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Abdominal wall and stomach perforation following accidental electrocution with high tension wire: A unique case
The Journal
of Emergency
Medicine,
Vol 11, pp 141-l
PrInted in the USA
45, 1993
Copyright
0 1993 Pergamon
Press Ltd.
ABDOMINAL WALL AND STOMACH PERFORATION FOLLOWING ACCIDENTAL ELECTROCUTION WITH HIGH TENSION WIRE: A UNIQUE CASE Sunil Kumar, MB, BS, MS, Shaji Thomas, MB, BS, MS, DNB, and Sanjeev Lehri, MB, BS Department of General Surgery, University College of Medical Sciences-cum- Guru Teg Bahadur Hospital. Shahdara, Delhi, India Reprint Address: Dr. Sunil Kumar, A - 593, Shastri Nagar, Delhi - 110 052, India
0 Abstract-The usual form of direct gastrointestinal injury following high-tension electric injury is widespread necrosis of the colon or the small intestine. It usually occurs in combination with extensive electric burns of the overlying abdominal wall. We report a case of immediate postelectrocution abdominal wall and stomach perforation following high tension electric injury. The total absence of coagulation necrosis of the stomach or other portions of the gastrointestinal tract and the absence of bums of the abdominal wall were other unique features of the case reported. The patient was successfullytreated.
of the abdominal wall and stomach following hightension electric injury. The perforation of the abdominal wall and the stomach after accidental electrocution is seen for the first time. Additionally, the presence of other unique features prompted the authors to report the case. Challenges involved in the early diagnosis and the treatment of these intraabdominal hollow viscus injuries and the probable mechanism responsible for different types of these injuries are discussed.
0 Keywords-abdominal wall perforation; evisceration; electrical burns; stomach perforation
CASE REPORT
An l&year-old male was brought to the casualty department of our hospital in the middle of the night with a history of accidental electrocution from a high-tension (11,000 volts) electric wire. He was a laborer and was unloading damp sand from a truck while standing over the truck parked in the compound of an electric power station. During this process he accidentally touched a low-hanging wire with his left hand, resulting in entry of high voltage current via the left index finger. Immediately after the electrocution the patient became unconscious and had one generalized convulsion. This was followed by a number of episodes of vomiting. He was rushed to a nearby first-aid center. The doctor at the firstaid center noticed the abdominal wall perforation and evisceration. Therefore, he referred the patient to our hospital after starting an intravenous drip. The patient arrived at the hospital 3 hours after electrocution.
INTRODUCTION
Gastrointestinal complications following accidental high tension electric injuries (excluding lightning) are mostly indirect and include self-limiting nausea, vomiting, intestinal colic, abdominal distension, Curling’s ulcers, and paralytic ileus (1). Intraabdominal hollow viscus injuries directly attributable to electric current are extremely rare and generally take the form of hemorrhagic necrosis of a segment of the gut, with or without its delayed perforation. A review of the literature of the last 70 years revealed eight such cases (Table 1). For reasons not known, the colon and the small intestine were the commonest segment of the gut involved. The majority of these patients had associated extensive electric burns of the overlying abdominal wall. The authors recently treated a case of perforation
Clinical Communications, focusing primarily on adult emergencies, is coordinated by Ron Walls, MD, of Vancouver General Hospital, Vancouver, BC, Canada. 0736-4679/93 $6.00 + .OO RECEIVED: 2 December 1991; FINAL SUBMISSION RECEIVED: 1 June 1992;
w
ACCEPTED:
26 June 1992
141
142
Sunil Kumar, Shaji Thomas, Sanjeev
Table 1. lntra Abdominal Case No.
Ref. No.
Hollow Viscus Injuries Directly Due to High-Tension Author
Year
GIT Lesion small bowel necrosis & perforation gallbladder necrosis gallbladder necrosis small intestine + sigmoid colon necrosis & perforation sigmoid colon necrosis & perforation gallbladder necrosis small intestine necrosis & perforation small bowel & sigmoid colon necrosis
1
5
Simonin
1927
2 3 4
6 1 7
Smith & Rank Taylor et al. Almgard et al.
