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Cards: AV Endocarditis presenting as back pain

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Morning Report<br />

April 10th, 2012<br />

Roderick Deaño<br />

Jack Ende, MD<br />

Parker Ward, MD


MKSAP<br />

A 51-year-old woman is evaluated during a routine<br />

physical examination. She h<strong>as</strong> no history of hypertension<br />

and h<strong>as</strong> never used tobacco. There is no family history<br />

of heart dise<strong>as</strong>e. Her only medication is daily oral<br />

conjugated estrogens combined with<br />

medroxyprogesterone acetate for intolerable hot flushes.<br />

Physical examination is normal. BMI is 31. A f<strong>as</strong>ting lipid<br />

panel is obtained with the following results: total<br />

cholesterol, 218 mg/dL (5.65 mmol/L); HDL cholesterol,<br />

42 mg/dL (1.09 mmol/L); LDL cholesterol, 128 mg/dL<br />

(3.32 mmol/L); triglycerides, 240 mg/dL (2.71 mmol/L).


Which of the following is the most<br />

appropriate next step in the<br />

management of this patient?<br />

A. Calculate<br />

Framingham risk score<br />

B. Calculate non-HDL<br />

cholesterol level<br />

C. Prescribe<br />

atorv<strong>as</strong>tatin<br />

D. Prescribe<br />

gemfibrozil<br />

0% 0% 0% 0%<br />

1 2 3 4


The most appropriate management option for this patient is to calculate her non-HDL cholesterol<br />

level. This patient h<strong>as</strong> a high triglyceride level (>200 mg/dL [2.26 mmol/L]). According to the Adult<br />

Treatment Panel III guidelines, the next step in the management of a patient with a triglyceride<br />

level between 200 mg/dL and 500 mg/dL (2.26 and 5.65 mmol/L) is to calculate non-HDL<br />

cholesterol (total cholesterol minus HDL cholesterol) to determine whether triglyceride-lowering<br />

medication is indicated. In addition, reversible causes of hypertriglyceridemia should be sought.<br />

These include excessive alcohol intake, obesity, high carbohydrate intake, physical inactivity, type<br />

2 diabetes mellitus, renal dise<strong>as</strong>e, and certain medications (corticosteroids, β-blockers, estrogens,<br />

and prote<strong>as</strong>e inhibitors).<br />

LDL cholesterol goal is b<strong>as</strong>ed on the presence or absence of five major risk factors (smoking,<br />

hypertension, older age, low HDL cholesterol, family history of premature coronary artery<br />

dise<strong>as</strong>e). This patient does not have any of these risk factors; therefore, her LDL cholesterol goal<br />

is 160 mg/dL (4.14 mmol/L), and she does not need a statin.<br />

The second therapeutic target is the non-HDL cholesterol. The non-HDL cholesterol goal is set at<br />

the LDL goal plus 30 mg/dL (0.78 mmol/L); therefore, her non-HDL cholesterol goal is 190 mg/dL<br />

(4.92 mmol/L). This patient’s non-HDL cholesterol level is 176 mg/dL (4.56 mmol/L); therefore,<br />

triglyceride-lowering medication (gemfibrozil or other fibrate medication) is not indicated.<br />

Triglyceride-lowering medication should be considered in patients with a personal or family history<br />

of premature coronary artery dise<strong>as</strong>e regardless of non-HDL cholesterol level. The patient<br />

presented h<strong>as</strong> no family history of premature coronary artery dise<strong>as</strong>e.<br />

The Framingham risk score, used to further stratify some patients with elevated LDL cholesterol,<br />

does not have to be calculated in this patient because her LDL cholesterol of 128 mg/dL (3.32<br />

mmol/L) is below the goal of 160 mg/dL (4.14 mmol/L). Calculating the Framingham risk score is<br />

most helpful in making management decisions when patients have an LDL cholesterol level above<br />

their target goal.


61yom presents to your PCP<br />

clinic:<br />

“Doc, I have this <strong>pain</strong> in my<br />

lower <strong>back</strong>.”


