Overall erectile dysfunction pills philippines order 40 mg cialis extra dosage overnight delivery, small isolated ventricular septal defects are difficult to detect prenatally impotence forum cialis extra dosage 50mg with mastercard, and both false positive and false negative diagnoses have been made erectile dysfunction treatments vacuum discount generic cialis extra dosage uk. Ventricular Septal Defects In dubious cases impotence in women generic 200 mg cialis extra dosage with amex, Color Doppler may be useful impotence pills for men purchase discount cialis extra dosage, in that many ventricular septal defects are associated with a demonstrable left to right shunt erectile dysfunction treatment boots purchase cialis extra dosage 50 mg amex. Prognosis Ventricular septal defects are not associated with hemodynamic compromise in utero because the right and left ventricular pressures are very similar and the degree of shunting should be minimal impotence only with wife order cialis extra dosage 100 mg without prescription. Large defects present with congestive heart failure at 2-8 weeks of life and require medical treatment (digoxin and diuretics) erectile dysfunction pump surgery cheap cialis extra dosage 40 mg mastercard. Rarely very large defects, associated with massive left to right shunt, can be associated with congestive heart failure soon after birth. If medical treatment fails surgical closure is undertaken; survival from surgery is more than 90% and survivors have a normal life expectancy and normal exercise tolerance. Abnormal development of these structures is commonly referred to as endocardial cushion defects, atrioventricular canal or atrioventricular septal defects. In the complete form, persistent common atrioventricular canal, the tricuspid and mitral valve are fused in a large single atrioventricular valve that opens above and bridges the two ventricles. In the complete form of atrioventricular canal, the common atrioventricular valve may be incompetent, and systolic blood regurgitation from the ventricles to the atria may give rise to congestive heart failure. Prevalence Atrioventricular septal defects, which represent about 7% of all congenital heart defects, are found in about 1 per 3, 000 births. Diagnosis Antenatal echocardiographic diagnosis of complete atrioventricular septal defects is usually easy. Color Doppler ultrasound can be useful, in that it facilitates the visualization of the central opening of the single atrioventricular valve. In such cases, Color and pulsed Doppler ultrasound allow one to identify the regurgitant jet. The main clue is the absence of the atrial septum below the level of the foramen ovalis. Another useful hint is the demonstration that the tricuspid and mitral valves attach at the same level at the crest of the septum. This apical displacement of the mitral valve elongates the left ventricular outflow tract. The atrial septal defect is of the ostium primum type (since the septum secundum is not affected) and thus is close to the crest of the interventricular septum. Prognosis Atrioventricular septal defects will usually be encountered either in fetuses with chromosomal aberrations (50% of cases are associated with aneuploidy, 60% being trisomy 21, 25% trisomy 18) or in fetuses with cardiosplenic syndromes. In the former cases, an atrioventricular septal defect is frequently found in association with extra-cardiac anomalies. In the latter cases, multiple cardiac anomalies and abnormal disposition of the abdominal organs are almost the rule. However, the presence of atrioventricular valve insufficiency may lead to intrauterine heart failure. The prognosis of atrioventricular septal defects is poor when detected in utero, probably because of the high frequency of associated anomalies in antenatal series. About 50% of untreated infants die within the first year of life from heart failure, arrhythmias and pulmonary hypertention due to right-to-left shunting (Eisenmenger syndrome). Survival after surgical closure (which is usually carried out in the sixth month of life) is more than 90% but in about 10% of patients a second operation for atrioventricular valve repair or replacement is necessary. Therefore, univentricular heart includes both those cases in which two atrial chambers are connected, by either two distinct atrioventricular valves or by a common one, to a main ventricular chamber (double-inlet single ventricle) as well as those cases in which, because of the absence of one atrioventricular connection (tricuspid or mitral atresia), one of the ventricular chambers is either rudimentary or absent. Diagnosis In double-inlet single ventricle, two separate atrioventricular valves are seen opening into a single ventricular cavity without evidence of the interventricular septum. In mitral / tricuspid atresia, there is only one atrioventricular valve connected to a main ventricular chamber. A small rudimentary ventricular chamber lacking of atrioventricular connection is a frequent but not constant finding. Demonstration of two patent great arteries arising from the ventricle allows a differential diagnosis from hypoplastic ventricles (hypoplastic left heart syndrome, pulmonary atresia with intact ventricular septum). Prognosis Surgical treatment (the Fontan procedure) involves separation of the systemic circulations by anastomosing the superior and inferior vena cava directly to the pulmonary artery. The survivors from this procedure often have long term complications including arrhythmias, thrombus formation and protein-losing enteropathy. Supravalvar aortic stenosis can be due to one of three anatomic defects: a membrane (usually placed above the sinuses of Valsalva), a localized narrowing of the ascending aorta (hourglass deformity) or a diffuse narrowing involving the aortic arch and branching arteries (tubular variety). The valvar form of aortic stenosis can be due to dysplastic, thickened aortic cusps or fusion of the commissure between the cusps. The subaortic forms include a fixed type, representing the consequence of a fibrous or fibromuscular obstruction, and a dynamic type, which is due to a thickened ventricular septum obstructing the outflow tract of the left ventricle. The latter is also known as asymmetric septal hypertrophy or idiopathic hypertrophic subaortic stenosis. A transient form of dynamic obstruction of the left outflow tract is seen in infants of diabetic mothers, and is probably the consequence of fetal hyperglycemia and hyperinsulinemia. Prevalence Aortic stenosis, which represents 3% of all congenital heart defects, is found in about 1 per 7, 000 births. Diagnosis Most cases of mild to moderate aortic stenosis are probably not amenable to early prenatal diagnosis. Severe valvar aortic stenosis of the fetus is usually associated with a hypertrophic left ventricle. Within the ascending aorta (that can be small or enlarged) pulsed Doppler demonstrates increased peak velocity (usually in excess of 1 m/sec). At the Color Doppler