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Bacterial Meningitis A Case presentation for the requirement of Internal Medicine Residency Training

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“Brain under Siege: The Dangers of Traumatic Brain infections” Dr. Don Jayric V. Depalobos 2nd Year Internal Medicine Resident Ospital Ng Palawan Subspecialty Conference on Infectious Diseases
OBJECTIVES To present a case of a 21/M who was brought due to upward rolling of eyeballs and stiffening of extremities with associated headache, and fever To discuss approach to patient presenting with upward rolling of eyeballs and stiffening of extremities with associated headache, and fever To Identify treatment and management algorithms for patients with the said condition
CASE PRESENTATION 01 COURSE IN THE WARD 02 DISCUSSION AND CONCETP MAP 03 ASSESSMENT AND DIFFERENTIAL DIAGNOSIS 04 TAKE AWAY 05 REFERENCES 06 TABLE OF CONTENTS
CASE PRESENTATION J.G. 21/M Single Sta Monica, PPPC Admitted on February 7, 2025 Informant: Father 85% Reliability Chief Complaint: (+) Stiffening of extremities and upward rolling of eyeballs
HISTORY OF PRESENT ILLNESS (+) Increasing severity of headache (+) Fever (+)Decrease d sensorium (+)headache Sought consult at BDH Started Ceftriaxone 2gm IV Mannitol 100cc IV Paracetamol 600mg IV (+) Stiffening of extremities and upward rolling of eyeballs No consult done. No meds taken. 3 days pta 1 day pta Few hours pta
Past Medical History (+) MVA Oct 2024 sustained frontal bone fracture (+) Primary Complex Personal/ Social History 2.5 pack year smoker Occasional Alcoholic Beverage drinker Family Medical History (+)HPN – Both sides Vaccination History (+) COVID Vaccination Childhood vaccination was given but unrecalled if completed A C B D
PHYSICAL EXAMINATION Vital Signs: Vital Signs: BP 110/80 HR 65 RR 22 T 37.8 C Spo2 95% at 2lpm NC General Status: Awake, GCS 9 (E2V2M5), in mild respiratory distress. Confused, weak-looking. Head and Neck: (+) Nuchal Rigidity, (+) Kernig’s Sign, (-) Brudzinski Sign; No visible or palpable masses, depressions, or scarring. Hair is of normal texture and evenly distributed. No neck vein distention Non-erythematous, not enlarged tonsils EENT: (+) Preferential Gaze (Right); (+) Horizontal nystagmus; pink conjunctivae, Anicteric, Pink Palpebral Conjunctiva, No CLAD, No nystagmus Pupils equally reactive to light at 5mm, OU Fundoscopy: No papilledema
PHYSICAL EXAMINATION Chest and Lungs: Symmetrical Chest Wall Expansion, Clear Breath Sounds Cardiac: External chest is normal in appearance without lifts, heaves, or thrills. PMI is not visible and is palpated in the 5th intercostal space at the midclavicular line. Normal rate with normal rhythm. No murmurs, gallops, or rubs are auscultated. Abdomen: There are no visible lesions or scars. Umbilicus is normal without herniation. Bowel sounds are present and normoactive. Soft, symmetric, and non-tender without distention. No masses, hepatomegaly, or splenomegaly are noted.
PHYSICAL EXAMINATION Genitourinary: no masses or lesions noted. Skin and Extremities: No gross deformities noted on upper and lower extremities. Good and equal pulses, no tremors, no limitations on range of motions noted. Nails without wounds or lesions, Capillary refill time of <2s. Neurologic: CN are intact. No Brudzinski. (+) Kernig. (+) Nuchal Rigidity
PHYSICAL EXAMINATION Constitutional: generalized body malaise, (+)fever HEENT: No sore throat Skin: No caput medusae. No telangiectasia. (+) Bruises on IV insertion and injection sites Cardiovascular: (-)Palpitations, (-)Easy Fatigability Respiratory: Shortness of breath Gastrointestinal: no changes in bowel movement Genitourinary: no dysuria, flank pains, change in urination Neurologic: no sensory deficits or motor deficits
Initial Impression CNS Infection probably Bacterial secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess
Patient J.G. 21/M HEADACHE FEVER NUCHAL RIGIDITY and KERNIG’S SIGN HISTORY OF TRAUMA SEIZURES SENSORIUM CHANGES
DIFFERENTIAL DIAGNOSES Meningitis (Bacterial Vs Viral) Encephalitis Intracranial Mass Brain Abscess Cerebrovascular Disease
DIFFERENTIAL DIAGNOSES Differential Rule In Rule Out Meningitis Fever Headache Generalized body weakness/Prostration Drowsiness No focal deficit Neck Stiffness Kernig’s Altered Mental Status Cannot totally rule out Encephalitis Fever Altered Mental Status Cannot totally Rule Out Neck Stiffness Headache focal or diffuse neurologic signs and symptoms Intracranial Mass/Cerebral Abscess Headache Drowsiness Fever No neurologic deficit, usually unipolar unless massive/equal* CVA Headache Drowsiness No neurologic deficit, usually unipolar unless massive/equal*
DIFFERENTIAL DIAGNOSES
COURSE IN THE WARD
