Summary Of Exposure |
A) USES: This management is limited to the vipers of Africa and the surrounding region of most medical importance. Some geographic overlap may occur in this management with venomous snakes of the Middle East. Please refer to the SNAKES, MIDDLE-EASTERN management as appropriate. There are over 45 species that inhabit this region. In particular, the saw-scaled or carpet vipers (genus Echis), the puff adder (Bitis arietans), and the Gaboon viper (B. gabnonica) are of significant medical importance.
B) TOXICOLOGY: Snake venom varies in composition and quantity dependent on the species and size of the snake and the mechanical efficiency in which the bite occurred. Clinically important components of venom include proteolytic/procoagulant enzymes, cytolytic/necrotic toxins, hemolytic/myolytic phospholipase A2, neurotoxins, vasodilators and hemorrhagins.
C) EPIDEMIOLOGY: True epidemiologic data on African snakebites are difficult to ascertain. The World Health Organization estimates 100,000 envenomations and 5,000 deaths from African snakes (including Viperidae and Elapidae) annually in 2010. Because of the inaccuracies of reporting systems, the estimate of the annual incidence is as high as 1,000,000 bites with 500,000 envenomations and 20,000 deaths.
D) WITH POISONING/EXPOSURE
1) MILD TO MODERATE TOXICITY: LOCAL TISSUE INJURY: An estimated 20% to 50% of snake bites do not result in envenomation - "dry bite". Localized pain and swelling occur after envenomation by most species of vipers; localized bleeding is also relatively common and tissue necrosis may occur. SYSTEMIC EFFECTS: Nausea, vomiting and diarrhea are common.
2) SEVERE TOXICITY: LOCAL TISSUE INJURY: Tissue necrosis in severe envenomations may require surgical debridement and amputations. COAGULOPATHY: Thrombocytopenia, prolonged PT/INR and PTT, decreased fibrinogen levels, increased fibrin degradation products and inhibition of platelet aggregation are produced by the venom of many vipers. Direct damage to vascular endothelium in some species can also result in hemorrhage. Rarely, bites have led to thrombotic events and disseminated intravascular coagulopathy. Bleeding complications can include bleeding gums, hemoptysis, hematemesis, rectal bleeding, melena, hematuria, vaginal bleeding, and bleeding from old wound sites or venipuncture sites, and rarely intracranial hemorrhage. Rhadomyolysis can occur following severe envenomations. Multiple cases of compartment syndrome have been described after envenomation by B. arietans. Envenomations can produce hypotension which is mainly associated with hypovolemia but can occur from direct cardiotoxicity (B. arietans). Neurotoxicity has been reported infrequently. Both ischemic and hemorrhagic strokes have been reported with Cerastes cerastes.
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Vital Signs |
3.3.3) TEMPERATURE
A) WITH POISONING/EXPOSURE 1) Fever can develop in some cases of viper envenomation. a) In a small case study of 31 victims of viper bite, fever was reported in patients with E. carinatus or a B. arietans bite. Neutrophil leukocytosis was also present in some patients with fever (Pugh & Theakston, 1987).
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Heent |
3.4.3) EYES
A) WITH POISONING/EXPOSURE 1) PTOSIS may occur following viper envenomations. a) CASE REPORT: Bilateral ptosis developed in a young adult following an Echis pyramidum (carpet viper) bite. Symptoms developed within the first 3 days and resolved within one week following antivenom administration and supportive care (Gillissen et al, 1994).
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Cardiovascular |
3.5.2) CLINICAL EFFECTS
A) HYPOTENSIVE EPISODE 1) WITH POISONING/EXPOSURE a) SUMMARY: The venom of vipers in this region can produce hypotension. In victims of viper envenomation, hypotension is mainly associated with hypovolemia (Warrell, 1995; Blaylock, 2003).
b) PATHOPHYSIOLOGY: Viper venom can produce a decline in blood pressure by increasing vascular permeability leading to hypovolemia. Some species (i.e., B. gabonica, B. arietans) can have a direct effect on the heart and other species (i.e., B. arietans) can produce splanchnic vasodilatation, and autopharmacological release of vasodilators, such as bradykinin release in some species (e.g., V. palaestinae) (Warrell, 1995).
c) The almost immediate clinical improvement in blood pressure by the administration of antivenom following some viper envenomations (e.g., B. arietans) suggests a direct myocardial effect (Warrell, 1995).
d) CASE REPORT: A 43-year-old man developed episodic premature ventricular contractions and hypotension (80/50 mmHg) after being bitten on his left thumb by Bitis gabonica (gaboon viper). The patient also experienced ecchymosis and edema at the bite site, paresthesias extending to the mid wrist, and chest tightness. Following intravenous administration of 10 vials of antivenom, given over a six-hour period, and administration of diphenhydramine and hydrocortisone, the patient recovered and was discharged 3 days post-envenomation (Marsh et al, 2007).
