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Carotid artery puncture, airway obstruction and the laryngeal mask airway in a preeclamptic patient
International Journal of Obstetric Anesthesia (1996) 5, 194-191
8 1996 Pearson Professional Ltd
CASE REPORT
Carotid artery puncture, airway obstruction and the laryngeal mask airway in a preeclamptic patient C. R. Garcia-Rodriguez, S. M. Yentis Magi11 Department of Anaesthetics, Chelsea and Westminster Hospital, London, UK SUMMARY. We report a case of a preeclamptic patient with a difficult airway in whom attempted central venous cannulation led to inadvertent carotid artery puncture and dilatation causing immediate life threatening upper airway obstruction. The use of the laryngeal mask airway was life-saving on two occasions when other techniques of airway management had failed. We discuss the series of events that led to this critical incident and suggest areas in which management might have been improved.
Acute respiratory obstruction secondary to haematoma formation is a rare and potentially fatal complication following attempted central venous cannulation in both non-pregnantle3 and obstetric4 patients. In some such cases a cricothyroidotomy or emergency tracheostomy may be required.4 The laryngeal mask airway (LMA) has been successfully used in cases of failed or difficult intubation and it has been suggested that it should be available in all obstetric units.5 We describe a patient in whom multiple factors led to acute life-threatening respiratory obstruction, where the LMA was an essential part of management on two separate occasions.
observation and monitoring were required. Within 24 h the pain had become severe. Her arterial blood pressure (BP) was 130/90 mmHg and examination was normal other than slight tenderness in her back. Repeat CTG showed worsening fetal distress over the next 15 min, and a firm diagnosis of abruption was made. Immediate caesarean section (CS) was planned and 50 mg of ranitidine was given intravenously (i.v.). Investigations at this time (1800 h) were Hb 9.8 g/dl, platelet count 252 x log/l, sodium 140 mmol/l, potassium 4.4 mmol/l, urea 6.7 mmol/l and creatinine 88 mmoY1. The patient was frightened and refused to undergo any procedures. Her husband could not be found and a medical student fluent in Urdu explained that an emergency operation was needed, but she continued to refuse. Forty five minutes after the decision to operate her husband was located and by phone persuaded her to have the operation. During this time the CTG continued to deteriorate, whilst her diastolic BP remained 70-90 mmHg. She would not allow preoxgenation and refused sodium citrate. In view of the imminent death of the fetus and normal assessment of her airway, general anaesthesia (thiopentone 450 mg and suxamethonium 100 mg) was given without preoxygenation. The oxygen saturation (SpO,) fell rapidly after induction and laryngoscopy was difficult (Cormack & Lehane6 grade 3). Intubation by the senior registrar with a size 8.0 orotracheal tube was only possible after 45560 s with cricoid pressure relaxed and using a bougie, by which time the SpO, was 40% and there were multiple ectopics on the electrocardiogram. The intubation was noted to be traumatic. Once intubated, anaesthesia and surgery
CASE REPORT
A 64 kg 27-year-old primigravida of Pakistani origin was admitted at 35 weeks of an otherwise unremarkable pregnancy with a two day history of reduced fetal movements. She spoke no English and required her husband to be a translator. Previous anaesthetic records were unavailable. She had mild abdominal pain, was slightly tender in the right iliac fossa with a soft uterus and the cardiotocograph (CTG) was normal. The differential diagnosis included acute appendicitis and placental abruption and further C. R. Garcia-Rodriguez, Department of Anaesthetics, Royal Brompton Hospital, Sydney Street, S. M. Yentis, Magi11 Department of Anaesthetics, Chelsea and Westminster Hospital, London, SW10 9NH, UK.
