Bilateral Simple Orthotopic Ureteroceles in an Adult Male Complaining of Urgency and Pain on Urination

We report a case of a 38-year-old man with a simple orthotopic bilateral ureterocele and pain on urination that was improved by transurethral incision. His symptoms were present for 3 years since he first visited our hospital in 2012. Cystoscopy at our hospital revealed a simple bilateral ureterocele, and he was given an alpha blocker plus anticholinergic agent. The medication did not relieve his symptoms. Three years after his initial visit in 2012, he returned for a re-evaluation in May, 2015, because his symptoms had worsened. Computed Tomography (CT) showed normal locations of the bilateral ureteric orifices in the bladder, bilateral ureterocele with a right-sided predominance and a cobra head sign, and bilateral hydroureter. We performed a transurethral incision of his ureteroceles. Intraoperatively, we found that the urete-rocele on the right ureter entered the opening and expanded at the time of urine discharge. The symptoms significantly improved after the procedure.


Introduction
Simple ureterocele generally has few symptoms and is often treated conservatively [1] [2]. The most frequent symptoms are urinary tract infection, dysuria, palpable abdominal tumor, and vesicoureteral reflux (VUR). The majority of ureteroceles are related to duplex systems and are ectopic. Simple ureterocele usually remain asymptomatic and/or unrecognized in adults. We report a case of an adult male with simple orthotopic bilateral ureteroceles and pain on urination that was improved by transurethral incision. A 38-year-old man with a history of childhood asthma visited a community hospital complaining of urgency and pain on urination present for 3 years. Cystoscopy at our hospital revealed a simple bilateral ureterocele, and he was given an alpha blocker plus anticholinergic agent (Figure 1). The medication did not relieve his symptoms, and he experienced adverse effects including dizziness. The medication was thus discontinued, and he left our hospital.

Case Presentation
Three years after his initial visit in 2012, he returned for a re-evaluation in May, 2015, because his symptoms had worsened. Laboratory evaluation revealed white blood cells (WBC) 6300 cells/mL, hemoglobin 16.0 g/mL, hematocrit 45.1%, blood glucose 175 mg/dL, blood urea nitrogen 14.5 mg/dL, creatinine 0.73 mg/dL, and C-reactive protein 0.05 mg/dL; 0-1 WBC and 0-1 erythrocyte per high-power field were seen in his urine.
On cystoscopy, the bilateral ureterocele appeared larger than it was 3 years previously ( Figure 2). Computed Tomography (CT) showed normal locations of the bilateral ureteric orifices in the bladder, bilateral ureterocele with a right-sided predominance and a cobra head sign, and bilateral hydroureter ( Figure 3). The patient's symptoms were slightly relieved following prescription of tadalafil 5 mg/day. However, after requesting a consultation for further symptom relief, he consented to surgical treatment, and we performed a transurethral incision of his ureteroceles. Intraoperatively, we found that the ureterocele on the right ureter entered the opening and expanded at the time of urine discharge. The ureterocele on left side also entered the ureteric orifice, but was smaller than the one on the right (Figure 4). After performing the incision, we confirmed that, on both sides, the ureteric orifices did not act like golf holes to permit VUR after the operation. The symptoms significantly improved after the procedure, and the patient was satisfied with the outcome. No postoperative complications or pyelonephritis occurred, and the symptoms have not reappeared in the 3 months following surgery.  Ureteroceles are bilateral in 10% and occur in 80% in upper poles in duplex systems [4].
This case was a simple bilateral single system ureterocele located in a normal ureteric orifice. A simple ureterocele usually has few symptoms. Symptoms that lead to the discovery of a simple ureterocele include urinary tract infection, sharp pain caused by a calculus in the ureterocele, dysuria caused by a huge cele that obstructs the internal urethral orifice, or a palpable abdominal tumor that acts like a huge cele [5]. A case of prolapse of a simple ureterocele presenting as perineural tumor was reported in a young woman [6]. Treatment of simple ureteroceles is generally conservative. If recurring urinary tract infections caused by urinary tract obstruction, cannot be resolved by treatment with antibiotics or VUR, surgical treatment may be considered. Transurethral incision is often performed for ureteroceles, and VUR is a common surgical complication [7]. This patient's chief complaint was urgency and pain on urination, which rarely leads to suspicion of a uretocele. He had no episodes of repeated urinary tract infection or VUR, but based on the cystoscopy findings, we have concluded his symptoms might have been caused by expansion of the ureteroceles and tugging of the vesical trigon at the time of urine discharge. We also have concluded that the symptoms would have improved following removal of the ureteroceles. We performed the transurethral incision of the ureteroceles when the patient gave his consent after being told that his symptoms might not improve following the procedure. Considering the improvement of the symptoms and the patient's satisfaction with the outcome, we believe that the ureteroceles may have been responsible for the urinary symptoms.

Conclusion
We report the case of an adult male with simple orthotopic bilateral ureteroceles and pain on urination that was improved by transurethral incision.

