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.  [polldaddy poll=8210380]

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.[polldaddy poll=8206329]

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.[polldaddy poll=8191357]

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. [polldaddy poll=8191360]

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
025_ECG_12leads
http://www.elin.ttu.ee/mesel/Study/Courses/3240BME/Content/1_Bioelectricity/BME_2_bioelectric_signals.htm

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.  [polldaddy poll=8168396]

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. [polldaddy poll=8168406]

Question 3.  [polldaddy poll=8169897]

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.