Toxic Epidermal Necrolysis

Author: Victor Cohen, PharmD; Chief Editor: Michael Stuart Bronze,

http://emedicine.medscape.com/article/229698-overview

Background
Toxic epidermal necrolysis (TEN) is a potentially life-threatening dermatologic disorder
characterized by widespread erythema, necrosis, and bullous detachment of the epidermis and
mucous membranes, resulting in exfoliation and possible sepsis and/or death (see the image
below). Mucous membrane involvement can result in gastrointestinal hemorrhage, respiratory
failure, ocular abnormalities, and genitourinary complications.

TEN is most commonly drug induced. However, the disorder has other potential etiologies,
including infection, malignancy, and vaccinations (see Etiology). TEN is idiosyncratic, and
its occurrence is not easily predicted.
Some authors believe that Stevens-Johnson syndrome (SJS; also known as erythema
multiforme major) is a manifestation of the same process involved in TEN, with the latter
involving more extensive necrotic epidermal detachment. TEN involves more than 30% of
the body surface, whereas SJS involves less than 10% (see Differentials).
A classification system, based largely on the extent of epidermal detachment and morphology
of the skin lesions, aids in differentiating opposite spectrums of the same disease entity.[1] This
system comprises the following:

TEN with spots

TEN without spots

Overlap Stevens-Johnson syndrome and TEN (SJS-TEN)

TEN with spots is defined as widespread, irregularly shaped erythematous or purpuric

macules with blistering that occurs on all or part of the macule. Blisters become more
confluent and result in detachment of the epidermis and erosions on greater than 30% of the
body surface area. Mucosal surfaces are usually involved.

TEN without spots is defined as widespread, large areas of erythema with no discrete lesions.
Epidermal detachment is greater than 10% of the body surface area. Mucosal surfaces are
usually involved.
Overlap Stevens-Johnson syndrome and TEN (SJS-TEN) is characterized by widespread,
irregularly shaped erythematous or purpuric macules with blistering that occurs on all or part
of the macule. Blisters become confluent and result in detachment of the epidermis and
erosions on 10-29% of the body surface area.
TEN is a clinical diagnosis, confirmed by histopathologic analysis of lesional skin (see
Clinical and Workup). The mainstay of treatment is supportive care until the epithelium
regenerates. Early transfer of patients to a burn or intensive care unit has been shown to
reduce the risk of infection, mortality rate, and length of hospitalization (see Treatment).
Historical background

Alan Lyell provided an early description of TEN in 1956, describing the condition as "an
eruption resembling scalding of the skin."[2] This dermatologic condition is characterized by
extensive epidermal loss suggestive of severe scalding. In that same year, Lang and Walker
reported a case of TEN.[3] The disorder was originally described by Debre et al in 1939 in
French as l'erythrodermie bulleuses avec epidermolyse.[4]
Lyell later reclassified the conditions of 2 of his patients as having staphylococcal scalded
skin syndrome,[5] which is due to Staphylococcus aureus infection rather than to a probable
drug hypersensitivity-type reaction. Histopathologic analysis of the skin remains the main
tool for discrimination between the two conditions.
Patient education

Patients who have had TEN must be counseled regarding the likely causative medication or
agent, and they must be advised to avoid these medications and those of the same or similar
classes in the future. Cross-reactivity may occur with agents that chemically resemble the
causative agent. Patients must call a pharmacist whenever they start a new prescription.
Genetic factors are suspected in drug-induced blistering disorders, and blood relatives of the
patient also should not use the suspected drug.
For patient education information, see the Skin, Hair, and Nails Center, as well as LifeThreatening Skin Rashes.

Pathophysiology
The pathophysiology of TEN has not been fully elucidated; however, various theories have
received wide acceptance. TEN is believed to be an immune-related cytotoxic reaction aimed
at destroying keratinocytes that express a foreign antigen.
TEN mimics a hypersensitivity reaction, with its characteristic delayed reaction to an initial
exposure and an increasingly rapid reaction with repeated exposure.

The widespread epidermolysis and blistering of TEN results from keratinocyte apoptosisan
organized series of biochemical reactions leading to cell changes and cell death.[6] However,
the number of inflammatory T cells in the skin of patients with TEN is variable and perhaps
too low to explain the widespread destruction.[7]
There is evidence supporting several immunopathologic pathways leading to keratinocyte
apoptosis in TEN, including the following:

Fas ligand activation on keratinocyte membranes leading to death

receptormediated apoptosis[8]

Release of destructive proteins (perforin and granzyme B) from cytotoxic T

lymphocytes (CTLs) generated from an interaction with cells expressing
major histocompatability complex (MHC) class I[9]

Overproduction of T cell and/or macrophage-derived cytokines

(interferon- [INF-], tumor necrosis factor- [TNF-], and various
interleukins)[10, 11]

Drug-induced secretion of granulysin from CTLs, natural killer cells, and

natural killer T cells[12]

Precisely how the inciting agent triggers the proposed pathways is yet to be elucidated.

Etiology
TEN can be induced by drugs or infection or can be idiopathic. Medications are the major
precipitating cause. Numerous medications have been implicated,[13] including antibiotics,
antiepileptic drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), ampicillin, allopurinol,
corticosteroids (topical and systemic), and the antiretroviral drugs nevirapine and abacavir.
Antibacterial drugs associated with TEN include the following:

Sulfonamides (4.5 cases per million users per week)

Chloramphenicol

Macrolides (eg, erythromycin)

Penicillins

Quinolones (eg, ciprofloxacin,[14] trovafloxacin[15] )

Anticonvulsants associated with TEN include the following:

Phenobarbital

Phenytoin[16]

Carbamazepine

Valproic acid

Lamotrigine

TEN in patients taking anticonvulsants has most often been reported within 2 months of
starting the drug. However, some cases associated with long-term use have been reported.
NSAIDs associated with TEN include the following:

Phenylbutazone and oxybutazone - Implicated most commonly, although

they are no longer available in the United States

Oxicams (eg, piroxicam, tenoxicam) - Implicated more often than other

NSAIDs

Ibuprofen

Indomethacin

Sulindac

Tolmetin

With allopurinol, risk is not constant over time. Patients have a 5.5 relative risk. However,
during the first 2 months of therapy, the relative risk is 52, and the long-term therapy risk is
0.5.
No laboratory test is able to confirm a specific drug etiology. A causal link is suggested when
TEN occurs during the first 4 weeks of medication therapy, usually between 1 and 3 weeks.
Drugs with longer half-lives and those with circulating active metabolites may result in more
fulminant disease.
Infectious agents (ie, Mycoplasma pneumoniae, herpes virus, hepatitis A), immunizations,
and bone marrow or solid organ transplantation have also been associated with TEN.

