Fioricet

Tetanus is an acute, often fatal infectious disease caused by an exotoxin produced by Clostridium tetani, a spore-forming bacteria. Classic symptoms include generalized rigidity and convulsive spasms of the skeletal muscles. The muscle stiffness commonly involves the jaw and neck, and then becomes widespread. C. tetani usually enters the body through a puncture wound. The spores germinate in the anaerobic conditions, and toxins, including tetanospasmin, are produced. The toxins travel through the body via the blood and lymphatics, and act at several central nervous system sites including peripheral motor end plates, spinal cord, brain, and sympathetic nervous system. Tetanus toxin interferes with neurotransmitter release, blocking inhibitor impulses and resulting in unopposed muscle contraction and spasm. Seizures can occur as well.1 Diagnosing tetanus in modern medicine is particularly challenging because it mimics other infectious disease processes and is considered preventable in today's world.

Case History

L. L., a 44-year-old female in otherwise good health, was cleaning debris from a creek on her land. The shallow and muddy creek water was drainage from the surrounding land and nearby road, and most likely contained animal feces. The patient was removing rocks from the creek bed when she accidentally grasped a piece of barbed wire concealed by the murky water. This led to four cuts to the palmer surface of four fingers on her right hand. She cleaned the injury with an antibacterial soap and immediately continued working in the creek, submerging her hand in the dirty water.

Twenty-seven days later, L.L. awoke with a severe headache. Although she has a history of migraine headaches, this had never happened. Her bilateral temporal pain, however, was usual for her episodes of migraine headaches. By mid-morning, her headache was so severe that she presented to the emergency room (ER). She received one Demerol injection and was released. Approximately 6 hours later, her headache worsened and the left side of her jaw became painful and slightly swollen. She returned to the ER. She received another Demerol injection for pain and Augmentin for jaw swelling, and was released.

After 7 hours at home, she awoke with severe left jaw swelling, inability to open her mouth, and difficulty breathing. She returned to the ER for the third time. At this visit, she received facial radiographs and a computerized tomography (CT) scan, which showed soft tissue swelling. She was given Versed for the CT scan. The patient was admitted to the intensive care unit with a diagnosis of obstructed airway. Consults to pulmonology, ear, nose, and throat (ENT), and infectious disease departments revealed no specific etiology. Treatment included pain medication, steroids, and ice to her jaw. Oral surgery was also consulted because a tooth abscess could possibly cause jaw swelling and difficulty opening the mouth. The patient was discharged with oral pain medication, antibiotics and a follow-up appointment with the ENT physician 10 days later.

At home, L.L. began to experience muscle spasms, twitching, headache, low-grade fever, fatigue, and general aching. She described her fingers on both hands contracting in a "claw-like" position. She attempted to contact the ENT provider, but was unsuccessful. Four days later, when she did see the ENT provider, no change in the treatment plan was made.

A nurse practitioner (NP) saw her the following day for a refill of Fioricet. L.L. relayed her recent medical situation and stated she was still not feeling well. After performing a thorough medical history and listening to the patient's description of the events, the NP suspected tetanus. She ordered tetanus diphtheria booster and referred the patient to another ENT physician for a definitive plan of care. The next day, the patient saw the ENT provider who, based on her history, diagnosed her with tetanus. No further treatment was indicated.

Over the next 4 months, the patient continued to experience jaw swelling, neck stiffness, and muscle tightness, particularly in her arms, legs, fingers, toes, and occasionally in her face. During this time, she was treated with Cipro and Levaquin for the tetanus infection, and Robaxin for muscle spasms. She also noted a painful lump in the left side of her neck, which reached the size of a lemon. It was diagnosed as an infected parotid gland, without a specific etiology. The salivary glands also showed chronic inflammation. The patient was given the option to have it surgically removed, which she declined at that time. Six months later, she had the mass removed, with no tetanus on biopsy. After another 5 months, the mass returned, and she decided to once again have it surgically removed.

* Past Medical History

L L. had a history of tension/migraine headaches that began in 1987 following an episode of viral meningitis. Treatment included opioids and muscle relaxants. She had a 24-year half a pack per day smoking history. Past medical history was not significant for tetanus. Her last tetanus booster was in 1986, and before that, in 1965.