Correspondence to S. M. Yentis. 194
Carotid artery puncture, airway obstruction and the laryngeal mask airway proceeded normally. Her lungs were ventilated with oxygen, nitrous oxide and isoflurane, and her stomach was emptied via an orogastric tube. She received atracurium 40 mg and morphine 5 mg i.v. peroperatively. The diagnosis of abruption was confirmed and a live male was delivered with Apgar scores of 2 and 7 at 1 and 5 min respectively. During the operation she received 1 L of Hartmann’s solution and 500 ml of Haemaccel, and her diastolic BP varied between 75 and 95 mmHg. Her trachea was extubated when she was awake and on her left side. Slight inspiratory stridor resolved after 2-3 min. Postoperatively she received a further 10 mg of morphine i.v. in divided doses, and the SpO, and non-invasive BP were monitored. Heparin 5000 U 12 hourly was started and 40% oxygen given overnight. Over the next 12 h the SpO, remained 99-100X and pulse rate 90-l 1S/min but her BP increased from 120/70 mmHg to 180/108 mmHg. Urine output fell from 4%50 ml/h to 12-l 3 ml/h with heavy proteinuria despite receiving 2 L of crystalloid over this time. On examination her jugular venous pressure was not raised and she had normal breath sounds, and mild but generalized oedema. She also had marked sublingual swelling, presumed to be from the difficult laryngoscopy, but was breathing easily with no signs of respiratory obstruction. A diagnosis of preeclampsia was made and she was started on sublingual nifedipine and then intravenous hydralazine. After 500 ml of colloid her urine output was still poor and it was therefore decided that central venous pressure monitoring was needed to guide further fluid therapy. Laboratory tests at this time (0900 h) were as follows: Hb 8.7 g/dl, white cells 40.6 x 10% platelets 138 x 109/1, prothrombin time (PT) 16 s (normal 12.516.5 s), activated partial thromboplastin time (APPT) 39 s (normal 27-38 s), thrombin time (TT) 13 s (normal 12-15 s), sodium 139 mmol/l, potassium 4.6 mmol/l, urea 8.0 mmol/l, creatinine 120 mmol/l (and though not available at the time urate 0.64 mmol/l [normal 0.17-0.371). The procedure was explained via her husband and was carried out by the anaesthetic registrar. Identification of the right internal jugular vein was difficult partly because of movement related to anxiety. At 1100 h using the Seldinger technique and self sealing syringe (Arrow kit size 7 Fr) a vessel was located and dilated. On removing the dilator there was obvious arterial bleeding from the site, the wire was removed and firm pressure applied. Approximately 30 s later the patient became agitated throwing off all monitors and developed signs of acute respiratory obstruction. There was a large swelling on the right side of her neck which extended into the tissues of her face, jaw and tongue. She then became cyanosed and
195
rapidly lost consciousness. Ventilation using a bag, mask and Guedel airway was impossible. Suxamethonium 100 mg was given i.v. to aid ventilation in case laryngeal spasm was contributing to the obstruction, and to aid laryngoscopy. The larynx could not be seen because of tense pharyngeal tissues and an extremely swollen tongue, and intubation was unsuccessful. A size 3 LMA was inserted which immediately allowed ventilation and the SpO, increased from 40% to 92%. After sedation and further paralysis and with an ear, nose and throat surgeon standing by, further intubation attempts were made by a senior anaesthetist. Because of blood and secretions in the pharynx fibreoptic intubation was unsuccessful. After several unsuccessful attempts at intubation under direct vision, (laryngoscopy was now grade 4) an orotracheal tube was placed blindly and correct position confirmed with the fibreoptic laryngoscope. She was transferred to the intensive care unit for ventilation. A chest radiograph showed a large right para-tracheal swelling. Haematology 2 h after the event (1300 h) was as follows: Hb 5.8 g/dl, white cells 27.9 x 106/1, platelets 70 x 109/1,PT 20 s, APTT 50 s, TT 18 s. Over the next 2 days she developed generalized oedema and acute oliguric renal failure with a peak urea 34 mmol/l and creatinine 275 mmolll. The coagulopathy resolved with transfusion of blood, FFP, platelets and cryoprecipitate. She was cardiovascularly stable and did not require further antihypertensive treatment. Her respiratory function was good but she developed left lower lobe consolidation and continued to need ventilation for upper airway swelling. She was scheduled to undergo elective tracheostomy but on day 11 of her intensive care unit (ICU) admission the tracheal tube became dislodged resulting in complete upper airway obstruction. Ventilation by face mask was again unsuccessful and laryngoscopy was grade 4; fortunately a size 3 LMA allowed easy ventilation. Fibreoptic laryngoscopy through the LMA showed oedematous vocal cords with erosions of the posterior 2-3 mm with a normal bronchial anatomy. Using the LMA for ventilation, a percutaneous tracheostomy was performed and a size 7.0 cuffed tracheostomy tube passed and sutured in position. Her renal function improved over the next 2 days but the glossal swelling persisted until day 20 when the cuff could be deflated and a minitracheostomy tube substituted. She had no family history of angioedema and C 1, C3 and C4 esterase inhibitor studies were normal. She made a full recovery, was discharged from hospital 30 days after admission and has remained well since. Subsequent examination of her previous anaesthetic notes, unavailable at the time of CS, revealed a grade 3 laryngoscopy 3 years before. Her baby was admitted to the neonatal ICU and
196 International
Journal of Obstetric Anesthesia
received i.v. colloids. He stayed from day 2 only because his mother was a patient on ICU and has remained well since.
