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Altered Mental Status
- 1. ALTERED MENTAL STATUS Danilo Vitorovic, M.D. Chief resident. Department of Neurology Loyola University Medical Center 2012.
- 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. Altered Mental Status ⢠Change in consciousness ⢠Confusion ⢠Organic Brain Syndrome ⢠Change in Mental Status ⢠Decreased Level of Consciousness
- 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. 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. Altered Mental Status: Diagnostic and Management 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. 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. 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. 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. Consciousness ⢠State of full awareness of the self and oneâs 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. 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
- 13. 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
- 14. Examination of Patient with Impaired Consciousness ⢠Arousal ⢠Attention and Alertness ⢠Orientation and Grasp ⢠Cognition ⢠Memory ⢠Affect ⢠Perception
- 15. Differential Diagnosis of AMS ⢠Focal brain lesion(s) ⢠Diffuse brain injury ⢠Psychogenic causes
- 16. 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
- 17. 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
- 18. Differential Diagnosis of AMS ⢠Focal brain lesion(s) ⢠Diffuse brain injury ⢠Psychogenic causes Conversion reaction Catatonia Psychogenic seizures Cerebellar cognitive affective syndrome
- 19. 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
- 20. 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
- 21. 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
- 22. Deprivation of oxygen, substrate of metabolic cofactors ⢠Hypoxia and Ischemia ⢠Hypoglycemia ⢠Thiamine deficiency ⢠Niacin deficiency ⢠Pyridoxine deficiency
- 23. 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
- 24. 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
- 25. 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
- 26. 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
- 27. 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
- 28. Hypoglycemia ⢠Causes: ⢠diabetes mellitus ⢠oral hypoglycemic agents ⢠insulin ⢠alcohol ⢠floroqunolones in combination with hypoglycemic agents (both insulin and oral)
- 29. Hypoglycemia ⢠Clinical presentation ⢠Delirium ⢠Coma with signs of multifocal brainstem dysfunction ⢠Stroke-like presentation ⢠Generalized convulsions ⢠Diagnosis ⢠Fingerstick glucose measurement ⢠Treatment ⢠D50 ⢠Octreotide
- 30. 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
- 31. 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
- 32. Toxicity of Endogenous Products ⢠Liver failure ⢠Kidney failure ⢠Respiratory failure ⢠Pancreatic disease
- 33. Liver Failure: Hepatic Encephalopathy ⢠Acute Liver Failure ⢠brain edema ď increased intracranial pressure ď herniation ⢠Chronic Liver Failure ⢠triggers: infection, GI bleed, high protein intake ⢠Alzheimer type-2 astrocytes ⢠ammonia ď glutamine
- 34. Liver Failure: Hepatic Encephalopathy ⢠Clinical Presentation ⢠apathetic delirium ⢠hyperventilation ⢠small, reactive pupils ⢠tonic gaze deviation ⢠nystagmus ⢠paresis (hemiplegia, paraplegia) ⢠seizures ⢠asterixis
- 35. 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
- 36. 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
- 37. Kidney Failure: Uremic Encephalopathy ⢠Diagnosis ⢠Elevation of BUN and Cr ⢠CSF studies: increased ICP, lymphocytic pleocytosis and proteinorachia ⢠Treatment ⢠hemodialysis
- 38. 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
- 39. Respiratory Failure: Pulm Encephalopathy ⢠Pathophysiology ⢠hypercapnia (correlates to the neurologic symptoms) ⢠hypoxemia ⢠Clinical presentation ⢠confusion ⢠somnolencce ⢠headache
- 40. Respiratory Failure: Pulm Encephalopathy ⢠Diagnosis ⢠high level of clinical suspicion (especially in COPD patient) ⢠Treatment ⢠Ventilator support
- 41. Respiratory Failure: Pulm Encephalopathy ⢠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