Case Report
A 35-year-old married female presented to us with history of hemoptysis of six months duration. There was no other history of excessive cough or fever. A chest X-Ray ( Figure 1& Figure 2) showed, to our utter surprise, a nasal ring in the upper zone of right lung with evidence of mild bronchiectatic changes in the right lung. On close interrogation, the patient did remember losing this ring about eight years back while asleep at night and had been searching for it since next day morning. The patient was unaware of having aspirated nasal ring as she did not experience any symptoms of choking, coughing or respiratory distress. She remained asymptomatic for next eight years except for occasional episodes of upper respiratory tract infections and fever off and on, which were ignored by her primary care physician.
On admission, a computerised tomography scan of chest was performed, which revealed collapse of right upper lobe with bronchiectatic changes (the CT scan images are however not available) .Bronchoscopic removal of the foreign body was attempted but was not successful, as the foreign body was deeply impacted in the right upper lobe. A decision was taken to proceed with right upper lobectomy. The procedure was performed via a standard right postero-lateral thoracotomy. During the procedure, the upper lobe bronchus was encircled and divided carefully to recover the offending ring ( Figure 3). The patient had an uneventful post-operative recovery and is doing well on last follow-up which was 6 months after the surgery.

Discussion
Foreign body aspiration refers to the inhalation of solid and liquid material in to the airways. The foreign body may be lodged in to the main bronchus and its branches and may even reach the lungs. The right main bronchus is frequently implicated because of more vertical path. The upper lobe and the superior segment of the lower lobes are thus commonly affected when the patients are in recumbent position. Foreign body aspiration is a common accident in childhood with a high incidence of mortality and morbidity. Children between one to three years of age are more vulnerable [4] [5], due to their lack of dentition and inherent nature to explore their world by putting objects in their mouth. The other age group which is affected by foreign body aspiration is elderly people with poor dentition and with altered sensorium, such as with history of drug or alcohol use. It is extremely rare to find foreign bodies in young healthy adults, as in our case, and that too without producing any apparent symptoms.
Many varieties of foreign bodies may be inhaled, with organic foreign bodies being more common than inorganic (67% versus 33%) [6]. The severity of signs and symptoms depend on site, size, composition and duration of lodgement of the foreign body.
Organic foreign bodies are more dangerous as compared to metallic ones due to the severe lipoid reaction caused by them. Amongst the inorganic foreign bodies those with sharp edges cause early symptoms. Longer the foreign body stays in the airway, the more likely it is to migrate distally and to give rise to inflammatory reactions, granulation and impaction. This is what happened in our case, because of which bronchoscopic removal was unsuccessful.
Diagnostic imaging plays a variable role. Most of the foreign bodies are not radiopaque. Plain films, therefore, may be fallacious unless they are taken in full expiratory phase. On expiration, air trapping, obstructive emphysema and mediastinal shift may be documented as corroborative evidences. When chest radiograph is normal but suspicion is high helical CT and virtual bronchoscopy can be considered [7].
The rigid bronchoscope remains the gold standard for safe removal of tracheobronchial foreign body [8]. Surgery is very rarely called for. In our case, the only feasible option was a lobectomy as endoscopic removal had failed due to the chronicity of the foreign body and the patient was having hemoptysis due to bronchiectatic changes in the lung.
Informed consent was taken from the patient to report this case. The type of foreign body reported here is not unusual but the course of events is. Often patients have remembered the history of inhalation. However, in our case the patient missed both the in-halation and signs and symptoms of aspiration. Probably inert gold material had minimal tissue reaction and the metallic object allowed the movement of air in the lung without complete obstruction. She did not have any predisposing factors either like advanced age, neurological disorders, alcohol consumption, poor dentition and sedative use [9] [10]. Diagnosis was delayed for eight long years probably due to incomplete ob-struction of the airway. Gradually patient may have developed bronchiectatic changes, due to chronic irritation by the foreign body, superimposed with some lower respiratory tract infection which led to delayed presentation with hemoptysis and the ultimate penalty was in the form of lobectomy.
What makes this case unusual is the rather delayed and innocuous presentation after aspiration of such a large foreign object. It emphasizes the fact that healthy adults may tolerate aspiration of foreign bodies for a long time without acute life-threatening consequences. This case shows the importance of further investigation in patients with obstructive airway disease who are unresponsive to routine therapies. Although the diagnosis of foreign body aspiration could be established rather easily in our case due to the radio-opaque nature of the object, this might be particularly difficult in others particularly those with aspiration of radiolucent foreign bodies. The inclusion of foreign body aspiration in the differential diagnosis for such patients allows for early recognition and appropriate management, thereby decreasing the incidence of costly and unnecessary complications. This unusual case emphasizes the need to maintaining a high index of suspicion when an adult presents with chronic complaints of upper respiratory tract infection without any obvious reasons and highlights the need to create awareness about this potentially avoidable situation at the level of general practitioners.

