Transcript ITE Review: Allergy and Immune Disorders

ITE Review: Allergy
and Immune Disorders
Angela M. Pugliese MD
Henry Ford Hospital
Department of Emergency Medicine
ALLERGY
Allergy
• 4 types of hypersensitivity reactions
• 1. Anaphylactic
• IgE mediated with degranulation from mast cells
• 2. Cytotoxic
• IgG or IgM antibiodies react with cell antigens and activate
complement
• ie: autoimmune hemolytic anemia, goodpasture’s
• 3. Immune Complex
• immune complex deposition resulting in complement activation
• ie: serum sickness, SLE, RA
• 4. Cell-mediated
• activated T-cells against cell surface bound antigens
• ie: contact dermatitis
Angioedema
• edema of deeper layers of skin that is non-pruritic
• can cause burning, pain or numbness
• Drug induce vs Hereditary
• Drug induced
• ACE inhibitors: not IgE mediated
• anti-histamines and steroids haven’t shown clear benefit
• tx includes airway protection and possible racemic epi
• Hereditary
• C1-esterase inhibitor deficiency
• tx is also airway protection, but can also give frozen plasma
• consider high dose epi, danazol and stanozolol
Anaphylaxis
• IgE mediated, immediate hypersensitivity reaction to antigen
• abrupt onset of symptoms to SENSITIZED patient involving 2
or more organ systems
• pts on beta-blockers have more severe reactions
• Presenting Symptoms: rash, “lump” in throat, wheezing,
N/V/D, hypotension, pulmonary edema
• most serious reactions tend to occur within minute but can
have relapse of symptoms within 4-8 hours
Anaphylaxis Treatment
• EPINEPHRINE – MUST KNOW DOSES
• stop or remove offending agent, protect airway
• also give H1 blockers, steroids, nebs and consider glucagon for
patients on b-blockers who are refractory
Anaphylaxis Disposition
• Usually admission for observation or continued treatment
• Consider discharge only in mild cases
•
•
•
•
no hemodynamic instability
no airway involvement
complete resolution of symptoms to ED treatment
no relapse after 6 hour observation
Anaphylactoid Reaction
• Direct release of mediators, do not require prior exposure like
anaphylaxis (but otherwise can think of as the same)
• Treatment is same as anaphylaxis
• Most common offending agents
•
•
•
•
IV dye
ASA
NSAIDs
codeine
Erythema Multiforme
• more severe variant of an urticarial reaction
• Iris or target Lesions
• Common Drug Offenders
•
•
•
•
•
PCN
Sulfa
Cephalosporins
tetracycline
phenytoin
Stevens-Johnson Syndrome
• severe, potentially fatal form of erythema multiforme
• Characterized by bullae, mucus membrane lesions and
multisystem involvement
• Bactrim and Herpes Simplex
are common causes
Jarish-Herxheimer Reaction
• febrile reaction to parasitic or bacterial antigens that are
release when organism is killed
• occurs 2-12 hours after initiation of antibiotics, lasts less than
48 hours
• Tx is supportive: give antipyretics and consider steroids
occasionally
Adverse Food Reactions
• DIRECT HISTAMINE RELEASE: causes flushing, bronchospasm,
urticarial rash and hypotension
• Preservatives, food enhancers, dyes and allergens cause this
• Sulfites (preservatives): asthmatics are more sensitive,
commonly found in packaged salad, shrimp, pickles, dried
fruit, sausages, cheese, wine and fruit juices
• Scombroidosis: food toxin from spoiled salt water fish, has
peppery taste, usually doesn’t have bronchospasm or
hypotension
Immunology
General Priciples
• Innate vs Adaptive immunity
• Antibodies
• IgM: first to appear, serves as marker for early acute infection
• IgA: predominates in secretions and GI fluid, inhibits cell adherence
to pathogens
• IgE: found in mast cells and basophils, responsible for
hypersensitivity responses
• IgG: 75% of total immunoglobulin mass, crosses placenta and provide
fetal immunity for first 6 months of life, deficiencies lead to infections
with encapsulated organisms
• Cell Mediate Immunity
• T-cells, natural killer cells and macrophages
