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Malignant hyperthermia(MH)

MedGen UID:
1830388
Concept ID:
C5779784
Pathologic Function
Synonyms: HYPERPYREXIA, MALIGNANT; MH
SNOMED CT: Malignant hyperthermia (405501007); MH - malignant hyperpyrexia (405501007); MHS - malignant hyperthermia susceptibility (405501007)
 
Related genes: RYR1, CACNA1S
 
HPO: HP:0002047
OMIM®: 145600

Definition

Malignant hyperthermia is characterized by a rapid increase in temperature to 39-42 degrees C. Malignant hyperthermia may occur in response to either inhalational anesthetics such as halothane, to muscle relaxants such as succinylcholine, or to exercise. [from HPO]

Term Hierarchy

Conditions with this feature

SUDDEN INFANT DEATH SYNDROME
MedGen UID:
52548
Concept ID:
C0038644
Disease or Syndrome
Sudden infant death syndrome (SIDS) is a diagnosis of exclusion which should be made only after a thorough autopsy without identification of a specific cause of death (Mage and Donner, 2004). Weese-Mayer et al. (2007) provided a detailed review of genetic factors that have been implicated in SIDS. The authors concluded that SIDS represents more than 1 entity and has a heterogeneous etiology most likely involving several different genetically controlled metabolic pathways.
Freeman-Sheldon syndrome
MedGen UID:
120516
Concept ID:
C0265224
Disease or Syndrome
Freeman-Sheldon syndrome (FSS), or DA2A, is phenotypically similar to DA1. In addition to contractures of the hands and feet, FSS is characterized by oropharyngeal abnormalities, scoliosis, and a distinctive face that includes a very small oral orifice (often only a few millimeters in diameter at birth), puckered lips, and an H-shaped dimple of the chin; hence, FSS has been called 'whistling face syndrome.' The limb phenotypes of DA1 and FSS may be so similar that they can only be distinguished by the differences in facial morphology (summary by Bamshad et al., 2009). For a general phenotypic description and a discussion of genetic heterogeneity of distal arthrogryposis, see DA1 (108120).
Brody myopathy
MedGen UID:
371441
Concept ID:
C1832918
Disease or Syndrome
Brody disease (BROD) is an autosomal recessive skeletal muscle disorder characterized by exercise-induced muscle stiffness and cramps primarily affecting the arms, legs, and eyelids, although more generalized muscle involvement may also occur. Symptom onset is most often in the first decade, but many patients present and are diagnosed later in life. Skeletal muscle biopsy typically shows variation in fiber size, increased internal nuclei, and atrophy of type II muscle fibers. Rare patients have been reported to develop malignant hyperthermia after administration of anesthesia, suggesting that patients with the disorder should be tested. The disorder results from defective relaxation of fast-twitch (type II) skeletal muscle fibers due to defects in calcium homeostasis and reuptake in the muscle fiber (summary by Odermatt et al., 2000 and Molenaar et al., 2020).
Malignant hyperthermia, susceptibility to, 4
MedGen UID:
324944
Concept ID:
C1838102
Finding
Malignant hyperthermia susceptibility (MHS) is a pharmacogenetic disorder of skeletal muscle calcium regulation associated with uncontrolled skeletal muscle hypermetabolism. Manifestations of malignant hyperthermia (MH) are precipitated by certain volatile anesthetics (i.e., halothane, isoflurane, sevoflurane, desflurane, enflurane), either alone or in conjunction with a depolarizing muscle relaxant (specifically, succinylcholine). The triggering substances cause uncontrolled release of calcium from the sarcoplasmic reticulum and may promote entry of extracellular calcium into the myoplasm, causing contracture of skeletal muscles, glycogenolysis, and increased cellular metabolism, resulting in production of heat and excess lactate. Affected individuals experience acidosis, hypercapnia, tachycardia, hyperthermia, muscle rigidity, compartment syndrome, rhabdomyolysis with subsequent increase in serum creatine kinase (CK) concentration, hyperkalemia with a risk for cardiac arrhythmia or even cardiac arrest, and myoglobinuria with a risk for renal failure. In nearly all cases, the first manifestations of MH (tachycardia and tachypnea) occur in the operating room; however, MH may also occur in the early postoperative period. There is mounting evidence that some individuals with MHS will also develop MH with exercise and/or on exposure to hot environments. Without proper and prompt treatment with dantrolene sodium, mortality is extremely high.