DISCUSSION This case illustrates how several different problems can compound to produce a disastrous clinical situation. Once she had agreed to the emergency CS this patient posed a major dilemma to the anaesthetist. The options available at the time were (1) attempt regional blockade in a frightened, uncooperative patient with whom effective communication was impossible, or (2) proceed to a general anaesthetic without preoxygenation or antacid therapy. It was felt that option (1) was unlikely to succeed, although well prepared foreign speaking patients can have successful regional techniques. In retrospect it would have been better to have obtained consent for surgery and anaesthesia, with full explanation, when the patient was first admitted. It is hard to know, when carrying out a procedure that a patient has consented to, how forceful one can or should be when implementing a part of it when patient safety is compromised. Could she have been made to accept sodium citrate and preoxygenation? Respiratory obstruction in obstetric patients has usually been described after extubation following CS without prior warning signs of stridor or respiratory distress.7,8 Despite the early resolution of stridor immediately after extubation in our patient, it is possible that she did have some residual airway obstruction but manifested no signs of this. Pharyngeal oedema in pregnancy may be the first sign of preeclampsia9 whilst laryngeal oedema may occur in preeclampsia,lO prolonged strenuous labour,” overhydration with rapid weight gainI upper respiratory tract infection’ and Cl esterase inhibitor deficiency.14 Accessing a central vein via a peripheral or external jugular vein is safer than a direct approach but with a lower success rate.15 The internal jugular venous route is the preferred choice for most anaesthetists but carotid artery puncture occurs in up to 6% of cannulation attempts, 15-**increasing in frequency with inexperienced operators. I6 However, clinically significant haematoma formation is rare even in patients with coagulopathies. l8 Verification of arterial puncture by the force or colour of blood flow is not always reliable leading to dilation or catheter insertion in about 1 in 2000 cannulation attempts]’ which can be fatal due to haemorrhage. Our patient had normal coagulation tests and a falling but normal platelet count 2 h before attempted cannulation, but abnormal tests shortly
afterwards. Perhaps a more recent blood count and coagulation screen would have revealed abnormalities, however the rapid fall in platelet count from 252 to 138 x lo9 in 15 h is most significant. It is the combination of a coagulopathy and arterial dilatation that has led to rapid catastrophic airway obstruction requiring immediate intubation in non-pregnant patients.2 The design of the triple lumen catheter kit used in this case allowed a Seldindger wire to be placed in the carotid artery without disconnecting the syringe from the cannulating needle, which might have indicated arterial puncture. When arterial catheterization occurs, it has been recommended that the catheter be left in place and the hole in the artery closed surgically. Our patient suffered respiratory arrest 30 s after carotid artery dilatation, whereas Randalls & Toomey,4 described a pregnant patient with coagulopathy, in whom carotid artery puncture was associated with complete respiratory obstruction several hours later, suggesting that differing mechanisms of airway obstruction may exist. Haematoma formation in the neck may lead to obstruction of venous drainage causing laryngeal oedema or else extravasation of blood into pharyngeal soft tissues may cause obstruction above the level of the larynx over a much shorter period of time. Despite the paratracheal swelling illustrated on the chest X-ray, the fact that the LMA was successful suggests that the airway obstruction was predominantly supraglottic. This would also fit with the observation of a grossly swollen tongue and pharyngeal tissues. The fibreoptic laryngoscope is difficult to use when there is trauma of the airway with much bleeding but fibreoptic intubation through the LMA might have been successful obviating the need to remove and reinsert it between intubation attempts. Blind nasal intubation would have been unlikely to succeed in the presence of an enlarged tongue pushing posteriorly and would have risked further bleeding. The establishment of a surgical airway would have been very difficult even in