Wednesday, August 26, 2009
Three Classes of Calcium Channel Blockers
• Phenylalkylamines (verapamil):
o Vasodilation resulting in a decrease in blood pressure (BP)
o Negative chronotropic and inotropic effects: reflex tachycardia not seen with a drop in BP.
• Dihydropyridine (nifedipine):
o Decreased vascular resistance resulting in a drop in BP
o Little negative inotropic effect: reflex tachycardia occurs.
• Benzodiazepine (diltiazem):
o Decreased peripheral vascular resistance leading to a decrease in BP
o Heart rate (HR) and cardiac output initially increased
o Direct negative chronotropic effect, which leads to a fall in HR
Effects of Calcium Channel Blockade
• Calcium plays key role in cardiac and smooth muscle contractility.
• Calcium channel blockers (CCBs) prevent:
o The entry of calcium, resulting in a lack of muscle contraction
o The normal release of insulin from pancreatic islet cells, resulting in hyperglycemia
Signs and Symptoms
o Reflex tachycardia (dihydropyridine)
o Conduction abnormalities/heart blocks
o CNS depression
• Bradycardia (tachycardia with nifedipine)
• Conduction delays: QRS-complex prolongation
• Heart blocks
• Ionized calcium level when administering calcium
• Digoxin level if patient taking digoxin (dictate safety of calcium administration)
• Electrolytes, BUN, creatinine, glucose:
o Hyperglycemia/metabolic acidosis may occur.
• Toxicology screen if coingestants suspected
• Î²-Blocker toxicity
• Clonidine toxicity
• Digitalis toxicity
• Acute myocardial infarction with heart block
• Transport pill/pill bottles to ED.
• Calcium for bradycardic/unstable patient with confirmed CCB overdose
Airway, breathing, circulation (ABCs):
• Airway protection as indicated
• Supplemental oxygen as needed
• 0.9% normal saline (NS) IV access
• Hemodynamic monitoring
• Heart rate >60 beats/minute
• Systolic BP >90 mm Hg
• Adequate urine output
• Improving level of consciousness
• Syrup of ipecac: contraindicated in the ED
• Activated charcoal:
o May be helpful, especially in the presence of coingestants
• Whole bowel irrigation:
o Beneficial with ingestion of sustained-release preparations
o Contraindicated in hemodynamically unstable patients
• First-line agent for CCB toxicity
• Calcium chloride (10%):
o Contains 1.36 mEq Ca2+/mL (three times more calcium than calcium gluconate)
o Can cause tissue necrosis and sloughing with extravasation
o Very irritating to veins
• Calcium gluconate (10%):
o Contains 0.45 mEq Ca2+/mL
o Does not cause tissue necrosis as calcium chloride does
o Calcium gluconate: preferred agent in an acidemic patient
• Follow serum calcium levels if repeated doses of calcium administered.
• Contraindicated in digoxin toxicity because calcium can produce serious adverse effects in digoxin toxicity
• IV fluids:
o Administer cautiously in the hypotensive patient.
o Swan-Ganz catheter or central venous pressure (CVP) monitoring to help follow volume status
• Atropine usually ineffective
• Pressor agents:
o No clear evidence that one agent is more effective than another
o Institute invasive monitoring to help guide treatment.
Î²1-Receptor agonist at low doses, which causes a positive inotropic effect on the myocardium
Î±-Receptor agonist at higher doses, which leads to vasoconstriction
Potent Î±- and Î²-receptor agonist
o Promotes cAMP production through a receptor site other than the Î²-receptor
o May cause nausea and vomiting
o Mix with NS or 5% dextrose in water.
o Selective phosphodiesterase III inhibitor
o Indirectly increases cAMP
• Electrical pacing: when other treatment options have failed
o Promotes more efficient myocardial metabolism
• Hypertonic sodium bicarbonate:
o Potential treatment in the future
• Amrinone: loading dose 0.75 mg/kg; maintenance drip 2-20 µg/kg/min; titrate for effect
• Atropine: 0.5 mg (peds: 0.02 mg/kg) IV; repeat 0.5-1.0 mg IV (peds: 0.04 mg/kg)
• Calcium chloride: 10 mL of 10% solution slow IVP (peds: 0.2-0.25 mL/kg; repeat in 10 minutes if necessary) followed by infusion 20-50 mg/kg/h
• Calcium gluconate: 10 mL of 10% solution slow IVP (peds: 1 mL/kg; may repeat in 10 minutes if necessary)
• Dopamine: 2-20 µg/kg/min; titrate to effect
• Epinephrine: 2 µg/min (peds: 0.1 µg/kg/min); titrate to effect
• Glucagon: 3.5-5 mg (peds: 0.03-0.1 mg/kg) IV bolus followed by 70 µg/kg/h infusion
• GoLYTELY WBI: 2 L/h PO or by nasogastric tube (NGT) for 4-6 hours or until rectal effluent is clear (peds: 40 mL/kg/h)
• Insulin: 1 IU/kg bolus IV followed by 0.5-1.0 IU/kg/h titrated to clinical response
• Admit symptomatic patients to a monitored bed for hemodynamic monitoring.
