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Senoir 21-2 > EM Block I > Flashcards

EM Block I Flashcards

1
Q

Define coma

A

is characterized by failure of both arousal and content functions of consciousness.

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2
Q

Define delirium

A

Delirium refers to an acute state of fluctuating attention and change in cognition

Can happen over minutes

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3
Q

Define Dementia

A

Dementia is a chronic disorder of deteriorating cognition.

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4
Q

What are 5 DDx for “acute brain failure”

A 
Primary Intracranial Dz 
Systemic Dz 
Exogenous toxins 
Drug Withdrawal 
Major Trauma or Surgery
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5
Q

What are the hallmarks of delirium

A

Disordered attention and acute fluctuations

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6
Q

What is the W/u for Delirium

A 
Serum Electrolytes
Hepatic and Renal Studies 
UA/ HcG 
CBC 
CXR 
\+/- CT (if stroke or bleed) 
\+/- LP
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7
Q

Define Non convulsive status epilepticus

A

May persist for hours or even months after a seizure. There is no post ictal state and they remain altered.

So if you have a patient with a history of seizures or epilepsy that does not wake back up from a seizure, this should raise your suspicion and you must act.

An electroencephalography (EEG) are required for recognition!!! (More on this in the seizure lecture…)

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8
Q

What is the standard of care approach to delirium

A

Nonpharmacologic approaches to delirium are the standard of care.

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9
Q

Do we use physical restraints on the elderly

A

NO, we give them drugs!

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10
Q

What is the initial Rx of choice for acute delirium

A

Haloperidol is a frequent initial choice at a dose of 5 to 10 milligrams PO, IM, or IV, with reduced dosing of 1 to 2 milligrams in older adults.

Avoid giving Benzos to the elderly

In younger Pts, B52!
Benadryl 50mg,
Haldol 5mg
Ativan 2mg

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11
Q

If giving B52, what must you monitor for

A

ETCO2

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12
Q

When do you admit a pt with delirium

A

Admit the patient with delirium to the hospital for further treatment and additional diagnostic testing, unless a readily reversible cause for the acute mental status change is discovered and treatment initiated.

Consider resources in the home or healthcare facility, and the patient’s safety.

If you feel that the patient may not have great resource listed above, then admit.

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13
Q

If a pt presents with abrupt onset of a sentinel event with underlying dementia

What should you think

A

The abrupt onset of symptoms or rapidly progressive symptoms should prompt a search for other diagnoses, including delirium.

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14
Q

What is the general W/u for dementia

A 
CBC
 CMP 
UA 
Thyroid Function Tests 
CXR 
\+/- CT

Serum B12
Serum Syphillis
HIV test

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15
Q

what are three conditions that can cause rapid cognitive decline

A

urinary tract infection, congestive heart failure, and hypothyroidism
… are just a few of the conditions that may cause a patient with mild dementia to show rapid decline!

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16
Q

When should you ever use antipsychotics in dementia pts

A

Antipsychotics, black box warning against use for behavioral and psychiatric symptoms of dementia

Reserve consideration of antipsychotic use for patients with significant risk of harm to self and others.

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17
Q

How is vascular dementia treated

A

Treatment of vascular dementia is limited to treatment of risk factors, including hypertension, tobacco use, glucose control and cholesterol.

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18
Q

If you see excessively large ventricles on Head CT mean

A

Normal pressure hydrocephalus

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19
Q

What is Uncal Herniation

A

medial temporal lobe shifts to compress the upper brainstem, which results in progressive drowsiness followed by unresponsiveness.

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20
Q

A pt presents iwth ipsilateral pupil sluggish that eventually becomes dilated and non reactive
With ipsilateral hemiparesis

Think

A

Uncal Herniation

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21
Q

How does a central herniation present

A

A mid line shift without herniation

With a Progressive loss of consciousness, loss of brainstem reflexes, decorticate posturing, and irregular respiration.

