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. 2024 Oct 8;111(6):1178–1183. doi: 10.4269/ajtmh.24-0163

Myocardial Ischemia after Severe Scorpion Envenomation: A Narrative Review

Mabrouk Bahloul 1,*, Karama Bouchaala 1, Kamilia Chtara 1, Sana Kharrat 1, Mounir Bouaziz 1
PMCID: PMC11619508  PMID: 39378865

ABSTRACT.

Myocardial ischemia after severe scorpion envenomation is rarely reported. The aim of this review was to elaborate on a review of myocardial ischemia after severe scorpion envenomation and to detail the mechanism of this myocardial hypoperfusion. We used the PubMed database and entered the following keywords in MeSH research: scorpion envenomation, myocardial ischemia, myocardial perfusion scintigraphy, echocardiography, and troponins. The literature analysis confirmed that severe scorpion envenomation can be complicated by temporary myocardial ischemia, based on electrocardiographic, histopathologic, echocardiographic, myocardial perfusion scintigraphy, and biological studies. The correlation between clinical manifestations, laboratory and electrocardiographic evidence of myocardial damage, echocardiographic studies, perfusion scintigraphy abnormalities, and histopathologic findings are suggestive of lesions of cardiac fibers secondary to myocardial ischemia. Myocardial hypoperfusion may be due to multiple factors. First, catecholamine storms can induce microvascular constriction. On the other hand, the release of catecholamines through a complex neurohormonal interaction with other neuropeptides and cytokine release can produce/induce major coronary microvascular constriction and/or microvascular injury, leading to microvascular acute coronary syndrome with Takotsubo cardiomyopathy. The management of severe scorpion envenomation with severe myocardial failure and pulmonary edema is based on oxygen with invasive or noninvasive ventilator support. Dobutamine improves cardiac function after scorpion envenomation. Antiplatelet therapy is not recommended. In conclusion, severe scorpion envenomation can be complicated by temporary myocardial ischemia, which can be due to multiple factors.

INTRODUCTION

Scorpion envenomation is a common intoxication in tropical and subtropical areas.1 Severe cases of scorpion envenomation can lead to admission to the intensive care unit (ICU). The severity of the clinical manifestation is due essentially to cardiopulmonary damage. Indeed, cardiorespiratory manifestations, mainly cardiogenic shock and acute pulmonary edema, represent the main causes of ICU admission and death after scorpion envenomation.2 Their mechanism remains unclear, and multiple conclusions are discussed and reported in the literature.2 Moreover, the nature of scorpion envenomation–related cardiomyopathy is still the subject of much debate. Indeed, at least three mechanisms, namely adrenergic myocarditis, toxic myocarditis, and myocardial ischemia, have been discussed and debated in the literature.3–7

Although myocardial ischemia is rarely reported after scorpion envenomation, some studies have shown that severe scorpion envenomation may be associated with myocardial perfusion disturbance, leading to myocardial ischemia.8–13 This hypothesis was advanced in some electrocardiographic (ECG),8–10 histopathologic,14 echocardiographic,6,12 coronary angiogram,15 myocardial perfusion scintigraphy,11,12,16,17 and biological13,18 studies.

As a result, we found it interesting to elaborate on this review about myocardial ischemia after severe scorpion envenomation. This review aimed to analyze the most severe form of scorpion envenomation complicated by myocardial ischemia and to detail the mechanism of this myocardial hypoperfusion.

MATERIALS AND METHODS

We used the PubMed database and entered the following keywords in MeSH research: scorpion envenomation, myocardial ischemia, myocardial perfusion scintigraphy, echocardiography, and troponins. Our PubMed search strategy was to search with the keywords assembled as follows: [scorpionic envenomation AND (myocardial ischemia OR myocardial perfusion OR scintigraphy OR echocardiography OR troponin)]. We included only published studies with the full text available in English or French. All the studies that were reported as only an abstract, those with no accessible full text, and all review papers were excluded. Finally, the last reference list was defined based on the significance of each paper to the scope of this review according to our judgment.

