Intern Report 6.5

Case Presentation by Dr. Laura Smylie

History of Present Illness:

50 year old male complaining of being “sick” for the past three to four days. He stated he began feeling generally poorly with an associated pain in his left shoulder. He states the pain is sharp in nature and he denies trauma to the area. The pain radiates to the axilla and is sharp and pulling in that area. He denies chest pain. He has been feeling hot and cold but has not taken his temperature at home. He has been diaphoretic. He has a mild nonproductive cough. He denies abdominal pain, nausea or vomiting. He denies shortness of breath.

Review of systems negative except as detailed in the HPI.

Past Medical History: No hypertension

Past Surgical History: none

Medications: None

Allergies: No known drug allergies

Family History: Negative for hypertension.

Primary care physician: None

Social History: Positive for tobacco use and IVDA. Denies alcohol use.

Physical Exam:

Vitals: T 39.5 rectal, HR 98 regular, BP 180/80, RR 24, Pulse ox 97% room air

Constitution: Thin male, alert, in no apparent distress.

Head: Normocephalic, atraumatic

Eyes: Pupils equal, round and reactive to light. Sclera nonicteric. Conjunctiva pictured below.

ENT: Mucous membranes slightly dry. No erythema in the posterior pharynx or tonsillar exudates.

Neck is supple. Trachea midline. No JVD.

Respiratory: Normal respiratory effort. Clear inspiration. Few scattered rales in bilateral bases, no wheezing. Good air exchange.

Cardiovascular: Regular rate and rhythm. 3/6 systolic murmur at the sternal edge. No gallop. Pulses were equal in the extremities.

Chest wall: Nontender.

Abdomen: Soft, nontender, nondistended. No rebounding or guarding.

Musculoskeletal: Right side extremities unremarkable. He has full range of motion at the right shoulder. No erythema or warmth over the left shoulder. No swelling, no tenderness of the clavicle. No tenderness over the AC joint. Some pain with passive motion but full range of motion present.

Skin: Warm and dry. No rashes or lesions.

Neurologic: Alert and orient to person, place and time. Cranial nerves II-VII intact. Gait is narrow and steady. Normal Speech, Strenght 5/5 upper and lower extremities both proximal and distal muscle groups

Picture 1:

6.5-1

 Medical Course:

IV access was established. Blood was sent for analysis. Blood cultures were sent and are pending.

CBC: 7.4\14.9/139

Electrolytes: 139 | 92 | 27

3.5 | 22 | 1.0

Questions:

1)Which one test is most likely to solidify the diagnosis:

a) ECG

b) 2 view chest x-ray

c) Echo – usually needs to be TEE (where do blood culture fall in the diagnostic workup?)

d) This is a clinical diagnosis

2) Given this patients most likely diagnosis, what is the most commonly found physical finding :

a) Murmur

b) Conjunctival hemorrhage/petechiae

c) Splenomegaly

d) Fever

3) The most appropriate initial empiric therapy for the patient in this case is:

a) Penicillin G + nafcillin

b) Vancomycin alone

c) Vancomycin + gentamicin

d) Vancopime

 

 

Answers:

 

  1. C. echo
  2. D. fever
  3. B vancomycin aloneNICE guidelines published in 2008 made an even more radical departure from the past.22 They do not recommend antibiotic prophylaxis for dental, or non-dental procedures (eg, respiratory, gastrointestinal, and genitourinary)

 

Discussion:

 

This patient’s history of IV drug abuse and fever should bring infective endocarditis near the top of the differential diagnosis. The physical exam finding of cardiac murmur should further heighten suspicion. The finding of conjunctival petechiae should reinforce this suspicion – although this vascular finding is not pathognomonic for endocarditis, it is one of the minor criteria that can help make the diagnosis. The most common physical finding is fever – up to 30% of those with endocarditis do not present with murmur, although the vast majority do have a murmur at some point in their disease course.

 

 

 

6.5-1

 

Conjunctival hemorrhage – septic emboli

 

 

 

Infective endocarditis is an infection of the endocardial surface of the heart, most commonly one or more of the cardiac valves, but can also include a septal defect or the mural endocardium itself. The pathophysiology of this disease is classically a valve with mechanical damage at which a sterile thrombus initially forms, which then becomes infected when a subclinical bacteremia is induced (ie, with IV drug injection, after dental procedures, endoscopy, cystoscopy, etc). IV drug users may have damaged valves secondary to contaminants in drugs such as talc. Valves also can become damaged with age secondary to degenerative changes.

 

 

 

Incidence and Risk:

 

The incidence of infective endocarditis varies widely depending on which part of the country in which you practice – it is very dependent on the prevalence of high risk indiviuals in the specific population. What is clear is that over 50% of those diagnosed with endocarditis are over the age of 60.