Admission Day (ER) (February 6, 2025) Subjective Objective Assessment Plan Headache 9/10 Changes in behavior Awake GCS 9 (E2V2M5) Vital Signs: BP 120/90 HR 82 RR 20 T 38 Spo2 99% at 3lpm Pupils equally reactive to light at 5mm, OU Preferential gaze Nuchal Rigidity SCWE CBS AP NRRR Soft nontender abdomen FEP no edema <2s CRT CNS Infection probably Bacterial secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess; MVA Self crash with Multiple Skull Fracture Oct 2024 Diet: OF 1,400 kcal in 6 divided feedings IVF: PNSS 1L x 100cc/hour Diagnostics: RBS CBC Na K Crea BUN, Chest Xray, Cranial Ct Scan with Contrast 12 Lead ECG, UA Plain Cranial CT Scan was done outside Therapeutics: Ceftriaxone 2gm IV q12 Mannitol 100cc IV q6 Diazepam 5mg IV PRN for frank seizures Paracetamol 300mg IV q4 PRN O2 at 2-3lpm via NC IFC Inserted NGT Inserted Vital Signs q2 Neuro Vital Signs q2 I&O q shift
Admission Day (WARD) (February 7, 2025) Subjective Objective Assessment Plan Headache 9/10 Changes in behavior Awake GCS 9 (E2V2M5) Vital Signs: BP 110/80 HR 65 RR 22 T 37.8 Spo2 95% at 3lpm Pupils equally reactive to light at 5mm, OU Preferential gaze Nuchal Rigidity SCWE CBS AP NRRR Soft nontender abdomen FEP no edema <2s CRT CNS Infection probably Bacterial secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess; MVA Self crash with Multiple Skull Fracture Oct 2024 Diet: OF 1,400 kcal in 6 divided feedings IVF: PNSS 1L x 100cc/hour Additional Diagnostics: Blood Culture x 2 sites Procalcitonin iCa, Mg, FBS CBG q6 CSF Analysis/Lumbar Tap Contrast-enhanced Cranial CT Scan Therapeutics: Vancomycin 1gm + 100cc PNSS IV to run for 4 hours q12 Dexamethasone 10mg IV q6 x 4 days Omeprazole 40mg IV q12 Father apprised of Pt’s condition and prognosis Referred to IDS Service LDH, BSMP, Dengue Duo, ABG CSF Fluid Gene Xpert
CBC 02/06 02/11 Hgb 158 130 Hct 49.7 40.4 RBC 6.0 5.1 WBC 37.1 7.1 Platelet 297 296 Segmenters 85 58.4 Lymphocytes 2.1 16.6 Monocytes 6.2 10.1 Eosinophils 1.5 12.3 Basophils 0.0 0.2 MCV 82.5 78.6 MCH 26.1 25.3 MCHC 31.7 32.2 MPV 7.5 82. RDW-SD 45.6 39.6 RDW-CV 15.3 15.5 Chem 02/06 02/08 02/11 02/14 Na 137.8 152.6 143.9 K 3.88 4.10 3.99 Crea 90.5 55 35 BUN 5.88 4.24 1.85 eGFR Procalcitonin 45.69 D2 Abx 7.159 D5 Abx 0.777 D8 Abx RBS 131 iCa 0.84 Mg 1.16 SGPT 10.3 SGOT 20.6 LDH 187 PT 17.8 INR 1.43 BSMP NMPS
Skull Xray PA 2/7/25 Findings: A depressed fracture is seen involving the midline frontal bones with overlying soft tissue swelling. The rest of the calvarium is normal with symmetrical appearance. Impression: Depressed Fracture is seen involving the midline frontal Chest Xray PA 2/7/25 Findings: Bilateral Hilar fullness with accentuation of bronchovascular markings is noted. The rest of the lungs show no active parenchymal opacities. The heart is not enlarged. The diaphragm, sulci, and bony thorax are intact. Impression: Signs of Pulmonary Congestion. Intercurrent Pneumonia is not ruled out.
12 Lead ECG 02/06/2025 Rate 65 Regular Sinus Rhythm No Chamber enlargement No axis deviation Normal Sinus Rhythm
Contrast-enhanced Cranial CT Scan 02/07/2025
02/13 CSF Gene Xpert (2/12/25) MTB not detected Gram Stain (02/08/25) Organism: Gram (+) Cocci in Singles – Rare Epithelial: 0-1/LPO Pus Cells: 0-1/HPO Blood and SCF Culture No Growth CSF Cell Count WBC 0.80 cells/cu mm CSF Differential Count PMN 56% MNC 44% ABG 2/8/25 pH 7.56 CO2 18.5 O2 126.2 HCO3 17 Partially Compensated Respiratory Alkalosis with Overcorrected OXygenation
Hospital Day 1-3 (February 8-10, 2025) Subjective Objective Assessment Plan On/Off Headache 9/10 Changes in behavior (+)Nausea Ceftriaxone Day 3 Vancomycin Day 3 Awake GCS 14 (E4V4M6) Vital Signs: BP 110/60 HR 63 RR 22 T 36.1 Spo2 98% at 3lpm Pupils equally reactive to light at 5mm, OU Preferential gaze Nuchal Rigidity SCWE CBS AP NRRR Soft nontender abdomen FEP no edema <2s CRT iCa 0.84 Fundoscopy: pale pink 1.5mm disk with sharp flat margin. Cup is within the disk. Vessels are enlarged and prominent CNS Infection probably Bacterial secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess; MVA Self crash with Multiple Skull Fracture Oct 2024; Hypocalcemia Calcium Gluconate 10ml SIVP now Nimodipine 30mg tab 2 tabs q4 Metoclopramide 10mg SIVP q8 PRN Lumbar Tap was done IDS Rounds: Increase Mannitol to 150cc q4 For repeat Procalcitonin
CBC 02/06 02/11 Hgb 158 130 Hct 49.7 40.4 RBC 6.0 5.1 WBC 37.1 7.1 Platelet 297 296 Segmenters 85 58.4 Lymphocytes 2.1 16.6 Monocytes 6.2 10.1 Eosinophils 1.5 12.3 Basophils 0.0 0.2 MCV 82.5 78.6 MCH 26.1 25.3 MCHC 31.7 32.2 MPV 7.5 82. RDW-SD 45.6 39.6 RDW-CV 15.3 15.5 Chem 02/06 02/08 02/11 02/14 Na 137.8 152.6 143.9 K 3.88 4.10 3.99 Crea 90.5 55 35 BUN 5.88 4.24 1.85 eGFR Procalcitonin 45.69 D2 Abx 7.159 D5 Abx 0.777 D8 Abx RBS 131 iCa 0.84 Mg 1.16 SGPT 10.3 SGOT 20.6 LDH 187 PT 17.8 INR 1.43 BSMP NMPS
Hospital Day 5-7 (February 11-14, 2025) Subjective Objective Assessment Plan No nuchal Rigidity No Headache No fever Ceftriaxone Day 4 Vancomycin Day 4 Awake GCS 15 (E4V5M6) Vital Signs: BP 120/70 HR 58 RR 220 T 36.5 Spo2 98% at room air Pupils equally reactive to light at 5mm, OU SCWE CBS AP NRRR Soft nontender abdomen FEP no edema <2s CRT Procalcitonin 7.159 from 45 Bacterial Meningitis secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess; MVA Self crash with Multiple Skull Fracture Oct 2024 Titrate down Mannitol To Complete Antibiotics to 10 days
