Unique presentation of cricoid cartilage fracture causing intermittent dyspnea without preceding trauma.

Cricoid cartilage fracture is generally caused by significant neck trauma and causes continuous dyspnea, neck pain, or hoarseness developing immediately after the traumatic episode. A 69-year-old woman without any history of trauma was admitted to our hospital with intermittent dyspnea. Six months before admission she had started to complain of dyspnea occurring several times a month without warning, improving spontaneously within a few hours without treatment. Her primary care doctor diagnosed asthma and she was treated with inhaled short-acting beta agonists and glucocorticoids, without improvement. On initial evaluation at our hospital, the cause of dyspnea was unclear. Laryngoscopy was performed, which excluded vocal cord dysfunction. A further attack of dyspnea occurred on the fourth admission day. Stridor was evident during the attack, and bronchoscopy revealed subglottic narrowing of the trachea on both inspiration and expiration with no mass or foreign objects. Computed tomography (CT) of the neck revealed cricoid cartilage fracture causing airway narrowing and dyspnea. She was orally intubated, and tracheostomy was performed 2 weeks later to maintain her airway, which resolved her dyspnea. This patient's presentation was unique in two aspects. First, there was no history of trauma that may cause her cricoid cartilage fracture. Second, her symptoms of dyspnea were intermittent rather than continuous. These aspects led to suspicions of other diseases such as asthma or vocal cord dysfunction, thus delaying the diagnosis. Cricoid cartilage fracture should be considered in patients with dyspnea of unknown cause, irrespective of continuous or intermittent symptoms and preceding traumatic episodes.

Chronic obstructive pulmonary disease in heart failure: accurate diagnosis and treatment.

Coincidence of COPD and heart failure (HF) is challenging as both diseases interact on multiple levels with each other, and thus impact significantly on diagnosis, disease severity classification, and choice of medical therapy. The current overview aims to educate caregivers involved in the daily management of patients with HF and (possibly) concurrent COPD in how to deal with clinically relevant issues such as interpreting spirometry, the potential role of extensive pulmonary function testing, and finally, the potential beneficial, but also detrimental effects of medication used for HF and COPD on either disease.

Diagnosis of elderly patients with heart failure.

The prevalence and mortality of heart failure (HF) increase with age. As a result, the early diagnosis of HF in this population is useful to reduce cardiovascular morbidity and probably mortality. However, the diagnosis of HF in the elderly is a challenge. These challenges arise from the under-representation of elderly patients in diagnostic studies and clinical trials, the increasing prevalence of HF with relatively normal ejection fraction, the difficulty in accurate diagnosis, the underuse of diagnostic tests, and the presence of co-morbidities. Particularly in the elderly, symptoms and signs of HF may be atypical and can be simulated or disguised by co-morbidities such as respiratory disease, obesity, and venous insufficiency. This review aims to provide a practical clinical approach for the diagnosis of older patients with HF based on the scarce available evidence and our clinical experience. Therefore, it should be interpreted in many aspects as an opinion paper with practical implications. The most useful clinical symptoms are orthopnoea and paroxysmal nocturnal dyspnoea. However, confirmation of the diagnosis always requires further tests. Although natriuretic peptides accurately exclude cardiac dysfunction as a cause of symptoms, the optimal cut-off level for ruling out HF in elderly patients with other co-morbidities is still not clear. In our opinion, echocardiography should be performed in all elderly patients to confirm the diagnosis of HF, except in those cases with low clinical probability and a concentration of brain natriuretic peptide (BNP) or N-terminal proBNP (NT-proBNP) lower than 100 or 400 pg/mL, respectively.

If at first you do not succeed, think again!

The authors describe a case of platypnoea orthodeoxia syndrome in an 83-year-old man with a fenestrated atrial septal defect and severe coronary artery disease. The patient had been admitted to hospital six times in the previous year with acute breathlessness, attributed to paroxysmal atrial fibrillation. The patient's symptoms resolved completely following surgical repair of the defect and coronary artery bypass grafting.

Dyspnoeic dysphasia: a series of unfortunate events.