 

Presentation is most often a febrile patient who is high risk. Those at high risk include:

 

  • IV drug users (as in the case presented here),

 

  • Patients with prosthetic heart valves,

 

  • Unrepaired cyanotic congenital heart disease (which includes palliative shunts and conduits),

 

  • Completely repaired congenital heart defects with prosthesis during the first 6 months after the procedure,

 

  • Repaired congenital heart disease with residual defect at or adjacent to the site of the prosthetic device, and

 

  • Cardiac valvulopathy in a transplanted heart.

 

Diagnosis:

 

The Duke Criteria are widely accepted to stratify patients with suspected infective endocarditis into three categories: Definite, Possible, and Rejected. These criteria have been validated multiple times after the original study of 69 patients. Although there have been proposed updates to these criteria (including any s. aureus bacteremia in high risk patients as a major criteria), the original Duke Criteria are 95% sensitive and 99% specific.

 

Major Criteria include:

 

  • Positive blood cultures (of typical pathogens) from >=two sites
  • Definitive evidence of endocardial involvement by echo, including endocardial vegetation, paravalvular abscess, new partial dehiscence of prosthetic valve or new valvular regurgitation
  • *It has been proposed to add S.Aureus positive bacteremia

 

Minor Criteria include:

 

  • Predisposition defined as a predisposing heart condition (as described above) or IVDA
  • Vascular phenomena including arterial emboli, septic pulmonary infarcts, mycotic aneurysm, conjunctival hemorrhages, or Janeway lesions.
  • Immunologic phenomena including Osler’s nodes, Roth’s spots, and rheumatoid factor
  • Microbiologic evidence, ie single positive blood culture
  • Echocardiogram findings “consistent with endocarditis but do not meet major criteria” *(with the advancement of technology and widespread availability of TEE, it has been proposed to take this off)

 

 6.5-2

 

 Roth spots – retinal hemorrhage with central pallor

 

 

 6.5-3

 

Splinter hemorrhage – septic emboli seen under nails

 

 6.5-4

 

Osler’s nodes – Painful lesions seen on finger/toe pads (caused by immune complexes)

 

Janeway Lesions – nontender lesions on the palms/soles (septic emboli)

 

6.5-5

 

Mycotic aneurysm of MCA seen on noncontrast head CT – (although any artery can be affected, intracranial arteries are most often involved followed by visceral arteries and then arteries supplying extremities.)

 

 

Definite Endocarditis – any one of the following combinations of clinical findings:

 

  1. Two major clinical criteria
  2. One major and any three minor criteria
  3. Five minor criteria

 

Possible Endocarditis – any one of the following combinations of clinical findings:

 

  1. One major and one or two minor criteria
  2. Three minor criteria

 

Rejected Endocarditis – any one of the following are present:

 

  1. A firm alternative diagnosis
  2. Resolution of clinical manifestations occurring after <= 4 days of antibiotic therapy
  3. Clinical criteria for possible or definite endocarditis is not met.

 

 

 

Antimicrobial therapy:

 

Most common pathogens: S. aureus (32%); s. viridans (18%); enterococci (11%); coagulase negative staph (11%), Streptococcus bovis (7%); other strep (5%); non-HACEK gram-negatives (2%); fungi (2%); HACEK – Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae (2%)

 

 

 

Choice of empiric antibiotics depends on the patient’s main risk factor for endocarditis. For patients with a native valve who are not IV drug users, the best choice is:

 

  • Penicillin G 5 million units IV q4h + nafcillin 2g IV q4h

OR

  • Vancomycin 15mg/kg IV q 12h

AND

  • Gentamicin 1mg/kg IV q8h

 

For patients with a native valve who are IVDA:

 

  • Vancomycin 15mg/kg IV q12h

 

For patients with prosthetic valve:

 

  • Vancomycin 15mg/kg IV q12 + Gentamicin 1mg/kg IV q8h

 

Complications:

 

  •  Heart failure is linked to infective endocarditis and is a complication associated with poorer outcomes. Whether the patient’s CHF is a result of endocarditis or a separate preceding entity, patients tend to have increased mortality.
  • Extension of endocarditis beyond the valve’s annulus is also associated with a significantly higher mortality.
  • Mycotic aneurysms, if present intracranially, are associated with a 60% mortality.

 

 

 

 

 

Prophylaxis to prevent Endocarditis during procedures in the ED:

 

  • NICE (National Institute for Health and Clinical Excellence) guidelines published in 2008 do not recommend antibiotic prophylaxis for dental, or non-dental procedures (eg, respiratory, gastrointestinal, and genitourinary)
  • The American Heart Association also published guidelines against prophylaxis even in high risk populations in 2007.

