Mental status Kamal Shemisa pgy3



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Mental status


Objectives

  • Definitions

  • Neurological Examination

  • Clinical Presentation

  • Diagnostic Evaluation

  • Encephalopathy vs. Structural Lesions

  • Case Vignette’s

  • Conclusions



Clinical Vignette

  • 65 yo male HF hospitalized overnight for “volume overload” with plans to diurese.

  • You are called because he’s unresponsive and difficult to arouse.

  • You patiently ask the nurse to obtain a set of vital signs and tell him that you will be there to assess the patient.





Clinical Vignette

  • The read the note from last night and its somewhat helpful…

  • Pmhx- Heart failure, HTN, DM2, atrial fibrillation, Hypothyroidism, OSA, remote hx of prostate cancer.

  • The Hx obtained from the family last evening was that he was developing progressive dyspnea, abdominal distention, decreased appetite and lethargy the past few days. He also was urinating infrequently.



Exam

  • Neuro: unchanged; you verify the findings

  • HEENT: The face appears symmetric, the pupils are small but reactive, mucous membranes are dry, conjunctivae are pale, pharynx is unremarkable

  • Neck: obese, JVP is elevated, accessory muscle use is noted, negative nuchal rigidity

  • Cardio: tachycardic and irregular, -mgr

  • Lungs: Tachypneic taking shallow breaths; BS are heard bilaterally, crackles and rhonchi are heard over the right anterior chest wall

  • Abdomen: is large; BS are present but diminished, the abdomen and flanks are soft and non-tender, the liver is large; there is presacral edema; there are no bruits or pulsatile masses.

  • Extremities are tepid to touch; there +4 edema in the lower extremities, with a tender erythematous region over the dorsum of the foot.



What do you do next?

  • Answer the following questions

  • Is the cause of the patients alteration in mental status a reversible one i.e. metabolic etiology?

  • Or is there a structural etiology or primary brain disorder, responsible for the patient’s AMS

    • i.e. stroke, meningitis, mass lesion, or hydrocephalus?


Differential Diagnosis?



  • What laboratory should be obtained?



  • What Imaging is appropriate?



Acutely Altered States of Consciousness

  • Clouding of consciousness

    • Minimally reduced wakefulness or awareness


Terminology

  • Delerium: charac. Misperception of sensory stimul, vivid hallucinations

  • Obtundation: Mild to moderate reduction in alertness, lesser interest in the environment.

  • Stupor: (to be stunned), deep sleep unresponsiveness requiring vigorous stimulation to arouse.

  • Coma: deep sleep, a state of unresponsiveness and cannot be aroused.



Disorders of Consciousness

  • Acute

    • Clouding
    • Delirium
    • Obtundation
    • Stupor
    • Coma
    • Locked in




Answer

  • COMA!



Physiology behind the Arousal

  • Ascending Arousal System

    • Projections from the mesopontine tegmentum to the forebrain
    • Pedunculopontine and laterodorsal tegmental
    • to the paramedian midbrain reticular formation to nuclei in the thalamus (later to the cortex)
    • Physiology
    • 1) tonic variations are seen via EEG monitoring; ex. in REM PP and LDT are firing fastest
    • 2) Varied responses are due to cholinergic, monoamine, and GABA receptors


Physiological State

  • In physiological states the Central Nervous System relies on sufficient

    • Cerebral blood flow
    • Oxygenation
    • Glucose
    • Electrolyte and Osmotic homeostasis
    • Pharmacokinetics
    • Sterile environment
    • CSF hydrodynamics and pressure balances in a closed container.


History

  • From relatives, friends, attendants

  • Onset

  • Recent complaints of headache

  • Recent injury

  • Prior medical illness

  • Psychiatric history

  • Access to drugs



General exam

  • Vitals

  • Evidence of trauma

  • Acute or chronic systemic illness

  • Drug ingestion?

  • Nuchal rigidity



General Exam

  • Signs of head trauma; otorrhea, hemotympanum, raccoon eyes, battle sign

  • Nuchal rigidity or Brudzinski’s

  • Papilladema?

