anaphylaxix due to intravenous administration of diclofenac

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    PRESENTED TO:Mrs. VAISHALI SIDDHARTHASSO. PREOFESSOR,BVCON,PUNE.PRESENTED BY:Mr. STAWAN CHOUGULES.Y.M.Sc. NURSING

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    RANJU SINGH,ET.AL.,

    DEPARTMENT OF ANESTHESIOLOGY

    AND CRITICAL CARE,

    LADY HARDINGE MEDICAL

    COLLEGE & ASSOCIATED HOSPITALS,

    NEW DELHI 110 001, INDIA

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    Diclofenac sodium is aNSAID.

    Commonly routes ofDiclofenac administration.

    Anaphylaxis has beenrarely reported withintravenous administration.

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    A 25-year-old primigravida female wasadmitted with complaints of severe pain inthe abdomen for 2 days and bleeding pervaginum for 1 day.

    Vital Signs :

    1. PR : 150/MIN

    2. BP : 84/56 mmhg

    3. SPO2 : 95 % DIAGNOSED : Ruptured Ectopic Pregnancy

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    Operated for Emergency ExploratoryLaparotomy.

    Elective Intubation was done.

    VITAL SIGN :1. PR : 108/minute,

    2. BP : 112/84 mmHg

    3. SpO2 on Ventilation : 100%.

    4 Hours after Extubation IV Diclofenac 75 mgwas started in 100 ml of normal saline forpostoperative analgesia.

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    About 2025 minutes after starting theinfusion, the patient complained of tightnessin her chest, palpitations and shortness ofbreath.

    VITAL SIGNS :

    1. SPO2 : 55% & increased to 72% onadministration of oxygen (FiO2 of 100)

    2. PR : 183/min3. BP : 80/40 mmhg

    4. RR : 40/min

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    On examination, extremities were cold andauscultation of chest revealed bilateralRonchi.

    ABG :

    1. pH 7.47,

    2. Po2 : 32 mm of Hg

    3. pCO2:37 mm Hg

    Type I respiratory failure.

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    In view of these findings, pulmonary embolusor anaphylaxis to IV Diclofenac wassuspected.

    Infusion of Diclofenac was stopped.

    Adrenaline (0.5 ml of 1:10,000) was injected.

    Patient was intubated.

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    Fluids were infused rapidly and vasopressorsupport (inj. dopamine 10 g/kg/minute) wasstarted.

    Enoxaparin sodium 40 mg SC.

    Inj. Methylprednisolone (250 mg IV)

    Inj. Pheniramine (25 mg IV)

    Inj. Deriphylline (200 mg IV)

    Nebulization with Salbutamol.

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    VITAL SIGNS :1. SPO2 : 92%2. FiO2 : 1.03. BP : 113/64 mmhg4. PR : 85/min X-RAY : Bilateral Pneumonitis Lab Test :

    1. D-dimer : 3.8 mg/l ELEVATED2. fibrinogen : 5.1 g/l3. PT (INR 1.3)4. Hemogram,Sr. Biochemistry & Sr. Troponin

    T levels NORMAL

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    5. Serum Tryptase : 27 ng/ml6. Ethyl Histamine : 147 ng/mol

    7. CT Pulmonary Angiography : BilateralPneumonitis and no evidence of pulmonaryembolism.

    8. CT venography of leg and pelvic veins : Didnot reveal any evidence of deep vein thrombosis.

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    The patients general condition andhemodynamic parameters improved gradually.

    Extubated after 24 hours.

    She was discharged from the ICU to the wardthe next day.

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    NSAIDs are amongst the most frequently useddrugs.

    Anaphylaxis to Diclofenac is an Idiosyncraticreaction and is a rare event.

    Safety data from clinical trials in the UnitedStates have shown that Diclofenac Sodiumhas lower rates of adverse reactions than any

    of the other comparative NSAIDs.

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    Anaphylactic reactions have been reported totrigger cardiovascular events, includingmyocardial infarction and acute coronarysyndromes, even in patients with normal

    coronary vasculature.

    Pulmonary embolism can present with a widerange of clinical features many of which can alsobe seen in anaphylaxis.

    Both guidelines on pulmonary embolism andanaphylaxis emphasize the need for carefulassessment of probability in making the

    diagnosis.

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    Tryptase, released by mast cells together withhistamine and serves as a Marker of mast cellactivation.

    Another marker is urinary methyl histamine, ametabolite of histamine that has a longer half-life than histamine (23 hours).

    With these markers, a retrospective diagnosis

    can be made after the initial treatment of thepatient.

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    Serum Tryptase levels(normally

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    D-dimer testing is useful in excludingpulmonary embolism in patients, when usedwith assessment of clinical probability.

    However, it has poor specificity and is elevatedin a variety of settings, including anaphylaxis,due to activation of the coagulation pathway byallergic mechanisms.

    The pulmonary infiltrates seen in our patientwere probably caused by Diclofenacadministration as has been reported earlier.

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    Careful clinical assessment is important so thatappropriate treatment can be institutedpromptly.

    Epinephrine is the first and most important

    treatment for anaphylaxis. Also, an association between early

    anticoagulation and reduced mortality forpatients with acute pulmonary embolism has

    been noted. So anticoagulation can be started empirically

    when clinical features suggest acute pulmonaryembolism in a patient

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    This is a rare case of anaphylactic reactiondeveloping due to IV Diclofenac.

    IV Diclofenac sodium is a safe and widelyused drug, severe and potentially fatalanaphylactic reactions may occur with its use.

    Due to features resembling pulmonaryembolism, clinicians should be aware of this

    serious, albeit rare, complication of IVDiclofenac to enable them to make a correctand timely diagnosis

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    1. http://www.ijccm.org/temp/IJCCM15137-4657883_125618.pdf2. http://www.ijccm.org/article.asp?issn=09725229;year=2011;volume=15;issue=1;spage=37;epag

    e=39;aulast=Singh3. http://en.wikipedia.org/wiki/Mast_cell4. Denise F. Polit,et.al.,Essentials of NursingResearch,wolter kluver;third edition;2011.