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Pulmonary edema

MedGen UID:
11026
Concept ID:
C0034063
Pathologic Function
Synonyms: Edema, Pulmonary; Edemas, Pulmonary; Lung, Wet; Lungs, Wet; Pulmonary Edema; Pulmonary Edemas; Wet Lung; Wet Lungs
SNOMED CT: Pulmonary edema (19242006)
 
HPO: HP:0100598
Monarch Initiative: MONDO:0006932

Definition

Fluid accumulation in the lungs. [from HPO]

Conditions with this feature

Pulmonary hypertension due to chronic exposure to high altitude
MedGen UID:
83314
Concept ID:
C0340552
Disease or Syndrome
Lethal congenital glycogen storage disease of heart
MedGen UID:
337919
Concept ID:
C1849813
Disease or Syndrome
A rare glycogen storage disease with fetal or neonatal onset of severe cardiomyopathy with non-lysosomal glycogen accumulation and fatal outcome in infancy. Patients present with massive cardiomegaly, severe cardiac and respiratory complications and failure to thrive. Non-specific facial dysmorphism, bilateral cataracts, macroglossia, hydrocephalus, enlarged kidneys and skeletal muscle involvement have been reported in some cases.
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.
Hypertrophic cardiomyopathy 4
MedGen UID:
350526
Concept ID:
C1861862
Disease or Syndrome
Nonfamilial hypertrophic cardiomyopathy tends to be milder. This form typically begins later in life than familial hypertrophic cardiomyopathy, and affected individuals have a lower risk of serious cardiac events and sudden death than people with the familial form.\n\nThe symptoms of familial hypertrophic cardiomyopathy are variable, even within the same family. Many affected individuals have no symptoms. Other people with familial hypertrophic cardiomyopathy may experience chest pain; shortness of breath, especially with physical exertion; a sensation of fluttering or pounding in the chest (palpitations); lightheadedness; dizziness; and fainting.\n\nIn familial hypertrophic cardiomyopathy, cardiac thickening usually occurs in the interventricular septum, which is the muscular wall that separates the lower left chamber of the heart (the left ventricle) from the lower right chamber (the right ventricle). In some people, thickening of the interventricular septum impedes the flow of oxygen-rich blood from the heart, which may lead to an abnormal heart sound during a heartbeat (heart murmur) and other signs and symptoms of the condition. Other affected individuals do not have physical obstruction of blood flow, but the pumping of blood is less efficient, which can also lead to symptoms of the condition. Familial hypertrophic cardiomyopathy often begins in adolescence or young adulthood, although it can develop at any time throughout life.\n\nWhile most people with familial hypertrophic cardiomyopathy are symptom-free or have only mild symptoms, this condition can have serious consequences. It can cause abnormal heart rhythms (arrhythmias) that may be life threatening. People with familial hypertrophic cardiomyopathy have an increased risk of sudden death, even if they have no other symptoms of the condition. A small number of affected individuals develop potentially fatal heart failure, which may require heart transplantation.\n\nHypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. When multiple members of a family have the condition, it is known as familial hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy also occurs in people with no family history; these cases are considered nonfamilial hypertrophic cardiomyopathy. 
Respiratory distress syndrome in premature infants
MedGen UID:
368840
Concept ID:
C1968593
Disease or Syndrome
