Splenic Infarct, Atrial Fibrillation

Morning report
Resident: Bijan
Ghassemieh
Faculty
Discussant: Dr.
Kirk Spencer

45 year-old asymptomatic man, history of sudden
cardiac death in the family: what’s the syndrome?

MKSAP
A 43-year-old man is evaluated during a routine examination. He
has a history of a cardiac murmur diagnosed during childhood.
He exercises regularly without restriction to activity and has no
history of syncope, presyncope, palpitations, or edema. He is on
no medications.
On physical examination, he is afebrile, blood pressure is
120/64 mm Hg, pulse is 80/min and regular, and respiration
rate is 16/min. BMI is 25. He appears well. Cardiac examination
reveals a normal S1 and a physiologically split S2. There is a
grade 2/6 decrescendo diastolic murmur at the left sternal
border. Distal pulses are brisk. There is no pedal edema.

MKSAP
A transthoracic echocardiogram demonstrates normal ventricular
size and function, with ejection fraction of 60% to 65%. There is a
bicuspid aortic valve with moderate regurgitation. The proximal
ascending aorta diameter measures 4.2 cm. Pulmonary pressure
estimates are in the normal range.

MKSAP
Which of the following is the most appropriate management
option for this patient?
A. Antibiotic prophylaxis prior to dental procedures
B. Clinical follow-up in 1 year
C. Surgical referral for aortic valve replacement
D. Transesophageal echocardiography

A.
B.
C.
D.
Please make your selection...
Antibiotic prophylaxis prior
to dental procedures
Clinical follow-up in 1 year
Surgical referral for aortic
valve replacement
Transesophageal
echocardiography
25% 25% 25% 25%
A. B. C. D.

MKSAP
Because a bicuspid valve is subject to higher mechanical and shear stress than
a tricuspid valve, the disease process of progressive calcification is
accelerated, and clinical presentation tends to be earlier—in the fourth or fifth
decades of life. This patient has a bicuspid aortic valve with moderate aortic
regurgitation. Echocardiography demonstrates normal left ventricular size and
systolic function. Pulmonary pressures are in the normal range, and there is no
evidence of adverse hemodynamic effects of valve regurgitation on the
ventricle (ventricular size and function are normal). No specific treatment is
needed at this time. However, because worsening of aortic regurgitation can be
insidious, routine clinical follow-up is indicated in at least yearly intervals,
typically with repeat transthoracic echocardiography to monitor for disease
progression. The presence of a bicuspid aortic valve is associated with
ascending aorta dilation, and TTE can also monitor for aortic enlargement.
Most patients with bicuspid valves will eventually develop significant
abnormalities—aortic stenosis, regurgitation, or aortic root dilation or
dissection—that require surgery.

69 y.o. Male Presents to ED
With FEVER and Abdominal
Pain

HPI
Pain History:
Location: Diffuse throughout abdomen, worse in LUQ
Onset: 2 day ago
Positional: No
Quality: Sharp, constant
Radiation: None
Severity: 7/10
Timing: Constant, not spasmodic
Aggravating: nothing identified (no change with eating)
Alleviating: nothing
GEN: +fevers. No chills, weight loss, sweats
HEENT: ROS negative
CV: No chest pain, palpitations, lightheadedness, orthopnea, PND, LE edema
PULM: No SOB, cough, pleuritic chest pain
GI: + abd px. No nausea, vomiting, diarrhea, constipation, blood in his stool, jaundice,
or pruritis
GU: No frequency, dysuria

PAST MEDICAL/SURGICAL HISTORY
DM
HTN
Complete heart block s/p
MEDICATIONS
HCTZ 25 mg daily
Pantoprazole 40 mg PO daily
Metformin 500 mg PO BID
FAMILY HISTORY: Non-contributory
Medical HIstory
dual chamber pacemaker in 2007
SOCIAL HISTORY: Retired pit-boss. History of moderate alcohol use, quit many
years ago. 25 pack years, quit 5 years ago. No travel or sick contacts.

