Scorpion sting (Scorpion Envenomation)

Subject: Scorpion sting (Scorpion Envenomation) 11/8/2010, 4:23 am

Introduction

Background

Scorpion
stings are a major public health problem in many underdeveloped
tropical countries. For every person killed by a poisonous snake, 10 are
killed by a poisonous scorpion. In Mexico, 1000 deaths from scorpion
stings occur per year. In the United States, only 4 deaths in 11 years
have occurred as a result of scorpion stings. Furthermore, scorpions can
be found outside their normal range of distribution, ie, when they
accidentally crawl into luggage, boxes, containers, or shoes and are
unwittingly transported home via human travelers.A scorpion has a
flattened elongated body and can easily hide in cracks. It has 4 pairs
of legs, a pair of claws, and a segmented tail that has a poisonous
spike at the end. Scorpions vary in size from 1-20 cm in length.Out
of 1500 scorpion species, 50 are dangerous to humans. Scorpion stings
cause a wide range of conditions, from severe local skin reactions to
neurologic, respiratory, and cardiovascular collapse. Envenomation from
most scorpions results in a simple, painful, local reaction that can be
treated with analgesics, antihistamines, and symptomatic/supportive
care. This article focuses on scorpions that generally are considered
more dangerous to humans.

Scorpion sting (Scorpion Envenomation) 756148-768477-168230-1649414tn

Scorpion sting (Scorpion Envenomation) 756148-768477-168230-1649414tn

Scorpions from the family Buthidae (which
includes almost all of the potentially lethal scorpions)
generally can be identified by the triangular sternal plate. In
other families of scorpions, this feature is more square or
pentagonal. Photo by Sean Bush, MD.

Mortality/Morbidity

Accurate
worldwide data do not exist. The underreporting of scorpion stings is
frequent because most envenomations occur in desert and jungle areas
that do not have large medical facilities. Furthermore, reporting is not
required.Most deaths occur during the first 24 hours after the sting and are secondary to respiratory or cardiovascular failure.The
highest reported mortality rate is recorded in data from Mexico, with
estimates as high as 1000 deaths in 1 year. In the United States, 4
deaths were reported in an 11-year period according to one source.²However,
no deaths were reported to the American Association of Poison Control
Centers from 1983 to 1999. Only one death from the Arizona bark scorpion
(C sculpturatus) has been reported since 1964.³Ironically, the highest and lowest mortality estimates are associated with different species within the same genus of scorpion (Centruroides). Children
and elderly persons are at the greatest risk for morbidity and
mortality. A smaller child, a lower body weight, and a larger ratio of
venom to body weight lead to a more severe reaction. A mortality rate of
20% is reported in untreated babies, 10% in untreated school-aged
children, and 1% in untreated adults.In terms of venom lethality, the venom of Androctonus australis and Leiurus quinquestriatus are the most toxic. C sculpturatus venom is low in toxicity compared with most scorpions of medical importance.Furthermore,
patients in rural areas tend to fare worse than patients in urban areas
because of the delay in getting medical help due to a longer travel
time to medical centers. Fortunately, better public education, improved
control of the scorpion population, increased supportive therapies, and
more technologically advanced intensive care units have combined to
produce a substantial decrease in mortality from these envenomations. Race

No
racial predilection exists. Any differences in individual reactions to
the scorpion sting are a reflection of that individual's genetic
composition rather than race. Sex

Females are more susceptible than males to the same amount of scorpion venom because of their lower body weight. Age

While
adults are stung more often than children, children are more likely to
develop a more rapid progression and increased severity of symptoms
because of their lower body weight. Furthermore, elderly persons are
more susceptible to stings because of their decreased physiologic
reserves and increased debilitation.

Subject: Re: Scorpion sting (Scorpion Envenomation) 11/8/2010, 4:31 am

Clinical

History

For patients presenting with scorpion stings, ascertaining the following is essential:
- 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.