• Admit all patients who ingested sustained-release CCBs for 24 hours of observation and monitoring owing to the potential delay in symptoms.
Discharge asymptomatic patients 8 hours after ingestion of immediate-release preparation.
1. Boyer EW, Shannon MW. Treatment of calcium channel blocker intoxication with insulin infusion. New Engl J Med. 2001;344:1721-1722.
2. Kalman S, Berg S, Lisander B. Combined overdose with verapamil and atenolol: treatment with high doses of adrenergic agonists. Acta Anaesthesiol Scand. 1998;45:379-382.
3. Salhanick SD, Shannon MW. Management of calcium channel antagonist overdose. Drug Safety. 2003;26:65-79.
4. Tanen DA, Ruha AM, Curry SC, et al. Hypertonic sodium bicarbonate is effective in the acute management of verapamil toxicity in swine model. Ann Emerg Med. 2000;36:547-553.
Friday, August 21, 2009
• The median nerve, flexor digitorum profundus, flexor digitorum superficialis, and flexor pollicis longus are located in the carpal tunnel.
• Area bound by the carpal bones and the transverse carpal ligament
• Compression of the median nerve causes symptoms.
• Occupational/overuse syndromes-high impact, repetitive motion
• Pregnancy, birth control pills
• Granulomatous disease: tuberculosis, sarcoidosis
• Mass lesions with median nerve compression
• Multiple myeloma
• Rheumatoid arthritis
• Endocrine disorders: hypothyroidism, diabetes mellitus, acromegaly
• Chronic hemodialysis
• Idiopathic cause rare in children; most cases have correctable cause including:
o Hamartoma of the median nerve
o Anomalous flexor digitorum superficialis (FDS)
o Hemophilia with hematoma
Signs and Symptoms
• Numbness/paresthesias in median nerve distribution:
o Thumb, index, middle, and radial aspect of ring finger
o Location: wrist or hand, sometimes radiating to elbow, forearm, or shoulder
o Often worse at night-relieved by shaking out the hand
o Exacerbated by repetitive wrist movement and by activities in which the wrist is flexed (e.g., driving)
• Weakness of the abductor pollicis brevis and opponens muscles:
o Innervated by the recurrent branch of the median nerve
o Patient may complain of dropping things or having decreased fine motor control.
o Sensitivity of 29%; specificity of 80%, on average
• Loss of two-point discrimination:
o Late finding, highly specific
o Sensitivity of 24%; specificity of 94%
• Atrophy of thenar muscles:
o Late finding, highly specific
o Sensitivity of 18%; specificity of 94%
• History of characteristic nocturnal pain and paresthesias in the median nerve distribution.
• Muscle weakness and thenar wasting are later findings.
• Provocative testing:
o Phalen test:
Wrist flexion for 60 seconds produces numbness or tingling in the median nerve distribution.
Sensitivity of 68%; specificity of 73%
o Tinel sign:
Gentle tapping over the median nerve at wrist produces tingling in the fingers in the median nerve distribution.
Sensitivity of 50%; specificity of 77%
o Carpal compression test:
Thumb pressure applied over the proximal carpal ligament produces tingling in the fingers in the median nerve distribution.
Sensitivity of 64%; specificity of 83%
o Tourniquet test:
Blood pressure (BP) cuff inflated to just above the patient's systolic blood pressure for 2 minutes produces paresthesias in the median nerve distribution.
Sensitivity of 59%; specificity of 61%
• Not indicated in most cases
• Thyroid function studies; rheumatoid factor and immune panel if indicated by history and physical exam
• Wrist radiograph if trauma or degenerative arthritis suspected
• CT in select cases:
o May show encroachment of carpal tunnel
• MRI displays the soft tissues well but may not be justified in ED owing to time and cost:
o Findings: palmar bowing of transcarpal ligament, flattened median nerve, median nerve or synovial swelling, fluid in carpal tunnel, signal abnormality of median nerve
• Ultrasound can be diagnostic:
o Findings: median nerve swelling at proximal canal, median nerve flattening at distal canal, bowing of transcarpal ligament
Nerve conduction studies and electromyography are criterion standard tests.
