june 21, 2012 balderama-mendieta

June 21, 2012Balderama-Mendieta

OBJECTIVES Identify pertinent findings from the history

and physical examination that would contribute to the diagnosis of peripartum cardiomyopathy

Provide a systematic approach in diagnosing patients with peripartum cardiomyopathyDetermine supportive diagnostic

examinationsArrive at a definitive diagnosis

Learn how to conservatively manage patients with peripartum cardiomyopathy

Patient Profile

JT 32 year-old , Female Single, Filipino, Roman

Catholic From Quezon City Admitted for the 1st time at our

institution on November 30, 2011

Patient Profile

Merchandiser Denies intake of alcoholic beverages Denies smoking and taking illicit

drugs

Patient Profile

Rents the 1st floor of a 4-storey studio type apartment

Sufficient source of water and electricity in the neighbourhood

Garbage collected twice a week

Chief Complaint

Difficulty of breathing of 6 days duration

Source and Reliability The patient herself with fair (70%)

reliability

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Chart Title

Difficulty of Breath-ing

2 pillow orthopnea

Paroxysmal Nocturnal Dysp-neaEasy Fatigability

Elevated BP 170/40

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2 pillow orthopnea


Elevated BP 170/40

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2 pillow orthopnea


Elevated BP 170/40

TemporalProfile

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2 pillow orthopnea


Elevated BP 170/40

Past Medical History Unremarkable

Maternal History

Menstrual History Menarche at 16 y/o, regular, 28-day cycle,

3 days duration, moderately soaked, 3 pads per day, no dysmenorrhea

Obstetrical History: G2P1 (1011) G1- 2004, Spontaneous abortion G2- 2011, LFT male via NSD, delivered at

a lying-in-clinic by a mid-wife, the patient had regular pre-natal check-up

Gynecologic History History of pelvic infection, UTI at 16 3/7

weeks AOG of G2 (treated with Cefuroxime 500 mg/tab BID, resolved)

Sexual History Coitarche at 23 y/o, 2 SP, no post coital

bleeding or dyspareunia Contraceptives History

None

Family History

Hypertension, CVD, and asthma – paternal and maternal sides

Review of SystemsGeneral No significant weight loss, weight gain

Skin No lumps, no sores, no itching, no changes in color; no changes in hair or nails, no changes in size or color of moles

Head No headache, no head injury, no dizziness and no light-headedness

Eyes No icteric sclerae, no pale palpebral conjunctivae

Ears Unremarkable

Nose No frequent colds, no discharge, no itching, no nosebleed

Throat No dentures, no hoarseness, no dry mouth, no frequent sore throats

Neck No swollen glands, anterior neck mass, no lumps, no pain and stiffness

Review of Systems

Respiratory No cough, no hemoptysis, no dyspnea, no wheezing, no tuberculosis

Gastrointestinal

No dysphagia, no nausea and vomiting, no melena, no jaundice, no indigestion, no fatty food intolerance, no acholic stool, no changes in bowel movement

Urinary No polyuria, no nocturia; no hematuria, no retention, no bleeding

Review of SystemsGenitoreproductive

gravidum striae, linea nigra, gravid uterus

Musculoskeletal swelling both feet, no redness, no history of trauma

Psychiatric No nervousness, no tension, no mood changes, no depression, no memory change

Neurologic Unremarkable

Hematologic No anemia, no easy bruising or bleeding

Endocrine No excessive sweating, no excessive thirst or hunger

PHYSICAL EXAMINATION

Admitting Physical Examination

General Survey

Awake, alert, ambulatory, weak-looking, ectomorph, in cardiorespiratory distress

Vital Signs

BP 130/90; HR 109bpm; RR 34 cpm; 36.1C


Anthropometrics Height: 157 cm Weight: 48 kg BMI: 19.5

HEENT Anicteric sclerae, pink palpebral conjunctivae, no tonsillopharyngeal congestion, no cervical lymphadenopathies, distended neck veins


Chest/Lungs Equal chest expansion, dullness noted on both lower lung fields, decrease vocal fremitus on both lateral fields, decrease breath sounds on both lower lung field, noted with bibasal crackles


Heart Adynamic precordium, tachycardic, irregular rhythm, distinct S1 and S2, PMI at 5th ICS, MCL, no murmurs, no S3 gallops

Abdomen Globular, soft abdomen, NABS, no tenderness, no palpable masses


Extremities Grade 3/5 pulses on all extremities, Grade 2 bipedal edema, cold extremities, no cyanosis

MSE Intact

Cranial Nerves

Intact

SALIENT FEATURES

Salient Features

32-year-old female Recently delivered a full term

baby boy Difficulty of breathing Orthopnea Paroxysmal nocturnal dyspnea Easy fatigability Bipedal edema

Salient FeaturesEuthyroidIn cardiorespiratory distress BP 130/90; HR 109bpm; RR 25bpmBMI: 19.5Distended neck veinsSubcostal retractionsDullness noted on both lower lung fields