RESULTS

According to our search strategy using assembled keywords, 85 articles were identified. According to our selected criteria, 62 articles were excluded and 23 articles were used in this current review8–30 (Table 1). Figure 1 shows the study flowchart.

Table 1.

Summary of all included studies

Authors/Year Type of Study Diagnostic Tools Used Age of the Patients Symptoms Reported Scorpion Species
Bawaskar et al.8 Case Report Electrocardiography Young (not precise) Respiratory Distress Not Precise
Ramalingam et al.9 Case Report Electrocardiography/C. Angiogram 50 Years Respiratory Distress Red Scorpion
Patra et al.10 Case Report Electrocardiography/C. Angiogram 65 Years Shock Not Precise
Cupo et al.11 Case Reports (12 children) Myocardial Perfusion Scintigraphy 1–12 Years Respiratory Distress Tityus serrulatus
Bahloul et al.12 Brief Reports (6 patients) Electrocardiography/Echocardiography/Myocardial Perfusion Scintigraphy 6–29 Years Shock/Respiratory Distress Androctonus australis
Chakroun-Walha et al.13 Retrospective (132 patients) Electrocardiogram/Troponin Dosage 31.3 ± 24.4 Years Respiratory Distress A. australis/Buthus occitanus
Gueron and Yaron14 Retrospective (34 patients) Electrocardiography/Histopathologic Findings 1–65 Years Respiratory Distress/Shock Buthus quinquestriatus
Köse and Yildirim15 Case Report Electrocardiography/C. Angiogram 54 Years Respiratory Distress Mesobuthus gibbosus
Gueron et al.16 Case Reports (5 children) Echocardiographic/Radionuclide Angiographic 1–14 Years Respiratory Distress/Shock Leiurus quinquestriatus
Rahav and Weiss17 Case Reports (2 children) Radionuclide Ventriculography 9 and 28 Years Respiratory Distress Yellow Scorpion
Meki et al.18 Prospective (41 children) Dosage of Troponin 7–14 Years Respiratory Distress/Shock B. occitanus/L. quinqestratus
Goyffon et al.19 Retrospective (717 patients) Electrocardiography 241 Patients <15 Years Respiratory Distress/Shock A. australis/B. occitanus
Katwaroo et al.20 Case Report Electrocardiography/C. Angiogram 59 Years Arterial Hypertension Tityus trinitatis
Baykan et al.21 Case Report Electrocardiography/C. Angiogram 55 Years Respiratory Distress Not Precise
Figueiredo et al.22 Prospective (15 children) Electrocardiography/Myocardial Perfusion Scintigraphy 7.6 ± 4.3 Years Respiratory Distress/Shock Not Precise
Sagarad et al.23 Prospective (84 children) Electrocardiography/Troponin Dosage Children in 85.6% S. Manifestations (85.7%) Not Precise
Sagarad et al.24 Prospective (84 children) Echocardiography/Troponin Dosage Mostly Children S. Manifestations Not Precise
Amaral et al.25 Case Reports (6 children) Electrocardiography/Echocardiographic and Histopathologic Findings 3–9 Years Respiratory Distress T. serrulatus
Cupo et al.26 Case Reports (4 children) Electrocardiography/Echocardiographic and Histopathologic Findings 4–6 Years Respiratory Distress T. serrulatus
Daisley et al.27 Case Reports (4 children) Histopathologic Findings 3–7 Years Respiratory Distress T. trinitatis
Abroug et al.28 Case Reports (2 patients) Electrocardiography/Troponin Dosage Echocardiographic/CMR 36 and 45 Years Respiratory Distress A. australis
Miranda et al.29 Case Report (1patient) Electrocardiography/Troponin Dosage Echocardiographic/CMR 7 Years Respiratory Distress T. serrulatus
Ben Jemaa et al.30 Case Report (1patient) Electrocardiography/Troponin Dosage Echocardiographic/CMR 26 Years Respiratory Distress A. australis
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C. angiogram = coronary angiogram; CMR = cardiac magnetic resonance; S. manifestations = systemic manifestations.

