| Anaphylaxis |
| Classification and external resources |
Angioedema of the face such that the boy cannot open his eyes. This reaction was caused by an allergen exposure. |
| ICD-10 |
T78.2 |
| ICD-9 |
995.0 |
| DiseasesDB |
29153 |
| MedlinePlus |
000844 |
| eMedicine |
med/128 |
| MeSH |
D000707 |
Anaphylaxis is a serious allergic reaction that is rapid in onset and may cause death.[1] It typically causes a number of symptoms including an itchy rash, throat swelling, and low blood pressure. Common causes include insect bites/stings, foods, and medications.
On a pathophysiologic level, anaphylaxis is caused by the release of mediators from certain types of white blood cells triggered either by immunologic or non-immunologic mechanisms. It is diagnosed based on the presenting symptoms and signs. The primary treatment is injection of epinephrine, with other measures being complementary.
Worldwide 0.05–2% of people are estimated to have anaphylaxis at some point in their life and rates appear to be increasing.[2] The term comes from the Greek words ἀνά ana, against, and φύλαξις phylaxis, protection.
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Contents
- 1 Signs and symptoms
- 1.1 Skin
- 1.2 Respiratory
- 1.3 Cardiac
- 1.4 Other
- 2 Causes
- 2.1 Food
- 2.2 Medication
- 2.3 Venom
- 2.4 Risk factors
- 3 Pathophysiology
- 3.1 Immunologic
- 3.2 Non-immunologic
- 4 Diagnosis
- 4.1 Classification
- 4.2 Allergy testing
- 4.3 Differential diagnosis
- 4.4 Post-mortem findings
- 5 Prevention
- 6 Management
- 6.1 Epinephrine
- 6.2 Adjuncts
- 6.3 Preparedness
- 7 Prognosis
- 8 Epidemiology
- 9 History
- 10 Research
- 11 References
- 12 External links
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Signs and symptoms
Signs and symptoms of anaphylaxis.
Anaphylaxis typically presents with many different symptoms over minutes or hours[3][4] with an average onset of 5 to 30 minutes if exposure is intravenous and 2 hours for foods.[5] The most common areas affected include: skin (80–90%), respiratory (70%), gastrointestinal (30–45%), heart and vasculature (10–45%), and central nervous system (10–15%)[4] with usually two or more being involved.[2]
Skin
Hives and flushing on the back of a person with anaphylaxis
Symptoms typically include generalized hives, itchiness, flushing or swelling of the lips.[6] Those with swelling or angioedema may describe a burning sensation of the skin rather than itchiness.[5] Swelling of the tongue or throat occurs in up to about 20% of cases.[7] Other features may include a runny nose and swelling of the conjunctiva.[8] The skin may also be blue tinged because of lack of oxygen.[8]
Respiratory
Respiratory symptoms and signs that may be present, including shortness of breath, wheezes or stridor.[6] The wheezing is typically caused by spasms of the bronchial muscles[9] while stridor is related to upper airway obstruction secondary to swelling.[8] Hoarseness, pain with swallowing, or a cough may also occur.[5]
Cardiac
Coronary artery spasm may occur with subsequent myocardial infarction, dysrhythmia, or cardiac arrest.[4][2] Those with underlying coronary disease are at greater risk of cardiac effects from anaphylaxis.[9] The coronary spasm is related to the presence of histamine-releasing cells in the heart.[9] While a fast heart rate caused by low blood pressure is more common,[8] a Bezold–Jarisch reflex has been described in 10% of cases, where a slow heart rate is associated with low blood pressure.[10] A drop in blood pressure or shock (either distributive or cardiogenic) may cause the feeling of lightheadedness or loss of consciousness.[9] Rarely very low blood pressure may be the only sign of anaphylaxis.[7]
Other
Gastrointestinal symptoms may include crampy abdominal pain, diarrhea, and vomiting.[6] There may be confusion, a loss of bladder control or pelvic pain similar to that of uterine cramps.[6][8] Dilation of blood vessels around the brain may cause headaches.[5] A feeling of anxiety or of "impending doom" has also been described.[2]
Causes
Anaphylaxis can occur in response to almost any foreign substance.[11] Common triggers include venom from insect bites or stings, foods, and medication.[10][12] Foods are the most common trigger in children and young adults while medications and insect bites and stings are more common in older adults.[2] Less common causes include: physical factors, biological agents such as semen, latex, hormonal changes, food additives such as monosodium glutamate and food colors, and topical medications.[8] Physical factors such as exercise (known as exercise-induced anaphylaxis) or temperature (either hot or cold) may also act as triggers through their direct effects on mast cells.[2][13] Exercise induced events are frequently associated with the ingestion of certain foods.[5] During anesthesia, neuromuscular blocking agents, antibiotics, and latex are the most common causes.[14] The cause remains unknown in 32-50% of cases, referred to as "idiopathic anaphylaxis".[15]
