Antivenom dosage guidelines -
The administration of adrenaline and hydrocortisone may be repeated if necessary. When symptoms of snakebite are severe it may not be advisable to wait for 30 minutes to observe reactions to test-dose of serum. In such cases it may be better to inject 1 ml. of adrenaline intramuscularly at the same time as the serum in order to lessen the risk of anaphylaxis.
Half the dose of adrenaline may be repeated 15 minutes later if necessary. Infection in Children - Part 3. Drug Categories. Drug Index. Drugs Category.
Drugs A to Z. Anti-Snake Venom Synonyms : ASV, Snake Antivenom Serum Mechanism : Snake venoms are complex mixtures of enzymatic proteins and different toxins. Indication : Snake bite Contraindications : Before injection of Anti-Snake Venom Serum, history of prior injections of serum e.
Dosing : 10 vials of polyvalent vials of ASV as the initial dose. For severe envenomation, can give almost upto 50 vials. Should be given IV over 1 hour. Join Us.
Partner Sites HIV in Childern Vaccine Reminder Pediatric Oncall Journal. New Arrival Infection in Children - Part 3. Other Pediatric Oncall Books. Copyright © - Pediatric Oncall All Rights Reserved. All trademarks used are the properties of their respective owners. The dose of antivenom is defined as the amount administered before the first available post-antivenom blood sample for venom-specific enzyme immunoassay.
Polyvalent antivenom contains on average the equivalent of eight vials of brown snake antivenom, based on a study of CSL terrestrial snake antivenoms.
The total dose was also calculated for each patient receiving further antivenom. Methods for the enzyme immunoassay have previously been described. The limit of detection for brown snake venom was 0.
The peak pre-antivenom venom concentration is reported where available. An enzyme immunoassay using labelled anti-Horse IgG was also used to detect antivenom in patient serum to confirm antivenom administration. For the enzyme immunoassay standard curves were fitted by linear and non-linear regression using both Excel and Prism 5.
com ]. There were possible brown snake bites recruited to ASP and of these were definite brown snake bites by our definition and included in our analysis, 13 of which were non-envenomed. Of the excluded patients, 73 patients had no pre-antivenom serum available for testing and four patients had no brown snake venom detected but had either Notechis sp.
or Tropidechis carinatus venom detected. The snake was identified in 20 of the envenomed patients. Demographics of the patients with definite brown snake envenoming are summarised in Table 1. The distribution of bite locations is shown in Figure 2.
Most bites occurred in Queensland, Western Australia and New South Wales with only one case in Victoria. Most patients were bitten while undertaking yard work or gardening 40 , when walking or in the bush 44 , or intentionally interacting with the snake 41 ; only eight patients were bitten indoors.
The clinical effects of the envenomed patients are summarised in Table 2. The grouping of patients into each clinical syndromes including the numbers in each group is shown in Figure 3. The median time to recovery of complete VICC to an INR of less than 2 was Three patients died with an INR greater than 2 and one patient was discharged with an INR of 3.
Twenty two patients were discharged with an INR of 1. Major haemorrhage occurred in five cases, three gastrointestinal haemorrhages and two intracranial haemorrhages both associated with hypertension.
Table 4 provides a comparison between patients with VICC and partial VICC which shows that more severe effects occurred in patients with complete VICC except thrombotic microangiopathy which occurred with similar frequency in partial VICC.
In 19 patients with a known time of collapse this occurred a median of 30 minutes range: 2 to 90 min after the bite.
Cardiac arrest occurred in seven patients with collapse and four of these were fatal. Non-fatal cardiac arrests received prompt cardiopulmonary resuscitation. Eight patients of the 37 had generalised seizures, seven of which were hypotensive immediately prior to the seizure.
No ventricular arrhythmias were reported at the time of collapse or cardiac arrest. Two patients had atrial fibrillation. ECG and troponins were not routinely done in all patients.
Three patients with early collapse had abnormal electrocardiograms ST segment depression, atrial fibrillation and widespread T wave inversions. Troponin was measured in only 24 patients; the median troponin was somewhat higher in the 12 who had collapsed than the 12 who did not [0.
One patient developed acute renal impairment without significant thrombocytopenia but had severe environmental hyperthermia. Another nine patients had an abnormal creatinine without all the features of thrombotic microangiopathy. Two patients had mild neurotoxicity. One developed ptosis prior to having an intracerebral haemorrhage.
