Article

Consideration of C-reactive protein and polyserositis in systemic lupus erythematosus presenting with cardiac symptoms

Correspondence / American Journal of Emergency Medicine 33 (2015) 108122 115

Figure. Randomization flow chart. Supplementary data.

Table

Compression and Ventilation parameters (observation period, 8 minutes)

CC parameter

CP a

Standard BLS

P

effective compressions (%) b

69.5 +- 18.4

34.6 +- 25.3

b.001

Compression depth (millimeters)

49.5 +- 21.4

40.6 +- 11.2

b.001

Compression too shallow (b50 mm) (%)

14.5 +- 11.6

31.3 +- 19.4

b.001

Compression too deep (N 60 mm)(%)

4.9 +- 3.5

14.5 +- 11.2

b.001

Compression rate [min-1]

102 +- 11.4

125.4 +- 23.3

b.001

Incorrect decompressions (%)

4.6 +- 3.2

8.5 +- 7.2

b.001

Incorrect pressure point (%)

7.5 +- 6.2

9.2 +- 8.3

.234

Absolute hands-off time (s) c

59.6 +- 25

140 +- 43

b.001

Abbreviation: NS, not statistically significant. Data are presented as mean +- SD.

a CardioPump Manual CPR Device (with metronome).

b Effective compression was defined as compression with correct depth (50-60 mm), compete decompression, and correct hand position

c Absolute hands-off time was defined as the sum of all periods during which no hand was placed on the chest minUS time used for patient ventilation.

References

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  2. Kovic I, Lulic D, Lulic I. CPR PRO(R) device reduces rescuer fatigue during continu- ous chest compression cardiopulmonary resuscitation: a randomized crossover trial using a manikin model. J Emerg Med 2013;45(4):570-7. http://dx.doi.org/ 10.1016/j.jemermed.2013.04.021.
  3. Hellevuo H, Sainio M, Huhtala H, Olkkola KT, Tenhunen J, Hoppu S. The quality of manual chest compressions during transport–effect of the mattress assessed by dual accelerometers. Acta Anaesthesiol Scand 2014;58(3):323-8. http://dx.doi.org/ 10.1111/aas.12245.
  4. Zapletal B, Greif R, Stumpf D, Nierscher FJ, Frantal S, Haugk M, et al. Comparing three CPR Feedback devices and standard BLS in a single rescuer scenario: a randomised simulation study. Resuscitation 2014;85(4):560-6. http://dx.doi. org/10.1016/j.resuscitation.2013.10.028.
  5. Yeung J, Davies R, Gao F, Perkins GD. A randomised control trial of prompt and feedback de- vices and their impact on Quality of chest compressions–a simulation study. Resuscitation 2014;85(4):553-9. http://dx.doi.org/10.1016/j.resuscitation.2014.01.015.

    Consideration of C-reactive protein and

    polyserositis in systemic lupus erythematosus presenting with cardiac symptoms?

    To the Editor,

    We read with interest the article entitled “Systemic lupus erythemato- sus presenting with cardiac symptoms” by Chen et al [1]. The authors reported on the characteristics of 8 cases of previously undiagnosed systemic lupus erythematosus who presented with cardiac symptoms. We welcome the information and its relevance; however, we think that 2 aspects of the analysis deserve discussion.

    In their analysis, the authors asserted that elevated levels of C-reactive protein (CRP) and antibodies to double stranded DNA (anti-dsDNA), as well as decreased complement C3 and C4 levels indicate generalized in- flammation and immunological activity. This was reported as consistent with previous data [2]; however, although the referenced study noted the association of increased immunological activity with elevated anti- dsDNA and decreased complement levels, it did not report on association with CRP. We also note that the combination of a low B-type natriuretic peptide (Brain natriuretic peptide and elevated CRP levels was used as prima facie evidence that serositis, instead of heart failure, was the Underlying etiology of the pericardial and Pleural effusions.

    We would like to point out that although CRP is an inflammatory marker, it has an intriguing relation to SLE disease activity. Contrary to the authors’ assertion that elevated levels of CRP are associated with generalized inflammation and SLE disease activity, it is well recognized that CRP is often normal or only mildly elevated in patients with active SLE [3,4]. There are many hypotheses concerning this phenomenon, but the explanation is still unknown. Serositis, polyarthritis, and nephritis are perhaps the few manifestations of SLE reported to cause an elevated CRP. Curiously, in patients with SLE, the CRP level responds to intercurrent infection as expected. One must also consider the influence of confounding

    ? The authors report no conflicts of interest, and no sources of funding are applicable to this article.

    116 Correspondence / American Journal of Emergency Medicine 33 (2015) 108122

    factors (2 patients were smokers, for instance) known to affect CRP level. Given this information, although the authors reported that 100% of patients had elevated CRP and the elevated CRP was used to rule in serositis, we propose that, in SLE, the CRP level is not as sensitive as it would appear here. Thus, the physician must be aware of this complex re- lationship, knowing that the predictive value of an elevated conventional CRP assay on SLE disease activity and cardiovascular risk is still limited at present.