Food
Many foods can trigger anaphylaxis; this may occur upon the first known ingestion.[10] Common triggering foods vary around the world. In Western cultures, ingestion of or exposure to peanuts, wheat, tree nuts, shellfish, fish, milk, and eggs are the most prevalent causes.[4][2] Sesame is common in the Middle East, while rice and chickpea are frequently encountered as sources of anaphylaxis in Asia.[2] Severe cases are usually caused by ingesting the allergen,[10] but some people experience a severe reaction upon contact. Children can outgrow their allergies. By age 16, 80% of children with anaphylaxis to milk or eggs and 20% who experience isolated anaphylaxis to peanuts can tolerate these foods.[11]
Medication
Any medication may potentially trigger anaphylaxis. The most common are β-lactam antibiotics (such as penicillin) followed by aspirin and NSAIDs.[4][16] Other antibiotics are implicated less frequently and the reactions to NSAIDs are agent specific meaning that if one is allergic to one NSAID they can typically tolerate a different one.[16] Other relatively common causes include chemotherapy, vaccines, protamine and herbal preparations.[2][16] Some medications (vancomycin, morphine, x-ray contrast among others) cause anaphylaxis by directly triggering mast cell degranulation.[10]
The frequency of a reaction to an agent partly depends on the frequency of its use and partly on its intrinsic properties.[17] Anaphylaxis to penicillins or cephalosporins only occurs after they bind to proteins inside the body with some agents binding more easily than other.[5] Anaphylaxis to penicillin occurs once in every 2,000 to 10,000 courses of treatment, with death occurring in less than one in every 50,000 courses of treatment.[5] Anaphylaxis to aspirin and NSAIDs occurs in about one in every 50,000 persons.[5] If someone has a reaction to penicillins their risk of a reaction to cephalosporins is greater but still less than one in 1000.[5] The old radiocontrast agents caused reactions in 1% of cases while the newer lower osmolar agents cause reactions in 0.04% of cases.[17]
Venom
Venom from stinging or biting insects such as Hymenoptera (bees and wasps) or Triatominae (kissing bugs) may induce anaphylaxis in susceptible people.[4][18] Previous systemic reactions, which are anything more than a local reaction around the site of the sting, are a risk factor for future anaphylaxis;[19][20] however, half of fatalities have had no previous systemic reaction.[21]
Risk factors
People with atopic diseases such as asthma, eczema, or allergic rhinitis are at high risk of anaphylaxis from food, latex, and radiocontrast but not from injectable medications or stings.[2][10] One study in children found that 60% had a history of previous atopic diseases, and of those who die from anaphylaxis more than 90% have asthma.[10] Those with mastocytosis or of a higher socioeconomic status are at increased risk.[2][10] The longer the time since the last exposure to the agent in question the lower the risk.[5]
Pathophysiology
Anaphylaxis is a severe allergic reaction of rapid onset affecting many body systems.[1][22] It is due to the release of inflammatory mediators and cytokines from mast cells and basophils, typically due to an immunologic reaction but sometimes non-immunologic mechanism.[22]
Immunologic
In the immunologic mechanism, immunoglobulin E (IgE) binds to the antigen (the foreign material that provokes the allergic reaction). Antigen-bound IgE then activates FcεRI receptors on mast cells and basophils. This leads to the release of inflammatory mediators such as histamine. These mediators subsequently increase the contraction of bronchial smooth muscles, trigger vasodilation, increase the leakage of fluid from blood vessels, and cause heart muscle depression.[5][22] There is also an immunologic mechanism that does not rely on IgE, but it is not known if this occurs in humans.[22]
Non-immunologic
Non-immunologic mechanisms involved substances that directly cause the degranulation of mast cells and basophils. These include agents such as contrast medium, opioids, temperature (hot or cold), and vibration.[13][22]
Diagnosis
Anaphylaxis is diagnosed based on clinical criteria.[2] When any one of the following three occurs within minutes/hours of exposure to an allergen there is a high likelihood of anaphylaxis:[2]
