Doctorz

Viral Meningitis

2009-04-06T04:24:00.000-07:00

Aseptic Meningitis
Steven Wilson, M.D.

I. Background
A.Terminology. Aseptic meningitis refers to subarachnoid inflammation from any cause other than pyogenic bacteria or fungi. The differential includes viruses, other microorganisms, and non-infectious causes. Sinc most cases are caused by viruses, the terms "aseptic" and "viral" meningitis are often used synonymously
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Viral Hepatitis Update

2009-04-06T04:15:00.000-07:00

Spencer Wilson, MD
Acute viral hepatitis has been defined as a systemic viral infection in which there is hepatocellular necrosis and inflammation. There are characteristic clinical, biochemical, immuno-serologic, and morphologic features. There are five major viruses: Hepatitis A virus (HAV), hepatitis B virus (HBV), Hepatitis C virus (HCV), hepatitis D virus (delta Virus, HDV), and Hepatitis E virus (enterically transmitted, epidemic non-A, non-B hepatitis, HEV). Chronic viral hepatitis is a necro-inflammatory disorder of the liver initiated by viruses and persisting for longer than six months. It occurs in association with HBV, HCV, and delta virus infection. In contrast, patients with acute hepatitis A and hepatitis E virus infection have no propensity whatsoever to develop a chronic carrier state or chronic liver disease.

Hepatitis A
The hepatitis A virus (HAV) is a 27 nm RNA virus classified as an enterovirus and belonging to the picornovirus family The nucleic acid of HAV is single-stranded RNA and. to date, only a Single serotype has been identified. The virus is stable for several months at 40cbut can be inactivated by exposure to heat to 100BC for five minutes. The virus can be transmitted to chimpanzees and marmosets and has been recently grown in tissue culture.
Susceptibility to HAV infection increases linearly with age and bears an inverse correlation to socioeconomic status. In major metropolitan centers in the United States, 50% of persons 50 years of age or older have detectable antibody to HAV. HAV is spread predominantly by the fecal-oral route via contaminated food and water. Overcrowding, poor hygiene, and poor sanitation favor the spread of this infection. A chronic viremic or fecal carrier state does not occur. Hence, patients are only transiently infectious. Viremia and fecal shedding occur over a short and finite period of time lasting several days to a few weeks. Transmission occurs via serial spread from one infected individual to another susceptible individual. Parenteral transmission of hepatitis A infection is extremely rare. Intravenous drug users, dialysis patients, transfusion recipients, and health care workers are not at increased risk of infection. Acquisition of HAV secondary to frequent oral-anal sexual contact has been documented in homosexual men.
The diagnosis is accomplished by testing the serum for antibody to hepatitis A. The IgM antibody appears during the acute phase and is detected by immune adherence hemagglutination, as well as by radioimmunoassay and usually disappears within 4 to 12 weeks. Persistent anti-HAV IgG antibody, is then detectable and confers homologous immunity. Fecal shedding of the hepatitis A virus occurs in the early phase of the illness. HAV is detected in stool during the first week of infection in 50% of patients, during the second week in 25% of patients, and in the third and fourth weeks only rarely.
In the United States, HAV is responsible for 25% of sporadic cases of hepatitis. In most persons, the disorder is mild, self-limited, and anicteric. Constitutional symptoms of fever, malaise, and anorexia are common and an abrupt onset is characteristic. If the patient develops jaundice, the urine may darken and the stool may lighten a few days before the onset of jaundice. When jaundice begins, the other symptoms usually subside. Tender hepatomegaly is common. Splenomegaly and lymphadenopathy are present in less than a third of patients.
Hepatitis A has an incubation period is 15 to 50 days. The virus is present in the blood stream for a short final period of time. The viremic phase is very short lived. It is shed in the stool for a short period of time. The majority of individuals do not develop jaundice. The ratio of anicteric hepatitis to jaundice is 20 to 1. Patients recover by in large. There are 2 antibodies, which are the IgM and the IgG. The way to make the diagnosis of acute hepatitis A is to look at a single sample of serum and if it is positive for IgM Anti-HV your patient with acute hepatitis has acute hepatitis A infection. IgG antibody appears during the convalescence phase, and confers life long immunity. There are 3 variants of hepatitis A virus infection which are cholestatic hepatitis, relapsing, and fulminant. Fulminant occurs rarely but can lead to fatalities and the only treatment in that setting is to do a liver transplant. Cholestatic hepatitis occurs more often in middle-aged or elderly individuals. They can have bilirubins in excess of 20 or 30 mg/dL. They develop marked pruritus. We can do an IgM antibody and make the diagnosis of acute hepatitis A. The patient has a bilirubin of 30, so we can get an ultrasound and make sure the bile ducts are not dilated and make the diagnosis of hepatitis A infection. This is the one time to consider a short course of corticosteroids. Prednisone, 30 or 40 mg, for week and then taper it, will significantly truncate or abrogate the illness.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Surgery Documentation

2009-04-06T04:08:00.000-07:00

Surgical Documentation
S. E. Wilson, MD
Surgical History and Physical Examination
Identifying Data: Patient's name, age, race, sex; referring physician.
Chief Compliant: Reason given by patient for seeking surgical care and the duration of the symptom. History of Present Illness (HPI): Describe the course of the patient's illness, including when it began, character of the symptoms; pain onset (gradual or rapid), precise character of pain (constant, intermittent, cramping, stabbing, radiating); other factors associated with pain (defecation, urination, eating, strenuous activities); location where the symptoms began; aggravating or relieving factors. Vomiting (color, character, blood, coffee-ground emesis, frequency, associated pain). Change in bowel habits; rectal bleeding, character of blood (clots, bright or dark red), trauma; recent weight loss or anorexia; other related diseases; past diagnostic testing. Past Medical History (PMH): Previous operations and indications; dates and types of procedures; serious injuries, hospitalizations; diabetes, hypertension, peptic ulcer disease, asthma, heart disease; hernia, gallstones. Medications: Aspirin, anticoagulants, hypertensive and cardiac medications, diuretics. Allergies: Penicillin, codeine, iodine. Family History: Medical problems in relatives. Family history of colon cancer, cardiovascular disease. Social History: Alcohol, smoking, drug usage, occupation, daily activity.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Pediatric History

2009-04-06T03:34:00.000-07:00

Identifying Data: Patient's name, age, sex; significant medical conditions,
informant (parent).

Chief Compliant (CC): Reason that the child is seeking medical care and
duration of the symptom.

History of Present Illness (HPI): Describe the course of the patient's illness,
including when and how it began, character of the symptoms; aggravating or
alleviating factors; pertinent positives and negatives, past diagnostic testing.

Past Medical History (PMH): Medical problems, hospitalizations, operations;
asthma, diabetes.

Perinatal History: Gestational age at birth, obstetrical complications, type of
delivery, birth weight, Apgar scores, complications (eg, infection, jaundice),
length of hospital stay.

Medications: Names and dosages.

Nutrition: Type of diet, amount taken each feed, change in feeding habits.

Developmental History: Age at attainment of important milestones (walking,
talking, self-care). Relationships with siblings, peers, adults. School grade and
performance, behavioral problems.

Immunizations: Up-to-date?
Allergies: Penicillin, codeine?
Family History: Medical problems in family, including the patient's disorder;
diabetes, seizures, asthma, allergies, cancer, cardiac, renal or GI disease,
tuberculosis, smoking.

Social History: Family situation, alcohol, smoking, drugs, sexual activity.
Parental level of education. Safety: Child car seats, smoke detectors, bicycle
helmets.

Review of Systems (ROS)
General: Overall health, weight loss, behavioral changes, fever, fatigue. Skin: Rashes, moles, bruising, lumps/bumps, nail/hair changes. Eyes: Visual problems, eye pain.
Ear, nose, throat: Frequency of colds, pharyngitis, otitis media. Lungs: Cough, shortness of breath, wheezing. Cardiovascular: Chest pain, murmurs, syncope.
Gastrointestinal: Nausea/vomiting, spitting up, diarrhea, recurrent abdominal pain, constipation, blood in stools.
Genitourinary: Dysuria, hematuria, polyuria, vaginal discharge, STDs. Musculoskeletal: Weakness, joint pain, gait abnormalities, scoliosis. Neurological: Headache, seizures.
Endocrine: Growth delay, polyphagia, excessive thirst/fluid intake, menses duration, amount of flow.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Outpatient and Primary Care Medicine

2009-04-06T03:28:00.000-07:00

Cardiovascular Disorders

Stable Angina Pectoris

Angina pectoris is a symptom complex caused by myocardial ischemia. Stable angina refers to chest discomfort that occurs predictably and reproducibly at a certain level of exertion and is relieved with rest or nitroglycerin. Unstable angina includes new onset of chest pain, progressing effort angina, rest angina, post-myocardial infarction angina, and angina after revascularization.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Nutrition Infant

2009-04-06T03:16:00.000-07:00

Nutrition for the Term Infant
Breast milk is universally recommended as the preferred source of infant nutrition, in part because of its superior nutrient and immunologic properties. Successful breast feeding requires nursing on demand, prevention of sore nipples and convenient access to medical advice. For mothers relying on bottle feeding, cow's-milk-based formula is the preferred choice. Because soy-based formulas are lactose-free, they may be tolerated by infants who are allergic to cow's-milk protein. Protein hydrolysate formulas should be used only in infants who cannot tolerate cow's-milk-based or soy-based formulas. Low-iron formulas and whole cow's milk should not be used during the first year. Breast-fed infants rarely require vitamin supplementation. Fluoride supplementation is no longer recommended for infants less than six months of age.

Benefits of Breast Feeding
Breast milk is universally recognized as the preferred source of infant nutrition, and the nutritional advantages of breast milk have been well documented. Colos-trum, the first milk produced after delivery, provides an initial dose of enzymes that promote gut maturation, facilitate digestion and stimulate passage of meco-nium. Colostrum is also high in protein, primarily because of high levels of im-munoglobulins and secretory IgA. The protein in human milk is ideal not only for absorption, but also for utilization, especially by the rapidly developing infant brain. Human milk also contains predominantly polyunsaturated fats with stable amounts of cholesterol, an important constituent of brain and nerve tissue.
Human milk also protects against infection by providing cellular immunity through macrophages and humoral factors, such as antibodies. Numerous studies have verified that breast-fed infants have a lower incidence of bacterial and viral illnesses than bottle-fed infants. This low incidence is of particular clinical significance in developing nations? Ongoing research suggests that breast feeding may provide immuno-logic protection against diabetes mellitus, cancer and lymphoma. Finally, breast feeding has been found to provide protection from allergic diseases, including eczema, asthma and allergic rhinitis. This protection is most likely the result of breast milk decreasing intestinal permeability to large, allergenic molecules.
Recognizing these as well as other advantages, the American Academy of Family Physicians (AAFP) and the American Academy of Pediatrics (AAP) have identified breast milk as the preferred source of infant nutrition. In addition, the U.S. Public Health Service (USPHS) has established a national goal that, by the turn of the century, 75 percent of new mothers will be breast-feeding at the time of hospital discharge. Despite an emphasis on breast feeding by both private and government organizations, only 54 percent of U.S. mothers initiate breast feeding, and fewer than half of these mothers continue nursing for at least six months. Clearly, all health care providers should actively promote breast feeding if the goal set by the USPHS is to be accomplished.
To successfully promote breast feeding, family physicians should consider the influence of marketing campaigns aimed at expectant and new mothers by the manufacturers of infant formulas. Historically, their dogged marketing efforts have included the distribution of free cases of infant formula to expectant mothers, as well as the inclusion of formula samples in commercial hospital discharge packs designed for breast-fed infants. Physicians must work proactively to weigh the risks and benefits of promotional materials and develop appropriate policies governing their distribution in their hospitals or academic institutions.

Counseling Strategies
Breast feeding should be initiated as soon after delivery as possible, and mothers should be encouraged to nurse on demand, usually eight to 10 times a day.

Signs of Successful Breast Feeding
Audible swallowing
Eight to 10 feedings per day
Six to eight wet diapers per day
Three to five bowel movements per day
Infant regains birth weight by two weeks of age

This strategy enables the milk supply to quickly become well established. Table 1 lists reassuring signs of successful breast feeding, which can be used to assess the infant's nutritional intake as well as to bolster the new mother's confidence in her breast-feeding success. Supplemental formula feedings should be discouraged in the early postpartum period, since they may result in a decreased milk supply or infant confusion between the artificial and maternal nipples?
The first weeks of nursing represent a pivotal time for success or failure of breast feeding. And with the trend toward increasingly abbreviated inpatient stays, nursing mothers will be relying more than ever before on their physicians and office staff to provide much of the breast-feeding counseling that previously took place in the hospital.
To be successful, nursing mothers must learn proper positioning of the infant. Since sore nipples can derail even the best intentions to breast feed, nursing mothers should learn techniques for preventing sore nipples, such as varying the nursing position and using the little finger to break the infant's suction before removing the infant from the breast. Should these efforts fail to prevent soreness, mothers should have quick access to effective treatment regimens.
The ability of the breast-feeding couple to weather difficulties and setbacks can be enhanced by close contact with a responsive physician and office staff. Early physician visits, home nursing visits and even telephone contacts can provide opportunities to offer support and guidance to nursing mothers? For example, a staff member might routinely call nursing mothers the day after hospital discharge. The physician's office environment can be structured to allow privacy and comfort for nursing mothers. Often this can be accomplished by simply making an examination room available.

Once nursing is well established, the physician should encourage the mother to continue nursing throughout the infant's first year of life. Physicians should avoid recommending unnecessary disruptions in breast feeding. Recent guidelines on the management of hyperbilirubinemia in the healthy term newborn, for example, discourage the interruption of breast feeding and, instead, provide the option of frequent breast feeding.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Non-invasive Cardiac Imaging

2009-04-06T02:58:00.000-07:00

Janet Wong, M.D.

Chest X-Ray
The chest X-ray provides information about the size and configuration of the heart and great vessels, as well as pulmonary vasculature, and pleural effusions. Cardiac chamber dilation, rather than wall thickening is generally perceived as an alteration in cardiac silhouette. Routinely posteroanterior (PA) and lateral chest films are obtained. Enlargement of the fight atrium may cause bulging of the heart to the fight on the PA film, while fight ventricular enlargement is generally perceived as a filling of the anterior clear space on the lateral film. Left atrial enlargement may be detected by an upward displacement of the left main-stem bronchus, or posterior displacement of the barium filled esophagus on lateral films. Left ventricular enlargement is the most common finding on chest x-ray, generally results in an increased cardiothoracic ratio (> 0.50). Pericardial effusions may be suspected by an enlarged cardiac silhouette with "water bottle" appearance. Fluoroscopy, more often performed in the cardiac catheterization suite, generally confirms minimal motion of cardiac borders. Fluoroscopy is also more sensitive for detection of cardiac valve calcium as well as epicardial calcium (see cine CT). The chest x-ray is also helpful to demonstrate upper zone redistribution, pleural effusions, and Kerley B-lines indicative of congestive heart failure.

Echocardiography
Echocardiography uses ultrasound to image the heart and great vessels. It is widely regarded as the technique of choice for evaluation of suspected valvular heart disease. Its ease of use, high temporal and spatial resolution, and lack of complications also makes it ideal for assessment of cardiac chamber size and systolic function, though comprehensive left ventricular endocardial borders may be difficult to identify in a significant minority (20%) of patients. Three general types of studies may be performed, M-mode echocardiography, two-dimensional (2D) echocardiography, and Doppler echocardiography. M-mode and 2D imaging are useful for quantifying chamber sizes, ventricular systolic function, wall thickness, and valvular morphology while Doppler echocardiography, which measures blood flow velocity and includes pulsed wave, continuous wave and color Doppler methods, is most valuable for assessing valvular function.

Quantitative data regarding left ventricular wall thickness and chamber dimensions are generally measured using M-mode methods, a technique which uses very high temporal (>1000 Hz) resolution, while qualitative global and regional left ventricular systolic function is generally best appreciated using 2D methods. Automated endocardial edge-detection techniques have recently been introduced for "real-time" analysis of global systolic indices, but these algorithms make many assumptions regarding the ventricular geometry (symmetry) which may not be applicable to the individual patient. Complications of myocardial infarction such as left ventricular aneurysm or left ventricular apical thrombi are readily identified by 2D transthoracic echocardiography. The crescent shaped right ventricle is more difficult to assess, and only qualitative analyses from 2D data are generally used. Left atrial chamber size may also be quantified by 2D transthoracic echocardiography. While left ventricular thrombi are easily appreciated from transthoracic approaches, left atrial thrombi are best visualized using The physical examination provides a tremendous amount of information we get from that. Just the general appearance of our patients. Is there evidence of peripheral cyanosis? Are they dyspneic? Is there evidence of exophthalmus, the fundi? Again, in patients with hypertension especially diabetes. Looking at jugular venous distension. Examining the carotid pulse. Is it delayed, is there a bi-fib pulse - the bi-fib pulse being suggestive of a hypertrophic obstructive cardiomyopathy? Examining the lungs for rales, effusions. The heart for PMI as well as murmurs. It is important in your patients to have the patients turn in the left lateral decubitus position to hear mitral murmurs and if you are concerned about aortic insufficiency, certainly have them sit up and forward with an exhalation examination. Finally, the abdominal examination - ascites, organomegaly and the extremities.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Newborn Care

2009-04-06T02:53:00.000-07:00

Routine testing of the fetus in utero start early in pregnancy with the mother having a hemoglobin and hematocrit, a urinalysis, blood group, an Rh determination, an antibody screen, rubella titer measurement, syphilis screen, cervical cytology, and hepatitis B virus screen..
As pregnancy goes on, an ultrasound should be done between 8 and 18 weeks if it's being used for dating purposes. Also, for an amniocentesis for diagnostic purposes. Chorionic villus biopsy sampling, of course, is also for chromosome imbalances and should also be done prior to 18 weeks. Maternal serum alpha-fetoprotein screening for neural tube defects should be done between 16 and 18 weeks. If the initial value is elevated, then it should be repeated. Subsequently, if that one is elevated, then an amniotic fluid alpha-fetoprotein should be done.
At 26-28 weeks, diabetes screening is recommended and repeat hemoglobin in the mother. An antibody test for Rh negative patients should be done by 28 weeks and prophylactic administration of RhoGAM should be done at that time. An ultrasound can be repeated at 32-36 weeks if one is suspicious of congenital malformations or for identification of sex, although it is very important to recognize that that is not a completely accurate test.
Prenatal diagnostic tests for birth defects. Cytogenetic indications are generally advanced maternal age; previous offspring with chromosome abnormality, especially trisomy; chromosome abnormality in either parent, especially if there is translocation such as in Down's syndrome; a need to determine the fetal sex when there is a family history of serious X-linked disease. Also, if there is a single gene disorder in a sibling or carrier or multifactorial disorders in first-degree relatives.
Documentation of dates. This should be done by the presence of fetal heart tones for 20 weeks by nonelectronic stethoscope, or 30 weeks by a Doppler ultrasound, or a positive pregnancy test of 36 weeks duration, or an ultrasound examination documenting a crown rump length between 6-11 weeks, or an evaluation at 12-20 weeks that confirms the clinical history and physical examination. An assessment of continued growth includes crown rump length, femur length, chest/abdominal circumference, and head circumference. Of course, the point here is to identify the baby's continued growth in utero. The femur length is really a very accurate tool to use in length of gestation throughout pregnancy.
In the absence of documenting length of pregnancy by any of the aforementioned methods above, the assessment of the fetal pulmonary maturity should be done when the pregnancy has to be induced, one of the most common tests to do this is a phosphatidylglycerol (PG) and if there is fetal maturity the presence of PG is positive. An L:S ratio is somewhat more accurate. It takes a longer period of time. An L:S ratio greater than two is equal to maturity. Other tests that are done, somewhat less commonly but are fairly reliable, are the foam stability index and a Delta OD 650 with a value greater than 0.15 indicating maturity.
Assessment of placental integrity is being done more and more frequently by our OB colleagues by ultrasound and by Doppler studies of blood flow. We can grade the placenta by ultrasound and determine whether or not there is calcium deposition, get a rough idea of the size placenta and whether or not placental function is normal with flow studies. There are two indices, the pulsatility index and BD index that are calculated and two ratios, systolic and diastolic and diastolic over average ratios that are being assessed as obstetricians evaluate blood flow through the umbilical vein. Absence of diastolic flow is a very bad prognostic sign suggesting that the fetus is not being perfused well and may well be better off out than in.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Manual of HIV AIDS

2009-04-06T02:37:00.000-07:00

Clinical Care of the HIV-Infected Patient

Primary HIV Infection

Acute retroviral syndrome occurs at the time the infection is acquired in 60% to 80% of HIV-infected persons. The illness resembles infectious mononucleosis from infection with Epstein-Barr virus (EBV). Risk factors fortransmission of HIV include history of a sexually transmitted disease, especially genital ulcers; unprotected anal or genital intercourse; and multiple sexual partners.
I. Clinical signs and symptoms

The period between acquisition of HIV and onset of symptoms is about 14 days, and the characteristic signs and symptoms range from a mild fever and sore throat to a severe mononucleosis-type syndrome with high spiking fevers and a measles-like rash.