Experience Summary
In conclusion, bronchoaspiration of foreign bodies by adults is rare. However, it is important to suspect bronchoaspiration of a foreign body in the presence of suggestive symptoms. In adults, respiratory infection (acute or recurrent pneumonia) is the most common clinical presentation. Chest radiography is not always useful for diagnosis.
Sometimes metallic foreign bodies can be observed, but other times only indirect signs of alveolar infiltrate are present. Surgical treatment is reserved for cases in which bronchoscopy is unsuccessful or there are irreversible bronchial or lung complications.

Introduction
Apical hypertrophic cardiomyopathy (apical HCM) is an atypical phenotype of nonobstructive HCM (hypertrophic cardiomyopathy) and it is more prevalent in Japanese people [1]. Usually it is considered as a benign condition and is detected incidentally by echocardiography.

Review of Literature
Apical HCM was first described in Japan. Sakamoto  leagues [4] used echocardiography in a cohort of 264 patients to define the imaging characteristics and Chen et al. [5] utilized 2D echocardiography to further classify apical HCM and to assess the wall thickness. Kitaoka  [7] of non-Japanese population. It is rare in the West (1 to 11%) [8], but more common in oriental people and accounts for 13% -41% of all variants of HCM among Asian individuals [9], 16% -41% of entire HCM population in Chinese [10] and 24.5% of all HCM in Taiwan [11]. Sakamoto et al. noticed the benign prognosis of apical HCM in a study on 200 patients in Japan [12].
Published Indian studies are limited for comparison, so this case had been reported.

Case Report
A 54-year-old asymptomatic male was referred for echocardiographic evaluation due to an LVH (left ventricular hypertrophy) pattern of ECG changes as shown in Figure 1 and a normal X-Ray chest as in Figure

Etiopathogenesis
Hypertrophic cardiomyopathy (HCM) is the most common genetically transmitted cardiovascular disease and it is usually familial with heterogeneous expression. Several disease-causing mutations in genes encoding proteins of the sarcomere have been reported [13]. A family history is more common in patients with asymmetric septal hypertrophy (ASH) than with apical hypertrophic cardiomyopathy (AHCM). Apical hypertrophic cardiomyopathy is frequently sporadic, a few families have been reported with autosomal dominant inheritance and a sarcomere gene mutation in the alphacardiac actin gene (Glu101Lys) has been shown to consistently producing the apical HCM phenotype [14]. Alpha and beta cardiac myosin heavy chain (MHC) mutations affect the polypeptides crucial to the structure of myofibrils and might be responsible for the myocyte and myofibrillar disarray, characteristic of familial HCM. The cause of sporadic apical HCM is unknown, but genetic, racial and even environmental factors could be responsible and many have lesser degree of hypertrophy, the outflow gradients are usually lacking, symptoms are often absent and the disease is detected only by echo- cardiography. An association with HLA-DR 2 antigen in patients with apical HCM was recently reported in Japan [15]. Other investigators consider a secondary genesis as the underlying pathogenetic mechanism, i.e., hypertension or heavy physical exercise [16].

Morphological Types of Apical HCM
According to the distribution of hypertrophied musculature, the morphologic sub classification as "true apical" phenotype (hypertrophy of only the apical segment below the papillary muscle) and "distal-dominant" phenotype (hypertrophy extended into the middle LV segments) have been recently recognized in North America [24]. Mid ventricular obstruction or apical obliteration was frequently found in patients with distaldominant form and it is more often symptomatic and more likely to develop cardi-  (apical segment only) and "mixed form" (hypertrophy extending into other segments) [25]. Based on CMR (cardiac magnetic resonance) imaging, apical HCM is divided into 3 types as true apical form, a type with additional asymmetric involvement of ventricular wall segments and a type with symmetric involvement of ventricular wall segments.
Generally, apical HCM is divided into two groups as isolated asymmetric apical HCM (pure AHCM) and co-existent hypertrophy of interventricular septum (mixed AHCM) [26]. The pure form is predominant in Japanese, while the mixed form has been linked to Caucasian patients [27] [28].
A relatively normal-sized, diffusely hypokinetic left ventricle with an unexplained, pathological hypertrophy is termed as "burned-out" hypertrophic cardiomyopathy.

