Altered Mental Status

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Altered Mental Status

  1. 1. ALTERED MENTALSTATUS Danilo Vitorovic, M.D. Chief resident. Department of Neurology Loyola University Medical Center 2012.
  2. 2. Objectives• Understanding Consciousness • Anatomy and Pathophysiology• Differential diagnosis of Altered Mental Status • Navigating effectively through differential• Clinical presentation, diagnosis and treatment • Recognizing subtle clinical changes and choosing right imaging/laboratory modality • Initiating treatment early in the process
  3. 3. Altered Mental Status• Change in consciousness• Confusion• Organic Brain Syndrome• Change in Mental Status• Decreased Level of Consciousness
  4. 4. Altered Mental Status (AMS)• Defined as impairment of: • Arousal • Cognition • Behavior• Delirium • Disturbance of consciousness (awareness and attention) • Impaired cognition and/or perception • Acute onset and fluctuating course • Caused by general medical condition, substance abuse or multifactorial
  5. 5. Epidemiology• ED Patients >65 years of age • 25% has alteration in mental status • 26% has minimal cognitive impairment • 34% has moderate cognitive impairment • 40% cognitively intact
  6. 6. Altered Mental Status: Diagnostic andManagement Challenge• Patient • not able to clearly communicate problems • patient frustration• Caregiver • difficult to approach patient • difficult to provide focused care • apprehensive family • caregiver frustration• Diagnosis and Treatment • correct diagnosis and appropriate treatment frequently delayed
  7. 7. Case 1.• 62 year old right handed man presents to ED with difficulty speaking for one day: • tries to explain events of the previous day but words are unintelligible and appears confused • BP 156/93mmHg HR 87/min RR 13/min O2 Sat 97% RA • does not move his right hand
  8. 8. Case 2.• 47 year old man with past medical history significant for hypertension, hyperlipidemia and diabetes presents to ED for brief episode of chest pain • during the examination by ED Attending, patient developed slurred speech and right sided weakness • BP 146/92 mmHg HR 91/min RR 18/min O2 Sat 99% RA • right arm biceps, brachioradialis and triceps hyporeflexia
  9. 9. Case 3.• 27 year old woman without significant past medical history presents to ED with inability to speak for the last 90 minutes • sudden onset during party • BP 107/69 mmHg HR 73/min RR 12/min O2 Sat 100% RA • other than inability to speak, no other neurologic deficits
  10. 10. Consciousness• State of full awareness of the self and one’s relationship to environment• Components: • Arousal • degree of sensory stimulation necessary to keep patient awake • Content • cognitive (language, face recognition, space awareness) • affective (appropriateness of affect)
  11. 11. Consciousness• Anatomy • Pontine reticular activating system • mesopontine tegmentum (pedunculopontine and letarodorsal tegmental nuclei) • Midbrain reticular activating system • paramedian midbrain reticular formation and monoamine neurons (noradrenergic, serotoninergic and dopaminergic) • Hypothalamus • lateral hypothalamic area (orexin) and histaminergic neurons • Thalamus • midline, intralaminar and reticular nuclei • Diffuse cortical projections
  12. 12. Pathophysiology of Impaired Consciousness• Ascending Reticular Activating System (ARAS) lesion • suspect focal compressive/destructive lesion• Bilateral diffuse hemispheric dysfunction • toxic/metabolic derangements • interplay between global process and local susceptibility
  13. 13. Examination of Patient with Impaired Consciousness• Arousal• Attention and Alertness• Orientation and Grasp• Cognition• Memory• Affect• Perception
