Study guide
Acute CNS Infections, Encephalitis & Inflammatory Emergencies
ABPN Neurocritical Care Study Guide Exam
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1 Chapter 1: Neurologic Examination & Coma Assessment in the ICU
Current Examination, Blueprint & Preparation Neurologic Examination in Critically Ill Patients Coma Evaluation & Consciousness Alterations Delirium & Toxic-Metabolic Encephalopathy in the ICU
2 Chapter 2: Cerebral Physiology & Intracranial Dynamics
Cerebral Blood Flow, Metabolism & Autoregulation Intracranial Pressure & Compliance Cerebral Edema & Herniation Syndromes
3 Chapter 3: Intracranial Hypertension & Cerebral Perfusion Management
Tiered ICP Management Protocols Hyperosmolar Therapy & Fluid Management Advanced & Refractory ICP Interventions
4 Chapter 4: Airway, Mechanical Ventilation & Pulmonary ICU Management
Emergency Airway Management & Neuro-Intubation Mechanical Ventilation Strategies in Acute Brain Injury Tracheostomy & Ventilator Weaning in Neurocritical Care Pulmonary Complications in the Neuro-ICU Obstructive Lung Disease, Pulmonary Hypertension & Bronchoscopy
5 Chapter 5: Hemodynamics, Shock & Cardiovascular Management
Hemodynamic Monitoring & Blood Pressure Targets Vasoactive Agents: Inotropes, Vasopressors & Antihypertensives Cardiac Complications of Brain Injury
6 Chapter 6: Neuropharmacology, Analgesia & Sedation
ICU Sedation & Analgesia Neuromuscular Blockade & Monitoring Propofol Infusion Syndrome & Drug Toxicities Antiseizure Drug Pharmacology in the ICU
7 Bleeding, Thrombosis & Hematologic Emergencies
Warfarin & Heparin Reversal Direct Oral Anticoagulant (DOAC) Reversal Antiplatelet Management & Platelet Dysfunction Venous Thromboembolism Prophylaxis & Management Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity
8 Chapter 8: Systemic ICU Care, Fluids, Electrolytes & Endocrine
Hyponatremia & Osmoregulation: SIADH vs Cerebral Salt Wasting Diabetes Insipidus, Hypernatremia & Endocrine Crises Critical Care Prophylaxis, Nutrition & Infection Prevention
9 Systemic Trauma & Environmental Injury
Polytrauma, Chest Injury & Abdominal Hemorrhage Burns, Electrical Injury & Hanging
10 Cardiac Emergencies & Mechanical Support
IABP, Ventricular Devices & ECMO Acute Coronary, Valvular, Rhythm & Aortic Emergencies
11 Kidney Injury, Acid–Base & Renal Replacement
Acute Kidney Injury & Renal Drug Clearance Acid–Base Disorders, Electrolytes & Renal Replacement
12 Systemic Infection & Endocrine Emergencies
Sepsis, Endocarditis & Antimicrobial Principles Thyroid, Adrenal & Dysglycemic Emergencies
13 Gastrointestinal & Hepatic Emergencies
Acute Abdomen, GI Bleeding & Abdominal Compartment Syndrome Acute Liver Failure, Cirrhosis & Hepatic Drug Effects
14 Chapter 9: Neuroimaging in the Neuro-ICU
Non-Contrast CT & CT Angiography CT Perfusion & Advanced Perfusion Imaging Magnetic Resonance Imaging in Critical Illness
15 Chapter 10: Electrophysiology & Neuromonitoring
Continuous EEG & ACNS Standardized Critical Care Terminology Invasive Neuromonitoring: ICP & External Ventricular Drains Multimodal Monitoring: PbtO2, Microdialysis & Transcranial Doppler
16 Angiography, Electrodiagnosis & CSF Analysis
Conventional Angiography & Cranial–Spinal Shunts EMG, Nerve Conduction & Acute Muscle Disease CSF Analysis: Infection, Inflammation & Hemorrhage
17 Chapter 11: Bedside Procedures, Ultrasound & Death by Neurologic Criteria
Critical Care Procedural Skills Critical Care Ultrasound & Echocardiography Determination of Death by Neurologic Criteria