experienced hands because of haematoma and loss of anatomical landmarks. The LMA has been used successfully in the management of suspected difficult intubation and in cases of failed intubation with inadequate bag and mask ventilation in both obstetric and non-pregnant patients.1g-22 In our patient the LMA proved life-saving on two separate occasions; in addition it allowed airway management for fibreoptic assisted percutaneous tracheostomy as has been previously reported.23 The common theme in critical incidents is a succession of mostly avoidable minor problems or accidents that go unrecognised or uncorrected.” Patient education and early consent for CS should be considered in
Carotid artery puncture, airway obstruction and the laryngeal mask airway foreign-only speaking patients with problems during pregnancy or labour. Obtaining the non-obstetric medical notes containing documentation of a previous difficult intubation would have increased awareness of airway problems at CS. Post-extubation stridor and a falling platelet count warning of worsening preeclampsia, attempted central venous cannulation without calling on senior expertise and lack of recognizing arterial puncture leading to dilation, were events which contributed to an avoidable incident. These have since been addressed in the development or improvement of guidelines on the labour ward. In particular these include improved plans for managing foreign-only speaking patients, well defined criteria for the diagnosis and management of preeclampsia, indications for central venous monitoring, stressing the place of peripheral placement of central lines, early involvement of senior anaesthestists and the ready availability of the LMA in all sites where obstetric anaesthesia is practised. REFERENCES
1. Knoblanche G E. Respiratory obstruction due to haematoma following internal jugular vein cannulation. Anaesth Intens Care 1979; 7: 286. 2. Weimann J, Frass M, Traindl 0, Pidlich J, Leithner C, Acute upper airway obstruction caused by cervical hematoma as a complication of an internal jugular vein catheter. Acta Medica Austriaca 1990; 17: 77-79. 3. O’Leary A M. Acute upper airway obstruction due to arterial puncture during percutaneous central venous cannulation of the subclavian vein, Anesthesiology 1990; 73: 780-782. 4. Randalls B. Toomey P J. Laryngeal oedema from a neck haematoma. Anaesthesia 1990; 45: 850-852. 5. Brimacombe J, Berry A. The laryngeal mask airway for obstetric anaesthesia and neonatal resuscitation. International Journal of Obstetric Anesthesia 1994; 3: 211-218. Cormdck R S, Lehane J. Difficult tracheal intubation in obstetrics. Anaesthesia 1984; 39: 1105-l 111. Seager S J, Macdonald R. Laryngeal oedema and preeclampsia. Anaesthesia 1980; 35: 360-362. Rocke D A, Scoones G P. Rapidly progressive laryngeal
9. 10. 11. 12. 13. 14. 15.
16.
17. 18.
19. 20. 21. 22. 23.
24.
197
oedema associated with pregnancy aggravated hypertension. Anaesthesia 1992; 47: 141-143. Heller P J, Scheider E P, Marx G F. Pharyngolatyngeal edema presenting as a symptom in pre-eclampsia. Obstet Gynecol 1983; 62: 523-525. Brock-Utne J G, Downing J W, Seedat F. Laryngeal oedema associated with pre-eclamptic toxaemia. Anaesthesia 1977; 32: 556558. McKenzie A I. Laryngeal oedema complicating obstetric anaesthesia. Anaesthesia 1978; 33: 271. Proctor A J M, White J B. Laryngeal oedema in pregnancy. Anaesthesia 1983; 38: 1676. Spotoft H, Christensen P. Laryngeal oedema accompanying weight gain in pregnancy. Anaesthesia 198 1; 36: 7 I. Peters M, Ryley D, Lockwood C. Hereditary angioedema and immunoglobulin A. A deficiency in pregnancy. Obstet Gynecol 1988; 72: 454455. Belani K G, Buckley J J, Gordon J R, Castaneda W. Percutaneous central venous line placement: A comparison of the internal and external jugular vein routes. Anesth Analg 1980; 59: 4&44. Sznajder J I, Zveibil F R, Bitterman H, Weiner P, Bursztein S. Central vein catheterisation: failure and complication rates by three percutaneous approaches. Arch Intern Med 1986; 146: 259-261. Schwartz A J, Jobes D R, Greenhow E, Stephenson L W. Ellison N. Carotid artery puncture with internal jugular cannulation. Anesthesiology 1979; S160: 511. Goldfarb G, Lebrec D. Percutaneous cannulation of the internal jugular vein in patients with coagulopathies, an experience based on 1000 attempts. Anesthesiology 1982; 56: 321-323. Chadwick I S, Vohra A. Anaesthesia for emergency caesarean section using the Brain laryngeal mask airway. Anaesthesia 1989; 