Care of the Cirrhotic Patient: How to keep them compensated?
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Transcript Care of the Cirrhotic Patient: How to keep them compensated?
Mortality & morbidity
conference
Ana Mae Quintal-Quetua, M.D.
Mary Antoniette Tan, M.D.
Case Objectives
To present a case of a patient with
Myelodysplastic Syndrome who had multiple
medical problems, and developed acute STelevation myocardial infarction
To discuss the management and treatment
options for a patient with MDS who had STEMI
Hematologic- overview of AA and MDS
Cardiac
Patient Data
M.L.
61 years old
Female
Known HPN, on Diltiazem
Known asthmatic
Non-diabetic
Obese class II
Patient Data
March 2009, 2nd week - consult at MMC for
pancytopenia; BMA done
Bone Marrow cytology report (Mar-17-09)
60-70% marrow hypercellularity with erythroid
hyperplasia and mild dyserythropoiesis
Diagnostic comment: correlation with cytogenetic
studies for chromosomal haploinsufficiency is
recommended
Started on Prednisone; platelet counts improve with
increased doses
Patient Data
March 2009, 4th week- sought 2nd opinion at
SLMC; 2nd BMA done
Bone Marrow cytology report (Apr-03-09)
5-10% marrow hypocellularity with pancytopenia
with relative lymphocytosis; marrow space
occupied mainly by fibroadipose tissue
Cellular smears with dyserythropoiesis and
dysgranulopoiesis
Conclusion: Thrombocytopenia secondary to Severe
Aplastic Anemia , cannot rule out low-grade Hypoplastic
Myelodysplastic Syndrome
Patient Data
April 5- 9, 2009 - admitted at MMC for ATG
administration (with Solumedrol) and was started
on Cyclosporine 300mg OD; discharged stable
April 2009, 4th week - Prednisone dose was
increased up to 100mg OD
Steroid-induced hyperglycemia, on Humulin R 80-2 and Humulin N 28-0-10
History of Present Illness
3 days PTA, (+) productive cough, throat
irritation and hoarseness but (-) fever, DOB,
chest pain, bleeding
12 hours PTA, (+) blood-tinged sputum
May 6, 2009 - admitted for blood transfusion
due to decreased platelet count (PC 10,000)
Physical Examination on Admission
General
Survey
Conscious, coherent, ambulatory, not in respiratory distress
Vital Signs
BP = 110/70
BMI = 31kg/m2
HEENT
Anicteric sclerae, pale palpebral conjunctivae, (+) TPC with whitish
plaques on pharyngeal mucosa, (-) CLAD
HR = 78 bpm
RR = 20 cpm
Temp = 37.0C
Chest/ Lungs Clear breath sounds, symmetric chest expansion, no rales or
wheezes
CVS
Adynamic precordium, normal rate, regular rhythm, distinct S1 and
S2, no murmurs
Abdomen
Flabby, soft, normoactive bowel sounds, (-) masses or tenderness,
no splenomegaly
Extremities
Full and equal pulses, no pedal edema, no cyanosis, no clubbing
Admitting Impression
Severe Aplastic Anemia vs Hypoplastic
Myelodysplastic Syndrome
Upper Respiratory Tract Infection vs
Community Acquired Pneumonia
Laryngitis, Oral Candidiasis
COURSE IN THE WARDS
PROBLEM-BASED
1. Pancytopenia
BM biopsy (May-29-09, MMC)
10-20% hypocellularity with panhypoplasia,
dyserythropoiesis, left- shift granulocytic
maturation focal collagen fibrosis, Inc Iron
stores
CONCLUSION: presence of significant
dysplasia favors a diagnosis of Hypocellular
Myelodysplatic Syndrome
MYELODYSPLASTIC
SYNDROME
APLASTIC ANEMIA
Ineffective
Marrow failure secondary
hematopoiesis due to
abnormal differentiation
and maturation, leading
to bone marrow failure
Peripheral cytopenia,
dysfunctional blood
elements
Possibility of leukemic
conversion
to inability to produce
blood cell components
Maybe immune- mediated
(T- cells) or due to direct
bone marrow injury (drugs,
chemicals)
Pancytopenia, Bone
marrow hypocellularity
MYELODYSPLASTIC
SYNDROME
Bone marrow maybe