The main cause of respiratory distress syndrome (RDS) in premature infants is a developmental deficiency of pulmonary surfactant. The frequency of RDS is inversely proportional to gestational age. However, not all infants born prematurely develop RDS, suggesting that there may be susceptibility factors. Because multiple factors can contribute to the pathogenesis of RDS specifically in premature infants, the etiology is considered to be multifactorial (summaries by Ramet et al., 2000; Clark and Clark, 2005). Pathogenic germline mutations in several genes involved in surfactant metabolism, including SFTPB (178640) and SFTPC (178620), can cause clinical features of respiratory distress syndrome in term neonates, children, and adults, disorders referred to as 'surfactant metabolism dysfunction' (see, e.g., SMDP1, 265120). Susceptibility to the development of RDS in premature infants may be associated with polymorphisms in surfactant genes, such as surfactant protein A1 (SFTPA1; 178630), SFTPB, and SFTPC (see MOLECULAR GENETICS).
Familial amyloid neuropathy
MedGen UID:
414031
Concept ID:
C2751492
Disease or Syndrome
Hereditary transthyretin (ATTR) amyloidosis is characterized by a slowly progressive peripheral sensorimotor and/or autonomic neuropathy as well as non-neuropathic changes of cardiomyopathy, nephropathy, vitreous opacities, and CNS amyloidosis. The disease usually begins in the third to fifth decade in persons from endemic foci in Portugal and Japan; onset is later in persons from other areas. Typically, sensory neuropathy starts in the lower extremities with paresthesias and hypesthesias of the feet, followed within a few years by motor neuropathy. In some persons, particularly those with early-onset disease, autonomic neuropathy is the first manifestation of the condition; findings can include: orthostatic hypotension, constipation alternating with diarrhea, attacks of nausea and vomiting, delayed gastric emptying, sexual impotence, anhidrosis, and urinary retention or incontinence. Cardiac amyloidosis is mainly characterized by progressive cardiomyopathy. Individuals with leptomeningeal amyloidosis may have the following CNS findings: dementia, psychosis, visual impairment, headache, seizures, motor paresis, ataxia, myelopathy, hydrocephalus, or intracranial hemorrhage.
Ogden syndrome
MedGen UID:
477078
Concept ID:
C3275447
Disease or Syndrome
Ogden syndrome (OGDNS) is an X-linked neurodevelopmental disorder characterized by postnatal growth failure, severely delayed psychomotor development, variable dysmorphic features, and hypotonia. Many patients also have cardiac malformations or arrhythmias (summary by Popp et al., 2015).
Lymphatic malformation 7
MedGen UID:
934596
Concept ID:
C4310629
Disease or Syndrome
LMPHM7 is an autosomal dominant disorder with variable expressivity. Some patients may develop severe nonimmune lymphatic-related hydrops fetalis (LRHF) in utero, resulting in early death, whereas others may have milder manifestations, such as atrial septal defect (ASD) or varicose veins as adults. The hydrops and/or swelling improves spontaneously in those who survive the neonatal period (summary by Martin-Almedina et al., 2016). For a discussion of genetic heterogeneity of lymphatic malformation, see 153100.
Liver disease, severe congenital
MedGen UID:
1823968
Concept ID:
C5774195
Disease or Syndrome
Severe congenital liver disease (SCOLIV) is an autosomal recessive disorder characterized by the onset of progressive hepatic dysfunction usually in the first years of life. Affected individuals show feeding difficulties with failure to thrive and features such as jaundice, hepatomegaly, and abdominal distension. Laboratory workup is consistent with hepatic insufficiency and may also show coagulation defects, anemia, or metabolic disturbances. Cirrhosis and hypernodularity are commonly observed on liver biopsy. Many patients die of liver failure in early childhood (Moreno Traspas et al., 2022).

