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Fransciscus Ginting, Restuti, Endang, Tambar Kembaren, Yosia Ginting, Ricky Rivalino Sitepu

Tropical Infenction Medicine - Internal Medicine Department

Medical Faculty North Sumatera University - RSUP. H. Adam Malik Medan


Several unique clinical syndromes are associated with snake bites. Hemmorraghic
symptoms and renal failure are frequent accompaniment of snakebite. A case of a 60-year-old
man who presented to the emergency department with complaints of a massive swelling and
ecchymosis of the involved proximity. He also developed acute kidney injury (AKI) which were
shown from increasing serum creatinine level. He was given polyvalent anti venom and later
heparin injection. A week after following treatment, his renal function was corrected and a
noticeable reduction in leg swelling were seen.
The aim of this report is to give information of any common pathological disorder
following snake bites.

Keywords : Renal failure, DIC, Snake bite.


Snake bites are uncommon cases in Medan however its morbidity and mortality is a serious
problem since it may cause multiple organs failures. Several clinical syndrome are resulting from the
effects of the toxins in snake venoms. The important clinical effects include neurotoxicity,
coagulopathy, myotoxicity, local necrosis, and renal toxicity. Renal failure and coagulopathy are the
most important effects and occurs in many species of venomous snake with the prevalence of up to
30% and 5% respectively [1, 2].
The mechanism of coagulation activation in venom induced consumption coagulopathy
(VICC) differs from disseminated intravascular coagulopathy (DIC). DIC results from several
different mechanisms that result in fibrin deposition. The activation in DIC is mediated by the tissue
factor/factor VIIa pathway while in VICC is usually due to the snake procoagulant toxin. A major
difference between VICC and DIC is that in VICC there is no obvious fibrin deposition and
microvascular thrombotic obstruction. Thus VICC is usually only complicated by bleeding, whereas
DIC is characterized by both end-organ failure resulting from microvascular thrombi as well as
bleeding complications [3, 4].
The pathogenesis of renal failure in snake bites includes several causes such DIC,
hypotension, hemolysis, hemoglobinuria, rhabdomyolysis as well as direct cytotoxic effect of the
venom. The histopathological findings on kidney biopsy are variable; acute tubular necrosis is the

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most common and is observed in 7080% of patients [5].
The clinical effects of snake-bites are varied depending on the range of activities of the venom. It
can cause either local effect, i.e. swelling, pain, bleeding, blistering, lymph node enlargement, and
necrosis in the bitten area; and it can also cause systemic symptoms, i.e. nausea, vomiting, malaise, and
drowsiness. Additionally, it could possibly affect cardiovascular causing shock and arrhythmia,
neurology which lead to paralysis of respiratory muscle, hemorrhagic disturbance, and renal failure [6].
The diagnosis of snake bite or determination of which snake is responsible for envenoming of a
victim can be conveniently divided into clinical diagnosis and laboratory diagnosis. Clinical diagnosis
depends upon recognising specific signs of envenoming in the patient. This includes local signs such as
swelling, blistering, and local necrosis. More importantly for accurate diagnosis, systemic signs, such as
haemorrhage, incoagulable blood, and hypovolaemic shock, are common mainly in viper bite, whereas
neurotoxic signs occur primarily in elapid bite, and rhabdomyolyis (muscle damage) in sea snake bite
[6, 7].
The aim of treatment are to retard systemic absorption of venom, neutralizes venoms, prevent
and controlling any complications. Recommended first-aid methods are to immobilized the whole of
patients body, apply pressure pad on proximal and distal of bitten area, and avoid any with the bite
wound (incisions, rubbing, vigorous cleaning, massage, application of herbs or chemicals) [8].
Antivenom should be given only to patients in whom its benefits are considered likely to
exceed its risks. Since antivenom is relatively costly and often in limited supply, it should not be
used indiscriminately. It consist of immunoglobulin that were purified from horse or donkey that will
neutralized particular venom. Antivenom is given if patient develop sign of systemic envenoming
including haemostatic abnormalities, neurotoxic, cardiovascular abnormalities, kidney failure. It can
also be given if there are severe local envenoming such as rapid extension of swelling. The dose vary
between 5-25 vials according to the severity [8].