  14. 14. Differential Diagnosis of AMS• Focal brain lesion(s)• Diffuse brain injury• Psychogenic causes
  15. 15. Differential Diagnosis of AMS• Focal brain lesion(s) Epidural hematoma Subdural hematoma• Diffuse brain injury Epidural abscess• Psychogenic causes Subarachnoid hemorrhage Intracerebral hemorrhage Intracerebral tumors Intracerebral abscesses Large hemispheric strokes Brainstem lesions
  16. 16. Differential Diagnosis of AMS• Focal brain lesion(s)• Diffuse brain injury Deprivation of oxygen, substrate or metabolic cofactors• Psychogenic causes Toxicity of endogenous products Toxicity of exogenous products Infections or inflammation of CNS Abnormalities of ionic or acid-base environment of CNS Disorders of temperature regulation Primary neuronal or glial disorders Miscellaneous disorders of unknown cause
  17. 17. Differential Diagnosis of AMS• Focal brain lesion(s)• Diffuse brain injury• Psychogenic causes Conversion reaction Catatonia Psychogenic seizures Cerebellar cognitive affective syndrome
  18. 18. Case 1.• 62 year old right handed man presents to ED with difficulty speaking for one day: • tries to explain events of the previous day but words are unintelligible and appears confused • BP 156/93mmHg HR 87/min RR 13/min O2 Sat 97% RA • does not move his right hand
  19. 19. Case 2.• 47 year old man with past medical history significant for hypertension, hyperlipidemia and diabetes presents to ED for brief episode of chest pain • during the examination by ED Attending, patient developed slurred speech and right sided weakness • BP 146/92 mmHg HR 91/min RR 18/min O2 Sat 99% RA • right arm biceps, brachioradialis and triceps hyporeflexia
  20. 20. Case 3.• 27 year old woman without significant past medical history presents to ED with inability to speak for the last 90 minutes • sudden onset during party • BP 107/69 mmHg HR 73/min RR 12/min O2 Sat 100% RA • other than inability to speak, no other neurologic deficits
  21. 21. Deprivation of oxygen, substrate of metabolic cofactors• Hypoxia and Ischemia• Hypoglycemia• Thiamine deficiency• Niacin deficiency• Pyridoxine deficiency
  22. 22. Hypoxia and Ischemia• Causes: • Hypoxia • hypoxic hypoxia • anemic hypoxia • ischemic hypoxia • hystotoxic hypoxia • Acute ischemia • Intermittent/Sustained Hypoxia • posterior reversible leukoencephalopathy • disseminated intravascular coagulation • cerebral malaria • fat embolism • cardiopulmonary bypass surgery
  23. 23. Hypoxia and Ischemia• Clinical presentation: • Immediate presentation • loss of consciousness • generalized convulsion • pupillary dilatation • generalized weakness • extensor plantar responses • Delayed presentation • delayed post-anoxic encephalopathy • delayed coma after hypoxia • intention myoclonus
  24. 24. Hypoxia and Ischemia• Clinical presentation: • Immediate presentation • loss of consciousness Delayed Post-Anoxic Encephalopathy • generalized convulsion • pupillary dilatation • generalized weakness - Onset between 4 and 14 days after insult • extensor plantar responses - Patients become irritable, apathetic, confused • Delayed presentation - Diagnosis: Clinical presentation and MRI imaging • delayed post-anoxic encephalopathy - Treatment: Expectant • delayed coma after hypoxia - Prognosis: • intention myoclonus usually complete resolution within a year
  25. 25. Hypoxia and Ischemia• Clinical presentation: • Immediate presentation Delayed • loss of consciousness Coma After Hypoxia • generalized convulsion • pupillary dilatation - Onset after variable lucid interval • generalized weakness • extensor - Patients lapse plantar responses into coma without focal signs - Diagnosis: Clinical presentation and MRI imaging • Delayed presentation - Treatment: Bed rest after hypoxia might be • delayed post-anoxic encephalopathy • delayed coma after hypoxia preventative • intention myoclonus - Prognosis: Poor
