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Prolonged partial thromboplastin time

MedGen UID:
66815
Concept ID:
C0240671
Finding
Synonyms: Prolonged activated partial thromboplastin time; Prolonged PTT; PTT prolonged
SNOMED CT: Partial thromboplastin time increased (409675001)
 
HPO: HP:0003645

Definition

Increased time to coagulation in the partial thromboplastin time (PTT) test, a measure of the intrinsic and common coagulation pathways. Phospholipid, and activator, and calcium are mixed into an anticoagulated plasma sample, and the time is measured until a thrombus forms. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVProlonged partial thromboplastin time

Conditions with this feature

Hereditary factor IX deficiency disease
MedGen UID:
945
Concept ID:
C0008533
Disease or Syndrome
Hemophilia B is characterized by deficiency in factor IX clotting activity that results in prolonged oozing after injuries, tooth extractions, or surgery, and delayed or recurrent bleeding prior to complete wound healing. The age of diagnosis and frequency of bleeding episodes are related to the level of factor IX clotting activity. In individuals with severe hemophilia B, spontaneous joint or deep-muscle bleeding is the most frequent sign. Individuals with severe hemophilia B are usually diagnosed during the first two years of life; without prophylactic treatment, they may average up to two to five spontaneous bleeding episodes each month. Individuals with moderate hemophilia B seldom have spontaneous bleeding; however, they do have prolonged or delayed oozing after relatively minor trauma and are usually diagnosed before age five to six years; the frequency of bleeding episodes varies from once a month to once a year. Individuals with mild hemophilia B do not have spontaneous bleeding episodes; however, without pre- and postoperative treatment, abnormal bleeding occurs with surgery or tooth extractions; the frequency of bleeding may vary from once a year to once every ten years. Individuals with mild hemophilia B are often not diagnosed until later in life. In any individual with hemophilia B, bleeding episodes may be more frequent in childhood and adolescence than in adulthood. Approximately 30% of heterozygous females have factor IX clotting activity lower than 40% and are at risk for bleeding (even if the affected family member has mild hemophilia B), although symptoms are usually mild. After major trauma or invasive procedures, prolonged or excessive bleeding usually occurs, regardless of severity.
Congenital factor V deficiency
MedGen UID:
4633
Concept ID:
C0015499
Disease or Syndrome
Factor V deficiency is a rare autosomal recessive bleeding disorder with variable phenotypic expression (summary by van Wijk et al., 2001).
Hereditary factor XI deficiency disease
MedGen UID:
8770
Concept ID:
C0015523
Disease or Syndrome
Factor XI deficiency is an autosomal bleeding disorder characterized by reduced levels of factor XI in plasma (less than 15 IU/dL). Bleeding occurs mainly after trauma or surgery. On the basis of the concordance or discordance of F11 antigen and activity, the disorder is classified into the more frequent cross-reactive negative (CRM-) and the rarer CRM positive (CRM+) (summary by Duga and Salomon, 2009).
Factor XII deficiency disease
MedGen UID:
8772
Concept ID:
C0015526
Disease or Syndrome
Decreased activity of coagulation factor XII. Factor XII (fXII) is part of the intrinsic coagulation pathway and binds to exposed collagen at site of vessel wall injury, activated by high-MW kininogen and kallikrein, thereby initiating the coagulation cascade.
Hereditary factor VIII deficiency disease
MedGen UID:
5501
Concept ID:
C0019069
Disease or Syndrome
Hemophilia A is characterized by deficiency in factor VIII clotting activity that results in prolonged oozing after injuries, tooth extractions, or surgery, and delayed or recurrent bleeding prior to complete wound healing. The age of diagnosis and frequency of bleeding episodes are related to the level of factor VIII clotting activity. Individuals with severe hemophilia A are usually diagnosed during the first two years of life following oral or soft tissue bleeding either with procedures or due to a known family history of hemophilia. Without prophylactic treatment, individuals may average up to two to five spontaneous bleeding episodes each month including spontaneous joint bleeds or deep-muscle hematomas, and prolonged bleeding or excessive pain and swelling from minor injuries, surgery, and tooth extractions. Individuals with moderate hemophilia A seldom have spontaneous bleeding, although it varies between individuals; however, they do have prolonged or delayed bleeding after relatively minor trauma and are usually diagnosed before age five to six years; the frequency of bleeding episodes varies, usually