B. In those patients with symptomatic seroconversion, the five most common signs and symptoms are fever, fatigue, pharyngitis, weight loss, and myalgias. Characteristic symptoms of acute retroviral syndrome occur in 50% to 90% of patients.

.... CLICK HERE TO DOWNLOAD FULL ARTICLE

Lung Cancer

2009-04-06T02:33:00.000-07:00

Kenneth Albert, MD
Lung cancer is not the most common cancer in either men or women. Prostate cancer is certainly number one in men and breast cancer is number one in women. It cuts lung cancer at approximately half; so you can see breast cancer is much more common than lung cancer. However, if you look at the deaths from cancer, lung cancer, it is by far the biggest killer in both men and women.
If you look at the changing incidence of lung cancer in men, the United Kingdom is actually decreasing quite substantially from the earlier 1960s and '70s. In the United States, it actually leveled off in the 1980s, and it has started to decline in the last couple of years, and in France it is still rising. So it really just depends on where you are and on your habits. In women, the United States is still going up. It hasn't showed any sign of leveling off. The United Kingdom has already leveled off and started to decline a little bit. In France, it is has always been low.
Types of lung cancer. There are two major types: non-small cell and small cell. Approximately 75-80% of the tumors that we see are non-small cell, while only 20-25% are small cell itself. If we look at the small cell subtypes, previously the vast majority of those particularly with the disease found in males was squamous cell cancer, but more recently the majority of them are adenocarcinomas, and 40% of all lung cancers are adenocarcinomas. So this has really shot up and changed the nature of the disease as well. Squamous cell is only 17% of all lung cancers.
In smokers, particularly males, squamous cell is a fairly predominant tumor type. But if we look at nonsmokers, adenocarcinoma is by far the most common subtype. The same is true of females, even to a greater extent. In smokers, adenocarcinoma is more common in females.
....CLICK HERE TO DOWNLOAD FULL ARTICLES

Liver Disease

2009-04-06T02:25:00.000-07:00

Laboratory Tests And Diagnostic Procedures in Hepatobiliary Disease

Patricia Liu, M.D.
Liver function tests are best utilized in concert with the clinical situation and in conjunction with serial determinations to ascertain the cause or evolution of the hepatic disorder. In addition, stool and urine tests, radionuclide imaging, contrast cholangiography (transhepatic cholangiography and endoscopic retrograde cholangiopancreatography), and histological assessment (liver biopsy) are often utilized to delineate the nature of the liver disease.

Serum Enzymes (Serum Aminotransferase Transaminases)
Serum glutamic oxaloacetic transaminase, also referred to as aspartate aminotransferase, and serum glutamic pyruvic transaminase, also called alanine aminotransferase (AST and ALT) are commonly employed to ascertain liver function. Striking elevations in the serum levels of these two enzymes are encountered in acute viral hepatitis, acute drug- or toxin-induced liver damage, and ischemic hepatitis. In addition, levels exceeding 500 IU/L and, on rare occasions, 1,000 IU/L can also be seen in patients with severe chronic active hepatitis, transiently in patients with common bile duct stones, and in patients with Budd-Chiari and veno-occlusive disease.
There are a number of important hepatic disorders in which the serum AST and ALT are normal or minimally elevated . These include idiopathic genetic hemochromatosis, methotrexate-induced liver injury, liver dysfunction due to amiodarone, the liver disease associated with jejunal ileal bypass surgery, and patients with chronic hepatitis C virus infection.
The ratio of AST and ALT is also sometimes of value in clinical practice. A ratio greater than 2 with both AST and ALT being less than 300 IU/L is characteristic of alcoholic liver disease.
On rare occasions, if both the AST and ALT are elevated, patients are subjected to a liver biopsy after a very thorough serologic workup only to find that the liver histology is completely normal. It is very important to exclude a primary muscle disorder in such patients since not only the AST but also the ALT can be elevated in patients with muscle disorders.

Serum Alkaline Phosphatase
The sources of serum alkaline phosphatase include liver, bone, small intestine, placenta, and, on rare occasions, tumors capable of producing alkaline phosphatase.
In general, patients with cholestasis have increased levels. However, the level of serum alkaline phosphatase is not helpful in distinguishing intrahepatic from extrahepatic cholestasis. Rarely, patients with hypernephroma and Hodgkin's disease have elevated levels in the absence of liver involvement. Also, patients with Wilson's disease often have normal values.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Intestinal Obstruction in the Newborn

2009-04-06T02:18:00.000-07:00

Obstruction of an infant's gastrointestinal (GI) tract can occur anywhere from the esophagus to the anus. For purposes of this review, the newborn infant will be defined as an infant from birth to 30 days of age. Both congenital and acquired obstructions will be addressed. In each instance, the epidemiology, pathogenesis, clinical aspects, and management of the disorder will be considered.

Esophageal Atresia

EPIDEMIOLOGY AND PATHOGENESIS
Esophageal atresia, or interruption of the esophagus, generally occurs in association with a tracheoesophageal fistula (EA -- TEF). The most common anatomic arrangement is a blind proximal esophageal pouch that has a distal tracheoesophageal fistula (Figure 1). This is seen in 85% to 90% of infants who have this anomaly. Seen less commonly is pure esophageal atresia that does not have a tracheoesophageal fistula and tracheoesophageal fistula that does not have an esophageal atresia (H-type tracheoesophageal fistula). These latter two conditions occur in approximately 10% of newborns who have these types of anomalies. Other anatomic arrangements, such as an esophageal atresia that has a fistula between the upper pouch and trachea or esophageal atresia that has a fistula to both pouches, are seen in only a tiny fraction of these infants.
EA -- TEF occurs in approximately 1 in 4000 live births. There have been numerous reports of siblings who have EA -- TEF as well as reports of the anomaly in identical twins. Also reported, however, are many instances of identical twins in which one has the anomaly and the other has been spared. It is well recognized that esophageal atresia is a frequent component of the VATER association as well as other malformations, suggesting that the anomaly also might result from a specific teratogen in the developing fetus.
It commonly is believed that interruption of the events responsible for the elongation and separation of the esophageal and tracheal tubes during the fourth week of development leads to the development of this anomaly.

PRESENTATION
Infants who have EA -- TEF commonly will present in the nursery having an excessive amount of saliva. The saliva pools in the blind proximal esophageal pouch and is either regurgitated or continuously dribbled from the infant's mouth. The infant's first feeding will not be tolerated; the formula, which is, of course, not bile-stained, will be regurgitated immediately. Because these infants most commonly have a distal tracheoesophageal fistula, air enters their GI tracts through the fistula, and the abdomen will not be scaphoid. Indeed, the infant who is ventilated may well have air forced into his or her GI tract via the fistula, causing distension. Such an infant's respiratory difficulty, thus, may be compounded by the gastric distention leading to diaphragmatic elevation. In pure esophageal atresia that has no fistula, no air will enter the GI tract, and the infant will have a scaphoid abdomen.

DIAGNOSIS
The diagnosis of esophageal atresia can be made by attempting to pass a firm catheter through the mouth and into the esophagus. Obstruction to passage of the catheter, which should not be "forced," suggests the anomaly, and a chest radiograph usually will confirm the diagnosis via the presence of the coiled catheter sitting within the proximal esophageal pouch. Air injected into the catheter provides an excellent "contrast" agent to help confirm the diagnosis. The use of a true contrast agent generally is not recommended because the infant will be at risk of aspirating the agent and acquiring a chemical pneumonitis. In the rare instance in which contrast is required, 1 mL or less of a water-soluble agent can be injected into the pouch and then withdrawn immediately once the diagnosis has been confirmed. Air in the GI tract confirms the presence of the distal tracheoesophageal fistula.

MANAGEMENT
Appropriate management of these babies begins at the time of diagnosis. A significant risk to the infants is the potential for gastric juice to pass upward in the distal esophagus and traverse the tracheoesophageal fistula where it may be aspirated, resulting in the development of chemical pneumonitis. These infants need to have a sump catheter placed immediately into the upper pouch and into the head up position at an angle of at least 45 degrees. This will help minimize the aspiration of saliva and the chance of gastric juice soiling the lungs.
As a general rule, all newborns whose GI tracts are obstructed should have intravenous fluids instituted and antibiotics begun. If the neonate is not at a surgical center, transport needs to be arranged as soon as possible.
In infants who have EA -- TEF, immediate primary repair generally is undertaken in those weighing as little as 1200 g. An infant presenting with significant pneumonia or other major congenital anomalies will require a more individualized approach; a staged repair via an initial gastrostomy may be performed in an infant who has EA -- TEF and is ill. The infant can be allowed to improve or to be evaluated for other anomalies prior to performing definitive repair.
Infants who have pure esophageal atresia generally are unable to have a primary repair performed in the newborn period because the distance between the two ends of the esophagus is too great. These infants require a gastrostomy and either exteriorization of the esophagus with a later esophageal substitution procedure (reverse gastric tube, colon interposition) or serial attempts at dilatation of the two ends of the esophagus with a later attempt at a primary anastomosis. Although conceptually more attractive, the latter option requires a prolonged initial hospitalization and has an attendant ongoing risk of aspiration.
The prognosis for most babies is excellent; only a few sick infants who have serious coexisting anomalies, are of extreme low birth weight, and have persistent pulmonary disease have a diminished chance for survival. It is not at all uncommon for the infant to develop a relative narrowing or stricturing at the anastomotic site, which does not become evident until the child is advanced to solid foods. Generally, this problem is managed easily with esophageal dilatation. The infants also may have problems with esophageal motility that mimics a stricture. This is determined easily by a contrast swallow radiograph.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Infectious Diseases

2009-04-06T02:11:00.000-07:00

HHV-6 and HHV-7 actually causes infection at a little older age and
more towards the second year of life rather than the first year of life
as we see with HHV-6.
HHV-8 doesn't affect many children. In the past couple of years it has
been described and identified. it is nearly
universally present in all cases of Kaposi's sarcoma tissues. It is also found in AIDS related B- cell
lymphomas that are based in body cavities, and many of those had coinfection with Epstein-Barr virus it isthought that it may actually be necessary to have the HHV-8 for transformation of a
precursor cell that proliferates monoclonally and causes these tumors.
Focusing on HHV-6, a little about the epidemiology and transmission. Roseola was first described in 1913. In 1950, transmissibility
was actually demonstrated although it wasn't until 1986 that the
particular virus was identified. We know that we see these infections year-round and there is worldwide distribution. There is antibody present in 85% of pregnant women with active transport across the placenta. Hence, in the very early weeks, the infants are protected. The antibody declines in the first five months of life to a low of 6%,
then increases to its highest seroprevalence of 86% at one year. So,
by one year of age, most infants have an HHV-6 infection. Titers fall after 40 years of age and there is increased prevalence of IgM six months to one year of age. Saliva is the most likely route of transmission. There is no congenital/perinatal symptom that has been described, and this virus has not been found in breast milk.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Infectious Conjunctivitis

2009-04-05T16:23:00.000-07:00

Infectious conjunctivitis is one of the most common causes of red eye. Infectious conjunctivitis is commonly caused by bacterial or viral infection.
I. Pathophysiology
A. The clinical term "red eye" is applied to a variety of distinct infectious or inflammatory
diseases of the eye. Conjunctivitis is the most common cause of red eye. Conjunctivitis
consists of inflammation of the conjunctiva, which is caused by a broad group of conditions.
The inflammation can be infectious or noninfectious in origin.
B. Most frequently, conjunctivitis is caused by a bacterial or viral infection. Sexually
transmitted diseases such as chlamydial infection and gonorrhea are less common causes
of conjunctivitis. Ocular allergy is a major cause of chronic conjunctivitis.

II. Clinical Evaluation of Conjunctivitis
A. An ocular, medical and medication history should establish whether the condition is acute,
subacute, chronic or recurrent, whether it is unilateral or bilateral.
B. Discharge
1. A serous discharge (watery) is most commonly associated with viral or allergic ocular
conditions.
2. A mucoid (stringy or ropy) discharge is highly characteristic of allergy or dry eyes.
3. A mucopurulent or purulent discharge, often associated with morning crusting and
difficulty opening the eyelids, strongly suggests a bacterial infection. The possibility of
Neisseria gonorrhoeae infection should be considered when the discharge is copiously
purulent.
C. Itching is highly suggestive of allergic conjunctivitis. In general, a red eye in the absence
of itching is not caused by ocular allergy. A history of recurrent itching or a personal or
family history of hay fever, allergic rhinitis, asthma or atopic dermatitis is also consistent
with an ocular allergy.
D. Unilateral or Bilateral Conjunctivitis
1. Allergic conjunctivitis is almost always secondary to environmental allergens and,
therefore, usually presents with bilateral symptoms. Infections caused by viruses and
bacteria are transmissible by eye-hand contact. Often, these infections initially
present in one eye, with the second eye becoming involved a few days later.
2. Pain, Photophobia and Blurred Vision
a. Pain and photophobia do not usually occur with conjunctivitis, and these findings
suggest an ocular or orbital disease processes, including uveitis, keratitis, acute
glaucoma and orbital cellulitis.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

History and Physical Exam

2009-04-05T16:08:00.000-07:00

Medical Documentation
History and Physical Examination

Identifying Data: Patient's name; age, race, sex. List the patient’s significant medical problems. Name of informant (patient, relative).
Chief Compliant: Reason given by patient for seeking medical care and the duration of the symptom. List all of the patients medical problems.
History of Present Illness (HPI): Describe the course of the patient's illness, including when it began, character of the symptoms, location where the symptoms began; aggravating or alleviating factors; pertinent positives and negatives. Describe past illnesses or surgeries, and past diagnostic testing.
Past Medical History (PMH): Past diseases, surgeries, hospitalizations; medical problems; history of diabetes, hypertension, peptic ulcer disease, asthma, myocardial infarction, cancer. In children include birth history, prenatal history, immunizations, and type of feedings.
Medications:
Allergies: Penicillin, codeine?
Family History: Medical problems in family, including the
patient's disorder. Asthma, coronary artery disease,
heart failure, cancer, tuberculosis. Social History: Alcohol, smoking, drug usage. Marital
status, employment situation. Level of education.
Review of Systems (ROS):
General: Weight gain or loss, loss of appetite, fever, chills, fatigue, night sweats. Skin: Rashes, skin discolorations. Head: Headaches, dizziness, masses, seizures. Eyes: Visual changes, eye pain. Ears: Tinnitus, vertigo, hearing loss. Nose: Nose bleeds, discharge, sinus diseases. Mouth and Throat: Dental disease, hoarseness, throat pain.
Respiratory: Cough, shortness of breath, sputum (color).
Cardiovascular: Chest pain, orthopnea, paroxysmal nocturnal dyspnea; dyspnea on exertion, claudication, edema, valvular disease.
Gastrointestinal: Dysphagia, abdominal pain, nausea, vomiting, hematemesis, diarrhea, constipation, melena (black tarry stools), hematochezia (bright red blood per rectum).
Genitourinary: Dysuria, frequency, hesitancy, hematuria, discharge.
Gynecological: Gravida/para, abortions, last menstrual period (frequency, duration), age of menarche, menopause; dysmenorrhea, contraception, vaginal bleeding, breast masses.
Endocrine: Polyuria, polydipsia, skin or hair changes, heat intolerance.
Musculoskeletal: Joint pain or swelling, arthritis, myalgias.
Skin and Lymphatics: Easy bruising, lymphadenopathy.
Neuropsychiatric: Weakness, seizures, memory changes, depression.

Physical Examination
General appearance: Note whether the patient appears
ill, well, or malnourished. Vital Signs: Temperature, heart rate, respirations, blood
pressure. Skin: Rashes, scars, moles, capillary refill (in seconds). Lymph Nodes: Cervical, supraclavicular, axillary, inguinal
nodes; size, tenderness. Head: Bruising, masses. Check fontanels in pediatric
patients. Eyes: Pupils equal round and react to light and accommodation (PERRLA); extra ocular movements intact (EOMI), and visual fields. Funduscopy (papilledema, arteriovenous nicking, hemorrhages, exudates); scleral icterus, ptosis.
Ears: Acuity, tympanic membranes (dull, shiny, intact, injected, bulging).
Mouth and Throat: Mucus membrane color and moisture; oral lesions, dentition, pharynx, tonsils.
Neck: Jugulovenous distention (JVD) at a 45 degree incline, thyromegaly, lymphadenopathy, masses, bruits, abdominojugular reflux.
Chest: Equal expansion, tactile fremitus, percussion, auscultation, rhonchi, crackles, rubs, breath sounds, egophony, whispered pectoriloquy.
Heart: Point of maximal impulse (PMI), thrills (palpable turbulence); regular rate and rhythm (RRR), first and second heart sounds (S1, S2); gallops (S3, S4), murmurs (grade 1-6), pulses (graded 0-2+).
Breast: Dimpling, tenderness, masses, nipple discharge; axillary masses.
Abdomen: Contour (flat, scaphoid, obese, distended); scars, bowel sounds, bruits, tenderness, masses, liver span by percussion; hepatomegaly, splenomegaly; guarding, rebound, percussion note (tympanic), costovertebral angle tenderness (CVAT), suprapubic tenderness.
Genitourinary: Inguinal masses, hernias, scrotum, testicles, varicoceles.
Pelvic Examination: Vaginal mucosa, cervical discharge, uterine size, masses, adnexal masses, ovaries.
Extremities: Joint swelling, range of motion, edema (grade 1-4+); cyanosis, clubbing, edema (CCE); pulses (radial, ulnar, femoral, popliteal, posterior tibial, dorsalis pedis; simultaneous palpation of radial and femoral pulses).
Rectal Examination: Sphincter tone, masses, fissures; test for occult blood, prostate (nodules, tenderness, size).
Neurological: Mental status and affect; gait, strength (graded 0-5); touch sensation, pressure, pain, position and vibration; deep tendon reflexes (biceps, triceps, patellar, ankle; graded 0-4+); Romberg test (ability to stand erect with arms outstretched and eyes closed).
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Herpes Simplex Infections

2009-04-05T16:04:00.001-07:00

HSV Infections
Asymptomatic, mucocutaneous, neonatal, CNS, latent
Type 1: gingivostomatitis, whitlow, keratoconjunctivitis, encephalitis, eczema
herpeticum
Type 2: genital HSV, meningitis
Classification: primary; non primary, first episode; recurrent, reinfection Latency: sensory or autonomic neurons; LATS Reactivations: trauma, sunlight, stress (despite antibodies) Host: normal vs. immunocompromised

Neonatal HSV Infections
Congenital 5%; most HSV 2 (poorer prognosis)
Most mothers asymptomatic; antibodies may modify
Attack rate after primary maternal infection over 50% (> 10 times
than after recurrent infection) Cesarean section controversial in women with recurrent HSV at delivery Culture baby (eye, skin, throat) after 24 hours old Categories, prognosis: skin/eye/mouth, CNS, disseminated Symptoms: skin vesicles, fever, intractable seizures, pneumonia, DIC, conjunctivitis, recurrent skin vesicles after therapy
.... CLICK HERE TO DOWNLOAD FULL ARTICLE

Head Injury

2009-04-05T15:45:00.000-07:00

Trauma is the most common cause of death in young people, and head injury accounts for almost half of these trauma-related deaths. The prognosis following head injury depends upon the site and severity of brain damage. Some guide to prognosis is provided by the mental status, since loss of consciousness for more than 1 or 2 minutes implies a worse prognosis than otherwise. Similarly, the degree of retrograde and posttraumatic amnesia provides an indication of the severity of injury and thus of the prognosis. Absence of skull fracture does not exclude the possibility of severe head injury. During the physical examination, special attention should be given to the level of consciousness and extent of any brain stem dysfunction. Note: Patients who have lost consciousness for 2 minutes or more following head injury should be admitted to the hospital for observation, as should patients with focal neurologic deficits, lethargy, or skull fractures. If admission is declined, responsible family members should be given clear instructions about the need for, and manner of, checking on them at regular (hourly) intervals and for obtaining additional medical help if necessary.
Skull radiographs or CT scans may provide evidence of fractures. Because injury to the spine may have accompanied head trauma, cervical spine radiographs (especially in the lateral projection) should always be obtained in comatose patients and in patients with severe neck pain or a deficit possibly related to cord compression. CT scanning has an important role in demonstrating intracranial hemorrhage and may also provide evidence of cerebral edema and displacement of midline structures.
Cerebral Injuries
These are summarized in Table 24–5 along with comments about treatment. Increased intracranial pressure may result from ventilatory obstruction, abnormal neck position, seizures, dilutional hyponatremia, or cerebral edema; an intracranial hematoma requiring surgical evacuation may also be responsible. Other measures that may be necessary to reduce intracranial pressure include induced hyperventilation, intravenous mannitol infusion, and intravenous furosemide; corticosteroids provide no benefit in this context.
Table 24–5. Acute cerebral sequelae of head injury.

