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Sympathetic hyperactivity, respiratory failure, pruritus, and anesthesia after unintentional epidural injection of potassium chloride: Case report
Regional Anesthesia and Pain Medicine23(2): 219-222, 1998
Sympathetic Hyperactivity, Respiratory Failure, Pruritus, and Anesthesia After Unintentional Epidural Injection of Potassium Chloride: Case Report Paulo do Nascimento Jr., M.D., * Norma Sueli Pinheiro M6dolo, M.D., Ph.D., * Jose Fernando do Amaral Meletti, M.D.,* and Jose Reinaldo Cerqueira Braz, M.D., Ph.D.*
Backgroundand Objectives. A combination of epidural and general anesthesia has been widely used to attenuate the surgical stress response and to provide postoperative analgesia. This case report illustrates the use of this anesthetic technique. Analgesia was induced with local anesthetic in the immediate postoperative period using unintentional 19.1 % potassium chloride (KCI) as diluent. Methods. An ASA I male patient was scheduled for surgical correction of idiopathic megaesophagus under continuous epidural anesthesia combined with general anesthesia. In the postoperative period, while preparing 10 mL 0.125% bupivacaine to be administered through the epidural catheter for pain control, 5 mL 19.1 % KCI was unintentionally used as diluent, resulting in a 9.55% potassium solution concentration. Results. The patient developed warmness of the lower limbs, tachycardia, hypertension, intense pruritus on the chest, agitation, exacerbation of sensory and motor blocks, and respiratory failure secondary to pulmonary edema, requiring ventilatory support. Total recovery was observed after 24 hours. Conclusions. Epidurally injected potassium leads to severe clinical manifestations caused by autonomic dysfunction, spinal cord irritation, and possible release of histamine. Despite continuous recommendations, ampule misidentification still happens in hospitals, frequently leading to serious accidents. Reg Anesth Pain Med1998: 23: 219-222. Key words: unintentional injection, sympathetic hyperactivity, respiratory failure, pruritus, potassium chloride, combined epidural and general anesthesia.
The combination of epidural and general anesthesia to attenuate the surgical stress response has ·From the Department of Anesthesia, Faculdade de Medicina de Botucatu, Sao Paulo, Brazil. Accepted for publication September 20, 1997. Reprint requests: Paulo do Nascimento Jr., M.D., Departamento de Ancstesiologla, Faculdade de Mcdlcina de BotucatuUNESP, Distrito de Rublao Junior sln, 18.618·970·Botucatu, SP, Brazil. Copyright CD 1998 by the American Society of Regional Anesthesia. 0146·521X/98/2302·0019$5.0010
been widely used. This technique allows prolongation of postoperative pain control with epidural administration of opioids and local anesthetics (14). Serious complications associated with unintentional administration of drugs into the epidural space have previously been reported (5-11). However, there are only a few cases related to the unintentional epidural injection of potassium chloride (KCI) in different concentrations, leading to temporary or permanent sensory and motor deficits (711). We report a case of combined epidural and
220
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general anesthesia in a patient in who received 19.1 % KCI unintentionally.
