Air embolism during anaesthesia for shoulder arthroscopy

British Journal of Anaesthesia 85 (6): 911±13 (2000)

CASE REPORTS Survivors of childhood cancers: implications for obstetric anaesthesia H. Gorton1*, R. Wilson2, A. Robinson2 and G. Lyons2 1

Academic Unit of Anaesthesia, Leeds General In®rmary, Leeds LS1 3EX, UK. 2Obstetric Anaesthesia, St James's University Hospital, Leeds LS9 7TF, UK *Corresponding author Treatment of many childhood malignancies involves surgery, radiotherapy and chemotherapy. If the child survives, normal physical development can be impaired and abnormalities with anaesthetic implications may be present. We discuss two women with a range of problems who presented for obstetric anaesthesia, having survived childhood malignancies. Common features included anthracycline cardiotoxicity and short stature. Both patients received incremental spinal anaesthesia in order to titrate the dose of local anaesthetic required to produce an adequate block height and to minimize cardiovascular instability. Br J Anaesth 2000; 85: 911±13 Keywords: anaesthesia, obstetric; children, cancer; anaesthetic techniques, epidural Accepted for publication: July 20, 2000

Modern, aggressive treatment of paediatric malignancies has enabled survival into adulthood. There is a small but increasing cohort of women of reproductive age who were treated with chemotherapy, radiotherapy and surgery in childhood. Although infertility and pregnancy loss are more common in such women, a signi®cant number of them have successful pregnancies.1 The consequences of chemotherapy, radiation and surgery will differ according to the site of the malignancy treated, but presentations in adulthood have common features. We present two women who survived childhood cancer and illustrate some of the dif®culties that were encountered. The infants of both women were delivered by elective Caesarean section and both women requested regional anaesthesia.

Case 1 A 25-yr-old primipara presented to the anaesthesia clinic before elective Caesarean section at 34 weeks of gestation. At the age of 10 months, a mass around the right adrenal had been diagnosed as stage IV neuroblastoma. She had been treated with nephrectomy, adrenalectomy, radiotherapy and chemotherapy (vincristine, cyclophosphamide and doxorubicin). She was short in stature (145 cm, 4 ft 10 inches), and had a deformity of her right hip and a signi®cant thoracolumbar scoliosis, which was not severe enough to

limit respiratory function; pulmonary function tests had not been performed. She had suffered anthracycline cardiotoxicity, a dose-dependent complication of therapy with doxorubicin and daunorubicin. There was myocyte damage resulting from the production of free radicals, and cardiac growth was impaired.2 Echocardiography 3 days before the operation demonstrated an ejection fraction of 45% and fractional shortening of 22%. Increasing breathlessness during pregnancy was ascribed to worsening cardiac function, for which she was taking lisinopril 7.5 mg daily. She was hypertensive (130/100 mm Hg), and methyldopa 250 mg twice daily had been added during pregnancy as the hypertension worsened. Renal function was normal. Because of her problems, her obstetrician had already chosen Caesarean delivery, and she requested regional anaesthesia. Two doses of dexamethasone 4 mg were given before delivery in an attempt to improve fetal lung maturity. From the history and examination in the clinic, it was felt that reduced cardiac reserve posed the greatest anaesthetic problem, and that technical dif®culty with regional block arising from scoliosis was a secondary concern. No respiratory problems were anticipated, and further investigations were not thought to be necessary. The plan agreed upon for anaesthesia was to use an incremental subarachnoid technique, with invasive arterial monitoring but without a pulmonary artery ¯otation catheter.

Ó The Board of Management and Trustees of the British Journal of Anaesthesia 2000

Gorton et al.

Before operation, a 20-gauge cannula was inserted into the left radial artery, and a 16-gauge i.v. cannula was inserted into a forearm vein. An infusion of Gelofusine (B. Braun Medical Ltd, Aylesbury, UK) 500 ml was commenced. Further monitoring included ECG and pulse oximetry. In the sitting position, a 26-gauge Quincke spinal needle was inserted with dif®culty into the L3/4 interspace. A 32-gauge catheter (TFX Medical, Lurgan, N. Ireland) was then inserted and the needle removed. Two centimetres of catheter was placed in the subarachnoid space. Initially, 0.5% w/v hyperbaric bupivacaine 1 ml and diamorphine 0.4 mg were injected whilst the patient was sitting. A further 500 ml of Gelofusine containing ephedrine 30 mg was commenced. The patient was then moved into a tilted left supine position. After 10 min, plain bupivacaine 2.5 mg was injected. Sensation was blocked up to T6 on the right and T4 on the left. Caesarean section was performed without incident. Transient hypotension (systolic pressure of 60 mm Hg) occurred on administration of a test dose of Syntocinon 1 IU, and no further oxytocic was given. A live female baby weighing 2 kg was delivered. Apgar scores at 1 and 5 min were 8 and 9 respectively, and the umbilical arterial pH was 7.36. For postoperative analgesia, the patient received diclofenac 100 mg per rectum, and thereafter up to 150 mg orally per day, and paracetamol 1000 mg/codeine 60 mg as required to a maximum of six doses per day. The intrathecal catheter was removed in the recovery ward 2 h after operation. We continued invasive monitoring for 24 h after delivery and the patient was stable throughout this period. Blood loss at delivery was estimated at 500 ml, but the haemoglobin had decreased to 8.1 g dl±1 on the ®rst postoperative day and 3 units of blood was transfused. The patient was seen by an anaesthetist for three consecutive days to identify complications of regional block. No such complications were apparent. The mother and baby were discharged home after 5 days. Antihypertensive medication was continued on discharge.

Case 2 A 24-yr-old primipara presented at 33 weeks for urgent Caesarean section with only a few hours' notice. The membranes had ruptured prematurely and markers of infection, especially raised C-reactive protein (11 mg litre±1), were causing increasing concern about chorioamnionitis. The patient was apyrexial and had no other clinical signs of systemic infection. The patient had been treated successfully with radiotherapy and chemotherapy for rhabdomyosarcoma of the pharynx as a child. She had been informed that the treatment would result in infertility, so did not use contraception and the pregnancy was unplanned. She requested regional anaesthesia. On examination she was of short stature (147 cm, 4 ft 11 inches) and had mandibular hypoplasia, which was considered likely to cause dif®culty with intubation

(Mallampati grade 2). There was little opportunity for further investigation. Cardiomyopathy secondary to an unknown anthracycline had been diagnosed previously and mid-trimester echocardiography demonstrated an ejection fraction of 60% and fractional shortening of 23%. Her medical history included fractured lumbar spine, for which no details were available. She was taking thyroxine because treatment had resulted in thyroid hypoplasia. An incremental subarachnoid technique was chosen. In case regional anaesthesia was not successful, facilities for awake ®bre-optic intubation were available. Before the block, monitoring with ECG, non-invasive arterial blood pressure and pulse oximeter were established. An i.v. cannula was placed in a forearm vein and Gelofusine 500 ml was given. In the absence of signs and symptoms of heart failure, invasive monitoring was considered unnecessary. Aseptic techniques were used, including gown, hat and mask. The skin was prepared with alcohol solution. We used a needle-through-needle technique with a Spinocath kit (B. Braun Medical, Melsungen, Germany). An 18-gauge Tuohy needle was placed in the epidural space and a 24-gauge catheter was threaded over a 29-gauge Quincke spinal needle passed intrathecally. Both needles were then withdrawn. An i.v. infusion of ephedrine 30 mg in Gelofusine 500 ml was begun with the ®rst intrathecal injection. Three increments of 0.5% w/v hyperbaric bupivacaine were given (10 mg in total), together with 0.5% w/v plain bupivacaine 4 mg, and diamorphine 0.4 mg, without achieving a satisfactory block. At this point it was decided that the tip of the catheter might be positioned in a caudad direction and the catheter was withdrawn 2 cm. Hyperbaric bupivacaine 0.5% w/v 2.5 mg and 0.5% w/v plain bupivacaine 5 mg were then given, producing excellent anaesthesia with abolition of sensation bilaterally to T5. There was no haemodynamic disturbance, and the patient was stable throughout. A female baby was delivered, and the umbilical arterial pH was 7.28. Syntocinon 10 units was given slowly via the i.v. infusion on delivery, without detectable hypotension. Prophylactic cefuroxime 750 mg and metronidazole 500 mg were given i.v. in the operating theatre and continued orally for 5 days. Postoperative analgesia consisted of diclofenac and paracetamol/codeine. The estimated blood loss at delivery was 700 ml. The intrathecal catheter was removed in the recovery ward. The next day, haemoglobin was recorded as 9.8 g dl±1 and 3 units of blood was transfused. An anaesthetist visited the patient for 3 days to identify complications of regional blockade. The mother and baby were discharged home after 5 days.

Discussion Despite different original pathologies, these two survivors of paediatric malignancy have common features.