The toxicity, variation, and duration of the symptoms depends on the following factors:
- 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
- Presence of comorbidities
- Treatment effectiveness

Generally,
intrathecal and intravenous routes have immediate effects, while
subcutaneous and intramuscular routes take effect several minutes to
hours later.
Nonlethal scorpion species tend to produce local
reactions similar to a hymenopteran sting, while lethal scorpion species
tend to produce systemic symptoms. The duration to progress to systemic
symptoms ranges from 5 minutes to 4 hours after the sting. The symptoms
generally persist for 10-48 hours.

Physical

Local tissue effects vary among species.
- Minimal local tissue effects are present with Centruroides envenomation.
- Significant local tissue reaction rules out C exilicauda envenomation.
- Tapping over the injury site (ie, tap test) may cause severe pain after a sting by C exilicauda.

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 are common causes of mortality.
Pulmonary edema has been described and may be 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.

Somatic effects include the following:
- Restlessness and involuntary muscle jerking that can be mistaken for seizures have been described.
- Presence of true seizures in Centruroides
  envenomation is controversial and has not been proven to occur.
  Seizures are described in association with other scorpion envenomations.

Cerebral
infarction, cerebral thrombosis, and acute hypertensive encephalopathy
have been described with a variety of Buthidae scorpion envenomations.
The
signs of the envenomation are determined by the scorpion species, venom
composition, and the victim's physiological reaction to the venom. The
signs occur within a few minutes after the sting and usually progress to
a maximum severity within 5 hours. The signs last for 24-72 hours and
do not have an apparent sequence. Thus, predicting the evolution of
signs over time is difficult. Furthermore, a false recovery followed by a
total relapse is common.
A person who has been stung by a
scorpion usually has 4 signs, with the most common being mydriasis,
nystagmus, hypersalivation, dysphagia, and restlessness. 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.
Furthermore, they may display a restlessness that is out of proportion
when compared to any other disease. A child's symptoms have been
described as inconsolable crying; uncontrollable jerking of the
extremities; and chaotic thrashing, flailing, and writhing combined with
contorted facial grimaces. The symptoms mimic a centrally mediated
seizure, but the patient is awake and alert the entire time.
The grading of these scorpion envenomations depends on whether or not neurological signs predominate and is as follows:

Nonneurological 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%)

Local signs
- Neurotoxic local effects
  - Local
    evidence of a sting may be minimal or absent in as many as 50% of cases
    of neurotoxic scorpion stings. In fact, tissue necrosis is rarely
    found.
  - A sharp burning pain sensation at the sting site,
    followed by pruritus, erythema, local tissue swelling, and ascending
    hyperesthesia, may be reported. This paresthesia feels like an electric
    current, persists for several weeks, and is the last symptom to resolve
    before the victim recovers.
  - The tap test is administered by
    tapping at the sting site. A positive result is when the paresthesia
    worsens with the tapping because the site is hypersensitive to touch and
    temperature. In fact, wearing clothing over the area and sudden changes
    in temperature exacerbate the symptoms. Tapping over the injury site
    (ie, tap test) may cause severe pain after a sting by C exilicauda.
- Cytotoxic local effects
  - A macule or papule appears initially at the sting site, occurring within the first hour of the sting.
  - The diameter of the lesion is dependent on the quantity of venom injected.
  - The lesion progresses to a purpuric plague that will necrose and ulcerate.
  - Lymphangitis results from the transfer of the venom through the lymphatic vessels.
- Nonlethal local effects
  - Pain, erythema, induration, and wheal may be present.
  - These are secondary to venom activation of kinins and slow-releasing substances.
  - Local tissue effects vary among species. Minimal local tissue effects are present with Centruroides envenomation. Significant local tissue reaction rules out C exilicauda envenomation.

