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Altered Mental Status and Coma November 15, 2005 Tintinalli Chapter 229 Dr. Hadcock Slides by Scott Gunderson.

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Presentation on theme: "Altered Mental Status and Coma November 15, 2005 Tintinalli Chapter 229 Dr. Hadcock Slides by Scott Gunderson."— Presentation transcript:

1 Altered Mental Status and Coma November 15, 2005 Tintinalli Chapter 229 Dr. Hadcock Slides by Scott Gunderson

2 Altered Mental Status Arousal Function Arousal Function Content of Consciousness Content of Consciousness Or both Or both

3 Arousal Function Reticular activating system Reticular activating system Midbrain Midbrain Pons Pons Medulla Medulla

4

5 Content of Consciousness Cerebral cortex Cerebral cortex Emotions Emotions Reasoning Reasoning Self-awareness Self-awareness Spatial relationships Spatial relationships

6 Delirium

7 Delirium Acute confusional state with impaired alertness Acute confusional state with impaired alertness Alerting functions Alerting functions Overworking or underworking Overworking or underworking Difficulty focusing, shifting or sustaining attention Difficulty focusing, shifting or sustaining attention Formal definition includes: Formal definition includes: Fluctuating confusion Fluctuating confusion Disturbed sleep wake cycle Disturbed sleep wake cycle

8 Pathophysiology 4 general causes 4 general causes 1. Primary intracranial disease 2. Systemic disease affecting CNS 3. Exogenous toxins 4. Drug withdrawal

9 Clinical Features Onset is within days Onset is within days 3 general variants of activity and alertness 3 general variants of activity and alertness 1. Hypoalert-hypoactive 2. Hyperalert-hyperactive 3. Mixed – May cycle rapidly between hyperactive and hypoactive.

10 Clinical Features Altered sleep wake cycles Altered sleep wake cycles “Sundowning” “Sundowning” Tremor, tachycardia, diaphoresis, outbursts, delusions, hallucinations may occur Tremor, tachycardia, diaphoresis, outbursts, delusions, hallucinations may occur

11 Diagnosis Diagnosis primarily by history Diagnosis primarily by history Physical exam to look for causes Physical exam to look for causes Additional testing to identify a cause Additional testing to identify a cause Labs: CMP, CBC, UA Labs: CMP, CBC, UA +/- lumbar puncture +/- lumbar puncture Radiology: CXR and head CT Radiology: CXR and head CT MMSE MMSE

12 Treatment Treat the underlying cause (Table 229-5) Treat the underlying cause (Table 229-5) Infections: pneumonia, UTI, meningitis, sepsis Infections: pneumonia, UTI, meningitis, sepsis Metabolic: hypoglycemia, electrolytes, hepatic, thyroid disorders, ETOH, or drugs Metabolic: hypoglycemia, electrolytes, hepatic, thyroid disorders, ETOH, or drugs Neurologic: CVA, TIA, seizure, intracranial hemorrhage or mass Neurologic: CVA, TIA, seizure, intracranial hemorrhage or mass Cardiopulmonary: CHF, MI, PE, hypoxia Cardiopulmonary: CHF, MI, PE, hypoxia Drug related: Narcotics, sedatives, muscle relaxants, antiemetics, digoxin Drug related: Narcotics, sedatives, muscle relaxants, antiemetics, digoxin

13 Treatment Sedation Sedation Haloperidol Haloperidol Lorazepam Lorazepam Confinement or restraints as appropriate Confinement or restraints as appropriate Admit unless rapidly reversible cause is identified Admit unless rapidly reversible cause is identified

14 Dementia

15 Dementia 2 main types 2 main types Dementia of Alzheimer disease Dementia of Alzheimer disease Vascular dementias Vascular dementias Insidious loss of mental capacity Insidious loss of mental capacity Rapidly progressing or abrupt onset indicates another organic cause Rapidly progressing or abrupt onset indicates another organic cause Behavior problems are common Behavior problems are common

16 Pathophysiology Majority of causes are from Alzheimer’s Majority of causes are from Alzheimer’s Etiology is poorly understood Etiology is poorly understood Reduced number of neurons in the cortex Reduced number of neurons in the cortex Amyloid deposition Amyloid deposition Neurofibrillary tangles and plaques Neurofibrillary tangles and plaques Vascular Dementia Vascular Dementia Multiple infarctions Multiple infarctions

