Brain injury due to anaphylactic shock: broadening manifestations of <scp>K</scp>ounis syndrome

Soufras, George D.; Kounis, George N.; Kounis, Nicholas G.

doi:10.1111/iej.12152

Cited by 15 publications

(12 citation statements)

References 23 publications

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“…Currently, allergic angina and allergic myocardial infarction constitute coronary artery disorders that might be caused by numerous and continuously increasing causes, accompanied with broadening clinical symptoms and signs, via multi-organ arterial system involvement in patients of any age and consisting a wide spectrum of mast cell-associated disorders (2,8,9,10,11,12,13,14,15).…”

mentioning

confidence: 99%

Kounis Syndrome—not a Single-organ Arterial Disorder but a Multisystem and Multidisciplinary Disease

Kounis¹,

Koniari²,

Velissaris³

et al. 2019

Balkan Med J

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Coronary symptoms associated with conditions related to mast cell activation and inflammatory cell interactions, such as those involving T-lymphocytes and macrophages, further inducing allergic, hypersensitivity, anaphylactic, or anaphylactic insults, are currently referred to as the Kounis syndrome. Kounis syndrome is caused by inflammatory mediators released during allergic insults, postinflammatory cell activation, and interactions via multidirectional stimuli. A platelet subset of 20% with high-and low-affinity IgE surface receptors is also involved in this process. Kounis syndrome is not just a single-organ but also a complex multisystem and multiorgan arterial clinical condition; it affects the coronary, mesenteric, and cerebral arteries and is accompanied by allergy-hypersensitivityanaphylaxis involving the skin, respiratory, and vascular systems in the context of anesthesia, surgery, radiology, oncology, or even dental and psychiatric medicine; further, it has significantly influences both morbidity and mortality. Kounis syndrome might be caused by numerous and continuously increasing causes, with broad clinical symptoms and signs, via multi-organ arterial system involvement, in patients of any age, thereby demonstrating predominant anaphylactic features in terms of a wide spectrum of mast cell-association disorders. Cardiac symptoms, such as chest pain, coronary vasospasm, angina pectoris, myocardial infarction, stent thrombosis, acute cardiac failure, and sudden cardiac death associated with subclinical, clinical, acute, or chronic allergic reactions, constitute the clinical manifestations of this syndrome. Since its first description, a common pathway between allergic and non-allergic coronary events has been demonstrated. The hypothesis is based on the existence of a much higher degree of mast cell degranulation at plaque erosion or rupture sites compared with at the adjacent areas or even more distant segments in post-acute myocardial infarction of non-allergic etiology. Although mast cell activation, differentiation, and mediator release takes days or weeks, the mast cell degranulation may occur just before any acute coronary event, further resulting in coronary artery vasoconstriction and atheromatous plaque rupture. It seems that medications and natural molecules stabilizing the mast cell membrane as well as monoclonal antibodies protecting the mast cell surface can emerge as novel therapeutic modalities for acute coronary and cerebrovascular event prevention.

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mentioning

confidence: 99%

Kounis Syndrome—not a Single-organ Arterial Disorder but a Multisystem and Multidisciplinary Disease

Kounis¹,

Koniari²,

Velissaris³

et al. 2019

Balkan Med J

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“…Although mucocutaneous symptoms are reported in 80% to 90% of cases of anaphylaxis in general, [10,11] only about 30% of the DIA litigation cases in our study involved mucocutaneous symptoms, suggesting that in many cases reaching the diagnosis of anaphylaxis were relatively difficult. [26–29] In contrast, although cardiovascular symptoms are reported in up to 45% of cases of anaphylaxis, [7] more than 90% of cases in this study involved cardiovascular symptoms, and most cases were accompanied by cardiac arrest. Neurologic symptoms were also recognized more frequently in this study than in previous reports (up to 15%).…”