hypercellular, hypocellular
or normal
Cytogenetic abnormality
involving chromosome 5,
7, 11, 12 and 20 deletions,
and/or trisomy 8
Recurrent chromosome
deletions Loss of tumor
suppressor genes are
involved in the
pathogenic process
APLASTIC ANEMIA
Bone marrow consists
primarily of fatty space
and stromal cells
Evolution of AA to MDS/
AML is marked with
increased proliferative
activity +/- development of
cytogenetic abnormalities
9% risk of developing to
AML
Differentiating AA from Hypoplastic MDS:
Diagnosis dictates management and prognosis
A hypocellular bone marrow is seen in 20%
of MDS , which maybe confused with AA
Hypoplastic MDS- cytopenia, marrow
dysplasia and marrow hypocellularity
Incidence of 7.7% among a large series of
MDS patients evaluated
Increase in mast cells and lymphoid cells
Cytogenetic studies: changes in chromosome
7, especially monosomy 7
3/5 cases transforming from AA to H- MDS
showed monosomy 7
Monosomy 7 found in Hypoplastic MDS
indicates a poor prognosis, with patients
progressing to refractory cytopenia, with 80%
risk of evolving into Acute Myeloid Leukemia
Trisomy 8- immune pathophysiology; often
responds clinically to immunosuppressive Tx
International Prognostic
Scoring System
Treatment Algorithm
Treatment
MYELODYSPLASTIC
Poor response to
cytotoxic chemotherapy
Stem Cell
Transplantation offers
cure, 50% survival rate at
3 yrs
Demthylating agentsPyrimidine analogues
(Azacitidine, Decitabine)
Lenalidomide,
Cyclosporine, ATG, GCSF
APLASTIC ANEMIA
Immunosuppression:
Combination of
Cyclosporine & AntiThymocyte Globulin
Stem Cell
Transplantation
Supportive - transfusion
1. Pancytopenia
ISSUES
Hemoglobin: 6.3 – 12.4 g/dl
WBC: 410 – 5,100
Platelet count: 2,000 – 160,000
Persistent pancytopenia despite multiple
blood transfusion and repeated GCSF admin.
Risk for severe infection, hemodynamic
instability and bleeding
1. Pancytopenia
MANAGEMENT
Multiple transfusion of blood products
ATG
Cyclosporine
Repeated GCSF administration
Steroid administration
Erythropoietin, thrombopoietin
Vitamin K and tranexamic acid
administration
Effect of Multiple Blood
Transfusion
Supportive therapy: PLT transfusion
However, repeated PLT transfusion may fail
to show the desired increment in PLT counts
PLT refractoriness develop in 30-70%; maybe
due to the underlying condition (fever, sepsis,
drugs) or it may be due to alloimmunization
Patients with transfusion failure due to HLAantibodies may be given HLA- matched PLT
components
1. Pancytopenia
ETIOLOGY
Thrombocytopenia secondary to Severe
Hypoplastic Myelodysplastic Syndrome
Platelet refractoriness secondary to
multiple blood transfusion
Unresolving Sepsis secondary to
Pneumonia in the Immunocompromised
2. Pneumonia and Fungal Laryngitis
in the Immunocompromised
ISSUES
Severe infection; sepsis
Unresolving lung infiltrates and persistent
pleural effusion
Persistent wheezing/bronchospasm sec. to
hyperreactive airways
2. Pneumonia and Fungal Laryngitis
in the Immunocompromised
MANAGEMENT
Sputum cultures, blood cultures
Chest radiographs, chest UTZ, chest CT scan
Attempted thoracentesis/chest pigtail insertion
Use of broad-spectrum antibiotics, antifungals,
antivirals
Inhaled and systemic bronchodilators and
mucolytics; steroid administration
CT scan of the chest, plain
(May 31, 2009)
Pneumonia, left lower lobe
Soft tissue density in the LUL and pulmonary
nodular opacities in the right lung may still be
related to the infectious process
Subcentimeter granuloma, RLL
Minimal pleural effusion, left
Calcified lymph nodes, right paratracheal and
right hilar regions. These were already noted in
the study of April 4, 2009.
