Academic literature on the topic 'Respiratory Therapy – instrumentation – Examination Questions'

The multifactorial nature of subacute cough, combined with the anatomical and physiological characteristics of preschool children, the impossibility of their full examination in outpatient practice, complicates its diagnosis. An algorithm for the differential diagnosis of acute respiratory infections accompanied by subacute cough in preschool children has been developed, it can contribute to the early identification of its causes and targeted treatment of the disease that caused the cough. A sequence of diagnostic measures is proposed, it includes anamnesis of life and diseases with a list of key questions that should be asked when collecting anamnesis in children with prolonged cough; objective examination of the child; determination of the tactics of further management (inpatient or outpatient); the choice of therapy that is comparable to the intended diagnosis; and evaluation of ongoing therapy. The emphasis is made on the importance of a full-fledged collection of anamnesis, taking into account the data of the time and conditions of the disease, and clinical data for making a presumptive diagnosis in an outpatient practice. It is recommended to carry out trial therapy if the diagnosis is difficult. The article presents modern approaches to the diagnosis of bronchial asthma in children with recurrent virus-induced vising. The modern approaches to the diagnosis and treatment of acute respiratory infections of the upper and lower respiratory tract are outlined in accordance with the principles of evidence-based medicine. It is noted that the most effective methods of treating cough are etiological and pathogenetic approaches, which consist in eliminating or weakening the action of factors that cause cough. It is emphasized that if treatment is impossible or insufficient, symptomatic cough therapy should be carried out. The main directions of symptomatic treatment of cough have been substantiated, which include measures to improve the drainage function of the lungs and restore adequate mucociliary clearance. The expediency of using ambroxol and acetylcysteine preparations was confirmed. Attention is also paid to the use of centrally acting antitussives. Discussion of the problem «to treat or not to treat subacute cough in acute respiratory infection of the upper respiratory tract» from the standpoint of evidence-based medicine is shown. No conflict of interest was declared by the authors. Key words: children, subacute cough, acute respiratory infections.

Bronchopulmonary dysplasia (BPD) is a morbidity of prematurity with implications for respiratory and neurologic health into adulthood. Multiple risk factors contribute to the development of BPD leading to examination of various prevention strategies. The roles of systemic corticosteroids and caffeine have been addressed by the American Academy of Pediatrics. The place in therapy of other agents commonly utilized in clinical practice remains unclear. Inhaled nitric oxide has been the subject of numerous large, randomized controlled trials in preterm infants. Despite sound rationale, these trials have largely failed to document benefit, suggesting a limited role for inhaled nitric oxide therapy in the preterm population. In contrast, intramuscular vitamin A has been documented to reduce the incidence of BPD in randomized trials. However, the invasiveness and the sporadic availability of this therapy have led to decreased utilization. All macrolide antibiotics do not appear to have a similar impact on the incidence of BPD; however, azithromycin administered to infants colonized with Ureaplasma may have impact. Questions remain about the optimal dosing approach and long-term safety of this intervention. Finally, diuretic therapy is widely used in clinical practice despite significant toxicities and limited data supporting a role in BPD prevention. Taken together, available data suggest that caffeine and selective use of corticosteroids remain the mainstays of pharmacologic BPD prevention.

The global pandemic known as coronavirus disease 2019 (COVID-19) was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This review article presents the taxonomy of SARS-CoV-2 coronaviruses, which have been classified as the seventh known human pathogenic coronavirus. The etiology of COVID-19 is also briefly discussed. Selected characteristics of SARS-CoV-2, SARS-CoV, and HCoV-NL63 are compared in the article. The angiotensin converting enzyme-2 (ACE-2) has been identified as the receptor for the SARS-CoV-2 viral entry. ACE2 is well-known as a counter-regulator of the renin-angiotensin system (RAAS) and plays a key role in the cardiovascular system. In the therapy of patients with COVID-19, there has been a concern about the use of RAAS inhibitors. As a result, it is hypothesized that ACE inhibitors do not directly affect ACE2 activity in clinical use. Coronaviruses are zoonotic RNA viruses. Identification of the primary causative agent of the SARS-CoV-2 is essential. Sequencing showed that the genome of the Bat CoVRaTG13 virus found in bats matches the genome of up to (96.2%) of SARS-CoV-2 virus. Sufficient knowledge of the molecular and biological mechanisms along with reliable information related to SARS-CoV-2 gives hope for a quick solution to epidemiological questions and therapeutic processes.