A 60-year-old healthy male was bitten on the lower calf of his left foot by a mid-sized snake
as he was walking through rice field. Patient did not know the species of the snake, it was described
as a one meter long green-coloured snake. There was immediate pain around the fang marks, to
which he applied water and then tying tight bands around the limb. Within 2-3 hours after incident
he was brought to Adam Malik hospital.
At admission, patients vital sign showed sensorium compos mentis, blood pressure of
140/80 mmHg, pulse frequency 82x / minute regular, respiratory frequency 22x / min, the
temperature of 37,5C. Nutritional status of BMI is 26.6 kg / m2 which is overweight. Physical
examination revealed swelling and tenderness of the left lower leg. Patient also developed numerous
ecchymosis around the fang marks (Picture 1). Other physical examination are within normal limit.
From laboratory examination: Hb 10.90 g / dl, leukocytes 13,240 / mm3, platelets 15,000 /
mm3, neu/lim/mo/eo/bas: 75.9/8.2/14.6/1.1/0.2. Urea 163.50 mg/ dl, creatinine 5.5 mg / dl, uric acid:
6.2 mg / dl, Na: 136 meg / L, K: 4.5 meg / L, Cl: 107 meg/ L, albumin: 3.1 g/L, KGD adr: 97.5 mg/dL,
Thorax X-ray and ECG examination showed cardiomegaly, suggesting that patient has chronic
hypertension. Patient were then given fluid resuscitation, followed by 1 vial of antivenom or SABU
(serum anti bisa ular), antibiotic, and analgesics.
The following day, patient developed more ecchymosis which developed into hematoma.
Hemorrhagic screening test revealed prolonged protrombin time: 80.0 (control: 13.6); INR: >6.0; APTT:

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>120.0 (control: 32.8); and trombin time: 81.7 (control: 17.0); Fibrinogen: 485 mg/dl (150-440); D-
dimer: 770 (normal: <500). DIC scores were calculated with the result of 6 (normal: 1-4), indicating
probability of DIC. Additional treatment of heparin were added at 5000 IU for every 12 hours.
On the fourth day of hospital admission, patient showed general improvement. The leg
swelling and hematoma markedly decreased. Patient still felt minimal pain but able to move around.
Blood examination slight decreased in hemoglobin, but others blood component showed good
improvement (Table 1). Patient were discharge on the next day.

(a) (b)
Picture 1. (a) Site of the wound, on the lower cruris. (b) Hematoma developed one day after hostipal admission.

Table 1. Result of blood examination

Hematology 1st Day 4th Day
Hb 10.9 g/dl 7.6 g/dl
Leukocytes 13,240 /mm3 12,590 /mm3
platelets 15,000 / mm3 160,000/mm3
Neutrofil 75.9 % 61.0 %
Limfosit 8.2 % 12.6 %
Monosit 14.6 % 16.4 %
Eosinofil 1.1 % 9.4 %
Basofil 0.2 % 0.6 %
Ureum 163.50 mg/dl 73.1 mg/dl
Creatinine 5.50 mg/dl 1.83 mg/dl
Prothrombin 80.0 (control: 13.6) 20.3 (control: 13.6)

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INR > 6.0 1.52
APTT >120.0 (control: 32.8) 35.5 (control: 32.8)
Thrombin time 81.7 (control: 17.0) 80 (control: 17.5)
Fibrinogen 485 mg/dl (n: 150-440) 420 mg/dl
D-dimer 770 ng/ml (n: <500) 710 ng/ml
Electrolite Na: 136; K: 4.5; Cl: 107 -


