A Methamphetamine User with a Serious Underlying Syndrome: Case Presentation

Mark P. Brady, PA-C Contributor Information

March 18, 2013


A 45-year-old woman presents to the emergency department with complaints of mouth pain and fever that have been present for approximately 1 week. She denies any recent history of trauma. Social history is significant for tobacco, alcohol, methamphetamine, cocaine, and intravenous drug use. The patient's oral examination reveals severe dental decay and enamel erosion, as well as dental fractures and loss of teeth (shown). What is this cause of this oral condition?

Image courtesy of Wikipedia Commons.

Slide 1.

Answer: "Meth mouth" caused by methamphetamine use

Inhaling methamphetamine produces acid that weakens tooth enamel, causes the mouth to dry out, and reduces the amount of saliva protecting the teeth. Users crave carbonated drinks and snacks, and they rarely brush or floss. The cachectic patient is given supplemental oxygen and a peripheral IV; routine labs, blood cultures, and vital signs (shown) are obtained. She appears agitated with tachypnea, reports recent subjective fevers and chills with chronic cough, and requests pain medication.

Slide 2.

The patient has no surgical history and denies known sick contacts or recent travel. She takes no prescribed medications and denies allergies to medication. She does admit to dyspnea on exertion and to several episodes of chest pain over the past week. However, she is currently free of chest pain. How would you interpret the patient's electrocardiogram (ECG) tracing (shown)?

Slide 3.

Answer: The ECG shows evidence of sinus tachycardia with ventricular rate of 112 bpm. Diffuse concave-upward ST-segment elevation (yellow arrows), ST-segment depression in aVR (blue arrow), and PR-segment depression (often best demonstrated in leads II and V3) are shown. These findings are most consistent with stage 1 of acute pericarditis, initially thought secondary to hematogenous seeding from gingival and dental infection. Note the lack of reciprocal ST-segment changes, an important feature that differentiates acute pericarditis from acute myocardial infarction.

Slide 4.

The patient is started on nonsteroidal anti-inflammatory drugs. A quick bedside ultrasound, performed through the subxiphoid window, rules out a pericardial effusion. The ultrasonogram (shown) demonstrates a normal subcostal 4-chamber view of the heart. The pericardium is brightly reflective (echogenic or white in appearance). Abbreviations: LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Slide 5.

The patient's laboratory results are shown. She appears mildly tachypneic and dyspneic, even though her lungs were initially clear upon auscultation. Her cardiac exam reveals III/VI diastolic murmur, heard best at the left sternal border. The patient's abdominal exam is unremarkable: soft and nondistended without guarding or rebound. No palpable hepatosplenomegaly is evident. The patient has multiple track marks on her bilateral forearms from IV drug use.

Slide 6.

A chest radiograph is performed and reveals a peripheral wedge-shaped infiltrate referred to as "Hampton's hump" (arrow). What is Hampton's hump? What additional confirmatory imaging findings should you obtain?

Slide 7.

Answer: Hampton's hump is an opacification in the lung due to pulmonary embolism and lung infarction. CT angiography of the chest can confirm the findings. CT chest angiogram in this patient reveals an intraluminal filling defect that occluded the anterior basal segmental artery of the right lower lobe (shown). In addition, an infarction of the corresponding lung is present, which is indicated by a triangular, pleura-based consolidation (Hampton's hump, arrow).

Slide 8.

Immediate therapeutic anticoagulation therapy with heparin is initiated. In patients with a pulmonary embolism, anticoagulation reduces mortality rates from 30% to less than 10%. A more thorough repeat physical examination provides some additional skin findings of what appear to be petechial lesions on the palms (shown).

Slide 9.

The patient is also noted to have nonblanching, petechial lesions on the toes (shown). What might this skin manifestation represent in this patient?

Slide 10.

Answer: The initial image revealed petechial lesions that were caused, in this patient, by septic emboli. These petechial lesions, also known as Janeway lesions, can coalesce to form retiform purpura (shown), which is characterized by stellate infarcts that merge into a netlike pattern.

Slide 11.

The patient is also noted to have dark red linear lesions in the nail beds (arrow). What are these lesions? What might these findings prompt a clinician to further consider as possible disease processes?

Slide 12.

Answer: Subungual splinter hemorrhages are caused by hemorrhage of the distal capillary loop and are common in subacute infective endocarditis, but may also be seen in patients with vasculitis, nail trauma, systemic lupus erythematosus, trichinosis, pityriasis rubra pilaris, psoriasis, and renal failure. Osler's nodes (shown) are painful, erythematous nodules, most commonly found on the pulp of fingers and toes. Osler's nodes are most often associated with subacute bacterial endocarditis and infection from S. viridans.

Slide 13.

After a few hours in the emergency department, despite anticoagulation and supplemental oxygen, the patient becomes increasingly dyspneic, tachypneic, and hypoxic. A repeat portable chest radiograph is obtained (shown). What is your interpretation of this chest radiograph? What findings are indicated in the region inside the circle? What findings are indicated by the arrow?

Image courtesy of Wikipedia Commons.

Slide 14.