Epidemiology
In the United States, the annual frequency of TEN is reported to be 0.22-1.23 cases per
100,000 population. In the HIV-positive population, the incidence of TEN increases to 1 case
per thousand per year.[17]
Worldwide, the average annual incidence of TEN is 0.4-1.3 cases per million population.[18] In
1992, the cumulative incidence of TEN and SJS in Germany was 1.9 cases per million
population. A French survey of dermatologists and health care facilities reported an annual
incidence of 1 case per million population.

Race-, sex-, and age-related demographics

A genetic predilection toward carbamazepine-induced TEN has been observed in HLAB*1502positive Han Chinese patients.[19] The US Food and Drug Administration
recommends screening for the HLA-B*1502 allele before initiating carbamazepine in patients
of Asian ancestry.[20]
For unclear reasons, TEN appears to have a predilection for females. The female-to-male
ratio is 1.5:1.[21]
TEN may occur in all age groups; however, the mean age of patients with TEN is reported to
be between 46 and 63 years. Infection is more commonly implicated as an etiology in
children, whereas medication exposure is more common in adults. Elderly persons may be at
greater risk because of their tendency to use multiple medications.

Prognosis
The estimated mortality associated with TEN varies widely in different reports, from 10-70%.
Outcome depends in part on the quality of care and the rapidity with which treatment is
initiated.
Septicemia and multisystem organ failure are the primary causes of death. Epithelial loss
results in vulnerability to bacterial and fungal infections. Sloughing of stratified epithelium of
mucosal membranes can result in GI hemorrhage, respiratory failure, ocular abnormalities,
and genitourinary lesions. Significant fluid loss from extensive skin exfoliation and an
inability to tolerate oral intake can lead to hypovolemia, acute tubular necrosis, and shock.
Age, extent of epidermal involvement, and serum urea level are said to be the most important
prognostic factors in TEN.[22] Mortality rates in children are much lower than in adults.[23]
Elderly patients have a poor prognosis.
Other negative prognostic factors include the following:

Elevated blood urea nitrogen (BUN) and serum creatinine levels

Respiratory failure

Multiple drugs

Thrombocytopenia

Lymphopenia

Neutropenia

Leukopenia

Sepsis

Severity-of-illness score

A severity-of-illness score that estimates the risk of death in TEN (SCORTEN) has been
developed and validated.[24] Each of the following independent prognostic factors is given a
score of 1:

Age >40 years

Heart rate >120 beats per minute

Cancer or hematologic malignancy

Involved body surface area >10%

Blood urea nitrogen level >10 mmol/L (28 mg/dL)

Serum bicarbonate level < 20 mmol/L (20 mEq/L)

Blood glucose level >14 mmol/L (252 mg/dL)

The number of positive criteria and the corresponding mortality rates are as follows:

0: 1 to 3%

2: 12%

3: 35%

4: 58%

5 or more: 90%

Sequelae

Major sequelae are generally limited to the affected organ systems (ie, the skin and mucosal
membranes).
Cutaneous sequelae of TEN include the following:

Changes in skin pigment (hypopigmentation or hyperpigmentation; sun

exposure must be avoided for several months because ultraviolet light can
worsen hyperpigmentation; sunblock is recommended)

Nail loss and nail dystrophy

Hypohidrosis (inability to sweat)

Scarring, alopecia, and hypertrophic scarring

Dermal desiccation, causing deep dermal wounds

Chronic xerostomia

Esophageal strictures

Vulvovaginal synechiae

Phimosis

Chronic erosion of the mouth and genitalia

Ocular complications generally result from abnormal keratinization of the tarsal conjunctiva.
A Sjogrenlike syndrome with decreased lacrimal secretion causes dry eye and predisposes to
corneal abrasions and corneal scarring with neovascularization. In addition, patients have
been reported to have palpebral synechiae, entropion, or symblepharon (adhesion of the
eyelids).[25]
A study by Power and colleagues found that 50% of patients with TEN developed ocular
complications.[26] Patients treated with steroids fared no better than those treated without
steroids. Therefore, TEN remains a common cause of visual loss in a significant number of
patients. Ultimately, 5-9% of patients can become blind as a result of some of these
complications.

History
Patients with toxic epidermal necrolysis (TEN) may describe an influenzalike prodrome
characterized by the following:

Malaise

Rash

Fever

Cough

Arthralgia

Myalgia

Rhinitis

Headache

Anorexia

Nausea and vomiting, with or without diarrhea

Other prodromal signs and symptoms include conjunctivitis (32%), pharyngitis (25%), and
pruritus (28%). The prodrome typically lasts from 1 day to as long as 3 weeks.

The cutaneous eruption begins as a poorly defined, erythematous macular rash with purpuric
centers. Over a period of hours to days, the rash coalesces to form flaccid blisters and
sheetlike epidermal detachment. The lesions predominate on the torso and face, sparing the
scalp. Pain at the site of the skin lesions is often the predominating symptom and is often out
of proportion to physical findings in early disease.
Mucous membrane erosions (seen in 90% of cases) generally precede the skin lesions by 1-3
days. The most frequently affected mucosal membrane is the oropharynx, followed by the
eyes and genitalia. Oral cavity involvement typically presents as a sore or burning sensation.
Intake may be limited because of pain associated with the oropharyngeal lesions.
Ocular manifestations range from acute conjunctivitis to corneal erosions and ulcers. Genital
involvement may result in painful urination. Other mucosal surfaces such as the esophagus,
intestinal tract, or respiratory epithelium may be affected. Bronchial epithelial sloughing may
result in dyspnea and hypoxemia.
Most cases of TEN are drug induced, typically occurring within 1-3 weeks of therapy
initiation and rarely occurring after more than 8 weeks. Therefore, a detailed medication
history, focusing on medications that have been recently started, is a vital component of the
patient's history.
More than 220 different medications have been suggested. The most commonly implicated
agents include the following:

Sulfonamide antibiotics

Antiepileptic drugs

Oxicam nonsteroidal anti-inflammatory drugs

Allopurinol

Nevirapine

Abacavir

Lamotrigine

Fewer than 5% of patients report no history of medication use

Physical Examination
Vital signs in toxic epidermal necrolysis may include hyperpyrexia, hypotension secondary to
hypovolemia, and tachycardia.