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Obstetric anaesthia in survivors of childhood cancer

Anthracyclines are a family of cytotoxic antibiotics. Anthracycline cardiomyopathy is a dose-dependent complication of therapy with doxorubicin and daunorubicin, which damages myocytes and impairs cardiac growth.2 If given in childhood, normal cardiac growth is impaired, leading to permanent cardiac dysfunction. The toxicity has been attributed to the production of free radicals. The incidence of cardiomyopathy after chemotherapy is unknown, and whether a safe dose exists has not been clari®ed. Changes are irreversible and are characterized by a poorly compliant myocardium3 that is likely to respond poorly to changes in preload and afterload. Diagnosis is made clinically, using echocardiography or cardiac catheterization, but may be con®rmed histologically, showing hypertrophy and ®brosis of myocytes.3 Both our patients had impairment of left ventricular function, but one woman was symptomatic with breathlessness, indicating a degree of cardiac failure. Her limited cardiac reserve presumably accounted for the hypotension after administration of 1 unit of Syntocinon. We did not think it advisable to give a further dose. Our second patient, despite a fractional shortening of 23%, was asymptomatic and tolerated Syntocinon well. Clinical assessment correctly identi®ed which woman posed the greater risk. The long-term prognosis of this condition may be poor, and transplantation has been required.4

resistance signi®cantly and increase afterload.9 Syntocinon, a synthetic form of the naturally occurring oxytocin, has greater cardiac stability, but is known to cause hypotension with bolus administration.10 The mechanism for this is debatable. Possible causes are a reduction in venous pressure, a decrease in vascular resistance, and negative inotropy, or a combination of these.10 Death at Caesarean section has occurred after bolus administration of Syntocinon in a woman with congenital heart disease.11 Our experience demonstrates that even minute doses of Syntocinon can cause worrying hypotension in the presence of poor myocardial function. It has been suggested that slow infusion of Syntocinon may reduce the incidence of hypotension.9 Cardiac output monitoring is justi®ed when effects are predicted to be severe. Survivors of childhood cancers will present with increasing frequency for obstetric anaesthesia both to regional centres and to district general hospitals. It is likely that these women will have abnormalities affecting anaesthesia and a management plan should be made in the antenatal period. Adult survivors with lifelong cardiac impairment secondary to anthracyclines are an emerging problem. The ®rst exposure of young adult cancer survivors to anaesthesia may occur with their ®rst pregnancy, and the obstetric anaesthetist may be the ®rst to test cardiac performance and to deal with the sequelae of their treatments.

Scoliosis and short stature

References

Anthracycline cardiotoxicity

Scoliosis can be a cause of short stature. In our ®rst case, the scoliosis was presumed to be secondary to radiation-induced hip deformity. The spine may also be affected during the irradiation of midline tumours,5 and deformity, white matter injury, osteoporosis and epidural space scarring has been documented.5 Norris recommended one dose of single-shot intrathecal local anaesthetic for regional block, assuming normal anatomy, but of the 50 women included in that study only one was less than 150 cm tall.6 Scoliosis and short stature can cause uncertainty about the dose of intrathecal local anaesthetic required. Our solution to potential problems within the epidural space is to use an intrathecal approach, and because of uncertainties over dose we titrated the local anaesthetic through an indwelling catheter. This had the added advantage of a slow onset of block, avoiding cardiovascular upset.7 An additional factor in our choice was that we have signi®cant experience with Caesarean delivery in scoliotics using continuous intrathecal anaesthesia.8

Oxytocics Oxytocics are used to provide uterine contraction and haemostasis after delivery. Two drugs are commonly used for this purpose: ergometrine and Syntocinon, singly or in combination. Ergometrine, an ergotamine alkaloid, is a powerful oxytocic but is known to raise systemic vascular 913

1 Byrne J. Infertility and premature menopause in childhood cancer survivors. Med Ped Oncol 1999; 33: 24±8 2 Green M. Anthracycline cardiotoxicity, no longer an issue? Ann Oncol 1998; 9: 691±3 3 Lipshultz SE, Colan SD, Gelber RD, Perez-Atayde AR, Sallan SE, Sanders SP. Late cardiac effects of doxorubicin therapy for acute lymphoblastic leukemia in childhood. N Engl J Med 1991; 324: 808±15 4 Levitt G, Bunch K, Rogers CA, Whitehead B. Cardiac transplantation in childhood cancer survivors in Great Britain. Eur J Cancer 1996; 32A: 826±30 5 Hilton AR, Lockhart EM, Penning DH. Epidural analgesia in parturients with previous spinal irradiation. Can J Anaesth 1998; 45: 884±7 6 Norris MC. Height, weight and the spread of spinal anaesthesia for cesarean section. Anesth Analg 1988; 67: 555±8 7 Moran DH, Johnson MD. Continuous spinal anesthesia with combined hyperbaric and isobaric bupivacaine in a patient with scoliosis. Anesth Analg 1990; 70: 445±7 8 Lyons G, Gorton H. Scoliosis and spinal surgery: use of spinal catheter for delivery. Eur J Anaesth 2000; 17 (Suppl. 19): A499 9 Rocke DA, Rout CC. Anaesthesia and cardiac disease. In: Norris MC, ed. Obstetric Anaesthesia, edn 2. Philadelphia: Lippincott, 1999; 441±52 10 Dennehy KC, Rosaeg OP, Cicutti NJ, Krepski B, Sylvain JP. Oxytocin injection after caesarean delivery: intravenous or intramyometrial? Can J Anaesth 1998; 45: 635±8 11 Department of Health. Report on con®dential enquiries into maternal deaths in the United Kingdom 1979±1981. London: HMSO, 1986


Prolonged vecuronium neuromuscular blockade associated with Charcot Marie Tooth neuropathy D. Pogson1*, J. Telfer2 and S. Wimbush2 1

Department of Anaesthesia, Derriford Hospital, Plymouth PL6 8DH, UK. 2Department of Anaesthesia, Royal Cornwall Hospital, Truro TR1 3LJ, UK *Corresponding author

Charcot Marie Tooth (CMT) disease comprises a group of disorders characterized by progressive distal muscle weakness and wasting. Review of the anaesthetic literature produced con¯icting reports concerning the responses to neuromuscular blocking drugs in these patients. We describe a case in which vecuronium 0.11 mg kg±1 produced prolonged neuromuscular blockade lasting 115 min in a patient with the condition. Conduction velocity in the facial nerve is usually less affected than the ulnar or peroneal nerve in CMT patients. This nerve may be more useful in monitoring neuromuscular blockade, both in titrating the dose of neuromuscular blocking drug and ensuring adequate reversal at the end of a procedure. Recent advances in molecular biology have enabled identi®cation of the underlying genetic abnormalities and pathophysiology of CMT. These advances are reviewed and implications of CMT for the anaesthetist discussed. Br J Anaesth 2000; 85: 914±17 Keywords: neuromuscular block, vecuronium; complications, Charcot Marie Tooth disease Accepted for publication: July 10, 2000

Charcot Marie Tooth (CMT) neuropathy affects 1 in 2500 people and accounts for a large proportion of the neuropathic diseases encountered in clinical practice.1 The condition causes atrophy and weakness of the distal muscles due to diminished nerve conduction. The spectrum of severity varies from asymptomatic individuals to those with severe limb abnormalities requiring corrective surgery. There are few descriptions of the anaesthetic management of patients with CMT. Both prolonged and attenuated responses to neuromuscular blocking drugs have been described.2-5 Such variation between patients may be accounted for by variations in disease severity. Autosomal dominant and X-linked genetic defects may occur in these patients, resulting in point mutations or multiple expression of genes encoding myelin proteins.6 Axonal loss or demyelination occurs, enabling classi®cation of CMT according to nerve biopsy and conduction studies.7 CMT is now considered to be a heterogeneous group of polyneuropathies. The severity of symptoms may differ between the subtypes. It is appropriate to review recent advances in our understanding of the condition and the anaesthetic experience that has been described.

Case report A 59-yr-old, 74 kg male with CMT neuropathy presented with a fractured right proximal ®bula and distal tibia, requiring open reduction and internal ®xation with a tibial nail. The patient had been diagnosed as having CMT in May 1987 in a medical report for retirement on the grounds of ill health. The diagnosis was made on clinical grounds, with examination revealing high foot arches and distal muscle wasting involving the forearms, interossei in the hands, and all muscles below the knee. His arm tendon re¯exes were brisk and symmetrical but knee and ankle jerks were absent with ¯exor plantar responses. Sensation was normal and there was no ataxia. He described himself as always having been weak. He had no siblings but described his father as having been of the same build. Electromyography had not been performed. The patient underwent L5-S1 discectomy in 1983, receiving thiopental 225 mg, tubocurarine 40 mg and halothane. The operation lasted 75 min. There was no comment in the anaesthetic record regarding reversal of residual neuromuscular blockade, nor were any problems recorded. In 1996, he underwent insertion of a dynamic hip screw of his left femur and received midazolam 2 mg, propofol 100 mg, and atracurium 30 mg at


