VAPAGuide - Biomedical database - Terrestrial snakes, Pit vipers - Bothrops spp.

Clinic

Bothrops asper

Studies

Mexico, Costa Rica, Belize, Guatemala, Nicaragua

Hardy 1992c: 9 B. asper bites; identification: morphological. Mexico 4/9, Costa Rica 2/9, Belize 1/9, Guatemala 1/9, Nicaragua 1/9.
Classification based on local and systemic effects of envenoming:

No envenoming 1/9.
Mild envenoming 0/9.
Moderately severe envenoming 2/9.
Severe envenoming 6/9.

Case reports

Canal Zone

Jutzy et al. 1953: 2 cases; identification morphological.

Sass 1979: 1 case; identification criteria not given.

Costa Rica
Clark 1928: 3 cases; identification morphological.
Rotter 1938: 3 cases; identification: very probably B. asper.

Guatemala
Clark 1928: 1 case; identification morphological.

Honduras
Phelps 1926: 1 case; identification morphological.
Nutter 1926: 3 cases; identification morphological.

Panama
Clark 1928: 1 case; identification morphological.
Kornalik and Vorlova 1990: 1 case; identification morphological; 2-month-old snake; no antivenom treatment; replacement therapy and plasmapheresis.

Regional differences in symptoms of envenoming

No comparative clinical studies available. However, large regional differences in venom composition between Atlantic and Pacific populations lead to an expectation of differences in the clinical effects of the venoms (Aragon and Gubensek 1981).

Effect of ontogenetic differences in venom composition on the symptoms of envenoming
See below, 1. Haemostasis.

Signs & symptoms

Autopharmacological effects

Vomiting 3/4 (Nutter 1926, Phelps 1926).

Local effects

Minimal local effects (Kornalik and Vorlova 1990).

Local pain, marked local swelling, sometimes affecting the whole extremity (4/4). In one patient swelling of the whole leg within 2 h; local necrosis 1/4 (Nutter 1926; Phelps 1926).

Marked local swelling, sometimes affecting the whole extremity (4/5), blistering 1/5 (Clark 1928).

Minimal local swelling (venom was probably injected directly into the saphenous vein) (Sass 1979).

Haemostatic effects

Gingival bleeding, haemoptysis, haematuria (starting 4 h after the bite); duration of the haemostatic defect 12 days (Kornalik and Vorlova 1990).

Gingival bleeding 3/4, haematemesis 2/4 (Nutter 1926, Phelps 1926).

Other signs & symptoms

Generalised cerebral seizures (venom was probably injected directly into the saphenous vein) (Sass 1979).

Morbidity

Irreversible local damage (3/9), 1 of these 3 patients had to have an amputation of the lower leg; all patients who had signs of envenoming had received antivenom (Hardy 1992c).

Local necrosis (1/4); all patients had received antivenom (Nutter 1926, Phelps 1926). Irreversible damage seems to occur particularly in those patients who have a very tight tourniquet applied (Sass 1979) (Sass argues on the basis that 90% of the bites he observed could be attributed to B. asper).

Case fatality rate

0/9; all patients with signs of envenoming had received antivenom (Hardy 1992c).
0/4; all had received antivenom (Nutter 1926, Phelps 1926).
1/5; this patient had received antivenom (Clark 1928).

3 fatalities (autopsy findings: intracranial haemorrhage 2/3, in 1 of these 2 patients bleeding in the renal pelvis of both kidneys was also found) (Rotter 1938).

2 fatalities (autopsy findings: intracranial haemorrhage 1/2, gastrointestinal bleeding 1/2) (Jutzy et al. 1953).

Laboratory and physical investigations

1. Haemostasis
Studies
Costa Rica
Barrantes et al. 1985: 18 B. asper bites.
Classification:

asymptomatic: no symptoms or very minor local swelling (3/18),
mild envenoming: marked local swelling, no bleeding (4/18),
moderately severe envenoming: local swelling with necrosis, bleeding (4/18),
severe envenoming: local swelling with necrosis and bleeding as well as additional vascular damage (7/18).