In cardiorespiratory distress BP 130/90; HR 109bpm; RR 34 bpm BMI: 19.5 Distended neck veins Dullness noted on both lower lung

fields Decrease vocal fremitus on both

lateral fields

Salient FeaturesEuthyroidIn cardiorespiratory distress BP 130/90; HR 109bpm; RR 25bpmBMI: 19.5Distended neck veinsSubcostal retractionsDullness noted on both lower lung fields

Decrease breath sounds on both lower lung field

Noted with bibasal crackles Tachycardic Irregular rhythm Grade 2 bipedal edema

ADMITTINGIMPRESSION

CONGESTIVE HEART FAILURE

PROBABLY SECONDARY TO PERIPARTUM CARDIOMYOPATHY

R/O PNEUMONIA, SEVERE PRE-ECLAMPSIA

CASE DISCUSSION

Harrisons 18th ed.

of:

Salient features

32-year-old female Recently delivered a full term baby

boy Difficulty of breathing Orthopnea Paroxysmal nocturnal dyspnea Easy fatigability Bipedal edema

of:

Salient features

In cardiorespiratory distress Distended neck veins Dullness noted on both lower

lung fields Decrease vocal fremitus on both

lateral fields

of:

Salient features Decrease breath sounds on both lower lung

field Noted with bibasal crackles Tachycardic Irregular rhythm Grade 2 bipedal edema

:

of:

Chest Xray

of:

Framingham Criteria MAJOR Paroxysmal

nocturnal dyspnea Neck vein distention Rales Radiographic

cardiomegaly Acute pulmonary

edema S3 gallop Increased central

venous pressure (>16 cm H2O at right atrium)

Hepatojugular reflux Weight loss >4.5 kg in

5 days in response to treatment

MINOR Bilateral ankle

edema Nocturnal cough Dyspnea on ordinary

exertion Hepatomegaly Pleural effusion Decrease in vital

capacity by one third from maximum recorded

Tachycardia (heart

rate>120 beats/min.)

of:

Peripartum Cardiomyopathy

Sliwa K, Hilfiker-Kleiner D, Petrie M, et.al. Current State of knowledge on aetiology, diagnosis, management, and therapy of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Working Group on Peripartum Cardiomyopathy. European Journal of Heart Failure (2010) 12, 767–778

of:

Epidemiology

4% of all cardiomyopathies Incidence:

Geographic variations exist1 in 500–4000 in the USA1 in 1000 in South Africa1 in 300 in Haiti

Mielniczuk LM, Williams K, Davis DR, Tang AS, Lemery R, Green MS, Gollob MH, Haddad H, Birnie DH. Frequency of peripartum cardiomyopathy. Am J Cardiol 2006;97:1765–1768

of:

Epidemiology

CDC Pregnancy Related Mortality Surveillance 1991-1999Leading Causes of Maternal Mortality:

○ Embolism – 20%○ Hemorrhage – 17%○ Hypertension – 16%○ Peripartum Cardiomyopathy- 9%*


of:

Epidemiology

• 78% present within the first 4 months postpartum• Only 9% may present in the last month of pregnancy


of:

Etiology Etiology of this disorder is unclear. Proposed mechanisms:

nutritional deficienciesgenetic disordersviral or autoimmune etiologieshormonal problemsvolume overloadalcoholphysiologic stress of pregnancyunmasking of latent idiopathic dilated

cardiomyopathy

Fuster V, Alexander R, O’Rourke, et.al. Hurst’s THE HEART. Chapter 32: Myocarditis and Specific Cardiomyopathies. 12th Edition.

Clinical Presentations

Third heart sound (S3): 92% Fourth heart sound (S4) Tricuspid or mitral insufficiency

murmurs: 43% Displaced apical impulse: 72% Edema Rales Ascites Hepatomegaly Jugular venous distensionFuster V, Alexander R, O’Rourke, et.al. Hurst’s THE HEART. Chapter 32: Myocarditis and Specific Cardiomyopathies. 12th Edition.

Alogorithm


Diagnostics

Electrocardiogramor

β-type Natriuretic Peptideand

Cardiac Imaging:EchocardiographyCardiac MRI


Patient’s ECG

PPCM ECG

LVH: 66%NSSTTWC: 96%

Desai D, Moodley J, Naidoo D. Peripartum cardiomyopathy: experiences at King Edward VIII Hospital, Durban, South Africa and a review of the literature. Trop Doct 1995;25:118–123

BNP As a result of elevated LV end-diastolic

pressure due to systolic dysfunction, patients with PPCM commonly have an increased plasma concentration of B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP).

