Aseptic meningitis is an illness characterized by serous inflammation of the linings of the brain (i.e., meninges), usually with an accompanying mononuclear pleocytosis. Clinical manifestations vary, with headache and fever predominating. The illness is usually mild and runs its course without treatment; however, some cases can be severe and life threatening.
Aseptic meningitis syndrome is not caused by pyogenic bacteria. Although it is usually caused by certain viruses, it has a number of other etiologies as well, both infectious and noninfectious. Hence, the term aseptic meningitis is no longer synonymous with viral meningitis, although the two are still often used interchangeably.
The epidemiologic setting (e.g., time of year, geographic locale, exposure to insects, diseases prevalent in the local community) and accompanying systemic manifestations may be helpful in making a presumptive diagnosis. However, with a few exceptions, the clinical and laboratory findings accompanying acute viral meningitis are insufficiently distinct to allow an etiologic diagnosis, and distinguishing these disorders from a number of nonviral diseases may be difficult.
Treatment varies with the cause. No specific pharmacologic treatment is available for most cases of viral meningitis; these patients are managed with supportive therapy, which includes analgesics, antinausea medications, intravenous fluids, and prevention and treatment of complications.
Overall, viral infection is the most common form of aseptic meningitis, and enteroviruses are the most common viral cause. Enteroviruses are small, nonenveloped RNA viruses of the picornavirus family with various serotypes. More than 50 subtypes have been linked with meningitis. Coxsackieviruses and echoviruses, which are enteroviruses, account for approximately half of cases of aseptic meningitis.
Certain enteroviruses (e.g., coxsackievirus B5, echovirus 6, 9, and 30) are more likely to cause meningitis outbreaks, while others (coxsackie A9, B3, and B4) are mostly endemic.[1, 2, 3] The incidence of infections from enteroviruses increases in the summer and early fall. Transmission occurs by hand-to-mouth contact and to a lesser extent by respiratory and fecal routes.
Herpesviruses, both herpes labialis (HSV-1) and genital herpes (HSV-2), can cause meningitis in children and especially infants. Varicella-zoster virus, another herpesvirus, causes encephalitis but only in immunocompromised persons.
Mumps was a common cause of aseptic meningitis in the United States until mumps vaccination came into use. In several countries, mumps virus remains a common pathogen in aseptic meningitis. It is spread by respiratory secretions, with increased incidence in the spring.
Aseptic meningitis from HIV occurs mostly at the time of seroconversion. HIV spreads to the meninges hematogenously, while rabies, polio, and herpesviruses are neurotrophic (i.e., spread through neurons).
Aseptic meningitis from arboviruses follows geographic and seasonal patterns determined by the life cycle of arthropod vectors, animal reservoirs, and their contact with human subjects. Eastern equine encephalitis virus (EEEV) usually is observed in Atlantic and Gulf regions, whereas western equine encephalitis virus (WEEV) is prevalent in the western part of the United States. WEEV is responsible for more aseptic meningitis cases than EEEV.
Approximately 15% of St Louis encephalitis virus (SLEV) infections result in meningitis. In children, this incidence is as high as 60%. SLEV infection can occur in both rural and urban areas. In the rural setting, the infection from SLEV tends to follow the same pattern as WEEV infection. Conversely, in urban settings, outbreaks tend to be more explosive.
Approximately 18% of people infected with Colorado tick fever develop meningitis. This disease primarily occurs in the Rocky Mountain region, which is the habitat of Dermacentor andersoni ticks whose bite transmits the virus.
Infection with Venezuelan equine encephalitis virus initially leads to influenza-like illness in most people. Only 3% of infected persons are known to develop acute meningitis. This virus has spread into Florida and some southwestern states. LCMV, an arenavirus, is an extremely rare cause of meningitis. Transmission of LCMV infection occurs by contact with dust or food contaminated by excreta of rodents. Cases tend to be more common in the winter. Human infections have been seen in both laboratory and home settings.
Brucellosis is an infection with a bacterium of one of the Brucella species, usually Brucella abortus (cattle), Brucella melitensis, Brucella ovis (sheep, goats), Brucella suis (pigs), or rarely Brucella canis (dogs). Its distribution is worldwide, but it is most common in the Mediterranean regions, Africa, the Middle East, India, Central Asia, Mexico, and Central and South America.