Case Report A 23-year-old, 1.63-m, 76-kg male patient (ASA Physical Status I) was scheduled for antireflux valve surgery due to idiopathic megaesophagus. Adequate physical condition and normal vital signs were observed before anesthesia. Electrocardlography, noninvasive blood pressure, pulse oximetry, and capnometry were monitored during surgery. Lumbar epidural anesthesia was performed at the L3-L4 space via a 17-gauge Tuohy needle. Epidural space was located via loss of resistance to air. Twenty milliliters of 0.5% bupivacaine with epinephrine (1:200,000) were slowly injected, followed by the insertion of a catheter into the epidural space. The patient was placed in the supine position and an additional 10 mL of the same local anesthetic solution was injected via the epidural catheter. When the sensory block reached a T8 level and stable hemodynamic conditions were observed, general anesthesia was induced with 400 mg thiopental, 500 p.g fentanyl, and 7 mg pancuronium bromide. After tracheal intubation, anesthesia was maintained with 02/N20 (50%/50%) and halothane in concentrations ranging from 0.3-0.5%. There were no intraoperative complications. In the recovery room the patient remained hemodynamically stable and was extubated after reversal of neuromuscular relaxants (1 mg atropine and 1.5 mg neostigmine). After complaining of moderate pain, 10 mL 0.125% bupivacaine was believed to have been injected into the epidural catheter to provide postoperative analgesia. After 30 minutes, the patient reported intense warmth in the lower limbs and developed a tachycardia (heart rate reaching 180 beats/min), a severe headache, hypertension (240/120 mm Hg), intensive pruritus on the chest, a complete sensory block at the level of TIO, and grade 3 motor block according to Bromage scale (12). The patient was then medicated with 1 g dipyrone intravenous, 5 mg metoprolol intravenous, 10 mg nifedipine sublingual, and 25 mg promethazine intravenous. After that, we observed that 5 mL 19.1 % KCI had been unintentionally used as the epidural diluent, resulting in injection of a 9.55% potassium and 0.125% bupivacaine solution. Hydrocortisone (200 mg intravenous) was administered, and the patient was sedated with a continuous infusion of propofol 60 p.g/kg/min for approximately 2 hours due to the patient's intense pruritus. During sedation, the patient remained
asleep with a brisk response to a loud auditory stimulus (level 4 according to Ramsay sedation scale) (13). After 5 hours, there was a total regression of the block, pruritus was less intense; however, tachycardia, hypertension, dyspnea, increased bronchial secretion, and decrease of Sp02 to 94%, in spite of O 2 administration via facial mask (5 Llmin) was observed. At this time, arterial blood gases analysis showed pH, 7.38; p02' 87 mm Hg; pC0 2, 34 mm Hg; and HC0 3 = 21 mmollL. Serum sodium and potassium concentrations were within the normal range (Na+, 142 mmollL; K+, 3.6 mmol/L). Chest radiographshowed bilateral diffuse pulmonary infiltrates. Pulmonary function deteriorated and 10 hours later the patient developed respiratory failure requiring tracheal intubation, sedation, and ventilatory support. The patient was extubated 24 hours later, with normalization of pulmonary and cardiovascular function. Other postoperative complications included development of a pneumothorax after percutaneous catheterization of the right subclavian vein in the intensive care unit and dehiscence of his abdominal wall. He underwent spinal anesthesia without complications for repair of his abdomen 6 days later.
Discussion It is a common practice to dilute local anesthetics and opioids to be used epidurally with saline (14). The use of wrong ampules is still a common and serious problem and is caused by several factors: Similarity between ampules (considered a "problem inherent to the equipment"), lack of attention, lack of care in storing similar ampules in different places, and fatigue of the healthcare staff (15). Such factors, isolated or in combination, contributed to the unintentional use of 19.1 % KCI as epidural drug diluent, leading to an exacerbation of sensory and motor blocks, tachycardia, hypertension, and respiratory failure. Potassium speeds the onset and intensifies sensory and motor blocks because it reduces the resting potential of the neuronal membrane and potentiates the depolarization of the cell membrane (10,16,17). Occasionally, the epidural injection of KCI is followed by severe pain caused by the hyperosmolarity of the solution and an irritatingeffect on the cell membrane (10,11). In this case, as 5 mL 19.1 % KCI was diluted with 5 mL 0.25% bupivacaine, the final concentration (9.55%) appeared to be insufficient to cause pain. In addition, the local anesthetic itself may have induced some analgesia during the solution administration. The intense
Effects of Unintentional Epidural Injection of Potassium Chloride
•
Nascimento et al. 221
Table 1. Potassium Chloride: Final Concentration and Dosages Unintentionally Administered Epidurally and Its Consequences Concentrations and Dosages of KCI
Epidural Anesthetics
6.43%, 900 mg 11.25%, 2250 mg 0.2%, 1.1-1.5 mg 15%, 1500 mg 15%, 1500 mg (two cases)
Lidocaine (1.15%) Bupivacaine (0.125%), morphine Fentanyl. diazepam Sufentanil Morphine
7.45%, 372 mg (two cases) 9.55%, 955 mg
Lidocairie (1%) Bupivacaine (0.125%)
Time and Level of Block Onset*
Time of Block Recovery
Treatment with Steroids
Reference
not report few minutes, T7 15 min, TIO 2 hours, TIt Few minutes, T4 (case I), and TIl (case 2) Few minutes, TIl (both) 30 minutes, TIO
6h
Yes No No§ Yes Yes
3 7 8 9 10
2h (both)
Yes"
11
5h
Yes
This report (1998)
t
5.5 h 12 h 14h(casel) 18 h (case 2)
* Sensory and motor block. t Sensory block only. t Permanent neurologic damage below T7. § Use of epidural saline. II The original purpose of epidural injection was to use corticosteroids and anesthetics to treat chronic pain in both cases.