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22
Q

How do you determine CPP

A

Cerebral perfusion pressure is equal to the mean arterial pressure minus the ICP
(cerebral perfusion pressure = mean arterial pressure – ICP)

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23
Q

In a hemispheric hemorrhage where do the eyes deviate

A

Hemispheric hemorrhage and midline shift may have decreased muscle tone on the side of the hemiparesis.
(Like a stroke)

The eyes may conjugately deviate toward the side of the hemorrhage.

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24
Q

What is the major DDx finding in toxic metabolic coma

A

Should be no focal or unilateral neurological deficits on exam.
-No hemiparesis
= Pupils may be small but reactive because it mainly preserved in toxic-metabolic comas.

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25
Q

A pt presents with small but reactive pupils and in a coma with resp depression.. think

A

Narc OD

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26
Q

Define Cushings triad

A

Brady HR
Irregular RR
Widened Pulse pressure ( HOTN)

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27
Q

If a mass presses on the supratentorial space of the brain what happens

A

Coma caused by lesions of the hemispheres, or supratentorial (above the tentorium) masses, may present with progressive hemiparesis or asymmetric muscle tone and reflexes.

Ie: Uncal herniation

S/S Cushings reflex

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28
Q

If a pt presents with dual pinpoint size pupils

Think herniation where

A

pontine hemorrhage, which may present with the unique signs of pinpoint-sized pupils.

A Infratentorial hemorrhages

Swelling in the posterior fossa

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29
Q

How can you rule out pseudo coma

A

Avoidance of gaze by the pt

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30
Q

What is the imaging of choice for brain hem

A

Non-Contrasted Head CT is the neuroimaging procedure of choice.

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31
Q

If subarachnoid hemorrhage or CNS infection is suspected but the CT in NML what is the next step

A

LP

Or if suspected basalir artery thrombosis get a MRI and look for a hyper dense basilar artery

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32
Q

What is the time frame for NSE

A

If the motor activity of the seizure stops and the patient does not awaken within 30 minutes, then consider nonconvulsive status epilepticus.

Obtain neurologic consultation and electroencephalography.

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33
Q

What are the first steps in treating ICP

A

HOB 30*

HYPERTONIC OR MANNITOL

IF there is a tumor? THen Dexamethasone
(only from consult instructions)

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34
Q

What are the downstream effects of DKA

A

HYPERGL
Prerenal azotemia
Ketone Formations
Wide Anion Gap Met acidosis

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35
Q

What are the 8 “I”s of DKA

A 
infection 
Infarction (MI) 
Infraction (noncompliance) 
Infant 
Ischemic (CVA) 
Illegal drugs 
Iatrogenic 
Idiopathic
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36
Q

What causes N/V in DKA

A

High acidity causes the release of prostaglandins which lead to N/V and Abdominal PAIN

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37
Q

What is the better menearles of AMS in DKA, osmolality or ph or glucose?

A

OSM

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38
Q

What is the W/u for DKA

A

Bed side gl

VBG (measure pH) 
CMP 
CBC 
Anion Gap 
ABG
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39
Q

Which is the better marker for determining severity of DKA

Biacrab ?
Or glucose levels?

A

Bi-carb

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40
Q

What is the order of tx in DKA

A
  1. Volume first and foremost
  2. Correction of K+ deficits
  3. Insulin administration
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41
Q

What is the bolus rate for NS in DKA

A

20ml/kg/hr

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42
Q

in DKA, once the glucose reaches 250 what must be changed in the Tx

A

Switch to 5% dextrose

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43
Q

How is fluid managed in the DKA pt

A

20ml/kg/hr

First 2L / 0-2hours
The next 2L/ 2-6 hrs
Additional 2L/ 6-12 hours

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44
Q

What is the most severe electrolyte abNML in DKA

A

Rapid development of severe hypokalemia is potentially the most life-threatening electrolyte derangement during the treatment of DKA (not glucose management)

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45
Q

When should K be withheld in DKA

When should Insulin be withheld in DKA

A

IF the K is below 3.3 hold insulin and give K

If the K is above 5.2 then hold K and give insulin

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46
Q

What is the definition of DKA resolution

A

Glucose <200 mg/dL & 2 of the following:

  • Bicarbonate level >15 mEq/L
  • Venous pH >7.3
  • Normal calculated anion gap (Closed Gap)
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47
Q

WHere do all DKA pts go

A

ICU

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48
Q

A headache that occurs while execution, heavy lifting, vomitting, sneezing, and straining

Think?