Scalp Injuries and Skull Fractures
Scalp lacerations and depressed or compound depressed skull fractures should be treated surgically as appropriate. Simple skull fractures require no specific treatment. The clinical signs of basilar skull fracture include bruising about the orbit (raccoon sign), blood in the external auditory meatus (Battle's sign), and leakage of cerebrospinal fluid (which can be identified by its glucose content) from the ear or nose. Cranial nerve palsies (involving especially the first, second, third, fourth, fifth, seventh, and eighth nerves in any combination) may also occur. If there is any leakage of cerebrospinal fluid, conservative treatment, with elevation of the head, restriction of fluids, and administration of acetazolamide (250 mg four times daily), is often helpful; but if the leak continues for more than a few days, lumbar subarachnoid drainage may be necessary. Antibiotics are given if infection occurs, based on culture and sensitivity studies. Only very occasional patients require intracranial repair of the dural defect because of persistence of the leak or recurrent meningitis.

Late Complications of Head Injury
The relationship of chronic subdural hemorrhage to head injury is not always clear. In many elderly persons there is no history of trauma, but in other cases a head injury, often trivial, precedes the onset of symptoms by several weeks. The clinical presentation is usually with mental changes such as slowness, drowsiness, headache, confusion, memory disturbances, personality change, or even dementia. Focal neurologic deficits such as hemiparesis or hemisensory disturbance may also occur but are less common. CT scan is an important means of detecting the hematoma, which is sometimes bilateral. Treatment is by surgical evacuation to prevent cerebral compression and tentorial herniation.
Normal-pressure hydrocephalus may follow head injury, subarachnoid hemorrhage, or meningoencephalitis.
Other late complications of head injury include posttraumatic seizure disorder and posttraumatic headache.
10240:31:1 Alexander MP: Mild traumatic brain injury: Pathophysiology, natural history, and clinical management. Neurology 1995;45:1253. 10240:31:2 Miller JD: Head injury. J Neurol Neurosurg Psychiatry 1993;56:440. (Pathophysiology, evaluation, management, and monitoring of head injury.)

Handbook of Skin Diseases

2009-04-05T15:25:00.000-07:00

Rosacea

Rosacea is a congestive blushing and
flushing reaction of the central areas of
the face. It is usually associated with an
acneiform component (papules,
pustules, and oily skin). It usually
occurs in middle-aged and older people.
The cheeks, nose, and chin, on the
entire face, may have a rosy hue.
Burning or stinging often accompanies
episodes of flushing. It is much more
common than lupus erythematosus, with which it is often confused. Rosacea
is distinguished from acne by age, the presence of the vascular component, and
the absence of comedones.

Folliculitis

Folliculitis is characterized by red-ringed papules and pustules at hair follicles. Gram-negative folliculitis may be spread by contaminated hot tubs. Gram stain and culture will help to differentiate bacterial from non-bacterial folliculitis. History is important for pinpointing the cause of non-bacterial folliculitis.

Impetigo

Superficial honey-colored serous crusts are characteristic of this disorder. It is usually caused by a staphylococcus infection. Culture is rarely reliable.

.... CLICK HERE TO DOWNLOAD FULL ARTICLE

Gynecology and Obstetrics

2009-04-05T15:19:00.000-07:00

Surgical Documentation for Gynecology

Gynecologic Surgical History
Identifying Data. Age, gravida (number of pregnancies), para (number of deliveries).
Chief Compliant. Reason given by patient for seeking surgical care.
History of Present Illness (HPI). Describe the course of the patient's illness, including when it began, character of the symptoms; pain onset (gradual or rapid), character of pain (constant, intermittent, cramping, radiating); other factors associated with pain (urination, eating, strenuous activities); aggravating or relieving factors. Other related diseases; past diagnostic testing. Obstetrical History. Past pregnancies, durations and outcomes, preterm deliveries, operative deliveries. Gynecologic History: Last menstrual period, length of regular cycle.
Past Medical History (PMH). Past medical problems, previous surgeries, hospitalizations, diabetes, hypertension, asthma, heart disease.
Medications. Cardiac medications, oral contraceptives, estrogen.
Allergies. Penicillin, codeine. Family History. Medical problems in relatives. Social History. Alcohol, smoking, drug usage, occupation. Review of Systems (ROS):
General: Fever, fatigue, night sweats.
HEENT: Headaches, masses, dizziness.
Respiratory: Cough, sputum, dyspnea.
Cardiovascular: Chest pain, extremity edema.
Gastrointestinal: Vomiting, abdominal pain, melena
(black tarry stools), hematochezia (bright red blood per
rectum).
Genitourinary: Dysuria, hematuria, discharge.
Skin: Easy bruising, bleeding tendencies.
Gynecologic Physical Examination
General:
Vital Signs: Temperature, respirations, heart rate, blood pressure.
Eyes: Pupils equally round and react to light and accommodation (PERRLA); extraocular movements intact (EOMI). Neck: Jugular venous distention (JVD), thyromegaly,
masses, lymphadenopathy. Chest: Equal expansion, rales, breath sounds. Heart: Regular rate and rhythm (RRR), first and second heart sounds, murmurs.
Breast: Skin retractions, masses (mobile, fixed), erythema, axillary or supraclavicular node enlargement. Abdomen: Scars, bowel sounds, masses, hepatosplenomegaly, guarding, rebound, costovertebral angle tenderness, hernias. Genitourinary: Urethral discharge, uterus, adnexa, ovaries, cervix. Extremities: Cyanosis, clubbing, edema. Neurological: Mental status, strength, tendon reflexes,
sensory testing. Laboratory Evaluation: Electrolytes, glucose, liver function tests, INR/PTT, CBC with differential; X-rays, ECG (if >35 yrs or cardiovascular disease), urinalysis. Assessment and Plan: Assign a number to each problem. Discuss each problem, and describe surgical plans for each numbered problem, including preoperative testing,
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Genetics and Fetal Development

2009-04-05T15:16:00.000-07:00

There are three sources of chromosome abnormalities that occur during the course of pregnancy. Primarily during the formation of oocytes and spermatozoa during gametogenesis, during the course of fertilization with the fusion of the oocyte and the sperm and in the postzygotic period. The consequences of any kind of chromosome abnormality usually is on a preimplantation death, implantation failure, spontaneous abortion, stillbirth or an infant born with birth defects.
15% of the population identified in a clinically identified pregnancy spontaneously aborts of which 60-70% are due to chromosome abnormalities. We have now begun to define the incidence of chromosome abnormalities prior to the third week of gestation and have found surprisingly that a significant number of pregnancies are lost following implantation. It is estimated that as many as 70% of all conceptions that are identified through in vitro fertilization programs, for example, may be carrying a chromosome abnormality. The significance of that is such that one of my colleagues remarked that "it is a miracle that any one of us is in this room." Following the 12th week of pregnancy, in the second and third periods of gestation, the incidence of stillbirths may be 5-10% and again chromosome abnormalities play a significant role in each of these stages.
There are three classes of chromosome abnormalities that we will briefly discuss with you. Aneuploidy which is defined as a gain or loss of single whole chromosomes. Polyploidy in which you have an additional set or sets of chromosomes. In the human, the chromosome complement consists of 23 different kinds of chromosomes so we have speak of triploidy with 69 chromosomes and tetraploidy with 92 chromosomes. Then there are instances where chromosomal rearrangements occur. The chromosomes physically break and heal or restitute in new forms or arrangements.
This is a normal karyotype in which to emphasize to you that indeed there are 46 chromosomes, 22 pairs of non-sex chromosomes or autosomes and an X and a Y constituting a male. It is possible for us using various kinds of stains to identify not only individual chromosomes from one another, but gains and losses of specific segments of chromosomes as well. Then you are looking at what constitutes G-banding in which they use trypsin and a Giemsa staining.
In the case of aneuploidy, and the next set of slides will briefly illustrate each of the classes of chromosome aberrations, there are three chromosomes and the total count is now 47 instead of the normal number of 46. This is the characteristic karyotype associated with trisomy 21 in which there is in all of the cells presumably an extra chromosome 21.
Triploidy. Each chromosome is represented 3 times throughout the entire complement and so the total chromosome number is 69 and this is an example of polyploidy. Another example of polyploidy is shown in this lower segment in which the total chromosome count is 92, an example of tetraploidy. Each chromosome has its own particular pair. Tetraploidy characteristically arises after the first postzygotic cleavage in which the chromosomes divide but the cytoplasm does not, so the chromosome number immediately goes from 46 to 92. The cell fails to divide, to form two daughter cells. You still have only one parental cell remaining but now the chromosome number has been immediately doubled. Invariably, this will lead to a missed abortion early in the first trimester although again, for all of the statements we make, there are exceptions. There have been a few, a small number of examples of diploid, tetraploid mosaic infants born with birth defects presumably associated with the fact that a portion of their cells now have a doubling of their chromosome number.
Breakage of the chromosome at two particular sites on either of the two arms and the broken ends of the long part healing and forming this ring. It also means, of course, that pieces or segments of genetic material have been lost in the formation of this ring chromosome thereby leading to chromosome and genetic imbalance and will be associated with either spontaneous abortions, stillbirth or an infant born with a genetic abnormality.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

General Pediatrics 2

2009-04-05T15:07:00.000-07:00

In children there is a physiologic anemia. Often it occurs - it peaks between 2 and 3 months of age. Most children will get down to a range of around 11 in about 3 months. Some people advocate screening between 9 and 12 months. It’s a peak age for iron deficiency if they have switched off iron formulas. Some people advocate 24 months. Another point is that if you do a peripheral hematocrit it could be lower than central so that if they are anemic, you should probably do a central test. Just a picture of a tiny child that can show up. Pale mucous membrane, pale skin. You see what are called red lines, concentrated dense lines at the growth centers.
Lead Poisoning. In the 1980’s the average lead level was about 12. In 1991 the average lead level in our population was 3. Leaded paint has been eliminated for the most part in this country, but even today some paint is still leaded. Leaded gasoline, industrial lead, and car batteries and then all this miscellaneous. Sometime lead-containing ceramic vessels. The point is that young children are particularly at risk for lead poisoning because of their hand-to-mouth exposure. And also through the respiratory tract. In the past we used to use the erythrocyte protoporphyrin test as a screen. It’s no longer recommended. It was only useful when sort of there were a lot of levels above 30. Venous lead level is the test to use. You do a finger first and then you do a venipuncture if it’s elevated. And the big news is, as most of you know this, is that we have
lowered our level of what’s acceptable. Any child that’s screened that has a level of 10, an environmental assessment needs to be done.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Family Medicine

2009-04-05T14:57:00.000-07:00

INTERNAL MEDICINE
Medical Documentation

History and Physical Examination
Identifying Data: Patient's name; age, race, sex. List the patient’s significant medical problems. Name of informant (patient, relative).
Chief Compliant: Reason given by patient for seeking medical care and the duration of the symptom. List all of the patients medical problems.
History of Present Illness (HPI): Describe the course of the patient's illness, including when it began, character of the symptoms, location where the symptoms began; aggravating or alleviating factors; pertinent positives and negatives. Describe past illnesses or surgeries, and past diagnostic testing.
Past Medical History (PMH): Past diseases, surgeries, hospitalizations; medical problems; history of diabetes, hypertension, peptic ulcer disease, asthma, myocardial infarction, cancer. In children include birth history, prenatal history, immunizations, and type of feedings.
Medications:
Allergies: Penicillin, codeine?
Family History: Medical problems in family, including the
patient's disorder. Asthma, coronary artery disease,
heart failure, cancer, tuberculosis. Social History: Alcohol, smoking, drug usage. Marital
status, employment situation. Level of education.
Review of Systems (ROS):
General: Weight gain or loss, loss of appetite, fever, chills, fatigue, night sweats. Skin: Rashes, skin discolorations. Head: Headaches, dizziness, masses, seizures. Eyes: Visual changes, eye pain. Ears: Tinnitus, vertigo, hearing loss. Nose: Nose bleeds, discharge, sinus diseases. Mouth and Throat: Dental disease, hoarseness, throat pain.
Respiratory: Cough, shortness of breath, sputum (color).
Cardiovascular: Chest pain, orthopnea, paroxysmal nocturnal dyspnea; dyspnea on exertion, claudication, edema, valvular disease.
Gastrointestinal: Dysphagia, abdominal pain, nausea, vomiting, hematemesis, diarrhea, constipation, melena (black tarry stools), hematochezia (bright red blood per rectum).
Genitourinary: Dysuria, frequency, hesitancy, hematuria, discharge.
Gynecological: Gravida/para, abortions, last menstrual period (frequency, duration), age of menarche, menopause; dysmenorrhea, contraception, vaginal bleeding, breast masses.
Endocrine: Polyuria, polydipsia, skin or hair changes, heat intolerance.
Musculoskeletal: Joint pain or swelling, arthritis, myalgias.
Skin and Lymphatics: Easy bruising, lymphadenopathy.
Neuropsychiatric: Weakness, seizures, memory changes, depression.
Physical Examination
General appearance: Note whether the patient appears ill, well, or malnourished.
Vital Signs: Temperature, heart rate, respirations, blood pressure.
Skin: Rashes, scars, moles, capillary refill (in seconds).
Lymph Nodes: Cervical, supraclavicular, axillary, inguinal nodes; size, tenderness.
Head: Bruising, masses. Check fontanels in pediatric patients.
Eyes: Pupils equal round and react to light and accommodation (PERRLA); extra ocular movements intact (EOMI), and visual fields. Funduscopy (papilledema, arteriovenous nicking, hemorrhages, exudates); scleral icterus, ptosis.
Ears: Acuity, tympanic membranes (dull, shiny, intact, injected, bulging).
Mouth and Throat: Mucus membrane color and moisture; oral lesions, dentition, pharynx, tonsils.
Neck: Jugulovenous distention (JVD) at a 45 degree incline, thyromegaly, lymphadenopathy, masses, bruits, abdominojugular reflux.
Chest: Equal expansion, tactile fremitus, percussion, auscultation, rhonchi, crackles, rubs, breath sounds, egophony, whispered pectoriloquy.
Heart: Point of maximal impulse (PMI), thrills (palpable turbulence); regular rate and rhythm (RRR), first and second heart sounds (S1, S2); gallops (S3, S4), murmurs (grade 1-6), pulses (graded 0-2+).
Breast: Dimpling, tenderness, masses, nipple discharge; axillary masses.
Abdomen: Contour (flat, scaphoid, obese, distended); scars, bowel sounds, bruits, tenderness, masses, liver span by percussion; hepatomegaly, splenomegaly; guarding, rebound, percussion note (tympanic), costovertebral angle tenderness (CVAT), suprapubic tenderness.
Genitourinary: Inguinal masses, hernias, scrotum, testicles, varicoceles.
Pelvic Examination: Vaginal mucosa, cervical discharge, uterine size, masses, adnexal masses, ovaries.
...... CLICK HERE TO DOWNLOAD FULL ARTICLE

Emergency Care - Injuries - Poisonings

2009-04-05T01:07:00.000-07:00

Cervical spine injuries are uncommon in children. They are really not that uncommon in children, but because injuries to the C-spine in childhood are usually to the upper C-spine, they are frequently fatal. So if we were to look at trauma related fatalities
in young children, we would find quite a number of upper C- to see a child come in with a C-spine injury without a terribly morbid series of other injuries. The typical frontal impact in an automobile accident, where the head comes forward, that fulcrum being higher in the C-spine causes the injuries to be C1,C2 or C3 in a vast majority of children less than eight years of age. Once they are over eight, that fulcrum is down around C6. And after eight years of age, you'll see more of an adult pattern of C-spine injuries in children.
Every child who has had a bump on the head does not need C-
spine x-rays. We frequently will "clear" a C-spine clinically. However, if there is any question, we'll leave the collar in place and we will do radiographs. First of all, the child needs a normal level of consciousness. And people ask, "At what age does a child really have a normal level of consciousness?" A cooperative
four or five-year-old who can tell us that the
neck doesn't
hurt is in many cases a child whose neck can be cleared clinically. But again, the younger they are and the less cooperative, the less likely we are to trust the clinical approach for clearing
the C-spine after
a significant head injury. Of course, we want a
normal neurological examination. No neck pain and no neck tenderness. Any serious injury, any femur fracture or another very painful injury, can cause endogenous endorphin release and can cause a child to really be distracted from the neck injury. And so when a child says there is no neck pain when there is another very serious painful injury, we don't trust that the absence of reporting really means that the neck is not injured.
And then once we have gone through
these various parameters
we'll ask a child to fully move the neck voluntarily. If we've met
all of these criteria,
then we'll take the C-spine collar off
The presence of a collar when a child arrives to the Emergency Department does not obligate one to obtain C-spine films. Conversely, the fact that a child arrived in the Emergency Department without a collar doesn't mean it is inappropriate for
you to put one on if you think
is indicated. So we are not
required to continue what are perhaps the mistakes of others. I
would use your own independent judgement to determine whether
or not a collar should be placed or perhaps can be removed without radiographs.
....CLICK HERE TO DOWNLOAD FULL ARTICLE

Critical Care Medicine

2009-04-05T00:48:00.000-07:00

Critical and Cardiac Care Patient Management
T. Scott Gallacher, MD, MS
Critical Care History and Physical Examination
Chief complaint: Reason for admission to the ICU.
History of present illness: This section should included pertinent chronological events leading up to the hospitalization. It should include events during hospitalization and eventual admission to the ICU.
Prior cardiac history: Angina (stable, unstable, changes in frequency), exacerbating factors (exertional, rest angina). History of myocardial infarction, heart failure, coronary artery bypass graft surgery, angioplasty. Previous exercise treadmill testing, ECHO, ejection fraction. Request old ECG, ECHO, impedance cardiography, stress test results, and angiographic studies.
Chest pain characteristics:
A.Pain: Quality of pain, pressure, squeezing, tightness
B.Onset of pain: Exertional, awakening from sleep,
relationship to activities of daily living (ADLs), such as
eating, walking, bathing, and grooming.
C.Severity and quality: Pressure, tightness, sharp,
pleuritic
D.Radiation: Arm, jaw, shoulder
E.Associated symptoms: Diaphoresis, dyspnea, back
pain, GI symptoms.
F.Duration: Minutes, hours, days.
G.Relieving factors: Nitroclycerine, rest.
Cardiac risk factors: Age, male, diabetes, hypercholesteremia, low HDL, hypertension, smoking, previous coronary artery disease, family history of arteriosclerosis (eg, myocardial infarction in males less than 50 years old, stroke).
Congestive heart failure symptoms: Orthopnea (number of pillows), paroxysmal nocturnal dyspnea, dyspnea on exertional, edema.
Peripheral vascular disease symptoms: Claudication, transient ischemic attack, cerebral vascular accident.
COPD exacerbation symptoms: Shortness of breath, fever, chills, wheezing, sputum production, hemoptysis (quantify), corticosteroid use, previous intubation.
Past medical history: Peptic ulcer disease, renal disease, diabetes, COPD. Functional status prior to hospitalization.
Medications: Dose and frequency. Use of nitroglycerine, beta-agonist, steroids.
Allergies: Penicillin, contrast dye, aspirin; describe the specific reaction (eg, anaphylaxis, wheezing, rash, hypotension).
Social history: Tobacco use, alcohol consumption, intravenous drug use.
Review of systems: Review symptoms related to each
organ system.
Critical Care Physical Examination
Vital signs:
Temperature, pulse, respiratory rate, BP (vital signs
should be given in ranges)
Input/Output: IV fluid volume/urine output.
Special parameters: Oxygen saturation, pulmonary
artery wedge pressure (PAWP), systemic vascular
resistance (SVR), ventilator settings, impedance
cardiography. General: Mental status, Glasgow coma score, degree of distress.
HEENT: PERRLA, EOMI, carotid pulse. Lungs: Inspection, percussion, auscultation for wheezes, crackles.
Cardiac: Lateral displacement of point of maximal impulse; irregular rate,, irregular rhythm (atrial fibrillation); S3 gallop (LV dilation), S4 (myocardial infarction), holosystolic apex murmur (mitral regurgitation). Cardiac murmurs: 1/6 = faint; 2/6 = clear; 3/6 - loud; 4/6 = palpable; 5/6 = heard with stethoscope off the chest; 6/6 = heard without stethoscope.
Abdomen: Bowel sounds normoactive, abdomen soft and nontender.
Extremities: Cyanosis, clubbing, edema, peripheral pulses 2+.
Skin: Capillary refill, skin turgor. Neuro
Deficits in strength, sensation.
Deep tendon reflexes: 0 = absent; 1 = diminished; 2 =
normal; 3 = brisk; 4 = hyperactive clonus. Motor Strength: 0 = no contractility; 1 = contractility but no joint motion; 2 = motion without gravity; 3 = motion against gravity; 4 = motion against some resistance; 5 = motion against full resistance (normal). Labs: CBC, INR/PTT; chem 7, chem 12, Mg, pH/pCO2/pO2. CXR, ECG, impedance cardiography, other diagnostic studies.
Impression/Problem list: Discuss diagnosis and plan for each problem by system.
Neurologic Problems: List and discuss neurologic problems
Pulmonary Problems: Ventilator management. Cardiac Problems: Arrhythmia, chest pain, angina. GI Problems: H2 blockers, nasogastric tubes, nutrition. Genitourinary Problems: Fluid status: IV fluids, electrolyte therapy.
Renal Problems: Check BUN, creatinine. Monitor fluids and electrolytes. Monitor inputs and outputs. Hematologic Problems: Blood or blood products, DVT prophylaxis, check hematocrit/hemoglobin. Infectious Disease: Plans for antibiotic therapy; antibiotic day number, culture results.
Endocrine/Nutrition: Serum glucose control, parenteral or enteral nutrition, diet.
Admission Check List
1. Call and request old chart, ECG, and x-rays.
2. Stat labs: CBC, chem 7, cardiac enzymes (myoglobin, troponin, CPK), INR, PTT, C&S, ABG, UA, cardiac enzymes (myoglobin, troponin, CPK).
3. Labs: Toxicology screens and drug levels.
4. Cultures: Blood culture x 2, urine and sputum culture (before initiating antibiotics), sputum Gram stain, urinalysis............
5. CXR, ECG, diagnostic studies.
6. Discuss case with resident, attending, and family.
Critical Care Progress Note
ICU Day Number:
Antibiotic Day Number:
Subjective: Patient is awake and alert. Note any events
that occurred overnight.
Objective: Temperature, maximum temperature, pulse,
respiratory rate, BP, 24- hr input and output, pulmonary
artery pressure, pulmonary capillary wedge pressure,
cardiac output.
Lungs: Clear bilaterally
Cardiac: Regular rate and rhythm, no murmur, no rubs.
Abdomen: Bowel sounds normoactive, soft-nontender.
Neuro: No local deficits in strength, sensation.
Extremities: No cyanosis, clubbing, edema, peripheral
pulses 2+.
Labs: CBC, ABG, chem 7.
ECG: Chest x-ray:
Impression and Plan: Give an overall impression, and
then discuss impression and plan by organ system:
Cardiovascular:
Pulmonary:
Neurological:
Gastrointestinal:
Renal:
Infectious:
Endocrine:
Nutrition:
Procedure Note
A procedure note should be written in the chart when a procedure is performed. Procedure notes are brief operative notes.
Procedure Note
Date and time:
Procedure:
Indications:
Patient Consent: Document that the indications,
risks and alternatives to the procedure were ex
plained to the patient. Note that the patient was
given the opportunity to ask questions and that the
patient consented to the procedure in writing.
Lab tests: Relevant labs, such as the INR and CBC
Anesthesia: Local with 2% lidocaine
Description of Procedure: Briefly describe the
procedure, including sterile prep, anesthesia
method, patient position, devices used, anatomic
location of procedure, and outcome.
Complications and Estimated Blood Loss (EBL): Disposition: Describe how the patient tolerated the
procedure. Specimens: Describe any specimens obtained and labs tests which were ordered. Name of Physician: Name of person performing procedure and supervising staff.
Discharge Note
The discharge note should be written in the patient’s chart prior to discharge.
Discharge Note
Date/time:
Diagnoses:
Treatment: Briefly describe treatment provided
during hospitalization, including surgical procedures
and antibiotic therapy.
Studies Performed: Electrocardiograms, CT scans,
CXR.
Discharge Medications: Follow-up Arrangements:
Fluids and Electrolytes
Maintenance Fluids Guidelines:
70 kg Adult: D5 1/4 NS with KCI 20 mEq/Liter at 125 mL/hr.
Specific Replacement Fluids for Specific Losses: Gastric (nasogastric tube, emesis): D5 1/2 NS with KCL 20 mEq/L.
Diarrhea: D5LR with KCI 15 mEq/liter. Provide 1 liter of replacement for each 1 kg or 2.2 lb of body weight lost.
Bile: D5LR with sodium bicarbonate 25 mEq/liter (1/2 amp).
Pancreatic: D5LR with sodium bicarbonate 50 mEq/liter (1 amp).
.... CLICK HERE TO DOWNLOAD FULL ARTICLE

