Clinmed: Emergency Medicine

Front 1

What does the primary survey consist of?

Back 1

airway, breathing, circulation, neurologic deficits

Front 2

What is the approach to the patient in the emergency room?

Back 2

classify as critical, emergent, nonurgent
stabilize if necessary
R/O most serious causes of presentation

Front 3

What is the range of the glascow coma scale?

Back 3

3-15
where 3 = coma or death
where 15 = normal

Front 4

Describe the glascow coma scale.

Back 4

Front 5

What is the clinical presentation and initial management of acetaminophen overdose?

Back 5

1. clinical presentation → asymptomatic or nausea, vomiting, anorexia, RUQ pain
2. draw 4-hour post-ingestion acetaminophen level, LFTs
3. draw another acetaminophen level 4-6 hours later if sustained-release acetaminophen ingested
4. assess likelihood of hepatic toxicity based on clinical exam, acetaminophen level, LFTs
5. toxic dose of acetaminophen is >150mg/kg in children and 7g in adults
6. hepatic toxicity occurs 24-72 hours after ingestion and may be manifested by nausea, vomiting, anorexia, jaundice, RUQ pain, and ↑ LFTs
7. give activated charcoal
8. give N-acetylcysteine within 12-16 hours of ingestion if acetaminophen level >150 micrograms/mL
9. do not delay N-acetylcysteine if high suspicious and acetaminophen level not ready
10. obtain salicylate level since often ingested simultaneously
11. hospitalize if require N-acetylcysteine therapy or evidence of hepatic toxicity

Front 6

What is the clinical presentation and initial management of amphetamine overdose?

Back 6

1. CNS stimulant
2. clinical presentation → sympathetic hyperactivity → euphoria, restlessness, psychosis, palpitations, HTN, hyperthermia, mydriasis, ↑ muscle tone, arrhythmias, seizures
3. hyperthermia and seizures may result in rhabdomyolysis and myoglobinuria
4. peak toxicity within 2-3 hours if oral and 30 minutes if IV or IM
5. serum drug levels are of little value and measures to enhance elimination do not alter outcome
6. treatment is supportive
7. monitor temp and start cooling blanket if hyperthermia
8. give diazepam if severe agitation, psychosis, or seizure
9. give nitroprusside if diastolic BP >120
10. may give propranolol if tachycardia or ventricular arrhythmias
11. get urine for myoglobin
12. get EKG, cardiac enzymes if chest pain
13. get CT if seizures
14. hospitalize if psychosis, HTN, hyperthermia, chest pain, arrhythmias, or prolonged symptoms

Front 7

What is the clinical presentation and intitial management of salicylate toxicity?

Back 7

1. weak acid
2. clinical presentation → nausea, vomiting, tinnitus, listlessness, hyperventilation, hyperpnea, hyperthermia, respiratory alkalosis followed by severe metabolic acidosis, hypokalemia, hypoglycemia, seizures, hyperpyrexia, coma
3. presentation of sub acute toxicity often occurs in very young and very old and manifests as dehydration, obtundation, acidosis, cerebral and pulmonary edema, death
4. toxicity at >150 mg/kg
5. half life may increase from 2 to 20 hours at toxic levels
6. get salicylate level and repeat every 4-6 hours
7. give activated charcoal
8. additional activated charcoal and whole bowel irrigation if enteric-coated aspirin ingested
9. give IV crystalloid solution to correct dehydration
10. give sodium bicarbonate to correct acidosis
11. give glucose to correct hypoglycemia
12. give vitamin K IM if hypoprothombinemia
13. hemodialysis if persistent seizures, acidosis fails to respond to tx, cerebral or pulmonary edema
14. hospitalize all patients

Front 8

What is the clinical presentation and intitial management of TCA overdose?

Back 8

1. anticholinergic
2. clinical presentation → agitation, hallucinations, dry mouth, hypotension, tachycardia, mydriasis, twitching, myoclonic jerk, seizures, coma
3. toxic dose is 5mg/kg
4. 10-30 hour half-life
5. give activated charcoal within 1 hour of ingestion
6. get serial EKG for 6 hours – possible QRS widening, AV block, ventricular arrhythmias, torsades
7. treat hypotension with colloid solutions and sodium bicarbonate
8. treat ventricular arrhythmias and AV block with sodium bicarbonate
9. treat seizures with diazepam
10. hospitalize all patients

Front 9

Define concussion.

Back 9

trauma-induced alteration in mental status that may or may not include loss of consciousness

Front 10

Describe concussion grading.

Back 10

GRADE I:
transient confusion, no loss of consciousness, symptoms last <15 minutes
stop activity
may return after asymptomatic for 15 minutes

GRADE 2:
transient confusion, no loss of consciousness, symptoms last >15 minutes
stop activity
may return to activity if asymptomatic for 1 week

GRADE 3:
loss of consciousness
stop activity and go to ER
may return to activity if asymptomatic for 1 week + LOC only seconds long
may return to activity if asymptomatic for 2 weeks + LOC 1 minutes long

Front 11

What is the management of a concussion?

