TENS: Toxic Epidermal Necrosis Syndrome (3 CEs)

Written By: Kristi Hudson RN MSN CCRN

Written On: 9/29/06

Updated: September 11, 2009

Course Description:

This course is designed to provide and overview of the care and management of the patient diagnosed with Toxic Epidermal Necrosis Syndrome (TENS). Focus will be placed on the pathophysiology, causes, diagnosis and symptoms of TENS. Medical treatment options, as well as nursing assessment and interventions will be presented. NANDA nursing diagnosis and expected outcomes appropriate for the patient with TENS will be the final focus of this course.

Course Objectives:

Upon completion of this course the student will be able to:

• Describe the pathophysiology of TENS.
• List 2 major causes of TENS.
• Discuss how TENS is diagnosed.
• Describe 3 common symptoms associated with TENS.
• Explain the medical treatment options for TENS.
• Describe the nursing care and management for the patient with TENS.
• State 3 appropriate nursing diagnoses/expected outcomes for the patient with TENS.

Pathophysiology

Although the pathophysiology is not completed understood; TENS is believed to be an immune-related cytotoxic reaction aimed at destroying keratinocytes (Note: 90% of all epidermal cells are keratinocytes). The condition that is caused by this cytotoxic reaction mimics a “hypersensitivity” reaction to the skin that increases rapidly with continued insult or exposure from the initial causative agent.  The onset of this syndrome initially develops slowly, but once activated, this syndrome progresses very rapidly. 

Causes:

All of the following are thought to be possible causes of TENS:

• Adverse drug reaction (most common cause).
• Vaccinations.
• Malignant disorders.
• Graft vs. host disease.
• A considerable increase in TENS has been noted with HIV patients who take trimethoprim-suphamethoxazole (used for treatment of pneumocystis).

Causative Drugs Associated with the Development of TENS:

• Sulphonamnides
• Aminopenicillin
• Quinolones
• Cepahlosporins
• Carbamazepine
• Phenobarbital
• Dilantin
• NSAIDS
• Allopurinol
• Some corticoidsteriods

Diagnosis:

In advanced stages, the diagnosis of TENS is not difficult. A biopsy test that shows necrosis of “basal layer cells” without massive inflammatory infiltration into the dermis is confirmatory for TENS. In very late stages, it is possible to see necrosis of the keratinocytes involving the epidermis with diffuse detachment of the epidermis at the level of the basal membrane.

Clinical Presentation (symptoms):

After contact with the causative agent (again most likely a drug reaction); TENS can take from 1-45 days (the average is 14 days) before symptoms occur. The following describes the phases of presenting symptoms:

• The first phase is known as the “prodromal or flu like phase” (fever, rhinitis, cough, thoracic pain, anorexia and malaise).
• The second phase is known as the “acute phase” with skin involvement (itching, painful eruptions on the face and upper trunk that travel to the rest of the body).
• The third phase is known as the “spreading phase” (the initial lesions rapidly develop in bullae filled with serous fluid that form large plaques of necrotic epidermis that detach from the underlying dermis).
• Simultaneously during the spreading phase; the presence of Nikolsky’s sign (skin reddens, collect fluid underneath, rubs off and leaves a red and raw base). 
• The final phase is the “epidermal necrolysis” phase in which the entire body (except for the scalp) presents an exudative dark red dermis that loosens from the epidermal layer resulting in discharge of body fluids, protein and electrolytes.

Note: if untreated the loss of fluid and electrolytes through the dermis can lead to hemodynamic instability, hypovolemia and renal failure.

Medical Treatment Options:

Medical management of TENS requires early diagnosis with early withdrawal of causative agent and prompt treatment. The later the causative factor is identified and removed, the higher the mortality and/or morbidity. After removing the causative agent, the steps to treatment for TENS is as follows:

• Transfer to an Intensive Care Unit (preferably a burn unit as prompt intervention decreases the risk of infection and mortality).
• IV fluid replacement (saline solutions).
• Monitoring of environmental temperature (30 to 32 degrees C).
• Careful and aseptic handling (sterile field for all procedures).
• Avoidance of adhesive materials (tape and dressings).
• Peripheral IV’s should be placed distal to the affected area when possible.
• Initiation of Nutrition (oral or nasogastric).
• Anticoagulation therapy (Thromboembolism can cause morbidity/death).
• Prevention of stress ulcers (meds and enteral feeds can help prevent this).
• Physical Therapy.
• Pain management.
• Stress and anxiety management.
• Pulmonary care (aerosols, bronchial aspiration precautions.
• Phosphorus levels (Hypophosphatemia is frequent and can contribute to glycemia or muscular dysfunction).
• Regular changing of all catheters with cultures.
• Bacterial cultures of skin lesions on day one and every 48 hours after.
• Bacterial counts determine need for antibiotics.
• Insulin when hyperglycemia leads to overt glycosuria or increased osmolarity.
• Oxandrolone and human growth factor are thought to be effective in decreasing hypercatabolism.
• Ornithine alpha-ketoglutarate is thought to reduce healing time.
• Ascorbic acid (66 mg/kg/hour) for the first 24 hours is thought to reduce the need for fluid volume replacement.
• Topical management includes topical antiseptics (0.5% silver nitrate or 0.5% Chlorhexidine for example).
• Dressings vary from petroleum gauze to polyvidoneiodine or hydrogels.
• Large operative debridement with possible skin grafting.
• Prevention of ocular sequelae requires daily eye exams by an ophthalmologist (eye drops, physiologic saline or antibiotic are often instilled q 2 hours.
• Oral and nasal crusts are removed and mouth is sprayed with antiseptics q 4 hours.
• The use of corticoidsteriods is highly debated, but remains a mainstay in the treatment of TENS.

