Summary Of Exposure |
A) BACKGROUND: This management is limited to the discussion of Vipers of Asia and those species of most medical importance to this region. Please refer to the management ASIAN SNAKES-ELAPIDAE for further information regarding elapids of this region. Sea snakes will NOT be discussed here. Please refer to the SEA SNAKES management for further information. B) VIPERS: Vipers (family Viperidae) are venomous snakes which include 2 subfamilies: true vipers (Vipernae) and pit vipers (Crotalinae). Although these species are limited to a geographical area, bites from exotic species may occur outside their native region in reptile handlers, zoo personnel and amateur herpetologists. C) TOXICOLOGY: Venoms contain a wide variety of enzymes and proteins. Tissue necrosis is caused by proteolytic enzymes and phospholipases in venom. Procoagulants induce thrombin formation and depletion of clotting factors resulting in coagulopathy. Phospholipase A2 are believed to be responsible for neurotoxicity and rhabdomyolysis. D) EPIDEMIOLOGY: Several species of vipers, notably the Russell's viper (D. russelii), the mamushis (genus Agkistrodon (Gloydius)), the habus (genus Trimeresurus) and pit vipers (genera Calloselasma and Trimeresurus) can cause significant morbidity and mortality in endemic regions. E) WITH POISONING/EXPOSURE
1) LOCAL TISSUE INJURY: Localized pain and swelling occur after envenomation by most species of vipers; localized bleeding is also relatively common and tissue necrosis can occur. 2) COAGULOPATHY: Hemorrhagic effects, including thrombocytopenia, prolonged PT/INR and PTT, decreased fibrinogen levels and elevated fibrin split products, are produced by the venom of many vipers. Coagulopathy can result in bleeding from gums, wounds or venipuncture sites, hemoptysis, hematemesis, rectal bleeding, melena, hematuria, vaginal bleeding, and intracranial hemorrhage. 3) SYSTEMIC EFFECTS: Other systemic effects can include: nausea, vomiting, hypotension, shock, disseminated intravascular coagulopathy, and hemolysis. The Daboia (Vipera russelii) is unique in that it is able to produce both hemorrhagic and neurotoxic effects. Acute renal failure and adrenal insufficiency have also been associated with D. russelii and some pit viper envenomations. 4) ONSET: Immediate severe pain, erythema and swelling can occur after a bite. Generally, symptoms develop within 30 minutes of a pit viper envenomation. Venom can be rapidly absorbed and systemic effects (coagulopathy) can develop within 24 hours. In general, the later the onset of systemic symptoms the better the prognosis (ie, less venom absorbed). 5) LONG-TERM EFFECTS: Bites can result in local tissue loss and necrosis which may require surgical debridement or amputation in some cases. Compartment syndrome is possible. Ongoing chronic ulceration, infection, osteomyelitis or arthritis may result in permanent disability. Chronic renal failure, chronic diabetes insipidus, or chronic neurologic injury as a result of intracranial hemorrhage are also reported.
|
Heent |
3.4.3) EYES
A) WITH POISONING/EXPOSURE 1) CASE REPORT: A 34-year-old man was bitten by a Deinagkistrodon acutus (formerly Agkistrodon actus) in the eye, and developed no light perception in that eye. At 4.5 hours after exposure, effects included: periorbital ecchymoses, facial edema, massive subconjunctival hemorrhage, severe corneal edema, and exophthalmos of the right eye. The patient was intubated for progressive facial edema and airway management and received 2 vials of D. acutus antivenom. Six hours after exposure, the eye continued to bleed and necrosis of the surrounding conjunctiva, Tenon capsule, episclera, and sclera were observed; treatment consisted of evisceration of the eye to minimize the effects of the venom (Chen et al, 2005). 2) CASE REPORT: Bilateral ptosis and angioedema of the eyelid, without vision loss, were reported in a 31-year-old man following envenomation by Eristicophis macmahonii (Asian sand viper). The patient recovered with supportive therapy, including administration of antihistamines and IV steroids (denEndenErwin & Emmanuel, 2005).
|
Cardiovascular |
3.5.1) SUMMARY
A) WITH POISONING/EXPOSURE 1) Cardiovascular toxicity may result in hypotension, shock and circulatory collapse and ECG abnormalities.