B) SHOCK 1) WITH POISONING/EXPOSURE a) Shock can be a clinical feature of the genus Bitis (B. arietans {puff adder} and B. gabonica {Gaboon viper}) envenomations. In victims of viper envenomation, shock was mainly associated with hypovolemia (Warrell, 1995). b) INCIDENCE: B. gabonica bites are more likely to produce severe cardiovascular effects than are B. arietans bites (Warrell, 1995). 1) Envenomations by the genus Echis (saw-scaled or carpet vipers) can produce shock, but it has been reported infrequently. Likewise, the genus Vipera (typical old world vipers) can cause severe systemic effects which may include shock.
c) CASE REPORT: A 40-year-old man experienced hypotensive shock approximately 2.5 hours following envenomation by M. lebetina lebetina (blunt-nosed viper). Antivenom was not available; the patient recovered with supportive care (Gocmen et al, 2006). C) CONDUCTION DISORDER OF THE HEART 1) WITH POISONING/EXPOSURE a) The following dysrhythmias have been associated with B. arietans (puff adder) and B. gabonica (Gaboon viper) envenomations: bradycardia, atrial tachycardia with ectopic beats, and ECG changes associated with myocardial damage (Warrell, 1995).
b) The almost immediate clinical improvement in bradycardia by the administration of antivenom following some viper envenomations (e.g., B. arietans) suggests a direct myocardial effect (Warrell, 1995).
c) CASE REPORT: A 43-year-old man developed episodic premature ventricular contractions and hypotension (80/50 mmHg) after being bitten on his left thumb by Bitis gabonica (gaboon viper). The patient also experienced ecchymosis and edema at the bite site, paresthesias extending to the mid wrist, and chest tightness. Following intravenous administration of 10 vials of antivenom, given over a six-hour period, and administration of diphenhydramine and hydrocortisone, the patient recovered and was discharged 3 days post-envenomation (Marsh et al, 2007).
D) HYPERTENSIVE DISORDER 1) WITH POISONING/EXPOSURE a) CASE REPORT: Hypertension (180/100 mmHg) was reported in a 57-year-old man within 24 hours following envenomation from Proatheris supercilius (Lowland Swamp viper) (Valenta et al, 2008).
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Respiratory |
3.6.2) CLINICAL EFFECTS
A) DYSPNEA 1) WITH POISONING/EXPOSURE a) CASE REPORT: A 40-year-old man experienced uncontrolled movements of his arms and legs, faintness, tremors, dyspnea, tachycardia, and sweating approximately 2.5 hours after being bitten on the finger of his right hand by a blunt-nosed viper (M. lebetina lebetina). The symptoms spontaneously disappeared 20 minutes later (Gocmen et al, 2006).
B) PULMONARY EMBOLISM 1) WITH POISONING/EXPOSURE a) CASE REPORT: A 16-year-old adolescent experienced dyspnea and severe pleuritic chest pain following a 1-week hospitalization for a snake bite from an Egyptian sand viper (Cerastes cerastes). Chest radiograph was normal; however, a pulmonary angiogram confirmed the presence of an embolus in the left pulmonary artery. Symptoms persisted despite heparin administration, and an intermittent fever (38.9 degrees C) developed. Further complications ensued, including pleural effusion and a clostridial infection. With supportive therapy, the patient recovered and was discharged (Halkin et al, 1997).
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Neurologic |
3.7.2) CLINICAL EFFECTS
A) CENTRAL NERVOUS SYSTEM FINDING 1) WITH POISONING/EXPOSURE a) Neurotoxicity is not a typical feature of viper envenomation. b) The following neurotoxic effects have been reported for specific African vipers (Warrell, 1995): 1) B. gabonica (gaboon viper): Some reports of dizziness, blurred vision and difficulty with visual accommodation have occurred, but ptosis (a common clinical feature of neurotoxicity following elapid envenomation) has not been reported.
