Babar, I

Bashir, S

Shah, S M

English

eCommons@AKU

eCommons@AKUDepartment of Anaesthesia Medical College, PakistanJune 2000Incidence and pattern of Thrombocy to penia incardiac surgery patientsS BashirS M. ShahI BabarFollow this and additional works at: https://ecommons.aku.edu/pakistan_fhs_mc_anaesthPart of the Anesthesia and Analgesia Commons, and the Anesthesiology CommonsRecommended CitationBashir, S., Shah, S. M., Babar, I. (2000). Incidence and pattern of Thrombocy to penia in cardiac surgery patients. Journal of PakistanMedical Association, 50(6), 207-209.Available at: https://ecommons.aku.edu/pakistan_fhs_mc_anaesth/334Allopurinol Induced Stevens-Johnson Syndrome: A Case ReportShahida Bashir,Syed Mahmood Ali Shah ( Medical Student, Department of Medicine, The Aga Khan University, Karachi. ) ijlal Babar ( Medical Student Anaesthesia, The Aga Khan University, Karachi. ) Introduction Adverse cutaneous reactions to drugs are freqilent, affecting 2 to 3 percent of hospitalised patients1.Stevens-Johnson syndrome is a rare, life-threatening drug-induced cutaneous reaction2. Epidermalnecrosis causes erosions of the mucous membranes, extensive detachment of the epidermis, and severeconstitutional symptoms2,3 Drugs are an important cause of Stevens-Johnson syndrome, but infectionsor a combination of drugs and infections has also been implicated4.Although sonic drugs are clearly more often responsible than others, all drugs, especially thoseintroduced within one month of the reaction, should be considered suspect3. A limited number of drugsincluding sulfonamides, anticonvulsant agents, and allopurinol are consistently associated with thissyndrome; whether nonsteroida! anti-inflammatory drugs (NSAIDs), analgesic agents, andnonsulfonamide antibiotics are associated with it is controversial2. Allopurinol, which is most oftenadministered for long periods, is frequently cited as a cause of Stevens-Johnson syndrome2,3 The risk isnot constant over time. We report a case of allopurino induced Stevens Johnson syndrome presentingafter drug usage for 3 weeks.Case ReportReport A 65-year old lady with no known co-morbids except joint pains since 4 months presented to theEmergency Room (ER) of The Aga Khan University Hospital (AKUH) complaining of amaculopapular rash, high grade fever of 38.8°C, loose motions since one week, and vomiting since themorning of presentation. A provisional diagnosis of drug-induced reaction, or viral infection was made.Her skin lesions were irregular erythematous and purpuric macules; later they became papular,followed by development of blisters and weeping lesions and eventually extensive desquamation. Thedistribution of the rash was widespread involving the face, eyelids, oropharynx and trunk. At least 36%of the body surface area was involved. The conjunctiva were congested and oedematous but there wasno corneal erosion or symblepheron/synech iae formation. Painful ulcers were present on the lips andthe palate. The lesions first erupted on the mucous membranes and then extended all over the body. Thecutaneous lesions emerged dramatically all together.During her hospital stay the blisters ruptured with raw ulceration and there was extensive skindenudation. Crusting developed on the lips. However, the skin did not peel off in >3 cm sheets. lesions.No prior history of such a reaction was reported. Her past medical history was unremarkable except forjoint pains for the last 3 months for which she had been on several non-steroidal anti—inflammatorydrugs (NSA I Ds) like Loxoprofen Na, Naproxen, Diclofenac, lbuprofen and Azapropazone. All thesewere discontinued 4 weeks prior to presentation, and allopurinol 300 rng BID was started only threeweeks back, as her serum uric acid level had been discovered to be high.The hospital management was conservative, and she was taken care of in isolation. She was treatedwith systemic prednisolone 60 mg/ day, tapered off in 15 days. Cutaneous lesions were taken care ofwith topical therapy and local anaesthetic creams. Topical antibiotics like sofra tulle dressings wereapplied on the wounds. Adequate hydration and nutrition were ensured with intravenous fluids and ahigh protein diet.Discussion Stevens-Johnson syndrome is a rare but severe blistering mucocutaneous disease with a high rate ofmorbidity and mortality3,5-7 Mortality rates are below 5 percent for Stevens-Johnson syndrome butabout 30 percent for