• Cervical nerve root compression:
o Origin of median nerve is at the sixth and seventh cervical roots.
o Symptoms are aggravated by erect posture and neck movement.
• Hand-arm vibration syndrome:
o Characterized by Raynaud, numbness and tingling in ulnar and median nerve distributions when exposed to cold or vibration, weakened grip, and upper extremity myalgias
o Associated with prolonged exposure to vibration
• Thoracic outlet obstruction
• Osteoarthritis of the first carpometacarpal joint
• Brachial plexitis
• Generalized neuropathy
• Splint wrist in neutral position (0 degrees).
• Aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs)
• Avoidance of repetitive wrist movement
• Wrist splint to be worn at night until follow-up
• Apply heat to involved wrists heating pad, hot water bottle, low-level heat wraps
• Referral to occupational medicine for ergometric testing if caused by repetitive motion, and tendon gliding or nerve gliding exercises
• May need referral to a hand surgeon for consideration of surgical release of transverse carpal ligament using either open or endoscopic technique
• NSAIDs (there are many choices; a few are listed below):
o Ibuprofen: 600 mg (peds: 5-10 mg/kg) PO q6h
o Ketorolac: 30 mg IV or IM q6h or 10 mg PO q4h-q6h
o Diclofenac: 50 mg PO b.i.d. or t.i.d.
o Piroxicam: 20 mg PO daily
• Local corticosteroid injection provides transient relief in two thirds of patients (many different regimens):
o Hydrocortisone: 25-100 mg
o Methylprednisolone: 40 mg
o Prednisolone suspension: 20-40 mg
o Triamcinolone: 20 mg
Discharge to home with appropriate referral to either patient's primary care physician or directly to a specialist in occupational medicine or hand surgery.
1. Al-Qattan MM, Thompson HG, Clarke HM. Carpal tunnel syndrome in children and adolescents with no history of trauma. J Hand Surg. 1996;21B(1):108-111.
2. Kanaan N, Sawaya RA. Carpal tunnel syndrome: modern diagnostic and management techniques. Br J Gen Pract. 2001;51:311-314.
3. MacDermid JC, Wessel J. Clinical diagnosis of carpal tunnel syndrome: a systematic review. J Hand Ther. 2004;17(2):309-319.
4. Michlovitz SL. Conservative interventions for carpal tunnel syndrome. J Orthop Sports Phys Ther. 2004;34(10):589-600.
5. O'Gradaigh D, Merry P. Corticosteroid injection for the treatment of carpal tunnel syndrome. Ann Rheum Dis. 2000;59:918-919.
6. Sternbach G. The carpal tunnel syndrome. J Emerg Med. 1999;17:519-523.
7. Whitley JM, McDonnell DE. Carpal tunnel syndrome. A guide to prompt intervention. Postgrad Med. 1995;97(1):89-96.
Wednesday, August 19, 2009
• Acute, idiopathic peripheral palsy of CN VII (facial nerve)
• Complete recovery in 85% of cases without treatment
• Degree of deficit correlates with prognosis:
o Complete lesions have poorest prognosis.
o Partial lesions often have excellent results.
• Recovery usually begins within 2 weeks (often taste returns first) and is complete by 2-3 months:
o Advanced age and slow recovery are poor prognosticators.
• Affects men and women equally
• Age predominance between the third and fifth decade (may occur at any age)
• Incidence 15-40 per 100,000 per year
• Innervation to each side of forehead is from both motor cortices:
o Unilateral cortical processes do not completely disrupt motor activity of forehead.
o Only peripheral or brainstem lesion can interrupt motor function of just one side of forehead.
• Idiopathic by definition, but viral cause (particularly herpes simplex) suspected
• Lyme disease, infectious mononucleosis (Epstein-Barr virus [EBV] infection), varicella-zoster infections, and others may cause peripheral seventh nerve palsy.
• Mechanism: edema and nerve degeneration within stylomastoid foramen
Signs and Symptoms
• Sudden onset of unilateral facial droop, incomplete eyelid closure, and loss of forehead muscle tone:
o Maximal deficit by 5 days in almost all cases (2 days in 50%)
• If forehead muscle tone is not lost, a central lesion is strongly implied (i.e., this is not Bell's palsy)
• Tearing (68%) or dryness of eye (16%) and less frequent blinking on affected side
• The Bell phenomenon (upward rolling of the eye on attempted lid closure) may be seen.