Child Maltreatment and Abusebuse

2009-04-05T00:41:00.000-07:00

Child abuse or neglect, or the newer term “child maltreatment,” encompasses abusive as well as neglect issues.
Child maltreatment is legally defined as the physical or mental injury, sexual abuse or exploitation, negligent treatment or maltreatment of a child under the age of 18, by a person responsible for the child's welfare and under circumstances which indicate that child's health or welfare is harmed or threatened thereby. Child maltreatment is divided into physical abuse, sexual abuse, neglect, which is a big category, and then emotional abuse.
Every year there are about 2,000 fatalities from child abuse. There are about 20,000 children who are killed or permanently disabled from child abuse. There are another 141,000 who are seriously injured, many of whom have to be hospitalized. Overall, there are roughly 1 million substantiated instances. It involves about 2.9 million reports on 1.9 million children with about 1 million cases are substantiated as maltreatment. 1.9 million children are reported as victims with 1.6 million investigations.
..... CLICK HERE TO DOWNLOAD FULL ARTICLE

Chemotherapy

2009-04-05T00:34:00.000-07:00

Cancer Chemotherapy
Cytotoxic drugs, hormones, antihormones, and biologic agents have become increasingly effective means of treating cancer. Many patients are treated on protocols to provide optimal therapy for refractory or poorly responsive malignancies. Treatment may be inadequate or ineffective because of drug resistance of the tumor cells. This has been attributed to spontaneous genetic mutations in subpopulations of cancer cells prior to exposure to chemotherapy. After chemotherapy has eliminated the sensitive cells, the resistant subpopulation grows to become the predominant cell type (Goldie-Coldman hypothesis). This has been the basis of alternating non-cross-resistant chemotherapy regimens.
Molecular mechanisms of drug resistance are now the subject of intense study. In many instances, specific drug resistance results from an amplification in the number of gene copies for an enzyme inhibited by a specific chemotherapeutic agent. A more general form of "multidrug resistance" (MDR) has been described in association with expression of a gene (MDR1) encoding a transmembrane glycoprotein of MW 170 (P-glycoprotein) on tumor cells. This protein is an energy-dependent transport pump that facilitates drug efflux from tumor cells and promotes resistance to a broad spectrum of unrelated cancer drugs. Acquired multidrug resistance in multiple myeloma and lymphoma has been reversed clinically by adding the calcium channel blocker verapamil to chemotherapy regimens. Unfortunately, the doses of verapamil required to overcome drug resistance are associated with cardiovascular side effects. High doses of cyclosporine appear to increase the cytotoxicity of etoposide both in vitro and in vivo, probably by inhibiting the function of P-glycoprotein. The use of cyclosporine to enhance the effect of etoposide in purging resistant tumor cells in vitro from autologous bone marrow is under investigation. Cyclosporine has also been shown to enhance the cytotoxic effect of multiagent chemotherapy against resistant multiple myeloma. Verapamil and cyclosporine increase the accumulation and cytotoxicity of daunorubicin in myeloid leukemia cells, enhancing cell kill. MDR modulators will need to be both less toxic and more potent to be clinically useful. An example is the cyclosporine analog PSC 833, with little of the immunosuppressive effects or renal toxicities of cyclosporine but with five- to tenfold greater MDR-modulating activity.
Chemotherapy is used to cure a small percentage of malignancies, as adjuvant therapy to decrease the rate of relapse or improve the disease-free interval, and to palliate symptoms in some patients with incurable malignancies. In addition, chemotherapy may play a role as preoperative or "neoadjuvant" therapy to reduce the size and extent of the primary tumor, thereby allowing complete excision at the time of surgery. Chemotherapy was first shown to be curative in the treatment of advanced stages of choriocarcinoma in women. It is also curative in Hodgkin's disease, diffuse large-cell and some high-grade lymphomas (including Burkitt's), carcinoma of the testis, some cases of acute leukemia, and embryonal rhabdomyosarcoma. When combined with initial surgery—and in some instances with irradiation—chemotherapy increases the cure rate in Wilms' tumor and increases the rate of long-term control and cure of breast cancer, colon cancer, rectal cancer, and osteogenic sarcomas. Combination chemotherapy provides palliation and prolongation of survival in adults with Hodgkin's disease, non-Hodgkin's lymphoma, mycosis fungoides, multiple myeloma and macroglobulinemia, acute and chronic leukemias, and breast, ovary, and small-cell lung carcinoma as well as carcinoid. Patients with incurable tumors who desire aggressive treatment should be referred for experimental protocol therapy. Tumor cell vaccines combined with immune adjuncts are under investigation as specific immunotherapy for chemotherapy-resistant tumors such as malignant melanoma.
High-dose chemotherapy followed by bone marrow transplantation is curative therapy for various types of leukemia, multiple myeloma, and high-risk lymphoma and testicular cancer. Allogeneic or autologous bone marrow or peripheral blood stem cells with or without ex vivo purging is used depending on the disease. The use of growth factors and blood stem cells has decreased the toxicity and cost of bone marrow transplantation. Autologous transplantation may now be used with low morbidity and mortality on selected patients up to age 70. In addition, dose-intense chemotherapy regimens with autologous bone marrow or peripheral blood progenitor cell rescue are currently being investigated in the high-risk adjuvant or early relapse setting for patients with carcinoma of the breast and ovaries. A small study suggests that intensive doses of chemotherapy followed by bone marrow or peripheral blood stem cell infusion in incurable diseases such as metastatic breast cancer may prolong survival. It is possible that this aggressive approach may be useful even when "cure" is not the objective.
While most anticancer drugs are used systemically, there are selected indications for local or regional administration. Regional administration involves direct infusion of active chemotherapeutic agents into the tumor site (eg, intravesical therapy, intraperitoneal therapy, hepatic artery infusion with or without embolization of the main blood supply of the tumor). These treatments can result in palliation and prolonged survival.
A summary of the types of cancer responsive to chemotherapy and the current treatments of choice is offered in Table 4–3. In some instances (eg, Hodgkin's disease), optimal therapy may require a combination of therapeutic resources, eg, radiation plus chemotherapy rather than either modality alone. Patients with stages I, II, and IIIA Hodgkin's disease are often treated with radiation alone, avoiding the potential toxicity of systemic chemotherapy. A small percentage of these patients may require chemotherapy later for disease recurrence.
... CLICK HERE TO DOWNLOAD FULL ARTICLE

Cerebral Palsy

2009-04-05T00:31:00.000-07:00

Cerebral palsy (CP) is defined as a nonprogressive disorder of posture and movement, often associated with epilepsy and abnormalities of speech, vision, and intellect resulting from a defect or lesion of the developing brain. CP is a common disorder, with an estimated prevalence of 2/1,000 population.

EPIDEMIOLOGY AND ETIOLOGY. The reported the prevalence rate of CP is 4/1,000 live births. Birth asphyxia was an uncommon cause of CP; moreover, most high-risk pregnancies resulted in neurologically normal children. Although a cause for CP could not be identified in most cases, a substantial number of children with CP had congenital anomalies external to the central nervous system (CNS), which may have placed them at increased risk for developing asphyxia during the perinatal period. An Australian study comparing children with spastic CP with a group of matched controls had similar findings. Less than 10% of children with CP had evidence of intrapartum asphyxia. Although the increased survival of premature infants from improved perinatal care has resulted in more children with CP, the rate did not increase. These studies suggest that future developments aimed at enhancing perinatal care will have minimal impact on the incidence of CP and that research might be directed more profitably to the field of developmental biology in order to understand the pathogenesis of CP.

CLINICAL MANIFESTATIONS. CP may be classified by a description of the motor handicap in terms of physiologic, topographic, and etiologic categories and functional capacity. The physiologic classification identifies the major motor abnormality, whereas the topographic taxonomy indicates the involved extremities. CP is also commonly associated with a spectrum of developmental disabilities, including mental retardation, epilepsy, and visual, hearing, speech, cognitive, and behavioral abnormalities. The motor handicap may be the least of the child's problems.
Infants with spastic hemiplegia have decreased spontaneous movements on the affected side and show hand preference at a very early age. The arm is often more involved than the leg, and difficulty in hand manipulation is obvious by 1 yr of age. Walking is usually delayed until 18–24 mo, and a circumductive gait is apparent. Examination of the extremities may show growth arrest, particularly in the hand and thumbnail, especially if the contralateral parietal lobe is abnormal, because extremity growth is influenced by this area of the brain. Spasticity is apparent in the affected extremities, particularly the ankle, causing an equinovarus deformity of the foot. The child often walks on tiptoes because of the increased tone, and the affected upper extremity assumes a dystonic posture when the child runs. Ankle clonus and a Babinski sign may be present; the deep tendon reflexes are increased; and weakness of the hand and foot dorsiflexors is evident. About one third of patients with spastic hemiplegia have a seizure disorder that usually develops during the first year or two, and approximately 25% have cognitive abnormalities including mental retardation. A computed tomography (CT) scan or magnetic resonance imaging (MRI) may show an atrophic cerebral hemisphere with a dilated lateral ventricle contralateral to the side of the affected extremities. Intrauterine thromboembolism with focal cerebral infarction may be one etiology; CT or MRI at birth in infants with focal seizures often demonstrates the area of infarction.

Spastic diplegia refers to bilateral spasticity of the legs. The first indication of spastic diplegia is often noted when the infant begins to crawl. The child uses the arms in a normal reciprocal fashion but tends to drag the legs behind more as a rudder (commando crawl) rather than using the normal four-stance crawling movement. If the spasticity is severe, the application of a diaper is difficult owing to excessive adduction of the hips. Examination of the child reveals spasticity in the legs with brisk reflexes, ankle clonus, and a bilateral Babinski sign. When the child is suspended by the axillae, a scissoring posture of the lower extremities is maintained. Walking is significantly delayed; the feet are held in a position of equinovarus; and the child walks on tiptoes. Severe spastic diplegia is characterized by disuse atrophy and impaired growth of the lower extremities and by disproportionate growth with normal development of the upper torso. The prognosis for normal intellectual development is excellent for these patients, and the likelihood of seizures is minimal. The most common neuropathologic finding is periventricular leukomalacia, particularly in the area where fibers innervating the legs course through the internal capsule. This lesion is noted among premature infants.
Spastic quadriplegia is the most severe form of CP because of marked motor impairment of all extremities and the high association with mental retardation and seizures. Swallowing difficulties are common owing to supranuclear bulbar palsies and often lead to aspiration pneumonia. At autopsy, the central white matter is disrupted by areas of necrotic degeneration that may coalesce into cystic cavities. Neurologic examination shows increased tone and spasticity in all extremities, decreased spontaneous movements, brisk reflexes, and plantar extensor responses. Flexion contractures of the knees and elbows are often present by late childhood. Associated developmental disabilities, including speech and visual abnormalities, are particularly prevalent in this group of children. Children with spastic quadriparesis often have evidence of athetosis and may be classified as mixed CP.
Athetoid CP is relatively rare, especially since the advent of aggressive management of hyperbilirubinemia and the prevention of kernicterus. These infants are characteristically hypotonic and have poor head control and marked head lag. Feeding may be difficult, and tongue thrust and drooling may be prominent. The athetoid movements may not become evident until 1 yr of age and tend to coincide with hypermyelination of the basal ganglia, a phenomenon called status marmoratus. Speech is typically affected owing to involvement of the oropharyngeal muscles. Sentences are slurred, and voice modulation is impaired. Generally, upper motor neuron signs are not present, seizures are uncommon, and intellect is preserved in most patients. DIAGNOSIS. A thorough history and physical examination should eliminate a progressive disorder of the CNS, including degenerative diseases, spinal cord tumor, or muscular dystrophy. Depending on the severity and the nature of the neurologic abnormalities, a baseline electroencephalogram (EEG) and CT scan may be indicated to determine the location and extent of structural lesions or associated congenital malformations. Additional studies may include tests of hearing and visual function. As CP is usually associated with a wide spectrum of developmental disorders, a multidisciplinary approach is most helpful in the assessment and management of such children.

TREATMENT. Parents should be taught how to handle their child in daily activities such as feeding, carrying, dressing, bathing, and playing in ways that will limit the effects of abnormal muscle tone. They also need to be instructed in the supervision of a series of exercises designed to prevent the development of contractures, especially a tight Achilles tendon. There is no proof that physical or occupational therapy will prevent the development of CP in the infant at risk or that it will correct the neurologic deficit, but there is ample evidence that therapy optimizes the development of the abnormal child. The child with spastic diplegia is treated initially with the assistance of adaptive equipment, such as walkers, poles, and standing frames. If the patient has marked spasticity of the lower extremities or if there is evidence of hip dislocation, consideration should be given to performing surgical soft-tissue procedures that reduce muscle spasm around the hip girdle, including an adductor tenotomy or psoas transfer and release. A rhizotomy procedure in which the roots of the spinal nerves are divided has produced considerable improvement in selected patients with severe spastic diplegia. A tight heel cord in a child with spastic hemiplegia may be treated surgically by tenotomy of the Achilles tendon. The quadriplegic patient is managed with motorized wheelchairs, special feeding devices, modified typewriters, and customized seating arrangements. Communication skills may be enhanced by the use of Bliss symbols, talking typewriters, and specially adapted computers including artificial intelligence computers to augment motor and language function. Significant behavior problems may substantially interfere with the development of a child with CP; their early identification and management are important, and the assistance of the psychologist or psychiatrist may be necessary. Learning and attention deficit disorders and mental retardation are assessed and managed by a psychologist and educator. Strabismus, nystagmus, and optic atrophy are common in children with CP; thus, an ophthalmologist should be included in the initial assessment. Lower urinary tract dysfunction should receive prompt assessment and treatment. Several drugs have been utilized to treat spasticity, including dantrolene sodium, the benzodiazepines, and baclofen. These medications are generally ineffective but should be considered if severe spasticity is not controlled by other measures. Intrathecal baclofen has been used successfully in selected children with severe spasticity. This experimental therapy requires a team approach and constant follow-up for complications of the infusion pumping mechanism and infection. Botulinum toxin is undergoing study for the management of spasticity in specific muscle groups, and the preliminary findings show a positive response in those patients studied. Occasionally, patients with incapacitating athetosis will respond to levodopa, and children with dystonia may benefit from carbamazepine or trihexyphenidyl.

Carpal Tunnel Syndrome

2009-04-05T00:29:00.000-07:00

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.

Cardiovascular Disorders in Pediatrics

2009-04-05T00:21:00.000-07:00

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

Cardiac Infections

2009-04-05T00:18:00.000-07:00

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

Bone and Joint Infections

2009-04-05T00:13:00.000-07:00

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

Attention Deficit Disorder and Learning Disorders

2009-04-05T00:06:00.000-07:00

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

Antiviral Agents

2009-04-04T23:49:00.000-07:00

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

Antifungal Therapy

2009-04-04T23:38:00.000-07:00

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

Antibiotics and Outpatient Infections.pdf

2009-04-04T23:36:00.000-07:00

When you are choosing an agent to use, you are looking at what clinical symptoms the patient has, who is this patient, an immunocompromised or normal host. You are taking a little bit more of a detailed history to include infectious risks, and you are thinking about the antibiotic itself.
In a clinical syndrome, you are trying to identify what is the predominant symptom and signs. You are trying to see where the site of infection is. Is this infection in the joint? Is this infection in the bone? Where are we treating this infection? Does this patient have a central nervous system infection? Then, identify the disease process because if you identify that this is osteomyelitis, it is a little bit different than if you think that the patient has pyogenic arthritis. The causative organisms might change and then what you need do, is you need to think of what the disease is, what are the most likely pathogens associated with this disease and what is their susceptibility pattern in the area where you practice. This is essential. To pick a drug, you have to know what organism you are dealing with. Because if not, you are really doing it blindly. So you have to have an idea of what organisms cause what specific diseases so that then you can make a good choice about antibiotic therapy.
When you look at hosts, you need to know the age of the patient. A 10-year-old is different from a neonate. The pathogens are different. Think about underlying conditions. Is this a patient with cystic fibrosis with pneumonia, or is this a well child with pneumonia? Different pathogens. So you are thinking about that host. Does this patient have an indwelling catheter? Does the patient have a prosthetic heart valve? All these things make it a little different to know which antibiotic to choose. Then, is the patient malnourished because that might be a cause for immunodeficiency.
When you are looking at a focused history, you need to know if the patient you are seeing with fever for 10 days has just come back from a safari in Africa, or is this a patient who has just been in the community where there is a lot of influenza. So you are going to ask about travel, about exposure to people who have contagious diseases such as tuberculosis, or whether the child is exposed to more infections because he is in daycare. Are immunizations up to date? That is very important. That patient may have measles if they have never been immunized and there is an increase in your community of Hemophilus influenza type E,. which is now very rare but can occur. Is this adolescent an IV drug abuser? Unfortunately, this happens occasionally and it brings in another set of organisms and diseases we have to think about, and then sexual activity brings up another whole host of organisms and disease processes.
.... CLICK HERE TO DOWNLOAD FUL ARTICLE