Vercuronium and Charcot Marie Tooth neuropathy

induction followed by atracurium 10 mg after 30 min. This operation lasted 50 min. Acetylcholinesterase inhibitors were not given. On neither occasion was any neuromuscular monitoring used. No adverse events or clinical evidence of prolonged neuromuscular block were noted. After his hip fracture, a diagnosis of osteoporosis was made using bone density studies. He received alendronate 10 mg day±1 and calcium supplementation. His corrected serum calcium was 2.59 mmol litre±1 with an inorganic phosphate of 1.00 mmol litre±1 prior to this operation. Serum potassium was 4.6 mmol litre±1. On this occasion the patient was unpremedicated. He received morphine 10 mg and thiopental 350 mg at induction. Vecuronium 0.11 mg kg±1 was administered and after 2 min the trachea was intubated easily with a size 9 mm cuffed oral tracheal tube. Anaesthesia was maintained with iso¯urane 1% in nitrous oxide/oxygen 2:1. No further opiates were given. A peripheral nerve stimulator was not used at the outset because no problems had been identi®ed from the previous anaesthetic records. The operation lasted approximately 115 min, during which time no further drugs were given. At the end of the procedure the lungs were ventilated with FIO2 1.0 and the patient received neostigmine 2.5 mg with glycopyrrolate 500 mg. A peripheral nerve stimulator was not used at this stage. It was felt that suf®cient time had passed since induction for recovery from neuromuscular blockade to occur. Spontaneous diaphragmatic breathing with an adequate tidal volume followed and the tracheal tube was removed uneventfully although the patient was not fully conscious. He was then transferred to the recovery room with oxygen administered by facemask. In recovery, the patient became anxious and distressed, with signs of incomplete reversal of neuromuscular block including twitching of the limbs and uncoordinated movements. Oxygenation and ventilation remained normal. A peripheral nerve stimulator was applied ®rst to the right ulnar nerve. Trains of four stimuli were applied. There was a palpable twitch response to the ®rst stimulus only. As clinically obvious muscle wasting was present in the forearm muscles the nerve stimulator was applied to the right facial nerve. Again, a twitch response was only visible to the ®rst stimulus of the train of four. Double burst stimulation was not used as partial reversal was clinically obvious and it was felt this would subject the patient to further distress. A second dose of neostigmine 2.5 mg was given, resulting in all four twitches of the train of four response in the facial muscles being visible within 2 min. The patient's condition improved and he was transferred to the high dependency unit for overnight observation and returned to the ward on the next day.

Discussion Charcot Marie Tooth neuropathy comprises a heterogeneous group of peripheral nerve diseases affecting adults and children.7 There is a typical clinical picture with distal muscle weakness and atrophy affecting the intrinsic muscles of the foot, the peronei and tibialis anterior. Both motor and sensory function may be affected. Deep tendon re¯exes are diminished or absent. There is a spectrum of clinical presentation from severe atrophy with limb abnormality to pes cavus. A signi®cant proportion of CMT patients are not identi®ed because their symptoms do not cause them to consult a doctor. Most patients with the condition have manifestations by their second decade, seldom presenting after 30 yr. Upper limb involvement tends to occur later. Clinical studies in CMT families using nerve biopsies and nerve conduction studies enabled a separation of these patients into two main groups.8 In CMT1 there is a marked reduction in nerve conduction velocity with demyelination; nerve conduction velocity in the ulnar, median and peroneal nerves is commonly half that in normal subjects.7 The muscle action potential amplitude is half normal, and the nerve latency three times as long on average; 25% of patients have clinically thickened peripheral nerves. Those adolescents with the slowest conduction velocities tended to have a worse neurological de®cit in later life. In CMT2 the nerve conduction velocity is normal or low normal.9 There is axonal loss but no prominent demyelination. In this type the clinical symptoms may present later, even in middle age. Although the features are similar to CMT1, there is said to be less upper limb involvement and the peripheral nerves are less enlarged. The two types cannot be distinguished solely on clinical grounds because there is such a range of severity of symptoms. Nerve conduction studies are often performed in the median or ulnar nerves because distal nerve degeneration is often complete in the lower limbs. In fact, motor nerve conduction velocity is commonly less than 60% normal in all nerves studied, including the facial nerve. Advances in molecular biology and gene mapping have enabled the underlying genetic abnormalities in CMT to be identi®ed. In the majority of cases of CMT1 and CMT2 the inheritance is autosomal dominant.10 There are also much rarer X-linked and autosomal recessive variants. CMT1 can be subdivided on the basis of the gene defect. In CMT1a there is a duplication at the 17p11, 2±12 locus. This area codes for the PMP22 gene resulting in multiple expression. PMP22 is a major component of peripheral nerve myelin. The result may be a new Schwann cell phenotype that has defective myelin stability and increased turnover.10 In CMT1b there are point mutations in the myelin protein P0 gene.6 This codes for the major myelin protein in peripheral nerves, accounting for 50% of the mass. It has been suggested that the neurological disability in CMT1b is worse than in CMT1a. In X-linked CMT (CMTX), which is clinically similar to CMT1, there are mutations in the

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connexin 32 gene. This encodes a gap junction channel protein that may play a role in transmission at nodes of Ranvier. Dejerine Sottas disease, or CMT3, is a severe variant with onset in infancy. There may be point mutations in the P0 or PMP22 genes. The clinical features overlap with severe CMT1. CMT2 accounts for 25% of cases.9 There does not appear to be a unifying genetic defect. As 1 in 2500 people has some form of CMT, it is surprising that case reports concerning anaesthesia in CMT sufferers are rare. In one report, the notes of seven patients under 16 yr who were anaesthetised over a 10 yr period were reviewed.11 These patients received both depolarizing and nondepolarizing neuromuscular blocking drugs. There were no recorded adverse effects of succinylcholine and no cases of prolonged response to a range of non-depolarising neuromuscular blocking drugs. However, the authors conceded that the methods used to assess neuromuscular function varied widely. Antognini reviewed the operative charts of 86 patients with CMT identi®ed by postal questionnaire to members of a CMT help group.12 In 161 surgical procedures on these patients anaesthetic complications were few, although the study is necessarily biased because non-responders are excluded. In addition, anaesthetic management and inclusion criteria for CMT could not be standardized. 48% of patients received succinylcholine with no recorded adverse effect. A paralysing dose of non-depolarizing neuromuscular blocking drug was used in 45% of patients. How neuromuscular block was monitored and reversed is not known. There were no descriptions of objective weakness or prolonged intubation. Despite the absence of adverse effects after succinylcholine, it would seem prudent to avoid this drug in CMT if possible as hyperkalaemia is well reported in other similar polyneuropathies and denervation injuries. There is no evidence to suggest that patients with CMT are susceptible to malignant hyperthermia. Another report studied 20 patients with CMT presenting for orthopaedic procedures.2 The authors found that CMT sufferers required less thiopental for induction than controls. The report is of interest because one female patient received vecuronium 0.07 mg kg±1 at induction and subsequently did not exhibit a normal twitch response or spontaneous ventilation for 280 min. In addition, the ulnar nerve twitch response was absent in six of the 20 patients. In these six patients, the facial nerve was used for evaluation of neuromuscular block. A review of the literature concerning anaesthesia for CMT revealed few detailed case reports. One describes prolonged arti®cial ventilation due to respiratory muscle involvement in pregnancy.13 Another describes a 17-yr-old who underwent anaesthesia on two occasions and showed no prolonged response to either mivacurium or atracurium.3 Baraka described a 16-yr-old girl who underwent a tendon transfer under general anaesthesia using vecuronium. In this case, the T4/T1 ratio recovered to 25% after 20 min and further supplementation was required. Residual neuromus-

cular blockade was readily reversed after 90 min. The author suggested that upregulation of acetylcholine receptors at the neuromuscular junction due to the generalized polyneuropathy might account for the resistance to vecuronium even in the presence of muscle weakness and atrophy.4 One case report demonstrated a potential dif®culty in monitoring neuromuscular block in CMT patients. In a 17yr-old neurosurgical patient, it was not possible to elicit responses from either tibial nerve following vecuronium 0.1 mg kg±1 after 100 min. The muscle response was either too delayed or too small in amplitude to be recorded.5 This is perhaps unsurprising as the tibial nerves are among the worst affected by demyelination in CMT. The use of peripheral nerve stimulators in CMT has been shown to be misleading if a nerve with delayed conduction or increased latency is chosen. One solution would be to monitor relaxation after induction using a less affected peripheral nerve such as the facial nerve. A suitable site for neuromuscular monitoring should be identi®ed before a neuromuscular blocking drug is administered. The drug can then be titrated to effect and adequate reversal identi®ed. Case reports have been described in the literature of patients with CMT undergoing central neural blockade without neurological sequelae.14 15 Posterior column demyelination has been noted in autopsies of some CMT patients, however. A balanced risk assessment in considering central blockade would seem prudent lest any deterioration be blamed on the anaesthetic technique. Autonomic neuropathy is not a major ®nding in CMT. It is usually limited to decreased sweating in the extremities. Autonomic neuropathy does not feature as a clinical problem in any anaesthetic case reports. Clinically palpable nerve enlargement occurs in 25% of patients with CMT 1. These patients may be at greater risk of positional nerve injuries due to pressure during prolonged procedures. In addition, the use of regional blockade in areas such as the elbow may carry additional risk. Given the incidence of CMT and the fact that many cases go unrecognized, it would seem that anaesthesia for these patients must be generally uneventful. The cases presenting for corrective limb surgery must be the worst affected and yet adverse events are seldom described.

