Daych Chongnarungsin

Lead perforation: an uncommon cause of chest pain in a patient with pacemaker.

Fig. 1. Pacemaker wire in the right ventricle close to the apex, also note moderate sized pericardial effusion. We thank Chen et al. [1] for their article regarding right ventricular septal perforation from an active fixation lead. This was very interesting, as usual for International Journal of Cardiology. We also recently had a 56-year-oldmalewhopresented to our emergency department with a 30-minute history of midsternal, stabbing chest pain. He underwent permanent pacemaker insertion 2 days prior to this presentation for third degree heart block. His vital signs and physical examination were unremarkable. His chest X-ray showed stable cardiomegaly without any pulmonary pathology. Electrocardiography revealed old left bundle branch block with a paced rhythm. Bedside transthoracic echocardiography was urgently obtained, revealing a moderate sized circumferential pericardial effusion and displacement of right ventricular (RV) pacer lead perforating through the apex (Figs. 1 and 2). The patient underwent emergent cardiac surgery which revealed 250 ml of blood in the pericardial space. His pacemaker wire was pulled back. The patient had an uncomplicated post-op course and was discharged to home in a stable condition. Lead perforation is an infrequent but potentially fatal complication of pacemaker implantation with published rate of 0.1–0.8% [2,3]. Patients with this complication typically present with recurring, stabbing chest pain and usually present within 1 month after implantation [3,4]. Transthoracic echocardiography is the initial diagnostic test of choice as it usually provides a clear visualization of the position of the lead tip as well as associated pericardial effusion. Chest computed tomography scan can be used if the initial echocardiography is not diagnostic [5]. Management of lead perforation depends on the patients hemodynamic status. In a patient with hemodynamic instability or with rapid progression of pericardial effusion, surgical repair is generally mandated while simple direct traction with close echocardiographic

Vitamin D deficiency and cardiovascular disease

We read with interest the article by Guessous et al. [1]. The author described an excellent study on vitamin D levels and associated factors. The author mentioned the association between vitamin D and cardiovascular disease, which we found fascinating, and we would like to emphasise the topic. Cardiovascular disease (CVD) is the leading cause of death in the United States. There is an increasing interest in using vitamin D levels as a novel marker for CVD [2], because epidemiological data have shown a strong correlation between the risk of CVD and vitamin D deficiency. A cross-sectional analysis of the NHANES database showed a higher prevalence of CVD among individuals with low levels of 25-hydroxy [25(OH)] vitamin D [3]. The mechanism leading to the increased cardiovascular risk is not clearly understood; however, patients with vitamin D deficiency were found to have upregulation of the renin angiotensin aldosterone system (RAAS). The relationship between vitamin D deficiency and upregulation of the RAAS was also found in a large epidemiological study of 3,000 patients [4]. A recent meta-analysis involving 19 prospective studies (6,123 CVD cases) also showed increased CVD risk in patients with serum 25(OH)-vitamin D levels of 20–60 nmol/L [5]. Though multiple lines of evidence suggest a link between low vitamin D levels and increased risk of CVD, multiple interventional trials have failed to reveal any significant benefit of vitamin D supplementation [6–7]. There is also no benefit of vitamin D supplementation in improvement of diastolic function and regression of left ventricular hypertrophy [8]. Further studies are needed to establish the effect of vitamin D supplementation on CVD risk. Correspondence: Wisit Cheungpasitporn, MD, Department of Medicine, Bassett Medical Center, USA-Cooperstown, New York 13326, wisit.cheungpasitporn[at]bassett.org

Pulmonary blastomycosis: a new endemic area in New York state

We describe three cases of pulmonary blastomycosis in patients from central New York State (NYS). Two of these cases occurred in 2012, and in patients who resided in the same county. Moreover, two of these cases manifested with acute respiratory distress syndrome and survived. Interestingly, one of the two received corticosteroids and was extubated within 1 week. To the best of our knowledge, these are the first cases of human blastomycosis to be reported from NYS and we propose that corticosteroids administration might reduce hospitalisation time and ventilator‐associated complications, even though it is not currently recommended in standard treatment.