Figure 1.

Figure 1.

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Study flow chart. Mechanisms of myocardial ischemia and management of severe scorpion envenomation with severe myocardial failure.

The literature analysis confirmed that complication of severe scorpion envenomation by myocardial ischemia is well established. This hypothesis was advanced in some ECG,8–10 histopathologic,14 echocardiographic,6,12 coronary angiogram,15 myocardial perfusion scintigraphy,11,12,16,17 and biological13,18 studies.

Electrocardiographic studies.

Electrocardiographic disorders after severe scorpion envenomation are common (84% of cases).1,8–10,14,19 They are polymorphic and nonspecific, associated with rhythm abnormalities (sinus tachycardia or bradycardia, atrial or ventricular fibrillation, and supraventricular tachycardia), disorders of conduction (first degree of atrioventricular block, junctional rhythm, bundle branch block), and repolarization disorders (ST changes). ST-T changes, including ST-segment elevation or depression, T inversion, or tall T waves, were present in 64.6% of cases after severe scorpion envenomation.6 More rarely, Q waves, which can be indicators of myocardial necrosis, have been observed.20

In one prospective study including six patients with severe SE, Bahloul et al.12 analyzed myocardial perfusion to determine myocardial ischemia. In this study, the most common ECG abnormality observed was tachycardia (>110 beats/minute) (100%). The T-wave change was detected in four patients, ST-segment depression or elevation in two patients, and right bundle branch block in one. Moreover, ECG changes observed in all patients were associated with echocardiographic abnormalities.12 Finally, they found a good association between myocardial hypoperfusion grade and localization and the abnormal localization shown by echocardiography and electrocardiography compared with a normal wall. However, it appears that the frequency of pathologic Q waves was underestimated in the literature.31 In fact, in a retrospective study involving 59 children with acute myocarditis admitted between January 2016 and July 2021, pathologic Q waves were found in 52.5% of the patients.31 Moreover, in the last study,31 the presence of Q waves was associated with higher troponin I values (499 versus 145 ng/L; P  = 0.011) and longer hospital stays (13 versus 9 days; P  = 0.020) than the non–Q-wave group. Moreover, the Q-wave myocarditis group also required higher doses of inotropic or vasoactive drugs and mechanical ventilation compared with non–Q-wave patients. Finally, all patients who died or were discharged with a left ventricular ejection fraction <30% fit into the Q-wave group. On the other hand, an authentic acute coronary syndrome after a severe scorpion sting was also reported.20,21 More recently, Bawaskar et al.8 reported an ST-segment elevation in a young patient after severe scorpion envenomation. The follow-up ECG done at 48 hours showed the nonappearance of Q waves or T-wave inversion in the leads that previously showed ST-segment elevation; cardiac enzyme measure was not conducted.

Echocardiographic studies.

Severe scorpion envenomation is usually associated with cardiac manifestations that can progress to heart failure. Echocardiography findings observed in most studies were regional or global hypokinesia, decreased left ventricular ejection fraction, and decreased fractional shortening.6 In one prospective study, Bahloul et al.12 included six patients admitted for severe scorpion envenomation with pulmonary edema over a period of 1 year. All included patients exhibited evidence of ischemic myocardial damage confirmed by electrocardiography, myocardial perfusion scintigraphy, and echocardiography. In this study,12 the diagnosis of myocardial ischemia was established on the clinical presence of pulmonary edema, the presence of segmental hypokinesia in echocardiography, T-wave change, and/or RST abnormalities on the ECG study associated with myocardial scintigraphic abnormalities.

Radionuclide ventriculography was abnormal in all included patients,12 and 201Tl scintigraphy showed evidence of myocardial hypoperfusion in all cases. The severe myocardial perfusion defects were located in the wall segments, with motion abnormalities shown by echocardiography. The investigators of this research concluded that motion abnormalities shown by echocardiography were due to severe myocardial hypoperfusion.

