NEW ONSET FEVER AND SEIZURE

Sonya, Royd and Rick

Trigger 1

PC: 67 y.o. ♀ ϖ fever, seizures and altered

conciousness HPC:

Husband states she’s been ill for 2 days ϖ fever, headache,

fatigue. Morning, tried to wake, confused, incoherent, 2

x tonic-clonic seizures lasting 2-3mins. Occurred < 1hr ago

Has not regained normal mentation

Trigger 1

PMHx No seizures or headaches Nothing significant to report (NSTR)

PSHx NSTR

Meds HRT, Ca supp, paracetamol (during illness)

SHx Married, homemaker, 4 adult kids. 2 x glasses wine an evening

FHx IHD

Q1 How would you summarise the case thus far?

Q2 What is your differential diagnosis? (List at least three possibilities)

Q3 What signs would you look for on examination and laboratory tests will you order to aid in diagnosis?

Q4 Name the most common organisms responsible for bacterial meningitis in developed countries and the most common organisms in her age group, in children, in immunocompromised? Most common:

N. meningitidis, S. pneumoniae, H. influenzae Most common in elderly:

S. pneumoniae, L. monocytogenes Most common in healthy children:

N. meningitidis, S. pneumoniae Most common in neonates:

E. coli, group B streptococci Most common in adolescents/young adults:

N. meningitidis

Q5 Discuss the typical CSF findings in acute bacterial meningitis and four circumstances under which these typical CSF findings may be absent.

Typical: raised opening pressure; polymorphonuclear leukocytosis; decreased relative glucose; increased protein; Gram stain is often positive; culture is usually positive; latex agglutination can be positive

Generally dominated by PMNs, but can be dominated by lymphocytes

Atypical CSF results can occur if Early presentation Recent prior antibiotic therapy Partially-treated meningitis Neutropenia L. monocytogenes: lymphocytosis (not polymorphonuclear

leukocytosis) Tuberculous meningitis: mononuclear pleocytosis; hard to detect

acid-fast bacilli

Q6 Discuss the differences in clinical presentation of bacterial and viral meningitis.

Bacterial meningitis: fever + headache + nuchal rigidity (positive Kernig’s and Brudzinski’s signs) Also can have dec consciousness, seizures, raised

ICP, stroke Certain bacteria (esp N. meningitidis) can cause skin

manifestations (petechiae, purpura) Viral meningitis: fever + headache + signs of

meningeal irritation + inflammatory CSF profile Unlikely to have profoundly altered

consciousness

Trigger 2

Ex T 38.8 ̊C BP 110/70 HR 120 RR 20 No skin or nail lesions, CVS - no murmurs, Lungs clear, Abdomen soft, no organomegaly CNS: PERLA, moves eyes conjugately in all directions,

corneal reflexes present bilaterally, gag reflex intact Motor: moving all four limbs spontaneously Co-ordination: no tremor or nystagmus Reflexes : 2+ throughout. Babinski signs present

bilaterally Sensory: withdrawals all four limbs to touch

Trigger 2

Lumbar Puncture:

Opening pressure: 230mm H 2O (60 - 180 mm H 2O)

Appearance: cloudy

WBC: 100 cells/mm 3(<5) 65%lymphs, 25% PMNs, 10% monos

RBC: 100 cells/mm 3 (none - few)

Protein: 85mg/dL (15-40)

Glucose: 60mg/dL (50 - 70 ½ to 2/3 blood glucose level)

Q7 What is the most likely diagnosis? Why?

Viral encephalitis Febrile illness ϖ signs of meningitis (???) and altered

level of consciousness Pg 1155 of Kumar and Clark:

*some polymorphs may be seen in the early stages of viral meningitis and encephalitis.

~20% of pt’s ϖ encephalitis have sig. #’s of RBC’s in LP

Normal Viral Pyogenic Tuberculosis

Appearance Crystal Clear Clear/Turbid Turbid/Purulent

Turbid/Viscous

Mononuclear cells

<5/mm 3 10-100/mm 3 <50/mm 3 100-300/mm 3

Polymorph cells

Nil Nil* 200-300/mm 3

0-200/mm 3

Protein 0.2 - 0.4 g/L 0.4 – 0.8 g/L 0.5 - 2.0 g/L 0.5 – 3.0 g/L

Glucose 2/3 – ½ BGL > ½ BGL < ½ BGL < ½ BGL

Q8 What additional tests can be ordered to aid in diagnosis?

CT/MRI to determine extent of brain oedema

Polymerase Chain Reaction to determine virus Majority of cases remain undefined

EEG (slow wave changes) Viral serology (in blood and CSF) Brain biopsy (only occasionally required)

Q9 Discuss the aetiology, course, treatment, prognosis/complications of viral encephalitis.

Aetiology: The list is long and distinguished HSV-1, Arthropod borne/Arbovirus (West Nile (WNV), St Louis, Japanese encephalitis (JEV))

Course: Many mild ϖ recovery Otherwise, Sx develop over hrsdays. If recovery occurs, from coma = gradual days weeks.

Complete <1yr Treatment:

Empirically or known HSV: Aciclovir – Active form inhibits DNA polymerase. (Pg 687 R&D) aciclovir 10 mg/kg IV, 8-hourly for at least 14 days (adjust dose for renal function)

Tailored to the organism. Anticonvulsants for seizures. Supportive care for fluids and electrolytes, DIC, GIT bleed, cardioresp

monitoring and cerebral oedema. Prophylaxis: immunisation vs JEV and others. Hand washing. Caesarean. Mozzie control.

Prognosis: Related to age of patient (<5yo), agent (HSV) and level of consciousness at time of therapy. Diffuse cerebral oedema/ intractable seizures poor neurolgic recovery and ↑ risk of mortality HSV-1 = 19% (14%)mortality. Survivors: 42% severe sequelae, 46% no – minor seq. Self-limited seizure activity rapid recovery

Complications: Depends on the nasty Severe neurologic sequlae rare presentation Residual seizure disorder (epilepsy – HSV-1 = 24%/survivors) Neuropsychiatric (HSV-1 = 22%/survivors) Cognitive impairment, personality or behaviour change Blindness, Weakness Hyper/hypokinetic movt disorders: tremor, myoclonus, parkinsonism, paresis, ataxia