Clinical Presentation
Clinical expression of apical HCM is highly variable. Apical HCM may manifest early in adulthood [29] and most series reported a mean age of atleast 41 years [30]. About 54% of patients with apical HCM are symptomatic and the most common symptoms are chest pain, followed by palpitations, dyspnea and syncope. According to one large published series, AHCM presented with atypical chest pain (14%), palpitations (10%), dyspnea (6%), presyncope/syncope (6%) [31]. Atypical chest pain is the most frequent symptom and typical angina may also occur due to diminished vasodilaltory reserve.
Atrial fibrillation (12%), apical myocardial infarction (10%), ventricular arrhythmia and apical thrombosis with subsequent embolization may occur up to 33% of cases [32]. [33]. The mismatch between fixed epicardial blood supply and large muscle mass leads to sustained myocardial ischemia and necrosis resulting apical aneurysm which may complicate with ventricular tachycardia. A 65-year-old Indian woman having apical aneurysm and presented with long standing angina had been reported [34].
Apical hypokinesis and aneurysm formation may also result from midventricular (mid-cavity) obstructive type of hypertrophic cardiomyopathy and transient LV (left ventricular) apical ballooning, a characteristic feature of Takotsubo cardiomyopathy (stress cardiomyopathy or apical ballooning syndrome or broken-heart syndrome) which was originally described in Japan in 1990 and it is most commonly seen in elderly post-menopausal women, characterized by ST segment elevation in anterior precordial leads with elevated cardiac enzymes and may be due to excess catecholamines (diffuse microvascular spasm or dysfunction, resulting myocardial stunning or direct myocardial toxicity), coronary vasospasm and triggered by emotional or physical stress.
It may presents with sudden onset of chest discomfort, shortness of breath and reversible within weeks to months. A criteria formulated by Mayo clinic as regional hypokineses with ECG evidence of ST-segment elevation in the absence of obstructive coronary artery disease, pheochromocytoma or myocarditis to diagnose this condition.
During the event, the shape of LV cavity resembles the fishing pot of Japanese (Tako-tsubo) to trap octopuses and so it is called as Takotsubo cardiomyopathy. The typical form of this cardiomyopathy is apical type, characterized by systolic apical ballooning with hypokineses of apical and mid segments and hyperkineses of basal walls. The atypical variants such as mid-ventricular type (hypokineses restricted to mid-ventricle with sparing of apex), basal type (hypokineses of base with sparing of mid-ventricle and apex), focal type (dysfunction of a segment, usually anterolateral) and global type (global hypokineses) were also described.

ECG Features
The most common ECG findings are negative T waves in the precordial leads, found in 93% of patients (a depth >10 mm in 47%) and a documented left ventricular hypertro-phy on imaging is seen in 65% of patients with HCM. Giant T wave negativity (defined as depth or voltage >1 mV or 1.2 mV in any of the leads) in the left precordial leads is the hallmark feature of apical HCM as a result of balance of electrical forces emanating from the left versus the right ventricle [35] [36]. Altered repolarization changes of ventricular myocardium may produce ST segment/ T wave changes in 70% of cases of left ventricular hypertrophy. There is significant variability on manifestation of strain pattern as minimally inverted or >5 mm depth, asymmetric T waves with rapid return to baseline and terminal positivity, depression of the J point, T wave inversion in lead V 6 > 3 mm and greater in V 6 than V 4 [37] and high QRS voltage (R in V 5 > 26 mm, S in V 1 + R in V 5 ≥ 35 mm -positive Sokolow-Lyon index as a sign of LVH).
In apical HCM, larger degree of T wave inversions are seen and it's depth does not correlate with severity of apical hypertrophy [38]. Presence of giant T wave inversions in Japanese HCM patients has been identified as a predictor of favourable outcome and it is more common in sporadic cases of apical HCM. Reports from outside Asia would suggest, however, that apical hypertrophy is uncommonly accompanied by marked T wave inversion and associated with adverse outcome in some patients. This heterogeneous morphologic expression even in first degree relatives is due to great dissimilarity in the pattern of left ventricular wall thickening [39]. In some non-Japanese studies, T wave negativity was often less pronounced and not necessarily localized to the precordial leads [40].
Abnormal ECG changes and no echocardiographic evidence of hypertrophic cadiomyopathy is seen in some patients due to abnormal gene in first degree relatives and called as carrier or preclinical state of hypertrophic cardiomyopathy. Incidence of deep T inversion may diminish considerably with advancing age. Myocardial infarction with a secondary apical LV aneurysm may occur in 10% of cases, that might determine the disappearance of the giant T waves in apical HCM and the "spade" shaped LV configuration may become "bottle-gourd "shaped. In normal variant of hypertrophic cardiomyopathy (HCM), the LV (left ventricular) cavity is usually "banana" shaped. However, in some cases, non-giant T waves may become a giant one on later life. The T wave changes associated with ischemia are usually narrow and symmetric (deep T wave inversion) and "CVA (cerebrovascular accident)-T wave pattern" is associated with marked QT prolongation especially in subarachnoid hemorrhage.

