Summer Breaks

Getting set for a season of bumps, bruises and bites.

The weather is beautiful, the kids are out of school, it’s grilling season and you can’t wait to get to the beach. Summer is finally here! Though this season is a great time for outdoor and family activities, summer brings with it the potential for several injuries. We’ll take you case by case through some of these summertime injuries.

Case 1: A 6-year-old male presents with his mother after a bee sting to his left forearm. It appears the stinger remains in his arm and the sting is surrounded by erythema, with approximate diameter 5 cm. He denies shortness of breath, nausea/vomiting or any other symptoms besides pain over the site.

Bee/Wasp Stings

Bees, vespids (wasps and hornets) and fire ants belong to the Hymenoptera order. Bees and vespids are responsible for more than 25% of all annual envenomations in the U.S., with over 50 deaths per year and 10% of anaphylaxis cases due to these stings.^1-4 Systemic reactions occur in 1% of patients stung.(^1,3) Upon stinging, bees lose their stinger and die, but their venom (mainly consisting of protein) results in a higher histamine release than other hymenoptera venom.(^1,3) Vespids with their unbarbed stingers may sting multiple times. Thankfully, there is little cross-reactivity between bee and vespid venom, meaning those who are allergic to bees may not have an allergy to wasp venom.(^1,3) There are four primary reactions, demonstrated in Table 1.^1,3,5

Table 1

Reaction Type	Characteristics
Local	– Most common type, result from vasoactive effects, generally mild – Pain, erythema, edema, pruritis. – If occurs in the mouth/throat, may result in airway swelling.
Toxic	– More common with multiple stings (Africanized honey bee). – Lethal dose is 20 stings/kg (related to number of stings). – May resemble anaphylaxis, but vomiting, diarrhea and lightheadedness are common, as well as headache, fever, spasms and edema. – Hepatic failure, DIC, rhabdomyolysis, stroke, myocardial infarction and intracranial bleed can occur.
Anaphylaxis	– Generalized reaction due to Ig-E regulated mechanism, typically with prior exposure. – No correlation with number of stings. – Fatalities are due to airway obstruction and anaphylactic shock. – Typically occur within 10 minutes, with almost all within six hours. – Airway symptoms, wheezing, swelling, abdominal pain/vomiting/diarrhea, fever, dyspnea and hives.
Delayed	– Serum sickness-like: fever, headache, urticaria, lymphadenopathy, malaise and polyarthritis. – Immune complex mediated reaction that occurs 1-2 weeks after sting

 

Management of these reactions revolves around rapid evaluation for life-threatening anaphylaxis, followed by the treatment we all love if anaphylaxis is present — epinephrine.(^1,3,7,8) If the airway is involved, airway intervention is vital. Antihistamines (H1 and H2 antagonists) are recommended, along with corticosteroids and IV fluids for anaphylaxis. Milder, local reactions are treated with antihistamines, ice and acetaminophen/ibuprofen.(^1,3,7,8) Toxic and delayed reactions may be severe, with treatment based on the patient’s condition.

What about removing the stinger for bee stings? The stinger should be removed as soon as able. Prior recommendations included scraping the stinger with lateral pressure and avoiding squeezing the venom gland. However, recent literature suggests this is not needed, as the stinger releases almost all of its venom within seconds of the initial sting.(^1,3,5) Thus, use what you can, whether it be tweezers or the traditional scraping. Skin infections of a local reaction following a sting are very rare. Local reactions typically last for two to three days and resolve.(^1,3,5,6) Antibiotics are not needed for these patients. More importantly, any concern for an allergic reaction warrants discharge with and instructions to use a portable epinephrine kit. Referral to an allergist is beneficial for patients who experienced anaphylaxis or a severe reaction.

Fire Ants

There are two species of fire ants currently in the U.S., originally imported from South America. These organisms are 2-5 mm in size with a red color and they live in colonies in warmer environments.(^1,3,5) Fire ants attack in swarms with multiple stings consisting of an alkaloid venom.(^1,5) Patients are stung most commonly along the lower extremities. Interestingly, stings occur in two phases: first a bite and then the ant arches its body and swivels to sting the victim repeatedly.(^1,3,5) The stings result in a sharp pain with wheals/papules around central hemorrhagic punctures.

The reaction may resolve within an hour, but pustules develop over a day, which then slough over the following two to three days. Close to 25% of patients experience more severe local reactions with edema, erythema and induration, which may reach over 5 cm in diameter.(^1,3,5,8) This reaction typically lasts for up to three days and resembles cellulitis. Venom can sensitize patients to future attacks, which may be worse.(^1,9) Treatment of local reactions includes topical glucocorticoids and oral antihistamines, with ice and cleaning of the area. Antibiotics are not recommended, even with severe local infections. If the redness worsens after three days and the patient develops fever, superinfection may be present.

Case 2: A 23-year-old female presents after sunbathing. Unfortunately, she fell asleep outside in the prone positions for several hours and presents with severe pain and “the worst sunburn of my life.” Her entire back is erythematous with several small blisters. She denies other symptoms. The sunburn blanches to pressure.

Severe Sunburn

Burns come in all shapes and sizes, with thermal burns the most common. Most are associated with risky behavior, inattention or inadequate protection, and the majority of patients with burns never come to an ED. Sunburn is no exception. The type of thermal burn occurs in up to 80% of outdoor workers per year, with most sunburns occurring before age 18 years.(^10-12) Over 35% of adults and 69% of adolescents in the U.S. experience sunburn annually, with higher rates in males, whites, young adults and high-income groups.(¹²⁾ There’s even a classification system (Fitzpatrick skin types) for those at risk for sunburn!(¹³⁾ Most of these thermal injuries are superficial, though those unlucky patients with sunburn can experience intense pain.