    Secondly, we comment on the frequent occurrence of coexisting pericardial and pleural effusions in SLE disease presentation. This correlation was explained by the authors as a generalized serositis. In SLE, the pathogenesis of serositis is thought to involve immune complex deposition stimulating an inflammatory reaction [5]. Although this can simultaneously affect both the pleura and pericardium, we draw attention to the fact that outside of autoimmune serositis, there is a strong link between pericardial disease and pleural effusion, in particu- lar, a predominantly left-sided effusion [6,7]. It would be interesting for the authors to have reported if the coexistent pleural effusions were predominantly left sided. This little-known association is clinically important for emergency physicians. The finding of increased trans- verse cardiac diameter and a left-sided pleural effusion on imaging should arouse suspicion of pericardial disease. This can be an early clue to a pericardial effusion, which can otherwise be silently progressing to tamponade physiology. Furthermore, this association is important to recognize as a small pericardial effusion in existence with a large pleural effusion can produce cardiac tamponade, which may actually resolve with pleural tap [8,9].

    In conclusion, physicians must always consider SLE as a differential in patients presenting with cardiac symptoms in the appropriate Clinical context. This involves appropriate laboratory investigations, with cautious interpretation of CRP levels, and remembering the link between pericardial and pleural effusions when interpreting imaging and instituting management.

    Satish Maharaj, MBBS? Simone Chang, MBBS

    Eric Williams Medical Sciences Complex, University of the West Indies

    Trinidad and Tobago

    ?Corresponding author. Eric Williams Medical Sciences Complex University of the West Indies, Champs Fleurs, Trinidad and Tobago

    E-mail-address: [email protected] http://dx.doi.org/10.1016/j.ajem.2014.10.026

    References

    Chen PY, Chang CH, Hsu CC, Liao YY, Chen KT. Systemic lupus erythematosus present- ing with cardiac symptoms. Am J Emerg Med 2014;32(9):1117-9.

  6. Law WG, Thong BY, Lian TY, Kong KO, Chng HH. Acute lupus myocarditis: clinical features and outcome of an oriental case series. Lupus 2005;14:827-31.
  7. Mok CC, Birmingham DJ, Rovin BH. High sensitivity C-reactive protein, disease activity and Cardiovascular risk factors in systemic lupus erythematosus. Arthritis Care Res 2013;65(3):441-7.
  8. ter Borg EJ, Horst G, Limburg PC, van Rijswijk MH, Kallenberg CG. C-reactive protein levels during disease exacerbations and infections in systemic lupus erythematosus: a prospective longitudinal study. J Rheumatol 1990;17:1642-8.
  9. Tincani A, Rebaioli CB, Taglietti M, Shoenfeld Y. Heart involvement in systemic lupus erythematosus, anti-phospholipid syndrome and neonatal lupus. Rheumatology 2006;45(Supplement 4):iv8-iv13.
  10. Eisenberg MJ, Dunn MM, Kanth N, Gamsu G, Schiller NB. Diagnostic value of chest radiography for pericardial effusion. J Am Coll Cardiol 1993;22:588-93.
  11. Weiss JM, Spodick DH. Association of left pleural effusion with pericardial disease. N Engl J Med 1983;308:696-7.
  12. Traylor JJ, Chan K, Wong I, Roxas JN, Chandraratna PA. Large pleural effusions produc- ing signs of cardiac tamponade resolved by thoracentesis. Am J Cardiol 2002;89(1): 106-8.
  13. Kaplan LM, Epstein SK, Schwartz SL, Cao QL, Pandian NG. Clinical, echocardiographic, and hemodynamic evidence of cardiac tamponade caused by large pleural effusions. Am J Respir Crit Care Med 1995;151(3 Pt 1):904-8.

    noninvasive ventilation during procedural sedation in the ED: a case series?,??

    To the Editor,

    Procedural sedation and analgesia (PSA) is the administration of sed- ative, analgesic, or dissociative agents to facilitate painful or unpleasant procedures. The most important complication during PSA is hypoventilation, which may result from compromise of the airway or re- spiratory drive. Although emergency physicians have a conclusive record of safety in using a variety of PSA agents to facilitate painful procedures across the sedation continuum [1], emergency departments (EDs) serve an aging population that is burdened with high rates of obesity [2,3]; emergency providers are therefore more likely to perform PSA on pa- tients with high anesthetic risk. Noninvasive ventilation has emerged as a valuable, intubation-sparing therapy in the management of various types of respiratory failure [4] and also as an effective treat- ment in patients with obstructive Sleep apnea [5]. The pathophysiology of these conditions pertains to PSA, where patients who require deep sedation may develop central hypoventilation or airway ob- struction [6-8]. Noninvasive ventilation may therefore offer addi- tional safety during PSA, especially in patients predisposed to these

    Fig. 1. a, NIV setup AP. b, NIV setup oblique.

    ? This work has been presented at no meetings nor funded by any grants or other financial support. Authors Strayer and Caputo acknowledge no financial support and no conflicts pertinent to the preparation of this manuscript.

    ?? RJS and NDC conceived the study and designed the case series. NDC supervised the

    conduct of the trial and data acquisition. RJS drafted the manuscript. NDC contributed substantially to its revision. RJS takes responsibility for the paper as a whole.

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