Carpal tunnel syndrome is a common disorder characterized by pain, burning , and tingling of the palmar surface of the hand, resulting from compression of the median nerve between the carpal ligament and other structures within the carpal tunnel (entrapment neuropathy). The volume of the contents of the tunnel can be increased by organic lesions such as synovitis of the tendon sheaths or carpal joints, recent or malhealed fractures, tumors, and occasionally congenital anomalies. Even though no anatomic lesion is apparent, flattening or even circumferential constriction of the median nerve may be observed during operative section of the ligament. The disorder may occur in pregnancy, is seen in individuals with a history of repetitive use of the hands, and may follow injuries of the wrists. A familial type of carpal tunnel syndrome has been reported in which no etiologic factor can be identified.
Carpal tunnel syndrome can also be a feature of many systemic diseases: rheumatoid arthritis and other rheumatic disorders (inflammatory tenosynovitis); myxedema, amyloidosis, sarcoidosis, and leukemia (tissue infiltration); acromegaly; hyperparathyroidism, hypocalcemia, and diabetes mellitus.
Clinical Findings
Pain in the distribution of the median nerve, which may be burning and tingling (acroparesthesia), is the initial symptom. Aching pain may radiate proximally into the forearm and occasionally proximally to the shoulder, neck, and chest. Pain is exacerbated by manual activity, particularly by extremes of volar flexion or dorsiflexion of the wrist. It may be most bothersome at night. Impairment of sensation in the median nerve distribution may not be apparent. Subtle disparity between the affected and opposite sides can be demonstrated by testing for two-point discrimination or by requiring the patient to identify different textures of cloth by rubbing them between the tips of the thumb and the index finger. Tinel's or Phalen's sign may be positive. (Tinel's sign is tingling or shock-like pain on volar wrist percussion; Phalen's sign, pain or paresthesia in the distribution of the median nerve when the patient flexes both wrists to 90 degrees with the dorsal aspects of the hands held in apposition for 60 seconds.) The carpal compression test, performed by applying direct pressure on the carpal tunnel, may be more sensitive and specific than the Tinel and Phalen tests. Muscle weakness or atrophy, especially of the abductor pollicis brevis, appears later than sensory disturbances. Useful special examinations include electromyography and determinations of segmental sensory and motor conduction delay. Distal median sensory conduction delay may be evident before motor delay.
Differential Diagnosis
This syndrome should be differentiated from other cervicobrachial pain syndromes, from compression syndromes of the median nerve in the forearm or arm, and from mononeuritis multiplex. When left-sided, it may be confused with angina pectoris.
Treatment
Treatment is directed toward relief of pressure on the median nerve. When a primary lesion is discovered, specific treatment should be given. When soft tissue swelling is a cause, elevation of the extremity may relieve symptoms. Splinting of the hand and forearm at night may be beneficial. Injection of corticosteroid into the carpal tunnel can alleviate symptoms in some patients, particularly those with synovitis of the wrist. To reduce the chance of nerve injury, this injection should be performed by a physician thoroughly familiar with the anatomy of the carpal tunnel. Operative division of the volar carpal ligament gives lasting relief from pain, which usually subsides within a few days. Muscle strength returns gradually, but complete recovery cannot be expected when atrophy is pronounced.
Sunday, April 5, 2009
Cardiovascular Disorders in Pediatrics
Congenital heart disease occurs in about 1% of children. Heart murmurs are much more common, and may be heard in virtually every child if examined carefully.
I. Clinical Evaluation of Cardiovascular Disorders
A. History
1. For neonates, a history of feeding problems, cyanosis, tachypnea, irritability or grunting respirations may indicate serious cardiac pathology. A history of feeding less than 2 ounces at each feeding in a term infant may indicate pathology. A family history of congenital heart disease may be helpful, but the
incidence of congenital heart disease in families where the mother has
congenital heart disease is only 5-10%. 2. For older children, it is unusual for a pathologic murmur to present for the first time outside of infancy. Two notable exceptions are hypertrophic cardiomyopathy and murmurs associated with dilated cardiomyopathy.
Symptoms which indicate serious pathology include exercise-induced chest pain, exercise induced syncope, or cyanosis. Easy fatigability is non specific, and not helpful in differentiating pathologic from non-pathologic murmurs.
B. Physical Examination
1. Congenital heart disease is more common in infants with congenital anomalies.
Trisomy 21. The incidence of heart disease is about 50% in these children. Anomalies include
ventricular septal defects, atrioventricular canal defects,
and patent ductus arteriosus.
b. Trisomy 18. The incidence of heart disease is almost 100%in these children. Ventricular septal
defect is the most common anomaly.
c. Trisomy 13. The incidence of heart disease is about 80%, usually VSD.
d. Turner syndrome (coarctation, hypertension), Marfan syndrome (aortic
aneurysms), and Noonan syndrome (pulmonic stenosis, coarctation) are other congenital
anomalies.
2. Growth parameters may suggest failure to thrive that is caused by cardiovascular disease. Infants with cardiovascular disease usually have a
normal head circumference, and height may be normal, but the weight is usually lower than anticipated.