• Subjective â€œnumbnessâ€� of the affected side
• Abnormal taste, drooling
• Hyperacusis (sensitivity to loud sounds)
• Fullness or pain behind mastoid
• Viral prodrome frequently reported
• Diagnosis is clinical and based on history and physical exam.
• Motor weakness isolated to seventh nerve distribution:
o Involves both upper and lower face
• An otherwise normal neurologic exam including all cranial nerves and extremity motor function
• Not helpful in diagnosis of Bell's palsy
• Lyme titers are useful when Lyme disease is suspected or in endemic area
• Tests for mononucleosis (CBC, Monospot) if EBV infection suspected
• Not helpful in diagnosis of Bell's palsy
• CNS imaging (CT, MRI) useful if CNS pathology is suspected
• Brainstem events (mass, bleed, infarct) affecting CN VII almost always involve CN VI (abnormal EOM) and may affect long motor tracts:
o There have been (rare) case reports of isolated CN VII palsy from brainstem disease.
• Lyme disease: history of tick bite, erythema migrans rash, or endemic area
• Zoster (Ramsay-Hunt syndrome): Look for herpetic vesicles, inquire about tinnitus or vertigo.
• Infectious mononucleosis: look for pharyngitis, posterior cervical adenopathy
• Tumors: parotid, bone, or metastatic masses, acoustic neuroma (deafness)
• Trauma: Skull fracture or penetrating facial injury may damage CN VII.
• Middle ear or mastoid surgery or infection, cholesteatoma
• Meningeal infection
• Guillain-BarrÃ© syndrome: other neurologic deficits (e.g., ascending motor weakness or diminished deep tendon reflexes [DTRs] present)
• Basilar artery aneurysm; other CN deficits should be present.
• Bilateral peripheral CN VII palsy: Consider multiple sclerosis, sarcoid, leukemia, and Guillain-BarrÃ© idiopathic (Bell's) palsy may be bilateral in rare cases.
• Bell's palsy may reoccur; treatment is unchanged.
Patients with an isolated peripheral CN VII palsy are stable.
• Oral steroids may hasten recovery if started within 1 week of onset:
o Complications of therapy are rare and treatment is recommended by many authors.
o Some meta-analyses question efficacy.
• Corneal damage may result from incomplete eyelid closure:
o Lubricating and hydrating ophthalmic preparations is essential/
o Eyelid taping at night
• Acyclovir with steroids may be effective in improving functional nerve recovery:
o Initiate within 72 hours of symptom onset.
• Suspected Lyme disease should be treated with doxycycline or amoxicillin.
• Surgical decompression may be indicated for complete lesions that do not improve; this is controversial.
• Acyclovir: 400 mg five times per day PO for 7 days (peds: no data to support its use) or valacyclovir 1 g PO for 7 days
• Lacri-Lube: at bedtime and PRN; dryness/irritation in affected eye (or equivalent)
• Prednisone: 30-40 mg PO b.i.d. (or 60 mg PO daily) for 5 days, then taper over 5 days; total 10 days of therapy (peds: 2 mg/kg/d PO [max. 60 mg])
Isolated peripheral CN VII palsy does not require admission.
• Isolated peripheral CN VII palsy may be treated on outpatient basis.
• Follow-up should be within 1 week.
1. Adour K, et al. Bell's palsy treatment with acyclovir and prednisone compared with prednisone alone. Ann Otol Rhinol Laryngol. 1996;105:371-378.
2. Austin JR, et al. Idiopathic facial nerve paralysis: a randomized double blind controlled study of placebo versus prednisone. Laryngoscope. 1993;103:1326-1333.
3. Gilden D. Bell's palsy. N Engl J Med. 2004; 351:1323-1231.
4. Grogan PM, et al. Practice parameter: steroids, acyclovir, and surgery for Bell's palsy (an evidence-based review). Neurology. 2001; 56(7):830-836.
5. Ramsey JR, et al. Corticosteroid treatment for idiopathic facial nerve paralysis: a meta-analysis. Laryngoscope. 2000;110:335-341.
6. Salinas R, Alvarez G, Ferreira J. Corticosteroids for Bell's palsy (idiopathic facial paralysis). Cochrane Database Syst Rev. 2004;4:CD001942.