Professional guidelines

PubMed

Daily JP, Minuti A, Khan N
JAMA 2022 Aug 2;328(5):460-471. doi: 10.1001/jama.2022.12366. PMID: 35916842
Overton E, Tobes D, Lee A
Best Pract Res Clin Anaesthesiol 2022 May;36(1):107-121. Epub 2022 Feb 10 doi: 10.1016/j.bpa.2022.02.003. PMID: 35659948
Saguil A, Fargo MV
Am Fam Physician 2020 Jun 15;101(12):730-738. PMID: 32538594

Recent clinical studies

Etiology

Dobbe L, Rahman R, Elmassry M, Paz P, Nugent K
Am J Med Sci 2019 Dec;358(6):389-397. Epub 2019 Oct 1 doi: 10.1016/j.amjms.2019.09.011. PMID: 31813466
Roubinian N
Hematology Am Soc Hematol Educ Program 2018 Nov 30;2018(1):585-594. Epub 2018 Dec 14 doi: 10.1182/asheducation-2018.1.585. PMID: 30570487Free PMC Article
Assaad S, Kratzert WB, Shelley B, Friedman MB, Perrino A Jr
J Cardiothorac Vasc Anesth 2018 Apr;32(2):901-914. Epub 2017 Aug 19 doi: 10.1053/j.jvca.2017.08.028. PMID: 29174750
Clark AL, Cleland JG
Nat Rev Cardiol 2013 Mar;10(3):156-70. Epub 2013 Jan 15 doi: 10.1038/nrcardio.2012.191. PMID: 23319101
Rimoldi SF, Yuzefpolskaya M, Allemann Y, Messerli F
Prog Cardiovasc Dis 2009 Nov-Dec;52(3):249-59. doi: 10.1016/j.pcad.2009.10.002. PMID: 19917337

Diagnosis

Ingbar DH
Curr Opin Crit Care 2019 Aug;25(4):371-378. doi: 10.1097/MCC.0000000000000626. PMID: 31116110
Assaad S, Kratzert WB, Shelley B, Friedman MB, Perrino A Jr
J Cardiothorac Vasc Anesth 2018 Apr;32(2):901-914. Epub 2017 Aug 19 doi: 10.1053/j.jvca.2017.08.028. PMID: 29174750
Busl KM, Bleck TP
Crit Care Med 2015 Aug;43(8):1710-5. doi: 10.1097/CCM.0000000000001101. PMID: 26066018
Murray JF
Int J Tuberc Lung Dis 2011 Feb;15(2):155-60, i. PMID: 21219673
Rimoldi SF, Yuzefpolskaya M, Allemann Y, Messerli F
Prog Cardiovasc Dis 2009 Nov-Dec;52(3):249-59. doi: 10.1016/j.pcad.2009.10.002. PMID: 19917337

Therapy

McMahon BA, Chawla LS
Ren Fail 2021 Dec;43(1):830-839. doi: 10.1080/0886022X.2021.1906701. PMID: 33971784Free PMC Article
Permpikul C, Tongyoo S, Viarasilpa T, Trainarongsakul T, Chakorn T, Udompanturak S
Am J Respir Crit Care Med 2019 May 1;199(9):1097-1105. doi: 10.1164/rccm.201806-1034OC. PMID: 30704260
Matthay MA, Ware LB, Zimmerman GA
J Clin Invest 2012 Aug;122(8):2731-40. Epub 2012 Aug 1 doi: 10.1172/JCI60331. PMID: 22850883Free PMC Article
Carson JL, Grossman BJ, Kleinman S, Tinmouth AT, Marques MB, Fung MK, Holcomb JB, Illoh O, Kaplan LJ, Katz LM, Rao SV, Roback JD, Shander A, Tobian AA, Weinstein R, Swinton McLaughlin LG, Djulbegovic B; Clinical Transfusion Medicine Committee of the AABB
Ann Intern Med 2012 Jul 3;157(1):49-58. doi: 10.7326/0003-4819-157-1-201206190-00429. PMID: 22751760
Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, Lamy M, Legall JR, Morris A, Spragg R
Am J Respir Crit Care Med 1994 Mar;149(3 Pt 1):818-24. doi: 10.1164/ajrccm.149.3.7509706. PMID: 7509706

Prognosis

Ufuk F, Bayraktaroğlu S, Rüksan Ütebey A
Diagn Interv Radiol 2023 Jan 31;29(1):80-90. Epub 2022 Nov 29 doi: 10.5152/dir.2022.21614. PMID: 36960496Free PMC Article
Domínguez-Rodríguez A, Suero-Mendez C, Burillo-Putze G, Gil V, Calvo-Rodriguez R, Piñera-Salmeron P, Llorens P, Martín-Sánchez FJ, Abreu-Gonzalez P, Miró Ò; MIMO (MIdazolam versus MOrphine) Trial Investigators
Eur J Heart Fail 2022 Oct;24(10):1953-1962. Epub 2022 Jul 16 doi: 10.1002/ejhf.2602. PMID: 35780488
Li X, Liu C, Mao Z, Li Q, Zhou F
Crit Care 2021 Jan 6;25(1):15. doi: 10.1186/s13054-020-03451-y. PMID: 33407756Free PMC Article
Volk C, Spiro J, Boswell G, Lindholm P, Schwartz J, Wilson Z, Burger S, Tripp M
Chest 2021 May;159(5):1934-1941. Epub 2020 Nov 25 doi: 10.1016/j.chest.2020.11.019. PMID: 33245874
Netzer N, Strohl K, Faulhaber M, Gatterer H, Burtscher M
J Travel Med 2013 Jul-Aug;20(4):247-55. Epub 2013 Mar 11 doi: 10.1111/jtm.12017. PMID: 23809076