Abstract Introduction: The combination of fludarabine, cyclophoshamide and rituximab (FCR) represents the current standard of treatment of fit patients with chronic lymphocytic leukemia (CLL). However, despite the success of the FCR regimen, a number of questions exist on its optimal administration as well as on its short and long term toxicity. As a consequence, in the daily practice (Knauf et al, Hematological Oncology, 2015) less intensive regimens such as bendamustine plus rituximab (BR) are often adopted also in fit patients. Most data on the FCR regimen derive from clinical trials, while data from real life are poor. Methods: Here we report our experience on a series of 50 previously untreated patients with CLL, managed with FCR at a single institution in Italy. Patients were programmed to receive 6 courses plus 2 additional rituximab infusions. The median age of the whole patient population was 60 years (range 41-75), there were 29 males (58%) and 21 females (42%). 44 patients (88 %) received the classical schedule (Fludarabine 25 mg/sqm and Cyclophosphamide 250 mg/sqm, on days 1-3) , while 6 patients (12%), all aged over 70 years, were given FCR-lite (Fludarabine 15 mg/sqm and Cyclophosphamide 200 mg/sqm). In all patients Rituximab was given at 375 mg/sqm on course 1, and 500 mg/sqm infusions 2 to 6. According to Binet staging system, 20 patients were in stage B and 30 in stage C. Patients were carefully selected according to the absence of hepatic, cardiac, renal and respiratory comorbidity and medical judgment (go patients). 40 patients were evaluable for cytogenetic examination (FISH) and none of them had 17 p abnormality. Results: Overall, 46 patients (92%) received the 6 programmed FCR courses, while in four patients therapy was stopped after 1, 2, 4 and 5 courses due to unexplained cytopenia, while CLL cells were undetectable in the bone marrow. Overall response rate was 90 % (74 % CR, 16 % PR) The median duration of response was 30 months, after a median follow up of 38 months. 8 patients have relapsed from CR achievement and 2 of them achieved sustained response with BR, one is on treatment with ibrutinib, while 5 were refractory to salvage therapy. 5 patients died in the setting of refractory disease, 44 are alive and one has been lost to follow-up. Major toxicities (grade 3-4) included: neutropenia registered in 25 patients (50 %), needing G-CSF administration in all cases and producing delay in the administration in 35 % of patients; anemia requiring blood transfusions was registered in 10% of the cases, while no patient required platelet units. Hepatitis B and Herpes Zoster virus reactivation occurred in 1 (2%) and 2 patients (4%), respectively. Overall, 5 patients were hospitalized, all because of febrile neutropenia successfully managed with antibiotic therapy and G-CSF. Conclusions: We conclude that FCR in the "real life" is effective and well tolerated in patients with advanced CLL, provided that a careful evaluation of is made as to eligibility to therapy, mainly in terms of absence of comorbidities. This work was supported by AIL Napoli, "Sezione Bruno Rotoli". Disclosures No relevant conflicts of interest to declare.

