complete airway obstruction during awake fibreoptic intubation

CASE REPORT

Epidural abscess following epidural steroid and localanaesthetic injection

J. W. Knight, J. J. Cordingley and M. G. A. Palazzo

Department of Intensive Care, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UK

SummaryEpidural abscess is a well-recognised but rare complication of epidural catheter placement. Wehave found only five previous reports of epidural abscess from noncatheter-related administrationof steroids and/or local anaesthetic. We describe a further case which led to critical illness andemphasise the association between diabetes mellitus and epidural infection.

Keywords Anaesthetic techniques, regional; epidural, caudal. Complications; epidural abscess, paraplegia,diabetes.

......................................................................................Correspondence to: Dr M. G. A. PalazzoAccepted: 21 January 1997

Case history

A 53-year-old man, with noninsulin-dependent diabetesmellitus, was referred for specialist opinion by his generalpractitioner because of right buttock pain radiating intothe posterolateral thigh and calf.

Examination revealed straight leg raising limited to 758on the left and 558 on the right. Knee reflexes were presentand equal but ankle reflexes were absent. The plantarresponses were equivocal and power was normal in bothlegs. A clinical diagnosis was made of lumbosacral nerveroot compression due to intervertebral disc pathology anda caudal epidural injection was performed.

A mixture of procaine hydrochloride and triamcinoloneacetonide (unlicensed for epidural use) was drawn up fromnew sterile vials, the tops of which had been swabbed with0.5% chlorhexidine in 70% spirit and allowed to dry. Theskin was cleaned with 0.5% chlorhexidine in 70% spiritand allowed to dry. A new sterile 2’’ 21G needle wasintroduced through the sacral hiatus using a no-touchtechnique (without the use of gloves, gown or mask). Atotal of 22 ml of 0.5% procaine hydrochloride with 80 mgof triamcinolone acetonide was slowly injected into theepidural space. After an initial administration of 10 ml,continued injection produced bilateral leg pain. However,within minutes of completing the procedure re-exami-nation revealed that straight leg raising was full and pain-free at 858.

Four days later a lumbar MRI scan demonstrated amodest right posterolateral protrusion of the L4/5 discimpinging upon the L5 nerve root.

On review 3 weeks later the patient reported significantcoccygeal pain which had made sitting difficult. In addi-tion he had experienced 4 days of bilateral leg pain,radiating into the posterior thighs and calves which hadnecessitated bed rest. Examination revealed pain-freespinal movements and straight leg raising was pain-freeat 808. His neurological status was unremarkable except forabsent ankle reflexes. A further caudal injection wasperformed in an identical way to the first, includingdrug volume and dosage. However, bilateral leg pain wasprovoked after 5 ml had been injected.

The following day he felt feverish and had a headache.He developed rigors and was admitted to hospital 3 daysafter the second epidural injection. On examination hewas afebrile, had a stiff neck but no focal neurologicalsigns. His bladder was distended. Haematological investi-gation showed a white blood cell count of 24.6 × 109.lÿ1

with 91% neutrophils. The erythrocyte sedimentation ratewas 70 mm.hÿ1, platelets 260 ×109.lÿ1, haemoglobin con-centration 14.6 g.dlÿ1 and blood glucose 18.2 mmol.lÿ1.Meningitis was suspected. An MRI scan of the head wasnormal and lumbar scans were inconclusive. A lumbarpuncture was attempted in the L4/5 region which resultedin aspiration of frank pus. Immediate microscopy showed alarge number of Gram-positive cocci.

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An L4/5 and L5/S1 bilateral foraminal and nerve rootcanal decompression was performed urgently. At opera-tion there was an extensive epidural abscess extendingfrom the lower lumbar to the upper thoracic region. Puswas also found in the intradural space. The epidural abscesswas flushed with gentamicin 80 mg in saline using a finecatheter and intravenous antibiotics started (flucloxacillin2 g 4-hourly and fusidic acid 500 mg 8-hourly). Bloodculture taken on the day of admission and the extraduralpus grew Staphylococcus aureus, sensitive to penicillin.

Postoperatively his conscious level deteriorated and herequired tracheal intubation and intermittent positivepressure ventilation. Examination revealed loss of motorfunction in the legs with absent reflexes and lax analsphincter tone. MRI scan demonstrated a subdural collec-tion in the cervical and upper thoracic region and acisternal tap produced turbid cerebrospinal fluid.

Four days after the initial operation he had a C3/4

laminectomy and hemifacetectomy. Large volumes ofextradural and subdural pus were drained. The lumbarwound was re-opened and a laminectomy of L4 and L5

performed with further drainage. Culture of the pus againgrew Staphylococcus aureus.

Following the second operation he was transferred forintensive care management. He remained comatose for 7weeks during which time his illness was complicated byacute renal failure requiring haemofiltration and a largeupper gastrointestinal bleed managed by truncal vagotomy,pyloroplasty and ligation of the gastroduodenal artery.

