4`•. Acta Med Kinki Univ
• Vol. 36, No. 1 41-44, 2011
A suspected case of anaphylaxis
adrenocorticosteroids
due to
Tatsushige Iwamoto, Hiroshi
Masahiro Morimoto, Mitsuo Morimoto, Uno, Keiji Uehara and Shinichi Nakao
Toru Shirai,
Department of Anesthesiology, Kinki Osakasayama, Osaka
University Faculty of Medicine, 589-8511, Japan
Abstract
We encountered a case suspected as ana- phylaxis due to treatment with dexamethasone phosphate in a patient with left median nerve injury. In this case, past use of adrenocorticos-
teroids, such as methylprednisolone succinate injections and inhaled fluticasone propionate, had not caused any abnormalities ; however, anaphylaxis-like symptoms occurred following
use of dexamethasone phosphate during intra- venous regional sympathetic block. We report anaphylaxis-like symptoms occurred when dex- amethasone phosphate was administered.
Key words : anaphylaxis, adrenocorticoster- oids, dexamethasone phosphate, intravenous regional sympathetic block
Introduction
Adrenocorticosteroids are an essential medica- tion in the treatment of anaphylaxis. Since Mendelson et al. reported anaphylaxis, the synoptome of which were hives and breathing difficulty associated with adrenocorticosteroid use in 1974, cases of hypersensitivity to steroid drugs have been receiving more attention.2'3
We report herein a case of deafferentation pain due to a severed left median nerve in which anaphylaxis-like symptoms occurred when dex- amethasone phosphate was administered during intravenous regional sympathetic block (IRSB).
Case Report
The patient was a 35-year-old woman with a history of somatization disorder, panic disorder and borderline personality disorder, who had been brought to the emergency medical center of our hospital three times with acute drug intoxica- tion (overdose of sleeping medications). In addition, she had been receiving fluticasone propionate as a spray for 1 year as a treatment
for bronchial asthma.
When the patient was 34 years old in April, she had severed the left median nerve in a suicide attempt and underwent neurorrhaphy of the median nerve in the Department of Plastic and Reconstructive Surgery of our hospital in July, 17. The patient experienced numbness and hypoesthesia from the wound to the nerve periphery immediately after the operation and underwent neurolysis in July, 31 for pain relief.
Postoperatively, as the patient reported a painful sensation, as if electricity was running down to the left palm, she was referred to our department 3 months after the first surgery.
At the time of the first examination, the patient complained of an electric-shock-like pain in the left palm ; however, no evidence of decal- cification or atrophy of the upper bones of the left hand was apparent on radiography (Fig. 1).
In addition, the injury was class 2 on the Cornell medical index (CMI). Based on radiographic findings and localized symptoms from the wound to the peripheral region of the median nerve (Fig. 2), we diagnosed her symotoms as deafferentation pain resulting from distal medial
Received January 12, 2010 ; Accepted January 27, 2011
41
T. Iwamoto et al.
V
Fig. 1
JF
r-
r.
Radiography at the time of first examination.
No signs of atrophy or decalcification were apparent in bones of the left hand.
Fig. 2 Schema at the time of first examination
The patient experienced numbness and hypoesthesia in the area from the wound to the nerve periphery (area innervated by the median nerve).
Discussion
neuropathy. Treatment with amitriptyline hydrochloride (10 mg/day) and gabapentin(600 mg/day) was initiated, and IRSB (2% lidocaine 5 ml, reserpine 1 mg, saline solution 15 ml) was performed.
We increased the dosage of her oral medica- tions during follow-up ; however, as the effect was insufficient, dexamethasone phosphate was added to the drug mixture during IRSB on September, 2. Immediately after administration of dexamethasone phosphate (4 mg), the patient complained of an itching sensation of the left upper extremity. This itching sensation was abated after intramuscular injection of hydox- yzine (25 mg) ; however, after removal of the tourniquet, the patient began wheezing and we administered aminophylline (75 mg) intravenously, since stable hemodynamic comfir- med and steroid allergy was suspected. Wheez- ing abated after 15 min, during which time no marked changes in electrocardiography, blood pressure or peripheral artery oxygen saturation were apparent. (Fig. 3)
Medications commonly known to cause ana- phylaxis include antibiotics and analgesic anti- pyretics.4 Treatments for anaphylaxis include intramuscular injections and intravenous injec- tions of epinephrine, fluid resuscitation treat- ment, antihistamine medication, bronchodilators (beta-adrenergic receptor agonists), adrenocor- ticosteroids, and glucagon injections. If the patient is in a state of cardiopulmonary arrest, immediate cardiopulmonary resuscitation and advanced cardiac life support are necessary.5'6
Conversely, case reports on anaphylaxis caused by adrenocorticosteroids (an anaphylaxis treatment) have become fairly common in recent years. Mendelson et al. were the first to report a case of hives and exacerbation of asthma due to intravenous injection of methylprednisolone suc- cinate in 1974. Taniguchi et al.' reported that the mechanism of hypersensitivity to this injecta- ble steroid medication is caused by sensitivity to the esterified structure of the drug. As adrenocorticosteroid crystals are difficult to dis- solve in water, esterification is needed to increase water solubility for injection purposes. Succinic
42
A suspected case of anaphylaxis due to adrenocorticosteroids
diagnosed distal medial neuropathy
IRSB(2% lidocaine 5 ml, resepine 1 mg, saline solution 15 ml)
•
2 month : V
Ineffective
IRSB(2% lidocaine 5 ml, reserpine 1 mg, saline solution 15 ml, dexamethasone phosphate 4mg)
immediately
itching sensation on the left upper extremity 4— hydoxyzine(25mg) i,m,
1
Itching resolution
/
Fig. 3
removal of the tourniquet
wheezing
aminophylline(75mg) i,v, 15 min
Wheezing abated Therapeutic process
IRSB (intravenous regional sympathetic block), i,m, (intramuscular injection) i,v, (intravenous injection) During which time no marked changes in electrocar- diography, blood pressure or peripheral artery oxy- gen saturation were apparent.
acid, phosphate, and ester acetate all are be used to achieve esterification, but Freedman et al.8 reported that esterification using succinic acid produces the greatest frequency of anaphylaxis- like symptoms.