Transthoracic Echocardiography
The preferred initial imaging test is Transthoracic Echocardiography and it is the most frequently utilized diagnostic modality [41]. Hypertrophy (apical or elsewhere) is de-fined as a compacted myocardial wall thickness in diastole greater than or equal to 14 mm and it is 15 mm as a threshold in conventional echocardiographic measurements, which was performed perpendicular to the axis of the wall and at the point of maximal thickness in short axis view at apical level as shown in Figure 9. In apical hypertrophic cardiomyopathy, the asymmetric hypertrophy of the left ventricle is predominantly confined to LV apex as shown in Figures 3-10, with a maximal apical thickness ≥15 mm and a ratio of maximal apical to posterior wall thickness ≥1.5 based on two dimensional echocardiography is a diagnostic criterion of apical HCM [42]. Figure 9 shows the maximal apical thickness of 37.5 mm and a ratio of maximal apical to posterior wall thickness (10.2 mm) 3.7:1 (>1.5:1) in short axis view, satisfying the diagnosis of apical HCM in this patient.
Relative hypertrophy was defined as the absence of hypertrophy (wall thickness <14 mm) but with the apical wall thickness greater than the basal thickness (apex:base ratio (ABR) wall thickness >1). An apical-to-basal LV wall thickness ratio of 1.3 -1.5 is diagnostic of apical HCM [43] and in this patient, it is 2:1 in parasternal long axis view as shown in Figure 8.
Apical HCM is characterized as concentric, circumferential hypertrophy of the entire apex due to apical left ventricular thickening of the anterior and posterior walls, resulting in a spade-like morphology of the left ventricular cavity during end diastole in LV long axis view of MRI and RAO projection of angiography. A subtype of apical HCM in which the distribution of hypertrophied myocardium proved to be confined to the apical lateral wall (AAH-asymmetric apical hypertrophy) and cannot be evaluated in long axis MRI or RAO projection in angiography and this subtype was called as nonspade apical HCM in short axis images of MRI [44]. A recent long-term study showed that patients with non-spade apical HCM may develop the typical spade-like configuration after some years [45]. Thus, the non-spade type is possibly an early stage of apical HCM and giant negative T waves are common in both types.
A criteria was formulated to diagnose apical HCM in a distinct phenotype [46]  The presence of two or more of four minor criteria is the supportive evidence of apical HCM. The differential features of Japanese and non-Japanese type of apical HCM is shown in the Table 1 given below.
In transthoracic echocardiography, the lateral wall hypertrophy is more than the Segmental distribution may occur. Basal septal hypertrophy producing sub aortic obstruction in 50%, mid-septal hypertrophy with mid-cavity obstruction in 25%, apical septal hypertrophy with apical obliteration in 25% of cases. Occasionally, papillary muscle hypertrophy alone may be seen Apical wall thickness lesser degree More than Japanese in Americans apical septum and producing a classical "ace of spades sign" in apical four chamber [47] views as shown in Figure 3 and Figure 4. In apical long axis view as shown in Figure 7 and parasternal long axis view as in Figure  Lateral wall thickening was smooth, homogeneous, non-trabeculated in apical HCM and thus differentiated from non-compacted LV (left ventricular) cardiomyopathy and apical HCM may mimic as apical LV thrombus which may be associated with wall motion abnormality. It can also mimic LV EMF (Endomyocardial fibrosis), but EMF is characterized with firm, rolled edges and a rugose surface over the endocardium.

Treatment
Apical HCM is generally associated with good prognosis in both Asian and Caucasian population and a long-term mortality is 0.1% per year. The approach to management of apical HCM depends on symptoms and risk of sudden cardiac death (SCD). There is lesser incidence of sudden cardiac death in apical variant, compared to patients with normal variant HCM.
In asymptomatic patients, no specific therapy has been outlined, but counseling is certainly recommended for symptomatic monitoring to notice any syncope or presyncopal events on follow up. The medical regimen in symptomatic patients primarily consists of beta-blockers, which have been shown to decrease symptoms as well as overall mortality [48].
The major clinical features associated with increased risk of SCD in HCM patients are non-sustained ventricular tachycardia, maximum LV wall thickness of ≥3 cm, family history of SCD at younger age, unexplained syncope, abnormal BP response during exercise and increased left atrial diameter (>36 mm) as a potential SCD risk modifier. Current guidelines do not recommend ICD (implantable cardioverter defibrillator) implantation as a primary prevention for SCD in apical HCM and these clinical features should be used to assess the prognosis on follow up.
In apical HCM complicated with apical aneurysm formation, the size and symptoms of the aneurysm were ameliorated by sub selective coronary angiography and alcohol injection into the small vessels supplying a limited segment of mid-LV obstructive muscle. Others have reported the use of surgical apical myectomy in similar circumstances [49].
An increased apical thickness of 55.3 mm indicate massive hypertrophy (>50 mm [50]) and LA dilatation (51.2 mm) predict this patient as a high risk category and so close monitoring is recommended in cardiologic clinic.