38 patients with PPCM were compared with 21 healthy mothers post-partum: PPCM mothers: all had abnormal NT-proBNP

plasma levels (mean 1727.2 fmol/mL) Healthy mothers: mean 339.5 fmol/mL P < 0.0001


Patient’s Echocardiography

PPCM Echocardiography

Most widely available imaging modality

Echocardiography should be repeated before patient discharge and at 6 weeks, 6 months, and annually to evaluate the efficacy of medical treatment



• Patient with persistent left ventricular dysfunction after pregnancy • Left ventricular and left atrial dilatation• There is a thrombus at the left ventricular apex


Peripartum Cardiomyopathy(Post-partum)

Repeat Echo 6 weeks after delivery

Pathophysiology

Prolactin Cleavage and its role in PPCM

Previous studies have attributed PPCM to the following causesInflammationAutoimmune processesApoptosisImpaired cardiac microvasclatureProlactin cleavage

A study though by Hilfer-Kleiner et.al states that proteolytic cleavage of prolactin, brought upon most likely by peri/postpartum oxidative stress is the specific pathomechanism invloved in PPCMPro- apoptoticPro-inflammatory

16kDa prolactinDecrease in cardiac

densityInc. cardiac apoptosisAttenuates cardiac func.Promotes LV dilatation

Where does this happen? The process requires an acidic

environment (Cruz-Soto et al.) It is postulated that cleavage

occurs in acidic intracellular compartments

Lactotrophs being the most likely located in the adenohypophyseal area of the pituitary gland

Vasoinhibins Peptides that result from the cleavage of

full length prolactinAct on endothelial cells inhibiting proliferationReduce vasodilatation and vasopermeabilityPromote apoptosis-mediated vascular

regressionNatural inhibitors of the angiogenesis process

This is attributed to Cathepsin DDistributed in intracellular vesicles including

lysosomes and phagosomes

Lactotrophs Prolactin secreting cells, acidophilic Secretory granules have a pH of 5.3

and contain cathepsin D The cleavage process is inhibited by

Pepstatin A IN the case of PPCM with enough

production of 16kDa and stimulation for prolactin release there can be regulated release of 16kDa from the anterior pituitary lobe

Management Treatment is essentially the same with

dilated cardiomyopathy Goals:1. To reduce to amount of volume returning

to the heart (preload reduction)2. To decrease the resistance against which

the heart must pump (afterload reduction)

3. To increase the contractile force of the heart (inotropy).

Preload and afterload reductionLoop diuretics (caution in women with

preeclampsia)Hydralazine, nitrates and beta blockers

InotropyDigoxin (unless contraindicated)Dobutamine, dopamine, milrinone

Prophylaxis for thromboembolismLow dose heparin

Immunosuppressive therapy may be needed if peripartum cardiomyopathy is considered to be the result of myocarditis.

Patients should have a low sodium diet (≤ 4 gm) and fluid restriction (≤2L).

Activity should only be limited depending on the patient’s symptoms.

Cardiac transplantation and left ventricular assist devices are considered for women with progressive left ventricular dysfunction or deterioration despite medical therapy, however since most patients improve over time, surgical therapy should be delayed if possible.

Suggested Treatment Plan1. Institute ACE inhibitor therapy with

enalapril 5 mg twice daily and titrate up to a maximum dose of 20 mg twice daily, yet maintain SBP to 100 -110 mm Hg.

2. Start digoxin to achieve a serum level of 1 to 2 ng/dl.

3. Start diuretic therapy (furosemide 20 to 40 mg once daily) to control symptoms related to volume excess.

*Peripartum cardiomyopathy: A comprehensive reviewAmerican Journal of Obstetrics and Gynecology - Volume 178, Issue 2 (February 1998)

http://www.mdconsult.com/das/journallist/view/339651407-2/home/0002-9378/0?issn=0002-9378

http://www.mdconsult.com/das/journallist/view/339651407-2/issue/5932?ANCHOR=102803&issn=0002-9378

4. Start low-dose beta-blocker therapy (i.e., metoprolol 12.5 mg twice daily) and titrate for heart rate 80 to 100 beats/min.

5. Add additional vasodilator agents as needed to control systemic blood pressure (e.g., goal is systolic blood pressure 110 mm Hg).

6. Monitor ambulation for 24 to 48 hours.

7. Dietary consultation for fluid-restricted, low-salt diet.

8. Detailed patient education and counseling.

9. Referral to exercise rehabilitation program.

10. Vigilant follow-up to include measure of cardiac function within 3 to 6 months of treatment onset.

Prognosis Prognosis depends on return to normal left

ventricular function after the first episode of CHF.

In a study by Damaskis et al, they have observed that if the congestive cardiomyopathy persists after 6 months, it is likely irreversible and associated with a worse survival.

Recent studies have found that 30% of patients return to their baseline function after 6 months if given timely medical treatment.

Prognosis Mortality rate is 10% and the usual

causes of death include progressive heart failure, arrhythmia, or thromboembolism.

Patients who have peripartum cardiomyopathy are advised to avoid subsequent pregnancies due to concerns about the hearts inability to handle the increased cardiovascular workload during pregnancy.

Summary • PPCM –Dilated myopathy• Presents 36 weeks GA – 5

months Postpartum • 1:3000-4000 pregnancies• Increased maternal

mortality• Symptoms:

– Dyspnea, Edema, Orthopnea

• Dx: EKG and Echocardiogram

• Tx: Diuretics, B-blockers, ACEI, Anticoagulants

• Prognosis varies• Consult, consult, consult

june 21, 2012 balderama-mendieta

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