Pulmonary embolism

My patient with pulmonary embolism also reports new-onset hiccups. Are the two conditions related?

FA Manian MD, MPH, , , , Leave a comment

Hiccups (AKA singultus) are due to the involuntary contraction of the inspiratory muscles, especially the diaphragm. The hiccup reflex involves an afferent limb ( eg, the phrenic and vagus nerves, sympathetic fibers from T6-T12,  brainstem) and an efferent limb, primarily the phrenic nerve1,2.  Thus, the irritation of any part of the arc in the head, neck, chest, or abdomen may potentially lead to hiccups.

Conditions involving the chest cavity that may be associated with hiccups include lung cancer, GERD, herpetic esophagitis, myocardial ischemia, bronchitis, empyema, lung masses, pneumonia, pleuritis, and pacemaker lead injury 1-3.

Reports of patients with PE and persistent hiccups (lasting longer than 48 h) have also appeared in the literature1,3. Of interest, in a report involving 3 patients, 2 had submassive or “large” PE, with one displaying the classic EKG changes of S1Q3T3; the size of PE in another was not reported1.  In another case report, PE was “not small” and involved the anterior and lateral lower lobe segments of pulmonary artery2.  Although the exact mechanism of PE causing hiccups is not clear, irritation of the afferent or efferent limb of the reflex arc in the chest has been postulated.  

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References

  1. Hassen GW, Singh MM, Kalantari H, et al. Persistent hiccups as a rare presenting symptom of pulmonary embolism. West J Emerg Med 202;13:479-483.
  2. Durning SJ, Shaw DJ, Oliva AJ et al. Persistent hiccups as the presenting symptom of a pulmonary embolism. Chest Disease Reports 2012;2:e2.
  3. Buyukhatipoglu H, Sezen Y, Yildiz A, et al. Hiccups as a sign of chronic myocardial ischemia. S Med J 2010;103: 1184-85.
My patient with pulmonary embolism also reports new-onset hiccups. Are the two conditions related?

Should I routinely consider the possibility of pulmonary embolism (PE) in my patients hospitalized for syncope?

FA Manian MD, MPH, , , , , , Leave a comment

Syncope is a well-known initial manifestation of pulmonary embolism (PE)1.  However, given the varied causes of syncope, determining the prevalence of PE among patients hospitalized for syncope is important.   

A multicenter prospective study2 enrolled 560 patients not already on anticoagulation who were hospitalized for a first episode syncope.  Of patients who had either a high pretest probability for PE, positive D-dimer assay or both, PE was diagnosed in 17%, or nearly 1 of 6 of enrolled patients, based on CT or ventilation/perfusion scan. PE was found more frequently among patients with syncope of undetermined cause than those with an alternative explanation (25.4% vs 12.7%). 

Another multicenter prospective study (2019), however, found a much lower prevalence of PE (0.6%) among patients evaluated in the ED for syncope, including those who were not hospitalized.3 A related commentary on the article reported a prevalence of 4.1% in the total study population, assuming a “worst-case scenario calculation.” 4 

Given these divergent results, perhaps the best advice is to consider PE as cause of syncope in the proper context and minimize overtesting when suspicion remains low.

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References 

  1. Thames MD, Alpert JS, Dalen JE. Syncope in patients with pulmonary embolism. JAMA 1977;238:2509-2511. https://www.ncbi.nlm.nih.gov/pubmed/578884
  2. Prandoni P, Lensing AWA, Prins MH, et al. Prevalence of pulmonary embolism among patients hospitalized for syncope. N Engl J Med 2016;375:1524-31. http://www.nejm.org/doi/full/10.1056/NEJMoa1602172
  3. Thiruganasambandamoorthy V, Sivilotti MLA, Rowe BH, et al. Prevalence of pulmonary embolism among emergency department patients with syncope: a multicenter prospective cohort study [published online January 25, 2019]. Ann Emerg Med. doi:10.106/j.annemergmed.2018. https://www.annemergmed.com/article/S0196-0644(18)31535-X/fulltext
  4. Anonymous. Pulmonary embolism uncommon in syncope hospitalizations. Pulmonology Advisor. February 6, 2019.  https://www.pulmonologyadvisor.com/pulmonary-embolism-uncommon-in-syncope-hospitalizations/printarticle/832069/

 

Contributed in part by Rebecca Berger  MD, Department of Medicine, Mass General Hospital, Boston, MA

 

Should I routinely consider the possibility of pulmonary embolism (PE) in my patients hospitalized for syncope?