Importantly, superficial burns do not count in total body surface area, so this patient with pain over the back due to her burn actually has a 0% TBSA.(¹⁴⁾ Use of lotions to keep the skin moist (hydrating lotions or aloe vera), NSAIDs and acetaminophen may assist in healing and analgesia, but most patients will never require burn center or even physician care.(¹⁴⁾ Superficial partial-thickness or deep partial-thickness burns are rare with sunburn, but these are associated with long healing times and may require topical antibacterials.(¹⁴⁾

Emergency physicians can have a major impact just with counseling. A significant problem associated with sunburns is not the initial burn, but the risk of skin cancer, which is the most common cancer in the U.S. (2 million patients per year), including melanoma and nonmelanoma skin cancers.(^15-17) Exposure to ultraviolet radiation is the primary risk factor, with as little as five sunburns increasing risk.(^16,17) This brings us to prevention.

Risk of sunburn and the potential cancer can be decreased with sunscreen, which may prevent cancer by more than 10 years.(¹⁸⁾ Patients should use sunscreen with protection against UVA and UVB, but they should not use sunscreen to prolong exposure. Clothing and hats are still the best protection against sunburn.(^15,18) Sunscreen with SPF 100+ may be more effective than lower SPF in total protection from sunburn, as well as decreased cumulative damage.(^19,20) Avoiding the sun at peak times and using other protective measures such as clothing can reduce cancer risk by 80%.(²¹⁾

Case 3: A 52-year-old male presents with a laceration over his right lower leg. He was jet skiing in the local lake, and he thinks he cut his leg on a branch earlier in the day. The site surrounding his laceration is erythematous and warm. The patient denies any liver or renal issues and his vital signs are normal.

Punctures/Lacerations from fresh water or salt water

Personal watercraft include jet skis and wave runners, defined by a water vehicle under 13 feet in length and operated by a person on the body of the vehicle.(^22,23) As more people use these vehicles, injury rates increase.(^22,23) These injuries can range in severity, including contusion, laceration, traumatic amputation and even death. We will focus on the laceration for this case. Injuries in fresh or saltwater are exposed to a variety of bacteria that are not usually found in other wounds. Lacerations are associated with higher rates of infection and morbidity in fresh and saltwater.(^24-27) Though organisms such as Vibrio, Aeromonas, Erysipelothrix and Mycobacterium marinum may result in infection, other more common causes of infection occur (think Staph and Strep species).(^24-27)  Table 2 provides you a brief summary of the microbes, with characteristics and antibiotic regimens.(^28-31)

Table 2 – Fresh and Saltwater Organisms

Organism	Characteristics	Treatment
Vibrio species	– Anaerobic gram-negative bacteria found in ocean and freshwater. – Associated with shark and stingray exposure. – May result in necrotizing fasciitis, sepsis, and osteomyelitis. – Higher risk in those with liver disease, alcoholism, diabetes, malignancy and renal disease.	– Surgical debridement – Doxycycline every 12 hours + Ceftazidime OR Ciprofloxacin 400 mg IV OR Levofloxacin 500 mg IV – Glycylcycline class is efficacious (Tigecycline)
Aeromonas species	– Facultative anaerobic gram-negative bacteria. – Found in freshwater, most commonly from contamination of open wound (especially alligator and crocodile bites). – Presents as localized cellulitis first, then may progress to gangrene, necrotizing fasciitis, osteomyelitis.	– Irrigation and debridement – Ciprofloxacin OR Levofloxacin OR 3rd/4th generation cephalosporin – Hyperbaric oxygen may benefit in severe cases
Erysipelothrix species	– Gram-positive rod found in saltwater – Most commonly infects those who handle fish – Self-limited infection with itching and pain and injury site – May progress to septic arthritis, endocarditis, sepsis	– Cutaneous: Penicillin V, Cephalexin, OR Ciprofloxacin – Systemic (sepsis, endocarditis): Penicillin G, Ceftriaxone, OR Ciprofloxacin
Mycobacterium marinum	– Atypical mycobacterium found in freshwater and saltwater – Starts with minor abrasion over bony prominence from handling fish – Symptoms include erythema, painless papules, and local granuloma weeks to months after injury – Infection may worsen to tenosynovitis, septic arthritis and osteomyelitis	– Surgical debridement for severe, deep infections – Clarithromycin, Minocycline, Bactrim, OR Rifampin with Ethambutol

 

Caring for these wounds includes adequate history, exam evaluating the wound and for foreign bodies, and neurovascular status.(^25,26) Accurate history is important and should focus on the type of exposure and symptoms, as well as comorbidities. Severe lacerations require immediate hemostatic control and hemodynamic resuscitation. Tetanus prophylaxis and antibiotics (Table 1) are also recommended.

For stable patients, irrigation of the wound with debridement of any necrotic tissue is needed to optimize outcomes. Most small, superficial wounds should be left open and larger wounds may need packing and delayed closure.(^27-29) Vibrio infections in particular require debridement, and any wound with cellulitis exposed to saltwater is likely due to Vibrio.(³¹⁾ The same goes for freshwater exposure and Aeromonas.(^25-27)

Venomous attacks

Not only do you have to worry about atypical microbes, but venomous marine life can also result in significant injury, including stinging fish, stingrays, sea urchins and coral. These injuries are usually associated with pain and localized subcutaneous swelling.(^25-27) Unfortunately, the venom may result in more severe injuries and even hemodynamic or respiratory collapse from anaphylaxis.(^25,26)

Stinging fish, stingrays and sea urchins have spines with heat-labile venom. These spines can be difficult to treat and may penetrate through a wetsuit with severe pain.(^32-35) At the scene, the spine should be left in place, though the spine often results in severe pain and muscle spasm. Hot water immersion (at 45C or 113F for 30- to 90-minutes) can inactivate the venom and reduce pain.(^25,26,35) Imaging with radiographs of the affected body part are recommended to evaluate the location and depth of the spine though ultrasound and CT may also be used.

Removal of the spine is needed, which will require local anesthetic, or better yet, regional anesthesia.(^34-36) Once the spine is removed, the wound should be left open and antibiotics provided.(^32-36) Sea urchin injuries may result in discoloration of the skin, which can be due to dye or retained spine. Importantly, the patient should be observed for several hours to evaluate for reaction to the venom. If the injury is near a vital organ, imaging (CT) is recommended, and if near a joint, consult orthopedics as these wounds are associated with septic arthritis.

Jellyfish are an entity to themselves, with several classifications and stinging organelles. Cnidocysts possess coiled thread tubes with venom laden darts (contained by cnidocytes, or stinging cells) that anchor in the skin.(^25,26) The most lethal jellyfish is the box jellyfish, which may result in rapid blistering, hypotension, spasms and cardiac arrest within one to two minutes.(^25,26,37) Other jellyfish stings are painful, but not as deadly.

Patients can actually be sensitized to jellyfish stings, with future reactions more severe than prior. Localized pain and erythema are typical and last approximately one day. Larval form contact can cause seabather’s eruption, which is pruritic papules that look like bug bites in a swim suit distribution.(³⁸⁾ Topical decontaminants are tricky, as fresh water, cold water and abrasion are not recommended for stings.

Remember the old myth of using urine? Well, since urine is typically hypotonic, this may result in cnidocyte discharge and pain, but you have several other options such as vinegar, salt water, lidocaine and others.(^25,39) Topical lidocaine is probably best, based on a 2013 Cochrane Review.(³⁹⁾ For inflammatory reactions, topical steroids can be used. If severe, systemic steroids are recommended. The box jellyfish envenomation requires antivenom.(^25,26)

Finally, fire coral and Portuguese man-of-war can cause intense, immediate pain and urticaria, with local symptoms resolving in 72 hours.(^40,41) However, systemic symptoms may include vomiting, cramps, dyspnea, anxiety, abdominal pain and headache. Acetic acid should be applied to the wound, and steroid cream and oral antihistamines provide further relief.

Case 4: A 27-year-old male presents with forearm pain and deformity after falling from a paddle board. He and some friends were drinking earlier. He is neurovascularly intact, but his distal forearm is mildly deformed.

Paddleboard and Surfboard Injuries

Paddleboard and surfboard injuries are increasing in frequency, with head and lower extremity injuries the most common sites.(^42,43) Injuries are commonly due to collision with the board (over 30%), but injuries due to rocks and coral (15%) or waves (> 10%) also occur.(^42,43)

Lacerations and contusions/bruises are the most common injuries. However, most patients never seek care. Most major sporting societies recommend protective gear for water sports, but as we know, these aren’t always followed.

Most injuries occur in heavier waves.(^42-45) Paddleboard injuries more commonly involve the lower extremities (sprains and contusions), while surfboards can also cause significant head or trunk injury.(^42-45) We all know how to care for these types of injuries (remember all that orthopedic expertise?), but what about more severe injuries?

Despite most injuries not being severe, water sports can be associated with major injuries, with drowning the most common cause of death. Major head or spine injuries can also result, though these are found in less than 3% of patients.(^42-45) A recent EM:RAP segment discussed surfer’s myelopathy,(⁴⁶⁾ which typically affects young, healthy patients who have no known spinal disease.

It may present with cauda equina-like symptoms such as bladder incontinence, though usually it first occurs with back pain.(^47,48) This is likely due to protracted hypertension of the back with potential mechanisms including perforating vessel avulsion, vasospasm or kinking of the artery of Adamkiewicz and ischemic damage.

This pain may rapidly progress, with 50% of cases with complete injury never walking again. An incomplete myelopathy is more common and may improve within 24 hours of onset. More severe injuries may require weeks to months to heal, with some never recovering.(^47,48)

This is one of those times to break out the MRI for diagnosis.(^47,48)  Steroids can be used for treatment, but currently, there are no specific guidelines. Strict blood pressure targets, imaging results and corticosteroid use do not definitively improve outcomes, so if this injury is suspected, get in touch with your neurosurgeon.(^47,48)

Case 5 Part A: A 25-year-old female presents with several bites which are red and raised. She spent the weekend at a lake, and she is asking about malaria-borne diseases. She denies any systemic symptoms and has a normal physical exam except for several 0.5 cm diameter raised red lesions consistent with a mosquito bite.

Hands down, mosquitoes are one of the deadliest creatures in the world due to their ability to spread diseases. They are associated with millions of deaths per year and over half of the world’s population living in endemic locations of Aedes aegypti (which transmits zika, dengue, chikungunya and yellow fever) (Table 3).(⁴⁹⁾ The world has seen the rise of zika, dengu and chikungunya recently, with dengue alone demonstrating a 30-fold increase within the past 30 years.