from once a month to once a year. Individuals with mild hemophilia A do not have spontaneous bleeding episodes; however, without pre- and postoperative treatment, abnormal bleeding occurs with surgery or tooth extractions; the frequency of bleeding episodes varies widely, typically from once a year to once every ten years. Individuals with mild hemophilia A are often not diagnosed until later in life. Approximately 30% of heterozygous females have factor VIII clotting activity below 40% and are at risk for bleeding (even if males in the family are only mildly affected). After major trauma or invasive procedures, prolonged or excessive bleeding usually occurs, regardless of severity. In addition, 25% of heterozygous females with normal factor VIII clotting activity report an increased bleeding tendency.
Tyrosinemia type I
MedGen UID:
75688
Concept ID:
C0268490
Disease or Syndrome
Untreated tyrosinemia type I usually presents either in young infants with severe liver involvement or later in the first year with liver dysfunction and renal tubular dysfunction associated with growth failure and rickets. Untreated children may have repeated, often unrecognized, neurologic crises lasting one to seven days that can include change in mental status, abdominal pain, peripheral neuropathy, and/or respiratory failure requiring mechanical ventilation. Death in the untreated child usually occurs before age ten years, typically from liver failure, neurologic crisis, or hepatocellular carcinoma. Combined treatment with nitisinone and a low-tyrosine diet has resulted in a greater than 90% survival rate, normal growth, improved liver function, prevention of cirrhosis, correction of renal tubular acidosis, and improvement in secondary rickets.
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 factor X deficiency disease
MedGen UID:
543976
Concept ID:
C0272327
Disease or Syndrome
A rare inherited bleeding disorder with a decreased antigen and/or activity of factor X (FX) and characterized by mild to severe bleeding symptoms.
High molecular weight kininogen deficiency
MedGen UID:
75780
Concept ID:
C0272340
Disease or Syndrome
High molecular weight kininogen (HMWK) deficiency is an autosomal recessive coagulation defect. It is known by a variety of names, including Fitzgerald trait, Flaujeac trait, and Williams trait. Patients with HWMK deficiency do not have a hemorrhagic tendency, but they exhibit abnormal surface-mediated activation of fibrinolysis. Fitzgerald trait represents a 'true' deficiency of HMWK, whereas Flaujeac and Williams traits represent total kininogen deficiency, in which both HMWK and low molecular weight kininogen (LMWK) are deficient. HMWK and LMWK are both encoded by the KNG1 gene (612358) (Bick, 2002; Takagaki et al., 1985).
PMM2-congenital disorder of glycosylation
MedGen UID:
138111
Concept ID:
C0349653
Disease or Syndrome
PMM2-CDG, the most common of a group of disorders of abnormal glycosylation of N-linked oligosaccharides, is divided into three clinical stages: infantile multisystem, late-infantile and childhood ataxia–intellectual disability, and adult stable disability. The clinical manifestations and course are highly variable, ranging from infants who die in the first year of life to mildly affected adults. Clinical findings tend to be similar in sibs. In the infantile multisystem presentation, infants show axial hypotonia, hyporeflexia, esotropia, and developmental delay. Feeding problems, vomiting, faltering growth, and developmental delay are frequently seen. Subcutaneous fat may be excessive over the buttocks and suprapubic region. Two distinct clinical courses are observed: (1) a nonfatal neurologic course with faltering growth, strabismus, developmental delay, cerebellar hypoplasia, and hepatopathy in infancy followed by neuropathy and retinitis pigmentosa in the first or second decade; and (2) a more severe neurologic-multivisceral course with approximately 20% mortality in the first year of life. The late-infantile and childhood ataxia–intellectual disability stage, which begins between ages three and ten years, is characterized by hypotonia, ataxia, severely delayed language and motor development, inability to walk, and IQ of 40 to 70; other findings include seizures, stroke-like episodes or transient unilateral loss of function, coagulopathy, retinitis pigmentosa, joint contractures, and skeletal deformities. In the adult stable disability stage, intellectual ability is stable; peripheral neuropathy is variable, progressive retinitis pigmentosa and myopia are seen, thoracic and spinal deformities with osteoporosis worsen, and premature aging is observed; females may lack secondary sexual development and males may exhibit decreased testicular volume. Hypogonadotropic hypogonadism and coagulopathy may occur. The risk for deep venous thrombosis is increased.
