In 1995, Kilka and colleagues described the infraclavicular vertical brachial plexus blockade approach as a safe and successful method for upper limb anaesthesia . Owing to the rapid and complete blockade of the entire upper extremity, this technique has received increasing acceptance, despite reports of pneumothorax . However, the incidence of pneumothorax may be expected to be very low when the needle is placed according to Kilka and colleagues' original description . We report on two patients who developed transient respiratory compromise associated with infraclavicular vertical brachial plexus blockade resulting from ipsilateral paralysis of the diaphragm.
The first patient was an 84-yr-old female, 74 kg body weight, who presented for surgery of the left forearm. She had arterial hypertension, pulmonary emphysema and myocardial insufficiency (NYHA II); a preoperative chest radiograph was normal. Standard monitoring was established; heart rate (HR) 90 beats min−1, arterial pressure 170/95 mmHg, SpO2 92% during room air breathing and 97% with 3 L min−1 oxygen via a nasal cannula. Intravenous (i.v.) access was established and slight sedation was provided with midazolam 2 mg i.v. Blockade of the brachial plexus was achieved in the supine position at the site recommended by Kilka and colleagues . In brief, the puncture site was established midway between the ventral process of the acromion and the jugular fossa - caudal in immediate proximity of the clavicle. Following local anaesthesia (mepivacaine 1% 2 mL), the needle (Stimuplex D®, 25-G, 55 mm; Braun, Germany) was advanced in a strictly vertical direction (i.e. the stretcher, rather than the patient's skin, was used as plane of reference). Muscular contractions were elicited in extender and flexor muscles of the left forearm using a nerve stimulator at 0.1 ms and 0.8 mA (Stimuplex HNS 11®; Braun, Germany). After reduction of the current to 0.3 mA and negative aspiration control, we injected prilocaine 1% 40 mL (400 mg) for rapid onset of analgesia and ropivacaine 0.75% 10 mL (75 mg) for prolonged postoperative pain relief. Adequate neural blockade of the left forearm was achieved after approximately 10 min. Twenty minutes after the injection, the patient developed expiratory stridor and dyspnoea with a respiratory rate of 22 breaths min−1. Peripheral oxygen saturation decreased to 89%, although the patient was receiving oxygen 3 L min−1 through the nasal cannula. Oxygen flow was increased to 5 L min−1 by a facemask leading to an increase in the saturation to 96%. Dyspnoea diminished almost completely within a few minutes. Auscultation revealed decreased breathing sounds over the left lung. A chest radiograph was taken immediately, which showed an elevated left diaphragm; a pneumothorax and other lung-related pathology was excluded by an experienced radiologist. Surgery was carried out without any problem. The patient remained in a stable condition and was monitored over 2 h. She was discharged to the ward with stable vital signs and without any apparent discomfort. The neural blockade of the brachial plexus lasted for 7 h.
The second patient was a 47-yr-old female who was scheduled for surgery of the right forearm with regional anaesthesia. The medical history revealed arterial hypertension, gastric reflux disease and obesity (weight 82 kg, height 158 cm). A previous chest radiograph was normal. She received oxazepam 10 mg orally for premedication. Standard monitoring was established: HR 70 beats min−1, arterial pressure 115/70 mmHg, SpO2, breathing room air, 97%. Then an infraclavicular vertical brachial plexus blockade was achieved in the supine position as described for the first patient; using the same procedure, prilocaine 1% 40 mL followed by ropivacaine 0.75% 10 mL was injected. Ten minutes after the injection, the patient developed dyspnoea (respiratory rate 25 breaths min−1) and her oxygen saturation decreased. Oxygen was given through a nasal cannula (3 L min−1) and it resulted in a return of SpO2 to baseline values and the dyspnoea resolved. A chest radiograph revealed an elevated right diaphragm. As with the first patient, a pneumothorax and other lung-related pathology were excluded by an experienced radiologist. The patient had no further discomfort or impairment of vital signs. One hour after surgery she was discharged from the recovery room to the ward in stable condition. After an additional 4 h, the neural blockade of the brachial plexus resolved (total duration of the block was 6 h).
Both patients presented with transient respiratory compromise after infraclavicular vertical brachial plexus blockade. Pneumothorax was excluded in both cases. Thus, respiratory compromise was probably caused by a paresis of the ipsilateral diaphragm. An infraclavicular vertical brachial plexus blockade may induce blockade of the phrenic nerve, leading to a paralysis of the ipsilateral diaphragm, which may subsequently cause dyspnoca in susceptible patients.
The incidence of hemidiaphragmatic paralysis due to phrenic nerve block after interscalene brachial plexus anaesthesia was almost 100% . Healthy patients are usually unaware of the presence of a paralysed hemidiaphragm and tolerate an unilateral phrenic nerve block without problems . Even the function of only one-half of the diaphragm can generate sufficient negative intrathoracic pressure to ensure adequate respiration at rest . To our knowledge there are no reports on the incidence of unilateral paralysis of the phrenic nerve after infraclavicular vertical brachial plexus blockade, and only one case report has been published recently .
In contrast to healthy individuals, the clinical appearance of dyspnoea in our patients may have resulted from a combination of several factors. Both patients received benzodiazepines for sedation, yet remained co-operative and alert throughout the entire clinical course, suggesting that the contribution of the premedication was limited. The first patient had pulmonary emphysema, which may have been an important cofactor regarding the observed symptoms. In patients with parenchymal destruction, adequate diaphragmatic function is important for sufficient gas exchange, and a 50% loss of function may result in significant impairment . Obesity, observed in our second patient, is associated with the mass of the abdominal shifting the diaphragm more cephalad (in the supine position), thereby reducing functional residual capacity and respiratory function . Thus, both patients had decreased pulmonary reserves before the infraclavicular vertical brachial plexus blockade.
In patients with decreased pulmonary reserve, the use of infraclavicular vertical brachial plexus blockade should therefore be restricted. If appropriate for the planned surgical procedure, these patients are likely to benefit from the axillary approach to the brachial plexus, thus avoiding the risk of phrenic nerve paresis. We believe that the central spread of the local anaesthetic from the site of the injection towards the phrenic nerve was most likely responsible for the observed symptoms. The onset of dyspnoea was delayed compared with the manifestation of the sensomotor blockade. In addition, the respiratory symptoms resolved 4-5 h earlier than the neural blockade of the brachial plexus. We may speculate that a smaller volume of the local anaesthetic may reduce the risk of a subsequent block of the phrenic nerve.
In summary, we report on two cases of transient respiratory compromise following infraclavicular vertical brachial plexus blockade, most probably due to an ipsilateral phrenic nerve anaesthesia and subsequent paralysis of the hemidiaphragm. Our findings emphasize the risk of respiratory impairment associated with this regional anaesthetic technique. In patients with reduced pulmonary reserve, this risk should be weighed carefully against the benefits.
F. M. Heid
A. M. Brambrink
Clinic of Anaesthesiology; Johannes Gutenberg-University Hospital; Mainz, Germany
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