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Myocardial damage after a scorpion sting: Long-term echocardiographic follow-up
Abstract
A seven-year-old girl, stung by a scorpion, was hospitalized in a confused state with signs of myocarditis and pulmonary edema. In spite of clinical improvement within 24 h, 14 serial echocardiograms and electrocardiograms performed during a four-month period showed severe changes. There have been no previously published reports of echocardiographic studies showing myocardial changes after a scorpion sting.
... Nouira et al. [56] have found that just like LV, RV function gets impaired in scorpion myocarditis. Echocardiography findings in the studies included regional or global hypokinesia [13,26,34,[36][37][38]45,48,51,52,54,57,59,61,62,67,71,72,[75][76][77]79,81,[83][84][85][86][87]90,91], chamber dilation [45,53,59,68,69,73,76,80], decreased left ventricular ejection fraction (LVEF) [13,14,18,26,34,[36][37][38][39][40][41]45,46,48,49,[51][52][53][54][55][57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][77][78][79][80][81][82][83][84][85][86][87][88][89][90][91][92][93], decreased fractional shortening (FS) [37,38,41,48,49,51,53,55,62,73,80,92], right ventricular (RV) dysfunction [56, 60,90], and mitral or tricuspid regurgitation [13,26,34,36,37,45,48,51,57,73,[75][76][77]79,80,82,83,87,89]. ...
... Nouira et al. [56] have found that just like LV, RV function gets impaired in scorpion myocarditis. Echocardiography findings in the studies included regional or global hypokinesia [13,26,34,[36][37][38]45,48,51,52,54,57,59,61,62,67,71,72,[75][76][77]79,81,[83][84][85][86][87]90,91], chamber dilation [45,53,59,68,69,73,76,80], decreased left ventricular ejection fraction (LVEF) [13,14,18,26,34,[36][37][38][39][40][41]45,46,48,49,[51][52][53][54][55][57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][77][78][79][80][81][82][83][84][85][86][87][88][89][90][91][92][93], decreased fractional shortening (FS) [37,38,41,48,49,51,53,55,62,73,80,92], right ventricular (RV) dysfunction [56, 60,90], and mitral or tricuspid regurgitation [13,26,34,36,37,45,48,51,57,73,[75][76][77]79,80,82,83,87,89]. ...
... Several treatment strategies were presented in the literature. Scorpion antivenom (SAV) [36][37][38][42][43][44]49,55,56,61,62,65,66,69,74,75,78,80,81,84,85,87,88] was used in most of the studies. Tetanus prophylaxis in the form of tetanus toxoid was also used [42,65,87]. ...
Background
Scorpion envenomation is associated with several complications. One of the most serious complications is the cardiac involvement in the form of myocarditis that remains the main reason for mortalities associated with scorpion envenomation. The present review aims to elucidate clinical and paraclinical findings associated with scorpion-related myocarditis, and to explore different management strategies and subsequent outcomes.
Methods
We searched PubMed, Web of Science, Scopus, and Google Scholar for articles related to keywords of myocarditis associated with scorpion envenomation up to May 1, 2022. Each article was carefully reviewed by two independent researchers. In case of disagreement for inclusion, we sought a third researcher opinion.
Results
A total of 703 cases from 30 case reports and 34 case series were included in our review. Myocarditis associated with scorpion envenomation was usually reported in children presenting with cardiopulmonary symptoms including pulmonary edema (60.7%) and shock or hypotension (45.8%). The most common ECG findings are sinus tachycardia (82%) followed by ST-T changes (64.6%). The management typically included inotropes (especially dobutamine), prazosin, diuretics, nitroglycerine and digoxin, when indicated. Mechanical ventilation was required in 36.7% of the patients. Mortality in confirmed scorpion-related myocarditis cases is estimated at 7.3%. Almost all survived cases showed rapid recovery and improvement in the left ventricular function.
Conclusion
Even though myocarditis associated with scorpion envenomation is rare, it remains a serious and in some of cases a fatal consequence of scorpion sting. In case of relative presentations, particularly in envenomed children, diagnosis of myocarditis should be considered. Early screening using serial cardiac markers and echocardiography can guide the treatment. Prompt treatment that focuses on cardiogenic shock and pulmonary edema usually results in a favorable outcome.
... Evidences of myocardial insult include electrocardiographic, echocardiographic and laboratory alterations that simulate acute myocardial infarction (26). The main electrocardiographic findings described in the literature are sinusal tachycardia with premature ventricular complexes, wandering pacemaker, depression of ST segment, and atrial-ventricular blockade, among others (3,10,11,13,17,23,25,43,44). ...