Hospital Day 8-12 (February 15-18, 2025) Subjective Objective Assessment Plan No nuchal Rigidity No Headache No fever Ceftriaxone Day 10 Vancomycin Day 10 Awake GCS 15 (E4V5M6) Vital Signs: BP 100/60 HR 67 RR 21 T 36.7 Spo2 98% at room air Pupils equally reactive to light at 5mm, OU SCWE CBS AP NRRR Soft nontender abdomen FEP no edema <2s CRT Procalcitonin 0.77 from 7,159 CNS Infection probably Bacterial secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess; MVA Self crash with Multiple Skull Fracture Oct 2024 Titrate down Mannitol To Complete Antibiotics to 10 days Patient was then sent home Improved Home Meds: Clindamycin
Final Diagnosis Bacterial Meningitis secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident
Bacterial Meningitis Bacterial meningitis is an acute purulent infection within the sub- arachnoid space (SAS). It is associated with a CNS inflammatory reaction that may result in decreased consciousness, seizures, raised intracranial pressure (ICP), and stroke. The meninges, SAS, and brain parenchyma are all frequently involved in the inflammatory reaction (meningoencephalitis). Harrison’s Principles of Internal Medicine 21st Edit
Bacterial meningitis is the most common form of suppurative CNS infection, with an annual incidence in the United States of >2.5 cases/100,000 population. • Streptococcus pneumoniae (~50%) • Neisseria meningitidis (~25%) • Group B streptococci (~15%) • Listeria monocytogenes (~10%) • Haemophilus influenzae type b accounts for <10% of cases of bacterial meningitis in most series. • N. meningitidis is the causative organism of recurring epidemics of men- ingitis every 8–12 years. Epidemiology Harrison’s Principles of Internal Medicine 21st Edit
In 1999, the CNS Infection Council of the Philippine Neurological Association did a study to determine the spectrum of CNS infections seen in this country by combining the census of all the neurology training institutions. Epidemiology The PCP Textbook of Internal Medicine 1st Edition
1. Bacterial or Pyogenic 2. Tuberculous 3. Viral 4. Fungal (mostly cryptococcal) A. Acute - Less than a week B. Sub-Acute – 1-2 weeks C. Chronic – More then 2 weeks Major Types of Meningitis The PCP Textbook of Internal Medicine 1st Edition
Approach to Suspected Meningitis 1. Is this Meningitis or Encephalitis? Meningitis - fever, headache, neck rigidity, no focal signs, relative preservation of mentation or consciousness. "Patient can relate to you his history" (Proceed to #2) Encephalitis - fever + (mental, behavioral or sensorial change), the latter occurring at the onset of the illness, acute course (Proceed to # 4)
Approach to Suspected Meningitis 2. If this is a meningitic syndrome, classify according to acute, subacute, or chronic. Acute: < 1 week course Subacute: 1 to 2 weeks Chronic: > 2 weeks
Approach to Suspected Meningitis 3. What major type of meningitis would it likely be? If acute - bacterial or viral If chronic - TB or fungal If subacute - consider all 4
Approach to Suspected Meningitis 4. Look for the following before doing an LP - focal signs, papilledema, signs of herniation.
Approach to Suspected Meningitis Recommended criteria for adult patients with suspected bacterial meningitis who should undergo CT prior to lumbar puncture
Approach to Suspected Meningitis 5. If any of the above are present, do first a CT scan or MRI to rule out a mass lesion. If none of the above are present, proceed with an LP. 6. If a mass lesion (e.g., abscess, tumor) is seen on neuroimaging, treat accordingly. Don't do a tap. 7. If no mass lesion is seen on CT or MRI, proceed with LP.
Approach to Suspected Meningitis 8. Lumbar puncture: Measure opening pressure. If > 300 mm H,0, run Mannitol first until pressure drops to at 300 mmH2O before withdrawing fluid. For adults, take 10 cc or more divided as follows: 1st bottle - 2 cc for protein and glucose 2nd bottle - 7 cc for microbiological studies. Reserve for Cryptococcal antigen latex agglutination test (CALAS) and other studies. To the sediment, do G/S, C/S, India ink smear, Saboraud's culture, TB culture. 3rd bottle - 1 cc - cell count with differential 4th bottle - 1 cc or more - for other studies as indicated by clinical suspicion (e.g., PCR for herpes, biofilm array for meningitis-en-cephalitis panel, etc) CSF lactate concentrations of >4.2 mmol/L were considered to be a positive discriminative factor for bacterial meningitis
Approach to Suspected Meningitis 9. Look at the routine CSF picture (WBC, differential, sugar, protein) to determine major type of meningitis one (bacterial, TB or fungal, viral)
Approach to Suspected Meningitis 10. If stains are positive, treat accordingly. Correlate with CSF picture. G/S: (+ ) for bacteria - start empiric treatment. India ink smear: round to oval organisms with a double refractile wall - treat for Cryptococcus. A (+) AFB smear from the CSP is extremely rare in the Philippine setting.