- Involvement of the skin or mucosal tissue plus either respiratory difficulty or a low blood pressure
- Two or more of the following symptoms:-
- a. Involvement of the skin or mucosa
- b. Respiratory difficulties
- c. Low blood pressure
- d. Gastrointestinal symptoms
- Low blood pressure after exposure to a known allergen
During an attack, blood tests for tryptase or histamine (released from mast cells) might be useful in diagnosing anaphylaxis due to insect stings or medications. However these tests are of limited utility if the cause is food or if the person has a normal blood pressure,[2] and they are not specific for the diagnosis.[11]
Classification
There are three main classifications of anaphylaxis. Anaphylactic shock is associated with systemic vasodilation that causes low blood pressure which is by definition 30% lower than the person's baseline or below standard values.[7] Biphasic anaphylaxis is the recurrence of symptoms within 1–72 hours with no further exposure to the allergen.[2] Reports of incidence vary, with some studies claiming as many as 20% of cases.[23] The recurrence typically occurs within 8 hours.[10] It is managed in the same manner as anaphylaxis.[4] Pseudoanaphylaxis or anaphylactoid reactions are a type of anaphylaxis that does not involve an allergic reaction but is due to direct mast cell degranulation.[10][24] Non-immune anaphylaxis is the current term use by the World Allergy Organization[24] with some recommending that the old terminology no longer be used.[10]
Allergy testing
Skin allergy testing being carried out on the right arm
Allergy testing may help in determining the trigger. Skin allergy testing (such as patch testing) is available for certain foods and venoms.[11] Blood testing for specific IgE can be useful to confirm milk, egg, peanut, tree nut and fish allergies.[11] Skin testing is available to confirm penicillin allergies but is not available for other medications.[11] Non-immune forms of anaphylaxis can only be determined by history or exposure to the allergen in question, and not by skin or blood testing.[24]
Differential diagnosis
It can sometimes be difficult to distinguish anaphylaxis from asthma, syncopy, and panic attacks.[2] Asthma however typically does not entail itching or gastrointestinal symptoms, syncope presents with pallor rather than a rash, and a panic attack may have flushing but does not have hives.[2] Other conditions that may present similarly include: scrombroidosis and anisakiasis.[10]
Post-mortem findings
In a person who died from anaphylaxis, autopsy may show an "empty heart" attributed to reduced venous return from vasodilation and redistribution of intravascular volume from the central to the peripheral compartment.[25] Other signs are laryngeal edema, eosinophilia in lungs, heart and tissues, and evidence of myocardial hypoperfusion.[26] Laboratory findings could detect increased levels of serum tryptase, increase in total and specific IgE serum levels.[26]
Prevention
Avoidance of the trigger of anaphylaxis is recommended. In cases where this may not be possible, desensitization may be an option. Immunotherapy with Hymenoptera venoms is effective at desensitizing 80–90% of adults and 98% of children against allergies to bees, wasps, hornets, yellowjackets, and fire ants. Oral immunotherapy may be effective at desensitizing some people to certain food including milk, eggs, nuts and peanuts; however adverse effects are common. Desensitization is also possible for many medications, however it is advised that most people simply avoid the agent in question. In those who react to latex it may be important to avoid cross-reactive foods such as avocados, bananas, and potatoes among others.[2]
Management
Anaphylaxis is a medical emergency that may require resuscitation measures such as airway management, supplemental oxygen, large volumes of intravenous fluids, and close monitoring.[4] Administration of epinephrine is the treatment of choice with antihistamines and steroids often used as adjuncts.[2] A period of in hospital observation for between 2 and 24 hours is recommended for people once they have returned to normal due to concerns of biphasic anaphylaxis.[5][10][23][27]
Epinephrine
An old version of an EpiPen auto-injector
Epinephrine (adrenaline) is the primary treatment for anaphylaxis with no absolute contraindication to its use.[4] It is recommended that an epinephrine solution be given intramuscularly into the mid anterolateral thigh as soon as the diagnosis is suspected. The injection may be repeated every 5 to 15 minutes if there is insufficient response.[2] A second dose is needed in 16-35% of episodes[10] with more than two doses rarely required.[2] The intramuscular route is preferred over subcutaneous administration because the latter may have delayed absorption.[28] Minor adverse effects from epinephrine include tremors, anxiety, headaches, and palpitations.[2]