A

SAH or arterial dissection of the carotid or vertebrobasilar circulation- ALWAYS!!!

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49
Q

A headache that is associated with valsalva should make you think /?

A

possible intracranial abnormality such as mass/tumor.

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50
Q

Do migraines increase or decrease with age

A

Decreases with age

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51
Q

Does absence of fever rule out infection with a headache

A

NO!

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52
Q

What is meningismus

A

Pain with flexion of the neck

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53
Q

What family history finding is important in headache W/u

A

Known aneurysm or sudden death in first-degree relatives with intracranial aneurysm (3-5 times higher than in those without a family history)- so ask about FMH!!

PMH/FMH of autosomal dominant polycystic kidney disease also increases the risk for intracranial aneurysm

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54
Q

What is the abnormal number for glaucoma

A

> 21

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55
Q

When doing a W/u for a HA

What is the imaging to look at arterial dz

A

MRA

CTA right away

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56
Q

What are the Dx and Tx uses of LP

A

Dx: Meningitis, SAH, intracranial hypotension, carcinomatous meningitis

Tx: Pseudotumor cerebri

(However, we do not routinely just draw CSF off of people if we can weight manage or medically manage them.)

Ideally, perform the LP in the lateral decubitus position to allow for the accurate measurement of opening pressure

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57
Q

When is it safe to do a LP without imaging

A

Safe to proceed with LP without prior imaging if…
- No history of immunosuppression
(HIV, AIDS, CX, DMARDS)
-Normal sensorium
(AWOX4)
-No focal neurologic deficits

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58
Q

Should ABX be delayed for the results of an LP

A

NO!

If:  Deteriorating or altered level of consciousness 
(particularly a GCS ≤ 11)
Brainstem signs 
(including pupillary changes, posturing, or irregular respirations)
 Focal neurologic deficit
 Recent seizure
 Preexisting neurologic disorder
 Immunocompromised state

Then do not delay ABX initiation

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59
Q

What is the classic triad of Meningitis

A

Definition:
Headache + classic triad
(fever, altered mentation & neck stiffness)

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60
Q

What is the common cause of Bac Meningitis in the military

A

N. meningitis

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61
Q

Should you ever withhold empiric ABX in meningitis

A

NO

Never withhold empiric antibiotic therapy in order to collect fluid sample

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62
Q

What are the C/I for LP

A

Do not perform if there is coagulopathy or use extreme caution
-Platelet <20,000/µL or INR ≥ 1.5

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63
Q

When should you perform a Head Ct before LP in Bac Meningitidis

A

Complete a Head Ct before LP if you have concerns for possible herniation.

Perform LP as soon as possible to secure the diagnosis (if safe… if not, give empiric AB’s and move on)

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64
Q

What are the empiric ABX for 18-49yo in Bac Meningitis

A

18 – 49 yo
-Ceftriaxone 2gm IV PLUS -Vancomycin 15mg/kg IV

Covers S. pneumoniae and N. meningiditis

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65
Q

What is the empiric ABX for BAc Meningitis in pts older than 50

A

Same ABX but add Ampicillin

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66
Q

When shoudl dexamethasone be used in Bac meniginits

A

Dexamethasone before or with 1st dose of antibiotics to reduce inflammation

Before or with reduces hearing loss and neurological sequelae (neurological deficits).