The past three years have seen an overwhelming increase in the number of dysphonic patients in our clinics. This phenomenon goes hand in hand with increased opening of call centers nationwide and increased demand for teachers, singers and performers abroad. This article discusses simple steps for the Otolaryngologist interested in evaluating these patients with different voice demands. It is important to recognize these common voice problems and address them promptly, or to refer them accordingly to Voice Centers if necessary. Chief Complaint The most common chief complaint is change in the quality of the voice or hoarseness. Hoarseness means a change in the perception of one’s voice, described as harsh, raspy, “paos” or “malat.” Other complaints include breathiness, throat pain, neck pain, inability and unrealibility to reach high notes. Inability to reach high notes suggests edema of the vocal folds making them more plump, as can be found in reflux laryngitis, allergies, or smoking. Lesions such as nodules, polyps and cysts cannot be discounted because they prevent vocal fold closure especially during high notes1 Throat and neck pain without an accompanying history of infection may suggest muscle tension dysphonia, especially in a voice professional who later develops maladaptive ways of talking that could strain other throat and neck muscles in an effort to speak.2 Frequent throat clearing, a sensation of phlegm in the throat and cough are also important chief complaints that may lead the otolaryngologist to the cause of the voice problem. In the absence of upper respiratory tract infections and post-nasal discharge, these could be suggestive of laryngopharyngeal reflux.3 History Does the hoarseness occur on and off? Was it sudden? After shouting in a basketball event? Is it becoming worse and permanent? What triggers or relieves it? Intermittent hoarseness could be due to voice abuse and misuse especially in a voice professional. Sudden hoarseness especially after watching a basketball event could be suggestive of vocal fold hemorrhage. A voice problem becoming worse and permanent could be a growing polyp or cyst, vocal fold paralysis in laryngeal cancer or thyroid cancer. A long lecture triggering the hoarseness and rest relieving it may suggest soft nodules, or Reinke’s edema due to vocal fold trauma of voice abuse and misuse. To begin with, it is important to know the occupation of our patient. Is our patient a voice professional- someone who uses his or her voice for a living? Voice demands at work contribute to voice change significantly and voice abuse and misuse is one of the most common causes of hoarseness. What are the other associated symptoms? Medical problems like a recent bout of upper respiratory tract infection and allergies are among the most common causes of hoarseness and should not be discounted immediately. Symptoms of hyperacidity are also significant.4 Is there a history of breathiness and difficulty of breathing? Voice fatigue, tremor, hypo or hypernasal voice? Choking, globus, odynophagia or dysphagia? Neck pain or head and neck trauma? These questions can give clues to the clinician regarding the possible cause of the problem. Past Medical History Asthma, COPD, pulmonary malignancy are associated with voice changes due to decreased airflow. Gastric ulcers and GERD can be suggestive of associated laryngopharyngeal reflux disease changing the vocal fold mucosa leading to voice change.3 Parkinsonism, myasthenia, traumatic brain injury and movement disorders can cause tremors, weakness or strained voice quality. Rheumatoid arthritis, SLE, and other autoimmune disorders can cause voice changes such as paralysis in RA. Endocrine problems such as hypothyroidism can cause edema of the vocal folds leading to decrease in pitch. Thyroid cancer can cause vocal fold paralysis. A history of radiation secondary to malignancies in the head and neck can cause vocal fold scarring leading to voice change.1 Personality and psychiatric disorders also lead to diagnosis. The outgoing, type A personality usually has vocal fold nodules; while inhibited and shy persons have functional dysphonias.5 Traumatic life events are also very important to take note of. History of surgery for neck trauma, thyroid nodules or malignancies, spine, cardiac, pulmonary and brain surgeries or previous endotracheal intubation can cause voice changes, usually related to vocal fold mobility problems. 