44: 261-262. McClune S, Regan M, Moore J. Laryngeal mask airway for caesarean section. Anaesthesia 1990; 45: 2277228. Caulder I, Ordman A J, Jackowski A, Crockard H A. The Brain laryngeal mask airway; an alternative to emergency tracheal intubation. Anaesthesia 1990; 45: 137-139. De Mello W F, Kokan M. The laryngeal mask in failed intubation. Anaesthesia 1990; 45: 689-690. Dexter T J. The laryngeal mask airway: a method to improve visualisation of the trachea and larynx during fibreoptic assisted percutaneous tracheostomy. Anaesth Intens Care 1994; 22: 35-39. Runciman W B, Sellen A, Webb R K et al. Errors, Incidents and accidents in anaesthetic practice. Anaesth Intens Care 1993; 21: 506519.
8 1996 Pearson Professional Ltd
CASE REPORT
Carotid artery puncture, airway obstruction and the laryngeal mask airway in a preeclamptic patient C. R. Garcia-Rodriguez, S. M. Yentis Magi11 Department of Anaesthetics, Chelsea and Westminster Hospital, London, UK SUMMARY. We report a case of a preeclamptic patient with a difficult airway in whom attempted central venous cannulation led to inadvertent carotid artery puncture and dilatation causing immediate life threatening upper airway obstruction. The use of the laryngeal mask airway was life-saving on two occasions when other techniques of airway management had failed. We discuss the series of events that led to this critical incident and suggest areas in which management might have been improved.
Acute respiratory obstruction secondary to haematoma formation is a rare and potentially fatal complication following attempted central venous cannulation in both non-pregnantle3 and obstetric4 patients. In some such cases a cricothyroidotomy or emergency tracheostomy may be required.4 The laryngeal mask airway (LMA) has been successfully used in cases of failed or difficult intubation and it has been suggested that it should be available in all obstetric units.5 We describe a patient in whom multiple factors led to acute life-threatening respiratory obstruction, where the LMA was an essential part of management on two separate occasions.
observation and monitoring were required. Within 24 h the pain had become severe. Her arterial blood pressure (BP) was 130/90 mmHg and examination was normal other than slight tenderness in her back. Repeat CTG showed worsening fetal distress over the next 15 min, and a firm diagnosis of abruption was made. Immediate caesarean section (CS) was planned and 50 mg of ranitidine was given intravenously (i.v.). Investigations at this time (1800 h) were Hb 9.8 g/dl, platelet count 252 x log/l, sodium 140 mmol/l, potassium 4.4 mmol/l, urea 6.7 mmol/l and creatinine 88 mmoY1. The patient was frightened and refused to undergo any procedures. Her husband could not be found and a medical student fluent in Urdu explained that an emergency operation was needed, but she continued to refuse. Forty five minutes after the decision to operate her husband was located and by phone persuaded her to have the operation. During this time the CTG continued to deteriorate, whilst her diastolic BP remained 70-90 mmHg. She would not allow preoxgenation and refused sodium citrate. In view of the imminent death of the fetus and normal assessment of her airway, general anaesthesia (thiopentone 450 mg and suxamethonium 100 mg) was given without preoxygenation. The oxygen saturation (SpO,) fell rapidly after induction and laryngoscopy was difficult (Cormack & Lehane6 grade 3). Intubation by the senior registrar with a size 8.0 orotracheal tube was only possible after 45560 s with cricoid pressure relaxed and using a bougie, by which time the SpO, was 40% and there were multiple ectopics on the electrocardiogram. The intubation was noted to be traumatic. Once intubated, anaesthesia and surgery
CASE REPORT
A 64 kg 27-year-old primigravida of Pakistani origin was admitted at 35 weeks of an otherwise unremarkable pregnancy with a two day history of reduced fetal movements. She spoke no English and required her husband to be a translator. Previous anaesthetic records were unavailable. She had mild abdominal pain, was slightly tender in the right iliac fossa with a soft uterus and the cardiotocograph (CTG) was normal. The differential diagnosis included acute appendicitis and placental abruption and further C. R. Garcia-Rodriguez, Department of Anaesthetics, Royal Brompton Hospital, Sydney Street, S. M. Yentis, Magi11 Department of Anaesthetics, Chelsea and Westminster Hospital, London, SW10 9NH, UK.
