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Hypotension, myocardial infarction, and coagulopathy following gila monster bite
The Journal
of Emergency
Medicine,
Vol. 7. pp. 37-40,
Printed in the USA
1989
l
Copyright
0 1989 Pergamon
Press plc
HYPOTENSION, MYOCARDIAL -INFARCTION, AND COAGULOPATHY FOLLOWING GILA MONSTER BITE Charles A. Preston. Louisiana
State University
School
of Medicine,
Reprint address: Charles
Department of Medicine, Section A. Preston, MD, 124 Layburn
q Abstract-We report a 23-year-old man who developed life threatening hypotension, myocardial infarction, coagulopatby, and renal failure following the bite of a Gila monster (Heloderma suspecturn). These are previously unreported complications in humans. The patient recovered after fluid resuscitation and treatment with pressor agents.
of Emergency Court, Gretna,
Medicine, LA 70056
New
Orleans,
Louisiana
CASE REPORT A 23-year-old amateur herpetologist presented to the emergency department complaining of a Gila monster bite to the left forearm. He arrived four hours after the bite complaining of pain and swelling in the left forearm as well as general malaise. He had no history of any previous reptile envenomation. The physical examination revealed an athlecticallybuilt male in obvious distress. His blood pressure was 76/54, pulse 140/min and respirations 18/min. The skin was cool and diaphoretic. Examination of the extremities revealed a bite on the volar aspect of the mid left forearm. The fifteen teeth marks penetrated the dermis and were surrounded by an area of erythema and edema approximately 20 cm by 8 cm. No significant ecchymosis was noted. The vascular and neuromuscular examinations were normal. A fluid challenge of 1000 cc was administered and resulted in a blood pressure of 110 mmHg systolic and a pulse of 11Yminute. He was given 0.3 cc epinephrine (1 : 1000) subcutaneously, and 50 mg diphenhydramine and 0.5 cc tetanus toxoid intramuscularly. Due to the development of multifocal premature ventricular contractions, the patient was given 70 mg of lidocaine by intravenous bolus and begun on a maintenance drip at 2 mg/min. The arm was elevated, the wound cleansed, probed, x-ray studies performed, and found to be free of teeth. The blood pressure remained very labile, dropping at the range of 60 to 80 mmHg systolic, and the patient remained anuric despite 3.5 liters of crystalloid fluid resuscita-
0 Keywords - hypotension; myocardial infarction, coagulopathy, Gila monster
INTRODUCTION The Gila monster (Heloderma suspecturn) is well known for its forceful and tenacious bite. This slow moving reptile, indigenous to the southwestern United States, also has a powerful venom, which is reported to cause local pain, anaphylactic reaction, and rarely, hypotension (1,2). It is not generally believed to affect the coagulation system (2,3). Heloderma suspecturn and it close relative Heloderma horridum both belong to the Order Squamata, which also includes venomous snakes. Additionally the biochemistry of snake venom and Gila monster venom are somewhat similar in that they both contain L-amino acid oxidase activity, phospholipase AZ, hyaluronidase, protease, kallikrein and seritonin (2,4,5).
We recently treated a young man who suffered severe, refractory hypotension, coagulopathy, renal failure, and myocardial infarction secondary to Heloderma suspecturn envenomation. = w
MD
Toxicology-one of the most critical and challenging areas confronting the emergency department staff -is coordinated by Kenneth Kulig, MD, of the Rocky Mountain Poison Center.