... Echocardiographic studies reveal impaired ventricular function and ejection fraction with variable degrees of hypokinesis, resembling the clinical signs of dilated cardiomyopathy (3,10,11,13,25,26,29,44). Ventricular dysfunction is clearly demonstrated by radioisotopic ventriculography, evidencing reduced values of ventricular ejection fraction associated with severe alteration in the regional parietal movement (21). ...
... These possible mechanisms could be demonstrated by the reduction in the number of red blood cells in G2 during the three moments observed after envenomation, since these animals did not present clinically significant dehydration. Leukocytosis in victims of scorpionism is reported in many studies (2,3,10,11,13,23,25,31), being justified by neutrophilia due to mobilization of neutrophils from the bone marrow to the blood compartment (9). The animals studied demonstrated leukocytosis with neutrophilia and lymphopenia, which was sufficiently evident in G1 and mild in G2, characterizing the occurrence of "stress leucogram", which could be caused by the release of catecholamines described in scorpionism. ...
Scorpionism is a common problem that occurs in tropical and subtropical countries and assumes great medical-sanitary importance due to its fatal effect on sensitive individuals, being able to lead children and aged people to death. The envenomation lethal potential is responsible for the serious cardiopulmonary alterations the scorpion toxin produces in its victims. The present research evaluated the effects of Tityus serrulatus venom on dogs, using two distinct doses: a dose that simulates natural envenomation (0.4 mg/total dose), and an experimental dose (0.25 mg/kg). General clinical signs were observed at different moments after envenomation, and specific data related to the cardiopulmonary system were evaluated by systemic arterial pressure measurement, CK-MB enzymatic activity dosage, and radiographic, electrocardiographic and echocardiographic examinations. Results demonstrated that the scorpion venom, in experimental doses, was able to cause acute and reversible cardiac injury in few days, and, in the dose that simulated natural accident, it produced clinical signs of light envenomation, such as local pain, hyperesthesia, sialorrhea, vomiting, diarrhea, sneeze and prostration.
... Cardiac ischemia is expressed by transient elevation of cardiac enzymes [38,48] and electrocardiograms with depressed or elevated ST segment, Q waves in leads I and aVL, prolonged QT c intervals, and peaked T waves [38]. Cardiac dysfunction is evidenced on echocardiography as diminished global wall motion with decreased systolic left ventricular performance and diminished ejection fraction [49][50][51]. Left ventricular dysfunction also has been shown by cardiac radionuclide scan [50]. Transient elevation of pancreatic enzymes has been reported [42]. ...
Scorpions are arthropods with a hard exoskeleton, two anterior pinching claws, and a tail ending with a bulbous enlargement. The poison gland and the stinger are located at the distal part of the tail. The tail is long and able to arch over the head, allowing the stinger to hit the prey grasped between the claws [1]. Scorpions are among the oldest creatures on earth. Their habitat is warm and arid areas, as reflected in their first mentioning in the Bible: “He led you through the vast and dreadful desert, that thirsty and waterless land, with venomous snakes and scorpions” [2]. The scorpion is a nocturnal animal that hibernates in winter and is active in the warm seasons [3].
Scorpions are arthropods with a hard exoskeleton, two anterior pinching claws, and a tail ending with a bulbous enlargement. The poison gland and the stinger are located at the distal part of the tail. The tail is long and able to arch over the head, allowing the stinger to hit the prey grasped between the claws [1]. Scorpions are among the oldest creatures on earth. Their habitat is warm and arid areas, as reflected in their first mentioning in the Bible: “He led you through the vast and dreadful desert, that thirsty and waterless land, with venomous snakes and scorpions” [2]. The scorpion is a nocturnal animal that hibernates in winter and is active in the warm seasons [3].
Animal poisons induce myocardial damage after envenomation. Those capable of producing toxins in their salivary gland and delivering them through biting or stinging are referred to as venomous animals. Snakes and arthropods, such as scorpions, spiders, and hymenoptera (e.g., bee, wasp), are common worldwide and envenomation of these species causes cardiac toxicity. This chapter focuses on the cardiac complications induced by the envenomation from snakes and arthropods.
