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Epidural Analgesia Associated With a Fatal Outcome in a Patient With an Unrecognized Brain Tumour

Posted on: Saturday, 8 January 2005, 03:00 CST

SUMMARY

A fatality associated with epidural analgesia in a patient with an unsuspected brain tumour has not been reported in the literature. We describe a case of postoperative lumbar epidural analgesia in a 54-year-old female patient who had an undiagnosed brain tumour and a fatal outcome postoperatively. The factors that potentially contributed to this mishap and the possible alternative management of this patient are discussed.

Key Words: ANALGESIA, EPIDURAL: brain, tumour; headache; postoperative complications

Epidural analgesia is widely used for the management of postoperative pain1,2 and its complications are well known3. In patients with increased intracranial pressure (ICP), epidural analgesia is generally considered to be relatively contraindicated, due to the effect of epidural injection and the potential effects of possible dural puncture4,5. After epidural injection, not only pressure effects from the fluid volume load across the epidural space, but also respiratory depression induced by the epidural opioid, might directly or indirectly precipitate an increase in ICP. We report a case of an unexpected postoperative death where lumbar epidural analgesia for postoperative pain control was used in a patient with an undiagnosed brain tumour.

CASE HISTORY

The patient was a 54-year-old female (166 cm, 59 kg) who had had a palpable pelvic mass for five years. Her past history was otherwise unremarkable except for chronic headache of one year duration that had been treated with paracetamol. She had no symptoms suggestive of neurological disease. The patient sought treatment when she experienced expansion of her pelvic mass and hypermenorrhoea.

Physical examination on her admission to a local obstetric and gynaecological hospital was notable for the palpation of the parametrium and adnexae. This demonstrated a huge pelvic mass equivalent to 18 weeks gestational size. A uterine myoma (12 cm in diameter) with cystic degeneration was evident on an abdominal ultrasound. Therefore, total abdominal hysterectomy was scheduled for the next day. The preoperative assessment and examination was normal except for anaemia (haemoglobin 7.4 g/dl). She was given a blood transfusion of one unit of packed red blood cells.

On her arrival in the operating room, epidural analgesia for postoperative pain control was established. With the patient in a lateral position, an epidural catheter was inserted uneventfully in the interspace between L3 and L4, using an 18-gauge Tuohy needle. Two per cent lignocaine (2 ml) was administered as a test dose. A 10 ml loading dose of 0.25% bupivacaine and 2 mg morphine was injected via an epidural catheter; each 5 ml was given over a 20 to 30 second period. The combined volume of the test and loading dose administered was 12 ml. The patient had no complaints and her vital signs remained stable throughout. Following premedication with glycopyrrolate 0.2 mg and preoxygenation, general anaesthesia was induced with fentanyl 150 g, thiopentone 360 mg, and atracurium 30 mg. Tracheal intubation proceeded smoothly. Anaesthesia was maintained with isoflurane in oxygen (inspired oxygen fraction [F^sub i^O^sub 2^] 0.6), and end-tidal carbon dioxide (CO2) was maintained between 28 and 30 mmHg. Her vital signs were stable intraoperatively, the blood pressure fluctuating around 110/60 mmHg and heart rate 60-80 beats/min. After regaining muscle function and wakening two hours later, the patient was extubated in the operating room. The total fluid input intraoperatively was 1100 ml Ringer's solution and the fluid output 150 ml of blood and 50 ml of urine.

