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Scorpion Envenomation


Scorpions vary in size from 1-20 cm in length Out of 1500 scorpion species, 50 are dangerous to humans. Almost all of these lethal scorpions, except the Hemiscorpius species, belong to the scorpion family called the Buthidae. The Buthidae family is characterized by a triangular-shaped sternum, as opposed to the pentagonal-shaped sternum found in the other 5 scorpion families.

scorpions are not aggressive. They do not hunt for prey; they wait for it

 amount of venom ejected, is usually 0.1-0.6 mg.  Venom deposited via the intravenous route can cause symptoms only 4-7 minutes after the injection, with a peak tissue concentration in 30 minutes and an overall toxin elimination half-life of 4.2-13.4 hours through the urine  The venom is composed of varying concentrations of neurotoxin, cardiotoxin, nephrotoxin, hemolytic toxin, phosphodiesterases, phospholipases, hyaluronidases, glycosaminoglycans, histamine, serotonin, tryptophan, and cytokine releasers  The binding of these neurotoxins to the host is reversible

Clinical Presentation
Time of envenomation Nature of the incident Description of the scorpion: Specimen identification by an entomologist may be helpful (if the scorpion can be captured safely). Local and systemic symptoms: Pain and paresthesias often are present. Nausea and vomiting are common Scorpion species Scorpion age, size, and nutritional status Healthiness of the scorpion's stinging apparatus (telson) Number of stings and quantity of venom injected Depth of the sting penetration Composition of the venom Site of envenomation: Closer proximity of the sting to the head and torso results in quicker venom absorption into the central circulation and a quicker onset of symptoms. Age of the victim Health of the victim Weight of the victim relative to amount of venom

 The toxicity, and duration of the symptoms depends on the following factors:

Clinical manifestations
 Local tissue effects vary among species  Tachycardia and other dysrhythmias are caused by autonomic effects primarily, although direct myocardial toxicity with arrhythmogenic effects has been described  Hypertension or hypotension may be present.  The patient may have hyperthermia.  Respiratory arrest and loss of protective airway reflexes  Pulmonary edema secondary to cardiogenic causes and to increased capillary permeability  Autonomic effects include the following:
 Sympathetic overdrive symptoms predominate, causing tachycardia, hypertension, hyperthermia, and pulmonary edema.  Parasympathetic symptoms include hypotension, bradycardia, salivation, lacrimation, urination, defecation, and gastric emptying

Cranial nerve effects include the following:

Classic roving or rotary eye movements, blurred vision, tongue fasciculations, and loss of pharyngeal muscle control may be observed. Difficulty swallowing combined with excessive salivary secretions may lead to respiratory difficulty

Cerebral infarction, cerebral thrombosis, and acute hypertensive encephalopathy have been described The mode of death is usually via respiratory failure secondary to anaphylaxis, bronchoconstriction, bronchorrhea, pharyngeal secretions, and/or diaphragmatic paralysis, even though venom-induced multiorgan failure plays a large role.

Children present with the same symptoms and signs as adults, except their symptoms are more severe and protracted

Nonneurologic systemic signs

1. Cardiovascular signs:Usually follow a pattern of a hyperdynamic phase followed by a hypodynamic phase .
Hypertension is described as follows: Secondary to catecholamine and renin stimulation Observed as early as within 4 minutes after the sting Lasts a few hours High enough to produce hypertensive encephalopathy Hypotension - Less common and occurs secondary to excess acetylcholine or catecholamine depletion

Tachycardia is greater than 130 beats per minute, although bradycardia can be observed. Transient apical pansystolic murmur is consistent with papillary muscle damage. Cardiovascular collapse occurs secondary to toxin induced myocarditis biventricular dysfunction and profuse loss of fluids from sweating, vomiting, diarrhea, and hypersalivation  Mild envenomation - Vascular effect with vasoconstriction hypertension  Moderate envenomation - Left ventricular failure hypotension with and without an elevated pulmonary artery wedge pressure, depending on fluid status of the patient  Severe envenomation - Biventricular cardiogenic shock

2. Respiratory signs:
 Tachypnea may be present.  Pulmonary edema with hemoptysis and a normal-sized heart is observed in 7-32% of respiratory cases. This is secondary to a direct toxin-induced increased pulmonary vessel permeability effect and is also secondary to catecholamine-induced effects of hypoxia  Respiratory failure may occur secondary to diaphragm paralysis, alveolar hypoventilation, and bronchorrhea

3. Allergic signs:
 Patients may have urticaria.  Angioedema is reported.  Patients may present with bronchospasm.  Anaphylaxis is possible.