Lower Back Pain – Persistent, non-radiating;<br />

happening for two months, non-exertional, no<br />

trauma to area, no distal paresthesi<strong>as</strong>,<br />

incontinence or lower extremity weakness. Not<br />

relieved with lying down or OTC NSAIDS. No<br />

F/C, no weight loss<br />

L UE Weakness – starting 3 days ago while<br />

changing his clothes, w no par<strong>as</strong>thesi<strong>as</strong> or<br />

decre<strong>as</strong>e sensation<br />

Went to OSH ED, CT Head w<strong>as</strong> negative<br />

Presents bc LUE weakness still persists


PMH:<br />

ESRD x 10 yrs – MWF HD;<br />

secondary to HTN<br />

R Femoral Tunneled<br />

catheter<br />

HTN<br />

PE – diagnosed OSH 9<br />

months ago on coumadin<br />

(unclear if had<br />

hypercoagulable w/u)<br />

? CVA (per history) approx<br />

20 yrs ago w resolved R<br />

sided weakness<br />

OSA on CPAP<br />

H&P<br />

NKDA<br />

MEDS: Albuterol prn; Renvela<br />

TID; Nifedipine 60 mg qday;<br />

diazepam 5mg qhs; vit D;<br />

coumadin<br />

Social Hx: former security<br />

guard; separated w 5 healthy<br />

children; former crack use<br />

(smoked); l<strong>as</strong>t use 2 yrs ago;<br />

no IVDU; never smoker; quit<br />

ETOH, used to drink 1 pint<br />

every other week w three<br />

friends<br />

FH: non-contributory


Differential?


focused history and physical examination to help place patients with<br />

low <strong>back</strong> <strong>pain</strong> into 1 of 3 broad categories:<br />

nonspecific low <strong>back</strong> <strong>pain</strong>,<br />

<strong>back</strong> <strong>pain</strong> potentially <strong>as</strong>sociated with radiculopathy or spinal<br />

stenosis,<br />

or <strong>back</strong> <strong>pain</strong> potentially <strong>as</strong>sociated with another specific spinal<br />

cause.<br />

no routine imaging or other diagnostic tests in patients with<br />

nonspecific low <strong>back</strong> <strong>pain</strong><br />

diagnostic imaging for low <strong>back</strong> <strong>pain</strong> when severe or progressive<br />

neurologic deficits are present or when serious underlying conditions<br />

are suspected<br />

evaluate patients with persistent low <strong>back</strong> <strong>pain</strong> and signs or<br />

symptoms of radiculopathy or spinal stenosis with MRI or CT only if<br />

candidates for surgery or epidural


Physical Exam<br />

VS: AF (36), HR 89 BP 101/40 RR 20 94% on 2L<br />

GEN: AAM, looks appropriate age, no acute distress<br />

HEENT: NC/AT EOMI PERRL, Anicteric clear O/P; no<br />

supraclavicular/axillary LAD, no thyromegaly<br />

Chest: CTAB, No W/R<br />

CV: RRR, Nl S1, S2, Di<strong>as</strong>tolic murmur; JVP 12cm above RA, 2+<br />

radial/dp pulses, warm extremities w good cap refill. Nl carotid upstroke<br />

Abd: soft obese, NTND, +BS<br />

Ext: No LE Edema; warm extremities; erythema around the R femoral<br />

catheter<br />

Neuro: CNII-XII intact, A&O x3; no focal deficits; normal sensation; no T<br />

in the cervical/thoracic/lumbar spine<br />

Musk: 5/5 Strength LE BL; 4/5 LUE; 5/5 RUE;<br />

Skin: no r<strong>as</strong>hes; no track marks in UE’s.


What initial diagnostics<br />

to you want to order?