1946 1962 1985
5
7
Almgard et al.
1965
6 7
8 9
DiVicenti et al. Xuewei & Zongdian
1969 1981
8
10
Branday et al.
1989
By this time the patient had regained consciousness, though he was still confused and disoriented. His pulse rate was 90 beats/minute. His blood pressure was 124/70 torr. His pupils were moderately dilated, but equal in size and reactive to light. There was no external evidence of head injury. Examination of the respiratory system revealed no abnormality. A 1Zlead electrocardiogram was also within normal limits. An irregular gaping wound 2 cm x 3 cm in size, with loops of viable small intestine and omenturn prolapsing out, was seen in the epigastrium. Undigested, dried-up food particles were also seen near the epigastric wound. The margins of the epigastric wound showed charring and blackening with no active bleeding. Characteristic extensive electric burns of the abdomen were absent. Besides these abdominal findings, characteristic electric burns were present on the left index finger, the right elbow joint, and the right knee. The patient was sedated by 5 mg intravenous Diazepam. Ringer’s lactate 1000 mL was given intravenously at a fast rate (within 1 hour), following which the patient passed approximately 200 mL of clear urine. The antibiotic therapy, consisting of injection ampicillin 500 mg every 6 hours, injection gentamycin 60 mg every 8 hours, and injection metrogyl500 mg every 8 hours, was begun intravenously and immediate laparotomy was planned. The laparotomy was performed via a midline supraumbilical incision. An irregular perforation 3 cm x 4 cm in size was found in the anterior wall of the stomach in the region of its body, directly underneath the epigastric wound. The margins of the perforation in the stomach were also charred and blackened with no active bleeding. There was no necrosis of the stomach wall. Other viscera were entirely normal. Peritoneal contamination was minimal. The stomach perforation was repaired in two layers using standard technique after debridement of the edges.
Lehri
Electric Current Abdominal wall burn
Diagnosis
(+I
postmortem
died
antemortem postmortem antemortem
survived died died
antemortem
survived
postmortem antemortem
died survived
antemortem
died
:;,’ (+I (+) (+I (+) (+I
End Result
The epigastric wound was also repaired in layers after debridement. The laparotomy was concluded after a thorough peritoneal lavage and drainage. The burn wounds over the limbs were debrided and dressed daily, and left to heal by secondary intention. The patient showed progressive improvement. Ryle’s tube aspiration was discontinued on the 4th postoperative day when the bowel sounds returned and the patient passed flatus. Peritoneal drains were also removed the same day. Oral feeds were started on the 5th postoperative day. The abdominal wound healed without any complications. The urine output, the respiratory system, and the cardiovascular system remained normal throughout. The disorientation and confusion exhibited by the patient at the time of admission cleared by the second postoperative day. The patient was discharged on the 9th postoperative day in a perfect state of health. DISCUSSION
High-tension electric injuries (excluding lightning) generally occur in electric workers. Most of the time the current enters and leaves via the extremities, inflicting maximum tissue damage at these sites. This accounts for a large number of amputations these patients must undergo (2). Since these patients are generally seriously ill, they are prone to certain indirect gastrointestinal complications such as nausea, vomiting, intestinal colic, abdominal distension, paralytic ileus, and Curling’s ulcers (I). The incidence of these indirect gastrointestinal complications varies from 6% (3) to 25% (4). Rarely, as a direct consequence to the electric current, injury of the abdominal viscera can result, requiring operative intervention. As shown in Table 1, over the last 70 years, 8 cases with intraabdominal hollow viscus injury (1,510) and 2 related to the solid organs, one each of the
143
Accidental Electrocution
pancreas (11) and the liver (12), due to high-tension electric accident are on record in the world’s literature. All except one of these patients (6) also sustained extensive burns of the overlying abdominal wall. The colon and the small intestine were affected an equal number of times. The gallbladder was involved in 2 cases. Pathologically, all the cases had widespread necrosis, with or without perforation, of the affected gastrointestinal segment. In comparison to these historical findings, the case presented here had several unique features. An immediate perforation of the abdominal wall occurred. Only the margins of the gaping wound in the abdomen were charred and blackened. Extensive burns of the abdominal wall, noted in 7 of 8 cases presented in Table 1, were altogether missing in the present case. Immediate