Congenital disorder of glycosylation type 1E
MedGen UID:
324784
Concept ID:
C1837396
Disease or Syndrome
Congenital disorders of glycosylation (CDGs) are metabolic deficiencies in glycoprotein biosynthesis that usually cause severe mental and psychomotor retardation. Different forms of CDGs can be recognized by altered isoelectric focusing (IEF) patterns of serum transferrin. For a general discussion of CDGs, see CDG Ia (212065) and CDG Ib (602579).
ALG2-congenital disorder of glycosylation
MedGen UID:
334618
Concept ID:
C1842836
Disease or Syndrome
Congenital disorder of glycosylation type Ii (CDG1I) is a rare autosomal recessive disorder characterized by neurologic involvement, including a convulsive syndrome of unknown origin, axial hypotonia, and mental and motor regression (summary by Papazoglu et al., 2021). For a general discussion of CDGs, see CDG1A (212065).
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.
Noonan syndrome 4
MedGen UID:
339908
Concept ID:
C1853120
Disease or Syndrome
Noonan syndrome (NS) is characterized by characteristic facies, short stature, congenital heart defect, and developmental delay of variable degree. Other findings can include broad or webbed neck, unusual chest shape with superior pectus carinatum and inferior pectus excavatum, cryptorchidism, varied coagulation defects, lymphatic dysplasias, and ocular abnormalities. Although birth length is usually normal, final adult height approaches the lower limit of normal. Congenital heart disease occurs in 50%-80% of individuals. Pulmonary valve stenosis, often with dysplasia, is the most common heart defect and is found in 20%-50% of individuals. Hypertrophic cardiomyopathy, found in 20%-30% of individuals, may be present at birth or develop in infancy or childhood. Other structural defects include atrial and ventricular septal defects, branch pulmonary artery stenosis, and tetralogy of Fallot. Up to one fourth of affected individuals have mild intellectual disability, and language impairments in general are more common in NS than in the general population.
Congenital lactic acidosis, Saguenay-Lac-Saint-Jean type
MedGen UID:
387801
Concept ID:
C1857355
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 5 (MC4DN5) is an autosomal recessive severe metabolic multisystemic disorder with onset in infancy. Features include delayed psychomotor development, impaired intellectual development with speech delay, mild dysmorphic facial features, hypotonia, ataxia, and seizures. There is increased serum lactate and episodic hypoglycemia. Some patients may have cardiomyopathy, abnormal breathing, or liver abnormalities, reflecting systemic involvement. Brain imaging shows lesions in the brainstem and basal ganglia, consistent with a diagnosis of Leigh syndrome (see 256000). Affected individuals tend to have episodic metabolic and/or neurologic crises in early childhood, which often lead to early death (summary by Debray et al., 2011). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Congenital bile acid synthesis defect 4
MedGen UID:
388039
Concept ID:
C1858328
Disease or Syndrome
Congenital bile acid synthesis defect type 4 (BAS defect type 4) is an anomaly of bile acid synthesis (see this term) characterized by mild cholestatic liver disease, fat malabsorption and/or neurological disease.
Celiac disease, susceptibility to, 1
MedGen UID:
395227
Concept ID:
C1859310
Finding
Celiac disease is a systemic autoimmune disease that can be associated with gastrointestinal findings (diarrhea, malabsorption, abdominal pain and distension, bloating, vomiting, and weight loss) and/or highly variable non-gastrointestinal findings (dermatitis herpetiformis, chronic fatigue, joint pain/inflammation, iron deficiency anemia, migraines, depression, attention-deficit disorder, epilepsy, osteoporosis/osteopenia, infertility and/or recurrent fetal loss, vitamin deficiencies, short stature, failure to thrive, delayed puberty, dental enamel defects, and autoimmune disorders). Classic celiac disease, characterized by mild to severe gastrointestinal symptoms, is less common than non-classic celiac disease, characterized by absence of gastrointestinal symptoms.
Thrombophilia due to activated protein C resistance
MedGen UID:
396074
Concept ID:
C1861171
Disease or Syndrome