Snake venoms are complex mixtures of toxic materials, some of which are coagulant or
fibrinolytic or both. Venoms of Viperidae, for example, contain serine proteases and other
procoagulant enzymes that are thrombin-like or activate factor X, prothrombin and other clotting
factors. These enzymes stimulate blood clotting with formation of fibrin in the blood stream.
However, this process results in incoagulable blood because most of the fibrin clot is broken down
immediately by the bodys own plasmin fibrinolytic system and, sometimes within 30 minutes of the
bite, the levels of clotting factors are so depleted consumption coagulopathy that the blood will not
clot. Some venoms contains toxins that activate factors V, X, IX and XIII, fibrinolysis, protein C,
platelet aggregation, anticoagulation and haemorrhage (see Picture 2. [9, 10]
Based on World Health Organizations (WHO), bleeding and clotting disturbances usually
respond satisfactorily to treatment with specific antivenom, but the dose may need to be repeated
several times, at six hourly intervals. Heparin and antifibrinolytic agents are ineffective against
venom-induced thrombin and may cause bleeding on its own account. It should never be used in
cases of snake-bite. In severe bleeding, restoration of coagulability and platelet function can be done
by giving fresh frozen plasma, cryoprecipitate (fibrinogen, factor VIII), fresh whole blood or platelet
concentrates. [11]
In this case, patient had prolonged prothrombin time, decreased platelet count, and increased
in fibrin-related marker, resulting in DIC score of 6 which is compatible with overt DIC. Patient
were given heparin, which according to WHO is either ineffective or contraindicated. The DIC-like
symptoms were almost certainly just a consumption coagulopathy that happened hours after patient
was bitten. Consumption coagulopathy were probably would be resolved even without heparin.
According to Indonesia Department of Health (Depkes), anti-venom should be given at least
3 hours after incident. The amount can be varied from 5-25 vials depending on the degree of the
severity (see Table 2). On 0th and 1st degree, anti-venom is not necessary, but patient should be
monitored to see if the condition were worsen. 2nd degree of snake bite need 5-15 vials of anti-
venom. 3rd degree of snake bite need 15-20 vials of anti-venom, and 4th degree need at least 25 vials
of anti-venom. Supportive therapy should be given in all case of snake bite. [12]
Patient had symptoms of moderate internal bleeding. In this case, patient should at least
classified on 3rd degree of snake bite and received no less than 15 vials of anti-venom. However,
only 1 vial of anti-venom was administered to patient. The lack of anti-venom might be the reason
that the bleeding was worsened on the following days. [12]
The renal failure that patient suffered was probably the result of rhabdomyolysis. Myoglobin
and potassium released from damaged skeletal muscle may cause renal failure. In some cases, the
renal failure is attributed to tubular necrosis and cortical necrosis. Acute kidney injury (AKI) usually

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happened in 5-30% of the victims of viper poisoning. There is no specific treatment needed, and
symptoms usually gone in few days.

Table 2. Snake-bite classification based on Schwartz (Depkes 2001) [12]

Derajat Venerasi Luka Nyeri Edema/Eritema Sistemik
0 0 + +/- < 3cm/12 jam 0
I +/- + - 3-12 cm/12 jam 0
II + + +++ > 12-25 cm/12 jam + Neurotoksik, mual, pusing,
III + + +++ > 25 cm/12 jam ++ Petekie, syok, ekhimosis
IV +++ + +++ > Ekstremitas ++ gagal ginjal akut, koma,

Picture 2. Different type of snake has venom that could induced coagulation


A reported case of snake bite where patient developed renal failure and hematologic disorder.
Diagnosis was made based on clinical manifestations, diagnostic physical examination, laboratory
tests, ultrasound kidney and urinary tract as well as the CT Scan Whole Abdomen and conservative
therapy. Patients was discharged with clinical and laboratory improvement. Then the patient is
recommended to control outpatient treatment to Poli Penyakit Tropik dan Infeksi.

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