Nine weeks post intensive care admission he was awakebut intermittently confused. Neurological examinationshowed normal power in his right arm and limited move-ment in his left arm and no motor function in his legs. Sixmonths later he remains paraplegic, but has normal powerin both arms. His mental state has returned to normalother than occasional periods of forgetfulness.

Discussion

Epidural abscess is extremely rare. However, it is anincreasingly common described complication of epidurallocal anaesthetic and/or steroid administration. Mostreported cases are associated with the use of epiduralcatheters. In addition to the case described we havefound only five other reports of noncatheter-relatedepidural abscess associated with epidural steroid or localanaesthetic administration. All cases involved the use ofsteroids and in three patients there were multiple injections[1–5]. The aetiology, clinical features, investigations andtreatment of epidural abscess have been reviewed pre-viously by a number of authors [4, 6–10].

Infection may follow direct inoculation of organisms fromthe patients’ or doctors’ flora, or from haematogenous

spread. Epidural haematomas, the result of local trauma,are thought to predispose to blood-borne infection andthis may account for the association between local backtrauma and the development of idiopathic epiduralabscesses. In most cases the infective organism is Staphylo-coccus aureus [11]. Our case report highlights the extensivearea that these abscesses can occupy since pus wasidentified in the cervical, thoracic and lower lumbarregions.

As in our own case, two of the five previously reportedcases have been in noninsulin-dependent diabetics. Dia-betics are well known to be at risk of infection particularlywhen diabetes is poorly controlled. Colonisation of theskin and nose by Staphylococcus aureus has been found to beinversely correlated with markers of glycaemic control[12]. Neutrophil bactericidal activity is also impaired indiabetics particularly in those with poor control [13].

In several reported series of epidural abscesses of mixedaetiologies diabetes mellitus has been an associated factor.Baker et al. reported diabetes in five of 39 patients andMaslen et al. in 18 of 28 patients [8, 11]. Maslen et al., ina literature search of other series of epidural abscesses,found that 16 of 254 cases had associated diabetes mellitus[8].

Prevention of epidural abscess after epidural injectionincludes use of an aseptic technique. Since direct intro-duction of bacteria is not the sole mechanism for this typeof infection, an aseptic technique by itself may notnecessarily prevent epidural abscesses. Despite this com-plication being rare there may be a case for prophylacticantistaphylococcal antibiotic therapy for all diabeticshaving epidural steroid administration.

References

1 Goucke CR, Graziotti P. Extradural abscess following localanaesthetic and steroid injection for chronic low back pain.British Journal of Anaesthesia 1990; 65: 427–9.

2 Chan ST, Leung S. Spinal epidural abscess following steroidinjection for sciatica. Spine 1989; 14: 106–8.

3 Waldman SD. Cervical epidural abscess after cervicalepidural nerve block with steroids [letter]. Anesthesia andAnalgesia 1991; 72: 717–18.

4 Bromage PR. Spinal extradural abscess: pursuit ofvigilance. British Journal of Anaesthesia 1993; 70: 471–3.

5 Mamourian AC, Dickman CA, Drayer BP, Sonntag VK.Spinal epidural abscess: three cases following spinal epiduralinjection demonstrated with magnetic resonance imaging.Anesthesiology 1993; 78: 204–7.

6 McGee-Collett M, Johnston IH. Spinal epidural abscess:presentation and treatment. A report of 21 cases. MedicalJournal of Australia 1991; 155: 14–17.

7 Danner RL, Hartman BJ. Update on spinal epiduralabscess: 35 cases and review of the literature. Reviews ofInfectious Diseases 1987; 9: 265–74.

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8 Maslen DR, Jones SR, Crislip MA, Bracis R, Dworkin RJ,Flemming JE. Spinal epidural abscess. Optimizing patientcare. Archives of Internal Medicine 1993; 153: 1713–21.

9 Borum SE, McLeskey CH, Williamson JB, Harris FS,Knight AB. Epidural abscess after obstetric epiduralanalgesia. Anesthesiology 1995; 82: 1523–6.

10 Ngan Kee WD, Jones MR, Thomas P, Worth RJ.Extradural abscess complicating extradural anaesthesia forCaesarean section. British Journal of Anaesthesia 1992; 69:647–52.

11 Baker AS, Ojemann RG, Swartz MN, Richardson EPJR.Spinal epidural abscess. New England Journal of Medicine1975; 293: 463– 468.

12 Lipsky BA, Pecoraro RE, Chen MS, Koepsell TD. Factorsaffecting staphylococcal colonization among NIDDMoutpatients. Diabetes Care 1987; 10: 483–6.

13 Reeves W, Wilson R. Infection, immunity and diabetes.In: Alberti K, Defronzo H, Keen H, Zimmet P, eds.International Textbook of Diabetes Mellitus. New York: JohnWiley & Sons Ltd, 1992: 1165–71.