 

 

Clinical Pearls:

  • In patients presenting with fever and IVDA or some cardiac history, keep infective endocarditis high on the differential and look for clues on physical exam to confirm diagnosis
  • Infective Endocarditis can be definitively diagnosed in the ED! An echo positive for valvular vegetation and significant physical findings with and IVDAer and fever.
  • However, ALWAYS SEND AT LEAST TWO BLOOD CULTURES (some sources say three from three different sites) – this will help our colleagues tailor the therapy appropriately once the pathogen has been identified and susceptibilities are available.

References:

“Diagnosis, Antimicrobial Therapy, and Management of Complications: A Statement for Healthcare Professionals From the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association—Executive Summary: Endorsed by the Infectious Diseases Society of America.” Circulation. 2005; 111: 3167-3184

Garg SJ, Sivalingam A, Bolling J, Goldberg R, Sivalingam J, Magargal L. Ocular Abnormalities in Acquired Heart Disease. Duane’s Ophthalmology. 2006. Vol 5. http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v5/v5c022.html

The Hand in Pathology. Stanford School of Medicine. Stanfordmedicine35.stanford.edu/the25/hand.html

Lee W, Mossop P, Little A, Fitt G, Vrazas J, Hoang J, Hennessy O. Infected (Mycotic) Aneurysms: Spectrum of Imaging Appearances and Management. RadioGraphics, 28, 1853-1868. November 2008.

Li JS, Sexton DJ, Mick N, Nettles R, Fowler VG Jr, Ryan T, Bashore T, Corey GR. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clinical Dis. 2000 Apr; 30(4):633-8.

Infective Endocarditis.  Rosen’s Emergency Medicine.  7th edition.  2010.  Print.

 

Morrison’s Pouch V2.1

morrisons-pouch-redo2

Case Presented by: Dr. Meredith Hill

CC: “I can’t breath”

70-year-old man with a PMH of HTN who presents with shortness of breath. He states that he is increasingly short of breath over the last 3 weeks, and is significantly worse today. The patient complains of orthopnea and new bilateral lower extremity edema. He states he takes multiple medication, but ran out of them a few days ago. The patient denies chest pain, nausea, vomiting and abdominal pain. He denies fever and chills. Patient has a history of smoking, but quit several years ago.

Physical Exam:

VS: BP 182/104, HR 95, RR 22, Temp 36.1, Pulse ox 97 % on room air

General: Acute respiratory distress

Consitutional: Well-developed, well-nourished, pt in mild respiratory distress and can speak about 4-5 words at a time.

Respiratory: Decreased air entry at the bases, bilaterally. Accessory muscle use. No wheezing, but  faint crackles heard bilaterally.

Cardiovascular: Regular rate and rhythm. Normal heart sounds – S1/S2 positive, no murmurs, rubs, or gallops. Good peripheral pulses felt in bilateral upper extremities, capillary refill is less than two seconds. 3+ pitting edema bilaterally.  No JVD appreciated

DDX

Heart failure

COPD exacerbation

Pneumonia

Pneumothorax

Pulmonary Embolism

Acute coronary syndrome

Question:

How can we use ultrasound to differentiate causes of this patient’s acute dyspnea?

Discussion:

The BLUE protocol can be used to assess this patient’s dyspnea. The linear array probe is used to assess 3 lung zones on each hemithorax. Make sure the probe indicator goes toward the patient’s head. You are looking for a view between 2 ribs.  Maximizing the depth will also help.

1

2

You begin by ruling out pneumothorax. This is achieved by identifying lung sliding and assessing for A and B lines (Figure B and C).

A-lines (Figure B) are parallel to the lung pleura and B-lines (Figure C) are perpendicular.  B-lines indicate subpleural interstitial edema. If a dyspneic patient has A lines in bilateral lung fields then pneumonia and pulmonary edema can be ruled out. If you identify bilateral B lines, then pulmonary edema may be the cause of the dyspnea. Identification of both A and B line may represent pneumonia.  If you see the right lung with predominate A lines and the left with B lines (or vice versa) there is an increased likelihood for pneumonia.

3

4

You cannot really appreciate the sliding of the pleura in these still images but if you wanted to switch to M mode (Figure D) to assess for the “seashore” sign you could also use this to r/o PTX.