  • Skin exam: assess for rash, petechia, needle marks, jaundice, bullae

  • Cardiac exam: murmurs, bruits



The neurologic exam

  • Assess the level of consciousness

  • Hemodynamics

  • The pattern of breathing

  • The size and reactivity of the pupils

  • The eye movements and oculovestibular responses

  • The skeletal motor responses



Coma Scales

  • Glasgow coma scale: 13 mild, 9-12 moderate, <8 severe.

  • AVPU: alert ?, voice?, pain?, UR?

  • ACDU: Alert?, confused?, drowsy?, UR?



Exam

  • Methods to elicit response

    • Supra-orbital ridge
    • Nail beds
    • Sternum
    • TM joints


What does it mean?

  • The level of response is important to the initial consideration of the depth of impairment of consciousness.

  • Patients responding to voice or light shaking are lethargic or obtunded

  • Patient whose best response to deep pain is to push the examiner’s arm away is considered to be stuporous with localizing responses.



Cerebral Circulation

  • Is the brain receiving adequate blood flow

    • CPP=MAP-ICP
    • Cerebral autoregulation regulates perfusion to the brain over a wide range of blood pressures.
    • CPP is regulated by head position, MAP aug., CSF drainage, CO2 regulation


Circulation

  • Neurogenic Shock: Damage to the descending sympathetics pathway that support blood pressure may result in a fall in blood pressure.

  • Stokes-Adams attacks: periods of brief loss of consciousness due to lack of adequate cerebral perfusion. (baroreceptor dysfunction)

  • Cushings reflex: Lesions that result in stimulation of the sympatho-excitatory system may cause an increase in blood pressure (ischemia, delerium [amygdala-thalamus]).



Circulation

  • The brain tightly controls circulation.

  • The brain acts through the Autonomic nervous system to adjust systemic arterial pressure



Respirations

  • Breathing is a sensorimotor act

  • Respiratory Rhythm is an intrinsic property of the brainstem (ventro-lateral medulla).

    • Vagus, GP nerves: respond to stretch and chemoreceptors- (influence RR and TV)
    • Forebrain can alter respiratons by emotional centers.


Respirations

  • Cheyne-stokes- alt. hyperpnea with apnea

  • Hyperventilation (Kussmaul’s): sepsis, hepatic coma, metabolic acidosis, [SAH, gliomas (localized acidosis)]

  • Apneustic: end resp. pauses of 2-3 sec; Pontine infarct, TT herniation

  • Ataxic: irregular gasping bilateral medullary lesions



Cheyne-Stokes

  • The Brain Stem is intact

  • Hyperpnea phase lasts longer than apnea

  • When Medullary sensors sense oxygen and increases in carbon dioxide tension reduce the rate and TV

  • Alveolar carbon dioxide reaches even higher levels ramping up of respiration as the brain sees rising carbon dioxide

  • By the time the brain begins to see a fall in CO2 the levels in the alveoli are too low.

  • Low level of carbon dioxide reaches the brain, respirations slow or even cease.



continued

  • Understand the feed back loop between alveolar ventilation and brain chemoreceptors are influenced by:

    • Circulatory delays (heart failure)
    • Bilateral forebrain impairment: i.e. diffuse metabolic process such as uremia, hepatic failure, or bilateral damage Diencephalic displacement.


Pupils

  • Abnormalities of pupillary responses are of great localizing value.

  • Single most important physical sign in differentiating metabolic from structural coma.



Pupils

  • Most pupillary responses are brisk but some slow: illuminate the eye for 10 seconds.

  • Consensual responses are normal

  • Paradoxical dilation: (APD): lesion of the optic nerve or retina.



Pupils

  • Small Reactive: Metabolic encephalopathy, Diencephalic Injuries

  • Unilateral dilated and UR: Pcom An, temporal lobe herniation.

  • Unilateral Small: Horner’s i.e sympathetic lesionCavernous sinus, ICA lesion, stellate ganglion.