RECEIVED: 26 October 1987; SECOND SUBMISSION RECEIVED: 25 February 1988 ACCEPTED: 3 March 1988 37
0736-4679189 $3.00 + .OO
38
Charles A. Preston
tion. The patient was then transferred to the Intensive Care Unit for invasive monitoring and pressor therapy with dopamine hydrochloride. The admission laboratory determinations included arterial blood gases on 5 liters of oxygen by nasal cannula. This revealed a pH 7.27, p0, 104, pC0, 32, HCO, 15. The white blood cell count was 48,300/ ccm, hematocrit 57.6%, and hemaglobin 18.6 gm/dL. The initial platelet count was 171,0OO/ccm. A prothrombin time of 17.6 seconds (control 11.0-13.0) and a partial thromboplastin time of 54 seconds (control 21-32) were observed. Serum electrolytes were remarkable for a potassium of 2.3 mEq/L and a CO, of 18 mEq/L. The admission electrocardiogram revealed changes consistent with acute anterolateral myocardial infarction (Figure 1). A persistent coagulopathy was noted in the form of elevated PT and PTT, the appearance of fibrin split products greater than 40 mcg/dL (normal O-10 mcg/dL), a decrease in fibrin to 68 mg/dL, and a fall in the platelet count to 62,00O/ccm. This did not result in any observable bleeding. Additionally the BUN and creatinine were elevated to 23 mg/dL and 3.0 mg/dL, respectively (normals 8-20 and 0.8-2.0). A marked increase in the lactate dehydrogenase to 8297 IU and creatinine phosphokinase to 4697 IU was observed. The patient developed a LDH, > LDH, pattern but did not have CPK-MB bands detected. A technetium scan of the heart, however, was consistent with myocardial infarction of the lateral wall of the left ventricle. Hemodynamic stability and a return of adequate urine output was obtained within the first 16 hours of hospitalization, and the patient was weaned from dopamine and lidocaine. Two units of fresh frozen plasma were given on the second hospital day in response to the developing coagulopathy. The erythema and edema of the forearm progressed to the level of the axilla in the first 24 hours and then resolved over the next three days. Further laboratory values normalized, the patient continued to improve clinically and was discharged home on the seventh hospital day on Keflex (cephalexin) and Naprosyn (naproxen).
DISCUSSION
The Gila monster is a large slow moving nocturnal reptile that naturally inhabits the Great Sonoran Desert area of Arizona and Mexico and has also been reported to be found in Utah and Nevada. Nevertheless, because the animals represent a prize to amateur collectors, Gila monster bites may be encountered anywhere in the United States.
The venom of Heloderma suspectum is produced in paired inferior labial glands. Each gland contains several lobes with separate ducts that carry the venom to the base of sharp, grooved, recurved teeth. The victim is envenomated by means of capillary action during extended chewing. Russell reports and approximate 60 % envenomation rate (2). Gila monster venom, like that of venomous snakes, represents a complex mixture of proteins including hyaluronidase (or spreading factor), phospholipase A,, kinin releasing activity, L-amino acid oxidase activity, and proteolytic enzymes. Phospholipase A, splits lecithin to isolecithin thereby weakening cell membranes. L-amino acid oxidase acts like thrombin and splits fibrinogen leading to platelet trapping and clot formation. When administered to test animals, the venom has been shown to cause dyspnea, respiratory arrest, gastrointestinal hemorrhage, and pulmonary edema. As in snake envenomation, one may see increased capillary leakage and third space fluid losses. Severe hypotension, tachycardia, and an immediate decrease in carotid bloodflow have been demonstrated in dogs following envenomation from a gila monster, However, the venom was not observed to have any effect on the coagulation system of the dog or cat (4). Treatment of the Gila monster bite begins with disengagement of the animal. Many methods for disengagement have appeared in the literature including placing a stick in the jaws and prying open, cutting the strong masseter muscles with a sharp knife, or immersion of the extremity with attached animal in cold water (1,3,6). Also reported are the rather unwise suggestions of grabbing the animal by the tail and tugging, pouring gasoline in the animal’s mouth, or applying a flame to its chin (3). Local wound care including cleansing of the wound, probing the teeth marks with a 25 gauge needle, and removal of teeth fragments should be carried out. Tetanus prophylaxis should be administered when appropriate. The usual presenting complaints for Gila monster bite include local pain and swelling at the site of injury. The pain may be severe, radiating up the extremity for 3 to 5 hours, but usually subsides within 8 hours. Edema may be present in as short a time as 15 minutes, and cyanosis may appear around the wound. The patient may be diaphoretic. One textbook states: “in humans severe hypotension is rarely observed and no coagulation defects have been noted” (2). Russell reports “no evidence to date suggests the venom alters blood coagulation” (3). This case not only demonstrates a coagulopathy but a severe refractory hypotension most likely resulting in myocardial infarction and renal insult in this otherwise young, healthy
I I
40
Charles A. Preston
patient. These are previously unreported complications from Gila monster envenomation. Hypotension and coagulopathy are well known to occur in snake envenomation. The hypotension usually responds to crystalloid resuscitation but in severe cases, such as the one presented here, colloid fluid resuscitation and pressor therapy may be warranted (3). Additionally, the physician should be aware that coagulopathy may occur so that appropriate action may be taken if bleeding occurs. There is no commercially available antivenom for Gila monster poisoning.
