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Biomedical subjects

R Ritz

Publications and source records attributed to R Ritz.

At least 19 recordsLinked to original sources

[Cocaine poisoning from transport of the drug in the gastrointestinal tract (the body-packer syndrome)].

Three days after arriving in Switzerland from Bolivia a 35-year-old man presented at a casualty department. He was anxious, agitated and hallucinating, and he expressed delusional ideas of being poisoned. As a general physical examination was without abnormal findings he was thought to suffer from a psychiatric disorder. It was only when he had evacuated in stool a long oval foreign body, packed in plastic sheeting and filled with a dark paste, that cocaine poisoning due to cocaine transport in the gastrointestinal tract (body packer syndrome) was suspected. Plain X-ray of the abdomen revealed numerous regular structures of poor X-ray contrast and the urine contained cocaine metabolites, confirming the tentative diagnosis. As the patient's state of consciousness deteriorated and he had a grand mal seizure, an emergency laparotomy was performed. 78 packages (two of them had opened) were removed by gastro- and caecotomy. Total cocaine weight was 650 g. He was discharged from hospital after 11 days, free of symptoms.

Adult

[Anti-arrhythmia treatment using L-carnitine in acute myocardial infarct].

Carnitine, a quaternary amine (3-hydroxy-4-N-trimethylaminobutyric acid), plays an important physiologic role in fatty acid transport and metabolism as well as in energy production of the myocardial cell. L-carnitine in high doses has been postulated to have an antiarrhythmic effect and this has also been clinically proven. We studied 20 patients with acute myocardial infarction (AMI), 4-12 hours after onset of pain. The patients were randomized and treated double-blind with 5 g L-carnitine (n = 12) or placebo (n = 8) at hours 0, 12, 24, 36, and with 2 x 3 g on days 3 to 7 by intravenous infusion over 2 hours. The two groups were similar for age, sex, infarct site, maximum CPK and conventional antiarrhythmic therapy. 24-hour Holter-ECG was performed on days 1, 2 and 7 and showed no significant difference between the two groups with respect to incidence of ventricular premature beats (VPB) per hour. On the second day following AMI, however, only 4 of 12 carnitine-treated patients showed high-grade VPB (Lown IVa and IVb), in comparison with 7 of 8 patients in the placebo group. The difference is significant: p = 0.028 (Fisher's Exact Test). Carnitine was well tolerated and the efficacy demonstrated on the second day following AMI must be interpreted with caution.

Aged

[Acute left heart insufficiency: possible leading symptom of a pheochromocytoma].

A 42-year-old patient with acute left-ventricular failure is described in whom pheochromocytoma was diagnosed only after prolonged and fruitless efforts. Pheochromocytoma may present without the typical features of paroxysmal or sustained hypertension, headache, increased sweating, and palpitations. Therefore, in cases of acute left-sided cardiac failure of primarily undetermined origin, pheochromocytoma should be considered in differential diagnosis.

Acute Disease

Possible risk for cardiac arrhythmia related to intravenous erythromycin.

OBJECTIVE: To evaluate the incidence of prolongation of the rate-corrected electrocardiographic QT interval (QTc) and of ventricular arrhythmia associated with intravenous administration of erythromycin lactobionate. DESIGN: A consecutive series of 7 critically ill patients treated with intravenous erythromycin for severe pneumonia. SETTING: A medical intensive care unit of a university hospital. MEASUREMENTS AND RESULTS: Registration of QTc duration before and after intravenous administration of erythromycin as a short infusion. Blood chemistry, hemodynamic variables, arrhythmias, and co-medications were recorded. Evaluation of at least 10 ECG intervals by 2 experienced investigators who were blinded as to the time of drug administration. If several measurements were performed in the same patient, only the mean value was used for further analysis. During 12 of 13 drug administrations studied in 7 patients QTc prolongation was observed. The extent of QTc prolongation was significantly correlated with the infusion rate (mg/min, r = 0.765, p = 0.05). In 3 patients ventricular arrhythmia occurred in close temporal relation to the erythromycin infusion; two of them developed ventricular fibrillation shortly after the first and second dose of erythromycin, respectively, and died within 3 h. CONCLUSION: In critically ill patients erythromycin-induced QTc prolongation is a frequent pharmacologic effect correlated with erythromycin infusion rate. To avoid changes in electrocardiographic intervals and thereby possibly potentially life-threatening ventricular arrhythmia administration with the lowest possible infusion rate and close cardiac rhythm monitoring are advisable in these patients.

