Emergency Flashcards

1
Q

Anaphylaxis

A

-Severe, life-threatening allergic reaction
• Not all allergic reactions will cause anaphylaxis
• Severe allergic reactions can lead to anaphylaxis
– Chemical cascade causes the body to go into shock
– Type I Reaction (IgE)
• Mediated release of histamine and others from mast cells and basophils
– Occurs from seconds

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2
Q

Signs and symptoms/diagnosis of anaphylaxis

A

– General appearance/vital signs
• Restless and anxious
– Dermatological
• Generalized or local erythema, urticaria, cutaneous injection or pruritis, warmth, angioedema
– Ocular
• Conjunctival injection, pruritis, ecchymosis
– Cardiovascular
• Hypotension & weak and rapid pulse
– Respiratory
• Congestion, coryza, rhinorrhea, sneezing, throat tightness, wheezing, hoarseness, dyspnea
Gastrointestinal
• Nausea, vomiting, diarrhea, bloating, cramps, dysphagia
– Neurological
• Dizziness, headache, blurred vision, syncope, seizure, depressed level of consciousness, agitation, combative, altered mental status
– Other
• Metallic taste, feeling of impending doom

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3
Q

Causes of anaphylaxis

A

Food allergies
• Peanuts, tree nuts, fish, shellfish, milk
– Medications
• Antibiotics, aspirin, OTC pain relievers, IV contrast
– Venom
• Bees, yellow jackets, wasps, fire ants, hornets – Material
• Latex, plastics
– Activity
• Aerobic exercise (jogging)

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4
Q

Risk factors for anaphylaxis

A

-Previous anaphylaxis
– Allergies or asthma
– Heart disease
– Mastocytosis (accumulation of specific white blood cell)

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5
Q

Differential diagnosis for anaphylaxis

A
-Vasovagal*
– Hereditary angioedema
– Malignant carcinoid syndrome
– Medullary thyroid carcinoma
– Pheochromocytoma
– Systemic mastocytosis
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6
Q

Testing for anaphylaxis

A

-Serum tryptase
• Confirm diagnosis – Urinary 24h histamine
• Diagnose recurrent anaphylaxis – Urinary 24h 5-hydroxyindoleacetic acid level
• R/O malignant carcinoid syndrome – In vitro IgE tests/skin tests
• Determine food, medication, and causes of IgE-independent reactions

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7
Q

Managment of anaphylaxis: non pharmacological

A
  • Airway management (ventilator with bag/valve/mask/intubation)
  • High-flow oxygen
  • Cardiac monitoring and pulse oximetry
  • IV access
  • Fluid resuscitation with isotonic crystalloid solution
  • Supine position with legs elevated
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8
Q

Pharmacological managment of anaphylaxis

A
• Adrenergic agonist
– Epinephrine 
• Antihistamines
– Diphenhydramine, hydroxyzine 
• H2 receptor antagonists
– Cimetidine, ranitidine, famotidine 
• Bronchodilators
– Albuterol
•Corticosteroids
– Methylprednisolone, prednisone 
• Positive inotropic agents
– Glucagon 
• Vasopressors
– Dopamine
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9
Q

Surgical management of anaphylaxis

A
  • Cricothyrotomy

* Catheter jet ventilation

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10
Q

In office management of anaphylaxis

A
  • Call 911
  • Use an Epipen
  • Lie the patient down with legs elevated** (Why? Get blood to brain. If not they will go into a full blown seizure)
  • Administer albuterol and then oxygen
  • Check pulse/breathing and perform CPR if needed
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11
Q

Vasovagal syncope

A

-Also called neurocardiogenic syncope or reflex syncope
– Response is controlled by the vagus nerve (CNX)
• Breathing, sweating, regulating heart rate, emptying food from stomach
• Involuntary body functions are controlled by parasympathetic nervous system
– Certain triggers inducing extreme stress leading to syncope
• Triggers → bradycardia/hypotension/hyperhidrosis → reduced blood to the brain → syncope

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12
Q

Signs and symptoms/diagnosis of vasovagal syncope

A
-General appearance/vital signs 
• Jerky, abnormal movements
– Dermatological
• Pale skin, felling of warmth, cold/clammy sweat 
– Ocular
• Dilated pupils 
– Cardiovascular
• Hypotension & weak and slow pulse 
– Respiratory
• Yawning
-Gastrointestinal
• Nausea, vomiting 
– Neurological
• Dizziness, tunnel vision, lightheadedness, blurred vision, syncope
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13
Q

Causes of vasovagal syncope

A
  • Excessive standing
  • Heat exposure
  • Seeing blood or needles
  • Having blood drawn
  • Fear of injury
  • Straining
  • Tonometry
  • Bright lights
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14
Q

Differential diagnosis of vasovagal syncope

A
– Anaphylaxis
– Cardiac syncope (unknown cause of syncope have a 30% increase in death vs vasovagal
have no increased risk of death) 
– Hemorrhage 
– Pulmonary embolism 
– Carotid sinus hypersensitivity 
– Orthostasis 
– Medications 
– Metabolic 
– Seizure
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15
Q

Testing for vasovagal syncope

A
– Electrocardiogram
– Echocardiogram
– Exercise stress test
– Blood tests
– Neurological studies
– Tilt table (done after heart problems are r/o)
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16
Q

Non pharm management of vasovagal syncope

A
  • Foot exercises
  • Compression stockings
  • Increased salt intake
  • Increased fluid intake
17
Q

