UMEM Educational Pearls

Pulseless Electrical Activity (PEA)

ACLS algorithm for PEA focuses on memorizing the “ H's & T's" without a systematic approach on how to evaluate & treat the possible etiologies

A modified approach to PEA focuses on “cause-specific” interventions utilizing two simple tools: ECG and Bedside Ultrasound (US)

Simplified PEA Algorithm

♦1st obtain the ECG and assess the QRS-complex length (narrow vs. wide)

♦ A narrow QRS-complex suggests a mechanical problem:  RV inflow or outflow obstruction

Utilize bedside US to assess for RV collapsibility vs. dilation

A collapsed RV suggests tamponade, tension PTX or mechanical hyperinflation

A dilated RV suggests PE

The above listed etiologies all have a preserved/hyperdynamic LV Tx begins w/aggressive IVF’s followed by “cause-specific” therapy: pericardiocentesis, needle decompression, forced expiration/vent management, and thrombolysis respectively

♦ A wide QRS-complex suggests a metabolic (hyperK/acidosis/toxins), ischemic, or LV problem

Utilize bedside US to assess for LV hypokinesis/akinesis

For metabolic/toxic etiologies treat w/calcium chloride and sodium bicarbonate +/- vasopressors

For ischemia and LV failure treat w/cardiac cath. vs. thrombolysis +/- vasopressors/inotropes

♦Trauma and several other etiologies of PEA that are seldom forgotten in any critically ill patient (hypothermia, hypoxia, and hypoglycemia) are not included in this algorithm.

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Background

The ACLS recommendation for epinephrine dosing in most cardiac arrest cases is 1 mg every 3-5 minutes. This dosing interval is largely based on expert opinion.

Primary Outcome

A new study reviewed 21,000 in-hospital cardiac arrest (IHCA) cases from the Get With the Guidelines-Resuscitation registry. The authors sought to examine the association between epinephrine dosing period and survival to hospital discharge in adults with an IHCA.

Methods

• For 6 to <7 min/dose, adjusted OR, 1.41 (95%CI: 1.12, 1.78)
• For 7 to <8 min/dose, adjusted OR, 1.30 (95%CI: 1.02, 1.65)
• For 8 to <9 min/dose, adjusted OR, 1.79 (95%CI: 1.38, 2.32)
• For 9 to<10 min/dose, adjusted OR, 2.17 (95%CI: 1.62, 2.92)

This pattern was consistent for both shockable and non-shockable cardiac arrest rhythms.

• This study only included in-hospital cardiac arrests.
• The data was retrospectively reviewed from a registry of prospectively collected data.
• This is certainly an interesting finding that needs to be explored further.
• Given that epinephrine in cardiac arrest has never been proven to work (and may cause harm), it's not too suprising that giving less of a potentially harmful drug portends better outcomes.

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Acid and Alkali burns are all known for their caustic cellular injury to local tissue. Acid burns and specifically hydrofluoric acid has systemic toxicity. HF can be lethal even if there is only a 5-10% total body surface area burn. You can find HF in brick cleaner, glass etching and wheel cleaner. They main metabolic derangement is hypocalcemia which can lead to cardiac dysrrhythmias and death.

Treatment has ranged from IV calcium or even intra-arterial calcium in the affected limb to treat the local severe pain associated with an HF burn. Checking a serum calcium to be sure IV calcium replacement is also necessary.

Remember HF -> severe pain, minimal tissue damage, hypocalcemia, hyokalemia, dysrrhythmias

Bottom Line:

• Routine immunizations (make sure you don’t need boosters!) : Hep A/B, Tetanus, Measles, Influenza
• Vaccines for disaster relief purposes where sanitation is a concern: typhoid, cholera
• Japanese encephalitis if you plan to be rural areas for > 1 month or spend substantial time outdoors
• Rabies if you might encounter animal bites, bats
• Yellow fever
• Malaria prophylaxis (not really a vaccine but necessary)

University of Maryland Section of Global Emergency Health

Author: Veronica Pei

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Intensive BP Control in Spontaneous Intracranial Hemorrhage

Managing the patient with hypertensive emergency in the setting of spontaneous intracerebral hemorrhage (ICH) is often a challenge.  Current guidelines from the American Stroke Association are to target an SBP of between 160 - 180 mm Hg with continuous or intermittent IV antihypertensives.  Continuous infusions are recommended for patients with an initial SBP > 200 mm Hg.
 

An emerging concept is that rapid and aggressive BP control (target SBP of 140) may reduce hematoma formation, secondary edema, & improve outcomes.
 

