Go to start page
V1.2.0 (T12376)
Disclaimer & Information
Show Mindmap
Poisonous animals
Cnidarians (Jellyfish, Corals and Anemones)
Venomous fish
Hymenopterans (Bees, Wasps and Ants)
Sea snakes
Terrestrial snakes
Miscellaneous animals
North America
Mexico and Central America
South America and the West Indies
North Africa, Near and Middle East
Central and Southern Africa
The Far East
Indian Subcontinent and Southeast Asia
Australia and the Pacific Islands



Echis carinatus sochureki


Kashmir, India
Bhat 1974: 117 E. carinatus bites; identification: a total of 310 viper bites are discussed in this study. The snake that caused the bite was identified morphologically in 121 cases: E. carinatus 117/310, V. russelli 4/310. Thus 96.7% of the snakes brought in by patients were E. carinatus and 3.3% were V. russelli. In this region, clinical criteria do not aid in the differentiation of the type of viper that caused the bite. However, with certain qualifications, the snakes brought in by patients in this study can be considered a representative sample that gives an idea of the prevalence of these snakes as the cause of snakebites.

Classification of the severity of envenoming caused by verified E. carinatus bites:

Systemic envenoming

  • mild envenoming (impaired haemostasis) 16/117,
  • moderately severe envenoming (incoagulable blood) 22/117, 
  • severe envenoming (haemorrhaging) 79/117.

All other data discussed in this study refer to the total number of observed cases (310). Assuming that the sample of herpetologically identified snakes (121/310), of which 96.7% were E. carinatus bites, is representative, the data from this study concerning the total number of bites provide a good approximation of the clinical picture and course of E. carinatus envenoming in Kashmir.

Signs & symptoms

Autopharmacological effects

Vomiting 118/310, in connection with antivenom administration 47/118. In the remaining cases information on the time point at which vomiting occurred and other signs and symptoms do not make it likely that there was an autopharmacological cause. Bronchospasm and dyspnoea 13/310 (Bhat 1974).

Local effects

Slight pain in the region of the bite, duration <24 h (65/310) (Bhat 1974).

Swelling 248/310. The swelling was particularly marked in those patients who had had tourniquets applied or whose wound had been incised (162/310); in the remaining 148/310 only 86/310 had noticeable swelling, 62/310 merely had local oedema. Onset of swelling shortly after the bite, at the latest after 24 h. Regional lymph node swelling 84/310. Blistering, diameter <1 cm to several cm (130/310). Necroses 0/130.

42% of the patients with systemic envenoming who had had no local intervention did not develop local swelling (Bhat 1974).

Haemostatic effects

Systemic bleeding 202/310, interval between the bite and onset of bleeding: 1–6 h: 6/202; 7–48 h: 168/202; 25–48 h: 44/202; >48 h: 28/202.

Hypovolaemic schock as a consequence of haemorrhaging 6/310; all 6 were not hospitalised until >2 days after the bite.

Bleeding from bite wounds 108/310, severe and persistent if an incision had been made. Many of these patients required blood transfusions. Ecchymosis 133/310, gingival bleeding 40/310, haematemesis 37/310, bleeding per rectum 6/310, haemorrhoidal bleeding 6/310, epistaxis 22/310, haemoptysis 87/310, haematuria, microscopic 242/310, macroscopic 102/310, subarachnoid haemorrhage 6/310, of whom 2 died (Bhat 1974).

Other signs & symptoms

Upper abdominal pain 115/310 (Bhat 1974).


Necroses 0/310, local infections 79/310; all of these patients had had their wound incised after the bite. Total number of incisions 84/310. Osteomyelitis 3/310; all of these patients had had their wound incised after the bite (Bhat 1974).

Case fatality rate

4/117 (3,4 %) of treated patients. Causes of death in patients definitely bitten by E. carinatus: cardiovascular failure as a consequence of blood loss 2/4, subarachnoid haemorrhage 1/4, septic shock? 1/4 (Bhat 1974).

