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• W4206351720 abstract "EDITOR: Failure of noninvasive treatment in status asthmaticus is seen in about 1% of patients and requires mechanical ventilation of the lungs. Nevertheless, the overall status of patients is not always improved [1]. In some patients it is impossible to control severe status asthmaticus despite conventional treatment and properly managed ventilatory support. Stellate ganglion block and blockade of the thoracic part of the sympathetic trunk (continuous epidural anaesthesia) have been advocated to treat status asthmaticus [2]. To the best of our knowledge there are only a few reports of the use of sympathetic block in the management or prevention of this condition [2,3]. Since it takes more than 30 min to achieve any therapeutic effect we decided it was quicker to perform high subarachnoid blocks through the L3-4 space in our patients described below. Although from the theoretical point of view, any reduction of sympathetic activity is more likely to increase bronchospasm, thus acting adversely in patients with status asthmaticus, this does not occur in practice and the block is surprisingly effective. Possible mechanisms of beneficial action include: (a) an interruption of the vicious circle that promotes bronchospasm through the afferent reflex arc that transfers sensory impulses from the respiratory tract; (b) improved oxygenation of arterial blood due to increased pulmonary blood flow; (c) decreased alveolar surface tension and increased lung compliance. The block is both simple to perform and immediate in its action. Its extent depends on the patient's position, body weight, volume of drug and rate of infusion; relief of the bronchospasm is a benefit. Three females aged 50, 47 and 37 years developed severe bronchospasm resistant to classical treatment (glucocorticoids, β2-mimetic agents and methylxanthines, deep sedation and muscle relaxation, and finally use of halothane in the respired gas mixture) [4]. The causes of the status asthmaticus in the three patients were atopic asthma, an intratracheal intubation-induced reaction and bronchiolitis. The patient with bronchiolitis had needed cardiopulmonary resuscitation on her way to hospital, following cardiac arrest due to asphyxia. The extreme bronchospasm made mechanical ventilatory support impossible. Inflation of the lungs was achieved using an Ambu bag, while a second person manually squeezed air out of the chest (by applications of firm, long-lasting pressure downwards on the wall of the thorax). The bronchospasm in our three patients was so severe that only 4-5 respiratory cycles per minute were possible. Rapid administration of intravenous (i.v.) epinephrine, 1 mg per 500 mL of crystalloid, resulted in some improvement. After about 20 min of respiratory support using the Ambu bag and continuous epinephrine infusion the bronchospasm decreased enough to allow artificial ventilation with the lung ventilator (tidal volume 8 mL kg−1; frequency 6 min−1; peak flow 30 L min−1). The peak inspiratory pressures ranged from 50 to 60 cmH2O. Our attempts to reduce the rate of the epinephrine infusions in our three patients resulted in worsening of the bronchospasm. We therefore decided to try high subarachnoid blocks. We kept the epinephrine infusions running, at a rate depending on arterial pressure, while we performed the blocks. With the patients in the lateral decubitus position, a 22 G needle was inserted into the subarachnoid space at L3-4. After withdrawal of cerebrospinal fluid, 4 mL of 5% lidocaine solution (Grave Lignocaine, Polfa, Poland) was injected into the subarachnoid space with the patients tilted about 30° head down. When the injection was complete the patients were turned into the supine position but still kept head down for the next 15 min. We administered i.v. crystalloid solutions during the procedure. In two patients the bronchospasm decreased several minutes after the blockade, and subsided within the hour. In the third patient the high subarachnoid block only resulted in a reduction of peak inspiratory pressure. However, this was enough to allow mechanical ventilation of the lungs; in this patient we had previously unsuccessfully attempted a stellate ganglion block before attempting the TSB. All patients received 3 L of electrolyte i.v. during the first hour after the high subarachnoid block. Persistent hypotension in one patient (who had bronchiolitis) was the only complication of the high subarachnoid block despite intensive compensation of relative oligaemia. In the remaining two patients only a short period of arterial hypotension occurred. Our three patients with these high subarachnoid blocks were flaccid, with dilated fixed pupils; body temperature was 36°C. These signs subsided over the next 8 h and the hypotonia gradually improved. The bronchospasm did not recur in two of the patients and their psycho-neurological status was considered normal. Bronchospasm - due to bronchiolitis - subsided in the third patient only after removal of mucopurulent plugs from the lungs. She was referred to the Neurology Department 21 days later with symptoms of brain damage. It is difficult to know whether this was a result of the cardiac arrest in the pre-hospital period, or from difficulties in controlling arterial pressure after the TSB. In conclusion, the bronchospasm subsided during subarachnoid anaesthesia under circumstances that could be considered as life-threatening. One must always be aware of the need to maintain an adequate circulation in the face of a high subarachnoid block. C. PAKULSKI Department of Anaesthesiology and Intensive Care, University School of Medicine, Szczecin, Poland A. ŚWINIARSKI G. JASZCZYK Department of Anaesthesiology and Intensive Care, General Hospital, Szczecin, Poland" @default.
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• W4206351720 date "2000-09-01" @default.
• W4206351720 modified "2023-09-27" @default.
• W4206351720 title "High subarachnoid block for severe bronchospasm" @default.
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