examination, high velocity and turbulence results in aliasing, with a mosaic of colors. Severe aortic stenosis may result in atrioventricular valve insufficiency and intrauterine heart failure. Asymmetric septal hypertrophy and hypertrophic cardiomyopathy of fetuses of diabetic mothers resulting in subaortic stenosis has been occasionally diagnosed by demonstrating an unusual thickness of the ventricular septum. Prognosis Depending upon the severity of the aortic stenosis, the association of left ventricular pressure overload and subendocardial ischemia, due to decrease in coronary perfusion, may lead to intrauterine impairment of cardiac function. Subvalvular and subaortic forms are not generally manifested in the neonatal period. Conversely, the valvar type can be a cause of congestive heart failure in the newborn and fetus as well. Although there is concern that cases seen in early gestation may progress in severity, the lesion usually remains stable. If the left ventricular function is adequate balloon valvuloplasty is carried out in the neonatal period and in about 50% of cases surgery is necessary within the first 10 years of life because of aortic insufficiency or residual stenosis. If left ventricular function is inadequate a Norwood-type of repair is necessary (see hypoplastic left heart). Fetal therapy Antenatal transventricular balloon valvuloplasty has been attempted in a handful of cases but the results are uncertain. Cardiac anomalies are present in 90% of the cases and include aortic stenosis and insufficiency, ventricular septal defect, atrial septal defect, transposition of the great arteries, truncus and double outlet right ventricle. Non-cardiac anomalies include diaphragmatic hernia, Turner syndrome but not Noonan syndrome. Diagnosis Coarctation may be a postnatal event, and this limits prenatal diagnosis in many cases. It should be suspected when the right ventricle is enlarged (right ventricle to left ventricle ratio of more than 1. Narrowing of the isthmus, or the presence of a shelf are often difficult to demonstrate because in the fetus aortic arch and ductal arch are close and are difficult to distinguish. In most cases, coarctation can only be suspected in utero and a certain diagnosis must be delayed until after birth. Prognosis Critical coarctation is fatal in the neonatal period after closure of the ductus and therefore prostaglandin therapy is necessary to maintain a patent ductus. Surgery (which involves excision of the narrowed segment and end-to-end anastomosis) is associated with a mortality of about 10% and the incidence of restenosis in survivors (requiring further surgical repair) is about 15%. It may be isolated or associated with intracardiac lesions that cause obstruction to the blood flow from the left heart (aortic stenosis, aortic atresia, malaligned ventricular septal defects). Associated extracardiac anomalies are frequent and include DiGeorge syndrome (association of thymic aplasia, type B interruption and hypoplastic mandible), holoprosencephaly, cleft lip/palate, esophageal atresia, duplicated stomach, diaphragmatic hernia, horseshoe kidneys, bilateral renal agenesis, oligodactyly, claw hand and syrenomelia. Diagnosis Interrupted aortic arch should always be considered when intracardiac lesions diverting blood flow from the left to the right heart are encountered (aortic stenosis and atresia in particular). Isolated interruption of the aortic arch is often encountered with enlargement of the right ventricle (right ventricle to left ventricle ratio of more than 1. As the sonographic access to the arch is difficult, the diagnosis is not always possible. The characteristic finding of an ascending aorta more vertical than usually, and the impossibility to demonstrate a connection with the descending aorta suggest the diagnosis. The initial treatment is the same as for any anomalies in which the perfusion is ductus dependent: prostaglandin E. Blood flow to the head and neck vessels and coronary artery is supplied in a retrograde manner via the ductus arteriosus. Diagnosis Prenatal echocardiographic diagnosis of the syndrome depends on the demonstration of a diminutive left ventricle and ascending aorta. In most cases, the ultrasound appearance is self-explanatory, and the diagnosis an easy one. There is however a broad spectrum of hypoplasia of the left ventricle and in some cases the ventricular cavity is almost normal in size. As the four-chamber view is almost normal, we anticipate that these cases will be certainly missed in most routine surveys of fetal anatomy. At a closer scrutiny, however, the movement of the mitral valve appears severely impaired to non-existent, ventricular contractility is obviously decreased, and the ventricle often displays an internal echogenic lining that is probably due to endocardial fibroelastosis. The definitive diagnosis of the syndrome depends on the demonstration of hypoplasia of the ascending aorta and atresia of the aortic valve. Color flow mapping is an extremely useful adjunct to the real-time examination, in that it allows the demonstration of absent to severely decreased mitral valve flow and of retrograde blood flow within the ascending aorta and aortic arch. The patency of the ductus arteriosus allows adequate perfusion of the head and neck vessels. Intrauterine growth may be normal, and the onset of symptoms most frequently occurs after birth. The prognosis for infants with hypoplastic left heart syndrome is extremely poor and this lesion is responsible for 25 % of cardiac deaths in the first week of life. In the neonatal period prostaglandin therapy is given to maintain ductal patency but still congestive heart failure develops within 24 hours of life. Options for surgery include cardiac transplantation in the neonatal period (with an 80% 5-year survival) and the three-staged Norwood repair. Stage 1 involves anastomosis of the pulmonary artery to the aortic arch for systemic outflow, placement of systemic-to-pulmonary arterial shunt to provide pulmonary blood flow, and arterial septectomy to ensure unobstructed pulmonary venous return; the mortality from the procedure is about 30%. Stage 2 (which is usually carried out in the sixth month of life) involves anastomosis of the superior vena cava to the pulmonary arteries. The overall 2-year survival with the Norwood repair is about 50% but more than 50% of survivors have neurodevelopmental delay. Diagnosis the most common form of pulmonary stenosis is the valvar type, due to the fusion of the pulmonary leaflets. The work of the right ventricle is increased, as well as the pressure, leading to hypertrophy of the ventricular walls. The same considerations formulated for the prenatal diagnosis of aortic stenosis are valid for pulmonic stenosis as well. A handful of cases recognized in utero have been reported in the literature thus far, mostly severe types with enlargement of the right ventricle and/or post stenotic enlargement or hypoplasia of the pulmonary