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.

 

Episode 5 – Psychiatry & Increased ICP

Episode 5 – Psychiatry & Increased Intracranial Pressure (iTunes or Listen Here

The Free Open Access Medical Education (FOAM)

Academic Life in Emergency Medicine -Atypical Antipsychotic Medication Re-initiation in the Emergency Department

  • Determine how long the patient has been without their atypical antipsychotic.
  • Consider dosing reductions in patients who have been without their medications for more than a few doses or in patients at higher doses.
  • Look up the recommendations.

(more…)

Episode 4 – Transfusions and Ingested Foreign Bodies

Episode 4 – Transfusion Emergencies (iTunes or Listen Here

The Free Open Access Medical Education (FOAM) –from Dr. Ryan Radecki’s erudite blog, Emergency Medicine Literature of Note..

Infections & Transfusions” – a JAMA meta-analysis found that higher hemoglobin targets were associated with an increased incidence of infection with a number needed to harm of 20-38.  The  group with a target level of 7-9 g/dL had an infection rate of 11.8% (95% CI, 7.0%-16.7%)  compared with an infectious complication rate of 16.9% (95% CI, 8.9%-25.4%) in the “liberally” transfused group.

Grilling Injuries on Memorial Day” – Grilling isn’t risk free.  Dr. Radecki reviewed a case series of six individuals who presented in one year to a hospital after ingesting meat cooked on a grill.  Three patients had neck pain with wire grill bristles removed via laryngoscopy and three had abdominal pain necessitating removal – 2 by colonoscopy and 1 with urgent surgery secondary to intestinal perforation.

The Bread and Butter

We summarize some key topics from the following readings,  Tintinalli (7e) Chapters 233; Rosen’s (8e) Chapter 7…but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Transfusion Reactions

Immediate Reactions – great FOAM summary from Life in the Fast Lane: Transfusion Risks, Transfusion Reactions 

Screen Shot 2014-06-08 at 9.39.12 PM

 

 

 

 

 

 

 

The Ones Our Patients Care About (Infectious – statistics are US based)

  • Bacterial contamination is rare: 1/500,000 – 1/1,000,000
    • Most common pathogen: Yersinia Entercolitica
  • More common in platelets: 1/1000-1/2000 per Rosen, CDC, and the AABB  (Tintinalli cites 1 in 6 million)
  • Most Common virus: Parvovirus B19 (1 in 10,000).  The others are very very rare: HIV and Hepatitis C > 1 in 1 million, Hepatitis B 1 in 100,000-200,000

Ingested Foreign Bodies

  • Beware the button battery. These can cause necrosis within hours in the esophagus and must be removed ASAP.
  • Objects that are irregular, very sharp, or have dimensions greater than 2.5cm in width or 6 cm in length that are still in the stomach or duodenum – call GI to have these removed via endoscopy.

Generously donated Rosh Review questions (scroll for answers)

Question 1 A 55-year-old woman is receiving a blood transfusion due to persistent vaginal bleeding and a hemoglobin of 5 mg/dL. While receiving the transfusion, she develops fever, chills, back pain, pain at the site of transfusion, and tachycardia. 

Question 2 A 28-year-old man presents with a 1-day history of rectal bleeding. In the ED, he is hypotensive, thrombocytopenic, and is found to be passing melena. He receives a transfusion of platelets and packed red blood cells as part of his resuscitation. Twenty minutes after the start of his platelet transfusion, his BP is 90 mm Hg systolic, he becomes dyspneic, and his oxygen saturation drops from 99% on room air to 91% on 2L of oxygen supplementation. On exam, you note rales at the lung apices and that he is using accessory muscles to breathe. His chest radiograph shows diffuse interstitial infiltrates. 

Question 3 

 

References:

Emery M.  Blood and Blood Products.  Rosen’s Emergency Medicine. 2014: 8th ed. p 75-80.e2

Coil CJ, Santen SA.  Transfusion Therapy  Tintinalli’s Emergency Medicine: A Comprehensive Review. 7th ed.

Hillyer CD, Josephson CD, Blajchman MA, et al. Bacterial contamination of blood components: risks, strategies, and regulation: joint ASH and AABB educational session in transfusion medicine. Hematology Am Soc Hematol Educ Program. 2003:575-89.

