This case presentation describes a 42-year-old pregnant woman, 28 weeks gestation, who presented with shortness of breath. She reported dyspnea on exertion that had progressively worsened since her first trimester. Physical exam, labs, ECG, CXR, echo, and MRI were performed. Echo showed a moderate pericardial effusion. Pericardiocentesis was performed and fluid analysis found no organisms. A small residual effusion remained on follow up echo. The patient was diagnosed with a pericardial effusion likely related to her Hodgkin's lymphoma.

1. Case presentation
Diana Girnita, MD, PhD
The Christ Hospital

2. CC: shortness of breath
42 yo Caucasian F pregnant, (P2G2) 28 weeks, seen by cardiology for
dyspnea on exertion, since her first trimester of pregnancy that got
progressively worse.
▪ In the last month, DOE with walking the length of 2 rooms, walking up the
stairs and sometimes at rest.
▪ Orthopnea episodes in the middle of the night.
▪ Pressure in the mid -chest, rated 2/10, constant, not irradiating, not
accentuated by inspiration.
▪ Not feeling comfortable to lay flat in bed and will use up to 3 pillows to
sleep
▪ Denies palpitations, cough, flu like symptoms, sick contacts or recent
travel.
▪ At 21 weeks of pregnancy was dg with Hodgkin lymphoma, but
chemotherapy was currently postponed close to her delivery term.
▪ Had no similar complains with previous pregnancy, although had pedal
edema.

3. PMH
 Allergy
 Hodgkin Lymphoma stage IIA
PMS
▪ Hx appendectomy
▪ D&c after delivery
▪ Cesarean delivery
Allergies : Ciprofloxacin (Hives)

4. SH: Former Smoker -- 0.5 packs/day
FH: father with LAD infarction (died in
the 40’s)
Home Medication
▪ cetirizine (ZYRTEC) 10 mg PO
▪ PRENATAL VITAMINS-IRON-FA PO

5. ROS
▪ Constitutional: No fevers, chills, or weight loss.
▪ Skin: no skin, hair, nail changes, rash or pruritis
▪ Neurologic: No syncope, weakness, seizure disorder, headaches or gait
abnormalities.
▪ Endocrine: No history of DM, HLD, thyroid disorder
▪ Eyes: No blurred vision
▪ Cardiovascular: + SOB, No palpitations. No claudication.
▪ Respiratory: + SOB , no wheezing, coughing, asthma, COPD or chronic
bronchitis
▪ Gastrointestinal: No change in appetite, dysphagia, N/V/D/C
▪ Psychiatric: No depressed mood / anxiety/No memory loss or altered
mental status

6. Vital signs
▪ BP 127/70
▪ Pulse 83
▪ Temp 97.7 °F (36.5 °C) (Oral)
▪ Resp 18
▪ SpO2 95%

7. PHYSICAL EXAM
▪ Constitutional: NAD, Non-toxic appearance
▪ HEENT: NC/AT, Bilateral external ears, oropharynx moist, nose
normal. Eyes normal. L side submandibular
lymphadenopathy
▪ Neck: Normal ROM, No JVD, carotid upstrokes are preserved
without audible bruits.
▪ Cardiovascular: RRR, Normal S1 and S2. No rubs, gallops, or
murmurs.
▪ Lungs: Clear to auscultation.
▪ GI: BS normal, Soft, No tenderness, No masses, No pulsatile
masses. No spleno/ hepatomegaly
▪ Extremities: Intact distal pulses, No pedal edema, No
tenderness.
▪ Neurologic: Alert & oriented x 3, Normal motor function,
Normal sensory function, No focal deficits.

8. Labs
▪ Hb 12, Ht 34, WBC 10, Platelets 235
▪ EP1: Na133, K 4.3, Co2 18, AG 10, Bun 6,
Cr 0.52, GFR 138
▪ Alk phosp 96
▪ Albumin 3.4
▪ Chol 184, HDL 39, LDL 128, TG
▪ ESR 82

9. ECG

10. CXR

11. CXR
CXR 8/17 Large mediastinal and hilar
lymphadenopathy ; does not appear to be
significantly changed.
CXR 09/06 Little change since August,
2012 with a mediastinal and bilateral hilar
lymphadenopathy consistent with clinically
reported Hodgkin's lymphoma. No
evidence of acute cardiopulmonary
disease.

