At the 7AM turnover, you are signed out a 22 y/o female who is ‘likely high on drugs’.
EMS notes they were called for altered mental status, and on their arrival she was disoriented and crying out, and they were having problems getting her to answer simple questions. She was in the upstairs bathroom, and there was a party going on downstairs. She denied any drug or alcohol ingestion, but they felt she was high on drugs based on ‘how she is acting’.
The previous doc notes the urine drug screen is pending. He notes she will answer questions, but not consistently. At times she just rocks back and forth and is very agitated, but then she goes to sleep. She is easily arousable. She has vomited several times. He is having a hard time getting a history from the patient, but her sister and boyfriend are in the room. The previous ED doctor did order some Ativan and Zofran.
After turnover, you approach the pateins room and find her sitting on a chair with her chest, head and arms on the cot, lights off, towel over her head. Her sister and boyfriend are in the room. Her sister tells you there was a party at their house, but the patient did not participate. She actually went to bed early, and then woke up once to come down stairs and ask them to turn the music down. About 1 hour later her boyfriend heard her moaning in the bathroom. She was vomiting and when he tried to talk to her, she couldn’t answer. “It’s like she was trying to say the words, but they wouldn’t come out!” he added. “I could tell she was really frustrated when she was trying to talk, then eventually she would scream in frustration.“
During your interview, she has no word finding problem, has clear speech, but speaks slowly. Previous to this morning she was fine, ROS (review of systems) negative prior to this AM. After the event in the bathroom, she seemed to have times when she could talk, and she complained of a headache and ‘not feeling right.’ She had vomited several times, no blood or coffee grounds. She notes the light bothers her, but other ROS negative. She denied any ingestion.
PMH: Vaginal infection on Metronidazole, no other medical problems. SH: Smoker, no drug or alcohol abuse, works in a shipping company.
PE: WDWN female, lying quietly half prone on the cot. A towel is over the top of her head. 100/60 HR=55 RR=18 Temp=98.4 Sat=98%
HEENT: Photophobia is noted, but pupils are round and reactive. She cannot tolerate a fundoscopic exam. Otherwise negative exam, neck supple
Heart/lung/abdomen/skin exam negative
Neurologic: Cranial nerves, motor, and sensory exam normal. Mental status: Oriented x 3, speech slow but clear. Gait wide based but Romberg negative. Finger to nose test is normal. Negative Kernigs and Brudzinski signs, Babinski downgoing, and slight hyperreflexia with 3 beats of clonus at ankle bilaterally.
Urine drug screen is negative. A CT scan is ordered along with a basic metabolic panel and CBC. Patient is more bradycardic with heart rate down to 38 at times (sinus bradycardia). Blood pressure occasionally dropping to systolic of 80, but responding to fluid bolus’s. Heart rate increases with stimulation of patient. CT and metabolic panel are normal. CBC shows WBC 13.9K (normal upper limit is 11.0K), along with mild anemia (Hbg=11.0).
1. How do you test for Kernigs and Brudzinski signs? How often is it positive in a patient with bacterial meningitis?
The Kernig sign is performed in a supine patient by flexing the hip to 90° while the knee is flexed at 90°. Then an attempt to further extend the knee produces pain in the hamstrings and resistance to further extension. The Brudzinski sign is performed by passively flexing the neck while the patient is in a supine position with extremities extended. If this maneuver produces flexion of the hips then the Brudzinski sign is positive and the patient has meningeal irritation. One source estimated approximately 50% of adults with bacterial meningitis will show signs of meningeal irritation such as nuchal rigidity and/or positive Kernig and Brudzinski sign. (1)
2. How specific is the triad of fever, headache, and altered mental status for bacterial meningitis?
According to one source, 85% of adults and children with bacterial meningitis will have the classic triad.(2) Fever is the most common (95%).(2) Although the specificity of this triad is poor, the negative predictive value of these symptoms is high (absence of fever, neck stiffness, OR altered mental status eliminates the diagnosis in 99% of cases).(3)
3. Which organisms causing pediatric bacterial meningitis have the highest mortality rate?
The overall mortality rate for pediatric meningitis is 5-10%, and varies based on age of the patient (neonatal meningitis mortality higher than older children). Past the neonatal age, S pneumonia has the highest mortality rate (26-30%), with H influenza type B next at 7.7-10% and N meningitides has the lowest mortality rate at 3.5-10%. (4) Prior to this case, I had assumed it was N. meningitides.
