Clinic: Calloselasma rhodostoma

Examine for venom effects

Autopharmacological effects

Nausea, vomiting
Sweating
Urticaria, angiooedema
Arterial hypotension / hypovolaemic shock (transient, recurrent; immediate; delayed (CLS))
Diarrhoea
Bronchospasm

Local Effects

Pain
Tender local (spreading) swelling
Blistering
Lymphangiopathy and lymphadenopathy
Necrotic skin

Haematological effects

Clotting disturbances:
- Bleeding from the fang marks and from injuries, in particular ones that are not located in the region in which venom application occurred.
- Bleeding into the skin (ecchymosis, petechiae)
- Gingival bleeding, bleeding from the nose, conjunctiva, haematemeis, bleeding per rectum, including melaena, haematuria, haemoptysis.
- Oliguria, anuria (VICC / AKI)
Bleeding and/or haemolytic anaemia:
- Arterial hypotension (haemorrhagic shock)
- Acute abdomen (intra-abdominal bleeding!)
- Loin pain/renal bed sensitive to percussion (ischaemia, renal haemorrhage!)
- Local neurological signs, meningism, coma (intracranial bleeding!)
- Pale sclera (bleeding, haemolysis!)
- Oliguria, anuria (arterial hypotension / AKI!)

Species-specific envenoming pattern

The assessment of the envenoming pattern is based on the data from publication in which the identification of the snakes is clearly specified and in accordance with accepted criteria.

	Local effects¹	Haematological effects
		Bleeding²	Coagulopathy³
Calloselasma rhodostoma

¹Local effects
A study of Reid et al. (1963a) and Warrell et al. (1986) established the principle features of Calloselasma rhodostoma envenoming (see 'Species-specific evidence', below).

Local pain is correlated with the degree of severity of the envenoming (Reid et al. 1963a).
No swelling or only minor local swelling practically excludes a clinically relevant injection of venom. Swelling began within minutes after the bite, maximum after 24–48 h (in all patients ≥75% of the maximum extent of the local swelling was reached after 12 h) (Reid et al. 1963a).
Local necrosis in around 10% of envenomend patients (Reid et al. 1963a).

Haematological effects

²Bleeding

Systemic bleeding in around 15% of envenomned patients (Reid et al. 1963a).
Haemoptysis as early as 30 minuntes after the bite (Reid et al. 1963a). Haemoptysis observed most notably in patients with pulmonary cavities (tuberculosis) (Warrell 1993, pers. comm.).
Discoid ecchymosis, gingival bleeding, persistent oozing of blood from the site of the bite, Haematemesis, macroscopic haematuria, intracerebral haemorrhage, shock. (Reid et al. 1963a)
The cause of significant anaemia was generally loss of erythrocytes into the bitten extremity (Reid et al. 1963a, Warrell et al. 1986).
Time course of clinical signs see 'Species-specific evidence' 'Haematological effects' below.

³Coagulopathy

The time until the incoagulability of the blood became evident on laboratory tests (clotting time) varied greatly. In patients who still had coagulable blood at the initial investigation, the blood became incoagulable after a period of between several hours and 2–3 days.
Incoagulability of the blood can re-occur after a long latency period.
In order to detect and treat relapses, patients should be kept in hospital for at least 5 days after initial treatment, and coagulation should continue to be investigated twice daily (Warrell et al. 1986).
Patients whose only symptom is incoagulable blood appear remarkably well, and the risk of systemic bleeding (excluding blood loss into the area of local swelling) appears to be small (Reid et al. 1963a, Reid and Chan 1968). This seems to apply at least to hospitalised patients, but not necessarily to patients who engage in physical labour despite incoagulability of the blood, especially if they are exposed to trauma while working (Warrell et al. 1986).

Type of haemostatic defect
Defibrin(ogen)ation due to a fibrinogen-coagulating ("thrombin-like") enzyme (Arvin); thombocytopenia.
Haemostatic parameters
See Section 'Species-specific evidence', 'Haemostatic parameters' below.

Morbidity
See section 'species-specific evidence' below.

Case fatality rate

See section 'species-specific evidence' below.

Clinical management

First Aid

Release of any type of tourniquet follow link above.

Local treatment

Pain control
Tetanus prophylaxis
Standard wound care
WHO (2010, 2016)

Systemic supportive treatment

A general understanding of emergency medicine is required, or can be found in emergency medicine guidelines, e.g. ABCDE approach, WHO-ICRC Basic Emergency Care.