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67
Q

What is the most common cause of SAH

A

Ruptured Aneurysm

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68
Q

What is the 1st step in evaluation of SAH

A

Non Con CT

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69
Q

What is xanthocromia

A

yellow appearance of the CSF due to the enzymatic breakdown of blood by bilirubin

Which means a SAH

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70
Q

When shoudl patients always receive a CT with a SAH or ICH

A

Elderly, chronic alcohol and substance abuse, and those on antiplatelets & anticoagulants (No trauma)

Patients receiving antiplatelets and anticoagulants should be screened using head CT, regardless of symptoms!!

If they say they have a headache and they are on the above medications, you will scan!!

71
Q

Acute headache + vestibular symptoms (vertigo or ataxia)—> consider…

A

Cerebellar hem

72
Q

What is the study of choice for detecting Brian tumors

A

MRI with and without gadolinium (contrast) is the study of choice for detecting brain tumors

73
Q

A periparturm woman presents with recent surgical history and new headache onset

Think

A

Central Venous Thrombosis

74
Q

What is the Def Dx for Central Venous thrombosis made with

A

In the presence of abnormal imaging (NCHCT), focal neurologic deficit (Numbness, tingling, weakness), or AMS, the definitive diagnosis of cerebral venous thrombosis made with magnetic resonance venography.

75
Q

A pt with an elevated LP with out suspicion of meningitis think ?

A

Central Venous Thrombosis

Prompt MR venography and consult neuro

76
Q

50 yo female presents with fatigue, fever, Jaw claudiacaition and Transient vision loss
Elevated ESR.
Think ?

A

Giant Cell Temp Arteritis

Also check IOP to exclude glaucoma

77
Q

How do you confirm temp arteritis

A

Bx

78
Q

What is the most common non life threatening headache in the ED

A

Migraine

79
Q

What is the treatment for migraines in the ED

A

In the ED, most have failed abortive therapy (triptans)
& require rescue therapy and they need your help.
Initial treatment:
- IV hydration
- IV treatment with NSAIDs and dopamine receptor antagonist (droperidol or metoclopramide)

Combine with antihistamine (diphenhydramine 25 - 50 mg IV)
— Treats akathisias from antiemetics

Dexamethasone for D/c home

80
Q

What drugs are contraindicated for pregnancy migraines

A

Triptans, Ergotamines, and Combo agents with caffeine’s and isomtheptene

81
Q

Idiopathic intracranial hypertension is most common to what demographic

A

Most common to obese women between 20-44 years old

82
Q

34 year old obese female presents with HA, visual obsucruations, back pain, and pulsátiles tinnitus

Think what major HA cause that you CAN NOT MISS

A

Idiopathic intracranial hypertension

83
Q

If the pt has no papilledema or Abducens nerve palsy, what three findings do you need to Dx Idiopathinc Intracranial hypertension

A

dx without papilledema can be made if at least 3 of the following neuroimaging findings are present:

  • Empty sella
  • Flattening of the posterior aspect of the globe
  • Distention of the perioptic subarachnoid space
  • Transverse venous sinus stenosis
84
Q

What is necessary to make the Dx for Idiopathic intracranial HTN

A

LP!

Target pressure of 15 - 20cm H2O
In general, removal of 1mL of CSF will ↓ CSF pressure by ~1cm H2O
1 for 1

85
Q

What is the treatment for idiopathic intracranial HTN

A

Acetazolamide can lower ICP and decrease the symptoms
— Treatment is started at 250 to 500mg BID

Treatment is focused on preservation of vision

86
Q

What is the treatment for a cluster headache

A

Treatment: First Line: 100% oxygen at 12 L/min for 15 minutes through a NRB facemask
- Sumatriptan (6 mg SC) can also be used

87
Q

How does Epi reduce further mediator releases in anaphylaxis

A

B2 stimulation

88
Q

How does B blockers effect anaphylaxis

A

Concurrent use of β-blockers is a risk factor for severe prolonged anaphylaxis-

Glucagon* is the reversal agent for Beta Blockers.