perforation of the stomach as a direct complication of high-tension electric injury is also reported for the first time. Extensive necrosis of the involved viscera (the stomach in the present case), otherwise so characteristic of the electric injury, was conspicuously absent, and only the margins of the perforation of the stomach were charred and blackened. The high-tension electric current is believed to cause tissue damage by coagulation necrosis due to conversion of the electric energy into heat energy (13). The amount of heat generated during passage of the current depends on the resistance of the tissue. According to Hunt and co-workers (14), the resistance in the large caliber vessels is low and the flow of blood fast. Thus, in the large-calibered vessels, a low amount of heat is generated and its dissipation is rapid. Therefore, damage to the large vessels (e.g., the aorta) is negligible. In contrast, in the smaller vessels (e.g., the branches of the superior mesentric artery), the resistance is high, resulting in more heat generation, and the blood flow is slow, resulting in slow dissipation of the heat. This results in coagulation necrosis of the smaller vessels, and infarction of the concerned bowel segment. This is believed to be the principal mechanism of injury to the intraabdominal viscera due to accidental electrocution. It has been suggested that the widespread infarction of the intraabdominal organs could also result from prolonged use of the vasoconstrictors used for treatment of shock (1). In the case reported, the perforation of the abdominal wall and the stomach occurred immediately after the electrocution, and the extensive burns of the abdominal wall and the stomach were missing altogether. The hypothesis proposed by Taylor and colleagues (1) remains unproven. Thus, the aforementioned mechanisms cannot explain the injuries seen in the case reported.
EC : ELECTRIC VN : VAGUS
CURRENT NERVE
SC : STOMACH CA
CONTRACTION
: COMPRESSED
AIR
(a)
SR
SP
SR : STOMACH
RELAXATION
EA : EXPANDING SP : STOMACH
AIR PERFORATION
(W Figure 1. Probable mechanism proposed for the perforation of the abdominal wall and the stomach after electrocution in this patient. a) Transmission of the current to the stomach via the vagus nerves caused vigorous peristalsis of the stomach. This caused compression and displacement of the air trapped in the stomach. b) After the passage of the current, the stomach relaxed resulting in rapid m-expansion of the previously compressed air. This is belleved to have caused perforation of the stomach and the abdominal wall.
Hanson and McIlwraith (15) reported one case of lung contusion and one case of colonic contusion following electrocution due to lightning. They suggested that when a discharge of enormous potential
144
Sunil Kumar, Shaji Thomas, Sanjeev Lehri
(such as lightning) takes place, the atmospheric air is expanded and displaced, and the return of this air causes the blast like effect due to generation of pressure waves. This is akin to the “explosion effect” seen with explosive devices. In simple terms, this is like an impact from the outside causing internal visceral damage such as lung contusion, intestinal contusion, and subarachnoid or cerebral hemorrhage. However, this mechanism cannot explain the perforation of the stomach and the abdominal wall seen in our case either. In our case, the high voltage current traveling via the vagus nerves probably caused violent contraction of the stomach, with the result that the air that is normally present in the stomach was compressed and displaced. When the stomach relaxed after the passage of the current, the compressed air within the stomach rapidly and forcefully re-expanded, causing perforation of the stomach and the anterior abdominal wall. This is like an explosion from within (Figures la and lb). The presence of perforation of the abdominal wall and the stomach with negligible electric burns of the anterior abdominal wall and stomach are probably best explained by this hypothesis. Diagnosis of the intra-abdominal visceral injury in the present case was apparent, as was the need for the laparotomy. However, in general, the diagnosis of the intra-abdominal injury, as well as the decision for the laparotomy, is quite a difficult and challenging task in patients with electric injuries. In the majority of the patients shown in Table 1 the diagnosis was either delayed (up to 2 weeks) or made at autopsy. For this reason, a number of authors have advocated mandatory early laparotomy, especially in cases with the full-thickness electric burns of the abdominal wall. In these cases the signs of peritonitis may be masked by the burns of the overlying abdominal wall. In cases without any electric burns of the abdominal wall, careful observation for the signs of peritonitis is advocated. The laparotomy should be performed subsequently if signs of peritonitis appear.