12. MRI abdomen
1. No definite abdominal or retroperitoneal
lymphadenopathy.
2. Partial visualization of mediastinal
lymphadenopathy.
3. Left cardiophrenic lymphadenopathy.
4. Borderline splenomegaly.

13. ECHO 9/5
▪ Left ventricle: The cavity size was normal. Wall
thickness was normal.
▪ Systolic function was mildly reduced. The estimated
ejection fraction was 45%. Hypokinesis of the
anteroseptal and inferoseptal myocardium.
▪ Left ventricular diastolic function parameters were
normal.
▪ Pericardium, extracardiac: A moderate pericardial
effusion was identified circumferential to the heart.
There was no evidence of hemodynamic compromise.
There was no chamber collapse.
▪ Respirophasic change in stroke volume was normal.

14. Cardiology was consulted

15. Diagnostic approach
▪ Pericardiocentesis.
▪ Impression: Moderate to large pericardial
effusion
▪ The fluid was noted to be clear yellow-
placement of the pericardial catheter
▪ A repeat echo demonstrated resolution of the
effusion

16. Pericardial effusion features
9/7/2012
Clarity, Fluid Cloudy
Lymphs, Fluid 85
Macrophage count 4
Neutrophil Count, Fluid 11
Nucl Cell, Fluid 3286
RBC, Fluid 2681
LDH 203
Glucose 83
CEA <0.5
MICRO
No AFB isolated
No fungus isolated
Routine Cx- no
organism seen
Anaerobes- pending
Cytology pending

17. ECHO 9/8 at discharge
▪ Left ventricle: The cavity size was normal. Wall
thickness was normal.
▪ Systolic function was normal.
▪ The estimated EF 55% to 60%.
▪ Wall motion was normal; there were no regional
wall motion abnormalities.
▪ Pericardium, extracardiac: A small, free-flowing
pericardial effusion was identified circumferential
to the heart.

18. Pericardial
effusion

19. Pericardial effusion
▪ is an accumulation of fluid in the pericardial space, with or
without associated pericarditis.

20. Pericardial effusion
▪ can develop in patients with acute pericarditis or
in association with a variety of systemic disorders.
▪ important implications
▪ for prognosis (pts with intrathoracic neoplasm)
▪ for diagnosis (myopericarditis or acute pericarditis)
▪ or both (as in Ao ascending dissection).

21. Etiology
▪ Idiopathic
▪ Infections
A. Viral - Coxsackie, echo, adeno, EBV, CMV, influenza, varicella,
rubella, HIV, hepatitis B, mumps, parvovirus B19
B. Bacterial - Staph, Strep, Haemophilus, Neisseria, Chlamydia,
Legionella, TB, Salmonella, Lyme disease.
C. Mycoplasma
D. Fungal - Histoplasmosis, aspergillosis, blastomycosis,
coccidiodomycosis, actinomycosis, nocardia, candida
E. Parasitic - Echinococcus, amebiasis, toxoplasmosis

22. Etiology
▪ Cardiac
A. Early infarction pericarditis
B. Late postcardiac injury syndrome (Dressler's
syndrome)
C. Myocarditis
D. Dissecting aortic aneurysm
▪ Trauma
▪ Iatrogenic - Catheter and pacemaker perforations,
cardiopulmonary resuscitation, post-thoracic surgery
▪ Malignancy

23. Etiology
▪ Autoimmune
A. Rheumatic diseases – SLE, RA, MCTD,scleroderma
B. Wegener's granulomatosis, PAN, sarcoidosis, IBD
(Crohn's, ulcerative colitis), Whipple's, giant cell
arteritis, Behcet's disease, rheumatic fever
▪ Drugs (Procainamide, isoniazid, or hydralazine,cromolyn
sodium, dantrolene, anticoagulants, thrombolytics,
phenytoin, penicillin, phenylbutazone, doxorubicin)
▪ Metabolic (Hypothyroidism - primarily pericardial effusion,
Uremia, Ovarian hyperstimulation syndrome)

24. Diagnostic approach
▪History (suspect in all cases of acute
pericarditis)
▪ECG
▪CXR/ CT chest
▪Echo is required for establishing dg

25. ECG - Electrical alternans.
▪ beat-to-beat shift in
the QRS (and
sometimes the P
wave) axis,
amplitude, and/or
morphology.
▪ occurs in
association with
swinging of the
heart, usually in a
large pericardial
effusion