The second had unusual and fluctuating neurological findings including ptosis, lateral gaze diplopia, bulbar weakness, dysphonia and facial weakness. Venom concentrations and clinical effects were similar between the three groupings of brown snakes Eastern or P. textilis , Northern and Western; Table 5 except more cases of hypotensive collapse and cardiac arrest occurred in the eastern group.
A urine sVDK was done in 45 patients and was positive for brown snake venom in 40 and negative in 5. Pre-treatment serum samples were available in envenomed cases and eight non-envenomed patients.
Venom was not detected in any of the eight non-envenomed patients. The median peak venom concentration in the envenomed patients was 1. There were no significant differences in brown snake venom concentrations between different groups of Pseudonaja sp.
There was a significant difference in peak venom concentrations between patients who developed complete VICC compared with partial VICC Table 5. The median peak concentration in patients developing collapse, cardiac arrest or death was not notably higher than for other patients Table 6.
Antivenom was given in envenomed patients with a median initial dose of two vials IQR 2 to 5, Range 1 to Further doses were given in 25 patients and the total dose in all patients was a median of two vials IQR 2 to 5, Range 1 to Twenty five patients received only one vial of antivenom initially, and five of these received a second dose of one vial 3 , two vials 1 and eight vials 1.
Clinical effects were similar in patients receiving an initial dose of one vial compared with more than one vial, including the frequency of collapse.
Outcomes were similar between patients receiving an initial dose or a total dose of one vial and those receiving greater than one vial, including the time to recovery of VICC Figure 4 and Figure 5. The median brown snake venom concentration of those receiving an initial dose of one vial was not significantly different to those receiving more than one vial [0.
Post-treatment samples were available in patients given antivenom. Free venom was not detected in patients, including in 16 patients after only one vial of antivenom. Three patients had low concentrations of venom detected post-antivenom 0.
Thirty eight of the 73 excluded possible brown snake bites had post-treatment samples available and free venom was not detected in any, including 12 patients receiving one vial of antivenom.
Eight envenomed patients were not given antivenom, seven had only partial VICC and one presented late with VICC. The venom concentrations for 5 of the 8 patients who had serial blood samples available shows venom concentrations decreasing over 20 to 40 hours Figure 6.
Four patients had anaphylaxis and 13 had skin-only reactions. There were no severe cases of anaphylaxis. Neurotoxicity was mild and rare, and myotoxicity did not occur.
Cardiovascular effects were common with hypotensive collapse occurring in over a quarter of patients, although non-fatal and fatal cardiac arrests were uncommon.
Deaths in all but one case were attributed to early pre-hospital collapse and cardiac arrest. Clinical outcomes following one vial of antivenom were similar to those found with larger doses and venom was only detected in three cases following antivenom and these concentrations were very low and the coagulopathy was improving Table 5.
The study emphasizes the importance of cardiovascular effects in brown snake envenoming. Although these effects are well recognised in brown snake envenoming the frequency and severity have not been well quantified in the past.
A recent animal study suggests that the collapse in Australasian elapids is a result of hypotension following vasodilation due to the release of endogenous mediators, and is not cardiac in origin. Unfortunately ECGs and troponins were not routinely collected, but there were moderately elevated troponins in patients with collapse, and these appeared generally higher than those seen in patients who did not have a collapse.
Further detailed investigation of patients with and without collapse is required to determine if the elevated troponin is secondary to the collapse, rather than a primary cardiac event.
The study also confirmed that neurotoxicity was rare in brown snake envenoming in humans, and only results in minor effects.
This is consistent with recent studies of brown snake venom, [24] which showed the presynaptic neurotoxin in brown snake venom is far less potent than that in taipan venom, and constitutes a much smaller proportion of the venom.
The study demonstrates some of the difficulties with correlating the clinical effects in humans with the composition of the venom.
A number of studies have identified the important venom proteins in P. textilis venom. Pseutarin C is a potent procoagulant in vitro [27] and is the cause of VICC seen in patients in this study.
However, some toxins identified in the venom, such as the presynaptic neurotoxin textilotoxin, and other long and short chain post-synaptic neurotoxins, do not appear to play an important role in human envenoming as evidenced by the lack of neurotoxicity in the majority of patients.