Persons at highest risk of brucellosis are those who work with animals that are infected, such as veterinarians and ranchers, and persons who consume raw milk or cheeses made with raw milk. Brucellosis also may be transmitted to humans if they are exposed inadvertently to live brucellosis vaccine by a needlestick or other accident.
The incidence in the United States is fewer than 0.5 cases per 100,000 population.
The incidence of drug-induced meningitis (DIAM) is unknown. Many antimicrobials can cause the disorder (e.g., trimethoprim-sulfamethoxazole, ciprofloxacin, cephalexin, metronidazole, amoxicillin, penicillin, isoniazid). Other drugs that have been associated with DIAM include NSAIDs, ranitidine, carbamazepine, vaccines against hepatitis B and mumps, immunoglobulins, radiographic agents, and muromonab-CD3.
DIAM may recur with re-exposure to the offending agent. Green et al reported a case of lamotrigine-induced aseptic meningitis, with a second episode on rechallenge with lamotrigine.[5]
The pathogenic mechanisms of DIAM are diverse and presumably differ from drug to drug. There are two proposed mechanisms: direct meningeal irritation by the intrathecal drug and hypersensitivity reactions to the drug (type III and IV). In type III hypersensitivity reactions, the drug or its metabolite forms a complex with antibodies in the serum, in turn activating the complement cascade. In type IV reactions, T helper cells, after previous sensitization, are recruited to the site of inflammation.[6]
DIAM from muromonab (OKT3) is believed to be mediated, at least in part, by cytokine release. Why such reactions are confined selectively to the CSF compartment is unclear.
Aseptic meningitis—along with cerebral vasospasm or ischemic encephalopathy—has been reported with intravenous immunoglobulin (IVIg) therapy.[7] Jarius et al strongly suggest that in vivo activation of TNF-alpha–primed neutrophils by atypical antineutrophil cytoplasmic antibodies (ANCAs) of IVIg may contribute to these side effects.[8]
Patients with systemic lupus erythematosus are especially susceptible to aseptic meningitis. In these patients, the disorder is often precipitated by drugs.
The exact etiology of this condition remains uncertain. Originally, the Vogt-Koyanagi syndrome was described independently of the Harada syndrome. However, the clinical manifestations of both overlap sufficiently to justify their combination into a single entity.
The cause of Behçet syndrome remains uncertain. CNS manifestations occur in 18% of patients with Behçet syndrome.
Mollaret meningitis is a recurrent disorder whose causative agent remains unknown. However, recent data suggest that herpes simplex virus (HSV-2 and, less frequently, HSV-1) may cause some if not most cases.
Patients have developed febrile meningeal syndromes shortly after undergoing embolization of cerebral aneurysms with hydrogel-coated coils.[9]
Postoperative aseptic meningitis was first described by Cushing in 1925,[10] though the mechanisms remain unclear.
Go to Meningitis, Meningococcal Meningitis, Staphylococcal Meningitis, Haemophilus Meningitis, Viral Meningitis, and Tuberculous Meningitis for more complete information on these topics.
Aseptic meningitis may be caused by viruses, bacteria, fungi, parasites, drugs, systemic diseases, and miscellaneous other conditions.
Viral causes include the following:
Bacterial causes are as follows:
Fungal causes are as follows:
Parasites that can cause aseptic meningitis are as follows:
Drugs that can cause aseptic meningitis include the following:
Systemic diseases that can cause aseptic meningitis include the following:
Miscellaneous causes include the following:
Viral meningitis is a relatively common disorder. In Olmsted County, Minnesota, the incidence of viral meningitis was 10.9 per 100,000 person-years from 1950 to 1981, with most cases occurring in the summer months.[4] The incidence of aseptic meningitis has been reported as 11 per 100,000 person-years, compared with a rate of 8.6 per 100,000 for bacterial meningitis. In the United States, a specific cause is usually identifiable in 10-15% of cases of meningitis.
Aseptic meningitis is usually a benign disease. Rates of morbidity and mortality are low, except among neonates. Most patients experience full recovery in 5-14 days after onset of symptoms. Fatigue, light-headedness, and asthenia may persist for months in some cases, however.