26. ECG - Low voltage QRS

27. Low voltage
▪ is probably due to short-circuiting of cardiac potentials by the
fluid surrounding the heart.
▪ Defined as
▪ QRS complexes ≤5 mm (0.5 mV) in all of the limb leads.
▪ +/-- low voltage in the chest leads, QRS amplitude of ≤10 mm
in V1 to V6

28. CXR

29. CT chest

30. ECHO –confirms the diagnosis
▪ Small
collections of
pericardial fluid
can be
physiologic if
visible during
ventricular
systole.
▪ Effusions > 25
to 50 mL are
seen as an
echo-free space
throughout the
cardiac cycle

31. ECHO

32. Hemodynamic compromise
assesment
▪ Factors that determine the degree of hemodynamic compromise
include
the volume of pericardial fluid
the rate at which the effusion accumulates
whether or not the pericardium is scarred or
adherent.

33. Acute vs subacute cardiac tamponade
ACUTE
▪ Sudden onset
▪ chest pain and dyspnea, and
is life-threatening if not
promptly treated.
▪ JVD markedly elevated
▪ Hypotension due to the decline
in CO
▪ heart sounds muted.
▪ effusion is relatively small.
SUBACUTE
▪ less dramatic process.
▪ asymptomatic or c/o dyspnea,
chest discomfort or fullness,
fatiguability.
▪ Peripheral edema in chronic
tamponade.
▪ Hypotension with a narrow
pulse pressure (limited stroke
volume)/ preexisting HTN may
remain hypertensive due to the
increased sympathetic activity

34. Acute vs subacute cardiac tamponade

35. Question no. 1
▪ 67 yo M is evaluated for an asymptomatic large pericardial effusion that has
persisted for 4 months. He denies chest pain, dyspnea, fever, chills, cough,
edema, and weight loss. He has a 30-year history of HTN which he takes
amlodipine. CXR performed 4 months ago to evaluate chronic cough
demonstrated an enlarged cardiac silhouette. Lab results at that time
included normal CBC, electrolytes, creatinine, BUN, TSH. ANA and PPD were
negative. Chest CT scan was normal. Echo performed 4 and 2 months ago
showed a moderate pericardial effusion, no evidence of tamponade, and
normal left and right ventricular function and size.
▪ PE: temp is normal, BP 135/75 mm Hg, HR 76/min, RR 16/min. Estimated
CVP less than 5 cm H2O. Cardiac examination reveals muffled heart sounds,
an absent apical impulse, and no pericardial friction rub. Pulmonary
auscultation reveals normal breath sounds.
▪ Echo shows a large circumferential pericardial effusion and no findings of
tamponade, and is otherwise without change from 4 and 2 months ago.

36. Which of the following is the most
appropriate next step in management?
A. Colchicine
B. Indomethacin
C. Pericardiectomy
D. Pericardiocentesis
E. Prednisone

37. Answer
▪ Correct : D
▪ A pericardiocenthesis should be done when an
idiopathic pericardial effusion persists more
then 3 months.
▪ An idiopathic pericardial effusion lasting less
than 3 months in a stable patient requires no
specific therapy, but serial echocardiography
based on clinical status, as was done in this
patient, is advisable.

38. Cardiac tamponade – clinical features to
look for:
▪ sinus tachycardia, even in the absence of frank hypotension,
may indicate significant hemodynamic compromise from
tamponade and serve as an indication for immediate
pericardiocentesis.
▪ Elevated jugular venous pressure
▪ Pulsus paradoxus — defined as an abnormally large decrease
in systolic blood pressure (>10 mmHg) on inspirations
▪ Pericardial rub
▪ Kussmaul's sign — is the absence of an inspiratory decline in
jugular venous pressure

39. Pulsus paradoxus

40. Question no. 2
▪ A 45 yo M is evaluated in ED for 3-day history of progressively
worsening dyspnea on exertion to the point that he is unable to walk
more than one block without resting. He has had sharp intermittent
pleuritic chest pain and a nonproductive cough with myalgias and
malaise for 7 days and has had orthostatic dizziness for 2 days. He is
taking no medications.
▪ On PE: temp- 37.7°C (99.9 °F), BP 88/44 mmHg, HR- 125/min, and
RR 29/min; BMI is 27. O2 sats at RA is 95%. Pulsus paradoxus is 15
mm Hg. Estimated central venous pressure is 10 cm H2O. Cardiac
examination discloses muffled heart sounds with no rubs. Lung
auscultation reveals normal breath sounds and no crackles. There is
2+ pedal edema. BP and HR are unchanged after a 500-mL
intravenous normal saline challenge.