In another echocardiographic and radionuclide angiographic study, Gueron et al.16 included five severely hypertensive children, one of them in respiratory failure and another who had pulmonary edema after a scorpion envenomation with Leiurus quinquestriatus. Abnormal echocardiography on admission was observed in three patients. Poorly contracting wall motion with decreased systolic left ventricular performance and normal wall thickness was present in three children. The radionuclide angiograms confirmed the poorly contracting left ventricle in the same patients. There was a good correlation between wall segments and motion abnormalities, as shown by echocardiography and radionuclide angiographic exploration. In this study,16 high levels of cardiac enzymes on admission were found in most of the patients, with normalization of their values at the time of discharge.

The good correlation between echocardiographic, ECG, myocardial perfusion scintigraphy, and radionuclide angiographic abnormalities observed in the above-mentioned studies12,16 supports the hypothesis of myocardial hypoperfusion in severe scorpion envenomation.

Myocardial perfusion scintigraphy studies.

The presence of myocardial ischemia explaining left ventricular dysfunction after scorpion envenomation is to be considered whenever ECG, biological, and echocardiogram abnormalities suggest ischemic alterations. Moreover, to the best of our knowledge, only three published studies explored myocardial perfusion with myocardial perfusion scintigraphy.11,12,22 In all, 33 young patients admitted for severe scorpion envenomation were included in these studies.11,12,22 All included patients underwent myocardial perfusion scintigraphy with the administration of technetium-99m. The main result of all studies11,12,22 is that myocardial perfusion abnormalities are common in severe scorpion envenomation, and there was a good correlation between myocardial perfusion defects and contractile dysfunction. Recovery of contractility was correlated with the reversibility of perfusion defects. Moreover, there was a good correlation between T-wave change and/or RST abnormalities in ECG studies and myocardial scintigraphy abnormalities. These findings suggest the participation of myocardial perfusion abnormalities in the pathophysiology of this form of acute ventricular failure.

Biological findings.

Nowadays, it is a well-established fact that levels of troponin I and T are the biomarkers of choice for the detection of cardiac injury and myocardial infarction.32 Many published studies13,18,23 have shown that troponin measurement can represent a consistent device in the detection of cardiac dysfunction in severely scorpion-envenomed patients. The first study showing a substantial correlation between high levels of troponin on admission, and myocardial injury in scorpion envenomation was established by Meki et al.18 The latter study18 included 41 children admitted to a pediatric ICU in upper Egypt, and the authors found a 100% specificity and sensitivity of high levels of troponin for the diagnosis of myocardial injury in relation to echography findings in the envenomed victims. In another more recently published study,13 Chakroun-Walha et al.13 established that the mean troponin level was higher in patients with clinical manifestations of left ventricular dysfunction. Troponin levels were significantly higher in patients with a positive T wave on electrocardiogram. In another study, Sagarad et al.24 found a good correlation between elevated cardiac troponin levels and echocardiographic evidence of severe myocarditis in scorpion sting envenomation. The correlation between high levels of troponin on admission and myocardial injury due to myocardial perfusion abnormalities in scorpion envenomation was established.11,12,22 In one study conducted on 12 nonconsecutive children admitted to the emergency department for severe scorpion envenomation, Cupo et al.11 found a significant correlation between the clinical manifestations, the severity of myocardial perfusion changes, ECG abnormalities, and distribution of wall motion. Moreover, all included patients except two showed increased troponin I levels, suggesting the ischemic origin of this biological disturbance. Finally, in one study including 15 patients for severe scorpion envenomation, Figueiredo et al.22 found that ECG abnormalities were common in their case series, and in some cases, they were similar to those found in acute myocardial infarction. Significant elevations of enzyme levels creatine phosphokinase-MB were observed in most of the patients.