2) B. atropos (berg adder): Neurotoxic effects may develop and last several hours or up to a week.
3) E. pyramidum (Egyptian carpet viper): Neurotoxicity has been reported.
4) Neurotoxin venom has been found in the venoms of the following: B. caudalis (horned adder) and the B. atropos (berg adder); V. palaestinae (Palestine viper) has a neurotoxic polypeptide that can act directly on the medulla.
5) Coma was reported in 2 patients (a 9-year-old boy and a 26-year-old man) who presented to the hospital 69 and 95 hours, respectively, after being bitten by Echis ocellatus. Despite administration of antivenom, both patients died within 2 days after presentation (Einterz & Bates, 2003).
c) CASE REPORT: Bilateral ptosis developed in a young adult following an Echis pyramidum (carpet viper) bite. Symptoms developed within the first 3 days and resolved within one week following antivenom administration and supportive care (Gillissen et al, 1994). d) CASE REPORT: A research scientist developed facial and tongue numbness after using her bare hands to remove residual petroleum jelly from a dish that had previously contained dendrotoxin and then rubbing her eye. Dendrotoxin is derived from the venom of the green mamba (Dendroaspis angusticeps). Weakness on superior gaze and tongue fasciculations were present. Signs and symptoms resolved within 12 hours (Munday et al, 2003). e) CASE REPORT: A 40-year-old man experienced uncontrolled movements of his arms and legs, faintness, tremors, dyspnea, tachycardia, and sweating approximately 2.5 hours after being bitten on the finger of his right hand by a blunt-nosed viper (M. lebetina lebetina). The symptoms spontaneously disappeared 20 minutes later (Gocmen et al, 2006). B) CEREBRAL HEMORRHAGE 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Thrombosis has been reported following viper exposure infrequently and has produced hemorrhagic and ischemic stroke (Rebahi et al, 2014; Aissaoui et al, 2013; Pugh & Theakston, 1987).
b) CASE REPORT 1) CERASTES CERASTES (Desert-horned or Egyptian sand viper): Three patients developed acute ischemic cerebrovascular events after severe envenomation by C. cerastes vipers (Rebahi et al, 2014). a) A 32-year-old woman was bitten by a horned viper on her hand and the following day developed tonic-clonic seizures. Upon admission she had a Glasgow Coma Scale score of 12 and spontaneous bleeding of the gums. Her CNS function further declined (GCS 8) and she was electively intubated and ventilated. Two days after envenomation, a CT of the brain showed an extensive infarction of the brain including frontal, temporal, and parietal lobes with cerebral edema. She also had laboratory evidence of disseminated intravascular coagulation. Despite supportive care, her CNS function did not improve and she died (Rebahi et al, 2014).
b) A 5-year-old girl was hospitalized with confusion, polypnea, and compartment syndrome in her lower limb 4 days after being bitten by a C. cerastes viper. She required immediate intubation and ventilation. Coagulation studies were abnormal. A CT scan of the brain showed an extensive frontal-parieto-occipital ischemic stroke. Although she received supportive care, her neurologic function continued to decline and she died on day 7 (Rebahi et al, 2014).
c) A 51-year-old man was bitten by a C. cerastes viper and early on developed compartment syndrome of his right limb, hemodynamic shock, rhabdomyolysis and hyperkalemia. He also had evidence of DIC. A fasciotomy was performed and 48 hours later his neurologic function declined and his Glasgow Coma Scale score dropped to 10. A CT scan of brain showed acute bilateral cerebral infarctions in internal capsules. He was intubated and ventilated and successfully extubated on day 7. He gradually recovered and his neurologic function was normal at 3 months (Rebahi et al, 2014).
2) ECHIS CARINATUS (carpet viper): A 65-year-old woman who arrived several hours after receiving a bite by an E. carinatus (carpet viper) was drowsy on admission and later died from a subarachnoid hemorrhage (Pugh & Theakston, 1987). C) PARESTHESIA 1) WITH POISONING/EXPOSURE a) CASE REPORT: Paresthesias, extending to the mid-wrist, occurred in a 43-year-old man who was bitten on his left thumb by B. gabonica (gaboon viper) (Marsh et al, 2007).