The quantity and potency of the textilotoxin explains the lack of neurotoxicity in part. textilis venom, such as textilinin, [25] do not appear to play a role in human envenoming.
Finally, further study is required to determine the toxic mechanisms and specific toxins that cause the cardiovascular effects and thrombotic microangiopathy, which we have shown to be characteristic of brown snake envenoming.
The geographical distribution of brown snake envenoming was notable with only one case in Victoria. Most brown snake bites occurred in North-Eastern Australia and Western Australia Figure 2 and in these regions brown snake envenoming is likely to be the most important cause of snake envenoming.
A comparison of three Pseudonaja groupings suggests that they are similar clinically and produce similar venom concentrations, which refutes previous suggestions that brown snakes from Western Australia cause more severe envenoming or inject more venom. Published opinions and guidelines have offered conflicting advice on antivenom dosing.
Previous recommendations of larger doses of brown snake antivenom have been based on either the incorrect assumption that ongoing coagulopathy is due to inadequate antivenom, [5] or that the average venom yield used for calculating antivenom quantities was lower than that found in more recent milking studies.
We were unable to determine the proportion of brown snake bites that result in envenoming. The small proportion of non-envenomed cases in this series was due to the fact that if venom was not detected in blood most patients were excluded. Snake collection and identification by an expert was uncommon.
Another limitation is the lack of routine cardiovascular investigation, including the regular collection of ECG and troponin data that were not specifically part of the research protocol or current clinical practice. In future it will be important for troponins and ECGs to be done in patients following collapse.
This series confirms that VICC occurs in all brown snake envenoming cases, and over a third of patients develop complications related to envenoming early collapse, major haemorrhage, thrombotic microangiopathy.
We acknowledge the many referrals from the National Poison Centre Network and clinical toxicologists and help of the many other nurses, doctors and laboratory staff in recruiting patients and collecting samples.
We thank Leonie Calver for her help in recruiting and randomising patients; Renai Kearney for data entry and follow up of patient information and medical records; and Ellen MacDonald for assistance in ethics applications and data collection.
We also thank Joseph Sambono and Jenna Allen for reading the manuscript. Conceived and designed the experiments: GKI SGAB BJC NAB.
Performed the experiments: GA GKI SGAB NAB JW BJC CBP MAO. Analyzed the data: GA GKI NAB SGAB. Wrote the paper: GA GKI MAO NAB SGAB JW BJC CBP. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field.
Article Authors Metrics Comments Media Coverage Reader Comments Figures. Abstract Background Snakebite is a global health issue and treatment with antivenom continues to be problematic. Methods and Finding This was a prospective observational study of definite brown snake envenoming from the Australian Snakebite Project ASP based on snake identification or specific enzyme immunoassay for Pseudonaja venom.
Conclusions Envenoming by brown snakes causes VICC and over a third of patients had serious complications including major haemorrhage, collapse and microangiopathy. Burdmann, University of Sao Paulo Medical School, Brazil Received: August 2, ; Accepted: November 29, ; Published: December 28, Copyright: © Allen et al.
Introduction Snake envenoming is a major problem in many parts of the world. Download: PPT. Figure 1. Brown snake Pseudonaja textilis. Photo taken by Gunther Schmida.
Methods This study was part of the Australian snakebite project ASP which prospectively recruits suspected and definite snake bite patients from more than one hundred hospitals across Australia and referrals from all major Australian poison centres.
Results There were possible brown snake bites recruited to ASP and of these were definite brown snake bites by our definition and included in our analysis, 13 of which were non-envenomed.
Figure 2. Table 1. Demographic features of definite brown snake envenoming cases. Figure 3. Number of patients with partial or complete venom induced consumption coagulopathy VICC , collapse or no collapse, thrombotic microangiopathy TMA , major haemorrhage and death.
Table 2. Clinical features of the patients with definite brown snake envenoming. Table 3. Details of the six deaths from brown snake envenoming. Table 4.