18 Chapter 12: Acute Ischemic Stroke & Reperfusion Therapies
Acute Ischemic Stroke Management & Thrombolysis Endovascular Thrombectomy & Large Vessel Occlusion Malignant Hemispheric & Cerebellar Infarction
19 Chapter 13: Spontaneous Intracerebral Hemorrhage & Intraventricular Hemorrhage
Acute Intraparenchymal Hemorrhage Management Intraventricular Hemorrhage & Hydrocephalus Surgical Evacuation & Minimally Invasive Surgery in ICH
20 Chapter 14: Aneurysmal Subarachnoid Hemorrhage & Delayed Cerebral Ischemia
Aneurysmal Subarachnoid Hemorrhage: Acute Resuscitation & Securing Delayed Cerebral Ischemia & Cerebral Vasospasm Non-Aneurysmal Subarachnoid Hemorrhage & Vascular Malformations
21 Venous, Spinal & Traumatic Vascular Disease
Cerebral Venous Thrombosis & Spinal Cord Infarction Traumatic Dissection, Carotid–Cavernous Fistula & Penetrating Injury
22 Chapter 15: Traumatic Brain & Spinal Cord Injury
Severe Traumatic Brain Injury & Contusions Acute Traumatic Spinal Cord Injury & Neurogenic Shock Spine Trauma, Fractures & Cord Syndromes
23 Chapter 16: Status Epilepticus, Seizures & Neuromuscular Emergencies
Status Epilepticus: Convulsive & Non-Convulsive Refractory & Super-Refractory Status Epilepticus Acute Neuromuscular Respiratory Failure
24 Chapter 17: Post-Cardiac Arrest Care, CNS Infections & Encephalitis
Targeted Temperature Management & Post-Cardiac Arrest Care Post-Cardiac Arrest Neuroprognostication Acute CNS Infections, Encephalitis & Inflammatory Emergencies
25 Neuroinflammation & Neurooncology
Fulminant Demyelination & Autoimmune Encephalitis Brain, Spinal & Leptomeningeal Cancer Emergencies
26 Pregnancy, Transplantation & Pediatric Care
Pregnancy, Postpartum & Post-Transplant Neurologic Care Pediatric Neurocritical Care
27 Chapter 18: Neurosurgical & Perioperative Emergencies
Postoperative Neurosurgical Complications Device Complications: EVDs, Shunts & ICP Monitors Cerebral Hyperperfusion Syndrome & Post-Interventional Emergencies
28 Chapter 19: Ethics, Palliative Care & Organ Donation in the Neuro-ICU
Communication, Surrogate Decision-Making & Conflict Resolution Neuroprognostication Ethics, Withdrawal of Life Support & Palliative Care Organ Donation & Management of the Deceased Donor
Acute CNS Infections, Encephalitis & Inflammatory Emergencies
Key Takeaways Explain This Topic AI
Suspected bacterial meningitis requires prompt empiric antimicrobials; imaging or an unsafe/delayed LP must not postpone necessary treatment.
Listeria risk changes empiric coverage, and healthcare-associated CNS infection requires a different resistance-aware regimen.
For suspected HSV encephalitis, start acyclovir promptly with renal and hydration precautions; repeat an early negative PCR when suspicion remains high.
Autoimmune encephalitis, PRES, RCVS, infection, and toxic-metabolic disease overlap clinically and require phenotype-based investigation.
PRES can coexist with infarction or hemorrhage; avoid glucocorticoids as RCVS treatment and do not promise that calcium-channel blockers prevent its strokes.
Last updated: October 2026
Acute CNS Infections, Encephalitis & Inflammatory Emergencies
Acute infectious, inflammatory, and neurovascular encephalopathies are life-threatening neurological catastrophes frequently admitted to the neurocritical care unit. Rapid recognition, diagnostic lumbar puncture ( L P LP L P ), tailored neuroimaging, and emergent pathogen-directed or immunosuppressive therapy are essential to prevent irreversible neurological disability and death.