Recently published, the INTERACT 2 trial (n=2,829) compared intensive BP control (target SBP < 140 within 1 hour) to standard therapy (target SBP < 180) found:

• No difference in mortality (11.9% vs 12%, respectively)
• Improved functional status (secondary outcome) with intensive BP control
• Intensive lowering of BP in patients with acute ICH appears safe 

Study flaws: Patients treated with multiple drugs - combinations of urapadil, labetalol, nicardipine, nitrates, hydralazine, and diuretics.  Management variability away from protocol seemed high. (Interesting editorial)
 

A Post-hoc analysis of the INTERACT 2 published just this month suggests that large fluctuations in SBP (>14 mmHg) during the first 24 hours may increase risk of death & major disability at 90 days.

Bottom Line:  INTERACT 2 was a large RCT but not a great study (keep on the look out for ATACH II).  However, in patients with spontaneous ICH, consider early initiation of an antihypertensive drip (preferably nicardipine) in the ED to reduce blood pressure fluctuations early with a target SBP of 140 mmHg.

Follow me on Twitter: @JohnGreenwoodMD

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Question

50 year-old with facial weakness and dysarthria. What's the diagnosis?

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The clinical examination is often unreliable in ruling out septic arthritis in the ED.

 Diagnostic arthrocentesis is often performed.

Traditional teaching involved very high WBC count thresholds as part of diagnosis.

In one 2009 study, synovial leukocyte counts in cases of MRSA were often less than 25,000 cells/uL

Have a low threshold for empiric antibioitics even in the face of low WBC counts (and incredulous consultants)

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Passive leg raise (PLR) has been studied in adults as a bedside tool to predict volume responsiveness (see previous pearls from 5/7/13 and 6/17/2008). Can this be applied to children?
 
A single center prospective study looked at 40 intensive care patients ranging in age from 1 month to 12.5 years.  They used a noninvasive monitoring system that could measure heart rate, stroke volume and cardiac output.  These parameters were measured at a baseline, after PLR, after another baseline and after a 10 ml/kg bolus.
 
Overall, changes in the cardiac index varied with PLR.  However, there was a statistically significant correlation in children over 5 years showing an increase in cardiac index with PLR and with a fluid bolus.
 
Bottom line:  In children older then 5 years, PLR can be a quick bedside tool to assess for fluid responsiveness, especially if worried about fluid overload and in an under served area.

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General Information:

• Hepatitis B virus (HBV) is a common cause of cirrhosis, end-stage liver disease, and hepatocellular carcinoma, particularly in areas of the world where infection rates are high.
• More than 240 million people have chronic HBV infections and about 600,000 people die every year due to the acute or chronic consequences.
• The antiviral tenofovir (used in HIV treatment) has shown recent promise in not only prolonging progression to cirrhosis but actually reversing cirrhosis.
• Phase III trial results of 5 years of tenofovir treatment showed an 87% improvement in histology. Notably, of the 96 patients with cirrhosis prior to treatment, 74% were no longer cirrhotic at year 5 of therapy and only 2 went on to decompensated liver disease.

Bottom Line:

Tenofovir has already become standard therapy for HIV (contained in Truvada and Atripla). This HBV study shows promise that this drug can not only decrease progression of disease but also reverse the cirrhosis associated with long-term infection. Given the prevalence of chronic HBV, larger scale role-out of this drug could markedly change the epidemiologic landscape of morbidity and mortality due to hepatitis B.

University of Maryland Section of Global Emergency Health

Author: Emilie J.B. Calvello

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• The well-known effects of cocaine toxicity include seizures, cardiac ischemia, and rhabdomyolysis. Abdominal pain, however, is a lesser known side-effect and may occur secondary to ischemia, infarction or perforation of the gastrointestinal tract; such cases tend to occur in younger people without known risk factors for ischemia.
• Ischemia may occur from the direct vasoconstrictive effects of cocaine, but may also occur from its pro-thrombotic effects on the mesenteric vessels; although any segment of the GI tract may be involved, the small bowel is most often affected.
• Symptoms may vary from mild abdominal pain to bloody diarrhea. Physical exam may reveal peritoneal signs if perforation occurs.
• CT scan of the abdomen may reveal the diagnosis although angiography may required for diagnosis or to guide revascularization.
• Management may vary from conservative (i.e., bowel rest and antibiotics) to surgical exploration and bowel resection in selected cases.

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Question

44 year-old construction worker fell off a ladder and presents with elbow pain. What's the diagnosis and what is the most commonly associated nerve injury? 