Approach to Suspected Meningitis On the basis of the available evidence on the use of adjunctive dexamethasone in adults, we recommend use of dexamethasone (0.15 mg/kg q6h for 2–4 days with the first dose administered 10–20 min before, or at least concomitant with, the first dose of antimicrobial therapy) in adults with suspected or proven pneumococcal meningitis (A-I). Infectious Disease Society of America (IDSA)
Approach to Suspected Meningitis 11. If CS picture is compatible with bacterial meningitis, and the stains are negative, treat empirically for bacterial meningitis. 12. If stains are negative, and CSF picture is compatible with TB or fungal meningitis, presume TB and treat as such. 13. If cryptococcal antigen latex agglutination system (CALAS) is (+), but India ink is (-) for cryptococcus, repeat tap the next day for India ink and CALAS because the test has a 10% false positivity rate. If CALAS is again (+) and India ink remains negative, one can treat presumptively as cryptococcal meningitis. If CALAS is negative, cryptococcal meningitis can virtually be ruled out (CALAS negative predictive value is 100% by the local validation study of the author), so long as the India ink stain and culture are negative.
Approach to Suspected Meningitis 14. When cultures show an isolate (bacteria, TB, cryptococcus), treat accordingly using drugs specific for the isolated etiologic organism and guided by sensitivity results.
Approach to Suspected Meningitis
Approach to Suspected Meningitis 15. If clinical and CS picture is compatible with viral meningitis, treat symptomatically. 16. If clinical diagnosis is ENCEPHALITIS the main task is to determine if this is HERPES SIMPLEX OR NON-HERPES SIMPLEX, because only the former (and possibly Varicella- zoster and Epstein-Barr) have been proven to be treatable.
Approach to Suspected Meningitis 17. Do LP for CSF analysis as for meningitis, but reserve at least 1 cc for Polymerase Chain Reaction (PCR) or biofilm array meningitis/ encephalitis panel for herpes and other viruses. 18. EEG, CT and MRI should be done as quickly as possible to detect focal abnormalities in the fronto-temporal lobes, which support a diagnosis of herpes simplex. a. EEG - periodic sharps or spikes from one or both frontal and/or temporal lobes. b. CT / MRI - focal abnormalities at the frontal, temporal or cingulate areas (MRI is more sensitive than CT).
Approach to Suspected Meningitis 19. If routine CS picture is compatible with a viral encephalitis and/or EEG and neuroimaging is/are suggestive of herpes, start presumptive treatment for herpes with IV acyclovir. 20. If PCR for herpes turns out negative, discontinue acyclovir unless zoster or EBV encephalitis is suspected, or EEG, CT or MRI shows focal abnormalities suggestive of herpes. Continuing with acyclovir therapy for herpes is an option despite absence of evidence for herpes if the clinician believes or wants to give the patient the potential benefit of acyclovir treatment. 21. For CMV-related CNS infections, ganciclovir and foscarnet may be tried. 22. For California encephalitis, adenovirus, rotavirus, LCMV and other arenavirus encephalitis: may try IV rivabirin.
Diagnosis of Bacterial Meningitis The classic CSF abnormalities in bacterial meningitis are: (1) Polymorphonuclear (PMN) leukocytosis (>100 cells/μL in 90%) (2) Decreased glucose concentration (<2.2 mmol/L [<40 mg/dL] and/or CSF/serum glucose ratio of <0.4 in ~60%) (3) Increased protein concentration (>0.45 g/L [>45 mg/dL] in 90%), (4) Increased opening pressure (>180 mmH2O in 90%). CSF bacterial cultures are positive in >70% of patients, and CSF Gram’s stain demonstrates organisms in >60%.
PATHOPHYSIOLOGY
Increased Intracranial Pressure Emergency treatment of increased ICP includes elevation of the patient’s head to 30–45°, intubation, and hyperventilation (PaCO2 25–30 mmHg), and mannitol. Patients with increased ICP should be managed in an intensive care unit; accurate ICP measurements are best obtained with an ICP monitoring device.
Increased Intracranial Pressure
PROGNOSIS Mortality Rate for Bacterial Meningitis: 3–7% for meningitis caused by H. influenzae, N. meningitidis, or group B streptococci; 15% for that due to L. monocytogenes; 20% for S. pneumoniae. In general, the risk of death from bacterial meningitis increases with (1) decreased level of consciousness on admission (2) onset of seizures within 24 h of admission (3) signs of increased ICP (4) young age (infancy) and age >50 (5) the presence of comorbid conditions including shock and/or the need for mechanical ventilation, (6) delay in the initiation of treatment. Decreased CSF glucose concentration (<2.2 mmol/L [<40 mg/dL]) and markedly increased CSF protein concentration (>3 g/L [> 300 mg/dL]) have been predictive of increased mortality and poorer outcomes in some series. Moderate or severe sequelae
CONCEPT MAP History of Trauma
TAKE AWAY… • Meningitis is a devastating disease with a high case fatality rate, which can lead to serious long-term complications (sequelae). • Meningitis remains a major global public-health challenge. • Many organisms can cause meningitis, including bacteria, viruses, fungi and parasites. • Bacterial meningitis is of particular concern. Around 1 in 6 people who get this type of meningitis die and 1 in 5 have severe complications. • Safe affordable vaccines are the most effective way to deliver long-lasting protection.
REFERENCES

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Bacterial Meningitis A Case presentation for the requirement of Internal Medicine Residency Training

  • 1.
    “Brain under Siege: TheDangers of Traumatic Brain infections” Dr. Don Jayric V. Depalobos 2nd Year Internal Medicine Resident Ospital Ng Palawan Subspecialty Conference on Infectious Diseases
  • 2.