  • Midposition fixed: Midbrain; fixed mid or dilated (symp. Preserved).

  • Pontine tegmental injury results in pinpoint pupils.

  • Lateral Medullary tegmentum: cause ipsilateral central Horner’s syndrome.



Pupils

  • Assess the level simultaneously with respirations…



continued



Oculomotor response

  • Assesses brainstem function:

  • Blepharospasm- strong resistance to eyelid opening is voluntary; not truly in coma. (frontal lobes intact)

  • Spontaneous blinking lost in coma. However can be present in PVS

  • Corneal reflex: elicited with cotton wisp or sterile saline eye drops: closure of the eyelids and elevation of the eyes suggest preservation of the brainstem spinal V nucleus and facial nuclei.



Oculomotor Responses

  • Eye movements are smooth and conjugate.

  • Vestibulo-ocular responses: nl responses generated is for eyes to rotate counter to the direction of the examiner’s movement. i.e. Doll’s Eyes.

  • Nl responses in both horizontal and vertical suggest intact brainstem function.



Vestibulo-ocular responses

  • Unusual to have normal VOR in structural causes of coma.

  • Exaggerated responses to OC stim. do occur particularly due to hepatic failure.



Vestibulocular Reflex

  • When do we do caloric testing???

    • Patients who are deeply comatose may respond sluggishly or not at all to OC stim.
    • 50 ml syringe with plastic IV catheter is gently advanced until it is near the TM. Infuse at a rate 10 ml/minute until the response is obtained.


CWC

  • Video

    • http://www.youtube.com/watch?v=H4iQkFUgG6k


VOR and CWC

  • Metabolic encephalopathy- VOR is nl

  • Right lateral pontine lesion-conjugate gaze paralysis on right and nl. VOC on left.

  • MLF lesion or bilateral INO- absent conjugate gaze with single eye deviation on VOCR side elicited

  • Paramedian pontine lesion- 11/2 syndrome

  • Midbrain lesion-bilateral paralysis



Continued

  • Roving eye movements (ping-pong gaze): metabolic encephalopathy.

  • Nystagmus: abnormal if irregular jerks present, convergence nystagmus.

    • Typically seen dorsal midbrain lesions


Motor Responses

  • Assess tone:

  • Spastic rigidity: spastic catchParkinsons

    • Quick passive movement triggers rigidity
  • Paratonic rigidity: metabolic encephalopathy

    • Increases with intensity of passive movement, as if the patient willfully resists the examiner.


Motor responses

  • Muscle stretch reflexes- may be increased who are drowsy or confused.

  • Cutaneous reflexes: cremasteric/abdominal reflexes

  • Prefrontal cutaneous reflexes: “frontal release reflexes” or primitive reflexes also emerge in drowsy patients with.

    • Rooting
    • Snout
    • Glabellar
    • Palmomental
    • Grasp (specific to bilateral frontal impairment)


Motor response

  • Appropriate responses are ones that attempt to escape the stimulus: withdrawing.

  • Likewise facial grimacing, increasing blood pressure, pupillary dilation, movement of the contralateral side.

  • Inappropriate responses: posturing



Motor Responses



Diagnostic testing

  • Evaluate metabolic etiologies

    • Glucose
    • Electrolytes
    • Hepatic function panel
    • Toxin/drug screens
    • Arterial blood gas
    • urinalysis


Metabolic Abnormalities

  • Hypo/hyper glycemia

  • Acid/base derangements

  • Hypo/hypercapnia

  • Hpoxia

  • Liver disease (hyperammonia)

  • Renal Disease (uremia)

  • Pancreatic Encephalopathy

  • Endocrinopathy

  • Toxins: Sedatives, opiates, ethanol intoxication

  • Electrolyte

  • Hypo/hyperthermia

  • Nutritional: Wernicke’s



Clinical Vignette

  • The read the note from last night and its somewhat helpful…

  • Pmhx- Heart failure, HTN, DM2, atrial fibrillation, Hypothyroidism, OSA, remote hx of prostate cancer.

