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Sepsis

MedGen UID:
48626
Concept ID:
C0036690
Disease or Syndrome
Synonyms: Blood Poisoning; Blood Poisonings; Poisoning, Blood; Poisonings, Blood; Septicemia; Septicemias
 
HPO: HP:0100806

Definition

Systemic inflammatory response to infection. [from HPO]

Conditions with this feature

Wiskott-Aldrich syndrome
MedGen UID:
21921
Concept ID:
C0043194
Disease or Syndrome
The WAS-related disorders, which include Wiskott-Aldrich syndrome, X-linked thrombocytopenia (XLT), and X-linked congenital neutropenia (XLN), are a spectrum of disorders of hematopoietic cells, with predominant defects of platelets and lymphocytes caused by pathogenic variants in WAS. WAS-related disorders usually present in infancy. Affected males have thrombocytopenia with intermittent mucosal bleeding, bloody diarrhea, and intermittent or chronic petechiae and purpura; eczema; and recurrent bacterial and viral infections, particularly of the ear. At least 40% of those who survive the early complications develop one or more autoimmune conditions including hemolytic anemia, immune thrombocytopenic purpura, immune-mediated neutropenia, rheumatoid arthritis, vasculitis, and immune-mediated damage to the kidneys and liver. Individuals with a WAS-related disorder, particularly those who have been exposed to Epstein-Barr virus (EBV), are at increased risk of developing lymphomas, which often occur in unusual, extranodal locations including the brain, lung, or gastrointestinal tract. Males with XLT have thrombocytopenia with small platelets; other complications of Wiskott-Aldrich syndrome, including eczema and immune dysfunction, are usually mild or absent. Males with XLN have congenital neutropenia, myeloid dysplasia, and lymphoid cell abnormalities.
X-linked agammaglobulinemia
MedGen UID:
65123
Concept ID:
C0221026
Disease or Syndrome
X-linked agammaglobulinemia (XLA) is characterized by recurrent bacterial infections in affected males in the first two years of life. Recurrent otitis is the most common infection prior to diagnosis. Conjunctivitis, sinopulmonary infections, diarrhea, and skin infections are also frequently seen. Approximately 60% of individuals with XLA are recognized as having immunodeficiency when they develop a severe, life-threatening infection such as pneumonia, empyema, meningitis, sepsis, cellulitis, or septic arthritis. S pneumoniae and H influenzae are the most common organisms found prior to diagnosis and may continue to cause sinusitis and otitis after diagnosis and the initiation of gammaglobulin substitution therapy. Severe, difficult-to-treat enteroviral infections (often manifest as dermatomyositis or chronic meningoencephalitis) can be prevented by this treatment. The prognosis for individuals with XLA has improved markedly in the last 25 years as a result of earlier diagnosis, the development of preparations of gammaglobulin that allow normal concentrations of serum IgG to be achieved, and more liberal use of antibiotics.
Reticular dysgenesis
MedGen UID:
124417
Concept ID:
C0272167
Disease or Syndrome
Reticular dysgenesis is the most severe form of severe combined immunodeficiency (SCID; see this term) and is characterized by bilateral sensorineural deafness and a lack of innate and adaptive immune functions leading to fatal septicemia within days after birth if not treated.
Hyper-IgM syndrome type 1
MedGen UID:
96019
Concept ID:
C0398689
Disease or Syndrome
X-linked hyper IgM syndrome (HIGM1), a disorder of abnormal T- and B-cell function, is characterized by low serum concentrations of IgG, IgA, and IgE with normal or elevated serum concentrations of IgM. Mitogen proliferation may be normal, but NK- and T-cell cytotoxicity can be impaired. Antigen-specific responses are usually decreased or absent. Total numbers of B cells are normal but there is a marked reduction of class-switched memory B cells. Defective oxidative burst of both neutrophils and macrophages has been reported. The range of clinical findings varies, even within the same family. More than 50% of males with HIGM1 develop symptoms by age one year, and more than 90% are symptomatic by age four years. HIGM1 usually presents in infancy with recurrent upper- and lower-respiratory tract bacterial infections, opportunistic infections including Pneumocystis jirovecii pneumonia, and recurrent or protracted diarrhea that can be infectious or noninfectious and is associated with failure to thrive. Neutropenia is common; thrombocytopenia and anemia are less commonly seen. Autoimmune and/or inflammatory disorders (such as sclerosing cholangitis) as well as increased risk for neoplasms have been reported as medical complications of this disorder. Significant neurologic complications, often the result of a CNS infection, are seen in 5%-15% of affected males. Liver disease, a serious complication of HIGM1 once observed in more than 80% of affected males by age 20 years, may be decreasing with adequate screening and treatment of Cryptosporidium infection.