Skin examination

Skin lesions begin as painful/burning, warm, erythematous, morbilliform macules that are
initially discrete. They begin symmetrically on the face and thorax before spreading to the
entire body. The skin lesions coalesce and fill with fluid-producing large, flaccid blisters. The
epidermis sloughs in sheets, leaving a characteristic moist, denuded dermis (see images
below). Conjunctivitis and denudation and erosions of other mucous membranes precede
epidermal necrolysis.
A positive Nikolsky sign is evident when the application of slight lateral pressure to the
epidermal surface results in the epidermis easily separating from its underlying surface.
The usual course is an intense erythema that progresses rapidly to epidermolysis and stops
within 2-3 days. Dermatologic recovery typically takes 1-3 weeks, with mucosal lesions
taking longer. Rarely, necrolysis recurs in areas that began to heal.
Involvement of the oral mucosa results in edema and erythema, followed by blistering.
Ruptured blisters may form extensive hemorrhagic erosions with grayish white
pseudomembranes or shallow aphthouslike ulcers. Hemorrhagic crusting of the lips is a
common finding (as seen in the image below).
Ocular involvement varies in severity and can result in mild inflammation, conjunctival
erosion, purulent exudates, or pseudomembrane formation.
Involvement of respiratory epithelium may result in bronchial hypersecretion, hypoxemia,
interstitial infiltrates, pulmonary edema, bacterial pneumonia, or bronchiolitis obliterans.

Complications
Numerous complications of TEN can arise as a result of the widespread cutaneous and
mucosal membrane inflammation and necrosis. Stomatitis and mucositis, which are painful
and hinder oral intake, can place patients at risk for dehydration and malnutrition.
Epithelial loss predisposes to septicemia (Pseudomonas aeruginosa, Staphylococcus aureus,
gram-negative species, and Candida albicans). Renal hypoperfusion, acute tubular necrosis,
and renal insufficiency may develop subsequent to septic shock.
Ulceration of various mucosal membranes may result in pain, scarring, and stricture
formation. Affected surfaces include oral, ocular, and urogenital mucosa. Barrera and
colleagues reported a case of hypopharyngeal stenosis and dysphagia with recurrent
aspiration.[27] Miscellaneous complications include hypovolemia, massive gut bleeding, and
pulmonary emboli.
Mild-to-severe eye complications can occur, such as the following:

Lid edema

Persistent dry eyes

Chronic photosensitivity

Conjunctivitis

Keratitis

Conjunctival fornix foreshortening

Ectropion or entropion with subsequent trichiasis

Symblepharon

Corneal ulceration and scarring

Blindness

Pulmonary complications may occur. Mucous retention and sloughing of tracheobronchial

mucosa may occur, with aspiration of mucosal debris. Pneumonia and pneumonitis are
common and sometimes fatal complications of TEN. Pulmonary embolism and acute
respiratory distress syndrome (ARDS) have also been reported.
GI hemorrhage results from intestinal inflammation.

Diagnostic Considerations
Toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS) are considered to be
a single disease entity differing in severity. There is debate whether TEN and SJS are part of a
spectrum of disorders including erythema multiforme major (EMM); however, it is widely
accepted that SJS and TEN are distinct entities differing in etiology, clinical manifestations,
histopathology, treatment, and prognosis.
EMM is characterized by typical target lesions (at least 3 concentric rings) with or without
blister formation in a symmetric, predominantly acral distribution. In contrast, the skin
lesions of SJS and TEN are predominately central (trunk and face), consisting of blisters that
arise on erythematous or purpuric macules and involve 2 or more mucosal surfaces.
Histopathologic examination is necessary in differentiating these disorders from other severe
bullous skin diseases, including the following[28] :

Staphylococcal scalded skin syndrome

Toxic shock syndrome

Phototoxic skin reactions

Drug reaction with eosinophilia

Acute generalized exanthematous pustulosis

Paraneoplastic pemphigus

TEN and SJS are characterized by apoptotic keratinocyte cell death in the epidermis with
dermal-epidermal separation that results in bullae formation.
Other problems to be considered in the differential diagnosis of TEN include the following:

Cauterization burns

Caustic agents

Drug reaction with eosinophilia

Generalized bullous fixed eruption

Kerosene and paraffin burns

Approach Considerations
TEN is a clinical diagnosis, confirmed by histopathologic analysis of lesional skin. Early
involvement of a dermatologist and dermatopathologist is recommended. Skin biopsy,
harvested at the earliest possible stage, is important in establishing an accurate diagnosis and
directing specific therapeutic modalities.
Necrotic keratinocytes with full-thickness epithelial necrosis and detachment is consistent
with the diagnosis of TEN. Perivascular and scattered lymphocytic infiltration of the dermis
is sometimes demonstrated, although the underlying dermis is not greatly altered.
No definitive or specific emergent laboratory tests are indicated for TEN. Basic laboratory
tests may be helpful in planning symptomatic or supportive therapy. Surveillance cultures of
blood, skin, and urine should be obtained.
Imaging studies are not indicated for the diagnosis of TEN. Chest radiography should be
performed in the setting of respiratory distress because tracheobronchial inflammation may
predispose to diffuse interstitial pulmonary disease or pneumonia.

Blood Studies
Hematology studies include the following:

Complete blood count (CBC) and differential

Circulating immune complexes

Erythrocyte sedimentation rate

Leukopenia is common, whether a result of TEN itself or of bacteremia, as is a

normochromic normocytic anemia. Eosinophilia may be present. Less often,
thrombocytopenia, neutropenia, and bandemia may occur. Neutropenia is an unfavorable
prognostic sign.
In the acute phase, there are transient decreases of peripheral CD4+ T lymphocytes and
reduced allogeneic and natural killer cell cytotoxicity, which returns to normal in 7-10 days.
Coagulation studies may include prothrombin time/international normalized ratio (INR) and
activated partial thromboplastin time.
Chemistry to assess fluid and electrolyte losses include the following:

Albumin

Blood urea nitrogen

Total protein

As toxic epidermal necrolysis progresses, multiple organs are affected, causing other
abnormalities in laboratory test results. Diffuse skin involvement may cause significant fluid
loss and electrolyte abnormalities.