3. Blood pressure determination. All children 3 years of age and older should have their blood pressure measured on a yearly basis. The blood pressure cuff should be appropriate for the patient’s size. The width of the cuff should be at least 2/3 the length of the upper arm, and the bladder should be long enough to almost encircle the upper arm. Blood pressure levels vary depending on the
age of the child, and hypertension is defined as a blood pressure consistently greater than the 95th percentile for age.
a. Presenting symptoms of severe hypertension in infants include congestive heart failure
(caused by coarctation), respiratory distress, and failure to thrive.
b. Symptoms of severe hypertension in older children may include headache, nausea, vomiting,
mental status changes, and epistaxis.
4. Cardiovascular Examination
a. Inspection
(1) Conditions that cause cardiac enlargement (ventricular septal defect,
The recommendations in blood pressure management are from the National High Blood Pressure Education Project provides tables that will give you normal data for blood pressure that varies by age, by height of the patient. Blood pressure should be measured in all children greater than three years of
age. Blood pressure should be measured from the patient's right arm after they
have been sitting in a quiet room for three to five minutes. Blood pressure should be measured twice and the results averaged, and the blood pressure should be measured with an appropriate size cuff. The simplest way to remember that is to try and get the largest cuff you can get on the child's arm.
They recommend that in a pediatric practice you have six cuffs. Three small
cuffs, one adult cuff, a large adult cuff and then a thigh cuff.
For definition of the diastolic blood pressure, the fifth Korotkoff sound is used. The fifth sound is when the sound totally disappears. There are patients in
whom the fifth Korotkoff sound never occurs. In other words, the sound never disappears, but then if it goes all the way down to zero, they don't have diastolic
hypertension, which makes sense.
Hypertension is defined as a child that has an average systolic or diastolic
blood pressure greater than the 95th percentile on three separate occasions, not all done in the same day. So don't rush into the diagnosis of hypertension.
Most children that have modest elevations in blood pressure are overweight and possibly have a family history of high blood pressure. Those people might get just a very basic routine screening evaluation which might include a urinalysis (looking for casts, hematuria, proteinuria), a BUN creatinine, looking
for elevation of creatinine consistent with renal disease, and also a good
cardiac physical exam, feeling femoral pulses. Those people would be treated with weight reduction, dietary restrictions, and emphasis on physical activity. Patients should not be restricted from physical activity because of mild elevations in blood pressure.
People that have significantly elevated blood pressure, and these are the people in the 99th and above percentile, frequently have underlying disease that is causing their hypertension. It is not idiopathic or familial hypertension. The two organ systems that are most commonly implicated are the renal
system and the cardiovascular system. Remember to listen for bruits over the abdomen because renal artery stenosis is a fairly common cause of significant
hypertension in children, and remember to feel the femoral pulses.
Now, I am going to briefly go over the cardiovascular exam, specifically the acyanotic category for an atrioseptal defect (ASD). In order to diagnose an
ASD it is not what is outside your ears that is most important. It is what is
between your ears that is most important. You need to know what you are listening for. If you can do a good ASD exam, then you know how to use your stethoscope. If you can rule out an ASD every time you listen to a patient, you will refer many fewer functional murmurs for evaluation, and you will miss many
fewer ASDs.
..... CLICK HERE TO DOWNLOAD FULL ARTICLE
I. Clinical Evaluation of Cardiovascular Disorders
A. History
1. For neonates, a history of feeding problems, cyanosis, tachypnea, irritability or grunting respirations may indicate serious cardiac pathology. A history of feeding less than 2 ounces at each feeding in a term infant may indicate pathology. A family history of congenital heart disease may be helpful, but the
incidence of congenital heart disease in families where the mother has
congenital heart disease is only 5-10%. 2. For older children, it is unusual for a pathologic murmur to present for the first time outside of infancy. Two notable exceptions are hypertrophic cardiomyopathy and murmurs associated with dilated cardiomyopathy.
Symptoms which indicate serious pathology include exercise-induced chest pain, exercise induced syncope, or cyanosis. Easy fatigability is non specific, and not helpful in differentiating pathologic from non-pathologic murmurs.
B. Physical Examination
1. Congenital heart disease is more common in infants with congenital anomalies.
Trisomy 21. The incidence of heart disease is about 50% in these children. Anomalies include
ventricular septal defects, atrioventricular canal defects,
and patent ductus arteriosus.
b. Trisomy 18. The incidence of heart disease is almost 100%in these children. Ventricular septal
defect is the most common anomaly.
c. Trisomy 13. The incidence of heart disease is about 80%, usually VSD.
d. Turner syndrome (coarctation, hypertension), Marfan syndrome (aortic
aneurysms), and Noonan syndrome (pulmonic stenosis, coarctation) are other congenital
anomalies.
2. Growth parameters may suggest failure to thrive that is caused by cardiovascular disease. Infants with cardiovascular disease usually have a
normal head circumference, and height may be normal, but the weight is usually lower than anticipated.