Type of haemostatic defect

Venom composition varies between juvenile and adult Bothrops spp. (Meier 1986, Kornalik and Taborska 1988).

Juvenile B. asper: defibrinogenation via prothrombin activation with secondary fibrinolysis (Hofmann and Bon 1987, Kornalik and Vorlova 1990).

Adult B. asper: defibrinogenation via direct fibrinogen-coagulating (thrombin-like) activity with secondary fibrinolysis (Kornalik and Vorlova 1990).

The haemorrhagins contained in the venom appear to have a chiefly local effect and to not contribute systemically to an increase in the risk of haemorrhage (Kornalik and Hladovec 1989, Kornalik and Vorlova 1990).

Haemostatic parameters

Overview haemostasis

(FSP)

aPTT

FSP

VIII

XIII

ATIII

tPA

α₂AP

Essential

bed-side

tests

Tests for full clinical assessment

Tests for research purposes

H	haemorhagic effects
+	definite evidence in human envenoming
CT	full blood clotting test
(FSP)	FSP rapid test
Tc	platlets
PT	prothrombin time
aPTT	partial thromboplastin time

TT	thrombin time
I	fibrinogen
FSP	fibrinogen split products
D	D-dimer
II, V, VII, X, XIII
	clotting factors
PC	protein C
ATIII	antithrombin III

PI	plasminogen
tPA	tissue plasmin activator
α₂AP	α₂-antiplasmin

In this overview, the deviations from normal are recorded for those haemostasis para- meters only, for which good evidence is documented in the literature.

A	Clotting time ↑.
B	PT, aPTT: Asymptomatic 3/18: PT 80 ± 20%; aPTT 51 ± 6 s (Barrantes et al. 1985). Mild envenoming 4/18: PT 38 ± 48%; aPTT 167 ± 154 s (Barrantes et al. 1985). Moderately severe envenoming 4/18: PT 12 ± 24%; aPTT 242 ± 117 s. (Barrantes et al. 1985). Severe envenoming 7/18: PT 21 ± 26%; aPTT 199 ± 127 s (Barrantes et al. 1985). PT and aPTT ↑; normalisation from the 8th day after the bite (no antivenom treatment; replacement therapy and plasmapheresis) (Kornalik and Vorlova 1990).
C	Fibrinogen: "Asymptomatic" 3/18: 101 ± 40 mg/100 ml (normal: 290 ± 60 mg/100 ml) (Barrantes et al. 1985). Mild envenoming 4/18: 85 ± 100 mg/100 ml (normal: 290 ± 60 mg/100 ml) (Barrantes et al. 1985). Moderately severe envenoming 4/18: 9 ± 0.5 mg/100 ml (normal: 290 ± 60 mg/100 ml) (Barrantes et al. 1985). Severe envenoming 7/18: 64 ± 99 mg/100 ml (normal: 290 ± 60 mg/100 ml) (Barrantes et al. 1985). Fibrinogen <0.5 g/l; continuous increase in fibrinogen from the 8th day after the bite, normal levels from the 12th day (no antivenom treatment; replacement therapy and plasmapheresis) (Kornalik and Vorlova 1990) (see also below, Symptomatic treatment).
D	FSP: "Asymptomatic" 3/18: 640 μg/ml (1/3), <10 μg/ml (2/3) (Barrantes et al. 1985). Mild envenoming 4/18: 5,540 ± 10,217 μg/ml (normal <10 μg/ml) (Barrantes et al. 1985). Moderately severe envenoming 4/18: 11,600 ± 19,600 μg/ml (normal <10 μg/ml) (Barrantes et al. 1985). Severe envenoming 7/18: 1,074 ± 1,032 μg/ml (normal <10 μg/ml) (Barrantes et al. 1985). FSP >40 μg/ml (normal <10 μg/ml) (no antivenom treatment; replacement therapy and plasmapheresis) (Kornalik and Vorlova 1990).
E	Platelets: "Asymptomatic" 3/18: >170,000/mm³ (Barrantes et al. 1985). Mild envenoming 4/18: >180,000/mm³ (Barrantes et al. 1985). Moderately severe envenoming 4/18: >195,000/mm³ (Barrantes et al. 1985). Severe envenoming 7/18: >220,000/mm³ (Barrantes et al. 1985). Platelets normal (no antivenom treatment; replacement therapy and plasmapheresis) (Kornalik and Vorlova 1990).
F	Clotting factors: "Asymptomatic" 3/18: II: 66 ± 29% (normal 95 ± 8%); V: 63 ± 35% (normal 95 ± 8%); VIII: 66 ± 12% (normal 100 ± 25%); IX: 70 ± 4% (normal 95 ± 18%); X: 75 ± 30% (normal 95 ± 8%) (Barrantes et al. 1985). Mild envenoming 4/18: II: 71 ± 25% (normal 95 ± 8%); V: 50 ± 36% (normal 95 ± 8%); VIII: 123 ± 46% (normal 100 ± 25%); IX: 77 ± 22% (normal 95 ± 18%); X: 81 ± 19% (normal 95 ± 8%) (Barrantes et al. 1985). Moderately severe envenoming 4/18: II: 16 ± 15% (normal 95 ± 8%); V: 24 ± 19% (normal 95 ± 8%); VIII: 27 ± 14% (normal 100 ± 25%); IX: 61 ± 17% (normal 95 ± 18%); X: 68 ± 17% (normal 95 ± 8%) (Barrantes et al. 1985). Severe envenoming 7/18: II 25 ± 17% (normal 95 ± 8%); V: 41 ± 25% (normal 95 ± 8%); VIII: 70 ± 40% (normal 100 ± 25%); IX: 71 ± 22% (normal 95 ± 18%); X: 70 ± 40% (normal 95 ± 8%) (Barrantes et al. 1985). Factors II, IX and X <20% (Kornalik and Vorlova 1990).
G	Inhibitors: "Asymptomatic" 3/18: ATIII 97 ± 8% (normal 100 ± 10%) (Barrantes et al. 1985). Mild envenoming 4/18: ATIII 84 ± 12% (normal 100 ± 10%) (Barrantes et al. 1985). Moderately severe envenoming 4/18: ATIII 76 ± 15% (normal 100 ± 10%) (Barrantes et al. 1985). Severe envenoming 7/18: ATIII 75 ± 7% (normal 100 ± 10%) (Barrantes et al. 1985).

