PEDIATRIC TIP In children younger than age 2, fever, vomiting, nonspecific abdominal complaints, or failure to thrive may be the only signs of acute pyelonephritis.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Nephrotic syndrome:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
The dominant clinical feature of nephrotic syndrome is mild to severe dependent edema of the ankles or sacrum, or periorbital edema, especially in children. Edema may lead to ascites, pleural effusion, and swollen external genitalia. Accompanying symptoms may include orthostatic hypotension, lethargy, anorexia, depression, and pallor. Major complications are malnutrition, infection, coagulation disorders, thromboembolic vascular occlusion, and accelerated atherosclerosis.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Acute respiratory failure in COPD:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
In patients who have COPD with ARF, increased ventilation-perfusion mismatch and reduced alveolar ventilation decrease PaO2 (hypoxemia) and increase Paco2 (hypercapnia). This rise in carbon dioxide (CO2) lowers the pH. The resulting hypoxemia and acidemia affect all body organs, especially the CNS and the respiratory and cardiovascular systems.
Specific symptoms vary with the underlying cause of ARF but may include these systems:
❑ Respiratory — Rate may be increased, decreased, or normal depending on the cause; respirations may be shallow, deep, or alternate between the two; and air hunger may occur. Cyanosis may or may not be present, depending on the hemoglobin (Hb) level and arterial oxygenation. Auscultation of the chest may reveal crackles, rhonchi, wheezing, or diminished breath sounds.
❑ CNS — When hypoxemia and hypercapnia occur, the patient may show evidence of restlessness, confusion, loss of concentration, irritability, tremulousness, diminished tendon reflexes, and papilledema; he may slip into a coma.
❑ Cardiovascular — Tachycardia, with increased cardiac output and mildly elevated blood pressure secondary to adrenal release of catecholamine, occurs early in response to low PaO2. With myocardial hypoxia, arrhythmias may develop. Pulmonary hypertension, secondary to pulmonary capillary vasoconstriction, may cause increased pressures on the right side of the heart, elevated jugular veins, an enlarged liver, and peripheral edema. Stresses on the heart may precipitate cardiac failure.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Infant respiratory distress syndrome:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
Although a neonate with IRDS may breathe normally at first, he usually develops rapid, shallow respirations within minutes or hours of birth, with intercostal, subcostal, or sternal retractions, nasal flaring, and audible expiratory grunting. This grunting is a natural compensatory mechanism designed to produce positive end-expiratory pressure (PEEP) and prevent further alveolar collapse.
Severe disease is marked by apnea, bradycardia, and cyanosis (from hypoxemia, left-to-right shunting through the foramen ovale, or right-to-left intrapulmonary shunting through atelectatic regions of the lung). Other clinical features include pallor, frothy sputum, and low body temperature as a result of an immature nervous system and the absence of subcutaneous fat.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Acute poststreptococcal glomerulonephritis:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
APSGN begins within 1 to 3 weeks after untreated pharyngitis. Symptoms include mild to moderate edema, oliguria (less than 400 ml/24 hours), proteinuria, azotemia, hematuria, and fatigue. Mild to severe hypertension may result from either sodium or water retention (due to decreased GFR) or inappropriate renin release. Heart failure from hypervolemia leads to pulmonary edema.
PEDIATRIC TIP The presenting features of APSGN in children may be encephalopathy with seizures and focal neurological deficits.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Acute respiratory distress syndrome:
Signs and Symptoms
(Professional Guide to Diseases (Eighth Edition))
Rapid, shallow breathing; dyspnea, crackles, rhonchi; hypoxemia; bilateral infiltrates on chest X-ray
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Acute respiratory failure:
Signs and Symptoms
(Professional Guide to Diseases (Eighth Edition))
Shallow or deep respirations (or both), air hunger, cyanosis, adventitious breath sounds, confusion, decreased level of consciousness, tachycardia, pulmonary hypertension, irritability, decreased reflexes
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Respiratory alkalosis:
Signs and Symptoms
(Professional Guide to Diseases (Eighth Edition))
Deep, rapid breathing; dizziness; agitation; circumoral and peripheral paresthesia; carpopedal spasms; twitching; muscle weakness; seizures; arrhythmias
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Respiratory syncytial virus infection:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
Clinical features of RSV infection vary in severity from mild, coldlike symptoms to bronchiolitis or bronchopneumonia and, in a few patients, severe, life-threatening lower respiratory tract infections. Symptoms usually include coughing, wheezing, malaise, pharyngitis, dyspnea, and inflamed mucous membranes in the nose and throat. Reinfection is common, producing milder symptoms than the primary infection.