artery. However, cases with enlarged right ventricle and atrium have been described with unusual frequency in prenatal series. Although these series are small, it is possible that the discrepancy with the pediatric literature is due to the very high perinatal loss rate that is found in "dilated" cases. Enlargement of the ventricle and atrium is probably the consequence of tricuspid insufficiency. Prognosis Patients with mild stenosis are asymptomatic and there is no need for intervention. Patients with severe stenosis, right ventricular overload may result in congestive heart failure and require balloon valvuloplasty in the neonatal period with excellent survival and normal long-term prognosis. Fetuses with pulmonary atresia and an enlarged right heart have a very high degree of perinatal mortality. Infants with right ventricular hypoplasia require biventricular surgical repair and the mortality is about 40%. The posterior and septal leaflets are elongated and tethered below their normal level of attachment on the annulus or displaced apically, away from the annulus, down to the junction between the inlet and trabecular portion of the right ventricle. The resulting configuration is that of a considerably enlarged right atrium at the expense of the right ventricle. The portion of the right ventricle that is ceded to the right atrium is called the atrialized inlet of the right ventricle. Associated anomalies include atrial septal defect, pulmonary atresia, ventricular septal defect, and supraventricular tachycardia. Diagnosis the characteristic finding is that of a massively enlarged right atrium, a small right ventricle, and a small pulmonary artery. About 25% of the cases have supraventricular tachycardia (from re-entrant impulse), atrial fibrillation or atrial flutter. Differential diagnosis from pulmonary atresia with intact ventricular septum and a regurgitant tricuspid valve or isolated tricuspid valve insufficiency is difficult and may be impossible antenatally. This probably reflects that the prenatal variety is more severe than the one detected in children or adults. They account for 20-30% of all cardiac anomalies and are the leading cause of symptomatic cyanotic heart disease in the first year of life. Given the parallel model of fetal circulation, conotruncal anomalies are well tolerated in utero. The clinical presentation occurs usually hours to days after delivery, and is often severe, representing a true emergency and leading to considerable morbidity and mortality. Two ventricles of adequate size and two great vessels are commonly present giving the premise for biventricular surgical correction. The outcome is indeed much more favorable than with most of the other cardiac defects that are detected antenatally. Nevertheless, despite improvement in the technology of diagnostic ultrasound, the recognition of these anomalies remains difficult. A specific diagnosis requires meticulous scanning and at times may represent a challenge even for experienced sonologists. Referral centers with special expertise in fetal echocardiography have indeed reported both false positive and false negative diagnoses. There is a typical association between conotruncal anomalies and 22q11 deletion, a condition associated with long term implications, including immune deficits, neurological development and speech, that may not be apparent in neonatal life. Associated cardiac lesions are present in about 50% of cases, including ventricular septal defects (which can occur anywhere in the ventricular septum), pulmonary stenosis, unbalanced ventricular size ("complex transpositions"), anomalies of the mitral valve, which can be straddling or overriding. There are three types of complete transposition: those with intact ventricular septum with or without pulmonary stenosis, those with ventricular septal defects and those with ventricular septal defect and pulmonary stenosis. Prevalence Transposition of the great arteries is found in about 1 per 5, 000 births. Diagnosis Complete transposition is probably one of the most difficult cardiac lesions to recognize in utero. In most cases the four-chamber view is normal, and the cardiac cavities and the vessels have normal appearance. A clue to the diagnosis is the demonstration that the two great vessels do not cross but arise parallel from the base of the heart. The most useful echocardiographic view however is the left heart view demonstrating that the vessel connected to the left ventricle has a posterior course and bifurcates into the two pulmonary arteries. Conversely, the vessel connected to the right ventricle has a long upward course and gives rise to the brachio-cephalic vessels. Difficulties may arise in the case of huge malalignment ventricular septal defect with overriding of the posterior semilunar root. This combination makes the differentiation with double outlet right ventricle very difficult. Corrected transposition is characterized by a double discordance, at the atrio-ventricular and ventriculo-arterial level. The left atrium is connected to the right ventricle, which is in turn connected to the ascending aorta. Conversely, the right atrium is connected with the right ventricle, which is in turn connected to the ascending aorta. The derangement of the conduction tissue secondary to malalignment of the atrial and ventricular septa may result in dysrhythmias, namely complete atrioventricular block. For diagnostic purposes, the identification of the peculiar difference of ventricular morphology (moderator band, papillary muscles, insertion of the atrioventricular valves) has a prominent role. Demonstration that the pulmonary veins are connected to an atrium which is in turn connected with a ventricle that has the moderator band at the apex is an important clue, that is furthermore potentially identifiable even in a simple four-chamber view. Diagnosis requires meticulous scanning to carefully assess all cardiac connections, by using the same views described for the complete form. Prognosis As anticipated from the parallel model of fetal circulation, complete transposition is uneventful in utero. After birth, survival depends on the amount and size of the mixing of the two otherwise independent circulations. Patients with transposition and an intact ventricular septum present shortly after birth with cyanosis and deteriorate rapidly. Clinical presentation may be delayed up to 2-4 weeks, and usually occurs with signs of congestive heart failure. When severe stenosis of the pulmonary artery is associated with a ventricular septal defect, symptoms are similar to patients with tetralogy of Fallot.