Nursing Care and Management:

The following table describes the major areas of focus for nursing:

Organ/System	Nursing Care
Eye	Meticulous eye care including saline rinses and proper lubrication (as often as q 1-2 hours).
Lungs	Sore throat or pharyngitis are seen early with TENS patients, mucosal sloughing occurs and intubation is often required. ET tube care and frequent suctioning required. Incentive spirometer (for patients who are not yet intubated) and frequent TCDB.
GI Tract	Mucosal sloughing can occur at the lips, mouth esophagus, stomach and rectum. Antacids, early nutritional support (prevents negative nitrogen balance and promotes wound healing). TPN for those who cannot tolerate oral or enteral feeding.
GU Tract	Mucosal sloughing leads to UTI’s in 37% of patients and renal failure in 17%. Foley and close monitoring of I&O.
Skin	Proper wound care and dressing changes BID and PRN. Assure adequate pain management during wound and skin care. Be sure to avoid hypothermia during wound care. Warmed IV’s and heat lamps may help.
Metabolic	Aggressively treat and maintain fluid and electrolyte balance.
Immune	Strict adherence of hand hygiene and other infection control procedures. Culture all purulent drainage.
Neuropsych	Anxiety, depression and altered body image must be assessed for and treated promptly and often.

Additional Nursing Interventions Include:

• In collaboration with physical and occupational therapy, splinting and proper positioning (to maintain joints and extremities in neutral positions).
• Pain management to include IV narcotics must be a priority.
• Frequent vital signs assessment (with emphasis on respiratory status).
• Monitoring of ABG’s.
• Elevate HOB to 30 degrees.
• Daily Chest X-rays.
• Monitor closely for signs of Hypovolemic shock (PAWP, CVP).

NANDA Nursing Diagnosis:

Nursing Diagnosis	Expected Outcome
Ineffective Airway	Po2 > 90 mmHg. PCo2 < 40 mmHg. O2 Sat > 95%. Resp. Rate 16-20. Ability to move secretions. Clear to white secretions.’ Absence of dyspnea or respiratory distress.
Fluid Volume Deficit	Urine output 30-50 ml per hour Stable vital sounds. No signs or symptoms of hypovolemia.
Alteration in Comfort: Pain	Pt. is able to identify factors that contribute to pain. Pt. is able to scale pain effectively. No respiratory distress. Able to participate in treatment plan.
High Risk for Infection	Absence of infected tissue. Vital signs stable (a-febrile). Negative blood and tissue cultures.
Impaired Skin Integrity	No increase is tissue damage. Skin shows signs of granulation and healing. Any Skin grafting is healing. No sign of infection to tissue. Frequent turning and preventative care.
High Risk for Aspiration	No aspiration of gastric contents. Stable respiratory status.
High Risk for Nutritional Deficit	Consumption of daily nutritional requirements adequate. Positive nitrogen balance. Wounds healing.
High Risk for Hypothermia	Rectal and core temp remains between 37.2-37.8 degrees C.
Ineffective Patient/Family Coping	Patient/family verbalize goals of treatment. Patient/family demonstrate knowledge of support systems. Patient/ family able to express fears and concerns.

References

Marini, J., J. MD. Wheeler, A., P. (2009). Critical care medicine: the essentials. (4th ed.). Lippincott, Williams & Wilkins. Philadelphia

Hargrove-Huttel, R., A. (2008). Lippincott’s review series: medical-surgical nursing. (2nd ed.). Lippincott, Williams & Wilkens. Philadelphia

Brambilla, G., Brucato, F., Angrisano, A., & Palmieri, G. (2002). Treatment of toxic epidermal necrolysis (TEN). Annuals of Burns and Fire Disasters. Vol. 15-n. 1. Retrieved on September 28, 2006 at:

http://www.medbc.com/annals/review/vol_15/num_1/text/vol15n1p17.asp

Ghislain, P., MD., &  Roujeau, J., MD. Treatment of severe drug reaction: Steven Johnson’s Syndrome, TENS and hypersensitivity syndrome. Dermatology Online Journal. (2002). 8(1): 5. Retrieved on September 28, 2006 at:

http://dermatology.cdlib.org/DOJvol8num1/reviews/drugrxn/ghislain.html

Melander, S., D., (2004). Case studies in critical care nursing: A guide to application and review. (Chap. 27).  Saunders, Philadelphia.

Riobom, F., Diogo, C., Telels, L., & Cruzeiro, C. (2004). Toxic epidermal necrolysis – Lyell’s syndrome. Annuals of Burns and Fire Disasters. Vol 17 n. 2. Retrieved on September 28, 2006 at:

 http://www.medbc.com/annals/review/vol_17/num_2/text/vol17n2p90.asp

Sacchidanand, S. (2002). Toxic epidermal necrolysis: A brief review. Retrieved on September 38, 2006 at:

 http://www.bangalorederma.com/toxic.htm

Web MD. (2006). Excerpts from Toxic Epidural Necrosis. Retrieved on September 28, 2006 at:

http://www.emedicine.com/med/byname/toxic-epidermal-necrolysis.htm

Wooten, J. (2001). Toxic epidermal necrolysis. RN. Vol. 64; No. 10. Retrieved on September 20, 2006 at: www.rn.com