Studies

Hardy 1983: 15 Crotalus scutulatus scutulatus bites; identification: morphological by the author (13/15), photographed dead snakes were identified by the author (2/15). All 15 accidents occurred in southern Arizona. Patients were treated in hospitals in Tucson, Phoenix and Wickenburg. In geographical terms, 12/15 patients were bitten by "type B" snakes, 2 by snakes in the borderland between "type A" and "type B" and 1 by a "type A" snake (this was the only patient to have neurological symptoms: ptosis, see below).

Classification:

• only local envenoming 8/15,
• systemic envenoming (arterial hypotension, plasma fibrinogen ↓, FSP ↑, platelets ↓, neurotoxic signs of envenoming) 8/15.

Case reports

Rhoten and Gennaro 1968: 1 Crotalus scutulatus scutulatus bite; identification: morphological.

Clark et al 1997: 1 Crotalus scutulatus scutulatus bite; identification: morphological.

 

Geographical variation in venom composition and associated symptoms

"Type A": venom contains "Mojave toxin", a presynaptically active neurotoxin, but no proteolytic or haemorrhagic components (Glenn et al. 1983).

"Type B": venom does not contain "Mojave toxin", but does have proteolytic and haemorrhagic components (Glenn et al. 1983).

Signs & symptoms

Autopharmacological effects

Hypotension: adults <80 mmHg systolic, children (<6 years) <60 mmHg systolic upon admission to hospital (3/15) (Hardy 1983).

Nausea, vomiting, uncontrollable bowel movements (Rhoten and Gennaro 1968).

Local effects

Strong local pain (Rhoten and Gennaro 1968).

Swelling, local to a maximum extending from the bitten extremity to the trunk 15/15, local ecchymosis 10/15, blistering 6/15, necroses 3/15 (Hardy 1983).

Swelling of the entire bitten extremity. Regional lymph node enlargement (Rhoten and Gennaro 1968).

Edema and tenderness of the bitten finger, the hand and the distal forearm and lymphangitis and tenderness to the axilla within 1 hour after the bite (Clark et el 1997).

Haemostatic effects

See below, "Laboratory and physical investigations".

Neurological effects

Ptosis 1/15. Commencing 36 h after the bite, duration 18 h (this patient, a 4-year-old boy, had only swelling locally and no ecchymosis or blistering) (Hardy 1983). Within 5 minutes after the bite oral and facial paesthesia, within further 30 minutes onset of fasciculations and weakness of the tongue, arms, hands and legs. On arrivel in the emergency department 1 hour after the bite dysphasia, fasciculation of the face, tongue and all extremities (Clark et al 1997).

Morbidity

Sequelae were confined to necroses on the fingers where the bite had occurred. Outcome in 3/15 patients who developed necroses: amputation of a finger 1/3, contracture of a finger (patient refused medical treatment) 1/3, primary healing 1/3 (Hardy 1983).

Case fatality rate

0/15 (Hardy 1983).

Laboratory and physical investigations

1. Haemostasis
Type of haemostatic defect
Fibrin(ogen)olytic activity in vitro (Denson et al. 1972).

Haemostatic parameters

Overview haemostasis

B

H

CT

(FSP)

Tc

PT

aPTT

TT

I

FSP

D

II

V

VIII

X

XIII

PC

ATIII

PI

tPA

α2AP

C

A

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	Fibrinogen: slight decrease 3/13 (Hardy 1983).
B	FSP: increased 3/6 (Hardy 1983).
C	Platelets: decreased 2/13 (Hardy 1983). Thrombopaenia (Rhoten and Gennaro 1968, Clark et el 1997).

2. Renal function values

Creatinine increased 1/15; 1.8 mg/dl 14 h after the bite, 0.8 mg/dl 42 h after the bite (normal value 0.3–1.3 mg/dl). The patient was hypotensive upon admission to hospital (Hardy 1983). Obviously pre-renal cause of the renal dysfunction.

Treatment (symptomatic)

Arterial hypotension: i.v. fluid replacement (15/15) and antivenom rapidly improved the arterial hypotension (Hardy 1983).

Treatment (specific)

Antivenoms

1. Crotalidae Polyvalent Immune Fab Antivenom, ovine (immunized with Crotalus adamanteus, Crotalus atrox, Crotaus scutulatus ssp. and Agkistrodon piscivorus) / CroFab™, Savage Laboratories, Melville, New York

 

see Crotalus sp.

 

Case report

Initial dose 6 vials of antivenom: during the infusion of antivenom substantial decrease of paresthesia and fasciculations. Return of normal speech. By the time the infusion of the second 6 vials had been completed, fasciculation had disappeared. Platelet count returned to normal within one hour after antivenom infusion. Follow-ups on day 2, 4 and 12 after discharge: full resolution of all symptoms and signs of envenomation (Clark et al 1997).

 

2. Wyeth antivenom (Crotalidae), polyvalent, Philadelphia, USA (no longer in use)

Studies

Clinical experiences are reported in the work of Hardy 1983: 13/15 received antivenom. Antivenom treatment was commenced on average 3.4 h after the bite. Mean dose administered 7.8 vials (Hardy 1983).

Efficacy

1. Only slight effect on neurological effects of the venom (Glenn and Straight 1978). Production of an antivenom including "venom A" or "Mojave toxin" would be useful (Glenn et al. 1983).
2. The current state of knowledge does not enable any conclusions with regard to the effect on haemostatic defects (Hardy 1983).

Adverse reactions

Acute: generalised urticaria and hypotension 1/13, urticaria, cramping abdominal pain, bradycardia 1/13.

Delayed: serum sickness 4/13; no symptoms 2/13, no details 7/13 (Hardy 1983).