3.5.2) CLINICAL EFFECTS
A) HYPOTENSIVE EPISODE 1) WITH POISONING/EXPOSURE a) Systemic envenomation by Daboia russelii (Russell's Viper) can produce a complex of clinical symptoms which includes hypotension (Than et al, 1991; Swe et al, 1997). b) FATALITIES: Hypotension has been responsible for 38% of deaths related to D. russelii envenomation (Swe et al, 1997). c) PATHOLOGY: Alterations in blood cortisol concentrations may have a role in producing hypotension. Steroid therapy (given at the onset of hypotension) appeared to be effective in stabilizing 3 patients with hypotension after D. russelii envenomation (Swe et al, 1997).
B) SHOCK 1) WITH POISONING/EXPOSURE a) D. russelii: Circulatory shock can occur after a D. russelii bite. Early symptoms may be related to vasodilatation with decreased peripheral vascular resistance. Persistent symptoms may then result from ongoing hemorrhage and massive necrosis of the pituitary and/or adrenal glands (Swe et al, 1997).
C) TAKOTSUBO CARDIOMYOPATHY 1) WITH POISONING/EXPOSURE a) CASE REPORT: Stress-induced cardiomyopathy (ie transient left ventricular apical ballooning syndrome) was reported in a 56-year-old woman after being bitten by a presumed Gloydius blomhoffi on her foot. An ECG showed negative T waves in various leads and an echocardiogram was performed showing abnormal left ventricular systolic function with apical akinesis and a hyperdynamic basal segment of the left ventricle. Hemodynamic abnormalities or arrhythmias did not develop. By day 4, the ECG and echocardiogram were both normal (Murase & Takagi, 2012).
D) ELECTROCARDIOGRAM ABNORMAL 1) WITH POISONING/EXPOSURE a) SUMMARY: Envenomation by some vipers can result in direct myocardial toxicity as noted by cardiac dysrhythmias or abnormal ECG findings (Meier & White, 1995).
|
Respiratory |
3.6.2) CLINICAL EFFECTS
A) RESPIRATORY FAILURE 1) WITH POISONING/EXPOSURE a) Although respiratory insufficiency is NOT usually a characteristic of a viper envenomation, D. russelii (Russell's Viper) envenomation can rarely result in respiratory and generalized flaccid paralysis (Anon, 1999).
B) DYSPNEA 1) WITH POISONING/EXPOSURE a) CASE REPORT: Dyspnea without bronchospasms was reported in a 31-year-old man following envenomation by an Asian sand viper (Eristicophis macmahonii) (denEndenErwin & Emmanuel, 2005).
|
Neurologic |
3.7.1) SUMMARY
A) WITH POISONING/EXPOSURE 1) Although neurotoxicity is more frequently associated with elapid exposure, it has occasionally been reported after daboia russelii bites. It primarily consists of cranial neuropathies; generalized flaccid paralysis and respiratory failure are rare. 2) Permanent neurological damage may occur secondary to intracranial bleeding in patients with coagulopathy.
3.7.2) CLINICAL EFFECTS
A) CEREBRAL HEMORRHAGE 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Facial palsy, generalized paralysis and coma may occur secondary to cerebral hemorrhage in patients with severe coagulopathies (Kuo & Wu, 1972; Anon, 1999).
b) CASE REPORTS 1) Deteriorated mental function, facial palsy and paralysis were thought to be secondary to cerebral hemorrhage in a 41-year-old female bitten by a T. mucrosquamatus (Chinese Habu). The patient responded well to symptomatic care and physical therapy (Kuo & Wu, 1972). 2) Viper bites with coagulopathy have resulted in fatal cerebral hemorrhage. Two adults died after a bite by a D. russelii (Russell's Viper) and a T. albolabris; one patient developed frontal and subarachnoid hemorrhage, while the other had a fatal cerebrovascular accident despite supportive care (Cockram et al, 1990). 3) A 24-year-old woman experienced a severe headache approximately 7 hours after being bitten on her left foot by Echis sochureki (saw-scaled viper). Fourteen hours post-envenomation the patient became comatose with mydriasis of the right eye and complete hemiplegia on her left side. A 20-minute whole blood clotting test (20-WBCT) showed incoagulability of her blood and a CT scan showed the presence of a subdural hematoma. Treatment consisted of continuous intravenous infusion of polyvalent antivenom (total number of vials given=16). A repeat 20-WBCT, performed 6 hours after the first clotting test, showed coagulable blood. Following fronto-temporal burr hole placement and removal of approximately 100 mL of clot, the patient's condition gradually improved and she was subsequently discharged 20 days post-envenomation with moderate residual weakness of the left side of her body (Kochar et al, 2007).