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Gastrointestinal |
3.8.2) CLINICAL EFFECTS
A) NAUSEA, VOMITING AND DIARRHEA 1) WITH POISONING/EXPOSURE a) Generalized symptoms of nausea, vomiting, abdominal pain or diarrhea may be present after a viper envenomation (Valenta et al, 2008; Marsh et al, 2007; Mebs et al, 1998; Warrell, 1995; Pugh & Theakston, 1987).
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Genitourinary |
3.10.2) CLINICAL EFFECTS
A) ACUTE RENAL FAILURE SYNDROME 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Acute renal failure has been reported after bites by vipers (e.g., Echis pyramidum {carpet viper})(Gillissen et al, 1994), and is characteristic of severe envenomation (Warrell, 1995).
b) CASE REPORTS 1) E. pyramidum (carpet viper): Renal impairment (serum creatinine (mg/dL) 1.1 on admission increasing to 4.8 on hospital day 3 and blood urea (mg/dL) of 7 increasing to 70 on hospital day 4) was reported in a 22-year-old man after envenomation by a carpet viper. Laboratory studies improved within 7 days of envenomation and dialysis was not necessary (Gillissen et al, 1994).
2) Atheris chlorechis (Western bush viper): Thrombocytopenia, severe coagulopathy with profound blood loss, and acute renal failure occurred in a 26-year-old man who was bitten on his left index finger by a Western bush viper (A. chlorechis). Laboratory analysis revealed a urea level and a serum creatinine level that peaked at 17.2 mmol/L (normal 3.3 to 6.7 mmol/L) and 314 mcmol/L (normal 62 to 106 mcmol/L), respectively, at approximately 17.5 hours post-envenomation. Following antivenom administration and supportive treatment, including hemodialysis, the patient gradually recovered (Top et al, 2006).
3) Proatheris superciliaris: A 57-year-old man developed oliguria (10 to 15 mL/hour) following envenomation by a Lowland swamp viper (P. superciliaris). Laboratory data revealed serum creatinine and BUN levels that peaked at 617 mcmol/L and 25.3 mmol/L, respectively, 8 days post-envenomation. Following continuous venovenous hemodiafiltration (CVVHDF) and intermittent hemodialysis, the patient gradually recovered (Valenta et al, 2008). Another patient developed renal insufficiency with oliguria, elevated serum creatinine and BUN levels, and hemoglobinuria following envenomation by P. superciliaris. The patient's renal function gradually improved following daily plasmapheresis treatments over a 7-day period (Keyler, 2008).
B) BLOOD IN URINE 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Hematuria may develop in victims of viper envenomations with severe coagulopathy or thrombocytopenia (Pugh & Theakston, 1987).
b) CASE REPORTS 1) C. maculatus (Western rhombic night adder): Transient hematuria has been reported in victims of C. maculatus bites; no intervention was required and hematuria resolved spontaneously (Pugh & Theakston, 1987).
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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.
3.13.2) CLINICAL EFFECTS
A) BLOOD COAGULATION PATHWAY FINDING 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Coagulopathy with thrombocytopenia, prolonged PT/INR and PTT, increased fibrin degradation products and decreased fibrinogen are common manifestations of moderate to severe envenomation. Coagulation disorders that are produced by vipers are usually reversed when antivenom is administered promptly (Marsh et al, 2007; Hantson et al, 2003; Pugh & Theakston, 1987; Warrell, 1995).
2) CASE REPORT: A 57-year-old man developed coagulopathy with a prolonged PT/INR and a decreased fibrinogen concentration, thrombocytopenia, and hemolysis after being bitten by Proatheris superciliaris. There is no specific antivenom available; the patient's laboratory values normalized following administration of fresh frozen plasma, platelets and packed red cells (Valenta et al, 2008).
3) CASE REPORT: A 34-year-old man was bitten by a green bush viper (Atheris squamiger) and within 90 minutes developed coagulopathy with a prolonged PT (greater than 100 sec; normal 15 to 20 sec) and PTT (greater than 180 sec; normal 26 to 40 sec) and a decreased plasma fibrinogen concentration (less than 0.5 g/L; normal 1.5 to 3 g/L), thrombocytopenia, and leukocytosis. No specific antivenom was available; the patient gradually recovered following supportive therapy (Mebs et al, 1998).
B) THROMBOCYTOPENIC DISORDER 1) WITH POISONING/EXPOSURE a) SUMMARY 1) Thrombocytopenia has developed after viper envenomations (Keyler, 2008; Valenta et al, 2008; Top et al, 2006; Mebs et al, 1998; Pugh & Theakston, 1987).