3. Blood pressure determination. All children 3 years of age and older should have their blood pressure measured on a yearly basis. The blood pressure cuff should be appropriate for the patient’s size. The width of the cuff should be at least 2/3 the length of the upper arm, and the bladder should be long enough to almost encircle the upper arm. Blood pressure levels vary depending on the
age of the child, and hypertension is defined as a blood pressure consistently greater than the 95th percentile for age.
a. Presenting symptoms of severe hypertension in infants include congestive heart failure
(caused by coarctation), respiratory distress, and failure to thrive.
b. Symptoms of severe hypertension in older children may include headache, nausea, vomiting,
mental status changes, and epistaxis.
4. Cardiovascular Examination
a. Inspection
(1) Conditions that cause cardiac enlargement (ventricular septal defect,
The recommendations in blood pressure management are from the National High Blood Pressure Education Project provides tables that will give you normal data for blood pressure that varies by age, by height of the patient. Blood pressure should be measured in all children greater than three years of
age. Blood pressure should be measured from the patient's right arm after they
have been sitting in a quiet room for three to five minutes. Blood pressure should be measured twice and the results averaged, and the blood pressure should be measured with an appropriate size cuff. The simplest way to remember that is to try and get the largest cuff you can get on the child's arm.
They recommend that in a pediatric practice you have six cuffs. Three small
cuffs, one adult cuff, a large adult cuff and then a thigh cuff.
For definition of the diastolic blood pressure, the fifth Korotkoff sound is used. The fifth sound is when the sound totally disappears. There are patients in
whom the fifth Korotkoff sound never occurs. In other words, the sound never disappears, but then if it goes all the way down to zero, they don't have diastolic
hypertension, which makes sense.
Hypertension is defined as a child that has an average systolic or diastolic
blood pressure greater than the 95th percentile on three separate occasions, not all done in the same day. So don't rush into the diagnosis of hypertension.
Most children that have modest elevations in blood pressure are overweight and possibly have a family history of high blood pressure. Those people might get just a very basic routine screening evaluation which might include a urinalysis (looking for casts, hematuria, proteinuria), a BUN creatinine, looking
for elevation of creatinine consistent with renal disease, and also a good
cardiac physical exam, feeling femoral pulses. Those people would be treated with weight reduction, dietary restrictions, and emphasis on physical activity. Patients should not be restricted from physical activity because of mild elevations in blood pressure.
People that have significantly elevated blood pressure, and these are the people in the 99th and above percentile, frequently have underlying disease that is causing their hypertension. It is not idiopathic or familial hypertension. The two organ systems that are most commonly implicated are the renal
system and the cardiovascular system. Remember to listen for bruits over the abdomen because renal artery stenosis is a fairly common cause of significant
hypertension in children, and remember to feel the femoral pulses.
Now, I am going to briefly go over the cardiovascular exam, specifically the acyanotic category for an atrioseptal defect (ASD). In order to diagnose an
ASD it is not what is outside your ears that is most important. It is what is
between your ears that is most important. You need to know what you are listening for. If you can do a good ASD exam, then you know how to use your stethoscope. If you can rule out an ASD every time you listen to a patient, you will refer many fewer functional murmurs for evaluation, and you will miss many
fewer ASDs.
..... CLICK HERE TO DOWNLOAD FULL ARTICLE
Cardiac Infections
Infective endocarditis. Streptococci and Staphylococci make up a very large fraction of cases of infective endocarditis, with Streptococci accounting for 50 to 60% of such infections and Staphylococci accounting for another
25%.
The viridans group of Streptococci includes the nutritionally variant organism which now has a new genus. They are now called abiotrophia. Abiotrophia defectivus. These are organisms that look like a viridans or any green hemolytic Streptococci that have unusual nutritional requirements.
Enterococci. Enterococcal infections are much less common in kids then they are in adults, and it is certainly true for endocarditis.
Occasionally, we have seen other Streptococcal organisms. Strep pneumoniae in beta hemolytic Streptococci, such as group C and T, Bs occasionally. So, this is the predominant group of origin. The two situations in which Staphylococci are particularly common, as far as this hemolytic carditis, are in the postoperative patient and in the patient who developed endocarditis in a normal heart.
The other common group of endocarditis agents that must be mentioned are the HACEK group. They account for 5 to 10% of cases of endocarditis.
About 5 % of cases of endocarditis are caused by other agents. Fungi, particularly Candida.
Aerobic gram negatives are not common in endocarditis, except occasionally in line-associated infections and in IV drug abusers; 3 to 5% of endocarditis is culture negative endocarditis and we will talk a little bit about that later on.
Pathogenesis of this disease. There is turbulent blood flow. In pediatric
lesions very often there is a jet effect, and in addition to the jet effect there is also non linear blood flow and eddies of blood. As a consequence of the jet effect, there is often endothelial disruption that occurs, which cumulates the development of the sterile fibrin-platelet thrombus in this area of endothelial damage or disruption. This is an outstanding place for "stray bacteremia" to settle out of the few organisms that become entrapped in this sterile fibrin-platelet fibrin. The slower the blood flow, the greater the opportunity for such organisms to be entrapped.