From 1985 to 1991, 950 cases of scorpion stings were admitted and treated with 0 to 1 ampule of scorpion antivenom at King Fahd Hospital, Al Baha. Antivenom policy was changed in mid 1991, therefore, from January, 1992 to December, 1998, 968 admitted cases of scorpion stings were treated with 5 or more ampules of antivenom. All patients with severe envenomation and pulmonary edema were treated in the intensive care unit. The protocol of treatment had remained the same (1985 - 1998), except for prompt high antivenom dosage. The occurrence of pulmonary edema and cardio-pulmonary arrest in the two years preceeding the policy change (1990-1991) was compared with the period when high dose serotherapy was made mandatory (1992-1998). After the new antivenom dose, mortality rate fell from 16 of 950 (1.7 %) to 0 to 968 (p=0.00015); occurrence of pulmonary edema decreased from 18 of 162 (11.1%) in 1990-1991 to 12 of 968 (1.2 %) in 1992-1998 (p<0.001) and cardio-pulmonary arrest from 7.4 % to 0.4 % (p<0.001). The last death recorded due to scorpion sting was of a patient in 1991 who had received no antivenom. The excellent outcome is attributed to scorpion antivenom.
From 1985 to 1991, 950 cases of scorpion stings were admitted and treated with 0 to 1 ampule of scorpion antivenom at King Fahd Hospital, Al Baha. Antivenom policy was changed in mid 1991, therefore, from January, 1992 to December, 1998, 968 admitted cases of scorpion stings were treated with 5 or more ampules of antivenom. All patients with severe envenomation and pulmonary edema were treated in the intensive care unit. The protocol of treatment had remained the same (1985 - 1998), except for prompt high antivenom dosage. The occurrence of pulmonary edema and cardio-pulmonary arrest in the two years preceeding the policy change (1990-1991) was compared with the period when high dose serotherapy was made mandatory (1992-1998). After the new antivenom dose, mortality rate fell from 16 of 950 (1.7 %) to 0 of 968 (p=0.00015); occurrence of pulmonary edema decreased from 18 of 162 (11.1 %) in 1990-1991 to 12 of 968 (1.2 %) in 1992-1998 (p<0.001) and cardio-pulmonary arrest from 7.4 % to 0.4 % (p<0.001). The last death recorded due to scorpion sting was of a patient in 1991 who had received no antivenom. The excellent outcome is attributed to scorpion antivenom.
Scorpion sting may cause myocardial injury and heart failure (HF). Clinical signs of failure may develop several hours or even days after the sting, while electrocardiography (ECG) and blood examination soon after the sting may be normal. We sought to examine whether normal echocardiographic (echo) examination performed shortly after hospital arrival would exclude subsequent HF. We also sought to check if blood troponin and natriuretic peptide values measured shortly after arrival may predict or exclude subsequent HF. Natriuretic peptide activities have not been measured in scorpion sting victims. We also wanted to check if HF occurs in envenomated young infants. In a 3-year prospective study we looked at the demographic, clinical, laboratory, ECG, and echo data of all patients with general envenomation who arrived at the emergency department (ED) after scorpion sting. Clinical, laboratory, ECG, and echo results on arrival and 24 hours after arrival were checked and compared between groups of patients with normal and abnormal echo on arrival. We then looked for differences in clinical course, therapy, and outcome between groups. The study included 98 children aged 80 days to 19 years (median 53.1 months), 25 were below the age of 2 years. Envenomation by the "yellow scorpion" Leiurus quinquestriatus was suspected in 74 cases. Median time between sting and ED arrival was 80 minutes. Echo was performed on arrival in 93 of the 98 patients, (in 5 occasions it was not performed or not recorded) 74 were normal and 19 were abnormal. Abnormal echo included hypokinesia and low fractional shortening and ejection fraction of the left ventricle. Clinical signs, abnormal ECG, and laboratory results were not discriminative between groups on arrival. Mean troponin T was higher in patients with abnormal echo, but within normal range in 13 of the 19 patients with abnormal echo and above normal in 2 of the 74 patients with normal echo - missing sensitivity and specificity. Mean N-terminal pro B-type natriuretic peptide was above normal in both groups but within normal range in 5 patients with abnormal echo and above normal range in 24 patients with normal echo - missing sensitivity and specificity. None of the patients with normal echo had subsequent HF and none of the children younger than 2 years of age had HF. All patients survived the intoxication and were discharged home without sequel. We conclude that early echo examination is an important procedure. In our study, normal examination excluded subsequent HF. Abnormal examination accelerated cardiac therapy which might have contributed to our favorable outcome. HF did not occur in infants younger than two years of age.
Scorpion envenomation is quite common in India, southeast Asia, the U.S. southwest, and Israel (in the Negev and around Jerusalem). Yellow scorpion is considered the most dangerous scorpion that causes cardiac toxicity. Two patients are described, who lived in a nonendemic area of yellow scorpions and were envenomated by the black scorpion. Both suffered temporary cardiac involvement (manifested by electrocardiographic changes) which reverted to a normal pattern within 24 h. These are the first two cases that have been reported (from black scorpion envenomation) and indicate that the toxin of the black scorpion is also cardiotoxic, but much less than the “yellow scorpion” toxin.