To evaluate for pulmonary embolism, a quick way to reduce the likelihood of the diagnosis is to evaluate for a DVT since most PEs originate from lower extremity DVTs.  Begin the scan by placing gel to the groin and medial thigh at a distance about 10 centimeters distal to the inguinal crease and identify the common femoral vein. Check for compressibility. Scan distally and check for compressibility at the junction of the superficial femoral vein and deep femoral vein.  Subsequently, move down to the popliteal vein, starting 2 cm proximal to the knee, compressing 3 separate times until you see the trifercation of the the popliteal vein into the anterior tibial vein, the posterior tibial vein, and the peroneal vein. If you confirm the presence of a DVT and identified an A-line on chest ultrasound, your suspicion for pulmonary embolism should increase.

http://www.youtube.com/watch?v=FHerMNhCR54

In the case above, the bedside US revealed B lines in all lung fields and negative DVT scan.  The patient was diagnosed with an acute exacerbation of heart failure.

Source: Lichtenstein et al. Relevance of Lung Ultrasound in the Diagnosis of Acute Respiratory Failure: The BLUE Protocol. CHEST July 2008 vol. 134 no. 1 117-125.

5

Intern Report 6.4

Case Presentation by Dr. Daniel Hutchens

History of Present Illness:

A 52 year old man with a past medical history of hypertension presents to the ED with complaints of acute onset chest pain for 8 hours.  The patient was sitting at home when it started and denies any exertional component.  The pain is sharp, located retrosternally, and radiates to the left neck and shoulder.  The pain is worse during inspiration and when lying flat, and is relieved by sitting upright and leaning forward.  Patient took his blood pressure medication at home and did not feel relief so he came to the ED.  He does not take aspirin.  He feels SOB and states that he had a URI 1 week ago.  There has been no recent travel.  He states toward the end of the exam that he is worried about the cost of his care as he just lost his job.

Review of Systems:

Admits to a mild cough and occasional dizziness, otherwise negative except as per HPI.

Past Medical History: Hypertension

Past Surgical History: No surgical history

Medications: HCTZ

Allergies: NKDA

Social History: Denies tobacco, occasional alcohol, occasional marijuana

Family History: HTN, father with an acute MI (AMI) at 65

Physical Examination:

VS: BP 142/92 mmHg, HR 110, RR 20, O2 Sat 97% on room air, Temp 38.0°C
Head: Atraumatic
ENT: PERRLA, EOMI, throat is non-erythematous
Neck: Supple, no carotid bruits
Heart: RRR, there is a high pitched scratching sound heard that remains with suspension of respiration
Lungs: CTAB, no wheezing, no rales, ronchi are heard that remain with suspension of respiration
Abdomen: Soft, nontender, nondistended, positive bowel sounds
Skin: No rash
Neurologic: Gait is normal.

IV access was established; patient was put on oxygen, cardiac monitoring, and given an aspirin.  12 lead EKG was obtained.

ECG 6.4

A line was placed and labs were sent including a BMP, CBC, coagulation panel, and troponin.  CXR was obtained.

cxr 6.4

Cardiac ultrasound (US) was performed at the bedside.

us 6.4

Labs came back and Troponin I was <0.017.  Serum electrolytes as well as BUN and Cr were wnl.  CBC and coagulation studies were wnl.

Questions:

1.) What is the best treatment in this patient’s case?
a. Indomethacin
b. Ibuprofen
c. Colchicine
d. Prednisone

2.) What is a distinguishing factor for acute pericarditis vs. AMI on EKG?
a. PR interval elevation
b. Inverted T waves in the anterior and inferior leads
c. ST-segment depressions in the precordial leads with reciprocal changes
d. Diffuse ST-segment elevations with no reciprocal changes

3.) How can you use serum biomarkers with EKG to help diagnose acute pericarditis over AMI?
a. Biomarker elevation will be moderate compared to what would be expected in AMI given the EKG findings
b. Biomarker elevation will be higher compared to what would be expected in AMI given the EKG findings
c. Biomarker elevation is never seen in acute pericarditis
d. There is no relation between biomarker elevation and EKG findings in acute pericarditis

 

Answers to the questions:

1.) b. Ibuprofen

2.) d. Diffuse ST elevations with no reciprocal changes

3.) a. Biomarker elevation will be moderate compared to what would be expected given the EKG findings

Discussion:

The characteristics of this patient’s pain, the physical exam finding of a friction rub, and the EKG findings make the most likely diagnosis acute pericarditis.  Acute pericarditis is classified as chest pain for <6 weeks and can resemble cardiac ischemia.  It is often severe, retrosternal and left precordial, and referred to the neck, arms, or left shoulder.  Pain is often pleuritic but sometimes it is a steady, constricting pain that radiates into either arm.  Characteristically, pericardial pain is relieved by sitting up and leaning forward, something you would not see classically with AMI.  EKG changes in acute pericarditis will show diffuse, concave ST elevation across multiple leads, usually with PR depression early, then isometric T-waves progressing to ST depression.  This is in contrast to EKG changes in AMI, where you would expect more convex ST elevations present in anatomically contiguous leads with reciprocal changes.  Acute pericarditis is often accompanied by some degree of myocarditis causing serum biomarkers (troponin) to rise, termed myopericarditis.  These elevations, if they occur, are often quite modest compared to the elevations in AMI given the extensive EKG findings of ST-segment elevation.