Bilateral putaminal hemorrhages: serious complication of methanol intoxication.

Context: Methanol intoxication is a life-threatening condition. Hallmark of clinical presentations include severe wide anion gap metabolic acidosis with very high serum osmolar gap and visual complication. Case Report: We report a case of severe methanol intoxication with bilateral putaminal hemorrhage, an uncommon serious complication. A 56-year-old man presented with altered mental status. Fundus examination showed optic disc edema. Arterial Blood Gas (ABG) revealed severe anion gap metabolic acidosis with osmolal gap. Head computed tomography (CT) showed hypodense lesions in basal ganglia bilaterally. Hemodialysis and intravenous fomepizole were initiated. Serum methanol level was significantly elevated. Unfortunately, patient was lethargic 2 weeks after discharge. Repeated CT of head demonstrated new putaminal hemorrhages. Conclusion: Bilateral putaminal hemorrhage is an uncommon but serious complication in methanol intoxication. Clinicians should have high index of suspicion for putaminal hemorrhage when patients with recent methanol intoxication present with altered mental status.

A rare case of ecthyma gangrenosum associated with methicillin-resistant Staphylococcus aureus infection

Ecthyma gangrenosum (EG) is a well-recognized dermatological condition caused by gram-negative bacillary infection, particularly Pseudomonas aeruginosa. Association with gram-positive cocci is very rarely reported in the literature. To the best of our knowledge, we describe the third case of EG caused by methicillin-resistant Staphylococcus aureus in a patient with AIDS who presented with multiple typical necrotic lesions.

Unveiling the hidden eagle: acute parotitis-induced eagle syndrome.

Context: A cervicofacial pain and foreign body sensation in pharynx associated with styloid process elongation is called Eagle syndrome. Typically, this syndrome is provoked by tonsillectomy or trauma. We report the first case of acute parotitis-induced Eagle syndrome. Case Report: A 65-year-old woman presented with right facial pain. CT scan of neck revealed asymmetric enhancement of the right parotid gland compatible with acute parotitis. All inflammation was resolved with antibiotics. However, the patient complained of pain in right mandibular region out of proportion to inflammation. Review CT found to have an asymmetrically long right styloid process measures. The diagnosis of acute parotitis-induced Eagle syndrome was established. Conclusion: Physicians should have a high index of suspicion for Eagle syndrome in patients with atypical neck pain and elongated styloid process since another significant manifestation of Eagle syndrome is carotid artery compression leading to recurrent syncope or stroke.

White willow bark induced acute respiratory distress syndrome

Dear Editor, A 61-year-old female with the past medical history of hypertension and osteoarthritis presented to Emergency Department with sudden onset of shortness of breath and non-productive cough 30 min, after taking white willow bark supplement. The patient denied any history of the drug or supplement allergy. Pulse oximetry demonstrated oxygen desaturation; SpO2 of 75% on ambient air and 94% on nasal cannula with the flow of oxygen 20 L/min. Arterial blood gas although on FiO2 of 100% showed severe hypoxemia with the high A-a gradient, metabolic acidosis with respiratory compensation (pH 7.28, PCO2 36 mmHg, PaO2 75 mmHg, and HCO3 19 mmol/L). Blood tests demonstrated evidence of wide anion gap (AG) metabolic acidosis (AG 14 mmol/L) from lactic acidosis (lactic acid 4.9 mmol/L) with the normal gap metabolic acidosis (∆AG/∆Bicarb = 0.4) and the patient had no osmolal gap. Furthermore, serum ketone and salicylate levels were undetectable and her chest X-ray showed bilateral interstitial infiltrates [Figure 1]. Transthoracic echocardiogram revealed normal systolic and diastolic function. The diagnosis of acute hypoxic respiratory failure secondary to severe acute respiratory distress syndrome (ARDS) from reaction to white willow bark was made; the PaO2/FiO2 of 75 mmHg. The patient was promptly started on intravenous venous methylprednisolone and oral antihistamines including diphenhydramine and ranitidine. The patient responded well with our treatment and her oxygen requirement gradually improved from 94% on FiO2 of 100% to 95% on room air. Lactic acidosis also subsided after maintaining adequate oxygenation. Figure 1 Chest X-ray demonstrated bilateral interstitial infiltrates The use of white willow bark supplement was first reported back to the time of Hippocrates (400 BC) when patients were advised to chew on the bark for pain relief and fever reduction. Willow bark is also included in weight-loss products.[1] There have been a remarkably small number of reported cases of adverse reactions to willow bark extract. These adverse drug reactions are usually mild (maculopapular rashes). White willow bark induced anaphylaxis is rare; however, a few cases have been reported.[2,3] To our knowledge, this is the first report of white willow bark induced ARDS. People who are allergic or sensitive to salicylates (such as aspirin) should not use willow bark.