People on β-blockers may be resistant to the effects of epinephrine.[10] In this situation if epinephrine is not effective intravenous glucagon can be administered which has a mechanism of action independent of β-receptors.[10]
If necessary, it can also be given intravenously using a dilute epinephrine solution. Intravenous epinephrine however has been associated both with dysrhythmia and myocardial infarction.[29] Epinephrine autoinjector used for self-administration typically in two doses, one for adults or children who weigh more than 25 kg and one for children who weigh 10 to 25 kg.[30]
Adjuncts
Antihistamines (both H1 and H2), while commonly used and assumed effective based on theoretical reasoning, are poorly supported by evidence. A 2007 Cochrane review did not find any good-quality studies upon which to base recommendations[31] and they are not believed to have an effect on airway edema or spasm.[10] Corticosteroids are unlikely to make a difference in the current episode of anaphylaxis, but may be used in the hope of decreasing the risk of biphasic anaphylaxis. Their prophylactic effectiveness in these situations is uncertain.[23] Nebulized salbutamol may be effective for bronchospasm that does not resolve with epinephrine.[10] Methylene blue has been used in those not responsive to other measures due to its presumed effect of relaxing smooth muscle.[10]
Preparedness
People prone to anaphylaxis are advised to have an "allergy action plan", and parents are advised to inform schools of their children's allergies and what to do in case of an anaphylactic emergency.[32] The action plan usually includes use of epinephrine auto-injectors, the recommendation to wear a medical alert bracelet, and counseling on avoidance of triggers.[32] Immunotherapy is available for certain triggers to prevent future episodes of anaphylaxis. A multi-year course of subcutaneous desensitization has been found effective against stinging insects, while oral desensitization is effective for many foods.[4]
Prognosis
In those in whom the cause is known and prompt treatment is available, the prognosis is good.[33] Even if the cause is unknown, if appropriate preventative medication is available, the prognosis is generally good.[5] If death occurs, it is usually due to either respiratory (typically asphyxia) or cardiovascular causes (shock),[10][22] with 0.7–20% of cases causing death.[5][9] There have been cases of death occurring within minutes.[2] Outcomes in those with exercise-induced anaphylaxis are typically good, with fewer and less severe episodes as people get older.[15]
Epidemiology
The incidence of anaphylaxis is 4–5 per 100,000 persons per year,[10] with a lifetime risk of 0.5–2%.[2] Rates appear to be increasing: incidence in the 1980s was approximately 20 per 100,000 per year, while in the 1990s it was 50 per 100,000 per year.[4] The increase appears to be primarily for food-induced anaphylaxis.[34] The risk is greatest in young people and females.[4][10]
Currently, anaphylaxis leads to 500–1,000 deaths per year (2.4 per million) in the United States, 20 deaths per year in the United Kingdom (0.33 per million), and 15 deaths per year in Australia (0.64 per million).[10] Mortality rates have decreased between the 1970s and 2000s.[35] In Australia, death from food-induced anaphylaxis occur primarily in women while deaths due to insect bites primarily occur in males.[10] Death from anaphylaxis is most commonly triggered by medications.[10]
History
The term "aphylaxis" was coined by Charles Richet in 1902 and later changed to "anaphylaxis" due to its nicer quality of speech.[11] He was subsequently awarded the Nobel Prize in Medicine and Physiology for his work on anaphylaxis in 1913.[5] The phenomenon itself however has been described since ancient times.[24] The term comes from the Greek words ἀνά ana, against, and φύλαξις phylaxis, protection.[36]
Research
There are ongoing efforts to develop sublingual epinephrine to treat anaphylaxis.[10] Subcutaneous injection of the anti-IgE antibody omalizumab is being studied as a method of preventing recurrence, but it is not yet recommended.[2][37]
References
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- ^ a b c d Sampson HA, Muñoz-Furlong A, Campbell RL, et al. (February 2006). "Second symposium on the definition and management of anaphylaxis: summary report—Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium". J. Allergy Clin. Immunol. 117 (2): 391–7. doi:10.1016/j.jaci.2005.12.1303. PMID 16461139.
