2-year-old with tuberculous meningitis: a case study.
Neurological nursing (Case studies)
Meningitis (Care and treatment)
|Publication:||Name: Journal of Neuroscience Nursing Publisher: American Association of Neuroscience Nurses Audience: Professional Format: Magazine/Journal Subject: Health care industry Copyright: COPYRIGHT 2004 American Association of Neuroscience Nurses ISSN: 0888-0395|
|Issue:||Date: April, 2004 Source Volume: 36 Source Issue: 2|
Tuberculous meningitis (TBM) may occur with tuberculosis infection,
and young children are more prone to this disease. The clinical
manifestations, time course, and treatment of TBM are unlike those of
other types of meningitis, and the disease presents unique challenges
for nurses caring for these patients. This case study highlights the
typical presentation, course, and management of TBM in a pediatric
patient and provides an overview of this devastating disease. Specific
nursing issues related to the care of these children are outlined.
Although tuberculous meningitis (TBM) is uncommon, it can have devastating consequences. Early diagnosis of TBM can be difficult, because signs and symptoms often are vague early in the disease. Without treatment, however, the disease can be fatal in 3 to 4 weeks (Starke & Smith, 1998). There is minimal nursing literature on the subject, yet nurses play an important role in managing these patients. The following case study presents a previously healthy child who developed tuberculous meningitis and did well following appropriate diagnosis and treatment.
N.T., a previously healthy 2-year-old girl, presented to her pediatrician with a 10-day history of progressive fevers (99-102[degrees]F), mild lethargy, and irritability. Urine and blood tests were performed, and the patient was placed on amoxicillin. During the next 5 days, N.T.'s lethargy worsened and her mother felt she was somewhat cross-eyed. N.T. was admitted to the hospital for further evaluation and management.
Upon admission, N.T. was irritable and inconsolable. She was moving all extremities, her pupils were equal and reactive to light, she had mild nuchal rigidity, and she was febrile to 102[degrees]F. A computed tomography (CT) scan and lumbar puncture were performed. The CT scan revealed communicating hydrocephalus. The lumbar puncture revealed slightly cloudy cerebrospinal fluid (CSF) with the following CSF results: red blood cells = 125; white blood cells (WBCs) = 615 (82% lymphocytes, 16% monocytes, and 2% polys); protein = 278 mg/dl; and glucose-13 mg/dl. Gram stain was negative. The CSF was sent for numerous studies, including acid fast bacillus (AFB). Although initial CSF cultures and AFB smear were negative, N.T. was given a presumed diagnosis of tuberculous meningitis. She was placed on isoniazid (INH), streptomycin, pyrazinamide, and rifampin, in addition to ceftriaxone, vancomycin, and dexamethasone. A purified protein derivative (PPD) was placed, and a chest X ray was performed, both of which were negative for tuberculosis (TB).
On the morning following admission, N.T. became lethargic, bradycardic, and hypertensive. An external ventricular drain was placed, and N.T. rapidly stabilized after drainage of CSF. A magnetic resonance imaging (MRI) scan revealed extensive gadolinium enhancement throughout the basal cisterns and meninges. N.T. continued to improve, and within 10 days she underwent placement of a ventriculo-peritoneal shunt for hydrocephalus and placement of a Broviac catheter for long-term antibiotic therapy.
N.T. was discharged after 15 days with no apparent neurological deficit. Discharge medications included intravenous (IV) streptomycin for 2 months; isoniazid, rifampin, and pyrazinamide for 12-18 months; and tapering doses of dexamethasone. After discharge, N.T. and her family were followed by the public health department, a home health nursing agency, and a pediatric infectious diseases clinic. A repeat PPD, placed after the discontinuation of steroids, was positive with 11 mm induration. The CSF culture grew Mycobacterium tuberculosis 5 weeks after discharge from the hospital. The organism was sensitive to the prescribed antibiotics. Both of N.T.'s parents had a positive reaction to PPD testing and were placed on appropriate antibiotics. Follow-up investigation by the public health department could not determine the source of the infection. It was believed the parents and child were exposed at the same time, however.
Meningitis is a serious complication of tuberuculosis (TB) infection. TBM usually is seen in children who have not previously been diagnosed with TB (Krugman, Katz, Gershon, & Wilfert, 1992). Because it takes 2 to 6 months to develop after the initial tuberculosis infection, TBM is almost never seen in infants younger than 4 months. TBM is estimated to occur in 1 of every 300 untreated cases of TB and is most common in children younger than 6 years (Starke & Smith, 1998).