Neurologic
signs: Most of the symptoms are due to either the release of
catecholamines from the adrenal glands (sympathetic nerves) or the
release of acetylcholine from postganglionic parasympathetic neurons.
One study by Freire-Maia et al (1974) found that the adrenergic signs
occur at a low venom dose, while cholinergic signs occur at high venom
dose concentrations (ie, >40 mcg/100 g in Tityus serrulatus scorpion venom).⁴Furthermore,
the adrenergic phase tended to be more dependent on the venom dose than
the cholinergic phase. However, dual manifestations of the adrenergic
and cholinergic signs are possible because of varying organ system
sensitivities to these neurotransmitters.
- Central nervous system signs
  - Thalamus-induced systemic paresthesia occurs in all 4 limbs.
  - Patients experience venom-induced cerebral thrombosis strokes.
  - The level of consciousness is altered, especially with restlessness, confusion, or delirium.
  - Patients have abnormal behavior.
  - Ataxia is also a sign.
- Autonomic nervous system signs - Predominately sympathetic signs, parasympathetic signs, or a combination of signs
  - Sympathetic signs
    - Hyperthermia
    - Tachypnea
    - Tachycardia
    - Hypertension
    - Arrhythmia
    - Hyperkinetic pulmonary edema
    - Hyperglycemia
    - Diaphoresis
    - Piloerection
    - Restlessness and apprehension
    - Hyperexcitability and convulsions
  - Parasympathetic signs
    - Bronchoconstriction
    - Bradycardia
    - Hypotension
    - Salivation, lacrimation, urination, diarrhea, and gastric emesis (SLUDGE)
    - Rhinorrhea and bronchorrhea
    - Goose pimple skin
    - Loss of bowel and bladder control
    - Priapism
    - Dysphagia
    - Miosis
    - Generalized weakness
  - Somatic signs
    - Rigid spastic muscle of the limbs and torso
    - Involuntary muscle spasm, twitching, clonus, and contractures
    - Alternating opisthotonos and opisthotonus from inactivation of sodium channels, leading to increased sodium and calcium uptake
    - Increased tendon reflexes, especially prolongation of the relaxation phase
    - Piloerection accompanied by goose pimples
- Cranial nerve signs
  - Classic rotary eye movement may result in ptosis, nystagmus, and blurred vision.
  - Mydriasis is a sign.
  - Patients may have tongue fasciculations.
  - Dysphagia, dysarthria, and stridor occur secondary to pharyngeal reflex loss or muscle spasm.
  - Patients may present with excessive salivation and drooling.
- Peripheral
  nervous system signs - Intense local burning pain with minimal swelling
  at sting site, followed by ascending numbness and tingling, then
  paralysis and convulsions

Nonneurologic systemic signs
- 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 biventricular dysfunction and profuse loss
    of fluids from sweating, vomiting, diarrhea, and hypersalivation.
    - Observed in 7-38% of cardiovascular cases
    - 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
    - Cardiac
      dysfunctions attributed to catecholamine-induced increases in
      myocardial metabolism oxygen demand (leading to myocardial
      ischemia–induced myocardial hypoperfusion) and to the direct effects of
      the toxin (leading to myocarditis)
- 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 and intracellular calcium
    accumulation, which leads to a decrease in left ventricular compliance
    with resultant ventricular dilation and diastolic dysfunction.
  - Respiratory failure may occur secondary to diaphragm paralysis, alveolar hypoventilation, and bronchorrhea.
- Allergic signs
  - Patients may have urticaria.
  - Angioedema is reported.
  - Patients may present with bronchospasm.
  - Anaphylaxis is possible.
- 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
- 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. One small study by
    Bawaskar (1982) found a positive prognostic correlation to the
    development of cardiac manifestations following scorpion stings.⁵
- Hematological signs
  - Platelet aggregation may occur because of catecholamine stimulation.
  - Disseminated intravascular coagulation with massive hemorrhage may result from venom-induced defibrination.
- 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.
- Pregnancy signs - Toxin-induced uterine contraction
- Symptoms predictive of hospital admission
  - Priapism (odds ratio 150.59)
  - Vomiting (odds ratio 15.82)
  - Systolic blood pressure (SBP) greater than 160 (odds ratio 13.38)
  - Temperature greater than 38º C (odds ratio 3.66)
  - Heart rate greater than 100 beats per minute (odds ratio 3.35)