Scorpion envenomation (SE) is a public health problem in many regions of the world. It is a lifethreatening accident by the dreadful cardiorespiratory consequences where pulmonary edema is the main feature. Pathogenesis of cardiorespiratory consequences of SE has not been clearly identified until recently. Although most previous studies suggested a hemodynamic origin for scorpion envenomation's induced pulmonary edema, the mechanism of cardiac dysfunction remains unclear. The purpose of this study was to assess the cardiorespiratory consequences of severe SE manifested by pulmonary edema. Accordingly, a hemodynamic study was carried out in 22 patients victims of pulmonary edema following scorpion sting. In nine patients, an echocardiographic study was also performed to characterize the effects of scorpion envenomation on left ventricular diastolic and systolic functions. Eight among these patients were investigated with a fast-response thermodilution catheter in order to assess the right ventricular function. All patients had increased pulmonary artery occluded pressure (mean 24 ± 3 mmHg) pointing to left ventricular dysfunction as the cause of pulmonary edema. Right ventricular ejection fraction and echo-doppler studies showed that cardiac dysfunction involved both left and right ventricules mainly by a reduction in myocardial contractility. These findings argue against catecholamines discharge or myocardial ischemia as the cause of cardiac dysfunction. Whatever the mechanism involved, cardiac dysfunction seen after SE responded favorably to inotropic support in patients who survived (n = 18). We conclude that scorpion envenomation's induced pulmonary edema is related to a diffuse and reversible cardiomyopathy.
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Whipple’s disease (“intestinal lipodystrophy”) is sometimes associated with myocarditis with periodic acid-Schiff-positive
macrophages in the myocardium, pericardium, and heart valves.
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Fabry’s disease is an X-linked disorder of glycosphingolipid metabolism resulting from a deficiency in the enzyme, ceramide
trihexosidase. Patients with the cardiac variant have mild, late onset of the disease primarily limited to the heart with
progressive involvement of the heart with aging leading to death. These patients often have mutations in the X-galactosidase
gene. Cardiac involvement includes the myocardium, conducting tissue, small arteries resulting in their occlusion, and valves,
especially the mitral valve.
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Gaucher’s disease is an inherited disease of glycoceramide metabolism caused by a deficiency of the enzyme β-glucosidase,
resulting in the accumulation of cerebrosides in the myocardium, liver, spleen, bone marrow, lymph nodes, and brain. Myocardial
infiltration of the left ventricle by cells laden with cerebroside results in reduced left ventricle (LV) compliance, entailing
increased stiffness, LV dysfunction, myocardial hemorrhage, pericardial calcification, and calcification of left heart valves.
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Severe and sustained thiamine defi ciency for at least 3 months occurs in individuals who drink heavily and eat high carbohydrate
diets. It may lead to beriberi heart disease, initially characterized by a high output state with biventricular failure converting
later to a low cardiac output state with peripheral vasoconstriction.
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Carnitine, selenium, and taurine deficiency may lead to a dilated cardiomyopathy, and carnitine deficiency may also lead to
hypertrophic cardiomyopathy in children.
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Starvation may lead to a dilated cardiomyopathy and chronic congestive heart failure (CHF).
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Severe hypocalcemia and hypomagnesemia may lead to depressions in cardiac contractility and decreased responsiveness to cardiac
medications that cause positive inotropic responses related to increasing intracellular cardiac calcium concentrations. Both
electrolyte abnormalities also lead to prolongations of the QT interval predisposing to cardiac arrhythmias of the torsades
de pointes type.
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Insect bites and stings and snake bites occasionally cause hypersensitivity responses that may include myocardial infarction
or serious cardiac arrhythmias.
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Doxorubicin (Adriamycin) given in doses of 450 mg/m2 or greater may cause a dilated cardiomyopathy. When combined with radiation therapy to the chest or other chemotherapeutic
agents, lower doses of Adriamycin sometimes may exert similar effects. Patients should have their left ventricular ejection
fractions (LVEFs) measured before and at intervals after beginning Adriamycin by echocardiography or magnetic resonance imaging
(MRI) and the drug discontinued with a fall in the patient’s LVEF into the 40% to 50% range. If this is done, the LVEF may
return to normal values with time.
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Giant cell myocarditis is characterized by multinucleated giant cells in the myocardium leading to cardiomegaly and fulminant
heart failure. Young and middle-aged adults are most commonly affected. On occasion, corticosteroids and other immunosuppressant
agents have resulted in clinical remissions.