Follow SAMPLE & ABCDE ApproAch

Comprehensive ABCDE approach

ICRC Basic Emergency Care: approach to the acutely ill and injured (SAMPLE and ABCDE approach: first module)

Obey Calloselasma rhodostoma - specific features

see

'Species-specific envenoming pattern' above

and

Guidelines for the Management of Snakebites, WHO Regional Office SE Asia

Key issues

See

Footnotes above
Species-specific evidence below

Specific treatment (antivenoms)

References

see also references in section 'species specific evidence' (below).

Reid, H. A., K. E. Chan (1968) The paradox in therapeutic defibrination. Lancet I: 485-486
WHO-ICRC Basic Emergency Care: approach tothe acutely ill and injured (2018)
https://www.who.int/publications-detail-redirect/basic-emergency-care-approach-to-the-acutely-ill-and-injured
WHO ABCDE Approach
https://cdn.who.int/media/docs/default-source/integrated-health-services-(ihs)/csy/bec-quick-cards/becp-edu29-pdf-en-finl.pdf?sfvrsn=2532d61b_2
WHO (2010) Wound and lymphoedema management. WHO/HTM/NTD/GBUI/20101 I. 2010. https://www.who.int/publications/i/item/9789241599139
WHO (2016) Guidelines for the management of snakebites. 2^nd edition. https://www.who.int/publications/i/item/9789290225300
WHO Snakebite Information and Data Platform
https://www.who.int/teams/control-of-neglected-tropical-diseases/snakebite-envenoming/snakebite-information-and-data-platform
Warrell DA. Venomous and poisonous animals. In: Farrar J, Garcia PJ, Hotez T, Junghanss T, Kang G, Laloo D (eds.). Manson’s tropical diseases. 24th ed. Elsevier; 2023.
Warrell DA, Williams DJ. Clinical aspects of snakebite envenoming and its treatment in low-resource settings. Lancet. 2023 Apr 22;401(10385):1382-1398. PMID: 36931290. https://doi.org/10.1016/s0140-6736(23)00002-8

Species-specific evidence

Calloselasma rhodostoma

Malaysia

Reid et al. (1963a)
Systemic envenoming (haemostatic defect) 97/250:
250 verified Calloselasma rhodostoma bites; identification: criteria not specified.
Classification
Local envenoming
- - None (no local swelling) 48/250.
  - Negligible (maximum extent of local swelling ≤1 cm difference in circumference between the bitten and healthy extremity) (24/250).
  - Mild (maximum extent of local swelling >1 to <4 cm difference in circumference between the bitten and healthy extremity, no necrosis) (57/250).
  - Moderate (maximum extent of local swelling >4 cm difference in circumference between the bitten and healthy extremity, no necrosis) (94/250).
  - Necrosis 27/250

Systemic envenoming

- - None (no haemostatic defect) 56/250.
  - Mild: haemostasis with impaired clot formation (Reid et al. 1963b) 28/250.
  - Moderate (incoagulable blood) 32/250.
  - Severe (haemorrhagic syndrome) 37/250.

Overall, incoagulability of the blood does not appear to be associated with a high risk of systemic bleeding (excluding blood loss into the local swelling), at least not in hospitalised patients. However, this is not necessarily the case for patients who engage in physical labour despite incoagulability of the blood, especially if they are exposed to trauma while working (Warrell et al. 1986).

Thailand

Warrell et al. (1986)
46 Calloselasma rhodostoma bites; identification: morphological or immunological with ELISA (Ho et al. 1986a). All patients had incoagulable blood as a sign of systemic envenoming.

Brown and Brown (1987)
1 Calloselasma rhodostoma bite; identification: ELISA.

Brown and Brown (1988)
1 Calloselasma rhodostoma bite; identification: initially incorrectly identified as a Vipera russelli bite and treated with monospecific Russell's viper antivenom, QSMI. Identification of the snake revised and successful treatment with Malayan pitviper antivenom, QSMI.

Signs & symptoms

Autopharmacological effects

Gastrointestinal, pulmonary and cutaneous signs and symptoms that could be caused by autopharmacological processes were rarely or never observed (Reid et al. 1963a).