Correspondence to S. M. Yentis. 194
Carotid artery puncture, airway obstruction and the laryngeal mask airway proceeded normally. Her lungs were ventilated with oxygen, nitrous oxide and isoflurane, and her stomach was emptied via an orogastric tube. She received atracurium 40 mg and morphine 5 mg i.v. peroperatively. The diagnosis of abruption was confirmed and a live male was delivered with Apgar scores of 2 and 7 at 1 and 5 min respectively. During the operation she received 1 L of Hartmann’s solution and 500 ml of Haemaccel, and her diastolic BP varied between 75 and 95 mmHg. Her trachea was extubated when she was awake and on her left side. Slight inspiratory stridor resolved after 2-3 min. Postoperatively she received a further 10 mg of morphine i.v. in divided doses, and the SpO, and non-invasive BP were monitored. Heparin 5000 U 12 hourly was started and 40% oxygen given overnight. Over the next 12 h the SpO, remained 99-100X and pulse rate 90-l 1S/min but her BP increased from 120/70 mmHg to 180/108 mmHg. Urine output fell from 4%50 ml/h to 12-l 3 ml/h with heavy proteinuria despite receiving 2 L of crystalloid over this time. On examination her jugular venous pressure was not raised and she had normal breath sounds, and mild but generalized oedema. She also had marked sublingual swelling, presumed to be from the difficult laryngoscopy, but was breathing easily with no signs of respiratory obstruction. A diagnosis of preeclampsia was made and she was started on sublingual nifedipine and then intravenous hydralazine. After 500 ml of colloid her urine output was still poor and it was therefore decided that central venous pressure monitoring was needed to guide further fluid therapy. Laboratory tests at this time (0900 h) were as follows: Hb 8.7 g/dl, white cells 40.6 x 10% platelets 138 x 109/1, prothrombin time (PT) 16 s (normal 12.516.5 s), activated partial thromboplastin time (APPT) 39 s (normal 27-38 s), thrombin time (TT) 13 s (normal 12-15 s), sodium 139 mmol/l, potassium 4.6 mmol/l, urea 8.0 mmol/l, creatinine 120 mmol/l (and though not available at the time urate 0.64 mmol/l [normal 0.17-0.371). The procedure was explained via her husband and was carried out by the anaesthetic registrar. Identification of the right internal jugular vein was difficult partly because of movement related to anxiety. At 1100 h using the Seldinger technique and self sealing syringe (Arrow kit size 7 Fr) a vessel was located and dilated. On removing the dilator there was obvious arterial bleeding from the site, the wire was removed and firm pressure applied. Approximately 30 s later the patient became agitated throwing off all monitors and developed signs of acute respiratory obstruction. There was a large swelling on the right side of her neck which extended into the tissues of her face, jaw and tongue. She then became cyanosed and
195
rapidly lost consciousness. Ventilation using a bag, mask and Guedel airway was impossible. Suxamethonium 100 mg was given i.v. to aid ventilation in case laryngeal spasm was contributing to the obstruction, and to aid laryngoscopy. The larynx could not be seen because of tense pharyngeal tissues and an extremely swollen tongue, and intubation was unsuccessful. A size 3 LMA was inserted which immediately allowed ventilation and the SpO, increased from 40% to 92%. After sedation and further paralysis and with an ear, nose and throat surgeon standing by, further intubation attempts were made by a senior anaesthetist. Because of blood and secretions in the pharynx fibreoptic intubation was unsuccessful. After several unsuccessful attempts at intubation under direct vision, (laryngoscopy was now grade 4) an orotracheal tube was placed blindly and correct position confirmed with the fibreoptic laryngoscope. She was transferred to the intensive care unit for ventilation. A chest radiograph showed a large right para-tracheal swelling. Haematology 2 h after the event (1300 h) was as follows: Hb 5.8 g/dl, white cells 27.9 x 106/1, platelets 70 x 109/1,PT 20 s, APTT 50 s, TT 18 s. Over the next 2 days she developed generalized oedema and acute oliguric renal failure with a peak urea 34 mmol/l and creatinine 275 mmolll. The coagulopathy resolved with transfusion of blood, FFP, platelets and cryoprecipitate. She was cardiovascularly stable and did not require further antihypertensive treatment. Her respiratory function was good but she developed