomino-cervical (transhiatal) resection was favored (n = 17) with no instance of anastomotic insufficiency and with 2 cases only of locoregional recurrence. In a case of spontaneous esophageal perforation (Boerhaave) primary suture through an abdomino-transhiatal approach was successful. The interdisciplinary intensive care, necessary in surgery of the esophagus, may be of a high standard in the district hospital.

Adenocarcinoma↗
PubMed1996

[Iatrogenic falls].

One third of community-dwelling people, aged 65 years and over, experience a fall each year, and for institutionalized persons the fall frequency is 1.6 times a year. A fracture results in 5% of falls, one in five of which is a hip fracture. In view of this epidemic among the elderly it is obvious that preventive measures are needed. From the patient's history and the clinical assessment a risk of falls can be defined and this should influence decisions regarding drug treatment. Anamnestic data from relatives or neighbours can be important clues to the circumstances of a fall. Supine and standing blood pressure readings (orthostatic drop?) and testing of mobility provide relevant clinical information. To reduce the fall risk in elderly people, drug therapy should not induce daytime fatigue, sedation or drowsiness. Confusion and orthostatic blood pressure drop should be avoided. Long-term drug therapy should be modified or interrupted during acute illness. Electrolyte imbalance should be prevented.

Accidental Falls↗
PubMed1995

Plasma potassium response to acute respiratory alkalosis.

Acute respiratory alkalosis (hyperventilation) occurs in clinical settings associated with electrolyte-induced complications such as cardiac arrhythmias (such as myocardial infarction, sepsis, hypoxemia, cocaine abuse). To evaluate the direction, magnitude and mechanisms of plasma potassium changes, acute respiratory alkalosis was induced by voluntary hyperventilation for 20 (18 and 36 liter/min) and 35 minutes (18 liter/min). The plasma potassium response to acute respiratory alkalosis was compared to time control, isocapnic and isobicarbonatemic (hypocapnic) hyperventilation as well as beta- and alpha-adrenergic receptor blockade by timolol and phentolamine. Hypocapnic hypobicarbonatemic hyperventilation (standard acute respiratory alkalosis) at 18 or 36 liter/min (delta PCO2-16 and -22.5 mm Hg, respectively) resulted in significant increases in plasma potassium (ca + 0.3 mmol/liter) and catecholamine concentrations. During recovery (post-hyperventilation), a ventilation-rate-dependent hypokalemic overshoot was observed. Alpha-adrenoreceptor blockade obliterated, and beta-adrenoreceptor blockade enhanced the hyperkalemic response. The hyperkalemic response was prevented under isocapnic and isobicarbonatemic hypocapnic hyperventilation. During these conditions, plasma catecholamine concentrations did not change. In conclusion, acute respiratory alkalosis results in a clinically significant increase in plasma potassium. The hyperkalemic response is mediated by enhanced alpha-adrenergic activity and counterregulated partly by beta-adrenergic stimulation. The increased catecholamine concentrations are accounted for by the decrease in plasma bicarbonate.

Acute Disease↗
PubMed1994

[Hypokalemia in the course of a Bartter syndrome].

We report on diagnostic and differential diagnostic considerations in the case of a 30 year old Italian woman with hypokalemic alkalosis, fatigue and muscular weakness. The symptoms were caused by a Bartter syndrome with distinctly increased renin but almost normal aldosterone levels in the serum and increased aldosterone values in the urine.

Adult↗
PubMed1994

Hyperventilation-induced changes of blood cell counts depend on hypocapnia.

Voluntary hyperventilation for 20 min causes haemoconcentration and an increase of white blood cell and thrombocyte numbers. In this study, we investigated whether these changes depend on the changes of blood gases or on the muscle work of breathing. A group of 12 healthy medical students breathed 36 l.min-1 of air, or air with 5% CO2 for a period of 20 min. The partial pressure of CO2 decreased by 21.4 mmHg (2.85 kPa; P < 0.001) with air and by 4.1 mmHg (0.55 kPa; P < 0.005) with CO2 enriched air. This was accompanied by haemoconcentration of 8.9% with air (P < 0.01) and of 1.6% with CO2 enriched air (P < 0.05), an increase in the lymphocyte count of 42% with air (P < 0.001) and no change with CO2 enriched air, and an increase of the platelet number of 8.4% with air (P < 0.01) and no change with CO2 enriched air. The number of neutrophil granulocytes did not change during the experiments, but 75 min after deep breathing of air, band-formed neutrophils had increased by 82% (P < 0.025), whereas they were unchanged 75 min after the experiment with CO2 enriched air. Adrenaline and noradrenaline increased by 360% and 151% during the experiment with air, but remained unchanged with CO2 enriched air. It was concluded that the changes in the white blood cell and platelet counts and of the plasma catecholamine concentrations during and after voluntary hyperventilation for 20 min were consequences of marked hypocapnic alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Leiomyosarcoma in the thyroid gland--primary tumor or metastasis?].

In a 69-year-old female patient a moderately pleomorphic spindle-cell thyroid tumour measuring 5 cm in diameter was initially misinterpreted as primary anaplastic thyroid carcinoma. During clinical investigations to elucidate the cause of severe anaemia, 17 months later an ulcerated duodenal leiomyosarcoma was detected and removed by duodenopancreatectomy. Reevaluation of the thyroid nodule led to revision of the initial diagnosis to metastatic leiomyosarcoma. Six months later the patient died from cerebral stroke. Autopsy findings confirmed the diagnosis of primary leiomyosarcoma of the duodenum with initial manifestation as thyroid metastasis.

Aged↗
PubMed1993

[Stability of blood sedimentation rate following repeated mixing of the blood in a vacutainer tube (Seditainer)].

The stability of the sedimentation rate (read at 1 hour) was tested after repetitive mixing of the blood in the same Vacutainer Sedimentation tube ("Seditainer", Becton-Dickinson). The results of 275 sedimentation probes were collected by the nursing staff during routine clinical work on 5 internal medical wards. Sequential sedimentation tests with the same tube after mixing the blood by 6 inversions for the first run and 10 inversions for the second run, or 10 inversions for the first run and 6 inversions for the second, gave identical results. This shows that 6 inversions provide sufficient mixing of the blood. Our definition of one inversion includes turning of the tube axis by 180 degrees plus turning back to the original (vertical) position. If only 3 inversions were performed, the results were less consistent with those after 6 inversions. In 38 of 623 sedimentation runs the readings were too late by 7.6 +/- 4.7 minutes. The corresponding sedimentation rates were 113 +/- 24% of the control values read in time. In 17 of the 275 probes (6.2%) it was the first sedimentation run which was read too late. This shows that repetitions of the sedimentation test may be necessary in routine clinical work. The study clearly demonstrates that repetition is possible with the original sedimentation probe, which provides a reliable result if the blood is remixed by 6 inversions.

Blood Sedimentation↗
PubMed1993

[Panic attacks].

A panic attack is characterized by the abrupt onset of apprehension or fear, accompanied by symptoms such as dyspnea, palpitations, chest pain, dizziness, sweating, the feeling of going mad or the fear of dying. The feeling of anxiety often recedes into the background and such patients present to nonpsychiatric physicians with mainly somatic symptoms. The consequences of frequent panic attacks, named panic disorder, are agoraphobia with impairment of psychic and social functioning, increased prevalence of alcohol abuse, depression and, in particular, suicidal attempts. It is of the utmost importance that physicians recognize the somatic symptoms of panic anxiety and plan integrated treatment. The main therapeutic resources at present include antidepressants, selected benzodiazepines and behavioral treatments and are very successful in improving panic attacks and their consequences, which may long go undiagnosed.

Agoraphobia↗
PubMed1990

[Acute hepatitis following administration of fansidar].

Since 1971 pyrimethamine-sulfadoxine (Fansidar, Roche) has been used worldwide for prophylaxis and therapy of chloroquine resistant Plasmodium falciparum malaria. The drug monitoring team of the producing firm has received reports of a number of cutaneous adverse reactions, some severe, and a few even with fatal outcome. Liver reactions were also encountered, with severe cases only in the recent literature. We report on two patients with hepatitis in temporal relationship to pyrimethamine-sulfadoxine, the first with a second event after later exposure to the same drug. After discontinuing the medication the liver function abnormalities returned to normal limits within a few weeks. Liver biopsy and a positive lymphocyte transformation test against sulfadoxine, a component of Fansidar, strongly suggest that Fansidar was the cause of hepatic injury.

Adult↗
PubMed1990

Myocardial infarction during a football game: empiric estimation of the contribution of skeletal muscle damage to the serum creatine kinase activity.

A 40-year-old untrained participant of a competitive football game experienced chest pain after 20 minutes of playing time. An acute anterior myocardial infarction was diagnosed by electrocardiographic criteria and the creatine kinase rose to its maximum of 3900 U/l (normal range less than 125 U/l) by 24 h with a CK-MB fraction of 6.1%. In order to estimate the contribution of skeletal muscular work to CK activity, the course of CK activity was prospectively measured in 11 untrained participants of a competitive football game, who had normal electrocardiographic findings on exercise testing. Individual peak values of CK correlated positively (p less than 0.01) with the time spent in play. Based on this observation we could estimate that, at most, 14% of the total CK was contributed by skeletal muscle damage in our patient. When total CK was elevated above 125 U/l, the percentage of CK-MB activity did not exceed 6% of total CK in any case. 3-methylhistidine, methylhistidine, an indicator of contractile protein turnover and creatinine were prospectively determined in spot urine samples before the game and for up to 48 h after the game. 3-methylhistidine/creatinine ratios did not change from baseline after the game and no correlation with CK was found. Urine 3-methylhistidine/creatinine, measured within 48 h after a football game, does not contribute to the quantification of skeletal muscle damage.

Adult↗
PubMed1989

[Giant adenoma of Brunner's glands].

Bleeding, obstruction and invagination are the common symptoms of large polyps in the duodenal bulb. We present 2 patients with a large ulcerated Brunner's gland adenoma. The clinical findings were acute bleeding and nonspecific upper gastrointestinal symptoms. The treatment was surgical due to a suspect histological finding in one case, a thick stalk in the other, and the fact that endoscopic polypectomy is a much higher risk procedure in the duodenum than in the colon.

Adenoma↗
PubMed1988

[Amiodarone].

The extraordinary antiarrhythmic efficacy of amiodarone has been well documented in the last few years. Parallel investigations of the electrophysiologic influence of this iodinated benzofuran derivative on myocardial tissue showed that repolarizing as well as depolarizing currents are inhibited. However, the detailed electrochemical aspects of these effects are only partly understood. Likewise, ideas on causes of the differences in hemodynamic and electrophysiologic actions of oral and intravenous amiodarone are still speculative. An understanding of the actions of amiodarone is particularly difficult to achieve because of the unique pharmacokinetics of the drug: it resides in extra-plasmatic compartments for months after discontinuation of treatment, a fact which explains, for example, the lack of an established dose/response relationship. Replacement of amiodarone by another antiarrhythmic drug in the same patient may be problematic, because pharmacokinetic and pharmacodynamic interactions of residual amiodarone with the new antiarrhythmic drug are to be expected. Therefore, amiodarone should be prescribed only in cases where other treatment has failed. This is also advisable in view of the long list of amiodarone-induced adverse reactions. Determinations of plasma concentrations of amiodarone and desethylamiodarone may be useful in some instances, but must never replace clinical evaluation of antiarrhythmic drug efficacy. Although the incidence of some amiodarone-induced adverse reactions increases with dosage and serum drug level, dose-independent factors may play a role in the rare but serious pulmonary and hepatic side effects.

Amiodarone↗
PubMed1988

[Severe complications during enalapril therapy for heart insufficiency].

In 3 patients with severe cardiac failure high dose therapy with the ACE inhibitor enalapril was instituted during a state of extracellular volume depletion. Severe arterial hypotension with reversible renal insufficiency developed in all the patients. In two the hypovolemia was induced by diuretic treatment and in one by an acute infection with diarrhea. The latter patient also developed life-threatening hyperkalemia with cardiac arrest since he was also receiving spironolactone and potassium supplements. These cases demonstrate that ACE inhibitors should not be instituted during extracellular volume depletion and their initial dosage should be low. The dangerous combination of ACE inhibitors with spironolactone and potassium supplements should be avoided wherever possible.

Acute Kidney Injury↗
PubMed1988

Mechanisms of the haematological changes induced by hyperventilation.

During voluntary hyperventilation an increase in the lymphocyte and thrombocyte counts occurs, paralleled by an increase in plasma epinephrine and norepinephrine. All these changes are rapidly reversible after hyperventilation and are followed by an increase in the neutrophil granulocyte count. The pathophysiological mechanisms of these changes were investigated by comparison of the hyperventilation-induced changes of the blood picture in 11 normal, 9 splenectomized and 12 beta-blocked volunteers. Splenectomy did not affect the hyperventilation-induced mobilization of lymphocytes and neutrophils but totally suppressed the change in the thrombocyte count. beta-blockade by 80 mg propranolol did not suppress the hyperventilation-induced increase in neutrophils. It reduced the absolute increase of lymphocytes and thrombocytes by half, but it also increased the baseline counts of these cells. The study shows that hyperventilation mobilizes thrombocytes from the spleen but not from extralienal pools, and that lymphocytes and neutrophils are mobilized from extralienal pools. Whereas neutrophil mobilization is not suppressed by beta-blockade, the reduction of hyperventilation-induced mobilization of lymphocytes and thrombocytes may be due to a reduction in the size of the mobilizable cell pools, and therefore cannot be interpreted as a sure indication that adrenergic mechanisms are involved in their hyperventilation-induced mobilization.

Adult↗