31 Flashcards
Conjunctivitis
Presentation
Etiology
Different types
Conjunctivitis is any inflammation of the conjunctiva.
Presentation
The conjunctiva appears red and swollen, with some mild lid edema.
Depending on the type of conjunctivitis there is also either watery or purulent drainage associated. (Link to a photo showing a child with conjunctivitis.)
Etiology
Conjunctivitis can be caused by:
Allergies
Chemical irritation, or
Infection.
Consider allergy in a child who has bilateral red, watery eyes, and who complains of itchiness and irritation. Discharge in allergic conjunctivitis tends to be mucoid and ropey. There is usually a history of hypersensitive reactions to seasonal allergens, such as pollens and molds, or to perennials such as dust mites and animal dander.
Infectious Conjunctivitis
Often difficult to distinguish bacterial from viral conjunctivitis on clinical presentation.
Children younger than 6 are more likely to have a bacterial than a viral infection.
Both produce conjunctival redness and itching.
Bacterial conjunctivitis is more likely to be bilateral and to cause a purulent exudate with eyelids crusted closed upon waking.
Both viral and bacterial tend to begin in one eye, but both may spread to the other eye.
Adenovirus conjunctivitis frequently becomes bilateral and may be associated with pharyngitis and pre-auricular lymphadenopathy.
Presentations of periorbital swelling 5
Seasonal/perennial allergic conjunctivitis
May be associated with pruritis and mucoid discharge
Often associated sneezing, itchy nose, and clear rhinorrhea
On exam there may be allergic shiners (dark circles under the eyes), Dennie’s lines (an extra crease below the lower eyelid), and cobblestoning of the conjunctiva (fine bumps on the conjunctival mucosa).
Link to a photo of a child with allergic eye swelling.
URI
Usually concurrent findings of nasal congestion, cough, and/or pharyngitis.
Sinusitis (ethmoid, frontal, or maxillary)
Swelling with or without redness also can result from inflammatory edema (usually painless swelling thought to result from the obstruction of venous drainage from periorbital structures into veins that pass through the sinuses because the veins are partially blocked by inflamed tissues in the sinuses)
May be associated nasal congestion, headache, and cough.
(Inflammatory edema can also occur in the setting of a URI or allergic rhinitis.)
Acute allergic reaction
Usually abrupt in onset
Often accompanied by an urticarial rash
May be swelling of other parts of the face as well, including the lips, tongue, and other oropharyngeal structures that can compromise the airway.
Link to a picture of a child whose allergic reaction has caused facial swelling and an urticarial rash.
Cellulitis
Edema is usually unilateral and usually erythematous.
Often accompanied by a history of a local insect bite, trauma, or infection
May also extend from another site of infection, such as sinusitis
Most often caused today by pneumococci (strep pneumoniae) , Moraxella catarrhalis, or non-typable Haemophilus influenzae
Incidence of Haemophilus influenzae type B has dropped markedly since the introduction of the Hib vaccine.
Link to a photo of a child with periorbital cellulitis.
Differential dx for fatigue, periorbital edema and abdominal distention 6
Nephrotic syndrome
Periorbital edema is often the first sign of hypoalbuminemia, which may be caused by nephrotic syndrome.
Abdominal distention can be caused by ascites, which is seen in hypoalbuminemic states such as can occur in nephrotic syndrome.
Ascites can lead to fatigue and poor appetite.
Allergic reaction
Periorbital swelling can be caused by an allergic reaction.
An allergic reaction is usually abrupt in onset and often accompanied by a urticarial rash.
Acute glomerulonephritis
Periorbital edema is often the first sign of hypoalbuminemia, which may be caused by glomerulonephritis.
Abdominal distention can be caused by ascites, which is seen in hypoalbuminemic states such as can occur in glomerulonephritis.
Ascites can lead to fatigue and poor appetite.
Congestive heart failure (CHF)
Although not often seen in children with congestive heart failure, edema is common in adults with heart failure.
Hepatomegaly is a common finding in CHF and could present as abdominal distention.