Table 3 – Mosquito-Borne Diseases

Infection	Transmission	Presentation	Diagnosis/Assessment	Treatment
Chikungunya(49-51) (Americas, Africa, Asia, Europe, Indian subcontinent)	Virus transmitted by female Aedes, bites during daylight with peaks at dawn/dusk	Fever (up to 105 F), chills, conjunctivitis, severe joint and muscle pain, headache, rash, nausea   May have saddle-back fever, or fever after 1-2 days after afebrile period Joint pain typically debilitating, varied duration	Tourniquet test positive in some (inflate BP cuff on upper arm between diastolic and systolic pressures for five minutes – positive if > 20 petechiae per square inch) Lymphocytopenia, elevated LFTs, worsening renal function Confirmation includes viral testing (PCR, viral culture, IgM/IgG antibodies)	Treat symptoms and rehydrate   Treat arthralgias with NSAIDS (after dengue is excluded) Symptoms usually resolve within 10 days
Dengue(49,52-54)   (Latin America and U.S., Europe, Africa, Asia)	Virus transmitted by Aedes, bites during daylight	Febrile phase: high fever, GI symptoms, rash, pulse temperature dissociation, headache, retroorbital pain   Critical phase: less common (pediatric, elderly), biphasic fever curve, hepatomegaly, vascular leak, hemoconcentration, pleural effusions, lethargy, ascites, vomiting, abdominal pain, skin/mucosal bleeding, hematuria Severe dengue (shock syndrome): shock, hemorrhage, hypothermia, respiratory distress	Tourniquet test often positive (see above)   Hemoconcentration, neutropenia, thrombocytopenia, elevated LFTs Severe: increased Hct, prolonged PT/PTT, low serum protein, decreased fibrinogen   Diagnosis with IgG/IgM, dengue viral antigen detection	Treat symptoms and rehydrate; mortality < 1% if diagnosed early, though severe dengue has mortality 20% Support care with acetaminophen, but avoid aspirin, NSAIDs, and steroids Bleeding patients may need transfusion   Dengue vaccine is licensed in several countries for those who are 9-45 years living in endemic areas
Malaria (49,55-57)   (Over 95 countries and territories, 3.2 billion at risk, Africa possesses greatest risk)	Protozoa transmitted by female Anopheles; Plasmodium falciparum most prevalent and deadliest	If non-immune, symptoms appear seven days after bite   Fever, headache, chills, rigors, vomiting (paroxysms may occur every 48-72 hours, based on species)	Severe: anemia, metabolic acidosis, renal failure, elevated LFTs, thrombocytopenia, elevated LDH, atypical lymphocytes, hyponatremia Diagnosis: thick and thin smears (if negative, repeat BID for two to three days, rapid antigen testing	P. falciparum almost always fatal without therapy   Uncomplicated: no organ dysfunction, < 5% parasitemia, PO tolerant   – Artemether + lumefantrine, amodiaquine or mefloquine – Dihydroartemisinin + piperaquine – Artesunate + sulfadoxine-pyrimethamine   Severe: organ dysfunction, cerebral malaria, high parasitemia; begin treatment if suspicious even with negative smear; start IV therapy for > 24 hours, then three days PO – Artesunate – Quinidine (associated with hypoglycemia)
West Nile(49,58-60)   (Africa, Europe, Middle East, North America, West Asia)   Associated with encephalitis: Murray Valley, St. Louis, Kunjin Japanese	Virus transmitted by Culex, mosquitoes feed on infected birds and transmit to horses and humans	80% are asymptomatic; 20% develop severe disease (West Nile Fever) with headache, high fever, altered mental status, neck stiffness, weakness, paralysis Patients > 50 years, immunocompromised are at highest risk	WBC normal or elevated, CSF pleocytosis with lymphocytosis, hyponatremia   Diagnosis with blood or CSF IgM, 4-fold increase in antibodies	Symptomatic therapy; no studies have supported ribavirin, IVIG, interferon, steroids, osmotic agents   Admission for those with West Nile virus
Yellow Fever(49,61,62)   (Africa, Latin America)   Mosquitoes infect monkeys, then humans	Virus transmitted by Aedes and Haemagogus, bites mostly during day	Fever, muscle pains, backache, headache, chills, anorexia, GI symptoms, then remission   15% develop severe, toxic phase with high fever, jaundice, abdominal pain, vomiting, worsening renal function, hemorrhage (from mouth, nose, eyes, GI tract)	Toxic phase: worsening renal function and LFTs, neutropenia, elevated PT/PTT, reduced fibrinogen	Symptomatic therapy, transfusion may be needed for toxic disease with bleeding   Dialysis required for renal failure   Avoid salicylates and NSAIDs   Vaccine available and can provide life-long immunity
Zika(49,63,64)   (Africa, Americas, Asia, Pacific)   Greatest concern is microcephaly from vertical transmission during pregnancy	Virus transmitted by Aedes, perinatal, and sexual intercourse; bites during the day	80% are asymptomatic; symptoms can include fever, rash, conjunctivitis, arthralgia, myalgia, headache Symptoms usually mild if they occur   Rash is widespread, maculopapular	Diagnosis with PCR or IgM	Disease is self-limited and mild; no specific therapy   Supportive care and hydration

 

Prevention is a major component of reducing mosquito-borne diseases. Patients should use repellants, long-sleeve shirts and pants, and closed-in rooms.(^49,65) Though sanitation or city departments may use spraying to kill mosquitoes, this is probably not helpful. Removing free standing, stagnant pools of water can reduce mosquito breeding.(⁴⁹⁾

Regarding zika virus in particular, patients should avoid travel to regions with active virus. The CDC recommends sexual abstinence or regular condom use as well. Women with zika should wait at least two months after any symptom onset before trying to get pregnant, and men should wait at least six months.(^49,64,65)

Case 5 Part B: A 42-year-old male presents with an enlarging rash over his right lower calf. He was wearing shorts while hiking in Minnesota. He does not recall a tick bite.