Antibiotic Toxicities Agents

2009-04-04T23:21:00.000-07:00

Aminoglycosides. These are used for gram-negative infections.
Most of them have some gram-positive activity, but you would never use it for a gram-positive infection unless you're using it with other drugs. The most common that we still use in kids is gentamicin, also tobramycin, not much with kanamycin, even less with streptomycin. Pulmonologist are using inhaled tobra for some CS patients. The main type of toxicities that we see from aminoglycosides are ototoxicity and nephrotoxicity.
There are two kinds of toxicity to the ear. The direct ototoxicity is actually destruction of the cochlear hair cells and it produces a
high-frequency, irreversible hearing loss. This can occur early. It can occur late. It can occur after you've gone through you're
therapy. It's most commonly seen with amikacin and kanamycin. The vestibular dysfunction, which causes damage to the vestibular hair cells is most commonly seen with gentamicin and streptomycin. These can occur at any time during therapy.
Risk factors. The very young and the very old. Those may be some people to worry about. Ototoxicity is usually directly related to the peak level that you get. So, if you give 10 x the dose of
aminoglycoside, that's the kind of patient that I would worry about
their ears. If something could happen to their ears. Pre-existing renal disease, obviously if you are not getting rid of it and you're having high peaks for whatever reason you're not following them and you don't check peaks and troughs, there is a data suggesting that maybe we don't need to do that all the time anymore and maybe it doesn't really suggest efficiency of therapy. Let's say your patient had renal disease that you didn't pay attention, so you're getting too much of it producing high peaks. If you use other agents which also have Ototoxic potential in combination vancomycin and
other loop diuretics. Prior exposure to aminoglycosides or loud sound. Again, the very young, the very old. If you have a hereditary tendency for any ear problems you need to be concerned with
aminoglycosides and the exact amount of ototoxicity we always think is rare in infants but they're hard to evaluate, especially the premature infants. All premature infants should get their hearing screened usually before they leave the premature nursery and I talk about the micro-preemies. The 500 to 1000 gm infants, but if they have hearing loss was it to the multiple courses of aminoglycosides they got or the fact that they had intraventricular hemorrhage or a
brain abscess or was it the fact that they were exposed to multiple loud noises. So the exact mechanism is not well known.
Nephrotoxicity, I think of the patients who had high troughs. They're not clearing their aminoglycoside. They really need to be on it twice a day which is clearly just enough to get their peaks down but still
maintains a very high level which is hurting their kidneys as time
goes by. What we see is a gradual onset which could complete the kidney shut down. Usually we'll see elevations of BUN or creatine or hypertension and excessive urine protein. Risk for nephrotoxicity. Again, high doses or prolonged courses of therapy, especially for hemoglobin. Liver disease, concurrent use of other nephrotoxic medications, again, vancomycin, salt and water deprivation.
With each kind of drug we are going to talk about adverse effects and drug interactions. The interactions, mostly we worry about increased nephrotoxicity. Again, increased nephrotoxicity when you
use aminoglycosides in combination with all other potential
nephrotoxicity drugs. Cyclosporine, amphotericin B, some of the loop diuretics, indomethacin, most people don't realize that cephalothin is one of those. One of the interesting things aminoglycosides do or potentially potentiate is the respiratory suppression of nondepolarizing neuromuscular agents, but if you think about it too, in the old days before the cephalosporins when we used ampicillin and gentamicin exclusively when the newborn babies came in or you had the baby that presented with a little constipation, some cranial nerve findings, just kind of being floppy,
you put him on amp and gent and all of a sudden boom they got a lot worse, so it potentiates that neuromuscular blockade. I don't think anybody's going to use a lot of oral kanamycin, but oral
kanamycin and methotrexate can increase methotrexate toxicity.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE

Allergic Disorders

2009-04-04T23:09:00.000-07:00

Allergic illnesses have a significant impact that allergic diseases have on children's health and quality of life. Allergic diseases, including asthma, are among the major causes of chronic illnesses in the United States, affecting approximately 50 million patients or as many as one in five children. The economic impact is enormous; asthma alone is estimated to cost more than 6.2 billion dollars of health care expenditures annually. Of all the chronic illnesses, allergic respiratory problems, including allergic asthma, is the most common cause of school absenteeism. Even though allergic disease usually is not fatal, death can result as a consequence of allergic anaphylaxis related to medication, food, or insect venom allergy or from a complication of asthma. Therefore, the pediatrician must be capable of diagnosing allergic disease so as to institute appropriate management. This review will emphasize those clinical diagnostic features ascertained by history and physical examination as well as the appropriate laboratory studies useful in the diagnosis of respiratory (inhalant) and gastrointestinal (food) allergy.

General Features of Allergic Diseases
Allergic diseases are immunoglobulin E (IgE)-mediated immunologic illnesses that can affect any of the body's major organ systems either individually or collectively. Typically, children are not born having allergies because maternal IgE normally does not cross the placenta. In rare instances, neonates and young infants who apparently were sensitized in utero have been born with specific IgE to foods and had allergic reactions to those foods. Development of an allergy requires a familial predisposition and repeat exposure to an allergen (antigen) that provokes specific IgE antibody.
Epidemiologic surveys indicate that the familial trait for allergy is inherited as autosomal recessive. Whereas the frequency of positive allergy skin tests is similar in boys and girls, asthma is twice as common in males as in females prior to adolescence, but it appears equal in prevalence thereafter. A specific immune response gene has been identified for IgE antibody synthesis in rodents, but it has not yet been demonstrated conclusively in humans. With the recent advances in molecular genetics, it is anticipated that the genetic basis of allergy will be understood better in the near future.
Allergens sensitize by several potential routes and are categorized as inhalants, ingestants, injectants, and contactants (Table 1). It is important for the physician to define the route by which any specific allergen provokes clinical allergy in individual patients.
Of the inhalant IgE-mediated allergies, allergic rhinitis is by far the most common, affecting approximately 15% of all children. Asthma, of which 80% has an allergic inhalant basis, occurs in more than 5% of children. Gastrointestinal (ingestant) allergy typically is associated with food allergy; however, ingestants also may provoke urticaria and atopic dermatitis and less often may trigger respiratory symptoms. Anaphylaxis is a systemic generalized allergic response consisting of hypotension, urticaria, and angioedema as well as upper and lower airway obstruction; it can be caused by severe allergic reactions to foods (ingestant), insect venom stings (injectant), or medications (ingestant, injectant, or contactant).
Although incriminated anecdotally as the cause for hyperactivity, poor school performance, learning disabilities, or abnormal child behavior, there are no definitive, appropriately controlled studies that document an IgE allergic etiology for these predominantly psychosocial or educational problems. The possibility that overgrowth of a yeast such as Candida is important in the pathogenesis of allergy never has been substantiated. The concept of such a candidal syndrome in the context of abnormal child behavior has no validity, and antifungal therapy in the absence of overt clinical candidal infection should be discouraged.

Inhalant Allergy
Microscopic inhaled airborne allergens are responsible for most respiratory allergy (Table 2). In temperate climates, seasonal allergic rhinitis is induced by tree pollens in the early spring, grass pollens in the late spring and early summer, and ragweed in the late summer and early fall. Because of geographic differences in the US, clinicians must become familiar with the pollination patterns in their individual regions. Hay fever is an inappropriate term for allergic rhinitis because these patients neither are allergic to hay nor have fever. Flowering vegetation, such as roses and fruit blossoms, rarely cause allergy because these pollens are too heavy to become airborne; their germination is facilitated by bees and other insects. Fungi (mold) spores may be important outdoor aeroallergens in humid climates throughout the year, but their numbers decrease once there is significant frost in temperate climates. Fungi can be important indoor perennial allergens in damp environments. In perennial allergic rhinitis, house dust, animals, and molds all may be significant indoor inhalant allergens. The principal allergens in house dust are the cuticles and feces of the microscopic house dust mite Dermatophagoides. Animal allergens, such as epidermal danders, salivary proteins, urinary proteins, feces, and feathers, especially from pets such as cats, dogs, and birds are important because about 50% of households in the US have indoor animal pets. Food allergens are of lesser importance in the etiology of allergic rhinitis but cannot be ignored, especially in young children. Patients can be sensitive to one or multiple allergens. Certain individuals react to miniscule amounts of inhaled allergens, while others tolerate a large allergen dose before developing symptoms.
In addition to allergens, viral infections, aerosolized cosmetics, cigarette smoke, industrial fumes, and changes in temperature, humidity, and barometric pressure contribute to exacerbation of both upper and lower respiratory tract symptoms in the allergic child. Psychologic and social stresses also can enhance symptoms. The importance of these additional contributory factors varies greatly from patient to patient but should not be ignored when evaluating any individual.
Symptoms of nasal allergy consist of frequent sneezing, nasal pruritus, watery rhinorrhea, and often, nasal obstruction. Patients also may complain of red, itchy eyes as well as itchy throat and ears. If there is nasal obstruction, the patient will be a mouth breather and snoring can be a bedtime symptom; smell and taste also may be lost. Increased symptoms frequently are noted with increased exposure to the responsible allergen, such as after cutting grass or sleeping on a feather pillow.
When an allergic reaction develops, clear nasal secretions will be evident, and the nasal mucous membranes will become edematous without much erythema. The mucosa appear boggy and blue-gray. With continued exposure to the allergen, the turbinates will appear swollen and can obstruct the nasal airway. Conjunctival edema, itch, tearing, and hyperemia are frequent findings in patients who have associated allergic conjunctivitis. Patients who have allergic rhinitis, particularly children who have significant nasal obstruction and venous congestion, also may demonstrate edema and darkening of the tissues beneath the eyes. These so-called "shiners" are not pathognomonic for allergic rhinitis because they also can be seen in patients who have chronic rhinitis and/or sinusitis. Thick, purulent secretions indicate the presence of infection, including the possibility of sinusitis.

DIAGNOSTIC TESTS
Nonspecific Allergy Tests
Many pediatricians believe in the need for a screening test for allergy. Blood eosinophilia and total serum IgE levels have been proposed as screening tests, but they have relatively low sensitivity and should be used selectively (Table 3). The nasal secretions or sputum of patients who have a respiratory allergy contain increased numbers of eosinophils, which forms the basis of a useful nonspecific test, although not one that will identify any specific allergen etiology. Eosinophilia may not be present in patients who have not been exposed to allergens recently or who have a superimposed upper respiratory tract infection. Both systemic and inhaled steroids can reduce eosinophilia in secretions significantly; antihistamines have no direct effect on eosinophils.
The usefulness of nasal eosinophilia as a diagnostic test depends in large part on the technique used to obtain the specimens to prepare the slides for examination. Patients should expel nasal secretions onto wax paper or parafilm; secretions then are spread on a microscope slide, stained, and eosinophils counted under a microscope. It is difficult to quantify nasal eosinophilia accurately, although a finding of more than 3% eosinophils on stained smear of expelled nasal or bronchial secretions is considered increased. Because cotton or nylon nasal swabs trap secretions, they are not recommended for collecting secretions, except in the young child who will not or cannot expel secretions by blowing the nose. Peripheral blood eosinophilia is observed in allergic asthma but less commonly in allergic rhinitis. Blood eosinophilia is more frequent in atopic dermatitis and other conditions, such as parasite infection.
Total serum IgE is elevated in about 60% of patients who have allergic asthma but only in 30% of those who have allergic rhinitis. Unfortunately, commercial laboratories have promoted tests of total serum IgE excessively, but its usefulness in screening for allergy is limited to positive tests only because more than 60% of patients who have nasal allergy will have normal levels of total serum IgE.
.... CLICK HERE TO DOWNLOAD FULL ARTICLE

Adolescent Medicine

2009-04-04T22:49:00.000-07:00

Pubescence is a dynamic process that takes two and a half to five years to complete. The word pubescence is used, instead of puberty, because pubescence implies that it is an extended process. Puberty is a process. Also, remember that individuals may start the growth spurt early. Two young men, fourteen years of age, they have different growth patterns. And the implications of that are terrific among the adolescents themselves. The nice thing that we can do for smaller adolescent, is that we can assure him that when he comes back for the 10 year reunion, that he is probably going to be taller than the guy that started developing early.
As far as physical development, the first sign of pubescence in males is usually testicular enlargement. It usually starts around 11½ years of age. The first sign of pubescence in females is breast bud development with the usual onset is somewhere between eight and 14 years of age.
Another important concept from the growth and development standpoint is the sequence of secondary sexual characteristics. In males, that sequence is the following: testicular growth, pubarche, penile growth, and finally peak height velocity. From the graph over here, you can see that for females, peak height velocity occurs much earlier, about two years earlier than males. Remember too, that menarche usually occurs around two years after thelarche, or the onset of breast bud development, and it usually is a sexual maturity rating of 4 for females. Girls height rarely increases more than a couple of inches after menarche.Tanner staging. This is the breast staging with stage 1, the top two pictures, lateral and AP being Tanner stage 1, which is really just childlike. No palpable glands. Tanner stage 2 with a breast lump right under the breast bud directly below the areola. Tanner stage 3 being when the breast extends beyond the areola and is palpable beyond the areola. Stage 4 is when we get the typical mound on mound configuration. The first mound is actually the gland of the breast itself and the second mound is where the areola and the nipple form one complex that becomes the second mound on top of the first mound. And finally, stage 5, or the mature breast of the female where the puffiness of the areola goes away and the areola becomes contiguous with the skin of the rest of the breast with a protuberant nipple.
Another common finding in most of your practices and certainly in the adolescent medicine world is that we see a lot of gynecomastia in males. It is very common. Some estimates say that at least 25% of males have gynecomastia to some extent or another. And certainly it can also be represented in the female population as simple breast asymmetry and there will be a huge disparity between one breast and the other, which from a psychological standpoint can be traumatizing to the adolescent female. We may need to refer those girls either for reduction or augmentation of one of the breasts.
Gynecomastia in males can certainly change a lot of habits, including whether they decide to dress a certain way. One of the common things is that the guy wears a very tight T-shirt with lots of layers over to totally disguise the prominence of the breast. The other thing we hear is that physical activity changes. That they stop going swimming. If the P.E. at school requires that they take a shower with everybody, they avoid P.E. at all costs. Go to the showers as everyone else is getting dressed which makes them late to class and therefore they're constantly tardy. Gynecomastia in males will resolve within a year or two. Most of the time you don't need to do anything but give a little reassurance. Rarely, we will send someone over for plastic surgery. When they are Tanner stage 4 or sexual maturity rating of 4 and preferably even 5, but it depends again upon how psychologically traumatizing the gynecomastia has Pubic area. Prepubertal or stage 1 is basically no hair. These are two pictures of stage 2. I think if you look closely you can see a little bit of hair here and a little more here. Stage 3 is when the dense hair is in very circumscribed limits and moving on to 4, where basically the mons area is filled out with dense, curly hair, and then 5 where the hair extends onto the thighs or upwards toward the umbilicus.
.... C LICK HERE TO DOWNLOAD FULL ARTICLE

Acute Renal Failure Treatment

2009-04-04T22:39:00.000-07:00

General Therapy for Acute Renal Failure
Treatment of acute renal failure usually should be conservative and largely supportive. It requires careful and precise management. All patients will require close monitoring, many of them within intensive care settings.
Supportive care includes stabilizing the patient, monitoring input and output strictly, weighing daily, determining electrolyte values frequently, preventing sepsis via reducing the number of intravenous lines and removing an indwelling urinary catheter, culturing periodically, and using antibiotics when indicated clinically. It is important to adjust medication dosage according to renal function and to avoid nephrotoxins whenever possible. Because serum creatinine values increase daily, it is best to calculate drug doses based on GFR <10 style="font-weight: bold;">THERAPY FOR PRERENAL FAILURE
Rapid volume replacement and treatment of the underlying condition that resulted in prerenal failure are the cornerstones of therapy. Initial fluid administration of isotonic saline (0.9%) or 5% albumin (10 to 20 mL/kg per dose) should be used to restore intravascular volume. This can be both a diagnostic and a therapeutic trial. Fluid administration also can convert oliguric to nonoliguric renal failure in its early stage.
Unless a patient is suffering congestive heart failure (CHF), fluid administration should be repeated, followed by the use of loop diuretics, including furosemide (2 to 5 mg/kg per dose) or bumetanide (0.25 to 0.5 mg/dose IV). After each bolus, the patient's volume needs to be reevaluated. Response to the therapy will be indicated by a urine output of greater than 1 to 3 mL/kg per hour.
Patients who have CHF will need inotropic support, such as dopamine (5 µg/kg per minute IV), dobutamine (5 to 20 µg/kg per minute), or digoxin. Therapeutic digitalis values should be achieved slowly and the maintenance dose reduced as dictated by renal function (Table 6).
THERAPY FOR POSTRENAL FAILURE
Therapy for postrenal failure includes removal of obstruction by decompression or diversion of the urinary tract, stabilization of electrolyte abnormalities, management of postobstructive diuresis, and therapy for voiding dysfunction and for urinary tract infection. Surgical intervention will require urologic consultation. The site of the obstruction will determine the approach: placement of a Foley catheter, vesicostomy, ureteral catheters (stents), or nephrostomy tubes. Prompt relief of a partial obstruction is indicated in cases of severe pain, where the possibilities for severe renal damage predominate, and whenever there is a history of frequent urinary tract infections.
Postobstructive diuresis is characterized by marked polyuria. The excessive excretions of salt and water may result in hypokalemia, hyponatremia, and hypotension and lead to collapse. Fluid replacement should be guided by what is excreted and based on frequent measurements of urine volume, urinary electrolytes, and serum electrolytes, including calcium and phosphorus.
THERAPY FOR ESTABLISHED RENAL FAILURE
Maintaining Balance of Fluid and Electrolytes
In a euvolemic state, fluid intake, including water generated from endogenous metabolism (insensible fluid gain), is balanced by fluid output. Most of the fluid output involves sensible fluid losses by urine, stool, and sweat and insensible losses by water evaporation from the skin and respiratory tract. Only small amounts of water normally are lost in the stool (100 to 150 mL/d), and fluid loss by sweat is minimal. Therefore, patients who are in ARF should have fluid restricted to net insensible water loss (insensible losses minus endogenous water production, which is 400 mL/m² per day or 25% to 30% of caloric expenditure) plus all measured fluid losses (urine output, gastrointestinal losses, chest tube drainage). Net insensible loss should be restored with 5% to 10% dextrose in water (D5%W - D10%W). Urine output should be replaced with fluid that has the composition and quantity of these losses. Usually, normal saline (0.45% NS) mL for mL of losses every 4 to 6 hours is appropriate. If this therapy is sufficient, the patient will lose 0.5% to 1% of body weight per day over the initial few days. The patient should be weighed at leastonce daily, and input and output should be monitored strictly, with clinical status assessed constantly. Once urine output begins to rise, fluid intake should be increased. Fluid balance is easier to manage in children who have nonoliguric renal failure. Dialysis is indicated in the case of a severe fluid overload
..... CLICK HERE TO DOWNLOAD FULL ARTICLE

Acute Renal Failure Diagnosis

2009-04-04T22:24:00.000-07:00

Diagnosis of Acute Renal Failure
Although acute renal failure (ARF) is relatively uncommon, its mortality rate is potentially so high that it is important to recognize this condition in children. Rapid deterioration of renal function is caused by numerous insults and results in typical findings, including extracellular volume expansion, hyperkalemia, hypertension, metabolic acidosis, and azotemia. It usually is reversible, with the majority of patients recovering completely. However, ARF can lead to residual impairment of renal function and progress to end-stage renal disease and death. Conservative medical treatment often is life-saving.

Definition
ARF represents the rapidly progressive (within several hours or days) cessation of renal function, which results in the inability of the kidney to control body homeostasis, manifesting in retention of nitrogenous waste products (azotemia) and fluid and electrolyte imbalance. On the basis of pathophysiologic process, ARF has been divided broadly into three diagnostic categories: prerenal, intrarenal (organic-intrinsic), and postrenal failure (Table 1). Prerenal and early postrenal failures are renal functional disorders and responses of a structurally intact kidney to extrarenal processes. These forms of renal dysfunction recover rapidly as soon as the cause is reversed. However, if these two disorders are not recognized in time, persist too long, or are treated inadequately, they can result in intrinsic renal failure. Intrinsic or organic renal failure is caused by structural changes within the kidney. It is potentially reversible but requires an extended period of recovery.

Etiology
Prerenal failure is the most common form of ARF in children. The main process in the development of prerenal failure is hypoperfusion of the kidney, secondary to reduced effective plasma volume or heart failure. Numerous underlying conditions can lead to prerenal failure (Table 1). In children, the most common causes are hypovolemia secondary to gastrointestinal losses, the state of shock, and postoperative conditions. For example, ARF may occur after heart surgery when the aorta is cross-clamped or following prolonged cardiopulmonary bypass time.
A variety of renal disorders and insulting events can contribute to the development of intrinsic renal failure (Table 1). Among these are acute glomerulonephritis and vasculitis of childhood, acute tubular necrosis, and acute interstitial nephritis.
Acute tubular necrosis (ATN) is the most common cause of intrinsic renal failure. It is associated with necrosis of the tubular epithelium following hypoxic or nephrotoxic injury. Various substances, including ethylene glycol, heavy metals, hydrocarbons, and certain antibiotics, including cephalosporins, aminoglycosides, sulfonamides, methicillin, and colistin, are potent nephrotoxins. Aminoglycoside-induced acute renal failure occurs typically 5 days after drug administration and represents a dose-dependent phenomenon.
Radiologic contrast material of the ionic type can cause ARF, usually within 24 hours after exposure, especially in individuals who are dehydrated, have diabetes mellitus, or have preexisting renal insufficiency. Primary diseases of the glomeruli and small blood vessels of the kidney may present with rapidly progressive ARF (Table 1). Large vessel diseases (renal artery thrombosis or embolism, renal vein thrombosis) are uncommon. Acute interstitial nephritis usually results from immune-mediated drug sensitivity or infection.
Postrenal failure is a less frequent cause of ARF in children. It presents as an abrupt decline in glomerular filtration rate (GFR) secondary to lower tract obstruction or bilateral upper tract obstructions, unless the patient has a single kidney. Obstruction can be secondary to structural, congenital, or acquired anomalies of the urinary tract, including posterior urethral valve, ectopic ureter, aberrant vessels, or stones, or may result from functional abnormalities such as neurogenic bladder. Uric acid, the end product of purine metabolism, is insoluble at high concentrations in an acidic medium; during rapid cellular lysis before or after chemotherapy it often will precipitate in a distal nephron and cause renal obstruction. Depending on localization, obstruction can be extrinsic or intrinsic, at the level of the collecting duct, pelvis, ureter, bladder, urethra, or meatus (Table 1).