Local effects

Local pain is correlated with the degree of severity of the envenoming.
No swelling or only minor local swelling practically excludes a clinically relevant injection of venom. Swelling began within minutes after the bite, maximum after 24–48 h (in all patients ≥75% of the maximum extent of the local swelling was reached after 12 h).
Very good correlation of the difference in circumference between the bitten and healthy extremity and the extent of the swelling with the amount of venom injected and the degree of systemic envenoming:

Difference in circumference and systemic envenoming: difference in circumference at the initial investigation of the patient in cm < the number of hours since the bite, or maximum difference in circumference <3 cm: exclusion of severe systemic envenoming. In contrast, a third of the patients with a difference in circumference of 4–8 cm and all of those with a difference in circumference of ≥9 cm had severe systemic envenoming.
Extent of the swelling and systemic envenoming: 32/33 patients with swelling that extended beyond the level of the knee proximally and 8/12 who had swelling that extended beyond the level of the elbow proximally developed severe systemic envenoming. In contrast, 86 patients in whom the swelling was confined to the area below the knee or elbow, respectively, did not develop severe systemic envenoming.
Extravasation, blistering (haemorrhagin activity) and systemic envenoming: extensive blistering is a reliable sign of injection of a large amount of venom: 5/6 patients with this clinical sign had severe systemic envenoming, 1/6 moderate envenoming. Extravasation of erythrocytes and plasma leads to discolouration of the skin, but in dark skin this is barely discernible.

Local necroses 27/250, but these were more common with bites on the toes and fingers. Bacterial infections practically never occur if there is no necrosis (Reid et al. 1963a).

Haemologocal effects

Systemic bleeding 37/250, by definition all patients with severe systemic envenoming.
Haemoptysis 29/37, at the earliest 30 min after the bite, for a maximum of 4 days (this clinical sign probably overestimated, as in a large proportion of these patients, the blood actually originated exclusively from the oral cavity). Haemoptysis observed most notably in patients with pulmonary cavities (tuberculosis) (Warrell 1993, pers. comm.).
Discoid ecchymosis 21/37, at the earliest 2 ¾ h after the bite, for a maximum of 3 days.
Gingival bleeding 17/37, at the earliest 2 ¾ h after the bite, maximum duration 3 days.
Persistent oozing of blood from the site of the bite 11/37.
Haematemesis 3/37, at the earliest 2 h after the bite, for a maximum of 1 day. Macroscopic haematuria 1/37, 24 h after the bite, for 3 days. Intracerebral haemorrhage 1/37, 36 h after the bite, patient died. Shock 8/37; if the shock occurred late (>24 h), the most probable cause was hypovolaemia (fluid and erythrocyte loss into the region of the swelling). If the state of shock occurred before the bitten extremity was noticeably swollen, then other mechanisms must be assumed to have caused it. The patients with shock responded extremely well to antivenom treatment (Reid et al. 1963a).

Neurological effects

Neurological symptoms and clinical signs due to a direct effect of toxin were not observed in >1,000 cases (Reid et al. 1963a).

Renal effects

Rare and, if present, secondary (arterial hypotension) (Reid et al. 1963a).

Other signs & symptoms

Fever 12/250, of whom 5/12 had severe and 7/12 moderately severe systemic envenoming (Reid et al. 1963a).

Morbidity

The local necrotising effect of the venom is a common cause of morbidity. Gangrene can lead to the loss of toes, fingers or whole extremities; chronic infections (osteomyelitis) can occur (Warrell et al. 1986).
Local necroses occur chiefly with bites on the fingers and toes and if tourniquets are used.
If there is no necrosis, healing starts quickly. In these cases the time it takes for the swelling to subside is practically identical to the time it takes for complete recovery of the bitten extremity: these time periods range from an average of 3.6 days (1–10 days) for swelling to subside and complete recovery in patients with negligible local envenoming and up to 22.3 days (8–42 days) in patients with severe systemic envenoming. If necroses occur, the time to complete recovery is drastically increased to an average of 67.6 days (13–322 days) (Reid et al. 1963a). Infections complicate the course of recovery in patients with necroses.
Of 46 patients treated with TRC, GPO or Twyford antivenom, a 5-year-old girl developed local necrosis to such an extent that residual deformity and loss of function were expected. In 1 patient a necrotic toe had to be amputated. One patient suffered peroneal paralysis; fasciotomy was indicated but
the patient refused the operation. 3 patients developed necroses of ≤9 cm² (Warrell et al. 1986).
Intracerebral haemorrhages with permanent neurological deficits are very rare.
Overall, incoagulability of the blood does not appear to be associated with a high risk of systemic bleeding (excluding blood loss into the local swelling), at least not in hospitalised patients. However, this is not necessarily the case for patients who engage in physical labour despite incoagulability of the blood, especially if they are exposed to trauma while working (Warrell et al. 1986).