warmth in the lower limbs was probably related to the sensory alterations due to the neurologic block and to the vasodilatation caused by the sympathetic block (3). According to previous publications, the clinical symptoms may appear a few minutes after the unintentional epidural injection of KCI. However, in this and other reports detailed in Table I, there were cases with later onset of symptoms (8,9). It is possible that this patient had sensory and motor block few minutes after the epidural injection too. However, he had no pain, and help was necessary about 30 minutes later when the clinical changes were observed. Fortunately, there was complete recovery of the patient's neurologic function, even after 955 mg of KCI was administered. As seen in previous reports and as shown in Table I, clinical recovery seems to be based more on the total KCI dose than its concentration (7-11). Shanker et al. (1985) reported irreversible paraplegia and a patient'S death, 6 months following the unintentional injection of 2250 mg of an 11.25% KCI solution (7). These authors believed that permanent neurologic damage might have been caused by the high extracellular concentration of potassium and its hyperosmolar effect at the spinal cord. There was no report of corticosteroid use, and the intense inflammatory response may have produced neuronal injury. We believe the autonomic alterations produced (tachycardia and hypertension) are related to the cephalad diffusion of potassium in the cerebrospinal fluid (CSF), causing sympathetic stimulation at higher spinal levels (potassium solution also potentiates the depolarization of the sympathetic neurons) (7,9,10). In this case, an intense release of histamine is believed to have occurred, causing pruritus and pulmonary edema (18). It is possible that
the pulmonary edema caused by histamine release started at the same time as pruritus did, but was clinically apparent only 5 hours later. Potassium concentration in CSF was not measured and may vary according to the spinal level at which the KCI was injected and impacted by the diffusion of the solution via CSF flow (19). The treatment was designed to decrease the sympathetic response, and to reduce pruritus and agitation. It is possible that systemic corticosteroids, due to their antiinflammatory action, may have helped decreased the irritability and edema caused by KCI (20,21). Reports also suggest that epidural corticosteroids may decrease the effects of epidural KCI (10). We believe that the use of epidural saline in an attempt to reduce the local concentration of KCI may raise the sensory level of the block, and we do not recommend it (8,9). Although multiple studies report unintentional injections caused by the use of the wrong ampules and solutions, such problems still persist. Recommendations to double-check ampule labels need to be emphasized. We believe solutions such as KCI which may lead to serious problems when unintentionally injected should be stored in special places.
References 1. Poon KS, Chang WK, Chen YC, Chan KH, Lee TY.
Evaluation of stress response 10 surgery under general anesthesia combined with spinal analgesia. Acta Anaesthesiol Sin 1995: 33: 85-90. 2. Davies Ml, Silbert BS, Mooney Pl, Dysart RH, Meads AC. Combined epidural and general anaesthesia versus general anaesthesia for abdominal aortic surgery: A prospective randomized trial. Anaesth Intens Care 1993: 21: 790-794.
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3. Bromage PRo Epidural analgesia. Philadelphia, W.B. Saunders. 1978: 394-396. 4. Suwanchinda V, Yok-Dbol B, Prakanrattana D, Udomphunthurak S. Combined thoracic epidural with light general anesthesia for thimectomy' in myasthenia gravis. J Med Assoc Thai 1995: 78: 605-610. 5. Forestner JE, Raj PP. Inadvertent epidural injection of thiopental: A case report. Anesth Analg 1975: 54: 406-407. 6. Cay DL. Accidental epidural thiopentone. Anaesth Intens Care 1984: 12: 61-63. 7. Shanker KB, Palkar NV, Nishkala R. Paraplegia following epidural potassium chloride. Anaesthesia 1985: 40: 45-47. 8. Lin D, Becker K. Shapiro HM. Neurologic changes following epidural injection of potassium chloride and diazepam: A case report with laboratory correlations. Anesthesiology 1986: 65: 210-212. 9. Tessler MJ, White I, Naugler-Colville M, Biehl DR. Inadvertent epidural administration of potassium chloride: A case report. Can J Anaesth 1988: 35: 631633. 10. Liu K, Chia YY. Inadvertent epidural injection of potassium chloride. Report of two cases. Acta Anaesthesiol Scand 1995: 39: 1134-1137. 11. Vercauteren M, Saldien V. Epidural injection of potassium hydrochloride. Acta Anaesthesiol Scand 1996: 40: 505. 12. Bromage PRo A comparison of the hydrochloride and carbon dioxide salts of lidocaine and prilocainc in epidural analgesia. Acta Anaesthesiol Scand 1965: 16: S55-S69.