4. Gastrointestinal signs Patients may present with

excessive salivation. Dysphagia is possible. Nausea and vomiting are reported. Gastric hyperdistention occurs secondary to vagal stimulation. Increased gastric acid output may lead to gastric ulcers. Acute pancreatitis may lead to hyperglycemia. Liver glycogenolysis may occur from catecholamine stimulation. Toxic hepatitis

5. Genitourinary signs: Patients have decreased

renal plasma flow.

Toxin-induced acute tubular necrosis renal failure may occur. Rhabdomyolysis renal failure may result from venom-induced excessive motor activity. Priapism may occur secondary to cholinergic stimulation

6. Metabolic signs

Hyperglycemia may occur from

catecholamine-induced hepatic glycogenolysis, pancreatitis, and insulin inhibition. Increased lactic acidosis may occur from hypoxia and venom-induced increased lactase dehydrogenase activity. Patients may have an electrolyte imbalance and dehydration from hypersalivation, vomiting, diaphoresis, and diarrhea

Laboratory Studies
Obtain a CBC count for leukocytosis and hemolysis Electrolyte evaluation Coagulation parameters Glucose levels should be measured Creatine kinase and urinalysis aspartate aminotransferase and alanine aminotransferase levels Obtain arterial blood gas chest radiograph Echocardiography ,EEG

Medical Care
individualize management of scorpion stings Local treatment is discussed as follows:
A negative-pressure extraction Use ice bags to reduce pain and to slow the absorption of venom
Immobilize the affected part in a functional position below the level of the heart to delay venom absorption.

Calm the patient to lower the heart rate and blood pressure For medical delay secondary to remoteness, consider applying a lymphatic-venous compression wrap 1 inch proximal to the sting site to reduce superficial venous and lymphatic flow of the venom but not to stop the arterial flow. Only remove this wrap when the provider is ready to administer systemic support Apply a topical or local anesthetic agent to the wound to decrease paresthesia Administer tetanus prophylaxis Administer systemic antibiotics if signs of secondary infection occur. Administer muscle relaxants for severe muscle spasms (ie, benzodiazepines.)

predominance Mild - Local signs Moderate - Ascending local signs or mild systemic signs Severe - Life-threatening systemic signs

Neurologic predominance:
Grade I - Local pain or paresthesia at the sting site (83%) Grade II - Pain or paresthesia that has traveled from the sting site (9.1%) Grade III - Either cranial nerve or somatic neuromuscular dysfunction (4.7%) Grade IV - Both cranial nerve and somatic neuromuscular dysfunction (3%)

Systemic treatment is instituted by directing supportive care toward the organ specifically affected by the venom:

Establish airway, breathing, and circulation

Monitor vital signs (eg, pulse oximetry; heart rate, blood pressure, and respiratory rate monitor). Administer oxygen.

Administer intravenous fluids For hyperdynamic cardiovascular changes, administration of a combination of betablockers with sympathetic alpha-blockers is most effective in reversing this venominduced effect nitrates can be used for hypertension and myocardial ischemia. For hypodynamic cardiac changes, a titrated monitored fluid infusion with afterload reduction helps reduce mortality. A diuretic may be used for pulmonary edema in the absence of hypovolemia, but an afterload reducer, such as prazosin, nifedipine, nitroprusside, hydralazine, or angiotensin-converting enzyme inhibitors, is better. Insulin administration in scorpion envenomation animal experiments has helped the vital organs to use metabolic substrates more efficiently, thus preventing venominduced multiorgan failure

The use of steroids to decrease shock and edema is of unproven benefit.

Antivenom is the treatment of choice after stabilization and supportive care. Because of the heterogeneity of venom composition between different scorpion species, one specie s antivenom will have limited effect on another scorpion specie s venom. Thus, correct scorpion species identification is a prerequisite for proper antivenom treatment Antivenins Composed of venom-specific F(ab )2 fragments of immunoglobulin G (IgG) that bind and neutralize venom toxins, facilitating redistribution away from target tissues and elimination from the body