- 42. Toxicity of Exogenous Products ⢠Sedative drugs ⢠Acid poisons ⢠Psychotropic drugs ⢠Miscellaneous medications
- 43. Toxicity of Exogenous Products ⢠Sedative drugs ⢠Benzodiazepines ⢠Barbiturates ⢠Ethanol ⢠Opiates ⢠Acid poisons ⢠Psychotropic drugs ⢠Miscellaneous medications
- 44. Toxicity of Exogenous Products ⢠Sedative drugs ⢠Acid poisons ⢠Paraldehyde ⢠Methyl alcohol ⢠Ethylene glucol ⢠Ammonium chloride ⢠Psychotropic drugs ⢠Miscellaneous medications
- 45. 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
- 46. Toxicity of Exogenous Products ⢠Sedative drugs ⢠Acid poisons ⢠Psychotropic drugs ⢠Miscellaneous medications ⢠Penicillin ⢠Antiepileptic medications ⢠Steroids ⢠Cardiac glycosides ⢠Trace metals ⢠Organic phosphates ⢠Cyanide ⢠Salicylate
- 47. CNS Infections ⢠Acute bacterial leptomeningitis ⢠Chronic bacterial meningitis ⢠Acute viral encephalitis ⢠Acute toxic encephalopathy during viral infection
- 48. Systemic Infection ⢠Etiology ⢠Systemic infections: most commonly UTI and pneumonia ⢠Mechanism ⢠peripheral cytokine release: IL-1, IL 6, TNF- ι ⢠activation of microglia in CNS inflamation ⢠Clinical presentation ⢠alteration in mental status ⢠Management ⢠Treatment of underlying condition ⢠Avoidance of anticholinergic drugs
- 49. 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
- 50. Acute Bacterial Leptomeningitis ⢠Clinical presentation: ⢠fever ⢠nuchal rigidity ⢠headache ⢠alteration of mental status ⢠papilledema ⢠focal neurological signs ⢠cerebral herniation
- 51. Acute Bacterial Leptomeningitis ⢠Diagnostic and therapeutic approach: ⢠blood cultures draw ⢠initiation of broad spectrum antibiotics ⢠CT head ⢠lumbar puncture
- 52. Chronic Bacterial Meningitis ⢠Tuberculous meningitis ⢠Syphilis ⢠Lyme disease ⢠Nocardia ⢠Actinomyces ⢠Whippleâs disease
- 53. Chronic Bacterial Meningitis ⢠Tuberculous meningitis ⢠Whippleâs disease
- 54. 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 ⢠Whippleâs disease
- 55. Chronic Bacterial Meningitis ⢠Tuberculous meningitis ⢠Whippleâs disease
- 56. Chronic Bacterial Meningitis ⢠Tuberculous meningitis ⢠Whippleâs 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
- 57. Viral Encephalitis ⢠Herpes encephalitis ⢠Eastern equine encephalitis ⢠Western equine encephalitis ⢠St. Louis encephalitis ⢠West Nile encephalitis
- 58. Viral Encephalitis ⢠Herpes encephalitis ⢠Eastern equine encephalitis ⢠Western equine encephalitis ⢠St. Louis encephalitis ⢠West Nile encephalitis
- 59. 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
- 60. 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
- 61. 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 ⢠Reyeâs syndrome: ⢠precipitated by administration of aspirin in context of viral illness ⢠increased ICP ⢠fatty degeneration of viscera
- 62. Inflammatory Encephalopathies ⢠Granulomatous CNS angiitis ⢠Systemic lupus erythematosus ⢠Varicella-Zoster Vasculitis ⢠Behcetâs syndrome ⢠CADASIL
- 63. 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 ⢠Behcetâs syndrome ⢠CADASIL
- 64. Inflammatory Encephalopathies ⢠Granulomatous CNS angiitis ⢠Systemic lupus erythematosus ⢠CNS vasculitis ⢠Thromboembolic events due to hypercoagulable state ⢠Libman-Sachs endocarditis ⢠Varicella-Zoster Vasculitis ⢠Behcetâs syndrome ⢠CADASIL
- 65. 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 ⢠Behcetâs syndrome ⢠CADASIL
- 66. Inflammatory Encephalopathies ⢠Granulomatous CNS angiitis ⢠Systemic lupus erythematosus ⢠Varicella-Zoster Vasculitis ⢠Behcetâs 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
- 67. Inflammatory Encephalopathies ⢠Granulomatous CNS angiitis ⢠Systemic lupus erythematosus ⢠Varicella-Zoster Vasculitis ⢠Behcetâs syndrome ⢠CADASIL ⢠Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy ⢠Clinical presentation: ⢠Migraine headache with aura ⢠Recurrent ischemic strokes ⢠Behavioral changes ⢠Cognitive imparment
- 68. Primary neuronal or glial disorders ⢠Prion diseases ⢠Gliomatosis cerebri ⢠Progressive multifocal leukoencephalopathy
- 69. Miscellaneous Causes of AMS ⢠Drug withdrawal delirium ⢠Postoperative delirium ⢠Intensive Care Unit delirium ⢠Drug induced delirium
- 70. 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