1 Medications such as inhalational steroids for asthma can cause fungal laryngitis. ARB and ACE inhibitors for hypertension can cause non specific vocal fold masses. Antitussives, decongestants, antihistamines and Vitamin C are known to cause dryness of the vocal folds. Pills with sexual hormones can cause either elevations or decreases in pitch.6 Smoking can cause polypoid conditions in the vocal folds, pre-malignant or malignant changes. Intake of alcohol, diet and lifestyle can contribute to reflux problems and dysphonia. Physical Examination Hearing the patient and forming a subjective impression of the patient’s voice should automatically be part of the interview process. Ranking the voice according to a standard scale is subjective but becomes increasingly reproducible and precise with training and experience. Voice can be evaluated according to pitch, loudness, and vocal quality. Pitch is the highness or lowness of the voice. Is the speaking voice too low for the soprano? This could be the problem why a trained singer would have dysphonia. Does the woman sound like a man over the phone? This could be Reinke’s edema, maybe she is a smoker as well. Does the adult male suddenly speak with elevated pitch? This could be vocal fold paralysis. Loudness is the power of the voice. This is due to the source of power, the lungs. Posture, type of breathing, technique or training can affect this. Systemic problems like generalized weakness and cachexia are contributory. Of course pulmonary problems can contribute to decreased power. Voice quality can be evaluated using the GRBAS system.7 Just hearing the voice and using this system is helpful in making an impression. G- grade R- roughness B- breathiness A- asthenia S- strain GRBAS uses a 0 to 3 scale (0= normal or absence of deviance; 1=slight deviance; 2=moderate deviance; 3= severe deviance). Grade relates to the overall voice quality, integrating all deviant components GRBAS Sounds Probable Conditions Roughness Grainy quality; diplophonic Vocal fold masses such as nodules, polyps, cysts, laryngitis Breathiness Airy Unilateral paralysis, bowing, atrophy, abductor spasmodic dysphonia Asthenia No voice Bilateral paralysis in paramedian position, vocal fold atrophy Strain Tight quality Abductor spasmodic dysphonia, muscle tension dysphonia Head and Neck Examination Palpating the neck, especially the base of the tongue, and neck muscles which are tense and tender can be suggestive of an ongoing muscle tension dysphonia as a cause of the voice change.8 Thyroid masses, neck nodes, etc can be helpful in leading the clinician to a diagnosis. Visualizing the larynx has evolved as advances in technology have improved the understanding of vocal fold anatomy, physiology and voice production. At present, there is no single laryngeal examination tool that is superior to the others. What is important is that it gives a thorough visualization of the anatomy and a good functional evaluation of the larynx. Selecting the appropriate instrumentation will be possible if we recognize the advantages and limitations of the diagnostic tool we are using.9 Sometimes, a combination of these tools is important to make an accurate diagnosis. Advantages and Limitations of the Different Instruments to Visualize the Larynx Instrument Advantages Limitations Indirect Mirror Laryngoscopy Readily available; inexpensive Gives a gross idea of the anatomy; mobility; mucus; and mass (if big enough) Limited in patients who are hypergag; patient is not in a normal physiologic position; hard to detect paresis and small lesions Transnasal Flexible laryngoscopy Helpful for hypergag patients; patients physiology involving the tongue, pharynx and palate are well visualized; can assess paresis from paralysis; can be recorded for review Small lesions are hard to differentiate; color might not be reliable depending on the camera; may be expensive Rigid 70 or 90 degrees laryngoscope Extremely clear and magnified view; less expensive; can be recorded for review Limited in patients who are hypergag; patient is not in a normal physiologic position; hard to detect paresis and muscle tension dysphonia Videostroboscopy10 Provides a slow motion evaluation of vocal fold vibratory pattern, closure, mucosal wave; can differentiate benign vocal fold lesions Expensive; requires additional training Some helpful vocal tasks when using a flexible scope: Task Endoscopic Findings /ii/ Adduction Sniff Abduction Hee-hee-hee Either decreased adduction or abduction Sniff then /ii/ Fatigues the vocal folds; detects paresis/ weakness /ii/ glide form low to high pitch ability to lengthen the vocal folds Despite technological advances in laryngology, a good history and physical examination are still crucial in the diagnosis of voice disorders. Certain clues can be provided by a good history that especially point to a hoarse patient. Because no single instrument is superior for visualization of the larynx, it is important to recognize the advantages and limitations of each.