My patient with significant dyspnea appears to have an acute exacerbation of his chronic obstructive pulmonary disease (AE-COPD). How often do AE-COPD and pulmonary embolism (PE) coexist?

FA Manian MD, MPH, , , , , , , , , , Leave a comment

Simultaneous presence of PE in patients with AE-COPD is not rare, particularly in those with unexplained AE-COPD.

A recent systematic review and meta-analysis reported a pooled PE prevalence of 16.1% (95% C.I. 8.3%-25.8%) in unexplained AE-COPD, with 68% of emboli found in the main pulmonary arteries, lobar arteries or inter-lobar arteries (i.e. not subsegmental); the pooled prevalence of deep venous thrombosis (DVT) was 10.5% (95% C.I. 4.3%-19.0%) 1. Pleuritic chest pain and signs of cardiac failure were associated with AE-COPD, while symptoms suggestive of a respiratory tract infection argued against PE.

It remains unclear, however, if the threshold for evaluation of venous thromboembolism (VTE) should necessarily differ between patients with explained vs unexplained AE-COPD.

In one small study, the prevalence of VTE in “unexplained” AE-COPD was significantly higher (25%) than “explained” AE-COPD (including cases with  tracheobronchitis, pneumonia, cardiac disorders, exposure to irritant inhalants, and lack of compliance with treatment), but the VTE prevalence for the latter group was still 8.4%2.  Serum D-dimer level and Wells criteria may help exclude VTE in this patient population.

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References

  1. Aleva FE, Voets LWLM, Simons SO, et al. Prevalence and localization of pulmonary embolism in unexplained acute exacerbations of COPD: A systematic review and meta-analysis. CHEST (2016), doi: 10.1016/j.chest.2016.07.034.
  2. Gunen H, Gulbas G, In E, Yetkin O, Hacievliyagil SS. Venous thromboemboli and exacerbations of COPD. Eur Respir J 2010;35:1243-1248.

 

Contributed by Jeff Greenwald, MD, Core Educator Faculty, Department of Medicine, Massachusetts General Hospital

My patient with significant dyspnea appears to have an acute exacerbation of his chronic obstructive pulmonary disease (AE-COPD). How often do AE-COPD and pulmonary embolism (PE) coexist?

What complication of Behçet’s syndrome carries the highest mortality?

FA Manian MD, MPH, , , Leave a comment

Behçet’s syndrome may cause life-threatening hemoptysis due to pulmonary artery aneurysms.1 In a cohort of 387  patients with such syndrome followed for over 20 years, massive hemoptysis was the leading cause of death, found most commonly early in the course of the disease among young men.2 Conversely, the one-year mortality of pulmonary artery aneurysm in Behçet’s may be greater than 50%.1 Behçet’s syndrome is the only vasculitic disease with a proclivity for large pulmonary vessels, while its less frequent pulmonary manifestations, such as fibrosis and thrombosis, overlap with other small vessel vasculitides.3 Beware that the initial presentation of pulmonary aneurysm rupture may be confused with that of pulmonary embolism, with potential for fatal complications from anticoagulation.1 CT angiogram should help in distinguishing the two conditions.

 

References 

  1. Uzun O, Akpolat T, Erkan L. Pulmonary vasculitis in behcet disease: a cumulative analysis. Chest. 2005;127(6):2243-2253.
  2. Kural-Seyahi E, Fresko I, Seyahi N, et al. The long-term mortality and morbidity of Behçet syndrome: a 2-decade outcome survey of 387 patients followed at a dedicated center. Medicine (Baltimore). 2003;82(1):60-76.
  3. Hamuryudan V, Er T, Seyahi E, et al. Pulmonary artery aneurysms in Behçet syndrome. Am J Med. 2004;117(11):867-870.

 

Contributed by Sam Slavin, Harvard Medical Student

What complication of Behçet’s syndrome carries the highest mortality?

My patient with chronic alcoholism is showing signs of alcohol withdrawal even though his blood alcohol level (BAL) is still elevated. Is this possible?