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Early Atherosclerosis Detection

50 middle-aged asymptomatic subjects free of vascular disease underwent carotid ultrasound (CUS) for risk stratification were also invited to undergo coronary computed tomography angiography (CCTA) or coronary artery calcium score (CAC) to identify which of the 3 imaging modalities was best at identification of early atherosclerosis

Atherosclerosis was observed in 28%, 78%, and 90% of subjects using CAC, CCTA, and CUS, respectively

36 patients with a CAC score = 0, 69% and 86% had atherosclerosis on CCTA and CUS, respectively

Concordance between modalities was highly variable

CUS and CCTA detection of plaque were significantly more sensitive than CAC 

Considering the prevalence of subclinical disease on CUS and CCTA, the threshold at which to treat warrants further research

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Inborn errors of metabolism (IEM) are rare, each typically affecting 1 in 5000 to 1 in 100,000 children, BUT collectively these disorders are more common because there are so many. If you are lucky…when they present to the ED they come with a letter from Dr. Greene (our world renowned metabolic geneticist) detailing exactly what to do. The rest of the time…you are on your own. Think about IEM in any neonate or child with history of feeding difficulties, failure to thrive, recurrent vomiting, unexplained altered mental status and/or acidosis. Pay particular attention to feeding difficulties that appear with changes in diet: switch from soy to cow’s milk formula (galactose), addition of juice or fruit or certain soy formulas (fructose), switch from breast milk to formula or foods (increased protein load), and longer fasting periods from sleeping or illness.

For this pearl, we will focus on primary hyperammonemia from an enzymatic block in ammonia metabolism within the urea cycle. It is important to remember that secondary hyperammonemia can result from metabolic defects such as organic acid disorders, fatty acid oxidation disorders, drugs that interfere with urea cycle, or severe liver disease. Amino acids liberated from excess protein breakdown (stress of newborn period, infection, injury, dehydration, surgery, or increased intake) release nitrogen which circulates as ammonia. Ammonia is then converted to urea via the urea cycle and excreted in the urine. With urea cycle defects (UCD) there is an enzymatic block in the cycle that results in accumulation of ammonia which has toxic effects on the CNS especially cerebral edema. The most common UCD is ornithine transcarbamylase deficiency followed by argininosuccinic academia, and citrullinemia.

Clinical presentation includes poor feeding, lethargy, tachypnea, hypothermia, irritability, vomiting, ataxia, seizures, hepatomegaly, and coma. Hyperammonemic crises in neonates mimic sepsis! If you think about an IEM in your differential, send plasma ammonia (1.5 mL sodium-heparin tube on ice STAT), plasma amino acids, and urine organic acids. Other helpful labs include blood gas, CMP, urinalysis (looking at ketones), lactate, plasma acylcarnitines, and newborn screen if not already sent. Plasma ammonia is a direct index of CNS toxicity and important to follow for acute management. Serum level > 150 in sick neonate or > 100 in sick infant/child is concerning for IEM. The presence of hyperammonemia and respiratory alkalosis suggest urea cycle defect. The presence of metabolic acidosis and hyperammonemia suggests organic acid disorder.

Immediate treatment of hyperammonemia is critical to prevent neurologic damage. Cognitive outcome is inversely related to the number of days of neonatal coma caused by the cerebral edema.

1. Stop all protein intake! You need to stop catabolism.

2. Start D10 at 1.5 times maintenance rate with GIR at least 6-8. Start intralipids 1-3g/kg/day when able (typically in the ICU after central line placed).

3. Give ammonia scavenger medications sodium benzoate and sodium phenylacetate. These are available commercially as Ammonul.

     a. 0-20kg: 2.5mL/kg IV bolus over 90 min followed by same dose as 24 hr infusion

     b. >20kg: 55 mL/m2 IV bolus over 90 min followed by same dose as 24 hr infusion

4. HEMODIALYSIS! Dialysis is the most effective way to remove ammonia and should be done when level > 300. The decision to hemodialyze is crucial in preventing irreversible CNS damage; when in doubt in the face of elevated ammonia, HEMODIALYZE!

Seizures can be the presenting manifestation of acute poisoning in children.

A 3-year data set from the Toxicology Investigators Consortium (ToxIC) Case Registry identified 142 cases of drug-induced seizures in children < 18 years old. 75% were teenagers.

Antidepressants were most commonly associated with causing seizures, especially bupropion and citalopram. Diphenhydramine was also a commonly identified cause.

The authors conclude that clinicians managing teenagers presenting with seizures should have a high index of suspicion for intentional ingestion of antidepressants.

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• The American College of Emergency Physicians recently released the 2014 National Report Card on America’s Emergency Care Environment.
  • This comprehensive, state-by-state report card evaluates the support for emergency care in the United States.
• One area to highlight from the Report Card is the issue of emergency department (ED) crowding.
  • Crowding primarily results from keeping admitted patients in the ED for hours while waiting for an inpatient bed. This happens not only in the U.S., but in many other countries as well.
• For the U.S. overall, the median time from ED arrival to ED departure for admitted patients was 272 minutes (approximately 4.5 hours).
  • However, median times for individual states ranged from the best time of 176 minutes (approximately 3 hours) to 452 minutes (approximately 7.5 hours).