There are two presentations of infective endocarditis. The patient who
presents acutely is very sick with high fever and very toxic. They may be in congestive failure, and this is the situation where most often one would expect to find Staph aureus as the etiologic agent of the endocarditis. Situations where this presentation is most common is in a patient in the early postoperative phase, who has recently had heart surgery and had lines in place, or the unusual patient who presents with endocarditis with a normal heart without any obvious antecedent event. Other patients who are not postoperative but who have indwelling lines may also become infected with Staph aureus.
The other rather distinctive presentation, and more common presentation of endocarditis, is a much more insidious one. Patients may have low-grade fever or no fever, they are non-toxic. They do not feel very well, they have malaise, decreased energy. These infections are most commonly due to the viridans Streptococci. The HACEK group and fungi also produce infections that are more insidious and subacute in their presentations. Of course, we have patients who do not quite fit exactly in this category.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
25%.
The viridans group of Streptococci includes the nutritionally variant organism which now has a new genus. They are now called abiotrophia. Abiotrophia defectivus. These are organisms that look like a viridans or any green hemolytic Streptococci that have unusual nutritional requirements.
Enterococci. Enterococcal infections are much less common in kids then they are in adults, and it is certainly true for endocarditis.
Occasionally, we have seen other Streptococcal organisms. Strep pneumoniae in beta hemolytic Streptococci, such as group C and T, Bs occasionally. So, this is the predominant group of origin. The two situations in which Staphylococci are particularly common, as far as this hemolytic carditis, are in the postoperative patient and in the patient who developed endocarditis in a normal heart.
The other common group of endocarditis agents that must be mentioned are the HACEK group. They account for 5 to 10% of cases of endocarditis.
About 5 % of cases of endocarditis are caused by other agents. Fungi, particularly Candida.
Aerobic gram negatives are not common in endocarditis, except occasionally in line-associated infections and in IV drug abusers; 3 to 5% of endocarditis is culture negative endocarditis and we will talk a little bit about that later on.
Pathogenesis of this disease. There is turbulent blood flow. In pediatric
lesions very often there is a jet effect, and in addition to the jet effect there is also non linear blood flow and eddies of blood. As a consequence of the jet effect, there is often endothelial disruption that occurs, which cumulates the development of the sterile fibrin-platelet thrombus in this area of endothelial damage or disruption. This is an outstanding place for "stray bacteremia" to settle out of the few organisms that become entrapped in this sterile fibrin-platelet fibrin. The slower the blood flow, the greater the opportunity for such organisms to be entrapped.
There are two presentations of infective endocarditis. The patient who
presents acutely is very sick with high fever and very toxic. They may be in congestive failure, and this is the situation where most often one would expect to find Staph aureus as the etiologic agent of the endocarditis. Situations where this presentation is most common is in a patient in the early postoperative phase, who has recently had heart surgery and had lines in place, or the unusual patient who presents with endocarditis with a normal heart without any obvious antecedent event. Other patients who are not postoperative but who have indwelling lines may also become infected with Staph aureus.
The other rather distinctive presentation, and more common presentation of endocarditis, is a much more insidious one. Patients may have low-grade fever or no fever, they are non-toxic. They do not feel very well, they have malaise, decreased energy. These infections are most commonly due to the viridans Streptococci. The HACEK group and fungi also produce infections that are more insidious and subacute in their presentations. Of course, we have patients who do not quite fit exactly in this category.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
Bone and Joint Infections
There are three different routes of infection in children. The most common seems to be the hematogenesis route, which gains entry into the bone from the blood stream. Less commonly is by direct inoculation and this can be a puncture wound, such as stepping on a nail or something. This can also occur following trauma or surgery. Finally, a particular spread, which is really rare in children and seems to be more common in adults with various disabilities, especially alterations in blood flow.
What is thought to happen from the hematogenesis standpoint is that the during a course of bacteremia, as the organisms enter into the bone through the nutrient artery towards the growth plate, there are these loose capillaries that are said to have sluggish blood flow in them. It is also thought that maybe there is a fully developed reticulum within this system. There does seem to be evidence of low oxygen within the metaphysis, and we always hear about this preceding history of trauma as a possibly predisposing factor. Perhaps this is simply disruptive blood flow, but the history of trauma to children is common, and it is hard to know what really this is contributing to the pathogenesis.
The nutrient artery penetrates into the diaphysis of the bone, moving up into the metaphysis and making a hairpin turn at the epiphysis. This is why it is in a long individual, at least for the tubular long bones, that osteomyelitis is more common at the ends of the bones because of these here hairpin turns.
More recently there is some evidence in animals, specifically chickens, who actually can develop osteomyelitis spontaneously. A chicken strain of Staphylococcus aureus that appears at the endothelium within the capillaries of bones have gaps, and it looks as if the organisms can actually access the capillary system to these particular gaps. If you take a Staph aureus and inject it into the blood of the chicken, within 12 hours you can see bacteria in some of these capillaries, and subsequently a day or two later, evidence of infection at the metaphyseal epiphyseal junction. So this is sort of an interesting animal experiment, perhaps showing that these epithelial gaps, at least in chickens, play some role.
