My patient recently underwent total knee arthroplasty (TKA) and is now found to have a Baker’s cyst. Is Baker’s cyst a postoperative complication of TKA?

Not likely! There is no evidence that TKA causes Baker’s cyst (also known as popliteal cyst). Instead, the finding of Baker’s cyst following TKA may be best explained by its well-known association with osteoarthritis, one of the main indications for TKA.1,6,7

In a study of 2025 patients who underwent primary TKA, 0.6% were diagnosed with Baker’s cysts within 6 weeks to 2 years postoperatively (75% symptomatic), but whether the cysts were present prior to TKA was unclear. There was no reported association between surgical technique or perioperative course and Baker’s cyst diagnosis.9

Actually, there might be a correlation between TKA and Baker’s cyst resolution.2,3 Among patients with known cysts preoperatively, 15% and 67% of patients may experience resolution of the cyst at 1 year and 4-6 years following surgery, respectively. 2,3

A Baker’s cyst is a fluid-filled pocket in the posterior aspect of the knee, typically seen in adults with degenerative changes in the patellofemoral joint, as may occur with meniscal tears and arthritis. When symptomatic, it can be treated non-operatively with ultrasound-guided aspiration and corticosteroid injection or operatively with surgical excision or attempted repair of the underlying defect. 4,8

 

Bonus Pearl: Did you know that the ‘crescent sign’ (bruising below the medial malleolus associated with fluid from ruptured cyst moving inferiorly toward the ankle) was first described in 1976 and may help distinguish calf pain due to Baker’s cyst from that of deep venous thrombophlebitis? 5

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 Contributed by Anamika Veeramani, Medical Student, Harvard Medical School

 

References

  1. Guermazi A., Hayashi D., Roemer F, et al. Cyst-like lesions of the knee joint and their relation to incident knee pain and development of radiographic osteoarthritis: The MOST study. Osteoarthritis and Cartilage 2010; 18:1386-1392. doi:10.1016/j.joca.2010.08.015. https://pubmed.ncbi.nlm.nih.gov/20816978/
  2. Hommel H., Becker R., Fennema P., et al. (2020). The fate of Baker’s cysts at mid-term follow-up after total knee arthroplasty. The Bone & Joint Journal, 2020;102-B(1):132-136. doi:10.1302/0301-620x.102b1.bjj-2019-0273.r2. https://pubmed.ncbi.nlm.nih.gov/31888367/
  3. Hommel, H., Perka, C., Kopf, S. The fate of Baker’s cyst after total knee arthroplasty. The Bone & Joint Journal 2016;98-B(9):1185-1188. doi:10.1302/0301-620x.98b9.37748. https://pubmed.ncbi.nlm.nih.gov/27587518/
  4. Leib AD, Roshan A, Foris LA, et al. Baker’s Cyst. [Updated 2020 Mar 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430774/
  5. Mizumoto, J. The crescent sign of ruptured baker’s cyst. Journal of General Family Medicine, 2019;20(5): 215-216. doi: 10.1002/jgf2.261. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6732489/
  6. Rupp, S., Seil, R., Jochum, P., & Kohn, D. Popliteal Cysts in Adults. The American Journal of Sports Medicine 2002; 30(1): 112-115. doi:10.1177/03635465020300010401. https://pubmed.ncbi.nlm.nih.gov/11799006/
  7. Sansone, V., Ponti, A. D., Paluello, G. M., & Maschio, A. D. Popliteal cysts and associated disorders of the knee. International Orthopaedics 1995;19(5): 275-279. doi:10.1007/bf00181107. https://pubmed.ncbi.nlm.nih.gov/8567131/
  8. Smith, M., Lesniak, B., Baraga, M., Kaplan, L., Jose, J. Treatment of Popliteal (Baker) Cysts with Ultrasound-Guided Aspiration, Fenestration and Injection: Long-term Follow-up. Sports Health 2015; 7(5): 409-414. doi: 10.1177/1941738115585520. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547114/
  9. Tofte, J. N., Holte, A. J., & Noiseaux, N. Popliteal (Baker’s) Cysts in the Setting of Primary Knee Arthroplasty. The Iowa Orthopedic Journal 2017;37:177-180. https://pubmed.ncbi.nlm.nih.gov/28852354/

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My patient recently underwent total knee arthroplasty (TKA) and is now found to have a Baker’s cyst. Is Baker’s cyst a postoperative complication of TKA?

