Unipen

Patients with markedly altered mental status and neurologic deficit are commonly encountered by primary care physicians. The underlying etiologies of altered mental status are often associated with significant morbidity and mortality, and patients with new-onset altered mental status or neurologic deficit require a complete and rapid evaluation.

Initial Evaluation and Management

Since cardiopulmonary stabilization is the first priority in emergency management, the initial evaluation should begin with an assessment of airway, breathing and circulatory status (the "ABCs"). It is occasionally necessary to intubate patients with altered mental status before it is safe to continue the evaluative process. Several methods of achieving endotracheal intubation are available to the physician. Rapid sequence intubation with paralytic agents has become a popular method of accomplishing endotracheal intubation.[1] With proper education and training, physicians can use this method to facilitate safe and expeditious intubation. Rapid sequence intubation reduces the increase in gastric, ocular and intracranial pressure caused by intubation; it makes intubation easier by decreasing muscular resistance, and it decreases the risk of aspiration.[2] Table 1 lists the general steps in preparing a patient for rapid sequence intubation.

TABLE 1

Rapid Sequence Intubation Protocol

There are several antidotes for specific ingestions, and these may be required for hemodynamic stabilization. Table 3 lists several of these antidotes.[6]

Central Nervous System Infections

Several types of central nervous system infections may cause altered mental status, including bacterial meningitis and, less frequently, cerebral abscess, subdural empyema and encephalitis.

BACTERIAL MENINGITIS

The etiology of meningitis varies among different age groups.[15,16] During the neonatal period, Escherichia coli, Klebsiella pneumoniae and group B streptococcus predominate; Listeria monocytogenes is also an important pathogen. Streptococcus pneumoniae and Neisseria meningitidis are the predominant pathogens in older infants and young children, with the incidence of cases due to Haemophilus influenzae type b being markedly reduced since the introduction of an effective vaccine (Hibtiter, Pedvaxhib, Prohibit) several years ago. Adults are also affected primarily by S. pneumoniae and N. meningitidis; however, organisms such as Staphylococcus aureus, viridans streptococci, E. coli and K. pneumoniae are also responsible in certain situations.

Antibiotic therapy should not be withheld pending lumbar puncture in patients who are comatose, obtunded or in septic shock. Ampicillin and ceftriaxone (Rocephin) provide good initial antibiotic coverage in patients with suspected meningitis until cerebrospinal fluid can be obtained for Gram stain and culture. Vancomycin (Vancocin, Vancoled) should also be used in areas where drug-resistant S. pneumoniae is prevalent. Antibiotics are then tailored to the specific organisms recovered. Two sets of blood cultures should also be obtained. Cerebral CT scans are obtained to exclude cerebral edema or mass lesions in adult patients with suspected meningitis before performing lumbar punctures. Cerebrospinal fluid is sent for Gram stain, blood cell count determination with differential, and determination of glucose and protein. In patients who have been treated recently with antibiotics, sterile cerebrospinal fluid cultures may confound the diagnosis of bacterial meningitis and, in these patients, it is probably safest to continue an antibiotic regimen for 10 to 14 days.[16]

Although dexamethasone (Decadron, Dexameth, Dexone) administration has been shown to decrease deafness among children with meningitis caused by H. influenzae,[17] the marked decline in the prevalence of this organism since the advent of the Haemophilus b conjugate vaccine, combined with the lack of evidence that steroids are beneficial in adults, suggests a limited role for dexamethasone in the treatment of meningitis at present.[16,18]

CEREBRAL ABSCESS

Brain abscesses may arise following open skull trauma, meningitis or bacteremia, or they may result from the direct spread of infection from the ears, sinuses, teeth or facial skin.19 In addition, lesions may be metastatic as a result of endocarditis, sepsis or congenital heart disease. Anaerobic bacteria are important pathogens in brain abscesses.[20] The typical organisms recovered from cerebral abscesses are those reflecting the more common etiologies such as sinusitis, otitis media and dental infections.[19] These organisms include S. pneumoniae, H. influenzae, Moraxella catarrhalis, group A streptococci and anaerobes. S. aureus may also be involved in chronic sinusitis.

The most frequent presentations include headache, fever, vomiting and, occasionally, obtusion, seizure and hemiparesis.[19,20] Symptoms may persist for weeks before diagnosis.[20] Cerebral CT with contrast is used to make the diagnosis, and CT can provide evidence of mass effect, edema and the possible source of the abscess, such as sinusitis.[16] Because of the risk of herniation and because it offers no useful information once the diagnosis of abscess is made, lumbar puncture should not be performed in patients with a cerebral abscess.[20]

Initial antibiotic therapy must be broad, and a combination of penicillin, a third-generation cephalosporin and metronidazole (Flagyl) is a good empiric choice.[19] Generally, four to six weeks of intravenous antibiotic therapy are required for resolution of the infection.[16,19] Often, surgical drainage of the lesion and culture of the aspirated fluid are necessary for complete recovery.[20]