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Lower mortality in patients with defects: Anatomical and biomechanical considera scapular fractures erectile dysfunction tips generic cialis extra dosage 100 mg on-line. For more than 32 additional continuing education articles on orthopaedic nursing topics, go to nursingcenter. A study [1] estimated annual incidence of nerve injury procedure such as intramuscular injection or routine venipuncture was 3. However, it should not be overlooked, because neuro involved upper limb) in children under 15 years of age. Other logical injury may cause not only minor transient pain but also severe sensory disturbance, hand deformity and motor dysfunction studies on the blood donors showed that the incidence of with poor recovery. Recognizing competent level of anatomy and needle-related nerve injuries ranged from 1/1, 400 to 1/6, 300 adept skill of needle placement are crucial in order to prevent this donations [2, 3]. If a patient notices any experience of abnormal pain or paresthesia during the needle procedures, an administrator these procedures, it may be underreported due to the lack of should be alert to the possibility of nerve injury and should withdraw recognition and diagnosis. Careful monitoring of the injection site for Several mechanisms are associated with injection-related hours is required for early detection of nerve injury. The present article reviews upper limb nerve injuries caused Intramuscular injection into the upper limb is a popular by intramuscular injection or routine venipuncture including clinical technique for vaccination or other drug administration. However, these procedures are not always safe and may cause nerve injuries in various degrees. Search terms were comprised of the specific upper limb nerve, Received: December 29, 2016. As it forms anterior and posterior branches beneath the deltoid the axillary nerve courses beneath the deltoid muscle and muscle. It innervates the deltoid and teres minor muscles, and supplies the muscle, it is clearly vulnerable to needle injury. Although deltoid intramuscular injection is considered a Reports routine clinical procedure, occasionally it is performed the axillary nerve could be damaged by intramuscular incorrectly. Excessive proximal site could lead to bursa injection, while excessive distal site could lead to nerve damage or injection Presentation into vessels [11, 12]. So, a deltoid injection near 5 cm below the acromion pure motor branch of the axillary nerve is injured, the patient may injure the axillary nerve. Therefore, unfor Deltoid intramuscular injection technique tunately, no site offers an absolute protection against at-risk the suitable intramuscular injection site in upper limb is the structures [7, 11, 13]. The deltoid is a triangular-shaped muscle that originates from the lateral one third of the clavicle, the. Hyun Jung Kim, et al:Upper limb nerve injuries by injection 105 the deltoid intramuscular injection is not recommended in dorsum in the hand and fingers [5, 16]. Even in Reports adults, it is not recommended in patients who are thin with debilitating diseases as the same reason. Additionally, the the radial nerve is the most commonly injured nerve in the number and volume of injections should be limited due to its upper extremity after intramuscular injection. It is important to recognize the possibility of nerve injury Venipuncture near or at the elbow level can also involve the following an intramuscular injection. Edwards and Fleming [19] described a patient any abnormal pain or paresthesia during the injection, the with a complete radial nerve palsy after the cephalic vein needle should be immediately withdrawn. Two to four hourly post puncture of the radial nerve through the extensor carpi radialis injection observation of the injection site is recommended [12]. It descends down the posterior aspect of the humerus along the radial groove and wraps around the humerus in a lateral direction. Then it moves anteriorly over the lateral epicondyle of the humerus and passes the antecubital fossa. It provides motor innervation to the posterior compartment of the arm and forearm responsible for extension of the elbow, wrist and fingers. It also provides sensory innervation to the posterior arm, posterior forearm, and lateral two-thirds of the Table 1. Recommendation of Needle Length for Deltoid Intramuscular Injection in Adults Needle length Weight Male Female < 60 kg 5/8 inch (16 mm) 5/8 inch (16 mm). Simple sensory reported an arm level ulnar nerve injury caused by a jet deficits without pain may be functionally less significant injection for vaccination. Relatively small size of the patient because they involve the anatomical snuffbox and the radial and small muscle mass were the deduced causes of the nerve dorsum of the hand. Excessive arm rotation by the operator during the when extending the forearm, wrist, and fingers. Prevention Presentation the radial nerve locates very superficially in the middle As other nerve injuries, pain is the most frequent symptom third of the lateral aspect of the arm. The symptoms could include numbness, intramuscular injection into this site could result in damaging paresthesia, hypoesthesia and other sensory disturbance in the the nerve. Motor function injury could result in weakness should be selected midway between the acromion and deltoid of finger abduction and adduction, fourth and fifth finger tuberosity of humerus, i. Atrophy of For venipuncture near the elbow level, selection of an hypothenar eminence and interosseous muscles is also a injection site and a proper needle procedure are important. Superficial location of the ulnar nerve under the plexus formed by C8 and T1 spinal roots. Patients that lack a position medial to the axillary and brachial arteries in the subcutaneous tissue and muscle could face more vulnerability upper arm and descends on the posteromedial aspect of the to this traumatic injury. It innervates most of the intrinsic muscles of the prevented by administering the injection by properly trained hand, and muscles of the flexor carpi ulnaris and medial half staff that holds sufficient anatomical knowledge [21, 22]. Reports Anatomy Injection-related ulnar nerve injury seems to be relatively the median nerve arises from the lateral and medial cords rare. Geiringer and Leonard [21] reported 2 and enters the anterior compartment of the forearm via the cases of ulnar nerve injury at the arm level who received antecubital fossa. It provides motor innervation to anterior intramuscular injection for immunization. The patients were compartment of the forearm responsible for flexion of the asked to fixate their hands on the hips and rotate their arms. It is a pure motor nerve to the flexor Hyun Jung Kim, et al:Upper limb nerve injuries by injection 107 pollicis longus, flexor digitorum profundus to the index and beds [27-29]. Reports Reports There are several case reports of the superficial branch of Kohn et al. The patient intermittently received intravenous blood sampling in dorsolateral side near the wrist [28-33]. A large hematoma was developed after an antecubital Horowitz [34] examined 11 patients with nerve injuries venipuncture and the median nerve was found to be following routine venipuncture. Presentation peripherally inserted central catheter line insertion into the antecubital