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Anaphylaxis with intravenous gammaglobulin
874
Anaphylaxis with intravenous gammaglobulin SIR,-Dr Hachimi-Idrissi and colleagues (July 7,
p
55) report
a
immune-complex reaction to intravenous gammaglobulin (IVIG) in a patient with IgG, subclass deficiency. They state that anaphylactoid reactions have been noted mainly in patients with hypogammaglobulinaemia or agammaglobulinaemia. We agree, having lately had experience of a 45-year-old man with acquired hypogammaglobulinaemia who had an anaphylactoid reaction during his first infusion with IVIG. Subsequent testing revealed anti-IgA antibodies in his serum, pointing to a risk of such reactions during gammaglobulin infusions in patients with anti-IgA
severe
doctors should be wary of the potential toxic effects in young children. Inadvertent antimotility drug use can be partly avoided by ensuring that clinicians are aware of the spectrum of pharmacological properties of any particular agent. Unfortunately, despite such knowledge, some individual patients may still be prescribed these agents if the benefit of analgesia outweighs the possibility of aggravating the enteropathy. This difficulty should promote the development of analgesics or antinauseants that are devoid of antimotility properties. Division of Medical Microbiology, Departments of Pathology and Pediatrics, British Columbia’s Children’s Hospital, Vancouver, Canada V6H 3V4
N. CIMOLAI J. E. CARTER
antibodies.
Autologous antibodies are present in up to 40% of patients with IgA deficiency,’ and these individuals have a high risk of adverse reactions during the infusion of any preparation containing IgA. Commercial IVIG may contain as much as 150 Ilg/ml IgA.2 These preparations are increasingly used in the treatment of various diseases such as primary immunodeficiency, Kawasaki disease, Guillain-Barre syndrome, and myasthenia gravis.3Since the prevalence of IgA deficiency in the general population is 1 in 700, the potential for severe reactions will rise with the increasing use of IVIG. We advise caution in the use of IVIG and suggest that all patients be screened for IgA antibodies before transfusion. IVIG should only be used for the treatment of conditions for which it has been shown to be effective. Department of Immunology, Royal Victoria Hospital, Belfast BT126BN, UK
D. R. MCCLUSKEY N. A. M. BOYD
L, Persson MAA, Smith CIE. Anti-Iga in selective IgA deficiency. Scand J Immunol 1983; 18: 509-13 2. Apfelzweig R, Piszkiewicz D, Hooper JA. Immunoglobulin A concentrations in commercial immune globulins. J Clin Immunol 1987; 7: 46-50 3. Berkman SA, Lee ML, Gale RP. Clinical uses of intravenous immunoglobulin. Ann 1. Hammarstrom
Intern Med 1990; 112: 278-92.
Antimotility agents for paediatric
use
SIR,-Dr Bhutta and Dr Khwaja (Aug 4, p 314) highlight a direct toxic effect of antimotility agents in young children. Although Bhutta notes a widespread use of these pharmacological agents in developing countries, our experience suggests that their use is also common in the western world. We have lately drawn attention to another end of the spectrum of adverse effects-namely, the potential of these pharmacological agents to worsen an infectious diarrhoeal disease and its complications.’ The impedance of bowel motility alters one of the body’s natural defence mechanisms. In the context of presumably toxin-mediated illness-ie, verotoxic Escherichia coli-associated enteritis and haemolytic-uraemic syndrome (HUS)—we postulate that antimotility agents quantitatively enhance the absorption of toxin and lead to the systematic complications of HUS. The association of antimotility agents with the worsening of some infectious enteritides is, however, not noveJ.2,3 Although much of the prescribed antimotility drug use is intended to benefit the enteritis, there is also considerable inadvertent use of agents with antimotility properties. Two categories of the latter drugs include some analgesics and antinauseants. Codeine and morphine both have significant bowel antimotility properties and may be used to treat the abdominal colic associated with infectious enteritides. Antinauseants such as dimenhydrinate or some phenothiazines may be used to mitigate the nausea and/or emesis that is also associated with enteric disease. Some of these agents are available in suppository formulations which potentially deliver large doses directly to the large bowel. Combinations of these drugs could superimpose antimotility action. For the doctor treating children with presumed acute infectious enteritides, the use of antimotility agents should not be encouraged. For patients with chronic diseases where antimotility agents are of value--eg, some diarrhoeas associated with bowel resections-
1. Cirnolai N, Carter JE, Morrison BJ, Anderson JD. Risk factors for the progression of Escherichia coli. O157.H7 enteritis to hemolytic-uremic syndrome J Pediatr 1990, 116: 589-92 2. Dupont HL, Hornick RB. Adverse effect of Lomotil therapy in shigellosis JAMA 1973; 226: 1525-28. 3. Novak E, Lee JG, Seckman CE, et al Unfavourable effect of atropine-diphenoxylate (Lomotil) therapy in lincomycin-caused diarrhea. JAMA 1976, 235: 1451-54
Intra-articular