B) CEREBRAL INFARCTION 1) WITH POISONING/EXPOSURE a) CASE REPORT: A 55-year-old man was bitten on the toe by a Russell's viper and developed coagulopathy (initial clotting time was more than an hour). Ten vials of equine polyvalent antisnake venin (ASV) was given along with other wound care and prophylactic parenteral ampicillin and metronidazole. An additional, 16 vials of ASV was given over the next 8 hours. The following day, his coagulation studies were normal but he continued to have a prolonged clotting time and remained drowsy. An intracranial bleed was suspected due to ongoing disorientation, restlessness and prolonged clotting time. A MRI of the brain showed bilateral thalamic infarcts. Gradually, over the next week he clinically improved and his neurologic function returned to normal. He continued to do well 6 months later (Ittyachen & Jose, 2012).
C) CENTRAL NERVOUS SYSTEM FINDING 1) WITH POISONING/EXPOSURE a) Sleepiness and dizziness have been reported after a bite by a Daboia (Vipera) russelii and a T. mucrosquamatus (Chinese Habu) (Kuo & Wu, 1972).
D) PARALYSIS 1) WITH POISONING/EXPOSURE a) Generalized flaccid paralysis can develop after envenomation by a D. russelii (Russell's Viper) (Anon, 1999). Muscle paralysis, however, is NOT a characteristic of other viper envenomations.
E) PARESTHESIA 1) WITH POISONING/EXPOSURE a) CASE REPORT: A 31-year-old man was bitten by Eristicophis macmahonii (Asian sand viper) on the tip of the third finger of his left hand, and subsequently developed paresthesias in his contralateral arm and fingers. The patient also experienced a skin rash, edema, generalized tremors, muscular weakness, dyspnea, dysphagia, dry mouth, and bilateral ptosis. The patient recovered following supportive care (denEndenErwin & Emmanuel, 2005).
F) HEADACHE 1) WITH POISONING/EXPOSURE a) Headaches were reported following envenomation by H. hypnale (hump-nosed pit viper) and Echis sochureki (saw-scaled viper) (Joseph et al, 2007; Kochar et al, 2007).
|
Gastrointestinal |
3.8.1) SUMMARY
A) WITH POISONING/EXPOSURE 1) Nausea, vomiting, or abdominal pain may develop after a bite. Intestinal necrosis has been reported infrequently following envenomation.
3.8.2) CLINICAL EFFECTS
A) NAUSEA AND VOMITING 1) WITH POISONING/EXPOSURE a) Generalized symptoms of nausea, vomiting or abdominal pain may be present after a viper envenomation (Joseph et al, 2007; denEndenErwin & Emmanuel, 2005; Anon, 1999). b) INCIDENCE: Vomiting occurred in 11 of 12 patients following envenomation by Echis sochureki (saw-scaled viper) (Kochar et al, 2007).
B) COLITIS 1) WITH POISONING/EXPOSURE a) CASE REPORT 1) A 57-year-old man was bitten by an Agkistrodon blomhoffii (Japanese Mamushi) and initially developed severe abdominal pain, frequent tarry stools and abdominal distension. The patient's hospital course was complicated by disseminated intravascular coagulation (DIC) and acute renal failure. It has been suggested that DIC may have been responsible for gastrointestinal tract occlusion of small vessels which produces intestinal necrosis. On day 125, stenotic lesions of the descending colon were resected and a right hemicolectomy performed; histologic evidence of ischemic colitis was present. The patient recovered, and 12 months later he remained asymptomatic (Iwakiri et al, 1995).
C) APTYALISM 1) WITH POISONING/EXPOSURE a) CASE REPORT: A very dry mouth and dysphagia were reported in a 31-year-old man who was bitten by an Asian sand viper (Eristicophis macmahonii) (denEndenErwin & Emmanuel, 2005).
|
Genitourinary |
3.10.2) CLINICAL EFFECTS
A) ACUTE RENAL FAILURE SYNDROME 1) WITH POISONING/EXPOSURE a) SUMMARY 1) SUMMARY: Acute renal failure requiring dialysis (peritoneal or hemodialysis) has been reported after bites by vipers (e.g., Agkistrodon blomhoffii {pit viper}, A. halys {pit viper}, Daboia russelii, H. hypnale {pit viper}) (Joseph et al, 2007; Swe et al, 1997; Iwakiri et al, 1995; Than et al, 1991; Moore, 1977) . a) Acute renal failure is often associated with the presence of DIC which results in severe renal tubular and cortical necrosis with widespread microvascular fibrin deposition (microthrombi). It is suggested, however, that a direct toxic effect produced by the venom of D. russelii (Russell's Viper) may produce renal damage (Aung et al, 1998). b) Moore (1977) reported that acute renal failure developed in two patients without DIC or circulatory shock; it was suggested that renal failure were caused by myoglobinuria and possibly due to the direct effects of the venom.