The patient was alert and her vital signs were stable when she entered the recovery unit. She started to use her patient- controlled epidural analgesia (PCEA) device (Abbott AIM plus, Abbott Laboratories, North Chicago, Illinois). The PCEA regimen used bupivacaine 0.0625% combined with morphine 0.02 mg/ml, at 2 ml/h basal infusion rate, with a 1 ml demand and a 20-minute lockout interval. Two hours later, when the patient was transferred to a general ward, her condition was stable and her mental status was clear. Later that evening, about six hours after leaving the recovery unit, an anaesthetist routinely evaluated her condition. She was found to be lethargic, but could be roused. The level of sedation (as evaluated by the Ramsay Sedation Scale) was 4 (asleep, brisk response to loud auditory stimuli)6. Moderate dizziness and nausea, without wound pain, were also noted. The basal infusion rate was decreased from 2.0 to 1.2 ml/h, and the patient observed closely. Three hours later she was reported to "choke" while in a sitting position and suffered a respiratory arrest followed by sudden loss of consciousness. She was given 100% oxygen and manually ventilated with an Ambu bag and facemask. An electrocardiographic monitor showed sinus bradycardia, followed by asystole. Tracheal intubation and external cardiac massage were performed and intravenous adrenaline given immediately. The cardiac rhythm returned to sinus rhythm after 15 minutes of resuscitation. However, by that time both pupils were dilated with absence of light reflex. During resuscitation, there was no evidence of aspiration and naloxone was not administered because she was intubated and manually ventilated. Throughout the period from initiation of PCEA to this event (11 hours), the total volume of epidural solution administered was 24.1 ml (15 mg bupivacaine and 0.5 mg morphine). The patient was transferred to our institution for further management. When she arrived in our surgical intensive care unit, her Glasgow Coma Scale determination was 3. Brain stem reflexes were absent. Her arterial blood pressure was unstable despite high-dose inotropes.

The next morning, a friend of the patient brought in a health evaluation that had been completed two days prior to surgery, at a centre different from that at which she was subsequently admitted. This report included a computerized tomography scan of the brain (Figure 1) showing a huge mass in the right frontal region and obstructive hydrocephalus. The hospital at which the patient had surgery and postoperative epidural analgesia had been unaware of these findings. Due to her persistent vegetative state and poor prognosis, her treatment was supportive and she died 35 days later. An autopsy was not performed.

FIGURE 1: A large cerebral tumour with perifocal oedema on the right side of the frontal region and shift of the midline structures to the left, seen on computerized tomography scan.

DISCUSSION

We present a rare case of a fatality in a patient with an undiagnosed brain tumour who was receiving epidural analgesia. In this case, fatal brain herniation may have occurred at any time during hospitalization, because of tumour growth or swelling and brainstem compression. We consider that several factors, including epidural analgesia, may have contributed to deterioration.

First, volume loading of the lumbar epidural space can increase ICP4. This adverse effect appears more pronounced in patients with persistently high ICP5. Second, epidural-induced sympathectomy causes peripheral vasodilation, which could result in cerebral hypoperfusion and aggravate brainstem ischemia. Third, cephalic movement of epidural morphine may cause delayed respiratory depression, resulting in hypercarbia and further increase of ICP. Such depression characteristically occurs six to twelve hours following epidural administration of morphine7, the interval from epidural administration to deteriorating conscious state in this patient being 10 hours. The level of consciousness is considered the most reliable clinical sign of respiratory depression8. It is doubtful whether the dose of opioid given (2.5 mg morphine over the whole clinical course) could have caused sufficient respiratory depression to produce this fatal episode9,10. However, in a patient with a pre-existent brain tumour, even mild respiratory depression can precipitate a rise in ICP, accelerating the progress of fatal cerebral herniation. One or all of these factors may explain our patient's sudden respiratory arrest and cardiovascular collapse.

Another consideration is whether perioperative intravenous infusion was an aggravating factor for cerebral tumour swelling or peritumour oedema. Patients with cerebral oedema as a consequence of a brain tumour inevitably have disruption of the blood-brain barrier that allows fluid movement into brain tissue. Although in this case the fluid input and output was balanced perioperatively, fluid shifts and reactive postoperative cerebral oedema may develop. In addition, haemorrhage within the brain tumour could occur.

The patient had no preoperative neurological symptoms except chronic headache. She was alert and had performed daily activity, which required muscle strength and coordination, normally. Brain tumours may attain a large size due to a slow growth rate. This enables the intracranial contents to accommodate to the slowly evolving mass lesion, prior to the appearance of a clinically detectable neurological deficit11. Thus, anaesthetists who recommend epidural analgesia for patients with chronic headache should be aware that this symptom may be caused by a brain tumour. More importantly, a fatal event such as this might have been preventable had a detailed his\tory and thorough physical examination, including neurological evaluation, been performed. Elective surgery for total abdominal hysterectomy would have been cancelled if the surgeon or anaesthetist had been aware of the patient's pre-existent brain tumour. Furthermore, alternative therapies by neurosurgery and the use of osmotic agents and corticosteroid to reduce her ICP could have been employed.

