13. Confusion Flashcards

(37 cards)

1
Q

Emergent causes of confusion: 5

A

-hypoglycemia<br></br>hypoxemia<br></br>hypotension<br></br>sepsis<br></br>toxic ingestion

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2
Q

Confusion, indicates an acute impairment of higher cerebral function - memory, attention awarenes

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3
Q

<span>the characteristic disturbance in confusion is to the content portion of consciousness, resulting in abnormalities of attention and awareness. </span>

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4
Q

<span>Four major groups of disorders encompass most causes of confusion: (1) systemic diseases secondarily affecting the CNS; (2) primary intracranial disease; (3) exogenous toxins; and (4) drug withdrawal states</span>

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5
Q

Emergent ddx for confusion: 

A

<ul><li><ul><li>•&nbsp;<div>Primary intracranial disease</div><ul><li><div>Seizure/nonconvulsive status epilepticus</div></li><li><div>Traumatic brain injury</div></li><li><div>Hypertensive encephalopathy</div></li></ul><div></div></li><li>•&nbsp;<div>Systemic diseases secondarily affecting the central nervous system</div><ul><li><div>Sepsis</div></li><li><div>Hepatic encephalopathy</div></li><li><div>Uremia/renal failure</div></li><li><div>Hyperthermia/hypothermia</div></li><li><div>Endocrinopathy</div></li><li><div>Nutritional deficiency</div></li></ul><div></div></li><li>•&nbsp;<div>Exogenous toxins</div></li><li><div>Sedatives/hallucinogens</div></li><li><div>Ethanol/toxic alcohols</div></li><li><div>Narcotics</div></li><li><div>Antihistamines</div></li></ul><div></div></li><li>•&nbsp;<div>Drug withdrawal</div><ul><li><div>Alcohol</div></li><li><div>Drugs of abuse</div></li></ul></li></ul>

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6
Q

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7
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<img></img>

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<img></img>

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8
Q

<span>CNS causes of confusion include stroke, seizure, and infection. Focal cortical dysfunction, such as from tumor or stroke, may present as confusion when receptive or expressive dysphasia is present. </span>

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9
Q

<span> Subcortical or brainstem dysfunction usually results in a diminished level of alertness, rather than confusion. Frontal lobe dysfunction from stroke, trauma, or tumor may result in personality changes and the report of confusion by family or friends. Postictal state or nonconvulsive or petit mal status epilepticus may present with acute confusion. </span>

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10
Q

<span>Atypical migraines or migraine variants may present with confusion alone. Meningitis and encephalitis cause alterations of consciousness, often with other signs of infection. Neuroimaging or other diagnostic studies may be required to narrow the differential in these cases.</span>

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11
Q

<span>patient with confusion is evaluated through a focused history, physical examination, and rapid bedside screening assessment tools. Response to specific therapies (e.g., dextrose, naloxone) may identify critical causes.</span>

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12
Q

<span>Examples of pivotal historical findings that provide the key to the diagnosis include new medications, infection symptoms, history of head trauma, history of seizures, history of migraines, and time course of symptom onset.</span>

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13
Q

<span>. Examples of pivotal physical findings include vital sign abnormalities, evidence of trauma, focal neurologic deficits, loss of attention, preservation of orientation, and presence of a toxic syndrome</span>

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14
Q

<span>An essential goal of the history is to determine the baseline level of neurologic function for the particular patient, and when the patient last exhibited their baseline thinking and behavior.</span>

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15
Q

<span>The initial task in evaluating the patient is to define the symptoms and severity of confusion. The specific behaviors that are of concern to the patient or caregivers should be delineated. Often, the family is the most valuable source for information;</span>

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16
Q

<span>The duration of the confusion, recent changes in medications, and recent illnesses are important points in the clinical history. A history of previous episodes that have resolved spontaneous may be a clue to petit mal status or confusional migraine</span>

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<span>Hallucinations may occur in delirium and are classically visual, unlike the auditory hallucinations associated with schizophrenia. A history of medication or substance abuse and any recent changes, especially cessation of benzodiazepines or ethanol, should be sought.</span>

17
Q

PE:<br></br><span>The general physical examination may suggest a cause of confusion or altered mental status, such as asterixis and jaundice in liver dysfunction, fever and dysuria in urinary tract infection, or injection marks from illicit drug use. New focal neurologic findings suggest a possible mass lesion or stroke, but these would manifest with confusion only if global cortical dysfunction were caused by surrounding cerebral edema or elevated intracranial pressure by severe mass effect.</span>

18
Q

PE: <span>Aphasia, fluent or nonfluent, is a focal sign suggesting a lesion in the dominant cerebral hemisphere. In confusional states, speech may be abnormal and is often incoherent, and the rate of speech may be rapid or slowed. Identification of the elements of a “toxidrome,” such as serotonin syndrome, may assist in the identification of a drug effect as the cause of confusion, prompting intervention or consultation.</span>

19
Q

<span>. Studies have shown that delirium in older adults often goes unrecognized unless a structured assessment is performed.</span>

20
Q

Delirium triage scale<br></br><span>The DTS assesses level of consciousness using the Richmond Agitation and Sedation Scale (RASS) and assesses attention by a simple question (backward spelling of five-letter word, such as “LUNCH” or “WORLD” with positive result for more than one error). The screening test can be performed in less than 20 seconds</span>

21
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22
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23
Q

