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A 31-year-old female asthmatic patient received an infusion of metamizole and tramadol for chronic pain at a GP surgery. After a few minutes, the patient developed breaing difficulties and died in spite of resuscitation measures. The general practitioner was suspected of medical malpractice. Medico-legal investigations confirmed the assumption that death was caused by anaphylacitic shock. In spite of temporary intubation into the oesophagus no evidence of medical malpractice was found, however.

Acute rhabdomyolysis is a rare complication in patients with status asthmaticus receiving mechanical ventilation. Individual reports implicate several factors, whereby the simultaneous use of high-dose glucocorticoids and non-depolarizing muscle blocking agents appears to be the major patho-physiological mechanism. A 48 year-old female patient with a 3-year history of granulomatous vasculitis Churg-Strauss was admitted to the intensive care unit (ICU) due to severe status asthmaticus, which necessitated endotracheal intubation and mechanical ventilation. Antiobstructive therapy consisted of beta 2-sympathomimetics, theophylline and high-dose intravenous prednisolone (5440 mg in 10 days). Additionally, the patient was treated with non-depolarizing muscle blocking agents (atracurium 2070 mg over 7 days). Six days after admission to the ICU the patient developed severe rhabdomyolysis, with an increased creatine kinase (CK) level and myoglobinuria. The maximum CK value occurred 12 days after ICU admission (3810 U/l), accompanied by a serum myoglobin level of 13,900 ng/ml. 5 days after cessation of muscle relaxant therapy and reduction of intravenous glucocorticoids, the serum CK level decreased, reaching normal values 9 days later.

A case report of an intraoperative asthmatic state that was untreatable by conservative methods is described. These methods include elevation of the patient's chest, ventilation with pure oxygen, and administration of volatile anaesthetics, bronchodilative drugs and corticoids. If the patient does not respond to conventional therapy, the bronchial smooth muscle relaxant effect of ketamine should be used.

Intensive therapy of a patient with status asthmaticus must lead to a reduction of vital threat by improving respiratory and cardiac functions. Because of the bronchodilating effect of ketamine, analgesic sedation with ketamine and benzodiazepines is extremely useful for prolonged ventilation. At the beginning of this treatment it can be necessary to supplement the continuous intravenous infusion of ketamine and diazepam or ketamine and midazolam with small bolus doses of up to 3.5 mg/kg/h of ketamine. Experience has shown that the combination of ketamine and midazolam has better controllability. In some of our patients the bronchodilating effect of ketamine was not sufficient and therefore ventilation with halothane was necessary at least intermittently. In contrast to halothane, ketamine can be combined with vasodilators and sympathomimetics as our own experience has shown. The combined application of ketamine with glycerol trinitrate or sodium nitroprusside is indicated in the event of pulmonary or general hypertension. The use of sympathomimetics--mainly beta-sympathomimetics--antagonizes the negative inotropic effect of ketamine, improves the circulatory system and leads to a direct bronchodilating effect. Progress in treatment was mainly achieved by continuous intravenous infusions of terbutaline (Bricanyl). Aminophylline is very compatible with ketamine, but because of its stimulating effect the use of aminophylline seems to be reasonable only during weaning from the ventilator. Control of the usually deep analgesic sedation and an accompanying optimum drug therapy are only possible with complete cardiorespiratory monitoring including invasive blood pressure measurement and catheterization of the pulmonary artery. In our clinic 24 patients with status asthmaticus were treated. Sixteen asthmatic patients were treated with analgesic sedation using ketamine and benzodiazepines, three of them without intubation and ventilation. In spite of the life-threatening situation and reanimation before admission to the intensive care unit, only one patient died. Our experience has shown that intensive therapy including analgesic sedation with ketamine and benzodiazepines, optimized by application of sympathomimetics and vasodilators, is suitable for overcoming the life-threatening situation of patients with status asthmaticus.