Biopsy
A skin biopsy specimen must be obtained. In experienced hands, a frozen section specimen
expedites matters. Results are very useful in differentiating TEN from other dermatologic
disorders.
Histologically, TEN is characterized by full-thickness epidermal necrosis with little evidence
of epidermal or dermal inflammation. Epidermal detachment and sloughing may be evident.
Satellite cell necrosis may be visible early, progressing to extensive eosinophilic necrosis.
Treatmen & management

Prehospital Care
Prehospital care for patients with TEN is similar to that for patients with burns. Supplement
with oxygen by face-mask as needed; do not perform prophylactic tracheal intubation.
Prevent hypothermia with rewarming devices and blankets.
In severe TEN, the barrier function of the skin is compromised. Thus, contamination and
evaporation must be minimized. The patient should be treated similarly to one with extensive
burns, that is, with the application of sterile coverings. Fluid and pulmonary status must be
carefully monitored.

Emergency Department Care

For the emergency physician, the two most important elements in the treatment of TEN are
discontinuation of the offending drug and admission to a burn unit.[31] Evidence suggests that
rapid institution of these two measures is associated with a more favorable prognosis.[32, 33]
Emergency department care should be directed toward the following:

Maintaining fluid and electrolyte homeostasis

Mitigating temperature loss

Providing adequate analgesia

Preventing secondary infection

Aggressive fluid and electrolyte management, pain control, and meticulous skin care are
important. Fluid resuscitation with crystalloids should follow standard guidelines used for
burn patients. However, patients with TEN typically require less aggressive fluid replacement
than that of burn patients because of less severe microvascular injury.
A goal of resuscitation should be to maintain sufficient mean arterial blood pressure (ABP
>65 mm Hg), central venous pressure (CVP 8-12 mm Hg), and central oxygenation (Svco2
>70%) for adequate tissue perfusion and renal perfusion.[21] Fluid management should be
based on the physiologic endpoint of urine output of 0.5-1 mL/kg/h.[31]
Patients with extensive skin involvement require reverse isolation and a sterile environment.
Areas of skin erosion should be covered with nonadherent protective dressings such as
petrolatum gauze. Respiratory distress may result from mucosal sloughing and edema and
may necessitate endotracheal intubation and ventilation.

Approach Considerations
Management of toxic epidermal necrolysis (TEN) requires prompt recognition of the disorder
and withdrawal of all potential causative agents. The mainstay of treatment is supportive care
until the epithelium regenerates. Supportive measures include isolation, fluid and electrolyte
balance, nutritional support, pain management, and protective dressings. Early transfer of
patients to a burn or intensive care unit has been shown to reduce the risk of infection,
mortality rate, and length of hospitalization.
Withdraw the offending agent, if one is identified, as soon as possible. One observational
study showed a reduction in mortality from 26% to 5% when the implicated drugs with short
elimination half-lives were withdrawn no later than the day the blisters or erosions first
developed.
No controlled prospective treatment studies or generally accepted guidelines exist. In 1991,
Avakian and colleagues published the University of Florida treatment protocol for toxic

epidermal necrolysis.[29] In 2007, these guidelines were revised by Fromowitz and colleagues.
[30]
The guidelines are as follows:
Monitor fluids and electrolytes. Administer fluids and titrate based on central venous pressure
and urine output; on average, 3-4 L are needed in patients with 50% of the body surface area
affected.
Parenteral nutrition or nutrition provided enterally via a soft-fine bore nasogastric tube is
usually needed. Start total parenteral nutrition in patients unable to take nourishment. Early
and continuous enteral nutrition reduces the risk of stress ulcers, reduces bacterial
translocation and enterogenic infection, and allows earlier discontinuation of venous lines.

Supportive Systemic Therapy

The patient should be placed in a heated environment to enhance reepithelialization.
However, this may enhance water losses, and appropriate hydration must be maintained.
Institute a bed warmer.
Saline applied to skin hourly is important, and then emollients are smeared. Chlorhexidine
solution is used to bathe the patient's skin. Chlorhexidine mouthwash is administered 4 times
a day, and white petrolatum is administered to the lips. Rinse the patients mouth frequently
and apply a topical anesthetic or spray for buccal pain.
Provide daily physical therapy for range-of-motion exercises.
Place a Foley catheter and nasogastric tube only when needed.
Energy requirements for patients with TEN must be carefully calculated and nutritional
support provided. Protein loss can be significant.[23]
Patients with mucosal vulnerability may have severe bleeding complications. Coagulation
factors and blood counts should be held within the normal ranges, and transfusion of red
cells, platelets, and plasma products should be considered when necessary.[21]
Ocular complications are common and can be debilitating. Early consultation with an
ophthalmologist is recommended to assess and minimize the risk of ocular damage.
Treatments with topical lubricants/antibiotics and steroid drops are often needed.
Wound care

Meticulous wound care is necessary to prevent secondary infection. Debate continues in the
literature regarding whether or not to debride the wounds associated with toxic epidermal
necrolysis. To date, no conclusive evidence supports early, late, or no debridement of the
wounds. Cutaneous lesions heal in approximately 2 weeks; mucosal membrane lesions take
longer.

If debridement of necrotic and desquamation areas is chosen, it is performed with the patient
under general anesthesia. Apply porcine xenografts to involved areas.
Provide hydrotherapy (whirlpool) twice a day. Repair and replace porcine xenografts. Apply
Kerlix dressings soaked in silver nitrate 0.5% to involved areas after each whirlpool session.
Pharmacologic therapies

Emergence of resistance precludes the use of prophylactic antibiotics. Bacterial sampling of

skin lesions should be performed the first day and every 48 hours. Indicators for antibiotic
treatment include increased number of bacteria cultured from the skin with selection of a
single strain, sudden decrease in temperature, or deterioration of the patient's condition.
Empiric antimicrobial therapy should include broad-spectrum antimicrobials that cover gramnegative, gram-positive, and anaerobic organisms. phylococcus aureus is the main bacteria
present during the first days, with gram-negative strains appearing later. If staphylococcal
infection is involved, administer an appropriate antistaphylococcal agent (ie,
nafcillin/oxacillin for methicillin-sensitive organisms or vancomycin for methicillin-resistant
organisms).
Provide pain relief with patient-controlled analgesia (PCA). Opiate analgesics for skin pain
and anxiety are essential for comforting patients. Hydroxyzine may be used to relieve the
intense pruritus that may occur when reepithelialization begins.
Patients remain nonambulatory until skin begins to heal. Until that time, anticoagulant
therapy is imperative. Heparin is indicated for prophylaxis of thromboembolic events.
Apply chloramphenicol ointment to prevent infection. Silver sulfadiazine should be avoided
because it is a sulfonamide derivative and may precipitate TEN. Silver compounds not
utilizing sulfadiazine or other sulfa medications should be used because they assist in wound
healing and prevent infection and bacterial growth.
No specific treatment modality has been proven effective, including the following:

