Anatomy, Article

Confidence intervals and adjusted odds ratios: a commend on interpreting the results of Killip classification and glucose levels

Fig. 1 Photograph of the AWS laryngoscope. The device is held in the left hand and passed into the mouth over the tongue, and the tip is placed under the epiglottis.

patients at increased risk for difficult intubation [7]. It is quick to learn [8], it can be used for awake tracheal intubation [9], and it requires less sedative drugs than DL, which is a very important issue in airway management of critically ill hypotensive patients. Further studies are required to determine the role of Pentax AWS in ICU in light of some of the current limitations of a fixed PBlade’s size and curvature.

Ruggero M. Corso MD Emanuele Piraccini MD Marina Terzitta MD

Juana L. Chanis Vargas MD Stefano Gaetani MD Carmen Rotondo MD Vanni Agnoletti MD Giorgio Gambale MD Department of Emergency

Anaesthesia and Intensive Care Section

G.B. Morgagni-PierantoniHospital

Forli 47100, Italy

doi:10.1016/j.ajem.2011.05.023

References

  1. Koyama J, Aoyama T, Kusano Y, et al. Description and first clinical application of Airway Scope for tracheal intubation. J Neurosurg Anesthesiol 2006;18:247-50.
  2. Asai T, Liu EH, Matsumoto S, et al. Use of the Pentax-AWS in 293 patients with Difficult airways. Anesthesiology 2009;110:898-904.
  3. Hirabayashi Y, Seo N. Airway scope: early clinical experience in 405 patients. J Anesth 2008;22:81-5.
  4. Suzuki A, Toyama Y, Katsumi N, et al. The Pentax-AWS((R)) rigid indirect video laryngoscope: clinical assessment of performance in 320 cases. Anaesthesia 2008;63:641-7.
  5. Jaber S, Amraoui J, Lefrant JY, et al. Clinical practice and risk factors for immediate complications of endotracheal intubation in the intensive care unit: a prospective, multiple-center study. Crit Care Med 2006;34: 2355-61.
  6. Maruyama K, Yamada T, Kawakami R, et al. Upper cervical spine movement during intubation: fluoroscopic comparison of the AirWay Scope, McCoy laryngoscope, and Macintosh laryngoscope. Br J Anaesth 2008;100:120-4.
  7. Malik MA, Subramaniam R, Maharaj CH, et al. Randomized controlled trial of the Pentax AWS, Glidescope, and Macintosh laryngoscopes in predicted difficult intubation. Br J Anaesth 2009;103(5):761-8.
  8. Liu L, Tanigawa K, Kusunoki S, et al. Tracheal intubation of a difficult airway using Airway Scope, Airtraq, and Macintosh laryngoscope: a comparative manikin study of inexperienced personnel. Anesth Analg 2010;110(4):1049-55.
  9. Asai T. Pentax-AWS videolaryngoscope for awake nasal intubation in patients with unstable necks. Br J Anaesth 2010;104(1):108-11.

Confidence intervals and adjusted odds ratios: a commend on interpreting the results of Killip classification and glucose levels

To the Editor,

I have read with great pleasure the letters by Lina et al

[1] and Cheng [2] about the article investigating the relationship between Killip classification and glucose levels in patients with acute myocardial infarction by Cheng and Yen [3].

Lina et al [1] claimed that the width confidence intervals (CIs) of glucose levels of Killip classes make the difference insignificant despite significant result by 1-way analysis of variance, and Cheng [2] accepted this claim and stated that it could be due to the limited sample size. However, the statistical significance by CIs is calculated whether the difference between 2 means includes zero; and when we look at the glucose levels of Killip class 1 (186.8 +- 82.5) and Killip class 4 (236.2 +- 115.5), we get a difference of 49.4 with a 95% CI of 19.4 to 79.4, which has a P value of .0014. This P value is significant even with the Bonferroni correction. So, the statistical significance of differences between 2 means calculated by CIs is not related to the width of the CI but the CI of differences including zero or not.

If we look for a relation between Killip class and glucose levels, we have to adjust the ratios according to the diabetes mellitus rates, which differ between Killip classes (31.9%, 33.3%, 34.8%, and 49%, respectively); and if we want to get the real relationship between glucose levels and 1-year mortality, we have to perform a logistic regression analysis including Killip classes, diabetes rates, and glucose levels

and also other related variables to mortality to get the adjusted odds ratios for all the independent variables.