Aged

Absence of nitroglycerin-induced heparin resistance in healthy volunteers.

A previously described nitroglycerin-induced heparin resistance could not be verified by in-vitro experiments or in a randomized, double-blind, crossover trial in healthy volunteers. A clinically relevant attenuation of the anticoagulant effect of a heparin bolus (40 U.kg-1) by a concomitant infusion of nitroglycerin (100 micrograms.min-1) was absent. Activated partial thromboplastin time was not significantly different under nitroglycerin infusion as compared to placebo after heparin injection. Concentrations and activities of antithrombin III and heparin cofactor II remained unchanged during nitroglycerin infusion. An interaction of these two frequently combined drugs in patients with active thromboembolic disease or after a prolonged concomitant intravenous administration cannot be ruled out. Since this is of clinical importance, further studies must clarify a possible nitroglycerin-induced heparin resistance.

Adult

Rapid reversal of heart failure in a patient with phaeochromocytoma and catecholamine-induced cardiomyopathy who was treated with captopril.

A patient with a phaeochromocytoma and severe left ventricular heart failure caused by a catecholamine-induced cardiomyopathy is described. The clinical signs of congestive heart failure resolved rapidly on treatment with captopril and myocardial performance became normal within two weeks of medical treatment with captopril for one week and with captopril in combination with phenoxybenzamine for another week.

Acute Disease

[Are ECG criteria for indications for thrombolysis in acute myocardial infarct defined too narrowly?].

BACKGROUND: Despite the advantages of fibrinolytic therapy in acute myocardial infarction only about 20% of these patients receive this therapy. We studied patients excluded from fibrinolysis to identify subgroups with high mortality, which could derive benefit from more liberal interpretation of the indications for fibrinolytic therapy. METHODS: Retrospective chart review to identify patients with acute myocardial infarction in our coronary care unit 7/88-7/89. All patients received a questionnaire one year after this myocardial infarction. Patients not answering the questionnaire were contacted by phone or the information was sought from their physician. Indications for thrombolysis (with streptokinase or rTPA) were ST elevations of greater than or equal to 2 mm in greater than 2 adjacent leads and the absence of contraindications. RESULTS: In 231/242 (95%) of the identified patients a complete follow-up was obtained, 32% were age greater than 70 years, 30% were admitted greater than 6 h after the beginning of the symptoms, 64% did not fulfil the ECG criteria for thrombolysis, 21% (49/231) received thrombolytic therapy. The mortality after one year was 20.3% in patients not treated with thrombolysis and 8.2% in patients with thrombolysis (difference 12.1%, 95% confidence interval 2.9-21.3%, p = 0.048). Patients with preceding old infarctions (n = 58) fulfilled the ECG criteria for thrombolysis in a significantly smaller proportion (21% vs 41%, p = 0.004). Of all patients 12% were excluded from thrombolytic therapy due to a negative initial ECG and yet developed a Q ware infarction. The one year mortality of patients not given thrombolysis and with a Q wave infarction was 24% (22/93, p = 0.02 as compared to patients with thrombolysis), in patients with non Q wave infarction it was 13% (11/82, p = 0.41) and in patients with ambiguous ECG it was 57% (4/7, p = 0.006). The mortality in patients with a preceding infarction was 31% and significantly higher than in patients with a first infarction (16%, p = 0.049) and in patients receiving thrombolysis (8.2%, p = 0.005). CONCLUSIONS: By excluding patients with acute myocardial infarction from thrombolytic therapy a group with high first year mortality is selected. Most patients are excluded because of an initial ECG not showing enough ischemia to fulfil the criteria for thrombolytic therapy. A prospective study of thrombolytic therapy using less rigid ECG criteria in the subgroups with the highest mortality (patients with preceding myocardial infarction or ambiguous ECG) seems necessary.