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Carcinoid heart disease is usually associated with carcinoid tumors of the ileum that invade the liver and metastasize to
the heart, leading to tricuspid stenosis and insufficiency or pulmonary valvular stenosis and insufficiency. The tumor produces
serotonin and bradykinin in excess, leading to wheezing, spontaneous flushing, and diarrhea.
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Patients with profound hypothermia may have a characteristic deflection of the terminal portion of the QRS pattern known as
the Osborne wave.
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Left ventricle noncompaction is characterized by a spongy morphology appearance that involves the distal apical LV with deep
intratrabecular recesses or sinusoids. Clinical problems resulting from this entity include LV dysfunction with CHF, arrhythmias,
and emboli.
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Arrhythmogenic right ventricular dysplasia (ARVD/C) is an inherited disease of heart muscle associated with ventricular arrhythmias
and sudden death.
Adrenal insufficiency is defined by impaired secretion of adrenocortical hormones. It is classified upon the etiology in primary and secondary. Rapid recognition and therapy of adrenocortical crisis are critical to survival. Patients often have nonspecific symptoms: anorexia, vomiting, weakness, fatigue and lethargy. They are followed by hypotension, shock, hypoglicemia, hyponatremia and hyperkalemia. All patients with adrenal insufficiency require urgent fluid reposition, correction of hypoglycemia and glucocorticoid replacement, in order to avoid serious consequences of adrenal crisis. After initial crisis treatment, maintenance dose of corticoids should be indicated. Mineralocorticoids replacement, if necessary, should also be initiated.
In Argentina, scorpion poisoning is an entity with high morbidity and mortality mainly produced by Tityus trivitatus sting. This species is distributed all around the center and north of the country. Clinical manifestations range from local pain and paresthesia to multisystemic failure followed by death. Diagnosis is done by recognizing clinical features, and is reinforced by the history of a sting and the identification of the scorpion. Specifc treatment is antitoxic serum. We strongly recommend preventive measures to keep scorpions far from building areas. At present, a new species, Tityus confluens, arouses in association with lethal events.
The present study characterized envenomation in young rats by Tityus fasciolatus, an endemic scorpion to Central Brazilian and state of Minas Gerais. Electrocardiographic examinations were performed prior to treatment and every 5 min during the first 30 min after envenomation. The cardiac blood profile [creatine kinase, CK isoenzyme MB, lactate dehydrogenase, aspartate aminotransferase and troponina] together with macroscopic and microscopic alterations in the lungs and heart were evaluated. Envenomated animals showed ECG changes suggesting electrolytic imbalance, myocarditis and venom interference on the conduction tissue. Biochemical analyses indicated myocardial damage with high levels of CK, CK-MB and LDH. Macroscopic and microscopic findings included detection of pulmonary haemorrhages. In conclusion, T. fasciolatus venom leads to acute cardio-respiratory changes in young rats.
Cardiac function was evaluated by serial echocardiography in 30 children affected by scorpion stings. They could be separated into two groups on the basis of the initial echocardiogram. Group 1, consisting of 18 children, had normal left ventricular function, whereas group 2, consisting of 12 children, showed compromised left ventricular function (ejection fraction less than 0.55; fractional shortening less than 27%). In group 2 the left ventricular end-systolic dimension was increased significantly and the interventricular septal thickening fraction was depressed significantly, compared with group 1. Nine children in group 2 showed improvement in all measurements of contractility, usually within 24 to 48 hours. Of the remaining children, one showed no echocardiographic changes and subsequently died. Another child made a slow improvement over several weeks. We conclude that myocardial toxicity is a common and serious complication of scorpion stings in children. Systolic function appears to be affected predominantly. Serial echocardiography is useful to follow changes in left ventricular function, which are generally matched by clinical improvement. Patients who fail to improve within 24 to 48 hours require particularly close observation.
Scorpion envenomation is a common medical problem and life hazard in many countries of the world. Scientific investigations have addressed the interrelationship between the stimulatory effects of the venom on the autonomic nervous system and adrenals and the subsequent effects of released transmitters on the cardiovascular system. A number of clinical cardiovascular syndromes may dominate the initial clinical presentation after envenomation: the syndromes usually vary with the age of the victim, the size of the offender and the season. Central nervous system dysfunction is seen in children but rarely observed in adults; if accompanied by severe hypertension the clinical picture is consistent with acute hypertensive encephalopathy. Heart failure, pulmonary edema or a shock-like syndrome has been observed in 25% and hypertension in 30% to 77% of our patients. The electrocardiographic abnormalities recorded in the majority of the patients after envenomation include an "acute myocardial infarction-like pattern." Rhythm disturbances are frequent but conduction abnormalities are rare. Echocardiographic, radionuclide and experimental hemodynamic observations have provided evidence that heart failure and pulmonary edema after envenomation are multifactorial with diminished systolic performance following the initially increased left ventricular contractility and decreased ventricular diastolic compliance. Clinical laboratory data reporting increased catecholamine metabolite excretion and elevated plasma renin and aldosterone are consistent with the stimulatory effects of the venom on the autonomic nervous system. Treatment, including our experience with vasodilators and calcium channel blockers, is reviewed.