2) CASE SERIES: In a review of 13 victims of E. carinatus envenomation, only 2 developed mild symptoms of thrombocytopenia (Pugh & Theakston, 1987).
C) ECCHYMOSIS 1) WITH POISONING/EXPOSURE a) CASE REPORTS 1) Twenty hours after a snake bite on the finger (antivenom not available), ecchymosis extended into the axilla and chest wall of a man envenomated by a B. arietans (puff adder). No further progression of ecchymosis occurred after receiving antivenom (Bey et al, 1997).
2) Ecchymosis was reported in two patients following envenomation by a B. gabonica (gaboon viper) (Marsh et al, 2007). In one of the patients, a 43-year-old man, the ecchymosis was localized, occurring at the base of the left thumb. In the other patient, a 33-year-old woman who was found dead approximately 3 days following envenomation, the ecchymosis was more generalized, appearing at the head, trunk, and extremities, indicating extensive internal bleeding.
3) Ecchymoses of the upper arm, deltoid, and pectoral areas were reported in a 33-year-old man who was bitten on his left hand by M. lebetina (levantine viper) (Sharma et al, 2008).
D) HEMORRHAGE 1) WITH POISONING/EXPOSURE a) SUMMARY: Hematological effects can result in bleeding from multiple sites (e.g., bleeding gums, hemoptysis, hematemesis, rectal bleeding, melena, hematuria, vaginal bleeding, and bleeding from old wound sites or venipuncture sites) (Marsh et al, 2007; Top et al, 2006; Einterz & Bates, 2003; Gillissen et al, 1994). The Echis species can produce spontaneous bleeding and incoagulable blood (Pugh & Theakston, 1987) (Mebs et al, 1988). 1) INCIDENCE: In a small case series of 26 viper bites, all victims of an E. carinatus bite developed spontaneous bleeding; the mean onset was 8 hours after the bite with a range of 0.5 to 25 hours. The most frequent site of bleeding was the gingival sulcus (Pugh & Theakston, 1987).
b) CASE REPORTS 1) ECHIS a) E. pyramidum (carpet viper) - Moderate bleeding from the gums, gastrointestinal tract, urinary tract, trachea and injection sites was reported in a 22-year-old man 24 hours after receiving a bite from a carpet viper. The bleeding persisted for 4 days. Despite antivenom administration the patient required two blood transfusions to correct the anemia (Hgb 14.3 g/dL on admission to 6.9 g/dL on the 8th day after the bite). Symptoms stabilized and the patient was discharged on day 17 (Gillissen et al, 1994). b) In a case series of 13 victims of E. carinatus bites that responded to antivenom therapy, all patients had incoagulable blood at the time of admission with normal clotting occurring 12 to 54 hours after antivenom administration; spontaneous bleeding stopped between 2 and 20 hours after antivenom therapy. 1) In patients with delayed or failed response to antivenom administration, spontaneous bleeding continued in 6 of 7 patients up to 36 hours after admission (Pugh & Theakston, 1987).
c) In a series of 59 patients who were bitten by E. ocellatus, 5 patients who presented 2 hours or less after envenomation were not bleeding at the time of presentation, 14 of 22 patients (64%) presenting 2 to 5 hours after envenomation were bleeding, and 25 of 32 patients (68%) presenting 6 hours or more after envenomation were bleeding at the time of presentation (Einterz & Bates, 2003). All 8 patients who died presented with life threatening complications related to bleeding, 5 with neurologic findings suggesting intracranial or meningeal bleeding, 3 with intra-abdominal or gastrointestinal bleeding, and 1 with acute airway obstruction from tongue and sublingual bleeding. 2) Bitis gabonica (gaboon viper): A 55-year-old man with suspected gaboon viper envenomation developed hypotension, severe coagulopathy (fibrinogen not measurable, D-dimer 8,000, INR >7), anemia (hematocrit 16%), and multiple hematomas, bleeding at puncture sites and hemoperitoneum. Coagulopathy did not correct with administration of 8 units fresh frozen plasma and 2 grams of fibrinogen, but rapidly corrected after 2 vials of trivalent antivenom (Hantson et al, 2003). 