Currarino triad
MedGen UID:
323460
Concept ID:
C1531773
Disease or Syndrome
Currarino syndrome (CS) is a rare congenital disease characterized by the triad of anorectal malformations (ARMs) (usually anal stenosis), presacral mass (commonly anterior sacral meningocele (ASM) or teratoma) and sacral anomalies (i.e. total or partial agenesis of the sacrum and coccyx or deformity of the sacral vertebrae).
Heme oxygenase 1 deficiency
MedGen UID:
333882
Concept ID:
C1841651
Disease or Syndrome
Heme oxygenase-1 deficiency (HMOX1D) is a rare autosomal recessive disorder with a complex clinical presentation including direct antibody negative hemolytic anemia, low bilirubin, and hyperinflammation (summary by Chau et al., 2020). Other features may include asplenia and nephritis (Radhakrishnan et al., 2011).
Granulocytopenia with immunoglobulin abnormality
MedGen UID:
383874
Concept ID:
C1856263
Disease or Syndrome
Immunodeficiency-59 is an autosomal recessive primary immunologic disorder characterized by combined immunodeficiency and recurrent septic infections of the respiratory tract, skin, and mucous membranes, as well as disturbed glucose metabolism. Granulocytopenia and B-cell and dentritic cell deficiency are present (Haapaniemi et al., 2017).
Pyogenic bacterial infections due to MyD88 deficiency
MedGen UID:
383023
Concept ID:
C2677092
Disease or Syndrome
Immunodeficiency-68 (IMD68) is an autosomal recessive primary immunodeficiency characterized by severe systemic and invasive bacterial infections beginning in infancy or early childhood. The most common organisms implicated are Streptococcus pneumoniae, Staphylococcus aureus, and Pseudomonas, although other organisms may be observed. IMD68 is life-threatening in infancy and early childhood. The first invasive infection typically occurs before 2 years of age, with meningitis and upper respiratory infections being common manifestations. The mortality rate in early childhood is high, with most deaths occurring before 8 years of age. Affected individuals have an impaired inflammatory response to infection, including lack of fever and neutropenia, although erythrocyte sedimentation rate (ESR) and C-reactive protein may be elevated. General immunologic workup tends to be normal, with normal levels of B cells, T cells, and NK cells. However, more detailed studies indicate impaired cytokine response to lipopolysaccharide (LPS) and IL1B (147720) stimulation; response to TNFA (191160) is usually normal. Patients have good antibody responses to most vaccinations. Viral, fungal, and parasitic infections are generally not observed. Early detection is critical in early childhood because prophylactic treatment with IVIg or certain antibiotics is effective; the disorder tends to improve naturally around adolescence. At the molecular level, IMD68 results from impaired function of selective Toll receptor (see TLR4, 603030)/IL1R (see IL1R1; 147810) signaling pathways that ultimately activate NFKB (164011) to produce cytokines (summary by Picard et al., 2010). See also IMD67 (607676), caused by mutation in the IRAK4 gene (602170), which shows a similar phenotype to IMD68. As the MYD88 and IRAK4 genes interact in the same intracellular signaling pathway, the clinical and cellular features are almost indistinguishable (summary by Picard et al., 2010).
Leukocyte adhesion deficiency 3
MedGen UID:
411605
Concept ID:
C2748536
Disease or Syndrome
Leukocyte adhesion deficiency-3 (LAD3), also known as LAD1 variant (LAD1V), is an autosomal recessive disorder characterized by LAD1 (116920)-like immune deficiency and Glanzmann thrombasthenia (GT; 273800)-like bleeding problems. LAD3 results from mutations in FERMT3, or KINDLIN3, which encodes an intracellular protein that interacts with beta-integrins in hematopoietic cells. In LAD3, the adhesive functions of integrins on both leukocytes and platelets are disrupted, most likely due to defects in activation-dependent alterations of surface integrins that enable high-avidity binding to ligands on target cells, a process termed 'inside-out signaling' (Svensson et al., 2009; Zimmerman, 2009). For a discussion of genetic heterogeneity of leukocyte adhesion deficiency, see 116920.
Autosomal recessive severe congenital neutropenia due to G6PC3 deficiency
MedGen UID:
414066
Concept ID:
C2751630
Disease or Syndrome