In summary, the presence of ECG alterations evocative of myocardial ischemia and damage, the presence of myocardial perfusion abnormalities, the good correlation between myocardial perfusion defects and contractile dysfunction, and elevation of serum enzyme levels are suggestive of lesions of cardiac fibers secondary to myocardial ischemia.11,12,22

Histopathologic findings.

The literature analysis showed that only four studies investigated histopathologic findings in the autopsy of victims of severe scorpion envenomation.14,25–27 Most of the histopathologic findings were interstitial edema, dilation of chambers, inflammatory infiltrates, and foci of hemorrhage.14,25–27 However, myocardial necrosis with necrosis of single or small groups of muscle fibers was reported (in two studies)14,27 in fatal cases of young patients after severe scorpion envenomation. The clinical manifestations, laboratory and ECG evidence of myocardial damage, and histopathologic findings are suggestive of lesions of cardiac fibers secondary to myocardial ischemia in the described fatal cases.14,27 Table 1 summarizes all the articles included in this study.

In summary, the literature analysis confirmed that severe scorpion envenomation can be complicated by temporary functional myocardial ischemia. This finding was based on ECG, histopathologic, echocardiographic, myocardial perfusion scintigraphy, and biological studies. The correlation between clinical manifestations, laboratory and ECG evidence of myocardial damage, echocardiographic studies, perfusion scintigraphy abnormalities, and histopathologic findings is suggestive of lesions of cardiac fibers secondary to myocardial ischemia. Moreover, the presence of a nearby association between systolic ventricular dysfunction and disease of myocardial perfusion in some studies suggests the participation of transitory myocardial ischemia in the mechanism of this form of acute reversible heart failure. For these reasons, we think that myocardial ischemia can contribute to transitory cardiac dysfunction in severe scorpion envenomation.

DISCUSSION

Mechanisms of myocardial ischemia.

Myocardial ischemia as a pathophysiologic mechanism seems to be particularly observed in severe scorpion envenomation with cardiorespiratory manifestation. Myocardial hypoperfusion after scorpion envenomation can be explained by the effects of adrenergic hyperstimulation on the myocardium arteries. Thus, coronary vasoconstriction can be related to a direct vasoconstrictive effect of different substances (e.g., catecholamines) in the coronary arteries33 and/or secondary hypoperfusion induced by endothelial dysfunction. In fact, it is a well-established fact that severe scorpion envenomation leads to a significant (30- to 40-fold) increase in plasma epinephrine and norepinephrine levels.34,35

In addition, it was well proven that severe scorpion envenomation is associated with a storm of high levels of cytokines (interleukins [IL]-1α, IL-6, IL-10, tumor necrosis factor-α, IL1-β).36 This leads to microvascular injury or vasospastic responses in the coronary arteries37,38 and may explain the coronary vasospasm and the myocardial hypoperfusion (Supplemental Figure 2). Moreover, cardiac failure can provoke gut hypoperfusion and cytokine release,2,4,7 leading to a vicious spiral that may worsen cardiac manifestations. Accordingly, urgent management, including circulatory and hemodynamic correction, is necessary.

As a consequence, we can conclude that myocardial hypoperfusion may be due to multiple factors. First, catecholamine storms can induce microvascular constriction through the stimulation of alpha receptors at the coronary arteries, leading to hypoperfusion, ischemia, and myocardial stunning. On the other hand, catecholamines release—by a complex neurohormonal interaction with other neuropeptides (such as neuropeptide Y, endothelin-1)35 and cytokine release—can induce a major coronary microvascular constriction and/or microvascular injury, leading to microvascular acute coronary syndrome with Takotsubo cardiomyopathy.28–30 Thus, tachycardia, vasospasm, and hypoxemia, whatever the mechanism, can provoke functional myocardial ischemia or worsen myocardial ischemic damage. All these mechanisms trigger cardiac dysfunction and pulmonary edema with hypoxemia, which may aggravate ischemic manifestations.