fossa [23, 25, 26]. Direct superficial branch of the radial nerve injury by needle or catheter induces immediate pain and paresthesia in the Presentation dorsolateral surface of the distal forearm radiating to the Proximal median nerve lesion induces functional loss of dorsum of the hand. Because this nerve is a pure sensory forearm pronation and flexion of the wrist and fingers with nerve, its injury does not affect muscle atrophy or weakness median nerve distribution sensory disturbance. Many previous sheet of paper using their thumb and the index fingers reports state conservative treatment was not successful and [23, 25, 26]. Prevention For venipuncture near the elbow level, cautious selection of an injection site and proper needle procedures are important. Additionally, Superficial branch of the radial nerve injury the position of forearm pronation and wrist flexion during the venipuncture restricts the movement of the nerve and makes it 1. Superficial branch of the radial nerve divides from the main It is difficult to choose particular venipuncture site in the radial nerve distal from the elbow. It runs down on the radial dorsolateral forearm to avoid superficial branch of the radial side of the forearm beneath the brachioradialis muscle. In this subcutaneous plane, the the randomly located nerve and vein crossing zones, where the nerve lies close to the cephalic vein. They suggested that the which gives nerve supply to dorsal aspect of the thumb, index cephalic vein should be punctured above the emergence of the finger, and radial side of the middle finger except the nail superficial branch of the radial nerve, at least 12 cm above 108 Anesth Pain Med Vol. Other studies also There are also several case reports of the medial or lateral recommended that cephalic venipuncture at wrist should be antebrachial cutaneous nerve injury after routine venipuncture avoided in the distal second quarter of the forearm and should in the antecubital fossa [37-40]. Horowitz [34] examined 11 be located 55 mm more proximal area from radial styloid patients with nerve injury after routine venipuncture. Presentation the medial antebrachial cutaneous nerve arises from the Direct nerve injury results in immediate shooting and medial cord of the brachial plexus. It runs down the ulnar side electric-type pain on the medial or lateral aspect of the of the arm medial to the brachial artery and pierces the deep forearm, according to the affected nerve [37-39]. But, in case fascia with the basilic vein above the medial epicondyle of the of a nerve injury due to subcutaneous extravasation of drugs humerus. A study of nerve injuries on the blood donors, the symptom the lateral antebrachial cutaneous nerve originates from the of pain occurred at venipuncture (24%), during the bleeding musculocutaneous nerve. Venipuncture technique in the antecubital fossa the reports about the incidence of venipuncture-related Venipuncture in the antecubital fossa is a routine procedure medial/lateral antebrachial cutaneous nerve injuries are limited. However, the anatomical rela Although particular nerves were not specified, two studies on tionships of superficial veins and cutaneous nerves in this area the blood donors showed that the incidence of needle-related are in close proximity. The nerves and the veins are located nerve injury rages from 1/1, 400 to 1/6, 300 donations [2, 3]. Median cubital vein is the first choice for a routine venipuncture in the antecubital fossa. Although no single area suitable for all individuals was identified due to a wide variation of the distribution of cutaneous veins and nerves, they suggested a puncture of the median cubital vein near the cephalic vein is the least likely site to be damaged. If the median cubital vein is unavailable or unsuitable, then the cephalic and basilic vein could be attempted carefully. However, the area just lateral to the biceps tendon at the elbow should be avoided to prevent the lateral antebrachial cutaneous nerve injury [40, 43]. Median cubital vein near the cephalic vein is the first choice for a routine runs the risk of damaging nerve or artery and is usually more venipuncture to cause nerve damage least likely. Hyun Jung Kim, et al:Upper limb nerve injuries by injection 109 During the venipuncture, needle should be inserted as lesion in continuity. Upper limb nerve injuries caused by intramuscular injection Nonetheless, even after a non-traumatic and satisfactory or routine venipuncture is rare, but it could lead to severe venipuncture, the risk of nerve damage still exists due to the impairment of sensory and motor function with poor recovery. Therefore, the patient should be encouraged to placement can hugely contribute to the prevention of immediately inform any experience of abnormal pain or intramuscular nerve injuries. If there is any notice, the possibility of nerve injuries during these procedures and to needle should be immediately withdrawn. Incidence achieved a full recovery and some patients had only a mild/ of traumatic injection neuropathy among children in Pakistan. Vox Sang 2008; 94: suffered pain/sensory change more than 1 year and 10% of 132-7. J Int the management is generally similar to that of other nerve Med Res 2014; 42: 887-97. After nerve injury, axonal regeneration is a complication after nerve block or vessel puncture. Korean J Pain proceeding and initial symptoms are gradually improved over 2014; 27: 210-8. Iatrogenic axillary could be observed for several months with conservative neuropathy after intramuscular injection of the deltoid muscle. It includes medications for acute neuropathic pain J Phys Med Rehabil 2007; 86: 507-11. Mapping such as opioids, non-opioid analgesics, adjuvant analgesics and the axillary nerve within the deltoid muscle. J Res Med Sci 2008; However, early surgical exploration without waiting axonal 13: 244-7. Axillary nerve injury caused by intradeltoid muscular or severe neuromotor functional loss. Surgical technique of neurolysis is research review and guideline for evidence-based practice. Appl indicated when nerve action potential is present across a nerve Nurs Res 2002; 15: 149-62. Surg Radiol Anat 2010; 32: branch of the radial nerve after intravenous cannulation. Peripheral nerve injury from General recommendations on immunization recommendations intravenous cannulation: a case report. Peripheral nerve injury and causalgia secondary to Implications for needle length in adult immunization. Nerve Superficial radial nerve and cephalic vein: an anatomic study by injuries following intramuscular injections: a clinical and cadaver dissection. Radial nerve palsy at the elbow cutaneous nerve of forearm after venous cannulation: a case report following venipuncture-case report. Traumatic ulnar neuropathy from jet of upper extremity superficial veins and nerves, and clinical injection: case report. Early changes sensory branches of the radial nerve: How can nerve lesions during following injection injury of peripheral