The surgery in these cases should be aggressive. Bowel resection should be done through the clearly healthy areas and any area of doubtful viability should be included. Resection-anastomosis is advised in cases with necrosis of the small intestine. However, in cases with infarction of the large bowel, a protective proximal colostomy after primary resection-anastomosis or exteriorization of the resected ends should be the rule (13). Some authors have advocated a routine second look laparotomy after 48 to 72 hours because of the high incidence of extension of bowel necrosis and anastomotic leak (16). Mortality in these patients is high (5 of the 8 patients reported in Table 1 died). The deaths in the immediate postelectrocution period are primarily due to cardiorespiratory arrest, and the deaths in the late first week or early second week period are primarily due to acute renal failure (1). The incidence of acute renal failure and the resultant mortality was as high as 26% in the series by Taylor and colleagues (1). In the series reported by DiVincenti and colleagues (8), the incidence of acute renal failure was 11%. Although the exact etiology of renal damage is not known, Pearl (17) has suggested that this may be due to the toxic products of abnormal protein cleavage (hemoglobinuria and myoglobinuria). In addition, renal damage may also be caused by the initial shock period, with late or inadequate resuscitation (8). Therefore, the best method of avoiding acute renal failure and associated mortality is early and vigorous fluid resuscitation. It is easy for the inexperienced to underestimate the extent of deep tissue necrosis due to electrical injuries and thus underestimate the fluid needs of these patients. Therefore, the measurement of central venous pressure and hourly urine output should be used in monitoring the adequacy of the fluid resuscitation. The urine should be kept in the range of alkaline pH for prevention of acute renal failure due to hemoglobinuria and myoglobinuria. With these precautions Solem and colleagues (2) were able to reduce the incidence of acute renal failure to 1.5%.
REFERENCES 1. Taylor PH, Pugsley LQ, Vogel EH. The intriguing electrical burn: a review of thirty-one electrical burn cases. J Trauma. 1962;2:309-26. 2. Solem L, Fischer RP, Strate RG. The natural history of electrical injury. J Trauma. 1977;17:487-92. 3. Butler ED, Grant TD. Electrical injuries, with special reference to the upper extremities. Am J Surg. 1977;134:95-101. 4. Wilkinson C, Wood M. High voltage electric injury. Am J Surg. 1978;136:693-6. 5. Simonin T. Electrocution par courant de 12,000 volts: Brulures electriques abdominointestinales. Ann de med leg. 1927; 7:339-44.
6. Smith J, Rank BK. A case of severe electric burns with an unusual sequence of complications. Brit J Surg. 1946;33:365-8. 7. AImgard L, Liljedahl S, Nylen B. Electric burns of the abdomen. Acta Chir Stand. 1965;130:550-9. 8. DiVincenti FC, Moncrief JA, Pruitt BA. Electrical injuries: a review of 65 cases. J Trauma. 1%9;9:497-507. 9. Xuewei W, Zongdian Y. Successful treatment of a case of electric abdominal burn complicated by intestinal perforation. Chin Med J. 1981;94:181-4. 10. Branday JM, DuQuesnay DR, Yessing MT, Duncan ND. Visceral complications of electric burn injury: a report of 2 cases with review of the literature. WI Med J. 1989;38:110-3.