morphine for pain after knee arthroscopy
SIR,-Traditional thought has associated analgesic effects of opioids with actions upon the central nervous systems (CNS). Recently, however, the notion that anti-nociception can be brought about by activation of opioid receptors outside the CNS has gained more widespread recognition. Animal studies have demonstrated morphine receptors in chronically inflamed joints.’The presence of these receptors and their efficacy in the clinical setting was evaluated in seven patients undergoing bilateral video arthroscopy and lateral release. At the end of surgery, under general anaesthesia, one knee was injected with 20 ml 0-25 % bupivacaine and the other knee was injected with 20 ml saline with 1 mg morphine sulphate. Pain was assessed by patient on a visual analogue scale (VAS) up to 10. Narcotic requirements were monitored. Patients complained of severe pain in the knee injected with morphine on admission to the recovery room (VAS 8-5). They required an average of 125 pg of fentanyl intravenously for control of knee pain, while the knee injected with bupivacaine was pain-free. After an hour, the pain in the knee injected with morphine decreased to a VAS of 2, whereas, pain score for the knee injected with bupivacaine was 1. No patient required narcotics until mobilisation, about 3 hours after surgery. Patients had severe discomfort (VAS 6-5) in the knee injected with bupivacaine and needed an average of 75 mg of intramuscular pethidine to facilitate mobilisation. The knee injected with morphine had a VAS of only 2 and no further narcotics were needed. For the next 3 days, five out of seven patients assessed the knee injected with morphine as pain-free or they were able to use it with less discomfort than the knee injected with bupivacaine (VAS 2-5 vs 6-5). These results indicate that morphine injected into the knee joint is an adequate treatment modality of postoperative pain after knee
arthroscopy. Study done at surgical services, Long Beach Community Hospital, Long Beach, California. Department of Anaesthesiology, University of California, Los Angeles, Los Angeles, California, USA
GEORGE F. KHOURY
Department of Anaesthesiology, Klinikum Grosshadern, University of Munich,
Munich, Germany
CHRISTOPHER STEIN
Department of Orthopaedic Surgery, USC County Medical Center, Los Angeles, California
DOUGLAS E. GARLAND
1. Stem
C, Millan MJ, Shippenberg TS, et al. Peripheral opioid receptors mediating antinociception inflammation, evidence for involvement of mu, delta and kappa receptors.J Pharmacol Exp Ther 1989, 248: 1269-75.
Anaphylaxis with intravenous gammaglobulin SIR,-Dr Hachimi-Idrissi and colleagues (July 7,
p
55) report
a
immune-complex reaction to intravenous gammaglobulin (IVIG) in a patient with IgG, subclass deficiency. They state that anaphylactoid reactions have been noted mainly in patients with hypogammaglobulinaemia or agammaglobulinaemia. We agree, having lately had experience of a 45-year-old man with acquired hypogammaglobulinaemia who had an anaphylactoid reaction during his first infusion with IVIG. Subsequent testing revealed anti-IgA antibodies in his serum, pointing to a risk of such reactions during gammaglobulin infusions in patients with anti-IgA
severe
doctors should be wary of the potential toxic effects in young children. Inadvertent antimotility drug use can be partly avoided by ensuring that clinicians are aware of the spectrum of pharmacological properties of any particular agent. Unfortunately, despite such knowledge, some individual patients may still be prescribed these agents if the benefit of analgesia outweighs the possibility of aggravating the enteropathy. This difficulty should promote the development of analgesics or antinauseants that are devoid of antimotility properties. Division of Medical Microbiology, Departments of Pathology and Pediatrics, British Columbia’s Children’s Hospital, Vancouver, Canada V6H 3V4
N. CIMOLAI J. E. CARTER
antibodies.
Autologous antibodies are present in up to 40% of patients with IgA deficiency,’ and these individuals have a high risk of adverse reactions during the infusion of any preparation containing IgA. Commercial IVIG may contain as much as 150 Ilg/ml IgA.2 These preparations are increasingly used in the treatment of various diseases such as primary immunodeficiency, Kawasaki disease, Guillain-Barre syndrome, and myasthenia gravis.3Since the prevalence of IgA deficiency in the general population is 1 in 700, the potential for severe reactions will rise with the increasing use of IVIG. We advise caution in the use of IVIG and suggest that all patients be screened for IgA antibodies before transfusion. IVIG should only be used for the treatment of conditions for which it has been shown to be effective. Department of Immunology, Royal Victoria Hospital, Belfast BT126BN, UK
D. R. MCCLUSKEY N. A. M. BOYD
L, Persson MAA, Smith CIE. Anti-Iga in selective IgA deficiency. Scand J Immunol 1983; 18: 509-13 2. Apfelzweig R, Piszkiewicz D, Hooper JA. Immunoglobulin A concentrations in commercial immune globulins. J Clin Immunol 1987; 7: 46-50 3. Berkman SA, Lee ML, Gale RP. Clinical uses of intravenous immunoglobulin. Ann 1. Hammarstrom
Intern Med 1990; 112: 278-92.
