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Ecchymosis

MedGen UID:
8524
Concept ID:
C0013491
Finding; Pathologic Function
Synonym: Ecchymoses
SNOMED CT: Ecchymosis (77643000); Ecchymoses (77643000); Ecchymosis (302227002)
 
HPO: HP:0031364

Definition

A purpuric lesion that is larger than 1 cm in diameter. [from HPO]

Conditions with this feature

Glanzmann thrombasthenia
MedGen UID:
52736
Concept ID:
C0040015
Disease or Syndrome
Glanzmann thrombasthenia is a bleeding disorder that is characterized by prolonged or spontaneous bleeding starting from birth. People with Glanzmann thrombasthenia tend to bruise easily, have frequent nosebleeds (epistaxis), and may bleed from the gums. They may also develop red or purple spots on the skin caused by bleeding underneath the skin (petechiae) or swelling caused by bleeding within tissues (hematoma). Glanzmann thrombasthenia can also cause prolonged bleeding following injury, trauma, or surgery (including dental work). Women with this condition can have prolonged and sometimes abnormally heavy menstrual bleeding. Affected women also have an increased risk of excessive blood loss during pregnancy and childbirth.\n\nAbout a quarter of individuals with Glanzmann thrombasthenia have bleeding in the gastrointestinal tract, which often occurs later in life. Rarely, affected individuals have bleeding inside the skull (intracranial hemorrhage) or joints (hemarthrosis).\n\nThe severity and frequency of the bleeding episodes in Glanzmann thrombasthenia can vary greatly among affected individuals, even in the same family. Spontaneous bleeding tends to become less frequent with age.
Pituitary dependent hypercortisolism
MedGen UID:
66381
Concept ID:
C0221406
Disease or Syndrome
AIP familial isolated pituitary adenoma (AIP-FIPA) is defined as the presence of an AIP germline pathogenic variant in an individual with a pituitary adenoma (regardless of family history). The most commonly occurring pituitary adenomas in this disorder are growth hormone-secreting adenomas (somatotropinoma), followed by prolactin-secreting adenomas (prolactinoma), growth hormone and prolactin co-secreting adenomas (somatomammotropinoma), and nonfunctioning pituitary adenomas (NFPA). Rarely TSH-secreting adenomas (thyrotropinomas) are observed. Clinical findings result from excess hormone secretion, lack of hormone secretion, and/or mass effects (e.g., headaches, visual field loss). Within the same family, pituitary adenomas can be of the same or different type. Age of onset in AIP-FIPA is usually in the second or third decade.
Ehlers-Danlos syndrome, type 4
MedGen UID:
82790
Concept ID:
C0268338
Disease or Syndrome
Vascular Ehlers-Danlos syndrome (vEDS) is characterized by arterial, intestinal, and/or uterine fragility; thin, translucent skin; easy bruising; characteristic facial appearance (thin vermilion of the lips, micrognathia, narrow nose, prominent eyes); and an aged appearance to the extremities, particularly the hands. Vascular dissection or rupture, gastrointestinal perforation, or organ rupture are the presenting signs in most adults with vEDS. Arterial rupture may be preceded by aneurysm, arteriovenous fistulae, or dissection but also may occur spontaneously. The majority (60%) of individuals with vEDS who are diagnosed before age 18 years are identified because of a positive family history. Neonates may present with clubfoot, hip dislocation, limb deficiency, and/or amniotic bands. Approximately half of children tested for vEDS in the absence of a positive family history present with a major complication at an average age of 11 years. Four minor diagnostic features – distal joint hypermobility, easy bruising, thin skin, and clubfeet – are most often present in those children ascertained without a major complication.
Congenital prothrombin deficiency
MedGen UID:
124425
Concept ID:
C0272317
Disease or Syndrome
