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 alBenklefat ].

  • 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. 

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. 

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. 

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. 

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.

Episode 9 – Pregnancy Emergencies

Episode 9 (iTunes or listen here)

The Free Open Access Medical education (FOAM)

We review Dr. Scott Weingart’s Practical Evidence Podcast #3 – ACEP 2012 Management of Early Pregnancy, in which he summaries the ACEP 2012 Clinical Policy on this topic.

  • The discriminatory zone is out.  Get ultrasounds in pregnant patients, regardless of the quantitative beta-hCG.
  • A certain beta-hCG level can not be used to rule in or rule out ectopic pregnancy or viable intrauterine pregnancy (IUP), get the ultrasound and ensure you identify the uterus.
  • If an ultrasound (including radiology’s formal ultrasound) is indeterminate for ectopic versus IUP, that patient should have a repeat ultrasound and follow up with OB within 48 hours.

A good FOAM ectopic rule out pathway

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapters 102-105; Rosen’s 8(e) Chapter 178 but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

 Bleeding after the First Trimester

 The two things we worry about the most are placental abruption and placenta previa.

Placental Abruption – premature separation of the placenta from the uterine lining.

  • Classic presentation: painful vaginal bleeding.
  • Actual presentation: 30% do not have vaginal bleeding, uterine pain/tenderness, back pain, hypotension, nausea.
  • Risk factors: hypertension, previous abruption, uterine scar, cocaine, smoking, blunt trauma, older age
  • Diagnosis: Ultrasound, clinical suspicion, MRI. Note – Ultrasound is specific but NOT sensitive.
  • Management: Intravenous access, hemoglobin, type and screen, coagulation panel, resuscitation, ultrasound, likely call OB.

Placenta Previa – implantation of the placenta over the cervical os.

  • Classic presentation: painless vaginal bleeding
  • Diagnosis: Ultrasound
  • Management is the same as for abruption but do NOT do a speculum or cervical exam unless there is no OB service.

Abdominal Pain in Pregnancy

Pregnant women are at risk for the same abdominal emergencies as everyone else – appendicitis, cholecystitis, and pyelonephritis but they’re also at risk for some special pregnancy related issues.

Septic Abortion –  evidence of infection with any type of abortion, often due to unsanitary abortions or retained products of conception

  • Presentation: fever, uterine tenderness at under 20 weeks of gestation
  • Treatment: Ampicillin 3g IV, gentamicin 1-2 mg/kg IV, stat OB consult for source control

Chorioamnionitis – infection or inflammation of the placenta and fetal membranes, often after 16 weeks of gestation

  • Presentation: fever, uterine tenderness, fever/maternal tachycardia, sepsis
  • Risk factors: preterm labor
  • Treatment: Ampicillin 3g IV, gentamicin 1-2 mg/kg IV, stat OB consult for source control

HELLP syndrome – hemolysis, elevated liver enzymes, low platelets.

  • Diagnostics: CBC with schistocytes, Platelets <100,000, Elevated transaminases, Normal or elevated BUN/creatinine, abnormal coagulation profile.  CT abdomen/pelvis if patient hemodynamically stable.
  • Complications: liver hematoma, splenic or liver rupture.
  • Management: Magnesium, control of blood pressure (labetalol, hydralazine), correction of coagulopathy, delivery of the fetus.

Pre-Eclampsia/Eclampsia

New onset hypertension (BP >140/90) after 20 weeks of gestation in a previously normotensive patient plus one of the following: proteinuria or end organ dysfunction (pulmonary edema, renal dysfunction, visual changes, etc). Eclampsia is a sequelae of pre-eclampsia, like HELLP syndrome, characterized by seizures and coma.

  • Control seizures with magnesium
  • Control BP if DBP >105 mmHg
  • Check for organi injury (CBC/platelet count, transaminases, BUN/Creatinine)

Generously donated Rosh Review questions (scroll for answers)

Question 1. A 27-year-old woman 32 weeks pregnant presents with bright-red vaginal bleeding for 1 day. The patient denies any pain and is not tender on abdominal exam. Her vital signs are BP 115/70, HR 90, and RR 16.  