A pericardial friction rub will be audible in anywhere from 50-85% of patients with acute pericarditis and is pathognomonic.  It will have a rasping, scratching, or grating quality.  The best way to hear it is to have the patient sit up and lean forward while placing your stethoscope over the lower sternal edge or apex.  It is heard best at end-expiration and won’t disappear with cessation of respirations as would a pleural rub.  More than 50% of rubs are triphasic and will include an atrial systolic rub preceding S1, a ventricular systolic rub occurring between S1 and S2, and an early diastolic rub occurring after S2.  It is not uncommon for patients with acute pericarditis to have a pericardial effusion and a pericardial friction rub can be heard at the start.  After enough effusion has accumulated the rub will disappear.  US is the best initial test which will show free fluid in the pericardial space.  The US from the case shows a small pericardial effusion near the right atrium.

Within the diagnosis of acute pericarditis it is necessary to determine an underlying cause.  Different etiologies of are grouped into infectious, noninfectious, or autoimmune.  Infectious etiologies include: viral (1-10% of cases, peaks in spring and fall); pyogenic (bacterial from direct pulmonary extension, hematogenous spread, myocardial abscess/endocarditis, post-surgery); tuberculous (suspect in high risk groups and developing countries).  Noninfectious etiologies include: post-MI (Dressler’s syndrome); uremia (usually secondary to ESRD or dialysis, will often have normal EKG because little epicardial inflammation occurs); neoplastic (both primary and metastatic); myxedematraumaticaortic dissectionsarcoidosis.  Autoimmune etiologies include: rheumatic feverSLERAsclerodermaWegener’s granulomatosisdrug-induced (procainamide, hydralazine, phenytoin, isoniazide, minoxidil, anticoagulants).  An idiopathic cause is responsible for 26-28% of acute pericarditis diagnoses and is the most common etiology given.  Many idiopathic cases are likely due to undiagnosed viral infections.

Pericardiocentesis is indicated in patients with effusions larger than 250 mL, effusions where the size increases despite intensive dialysis for 10-14 days, or effusions with evidence of tamponade.  The procedure can be performed with or without US guidance, although if it is available US should be used.  Before you perform the procedure you should ensure the patient has IV access, is receiving supplemental oxygen, is connected to a cardiac monitor, and continuous pulse oximetry.  If time permits you can place an NG tube to decompress the stomach and reduce the risk of a gastric perforation.  Either subxyphoid or left sternocostal margin approaches are most often used.  The procedure should be performed in a sterile fashion using a spinal needle connected to a syringe with the patient supine if there’s no US guidance, and at 30-45 degrees head elevation if there is.  When you’re not using US the needle should be inserted at a 45 degree angle to the abdominal wall and directed toward the left shoulder.  With US guidance, insert the needle at a 15-20 degree angle and direct it just under the rib cage toward the left should.  The needle is inserted ~5cm while applying negative pressure to the syringe until a return of fluid is noted or a change on the EKG strip is seen.  If the EKG pattern shows cardiac injury (ST segment elevation) then you have gone too far, are in direct contact with the myocardium, and should withdraw the needle until the pattern has returned to normal.  Withdraw as much fluid as possible.  Complications of this procedure are production of pericardial tamponade, laceration of a coronary artery, and induction of cardiac dysrhythmias.  Pericardial fluid should be analyzed for red and white blood cells, cytologic studies for cancer, microscopic studies, and cultures.  Fluid that returns as an exudate is likely from an inflammatory cause (most commonly viral).  Transudative fluid is seen in pressure-related conditions such as congestive heart failure.  If red blood cells are seen in the fluid this could represent a complication from acute rheumatic fever, post-cardiac injury, or renal failure (such as in uremic pericarditis).  If adenosine-deaminase activity is high, tuberculous pericarditis should be suspected.