Antimotility agents for paediatric
use
SIR,-Dr Bhutta and Dr Khwaja (Aug 4, p 314) highlight a direct toxic effect of antimotility agents in young children. Although Bhutta notes a widespread use of these pharmacological agents in developing countries, our experience suggests that their use is also common in the western world. We have lately drawn attention to another end of the spectrum of adverse effects-namely, the potential of these pharmacological agents to worsen an infectious diarrhoeal disease and its complications.’ The impedance of bowel motility alters one of the body’s natural defence mechanisms. In the context of presumably toxin-mediated illness-ie, verotoxic Escherichia coli-associated enteritis and haemolytic-uraemic syndrome (HUS)—we postulate that antimotility agents quantitatively enhance the absorption of toxin and lead to the systematic complications of HUS. The association of antimotility agents with the worsening of some infectious enteritides is, however, not noveJ.2,3 Although much of the prescribed antimotility drug use is intended to benefit the enteritis, there is also considerable inadvertent use of agents with antimotility properties. Two categories of the latter drugs include some analgesics and antinauseants. Codeine and morphine both have significant bowel antimotility properties and may be used to treat the abdominal colic associated with infectious enteritides. Antinauseants such as dimenhydrinate or some phenothiazines may be used to mitigate the nausea and/or emesis that is also associated with enteric disease. Some of these agents are available in suppository formulations which potentially deliver large doses directly to the large bowel. Combinations of these drugs could superimpose antimotility action. For the doctor treating children with presumed acute infectious enteritides, the use of antimotility agents should not be encouraged. For patients with chronic diseases where antimotility agents are of value--eg, some diarrhoeas associated with bowel resections-
1. Cirnolai N, Carter JE, Morrison BJ, Anderson JD. Risk factors for the progression of Escherichia coli. O157.H7 enteritis to hemolytic-uremic syndrome J Pediatr 1990, 116: 589-92 2. Dupont HL, Hornick RB. Adverse effect of Lomotil therapy in shigellosis JAMA 1973; 226: 1525-28. 3. Novak E, Lee JG, Seckman CE, et al Unfavourable effect of atropine-diphenoxylate (Lomotil) therapy in lincomycin-caused diarrhea. JAMA 1976, 235: 1451-54
Intra-articular
morphine for pain after knee arthroscopy
SIR,-Traditional thought has associated analgesic effects of opioids with actions upon the central nervous systems (CNS). Recently, however, the notion that anti-nociception can be brought about by activation of opioid receptors outside the CNS has gained more widespread recognition. Animal studies have demonstrated morphine receptors in chronically inflamed joints.’The presence of these receptors and their efficacy in the clinical setting was evaluated in seven patients undergoing bilateral video arthroscopy and lateral release. At the end of surgery, under general anaesthesia, one knee was injected with 20 ml 0-25 % bupivacaine and the other knee was injected with 20 ml saline with 1 mg morphine sulphate. Pain was assessed by patient on a visual analogue scale (VAS) up to 10. Narcotic requirements were monitored. Patients complained of severe pain in the knee injected with morphine on admission to the recovery room (VAS 8-5). They required an average of 125 pg of fentanyl intravenously for control of knee pain, while the knee injected with bupivacaine was pain-free. After an hour, the pain in the knee injected with morphine decreased to a VAS of 2, whereas, pain score for the knee injected with bupivacaine was 1. No patient required narcotics until mobilisation, about 3 hours after surgery. Patients had severe discomfort (VAS 6-5) in the knee injected with bupivacaine and needed an average of 75 mg of intramuscular pethidine to facilitate mobilisation. The knee injected with morphine had a VAS of only 2 and no further narcotics were needed. For the next 3 days, five out of seven patients assessed the knee injected with morphine as pain-free or they were able to use it with less discomfort than the knee injected with bupivacaine (VAS 2-5 vs 6-5). These results indicate that morphine injected into the knee joint is an adequate treatment modality of postoperative pain after knee
arthroscopy. Study done at surgical services, Long Beach Community Hospital, Long Beach, California. Department of Anaesthesiology, University of California, Los Angeles, Los Angeles, California, USA
GEORGE F. KHOURY
Department of Anaesthesiology, Klinikum Grosshadern, University of Munich,
Munich, Germany
CHRISTOPHER STEIN
Department of Orthopaedic Surgery, USC County Medical Center, Los Angeles, California
DOUGLAS E. GARLAND
1. Stem
C, Millan MJ, Shippenberg TS, et al. Peripheral opioid receptors mediating antinociception inflammation, evidence for involvement of mu, delta and kappa receptors.J Pharmacol Exp Ther 1989, 248: 1269-75.