    OBJECTIVES To present acase of a 21/M who was brought due to upward rolling of eyeballs and stiffening of extremities with associated headache, and fever To discuss approach to patient presenting with upward rolling of eyeballs and stiffening of extremities with associated headache, and fever To Identify treatment and management algorithms for patients with the said condition
  • 3.
    CASE PRESENTATION 01 COURSE INTHE WARD 02 DISCUSSION AND CONCETP MAP 03 ASSESSMENT AND DIFFERENTIAL DIAGNOSIS 04 TAKE AWAY 05 REFERENCES 06 TABLE OF CONTENTS
  • 4.
    CASE PRESENTATION J.G. 21/M Single Sta Monica, PPPC Admittedon February 7, 2025 Informant: Father 85% Reliability Chief Complaint: (+) Stiffening of extremities and upward rolling of eyeballs
  • 5.
    HISTORY OF PRESENTILLNESS (+) Increasing severity of headache (+) Fever (+)Decrease d sensorium (+)headache Sought consult at BDH Started Ceftriaxone 2gm IV Mannitol 100cc IV Paracetamol 600mg IV (+) Stiffening of extremities and upward rolling of eyeballs No consult done. No meds taken. 3 days pta 1 day pta Few hours pta
  • 6.
    Past Medical History (+) MVAOct 2024 sustained frontal bone fracture (+) Primary Complex Personal/ Social History 2.5 pack year smoker Occasional Alcoholic Beverage drinker Family Medical History (+)HPN – Both sides Vaccination History (+) COVID Vaccination Childhood vaccination was given but unrecalled if completed A C B D
  • 7.
    PHYSICAL EXAMINATION Vital Signs:Vital Signs: BP 110/80 HR 65 RR 22 T 37.8 C Spo2 95% at 2lpm NC General Status: Awake, GCS 9 (E2V2M5), in mild respiratory distress. Confused, weak-looking. Head and Neck: (+) Nuchal Rigidity, (+) Kernig’s Sign, (-) Brudzinski Sign; No visible or palpable masses, depressions, or scarring. Hair is of normal texture and evenly distributed. No neck vein distention Non-erythematous, not enlarged tonsils EENT: (+) Preferential Gaze (Right); (+) Horizontal nystagmus; pink conjunctivae, Anicteric, Pink Palpebral Conjunctiva, No CLAD, No nystagmus Pupils equally reactive to light at 5mm, OU Fundoscopy: No papilledema
  • 8.
    PHYSICAL EXAMINATION Chest andLungs: Symmetrical Chest Wall Expansion, Clear Breath Sounds Cardiac: External chest is normal in appearance without lifts, heaves, or thrills. PMI is not visible and is palpated in the 5th intercostal space at the midclavicular line. Normal rate with normal rhythm. No murmurs, gallops, or rubs are auscultated. Abdomen: There are no visible lesions or scars. Umbilicus is normal without herniation. Bowel sounds are present and normoactive. Soft, symmetric, and non-tender without distention. No masses, hepatomegaly, or splenomegaly are noted.
  • 9.
    PHYSICAL EXAMINATION Genitourinary: nomasses or lesions noted. Skin and Extremities: No gross deformities noted on upper and lower extremities. Good and equal pulses, no tremors, no limitations on range of motions noted. Nails without wounds or lesions, Capillary refill time of <2s. Neurologic: CN are intact. No Brudzinski. (+) Kernig. (+) Nuchal Rigidity
  • 10.
    PHYSICAL EXAMINATION Constitutional: generalizedbody malaise, (+)fever HEENT: No sore throat Skin: No caput medusae. No telangiectasia. (+) Bruises on IV insertion and injection sites Cardiovascular: (-)Palpitations, (-)Easy Fatigability Respiratory: Shortness of breath Gastrointestinal: no changes in bowel movement Genitourinary: no dysuria, flank pains, change in urination Neurologic: no sensory deficits or motor deficits
  • 11.
    Initial Impression CNS Infectionprobably Bacterial secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess
  • 12.
    Patient J.G. 21/M HEADACHEFEVER NUCHAL RIGIDITY and KERNIG’S SIGN HISTORY OF TRAUMA SEIZURES SENSORIUM CHANGES
  • 13.
    DIFFERENTIAL DIAGNOSES Meningitis (BacterialVs Viral) Encephalitis Intracranial Mass Brain Abscess Cerebrovascular Disease
  • 14.
    DIFFERENTIAL DIAGNOSES Differential RuleIn Rule Out Meningitis Fever Headache Generalized body weakness/Prostration Drowsiness No focal deficit Neck Stiffness Kernig’s Altered Mental Status Cannot totally rule out Encephalitis Fever Altered Mental Status Cannot totally Rule Out Neck Stiffness Headache focal or diffuse neurologic signs and symptoms Intracranial Mass/Cerebral Abscess Headache Drowsiness Fever No neurologic deficit, usually unipolar unless massive/equal* CVA Headache Drowsiness No neurologic deficit, usually unipolar unless massive/equal*
  • 15.
  • 16.
  • 17.
    Admission Day (ER) (February6, 2025) Subjective Objective Assessment Plan Headache 9/10 Changes in behavior Awake GCS 9 (E2V2M5) Vital Signs: BP 120/90 HR 82 RR 20 T 38 Spo2 99% at 3lpm Pupils equally reactive to light at 5mm, OU Preferential gaze Nuchal Rigidity SCWE CBS AP NRRR Soft nontender abdomen FEP no edema <2s CRT CNS Infection probably Bacterial secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess; MVA Self crash with Multiple Skull Fracture Oct 2024 Diet: OF 1,400 kcal in 6 divided feedings IVF: PNSS 1L x 100cc/hour Diagnostics: RBS CBC Na K Crea BUN, Chest Xray, Cranial Ct Scan with Contrast 12 Lead ECG, UA Plain Cranial CT Scan was done outside Therapeutics: Ceftriaxone 2gm IV q12 Mannitol 100cc IV q6 Diazepam 5mg IV PRN for frank seizures Paracetamol 300mg IV q4 PRN O2 at 2-3lpm via NC IFC Inserted NGT Inserted Vital Signs q2 Neuro Vital Signs q2 I&O q shift
  • 18.
