Dott. Maurizio M. Ciammaichella
Dirigente Medico
Responsabile UAS “Trombosi Venosa Profonda ed Embolia Polmonare”
Responsabile CDF BLSD IRC “Emersan Lateranum”
U.O.C. Medicina Interna I° per l'Urgenza
(Direttore: Dott. G. Cerqua)
A.C.O. S. Giovanni - Addolorata - Roma
 

 

PERICARDITIS AND CARDIAC TAMPONADE

 

KEY-WORDS: Pericarditis and cardiac tamponade

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INTRODUCTION
CLINICAL
WORKUP
TREATMENT
MEDICATION
FOLLOW-UP
MISCELLANEOUS
BIBLIOGRAPHY


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INTRODUCTION

Background: Pericarditis and cardiac tamponade are clinical problems involving the potential space surrounding the heart or pericardium. Pericarditis is one cause of fluid accumulation in this potential space while cardiac tamponade is the hemodynamic result of fluid accumulation.

The use of limited echocardiography by emergency physicians has enhanced the diagnosis of cardiac tamponade from a variety of causes, including trauma, infectious and other noninfectious causes.

 

Pathophysiology: The pericardium consists of two layers, an outer fibrous layer and an inner serous layer. The potential space produced by these layers contains approximately 20 cc of fluid with similar electrolyte and protein profiles to plasma. Approximately 120 cc of additional fluid can accumulate in the pericardium without an increase in pressure. Further fluid accumulation can result in marked increases in pericardial pressure resulting in decreased cardiac output and hypotension. The rapidity of fluid accumulation influences the hemodynamic effect.
.

Frequency:

  • In the U.S.: reported incidence of acute pericardial tamponade is approximately 2% of penetrating trauma. It is rarely seen in blunt chest trauma.

.Mortality/Morbidity: The early diagnosis of significant pericardial and cardiac injuries can prevent morbidity and enhance survival.

  • Penetrating cardiac injury - Immediate identification of penetrating cardiac injuries via ED echocardiography can improve survival rate and neurologic outcome.
  • Nontraumatic pericardial effusion - Prompt identification utilizing ED bedside echocardiography streamlines appropriate therapy and disposition.

Sex: Pericarditis, Male > Female

 

Age: Pericarditis, predominant in adolescents and young adults

 


CLINICALPATHOPHYSIOLOGY

History:

  • Pericarditis
    • The most common symptom of acute pericarditis is precordial or retrosternal chest pain, usually described as sharp or stabbing.
    • This pain may be of sudden or gradual onset and may radiate to the back (left trapezial ridge), neck, left shoulder, or arm.
    • Movement or inspiration may aggravate the pain.
    • It can be most severe when the patient is supine and can be relieved when the patient leans forward while sitting.
    • Common associated signs and symptoms include a low-grade intermittent fever, dyspnea, and dysphagia.
  • Pericardial tamponade
    • Patients may present subacutely with symptoms of anxiety, dyspnea, fatigue, or altered mental status.
    • Patients may have a history of medical illnesses associated with pericardial involvement, particularly end-stage renal disease (ESRD).
    • Traumatic tamponade may present with acute dyspnea or altered mental status.

Physical:

  • Pericarditis
    • The most common and important physical finding is a pericardial friction rub, which is best heard at the lower left sternal border or apex when the patient is sitting forward, or when on hands and knees. It may be transient from one hour to the next.
    • Fever
    • Cardiac arrhythmias
    • Tachypnea
    • Distended jugular neck veins (DJV)
    • Cyanosis
    • Relative or absolute hypotension
    • Ewart's sign (dullness and bronchial breathing between the tip of the left scapula and the vertebral column)
    • Varying degrees of consciousness
    • Pulsus paradoxus (greater than 10 mm Hg decrease in systolic pressure with inspiration)
    • Hepatomegaly, ascites
  • Cardiac tamponade
    • Beck's triad (Jugular venous distention, hypotension, and muffled heart sounds)
    • Pulsus paradoxus
    • Measurement by careful auscultation during the lowering of the pressure in the blood pressure cuff. The first sphygmomanometer reading is recorded at the point when beats are audible during expiration. The second reading is taken when each beat is audible. If the difference between the two readings is greater than 10 mm Hg, pulsus paradoxus is present.