Is intermittent pneumatic compression effective in reducing the risk of deep vein thrombosis in non-surgical hospitalized patients at high risk of major bleed?

The weight of the evidence to date suggests that intermittent pneumatic compression (IPC) is effective in reducing the risk of deep venous thrombosis (DVT) in hospitalized patients with stroke. 1,2 Whether IPC is also effective in non-surgical hospitalized patients without stroke at high risk of DVT and major bleed needs further studies.

A 2013 multicenter randomized trial (CLOTS 3) involving over 2,000 immobile hospitalized patients post-stroke found a significantly lower risk of DVT in proximal veins or any symptomatic DVT in the proximal veins within 30 days of randomization (8.5% vs 12.1%; absolute reduction risk 3.6%, 95% C.I. 1.4-5.8). Of note, the rate of concurrent heparin or low molecular weight heparin (LMWH) prophylaxis was similar between the 2 groups (17%). 1

A meta-analysis including the CLOTS 3 study and 2 other smaller trials 2 in patients with stroke found a risk reduction for proximal DVT (O.R. 0.66, 95% C.I 0.52-0.84) with nearly significant reduction in deaths by the end of the treatment period (O.R. 0.81, 95% 0.65-1.01).1

Although IPC may also be effective in non-surgical hospitalized patients without stroke but at high risk of DVT and bleed, proper trials in this patient population is lacking. In fact, the 2012 American College of Chest Physicians guidelines on antithrombotic therapy and prevention of thrombosis classifies use of IPC in preventing DVT’s in non-surgical acutely ill hospitalized patients as category 2C recommendation (weak, low quality evidence). 3

The patient population and methodology of above studies should be distinguished from those of a 2019 published trial involving only critically ill patients—all receiving pharmacologic thromboprophylaxis—which reported no reduction in the incidence of proximal lower-limb DVT with the addition of IPC. 4

 

Bonus Pearl: Did you know that venous thromboembolism has been reported in up to 42% of hospitalized patients who have had a stroke? 1

 

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References

  1. Dennis M, Sandercock P, Reid J, et al. Effectiveness of intermittent pneumatic compression in reduction of risk of deep vein thrombosis in patients who have had a stroke (CLOTS 3): a multicenter randomized controlled trial. Lancet 2013;382:516-24. https://www.thelancet.com/cms/10.1016/S0140-6736(13)61050-8/attachment/1a0438d2-86eb-4da1-8bdb-92c0aec18b8d/mmc1.pdf
  2. Naccarato M, Chiodo Grandi F, Dennis M, et al. Physical methods for preventing deep vein thrombosis in stroke. Cochrance Database Syst Rev 2010;8:CD001922. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD001922.pub3/full
  3. Guyatt GH, Akl EA, Crowther M, et al. Executive summary: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. CHEST 2012;141 (suppl):7S-47S. http://www.sphcs.org/workfiles/CardiacVascular/7S-full.pdf
  4. Arabi YM, Al-Hameed F, Burns KEA, et al. Adjunctive intermittent pneumatic compression for venous thromboprophylaxis. N Engl J Med 2019;380:1305-15. https://pubmed.ncbi.nlm.nih.gov/30779530/

 

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Is intermittent pneumatic compression effective in reducing the risk of deep vein thrombosis in non-surgical hospitalized patients at high risk of major bleed?

What’s the evidence that patients with Covid-19 are at high risk of blood clots?

Although we often think of it as a respiratory disease, emerging evidence suggests that Covid-19, particularly when severe,  is also associated with high risk of thrombotic events, including pulmonary embolism, venous thrombosis, and arterial thrombotic events.1

A Chinese study found that ICU patients with severe Covid-19 had a venous thromboembolism (VTE) incidence of 25%, with disseminated intravascular coagulopathy (DIC) found in the majority of fatal cases.2

A prospective Dutch study involving critically ill ICU patients with Covid-19 reported VTE in 27% and arterial thrombotic events in another 3.7%, despite standard VTE prophylaxis.3 The authors suggested the use of “high prophylactic doses” of anticoagulants in these patients due to concern over hypercoagulability.