Another factor in the development of osteomyelitis, at least relating to Staphylococcus aureus, is the organism that produces this sort of slimy stuff seems to make it more adherent to various portions of the bones and thus more commonly associated with osteomyelitis than those other organs.
Microbial etiology of osteomyelitis. In the neonate, the organisms most commonly associated with osteomyelitis are typically Group B streptococcus and Staphylococcus aureus. Very small babies may involve for various gram negative bacteria and certainly cause osteomyelitis as well as some other bacteria. In the infant and older child, Staphylococcus aureus is the most common cause. Streptococcus is the second most common.
Highly encapsulated organisms are unusual causes of osteomyelitis, but 3 to 5% of patients with acute osteomyelitis will have pneumococcus as the etiology.
In the older child, the same types of organisms are seen. Salmonella is an important pathogen in patients with sickle cell anemia.
With penetrating injuries, organisms associated with the soil or the skin or on clothes can of course lead to infection. Some of these injuries, such as injuries associated with lawn mower trauma, can grind the soil-type organism into the skin and ultimately into the bone.
Now, sacroiliitis is not necessarily specifically an osteo, it is an osteo-like illness we must keep in mind, especially in dealing with certain populations, especially those who are likely to ingest under pasteurized or nonpasteurized dairy products.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
What is thought to happen from the hematogenesis standpoint is that the during a course of bacteremia, as the organisms enter into the bone through the nutrient artery towards the growth plate, there are these loose capillaries that are said to have sluggish blood flow in them. It is also thought that maybe there is a fully developed reticulum within this system. There does seem to be evidence of low oxygen within the metaphysis, and we always hear about this preceding history of trauma as a possibly predisposing factor. Perhaps this is simply disruptive blood flow, but the history of trauma to children is common, and it is hard to know what really this is contributing to the pathogenesis.
The nutrient artery penetrates into the diaphysis of the bone, moving up into the metaphysis and making a hairpin turn at the epiphysis. This is why it is in a long individual, at least for the tubular long bones, that osteomyelitis is more common at the ends of the bones because of these here hairpin turns.
More recently there is some evidence in animals, specifically chickens, who actually can develop osteomyelitis spontaneously. A chicken strain of Staphylococcus aureus that appears at the endothelium within the capillaries of bones have gaps, and it looks as if the organisms can actually access the capillary system to these particular gaps. If you take a Staph aureus and inject it into the blood of the chicken, within 12 hours you can see bacteria in some of these capillaries, and subsequently a day or two later, evidence of infection at the metaphyseal epiphyseal junction. So this is sort of an interesting animal experiment, perhaps showing that these epithelial gaps, at least in chickens, play some role.
Another factor in the development of osteomyelitis, at least relating to Staphylococcus aureus, is the organism that produces this sort of slimy stuff seems to make it more adherent to various portions of the bones and thus more commonly associated with osteomyelitis than those other organs.
Microbial etiology of osteomyelitis. In the neonate, the organisms most commonly associated with osteomyelitis are typically Group B streptococcus and Staphylococcus aureus. Very small babies may involve for various gram negative bacteria and certainly cause osteomyelitis as well as some other bacteria. In the infant and older child, Staphylococcus aureus is the most common cause. Streptococcus is the second most common.
Highly encapsulated organisms are unusual causes of osteomyelitis, but 3 to 5% of patients with acute osteomyelitis will have pneumococcus as the etiology.
In the older child, the same types of organisms are seen. Salmonella is an important pathogen in patients with sickle cell anemia.
With penetrating injuries, organisms associated with the soil or the skin or on clothes can of course lead to infection. Some of these injuries, such as injuries associated with lawn mower trauma, can grind the soil-type organism into the skin and ultimately into the bone.
Now, sacroiliitis is not necessarily specifically an osteo, it is an osteo-like illness we must keep in mind, especially in dealing with certain populations, especially those who are likely to ingest under pasteurized or nonpasteurized dairy products.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
Attention Deficit Disorder and Learning Disorders
Attention and learning disorders in children are very common
problems. Primary care pediatricians should be the ones to make the
diagnosis and do the treatment in the majority of children. You do not need a specialist in developmental/behavioral pediatrics to treat most kids or diagnose most kids with ADHD.
ADHD and the new DSM IV criteria. ADHD is defined as a persistent, that is more than 6 month cluster of behaviors. It's a behavioral cluster that has to have been going on for awhile - it can't just have started last week or last month. The behaviors are more frequent and more severe than most children at a comparable developmental level. This is very subjective, and part of the whole problem with diagnosing ADHD is there is no one way to make the diagnosis. There is no specific test. It is defined as behavior that is just more frequent and more severe than most children at a comparable level. It has to begin before seven years of age. It is not something that begins later on.