  26. 26. Hypoxia and Ischemia• Clinical presentation: • Immediate presentation Intention Myoclonus • loss of consciousness • generalized convulsion - Occurs • pupillary dilatation in 40% of patients who do not regain • generalized weakness consciousness after episode of severe hypoxia • extensor plantar responses - Origin: cortical or subcortical • Delayed presentation - Presentation: dysarthria, myoclonic jerks • delayed post-anoxic encephalopathy - Diagnosis: EEG • delayed coma after hypoxia - Treatment: • intention myoclonus levetiracetam/5-hydroxytryptofan - Prognosis: Poor
  27. 27. Hypoglycemia• Causes: • diabetes mellitus • oral hypoglycemic agents • insulin • alcohol • floroqunolones in combination with hypoglycemic agents (both insulin and oral)
  28. 28. Hypoglycemia• Clinical presentation • Delirium • Coma with signs of multifocal brainstem dysfunction • Stroke-like presentation • Generalized convulsions• Diagnosis • Fingerstick glucose measurement• Treatment • D50 • Octreotide
  29. 29. Thiamine deficiency• Causes • Glucose infusions without thiamine • Alcoholism • Pregnancy (emesis gravidarum) • Bariatric surgery• Pathophysiology • Selective damage of • mammillary bodies • medio-dorsal nucleus of thalamus • periaqueductal gray matter • oculomotor nuclei
  30. 30. Thiamine deficiency• Clinical presentation • confusion/delirium/stupor • memory impairment • anisocoria • nystagmus • ophthalmoplegia • ataxia • autonomic insufficiency• Diagnosis • clinical presentation • MRI brain• Treatment • Thiamine supplementation (IV form preferred): no actual dose established
  31. 31. Toxicity of Endogenous Products• Liver failure• Kidney failure• Respiratory failure• Pancreatic disease
  32. 32. Liver Failure: Hepatic Encephalopathy• Acute Liver Failure • brain edema  increased intracranial pressure  herniation• Chronic Liver Failure • triggers: infection, GI bleed, high protein intake • Alzheimer type-2 astrocytes • ammonia  glutamine
  33. 33. Liver Failure: Hepatic Encephalopathy• Clinical Presentation • apathetic delirium • hyperventilation • small, reactive pupils • tonic gaze deviation • nystagmus • paresis (hemiplegia, paraplegia) • seizures • asterixis
  34. 34. Liver Failure: Hepatic Encephalopathy• Diagnosis • Clinical presentation and stigmata of liver disease • MRI brain • CSF analysis: glutamine and alpha-ketoglutaramate• Treatment • Lactulose • Rifaximin • Neomycin • Liver transplantation • Diet: caution
  35. 35. Kidney Failure: Uremic Encephalopathy• Etiology • no clear inciting factor • considering intracranial calcium level changes, 1-guanadino compounds and tryptophan• Clinical presentation • decreased alertness • hyperventilation • motor hyperactivity (including multifocal myoclonus) • muscle stretch reflexes asymetry • seizures (frequently provoked by cephalosporins) • metabolic acidosis
  36. 36. Kidney Failure: Uremic Encephalopathy• Diagnosis • Elevation of BUN and Cr • CSF studies: increased ICP, lymphocytic pleocytosis and proteinorachia• Treatment • hemodialysis
  37. 37. Kidney Failure: Uremic Encephalopathy• Diagnosis • Elevation of BUN and Cr • CSF studies: increased ICP, lymphocytic pleocytosis and proteinorachia Dialysis Dysequlibrium Syndrome• Treatment - Usually occurs during the first treatment • hemodialysis - Presents with headache, nausea, muscle weakness and cramps, fatigue - Asterixis, myoclonus, seizure, death - Prevention: slow hemodialysis, mannitol
  38. 38. Respiratory Failure: Pulm Encephalopathy• Pathophysiology • hypercapnia (correlates to the neurologic symptoms) • hypoxemia• Clinical presentation • confusion • somnolencce • headache
