Noon conference talk by Mathini Mohanachandran

1. Noon Conference
7/9/18

3. Defining terms
 Encephalopathy- global cerebral dysfunction

4. The Rational Clinical Examination
Copyright © American Medical Association. All rights reserved. | JAMA | McGraw-Hill Education
©©
Delirium – Key Features
 Acute onset
 Fluctuating course
 Inattention
 Disorganized thinking
 Altered level of consciousness
 Disorientation
 Memory impairment
 Perceptual disturbances
 Decreased/increased psychomotor activity
 Disturbed sleep-wake cycle

5. Delirium
 Risk factors: Age, structural brain disease, sensory impairment
 Precipitating factors
 Sepsis
 CNS infections
 Medications
 Toxins
 Metabolic abnormalities
 Environment

6. The Rational Clinical Examination
Copyright © American Medical Association. All rights reserved. | JAMA | McGraw-Hill Education
©©
Bedside Tools – CAM
 4 features
1. Acute onset and fluctuating course
2. Inattention
3. Disorganized thinking
4. Altered level of consciousness
 Features 1 and 2 must be present and either 3 or 4 must be present
Confusion Assessment Method (CAM)

7. The Rational Clinical Examination
Copyright © American Medical Association. All rights reserved. | JAMA | McGraw-Hill Education
©©
Method
Examiner
Specialty Finding
LR+
(95% CI)
LR–
(95% CI)
Global
Attentiveness
Rating
Geriatrician > 7 cm
on scale
65
(9.3-458)
0.06
(0.01-0.38)
Confusion
Assessment
Method
Nurses Positive 7.3
(1.9-27)
0.08
(0.03-0.21)
Confusion
Assessment
Method
Physicians Positive 19
(6.7-51)
0.19
(0.13-0.27)
Mini-Mental
Status
Examination
Trained
research
psychologist
< 24
points
1.6
(1.2-2.0)
0.12
(0.04-0.38)
©

8. The Rational Clinical Examination
Copyright © American Medical Association. All rights reserved. | JAMA | McGraw-Hill Education
©©
Nomogram for Interpreting LR

9. Defining terms
 Encephalopathy- global cerebral dysfunction
 Delirium
 Encephalitis – infectious or post-infectious

10. VZV Encephalitis

11. Pathophysiology
 Following primary infection, herpes zoster virus latent in dorsal root,
autonomic and cranial nerve ganglia
 Following reactivation, virus travels back along nerve->redevelopment
of rash
 CNS
 Transaxonal spread v hematogenous
 Vasculopathy

12. Epidemiology
 Shingles- 4 cases /1000 people per year
 Meningoencephalitis- 0.5%
 Risk factors: age (>50), immunosuppression (malignancy, HIV,
immunosuppressive treatments)
-Up to 10 cases/1000 people per year for age >60 years

13. Clinical Presentation
 Rash- erythematous vesicles, typically 1-2 dermatomes

15. Clinical Presentation
 Rash- erythematous vesicles, typically 1-2 dermatomes
 Disseminated zoster- presenting in 3 or more dermatomes or
crossing midline
 Only present in 2/3 of CNS presentations of VZV infection
 CNS symptoms may present before or after the rash- days to weeks
 Encephalitis- altered cognition, seizures, focal neurological signs –
motor/sensory deficits

16. Diagnosis
 PCR
 Direct fluorescence antibody
 Viral culture
 Encephalitis
 CSF – normal WBC, elevated CSF/serum albumin levels
 May resemble viral meningitis if meningoencephalitis
 Positive PCR, positive antibodies
 PCR – negative within 1-3 weeks of onset of symptoms
 Imaging- typically clear
 -MRI- may have cortical and deep ischemic lesions

17. CSF
parameter
Opening
pressure
Leukocyte
count
Leukocyte
predominance
Glucose Protein
Viral
meningitis
≤250 mm
H2O
50-1000/µL Lymphocytes >45 mg/dL < 200 mg/dL
Bacterial
meningitis
200-500 mm
H2O
1000-
5000/µL
Neutrophils <40 mg/dL 100-500
mg/dL

18. Treatment/Prognosis
 Acyclovir 10-15 mg/kg q8hr x at least 14 days
 Up to 20% mortality
 Residual neurological deficits
 Cognitive slowing
 Impaired memory and executive function
 Behavioral changes

19. Delirium VZV encephalitis Bacterial meningitis
Pathophysiology Unknown-possibly impaired
higher order cortical
function
Reactivation of virus-
>retrograde movement
along axons-
>vasculopathy
Hematologic spread of
infection to meninges
Epidemiology/risk
factors
Age, structural brain
disease, precipitating
factor- sepsis
Age,
immunosuppression
Age,
immunosuppression,
recent surgery,
ventricular drains
Clinical presentation Acute, fluctuating,
inattention, disorganized
thinking
Rash (2/3 cases),
altered cognition,
sensory/motor deficits,
seizures
Fever, headache,
meningmus, altered
Diagnosis Clinical, CAM CSF PCR, antibodies CSF – elevated WBC,
protein, low glucose,
gram stain, culture
Treatment Treat underlying
precipitating factors,
nonpharmacologic
interventions, haloperidol
Acyclovir Ceftriaxone,
vancomycin ± ampicillin

20.  -Grahn A, Studahl M. Varicella-sozter infections of the central nervous system
– prognosis, diagnostics and treatment. J Infect. 2015 Sep;71(3):281-93.
 Nagel MA, Gliden D. Neurological complications of varicella zoster virus
reactivation. Curr Opin Neurol. 2014 Jun;27(3):356-60.
 Saylor D, Takur K, Venkatesan A. Acute encephalitis in the
immunocompromised individual. Curr Opin Infect Dis. 2015 Aug;28(4):330-6.