X-linked lethal multiple pterygium syndrome
MedGen UID:
374225
Concept ID:
C1839440
Disease or Syndrome
X-linked lethal multiple pterygium syndrome is a rare, genetic, developmental defect during embryogenesis characterized by the typical lethal multiple pterygium syndrome presentation (comprising of multiple pterygia, severe arthrogryposis, cleft palate, cystic hygromata and/or fetal hydrops, skeletal abnormalities and fetal death in the 2nd or 3rd trimester) with an X-linked pattern of inheritance.
King Denborough syndrome
MedGen UID:
327082
Concept ID:
C1840365
Disease or Syndrome
King-Denborough syndrome (KDS) is an autosomal dominant disorder characterized by the triad of congenital myopathy, dysmorphic features, and susceptibility to malignant hyperthermia (summary by Dowling et al., 2011).
Bailey-Bloch congenital myopathy
MedGen UID:
340586
Concept ID:
C1850625
Disease or Syndrome
STAC3 disorder is characterized by congenital myopathy, musculoskeletal involvement of the trunk and extremities, feeding difficulties, and delayed motor milestones. Most affected individuals have weakness with myopathic facies, scoliosis, kyphosis or kyphoscoliosis, and contractures. Other common findings are ptosis, abnormalities of the palate (including cleft palate), and short stature. Risk for malignant hyperthermia susceptibility and restrictive lung disease are increased. Intellect is typically normal. Originally described in individuals from the Lumbee Native American tribe (an admixture of Cheraw Indian, English, and African American ancestry) in the state of North Carolina and reported as Native American myopathy, STAC3 disorder has now been identified in numerous other populations worldwide.
Lethal multiple pterygium syndrome
MedGen UID:
381473
Concept ID:
C1854678
Disease or Syndrome
Lethal multiple pterygium syndrome has many of the same signs and symptoms as the Escobar type. In addition, affected fetuses may develop a buildup of excess fluid in the body (hydrops fetalis) or a fluid-filled sac typically found on the back of the neck (cystic hygroma). Individuals with this type have severe arthrogryposis. Lethal multiple pterygium syndrome is associated with abnormalities such as underdevelopment (hypoplasia) of the heart, lung, or brain; twisting of the intestines (intestinal malrotation); kidney abnormalities; an opening in the roof of the mouth (a cleft palate); and an unusually small head size (microcephaly). Affected individuals may also develop a hole in the muscle that separates the abdomen from the chest cavity (the diaphragm), a condition called a congenital diaphragmatic hernia. Lethal multiple pterygium syndrome is typically fatal in the second or third trimester of pregnancy.\n\nIn people with multiple pterygium syndrome, Escobar type, the webbing typically affects the skin of the neck, fingers, forearms, inner thighs, and backs of the knee. People with this type may also have arthrogryposis. A side-to-side curvature of the spine (scoliosis) is sometimes seen. Affected individuals may also have respiratory distress at birth due to underdeveloped lungs (lung hypoplasia). People with multiple pterygium syndrome, Escobar type usually have distinctive facial features including droopy eyelids (ptosis), outside corners of the eyes that point downward (downslanting palpebral fissures), skin folds covering the inner corner of the eyes (epicanthal folds), a small jaw, and low-set ears. Males with this condition can have undescended testes (cryptorchidism). This condition does not worsen after birth, and affected individuals typically do not have muscle weakness later in life.\n\nThe two forms of multiple pterygium syndrome are differentiated by the severity of their symptoms. Multiple pterygium syndrome, Escobar type (sometimes referred to as Escobar syndrome) is the milder of the two types. Lethal multiple pterygium syndrome is fatal before birth or very soon after birth.\n\nMultiple pterygium syndrome is a condition that is evident before birth with webbing of the skin (pterygium) at the joints and a lack of muscle movement (akinesia) before birth. Akinesia frequently results in muscle weakness and joint deformities called contractures that restrict the movement of joints (arthrogryposis). As a result, multiple pterygium syndrome can lead to further problems with movement such as arms and legs that cannot fully extend.
Multiple pterygium-malignant hyperthermia syndrome
MedGen UID:
347490
Concept ID:
C1857576
