Multiple choice (choose 1 answer)
1. Which of the following classes of antibiotics is associated with peripheral neuropathy?
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
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
Multiple choice questions:1=d; 2=a;3=a;4=d;5=c
True or false questions:1=True; 2,3,4,5=False
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.
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
Contributed by Hanny Al-Samkari, MD, Mass General Hospital, Boston, MA
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Continue reading “Is there any utility to laboratory testing for inherited thrombophilia or antiphospholipid syndrome in my hospitalized patient with unprovoked acute pulmonary embolism?”
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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
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 2 . 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.
- 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
- 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/
- 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
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.
- 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.
- Durning SJ, Shaw DJ, Oliva AJ et al. Persistent hiccups as the presenting symptom of a pulmonary embolism. Chest Disease Reports 2012;2:e2.
- Buyukhatipoglu H, Sezen Y, Yildiz A, et al. Hiccups as a sign of chronic myocardial ischemia. S Med J 2010;103: 1184-85.
Lead aVR is often “neglected” because of its non-adjacent location to other EKG leads (Fig 1) and poor awareness of its potential utility in detecting myocardial ischemia.
In acute coronary syndrome (ACS), ST-elevation (STE) in aVR (≥1mm) with diffuse ST depression in other leads (Fig 2) is usually a sign of severe left main coronary artery (LMCA), proximal left anterior descending (LAD), or 3-vessel coronary disease, and is associated with poor prognosis1-3. In some patients with LMCA thrombosis, the EKG changes may be non-specific but STE in aVR should still raise suspicion for ischemia1. Possible mechanisms for STE in aVR include diffuse anterolateral subendocardial ischemia or transmural infarction of the basal portion of the heart.
The possibility of an anatomical variant of the Purkinje fibers leading to the absence of STE in the anterior leads in some patients with transmural anterior infarction is another reason to pay attention to aVR.
Fig 1. Standard EKG limb leads. Note that aVR is “in the fringes”.
Fig 2. 35 year old female with ACS due to LMCA spasm. Note STE in aVR with ST segment depression in leads V3-6, I, aVL, II, and aVF (Courtesy National Library of Medicine)
- Kossaify A. ST segment elevation in aVR: clinical syndrome in acute coronary syndrome. Clin Med Insights: Case Reports 2013:6.
- Kireyev D, Arkhipov MV, Zador ST. Clinical utility of aVR-the neglected electrocardiographic lead. Ann Noninvasive Electrocardiol 2010;15:175-180.
- Wong –CK, Gao W, Stewart RAH, et al. aVR ST elevation: an important but neglected sign in ST elevation acute myocardial infarction. Eur Heart J 2010;31:1845-1853.
- De Winter RJ, Verouden NJ, Wellens HJ, et al. A new ECG sign of proximal LAD occlusion. N Engl J Med 2008;359:2071-3.
There are no randomized-controlled studies that examine the effectiveness of VTE prophylaxis in debilitated patients following discharge from the hospital, and currently the literature does not recommend prophylaxis for chronic immobility as a single risk factor for VTE (1). However, given the expected morbidity, potential mortality and hospital readmission associated with VTE, prophylaxis should be considered in residents of LTFs with the following comorbidities (2):
- Acute exacerbation of congestive heart failure
- Acute exacerbation of chronic obstructive pulmonary disease
- Acute infection (e. g. pneumonia, urosepsis, skin and soft tissue infections, infectious diarrhea)
- Acute exacerbation of inflammatory/autoimmune diseases
Unless contraindicated, patients should receive prophylactic doses of unfractionated heparin, enoxaparin, or other approved drugs. Mechanical VTE prophylaxis should be used only when the risk of bleeding is considered unacceptably high or when there are drug intolerances or adverse effects.
The need for VTE prophylaxis should be reassessed regularly taking into account patient’s overall health status, mobility, drug tolerance and goals of care.
- Pai M, Douketis JD. Preventing venous thromboembolism in long-term care residents: Cautious advice based on limited data. Cleveland Clin J Med 2010;77: 123-130. https://www.ncbi.nlm.nih.gov/pubmed/20124270
- Robinson Am. Venous thromboembolism prophylaxis for chronically immobilized long-term care residents. Ann Long-Term Care 2013;10:30. https://www.managedhealthcareconnect.com/article/venous-thromboembolism-prophylaxis-chronically-immobilized-long-term-care-residents