Causes:

  • Acute pericarditis
    • Serous pericarditis - Usually caused by noninfectious inflammation, such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The fluid will demonstrate few PMNs, lymphocytes, or histiocytes. The usual volume is 50-200 mL and accumulates slowly. Fibrous adhesions rarely occur.
    • Fibrous and serofibrinous pericarditis - These two types represent the same basic process and are the most frequent type of pericarditis. Common causes are acute myocardial infarction (AMI), postinfarction (Dressler's syndrome), uremia, radiation, RA, SLE and trauma. Severe infections may also cause a fibrinous reaction, as does routine cardiac surgery.
    • Purulent/suppurative pericarditis - Infection is the most common cause. Organisms may arise from direct extension, hematogenous seeding, lymphatic extension, or by direct introduction during cardiotomy. Immunosuppression facilitates this condition. The fluid usually is 400-500 mL in volume and shows a thin to creamy pus. Clinical features include fever, chills, and spiking temperatures. Constrictive pericarditis is a serious potential complication.
    • Hemorrhagic pericarditis - Blood mixed with a fibrinous or suppurative effusion most commonly is caused by tuberculosis or direct neoplastic invasion. It also can occur in severe bacterial infections or in patients with a bleeding diathesis. It is common after cardiac surgery and may cause tamponade. The clinical significance is similar to suppurative pericarditis.
    • Caseous pericarditis - Until proven otherwise, caseation within the pericardial sac is tuberculous in origin. Untreated, this is the most common antecedent to chronic constrictive, fibrocalcific pericarditis.
  • Chronic pericarditis
    • Adhesive mediastinopericarditis - This reaction usually follows suppurative or caseous pericarditis, cardiac surgery, or irradiation. It rarely is caused by a simple fibrinous exudate. The pericardial potential space is obliterated and the subsequently there is adhesion of the external surface of the parietal layer to the surrounding structures. Clinically, systolic contraction of the ribcage and diaphragm, and pulsus paradoxus may be observed. The increased workload may cause massive hypertrophy and dilatation, which can mimic an idiopathic cardiomyopathy.
    • Constrictive pericarditis - This usually is caused by suppurative, caseous, or hemorrhagic pericarditis. The heart may become encased in a 0.5- 1.0 cm thick layer of scar or calcification (concretio cordis), resembling a plaster mold. Contrary to clinical findings in adhesive mediastinopericarditis, the heart cannot hypertrophy or dilate because of insufficient space.
  • Cardiac tamponade
    • Penetrating cardiac injuries - Identification of any pericardial fluid in the setting of penetrating injury to the thorax or upper abdomen requires aggressive resuscitation.
    • Hemopericardium is the most common feature of penetrating cardiac injuries. In acute massive hemopericardium, there is insufficient time for defibrination to occur. The hemopericardium organizes and may partially clot resulting in a pericardial hematoma. The hematoma may appear echogenic instead of echo-free.
    • Iatrogenic causes - Potential sources of perforation include central line placement (CVP), pacemaker insertion, cardiac catheterization, sternal bone marrow biopsies, and pericardiocentesis.
    • The right atrium is the most common site of perforation from catheter placement. Perforation as well as direct infusion of fluids through the catheter can cause tamponade.
    • Delayed tamponade has occurred secondary to catheter misplacement (hours to days).


WORKUP

Lab Studies:

  • Complete blood count (CBC) with differential
  • Elevated erythrocyte sedimentation rate (ESR)
  • Creatinine phosphokinase (CPK) and isoenzymes
  • Elevated lactate dehydrogenase (LDH) and serum glutamic-oxaloacetic acid (SGOT)

.Imaging Studies:

  • Chest radiography
    • Not helpful in uncomplicated viral pericarditis. A water-bottle shaped heart can be seen with excessive pericardial fluid accumulation.
    • In cardiac tamponade (or large effusions), the chest x-ray may demonstrate an enlarged cardiac silhouette after 200-250 mL of fluid accumulation. This occurs in patients with slow fluid accumulation, compared to a normal cardiac silhouette seen in patients with rapid accumulation and tamponade.
  • Limited echocardiography
    • In pericarditis, the pericardium may have a normal appearance, without evidence of fluid accumulation.
    • If no pericardial effusion is noted, stable patients with presumptive viral pericarditis may be discharged with appropriate instructions and follow-up care.
    • The emergency nature of blunt and penetrating trauma often does not allow emergency sonographers to assess pericardial fluid to the same degree as traditional echocardiographers.
    • Echocardiographers utilize M-mode to evaluate pericardial fluid and timing during the cardiac cycle.
    • Emergency sonographers essentially note the presence or absence of pericardial fluid and may comment on the amount of fluid.
    • Very small effusions are located posterior and inferior to the left ventricle.
    • Moderate effusions extend toward the apex of the heart and large effusions circumscribe the heart.
    • It may be difficult for the emergency sonographer to utilize the classic textbook sonographic findings of tamponade, as the trauma patient is often tachycardic and the exam abbreviated.
    • The amount of fluid present is important to note. It should be a large effusion with fluid surrounding the heart.
    • A swinging heart may be present. This is characterized as counter-clockwise rotational movement, which occurs in addition to the triangular movement of the heart producing a dance-like motion.
    • A dilated inferior vena cava without inspiratory collapse (plethora) is highly suggestive of tamponade.

