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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Monday, April 6, 2009
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.
....CLICK HERE TO DOWNLOAD FULL ARTICLE
Patricia Liu, M.D.
Liver function tests are best utilized in concert with the clinical situation and in conjunction with serial determinations to ascertain the cause or evolution of the hepatic disorder. In addition, stool and urine tests, radionuclide imaging, contrast cholangiography (transhepatic cholangiography and endoscopic retrograde cholangiopancreatography), and histological assessment (liver biopsy) are often utilized to delineate the nature of the liver disease.
Serum Enzymes (Serum Aminotransferase Transaminases)
Serum glutamic oxaloacetic transaminase, also referred to as aspartate aminotransferase, and serum glutamic pyruvic transaminase, also called alanine aminotransferase (AST and ALT) are commonly employed to ascertain liver function. Striking elevations in the serum levels of these two enzymes are encountered in acute viral hepatitis, acute drug- or toxin-induced liver damage, and ischemic hepatitis. In addition, levels exceeding 500 IU/L and, on rare occasions, 1,000 IU/L can also be seen in patients with severe chronic active hepatitis, transiently in patients with common bile duct stones, and in patients with Budd-Chiari and veno-occlusive disease.
There are a number of important hepatic disorders in which the serum AST and ALT are normal or minimally elevated . These include idiopathic genetic hemochromatosis, methotrexate-induced liver injury, liver dysfunction due to amiodarone, the liver disease associated with jejunal ileal bypass surgery, and patients with chronic hepatitis C virus infection.
The ratio of AST and ALT is also sometimes of value in clinical practice. A ratio greater than 2 with both AST and ALT being less than 300 IU/L is characteristic of alcoholic liver disease.
On rare occasions, if both the AST and ALT are elevated, patients are subjected to a liver biopsy after a very thorough serologic workup only to find that the liver histology is completely normal. It is very important to exclude a primary muscle disorder in such patients since not only the AST but also the ALT can be elevated in patients with muscle disorders.
Serum Alkaline Phosphatase
The sources of serum alkaline phosphatase include liver, bone, small intestine, placenta, and, on rare occasions, tumors capable of producing alkaline phosphatase.
In general, patients with cholestasis have increased levels. However, the level of serum alkaline phosphatase is not helpful in distinguishing intrahepatic from extrahepatic cholestasis. Rarely, patients with hypernephroma and Hodgkin's disease have elevated levels in the absence of liver involvement. Also, patients with Wilson's disease often have normal values.
....CLICK HERE TO DOWNLOAD FULL ARTICLE
Intestinal Obstruction in the Newborn
Obstruction of an infant's gastrointestinal (GI) tract can occur anywhere from the esophagus to the anus. For purposes of this review, the newborn infant will be defined as an infant from birth to 30 days of age. Both congenital and acquired obstructions will be addressed. In each instance, the epidemiology, pathogenesis, clinical aspects, and management of the disorder will be considered.
Esophageal Atresia
EPIDEMIOLOGY AND PATHOGENESIS
Esophageal atresia, or interruption of the esophagus, generally occurs in association with a tracheoesophageal fistula (EA -- TEF). The most common anatomic arrangement is a blind proximal esophageal pouch that has a distal tracheoesophageal fistula (Figure 1). This is seen in 85% to 90% of infants who have this anomaly. Seen less commonly is pure esophageal atresia that does not have a tracheoesophageal fistula and tracheoesophageal fistula that does not have an esophageal atresia (H-type tracheoesophageal fistula). These latter two conditions occur in approximately 10% of newborns who have these types of anomalies. Other anatomic arrangements, such as an esophageal atresia that has a fistula between the upper pouch and trachea or esophageal atresia that has a fistula to both pouches, are seen in only a tiny fraction of these infants.
EA -- TEF occurs in approximately 1 in 4000 live births. There have been numerous reports of siblings who have EA -- TEF as well as reports of the anomaly in identical twins. Also reported, however, are many instances of identical twins in which one has the anomaly and the other has been spared. It is well recognized that esophageal atresia is a frequent component of the VATER association as well as other malformations, suggesting that the anomaly also might result from a specific teratogen in the developing fetus.
It commonly is believed that interruption of the events responsible for the elongation and separation of the esophageal and tracheal tubes during the fourth week of development leads to the development of this anomaly.