Factor V Leiden thrombophilia is characterized by a poor anticoagulant response to activated protein C (APC) and an increased risk for venous thromboembolism (VTE). Deep vein thrombosis (DVT) is the most common VTE, with the legs being the most common site. Thrombosis in unusual locations is less common. Evidence suggests that heterozygosity for the Leiden variant has at most a modest effect on risk for recurrent thrombosis after initial treatment of a first VTE. It is unlikely that factor V Leiden thrombophilia (i.e., heterozygosity or homozygosity for the Leiden variant) is a major factor contributing to pregnancy loss and other adverse pregnancy outcomes (preeclampsia, fetal growth restriction, and placental abruption). The clinical expression of factor V Leiden thrombophilia is influenced by the following: The number of Leiden variants (heterozygotes have a slightly increased risk for venous thrombosis; homozygotes have a much greater thrombotic risk). Coexisting genetic thrombophilic disorders, which have a supra-additive effect on overall thrombotic risk. Acquired thrombophilic disorders: antiphospholipid antibody (APLA) syndrome, paroxysmal nocturnal hemoglobinuria, myeloproliferative disorders, and increased levels of clotting factors. Circumstantial risk factors including but not limited to pregnancy, central venous catheters, travel, combined oral contraceptive (COC) use and other combined contraceptives, oral hormone replacement therapy (HRT), selective estrogen receptor modulators (SERMs), obesity, leg injury, and advancing age.
Bone fragility with contractures, arterial rupture, and deafness
MedGen UID:
382811
Concept ID:
C2676285
Disease or Syndrome
BCARD syndrome is an autosomal recessive connective tissue disorder characterized by bone abnormalities, including low bone mineral density, scoliosis, contractures of the fingers and other joints, prominent knees, and rare pathologic fractures; cataract and other ocular abnormalities, including high myopia, optically empty vitreous, and risk for retinal detachment; risk of arterial rupture due to vascular aneurysm or dissection; and sensorineural deafness. Affected individuals also exhibit recognizable craniofacial dysmorphisms, and variable skin features have been observed, including reduced palmar creases, soft skin with easy bruising, and blistering. Developmental delay, which is present in most patients, may be attributable to sensory deficits or medical complications (Ewans et al., 2019).
PGM1-congenital disorder of glycosylation
MedGen UID:
414536
Concept ID:
C2752015
Disease or Syndrome
Congenital disorder of glycosylation type It (CDG1T) is an autosomal recessive disorder characterized by a wide range of clinical manifestations and severity. The most common features include cleft lip and bifid uvula, apparent at birth, followed by hepatopathy, intermittent hypoglycemia, short stature, and exercise intolerance, often accompanied by increased serum creatine kinase. Less common features include rhabdomyolysis, dilated cardiomyopathy, and hypogonadotropic hypogonadism (summary by Tegtmeyer et al., 2014). For a discussion of the classification of CDGs, see CDG1A (212065).
ALG12-congenital disorder of glycosylation
MedGen UID:
443954
Concept ID:
C2931001
Disease or Syndrome
Congenital disorders of glycosylation (CDG), previously called carbohydrate-deficient glycoprotein syndromes (CDGSs), are a group of hereditary multisystem disorders first recognized by Jaeken et al. (1980). The characteristic biochemical abnormality of CDGs is the hypoglycosylation of glycoproteins, which is routinely determined by isoelectric focusing (IEF) of serum transferrin. Type I CDG comprises those disorders in which there is a defect in the assembly of lipid-linked oligosaccharides or their transfer onto nascent glycoproteins, whereas type II CDG comprises defects of trimming, elongation, and processing of protein-bound glycans. CDG1G is a multisystem disorder characterized by impaired psychomotor development, dysmorphic features, failure to thrive, male genital hypoplasia, coagulation abnormalities, and immune deficiency. More variable features include skeletal dysplasia, cardiac anomalies, ocular abnormalities, and sensorineural hearing loss. Some patients die in the early neonatal or infantile period, whereas others are mildly affected and live to adulthood (summary by Tahata et al., 2019). For a general discussion of CDGs, see CDG1A (212065).
B4GALT1-congenital disorder of glycosylation
MedGen UID:
419310
Concept ID:
C2931009
Disease or Syndrome
Congenital disorders of glycosylation (CDG) are a group of hereditary multisystem disorders that are commonly associated with severe psychomotor and mental retardation. The characteristic biochemical abnormality of CDGs is the hypoglycosylation of glycoproteins, which is routinely determined by isoelectric focusing (IEF) of serum transferrin. Type I CDG comprises those disorders in which there is a defect in the assembly of lipid-linked oligosaccharides or their transfer onto nascent glycoproteins, whereas type II CDG comprises defects of trimming, elongation, and processing of protein-bound glycans (summary by Hansske et al., 2002). For a general discussion of CDGs, see CDG1A (212065).
Noonan syndrome 10
MedGen UID:
902892
Concept ID:
C4225280
Disease or Syndrome
