In North America, bites and stings by arthropods occur frequently. Approximately 50,000 bites or stings occur every year, with about half of these caused by spiders. There are more than 41,000 species of spiders,¹ most of which cannot inflict serious bites to humans.² The majority of exposures are unnoticed and do not need treatment. There are a few medically relevant spiders that produce toxic venoms, which can lead to local reactions, systemic illnesses, and neurotoxicity.

ANATOMY

The Latrodectus genus of spiders includes five primary species found in North America: Latrodectus bishop, L. geometricus, L. hesperus, L. variolus, and L. mactans.² They live in dimly lit, secluded areas such as woodpiles, barns, and stone walls. They are present in every US state except Alaska.³ Black widows are described as shiny jet black with a characteristic red hourglass mark on the ventral aspect of the abdomen (Fig. 135-1). The red hourglass is specific to L. mactans, and other species have distinctive ventral markings such as triangles and spots. There is a seasonal variation in the number of black widow bites, starting to rise in spring, peaking in September, and reaching a nadir in January and February.³

PATHOPHYSIOLOGY

Black widows are overall shy, nocturnal, and only bite when their web is disturbed. The female black widow is generally considered poisonous to humans. The male black widow spider, with its smaller jaw and minimal venom, is not significantly poisonous to humans. These spiders use striated muscles to control the amount of venom they inject, and about 15% of bites do not deliver venom.⁴ The venom’s toxicity is due to the presence of α-latrotoxin. This toxin facilitates exocytosis of synaptic vesicles and the release of the neurotransmitters norepinephrine, γ-aminobutyric acid, and acetylcholine.⁵ The toxin also causes degeneration of motor end plates, resulting in denervation. The venom destabilizes nerve cell membranes by opening ion channels, causing a massive influx of calcium into the cell, which may lead to hypocalcemia.

CLINICAL PRESENTATION

Latrodectism is the clinical syndrome that follows a black widow bite. The bite produces a pinprick sensation that often goes unnoticed. Within the first few hours, local irritation may develop, including erythema, urticaria, or a characteristic halo-shaped target lesion. These local symptoms may be followed by generalized symptoms of pain and muscle spasms in the chest, abdomen, and lower back. Abdominal rigidity can be quite severe and may even be mistaken as a surgical emergency, especially in children who are often unable to provide a preceding history of a bite.^6,7 According to one study, signs and symptoms in infants were wound erythema, irritability, constant crying, sialorrhea, agitation, and seizures. Elementary school–aged children and adolescents described pain on the wound site, abdominal and thoracic pain, muscle spasms, and fine tremors.⁸ About one-third of patients will go on to have systemic symptoms.¹ These include hypertension, sweating, salivation, dyspnea with increased bronchosecretions, and convulsions. Less common effects include myocarditis,⁹ compartment syndrome of the upper extremity,¹⁰ and priapism.¹¹ Death is rare, with no cases reported in the United States and only two in the worldwide literature from black widow envenomation alone.^12–14 Symptoms of latrodectism typically last days, but patients can have intermittent muscle weakness and spasms for weeks.

MANAGEMENT

Local wound care is appropriate, and pain at the bite site may be relieved with early application of ice. Tetanus immunization should be updated, but antibiotics are unnecessary unless there is evidence of a wound infection. Oral and parenteral analgesics, such as morphine, may be used if pain is severe. Muscle spasms may require administration of benzodiazepines.

In the past, administration of calcium gluconate was considered given the concern for hypocalcemia following a black widow envenomation. This practice is currently not advocated, as studies have proven no benefit to the administration of calcium.^6,15

In extreme cases with severe symptoms, Latrodectus antivenom is recommended.¹⁶ Currently, only one antivenom is available in the United States, Black Widow Antivenin^® (Merck). This is a horse serum–derived product containing IgG antibodies to L. mactans venom. The use of Latrodectus-specific antivenom is restricted to patients with severe envenomation (e.g., hypertensive crisis or intractable pain), no allergic contraindications, and in whom opioids and benzodiazepines are ineffective. Young children and elderly patients with severe toxicity should receive antivenom early in the clinical course. There has traditionally been reluctance to use antivenom because of concern for anaphylaxis. Two recent reviews of antivenom use in the United States have demonstrated low rates of adverse reactions.^3,13 In the medical literature, there have only been two deaths reported after black widow antivenom administration.^6,17 Patients receiving antivenom may experience flu-like symptoms or serum sickness for 1 to 3 weeks following treatment. This entity is generally self-limited and responsive to antihistamines and steroids.

DISPOSITION

Any symptomatic pediatric patient who has suffered a bite from a black widow spider should be admitted for observation and pain control. If there is cardiopulmonary compromise or convulsions, the child should be admitted to the intensive care unit for stabilization and antivenom administration.

The six species of recluse spiders in North America are Loxosceles arizonica, L. deserta, L. devia, L. laeta, L. rufescens, and L. reclusa. Of these, L. reclusa is the most common. These spiders are known to be reclusive nocturnal hunters and are more active from April to October.^18,19 Their webs are scant and ill defined. Victims typically are bitten on the extremities while rummaging in confined spaces such as a closet or an attic while putting on a shoe or using a blanket that a spider is trapped in.