SUBDURAL EMPYEMA

Subdural space purulent collections generally arise from the same processes involved in the formation of cerebral abscesses.[15,16] Therefore, the responsible organisms include S. aureus, streptococci, H. influenzae and anaerobes. Subdural empyema can be difficult to diagnose. These lesions may be very large but not very thick, so they may be missed on routine CT scanning. MRI is diagnostically superior to CT in locating these lesions.[16]

Initial management includes antibiotic therapy with a third-generation cephalosporin, nafcillin (Nafcil, Nallpen, Unipen) and metronidazole. Immediate neurosurgical consultation is required, as the mass effect by these collections necessitates evacuation.[15] Lumbar puncture is again contraindicated because of the possibility of herniation and because of its limited diagnostic utility in this setting.[16]

VIRAL ENCEPHALITIS

Inflammation of the cerebral tissue may occur after infection with several different types of viruses, notably, herpes simplex virus and arboviruses.[15,16] On occasion, no etiology is ever determined. Fever, headache and confusion are the typical presenting features.[15] Speech, along with hand and facial function, may be affected in patients with herpes simplex virus infection, since the organism has a predilection for the temporal lobes. CT scanning with contrast may reveal uptake in the temporal lobe. A 14-day course of acyclovir (Zovirax) is indicated in patients with suspected herpes simplex virus encephalitis; this treatment has reduced mortality by 30 percent.[15,16] Arboviral illnesses tend to occur in the summer and fall, and may occur in epidemics. Treatment is supportive in these patients.[15]

REFERENCES

[1.] Walls RM. Rapid-sequence intubation in head trauma. Ann Emerg Med 1993;22:1008-13.

[2.] Walker LA. Using rapid sequence intubation to facilitate tracheal intubation. Emerg Med Rep 1993; 14:125-32.

[3.] Elliott SE, Wang RY. Toxicologic syndromes in the elderly: recognition and management of drug-related adverse events. Emerg Med Rep 1995; 16:49-58.

[4.] Pond SM, Lewis-Driver DJ, Williams GM, Green AC, Stevenson NW. Gastric emptying in acute overdose: a prospective randomised controlled trial. Med J Aust 1995;163:345-9.

[5.] Perrone J, Hoffman RS, Goldfrank LR. Special considerations in gastrointestinal decontamination. Emerg Med Clin North Am 1994;12:285-99.

[6.] Ellenhorn MJ, Barceloux DG. Medical toxicology: diagnosis and treatment of human poisoning. New York: Elsevier, 1988:75-82.

[7.] Wisner DH, Victor NS, Holcroft JW. Priorities in the management of multiple trauma: intracranial versus intra-abdominal injury. J Trauma 1993;35: 271-6.

[8.] Lehman LB. Intracranial pressure monitoring and treatment: a contemporary view. Ann Emerg Med 1990;19:295-303.

[9.] White RJ, Likavec MJ. The diagnosis and initial management of head injury. N Engl J Med 1992; 327:1507-11.

[10.] Kwan AL, Howng SL, Sun ZM, Lin CN. Delayed onset of traumatic epidural hematoma. Kao Hsiung I Hsueh Ko Hsueh Tsa Chih 1989;5:683-7.

[11.] Rappaport ZH, Shaked I, Tadmor R. Delayed epidural hematoma demonstrated by computed tomography: case report. Neurosurgery 1982;10: 487-9.

[12.] Smucker WD, Disabato JA, Krishen AE. Systematic approach to diagnosis and initial management of stroke. Am Fam Physician 1995;52:225-34.

[13.] Humphrey PR. Management of transient ischaemic attacks and stroke. Postgrad Med J 1995; 71:577-84.

[4.] Coull BM, Levine SR, Brey RL. The role of anti-phospholipid antibodies in stroke. Neurol Clin 1992;10:125-43.

[15.] Anderson M. Management of cerebral infection. J Neurol Neurosurg Psychiatry 1993;56:1243-58 [Published erratum appears in J Neurol Neurosurg Psychiatry 1994;58:877 and 1994;57:13021.

[16.] Luby JP. Infections of the central nervous system. Am J Med Sci 1992;304:379-91.

[17.] Wald ER, Kaplan SL, Mason EO jr, Sabo D, Ross L, Arditi M, et al. Dexamethasone therapy for children with bacterial meningitis. Meningitis Study Group. Pediatrics 1995;95:21-8.

[18.] Prober CG. The role of steroids in the management of children with bacterial meningitis. Pediatrics 1995;95:29-31.

[19.] Woods CR Jr. Brain abscess and other intracranial suppurative complications. Adv Pediatr Infect Dis 1995;10:41-79.

[20.] Yang SY, Zhao CS. Review of 140 patients with brain abscess. Surg Neurol 1993;39:290-6.

The Authors

PETER C. FERRERA, m.d. is attending physician at Albany (N.Y.) Medical Center. He graduated from the University of Vermont College of Medicine, Burlington, and completed a residency in emergency medicine at Albany Medical Center.

LISA CHAN, m.d. is currently attending physician and director of the emergency medicine clerkship for the medical students at Albany Medical Center. She graduated from State University of New York at Stony Brook and completed a residency in emergency medicine at Albany Medical Center.

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