89
Q

How does glucagon effect B receptors

A

*Glucagon activates adenyl cyclase and exerts an inotropic and chronotropic effect by a pathway that bypasses the b receptors.

90
Q

What are the components of Hymenoptera venom

A

Histamine
Melittin- cause degranulation of basophils and mast cells
Phospholipase and hyaluronidase

91
Q

What is the most common response to a Hymenoptera sting?

A

is a transient local reaction.

Localized itching, pain, erythema, and swelling are common.

92
Q

What is the diff between brown recluse and black widows

A

Black widows are painful!

93
Q

What is the cause of death within the first hour from Hymenoptera stings

A

Fatalities that occur within the first hour after the sting usually result from airway obstruction or hypotension.

In general, the shorter the interval between the sting and the onset of symptoms, the more severe is the reaction!!

94
Q

What is the treatment for Hymenoptera stings

A

Immediate removal

Pain and nsaids

Elevation of the limb

+/- corticosteroids

95
Q

What is the Tx for a Scorpion sting

A

Anti venom and send them up stairs

96
Q

What is the mainstay of therapy for snake bites

A

Anti venom

97
Q

What is the anti venom used in the US

A

Crotalidae Polyvalent Immune Fab (Ovine) (FabAV) is used in the United States.

98
Q

Define SZR

A

Temp abnormality in muscle tone and movements, behaviors, sensations or states of awareness

99
Q

Define status epilepticus

A

Status epilepticus-

seizure activity for ≥5 min or ≥2 seizures without regaining consciousness between seizures

100
Q

Define refractory status epileptic-us

A

Refractory status epilepticus- persistent seizure activity despite the IV administration of adequate amounts of 2 antiepileptic agents!

101
Q

Define Generalized SZR

A

Nearly simultaneous activation of the entire cerebral cortex

Begins with abrupt loss of consciousness!

LOC may be the only clinical manifestation of the seizure

Variety of motor manifestations including Tonic Clonic or jerking rythmatic movements

102
Q

Define Generalized Absence SZR

A

Very brief, generally lasting only a few seconds

Sudden altered consciousness but no change in postural tone

Appear confused, detached, or withdrawn, and current activity ceases

May stare or have twitching of the eyelids

May not respond to voice or to other stimulation

May exhibit involuntary movements or lose continence

103
Q

Define partial focal SZR

A

Electrical discharges beginning in a localized region of the cerebral cortex

May remain localized or may spread to involve nearby cortical regions or the entire cortex

More likely to be secondary to a localized structural lesion of the brain

104
Q

Define Partial Focal Simple SZR

A

Seizure remains localized

Consciousness and mentation are not affected

Possible to deduce the likely location of the initial cortical discharge from the clinical features at the onset of the attack

Tonic/clonic movements limited to one extremity —>motor cortex focus

Visual symptoms—> occipital focus

Olfactory or gustatory hallucinations—> medial temporal lobe focus

Secondary generalization: sensory phenomena (aka auras) are often the initial symptoms of attacks that then become more widespread

105
Q

Define Partial Focal Complex SZR

A

Seizures in which consciousness or mentation is affected

Often caused by a focal discharge originating in the temporal lobe
(aka temporal lobe seizures)

Commonly misdiagnosed as psychiatric problems because symptoms can be so bizarre

Previously referred to as psychomotor seizures

106
Q

What is the number one most likely cause of SZR

A

1 missed doses of antiepileptic medications

#2 Recent alterations in medication

 Sleep deprivation
 Increased strenuous activity
 Infection
 Electrolyte disturbances
 Alcohol or substance use or withdrawal
107
Q

Persistent, severe, or sudden HA with seizure, suggest intracranial pathology.

What should you do

A

Scan ‘em with Non Contrast head Ct (Screening)

108
Q

What is the 1st step in AMS

A

POC gl

109
Q

Define Todd’s paralysis

A

Todd’s paralysis: transient focal deficit (usually unilateral) following a simple or complex focal seizure.

