Medical Image of the Week: Wolff-Parkinson-White Syndrome

Figure 1. Presenting EKG with supraventricular tachycardia at rate of 232.

Figure 2. Post-conversion EKG demonstrating a short PR interval, slurring of the initial QRS upslope (delta wave), widened QRS, and ST-T repolarization change; characteristic of Wolff-Parkinson-White Syndrome.

A 38-year-old man developed sustained rapid heart rate while rock climbing. The patient reported that he had experienced rare bouts of self-limited palpitations in the past. Blood pressure on arrival to the emergency department was 112/ 65 mm Hg. The patient’s initial EKG demonstrated a regular, narrow complex supraventricular tachycardia, with a rate of 232 (Figure 1). Intravenous adenosine was administered with no change in his rate or rhythm. The patient then received amiodarone by intravenous bolus, with subsequent conversion to sinus rhythm (Figure 2).

Wolff-Parkinson-White (WPW) syndrome is a congenital cardiac condition present in approximately 0.15% of the general population. WPW is characterized by the abnormal presence of conduction tissue that creates an accessory atrioventricular pathway and thus potentiates reentrant tachycardia (1). The classic resting EKG findings in WPW are: a shortened PR interval (less than 0.12 seconds), an indistinct initial upslope of the QRS complex (known as the delta wave), a widened QRS complex (0.12 seconds or greater), and ST-T repolarization changes (2). In WPW presenting as a narrow complex tachycardia without hypotension, the initial treatment is adenosine or a calcium channel blocker, followed by amiodarone if unsuccessful. If the presenting rhythm is atrial fibrillation, atrial flutter, or an undefined wide complex tachycardia without hypotension, amiodarone is used. A hemodynamically unstable rhythm warrants immediate electrical cardioversion. Definitive evaluation and treatment of WPW requires electrophysiologic mapping and subsequent ablation of the accessory pathway.

Charles Van Hook MD, Cristina Demian MD, Douglas Tangel MD, Jennifer Blair MD, and Lisa Patel MD

Avista Adventist Hospital

Louisville, Colorado USA

References

1. Katritsis DG, Camm AJ. Atrioventricular nodal reentrant tachycardia. Circulation. 2010 Aug 24;122(8):831-40. [CrossRef] [PubMed]
2. Mark DG, Brady WJ, Pines JM. Preexcitation syndromes: diagnostic consideration in the ED. Am J Emerg Med. 2009 Sep;27(7):878-88. [CrossRef] [PubMed]
3. Khairy P, Van Hare GF, Balaji S, et al. PACES/HRS expert consensus statement on the recognition and management of arrhythmias in adult congenital heart disease. Heart Rhythm. 2014 Oct;11(10):e102-65. [CrossRef] [PubMed]

Cite as: Van Hook C, Demian C, Tangel D, Blair J, Patel L. Medical image of the week: Wolff-Parkinson-White syndrome. Southwest J Pulm Crit Care. 2017;14(4):164-5. doi: https://doi.org/10.13175/swjpcc046-17 PDF 

Medical Image of the Week: Acute Amiodarone Pulmonary Toxicity

Figure 1. Chest X-ray showing diffuse interstitial markings, right upper lobe consolidation, small pleural effusions, thoracotomy wires and external leads.

Figure 2. Axial image of the thoracic CT scan showing increased interstitial markings, ground glass opacities and bilateral pleural effusions.

A 71 year old man with a medical history significant for chronic obstructive pulmonary disease, coronary artery disease with post-operative status coronary artery bypass grafting, heart failure with reduced ejection fraction (25%) and atrial fibrillation/flutter underwent an elective ablation of the tachyarrhythmia at another facility and was prescribed amiodarone post procedure. He started complaining of cough and dyspnea one day post procedure and was empirically treated with 2 weeks of broad spectrum antibiotics. He subsequently was transferred to our facility due to worsening symptoms. He also complained of nausea, anorexia with resultant weight loss since starting amiodarone, which was stopped 5 days prior to transfer. Infectious work up was negative.

On arrival to our facility, he was diagnosed with small sub-segmental pulmonary emboli, pulmonary edema and possible acute amiodarone toxicity. His was profoundly hypoxic requiring high flow nasal cannula or 100% non-rebreather mask at all times. His symptoms persisted despite antibiotics, diuresis, anticoagulation and heart rate control. Steroid therapy was then initiated for acute amiodarone toxicity. Although he reported some improvement in symptoms 2-3 days after initiation of steroids, his oxygen requirement did not improve. Unfortunately he suffered a cardiac arrest on day 10 of admission and did not survive.