SUMMARY We report a cause of a previously healthy male who developed profound hypotension, myocardial infarction, coagulopathy, and renal failure following Gila monster bite. The venom of the Gila monster induces a hypovolemic shock syndrome due to excessive third space losses and has some direct physiologic toxicity. It is our belief that this patient suffered significant morbidity as a result of the profound and prolonged hypotension, but direct venom cardiotoxicity and nephrotoxicity cannot be excluded.
REFERENCES 1. Piacentine J, Curry C, Ryan P. Life threatening anaphylaxis following gila monster bite. Ann Emerg Med. 1986;15:147-9. 2. Russell FE. Venomous snake bites. In Auerbach PS, Geehr EC, eds.: Management of wilderness and environmental emergenties. New York: Macmillian; 1983:370-2. 3. Russell FE, Bogert CM. Gila monster, its biology, venom and bite, a review. Toxicon. 1981;19:341-59. 4. Gila monster venoms. In Tu AT, ed. Venoms: chemistry and
molecular biology. New York: John Wiley and Sons; 1977:5314. 5. Wingert WA. Audio digest emergency medicine. May 19, 1986. 3, 10. 6. Burnett JW, Calton, GJ, Morgan RJ. Gila monster bites. Cutis. April, 1985:323. 7. Cooke E, Loeb L. The venom of Heloderma. Washington, DC: Carnegie Institute; 1913:51.
of Emergency
Medicine,
Vol. 7. pp. 37-40,
Printed in the USA
1989
l
Copyright
0 1989 Pergamon
Press plc
HYPOTENSION, MYOCARDIAL -INFARCTION, AND COAGULOPATHY FOLLOWING GILA MONSTER BITE Charles A. Preston. Louisiana
State University
School
of Medicine,
Reprint address: Charles
Department of Medicine, Section A. Preston, MD, 124 Layburn
q Abstract-We report a 23-year-old man who developed life threatening hypotension, myocardial infarction, coagulopatby, and renal failure following the bite of a Gila monster (Heloderma suspecturn). These are previously unreported complications in humans. The patient recovered after fluid resuscitation and treatment with pressor agents.
of Emergency Court, Gretna,
Medicine, LA 70056
New
Orleans,
Louisiana
CASE REPORT A 23-year-old amateur herpetologist presented to the emergency department complaining of a Gila monster bite to the left forearm. He arrived four hours after the bite complaining of pain and swelling in the left forearm as well as general malaise. He had no history of any previous reptile envenomation. The physical examination revealed an athlecticallybuilt male in obvious distress. His blood pressure was 76/54, pulse 140/min and respirations 18/min. The skin was cool and diaphoretic. Examination of the extremities revealed a bite on the volar aspect of the mid left forearm. The fifteen teeth marks penetrated the dermis and were surrounded by an area of erythema and edema approximately 20 cm by 8 cm. No significant ecchymosis was noted. The vascular and neuromuscular examinations were normal. A fluid challenge of 1000 cc was administered and resulted in a blood pressure of 110 mmHg systolic and a pulse of 11Yminute. He was given 0.3 cc epinephrine (1 : 1000) subcutaneously, and 50 mg diphenhydramine and 0.5 cc tetanus toxoid intramuscularly. Due to the development of multifocal premature ventricular contractions, the patient was given 70 mg of lidocaine by intravenous bolus and begun on a maintenance drip at 2 mg/min. The arm was elevated, the wound cleansed, probed, x-ray studies performed, and found to be free of teeth. The blood pressure remained very labile, dropping at the range of 60 to 80 mmHg systolic, and the patient remained anuric despite 3.5 liters of crystalloid fluid resuscita-
0 Keywords - hypotension; myocardial infarction, coagulopathy, Gila monster
INTRODUCTION The Gila monster (Heloderma suspecturn) is well known for its forceful and tenacious bite. This slow moving reptile, indigenous to the southwestern United States, also has a powerful venom, which is reported to cause local pain, anaphylactic reaction, and rarely, hypotension (1,2). It is not generally believed to affect the coagulation system (2,3). Heloderma suspecturn and it close relative Heloderma horridum both belong to the Order Squamata, which also includes venomous snakes. Additionally the biochemistry of snake venom and Gila monster venom are somewhat similar in that they both contain L-amino acid oxidase activity, phospholipase AZ, hyaluronidase, protease, kallikrein and seritonin (2,4,5).