Question 2.  A 26-year-old woman presents with abdominal cramping after a positive home pregnancy test. Her vitals are T 98.7°F, HR 94, BP 110/66, RR 18, oxygen saturation 97%. Her exam is unremarkable. Labs reveal a serum beta HCG of 1000 mIU and she is Rh positive. She states that the pregnancy is wanted. An ultrasound is performed as seen below.

More FOAM on vaginal bleeding:

Answers.

1. A. Placenta previa is characterized by painless, fresh vaginal bleeding in late pregnancy. Placenta previa occurs in 1% of pregnancies and is defined as a placenta that extends near, partially over, or completely over the cervical os. These patients are at an increased risk for life-threatening hemorrhage. As a result, the first step in management of placental previa is to obtain intravenous access in anticipation of fluid resuscitation and possible transfusion. Obstetrical consultation is also advised.

2.  D. This patient presents with abdominal pain and a positive pregnancy test raising the concern for an ectopic pregnancy. Ectopic pregnancy complicates about 1.5 – 2.0% of pregnancies and is potentially life threatening. There are a number of risk factors for ectopic pregnancy including pelvic inflammatory disease, prior tubal surgery and previous ectopic pregnancy. This patient has an early pregnancy based on the low beta hCG. The transvaginal ultrasound shows an early gestational sac without a yolk sac or fetal pole within the uterus. This ultrasound does not rule out the diagnosis of an ectopic pregnancy as an ectopic pregnancy can cause a decidual reaction in the uterus, which appears similar to an early gestational sac. The definitive ultrasound finding for an intrauterine pregnancy would be the presence of a yolk sac or fetal pole. It is expected that above the discriminatory hCG zone of 1500-2500 mIU, a definitive IUP should be identified. Patients with a beta hCG below the discriminatory zone without a definitive IUP can be managed conservatively with repeat hCG level in 48 hours (the level should double every 48 hours) and repeat ultrasound.

Episode 8 – Acid-Base and Hyponatremia

Episode 8 (iTunes or Listen Here)

The Free Open Access Medical education (FOAM)

This week we review Dr. David Story’s talk from SMACC GOLD, “Is Chloride a Poison?”  Dr. Story discusses the Stewart ion approach to acid-base, driven by the independent variable, the Strong Ion Difference (SID), which is the difference between the sums of concentrations of the strong cations and strong ions (typically Sodium and Chloride). He also reviews literature that suggests that there may be morbidity and even mortality associated with large volume infusions of 0.9% NaCl (NS), although more research is required in this arena to determine the patient oriented sequelae. Perhaps we should be using more balanced solutions such as lactated ringers (LR).

Also, SMACC  is awesome, listen to the talks from SMACC GOLD and come meet us in Chicago next June!

Literature on the topic:

Other FOAM Acid-Base Resources:

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapters 19,21; Rosen’s (3e) Chapters 124, 125 …but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

IV Fluids – Know the Composition (PV card from ALiEM)

Red - Too Much, Yellow - Too Little, Green - Just Right

Red – Too Much, Yellow – Too Little, Green – Just Right

Costs – NS (0.9%) is the cheapest, coming in at just over a US dollar per Liter and LR is slightly more expensive (most estimates are approximately $0.50 more per liter).  Plasma-lyte is more expensive, costing several dollars more per liter.

Downsides of Normal Saline (NS, 0.9%)

  • Hypertonic, hypernatremic, hyperchloremic – it has a little too much of everything and is acidic, with a pH of 5.0 [1]
  • The SID (Strong Ion Difference) of NS is 0, far less than the physiologic or normal SID of 38.  This is where the non-anion gap acidosis comes into play [1].

Caution with Lactated Ringers (LR)

  • LR contains calcium and some labs studies have shown that this may cause clotting; thus, major societies say LR is incompatible with blood products.  There are some studies to show that this may not be as big of a deal as previously thought: Albert et alCull et alLorenzo et al.
  • May interfere with Lactate clearance -A study of healthy individuals demonstrated that LR did not affect serum lactate levels [2].  However, often we are doing these large volume resuscitations in the critically ill who may have hepatic insufficiency and, thereby, reduced lactate clearance.  There is worry that LR may increase the serum lactate, making it difficult to gauge resuscitation by lactate clearance.  Paul Marino’s ICU Book states that significant skewing of the lactate is unlikely unless the patient’s ability to hepatically clear lactate is nil and the patient has gotten several liters of LR [1].

