Myopathy, Neuropathy, CNS Infections Rachel Garvin, MD Assistant Professor, Neurocritical Care Department of Neurosurgery

Objectives Describe critical care myopathy and neuropathy, causes, diagnosis and management Describe CNS infections, diagnosis and management

Critical Illness Polyneuropathy (CIP) and Myopathy (CIM) Seen in conjunction with severe sepsis and prolonged use of neuromuscular blockade +/- steroids Seen in up to 40% of ICU patients

CIM/CIP First sign is often inability to wean from ventilator Not usually noted until patient at least 2 weeks on ventilator Severe diffuse weakness and muscle wasting

CIP Diagnosis by EMG Axonal degeneration of motor and sensory fibers CK is normal Muscle biopsy shows denervation atrohpy

CIM EMG shows myopathic muscle units Elevated serum CK Biopsy shows myopathy with loss of myosin

Recovery/Management No specific treatment – supportive care Range of levels of recovery

CNS INFECTIONS

CNS Infections Meningitis/Ventriculitis Encephalitis Brain Abscess

Meningitis Bacterial (septic) vs Other infectious or inflammatory (aseptic) Most often caused by bacteremia that seeds meninges by crossing BBB and multiplying in CSF Ventriculitis more common in those with ventricular drains/shunts Cerebral edema can occur d/t inflammatory effects of infection leading to vasogenic and cytotoxic edema

Meningitis Classic signs of fever, HA and meningismus may not always be present (esp. elderly) Also seen with photophobia, N/V, altered consciousness Pathogens dependent on: ◦ Adult in community: strep pneumo, neisseria, listeria ◦ Hospitalized patient: gram negatives

Meningitis Dx: LP Elevated opening pressure (>20cmH2O) Increased protein (>100mg/dl) Decreased glucose (<40% serum level) Elevated nucleated cell count (usually >100)

Complications SIADH (50% of cases) Seizures Elevated ICP  risk of herniation

Treatment Abx appropriate to pathogen Ensure appropriate CNS dosing Duration from days depending on pathogen

Encephalitis Infection of brain parenchyma Multiple modes of infection Most are hematogenous spread except for HSV and rabies which spread via neurons Most are viral

Encephalitis: Presentation Varies as certain infections have certain locations they affect: HSV: inf/medial temporal lobes and orbito-frontal cortex Arboviruses (West Nile, equine): cortical gray matter, brainstem and thalamic nuclei Japanese B virus: brainstem nuclei and basal ganglia

Encephalitis: Diagnosis History and physical Neuroimaging: CT and MRI LP: many present as meningoencephalitis HSV PCR may be falsely negative in first 48 hours and then again 10 days after infection Other viruses: IgM in CSF, viral culture from blood, tissue or CSF

Encephalitis: Treatment and Outcomes Only treatment for HSV with Acyclovir for 14 days Other viruses are supportive care only

Brain Abscess Encapsulated collection of pus within brain parenchyma Risk factors include: head and neck infections, penetrating head injury, immunocompromised state Presentation often non-specific but can have symptoms related to location of abscess

Brain Abscess: Pathophysiology Begins as a cerebritis, day 1-3 with surrounding inflammation and edema 1 week into infection, central necrosis develops By 14 days, fibrous capsule apparent which becomes more established

Brain Abscess: Diagnosis History and Physical CT + contrast MRI Needle-guided aspiration

Braun Abscess: Complications Seizures are most common morbidity (up to 70%) Abscess rupture leading to meningitis/ventriculitis Formation of subdural empyema, epidural abscess, septic thrombophlebitis

Brain Abscess: Treatment IV abx based on pathogen or presumed source (otitis, odontogenic) Surgical drainage

CNS Fungal Infections Seen mostly in immunocompromised patients Can present in any form (meningitis  abscess) Often difficult to grow in culture Treatment with ampho B