Prothrombin deficiency is an extremely rare autosomal recessive bleeding disorder characterized by low levels of circulating prothrombin; it affects about 1 in 2,000,000 individuals. There are 2 main types: type I deficiency, known as true prothrombin deficiency or 'hypoprothrombinemia,' is defined as plasma levels of prothrombin being less than 10% of normal with a concomitant decrease in activity. These patients have severe bleeding from birth, including umbilical cord hemorrhage, hematomas, ecchymoses, hematuria, mucosal bleeding, hemarthroses, intracranial bleeding, gastrointestinal bleeding, and menorrhagia. Type II deficiency, known as 'dysprothrombinemia,' is characterized by normal or low-normal synthesis of a dysfunctional protein. Bleeding symptoms are more variable, depending on the amount of residual functional activity. Variant prothrombin gene alleles can result in 'hypoprothrombinemia' or 'dysprothrombinemia,' and individuals who are compound heterozygous for these 2 types of alleles have variable manifestations. Heterozygous mutation carriers, who have plasma levels between 40 and 60% of normal, are usually asymptomatic, but can show bleeding after tooth extraction or surgical procedures (review by Lancellotti and De Cristofaro, 2009).
Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1
MedGen UID:
321945
Concept ID:
C1832388
Disease or Syndrome
RUNX1 familial platelet disorder with associated myeloid malignancies (RUNX1-FPDMM) is characterized by prolonged bleeding and/or easy bruising and an increased risk of developing a hematologic malignancy. RUNX1-FPDMM is characterized by thrombocytopenia with normal platelet size; bleeding is often greater than expected due to qualitative platelet dysfunction. Myeloid malignancies are the most common, including acute myelogenous leukemia (and myelodysplastic syndrome. T- and B-cell acute lymphoblastic leukemias and lymphomas have also been reported, as well as skin manifestations (e.g., eczema, psoriasis).
Vitamin K-dependent clotting factors, combined deficiency of, type 1
MedGen UID:
376381
Concept ID:
C1848534
Disease or Syndrome
Deficiency of all vitamin K-dependent clotting factors leads to a bleeding tendency that is usually reversed by oral administration of vitamin K. Acquired forms of the disorder can be caused by intestinal malabsorption of vitamin K. Familial multiple coagulation factor deficiency is rare. Clinical symptoms of the disease include episodes of intracranial hemorrhage in the first weeks of life, sometimes leading to a fatal outcome. The pathomechanism is based on a reduced hepatic gamma-carboxylation of glutamic acid residues of all vitamin K-dependent blood coagulation factors, as well as the anticoagulant factors protein C (612283) and protein S (176880). Posttranslational gamma-carboxylation of proteins enables the calcium-dependent attachment of the proteins to the phospholipid bilayer of membranes, an essential prerequisite for blood coagulation. Vitamin K1 acts as a cofactor for the vitamin K-dependent carboxylase in liver microsomes, GGCX. Genetic Heterogeneity of Combined Deficiency of Vitamin K-Dependent Clotting Factors Combined deficiency of vitamin K-dependent clotting factors-2 (VKFCD2; 607473) is caused by mutation in the gene encoding vitamin K epoxide reductase (VKORC1; 608547) on chromosome 16p11.
Platelet-type bleeding disorder 8
MedGen UID:
344008
Concept ID:
C1853278
Disease or Syndrome
Platelet-type bleeding disorder-8 (BDPLT8) is an autosomal recessive condition characterized by mild to moderate mucocutaneous bleeding and excessive bleeding after surgery or trauma. The defect is due to the inability of ADP to induce platelet aggregation (review by Cattaneo, 2011).
Platelet-type bleeding disorder 17
MedGen UID:
396078
Concept ID:
C1861194
Disease or Syndrome
Platelet-type bleeding disorder-17 is an autosomal dominant disorder characterized by increased bleeding tendency due to abnormal platelet function. It is a type of 'gray platelet syndrome' because the platelets appear abnormal on light microscopy. Electron microscopy shows decreased or absent alpha-granules within platelets, and bone marrow biopsy shows increased numbers of abnormal megakaryocytes, suggesting a defect in megakaryopoiesis and platelet production. The bleeding severity is variable (summary by Monteferrario et al., 2014).
Ehlers-Danlos syndrome, musculocontractural type
MedGen UID:
356497
Concept ID:
C1866294
Disease or Syndrome