CASE REPORT

Caesarean section in a parturient with respiratory failurecaused by cystic fibrosis

D. Bose,1 S. M. Yentis2 and N. J. Fauvel2

1 Department of Anaesthesia, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK2 Magill Department of Anaesthetics, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, UK

SummaryWe describe a 27-year-old primigravida suffering from cystic fibrosis. Her chest was colonised withBurkholderia cepacia and she was in respiratory failure for which she required constant nasalintermittent positive pressure ventilation. In view of her rapid deterioration, Caesarean section wasperformed under epidural anaesthesia at 25 weeks gestation. A live 790-g boy was delivered.Post-operatively she made steady progress for 5 days although still requiring nasal ventilatorysupport. Thereafter she developed pneumonia and required tracheal intubation and ventilation onthe eighth day. Her increasing hypoxaemia and pulmonary hypertension failed to respond to anytherapy including inhaled nitric oxide and she died on the tenth postoperative day.

Keywords Complications; cystic fibrosis. Anaesthesia; obstetric. Anaesthetic techniques, regional; epidural.

......................................................................................Correspondence to: Dr D. BoseAccepted 7 January 1997

Cystic fibrosis is an autosomal recessive disease, charac-terised by abnormally thick secretion from mucous glands.It occurs predominantly in Caucasians with a frequency of1:1600 births, although the gene frequency is 1:22 [1].Although both sexes are equally affected, males survivelonger than females [2]. With improvements in manage-ment, increasing numbers of patients are now surviving toadulthood and presenting for childbirth. Although theanaesthetic management for Caesarean section in patientswith cystic fibrosis has been described [3], management ofpatients with severe respiratory impediment has not beenreported. We describe a patient with cystic fibrosis with

respiratory failure who presented for Caesarean sectionbecause of worsening respiratory function.

Case history

A 27-year-old primigravida was referred from anotherhospital at 25 weeks gestation, in severe respiratory failure.She had been diagnosed as having cystic fibrosis at 2 yearsof age following recurrent chest infections. Over the yearsshe required multiple admissions for respiratory infections,but on no occasion did she need intensive care treat-ment. She was under the continuing care of a specialist

Case reports Anaesthesia, 1997, 52, pages 576–585................................................................................................................................................................................................................................................


respiratory unit in another hospital. At 20 years of age sheunderwent an uneventful general anaesthetic for evacua-tion of retained products of conception following aspontaneous abortion. She was known to have had pul-monary colonisation since then with Burkholderia cepaciaand Staphylococcus aureus, despite many courses of antibio-tics. She was determined to have a baby and, having beenturned down for adoption, became pregnant again aged 26years, despite medical advice against pregnancy and anestimated maximum life expectancy of 18 months at thistime. At 15 weeks gestation her respiratory functiondeteriorated. She was started on ceftazidime and requiredoxygen therapy overnight for the first time in her life.Termination of pregnancy was discussed but she refused.She was treated with temocillin and nebulised recombi-nant human deoxyribonuclease (DNase) but her respira-tory function continued to deteriorate (Table 1).

By 22 weeks the patient’s lung function had deterio-rated markedly and sputum culture revealed a floridgrowth of B. cepacia and S. aureus for which she receivedphysiotherapy using a Bird Mark 7 ventilator. Her respira-tion was supported at night with nasal continuous positiveairway pressure (CPAP) initially, subsequently changed tonasal bilevel positive airway pressure ventilation (BIPAP)with a ‘Nippy’ Mark1 ventilator (Friday Medical). Sheaccepted the nasal ventilation well but became increasinglydependent, eventually requiring it constantly to maintainadequate gas exchange (Table 1). There was no evidenceof pulmonary hypertension on electrocardiogram (ECG)or chest X-ray. By the 23rd week she was losing weightand unable to eat and total parenteral nutrition (TPN) wasstarted. Again termination was discussed, but was declined.At 24 weeks she developed pancreatitis with increasingbreathlessness. The pancreatitis settled over the nextweek but, in view of the increasing likelihood of urgentdelivery, she was transferred to our hospital because of the

availability of adult and neonatal intensive care unit (ICU)facilities on the same site.

On arrival she was tired but alert and orientated, withrespiratory rate 24 breath.minÿ1 and able to speak com-plete sentences on nasal BIPAP. Her drug therapy com-prised flucloxacillin, gentamicin, temocillin, ceftazidime,pethidine, metoclopramide, ranitidine, hydrocortisone,terbutaline and nebulised DNase.

After discussion between the patient, her family, obste-tricians, intensivists, neonatologists, anaesthetists and res-piratory physicians, it was decided to prolong pregnancyby a few days if possible provided that her condition did notdeteriorate, to increase the baby’s chance of survival.Arrangements were made for immediate Caesarean sectionif deterioration occurred. She had already received steroidsto enhance fetal lung maturity prior to transfer. After 2 moredays of constant support with nasal BIPAP she becameincreasingly exhausted and a decision was made to proceedto Caesarean section. At that time, she was totally dependenton nasal BIPAP and was unable to lie flatter than 608 to thehorizontal. Her arterial blood gases had deteriorated (PaO2

10.1 kPa, PaCO2 9.1 kPa; Table 1). She had a heart rate of120 beat.minÿ1, blood pressure of 130/70 mmHg andrespiratory rate of 24 breath.minÿ1.