Reports have also described hypersensitivity to additives present in adrenocorticosteroid medica- tions as the cause of anaphylaxis-like symptoms.
Schorr et al.9 reported additives, namely the preservative paraben (Solu-Cortef®, Hydrocor- tone®, Decadron®), as a cause of adverse reac- tions. Prenner et al." reported that sulfur- containing antioxidants (Hydrocortone®, Deca- dron®, Rinderon®) caused reactions. We show the table of various adrenocorticosteroid drugs.
(Table 1)
Reactions to the steroid structure of adrenocorticosteroids have also been reported.
Freedman et al.8 proposed a hypothesis that
low-molecular-mass substances such as steroids showed be bound to a different, high-molecular- mass substance in order to cause an allergic reaction. In this way, steroids act as haptens to induce allergic reactions ; within this class of allergens, reactions due to hydrocortisone are the most common.
In the present case, no allergic reactions were induced by inhaled fluticasone propionate and intravenously injected methylprednisolone suc- cinate. However, the patient had the history feelings of illness by external use of betameth- asone butyrate propionate, and anaphylaxis-like symptoms due to the use of dexamethasone phosphate during IRSB. Judging from these reactions, the esterified structure or additives may have caused the anaphylaxis-like symptoms.
Moreover, the patient had a history of asthma. It is generally presumed that paitients with aspirin- induced asthma are also susceptible to not only to analgesic antipyretics, but also to other medi- cations, preservatives and coloring agents, and may thus be potentially hypersensitive to suc- cinate compounds.' Use of steroid phosphate esters in aspirin-induced asthma patients is regar- ded as safe ; however, the use of steroid phos- phate esters in the present case caused anaphylax- is and cannot be considered safe.
These findings suggest that adrenocorticoster- oids primarily used as anaphylaxis treatment have the possibility of causing anaphylaxis-like symptoms. If symptoms worsen following the administration, medication must be immediately changed to another adrenocorticosteroid and antihistamine. In addition, follow-up may be necessary.
In this case, we hoped to investigate the under- lying cause of this reaction through histamine release tests and immunoglobulin E measure- ments, but were unable to perform a complete evaluation as the patient declined to participate.
The patient underwent another neurolysis proce- dure 2 years after the first occurrence of symp- toms, but has yet to achieve any improvement in the condition of the left palm area and the symptoms remain.
Conclusion
Adrenocorticosteroids are an effective treat- ment for anaphylaxis-like symptoms, but have the potential to cause anaphylaxis-like symp- toms. Sufficient caution must thus be exercised
43
T. Iwamoto et al.
Table Assortment in various adrenocorticosteroid drugs
Drug (INN) Drug (trade name) assortment Additives
Hydrocortisone sodium
succinate Solu-Cortef®
Saxizon®
bulk
solution bulk solution
Methylparaben, Propylparaben
Hydrocortisone sodium
phosphate Hydorocotone®
Phosphate®
Cleiton®
bulk
liquid
Methylparaben, Propylparaben sodium
Hydrogen sulfite
Creatinine Xylitol Benzethonium chloride Prednisolone sodium
succinate
Predonine® bulk
Methylprednisolone sodium succinate
Solu-medrol® bulk
solution
Lactose
Dexamethasone
Decadron® liquid
Methylparaben Propylparaben sodium
Hydrogen sulfite
Creatinine Betamethasone
Rinderon® liquid Sodium sulfite
D-sorbitol
during administration. As soon as an adverse reaction following adrenocorticosteroid use is detected, hypersensitivity to adrenocorticoster- oids should be suspected and addressed immedi- ately. In addition, there is a wide range of possible causes of adrenocorticosteroid hypersen- sitivity and the underlying cause may be different in each case. A clear definition of which medica- tions elicit hypersensitivity reactions and which may be used to treat the patient is required on a case-by-case basis ; thesefore, sharing informa- tion is required to prevent anaphylaxis.
References
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2. Moreno Escobosa MC, Cruz Granados S, Moya Quesada MC, Amat Lopez J (2008) Anaphylaxis due to methylprednisolone. J Investig Allergol Clin Immunol 18 : 407-408
3. Ventura MT, Calogiuri GF, Matino MG, Dagnello
M, Buquicchio R, Foti C, Di Corato R (2003) Alterna- tive glucocorticoids for use in cases of adverse reaction to systemic glucocorticoids : a study on 10 patients. Br J Dermatol 148 : 139-141
4. Tang AW (2003) A practical guide to anaphylaxis.
Am Fam Physician 68 : 1325-1332
5. Project Team of The Resuscitation Council (UK) (2001) Update on the emergency medical treatment of anaphylactic reactions for first medical responders and for community nurses. Emerg Med J 18 : 393-395 6. Hughes G, Fitzharris P (1999) Managing acute ana-
phylaxis. New guidelines emphasise importance of intramuscular adrenaline. BMJ 319 : 1-2
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8. Freedman MD, Schocket AL, Chapel N, Gerber JG (1981) Anaphylaxis after intravenous methylpred- nisolone administration. JAMA 245: 607-608 9. Schorr WF (1968) Paraben allergy. A cause of
intractable dermatitis. JAMA 204: 859-862
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