2) According to a retrospective analysis of snakebites admitted to a hospital in northwest India during January of 1997 to December of 2001, acute renal failure was reported in 39 of 52 patients (75%) following viper envenomations, with 33 of the 39 patients (84.6%) requiring dialysis (Sharma et al, 2005). b) DABOIA RUSSELII 1) INCIDENCE: In a case series of 24 patients with systemic envenomation, 10 patients developed mild renal dysfunction, but recovered with antivenom treatment alone. Of 5 patients who had developed oliguric acute renal failure, peritoneal dialysis was required. 2) FATALITIES: Oliguric acute renal failure is responsible for 44% of deaths related to envenomation (Swe et al, 1997) and is the most common cause of death in D. russelii (Russell's Viper) envenomations (Aung et al, 1998). 3) PATHOLOGY: The acute renal failure which can develop resembles that of acute tubular necrosis. The onset of renal damage may begin within several hours of a bite with onset noted by the presence of proteinuria, and the possible disruption of urine flow. The authors have suggested that the administration of antivenom does NOT alter the course of severe renal damage; therefore, the treatment of choice is dialysis which corrects the underlying pathology: acute reversible tubular necrosis (Than et al, 1991). 4) ANTIVENOM: A study was performed comparing 12 patients with Russel's viper envenomation who received antivenom early (within 6 hours of bite) with 19 historic controls who received late or no antivenom. Six of the 12 cases who received early antivenom treatment developed acute renal failure (50%) as compared to 14 of the 19 cases who received either late or no antivenom treatment (73.7%). The severity of renal failure was less in patients who were given early antivenom treatment as compared with late or no antivenom treatment (hemodialysis needed: 2 (16.7%) vs 10 (52.6%), respectively). This suggests that early intervention with antivenom treatment MAY impact renal function after envenomation, but the use of historic controls precludes confidence in this conclusion (Hung et al, 2006).
c) HYPNALE HYPNALE 1) CASE REPORT: A 54-year-old man experienced decreased urine output approximately 22 hours after being bitten by Hypnale hypnale (hump-nosed pit viper). Laboratory analysis revealed elevated serum creatinine and BUN concentrations, peaking at 7 mg/dL and 110 mg/dL, respectively, and urinalysis showed proteinuria. The patient's renal function improved, with his serum creatinine level decreasing to 2 mg/dL, after receiving 15 sessions of alternate day hemodialysis (Joseph et al, 2007).
|
Hematologic |
3.13.1) SUMMARY
A) WITH POISONING/EXPOSURE 1) Coagulopathy with thrombocytopenia, prolonged PT/INR and PTT, increased fibrin degradation products and decreased fibrinogen are common manifestations of moderate to severe envenomation. Localized and spontaneous systemic bleeding have been reported after viper bites. 2) Intravascular hemolysis may occur with Russell's Viper envenomation.
3.13.2) CLINICAL EFFECTS
A) BLOOD COAGULATION PATHWAY FINDING 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Disseminated intravascular coagulation (DIC) may develop after viper envenomation (Sharma et al, 2005; Anon, 1999). Disorders of platelet aggregation and the coagulation-fibrinolysis system have been observed in patients with snakebites from Daboia (Vipera) russelii, genus Trimeresurus, and the Agkistrodon blomhoffii and A. halys species (Chan et al, 1993; Chan et al, 1993a) (Iwarkiri et al, 1995)(Li et al, 2000). 2) Coagulation disorders produced by vipers are promptly reversed by antivenom administration (Rojnuckarin et al, 1998; Hung et al, 2006).