Other types of Ehlers-Danlos syndrome have additional signs and symptoms. The cardiac-valvular type causes severe problems with the valves that control the movement of blood through the heart. People with the kyphoscoliotic type experience severe curvature of the spine that worsens over time and can interfere with breathing by restricting lung expansion. A type of Ehlers-Danlos syndrome called brittle cornea syndrome is characterized by thinness of the clear covering of the eye (the cornea) and other eye abnormalities. The spondylodysplastic type features short stature and skeletal abnormalities such as abnormally curved (bowed) limbs. Abnormalities of muscles, including hypotonia and permanently bent joints (contractures), are among the characteristic signs of the musculocontractural and myopathic forms of Ehlers-Danlos syndrome. The periodontal type causes abnormalities of the teeth and gums.\n\nBleeding problems are common in the vascular type of Ehlers-Danlos syndrome and are caused by unpredictable tearing (rupture) of blood vessels and organs. These complications can lead to easy bruising, internal bleeding, a hole in the wall of the intestine (intestinal perforation), or stroke. During pregnancy, women with vascular Ehlers-Danlos syndrome may experience rupture of the uterus. Additional forms of Ehlers-Danlos syndrome that involve rupture of the blood vessels include the kyphoscoliotic, classical, and classical-like types.\n\nMany people with the Ehlers-Danlos syndromes have soft, velvety skin that is highly stretchy (elastic) and fragile. Affected individuals tend to bruise easily, and some types of the condition also cause abnormal scarring. People with the classical form of Ehlers-Danlos syndrome experience wounds that split open with little bleeding and leave scars that widen over time to create characteristic "cigarette paper" scars. The dermatosparaxis type of the disorder is characterized by loose skin that sags and wrinkles, and extra (redundant) folds of skin may be present.\n\nAn unusually large range of joint movement (hypermobility) occurs in most forms of Ehlers-Danlos syndrome, and it is a hallmark feature of the hypermobile type. Infants and children with hypermobility often have weak muscle tone (hypotonia), which can delay the development of motor skills such as sitting, standing, and walking. The loose joints are unstable and prone to dislocation and chronic pain. In the arthrochalasia type of Ehlers-Danlos syndrome, infants have hypermobility and dislocations of both hips at birth.\n\nThe various forms of Ehlers-Danlos syndrome have been classified in several different ways. Originally, 11 forms of Ehlers-Danlos syndrome were named using Roman numerals to indicate the types (type I, type II, and so on). In 1997, researchers proposed a simpler classification (the Villefranche nomenclature) that reduced the number of types to six and gave them descriptive names based on their major features. In 2017, the classification was updated to include rare forms of Ehlers-Danlos syndrome that were identified more recently. The 2017 classification describes 13 types of Ehlers-Danlos syndrome.\n\nEhlers-Danlos syndrome is a group of disorders that affect connective tissues supporting the skin, bones, blood vessels, and many other organs and tissues. Defects in connective tissues cause the signs and symptoms of these conditions, which range from mildly loose joints to life-threatening complications.
Factor XIII, b subunit, deficiency of
MedGen UID:
442490
Concept ID:
C2750481
Finding
Factor XIII deficiency is an autosomal recessive hematologic disorder characterized by increased bleeding and poor wound healing. Most cases of congenital factor XIII deficiency result from mutation in the A subunit (Kangsadalampai et al., 1999). Ichinose et al. (1996, 2000) proposed a classification of factor XIII deficiency: XIIIA deficiency (formerly 'type II' F13 deficiency) and XIIIB deficiency (formerly 'type I' F13 deficiency), as well as a possible combined deficiency of the 2.
Factor XIII, A subunit, deficiency of
MedGen UID:
442497
Concept ID:
C2750514
Disease or Syndrome
Factor XIII deficiency is an autosomal recessive hematologic disorder characterized by increased bleeding and poor wound healing. Most cases of congenital factor XIII deficiency result from mutation in the A subunit (Kangsadalampai et al., 1999). Ichinose et al. (1996, 2000) proposed a classification of factor XIII deficiency: XIIIA deficiency (formerly 'type II' F13 deficiency) and XIIIB deficiency (formerly 'type I' F13 deficiency), as well as a possible combined deficiency of the 2.
Hermansky-Pudlak syndrome 1
MedGen UID:
419514
Concept ID:
C2931875
Disease or Syndrome
Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, a bleeding diathesis, and, in some individuals, pulmonary fibrosis, granulomatous colitis, or immunodeficiency. Ocular findings include reduced iris pigment with iris transillumination, reduced retinal pigment, foveal hypoplasia with significant reduction in visual acuity (usually in the range of 20/50 to 20/400), nystagmus, and increased crossing of the optic nerve fibers. Hair color ranges from white to brown; skin color ranges from white to olive and is usually a shade lighter than that of other family members. The bleeding diathesis can result in variable bruising, epistaxis, gingival bleeding, postpartum hemorrhage, colonic bleeding, and prolonged bleeding with menses or after tooth extraction, circumcision, and other surgeries. Pulmonary fibrosis, a restrictive lung disease, typically causes symptoms in the early thirties and can progress to death within a decade. Granulomatous colitis is severe in about 15% of affected individuals. Neutropenia and/or immune defects occur primarily in individuals with pathogenic variants in AP3B1 and AP3D1.
Bernard-Soulier syndrome, type A2, autosomal dominant
MedGen UID:
478706
Concept ID:
C3277076
Disease or Syndrome
Autosomal dominant Bernard-Soulier syndrome type A2 (BSSA2) is characterized by chronic macrothrombocytopenia with mild or no clinical symptoms, normal platelet function, and normal megakaryocyte count. When present, clinical findings include excessive ecchymoses, frequent epistaxis, gingival bleeding, prolonged menstrual periods, or prolonged bleeding after tooth extraction (Savoia et al., 2001). Genetic Heterogeneity of Bernard-Soulier Syndrome Homozygous or compound heterozygous mutations in the GP1BA gene cause classic autosomal recessive Bernard-Soulier syndrome (BSSA1; 231200).
Bleeding disorder, platelet-type, 13, susceptibility to
MedGen UID:
481244
Concept ID:
C3279614
Finding
Susceptibility to platelet-type bleeding disorder-13 is due to a defective thromboxane A2 receptor on platelets. The susceptibility is inherited in an autosomal dominant pattern, but clinical features, including mild mucocutaneous bleeding, occur only in the presence of a 'second hit' affecting platelet function; this second hit may be either in the TBXA2R gene or in another gene affecting the coagulation cascade (summary by Mumford et al., 2010).
Platelet-type bleeding disorder 11
MedGen UID:
481750
Concept ID:
C3280120
Disease or Syndrome
Platelet-type bleeding disorder-11 is an autosomal recessive mild to moderate bleeding disorder caused by defective platelet activation and aggregation in response to collagen (summary by Dumont et al., 2009).
Hermansky-Pudlak syndrome 6
MedGen UID:
854714
Concept ID:
C3888007
Disease or Syndrome
Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, a bleeding diathesis, and, in some individuals, pulmonary fibrosis, granulomatous colitis, or immunodeficiency. Ocular findings include reduced iris pigment with iris transillumination, reduced retinal pigment, foveal hypoplasia with significant reduction in visual acuity (usually in the range of 20/50 to 20/400), nystagmus, and increased crossing of the optic nerve fibers. Hair color ranges from white to brown; skin color ranges from white to olive and is usually a shade lighter than that of other family members. The bleeding diathesis can result in variable bruising, epistaxis, gingival bleeding, postpartum hemorrhage, colonic bleeding, and prolonged bleeding with menses or after tooth extraction, circumcision, and other surgeries. Pulmonary fibrosis, a restrictive lung disease, typically causes symptoms in the early thirties and can progress to death within a decade. Granulomatous colitis is severe in about 15% of affected individuals. Neutropenia and/or immune defects occur primarily in individuals with pathogenic variants in AP3B1 and AP3D1.
Portal hypertension, noncirrhotic, 2
MedGen UID:
1794158
Concept ID:
C5561948
Disease or Syndrome
Noncirrhotic portal hypertension-2 (NCPH2) is an autosomal recessive disorder characterized by signs of liver dysfunction that become apparent in the first decades of life. Affected individuals have jaundice, hyperbilirubinemia, pancytopenia, including neutropenia, lymphopenia, and thrombocytopenia, hepatosplenomegaly, and esophageal varices. Some patients may have recurrent infections or features suggestive of an immunodeficiency. Liver biopsy is notable for the absence of cirrhosis and the presence of nodular regeneration. Liver sinusoidal endothelial cells (LSECs) have abnormal expression of CD34 (142230) (summary by Drzewiecki et al., 2021). For a discussion of genetic heterogeneity of NCPH, see 617068.