Noonan syndrome (NS) is characterized by characteristic facies, short stature, congenital heart defect, and developmental delay of variable degree. Other findings can include broad or webbed neck, unusual chest shape with superior pectus carinatum and inferior pectus excavatum, cryptorchidism, varied coagulation defects, lymphatic dysplasias, and ocular abnormalities. Although birth length is usually normal, final adult height approaches the lower limit of normal. Congenital heart disease occurs in 50%-80% of individuals. Pulmonary valve stenosis, often with dysplasia, is the most common heart defect and is found in 20%-50% of individuals. Hypertrophic cardiomyopathy, found in 20%-30% of individuals, may be present at birth or develop in infancy or childhood. Other structural defects include atrial and ventricular septal defects, branch pulmonary artery stenosis, and tetralogy of Fallot. Up to one fourth of affected individuals have mild intellectual disability, and language impairments in general are more common in NS than in the general population.
Congenital bile acid synthesis defect 5
MedGen UID:
904751
Concept ID:
C4225390
Congenital Abnormality
Any congenital bile acid synthesis defect in which the cause of the disease is a mutation in the ABCD3 gene.
Developmental and epileptic encephalopathy, 36
MedGen UID:
1382656
Concept ID:
C4317295
Disease or Syndrome
Developmental and epileptic encephalopathy-36 (DEE36) is an X-linked neurodevelopmental disorder characterized by the onset of seizures at a mean age of 6.5 months. Most patients present with infantile spasms associated with hypsarrhythmia on EEG, consistent with a clinical diagnosis of West syndrome. The seizures tend to be refractory to treatment, although some patients may respond to benzodiazepines or a ketogenic diet. Affected individuals have severely delayed psychomotor development with poor motor function, severe intellectual disability, poor or absent speech, and limited eye contact. More variable features include feeding difficulties sometimes requiring tube feeding, ocular defects including cortical visual impairment, dysmorphic facial features, and scoliosis or osteopenia. The vast majority of patients reported have been females, although rare affected males with a similar phenotype have been described. Most patients show normal N-glycosylation on transferrin isoelectric focusing, but some show abnormal N-glycosylation consistent with CDG type I (summary by Ng et al., 2020). For a general phenotypic description and a discussion of genetic heterogeneity of DEE, see 308350. For a discussion of the classification of CDGs, see CDG1A (212065).
Familial hemophagocytic lymphohistiocytosis type 1
MedGen UID:
1642840
Concept ID:
C4551514
Disease or Syndrome
Familial Hemophagocytic lymphohistiocytosis (FHL) is a rare primary immunodeficiency characterized by a macrophage activation syndrome with an onset usually occurring within a few months or less common several years after birth.
Shwachman-Diamond syndrome 2
MedGen UID:
1634617
Concept ID:
C4693704
Disease or Syndrome
Shwachman-Diamond syndrome (SDS) is characterized by: exocrine pancreatic dysfunction with malabsorption, malnutrition, and growth failure; hematologic abnormalities with single- or multilineage cytopenias and susceptibility to myelodysplasia syndrome (MDS) and acute myelogeneous leukemia (AML); and bone abnormalities. In almost all affected children, persistent or intermittent neutropenia is a common presenting finding, often before the diagnosis of SDS is made. Short stature and recurrent infections are common.
Congenital disorder of glycosylation, type IIw
MedGen UID:
1794196
Concept ID:
C5561986
Disease or Syndrome
Congenital disorder of glycosylation type IIw (CDG2W) is an autosomal dominant metabolic disorder characterized by liver dysfunction, coagulation deficiencies, and profound abnormalities in N-glycosylation of serum specific proteins. All reported patients carry the same mutation (602671.0017) (summary by Ng et al., 2021). For an overview of congenital disorders of glycosylation, see CDG1A (212065) and CDG2A (212066).
Cholestasis, progressive familial intrahepatic, 12
MedGen UID:
1824084
Concept ID:
C5774311
Disease or Syndrome
Progressive familial intrahepatic cholestasis-12 (PFIC12) is characterized by neonatal-onset jaundice and conjugated hyperbilirubinemia, associated with intense pruritus. Transaminases are mildly elevated but GGT (see 612346) is normal. Hepatosplenomegaly and mildly prolonged activated partial thromboplastin time (APTT) have been observed in some patients (Qiu et al., 2019).
Inherited prekallikrein deficiency
MedGen UID:
987194
Concept ID:
CN305372
Disease or Syndrome
Prekallikrein deficiency (PKKD) is a rare asymptomatic clotting defect characterized by prolongation of activated partial thromboplastin time (summary by Saito et al., 1981).