Plasmapheresis

Corticosteroids

Cyclophosphamide

Cyclosporine

Tumor necrosis factoralpha (TNF-alpha) inhibitors

Intravenous immune globulin (IVIg)[6]

Multiple studies of these modalities have been completed, and multiple studies are ongoing.
Completed studies have shown that either the risk of the medication outweighs the benefit or
the data are inconclusive to support its utilization. Therefore, there is a significant need for
randomized control studies to further evaluate potential treatment modalities in TEN.
Corticosteroids are commonly used to control progression of TEN, but this is highly
controversial. In some studies, corticosteroids have increased the incidence of mortality.
Consider the use of plasmapheresis, if available, daily for 3 days. Although prospective
randomized studies have not been performed, limited data suggest that plasmapheresis may
enhance elimination of the drug or offending agent or inflammatory mediators such as
cytokines and should be considered.[34]
AntiTNF- treatment has been reported to rapidly resolve skin lesions due to TEN. TNF- is
strongly expressed in keratinocytes and macrophages of lesional skin, and high
concentrations are found in cutaneous blister fluid.
Sucrose-depleted IVIg 1 g/kg/d (infused over 4 h) for 3 days may be beneficial if started
within 48-72 hours of bulla onset. If more than 72 hours have elapsed since the onset of bulla
but TEN is still actively progressing, with new lesions, IVIg may still be useful.

Consultations
Most patients with TEN require specialized care under the direction of a team of physicians
with experience in handling this disorder. Burn-unit care represents an option worthy of
serious consideration.
Required consultations may include the following:

A dermatologist is consulted to identify and to confirm the diagnosis of

TEN

A plastic surgeon is consulted to debride areas of skin necrosis, as

indicated

An ophthalmologist is consulted for assisting in the treatment of ocular

manifestations and preventing long-term sequelae

An internal medicine specialist is consulted to assist in patient treatment

Consultation with a respiratory medicine specialist may be important,

since respiratory mucosa may slough; establishment of pulmonary toilet
may be advisable

Otolaryngologic or urologic consultation may be helpful in patients with

significant mucous membrane involvement of those areas

Medication Summary
The goals of pharmacotherapy in toxic epidermal necrolysis (TEN) are to reduce morbidity
and to prevent complications. No specific treatment modality has been proven effective, but
agents such as crystalloids, antibiotics, antihistamines, anticoagulants, analgesics, and
antiseptic agents are important for supportive care. Use of corticosteroids is controversial.

Crystalloids
Class Summary

Fluid resuscitation is critical in TEN. In cases of acute skin failure, insensible losses may be
enormous, and repletion of water loss is essential.
Isotonic sodium chloride 0.9%

Patients with TEN are at serious risk of dehydration, which may complicate their condition.
For example, water losses in a hypercatabolic state result in hypoalbuminemia and reduced
renal perfusion. This leads to acute renal failure; therefore, maintaining intravascular volume
is paramount. The rate of intravenous repletion should be titrated based on urine output or
central venous pressure.

Antibiotics
Class Summary

Patients with TEN lose their epidermis, a major barrier to invading organisms. If patients
become infected, morbidity is enhanced. Staphylococcus aureus is the main bacteria present
during the first days, with gram-negative strains appearing later.
Case reports of Klebsiella species,[35] Escherichia coli, and Pseudomonas species recovered
from patients with TEN have created concern about the possible polymicrobial nature of
sepsis associated with this condition. Therefore, good gram-negative coverage may be
necessary.
Nafcillin

Nafcillin covers most common skin organisms (eg, Staphylococcus, Streptococcus). If patient
has allergy to penicillin or if methicillin-resistant S aureus (MRSA) is present on skin culture,
use vancomycin.

osing & Uses

AdultPediatric
Dosing Forms & Strengths
Usual

500 mg IV/IM q4-6hr

Severe Infections

1 g IV/IM q4hr
Staphylococcal Endocarditis

2 g IV q4hr x4-6 weeks; may be longer and may add rifampin and gentamicin if prosthetics
present
Other Indications & Uses

Infections resistant to penicillin G: Staph, strep, Staphylococcus aureus, Staphylococcus

epidermidis

Adverse Effects
1-10%

Hypersensitivity
Neutropenia
Interstitial nephritis
Possible hypokalemia
<1%

Neurotoxicity (high doses)

Pseudomembranous colitis
Phlebitis (oxacillin preferred in peds)

Contraindications & Cautions

Contraindications

Allergy to penicillins, cephalosporins, imipenem

Cautions

Evaluate renal, hepatic, hematologic systems periodically during prolonged treatment

To optimize therapy, determine causative organisms and susceptibility; > 10 d treatment to
eliminate infection and prevent sequelae (eg, endocarditis, rheumatic fever); take cultures
after treatment to confirm that infection is eradicated

Pregnancy & Lactation

Pregnancy Category: B
Lactation: excreted into breast milk; use caution

Pharmacology
Half-Life: 0.5-1.5 hr
Peak Plasma Time: 0.5-1 hr
Absorption: poorly absorbed orally
Distribution: in fluid, bone, bile, crosses placenta
Vd 0.5-1.5 L/kg
Metabolism: liver
Elimination: hepatic, renal
Enzymes induced: hepatic CYP3A4
Mechanism of Action

Initial therapy for suspected penicillin G-resistant streptococcal or staphylococcal infections.

Use parenteral therapy initially in severe infections. Change to oral therapy as condition
warrants.
Due to thrombophlebitis, particularly in the elderly, administer parenterally only for short
term (1-2 d); change to oral route as clinically indicated.