TB is contracted via respiratory spread from an infected person. TBM occurs as tubercle bacilli are distributed into the central nervous system (CNS) during lymphohematogenous spread of tuberculosis, probably during the incubation period. Because tubercle bacilli do not multiply as quickly in nervous tissue as in other areas of the body such as the lung, CNS manifestations are delayed after the initial TB infection (Starke & Smith, 1998). Small TB plaques, which are initially contained, develop in the brain and meninges. These plaques discharge tubercle bacilli directly into the subarachnoid space, causing a thick, gelatinous exudate to line the brain and meninges and infiltrate the meningeal arteries and veins. This exudate has a predilection for accumulating at the base of the brain, leading frequently to involvement of the cranial nerves and the optic chiasm. The subsequent inflammation, edema, and obstruction can interfere with the flow and absorption of CSF, resulting in hydrocephalus, and can cause obstruction of small vessels, resulting in vasculitis and infarction. In addition to causing TBM, TB infection in the CNS also can cause serous meningitis, tuberculomas, brain abscesses, and spinal leptomeningitis (Starke & Smith, 1998).
As happened in N.T.'s case, TBM has a gradual onset and initial symptoms can be vague. Patients usually present with fever, malaise, anorexia, and irritability, and at this point, a patient often is not diagnosed with meningitis (Waecker & Connor, 1990). As intracranial pressure (ICP) increases, patients develop vomiting, lethargy, headaches, and personality changes, as well as cranial nerve palsies and nuchal rigidity. Later signs include seizures, coma, and irregular pulse and respirations. Hyponatremia also can be observed.
TBM has been classified into three stages based on neurological status. In Stage I, the patient has a nonspecific febrile illness without neurological signs. In Stage II, the patient has an altered sensorium (e.g., lethargy, confusion) with focal neurological signs. In Stage III, patients are unresponsive and have signs and symptoms of significantly elevated ICP, such as irregular vital signs (Hosoglu et al., 2002; Waecker & Connor, 1990; Yaramis et al., 1998).
Besides close evaluation of the patient's signs and symptoms, the workup for suspected TBM includes a thorough family and social history. It is important to recognize those children who are at the greatest risk for developing tuberculosis (American Lung Association, 2002):
* children living with an adult who has active TB or who is at risk for contracting TB
* immunocompromised children (including those with HW infection)
* children born in a country with a high prevalence of TB
* children from medically underserved communities
Having a family member with active TB is an important epidemiological finding and is helpful in strongly suggesting the diagnosis early in the course of the disease (Waecker & Connor, 1990).
Further workup for TBM includes placement of a TB test such as a PPD, a lumbar puncture, and a CT scan or MRI scan of the head. The typical CSF profile contains 50 to 500 WBCs, with lymphocytes predominant, very low glucose, and very high protein, usually out of proportion to the WBC count (Krugman et al., 1992; Yaramis et al., 1998). N.T.'s initial CSF profile was consistent with TBM, Including the fact that the gram stain was negative. CSF cultures for tubercle bacilli (AFB) should be sent, but results may not return for a long time. A chest X ray is performed to rule out pulmonary TB. In N.T.'s case, the chest X ray was negative. Gastric and sputum specimens for culture and AFB also may assist in the diagnosis of TB (Doerr, Starke, & Ong, 1995).
Typical findings on MRI or CT show ventriculomegaly in more than 50% of the patients, and one study showed hydrocephalus in 100% of patients (Barkovich, 1995; Doerr et al., 1995; Hosoglu et al., 2002; Tung et al., 2002). Basal cisterns show marked enhancement on CT and MRI, and noncontrast scans may show the exudate appearing as soft tissue density filling the cisterns. Infarcts may also be seen (Barkovich, 1995). Fig 1 and 2 show N.T.'s diffuse meningeal enhancement and hydrocephalus.
[FIGURES 1-2 OMITTED]
The Centers for Disease Control and Prevention (1994) recommends a minimum of 12 months of therapy to treat TBM. The drug regimen usually consists of isoniazid, rifampin, and pyrazinamide for patients with susceptible organisms. Because drug resistance is a possibility, either ethambutol or streptomycin is given initially until susceptibility studies are available. Ethambutol may cause visual impairment; therefore, streptomycin usually is given to children younger than 8 years because monitoring visual acuity can be difficult. N.T.'s treatment followed these CDC guidelines. Although intramuscular (IM) injection often is the recommended route for streptomycin, it is painful. IV administration is a viable alternative and has been used successfully (Morris & Cooper, 1994). N.T.'s parents--given the choice of daily IM administration or IV administration via Broviac catheter--chose the IV route. The IV route often is much easier for children and their families.