Most importantly, it has to be manifested in two or more settings: school or work and home. If you just have these behaviors occurring in one setting only, that is not ADHD. If it is only at home and not at school, it is not ADHD. If it is only at school and not at home, that is not ADHD. You should be thinking of other parts of your differential diagnosis. So, ADHD has to occur in at least two or more settings.
Finally to make the diagnosis, it has to cause clinically significant dysfunction in the social, academic, occupational, or family setting. There are some kids you'll see, that you will say to yourself, "this kid has ADHD. He's wild." But, he's doing great. He has friends. He's doing well in school. The school has adapted to him. The family has
adapted to him. You might not make the diagnosis in that child because there is not a clinically significant dysfunction. With the same
child in another setting who has a lot of problems in school and at home, you might make the diagnosis. So the diagnosis of ADHD is tough because there are these subjective features. And even among
experts, so-called experts, people will disagree with the diagnosis.
careless mistakes in school work, work outside the home, or in other activities. They often have difficulty sustaining attention in tasks or
play activities. What is important is sustaining attention when it is not easy to sustain attention, when it takes a little more effort, that is when ADHD shows up. The parents say, "He can play Nintendo for two
hours." and therefore he doesn't have ADHD. But that is not true.
The DSM IV criteria. For inattention, you have to have six or more of the following. One fails to give close attention to details or makes
careless mistakes in school work, work outside the home, or in other activities. They often have difficulty sustaining attention in tasks or
play activities. What is important is sustaining attention when it is not easy to sustain attention, when it takes a little more effort, that is when ADHD shows up. The parents say, "He can play Nintendo for two
hours." and therefore he doesn't have ADHD. But that is not true.
Because think of the kind of attention that it takes to play Nintendo. Whereas you have to pay attention to what's going on it is always changing. You are not sitting laboriously studying one thing or looking
at a number of things as you do in school. Does not seem to listen when spoken to directly.
Often does not follow through on instructions and fails to finish schoolwork, chores or duties in the workplace (not because of
oppositional behavior or inability to understand directions). He just can't get things done. Keeps trying a million projects, none of which get completed on time, if they get completed at all. Often has difficul-
ties organizing tasks and activities. And often avoids, dislikes or is
reluctant to engage in tasks that require sustained mental effort, such as schoolwork, homework.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
problems. Primary care pediatricians should be the ones to make the
diagnosis and do the treatment in the majority of children. You do not need a specialist in developmental/behavioral pediatrics to treat most kids or diagnose most kids with ADHD.
ADHD and the new DSM IV criteria. ADHD is defined as a persistent, that is more than 6 month cluster of behaviors. It's a behavioral cluster that has to have been going on for awhile - it can't just have started last week or last month. The behaviors are more frequent and more severe than most children at a comparable developmental level. This is very subjective, and part of the whole problem with diagnosing ADHD is there is no one way to make the diagnosis. There is no specific test. It is defined as behavior that is just more frequent and more severe than most children at a comparable level. It has to begin before seven years of age. It is not something that begins later on.
Most importantly, it has to be manifested in two or more settings: school or work and home. If you just have these behaviors occurring in one setting only, that is not ADHD. If it is only at home and not at school, it is not ADHD. If it is only at school and not at home, that is not ADHD. You should be thinking of other parts of your differential diagnosis. So, ADHD has to occur in at least two or more settings.
Finally to make the diagnosis, it has to cause clinically significant dysfunction in the social, academic, occupational, or family setting. There are some kids you'll see, that you will say to yourself, "this kid has ADHD. He's wild." But, he's doing great. He has friends. He's doing well in school. The school has adapted to him. The family has
adapted to him. You might not make the diagnosis in that child because there is not a clinically significant dysfunction. With the same
child in another setting who has a lot of problems in school and at home, you might make the diagnosis. So the diagnosis of ADHD is tough because there are these subjective features. And even among
experts, so-called experts, people will disagree with the diagnosis.
careless mistakes in school work, work outside the home, or in other activities. They often have difficulty sustaining attention in tasks or
play activities. What is important is sustaining attention when it is not easy to sustain attention, when it takes a little more effort, that is when ADHD shows up. The parents say, "He can play Nintendo for two
hours." and therefore he doesn't have ADHD. But that is not true.
The DSM IV criteria. For inattention, you have to have six or more of the following. One fails to give close attention to details or makes
careless mistakes in school work, work outside the home, or in other activities. They often have difficulty sustaining attention in tasks or
play activities. What is important is sustaining attention when it is not easy to sustain attention, when it takes a little more effort, that is when ADHD shows up. The parents say, "He can play Nintendo for two
hours." and therefore he doesn't have ADHD. But that is not true.
Because think of the kind of attention that it takes to play Nintendo. Whereas you have to pay attention to what's going on it is always changing. You are not sitting laboriously studying one thing or looking
at a number of things as you do in school. Does not seem to listen when spoken to directly.