b) PREDICTORS: T. albolabris and T. macrops (green pit vipers): Systemic bleeding was found to occur more often if the bite occurred at a site other than the fingers or toes (venom NOT well absorbed from the digits); a requirement for antivenom within 24 hours, and prolonged venous clotting time and thrombocytopenia (Rojnuckarin et al, 1998). c) SEVERITY: Serious morbidity and mortality may result from the development of DIC. Fatalities have been reported secondary to the hemorrhagic effects of a viper envenomation (Kuo & Wu, 1972). d) INCIDENCE 1) In a national hospital-based survey of snake bites in Thailand, the following clinical features related to hematological disorders were reported (Viravan et al, 1992): a) Calloselasma rhodostoma (Malayan Pit Viper): Incoagulable blood was reported in 57 (38.8%) of 147 cases; b) T. albolabris: Incoagulable blood in 13 (20.6%) of 63 cases; c) D. russelii: Incoagulable blood in 19 (27.9%) of 68 cases.
2) E. SOCHUREKI: Incoagulable blood was reported in all 12 patients bitten by Echis sochureki (saw-scaled viper) in Rajasthan, India (Kochar et al, 2007). 3) H. HYPNALE: Incoagulable blood was reported in patients approximately 12 to 24 hours following envenomation by Hypnale hypnale (hump-nose pit viper) (Joseph et al, 2007). e) CASE REPORTS 1) A patient developed DIC after a bite by a A. blomhoffii (Japanese Mamushi), which resulted in the development of renal cortical necrosis and ischemic injury to the colon resulting in bowel resection (Iwarkiri et al, 1995). 2) Defibrination (prolonged clotting time greater than 30 minutes) occurred in a 27-year-old man who was bitten by a snake suspected to be from the Viperidae family. Despite receiving a total of 30 units of antivenom (300 mL) over a 6-day period, the patient's clotting time continued to be greater than 30 minutes and his prothrombin time was more than 1 minute; however, there was no evidence of bleeding from any site. On the 7th day post-envenomation, the patient's clotting time returned to normal and the patient was subsequently discharged (Jacob, 2006). The authors speculate that the continued defibrination may have been either due to unneutralized venom components or that, even though the snake was believed to be from the Viperidae family, the antivenom used was not specific for that particular species of snake.
f) CASE SERIES 1) In a series of 21 cases of envenomation by T. albolabris, 86% (n=18) of the victims had increased blood concentrations of fibrin degradation products (FDP) ranging from 10 to 40 mcg/L (normal: less than 10 mcg/L) and 28% (n=10) had thrombocytopenia or prolonged prothrombin time (PT), activated partial thromboplastin time (APTT) and thrombin time (TT). No patient in this study received antivenom and coagulation abnormalities were corrected with replacement therapy (i.e., platelet transfusions and fresh frozen plasma) (Chan et al, 1993a).
B) THROMBOCYTOPENIC DISORDER 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Thrombocytopenia has developed after viper envenomation (Joseph et al, 2007; Kochar et al, 2007; Hung et al, 2006; Rojnuckarin et al, 1998; Chan et al, 1993) .
b) CASE SERIES 1) In a review of 242 cases of venomous snakebites, of those who developed hematologic abnormalities (10% (n=24)), thrombocytopenia was the most common abnormality reported along with excessive fibrinolysis and defibrination (Cockram et al, 1990). 2) In a retrospective study of 30 patients with green pit viper envenomation, platelet counts and mean platelet volume were lower in envenomated patients than control subjects (Soogarun et al, 2003).
C) COAG./BLEEDING TESTS ABNORMAL 1) WITH POISONING/EXPOSURE a) CASE REPORTS 1) Prolonged bleeding, oozing (more than 24 hours) and ecchymosis have been reported after viper bites (e.g., Agkistrodon acutus, Japanese Mamushi, and genus Trimeresurus {T. albolabris, T. macrops}) (Kuo & Wu, 1972; Hutton et al, 1990). 2) Severe coagulopathy (PT >60 seconds, INR >4.5, APTT >150 seconds) was reported in a 6-year-old girl 4 days after being bitten by T. albolabris (white-lipped green pit viper). Initially, the patient had been given Agkistrodon halys antivenin with no clinical improvement; however the coagulopathy completely resolved within 2 days after receiving 5 vials of Green Pit Viper antivenin (Yang et al, 2007).
b) INCIDENCE 1) Of 29 patients with snakebites by T. albolabris or T. macrops, 58% of patients developed localized bruising (Hutton et al, 1990).