4. How often will a patient with elevated intracranial pressure have papilledema?
Papilledema takes hours to develop, and may only be present in 1/3 of patients with elevated ICP (intracranial pressure).
5. What organisms cause viral meningitis?
In approximately 1/3 of meningitis cases, no virus is identified.(5) Of the virus’s that are identified, more than 85% of viral meningitis cases are caused by non-polio enteroviruses (echovirus, coxsackievirus, and others).(5) These virus’s usually enter the host via a fecal/oral route but can enter through a respiratory route. Associated clinical findings in these infections include pharyngitis, pleurodynia, rash and pericarditis.
Arboviruses account for another 5% I North America (5). They are ‘ARthropod-BOrne’ or in other words, blood sucking arthropods (usually mosquitoes) are the vectors for transmission. Seizures are more common with arboviral meningitis, compared to other viruses. St. Louis encephalitis virus is the most common cause of arboviral meningitis in the USA.
The herpes virus causes another 4% of infections. When associated with encephalitis, the mortality rate can be as high as 70% in untreated patients and 6-11% in those treated with acyclovir. In treated surviving patients with Herpes encephalitis, 38% have no or only mild neurologic deficits, 9% have moderate and 53% have severe deficits! (6)
Outcome:
Patient had LP performed after CT was unremarkable. CSF showed 0 RBC, 248 WBC (98% lymphs), Glucose 62 mg/dl, Total Protein 80 mg/dl. CBC revealed a WBC count of 12.7K. Patient was started on Acyclovir, Vancomycin and Ceftriaxone in the ED and admitted. Cultures, gram stain, and viral markers all negative. Symptoms (bradycardia, headache, photophobia, vomiting, gait problem, speech problem) improved over 12 hours after starting medications. Acyclovir and antibiotics were stopped the next morning when all tests were negative (WBC ct normalized) and patient discharged with diagnosis of aseptic meningitis. She returned 3 days later with a similar presentation (speech and gait problem, headache, vomiting and photophobia, and was again bradycardic with an elevated WBC at 14K), LP at that time revealed 275 WBC, all lymphocytes. Acyclovir was restarted, and symptoms resolved over 12 hours. WBC normalized. All repeat tests on CSF revealed no identifiable cause for the meningo-encephalitis. Acyclovir was stopped and patient discharged. She returned again 3 days later with the exact same presentation. Acyclovir was not started and she was watched for 12 hours with no improvement in her symptoms. After 12 hours of continued symptoms, and because of persistent sinus bradycardia to the 30’s with occasional hypotension, she was restarted on Acyclovir and after 12 hours symptoms were again resolved, and WBC ct normalized next day. This time patient was discharged with 21 days of acyclovir IV, and recovered uneventfully.
Although it’s not clear exactly what virus was causing her meningo-encephalitis, clearly it responded to acyclovir. She has no neurologic deficits on follow up.
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References:
1. Moses S. Meningitis: acute bacterial meningitis. Accessed February 8, 2011. Available at http://www.fpnotebook.com/neuro/ID/Mngts.htm.
2. Scheld WM, Koedel U, Nathan B, Pfister HW. Pathophysiology of Bacterial Meningitis: Mechanism(s) of Neuronal Injury. J Infect Dis. Dec 1 2002;186 Suppl 2:S225-33.
3. Fazonable R, Cavaliere R, Cuna B. Meningitis. Emedicine Jul 7, 2011. Accessed at: http://emedicine.medscape.com/article/232915-clinical
4. Hom J, Felter RA, Bachur R. Pediatric Meningitis and Encephalitis, Emedicine. April 19, 2011. Accessed at: Moses S. Meningitis: Acute Bacterial Meningitis. Accessed February 8, 2011. http://emedicine.medscape.com/article/802760-overview#showall
5. Wan C, Vokshoor A. Viral Meningitis, Emedicine Mar 29, 2011. Accessed at: http://emedicine.medscape.com/article/1168529-overview#showall
6. Anderson WE, Herpes Simplex Encephalitis, Emedicine Jun 17, 2011, accessed at: http://emedicine.medscape.com/article/1165183-clinical#showall