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Clinic

 

Oxyuranus sp.

Studies

Papua New Guinea
Currie et al. 1992a: 149 O. scutellatus canni bites; identification: detection of venom antigen by ELISA (wound swab, serum, urine). Neurotoxic signs of envenoming were defined as ptosis or a more serious finding, coagulopathy as obvious bleeding and/or non-coagulable blood after 15 min on the whole-blood clotting test:

Classification:

  • clinical signs of envenoming: 110/149,
  • neurotoxic signs of envenoming and coagulopathy: 57/110,
  • only neurotoxic signs of envenoming: 32/110,
  • only coagulopathy: 13/110,
  • only regional lymphadenopathy: 8/110.

Lalloo et al. 1992a:  77 O. scutellatus canni bites; identification: detection of venom antigen by ELISA (wound swab/aspirate, serum) according to the method of Theakston et al. 1977, modified by Ho et al. 1986a; morphological 4/77; 58/77 (75%) of these patients had clinical signs of envenoming.

 

Lalloo et al. 1995:  166 O. scutellatus canni bites; identification: detection of venom antigen by ELISA. Clinical evidence of envenoming 139/166.

Case reports

Australia
Benn 1951:
1 Oxyuranus sp. bite; identification: morphological.
Brigden and Sutherland 1981: 1 Oxyuranus sp. bite; identification: ELISA.
Covacevich et al. 1988:
1 O. microlepidotus bite; identification: morphological.
Flecker 1940: 1 Oxyuranus sp. bite; identification: identity verified with near certainty.
King  and Smith 1991: 1 Oxyuranus sp. bite; identification: ELISA.
Mirtschin et al. 1984:
1 Oxyuranus microlepidotus bite; identification: morphological.
Reid and Flecker 1950: 1 Oxyuranus sp. bite; identification: morphological.
Sutherland et al. 1980: 1 Oxyuranus sp. bite; identification: RIA.
Trinca 1969:
1 O. scutelatus bite; identification: morphological.
White 1987b: 2 Oxyuranus sp. bites; identification: ELISA.
White 1992:
3 Oxyuranus sp. bites; identification: morphological.  

Papua New Guinea
Campbell 1967: 6 O. scutellatus canni bites; identification: morphological 2/6; described by the patient 4/6.

Signs & symptoms

Autopharmacological effects

Vomiting within 85 min (median) 57/95, abdominal pain within 90 min (median) 82/102, headache within 120 min (median) 73/97, collapse within 15 min (median) 23/97 (Currie et al. 1992a).

Nausea 3/3, vomiting 3/3, headache 3/3, collapse and loss of consciousness in the early period after the bite 2/3 (White 1992).

Vomiting 65% (Lalloo et al. 1995).

Local effects

Local lymphadenopathy (84%) (Lalloo et al. 1992a).

Painful lymph nodes within 90 min (median) 99/104 (Currie et al. 1992a).

Local pain 3/3, local swelling 1/3 (White 1992).

Swelling at the bite site 2%, tender lymph node 91% (Lalloo et al. 1995).

Haemostatic effects

Gingival bleeding (17%) (Lalloo et al. 1992a).

Clinically evident bleeding within 105 min (median) 48/110 (Currie et al. 1992a).

Bleeding bite site 7%, systemic bleeding 35% (Lalloo et al. 1995).

Neurological effects

Neurological signs of envenoming (86%), endotracheal intubation and ventilation (26%) (Lalloo et al. 1992a).

Neurological signs of envenoming within 390 min (median) 89/110: ptosis 88/89, ophthalmoplegia 73/89, bulbar paralysis 53/89, endotracheal intubation 32/89, artificial respiration 29/89 (Currie et al. 1992a).

Signs of paralysis 2/3, one of these patients required artificial respiration (White 1992).

Ptosis 85%, ophthalmoplegia 77%, diminished hand grip 58%, in need of intubation and ventilation 37% (Lalloo et al. 1995).

Muscular effects

See Laboratory and physical investigations below.

Cardiac effects

See Laboratory and physical investigations below.

Renal effects

See Laboratory and physical investigations below.

Morbidity

3/77 patients, of whom 58 showed clinical signs of envenoming, had persistent altered sensibility in the area around the bite after being bitten by Oxyuranus scutellatus canni (Lalloo et al. 1992a).

Case fatality rate

1/77 patients, of whom 58 showed clinical signs of envenoming, died after being bitten by Oxyuranus scutellatus canni (Lalloo et al. 1992a).

8/149 patients, of whom 110 showed clinical signs of envenoming, died after being bitten by Oxyuranus scutellatus canni. 6 of the 8 deaths occurred in children <15 years. All fatalities were associated with neurological consequences of envenoming: in connection with delayed endotracheal intubation 5/8; in connection with a blocked endotracheal tube 4/8. All 8 patients had clinical signs of aspiration pneumonia (Currie et al. 1992a).

4.3% (attributable mainly to the use of mechanical ventilation) (Lalloo et al. 1995).

Laboratory and physical investigations

1. Haemostasis
Studies
Lalloo et al. 1992b: 13 Oxyuranus scutellatus canni bites; identification: detection of venom antigen by ELISA (wound swab/aspirate, serum). All patients had non-coagulable blood.

Lalloo et al. 1997: 87 Oxyuranus scutellatus canni bites; identification: detection of venom antigen by ELISA.

 

Type of haemostatic defect
Consumptive coagulopathy (DIC) (defibrin(ogen)ation) (Lalloo et al. 1992b) due to prothrombin activator, whose activity is increased by Ca2+ and phospholipids, but not by factor Va (Denson 1968, Pirkle et al. 1972, Speiger et al. 1986).