D) BLEEDING 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Hematological effects can result in bleeding from multiple sites (e.g., bleeding gums, hemoptysis, hematemesis, rectal bleeding, melena, hematuria, vaginal bleeding, old wound sites or venipuncture sites) (Kochar et al, 2007; Sharma et al, 2005; Anon, 1999). Evidence of generalized petechial hemorrhage may be noted (Buranasin, 1993).
b) INCIDENCE 1) TRIMERESURUS a) In a case series of 72 victims of Trimeresurus sp. bites, 52 cases developed only localized symptoms while coagulopathies were reported in 25 victims (34.7%). Of those 25 victims, 7 showed evidence of systemic bleeding (i.e., hematemesis, hematuria, bleeding gums, and generalized petechial hemorrhage). In all cases, hematologic disturbances resolved within 5 to 6 hours after antivenom administration (Buranasin, 1993). b) T. albolabris or T. macrops (Green Pit Vipers): Of 271 moderate to severely envenomated patients, 17.3% developed systemic bleeding (Rojnuckarin et al, 1998).
2) E. SOCHUREKI a) E. SOCHUREKI: Systemic bleeding was reported in 7 of 12 patients following envenomation by Echis sochureki (saw-scaled viper) (Kochar et al, 2007).
c) CASE REPORTS 1) AGKISTRODON ACUTUS a) PEDIATRIC: A 10-year-old girl developed bleeding from the nose, gingiva, eponychium and other abrasion sites approximately 24 hours after envenomation. Anemia was present (Hgb 7.93 grams/dL), along with hematuria. Bleeding time was prolonged greater than 1 hour without clotting. The patient responded to antivenom therapy; oozing from local wound sites stopped within 12 hours. Symptomatic care also included a blood transfusion (Kuo & Wu, 1972).
E) LEUKOCYTOSIS 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Leukocytosis may occur after viper envenomation. Bites by the following species have resulted in leukocytosis: A. acutus (Japanese Mamushi) T. albolabris (White-lipped Green Pit Viper) and T. stejnegeri (Green Habu) (Chen et al, 2007; Chan et al, 1993; Kuo & Wu, 1972).
b) INCIDENCE 1) T. albolabris: Of 30 patients envenomated, 8 developed leukocytosis (Chan et al, 1993).
F) HEMOLYSIS 1) WITH POISONING/EXPOSURE a) Hemolysis has been reported following Russell's viper (D. russelli siamensis) envenomations (Hung et al, 2006).
|
Dermatologic |
3.14.1) SUMMARY
A) WITH POISONING/EXPOSURE 1) Localized pain and swelling are reported after envenomation from most species, blebs and ecchymosis may be seen. 2) Severe tissue injury resulting in necrosis, gangrene, compartment syndrome and permanent disability have developed.
3.14.2) CLINICAL EFFECTS
A) EDEMA 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Swelling and erythema are likely to occur following any viper envenomation (Anon, 1999) (Warrell et al, 1992) (Kuo & Wu, 1972). Swelling may progress and involve the entire affected limb and include the regional lymphatic system (denEndenErwin & Emmanuel, 2005; Meier & White, 1995). In one case report, envenomation by a juvenile A. rhodostoma (Pit Viper) produced only local swelling and erythema; no systemic effects were reported (Vest & Kardong, 1980).
b) LOCALIZED EFFECTS 1) A. rhodostoma: A bite by a juvenile pit viper (A. rhodostoma) produced swelling in the affected hand and arm which began to resolve within 12 hours of the bite. The authors suggested that the relatively minor side effects were due to the limited quantity of venom available which was NOT sufficient to produce systemic envenomation (Vest & Kardong, 1980). 2) In a national hospital-based survey of snakebites in Thailand, bites from T. macrops, T. purpureomaculatus, T. wagleri caused only mild local swelling and no serious systemic effects (Viravan et al, 1992). 3) Pain and localized swelling were reported in 11 of 12 patients who were bitten by E. sochureki (Kochar et al, 2007) and in 5 patients following envenomation by H. hypnale (hump-nosed pit viper) (Joseph et al, 2007).
c) REGIONAL EFFECTS 1) Of 29 patients with snakebites by T. albolabris or T. macrops, swelling spread to include greater than half the bitten limb in 46% of patients and 46% of patients developed tender enlargement of local lymph nodes (Hutton et al, 1990). 2) CASE REPORT: A 6-year-old child, who was bitten on her right foot by Trimeresurus albolabris (white-lipped green pit viper), developed swelling of her right foot that progressed to her knee over the next 12 hours. Within 24 hours, the swelling had progressed to her mid thigh, and blisters had developed near the site of the bite (Yang et al, 2007). 3) CASE REPORT: A 25-year-old woman developed swelling which spread from the foot to the ankle area within 30 minutes of being bitten by a T. kanburiensis. Within 2 hours, edema had spread to the mid calf area and, 24 hours after exposure it had reached the mid thigh area; eventually it extended into the flank area. The patient was treated symptomatically, and was discharged 4 days after the bite with no evidence of permanent sequelae (Warrell et al, 1992).