toxic epidermal necrolysis 3. The typical interval from beginning of drug therapyto onset of reaction is 1-3 weeks, but is shorter with rechallenge2,5,6.In Stevens-Johnson syndrome, the individual lesions are <3 cni in diameter, there is involvement of atleast 2 mucous membranes, >10% of the body area is involved and there may be typical or atypicaltarget lesions. Toxic epidermal necrolysis is characterized by bullae and! or erosions over 20% of bodyarea on an ciythematous base, the skin peels off in >3 cm sheets, the Nikolskv’s sign is positive, thereare frequent areas of confluent erythema, and the fever is higher (>38° C)8. Lesions of the respiratorytract and gastrointestinal tract are present in nearly all cases of toxic epidermal necrolysis, butinfrequently in Stevens-Johnson syndrome (1 0-30%)3,5,7.The exact etiology is not confirmed. The recurrence of Stevens-Johnson syndrome within 48 hours ofrechallenge, (although the initial reaction occurs about 14 days after treatment is begun), argues againsta direct toxic effect and is more consistent with immunologic mechanisms3,6. The immunopathologicpattern of early lesions suggests a cell-mediated cytotoxic reaction against epidernial cells9,10.However, both type III (immune— complex) and type IV (cell-mediated) hypersensitivity reactionshave been implicated in the pathogenesis11.Patients often have underlying diseases A role for infection as a colactor has been postulated. but re islittle supporting evidence. Conditions that alter immunologic function, including systemic lupuserythematosus may increase risk13. A genetic predisposition is thought to exist.The complications are similar to those of extensive thermal burns. Massive transepidermal fluid losses,often with associated electrolyte imbalance may occur. Prerenal azotemia is common. A hypercatabolicstate sometimes with insu liii resistance, and diffuse interstitial pneumonitis leading to the adultrespiratory distress syndrome are possible sequelae. Ocular complications may include persistentphotophobia, burning eyes, visual impairment and even blindness.The main principles of therapy are the same as for thermal burns, including aggressive fluidreplacement, nutritional support, environmental temperature control, and antibiotics as indicated3,12Termination of nonessential drug therapy, local supportive care and ophthalmologic and dermaoiogicconSuJtatlOfls should also be considered3, Pain control, fluid replacement, aseptic handling, andavoidance of any adhesive material are important3. Treatment with antihistamines, antibiotics forsecondary infections, corticosteroids and mucous membrane regimen are recommended.Therapies that reduce morbidity associated with skin loss or accelerate regrowth of the skin are mostpromising3.Allopurinol a potent inhibitor of the synthesis of uric acid, is the drug most commonly prescribed forthe treatment of primary and secondary hyperuricem ia Generally the drug is well tolerated, although2% of patients develop a mildly pruritic rash. If allopurinol is administered together with ampicillin orin renal insufficiency this incidence may increase to 20%14. Impaired renal function and concomitantintake ol diuretics (especially thiazides) may be predisposing factors. Less common hut more severecutaneous intolerance reactions to allopurinol may occur, including exfoliative erythroderma, theStevens-Johnson syndrome, and the most severe reaction, toxic epidermal necrolysis14. These are oftenassociated with multisystemic disease such as immune complex vasculitis, eosinophilia hepatitis, andprogressive renal failure (allopurinol hypersensitivity syndrome)14.In view of the severe intolerance reactions that may result, the attitude towards prescription ofallopurinol ought to be reconsidered. It is often prescribed widely and indiscriminately even forasymptonlatic hyperuricaem Ia. The benefits of treatment with aliopurinol appear questionable inpatients with asymptomatic hyperuricern Ia and do not justify the risks associated with long-termadministration14, It should be prescribed with care, especially in patients with chronic renal failure whomay be prone to severe allopurino hypersensitivity reactions15.This case is illustrative of the considerable morbidity associated with irrational and indiscriminate drugusage. The problem is compounded by the fact that drugs that have a high incidence of side effects orsignificant risk of fatal