    Admission Day (WARD) (February7, 2025) Subjective Objective Assessment Plan Headache 9/10 Changes in behavior Awake GCS 9 (E2V2M5) Vital Signs: BP 110/80 HR 65 RR 22 T 37.8 Spo2 95% at 3lpm Pupils equally reactive to light at 5mm, OU Preferential gaze Nuchal Rigidity SCWE CBS AP NRRR Soft nontender abdomen FEP no edema <2s CRT CNS Infection probably Bacterial secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess; MVA Self crash with Multiple Skull Fracture Oct 2024 Diet: OF 1,400 kcal in 6 divided feedings IVF: PNSS 1L x 100cc/hour Additional Diagnostics: Blood Culture x 2 sites Procalcitonin iCa, Mg, FBS CBG q6 CSF Analysis/Lumbar Tap Contrast-enhanced Cranial CT Scan Therapeutics: Vancomycin 1gm + 100cc PNSS IV to run for 4 hours q12 Dexamethasone 10mg IV q6 x 4 days Omeprazole 40mg IV q12 Father apprised of Pt’s condition and prognosis Referred to IDS Service LDH, BSMP, Dengue Duo, ABG CSF Fluid Gene Xpert
  • 19.
    CBC 02/06 02/11 Hgb158 130 Hct 49.7 40.4 RBC 6.0 5.1 WBC 37.1 7.1 Platelet 297 296 Segmenters 85 58.4 Lymphocytes 2.1 16.6 Monocytes 6.2 10.1 Eosinophils 1.5 12.3 Basophils 0.0 0.2 MCV 82.5 78.6 MCH 26.1 25.3 MCHC 31.7 32.2 MPV 7.5 82. RDW-SD 45.6 39.6 RDW-CV 15.3 15.5 Chem 02/06 02/08 02/11 02/14 Na 137.8 152.6 143.9 K 3.88 4.10 3.99 Crea 90.5 55 35 BUN 5.88 4.24 1.85 eGFR Procalcitonin 45.69 D2 Abx 7.159 D5 Abx 0.777 D8 Abx RBS 131 iCa 0.84 Mg 1.16 SGPT 10.3 SGOT 20.6 LDH 187 PT 17.8 INR 1.43 BSMP NMPS
  • 20.
    Skull Xray PA2/7/25 Findings: A depressed fracture is seen involving the midline frontal bones with overlying soft tissue swelling. The rest of the calvarium is normal with symmetrical appearance. Impression: Depressed Fracture is seen involving the midline frontal Chest Xray PA 2/7/25 Findings: Bilateral Hilar fullness with accentuation of bronchovascular markings is noted. The rest of the lungs show no active parenchymal opacities. The heart is not enlarged. The diaphragm, sulci, and bony thorax are intact. Impression: Signs of Pulmonary Congestion. Intercurrent Pneumonia is not ruled out.
  • 21.
    12 Lead ECG02/06/2025 Rate 65 Regular Sinus Rhythm No Chamber enlargement No axis deviation Normal Sinus Rhythm
  • 22.
  • 23.
    02/13 CSF Gene Xpert (2/12/25) MTBnot detected Gram Stain (02/08/25) Organism: Gram (+) Cocci in Singles – Rare Epithelial: 0-1/LPO Pus Cells: 0-1/HPO Blood and SCF Culture No Growth CSF Cell Count WBC 0.80 cells/cu mm CSF Differential Count PMN 56% MNC 44% ABG 2/8/25 pH 7.56 CO2 18.5 O2 126.2 HCO3 17 Partially Compensated Respiratory Alkalosis with Overcorrected OXygenation
  • 24.
    Hospital Day 1-3 (February8-10, 2025) Subjective Objective Assessment Plan On/Off Headache 9/10 Changes in behavior (+)Nausea Ceftriaxone Day 3 Vancomycin Day 3 Awake GCS 14 (E4V4M6) Vital Signs: BP 110/60 HR 63 RR 22 T 36.1 Spo2 98% at 3lpm Pupils equally reactive to light at 5mm, OU Preferential gaze Nuchal Rigidity SCWE CBS AP NRRR Soft nontender abdomen FEP no edema <2s CRT iCa 0.84 Fundoscopy: pale pink 1.5mm disk with sharp flat margin. Cup is within the disk. Vessels are enlarged and prominent CNS Infection probably Bacterial secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess; MVA Self crash with Multiple Skull Fracture Oct 2024; Hypocalcemia Calcium Gluconate 10ml SIVP now Nimodipine 30mg tab 2 tabs q4 Metoclopramide 10mg SIVP q8 PRN Lumbar Tap was done IDS Rounds: Increase Mannitol to 150cc q4 For repeat Procalcitonin
  • 25.
    CBC 02/06 02/11 Hgb158 130 Hct 49.7 40.4 RBC 6.0 5.1 WBC 37.1 7.1 Platelet 297 296 Segmenters 85 58.4 Lymphocytes 2.1 16.6 Monocytes 6.2 10.1 Eosinophils 1.5 12.3 Basophils 0.0 0.2 MCV 82.5 78.6 MCH 26.1 25.3 MCHC 31.7 32.2 MPV 7.5 82. RDW-SD 45.6 39.6 RDW-CV 15.3 15.5 Chem 02/06 02/08 02/11 02/14 Na 137.8 152.6 143.9 K 3.88 4.10 3.99 Crea 90.5 55 35 BUN 5.88 4.24 1.85 eGFR Procalcitonin 45.69 D2 Abx 7.159 D5 Abx 0.777 D8 Abx RBS 131 iCa 0.84 Mg 1.16 SGPT 10.3 SGOT 20.6 LDH 187 PT 17.8 INR 1.43 BSMP NMPS
  • 26.