Seizures sometimes can complicate meningitis. Encephalitis may develop in some patients. The most common sequela following mumps meningoencephalitis is sensorineural deafness. Hydrocephalus from aqueductal stenosis has been reported as a late sequela of mumps meningitis and encephalitis in children.
The clinical manifestations of most acute viral meningitides may vary with the particular virus. Illness may be biphasic, with nonspecific constitutional symptoms followed by meningitis. The epidemiologic setting (e.g., time of year, geographic locale, exposure to insects, prevalent illnesses in the local community) and accompanying systemic manifestations may be helpful in making a presumptive diagnosis.
A detailed drug history is invaluable for identifying possible drug-induced aseptic meningitis, which has a clinical presentation indistinguishable from infectious meningitis. The drug history must include nonprescription medications such as ibuprofen.
The time course of acute viral meningitis varies. Onset may occur within a matter of hours after exposure or evolve more slowly over a few days. Usually, maximum deficit appears within 3-6 days after exposure. Persons infected with the viruses that commonly cause aseptic meningitis may remain infectious for weeks after contracting the virus.
Characteristic signs of acute viral meningitis include the following:
Focal signs, seizures, and profound lethargy are rarely features of aseptic meningitis. Occasionally, patients may exhibit altered levels of consciousness, including confusion and visual hallucinations.
Neck stiffness in meningitis is tested by gentle forward flexion of the neck with the patient lying in the supine position. Meningeal irritation also can be tested by the jolt accentuation of headache. This is elicited by asking the patient to turn his or her head horizontally at a frequency of 2-3 rotations per second. Worsening of a baseline headache represents a positive sign.
Severe meningeal irritation may result in the patient assuming the tripod position (termed Amoss sign or Hoyne sign) with the knees and hips flexed, the back arched lordotically, the neck extended, and the arms brought back to support the thorax.
When passive neck flexion in a supine patient results in flexion of the knees and hips, the Brudzinski sign is positive. Yet another Brudzinski sign, the contralateral reflex, is present if passive flexion of one hip and knee causes flexion of the contralateral leg.
Kernig sign is elicited with the patient lying supine and the hip flexed at 90°. A positive sign is present when extension of the knee from this position elicits resistance or pain in the lower back or posterior thigh.
Papilledema or absence of venous pulsations upon funduscopic examination indicates increased intracranial pressure.
Skin manifestations may suggest the diagnosis of aseptic meningitis from certain causes. Examples include the rash of varicella zoster, the genital lesions of HSV-2, or a mild maculopapular rash occurring in the summer and fall months with some enteroviruses.
Rash from enteroviral infections usually accompanies the onset of fever and persists for 4-10 days. In infections due to coxsackieviruses A5, 9, or 16 or echoviruses 4, 6, 9, 16, or 30, the rash is typically maculopapular and nonpruritic, may be confined to the face and trunk, or may involve extremities, including the palms and soles.
In coxsackievirus A16 and, rarely, in other group A serotype infections, a vesicular rash may involve the hands, feet, and oropharynx. Herpangina, characterized by gray vesicular lesions on the tonsillar fossae, soft palate, and uvula, can accompany infection caused by group A coxsackievirus. With echovirus 9 infections, a petechial rash resembling meningococcemia typically is observed.
The selection of blood tests is guided by the etiologic clues gleaned from the clinical evaluation. Tests that may be useful include the following:
Dubos et al found that measurement of blood procalcitonin (PCT) levels, in combination with other clinical and laboratory parameters, can help distinguish aseptic meningitis from bacterial meningitis. In a study of 198 consecutive children with acute meningitis (aged 29 days to 18 years), a PCT level ≥ 0.5-ng/mL indicated bacterial rather than aseptic meningitis with 99% sensitivity and 83% specificity.[12]
The following CSF studies may be considered:
Nucleic acid CSF tests are more sensitive than cultures in diagnosing enteroviral infections. There can be substantial cost savings and avoidance of unnecessary treatment of aseptic meningitis with antibiotics when the turnaround time for these tests is less than 24 hours.
A CSF protein level of 0.5 g/L or higher suggests bacterial rather than aseptic meningitis in children 28 days to 16 years old. However, this finding has relatively low sensitivity and specificity.[1, 13]
TNF alpha, which is a potent mediator of inflammation, has been demonstrated to have potential as a predictor of clinical outcome in children with acute bacterial meningitis. In one study, CSF levels of TNF alpha were markedly higher in children with acute bacterial meningitis than in controls. All patients with TNF alpha levels greater than 1500 pg/mL died.