Symptomology of specific scorpion species
- Mesobuthus, Tityus, and Leiurus - Tend to cause severe cardiovascular symptoms
- Centruroides - Tend to cause neurological symptoms
- Hemiscorpius - Tend to cause tissue necrosis

Subject: Re: Scorpion sting (Scorpion Envenomation) 11/8/2010, 5:03 am

Histologic Findings

The
local sting site shows mixed inflammatory cell infiltrates with
eosinophils scattered among collagen bundles in an edematous dermis.
Myocardial changes, which are most prominent at the papillary muscle and
subendocardial region, include focal myocardial necrosis; myofibril
destruction, especially at the I band; fine fatty deposits in the
cardiac muscle fibers; interstitial edema; and increased cellularity,
mainly lymphocytes and monocytes. Changes resemble interstitial
hypoxia-induced myocarditis caused by large doses of catecholamines.

Subject: Re: Scorpion sting (Scorpion Envenomation) 11/8/2010, 5:23 am

Treatment

Medical Care

Prehospital Care

Primary assessment of airway, breathing, and circulation takes precedence.
Few studies have evaluated the utility of most first aid.
The utility of negative pressure extraction devices has not been evaluated for scorpion stings.
Perform endotracheal intubation and vascular access as needed.

Emergency Department CareSupportive care is the backbone of treatment for systemic symptomatology.

Grades of Centruroides envenomation
- Grade I - Local pain and/or paresthesias at the site of envenomation
- Grade II - Pain and/or paresthesias remote from the site of the sting, in addition to local findings
- Grade III - Either cranial nerve/autonomic dysfunction or somatic skeletal neuromuscular dysfunction
  - Cranial
    nerve dysfunction - Blurred vision, roving eye movements,
    hypersalivation, tongue fasciculations, dysphagia, dysphonia, problems
    with upper airway
  - Somatic skeletal neuromuscular dysfunction -
    Restlessness, severe involuntary shaking or jerking of the extremities
    that may be mistaken for a seizure
- Grade IV - Combined cranial nerve/autonomic dysfunction and somatic nerve dysfunction

Androctonus australis Hector Hospitalization Score
- Priapism: +3
- Vomiting: +2
- SBP >160: +2
- Corticosteroid PTA: +2
- Temperature >38ºC: +1
- Heart rate >100 bpm: +1

Total ³2 = Hospitalization

Although
grading and scoring systems have been developed they are limited due to
species specificity and low degree a symptoms that would lead to
hospitalization or therapy.

Medical careBecause
the clinical manifestations and severity of the symptoms vary among
patients, individualize management of scorpion stings. Furthermore,
frequent patient monitoring allows earlier recognition of the
life-threatening problems of scorpion envenomation. Treatment generally
consists of moving the patient away from the scorpion and stabilizing
the patient's airway and vital signs, followed by administration of
antivenin and institution of symptomatic and local treatment.

Local treatment is discussed as follows:
- A
  negative-pressure extraction device (ie, the extractor) may be useful,
  although the benefit is unproven. The extractor creates a negative
  pressure of 1 atm. Apply it to the sting site after incision. Oral
  extraction is contraindicated.
- Use ice bags to reduce pain and
  to slow the absorption of venom via vasoconstriction. This is most
  effective during the first 2 hours following the sting.
- 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, thus limiting the spread of the venom.
- 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. The drawback of this wrap is that it
  may intensify the local effects of the venom.
- Apply a topical or local anesthetic agent to the wound to decrease paresthesia; this tends to be more effective than opiates.
- Administer local wound care and topical antibiotic to the wound.
- Administer tetanus prophylaxis.
- Administer systemic antibiotics if signs of secondary infection occur.
- Administer muscle relaxants for severe muscle spasms (ie, benzodiazepines.)