Objective: To assess the level of adherence to medical prescriptions and recommendations by patients with bronchial asthma (BA), in order to achieve control over the symptoms of the disease; to identify the most common factors of low adherence to BA therapy; to suggest strategies for optimizing treatment compliance. Methods: 92 children with a verified diagnosis of BA were examined. All patients underwent a general clinical, laboratory and instrumental examination, as well as an additional screening test with a mixture of respiratory allergens – the ImmunoCapPhadia® 250 method. The control of BA symptoms was assessed using ACT and ACQ tests. Adherence to BA therapy was assessed using a questionnaire. Results: Analysis of gender differences revealed that the proportion of male patients was 58%; female – 42%. The median age was 11 years. The average age of diagnosis of BA in children was 9 years. All patients were hospitalized during the period of exacerbation of the disease, the proportion of children with an attack of moderate BA – 87%; severe – 13%. An intermittent course of BA was observed in 28%; a persistent course in 72%. Analysis of ImmunoCap Phadia®250 data revealed that in 17.2% of cases class V sensitization prevailed, and the average values of allergen-specific IgE antibodies were 69.82 kU/L. Assessment of the level of control over asthma symptoms and the use of AST and ACQ tests revealed that partially controlled the course of BA was noted by 56% and uncontrolled over 46% of children. Analysis of the «Questionnaire of adherence to treatment of bronchial asthma (BA) in children», differences were found in the response to questions: «Do you experience difficulties in using the inhaler?» (χ2=8.952; p=0.003), «Was there any reluctance to take medications?» (χ2=4.715; p=0.03); «Does it happen that you forget to take drugs one/several days?» (χ2=5.093; p=0.025), «Are you satisfied with the prescribed therapy for BA?» (χ2=5.093; p=0.025). Conclusions: In order to achieve success in long-term control of the symptoms of BA in a patient, a comprehensive approach to the treatment and prevention of exacerbation of BA is required with an individual approach to each child, both from the doctor and from an adult who participates in the conduct and adherence to doctors appointments. Keywords: Asthma, children, adherence, compliance, symptom control.

An intramyocardial dissecting hematoma is a rare mechanical complication after an acute myocardial infarction that carries a high mortality rate. Because intramyocardial dissecting hematomas are associated with multiple cardiac complications, cardiac imaging is an integral component to guiding therapy. We present a case of an intramyocardial dissecting hematoma treated conservatively. Here we explore the role of surgery in patients with intramyocardial dissecting hematomas as well as issues of optimal medical management including the decision to anticoagulate. In conclusion, this report offers a unique commentary on a rare case of an intramyocardial dissecting hematoma.RésuméUn hématome disséquant intramyocardique est une rare complication mécanique après un infarctus aigu du myocarde qui comporte un taux élevé de mortalité. Parce que les hématomes dissection intramyocardique associés à de multiples complications cardiaques, l’imagerie cardiaque est une composante intégrale de guider le traitement. Nous présentons un cas d’hématome disséquant intramyocardique traités conservativement. Ici, nous examinons le rôle de la chirurgie chez les patients souffrant d’hématomes dissection intramyocardique ainsi que des questions de gestion médicale optimale y compris la décision d’anticoagulate. En conclusion, ce rapport offre un unique commentaire sur un cas rare d’un hématome disséquant intramyocardique.A dissecting intramyocardial hematoma is a rare mechanical complication after an acute myocardial infarction (AMI) that carries a high mortality rate. The pathophysiology of a dissecting intramyocardial hematoma involves hemorrhagic dissection through an area of necrotic tissue between the spiral myocardial fibres of the ventricle.1 Although most intramyocardial dissections occur in the left ventricle, the dissection plane can progress to lower pressure areas and involve the right ventricle as myocardial fibres are shared.1 Intramyocardial dissections are most commonly seen as a complication of an acute AMI, but have also been described following blunt chest trauma, and rarely, from cardiac echinococcus infections.2 Because intramyocardial hematomas are associated with multiple cardiac complications such as ventricular rupture, biventricular dysfunction, and thrombus formation, cardiac imaging is an integral component to guiding therapy. We present a case of intramyocardial dissection treated with conservative management.CaseA 58-year-old male presented to the emergency department with a one-day history of shortness of breath occurring at rest. Further history revealed progressive dyspnea with exertion over the prior two months and intermittent chest tightness. He denied symptoms