G6PC3 deficiency is characterized by severe congenital neutropenia which occurs in a phenotypic continuum that includes the following: Isolated severe congenital neutropenia (nonsyndromic). Classic G6PC3 deficiency (severe congenital neutropenia plus cardiovascular and/or urogenital abnormalities). Severe G6PC3 deficiency (classic G6PC3 deficiency plus involvement of non-myeloid hematopoietic cell lines, additional extra-hematologic features, and pulmonary hypertension; known as Dursun syndrome). Neutropenia usually presents with recurrent bacterial infections in the first few months of life. Intrauterine growth restriction (IUGR), failure to thrive (FTT), and poor postnatal growth are common. Other findings in classic and severe G6PC3 deficiency can include inflammatory bowel disease (IBD) resembling Crohn's disease, and endocrine disorders (growth hormone deficiency, hypogonadotropic hypogonadism, and delayed puberty).
Combined immunodeficiency due to LRBA deficiency
MedGen UID:
766426
Concept ID:
C3553512
Disease or Syndrome
Common variable immunodeficiency-8 with autoimmunity is an autosomal recessive disorder of immune dysregulation. Affected individuals have early childhood onset of recurrent infections, particularly respiratory infections, and also develop variable autoimmune disorders, including idiopathic thrombocytopenic purpura, autoimmune hemolytic anemia, and inflammatory bowel disease. The presentation and phenotype are highly variable, even within families (summary by Lopez-Herrera et al., 2012 and Alangari et al., 2012). Immunologic findings are also variable and may include decreased B cells, hypogammaglobulinemia, and deficiency of CD4+ T regulatory (Treg) cells (Charbonnier et al., 2015). For a general description and a discussion of genetic heterogeneity of common variable immunodeficiency, see CVID1 (607594).
Lymphoproliferative syndrome 2
MedGen UID:
767454
Concept ID:
C3554540
Disease or Syndrome
Lymphoproliferative syndrome-2, also known as CD27 deficiency, is an autosomal recessive immunodeficiency disorder associated with persistent symptomatic EBV viremia, hypogammaglobulinemia, and impairment in specific antibody function resulting from impaired T cell-dependent B-cell responses and T-cell dysfunction (summary by van Montfrans et al., 2012). The phenotype can vary significantly, from asymptomatic borderline-low hypogammaglobulinemia, to a full-blown symptomatic systemic inflammatory response with life-threatening EBV-related complications, including hemophagocytic lymphohistiocytosis, a lymphoproliferative disorder, and malignant lymphoma requiring stem cell transplantation (summary by Salzer et al., 2013). For a discussion of genetic heterogeneity of lymphoproliferative syndrome, see XLP1 (308240).
Autoimmune lymphoproliferative syndrome due to CTLA4 haploinsuffiency
MedGen UID:
863651
Concept ID:
C4015214
Disease or Syndrome
Immune dysregulation with autoimmunity, immunodeficiency, and lymphoproliferation (IDAIL) is an autosomal dominant complex immune disorder with highly variable presentation and clinical manifestations. Prominent features include recurrent infections often associated with hypogammaglobulinemia, autoimmune features such as autoimmune cytopenias, and abnormal lymphocytic infiltration of nonlymphoid organs, including the lungs, brain, and gastrointestinal tract, resulting in enteropathy. Laboratory studies often show lymphopenia and abnormal T and B cell subsets. The variable features are a result of impaired function of Treg cells, which play a role in immune homeostasis (summary by Kuehn et al., 2014; Schwab et al., 2018, and Lopez-Nevado et al., 2021). The disorder shows overlapping features with autoimmune lymphoproliferative syndrome (ALPS); for a general description and a discussion of genetic heterogeneity of ALPS, see 601859.
TFRC-related combined immunodeficiency
MedGen UID:
906483
Concept ID:
C4225219
Disease or Syndrome
A rare genetic combined T and B cell immunodeficiency characterized by life-threatening infections due to disrupted transferrin receptor 1 endocytosis, resulting in defective cellular iron transport and impaired T and B cell function. Patients present with early-onset chronic diarrhea, severe recurrent infections, and failure to thrive. Laboratory studies reveal hypo- or agammaglobulinemia, normal lymphocyte counts but decreased numbers of memory B cells, intermittent neutropenia and thrombocytopenia, and mild anemia (resistant to iron supplementation) with low mean corpuscular volume.
MIRAGE syndrome
MedGen UID:
924576
Concept ID:
C4284088
Disease or Syndrome
MIRAGE syndrome is an acronym for the major findings of myelodysplasia, infection, restriction of growth, adrenal hypoplasia, genital phenotypes, and enteropathy. Cytopenias are typically seen soon after birth; thrombocytopenia is the most common followed by anemia and pancytopenia. Recurrent infections from early infancy include pneumonia, urinary tract infection, gastroenteritis, meningitis, otitis media, dermatitis, subcutaneous abscess, and sepsis. Reported genital phenotypes in those with 46,XY karyotype included hypospadias, microphallus, bifid shawl scrotum, ambiguous genitalia, or complete female genitalia. Hypoplastic or dysgenetic ovaries have been reported in females. Gastrointestinal complications include chronic diarrhea and esophageal dysfunction. Moderate-to-severe developmental delay is reported in most affected individuals. Autonomic dysfunction and renal dysfunction are also reported.