An ICU French study also found high frequency of thrombotic complications in Covid-19 patients with ARDS, with 11.7% of patients having pulmonary embolism vs 2.1% in non-Covid-19 patients with ARDS. As with the Dutch study, thrombotic complications occurred despite standard prophylactic anticoagulation.4

Postmortem studies have also shown marked changes in lung microvasculature with the presence of microthrombi, with some calling it “pulmonary intravascular coagulopathy” to distinguish it from DIC.1

A NEJM letter reported 5 Covid-19 patients less than 50 years of age who presented with large vessel stroke symptoms without an alternative explanation.5 Of interest, 2 of these patients had no other symptoms suggestive of Covid-19.  A pre-print article from China reported an acute stroke incidence of 5% in hospitalized patients with Covid-19.6

The finding of a hypercoagulable state in patients with severe Covid-19 is not surprising given the frequent association of this infection with a high inflammatory state and the well-known capability of SARS-CoV-2 to attack the endothelial surfaces of blood vessels. High inflammatory state can promote activation of blood coagulation through release of inflammatory cytokines (eg, IL-6, IL-8, and TNF-alpha).1

Perhaps even more intriguing is the finding of extremely high levels of factor VIII found in some Covid-19 patients which could make them hypercoagulable.7 This phenomenon should be suspected when a patient appears to be resistant to anticoagulation by heparin based on aPTT but not based on anti-Xa assay.7

 Bonus pearl: Did you know that the overall incidence of VTE is lowest among Asians-Pacific islanders, followed by Hispanics and Caucasians, with highest rate among African-Americans? 1 ,8

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References

  1. Fogarty H, Townsend L, Cheallaigh CN, et al. COVID-19 coagulopathy in Caucasian patients. Br J Haematol 2020, https://onlinelibrary.wiley.com/doi/epdf/10.1111/bjh.16749
  2. Cui S, Chen S, Li X, et al. Huang C, Wang Y, Li X, et al. Prevalence of venous thromboembolism in patients with severe novel coronavirus pneumonia. J Thromb Haematol 2020, April 9. https://onlinelibrary.wiley.com/doi/epdf/10.1111/jth.14830
  3. Klok FA, Kruip MJHA, van der Meer NJM, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res 2020. https://www.sciencedirect.com/science/article/pii/S0049384820301201?via%3Dihub
  4. Helms J, Tacquard C, Severac F, et al. High risk of thrombosis in patients in severe SARS-CoV-2 infection: a multicenter prospective cohort study. Intensive Care Med 2020; https://www.esicm.org/wp-content/uploads/2020/04/863_author_proof.pdf
  5. Oxley TJ, Mocco J, Majidie S, et al. Large-vessel stroke as a presenting feature of Covid-19 in the young. N Engl J Med. 2020, April 28. https://www.nejm.org/doi/full/10.1056/NEJMc2009787?query=featured_home
  6. Li Y, Wang M. Acute cerebrovascular disease following COVID-19: A single center, retrospective, observational study. 2020. https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3550025
  7. Beun R, Kusadasi N, Sikma M, et al. Thromboembolic events and apparent heparin resistance in patients infected with SARS-CoV-2. Int J Lab Hematol 2020, April 20. https://onlinelibrary.wiley.com/doi/abs/10.1111/ijlh.13230
  8. White RH, Keenan CR. Effects of race and ethnicity on the incidence of venous thromboembolism. Thromb Res 2009;123 Suppl 4:S11-S17. doi:10.1016/S0049-3848(09)70136-7

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What’s the evidence that patients with Covid-19 are at high risk of blood clots?

Why is my diabetic patient complaining of arm pain and localized edema for couple of weeks without an obvious cause?

Aside from the usual suspects associated with a painful extremity (eg, trauma, deep venous thrombosis and soft tissue infections), think of spontaneous diabetic myonecrosis (DMN), also known as diabetic muscle infarction (1-3).

DMN is characterized by abrupt onset of painful swelling of the affected muscle, most often of the lower extremities, but also occasionally upper extremities. DMN occurs in patients with longstanding DM whose blood glucose control has deteriorated over time, often with nephropathy, retinopathy and/or neuropathy (1-3).

Couple of things to remember when considering DMN in your differential of a painful extremity. First, except for localized edema and tenderness over the involved muscle, the exam may be unremarkable. Specifically, there is no erythema or signs of compartment syndrome and fever is absent in the great majority of patients (~90%) (2). Even white blood cell count and creatine kinase (CK) are usually normal. The reason for normal CK at presentation is not clear but CK might have already peaked by the time of patient presentation (3). In contrast, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are usually elevated (>80%) (1).