    Hospital Day 5-7 (February11-14, 2025) Subjective Objective Assessment Plan No nuchal Rigidity No Headache No fever Ceftriaxone Day 4 Vancomycin Day 4 Awake GCS 15 (E4V5M6) Vital Signs: BP 120/70 HR 58 RR 220 T 36.5 Spo2 98% at room air Pupils equally reactive to light at 5mm, OU SCWE CBS AP NRRR Soft nontender abdomen FEP no edema <2s CRT Procalcitonin 7.159 from 45 Bacterial Meningitis secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess; MVA Self crash with Multiple Skull Fracture Oct 2024 Titrate down Mannitol To Complete Antibiotics to 10 days
  • 27.
    Hospital Day 8-12 (February15-18, 2025) Subjective Objective Assessment Plan No nuchal Rigidity No Headache No fever Ceftriaxone Day 10 Vancomycin Day 10 Awake GCS 15 (E4V5M6) Vital Signs: BP 100/60 HR 67 RR 21 T 36.7 Spo2 98% at room air Pupils equally reactive to light at 5mm, OU SCWE CBS AP NRRR Soft nontender abdomen FEP no edema <2s CRT Procalcitonin 0.77 from 7,159 CNS Infection probably Bacterial secondary to Multiple Skull Fracture secondary to Motor Vehicular Accident; Rule Out Brain Abscess; MVA Self crash with Multiple Skull Fracture Oct 2024 Titrate down Mannitol To Complete Antibiotics to 10 days Patient was then sent home Improved Home Meds: Clindamycin
  • 28.
    Final Diagnosis Bacterial Meningitissecondary to Multiple Skull Fracture secondary to Motor Vehicular Accident
  • 29.
    Bacterial Meningitis Bacterial meningitisis an acute purulent infection within the sub- arachnoid space (SAS). It is associated with a CNS inflammatory reaction that may result in decreased consciousness, seizures, raised intracranial pressure (ICP), and stroke. The meninges, SAS, and brain parenchyma are all frequently involved in the inflammatory reaction (meningoencephalitis). Harrison’s Principles of Internal Medicine 21st Edit
  • 31.
    Bacterial meningitis isthe most common form of suppurative CNS infection, with an annual incidence in the United States of >2.5 cases/100,000 population. • Streptococcus pneumoniae (~50%) • Neisseria meningitidis (~25%) • Group B streptococci (~15%) • Listeria monocytogenes (~10%) • Haemophilus influenzae type b accounts for <10% of cases of bacterial meningitis in most series. • N. meningitidis is the causative organism of recurring epidemics of men- ingitis every 8–12 years. Epidemiology Harrison’s Principles of Internal Medicine 21st Edit
  • 32.
    In 1999, theCNS Infection Council of the Philippine Neurological Association did a study to determine the spectrum of CNS infections seen in this country by combining the census of all the neurology training institutions. Epidemiology The PCP Textbook of Internal Medicine 1st Edition
  • 33.
    1. Bacterial orPyogenic 2. Tuberculous 3. Viral 4. Fungal (mostly cryptococcal) A. Acute - Less than a week B. Sub-Acute – 1-2 weeks C. Chronic – More then 2 weeks Major Types of Meningitis The PCP Textbook of Internal Medicine 1st Edition
  • 34.
    Approach to SuspectedMeningitis 1. Is this Meningitis or Encephalitis? Meningitis - fever, headache, neck rigidity, no focal signs, relative preservation of mentation or consciousness. "Patient can relate to you his history" (Proceed to #2) Encephalitis - fever + (mental, behavioral or sensorial change), the latter occurring at the onset of the illness, acute course (Proceed to # 4)
  • 35.
    Approach to SuspectedMeningitis 2. If this is a meningitic syndrome, classify according to acute, subacute, or chronic. Acute: < 1 week course Subacute: 1 to 2 weeks Chronic: > 2 weeks
  • 36.
    Approach to SuspectedMeningitis 3. What major type of meningitis would it likely be? If acute - bacterial or viral If chronic - TB or fungal If subacute - consider all 4
  • 37.
    Approach to SuspectedMeningitis 4. Look for the following before doing an LP - focal signs, papilledema, signs of herniation.
  • 38.
    Approach to SuspectedMeningitis Recommended criteria for adult patients with suspected bacterial meningitis who should undergo CT prior to lumbar puncture
  • 39.
    Approach to SuspectedMeningitis 5. If any of the above are present, do first a CT scan or MRI to rule out a mass lesion. If none of the above are present, proceed with an LP. 6. If a mass lesion (e.g., abscess, tumor) is seen on neuroimaging, treat accordingly. Don't do a tap. 7. If no mass lesion is seen on CT or MRI, proceed with LP.
  • 40.
    Approach to SuspectedMeningitis 8. Lumbar puncture: Measure opening pressure. If > 300 mm H,0, run Mannitol first until pressure drops to at 300 mmH2O before withdrawing fluid. For adults, take 10 cc or more divided as follows: 1st bottle - 2 cc for protein and glucose 2nd bottle - 7 cc for microbiological studies. Reserve for Cryptococcal antigen latex agglutination test (CALAS) and other studies. To the sediment, do G/S, C/S, India ink smear, Saboraud's culture, TB culture. 3rd bottle - 1 cc - cell count with differential 4th bottle - 1 cc or more - for other studies as indicated by clinical suspicion (e.g., PCR for herpes, biofilm array for meningitis-en-cephalitis panel, etc) CSF lactate concentrations of >4.2 mmol/L were considered to be a positive discriminative factor for bacterial meningitis
  • 41.
    Approach to SuspectedMeningitis 9. Look at the routine CSF picture (WBC, differential, sugar, protein) to determine major type of meningitis one (bacterial, TB or fungal, viral)
  • 42.