We recently treated a young man who suffered severe, refractory hypotension, coagulopathy, renal failure, and myocardial infarction secondary to Heloderma suspecturn envenomation. = w
MD
Toxicology-one of the most critical and challenging areas confronting the emergency department staff -is coordinated by Kenneth Kulig, MD, of the Rocky Mountain Poison Center.
RECEIVED: 26 October 1987; SECOND SUBMISSION RECEIVED: 25 February 1988 ACCEPTED: 3 March 1988 37
0736-4679189 $3.00 + .OO
38
Charles A. Preston
tion. The patient was then transferred to the Intensive Care Unit for invasive monitoring and pressor therapy with dopamine hydrochloride. The admission laboratory determinations included arterial blood gases on 5 liters of oxygen by nasal cannula. This revealed a pH 7.27, p0, 104, pC0, 32, HCO, 15. The white blood cell count was 48,300/ ccm, hematocrit 57.6%, and hemaglobin 18.6 gm/dL. The initial platelet count was 171,0OO/ccm. A prothrombin time of 17.6 seconds (control 11.0-13.0) and a partial thromboplastin time of 54 seconds (control 21-32) were observed. Serum electrolytes were remarkable for a potassium of 2.3 mEq/L and a CO, of 18 mEq/L. The admission electrocardiogram revealed changes consistent with acute anterolateral myocardial infarction (Figure 1). A persistent coagulopathy was noted in the form of elevated PT and PTT, the appearance of fibrin split products greater than 40 mcg/dL (normal O-10 mcg/dL), a decrease in fibrin to 68 mg/dL, and a fall in the platelet count to 62,00O/ccm. This did not result in any observable bleeding. Additionally the BUN and creatinine were elevated to 23 mg/dL and 3.0 mg/dL, respectively (normals 8-20 and 0.8-2.0). A marked increase in the lactate dehydrogenase to 8297 IU and creatinine phosphokinase to 4697 IU was observed. The patient developed a LDH, > LDH, pattern but did not have CPK-MB bands detected. A technetium scan of the heart, however, was consistent with myocardial infarction of the lateral wall of the left ventricle. Hemodynamic stability and a return of adequate urine output was obtained within the first 16 hours of hospitalization, and the patient was weaned from dopamine and lidocaine. Two units of fresh frozen plasma were given on the second hospital day in response to the developing coagulopathy. The erythema and edema of the forearm progressed to the level of the axilla in the first 24 hours and then resolved over the next three days. Further laboratory values normalized, the patient continued to improve clinically and was discharged home on the seventh hospital day on Keflex (cephalexin) and Naprosyn (naproxen).
DISCUSSION
The Gila monster is a large slow moving nocturnal reptile that naturally inhabits the Great Sonoran Desert area of Arizona and Mexico and has also been reported to be found in Utah and Nevada. Nevertheless, because the animals represent a prize to amateur collectors, Gila monster bites may be encountered anywhere in the United States.