Moreover, the literature analysis39 confirmed that three published studies28–30 reported four patients who met all the criteria of Takotsubo cardiomyopathy40 after severe scorpion envenomation. Indeed, all these patients developed a transient reversible left ventricular systolic dysfunction associated with tachycardia, ECG changes, minimal cardiac enzyme release, and transient myocardial hypoperfusion in the absence of coronary artery disease (young patients in all cases) after a positive history of scorpion envenomation.

However, Takotsubo syndrome is underestimated in patients who are victims of severe scorpion envenomation and suffer from cardiac failure. In fact, several patients included in previously reported studies,1,2,10–13,16,17 and who met all the criteria of Takotsubo cardiomyopathy were not categorized as having Takotsubo cardiomyopathy.

Management of myocardial ischemia after scorpion envenomation.

Although coronary microvascular constriction and/or microvascular injury leading to microvascular acute coronary syndrome with Takotsubo cardiomyopathy can explain myocardial ischemia after severe scorpion envenomation, the management of Takotsubo cardiomyopathy in this specific condition seems to be different from the international guidelines.41 In fact, the management of acute heart failure after Takotsubo cardiomyopathy is based on standard international guidelines, comprising oxygen and respiratory support, beta-blockers, mineralocorticoid receptor antagonists, and diuretics.41 However, victims of severe scorpion envenomation with acute heart failure are characterized by the presence of cardiogenic pulmonary and/or cardiogenic shock. As a consequence, beta-blockers, mineralocorticoid receptor antagonists, and diuretics cannot be used at this stage in this specific condition. The management of severe scorpion envenomation with severe myocardial failure and pulmonary edema is based on oxygen, with invasive or noninvasive ventilator support in patients with respiratory failure and/or cardiogenic shock.3,7 On the other hand, dobutamine (with a mean dose of 5–10 µg/kg per minute) improves cardiac function after scorpion envenomation.42–44

Finally, the literature review showed that no existing evidence supports lifelong antiplatelet therapy in patients with Takotsubo cardiomyopathy45 nor in myocardial ischemia after severe scorpion envenomation.3,7 For these reasons, antiplatelet therapy is not recommended.

In all, the mechanism of cardiac injury after scorpion envenoming is multifactorial, involving adrenergic, toxic, and ischemic mechanisms. Significant reversal of left ventricular dysfunction on echocardiogram or hemodynamic study is reached within approximately 1 week.3,4

This review confirmed that myocardial ischemia can contribute to transitory cardiac dysfunction in severe scorpion envenomation. However, some limitations of this review should be mentioned, such as the differences in diagnostic capabilities between studies, the variability in diagnostic criteria and their interpretation, gaps or missing data, and failure to look for factors favoring myocardial ischemia, such as a history of heart disease in some reported adult patients. Finally, this narrative review suffered from other limitations owing to the nature of this study type,46 which allowed researchers to describe what is known on a topic while conducting a subjective examination and critique of an entire body of literature. As a consequence, the last reference list was defined based on the significance of each paper to the scope of this review, as appreciated by the authors.

CONCLUSION

The literature analysis confirmed that severe scorpion envenomation can be complicated by temporary myocardial ischemia, which can be due to multiple factors. It can be due to coronary vasoconstriction secondary to a direct vasoconstrictive effect of different substances (e.g., catecholamines) in the coronary arteries and/or endothelial dysfunction due to a storm of high levels of cytokines, leading to microvascular acute coronary syndrome with Takotsubo cardiomyopathy. Antiplatelet therapy is not recommended in this specific condition.

Supplemental Materials

Supplemental Materials
tpmd240163.SD1.pdf (216.6KB, pdf)
DOI: 10.4269/ajtmh.24-0163

ACKNOWLEDGMENTS

The authors extend their sincere gratitude to Chokri Khalaf for meticulously correcting the errors and refining the language of this article. The American Society of Tropical Medicine and Hygiene (ASTMH) assisted with publication expenses.

Note: Supplemental material appears at www.ajtmh.org.

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tpmd240163.SD1.pdf (216.6KB, pdf)
DOI: 10.4269/ajtmh.24-0163

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