Mucopolysaccharidosis-like syndrome with congenital heart defects and hematopoietic disorders
MedGen UID:
934594
Concept ID:
C4310627
Disease or Syndrome
MPSPS is an autosomal recessive inborn error of metabolism resulting in a multisystem disorder with features of the mucopolysaccharidosis lysosomal storage diseases (see, e.g., 607016). Patients present in infancy or early childhood with respiratory difficulties, cardiac problems, anemia, dysostosis multiplex, renal involvement, coarse facies, and delayed psychomotor development. Most patients die of cardiorespiratory failure in the first years of life (summary by Kondo et al., 2017).
Specific granule deficiency 2
MedGen UID:
1371952
Concept ID:
C4479548
Disease or Syndrome
Specific granule deficiency-2 (SGD2) is an autosomal recessive immunologic disorder characterized by recurrent infections due to defective neutrophil development. Bone marrow findings include paucity of neutrophil granulocytes, absence of granule proteins in neutrophils, abnormal megakaryocytes, and features of progressive myelofibrosis with blasts. The disorder is apparent from infancy, and patients may die in early childhood unless they undergo hematopoietic stem cell transplantation. Most patients have additional findings, including delayed development, mild dysmorphic features, tooth abnormalities, and distal skeletal defects (Witzel et al., 2017). For a discussion of genetic heterogeneity of SGD, see SGD1 (245480).
Immunodeficiency 66
MedGen UID:
1717128
Concept ID:
C5394265
Disease or Syndrome
Immunodeficiency-66 (IMD66) is an autosomal recessive primary immune disorder caused by defective immune cell migration and chemotaxis resulting from defects in cytoskeletal actin dynamics. Neutrophils are primarily affected, although there may be defects in dendritic cells and T and B cells. The phenotype is characterized by onset of recurrent bacterial infections in infancy. Laboratory studies show normal levels of myeloid and lymphoid cells, but there may be mild thrombocytopenia (summary by Record et al., 2015).
Immunodeficiency 73b with defective neutrophil chemotaxis and lymphopenia
MedGen UID:
1740566
Concept ID:
C5436549
Disease or Syndrome
Immunodeficiency-73B with defective neutrophil chemotaxis (IMD73B) is an autosomal dominant immunologic disorder characterized by onset of recurrent infections in infancy or early childhood. Affected individuals develop respiratory infections, cellulitis, and severe invasive infections or sepsis; organisms include bacteria such as Staphylococcus, as well as viruses, fungi, and mycobacterial species. Laboratory studies show variable abnormalities, including B- and T-cell lymphopenia, decreased immunoglobulin subsets, decreased TRECs and dysfunctional T cells, decreased NK cells, neutropenia, and impaired neutrophil chemotaxis. Hematopoietic stem cell transplantation is curative (summary by Hsu et al., 2019; review by Lougaris et al., 2020). In a review of autosomal forms of chronic granulomatous disease (see 306400 for genetic heterogeneity of CGD), Roos et al. (2021) noted that patients with RAC2 mutations may manifest CGD-like symptoms due to defects in neutrophil NADPH oxidase activity.
Mitochondrial complex 4 deficiency, nuclear type 15
MedGen UID:
1773430
Concept ID:
C5436712
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 15 (MC4DN15) is an autosomal recessive multisystem metabolic disorder characterized by the onset of symptoms in infancy. Affected individuals show global developmental delay, poor feeding, short stature with microcephaly, proximal muscle weakness, and distal spasticity. Other manifestations include scoliosis, primary pulmonary hypertension, childhood-onset refractory seizures, and inability to walk. Brain imaging shows features consistent with Leigh syndrome (see 256000) and enlarged ventricles. Laboratory studies show increased serum and CSF lactate, as well as decreased levels and activity of mitochondrial respiratory complex IV (summary by Hallmann et al., 2016). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Megacystis-microcolon-intestinal hypoperistalsis syndrome 3
MedGen UID:
1780019
Concept ID:
C5543513
Disease or Syndrome
Megacystis microcolon intestinal hypoperistalsis syndrome (MMIHS) is a rare congenital defect of visceral smooth muscle, primarily affecting females who present at birth with functional obstruction of the intestine, microcolon, dilation of the bladder, and secondary hydronephrosis. Total parenteral nutrition, adequate intermittent catheterization of bladder, and surgical corrections for intestinal malrotation are frequent modes of treatment for this disease without which rapid death ensues. In some instances, multivisceral organ transplantation has been undertaken with some success. Despite these clinical interventions, MMIHS often leads to premature death due to complications of therapy (summary by Halim et al., 2017). For a discussion of genetic heterogeneity of MMIHS, see 249210.