• vital to control intracellular infections
• CD4 vs CD8 cells
SPECIFIC IMMUNOCOMPROMISED
STATES
•
•
•
•
•
•
•
Transplant
Cancer
Diabetes
Alcoholism and cirrhosis
Renal Failure
Splenectomy/Hyposplenia/Functional Asplenia
Pts on Immunosuppressive therapy
Transplant Patients
• Think – Rejection, infection, toxicity (to immunosuppressive
drugs)
• Infection is leading cause of death
• First month: mainly bacterial related to surgery, also think about
candida and HSV
• 1-6 months: think mainly CMV, also worry about EBV, hepatitis,
listeria and aspergillosis
• After 6 months: mainly chronic viral infections, can have
disseminated varicella-zoster, low threshold for IV acyclovir
Transplant Rejection
• 3 categories for rejection
• hyperacute: happens minutes to hours after surgery, irreversible
• acute: 1-12 weeks post-op, may be reversed
• chronic: progressive, insidious and irreversible
• Immunosuppressant (focus on toxicity)
• Cyclosporine: toxicity can cause vasoconstriction and renal
ischemia
• Cellcept (mycophenolate): side effects N/V/D, leukopenia
• Prograf: can be nephrotoxic or cause seizures and neuropathy
• Failure of transplant to take immunosuppressive meds should
be considered an emergency
Renal Transplant
• make sure to check for tenderness over allograft
• subtle elevation in creatinine can mean rejection
• Renal US with vascular flow analysis for evaluation
• tx is methylprednisolone
Lung Transplant
• search for infection, CXR can be non specific
• symptoms of subtle fever > 0.5 C above baseline should not be
ignored
• Can also have cough, dyspnea, chest tightness
• tx of rejection is methylprednisolone
Heart Transplant
• remember transplanted heart is DENERVATED
• no anginal chest pain
• no response to atropine
• Use isoproterenol
• watch closely for signs of heart failure, Mis present this
way………or with death
• Tx of rejection also methylprednisolone, can use dopa and
dobutamine for hypotension, ISOPROTERENOL for
bradydysrhythmias
Liver Transplant
• can present with fever, anorexia, abdominal pain, ascites,
color changes
• also consider vascular thrombosis, biliary leak or obstruction
and drug toxicity
• get hepatic US with vascular
• tx of rejection is methylprednisolone
Cancer Patients
• frequently have multiple immune defects
• neutropenia, impaired B & T cell function
• induced by chemo or the CA itself
• infection is much more common in acute leukemia, lymphoma
and multiple myeloma
• Listeria is common in CA patients with impaired cell mediated
immunity
• Pneumonia in neutropenic CA pts is usually from gram neg
bacteria early and fungal infections late
Neutropenia
• Definition
• neutrophil count less than 500 cell/mL
• Febrile neutropenia: above and fever of 38.3
• Usually from cytotoxic chemotherapy or radiation
• Incidence and Severity
• inversely proportional to neutrophil count
• directly proportional to duration
• Most common sites of infection
• lung, mouth and pharynx
• Bacteremia can occur without obvious source
Neutropenia
• Pneumonia and anorectal infections are more likely to associated
with bacteremia
• Gram positive bacteria are leading cause of infection
• Aspergillosis and candida are most common fungal infections
• Fever is frequently the only sign of infection
• Treatment:
• broad spectrum antibiotics in setting of fever or obvious infection
without fever
• Ampho B for fungal infections
• granulocyte colony-stimulating factor for high risk patients
Diabetes
• predisposed to infection from defects in immune functions, vascular
insufficiency and neuropathy (leads to wound neglect)
• Neutrophil and macrophage functions are impaired
• Cellular and humoral immunity are normal
• Infections with increased frequency
•
•
•
•
•
malignant otitis externa (pseudomonas)
rhinoncerbral zygomycosis (mucormycosis)
emphysematous cystitis
fournier’s
foot infections with osteo
Alcoholism and Cirrhosis
• predisposed to infection through…..
• direct immune suppression
• alterations in blood flow
• depression of mental status and delay in seeking care
• Cirrhotics have impaired hepatic clearance and killing of
bacteria as well as splenic hypofunction
• Common infections include spontaneous bacteremia
• also think sepsis from e. coli, klebsiella and salmonella
Renal Failure
• Infections are the 2nd most common cause of death after CAD
in CKD/ESRD patients
• Vascular access site infections and multiple defects in
immunity are the cause
• have generalized immune hyporesponsiveness
• humoral immunity affected: deficient IgG production
• have poor response to vaccinations
• Watch for peritonitis with PD patients
• 2/3 will have an episode within 1st year
Splenectomy/Hyposplenia/Functio
nal Asplenia
• primary site of IgM synthesis
• principle clearing site for strep pneumo
• higher rate of disseminated pneumococcal infections
• Overhwelming infections….
• from encapsulated organisms
• h. influenzae, n. meningitidis, gram neg bacilli
• more common in children, esp <2
• pts with underlying heme disorder (less so in trauma)
• usually have no obvious source
• Infections with babsia microti from ticks leads to severe and usually
fatal hemolysis
• Vaccination is very important in these patients
Immunosuppressives
• Steroids and company
• high dose steroids alter neutrophil, monocyte and lymphocyte
functions
• Suppress inflammation
• Cause profound depression of cell mediated immunity
• Most common infections from pyogenic bacteria
• ie. s. aureus, strep, gram neg bacilli
IMMUNE RELATED DISORDERS
•
•
•
•
•
Rheumatoid Arthritis
Lupus
Reiter’s Syndrome
Raynaud’s Disease
Vasculitis
Rheumatoid Arthritis
• associated with polyarticular joint pain
• Most common in women: related to HLA-DR haplotype
• Most commonly affects the hand (MCP and PIP joint), then
wrist and elbow
Lupus
• multisystem inflammatory disorder mediated by autoantibodies
• associated with symmetric polyarticular joint pain
• small and large joints
• Women 15-40 mainly affected
• Diagnosis: 4/11 of DOPAMINE RASH
• Can be drug induced; this is usually reversible
• HIPPS: hydralazine, INH, phyntoin, procainamide, sulfa
• Treatment
• Nsaids for joint pain, steroids for acute flare and immunosuppressive
therapy
Lupus Diagnosis
• DOPAMINE RASH
•
•
•
•
•
•
•
•
•
•
•
Discoid rash
Oral ulcers
Photosensitive rash
Arthritis
Malar rash
Immunologic criteria (positive anti-dsDNA, anti-Sm)
NEurologic or psych symptoms
Renal disease
Ana +
Serositis
Hematologic disorders
Reiter’s Syndrome
• Can’t see, can’t pee, can’t climb a tree
• classic triad: conjunctivitis, urethritis, arthritis
• Young males 15-35: with HLA-B27 antigen
• Usually proceeded by chlamydia, shigella or salmonella
infections
• Oligoarthritis develops 1-6 weeks after chlamydial urethritis,
affects weight bearing joints of lower extremities
• Treatment: Abx for urethritis, NSAIDS for arthritis,
immunosuppressives for recurrent ocular inflammation
Raynaud’s Disease
• Vasospasm of distal small arteries
• Bilateral triphasic response to cold or emotion
• fingers become white, blue, then red
• Resolves spontaneously, benign course
• avoid cold exposure
Vasculitis
• Inflammation and necrosis of blood vessels leading to tissue damage
• Temporal Arteritis:
•
•
•
•
involves branches of the carotid artery
presents with temporal HA, vision changes, scalp tenderness
Diagnose with temporal artery biopsy
ESR > 50 in pt with concerning symptoms should be started on
steroids
• leads to irreversible blindness if untreated
• Takayasu’s :
•
•
•
•
involves aorta and major branches
presents with finger ischemia and arm claudication
Diagnose with aortic arteriogram
Tx is steroids
Vasculitis
• Bechet Disease
• recurrent painful oral and genital ulcers
• diagnosis by biopsy
• tx: steroids and immunosuppression
• Polyarteritis Nodosa
• skin ulcers, nephritis, mesenteric ischemia
• diagnosis with biopsy of kidney or skin lesions
• tx: steroids and immunosuppression
Questions???