Clinical prediction guides

Houseman BS, Martinelli AN, Oliver WD, Devabhakthuni S, Mattu A
Am J Emerg Med 2023 Jan;63:74-78. Epub 2022 Oct 18 doi: 10.1016/j.ajem.2022.10.018. PMID: 36327753
Duan J, Chen L, Liu X, Bozbay S, Liu Y, Wang K, Esquinas AM, Shu W, Yang F, He D, Chen Q, Wei B, Chen B, Li L, Tang M, Yuan G, Ding F, Huang T, Zhang Z, Tang Z, Han X, Jiang L, Bai L, Hu W, Zhang R, Mina B
Crit Care 2022 Jul 3;26(1):196. doi: 10.1186/s13054-022-04060-7. PMID: 35786223Free PMC Article
Shakoori TA, Hafeez MM, Malik A
Acta Clin Croat 2020 Dec;59(4):740-744. doi: 10.20471/acc.2020.59.04.21. PMID: 34285445Free PMC Article
Girerd N, Seronde MF, Coiro S, Chouihed T, Bilbault P, Braun F, Kenizou D, Maillier B, Nazeyrollas P, Roul G, Fillieux L, Abraham WT, Januzzi J Jr, Sebbag L, Zannad F, Mebazaa A, Rossignol P; INI-CRCT, Great Network, and the EF-HF Group
JACC Heart Fail 2018 Apr;6(4):273-285. Epub 2017 Dec 6 doi: 10.1016/j.jchf.2017.09.023. PMID: 29226815
Siddall E, Khatri M, Radhakrishnan J
Kidney Int 2017 Jul;92(1):37-46. Epub 2017 Mar 17 doi: 10.1016/j.kint.2016.11.029. PMID: 28318633

Recent systematic reviews

Siddiqi TJ, Usman MS, Rashid AM, Javaid SS, Ahmed A, Clark D 3rd, Flack JM, Shimbo D, Choi E, Jones DW, Hall ME
J Am Heart Assoc 2023 Jul 18;12(14):e029355. Epub 2023 Jul 8 doi: 10.1161/JAHA.122.029355. PMID: 37421281Free PMC Article
Astarita A, Covella M, Vallelonga F, Cesareo M, Totaro S, Ventre L, Aprà F, Veglio F, Milan A
J Hypertens 2020 Jul;38(7):1203-1210. doi: 10.1097/HJH.0000000000002372. PMID: 32510905
Maw AM, Hassanin A, Ho PM, McInnes MDF, Moss A, Juarez-Colunga E, Soni NJ, Miglioranza MH, Platz E, DeSanto K, Sertich AP, Salame G, Daugherty SL
JAMA Netw Open 2019 Mar 1;2(3):e190703. doi: 10.1001/jamanetworkopen.2019.0703. PMID: 30874784Free PMC Article
Martindale JL, Wakai A, Collins SP, Levy PD, Diercks D, Hiestand BC, Fermann GJ, deSouza I, Sinert R
Acad Emerg Med 2016 Mar;23(3):223-42. Epub 2016 Feb 13 doi: 10.1111/acem.12878. PMID: 26910112
Carson JL, Grossman BJ, Kleinman S, Tinmouth AT, Marques MB, Fung MK, Holcomb JB, Illoh O, Kaplan LJ, Katz LM, Rao SV, Roback JD, Shander A, Tobian AA, Weinstein R, Swinton McLaughlin LG, Djulbegovic B; Clinical Transfusion Medicine Committee of the AABB
Ann Intern Med 2012 Jul 3;157(1):49-58. doi: 10.7326/0003-4819-157-1-201206190-00429. PMID: 22751760

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