Treatment includes empiric anti-inflammatory therapy for acute and recurrent pericarditis secondary to viral or idiopathic cases that are most commonly seen.  Currently, aspirin and NSAIDs are the mainstay of therapy.  An “attack dose” should be given for 1-2 weeks.  For aspirin this is 2-4 g/day, ibuprofen is 600mg TID, indomethacin is 50mg TID.  After the attack dose drug tapering may be considered.  Colchicine is added in autoimmune conditions and cases of recurrent pericarditis.  It interferes with WBC activity and is good for these cases.  Attack dose is not necessary with colchicines and 0.5mg BID can be given for 3 months if it’s the first attack or 6-12 months with recurrent attacks.  Corticosteroids should be reserved for difficult cases requiring multi-drug therapies and specific medical conditions.  This is because while they offer a fast remission, there is a higher risk of recurrences, prolonged course, and side effects with corticosteroids.  The corticosteroid of choice is prednisone and is dosed at 0.2-0.5 mg/kg/day.  Treatment length for aspirin, NSAIDs, and corticosteroids are usually until symptoms resolve and CRP normalizes.  If it is a uremic pericarditis aggressive dialysis is indicated and NSAID therapy will have little effect.  Corticosteroids can be used in these cases but typically don’t produce a response for 1-2 weeks.

Disposition depends on etiology.  For idiopathic acute pericarditis, high-dose NSAID therapy is the mainstay of treatment and should be continued for 1-4 weeks.  At a week’s time, however, if the current NSAID therapy is not working then the NSAID should be switched to another.  60% of patients will recover in 1 week and 80% by 3 weeks.  18% of patients can have recurrent pericarditis which warrants additional therapy with corticosteroids or colchicines.  Patients without clinically poor prognostic predictors (fever >38°C, subacute onset, immunosuppression, trauma, oral anticoagulant therapy, myopericarditis, severe pericardial effusion, cardiac tamponade) can be considered “low-risk cases” and assigned to outpatient treatment with high-dose oral NSAID therapy.  Otherwise, hospital admission is warranted with a consult to cardiology and any other subspecialties required (ex. In the case of uremic pericarditis you should also consult nephrology).

Clinical Pearls:

  • Suspect acute pericarditis if chest pain is sudden onset, relieved by sitting up and leaning forward, and is associated with a friction rub.
  • EKG in acute pericarditis will show diffuse ST-segment elevations with no reciprocal changes and PR depression early on.
  • Cardiac US should be performed in patients with acute pericarditis to rule out a pericardial effusion.
  • If a pericardial effusion is present, CXR may show a typical “water bottle” heart, where the heart is enlarged in the shape of a flask or water bottle.
  • Aspirin or NSAID therapies remain the mainstay of treatment for the majority of cases of acute pericarditis.  However, other etiologies should be investigated with each case and treated appropriately.

References:

Imazio M, Adler Y.  “Treatment with aspirin, NSAID, corticosteroids, and colchicines in acute and

recurrent pericarditis.”  Heart Fail Rev 4 Jun. 2012.  Pubmed.  Web.  16 Nov. 2012.

Imazio M, et al.  “Day-hospital treatment of acute pericarditis: a management program for outpatient

therapy.”  J Am Coll Cardiol.  2004; 43(6): 1042-46.

Longo D, et al.  “Acute Pericarditis.”  Harrison’s Online 18e: Part 10 Disorders of the Cardiovascular

System: Section 4 Disorders of the Heart: Chapter 239 Pericardial disease.  Web.  16 Nov. 2012.

Pericardial Disease (Pericarditis).  Rosen’s Emergency Medicine.  7th edition.  2010.  Print.

Spangler MD, Sean.  “Acute Pericarditis.”  Medscape Reference 10 Oct. 2011.  Medscape.  Web.  16 Nov.

2012.

Intern Report 6.3

 

Case Presentation by Dr. Heather Bowman

CC: “My legs and knees are swelling”

HPI: CG is a 93-year-old female with history of arthritis who comes to the to the emergency department stating that she is having leg and knee swelling.  She’s been unable to walk since last night.  She is unable to describe the quality or severity of the pain but she says “they’re killing her really bad”.  She says she’s had this before and they had put a needle in her knee last time.  Nothing makes the pain and swelling better or worse.  No trauma, fever or nausea or vomiting.