Acute Bacterial Meningitis
Acute bacterial meningitis is an inflammatory infection of the arachnoid membrane, subarachnoid space, and cerebrospinal fluid ( C S F CSF CSF ). Rapid bacterial proliferation and autolysis trigger massive release of cell wall components (peptidoglycan, teichoic acid, lipopolysaccharide), eliciting subarachnoid cytokine cascades ( I L - 1 IL\text{-}1 I L - 1 , T N F - α TNF\text{-}\alpha TNF - α ) that induce blood-brain barrier breakdown, purulent exudate accumulation, cerebral vasculitis, raised intracranial pressure, and secondary brain herniation.
Pathogen Stratification by Clinical Setting
Community-Acquired Adults ( 18 – 50 years 18\text{--}50\text{ years} 18 – 50 years ): Streptococcus pneumoniae ( 50 % – 60 % 50\%\text{--}60\% 50% – 60% ), Neisseria meningitidis ( 20 % – 30 % 20\%\text{--}30\% 20% – 30% ).
Older Adults ( > 50 years > 50\text{ years} > 50 years ), Immunocompromised, Alcoholism, Cirrhosis, Pregnancy: Streptococcus pneumoniae , Neisseria meningitidis , and L i s t e r i a m o n o c y t o g e n e s Listeria\ monocytogenes L i s t er ia m o n ocy t o g e n es ( 10 % – 15 % 10\%\text{--}15\% 10% – 15% ).
Post-Neurosurgical, External Ventricular Drains (EVD), Penetrating Head Trauma: Staphylococcus aureus , coagulase-negative staphylococci ( Staphylococcus epidermidis ), and aerobic Gram-negative bacilli ( Pseudomonas aeruginosa , Acinetobacter baumannii , Klebsiella pneumoniae , Enterobacter ).
Empiric Antimicrobial Regimens
Clinical Setting Common Pathogens Empiric Antimicrobial Regimen
Adult 18–50 years S. pneumoniae , N. meningitidis Ceftriaxone 2 g 2\text{ g} 2 g IV q12h (or Cefotaxime 2 g 2\text{ g} 2 g IV q4h) + Vancomycin 15 – 20 mg/kg 15\text{--}20\text{ mg/kg} 15 – 20 mg/kg IV q8–12h (trough 15 – 20 μ g/mL 15\text{--}20\text{ }\mu\text{g/mL} 15 – 20 μ g/mL )
Adult > 50 years, Immunocompromised, Pregnant S. pneumoniae , N. meningitidis , L. monocytogenes , Gram-negative bacilli Ceftriaxone 2 g 2\text{ g} 2 g IV q12h + Vancomycin 15 – 20 mg/kg 15\text{--}20\text{ mg/kg} 15 – 20 mg/kg IV q8–12h + Ampicillin 2 g 2\text{ g} 2 g IV q4h
Post-Neurosurgical / EVD-associated S. aureus , P. aeruginosa , Enterobacteriaceae Meropenem 2 g 2\text{ g} 2 g IV q8h (or Cefepime 2 g 2\text{ g} 2 g IV q8h) + Vancomycin 15 – 20 mg/kg 15\text{--}20\text{ mg/kg} 15 – 20 mg/kg IV q8–12h
Adjunctive Dexamethasone
Landmark Evidence (de Gans & van de Beek, NEJM 2002): In a multicenter randomized trial of 301 adults with acute bacterial meningitis, adjunctive dexamethasone reduced unfavorable outcomes from 25 % 25\% 25% to 15 % 15\% 15% ( p = 0.03 p = 0.03 p = 0.03 ) and reduced mortality from 15 % 15\% 15% to 7 % 7\% 7% ( p = 0.04 p = 0.04 p = 0.04 ), with the most profound mortality reduction in S t r e p t o c o c c u s p n e u m o n i a e Streptococcus\ pneumoniae St re pt ococc u s p n e u m o nia e meningitis ( 34 % to 14 % 34\%\text{ to }14\% 34% to 14% , p = 0.02 p = 0.02 p = 0.02 ).