The anaesthetic options were discussed fully with thepatient, her family and the various medical staff involved.Because of fears that postoperative weaning would beimpossible should tracheal intubation and intermittentpositive pressure ventilation (IPPV) be required, a regionaltechnique was chosen.

AnaesthesiaMonitoring consisted of pulse oximetry, ECG anddirect intra-arterial blood pressure measurement. A longfeeding intravenous catheter was already in place in theright cephalic vein. A 14G peripheral cannula was sited



Table 1 Lung function tests and arterial blood gases during pregnancy and following Caesarean section.

Gestation (weeks) Postoperative (days)

Pre- Intra-pregnant 16 21 22 22 24 operative 1 3 8 10

Ventilatory support none none none none BIPAP* BIPAP* Bird BIPAP* BIPAP* BIPAP* IPPV*F iO2 0.21 0.21 0.21 0.21 0.4 0.4 1.0 0.5 0.4 0.7 1.0FEV1; litres

(predicted – 2.86 l)0.89 0.43 0.64

FVC; litres(predicted – 3.28 l)

2.09 0.9 1.56

SpO2 98% 93% 92% 93% 99% 96% 85% 93% 94% 89% 85%PO2 (kPa) 7.8 7.8 8.54 22.8 10.1 7.3 10.7 10.4 9.3 11.2PCO2 (kPa) 4.95 6.09 6.81 9.1 10.6 10.9 9.6 12.6 24.9

* BIPAP = bilevel positive airway pressure; IPPV = intermittent positive pressure ventilation.

intravenously and 500 ml Hartmann’s solution preload wasgiven. A 16G epidural catheter was inserted in the sittingposition at L2–3, using the paramedian approach because ofpoor back flexion. After a test dose of 4 ml 1% lignocaine,she received a total of 30 ml 0.5% bupivacaine withfentanyl 25 mg in divided doses over 30 min to achieve alevel of T6 to light touch and T5 to cold. Nasal BIPAP wascontinued throughout the procedure; her SpO2 was 95–97% initially, falling to 90–95% at the start of surgery. Alower segment Caesarean section was performed with thepatient semisitting and tilted to the left. Surgery wasdifficult because the baby’s head was pushed down intothe pelvis; loops of small bowel kept obscuring the surgicalfield and there was marked pelvic venous distension.Although anaesthesia was adequate for skin incision anduterine manipulation, handling of the small bowel wasvery uncomfortable, requiring intravenous boluses ofketamine 5 mg to a total of 40 mg over 30 min. Oxygensaturation fell to 85–95% over the same period and herrespiratory support was changed from nasal BIPAP toflow-triggered support with 100% O2 using the BirdMark 7 ventilator. There was an initial improvement inSpO2 followed by a decline in oxygenation despite 150 mgaminophylline intravenously, as advised by her respiratoryphysicians. Arterial pressure was stable throughout theprocedure at around 120–140 mmHg systolic but shebecame more tachycardic towards the end of the surgerywith heart rate increasing from 120 to 170 beat.minÿ1.After delivery of a 790-g baby boy she was given 5 unitsof oxytocin intravenously over 10 min. Her respiratoryfunction remained stable but poor during the rest ofsurgery and she was transferred to the ICU totally depen-dent on the Bird for IPPV by mouthpiece, with no airadmixture.

Post-Caesarean sectionShe slowly improved over the next 12 h with intensivephysiotherapy and her arterial blood gases returning to thepre-operative values (Table 1). Nasal BIPAP was reinstatedand analgesia maintained with an epidural infusion of0.1% bupivacaine with 2 mg.mlÿ1 fentanyl, later changedto 0.25% bupivacaine.

She continued to improve, to the extent of sitting out ina chair by the 6th postoperative day by which time she waseating and drinking but still on supplementation withTPN. Epidural infusion continued until the 5th day; herwound was healthy and healing well and she was able tovisit her baby. However, on day 7th she developed a right-sided pneumonia with tachycardia, pyrexia and worseningrespiratory function. Despite antibiotic therapy and physio-therapy, she required tracheal intubation and IPPV onday 8 and rapidly deteriorated further. Pulmonary arterycatherisation revealed increasing pulmonary hypertension

and decreasing cardiac function. These were only tem-porarily relieved by inotropes, vasodilators and inhalednitric oxide. She died on the 10th postoperative day andpost-mortem examination revealed solid congested lungswith no evidence of aeration at all.

The baby stayed on the neonatal ICU for 7 weeks andsuffered from respiratory distress, bronchopulmonary dys-plasia, mild intraventricular haemorrhage and septicaemia.He was discharged to the father’s local hospital on nasaloxygen and intravenous caffeine.