Accidental Electrocution 11. Glazer AM. Pancreatic necrosis in electric shock. Arch Pathol. 1945;39:9-10. 12. Newsome TW, Curreri PW, Eurenius K. Visceral injuries-an unusual complication of an electrical burn. Arch Surg. 1972; 105:494-7. 13. Williams DB, Karl RC. Intestinal injury associated with lowvoltage electrocution. J Trauma. 1981;21:246-50. 14. Hunt JL, McManus WF, Honey WP, et al. Vascular lesions in acute electric injuries. J Trauma. 1974;14:461-73.
145 15. Hanson GC, McIlwraith GR. Lightning injury: two case histories and a review of management. Brit Med J. 1973;4: 271-4. 16. Baxter CR. Present concepts in the management of major electrical injury. Surg Clin North Am. 1970;50:1401-17. 17. Pearl FL. Electric shock: presentation of cases and review of literature. Arch Surg. 1933;27:227-49.
of Emergency
Medicine,
Vol 11, pp 141-l
PrInted in the USA
45, 1993
Copyright
0 1993 Pergamon
Press Ltd.
ABDOMINAL WALL AND STOMACH PERFORATION FOLLOWING ACCIDENTAL ELECTROCUTION WITH HIGH TENSION WIRE: A UNIQUE CASE Sunil Kumar, MB, BS, MS, Shaji Thomas, MB, BS, MS, DNB, and Sanjeev Lehri, MB, BS Department of General Surgery, University College of Medical Sciences-cum- Guru Teg Bahadur Hospital. Shahdara, Delhi, India Reprint Address: Dr. Sunil Kumar, A - 593, Shastri Nagar, Delhi - 110 052, India
0 Abstract-The usual form of direct gastrointestinal injury following high-tension electric injury is widespread necrosis of the colon or the small intestine. It usually occurs in combination with extensive electric burns of the overlying abdominal wall. We report a case of immediate postelectrocution abdominal wall and stomach perforation following high tension electric injury. The total absence of coagulation necrosis of the stomach or other portions of the gastrointestinal tract and the absence of bums of the abdominal wall were other unique features of the case reported. The patient was successfullytreated.
of the abdominal wall and stomach following hightension electric injury. The perforation of the abdominal wall and the stomach after accidental electrocution is seen for the first time. Additionally, the presence of other unique features prompted the authors to report the case. Challenges involved in the early diagnosis and the treatment of these intraabdominal hollow viscus injuries and the probable mechanism responsible for different types of these injuries are discussed.
0 Keywords-abdominal wall perforation; evisceration; electrical burns; stomach perforation
CASE REPORT
An l&year-old male was brought to the casualty department of our hospital in the middle of the night with a history of accidental electrocution from a high-tension (11,000 volts) electric wire. He was a laborer and was unloading damp sand from a truck while standing over the truck parked in the compound of an electric power station. During this process he accidentally touched a low-hanging wire with his left hand, resulting in entry of high voltage current via the left index finger. Immediately after the electrocution the patient became unconscious and had one generalized convulsion. This was followed by a number of episodes of vomiting. He was rushed to a nearby first-aid center. The doctor at the firstaid center noticed the abdominal wall perforation and evisceration. Therefore, he referred the patient to our hospital after starting an intravenous drip. The patient arrived at the hospital 3 hours after electrocution.
INTRODUCTION
Gastrointestinal complications following accidental high tension electric injuries (excluding lightning) are mostly indirect and include self-limiting nausea, vomiting, intestinal colic, abdominal distension, Curling’s ulcers, and paralytic ileus (1). Intraabdominal hollow viscus injuries directly attributable to electric current are extremely rare and generally take the form of hemorrhagic necrosis of a segment of the gut, with or without its delayed perforation. A review of the literature of the last 70 years revealed eight such cases (Table 1). For reasons not known, the colon and the small intestine were the commonest segment of the gut involved. The majority of these patients had associated extensive electric burns of the overlying abdominal wall. The authors recently treated a case of perforation
Clinical Communications, focusing primarily on adult emergencies, is coordinated by Ron Walls, MD, of Vancouver General Hospital, Vancouver, BC, Canada. 0736-4679/93 $6.00 + .OO RECEIVED: 2 December 1991; FINAL SUBMISSION RECEIVED: 1 June 1992;
w
ACCEPTED:
26 June 1992
141
142
Sunil Kumar, Shaji Thomas, Sanjeev
Table 1. lntra Abdominal Case No.