References

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1 Mendell J. Charcot Marie Tooth related disorders. Semin Neurol 1998; 18: 41±7 2 Kotani N, Hirota K, Anzawa N, Takamura K, Sakai T, Matsuki A. Motor and sensory disability has a strong relationship to induction dose of thiopental in patients with the hypertrophic variety of Charcot-Marie-Tooth syndrome. Anesth Analg 1996; 82: 182±6 3 Naguib M, Samarkandi A. Response to atracurium and mivacurium in a patient with Charcot Marie Tooth disease. Can J Anaesth 1998; 45: 56±9 4 Baraka A. Vecuronium neuromuscular block in a patient with Charcot Marie Tooth syndrome. Anesth Analg 1997; 84: 927±8

Severe unilateral bronchospasm mimicking inadvertent endobronchial intubation

5 Fiacchino F, Grandi L, Ciano C, Sghirlanzoni A. Unrecognised Charcot Marie Tooth disease: Diagnostic dif®culties in the assessment of recovery from paralysis. Anesth Analg 1995; 81: 199±201 6 Keller M, Chance P. Inherited neuropathies: from gene to disease. Brain Pathol 1999; 9: 327±41 7 Dyck P, Chance P, Lebo R, Carney J. Hereditary motor and sensory neuropathies. In: Dyck P, Thomas P, Eds. Peripheral Neuropathy. New York: Saunders, 1993; 1094±136 8 Dyck P, Lambert E. Lower motor and sensory neurone diseases with peroneal muscular atrophy. Neurologic, genetic and electrophysiological ®ndings in various neuronal degenerations. Arch Neurol (Chic) 1968; 18: 603±25 9 Thomas P, King R. The pathology of CMT disease and related disorders. Neuropath Appl Neurobiol 1996; 22: 269±84

10 Hannemann C, Muller H. Pathogenesis of CMT1a neuropathy. Trends Neurosci 1998; 21: 282±6 11 Greenberg R, Parker S. Anesthetic management for the child with Charcot Marie Tooth disease. Anesth Analg 1992; 74: 305±7 12 Antognini J. Anaesthesia for Charcot Marie Tooth disease: a review of 86 cases. Can J Anaesth 1992; 39: 398±400 13 Byrne D, Chappatte O, Spencer G, Raju K. Pregnancy complicated by Charcot Marie Tooth disease requiring intermittent ventilation. Br J Obstetr Gynaecol 1992; 99: 79±80 14 Reah G, Lyons GR, Wilson RC. Anaesthesia for caesarean section in a patient with Charcot Marie Tooth disease. Anaesthesia 1998; 53: 586±8 15 Scull T, Weeks S. Epidural analgesia for labour in a patient with Charcot Marie Tooth disease. Can J Anaesth 1996; 43: 1150±2


Severe unilateral bronchospasm mimicking inadvertent endobronchial intubation: a complication of the use of a topical lidocaine Laryngojet injector A. D. Farmery Nuf®eld Department of Anaesthetics, University of Oxford, Radcliffe In®rmary, Oxford OX2 6HE, UK A healthy young woman is described in whom the left chest was unable to be in¯ated after intubation. The differential diagnosis and management are discussed. Severe unilateral bronchospasm was probably caused by topical lidocaine injected at the vocal cords and, inadvertently, into the left main bronchus with a Laryngojet device. Br J Anaesth 2000; 85: 917±19. Key words: complications, bronchospasm; anaesthetics, local, lidocaine Accepted for publication: July 5, 2000

A healthy 19-yr-old woman, weighing 64 kg, was scheduled for angiography and alcohol sclerosis of a facial arteriovenous malformation. She had no history of chest disease but smoked 10 cigarettes per day. She received no premedication. Anaesthesia was induced slowly with midazolam 1.5 mg and propofol 110 mg, during which time she breathed oxygen. Anaesthesia was maintained with an infusion of propofol at 660 mg h±1 initially, reducing to 500 and 400 mg h±1 at 15 and 25 min respectively. Neuromuscular block was obtained with vecuronium. Before laryngoscopy, 40 mg of lignocaine was given i.v. A clear view of the larynx was obtained. The tip of a Laryngojet lidocaine (4%) injector was passed about 2 cm through the glottis, so that about half of the side-holes were above and half were below the cords. Five millilitres of solution were injected and the trachea was intubated with a

7.5 mm reinforced tracheal tube which was secured at 21 cm at the lips. On immediate inspection, both sides of the chest appeared to in¯ate equally and capnography revealed a normal waveform. The patient was transferred to the adjacent x-ray table and was ventilated with oxygen and air (FIO2 = 0.35) via a Bain system and a Nuf®eld 200 ventilator with a tidal volume of approximately 600 ml. Within 2 min of intubation the SpO2 had fallen from 100 to 90%. The inspired oxygen fraction was increased to 1 and the chest was re-examined. The right chest was expanding and breath sounds were vesicular with no wheeze. On the left, there was no expansion and there were no breath sounds or added sounds at all. Inadvertent right-sided endobronchial intubation was suspected. The tube position was rechecked. It remained at 21cm at the lips. The tube tip was checked immediately by dynamic x-ray screening and was


Farmery

seen 2 cm above the carina. A suction catheter was passed blindly down the tracheal tube. No secretions were aspirated and the left chest remained silent. The whole chest was then screened on X-ray. The right lung was seen to expand and accommodate the entire tidal volume. On the left there was no in¯ation of any lobe. The left hemidiaphragm was motionless and there was some basal collapse. Pneumothorax was excluded. Because the ventilatory abnormality was unclear, the procedure was discontinued, and a bronchoscopy was done to exclude an obstruction in the left main bronchus. This showed a normal bronchial tree on both sides to the level of the segmental bronchi, and no appreciable secretions. The left chest remained static. The SpO2 20 min after intubation remained at 90% with an FIO2 of 1, and the basal collapse had increased. Fifty micrograms of salbutamol was given intravenously. The PE¢CO2 rapidly increased from 5.2 to 6.3 kPa after 2 min. The alveolar plateau of the capnogram changed from virtually ¯at, to markedly up-sloping. The pulse rate increased from 85 to 110 min±1. There was now very slight expansion of the left chest and a marked expiratory wheeze. A further 50 mg of salbutamol was given. Within 3 min, expansion of the left and right chest was equal. The PE¢CO2 decreased to 5.0 kPa within a further 3 min and the capnogram plateau became almost ¯at again. The inspired oxygen fraction was reduced to 0.35 and the SpO2 remained at 98%. Given this marked improvement, the angiography proceeded and sclerosis of the arteriovenous malformation was done, taking approximately 1 h. After this, repeat screening of the chest showed both lungs expanding equally and complete resolution of the previous left basal collapse. The patient was extubated uneventfully and returned to the ward, where she was monitored closely. She displayed no wheeze or gas exchange de®cit.

Discussion Failure to ventilate one side of the chest after intubation of the trachea occurs commonly. Routine examination of the chest by inspection and auscultation after intubation will identify this and allow treatment before complications result. The most likely cause is unilateral endobronchial intubation, which is easily remedied by withdrawal of the tip of the tube into the trachea. In this case, it was unlikely that the tip of the tube was beyond the carina because its position at the lips seemed to be normal for the size of the patient. If attempts had been made to withdraw the tube until the left chest began to expand, this could have caused inadvertent extubation at a time when this could be least afforded. We had a unique radiographic opportunity to examine the causes and consequences of this incident without altering the tube position. Screening the tube tip position con®rmed the initial clinical belief that it was in the trachea. Screening the whole chest

showed no air entry to the left lung. If this were caused by large airway obstruction, say a large mucous plug, then it would have to be very proximal indeed. Blind passage of a suction catheter was predictably unhelpful and bronchoscopy excluded any airway obstruction as far down as the segmental bronchi. The patient's oxyhaemoglobin saturation remained at 90% with an FIO2 of 1. This is consistent with venous admixture of the order of 40±50%.1 The development of the basal atelectasis is of interest. Atelectasis in dependent dorsal regions is well known to occur during anaesthesia.2 3 It can occur very rapidly (within minutes) when patients have been preoxygenated4 or when lungs containing regions with a very low ventilation/perfusion ratio (V/Q) are ventilated with a high FIO2. Atelactasis is not easily visible on conventional X-ray imaging, but is detected with high sensitivity by CT scanning.5 This patient was only partially pre-oxygenated. However, when the oxyhaemoglobin saturation fell after intubation, the FIO2 was increased to 1. The whole of the left lung probably had a low V/Q, and the dependent dorsal regions more so. Even with screening that was relatively insensitive, atelectasis was noted and evolved over 20 min. In this case, the ventilatory abnormality was gross and unlikely to be missed. However, with a less obvious abnormality, if an increase in FIO2 restored a nearly normal SpO2, a prolonged anaesthetic might be permitted to proceed. Indeed, some anaesthetists use an FIO2 of 1 routinely. In such cases, the progressive development of atelectasis might impair postoperative lung function and gas exchange.6 There are three cases of `unilateral bronchospasm' listed in Medline (1966±2000). Two occurred after surgical procedures of the pleura (interpleural analgesia and pleurodesis)7 8 and one after subclavian vein puncture. Shantha7 reviews the likely mechanisms for unilateral bronchospasm. Bronchomotor tone depends on the balance of b-adrenergic and vagal parasympathetic out¯ow. Unilateral bronchospasm could result from (i) disproportionate sympathetic blockade, or (ii) stimulation of super®cial airway receptors supplied by vagal ®bres by any irritant.7 A direct sympathetic nerve supply to the bronchial smooth muscle has been questioned9 and it is unlikely that sympathetic blockade occurred in this case. The lignocaine given i.v. would be unlikely to cause signi®cantly large plasma concentrations, nor would it act unilaterally, and the topical lignocaine is unlikely to have penetrated such a deep and distant structure as the hilar plexus. The topical lignocaine may have stimulated airway receptors to produce vagally mediated bronchoconstriction. Atelectasis by a local neural bronchoconstrictor re¯ex can occur after a variety of lung insults, including pulmonary embolism and trauma.10 Constriction is not limited to the conducting airways, but is thought to be effected within the alveolar acinus by speci®c contractile interstitial cells, which are

918

Anaesthesia for Kartagener's syndrome

thought also to control local pulmonary capillary blood ¯ow and hence exert an effect on V/Q matching.11 Downes and colleagues12 13 showed that, in dogs, both aerosolized and i.v. lignocaine prevented the increase in airway resistance produced by an irritant citric acid aerosol, suggesting that lignocaine by either route blocked the re¯ex irritant response. They also showed that aerosolized lignocaine did not prevent allergic bronchospasm produced by inhalation of Ascaris antigen in previously sensitized animals. By contrast, Fish and Peterman14 showed that, in eight asthmatic subjects, rather than blocking re¯ex bronchoconstriction, aerosolized lignocaine (4%) actually caused it. They conclude that whilst topical lignocaine is theoretically capable of blocking neurogenic re¯exes, it may produce re¯ex bronchoconstriction in patients with asthma or hyperirritable airways. This patient was not asthmatic and had no history of recent upper respiratory tract infection. She was, however, a smoker and could have had hyperirritable airways. In addition, the drug was administered not as aerosolized mist but as a jet of liquid, which itself is likely to be more irritant. This case demonstrates a problem of a topical lignocaine delivery device which is capable of depositing a relatively large dose of the drug below the cords, and sending a jet of drug down either main bronchus or even both bronchi. It also demonstrates a risk of high inspired fractions of oxygen (in this case obligatorily) when the lung has signi®cant areas with very low V/Q ratios. The fortuitous use of instant X-ray screening allowed the tube position to be exonerated, and the value of ®bre-optic bronchoscopy in the differential diagnosis is highlighted.