left lower lobe consolidation and continued to need ventilation for upper airway swelling. She was scheduled to undergo elective tracheostomy but on day 11 of her intensive care unit (ICU) admission the tracheal tube became dislodged resulting in complete upper airway obstruction. Ventilation by face mask was again unsuccessful and laryngoscopy was grade 4; fortunately a size 3 LMA allowed easy ventilation. Fibreoptic laryngoscopy through the LMA showed oedematous vocal cords with erosions of the posterior 2-3 mm with a normal bronchial anatomy. Using the LMA for ventilation, a percutaneous tracheostomy was performed and a size 7.0 cuffed tracheostomy tube passed and sutured in position. Her renal function improved over the next 2 days but the glossal swelling persisted until day 20 when the cuff could be deflated and a minitracheostomy tube substituted. She had no family history of angioedema and C 1, C3 and C4 esterase inhibitor studies were normal. She made a full recovery, was discharged from hospital 30 days after admission and has remained well since. Subsequent examination of her previous anaesthetic notes, unavailable at the time of CS, revealed a grade 3 laryngoscopy 3 years before. Her baby was admitted to the neonatal ICU and
196 International
Journal of Obstetric Anesthesia
received i.v. colloids. He stayed from day 2 only because his mother was a patient on ICU and has remained well since.
DISCUSSION This case illustrates how several different problems can compound to produce a disastrous clinical situation. Once she had agreed to the emergency CS this patient posed a major dilemma to the anaesthetist. The options available at the time were (1) attempt regional blockade in a frightened, uncooperative patient with whom effective communication was impossible, or (2) proceed to a general anaesthetic without preoxygenation or antacid therapy. It was felt that option (1) was unlikely to succeed, although well prepared foreign speaking patients can have successful regional techniques. In retrospect it would have been better to have obtained consent for surgery and anaesthesia, with full explanation, when the patient was first admitted. It is hard to know, when carrying out a procedure that a patient has consented to, how forceful one can or should be when implementing a part of it when patient safety is compromised. Could she have been made to accept sodium citrate and preoxygenation? Respiratory obstruction in obstetric patients has usually been described after extubation following CS without prior warning signs of stridor or respiratory distress.7,8 Despite the early resolution of stridor immediately after extubation in our patient, it is possible that she did have some residual airway obstruction but manifested no signs of this. Pharyngeal oedema in pregnancy may be the first sign of preeclampsia9 whilst laryngeal oedema may occur in preeclampsia,lO prolonged strenuous labour,” overhydration with rapid weight gainI upper respiratory tract infection’ and Cl esterase inhibitor deficiency.14 Accessing a central vein via a peripheral or external jugular vein is safer than a direct approach but with a lower success rate.15 The internal jugular venous route is the preferred choice for most anaesthetists but carotid artery puncture occurs in up to 6% of cannulation attempts, 15-**increasing in frequency with inexperienced operators. I6 However, clinically significant haematoma formation is rare even in patients with coagulopathies. l8 Verification of arterial puncture by the force or colour of blood flow is not always reliable leading to dilation or catheter insertion in about 1 in 2000 cannulation attempts]’ which can be fatal due to haemorrhage. Our patient had normal coagulation tests and a falling but normal platelet count 2 h before attempted cannulation, but abnormal tests shortly