Pathophysiology
Prerenal dysfunction can lead to development of renal failure and is characterized by a decline in renal blood flow (RBF), GFR, and urine flow. After an acute reduction in effective intravascular volume, compensatory mechanisms of both the organism and the kidney will operate to counteract the volume loss and restore renal perfusion. Central activation of several neural and humoral responses occurs, including increased activity of the sympathetic system and the renin-angiotensin II-aldosterone system and enhanced release of antidiuretic hormone. Hemodynamic alterations within the kidney develop. An initial, short response of maximum dilatation of afferent arteriole is replaced by vasoconstriction. Blood flow is redistributed away from the renal cortex to juxtamedullary nephrons, which results in extensive tubular reabsorption of sodium, water, and urea.
With intense vasoconstriction, the kidney, acting as a blood reservoir, will shunt additional volumes of blood to the most vital organs (brain and heart); this response actually may be lifesaving in states of shock, blood loss, or severe dehydration. When the kidney has used these compensatory mechanisms fully, and the delivery of oxygen to the kidney remains critically impaired, acute necrosis of tubular cells occurs.
Injury due to ischemia or toxins is manifested by alterations in cellular metabolism. Cell detachment, desquamation, necrosis, and generation of intratubular debris and cast formations develop. The backward leak of tubular fluid across the injured tubular membrane and tubular obstruction results in further hemodynamic changes.
.......CLICK HERE TO DOWNLOAD FULL ARTICLE

Current Emergency Diagnosis

2009-04-03T14:42:00.001-07:00

WHAT IS EMERGENCY MEDICINE?

An emergency is commonly defined as any condition perceived by the prudent layperson—or someone on his or her behalf—as requiring immediate medical or surgical evaluation and treatment. Based on that definition, the American College of Emergency Physicians (ACEP) states that the practice of emergency medicine has the primary mission of evaluating, managing, and providing treatment to these patients with unexpected injury and illness.

So what does an emergency physician do? This specialist routinely provides care and makes medical treatment decisions based on real-time evaluation of a patient's history; physical findings; and many diagnostic studies, including multiple imaging modalities, laboratory tests, and electrocardiograms. The emergency physician needs an amalgam of skills to treat a wide variety of injuries and illnesses—ranging from the diagnosis of an upper respiratory infection or dermatologic condition to resuscitation and stabilization of the multiple trauma patient. Furthermore, these physicians must be able to practice emergency medicine on patients of all ages and not just in urban tertiary-care facilities. Clinical emergency medicine may be practiced in emergency departments, both rural and urban; urgent care clinics; and other settings such as at mass gathering incidents, through emergency medical services (EMS), and in hazardous material and bioterrorism situations.

Emergency medicine serves as the United States's health care safety net. It provides valuable clinical and administrative services to the health care delivery system, including care for the indigent and others who lack access to health care, and has evolved as the most visible and vital component of a patchwork of health care providers and facilities. These emergency departments have become the routine, and often the only, source of care for many of the uninsured, thereby acting as a critical safety net for our fragmented health care delivery system.

Finally, emergency departments are the only element of the health care system whose function has been delineated by federal law. Initially authorized in 1986, the Emergency Medical Treatment and Active Labor Act mandates that all emergency departments provide screening, stabilization, and appropriate transfer to all patients with any medical condition. Emergency medicine is often the last resort for many patients and frequently the access point for competent, comprehensive, and efficient medical care.

BIRTH & GROWTH OF EMERGENCY MEDICINE

By current popular opinion based on reality and dramatic television productions, emergency medicine appears to be at the forefront of medicine, providing compassionate and competent care by residency-trained emergency physicians. Unfortunately, this has not always been the case. The profession of emergency medicine is still quite young and continues to grow and mature. A brief timeline of emergency medicine growth is shown in Table 1-1. Since the first emergency medicine residency program began in 1970, the number of approved residency programs has increased dramatically (Table 1-2). Despite the rapid growth in emergency medicine residencies, a significant number of practitioners of emergency medicine are not residency trained or board certified (Table 1-3).

SCOPE OF PRACTICE

Emergency medicine physicians are faced with an ever-growing patient volume, decreasing inpatient bed availability, decreasing reimbursement, and increased litigation. However, these same physicians have the unique responsibility for being prudent stewards of a finite amount of health care resources. Based on that responsibility, the ACEP in 2002 endorsed the following:

• The best medical interest of the patient should be foremost in any clinical decision making process.

Criteria for appropriate use of finite resources should include:

1. Urgency of the patient's medical condition

2. Likelihood, magnitude, and duration of medical benefit to the patient

3. Burdens and cost of care to the patient

4. Cost to society

• Emergency physicians should not allocate health care resources on the basis of a patient's ability to pay, contribution to society, past use of resources, or responsibility for their medical condition.

In 2001, the ACEP Core Content Task Force II published its Model of Clinical Practice of Emergency Medicine. In this publication, the scope of practice of an emergency physician is well defined and yet quite expansive, to include care from the prehospital environment to prevention and education. Listed below are the tasks of the emergency physician as agreed upon by the task force.

Prehospital Care

Participate actively in prehospital care and education, provide direct patient care or on-line or off-line medical direction or interact with prehospital medical providers, and assimilate information from prehospital care into patient assessment and management.

Emergency Stabilization

Conduct primary assessment, and take appropriate steps to stabilize and provide treatment to patients.

Performance of Focused History & Physical Examination

Communicate effectively to interpret and evaluate the patient's symptoms and history; identify pertinent risk factors in the patient's history; provide a focused evaluation; interpret the patient's appearance, vital signs, and condition; recognize pertinent physical findings; and perform techniques required for conducting the exam.

Modifying Factors

Recognize age, gender, ethnicity, barriers to communication, socioeconomic status, underlying disease, and other factors that may affect patient management.

Professional & Legal Issues

Understand and apply principles of professionalism, ethics, and legal concepts pertinent to patient management.

Diagnostic Studies

Select and perform the most appropriate diagnostic studies, and interpret the results.

Diagnosis

Develop a differential diagnosis and establish the most likely diagnoses in light of the history, physical examination, interventions, and test results.

Therapeutic Interventions

Perform procedures and nonpharmacologic therapies, and counsel patients.

Pharmacotherapy

Select appropriate pharmacotherapy, recognize pharmacokinetic properties, and anticipate drug interactions and adverse effects.

Observation & Reassessment

Evaluate and reevaluate the effectiveness of a patient's treatment or therapy, including addressing complications and potential errors; and monitor, observe, manage, and maintain the stability of one or more patients who are at different stages in their workups.

Consultation & Disposition

Collaborate with physicians and other professionals to evaluate and provide treatment to patients; arrange appropriate placement and transfer if necessary; formulate a follow-up plan; and communicate effectively with patients, family, and involved health care members.

Prevention & Education

Apply epidemiologic information to patients at risk; conduct patient education; and select appropriate disease and injury prevention techniques.

Documentation

Communicate patient care information in a concise manner that facilitates quality care and coding.

Multitasking & Team Management

Prioritize multiple patients in the emergency department in order to provide optimal patient care; interact, coordinate, educate, and supervise all members of the patient management team; utilize appropriate hospital resources; and have familiarity with disaster management procedures.

Other "Tasks"

Emergency medicine has evolved to include much more than the above-mentioned "tasks." For the profession of emergency medicine to continue to progress, physicians must embrace the following responsibilities:

• Basic and clinical research

• Multidisciplinary and continuous medical education

• Injury prevention

• Disaster management and mass-gathering medicine

• Toxicology and regional Poison Control Center direction

• Hazardous material and bioterrorism management

• Hospital and EMS systems administration

PRINCIPLES OF EMERGENCY MEDICINE

It is often said that emergency department patients "don't read the textbook," meaning that their presentations do not fit nicely into specific textbook diagnoses or classical presentations of illness. However, a cornerstone of an emergency physician's practice is the recognition of patterns in a patient's presentation; therefore, the prudent physician must be a detective and scientist to muddle through the muck of vague signs and symptoms to find the pattern.

The principles of emergency medicine are simply questions that must be answered to provide effective care to patients who have entrusted emergency physicians with their care. The questions are not to be used as a cookbook approach to the management of these often complex medical and psychosocial issues but are a simple method to guide the prudent emergency physician through the quagmire of clinical emergency medicine.

A. Is the Patient About to Die?
Obviously, this is the first and most important question to answer. Every patient's presentation is quickly prioritized to one of the following acuities:

1. Critical—Patient has symptoms consistent with a life-threatening illness or injury with a high probability of death if immediate intervention is not begun.

2. Emergent—Patient has symptoms of illness or injury that may progress in severity if treatment is not begun quickly.

3. Nonurgent—Patient has symptoms that have a low probability of progression to a more serious condition.

Look for symptoms of a life-threatening emergency, not a specific disease entity. Anticipate impending life-threatening emergencies in the apparently stable patient.

B. What Steps Must Be Undertaken to Stabilize the Patient?
Act quickly to stabilize the critically ill or injured patient. Focus on the primary survey (airway, breathing, circulation, and neurologic deficits), and make necessary interventions as each issue is identified. Do not delay necessary primary interventions while awaiting completion of ancillary testing.

C. What Are the Most Potentially Serious Causes of the Patient's Presentation?
Thinking of the worst-case scenario, develop a mental list of the most deadly causes of the patient's presentation by asking, "What will kill my patient the fastest?" Once the list has been developed, the vital signs, history, physical examination, and ancillary assessments should identify or confirm those causes highest on the list.

D. Could There Be Multiple Causes of the Patient's Presentation?
In addition to constant reevaluation and reprioritization of the differential diagnosis, continually ask, "Is this all there is?" For example, is the new-onset seizure and hypoglycemia in an older diabetic patient from intentional or accidental medication overdose or perhaps worsening renal insufficiency? Is the near-syncope and abdominal pain in an apparently intoxicated college coed from a ruptured ectopic pregnancy or perhaps a ruptured spleen secondary to undisclosed physical abuse by her boyfriend? Frequent reassessment and thoughtful inquiry as to the multiple possibilities responsible for each patient's condition are imperative.

E. Can a Treatment Assist in the Diagnosis in an Otherwise Undifferentiated Illness?
Often in emergency medicine, treatment response foretells a diagnosis. A case in point is the unconscious patient with no available collateral history. The patient's response to empiric administration of naloxone will include or exclude narcotic overdose as a contributor to the obtundation. Referred to as the "diagnostic-therapeutic" concept, it underscores the emergency medicine philosophy that an established diagnosis is not a prerequisite to initiating appropriate treatment. Pitfalls can exist. For example, sublingual nitroglycerin and so-called GI cocktails can relieve symptoms of chest pain resulting from the same cause.

F. Is a Diagnosis Mandatory or Even Possible?
After emergent issues have been addressed, the patient and emergency physician are often left with an undifferentiated symptom complex. This frequently elicits an uncomfortable response by non-emergency-medicine-trained physicians. Become accustomed to and comfortable with the notion of determining the disposition for a nonemergent patient—having treated their symptoms and excluding emergency conditions-without a specific diagnosis.

G. Does This Patient Need To Be Admitted to the Hospital?
Having appropriately answered the preceding questions, make the bottom-line disposition decision. Once assessments and treatments are under way, decide whether an emergent condition exists. Consider other subtleties. Does the patient have timely, accessible follow-up? How far away from a medical facility does the patient live? Are unresolved abuse or self-care issues involved? Are you, as the emergency physician, comfortable discharging the patient?

H. If the Patient Is Not Being Admitted, Is the Disposition Safe and Adequate for the Patient?
More frequently than not, patients are discharged home from the emergency department. However, many patients do not receive a specific diagnosis, and some symptoms may persist. Recommend appropriate follow-up, and provide written discharge instructions. Invite the patient back. Instruct the patient when to return for further evaluation should symptoms change or worsen. Provide the patient with information regarding treatment and diagnosis as well.

CONCLUSION

Since 1970, emergency medicine has seen a tremendous growth and increase in awareness of the unique aspects of the profession. It remains a challenging and fulfilling experience for many physicians and an appealing choice of specialties for medical students. As emergency medicine matures as a specialty, its importance as the United States's health care safety net and its integral status as front-line medicine will continue to expand and grow.

American College of Emergency Physicians: Definition of emergency medicine, as approved by the ACEP Board of Directors, April 2001. http://www.acep.org/3,411,0.html

American College of Emergency Physicians: Emergency medicine training, competency and professional practice principles position statement, as approved by the ACEP Board of Directors, November 2001. http://www.acep.org/3,5141,0.html

American College of Emergency Physicians: Emergency physician stewardship of finite resources, as approved by the ACEP Board of Directors, January 1997. http://www.acep.org/ 3,4245,0.html

American College of Emergency Physicians Core Content Task Force II: The Model of the Clinical Practice of Emergency Medicine. American College of Emergency Physicians, 2001.

Asplin BR, Sosnow PL, Yeh CS: "The Safety Net and Current Federal Health Care Policy." Defending America's Safety Net. American College of Emergency Physicians, 1999.

Current Diagnosis & Treatment in Orthopedics

2009-04-03T14:37:00.000-07:00

INTRODUCTION

Orthopedic surgery is the branch of medicine concerned with restoring and preserving the normal function of the musculoskeletal system. As such, it focuses on bones, joints, tendons, ligaments, muscles, and specialized tissues such as the intervertebral disk. Over the last half century, surgeons and investigators in the field of orthopedics have increasingly recognized the importance that engineering principles play both in understanding the normal behavior of musculoskeletal tissues and in designing implant systems to model the function of these tissues. The goals of the first portion of this chapter are to describe the biologic organization of the musculoskeletal tissues, examine the mechanical properties of the tissues in light of their biologic composition, and explore the material and design concepts required to fabricate implant systems with mechanical and biologic properties that will provide adequate function and longevity. The subject of the second portion of the chapter is gait analysis.

BASIC CONCEPTS & DEFINITIONS

Most biologic tissues are either porous materials or composite materials. A material such as bone has mechanical properties that are influenced markedly by the degree of porosity, defined as the degree of the material's volume that consists of void. For instance, the compressive strength of osteoporotic bone, which has increased porosity, is markedly decreased in comparison with the compressive strength of normal bone. Like composite materials, alloyed materials consist of two or more different materials that are intimately bound. Although composite materials can be physically or mechanically separated, alloyed materials cannot.

Generally, composites are made up of a matrix material, which absorbs energy and protects fibers from brittle failure, and a fiber, which strengthens and stiffens the matrix. The performance of the two materials together is superior to that of either material alone in terms of mechanical properties (eg, strength and elastic modulus) and other properties (eg, corrosion resistance). The mechanical properties of various types of composite materials differ, based on the percentage of each substance in the material and on the principal orientation of the fiber. The substances in combination, however, are always stronger for their weight than is either substance alone. Microscopically, bone is a composite material consisting of hydroxyapatite crystals and an organic matrix that contains collagen (the fibers).

The mechanical characteristics of a material are commonly described in terms of stress and strain. Stress is the force that a material is subjected to per unit of original area, and strain is the amount of deformation the material experiences per unit of original length in response to stress. These characteristics can be adequately estimated from a stress-strain curve (Figure 1-1), which plots the effect of a uniaxial stress on a simple test specimen made from a given material. Changes in the geometric dimensions of the material (eg, changes in the material's area or length) have no effect on the stress-strain curve for that material.

Mechanical characteristics can also be estimated from a load-elongation curve, in which the slope of the initial linear portion depicts the stiffness of a given material. Although similar in appearance to the stress-strain curve, the load-elongation curve for a given material can be altered by changes in the material's diameter (cross-sectional area) or length. For instance, doubling the diameter of a test specimen while maintaining the original length will double the stiffness because the increased diameter doubles the load to failure (ie, it doubles the force that a material can withstand in a single application) without changing the total elongation. Conversely, doubling the length of the test specimen while maintaining the original diameter will decrease the stiffness by half because doubling the length in turn doubles the elongation without changing the load to failure.

Because of this difference between the stress-strain curve and load-elongation curve, any comparison of the characteristics of specimens requires that the same type of curve be used in the evaluation. If the load-elongation curve is used, the geometric dimensions of the specimens must also be the same. In this chapter, subsequent discussions will pertain to the stress-strain curve, although differing terminology in the load-elongation curve will be noted parenthetically.

The initial linear or elastic portion of the stress-strain curve (see Figure 1-1) depicts the amount of stress a material can withstand before permanently deforming. The slope of this line is termed the modulus of elasticity (stiffness) of the material. A high modulus of elasticity indicates that the material is difficult to deform, whereas a low modulus indicates that the material is more pliable. The modulus of elasticity is an excellent basis on which different materials can be compared. When materials such as those used in implants are compared, however, it is important to remember that the modulus of elasticity is a property only of the material itself and not of the structure. Implant stiffness in bending—or, more correctly, flexural rigidity—is a function both of material elastic modulus and of design geometry.

The proportional limit, or sp, of a material is the stress at which permanent or plastic deformation begins. The proportional limit, however, is difficult to measure accurately for some materials. Therefore, a 0.2% strain offset line parallel to the linear region of the curve is constructed, as shown in Figure 1-1. The stress corresponding to this line is defined as the yield stress, or sy. If stress is removed after the initiation of plastic deformation (point A in Figure 1-1), only the elastic deformation denoted by the linear portion of the stress-strain curve is recovered. The ultimate tensile strength (failure load), or su, is the maximal stress that a material can withstand in a single application before it fails.

When subjected to repeated loading in a physiologic environment, a material may fail at stresses well below the ultimate tensile strength. The fatigue curve, or S-N curve, demonstrates the behavior of a metal during cyclic loading and is shown in Figure 1-2. Generally, as the number of cycles (N) increases, the amount of applied stress (S) that the metal can withstand before failure decreases. The endurance limit of a material is the maximal stress below which fatigue failure will never occur regardless of the number of cycles. Fatigue failure will occur if the combination of local peak stresses and number of loading cycles at that stress are excessive. Although most materials exhibit a lower stress at failure with cyclic loading, some do not, such as pyrolytic carbon, making it appropriate for high-cycle applications such as heart valves. Environmental conditions strongly influence fatigue behavior. The physiologic environment, which is corrosive, can significantly reduce the number of cycles to failure and the endurance limit of a material.

Materials can be evaluated in terms of ductility, toughness, viscoelasticity, friction, lubrication, and wear. These properties will be introduced here, and many of them will be explored in detail in subsequent sections.

Ductility is defined as the amount of deformation that a material undergoes before failure and is characterized in terms of total strain. A brittle material will fail with minimal strain caused by propagation because the yield stress is higher than the tensile stress. A ductile material, however, will fail only after markedly increased strain and decreased cross-sectional area. Polymethylmethacrylate (PMMA, a polymer) and ceramics are brittle materials, whereas metals exhibit relatively more ductility. Environmental conditions, especially changes in temperature, can alter the ductility of materials.

Toughness is defined as the energy imparted to a material to cause it to fracture and is measured by the total area under the stress-strain curve.

Because all biologic tissues are viscoelastic in nature, a thorough understanding of viscoelasticity is essential. A viscoelastic material is one that exhibits different properties when loaded at different strain rates. Thus, its mechanical properties are time-dependent. Bone, for example, absorbs more energy at fast loading rates, such as in high-speed motor vehicle accidents, than at slow loading rates, such as in recreational snow skiing.

Viscoelastic materials have three important properties: hysteresis, creep, and stress relaxation. When a viscoelastic material is subjected to cyclic loading, the stress-strain relationship during the loading process differs from that during the unloading process (Figure 1-3). This difference in stress-strain response is termed hysteresis. The deviation between loading and unloading processes is dependent on the degree of viscous behavior. The area between the two curves is a measure of the energy lost by internal friction during the loading process. Creep, which has also been called cold flow and is observed in polyethylene components, is defined as a deformation that occurs in a material under constant stress. Some deformation is permanent, persisting even when the stress is released. The constant strain associated with a decrease in stress over time is a result of stress relaxation, a phenomenon evident, for example, in the loosening of fracture fixation plates. The time necessary to attain creep, or stress relaxation equilibrium, is an inherent property of the material.

Friction refers to the resistance between two bodies when one slides over the other. Friction is greatest at slow rates and decreases with faster rates. This is because the surface asperities (peaks) tend to adhere to one another more strongly at slower rates. Mechanisms of lubrication reduce the friction between two surfaces. Several lubrication mechanisms are present in articular cartilage to overcome friction processes in normal joint motion. Similarly, mechanisms are present in polyethylene-metal articulations to overcome friction in joint replacements.