- ^ a b c Limsuwan, T; Demoly, P (2010 Jul). "Acute symptoms of drug hypersensitivity (urticaria, angioedema, anaphylaxis, anaphylactic shock).". The Medical clinics of North America 94 (4): 691–710, x. doi:10.1016/j.mcna.2010.03.007. PMID 20609858. http://smschile.cl/documentos/cursos2010/MedicalClinicsNorthAmerica/Acute%20Symptoms%20of%20Drug%20Hypersensitivity%20(Urticaria,%20Angioedema,%20Anaphylaxis,%20Anaphylactic%20Shock).pdf.
- ^ a b c d e f Brown, SG; Mullins, RJ, Gold, MS (2006 Sep 4). "Anaphylaxis: diagnosis and management.". The Medical journal of Australia 185 (5): 283–9. PMID 16948628.
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- ^ a b c d e f g h i j k l m n o p q r s t u v w x y z Lee, JK; Vadas, P (2011 Jul). "Anaphylaxis: mechanisms and management.". Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 41 (7): 923–38. doi:10.1111/j.1365-2222.2011.03779.x. PMID 21668816.
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- ^ a b editors, Marianne Gausche-Hill, Susan Fuchs, Loren Yamamoto, (2007). The pediatric emergency medicine resource (Rev. 4. ed. ed.). Sudbury, Mass.: Jones & Bartlett. pp. 69. ISBN 978-0-7637-4414-4. http://books.google.ca/books?id=lLVfDC2dh54C&pg=PA69.
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- ^ a b c Volcheck, Gerald W. (2009). Clinical allergy : diagnosis and management. Totowa, N.J.: Humana Press. pp. 442. ISBN 978-1-58829-616-0. http://books.google.ca/books?id=pWZLkZB7EW8C&pg=PA442.
- ^ a b Drain, KL; Volcheck, GW (2001). "Preventing and managing drug-induced anaphylaxis.". Drug safety : an international journal of medical toxicology and drug experience 24 (11): 843–53. PMID 11665871.
- ^ Klotz, JH; Dorn, PL, Logan, JL, Stevens, L, Pinnas, JL, Schmidt, JO, Klotz, SA (2010 Jun 15). ""Kissing bugs": potential disease vectors and cause of anaphylaxis.". Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 50 (12): 1629–34. doi:10.1086/652769. PMID 20462351.
- ^ Bilò, MB (2011 Jul). "Anaphylaxis caused by Hymenoptera stings: from epidemiology to treatment.". Allergy 66 Suppl 95: 35–7. doi:10.1111/j.1398-9995.2011.02630.x. PMID 21668850.
- ^ Cox, L; Larenas-Linnemann, D, Lockey, RF, Passalacqua, G (2010 Mar). "Speaking the same language: The World Allergy Organization Subcutaneous Immunotherapy Systemic Reaction Grading System.". The Journal of allergy and clinical immunology 125 (3): 569–74, 574.e1-574.e7. doi:10.1016/j.jaci.2009.10.060. PMID 20144472.