Laboratory and physical investigations

1. Haemostasis
Bhat 1974 (see above for a description of the study).
All patients (310) included in the study had a haemostatic defect (clotting time according to Lee and White).

Incoagulable blood 242/310, of these patients 188 had systemic bleeding. 14/310 with systemic bleeding had severe haemostatic defects, but not completely incoagulable blood.

Type of haemostatic defect

Disseminated intravascular coagulation induced by prothrombin activation and reactive (secondary) hyperfibrinolysis. Little intravascular fibrin deposition (this is reflected in the low incidence of renal function defects and microangiopathic haemolysis). Fibrin clearance appears to be very efficient. Haemorrhagic activity is present, which together with the coagulation defect is responsible for the systemic bleeding (see clinical entry for Echis ocellatus, Nigeria) (Warrell et al. 1977, Edgar et al. 1980).

Haemostatic parameters

Overview haemostasis




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
  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.



CT according to Lee and White

Increased (study inclusion criterion) 310/310, impaired or no clot formation on clot observation test.

At the time of hospitalisation no detectable coagulation defect with the available laboratory methods (clotting time according to Lee and White): 81/310. Development of impaired coagulation (clotting time according to Lee and White) within 6 h after the bite: 54/81, within 24 h after the bite: 5/81.

Symptoms of bleeding within 6 h after the bite 6/81, although 54/81 already showed impaired coagulability within this time period (Bhat 1974).

In patients who did not receive antivenom, incoagulability of the blood persisted on average for 10 days (Bhat 1974). Thus even for bites that have occurred some time previously, it is still necessary to determine the coagulability of the blood.



In the normal range in 34 patients with systemic bleeding (Bhat 1974).

2. Haemoglobin
116/202 patients with systemic bleeding had an average decrease in haemoglobin of 3.8 g/100 ml (Bhat 1974).

3. ECG
T wave inversion 23/310, all were gravely ill (secondary effect?). In 17 of these patients the ECG changes normalised, 6 died (Bhat 1974).

Treatment (symptomatic)

Blood transfusions
17/310 received blood transfusions and no antivenom. Coagulability was restored within 36 h in 16/17, but not permanently. The incoagulability of the blood in these patients persisted on average for 10 days (Bhat 1974).

Treatment (specific)

Polyvalent snake venom antiserum, Central Research Institute, Kasauli, India.


  • On average 80 ml (60–120 ml): restoration of blood coagulability within 24 h in 120/293 patients, 12 of whom had systemic bleeding.
  • On average 140 ml (120–160 ml) and an average of 3 (1–4) units of blood in 159/293 patients whose bleeding persisted for >24 h. With this treatment blood coagulability was restored within 48 h.
  • 250 ml and 5 units of blood in 6/293 patients whose bleeding persisted for up to 72 h.
  • 270 ml and 6 units of blood in 3/293 patients whose bleeding persisted for >72 h. Coagulability was restored within 4 days.


The success of antivenom treatment depends on the time interval between the bite and the start of treatment:

  • Treatment was commenced within 24 h after the bite in 137 patients: restoration of blood coagulability in 120 of these 137 patients within 24 h.
  • Treatment was commenced within 25–48 h after the bite in 159 patients: restoration of blood coagulability in 100 of these 159 patients within 25–48 h (Bhat 1974).

Efficacy with regard to the haemotoxic effect of the venom (coagulability): normalisation of blood coagulability (assessed by the measurement of clotting time according to Lee and White) within 24 h: 120/293 (12 of these 120 patients had clinically apparent bleeding); within 25–48 h: 159/293 (all 159 patients had clinically apparent bleeding); within 49–72 h: 6/293 (all 6 patients had clinically apparent bleeding); within 73–96 h: 3/293 (all 3 patients had clinically apparent bleeding). 5/293 died before the coagulation defect could be corrected (Bhat 1974).

Adverse reactions

Vomiting in connection with antivenom administration 47/293, immediate hypersensitivity 9/293 (mild), serum sickness 1/293 (Bhat 1974).