Otitis media is a common complication of RSV in infants. RSV has also been identified in patients with a variety of central nervous system disorders, such as meningitis and myelitis.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Chronic glomerulonephritis:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
Chronic glomerulonephritis typically develops insidiously and asymptomatically, usually over many years. At any time, however, it may suddenly become progressive, producing nephrotic syndrome, hypertension, proteinuria, and hematuria. In late stages of progressive chronic glomerulonephritis, it may accelerate to uremic symptoms, such as azotemia, nausea, vomiting, pruritus, dyspnea, malaise, and fatigability. Mild to severe edema and anemia may accompany these symptoms. Severe hypertension may cause cardiac hypertrophy, leading to heart failure, and may accelerate the development of advanced renal failure, eventually necessitating dialysis or transplantation.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Severe acute respiratory syndrome:
Signs and symptoms
(Professional Guide to Diseases (Eighth Edition))
The incubation period for SARS is typically 3 to 5 days but may last as long as 14 days. Initial signs and symptoms include fever, shortness of breath and other minor respiratory symptoms, general discomfort, headache, rigors, chills, myalgia, sore throat, and dry cough. Some individuals may develop diarrhea or a rash. Later complications include respiratory failure, liver failure, heart failure, myelodysplastic syndromes, and death.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Respiratory acidosis:
Signs and Symptoms
(Professional Guide to Diseases (Eighth Edition))
Confusion, apprehension, asterixis, coma, headache, dyspnea, tachypnea, papilledema, depressed reflexes, tachycardia, hypertension or hypotension, arrhythmias, vasodilation
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Nephrotic syndrome:
Signs and symptoms
(Handbook of Diseases)
The dominant sign of nephrotic syndrome is mild to severe dependent edema of the ankles or sacrum, or periorbital edema, especially in children. Such edema may lead to ascites, pleural effusion, weight gain, and high blood pressure. (See Pathophysiology of nephrotic syndrome.)
Accompanying signs and symptoms include orthostatic hypotension, lethargy, anorexia, depression, and pallor. Major complications are malnutrition, infection, coagulation disorders, thromboembolic vascular occlusion, and accelerated atherosclerosis.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Acute respiratory failure in COPD:
Signs and symptoms
(Handbook of Diseases)
In COPD patients with ARF, increased ventilation-perfusion mismatching and reduced alveolar ventilation decrease Pao2 (hypoxemia) and increase Paco2 (hypercapnia). This rise in carbon dioxide tension lowers the pH. The resulting hypoxemia and acidemia affect all body organs, especially the central nervous, respiratory, and cardiovascular systems. Specific symptoms vary with the underlying cause of ARF but can include any of the following:
Respiratory symptoms. The respiratory rate may be increased, decreased, or normal, depending on the cause; respirations may be shallow or deep, or they may alternate between the two; and air hunger may occur. Cyanosis may or may not be present, depending on the hemoglobin (Hb) level and arterial oxygenation. Auscultation of the chest may reveal crackles, rhonchi, wheezes, or diminished breath sounds.
CNS symptoms. The patient may show evidence of restlessness, confusion, loss of concentration, irritability, tremulousness, diminished tendon reflexes, and papilledema; he may slip into a coma.
Cardiovascular symptoms. Tachycardia, with increased cardiac output and mildly elevated blood pressure secondary to adrenal release of catecholamines, occurs early in response to a low Pao2.With myocardial hypoxia, arrhythmias may develop. Pulmonary hypertension also occurs.
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Source: Handbook of Diseases, 2003
Respiratory alkalosis:
Signs and symptoms
(Handbook of Diseases)
The cardinal sign of respiratory alkalosis is deep, rapid breathing, possibly exceeding 40 breaths/minute and much like the Kussmaul’s respirations that characterize diabetic acidosis.
Such hyperventilation usually leads to CNS and neuromuscular disturbances, such as light-headedness or dizziness (from below-normal carbon dioxide levels that decrease cerebral blood flow), agitation, circumoral and peripheral paresthesia, carpopedal spasms, twitching (possibly progressing to tetany), and muscle weakness. Severe respiratory alkalosis may cause cardiac arrhythmias that fail to respond to conventional treatment, seizures, or both.