Ref. No.
Hollow Viscus Injuries Directly Due to High-Tension Author
Year
GIT Lesion small bowel necrosis & perforation gallbladder necrosis gallbladder necrosis small intestine + sigmoid colon necrosis & perforation sigmoid colon necrosis & perforation gallbladder necrosis small intestine necrosis & perforation small bowel & sigmoid colon necrosis
1
5
Simonin
1927
2 3 4
6 1 7
Smith & Rank Taylor et al. Almgard et al.
1946 1962 1985
5
7
Almgard et al.
1965
6 7
8 9
DiVicenti et al. Xuewei & Zongdian
1969 1981
8
10
Branday et al.
1989
By this time the patient had regained consciousness, though he was still confused and disoriented. His pulse rate was 90 beats/minute. His blood pressure was 124/70 torr. His pupils were moderately dilated, but equal in size and reactive to light. There was no external evidence of head injury. Examination of the respiratory system revealed no abnormality. A 1Zlead electrocardiogram was also within normal limits. An irregular gaping wound 2 cm x 3 cm in size, with loops of viable small intestine and omenturn prolapsing out, was seen in the epigastrium. Undigested, dried-up food particles were also seen near the epigastric wound. The margins of the epigastric wound showed charring and blackening with no active bleeding. Characteristic extensive electric burns of the abdomen were absent. Besides these abdominal findings, characteristic electric burns were present on the left index finger, the right elbow joint, and the right knee. The patient was sedated by 5 mg intravenous Diazepam. Ringer’s lactate 1000 mL was given intravenously at a fast rate (within 1 hour), following which the patient passed approximately 200 mL of clear urine. The antibiotic therapy, consisting of injection ampicillin 500 mg every 6 hours, injection gentamycin 60 mg every 8 hours, and injection metrogyl500 mg every 8 hours, was begun intravenously and immediate laparotomy was planned. The laparotomy was performed via a midline supraumbilical incision. An irregular perforation 3 cm x 4 cm in size was found in the anterior wall of the stomach in the region of its body, directly underneath the epigastric wound. The margins of the perforation in the stomach were also charred and blackened with no active bleeding. There was no necrosis of the stomach wall. Other viscera were entirely normal. Peritoneal contamination was minimal. The stomach perforation was repaired in two layers using standard technique after debridement of the edges.
