The management of viper bites on the hand

Introduction

The Viperidae family is responsible for a majority of venomous snake bites in Anatolia (Okur et al., 2001). Although one species of the Elapidae family has been reported in Southeast Anatolia, no bites have been reported yet (Ugurtas et al., 2001). In Çukurova (Southern Anatolia), the typical venomous snakes found are Vipera ammodytes meridionalis and Vipera lebetina obtusa (Acikalin et al., 2008). If appropriate treatment is administered, there is a very low complication rate; otherwise, serious sequelae can occur (Al et al., 2010).

Bites by members of the Viperidae family tend to cause haematotoxic effects and symptoms of local toxicity. These include oedema, hyperaemia, ecchymosis, marks of teeth, blistering, pain, necrosis, and regional lymphadenopathy (Acikalin et al., 2008; Davidson and Schafer, 1994; Okur et al., 2012). Bites can result in amputation, acute renal failure, infection, compartment syndrome, and death (Acikalin et al., 2008; Al et al., 2010; Bozkurt et al., 2008; Ertem et al., 2005; Fırat et al., 2012).

It is not always possible to diagnose venomous snake bites by blood tests. Nonspecific findings are usually all that can be relied upon, with an increase in white blood-cell count (WBC), increased levels of lactate dehydrogenase (LDH), creatine kinase (CK), and tumour necrosis factor alpha (TNFα), and a decrease in haemoglobin levels (Acikalin and Gokel, 2011; Okur et al., 2012). The local signs associated with envenomation are prominent with Viperidae bites (Acikalin et al., 2008; Bozkurt et al., 2008). Antivenom therapy should be provided if hyperaemia continues and/or oedema does not regress. Haematological follow-up, along with the local findings, provide a clearer picture of the extent of envenomation and the possible treatment options. The initial signs of venomous snake bites in the blood are neutrophilia and leukocytosis. In addition, the haemoglobin level tends to increase before beginning to decrease after 4–6 h (Okur et al., 2012). After the immediate effects of the venom, the WBC begins to decrease to normal levels. However, this does not mean that the effects of the venom have been resolved completely.

The occurrence of specific enzymes in the venom plays a role in the clinical presentation (Al et al., 2010; Bozkurt et al., 2008; Okur et al., 2012). Hyaluronidase, one such enzyme present in the venom of the Viperidae family, accelerates the dissemination of venom through the tissues. Another enzyme is phospholipase A, which causes haemolysis by converting lecithin to lysolecitihin. These proteolytic enzymes destroy the endothelium of the vessels at the site of the snake bite, and are responsible for causing haemorrhagic oedema, blood leakage from the vessels, and systemic bleeding (Okur et al., 2012). In addition, the venom of V. lebetina contains serine, factor 5 activator, and metalloproteinase, which cause coagulation and fibrinolysis (Siigur et al., 2001). Moreover, kinin-releasing enzyme, another substance present in the venom of the Viperidae family, causes potent kinin production, hypotensive shock, and localized pain (Al-Joufi et al., 1991).

Although there is a consensus that antivenom therapy is required after a snake bite, there is no established protocol regarding the amount of antivenom that is required. The role of additional treatments in the prophylaxis of anaphylaxis owing to the antivenom and to prevent complications of Viperidae bites is also unclear. The results of treatment of Viperidae snake bites of the hand in our clinic is discussed in relation to these points.

Patients and methods

Between 2010 and 2012, 23 patients presenting with venomous snake bites to the hand were admitted to our clinic. Other snake bite admissions, which were caused by nonvenomous species, were not included in this study. Patients who were bitten at sites other than the hand or those who were treated or followed up by other hospitals were excluded. This study did not require institutional review board (IRB) approval because antivenom therapy is a standard treatment for venomous snake bite in our institution.