FA Manian MD, MPH, , , , , , Leave a comment

Absolutely! For patients with chronic alcohol dependence, any acute decline in their BAL may precipitate withdrawal (1).

For example, if a patient typically drinks enough alcohol on a daily basis to sustain a BAL of 350 mg/dl, any significant drop in BAL (e.g. down to 125 mg/dl) may be associated with early signs of withdrawal such as nervousness, tachycardia and elevated blood pressure.

Another scenario that could lead to withdrawal symptoms despite an elevated BAL involves patients who use both alcohol and benzodiazepines chronically. In such patients— because the 2 substances have cross-reactive effects on the brain— a significant reduction in the dose or frequency of benzodiazepines may also lead to withdrawal despite an elevated BAL.  Also remember that symptoms of benzodiazepine withdrawal may begin within 24 h or up to 2 weeks following its cessation (2).

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Reference

  1. Roffman JL, Stern TA.  Alcohol withdrawal in the setting of elevated blood alcohol levels. Prim Care Companion J Clin Psychiatry. 2006; 8(3):170-173 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1540391/
  2. Greenberg MI. Benzodiazepine withdrawal: potentially fatal, commonly missed, Emergency Medicine News 2001;23:18. https://journals.lww.com/em-news/pages/articleviewer.aspx?year=2001&issue=12000&article=00013&type=Fulltext

 

Contributed by Stephanie Meller, MD, Boston, MA

 

 

My patient with chronic alcoholism is showing signs of alcohol withdrawal even though his blood alcohol level (BAL) is still elevated. Is this possible?

How should I choose between the direct oral anticoagulants (DOACs)?

FA Manian MD, MPH, , , , Leave a comment

Although warfarin has long been the standard treatment for venous thromboembolism (VTE) and thomboprophylaxis in atrial fibrillation (AF), the need for its frequent monitoring, potential drug interactions, and narrow therapeutic window made it far from ideal.

Since 2009, DOACs have become viable alternative agents owing to their more predictable and safer pharmacological profiles. DOACs include several direct factor Xa inhibitors (apixaban, rivaroxaban, edoxaban) and a direct thrombin inhibitor (dabigatran). Approved indications include: (1) thromboprophylaxis in nonvalvular AF; (2) treatment of deep venous thrombosis or pulmonary embolism; and (3) primary prevention of postoperative VTE. 

Compared to warfarin, DOACs are associated with a reduced risk of intracranial hemorrhage, and in the case of apixaban, lower risk of gastrointestinal bleeding; rivaroxaban and edoxaban have been associated with a higher risk of gastrointestinal bleeding.  

Apixaban is also the only NOAC whose dose can be safely reduced in chronic kidney disease, including those on hemodialysis. 

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References

 

1. Baber U, Mastoris I, and Mehran R. Balancing ischaemia and bleeding risks with novel oral anticoagulants. Nat Rev Cardiol 2014;11:693-703.  https://www.ncbi.nlm.nih.gov/pubmed/25367652 

2. Ansell JE. Universal, class-specific, and drug-specific reversal agents for the new oral anticoagulants. J Thromb Thrombolysis 2016;41:248-52. https://www.ncbi.nlm.nih.gov/pubmed/26449414

 

Contributed by William L. Hwang, MD, Mass General Hospital, Boston, MA

How should I choose between the direct oral anticoagulants (DOACs)?

Can syncope be related to acute pulmonary embolism in the absence of hemodynamic instability or right ventricular failure?

FA Manian MD, MPH, , , , , , , , , Leave a comment

Although we often think of syncope caused by acute pulmonary embolism (APE) in the setting of submassive or massive APE and right ventricular failure or shock (1,2), less massive APE may potentially cause syncope as well by triggering a vaso-vagal reflex (3).

For sure, a significant association between submassive or massive APE and syncope has been reported (1,2).  More specifically, patients with syncope and APE may be more likely to have systolic blood pressure <90 mmHg, right ventricular dilation and right ventricular hypokinesis (1). Another study reported a higher rate of central embolism (83% vs 43%), right ventricular dysfunction (91% vs 68%) and troponin positivity (80% vs 39%), but not 30 day mortality (2).