• Most bites are from provoked animals
• Dog bite wounds:
o Large dogs inflict the most serious wounds (pit bulls cause the most human fatalities).
o Most fatalities in children (70%) due to bites to face/neck
o Dogs of family or friends account for most bites.
• Cat bite wounds:
o Majority from pets known to victim
o 50% infection rate in those seeking care
o Puncture wounds most frequent due to sharp thin teeth causing deep inoculation of bacteria
• Cat-scratch disease:
o Three of the following four criteria:
Cat contact, with presence of scratch or inoculation lesion of the skin, eye, or mucous membrane
Positive CSD skin test result
Characteristic lymph node histopathology
Negative results of laboratory studies for other causes of lymphadenopathy
• Rat bite wounds:
o Occur in laboratory personnel or children of low socioeconomic class
o Infection rate
o Rat bites rarely transmit rabies, and prophylaxis not routine
• Dog and cat bites:
o Pasteurella multocida is the major organism in both
Twice as likely to be found in cat bites than dog bites
Gram-negative aerobe found in up to 80% of cat infections
Infection appears in <24 hours
o Staphylococcus or Streptococcus
Infection appears in >24 hours
o Other organisms include anaerobes and Capnocytophaga canimorsus (dogs)
• Cat-scratch disease:
o Caused by Bartonella henselae
• Rat bites:
o Caused by Spirillum minus and Streptobacillus moniliformis
Signs and Symptoms
• Distribution of mammalian bites:
o Dog bites represent 80-90% of all bites.
o Cat bites represent 5-15% of all bites.
o Human bites represent 2-5% of all bites (see Human Bite chapter).
o Rat bites represent 2-3% of all bites.
• Dog bites:
Crush injuries (most common), tears, avulsions, punctures, and scratches
o Low rates of infection compared with cat and human bites
o Infections usually present with:
Malodorous gray discharge
• Cat bites:
Puncture wounds (most common)
o High infection rates (30-50%) due to deeper puncture wounds
• Cat-scratch disease:
o From the bite/scratch of a cat, dog, or monkey
o Small macule or vesicle that progresses to a papule
Begins several days (3-10) after inoculation
Resolves within several days or weeks
Regional lymphadenopathy occurs 3 weeks postinoculation
Resolves after 2-4 months
o Low-grade fever, malaise, headache
• Animal's behavior, provocation, location, ownership
• Time since attack
• Past medical history: conditions compromising immune function, allergies, and tetanus status
• Record the location and extent of all injuries.
• Document any swelling, crush injuries, or devitalized tissue.
• Note the range of motion of affected areas.
• Note the status of tendon and nerve function.
• Document any signs of infection, including regional adenopathy.
• Document any joint or bone involvement.
• Aerobic and anaerobic cultures from any infected bite wound
• Cultures not routinely indicated if wounds not clinically infected
• Cat-scratch disease
o Presence of elevated titers of Bartonella (Rochalimaea) henselae, or
o Positive reaction to cat-scratch antigen (CSA)
Inject 0.1 mL CSA intradermally
Induration at the site 48-72 hours later equal to or exceeding 5 mm is positive
Plain radiograph indications:
• Suspect foreign body, e.g., tooth
• Baseline film if a bone or joint space has been violated in evaluating for osteomyelitis
• For infection in proximity to a bone or joint space
• Human bite injuries: human teeth cause crush injuries and animal teeth cause more punctures and lacerations.
• Bite injuries from other animals
• CSD-caused lymphadenopathy:
o Reactive hyperplasia (leading cause of lymphadenopathy in children younger than 16 years)
o Infection, chronic lymphadenitis, drug reaction, malignancy, and congenital conditions
• Achieve hemostasis on any bleeding wound.
• Airway stabilization if bite located on face or neck
• Wound irrigation:
o Copious volumes of normal saline irrigation with an 18-gauge plastic catheter tip aimed in the direction of the puncture
o Avoid injection of saline through tissue planes due to force of irrigation
o Remove foreign material, necrotic skin tags, or devitalized tissues
o Do not debride puncture wounds
o Remove any eschar present so underlying pus may be expressed and irrigated
• Wound closure:
o Closing wounds increases risk of infection and must be balanced with scar formation and effect of leaving wound open to heal secondarily.
o Do not suture infected wounds or wounds >24 hours after injury.
o Repair of wounds >8 hours: controversial
o Close facial wounds (warn patient of high risk of infection).
o Infected wounds, those presenting >24 hours after the event, and deep hand wounds should be left open
o May approximate the wound edges with Steri-Strips and perform a delayed primary closure
• Antibiotic indications:
o Infected wounds
o Cat bites
o Hand injuries
o Severe wounds with crush injury
o Puncture wounds
o Full-thickness puncture of hand, face, or lower extremity
o Wounds requiring surgical debridement
o Wounds involving joints, tendons, ligaments, or fractures
o Immunocompromised patients
o Wounds presenting >8 hours after the event
• Elevate injured extremity.