Discussion

Patients with cystic fibrosis pose a special problem duringanaesthesia, mainly because of the pulmonary manifesta-tions. Failure to clear secretions leads to airway obstruc-tion, endobronchial infection and progressive restrictiveand obstructive pulmonary disease. An increased alveolar–arterial oxygen gradient leads to chronic hypoxaemiawhich may in turn cause right heart strain leading to corpulmonale. Pneumonia, bronchiectasis, atelectasis, abscesses,empyema, pneumothorax and haemoptysis may also occur[1]. The main organisms causing infection are Haemophilusinfluenzae and S. aureus initially and subsequently Gram-negative bacteria particularly Ps. aeruginosa [1]. Burkholderiacepacia (previously known as Pseudomonas cepacia) has recentlyemerged as an important pathogen in cystic fibrosispatients [4–7]. Death in cystic fibrosis is usually causedby extensive pulmonary infection leading to respiratoryfailure.

Cystic fibrosis may worsen during pregnancy [8], pos-sibly related to the effect of progesterone on sputumproduction [9] as well as the effect of the enlarginguterus on respiratory mechanics. Maternal mortalitywithin 6 months of delivery among pregnant cystic fibrosispatients has been reported to be as high as 7.7% [8, 10, 11]with perinatal mortality up to 8.5% [8, 10–12]. Pretermdelivery has been recorded in up to 21% of cases [8, 11,12]. The decision to become pregnant is difficult for cysticfibrosis patients because of the consequences of knowinglypassing on the defective gene to offspring and thedeleterious effect of pregnancy on respiratory function.Should respiratory embarrassment occur, any decision tocontinue or terminate pregnancy requires involvement ofphysicians, intensivists, obstetricians, paediatricians andanaesthetists in discussions with the family. Our patientand her husband were desperate to have children andunderstood the implications of this decision. The patient’shusband was tested preconception and found not tocarry the cystic fibrosis gene. Our patient was determinedto persist with pregnancy despite her worsening conditionand was well aware of the consequences.

Anaesthesia for our patient posed particular problems:



she had end-stage cystic fibrosis, was in respiratory failureand was also pregnant. Although there are reports ofpregnant patients with cystic fibrosis receiving anaesthesia,none was in respiratory failure [3, 10]. Indeed, we wereunable to find any reports of Caesarean section in respira-tory failure from any cause. Our options in this case weregeneral anaesthesia, local anaesthetic infiltration or aregional technique. Although general anaesthesia wouldallow better control of gas exchange and tracheobronchialtoilet we were concerned that postoperative weaning frommechanical ventilation would be impossible given pastexperiences of patients with end-stage cystic fibrosis [13,14, M. E. Hodson, personal communication]. Given ourpatient’s prepregnant life expectancy, IPPV could wellhave been a preterminal event. Local anaesthetic infiltra-tion is a technique rarely used now and expertise in its useis declining. In addition, it would have been difficult to dogiven the inability of the patient to lie flat and may nothave been sufficient during the difficult surgery.

Among the regional techniques we had the choice of asubarachnoid block, combined spinal–epidural anaesthesiaor continuous epidural alone. Subarachnoid block wasconsidered unsuitable because the patient was only com-fortable in a semirecumbent position and was unable to liesupine in bed, thus the level of block would have beenvery difficult to control. A rapid-onset high block couldalso have compromised her finely balanced respiratoryfunction. The patient was also harbouring a resistantbacterial chest infection and it was felt that any procedurewhich could increase the risks of bacterial meningitisshould be avoided. For the same reasons a combinedspinal–epidural technique was deemed unsuitable. Wesettled on cautious epidural anaesthesia as the method ofchoice, as we felt it would give the best chance of allowingsurgery whilst avoiding IPPV. One concern with thetechnique was further impairment of respiratory functionif the block was too extensive; a maximum level of T6

has been recommended for Caesarean section in patientswith cystic fibrosis [3]. Although epidural opioids maycause respiratory depression, the dose we used was smalland we hoped that it might compensate for the relativelylow level of block. In the event, the block was insufficientfor handling of the small bowel, but we were reluctant toextend the block further. In retrospect, although the doseof ketamine was small and we never lost verbal contactwith the patient, the ketamine may have contributed tothe gradual decline in her SpO2. However, the SpO2 hadalready fallen from its starting point before administrationof the ketamine.

On return to the ICU, the patient’s condition hadcertainly deteriorated markedly but she steadily improvedinitially and for a time there were hopes of prolongedrecovery. Indeed, her ability to see her baby and talk to her

family postoperatively was extremely important to thepatient, her husband and her family.

In retrospect, her respiratory function showed a relent-less decline from conception to her death (Table 1).Colonisation with B. cepacia is associated with a particu-larly poor outcome in cystic fibrosis [4, 15–17]. Despitebeing treated with temocillin to which B. cepacia is gen-erally known to respond [18], she continued to deterio-rate. Although the end result in our case was a tragicmaternal death, this case illustrates the importance of amultidisciplinary approach in the management of thesedesperately ill patients. Because survival to child-bearingage in cystic fibrosis continues to increase, physicians,obstetricians and anaesthetists may encounter morepatients like ours in the future.