1. C – Up to 20% of all transfusions may lead to some type of adverse reaction. Although most of these reactions are minor, some are life-threatening. The patient is having an acute intravascular hemolytic reaction. This occurs when the recipient’s antibodies recognize and induce hemolysis of the donor’s red blood cells and may result in activation of the coagulation system and disseminated intravascular coagulation. This type of reaction typically presents with back pain, pain at the site of transfusion,headache, fever, hypotension, dyspnea, tachycardia, chills, bronchospasm, pulmonary edema, bleeding, and development of renal failure. First, stop the transfusion. Then initiate intravenous hydration to maintain diuresis.

2.D- This patient is most likely suffering from transfusion-related acute lung injury (TRALI), one of the leading causes of transfusion-related mortality. It is most closely associated with platelet and fresh frozen plasma transfusions, though cases have been reported with packed red blood cells since there is some residual plasma in the packed cells. Symptoms begin abruptly during transfusion or within 6 hours and resemble adult respiratory distress syndrome with noncardiogenic pulmonary edema, dyspnea, hypoxemia, and bilateral infiltrates on chest radiograph.

3. A- The patient is experiencing an allergic reaction without serious signs or symptoms. The transfusion does not need to be stopped for such a reaction; an antihistamine will help to relieve symptoms.

Episode 3 – Ear Emergencies

Episode 3 – Ear Emergencies (iTunes

The Free Open Access Medical Education (FOAM) – SMART EM Pseudoaxioms 2 and Literature Update

The podcast reviews:

  • Bullous Myringitis, a painful infection of the tympanic membrane, is typically caused by viruses, strep. pneumoniae and moraxella and, less commonly, mycoplasma.  The boards have caught up with this. Check out this review by Mellick.
  • PHANTOM-S trial: Use of the STEMO (Stroke Emergency Mobile – an ambulance with neurologist and a CT scanner for suspected strokes) reduced mean alarm-to-treatment time by 25 minutes (95% CI, 20-29; P < .001) without an appreciable neurologic benefit for this intensive intervention.
  • An article by Gregg et al in the NEJM discussed incredible improvements in diabetes outcomes as a result of tight glycemic control. Dr. Newman asserts that much of this is secondary to dilution, as the definition of diabetes changed in 1997.  This resulted in more people with less severe disease being diagnosed with diabetes.

The Bread and Butter

We summarize some key topics from the following readings,  Tintinalli (7e) Chapters 237; Rosen’s (8e) Chapter 92.  A good read on common ear emergencies from EBMedicine…but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Bullous Myringitis

This is a painful infection characterized by bullae on the tympanic membrane (TM), which has a richly innervated outer epithelium (hence the severe otalgia). Patients may collect fluid behind their TM or have a concomitant otitis media.

Etiology: viruses, typical otitis media pathogens.  Mycoplasma and chlamydia have been associated with bullous myringitis but the association is unclear and these are not the most common causes.

Treatment: pain control, pain control, pain control.  Antibiotics are optional in most cases. But then again, antibiotics are not necessary in most cases of otitis media.  Both Rosen and Tintinalli are on board with this.

Perforated Tympanic Membrane

Photo:Didier Descouens (Wikimedia Commons)

Etiology: infection, trauma (q-tips, instrumentation), changes in pressure (diving, flying)

Treatment:  Keep the ear canal dry, follow up with ENT.  Most of these patients can go home.  If the injury is in the posteriorsuperior aspect of the TM or secondary to penetrating trauma, they should see ENT within 24 hours because they may have damage to the bones of the middle ear.

Auricular Hematoma

Etiology: Blunt trauma (often associated with boxing, fights, or termed “rugby ear“)

Treatment:  Incision, drainage, and compression dressing/splint.  Photo guide to repair.

Ototoxic Agents (great table in Tintialli 8 e, Ch 237, p1551)

Risk of hearing loss typically increases with exposure to medication (dose and length of use) and issues with clearance such as renal insufficiency may cause medications to hang around longer than anticipated or at higher levels.

Loop Diuretics: furosemide, bumetanide, ethacrynic acid

Salicylates (aspirin and quinine), NSAIDs

Antibiotics that end in -mycin or -micin: aminoglycosides (gentamicin), vancomycin, erythromycin

Chemotherapeutic agents: vincristine, vinblastine, cisplatin, carboplatin

Topical agents: ethanol, polymixin B, neomycin

Sudden Hearing Loss Differential Diagnosis 

Occurs over the span of three days.

Differential Diagnosis categories for any ailment can be remembered by the mnemonic VINDICATE

  • Vascular – sickle cell, polycythemia
  • Infectious/Inflammatory – viruses (zoster oticus or herpes, EBV, CMV, mumps), syphilis, labyrinthitis, temporal arteritis
  • Neoplasms – leukemia, masses,  acoustic neuroma
  • Drugs –  loop diuretics, antibiotics that end in -mycin or -micin (aminoglycosides like gentamicin, vancomycin, erythromycin), salicylates and NSAIDs, chemotherapeutic agents (cisplatin, carboplatin, vinblastine, vincristine, and topical agents (ethanol, polymyxin B, neomycin)
  • Iatrogenic/idiopathic – perforated TM, idiopathic endolymphatic hydrops (Meniere’s disease) – vertigo, hearing loss, tinnitus
  • Autoimmune -granulomatosis with polyangitis (Wegener’s)
  • Trauma – ruptured TM
  • Endocrine – diabetes, high cholesterol

Necrotizing Otitis Externa (Malignant Otitis Externa) – an infection that can turn into osteomyelitis of the skull

Presentation: otalgia, headache, and swelling and tenderness around the ear particularly in the setting of a prolonged course of otitis externa.  Diagnosis often requires CT scan to gauge involvement.

Epidemiology: Diabetics, immunocompromised

Etiology: Pseudomonas (90%)
Treatment:   Pediatrics- imipenem or an aminoglycoside and an antispeudomonal penicillin.  Adults – cephalosporin or quinolone

Dispo: Mild cases with good follow up can get oral quinolones as outpatients. More severe cases – admission, IV antibiotics, and perhaps surgical debridement.

Generously donated Rosh Review questions (scroll for answers)

Question 1.

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Question 2.

A 36-year-old woman presents to the ED complaining of decreased hearing and increased fullness to the right ear. Over the last week, she has used cotton-tipped applicators to attempt to remove cerumen from her right ear. On exam, you notice a cerumen-impacted external canal on the right. You irrigate the right ear with warm saline using an 18-gauge IV catheter and a plastic curette to remove the cerumen. During the procedure, the patient has sudden and complete hearing loss to the right ear. 

 

Question 3. A 16-year-old girl presents complaining of pain behind her left ear. She thought the pain was due to an ear infection and took three of her boyfriend’s leftover antibiotic tablets without seeing her primary care physician. Her ear pain improved for a couple of days, but now she is complaining of fever and discharge from the external auditory canal. Her vitals are T 38.4°C, BP 120/80, HR 108, and RR 18. On physical examination, she has postauricular tenderness, swelling, and erythema. You note purulent otorrhea through a perforated tympanic membrane. 

Answers:

1. D-Bullous myringitis was previously linked to Mycoplasma pneumoniae but it appears, based on middle ear aspirate culture results, that typical acute otitis media pathogens are the true cause. Among these, Streptococcus pneumoniae is most common.
2. C – The patient does not require admission (A) to the hospital. ENT care can be arranged for as an outpatient. Traumatic tympanic membrane perforations do not require otic antibiotics (B) unless the ear was contaminated such as from diving in seawater or the rupture is secondary to infection. The patient should receive more than ac otton ball (D) in her ear. Her management should include analgesia and ENT follow-up because complications of tympanic membrane rupture include facial nerve palsy, vertigo, and hearing loss.

3. C – This patient has necrotizing otitis externa.

References:

Silverberg M, Lucchesi M.  Common Disorders of the External, Middle, and Inner Ear.  Tintinalli’s Emergency Medicine, A Comprehensive Study Guide, ed 7. New York, McGraw-Hill, 2011, (Ch) 237:p 1556-1557.