  39. 39. Respiratory Failure: Pulm Encephalopathy• Diagnosis • high level of clinical suspicion (especially in COPD patient)• Treatment • Ventilator support
  40. 40. Respiratory Failure: PulmEncephalopathy• Diagnosis Complications of Initiation of Mechanical Ventilation in • high level of clinical suspicion (especially in COPD patient) Patient with Respiratory Failure• Treatment - Occurs after patient recovers from CO2 narcosis - Obtundation • Ventilator support - Multifocal myoclonus - Generalized seizures - Death - Prevention: gradual treatment of respiratory failure
  41. 41. Toxicity of Exogenous Products• Sedative drugs• Acid poisons• Psychotropic drugs• Miscellaneous medications
  42. 42. Toxicity of Exogenous Products• Sedative drugs • Benzodiazepines • Barbiturates • Ethanol • Opiates• Acid poisons• Psychotropic drugs• Miscellaneous medications
  43. 43. Toxicity of Exogenous Products• Sedative drugs• Acid poisons • Paraldehyde • Methyl alcohol • Ethylene glucol • Ammonium chloride• Psychotropic drugs• Miscellaneous medications
  44. 44. Toxicity of Exogenous Products• Sedative drugs• Acid poisons• Psychotropic drugs • Tricyclic antidepressants • Anticholinergic drugs • Antihistaminic drugs • Amphetamines • Lithium • MAO inhibitors • LSD and mescaline • Phencyclidine• Miscellaneous medications
  45. 45. Toxicity of Exogenous Products• Sedative drugs• Acid poisons• Psychotropic drugs• Miscellaneous medications • Penicillin • Antiepileptic medications • Steroids • Cardiac glycosides • Trace metals • Organic phosphates • Cyanide • Salicylate
  46. 46. CNS Infections• Acute bacterial leptomeningitis• Chronic bacterial meningitis• Acute viral encephalitis• Acute toxic encephalopathy during viral infection
  47. 47. Systemic Infection• Etiology • Systemic infections: most commonly UTI and pneumonia• Mechanism • peripheral cytokine release: IL-1, IL 6, TNF- α • activation of microglia in CNS inflamation• Clinical presentation • alteration in mental status• Management • Treatment of underlying condition • Avoidance of anticholinergic drugs
  48. 48. Acute Bacterial Leptomeningitis• Causative organisms: • Streoptococcus pneumoniae (51%) • Naiseria meningitis (37%) • Listeria monocytogenes (4%) • Staphylococcus aureus • Hemophilus influenzae• Pathophysiology: • contiguous versus hematogenic spread • inflammatory reactions (toxic excephalopathy) • cerebral edema and herniation
  49. 49. Acute Bacterial Leptomeningitis• Clinical presentation: • fever • nuchal rigidity • headache • alteration of mental status • papilledema • focal neurological signs • cerebral herniation
  50. 50. Acute Bacterial Leptomeningitis• Diagnostic and therapeutic approach: • blood cultures draw • initiation of broad spectrum antibiotics • CT head • lumbar puncture
  51. 51. Chronic Bacterial Meningitis• Tuberculous meningitis• Syphilis• Lyme disease• Nocardia• Actinomyces• Whipple’s disease
  52. 52. Chronic Bacterial Meningitis• Tuberculous meningitis• Whipple’s disease
  53. 53. Chronic Bacterial Meningitis• Tuberculous meningitis • Insidious onset in ~50% of patients • lethargy, stupor, coma • nuchal rigidity • CSF analysis: • lymphocytic pleocytosis (~1-500 WBC) • hyperproteinorachia (>100mg/dL) • oligoglucorachia (not less than 20mg/dL) • Treatment • long term antimycobacterial antibiotics• Whipple’s disease
  54. 54. Chronic Bacterial Meningitis• Tuberculous meningitis• Whipple’s disease
