Transcript Serum Sickness

Serum Sickness
Myra Lalas Pitt
Serum Sickness
First described by von Pirquet and Schick. They described an
illness that developed in some patients after they were given
horse serum antitoxin for diphtheria and Scarlet fever. The
illness developed a few weeks after administration of horse
serum antitoxin.
Cardinal features: rash, fever, and polyarthralgias or
polyarthritis, which begin 1-2 weeks after exposure to the
responsible agent.
Pathophysiology
Type III Hypersensitivity Reaction
1. Immune complex formation
2. Complement activation
3. Complement- independent mechanisms
Immune complexes in tissues can react directly with Fc gamma
receptors on neutrophils, mast cells, and phagocytes, leading to
release of cytokines, histamine, and other inflammatory
mediators even without complement.
Precipitin Curve
Serum-like sickness
May be caused by drugs, viral infections
Has different pathophysiology than serum sickness
Levels of circulating immune complexes and serum complement
are often unaffected
Commonly implicated drugs: Cefaclor Penicillin (amoxicillin)
Trimethoprim-sulfamethoxazole
Cefaclor and Bactrim
Metabolites toxic to lymphocytes. The predisposing drug
metabolism is genetically influenced.
Penicillin
May be caused by drug-specific immune complexes, not
complexes with heterologous serum proteins.
Signs and Symptoms
Arthralgias
Lymphadenopathy
Urticarial rash
Fever, when present, is typically low-grade.
Acute onset of joint pain, often leading to inability to walk
Differential Diagnoses
Viral Exanthem
Urticarial Vasculitis
Meningococcemia
Reactive Arthritis
Acute Rheumatic Fever
Lyme disease
Erythema Multiforme
Steven Johnson's Sydrome
Kawasaki's disease
JIA
Serum Sickness Rash
SJS rash
Lyme Disease
Meningococcemia Rash
Kawasaki
Labs
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CBC count with differential - Leukocytosis or
leukopenia, eosinophilia, or mild thrombocytopenia
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Erythrocyte sedimentation rate and C-reactive protein
levels - Usually slightly elevated

Urinalysis - Albuminuria, hematuria, active sediment

Blood urea nitrogen (BUN) and creatinine levels - May
be transiently elevated

C3, C4, CH50 - Depressed complement levels due to
complement consumption

If infectious etiology is to be ruled out, cultures,
titers should be obtained.
Treatment
Discontinuation of the offending agent
Supportive care
Antihistamines for urticaria
Nonsteroidal anti-inflammatory drugs (NSAIDs) for arthritis,
arthralgia, or both
Steroids (Prednisone or Methylprednisolone)- Patients with
higher fever (eg, temperature >38.5ºC), more severe arthritis and
arthralgias, or more extensive rashes including extensive vasculitic
rashes may be treated with short courses of glucocorticoids.
References
Brucculeri, M. et al. Serum sickness-like reaction associated
with cefazolin. BMC Clin Pharmacol. 2006; 6: 3.
Hay Jr., W. et al. Current Pediatric Diagnosis and Treatment,
15th ed. McGraw-Hill. 2001: pp. 958-960.
www.emedicine.com
www.uptodate.com
PREP Questions

You have been asked by a local school to provide
recommendations about the use of self-injectable
epinephrine for anaphylaxis. The school supervisor is
concerned about the increased incidence of peanut and
tree nut food allergy. School officials have requested
that each child who has a diagnosis of "food allergy"
have two self-injectable epinephrine devices at the
school nurse's office.
Of the following, the BEST response regarding
anaphylaxis is that
A. A patient should not receive a second dose of
epinephrine unless a clinician is present
B. Epinephrine reaches higher peak plasma
concentrations if injected into the thigh rather than the
arm
C. Families should keep one epinephrine autoinjector in
the car in case a reaction occurs after school
D. Skin manifestations (eg, flushing, itching, urticaria)
are rare in severe anaphylaxis
E. Subcutaneous injection of epinephrine is preferable to
intramuscular injection
In the past, outpatient administration of epinephrine was
subcutaneous, but research has demonstrated that
intramuscular injection, specifically in the thigh, is the
preferred route and location due to higher and faster
peak plasma concentration.
If epinephrine is administered, parents or school should
call emergency services to evaluate the child and
transport him or her to the ER for further evaluation.
The effects of a single dose of epinephrine typically last
for 5 to 15 minutes; up to 20% of individuals experiencing
anaphylaxis may require a second epinephrine dose.
When symptoms persist, a second (or third) dose should
be administered, even if the parent or school
professional still is awaiting the ambulance.