Case fatality rate

Mortality, which is chiefly caused by haemorrhages and secondary infections, is low (Warrell et al. 1986).
On the whole, incoagulability of the blood does not appear to be associated with a high risk of fatal systemic bleeding, at least not in hospitalised patients. However, this is not necessarily the case for patients who engage in physical labour despite incoagulability of the blood, especially if they are exposed to trauma while working (Warrell et al. 1986).
Before specific antivenom became available, the mortality rate in hospitalised patients was around 1% (Reid et al. 1963a). In the study of Reid et al. (1963a), of a total of 291 patients with verified Calloselasma rhodostoma bites, only 2 patients died, and their deaths could only be indirectly attributed to the snakebites. One patient died of tetanus and one from a combination of an anaphylactic reaction to the antivenom, an intracerebral haemorrhage and severe pre-existing anaemia.
In 23 fatalities due to Calloselasma rhodostoma bites recorded in northern Malaysia between 1955 and 1960, the average time between the bite and death was 64.6 h (5–240 h), the median time 32 h (Reid et al. 1963a).
Of 46 patients treated with TRC, GPO or Twyford antivenom, none died (Warrell et al. 1986).
According to a study of fatal snakebites in rural areas of Thailand, 13/46 were caused by Calloselasma rhodostoma (Looareesuwan et al. 1988).

Laboratory and physical investigations

1. Haemostasis
Studies

Hutton et al., in press: 10 Calloselasma rhodostoma bites; identification: criteria not specified.

Reid et al. 1963b: 29 patients with systemic envenoming due to verified Calloselasma rhodostoma bites:

moderate systemic envenoming 8/29,
severe systemic envenoming 21/29.

Haemostatic parameters investigated: clotting time according to Lee and White, bleeding time according to Ivy, tourniquet test, clot quality test, prothrombin time, thrombin time, fibrinogen, platelets.

Warrell et al. (1986)

Type of haemostatic defect
Defibrin(ogen)ation due to a fibrinogen-coagulating ("thrombin-like") enzyme (Arvin). It differs from thrombin in that it only splits the fibrinopeptide A from the Aα-chain and not the fibrinopeptide B from the Bβ-chain. It is not inhibited by ATIII (?) or the ATIII-heparin complex, does not activate factor XIII and does not induce platelet aggregation (Stocker 1990). An activator of factor X might also play a role (Denson 1969).
Thrombopaenia: the speed with which platelets increase again after antivenom treatment implies that sequestered platelets are re-entering the circulation, rather than there being a fresh release of platelets from the bone marrow. According to clinical criteria, the activation, aggregation and deposition of platelet complexes do not play a role (Hutton et al. 1990).

Haemostatic parameters

The time until the incoagulability of the blood became evident on laboratory tests (clotting time) varied greatly. In patients who still had coagulable blood at the initial investigation, the blood became incoagulable after a period of between several hours and 2–3 days.

The latency period until the incoagulability of the blood becomes detectable with the clotting time test can be explained by a state of equilibrium between the consumption and production of fibrinogen, a state which is maintained for variable periods of time (Ho et al. 1986b). That is why patients need to be hospitalised for a sufficient period of time after a Calloselasma rhodostoma bite, and coagulation needs to be investigated regularly. Clotting time should be assessed at least twice a day. If antivenom treatment is indicated and administered, clotting time is assessed every 6 h in order to confirm the efficacy of the antivenom treatment or to determine whether a further dose of antivenom is indicated. It must be noted, however, that there is a delay in the time it takes for the clotting time to return to normal compared to the disappearance of the venom from the bloodstream. This can be explained by the increase in fibrinogen, the speed of which may vary. As fibrinogen is an acute-phase protein, the speed with which it increases depends, among other factors, on the number of concurrent inflammatory reactions present that can accelerate this process (Hutton et al. 1990). The clotting time test is thus misleading if it is performed too early, i.e. antivenom may be administered althoughthere is no longer any venom in the circulation. Other haemostatic tests are more sensitive and better suited to determining the status of the dynamic process of the haemostatic defectat any given moment(fibrinogen, FSP, see below), but they also do not solve the problem completely and are much more complicated. This problem will only be solved when reliable and fast ELISA tests for detection of venom antigen levels in the serum are available (Ho et al. 1986b).