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Source: Handbook of Diseases, 2003
Respiratory distress syndrome:
Signs and symptoms
(Handbook of Diseases)
Although a neonate with respiratory distress syndrome may breathe normally at first, he usually develops rapid, shallow respirations within minutes or hours of birth, with intercostal, subcostal, or sternal retractions; nasal flaring; and audible expiratory grunting. This grunting is a natural compensatory mechanism designed to produce positive end-expiratory pressure (PEEP) and prevent further alveolar collapse.
The neonate may also display hypotension, peripheral edema, and oliguria; if he has severe disease, apnea, bradycardia, and cyanosis (from hypoxemia, left-to-right shunting through the foramen ovale, or right-to-left shunting through atelectatic regions of the lung) may be present. Other signs and symptoms include pallor, frothy sputum, and low body temperature as a result of an immature nervous system and the absence of subcutaneous fat.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Respiratory syncytial virus infection:
Signs and symptoms
(Handbook of Diseases)
Signs and symptoms of RSV infection vary in severity, ranging from mild coldlike symptoms to bronchiolitis or bronchopneumonia and, in a few patients, severe, life-threatening lower respiratory tract infections. Generally, signs and symptoms include coughing, wheezing, malaise, pharyngitis, dyspnea, and inflamed mucous membranes in the nose and throat.
Otitis media is a common complication of RSV in infants. RSV has also been identified in patients with various central nervous system disorders, such as meningitis and myelitis.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Pyelonephritis, acute:
Signs and symptoms
(Handbook of Diseases)
Typical clinical features include urgency, frequency, burning during urination, dysuria, nocturia, and hematuria (usually microscopic but may be gross). Urine may appear cloudy and have an ammoniacal or fishy odor. Other common symptoms include a temperature of 102° F (38.9° C) or higher, shaking chills, flank pain, anorexia, and general fatigue.
These signs and symptoms characteristically develop rapidly over a few hours or a few days. Although these symptoms may disappear within days, even without treatment, residual bacterial infection is likely and may cause later recurrence of symptoms.
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Source: Handbook of Diseases, 2003
Respiratory acidosis:
Signs and symptoms
(Handbook of Diseases)
Acute respiratory acidosis produces CNS disturbances that reflect changes in the pH of cerebrospinal fluid rather than increased carbon dioxide levels in cerebral circulation.
Effects range from restlessness, confusion, and apprehension to somnolence, with a fine or flapping tremor (asterixis), or coma. The patient may complain of headaches and exhibit dyspnea and tachypnea with papilledema and depressed reflexes. Unless the patient is receiving oxygen, hypoxemia accompanies respiratory acidosis.
This disorder may also cause cardiovascular abnormalities, such as tachycardia, hypertension, atrial and ventricular arrhythmias and, in severe acidosis, hypotension with vasodilation (bounding pulses and warm periphery).
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Glomerulonephritis:
Glomerulonephritis - signs & symptoms
(The 5-Minute Pediatric Consult)
- Macroscopic hematuria (dark brown urine)
- Sore throat
- Impetigo
- A prior upper respiratory infection that persists at least 1 week or skin lesions in the proceeding 3–4 weeks suggests acute poststreptococcal glomerulonephritis.
- An upper respiratory infection in the previous few days suggests IgA nephropathy.
- Reduced output of urine
- Dyspnea, fatigue, lethargy
- Headache
- Seizures (hypertensive encephalopathy)
- Symptoms of a systemic disease such as fever, rash (especially on the buttocks and legs, posteriorly), arthralgia, and weight loss
» READ BOOK EXCERPT ONLINE »
Source: The 5-Minute Pediatric Consult, 2008
Article Excerpts About Symptoms of Wegener's granulomatosis:
The initial symptoms of Wegener's granulomatosis are often
vague or nonspecific and frequently include upper respiratory
tract symptoms, joint pains, weakness, and fatigue.
Upper respiratory tract. The most common sign of
Wegener’s granulomatosis is involvement of the upper respiratory
tract, which occurs in nearly all patients. Symptoms include sinus
pain, discolored or bloody nasal drainage and, occasionally, nasal
ulcerations. A common manifestation of the disease is persistent
rhinorrhea ("runny nose") or other cold symptoms that do not
respond to standard treatment or that become progressively worse.
Rhinorrhea can result from nasal inflammation or sinus drainage
and can cause pain. A hole or perforation of the nasal septum may
develop, and collapse of the nasal bridge (called saddlenose
deformity) may occur in some individuals. Blockage of the
eustachian tubes, which are important for normal ear function, may
cause chronic ear problems and hearing loss. A secondary bacterial
infection can cause Wegener’s-related sinusitis (inflammation of
the sinuses) with congestion and chronic sinus pain.