In contrast, 1 study found that patients with syncope as a presenting symptom of APE did not show a more serious clinical picture (e.g. shock) than those without syncope (3), while another found EKG signs of acute right ventricle overload in only 25% of patients with syncope (4).  

So while massive APEs may be associated with syncope, they don’t seem to be a prerequisite for this condition.

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References

1.  Omar HR, Mirsaeidi M, Weinstock MB, et al. Syncope on presentation is a surrogate for submassive and massive acute pulmonary embolism. Am J Emerg Med 2018;36:297-300. https://www.ncbi.nlm.nih.gov/pubmed/29146419

2. Altinsoy B, Erboy F, Tanriverdi H, et al. Syncope as a presentation of acute pulmonary embolism. Ther Clin Risk Manag 2016;12:1023-28. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4930221/

3. Castelli R, Tarsia P, Tantardini G et al. Syncope in patients with pulmonary embolism: comparison between patients with syncope as the presenting symptom of pulmonary embolism and patients with pulmonary embolism without syncope. Vascular Medicine 2003;8:257-261. https://journals.sagepub.com/doi/abs/10.1191/1358863x03vm510oa

4. Miniati M, Cenci, Monti S, et al. Clinical presentation of acute pulmonary embolism: survey of 800 cases. PloS One 2012;7:e30891.

 

 

Can syncope be related to acute pulmonary embolism in the absence of hemodynamic instability or right ventricular failure?

Is anticoagulation (AC) therapy recommended for treatment of vein thrombosis of upper extremities?

FA Manian MD, MPH, , , , Leave a comment

The short answer is “yes” when deep veins, such as brachial, axillary or subclavian are involved; cephalic and basilic veins are superficial. Although some have suggested that isolated brachial vein thrombosis may be considered at low risk of complication, this assumption has not been corroborated by objective research (1).

There are no randomized trials of AC therapy in patients with upper extremity deep vein thrombosis (UEDVT).  However,  the American College of Chest Physicians has recommended a 3-month course of AC therapy similar to that of leg DVT for several reasons (1,2):

  •  UEDVT has generally been reported to have complications and consequences comparable to that of leg DVT
  •  Several small cohort studies suggest lower rates of recurrent DVT, PE, and bleeding when UEDVT is treated similar to leg DVT
  •  Known demonstrated benefit of AC therapy in leg DVT

In addition, post-thrombotic syndrome is relatively common (~1 in 5) among patients with UEDVT (3)

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References

1.  Hingorani A, Ascher E, Marks N, et al. Morbidity and mortality associated with brachial vein thrombosis. Ann Vasc Surg 2006; 20:297-299. https://www.ncbi.nlm.nih.gov/pubmed/16779509

2. Kearon C, Akl EA, Comerato AJ, et al. Antithrombotic therapy for VTE disease: American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis Panel. Antithrombotic therapy for VTE disease: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest 2012;141(suppl):419S-494S. https://www.ncbi.nlm.nih.gov/pubmed/22315268

3. Maynard G. Upper extremity deep vein thrombosis:A call to arms. JAMA Intern Med 2014;696-698. https://www.ncbi.nlm.nih.gov/pubmed/24638129

Is anticoagulation (AC) therapy recommended for treatment of vein thrombosis of upper extremities?

How good are arterial blood gases in ruling out pulmonary embolism (PE)?

FA Manian MD, MPH, , Leave a comment

Not as good as one would hope! 

In an often quoted study involving 768 patients with suspected PE who underwent angiography, a combination of normal A-a gradient (<20 mm Hg ), normal PaO2 (>80 mm Hg), and normal PaCO2 (>35 mm Hg) was examined to help exclude PE (1). Among patients with no known cardiopulmonary disease and normal values in all 3 parameters,  over 30% still had PE, while among those with cardiopulmonary disease and normal parameters 17% had PE.  

In short, normal arterial blood gases may make PE less likely, they do not by any means exclude the possibility of PE.

Reference

  1. Stein PD, Goldhaber SZ, Henry JW, et al. Arterial blood gas analysis in the assessment of suspected acute pulmonary embolism. CHEST 1996; 109:78-81. https://www.ncbi.nlm.nih.gov/pubmed/8549223

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How good are arterial blood gases in ruling out pulmonary embolism (PE)?