CASE REPORT OF A YOUNG OTHERWISE HEALTHY FEMALE WHO DEVELOPED ACUTE CORONARY SYNDROME (ACS) FOLLOWING DICLOFENAC INJECTION

1. ALLERGIC ACUTE CORONARY SYNDROME
By
Dr.K.Manievelraaman
Second Year PG
IIM, MMC & RGGGH
UNIT M1
Prof.Dr.C.Hariharan MD
Not a rare disease occurrence
But a rarely identified one

2. History
• Ms.V, a 21 year old female
• Resident of Chennai
• Unmarried
• Educated
• Well Built and Nourished
• No known co-morbidities
• Otherwise healthy person
• Never had a chest discomfort
• Never had any symptoms suggestive of cardiac or pulmonary
pathology

3. History - Continued
• History of outside food ingestion the previous day
• Visited nearby Private clinic for colicky abdominal pain – Intermittent and each
episode lasted <5mins
• Received Inj. Diclofenac I.M for pain relief
• After 10-15 mins of IM Injection, Patient developed
• Chest discomfort – retrosternal; tightness; non-radiating
• Urticarial rashes all over the body
• Giddiness
• IM Adrenaline 0.5cc given and IV Fluids started
• After 2 hours of observation, symptoms persisted; Patient referred to higher centre

4. On Arrival
• History noted
• Vitals checked
• BP: 90/60 mm of Hg
• HR: 120 beats/min
• RR: 24/min
• SpO2: 98 with Nasal O2
• Hypotension present
• Second shot of IM Adrenaline 0.5cc given along with isotonic fluid bolus

5. After an hour
• C/O Breathlessness developed –
• Worsened by lying flat (orthopnea)
• Lying flat elicits cough

6. Relevant Negative History
• No H/O Palpitations, Pedal edema, Abdominal distension
• No H/O dysphagia, vomiting, loose stools, LGI bleed, constipation, obstipation
• No H/O oliguria, dysuria
• No H/O LOC, Seizures
• No H/O suggestive of Rheumatologic Illness
• Personal H/O – No adverse social habits; No history of drug abuse
• Family H/O – No family history of MI, SCD.
• Previous H/O – No previous episodes of urticaria, drug allergy.

7. On Examination
• HR:96/min; BP:90/60mm Hg; RR:24/min; SpO2:98 on O2; JVP- not elevated
• Conscious, Oriented, Afebrile, Tachypneic
• NO {pallor, icterus, cyanosis, clubbing, lymphadenopathy, pedal edema}
• CVS – S1S2+ ; No murmur
• RS – Scattered Wheeze+ (expiratory); Bilateral Crackles+
• PA – soft; non tender; no organomegaly; no guarding/rigidity
• CNS – Conscious, Oriented; B/L pupils reactive; No focal deficits

8. Provisional Diagnosis
• Anaphylaxis – triggered by Diclofenac
• Anaphylactic Shock
• Pulmonary edema ( ? non-cardiogenic )

9. Basic Investigations
• CBC
• Hb – 13.5
• TC – 10000 (N-66; L-26)
• Platelet – 3.2 lakh
• RFT ( Urea, Creatinine) – Normal
• LFT (Bilirubin, AST,ALT, Albumin) – Normal
• SERUM ELECTROLYTES – Normal
• RBS -105mg/dl
• COAGULATION PROFILE – Within normal limits
• INR – 1.12

16. Other Investigations
• USG Abdomen:
• No significant abnormality
• IVC diameter : 1.8cm @ Hepatic vein entry level
• CXR – Bilateral perihilar haziness noted
• ECHO
• Poor ECHO window
• Global Hypokinesia
• No PE/Clot

19. Cardiogenic Pulmonary Edema

20. ECHO – AFTER ONE WEEK
• NORMAL SYSTOLIC FUNCTION

21. CORONARY ANGIOGRAPHY – AFTER 2 WEEKS
• NORMAL EPICARDIAL CORONARIES

22. MOST PROBABLE DIAGNOSIS
• Anaphylaxis --Trigger: Diclofenac (NSAID)
• Anaphylactic shock (recovered)
• Cardiogenic Pulmonary Edema
• Allergic NSTE-ACS (?Vasospasm; Non-obstructive coronaries)

23. Controversies and Substantiations
• Could ADRENALINE be the reason for ECG changes?
• Could SHOCK explain all these?
• Could initial abdominal pain itself be of cardiac origin?

25. Temporal correlation?

26. Why adrenaline less likely cause?
• NO TACHYCARDIA IN INITIAL ECG ( HR<100/min )
• Second dose of Adrenaline didn’t worsen it, rather ECG showed
regression of ischemic changes.
• Half life of adrenaline.

27. • On Discharging,
• Patient BP was 90/60 mm Hg
• No tachycardia
• No Tachypnea
• No Dyspnea
• No orthopnea
• When in IMCU,
• IVC diameter was 1.8cm
• Also, Colicky (Intermittent) nature of pain is unlikely to be of cardiac origin

30. THESE EVENTS COULD BE DUE TO
DIRECT EFFECTS
of ALLERGY on HEART

34. Inflammatory mediators - Cause or Result?
• Mast cell infiltration
• Circulating precursors
• Stress test induced Ischemia not accompanied by surge
• No histamine elevation with Acetylcholine induced vasospasm

35. Myocardial Ischemia – Primary or Secondary?
• Differentiation is clearly challenging; Both may co-exist
Systemic
vasodilation
Increased vascular
permeability
Decreased Venous
Return
Reduced CO
Coronary
hypoperfusion
Antigen
administration
ECG signs of
Myocardial
Ischemia
LVEDP rapidly
increased
BP started
declining
steadily after 4
mins
Unlikely in the
setting of decreased
venous return

36. Why not in all allergic episodes?
• Threshold level
• Baseline elevation à high risk
• Underlying mast cell disorder à high risk
• Increased incidence of IHD in atopic individuals and wheezers
• Use of ICS a/w reduced risk of IHD in asthmatics

40. Textbook References

41. Terminologies
• Obstructive Epicardial coronaries
• Non-Obstructive Epicardial coronaries
• Vasospasm à Prinzmetal’s Angina
• No vasospasm but persisting ECG findings of ischemia
à cardiac syndrome X
• ( ? Microvascular pathology )
Developing
in the
setting of
Allergy
+

42. Treatment options for KOUNIS SYNDROME
• Type 1 variant à Steroid, Antihistamine, Vasodilator, Mast Cell Stabilizers
• Type 2 variant à Standard ACS Rx protocol + Above
• Type 3 variant à Same as above + Aspiration of Intrastent thrombus

43. • Ranitidine may have a role.
• Due to it’s paraspecific action on H1 blockade.

45. Significance of recognizing this syndrome?
Possibility of new therapeutic modality to treat ACS

48. Thank You