Disease or Syndrome
An extremely rare arthrogryposis syndrome, described in only two pairs of siblings from two unrelated families to date, and characterized by the association of arthrogryposis, congenital torticollis, dysmorphic facial features (i.e. asymmetry of the face, myopathic facial movements, ptosis, posteriorly rotated ears, cleft palate), progressive scoliosis and episodes of malignant hyperthermia. There have been no further descriptions in the literature since 1988.
Malignant hyperthermia, susceptibility to, 5
MedGen UID:
356151
Concept ID:
C1866077
Finding
Malignant hyperthermia susceptibility (MHS) is a pharmacogenetic disorder of skeletal muscle calcium regulation associated with uncontrolled skeletal muscle hypermetabolism. Manifestations of malignant hyperthermia (MH) are precipitated by certain volatile anesthetics (i.e., halothane, isoflurane, sevoflurane, desflurane, enflurane), either alone or in conjunction with a depolarizing muscle relaxant (specifically, succinylcholine). The triggering substances cause uncontrolled release of calcium from the sarcoplasmic reticulum and may promote entry of extracellular calcium into the myoplasm, causing contracture of skeletal muscles, glycogenolysis, and increased cellular metabolism, resulting in production of heat and excess lactate. Affected individuals experience acidosis, hypercapnia, tachycardia, hyperthermia, muscle rigidity, compartment syndrome, rhabdomyolysis with subsequent increase in serum creatine kinase (CK) concentration, hyperkalemia with a risk for cardiac arrhythmia or even cardiac arrest, and myoglobinuria with a risk for renal failure. In nearly all cases, the first manifestations of MH (tachycardia and tachypnea) occur in the operating room; however, MH may also occur in the early postoperative period. There is mounting evidence that some individuals with MHS will also develop MH with exercise and/or on exposure to hot environments. Without proper and prompt treatment with dantrolene sodium, mortality is extremely high.
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).
Malignant hyperthermia, susceptibility to, 1
MedGen UID:
443948
Concept ID:
C2930980
Finding
Malignant hyperthermia susceptibility (MHS) is a pharmacogenetic disorder of skeletal muscle calcium regulation associated with uncontrolled skeletal muscle hypermetabolism. Manifestations of malignant hyperthermia (MH) are precipitated by certain volatile anesthetics (i.e., halothane, isoflurane, sevoflurane, desflurane, enflurane), either alone or in conjunction with a depolarizing muscle relaxant (specifically, succinylcholine). The triggering substances cause uncontrolled release of calcium from the sarcoplasmic reticulum and may promote entry of extracellular calcium into the myoplasm, causing contracture of skeletal muscles, glycogenolysis, and increased cellular metabolism, resulting in production of heat and excess lactate. Affected individuals experience acidosis, hypercapnia, tachycardia, hyperthermia, muscle rigidity, compartment syndrome, rhabdomyolysis with subsequent increase in serum creatine kinase (CK) concentration, hyperkalemia with a risk for cardiac arrhythmia or even cardiac arrest, and myoglobinuria with a risk for renal failure. In nearly all cases, the first manifestations of MH (tachycardia and tachypnea) occur in the operating room; however, MH may also occur in the early postoperative period. There is mounting evidence that some individuals with MHS will also develop MH with exercise and/or on exposure to hot environments. Without proper and prompt treatment with dantrolene sodium, mortality is extremely high.
Malignant hyperthermia, susceptibility to, 2
MedGen UID:
419301
Concept ID:
C2930981
Finding
Malignant hyperthermia susceptibility (MHS) is a pharmacogenetic disorder of skeletal muscle calcium regulation associated with uncontrolled skeletal muscle hypermetabolism. Manifestations of malignant hyperthermia (MH) are precipitated by certain volatile anesthetics (i.e., halothane, isoflurane, sevoflurane, desflurane, enflurane), either alone or in conjunction with a depolarizing muscle relaxant (specifically, succinylcholine). The triggering substances cause uncontrolled release of calcium from the sarcoplasmic reticulum and may promote entry of extracellular calcium into the myoplasm, causing contracture of skeletal muscles, glycogenolysis, and increased cellular metabolism, resulting in production of heat and excess lactate. Affected individuals experience acidosis, hypercapnia, tachycardia, hyperthermia, muscle rigidity, compartment syndrome, rhabdomyolysis with subsequent increase in serum creatine kinase (CK) concentration, hyperkalemia with a risk for cardiac arrhythmia or even cardiac arrest, and myoglobinuria with a risk for renal failure. In nearly all cases, the first manifestations of MH (tachycardia and tachypnea) occur in the operating room; however, MH may also occur in the early postoperative period. There is mounting evidence that some individuals with MHS will also develop MH with exercise and/or on exposure to hot environments. Without proper and prompt treatment with dantrolene sodium, mortality is extremely high.