3) Atheris chlorechis (Western bush viper): A 26-year-old man developed severe coagulopathy (PT greater than 120 sec; APTT greater than 200 sec) and blood loss approximately 7 hours after being bitten on his left index finger by a Western bush viper (Atheris chlorechis) and following performance of two fasciotomies. The patient's lab values normalized following treatment with fresh frozen plasma; however, his bleeding progressively worsened, with a blood loss of approximately 5 liters during the first six hours of his stay in ICU. His hemoglobin level and platelet count declined to a low of 3.7 mmol/L (normal 8.7 to 10.6 mmol/L) and 19 x 10(9)/L (normal 150 to 350 x 10(9)/L), respectively. Following administration of the antivenom, given approximately 12 hours post-envenomation, the patient's blood loss slowly diminished over the next several days (Top et al, 2006). E) DISSEMINATED INTRAVASCULAR COAGULATION 1) WITH POISONING/EXPOSURE a) CERASTES VIPERA (Sahara sand viper): A 3-year-old boy was bitten on the foot by a C. vipera (the snake was killed and identified at the hospital) and admitted 3 hours after exposure in generally good condition with a slightly elevated heart rate (122 beats/min). His foot was markedly swollen with blood oozing from the bite site. However, his foot continued to swell and his initial coagulation studies were abnormal. By the end of day 1, hemoglobin was 9.1, PT and PTT were immeasurably prolonged and reduced platelets were present along with oozing observed from the venipuncture site along with hematemesis and rectal bleeding consistent with disseminated intravascular coagulation (DIC). Treatment included fresh frozen plasma (FFP), cryoprecipitate, vitamin K, packed cells and IV platelets in repeated doses for 5 days. Despite repeated administration of blood products, coagulation studies remained abnormal requiring a total exchange transfusion (1200 mL of fresh blood) 3 days after envenomation. The child gradually improved and coagulation studies returned to normal 6 days after the bite. Polyvalent antivenom (a specific antivenom was not available) did not arrive until after the child had clinically improved and was not administered (Lifshitz et al, 2000).
b) CERASTES CERASTES: A 32-year-old woman was bitten by a horned viper on her hand and the following day developed tonic-clonic seizures. Upon admission she had a Glasgow Coma Scale score of 12 and spontaneous bleeding of the gums. Her CNS function further declined (GCS 8) and she was electively intubated and ventilated. Two days after envenomation, a CT of the brain showed an extensive infarction of the brain including frontal, temporal, and parietal lobes with cerebral edema. She also had laboratory evidence of disseminated intravascular coagulation. Despite supportive care, her CNS function did not improve and she died (Rebahi et al, 2014).
c) CERASTES CERASTES: A 51-year-old man was bitten by a C. cerastes viper and early on developed compartment syndrome of his right limb, hemodynamic shock, rhabdomyolysis and hyperkalemia. He also had evidence of DIC. A fasciotomy was performed and 48 hours later his neurologic function declined and his Glasgow Coma Scale score dropped to 10. A CT scan of brain showed acute bilateral cerebral infarctions in internal capsules. He was intubated and ventilated and successfully extubated on day 7. He gradually recovered and his neurologic function was normal at 3 months (Rebahi et al, 2014).
F) LEUKOCYTOSIS 1) WITH POISONING/EXPOSURE a) Leukocytosis may occur after viper envenomation. Bites by the E. carinatus (carpet viper) have resulted in neutrophil leukocytosis (Pugh & Theakston, 1987).
b) INCIDENCE: In a review of 13 patients with E. carinatus envenomation, 5 developed neutrophil leukocytosis (greater than 7600 mm(-3)) (Pugh & Theakston, 1987).
c) CASE REPORT: Leukocytosis was reported in a 34-year-old man approximately 90 minutes following envenomation by a green bush viper (Atheris squamiger). The leukocyte count gradually decreased after reaching a peak of 22,100/ mcL (Mebs et al, 1998).
G) THROMBOTIC MICROANGIOPATHY 1) WITH POISONING/EXPOSURE a) CASE REPORT: 27-year-old man was bitten by Proatheris superciliaris and subsequently developed microangiopathic hemolysis, thrombocytopenia, schistocytosis, an elevated LDH, and worsening renal function, all of which is consistent with a diagnosis of thrombotic microangiopathy. The patient gradually improved with daily plasmapheresis treatments over a 7-day period (Keyler, 2008).