nerves. This report provides information for clinicians and other health care providers about concerns that commonly arise when vaccinating persons of various ages. Providers and patients must navigate numerous issues, such as the timing of each dose, screening for contraindications and precautions, the number of vaccines to be administered, the educational needs of patients and parents, and interpreting and responding to adverse events. Vaccination providers help patients understand the substantial body of (occasionally conflicting) information about vaccination. This vaccination best practice guidance is intended for clinicians and other health care providers who vaccinate patients in varied settings, including hospitals, provider offices, pharmacies, schools, community health centers, and public health clinics. General Best Practice Guidelines for Immunization: Introduction Suggested citation: Ezeanolue E, Harriman K, Hunter P, Kroger A, Pellegrini C. The guidance is organized in the following 10 documents: 1) Timing and Spacing of Immunobiologics; 2) Contraindications and Precautions; 3) Preventing and Managing Adverse Reactions; 4) Vaccine Administration; 5) Storage and Handling of Immunobiologics; 6) Altered Immunocompetence; 7) Special Situations; 8) Vaccination Records; 9) Vaccination Programs; and 10) Vaccine Information Sources. This report will help vaccination providers to assess vaccine benefits and risks, use recommended administration practices, understand the most effective strategies for ensuring that vaccination coverage in the population remains high, and communicate the importance of vaccination to reduce the effects of vaccine-preventable disease. Conflict of interest information for those individuals who must report is available upon request to the corresponding author. This group includes professionals from academic medicine (pediatrics, family practice, and pharmacy); international (Canada), federal, and state public health professionals; and a member from the nongovernmental Immunization Action Coalition (see Appendix 2: Membership). This revision involved consensus-building based on new evidence from the published literature and opinion from subgroups of subject matter experts consulted on specific topics. The process by which the guidelines were drafted varied for each document; each document is therefore discussed individually below. Other issues related to timing and spacing of vaccinations were discussed between February 2012 and September 2014 over 7 meetings (in February 2012, June 2012, August 2012, November 2012, January 2013, January 2014, May 2014, and September 2014). The evidence supporting this document is based on a review of the published literature. The search and selection of studies was limited to English-language and human studies. The search and selection process yielded 20 publications, including review articles, observational studies, and letters to the editor. Selected members from this subgroup participated in the April 2013 main work group call. Major changes included 1) more descriptive characterization of anaphylactic allergy and 2) incorporation of protocols for managing adverse reactions.
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Editorial: Infectious complications: as skin preparation before blood culture: A randomized impotence and smoking buy cialis extra dosage 50 mg on-line, con A new practice advisory. The importance and implications of aseptic cerebral hemodynamics: Its infuences on intracranial pres techniques during regional anesthesia. Regional Anesthesia and sure, cerebral perfusion pressure, and cerebral oxygenation. Intensive care service: Nursing ing lumbar puncture cerebrospinal fuid lead in a patient with policy and procedures lumbar drain. Diagnostic lumbar puncture: Comparative study be or tincture of iodine are associated with low rates of blood tween 22-gauge pencil point and sharp bevel needle. Practice guidelines for the man puncture success rate in paediatric haematology-oncology agement of bacterial meningitis. Gather a 3 mL syringe, povidone-iodine swab, sterile 2x2 gauze, sterile gloves, and mask. Subsequent fushes must be done by the physician if initial fush does not result in catheter patency. Gather 3 ml syringe, sterile 2x2 gauze, povidone-iodine swab, sterile gloves, mask, sterile syringe and vial of preservative-free normal saline or preflled 10-ml preservative-free sterile normal saline syringe. Clamping tubing allows fush to move toward obstruction rather than toward collection chamber. Using strict aseptic technique, draw up 1 ml preservative-free normal saline into syringe. If fushing to clear obstruction between sample port and collection chamber, turn 8. Turning stopcock off to drainage catheter is critical to preventing stopcock between sample port and patient off to ventricular drain. Its is used mainly as an antiepileptic drug both as mono-therapy and as an adjunct in the control of partial and primary generalised epilepsy in adults and children above the 1-3 age of two. Effectiveness in migraine prophylaxis, trigeminal neuralgia, bipolar 4-8 disorders, depression and eating disorders has also been reported. In an open label study it has been show to be as effective as acetazolamide in the treatment of intracranial 11 hypertension. Topiramate is rapidly absorbed after oral administration and has a 13, 14 half life of 24 hours, being rapidly excreted in the urine. Its possible mechanism of reduction of intracranial pressure is related to its inhibition of carbonic anhydrase 15 11 activity and perhaps its induction of weight loss. Data collected from spontaneous reporting systems have identified one hundred and fifteen cases of ocular side effects which include acute-onset angle closure glaucoma, acute myopia, suprachoriodal effusions, peri-orbital oedema, scleritis, 16 blepharospasm, oculogyric crisis, nystagmus and diplopia. Patients present with blurred vision, headaches or nausea and vomiting with findings characteristic of an acute attack of angle closure glaucoma. Conventional and high 16-28 frequency ultrasound demonstrated choroidal or cilio-choroidal detachments. In patients on topiramate this was demonstrated by high frequency or standard ultrasound. Topiramate should be discontinued and an alternative prescribed in discussion with the primary physician. The initial treatment should include cycloplegia, in an attempt to displace the iris lens plane posteriorly, topical and systemic ocular hypotensives and topical steroids. Caution has been suggested with the use of acetazolamide, a sulfamated drug, concurrently with the continued use of topiramate for fear of inducing renal calculi and further ciliary body oedema. Laser peripheral iridotomy used in 23% of reported cases has not been uniformly effective in relieving the secondary angle closure and should be reserved for cases where the above 16-28 treatment fails. Rapid resolution of an attack has been reported with the use of 31 intravenous