Pharmacological managment of vasovagal syncope

A

• Beta-blockers
– Atenolol
• Counteracts the increase in serum epinephrine that occurs before syncope
• Mineralocorticoids
– Fludrocortisone acetate
• Treats hypotension
• Selective serotonin reuptake inhibitors
– Fluoxetine
• 5HT inhibits sympathetic neural outflow while increasing adrenal sympathetic stimulation
• Vasoconstrictors
– Disopyramide
• Decrease cardiac contractility and manages heart rate

18
Q

Surgical management of vasovagal syncope

A

Electrical pacemaker

19
Q

In office management of vasovagal syncope

A
  • Try to catch patient before they fall
  • Lie the patient down with legs elevated
  • Check pulse/breathing
  • Administer smelling salt
20
Q

Orbital compartment syndrome

A

– Rare but treatable complication of increased pressure within the orbital space
– Mostly secondary to facial trauma or a surgical procedure

21
Q

Anatomy of orbital compartment syndrome

A

– Globe and retrobulbar contents are in a cone-shaped fascial envelope bound by 7 bony
walls (except anteriorly in which the boundary is the orbital septum and eyelid).
– The medial and lateral canthal tendons attach the eyelids to the orbital rim
• Limits forward movement of the globe

22
Q

Pathophysiology of orbital compartment syndrome

A

– Increased tissue pressure in an enclosed space → decreased perfusion
• Pressure within the orbit exceeds the pressure of the central retinal artery → ischemia

23
Q

Causes of orbital compartment syndrome

A
– Causes
• Trauma
– After large-volume resuscitation, asphysxia syndrome 
• Surgery/procedures
– Extravasated contrast material, complications of spinal surgery in prone position
– Spontaneous bleeding 
• Infection 
• Tumor 
• Inflammation
– Graves
24
Q

Retrobulbar hematoma

A

• Most common cause of OCS
• Hemorrhage emanating from infraorbital artery/branch
• Most commonly occur as an ophthalmologic/maxillofacial postop
complication
• Retrobulbar blood causes large increase in pressure unless
decompressive drainage occurs (through orbital wall fractures into the
paranasal sinuses)
• Causes an anterior ischemic optic neuropathy

25
Q

Anteiror ischemic optic neuropathy from retrobulbar hematoma

A

– Central retinal artery has protection from compression (b/c of the position within
the optic nerve) and from increasing tissue pressure (b/c of its higher systolic
pressure)
– Prelaminar capillaries, peripapillary choroid, and postciliary arteries (lie
within muscle cones, have lower pressure, and enter the eye around the optic
nerve) do not have the same protection

26
Q

Subperiosteal hematoma

A

-Cause of orbital compartment syndrome
• Hemorrhage within the potential space between the periosteum and the bones
• Most commonly occurs after trauma
• Orbital emphysema from a sinus communication causes a 1-way valve which causes an increase
in pressure
• Causes an anterior ischemic optic neuropathy

27
Q

Prognosis of acute orbital compartment syndrome

A

– Visual acuity loss leads to permanent blindness if emergency decompressive surgery is
not initiated immediately
– Irreversible vision loss is expected with retinal ischemia that lasts more than 120 minutes

28
Q

History of acute orbital compartment syndrome

A
  • Increased IOP >40mmHg
  • Vision loss
  • Proptosis
  • Ophthalmoplegia
  • Diplopia
  • Ecchymosis
  • Chemosis
  • Papilledema
29
Q

History of chronic orbital compartment syndrome

A
  • Decreased VF
  • Nerve pallor
  • Cherry red macula
  • APD
30
Q

Differential diagnosis of orbital compartment syndrome

A
– Optic nerve decompression for traumatic optic neuropathy
– Graves
– Orbital neoplasm
– Lens dislocation
– Anterior ischemic optic neuropathy
– Globe rupture
– Retinal detachment
31
Q

Testing for orbital compartment syndrome

A

– Fundoscopy
– IOP
– CT/MRI
• If truly from acute orbital compartment syndrome then this could delay sight-saving therapy
• Imitate therapy first and then send for imaging

32
Q

Treatment for orbital compartment syndrome

A

Lateral canthotomy

Inferior cantholysis

33
Q

Indication for treatment of orbital compartment syndrome

A

• Primary criterion
– IOP >40mmHg
– Decreased visual acuity (if vision worsens, then immediate decompression is necessary)
– Proptosis (can evaluate patients who are unconscious who cannot perform visual acuity)
– Pain

• Secondary criterion (late signs)
– APD
– Ophthalmoplegia
– Cherry-red macula
– Optic nerve pallor
34
Q

Contraindications of orbital compartment syndrome

A

Suspected ruptured globe

35
Q

Emergency department care for OCS

A

– Osmotic agents and carbonic anhydrase inhibitors given
– High dose steroids
– Consult for emergency decompression surgery

36
Q

Lateral canthotomy

A

Inject into lateral canthus with lidocaine
Will hit orbital bone
Crush tissue, devascularize and decreases bleeding and gives a good line to cut the tissue
Does not relieve tension

37
Q

Inferior cantholysis

A
  • Done after the canthotomy
  • Cut tendon itself
  • pull lid down, cut tendon, allows eye to move forward
  • check IOP to make sure its reduced, if not, then you cut the superior tendon
  • coverwith guaze, dont suture yet
38
Q

Post procedure of OCS: IOP

A

– IOP
• Directly after inferior cantholysis • Mean reduction with surgery
– Canthotomy

39
Q

Post procedure for OCS: VA

A

• Check immediately after procedure
• Fails to improve
– Operative orbital decompression or hematoma evacuation should be considered