References 1 Nunn JF. Nunn's Applied Respiratory Physiology. Oxford: Butterworth Heinemann, 1993 2 Tokics L, Hedenstierna G, Svensson L, Brismar B, Cederlund T, Lundquist H, et al. V/Q distribution and correlation to atelectasis in anaesthetised paralyzed humans. J Appl Physiol 1996; 81: 1822±33 3 Hedenstierna G. Ventilation±perfusion relationships during anaesthesia. Thorax 1995; 50: 85±91 4 Joyce CJ, Williams AB. Kinetics of absorption atelectasis during anaesthesia: a mathematical model. J Appl Physiol 1999; 86: 1116±25 5 Hedenstierna G. Respiratory Measurement, 3rd Edn. London: BMJ Books, 1998 6 Lindberg P, Gunnarsson L, Tokics L, Secher E, Lundquist H, Brismar B, et al. Atelectasis and lung-function in the postoperative period. Acta Anaesthesiol Scand 1992; 36: 546±53 7 Shantha TR. Unilateral bronchospasm after interpleural analgesia. Anesth Analg 1991; 74: 291±3 8 Narr BJ, Fromme GA, Peters SG. Unilateral bronchospasm during pleurodesis in an asthmatic patient. Chest 1990; 98: 767±8 9 Richardson JB. Nerve supply to the lungs. Am Rev Respir Dis 1979; 119: 785±802. 10 de Takis G, Fenn GK, Jenkinson EL. Re¯ex pulmonary atelectasis. JAMA 1942; 120: 686±90 11 Kapanci Y, Assimacopoulos A, Irle C, Zwahlen A, Gabbiani G. `Contractile interstitial cells' in pulmonary alveolar septa: a possible regulator of ventilation/perfusion ratio? J Cell Biol 1974; 60: 375±92 12 Downes H, Gerber N, Hirshman CA. I.v. lidocaine in re¯ex and allergic bronchoconstriction. Br J Anaesth 1980; 52: 873±8 13 Downes H, Hirshman CA. Lidocaine aerosols do not prevent allergic bronchoconstriction. Anesth Analg 1981; 60: 28±32 14 Fish JE, Peterman VI. Effects of inhaled lidocaine on airway function in asthmatic subjects. Respiration 1979; 37: 201±7


Anaesthesia for Kartagener's syndrome J. Reidy1*, S. Sischy2 and V. Barrow3 1

Dunkeld Anaesthetic Practice PO Box 41203, Craighall 2024, Johannesburg, South Africa. 2 Cardiothoracic ICU Morningside Mediclinic, Private Bag X6, Bryanston, South Africa. 3 Sandton Mediclinic, Private Bag X1, Bryanston, South Africa *Corresponding author Kartagener's syndrome is a hereditary syndrome involving a combination of dextrocardia (situs inversus), bronchiectasis and sinusitis, transmitted as an autosomal recessive trait. We describe a patient who had three anaesthetics over a period of a few months. Discussion relates to anaesthetic considerations in the syndrome and to recent ®ndings relating to the molecular mechanisms of left-right development.


Reidy et al.

Br J Anaesth 2000; 85: 919±21 Keywords: complications, Kartagener's syndrome; complications situs inversus; anaesthesia, general Accepted for publication: June 5, 2000

A 27-yr-old female presented for surgery three times. She had Kartagener's syndrome.1 The ®rst operation was a left middle lobectomy for bronchiectasis. Some months later she complained of abdominal pain and her second operation revealed an ovarian adenocarcinoma. This operation was complicated by an episode of postoperative pneumonia. Two weeks later she had a total abdominal hysterectomy with bilateral salpingo-oophorectomy.

Case report The ®rst operationÐleft middle lobectomy The patient's main complaint was one of recurrent episodes of pneumonia. She also admitted to chronic sinusitis and volunteered the information that `her heart was on the wrong side but normal'. Examination revealed no clubbing; her apex beat was on the right side; auscultation of the heart sounds was normal and there were some crepitations and rhonchi mainly in the left axilla. Chest x-ray revealed dextrocardia and a right-sided stomach bubble. ECG demonstrated sinus rhythm and inversion of the P wave in lead 1 with a deep Q wave and inversion of the T wave. CT scan showed bronchiectasis that was most prominent in the left middle lobe. Lung function tests were normal and it was not considered necessary to do a blood gas study. She was admitted to the clinic for physiotherapy and scheduled for left middle lobectomy. Anaesthesia for thoracotomy and lobectomy was unremarkable apart from it seemed logical to use a right-sided double lumen tube as she had three lobes on the left and two on the right with the longer main bronchus on the right. General anaesthesia was induced with propofol and maintained with iso¯urane and sufentanil. For neuromuscular block we used vecuronium. Routine monitoring was enhanced by inserting a radial arterial line. The trachea was intubated with a right-sided 37 FG Mallinkrodt doublelumen tube and the lungs ventilated with a Servo Elema 900C ventilator. After surgery, the trachea was extubated and the patient returned to the ward. Her postoperative course was uneventful and she was sent home after a few days.

The second operationÐdiagnostic laparoscopy A few months later after the lobectomy the patient presented to a gynaecologist with abdominal pain. We were not involved with her management at this time. She had a general anaesthetic for laparoscopy that revealed adenocar-

cinoma of the ovary. Her postoperative course was complicated by an episode of left lower lobe pneumonia.

The third operationÐtotal abdominal hysterectomy and bilateral salpingo-oophorectomy Two weeks after the laparoscopic examination, the patient presented for total abdominal hysterectomy and bilateral salpingo-oophorectomy. In view of the fact that her last procedure had been complicated by pneumonia, spinal anaesthesia was chosen. She was sedated with midazolam 5 mg i.v. Spinal anaesthesia was given through a 25-gauge pencil point needle using 12.5 mg of hyperbaric bupivacaine. A continuous propofol infusion was used for sedation. Surgery was performed through a Pfannenstiel incision. The operation and postoperative period was uneventful.

Discussion Kartagener's syndrome is a variant of the immotile cilia syndrome.2 This has also been called primary ciliary dyskinesia and is a result of an autosomal recessive disorder of the microtubules of ciliated cells. Symptoms include male sterility, chronic or recurrent respiratory tract infection, and bronchiectasis because of the absence of mucociliary clearance. In 50% of patients situs inversus occurs and hence Kartagener's syndrome. It may become possible to link the occurrence of abnormal ciliary function and abnormal position of the body organs. It seems that genes determine the structure, function, and time of appearance of proteins in the embryo that in¯uence normal development and siting of the internal organs asymmetrically (situs solitus). On the left side of the embryo, near Hensen's node, a variety of proteins are secreted (Sonic Hedgehog, Nodal, Lefty and Pitx2). On the right side are others (Activin betaB, Snail and Fibroblast Growth factor-8).3 These normally in¯uence rotations, that lead to a left-sided heart and the usual position and structure of the lungs and abdominal organs. Abnormal genes and so abnormal proteins would lead to malpositions. Normal ciliary motion in the mouse node is anticlockwise and conceivably in¯uences the ¯ow of the proteins to their correct sites in the embryo. In the immotile cilia syndrome it is possible that abnormal distribution of the proteins occurs. Is this the reason that the dextrocardia of Kartagener's syndrome links with the immotile cilia syndrome, and also situs inversus?