41. ▪ Laboratory studies:
▪ Prothrombin time 12 s
▪ Activated partial thromboplastin time28 s
▪ Creatinine1.3 mg/dL (99.2 µmol/L); BUN 26 mg/dL (9.3
mmol/L)
▪ ECG: sinus tachycardia, diffuse low voltage, no ST-segment
shifts.
▪ ECHO: shows a large circumferential pericardial effusion, right
ventricular and atrial free wall diastolic collapse, normal LV
systolic function, and EF of 70%.
▪ CXR shows an enlarged cardiac silhouette and no pulmonary
infiltrates.

42. ▪ Which of the following is the most appropriate
treatment?
A.Dobutamine
B.Levofloxacin and tobramycin
C.Pericardiocentesis
D.Surgical pericardiectomy

43. Answer
▪ Correct answer: C
▪ This patient has examination findings that indicate
cardiac tamponade. Physical examination reveals
tachycardia, reduced blood pressure, distended
jugular veins, elevated pulsus paradoxus (>10 mm
Hg), and an unremarkable lung examination.

44. Malignant
pericardial
effusion

45. Etiology
▪ Neoplasm
A. Metastatic – Lung, breast Ca, Hodgkin, leukemia,
melanoma
B. Primary - rhabdomyosarcoma, teratoma, fibroma,
lipoma, leiomyoma, angioma
C. Paraneoplastic
▪ Radiation

46. Relative incidence of metastatic heart tumors in autopsy
studies for frequent primary neoplasms.
Reynen K et al. Ann Oncol 2004;15:375-381
European Society for Medical Oncology

47. ▪ J Thorac Cardiovasc Surg. 2011 Jan;141(1):34-8
▪ Wagner PL et al “Pericardial effusions in the cancer
population: prognostic factors after pericardial window
and the impact of paradoxical hemodynamic instability”
▪ Retrospective review of 179 pericardial windows performed for
pericardial effusion over a 5-year period (2004- 2009)
▪ RESULTS: The most common malignancies were
▪ lung (44%)
▪ breast (20%)
▪ hematologic (10%)
▪ gastrointestinal (7%)

48. ▪ Heart Fail Rev. 2012 May 26
▪ Karatolios K et al “Diagnostic value of biochemical
biomarkers in malignant and non-malignant
pericardial effusion”
▪ Biochemical parameters and tumor markers to discriminate
malignant from benign effusion in 105 pts
▪ Malignant pericardial effusions had significantly higher pericardial
fluid levels of the tumor markers CEA, CA 19-9, CA 72-4, SCC and
NSE as well as higher pericardial fluid hemoglobin (p < 0.001),
WBC, LDH

49. ▪ None of the biochemical or cell-count parameters
tested proved to be accurate enough for distinguishing
malignant from benign effusions.
▪ However, measurement of pericardial CA 72-4
levels offered a high diagnostic accuracy
for malignancy, particularly in bloody
pericardial effusions.

50. Cytology in pericardial effusions
▪ Cytology and pericardial biopsy — whenever there is a
reason to suspect malignancy.
▪ Especially important if the effusion is hemorrhagic, and
there is no history of antecedent trauma
▪ Negative cytology should not be used to exclude the
diagnosis of malignancy, particularly if the index of
suspicion is high
▪ A positive cytology may be predictive of a poorer
outcome

51. Outcome prediction
▪ Prognosis and status of the underlying malignancy — most
patients with a symptomatic malignant pericardial effusion
have a short life expectancy (median two to four months)
▪ Patients with breast cancer or hematologic malignancies
had a better median survival (9 and 17 months,
respectively) than those with lung cancer.

52. THANK YOU!
ALYSA
ANA

53. References
▪ MKSAP 15
▪ John Hopkins Internal medicine review book
▪ Up to date www.Uptodate.com
▪ Reynen K et al. Ann Oncol 2004;15:375-381
▪ Karatolios K et al “Diagnostic value of biochemical
biomarkers in malignant and non-malignant pericardial
effusion” Heart Fail Rev. 2012 May 26
▪ Wagner PL et al “Pericardial effusions in the cancer
population: prognostic factors after pericardial window and
the impact of paradoxical hemodynamic instability” J Thorac
Cardiovasc Surg. 2011 Jan;141(1):34-8