Other Tests:

  • Electrocardiography (ECG)
    • Electrical alternans is pathognomonic of cardiac tamponade and is characterized by changing levels of ECG voltage of the P wave, QRS complex, and T waves. This is a result of the heart swinging in a large effusion.
    • The ECG can be diagnostic in acute pericarditis and evolves in 4 stages. Only 50% of patients with pericarditis experience all 4 stages.
      • The first stage is characterized by ST-segment elevation with concave upward ST segments. It can be seen within hours of chest pain and lasting several days. The ST segment changes usually are noted in all leads except V1.
      • In the second stage, the ST segments return to baseline with T-wave flattening.
      • The third stage is distinguished by T-wave inversion without Q-wave formation.
      • The fourth stage is characterized by ECG normalization.
    • Another important ECG finding is PR segment depression, which has been reported in up to 80% of viral pericarditis cases.

.Procedures:

  • Limited echocardiography
    • Echocardiography is the diagnostic procedure of choice in patients with large effusions or tamponade.
    • Echocardiography is useful in determination of fluid, location, and direction of pericardiocentesis.
  • Pericardiocentesis
    • The traditional approach is the subxiphoid technique. This technique avoids injury to the coronary arteries.
      • The chest is prepared with Betadine and a 16- to 18-gauge catheter is introduced between the xiphoid and the left subcostal margin.
      • The catheter is directed toward the inferior tip of the left scapula with slow advancement and with negative pressure.
      • If fluid is found, the catheter is advanced and the needle withdrawn. Fluid is removed via the catheter.
      • The catheter may be sutured in place for subsequent use.
  • Echocardiographically guided pericardiocentesis
    • Echocardiographic guided pericardiocentesis has evolved over the past 20 years and is now considered the procedure of choice for removal of pericardial fluid. The technique for echocardiographic guided pericardiocentesis differs from traditional blind pericardiocentesis primarily in the site of needle entry.
    • The left chest wall has become the preferred location for needle entry under echo guidance. The intended needle trajectory is investigated with echo to confirm the optimal direction and depth for needle advancement. A 16-gauge needle (with polytef-sheath) is advanced in a straight line without side-to-side manipulation. Needle position can be established via echo while agitated sterile saline is injected.
    • The step-by-step approach for echo guided pericardiocentesis includes the following:
      • Assess the size, distribution, and ideal needle entry site and trajectory with a 2.5-5 MHz ultrasound transducer placed approximately 3- 5 cm from the parasternal border. Locate the point where the effusion is closest to the transducer as well as an area of maximal, pericardial fluid accumulation.
      • Assess or measure the distance from the skin to the pericardial space. The needle trajectory is established by the angle of the transducer. Keep this trajectory in your mind during the procedure.
      • Use a sterile skin prep like povidone-iodine and, if readily available, use a transparent sterile plastic sheet (one author recommends a Baxter drape, 1030) to allow imaging and a sterile field.
      • Place a sterile 16-gauge catheter on the predetermined location on the chest wall avoiding the inferior rib margin. Advance in the predetermined direction, angle, and depth. Advance 2 mm further once fluid is obtained. Consider leaving the catheter in place after removing the needle. If needed, a guidewire can be advanced through the catheter.
  • Central venous pressure (CVP) measurement
    • If echocardiography is unavailable, placement of a CVP line may demonstrate increased right-sided pressures. CVP measurements greater than 12- 14 mm Hg usually are found in cardiac tamponade.

 


TREATMENT



Prehospital Care:

  • Patients with chest pain, regardless of the etiology, should routinely be treated with oxygen and cardiac monitor.
  • Pericarditis - Routine care as for acute cardiac patients
  • Cardiac tamponade
    • The initial prehospital care is the same as for any major trauma victim. The diagnosis may be suspected based upon the location of penetrating wounds.
    • The possibility of a tension pneumothorax should be a consideration.

Emergency Department Care: The emergency care of the patient centers on prompt diagnosis and treatment of potentially life-threatening entities.