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Acute right-to-left interatrial shunt

The anaesthetic implications of Kartagener's syndrome are varied. The anaesthetist might be involved with patients who have sinus surgery, pulmonary surgery, infertility investigations or possibly cardiac surgery. Of primary importance will be assessment of pulmonary and cardiac structure and function, and also prevention of pulmonary complications in the bronchiectatic patient. Physiotherapy, postural drainage, antibiotics, bronchodilators and incentive spirometry all have a role perioperatively. Where possible, local or regional anaesthesia is to be preferred to general anaesthesia. In thoracic surgery, the anatomy of the bronchi should be considered before selecting a double lumen tube. Knowledge of the position of the abdominal organs and of the branching pattern of the main stem bronchi is important in categorizing malpositions; and these must be borne in mind. When dextrocardia occurs with situs inversus, the heart is most frequently normal. When dextrocardia occurs without situs inversus, when the visceral situs is indeterminate (situs ambiguus), or if isolated levocardia is present, associated, often complex, multiple anomalies are usually present.4 Dextrocardia with complete situs inversus occurs in approximately 2 per 10 000 births. The incidence of congenital heart disease is low being about 3%. Kartagener's syndrome will occur in about 20% of patients.5 Thus, the incidence being approximately 1 in 50 000 births. Our patient did not have an echocardiogram and on clinical grounds was assumed to have a totally normal heart. In contrast, dextrocardia with situs solitus or situs ambiguus is less common (1 per 20 000 births) and the incidence of congenital heart disease is extremely high, probably 90% or greater. Dextrocardia with situs solitus usually, although not invariably, associates with severe

complex cardiac abnormalities. They are most commonly transposition of the great arteries, double outlet right ventricle, ventricular septal defect, single ventricle and pulmonary stenosis or artresia.5 In patients with dextrocardia and situs ambiguus, polysplenia or asplenia may be present in association with complex multiple cardiac abnormalities. These include a combination of systemic and pulmonary venous abnormalities, defects in the ventricular and atrial septa and endocardial cushion defects. There may be pulmonary artery obstruction and maldevelopment of the great arteries.6 The incidence of isolated levocardia (a left-sided heart) with situs inversus is about 0.6% per 10 000 births and more than 90% have serious heart disease.5

References 1 Kartagener M. Zur pathogenese der bronchiektasien. 1. Bronchiektasien bei situs viscerum inversus. Bietr Kli Tuberk 1933; 83: 489 2 Rubin BK. Immotile cilia syndrome (primary ciliary dyskinesia) and in¯ammatory lung disease. Clin Chest Med 1988; 9: 657±68 3 Belmonte JCI. How the body tells left from right. Sci Am 1999; June: 38±43 4 Friedman WF. Congenital heart disease in the adult. In: Isselbacher KJ, Braunwald E, eds. Harrison's Principles of Medicine. 13th Edn. New York: McGraw-Hill Inc., 1994; 1046 5 Nugent EW. The pathology, abnormal physiology, clinical recognition, and medical and surgical treatment of congenital heart disease. In: Hurst, ed. The Heart. 7th Edn. New York: McGraw-Hill Inc., 1990; 178 6 Friedman WF. Congenital heart disease. In: Wintrobe MM, Thorn GW, eds. Harrison's Principles of Medicine. 6th Edn. New York: McGraw-Hill Inc., 1970; 1182


Acute right-to-left inter-atrial shunt; an important cause of profound hypoxia I. L. Marples1*, M. J. Heap1, S. K. Suvarna2 and G. H. Mills3 1

Department of Anaesthesia, 2Department of Histopathology, Northern General Hospital, Herries Road, Shef®eld S5 7AU, UK. 3University Department of Anaesthesia, `K' Floor, Royal Hallamshire Hospital, Glossop Road, Shef®eld S10 2JF, UK *Corresponding author Three patients presented to our intensive care unit over a 3-yr period with profound hypoxia resulting from acute right-to-left inter-atrial shunt (RLIAS). Patient 1 was a 67-yr-old male with an atrial septal defect who became hypoxic and developed the rare sign of platypnoea following elective repair of an abdominal aortic aneurysm (breathlessness made worse when upright and relieved by lying ¯at). Patient 2 was a 38-yr-old female who developed platypnoea and


Marples et al.

hypoxia secondary to a patent foramen ovale (PFO) and pericardial effusion. Patient 3 was a 46-yr-old male with a PFO who developed hypoxia without platypnoea because of multiple pulmonary emboli following right hemicolectomy. These case reports illustrate the need to consider RLIAS as a cause of hypoxia of sudden onset. Early use of bubble contrast echocardiography is indicated. Br J Anaesth 2000; 85: 921±5 Keywords: complications, hypoxia; heart, bubble contrast echocardiography; intensive care Accepted for publication: July 19, 2000

Shunting of blood across a defect between the two sides of the heart is usually directed by the left-to-right pressure gradient. A large and persistent left-to-right shunt can increase pulmonary blood ¯ow, which over months or years leads to microvascular changes, increased pulmonary vascular resistance and elevated pulmonary artery pressure. When the pulmonary arterial pressure approaches the systemic arterial pressure, the direction of the shunt reverses (the Eisenmenger syndrome). This chronic development of right-to-left shunt (RLIAS) is accompanied by electrocardiographic changes of atrial enlargement and right ventricular hypertrophy. Chest radiography reveals prominent pulmonary arteries.1 In contrast, the adult patient with an asymptomatic interatrial defect may develop an acute RLIAS following a cardiac or respiratory insult. Acute RLIAS is a separate clinical entity from the Eisenmenger syndrome. Acute RLIAS is often overlooked as a cause of hypoxia2 but early diagnosis can direct therapy and avoid unnecessary invasive investigations. The three cases reported here illustrate the need to consider RLIAS in the differential diagnosis and investigation of profound hypoxia.

2

Case reports Patient 1 A 67-yr-old man presented for elective repair of an abdominal aortic aneurysm. He had a past history of hypertension, transient ischaemic attacks and a left hemiparesis from which he had made a full recovery. His exercise tolerance was good and a preoperative multiple uptake-gated acquisition scan demonstrated a left ventricular ejection fraction of 67%. Anaesthesia and surgery were uneventful. The perioperative cardiac index was 3±4 litres min±1 m±2 and pulmonary arterial pressures ranged between 28/8 and 52/24 mm Hg. He required admission to intensive care unit (ICU) 3 days postoperatively with hypoxia (PaO =5 kPa) on room air, pulmonary oedema, blood pressure of 90/60 mm Hg and oliguria. He required tracheal intubation, positive pressure ventilation, diuretics and inotropes. His oxygenation improved, allowing tracheal extubation after 3 days but after 10 days his PaO was 5.65 kPa and PaCO 2.7 kPa on a FIO2 0.95. He also developed 2

2

2

platypnoea; that is he was unable to sit upright because of severe breathlessness but he was less breathless when lying ¯at, particularly in the left lateral decubitus position. Initially the underlying cause of this patient's hypoxia was not clear. Transthoracic echocardiography (TTE) demonstrated good left ventricular function, mild mitral regurgitation and septal hypertrophy. A lung perfusion scintographic scan showed no evidence of pulmonary embolism. Thoracic computerized tomography revealed non-speci®c bilateral shadowing of the lung ®elds consistent with adult respiratory distress syndrome (ARDS) or infection. Despite antibiotic therapy followed by a trial of prednisolone 70 mg day±1 for possible ARDS, he continued to deteriorate and required reintubation and positive pressure ventilation. A pulmonary artery ¯otation catheter demonstrated a cardiac index of 2.1 litres min±1 m±2, mean right atrial pressure of 8 mm Hg, mean pulmonary arterial pressure of 37 mm Hg and pulmonary artery occlusion pressure of 3 mm Hg. During inspired nitric oxide therapy at 20 p.p.m. the cardiac index increased to 3.8 litres min±1 m±2, the mean right atrial pressure was 4 mm Hg, mean pulmonary arterial pressure 34 mm Hg and pulmonary artery occlusion pressure 5 mm Hg. The PaO increased from 10.5 to 24.5 kPa on a FIO2 1.0. A cardiology opinion was sought concerning the possibility of an inter-atrial shunt, but this diagnosis was thought to be excluded by the absence of a persistent right-to-left pressure gradient; right atrial pressure range of 4±8 mm Hg with a pulmonary artery occlusion pressure range of 3±5 mm Hg. However, an inter-atrial defect was discovered fortuitously during pulmonary angiography when a catheter passed from the right atrium into the left atrium. Bubble contrast transoesophageal echocardiogram (TOE) demonstrated RLIAS with severe impairment of right ventricular function (Fig. 1). The patient became septicaemic and died on the 26th postoperative day. Post-mortem examination revealed a secundum ASD, absent superior vena cava and anomalous venous drainage via a dilated coronary sinus. The right ventricle appeared normal and the lungs were oedematous. On histological examination, there was mild pulmonary ®brosis but no features of ARDS, organizing pneumonia, or pulmonary hypertension.

922


function was good. Pericardial tap brought immediate relief of the patient's hypoxia; the PaO rising from 5.8 to 30.4 kPa, on oxygen 10 litres min±1 by facemask. 2

Patient 3 A 46-yr-old man presented with breathlessness 4 days after right hemicolectomy for caecal carcinoma. Axillary temperature was 38.5°C, he had a sinus tachycardia 135 beat min±1, arterial pressure 90/60 mm Hg and a respiratory rate of 32 breath min±1. PaO was 4.1 kPa and PaCO 4.2 kPa on room air. Oxygen at maximum ¯ow via a facemask did not improve his hypoxia and he was transferred to ICU. FIO2 0.9 with CPAP 5 cm H2O produced a PaO 7.5 kPa. The patient was not distressed despite his hypoxia and was able to tolerate lying ¯at for a pulmonary angiogram. Pulmonary angiogram revealed a large embolus in the left-upper lobe pulmonary artery with smaller emboli in the right middle lobe pulmonary artery and right pulmonary vessels peripherally. The catheter passed from the right atrium to the left atrium. Mean right atrial pressure was 13 mm Hg, left atrial pressure 11 mm Hg and mean pulmonary arterial pressure 27 mm Hg. Left pulmonary venous PO2 was 32.3 kPa but the radial arterial PaO was 6.24 kPa. A Green®eld inferior vena cava ®lter was deployed with its base at the level of the L3L4 disc space. A bolus of tissue plasminogen activator 5 mg i.v. plus an infusion of 5 mg h±1 was instituted. The patient's oxygenation improved over the next 3 days and thereafter his recovery was uneventful. 2

2

2

Fig 1 Transoesophageal echocardiogram using bubble contrast (Patient 1). Injected microbubbles are seen as white specks. The bubbles visible in the left atrium (LA), at the same time as the right atrium (RA) and right ventricle (RV), are indicative of RLIAS. An ASD is seen (arrow).