Ticks belong to the class Arachnida and are widely spread across North America. They are major vectors of disease, including the feared Rocky Mountain spotted fever (RMSF) and Lyme disease.(⁶⁶⁾ Tick bites are normally asymptomatic and painless.(^66,67) As with everything in medicine, history is key, especially concerning recent outdoor activity. Several ticks spread disease, including Dermacentor/Amblyomma (RMSF and tularemia) and Ixodes (Lyme and babesiosis) (Table 4).

Table 4 – Tick-Borne Diseases

Infection	Incubation	Presentation	Laboratory	Treatment
Anaplasmosis(66-69)   (Upper Midwest and NE U.S.)	1-2 weeks	Fever, chills, rigors, headache, malaise, myalgias, GI symptoms, cough, rash (rare)	Mild anemia and thrombocytopenia, leukopenia, elevated LFTs   Diagnosis: Whole blood PCR or four-fold change in IgG antibody titer	Adults: Doxycycline 100 mg BID daily   Pediatric: Doxycycline 2.2 mg/kg per dose BID
Babesiosis(66,69,70)   (Upper Midwest and NE U.S.)	1-9+ weeks	Fevers, chills, rigors, malaise, arthralgias, GI symptoms, dark urine   Less common: cough, sore throat   Mild hepatosplenomegaly and jaundice may occur	Decreased hematocrit due to hemolytic anemia, thrombocytopenia, increased BUN/Cr, mildly elevated LFTs   Diagnosis: Whole blood PCR, isolation from whole blood, or microscopy	Adults: – Atovaquone 750 mg BID and Azithromycin 500-1,000 mg on day one, 250-1,000 mg on days 2-10 – Clindamycin 600 mg PO BID and Quinine 650 mg PO Q 6-8 hours
Ehrlichiosis(66,67,71)   (Midwest, SE, and South-Central U.S., Eastern seaboard)	1-2 weeks	Fever, headache, chills, malaise, myalgias, GI symptoms, confusion, conjunctival injection, rash (common in children)	Thrombocytopenia, leukopenia, anemia (later), mildly elevated LFTs, morulae in acute stage (20% of patients)   Diagnosis: Whole blood PCR, four-fold increase in IgG	Adults: Doxycycline 100 mg BID daily   Pediatric: Doxycycline 2.2 mg/kg per dose BID
Lyme Disease(66,72-74)   (Upper Midwest, Northeast, and some West Coast states)	3-30 days	Localized: Erythema migrans with red ring-like of homogenous rash, flu symptoms, lymphadenopathy   Disseminated: Secondary annular rashes, flu symptoms, transient migratory arthritis, lymphadenopathy, migratory pain, conduction abnormalities (AV block), myocarditis or pericarditis   Neurologic: Bell palsy, meningitis, motor or sensory symptoms, cognitive difficulties   Others: Conjunctivitis, hepatitis, splenomegaly	Elevated ESER, mildly elevated LFTs, hematuria/proteinuria, CSF may show lymphocytic pleocytosis, elevated protein, normal glucose   Diagnosis: Organisms isolated from clinical specimen, IgM or IgG antibodies with two-tier testing (EIA or IFA followed by Western blot)   Serologic tests are often negative in first few weeks. If symptoms > one month, IgG should be used   Single antibody test cannot differentiate active vs. past infection	Adults: – Doxycycline 100 mg BID – Cefuroxime axetil 500 mg BID – Amoxicillin 500 mg TID   Pediatric: – Amoxicillin 50 mg/kg daily, divided TID – Doxycycline 4 mg/kg daily, divided BID – Cefuroxime axetil 30 mg/kg daily, divided BID
RMSF(66,75)   (Reported in entire contiguous U.S.)	2-14 days	Fevers, chills, headache, malaise, myalgia, GI symptoms, photophobia, focal neurologic symptoms   Maculopapular rash appears at two to five days after fever on wrists, forearms, ankles first and spreads to trunk (also palms and soles), though 10% of patients do not have rash   Petechial rash with red to purple spots are not seen until after six days of symptoms, sign of progression to severe disease	Thrombocytopenia, mildly elevated LFTs, hyponatremia   Diagnosis: four-fold change in IgG, DNA detection on skin biopsy using PCR, IHC staining from biopsy	Associated with significant complications and mortality if not treated   Adults: Doxycycline 100 mg BID daily Pediatric: Doxycycline 2.2 mg/kg per dose BID
Tularemia(66,76)   (All U.S. states except Hawaii)	3-5 days usually (range 1-21 days)	Fever, headache, chills, malaise, myalgias, fatigue, anorexia, cough, chest pain, sore throat   Ulceroglandular: lymphadenopathy, cutaneous ulcer   Oculoglandular: photophobia, lacrimation, conjunctivitis, cervical and submandibular lymphadenopathy   Oropharyngeal: throat pain, cervical and submandibular lymphadenopathy   Pneumonic: cough; substernal pain; pleuritic pain; hilar adenopathy, effusion, or infiltrate on xray   Typhoidal: any combination of general symptoms	Normal or elevated leukocytes and ESR, thrombocytopenia, hyponatremia, elevated LFTs, elevated CK, myoglobinuria, pyuria   Diagnosis: four-fold change in antibody titer, organism isolation from specimen, IFA	Adults: – Streptomycin 1 g IM BID – Gentamycin 5 mg/kg IM or IV daily – Ciprofloxacin 400 mg BID – Doxycycline 100 mg BID   Pediatric: – Streptomycin 15 mg/kg IM BID – Gentamicin 2.5 mg/kg IM or IV TID – Ciprofloxacin 15 mg/kg BID
Colorado Tick Fever(66,77)   (West U.S., SW Canada)	1-14 days	Fever, headache, chills, malaise, myalgias   Half have biphasic illness   Conjunctival injection, red throat, lymphadenopathy may be present   Maculopapular rash in 20%	Leukopenia, thrombocytopenia   Diagnosis: Culture and PCR during first two weeks, serologic assays after two weeks	No specific treatment (viral), supportive care
Tickborne Relapsing Fever(66)   (U.S. Midwest and West)	7 days, followed by recurring fevers that last 3 days, followed by no symptoms for 7 days	Headache, chills, malaise, myalgias, GI symptoms	Increased WBC, left shift, increased bilirubin, thrombocytopenia, elevated ESR, slightly elevated PT and PTT   Borrelia spirochetes in peripheral smear (serologic testing not standardized)	Adults: – Tetracycline 500 mg Q 6 hours or erythromycin 500 mg Q 6 hours – CNS involvement: ceftriaxone 2 g daily