Back 11

post-concussion symptoms include HA, dizziness, and memory problems
concussion self-limiting with post-concussion symptoms resolving within weeks to months

Front 12

BASILAR SKULL FX:

Back 12

ETIOLOGY:
skull fracture at base of skull, typically at petrous portion of temporal bone
caused by trauma

CLINICAL PRESENTATION:
raccoon eyes → periorbital ecchymosis
Battle sign → mastoid ecchymosis
CSF leak from ear or nose
hemotympanum
hearing loss

DIAGNOSTIC WORKUP:
non-contrast CT

EMERGENT MANAGEMENT:
admit for observation
neurosurgery consult if more serious intracranial abnormality present

Front 13

Back 13

Battle sign indicating basilar skull fx

Front 14

Any alteration of consciousness or amnesia to an event of injury requires?

Back 14

CT

Front 15

EPIDURAL HEMATOMA:

Back 15

ETIOLOGY:
collection of blood and clot between dura mater and bones of skull
bleeding source may be meningeal arteries (often middle meningeal artery) or occasionally dural venous sinuses
usually d/t head trauma

CLINICAL PRESENTATION:
brief loss of consciousness followed by transient lucid interval followed by rapid deterioration

DIAGNOSTIC WORKUP:
CT reveals biconvex (lens-shaped) hematoma

EMERGENT MANAGEMENT:
decompression to prevent brain herniation ASAP

Front 16

Back 16

epidural hematoma of right frontal lobe

Front 17

SUBDURAL HEMATOMA:

Back 17

ETIOLOGY:
collection of blood between dura mater and arachnoid mater
bleeding source is often bridging veins
may be acute, chronic, or acute on chronic
usually d/t brain atrophy
risk factors include elderly, alcoholism, anticoagulants, repeated head injuries

CLINICAL PRESENTATION:
HA, confusion, LOC
minimal neurologic deficit with chronic hematomas
neurologic deficits with acute hematomas

DIAGNOSTIC WORKUP:
CT reveals concave (crescent-shaped, conforms to underlying cerebral cortex) hematoma

EMERGENT MANAGEMENT:
neurosurgery consult

Front 18

Back 18

subdural hematoma of left hemisphere

Front 19

SUBARACHNOID HEMATOMA:

Back 19

ETIOLOGY:
collection of blood between subarchnoid mater and pia mater
causes include head trauma, AVM leading to an aneurysm, bleeding disorders, anticoagulants

CLINICAL PRESENTATION:
sudden severe HA - “worst HA of your life”

DIAGNOSTIC WORKUP:
CT → peripheral if traumatic; circle of willis if AVM
If CT negative, do LP
LP positive if blood present

EMERGENT MANAGEMENT:
may obstruct CSF and cause increased ICP
if asymptomatic → admit for observation
if altered consciousness or other neurological deficits → admit to critical care for ICP monitoring

Front 20

DIFFUSE AXONAL INJURY:

Back 20

ETIOLOGY:
blunt trauma → sudden acceleration/deceleration → diffuse neuronal shearing
blunt trauma may be d/t MVA, child abuse (shaken baby syndrome), fall, assault, etc

CLINICAL PRESENTATION:
post-traumatic coma
possible autonomic dysfunction → HTN, fever, sweating

DIAGNOSTIC WORKUP:
difficult to see on CT
CT may reveal blurring of the margin between gray and white matter, punctate cerebral hemorrhages or cerebral edema

EMERGENT MANAGEMENT:
lacks specific treatment
stabilize patient and prevent increasing ICP

Front 21

Back 21

pneumocephalus
AKA mount Fugi sign
presence of air or gas within cranial cavity

Front 22

SKULL FX:

Back 22

ETIOLOGY:
trauma

CLINICAL PRESENTATION:
closed skull fracture
open skull fracture → underlies scalp lacerations, palpable
depressed skull fracture → visible on inspection, palpable

DIAGNOSTIC WORKUP:
noncontrast CT
open skull fx likely if pneumocephalus present

EMERGENT MANAGEMENT:
R/O intracranial injuries
closed skull fx → observation for developing epidural hematoma
open skull fx → admit, surgical referral, consider antibiotics d/t high risk of infection
depressed skull fx → admit, surgical referral, consider antibiotics d/t high risk of infection if open fx

Front 23

Describe first-degree burn.

Back 23

involves epidermis
characterized by erythema, skin texture normal, pain
resolves in 5-10 days
no scarring

Front 24

Describe second-degree burn.

Back 24

SUPERFICIAL PARTIAL-THICKNESS:
extends into superficial (papillary) dermis
characterized by erythema, +/- blistering, skin edematous, pain
resolves in 10-21 days
minimal or no scarring

DEEP PARTIAL THICKNESS:
extends into deep (reticular) dermis
characterized by pink to white discoloration, skin thick, possible pain
resolves in 25-60 days
dense scarring

Front 25

Describe third-degree burn.

Back 25

extends through entire dermis
characterized by white, brown or black discoloration, skin leathery, no pain
no spontaneous healing

Front 26

Describe fourth-degree burn.