Lehri
Electric Current Abdominal wall burn
Diagnosis
(+I
postmortem
died
antemortem postmortem antemortem
survived died died
antemortem
survived
postmortem antemortem
died survived
antemortem
died
:;,’ (+I (+) (+I (+) (+I
End Result
The epigastric wound was also repaired in layers after debridement. The laparotomy was concluded after a thorough peritoneal lavage and drainage. The burn wounds over the limbs were debrided and dressed daily, and left to heal by secondary intention. The patient showed progressive improvement. Ryle’s tube aspiration was discontinued on the 4th postoperative day when the bowel sounds returned and the patient passed flatus. Peritoneal drains were also removed the same day. Oral feeds were started on the 5th postoperative day. The abdominal wound healed without any complications. The urine output, the respiratory system, and the cardiovascular system remained normal throughout. The disorientation and confusion exhibited by the patient at the time of admission cleared by the second postoperative day. The patient was discharged on the 9th postoperative day in a perfect state of health. DISCUSSION
High-tension electric injuries (excluding lightning) generally occur in electric workers. Most of the time the current enters and leaves via the extremities, inflicting maximum tissue damage at these sites. This accounts for a large number of amputations these patients must undergo (2). Since these patients are generally seriously ill, they are prone to certain indirect gastrointestinal complications such as nausea, vomiting, intestinal colic, abdominal distension, paralytic ileus, and Curling’s ulcers (I). The incidence of these indirect gastrointestinal complications varies from 6% (3) to 25% (4). Rarely, as a direct consequence to the electric current, injury of the abdominal viscera can result, requiring operative intervention. As shown in Table 1, over the last 70 years, 8 cases with intraabdominal hollow viscus injury (1,510) and 2 related to the solid organs, one each of the
143
Accidental Electrocution
pancreas (11) and the liver (12), due to high-tension electric accident are on record in the world’s literature. All except one of these patients (6) also sustained extensive burns of the overlying abdominal wall. The colon and the small intestine were affected an equal number of times. The gallbladder was involved in 2 cases. Pathologically, all the cases had widespread necrosis, with or without perforation, of the affected gastrointestinal segment. In comparison to these historical findings, the case presented here had several unique features. An immediate perforation of the abdominal wall occurred. Only the margins of the gaping wound in the abdomen were charred and blackened. Extensive burns of the abdominal wall, noted in 7 of 8 cases presented in Table 1, were altogether missing in the present case. Immediate perforation of the stomach as a direct complication of high-tension electric injury is also reported for the first time. Extensive necrosis of the involved viscera (the stomach in the present case), otherwise so characteristic of the electric injury, was conspicuously absent, and only the margins of the perforation of the stomach were charred and blackened. The high-tension electric current is believed to cause tissue damage by coagulation necrosis due to conversion of the electric energy into heat energy (13). The amount of heat generated during passage of the current depends on the resistance of the tissue. According to Hunt and co-workers (14), the resistance in the large caliber vessels is low and the flow of blood fast. Thus, in the large-calibered vessels, a low amount of heat is generated and its dissipation is rapid. Therefore, damage to the large vessels (e.g., the aorta) is negligible. In contrast, in the smaller vessels (e.g., the branches of the superior mesentric artery), the resistance is high, resulting in more heat generation, and the blood flow is slow, resulting in slow dissipation of the heat. This results in coagulation necrosis of the smaller vessels, and infarction of the concerned bowel segment. This is believed to be the principal mechanism of injury to the intraabdominal viscera due to accidental electrocution. It has been suggested that the widespread infarction of the intraabdominal organs could also result from prolonged use of the vasoconstrictors used for treatment of shock (1). In the case reported, the perforation of the abdominal wall and the stomach occurred immediately after the electrocution, and the extensive burns of the abdominal wall and the stomach were missing altogether. The hypothesis proposed by Taylor and colleagues (1) remains unproven. Thus, the aforementioned mechanisms cannot explain the injuries seen in the case reported.
EC : ELECTRIC VN : VAGUS
CURRENT NERVE
SC : STOMACH CA
CONTRACTION
: COMPRESSED
AIR
(a)
SR
SP
SR : STOMACH
RELAXATION
EA : EXPANDING SP : STOMACH
AIR PERFORATION
(W Figure 1. Probable mechanism proposed for the perforation of the abdominal wall and the stomach after electrocution in this patient. a) Transmission of the current to the stomach via the vagus nerves caused vigorous peristalsis of the stomach. This caused compression and displacement of the air trapped in the stomach. b) After the passage of the current, the stomach relaxed resulting in rapid m-expansion of the previously compressed air. This is belleved to have caused perforation of the stomach and the abdominal wall.