One would expect an abnormal cardiothoracic exam, with tachycardia, a murmur, or a gallop.
It is possible that shortness of breath, typical with CHF, may be difficult to distinguish from fatigue in the patient’s history.
Sinusitis
Periorbital swelling and redness (typically painless) can result from inflammatory edema secondary to ethmoid, frontal, or maxillary sinusitis.
Hepatic failure
Abdominal distention is an expected finding in liver failure, which causes generalized edema due to decreased production of albumin.
Fatigue would be expected.
Patients with hepatic failure are almost always markedly jaundiced.
Liver failure is a rare diagnosis in an otherwise healthy child.
What is anasarca
Where is it often seen in males and females
anasarca (severe generalized edema)
Edema in the labia - females
Edema in the scrotum - males
Organ systems that cause nonpitting edema 3
Heart
Kidneys
Liver
Nephrotic syndrome
Sxs
Most common form in children
4 lab findings
Edema and Weight Gain
Edema is the most prominent symptom of nephrotic syndrome.
Periorbital edema that improves when the child is upright is a common presenting finding.
The edema then becomes more generalized, leading to pitting edema, ascites, and weight gain.
The edema in nephrotic syndrome is usually due more to interstitial fluid accumulation rather than intravascular fluid overload (as is the case in acute glomerulonephritis). Therefore, hypertension does not usually occur. In severe cases patients may actually become hypotensive.
Other Symptoms
Patients may complain of nonspecific symptoms of increasing tiredness and decreased appetite due to interstitial fluid accumulation.
Most Common Form of Nephrotic Syndrome in Children
Minimal change disease is the most common cause of the nephrotic syndrome in children, accounting for 90 percent of cases under the age of 10.
The characteristic histologic finding in minimal change disease is fusion and diffuse effacement of the epithelial cell foot processes on electron microscopy.
As implied by the name, the nephron appears relatively normal on light microscopy.
Hypoalbuminemia
In nephrotic syndrome there is a major loss of albumin in the urine due to leaking through the defective capillary basement membrane.
There is evidence for increased loss of albumin due to problems with renal tubular reabsorption/metabolism and decreased synthesis of the protein in the liver.
Hyperlipidemia
In reaction to the decreased albumin, the liver is stimulated to make lipoproteins as well as albumin, which leads to hyperlipidemia and hypercholesterolemia.
There is also decreased lipid clearance from the circulation.
Hyponatremia in nephrotic syndrome is due to total body fluid overload (A) caused by excessive sodium and water retention. (Go back to the previous card for the pathophysiology.)
Pseudohyponatremia, caused by the hyperlipidemia (C), may also exist. This depends on how the lab measures sodium. Pseudohyponatremia will occur only if the lipids are high enough to cause the blood to have a milky appearance.
Evaluation of generalized edema 5
In a setting of apparent hypoalbuminemia, it is important to obtain studies that will determine whether there is loss of albumin in the urine or lack of production in the liver.
The following diagnostic tests are appropriate to narrow your differential or confirm your diagnosis:
Electrolytes, BUN, and creatinine
Provide an indication of renal function
AST, ALT, cholesterol, albumin, and triglycerides
Will reveal hepatic inflammation and/or impairment in hepatic synthetic function
C3 and C4 complement levels
Screens for hypocomplementemia (a finding associated with membranoproliferative glomerulonephritis, post-streptococcal glomerulonephritis, and systemic lupus erythematosus)
Streptozyme
A test that detects antibodies to streptococcal antigens
Will be positive in the setting of post-streptococcal glomerulonephritis
A CBC is useful in this case as well, although it will not lead to a specific diagnosis.
Pathogenesis of proteinuria in nephrotic syndrome 3 MOA
Causes of proteinuria 3
In nephrotic syndrome there is increased filtration of large proteins—predominantly albumin and some globulins—through the glomerular capillary wall, resulting in proteinuria. There are three possible mechanisms for this:
The loss of the polyanion charge characteristic of the normal capillary wall. All layers of the glomerular filtration surface have a negative surface charge due to proteoglycans such as heparin sulfate. Therefore, loss or reduction of this charge may permit large negatively charged proteins like albumin—previously blocked from leaking by electrostatic forces—to leak through the membrane.