MRI (without contrast in patients with renal insufficiency) is the imaging of choice with muscle enlargement and edema with hyperintense signal on T2-weighted images and other changes, including perifascial, perimuscular and or subcutaneous edema (1-3). Muscle biopsy is not currently recommended because of its adverse impact on time to symptomatic improvement. Non-surgical therapy, with rest, analgesia and glycemic control is usually recommended (1-3).

 
Though its exact cause is still unclear, atherosclerosis, diabetic microangiopathy, vasculitis with thrombosis and ischemia-reperfusion injury have been posited as potential precipitants for DMN. The role of anti-phospholipid syndrome, particularly in patients with type I DM, is unclear (1,2).

 
Bonus pearl: Did you know that symptoms of DMN may last for weeks with at least one-third of patients having a recurrence in the same muscle or elsewhere (1)?

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Reference
1. Horton WB, Taylor JS, Ragland TJ, et al. Diabetic muscle infarction: a systematic review. BMJ Open Diabetes Research and Care 2015;3:e000082.
2. Trujillo-Santos AJ. Diabetic muscle infarction. An underdiagnosed complication of long-standing diabetes. Diabetes Care 2003;26:211-15.
3. Diabetes muscle infarction in end-stage renal disease:A scoping review on epidemiology, diagnosis and treatment. World J Nephrol 2018;7:58-64.

Why is my diabetic patient complaining of arm pain and localized edema for couple of weeks without an obvious cause?

Should my patient with below-knee venous thrombosis receive anticoagulation?

In contrast to proximal lower extremity deep venous thrombosis for which anticoagulation (AC) is standard therapy, whether below-knee deep venous thrombosis (BKDVT) (eg,  involving peroneal, soleus, tibial, or gastrocnemius veins) should routinely receive AC is a matter of debate because of lack of solid supportive evidence. 1-3

The American College of Chest Physicians (ACCP) recommends AC for patients with BKDVT who are severely symptomatic or have risk factors for extension of the thrombus but this recommendation is based on low-quality scientific evidence (grade 2C or “weak”).3 For other patients, surveillance ultrasound is recommended in 2 weeks to exclude clot propagation more proximally, and therefore the need for AC.  Of course, decision regarding AC should be made in the context of the patient’s risk of serious bleeding.

The following facts about BKDVT may help in therapeutic decision making:1

  • Most cases resolve spontaneously without AC
  • The incidence of propagation varies from 3%-32%
  • Embolization is unlikely in the absence of extension into proximal veins

Also remember that clot propagation usually occurs within 2 weeks of initial diagnosis. That’s why surveillance ultrasound is recommended during this period when watchful waiting is preferred.

References 

  1. Fleck D, Albadawi H, Wallace A, etal. Below-knee deep vein thrombosis (DVT): diagnostic and treatment patterns. Cariovasc Diagn Ther 2017;7(Suppl3):S134-39. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5778527/
  2. Olson EJ, Zander AL, Van Gent J-M, et al. Below-knee deep vein thrombosis: An opportunity to prevent pulmonary embolism? J Trauma Acute Care Surg 2014;77:459-63. https://www.ncbi.nlm.nih.gov/pubmed/25159251
  3. Kearon C, Akl EA, Comerota AJ, et al. 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):e419S-e494S. https://www.ncbi.nlm.nih.gov/pubmed/22315268

 

Should my patient with below-knee venous thrombosis receive anticoagulation?

200 pearls and counting! Take the Pearls4Peers quiz #2!