In 17 patients, the bites were on the fingers. Nine patients described the snake as a ‘dun-coloured snake’. The snake was captured and brought in by one patient, with investigation revealing that it was a V. lebetina. Furthermore, as mentioned above, members of the Viperidae family, particularly V. ammodytes meridionalis and V. lebetina obtusa, are frequently found around the Çukurova area (Acikalin et al., 2008; Okur et al., 2012). Therefore, it was assumed that the snake bites were caused by members of the Viperidae family and antivenom was administered based on this. Because wounds were contaminated with soil containing animal faeces, 250 IU of tetanus immunoglobulin was also administered intramuscularly for tetanus prophylaxis in all patients. The patients were admitted and managed in a standard hospital room. In an attempt to prevent the formation of severe oedema and the spread of venom into the circulation, the bitten extremity was kept at the same level as the heart. For analgesia 500 mg paracetamol was administered and 1 mg/kg tramadol hydrochloride was given to those patients whose pain was not relieved.

Three criteria were considered in the diagnosis of snake bite and the initiation of antivenom therapy (Okur et al., 2012): visual confirmation of the snake by the patient or parents; local symptoms and signs; and the haematological features. The snake bite was considered to be a venomous snake bite when two of the three criteria were positive. In suspicious cases, the patients were observed for at least 6 h, and those without progressive symptoms of a venomous snake bite were then discharged. The treatment algorithm that had been created for snake bite envenomation was followed (Figure 1).

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Figure 1.

Treatment algorithm for snake bite envenomation.

Total blood count and routine biochemical analysis were done in all patients immediately after admission. Adrenaline (0.25 mg dissolved in 1 mL physiological serum) was injected subcutaneously into the arms of all patients with an increase in circumference of an extremity, in order to prevent marked sensitivity reactions caused by the snake antivenom. According to the decrease in haemoglobin level, one to two vials (10–20 mL) of European Viper Venom® (Intervax Biological, Zagreb, Croatia) mixed with 150 mL physiological serum was administered intravenously 5 min after the injection of adrenaline, over 45 min. European Viper Venom®, which is effective against the venoms of V. ammodytes, V. aspis, V. berus, V. lebetina, V. ursinii, and V. xanthina, is the most commonly used antivenom in Turkey. The dose of antivenom is the same in children and adults, so the same dose of antivenom was given to all patients.

The total blood count was repeated every 6 h for all patients. Failure to observe a decrease in the haemoglobin level over two consecutive blood counts, along with regression of oedema and hyperaemia, were used as criteria for discharge. From our experience in using these 6-hourly total blood count results, 10 mL of antivenom was injected if there was a 0–1 g/dl decrease in the haemoglobin levels, and 20 mL of antivenom if there was a decrease of more than 1 g/dl. The enzymes present in snake venom cause oedema and vasoconstriction (Bozkurt et al., 2008; Grace and Omer, 1980; Juckett and Hancox, 2002). For this reason, to increase the plasma volume and the diameter of blood vessels, 0.6 mg/kg/h of pentoxifylline in 10 ml/kg of dextran 40 (Rheomacrodex®, Medisan Pharmaceuticals, Parsippany, NJ, USA ) was administered over 24 h for 3 days to 16 of the 17 patients who were bitten in the fingers, in addition to the antivenom therapy.

Results

Thirteen patients were male and ten were female, and their mean age was 32 years (range 12–71). The average time of admissions after snake bite was 11 h (range 1–74). The average duration of hospitalization was 4 days (range 1–7). The average number of antivenom vials administered was six per patient (range 2–17). With regard to the laboratory results, the average values and ranges were: WBC 14700 mm³ (range 9600–21,000); haemoglobin levels 12.6 g/dl (range 10.2–14.2); platelet count 144,000 U/L (range 57,000–183,000); LDH levels 212 (range 81–567); and CK 230 (range 89–421).

None of the patients received a blood transfusion or underwent fasciotomy. There were no severe sensitivity reactions owing to the snake antivenom. However, one patient required a surgical procedure, a full thickness skin graft that was applied after debridement. Although this patient developed an infection, and required antibiotic therapy, no other patient developed an infection or required antibiotic therapy.