Amiodarone is a class B anti-arrhythmic used to treat multiple supraventricular and ventricular tachyarrhythmias. Its adverse effects are usually dose and duration dependent. Amiodarone pulmonary toxicity (APT) has been shown to correlate with total cumulative dose; however acute reactions to amiodarone toxicity have previously been reported. Men are at increased risk for APT, and this risk increases with age and those with pre-existing lung conditions. Diagnosis of APT is predominantly a diagnosis of exclusion; however laboratory tests may show leukocytosis with neutrophil predominance (as in our patient) and imaging may provide a clue for diagnosis. Chest x-ray reveals patchy or diffuse infiltrates, which may have predominance in the upper lobes, particularly the right upper lobe (as in our patient). A thoracic CT scan may show bilateral alveolar or interstitial infiltrates with higher attenuation, secondary to the iodine component of the drug. The current mainstay of treatment is discontinuation of the drug permanently along with steroid therapy typically, 40-60 mg of prednisone a day for an extended period of time.  

Konstantin Mazursky DO¹, Bhupinder Natt MD², Laura Meinke MD^1,2

¹Department of Internal Medicine.

²Division of Pulmonary, Critical Care, Allergy and Sleep

Banner-University Medical Center

Tucson AZ

Reference

1. Wolkove N, Baltzan M. Amiodarone pulmonary toxicity. Can Respir J. 2009;16(2):43-8. [PubMed] 

Cite as: Mazursky K, Natt B, Meinke L. Medical image of the week: acute amiodarone pulmonary toxicity. Southwest J Pulm Crit Care. 2015;11(4):189-90. doi: http://dx.doi.org/10.13175/swjpcc099-15 PDF

Medical Image of the Week: Increased Liver Attenuation

Figure 1. Coronal (A) and axial (B) CT scan without contrast demonstrating diffuse increase in hepatic density.

An 86-year old man had a non-contrast thoracic CT for evaluation of a chest x-ray abnormality. Incidentally, the CT scan showed diffuse increase in liver density with Hounsfield units of 105. The normal unenhanced attenuation value is between 55-65 Hounsfield units in a normal liver on CT scan without contrast (1).   Hepatic attenuation is reflected in Hounsfield values and depends on combinations of factors including the presence or absence (as well as phase) of IV contrast administration.

The patient had no known underlying liver disease and liver function studies were within normal limits.  Figure 1 shows coronal and axial views of the CT scan of the patient.

There are several intrinsic liver pathologies leading to diffuse changes in liver attenuation including (2):

• Deposits of certain metals seen in hemochromatosis, hemosiderosis, and Wilson’s disease.
• Glycogen storage disease(es)
• Medications/drugs including amiodarone and gold therapy (3-7).
• Previous Thorotrast administration – Thorotrast is a contrast agent used between 1930-1950 and was found to be carcinogenic and can cause hepatic angiosarcoma, cholangiocarcinoma, and hepatocellular carcinoma. It is retained in the reticulo-endothelial system for long periods of time (8).

After reviewing the patient’s case he had been on chronic amiodarone therapy and had not had exposures or clinical history related to any of the other above causes of increased hepatic density. Based on imaging and history it is suspected that patient’s diffuse increase in liver density is secondary to iodine infiltration from chronic amiodarone usage.

Allen Thomas MD, Sandra Till DO, and Jeremy Patterson RT

Phoenix VA Medical Center

References

1. Boll DT, Merkle EM. Diffuse liver disease: strategies for hepatic CT and MR imaging. Radiographics. 2009;29:1591-614. [CrossRef] [PubMed]
2. Weerakkody Y. Hepatic attenuation on CT. Radiopaedia. Available at: http://radiopaedia.org/articles/hepatic-attenuation-on-ct (accessed 2/6/14).
3. Markos J, Veronese ME, Nicholson MR, McLean S, Shevland JE. Value of hepatic computerized tomographic scanning during amiodarone therapy. Am J Cardiol. 1985;56(1):89-92. [CrossRef] [PubMed]
4. Nicholson AA, Caplin JL, Steventon DM. Measurement of tissue-bound amiodarone and its metabolites by computed tomography. Clin Radiol. 1994;49(1):14-8. [CrossRef] [PubMed]
5. De Maria M, De Simone G, Laconi A, Mercadante G, Pavone P, Rossi P. Gold storage in the liver; appearance on CT scans. Radiology. 1986;159(2):355-6. [PubMed] 
6. Goldman IS, Winkler ML, Raper SE, Barker ME, Keung E, Goldberg HI, Boyer TD. Increased hepatic density and phospolipidosis due to amiodarone. AJR Am J Roentgenol. 1985;144(3):541-6. [CrossRef] [PubMed] 
7. Kojima S, Kojima S, Ueno H, Takeya M, Ogawa H. Increased density of the liver and amiodarone-associated phospholipidosis. Cardiol Res Pract. 2009;2009:598940. [CrossRef] [PubMed]
8. Weber E, Laarbaui F, Michel L, Donckier J. Abdominal pain: do not forget Thorotrast! Postgrad Med J. 1995;71(836):367-8. [CrossRef] [PubMed] 

Reference as: Thomas AR, Till S, Patterson J. Medical image of the week: increased liver attenuation. Southwest J Pulm Crit Care. 2014;8(2):105-7. doi: http://dx.doi.org/10.13175/swjpcc011-14 PDF