Myopathy Neuropathy CNS Infections Rachel Garvin MD Assistant

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 (>20 cm. H 2 O) �Increased protein (>100 mg/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 14 -21 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: Ig. M 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