Discussion

This study demonstrated that the probability of necrosis was minimal when antivenom therapy along with 0.6 mg/kg/h pentoxifylline in 10 ml/kg dextran 40 was administered over 24 h for 3 days, continued even after the decrease in haemoglobin level ceased. The efficacy of antivenom was tracked by 6-hourly total blood counts.

It has been suggested in a previous study that antivenom therapy should be stopped when the decrease in haemoglobin levels ceases (Okur et al., 2012). By using the 6-hourly total blood counts, we observed that in 14 patients the haemoglobin levels continued to decrease even after recovery.

In a previous report, allergic reactions to antivenom therapy were observed in eight of 45 patients (Acikalin et al., 2008). In contrast, Bozkurt et al. (2008) reported that allergic reactions occur in about 40% of patients after snake bites. Another study has demonstrated that such adverse events to antivenom therapy can be minimized by the injection of subcutaneous adrenaline (0.25 mg) (Premawardhena et al., 1999). The routine use of subcutaneous adrenaline in our study may explain why hypersensitivity reactions were not observed in any of our patients.

Serious complications such as thrombophlebitis, compartment syndrome, amputation, and acute renal failure have been observed in a larger group of 79 patients (Al et al., 2010). In that study, three doses of antivenom were administered to eight patients, two doses to 22 patients, and only one dose to 49 patients. The incidence of these serious complications might be a consequence of the administration of this low dose of antivenom. In addition, soft tissue infection was observed in 39% of patients. However, such serious complications were not observed in our study and antibiotic treatment was used in only one patient who required surgery. Instead of relying on antibiotic therapy, good wound care might be sufficient, and surgical treatment is used only when necessary. In a study of 20 patients with peripheral snake bites, surgical treatment was required in 12 patients, with permanent damage observed in half of them (Bozkurt et al., 2008). The average number of antivenom vials administered to these 12 patients was 1.7. Although later admission of the patients (i.e. on the second and third days after snake bite) resulted in complications, it could be that the amount of antivenom provided was insufficient. In our opinion, antivenom is indicated in patients with envenomation symptoms for up to 1 week after a bite.

There is almost no subcutaneous adipose tissue in the hands, and the skin is also thin; thus, a snake can easily breach it with its teeth. In addition, there are many veins on the skin surface of hands, which allow venom to be passed easily into the circulation. The enzymes present in snake venom cause oedema and vasoconstriction (Bozkurt et al., 2008; Grace and Omer, 1980; Juckett and Hancox, 2002). For this reason, it is necessary to be more aggressive in the management of snake bites to the hand. The plasma volume and the diameter of blood vessels can be increased in patients by administration of dextran and a peripheral vasodilator. This administration is a common procedure in patients with circulatory problems, but this is the first report of its use for snake bites, to our knowledge. Although antivenom therapy decreases the enzyme activity of the venom, additional circulation-enhancing treatments might also help to mitigate its effects.

The probability of necrosis is high (67%) in peripheral snake bites (Ertem et al., 2005) but it occurred in only 4% in our study. If the snake bite is located on the extremities, the algorithm proposed by Okur et al. (2012) may be used for treatment. Unfortunately, necrosis may develop in distal snake bites even when antivenom therapy is given in a timely fashion and at appropriate doses. Nevertheless, the use of a peripheral vasodilator may decrease the rate of necrosis by increasing the circulation in the extremity. In our study, necrosis did not occur when 0.6 mg/kg/h pentoxifylline in 10 ml/kg dextran 40 was administered over 24 h for 3 days. Peripheral vasodilators were not administered to the patient who developed necrosis (Figure 2).

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Figure 2.

Appearance of necrosis on the finger and oedema on the hand.

Repetition of antivenom therapy is necessary to decrease the complication rates in patients with venomous snake bites. If the bite is on a distal extremity, such as the hand, more aggressive management is required. Moreover, the addition of a peripheral vasodilator to antivenom therapy may decrease the complication rates in cases where the bite is to the fingers.