3. Respiratory Failure
CAUSES
Severe infection (laryngeal candidiasis and
unesolving pneumonia) and sepsis in the
immunocompromised
Pulmonary congestion sec.to hypervolemia,
hypoalbuminemia
Persistent wheezing/bronchospasm sec. to
hyperreactive airways
Anemia
Airway and intrathoracic bleeding
Empyema/pyothorax considered
3. Respiratory Failure
MANAGEMENT
Alternating BIPAP and in-line neb.
Endotracheal intubation and subsequent
tracheostomy
Inhaled and systemic bronchodilators in
increased doses
Inhaled and systemic mucolytics
4. Hypoalbuminemia
CAUSES
Nutritional
Hepatic failure
ISSUES
Third spacing: congestion, effusion and edema
MANAGEMENT
Repeated IV infusions of 25% human albumin
5.
Hyperglycemia
CAUSES
Steroid-induced
Stress-induced
ISSUES
Risk for uncontrolled infection,
cardiovascular/coronary events
MANAGEMENT
CBG monitoring and insulin administration
6. Renal Failure
CAUSES
Sepsis
Decreased renal perfusion sec. to anemia
(shunting of blood away from the kidney
for protection of O2 delivery to vital
organs)
Drugs (Cyclosporine, Amphotericin,
antibiotics)
6. Renal Failure
ISSUES
Hypervolemia (increased BP and CVP 1419 cmH2O, edema) due to multiple
transfusions, steroid admin.
On the 22nd HD, (+) oliguria with rising
serum crea 2.0 from 0.9 mg/dl (est. crea
clearance 21 ml/min from 47 ml/min)
6. Renal Failure
MANAGEMENT
Dose adjustments of antibiotics and other
medications
12-hour urine collection
Diuresis (Furosemide, Spironolactone,
Bumetanide)
Subsequent hemodialysis
7. Abdominal Distension
CAUSES
Septic ileus
Ileus sec.to metabolic derangement
Pseudomembranous colitis considered
ISSUES
Increasing abdominal girth with intermittent
episodes of voluminous watery stools
7. Abdominal Distension
MANAGEMENT
NPO
Plain film of the abdomen
CT scan of the abdomen
Prokinetics, laxatives, enemas
Vancomycin per orem
Rectal tube insertion
Total parenteral nutrition
CT scan of the abdomen, plain
(May 31, 2009)
Ileus
Few descending colon diverticula
Distended gall bladder
Atrophic pancreas
Possible right renal cortical cyst
Subcentimeter appendicolith vs. inspissated
barium with no associated inflammatory
changes
The rest is normal
8.
Metabolic Encephalopathy
CAUSES
Sepsis
Electrolyte derangements
Hypovolemia episodes during
hemodialysis
Hepatic failure
8.
Metabolic Encephalopathy
MANAGEMENT
Referral to Neurology service on the 27th HD
Cranial MRI and MRA of intracranial vessels
requested
EEG showed encephalopathy probably sec. to
hypovolemia (hypotension episodes during
dialysis)
Correction of electrolyte abnormalities;
manage sepsis
9. Elevated Blood Pressure
(130-200/70-100 mmHg)
CAUSES
Volume overload sec. to multiple blood
transfusion, steroid use
Increased cardiac output sec. to tachycardia
Catecholamine release (stress-induced)
9. Elevated Blood Pressure
(130-200/70-100 mmHg)
MANAGEMENT
Ca-channel blockers (Amlodipine,
Nicardipine, Verapamil)
Clonidine
Diuresis
10. Tachycardia with PACs
and PVCs (100 – 180 bpm)
CAUSES
Sepsis/stress-induced
Anemia
Metabolic derangements (i.e. electrolyte
imbalance)
Bronchodilators in increased doses
10. Tachycardia with PACs
and PVCs (100 – 180 bpm)
MANAGEMENT
2D-echocardiogram with CFDS
Electrolyte correction
Beta-blockers (Metoprolol, Nebivolol)
Digoxin stat doses
Verapamil
Amiodarone
Ivabradine
Trimetazidine
2D-echocardiogram with CFDS
(baseline)
May 15, 2009 - Normal LV dimension with
NWMC, EF 75%; calcified non- coronary cusp
of aortic valve without restriction of motion.
