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Anaphylactic Shock Decreases Cerebral Blood Flow More Than What Would Be Expected From Severe Arterial Hypotension

Reply

Mertes, Paul-Michel; Zheng, Feng; Barthel, Grégoire; Alb, Ionel; Tabarna, Adriana; Thornton, Simon N.; Longrois, Dan; Audibert, Gérard; Malinovsky, Jean-Marc

Author Information
doi: 10.1097/SHK.0b013e31829173a6
Erratum

In the Authors’ Reply published on pages 463–464 of the May 2013 issue, the authors’ institutional affiliations were not correctly assigned. They should appear as follows:

Paul-Michel Mertes

Groupe Choc, Contrat AVENIR INSERM U961

Faculté de Médecine, Université de Lorraine

Vandluvre-lès-Nancy

Pôle Anesthésie, Réanimations Chirurgicales, SAMU

Hôpitaux Universitaires de Strasbourg, Strasbourg

Feng Zheng

Groupe Choc, Contrat AVENIR INSERM U961

Faculté de Médecine, Université de Lorraine

Vandluvre-lès-Nancy

Grégoire Barthel

Ionel Alb

Ionel Alb

Adriana Tabarna

Gérard Audibert

Département d’Anesthésie-Réanimation Chirurgicale

Centre Hospitalier Universitaire (CHU) Central, Nancy

Simon N. Thornton

INSERM U961, Faculté de Médecine, Université de Lorraine

Vandluvre-lés-Nancy

Dan Longrois

Département d’Anesthésie-Réanimation Chirurgicale

Hôpital Bichat-Claude Bernard, Unité INSERM U698

Assistance Publique-Hôpitaux de Paris

Université Paris Diderot, Sorbonne Paris Cité, Paris

Jean-Marc Malinovsky

Département d’Anesthésie-Réanimation

Chirurgicale, CHU de Reims, Reims, France

The publisher regrets the error.

Shock. 40(3):236, September 2013.

Reply

We are grateful to Dr Kounis and colleagues for their thoughtful insight to the pathophysiology of anaphylactic shock and their evaluation of our article entitled: “Anaphylactic Shock Decreases Cerebral Blood Flow More Than What Would Be Expected From Severe Arterial Hypotension” (1).

There is no doubt that myocardial dysfunction, probably related (but no exclusively) to coronary events, participates to the pathophysiology of severe forms of anaphylactic shock. Nevertheless, we have brought proof of vasodilatation and plasma extravasation (acutely increased hemoglobin concentration due to hemoconcentration) and therefore consider that both vascular (macro- and micro-)dysfunction, decreased circulating blood volume and myocardial dysfunction contribute, to the pathophysiology of severe forms of anaphylactic shock. In addition, our results demonstrate that anaphylactic shock impairs cerebral blood flow beyond its characteristic arterial hypotension, resulting in severe brain ischemia, which contributes to the pathophysiology of severe anaphylactic shock. We have also recently showed that impairment of cerebral blood flow may persist despite correction of arterial hypotension (2).

Our group considers that there are multiple mechanisms that may underline refractory anaphylactic shock both in animal (healthy) models and even more so in human clinical practice because of the interaction between the mediators of anaphylactic shock and the underlying chronic/acute comorbidities (3–6).

Among our working hypothesis is also the fact that because of the “explosive” pattern of anaphylactic shock, there is no time for cells to adapt to the acute decrease in oxygen delivery, and this, coupled to the persistent oxygen consumption, results in very rapid cellular energetic failure, which will concern all organs (including the brain and the heart) that have high basal metabolic requirements (7). In addition, Dr. Kounis and colleagues point to the fact that intracoronary thrombosis may occur. Activation of platelets is a credible link. We agree with Dr. Kounis that further research is necessary to investigate the mechanism of refractory anaphylactic shock and to propose new therapeutic approaches.

Paul-Michel Mertes

Feng Zheng

Grégoire Barthel

Ionel Alb

Adriana Tabarna

Simon N. Thornton

Dan Longrois

Gérard Audibert

Jean-Marc Malinovsky

Groupe Choc, Contrat AVENIR INSERM U961

Faculté de Médecine, Université de Lorraine

Vandœuvre-lès-Nancy

Pôle Anesthésie, Réanimations Chirurgicales, SAMU

Hôpitaux Universitaires de Strasbourg, Strasbourg

Département d’Anesthésie-Réanimation Chirurgicale

Centre Hospitalier Universitaire (CHU) Central, Nancy

INSERM U961, Faculté de Médecine, Université de Lorraine

Vandœuvre-lès-Nancy

Département d’Anesthésie-Réanimation Chirurgicale

Hôpital Bichat-Claude Bernard, Unité INSERM U698

Assistance Publique-Hôpitaux de Paris

Université Paris Diderot, Sorbonne Paris Cité, Paris

and Département d’Anesthésie-Réanimation

Chirurgicale, CHU de Reims, Reims, France

REFERENCES

1. Davidson J, Zheng F, Tajima K: Anaphylactic shock decreases cerebral blood flow more than what would be expected from severe arterial hypotension. Shock 38 (4): 429–435, 2012.
2. Zheng F, Bartel G, Collange O, Montémont C, Thornton SN, Longrois D, Levy B, Audibert G, Malinovsky JM, Mertes PM: Methylene blue and epinephrine: a synergetic association for anaphylactic shock treatment. Crit Care Med 41 (1): 195–204, 2013.
3. Chung MC, Walsh A, Dennis I: Trauma exposure characteristics, past traumatic life events, coping strategies, posttraumatic stress disorder, and psychiatric comorbidity among people with anaphylactic shock experience. Compr Psychiatry 52 (4): 394–404, 2011.
4. Stoevesandt J, Hain J, Kerstan A, Trautmann A: Over- and underestimated parameters in severe Hymenoptera venom-induced anaphylaxis: cardiovascular medication and absence of urticaria/angioedema. J Allergy Clin Immunol 130 (3): 698.e1–704.e1, 2012.
5. Mulla ZD, Ebrahim MS, Gonzalez JL: Anaphylaxis in the obstetric patient: analysis of a statewide hospital discharge database. Ann Allergy Asthma Immunol 104 (1): 55–59, 2010.
6. Greenberger PA, Rotskoff BD, Lifschultz B: Fatal anaphylaxis: postmortem findings and associated comorbid diseases. Ann Allergy Asthma Immunol 98 (3): 252–257, 2007.
7. Dewachter P, Jouan-Hereaux V, Franck P, Menu P, de Talancé N, Zannad F, Laxenaire MC, Longrois D, Mertes PM: Anaphylactic shock: a form of distributive shock without inhibition of oxygen consumption. Anesthesiology 103 (1): 40–49, 2005.
©2013The Shock Society