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CPC Conference Patient: RT May 16th, 2017

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Presentation on theme: "CPC Conference Patient: RT May 16th, 2017"— Presentation transcript:

1 CPC Conference Patient: RT May 16th, 2017
Neurology Resident: Michael Isfort Pathologist: Dr. Hamilton

2 HPI 58yo morbidly obese male with PMHx of chronic EtOH abuse, Afib not on AC, HTN transferred to PUH on 04/28/17 with falls, LBP, BLE weakness c/f spinal cord injury. Progressive weakness for around 1 year following fall, unable to get OOB on morning of admission. L>R hand numbness. Neck pain radiating to shoulders (months). Walker for around 1 month. PMHx: chronic EtOH abuse, Afib not on AC, HTN PSHX: CCY FHX: Non-contributory Social Hx: Long H/o EtOH abuse. Lives alone Meds: Coreg,, ibuprofen, lisinopril, omeprazole, Admitted 08/2016 for L hand abscess/cellulitis

3 Hospital course VS: T: AF, P 90s-100s (afib), BP 110s/90s, Wt 130kg
Exam: AOx3, RUE 4/5, LUE 4/5, RLE 4/5, LLE3.5, + hoffmans BL, 3+ BR LABS (04/28): BMP wnl, BUN 43, TBili 5.2, AST/ALT 230/550, CRP 5.5, WBC 12 with L shift/plts 29 MRI spine: C3-C4 osteophyte with mod canal stenosis, flattening of cord, ?cord signal motion degraded Abd US: Cirrhosis

4 MRI C spine

5 Hospital course (continued)
04/28: Admitted to NSGY, c-collar, dexamethasone PO, med clearance for ACDF 04/29: NH3: 120 04/30 and 05/01: Somnolent (Aox2), hypotensive, afebrile. NH > ?HE +lactulose/rifaximin. +HCV. L elbow erythematous, WBC 8.8/Plts 35 Cr 1.0->2.3, k 5.3, NH Transfer to TICU. Lasix and spironolactone. Ortho drained L olecranon bursitis, + MSSA + Vanco. BCx later grew MSSA 05/02: VTach, K 7.5/BUN119/Cr 3.7/Ph 6.5, Plts: 32, INR 2.3, CRP 11. Intubated. EKG with STEMI. Went into Vfib. ACLS started multiple epi rounds, defibrillations. Pronounced at on 03:16 on 05/02.

6 Autopsy (prelim) COD: Multisystem organ failure 2/2 renal/liver failure and MI, caused by sepsis. Cavities: Rib fracture x3 (CPR), 150mL of ascites in abd CV: LVH Resp: Lungs congested with bloody, frothy fluid Liver: Multiple nodules seen GI: Esophageal varices, pancreas with calcifications Renal: Kidneys with multiple pinpoint hemorrhages, white lesions in rnal cortex and medulla

7 Neurologic Complications of EtOH abuse
Acute: Intoxication Withdrawal Acute alcoholic neuropathy, Alcohol related compression neuropathies Acute alcoholic myopathy Chronic: Wernicke syndrome: B1 def. Cognitive disorder, ataxia, ophthalmoparesis Korsakoff syndrome: B1 def. Anterograde/retrograde amnesia Confabulation. Vacuous speech and abulia Alcohol related dementia Alcohol related cerebellar atophy Marchiafava-bignami disease PNS: Chronic alcoholic neuropathy, Chronic alcoholic myopathy

8 Neurologic Complications of EtOH abuse: Acute
Intoxication Facilitates GABA, Inhibits glutamate = CNS depression in reticular formation -> cerebellar hemispheres Blackout: impaired memory encoding possibly from direct hippocampal effect Withdrawal GABA downregulated and glutamate receptor upregulated -> excitatory Seizures, tremors, hallucinations, DTs (previous +autonomic dysfunction) WAS + BZDs: diazepam or lorazepam (severe) or oral chlordiazepoxide

9 Neurologic Complications of EtOH abuse: Chronic
Wernicke syndrome: B1 def. cognitive disorder, ataxia, ophthalmoparesis Decreased attention, impaired memory, disorientation, diminished speech Exam: Nystagmus, bilateral but asymmetric LR palsy, trunchal/gait ataxia, coma Imaging: Restricted diffusion/FLAIR signal in thalamus, hypothalamus (mammillary bodies), midbrain (PAG/oculomotor regions) and pons (abducens and medial vestibular nuclei_ Tx: Thiamine 1g IV/24hr Korsakoff syndrome: Anterograde/retrograde amnesia without EOM problems or impaired attention. Confabulation. Vacuous speech and abulia. Damage to both anterior thalamic nuclei and hypothalamus Tx: Thiamine

10 Neurologic Complications of EtOH abuse: Chronic
Alcoholic related dementia: Underdiagnosed with few neuropathologic hallmarks may have concurrent micronutrient def, trauma, hepatic insufficency Early cognitive decline. Overlap with other cognitive disorders, but more globally impaired Neurotoxic glutaminergic excitation -> neuronal loss in hippocampal and neocortical neurons. Reduced brain volume Marchiafava-bignami disease: Gait impairment, LOC, dysarthria, amnesia, cortical disconnect syndrome CC involvement especially splenium-> DWI changes Thiamine def Cerebellar degeneration: Most common complication of EtOH. Similar to Wernicke but does not recover Cerebellar vermis and WM loss

11 Neurologic Complications of EtOH abuse: Chronic
Chronic alcoholic neuropathy EtOH impairs retrograde axonal transport Slowly progressive sensory loss involve small fibers/nociception -> painful senory neuropathy and paresthesias. Later motor. + autonomic. Thiamine def neuropathy: large fiber, weakness/ataxia Exam: Length dependent sensory, loss of ankle jerks-> distal weakness NCS: Axonal sensori>motor neuropathy Chornic alcoholic myopathy: Affects 2% of western adults (most common skeletal muscle disease) Progressive proximal weakness/atrophy, normal CK, lose type II fibers Mostly skeletal myocytes also cardiomyocytes EMG: polyphasic waves and early recruitment, proximal denervation

12 Neurologic Complications of EtOH abuse: Chronic
Acute EtOH neuropathy: Acute to subacute. Axonal. Mimics GBS. EtOH related compression neuropathies: + peripheral neuropathy higher risk of compression. Conduction block or axonal loss Acute EtOH Myopathy: Mechanism: (1) impairs sarcolemma Ca channels (2) compromise sarcolemmal integrity Increased CK. Fiber necrosis and phagocytosis. Type I fibers. Toxic effect. Decr K or PO4. Glycolytic inhibition Could be cause of 20% of rhabdo cases. Follows binge Proximal pain and weakness. Bulbar involvement Recovers with nutrition, lytes, hydration

13 References: Noble JM, Weimer LH. Neurologic Complications of Alcoholism. Continuum. 2014; 20(3):

14 NEUROPATHOLOGY EXTERNAL GROSS EXAMINATION IS UNREMARKABLE FURTHER DISSECTION REVEALS NO ABNORMALITIES. (NO GROSS IMAGES) MICROSCOPIC EXAMINATION AND FINAL DIAGNOSIS: Alzheimer Type II astrocytes – swollen pale nucleus 1. Multiple microabscesses with gram-positive cocci (also found in heart, lungs and kidneys) 2. Hepatic encephalopathy, mild CD68 - macrophages Gram stain – G+ cocci

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