  • The Hx obtained from the family last evening was that he was developing progressive dyspnea, abdominal distention, decreased appetite and lethargy the past few days. He also was urinating infrequently.



Work up

  • 7.47/36/65

  • 131/5.2/94/22/35/2.2

  • Glucose-180

  • Lactate-4.5

  • Wbc-12.2

  • Troponin-1.5



Decision

  • You Decide to intubate and transfer to MICU!



Mechanisms of Structural coma

  • Structural coma occurs with injury to sarousal pathways through the brain.

    • Supratentorial lesions: compress the diencephalon.
    • Infratentorial lesions: compress the arousal structures


Neurological Imaging

  • CT- applied to anyone who does not a have an immediately obvious source of coma.

    • Obvious hemorrhages, fractures, remote cerebral infarction and hydrocephalus can be detected.
    • Disadvantage is detecting acute infarction as well as delaying care of a patient with impending transtentorial herniation (blown pupil, gaze palsy).


MRI

  • MRI: time consuming, but is often necessary.

  • DWI/ADC are the studies of choice for acute stroke here.

  • TI/T2/Flair in conjunction are suitable to detect acute hemorrhage.

  • MRA can reveal most stenoses, aneurysms or occlusions.

  • Use Gadolinium if you suspect metastatic disease or abscess



Herniation Syndromes

  • Uncal

  • Central

  • Subfalcine/cingulate

  • Transcalvarial

  • Upward

  • Tonsillar





Herniation

  • Usually results from imbalances of pressure between different compartments leading to tissue herniation.



Case Vignette 2

  • You are on Carpenter Team and are assigned a 35 yo patient with HIV. He has been complaining of headache, nausea and vomitting, and blurred vision. His CD4 count is 50.

    • What do you want to do next?




Ring Enhancing Lesions

  • Bacterial Abscess

  • Metastatic Disease: Adenocarcinoma

  • Primary CNS lymphoma

  • Primary CNS Neoplasm: Glioma

  • Post-radiation changes

  • HIV associated lesions: PML, CryptococcosToxoplasmosis, Tuberculoma, lymphoma

  • Post-operative changes



Case Vignette 3

  • You are on Eckel team and your patient overnight became acute unresponsive. His eyes are closed, pupils are pinpoint, downward gaze, and his breathing is irregular. You examine and you note decerebrate posturing.

    • Where is the lesion?




Clinical Vignette 4

  • You admit a patient on Weisman, she is a 58 yo female with recently diagnosed breast cancer undergoing her final cycle of high dose AC/herceptin chemo. She has felt increasingly unsteady, complains of blurred vision, lower extremity weakness. On exam she has papilladema, 4/5 strength in the legs, brisk patellar reflexes and bilateral babinski’s

    • Differential Diagnosis?




Clinical vignette 5

  • You are the resident on Wearn team and have admitted a 58 yo alcoholic male patient presents to you from the ED dehydrated in ARF after police find him in alley way naked and disheveled.

  • You notice however that his face is “well kept” on one side and the other half of his face is unshaven.

  • When you ask him to stand up and walk he falls to his left side.





Recap

  • Definitions

  • Neurological Examination

  • Clinical Presentation

  • Diagnostic Evaluation

  • Encephalopathy vs. Structural Lesions

  • Case Vignette’s

  • Conclusions



Kataloq: images -> current residents
images -> Мп г. Белгорода «Стоматологическая поликлиника №2» Информированное добровольное согласие на стоматологическое эндодонтическое лечение
images -> Задачами модуля являются
images -> Сагітальні аномалії прикусу. Дистальний прикус. Етіологія, патогенез, клініка та діагностика дистального прикусу
images -> Мп г. Белгорода «Стоматологическая поликлиника №2» Информированное добровольное согласие на проведение ортодонтического лечения
images -> Мп г. Белгорода «Стоматологическая поликлиника №2» Информированное добровольное согласие на пародонтологическое лечение
images -> Yazılım Eleştirisi
current residents -> 45 yo hispanic male with long standing cirrhosis due to HepC and Alcohol

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