Treatment needs to be initiated once there is suspicion TBM is a likely diagnosis, even in cases in which a chest X ray and PPD are negative (Waecker & Connor, 1990). A delay in treatment can lead to a poorer neurological outcome and increased mortality (Doerr et al., 1995; Starke & Smith, 1998; Waecker & Connor, 1990; Yaramis et al., 1998). Once treatment begins, close follow-up is needed to ensure the patient is responding to treatment and to evaluate changes in the medication regimen. Cultures and sensitivities can take weeks to be finalized.
Steroids are indicated for TBM as long as they are used in conjunction with anti-TB medications. Although steroids usually are contraindicated when a patient has an active infection, steroids help reduce the cerebral inflammation and vasculitis associated with TBM. Studies have shown that steroids can lessen long-term neurological deficits, such as intellectual impairment, and can decrease the mortality rate (Schoeman, Van Zyl, Laubscher & Donald, 1997; Starke & Smith, 1998).
If caught early (Stage I) and treated appropriately, survival is nearly 100%, although many patients may have some degree of intellectual impairment. Morbidity and mortality rates are higher when patients are treated in Stage II or Stage III (Starke & Smith, 1998). In the later stages of the disease (Stage II and Stage III), morbidity rates range from 15% to 94% and mortality rates range from 3% to 23%. Neurological sequelae from TBM include motor difficulties, infarcts, seizures, cranial nerve palsies, and cognitive impairment (Hosoglu et al., 2002; Mahadevan, Mahadevan, & Tiroumourougane Serane, 2002; Waecker & Connor, 1990). An advanced clinical stage at diagnosis (Stage III), age less than 3 years at diagnosis, or a delay in initiating treatment all lead to a poorer outcome (Doerr et al., 1995). N.T. was diagnosed and her treatment was started in Stage II. She continued to do very well upon discharge and was neurologically normal at 2 months following discharge.
Nurses play an important role in caring for patients with TBM and their families in both inpatient and outpatient settings. Nurses are involved in acute hospital management, as well as in the home health and public health areas, and in educating patients and their families.
Patients require aggressive medical management at the time of suspected diagnosis, and antibiotic treatment should be started as soon as possible. Patients need to be closely evaluated for signs and symptoms of elevated intracranial pressure, such as headaches, vomiting, irritability, lethargy, and unstable vital signs. Analgesics and sedatives may be necessary to manage the pain and irritability caused by meningeal irritation and elevated ICP. Patients may require external ventricular drainage and/or placement of a ventriculo-peritoneal shunt. Appropriate institutional policies for isolation need to be followed. Children who do not have a cough and who have negative sputum AFB smears do not need respiratory isolation (American Academy of Pediatrics, 2000).
As soon as possible after diagnosis, patients must be evaluated for possible sources of exposure to TB. This evaluation includes the family, any patient contacts, and any patient travel. Immediate family members need to be tested for TB and referred for treatment if they test positive for recent TB exposure or if they are diagnosed with TB. Further testing and follow-up require close involvement of public health staff. Public health staff should provide
* public health follow-up upon discharge
* further TB testing of patient contacts and referrals for treatment, if necessary
* follow-up PPDs on patients if the initial test was negative
* patient, family, and community education.
Families require extensive education about TBM, and they should be taught about the mechanism of disease transmission and the importance of the need for close follow-up after discharge. Families need to be taught about their medication regimen, including the reasons for their use, drug interactions, and possible side effects (Table 1). The importance of uninterrupted TB drug therapy cannot be overemphasized. One study showed a fivefold increase in mortality when patients had an interruption of 2 weeks or more in their treatment (Hosoglu et al., 2002). This point needs to be highlighted numerous times during discharge education, because continuing medications for a minimum of 1 year will be difficult for some families. This is especially true when patients have recovered from the acute illness and are doing well at home. A referral to a home health nursing agency may be helpful so a registered nurse can evaluate the patient's condition and medication compliance and troubleshoot problems that may arise. Additional educational needs include
* management of long-term venous access device (e.g., Broviac catheter, PICC line)
* administration of antibiotics
* signs and symptoms of shunt malfunction and infection, if ventriculo-peritoneal shunt was placed
* when to call their physician with concerns
* dates and times of follow-up appointments.