Patient 2 A 38-yr-old woman presented with platypnoea and cyanosis that developed over a period of 4 days. Sitting upright exacerbated her breathlessness and she was more comfortable when lying ¯at despite being profoundly hypoxic. She had a past history of chronic renal impairment and aortic incompetence. At presentation she was an inpatient recuperating from an episode of infective endocarditis and gastrointestinal bleeding for which she had required treatment in the ICU. On physical examination she was apyrexial, heart rate 110 beats min±1, arterial pressure 120/80 mm Hg and the jugular venous pressure was not elevated. An aortic murmur was present, but unchanged from previous examinations; respiratory rate was 20 b.p.m. and chest auscultation was normal. Arterial blood gases on a FIO2 0.6 were: pH 7.6, PaO 5.6 kPa, PaCO 3.8 kPa, base excess 6.3 mmol litre±1. A chest radiograph showed a small right pleural effusion. Lung perfusion scintographic scan demonstrated a single segment perfusion defect in the right mid-zone. A preliminary diagnosis of pulmonary embolism was made but the decision to anticoagulate was deferred until a pulmonary angiogram could be performed in view of her recent history of gastrointestinal haemorrhage. During pulmonary angiography, the catheter passed through a patent foramen ovale into the left atrium and left upper lobe pulmonary vein. Radio-opaque dye ¯owed from the right to the left atrium. Pulmonary arteriography demonstrated no emboli. Mean pulmonary arterial pressure was 12 mm Hg and mean right atrial pressure was 13 mm Hg compared with 8 mm Hg in the left atrium. Right atrial PO2 was 2.8 kPa and the left atrial PO2 was 5.5 kPa. Transthoracic echocardiogram revealed a right-sided pericardial effusion, 4.5 cm in depth, compressing the right ventricle. Left ventricular 2

2

2

Discussion Acute RLIAS is a rare but important cause of profound hypoxia. The pathophysiology of acute RLIAS arises from an inter-atrial defect coupled with a secondary cardiac or pulmonary insult. Patent foramen ovale, which occurs in approximately 30% of the adult population,3 is present in the majority of reported cases of acute RLIAS. ASD is present in the remainder. A rise in right atrial pressure above left atrial pressure may precipitate RLIAS. This can be the result of obstruction of pulmonary blood ¯ow by pulmonary embolus4 (Patient 3), increased transmural pressures in asthma,5 right ventricular hypokinesis following right ventricular infarction6 or coronary artery bypass grafting,7 or as a result of elevated PaCO in hemidiaphragmatic paresis.8 However, in similar cases right heart pressures can be normal, which indicates that other factors can induce RLIAS.4 9 10 Mechanical distortion of the heart can alter the relative positions of the atrial septum and the inferior vena cava (IVC) which then directs the ¯ow of blood from the IVC towards the inter-atrial defect and into the left atrium. Mediastinal shift following lung resection is the most commonly reported cause of RLIAS.11 Other causes of distortion of cardiac anatomy with no apparent right-to-left pressure gradient include thoracic trauma,12 rupture of the papillary muscles,13 after tuberculosis,14 thoracic aortic

923

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Marples et al.

aneurysm,15 pericardial effusion (Patient 2),16 and metastatic cardiac disease.17 The mechanism of RLIAS is unclear in cases of morbid obesity,18 cystic ®brosis,19 adult respiratory distress syndrome20 and exposure to low atmospheric pressure.21 22 Platypnoea is a sign that is strongly associated with RLIAS. This sign, ®rst described in 1949 and given the name platypnoea in 1969, occurs in approximately one quarter of reported cases of acute RLIAS.23 24 A corresponding postural change in oxygenation is known as orthodeoxia.25 RLIAS is often diagnosed unexpectedly during investigation for other causes of acute hypoxia.26 A pulmonary angiography catheter may pass through an inter-atrial defect, as occurred in our patients, but the angiogram may be reported as normal despite the presence of a signi®cant RLIAS.4 13 Lung perfusion scintigraphy indicates RLIAS when early activity is detected in the brain, myocardium and kidneys.27 It has been advocated as the investigation of choice28 but failed to detect RLIAS in our ®rst and second patients and in several other reported cases.2 4 29 Injection of radiolabelled microaggregates into the arm has resulted in a normal perfusion scan whereas injection into the foot demonstrated shunt because of preferential ¯ow from the IVC across the interatrial defect.30 Bubble contrast echocardiography has the greatest sensitivity for detecting RLIAS and has the advantage that it is a relatively non-invasive technique that can be performed at the bedside.1 31 32 A syringe ®lled with 9 ml saline and 1 ml air is agitated, macroscopic bubbles expelled and the remaining microbubble emulsion injected i.v. The test is positive if microbubbles are seen in the left atrium (Fig. 1) within two to three cycles of the initial appearance in the right atrium. Bubble contrast echocardiography has detected RLIAS as a ®rst line investigation15 22 33 and when preceding pulmonary angiogram and lung perfusion scintigram have both been falsely negative.2 12 29 Injection of contrast via the leg may increase the sensitivity of the test as most shunting occurs via the IVC.34 RLIAS is exacerbated when intrathoracic pressure is increased by PEEP in the arti®cially ventilated patient35 and during coughing or the Valsalva manoeuvre.31 Each of these manoeuvres can increase the likelihood of detecting RLIAS by echocardiography. Bubble contrast echocardiography is a safe technique widely reported in the investigation of chronic RLIAS, particularly in patients who are thought to have developed paradoxical embolism.36 37 Paradoxical embolism is not commonly associated with profound hypoxia as these patients present with systemic embolic phenomena. Patient 1 had a past history of cerebrovascular events and whether these were caused by paradoxical emboli is an interesting matter for conjecture. Treatment of RLIAS is treatment of the underlying cause and/or closure of the PFO or ASD. Successful closure of the inter-atrial defect is frequently reported38 although some

patients have died following its closure because of right heart failure.20 35 Temporary closure may be achieved with a balloon catheter10 but de®nitive closure requires either open surgery or a percutaneous technique using an occlusive device.6 Patient 1 developed acute RLIAS and platypnoea. The nature of the precipitating cause remains uncertain. However, the raised perioperative pulmonary arterial pressures and the subsequent bene®cial effect of nitric oxide suggests that pulmonary vasoconstriction was a contributing factor. The diagnosis of RLIAS was discounted because of the absence of a signi®cant right-to-left pressure gradient between the atria. By the time RLIAS was diagnosed, the patient's condition precluded surgical closure of his ASD. The use of bubble contrast during the patient's ®rst echocardiogram might have revealed the RLIAS early enough for surgery to be feasible. Patient 2 presented with platypnoea; as this is highly indicative of RLIAS, early use of bubble contrast echocardiography was indicated. A lung perfusion scintogram failed to detect it and was falsely positive for pulmonary embolism. RLIAS was discovered during pulmonary angiography when the catheter passed through a PFO. Early use of bubble contrast echocardiography might have saved the patient from these more invasive investigations. Patient 3 demonstrates that acute RLIAS can occur without platypnoea and without high pulmonary arterial pressures. In conclusion, the diagnosis of acute RLIAS should be considered in any patient with unexplained acute hypoxia particularly if platypnoea or orthodeoxia is present. Neither pulmonary hypertension nor a pressure gradient between the right and left atria need be present. Bubble contrast echocardiography is more sensitive in detecting RLIAS than more invasive techniques and should be performed early.