• Tetanus prophylaxis
• Not required if rabies not known or suspected
• Rodents (squirrels, hamsters, rats, mice) and rabbits rarely transmit the disease.
• Skunks, raccoons, bats, and foxes represent the major reservoir for rabies.
• Recommended in following situations:
o Dog or cat in rabies-known area unable to be quarantined for 10 days
o Previously healthy dog or cat becomes ill while being quarantined (and awaiting results of rabies fluorescent antibody test)
o An ill dog or cat while awaiting rabies test results (to be continued or halted based on results of rabies test)
• Active immunization:
o Human diploid cell vaccine (HDCV): 1 mL IM on days 1, 3, 7, 14, and 28 after exposure
• Passive immunization:
o Human rabies immune globulin (HRIG): 20 IU/kg
o Up to one half in area around wound with the rest IM
• Apply local heat to affected nodes.
• Avoid lymph node trauma.
• Disease usually self-limiting
• Antibiotics controversial, consider if severe disease is present or immunocompromised victim
• Amoxicillin/clavulanic acid (Augmentin): 500-875 mg (peds: 40 mg/kg/24 hr) PO b.i.d. (first line for all three animals)
• Ampicillin/sulbactam (Unasyn): 1.5-3.0 g IV q6h
• Cefoxitin (Mefoxin): 2.0 g IV q8h
• Cefuroxime axetil (Ceftin): 500 mg PO b.i.d.
• Clindamycin (Cleocin): 300 mg PO q6h; 900 mg IV q8h
• Ciprofloxacin (Cipro): 500 mg PO b.i.d.; 400 mg IV q12h
• Doxycycline (Vibramycin): 100 mg PO b.i.d.
• Imipenem/cilastatin (Primaxin): 0.5-1.0 g (peds: 50 mg/kg/24h) IV q6h
• Piperacillin/tazobactam (Zosyn): 3.375 g IV q6h
• Ticarcillin/clavulanic acid (Timentin): 3.1 g IV q6h
• Trimethoprim-sulfamethoxazole (Bactrim): 1 tablet (peds: 6-12 mg TMP, 30-60 mg SMX/kg/24h) PO b.i.d.
• All bites:
o Infected wounds at presentation
o Severe/advancing cellulitis/lymphangitis
o Signs of systemic infection
o Infected wounds that have failed to respond to outpatient (PO) antibiotics
• Cat-scratch disease:
o Prolonged fever, systemic symptoms, and/or marked lymphadenopathy
• Healthy patient with localized wound infection: discharge on antibiotics with 24-hour follow-up.
• 48-hour follow-up for noninfected wounds
1. Brook I. Microbiology and management of human and animal bite wound infections. Prim Care. 2003;30(1):25-39, v.
2. Galloway RE. Mammalian bites. J Emerg Med. 1998;6:325-331.
3. Griego RD, et al. Dog, cat, and human bites: a review. J Am Acad Dermatol. 1995;33: 1019-1029.
4. Klein JD. Cat scratch disease. Pediatr Rev 1994; 15(9):348-353.
5. Pickering L, Red Book: 2003 Report of the Committee on Infectious Diseases. Amer Academy of Pediatrics 2003. 26th edition.
6. Smith PF, et al. Treating mammalian bite wounds. J Clin Pharm Ther. 2000;25:85-99.
See also: Rabies
Burn injuries represent an acute disruption of the skin.
Burns can be classified into six categories:
- Scald = hot liquids, grease, or steam
- Contact = hot or cold surfaces
- Thermal = fire or flames
- Radiation burns
- Chemical burns
- Electrical burns
Signs and Symptoms
- Most burns will have external signs of integumentary damage.
- Inhalation injury:
- Facial burns
- Carbonaceous sputum
- Pharyngeal injection
- Singed nasal hair
- Electrical burns may have minimal external findings.
- Information from emergency medical services (EMS), family, friends, or witnesses may be required.