Acute Disease

Cilazapril in congestive heart failure. A pilot study.

The haemodynamic effects of a single dose of cilazapril 2.5 or 5 mg were studied in 33 patients with stable chronic congestive heart failure who were receiving digitalis and diuretics. Subsequently, a double-blind comparison of the haemodynamic and clinical effects of 3 months' treatment with cilazapril 1.25 to 5 mg daily or placebo in 24 evaluable patients revealed that the acute haemodynamic improvement produced by a single dose of cilazapril was maintained in patients receiving repeated administration of the drug, but not in those randomly allocated the placebo. Acute cilazapril significantly decreased mean arterial pressure, systemic vascular resistance, pulmonary capillary wedge pressure, pulmonary artery pressure and right atrial pressure, while cardiac index and stroke volume index increased at rest and during submaximal exercise. After 3 months' treatment 11 of 13 cilazapril recipients improved their New York Heart Association (NYHA) class compared with 2 of 11 patients treated with placebo. This functional improvement was paralleled by a patient-perceived improvement in general well-being.

Adult

[Echocardiography in emergency medicine: tool or toy?].

In cardiovascular emergency medicine echocardiography allows in many patients a quick and gentle bedside examination. In particular in patients with acute arterial hypotension, suspected or known acute coronary heart disease and its complications and in patients with acute heart failure due to valvular heart disease a valuable narrowing down of the differential diagnosis can be achieved by the use of echocardiography. However, the use of echocardiography in acutely ill patients demands highly skilled investigators to avoid potentially dangerous errors. The echocardiographic examination in intensive or emergency care patients represents an invaluable diagnostic tool today and becomes a toy only in inexperienced hands.

Cardiovascular Diseases

[Hyperkalemic emergency: causes, diagnosis and therapy].

Eight patients with life threatening hyperkalemia were treated in the intensive care unit over a period of 2 years. Serum potassium at admission was 7.1-11.2. Two patients had to be resuscitated and 3 exhibited quadriplegia or paralyses but were alert. Seven showed marked ECG change: in 5 the QRS-complexes were extremely broadened and in one case an AV-rhythm was observed; the atrial wave was absent in all 7 patients. Renal failure was present in 7 of 8 patients. In 6 of these 8 cases drugs were also involved in the development of hyperkalemia. The following therapeutic procedure is recommended for hyperkalemia: (1) injection of calcium, (2) inhalation or injection of beta 2-mimetics (well documented in the literature; clinical experience limited), (3) insulin and glucose i.v., (4) sodium bicarbonate, but only in case of metabolic acidosis, (5) hemodialysis, (6) cation exchange resins or furosemide in non-acute situations.

Acute Kidney Injury

[Short-term dobutamine therapy in severe cardiac insufficiency].