Calcified aortic walls; normal MV, TV, PV;
minimal pericardial effusion; color flow
Doppler= MR, mild; TR, mild; mild pulmonary
hypertension as evidenced by pulmonary
acceleration time of 100 msec; Doppler
evidence of impaired LV relaxation.
On the 35th hospital day…
Tracheostomy done
O2 desaturation noted ~ 90%
HR much controlled: 78 bpm
BP 104/55 mmHg
12-lead ECG post-trache showed: new Twave inversions at V1 – V3, ST-elevations
at II and AVF
Cardiac Enzymes
May 13: TCPK 60, CKMB 1.5, Trop I 0.08
June 10: TCPK 47, CKMB 7, Trop T 0.51
June 11: TCPK 29, CKMB 2.9, Trop I 0.37
May 13: serum BNP 4,071
2D-echocardiogram with CFDS
(repeat)
June 11, 2009 - concentric LVH with NWMC,
EF 55%; color flow Doppler = MR, mild;
Doppler evidence of LV diastolic dysfunction
(E/A velocity ratio and isovolumic relaxation
time); mild pulmonary hypertension by
pulmonary acceleration time 108 msec;
compared with previous study done may 15,
increase in LV wall thickness; no note of
pericardial effusion.
On the 41st hospital day…
While on hemodialysis, ST-segment
elevations were noted on cardiac monitor,
and patient had 3 episodes of HR 30s – 40s (5
– 10 secs)
BP = 100-130/60-80 mmHg
Awake, responsive
(-) chest pain
12-lead ECG showed….
11. STEMI
ISSUES
Risk factors: age, atherosclerosis, anemia,
obesity, HPN, hyperglycemia,
dyslipidemia, hemodialysis, multiple blood
transfusion (blood viscosity? increased
platelet aggregation? endothelial
damage?), heparin-induced
thrombocytopenia (?)
11. STEMI
MANAGEMENT
Nitroglycerin drip
Nicorandil 5mg/tab 1 tablet BID
Coronary angiogram
Options: anti-platelet and anti-coagulation
(?), PTCA (?)
Coronary Angiogram
Results:
Left ventriculogram – intentionally omitted due to
elevated LV EDP 31mmHg
Coro angio – L main coronary artery normally
patent; LAD normal; L circumflex has slow flow with
abrupt cut off distally which indicates an
endovascular thrombus; RCA is dominant and
normal.
Assessment: Coronary thrombus involving L
circumflex artery
Recommedation: Consider Cilostazol at low dose
50mg BID
How Was The Patient Managed?
Post- coronary angiography recommendations:
Interventional Cardiology - low-dose Cilostazol
50 mg BID
Cardiology – Enoxaparin 40mg SC OD
Hematology service, however, did not agree
Due to persistent pancytopenia, Interventional
Cardiology entertained the possibility of HIT,
and suggested discontinuation of Heparin and
use of Bilvalirudin and Aspirin 325 mg OD
Heparin- Induced Thrombocytopenia?
HIT is a pro-thrombotic, immune- mediated adverse
reaction to heparin therapy;
It should be suspected whenever the PLT falls at
least 50% and/ or thrombosis occurs between day 4
and 14 following initiation of heparin
Based on results reported by Warkentin et al. and a
meta- analysis of 15 studies, it appears that HIT
type II occurs in 1-3% of all patients receiving UFH &
in only 0.3- 0.8% receiving LMWH
Heparin-InducedThrombocytopenia?
When heparin is administered in the presence of
platelet factor 4 (PF4), an immune complex can form
and result in the production of anti-PF4/ Heparin
antibody (HIT antibody)
This complex initially causes PLT aggregation,
followed by a decrease in the PLT count (due to
consumption and elimination from the circulation) &
the development of thrombosis.