13. Ramsay MAE, Savege TM, Simpson BRJ, Goodwin R. Controlled sedation with alphaxalone-alphadolone. Br Med J 1974: 2: 656-659. 14. Birnbach DJ, Johnson MD, Arcario T, Datta S, Naulty JS, Ostheimer GW. Effect of diluent volume on analgesia produced by epidural fentanyl. Anesth Analg 1989: 68: 808-810. 15. Runciman WB, Sellen A. Webb RK. Williamson JA, Currie M, Morgan C, Russell WJ. Errors, incidents and accidents in anaesthetic practice. Anaesth Intens Care 1993: 21: 506-519. 16. Bromage PR, Burfoot MF. Quality of epidural blockade II: Influence of physicochemical factors; hyaluronidase and potassium. Br J Anaesth 1966: 38: 857-865. 17. Parris MR, Chamber WA. Effects of the addition of potassium to prilocaine or bupivacaine. Br JAnaesth 1986: 58: 297-300. 18. Garrison JC. Histamine, bradykinin. 5-hydroxytryptarnine, and their antagonists. In: Gilman AG, Rail TW, Nies AS, Taylor P, eds. The pharmacological basis of therapeutics, 8th ed. Elmsford, Pergamon Press, 1990: 575-582. 19. Bromage PRo Camporesi EM, Durant PA, Nielsen CH. Rostral spread of epidural morphine. Anesthesiology 1982: 56: 431-436. 20. Bogduk N. Back pain: Zygapophysial blocks and epidural steroids. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain, 2nd ed. Philadelphia, J.B. Lippincott, 1988: 946-950. 21. Hall ED. The neuroprotective pharmacology of rncthyprednisoone. J Neurosurg 1992: 76: 13-22.
Sympathetic Hyperactivity, Respiratory Failure, Pruritus, and Anesthesia After Unintentional Epidural Injection of Potassium Chloride: Case Report Paulo do Nascimento Jr., M.D., * Norma Sueli Pinheiro M6dolo, M.D., Ph.D., * Jose Fernando do Amaral Meletti, M.D.,* and Jose Reinaldo Cerqueira Braz, M.D., Ph.D.*
Backgroundand Objectives. A combination of epidural and general anesthesia has been widely used to attenuate the surgical stress response and to provide postoperative analgesia. This case report illustrates the use of this anesthetic technique. Analgesia was induced with local anesthetic in the immediate postoperative period using unintentional 19.1 % potassium chloride (KCI) as diluent. Methods. An ASA I male patient was scheduled for surgical correction of idiopathic megaesophagus under continuous epidural anesthesia combined with general anesthesia. In the postoperative period, while preparing 10 mL 0.125% bupivacaine to be administered through the epidural catheter for pain control, 5 mL 19.1 % KCI was unintentionally used as diluent, resulting in a 9.55% potassium solution concentration. Results. The patient developed warmness of the lower limbs, tachycardia, hypertension, intense pruritus on the chest, agitation, exacerbation of sensory and motor blocks, and respiratory failure secondary to pulmonary edema, requiring ventilatory support. Total recovery was observed after 24 hours. Conclusions. Epidurally injected potassium leads to severe clinical manifestations caused by autonomic dysfunction, spinal cord irritation, and possible release of histamine. Despite continuous recommendations, ampule misidentification still happens in hospitals, frequently leading to serious accidents. Reg Anesth Pain Med1998: 23: 219-222. Key words: unintentional injection, sympathetic hyperactivity, respiratory failure, pruritus, potassium chloride, combined epidural and general anesthesia.
The combination of epidural and general anesthesia to attenuate the surgical stress response has ·From the Department of Anesthesia, Faculdade de Medicina de Botucatu, Sao Paulo, Brazil. Accepted for publication September 20, 1997. Reprint requests: Paulo do Nascimento Jr., M.D., Departamento de Ancstesiologla, Faculdade de Mcdlcina de BotucatuUNESP, Distrito de Rublao Junior sln, 18.618·970·Botucatu, SP, Brazil. Copyright CD 1998 by the American Society of Regional Anesthesia. 0146·521X/98/2302·0019$5.0010
been widely used. This technique allows prolongation of postoperative pain control with epidural administration of opioids and local anesthetics (14). Serious complications associated with unintentional administration of drugs into the epidural space have previously been reported (5-11). However, there are only a few cases related to the unintentional epidural injection of potassium chloride (KCI) in different concentrations, leading to temporary or permanent sensory and motor deficits (711). We report a case of combined epidural and
220
Regional Anesthesia and Pain Medicine Vol. 23 No.2 March-April1998
general anesthesia in a patient in who received 19.1 % KCI unintentionally.
Case Report A 23-year-old, 1.63-m, 76-kg male patient (ASA Physical Status I) was scheduled for antireflux valve surgery due to idiopathic megaesophagus. Adequate physical condition and normal vital signs were observed before anesthesia. Electrocardlography, noninvasive blood pressure, pulse oximetry, and capnometry were monitored during surgery. Lumbar epidural anesthesia was performed at the L3-L4 space via a 17-gauge Tuohy needle. Epidural space was located via loss of resistance to air. Twenty milliliters of 0.5% bupivacaine with epinephrine (1:200,000) were slowly injected, followed by the insertion of a catheter into the epidural space. The patient was placed in the supine position and an additional 10 mL of the same local anesthetic solution was injected via the epidural catheter. When the sensory block reached a T8 level and stable hemodynamic conditions were observed, general anesthesia was induced with 400 mg thiopental, 500 p.g fentanyl, and 7 mg pancuronium bromide. After tracheal intubation, anesthesia was maintained with 02/N20 (50%/50%) and halothane in concentrations ranging from 0.3-0.5%. There were no intraoperative complications. In the recovery room the patient remained hemodynamically stable and was extubated after reversal of neuromuscular relaxants (1 mg atropine and 1.5 mg neostigmine). After complaining of moderate pain, 10 mL 0.125% bupivacaine was believed to have been injected into the epidural catheter to provide postoperative analgesia. After 30 minutes, the patient reported intense warmth in the lower limbs and developed a tachycardia (heart rate reaching 180 beats/min), a severe headache, hypertension (240/120 mm Hg), intensive pruritus on the chest, a complete sensory block at the level of TIO, and grade 3 motor block according to Bromage scale (12). The patient was then medicated with 1 g dipyrone intravenous, 5 mg metoprolol intravenous, 10 mg nifedipine sublingual, and 25 mg promethazine intravenous. After that, we observed that 5 mL 19.1 % KCI had been unintentionally used as the epidural diluent, resulting in injection of a 9.55% potassium and 0.125% bupivacaine solution. Hydrocortisone (200 mg intravenous) was administered, and the patient was sedated with a continuous infusion of propofol 60 p.g/kg/min for approximately 2 hours due to the patient's intense pruritus. During sedation, the patient remained
asleep with a brisk response to a loud auditory stimulus (level 4 according to Ramsay sedation scale) (13). After 5 hours, there was a total regression of the block, pruritus was less intense; however, tachycardia, hypertension, dyspnea, increased bronchial secretion, and decrease of Sp02 to 94%, in spite of O 2 administration via facial mask (5 Llmin) was observed. At this time, arterial blood gases analysis showed pH, 7.38; p02' 87 mm Hg; pC0 2, 34 mm Hg; and HC0 3 = 21 mmollL. Serum sodium and potassium concentrations were within the normal range (Na+, 142 mmollL; K+, 3.6 mmol/L). Chest radiographshowed bilateral diffuse pulmonary infiltrates. Pulmonary function deteriorated and 10 hours later the patient developed respiratory failure requiring tracheal intubation, sedation, and ventilatory support. The patient was extubated 24 hours later, with normalization of pulmonary and cardiovascular function. Other postoperative complications included development of a pneumothorax after percutaneous catheterization of the right subclavian vein in the intensive care unit and dehiscence of his abdominal wall. He underwent spinal anesthesia without complications for repair of his abdomen 6 days later.