Malignant hyperthermia, susceptibility to, 3
MedGen UID:
418956
Concept ID:
C2930982
Finding
Malignant hyperthermia susceptibility (MHS) is a pharmacogenetic disorder of skeletal muscle calcium regulation associated with uncontrolled skeletal muscle hypermetabolism. Manifestations of malignant hyperthermia (MH) are precipitated by certain volatile anesthetics (i.e., halothane, isoflurane, sevoflurane, desflurane, enflurane), either alone or in conjunction with a depolarizing muscle relaxant (specifically, succinylcholine). The triggering substances cause uncontrolled release of calcium from the sarcoplasmic reticulum and may promote entry of extracellular calcium into the myoplasm, causing contracture of skeletal muscles, glycogenolysis, and increased cellular metabolism, resulting in production of heat and excess lactate. Affected individuals experience acidosis, hypercapnia, tachycardia, hyperthermia, muscle rigidity, compartment syndrome, rhabdomyolysis with subsequent increase in serum creatine kinase (CK) concentration, hyperkalemia with a risk for cardiac arrhythmia or even cardiac arrest, and myoglobinuria with a risk for renal failure. In nearly all cases, the first manifestations of MH (tachycardia and tachypnea) occur in the operating room; however, MH may also occur in the early postoperative period. There is mounting evidence that some individuals with MHS will also develop MH with exercise and/or on exposure to hot environments. Without proper and prompt treatment with dantrolene sodium, mortality is extremely high.
Schwartz-Jampel syndrome type 1
MedGen UID:
1647990
Concept ID:
C4551479
Disease or Syndrome
Schwartz-Jampel syndrome is a rare condition characterized by permanent muscle stiffness (myotonia) and bone abnormalities known as chondrodysplasia. The signs and symptoms of this condition become apparent sometime after birth, usually in early childhood. Either muscle stiffness or chondrodysplasia can appear first. The muscle and bone abnormalities worsen in childhood, although most affected individuals have a normal lifespan. The specific features of Schwartz-Jampel syndrome vary widely.\n\nMyotonia involves continuous tensing (contraction) of muscles used for movement (skeletal muscles) throughout the body. This sustained muscle contraction causes stiffness that interferes with eating, sitting, walking, and other movements. Sustained contraction of muscles in the face leads to a fixed, "mask-like" facial expression with narrow eye openings (blepharophimosis) and pursed lips. This facial appearance is very specific to Schwartz-Jampel syndrome. Affected individuals may also be nearsighted and experience abnormal blinking or spasms of the eyelids (blepharospasm).\n\nChondrodysplasia affects the development of the skeleton, particularly the long bones in the arms and legs and the bones of the hips. These bones are shortened and unusually wide at the ends, so affected individuals have short stature. The long bones may also be abnormally curved (bowed). Other bone abnormalities associated with Schwartz-Jampel syndrome include a protruding chest (pectus carinatum), abnormal curvature of the spine, flattened bones of the spine (platyspondyly), and joint abnormalities called contractures that further restrict movement.\n\nResearchers originally described two types of Schwartz-Jampel syndrome. Type 1 has the signs and symptoms described above, while type 2 has more severe bone abnormalities and other health problems and is usually life-threatening in early infancy. Researchers have since discovered that the condition they thought was Schwartz-Jampel syndrome type 2 is actually part of another disorder, Stüve-Wiedemann syndrome, which is caused by mutations in a different gene. They have recommended that the designation Schwartz-Jampel syndrome type 2 no longer be used.