The cardiovascular manifestations after a Tityus serrulatus scorpion sting consist of arterial hypertension or hypotension, heart failure, pulmonary edema, shock and electrocardiographic changes.1 Pulmonary edema evoked by scorpion toxin has been attributed to left ventricular failure induced by the venom or to increased pulmonary vascular permeability produced by vasoactive substances that might be released by the venom.2 The demonstration of myocardial damage and depressed left ventricular systolic function in patients with pulmonary edema following scorpion sting could support the hypothesis that this severe complication is cardiogenic in origin. This report describes results of electrocardiographic, enzymatic and echocardiographic studies in 5 patients with severe envenomation after a Tityus serrulatus scorpion sting.
The echocardiographic and radionuclide angiographic abnormalities in children after scorpion envenomation with L. quinquestriatus, were evaluated. Five children were severely hypertensive, one of them in respiratory failure and another had pulmonary edema. The results revealed poor global contractility 12-15 hr after the sting in three patients. The radionuclide angiograms also revealed poor contractility with low ejection fraction. There was enzymatic evidence of myocardial damage. The changes observed in the echocardiograms and radionuclide angiograms were attributed to catecholamine induced myocardial ischemia. The abnormalities observed suggest that systolic dysfunction plays a role in the pathogenesis of heart failure in scorpion envenomation, in addition to a decrease of left ventricular compliance and increased impedance to left ventricular emptying. The beneficial effects of nifedipine in hypertension and other cardiovascular manifestations justify the routine use of afterload reduction in children with cardiovascular manifestations after scorpion envenomation.
Severe scorpion envenoming is characterized by cardiocirculatory failure which may lead to pulmonary oedema. These are the major causes of death among victims of scorpion stings. Involvement of the heart has been attributed to the massive release of catecholamines and/or to a direct toxic effect of the venom on cardiac fibres, while pulmonary oedema has been considered to be of cardiogenic or non-cardiogenic origin. We present here the clinical, laboratory, electrocardiographic and echocardiographic data of 12 victims of severe Tityus serrulatus stings. These patients had important echocardiographic evidence of moderate to severe left ventricular (LV) dysfunction with diffuse LV hypokinesia and reduced ejection fraction. Seven developed pulmonary oedema. The clinical course of all the patients was satisfactory and the laboratory, electrocardiographic and echocardiographic changes returned to normal, usually within 1 week of the sting. The important alterations detected by echocardiography as early as during the 1st few hours after the sting, taken together with the enzymatic and electrocardiographic data, confirm that LV dysfunction is responsible, either alone or in combination with other factors, for the cardiac insufficiency and pulmonary oedema encountered in scorpion envenoming.
Scorpion stings in Brazil are important not only because of their incidence but also for their potential ability to induce severe, and often fatal, clinical situations, especially among children. In this report we present the clinical and laboratory data of 4 patients victims of scorpion stings by T. serrulatus, who developed heart failure and pulmonary edema, with 3 of them dying within 24 hours of the sting. Anatomopathologic study of these patients revealed diffuse areas of myocardiocytolysis in addition to pulmonary edema. The surviving child presented enzymatic, electrocardiographic and echocardiographic changes compatible with severe cardiac involvement, which were reversed within 5 days. These findings reinforce the need for continuous monitoring of patients with severe scorpion envenoming during the hours immediately following the sting.
Acute pulmonary edema due to scorpion toxins has been attributed to acute left ventricular failure resulting from massive catecholamine release or myocardial damage induced by the venom.1–3 It has been proposed that pulmonary edema could also result from increased pulmonary vascular permeability produced by vasoactive substances that may be released by the venom.4 This report presents radiologic, electrocardiographic, enzymatic, echocardiographic and histopathologic evidence that support both cardiogenic and noncardiogenic factors in the pathogenesis of acute pulmonary edema after Tityus serrulatus scorpion sting in children.
To assess left ventricular function in patients presenting with pulmonary edema following scorpion envenomation.
Cohort study.
Medical intensive care unit of a teaching hospital.
Nine consecutive adult patients stung by Androctonus australis and presenting with pulmonary edema entered the study. Fourteen normal volunteers comprised the control group.