  • Stroke mimic!!!
  • Should resolve within 48 hours
110
Q

What is the lab w.u for SZR

A

Glucose 1st!

Med Hx/ Rx Hx

BMP, Lactate, Calcium, mag, hCG, Tox/drug Screen.

111
Q

when should you get a LP for a SZR

A

Febrile
Immunocompromised
SAH is suspected & the noncontrast head CT is normal

112
Q

When should you get a CT for a SZR

A

First-ever seizure or a change in established seizure- r/o structural lesion with a non contrasted head CT!

Non Contrasted CT of the C spine if suspicion of head or neck trauma (always treat head and C spine as a unit. Scan one, scan both!)

113
Q

When should you get an EEG in the ED for a SZR

A

Emergent EEG can be considered in the evaluation of:
Persistent, unexplained AMS to evaluate for nonconvulsive status epilepticus, subtle status epilepticus, paroxysmal attack when a seizure is suspected, or ongoing status epilepticus after chemical paralysis for intubation

114
Q

What is the MC Cause of SZR

A

Many occur because of failure to take anticonvulsant med as prescribed!! MC!

115
Q

Is phenytoin compatible with glucose containing solutions?

A

NO! Use NS

116
Q

Steps to treat Status epilepticus

A

Call Neuro And arrange for EEG

Order gl and BMP/CMP

Lactate
+/- hCG, TOX screen and Rx levels

Treat hyperthermia with passive cooling

Place Urinary Cath and insert NG tube

If suspected toxin then GI decon with NG tube, activated charcoal or irrigation

If suspected meningitis the enteric ABX

117
Q

What is the initial Rx for Status epilepticus

A

IV lorazepam

1-2 doses

And if needed: 
phenytoin 
Fosphenytoin 
Levietiracetam 
Valproate
118
Q

What is the treatment approach to Status Epilepticus that is refractory

A

Refractory: Persistent seizure activity despite two antiepileptic agents and >2 rounds of Benzos!
Usually exceeds 60 min

Iv Midazolam or Proprofol or Phenobarbital

DEF NEED TO INTUBTAE, ICU ADMIN, and CONTINOUS EEG

119
Q

How does mag reduce eclampsia SZR

A

The mechanism of action of magnesium sulfate is thought to trigger cerebral vasodilation,!!

thus reducing ischemia generated by cerebral vasospasm during an eclamptic event.

The substance also acts competitively in blocking the entry of calcium into synaptic endings, thereby altering neuromuscular transmission

120
Q

Define SIRS criterion

A

Fever greater than 38.3 or hypothermia below 36*

Pulse greater than 90
Tachypnea greater than 20
Leukocytes greater than 12,000 or less than 4,000

121
Q

What are the criterion for sepsis

A

Documented or suspected infection

With fever Or hypothermia 
Pulse greater than 90 
Tachypnea 
AMS 
Signif edema 
And hyperglycemia without DM 
\+ HOTN 
Oliguria 
Elevated Cr 
INR>1.5 
Ileus 
Hyperlactermia >4
122
Q

What is qSOFA

A 
Criteria include:
 Altered mental status
 Respiratory rate ≥22
 Systolic BP ≤100
 A score ≥2 indicates a high risk for poor outcomes

For sepsis

123
Q

What is the most extreme outcome of sepsis

A

DIC and death

124
Q

How does acute kidney injury present

A

Acute kidney injury can present with azotemia, oliguria, or anuria

125
Q

If you see marked elevations of transaminases or bilirubin, consider …

A

Septic shock due to biliary source of infection. (G-bag)

126
Q

What is the most common manifestation in the GI in sepsis

A

Ileus!