IV & IM Information
IV Incompatibilities

Additive: aminophylline(?), ascorbic acid, aztreonam, bleomycin, cytarabine, gentamicin,

hydrocortisone sodium succinate, methylprednisolone sodium succinate, promazine, vit
B/C(?)
Y-site: diltiazem(?), droperidol, insulin (regular), labetalol, meperidine(?), midazolam,
nalbuphine, pentazocine, vancomycin(?), verapamil
IV Compatibilities

Solution: compatible w/ most common solvents

Additive (partial list): dexamethasone sodium phosphate, diphenhydramine, heparin,
lidocaine, KCl, prochlorperazine, Na bicarb
Syringe: cimetidine, heparin
Y-site (partial list): acyclovir, atropine, diazepam, fentanyl, fluconazole, heparin, MgSO4,
morphine, propofol, zidovudine

IV/IM Preparation

IM/IV: reconstitute 1-2 g of drug w/ 3.4- 6.8 mL SWI/BWI/NS to 250 mg/mL

IV inj: further dilute w/ 15-30 mL SWI/NS
IV infusion: further dilute w/ IV solution according to Mfr's directions
Bulk Packages:

Reconstitute 10 g of drug w/ 93 mL SWI/NS to 100 mg/mL

THEN further dilute before administration

Not for direct IV injection

IV/IM Administration

IM: deep into large muscle

IV inj: slowly over 5-10 min
IV infusion: over at least 30-60 min
Gentamicin

Gentamicin is an aminoglycoside antibiotic for gram-negative coverage. It is used in

combination with both an agent against gram-positive organisms and one that covers
anaerobes. Third-generation cephalosporins, such as ceftazidime, and others with good gramnegative coverage are suitable alternatives. Adjust dose based on renal insufficiency

Dosing & Uses

AdultPediatric

Dosing regimens are numerous and are adjusted based on CrCl and changes in volume of
distribution, as well as body space into which agent needs to distribute. Dose of gentamicin
may be given IV/IM. Each regimen must be followed by at least trough level drawn on third
or fourth dose, 0.5 h before dosing; may draw peak level 0.5 h after 30-min infusion.
Dosing Forms & Strengths
Susceptible Infections

Conventional

1-2.5 mg/kg/dose IV/IM q8-12hr OR

3-6 mg/kg/day IV/IM divided q8hr

Surgical Infection Prophylaxis

Oral/pharyngeal: 1.5 mg/kg IV + clindamycin 600-900 mg IV

Ruptured viscus: 1.5 mg/kg IV q8hr + clindamycin 600 mg IV q6hr
Endocarditis Prophylaxis (GI, GU procedure)

1.5 mg/kg IV/IM <30 minutes before procedure + ampicillin or vancomycin

Recent AHA Guidelines recommend only for high risk patients
Extended Interval Dosing (q24hr+)

4-7 mg/kg/dose IV qDay

Base on lean body weight
Subsequent doses: consult pharmacist
Cystic Fibrosis

7.5-10.5 mg/kg/day IV/IM divided q8hr

Mycobacterium Infection (Orphan)

Gentamicin liposome injection: Treatment of disseminated Mycobacterium aviumintracellulare infection

Orphan indication sponsor

Liposome Company, Inc; One Research Way; Princeton, NJ 08540

Renal Impairment

Elderly

CrCl >90 mL/minutes and <60 years old: q8hr

CrCl 60-90 mL/minutes or >60 years old: q12hr

CrCl 25-60 mL/minutes: q24hr

CrCl 10-25 mL/minutes: q48hr

CrCl <10 mL/minutes: q72hr

Following dialysis in ESRD

Administration

Monitor: peak, trough, renal and auditory function

Peak 4-12 mg/L; trough 1-2 mg/L

Use ideal body weight for mg/kg/dose more accurate than total body weight
Other Indications & Uses

Usually first line aminoglycoside: Gram-neg. infection, P. aeruginosa, Proteus, E. coli,

Klebsiella, Enterobacter, Serratia, Citrocbacter, Staph

Adverse Effects
>10%

Neurotoxicity (vertigo, ataxia)

Gait instability
Ototoxicity (auditory, vestibular)
Nephrotoxicity (decr CrCl)
Nephrotoxicity if trough >2 mg/L
1-10%

Edema
Rash
Reddening of skin
Skin itching
<1%

Drowsiness
Headache
Pseudomotor cerebri
Photosensitivity
Allergic reaction
Erythema
Anorexia
Nausea/vomiting
Weight loss

Incr salivation
Enterocolitis
Granulocytopenia
Agranulocytosis
Thrombocytopenia
Elevated LFTs
Burning
Stinging
Tremors
Muscle cramps
Weakness
Dyspnea

Contraindications & Cautions

Black Box Warnings

Neurotoxicity, manifested as both bilateral auditory and vestibular ototoxicity, can occur in
patients with preexisting renal damage and in patients with normal renal function treated at
higher doses and/or for periods longer than those recommended. High-frequency deafness
usually occurs first and can be detected only by audiometric testing.
Aminoglycosides are potentially nephrotoxic. Risk is greater in patients with impaired renal
function and in those who receive high doses or prolonged therapy. Rarely, nephrotoxicity
may not become apparent until the first few days after cessation of therapy.
Use with caution in premature infants and neonates because of renal immaturity and the
resulting prolongation of serum half-life of the drug
Neuromuscular blockade and respiratory paralysis have been reported following parenteral
injection, topical instillation (as in orthopedic and abdominal irrigation or in local treatment
of empyema), and oral use of aminoglycosides, especially when given soon after anesthesia
or muscle relaxants. If blockage occurs, calcium salts may reverse these phenomena, but
mechanical respiratory assistance may be necessary.

Avoid concurrent or sequential use of neurotoxic and/or nephrotoxic drugs including other
aminoglycosides (eg, amikacin, streptomycin, neomycin, kanamycin, gentamicin,
paromomycin
Cumulative listing of drugs to avoid from all aminoglycoside package inserts includes
amphotericin B, bacitracin, cephaloridine, cisplatin, colistin, polymyxin B, vancomycin, and
viomycin. Avoid potent diuretics (eg, ethacrynic acid, furosemide) because they increase risk
of ototoxicity. When administered intravenously, diuretics may enhance aminoglycoside
toxicity by altering antibiotic concentrations in serum and tissue.
Contraindications

Prior aminoglycoside toxicity or hypersensitivity

Cautions

Risk of ototoxicity, neurotoxicity, nephrotoxicity

Endocarditis prophylaxis: use only for high risk patients, per recent AHA Guidelines
Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (not
on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular
transmission; adjust dose in renal impairment

Pregnancy & Lactation

Pregnancy Category: D
Lactation: enters breast milk; use with caution (AAP Committee states "compatible with
nursing")