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Dermatologic |
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 (Keyler, 2008; Valenta et al, 2008; Top et al, 2006; Bey et al, 1997). Swelling may be localized or progress to involve the entire affected limb and include the regional lymphatic system (Marsh et al, 2007; Meier & White, 1995a; Gillissen et al, 1994; Bey et al, 1997).
b) REGIONAL EFFECTS 1) B. arietans (puff adder): A 35-year-old man was bitten on his finger by a juvenile puff adder and developed immediate pain followed by edema and swelling which started minutes later. Due to a delay in antivenom administration, edema and ecchymosis extended into the axilla and chest wall over the next 20 hours; signs and symptoms responded to antivenom administration (Bey et al, 1997).
2) B. arietans (puff adder): A 50-year-old woman was admitted 16.5 hours after receiving a bite on the leg by a B. arietans and developed swelling in the entire leg with blistering and bruising around the bite site. Antivenom was given; blistering and swelling improved by the fourth day (Pugh & Theakston, 1987).
3) Macrovipera lebetina lebetina (blunt-nosed viper): A 40-year-old man was bitten on the finger of his right hand by a blunt-nosed viper (M. lebetina lebetina) and immediately experienced swelling of the finger. Within 3 hours post-envenomation, the swelling extended to the middle of his right arm. Antivenom was not available; the patient recovered with supportive care (Gocmen et al, 2006). Another patient, a 33-year-old man, who was also bitten by M. lebetina on his little finger of his left hand, developed swelling at the bite site that continued to progress from his left hand and arm to the left pectoral region over a period of 48 hours. Fasciotomy of the hand was performed in order to prevent ischemic damage (Sharma et al, 2008).
c) LOCALIZED EFFECTS 1) Bitis schneideri (Namaqua dwarf adder): An adult was bitten on the finger by a Namaqua dwarf adder and developed localized swelling of the finger and hand with only tenderness occurring in the axillary lymph node region. Swelling and pain remained and gradually lessened over days 5 through 14 with complete healing at 2 weeks. Supportive care included elevation, analgesics, and antibiotic therapy; antivenom was not used (Hurrell, 1981).
2) C. maculatus (Western rhombic night adder) - Local swelling occurred within 15 minutes of envenomation in 3 patients exposed. The authors noted that symptoms were limited to local pain and swelling only; symptoms resolved spontaneously without antivenom (Pugh & Theakston, 1987).
3) A 27-year-old man was bitten on his left index finger by Proatheris superciliaris and developed immediate swelling that extended to the dorsum of his right hand and up to the crease in his wrist (Keyler, 2008).
B) PAIN 1) WITH POISONING/EXPOSURE a) SUMMARY: Envenomation by vipers and adders usually produce immediate intense local pain (Hurrell, 1981; Pugh & Theakston, 1987; Bey et al, 1997; Top et al, 2006; Marsh et al, 2007; Keyler, 2008).
C) BLISTERING ERUPTION 1) WITH POISONING/EXPOSURE a) Local blistering may occur within 24 hours of a viper envenomation. 1) INCIDENCE: In a series of 26 patients with snakebites by E. carinatus, B. arietans, or C. maculatus, 3 patients (12%) developed local blistering (Pugh & Theakston, 1987).
D) SKIN NECROSIS 1) WITH POISONING/EXPOSURE a) Tissue necrosis can occur after viper envenomation and may require surgical debridement (Pugh & Theakston, 1987; Bey et al, 1997) or amputation (Sharma et al, 2008). Necrosis appears to be more prevalent after bites sustained on fingers or toes (Bey et al, 1997).
b) CASE REPORT: A 26-year-old man who was bitten on his left index finger by a Western bush viper (Atheris chlorechis) developed a small necrotic area at the bite site (Top et al, 2006).
c) CASE REPORT: A 27-year-old man was bitten on his left index finger by Proatheris superciliaris and, 36 hours later, developed necrosis from the base of the fingernail to the proximal interphalangeal joint. The necrosis remained localized, but required debridement and irrigation with saline and antibiotics (Keyler, 2008).
E) SWEATING 1) WITH POISONING/EXPOSURE a) CASE REPORT: A 40-year-old man experienced uncontrolled movements of his arms and legs, faintness, tremors, dyspnea, tachycardia, and sweating approximately 2.5 hours after being bitten on the finger of his right hand by a blunt-nosed viper (M. lebetina lebetina). The symptoms spontaneously disappeared 20 minutes later (Gocmen et al, 2006).