Metabolic acidosis may increase fibroblast growth factor-23 and cardiovascular mortality in the community

To the Editor: Thank you for the excellent study on fibroblast growth factor-23 (FGF23) and cardiovascular mortality by Ärnlöv et al.1 The authors demonstrated an interesting association between higher FGF23 and increased risk of all-cause and cardiovascular mortality in the community. However, an interesting topic that the authors did not mention about was the degree of metabolic acidosis in the study population. The authors stated that FGF23 becomes elevated in chronic kidney disease (CKD) because of the yet unknown pathological factor(s). We are wondering whether metabolic acidosis has a key role behind this effect. Recently, Krieger et al.2 found that metabolic acidosis directly increased FGF23 mRNA and protein in neonatal mouse bone. If we can confirm these results in humans with CKD, we might be able to decrease FGF23 and cardiovascular mortality by therapeutic interventions for metabolic acidosis.

Reported Cases of Recurrent Takotsubo Cardiomyopathy with Variant Forms of Left Ventricular Dysfunction

We read with great interest the article by Aggarwal and Krantz, entitled “Migratory takotsubo cardiomyopathy in the setting of cholecystitis.” This was a very interesting case presentation regarding stress-related cardiomyopathy involving variable myocardial segments at different time points. The author mentioned that this was the first reported case. After careful review, however, we found several reports in the literature of recurrent takotsubo cardiomyopathy with variable patterns of left ventricular dysfunction. In 2007, Blessing et al reported a 70-year-old man with recurrent takotsubo cardiomyopathy demonstrating basal area akinesis initially and apical ballooning on the second episode. In 2009, Izumo et al reported a 78-year-old male with recurrent takotsubo cardiomyopathy. At the first episode, the patient was found to have apical akinesis and basal hyperkinesis while at the second episode; 2 years later, he was found to have mid-ventricular akinesis combined with normal apical wall motion. In 2011, From et al presented a clinical image of a 65-year-old female with recurrent takotsubo cardiomyopathy manifesting as typical apical ballooning at the first episode and mid-ventricular variant at

Therapeutic hypothermia and effects on coagulopathy

We thank Camp-Rogers et al [1] for their excellent case study “Therapeutic hypothermia after profound accidental hypothermia and cardiac arrest.” This was a very interesting case report as usual for the American Journal of Emergency Medicine. The successful therapeutic hypothermia after cardiac arrest in humans was first described in the late 1950s [2]. This therapy has subsequently been recommended by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation and the American Heart Association as one of the mainstay treatment after cardiac arrest [3]. Screening for coagulopathy before initiating the hypothermic protocols is vital and should have been addressed in the case study. Hypothermia may cause significantly impaired homeostatic and coagulation pathways from the fact that the kinetics of enzyme activity are temperature dependent [4]. Coagulopathy is one of the relative contraindication for therapeutic hypothermia. Blood tests for prothrombin time/partial thromboplastin time, fibrinogen, and D-dimer should be considered at admission and every 6 hours during hypothermia treatment period.