The feasibility of heart transplantation has stimulated new interest in the therapy of severe refractory congestive heart failure even as an interim solution. We studied the hemodynamics, clinical efficacy and practical implications of a 72-hour dobutamine infusion in 11 patients with NYHA IV refractory congestive heart failure (age 40-73, average 55 years). The dose was 250-1000 micrograms/min, with the goal of increasing cardiac output by 30-50%. Changes in the pharmacokinetics of lidocaine were studied by single dose kinetics in 7 patients. Cardiac output increased from 2.94 +/- 0.68 to 4.77 +/- 1.1 l/min and stroke volume from 35 +/- 10 to 56 +/- 12 ml (p less than 0.001). Pulmonary capillary wedge pressure decreased from 28.5 +/- 5 to 21 +/- 6 and central venous pressure from 14 +/- 6 to 7 +/- 3 mm Hg (p less than 0.007). There was marked worsening of hemodynamics 24-48 h after starting dobutamine. However, after withdrawal of dobutamine a significantly higher cardiac output and stroke volume (3.73 +/- 0.43 l/min, 42 +/- 7 mm Hg. p less than 0.05) persisted. Both clearance and distribution volume of lidocaine increased, while half life decreased significantly (6.61 +/- 1.43 to 5.33 +/- 0.77 h. p less than 0.05). 9 of 11 patients developed Lown IVb ventricular arrhythmia, while in 4 massive diuresis occurred necessitating volume substitution. 6 patients left hospital clinically improved, 2 were transplanted and 3 patients died 1 day to 3 weeks after ending dobutamine. Dobutamine had salutary hemodynamic and clinical effects outlasting the duration of dobutamine therapy. Due to its arrhythmogenic effects it should be administered under ECG monitoring. In patients treated with lidocaine, upward dose adjustments may be necessary with improving hemodynamics.

Adult

Use of flumazenil in intoxicated patients with coma. A double-blind placebo-controlled study in ICU.

In a double-blind placebo-controlled prospective clinical trial we studied the efficacy and safety of the benzodiazepine antagonist, flumazenil. In 23 patients admitted to the Intensive Care Unit with coma due to overdose with benzodiazepines or other sedatives, flumazenil i.v. (up to 2 mg or placebo) was given. In 13 patients given flumazenil the Glasgow Coma Scale (GCS) increased significantly from 4.9 to 7.8 (p less than 0.05). Six of these 13 patients, including mainly benzodiazepine mono-intoxications, needed only one series of injections (up to 1.0 mg flumazenil); the GCS increased thereby from 4.5 to 10.7 within a maximum of 5 min (p less than 0.01). In the remaining 7 patients, needing two series of injections of flumazenil (up to 2.0 mg), GCS did not rise significantly and coma was related to intoxications with nonbenzodiazepine sedatives, flunitrazepam and in one patient, encephalitis. In the 10 patients receiving placebo, the GCS did not change. A significant increase in the GCS from 5.5 to 10.8 (p less than 0.001) was, however, observed when flumazenil (up to 1.0 mg) was given after placebo. In patients with EEG monitoring the changes in waveform pattern paralleled the clinical response. Effects could be detected within 1-2 min after flumazenil injection and lasted up to 45 min. There were no adverse reactions or benzodiazepine withdrawal symptoms. We conclude that flumazenil is an effective and safe drug in the treatment of benzodiazepine overdose. The use of flumazenil is of diagnostic value in mixed-drug intoxications or coma of unknown origin and is of therapeutic importance for reversal of benzodiazepine intoxications.

Adolescent

[Emergency coronary dilatation in acute myocardial infarct with contraindications to thrombolytic therapy: salvage of the myocardium by early intervention].

In 1986/87, emergency-PTCA in acute myocardial infarction was performed in 13 patients in whom thrombolysis was contraindicated. All infarct-related arteries could be opened with PTCA. Patency rate after one week was 94%. Reopening of the vessel resulted in immediate cessation of ischemic chest pain and in stable cardiac rhythm and hemodynamics. Prior cardiopulmonary resuscitation and/or cardiogenic shock did not influence short- or longterm outcome. In nine of eleven patients an improvement of left ventricular function was found after four to six months as compared to one to four weeks after PTCA. The functional result proved to be better if PTCA was performed early; PTCA within 90 minutes was associated with normal left ventricular function. Thus, PTCA is feasible as an emergency procedure in patients with acute myocardial infarction and contraindications to thrombolysis. It can salvage myocardium and improve or prevent severe infarct complications when performed early after onset of pain. Rapid hospital admission through the primary care physician importantly influences the outcome for these patients.

Adult