<span>Electrocardiography is indicated in older patients because myocardial infarction may manifest atypically as confusion.</span>

24
Q

testing for confusion:<br></br><br></br><div>Pulse oximetry may reveal hypoxia, or bedside glucose testing may reveal hypoglycemia or hyperglycemia. In the presence of fever, chest radiography and urinalysis often reveal the source of the infection causing the altered mentation. Serum chemistry tests for liver function may support a clinical diagnosis of hepatic encephalopathy, which does not require elevated serum ammonia level to be present. If there are clinical findings or a history suggestive of thyroid disease, thyroid-stimulating hormone (TSH) testing is indicated. Electrolyte testing can reveal either elevated or decreased sodium and calcium levels. Creatinine level and blood urea nitrogen levels may be elevated in renal failure and uremic encephalopathy.</div><div>Electrocardiography is indicated in older patients because myocardial infarction may manifest atypically as confusion. A complete blood count is unlikely to provide useful diagnostic clues unless profound anemia is suspected. White blood cell counts may be elevated, normal, or low, without specificity as to the presence or nature of a disorder. Blood gas testing may demonstrate acid-base disturbance or hypercarbia, although arterial, rather than venous, samples are rarely required unless pulse oximetry is not reliable.</div>

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If common and simple tests do not identify a cause, advanced diagnostic testing may be indicated. Selected drug and toxicologic testing may be ordered in this second tier of evaluation, although false-positive and false-negative results can occur. Caution should be applied before attributing mental status changes entirely to substance use in unclear cases. Blood and urine cultures are obtained in the febrile patient when hospital admission is anticipated and a clear infectious source is not evident. Paracentesis or thoracentesis may be appropriate if ascites or a new pleural effusion is present. Cranial computed tomography (CT) scanning is often done to screen for CNS lesions in the absence of another identified source of the confusion and in patients with focal neurologic findings on examination. Lumbar puncture may allow discovery or exclusion of CNS infection if no other source has been identified. Cerebrospinal fluid examination may clarify a diagnosis of meningitis, encephalitis, or subarachnoid hemorrhage.
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d/c vs admit and tx
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 If the patient remains unconscious or confused after a seizure, the possibility of ongoing or intermittent seizure activity should be entertained, and neurologic consultation and EEG should be considered. Nonconvulsive status epilepticus (NCSE) and convulsive subtle status epilepticus can present on a spectrum from confusion and abnormal behavior to deep coma, and these diagnoses carry significant morbidity if not diagnosed promptly.
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Empirical Management

Oral or intravenous (IV) glucose therapy is indicated if an abnormally low blood glucose level is discovered. In adults, one IV dose of dextrose (commonly 25 g as either a “D50” ampoule of 50 mL of 50% dextrose, or a prepared solution of 250 mL of 10% dextrose or similar product) is commonly administered, and the bedside glucose level is checked again. Thiamine, 100 mg IV, can be given at the time of dextrose administration if Wernicke encephalopathy is a concern. 
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Tx: Hypoxia and hypercarbia are addressed with noninvasive or invasive ventilation strategies tailored to the patient’s presentation. If a “toxidrome” is present, treatment is directed toward the specific toxin.
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Confused or agitated patients should be protected from harming themselves or others. Close observation may need to be supplemented by medications or physical restraint. Family members may offer valuable assistance in observing and comforting the patient. Environmental manipulations such as dim lighting or providing a quiet environment may be helpful. Confinement or physical restraint may be necessary at times but should be used with careful adherence to institutional guidelines. Use of physical restraints and bladder catheterization have been associated with prolonged duration of delirium.
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Antipsychotics have been studied extensively for chemical sedation of delirium in acutely ill patients, with conflicting data on efficacy. 6 Given a relatively rapid onset, availability of IV and intramuscular (IM) formulations, and some positive data from intensive care unit (ICU) populations, haloperidol may be the treatment of choice for acute confusion with agitation, at a dose of 1 to 5 mg, repeated up to every 15 minutes IV or every 30 minutes IM as needed to a maximum of 10 to 20 mg/day.
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ADverse effects of using haloperidol as confusion management: 
QT prolongation, acute dystonic reactions, and tardive dyskinesia, with chronic use, may occur. Haloperidol administration is associated with an increased risk of death in patients with Parkinson’s disease, which is why it is contraindicated in this patient population
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Atypical antipsychotics, including quetiapine, dosed as 25 to 50 mg per os (PO) 1 to 4 times daily, and olanzapine, dosed 5 to 10 mg IM every 2 to 4 hours to a maximum of 30 mg/day based on patient tolerability, have been studied for treatment of agitation as well, and may be effective in some cases.
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Age-appropriate antibiotic treatment for coverage of causes of sepsis tailored to the patient’s comorbidities may be considered in ill febrile patients while a definitive evaluation is in progress. If a CNS infection is suspected, age-guided empirical antibiotic treatment without delay for lumbar puncture is recommended.
35
n patients with history of epilepsy who have uncontrolled seizures or are suspected of being in nonconvulsive status epilepticus, empirical treatment with benzodiazepines may be considered, although this may cause increased somnolence. Other antiepileptics, such as levetiracetam IV, may be considered as well to rapidly achieve therapeutic plasma levels and prevent recurrence of seizures.
36
Prochlorperazine or other medications to treat migraine headache may be administered if confusional migraine is suspected.
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