Bishara et al found elevated levels of soluble triggering receptor expressed on myeloid cells (sTREM-1) in the CSF in 7 of 9 (78%) patients with culture-positive specimens and in 0 of 12 pati.e.nts with culture-negative specimens (sensitivity, 78%; specificity, 100%). This suggests that sTREM-1 is upregulated in the CSF of patients with bacterial meningitis with high specificity and that its presence can potentially assist in the diagnosis of bacterial meningitis.[14]
Mollaret cells (large endothelial cells) are considered by many to be the hallmark of Mollaret meningitis, although their presence in CSF is not pathognomonic. They may comprise 60-70% of cells in the CSF; however, they are usually present for only the first 24 hours and can be missed easily.
After the first 24 hours, the CSF shows a lymphocytic predominance with cell counts usually less than 3000/µL. Hypoglycorrhachia (i.e., low CSF glucose concentration) is reported in one third of the patients. CSF protein usually is elevated mildly.
Detection of enterovirus in stool specimens is an important adjunct study for diagnosing enteroviral infections in children.
The following imaging studies should be performed:
In the appropriate epidemiologic settings, consider an intradermal tuberculin test (purified protein derivative [PPD]) or other tests for tuberculosis.
Many patients who have aseptic meningitis can be cared for on an outpatient basis, but those who have profound headache, nausea, vomiting, or CSF pleocytosis with a polymorphonuclear leukocyte predominance should be admitted for observation. Antibiotic coverage for bacterial meningitis may be given, at the discretion of the managing clinician.
No specific treatment exists for most of the viruses that cause meningitis; therefore, management, for the most part, is supportive and includes analgesics, antinausea medications, intravenous fluids, and prevention and treatment of complications.
Headache and fever usually can be treated with judicious doses of acetaminophen. Severe hyperthermia (>40°C) may require vigorous therapy, but mild temperature elevation may serve as a natural defense mechanism, and some authors believe it should be left untreated.
Strict isolation is not necessary. When enteroviral infection is suspected, take precautions in handling stools and wash hands carefully. In patients with meningitis from measles, chickenpox, rubella, or mumps virus infections, the usual precaution of isolation from susceptible individuals should be observed.
For severe cases, meticulous care in an intensive care setting with respiratory and nutritional support is warranted. Remarkable recovery may be achieved in some patients who become comatose. Vigorous support and avoidance of complications are very important in these patients.
Given the potential for serious neurological morbidity and the persistently high mortality rates of bacterial meningitis, rapid institution of antibiotic coverage is essential when the diagnosis of bacterial meningitis is suspected. A third-generation intravenous cephalosporin is the customary choice.
Most studies suggest that rapid sterilization of CSF reduces mortality and long-term sequelae rates. Generally, if imaging studies are indicated before lumbar puncture, blood cultures and empiric antibiotic therapy should be instituted before the imaging studies; these are unlikely to decrease diagnostic sensitivity if CSF is tested for bacterial antigens.
A consensus conference recommended empirical antibiotic therapy for all patients with postoperative meningitis and treatment withdrawal after 48 or 72 hours if CSF culture results are negative.[15] This concept is not universally accepted. Zarrouk et al found that stopping antibiotic treatment after 3 days is effective and safe for patients with postoperative meningitis whose CSF culture results are negative.[16]
Effective antiviral therapy is available against HSV-1, varicella, and cytomegalovirus. In immunosuppressed patients, long-term therapy may be necessary.
Acyclovir is recommended for immunocompetent hosts with HSV-2 meningitis and a primary genital herpes infection. Valacyclovir and foscarnet are alternative antiviral agents.
In patients with Mollaret meningitis, acyclovir (intravenous or oral) or valacyclovir (oral only) are worthy of consideration for both therapy and prophylaxis.
For meningitis from the following pathogens, these specific agents are appropriate:
Antifungal agents of choice include amphotericin B, fluconazole, and flucytosine. For more information, see the Medscape article Meningitis.
In general, corticosteroids are avoided in aseptic meningitis because of their inhibitory effects on host immune responses. Occasionally, glucocorticoids, such as dexamethasone, are useful when meningitis is associated with signs of increased intracranial pressure.