Physical Exam
Vitals: T 38.3 HR 60 BP 130/67 RR 18 Sat 97% RA
GEN: Appears uncomfortable
HEENT: Sclerae anicteric. Oropharynx clear. No sinus tenderness or nasal
drainage.
CHEST: L chest pacemaker without surrounding erythema, tenderness, or
warmth
CV: RRR. 2/6 holosystolic murmur heard best at LUSB that does not increase
with inspiration (previously documented). No JVD. No LE edema. 2+ radial and
DP pulses bilaterally with good capillary refill
PULM: Breathing unlabored. CTA bilaterally
ABD: Flat abdomen. +BS. Soft. Mild diffuse tenderness, worse in LUQ. Displays
voluntary guarding in the LUQ, no rebound. No masses or organomegally
appreciated.
GU: Normal external genitalia. No inguinal hernia appreciated. No CVA
tenderness
LYMPH NODES: No appreciated cervical, supraclavicular, or inguinal LAD
EXT: No clubbing. No edema. Warm and well perfused. Otherwise unremarkable
NEURO: A+O X3. Strength and sensation grossly intact.
SKIN: No rash

136
4.5
17.0
104
23
12.4
28
1.2
154
Differential: 82% PMNs
What labs/studies would order next?
Initial studies
160
UA: unremarkable
LFTs: unremarkable
Lipase: normal
Coags: normal
Blood and urine cxs: Pending

CXR

EKG
Want anything else to workup his belly pain?

CT abdomen
New splenic broad wedge shaped hypodensities concerning for splenic
infarcts.

Uncommon
Clinical manifestations
Osler: LUQ pain, tenderness, swelling, and peritoneal friction rub
Retrospective review from Israel identified 26 patients over 12 years and
characterized the clinical findings as……
L sided abdominal pain in 48% (abd pain absent in 16%)
LUQ tenderness in 36% (abdominal tenderness absent in 32%)
Splenomegally: 32%
Fever in 36%
Nausea/vomiting: 32%
Elevated LDH: 71%
WBC > 12K: 56%
Splenic infarction
Why does he have this? What workup would you like?
Lawrence, et all. Splenic Infarction: an update on William
Osler’s observations. Isr Med Assoc J. 2010; 12(6):362

Differential Diagnosis of Splenic Infarction
Hunt DP et al. N Engl J Med 2010;363:1266-1274
Any more studies you
want now?

Clinical course
Patient admitted to the hospital, placed on broad spectrum antibiotics
(cefepime and vancomycin), and pain controlled with IV opiods.
On hospital day 3, his abdominal pain continued and he remained febrile.
Serial blood cultures remained negative. Rheumatologic studies were
unremarkable. CMV and EBV studies still pending. Hypercoaguable studies
were either negative or pending.
Despite negative blood cultures, consideration was given to
echocardiography to evaluate for endocarditis.

Modified Duke Criteria for the Diagnosis of Infective Endocarditis.
Mylonakis E,
Calderwood SB. N
Engl J Med
2001;345:1318-1330.

TEE

TEE Read:
- No evidence of vegetation
-
A left atrial
TEE
appendage thrombus is present.
- No mass or thrombus seen in the right atrium or right atrial
appendage.
There is a catheter in the coronary sinus consistent with
history of bi-ventricular pacer.
Where did this LA clot come from? How do you tie this in with
his abdominal pain?

Patient is started on a heparin ggt.
Patient course (cont)
At this point, the cardiology team is consulted to help determine the
etiology of his LA thrombus.
You are the resident on cardiology. As you are presenting the patient to
your attending on rounds, you pull up the patient’s old EKGs for
comparison

This is what you see . . . . Thoughts?

A-FIB AND CARDIOEMBOLIC RISK

OUR PATIENTS A-FIB WAS A BIT HARDER TO PICK UP
DUE TO HIS COMPLETE HEART BLOCK AND PACER

Explanation of the Threeand Four-Letter Designations for Commonly Used Pacing Modes.
Kusumoto FM, Goldschlager N. N Engl J Med 1996;334:89-99.

OUR PATIENTS RECENT EKGS

1.
2.
3.
A-sensed – sinus
rhythm, V-paced
A-sensed - Atrial
Fibrillation, V-paced
A-paced, V-paced
What is the Rhythm?

OUR PATIENTS RECENT EKGS

1.
2.
3.
A-sensed – sinus
rhythm, V-paced
A-sensed - atrial
fibrillation, V-paced
A-paced, V-paced
What is the Rhythm?

Our patients recent EKgs

1.
2.
3.
A-sensed – sinus
rhythm, V-paced
A-sensed - atrial
fibrillation, V-paced
A-paced, V-paced
What is the Rhythm?