Acknowledgment

We are grateful to Miss S. Bird for secretarial assistance.

References

1 Lane DJ, Weatherall DJ, Ledingham JGG, Warrell DA, eds.Cystic fibrosis. In: Oxford Textbook of Medicine, 3th edn.Oxford Medical Publications, 1996: 2746–55.

2 Corey M, Farewell V. Determinants of mortality fromcystic fibrosis in Canada, 1970–1989. American Journal ofEpidemiology 1996; 143: 1007–17.

3 Howell PR, Kent N, Douglas MJ. Anaesthesia for theparturiant with cystic fibrosis. International Journal ofObstetric Anesthesia 1993; 2: 152–8.

4 Whiteford ML, Wilkinson JD, McColl JH, et al. Outcomeof Burkholderia (Pseudomonas) cepacia colonisation in childrenwith cystic fibrosis following a hospital outbreak. Thorax1995; 50: 1194–8.

5 John M, Ecclestone E, Hunter E, Couroux P, Hussain Z.Epidemiology of Pseudomonas cepacia colonization amongpatients with cystic fibrosis. Pediatric Pulmonology 1994; 18:108–13.

6 Govan JR, Brown PH, Maddison J, et al. Evidence fortransmission of Pseudomonas cepacia by social contact incystic fibrosis. Lancet 1993; 342: 15–9.

7 Taylor RF, Gaya H, Hodson ME. Pseudomonas cepacia:pulmonary infection in patients with cystic fibrosis.Respiratory Medicine 1993; 87: 187–92.

8 Palmer J, Dillon Baker C, Tecklin JS, et al. Pregnancy inpatients with cystic fibrosis. Annals of Internal Medicine 1983;99: 596–600.

9 Cole BNL, Seltzer MH, Kassabian J, Abboud SE.Parenetral nutrition in a pregnant cystic fibrosis patient.Journal of Parenteral Enteral Nutrition 1987; 11: 205–7.

10 Corkey CWB, Newth CJL, Corey M, Levinson H.Pregnancy in cystic fibrosis: a better prognosis in patientswith pancreatic function. American Journal of Obstetrics &Gynecology 1981; 140: 737–42.

11 Canny GJ, Corey M, Livingstone RA, Carpenter S, Green



L, Levison H. Pregnancy and cystic fibrosis. Obsterics &tGynecology 1991; 77: 850–3.

12 Cohen LF, di Sant’Agnese PA, Friedlander J. Cystic fibrosisand pregnancy. A national survey. Lancet 1980; 2: 842–4.

13 Hodson ME, Madden BP, Steven MH, Tsang VT, YacoubMH. Non-invasive mechanical ventilation for cystic fibrosispatients – a potential bridge to transplantation. EuropeanRespiratory Journal 1991; 4: 524–7.

14 Davis PB, di Sant’Agnese PA. Assisted ventilation forpatients with cystic fibrosis Journal of the American MedicalAssociation 1978; 239: 1851–4.

15 Lewin LO, Byard PJ, Davis PB. Effect of Pseudomonascepacia colonization on survival and pulmonary function ofcystic fibrosis patients. Journal of Clinical Epidemiology 1990;43: 125–31.

16 Simpson IN, Finlay J, Winstanley DJ, et al. Multi-resistanceisolates possessing characteristics of both Burkholderia(Pseudomonas) cepacia and Burkholderia gladioli from patientswith cystic fibrosis. Journal of Antimicrobial Chemotherapy1994; 34: 353–61.

17 Tablan OC, Martone WJ, Doershuk cystic fibrosis, et al.Colonization of the respiratory tract with Pseudomonascepacia in cystic fibrosis. Risk factors and outcomes. Chest1987; 91:527–32.

18 Taylor RF, Gaya H, Hodson ME. Temocillin and cysticfibrosis: outcome of intravenous administration in patientsinfected with Pseudomonas cepacia. Journal of AntimicrobialChemotherapy 1992; 29: 341–4.

CASE REPORT

Complete airway obstruction during awakefibreoptic intubation

I. C. Shaw, E. A. Welchew, B. J. Harrison and S. Michael

The Departments of Anaesthetics and Surgery, The Northern General NHS Trust, Herries Road, Sheffield S5 7AU, UK

SummaryAwake fibreoptic intubation is well established as the optimum method of securing the airway inpatients in whom difficulty is anticipated. We report a patient undergoing awake fibreopticintubation in whom the use of topical local anaesthetic precipitated acute loss of the airway so thaturgent surgical intervention was required.

Keywords Intubation, tracheal; complications. Equipment; laryngoscope, fibreoptic.Airway; obstruction. Surgery; thyroidectomy, tracheostomy.