17 http://www-medlib.med.utah.edu/WebPath/CINJHTML/CINJ034.html

18 http://www-medlib.med.utah.edu/WebPath/CNSHTML/CNS178.html

19 http://www-medlib.med.utah.edu/WebPath/CNSHTML/CNS092.html

20 Clinical Features Memory impairment gradual & progressive Memory impairment gradual & progressive Recent memory affected greatest Recent memory affected greatest Impairment of memory and orientation with preserved motor and speech is characteristic Impairment of memory and orientation with preserved motor and speech is characteristic 3 stages 3 stages Mild–minor memory loss Mild–minor memory loss Moderate–memory now affecting social life Moderate–memory now affecting social life Severe–affecting ADL’s Severe–affecting ADL’s

21 Clinical Features Vascular dementia Vascular dementia Similar insidious onset Similar insidious onset May also have exam findings of exaggerated DTR’s or weakness that AD will not have. May also have exam findings of exaggerated DTR’s or weakness that AD will not have.

22 Diagnosis Diagnosis primarily by history Diagnosis primarily by history Usually no one specific event Usually no one specific event If single or multiple distinct events more likely to be vascular dementia If single or multiple distinct events more likely to be vascular dementia Labs to rule out other causes Labs to rule out other causes CBC, CMP, Thyroid, B12, RPR, +/- LP CBC, CMP, Thyroid, B12, RPR, +/- LP Radiology Radiology CT or MRI CT or MRI

23 Diagnosis Exacerbating factors Exacerbating factors UTI UTI CHF CHF Hypothyroidism Hypothyroidism Many others Many others

24 Treatment Primarily environmental or psychosocial Primarily environmental or psychosocial Pharmacologic Pharmacologic Antiphychotics Antiphychotics Mood stabilizers Mood stabilizers Cholinesterase inhibitors Cholinesterase inhibitors All have little use in the ED except to manage an acute exacerbation All have little use in the ED except to manage an acute exacerbation

25 Disposition New diagnosis entertained in the ED but further testing is needed New diagnosis entertained in the ED but further testing is needed Admit vs. outpatient follow up after treatable causes ruled out or addressed Admit vs. outpatient follow up after treatable causes ruled out or addressed Must consider safety of there environment when discharging. Must consider safety of there environment when discharging.

26 Coma

27 Coma State of reduced alertness and responsiveness from which you cannot be aroused State of reduced alertness and responsiveness from which you cannot be aroused Glasgow Coma Scale Glasgow Coma Scale Motor, verbal, eye opening Motor, verbal, eye opening

28 Motor Response ExampleScore Commands Follows simple commands 6 Localizes Pain Pulls examiner's hand away when pinched 5 Withdraws from Pain Pulls a part of body away when pinched 4 Abnormal Flexion Flexes body inappropriately to pain 3 Abnormal Extension Body becomes rigid in an extended position when examiner pinches him 2 No Response Has no motor response to pinch 1

29 Eye-Opening. Spontaneous Opens eyes on own 4 To Voice Opens eyes when asked to in a loud voice 3 To Pain Opens eyes when pinched 2 No Response Does not open eyes 1

30 Verbal Response (Talking). Orientated Carries on a conversation correctly and tells examiner where he is, who he is, and the month and year 5 Confused Conversation Seems confused or disoriented 4 Inappropriate Words Talks so examiner can understand him but makes no sense 3 Sounds Makes sounds that examiner cannot understand 2 No Response Makes no noise 1

31 Pathophysiology Global Global Hypoglycemia, hypoxia Hypoglycemia, hypoxia CNS CNS Brainstem disease Brainstem disease Bilateral cortical disease Bilateral cortical disease Unilateral should not present as coma Unilateral should not present as coma

32 Mass Lesions Causing Coma Secondary to compression of the brainstem Secondary to compression of the brainstem Primarily uncal vs. central Primarily uncal vs. central

33 Uncal herniation Medial temporal lobe compresses brainstem Medial temporal lobe compresses brainstem Decreased responsiveness going into a coma Decreased responsiveness going into a coma Ipsilateral pupil dilated and nonreactive Ipsilateral pupil dilated and nonreactive