127
Q

What is the common blood loss in GI in sepsis

A

Major blood loss secondary to UGI bleeding is rare in septic pts

Minor GI blood loss within 24 hours of developing severe sepsis can result from painless erosions in the mucosal layer of the stomach or duodenum (stress gastritis)

128
Q

What are the metabolic presentations of Sepsis

A

Elevated Lactate
Hyperglycemia
And/or Hypoglycemia

129
Q

A pt with a SBP less than 90 after an initial fluid bolus, with an evidence of EOD

Think

A

Septic Shock

130
Q

What is the common W/u for Sepsis

A 
CBC with platelet count
 Electrolytes
 (including calcium and glucose)
 Renal function panel 
 Lactic acid level 
 Liver function panel 
 Urinalysis
131
Q

Any on that comes in with sepsis, what W/u do you need to do for blood

A

Type and screen and type and cross for blood

Order a coug panel as well

132
Q

What is the tx approach to sepsis

A

Early recognition (vital signs, ABC’s)
Early infection control (AB’s)
Early reversal of hemodynamic compromise (fluids, pressors)

133
Q

Sepsis resus is based on what 5 criteria

A
  1. ABC’s
  2. Administering fluids! Get the body ready!!
  3. Adding adjunct therapies including vasopressors based on the conditions, +/-
  4. Infection Control (AB’s, surgery or identification of infectious etiology if any)
  5. Frequently assessing response! Is what you are doing, working, if not, now what?
134
Q

What is the 1st best choice for pressors in sepsis

A

NE

2nd line Vasopressin

135
Q

What is the most important reason to get a CT in Stroke Pts

A

Differentiate between ischemic and hemorrhagic stroke syndromes

136
Q

What is the most common cause of TIA

A

Thrombotic stroke

137
Q

What is the important baseline question in strokes

A

Last time seen normal

138
Q

what are the three criteria to Cincinnati stroke scale

A

facial droop
Arm drift
Speech

139
Q

A woman presents with generalize weakness and dizzyness

Think a-classical presentation for…

A

STROKE!

140
Q

The basal artery mostly feeds the..

A

Cerebellum

Problems here effect balance, coordination, taxia, and gait

141
Q

Todds paralysis is a DDX for

A

Stroke! Mimicer!

142
Q

What is the vessel most commonly involved in strokes

A

Middle cerebral artery

143
Q

How does a MCA stroke typically Present

A

Typically presents with hemiparesis, facial plegia, and sensory loss contralateral to the affected cortex

144
Q

If you see ataxia, nystagmus, AMS and vertigo

Think stroke where ?

A

Posterior cerebral artery infarction

145
Q

A patient presents with unilateral limb weakness, dizziness, dysarthria, diploplia, and HA

Think Stoke where?

A

Basically Artery Infarct

146
Q

What is the W/.u for a cerebellar infarct

A

if the initial noncontrasted head CT is unremarkable and the suspicion is very high, obtain an emergent diffusion-weighted MRI when this diagnosis is suspected.

147
Q

What demographic does Carotid & Vertebral Artery Dissection effect most

A

young and Middle Aged pt

148
Q

What are the presenting s/y for carotid/ .vertebral artery dissection

A

Unilateral fronto HA

Pulsatile, eye miosis, and ptosis

Partial horners syndrome with

149
Q

What is the W/u of new onset HA or neck pain what do we do next

A

Image neck vessels then CT angiogram

150
Q

How does a vertebral artery dissection typicall present

A

Dizzyness, vertigo, neck pain, HA In the occipital region

151
Q

What is the Image of Choice for Carotid and Vertebral artery dissection

A

CTA or MRA

152
Q

What are two methods of screening for delerium

A

Delirium triage screen and the confusion assessment method

153
Q

How do pts with vascular dementia present

A

Patients with vascular dementia often show similar neurocognitive symptoms but may have chronic neurologic physical deficits from prior cerebrovascular accidents.

154
Q

If a pt presents “wet and wobbly” with urinary incontinente and gait disturbance

Think

A

Normal pressure hydrocephalus

Dementia

155
Q

What kind of progression suggest vascular dementia

A

A fluctuating, stepped course suggests vascular dementia.