 

If a tick is attached, the physician needs to remove the tick and determine whether prophylaxis is warranted. To remove an alive tick, apply viscous lidocaine to the site and then use fine-tipped forceps to grasp as close to the head as possible. Pull the tick upwards with even pressure and try to avoid twisting/jerking movements (this increases risk of leaving tick mouthparts embedded in the skin).

If mouthparts are embedded, try to use tweezers to remove them, as they function as a nidus for infection. Once the tick is removed, wash the site with soap and water, and have the patient monitor the site for several days. Try to avoid heating the tick, which increases the risk of tick defecation (and infection).

Worsening redness after a tick bite warrants treatment with doxycycline for Lyme disease, as well as consideration of cellulitis.(^66,67,69)  So, what do we do about prophylaxis? You have three options, specifically for Lyme disease: watchful waiting, treat with doxycycline single dose 200 mg or treat with full course doxycycline.

Ticks attached for less than 24 hours have very low likelihood of transmitting Lyme disease. If the tick belongs to Ixodes scapularis (nymph or adult), doxycycline is not contraindicated, the tick was attached for > 36 hours, Lyme disease is prevalent in the area and the patient can receive prophylaxis within 72 hours after the tick was removed, prophylaxis with doxycycline 200 mg PO X 1 for adults and 4 mg/kg PO X1 for kids is recommended. For anaplasmosis, babesiosis, ehrlichiosis or RMSF, the CDC does not recommend prophylaxis. Tularemia prophylaxis is recommended in cases of laboratory exposure.(^66,67,69)

Prevention is important for tick-borne infections. Repellant with 20% (or more) DEET, picaridin or IR 3535 is recommended. Patients may also treat gear and clothing. Patients should wear long-sleeved shirts and pants with closed shoes. After exposure to outdoors, the patient should look closely for ticks (especially the underarms, belly button, knees, groin, hairline and scalp), followed by a shower.(⁶⁶⁾

Case 6: EMS brings in your next patient: a 33-year-old female surfer with severe left upper extremity lacerations. She thinks something knocked her off the surfboard, and upon entering the water, felt immediate pain and saw bleeding. She rapidly swam to shore, which was fortunately close. She is tachycardic, hypotensive, and tachypneic, but GCS is 15. EMS started an IV line in her other upper extremity and gave her 1 L NS. You take off the bandage, which appears red, and immediately see bleeding that rapidly worsens.

Shark Attacks

Yes, we saved the best for last. The movie JAWS brought to the forefront this primal fear. Sharks are one of the most dangerous marine predators, with a diet consisting mainly of seals and other fish. However, humans are not normally on a shark’s menu. Attacks on humans are rare, with 70-100 worldwide per year resulting in five deaths.(^78,79) Most are likely due to mistaken identity and most sharks bite once and leave after the first bite.(^80,81) Deaths usually result from drowning and/or hemorrhage.

Surfers are at higher risk, as from beneath a surfboard may appear similar to a seal. Most injuries involve the lower extremities, with truncal injuries accounting for 5% of total attacks.(^78,80,81) Unfortunately, shark attacks can result in severe damage due to several factors: sharp teeth that may serrate, large bite force, tearing action with shaking/rolling of the head, and other factors.(^82-84) Most shark bites pierce the skin and tear through soft tissue with an arc-shaped alignment. Shark teeth typically break off in the wound, resulting in morbidity later if not removed.(^82-84)

OK, so what do you do with the shark bite victim? These patients should be treated as any other patient with severe penetrating trauma, which we handle very well on a daily basis. Whether you use your ABCDE or MARCH (Massive hemorrhage, Airway, Respiratory, Circulation, Hypothermia, Head Injury) strategy, hemorrhage control should be your first goal with finding the bleeding source, applying direct pressure and using a tourniquet if bleeding is severe and using blood products.(^85,86)

The vast majority of bites require further care in the OR. Radiographs or further imaging is a must to evaluate for other injuries and broken teeth. Other long-term complications include neurovascular damage, bone fractures and infection.(^79,80,83) Antibiotics and tetanus prophylaxis are also typically needed, but in the severe injury, bleeding control and resuscitation are the goals.