Upon admission, all patients had right heart catheterization and, within the first 8 h, a Doppler echocardiographic study. Results of Doppler echocardiographic studies were compared to those of controls.
Usual hemodynamic information (heart and vascular pressures, derived data and tissue oxygenation parameters), left ventricular dimensions and indicators of systolic function, and Doppler-derived parameters of left ventricular filling and diastolic function were obtained upon admission. Serial echocardiographic measurements were repeated daily until full clinical recovery (eight patients) or death (one patient). All patients had a hemodynamic profile of acute congestive heart failure (mean PAOP = 24 +/- 2 mmHg; mean SVI = 22 +/- 7 ml/m2; mean CI = 2.5 +/- 0.5 l/min/m2). However, SVR were not increased (mean = 22 +/- 3 U/m2). Left ventricle was hypokinetic in all patients with transient mitral regurgitation present in five patients. Left ventricular systolic function was markedly depressed (FS = 12 +/- 6%; EF = 26 +/- 12%). An associated diastolic dysfunction is suggested by Doppler records of mitral inflow. Left ventricular systolic function evolved toward normalization within 6 +/- 2 days preceded by full clinical recovery.
These data suggest that pulmonary edema in scorpion envenomation is of hemodynamic origin and is related to a severe and prominent impairment of left ventricular systolic function.
The pathophysiology of the scorpion envenoming syndrome is reviewed with emphasis on the body systems commonly affected. Concepts of the mechanisms underlying venom action, as can be explained by the recently discovered effects on ionic channels, are discussed. The results of clinical analysis of cases of scorpion sting victims and animal experiments with scorpion envenomation supporting these concepts are presented. The pharmacokinetic characteristics of scorpion venoms and their correlation to the magnitude of toxic effects are presented in relation to the potentials of therapeutic intervention. The pharmacological basis of the therapeutic usefulness and toxicities of the drugs commonly used in the treatment of scorpion envenoming is also projected. Finally, the results of a successful nation-wide clinical study with serotherapy of scorpion envenoming are presented and evaluated.
In rat isolated atria, Androctonus australis (Aa), Leiurus quinquestriatus quinquestriatus (Lqq), and L. q. hebraceus (Lqh) venoms produced intense contracture, alterations in the force and frequency of the spontaneous atrial contractions, and delayed afterdepolarizations (DAD). It was shown by means of tetrodotoxin-induced blockade of neurotransmitter release that the contracture and DAD were produced by the action of the venoms on the atrial cell membrane (direct action) while alterations in the force and frequency of the spontaneous atrial contractions were caused by acetylcholine and norepinephrine released by the venoms (indirect action). The irregularities in the spontaneous contractions and DAD were suppressed by magnesium and lidocaine which, however, caused only a small reduction in the intensity of the atrial contracture. The venom-induced DAD was also abolished by ryanodine and intensified by an increase in [Ca2+]0. In anesthetized rats, Aa, Lqq, and Lqh venoms induced hypertension, arrhythmias, and T wave inversion. The arrhythmias included bradycardia, ventricular and supraventricular extrasystoles, unsustained and sustained ventricular tachycardia with torsade de pointes episodes. Magnesium and lidocaine abolished them, and magnesium also counteracted the hypertension. These results suggest that magnesium and lidocaine, particularly magnesium, may be useful in the treatment of the arrhythmias, hypertension, and other disorders associated with Buthinae scorpion envenomation.
Eight children aged 2-9 years, with signs and symptoms of severe scorpion envenoming by Tityus serrulatus were studied. All patients showed clinical manifestations of cardiac dysfunction, with ECG and echocardiographic alteration and five developed pulmonary edema. Troponin I levels were normal in all patients on admission, except for two who arrived later, and increased thereafter, with maximum values being observed 24-36 h after the sting. The detection of TnI in patients with severe scorpion envenoming, and the observed temporal pattern and serum levels meet the criteria established for the diagnosis of acute myocardial infarction. The rapid reversibility of cardiac dysfunction, together with the normalization of the enzymatic, ECG and echocardiographic data, indicates the occurrence of an acute myocardial lesion without underlying or associated coronary disease.
Scorpion sting in children is a hazardous and potentially lethal condition. Fifty-one infants and children were admitted to the Pediatric Departments at the Hadassah-Hebrew University Hospitals in Jerusalem, during a 5-year period, following scorpion sting. Fifteen (29.4%) had severe systemic signs of envenomation and two (3.9%) died. Analysis of our data showed that patients with severe toxicity were brought to the hospital after a significantly longer time lapse than were the patients with mild-to-moderate symptoms. The current management of children with scorpion envenomation consists of administration of specific antivenom and close surveillance in an intensive care unit, where vital signs and continuous cardiac monitoring enable early initiation of therapy for life-threatening complications, such as cardiac and respiratory failure, convulsions, or hypertension.