Patient transitioned from heparin to coumadin
Patient’s abdominal pain and fever resolved.
Infectious workup remained negative.
Source of splenic
PATIENT’S COURSE
infarcts presumed to be LA clot.
As you are explaining this to him, he has some questions….
and antibiotics stopped.

Why did the clot go to my spleen and not
somewhere else?
Go, A. S. et al. JAMA 2003;290:2685-2692

Can it still go somewhere else?
Leung, D et all. Thromboembolic Risk of Left Atrial Thrombus Detected
by Transesophageal Echocardiogram. American Journal of Cardiology.
79:5(626-629).

WHAT ABOUT THAT NEW BLOOD THINNER
THAT DOESN’T REQUIRE BLOOD DRAWS?
Clatanoff et all. Clinical Experience With
Coumarin Anticoagulants Warfarin and
Warfarin Sodium. Arch Intern Med.
1954;94(2):213-220

Warfarin:
Results in
biologically
inactive forms
of 2, 7, 9, 10
Pathways of Blood Coagulation during Hemostasis and Thrombosis
Furie B, Furie B. N Engl J Med 2008;359:938-949
ATIII, which heparin
activates
Direct 10a inhibitors
Direct
thrombin
inhibitors

RE-LY: Dabigatran vs Warfarin for A-fib: Cumulative Hazard Rates for the Primary Outcome of
Stroke or Systemic Embolism, According to Treatment Group
Connolly SJ et al. N Engl J Med 2009;361:1139-1151

RE-LY: Dabigtran vs Warfarin for A-fib: Safety Outcomes, According to Treatment Group
Connolly SJ et al. N Engl J Med 2009;361:1139-1151

ROCKET : Rivaroxaban vs. Warfarin: Cumulative Rates of the Primary End Point during Treatment and
after Discontinuation in the Intention-to-Treat Population.
Patel MR et al. N Engl J Med 2011;365:883-891

ROCKET: Rivaroxaban vs. Warfarin: Rates of Bleeding Events.
Patel MR et al. N Engl J Med 2011;365:883-891

ARISTOTLE: Apixaban vs. Warfarin for a-fib: Kaplan–Meier Curves for the Primary Efficacy
and Safety Outcomes.
Granger CB et al. N Engl J Med 2011;365:981-992

ARISTOTLE: Apixaban vs. Warfarin for A-fib: Bleeding Outcomes and Net Clinical Outcomes.
Granger CB et al. N Engl J Med 2011;365:981-992

RE-COVER: Dabigatran vs Warfarin for VTE: Cumulative Risk of Recurrent Venous
Thromboembolism or Related Death during 6 Months of Treatment among Patients Randomly
Assigned
Schulman S et al. N Engl J Med 2009;361:2342-2352

RE-COVER: Dabigatran vs. Warfarin for VTE: Cumulative Risks of a First Event of Major
Bleeding and of Any Bleeding among Patients Randomly Assigned
Schulman S et al. N Engl J Med 2009;361:2342-2352

Warfarin vs
Warfarin:
Pros
Tried and true (has been used for >50 years) at reducing risk of stroke
Cheap (but hidden cost of INR monitoring)
Reversible (vit K, FFP)
Can use to kill rats
Cons
Slow onset
Frequent INR monitoring
Multiple drug interactions
DTI’s and Apixiban
direct thrombin inhibitors and apixiban
Pros
As effective or more effective at preventing clots
Less bleeding complications
No need for monitoring
Faster onset than warfarin
Cons
Can’t reverse (with anything, even FFP); recent article in Circulation suggests rivaroxaban can be reversed with
“prothrombin complex concentrate”
Expensive (but no cost of INR monitoring)
New (post marketing side effects sure to come)
Utility in rat killing unproven

SUMMARY
DIFFERENTIAL AND WORKUP FOR SPLENIC INFARCTION
DON’T FORGET TO EVALUATE THE ATRIAL RHYTHM IN A PACED PATIENT
INCLUDE SYSTEMIC EMBOLI IN YOUR DIFFERENTIAL FOR SOMEONE
WITH A HISTORY OF A-FIB
NEW ANTICOAGULANTS FOR CARDIOEMBOLIC PROPHYLAXIS IN A-FIB