Meningitis from Vogt-Koyanagi-Harada syndrome responds to prednisone in moderate to high doses.
Seizures sometimes can complicate meningitis; however, prophylactic anticonvulsants are not recommended routinely. If seizures develop, they can be controlled with phenytoin and phenobarbital. If status epilepticus develops, appropriate therapy should be provided to prevent secondary brain injury.
If persistent cognitive problems occur after recovery from acute meningitis, especially residual suboptimal functioning in the workplace or in school, referral for formal neuropsychological testing clarifies the nature of the complaint both to the physician and to the patient and helps separate psychological adjustment factors from organic dysfunction.
Hand washing and other general good health measures may reduce the risk of developing an infection that can progress to meningitis.
Many of the causes of meningitis are communicable and, if one case of meningitis is diagnosed within a community, appropriate steps may need to be taken immediately to prevent the further spread of the disease. Since viruses that are passed in the stool cause most cases, people diagnosed with aseptic meningitis should be sure to wash their hands thoroughly after using the toilet. Always wash hands after changing diapers.
Effective vaccines are available for polio, measles, mumps, and rubella. Illnesses related to these viruses have declined dramatically in countries with effective vaccination strategies. Vaccination against Japanese encephalitis has been effective in controlling the infection in Asia. Rabies is the only infection in which the vaccine is given after exposure to the virus.
The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.
Clinical Context: Ceftriaxone is a third-generation cephalosporin with broad-spectrum gram-negative activity. It has lower efficacy against gram-positive organisms but has excellent activity against susceptible pneumococcal organisms. It exerts an antimicrobial effect by interfering with the synthesis of peptidoglycan, a major structural component of the bacterial cell wall. It is an excellent antibiotic for the empiric treatment of bacterial meningitis.
Clinical Context: Ceftazidime is a third-generation cephalosporin with broad-spectrum activity against gram-negative organisms, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. By binding to one or more of the penicillin-binding proteins, it arrests bacterial cell wall synthesis and inhibits bacterial replication.
Clinical Context: Cefotaxime is a third-generation cephalosporin that is used to treat suspected or documented bacterial meningitis caused by susceptible organisms, such as H influenzae or N meningitidis. Like other beta-lactam antibiotics, cefotaxime inhibits bacterial growth by arresting bacterial cell wall synthesis.
Clinical Context: Newer antibiotics are available, but aminoglycosides, such as gentamicin, remain significant in treating severe infections. Aminoglycosides inhibit protein synthesis by irreversibly binding to 30S ribosome. In meningitis or gram-negative meningitides, administer intrathecally because of poor CNS penetration. Dosing regimens are numerous; adjust the dose based on CrCl and changes in the volume of distribution.
Clinical Context: Doxycycline inhibits protein synthesis and, therefore, bacterial growth by binding with 30S and possibly 50S ribosomal subunits of susceptible bacteria.
These agents are used to treat or prevent infection caused by the most likely pathogen suspected or identified.
Clinical Context: A prodrug activated by cellular enzymes, acyclovir inhibits the activity of HSV-1, HSV-2, and varicella-zoster virus by competing for viral DNA polymerase and incorporation into viral DNA. Acyclovir is used in HSV meningitis.
Clinical Context: Foscarnet is an organic analog of inorganic pyrophosphate that inhibits the replication of known herpesviruses, including CMV, HSV-1, and HSV-2. It inhibits viral replication at the pyrophosphate-binding site on virus-specific DNA polymerases. Foscarnet is used to treat CMV meningitis in immunocompromised hosts at induction doses of 60 mg/kg IV q8h and maintenance doses of 90-120 mg/kg IV q24h.
Clinical Context: Valacyclovir is a prodrug rapidly converted to the active drug acyclovir. It is more expensive than acyclovir but has a more convenient dosing regimen. The adult dosage is 500 mg orally twice a day for 5-10 days.
Risk of hyperkalemia is increased in patients taking angiotensin-converting enzyme (ACE) inhibitors, cyclosporine, and potassium-sparing diuretics. Use with caution in patients with renal failure (decrease the dose) and patients also taking nephrotoxic drugs. Valacyclovir is associated with onset of hemolytic uremic syndrome. Valacyclovir is a pregnancy category B drug.