of typical angina. His medical history was significant for hypertension, hypercholesterolemia, and peripheral vascular disease with remote aorto-bifemoral bypass surgery. He had a 20-pack year history of smoking. His only medication on presentation was low-dose aspirin.On examination, his vital signs were as follows: temperature of 36.6°C, heart rate of 98 BPM, blood pressure of 131/105 mmHg, respiratory rate of 20, and an oxygen saturation of 99% on room air. His precordial examination was normal and there was no evidence of volume overload. Initial laboratory investigations showed a mildly elevated high-sensitivity troponin I which peaked at 39 ng/L. Chest radiography showed mild vascular redistribution but no evidence of overt heart failure. ECG showed sinus rhythm with poor R-wave progression but no ST-segment deviation or Q-waves to suggest a prior MI. The patient was subsequently admitted to hospital for further work-up of his shortness of breath.A transthoracic echocardiogram was performed which showed a dissecting intramyocardial hematoma from the mid segment of the left ventricular septum extending to the apex of the left ventricle (Figure 1 and Supplemental Videos 1 and2). The hematoma occupied approximately 50% of the left ventricular cavity, and the estimated left ventricular ejection fraction was 25–30%. The hematoma did not appear to receive any flow from the cavity of the left ventricle itself. There was no left ventricular thrombus identified. All other segments of the ventricle were either hypokinetic or akinetic and thinned. Surgical options were explored, but it was determined that the patient would be at excessive risk for morbidity and mortality with surgical resection of the hematoma due to the extent of left ventricular involvement. The patient was started on medical treatment for congestive heart failure. Due to the concern for myocardial rupture, no anticoagulation or anti-platelet therapies were given. Cardiac catheterization was not performed as there was no good option for revascularization.Six days later, cardiac magnetic resonance imaging (MRI) was performed to reassess the hematoma. The MRI identified a well-defined heterogeneity within the left ventricular mid to apical cavity extending into the apex, raising concern for an intramural dissecting hemorrhage of the myocardium or intracavitary thrombus (Supplemental Video 3). There was also late enhancement of the left ventricular septal and apical segments extending into the right ventricle, indicating an extensive left anterior descending artery territory AMI (Figure 2). Although it was unclear whether the thrombus was contained within the myocardium, anticoagulation was not pursued because of the concern that it would impair healing of, or potentially worsen, the hematoma. A repeat echocardiogram was performed two months after initial presentation, which showed an ejection fraction of 20–25%, a new large apical thrombus, and complete thrombosis of the intramyocardial dissection (Figure 3 and Video4). This was confirmed by cardiac MRI (Figure 4). The patient was subsequently started on warfarin therapy.Figure 1: Two-dimensional echocardiogram from four-chamber view showing the somewhat mobile intramyocardial dissecting hematoma occupying the distal one third of the LV cavity (arrow).Figure 2: Post-gadolinium enhanced cardiac MRI showing an extensive antero- septal and apical transmural MI (yellow arrow) extending into the apical part of the RV and the non-enhancing intramyocardial dissecting hematoma (red arrow). Figure 3: Two-dimensional echocardiogram from four-chamber view at follow-up showing a large wall-adherent apical thrombus (arrow).Figure 4: Post-gadolinium enhanced cardiac MRI confirming structure seen on echocardiogram was a showing a large, non-enhancing and wall-adherent apical thombus (arrow).DiscussionThis case describes a left ventricular dissecting intramyocardial hematoma which was likely the result of a late presenting AMI. Although coronary angiography was not performed to identify the culprit lesion, based on non-invasive imaging we suspect that the myocardial dissection originated in the left ventricle following an extensive antero-septal AMI.1,3 While the mild troponin elevation and lack of overt ischemic signs on electrocardiogram challenge this assertion, the severe regional hypokinesis and signs of ventricular thinning and remodelling on echocardiogram and MRI suggested infarcted tissue, likely in the LAD territory.There is limited data available on the appropriate management of dissecting intramyocardial hematomas following AMI. This is mainly due to their relative infrequency, with the literature limited to case reports and case series. Acute surgical options include application of pericardial patches or other prosthetic material (such as gore-tex or teflon felt), accompanied by excision of necrotic tissue, and coronary artery bypass grafting.1A case review in 1993 examined survival rates in 16 patients with intramyocardial hematomas treated either surgically or medically. This case review observed