Multiple choice (choose 1 answer)
1. Which of the following classes of antibiotics is associated with peripheral neuropathy?
a. Penicillins
b. Cephalosporins
c. Macrolides
d. Quinolones

 

 

2. The best time to test for inherited thrombophilia in a patient with acute deep venous thrombosis is…
a. At least 1 week after stopping anticoagulants and a minimum of 3 months of anticoagulation
b. Just before initiating anticoagulants
c. Once anticoagulation takes full effect
d. Any time, if suspected

 

 

3. All the following is true regarding brain MRI abnormalities following a seizure, except…
a. They are observed following status epilepticus only
b. They are often unilateral
c. They may occasionally be associated with leptomeningeal contrast enhancement
d. Abnormalities may persist for weeks or months

 

 

4. Which of the following is included in the quick SOFA criteria for sepsis?
a. Heart rate
b. Serum lactate
c. Temperature
d. Confusion

 

 

5. All of the following regarding iron replacement and infection is true, except…
a. Many common pathogens such as E.coli and Staphylococcus sp. depend on iron for their growth
b. Association of IV iron replacement and increased risk of infection has not been consistently demonstrated
c. A single randomized-controlled trial of IV iron in patients with active infection failed to show increased infectious complications or mortality with replacement
d. All of the above is true

 

True or false

1. Constipation may precede typical manifestations of Parkinson’s disease by 10 years or more
2. Urine Legionella antigen testing is >90% sensitive in legionnaire’s disease
3. Spontaneous coronary artery dissection should be particularly suspected in males over 50 years of age presenting with acute chest pain
4. Urine dipstick for detection of blood is >90% sensitive in identifying patients with rhabdomyolysis and CK >10,000 U/L
5. Diabetes is an independent risk factor for venous thrombophlebitis

 

 

 

Answer key
Multiple choice questions:1=d; 2=a;3=a;4=d;5=c
True or false questions:1=True; 2,3,4,5=False

 

200 pearls and counting! Take the Pearls4Peers quiz #2!

Is there any utility to laboratory testing for inherited thrombophilia or antiphospholipid syndrome in my hospitalized patient with unprovoked acute pulmonary embolism?

There is virtually no utility to obtaining heritable thrombophilia testing in acute hospital setting. In fact, there are potential harms due to false-positive and false-negative results which in turn may lead to increasing anxiety in the patient and added cost due to repeat testing.

As many tests obtained as part of this workup are functional assays—eg, the protein S, C, or antithrombin activity, and activated protein C resistance (often used to screen for factor V Leiden)— they are easily impacted by the physiologic effects of acute thrombosis as well as all anticoagulants.1

More importantly, testing for inherited thrombophilia will not impact management in the acute setting, as decisions regarding duration of anticoagulation are often made later in the outpatient setting. The proper time to evaluate the patient for inherited thrombophilias (if indicated) is at least one week following discontinuation of anticoagulation (minimum 3 months from the time of the index event). 2 

Testing for antiphospholipid syndrome (APS) may be considered in this setting though it should be noted that the lupus anticoagulant assay is impacted by nearly every anticoagulant, resulting in frequent false-positive results1, and therefore should be performed before initiation of these agents (or delayed until later if anticoagulation has already begun). A false-positive result has downstream implications as many patients with acute, uncomplicated venous thromboembolism (VTE) are discharged on a direct oral anticoagulant (DOAC), and antiphospholipid syndrome is currently considered a relative contraindication to the use of DOACs in VTE.

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 References
1. Moll, S. “Thrombophilia: Clinical-practical aspects.” J Thromb Thrombolysis 2015;39:367-78. https://www.ncbi.nlm.nih.gov/pubmed/25724822
2. Connors JM. “Thrombophilia Testing and Venous Thrombosis.” N Engl J Med 2017; 377:1177-1187. http://www.nejm.org/doi/full/10.1056/NEJMra1700365 

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

 

Is there any utility to laboratory testing for inherited thrombophilia or antiphospholipid syndrome in my hospitalized patient with unprovoked acute pulmonary embolism?

My patient with a thrombosed hemodialysis access is found to have an asymptomatic segmental pulmonary embolism following a vascular access declotting procedure. Does he need systemic anticoagulation?

There is no firm evidence either for or against the use of systemic anticoagulants (ACs) in patients with asymptomatic pulmonary embolism (PE) following hemodialysis vascular access declotting (HVAD).  

However, despite the common occurrence of asymptomatic PE following HVAD procedures (~40%), symptomatic PE—at times fatal—has also been reported in these patients1,2.