  55. 55. Chronic Bacterial Meningitis• Tuberculous meningitis• Whipple’s disease • Trophermyma whippleii • Affects middle aged man • Systemic sympoms and signs • weight loss, abdominal pain, diarrhea, arthralgias, uveitis • Neurologic symptoms and signs • oculomasticatory myorhythmia • ataxia • seizures (both focal and generalized) • CSF analysis • lymphocytic pleocytosis • can be normal • Treatment • antibiotics
  56. 56. Viral Encephalitis• Herpes encephalitis• Eastern equine encephalitis• Western equine encephalitis• St. Louis encephalitis• West Nile encephalitis
  57. 57. Viral Encephalitis• Herpes encephalitis• Eastern equine encephalitis• Western equine encephalitis• St. Louis encephalitis• West Nile encephalitis
  58. 58. Viral Encephalitis• Herpes encephalitis • Caused by Herpes Simples Virus type I • Clinical presentation • confusion, aphasia, behavioral changes • olfactory and/or gustatory hallucinations • focal neurological sings • partial complex seizures
  59. 59. Viral Encephalitis• Herpes encephalitis • Diagnosis • CSF analysis • Lymphocytic pleocytosis (~10-1000/mm3) • Hyperproteinorachia (up to 870mg/dL) • HSV PCR • MRI brain • Temporal lobe T2/FLAIR hyperintensities • Treatment • Acyclovir 10mg/kg every 8 hours for 2-3 weeks
  60. 60. Acute Toxic Encephalopathy During Viral Infection• Occurs in children age of 5 or younger• Systemic infection triggers acute onset of increased ICP• No CNS inflammatory markers• Reye’s syndrome: • precipitated by administration of aspirin in context of viral illness • increased ICP • fatty degeneration of viscera
  61. 61. Inflammatory Encephalopathies• Granulomatous CNS angiitis• Systemic lupus erythematosus• Varicella-Zoster Vasculitis• Behcet’s syndrome• CADASIL
  62. 62. Inflammatory Encephalopathies• Granulomatous CNS angiitis • associated with VZV infections, lymphoma, sarcoidosis, AA, infections • presents with headache, alteration in mental status, focal neurological sings and seizures• Systemic lupus erythematosus• Varicella-Zoster Vasculitis• Behcet’s syndrome• CADASIL
  63. 63. Inflammatory Encephalopathies• Granulomatous CNS angiitis• Systemic lupus erythematosus • CNS vasculitis • Thromboembolic events due to hypercoagulable state • Libman-Sachs endocarditis• Varicella-Zoster Vasculitis• Behcet’s syndrome• CADASIL
  64. 64. Inflammatory Encephalopathies• Granulomatous CNS angiitis• Systemic lupus erythematosus• Varicella-Zoster Vasculitis • Causes CNS vasculitis with ischemic strokes in immunocompetent pt • Diffuse encephalopathy in immunocompromised patient• Behcet’s syndrome• CADASIL
  65. 65. Inflammatory Encephalopathies• Granulomatous CNS angiitis• Systemic lupus erythematosus• Varicella-Zoster Vasculitis• Behcet’s syndrome • oral and genital ulcerations, anterior or posterior uveitis, skin lesions • primary neurologic symptoms: behavioral changes, AMS, diplopia, ataxia • CNS venous infarctions • increased ICP due to vena cava system thrombosis• CADASIL
  66. 66. Inflammatory Encephalopathies• Granulomatous CNS angiitis• Systemic lupus erythematosus• Varicella-Zoster Vasculitis• Behcet’s syndrome• CADASIL • Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy • Clinical presentation: • Migraine headache with aura • Recurrent ischemic strokes • Behavioral changes • Cognitive imparment
  67. 67. Primary neuronal or glial disorders• Prion diseases• Gliomatosis cerebri• Progressive multifocal leukoencephalopathy
  68. 68. Miscellaneous Causes of AMS• Drug withdrawal delirium• Postoperative delirium• Intensive Care Unit delirium• Drug induced delirium
  69. 69. Conclusion• Differentiation between structural and diffuse processes causing AMS• Exploring broad differential when approaching patient with AMS• Awareness of multiple causative processes occuring simultaneously• Importance of supportive care and early institution of treatment

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