Interactions

Adverse Effects

Warnings

Pregnancy

Pharmacology

Administration

Pricing & Images

Patient Handout

Pharmacology
Half-Life: 2-3 hr (NRF)
Protein Bound: <30%
Peak Plasma Time: IM 30-90 min; IV 30 min after 30 min infusion
Distribution: crosses placenta, relative diffusion from blood into CSF: minimal even with
inflammation, CSF: blood level ratio: normal meninges: nil; inflamed meninges: 10-30%
Vd: increased by edema, ascites, fluid overload; decreased w/ dehydration, neonates: 0.4-0.6
L/kg children: 0.3-0.35 L/kg adults: 0.2-0.3 L/kg
Excretion: urine (as unchanged drug), clearance: directly related to renal function
Mechanism of Action

Aminoglycoside antibiotic for gram-negative coverage bacteria including Pseudomonas

species. Synergistic with beta-lactamse against enterococci. Interferes with bacterial protein
synthesis by binding to 30S and 50S ribosomal subunits.

Antihistamines
Class Summary

Hydroxyzine may be used when reepithelialization begins because intense pruritus may
occur.
Hydroxyzine (Vistaril)

Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in

subcortical region of the central nervous system.

Dosing & Uses

AdultPediatricGeriatric
Dosing Forms & Strengths
Anxiety

Symptomatic relief of anxiety associated with psychoneurosis and as adjunct in organic

disease states
50-100 mg PO divided q6hr or 50-100 mg IM divided q4-6hr
Dosing considerations

Continuation of therapy for >4 months has not been studied; reassess
need for therapy periodically

Pruritus

Management of pruritus due to chronic urticaria, contact dermatoses, and histamine-mediated

pruritus
50-100 mg PO/IM divided q6-8hr
Preoperative Sedation

50-100 mg PO or 25-100 mg IM
Dosing considerations

If treatment is initiated IM, subsequent doses may be administered PO

Alcohol Withdrawal Syndrome

50-100 mg IM immediately; may be repeated q4-6hr PRN

Nausea & Vomiting

25-100 mg IM
Dosing Modifications

Hepatic impairment (primary biliary cirrhosis): Change frequency to daily

Adverse Effects
Frequency Not Defined

Bitter taste in mouth

CNS depression
Drowsiness
Sedation, ranging from mild drowsiness to deep sleep (most frequent)
Dizziness
Lassitude
Disturbed coordination
Muscular weakness
Restlessness, insomnia, tremors, euphoria, nervousness, delirium, palpitation, seizures
Epigastric distress
Anorexia

Nausea
Vomiting
Diarrhea
Constipation
Cholestasis, hepatitis, hepatic failure, hepatic function abnormality; jaundice is rare
Tachycardia, palpitation ECG changes (eg, widened QRS)
Arrhythmias (eg, extrasystole, heart block)
Hypotension
Hypertension
Dizziness, sedation, and hypotension may occur in geriatric patients
Dryness of mouth, nose, and throat
Dysuria
Urinary retention
Impotence
Vertigo
Visual disturbances
Blurred vision
Diplopia; tinnitus
Acute labyrinthitis
Insomnia
Tremors
Nervousness
Irritability

Facial dyskinesia
Tightness of chest
Thickening of bronchial secretions
Wheezing
Nasal stuffiness
Sweating
Chills
Early menses
Toxic psychosis
Headache
Faintness
Paresthesia
Agranulocytosis
Hemolytic anemia
Leukopenia
Thrombocytopenia
Pancytopenia

Contraindications & Cautions

Contraindications

Documented hypersensitivity
Cautions

Nursing mothers
May cause drowsiness; avoid driving or operating dangerous machinery
May cause oversedation and confusion in elderly patients; start on lower doses and monitor
closely

IM only for parenteral use; switch to PO ASAP

Pregnancy & Lactation

Pregnancy category: X in 1st trimester, C in 2nd and 3rd trimesters because there are no
adequate , manufacturer considers first-trimester use contraindicated on basis of lack of
adequate large, controlled, prospective studies of use in pregnant women and observed
teratogenic effects in mice and rats (though not rabbits); H1 antagonists typically not
recommended during last 2 weeks of gestation, because of association with retrolental
fibroplasia in premature babies
Lactation: Excretion in milk unknown; use with caution

Pharmacology
Mechanism of Action

H1-receptor antagonist with low to moderate antihistaminic properties; inhibits respiratory,

vascular, and GI smooth-muscle constriction
Moderate to high anticholinergic and antiemetic properties
Absorption

Onset: 15-30 min

Duration: Sedation, 4-6 hr; antipruritic, 1-12 hr; histamine-induced wheal and flare, 2-36 hr
Peak plasma time: 1-2 hr
Distribution

Vd: Adults, 16 L/kg; elderly, 23 L/kg

Metabolism

Metabolized by liver
Elimination

Half-life: Adults, 20 hr; elderly, 29 hr; hepatic dysfunction, 37 hr

Excretion: Urine

IV & IM Information
IM Incompatibilities

Additive: Aminophylline, amobarbital, chloramphenicol, ketorolac, penicillin G

sodium/potassium, pentobarbital, phenobarbital
Syringe: Aminophylline, dimenhydrinate, haloperidol, heparin, ketorolac, penicillin,
pentobarbital, phenytoin, ranitidine, vitamin B complex with C

IM Compatibilities

Additive (partial list): Cisplatin, cyclophosphamide, cytarabine, dimenhydrinate, etoposide,

lidocaine, methotrexate, nafcillin
Syringe (partial list): Atropine, buprenorphine, cimetidine, diphenhydramine, fentanyl,
glycopyrrolate, lidocaine, meperidine, midazolam, morphine, promethazine, scopolamine,
sufentanil

Anticoagulants
Class Summary

Heparin is indicated for prophylaxis of thromboembolic events. Patients with TEN remain
nonambulatory until skin begins to heal, and until that time, anticoagulant therapy is
imperative.
Heparin

Heparin augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin.
It does not actively lyse thrombus but is able to inhibit further thrombogenesis. Heparin
prevents reaccumulation of clot after spontaneous fibrinolysis. It is indicated for the
prevention of thromboembolic events.
Dosing & Uses
AdultPediatricGeriatric
Dosing Forms & Strengths
DVT & PE Prophylaxis