B) PAIN 1) WITH POISONING/EXPOSURE a) SUMMARY: Envenomation by vipers usually produces immediate pain (Warrell et al, 1992) (Chan et al, 1993; Anon, 1999; Jacob, 2006). A juvenile bite by a pit viper produced throbbing pain, but the duration of symptoms was less than would be expected following an adult envenomation (Vest & Kardong, 1980). b) INCIDENCE 1) T. ALBOLABRIS: In a case series of 31 victims of a Trimeresurus albolabris bite, all patients developed pain and swelling (Chan et al, 1993). 2) Pain and localized swelling were reported in 11 of 12 patients who were bitten by E. sochureki (Kochar et al, 2007) and in 5 patients following envenomation by H. hypnale (hump-nosed pit viper) (Joseph et al, 2007).
C) BLISTERING ERUPTION 1) WITH POISONING/EXPOSURE a) Local blistering may occur after viper envenomation. The presence of blisters is more likely to lead to necrosis and/or secondary infections in bites by T. albolabris or T. macrops (Green Pit Vipers) (Yang et al, 2007; Rojnuckarin et al, 1998). b) INCIDENCE 1) Of 29 patients with snakebites by T. albolabris or T. macrops, 6 patients developed localized blistering (Hutton et al, 1990). 2) Blistering occurred in 3 of 12 patients following envenomation by E. sochureki (Kochar et al, 2007).
D) SKIN NECROSIS 1) WITH POISONING/EXPOSURE a) Tissue necrosis can occur after viper envenomation (Hutton et al, 1990; denEndenErwin & Emmanuel, 2005). Necrosis was more likely to develop after bites sustained on fingers or toes by T. albolabris or T. macrops (Green Pit Vipers), due to poor systemic absorption of the venom (resulting in a higher concentration of localized venom) (Rojnuckarin et al, 1998). b) INCIDENCE 1) T. albolabris or T. macrops (Green Pit Vipers): Of 271 moderately to severely envenomated patients, 6.6% developed wound necrosis (Rojnuckarin et al, 1998). 2) Necrosis occurred in 2 of 12 patients following envenomation by E. sochureki (Kochar et al, 2007).
E) LOCAL INFECTION OF WOUND 1) WITH POISONING/EXPOSURE a) Localized infection can occur after viper envenomation. b) INCIDENCE 1) T. albolabris or T. macrops (Green Pit Vipers) - Of 271 moderately to severely envenomated patients, 5.5% developed secondary infection (Rojnuckarin et al, 1998).
F) ERUPTION 1) WITH POISONING/EXPOSURE a) CASE REPORT: A burning skin rash occurred in a 31-year-old man who was bitten by an Asian sand viper (Eristicophis macmahonii). The rash resolved with supportive treatment, including administration of antihistamines and IV steroids (denEndenErwin & Emmanuel, 2005).
|
Musculoskeletal |
3.15.1) SUMMARY
A) WITH POISONING/EXPOSURE 1) Rhabdomyolysis and myoglobinurias have been associated with D. russelii bites. 2) Compartment syndrome rarely develops after viper bites.
3.15.2) CLINICAL EFFECTS
A) RHABDOMYOLYSIS 1) WITH POISONING/EXPOSURE a) Rhabdomyolysis and myoglobinuria can develop after D. russelii (Russell's Viper) envenomation (Hung et al, 2006; Anon, 1999).
B) COMPARTMENT SYNDROME 1) WITH POISONING/EXPOSURE a) Severe local envenomation can result in severe swelling and local necrosis and, if left untreated, may progress to compartment syndromes, which is more likely to occur if a patient can NOT be treated with antivenom (Anon, 1999).