Paradoxical thrombosis in the presence of
thrombocytopenia is a hallmark of HIT
Heparin- Induced Thrombocytopenia?
Diagnostic tests include C-Serotonin Release Assay,
Platelet aggregation test, Heparin- induced platelet
aggregation test, ELISA
Treatment is prompt discontinuation of heparin
and use of an anti-thrombin agent (ie, Argatroban,
Bivalirudin) to prevent thrombotic complications
Associated thrombotic events frequently noted are
Deep Vein Thrombosis, Pulmonary
Thromboembolism, Mesenteric Arterial Thrombosis
Bivalirudin
Newer direct thrombin inhibitor; binds to the
substrate- binding site of thrombin, with high
affinity
Has a rapid, dose- dependent anticoagulation, with
half- life 25 minutes
Eliminated by the kidneys
As with all direct thrombin inhibitors, it has no
structural similarities to heparin and has no crossreactivity with HIT antibodies
Patient Outcome
Hematology service did not agree on the
diagnosis of HIT; however agreed on the use
of Aspirin 325 mg OD (only 1 dose was given)
3rd day post MI and post angiogram,
persistent pancytopenia and hemodynamic
instability
Ventricular fibrillation
After 4o minutes of CPR, patient expired
IS IT POSSIBLE TO DO
PERCUTANEOUS
CORONARY
INTERVENTIONS
IN PATIENTS WITH
MYELODYSPLASTIC
SYNDROME?
Myelodysplastic Syndrome &
Myocardial Infarction
The association of CAD and thrombocytopenia due
to MDS is rare, and published data on the
management of obstructive lesions through PCI is
limited
This presents a challenge to interventional
cardiology, because PCI requires preventing both
intracoronary thrombosis with antiplatelet agents,
and bleeding after the procedure
61/ M, known case of MDS, hypertensive,
presented with pressure- like chest pain,
Dx: Unstable Angina; submitted to coronary
angiography and stenting
Platelet count was 40,000;
prophylactic, 10 unit platelet transfusion 2 days
prior to coronary angiography
80% stenosis of the RCA and 30% in the LAD
After a 6- day Clopidogrel 75 mg OD regimen, and
2 hrs after another 10 unit PLT transfusion, stenting
DES of the RCA lesion was done
6F catheter, femoral approach; introducer was
removed 4 hrs after the procedure
100 IU/ kg Heparin during the procedure
Local compression for 20 minutes; no bleeding nor
hematoma was observed after the removal of
introducers
Discharged with Clopidogrel 75 mg OD to complete 30
days of continuous use.
Platelet count remained stable at 40,000 on Clopidogrel
6 months later, TMST showed ST depression in the
inferior leads; repeat coronary angiography showed a
70% in-stent stenosis; He refused another PCI
20 months after stenting, patient remained
asymptomatic, maintained on the same medication
(Clopidogrel 75 OD, propranolol 40 mg BID, Simvastatin
20 mg OD)
His last platelet count was 104,000
In spite of the low PLT, this patient evolved with
progressively unstable angina, suggesting that regardless
of the small number, platelet function remained normal,
thereby justifying the use of anti- platelet agents
Clopidogrel alone was the treatment of choice in this
study, since it is better tolerated than Ticlodipine
This case report suggest that PCI in patients with
thrombocytopenia is a safe procedure, provided that
prophylactic platelet transfusion is done, although
restenosis may occur
Management Dilemmas
Is it possible to do stent placement?
•Bare- Metal Stent vs Drug- Eluting
Stent?
If patient tolerates stent
implantation, is it possible to
maintain her on an anti- thrombotic
regimen?
•Single or Dual Anti- PLT therapy?
•ASA vs Clopidogrel vs Cilostazol?
• Dose and duration?