Neurologic, endocrine, and pancreatic disease, multisystem, infantile-onset 2
MedGen UID:
1778117
Concept ID:
C5543623
Disease or Syndrome
Infantile-onset multisystem neurologic, endocrine, and pancreatic disease-2 (IMNEPD2) is an autosomal recessive multisystemic disorder characterized by cholestatic hepatitis, poor feeding associated with poor overall growth, and hypoglycemia apparent from infancy. Most, but not all, patients have variable global developmental delay. Additional common features include sensorineural deafness, retinal abnormalities with visual defects, and hypotonia. Some patients have endocrine abnormalities, including hyperinsulinemic hypoglycemia, pancreatic dysfunction, hypothyroidism, and primary amenorrhea. Additional features may include hypertriglyceridemia, anemia, proteinuria, increased lactate, and recurrent infections. Brain imaging often shows dysmyelination, thin corpus callosum, cerebral atrophy, and white matter abnormalities. Although the clinical manifestations and severity of the disorder are highly variable, death in early childhood may occur (summary by Williams et al., 2019 and Zeiad et al., 2021). For a discussion of genetic heterogeneity of IMNEPD, see IMNEPD1 (616263).
Epidermolysis bullosa simplex 2d, generalized, intermediate or severe, autosomal recessive
MedGen UID:
1794224
Concept ID:
C5562014
Disease or Syndrome
Epidermolysis bullosa simplex (EBS) is characterized by fragility of the skin (and mucosal epithelia in some cases) that results in non-scarring blisters and erosions caused by minor mechanical trauma. The current classification of epidermolysis bullosa (EB) includes two major types and 17 minor subtypes of EBS; all share the common feature of blistering above the dermal-epidermal junction at the ultrastructural level. The four most common subtypes of EBS are the focus of this GeneReview: EBS, localized (EBS-loc; previously known as Weber-Cockayne type). EBS, generalized intermediate (EBS-gen intermed; previously known as Koebner type). EBS-with mottled pigmentation (EBS-MP). EBS, generalized severe (EBS-gen sev; previously known as Dowling-Meara type). The phenotypes for these subtypes range from relatively mild blistering of the hands and feet to more generalized blistering, which can be fatal. In EBS-loc, blisters are rarely present or minimal at birth and may occur on the knees and shins with crawling or on the feet at approximately age 18 months; some individuals manifest the disease in adolescence or early adulthood. Blisters are usually confined to the hands and feet, but can occur anywhere if trauma is significant. In EBS, gen intermed, blisters may be present at birth or develop within the first few months of life. Involvement is more widespread than in EBS-loc, but generally milder than in EBS-gen sev. In EBS-MP, skin fragility is evident at birth and clinically indistinguishable from EBS-gen sev; over time, progressive brown pigmentation interspersed with hypopigmented spots develops on the trunk and extremities, with the pigmentation disappearing in adult life. Focal palmar and plantar hyperkeratoses may occur. In EBS-gen sev, onset is usually at birth; severity varies greatly, both among and within families. Widespread and severe blistering and/or multiple grouped clumps of small blisters are typical and hemorrhagic blisters are common. Improvement occurs during mid- to late childhood. Progressive hyperkeratosis of the palms and soles begins in childhood and may be the major complaint of affected individuals in adult life. Nail dystrophy and milia are common. Both hyper- and hypopigmentation can occur. Mucosal involvement in EBS-gen sev may interfere with feeding, especially in neonates and infants. Blistering can be severe enough to result in neonatal or infant death.
Immunodeficiency 87 and autoimmunity
MedGen UID:
1794280
Concept ID:
C5562070
Disease or Syndrome
Immunodeficiency-87 and autoimmunity (IMD87) is an autosomal recessive immunologic disorder with wide phenotypic variation and severity. Affected individuals usually present in infancy or early childhood with increased susceptibility to infections, often Epstein-Barr virus (EBV), as well as with lymphadenopathy or autoimmune manifestations, predominantly hemolytic anemia. Laboratory studies may show low or normal lymphocyte numbers, often with skewed T-cell subset ratios. The disorder results primarily from defects in T-cell function, which causes both immunodeficiency and overall immune dysregulation (summary by Serwas et al., 2019 and Fournier et al., 2021).