References

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operative hypoxemia: demonstration with contrast twodimensional echocardiography. J Am Coll Cardiol 1985; 6: 920±2 Farber HW, Make B. Physiologic closure of a symptomatic patent foramen ovale with oxygen therapy. Am Rev Respir Dis 1985; 131: 181±3 Brydon C, Fawcett WJ, Treasure T, Clarke JT. Pulmonary embolus and patent foramen ovale: a rare cause of refractory hypoxaemia. Br J Anaesth 1993; 71: 298±300 Cox D, Taylor J, Nanda NC. Refractory hypoxemia in right ventricular infarction from right-to-left shunting via a patent foramen ovale: ef®cacy of contrast transesophageal echocardiography. Am J Med 1991; 91: 653±5 van Rossum P, Plokker HWM, Ascoop CAPL. Breathlessness and hypoxaemia in the upright position after right pneumonectomy. Eur Heart J 1988; 9: 1230±3 Pacht ER. Interatrial right-to-left shunting in the absence of elevated right-sided pressures after major trauma [letter]. Chest 1994; 105: 1614 Ribichini F, Conte R, Lioi A, Dellavalle A, Ugliengo G. Subacute tricuspid regurgitation with severe hypoxemia complicating blunt chest trauma. Chest 1996; 109: 289±91 Remy-Jardin M, Remy J, Wallaert B. Right-to-left shunting through a patent foramen ovale without pulmonary hypertension. Chest 1990; 97: 1250±2 Laybourne KA, Martin ET, Cooper RAS, Holman WL. Platypnea and orthodeoxia: shunting associated with an aortic aneurysm. J Thorac Cardiovasc Surg 1997; 113: 955±6 Klepper JI, Seifert F, Lawson WF, et al. Intracardiac right-to-left shunting following cardiac surgery. Am Heart J 1988; 116: 189±92 Gallerstein PE, Belluscio RL, Berger M, Onseng F, Jurado RA. Right-to-left intracardiac shunt: a unique presentation with metastatic cardiac disease. J Am Coll Cardiol 1984; 3: 865±67 Collop NA. Refractory hypoxaemia in a morbidly obese 28-yearold woman. Chest 1996; 109: 1101±2 Davidson A, Chandrasekaran K, Guida L, Holsclaw DS. Enhancement of hypoxemia by atrial shunting in cystic ®brosis. Chest 1990; 98: 543±5 Dewan NA, Gayasaddin M, Angelillo VA, O'Donohue WJ, Mohiuddin S. Persistent hypoxemia due to patent foramen ovale in a patient with adult respiratory distress syndrome. Chest 1986; 89: 611±13 Sorrentino M, Resnekov L. Patent foramen ovale associated with platypnea and orthodeoxia. Chest 1991; 100: 1157±8 Levine BD, Grayburn PA, Voyles WF, Greene ER, Roach RC, Hackett PH. Intracardiac shunting across a patent foramen ovale may exacerbate hypoxemia in high-altitude pulmonary edema. Ann Intern Med 1991; 114: 569±70 Burchell HB, Helmolz HF, Wood EH. Re¯ex orthostatic dyspnea

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Air embolism during anaesthesia for shoulder arthroscopy R. T. Hegde* and R. N. Avatgere Department of Anaesthesia, Queen's Hospital, Burton upon Trent DE13 0RB, UK *Corresponding author We report a case of venous air embolism during an elective shoulder arthroscopy in which air was used as a joint distending agent. Venous air embolism was diagnosed by the sudden decrease in the end-tidal carbon dioxide concentration. The patient suffered no serious complications of venous air embolism and made a full recovery. We present this case to make surgeons and anaesthetists aware of the possibility of gas/air embolism during elective arthroscopy, when gas/air is used to distend the joint. This case also illustrates that the endtidal carbon dioxide monitor, which is part of the standard anaesthetic monitoring system, is very sensitive in detecting venous air embolism. Br J Anaesth 2000; 85: 925±7 Keywords: surgery, arthroscopy; complications, air embolism; monitoring Accepted for publication: July 7, 2000

Venous air embolism is a known complication during anaesthesia for hip replacements, laparoscopies and operative procedures in which the operative site is above the level of the heart, as in neurosurgical and major head and neck procedures, especially in the sitting position. Although rare, venous gas embolism can occur during arthroscopy, when air or another gas is used to distend the joint. We are aware of only one report where air embolism occurred during shoulder arthroscopy. We report an additional case of air embolism during a diagnostic arthroscopy of a shoulder joint, during which the surgeon had injected 50 ml of air into the joint.

Case report A 28-yr-old man was scheduled for elective arthroscopy of the left shoulder and subacromial decompression. He had suffered left shoulder pain for 2 yr but there was no history of trauma to the joint. Two preoperative MRI scans had not shown any abnormalities in the joint. His health status was unremarkable, apart from a history of mild asthma for which he had not taken any medication in the previous 2 yr. He had undergone an uneventful general anaesthetic in the past for inguinal hernia repair. Anaesthesia was induced with propofol 200 mg, fentanyl 0.1 mg, and vecuronium bromide 10 mg. The trachea was intubated and ventilation of the lungs was controlled. Anaesthesia was maintained with sevo¯urane and nitrous oxide in oxygen. Morphine 10 mg and ondansetron 4 mg was administered. Routine monitoring included end tidal carbon dioxide measurements. The patient was placed in the beach chair position. After a stab incision in the skin, the arthroscope with a pointed trochar was introduced into the left shoulder joint. The joint was seen using the arthroscope

and 50 ml of air was injected into the joint by attaching a syringe with air to the in¯ow portal on the arthroscope. Within 1 min after the injection, a marked drecrease in the end tidal carbon dioxide (ETCO2) from 4.0 to 1.5 kPa was noted. The electrocardiogram showed a 1-mm rise in the ST segment, and the heart rate increased from 56 to 90 beats min±1. There were no changes either in the oxygen saturation or in the non-invasive blood pressure. An air embolism was suspected and the patient was placed horizontal and nitrous oxide discontinued. The end tidal carbon dioxide concentration returned to 4.0 kPa after 4 min. The surgical procedure was allowed to continue after ensuring the condition of the patient was stable and the ETCO2 concentration had returned to normal. There was an episode of bradycardia 15 min following the incident during which the heart rate decreased to 38 beats min±1. This responded to 0.6 mg of i.v. atropine. The patient made a full recovery from the anaesthetic at the end of the procedure, without any sequelae. He remained stable for the next 48 h and was discharged home.

Discussion Venous air embolism may occur during any operative procedure in which the operative site is above the level of the heart and non-collapsible veins are exposed to atmospheric pressure, or when air or any other gas is introduced under pressure into a body cavity. The clinical presentation and complications of venous air embolism depend on the dose and the speed of air entry into the vein and the ®ltering capacity of the lungs. Although venous air embolism of some degree is detected in all patients undergoing neurosurgical procedures in the sitting position,1 it is very rare in shoulder arthroscopy. Air


Air embolism during anaesthesia for shoulder arthroscopy

and other gases have been used to distend the joint in arthroscopy since 1921. Fatal pulmonary air embolism has been reported during arthroscopy of injured knee joints.2 3 It is presumed that air entered the circulation through the exposed venous sinuses in these cases. We are aware of only one case of venous air embolism during a shoulder arthroscopy.4 There are, however, theoretical risks of embolism during this procedure. In the beach chair position, used for shoulder operations, the operative site is higher than the right atrium. In addition, during arthroscopy the pressure inside the joint may be 5±10 times higher than the venous pressure and if a vein is punctured during insertion of the arthroscope, any agent used to distend the joint may enter the venous system. Because of the low morbidity and anaesthetic complication rate associated with shoulder arthroscopy, the procedure is performed as a day case in most hospitals. Air is commonly used as the joint distending agent because of the better view obtained, when compared with normal saline. The possible mechanisms of developing a venous air embolism during arthroscopy are: injection of air into an injured joint, where the air can get into the exposed venous sinuses because the intra-articular pressure during arthroscopy is high and may reach peak values of 300 mm Hg with sudden manipulation of the joint;5 or accidental injection of air into a vein in the joint. In our case there was no history of trauma, preoperative MRI scans showed no abnormalities in the joint and arthroscopy did not show any disruption in the joint surface. It is presumed that a vein was accidentally punctured during the stab incision or by the introduction of the arthroscope into the joint. The raised intra-articular pressure because of the injected air and the manipulation of the joint resulted in air entering an open vein. There are several reports in the anaesthetic literature where the use of sophisticated monitors to detect venous air embolism early in operations, with a high risk of development of venous air embolism, has resulted in a signi®cant reduction in morbidity and mortality. Transoesophageal echocardiography is the most sensitive monitor for early detection of venous air embolism (detects as little as 0.02 ml kg±1 of air).6 Others include pulmonary artery catheters, pre-cordial Doppler probe and ETCO2 and nitrogen measurements. For day case arthroscopies an inexpensive, non-invasive, sensitive and easy-to-use monitor is essential. The precordial Doppler probe meets the above criteria. It is very sensitive, but picks up interference from other sources. Before it becomes a useful tool for early detection of venous air embolism, familiarity with its use is essential. In most district general hospitals, however, capnography remains the main monitor for the early diagnosis of venous air embolism. It has fewer sources of interference than echocardiography and pre-cordial Doppler. It is widely used and is sensitive (sensitivity of 0.4 ml kg min±1),7 but is non-speci®c for air embolism. Above all, awareness of the

possibility of air embolism, a high index of suspicion and vigilance are most important in arthroscopy when air or other gases are used to distend the joint. Early detection of venous air embolism will allow for prompt treatment before serious clinical complications develop. A signi®cant venous air embolism will manifest as bronchospasm, hypoxaemia, hypercapnia, decreased ETCO2, hypotension, cardiac dysrhythmias and cardiovascular collapse, depending on the size of the embolus and the rate of entry of air into the veins. Management of clinical venous air embolism includes measures to prevent expansion of the embolus and further entry of air into the venous system. The operative site should be lowered below the level of the heart, if possible and ¯ooded with ¯uids while haemostasis is obtained. Nitrous oxide should be discontinued and oxygen increased to 100%. Blood pressure and central venous pressure should be supported with ¯uids, vasopressors and inotropes. If a large amount of air is entrained, the left lateral decubitus position may improve right ventricular out¯ow. Further treatment includes insertion of right atrial catheter and aspiration of air from the right side of the heart. In the event of cardiovascular collapse, cardiovascular resuscitation should be commenced. Prevention is the key to the management of venous air embolism. Patients at risk should be well hydrated in order to reduce the pressure gradient between the surgical site and the right atrium. Surgical haemostasis is essential at all times. Intravenous air is ®ve times more dangerous than carbon dioxide.8 Therefore, carbon dioxide or normal saline are safer agents for distension of joints during arthroscopy.

References

927

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