......................................................................................Correspondence to: Dr I. C. ShawAccepted: 8 January 1996

Awake fibreoptic intubation is well established as a techniquefor managing difficult intubation in an elective situation.However, it is not the answer to every airway problem. Wereport a patient with tracheal compression secondary to alarge goitre, in whom problems were encountered duringfibreoptic intubation because she had additional unexpectedabnormalities in the glottic region.

Case history

A 66-year-old female presented for elective excision ofa large recurrent thyroid goitre. She had gradually

developed her goitre over the previous 2 years and hadbeen experiencing increasing respiratory distress. At thepre-operative visit she said that she was unable to sleep onher back, a position in which she was unable to breathe.She preferred to sleep on her left side to minimise hersymptoms and professed to paroxysmal nocturnal dys-pnoea. These symptoms were attributed to her trachealcompression since there was no clinical or radiologicalevidence of left ventricular failure. For the previous 2 yearsshe had suffered from a persistent cough productive ofyellow sputum. Her exercise tolerance was approximately20 m. Examination of her airway revealed normal



dentition, a grade 2 Mallampati classification and markedtracheal deviation to the left. However, it was not obviousthat her trachea would be difficult to intubate. She wasgrossly obese, weighing 105 kg at a height of 1.55 m (bodymass index � 43) and suffered from an arthritic hip whichhad a limited flexion of 458. Further complicating heranaesthetic management was a long history of oesophagealreflux. Despite continuous use of omeprazole she haddeveloped an oesophageal stricture. Clinically she waseuthyroid; her current thyroid function test showed freeT4 16.2 pmol.lÿ1 (11–20), free T3 5.1 pmol.lÿ1 (3.1–5.4),THS < 0:03 mmol.lÿ1 (0.35–4.3).

A CT scan and chest X-ray showed a large mass arisingmainly from the right lobe of the thyroid but extendinginto the left lobe. The larynx was deviated to the left(Fig. 1). The mass extended retrosternally to the left of T3,deviated the trachea to the left and caused trachealcompression to a lumen of approximately 4 mm diameter(Fig. 2). An ENT consultant had reported that he had beenunable to view the vocal cords by either direct or fibreopticlaryngoscopy but had seen large supraglottic mucosal folds.

In view of her multiple problems it was decided that thesafest way to secure her airway was by an awake fibreoptictechnique. Elective tracheostomy and/or thyroidectomyusing local anaesthetic were out of the question because ofher obesity, the huge mass of the thyroid which extendedup to the cricoid cartilage, the deviation of the trachea andher inability to lie flat.

As well as her routine medications, for premedication

she received intramuscular hyoscine 400 mg 2 h pre-operatively in order to reduce secretions. In the anaes-thetic room full monitoring was established (baseline valueof SpO2 was 97% breathing air). Intravenous access wasgained and metoclopramide 10 mg was given intrave-nously. She was positioned with a 458 tilt, which was asfar as her arthritic hip would allow.

We planned to intubate orally to avoid bleeding, which isa recognised complication of nasal intubation. Bleeding mayobscure vision when using the fibreoptic laryngoscope,precipitate coughing and make intubation impossible. Themouth was prepared by spraying topical 10% lignocaine tothe tongue and oropharynx. At this point the patientbecame agitated and began struggling to maintain herown airway. Despite turning the patient on her left side,using chin lift, jaw thrust and a Guedel airway it was notpossible to maintain air entry. Her SpO2 decreased rapidlyto less than 80% and she became unconscious. In view ofthe difficulty in maintaining an airway, a laryngeal maskairway (LMA) was inserted, allowing adequate ventilationwhen continuous positive airway pressure via a Bainsystem was applied. This improved oxygenation andallowed the patient to recover. However, as she began towake up the airway was lost again thus leaving us nochoice but to induce anaesthesia using propofol 100 mg.Pulmonary ventilation was maintained with isoflurane1.5% in 100% oxygen allowing adequate oxygenationwith SpO2 > 93%. Fibreoptic laryngoscopy was then per-formed through the LMA. It was possible to see the



Figure 1 CT scan image at the level ofthe vocal cords showing the 5th cervicalvertebra. Anterior to this is the right lobeof the goitre causing deviation of thelarynx to the left.

epiglottis, the supraglottic mucosal folds and the aryte-noids but the vocal cords were not visible and intubationwas impossible.

Faced with the situation in which the patient’s airwaypatency was lost each time we tried to awaken her, wedecided to perform a percutaneous tracheostomy using theCiaglia technique. The displaced trachea could only bepalpated at the level of the cricothyroid membrane andattempts to locate it were made by passing a needle whilstaspirating for air. On several occasions the needle was feltto pass through cartilage but without aspiration of air,presumably due to the proximity of the walls of the com-pressed trachea. Eventually access was achieved, the open-ing was dilated and a size 6.0 mm cuffed tracheostomy tubewas inserted.

With the airway secured, further attempts at visualisingthe larynx were made using both the fibreoptic andMacintosh laryngoscope because we felt that oral intuba-tion would make surgical access easier. With difficulty anarrowed laryngeal inlet was seen, sufficient only to allowpassage of a size 10 gum elastic bougie. It was not possibleto advance a size 5.0 mm reinforced tracheal tube over thebougie and therefore surgery was performed using thepercutaneous tracheostomy tube.