PRESENTATION
Infants who have EA -- TEF commonly will present in the nursery having an excessive amount of saliva. The saliva pools in the blind proximal esophageal pouch and is either regurgitated or continuously dribbled from the infant's mouth. The infant's first feeding will not be tolerated; the formula, which is, of course, not bile-stained, will be regurgitated immediately. Because these infants most commonly have a distal tracheoesophageal fistula, air enters their GI tracts through the fistula, and the abdomen will not be scaphoid. Indeed, the infant who is ventilated may well have air forced into his or her GI tract via the fistula, causing distension. Such an infant's respiratory difficulty, thus, may be compounded by the gastric distention leading to diaphragmatic elevation. In pure esophageal atresia that has no fistula, no air will enter the GI tract, and the infant will have a scaphoid abdomen.
DIAGNOSIS
The diagnosis of esophageal atresia can be made by attempting to pass a firm catheter through the mouth and into the esophagus. Obstruction to passage of the catheter, which should not be "forced," suggests the anomaly, and a chest radiograph usually will confirm the diagnosis via the presence of the coiled catheter sitting within the proximal esophageal pouch. Air injected into the catheter provides an excellent "contrast" agent to help confirm the diagnosis. The use of a true contrast agent generally is not recommended because the infant will be at risk of aspirating the agent and acquiring a chemical pneumonitis. In the rare instance in which contrast is required, 1 mL or less of a water-soluble agent can be injected into the pouch and then withdrawn immediately once the diagnosis has been confirmed. Air in the GI tract confirms the presence of the distal tracheoesophageal fistula.
MANAGEMENT
Appropriate management of these babies begins at the time of diagnosis. A significant risk to the infants is the potential for gastric juice to pass upward in the distal esophagus and traverse the tracheoesophageal fistula where it may be aspirated, resulting in the development of chemical pneumonitis. These infants need to have a sump catheter placed immediately into the upper pouch and into the head up position at an angle of at least 45 degrees. This will help minimize the aspiration of saliva and the chance of gastric juice soiling the lungs.
As a general rule, all newborns whose GI tracts are obstructed should have intravenous fluids instituted and antibiotics begun. If the neonate is not at a surgical center, transport needs to be arranged as soon as possible.
In infants who have EA -- TEF, immediate primary repair generally is undertaken in those weighing as little as 1200 g. An infant presenting with significant pneumonia or other major congenital anomalies will require a more individualized approach; a staged repair via an initial gastrostomy may be performed in an infant who has EA -- TEF and is ill. The infant can be allowed to improve or to be evaluated for other anomalies prior to performing definitive repair.
Infants who have pure esophageal atresia generally are unable to have a primary repair performed in the newborn period because the distance between the two ends of the esophagus is too great. These infants require a gastrostomy and either exteriorization of the esophagus with a later esophageal substitution procedure (reverse gastric tube, colon interposition) or serial attempts at dilatation of the two ends of the esophagus with a later attempt at a primary anastomosis. Although conceptually more attractive, the latter option requires a prolonged initial hospitalization and has an attendant ongoing risk of aspiration.
The prognosis for most babies is excellent; only a few sick infants who have serious coexisting anomalies, are of extreme low birth weight, and have persistent pulmonary disease have a diminished chance for survival. It is not at all uncommon for the infant to develop a relative narrowing or stricturing at the anastomotic site, which does not become evident until the child is advanced to solid foods. Generally, this problem is managed easily with esophageal dilatation. The infants also may have problems with esophageal motility that mimics a stricture. This is determined easily by a contrast swallow radiograph.
....CLICK HERE TO DOWNLOAD FULL ARTICLE
Esophageal Atresia
EPIDEMIOLOGY AND PATHOGENESIS
Esophageal atresia, or interruption of the esophagus, generally occurs in association with a tracheoesophageal fistula (EA -- TEF). The most common anatomic arrangement is a blind proximal esophageal pouch that has a distal tracheoesophageal fistula (Figure 1). This is seen in 85% to 90% of infants who have this anomaly. Seen less commonly is pure esophageal atresia that does not have a tracheoesophageal fistula and tracheoesophageal fistula that does not have an esophageal atresia (H-type tracheoesophageal fistula). These latter two conditions occur in approximately 10% of newborns who have these types of anomalies. Other anatomic arrangements, such as an esophageal atresia that has a fistula between the upper pouch and trachea or esophageal atresia that has a fistula to both pouches, are seen in only a tiny fraction of these infants.