- Medical history, surgical history, medications, allergies, social history, tetanus immunization status
- Carbon monoxide poisoning with exposure to combustion
- Cyanide poisoning from burning wool, silk, nylon, and polyurethane found in furniture and paper
- Focus on airway, breathing first, then head-to-toe secondary survey for concurrent injuries.
- Evaluate face and oropharynx for signs of inhalation injury.
- Assess need for immobilization of cervical spine.
- Eye examination for corneal burns
- Determine severity of partial- and full-thickness burns by assessing size and depth of burn:
- Estimate surface area involved.
Specific patterns of injury may indicate nonaccidental injury (stockinglike or glovelike appearance of wounds, cigarette burns, etc.)
The severity of the burn should be assessed by determining the size and depth.
- Reported as percent involvement of total body surface area (TBSA) in one of three ways:
- 1. Rule of nines:
- TBSA of body parts is estimated by multiples of 9%; applies to adults only.
- Adult estimates of percentage of TBSA:
- Head and neck: 9
- Arms: right, 9; left, 9
- Legs: right, 18; left, 18
- Trunk: front, 18; back, 18
- Perineum, palms: 1
- In infants and children, the head contributes more to the percentage of TBSA and legs contribute less.
- Head and neck: 18
- Arms: right, 9; left, 9
- Legs: right, 14; left, 14
- Trunk: front, 18; back, 18
- 2. Lund and Browder chart, divides body into areas and assigns percentage of BSA based on age
- 3. Palm surface area, patient's palm is approximately 1% of TBSA:
- Estimate size in terms of number of patient's palms that cover burn.
- Helpful in assessing smaller, scattered burns
- Superficial or first-degree burns (epidermis only): local erythema and pain only, no blisters; healing occurs in several days
- Partial-thickness or second-degree burns (epidermis and dermis): divided into superficial partial-thickness and deep partial-thickness burns:
- Superficial partial-thickness: epidermis and superficial dermis:
- Skin is red, moist, painful, good capillary refill, develop blisters
- Heals in 14-21 days
- Deep partial-thickness: epidermis and deep dermis:
- Skin may be blistered, with dermis white to yellow; absent capillary refill, and pain sensation
- Heals via epithelialization within 3-12 weeks
- Full-thickness or third-degree burns (epidermis and dermis, extends into subcutaneous tissue):
- Skin is charred, leathery and pale, no blisters.
- Sensation absent
- Lesions will not heal spontaneously; needs surgical repair and skin grafting.
- Full-thickness burns with damage to underlying muscle or fourth-degree burns:
- Full-thickness plus involvement of underlying fascia, muscle, bone, and other tissues
- Requires extensive debridement
- Resultant disability
- For severe burns, obtain CBC, serum electrolytes, glucose, BUN, creatinine, and PT/PTT, type and cross-match, pregnancy test (female)
- Blood gas with carbon monoxide level for closed space or inhalation exposures
- Cyanide level if suspected
- Chest radiograph
- Fiber optic bronchoscopy to assess inhalation injury
- Electrical injury
- Chemical injury
- Associated trauma or intoxication
- Stop the burning process, remove smoldering clothes/jewelry.
- Establish patent airway; frequent reassessment:
- Intubate early for signs of respiratory distress.
- Initiate early IV fluid therapy.
- Relieve pain.
- Protect the wound with clean sheets.
- Transport to burn center (for major burns) if transport time shorter than 30 minutes.
- Immobilize spine if decreased sensorium or trauma.
- Airway control paramount:
- Early intubation for patients with signs of upper airway injury, significant nasolabial burns, or circumferential neck burns
- IV access, supplemental 100% oxygen, monitor, pulse oximetry
- Evaluation for concurrent injuries
- Provide adequate analgesia.
Fluid Resuscitation: Partial and Full-thickness Burns (>20% TBSA)
- Parkland formula: 4 mL of lactated Ringer solution or normal saline (NS) per kilogram per percentage of BSA burned IV; one half of this total is given in the first 8 hours and the remaining half over the next 16 hours:
- Example: 70-kg patient with a 40% TBSA burn requires 4 mL Ã— 70 kg Ã— 40% = 11,200 mL over 24 hours, with 5,600 mL over first 8 hours or 700 mL/h.
- For large burns, >20% TBSA, IV fluid therapy should be guided by invasive hemodynamic monitoring or urine output; maintain urine output of 0.5 to 1.0 mL/kg/h for adults and 1.0â€“1.5 mL/kg/h for children.
- Circumferential burn eschar may lead to neurovascular compromise:
- Monitor pulses; may need Doppler flow probe.