Professional guidelines

PubMed

Reed CR, Williamson H, Vatsaas C, Kamyszek R, Leraas HJ, Ray C, Otto J, Fitzgerald T, Agarwal S, Tracy ET
Surgery 2019 Jun;165(6):1108-1115. Epub 2019 Apr 23 doi: 10.1016/j.surg.2019.03.003. PMID: 31027837
Yang W, Shen Z, Peng G, Chen Y, Jiang S, Kang S, Wu J
Chin Med J (Engl) 2000 Jun;113(6):540-3. PMID: 11775876
Usta IM, Barton JR, Amon EA, Gonzalez A, Sibai BM
Am J Obstet Gynecol 1994 Nov;171(5):1342-7. doi: 10.1016/0002-9378(94)90158-9. PMID: 7977544

Recent clinical studies

Etiology

Guo F, Zhu X, Wu Z, Zhu L, Wu J, Zhang F
J Transl Med 2022 Jun 11;20(1):265. doi: 10.1186/s12967-022-03469-6. PMID: 35690822Free PMC Article
Reed CR, Williamson H, Vatsaas C, Kamyszek R, Leraas HJ, Ray C, Otto J, Fitzgerald T, Agarwal S, Tracy ET
Surgery 2019 Jun;165(6):1108-1115. Epub 2019 Apr 23 doi: 10.1016/j.surg.2019.03.003. PMID: 31027837
Willwerth BM, Harper MB, Mandl KD
Pediatr Emerg Care 2003 Aug;19(4):244-7. doi: 10.1097/01.pec.0000086233.54586.87. PMID: 12972821
Mor E, Jennings L, Gonwa TA, Holman MJ, Gibbs J, Solomon H, Goldstein RM, Husberg BS, Watemberg IA, Klintmalm GB
Surg Gynecol Obstet 1993 Mar;176(3):219-27. PMID: 8438192
Woods WG, Luban NL, Hilgartner MW, Miller DR
Am J Dis Child 1979 Jan;133(1):44-6. doi: 10.1001/archpedi.1979.02130010050008. PMID: 760511

Diagnosis

Duetz C, Houtenbos I, de Roij van Zuijdewijn CLM
Neth J Med 2019 Feb;77(2):84-85. PMID: 30895932
Yates SG, Fitts E, De Simone N, Sarode R
Transfus Apher Sci 2019 Feb;58(1):39-42. Epub 2018 Nov 22 doi: 10.1016/j.transci.2018.11.004. PMID: 30497857
Girolami A, Cosi E, Santarossa C, Ferrari S, Girolami B, Lombardi AM
Clin Appl Thromb Hemost 2018 Jan;24(1):33-40. Epub 2016 Dec 29 doi: 10.1177/1076029616686423. PMID: 28030967Free PMC Article
Willwerth BM, Harper MB, Mandl KD
Pediatr Emerg Care 2003 Aug;19(4):244-7. doi: 10.1097/01.pec.0000086233.54586.87. PMID: 12972821
Woods WG, Luban NL, Hilgartner MW, Miller DR
Am J Dis Child 1979 Jan;133(1):44-6. doi: 10.1001/archpedi.1979.02130010050008. PMID: 760511