The venom of Heloderma suspectum is produced in paired inferior labial glands. Each gland contains several lobes with separate ducts that carry the venom to the base of sharp, grooved, recurved teeth. The victim is envenomated by means of capillary action during extended chewing. Russell reports and approximate 60 % envenomation rate (2). Gila monster venom, like that of venomous snakes, represents a complex mixture of proteins including hyaluronidase (or spreading factor), phospholipase A,, kinin releasing activity, L-amino acid oxidase activity, and proteolytic enzymes. Phospholipase A, splits lecithin to isolecithin thereby weakening cell membranes. L-amino acid oxidase acts like thrombin and splits fibrinogen leading to platelet trapping and clot formation. When administered to test animals, the venom has been shown to cause dyspnea, respiratory arrest, gastrointestinal hemorrhage, and pulmonary edema. As in snake envenomation, one may see increased capillary leakage and third space fluid losses. Severe hypotension, tachycardia, and an immediate decrease in carotid bloodflow have been demonstrated in dogs following envenomation from a gila monster, However, the venom was not observed to have any effect on the coagulation system of the dog or cat (4). Treatment of the Gila monster bite begins with disengagement of the animal. Many methods for disengagement have appeared in the literature including placing a stick in the jaws and prying open, cutting the strong masseter muscles with a sharp knife, or immersion of the extremity with attached animal in cold water (1,3,6). Also reported are the rather unwise suggestions of grabbing the animal by the tail and tugging, pouring gasoline in the animal’s mouth, or applying a flame to its chin (3). Local wound care including cleansing of the wound, probing the teeth marks with a 25 gauge needle, and removal of teeth fragments should be carried out. Tetanus prophylaxis should be administered when appropriate. The usual presenting complaints for Gila monster bite include local pain and swelling at the site of injury. The pain may be severe, radiating up the extremity for 3 to 5 hours, but usually subsides within 8 hours. Edema may be present in as short a time as 15 minutes, and cyanosis may appear around the wound. The patient may be diaphoretic. One textbook states: “in humans severe hypotension is rarely observed and no coagulation defects have been noted” (2). Russell reports “no evidence to date suggests the venom alters blood coagulation” (3). This case not only demonstrates a coagulopathy but a severe refractory hypotension most likely resulting in myocardial infarction and renal insult in this otherwise young, healthy
I I
40
Charles A. Preston
patient. These are previously unreported complications from Gila monster envenomation. Hypotension and coagulopathy are well known to occur in snake envenomation. The hypotension usually responds to crystalloid resuscitation but in severe cases, such as the one presented here, colloid fluid resuscitation and pressor therapy may be warranted (3). Additionally, the physician should be aware that coagulopathy may occur so that appropriate action may be taken if bleeding occurs. There is no commercially available antivenom for Gila monster poisoning.
SUMMARY We report a cause of a previously healthy male who developed profound hypotension, myocardial infarction, coagulopathy, and renal failure following Gila monster bite. The venom of the Gila monster induces a hypovolemic shock syndrome due to excessive third space losses and has some direct physiologic toxicity. It is our belief that this patient suffered significant morbidity as a result of the profound and prolonged hypotension, but direct venom cardiotoxicity and nephrotoxicity cannot be excluded.
REFERENCES 1. Piacentine J, Curry C, Ryan P. Life threatening anaphylaxis following gila monster bite. Ann Emerg Med. 1986;15:147-9. 2. Russell FE. Venomous snake bites. In Auerbach PS, Geehr EC, eds.: Management of wilderness and environmental emergenties. New York: Macmillian; 1983:370-2. 3. Russell FE, Bogert CM. Gila monster, its biology, venom and bite, a review. Toxicon. 1981;19:341-59. 4. Gila monster venoms. In Tu AT, ed. Venoms: chemistry and
molecular biology. New York: John Wiley and Sons; 1977:5314. 5. Wingert WA. Audio digest emergency medicine. May 19, 1986. 3, 10. 6. Burnett JW, Calton, GJ, Morgan RJ. Gila monster bites. Cutis. April, 1985:323. 7. Cooke E, Loeb L. The venom of Heloderma. Washington, DC: Carnegie Institute; 1913:51.