Incoagulability of the blood can re-occur after a long latency period (see below). This is probably due to continued absorption of venom from a depot in the region of the bite or saturation of extravascular binding sites. Recurrent venom antigenaemia was detected with the aid of ELISA tests, both in the presence and absence of circulating antivenom.In order to detect and treat relapses, patients should be kept in hospital for at least 5 days after initial treatment, and coagulation should continue to be investigated twice daily (Warrell et al. 1986).

The coagulation disorder is the prominent sign of systemic envenoming due to Calloselasma rhodostoma. Incoagulable blood was observed as early as 30 min after the bite. In 43 patients who did not receive antivenom, the average duration of incoagulability of the blood in 8 patients with severe envenoming was 8.0 days (5–11 days), and in 24 patients with moderate envenoming it was 6.6 days (1–15 days) (Reid et al. 1963a). In the absence of specific treatment, the coagulation defect can persist for more than 3 weeks (Reid et al. 1963a).

Correlation between the degree of severity of the haemostatic defect and other systemic signs of envenoming: none of the patients with a mild (haemostasis with impaired clot formation) or moderate haemostatic defect (incoagulable blood) had additional signs of systemic envenoming (Reid et al. 1963a); in other words, there are no clinical signs or symptoms that initially point to a haemostatic defect, as long as it does not have a complicated course (haemorrhage).

Patients whose only symptom is incoagulable blood appear remarkably well, and the risk of systemic bleeding (excluding blood loss into the area of local swelling) appears to be small (Reid et al. 1963a, Reid and Chan 1968). This seems to apply at least to hospitalised patients, but not necessarily to patients who engage in physical labour despite incoagulability of the blood, especially if they are exposed to trauma while working (Warrell et al. 1986).

Haemorrhagic activity: haemorrhagins appear to be active primarily locally, i.e. in the region of the swelling.

Clotting time: 29/29 (study inclusion criterion) (Reid et al. 1963b). It is possible that a patient's blood may first become incoagulable as late as up to 72 h after the bite; in contrast, circulating antivenom (see ELISA) and increased serum FSP may be detectable significantly earlier.

In groups of patients with local signs of envenoming, increased clotting time was present in 69/202 (Reid et al. 1963a) and 57/147 (Viravan et al. 1992).

Platelets: marked thrombopaenia 27/29; 10,000–99,000/mm³ (Reid et al. 1963b). Determination of platelet count at the time of maximum defibrin(ogen)ation directly before administration of antivenom: <150,000/μl (7/10), of whom 4/7 <50,000/μl. The patients with platelets <50,000/μl all had systemic bleeding, but only 1/6 patients with a platelet count >50,000/μl. If the platelet count was low prior to antivenom treatment, it increased rapidly, i.e. within 3 h, after treatment was commenced. The speed of the platelet increase implies that sequestered platelets re-entered the circulation, rather than there having been a fresh release of platelets from the bone marrow. According to clinical criteria, the activation, aggregation and deposition of platelet complexes do not play a role. The platelet count should be taken into consideration when monitoring the course of the envenoming and assessing indications for antivenom treatment (Hutton et al., in press).

PT: increased 28/29 (Reid et al. 1963b).

TT: increased in all patients investigated (Reid et al. 1963b).

Fibrinogen: in all patients investigated 10–160 mg/100 ml, mean level 46.9 mg/100 ml (normal levels 140–420 mg/100 ml) (Reid et al. 1963b). Slow increase in fibrinogen after administration of antivenom (12–24 h) (Hutton et al. 1990).

FSP: on average 238 μg/ml (35–750 μg/ml; n = 15) (Warrell et al. 1986).
On average 550 μg/ml (10–750 μg/ml; n = 15) (Warrell et al. 1986).
On average 200 μg/ml (36–750 μg/ml; n = 16) (Warrell et al. 1986).

Increased FSP can be detectable early on, even if a patient's blood only becomes incoagulable as late as up to 72 h after the bite. This discrepancy may possibly be explained by a prolonged state of equilibrium between the synthesis and consumption of fibrinogen. As FSPs are eliminated from the bloodstream very rapidly, they are a good indicator for persistent or acute coagulation defects (Ho et al. 1986b).

2. Haemoglobin
32 patients were investigated, of whom 25 had severe and 7 moderate systemic envenoming. Hb decrease <1 g/100 ml: 8/32; 1.0–1.9 g/100 ml: 9/32; 2.0–2.9 g/100 ml: 7/32; 3.0–8.3 g/100 ml: 8/32 (Reid et al. 1963a).
The cause of significant anaemia was generally loss of erythrocytes into the bitten extremity (Reid et al. 1963a, Warrell et al. 1986).