- Elevate burned extremity.
- If circulation is compromised, escharotomy incisions on extremities should be made medially and laterally along the long axis of the limb just to the subcutaneous layer through the entire length of the burn eschar.
- A circumferential burn of the chest wall may prevent adequate ventilation unless escharotomy is performed:
- Make longitudinal incisions at anterior axillary line from the second rib to the level of the twelfth rib; connect with two transverse incisions across the chest.
- Cover the wounds with sterile moist saline dressings.
- If disposition is delayed, cleanse with sterile saline or poloxamer 188 product (e.g., Shur-Clens), debride blisters except those on palms or soles, and apply topical antibacterial agent (e.g., silver sulfadiazine, bacitracin, or mafenide acetate).
- Do not delay transfer to burn unit for wound care.
- Prophylactic antibiotics not indicated
Outpatient Management of Minor Burns
- Sterile technique for cleansing and debridement
- Remove loose, necrotic skin; debride broken, tense, or infected blisters.
- Topical antibacterial agents: (e.g., silver sulfadiazine, bacitracin, mafenide acetate) recommended in deep partial-thickness or full-thickness burns only
- Three-layer burn dressings should keep the wound moist and absorb exudate:
- Inner layer should be nonadherent porous mesh gauze saturated with a non-petroleum-based lubricant, or use a mild ointment (e.g., bacitracin or Polysporin) under a nonadherent porous gauze.
- The next layer should be fluffed coarse-mesh gauze.
- The outer wrap should keep the dressing in place without constricting.
- Dressings should be changed at least daily.
- Silver wound dressings (Silverlon and Acticoat):
- Thin coating of metallic silver applied to knitted fabric backing
- Requires dressing to remain moist
- May leave on for up to 3 days
- Parkland formula underestimates fluid requirements in children; the Galveston formula may be used instead: 5,000 mL/m2 BSA burned plus 2,000 mL/m2.
- TBSA of 5% dextrose in lactated Ringer solution IV over the first 24 hours, half in the first 8 hours and the other half over the next 16 hours
- Consider nonaccidental trauma, particularly with burns on the back of hands or feet, buttocks, the perineum, and the legs.
- Avoid hypothermia:
- Children have greater BSA/mass ratio and lose heat more rapidly.
- Avoid hypoglycemia:
- Children are more prone to hypoglycemia owing to limited glycogen stores.
- Significant morbidity to mother and child
- Fluid requirements may exceed estimations.
- Fetal monitoring and early obstetric consultation recommended
- Bacitracin ointment: Apply to wound one-four times per day.
- Mafenide (Sulfamylon) acetate cream: Apply to wound one or two times per day.
- Morphine: 0.1-0.2 mg/kg titrated to effect for pain control after shock
- Silverlon and Acticoat: Cut sheet to size of burn; moisten with sterile water.
- Silver sulfadiazine cream: Apply to wound one or two times per day.
- Tetanus toxoid or immunoglobulin: 0.5 mL IM; 250 U IM once along with toxoid
Injuries Requiring Admission
- Partial-thickness burns of noncritical areas (not the eyes, ears, face, hands, feet, or perineum) involving 10-20% of BSA in adults (older than 10 years and younger than 50 years)
- Partial-thickness burns of noncritical areas involving 5-10% of BSA in children younger than 10 years
- Suspicion of nonaccidental trauma
- Patients unable to care for wounds in outpatient setting (e.g., homeless patients)
Injuries Requiring Transfer and Admission to a Burn Center
- Partial-thickness and full-thickness burns involving ±10% of BSA in patients younger than 10 years or older than 50 years
- Partial-thickness and full-thickness burns over >20% of BSA in any patient
- Full-thickness burns involving >5% of BSA
- Partial-thickness and full-thickness of face, hands, feet, genitalia, perineum, or major joints
- Electrical burns, including lightning injury
- Significant chemical injury
- Inhalation injury
- Burn injury in patients with pre-existing illness that could complicate management
- Burn injury in patients with a concomitant trauma or social barrier
Partial-thickness burns of <15%>
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2. Holm C, et al. A clinical randomized study on the effects of invasive monitoring on burn resuscitation. Burns. 2004;30(8):798-807.
3. Kavanagh S, et al. Care of burn patients in the hospital. Burns. 2004;30(8):A2-6.
4. Schwartz LR. Thermal burns. In: Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw-Hill, 2004:1220-1226.
5. Tompkins D, et al. Care of out patient burns. Burns. 2004;30(8):A7-9.