Transthoracic Echocardiographic Screening
Echocardiographic screening of population was done in those individuals having ECG changes of LVH (left ventricular hypertrophy). A mixed form of apical HCM (with involvement of IVS) was found in a 65-year-old asymptomatic hypertensive female as shown in Figure 11, Figure 12 and a mid-cavity form of hypertrophic cardiomyopathy as shown in Figures 13 was detected in a 60-year-old aymptomatic normotensive male, having a similar ECG features of LVH in both cases. A mid-cavity type of HCM is also found in a 65-year-old asymptomatic normotensive female with a normal ECG pattern as shown in Figure 14 and Figure 15. Occasionally, papillary muscle hypertrophy alone may be seen as shown in Figure 16. An isolated basal hypertrophy of the interventricular septum in a 61-year-old, hypertensive male with normal ECG is detected by transthoracic echocardiography as shown in Figure 17.
A 60-year-old hypertensive woman having a mid-ventricular obstructive form of HCM with LVH (left ventricular hypertrophy) ECG pattern was observed and the gradient of obstruction may mimic apical dyskinesis with aneurysm as shown in Figures  18-22. The woman developed sudden onset of angina with an elevation in blood pressure up to 160/90 mmHg and cardiac enzymes (CK-MB fraction rises to 125 IU/Lnormal < 25 IU/L). The ECG during the event showed LVH (left ventricular hypertrophy) pattern with VPCs (ventricular premature complexes) as shown in Figure 22 and no evidence of ST-segment elevation and wall motion abnormalities, but with a mild increase in gradient of obstruction in the LV apex as shown in Figure 20 and Figure 21 and it was controlled with antihypertensive medications such as calcium channel blockers and anti-anginal drugs with nitrates. Coronary angiography and selective alcohol injection into the small vessels supplying the mid-segment of left ventricle is preferred in this patient to prevent further episodes. This type of mid-ventricular obstructive  form of HCM (hypertrophic cardiomyopathy) is frequently observed in elderly hyperensives with LVH (left ventricular) pattern of ECG changes and more prone to complications such as ischemia and infarction.

Genetic Screening
Genetic screening may be done in younger population if there is a family history of sudden death since hypertrophic cardiomyopathy (HCM) is the most common cause of  death in competitive athletes [51]. It is believed that hypertrophy in HCM is a compensatory phenomenon that occurs in response to mutant myosin protein peptide. By inhibiting transcription or translation of mRNA of this mutant allele, it is possible to induce regression of cardiac hypertrophy by abolishing the synthesis of this mutant peptide. The heart is capable to renew the proteins and the myosin, the longest lasting protein has a half-life of 5 days. There is an inherent potential for corrective resynthesis and inhibition of defective gene in adults and hypertrophy may revert it into normal within weeks to months. The ACE (angiotensin-converting enzyme) gene plays a remote role in the development of hypertrophy and ACE inhibitors may be given in those    individuals without outflow tract obstruction. The exact molecular pathogenesis of HCM is to be determined and so the definite therapy based on gene manipulation remains speculative.

Conclusion
The initial echocardiographic evaluation was sufficient to diagnose the patients with apical HCM [52]. Typical ECG changes are the signs of left ventricular hypertrophy such as pronounced negative T waves (>1 mV) in the precordial leads and a positive   The mixed and mid-cavity forms were detected in this region with a relatively benign and late onset disease in adult life. Mid-ventricular obstructive form with an anginal episode was also reported in an elderly hypertensive female at the age of 60 years old.

Introduction
The diaphragmatic hernia is defined by permanent or intermittent passage of the abdominal viscera in the chest by an abnormal diaphragmatic hole. This diaphragmatic hole may be abnormally far (Larrey slot, Bochdalek hernia) or abnormally enlarged (hiatal hernia). Hiatal hernias are due to movement of the gastroesophageal junction into the thorax. There are 3 types of hiatal hernia: • The most frequent (85% of cases) are sliding hernias.
• Hernias by rolling (5% of cases), in which the cardia is intra-abdominal and fundus in intrathoracic position. • Mixed hernias (10% of cases).
The rotating hiatal hernias do not cause gastroesophageal reflux or esophagitis.
The symptoms are related to the volume of the hernia, which can manifest as chest pain angina, respiratory symptom, sometimes chronic anemia. Complications are represented by gastrointestinal bleeding related to ulceration of the neck hernia (see necrosis and perforation of the collar, mediastinitis, and gastric volvulus). Because of the risk of complications, surgical indication arises when the diagnosis of hiatal hernia is made.
Given the rarity of this disease, we report the case of a patient admitted to our department for respiratory symptoms revealing hiatal hernia by rotation.

Case Report
Mrs. L A, 80 years old, with a history of dyslipidemia and type II diabetes put on oral anti-diabetic and placed under symptomatic treatment for gastroesophageal reflux 10 years ago. This patient was presented to the emergency room in an array of acute retrosternal chest pain, chronic dyspnea since 3 months, associated with a dry cough without hemoptysis nor dysphagia, nor hydatidoptysis or other respiratory or extra-respiratory signs associated. Clinical examination showed an obese patient with a BMI 26 kg/m 2 , tachypnea at 20 cycles/minute, cyanosis of the lips and extremities, 87% SaO 2 in the ambient air, without rattling in auscultation. The cardiac examination has not objectified abnomally outside except a tachycardia of 110 beats/minute. Ischemic heart disease was mentioned in the first place (according to age and cardiovascular risk factors presented by the patient). Troponin, ECG and echocardiography had not objectified signs for cardiac ischemia. Chest radiograph Figure 1 suggested the existence of some retrocardiac clarities, with horizontal air-fluid levels suggesting a diagnosis of a diaphragmatic hernia. After stabilization of the patient, a chest CT scan was requested ( Figure 2) showing a large defect of the left diaphragm with ascension through the esophageal hiatus of the large gastric tuberosity, of the 2/3 of the stomach and perigastric fat on retrocardiac region of the posteroinferior mediastinum. This CT aspect is suggestive of a hiatal hernia by rolling. Surgical treatment was proposed to the patient, but given the age and the medical history of the patient, surgery seemed to bring more risk than benefit. Therefore, we opted to keep it under strict surveillance to detect possible complications. A rhythm of regular monitoring has been proposed to the patient every 3 months. Lifestyle and dietary rules and anti reflux treatment have been proposed for the patient. The patient evolved well, no complications did not occur after 18 months.