Therapy

Guo F, Zhu X, Wu Z, Zhu L, Wu J, Zhang F
J Transl Med 2022 Jun 11;20(1):265. doi: 10.1186/s12967-022-03469-6. PMID: 35690822Free PMC Article
Minkowitz B, Lillie E, Ristic JR, Gregory JJ Jr
JBJS Case Connect 2019 Apr-Jun;9(2):e0275. doi: 10.2106/JBJS.CC.18.00275. PMID: 31167219
Sabanis N, Paschou E, Gavriilaki E, Kalaitzoglou A, Vasileiou S
Infect Dis (Lond) 2015;47(10):743-6. Epub 2015 May 8 doi: 10.3109/23744235.2015.1043942. PMID: 25951751
Blank SJ, Grindler DJ, Zerega J, Blinder M, Nussenbaum B
Otolaryngol Head Neck Surg 2014 Dec;151(6):967-71. Epub 2014 Sep 25 doi: 10.1177/0194599814552055. PMID: 25257903
Mor E, Jennings L, Gonwa TA, Holman MJ, Gibbs J, Solomon H, Goldstein RM, Husberg BS, Watemberg IA, Klintmalm GB
Surg Gynecol Obstet 1993 Mar;176(3):219-27. PMID: 8438192

Prognosis

Maillard O, Hirschinger D, Bénéteau S, Koumar Y, Vague A, Girerd R, DiAscia L, Jabot J, Cousty J, Randrianjohany A, Bertolotti A, Raffray L
PLoS One 2023;18(5):e0285900. Epub 2023 May 17 doi: 10.1371/journal.pone.0285900. PMID: 37195992Free PMC Article
Guo F, Zhu X, Wu Z, Zhu L, Wu J, Zhang F
J Transl Med 2022 Jun 11;20(1):265. doi: 10.1186/s12967-022-03469-6. PMID: 35690822Free PMC Article
Reed CR, Williamson H, Vatsaas C, Kamyszek R, Leraas HJ, Ray C, Otto J, Fitzgerald T, Agarwal S, Tracy ET
Surgery 2019 Jun;165(6):1108-1115. Epub 2019 Apr 23 doi: 10.1016/j.surg.2019.03.003. PMID: 31027837
Mor E, Jennings L, Gonwa TA, Holman MJ, Gibbs J, Solomon H, Goldstein RM, Husberg BS, Watemberg IA, Klintmalm GB
Surg Gynecol Obstet 1993 Mar;176(3):219-27. PMID: 8438192
Kusne S, Schwartz M, Breinig MK, Dummer JS, Lee RE, Selby R, Starzl TE, Simmons RL, Ho M
J Infect Dis 1991 May;163(5):1001-7. doi: 10.1093/infdis/163.5.1001. PMID: 1850439Free PMC Article

Clinical prediction guides

Maillard O, Hirschinger D, Bénéteau S, Koumar Y, Vague A, Girerd R, DiAscia L, Jabot J, Cousty J, Randrianjohany A, Bertolotti A, Raffray L
PLoS One 2023;18(5):e0285900. Epub 2023 May 17 doi: 10.1371/journal.pone.0285900. PMID: 37195992Free PMC Article
Guo F, Zhu X, Wu Z, Zhu L, Wu J, Zhang F
J Transl Med 2022 Jun 11;20(1):265. doi: 10.1186/s12967-022-03469-6. PMID: 35690822Free PMC Article
Reed CR, Williamson H, Vatsaas C, Kamyszek R, Leraas HJ, Ray C, Otto J, Fitzgerald T, Agarwal S, Tracy ET
Surgery 2019 Jun;165(6):1108-1115. Epub 2019 Apr 23 doi: 10.1016/j.surg.2019.03.003. PMID: 31027837
Felfernig M, Blaicher A, Kettner SC, Felfernig D, Acimovic S, Kozek-Langenecker SA
Eur J Anaesthesiol 2001 Jul;18(7):467-70. doi: 10.1046/j.1365-2346.2001.00869.x. PMID: 11437875
Woods WG, Luban NL, Hilgartner MW, Miller DR
Am J Dis Child 1979 Jan;133(1):44-6. doi: 10.1001/archpedi.1979.02130010050008. PMID: 760511

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