References

1. Erickson TB, Cheema N. Arthropod envenomation in North America. Emerg Med Clin N Am. 2017;35:355-375.
2. Forrester JA, Holstege CP, Forrester JD. Fatalities from venomous and nonvenomous animals in the United States (1999-2007). Wilderness Environ Med 2012;23(2):146–52.
3. Erickson T. North American arthropod envenomation and parasitism. In: Auerbach PS, editor. Wilderness medicine. 5th edition. Philadelphia: Mosby Elsevier; 2007. p. 2316.
4. Tankersley MS, Ledford DK. Stinging insect allergy: state of the art 2015. J Allergy Clin Immunol Pract 2015;3(3):315–22 [quiz: 323].
5. Fitzgerald KT, Flood AA. Hymenoptera stings. Clin Tech Small Anim Pract 2006; 21(4):194–204.
6. Mingomataj EC, Bakiri AH, Ibranji A, et al. Unusual reactions to hymenoptera stings: what should we keep in mind? Clin Rev Allergy Immunol 2014;47(1):91–9.
7. Lee JK, Vadas P. Anaphylaxis: mechanisms and management. Clin Exp Allergy 2011;41(7):923–38.
8. Kemp SF, deShazo RD, Moffitt JE, et al. Expanding habitat of the imported fire ant (Solenopsis invicta): a public health concern. J Allergy Clin Immunol 2000;105(4): 683–91.
9. Demain JG, Minaei AA, Tracy JM. Anaphylaxis and insect allergy. Curr Opin Allergy Clin Immunol 2010;10(4):318–22.
10. Reinau D, Weiss M, Meier CR, et al. Outdoor workers’ sun-related knowledge, attitudes and protective behaviours: a systematic review of cross-sectional and interventional studies. Br J Dermatol 2013;168(5):928–40.
11. Quatrano NA, Dinulos JG. Current principles of sunscreen use in children. Curr Opin Pediatr 2013;25:122–9. United States.
12. Buller DB, Cokkinides V, Hall I, et al. Prevalence of sunburn, sun protection, and indoor tanning behaviors among Americans: Review from national surveys and case studies of 3 states. J Am Acad Dermatol. 2011;65(5): S114.e1
13. Baron ED, Suggs AK. Introduction to photobiology. Dermatol Clin 2014;32(3): 255–66, vii.
14. Cleland H. Thermal burns – assessment and acute management in the general practice setting. Aust Fam Physician 2012;41(6):372–5.
15. Moyer VA. Behavioral counseling to prevent skin cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2012;157:59–65. United States.
16. Gallagher RP, Lee TK. Adverse effects of ultraviolet radiation: a brief review. Prog Biophys Mol Biol 2006;92:119–31. United Kingdom.
17. Gilchrest BA, Eller MS, Geller AC, et al. The pathogenesis of melanoma induced by ultraviolet radiation. N Engl J Med 1999;340(17):1341–8.
18. Green AC, Williams GM, Logan V, et al. Reduced melanoma after regular sunscreen use: randomized trial follow-up. J Clin Oncol 2011;29:257–63. United States.
19. Williams J, Maitra P, Atillasoy E, et al. High SPF sunscreen provides significant clinical benefit in actual use conditions: SPF 100+ is more effective than SPF 50+. J Am Acad Dermatol. 2017:AB154.
20. Williams J, Maitra P, Seo I, et al. High SPF sunscreen provides significantly better sunburn protection and reduces cumulative skin damage during a multiday beach clinical study: SPF 100+ is more effective than SPF 50+. J Am Acad Dermatol. 2017:AB154.
21. Balk SJ. Ultraviolet radiation: a hazard to children and adolescents. Pediatrics 2011;127:e791–817.
22. Branche CM, Conn JM, Annest JL. Personal watercraft-related injuries. A growing public health concern. JAMA 1997;279:663-5.
23. Gifford VB. Executive Summary. In: Guard USC, editor. 2015 Recreational Boating Statistics. Washington, D.C. U.S. Department of Homeland Security;2015. P. 1-82.
24. Kueh CSW, Kutarski P, Brunton M. Contaminated marine wounds— the risk of acquiring acute bacterial infection from marine recreational beaches. J Appl Bacteriol. 1992;73(5):412e420.
25. Hornbeak KB, Auerbach PS. Marine Envenomation. Emerg Med Clin N Am 2017;35: 321–337.
26. Auerbach PS. Envenomation by aquatic vertebrates. In: Auerbach PS, ed. Wilderness Medicine, 4th ed. St. Louis, MO: Mosby; 2001: 1488e1506.
27. Noonburg GE. Management of extremity trauma and related infections occurring in the aquatic environment. J Am Acad Orthop Surg. 2005;13(4):243e253.
28. Dennis L, Stevens, Alan L, et al; Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America, Clinical Infectious Diseases 2014;59(2):e10–e52.
29. Mosquito-borne diseases. World Health Organization. http://www.who.int/neglected_diseases/vector_ecology/mosquito-borne-diseases/en/ Accessed 06 April 2018.
30. Sam IC, AbuBakar S. Chikungunya virus infection. Med J Malaysia. 2006 Jun. 61(2):264-9.
31. Update: chikungunya fever diagnosed among international travelers–United States, 2006. MMWR Morb Mortal Wkly Rep. 2007 Mar 30. 56(12):276-7
32. World Health Organization. Dengue and severe dengue fact sheet. WHO. Available athttp://www.who.int/mediacentre/factsheets/fs117/en/. April 2017; Accessed 06 April 2018.
33. Halstead SB. Dengue. Lancet. 2007 Nov 10. 370(9599):1644-52.