In the absence of hard data and any contraindications, anticoagulation can be justified in our patient for the following reasons:

  • Asymptomatic segmental PE is commonly treated as symptomatic PE irrespective of setting2,3
  • Hemodialysis patients are often considered hypercoagulable due to a variety of factors eg, platelet activation due to extracorporeal circulation, anti-cardiolipin antibody, lupus anticoagulant, decreased protein C or S activity, and/or reduced anti-thrombin III activity4-7
  • Overall, chronic dialysis patients have higher incidence of PE compared to the general population8
  • There is no evidence that asymptomatic PE following HVAD has a more benign course compared to that in other settings
  • Untreated PE may be associated with repeated latent thrombosis or progression of thrombosis in the pulmonary artery5

 

References

  1. Calderon K, Jhaveri KD, Mossey R. Pulmonary embolism following thrombolysis of dialysis access: Is anticoagulation really necessary? Semin Dial 2010:23:522-25. https://www.ncbi.nlm.nih.gov/pubmed/21039878
  2. Sadjadi SA, Sharif-Hassanabadi M. Fatal pulmonary embolism after hemodialysis vascular access declotting. Am J Case Rep 2014;15:172-75. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4004792/pdf/amjcaserep-15-172.pdf
  3. Chiu V, O’Connell C. Management of the incidental pulmonary embolism. AJR 2017;208:485-88. http://www.ajronline.org/doi/pdf/10.2214/AJR.16.17201
  4. Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease: Chest guideline and expert panel report. CHEST 2016;149:315-52. http://journal.chestnet.org/article/S0012-3692(15)00335-9/fulltext
  5. Yamasaki K, Haruyama N, Taniguchi M, et al. Subacute pulmonary embolism in a hemodialysis patient, successfully treated with surgical thrombectomy. CEN Case Rep 2016;5:74-77 https://link.springer.com/article/10.1007/s13730-015-0195-9
  6. Nampoory MR, Das KC, Johny KV, et al. Hypercoagulability, a serious problem in patients with ESRD on maintenance hemodialysis, and its correction after kidney transplantation. Am J Kidney Dis 2003;42:797-805. https://www.ncbi.nlm.nih.gov/pubmed/14520631
  7. O’Shea SI, Lawson JH, Reddan D, et al. Hypercoagulable states and antithrombotic strategies in recurrent vascular access site thrombosis. J Vasc Surg 2003;38: 541-48. http://www.jvascsurg.org/article/S0741-5214(03)00321-5/pdf
  8. Tveit DP, Hypolite IO, Hshieh P, et al. Chronic dialysis patients have high risk for pulmonary embolism. Am J Kidney Dis 2002;39:1011-17. https://www.ncbi.nlm.nih.gov/pubmed/11979344
My patient with a thrombosed hemodialysis access is found to have an asymptomatic segmental pulmonary embolism following a vascular access declotting procedure. Does he need systemic anticoagulation?

Is diabetes mellitus (DM) an independent risk factor for venous thromboembolism (VTE)?

Although DM was originally thought to be an independent risk factor for DM1,2, more recent data suggest otherwise.

A population-based study involving residents of Olmsted County, Minnesota, calculated the incidence of VTE among patients with DM over a 25-year period and found it to be higher than that of controls .   However, in the same study, after controlling for hospitalization for major surgery or medical illness and nursing home confinement, no association between DM and VTE was found2  .  

A recent systematic review and meta-analysis of case-control and cohort studies involving over 1 million patients found no significant association between DM and VTE when controlled for common risk factors (eg, obesity, sedentary life style, smoking, hypertension, or dyslipidemia)3.  The authors concluded that DM and its complications are not independent risk factors for incident VTE.  

Thus, it appears that much of the risk of DVT in DM may be related to its comorbidities and the need for hospitalization, surgery or nursing home stay.

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 References

  1. Petrauskiene V, Falk M, Waernbaum I, et al. The risk of venous thromboembolism is markedly elevated in patients with diabetes. Diabetologia 2005;48:1017-21. https://www.ncbi.nlm.nih.gov/pubmed/15778859
  2. Heit JA, Leibson CL, Ashrani AA, et al. Is diabetes mellitus an independent risk factor for venous thromboembolism? A population-based case-control study. Thromb Vasc Biol 2009; 29:1399-1405. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735343/
  3. Gariani K, Mavrakanas T, Combescure C, et al. Is diabetes mellitus a risk factor for venous thromboembolism? A systematic review and meta-analysis of case-control and cohort studies. Eur J Intern Med 2016;28:52-58. https://www.ncbi.nlm.nih.gov/pubmed/26507303

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Is diabetes mellitus (DM) an independent risk factor for venous thromboembolism (VTE)?

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

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?