Lungs.The lungs are affected in most patients with
Wegener’s granulomatosis, although no symptoms may be present. If
symptoms are present, they include cough, hemoptysis (coughing up
of blood), shortness of breath, and chest discomfort.
Kidneys.Kidney involvement, which occurs in more than
three-fourths of patients, usually does not cause symptoms. If
detected by blood tests, proper treatment can be started,
preventing long-term damage to the kidneys.
Musculoskeletal system.Pain in the muscles and joints
or, occasionally, joint swelling affects two-thirds of patients
with Wegener’s granulomatosis. Although joint pain can be very
uncomfortable, it does not lead to permanent joint damage or
deformities.
Eyes.Wegener’s granulomatosis can affect the eyes in
several ways. Patients may develop conjunctivitis (inflammation of
the conjunctiva, the inner lining of the eyelid), scleritis
(inflammation of the scleral layer, the white part of the
eyeball), episcleritis (inflammation of the episcleral layer, the
outer surface of the sclera), or as an orbital mass lesion (sore
behind the eye globe). The symptoms of eye involvement include
redness, burning or pain in the eye. Double vision or a decrease
in vision are serious symptoms requiring immediate medical
attention.
Skin lesions.Nearly half of people with Wegener’s
granulomatosis develop skin lesions. These small red or purple
raised areas or blister-like lesions, ulcers, or nodules may or
may not be painful.
Other symptoms.Some patients
experience narrowing of the trachea (subglottic stenosis).
The symptoms can include voice change, hoarseness, shortness of
breath, or cough.
The nervous system and heart occasionally may be
affected. Fever and night sweats also may occur. However,
fever also may signal an underlying infection, often of the upper
respiratory tract.
Diagnosis
To treat people with Wegener’s granulomatosis most effectively,
doctors must diagnose the disease early in its course. There are
no blood tests that a doctor can use to diagnose Wegener’s
granulomatosis, but blood tests are important to rule out other
causes of illness and to determine which organ sites may be
affected. Most blood tests are nonspecific and can only suggest
that a person has an inflammatory process. Anemia (low red blood
cell count), elevated white blood cell count and platelet count,
and an elevated sedimentation rate are commonly found in people
with Wegener’s granulomatosis. If the kidneys are involved, red
blood cells and structures called red blood cell casts are visible
in the urine when viewed under a microscope, and the blood tests
measuring kidney function (creatinine and BUN) may show
abnormalities.
X-ray results can be very helpful in diagnosing Wegener’s
granulomatosis. People with lung involvement will have abnormal
chest x-rays, which may show one or many fluffy infiltrates, solid
nodules, or cavities. Sinus x-rays or computed tomography (CT)
scans in people with sinus involvement may show thickening of the
sinus lining.
Many patients with active Wegener's granulomatosis have a blood
test that reveals the presence of a specific type of antibody
called antineutrophil cytoplasmic antibodies (ANCA) (an antibody
is a disease-fighting protein). Although a positive ANCA test is
useful in supporting a suspected diagnosis of Wegener’s
granulomatosis, in most instances it is not used by itself to make
a diagnosis of this disorder. The ANCA test may be negative in
some patients with active Wegener’s granulomatosis.
Currently, the only definite way to diagnose Wegener’s
granulomatosis is by performing a biopsy of an involved organ site
(usually the sinuses, lung, or kidney). The tissue is examined
under the microscope to confirm the presence of vasculitis and
granulomas (a specific type of inflammation), which together are
diagnostic features of the disease. A biopsy is very important
both to confirm the presence of Wegener’s granulomatosis and also
to assure the absence of other disorders that may have similar
signs and symptoms.
Treatment
With the appropriate treatment, the outlook is good for
patients with Wegener’s granulomatosis. In a study of 158 patients
who were treated at the National Institutes of Health (NIH), 91
percent of them markedly improved. After 6 months to 24 years of
follow-up, 80 percent of the patients survived.
In most cases, standard therapy consists of a combination of a
glucocorticoid drug that reduces inflammation and a cytotoxic drug
that interferes with the abnormal growth of cells.