Professional guidelines

PubMed

Gauer RL, Whitaker DJ
Am Fam Physician 2022 Sep;106(3):288-298. PMID: 36126009
Verner I, Prag Naveh H, Bertossi D
Dermatol Ther 2019 May;32(3):e12861. Epub 2019 Mar 28 doi: 10.1111/dth.12861. PMID: 30758903
Momeni A, Gruber RP
Aesthet Surg J 2016 Oct;36(9):983-92. doi: 10.1093/asj/sjw093. PMID: 27651480

Recent clinical studies

Etiology

Li Y, Liao M, Zhu Y, Gao J, Song Y, Zhai Y, Zhu M, He Y, Dong W
Aesthet Surg J 2022 Mar 15;42(4):NP230-NP241. doi: 10.1093/asj/sjab387. PMID: 34758056Free PMC Article
Bachoo S, Batura D
Br J Hosp Med (Lond) 2021 Oct 2;82(10):1-9. Epub 2021 Oct 26 doi: 10.12968/hmed.2020.0715. PMID: 34726937
Carratola M, Hart CK
Semin Pediatr Surg 2021 Jun;30(3):151057. Epub 2021 May 21 doi: 10.1016/j.sempedsurg.2021.151057. PMID: 34172217
García-Chávez J, Majluf-Cruz A
Gac Med Mex 2020;156(1):67-77. doi: 10.24875/GMM.19005469. PMID: 32026881
Lee A, May A, Obremskey WT
J Am Acad Orthop Surg 2019 Mar 1;27(5):e199-e206. doi: 10.5435/JAAOS-D-17-00616. PMID: 30431504

Diagnosis

Guda VA, Brown ME, Palacios M
J Fam Pract 2022 Oct;71(8):E9-E11. doi: 10.12788/jfp.0492. PMID: 36508558
Ruiz R, Hintermann B
Foot Ankle Clin 2021 Jun;26(2):291-304. Epub 2021 Apr 17 doi: 10.1016/j.fcl.2021.03.004. PMID: 33990253
Sibaud V, Beylot-Barry M, Protin C, Vigarios E, Recher C, Ysebaert L
Am J Clin Dermatol 2020 Dec;21(6):799-812. doi: 10.1007/s40257-020-00535-x. PMID: 32613545
García-Chávez J, Majluf-Cruz A
Gac Med Mex 2020;156(1):67-77. doi: 10.24875/GMM.19005469. PMID: 32026881
Isbister GK, Fan HW
Lancet 2011 Dec 10;378(9808):2039-2047. Epub 2011 Jul 15 doi: 10.1016/S0140-6736(10)62230-1. PMID: 21762981

Therapy

Li Y, Liao M, Zhu Y, Gao J, Song Y, Zhai Y, Zhu M, He Y, Dong W
Aesthet Surg J 2022 Mar 15;42(4):NP230-NP241. doi: 10.1093/asj/sjab387. PMID: 34758056Free PMC Article
Şahan E, Boylu ME
Psychiatr Danub 2021 Spring;33(1):65-66. doi: 10.24869/psyd.2021.65. PMID: 33857043
Altunay ZO, Onerci M
J Craniofac Surg 2021 Mar-Apr 01;32(2):609-611. doi: 10.1097/SCS.0000000000006846. PMID: 33704992
Verner I, Prag Naveh H, Bertossi D
Dermatol Ther 2019 May;32(3):e12861. Epub 2019 Mar 28 doi: 10.1111/dth.12861. PMID: 30758903
Tasman AJ
Facial Plast Surg 2018 Feb;34(1):14-21. Epub 2018 Feb 6 doi: 10.1055/s-0037-1617444. PMID: 29409099