methylprednisolone and mannitol. As topiramate is a sulphamated preparation, the mechanism of acute myopia is similar to that reported with 36, 37 38, 39 sulphonamides and acetazolamide. The severity of ciliary body oedema, cilio-choroidal detachment and forward movement of the iris lens diaphragm stopping short of an acute attack of glaucoma causes myopia. Diplopia and Nystagmus have been reported in 14% to 15% of those patients on high doses of topiramate. Scleritis, including posterior scleritis has been reported in four cases, oculogyric crisis in two cases and single cases of blepharospasm, myokymia, 16, 40 periocular oedema, paresthesias and periocular pain. Weight loss has been reported in a group of patients treated with topiramate for idiopathic intracranial 11 hypertension. What advice can be given to patients or parents of children started on topiramate Parents of children or patients initiated on topiramate should be warned of the possible ocular side affects. In case of visual blurring or ocular pain initial advice from their local ophthalmologist should be encouraged. What should an ophthalmologist do when dealing with side effects associated with topiramate Patients referred to Ophthalmologists with blurring of vision or acute myopia should consider drug replacement following advice from a neurologist. Acute angle closure glaucoma should be managed with Withdrawal or replacement of topiramate with an alternative drug topical atropine drops and topical ocular hypotensives agents intravenous mannitol 15. A prospective pilot study using an ultrasound biomicroscope failed to show angle narrowing in a group of patients aged 18 years to 75 years over 41 a four week period. Long-term experience with topiramate as adjunctive therapy and as monotherapy in patients with partial onset seizures: retrospective survey of open-label treatment. Topiramate, carbamazepine and valproate monotherapy: double-blind comparison in newly diagnosed epilepsy. Topiramate in treatment of depressive and anger symptoms in female depressive patients: a randomized, double-blind, placebo-controlled study. Treatment of Idiopathic Intracranial hypertension:Topiramate vs Acetazolamide, an open label study. A review of its pharmacodynamic and pharmacokinetic properties and clinical efficacy in the management of epilepsy. Angle-closure glaucoma associated with ciliary body detachment in patients using topiramate. Topiramate in non-approved indications and acute myopia or angle closure glaucoma. Rapid Resolution of Topiramate induced Angle-closure Glaucoma with Mehtylprednisolone and Mannitol. Uveal effusion and secondary angle closure glaucoma associated with topiramate use. Acute myopia induced by topiramate: report of a case and review of the literature. Transient myopia, angle-closure glaucoma, and choroidal detachment after oral acetazolamide. The solution contains no bacteriostat, antimicrobial agent or added buffer (except for pH adjustment) and is intended only as a single-dose injection. The drug is freely filtered by the glomeruli with less than 10% tubular reabsorption; it is not secreted by tubular cells. Mannitol induces diuresis by elevating the osmolarity of the glomerular filtrate and thereby hindering tubular reabsorption of water. Reduction of high intraocular pressure when the pressure cannot be lowered by other means. Progressive heart failure or pulmonary congestion after institution of mannitol therapy. Renal complications, including irreversible renal failure have been reported in patients receiving mannitol. Patients with pre-existing renal disease, patients with conditions that put them at risk for renal failure, or those receiving potentially nephrotoxic drugs or other diuretics, are at increased risk for renal failure. The obligatory diuretic response following rapid infusion of 25% mannitol may further aggravate pre existing hemoconcentration. Serum sodium and potassium should be carefully monitored during mannitol administration. Accumulation of mannitol may result in overexpansion of the extracellular fluid which may intensify existing or latent congestive heart failure. With continued administration of mannitol, loss of water in excess of electrolytes can cause hypernatremia. Electrolyte measurements, including sodium and potassium are therefore of vital importance in monitoring the infusion of mannitol. Osmotic nephrosis, a reversible vacuolization of the tubules of no known clinical significance, may proceed to severe irreversible nephrosis, so that the renal function must be closely monitored during mannitol infusion. Mannitol injection may increase cerebral blood flow and the risk of postoperative bleeding in neurosurgical patients. Mannitol may increase the cerebral blood flow and worsen intracranial hypertension in children who develop a generalized cerebral hyperemia during the first 24 to 48 hours post injury. The cardiovascular status of the patient should be carefully evaluated before rapidly administering mannitol since sudden expansion of the extracellular fluid may lead to fulminating congestive heart failure. Shift of sodium-free intracellular fluid into the extracellular compartment following mannitol infusion may lower serum sodium concentration and aggravate pre-existing hyponatremia. By sustaining diuresis, mannitol administration may obscure and intensify inadequate hydration or hypovolemia. If it is essential that blood be given simultaneously, at least 20 mEq of sodium chloride should be added to each liter of mannitol solution to avoid pseudoagglutination. It is also not known whether mannitol injection can cause fetal harm when given to a pregnant woman or can affect reproduction. Because many drugs are excreted in human milk, caution should be exercised when mannitol is administered to a nursing woman. Reactions which may occur because of the solution or the technique of administration include febrile response, infection at the site of injection, venous thrombosis or phlebitis extending from the site of injection, extravasation and hypervolemia. If an adverse reaction does occur, discontinue the infusion, evaluate the patient, institute appropriate therapeutic countermeasures and save the remainder of the fluid for examination if deemed necessary. Repeated doses should not be given to patients with persistent oliguria as this can produce a hyperosmolar state and precipitate congestive heart failure and pulmonary edema due to volume overload. Careful evaluation must be made of the circulatory and renal reserve prior to and during administration of mannitol at the higher doses and rapid infusion rates. Careful attention must be paid to fluid and electrolyte balance, body weight, and total input and output before and after infusion of mannitol. Evidence of reduced cerebral spinal fluid pressure must be observed within 15 minutes after starting infusion. When used preoperatively, the dose should be given one to one and one-half hours before surgery to achieve maximal