The intravenous injection of Buthus minax venom into rabbits caused an initial brief bradycardia followed by tachycardia and then a prolonged bradycardia. The initial bradycardia is probably due to central vagal stimulation, while the tachycardia is possibly due to sympathetic stimulation and release of tissue catecholamines. The venom caused depression of the ST segment and symmetrical inversion of the T wave possibly due to coronary vasoconstriction leading to anterior wall infarction. Some of the electrocardiographic effects of the venom appeared to be mediated through hyperkalemia and hypocalcemia as evidenced from the tall, slender and peaked T wave, the wide QRS complex and the prolonged ST segment. The effect of the venom in causing sympathetic stimulation and release of tissue catecholamines seemed to mask the effects of electrolytes, since more pronounced effects were shown after blocking the B-adrenergic receptors with propranolol or depleting the catecholamine stores with reserpine. Treatment with atropine, aminophylline or the specific antivenin failed to protect the rabbits against the electrocardiographic effects of the venom.
Thirty-four patients with severe scorpion sting were reviewed and pertinent data related to the cardiovascular system such as hypertension, peripheral vascular collapse, congestive heart failure or pulmonary edema were analyzed. The electrocardiograms of 28 patients were reviewed; 14 patients showed "early myocardial infarction-like" pattern. The urinary catecholamine metabolites were investigated in 12 patients with scorpion sting. Vanylmandelic acid was elevated in seven patients and the total free epinephrine and norepinephrine in eight. Six of these 12 patients displayed the electrocardiographic "myocardial infarction-like" pattern. Nine patients died and the pathologic lesions of the myocardium were reviewed in seven. The causes of heart failure, pulmonary edema and the causes of the morphologic changes of the myocardium are discussed. It was concluded from our observations, as well from recent experimental studies, that the cardiovascular manifestations of the venom and morphologic abnormalities are related to the level of circulating catecholamines elicited by a direct effect of scorpion venom on the sympathetic system. These studies suggest that adrenergetic blockers should be used in the treatment of the cardiovascular manifestations of scorpion sting.
The hemodynamic effects of scorpion venom (Leiurus quinquestriatus) and the mechanism of heart failure were investigated in two groups of anesthetized spontaneously breathing dogs. The effects of different adrenergic and cholinergic blocking agents on the venom-induced hemodynamic changes were also evaluated. In one group the venom was given before autonomic nervous system blocking agents and in a second group propranolol, atropine, phentolamine and hexamethonium alone or in different combinations were given before the venom. Complete autonomic nervous system blockade was induced in two animals to evaluate a possible direct myocardial effect of venom.The venom, a powerful arrhythmogenic agent stimulating the autonomic sympathetic nervous system and adrenals, induced dramatic hemodynamic increases in left ventricular systolic and diastolic pressures, pulmonary and systemic arterial pressures and left ventricular contractility. The hemodynamic data show clearly for the first time that pulmonary edema in severe scorpion envenomation is cardiac in origin, thus emphasizing the importance of the abnormal left ventricular hemodynamics. Heart failure is most probably the result of the interaction of several mechanisms that include a catecholamine-induced decrease in left ventricular compliance and increased impedance to left ventricular emptying and cardiac arrhythmias, all of which may impede left ventricular filling. The combination of propranolol and phentolamine was the most effective blocking agent in reversing the venom-induced hemodynamic changes. However, atropine was effective only when the venom-induced cholinergic effects dominated the clinical picture.
A potentially lethal neurotoxin-producing scorpion, Centruroides sculpturatus, exists in the southwestern United States. The most common symptoms of envenomation of 24 patients included local pain, restlessness, and roving eye movements. In this series 80% of cases were in children less than 10 years of age. Pain at the site of the sting was a predominant symptom in the patient more than 10 years of age; however, extreme and perpetual restlessness was the most common symptom in the younger patient. The diagnosis in children is usually made by clinical presentation alone since the site of the sting cannot be identified and children may not communicate the history of the sting. The most commonly used chemotherapeutic agent is phenobarbital. There is no evidence, however, that this drug decreases morbidity or mortality, and massive doses of phenobarbital were associated with two respiratory arrests in this series. The nature of scorpions and their venoms is discussed. Research is needed regarding the use of sympathetic blocking agents in scorpion envenomation.
Hemodynamic electrocardiographic changes induced by scorpion venom
- K Braun
- S Stern
- S Werkson
- S Yalon
The Hegglin syndrome in myocarditis due to scorpion sting
- A Brand-Auraban
- A Rösler