EA -- TEF occurs in approximately 1 in 4000 live births. There have been numerous reports of siblings who have EA -- TEF as well as reports of the anomaly in identical twins. Also reported, however, are many instances of identical twins in which one has the anomaly and the other has been spared. It is well recognized that esophageal atresia is a frequent component of the VATER association as well as other malformations, suggesting that the anomaly also might result from a specific teratogen in the developing fetus.
It commonly is believed that interruption of the events responsible for the elongation and separation of the esophageal and tracheal tubes during the fourth week of development leads to the development of this anomaly.
PRESENTATION
Infants who have EA -- TEF commonly will present in the nursery having an excessive amount of saliva. The saliva pools in the blind proximal esophageal pouch and is either regurgitated or continuously dribbled from the infant's mouth. The infant's first feeding will not be tolerated; the formula, which is, of course, not bile-stained, will be regurgitated immediately. Because these infants most commonly have a distal tracheoesophageal fistula, air enters their GI tracts through the fistula, and the abdomen will not be scaphoid. Indeed, the infant who is ventilated may well have air forced into his or her GI tract via the fistula, causing distension. Such an infant's respiratory difficulty, thus, may be compounded by the gastric distention leading to diaphragmatic elevation. In pure esophageal atresia that has no fistula, no air will enter the GI tract, and the infant will have a scaphoid abdomen.
DIAGNOSIS
The diagnosis of esophageal atresia can be made by attempting to pass a firm catheter through the mouth and into the esophagus. Obstruction to passage of the catheter, which should not be "forced," suggests the anomaly, and a chest radiograph usually will confirm the diagnosis via the presence of the coiled catheter sitting within the proximal esophageal pouch. Air injected into the catheter provides an excellent "contrast" agent to help confirm the diagnosis. The use of a true contrast agent generally is not recommended because the infant will be at risk of aspirating the agent and acquiring a chemical pneumonitis. In the rare instance in which contrast is required, 1 mL or less of a water-soluble agent can be injected into the pouch and then withdrawn immediately once the diagnosis has been confirmed. Air in the GI tract confirms the presence of the distal tracheoesophageal fistula.
MANAGEMENT
Appropriate management of these babies begins at the time of diagnosis. A significant risk to the infants is the potential for gastric juice to pass upward in the distal esophagus and traverse the tracheoesophageal fistula where it may be aspirated, resulting in the development of chemical pneumonitis. These infants need to have a sump catheter placed immediately into the upper pouch and into the head up position at an angle of at least 45 degrees. This will help minimize the aspiration of saliva and the chance of gastric juice soiling the lungs.
As a general rule, all newborns whose GI tracts are obstructed should have intravenous fluids instituted and antibiotics begun. If the neonate is not at a surgical center, transport needs to be arranged as soon as possible.
In infants who have EA -- TEF, immediate primary repair generally is undertaken in those weighing as little as 1200 g. An infant presenting with significant pneumonia or other major congenital anomalies will require a more individualized approach; a staged repair via an initial gastrostomy may be performed in an infant who has EA -- TEF and is ill. The infant can be allowed to improve or to be evaluated for other anomalies prior to performing definitive repair.
Infants who have pure esophageal atresia generally are unable to have a primary repair performed in the newborn period because the distance between the two ends of the esophagus is too great. These infants require a gastrostomy and either exteriorization of the esophagus with a later esophageal substitution procedure (reverse gastric tube, colon interposition) or serial attempts at dilatation of the two ends of the esophagus with a later attempt at a primary anastomosis. Although conceptually more attractive, the latter option requires a prolonged initial hospitalization and has an attendant ongoing risk of aspiration.
The prognosis for most babies is excellent; only a few sick infants who have serious coexisting anomalies, are of extreme low birth weight, and have persistent pulmonary disease have a diminished chance for survival. It is not at all uncommon for the infant to develop a relative narrowing or stricturing at the anastomotic site, which does not become evident until the child is advanced to solid foods. Generally, this problem is managed easily with esophageal dilatation. The infants also may have problems with esophageal motility that mimics a stricture. This is determined easily by a contrast swallow radiograph.
....CLICK HERE TO DOWNLOAD FULL ARTICLE
Infectious Diseases
HHV-6 and HHV-7 actually causes infection at a little older age and
more towards the second year of life rather than the first year of life
as we see with HHV-6.
HHV-8 doesn't affect many children. In the past couple of years it has
been described and identified. it is nearly
universally present in all cases of Kaposi's sarcoma tissues. It is also found in AIDS related B- cell
lymphomas that are based in body cavities, and many of those had coinfection with Epstein-Barr virus it isthought that it may actually be necessary to have the HHV-8 for transformation of a
precursor cell that proliferates monoclonally and causes these tumors.