A patient presenting with acute severe asthma associated with protracted hypoventilation (paCO2 = 90 mmHg) and impaired consciousness underwent sedation and controlled mechanical ventilation. The peak airway pressure could be reduced by constant-volume mechanical ventilation and analgosedation with midazolam and ketamine. When the gas exchange had stabilized, the first attempt at weaning was made by synchronized intermittent mechanical ventilation (SIMV). After this and two other attempts had failed, the patient was given continuous sufentanil (0.8-1.0 micrograms/kg), as well as additional bolus injections of 2 micrograms/kg and 0.35 micrograms/kg for analgosedation. Controlled mechanical ventilation was replaced by the system of biphasic positive airway pressure (BIPAP). The mechanical ventilatory support was gradually reduced, as was the dose of continuous sufentanil. Extubation was possible at a dose of 0.2 micrograms/kg per h sufentanil and CPAP. From this case, it is not possible to determine whether the BIPAP system or the analgosedation with Sufentanil was the decisive factor in the therapeutic success. It may well have been the combination of both therapeutic measures that--in our opinion--supplemented each other in an ideal way.

For the treatment of severe attacks of asthma, too, inhalable beta 2-sympathomimetic agents form the basis of drug therapy. It is, further, necessary to apply these agents systemically together with theophylline, the best approach to pre-status and status asthmaticus being continuous i.v. application following a bolus administration (dose of beta 2-sympathomimetic 0.04 mg/kg x min, for theophylline 10-15 micrograms/kg x min). Furthermore, 50-200 mg prednisolone equivalent are administered i.v. Secretolysis and increased expectoration are ensured by a copious supply of liquids, inhalation of saline mists, administration of acetyl cysteine or ambroxol, together with physical-therapeutic measures. Also important is the administration of oxygen and the calming of the anxious, agitated patient by adopting a relaxed, calm approach and devoting the patient sufficient attention. The uncritical use of sedatives (cave: depressive effect on respiration) is to be rejected. If, despite increasing the dose of the beta 2-sympathomimetic agent (approx. 0.06 micrograms/kg x min), no improvement is seen after 1-2 hours, or if global respiratory failure develops or exhaustion of the respiratory musculature is threatening, intensive monitoring and care should be initiated. If necessary, the patient is intubated and ventilated; in therapy-refractory situations, bronchoalveolar lavage should be employed as an adjunctive measure.

Experiences in combined use of beta-adrenergic stimulants and cardioselective beta-receptor blocker Talinolol are reported in 3 patients in Status Asthmaticus. High dose Aminophyllintreatment in these 3 severe cases was insufficient, in 1 case it had to be finished because of toxic side effects respectively. For adrenergic stimulation in two cases Orciprenalin i.v. was given initially, in one case Terbutalinsulfat i.v. By cardioselective adrenergic blockade with low dose Talinolol it became possible to prevent cardiotoxic side effects in preexisting tachycardia and premature ventricular contractions. This combination treatment was continued successfully with Terbutalin and Talinolol p.o.

In eight patients with moderately severe bronchial obstruction intravenous bolus injection and continuous (four-hour) infusion of fenoterol (a beta 2-sympathomimetic) achieved a significant reduction in airway resistance after previous inhalation of the drug. Plasma levels of about 1.1 ng/ml were sufficiently effective. Intravenous administration of fenoterol gave a more rapid bronchospasmolytic response than theophylline-ethylenediamine (10 patients). In contrast to the latter drug, fenoterol caused a significant rise in heart rate. Intravenous fenoterol is thus an alternative to systemic theophylline administration for severe obstructive disorders of ventilation. Because of their additive effect, simultaneous and continuous intravenous administration of both drugs is recommended in the treatment of pre-status and status asthmaticus.

The present investigation provides evidence that the second messenger cyclic adenosine monophosphate (cAMP) shows a different reaction before and after treatment of asthmatic attack. 18 patients suffering from an asthmatic attack admitted to hospital as internal emergency cases were given intravenously 0.24 g theophylline-ethylenediamine (Euphyllin) and 10 mg benzoctamine. Blood was taken and cAMP-concentrations were tested during status asthmaticus, i.e. before theophylline was injected, and after symptoms had decreased. After injection of theophylline a relation could be shown between the clinical effect and a significant biochemical correlate. The cAMP-concentrations increased from 15.5 to 20.2 pmol/ml. The results are significant on the 1% level. It should be discussed whether there is a malfunction or a lack of receptors in asthmatic disease. The cAMP-concentrations found during status asthmaticus are low compared to those found during paroxysmal tachycardia (40 pmol/ml) and are slightly higher than those found in healthy persons. There was no depressant effect on respiration by benzoctamine; in spite of that good sedative component could be seen.