We describe a case of a 56 year old man with no previous medical history who presented with sudden onset dyspnoea, expressive dysphasia, and right arm sensory loss and paresis. A diagnosis of bilateral pulmonary embolism and transient cerebral ischaemic attack was confirmed by CT pulmonary angiogram and MRI. Paradoxical embolism through an occult patent foramen ovale (PFO) was subsequently proven by contrast echocardiography. This case highlights a number of short and long-term management conundrums, that to date are incompletely addressed by clinical trials. These include timing of anticoagulation in patients with both venous thromboembolism and cerebral infarction, and the risk:benefit ratio of surgical closure of patent foramen ovale.

Contralateral diaphragmatic palsy after subcortical middle cerebral artery infarction without capsular involvement.

Diaphragmatic palsy after acute stroke is a novel clinical entity and may result in a high incidence of respiratory dysfunction and pneumonia, which especially cause greater morbidity and mortality. Generally, internal capsule and complete middle cerebral artery (MCA) infarctions are major risk-factors for developing diaphragmatic palsy. Herein, we present a case with contralateral diaphragmatic palsy after a subcortical MCA infarction without capsular involvement. Dyspnea occurred after stroke, while a chest X-ray and CT study disclosed an elevated right hemidiaphragm without significant infiltration or patch of pneumonia. A phrenic nerve conduction study showed bilateral mild prolonged onset-latency without any significant right-left difference. This suggested a lesion causing diaphragmatic palsy was not in the phrenic nerve itself, but could possibly originate from an above central location (subcortical MCA infarction). We also discussed the role of transcranial magnetic stimulation study in the survey of central pathway and demonstrated diaphragmatic palsy-related orthopnea.

Assessing validity by comparing transition and static measures of dyspnea in patients with acute decompensated heart failure.

This study assessed the convergent validity of 2 dyspnea measures, the transition measure and the change measure, by comparing them with each other in patients admitted to the hospital with acute decompensated heart failure. Static measures of dyspnea were obtained at baseline (pre-static measure) and at time 1 hour and 4 hour (post-static measures). The change measure was calculated as the difference between the pre-static and post-static measures. Transition measures were obtained at time 1 hour and 4 hour. Visual analog scales and Likert scales were used. Both physicians and patients measured the dyspnea independently. A total of 112 patients had complete data sets at time 0 and 1 hour and 86 patients had complete data sets at all 3 time points. Correlations were calculated between the transition measures and static measures (pre-static, post-static, and change measure). Bland-Altman plots were generated and the mean difference and limits of agreement between the transition measures and the change measures were calculated. In general, short-term dyspnea assessment using transition measures and serial static measures can not be used to validate each other in this population of patients being admitted with acute decompensated heart failure.

Signo de Westermark como sospecha de tromboembolismo pulmonar / Westermark sign and suspicion of pulmonary thromboembolism

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The third heart sound for diagnosis of acute heart failure.

Dyspnea is a common presenting complaint in the emergency department (ED). Rapid identification of heart failure as the etiology leads to early implementation of targeted therapies. Although having only intermediate sensitivity, the S3 is a highly specific finding among older adults with heart failure. Identification of an S3 by routine auscultation can be problematic given the chaotic and noisy ED environment, patient comorbid conditions, and intolerance of ideal positioning for auscultation. Technologies using computerized analysis of digitally recorded heart tones have recently been developed to aid the clinician with bedside detection of abnormal heart sounds. Data using these technologies and their applications in the ED are reviewed as well as implications for future use and research.

Miocardiopatía chagásica: una causa de insuficiencia cardiaca de origen infeccioso / Chagasic myocardiopathy: an infectious etiology of congestive heart failure

Se presenta el caso de un paciente latinoamericano con una miocardiopatía dilatada secundaria a una enfermedad de Chagas crónica tratada satisfactoriamente con medidas de soporte cardiológico. La intención es aportar una nueva etiología de insuficiencia cardiaca hasta ahora poco frecuente en nuestro medio pero que posiblemente vaya a aumentar debido a las corrientes migratorias actuales

We present a case report to Latin-American patient with dilated cardiomyopathy due to chronic Chagas´ disease which treat with usually cardiologic support. We report a new aetiology of heart failure uncommon in our country but it would rise due to immigration from endemic countries