Back 26

extends through subcutaneous tissue, tendon, or bone
characterized by black or charred discoloration, dry skin, no pain
no spontaneous healing

Front 27

SUNBURN:

Back 27

1st-degree or 2nd-degree (superficial partial-thickness)
characterized by erythema +/- blistering
hx of sun or tanning booth exposure
no diagnostic workup
saline-soaked dressings, calamine lotion, and NSAIDs (ibuprofen) for pain relief
no scarring
RTC in 2-3 days if large blisters to monitor for secondary infection
admit if IV fluids and analgesics required
avoid prolonged sun exposure and wear sunscreen

Front 28

CHEMICAL BURNS:

Back 28

CLINICAL PRESENTATION:
usually d/t acids or alkalis, sometimes phosphorus or phenol
ascertain type of chemical, concentration
acid burns → partial-thickness, erythema, erosion, HCL stains skin black, nitric acid stains skin yellow, sulfuric acid stains skin brown
alkali burns → full-thickness, pale, leathery, slippery

DIAGNOSTIC WORKUP:
none

MANAGEMENT:
remove contaminated clothing
copious irrigation with large amounts of tap water ASAP
alkali burns may require emergency excision

PROGNOSIS:
size usually underestimated d/t slow development so reevaluate after 24-48 hours

Front 29

What are the 5 P's of compartment syndrome?

Back 29

pain, paresthesias, pallor, pulselessness, poikilothermia

Front 30

CHILBLAINS:

Back 30

Chilblains (Pernio)
d/t cold exposure but less severe that frostbite (no actual freezing of tissues)
most common in women, children, PVD
pruritic, red, violaceous lesions that usually form on face or extremities
+/- blistering, edema, lymphocytic vasculitis
elevate and allow to warm gradually at room temp
do not massage or apply heat

Front 31

DECOMPRESSION SICKNESS:

Back 31

RISK FACTORS:
scuba diving
inadequately pressurized airplane

CLINICAL PRESENTATION:
Type 1 = deep aching pain in large joints and extremities AKA “the bends”, cutaneous marmorata
Type 2 = cardiorespiratory (chest pain, SOB) or neurologic (ataxia, spinal paralysis, vertigo, visual or speech disturbance, cognitive deficits) symptoms

INITIAL MANAGEMENT:
100% O2 x 2 hours
mild analgesics
crystalloid IV fluids
recompression in hyperbaric chamber ASAP

Front 32

What is the most common infecting organism from cat scratches?

Back 32

pasteurella multocida

Front 33

What is the cause of cat scratch disease?

Back 33

bartonella henselae

Front 34

What do acid burns do?

Back 34

produce a coagulation necrosis

denature proteins → forming coagulum (AKA eschar) → limiting penetration

Front 35

What do alkali burns do?

Back 35

produce a liquefaction necrosis

denaturation of proteins
saponification of lipids which does not limit penetration

Front 36

Which are worse, acid or alkali burns?

Back 36

alkali
penetration not limited like in acid burns

Front 37

Back 37

allergic angioedema

Front 38

Why is angioedema a medical emergency?

Back 38

rapid swelling → airway obstruction

Front 39

What is treatment for allergic angioedema?

Back 39

epinephrine

Front 40

What are the indications for a drug screen?

Back 40

suspected substance abuse, overdose, or poisoning

Hint 40

Interpreting Laboratory Data p47

Front 41

What is a drug screen (AKA tox screen)?

Back 41

a qualitative test used to determine the presence of a specific substance or group of substances

Hint 41

Interpreting Laboratory Data p47

Front 42

How are drug screens categorized?

Back 42

1. tests included
2. preliminary vs. confirmatory

Hint 42

Interpreting Laboratory Data p48

Front 43

What factors should be considered when ordering a drug screen confirmation?

Back 43

1. Will result affect patient's care?
2. Will result be reported before patient discharge?
3. Is cost justified?
4. Are legal actions anticipated?

Hint 43

Interpreting Laboratory Data p48

Front 44

What should you order for drug screen confirmatory testing?

Back 44

GC-MS confirmation
(gas chromatography-mass spectrometry)

Hint 44

Interpreting Laboratory Data p49

Front 45

If a drug screen is negative, it means the drug was not present, true or false?

Back 45

false
it means the drug was not detected

Hint 45

Interpreting Laboratory Data p51

Front 46

What are possible reasons for negative drug screen?

Back 46

drug not taken
drug not part of drug screen panel
urine too dilute

Hint 46

Interpreting Laboratory Data p51

Front 47

What tests are in UDAS for Swedish?

Back 47

Amphetamines
Barbiturates
Benzodiazepines
Cannabinoids
Cocaine Metab.
Methadone
Opiates
Phencyclidine
THC Metabolite
Creatinine

Hint 47

Antrim

Front 48

What factors should be considered when ordering a drug screen in ER setting?

Back 48

1. Substances that exhibit delayed toxic symptoms (e.g. sustaine release agents)?
2. Multiple agents ingested?
3. Multiple agents found at scene?
If yes to any of the above, order drug screen

Hint 48

Interpreting Laboratory Data p49

Front 49

How does transfusion of one unit of RBCs affect HCT?

Back 49

raises HCT 4%

Hint 49

Current p518