Recent clinical studies

Etiology

Madushani RWMA, Patel V, Loftus T, Ren Y, Li HJ, Velez L, Wu Q, Adhikari L, Efron P, Segal M, Ozrazgat-Baslanti T, Rashidi P, Bihorac A; Sepsis and Critical Illness Research Center Investigators.
J Surg Res 2022 Sep;277:372-383. Epub 2022 May 12 doi: 10.1016/j.jss.2022.04.052. PMID: 35569215
Hammond NE, Kumar A, Kaur P, Tirupakuzhi Vijayaraghavan BK, Ghosh A, Grattan S, Jha V, Mathai D, Venkatesh B; Sepsis in India Prevalence Study (SIPS) Investigator Network.
Chest 2022 Jun;161(6):1543-1554. Epub 2022 Jan 31 doi: 10.1016/j.chest.2021.12.673. PMID: 35092747
Stallmach A, Kesselmeier M, Bauer M, Gramlich J, Finke K, Fischer A, Fleischmann-Struzek C, Heutelbeck A, Katzer K, Mutschke S, Pletz MW, Quickert S, Reinhart K, Stallmach Z, Walter M, Scherag A, Reuken PA
Infection 2022 Jun;50(3):661-669. Epub 2022 Jan 7 doi: 10.1007/s15010-021-01733-3. PMID: 34997542Free PMC Article
Becker AE, Teixeira SR, Lunig NA, Mondal A, Fitzgerald JC, Topjian AA, Weiss SL, Griffis H, Schramm SE, Traynor DM, Vossough A, Kirschen MP
Pediatr Neurol 2022 Mar;128:1-8. Epub 2021 Dec 13 doi: 10.1016/j.pediatrneurol.2021.12.001. PMID: 34992035
Fernández-Sarmiento J, De Souza DC, Martinez A, Nieto V, López-Herce J, Soares Lanziotti V, Arias López MDP, De Carvalho WB, Oliveira CF, Jaramillo-Bustamante JC, Díaz F, Yock-Corrales A, Ruvinsky S, Munaico M, Pavlicich V, Iramain R, Márquez MP, González G, Yunge M, Tonial C, Cruces P, Palacio G, Grela C, Slöcker-Barrio M, Campos-Miño S, González-Dambrauskas S, Sánchez-Pinto NL, Celiny García P, Jabornisky R
J Intensive Care Med 2022 Jun;37(6):753-763. Epub 2021 Nov 23 doi: 10.1177/08850666211054444. PMID: 34812664

