Read Rosen & Barkin's 5-Minute Emergency Medicine Consult Online

Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

Rosen & Barkin's 5-Minute Emergency Medicine Consult (52 page)

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
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  • Hemorrhoid
  • Perirectal Abscess
CODES
ICD9

565.0 Anal fissure

ICD10
  • K60.0 Acute anal fissure
  • K60.1 Chronic anal fissure
  • K60.2 Anal fissure, unspecified
ANAPHYLAXIS
Sean-Xavier Neath
BASICS
DESCRIPTION
  • An acute, widely distributed form of shock that occurs within minutes of exposure to antigen in a sensitized individual
  • ∼500–1,000 deaths are attributed annually in the US to anaphylaxis. There are ∼10,000 ER visits per month for anaphylaxis in the US
  • Involves release of bioactive molecules such as histamine, leukotrienes, and prostaglandins from inflammatory cells:
    • Mediator release results in increased vascular permeability, vasodilation, smooth-muscle contractions, and increased epithelial secretion.
    • Physiologically, this is manifested in a decrease in total peripheral resistance, venous return, and cardiac output, as well as intravascular volume depletion.
ETIOLOGY
  • IgE mediated:
    • Antibiotics, particularly penicillin family
    • Venoms, especially bee and wasp
    • Latex
    • Vaccines
    • Foodstuffs (shellfish, soybeans, peanuts, tree nuts, wheat, milk, eggs, nitrates/nitrites)
    • Monoclonal antibody therapeutics
  • Non-IgE mediated:
    • Iodine contrast media
    • Opiates
    • Vancomycin
Pediatric Considerations

In children, foods are an important trigger for IgE-mediated anaphylaxis:

  • Milk, egg, wheat, and soy (MEWS) are the most common food allergens.
  • Peanut allergies are increasingly common and can be more potent; children can develop anaphylaxis from residual peanut in a candy bar.
DIAGNOSIS
SIGNS AND SYMPTOMS
  • Symptoms begin within seconds to minutes after contact with an offending antigen.
  • Anaphylactic reactions almost always involve the skin or mucous membranes. >90% of patients have some combination of urticaria, erythema, pruritus, or angioedema.
  • Some patients may have an initial sensation of impending doom followed by more clearly definable symptomatology:
    • Respiratory: From sneezing and nasal congestion to frank bronchospasm and laryngeal edema
    • Cardiovascular: Hypotension, dysrhythmias, myocardial ischemia
    • Gastrointestinal: Nausea, vomiting, diarrhea
    • Ocular: Eye itching and tearing, conjunctival injection
    • Hematologic: Activation of intrinsic coagulation pathway sometimes leading to disseminated intravascular coagulation, thrombocytopenia
    • Neurologic: Seizures
History
  • Anaphylaxis is a clinical diagnosis.
  • A brief history should include previous history of allergy or anaphylaxis, as well as exposure to potential new triggers.
Physical-Exam
  • Usually will include alterations in a combination of any 2 or more of the following systems: Cutaneous, respiratory, gastrointestinal, or cardiovascular system
  • Hypotension or airway compromise is not always present at onset.
ESSENTIAL WORKUP
  • Diagnosis is made based on clinical symptoms.
  • It is important not to underestimate the potential severity of an allergic reaction in its early stages.
  • ECG should be done in patients with previous cardiac history or ischemic symptoms; consider routinely in the elderly.
DIAGNOSIS TESTS & NTERPRETATION
Lab

The diagnosis of anaphylaxis is made on clinical grounds; laboratory tests are usually not useful in aiding diagnosis in the acute setting. Tryptase levels remain elevated after an attack and can be useful for later confirmation of a suspected anaphylactic episode.

Imaging

Hyperinflation can be seen on CXR.