Discussion
Diaphragmatic hernia rotating or para esophageal hernia or hiatal firewall represents 5% of hiatal hernias. The hernia orifice has often variable diameter [1]. The omentum is uniquely the only herniated structure in almost all cases, the bag contains all or a part of the stomach, as the case of our patient. In fact, the content of the hernia sac depends on the volume of the hernia. In small hernia, only the gastric fundus is intrathoracic. In large hernias, all the stomach switches from the left to the right around the small curvature into the thorax, realizing volvulus organoaxial [2]. In the voluminous hernias  Usually the cardia remains in place with an intact ligament and a normal configuration of the His angle [3]. The gastro esophageal reflux is the most common symptom [4]. It is frequently observed in women 70 to 80 years as the case of our patient. Thoracic manifestations are the prerogative of young subjects, their appeared or worsened in postprandial and are frequently accompanied by intermittent symptoms of oesophageal or pyloric obstruction (dysphagia, vomiting) and often iron deficiency anemia with or without signs of digestive hemorrhage [5]. The respiratory symptoms can be present regardless of the size of the hernia, such as dyspnoea and chest pain that gets worse especially in postprandial, this was the case of our patient. The diagnosis is suggested by the presence of one or much retrocardiac clarity containing a hydroaeric level lateralized to the right when it is voluminous. This X-ray image increases in volume after in-gestion of a soft drink. It is usually accompanied by a disappearance of the gastric air pocket. The latter may still be in place, chest radio while revealing two clarities with hydro aeric level, one above, the other under diaphragmatic indicating a cascade stomach. When the hernia is large, it can be observed in addition to gastric hernia image, evocative clarities of colic hernia and/or opacity of a herniated spleen. So, any clarity of the postero-inferior mediastinum with hydro aeric level must lead to gastroesophageal transit that will affirm the diagnosis and eliminate other conditions sometimes evocated (bronchogenic cyst, abscess of the mediastinum…) [6]. In our patient, the diagnosis was suggested on chest radiograph, which showed the retro-cardiac clarities, which can be relevant to digestive clarities. CT allows affirming the epiploic hernia (a fat mass having an omental aspect occupying the postero-inferior mediastinum extending through the esophageal hiatus with intra abdominal omentum) [7]. In our patient, CT

Conclusion
The hiatal hernia by rolling remains fairly a rare disease. Diagnosis can be made by simple chest X-ray. We have to think about in case of gastroesophageal reflux with respiratory symptoms worsening especially in post-prandial. The treatment is surgical, and can avoid complications. But we must always consider the benefit risk before starting a surgical cure and prefer laparoscopy if it is available.

Conflicts of Interest
Authors declare they have no conflicts of interest.
fully treated by appropriate antibiotic treatment.

Case Report
A 53-year-old woman was brought by ambulance to the emergency department of our hospital due to fever and right shoulder pain for a few hours. She had no pertinent past medical history, family history, or recent history of overseas travel. However, she had been a smoker of 20 cigarettes per day for 30 years. On examination, her body temperature was 36.3˚C, blood pressure was 90/40 mmHg, pulse rate was 100 beats/min, respiratory rate was 22 breaths/min, and oxygen saturation was 97% at an oxygen support  A repeat chest CT scan on the 11th hospital day showed reduction of air space consolidation, but anew cavity formation was observed ( Figure 3). Although not detected in any of the specimens, co-infection with an anaerobe was suspected and intravenous clindamycin (CLDM) at 2.4 g/day was added and continued for 10 days. Follow-up chest radiograph and CT scan on the 24th hospital day revealed further improvement of the consolidation and resolution of the cavity (Figure 4). Intravenous CPFX was continued until discharge on the 28th hospital day and oral CPFX was prescribed for one more week after discharge. Six months after discharge, there were no clinical symptoms of recurrence and follow-up chest radiograph revealed resolution of the infiltrates ( Figure 5).