During the surgical procedure it was found that thetracheostomy tube had entered the trachea through thecricoid cartilage from its lateral aspect. An uneventfulthyroidectomy was performed and at the end a formal

tracheostomy was fashioned through the second trachealring and a size 8.0 mm cuffed tracheostomy tube wasinserted. The patient was sedated and her lungs ventilatedelectively overnight. The sedation was stopped the nextmorning and by deflating the cuff as she woke up she wasable to breathe past the tracheostomy tube and talk. Shewas reviewed by an ENT surgeon who performedfibreoptic laryngoscopy but again was unable to visualisethe vocal cords.

Discussion

Fibreoptic techniques represent a significant advance inthe management of difficult intubation and are particularlysuitable for use in the awake patient in an elective situation[1]. With a carefully prepared patient, on most occasions, itis possible to achieve intubation without undue distress ordiscomfort. However, in the presence of either anatomicalor pathological changes, passage of the fibreoptic laryngo-scope may be difficult. These include tumours, infectionor oedema, any of which may diminish the space betweenthe tongue and the posterior pharyngeal wall, externalmasses such as a thyroid goitre that cause compression anddistortion of the airway and glottic problems such as themucosal folds that we saw in this patient. Further to this,the presence of blood, pus or secretions in the airway maymake visualisation of the cords with the fibreopticlaryngoscope impossible.



Figure 2 CT scan image at the level ofthe 7th cervical vertebra showing trachealcompression, to an anteroposteriordiameter of 4 mm, by the goitre.

In this patient we were unlucky enough to encountertwo airway problems, the second of which was unexpected.Not only was there significant airway obstruction second-ary to the tracheal compression and distortion of herairway by the goitre but in addition she had abnormalpharyngeal/laryngeal anatomy which caused functionalobstruction, resulting in loss of the airway and inabilityto intubate. The presence of the supraglottic mucosal foldswas one of the most significant factors making inspectionof her vocal cords difficult both pre-operatively and, as itturned out, intra-operatively as well. Despite obtainingviews of the epiglottis and the arytenoids, it was impossibleto navigate the fibreoptic laryngoscope between them toachieve intubation.

Some authors have described cases where the LMA hadbeen inserted in the awake patient to facilitate intubationwith the fibreoptic laryngoscope [2, 3]. Asai [4] reported asimilar case to the one we faced in which both direct andfibreoptic laryngoscopy had failed. In this patient, how-ever, following the insertion of the LMA, intubation wasachieved in less than 90 s. It was suggested that the LMAmay make it easier to locate the laryngeal inlet. The LMAis designed to conform to the hypopharynx and to form aseal around the larynx. Thus, if it is possible to ventilate thelungs through the LMA it is likely that the larynx lieswithin the cuff.

The possible causes of the airway obstruction in thispatient include lignocaine allergy, laryngospasm or the lossof muscle tone of the tongue following the application oflocal anaesthetic. Allergy seems unlikely since the patienthad been exposed to lignocaine both before and after thisepisode without any problems. We feel that a combinationof laryngospasm secondary to irritation by the lignocainespray and loss of muscle tone as a result of its local

anaesthetic action contributed to the loss of the patient’sairway. The LMA insertion did alleviate the immediateairway problem but did not allow us to view the vocalcords and, therefore, we were forced to proceed to apercutaneous tracheostomy. Even with the airway secureorotracheal intubation by direct or fibreoptic laryngoscopywas impossible because of the marked anatomical distor-tion of the upper airway.

There are several lessons to be learned from this case.First of all, patients with a difficult airway undergoingawake fibreoptic laryngoscopy and intubation can stilldevelop life-threatening airway obstruction; therefore, itis important to ensure that a surgeon who has the skills toperform a tracheostomy is readily available. Secondly,although the LMA is a useful tool in establishing andmaintaining an airway, it cannot always be relied upon toassist intubation in these difficult cases. Finally, during apercutaneous tracheostomy technique in cases of trachealcompression it may be difficult to identify the tracheallumen because the diameter may be only 3–4 mm.

References

1 Morris IR. Fibreoptic intubation. Canadian Journal ofAnaesthesia 1994; 41: 996–1008.

2 Maltby JR, Loken RG, Beriault MT, Archer DP. Laryngealmask airway with mouth opening less than 20 mm. CanadianJournal of Anaesthesia 1995; 42: 1140–2.

3 Langenstein H. The laryngeal mask airway in the difficultintubation. The results of a prospective study (in German).Anaesthetist 1995; 44: 712–8.

4 Asai T. Use of the laryngeal mask for fibrescope-aidedtracheal intubation in an awake patient with a deviatedlarynx. Acta Anaesthesiologica Scandinavica 1994; 38: 615–6.



complete airway obstruction during awake fibreoptic intubation

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