Vol.11 /No: 1/ June 2002

 

   

 

 

ACUTE ANTERIOR MYOCARDIAL INFARCTION FOLLOWING ELECTROCUTION

*Omer A.A.,**Khalid M.K. and *Gehani A.A.
Departments of *Cardiology & Cardiovascular Surgery and**Accident & Emergency
Hamad Medical Corporation, Doha, Qatar

Introduction
Case Report

Discussion
References

Introduction:

Electrocution is a well known cause of cardiac arrest, mostly secondary to ventricular fibrillation. Acute myocardial infarction has been reported in a few cases although the pathogenesis is not clear. We report two cases of acute myocardial infarction after electrocution, both confirmed by electrocardiography and markedly elevated cardiac enzymes. Echocardiography showed cardiac damage evidenced by hypokinesia.

Case Report:

Case 1:

A twenty-five-year-old Nepali male was brought to the Emergency Department of Hamad General Hospital five minutes after electrocution and collapse at work. He was unconscious and pulseless; a cardiac monitor showed ventricular fibrillation. DC shocks reverted the rhythm to sinus. Total CPR time was two minutes. The patient was intubated and transferred to CCU. His vital signs were temp 37ºC, pulse 120/min, B.P. 90/50 mmHg.

Initial laboratory investigations showed a normal complete blood count, apart from a high WBC count of 13.6 x 109 / L; blood urea 10.5mmol/L (normal = 1.7- 8.3 mmol/L); serum creatinine 129 micromol/L (normal = 53-124 micromol/L).

ECG showed sinus rhythm, significant ST elevation in leads 1, avl, and V2-V4, (Figure 1). Echocardiography revealed diffuse left ventricular hypokinesia with akinetic left ventricular posterior wall and apex, severe left ventricular dysfunction with ejection fraction of 30%, no pericardial effusion, no valvular abnormality. Urgent coronary angiography revealed normal coronary arteries.

Figure 1:

Three days later the patient was successfully extubated. Neurological examination showed evidence of brain hypoxia while a CT scan was essentially normal

His cardiac enzymes over 72 hours are shown in Table 1.

Time

Initial

24 hours

32 hours

40 hours

50 hours

72 hours

CK

725 U/L

5342 U/L

11754 U/L

17610 U/L

12710 U/L

16100 U/L

CK-MB

23.3 ng/l

94.2 ng/l

104 ng/l

80.2 ng/l

36.9 ng/l

31.1 ng/l

Relative Index

3.2 %

1.8 %

0.9 %

0.5 %

0.3 %

0.2 %

Troponin T level was 31.6 ng/ml (normal. = 0.00 - 0.1 ng/ml).

Table 1

There was a dramatic improvement during hospitalization and he was discharged after seven days with good neurological recovery. Two months later his neurological examination was normal. His ECG showed slight ST elevation in leads V2-V4 (Figure 2), Repeated echocardiography showed normal Echo Doppler study with an ejection fraction of 66%.

Figure 2

Case 2:

A twenty-nine-year-old Indian male was brought to the emergency department unconscious 15 minutes after sustaining electrocution while dealing with a high voltage mainbox. He was unconscious, pulseless with dilated pupils. There was an electrical burn on the left hand. A cardiac monitor showed wide complex tachycardia.

A series of 200, 200, 360 joule DC shocks were delivered which reverted the rhythm to sinus. He was intubated and a 100mg IV bolus injection of lignocaine was given followed by infusion at a rate of 4 mg/ min. His ECG after cardioversion showed marked ST segment elevation in leads I, aVL, V2-V6 with ST depression in leads II, III, aVF consistent with extensive anterior myocardial infarction .

Initial laboratory investigations including urea, electrolytes, and creatinine were normal.

A series of cardiac enzymes is shown in Table 2.

Time

6 hours

14 hours

22 hours

48 hours

CPK

407 U/L

6890 U/L

9040 U/L

7150 U/L

CPK-MB

38.8 ng/L

340 ng/L

288 ng/L

54.8 ng/L

Relative index

9.5 %

4.9 %

3.18 %

0.7%

Troponin test was positive; serum cholesterol: 5.33 mmol/ L; triglyceride=1.43 mmol/ L.

Table 2

Echocardiography showed hypokinetic septum and apex with an ejection fraction of 64%.

He remained unconscious over the next seven days. His pupils were reactive to light with a positive corneal reflex. He developed generalized convulsions, which were controlled by intravenous diazepam and phenytoin. His serial ECG’s over the next seven days showed a gradual return of the ST segment to base line. He was extubated after ten days but his intellectual functions were impaired and he could move only by using a wheel chair. His family took him home to India and he was lost to follow up.

Discussion:

Acute myocardial infarction after electrocution has been reported in few cases but the pathogenesis is still debatable1 ,2. In all reported cases there was structural damage or stunning of the cardiac muscle, evidenced by hypokinesia on two-dimensional echocardiography or radionuclide isotope scan 5 . In the acute onset there is usually significant ST segment elevation in the ECG with marked enzyme elevation reflecting the myocardial insult. There is debate whether this enzyme elevation is due to associated rhabdomyolysis but the elevated troponin level and the normal blood urea, serum creatinine and electrolytes make this possibility unlikely.

The cases reported in this paper show evidence of acute myocardial infarction manifested by marked ST elevation in the ECG with significant rises in CPK-MB enzyme and troponin. The two-dimensional echocardiography shows hypokinesia in both cases and a reduced ejection fraction in the first case. The normal coronary angiography excludes the coincidence of coronary artery disease.

One case has been reported of myocardial infarction after electrical injury from diathermy equipment(1 ). The electric shock caused an anteroseptal myocardial infarction complicated by an apical aneurysm. Coronary angiography showed proximal occlusion of the left anterior descending artery and an apical aneurysm on ventriculography. The most probable mechanism is that electric current caused damage to the walls of the coronary arteries with direct thrombogenic effect. Myocardial infarction and rhabdomyolysis after a high voltage shock with successful resuscitation has been reported in a 25 year old man, working as a varnisher near power transmission lines, who sustained a 110,000 volt shock2 . Cardiac enzymes were markedly elevated; the ECG showed significant ST segment elevation in V2-V4. Coronary angiography was normal. Myocardial infarction after an injury by lightning has been reported also in one case3

Electric injury can affect many organ systems; the damage may result from the conversion of electric energy into heat4 . Radionuclide scintigraphy has been used to demonstrate myocardial damage after electrocution5 . A clear positive segment image on 99m TC-pyrophosphate scintigraphy and a defect on a 201- Thal SPECT scan at rest were found in a young man who suffered severe antero-apical myocardial necrosis caused by electrocution.

References:

1. Myocardial infarction caused by electric injury. Value of coronography, (in French); Ann Med Interne (Paris) 1985; 136(8): 659-62.

2. Myocardial infarct and rhabdomyolysis after a high-voltage accident with successful resuscitation. Dtsch Med Wochenschr 1997 Mar 27; 122(13); 400-6.

3. Heat and electrocution. A case of myocardial infarct after an electric injury by lightning. Arch Mal Coeur Vaiss 1971 Oct; 64(10); 1516-31.

4. Differential diagnosis of acute myocardial infarction caused by electrocution. Rev Esp Cardiol 1996 June; 49(6): 470-3.

5. Myocardial necrosis by electrocution; evaluation of noninvasive methods. J Nucl Med 1997 Feb; 38(2): 250-1.

CASE REPORT