Six of Digestive health supplements Promoting heart health with fruits species of venomous dosags found guirelines Promoting heart health with fruits are vuidelines Antivenom dosage guidelines most of the clinically significant envenomations in the country. These species are: Trimeresurus mucrosquamatus, Trimeresurus stejnegeri, Dosaye atra, Bungarus gujdelines, Deinagkistrodon acutus and Daboia russelii siamensis, which together can be subdivided into three groups based on their venom effects. Primary treatment consists of rapid administration of appropriate antivenoms. The present study aimed to identify a proper dose of antivenom for each snake group as well as to describe hemorrhagic, neurotoxic, and mixed effects of their venoms. A retrospective chart review identified 72 snakebite cases referred to an emergency department. Department of Emergency Medicine, Chonnam National University Hospital, Antiivenom National University Medical School, Gwangju, Korea. Objective This study aims to help Anntivenom domestic guidelines for administration of guideliines to envenomated Promoting heart health with fruits after Antvienom. Methods This Ahtivenom observational case Antivenom dosage guidelines comprised patients with snake envenomation. The GI meal ideas were Promoting heart health with fruits into two groups Antivenon to the need for additional antivenom after the initial treatment based on the traditional snakebite severity grading scale. Results The group requiring additional administration of antivenom showed a higher local effect score and a traditional snakebite severity grade at presentation, a shorter prothrombin and activated partial prothrombin time, a higher frequency of rhabdomyolysis and disseminated intravascular coagulopathy, and longer hospitalization than the group that did not need additional antivenom. The most common cause for additional administration was the progression of local symptoms. The independent factor that was associated with the need for additional antivenom was the local effect pain score odds ratio, 2.Video
Why I’ve Been Injecting Snake Venom for 30 YearsAntivenom dosage guidelines -
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View Topic. Font Size Small Normal Large. Snakebites worldwide: Management. Formulary drug information for this topic. No drug references linked in this topic. Find in topic Formulary Print Share. View in. Language Chinese English.
Author: Julian White, AM, MB, BS, MD, FACTM Section Editors: Daniel F Danzl, MD Michelle Ruha, MD Deputy Editor: Michael Ganetsky, MD Literature review current through: Jan This topic last updated: Jan 11, Venomous snakes are widely distributed around the world and clinical effects from envenomation can overlap to a great degree even among different families of snakes.
This topic will discuss the management of snakebites that occur worldwide, other than those by snakes found in the United States. FIRST AID Initial first aid of snake envenomation is directed at reducing the spread of venom and expediting transfer to an appropriate medical center.
In states such as Texas and Florida, a shortage of coral snake antivenom has put medical providers in a disturbing position. Because they do not want to waste the precious treatment, some doctors feel pressured to wait and see if a bite-victim shows symptoms of envenomation before administering antivenom.
However, the power of the treatment can be compromised by waiting. Although the World Health Organization includes snakebite antivenom on its List of Essential Medicines, the world is experiencing shortages of antivenom.
The populations hardest hit by the shortages tend to live and work in rural areas where highly venomous snakes are endemic, especially in less-developed nations with housing that allows for easier access by venomous snakes.
Hospitals currently face a multifaceted antivenom problem. Antivenom can be very expensive, a problem that is compounded when the product goes unused before its expiration date.
Many clinics do not have sufficient training in selecting the correct antivenom or administering the treatment. The challenges do not stop there: patients can suffer serious allergic reactions to antivenom, and medical supervision during treatment is important.
New monoclonal antibody antivenoms that cause fewer allergic reactions are being developed. However, because the CroFab product uses only a fragment of the cultured antibody, it causes fewer serious allergic reactions than older serum-based, whole antibody antivenoms.
Antivenom is one of those treatments that most of us never think about—until we suddenly and very desperately need it. Contemporary antivenoms made under strict controls are very effective. Yet, they remain out of reach for many victims who most need them. The Antibody Initiative Antivenom. Social Media Share Tools.
To skip the text and go directly to the objects, CLICK HERE The bite or sting of a highly venomous animal can inflict great suffering, including loss of limbs, paralysis, and an extremely painful death. CroFab is a monoclonal antibody antivenom used as an antidote to the venom of North American pit vipers, including rattlesnake, cottonmouth, and copperhead.
The Antibody Initiative What's an Antibody? Smallpox Diphtheria Tetanus Rabies Tuberculosis Antivenom Polio Whooping Cough MMR Influenza Disease, Allergy, and Immunotherapy Veterinary Diagnostics Monoclonal NYC Health Dept.
National Museum of American History Antivenin Nearctic Crotalidae - North American Anti-Snake-Bite Serum. National Museum of American History Antivenin Nearctic Crotalidae - North American Anti-Snake-Bite Serum - M National Museum of American History Antivenin - Latrodectus Mactans, Black Widow Spider - Lyovac.