  • Pericarditis - Ideally, echocardiography should be readily available to determine the presence or absence of a pericardial effusion.
  • If a small- to moderately-sized effusion is present, the patient should be admitted for observation and a serial echocardiography. If a large effusion is present, the stable patient may undergo an urgent pericardiocentesis or placement of a pericardial window.
  • Cardiad tamponade
    • Treatment depends upon stability. Unstable patients require immediate treatment of the increase in pericardial pressure with pericardiocentesis. Removing as little as 30-50 mL may produce dramatic hemodynamic improvement.
    • Patients may have subacute tamponade (intermittently decompressing) and may benefit from decompression in the operating room with cardiothoracic care available to treat cardiac injuries.

.Consultations:

  • Nontraumatic pericardial disease - internal medicine or cardiology
  • Traumatic pericardial injury - trauma or cardiothoracic surgery


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MEDICATION

SUMMARY

Patients with idiopathic or viral pericarditis should be treated symptomatically.

Drug Category: Non-Steroidal Anti-inflammatory Drugs (NSAIDs) - Since pericarditis primarily is due to inflammation, anti-inflammatory medications are considered the drugs of choice.

Drug Name

Ibuprofen - It is usually the DOC for the treatment of mild-to-moderate pain, if there are no contraindications.
It inhibits inflammatory reactions and pain, probably by decreasing the activity of the enzyme cyclo-oxygenase, which results in prostaglandin synthesis.

Adult Dose

400-800 mg PO q4-8h

Pediatric Dose

6 mo to 12 y: 10-70 mg/kg/d divided tid or qid; start at the lower end of the dosing range and titrate upward to a maximum of 2.4 g/d
Older than 12 y: same regimen as in adults

Contraindications

Avoid use in patients with documented hypersensitivity to ibuprofen. Because of potential cross-sensitivity to other NSAIDS, do not give these agents to patients whom aspirin, iodides or other NSAIDs induce hypersensitivity.

Interactions

Probenecid may increase the concentrations and possibly the toxicity of the NSAIDs. Ibuprofen may decrease the effect of loop diuretics when administered concurrently.
PT may increase when ibuprofen is administered concurrently with anticoagulants.
Ibuprofen and other NSAIDs may increase serum lithium levels and the risks of methotrexate toxicity.

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Use with caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function. Discontinue its use if there is gastric upset or GI bleeding

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Drug Name

Indomethacin - This is often considered the first choice. Indomethacin is rapidly absorbed. Metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation.

Adult Dose

25-50 mg PO q6h

Pediatric Dose

1-2 mg/kg/d in divided bid-qid; do not exceed 4 mg/kg/d or 150-200 mg/d

Contraindications

Avoid use in patients with documented hypersensitivity to ibuprofen. Because of potential cross-sensitivity to other NSAIDs, do not give these agents to patients whom aspirin, iodides, or other NSAIDs induce hypersensitivity. Also avoid in patients with GI bleed and renal insufficiency.

Interactions

Probenecid may increase the concentrations and possibly the toxicity of the NSAIDs. Indomethacin may decrease the effect of beta-blockers, hydralazine, and captopril. It may also decrease the diuretic effects of furosemide and thiazides.
It may prolong PT when administered concurrently with anticoagulants. Monitor PT closely and instruct patients to watch for signs and symptoms of bleeding.
Indomethacin may increase serum lithium levels and the risks of methotrexate toxicity such as stomatitis, bone marrow suppression, and nephrotoxicity.

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur. Patients with preexisting renal disease or compromised renal perfusion risk acute renal failure.
Low WBC counts occur rarely, are transient and usually return to normal while therapy continues. Persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuing the drug.

 

Drug Name

Ketoprofen - It is used for the relief of mild-to-moderate pain and inflammation.
Administer small dosages initially to patients with a small body size, those who are elderly, and those with renal or liver disease.
When administering this medication, doses higher than 75 mg do not increase its therapeutic effects. Administer high doses with caution and closely observe the patient for response.

Adult Dose

25-50 mg q6-8h prn; do not exceed 300 mg/d

Pediatric Dose

3 mo to 12 y: 0.11 mg/kg q6-8h
Older than 12 y: same regimen as in adults

Contraindications

Avoid use in patients with documented hypersensitivity to this medication drug or related products.

Interactions

Probenecid and lithium may increase the concentrations and, possibly, the toxicity of NSAIDs. Conversely, the effect of loop diuretics may decrease when administered concurrently with this drug.
PT may increase when ibuprofen is administered concurrently with anticoagulants. Monitor PT and patient closely. Instruct the patient to watch for signs and symptoms of bleeding.
Concurrent administration with phenytoin may increase serum phenytoin levels, resulting in an increase in pharmacologic and toxic effects of phenytoin.