Section: Discussionmentioning

confidence: 64%

Medical malpractice related to drug-induced anaphylaxis

Hyeon

Lee

Jang³

et al. 2019

Medicine

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Drug-induced anaphylaxis (DIA) is a highly paradoxical disorder involving a fatal response to medicines prescribed for therapeutic purposes. This study aimed to improve the awareness on DIA and to prevent errors through an analysis of lawsuit judgments. Sentenced judgments involving DIA from 1998 to 2017 using the database of the Korean Supreme Court Judgment System were collected. General characteristics, results, and recognized negligence of DIA litigation cases were analyzed. Of 27 lawsuit cases included, antibiotics (n = 6, 22.2%), radiocontrast media (n = 6, 22.2%), and non-steroidal anti-inflammatory drugs (n = 5, 18.5%) were the most common drugs that had caused DIA. Cardiac arrest was reported in 23 cases (85.2%). The median time interval from drug administration to diagnosis and from diagnosis to cardiac arrest were 7 (interquartile range, IQR = 0–35) and 5 minutes (IQR = 0–33), respectively, suggesting insufficient time to cope with anaphylaxis. Consequently, either death (n = 18, 66.7%) or ischemic brain injury (n = 9, 33.3%) occurred in all cases. Violation of duty of care was recognized in 19 cases (70.4%) with median awarded amount of $106,060 (IQR = $70,296–$168,363). The recognized negligence included inadequate observation after drug administration (n = 6), delayed or missed epinephrine administration (n = 6), ignoring a history of allergy or drug hypersensitivity (n = 6), and prescription error (n = 5). It is necessary to improve the awareness on DIA, because making a trivial error in any process of history taking, drug prescription and administration, observation, and/or emergency treatment may have fatal consequences that can lead to indemnity.

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“…The development of anaphylactic shock during post-SAH triple-H therapy induction is considered to be ill-timed. According to research reports on animal models [ 24 – 29 ], the direct action of anaphylactic mediators on the cerebral arterial system results in cerebral ischemia and brain injury. The decrease in cerebral blood flow is greater than what would be expected from the level of severity of arterial hypotension, which is attributed to the rapid and direct action of anaphylactic mediators on cerebral vessels [ 24 , 25 ].…”

Section: Discussionmentioning

confidence: 99%

“…According to research reports on animal models [ 24 – 29 ], the direct action of anaphylactic mediators on the cerebral arterial system results in cerebral ischemia and brain injury. The decrease in cerebral blood flow is greater than what would be expected from the level of severity of arterial hypotension, which is attributed to the rapid and direct action of anaphylactic mediators on cerebral vessels [ 24 , 25 ]. Even though blood pressure and cardiac output recover following anaphylactic shock, there is a risk of continued cerebral blood flow deterioration [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, mast cell activation by anaphylaxis causes a substantial release of vasoactive inflammatory cytokines. Mast cells resident within the cerebral microvasculature act on the basal membrane and damage the blood-brain barrier, resulting in brain edema [ 24 , 27 , 28 ]. When anaphylactic shock occurs in patients suffering from SAH, it is important to take special notice of harmful effects due to anaphylactic shock on cerebral circulation.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Severe Dextran-Induced Anaphylactic Shock during Induction of Hypertension-Hypervolemia-Hemodilution Therapy following Subarachnoid Hemorrhage

Shiratori¹,

Sato²,

Fukuzawa³

et al. 2015

Case Reports in Critical Care

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Dextran is a colloid effective for volume expansion; however, a possible side effect of its use is anaphylaxis. Dextran-induced anaphylactoid reaction (DIAR) is a rare but severe complication, with a small dose of dextran solution sufficient to induce anaphylaxis. An 86-year-old female who underwent clipping for a ruptured cerebral aneurysm was admitted to the intensive care unit. Prophylactic hypertension-hypervolemia-hemodilution therapy was induced for cerebral vasospasm following a subarachnoid hemorrhage. The patient went into severe shock after administration of dextran for volume expansion, and dextran administration was immediately discontinued. The volume administered at that time was only 0.8 mL at the most. After fluid resuscitation with a crystalloid solution, circulatory status began to recover. However, cerebral vasospasm occurred and the patient's neurological condition deteriorated. Five weeks after the shock, she was diagnosed with hypersensitivity to dextran by a skin test. When severe hypotension occurs after dextran administration, appropriate treatments for shock should be performed immediately with discontinuation of dextran solution. Although colloid administration is recommended in some guidelines and researches, it is necessary to consider concerning the indication for volume expansion as well as the risk of colloid administration.

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Brain injury due to anaphylactic shock: broadening manifestations of Kounis syndrome

Cited by 15 publications

References 23 publications

Kounis Syndrome—not a Single-organ Arterial Disorder but a Multisystem and Multidisciplinary Disease

Kounis Syndrome—not a Single-organ Arterial Disorder but a Multisystem and Multidisciplinary Disease

Medical malpractice related to drug-induced anaphylaxis

Severe Dextran-Induced Anaphylactic Shock during Induction of Hypertension-Hypervolemia-Hemodilution Therapy following Subarachnoid Hemorrhage

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