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BACKGROUND
Viperidae
Elapidae
Atractaspididae
PS) - has the ability to inject could use a modified teeth (canines).
In addition there constituent substances that are neurotoxic venom post synapse is bungarotoxin and cobrotoxin, which consists of 60-62 or 66-74 aminio acids and
phospholipase A subunit that release acetylcholine at the neuromuscular junction in the
peripheral nerves and prevents the release of neurotransmitters.
Increased vascular permeability if it continues will lead to shock or shock which if untreated
can lead to death. Often is neurotoxic venom that causes paralysis (paralysis) and cessation of
breathing, as well as cardiotoxic effect causes the heartbeat stops also affect the occurrence of
miotoksik.
4. PATHOGENESIS
Blood clotting disorders
Generally rattlesnake, usually containing serine proteases, metalloproteinases that interfere
with hemostasis by activating or inhibiting the coagulant factor or platelet and vascular
endothelial damage. Enzymes in snake venom binds to platelet receptors induce or inhibit
platelet aggregation. Procoagulant enzymes will activate prothrombin, factor V, X, XIII and
pasminogen endogenous. Combinations of anticoagulant activity, disruption of number and
platelet function and damage to the endothelial walls of the blood vessels resulting in severe
bleeding in patients,
Diseases of blood clotting (coagulation) marked defibrinasi associated with platelet counts. In
addition it can convert prothrombin to thrombin and reducing factor V, VII, protein C and
plasminogen.Tekanan in the cardiovascular system causing DIC or pressure in the heart
muscle.
NEUROTOXIC
Is neurotoxic venom that would hinder the excitation of peripheral neuromuscular junction in
various ways. So that the most frequent symptoms are drowsiness, indicating that there may
influence the central sedation associated with a small non-protein molecules contained in the
king cobra snake venom. Most of neurotoxins will result in pamanjangan effects of
acetylcholine, resulting paralysis symptoms such as ptosis, external ophtalmoplegia,
mydriasis, and depression airway and total flacid paralysis as in patients with Myastenia
Gravis. In addition there is a pattern that is difficult descending paralysis described in
pathophysiology.
hypotension
impaired vision, conjunctival edema (chemosis)
sweating and hypersalivation
arrhythmias, pulmonary edema, shock
Signs of spontaneous bleeding (petechiae, epistaxis, hemoptoe)
Paresthesia.
4. Status localist:
Imaging
Chest x-rays to see if there is pulmonary edema
Other
Looking for signs of compartment syndrome.
Diagnosis
- Anaphylaxis
- Deep vein thrombosis (DVT)
- Scorpion bites
- Septic shock
- Bee sting
- Infected wounds
Classification
The degree of snakebite:
1. Degree 0
- Former two canine bites - No systemic symptoms after 12 hours
- Swelling and minimal pain
2. Grade I (Minimal)
- Former two canine bites
- Swelling and redness with a diameter of 1-5 inches
- There is no systemic signs up to 12 hours
- Moderate to severe pain
3. Grade II (Moderate)
- Former two canine bites
- Severe pain, swelling and redness with a diameter of 6-12 inches in 12 hours
- Petechie, echimosis, perdarah to bite
- There are signs of systemic (nausea, vomiting, fever, enlargement of the lymph nodes)
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Anti-venom therapy was first introduced by Albert Calmette from the Pasteur Institute in
Saigon in 1890.1 There are two types of snakes are the first antitoxin made from horse serum
after horses injected with sublethal doses of snake venom. Antitoxin is then processed and
refined but still containing serum proteins that may still have antigenic properties. The second
type is recommended that the FDA in 2000 monovalent fragments of sheep immunoglobulin
purified to avoid antigenic proteins. 5
SABU should be given to the patient if necessary if a greater benefit. An indication of SABU:
- The existence of hemostatic abnormalities
Clinically the presence of spontaneous bleeding, coagulopathy (seen from the physiology of
hemostasis),
- Signs neurotoksis (ptosis, respiratory muscle paralysis)
- Abnormalities of cardiovascular (hypotension, shock, arrhythmias, abnormal ECG)
- Acute Kidney Injury (oliguria / anuria, increase in serum urea and creatinine or)
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Antibiotics
Analgesics
If necessary can be given strong analgesics such as opioids groups: pethidine with adult dose
of 50-100 mg, children 1-1.5 kg / kg or morphine at a dose of 5-10 mg adults and children
from 0.03 to 0.05 mg / kg.
6. Complications
The main causes of disability are things local necrosis and compartment syndrome. Extensive
necrosis may require action debridement or amputation due to damage to the deeper tissues.
At a later date can only arise osteomyelitis, and chronic ulcers. If after a snake bite had
occurred resulting in paralysis of the respiratory muscles and the brain hypoxia can result in
permanent neurological deficits.
7. Monitoring
In patients with respiratory failure may be given oxygen, intubation or manual bagging and
usually will repair within 1 month. Can also be given Anticholinesterase. Bed rest and
restriction of movement necessary to avoid trauma in patients with impaired hemostasis, can
be given a transfusion of FFP (Fresh Frozen Plasma) and cryoprecipitate with platelet
concentrate, but if no one can diebrikan Whole Blood. Sometimes required vasopressor
dopamine or norepinephrine similar in patients with shock or damage to the myocardium and
dialisi case of AKI. The presence of rhabdomyolysis resulting in metabolic acidosis as the
crush injury can be corrected with the appropriate dose of sodium bicarbonate.
REFFERENCE
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Oxford,
Prihatini, Trisnaningsih, Muchdor, U.N. Rachman. 2007. Penyebaran gumpalan
dalam pembuluh darah (disseminated intravascular coagulation) akibat racun gigitan
ular. Indonesian Journal of Clinical Pathology and Medical Laboratory, Vol. 14, No. 1,
November 2007.
Cribari, Cris. 2004. Management of Poisonous Snakebites. American College of
http://emedicine.medscape.com/article/168828-overview
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