Wear occurs whenever friction is present and is defined as the removal of surface material by mechanical motion. Wear is always observed between two moving surfaces, but lubrication mechanisms act to reduce the detrimental effects of excessive wear. Three types of wear mechanisms are apparent in normal and prosthetic joint motion: abrasive, adhesive, and three-body wear. Abrasive wear is the generation of material particles from a softer surface when it moves against a rougher, harder surface. An example of the product of abrasive wear is sawdust, which results from the movement of sandpaper against a wood surface. The amount of wear depends on factors such as contact stress, hardness, and finish of the bearing surfaces.

Adhesive wear results when a thin film of material is transferred from one bearing surface to the other. In prosthetic joints, the transfer film can be either polyethylene or the passivated (corrosion-resistant) layer of metal. Regardless of the material, wear occurs in the surface that loses the transfer film. If the particles from the transfer film are shed from the other surface as well, they behave as a third body and also result in wear.

Three-body wear occurs when another particle is located between two bearing surfaces. Cement particles act as third bodies in prosthetic joints. Implant designers continue to search for compatible substances that reduce friction at articulating surfaces and thereby reduce the amount of wear debris generated. Wear of polyethylene is the dominant problem in total joint replacement today because the wear debris generated is biologically active and leads to osteolysis.

BIOMECHANICS IN ORTHOPEDICS

Introduction

An analysis of the factors that influence normal and prosthetic joint function requires an understanding of free-body diagrams as well as the concepts of force, moment, and equilibrium.

Force, Moment, & Equilibrium

Forces and moments are vector quantities—that is, they are described by point of application, magnitude, and direction. A force represents the action of one body on another. The action may be applied directly (eg, via a push or a pull) or from a distance (eg, via gravity). A normal tensile or compressive force is applied perpendicular to a surface, whereas a shear force is applied parallel to a surface. A force that is applied eccentrically produces a moment.

The force generated by gravity on an object is the center of gravity. An object that is symmetric has its center of gravity in the geometrically centered position, whereas an object that is asymmetric has its center of gravity closer to its "heavier" end. The center of gravity for the human body is the resultant of the individual centers of gravity from each segment of the body. Therefore, as the body segments move, the center of gravity changes accordingly and may even lie outside the body in extreme positions, such as encountered in gymnastics. A moment is defined as the product of the quantity of force and the perpendicular distance between the line of action of the force and the center of rotation. A moment usually results in a rotation of the object about a fixed axis.

Newton's first law states that a body (or object) is in equilibrium if the sum of the forces and moments acting on the body are balanced; therefore, the sum of forces and moments for each direction must equal zero. The concept of equilibrium is important in understanding and determining force-body interactions, such as the increased joint reaction force occurring in an extended arm because of an external weight and such as the increased joint reaction force occurring in the hip at a specific moment during walking.

Free-Body Diagrams

A free-body diagram can be used to schematically represent all the forces and moments acting on a joint. The concepts of equilibrium can be extended to determine joint reaction or muscle forces for different conditions, as demonstrated in the following two examples.

Example 1: Determine the force on the abductor muscle of a person's hip joint (the abductor force, or FAB) and the joint reaction force (the FJ) when the person is standing on one leg. The weight of the trunk, both arms, and one leg is 5/6 of the total weight (w) of the person. As illustrated in Figure 1-4, this weight will tend to rotate the body about the femoral head and is counteracted by the pull of the abductor muscles on the pelvis. The necessary equation to solve for the abductor force, FAB, is as follows:

In solving the equation, assume that a = 5 cm and that b = 15 cm.

After this equation is solved, two of the three forces are known. The remaining force (the FJ) can be determined from a force triangle (see Figure 1-4), because according to Newton's first law, the sum of forces must equal zero.

Example 2: Determine the force on a person's deltoid muscle (the deltoid force, or FD) and the force of the joint acting about the shoulder (the joint force, or FJ) when the person holds a metal weight (w) at arm's length (Figure 1-5). The weight of the arm is ignored because only the increase in forces about the shoulder caused by the metal weight is to be determined. FD is determined by summing the moments about the joint center. The necessary equation is as follows:

In solving the equation, assume that a = 5 cm and that b = 60 cm.

After this equation is solved, a joint reaction force of 1150 N is determined using a force triangle (see Figure 1-5).

Moments of Inertia

The orientation of the bone's or implant's cross-sectional area with respect to the applied principal load also greatly influences the biomechanical performance. Bending and torsion occur in long bones and are important considerations in the design of implants. In general, the farther that material mass is distributed from the axis of bending or torsion while still retaining structural integrity, the more resistant the structure will be to bending or torsion. The area moment of inertia is a mathematical expression for resistance to bending, and the polar moment of inertia is a mathematical expression for resistance to torsion. Both types of moment of inertia relate the cross-sectional geometry and orientation of the object with respect to the applied axial load. The larger the area moment of inertia or the polar moment of inertia is, the less likely the material will fail. Figure 1-6 summarizes the area moments of inertia for representative shapes important to orthopedic surgery. Creating an open slot in an object will significantly decrease the polar moment of inertia of the object.

Knowledge of moments of inertia is important for understanding mechanical behavior in relation to object geometry. For instance, the length of the long bones predisposes them to high bending moments. Their tubular shape helps them resist bending in all directions, however. This resistance to bending is attributable to the large area moment of inertia because the majority of bone tissue is distributed away from the neutral axis. The concept of moment of inertia is crucial in the design of implants that are exposed to excessive bending and torsional stresses.

BIOLOGIC TISSUES IN ORTHOPEDICS

Introduction

The functions of the musculoskeletal system are to provide support for the body, to protect the vital organs, and to facilitate easy movement of joints. The bone, articular cartilage, tendon, ligament, and muscle all interact to fulfill these functions. The musculoskeletal tissues are integrally specialized to perform their duties and have excellent regenerative and reparative processes. They also adapt and undergo compositional changes in response to increased or decreased stress states. Specialized components of the musculoskeletal system, such as the intervertebral disk, are particularly suited for supporting large stress loads while resisting movement.

Bones

Bones are dynamic tissues that serve a variety of functions and have the ability to remodel to changes in internal and external stimuli. Bones provide support for the trunk and extremities, provide attachment to ligaments and tendons, protect vital organs, and act as a mineral and iron reservoir for the maintenance of homeostasis.

A. Structural Composition

Bone is a composite consisting of two types of material. The first material is an organic extracellular matrix that contains collagen, accounts for about 30-35% of the dry weight of bone, and is responsible for providing flexibility and resilience to the bone. The second material consists primarily of calcium and phosphorous salts, especially hydroxyapatite [Ca10(PO4)6(OH)2], accounts for about 65-70% of the dry weight of bone, and contributes to the hardness and rigidity of the bone. Microscopically, bone can be classified as either woven or lamellar.

Woven bone, which is also called primary bone, is characterized by a random arrangement of cells and collagen. Because of its relatively disoriented composition, woven bone demonstrates isotropic mechanical characteristics, with similar properties observed regardless of the direction of applied stress. Woven bone is associated with periods of rapid formation, such as the initial stages of fracture repair or biologic implant fixation. Woven bone, which has a low mineral content, remodels to lamellar bone.

Lamellar bone is a slower forming, mature bone that is characterized by an orderly cellular distribution and regular orientation of collagen fibers (Figure 1-7). The lamellae can be parallel to one another or concentrically organized around a vascular canal called a Haversian system or osteon. At the periphery of each osteon is a cement line, a narrow area containing ground substance primarily composed of glycosaminoglycans. Neither the canaliculi nor the collagen fibers cross the cement line. Biomechanically, the cement line is the weakest link in the microstructure of bone. The organized structure of lamellar bone makes it anisotropic, as seen in the fact that it is stronger during axial loading than it is during transverse, or shear, loading.

Bone can be classified macroscopically as cortical tissue and cancellous (trabecular) tissue. Both types are morphologically lamellar bone. Cortical tissue relies on osteons for cell communication. Because trabecular width is small, however, the canaliculi can communicate directly with blood vessels in the medullary canal. The basic differences between cortical tissue and cancellous tissue relate to porosity and apparent density. The porosity of cortical tissue typically ranges from 5% to 30%, and that of cancellous tissue ranges from 30% to 90%. The apparent density of cortical tissue is about 1.8 g/cm, and that of cancellous tissue typically ranges from 0.1 to 1.0 g/cm. The distinction between cortical tissue and cancellous tissue is arbitrary, however, and in biomechanical terms the two tissues are often considered as one material with a specific range in porosity and density.

The organization of cortical and cancellous tissue in bone allows for adaptation to function. Cortical tissue always surrounds cancellous tissue, but the relative quantity of each type of tissue varies with the functional requirements of the bone. In long bones, the cortical tissue of the diaphysis is arranged as a hollow cylinder to best resist bending. The metaphyseal region of the long bones flares to increase the bone volume and surface area in a manner that minimizes the stress of joint contact. The cancellous tissue in this region provides an intricate network that distributes weight-bearing forces and joint reaction forces into the bulk of the bone tissue.

B. Biomechanical Behavior

The mechanical properties of cortical bone differ from those of cancellous bone. Cortical bone is stiffer than cancellous bone. Cortical bone will fracture in vivo when the strain exceeds 2%, but cancellous bone does not until the strain exceeds 75%. The larger capacity for energy storage (area under the stress-strain curve) of cancellous bone is a function of porosity. Despite different stiffness values for cortical and cancellous bone, the following axiom is valid for all bone tissue: the compressive strength of the tissue is proportional to the square of the apparent density, and the elastic modulus or material stiffness of the tissue is proportional to the cube of the apparent density. Therefore, any increase in porosity, as occurs with aging, will decrease the apparent density of bone, and this in turn will decrease the compressive strength and elastic modulus of bone.

Variations in the strength and stiffness of bone also result from specimen orientation (longitudinal versus transverse) and loading configuration (tensile, compressive, or shear). Generally, the strength and stiffness of bone are greatest in the direction of the common load application (longitudinally for long bones). With regard to orientation, cortical bone (Figure 1-8) is strongest in the longitudinal direction. With regard to loading configuration, cortical bone is strongest in compression and weakest in shear.

Tensile loading is the application of equal and opposite forces (loads) outward from the surface. Maximal stresses are in a plane perpendicular to the load application and result in elongation of the material. Microscopic studies show that the tensile failure in bones with Haversian systems is caused by debonding of the cement lines and pull-out of the osteons. Bones with a large percentage of cancellous tissue demonstrate trabecular fracture with tensile loading.

The converse of tensile loading is compressive loading, which is defined as the application of equal and opposite forces toward the surface. Under compression, a material shortens and widens. Microscopic studies show that compressive failure occurs by oblique cracking of the osteons in cortical bone and of the trabeculae in cancellous bone. Vertebral fractures, especially associated with osteoporosis, are associated with compressive loading.

The application of either a tensile load or a compressive load produces a shear stress in the material. Shear loading is the application of a load parallel to a surface, and the deformation is angular. Clinical studies show that shear fractures are most common to regions with a large percentage of cancellous bone, such as the tibial plateau.

Bone is a viscoelastic material, and its mechanical behavior is therefore influenced by strain rate. Bones are approximately 50% stiffer at high strain rates than at low strain rates, and the load to failure nearly doubles at high strain rates. The result is a doubling of the stored energy at high strain rates. Clinical studies show that the loading rate influences the fracture pattern and the associated soft-tissue damage. Low strain rates, characterized by little stored energy, result in undisplaced fractures and no associated soft-tissue damage. High strain rates, however, are associated with massive damage to the bone and soft tissue owing to the marked increase in stored energy.

Bone fractures can be produced either from a single load that exceeds the ultimate tensile strength of the bone or from repeated loading that leads to fatigue failure. Because bone is self-repairing, fatigue fracture occurs only when the rate of microdamage resulting from repeated loading exceeds the intrinsic repair rate of the bone. Fatigue fractures are most common during strenuous activity when the muscles have become fatigued and are therefore unable to adequately store energy and absorb the stress imposed on the bone. When the muscles are fatigued, the bone is required to carry the increased stress.

Antibiotic Mechanisms

2009-04-03T14:31:00.000-07:00

Antifungals
Binds to ergosterol in fungal membranes, disrupting membrane permeability and transport functions, thereby allowing cations and macromolecules to leak out of the cell

Aztreonam
Binds to PCP's, inhibits peptidoglycan synthesis and is bactericidal for gram negative (no effect on gram pos and anaerobes) B-lactam resistant

Cephalosporins
B-lactam Bactericidal...Binds to PCP's and inhibits murein synthesis and cell wall production

Clindamycin
Binds to 50s subunit of bacterial ribosomes and suppresses protein synthesis by disrupting formation of 70s initiation complex and inhibits translocation step of peptide bond synthesis...gram + cocci and most anaerobes

Erythromycin
Inhibits protein synthesis by binding reversibly to 50s ribosomal subunits ...specifically inhibits translocation step of protein synthesis, where tRNA/amino acid complex moves from the acceptor site to the peptidyl site on the ribososmes

Gentamicin
Aminoglycoside bactericidal...enters by oxygen dependent active transport, binds to 30s and inhibits protein synthesis...interferes with initiation complex, induces misreading of mRNA, and breaks up polysomes...synergistics with B-lactams

Imipenem
B-lactam, binds to PCP's (many of which are transpeptidases for murein wall synthesis)...autolytic enzyme activation..broadest spectrum of all antibiotics

INH
Inhibits mycobacterial cell wall synthesis (specifically mycolic acids)

Metronidazole
Bioactivation of drug's nitro base by ferridoxin leads to cytotoxic agents which are bacteriocidal

Nafcillin
Penicillinase-resistant PCN...binds to PCP's inhibits cell wall synthesis..bulky nature prevents B-lactamase function

Neomycin
Enters by oxygen dependent active transport, binds to 30s and inhibits protein synthesis by interfering with initiation complex, misreading mRNA, breaks up polysomes

Nitrofurantoin
Bacteriostatic...urinary antiseptic...best if urine is acidic

Penicillin
Binds to PCP's which inhibits cell wall synthesis...autolytic enzyme activation leads to bactericidal activity on dividing bacteria

Rifampin
Inhibits DNA-dependent RNA polymerase of Mycobacteria by interacting with its B subunit...this suppresses RNA chain initiation

Quinolones
Inhibits DNA topoisomerase II (DNA gyrase)...bactericidal
Sulfa
Bactriostatic, structural analog of PABA and a competetive antagonist for dihydropteroate synthetase

Tetracycline
Bacteriostatic, bacteriocidal only at high concentrations...passively diffuses through hydrophilic channels and then an energy dependent active transport pumps the drug through the inner cytoplasmic membrane. Humans lack active transport and therefore are protected...drug then binds to 30s and prevents access of the aminoacyl tRNA to its acceptor site on the mRNA

Trimethoprim
Inhibits dihydrofolate reductase, thus preventing folic acid synthesis and therfore decreased production of thymine, purines, and amino acids and interferes with nucleic acid production.

Vancomycin
Binds with high affinity to D-alanyl-D-alanine portion of cell wall precursors and prevents polymerization of peptidoglycans. Bactericidal for dividing gram positives

Radiography

2009-04-03T14:16:00.000-07:00

This article illustrates the typical clinical and radiographic findings of patients with injuries to the cervical spine and discusses basic treatment guidelines. Cervical spine injuries are frequently seen in multitrauma patients and can be devastating injuries, particularly if not identified in a timely manner. The initial evaluation is both clinical (questioning about neck pain, palpating the neck, and neurologic examination) and radiographic, if indicated. All trauma patients should be effectively immobilized until a cervical spine injury is ruled out.
The initial radiographic work-up consists of anteroposterior, lateral, and open-mouth odontoid views. If the C7-T1 junction is not seen on plain radiographs, a swimmer’s view of the cervical spine should be obtained. If this view remains inadequate, a computed tomography (CT) scan through the nonvisualized vertebral bodies should be obtained. Depending on the type of injury, additional radiographic studies may be indicated. Early recognition of cervical spine injury and consultation of a spine specialist is imperative for a good neurologic outcome.
Atlanto-occipital dislocation
Frequency/incidence
Atlanto-occipital dislocation (AOD) is present in up to 1% of patients with cervical spine injuries. AOD has been found in 19% to 35% of autopsies of fatal cervical spine injuries. There is a higher incidence of AOD among children [1].
Signs and symptoms
AOD is typically fatal [1,2]. Mortality is most frequently from anoxia caused by respiratory arrest. Among survivors, more than 70% have an associated head injury [3]. Cranial nerve palsies (especially types VI, IX and XII) are seen in 50% of cases. Complete quadriplegia or brain-stem injury typically results in death. Brown-Sequard or central cord syndrome may also be observed. Patients will frequently deteriorate when placed in cervical traction. The patient may be completely neurologically intact and have a good outcome [1].
Etiology/pathophysiology
AOD is caused by violent trauma (typically, motor vehicle collision or pedestrian struck by car) and may be related to hyperextension with distraction [1,3]. In fatal cases, there is transection of the spinal cord; however, in cases in which the patient survived, there was angio-graphic evidence of vertebral artery injury at the C1 level where the artery penetrates the dura to become intracranial. From a mechanical view, the distal vertebral artery as well as the head is
freely moveable in AOD, causing the artery to be injured at the C1 level as the vertebral artery then becomes anchored to the spine within the transverse foramen. At autopsy, none of these patients had evidence for mechanical injury or transection of the cord [4].
Image of choice for diagnosis
Radiographic diagnosis is difficult, which frequently delays diagnosis. Plain lateral radiographs are typically the first test ordered. Plain radiographic techniques for diagnosing this entity include the Power’s ratio, and the X-line method [5]. The opisthion and basion are often difficult to identify on plain films, making thin-slice CT (3-mm cuts) with sagittal reconstruction a more accurate way of identifying AOD (see Power’s ratio in the Image hallmarks section). If suspicion is high, reformatted CT is the test of choice.
Image hallmarks
There is typically massive retropharyngeal soft tissue swelling (Fig. 1). On plain lateral radiographs, the Power’s ratio is frequently employed. The distance from the basion to the posterior arch of the atlas divided by the distance from the opisthion to anterior arch of atlas is greater than 1.0 in all cases of AOD. A Power’s ratio of less than 0.9 is normal, whereas ratios of 0.9 to 1.0 are borderline, representing 7% of the normal population and no cases of AOD [2].
Management
Initial treatment involves strict immobilization of the cervical spine. Patients are typically reduced and placed in a halo vest. It is typically recommended that the patient subsequently undergo posterior occipital to cervical fusion [1,3].

Atlantoaxial rotatory subluxation/dislocation
Frequency/incidence
Rotatory subluxation at the C1-2 joint is relatively uncommon. Signs and symptoms
Patients will frequently have torticollis, inability to rotate their head, facial flattening (if chronic), and upper cervical pain. The head position is sometimes described as ‘‘cock robin’’ (20° lateral tilt to one side, 20° rotation to the other side, and a slight flexion) [6].
Etiology/pathophysiology
Rotatory subluxation typically occurs in children because the facet joints are smaller and more steeply inclined, and children have a larger head-to-body ratio, making the joint prone to rotational damage [7]. It can be seen spontaneously, with minor or major trauma, and can occur in association with upper respiratory infections [6].

Studies On Low Blood Pressure

2009-04-03T14:03:00.000-07:00

Overview
In this chapter, we will show you how to locate peer-reviewed references and studies on low blood pressure.
The Combined Health Information Database
The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and low blood pressure, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “low blood pressure” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search:
• Heart in Uremia: Role of Hypertension, Hypotension, and Sleep Apnea
Source: American Journal of Kidney Diseases. 38(4 Supplement 1): S38-S46. October 2001.
Contact: Available from W.B. Saunders Company. Periodicals Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000.
Summary: Cardiovascular disease is the leading cause of morbidity (illness) and mortality (death) in patients with end stage renal (kidney) disease (ESRD). The causes of this morbidity and mortality include those usually found in the general population, those related to the uremic status, and those related to dialysis treatment. This article focuses on the specific roles of hypertension (high blood pressure), hypotension (lowblood pressure), anemia (low levels of hemoglobin, the oxygen carrying parts of the blood), hypoalbuminemia (low levels of protein in the blood), malnutrition, dyslipidemia (unhealthy levels of fats in the blood), reactive C protein, calcium-phosphate product, dialysis modalities (hemodialysis versus peritoneal dialysis), and hyperhomocysteinemia. The authors put special emphasis on hyperparathyroidism as a traditional toxin. The emergent role of sleep apnea has been confirmed in animal models as well as in humans studied using polysomnography. There are difficulties in diagnosing coronary disease, because angiography has some risks, is expensive, and should be reserved for patients having symptoms of heart failure, patients with diabetes mellitus, or patients entering a transplantation list. This allows patients with coronary disease to undergo revascularization (adding blood vessels) through coronary artery bypass (preferably) or percutaneous transluminal angioplasty. Patients for whom surgery is not appropriate should be treated using more traditional medical procedures. 2 figures. 1 table. 36 references.
• Achievement and Safety of a Low Blood Pressure Goal in Chronic Renal Disease: The Modification of Diet in Renal Disease Study Group
Source: Hypertension. 29(2): 641-650. February 1997.
Contact: Available from American Heart Association. 7272 Greenville Avenue, Dallas, TX 75231-4596.
Summary: The Modification of Diet in Renal Disease Study (MDRDS) showed a beneficial effect of a lower than usual blood pressure (BP) goal on the progression of renal disease in patients with proteinuria. This article reports on a study which analyzed the achieved BP, baseline characteristics that helped or hindered achievement of the BP goals, and safety of the BP interventions in the MDRDS. Patients (n = 585) were randomly assigned to either a usual or low BP goal (mean arterial pressure less than 107 or less than 92 mm Hg, respectively). Few patients had a history of cardiovascular disease. All antihypertensive agents were permitted, but angiotensin converting enzyme (ACE) inhibitors (with or without diuretics) followed by calcium channel blockers were preferred. The mean of the arterial pressures during followup in the low and usual BP groups was 93,.0 and 97.7 mm Hg, respectively. Followup BP was significantly higher in subgroups of patients with preexisting hypertension, baseline mean arterial pressure greater than 92 mm Hg, a diagnosis of polycystic kidney disease or glomerular diseases, baseline urinary protein excretion greater than 1 g per day, age greater than 61 years, and black race. The frequency of medication changes and incidence of symptoms of low BP were greater in the low BP group, but there were not significant differences between BP groups in stop points, hospitalizations, or death. When data from both groups were combined, each 1 mm Hg increase in followup systolic BP was associated with a 1.35 times greater risk of hospitalization for cardiovascular or cerebrovascular disease. The authors conclude that lower BP than usually recommended for the prevention of cardiovascular disease is achievable by several medication regimens without serious adverse effects in patients with chronic renal disease without cardiovascular disease. 1 figure. 7 tables. 40 references. (AA-M).
• Topsy-Turvy World of Postural Hypotension
Source: Diabetes Forecast. 52(3): 76-79. March 1999.
Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org.