2. Leucocytes
13,700 ± 5,100/mm³ (Barrantes et al. 1985).

First aid

See comment above in paragraph Morbidity.

Treatment (symptomatic)

Replacement therapy (fibrinogen, cryoprecipitate, vitamin K): cessation of bleeding within 12 h of every administration for 8 h, then renewed bleeding (Kornalik and Vorlova 1990).
Plasmapheresis: appears to have had a sustained effect on improvement of the haemostatic defect (Kornalik and Vorlova 1990).

Treatment (specific)

Antivenoms
Polyvalent antivenom, Instituto Clodomiro Picado, San Jose, Costa Rica;
Antibotropico, Instituto Butantan, São Paulo, Brazil.

Efficacy

With regard to local cytotoxicity: antivenom administration (i.m.) after the bite 5/9, later antivenom administration (i.v.) 8/9, i.e. all patients with signs of envenoming (see above); despite this 3/5 had permanent local damage, one of these patients had to have an amputation of the lower leg (no details regarding which antivenom was used) (Hardy 1992).
With regard to the formation of necroses: administration of antivenom has barely any effect on local swelling and formation of necroses, in particular local myonecroses (Gutierrez 1990, Gutierrez et al. 1981, Gutierrez et al. 1985).
With regard to the haemostatic effect: Polyvalent antivenom, Instituto Clodomiro Picado, San Jose, Costa Rica: 10–20 ml i.m. had no effect on the course of coagulation (13/18) (Barrantes et al. 1985).
Antibotropico, Instituto Butantan, São Paulo, Brazil: fibrinogen increase within hours of antivenom administration; PT and aPTT within the measurable range again within 1–2 h of antivenom administration (Sass 1979).