A shift in the capillary wall pore size in a direction permitting increased leaking of large molecules.
A change in the hemodynamic characteristics of capillary flow so there is a greater filtration of larger molecules.
Any disease causing inflammation of the renal parenchyma (nephritis) can cause proteinuria.
Pyelonephritis
White blood cells and white blood-cell casts would be seen with a urinary tract infection, which would cause a positive leukocyte esterase test on the dipstick.
Acute Glomerulonephritis
Acute glomerulonephritis results in varying degrees of proteinuria. Red blood cells and red blood cell casts would also be present, causing a positive heme test on the dipstick. Link to a photo of tea-colored urine from a patient with acute poststreptococcal glomerulonephritis.
Interstitial Nephritis
Interstitial nephritis can be associated with red and white blood cells in the urine, but not a massive degree of proteinuria. Interstitial nephritis is rare in children and usually caused by a medication such as the antibiotic methicillin (no longer available in the U.S.), NSAIDs, penicillins, cephalosporins, rifampin, sulfonamides, or infection.
Post streptococcal glomerulonephritis
Throat
Skin
Dx
Post-streptococcal Glomerulonephritis
When a patient presents with tea-colored urine, it is important to ask about recent throat and skin infections. Post-streptococcal glomerulonephritis (PSGN) may occur after a streptococcal infection of either throat or the skin, despite treatment with antibiotics.
Streptococcal Pharyngitis
Pharyngitis caused by Streptococcus pyogenes classically presents with sudden onset of fever, sore throat, headache, and abdominal pain with absence of rhinorrhea, congestion, or cough.
On exam, patients may have an exudative tonsillitis with palatal petechiae, strawberry tongue, tender anterior cervical lymph nodes, and sometimes an accentuation of skin lines in the flexor surfaces (Pastia’s lines) and a fine papular sandpaper-like rash (scarlitiniform rash).
Treating strep throat with antibiotics will prevent the complication of acute rheumatic fever, but will not prevent the occurrence of PSGN.
Streptococcal Skin Infection (Impetigo)
Classically there will be a golden honey-colored crust.
Common locations are under the nares or on insect bites or wounds.
Impetigo may be caused by S. pyogenes or staphylococcal species.
Treatment with topical or oral antibiotics will not prevent the occurrence of PSGN.
Diagnosis of Post-streptococcal Glomerulonephritis
A diagnosis of PSGN can be supported with: Elevated antistreptolysin-O (ASO) titer Positive streptozyme test Elevated anti-DNAase B antibodies, or Low C3
A complication of nephrotic syndrome and its RF
Venous thrombosis in nephrotic syndrome may involve any of the large veins of the body, including the sagittal sinus and pulmonary arteries. Renal venous thrombosis is a relatively frequent complication in adults.
Risk Factors
Factors predisposing to venous thrombosis include:
Urinary loss of proteins that inhibit coagulation (antithrombin III) or increased fibrinolysis
Destabilization of platelets by hyperlipidemia
Increased fibrinogen levels, and
Increased blood viscosity due to a rise in the hematocrit (especially if diuretics are used without albumin replacement).
Intense, prolonged therapeutic use of corticosteroids, which are themselves thrombogenic, adds to the risk of thrombosis for patients with nephrotic syndrome.
Testing for complement in suspected nephrotic syndrome
Complement
Complement levels, especially C3 and C4, are useful to determine if there is a secondary cause for nephrotic syndrome. Levels will be decreased in glomerulonephritis or nephrotic syndrome due to:
A collagen vascular disease (systemic lupus erythematosis [SLE])
A primary renal disease other than minimal change disease (membranoproliferative glomerulonephritis) or
An infectious etiology such as a recent group A strep infection (post streptococcal glomerulonephritis).