Discussion It is a common practice to dilute local anesthetics and opioids to be used epidurally with saline (14). The use of wrong ampules is still a common and serious problem and is caused by several factors: Similarity between ampules (considered a "problem inherent to the equipment"), lack of attention, lack of care in storing similar ampules in different places, and fatigue of the healthcare staff (15). Such factors, isolated or in combination, contributed to the unintentional use of 19.1 % KCI as epidural drug diluent, leading to an exacerbation of sensory and motor blocks, tachycardia, hypertension, and respiratory failure. Potassium speeds the onset and intensifies sensory and motor blocks because it reduces the resting potential of the neuronal membrane and potentiates the depolarization of the cell membrane (10,16,17). Occasionally, the epidural injection of KCI is followed by severe pain caused by the hyperosmolarity of the solution and an irritatingeffect on the cell membrane (10,11). In this case, as 5 mL 19.1 % KCI was diluted with 5 mL 0.25% bupivacaine, the final concentration (9.55%) appeared to be insufficient to cause pain. In addition, the local anesthetic itself may have induced some analgesia during the solution administration. The intense
Effects of Unintentional Epidural Injection of Potassium Chloride
•
Nascimento et al. 221
Table 1. Potassium Chloride: Final Concentration and Dosages Unintentionally Administered Epidurally and Its Consequences Concentrations and Dosages of KCI
Epidural Anesthetics
6.43%, 900 mg 11.25%, 2250 mg 0.2%, 1.1-1.5 mg 15%, 1500 mg 15%, 1500 mg (two cases)
Lidocaine (1.15%) Bupivacaine (0.125%), morphine Fentanyl. diazepam Sufentanil Morphine
7.45%, 372 mg (two cases) 9.55%, 955 mg
Lidocairie (1%) Bupivacaine (0.125%)
Time and Level of Block Onset*
Time of Block Recovery
Treatment with Steroids
Reference
not report few minutes, T7 15 min, TIO 2 hours, TIt Few minutes, T4 (case I), and TIl (case 2) Few minutes, TIl (both) 30 minutes, TIO
6h
Yes No No§ Yes Yes
3 7 8 9 10
2h (both)
Yes"
11
5h
Yes
This report (1998)
t
5.5 h 12 h 14h(casel) 18 h (case 2)
* Sensory and motor block. t Sensory block only. t Permanent neurologic damage below T7. § Use of epidural saline. II The original purpose of epidural injection was to use corticosteroids and anesthetics to treat chronic pain in both cases.
warmth in the lower limbs was probably related to the sensory alterations due to the neurologic block and to the vasodilatation caused by the sympathetic block (3). According to previous publications, the clinical symptoms may appear a few minutes after the unintentional epidural injection of KCI. However, in this and other reports detailed in Table I, there were cases with later onset of symptoms (8,9). It is possible that this patient had sensory and motor block few minutes after the epidural injection too. However, he had no pain, and help was necessary about 30 minutes later when the clinical changes were observed. Fortunately, there was complete recovery of the patient's neurologic function, even after 955 mg of KCI was administered. As seen in previous reports and as shown in Table I, clinical recovery seems to be based more on the total KCI dose than its concentration (7-11). Shanker et al. (1985) reported irreversible paraplegia and a patient'S death, 6 months following the unintentional injection of 2250 mg of an 11.25% KCI solution (7). These authors believed that permanent neurologic damage might have been caused by the high extracellular concentration of potassium and its hyperosmolar effect at the spinal cord. There was no report of corticosteroid use, and the intense inflammatory response may have produced neuronal injury. We believe the autonomic alterations produced (tachycardia and hypertension) are related to the cephalad diffusion of potassium in the cerebrospinal fluid (CSF), causing sympathetic stimulation at higher spinal levels (potassium solution also potentiates the depolarization of the sympathetic neurons) (7,9,10). In this case, an intense release of histamine is believed to have occurred, causing pruritus and pulmonary edema (18). It is possible that
the pulmonary edema caused by histamine release started at the same time as pruritus did, but was clinically apparent only 5 hours later. Potassium concentration in CSF was not measured and may vary according to the spinal level at which the KCI was injected and impacted by the diffusion of the solution via CSF flow (19). The treatment was designed to decrease the sympathetic response, and to reduce pruritus and agitation. It is possible that systemic corticosteroids, due to their antiinflammatory action, may have helped decreased the irritability and edema caused by KCI (20,21). Reports also suggest that epidural corticosteroids may decrease the effects of epidural KCI (10). We believe that the use of epidural saline in an attempt to reduce the local concentration of KCI may raise the sensory level of the block, and we do not recommend it (8,9). Although multiple studies report unintentional injections caused by the use of the wrong ampules and solutions, such problems still persist. Recommendations to double-check ampule labels need to be emphasized. We believe solutions such as KCI which may lead to serious problems when unintentionally injected should be stored in special places.