Hanson and McIlwraith (15) reported one case of lung contusion and one case of colonic contusion following electrocution due to lightning. They suggested that when a discharge of enormous potential
144
Sunil Kumar, Shaji Thomas, Sanjeev Lehri
(such as lightning) takes place, the atmospheric air is expanded and displaced, and the return of this air causes the blast like effect due to generation of pressure waves. This is akin to the “explosion effect” seen with explosive devices. In simple terms, this is like an impact from the outside causing internal visceral damage such as lung contusion, intestinal contusion, and subarachnoid or cerebral hemorrhage. However, this mechanism cannot explain the perforation of the stomach and the abdominal wall seen in our case either. In our case, the high voltage current traveling via the vagus nerves probably caused violent contraction of the stomach, with the result that the air that is normally present in the stomach was compressed and displaced. When the stomach relaxed after the passage of the current, the compressed air within the stomach rapidly and forcefully re-expanded, causing perforation of the stomach and the anterior abdominal wall. This is like an explosion from within (Figures la and lb). The presence of perforation of the abdominal wall and the stomach with negligible electric burns of the anterior abdominal wall and stomach are probably best explained by this hypothesis. Diagnosis of the intra-abdominal visceral injury in the present case was apparent, as was the need for the laparotomy. However, in general, the diagnosis of the intra-abdominal injury, as well as the decision for the laparotomy, is quite a difficult and challenging task in patients with electric injuries. In the majority of the patients shown in Table 1 the diagnosis was either delayed (up to 2 weeks) or made at autopsy. For this reason, a number of authors have advocated mandatory early laparotomy, especially in cases with the full-thickness electric burns of the abdominal wall. In these cases the signs of peritonitis may be masked by the burns of the overlying abdominal wall. In cases without any electric burns of the abdominal wall, careful observation for the signs of peritonitis is advocated. The laparotomy should be performed subsequently if signs of peritonitis appear.
The surgery in these cases should be aggressive. Bowel resection should be done through the clearly healthy areas and any area of doubtful viability should be included. Resection-anastomosis is advised in cases with necrosis of the small intestine. However, in cases with infarction of the large bowel, a protective proximal colostomy after primary resection-anastomosis or exteriorization of the resected ends should be the rule (13). Some authors have advocated a routine second look laparotomy after 48 to 72 hours because of the high incidence of extension of bowel necrosis and anastomotic leak (16). Mortality in these patients is high (5 of the 8 patients reported in Table 1 died). The deaths in the immediate postelectrocution period are primarily due to cardiorespiratory arrest, and the deaths in the late first week or early second week period are primarily due to acute renal failure (1). The incidence of acute renal failure and the resultant mortality was as high as 26% in the series by Taylor and colleagues (1). In the series reported by DiVincenti and colleagues (8), the incidence of acute renal failure was 11%. Although the exact etiology of renal damage is not known, Pearl (17) has suggested that this may be due to the toxic products of abnormal protein cleavage (hemoglobinuria and myoglobinuria). In addition, renal damage may also be caused by the initial shock period, with late or inadequate resuscitation (8). Therefore, the best method of avoiding acute renal failure and associated mortality is early and vigorous fluid resuscitation. It is easy for the inexperienced to underestimate the extent of deep tissue necrosis due to electrical injuries and thus underestimate the fluid needs of these patients. Therefore, the measurement of central venous pressure and hourly urine output should be used in monitoring the adequacy of the fluid resuscitation. The urine should be kept in the range of alkaline pH for prevention of acute renal failure due to hemoglobinuria and myoglobinuria. With these precautions Solem and colleagues (2) were able to reduce the incidence of acute renal failure to 1.5%.
REFERENCES 1. Taylor PH, Pugsley LQ, Vogel EH. The intriguing electrical burn: a review of thirty-one electrical burn cases. J Trauma. 1962;2:309-26. 2. Solem L, Fischer RP, Strate RG. The natural history of electrical injury. J Trauma. 1977;17:487-92. 3. Butler ED, Grant TD. Electrical injuries, with special reference to the upper extremities. Am J Surg. 1977;134:95-101. 4. Wilkinson C, Wood M. High voltage electric injury. Am J Surg. 1978;136:693-6. 5. Simonin T. Electrocution par courant de 12,000 volts: Brulures electriques abdominointestinales. Ann de med leg. 1927; 7:339-44.
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