C) OSTEOMYELITIS 1) WITH POISONING/EXPOSURE a) SUMMARY: Chronic osteomyelitis or arthritis may occur after an intraarticular viper envenomation (Anon, 1999). 1) CASE REPORT: A reptile handler developed osteomyelitis, and intraoperatively was found to have complete joint erosion of the proximal interphalangeal joint after envenomation by a T. flavomaculatus. Permanent joint immobility and intermittent pain was reported up to 16 months after the bite (Clark & Davidson, 1997).
|
Endocrine |
3.16.2) CLINICAL EFFECTS
A) ADRENAL CORTICAL HYPOFUNCTION 1) WITH POISONING/EXPOSURE a) D. RUSSELII: Bites by Russell's Vipers are able to produce acute adrenal/pituitary insufficiency which can result in clinical symptoms of shock and hypoglycemia (Anon, 1999).
B) HYPOPITUITARISM 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Acute and chronic hypopituitarism has been reported following a Russell's viper bite (Antonypillai et al, 2011).
b) PERSISTENT TOXICITY 1) A chronic phase that can occur months to years after a bite by a Russell's Viper can produce weakness, loss of secondary sexual hair, amenorrhea, testicular atrophy, and hypothyroidism (Anon, 1999). 2) CASE REPORT: A 49-year-old man from Sri Lanka was bitten by a Russel's viper on his left foot and developed acute symptoms of vomiting, blurred vision and coagulopathy within the first few hours. He was treated with Haffkine polyvalent anti-venom and required treatment for an early anaphylactic reaction but was discharged 2 days later. However, the patient continued to have persistent symptoms of fatigue, weakness, and reduced libido up to 3 years after envenomation. Pituitary function studies revealed steroid thyroid and gonadal axes deficiencies. Following treatment with hydrocortisone, levothyroxine and testosterone he was clinically improved 1 month later (Antonypillai et al, 2011). 3) PATHOGENESIS: Russell's viper envenomation can lead to acute and chronic hypopituitarism. It may be the result of focal hemorrhage and micro vascular thrombin deposition in the pituitary leading to hemorrhagic infarction of the anterior pituitary leading to acute and chronic pan-hypopituitarism (Antonypillai et al, 2011). 4) DIAGNOSIS: Chronic hypopituitarism can be diagnosed by the following studies: dynamic pituitary function tests, including insulin tolerance test, thyrotropin-releasing hormone stimulation test and luteinizing hormone-releasing hormone stimulation test (Antonypillai et al, 2011). 5) ONSET: In a study of 24 patients in Burma with a Russell's viper envenomation, the diagnosis of chronic hypopituitarism occurred within 6 months to 4 years after evenomation; symptoms developed as early as 4 weeks in some patients (Antonypillai et al, 2011).
C) HYPOGLYCEMIA 1) WITH POISONING/EXPOSURE a) Hypoglycemia may occur as a result of adrenal/pituitary insufficiency following a D. russelii (Russell's Viper) envenomation (Anon, 1999).
|
Reproductive |
3.20.1) SUMMARY
A) Intrauterine demise has been reported after envenomation by an asian viper. B) Three pregnant women, bitten by Trimeresurus stejnegeri (Green Habu snake), developed pain and swelling at the bite site, and mild leukocytosis. Two of the three women received equine-derived hemotoxic bivalent F(ab')2 antivenom without the development of any adverse effects. All three women delivered healthy babies without any evidence of subsequent developmental delays.
3.20.3) EFFECTS IN PREGNANCY
A) INTRAUTERINE FETAL DEATH 1) CASE REPORT - A 29-year-old woman who was 10 weeks pregnant was bitten by a viper (A. halys blomhoffii, mamushi) and developed swelling, mild rhabdomyolysis and paralysis of the right oculomotor nerve. One week prior to the bite, ultrasound had shown a live fetus. One week after exposure, ultrasound showed loss of the fetal heart beat and the woman underwent a D&C(Nasu et al, 2004).
B) LACK OF EFFECT 1) CASE SERIES - Three pregnant women, in various stages of pregnancy (ranging from 8 weeks to 28 weeks gestation), were bitten by Trimeresurus stejnegeri (Green Habu snake). All three women developed localized symptoms in the region of the envenomation site (pain, bleeding, swelling, ecchymosis) and mild leukocytosis. Two of the three women were given equine derived hemotoxic bivalent F(ab')2 antivenom without development of adverse effects. All 3 women recovered without sequelae and subsequently delivered healthy babies. Follow-up of the children, several years later, showed no developmental delays (Chen et al, 2007).
|