Focusing on HHV-6, a little about the epidemiology and transmission. Roseola was first described in 1913. In 1950, transmissibility
was actually demonstrated although it wasn't until 1986 that the
particular virus was identified. We know that we see these infections year-round and there is worldwide distribution. There is antibody present in 85% of pregnant women with active transport across the placenta. Hence, in the very early weeks, the infants are protected. The antibody declines in the first five months of life to a low of 6%,
then increases to its highest seroprevalence of 86% at one year. So,
by one year of age, most infants have an HHV-6 infection. Titers fall after 40 years of age and there is increased prevalence of IgM six months to one year of age. Saliva is the most likely route of transmission. There is no congenital/perinatal symptom that has been described, and this virus has not been found in breast milk.
....CLICK HERE TO DOWNLOAD FULL ARTICLE
more towards the second year of life rather than the first year of life
as we see with HHV-6.
HHV-8 doesn't affect many children. In the past couple of years it has
been described and identified. it is nearly
universally present in all cases of Kaposi's sarcoma tissues. It is also found in AIDS related B- cell
lymphomas that are based in body cavities, and many of those had coinfection with Epstein-Barr virus it isthought that it may actually be necessary to have the HHV-8 for transformation of a
precursor cell that proliferates monoclonally and causes these tumors.
Focusing on HHV-6, a little about the epidemiology and transmission. Roseola was first described in 1913. In 1950, transmissibility
was actually demonstrated although it wasn't until 1986 that the
particular virus was identified. We know that we see these infections year-round and there is worldwide distribution. There is antibody present in 85% of pregnant women with active transport across the placenta. Hence, in the very early weeks, the infants are protected. The antibody declines in the first five months of life to a low of 6%,
then increases to its highest seroprevalence of 86% at one year. So,
by one year of age, most infants have an HHV-6 infection. Titers fall after 40 years of age and there is increased prevalence of IgM six months to one year of age. Saliva is the most likely route of transmission. There is no congenital/perinatal symptom that has been described, and this virus has not been found in breast milk.
....CLICK HERE TO DOWNLOAD FULL ARTICLE
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.
....CLICK HERE TO DOWNLOAD FULL ARTICLE
I. Pathophysiology
A. The clinical term "red eye" is applied to a variety of distinct infectious or inflammatory
diseases of the eye. Conjunctivitis is the most common cause of red eye. Conjunctivitis
consists of inflammation of the conjunctiva, which is caused by a broad group of conditions.
The inflammation can be infectious or noninfectious in origin.
B. Most frequently, conjunctivitis is caused by a bacterial or viral infection. Sexually
transmitted diseases such as chlamydial infection and gonorrhea are less common causes
of conjunctivitis. Ocular allergy is a major cause of chronic conjunctivitis.
II. Clinical Evaluation of Conjunctivitis
A. An ocular, medical and medication history should establish whether the condition is acute,
subacute, chronic or recurrent, whether it is unilateral or bilateral.
B. Discharge
1. A serous discharge (watery) is most commonly associated with viral or allergic ocular
conditions.
2. A mucoid (stringy or ropy) discharge is highly characteristic of allergy or dry eyes.
3. A mucopurulent or purulent discharge, often associated with morning crusting and
difficulty opening the eyelids, strongly suggests a bacterial infection. The possibility of
Neisseria gonorrhoeae infection should be considered when the discharge is copiously
purulent.
C. Itching is highly suggestive of allergic conjunctivitis. In general, a red eye in the absence
of itching is not caused by ocular allergy. A history of recurrent itching or a personal or
family history of hay fever, allergic rhinitis, asthma or atopic dermatitis is also consistent
with an ocular allergy.
D. Unilateral or Bilateral Conjunctivitis
1. Allergic conjunctivitis is almost always secondary to environmental allergens and,
therefore, usually presents with bilateral symptoms. Infections caused by viruses and
bacteria are transmissible by eye-hand contact. Often, these infections initially
present in one eye, with the second eye becoming involved a few days later.
2. Pain, Photophobia and Blurred Vision
a. Pain and photophobia do not usually occur with conjunctivitis, and these findings
suggest an ocular or orbital disease processes, including uveitis, keratitis, acute
glaucoma and orbital cellulitis.
....CLICK HERE TO DOWNLOAD FULL ARTICLE
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