Cenker Eken MD Department of Emergency Medicine Akdeniz University Medical Faculty

Antalya, Turkey E-mail address: [email protected]

doi:10.1016/j.ajem.2011.05.025

References

  1. Lin GM, Li YH, Han CL. Letter for Killip classification and glucose level in patients with acute myocardial infarction. Am J Emerg Med 2011;29(4):462.
  2. Cheng HH. The authors respond. Am J Emerg Med 2011;29(4):462-3.
  3. Cheng HH, Yen PC. Killip classification and glucose level in patients with acute myocardial infarction. Am J Emerg Med 2010;28(8):853-6.

Anaphylaxis-induced hyperfibrinogenolysis and the risk of Kounis syndrome: the dual action of tryptase?

To the Editor,

In the very interesting report published in the Am J Emerg Med [1], a young lady had anaphylaxis after a wasp sting, and despite abnormalities in coagulation cascade with markedly increased prothrombin time and activated partial thrombo- plastin, neither bleeding nor Hepatic dysfunction was observed. The patient was discharged after treatment of anaphylaxis without administration of fresh-frozen plasma or antifibrino- lytics such as Tranexamic acid because the coagulation abnormalities were normalized spontaneously, and bleeding diathesis or thrombosis was absent. The authors thought that this unique case provides an interesting area of discussion.

Although biomarkers of Myocardial necrosis and electro- cardiographic changes were not given and allergic workup was not performed, tryptase levels were significantly elevated (initial level 200 ug/L). Therefore, in this patient, an abortive episode of type I variant of Kounis syndrome [2] cannot be excluded. The patient was treated with intravenous epinephrine. Indeed, epinephrine is the primary drug for anaphylaxis, but commercially available preparations of epinephrine contain sodium metabisulfite as a preservative, which is known to induce Allergic reactions [3]. For this reason, currently, sulfide-free epinephrine preparations are available [4]. Insect stings can induce Kounis syndrome, which combines cardiac events with conditions associated with mast cell activation, involving interrelated and inter-

acting inflammatory cells and including allergic or hyper- sensitivity and anaphylactic or anaphylactoid insults.

platelet activation and the ensuing coagulation cascade occur via stimulation of some known receptors on the platelet surface such as receptors for adenosine diphosphate, thromboxane, thrombin, serotonin, epinephrine, and some less-known receptors, which are associated with mast cell activation, such as receptors for histamine, high- and low- affinity immunoglobulin E receptors (FCe RI and FCe RII) and receptors for platelet-activating factor [5]. During activation, platelets change shape from discoid to spiculated form and release granules that contain proinflammatory (platelet factor 4, CD154 platelet-derived growth factor), prothrombotic (factor V, factor XI, platelet-activating inhib- itor-1), adhesive (thrombospondin, fibrinogen, P selectin, von Willebrand factor), and aggregatory mediators (serotonin, Ca2+, Mg2+, ATP, ADP) [6]. However, mast cell mediators are also associated with fibrinogenolysis. For example, tryp- tase can degrade fibrinogen [7] and can activate prourokinase [8]. Chymase can inactivate thrombin [9]. Moreover, mast cells are a unique and important source of heparin, which does not exhibit fibrinolytic activity but prevents coagulation by acting as a cofactor of antithrombin III. However, heparin has been described as a potent cofactor of tryptase and of tissue-type plasminogen activator [10,11]. Recent data pro- vide evidence that human tissue mast cells themselves are another important source of tissue plasminogen activator [12]. It is difficult to explain why anaphylaxis can be associated with either thrombotic or fibrinogenolytic events. Perhaps, mast cell clonality could explain this action, both thrombotic

[2] and fibrinogenolytic [1], on the coagulation cascade

? Conflict of interest: None declared.

Table 1 Tryptase dual action

Thrombotic action [2] Fibrinolytic action [1]

1. Activates the zymogen 1. Cleaves the ? and especially forms of metalloproteinases ? chain of fibrinogen, which such as interstitial regulate the removal of the collagenase, gelatinase, and thrombin cleavAge SIte and the stromelysin and can promote critical polymerization site,

plaque disruption or rupture

  1. Degrades the pericellular matrix components fibronectin and vitronectin and neuropeptides, such as vasoactive intestinal peptide and calcitonin gene-related peptide
  2. Activates neighboring cells by cleaving and activating

resulting in inhibition of clot formation

2. Degrades procoagulant proteins, which prevent fibrin deposition

3. Activates the single-chain urinary plasminogen activator

protease-activated receptor-2 (or prourokinase) and converts and thrombin receptors plasminogen into plasmin,

which degrades fibrinogen and other coagulation factors

4. Degrades high-density lipoprotein

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