Prognosis

Zhu HH, Qin YZ, Zhang ZL, Liu YJ, Wen LJ, You MJ, Zhang C, Such E, Luo H, Yuan HJ, Zhou HS, Liu HX, Xu R, Li J, Li JH, Hao JP, Jin J, Yu L, Zhang JY, Liu LP, Zhang LP, Huang RB, Shen SH, Gao SJ, Wang W, Yan XJ, Zhang XY, Du X, Chu XX, Yu YF, Wang Y, Mi YC, Lu Y, Cai Z, Su Z, Taussig DC, MacMahon S, Ball ED, Wang HY, Welch JS, Yin CC, Borthakur G, Sanz MA, Kantarjian HM, Huang JY, Hu J, Chen SN
Blood Adv 2023 Jul 11;7(13):2972-2982. doi: 10.1182/bloodadvances.2022008364. PMID: 36799929Free PMC Article
Sibaud V, Beylot-Barry M, Protin C, Vigarios E, Recher C, Ysebaert L
Am J Clin Dermatol 2020 Dec;21(6):799-812. doi: 10.1007/s40257-020-00535-x. PMID: 32613545
García-Chávez J, Majluf-Cruz A
Gac Med Mex 2020;156(1):67-77. doi: 10.24875/GMM.19005469. PMID: 32026881
Kassir M, Gupta M, Galadari H, Kroumpouzos G, Katsambas A, Lotti T, Vojvodic A, Grabbe S, Juchems E, Goldust M
J Cosmet Dermatol 2020 Mar;19(3):570-573. Epub 2019 Dec 30 doi: 10.1111/jocd.13266. PMID: 31889407
von Arx T, Tamura K, Yukiya O, Lozanoff S
Swiss Dent J 2018 May 14;128(5):382-392. doi: 10.61872/sdj-2018-05-01. PMID: 29734800

Clinical prediction guides

Aysel A, Karatan B, Müderris T
J Craniofac Surg 2022 Mar-Apr 01;33(2):661-664. doi: 10.1097/SCS.0000000000007692. PMID: 33867512
Achatz G, Schwabe K, Brill S, Zischek C, Schmidt R, Friemert B, Beltzer C
Eur J Trauma Emerg Surg 2022 Oct;48(5):3575-3589. Epub 2020 Jun 23 doi: 10.1007/s00068-020-01405-1. PMID: 32577779
Veronesi G, Virdi A, Leuzzi M, Gurioli C, Chessa MA, Guglielmo A, Neri I
Pediatr Dermatol 2021 Sep;38(5):1012-1019. Epub 2021 Sep 24 doi: 10.1111/pde.14771. PMID: 34561885
Cihantimur B, Aglamis O, Ozsular Y
Aesthetic Plast Surg 2021 Dec;45(6):2996-3002. Epub 2021 Aug 9 doi: 10.1007/s00266-021-02488-w. PMID: 34373975
Carratola M, Hart CK
Semin Pediatr Surg 2021 Jun;30(3):151057. Epub 2021 May 21 doi: 10.1016/j.sempedsurg.2021.151057. PMID: 34172217

Recent systematic reviews

Lucas JP, Allen M, Nguyen BK, Svider PF, Folbe AJ, Carron M
Facial Plast Surg Aesthet Med 2020 Nov/Dec;22(6):471-480. Epub 2020 Aug 10 doi: 10.1089/fpsam.2020.0029. PMID: 32779938
Boskabadi H, Rakhshanizadeh F, Zakerihamidi M
Arch Iran Med 2020 Feb 1;23(2):128-140. PMID: 32061076
Lee HS, Yoon HY, Kim IH, Hwang SH
Eur Arch Otorhinolaryngol 2017 Jul;274(7):2685-2694. Epub 2017 Mar 17 doi: 10.1007/s00405-017-4535-6. PMID: 28314960
Ong AA, Farhood Z, Kyle AR, Patel KG
Plast Reconstr Surg 2016 May;137(5):1448-1462. doi: 10.1097/PRS.0000000000002101. PMID: 27119920
Pulikkottil BJ, Dauwe P, Daniali L, Rohrich RJ
Plast Reconstr Surg 2013 Sep;132(3):352e-360e. doi: 10.1097/PRS.0b013e31829acc60. PMID: 23985647

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