reduction of intraocular pressure before operation. The urine is collected by catheter for a specific period of time and analyzed for mannitol excreted in mg per minute. A blood sample is drawn at the start and at the end of the time period and the concentration of mannitol determined in mg/mL of plasma. Normal clearance rates are approximately 125 mL/minute for men; 116 mL/minute for women. When infusing 25% mannitol concentrations, the administration set should include a filter. More rarely, it can occur in patients with intracranial hypertension, brain tumor, multiple sclerosis, migraine, Chiari malformation type I, and amyotrophic lateral sclerosis. Drug-induced yawning is an uncommon clinical condition and yawning in patients with autism or schizophrenia is very rare. Mais raramente, o bocejo pode ocorrer em pacientes com hipertensao intra-craniana, tumor cerebral, esclerose multipla, migranea, malformacao de Chiari tipo I, e esclerose lateral amiotrofca. O objetivo desta revisao foi descrever em detalhes a ocorrencia deste fenomeno em tais condicoes, sua fenomenologia e fsiopatologia. Yawning is considered an intriguing and fascinating phenomenon with an obscure etiopathogenesis. It involves opening the mouth wide and closing the eyelids while inhaling deeply and then exhaling more briefly. A yawn typically lasts 5-10 seconds (Figure 1)1, 2, 3, 4, 5, 6, 7 and is usu ally accompanied by retroflexion of the head and some times by elevation of the arms (known as pandiculation when occurring together). Human beings yawn with a fre quency of up to 28 times a day1, 2, 3, 4, 5, 6, 7, often after waking up and before falling asleep. Yawning is frequently contagious and is considered a sign of boredom or even disrespectful behavior in the presence of others8, 9, 10. In the 19th century, Charcot considered yawning an important clinical neuro logical sign, but for many years neurologists attached little importance to it8, 11. Nowadays, however, although yawn ing continues to be a largely under-appreciated behavior, chasmology, the study of yawning, has become the focus of considerable interest12. Received 26 February 2018; Received in fnal form 26 March 2018; Accepted 09 April 2018. In contrast, Gallup3 argued, in 2011, that the social/ A literature search was performed in Pubmed, for English communication hypothesis is unattractive and suggested language articles over the time period from 1992 to 2018, using that yawning is probably multifunctional across species. The initial references were selected using the following the thermoregulatory one, according to which yawning is a brain-cooling mechanism. In 2014, Walusinski14 proposed a main exclusion criteria: 1) duplicate articles; 2) articles unre lated to the purpose of the study; 3) articles unrelated to yawn new hypothesis, according to which yawning switches the ing; 4) articles not including sufcient relevant data. Tere is a high Phylogenetically, yawning is a very old behavior that can level of activity in the default-mode network when the mind be detected in most vertebrates from the fetal stages to old is not involved in specifc behavioral tasks, and a low level of age3, 4, 5, 8. Its meaning has been the subject of speculation since activity during focused attention14. In some cultures, it has been associated with Satan hypothesis, yawning is a homeostatic process that appears (Arab countries) and spirits (India), while Hippocrates asso when the default-mode network is active and sleepiness ciated it with apoplexy8. In the Hindu world, yawning in pub increases; yawning then disengages the default-mode net lic is a religious ofense. Since the 17th century, various expla work to promote the attentional network, which accelerates nations for its meaning have been put forward8. Curiously, in 1888, in his famous Lecons du Mardi and Eguibar13 hypothesized that there are three main neu a la Salpetriere, Charcot discussed the case of a 17-year-old ral pathways involved in the regulation of yawning (Figure 2). Her condi projecting from the paraventricular nucleus (one of the hypo tion was believed at the time to be associated with hysteria thalamic nuclei) to the hippocampus, pons, medulla and spi and oxygenation of the nervous centers8, 11. In a study published in 2011, Guggisberg is an expression of therapeutic dopaminergic activity, partic et al. According to to fatigue, tiredness, stress, overwork, lack of stimulation, Guggisberg et al. In general, it is associated with sleep hypothesis, contagious yawning is due to activation of a com deprivation during the night and drowsiness during the day plex network of brain areas associated with imitation, empa and often occurs when people are bored2, 3, 4, 10, 11, 21. Yawning is termed pathological, abnormal, or demonstrated activation in the ventromedial prefrontal cor excessive if it is spontaneous, more frequent than generally tex, suggesting that mirror neuron networks play a role in perceived as normal, compulsive, and not triggered by appro yawning. Since the latter study, various papers on the rela priate stimuli including fatigue or boredom. No consensus tionship between contagious behavior, such as yawning and defnition exists concerning the frequency of yawns. A recent itching/scratching, and the activation of mirror neurons and recommendation adopted the abnormal yawning frequency the neurological mechanism of social behavior have been as three yawns per 15 minutes to decrease the likelihood that published19, 20, 21. In 2014, Provine22 stated that contagious two subsequent, accidental yawns were counted as one epi behaviors such as yawning have mirror-like properties. Yawning in neurology 475 Yawning can be present in the clinical picture of sev structures27, 29. Yawning has tumor, intracranial hypertension, Chiari malformation type I been described in patients with locked-in syndrome due and epilepsy, and can be induced by drugs1, 11. Another potential cause of yawning in Yawning in sleep disorders patients with stroke is intracranial hypertension or even her In general, excessive yawning occurs more frequently niation27. They found a correlation between ischemic lesions in the insula and caudate nucleus and a period of abnormal yawn Excessive yawning in clinical conditions ing and suggested that the insula may be the main region of Other clinical conditions associated with yawning are the brain responsible for serotonin-mediated yawning23. Excessive yawn Occasionally, in patients with acute hemiplegia, the onset ing has also been reported in patients with depression and of yawning is associated with an involuntary raising of the can be caused by the many medications used in neurology, paralyzed arm31, 32. Parakinesia bra Drug-induced yawning chialis oscitans was probably frst described by Erasmus Drug-induced yawning represents a rare and frequently Darwin, the grandfather of Charles Darwin, in 1794, in his not very serious adverse side-efect11, 24.
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