5,000 units SC q8-12hr

DVT & PE Treatment

80 units/kg IV bolus, followed by continuous infusion of 18 units/kg/hr OR

5,000 units IV bolus, followed by continuous infusion of 1,300 units/hr OR

250 units/kg (alternatively 17,500 units) SC, followed by 250 units/kg q12hr
Acute Coronary Syndromes

PCI

Without GPIIb/IIIa inhibitor: Initial IV bolus of 70-100 units/kg (target ACT 250300 seconds)
With GPIIb/IIIa inhibitor: Initial IV bolus of 50-70 units/kg (target ACT > 200
seconds)

STEMI

If patient on fibrinolytics: IV bolus of 60 units/kg (max: 4,000 units), followed

by 12 units/kg/hr (max 1,000 units/hr) as continuous IV infusion
Dose should be adjusted to maintain aPTT of 50-70 seconds

Unstable Angina/NSTEMI

Initial IV bolus of 60-70 units/kg (max: 5,000 units), followed by initial IV

infusion of 12-15 units/kg/hr (max: 1,000 units/hr)
Dose should be adjusted to maintain aPTT of 50-70 seconds

Anticoagulation

Intermittent IV injection

10,000 units IV initially, then 50-70 units/kg (5,000-10,000 units) q4-6hr

Continuous IV infusion

5,000 units IV injection, followed by continuous IV infusion of 20,000-40,000

units/24hr

Catheter Patency

Indicated to prevent clot formation within venous and arterial catheters

Use 100 units/mL; instill enough volume to fill lumen of catheter

Amount and frequency depends on catheter volume and type
Peripheral heparin locks typically are flushed q6-8hr

Renal Impairment

No adjustment required
Hepatic Impairment

Caution is advised; dosage adjustment may be required

Adverse Effects
>10%

Heparin-induced thrombocytopenia, possibly delayed (10-30% )

Frequency Not Defined

Mild pain
Hematoma
Hemorrhage
Local irritation
Erythema
Injection site ulcer (after deep SC injection)
Increased liver aminotransferase
Anaphylaxis

Immune hypersensitivity reaction

Osteoporosis (long-term, high-dose use)

Contraindications & Cautions

Contraindications

Severe thrombocytopenia
Uncontrolled actuve bleeding (except DIC)
Conditions where coagulation tests cannot be performed at appropriate intervals
Cautions

Any risk factor for hemorrhage (eg, subacute bacterial endocarditis, blood dyscrasias,
menorrhagia, dissecting aneurysm major surgery, spinal anesthesia, hemophilia, GI ulcerative
lesions, liver disease, impaired hemostasis)
Heparin-induced thrombocytopenia may occur (with or without thrombosis); immunemediated reaction resulting from irreversible aggregation of platelets; monitor
thrombocytopenia of any degree, if platelet count falls below 100,000/m, discontinue
anticoagulants
Monitor therapy with aPTT
Heparin may prolong PT
History of allergy
Medication errors: Do not use heparin sodium injection as a catheter lock flush product;
heparin sodium injection is supplied in vials containing various strengths of heparin,
including vials that contain a highly concentrated solution of 10,000 units in 1 mL which
have been mistaken for 1 mL low-concentration catheter lock flush vials
Heparin preserved with benzyl alcohol

Do not administer if preserved with benzyl alcohol, to neonates, infants,

pregnant women, or breastfeeding women

Benzyl alcohol associated with serious adverse events and death,

particularly in pediatric patients (gasping syndrome; characterized by
central nervous system depression, metabolic acidosis, and gasping
respirations)

Pregnancy & Lactation

Pregnancy Category: C

Lactation: not excreted in breast milk; compatible

Pharmacology
Mechanism of Action

Mechanism for low dose: inactivates factor Xa and inhibits conversion of prothrombin to
thrombin
Mechanism for high dose: inactivates factors IX, X, XI,XII, thrombin, and inhibits
conversion of fibrinogen to fibrin
Also inhibits activation of factor VIII
Absorption

Bioavailability: 22-40%
Peak plasma time: 2-4 hr
Onset: Immediate (IV); 20-30 min (SC)
Distribuion

Protein bound: Extensive

Metabolism

Metabolism: Liver (partial); reticuloendothelial system (partial)

Metabolites: None
Elimination

Half-life: 60-90 minutes average (longer at higher doses)

Excretion: Urine
Dialyzable: No

IV & IM Information
IV Incompatibilities

Additive: dobutamine, erythromycin, gentamicin, haloperidol, hydrocortisone, meperidine,

morphine, vancomycin
Syringe: amiodarone, diazepam, erythromycin, gentamicin, haloperidol, meperidine,
morphine(?), vancomycin
Y-site: amiodarone, diazepam, dobutamine, gentamicin, haloperidol, vancomycin
Not spec: hydroxyzine, tetracycline

IV Compatibilities

Additive: aminophylline, ampho B, ampicillin, Ca gluconate, clindamycin, dopamine,

esmolol, furosemide, lidocaine, norepinephrine, KCl, Na bicarb, verapamil, vit B/C
Syringe: aminophylline, ampho B, ampicillin, atropine, cimetidine, clindamycin, dobutamine,
dopamine, epinephrine, furosemide, lidocaine, morphine(?), norepinephrine, Na bicarb,
verapamil
Y-site: aminophylline, ampicillin, atropine, Ca gluconate, cimetidine, clindamycin, dopamine,
epinephrine, erythromycin, esmolol, furosemide, hydrocortisone, lidocaine, norepinephrine,
meperidine, morphine, KCl, Na bicarb
IV Preparation

Recommended infusion concentration for most ps is 25,000 U in 500 mL D5W (50 U/mL
premixed infusion solution)
IV Administration

IV injection may be given undiluted or diluted in 50-100 mL NS or D5W

Infusion: dilute in NS, D5W or other compatible fluid
Continuous IV therapy is preferred because

Intermittent IV therapy produces a higher incidence of bleeding

abnormalities

Invert IV bag at least 6 times to

Ensure mixing

Prevent pooling of med

Use constant-rate IV infusion pump

Storage

Store heparin solns at room temp, do not freeze

Do not use if discolored/precipitates
Autoclavable

Analgesics
Class Summary

Opiate analgesics are important to alleviate pain and anxiety associated with TEN. Much like
treatment of a second-degree burn, the pain must not be ignored.

Morphine sulfate (Duramorph, Astramorph, MS Contin)

Morphine is the drug of choice for pain in patients with TEN. In case of allergy or
intolerability, meperidine or fentanyl may be used.