Dosing & Administration: 10 mg 10\text{ mg} 10 mg IV administered prior to or concurrently with the first dose of antimicrobial therapy , continued at 10 mg 10\text{ mg} 10 mg IV q6h for 4 days.
Clinical Nuances:
If the pathogen is proven to be Streptococcus pneumoniae , complete the full 4-day dexamethasone course.
If another pathogen ( N. meningitidis , L. monocytogenes , Gram-negative bacilli) or virus is identified, discontinue dexamethasone immediately.
If antimicrobial therapy has already been administered for several hours, the expected benefit of delayed steroid initiation is less certain; obtain infection-specific guidance rather than delaying antibiotics.
Diagnostic CSF Profiles in Meningitis & Encephalitis
Etiology Opening Pressure WBC Count (cells/ μ L \mu\text{L} μ L ) Differential Protein (mg/dL) CSF:Serum Glucose Ratio
Normal 100 – 200 mm H 2 O 100\text{--}200\text{ mm H}_2\text{O} 100 – 200 mm H 2 O < 5 < 5 < 5 > 95 % > 95\% > 95% Lymphocytes 15 – 45 15\text{--}45 15 – 45 > 0.60 > 0.60 > 0.60
Bacterial Meningitis Markedly elevated ( > 250 – 350 > 250\text{--}350 > 250 – 350 ) 1 , 000 – 10 , 000 + 1,000\text{--}10,000+ 1 , 000 – 10 , 000 + > 80 % > 80\% > 80% Neutrophils Markedly high ( 100 – 500 + 100\text{--}500+ 100 – 500 + ) Markedly low ( < 0.40 < 0.40 < 0.40 , often < 0.10 < 0.10 < 0.10 )
Viral Encephalitis / Meningitis Normal to mildly elevated 50 – 500 50\text{--}500 50 – 500 > 80 % > 80\% > 80% Lymphocytes Mildly elevated ( 50 – 100 50\text{--}100 50 – 100 ) Normal ( > 0.60 > 0.60 > 0.60 )
Fungal / Tuberculous Meningitis Moderately elevated ( > 200 – 300 > 200\text{--}300 > 200 – 300 ) 100 – 500 100\text{--}500 100 – 500 Lymphocytes / Mononuclear High ( 100 – 500 100\text{--}500 100 – 500 ) Low ( < 0.30 < 0.30 < 0.30 )
Autoimmune Encephalitis Normal 10 – 100 10\text{--}100 10 – 100 (mild) Lymphocytes (or normal) Mildly elevated ( 50 – 100 50\text{--}100 50 – 100 ) Normal ( > 0.60 > 0.60 > 0.60 )
Important
When acute bacterial meningitis is suspected, never delay antimicrobial administration for head CT or lumbar puncture. If a CT scan is required prior to LP (due to altered mental status, focal neurological deficits, new seizures, or papilledema), obtain blood cultures, administer IV dexamethasone 10 mg 10\text{ mg} 10 mg and empiric antibiotics immediately, and then transport the patient to CT.
- Viral Encephalitis: HSV-1 and Neurotropic Viruses
- Herpes Simplex Virus Encephalitis (HSV-1)
HSV-1 is the most common cause of non-epidemic sporadic viral encephalitis in developed nations, carrying > 70 % > 70\% > 70% mortality if untreated:
Pathophysiology: Retrograde axonal transport via olfactory tract or trigeminal sensory axons into limbic structures, producing asymmetric necrotizing, hemorrhagic encephalitis with marked predilection for the medial temporal lobes , insula, and inferior frontal lobes.
Clinical Presentation: Acute/subacute onset of fever, headache, altered mental status, bizarre behavioral changes, personality disintegration, olfactory/gustatory hallucinations, memory loss, and focal temporal lobe seizures with impaired awareness.