3. Leucocytes
In systemic envenoming on average considerably >10,000/μl (Warrell et al. 1986).

4. ELISA
- Determination of the serum antivenom concentration.
- Determination of the venom concentration (venom antigen level).
The serum venom antigen level at the initial investigation of the patient is correlated with the incidence of spontaneous systemic bleeding, the incoagulability of the blood and the plasma fibrinogen and FSP concentrations, as well as with the extent of local swelling and the occurrence of necroses (Ho et al. 1986b).

References

Brown, A. E., L. Brown (1987) Blood venom antigen levels after Malayan pit viper bite. Trans. roy. Soc. trop. Med. Hyg. 81: 548
Brown, L., A. E. Brown (1988) The problem of snake bite diagnosis: A case report and two-year hospital review. J. Med. Assoc. Thai. 71: 456-460
Denson, K. W. E. (1969) Coagulant and anticoagulant action of snake venoms. Toxicon 7: 5-11
Ho, M., D. A. Warrell, S. Looareesuwan, R. E. Phillips, P. Chanthavanich, J. Karbwang, W. Supanaranond, C. Virvan, R. A. Hutton, S. Vejcho (1986b) Clinical significance of venom antigen levels in patients envenomed by the Malayan pit viper (Calloselasma rhodostoma). Amer. J. trop. Med. Hyg. 35: 579-587
Hutton, R. A., S. Looareesuwan, M. Ho, K. Silamut, P. Chanthavanich, J. Karbwang, W. Supanaranond, S. Vejcho, C. Viravan, R. E. Phillips, D. A. Warrell (1990) Arboreal green pit vipers (genus Trimeresurus) of South-East Asia: bites by T. albolabris and T. macrops in Thailand and a review of the literature. Trans. roy. Soc. trop. Med. Hyg. 84: 866-874
Looareesuwan, S., C. Viravan, D. A. Warrell (1988) Factors contributing to fatal snake bite in the rural tropics: analysis of 46 cases in Thailand. Trans. roy. Soc. trop. Med. Hyg. 82: 930-934
Warrell, D. A., S. Looareesuwan, R. D. G. Theakston, R. E. Phillips, P. Chanthavanich, C. Viravan, W. Supanaranond, J. Karbwang, M. Ho, R. A. Hutton, S. Vejcho (1986) Randomized comparative trial of three monospecific antivenoms for bites by the Malayan pit viper (Calloselasma rhodostoma) in southern Thailand: Clinical and laboratory correlations . Amer. J. Trop. Med. Hyg. 35: 1235-1247
Reid, H. A., P. C. Thean, K. E. Chan, A. R. Baharom (1963a) Clinical effects of bites by Malayan viper (Ancistrodon rhodostoma). Lancet I: 617-621
Reid, H. A., K. E. Chan, P. C. Thean (1963b) Prolonged coagulation defect (defibrination syndrome) in Malayan viper bite. Lancet: 621-626
Stocker, K. F. (1990) Snake venom proteins affecting hemostasis and fibrinolysis. In Stocker, K. F.: Medical use of snake venom proteins. Boca Raton, CRC Press: 97-160
Viravan, C., S. Looareesuwan, W. Kosakarn, V. Wuthiekanun, C. J. McCarthy, A. F. Stimson, D. Bunnag, T. Harinasuta, D. A. Warrell (1992) A national hospital-based survey of snakes responsible for bites in Thailand. Trans. roy. Soc. trop. Med. Hyg. 86: 100-106

Clinic: Calloselasma rhodostoma

Examine for venom effects

Autopharmacological effects

Local Effects

Haematological effects

Species-specific envenoming pattern

Case fatality rate

Clinical management

See also Clinical Management: Indian Subcontinent and Southeast Asia

First Aid

Local treatment

Systemic supportive treatment

Follow SAMPLE & ABCDE ApproAch

Obey Calloselasma rhodostoma - specific features

Specific treatment (antivenoms)

References

Species-specific evidence

Calloselasma rhodostoma

Malaysia

Thailand

Signs & symptoms

Autopharmacological effects

Local effects

Haemologocal effects

Neurological effects

Renal effects

Other signs & symptoms

Morbidity

Case fatality rate

Laboratory and physical investigations

References