afterwards. Perhaps a more recent blood count and coagulation screen would have revealed abnormalities, however the rapid fall in platelet count from 252 to 138 x lo9 in 15 h is most significant. It is the combination of a coagulopathy and arterial dilatation that has led to rapid catastrophic airway obstruction requiring immediate intubation in non-pregnant patients.2 The design of the triple lumen catheter kit used in this case allowed a Seldindger wire to be placed in the carotid artery without disconnecting the syringe from the cannulating needle, which might have indicated arterial puncture. When arterial catheterization occurs, it has been recommended that the catheter be left in place and the hole in the artery closed surgically. Our patient suffered respiratory arrest 30 s after carotid artery dilatation, whereas Randalls & Toomey,4 described a pregnant patient with coagulopathy, in whom carotid artery puncture was associated with complete respiratory obstruction several hours later, suggesting that differing mechanisms of airway obstruction may exist. Haematoma formation in the neck may lead to obstruction of venous drainage causing laryngeal oedema or else extravasation of blood into pharyngeal soft tissues may cause obstruction above the level of the larynx over a much shorter period of time. Despite the paratracheal swelling illustrated on the chest X-ray, the fact that the LMA was successful suggests that the airway obstruction was predominantly supraglottic. This would also fit with the observation of a grossly swollen tongue and pharyngeal tissues. The fibreoptic laryngoscope is difficult to use when there is trauma of the airway with much bleeding but fibreoptic intubation through the LMA might have been successful obviating the need to remove and reinsert it between intubation attempts. Blind nasal intubation would have been unlikely to succeed in the presence of an enlarged tongue pushing posteriorly and would have risked further bleeding. The establishment of a surgical airway would have been very difficult even in experienced hands because of haematoma and loss of anatomical landmarks. The LMA has been used successfully in the management of suspected difficult intubation and in cases of failed intubation with inadequate bag and mask ventilation in both obstetric and non-pregnant patients.1g-22 In our patient the LMA proved life-saving on two separate occasions; in addition it allowed airway management for fibreoptic assisted percutaneous tracheostomy as has been previously reported.23 The common theme in critical incidents is a succession of mostly avoidable minor problems or accidents that go unrecognised or uncorrected.” Patient education and early consent for CS should be considered in
Carotid artery puncture, airway obstruction and the laryngeal mask airway foreign-only speaking patients with problems during pregnancy or labour. Obtaining the non-obstetric medical notes containing documentation of a previous difficult intubation would have increased awareness of airway problems at CS. Post-extubation stridor and a falling platelet count warning of worsening preeclampsia, attempted central venous cannulation without calling on senior expertise and lack of recognizing arterial puncture leading to dilation, were events which contributed to an avoidable incident. These have since been addressed in the development or improvement of guidelines on the labour ward. In particular these include improved plans for managing foreign-only speaking patients, well defined criteria for the diagnosis and management of preeclampsia, indications for central venous monitoring, stressing the place of peripheral placement of central lines, early involvement of senior anaesthestists and the ready availability of the LMA in all sites where obstetric anaesthesia is practised. REFERENCES
1. Knoblanche G E. Respiratory obstruction due to haematoma following internal jugular vein cannulation. Anaesth Intens Care 1979; 7: 286. 2. Weimann J, Frass M, Traindl 0, Pidlich J, Leithner C, Acute upper airway obstruction caused by cervical hematoma as a complication of an internal jugular vein catheter. Acta Medica Austriaca 1990; 17: 77-79. 3. O’Leary A M. Acute upper airway obstruction due to arterial puncture during percutaneous central venous cannulation of the subclavian vein, Anesthesiology 1990; 73: 780-782. 4. Randalls B. Toomey P J. Laryngeal oedema from a neck haematoma. Anaesthesia 1990; 45: 850-852. 5. Brimacombe J, Berry A. The laryngeal mask airway for obstetric anaesthesia and neonatal resuscitation. International Journal of Obstetric Anesthesia 1994; 3: 211-218. Cormdck R S, Lehane J. Difficult tracheal intubation in obstetrics. Anaesthesia 1984; 39: 1105-l 111. Seager S J, Macdonald R. Laryngeal oedema and preeclampsia. Anaesthesia 1980; 35: 360-362. Rocke D A, Scoones G P. Rapidly progressive laryngeal
9. 10. 11. 12. 13. 14. 15.
16.
17. 18.
19. 20. 21. 22. 23.
24.
197
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