Professional guidelines

PubMed

Gregory H, Weant KA
Adv Emerg Nurs J 2021 Apr-Jun 01;43(2):102-110. doi: 10.1097/TME.0000000000000344. PMID: 33915557
Hopkins PM, Girard T, Dalay S, Jenkins B, Thacker A, Patteril M, McGrady E
Anaesthesia 2021 May;76(5):655-664. Epub 2021 Jan 5 doi: 10.1111/anae.15317. PMID: 33399225
Laitano O, Leon LR, Roberts WO, Sawka MN
J Appl Physiol (1985) 2019 Nov 1;127(5):1338-1348. Epub 2019 Sep 23 doi: 10.1152/japplphysiol.00452.2019. PMID: 31545156

Recent clinical studies

Etiology

Gregory H, Weant KA
Adv Emerg Nurs J 2021 Apr-Jun 01;43(2):102-110. doi: 10.1097/TME.0000000000000344. PMID: 33915557
Hopkins PM, Girard T, Dalay S, Jenkins B, Thacker A, Patteril M, McGrady E
Anaesthesia 2021 May;76(5):655-664. Epub 2021 Jan 5 doi: 10.1111/anae.15317. PMID: 33399225
Rüffert H, Bastian B, Bendixen D, Girard T, Heiderich S, Hellblom A, Hopkins PM, Johannsen S, Snoeck MM, Urwyler A, Glahn KPE; European Malignant Hyperthermia Group
Br J Anaesth 2021 Jan;126(1):120-130. Epub 2020 Oct 31 doi: 10.1016/j.bja.2020.09.029. PMID: 33131754
Miller DM, Daly C, Aboelsaod EM, Gardner L, Hobson SJ, Riasat K, Shepherd S, Robinson RL, Bilmen JG, Gupta PK, Shaw MA, Hopkins PM
Br J Anaesth 2018 Oct;121(4):944-952. Epub 2018 Aug 17 doi: 10.1016/j.bja.2018.06.028. PMID: 30236257Free PMC Article
Rosenberg H, Davis M, James D, Pollock N, Stowell K
Orphanet J Rare Dis 2007 Apr 24;2:21. doi: 10.1186/1750-1172-2-21. PMID: 17456235Free PMC Article

Diagnosis

Gregory H, Weant KA
Adv Emerg Nurs J 2021 Apr-Jun 01;43(2):102-110. doi: 10.1097/TME.0000000000000344. PMID: 33915557
Hopkins PM, Girard T, Dalay S, Jenkins B, Thacker A, Patteril M, McGrady E
Anaesthesia 2021 May;76(5):655-664. Epub 2021 Jan 5 doi: 10.1111/anae.15317. PMID: 33399225
Kaur H, Katyal N, Yelam A, Kumar K, Srivastava H, Govindarajan R
Mo Med 2019 Mar-Apr;116(2):154-159. PMID: 31040503Free PMC Article
Sessler DI
Lancet 2016 Jun 25;387(10038):2655-2664. Epub 2016 Jan 8 doi: 10.1016/S0140-6736(15)00981-2. PMID: 26775126
Rosenberg H, Pollock N, Schiemann A, Bulger T, Stowell K
Orphanet J Rare Dis 2015 Aug 4;10:93. doi: 10.1186/s13023-015-0310-1. PMID: 26238698Free PMC Article

Therapy

Gregory H, Weant KA
Adv Emerg Nurs J 2021 Apr-Jun 01;43(2):102-110. doi: 10.1097/TME.0000000000000344. PMID: 33915557
Hopkins PM, Girard T, Dalay S, Jenkins B, Thacker A, Patteril M, McGrady E
Anaesthesia 2021 May;76(5):655-664. Epub 2021 Jan 5 doi: 10.1111/anae.15317. PMID: 33399225
Kaur H, Katyal N, Yelam A, Kumar K, Srivastava H, Govindarajan R
Mo Med 2019 Mar-Apr;116(2):154-159. PMID: 31040503Free PMC Article
Sessler DI
Lancet 2016 Jun 25;387(10038):2655-2664. Epub 2016 Jan 8 doi: 10.1016/S0140-6736(15)00981-2. PMID: 26775126
Nelson TE, Flewellen EH
N Engl J Med 1983 Aug 18;309(7):416-8. doi: 10.1056/NEJM198308183090706. PMID: 6348539

Prognosis

Tao M, Li J, Wang X, Tian X
Expert Opin Drug Saf 2021 Sep;20(9):1075-1085. Epub 2021 Apr 26 doi: 10.1080/14740338.2021.1919622. PMID: 33866917
Laitano O, Leon LR, Roberts WO, Sawka MN
J Appl Physiol (1985) 2019 Nov 1;127(5):1338-1348. Epub 2019 Sep 23 doi: 10.1152/japplphysiol.00452.2019. PMID: 31545156
Patton K, Borshoff DC
Anaesthesia 2018 Jan;73 Suppl 1:76-84. doi: 10.1111/anae.14143. PMID: 29313907
Amburgey K, Bailey A, Hwang JH, Tarnopolsky MA, Bonnemann CG, Medne L, Mathews KD, Collins J, Daube JR, Wellman GP, Callaghan B, Clarke NF, Dowling JJ
Orphanet J Rare Dis 2013 Aug 6;8:117. doi: 10.1186/1750-1172-8-117. PMID: 23919265Free PMC Article
Becker JH, Wu SC
J Am Podiatr Med Assoc 2010 Jul-Aug;100(4):281-90. doi: 10.7547/1000281. PMID: 20660880