Diagnostic Hallmarks:
Brain MRI: Asymmetric hyperintensity on T2/FLAIR and restricted diffusion on DWI in the medial temporal lobes, uncus, amygdala, and insular cortex. Petechial gyral hemorrhage may be evident on gradient-recalled echo ( G R E GRE GRE ) or susceptibility-weighted imaging ( S W I SWI S W I ).
cEEG: Lateralized Periodic Discharges ( L P D s LPDs L P Ds ) recurring every 1 – 2 seconds 1\text{--}2\text{ seconds} 1 – 2 seconds over the affected temporal lobe.
CSF Analysis: Lymphocytic pleocytosis ( 50 – 500 cells/ μ L 50\text{--}500\text{ cells/}\mu\text{L} 50 – 500 cells/ μ L ), elevated protein, elevated red blood cells ( R B C s RBCs RBC s ), and normal glucose. CSF HSV-1 PCR exhibits > 95 % > 95\% > 95% sensitivity and specificity. If early PCR ( < 48 hours < 48\text{ hours} < 48 hours ) is negative but clinical suspicion remains elevated, continue acyclovir and repeat LP at 3 – 7 days 3\text{--}7\text{ days} 3 – 7 days .
Empiric Management: Immediate Intravenous Acyclovir ( 10 mg/kg 10\text{ mg/kg} 10 mg/kg IV q8h with dosing weight, renal adjustment, and infusion plan selected according to the current protocol) for 14 – 21 days 14\text{--}21\text{ days} 14 – 21 days .
Clinical Pitfall: Acyclovir is insoluble in urine and precipitates in renal collecting tubules, causing acute obstructive crystal nephropathy. Infuse acyclovir slowly over at least 1 hour 1\text{ hour} 1 hour with appropriate hydration and renal monitoring while respecting cardiac, lung, and brain fluid constraints.
Other Neurotropic Viral Emergencies
Varicella Zoster Virus ( V Z V VZV V Z V ): Causes small- and large-vessel cerebral vasculopathy, producing multifocal ischemic and hemorrhagic strokes, aneurysmal dilatation, or temporal arteritis-like presentations. Treat with IV acyclovir when indicated; adjunctive steroids are a specialist, context-dependent decision with limited evidence rather than mandatory pulse treatment.
West Nile Virus ( W N V WNV W N V ): Neuroinvasive disease presents with fever, aseptic meningitis, encephalitis, and acute asymmetric flaccid paralysis caused by viral destruction of anterior horn cells (poliomyelitis-like syndrome). Patients exhibit prominent postural/action tremors, myoclonus, and parkinsonian rigidity. Brain MRI reveals T2/FLAIR hyperintensities in the substantia nigra, basal ganglia, and thalamus.
Distinguish Infectious and Immune Encephalitis
Psychiatric change, memory disturbance, seizures, dyskinesias, autonomic instability, and hypoventilation can indicate autoimmune encephalitis. Anti-NMDA receptor disease targets GluN1; LGI1 disease can produce brief faciobrachial dystonic seizures and hyponatremia; CASPR2 disease may combine encephalitis, neuromyotonia, dysautonomia, and severe insomnia. None of these patterns justifies omitting an infectious or toxic-metabolic evaluation. CSF and serum testing have different sensitivities and false-positive risks; interpret antibodies with the phenotype and appropriate paired testing.
MRI, EEG, CSF, and tumor screening support assessment. A normal MRI or initially mild CSF profile does not exclude immune disease. Tumor association varies with antibody, age, and sex. If a relevant tumor is present, coordinate treatment; removal is important but not a guaranteed immediate cure. First-line immunotherapy and escalation are expert-directed and depend on diagnosis, response, infection risk, and organ function. The dedicated immune-emergencies section develops this reasoning in detail rather than imposing a universal fixed drug sequence.