In conclusion, we report an unusual case of a patient with an unrecognized brain tumour, in whom lumbar epidural analgesia may possibly have precipitated a fatal event. Several other factors, including fluid shifts, tumour haemorrhage and disease progression may also have contributed. A detailed preoperative history and comprehensive physical examination might have resulted in diagnosis of the tumour and prevention of this tragedy.

REFERENCES

1. Liu SS, Allen HW, Olsson GL. Patient-controlled epidural analgesia with bupivacaine and fentanyl on hospital wards: prospective experience with 1030 surgical patients. Anesthesiology 1998; 88:688-695.

2. Flisberg P, Rudin A, Linner R, Lundberg CJ. Pain relief and safety after major surgery: a prospective study of epidural and intravenous analgesia in 2696 patients. Acta Anaesthesiol Scand 2003; 47:457-465.

3. Horlocker TT, Wedel DJ. Neurologic complications of spinal and epidural anesthesia. Reg Anesth Pain Med 2000; 25:83-98.

4. Grocott HP, Mutch WA. Epidural anesthesia and acutely increased intracranial pressure: lumbar epidural space hydrodynamics in a porcine model. Ancsthesiology 1996; 85:1086-1091.

5. Hilt H, Gramm HJ, Link J. Changes in intracranial pressure associated with extradural anaesthesia. Br J Anaesth 1986; 58:676- 680.

6. Ramsay MA, Savege TM, Simpson BR, Goodwin R. Controlled sedation with alphaxalone-alphadolone. Br Med J 1974; 2:656-659.

7. Kafer ER, Brown JT, Scott D et al. Biphasic depression of ventilatory responses to CO2 following epidural morphine. Anesthesiology 1983; 58:418-427.

8. Etches RC, Sandler AN, Daley WD. Respiratory depression and spinal opioids. Can J Anaesth 1989; 36:165-185.

9. Busch EH, Stedman PM. Epidural morphine for postoperative pain on medical-surgical wards: a clinical review. Anesthesiology 1987; 67:101-104.

10. Fuller JG, McMorland GH, Douglas MJ, Palmer L. Epidural morphine for analgesia after caesarean section: a report of 4880 patients. Can J Anaesth 1990; 37:636-640.

11. Vender JR, Black P, Natter HM, Katsetos CD. Post-anesthesia uncal herniation secondary to a previously unsuspected temporal glioma. J Forensic Sci 1995; 40:900-902.

H. J. TSAI*, M. Y. TSOU[dagger], C. M. HO[double dagger], S. K. TSAI

Departments of Anesthesiology, Taipei Veterans General Hospital, Mackay Memorial Hospital and National Yang-Ming University, Taipei, Taiwan

* M.D., Attending Anesthesiologist, Department of Anesthesiology, Mackay Memorial Hospital.

[dagger] M.D., Ph.D., Associate Professor and Chief in Division of Neuroanesthesia, Department of Anesthesiology, Taipci Veterans General Hospital and National Yang-Ming University.

[double dagger] M.D., Ph.D.,Associate Professor and Attending Anesthesiologist, Department of Anesthesiology, Taipei Veterans General Hospital and National Yang-Ming University.

M.D., Ph.D., Professor and Chairman, Department of Anesthesiology, Taipei Veterans General Hospital and National Yang- Ming University.

Address for reprints: Dr Chiu-Ming Ho, Department of Anesthesiology, Taipei Veterans General Hospital, No 201, Sec.2, Shpai Rd, Taipei 112, Taiwan.

Accepted for publication on September 2, 2004.

Copyright Australian Society of Anaesthetists Dec 2004

Source: Anaesthesia and Intensive Care

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