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Avoid use in patients diagnosed with GI disease, cardiovascular disease, renal or hepatic impairment, and patients receiving anticoagulants.

 

Drug Name

Naproxen - It is used for the relief of mild-to-moderate pain. It inhibits inflammatory reactions and pain by decreasing the activity of the enzyme cyclo-oxygenase, causing a decrease in prostaglandin synthesis.

Adult Dose

500 mg, followed by 250 mg q6-8h; do not exceed a 1.25 g/d

Pediatric Dose

Older than 2 y: 2.5 mg/kg/dose; do not exceed 10 mg/kg/d
Younger than 2 y: safety and efficacy have not been established

Contraindications

Avoid use in patients with documented hypersensitivity to this drug or related products.
Do not administer to patients diagnosed with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, and those at high risk of bleeding.

Interactions

Probenecid and lithium may increase the concentrations, and possibly, the toxicity of NSAIDs. Conversely, the effect of loop diuretics may decrease when administered concurrently with this drug.
PT may increase when naproxen is administered concurrently with anticoagulants. Monitor PT closely and instruct patients to watch for signs and symptoms of bleeding.
Concurrent administration with phenytoin may increase serum phenytoin levels, resulting in an increase in pharmacologic and toxic effects of phenytoin.

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur. It increases the risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion.
Low WBC counts occur rarely, and usually return to normal during ongoing therapy. Discontinuation of the therapy may be necessary if there is persistent leukopenia, granulocytopenia, or thrombocytopenia.
Exercise caution in patients that have anticoagulation defects or are receiving anticoagulant therapy.

 

.

FOLLOW-UP

Complications:

  • Recurrence of pericarditis
  • Noncompressive effusion
  • Chronic, constrictive pericarditis
  • Cardiac perforation at time of pericardiocentesis

 

Prognosis:

  • The prognosis for patients with pericarditis depends upon the etiology of the pericardial infection or inflammation as well as the presence of a pericardial effusion.
  • Cardiac tamponade
    • For penetrating injuries, the prognosis depends heavily upon the rapid identification of tamponade.
    • Favorable factors include minor perforations, isolated right ventricular wounds, systolic blood pressure greater than 50 mm Hg, and the presence of tamponade


MISCELLANEOUS

 

Medical/Legal Pitfalls:

  • Be careful not to confuse this disease entity with esophageal disorders, costochondritis, or other causes of noncardiac chest pain.
  • The potential misdiagnosis of pericarditis for acute myocardial infarction has lead to unfortunate complications when thrombolytic therapy has been given.
  • Tension pneumothorax may mimic cardiac tamponade. Trauma ultrasonography has limited this misdiagnosis.
  • Elevated CVP may be absent in patients with preexisting hypovolemia.
  • Rarely, air can enter the pericardium and obscure the sonographic evaluation.




BIBLIOGRAPHY

  • Debehnke DJ : Cardiac-related acute infectious disease. Emergency Cardiac Care 1994; 1 ed: 463-488.
  • Hauser AM: The emerging role of echocardiography in the emergency department. Ann Emerg Med 1989; 18: 1298-1303.
  • Horowitz MS, Schultz CS, Stinson EB: Sensitivity and specificity of echocardiographic diagnosis of pericardial effusion. Circulation 1974; 50: 239.
  • Markovchick V, Duffens KR: Cardiovascular Trauma. Rosen P., Barkin RM, et al., Emergency Medicine Concepts and Clinical Practice 1992; 3rd ed: 439-459.
  • Mayron R, Gaudio FE, Plummer D: Echocardiography performed by emergency physicians :Impact of diagnosis and therapy. Ann Emerg Med 1988; 17: 450-452.
  • Plummer D, Dick C, Ruiz E: Emergency department two-dimensional echocardiography in the diagnosis of nontraumatic cardiac rupture. Ann Emerg Med 1994; 23(6): 1333-1342.
  • Spodick DH: Pericarditis, pericardial effusion, cardiac tamponade and constriction. Crit Care Clin 1989; 5: 455.
  • Spodick DH: Differential diagnosis of acute pericarditis. Prog Cardiovasc Dis 1971; 14: 192.
  • Tsang TS, Freeman WK, Sinak LJ: Echocardiographically guided pericardiocentesis: evolution and state-of- the-art technique. Mayo Clin Proc 1998 Jul; PT - REVIEW, TUTORIAL(7): 647-52.