Answer: The patient's chest radiograph indicates acute pulmonary edema. Note enlarged heart size, apical vascular redistribution (region inside the circle on the previous slide), and small bilateral pleural effusions (arrow on the previous slide). A cardiology consult is ordered, and an echocardiogram is performed in the ED. A magnified portion of a parasternal long axis view from a transthoracic echocardiogram is shown. A small curvilinear vegetation on the mitral valve is indicated (arrow), raising the suspicion for infective endocarditis (IE). The patient likely developed congestive heart failure due to acute left-sided valvular insufficiency.

Slide 15.

The image shows bacterial endocarditis involving the mitral valve. The left ventricle of the heart has been opened to show mitral valve fibrin vegetations (arrow). IE is an endovascular microbial infection of cardiovascular structures (e.g., native valves, ventricular endocardium, or atrial endocardium), including endarteritis of the large intrathoracic vessels (e.g., in a patent ductus arteriosus, arteriovenous shunts, or coarctation of the aorta) or of intracardiac foreign bodies (e.g., prosthetic valves, pacemaker or implantable cardioverter defibrillator leads, surgically created conduits) facing the bloodstream.[1]

Image courtesy of Wikipedia Commons.

Slide 16.

The bicuspid aortic valve with IE is shown. Note the bulky vegetations on the ventricular surfaces in this excised valve, with distortion of the valve surfaces. Trauma to the heart's endothelial surface can result in a nonbacterial thrombotic endocarditis. The platelet/fibrin thrombus that develops can then be seeded by a transient bacteremia, resulting in IE. These infections can cause localized tissue destruction and result in emboli.

Slide 17.

This algorithm shows how to use echocardiogram for the evaluation of suspected endocarditis. IE is by far the most common cardiovascular infection worldwide. Despite medical and surgical advances, this condition remains associated with considerable mortality and morbidity.[2] Abbreviations: ATEE, transesophageal echocardiogram; TTE, transthoracic echocardiogram.

Slide 18.

The Duke criteria (shown) are used for the diagnosis of infective endocarditis. Clinical diagnosis requires either 2 major criteria, 1 major and 3 minor criteria, or 5 minor criteria from the table.[3]

Slide 19.

In this aortic valve with healed endocarditis, note the gaping hole with the fibrous rim (arrow) and a small strand at the free edge. The hole is at the line of closure. The affected valve is the left cusp. Note that the right noncoronary cusp (immediately to the left) demonstrates a small, multichanneled fenestration at the commissure, immediately adjacent to similar fenestrations in the left coronary cusp. These fenestrations are physiologic lesions occurring with age and are unrelated to endocarditis.

Slide 20.

This image shows endocarditis with mitral valve destruction and vegetation. Note the posterior leaflet of the mitral valve, with an irregular vegetation on the atrial surface, resulting in valve destruction at the commissure between the anterior leaflet and the posterior leaflet.

Slide 21.

The majority of subacute disease caused by S. viridans infection (arrow) is related to dental disease, specifically to transient bacteremia secondary to gingivitis. Despite medical and surgical advances, infective endocarditis has continued to be associated with significant morbidity and mortality. Antimicrobial resistance continues to create therapeutic management issues for this life-threatening illness.[4]

Image courtesy of Wikipedia Commons.

Slide 22.

A postrheumatic mitral valve with infective endocarditis is shown. Note the defect in the scarred valve, with focal surface hemorrhage. The patient in this case underwent aortic valve replacement because there was contiguous infection. Infective endocarditis is an uncommon disease that is critically important for clinicians in many disciplines to understand because it is uniformly fatal if it is not diagnosed and properly treated. If a timely diagnosis is made and proper treatment is provided, many patients can recover fully and return to their previous state of health.[5]

Slide 23.

Contributor Information


Mark P. Brady, PA-C
Adjunct Faculty and Preceptor
Physician Assistant Program
University of New England
Physician Assistant
Department of Emergency Medicine
Cambridge Hospital, Cambridge Health Alliance
Cambridge, Massachusetts

Disclosure: Mark P. Brady, PA-C, has disclosed no relevant financial relationships.


Michael Stuart Bronze, MD
Professor, Stewart G. Wolf Chair in Internal Medicine
Department of Medicine
University of Oklahoma Health Science Center
Oklahoma City, Oklahoma

Disclosure: Michael Stuart Bronze, MD, has disclosed no relevant financial


  1. Habib G, Hoen B, Tornos P, et al. Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Eur Heart J. 2009;30:2369-2413.
  2. Fedeli U, Schievano E, Buonfrate D, et al. Increasing incidence and mortality of infective endocarditis: a population-based study through a record-linkage system. BMC Infect Dis. 2011;11:48.
  3. Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med. 1994;96(3):200-209.
  4. Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis: 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: endorsed by the Infectious Diseases Society of America [errata, Circulation. 2007;116(21):e547; Circulation. 2005;112(15):2373; Circulation. 2008;118(12):e497; Circulation. 2007;115(15):e408]. Circulation. 2005;111(23):e394-e434.
  5. Brusch J. Infective Endocarditis: Management in the Era of Intravascular Devices. New York, NY: Informa Healthcare; 2007.