These agents interfere with viral replication; they weaken or abolish viral activity.
Clinical Context: A polyene antibiotic produced by a strain of S nodosus, this drug can be fungistatic or fungicidal. It binds to sterols, such as ergosterol, in the fungal cell membrane, causing intracellular components to leak with subsequent fungal cell death. The drug is used to treat severe systemic infection and meningitis caused by susceptible fungi (i.e., C albicans, H capsulatum, C neoformans). It is also available in liposomal (AmBisome) and lipid-complex (Abelcet) formulations. Amphotericin B does not penetrate the CSF well. Intrathecal amphotericin may be needed in addition.
Clinical Context: This agent is amphotericin B in phospholipid complexed form; it is a polyene antibiotic with poor oral availability. Amphotericin B is produced by a strain of Streptomyces nodosus; it can be fungistatic or fungicidal. The drug binds to sterols (e.g., ergosterol) in the fungal cell membrane, causing leakage of intracellular components and fungal cell death. Toxicity to human cells may occur via this same mechanism.
Clinical Context: Flucytosine is converted to fluorouracil after penetrating fungal cells and inhibits RNA and protein synthesis. It is active against candidal and cryptococcal species and is used in combination with amphotericin B.
Clinical Context: Fluconazole has fungistatic activity. It is a synthetic PO antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular membranes.
These agents are used in the management of infectious diseases caused by fungi.
Clinical Context: Rifampin is used in combination with other antituberculous drugs. It inhibits DNA-dependent bacterial, but not mammalian, RNA polymerase. Cross-resistance may occur
Clinical Context: Isoniazid is a first-line antituberculous drug that is used in combination with other antituberculous drugs to treat meningitis. It is usually administered for at least 12-24 months. A prophylactic dose of pyridoxine (6-50 mg/day) is recommended if peripheral neuropathies secondary to isoniazid therapy develop.
Clinical Context: Pyrazinamide is a pyrazine analog of nicotinamide; it may be bacteriostatic or bactericidal against M tuberculosis, depending on the drug concentration attained at the site of infection. Pyrazinamide's mechanism of action is unknown.
These agents are used in the management of mycobacterial disease in combination with other antitubercular agents.
Clinical Context: Dexamethasone has many pharmacologic benefits such as stabilizing cell and lysosomal membranes. It increases surfactant synthesis, increases serum vitamin A concentrations, inhibits prostaglandin and proinflammatory cytokines (e.g., TNF-alpha, IL-6, IL-2, and IFN-gamma). The timing of dexamethasone administration is crucial. If used, it should be administered before or with the first dose of antibacterial therapy. This is to counteract the initial inflammatory burst consequent to antibiotic-mediated bacterial killing. A more intense inflammatory reaction has been documented following the massive bacterial killing induced by antibiotics.
Clinical Context: Prednisone is an immunosuppressant used for treatment of autoimmune disorders; it may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. It stabilizes lysosomal membranes and suppresses lymphocyte and antibody production.
The use of steroids has been shown to improve the overall outcome of patients with certain types of bacterial meningitis, such as H influenzae, tuberculous, and pneumococcal meningitis. In general, corticosteroids are avoided but occasionally, glucocorticoids, such as dexamethasone, are useful when meningitis is associated with signs of increased intracranial pressure. If steroids are given, they should be administered prior to or during the administration of antimicrobial therapy. Meningitis from Vogt-Koyanagi-Harada syndrome responds to prednisone in moderate to high doses.
Clinical Context: Phenytoin works on the motor cortex, where it may inhibit the spread of seizure activity. The activity of brain stem centers responsible for the tonic phase of grand mal seizures may also be inhibited. Doses should be individualized. Doses of 15 mg/kg have been used.
Clinical Context: Phenobarbital elevates the seizure threshold, limits the spread of seizure activity, and is a sedative. Doses of 5-10 mg/kg have been recommended.
Anticonvulsants help to aggressively control seizures if present in acute meningitis, because seizure activity increases intracranial pressure.
Clinical Context: Acetaminophen is the drug of choice for managing pain or fever in patients who have documented hypersensitivity to aspirin or NSAIDs, who have upper gastrointestinal (GI) disease, or who are taking oral anticoagulants.
Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain.