Episode 12 – Back to Biphasics

(iTunes or listen here)

The Free Open Access Medical education (FOAM)

We review Episode 1 of Dr. Salim Rezaie’s REBEL Cast covering exposing the dogma behind biphasic anaphylaxis reactions.

Traditionally, we’re taught to observe patients in the Emergency Department (ED) for 4-6 hours to watch out for biphasic reactions, as the rate of biphasic reactions can approach 20%.

Grunau BE et al. Incidence of Clinically Important Biphasic Reactions in Emergency Department Patients with Allergic Reactions or Anaphylaxis. Ann of EM 2014; 63(6): 736 – 44.

  • Retrospective chart review of 430,000 visits
  • Anaphylaxis n=496 (2 had biphasic reactions, Allergic reactions n=2323 (3 had biphasic reactions)
  • No deaths, biphasic reactions occurred anywhere from 16 minutes into the ED stay to 6 days later

Rohacek M et al. Biphasic Anaphylactic Reactions: Occurrence and Mortality. Eur J All Clin Imm 2014; 69(6): 791 – 7.

  • Retrospective study in Europe of presentations to one hospital from 2001-2013 of n=1334 allergic reactions, n=524 anaphylaxis reactions
  • 2.3% (n=12) met criteria for clinically important biphasic reactions

Additional FOAM on the topic: The SGEM

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 27 ; Rosen’s 8(e) Chapter 119 but, the point isn’t to just take our word for it. Go enrich your fundamental understanding yourself!

Anaphylaxis

Diagnosis –

Two or more systems involved after likely allergen exposure (within hours):

  • Skin – generalized hives, itch-flush, swollen lips-tongue-uvula
  • Pulmonary – dyspnea, wheezing, bronchospasm, stridor
  • Cardiovascular -hypotension or associated symptoms (syncope, incontinence)
  • Gastrointestinal symptoms- crampy abdominal pain, vomiting

Hypotension after exposure to known allergen for that patient (minutes to several hours)also qualifies

Differential Diagnosis -vasovagal (most common mimicker), myocardial ischemia, status asthmaticus, epiglottitis, angioedema, foreign body, carcinoid, vocal cord dysfunction, drug reactions, psychogenic

Treatment –

Epinephrine. Commit the dose to memory and look up if, needed as this is a huge source of medication errors [Gaeta et al, Benklefat ].

  • Adults: 0.3mg, Pediatrics 0.01mg/kg of 1:1000 epinephrine intramuscular (IM) to lateral thigh (pediatric patients >30kg get the adult dose).
  • If repeated doses of IM epinephrine required and patient continues to remain hypotensive, start intravenous epinephrine. ALiEM’s post on making the dirty epi drip.

Adjuncts:

  • IV fluids for blood pressure/shock
  • Corticosteroids may help prevent recurrence although they take 4-6 hours to work, so are unhelpful in acute attacks [Choo et al]. Rosen recommends either prednisone 0.5-1mg/kg orally or methylprednisolone 80-125 mg IV. (You don’t have to give IV in all cases)
  • Histamine blockers (H1 and H2 such as diphenhydramine and famotidine, respectively) may help with the dermatologic symptoms and pruritis.
  • Glucagon in patients that aren’t responding or are on beta-blockers. ALiEM post.
  • Give patients that are going home a prescription for an EpiPen (for pediatric patients, have one parent go fill the script during the observation period) and show them how to use the autoinjector. These things are expensive and do expire, and there are some coupons out there to help out.

Disposition – Clearly patients with ongoing symptoms and/or shock should stay in the hospital. However, most patients can be discharged home once they are improved and the effects of the epinephrine have worn off. Tintinalli recommends about 4 hours, referencing a study by Brady et al from 2007. Interestingly, in this study there were 2 biphasic reactions that occurred at 20 hours and 46 hours after the initial ED visit. So, not sure how they came up with 4 hours.

FOAM Pearls Supported by the Literature and Rosenalli –

Iodine Allergy is not a thing.

Shellfish allergy does NOT put a patient at increased risk of contrast allergy more than any other allergen [Kaufman et al].

Cross-reactivity between penicillin and cephalosporins is often quoted at 10-20% but, in reality, is far less and a review demonstrates cross reactivity of 1% in patients reporting a penicillin allergy [Campagna et al]. Rosen’s agrees with this assessment and states that the overall cross reactivity is minimal. ALiEM post on this myth

ACE-Inhibitor Induced Angioedema

Cause: The vasodilation and non-pitting edema of the mucosal, dermal, and subcutaneous tissues thought to be mediated by the build up of bradykinin and substance P. Non-allergic, often asymmetric.

Presentation: Swelling of the lips, tongue, airway most often although it can also involve the genitals and viscera.

Treatment:

  • Stop the ACE-Inhibitor.
  • Active, anticipatory airway management. Perhaps, even an awake airway (The EMCrit Way, The Strayer Way).
  • Epinephrine, corticosteroids, and histamine blockers do not work. While fresh frozen plasma may work for hereditary angioedema, but it doesn’t really work in ACE-inhibitor angioedema and there’s no proven therapy [Winters et al].
  • Investigations underway for icatibant (bradykinin 2 receptor antagonist) Bas et al, Schmidt et al and Ecallantide (reversible kallikrein inhibitor)

Question 1. A 55-year old man who is taking several antihypertensive medications presents to the ED with nausea, vomiting, shortness of breath, and a rash after eating a home-cooked Thai meal at a friend’s house about 1 hour ago. The symptoms began within seconds of the first bite of his meal. Despite the patient being administered 2 doses of intramuscular epinephrine, diphenhydramine, dexamethasone, and crystalloid fluids, his blood pressure remains at 75/38 mm Hg.Which other medication should be considered in this patient?

  • A. Cimetidine
  • B. Glucagon
  • C. Norepinephrine
  • D. Octreotide

Question 2. A 55-year-old woman presents to the ED for swelling of her tongue and lips.

Photo: Rosh Review
Photo: Rosh Review

She recently started a new antihypertensive medication. Which of the following is the direct mediator for her condition?

  • A. Angiotensin
  • B. Bradykinin
  • C. C1-esterase inhibitor
  • D. Histamine

Answers.

1. B. The patient is experiencing an acute anaphylactic reaction, most likely to peanuts that are commonly found in Thai cooking. Although uncommon, patients taking beta-blocking agents for hypertension may exhibit refractory hypotension despite being administered fluids and epinephrine. This is because epinephrine acts by binding to adrenergic receptors, which includes beta-receptors. To circumvent the beta-receptor, glucagon can be administered, which will bypass the beta-adrenergic second messenger system, potentiate the circulating epinephrine, and help restore vasomotor tone.

Cimetidine (A) is an antihistamine. Although it may help in mild allergic reactions, it will not treat hypotension in severe anaphylaxis. In addition, cimetidine prolongs the metabolism of beta-blockers. Octreotide (D) may be used in management of esophageal variceal bleeding control, treatment of carcinoid syndrome, and refractory hypoglycemia after sulfonylurea-induced hypoglycemia. There is no role in anaphylaxis. Norepinephrine (C) also binds adrenergic receptors that may be inhibited in patients who take beta-blocking medications.
2. B. Angioedema is the clinical manifestation of transient, localized, nonpitting swelling of the subcutaneous layer of the skin or submucosal layer of the respiratory or gastrointestinal tracts. There are many cases of angioedema, but the condition is usually divided into hereditary, acquired, and drug-induced causes. Hereditary angioedema (HAE) is caused by deficiency or dysfunction of C1-esterase inhibitor and is usually precipitated by stress or trauma. Acquired angioedema is also due to deficiency or dysfunction of C1-esterase inhibitor, but is not due to a genetic cause; rather, it appears later in life. The exact etiology is unknown, but the condition is exceedingly rare. The most common cause of drug-induced angioedema is due to an adverse reaction from ACE inhibitors. When ACE is inhibited by medications, angiotensin I is not converted to angiotensin II, and bradykinin is not metabolized. It is thought that the increased level of bradykinin is responsible for angioedema induced by ACE inhibitors. Angioedema can result in severe airway compromise or, less commonly, compromise in the GI tract that is associated with abdominal pain. Evaluation should focus on ruling out laryngeal edema and airway compromise. Although direct visualization is best, asking the patient to phonate a high-pitched “E” is one quick way of assessing for laryngeal edema. If the patient is able to phonate a high-pitched “E,” then the presence of laryngeal edema is unlikely. Treatment is mainly supportive with special attention to airway protection. Angioedema caused by deficiency or dysfunction of C1-esterase inhibitor can be treated by replacing C1-esterase inhibitor with fresh frozen plasma or other recombinant agents.

Angiotensin (A) is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs (ACE inhibitors) that lower blood pressure. An elevated level of angiotensin is not responsible for angioedema. C1-esterase inhibitor (C) serves as the main regulator of the kallikrein-kinin system. As a result of decreased amounts of functional C1-INH, when the kallikrein-kinin system is activated, it is not kept in check. This leads to increased formation of bradykinin and the resultant increased vascular permeability and edema formation and is the cause of hereditary angioedema, not ACE-inhibitor induced angioedema. Histamine (D) has many roles in the body, but its primary role is within the immune system. Mast cells release histamine through a process known as degranulation when they have been sensitized with IgE antibodies and then come in contact with an appropriate antigen leading to the development of urticaria and pruritus.

 

Episode 12 – Back to Biphasics

(iTunes or listen here)

The Free Open Access Medical education (FOAM)

We review Episode 1 of Dr. Salim Rezaie’s REBEL Cast covering exposing the dogma behind biphasic anaphylaxis reactions.

Traditionally, we’re taught to observe patients in the Emergency Department (ED) for 4-6 hours to watch out for biphasic reactions, as the rate of biphasic reactions can approach 20%.

Grunau BE et al. Incidence of Clinically Important Biphasic Reactions in Emergency Department Patients with Allergic Reactions or Anaphylaxis. Ann of EM 2014; 63(6): 736 – 44.

  • Retrospective chart review of 430,000 visits
  • Anaphylaxis n=496 (2 had biphasic reactions, Allergic reactions n=2323 (3 had biphasic reactions)
  • No deaths, biphasic reactions occurred anywhere from 16 minutes into the ED stay to 6 days later

Rohacek M et al. Biphasic Anaphylactic Reactions: Occurrence and Mortality. Eur J All Clin Imm 2014; 69(6): 791 – 7.

  • Retrospective study in Europe of presentations to one hospital from 2001-2013 of n=1334 allergic reactions, n=524 anaphylaxis reactions
  • 2.3% (n=12) met criteria for clinically important biphasic reactions

Additional FOAM on the topic: The SGEM

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 27 ; Rosen’s 8(e) Chapter 119 but, the point isn’t to just take our word for it. Go enrich your fundamental understanding yourself!

Anaphylaxis

Diagnosis –

Two or more systems involved after likely allergen exposure (within hours):

  • Skin – generalized hives, itch-flush, swollen lips-tongue-uvula
  • Pulmonary – dyspnea, wheezing, bronchospasm, stridor
  • Cardiovascular -hypotension or associated symptoms (syncope, incontinence)
  • Gastrointestinal symptoms- crampy abdominal pain, vomiting

Hypotension after exposure to known allergen for that patient (minutes to several hours)also qualifies

Differential Diagnosis -vasovagal (most common mimicker), myocardial ischemia, status asthmaticus, epiglottitis, angioedema, foreign body, carcinoid, vocal cord dysfunction, drug reactions, psychogenic

Treatment –

Epinephrine. Commit the dose to memory and look up if, needed as this is a huge source of medication errors [Gaeta et al, Benklefat ].

  • Adults: 0.3mg, Pediatrics 0.01mg/kg of 1:1000 epinephrine intramuscular (IM) to lateral thigh (pediatric patients >30kg get the adult dose).
  • If repeated doses of IM epinephrine required and patient continues to remain hypotensive, start intravenous epinephrine. ALiEM’s post on making the dirty epi drip.

Adjuncts:

  • IV fluids for blood pressure/shock
  • Corticosteroids may help prevent recurrence although they take 4-6 hours to work, so are unhelpful in acute attacks [Choo et al]. Rosen recommends either prednisone 0.5-1mg/kg orally or methylprednisolone 80-125 mg IV. (You don’t have to give IV in all cases)
  • Histamine blockers (H1 and H2 such as diphenhydramine and famotidine, respectively) may help with the dermatologic symptoms and pruritis.
  • Glucagon in patients that aren’t responding or are on beta-blockers. ALiEM post.
  • Give patients that are going home a prescription for an EpiPen (for pediatric patients, have one parent go fill the script during the observation period) and show them how to use the autoinjector. These things are expensive and do expire, and there are some coupons out there to help out.

Disposition – Clearly patients with ongoing symptoms and/or shock should stay in the hospital. However, most patients can be discharged home once they are improved and the effects of the epinephrine have worn off. Tintinalli recommends about 4 hours, referencing a study by Brady et al from 2007. Interestingly, in this study there were 2 biphasic reactions that occurred at 20 hours and 46 hours after the initial ED visit. So, not sure how they came up with 4 hours.

FOAM Pearls Supported by the Literature and Rosenalli –

Iodine Allergy is not a thing.

Shellfish allergy does NOT put a patient at increased risk of contrast allergy more than any other allergen [Kaufman et al].

Cross-reactivity between penicillin and cephalosporins is often quoted at 10-20% but, in reality, is far less and a review demonstrates cross reactivity of 1% in patients reporting a penicillin allergy [Campagna et al]. Rosen’s agrees with this assessment and states that the overall cross reactivity is minimal. ALiEM post on this myth

ACE-Inhibitor Induced Angioedema

Cause: The vasodilation and non-pitting edema of the mucosal, dermal, and subcutaneous tissues thought to be mediated by the build up of bradykinin and substance P. Non-allergic, often asymmetric.

Presentation: Swelling of the lips, tongue, airway most often although it can also involve the genitals and viscera.

Treatment:

  • Stop the ACE-Inhibitor.
  • Active, anticipatory airway management. Perhaps, even an awake airway (The EMCrit Way, The Strayer Way).
  • Epinephrine, corticosteroids, and histamine blockers do not work. While fresh frozen plasma may work for hereditary angioedema, but it doesn’t really work in ACE-inhibitor angioedema and there’s no proven therapy [Winters et al].
  • Investigations underway for icatibant (bradykinin 2 receptor antagonist) Bas et al, Schmidt et al and Ecallantide (reversible kallikrein inhibitor)

Question 1. A 55-year old man who is taking several antihypertensive medications presents to the ED with nausea, vomiting, shortness of breath, and a rash after eating a home-cooked Thai meal at a friend’s house about 1 hour ago. The symptoms began within seconds of the first bite of his meal. Despite the patient being administered 2 doses of intramuscular epinephrine, diphenhydramine, dexamethasone, and crystalloid fluids, his blood pressure remains at 75/38 mm Hg.Which other medication should be considered in this patient?

  • A. Cimetidine
  • B. Glucagon
  • C. Norepinephrine
  • D. Octreotide

Question 2. A 55-year-old woman presents to the ED for swelling of her tongue and lips.

Photo: Rosh Review
Photo: Rosh Review

She recently started a new antihypertensive medication. Which of the following is the direct mediator for her condition?

  • A. Angiotensin
  • B. Bradykinin
  • C. C1-esterase inhibitor
  • D. Histamine

Answers.

1. B. The patient is experiencing an acute anaphylactic reaction, most likely to peanuts that are commonly found in Thai cooking. Although uncommon, patients taking beta-blocking agents for hypertension may exhibit refractory hypotension despite being administered fluids and epinephrine. This is because epinephrine acts by binding to adrenergic receptors, which includes beta-receptors. To circumvent the beta-receptor, glucagon can be administered, which will bypass the beta-adrenergic second messenger system, potentiate the circulating epinephrine, and help restore vasomotor tone.

Cimetidine (A) is an antihistamine. Although it may help in mild allergic reactions, it will not treat hypotension in severe anaphylaxis. In addition, cimetidine prolongs the metabolism of beta-blockers. Octreotide (D) may be used in management of esophageal variceal bleeding control, treatment of carcinoid syndrome, and refractory hypoglycemia after sulfonylurea-induced hypoglycemia. There is no role in anaphylaxis. Norepinephrine (C) also binds adrenergic receptors that may be inhibited in patients who take beta-blocking medications.
2. B. Angioedema is the clinical manifestation of transient, localized, nonpitting swelling of the subcutaneous layer of the skin or submucosal layer of the respiratory or gastrointestinal tracts. There are many cases of angioedema, but the condition is usually divided into hereditary, acquired, and drug-induced causes. Hereditary angioedema (HAE) is caused by deficiency or dysfunction of C1-esterase inhibitor and is usually precipitated by stress or trauma. Acquired angioedema is also due to deficiency or dysfunction of C1-esterase inhibitor, but is not due to a genetic cause; rather, it appears later in life. The exact etiology is unknown, but the condition is exceedingly rare. The most common cause of drug-induced angioedema is due to an adverse reaction from ACE inhibitors. When ACE is inhibited by medications, angiotensin I is not converted to angiotensin II, and bradykinin is not metabolized. It is thought that the increased level of bradykinin is responsible for angioedema induced by ACE inhibitors. Angioedema can result in severe airway compromise or, less commonly, compromise in the GI tract that is associated with abdominal pain. Evaluation should focus on ruling out laryngeal edema and airway compromise. Although direct visualization is best, asking the patient to phonate a high-pitched “E” is one quick way of assessing for laryngeal edema. If the patient is able to phonate a high-pitched “E,” then the presence of laryngeal edema is unlikely. Treatment is mainly supportive with special attention to airway protection. Angioedema caused by deficiency or dysfunction of C1-esterase inhibitor can be treated by replacing C1-esterase inhibitor with fresh frozen plasma or other recombinant agents.

Angiotensin (A) is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs (ACE inhibitors) that lower blood pressure. An elevated level of angiotensin is not responsible for angioedema. C1-esterase inhibitor (C) serves as the main regulator of the kallikrein-kinin system. As a result of decreased amounts of functional C1-INH, when the kallikrein-kinin system is activated, it is not kept in check. This leads to increased formation of bradykinin and the resultant increased vascular permeability and edema formation and is the cause of hereditary angioedema, not ACE-inhibitor induced angioedema. Histamine (D) has many roles in the body, but its primary role is within the immune system. Mast cells release histamine through a process known as degranulation when they have been sensitized with IgE antibodies and then come in contact with an appropriate antigen leading to the development of urticaria and pruritus.

 

Episode 11 – Ebola and Transmission Precaution Pearls

Episode 11 (iTunes or listen here)

The Free Open Access Medical education (FOAM)

We review Mount Sinai Emergency Medicine Residency’s blog post on Ebola. The Pearls:

  • Signs and symptoms of ebola: Fever (>101.5F, 41C), severe HA, myalgias, vomiting, abdominal pain, unexplained hemorrhage, hypotension plus an epidemiologic risk factor in the past 3 weeks.
  • Risk factors:  contact with blood or other body fluids of a patient known or suspected to have ebola, residence or travel to endemic areas, and direct handling of bats, rodents, or primates from disease endemic areas.
  • CDC recommends screening in those with :
    • percutaneous/mucous membrane exposure or direct skin contact with body fluids of a person with a confirmed or suspected case of ebola without appropriate personal protective equipment
    • laboratory processing of body fluids of suspected or confirmed ebola cases without appropriate PPE or standard biosafety precautions
    • participation in funeral rites or other direct exposure to human remains in the geographic area where the outbreak is occurring without appropriate personal protective equipment.
  • Personal protective equipment is key in prevention of ebola spread.  Ebola is not airborne but due to the case mortality rate, fear, and questionable history of aerosol transmission in the past, we treat it like it is.  Recommended protection in the United States:  fluid impermeable gown, N95 respirator, eye shield and in situations with large amounts of fluids -double gloving, disposable shoe covers, and leg coverings (CDC recommendations).

Check out the CDC website on Ebola

EMDocs post on Ebola

EMCRIT Ebola algorithm

 

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapters 157, 148  but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself! Airborne Precautions – used for patients known to be or suspected of being infected with organisms transmitted by airborne droplets and small particle residue (<5 micrometers) of evaporated droplets containing microorganisms that can be spread by air currents.

  • Require special, negative pressure rooms with special ventilation and filtration and the N95 respirators.
  • Limited movement of patient within the health care setting and in the ED they need to be in a room with the door closed.
  • Recommended for: Measles, Varicella, Tuberculosis

Droplet Precautions – used for patients known to have or suspected of having serious illnesses transmitted by large particle droplets (>5 micrometers) produced by the patient during talking, sneezing, or coughing or during procedures.

  • Use a mask and wash your hands.  N95 respirator recommended for procedures like bronchoscopy, suctioning, etc.
  • Non Sterile gown if one anticipates substantial contact with the patient or if the patient is incontinent or has wound drainage not contained by dressings.
  • Limit transportation and movement of the patient – they should wear a mask when transported throughout the hospital.
  • Recommended for: Serious infections, Pertussis, Parvovirus B19, Mumps, Rubella

Varicella – Herpes virus that causes chickenpox (primary infection) and a secondary reactivation (herpes zoster/shingles) as the virus may lie latent in dorsal root ganglia.

  • Use Airborne precautions as it’s spread via respiratory secretions but may also spread (although less infectious) from the fluid of the non-crusted vesicles.
  • Symptoms of chickenpox: fever, malaise, headache and a vesicular rash that appears in crops with lesions at varying stages, including papules, vesicles, and crusted lesions, predominantly on the torso and face.
  • Most infections are minor and self-limited but increased sequelae exist in the immunocompromised and elderly.  These subgroups may benefit from antivirals
  • Immunizations now prevalent although individuals can still get mild chickenpox after immunization.
  • Varicella-zoster immune globulin exists but use as postexposure prophylaxis is essentially limited to non-immune pregnant women and the severely immunosuppressed. Healthy non-immunue individuals can be vaccinated after exposure and, if they are high risk and develop symptoms, they can get antivirals.

Generously Donated Rosh Review Questions

Question 1. [polldaddy poll=8241932]

Question 2.  A 3-year-old boy presents to the ED with 3 days of fever, cough, and runny nose. On exam, you note conjunctival injection and an erythematous, nonblanching, nonvesicular, maculopapular rash behind his ears and on his hairline, with a few spots on his chest. [polldaddy poll=8241939]

References:

“Safe Management of Patients with Ebola Virus Disease (EVD) in U.S. Hospitals.”  CDC.  August 6, 2014

Cline DM.  “Chapter 157. Occupational Exposures, Infection Control, and Standard Precautions”  Tintinalli’s Emergency Medicine:  A Comprehensive Study Guide (2011).

Answers

1. Chickenpox is a highly contagious but generally benign and self-limited viral disease caused by the varicella-zoster virus (also known as human herpesvirus 3). The disease is characterized by the sudden onset of fever, malaise, and a pustular maculopapular rash that can occur anywhere on the skin or mucus membranes. The lesions then become vesiculated followed by scabbing over the course of 3-4 days before resolving. Skin lesions appear in crops with multiple lesions of various stages appearing on the skin at the same time. Uncomplicated infection is generally treated with supportive measures, including antipyretic, antipruritic, and pain control medications. Antivirals such as acyclovir, valacyclovir, and foscarnet may also be initiated in severe disease or immunosuppressed individuals. Parents should be cautioned to avoid giving their children aspirin or aspirin containing medications due to the risk of developing Reye’s syndrome.

The lesions of chickenpox appear suddenly rather than gradually (A). Smallpox lesions may appear similar to chickenpox lesions, however they are found in the same stage (B) of development. Rubella (German measles) is associated with the sudden onset of a maculopapular rash that first appears on the face then rapidly spreads inferiorly to the neck, trunk, and extremities and fades by the 3rd day (C).

2. Rubeola, or measles, is associated with fever and rash with cough, conjunctivitis, coryza, and Koplik spots. The characteristic rash is erythematous, nonblanching, and maculopapular. It begins on the head, usually behind the ears and around the hairline, with subsequent spread down the face, to the trunk, and extremities (centrifugal spread). The rash may coalesce into salmon-colored patches and typically disappears within 1 week. Koplik spots or pinpoint-sized white lesions on a red background that appear on the buccal mucosa opposite the molars are pathognomonic.

Roseola (A) is a viral infection with the onset of a rash that occurs upon resolution of a high fever. It is common in ages 6–18 months. Rubella (B) is often referred to as “three-day measles.” It is a mild illness, except for congenital infection, which can cause major birth defects. It is associated with fever, rash, and prominent lymphadenopathy, with tender posterior auricular, cervical, and occipital nodes. Varicella (D) (chicken pox) is associated with a flu-like illness and the formation of macules that progress to fluid-filled vesicles in an erythematous base (“dew drops on a rose petal”). Crops of lesions typically appear at the same time with vesicles in various stages of healing.

Episode 11 – Ebola and Transmission Precaution Pearls

Episode 11 (iTunes or listen here)

The Free Open Access Medical education (FOAM)

We review Mount Sinai Emergency Medicine Residency’s blog post on Ebola. The Pearls:

  • Signs and symptoms of ebola: Fever (>101.5F, 41C), severe HA, myalgias, vomiting, abdominal pain, unexplained hemorrhage, hypotension plus an epidemiologic risk factor in the past 3 weeks.
  • Risk factors:  contact with blood or other body fluids of a patient known or suspected to have ebola, residence or travel to endemic areas, and direct handling of bats, rodents, or primates from disease endemic areas.
  • CDC recommends screening in those with :
    • percutaneous/mucous membrane exposure or direct skin contact with body fluids of a person with a confirmed or suspected case of ebola without appropriate personal protective equipment
    • laboratory processing of body fluids of suspected or confirmed ebola cases without appropriate PPE or standard biosafety precautions
    • participation in funeral rites or other direct exposure to human remains in the geographic area where the outbreak is occurring without appropriate personal protective equipment.
  • Personal protective equipment is key in prevention of ebola spread.  Ebola is not airborne but due to the case mortality rate, fear, and questionable history of aerosol transmission in the past, we treat it like it is.  Recommended protection in the United States:  fluid impermeable gown, N95 respirator, eye shield and in situations with large amounts of fluids -double gloving, disposable shoe covers, and leg coverings (CDC recommendations).

Check out the CDC website on Ebola

EMDocs post on Ebola

EMCRIT Ebola algorithm

 

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapters 157, 148  but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself! Airborne Precautions – used for patients known to be or suspected of being infected with organisms transmitted by airborne droplets and small particle residue (<5 micrometers) of evaporated droplets containing microorganisms that can be spread by air currents.

  • Require special, negative pressure rooms with special ventilation and filtration and the N95 respirators.
  • Limited movement of patient within the health care setting and in the ED they need to be in a room with the door closed.
  • Recommended for: Measles, Varicella, Tuberculosis

Droplet Precautions – used for patients known to have or suspected of having serious illnesses transmitted by large particle droplets (>5 micrometers) produced by the patient during talking, sneezing, or coughing or during procedures.

  • Use a mask and wash your hands.  N95 respirator recommended for procedures like bronchoscopy, suctioning, etc.
  • Non Sterile gown if one anticipates substantial contact with the patient or if the patient is incontinent or has wound drainage not contained by dressings.
  • Limit transportation and movement of the patient – they should wear a mask when transported throughout the hospital.
  • Recommended for: Serious infections, Pertussis, Parvovirus B19, Mumps, Rubella

Varicella – Herpes virus that causes chickenpox (primary infection) and a secondary reactivation (herpes zoster/shingles) as the virus may lie latent in dorsal root ganglia.

  • Use Airborne precautions as it’s spread via respiratory secretions but may also spread (although less infectious) from the fluid of the non-crusted vesicles.
  • Symptoms of chickenpox: fever, malaise, headache and a vesicular rash that appears in crops with lesions at varying stages, including papules, vesicles, and crusted lesions, predominantly on the torso and face.
  • Most infections are minor and self-limited but increased sequelae exist in the immunocompromised and elderly.  These subgroups may benefit from antivirals
  • Immunizations now prevalent although individuals can still get mild chickenpox after immunization.
  • Varicella-zoster immune globulin exists but use as postexposure prophylaxis is essentially limited to non-immune pregnant women and the severely immunosuppressed. Healthy non-immunue individuals can be vaccinated after exposure and, if they are high risk and develop symptoms, they can get antivirals.

Generously Donated Rosh Review Questions

Question 1. [polldaddy poll=8241932]

Question 2.  A 3-year-old boy presents to the ED with 3 days of fever, cough, and runny nose. On exam, you note conjunctival injection and an erythematous, nonblanching, nonvesicular, maculopapular rash behind his ears and on his hairline, with a few spots on his chest. [polldaddy poll=8241939]

References:

“Safe Management of Patients with Ebola Virus Disease (EVD) in U.S. Hospitals.”  CDC.  August 6, 2014

Cline DM.  “Chapter 157. Occupational Exposures, Infection Control, and Standard Precautions”  Tintinalli’s Emergency Medicine:  A Comprehensive Study Guide (2011).

Answers

1. Chickenpox is a highly contagious but generally benign and self-limited viral disease caused by the varicella-zoster virus (also known as human herpesvirus 3). The disease is characterized by the sudden onset of fever, malaise, and a pustular maculopapular rash that can occur anywhere on the skin or mucus membranes. The lesions then become vesiculated followed by scabbing over the course of 3-4 days before resolving. Skin lesions appear in crops with multiple lesions of various stages appearing on the skin at the same time. Uncomplicated infection is generally treated with supportive measures, including antipyretic, antipruritic, and pain control medications. Antivirals such as acyclovir, valacyclovir, and foscarnet may also be initiated in severe disease or immunosuppressed individuals. Parents should be cautioned to avoid giving their children aspirin or aspirin containing medications due to the risk of developing Reye’s syndrome.

The lesions of chickenpox appear suddenly rather than gradually (A). Smallpox lesions may appear similar to chickenpox lesions, however they are found in the same stage (B) of development. Rubella (German measles) is associated with the sudden onset of a maculopapular rash that first appears on the face then rapidly spreads inferiorly to the neck, trunk, and extremities and fades by the 3rd day (C).

2. Rubeola, or measles, is associated with fever and rash with cough, conjunctivitis, coryza, and Koplik spots. The characteristic rash is erythematous, nonblanching, and maculopapular. It begins on the head, usually behind the ears and around the hairline, with subsequent spread down the face, to the trunk, and extremities (centrifugal spread). The rash may coalesce into salmon-colored patches and typically disappears within 1 week. Koplik spots or pinpoint-sized white lesions on a red background that appear on the buccal mucosa opposite the molars are pathognomonic.

Roseola (A) is a viral infection with the onset of a rash that occurs upon resolution of a high fever. It is common in ages 6–18 months. Rubella (B) is often referred to as “three-day measles.” It is a mild illness, except for congenital infection, which can cause major birth defects. It is associated with fever, rash, and prominent lymphadenopathy, with tender posterior auricular, cervical, and occipital nodes. Varicella (D) (chicken pox) is associated with a flu-like illness and the formation of macules that progress to fluid-filled vesicles in an erythematous base (“dew drops on a rose petal”). Crops of lesions typically appear at the same time with vesicles in various stages of healing.

Episode 10 – Pediatric GI Emergencies

Episode 10 (iTunes or listen here)

The Free Open Access Medical education (FOAM)

We review Dr. Natalie May’s brilliant post on the St. Emlyn’s blog, “When Sick Means Sick: Emesemantics and Vomiting in Kids”  in which she dissects emesis descriptors such as bilious, projectile, and coffee-ground.

The Pearls:

  • Ask for color descriptors or look at the emesis yourself rather rely on typical descriptors of emesis.
  • Bilious vomiting, medical speaking, means emesis that appears like cooked, green spinach – not the yellow color that parents often mean. While sometimes normal in older children with gastroenteritis, in neonates or anyone sick appearing, this represents a surgical emergency such as volvulus, malrotation, necrotizing enterocolitis etc.
Photo: Laurent Nguyen, Wikimedia Commons
Photo: Laurent Nguyen, Wikimedia Commons
  • Projectile vomiting – Most vomit is projected at least a short distance, so parents may say even reflux is projectile.  Observe a test feed to gauge whether a baby is vomiting or has true projectile vomiting which may represent idiopathic hypertrophic pyloric stenosis.
  • Coffee ground emesis – this is a blackish-brown gritty emesis but parents may mean any brown-ish vomit.  This is typically indicative of upper GI bleed, which is pretty rare in pediatric patients.

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapters 111,124; Rosen’s 8(e) Chapter 172 but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Neonatal Jaundice

Physiologic Jaundice – Jaundice in healthy, full-term newborns typically develops during the 2nd – 3rd day of life and resolves by the 5th or 6th day.  This occurs a little later in Asian and premature infants.

  • Mean peak total serum bilirubin is 6 mg/dL
  • Use the nomogram in infants >35 weeks gestational age to determine need for phototherapy

Non-physiologic Jaundice – bad.

  • Jaundice in the first 24 hours
  • Bilirubin rising faster than 5 mg/dL in 24 hours •Clinical jaundice >1 week
  • Direct bilirubin >2 mg/dL
  • In healthy term infants total serum bilirubin concentration >15 mg/dL (so remember: average of 6 but more than 15 is bad. But check out the nomogram in non-preemies).

Indirect Neonatal Jaundice – 3 main causes, listed below. Treatment is with phototherapy and mitigation of underlying causes.

  • Increased lysis – this can be due to lysis of red blood cells or sequestration of blood – ABO incompatibility, splenic sequestration, spherocytosis.
  • Decreased hepatic uptake/decreased conjugation – Immature transfer enzymes (babies grow out of this), breastmilk jaundice (lack certain enzymes, idiopathic hypertrophic pyloric stenosis (unclear why), as well as Gilberts, Crigler Najjar Syndrome
  • Increased enterohepatic uptake (i.e. too much reclaimed from the gut) – obstruction or breastfeeding jaundice (dehydrated babies who are breast feeding).

Direct Bilirubinemia

  • Etiology – biliary tree obstruction or biliary atresia, enzyme deficiencies (cystic fibrosis, alpha-1 antitrypsin deficiency, glycogen storage diseases)
  • Conjugated bilirubin is non-toxic so treat the underlying cause

Emergency Department Diagnostics:

  • Total and Fractionated Bilirubin,  Blood Type with Rh factor, Coomb’s test, blood count, Reticulocyte count, consider sepsis work-up .

More FOAM

Intussusception

Presentation: Abdominal pain, vomiting, bloody or guaiac positive stool.  The classic triad is not useful and present in 15-20%.  While intussusception is most common at approximately 1 year of age and, moreover 2 months -6 years, it can present at any time, including the elderly.

Etiology:  The bowel telescopes on itself and

Diagnosis:  Clinical, ultrasound (target sign), or diagnostic and therapeutic air contrast enema. It’s also reasonable to get plain films, if desired.

Treatment:  Air contrast enema in radiology results in approximately 60% success so most recommend a surgery consult in the event there’s a complication or failure in radiology.  Also, give these patients 20cc/kg fluid bolus and treat their pain.

More FOAM:

Generously donated Rosh Review questions (scroll for answers)

Question 1. A 10-month-old previously healthy boy presents with 1 day of bilious vomiting and fever. The patient is ill-appearing. Physical examination reveals a distended and diffusely tender abdomen with guarding and rebound. [polldaddy poll=8224476]

Question 2. A 2-year-old ex-33 week premature girl presents with vomiting, diarrhea and poor feeding. The patient has episodes of fussiness and inconsolable crying followed by periods of lethargy and sleeping. During periods of fussiness, the patient draws her legs up to her chest. [polldaddy poll=8225869]

Also, check out “Ketamine, The Album” – A musical written by and for emergency physicians as a tribute to ketamine

 

Answers.

1.Correct Answer ( A ) This patient presents with signs and symptoms concerning for an obstruction secondary to a volvulus and requires emergent surgical evaluation. Malrotation is a relatively common occurrence (1 in 500 live births) and about 75% of patients with malrotation will develop volvulus. During embryonic development, rotation of the gut arrests. This allows for the small bowel to twist around the superior mesenteric artery causing an acute obstruction. Patients will present with sudden onset of abdominal distension and bilious emesis. These infants will be ill-appearing and possibly toxic on presentation. Although a number of diagnostic modalities can be employed for definitive diagnosis, the priority in an ill-appearing infant with bilious emesis is emergent surgical consultation. All other interventions risk delaying definitive management. While waiting for the surgical consultation, the patient should have an IV placed, fluid resuscitation begun and a nasogastric tube placed for decompression of the stomach. Additionally, broad spectrum antibiotics should be administered. After consultation, an upper GI series may be obtained for definitive diagnosis.

Stool cultures (B) are useful when there is a suspicion for infectious process such as a parasitic or bacterial infection. Laboratory studies (C) will provide limited data and should not delay definitive management by a surgeon. The patient should receive intravenous hydration, not oral rehydration (D) as there is a high likelihood that this patient will be taken to the operating room. As such, the patient should be kept NPO.

2. D.  This patient presents with symptoms concerning for intussusception and should have an emergent ultrasound performed to make the diagnosis. Intussusception is defined as the telescoping of one segment of the intestine into another. It is the most common cause of obstruction in children younger than 2 years of age. The classic triadof intussusception is abdominal pain, vomiting and bloody stools but all three features are only present in about 33% of patients. Bowel movements may be loose with mucous and blood and appear like “currant jelly.” Often patients will have cycles of severe abdominal pain lasting 10 to 15 minutes during which they are inconsolable. These episodes are followed by periods of painlessness during which the child may be lethargic. Palpation of the abdomen may reveal a sausage-like mass in the right upper quadrant representing the actual intussusception. The lead point for the telescoping may be due to Henoch-Schonlein purpura vasculitis, Meckel’s divericulum, lymphoma or polyps in children over 5 years of age. In younger children, enlarge Peyer’s patches may be the culprit. These occur after viral infections. Ultrasound of the abdomen is the best initial modality for identifying the intussusception. It may reveal the classic findings of a target sign or “pseudokidney” sign. Sensitivity and specificity of ultrasound approach 100%.  Abdominal X-ray (A) may show intussusception but may be negative in up to 20% of patients. CT(B) and MRI (C) of the abdomen and pelvis  are also unreliable in the diagnosis.