- ^ Bilò, BM; Bonifazi, F (2008 Aug). "Epidemiology of insect-venom anaphylaxis.". Current opinion in allergy and clinical immunology 8 (4): 330–7. doi:10.1097/ACI.0b013e32830638c5. PMID 18596590.
- ^ a b c d e f Khan, BQ; Kemp, SF (2011 Aug). "Pathophysiology of anaphylaxis.". Current opinion in allergy and clinical immunology 11 (4): 319–25. doi:10.1097/ACI.0b013e3283481ab6. PMID 21659865.
- ^ a b c Lieberman P (September 2005). "Biphasic anaphylactic reactions". Ann. Allergy Asthma Immunol. 95 (3): 217–26; quiz 226, 258. doi:10.1016/S1081-1206(10)61217-3. PMID 16200811.
- ^ a b c d Ring, J; Behrendt, H, de Weck, A (2010). "History and classification of anaphylaxis.". Chemical immunology and allergy 95: 1–11. doi:10.1159/000315934. PMID 20519878. http://media.wiley.com/product_data/excerpt/42/04708611/0470861142.pdf.
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- ^ a b Da Broi, U; Moreschi, C (2011 Jan 30). "Post-mortem diagnosis of anaphylaxis: A difficult task in forensic medicine.". Forensic Science International 204 (1-3): 1–5. doi:10.1016/j.forsciint.2010.04.039. PMID 20684869.
- ^ "Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers" (PDF). Resuscitation Council (UK). January 2008. http://www.resus.org.uk/pages/reaction.pdf. Retrieved 2008-04-22.
- ^ Simons, KJ; Simons, FE (2010 Aug). "Epinephrine and its use in anaphylaxis: current issues.". Current opinion in allergy and clinical immunology 10 (4): 354–61. doi:10.1097/ACI.0b013e32833bc670. PMID 20543673.
- ^ Mueller, UR (2007 Aug). "Cardiovascular disease and anaphylaxis.". Current opinion in allergy and clinical immunology 7 (4): 337–41. doi:10.1097/ACI.0b013e328259c328. PMID 17620826.
- ^ Sicherer, SH; Simons, FE, Section on Allergy and Immunology, American Academy of, Pediatrics (2007 Mar). "Self-injectable epinephrine for first-aid management of anaphylaxis.". Pediatrics 119 (3): 638–46. doi:10.1542/peds.2006-3689. PMID 17332221.
- ^ Sheikh A, Ten Broek V, Brown SG, Simons FE (August 2007). "H1-antihistamines for the treatment of anaphylaxis: Cochrane systematic review". Allergy 62 (8): 830–7. doi:10.1111/j.1398-9995.2007.01435.x. PMID 17620060.
- ^ a b Martelli, A; Ghiglioni, D, Sarratud, T, Calcinai, E, Veehof, S, Terracciano, L, Fiocchi, A (2008 Aug). "Anaphylaxis in the emergency department: a paediatric perspective.". Current opinion in allergy and clinical immunology 8 (4): 321–9. doi:10.1097/ACI.0b013e328307a067. PMID 18596589.
- ^ Harris, edited by Jeffrey; Weisman, Micheal S. (2007). Head and neck manifestations of systemic disease. London: Informa Healthcare. pp. 325. ISBN 978-0-8493-4050-5. http://books.google.ca/books?id=31yUl-V90XoC&pg=PA325.