DIFFERENTIAL DIAGNOSIS
  • Pulmonary embolism
  • Acute MI
  • Airway obstruction
  • Asthma
  • Tension pneumothorax
  • NSAID reaction
  • Vasovagal collapse
  • Hereditary angioedema
  • Serum sickness
  • Systemic mastocytosis
  • Foreign body aspiration
  • Hypoglycemia
  • Pheochromocytoma
  • Carcinoid syndrome
TREATMENT
PRE HOSPITAL
  • IV access, O
    2
    , cardiac and pulse oximetry monitoring
  • Early intubation based on the initial progression of disease and response to treatment:
    • Laryngeal edema and spasm can progress rapidly.
    • Laryngeal edema can be managed with racemic epinephrine prior to intubation.
  • IM epinephrine can be administered en route even prior to establishment of an IV.
ALERT

Note that current guidelines advocate the use of IM over SC epinephrine

INITIAL STABILIZATION/THERAPY
  • ABCs
  • Assure adequate ventilation
  • Airway management:
    • Orotracheal intubation is the airway technique of choice.
    • If laryngeal edema, spasm, or soft tissue swelling present; consider using advanced airway adjuncts when available.
    • Consider blind nasotracheal intubation if soft tissue swelling prohibits an oral approach and there is absence of stridor.
    • Transtracheal jet insufflation or cricothyrotomy may be necessary to control the airway.
  • Epinephrine IM/IV or endotracheal administration:
    • Direct injection into the venous plexus at the base of the tongue is an option.
  • Volume resuscitation with crystalloids or colloids
ED TREATMENT/PROCEDURES
  • Continuous cardiac and vital sign monitoring until stable
  • Persistent bronchospasm can be treated with β
    2
    -agonist bronchodilators.
  • Hypotension should be treated with volume repletion. Vasopressors can provide additional support.
  • Antihistamines (both H
    1
    and H
    2
    blockers) have been shown to be helpful in preventing histamine interactions with target tissues.
  • Corticosteroids help prevent the progression or recurrence of anaphylaxis.
  • Glucagon is particularly useful in epinephrine-resistant anaphylaxis from β-adrenergic blocking agents.
MEDICATION
ALERT

A patient’s concomitant use of a β-blocker may antagonize the effects of epinephrine. For these patients consider glucagon as it increases intracellular cyclic adenosine monophosphate levels by a mechanism that does not depend upon β-receptors.

First Line
  • Diphenhydramine: Adults—50 mg IV; (peds: 1–2 mg/kg, not to t exceed 50 mg/dose) slow IVP
  • Epinephrine: 0.3–0.5 mg; use 1:1,000 dilution for IM route and 1:10,000 for IV route (peds: epinephrine 0.01 mg/kg SC/IV)
  • Hydrocortisone: Adults—500 mg IV (peds: 4–8 mg/kg/dose IV) OR
  • Methylprednisolone: Adult—125 mg IV (peds: 1–2 mg/kg IV) OR
  • Prednisone: Adult—60 mg PO (peds: 1 mg/kg PO)
  • Albuterol: 0.5 mL of 0.5% solution in 2.5 mL of isotonic saline by nebulizer
Second Line
  • Racemic epinephrine: 2.25% solution (0.5 mL placed in a nebulizer in 2.5 mL of normal saline)
  • Glucagon: Adults—1–2 mg IV/IM/SC
  • Ranitidine: Adult—50 mg IV (peds: 1 mg/kg)
    or
    cimetidine 300 mg IV
FOLLOW-UP
DISPOSITION
Admission Criteria
  • Intubated patients or patients in respiratory distress should be admitted to an intensive care unit setting.
  • A monitored inpatient bed may be necessary for the patient who has not had substantial response to initial therapy.
  • Patients with significant generalized reactions and persistent symptoms should be admitted for observation for 24 hr. Biphasic or late phase reactions are known to occur.
Discharge Criteria

Patients with complete resolution of symptoms may be discharged after several hours of ED observation.

Issues for Referral
  • Consultation with an allergist/immunologist is appropriate when desensitization to an antibiotic is being considered for the treatment of an infectious process.
  • When a patient at high risk for contrast reaction needs a contrast study, consultation with the radiologist regarding pretreatment and choice of contrast agent is appropriate.
BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
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