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
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Monday, April 6, 2009
Viral Hepatitis Update
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.
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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.
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Surgery Documentation
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.
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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.
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Pediatric History
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.
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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.
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Outpatient and Primary Care Medicine
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.
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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.
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Nutrition Infant
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
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
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.
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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.
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Newborn Care
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.
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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.
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Manual of HIV AIDS
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
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.
Lung Cancer
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.
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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.
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Liver Disease
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.
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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.
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Intestinal Obstruction in the Newborn
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.
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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.
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Infectious Diseases
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.
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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.
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Sunday, April 5, 2009
Infectious Conjunctivitis
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.
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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.
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History and Physical Exam
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).
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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).
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Herpes Simplex Infections
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
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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
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Head Injury
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.)
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
Rosacea
Impetigo
Superficial honey-colored serous crusts are characteristic of this disorder. It is usually caused by a staphylococcus infection. Culture is rarely reliable.
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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.
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.
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.
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Gynecology and Obstetrics
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,
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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,
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Genetics and Fetal Development
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.
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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.
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General Pediatrics 2
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.
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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.
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Family Medicine
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.
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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.
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Emergency Care - Injuries - Poisonings
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.
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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.
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Critical Care Medicine
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).
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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).
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Child Maltreatment and Abusebuse
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.
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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.
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Chemotherapy
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
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
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.
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.
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