ROS: Negative except as per HPI

PMH:Patient is a poor historian and is only able to say she has had Shingles, review of EMR shows patient has arthritis and A. fib., CAD status post stent, hypertension, CHF, stroke, diverticulitis and breast cancer

PSH:Patient denies, per EMR had coronary catheter and stent placement 2007

MEDICATIONS: Patient is unsure.  Per EMS has pantoprazole, Klor-Con, acetaminophen, aspirin furosemide, & ranitidine

ALLERGIES:Penicillin

SOCIAL HISTORY: Patient lives in a senior citizen home.  Reports has lots of support from her neighbors and her granddaughter

Physical Exam:

Vitals: Blood pressure was 155/86, pulse 90, respirations 16, febrile 38.2, satting 100% on room air

General: No Acute Distress, lying comfortably on stretcher

HEENT: PERRL, EOMI, very hard of hearing, mucous membranes dry

Cardiovascular: +S1, S2, no murmers, Radial and DP pulses symmetric

Respiratory: Clear to auscultation bilaterally

Gastrointestinal:  NT/ND

Musculoskeletal: Strength 4/5 in upper extremities and right leg, strength 4/5 left leg limited due to pain, effusion over both knees left greater than right, right knee has good range of motion, not warm or indurated. Left knee is warm not indurated, left knee range of motion limited at 45° due to pain

Skin: Intact

Neurologic:  patient can’t ambulate due to pain.

Labs/Radiograph

Electrolytes: Na=140, K=3.8, Cl=103, HCO3=27, BUN=20, Createnine=0.9, Glucose=101, Ca=9.3, Mg=2.1

CBC: WBC=8.5, Hgb=10.4, Platelets=182

Others: CRP=75.30, ESR=53

UA: 2-5 squamous cells, Specific gravity=1.015, blood=2+, protein=1+, Nitraes: positive, Leukocyte esterase 2+, RBC=5-10, WBC=20-50, bacteria=4+, trichomonas=neg

Cell count and differential, gram stain and bacterial culture, and the answer to question#3: pending

Complete R knee:

1.  Generalized osteopenia without identification of an acutely displaced fracture.

2.  Development of a moderate joint effusion.

3.  Severe osteoarthritis of the right knee

Complete L knee:

1.  Generalized osteopenia without identification of an acutely displaced fracture.

2.  Moderate to large joint effusion and soft tissue swelling.

3.  Advanced osteoarthritis of the left knee with findings suggesting loose intraarticular bodies.

Questions:

1. Which of the following is an absolute contraindication to arthrocentesis?

A. Infection of soft tissues over joint

B. Prosthetic joints

C. Confirmed Bacteremia

D. Hereditary bleeding diatheses

E. Patient on oral anticoagulants

 

2. Which is the correct pairing of organism and at risk population for septic arthritis?

A. N. Gonorrhoeae is the most common cause of septic arthritis for teens and patients >65yo.

B. Staph, strep, H. Influenzae, and E. coli are the most common cause of septic arthritis for kids

C. Salmonella is the most common cause of septic arthritis in patients with sickle cell

D. Staph aureus, Strep epidermidis, enterobacteriaceae and pseudomonus are most common causes in patient with a prosthetic joint

E. Gonococcal septic arthritis is more common in young males

 

3.  Besides cell count with differential, gram stain and bacterial culture and sensitivity, which other test is high yield for working up most joint effusions?  

A. Uric acid

B. Synovial protein

C. Crystal analysis

D.Synovial glucose

E. Lactate dehydrogenase

F. Rheumatoid factor

 

Answers:

1)    A

2)    D

3)    C

Discussion

1. Which of the following is an absolute contraindication to arthrocentesis?

A. Infection of soft tissues over joint-YES, arthrocentesis is absolutely contraindicated if infection of soft tissues over the joint is present.  However, remember joint may be warm, swollen and tender with acute arthritis and it is appropriate to perform arthrocentesis once you have eliminated cellulitis as the cause of this finding.

 B. Prosthetic joints-NO, while prosthetic joints are high risk for infection and you should avoid arthrocentesis if possible, if you suspect an infected prosthesis, you should perform an arthrocentesis.

C. Confirmed Bacteremia-NO, confirmed bacteremia is considered a relative contraindication because infection can spread to the joint, but it is not an absolute contraindication.

D. Hereditary bleeding diatheses -NO, hereditary bleeding tendency is also a relative contraindication.  However it is acceptable to do arthrocentesis to relieve a tense hemarthrosis in bleeding disorder such as hemophilia after infuse appropriate clotting factors

E. Patient on oral anticoagulants-NO, There is little data regarding arthrocentesis of patients on oral anticoagulants, however studies have demonstrated risk iatrogenic hemarthrosis is quite low, even with INR as high as 4.5.  Therefore when necessary is appropriate to perform arthrocentesis in patient on oral anticoagulants.

  

2. Which is the correct pairing of organism and at risk population for septic arthritis?

A. N. Gonorrhoeae is the most common cause of septic arthritis for teens and patients >65yo.  NO, While N. Gonorrhoeae is the most common cause of septic arthritis for teens and young adults, staphylococcus is more likely once a patient is >40yo.