Secondary fibrinolysis:

Primary fibrin(ogen)olysis (Marshall and Herrman 1983).

Fibrinogen-coagulating activity (Marshall and Herrman 1983).


Haemostatic parameters

Overview haemostasis
   
A
 
   
B
 
B
 
C
 
 
G
 
H
 
                   
 
H CT (FSP) Tc PT aPTT TT I FSP D II V VIII X XIII PC ATIII PI tPA α2AP
       
 
K
     
 
D
   
 
E
 
E
 
E
 
 
E
 
 
F
 
I
 
 
J
 

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

CT: blood non-coagulable (13/13) (Lalloo et al. 1992b).

B

PT, aPTT: increased or no clot formation (13/13) (Lalloo et al. 1992b).

C

TT: increased or no clot formation (13/13) (Lalloo et al. 1992b).

D

Fibrinogen: <0.2–0.6 g/l (13/13) (controls: 1.70–4.70 g/l) (Lalloo et al. 1992b).

E Clotting factors:
II 47.4 µg/dl  (n = 12) (mean; range 8–66) (controls: 88.7; 69–105),
V 5.4 µg/dl (n = 11) (mean; range 1–13) (controls: 80.2; 27–106),
VIII 10.6 µg/dl (n = 12) (mean; range 1–28) (controls: 74.6; 33–183), 
XIIIA  45.4 µg/dl (n = 10) (mean; range 12–79) (controls: 97.2; 63–135),
XIIIS 65.4 µg/dl (n = 10) (mean; range 45–97) (controls: 81.1; 60–106) (Lalloo et al. 1992b).
F

Inhibitors: ATIII (U/dl) (n = 12): mean 82.8 (range 42–14) (controls: 105.3; 92–125); protein C (U/dl) (n = 12): mean 43.3 (range 25–59) (controls: 107; 66–174) (Lalloo et al. 1992b).

G

FSP: 1,280–5,120 µg/dl (n = 9)  (controls: <10) (Lalloo et al. 1992b).

H

D-dimers: <5–250 µg/dl (n = 10) (controls: <0.2) (Lalloo et al. 1992b).

I

Plasminogen: (U/dl) (n = 13): mean 49 (range 18–72) (controls: 114; 98–147) (Lalloo et al. 1992b).

J

α2-Antiplasmin: (U/dl) (n = 12): mean 45 (range 29–85) (controls: 113.1; 98–163) (Lalloo et al. 1992b).

K

Platelets: <100,000/mm3 (4/10) (Lalloo et al. 1992b).

 

2. Creatinine phosphokinase (CPK)
Frequently elevated (Currie et al. 1992a).

CPK 19,600 IU/l; antivenom administration was greatly delayed in this patient (Brigden and Sutherland 1981).


3. Myoglobinuria

Observed occasionally (Currie et al. 1992a). Myoglobinuria (Brigden and Sutherland 1981).


4. Kidney function

Only a few patients had signs of impaired kidney function; acute renal failure (0/110) (Currie et al. 1992a). Acute renal failure (the patient had rhabdomyolysis) (Brigden and Sutherland 1981).

Impaired kidney function 2/3, one of these two required long-term dialysis (White 1992).

 

5. ELISA

See above.

6. ECG
ECG changes, which could be interpreted as an indication of cardiac effects of the venom, were observed occasionally (Currie et al. 1992a).

First aid

Tourniquets can delay the onset of neurological signs of envenoming and alter the course of the coagulopathy (Currie et al. 1992a).

Treatment (symptomatic)

  1. Endotracheal intubation and assisted/controlled ventilation (Currie et al. 1992a, Lalloo et al. 1992a),
  2.  A combination of clinical and electrophysiological variables was used to assess the effect of edrophonium and 3,4-diaminopyridine in patients with significant neurotoxicity. Both drugs produced minor electrophysiological and clinical changes in envenomed patients. This effect was maximal when the 2 drugs were used in combination, but was insufficient to be of significant clinical benefit. Neither drug can be recommended for use in the management of Papuan taipan bite.(Trevett et al. 1995b).
  3. Dialysis (White 1992, Brigden and Sutherland 1981).

Treatment (specific)

Antivenoms
Polyvalent (Australia-New Guinea), CSL, Parkville, Australia.
 
Studies

Lalloo et al. 1992a:  77 O. scutellatus canni bites; identification: detection of venom antigen by ELISA (wound swab/aspirate, serum); morphological 4/77; 58/77 of these patients had clinical signs of envenoming. 56/58 received antivenom: 13% 2 vials, all others 1 vial. 

Trevett et al. 1995a: 156 O. scutellatus canni bites; identification: detection of venom antigen by ELISA (wound swab/aspirate, serum).

 

Efficacy

  1. With regard to the haemostatic effect: antivenom treatment induced a reversal of the coagulation defect in nearly all patients within 6 h (Lalloo et al. 1992a). No difference was demostrated in the time of restoration of coagulability between the group which received antivenom before or after 4 h after the bite (Trevett et al. 1995a). Specific antivenom raised against Australian taipan venom was effective in stopping spontaneous systemic bleeding and restoring blood coagulability (Lalloo et al. 1995).
  2. With regard to the neurological signs of envenoming: in 15% of the patients treated with antivenom, neurological signs of envenoming first appeared during treatment, in 37% the neurological symptoms deteriorated with treatment (Lalloo et al. 1992a). The proportion of patients requiring intubation was significantly smaller, and the time to resolution of neurotoxicity and discharge from hospital significantly shorter, in patients receiving antivenom no more than 4 h after the bite (Trevett et al. 1995a). Specific antivenom raised against Australian taipan venom neither reversed nor prevented the evolution of paralysis even when given within a few hours of the bite  (Lalloo et al. 1995).