idiosyncrasy are commonly sold over the counter, especially in developingcountries16. Patients who develop Stevens-Johnson syndrome are in a precarious condition, and theirmanagement entails a great deal of vigilance. Fortunately, in this case appropriate surveillance led toconsiderable recovery, and the patient was discharged with strict instructions to avoid any possibleprecipitant drugs, and in particular allopurinol. the agent implicated in her recent predicament.Several case reports and studies substantiate the definite association between allopurinol usage and thedevelopment of Stevens Johnson syndrome15,17-20. However, no cases of al lopurino HinducedStevens-John son syndrome are cited in local literature. To our knowledge, our report describes the firstsuch case in the indigenous setting. It is imperative that this possible consequence be kept in mindwhilst prescribing this medicine, especially in individuals who are immunocompromised due tomultisvstern ic disease, or impaired renal function.References 1. Bigby M, Jick S. Jick H, et al. Drug- induced cutaneous rcactions: a report from the I3ostonCollaborative Drug Surveillance Program on 15,438 consecutive inpatients. 1975 to 1982. JAMA,l986;256:3358-63.2. Roujcau JC, Kelly JP, Naldi U, et at. Medication USC and the risk of Stevens-Johnson syndrome orToxic Epidermal Necrolysis. N. Eng. J. Med I 995;333:1600-07.3. Roujeau JC, Stem RS. Severe cutaneous adverse reactions to drugs N. EngI. J. Med., 1994,331:1272-85.4. Yetiv J7., Bianchine JR. Owen JA Jr. Etiologic factors of the Stevens-Johnson syndrome. South MedJ.. 980:73:599-602.5. Chan HL. Stem RS, Ainctt KA. Ct al. The inciidence of Erythema Multiforme. Stevens—JohnsonSyndrome, and Toxic Epidennat Necrolysis A population-based study with particular reference toreactions caused by drugs among outpatients: Arch. Dermatol., 1990; 26:43-47.6. Revuz J, Penso D, Roujeau JC, ct al. Toxic epidennal necrolysis: clinical findings and prognosisfactors in 87 patients. Arch. Dermatol 1987;123:1160-65.7. Schopf E, Siuhmer A, Rzany B, et at. Toxic epidermal Nccrolysis and Stevens-Johnson syndrome: anepidemiologic study from West Germans’, Arch. Dermatol., 1991;127:839-.12.8. Roujeau JC. Guillame JC, Fabre JR Toxic Epidermal Necrolysis (Lcll Syndrome); Incidence anddrug etiology in France. 1981-1985. Arch. Dermatol., 1990;126:37-42.9. Merot Y, Gravellese F., Guillen FJ. et al. Lymphocyte subsets and Langerhans cells in toxiccpiderntal necrolysis : report of a case. Arch Dermatol 1986:122:455-58.10. Correia 0, Delgado I., Ramos JP, et al. Cutaneous T-ccll recruitment in in toxic epidermalnecrotysis: further evidence of CD8 lymphocyte involvement. Arch. Dermatol., 1993;129:466-68.11. Stampien TM, Schwartz RA. Erythema multiforme Amer. Fain. Phys., 1992;46:1171-76.12. Lehrcr Bell KA, Kirsner RS, Tallman PG, et at. Treatment of the cutaneous involvement in Stevens-Johnson syndrome and toxic epidermal necrolysis with silver nitrate impregnated dressings. Arch,Dermatology, 1998; 34:877-79.13. Patterson R, Dykewicz MS, Gonzalzles A, et al Erythema multiforme and Stevens-Johnsonsyndrome. Descriptive ttnd therapeutic controversy. Chest, 1990:98:331-36.14. Aubock J, Fritsch P. Asvinptomatie hyperuricaemia and allopurinol induced toxic epidermalnecrolysis. Br. Med .J., 985;290:1969-70.15. Pennell DJ, Nunan To, 0-Doherty MJ, et at. Fatal Stevens—Johnson syndrome in a patient oncaptopril antI allopurinol. l,ancet, 1984;1:463.16. Trisha G. Drug prescription and Self-Medication in India: An Exploratory Survey. Soc. Sci. andMed 1987;25:307-18.17. Gonzalez U, Reyes F, Kershenovich J, et al. Hypersensitivity syndrome caused by allopurinol Acase of massive hepatic necrosis. Rev. Invest. Chin., 995:47:409-13.15. Huang RY, Liu-IIB, Wong CK. Stevens-Johnson syndrome:a review of 42 cases. Cluing I tiia IHsuch Tsa Chieh Taipei, 1993;51:225-30.19. Arellano F, Sacristan JA. Attopurinol hytsersensilivity syndrome: a review Ann. Pharmacother.,1993;27:337-43.20. Stratigos JD, Bartsokas SK, Capetanikas J. Further experiences of toxic epidermal necrolysisincriminating allopurinol, pyrazolone and derivatives. Br. J. Dermatol., 1972:86:564-67.

Incidence and pattern of Thrombocy to penia in cardiac surgery patients

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Incidence and pattern of Thrombocy to penia in cardiac surgery patients

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