CT Head<br />

Small focus of SAH isolated in R central<br />

sulcus w/o evidence of parenchymal<br />

edema<br />

Minimal small vessel dise<strong>as</strong>e of<br />

indeterminate age<br />

Pt admitted for SAH, in setting of<br />

therapeutic INR


5.1<br />

11.3<br />

Lab Tests<br />

156<br />

N 78; no bands<br />

7.7 3.5<br />

0.3 0.2/0.2<br />

15 7<br />

128<br />

138 93 23<br />

4.0 30 6.7 84<br />

INR 2.4<br />

BC’s Pending<br />

HIV pending<br />

UA neg<br />

Utox neg<br />

8.9<br />

2.1<br />

4.3


Chest Xray


TTE


TTE<br />

LV: nl size; mild LVH; nl EJF (60-65%); No<br />

WMA<br />

RV: moderately dilated; moderately<br />

reduced<br />

LA: mildly dilated and dilated IVC: nl RA<br />

Trace MR; trace TR; moderate AR<br />

Estimated RV: 53.5 + RA


Course Continues<br />

Admitted to Neuro ICU for SAH<br />

FFP Given to reverse INR<br />

L Femoral quinton exchanged over a wire for another HD<br />

Catheter, cultures sent<br />

BC from first day positive 2/2 for CONS (2 bottles) and<br />

Staph Hominus (1/2); HIV neg<br />

Pt h<strong>as</strong> incre<strong>as</strong>ed O2 requirement and now requiring<br />

intermittent BiPap for incre<strong>as</strong>ed WOB<br />

ABG 7.35/44/85/95% (on NRB 100%)<br />

Pt started on empiric Vanc/Cefepime<br />

CRP 124


Next Management Steps?


MRI Lumbar/Thoracic<br />

Abnl incre<strong>as</strong>ed signal intensity of<br />

intervertebral disk spaces @ T8-9 w<br />

<strong>as</strong>sociated adjacent marrow signal abnl of<br />

vertebral bodies raising concern for<br />

discitis/osteo; incre<strong>as</strong>ed signal intensity of<br />

intervertebral disc @ T7-T8


MRI Head<br />

Focus of restricted diffusion on R<br />

precentral gyrus of frontal lobe <strong>as</strong>sociated<br />

w parenchymal and subarachnoid<br />

hemorrhage; v<strong>as</strong>ogenic edema<br />

surrounding this region raises possibility of<br />

infected embolic stroke.


TEE


LV: nl performance<br />

TEE<br />

Atria: no m<strong>as</strong>s or thrombus<br />

Mild MR w moderate mitral annular<br />

calcification<br />

Trace TR<br />

Moderate-sized vegetation/m<strong>as</strong>s on <strong>AV</strong> 1<br />

1.2 cm pedunculated m<strong>as</strong>s on aortic<br />

leaflet c/w vegetation; severe AR


ECG


ECG<br />

Mobitz Type II <strong>AV</strong> Block and Sinus<br />

Bradycardia<br />

*Pt w<strong>as</strong> actually in Normal Sinus


Clinical Summary<br />

Pt h<strong>as</strong> likely mycotic aneurysm causing<br />

SAH, <strong>Endocarditis</strong> with Acute AR; discitis<br />

and osteomyelitis<br />

Pt is SOB with incre<strong>as</strong>ing oxygen<br />

requirement<br />

Now transferred to medicine service<br />

(CCU) for better coordination of medical<br />

care<br />

Next Management steps?


10-40% of patients with left sided endocarditis have<br />

neurologic complications<br />

Embolic CVA, ruptured mycotic aneurysm, TIA, meningitis, brain<br />

abscess, seizure<br />

Safety of cardiopulmonary byp<strong>as</strong>s w acute neurologic<br />

deficits (such <strong>as</strong> hemorrhage) and active endocarditis<br />

Reviewed charts and found 247 patients that underwent<br />

repair of valve for endocarditis<br />

34 had pre-operative neurologic deficits<br />

More neurologic deficits in pts who underwent surgery<br />

within 11 days of acute neurologic event<br />

Many of those patients were hemodynamically unstable and<br />

needed to go urgently


Clinical Management<br />

How would you manage the patient in the<br />

meantime: acute AR and endocarditis?<br />

What are some of the important things to<br />

watch for re: endocarditis?