ANATOMY

The brown recluse gets its name because of its brown- or fawn-colored body. It is approximately 1 to 5 cm in length, with a characteristic violin- or fiddle-shaped marking on the dorsal cephalothorax (Fig. 135-2). They have long, slender legs and have six eyes rather than eight, which is the norm for most other spiders, including the black widow.²⁰

PATHOPHYSIOLOGY

The venom of the recluse spider, per volume, is more potent than that of the rattlesnake and can cause extensive skin necrosis. The venom acts directly on the cell wall, causing immediate injury and cell death. It contains the calcium-dependent enzyme sphingomyelinase D that, along with C-reactive protein, has a direct lytic effect on red blood cells. Following cell wall damage, intravascular coagulation causes a cascade of clotting abnormalities and local polymorphonuclear leukocyte infiltration, culminating in a necrotic ulcer.

CLINICAL PRESENTATION

Most brown recluse bites occur in predawn hours and are often painless. The seasonality of brown recluse bites and the geographic area should be strongly considered when making this diagnosis. One study demonstrated that 43/45 brown recluse bites occurred between the months of April and October.¹⁸ L. reclusa is primarily found in south central United States.²¹ The clinical response to loxoscelism ranges from cutaneous irritation (necrotic arachnidism) to a life-threatening systemic reaction. Most signs and symptoms of envenomation are localized to the bite area.²² The majority (90%) result in nothing more than a local reaction and resolve spontaneously.²³ Within a few hours, the patient experiences itching, swelling, erythema, and tenderness over the bite site. Classically, erythema surrounds a dull, blue-gray macule circumscribed by a ring or halo of pallor. The color difference is important in identifying necrotic arachnidism. Gradually, over 3 to 4 days, the wound forms a necrotic base with a central black eschar. In 7 to 14 days, the wound develops a full necrotic ulceration.²⁴ Bites that are in fatty areas, such as the thigh or buttocks, tend to cause more extensive necrosis.²⁵ Some sources state that the diagnosis of necrotic arachnidism secondary to brown recluse spiders is over-reported in many case series due to inadequate documentation, and call for stricter diagnostic criteria.^26–28

The systemic reaction, which is much less common than the cutaneous reaction, is associated with a higher morbidity. The reaction rarely correlates with the severity of the cutaneous lesion. Within 24 to 72 hours following the envenomation, the patient experiences fever, chills, myalgias, and arthralgias. In severe systemic reactions, the patient may suffer coagulopathies, hypotension, jaundice, disseminated intravascular coagulation (DIC), convulsions, renal failure, and hemolytic anemia.^29,30 In rare cases, a patient may succumb to the systemic reaction.²³

The Hobo spider (Eratigena agrestis, formerly Tegenaria), originally from Europe and central Asia, now resides in the Pacific Northwest region of the United States and Canada.³¹ This spider should be included with Loxosceles species when discussing cases of necrotic arachnidism. Similar symptomatology leads many to incorrectly attribute hobo spider bites to that of the brown recluse, which is not indigenous to the northwest United States. This species exhibits an aggressive nature, biting with minor provocation.³² Hobo spiders are brown with gray markings and have a 7- to 14-mm body length and 27- to 45-mm leg span (Fig. 135-3). They live in moist, dark environments such as woodpiles or basements.

MANAGEMENT

The proper management of envenomation by the brown recluse or hobo spider depends on whether the reaction is local or systemic. It is difficult to predict which type of wound will eventually progress to a disfiguring necrotic ulcer, so appropriate wound care should be done for all suspected brown recluse wounds. Proper care includes wound cleansing, immobilization, and elevation of the affected extremity to reduce pain and swelling. Early application of ice to the bite area will lessen the local wound reaction, whereas heat will exacerbate the symptoms. Tetanus immunization should be updated, but antibiotics are only indicated if there is a secondary wound infection. Antihistamines and analgesics prove to be beneficial, especially in children. Many treatment modalities including dapsone, triamcinolone, diphenhydramine, electric shock, hyperbaric oxygen, colchicine, and trypsin have been studied but none have prevented the formation of an ulcerative lesion.³³

Early excision of ulcers and steroid injections are not recommended since studies have demonstrated that wound healing is slowed, and scarring is more severe as a result of those practices. Some complications of early surgical intervention include recurrent wound breakdown as well as long-term distal extremity dysfunction. Delayed excision of ulcers after the necrotic process has subsided (usually within 8 weeks), followed by secondary closure with skin grafting, is the preferred way of dealing with necrotic ulcers due to brown recluse bites. With appropriate wound care, most bite wounds heal well, with a 10 to 15% occurrence of major scarring.

Historically, the use of the polymorphonuclear leukocyte inhibitor, dapsone, was advocated to diminish scarring and subsequent surgical complications. Its use, however, has not proven effective in any large study with human or animal models.³⁴ Because of the potential for dapsone to induce methemoglobinemia and hemolytic anemia in children with G6PD deficiency, administration in pediatric patients is generally not advised. Another suggested method of treating expanding wound necrosis due to brown recluse spider bites is hyperbaric oxygen treatment. However, results with such treatment have been mixed, and little evidence exists to support its use.^23,34

Systemic effects of brown recluse spider bites are rare but can be life threatening, and should be treated aggressively. Although not proven in clinical trials, glucocorticoids may provide a protective effect on the RBC membrane, thus slowing hemolysis. The patient must be monitored closely for the development of DIC. Transfusion of red blood cells (RBCs) and platelets may be necessary. Plasma exchange for refractory hemolysis has been recently described following brown recluse spider envenomation.³⁵ Urine alkalinization with bicarbonate may lessen renal damage if the patient is experiencing acute hemolysis. Although it is not commercially available in the United States, there is ongoing research with brown recluse antivenom.³⁶ However, there is little evidence to support its efficacy, particularly against local effects.³⁷