Systemic treatment is instituted by directing supportive care toward the organ specifically affected by the venom.
- Establish airway, breathing, and circulation (ie, ABCs) to provide adequate airway, ventilation, and perfusion.
- Monitor vital signs (eg, pulse oximetry; heart rate, blood pressure, and respiratory rate monitor).
- Use invasive monitoring for patients who are unstable and hemodynamic.
- Administer oxygen.
- Administer
  intravenous fluids to help prevent hypovolemia from vomiting, diarrhea,
  sweating, hypersalivation, and insensible water loss from a tropical
  environment.
- Perform intubation and institute mechanical
  ventilation with end-tidal carbon dioxide monitoring for patients in
  respiratory distress.
- For hyperdynamic cardiovascular changes,
  administration of a combination of beta-blockers with sympathetic
  alpha-blockers is most effective in reversing this venom-induced effect.
  Avoid using beta-blockers alone because this leads to an unopposed
  alpha-adrenergic effect. Also, 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. Inotropic medications, such as digitalis, have little
  effect, while dopamine aggravates the myocardial damage through
  catecholaminelike actions. Dobutamine seems to be a better choice for
  the inotropic effect. Finally, a pressor such as norepinephrine can be
  used as a last resort to correct hypotension refractory to fluid
  therapy.
- Administer atropine to counter venom-induced parasympathomimetic effects.

Insulin
administration in scorpion envenomation animal experiments has helped
the vital organs to use metabolic substrates more efficiently, thus
preventing venom-induced multiorgan failure, especially cardiopulmonary
failure. Unfortunately, no human studies have been conducted.
Administer barbiturates and/or a benzodiazepine continuous infusion for severe excessive motor activity.
The use of steroids to decrease shock and edema is of unproven benefit.
Antivenin
is the treatment of choice after supportive care is established. The
quantity to be used is determined by the clinical severity of patients
and by their evolution over time. Unfortunately, predicting the
evolution of symptoms and, thus, the amount of antivenin that is needed
in the future, is difficult.
- The antivenin significantly
  decreases the level of circulating unbound venom within an hour. The
  persistence of symptoms after the administration of antivenin is due to
  the inability of the antivenin to neutralize scorpion toxins already
  bound to their target receptors.
- Time guidelines for the disappearance of symptoms after antivenin administration are as follows:
  - Centruroides antivenin: Severe neurologic symptoms reverse in 15-30 min. Mild-to-moderate neurologic symptoms reverse in 45-90 min.
  - Non-Centruroides
    antivenin: In the first hour, local pain abates. In 6-12 hours,
    agitation, sweating, and hyperglycemia abate. In 6-24 hours,
    cardiorespiratory symptoms abate.
- While an anaphylaxis
  reaction to the antivenin is possible, the patient is at lower risk for
  this than with other antivenins for other poisonous envenomations
  because of the huge release of catecholamines induced by the scorpion
  venom. However, the larger the dose of antivenin, the greater the chance
  for serum sickness.
- In a prospective, randomized, double-blind study, Boyer et al compared scorpion-specific F(ab')₂ antivenom (Anascorp, Centruroides [scorpion] immune F(ab)₂
  intravenous [equine], Instituto Bioclon) (n=8) with placebo (n=7) in
  children who developed neurotoxic symptoms following scorpion
  envenomation. Neuromotor abnormalities were present in all patients at
  baseline, and respiratory distress was present in 20%. Beginning 2 hours
  after treatment, symptom resolution differed significantly in the
  antivenom group compared with the placebo group. Plasma venom
  concentrations were undetectable and cessation of the neurologic
  syndrome occurred within 4 hours in 100% of antivenom recipients
  compared with 1 placebo recipient (p=0.001). In this study,
  scorpion-specific F(ab')₂ antivenom successfully treated the
  clinical syndrome, reducing the need for concomitant sedation and
  reducing circulatingunbound venom levels.⁶

A
vaccine preparation was tried in experimental animals but was not
pursued because of the need to prepare different antigens according to
different geographical areas and to different species of scorpions
living in the same area.
In some cases, be aware that meperidine
and morphine may potentiate the venom. Also, the concurrent use of
barbiturates and narcotics may add to the respiratory depression in
patients who have been envenomated.

Subject: Re: Scorpion sting (Scorpion Envenomation) 11/8/2010, 5:02 pm

http://emedicine.medscape.com/article/168230-treatment