Acute AR<br />

Circulation 2009, 119:3232-3241


Acute AR<br />

Chronic regurgitation of <strong>AV</strong> affords time for the ventricle<br />

to dilate to accommodate the regurgitant volume to<br />

maintain forward SV and CO<br />

LV does not compensate; initial compensatory<br />

tachycardia may preserve cardiac output initially, but<br />

eventually hypotension, organ failure, and other<br />

evidence of cardiogenic shock will develop.<br />

Pulmonary capillary wedge pressure incre<strong>as</strong>es abruptly and<br />

pulmonary edema develops<br />

Present with dyspnea, hemodynamic instability, and<br />

symptoms of shock, including weakness, dizziness, and<br />

AMS<br />

Circulation 2009, 119:3232-3241


Acute AR - Treatment<br />

Surgical Emergency<br />

Medically Stabilize until surgery<br />

Decre<strong>as</strong>e LVEDP<br />

Consider afterload reduction if BP can tolerate<br />

to improve forward flow<br />

Consider inotropic support to augment CO<br />

Griffin, Topol, 2009; Circulation 2009, 119:3232-3241


<strong>Endocarditis</strong> – Duke Criteria<br />

Circulation 2005, 111:e394-e434


<strong>Endocarditis</strong> - Complications<br />

CHF<br />

Embolization<br />

Higher rates with left sided vegetations; greater than 1cm in size<br />

Peri-annular extension of infection<br />

Occurs in the weakest portion of the annulus in native valve IE,<br />

near the membranous septum and <strong>AV</strong> Node<br />

Daily EKG for monitoring<br />

Splenic abscess<br />

Mycotic aneurysms<br />

septic embolization of vegetations to the arterial v<strong>as</strong>a v<strong>as</strong>orum<br />

or the intraluminal space, with subsequent spread of infection<br />

through the intima and outward through the vessel wall.<br />

Circulation 2005, 111:e394-e434


Hospital Course<br />

SCUF/CVVH for more fluid off<br />

Started v<strong>as</strong>odilators for afterload <strong>as</strong> BP<br />

tolerated<br />

Cath – non-obstructive Dise<strong>as</strong>e<br />

Repeat CTA head– no evidence of any<br />

aneurysm


Surgical Repair


Further Hospital Course<br />

Successful surgery with replacement with<br />

Tissue Aortic Valve<br />

Subsequent CTA Head negative for<br />

aneurysm<br />

CT PE positive for multiple segmental PE<br />

– started on heparin (and eventually<br />

coumadin) after cleared by Neuro<br />

Discharged on IV Vanc for 8 weeks to<br />

rehab


Take Home Points<br />

Low Back Pain workup<br />

Management of Acute AR<br />

Complications of <strong>Endocarditis</strong>


Thank you!


References<br />

1. Baddour, Wilson, et al. “Infective <strong>Endocarditis</strong>.” Circulation 2005,<br />

111:e394-e434<br />

2. Chou, R.; Q<strong>as</strong>em, Amir.; Vincenza, S, et al. “Diagnosis and Treatment of<br />

Low Back Pain: A Joint Clinical Practice Guideline from the American<br />

College of Physicians and the American Pain Society“. Ann Intern Med.<br />

2007;147:478-491<br />

3. Enriquez-Sarano M, Tajik AJ. “Clinical practice. Aortic regurgitation.” N<br />

Engl J Med. 2004 Oct 7;351(15):1539-46<br />

4. Gillinov AM, Shah RV, Curtis WE, Stuart RS, Cameron DE, Baumgartner<br />

WA, Greene PS. “Valve replacement in patients with endocarditis and<br />

acute neurologic deficit.” Ann Thorac Surg. 1996 Apr;61(4):1125-9<br />

5. Griffin, Topol, et al. Manual of Cardiov<strong>as</strong>cular Medicine. Third Edition.<br />

Wolters Kluwer. 2009<br />

6. Stout KK, Verrier ED. “Acute valvular regurgitation. Circulation. 2009 Jun<br />

30;119(25):3232-41. Review.<br />

7. UTD – “Low <strong>back</strong> <strong>pain</strong>.”


ADDENDUM


AR Table


DON’T FORGET TO<br />

SWIPE!!!

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