* Physical Examination

L.L was in no acute distress, afebrile at present time and vital signs were normal. HEENT-normocephalic, PERRLA, tympanic membranes and canals were normal, hearing was clinically normal, external nose normal, turbinates and mucosa normal, septum deviated to the right, with a fairly large spur. Lips and gums were normal. Her mouth was dry and virtually no saliva was noted. Oropharynx and oral cavity mucosa, tongue, hard and soft palate, and posterior pharyngeal wall were normal. Tonsillar fossae were normal. No anterior cervical adenopathy existed, but right post auricular lymphadenopathy and a 5 mm x 2 cm raised erythematous lesion on the back of the pinna were noted. Her trachea was midline, thyroid normal, and nonenlarged, without masses. L.L. was given a tetanus-diphtheria booster. Percocet was prescribed for her neck pain, Naprosyn for neck inflammation and mild headache, Flexeril for moderate headache, and Fioricet for severe headache pain.

* Differential Diagnosis

The differential diagnosis of tetanus can be extensive. Trismus (lockjaw) could also be attributed to tooth abscess, mandibular dislocation, or peritonsilar or rectopharyngeal abscess. Muscle spasms may be due to meningitis, dystonic reactions, acute abdomen, and strychnine poisoning. Priorities for treatment include airway management and cardiovascular stability. Ventilator support may be needed to prevent asphyxia from the continuous muscle spasm. Significant doses of Versed or Valium may be required to control tonic spasms and tetanic seizures and to induce muscle relaxation. These patients need to be monitored in an intensive care setting due to the rapid hemodynamic fluctuations.2

* Diagnosis

Diagnosis of tetanus is based on clinical findings. No laboratory or diagnostic tests are specific for tetanus; treatment is started when clinical diagnosis is considered. Wound cultures may be collected, but the yield for tetanus is inconclusive. Tetanus can be isolated from a wound in a nontetanus-infected individual, but it could also be negative in a wound from a patient with tetanus. Definite diagnosis for tetanus, therefore, is strictly based on the patient's clinical presentation.2

Clinical presentation in severe cases of generalized tetanus includes a triad of rigidity, muscle spasm, and autonomic dysfunction. The patient remains awake and alert throughout the course of the illness. Early symptoms include neck stiffness, sore throat, difficulty opening the mouth, and dysphagia. Jaw stiffness is followed by trismus or spasms of jaw muscles. This hyperrelexia includes rigidity and spasm of the abdominal, neck, and back muscles. As the spasm extends to the facial muscles, the typical expression, "risus sardonicus" is apparent. Minor stimuli may precipitate painful tonic clonic convulsions. Acute asphyxia may result from spasms of the glottis and respiratory muscles. Local tetanus is seen with lower toxin levels and peripheral injury. Muscle spasms are restricted to limited areas of the body, reducing the mortality rate. Cephalic tetanus must also be considered in those patients with symptoms of localized tetanus and head wounds. In cases of cephalic tetanus, paralysis vs. spasm predominates. In this case, the patient did experience acute respiratory distress and airway compromise.1

* Plan of Care

L.L.'s subsequent care after the diagnosis of tetanus was multifaceted. Antibiotics (Clindamycin, Cipro, Augmentin, Levaquin) were prescribed for the actual infection, and muscle relaxants (Flexeril) were given for the sporadic muscle spasms. L.L.'s pain was managed by Percocet, because she did not tolerate Oxycodone. For her neck inflammation, solumedrol was given intramuscularly, and oral Prednisone was prescribed for home use.

* Discussion

In cases of tetanus, the history of present illness usually includes a recognized wound that has been contaminated with soil, manure, or rusty metal. This wound may be trivial in nature, however, and the patient may not seek medical care. In 15% to 25% of cases, a recognized wound cannot be identified.3

The incubation period for tetanus ranges from three to 21 days. The length of the incubation period and severity of disease depends on the proximity of the wound to the central nervous system. If the injury is distal to the central nervous system, as in this case, the incubation will be longer. Furthermore, the probability of death is greater if the incubation period is short.1

L.L. did recall minor cuts to the right hand that occurred several weeks before the onset of her signs and symptoms. The patient reported cuts on her hand caused by contact with a rusty barbed wire in stagnant water. The patient also reported that her last immunization of tetanus was in 1986. Despite these clues and the patient's concerns that her signs and symptoms could be due to tetanus, she was originally diagnosed with submandibular gland infection.