- Reversible Neurovascular Encephalopathies: PRES and RCVS
- Posterior Reversible Encephalopathy Syndrome (PRES)
PRES is a clinicoradiological neurovascular syndrome characterized by failed cerebral autoregulation:
Pathophysiology: Acute severe blood pressure elevation exceeds the myogenic upper limit of cerebral autoregulation, causing arteriolar hyperperfusion, endothelial shear stress, blood-brain barrier breakdown, and extravasation of plasma and macromolecules into the interstitium ( vasogenic edema ). Vasogenic edema preferentially targets the parieto-occipital subcortical white matter because the posterior vertebrobasilar circulation possesses significantly less sympathetic adrenergic perivascular innervation compared to the carotid circulation.
Etiologies & Triggers: Hypertensive emergency, preeclampsia/eclampsia, calcineurin inhibitors ( tacrolimus , cyclosporine in solid organ transplant recipients), cytotoxic chemotherapy, and severe sepsis.
Clinical Presentation: Subacute encephalopathy, throbbing headache, generalized seizures ( 70 % – 80 % 70\%\text{--}80\% 70% – 80% ), visual disturbances (homonymous hemianopia, visual hallucinations, cortical blindness / Anton syndrome).
Neuroimaging: Brain MRI demonstrates symmetric hyperintensity on T2/FLAIR in parieto-occipital white matter. Apparent diffusion coefficient ( A D C ADC A D C ) mapping reveals facilitated diffusion (bright on ADC) , supporting vasogenic edema; restricted diffusion, infarction, or hemorrhage can coexist and must be assessed.
Management:
Controlled BP Reduction: Titrate IV labetalol, nicardipine, or clevidipine. Lower MAP by no more than 20 % – 25 % 20\%\text{--}25\% 20% – 25% within the first 2 hours to prevent secondary cerebral watershed ischemia.
Seizure Control & Toxin Withdrawal: Intravenous magnesium sulfate ( 4 – 6 g 4\text{--}6\text{ g} 4 – 6 g bolus then 1 – 2 g/h 1\text{--}2\text{ g/h} 1 – 2 g/h ) for eclampsia; immediately discontinue or reduce doses of calcineurin inhibitors or offending chemotherapeutic agents.
Reversible Cerebral Vasoconstriction Syndrome (RCVS)
RCVS is characterized by transient, reversible dysregulation of cerebral arterial tone:
Clinical Hallmark: Recurrent "thunderclap" headaches —sudden, explosive, agonizing headaches reaching maximal 10 / 10 10/10 10/10 intensity within seconds ("crashing waves"), recurring multiple times over 1 – 4 weeks 1\text{--}4\text{ weeks} 1 – 4 weeks . Often triggered by Valsalva, coughing, exertion, or emotional stress.
Triggers: Postpartum state, sympathomimetic and serotonergic vasoactive substances: SSRIs, SNRIs, nasal decongestants (pseudoephedrine), triptans, ergotamines, cocaine, amphetamines, and cannabis.
Complications: Non-aneurysmal convexity subarachnoid hemorrhage ( c S A H cSAH c S A H ) ( 30 % – 35 % 30\%\text{--}35\% 30% – 35% ), ischemic stroke in watershed distributions, and lobar intracerebral hemorrhage.
Imaging: CTA, MRA, or catheter DSA reveals diffuse, multifocal, segmental narrowing and ectasia ( "string of beads" appearance ) affecting medium and large cerebral arteries, which completely resolves on follow-up imaging within 3 months. Catheter angiography may be normal during the first 3 – 5 days 3\text{--}5\text{ days} 3 – 5 days (delayed vasoconstriction).
Therapy: Oral calcium channel blockers ( Nimodipine 60 mg 60\text{ mg} 60 mg q4h or Verapamil ) to relieve headache in selected patients; prevention of stroke or other complications is not established; strict cessation of all vasoactive medications.
Warning
Avoid glucocorticoids as treatment for RCVS: observational evidence associates them with worsening. Do not confuse RCVS with inflammatory vasculitis. A separate compelling steroid indication requires expert assessment rather than assuming the RCVS label resolves every competing risk.