34. Dengue. Available athttp://www.who.int/topics/dengue/en/. Accessed: October 20, 2011.
35. Centers for Disease Control and Prevention. Available athttp://www.cdc.gov/malaria. Accessed 06 April 2018.
36. Bailey JW, Williams J, Bain BJ, et al. Guideline: the laboratory diagnosis of malaria. General Haematology Task Force of the British Committee for Standards in Haematology.Br J Haematol. 2013 Dec. 163 (5):573-80.
37. Centers for Disease Control and Prevention. Malaria Diagnosis and Treatment in the United States. Available athttp://www.cdc.gov/malaria/diagnosis_treatment/index.html. Accessed 06 April 2018.
38. West Nile Virus.Centers for Disease Control and Prevention. Available at http://www.cdc.gov/ncidod/dvbid/westnile/prevention_info.htm#1. Accessed 06 April 2018.
39. Campbell GL, Marfin AA, Lanciotti RS, et al. West Nile virus. Lancet Infect Dis. 2002 Sep. 2(9):519-29.
40. West Nile virus and other arboviral diseases–United States, 2012. MMWR Morb Mortal Wkly Rep. 2013 Jun 28. 62(25):513-7.
41. Cleri DJ, Ricketti AJ, Porwancher RB, et al. Viral hemorrhagic fevers: current status of endemic disease and strategies for control. Infect Dis Clin North Am. 2006 Jun. 20(2):359-93, x.
42. World Health Organization. Yellow fever factsheet (revised in December 2009).Weekly Epidemiological Record. Jan 2010.
43. Roukens AH, Visser LG. Yellow fever vaccine: past, present and future. Expert Opin Biol Ther. 2008 Nov. 8(11):1787-95.
44. Centers for Disease Control and Prevention. Zika virus disease in the United States, 2015–2016. Centers for Disease Control and Prevention. Available athttp://www.cdc.gov/zika/geo/united-states.html. May 25, 2016; Accessed 06 April 2018.
45. Centers for Disease Control and Prevention. Guidelines for Travelers Visiting Friends and Family in Areas with Chikungunya, Dengue, or Zika. Centers for Disease Control and Prevention. Available athttp://wwwnc.cdc.gov/travel/page/travelers-vfr-chikungunya-dengue-zika. August 08, 2016; Accessed 06 April 2018.
46. Centers for Disease Control and Prevention. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever and other spotted fever group rickettsioses, ehrlichioses, and anaplasmosis—United States: a practical guide for health care and public health professionals. MMWR 2016; 65 (No. RR-2).
47. Gelfand JA, Vannier E. Ehrlichia chaffeensis (human monocytotropic ehrlichiosis), Anaplasma phagocytophilum (human granulocytotropic anaplasmosis) and other ehrlichiae. In: Mandell GL, Bennett JE, Dolin R, editors. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 6th ed. Philadelphia, PA: Churchill Livingstone; 2005. p. 2310–2318.
48. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis 2006; 43: 1089–1134.
49. Vannier E, Krause PJ. Human babesiosis. N Engl J Med 2012;366:2397–407.
50. Dumler JS, Madigan JE, Pusterla N, Bakken JS. Ehrlichioses in humans: epidemiology, clinical presentation, diagnosis, and treatment. Clin Infect Dis 2007 Jul 15;45 Suppl 1:S45–51.
51. Halperin JJ, Baker P, Wormser GP. Common misconceptions about Lyme disease. Am J Med 2013;126(3):264. Marques A. Lyme Disease: A Review. Curr Allergy Asthma Resp 2010, 10: 13-20.
52. Smith RP, Schoen RT, Rahn DW, et al. Clinical characteristics and treatment outcome of early Lyme disease in patients with microbiologically confirmed erythema migrans. Ann Intern Med 2002;136:421–8.
53. Stanek G, Wormser GP, Gray J, Strle F. Lyme borreliosis. Lancet 2012;379(9814):461-73.
54. Fischer M, Tsai TF. Coltiviruses (Colorado Tick Fever). In: Principles and Practice of Pediatric Infectious Diseases, 3rd edition. Eds: Long SS, Pickering LK, Prober CG. Elsevier 2008:1076–1078.
55. International Shark Attack File Statistics of Shark Attacks. Available at flmnh.ufl.edu/ fish/Sharks/Statistics/statistics.htm. Accessed 04 April 2018.
56. Ihama Y, Ninomiya K, Noguchi M, et al. Characteristic features of injuries due to shark attacks: A review of 12 cases. Legal Medicine. 2009;11:219-225.
57. Caldicott DG, Mahajani R, Kuhn M. The anatomy of a shark attack: a case report and review of the literature. Injury 2001;32:445–53.
58. Baldridge Jr HD, Williams J. Shark attack: feeding or fighting? Mil Med 1969;134:130–3.
59. Cirillo G, James H. Pattern association – a key to recognition of shark attacks. J Forensic Odontostomatol 2004;22:47–8.
60. Byard RW, Gilbert JD, Brown K. Pathologic features of fatal shark attacks. Am J Forensic Med Pathol 2000;21:225–9.
61. Makino Y, Tachihara K, Ageda S, et al. Peculiar circular and C-shaped injuries on a body from the sea. Am J Forensic Med Pathol 2004;25:169–71.
62. Butler FK,Bennett B, Wedmore CI. Tactical Combat Casualty Care and Wilderness Medicine: Advancing Trauma Care in Austere Environments. Emerg Med Clin North Am. 2017 May;35(2):391-407.
63. Butler FK Jr. TCCC J Spec Oper Med. Winter 2017;17(4):142-147.