Diagnosis

Madushani RWMA, Patel V, Loftus T, Ren Y, Li HJ, Velez L, Wu Q, Adhikari L, Efron P, Segal M, Ozrazgat-Baslanti T, Rashidi P, Bihorac A; Sepsis and Critical Illness Research Center Investigators.
J Surg Res 2022 Sep;277:372-383. Epub 2022 May 12 doi: 10.1016/j.jss.2022.04.052. PMID: 35569215
Hammond NE, Kumar A, Kaur P, Tirupakuzhi Vijayaraghavan BK, Ghosh A, Grattan S, Jha V, Mathai D, Venkatesh B; Sepsis in India Prevalence Study (SIPS) Investigator Network.
Chest 2022 Jun;161(6):1543-1554. Epub 2022 Jan 31 doi: 10.1016/j.chest.2021.12.673. PMID: 35092747
Deng H, Li J, Ali Shah A, Lin G, Chen H, Ouyang W
Int Immunopharmacol 2022 Mar;104:108518. Epub 2022 Jan 12 doi: 10.1016/j.intimp.2022.108518. PMID: 35032827
Stallmach A, Kesselmeier M, Bauer M, Gramlich J, Finke K, Fischer A, Fleischmann-Struzek C, Heutelbeck A, Katzer K, Mutschke S, Pletz MW, Quickert S, Reinhart K, Stallmach Z, Walter M, Scherag A, Reuken PA
Infection 2022 Jun;50(3):661-669. Epub 2022 Jan 7 doi: 10.1007/s15010-021-01733-3. PMID: 34997542Free PMC Article
Fernández-Sarmiento J, De Souza DC, Martinez A, Nieto V, López-Herce J, Soares Lanziotti V, Arias López MDP, De Carvalho WB, Oliveira CF, Jaramillo-Bustamante JC, Díaz F, Yock-Corrales A, Ruvinsky S, Munaico M, Pavlicich V, Iramain R, Márquez MP, González G, Yunge M, Tonial C, Cruces P, Palacio G, Grela C, Slöcker-Barrio M, Campos-Miño S, González-Dambrauskas S, Sánchez-Pinto NL, Celiny García P, Jabornisky R
J Intensive Care Med 2022 Jun;37(6):753-763. Epub 2021 Nov 23 doi: 10.1177/08850666211054444. PMID: 34812664

Therapy

Honda TJ, Kazemiparkouhi F, Henry TD, Suh HH
BMC Public Health 2022 Jun 18;22(1):1214. doi: 10.1186/s12889-022-13628-5. PMID: 35717154
Im Y, Kang D, Ko RE, Lee YJ, Lim SY, Park S, Na SJ, Chung CR, Park MH, Oh DK, Lim CM, Suh GY; Korean Sepsis Alliance (KSA) investigators.
Crit Care 2022 Jan 13;26(1):19. doi: 10.1186/s13054-021-03883-0. PMID: 35027073Free PMC Article
Menon K, Schlapbach LJ, Akech S, Argent A, Biban P, Carrol ED, Chiotos K, Jobayer Chisti M, Evans IVR, Inwald DP, Ishimine P, Kissoon N, Lodha R, Nadel S, Oliveira CF, Peters M, Sadeghirad B, Scott HF, de Souza DC, Tissieres P, Watson RS, Wiens MO, Wynn JL, Zimmerman JJ, Sorce LR; Pediatric Sepsis Definition Taskforce of the Society of Critical Care Medicine.
Crit Care Med 2022 Jan 1;50(1):21-36. doi: 10.1097/CCM.0000000000005294. PMID: 34612847Free PMC Article
de Souza DC, Gonçalves Martin J, Soares Lanziotti V, de Oliveira CF, Tonial C, de Carvalho WB, Roberto Fioretto J, Pedro Piva J, Juan Troster E, Siqueira Bossa A, Gregorini F, Ferreira J, Lubarino J, Biasi Cavalcanti A, Ribeiro Machado F; SPREAD PED Investigators and the Instituto Latino Americano de Sepsis Network.
Lancet Child Adolesc Health 2021 Dec;5(12):873-881. Epub 2021 Oct 29 doi: 10.1016/S2352-4642(21)00286-8. PMID: 34756191
Wang D, Li J, Sun Y, Ding X, Zhang X, Liu S, Han B, Wang H, Duan X, Sun T
Front Public Health 2021;9:754348. Epub 2021 Oct 15 doi: 10.3389/fpubh.2021.754348. PMID: 34722452Free PMC Article