Other secondary causes of nephrotic syndrome include Henoch Schoenlein purpura or IgA nephropathy (usually associated with significant hematuria) and lymphoma, which should be considered particularly if the presentation incudes lymphadenopathy and/or hepatosplenomegaly. Hepatitis B, HIV, and other infectious etiologies can also cause nephrotic syndrome, but would be expected to show other abnormalities in the liver enzymes and the CBC (and would have been considered if the medical history had revealed the patient to be in a high-risk population).
A negative ANA helps to rule out SLE and is recommended in the evaluation of children > 10 years old with nephrotic syndrome.
Normal complement levels and renal ultrasound—as well as a negative streptozyme test (a combination of antibody tests that detects a recent streptococcal infection)—help to rule out post-streptococcal glomerular disease.
Treatment of primary nephrotic syndrome 2
Corticosteroids
Children between the ages of 1 and 10 years without gross hematuria and with a normal serum complement level receive a trial of corticosteroids.
Sodium Restriction
During edema accumulation, the patient usually excretes less than 5 mEq of sodium per day. A diet of 50 mEq per day will result in the net gain of a kilogram of body water every 3 days. Current guidelines recommend sodium restriction to a level of 1500-2000 mg daily.
Combination of IV Furosemide and Albumin to Treat Symptomatic Edema
Combined use of furosemide and 25% albumin is recommended only for those children with symptomatic edema (particularly to relieve dyspnea and edema if these symptoms are causing discomfort, or, in boys, to reduce scrotal edema that may compromise testicular perfusion). In these cases, the albumin infusion should be followed with 1 to 2 mg/kg of furosemide to promote diuresis.
Note that treatment with IV furosemide alone is very dangerous in nephrotic syndrome because it could lower intravascular volume to dangerously low levels, precipitating shock and increasing the risk of venous thrombosis. And treatment with albumin alone may lead to pulmonary edema if the blood volume expands too rapidly.
Response to steroids then divides patients into three groups:
- Steroid responsive or
- Relapsing/steroid-dependent
Fortunately, more than 95% of children fall into these two groups (i.e., responsive to corticosteroid therapy):
Although relapses are common, the long-term prognosis is excellent for these children.
There may be repeated relapses until the disease resolves spontaneously toward the end of the second decade of life.
No long-term renal damage (even if relapses).
When in remission, the child is normal and may have unrestricted diet and activity, and it is generally unnecessary to test the urine for protein.
3. Steroid-resistant
Steroid-resistant patients (those who do not respond to steroids with elimination of proteinuria after 8 weeks of therapy) usually then undergo a renal biopsy.
Infectious complications of nephrotic syndrome
Prevention matters 3
During a nephrotic syndrome relapse with steroid use, patients are at high risk for infection. A high index of suspicion, prompt evaluation (including cultures of blood and peritoneal fluid), and early treatment with broad spectrum antibiotics to cover gram-positive and gram-negative organisms are critical to preventing life-threatening illness.
Increased Risk of Infection
An increased risk of bacterial infection during an episode of nephrotic syndrome may be due to any of the following:
Decreased immunoglobulin levels
Edema fluid acting as a culture medium
Protein deficiency
Decreased leukocyte bactericidal activity
Immunosuppression from steroids
Decreased splenic perfusion due to hypovolemia, and
Urinary loss of a complement factor (properdin factor B) that opsonizes certain bacteria.
Common Infectious Complications of Nephrotic Syndrome
Spontaneous peritonitis is one of the most frequent complications, with an insidious presentation of fever and minimal other findings (just as described in this scenario). Untreated it can lead to overwhelming sepsis and death, especially while the patient is on steroids. (Streptococcus pneumoniae is the most common pathogen causing peritonitis, but gram-negative bacteria can also be found.) Pneumonia Cellulitis Urinary tract infection Prevention
When in remission, patients should receive:
Polyvalent pneumococcal vaccine
Two doses of varicella vaccine (if not already immunized)
An annual influenza vaccine
Post strep glomerulonephritis buzz word
Tea colored urine is a buzz word
Nephritic syndrome sxs 3
Hematuria, hypertension, some proteinuria