34 Central Herniation Progressive loss of consciousness Progressive loss of consciousness Decorticate posturing Decorticate posturing Irregular respirations Irregular respirations

35 Increased Intracranial Pressure Localized vs. generalized Localized vs. generalized Cerebral blood flow constant with MAP of 50- 100 mm of Hg Cerebral blood flow constant with MAP of 50- 100 mm of Hg CPP = MAP – ICP CPP = MAP – ICP Cushing reflex of hypertension and bradycardia Cushing reflex of hypertension and bradycardia

36 Clinical Features Coma secondary to hemispheric hemorrhage may still have localizing features Coma secondary to hemispheric hemorrhage may still have localizing features Pupillary, muscle, and cranial nerve exam to determine central vs. focal Pupillary, muscle, and cranial nerve exam to determine central vs. focal Pupillary response generally preserved in toxic metabolic coma Pupillary response generally preserved in toxic metabolic coma

37 Diagnosis Stabilization diagnosis and treatment overlap Stabilization diagnosis and treatment overlap ABC’s ABC’s Lab,+/- LP Lab,+/- LP CT head CT head Examination Examination Focal vs. diffuse Focal vs. diffuse

38 Specific Issues C-spine immobilization if trauma suspected C-spine immobilization if trauma suspected Pediatric coma commonly ingestion, infection, or abuse Pediatric coma commonly ingestion, infection, or abuse Seizures Seizures Coma s/p seizure activity Coma s/p seizure activity “electromechanical dissociation of the brain and body” “electromechanical dissociation of the brain and body”

39 Treatment Reverse identifiable causes Reverse identifiable causes Glucose Glucose Thiamine prior if alcoholic Thiamine prior if alcoholic Naloxone Naloxone If signs or history of opioid use If signs or history of opioid use Flumazenil Flumazenil Only recommended if history of benzo use not as routine. Only recommended if history of benzo use not as routine.

40 Disposition Most cases will be admitted Most cases will be admitted Discharge rapidly reversible causes such as insulin induced hypoglycemia Discharge rapidly reversible causes such as insulin induced hypoglycemia Admit if unclear cause or poor follow-up Admit if unclear cause or poor follow-up

41 References Tintinalli, Judith E., Emergency Medicine a Comprehensive Study Guide. Sixth edition. McGrw-Hill Companies, Inc. 2004. Chapter 229. Altered Mental status and Coma. Huff, J. Stephen. Pages 1390-1397. Tintinalli, Judith E., Emergency Medicine a Comprehensive Study Guide. Sixth edition. McGrw-Hill Companies, Inc. 2004. Chapter 229. Altered Mental status and Coma. Huff, J. Stephen. Pages 1390-1397. Boon, Rosemary. “Sleeping Disorders.” http://home.iprimus.com.au/rboon/SleepingDisorders.htm. Accessed 11/14/05. Boon, Rosemary. “Sleeping Disorders.” http://home.iprimus.com.au/rboon/SleepingDisorders.htm. Accessed 11/14/05. Klatt, Edward C. University of Utah Webpath. http://www.medlib.med.utah.edu/WebPath/ Accessed 11/14/05. Klatt, Edward C. University of Utah Webpath. http://www.medlib.med.utah.edu/WebPath/ Accessed 11/14/05.

42 Questions 1. All of the following are features of delirium except: a. Fluctuating course b. Disordered attention c. Visual and/or auditory hallucinations d. Insidious onset over years 2. A fluctuating stepped course of mental impairment with focal neurologic signs is suggestive of: a. Vascular dementia b. Alzheimer’s dementia c. Delirium d. Parkinson’s disease

43 3. A patient arrives to the ED with an altered mental status. On examination he responds only to painful stimuli by withdrawing, opens his eyes only with pain, and only audible noises are moans. His GCS score is? a. 12 b. 10 c. 8 d. 4 4. (T/F) The reticular activating system responsible for arousal functions is located in the midbrain, pons, and medulla. 5. (T/F) Delirium always has an organic cause. Answers: 1-d, 2-a, 3-c, 4-T, 5-T


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