that only 10% of patients treated conservatively survived past 30 days in contrast to all patients treated surgically.1 While this may suggest that surgical management offers a better prognosis, the finding may have also been due to patients undergoing surgery being at lower risk (due to anatomic factors related to the hematoma or patient comorbidities) compared to those treated conservatively. Conversely, Vargas-Barron et al., examined 15 patients with intramyocardial dissections with a 12-month follow-up period, with 9 patients presenting with an apical free-wall dissection and 6 patients with dissections extending into the septum and/ or right ventricle.4 In the first group, all patients were treated conservatively with all patients surviving to follow up at one year, although 4 patients had worsening heart failure.4 In the second group, 80% of those treated surgically died, compared to 50% who underwent coronary angioplasty and 100% of those conservatively managed.4 This study suggests that conservative management may be a reasonable option in patients with less complicated hematomas, while those with more complicated features are at a high mortality risk irrespective of the course of treatment. While our patient likely fit into the latter group with a more extensive dissection, the primary reason for surgical exclusion was the extent of the hematoma without well-perfused residual tissue to surgically remodel the ventricle.Patients who are conservatively managed for an intramyocardial hematoma are at high risk for further major adverse events and require close follow-up. Concomitant heart failure secondary to MI can lead to left ventricular dysfunction and significant comorbidities, and treatment with proven heart failure medications is essential. Patients with a reduced ejection fraction are also at increased risk of apical thrombus formation.In patients with a myocardial dissection, the decision to anticoagulate must carefully balance the increased risk of stroke and possibility of dissection extension, a potentially devastating consequence. Studies investigating ventricular remodelling after an AMI suggest substantial remodelling, infarct thinning, and reduction of infarct extent typically occur within the first month of healing.5 Thus, deferring any anticoagulation for at least4 weeks may be prudent to allow for healing of the hematoma, as long as no clear indications (e.g., left ventricular thrombus) arise.In our patient, a follow-up echocardiogram performed after two months revealed a large apical thrombus, and anticoagulation was initiated at that point in time.Little is known about the long-term survival of conservatively treated dissecting intramyocardial hematomas. In a study of 8 patients with intramyocardial dissecting hematomas treated with medical management, six were alive at a mean follow up of 12 months.4 One case report has identified a case of a medically treated intramyocardial dissection with event free follow up extending to 40 months.6 Cases of prolonged survival seem to be related to a decrease in size or complete resolution of the hematoma, as was seen in our patient, underscoring the need for serial cardiac imaging both to determine prognosis and to guide therapeutic decisions.7 With improvement or resolution of the hematoma, the primary risks of morbidity and mortality will likely be related to heart failure as well as arrhythmias from scarring; long-term prognosis will depend on optimal heart failure management (e.g., evidence based heart failure medications and evaluating for implantable cardioverter defibrillator [ICD] and cardiac resynchronization therapy [CRT] placement). Finally, in appropriate patients, cardiac transplantation may be considered as a treatment option.References1. Pliam M, Sternlieb J. Intramyocardial dissecting hematoma: An unusual form of subacute cardiac rupture. J Cardiac Surg 1993;8(6):628–37.2. Sari I, Davutoglu V, Kucukdurmaz Z. Intramyocardial dissection after subacute anterior wall myocardial infarction: An unusual form ofmyocardial rupture with subsequent spontaneous healing. Echocardiography2007;25(2):228–30.3. Tighe D, Paul J, Maniet A, et al. Survival in infarct related intramyocardial dissection: Importance of early echocardiography and prompt surgery. Echocardiography 1997;14(4):403–8.4. Vargas-Barrón J, Roldán F, Romero-Cárdenas Á, et al. Dissecting intramyocardial hematoma: Clinical presentation, pathophysiology, outcomes and delineation by echocardiography. Echocardiography 2009;26(3):254–61.5. Hillenbrand H, Sandstede J, Störk S, et al. Remodeling of the infarct territory in the time course of infarct healing in humans. Magnetic Reson Mat Phys Biol Med 2011;24(5):277–84.6. Drozdz J, Kasprzak J, Krzeminska-Pakula M. Spontaneous closure (thrombosis) of the intramyocardial dissection: 40-month follow-up. J Am Soc Echocardio 2002;15(9):1023–24.7. Vargas-Barrón J, Romero-Cárdenas A, Roldán F, et al. Long-term follow-up of intramyocardial dissecting hematomas complicating acute myocardial infarction. J Am Soc Echocardio 2005;18(12):1422.e1–1422.e6.