    Approach to Suspected Meningitis 10.If stains are positive, treat accordingly. Correlate with CSF picture. G/S: (+ ) for bacteria - start empiric treatment. India ink smear: round to oval organisms with a double refractile wall - treat for Cryptococcus. A (+) AFB smear from the CSP is extremely rare in the Philippine setting.
  • 43.
    Approach to SuspectedMeningitis On the basis of the available evidence on the use of adjunctive dexamethasone in adults, we recommend use of dexamethasone (0.15 mg/kg q6h for 2–4 days with the first dose administered 10–20 min before, or at least concomitant with, the first dose of antimicrobial therapy) in adults with suspected or proven pneumococcal meningitis (A-I). Infectious Disease Society of America (IDSA)
  • 44.
    Approach to SuspectedMeningitis 11. If CS picture is compatible with bacterial meningitis, and the stains are negative, treat empirically for bacterial meningitis. 12. If stains are negative, and CSF picture is compatible with TB or fungal meningitis, presume TB and treat as such. 13. If cryptococcal antigen latex agglutination system (CALAS) is (+), but India ink is (-) for cryptococcus, repeat tap the next day for India ink and CALAS because the test has a 10% false positivity rate. If CALAS is again (+) and India ink remains negative, one can treat presumptively as cryptococcal meningitis. If CALAS is negative, cryptococcal meningitis can virtually be ruled out (CALAS negative predictive value is 100% by the local validation study of the author), so long as the India ink stain and culture are negative.
  • 45.
    Approach to SuspectedMeningitis 14. When cultures show an isolate (bacteria, TB, cryptococcus), treat accordingly using drugs specific for the isolated etiologic organism and guided by sensitivity results.
  • 46.
  • 47.
    Approach to SuspectedMeningitis 15. If clinical and CS picture is compatible with viral meningitis, treat symptomatically. 16. If clinical diagnosis is ENCEPHALITIS the main task is to determine if this is HERPES SIMPLEX OR NON-HERPES SIMPLEX, because only the former (and possibly Varicella- zoster and Epstein-Barr) have been proven to be treatable.
  • 48.
    Approach to SuspectedMeningitis 17. Do LP for CSF analysis as for meningitis, but reserve at least 1 cc for Polymerase Chain Reaction (PCR) or biofilm array meningitis/ encephalitis panel for herpes and other viruses. 18. EEG, CT and MRI should be done as quickly as possible to detect focal abnormalities in the fronto-temporal lobes, which support a diagnosis of herpes simplex. a. EEG - periodic sharps or spikes from one or both frontal and/or temporal lobes. b. CT / MRI - focal abnormalities at the frontal, temporal or cingulate areas (MRI is more sensitive than CT).
  • 49.
    Approach to SuspectedMeningitis 19. If routine CS picture is compatible with a viral encephalitis and/or EEG and neuroimaging is/are suggestive of herpes, start presumptive treatment for herpes with IV acyclovir. 20. If PCR for herpes turns out negative, discontinue acyclovir unless zoster or EBV encephalitis is suspected, or EEG, CT or MRI shows focal abnormalities suggestive of herpes. Continuing with acyclovir therapy for herpes is an option despite absence of evidence for herpes if the clinician believes or wants to give the patient the potential benefit of acyclovir treatment. 21. For CMV-related CNS infections, ganciclovir and foscarnet may be tried. 22. For California encephalitis, adenovirus, rotavirus, LCMV and other arenavirus encephalitis: may try IV rivabirin.
  • 50.
    Diagnosis of BacterialMeningitis The classic CSF abnormalities in bacterial meningitis are: (1) Polymorphonuclear (PMN) leukocytosis (>100 cells/μL in 90%) (2) Decreased glucose concentration (<2.2 mmol/L [<40 mg/dL] and/or CSF/serum glucose ratio of <0.4 in ~60%) (3) Increased protein concentration (>0.45 g/L [>45 mg/dL] in 90%), (4) Increased opening pressure (>180 mmH2O in 90%). CSF bacterial cultures are positive in >70% of patients, and CSF Gram’s stain demonstrates organisms in >60%.
  • 51.
  • 52.
    Increased Intracranial Pressure Emergencytreatment of increased ICP includes elevation of the patient’s head to 30–45°, intubation, and hyperventilation (PaCO2 25–30 mmHg), and mannitol. Patients with increased ICP should be managed in an intensive care unit; accurate ICP measurements are best obtained with an ICP monitoring device.
  • 53.
  • 54.
    PROGNOSIS Mortality Rate forBacterial Meningitis: 3–7% for meningitis caused by H. influenzae, N. meningitidis, or group B streptococci; 15% for that due to L. monocytogenes; 20% for S. pneumoniae. In general, the risk of death from bacterial meningitis increases with (1) decreased level of consciousness on admission (2) onset of seizures within 24 h of admission (3) signs of increased ICP (4) young age (infancy) and age >50 (5) the presence of comorbid conditions including shock and/or the need for mechanical ventilation, (6) delay in the initiation of treatment. Decreased CSF glucose concentration (<2.2 mmol/L [<40 mg/dL]) and markedly increased CSF protein concentration (>3 g/L [> 300 mg/dL]) have been predictive of increased mortality and poorer outcomes in some series. Moderate or severe sequelae
  • 55.
  • 56.
    TAKE AWAY… • Meningitisis a devastating disease with a high case fatality rate, which can lead to serious long-term complications (sequelae). • Meningitis remains a major global public-health challenge. • Many organisms can cause meningitis, including bacteria, viruses, fungi and parasites. • Bacterial meningitis is of particular concern. Around 1 in 6 people who get this type of meningitis die and 1 in 5 have severe complications. • Safe affordable vaccines are the most effective way to deliver long-lasting protection.
  • 57.

Editor's Notes

  • #3 Mmmmmmm,,.//’