Prednisone is the most common glucocorticoid drug (a steroid)
that is used. Prednisone is similar to hydrocortisone, the natural
glucocorticoid hormone produced by the body. It is chemically
different from the anabolic steroids that have been used by
athletes and is given in doses much higher than the body normally
produces. Prednisone is usually administered as a single morning
dose in an attempt to imitate how the body normally secretes
hydrocortisone. When the person’s illness improves, the prednisone
dose is gradually decreased and converted to an every other day
dosing schedule, usually over a period of 3 to 4 months. With
further improvement in the disease, the prednisone is very
gradually decreased and discontinued completely after
approximately 6 to 12 months. When prednisone is taken by mouth,
the body stops making its own natural hydrocortisone. As the
prednisone dose is gradually reduced the body will resume making
hydrocortisone again. It is extremely important that prednisone
never be stopped suddenly because the body requires prednisone (or
hydrocortisone) for its function and may not be able to
immediately make what it needs.
Cyclophosphamide (CytoxanÔ) is the most commonly used cytotoxic
drug. Cyclophosphamide is taken once a day by mouth. It is
important for a patient to take the drug all at once in the
morning followed by drinking a large amount of fluid. Although the
initial dose of cyclophosphamide is based on the patient’s weight
and kidney function, the doctor may adjust the dosage based on the
blood counts, which are monitored closely to be sure that the
white blood cell count is maintained at a safe level.
Cyclophosphamide is continued for a full year beyond that point at
which the disease has become quiet (is in remission). The dose of
cyclophosphamide is then decreased gradually and eventually
discontinued.
Cyclophosphamide and prednisone are both powerful drugs that
suppress the immune system. Although these medications are
beneficial in treating Wegener’s granulomatosis, patients and
their doctors should be aware that the drugs potentially have
serious side effects. Careful monitoring by the doctor is very
important. Because these drugs suppress the immune system, they
can affect the body’s ability to fight off infection. Patients
should report immediately any symptoms of infection and,
specifically, any fever to their doctors. Prednisone can cause
weight gain, cataracts, brittle bones, diabetes, and alterations
in mood and personality. Cyclophosphamide can cause bone marrow
suppression (lowering of blood counts), sterility, hemorrhagic
cystitis (bleeding from the bladder) as well as other serious side
effects.
Approximately half of people with Wegener’s granulomatosis may
experience a return (relapse) of their disease. This occurs most
frequently within two years of stopping medication, but
potentially can occur at any point both during treatment or after
stopping treatment. Thus, it is extremely important that patients
continue to see their physicians regularly, both while they are on
these medications, as well as after the medications have been
stopped. Even while on medication, many patients are able to lead
relatively normal lives and will remain in remission after therapy
has been stopped completely.
Research
Since the 1970s, research physicians at the National Institute
of Allergy and Infectious Diseases (NIAID), a component of NIH,
have been interested in Wegener’s granulomatosis. NIAID scientists
first introduced the combination of a glucocorticoid with
cyclophosphamide for treating people with this disease. This
dramatic breakthrough remains the standard of treatment. Despite
this, researchers realize that these medicines have serious side
effects and cannot be tolerated by all people. Therefore, NIH
researchers continue to study Wegener’s granulomatosis to
understand the causes of the disease and to develop new
treatments. NIAID is conducting several studies to investigate new
treatment regimens. These studies each have individual entry
criteria but are open to patients who have a definitive diagnosis
of Wegener’s granulomatosis and who have active disease.
Further Information
For information about enrolling in an NIAID clinical study at
NIH's facility in Bethesda, Maryland, the patient's personal
physician should call or write to:
Dr. Michael C. Sneller
Head, Immunologic Diseases
Section
or
Dr. Carol A. Langford
Immunologic Diseases
Section
Laboratory of Immunoregulation
National Institute of
Allergy and Infectious Diseases
National Institutes of
Health
Building 10, Room 11B-13, MSC 1876
10 Center
Drive
Bethesda, MD 20892-1876
301/496-1124
For more information on patient support groups, contact:
Wegener's Foundation, Inc.
Attention: Ms. Linda
Baltrusch
3705 South George Mason Drive
Suite 1813
South
Falls Church, VA 22041
703/931-5852
Wegener's Granolomatosis Support Group, Inc.
(International)
P.O. Box 28660
Kansas City, MO
64188-8660
800/277-WGSG (9474)
http://www.wgsg.org/
(Source: excerpt from Wegener's Granulomatosis, NIAID Fact Sheet: NIAID)
Wegener's granulomatosis as a Cause of Symptoms or Medical Conditions
When considering symptoms of Wegener's granulomatosis, it is also important to consider Wegener's granulomatosis as a possible cause of other medical conditions.
The Disease Database lists the following medical conditions that Wegener's granulomatosis may cause:
- (Source - Diseases Database)
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