Figure 4. Dog with diffuse swelling of the left forelimb, chest, neck, and face characteristic of pit viper envenomation. Tachycardia developed, prompting an additional pRBC transfusion. By day 4, the dog remained weak but was ambulatory.
On day 7 of hospitalization, progressive edema of the hindlimbs and ventrum developed, prompting steroid anti-inflammatory therapy based on concern for serum sickness. The dog developed phlebitis where the original catheter was placed, nausea and vomiting, and hyphema of the left eye.
These were managed with antibiotics, antiemetics with parenteral nutrition, and topical steroids and atropine, respectively. He made a full recovery despite severe envenomation. Pit vipers are known to inhabit the southeastern United States particularly North and South Carolina, Georgia, Florida, Alabama, Mississippi, and Louisiana.
In general, most snake bites occur in the spring and summer months, particularly between the months of June and October. Antivenom therapy is the only therapy proven to affect mortality in humans bitten by pit vipers.
It is often used alone or in conjunction with other therapies. The dog in this case required a significant volume of pRBCs owing to gastrointestinal hemorrhage combined with severe hemolysis, as well as plasma products for oncotic support. Three types of antivenom products are available, and understanding the differences in these products can aid clinical decision making.
All antivenoms are made by inoculating horses or sheep with venom from different snakes to create a polyvalent antibody product that provides improved venom neutralization for a variety of snake species. Hyperimmune plasma from the horse or sheep is harvested via plasmapheresis, producing antivenom after a series of processing steps.
Further classification of antivenoms depends on the processing steps. The antigen binding site is at the end of the Fab fragment; therefore, each step creates a smaller product that retains the ability to bind venom.
Figure 5. Antivenom types. A Whole IgG antibody with the fragment crystallizable Fc region made of 2 heavy chains, light chains, and antigen binding sites.
The whole IgG antibody creates IgG antivenom. C Further cleavage with papain creates Fab antivenom. Antivenom products available for treatment of dogs and cats bitten by pit vipers include whole, equine-derived antivenom crotalidae polyvalent ACP IgG Antivenin; Boehringer Ingelheim, bi-vetmedica.
com ; Rattler Antivenin; Mg Biologics, mgbiologics. com , and ovine-derived crotalidae polyvalent immune Fab antivenom CroFab; BTG International, crofab. com TABLE 1. Each product has differences in horse or sheep protein contamination, tissue penetration, and half-life.
In general, the smaller the molecular weight of the antivenom, the better tissue penetration is expected, and the shorter the half-life due to faster clearance from the body. IgG antivenom is available in both a powder form Antivenin and frozen liquid form Rattler Antivenin. Antivenin must be reconstituted prior to use, which can take 10 to 15 minutes or longer.
Once reconstituted, the product is further diluted in saline before administration and is typically administered over 30 minutes unless signs of allergic reaction develop.
Rattler Antivenin is a frozen product with a 3-year shelf life that does not require reconstitution or dilution and can be thawed in a warm water bath in 5 minutes. A blood filter should be used for administration according to the product label.
VenomVet is a liquid product, which eliminates the time delay for reconstitution, and should be diluted in crystalloid fluid before administration.
CroFab is a lyophilized powder and requires reconstitution with further dilution in mL 0. It is thought to be the least immunogenic antivenom available; however, this has yet to be determined in both human and veterinary medicine. There are no evidence-based guidelines in veterinary medicine to guide dosing of antivenom, and dosing schedules have largely been derived from human literature, clinical experience, and experimental studies.
Clinical decisions whether to administer additional vials are often made based on trends in the SSS. The SSS should be used with caution on initial presentation, as signs of envenomation take time. In cases of acute envenomation—when antivenom is most effective—the SSS may be low, but it can progress if the patient is left untreated.
Adverse reactions to antivenom administration can be acute or delayed.
To skip the text and go directly to Antvienom objects, CLICK HERE. The bite or sting Sosage a highly venomous animal Antivenkm Promoting heart health with fruits Antivebom suffering, including Antioxidant properties of limbs, paralysis, and guifelines extremely painful death. In the United States, envenomation the injection of venom usually happens during an encounter with a snake, spider, or insect. Antivenom is still produced by much the same method that was developed in the s to produce antitoxins for diphtheria and tetanus. An animal, such as a horse or goat, is injected with a small amount of venom.
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