Often does not follow through on instructions and fails to finish schoolwork, chores or duties in the workplace (not because of
oppositional behavior or inability to understand directions). He just can't get things done. Keeps trying a million projects, none of which get completed on time, if they get completed at all. Often has difficul-
ties organizing tasks and activities. And often avoids, dislikes or is
reluctant to engage in tasks that require sustained mental effort, such as schoolwork, homework.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
Saturday, April 4, 2009
Antiviral Agents
Amantadine and rimantadine have what is called an adamantyl cage structure. When the virus is endocytize into the cell, the influenza A membrane protein M2 is responsible for a transmembrane protein transport which increases the acidity inside of the cell and allows encoding. Both the adamantyl cage structure of amantadine and rimantadine interferes with this transmembrane protein hydrogen ion transport and, therefore, there can't be encoding of the virus. So, that is how these agents interfere with the influenza A virus replication. Blockage of the hydrogen ion channel reduces intracellular acidification which is necessary for fusion of the influenza A to the host cell endosomal membranes and release of viral RNA. Influenza B lacks the M2 protein and therefore influenza B is not inhibited by either amantadine or rimantadine.
Indications for amantadine and rimantadine. Prophylaxis of influenza A as well as treatment of influenza A. Now, for treatment of influenza A, efficacy is greatest if the medications are given within 48 hours from the onset of symptoms. Rimantadine does not have FDA indication for treatment in children. However, it is equally efficacious with amantadine. I would have no problems with using rimantadine in children for treatment if I was going to use the medication because it is certainly much safer than amantadine.
The indications for prophylaxis. Immunization with an appropriate influenza vaccine is the prevention method of choice. This method of choice may not be adequate when the circulating strain is not in the vaccine you may want to consider chemoprophylaxis. You may want to give rimantadine or amantadine simultaneously to the vaccine if the vaccine is delayed until the influenza A outbreak has occurred. This is particularly relevant if you have a child who currently now is receiving the vaccine that could lead for the first set of vaccines two doses four weeks apart. If you delayed it until the onset of the epidemic, you may need to do it with the amantadine and rimantadine for actually the entire six weeks because it will take four weeks to get the vaccines in and it takes about two weeks after the second dose to have an adequate immune response. So, if the vaccine was delayed, you can use the chemoprophylaxis.
tions or hospitals, or in home settings in which the child at risk for influenza related complications (children who have bronchopulmonary dysplasia or cystic fibrosis). If you have a child who can't take the vaccine, because they have anaphylaxis to egg protein or their age is less than six months, you may want to prophylax the individuals around that person in order to try to reduce the amount of disease. Another situation where prophylaxis would
Another indication for prophylaxis would be during an outbreak in institu-
tions or hospitals, or in home settings in which the child at risk for influenza related complications (children who have bronchopulmonary dysplasia or cystic fibrosis). If you have a child who can't take the vaccine, because they have anaphylaxis to egg protein or their age is less than six months, you may want to prophylax the individuals around that person in order to try to reduce the amount of disease. Another situation where prophylaxis would
be indicated is if you have a child who comes to your office who has influenza and they happen to have a sibling who is at risk for influenza related complications. It is better to prophylax the family members so that you can protect the at-risk child, because in general, most of the time, influenza is going to be a relatively benign disease for the healthy child and what you are trying to do is prevent disease in the child at risk.
......CLICK HERE TO DOWNLOAD FULL ARTICLE
Indications for amantadine and rimantadine. Prophylaxis of influenza A as well as treatment of influenza A. Now, for treatment of influenza A, efficacy is greatest if the medications are given within 48 hours from the onset of symptoms. Rimantadine does not have FDA indication for treatment in children. However, it is equally efficacious with amantadine. I would have no problems with using rimantadine in children for treatment if I was going to use the medication because it is certainly much safer than amantadine.
The indications for prophylaxis. Immunization with an appropriate influenza vaccine is the prevention method of choice. This method of choice may not be adequate when the circulating strain is not in the vaccine you may want to consider chemoprophylaxis. You may want to give rimantadine or amantadine simultaneously to the vaccine if the vaccine is delayed until the influenza A outbreak has occurred. This is particularly relevant if you have a child who currently now is receiving the vaccine that could lead for the first set of vaccines two doses four weeks apart. If you delayed it until the onset of the epidemic, you may need to do it with the amantadine and rimantadine for actually the entire six weeks because it will take four weeks to get the vaccines in and it takes about two weeks after the second dose to have an adequate immune response. So, if the vaccine was delayed, you can use the chemoprophylaxis.
tions or hospitals, or in home settings in which the child at risk for influenza related complications (children who have bronchopulmonary dysplasia or cystic fibrosis). If you have a child who can't take the vaccine, because they have anaphylaxis to egg protein or their age is less than six months, you may want to prophylax the individuals around that person in order to try to reduce the amount of disease. Another situation where prophylaxis would
Another indication for prophylaxis would be during an outbreak in institu-
tions or hospitals, or in home settings in which the child at risk for influenza related complications (children who have bronchopulmonary dysplasia or cystic fibrosis). If you have a child who can't take the vaccine, because they have anaphylaxis to egg protein or their age is less than six months, you may want to prophylax the individuals around that person in order to try to reduce the amount of disease. Another situation where prophylaxis would
be indicated is if you have a child who comes to your office who has influenza and they happen to have a sibling who is at risk for influenza related complications. It is better to prophylax the family members so that you can protect the at-risk child, because in general, most of the time, influenza is going to be a relatively benign disease for the healthy child and what you are trying to do is prevent disease in the child at risk.