156
Q

What is the motor portion of the GCS

A 
6- follow commands 
5- localizes pain 
4- withdrawals from pain 
3- flexion 
2- extension 
1 -none
157
Q

What is the verbal portion of the GCS

A 
5- A/O 
4- Confused 
3- Innapropartie words 
2- incomprehension 
1- none
158
Q

What is the eye portion of the GCS

A

4- spont
3- to command
2- to pain
1- none

159
Q

If the only finding on CT is a hyperdence basilar artery

Think

A

Suspect basilar artery thrombosis in a comatose patient with “normal” head CT, in which the only finding may be a hyperdense basilar artery.

MRI or cerebral angiography is needed to make the diagnosis of basilar artery thrombosis.

160
Q

What is the time frame to Tx stroke

A

Evaluate & decide treatment within 60 min (door to needle time) of the patient’s arrival in an ED

161
Q

When should a CT be done for Stroke

A

Obtain emergency non-contrast enhanced CT

Imaging done in ≤ 20 min of ED arrival

162
Q

What is the only imaging necessary prior to giving rTPa

A

Non con Ct

163
Q

If a pt is not a candidate for thrombolytics

Which is the treatment for Ischemic Stroke

A 
If patient NOT a candidate for thrombolytics or reperfusion
- Permissive hypertension
 -No attempts to lower BP unless 
 SBP is >220 mmHg or
 Diastolic is >120 mmHg

Or condition requiring acute BP lowering

Reduce BP by 10-15% over the first 24hrs

164
Q

What is the HTN goal for pts with ischemic stroke that meet the criteria for reprofusion

A

If a patient is a candidate for reperfusion
—Maintain BP <185/110

If the target BP cannot be met—>no longer a candidate for rtPA therapy
»permissive hypertension is allowed for perfusion of surrounding tissue.

165
Q

What are the HTN drugs used to lower BP before admin of rTPA

A

Labetalol or nicardipine

166
Q

When should asprin be used in the Tx of ischemic stroke

A

Current AHA/ASA guidelines recommend aspirin within 24 to 48 hours after stroke onset unless thrombolytics have been given within the last 24 hrs.

167
Q

What stroke scale score is commonly used as one of the criteria for rTPA admin

A

Between 4-22

168
Q

What is the inclusion exclusion criteria for rTPA in ischemic stroke

A

inclusion: Dx of Ischemic stroke
Onset less than 3hrs
Age older than 18

Exclusion:
Sig Head Trauma, Bleeding, Heparin within 48hours, high INR, low platelets, High Blood pressure, Using anticlotting agents, Low gl, Multilobular infarctions

169
Q

WHat is the W/u after admin of thrombolytics in strokes

A

Perform BP & neuro checks q 15 min for 2 hrs after starting the infusion

Do not give anticoagulants or antiplatelet agents in the initial 24 hrs following treatment

Admit patients to a specialized stroke unit or an ICU familiar with the use of thrombolytic drugs and neurologic monitoring

170
Q

Are pts with MCA strokes good candidates for rTPA

A

Patients with a massive middle cerebral artery-not candidates for thrombolytic therapy

80% mortality rate

May be candidates for decompressive surgery

171
Q

What is the ABCD2 score

A

Age greater than 60

Blood pressure 140/90

Clinical Features

Duration

Diabetes

172
Q

What is the tx approach to TIA

A

Aspirin plus Dipyridamole

+/- Clopidogrel

Decoagulate

173
Q

What is the most common cause of ischemic stroke in children

A

Sickle cell Dz

174
Q

Can you used rTPA in pregnancy

A

rtPA does not cross the placenta so you can use IV rTPA

ED treatment of stroke in pregnant women should ideally involve early consultation with obstetricians, stroke neurologists, and neonatologists

Senoir 21-2 (77 decks)

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