References 1. Poon KS, Chang WK, Chen YC, Chan KH, Lee TY.
Evaluation of stress response 10 surgery under general anesthesia combined with spinal analgesia. Acta Anaesthesiol Sin 1995: 33: 85-90. 2. Davies Ml, Silbert BS, Mooney Pl, Dysart RH, Meads AC. Combined epidural and general anaesthesia versus general anaesthesia for abdominal aortic surgery: A prospective randomized trial. Anaesth Intens Care 1993: 21: 790-794.
222
Regional Anesthesia and Pain Medicine Vol. 23 No.2 March-April1998
3. Bromage PRo Epidural analgesia. Philadelphia, W.B. Saunders. 1978: 394-396. 4. Suwanchinda V, Yok-Dbol B, Prakanrattana D, Udomphunthurak S. Combined thoracic epidural with light general anesthesia for thimectomy' in myasthenia gravis. J Med Assoc Thai 1995: 78: 605-610. 5. Forestner JE, Raj PP. Inadvertent epidural injection of thiopental: A case report. Anesth Analg 1975: 54: 406-407. 6. Cay DL. Accidental epidural thiopentone. Anaesth Intens Care 1984: 12: 61-63. 7. Shanker KB, Palkar NV, Nishkala R. Paraplegia following epidural potassium chloride. Anaesthesia 1985: 40: 45-47. 8. Lin D, Becker K. Shapiro HM. Neurologic changes following epidural injection of potassium chloride and diazepam: A case report with laboratory correlations. Anesthesiology 1986: 65: 210-212. 9. Tessler MJ, White I, Naugler-Colville M, Biehl DR. Inadvertent epidural administration of potassium chloride: A case report. Can J Anaesth 1988: 35: 631633. 10. Liu K, Chia YY. Inadvertent epidural injection of potassium chloride. Report of two cases. Acta Anaesthesiol Scand 1995: 39: 1134-1137. 11. Vercauteren M, Saldien V. Epidural injection of potassium hydrochloride. Acta Anaesthesiol Scand 1996: 40: 505. 12. Bromage PRo A comparison of the hydrochloride and carbon dioxide salts of lidocaine and prilocainc in epidural analgesia. Acta Anaesthesiol Scand 1965: 16: S55-S69.
13. Ramsay MAE, Savege TM, Simpson BRJ, Goodwin R. Controlled sedation with alphaxalone-alphadolone. Br Med J 1974: 2: 656-659. 14. Birnbach DJ, Johnson MD, Arcario T, Datta S, Naulty JS, Ostheimer GW. Effect of diluent volume on analgesia produced by epidural fentanyl. Anesth Analg 1989: 68: 808-810. 15. Runciman WB, Sellen A. Webb RK. Williamson JA, Currie M, Morgan C, Russell WJ. Errors, incidents and accidents in anaesthetic practice. Anaesth Intens Care 1993: 21: 506-519. 16. Bromage PR, Burfoot MF. Quality of epidural blockade II: Influence of physicochemical factors; hyaluronidase and potassium. Br J Anaesth 1966: 38: 857-865. 17. Parris MR, Chamber WA. Effects of the addition of potassium to prilocaine or bupivacaine. Br JAnaesth 1986: 58: 297-300. 18. Garrison JC. Histamine, bradykinin. 5-hydroxytryptarnine, and their antagonists. In: Gilman AG, Rail TW, Nies AS, Taylor P, eds. The pharmacological basis of therapeutics, 8th ed. Elmsford, Pergamon Press, 1990: 575-582. 19. Bromage PRo Camporesi EM, Durant PA, Nielsen CH. Rostral spread of epidural morphine. Anesthesiology 1982: 56: 431-436. 20. Bogduk N. Back pain: Zygapophysial blocks and epidural steroids. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain, 2nd ed. Philadelphia, J.B. Lippincott, 1988: 946-950. 21. Hall ED. The neuroprotective pharmacology of rncthyprednisoone. J Neurosurg 1992: 76: 13-22.