STENTS
Stents are used in the management of ACS and its
use has improved the outcomes of percutaneous
coronary revascularization
The metallic surface of the bare-metal stent (BMS)
can stimulate thrombosis before it becomes entirely
covered with endothelial tissues
Disadvantage: subsequent development of an instent restenosis due to significant loss of lumen
STENTS
Drug – eluting stents (DES) are believed to inhibit restenosis by inhibition of cytokine- mediated and GF-
mediated proliferation of lymphocytes and smooth
muscle cells
DES indicated for high- risk patients (diabetics, long
lesions, small vessels, presence of a thrombus)
DES and dual anti- PLT therapy with ASA and
Clopidogrel reduce stent re-thrombosis rates to <2%
However the consequences for patients with potential
bleeding conditions are potentially life- threatening
Drug- Eluting stents vs Bare metal stents: Off- label indications, A Propensity- score Matched Outcome Study
Stent Thrombosis
Catastrophic, mortality rate of 20-45%
Most commonly, about 1% occurs in the first
month after stent implantation ( subacute ) and
about 0.19% occur after a few months to a few
years ( late )
BMS are associated with higher incidence of
stent thrombosis compared to DES
Timing of thrombosis appears to be delayed in
DES (higher early stent thrombosis with BMS,
and late thrombosis with DES)
Drug- Eluting stents vs Bare metal stents: Off- label indications, A Propensity- score Matched Outcome Study
BMS or DES ?
DES is indicated in
high- risk patients:
diabetic, small vessel,
long lesion, presence of
a thrombus (off- label)
BMS - Shorter duration of
anti- platelet therapy
(minimum of 2 weeks to
1 month for those at risk
of bleeding) thereby
minimizing the risk of
bleeding
• However, BMS are prone
to early stent thrombosis
Aggressive: PCI
BMS has a shorter duration of anti- platelet therapy
(minimum of 2 weeks to 1 month for those at risk of
bleeding)
for post- BMS stent, Clopidogrel 75 mg OD for at least 1
month (ideally up to 1 year if not at risk for bleeding;
then it should be given for a minimum of 2 weeks if at
risk)
a lower dose of 75- 162 mg of ASA is reasonable (during
the initial period after stent placement) in patients at risk
of bleeding
Cilostazol has similar anti- PLT affects with less serious
side effects;
Use of
ANTI- PLATELET
AGENTS
in
Hematologic Patients
Literature reports on ITP patients who underwent
PTCA/ PCI, with use of anti-PLT:
62/M with PLT 3,000, underwent LAD stenting,
tolerated 4wks of ASA and 2wks of Clopidogrel;
no bleeding (Caputo, et al.)
68/F with PLT 22,000, underwent LAD stenting,
maintained on Ticlodipine, no bleeding (Kikuchi
et al.)
54/M with PLT 8,000, underwent BMS stenting,
given Enoxaparin; discontinued due to epistaxis
(Marques et al.)
77/M with PLT 70,000, underwent PTCA, on ASA
and Clopidogrel; discontinued due to petechiae
Use of Anti- Platelet Agents
ASPIRIN
Irreversible inhibition of COX-1, which prevents formation of
PGH2, the precursor of thromboxane A2
Patients with thrombocytopenia from whatever cause
(PLT 50,000) are at extremely high- risk of excessive
bleeding. Therefore, Aspirin is harmful in these patients
and should not be administered (Class III
RECOMMENDATION)
In those who underwent stent placement, a lower dose of
75- 162 mg of ASA is reasonable (during the initial period
after stent placement) in patients at risk of bleeding
The Society of Thoracic Surgeons Practice Guideline Series : ASA and other Anti- Platelet agents during operative coronary
revascularization, 2003
2007 Focused Update on STEMI Guideline
CLOPIDOGREL
Inhibits binding of PLT to ADP receptors
2007 STEMI guideline
• For STEMI patients not undergoing PCI (medical or
PTCA without stenting), treatment with Clopidogrel
75mg OD x 14 days
• Recommends all post- PCI stent patients receiving a
DES, Clopidogrel 75 mg OD for at least 12 months if
patient is not at high risk of bleeding; for post- BMS
stent, Clopidogrel 75 mg OD for at least 1 month
(ideally up to 1 year if not at risk for bleeding; then it
