ABBAS, FATIMAH FARMAILAH P January 21, 2021

NEUROLOGY MED-III

BLOOD AND CHOCOLATE

A 19-year-old female without known medical history was transported to our emergency
department because of coma.

She complained of fever over 39 °C and severe occipital headache the night before her
family found her unconscious. Physical examination revealed that her Glasgow coma scale was 6
(E1V1M4) with blood pressure of 128/72 mmHg, heart rate of 88 beats/min, and respiratory rate
of 19 breaths/min. Both pupils were 3.5 mm with a sluggish light reflex. Neurological examination
found no motor laterality or pathological reflex, except for nuchal rigidity.

A head CT scan revealed no focal region, but diffuse swelling of the brain. Her blood tests
showed elevated leukocytes (21,100 cells/μL) and C-reactive protein (20.6 mg/dL). A lumbar tap
was performed and turbid yellow spinal fluid was collected. Spinal fluid examination revealed
protein 394 mg/dl, glucose 0 mg/dl and a cell count of 10112/mm3 (96 % polymorphonuclear
leukocytes).

She was intubated and admitted to an intensive care unit. Due to poor study of the gram
staining, meropenem and vancomycin were administered right after IV dexamethasone. On day
8, N. meningitides was cultured from the spinal fluid collected on admission and antibiotic
therapy was changed to ampicillin. Brain MRI study was performed on day 10. Postcontrast T1-
weighted imaging showed enhanced subarachnoidal space of the cerebellum, typically along the
great horizontal fissure. Additionally, Diffusion-weighted imaging (DWI) found high intensity area
and SWI revealed multiple low-intensity spots in subarachoid space along the great horizontal
fissure. Since these spotty low-intensity areas in the cerebellum located nonlinearly and there
were no enhanced spots in the axial contrasted T1-weighted imaging, we confirmed that these
low-intensity signals were not telangiectasia, but microbleeds. Antibiotic management was
successful and her clinical symptoms improved. She was discharged on day 24 without
neurological deficits. A follow-up brain MRI was performed on day 42. SWI showed the regions
of multiple low-intensity spots in cerebellum persisted, but were disappearing. She had no
neurological deficits and complained no symptoms on day 42.
Brain magnetic resonance imaging of the patient. Postcontrast T1-weighted saggital and axial
imaging (a, b) showed enhancement in subarachoid space of cerebellum, typically in the great
horizontal fissure. Diffusion-weighted imaging (c) showed high-intensity area in the great
horizontal fissure. Susceptibility-weighted imaging (d) showed nonlinear multiple low intensity
spots. These multiple spots are not enhanced in axial postcontrast T1-weighted image (b). Follow
up MRI on day 42 showed that the multiple low-intensity spots persisted, but were disappearing
(e)
Clinical course of the case. The patient was managed successfully with antibiotics and
dexamethasone and discharged on day 24. MEPM, meropenem; VCM, vancomycin; TEIC,
teicoplanin; WBC, white blood cell; ICU, intensive care unit; ABPC, ampicillin
POINTS FOR DISCUSSION:

1. PROVIDE A CASE SUMMARY

A 19-year-old female without known medical history was transported to emergency department
because of coma. Blood tests have results of elevated leukocytes and C-reactive protein and
turbid yellow spinal fluid was collected on lumbar tap. Confirmation of the diagnosis of meningitis
was due to elevated protein levels and 0 mg/dl glucose with a cell count of 10112/mm3. Patient
was admitted to intensive care unit and were given Dexamethasone followed by meropenem and
vancomycin while causative agent was not established yet. After the spinal fluid collection, N. meningitides
was cultured and antibiotic therapy was changed to ampicillin. There was enhanced subarachnoid space of
cerebellum when postcontrast T1-weighted imaging was done and there was high intensity found on
diffusion-weighted imaging and multiple low-intensity areas in cerebellum or microbleed in susceptibility-
weighted imaging. The management done was successful that resulted in improved clinical
symptoms. No neurologic deficits were observed after day 24 so patient was discharged.

2. WHAT ARE THE SIGNS AND SYMPTOMS PRESENT IN THIS CASE POINTING TO A POSSIBLE
CNS INFECTION?
 Fever over 39 °C
 Severe occipital headache
 Unconscious the night before admission
 Leukocytes = 21,100 cells/μl
 C-reactive protein = 20.6 mg/dl
 Turbid yellow spinal fluid on lumbar tap
 Protein 394 mg/dl
 Glucose 0 mg/dl
 Cell count of 10112/mm3 (96 % polymorphonuclear leukocytes)

3. IN THIS CASE, IS IT POSSIBLE TO CLINICALLY DISTINGUISH MENINGITIS FROM

ENCEPHALITIS? PROVE YOUR POINT.