Discussion
P. aeruginosa is a frequent pathogen causing hospital-acquired pneumonia and healthcare-associated pneumonia [1] [3]. However, CAP secondary to P. aeruginosa is un-common, with an incidence of only 0.6%, as shown in Sibila's cohort study on 62,689 pneumonia patients aged ≥65 years old [4]. It is often rapidly progressive and may be fatal [4], with a 30-day mortality rate of 17.4% [4].
There have been only 12 case reports found in PubMed on P. aeruginosa CAP with septicemia in patients without comorbidities (Table 1) [3] [5]- [13]. The clinical characteristics of these cases were pleuritic chest pain and right upper lobe predilection; in addition, mortality rate was high. The outcome was shown to be dependent on initiation of appropriate antibiotic therapy against P. aeruginosa within the first 48 hours of  admission [14], therefore, timely appropriate empiric antibiotic treatment is crucial [14]. For this patient, we chose MEPM because the main target of treatment was septicemia due to lobar pneumonia and based on the presence of gram-negative rods on sputum. Gramstain is the most commonly performed microbiology test that can immediately identify the cause of a bacterial infection. Henderson et al. [10] suggest that P. aeruginosa CAP should be suspected in any patient who has gram-negative bacilli seen on sputum sample. Gram-negative bacteria include P. aeruginosa, which is reported to be one of the risk factors for death in CAP patients [15]. P. aeruginosa CAP may sometimes progressive to cavitary pneumonia [2] [3] or lung abscess; for the latter, anaerobes are the major pathogens involved and may co-infect    We experienced a rare case of P. aeruginosa CAP with septicemia in a previously healthy woman. The clinical course might be rapidly progressive and is often fatal. The choice of an initial empiric antibiotic treatment that is active against P. aeruginosa is critical in improving outcome.
Diastasis recti is a term used to describe a separation of the left and right sides of the abdominal wall of at least 2.7 centimeters [12]. It is a common result of childbearing caused by the repetitive stretching of the abdominal wall, which can result in midline or paraumbilical hernia [13]. Although it tends to be self-limiting postpartum, surgical intervention is often used for cosmetic purposes, as well as for hernia repair [14]. Exercise options are rare, but have been reported [15]. Even in cases where the diastasis recti improves, but doesn't resolve, after 6 months post-partum, the abdominal muscle strength does not return to normal [16]. Our case report details the management plan of a patient diagnosed with diastasis recti treated with prolotherapy. This report appears to be the first to document the use of prolotherapy to treat this common disorder.
Written informed consent was obtained from this patient to use her non-identifying information. Upon inspection of the patient's abdomen, a separation of the abdominal wall was apparent just superior to the umbilicus, measuring 2.9 mm. The patient was told by another provider that this separation would self-resolve approximately 6 months postpartum, but 8 months later it was still evident. The patient's desire was to correct this non-surgically. Figure 1 shows an illustration of this patient's diastasis recti.

Treatment
After she was informed of the potential benefits, risks, and complications associated with prolotherapy, the patient affirmed her intent to proceed with the procedure. A total of 4 injections were administered on the first treatment around the palpable site of supra umbilical muscle division. Solution was comprised of a combination of 6 mL of 50% dextrose, 3 mL of 1% lidocaine, and 1 mL of methylcobalamin (1000 mcg/mL).
Prolotherapy injections were administered every two weeks for a total of 7 prolotherapy sessions.
During the first 5 sessions, a total of 4 injections were used to administer the dextrose solution. For the final two prolotherapy sessions this decreased to 2 injections. The patient did not report and complications or side effects throughout the duration of treatment, and tolerated the injections well. Figure 2 shows prolotherapy injection points for this patient.

Outcome
Patient was re-evaluated at 14 weeks following the first prolotherapy session. Good approximation of the rectus abdominus was observed, with palpable closure measuring 0.5 cm, a decrease from the initial 2.9 cm.

Discussion
Although prolotherapy has been consistently used for chronic pain syndromes, due to its postulated mechanism of action, prolotherapy may be a novel way to treat diastasis recti when it is not self-limiting. This may be preferable to surgical options to repair any subsequent hernias or negative cosmetic impact.
It is important to also discuss the safety profile of prolotherapy. In a survey of approximately 500,000 patients treated for a variety of health conditions. They included 29 reports of a pneumothorax, 24 accounts allergic reactions, and 12 cases of hospitalization for an undisclosed reason [17]. Common side effects can include injection site redness and localized tenderness for 5 -7 days post-injection [1]. This track record makes prolotherapy a desirable intervention when compared to more invasive alternatives.
Over the course of the treatment presented in this case report, the patient was also prescribed various nutraceuticals based upon her symptoms and laboratory findings, including DHEA 5 mg b.i.d., pregnenolone 50mg daily, and cholecalciferol 10,000 mg daily. While it is possible that these nutraceutical interventions may have helped to play a part in the observed improvement in her diastasis recti, this has never been previously reported to do so in the literature.
Because this is a case report, there are limitations associated with this study design.
First, a lack of a control limits our ability to generalize or make assumptions on broader patient populations. Second, the apparent reduction in abdominal wall separation following prolotherapy could possibly be, however unlikely given the length of time this patient had the diagnosis, attributed to self-resolution over time as many of these cases do. Future studies on this topic could include testing multiple types of injection solutions to determine which work the best, as well as to compare against control patients to determine effectiveness compared to natural history.

Conclusion
In this case report, the treatment and the outcome of a patient with abdominal diastasis recti who received a therapeutic trial of dextrose prolotherapy were reported. Following this therapeutic trial, the patient's abdominal separation closed from 2.9 cm to 0.5 cm.
The patient will be followed to assess long-term benefits.