should be given for a minimum of 2 weeks if at risk)–
Level of evidence, B
• Premature discontinuation of Clopidogrel is
associated with a marked increase in risk of stent
thrombosis, & is the leading independent predictor
in multiple studies
• For every 100 patients treated with Clopidogrel +
ASA, 2 events of CV death, non- fatal MI, or stroke
will be prevented but 1 patient will suffer a major
bleed (ie, ICH)
1 Prevention of Premature Discontinuation of Dual anti- Platelet Therapy
2 AHA 2007 Focused Guideline on STEMI
3 CURE (Clopidogrel in Unstable angina to prevent Recurrent Event )Trial
Predictors of Thrombosis
CLINICAL
Advanced Age
Acute coronary Syndromes
Diabetes
Renal Failure
Low ejection Fraction
Premature Discontinuation of Dual anti- PLT Therapy in
Patients with Stents (Journal of AHA, 2007)
CILOSTAZOLPhosphodiesterase III inhibitor; anti- proliferative effect
Cilostazol for RESTenosis (CREST) clinical trial in
post BMS
Preliminary results suggested that Cilostazol
(phosphodiesterase III inhibitor) reduces
restenosis by nearly 40% over standard therapy
alone
It has similar anti- PLT affects with less serious
side effects (esp bleeding) ; common SE
include thrombocytopenia and leukopenia/
agranulocytosis
CILOSTAZOL
In the study “Triple vs Dual Anti- platelet Therapy
After Coronary Stenting”, addition of Cilostazol
resulted in further reduction of PLT activation due
to additional suppression of P- selectin (a marker
of PLT activity)
The rate of major bleeding was similar in both
groups
However, patients with known bleeding disorders
and PLT< 150T were excluded in the study
Recommended dose 100 mg BID, but may be
decreased to 50 BID if with concomittant use of
CYP450 inhibitors (ie, Diltiazem)
SINGLE ANTIPLATELET THERAPY
OR
DUAL ANTI- PLATELET
THERAPY
Current ACC/ AHA/ Society of Cardiovascular
Angiography & Interventions for prevention of
stent thrombosis post PCI
_________________________________________
At minimum, patients
should be treated with :
Clopidogrel 75 mg OD &
ASA 325 mg OD for
1 month after BMS,
3-6 months after DES,
and ideally up to 1 year if
they are not at risk for
bleeding
Dual Anti- PLT Therapy for Prevention of Ischemic
Cardiovascular Events & Stent Thrombosis
Use of a single antiplatelet regimen may
possibly reduce the
risk of bleeding
•Aspirin - 75- 162 mg is
reasonable (during the
initial period after stent
placement) in patients
at risk of bleeding
•Cilostazol has similar
anti- PLT affects with
less serious side effects;
Outcome
Hematology service agreed on Aspirin
325 mg OD
3rd day post angiogram, persistent
pancytopenia and hemodynamic
instability
ventricular fibrillation
After 45 minutes of CPR, patient
expired
Final Diagnoses
Cardiopulmonary Arrest sec.to Ventricular
Fibrillation post STEMI, anterolateral wall
Myelodysplastic Syndrome
Sepsis sec.to Pneumonia and Laryngeal
Candidiasis in the Immunocompromised
Acute Renal Failure, multifactorial
Steroid-induced Hyperglycemia
Hypertensive Atherosclerotic Cardiovascular
Disease
Arrhythmia is a serious complication of
STEMI
Possibility of another infarction may have
precipitated the arrhythmia
In retrospect, in an immunocompromised
patient with severe hematologic disorder
with a coronary artery thrombus, who was
septic, undergoing dialysis for acute renal
failure, with impending liver failure, would an
aggressive approach like PCI do more harm
than good?
CONCLUSION
It is apparent that any medical or surgical
intervention has both systematic and random
effects, some of which are beneficial and some
are unintended negative consequences
Therefore , the practice of medicine often
necessitates a probabilistic balancing of these
conflicting effects, and management should be
individualized, depending on the risk: benefit
ratio
Thank You
“….. The science of medicine becomes a structured
and organized way of using probability,
uncertainty, and facts in preventive medicine
and clinical care to best benefit the patient and
the community…”
-Jenicek, Foundations of Evidence- Based Medicine