B. Staph, strep, H. Influenzae, and E. coli are the most common cause of septic arthritis for kids.  NO, Staph, strep and E. coli are true but the incidence of H. flu has decreased to almost zero since the vaccine was developed.

C. Salmonella is the most common cause of septic arthritis in patients with sickle cell-NO, while salmonella is more prevalent in patients with sickle cell compared to the general population, the more common causes still predominate.

D. Staph aureus, Strep epidermidis, enterobacteriaceae and pseudomonus are most common causes in patient with a prosthetic joint-YES, true

E. Gonococcal septic arthritis is more common in young males-NO, while gonorrhea is more common in males, disseminated gonococcal infection is actually more common in women (4:1 prevalence), especially during pregnancy or after menstruation when the alkaline vaginal environment makes the organisms more resistant to the host defenses in the bloodstream and therefore more likely to disseminated and because infected women more likely to be asymptomatic.

3. Besides cell count with differential, gram stain & bacterial culture and sensitivity, which other test is high yield for working up most joint effusions?  

A. Uric acid-NO, Uric acid is not helpful for diagnosing acute gouty arthritis because it actually can normalize during acute phase

B. Synovial protein-NO, Synovial protein is unreliable in distinguishing inflammatory and infectious from noninfectious and therefore is no longer recommended.  Synovial protein had a sensitivity of 0.52 in one study, and ordering it is discouraged because it is likely to provide misleading or redundant information.

C. Crystal analysis-YES, Of the answers listed, crystal analysis is the best.  Remember to use a green top (liquid sodium heparin) to prevent clotting.  Calcium oxalate and lithium heparin anticoagulatns can introduce artificial crystals into the fluid.  Under a polarizing microscope, calcium pyrophosphate (gout) is a positively birefringent crystal (long axis is blue when parallel to the Z-axis and yellow when perpendicular to it).  Calcium pyrophosphate crystals are smaller than 10 micrometers and can be rods, rhomboids, plates or needle like.  Monosodium urate (pseudogout) is a negatively birefringent crystal (long axis is yellow when parallel to Z-axis and blue when perpendicular).  Urate crystals are needle shaped, and between 2-10 micrometers.   You can also see cholesterol crystals which are large, very bright, square or rectangular with broken corners.  As always, use the entire clinical picture and your clinical judgment when ruling out septic arthritis.  Patients with underlying joint disease are more likely to develop a septic arthritis and finding crystals does not eliminate an infectious cause.

 pict 6.3 

D.Synovial glucose, -NO, Glucose is unreliable in distinguishing inflammatory and infectious from noninfectious and therefore is no longer recommended.  Glucose had a sensitivity of 0.2 in one study, and ordering it is discouraged because it is likely to provide misleading or redundant information.

E. Lactate dehydrogenase-NO, Lactate dehydrogenase is also unreliable in distinguishing inflammatory and infectious from noninfectious and therefore is no longer recommended

F. Rheumatoid factor-NO, Rheumatoid factor is less frequently obtained than crystal analysis and has little diagnostic value in the ED, though it can be useful to the clinician providing follow up care.

Clinical Course and analysis:

We elected to drain the left knee since it had a larger fluid collection, was warm, and was limiting her range of motion.  Approximately 40ccs of fluid were aspirated from GC’s left knee.  Her fluid gram stain showed numerous PMNs but no organisms.  Elevation of PMNs is consistent with an inflammatory or septic arthritis.  Culture was negative x 4 days.  Gram stain or culture of an organism would confirm septic arthritis but lack of an organism does not rule out septic arthritis as organism is not always cultured.  Cell count with differential and fluid crystals were ordered, but never done.  ID saw the patient and thought she had an inflammatory arthritis and recommended continuation of ceftriaxone for UTI with discontinuation of vanco.  The primary team continued ceftriaxone and vanco and their discharge diagnosis was septic arthritis.

WBC, ESR and CRP are sensitive but non-specific screening tests.  ESR is elevated in 90% of septic arthritis and along with CRP can be used to track response to infection, although the admitting team did not re-order these tests.  WBC greater than 10,000 can suggest a systemic illness but is only elevated in 50% of septic arthritis cases and sterile inflammatory processes create a similar leukocytosis.  Her WBC was not elevated throughout her hospital stay.  Cultures from infectious foci can often demonstrate the bacteria responsible for septic arthritis.  Her urine culture did show >100,000 CFU of E. coli and if she did have septic arthritis this is a likely source.

References:

Marx, J. A., R. S. Hockberger, et al. (2010). Rosen’s emergency medicine: concepts and clinical practice, Mosby/Elsevier.

Roberts, J. R. and J. R. Hedges (2009). Clinical Procedures in Emergency Medicine E-Book, Elsevier Health Sciences