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 2 O ( mm H 2 O)  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 ( 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 NormalViralPyogenicTuberculosis AppearanceCrystal ClearClear/TurbidTurbid/PurulentTurbid/Viscous Mononuclear cells <5/mm /mm 3 <50/mm /mm 3 Polymorph cellsNilNil* /mm /mm 3 Protein g/L0.4 – 0.8 g/L g/L0.5 – 3.0 g/L Glucose2/3 – 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 hrs  days. 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