......CLICK HERE TO DOWNLOAD FULL ARTICLE
Antifungal Therapy
The topical antifungal agents are only useful for superficial mycoses. Griseofulvin is also useful for superficial mycoses and nothing else. Azoles are really the only antifungal agents which can go across the board and have utility in superficial, cutaneous and systemic mycoses. Among the polyenes, nystatin is useful only in superficial candidiasis, for example, such as thrush. Amphotericin B is typically reserved for more serious cutaneous disease and systemic therapy.
derivative, is quite useful in ringworm, provided it is not on the scalp, in tinea versicolor, and in candidiasis. Clotrimazole is a representative of the azole category, and it also is useful for all three types of superficial mycoses. Nystatin, on the other hand, is a polyene and of no utility in ringworm or tinea versicolor and must be reserved for superficial candidiasis such as thrush.
cutaneous mycoses. Now, here they are yet again. This is naftifine.
This is an allylamine derivative. The other allylamine that you may encounter is terbinafine and these of course, as allylamine derivatives, inhibit fungal metabolism very high up in the pathway of fungal cell-wall construction. They inhibit really the first step in the conversion of squalene to lanosterol. The imidazoles and the triazoles inhibit at a secondary step in the building of the fungal
cell wall. The imidazoles and the triazoles inhibit 14 alpha
demethylase, which mediates the conversion of lanosterol to ergosterol. The polyenes, nystatin (a topical antifungal agent) and amphotericin as (systemic antifungal agent), inhibit the actual synthesis of ergosterol, the major component of the fungal cell membrane.
superficial dermatophyte infections as well as for superficial
candidiasis. Such things as Candida diaper rash, mild intertrigo. The creams, the gels and solutions are very helpful in inflamed intertriginous areas such as the toe webs, the groin and the scrotum. Powder formulations are useful for milder lesions in the identical areas. If it’s wet, dry it, if it’s dry, wet it - so that if this is a wet diaper area then a powder may be very helpful. The powders,
like clotrimazole powders, the imidazole powders, are extremely useful in stoma infections. So if you have for example a cancer
patient with a colectomy or a child with short-gut syndrome who has a stoma and then has a bag. Those are typically very, very wet areas. Ointments and creams really don’t get the job done. The powders are very useful in those wet areas. Ointments in particular
are typically much too occlusive and the dermatophytes and particularly Candida love that sort of moist area. So usually I don’t
use the ointment formulations of these topical antifungals. The major exception to the use of topical antifungal agents are dermatophyte lesions of the head. Ringworm of the scalp, tinea capitus and kerion will require oral therapy, usually with
griseofulvin.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
derivative, is quite useful in ringworm, provided it is not on the scalp, in tinea versicolor, and in candidiasis. Clotrimazole is a representative of the azole category, and it also is useful for all three types of superficial mycoses. Nystatin, on the other hand, is a polyene and of no utility in ringworm or tinea versicolor and must be reserved for superficial candidiasis such as thrush.
cutaneous mycoses. Now, here they are yet again. This is naftifine.
This is an allylamine derivative. The other allylamine that you may encounter is terbinafine and these of course, as allylamine derivatives, inhibit fungal metabolism very high up in the pathway of fungal cell-wall construction. They inhibit really the first step in the conversion of squalene to lanosterol. The imidazoles and the triazoles inhibit at a secondary step in the building of the fungal
cell wall. The imidazoles and the triazoles inhibit 14 alpha
demethylase, which mediates the conversion of lanosterol to ergosterol. The polyenes, nystatin (a topical antifungal agent) and amphotericin as (systemic antifungal agent), inhibit the actual synthesis of ergosterol, the major component of the fungal cell membrane.
superficial dermatophyte infections as well as for superficial
candidiasis. Such things as Candida diaper rash, mild intertrigo. The creams, the gels and solutions are very helpful in inflamed intertriginous areas such as the toe webs, the groin and the scrotum. Powder formulations are useful for milder lesions in the identical areas. If it’s wet, dry it, if it’s dry, wet it - so that if this is a wet diaper area then a powder may be very helpful. The powders,
like clotrimazole powders, the imidazole powders, are extremely useful in stoma infections. So if you have for example a cancer
patient with a colectomy or a child with short-gut syndrome who has a stoma and then has a bag. Those are typically very, very wet areas. Ointments and creams really don’t get the job done. The powders are very useful in those wet areas. Ointments in particular
are typically much too occlusive and the dermatophytes and particularly Candida love that sort of moist area. So usually I don’t
use the ointment formulations of these topical antifungals. The major exception to the use of topical antifungal agents are dermatophyte lesions of the head. Ringworm of the scalp, tinea capitus and kerion will require oral therapy, usually with
griseofulvin.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE
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