Clinical prediction guides

Kushnir A, Todd JJ, Witherspoon JW, Yuan Q, Reiken S, Lin H, Munce RH, Wajsberg B, Melville Z, Clarke OB, Wedderburn-Pugh K, Wronska A, Razaqyar MS, Chrismer IC, Shelton MO, Mankodi A, Grunseich C, Tarnopolsky MA, Tanji K, Hirano M, Riazi S, Kraeva N, Voermans NC, Gruber A, Allen C, Meilleur KG, Marks AR
Acta Neuropathol 2020 Jun;139(6):1089-1104. Epub 2020 Mar 31 doi: 10.1007/s00401-020-02150-w. PMID: 32236737Free PMC Article
Laitano O, Leon LR, Roberts WO, Sawka MN
J Appl Physiol (1985) 2019 Nov 1;127(5):1338-1348. Epub 2019 Sep 23 doi: 10.1152/japplphysiol.00452.2019. PMID: 31545156
Saba R, Kaye AD, Urman RD
Anesthesiol Clin 2017 Jun;35(2):285-294. doi: 10.1016/j.anclin.2017.01.014. PMID: 28526149
Amburgey K, Bailey A, Hwang JH, Tarnopolsky MA, Bonnemann CG, Medne L, Mathews KD, Collins J, Daube JR, Wellman GP, Callaghan B, Clarke NF, Dowling JJ
Orphanet J Rare Dis 2013 Aug 6;8:117. doi: 10.1186/1750-1172-8-117. PMID: 23919265Free PMC Article
Demeyere R
Acta Anaesthesiol Belg 1978;29(1):101-20. PMID: 707024

Recent systematic reviews

Kruijt N, van den Bersselaar LR, Wijma J, Verbeeck W, Coenen MJH, Neville J, Snoeck M, Kamsteeg EJ, Jungbluth H, Kramers C, Voermans NC
Neuromuscul Disord 2020 Dec;30(12):949-958. Epub 2020 Oct 31 doi: 10.1016/j.nmd.2020.10.010. PMID: 33250373
Finsterer J, Scorza FA, Scorza CA
J Clin Neuromuscul Dis 2019 Dec;21(2):90-102. doi: 10.1097/CND.0000000000000269. PMID: 31743252
Larach MG, Klumpner TT, Brandom BW, Vaughn MT, Belani KG, Herlich A, Kim TW, Limoncelli J, Riazi S, Sivak EL, Capacchione J, Mashman D, Kheterpal S, Kooij F, Wilczak J, Soto R, Berris J, Price Z, Lins S, Coles P, Harris JM, Cummings KC 3rd, Berman MF, Nanamori M, Adelman BT, Wedeven C, LaGorio J, McCormick PJ, Tom S, Aziz MF, Coffman T, Ellis TA 2nd, Molina S, Peterson W, Mackey SC, van Klei WA, Ginde AA, Biggs DA, Neuman MD, Craft RM, Pace NL, Paganelli WC, Durieux ME, Nair BJ, Wanderer JP, Miller SA, Helsten DL, Turnbull ZA, Schonberger RB; Multicenter Perioperative Outcomes Group
Anesthesiology 2019 Jan;130(1):41-54. doi: 10.1097/ALN.0000000000002490. PMID: 30550426
Kraeva N, Sapa A, Dowling JJ, Riazi S
Can J Anaesth 2017 Jul;64(7):736-743. Epub 2017 Mar 21 doi: 10.1007/s12630-017-0865-5. PMID: 28326467
Metterlein T, Zink W, Kranke E, Haneya A, Graf B, Kranke P
J Thorac Cardiovasc Surg 2011 Jun;141(6):1488-95. Epub 2011 Mar 3 doi: 10.1016/j.jtcvs.2011.01.034. PMID: 21376345

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