Prognosis

Madushani RWMA, Patel V, Loftus T, Ren Y, Li HJ, Velez L, Wu Q, Adhikari L, Efron P, Segal M, Ozrazgat-Baslanti T, Rashidi P, Bihorac A; Sepsis and Critical Illness Research Center Investigators.
J Surg Res 2022 Sep;277:372-383. Epub 2022 May 12 doi: 10.1016/j.jss.2022.04.052. PMID: 35569215
Hammond NE, Kumar A, Kaur P, Tirupakuzhi Vijayaraghavan BK, Ghosh A, Grattan S, Jha V, Mathai D, Venkatesh B; Sepsis in India Prevalence Study (SIPS) Investigator Network.
Chest 2022 Jun;161(6):1543-1554. Epub 2022 Jan 31 doi: 10.1016/j.chest.2021.12.673. PMID: 35092747
Stallmach A, Kesselmeier M, Bauer M, Gramlich J, Finke K, Fischer A, Fleischmann-Struzek C, Heutelbeck A, Katzer K, Mutschke S, Pletz MW, Quickert S, Reinhart K, Stallmach Z, Walter M, Scherag A, Reuken PA
Infection 2022 Jun;50(3):661-669. Epub 2022 Jan 7 doi: 10.1007/s15010-021-01733-3. PMID: 34997542Free PMC Article
Becker AE, Teixeira SR, Lunig NA, Mondal A, Fitzgerald JC, Topjian AA, Weiss SL, Griffis H, Schramm SE, Traynor DM, Vossough A, Kirschen MP
Pediatr Neurol 2022 Mar;128:1-8. Epub 2021 Dec 13 doi: 10.1016/j.pediatrneurol.2021.12.001. PMID: 34992035
Lipatov K, Daniels CE, Park JG, Elmer J, Hanson AC, Madsen BE, Clements CM, Gajic O, Pickering BW, Herasevich V
Am J Emerg Med 2022 Jan;51:378-383. Epub 2021 Nov 11 doi: 10.1016/j.ajem.2021.09.086. PMID: 34823194

Clinical prediction guides

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Becker AE, Teixeira SR, Lunig NA, Mondal A, Fitzgerald JC, Topjian AA, Weiss SL, Griffis H, Schramm SE, Traynor DM, Vossough A, Kirschen MP
Pediatr Neurol 2022 Mar;128:1-8. Epub 2021 Dec 13 doi: 10.1016/j.pediatrneurol.2021.12.001. PMID: 34992035
Lipatov K, Daniels CE, Park JG, Elmer J, Hanson AC, Madsen BE, Clements CM, Gajic O, Pickering BW, Herasevich V
Am J Emerg Med 2022 Jan;51:378-383. Epub 2021 Nov 11 doi: 10.1016/j.ajem.2021.09.086. PMID: 34823194

Recent systematic reviews

Liu YC, Yao Y, Yu MM, Gao YL, Qi AL, Jiang TY, Chen ZS, Shou ST, Chai YF
BMC Infect Dis 2022 Jun 21;22(1):564. doi: 10.1186/s12879-022-07543-8. PMID: 35729526
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Menon K, Schlapbach LJ, Akech S, Argent A, Biban P, Carrol ED, Chiotos K, Jobayer Chisti M, Evans IVR, Inwald DP, Ishimine P, Kissoon N, Lodha R, Nadel S, Oliveira CF, Peters M, Sadeghirad B, Scott HF, de Souza DC, Tissieres P, Watson RS, Wiens MO, Wynn JL, Zimmerman JJ, Sorce LR; Pediatric Sepsis Definition Taskforce of the Society of Critical Care Medicine.
Crit Care Med 2022 Jan 1;50(1):21-36. doi: 10.1097/CCM.0000000000005294. PMID: 34612847Free PMC Article
Liang H, Song H, Zhai R, Song G, Li H, Ding X, Kan Q, Sun T
Front Immunol 2021;12:709155. Epub 2021 Aug 16 doi: 10.3389/fimmu.2021.709155. PMID: 34484209Free PMC Article
Karakike E, Giamarellos-Bourboulis EJ, Kyprianou M, Fleischmann-Struzek C, Pletz MW, Netea MG, Reinhart K, Kyriazopoulou E
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