* Treatment

The recommended treatment for tetanus is tetanus immune globulin (human) (TIG), which is given intramuscularly.4 Adults and children may receive one total dose of 3,000 to 5,000 U.4 Interestingly, most tetanus patients have either not been vaccinated, or have completed the primary series, but have not had a booster in the 10 years preceding their tetanus-inflicting events.5

Any wound found on a patient should be thoroughly cleaned and debrided if there is necrosis present. Provide supportive care and pharmacotherapy to stimuli minimize, which can provoke spasms. Sedation, paralysis, and mechanical ventilation are often used to control the tetanic spasms. All patients are to receive oral or intravenous metronidazole (30 mg/kg per day at 6 hour intervals). This is the antibiotic of choice to reduce the toxin-producing forms of C. tetani. Parenteral penicillin G (100, 000 U/kg per day at 6-hour intervals) can be administered as an alternative therapy. It is recommended that treatment be given for 10 to 14 days.4 Tetanus is preventable with routine vaccination and appropriate wound management.3

Primary tetanus immunization, commonly combined with diphtheria toxoid and acellular pertussis vaccine, is recommended for all persons between the ages of 6 weeks and 7 years who do not have any contraindications. Although toxoid efficacy has not been studied in a vaccine trial, it can be inferred that a complete tetanus toxoid series has a clinical efficacy of virtually 100%. Tetanus in persons who are fully immunized and whose last dose was within the preceding 10 years is extremely rare, and is evident by the fact that 0.02 cases of tetanus per 100,000 were reported in 1999.5 Routine boosters are recommended every 10 years to maintain the antitoxin level. To ensure protective antitoxin levels are sufficient in people who have a wound that is not clean or minor, a booster is recommended if the time from the last tetanus booster is 5 years or greater. Four doses at 2, 4, 6, and 15 to 18 months of age is considered primary series. Boosters are recommended at 4- to 6-years-old, then every 10 years.5

* Shortage of Tetanus Toxoid

In November 2000, the Centers for Disease Control (CDC) published a notice to readers regarding a shortage of tetanus and diphtheria toxoids. The temporary scarcity was attributed to two simultaneous events: 1) a decrease in the number of lots released by one manufacturer, and 2) a temporary decrease in vaccine inventory following routine maintenance actions that lasted longer than expected at another facility. Clinics were advised to prioritize their available supplies, and if Td was delayed, to initiate a callback system when the vaccine became available (see Table: "Vaccine Priority Recommendations").6 In May 2001, the CDC established guidelines to ensure vaccine availability for priority needs (see Tables: "CDC Guidelines" and "Recommendations for Wound Management").

* Conclusion

Although this particular case of tetanus was not affected by the vaccine shortage, it does elicit important patient care points. Tetanus status needs to be checked regularly and adequately recorded. NPs need to educate patients about the importance of completing the primary series and booster doses of tetanus and all other recommended vaccines. The final and most challenging point is to educate patients to appropriately seek care when injured. Proper wound management is essential, not only to prevent infection, but also to ensure that tetanus is prevented.

REFERENCES

1. Cook T M, Protheroe RT, Handel JM: Tetanus: a review of the literature. Br J Anaesth 2001, Vol. 87, 3477-487.

2. Tierney JR, McPhee SJ and Papadakis MA: Current medical diagnosis and treatment. Appleton and Lange, 2001.

3. CDC. Notice to readers: Deferral of routine booster doses of tetanus and diphtheria toxoids for adolescents and adults. MMWR 2001; 51 (20); 418-427.

4. Tierney LM, McPhee SJ, Papadakis MA: Tetanus. Current Medical Diagnosis and Treatment 2000, ed 39. The McGraw-Hill Companies, Inc, 2000, pp 1342-1343.

5. CDC. Epidemiology of vaccine-preventable diseases, course textbook, 6th ed. (2nd printing January 2001) pp.57-66.

6. CDC. Notice to readers: Shortage of tetanus and diphtheria toxiods. MMWR 2000; 49 (45); 1029-1030.

LTC Priscilla Quackenbush RN, MSN, NP

MAJ Shirley Tuorinsky RN, MSN, CRNA

MAJ Rebecca Rabb RN, MS

ABOUT THE AUTHORS

At the Munson Army Health Center, Ft. Leavenworth, Kan., LTC Priscilla Quackenbush was Deputy Comander for Nursing, MAJ Shirley Tuorinsky is Cheif of Anesthesia and Operative Services, and MAJ Rebecca Rabb was Cheif of Preventive Medicine.

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