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External links
- Anaphylaxis at the Open Directory Project
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Consequences of external causes (T66–T78, 990–995)
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| Temperature/radiation |
- elevated temperature
- Hyperthermia
- Heat syncope
- reduced temperature
- Hypothermia
- Immersion foot syndromes
- Trench foot
- Tropical immersion foot
- Warm water immersion foot
- Chilblains
- Frostbite
- Aerosol burn
- Cold intolerance
- Acrocyanosis
- Erythrocyanosis crurum
- radiation
- Radiation poisoning
- Radiation burn
- Chronic radiation keratosis
- Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy
- Radiation acne
- Radiation cancer
- Radiation recall reaction
- Radiation-induced erythema multiforme
- Radiation-induced hypertrophic scar
- Radiation-induced keloid
- Radiation-induced morphea
|
|
| Air |
- Hypoxia/Asphyxia
- Barotrauma
- Aerosinusitis
- Decompression sickness
- High altitude
- Altitude sickness
- Chronic mountain sickness
- HAPE
|
|
| Food |
|
|
| Maltreatment |
- Physical abuse
- Sexual abuse
- Psychological abuse
|
|
| Emesis |
- Motion sickness
- Seasickness
- Airsickness
- Space adaptation syndrome
|
|
| Adverse effect |
- Hypersensitivity
- Anaphylaxis
- Angioedema
- Allergy
- Arthus reaction
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|
| Other |
- Electric shock
- Drowning
- Lightning injury
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Ungrouped
skin conditions
resulting from
physical factors |
- Dermatosis neglecta
- Pinch mark
- Pseudoverrucous papules and nodules
- Sclerosing lymphangiitis
- Tropical anhidrotic asthenia
- UV-sensitive syndrome
- environmental skin conditions
- Electrical burn
- frictional/traumatic/sports
-
- Black heel and palm
- Equestrian perniosis
- Jogger's nipple
- Pulling boat hands
- Runner's rump
- Surfer's knots
- Tennis toe
- Vibration white finger
- Weathering nodule of ear
- Wrestler's ear
- Coral cut
- Painful fat herniation
- Uranium dermatosis
- iv use
-
- Skin pop scar
- Skin track
- Slap mark
- Pseudoacanthosis nigricans
- Narcotic dermopathy
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Immune disorders: hypersensitivity and autoimmune diseases (279.5–6)
|
|
Type I/allergy/atopy
(IgE) |
|
Foreign
|
Atopic dermatitis · Allergic urticaria · Hay fever · Allergic asthma · Anaphylaxis · Food allergy (Milk, Egg, Peanut, Tree nut, Seafood, Soy, Wheat), Penicillin allergy
|
|
|
Autoimmune
|
none
|
|
|
Type II/ADCC
(IgM, IgG) |
|
Foreign
|
Pernicious anemia · Hemolytic disease of the newborn
|
|
|
Autoimmune
|
|
Cytotoxic
|
Autoimmune hemolytic anemia · Idiopathic thrombocytopenic purpura · Bullous pemphigoid · Pemphigus vulgaris · Rheumatic fever · Goodpasture's syndrome
|
|
|
"Type 5"/receptor
|
Graves' disease · Myasthenia gravis
|
|
|
|
Type III
(Immune complex) |
|
Foreign
|
Henoch–Schönlein purpura · Hypersensitivity vasculitis · Reactive arthritis · Farmer's lung · Post-streptococcal glomerulonephritis · Serum sickness · Arthus reaction
|
|
|
Autoimmune
|
Systemic lupus erythematosus · Subacute bacterial endocarditis · Rheumatoid arthritis
|
|
|
Type IV/cell-mediated
(T-cells) |
|
Foreign
|
Allergic contact dermatitis · Mantoux test
|
|
|
Autoimmune
|
Diabetes mellitus type 1 · Hashimoto's thyroiditis · Guillain–Barré syndrome · Multiple sclerosis · Coeliac disease · Giant-cell arteritis
|
|
|
GVHD
|
Transfusion-associated graft versus host disease
|
|
|
Unknown/
multiple |
|
Foreign
|
Hypersensitivity pneumonitis (Allergic bronchopulmonary aspergillosis) · Transplant rejection · Latex allergy (I+IV)
|
|
|
Autoimmune
|
Sjögren's syndrome · Autoimmune hepatitis · Autoimmune polyendocrine syndrome (APS1, APS2) · Autoimmune adrenalitis · Systemic autoimmune disease
|
|
|
|
|
cell/phys/auag/auab/comp, igrc
|
|
|
|
|
|