Summary: This article discusses the problem of postural hypotension. The symptoms of this condition, which is low blood pressure caused by standing up, include dizziness, light-headedness, blurred vision, weakness, and fatigue. People who have diabetes may experience postural hypotension as a complication of autonomic neuropathy. As autonomic neuropathy progresses, the autonomic nervous system loses its reactive ability, so people who have this complication can experience rapidly changing highs and lows in blood pressure that make their head swim. The article explains how the body normally maintains blood pressure when a person stands and how it reacts in those who have autonomic neuropathy. Although physicians can perform some tests that will help determine if a person has postural hypotension, this condition is not something that physicians recognize well. If a diagnosis of postural hypotension is made, the next step is to figure out what is causing it and how to treat it. Regardless of whether autonomic neuropathy or other factors are the cause of postural hypotension, much of the treatment focuses on relieving the symptoms and removing factors that may aggravate the condition. Drugs may also be used to the condition. The article also addresses the issue of treating postural hypotension in people who also have hypertension and stresses the need to tailor treatment for postural hypotension to a person's specific needs.
• Low Blood Pressure and Incidence of Dementia in a Very Old Sample: Dependent on Initial Cognition
Source: JAGS. 47(6): 723-726. June 1999.
Summary: This population-based study of 304 nondemented people in Sweden, aged 75 to 96 years at baseline, examined whether initially low blood pressure is related to the incidence of dementia. DSM-III-R criteria were used for dementia with Hachinski's scale being used for a differential diagnosis between Alzheimer's disease (AD) and vascular dementia. Criteria for AD were similar to those of the NINCDS-ADRDA criteria. The diagnosis of dementia was given after consensus among three independent physicians. Arterial blood pressure, antihypertensive drug use, and medical histories were determined. The Cox proportional hazards regression model was used to calculate the relative risk of developing dementia in relation to baseline blood pressure levels. After an average of 3 years, 81 dementia cases were identified. Those with systolic pressure equal to or greater than 140 mm Hg had a significantly higher risk of dementia and AD. A baseline Mini-Mental State Examination (MMSE) of less than 24 significantly predicted the occurrence of dementia, and systolic pressure equal to or greater than 140 mm Hg was significantly related to MMSE scores of less than 24 at baseline. These results suggest that low blood pressure may be an early correlate of a dementing process, although researchers believe a causative effect cannot be definitely ruled out. 2 tables, 21 references. (AA-M).
Federally Funded Research on Low Blood Pressure
The U.S. Government supports a variety of research studies relating to low blood pressure. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable
database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions.
Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to low blood pressure.
For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore low blood pressure. The following is typical of the type of information found when searching the CRISP database for low blood pressure:
• Project Title: BIOCHEMISTRY AND GENETICS OF HYPERTENSION
Principal Investigator & Institution: Rapp, John P.; Professor and Chairman; Physiology/Molecular Medicine; Medical College of Ohio at Toledo Research & Grants Admin. Toledo, Oh 436145804
Timing: Fiscal Year 2001; Project Start 01-JUN-1988; Project End 30-MAY-2003
Summary: The overall objective is to identify-the loci which cause genetic differences in blood pressure in the rat. Because hypertension in animals and humans is a complex polygenic disease it can best be understood genetically in animals where controlled breeding is possible. We have focused our genetic studies on candidate genes in the inbred Dahl salt-hypertension sensitive (S) and inbred Dahl salt-hypertension resistant (R) rats. Genetic polymorphisms are sought at the DNA level in or near genetic loci thought (on the basis of their known biochemical/ physiological actions) to be relevant to blood pressure regulation. It is determined if a component of blood pressure and genotypes at the candidate locus cosegregate in populations derived from crosses of S and R, or S and other contrasting "control" strains. If so, this establishes the candidate locus (or an unknown closely linked locus) as a cause for genetic differences in blood pressure. DNA sequence analysis of the candidate alleles involved is then required to find a structural difference that is likely to have functional consequences with regard to blood pressure. If cosegregation is negative the candidate locus can be rejected as causing blood pressure differences provided the experiments have adequate statistical power and several different populations are studied. For candidate loci which cosegregate with blood pressure, the result will be con-firmed by the production of congenic strains. The low blood pressure allele from a control strain is transferred to the S genetic background by the standard genetic technique of repeated backcrossing to S with counter selection for the low blood pressure allele. The congenic S strain should have lower blood pressure than the parental S strain if in fact the allele transferred lowers blood pressure. "Double congenic" strains will be produced by crossing two single congenics each of which carries genes for low blood pressure at different loci on the S genetic background. Comparisons of blood pressure among double and single congenics with the parental S strain will allow definition of interactions between the loci involved. Initial studies show that such interactions are required for really high levels of genetically regulated blood pressure to be achieved. It is likely that understanding such complexity requires animal breeding techniques, and cannot be initially unraveled in work with humans.
Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

• Project Title: BLOOD PRESSURE CANDIDATE GENE SCREENING--A NEW PARADIGM
Principal Investigator & Institution: Cicila, George T.; Physiology/Molecular Medicine; Medical College of Ohio at Toledo Research & Grants Admin. Toledo, Oh 436145804
Timing: Fiscal Year 2001; Project Start 01-JUL-1999; Project End 30-JUN-2003
Summary: (Adapted from the Investigator's Abstract) The essential mechanisms (and the genes underlying them) leading to hypertension need identification for better understanding and treatment of this complex disorder. The most direct way of accomplishing this is to identify genes regulating blood pressure in animal models of genetic hypertension. The applicants have linked loci on rat chromosomes 3 and 7 to blood pressure quantitative trait loci (BP QTL) in a segregating population bred from inbred Dahl salt-sensitive (S) and salt-resistant (R) rats fed a high salt diet. Introgression of R-rat derived chromosomal regions containing these two QTLs into S rats resulted in congenic strains with significantly lower blood pressure and cardiac mass compared to S rats, confirming the presence of BP QTL in the introgressed regions of chromosomes 3 and 7. Similar methodology has been used by others to develop congenic strains carrying BP QTLs located on six other chromosomes, resulting in a panel of eight congenic strains derived from the Dahl rat model of blood pressure salt-sensitivity. The applicant hypothesizes that gene(s) underlying a given BP QTL may be differentially expressed in target organs/tissues. If so, such a gene should also be differentially regulated in congenic strains carrying different BP QTL. Gene(s) responsible for a QTL's effect should show a congenic strain-specific differential-pattern of expression in a target organ(s) and should map to the chromosomal interval carried by that particular congenic strain. Therefore, genes having such characteristics will be superior candidates as genes responsible for, at least in part, a specific BP QTL. The applicant proposes to identify candidate genes for BP QTL as follows: Differentially expressed genes will be identified in the kidneys of S and R rats, on both low NaCl (genetic-differences) and high NaCl diets (salt-responsive). Renal RNA expression of such differentially-expressed genes will be examined in a panel of congenic strains carrying Dahl rat BP QTL, where each strain carries a low blood pressure allele for a different BP QTL on a background of S-rat alleles. Genes having a congenic strain-specific pattern of differential gene expression will be mapped to determine their genomic location. Genes with a 1) congenic strain-specific pattern of differential gene expression and 2) mapping to the introgressed chromosomal region containing a specific BP QTL, will be considered strong candidates for the gene(s) responsible for blood pressure differences associated with this QTL. This new approach should accelerate the identification of strong candidate genes for particular BP QTL and, potentially, of new blood pressure regulatory mechanisms.
Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

Gale Encyclopedia of Surgery

2009-04-03T13:52:00.000-07:00

Abdominal ultrasound
Definition
Abdominal ultrasound uses high frequency sound waves to produce two-dimensional images of the body’s soft tissues, which are used for a variety of clinical applications, including diagnosis and guidance of treatment procedures. Ultrasound does not use ionizing radiation to produce images, and, in comparison to other diagnostic imaging modalities, it is inexpensive, safe, fast, and versatile.
Purpose
Abdominal ultrasound is used in the hospital radiology department and emergency department, as well as in physician offices, for a number of clinical applications. Ultrasound has a great advantage over x-ray imaging technologies in that it does not damage tissues with ionizing radiation. Ultrasound is also generally far better than plain x rays at distinguishing the subtle variations of soft tissue structures, and can be used in any of several modes, depending on the area of interest.
As an imaging tool, abdominal ultrasound generally is indicated for patients afflicted with chronic or acute abdominal pain; abdominal trauma; an obvious or suspected abdominal mass; symptoms of liver or biliary tract disease, pancreatic disease, gallstones, spleen disease, kidney disease, and urinary blockage; evaluation of ascites; or symptoms of an abdominal aortic aneurysm.
Specifically:
• Abdominal pain. Whether acute or chronic, pain can signal a serious problem—from organ malfunction or injury to the presence of malignant growths. Ultrasound scanning can help doctors quickly sort through potential causes when presented with general or ambiguous symptoms. All of the major abdominal organs can be studied for signs of disease that appear as changes in size, shape, or internal structure.

• Abdominal trauma. After a serious accident such as a car crash or a fall, internal bleeding from injured abdominal organs is often the most serious threat to survival. Neither the injuries nor the bleeding may be immediately apparent. Ultrasound is very useful as an initial scan when abdominal trauma is suspected, and it can be used to pinpoint the location, cause, and severity of hemorrhaging. In the case of puncture wounds, from a bullet for example, ultrasound can locate the foreign object and provide a preliminary survey of the damage. (CT scans are sometimes used in trauma settings.)
• Abdominal mass. Abnormal growths—tumors, cysts, abscesses, scar tissue, and accessory organs—can be located and tentatively identified with ultrasound. In particular, potentially malignant solid tumors can be distinguished from benign fluid-filled cysts. Masses and malformations in any organ or part of the abdomen can be found.
• Liver disease. The types and underlying causes of liver disease are numerous, though jaundice tends to be a general symptom. Sometimes, liver disease manifests as abnormal laboratory results, such as abnormal liver function tests. Ultrasound can differentiate between many of the types and causes of liver malfunction, and it is particularly good at identifying obstruction of the bile ducts and cirrhosis, which is characterized by abnormal fibrous growths and altered blood flow.
• Pancreatic disease. Inflammation of the pancreas— caused by, for example, abnormal fluid collections surrounding the organ (pseudocysts)—can be identified by ultrasound. Pancreatic stones (calculi), which can disrupt proper functioning, can also be detected.
• Gallstones. Gallstones are an extremely common cause of hospital admissions. In the non-emergency or non-acute setting, gallstones can present as abdominal pain, or fatty-food intolerance. These calculi can cause painful inflammation of the gallbladder and obstruct the bile ducts that carry digestive enzymes from the gallbladder and liver to the intestines. Gallstones are readily identifiable with ultrasound.

• Spleen disease. The spleen is particularly prone to injury during abdominal trauma. It may also become painfully inflamed when infected or cancerous. The spleen can become enlarged with some forms of liver disease.
• Kidney disease. The kidneys are also prone to traumatic injury and are the organs most likely to form calculi, which can block the flow of urine and cause further systemic problems. A variety of diseases causing distinct changes in kidney morphology can also lead to complete kidney failure. Ultrasound imaging has proved extremely useful in diagnosing kidney disorders, including blockage and obstruction.
• Abdominal aortic aneurysm. This is a bulging weak spot in the abdominal aorta, which supplies blood directly from the heart to the entire lower body. A ruptured aortic aneurysm is imminently life-threatening. However, it can be readily identified and monitored with ultrasound before acute complications result.
• Appendicitis. Ultrasound is useful in diagnosing appendicitis, which causes abdominal pain.
Ultrasound technology can also be used for treatment purposes, most frequently as a visual aid during surgical procedures—such as guiding needle placement to drain fluid from a cyst, or to guide biopsies.

Description
Ultrasound includes all sound waves above the frequency of human hearing—about 20 thousand hertz, or cycles per second. Medical ultrasound generally uses frequencies between one and 10 megahertz (1–10 MHz). Higher frequency ultrasound waves produce more detailed images, but they are also more readily absorbed and so cannot penetrate as deeply into the body. Abdominal ultrasound imaging is generally performed at frequencies between 2–5 MHz.
An ultrasound scanner consists of two parts: the transducer and the data processing unit. The transducer both produces the sound waves that penetrate the body and receives the reflected echoes. Transducers are built around piezoelectric ceramic chips. (Piezoelectric refers to electricity that is produced when you put pressure on certain crystals such as quartz.) These ceramic chips react to electric pulses by producing sound waves (trans-mitting) and react to sound waves by producing electric pulses (receiving). Bursts of high-frequency electric pulses supplied to the transducer cause it to produce the scanning sound waves. The transducer then receives the returning echoes, translates them back into electric puls es, and sends them to the data processing unit—a computer that organizes the data into an image on a television screen.
Because sound waves travel through all the body’s tissues at nearly the same speed—about 3,400 miles per hour—the microseconds it takes for each echo to be received can be plotted on the screen as a distance into the body. (The longer it takes to receive the echo, the farther away the reflective surface must be.) The relative strength of each echo, a function of the specific tissue or organ boundary that produced it, can be plotted as a point of varying brightness. In this way, the echoes are translated into an image.
Four different modes of ultrasound are used in medical imaging:
• A-mode. This is the simplest type of ultrasound in which a single transducer scans a line through the body with the echoes plotted on screen as a function of depth. This method is used to measure distances within the body and the size of internal organs.
• B-mode. In B-mode ultrasound, which is the most common use, a linear array of transducers simultaneously scans a plane through the body that can be viewed as a two-dimensional image on screen.
• M-Mode. The M stands for motion. A rapid sequence of B-mode scans whose images follow each other in sequence on screen enables doctors to see and measure range of motion, as the organ boundaries that produce reflections move relative to the probe. M-mode ultrasound has been put to particular use in studying heart motion.
• Doppler mode. Doppler ultrasonography includes the capability of accurately measuring velocities of moving material, such as blood in arteries and veins. The principle is the same as that used in radar guns that measure the speed of a car on the highway. Doppler capability is most often combined with B-mode scanning to produce images of blood vessels from which blood flow can be directly measured. This technique is used extensively to investigate valve defects, arteriosclerosis, and hypertension, particularly in the heart, but also in the abdominal aorta and the portal vein of the liver.
The actual procedure for a patient undergoing an abdominal ultrasound is relatively simple, regardless of the type of scan or its purpose. Fasting for at least eight hours prior to the procedure ensures that the stomach is empty and as small as possible, and that the intestines and bowels are relatively inactive. This also helps the gallbladder become more visible. Prior to scanning, an acoustic gel is applied to the skin of the patient’s abdomen to allow the ultrasound probe to glide easily across the skin and to better transmit and receive ultrasonic pulses. The probe is moved around the abdomen’s

surface to obtain different views of the target areas. The patient will likely be asked to change positions from side to side and to hold the breath as necessary to obtain the desired views. Usually, a scan will take from 20 to 45 minutes, depending on the patient’s condition and anatomical area being scanned.
Ultrasound scanners are available in different configurations, with different scanning features. Portable units, which weigh only a few pounds and can be carried by hand, are available for bedside use, office use, or use outside the hospital, such as at sporting events and in ambulances. Portable scanners range in cost from $10,000 to $50,000. Mobile ultrasound scanners, which can be pushed to the patient’s bedside and between hospital departments, are the most common configuration and range in cost from $100,000 to over $250,000, depending on the scanning features purchased.
Preparation
A patient undergoing abdominal ultrasound will be advised by his or her physician about what to expect and how to prepare. As mentioned above, preparations generally include fasting.
Aftercare
In general, no aftercare related to the abdominal ultrasound procedure itself is required. Discomfort during the procedure is minimal.
Risks
Properly performed, ultrasound imaging is virtually without risk or side effects.
Results
As a diagnostic imaging technique, a normal abdominal ultrasound is one that indicates the absence of the suspected condition that prompted the scan. For example, symptoms such as abdominal pain radiating to the back suggest the possibility of, among other things, an abdominal aortic aneurysm. An ultrasound scan that indicates the absence of an aneurysm would rule out this life-threatening condition and point to other, less serious causes.
Because abdominal ultrasound imaging is generally undertaken to confirm a suspected condition, the results of a scan often will confirm the diagnosis, be it kidney stones, cirrhosis of the liver, or an aortic aneurysm. At that point, appropriate medical treatment as prescribed by a patient’s physician is in order.
Ultrasound scanning should be performed by a registered and trained ultrasonographer, either a technologist or a physician (radiologist, obstetrician/gynecologist). Ultrasound scanning in the emergency department may be performed by an emergency medicine physician, who should have appropriate training and experience in ultrasonography.

HUMAN ANATOMY

2009-04-03T02:08:00.000-07:00

Human anatomy is the study of the structure of the human body and of its various parts. Physiology is the study of the function of those parts. A complete understanding of anatomy requires knowledge of physiology, and a comprehension of physiology, requires knowledge of anatomy.
Scientific and medical terminology has been developed to accurately explain the location and relationship of the parts of the body. A thorough understanding of these terms, is necessary for a clear comprehension of the location and function of body parts. If you do not know the exact meaning of these terms, you will be unable to successfully master human anatomy and physiology.

RELATIVE POSITIONS
Descriptions of the location of one part of the body in relation to another part of the body utilize terms of relative position. All of these terms assume that the body is in a standard position called the anatomical position. This posture of the body assumes that the body is facing the viewer, arms and legs down, and palms forward (Figure 1.1). Regardless of the actual position of the body and its parts, anatomical terminology is used as if the body were in anatomical position. Note: in anatomical position the body is facing you; therefore, the right side of the body will be on your left.
Anterior and Posterior. In humans the anterior structures are those at the front of the body such as the face and abdomen. The posterior features are those at the rear of the body, for example, the back and buttocks. The terms ventral and dorsal are sometimes used in place of anterior and posterior. Ventral is normally used of four-legged animals to refer to structures underneath, i.e. the belly. The word dorsal refers to the back.
Superior and Inferior. These two terms explain the vertical relationship between body parts. The Latin

SECTIONS
To view internal organs and understand their anatomy it is often helpful to cut or section them. There are three primary ways that an organ or the body can be cut to view its internal structure (Figure 1.3). A sagittal section is a cut which divides the body or organ into right and left portions. A special kind of sagittal section is a cut which passes through the imaginary midline of the body or organ. This cut is termed a midsagittal section. A frontal section is one which divides the structure into anterior and posterior parts (as if one had cut the "front all" off). Finally a transverse or cross section is a cut perpendicular to the midline dividing the body or organ into superior and inferior portions.

ABDOMINAL DIVISIONS
The location of organs which lie in the abdomen can be described using either the names of four quadrants (Figure 1.4A) or nine abdominal regions (Figure 1.4B). The four quadrants are named the upper right, lower right, upper left, and lower left quadrants. Remember that the right side of a body in anatomical position is on your left!
The nine abdominal surface areas are named as follows. The umbilical is located in the central region where the navel lies. Superior to this is the epigastric (epi =Gr. upon; gaster = Gr. belly) and below this is the hypogastric (hypo ■ Gr. under). The upper lateral regions are the right and left hypochondriacs (hypo = Gr. under; chondros Gr. ■ cartilage [of ribs]). (The Greeks thought that disease originated in this region, thus a person with many diseases was a "hypochondriac".) Inferior to the hypochondriac regions, lateral to the umbilicus region, are the two lumbar regions. Inferior to the lumbar regions are the right and left iliac regions. Remember that in anatomical position the right of a body facing you is on your left.

BODY CAVITIES
All of the internal organs (viscera) are located within body cavities (Figure 1.5). The two major cavities are the dorsal cavity and the ventral cavity. The dorsal cavity is divided..................