Encephalitis can mimic the clinical presentation of bacterial meningitis or vice versa.
Symptoms such as fever, headache, seizures and altered consciousness are nonspecific to
either diseases thus it is difficult to rely on clinical presentations only to clinically distinguish
encephalitis from meningitis especially this case is in the acute settings. In order to
distinguish both from each other, prompt investigations such as lumbar tap, neurologic
examination, blood tests, spinal fluid examination and imaging tests are done to establish
the diagnosis.
4. BASED ON YOUR READINGS, WHAT IS THE DIFFERENCE BETWEEN ENCEPHALOPATHY AND
ENCEPHALITIS?

Encephalopathy is a general term describing brain dysfunction that is diffuse, global or mutli-
focal or a damage or disease that affects the brain. There is a change in brain functions that
lead to an altered mental status and confusion. While encephalitis is a condition that refers
to inflammation of the brain that are caused either by infection, usually a virus. It is
presented by flu-like symptoms such as fever or headache, confusion, seizures or aphasia,
ataxia, involuntary movements and cranial nerve deficits.

5. BASED ON THE CLINICAL PRESENTATION, MAKE A LIST OF AT LEAST 5 CLOSEST

DIFFERENTIAL DIAGNOSIS AND PROVIDE RATIONALE FOR CHOSING SUCH

 HERPES SIMPLEX VIRUS ENCEPHALITIS

o it usually presents with fever, headache, focal neurologic deficits, altered
consciousness (dysphagia, hemiparesis) and focal or generalized seizures. The
CSF profile with this condition is a lymphocytic pleocytosis with a normal
glucose concentration, in contrast to the PMN pleocytosis and decreased
glucose level in meningitis.

 RICKETTSIAL DISEASE
o This disease may acutely present with high fever, prostration, myalgia,
headache, nausea, and vomiting but will develop rashes within 96h or the
onset of symptoms.

 EHRLICHIOSES
o Patients present with fever, headache, confusion, nausea and vomiting and
minority have a maculopapular or petechial rash. With laboratory
examination, leukopenia, thrombocytopenia, and anemia and mild to
moderate elevations in alanine aminotransferases, alkaline phosphatase and
lactate dehydrogenase are noted.

 SUBARACHNOID HEMORRHAGE
o Present with stiff neck and headache but without rash and fever

 SUBDURAL AND EPIDURAL EMPYEMA AND BRAIN ABSCESS

o It can be considered especially when neurologic findings are present.
6. MAKE A SIMPLE ALGORITHM REGARDING APPROACH TO THE CASE, FROM DIAGNOSIS TO
MANAGEMENT.

Suspected meningitis based on

history and examination

Rapid Physical Assessment

1. ABC
2. Level of consciousness

Initial Management
1. Obtain venous access
2. Cardiorespiratory monitoring
3. Laboratory examination
a. CBC with differential
b. Blood culture
c. Serum electrolytes, BUN,
creatinine, glucose, CRP

Start Empiric Therapy

(If causative agent is not identified)
(Dexamethasone & Antibiotics)

Lumbar puncture
Imaging Tests

CSF suggestive of
bacterial meningitis
YES NO

Start/Continue Empiric Therapy Continue Empiric therapy

(Dexamethasone & Antibiotics) and/or Reconsider Diagnosis

ALGORITHM OF SUSPECTED BACTERIAL MENINGITIS

7. WHAT ARE THE COMMON POSSIBLE COMPLICATIONS OF THIS CASE?

Possible complications includes involvement of intracranial vasculature (i.e. ischemic

infraction, sinus thrombosis and hemorrhagic complications) and microbleed although it is
rarely identified as a complication.

8. WHAT IS THE PROGNOSIS?

This case was reported as bacterial meningitis due to N. meningitides. The disease was
diagnosed early and early treatment and management was successful with improvement of
clinical symptoms. So for this case, the prognosis is good.

9. BONUS POINT: GUESS THE REASON FOR THE TITLE OF THIS CASE.

It is titled Blood and Chocolate since the causative agent, N. meningitides, can grow both in
a blood agar plate (BAP) and a chocolate agar plate (CAP)