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Musculoskeletal |
3.15.2) CLINICAL EFFECTS
A) COMPARTMENT SYNDROME 1) WITH POISONING/EXPOSURE a) Compartment syndrome is more likely to occur, especially in the anterior tibial fascial compartment, following bites in which venom is injected into a tight fascial compartment (Warrell, 1995). Compartment syndrome has been reported in 2 patients bitten by C. cerastes (Desert horned or Egyptian sand vipers) (Rebahi et al, 2014). b) CASE REPORT: A 16-year-old girl living in Kokstad was bitten by a B. arietans (puff adder) in both upper extremities (left finger and right hand) while sleeping and developed loss of sensory function, loss of opposition of the thumb and almost no movement at the joints. Polyvalent antivenom was given approximately 2 hours (upon hospital arrival) after envenomation. 1) The clinical impression of raised intracompartmental pressure (measuring of intracompartmental pressures was not possible at this hospital) was made. Bilateral carpal tunnel release was performed with operative findings of clotted blood found under the palmar fascia with edema at the carpel tunnel and cyanotic appearance of the nerve; 35 days after surgery the patient had full motor and sensory function of both hands (Schweitzer & Lewis, 1981).
c) CASE REPORT: A 15-year-old boy sustained a suspected puff adder (Bitis arietans) bite above the right ankle and presented 15 hours after envenomation with severe swelling of the leg into the chest wall, hypotension, anemia, and coagulopathy. The leg was tense below the knee with no pedal pulses. He was resuscitated with fluid and blood products and then developed severe hypotension after an attempt to administer antivenom. Antivenom was stopped and he received a four-compartment below-knee fasciotomy and an anterior thigh fasciotomy. Blood flow to the leg was not restored until the inguinal ligament was divided. He survived able to ambulate with a walking aid but lost most of the musculature of the anterior and peroneal compartments (Blaylock, 2003). |
Reproductive |
3.20.1) SUMMARY
A) Limited data are available regarding the effects of venom and antivenom on a human fetus. The risk of snake antivenom therapy in pregnancy is not available. Exposure may result in teratogenesis; mice and chicken embryos showed evidence of teratogenic effects after exposure to snake venom.
B) In a series of 10 pregnant women, who were bitten by E. ocellatus in their 20th to 36th week of gestation, all patients survived with antivenom therapy and supportive care; fetal loss was reported in only one of the 10 patients.
3.20.2) TERATOGENICITY
A) LACK OF INFORMATION 1) Limited data are available regarding the effects of venom and antivenom on a human fetus. Exposure may result in teratogenesis; mice and chicken embryos showed evidence of teratogenic effects after exposure to snake venom (Pantanowitz & Guidozzi, 1996).
3.20.3) EFFECTS IN PREGNANCY
A) LACK OF INFORMATION 1) Limited data are available regarding the effects of venom and antivenom on a human fetus; the risk of snake antivenom therapy in pregnancy is not available. In general, antivenom is recommended in pregnant women with systemic or progressive local effects of envenomation, especially in cases of coagulopathy because of the increased risk of bleeding (e.g., disseminated intravascular coagulopathy) associated with a depression of the fibrinolytic system that occurs normally during pregnancy (Pantanowitz & Guidozzi, 1996). 2) At the time of this review, it is unclear whether different types of venom, varying amounts of venom or routes of exposure have any effect on the developing fetus (Pantanowitz & Guidozzi, 1996). 3) ANIMAL STUDIES a) In animal studies, the isolated rat uterus was exposed to B. arietans venom and developed both increased frequency and amplitude of uterine contractions (Pantanowitz & Guidozzi, 1996).
B) STILLBIRTH 1) CASE REPORT - Stillbirth was reported in a 17-year-old girl who was 24 weeks pregnant and was bitten by E.ocellatus (carpet viper). The patient presented 6 days post-envenomation with severe swelling, anemia, epistaxis, melena, and bleeding at the gums. There were no fetal heart sounds at presentation. With antivenom therapy and supportive care, the patient recovered. It is believed that the delay in presentation may have directly contributed to the resulting stillbirth (Habib et al, 2008).
C) LACK OF EFFECT 1) In a series of 10 pregnant women, who were bitten by E. ocellatus, in their 20th to 36th week of gestation, all patients survived with antivenom therapy and supportive care; fetal loss was reported in only one of the 10 patients. It is believed that delayed presentation by the patient (6 days post-envenomation) may have contributed to the outcome (Habib et al, 2008).
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