FOAM Resources:

Hyponatremia  – Na+ <135 mEq/L

Symptoms: often asymptomatic but may see vague symptoms such as nausea, vomiting, myalgias, lethargy.  Values <120 mEq  more associated with symptoms and <113 mEq, may see seizures/coma.

Causes:

  • Hypovolemic – Extra-renal: dehydration (vomiting, diarrhea, small bowel obstruction, burns), infusion of hypotonic fluids, Renal: thiazide diuretics, Renal Tubular Acidosis, osmotic diuresis, aldosterone/mineralocorticoid deficiency
  • Euvolemic – SIADH (syndrome of inappropriate secretion of antidiuretic hormone), water intoxication, drugs (NSAIDs, APAP, TCAs, sulfonylureas, morphine, carbamazepine, etc), beer potomania
  • Hypervolemic – think organ failure and people who are third spacing fluids. Congestive Heart Failure, Liver Failure, Renal Failure

Other FOAM Hyponatremia Resources:

Generously donated Rosh Review questions (scroll for answers)

Question 1.

Question 2. A 23-year-old woman presents with seizures. The patient received 2 mg of lorazepam by EMS but continues to seize. Serum lab tests show the following: sodium 118, potassium 3.6, chloride 90, bicarbonate 21, BUN/Cr 10/1.0, glucose 89. 

Additional References:

1.Tizard, H.  Chapter 12: Colloid and Crystalloid Resuscitation.  Marino’s The ICU Book, ed 4.Lippincott Williams & Wilkins, 2007.

2.Didwania A, Miller J, Kassel D, Jet al. Effect of intravenous lactated Ringer’s solution infusion on the circulating lactate concentration: Part 3. Results of a prospective, randomized, double-blind, placebo-controlled trial.Crit Care Med. 1997 Nov;25(11):1851-4.

Answers.

1.C -The syndrome of inappropriate secretion of ADH (SIADH) is defined by the secretion of ADH in the absence of an appropriate physiologic stimulus. Its hallmark is an inappropriately concentrated urine, despite the presence of a low serum osmolality and a normal circulating blood volume. Causes of SIADH include central nervous system disorders, pulmonary disease, drugs, stress, pain, and surgery. Therefore, the above patient, with a known history of lung cancer and hyponatremia, most likely has SIADH and exhibits the following lab findings: serum osmolarity low, urine osmolarity high, urine sodium high. Psychogenic polydipsia (D) is a rare cause of euvolemic hyponatremia and is seen in psychiatric patients who consume large amounts of free water (in excess of 1 L/hr). This large consumption overwhelms the kidney’s ability to excrete free water. Patients will exhibit serum osmolarity low, urine osmolarity low, urine sodium low. Diabetes insipidus (B) results in the loss of large amounts of dilute urine from the loss of concentrating ability in the distal nephron. This may be due to a central cause—such as the lack of ADH secretion from the pituitary—or a nephrogenic cause—such as the lack of responsiveness to circulating ADH. Laboratory workup that invariably shows serum osmolarity high, urine osmolarity high, urine sodium low (A) rarely occurs.

2.A-This patient presents with prolonged seizure activity and hyponatremia and should emergently be treated withhypertonic saline. Hyponatremia is defined as a serum sodium level <135 mEq/L and is the second most common electrolyte abnormality after hypokalemia. The symptoms and signs of hyponatremia depend on the patient’s volume status, the cause and the rapidity of the change in serum sodium. Typically, patients with acute changes will have more severe symptoms including nausea, vomiting, confusion, stupor and seizures. Chronic hyponatremia will typically present with mild neurologic symptoms as well as lower serum sodium levels than acute hyponatremia. In patients without neurologic symptoms, volume status should be assessed and additional labs should be sent off to determine the cause of hyponatremia (urine sodium, osmolarity etc.). Patients with neurologic symptoms should be aggressively treated with 3% hypertonic saline. When correcting serum sodium, it is important to increase the serum sodium by no more than 0.5 mEq/L/hour and by no more than 10 – 12 mEq/day. More rapid changes can lead to central pontine myelinolysis, a crippling neurologic disease.

Episode 7 – Heart Failure

Episode 7 (iTunes or Listen Here)

The Free Open Access Medical Education (FOAM)

We review RAGE Podcast Episode 4 that awesomely covers nearly everything under the sun. A few of our favorite pearls:

Impact apnea -people who sustain traumatic brain injury often have associated apnea.  Support their airway because this could lead to arrest. Bystander support is crucial.

Right Ventricular Myocardial Infarction (RVMI)- Think about this in any inferior MI situation. Give fluids, these patients are preload dependent and need the cath lab.

Right Ventricular Heart Failure - OH CRAP.

  • Optimize Oxygenation, Hemodynamics, Contractility, Rate/rhythm, Afterload, and Preload
  • Give fluids, but not too much. Inotropes and vasopressors are often necessary. These guys like milrinone and epinephrine.

The Bread and Butter

We summarize some key topics from the following readings,  Tintinalli (7e) Chapters 53, 57; Rosen’s (8e) Chapters 78, 81…but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

RVMI - often associated with inferior MIs and can carry increased morbidity/mortality.

ECG pearls -

  • look for ST elevation in lead III greater than lead II or lead V1 (especially with ST depression in V2.
  • Right sided leads – elevation in V4R most specific but elevation in V3R-6R are indicative of RVMI.  Keep V1 and V2

Treatment – RVMI is preload dependent so they need fluid.  Too much fluid may cause the RV to impinge on the LV.

Acute Heart Failure (WikEM)

  • Give nitrates, which decrease preload, before diuretics.  Diuretics are only indicated in volume overloaded patients, and many patient simply have fluid shifts and are overall euvolemic or have decreased plasma volume.  Thus, in some patients, diuretics may be harmful.
  • Use non-invasive ventilation
  • BNP.  The boards and ACEP recommend it but randomized clinical trials have not consistently demonstrated a benefit in the Emergency Department (Carpenter et al)

Right vs Left Sided Heart Failure – this distinction is someone artificial as chambers are interdependent in series.

  • Left-sided failure – pulmonary symptoms (dyspnea and orthopnea)
  • Right-sided failure have systemic venous congestion(pedal edema and hepatomegaly)

High Output Failure – conditions with excess cardiac output

  • Causes – increased preload (excess mineralocorticoids, fluid/salt retention), decreased systemic vascular resistance (pregnancy, cirrhosis, severe anemia, beriberi, thyrotoxicosis, Paget’s disease, or vasodilator medications), or tachycardia and persistent beta-adrenergic stimulation.
  • Treatment – correct underlying cause

Generously donated Rosh Review questions (scroll for answers)

Question 1.  

Question 2. A 73-year-old man presents to the ED with progressive shortness of breath for two days without chest pain. The patient has a history of hypertension controlled with hydrochlorothiazide, but has been noncompliant with his medications. In the ED, his vital signs are BP 186/102, HR 108, RR 34, and oxygen saturation 90% on room air. On exam, the patient has pulmonary crackles midway up both lung fields, jugular venous distension, and pitting edema of his lower extremities. A chest X-ray depicts increased interstitial markings and an enlarged cardiac silhouette. An ECG shows sinus tachycardia. 

Question 3.  

References:

O’Brien JF.  Heart Failure.  Rosen’s Emergency Medicine (8e).  Chapter 81, 1075-1090.e7

Hollander JE, Diercks DB.  Chapter 53:  Acute Coronary Syndromes: Acute Myocardial Infarction and Unstable Angina.”Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011. p 367-385

Peacock WF.  Chapter 57: Congestive Heart Failure and Acute Pulmonary Edema. Failure. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011  p 404-414

 

Answers:

Question 1.  D. This patient presents with symptoms of acute decompensated heart failure (ADHF) and should be started on nitroglycerin therapy immediately. Patients with ADHF present with shortness of breath, increased work of breathing, tachycardia, hypoxia, crackles on lung examination and jugular venous distension. These patients experience acute worsening of left ventricular function and output secondary to a number of mechanisms including increased systemic vascular resistance. Therapy focuses on reduction of preload to decrease the flow of blood into the lungs and afterload reduction to increased the effectiveness of the left ventricle. Both of these goals can be accomplished through the administration of nitroglycerin. At lower doses, nitroglycerin acts as a peripheral vasodilator and increases venous capacitance leading to decreased preload. At higher doses, nitroglycerin causes arterial vasodilation leading to decreased afterload. Because of its rapid onset of action, nitroglycerin is the first line medication in patients with ADHF. Furosemide (A) may be useful in patients with volume overload and ADHF but this represents less than half of patients with ADHF. Additionally, the effects are delayed. Heparin (B) can be given in cases of ischemia induced ADHF but will not yield any immediate benefits. Morphine (C) was historically used as a preload reducer but has been associated with increased morbidity in patients with ADHF and is no longer recommended.

Question 2.   A .  This patient is in acute heart failure with pulmonary edema. The clinical presentation of heart failure includes shortness of breath, jugular venous distension, crackles and rales, peripheral edema, S3 gallop, orthopnea, and paroxysmal nocturnal dyspnea. A chest X-ray may show an enlarged cardiac silhouette, Kerley B lines suggesting pulmonary edema, and pulmonary vessel cephalization. Labs may show an elevated plasma brain natiuretic peptide (BNP). Management of heart failure with acute pulmonary edema begins with addressing the ABCs.Noninvasive respiratory therapy, such as bilevel positive airways pressure (BiPAP) or continuous positive pressure airway (CPAP) is the most appropriate next step in management. Noninvasive positive pressure ventilation increases oxygenation, decreases the worth of breathing, and decreases preload and afterload. In addition to BiPAP, adjunctive medications include nitrates, diuretics, morphine sulfate, and position the patient sitting up. Nitrates act as venous and arterial vasodilators and help to reduce preload and afterload. Morphine sulfate is thought to decrease oxygen consumption by decreasing catecholamines, decrease preload from mild vasodilator effects and decreases pain and anxiety. However, there are some studies that link the use of morphine sulfate to an increased mortality. Furosemide can be used in patients with evidence of fluid retention (JVD, extremity edema). Pulmonary edema secondary to heart failure usually responds well to preload and afterload reduction with noninvasive ventilation and nitroglycerin. If the patent continues to deteriorate then intubation (C) may be necessary. A myocardial infarction is less likely given the lack of chest pain and ECG that does not reveal ST-segment elevations. Therefore, activation of the cath lab (B) is unnecessary. Hydrochlorothiazide (D) has no role in the acute management of pulmonary edema. Once stabilized, the patient can resume his daily medications.

 

Question 3.  Correct Answer ( C ) Atrioventricular (AV) conduction blocks occur in 25%–30% of patients with acute myocardial infarction. A narrow complex third-degree AV block in the setting of an inferior wall MI is usually transient and resolves spontaneously. Other AV blocks associated with a favorable prognosis include first-degree heart block and second-degree Mobitz type I (Wenckebach). Patients with a new left bundle branch block (A) in the setting of an acute MI are more likely to develop CHF, AV block, and ventricular fibrillation and have an overall increased mortality. Left posterior hemiblock (B) is associated with a large infarct size, increased risk of cardiogenic shock, and increased mortality. A new right bundle branch (D)in the setting of an anterior wall MI is associated with an increased risk of developing complete AV block and cardiogenic shock.

Episode 6 – Hepatic Emergencies

Episode 6 – Liver Emergencies (iTunes or Listen Here

This episode is a response to Dr. Nick Genes tweet:

 Here’s the slideset he posted, filled with excellent pearls.

The Free Open Access Medical Education (FOAM)

We review a post from the Maryland Critical Care Project entitled  Chyle- coming to a paracentesis near you! The post reviews the etiology, epidemiology, and treatment for the rare but morbid chylous ascites.

For more excellent FOAM on liver emergencies:

The Bread and Butter

We summarize some key topics from the following readings,  Tintinalli (7e) Chapter 83; Rosen’s (8e) Chapter 90 …but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Spontaneous Bacterial Peritonitis

  • Diagnosis – paracentesis results revealing >1000 WBCs or >250 polymorphonuclear neutrophils (PMNs). Many patients lack abdominal pain or clear symptoms.  If a patient is sick and the benefit of identifying a source is likely to outweigh the benefit.
    • ACEP cites a relative contraindication of INR >2 [3]. Yet, the AASLD recommends that “coagulopathy should preclude paracentesis only when there is clinically evident hyperfibrinolysis (three-dimensional ecchymosis/hematoma) or clinically evident disseminated intravascular coagulation” [4].
    • Rosen’s supports giving blood products to reverse “significant coagulopathy” prior to paracentesis but note that the AASLD also does NOT support giving blood products to reverse coagulopathy prior to paracentesis, stating that “these patients regularly have normal global coagulation because of a balanced deficiency of procoagulants and anticoagulants[4].
  • Treatment – Third generation cephalosporin
  • Prevention – some patients are on prophylaxis for SBP (often norfloxacin or TMP-SMX).  In cirrhotic patients with upper gastrointestinal bleeds, some have found a number needed to treat (NNT) of 22 for mortality although only one study was placebo controlled.

Hepatic Encephalopathy (Calculator) – graded I-IV.  Remember, Grade II = asterixis, Grade IV is coma.

  • Diagnosis of exclusion – a high ammonia does not mean the patient has hepatic encephalopathy as the cause of their symptoms.
  • Check for precipitants – WikEM has a good list but it includes things like gastrointestinal bleed, electrolyte abnormalities (hyponatremia, hypokalemia), infection, drugs, etc.
  • Ammonia level does not correlate with degree or grade of encephalopathy.

Hepatotoxic Drugs – check out the tables in Rosen’s/Tintinalli.  The NIH website Liver Tox, is also quite helpful. A few highlights

  • Acetaminophen – we don’t cover this but it’s something that everyone needs to know (WikEM, Life in the Fast Lane).
  • Amoxicillin-clavulanate (mixed cholestatic and hepatocellular toxin, theorized to be mostly from the clavulanate) – per the NIH “currently the most common cause of drug induced liver disease in most large case series from the United States and Europe.”
  • Amiodarone, Buproprion
  • Cholestatic examples include haloperidol, verapamil, carbemazepine

MELD score – Quantifies end-stage liver disease for transplant planning

Generously donated Rosh Review questions (scroll for answers)

Question 1. A 54-year-old man is brought into the ED for altered mental status. He is markedly disoriented with confused speech and is unable to follow any commands. A musty odor is noticed when he breathes. Medical history is positive for IV drug abuse. 

Question 2. A 25-year-old previously healthy man presents to the ED with abdominal pain, weakness, confusion, and yellow discoloration of his skin. Laboratory studies reveal markedly elevated AST, ALT, total bilirubin, and serum creatinine. Review of his records shows that he was seen and discharged from the ED 3 days ago for vomiting, abdominal cramps, and watery diarrhea that he developed after a day of hiking in the woods. 

References:

1.O’Mara SR, Gebreyes K.  Chapter 83. Hpeatic Disorders, Jaundice, and Hepatic Failure. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011. p 566-574

2. Oyama L.  Chapter 90.  Diseases of the Liver and Biliary Tract .  Rosen’s Emergency Medicine, 8e.  2014.  p 1186-1204

3. Scheer D, Secko M, Mehta N.  Focus On: Ultrasound-Guided Paracentesis. November 1, 2012.

4. 3.  Runyon BA.  Management of Adult Patients with Ascites  Due to Cirrhosis: Update 2012.  (2013) doi: 10.1002/hep.00000

Answers.

1.  C – Grade I (A) is characterized by disordered sleep, irritability, depression, and mild cognitive dysfunction. Grade II (B) is characterized by lethargy, disorientation, confusion, personality changes, and asterixis. Grade IV (D) is characterized by coma.
2.B – Mushroom toxicity can be divided into 2 groups based on the onset symptoms: early onset toxicity and delayed onset toxicity. Symptom onset 0–4 hours after mushroom ingestion typically indicates a benign course, whereas delayed symptom onset (6–24 hours) is a marker for ingestion of mushrooms with potential for serious toxicity. The patient in the clinical scenario most likely ingested Amanita phalloides, aka the death cap mushroom, while on his hiking trip. This mushroom contains amatoxin, which causes fulminant hepatic failure over a course of days. Amatoxins are responsible for more than 90% of mushroom deaths worldwide. The classic presentation of amatoxin poisoning occurs in 3 phases: (1) delayed GI toxicity (abdominal cramping and diarrhea) 6–24 hours after ingestion; (2) a period of false recovery when the patient appears improved but liver enzymes rise; and (3) the final phase of markedly elevated transaminases, hyperbilirubinemia, DIC, and multiorgan failure 2–4 days after ingestion. Renal failure is also a hallmark. No antidote exists for amatoxin toxicity, and treatment involves supportive care. GI decontamination by activated charcoal may be of benefit, but hemodialysis is not effective.