Families need support during this time, because parents may be dealing with feelings of guilt over their child's illness and the way their child contracted TB. Parents may believe they transmitted the infection to their child or they allowed their child to be exposed to an infectious contact. The long-term management required for TBM and the possibility of neurological sequelae can be overwhelming. Some parents perceive there is a social stigma attached to TB, and this might make them feel isolated. Nurses need to approach patients and families with empathy, caring, and understanding. Nurses should try to learn about the patient's cultural background and ensure teaching is performed in the patient's native language to promote increased understanding and compliance.
TBM can be a devastating disease for patients and their families, but nurses can help make a difference in patient management. Early recognition and treatment of TBM is paramount, as is patient and family education and support.
The authors thank Dr. Dean A. Blumberg, associate professor, Pediatric Infectious Diseases, UC Davis Medical Center, for his review of this manuscript.
American Academy of Pediatrics. (2000). Tuberculosis. In L.K. Pickering (Ed.), 2000 Red Book.. Report of the Committee on Infectious Diseases (25th ed., pp. 593-613). Elk Grove Village, IL: Author.
American Lung Association. (2002). American Lung Association Fact Sheet: Pediatric tuberculosis. Retrieved February 13, 2003, from www.lungusa.org/diseases/pedtbfac.html.
Barkovich, J.H. (1995). Pediatric neuroimaging (2nd ed.). New York: Raven Press.
Buttaro, T.M., Ezell, B., & Gray, V. (1995). A care plan for children with tuberculosis. Public Health Nursing, 12(3), 181-188.
Centers for Disease Control and Prevention. (1994). Treatment of tuberculosis and tuberculosis infection in adults and children. American Thoracic Society Medical Section of the American Lung Association, American Journal of Respiratory and Critical Care Medicine, 149. Retrieved February 20, 2003, from http://www.cdc.gov.htm
Doerr, C.A., Starke, J.R., & Ong, L.T. (1995). Clinical and public health aspects of tuberculous meningitis in children. The Journal of Pediatrics, 127(1), 27-33.
Hosoglu, S., Geyik, M.F., Balik, I., Aygen, B., Erol, S., Ayghocel, T.G., et al. (2002). Predictors of outcome in patients with tuberculous meningitis. The International Journal of Tuberculosis and Lung Disease, 6(1), 64-70.
Krugman, S., Katz, S.L., Gershon, A.A., & Wilfert, C.M. (1992) Infectious Diseases of Children (9th ed.). Missouri: Mosby-Year Book.
Mahadevan, B., Mahadevan, S., & Tiroumourougane Serane, V. (2002). Prognostic factors in childhood tuberculous meningitis. Journal of Tropical Pediatrics, 48, 362-365.
Morris, J.T., & Cooper, R.H. (1994). Intravenous streptomycin: A useful route of administration. Clinical Infectious Diseases, 19, 1150-1151.
Schoeman, J.F., Van Zyl, L.E., Laubscher, J.A., & Donald. P.R. (1997). Effect of corticosteroids on intracranial pressure, computed tomographic findings and clinical outcome in young children with tuberculous meningitis. Pediatrics, 99(2), 226-231.
Starke, J.R., & Smith, M.D. (1998) Tuberculosis. In R.D.. Feigin, & J.D., Cherry (Eds.). Textbook of pediatric infectious diseases (4th ed., pp. 1210-1212). Philadelphia: Saunders Company.
Tung, Y.R., Lai, M.C., Lui, C.C., Tsai, K.L., Huang, L.T., Chang, Y.C., et al. (2002). Tuberculous meningitis in infancy. Pediatric Neurology, 27(4), 262-266.
Waecker. N,J., & Connor, J.D. (1990). Central nervous system tuberculosis in children: A review of 30 cases. The Pediatric Infectious Disease Journal, 9(8), 539-543.
Yaramis, A., Gurkan, F., Elevli, M., Soker, M., Haspolat, K., Kirbas, G., et al. (1998). Central nervous system tuberculosis in children: A review of 214 cases. Pediatrics, 102(5), retrieved February 20, 2002, from www.pediatrics.org
Questions or comments about this article may be directed to: Siobhan Geary, MS RN CNS CNRN, by phone at 916/733-6025 or by e-mail at firstname.lastname@example.org. She is a pediatric ICU clinical nurse specialist at Sutter Medical Center, Sacramento, CA.
Michelle Agnew, BSN RN, is a neuroscience nurse educator at Sutter Medical Center.
|Gale Copyright:||Copyright 2004 Gale, Cengage Learning. All rights reserved.|