Bottom line

ED crowding remains a critical problem in the US and globally.  It is frequently driven by the “boarding” of admitted patients.  Improved patient flow is needed to be able to take care of patients presenting with acute care needs.

University of Maryland Section of Global Emergency Health

Author: Jon Mark Hirshon, MD, MPH, PhD

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A 50yo man found dow in the snow was brought into our ER last week in cardiac arrest with a bladder temperature of 21° C. Let’s warm him up!

• Passive external warming (good for mild hypothermia > 34° C):  remove all wet clothing, use warm blankets, hot chocolate.
• Active external rewarming (Used for temp between 30-34° C): Radiant heat, electric blankets, Bair-Hugger. Disadvantages: “core temperature after drop” theory: drop in core temp because of peripheral vasodilatation. Therefore, focus on warming the chest and torso area.  May not occur with certain warming techniques.
• Active core rewarming (<30 °C, above techniques and several other options):

1. Heated humidified oxygen via mechanical ventilation at 42-46°
2. IV normal saline warmed to 41-43° C
3. Cardio-pulmonary bypass: 1-2° C increase every 5 minutes
4. ECMO (best option in cardiac arrest): Up to 4-6° C/hr. VV or VA ECMO. Provides Cardio-pulmonary support. Can continue CPR while placing a cannula.
5. CVVH: less costly, more available, 1-4°C/hr. Case reports only. 
6. Artic Sun; external rewarming pads: used in hypothermia protocols. Easy to use. Case reports only.

• Other methods (use if other methods are unavailable):

1. Pleural irrigation: one chest tube in the mid-clavicular line w saline at 42° and another chest tube in the post-axillary line and connected to a pleurovac.
2. Peritoneal lavage: 8 Fr catheter into the peritoneum using a standard paracentesis method. Use 40-45° C dialysate.
3. Gastric, bladder, colonic irrigations

We were able to get ROSC with CPR and ACLS and then used Artic Sun to re-warm successfully.

Other tips/tricks:

• Continue CPR while rewarming (This is debatable: monitor ECG for new rhythms)
• How warm is “warm and dead”? Probably around 32°C
• How fast to rewarm?  Would warm quickly in cardiac arrest and then 1-2° C/hr thereafter; (No good evidence here)
• Arrhythmias corrected by rewarming (bradycardia etc); no need for pacing
• Up to three defibrillations for V. fib/V. tach; hold if no benefit
• Can give epinephrine per ACLS protocol but would be cautious with further dosing
• Pressors: can use epinephrine drip cautiously for hypotension
• Cisaturacurium for paralysis w/ sedation to prevent shivering
• Rule out hypoglycemia, adrenal insufficiency, hypothyroidism, sepsis if patient does not rewarm as expected!
• Avoid IJ lines or irritating the myocardium with a guidewire.
• K>12 mmol /L: consider termination of CPR

Attachments

• 1402111256_nejm_hypothermia2012.pdf (581 Kb)

Question

25 year-old male presents after falling off his bicycle. He complains of pain in his right-hand (he is right-hand dominant). What's the diagnosis? 

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The importance of new ST-segment depressions (STD) and/or T wave inversions (TWI) in lead aVL have not been emphasized or well recognized across specialties. Computer-assisted ECG readings typically report these findings as normal or nonspecific. 

There is growing evidence that changes in lead aVL are abnormal, and that paying attention to that lead can be clinically useful. Reciprocal changes presenting as STD or TWI in lead aVL may be indicative of a significant coronary artery lesion and can sometimes be the only ECG manifestation of acute MI.  

STD in lead aVL is considered a sensitive marker for early inferior STEMI, and has been shown to help differentiate STEMI from pericarditis. Another recent retrospective study suggests that TWI in aVL might be associated with significant LAD lesions. 

Bottom Line: Paying close attention to subtle changes and abnormalities in lead aVL may help in early identification and initiation of therapy for patients who are having an acute MI.  

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Attachments

• 1402092205_TWI_in_aVL.pdf (112 Kb)

Overtraining syndrome

A maladaptive response to excessive exercise without adequate functional rest

-Results in disturbances of multiple body systems (neurologic, endocrinologic, immunologic and psychologic).

- May be caused by systemic inflammation and resultant neurohormonal changes
            - Multiple hypotheses exist

-Symptoms

Parasympathetic alterations: fatigue, depression, bradycardia

Sympathetic alterations: insomnia, irritability, agitation, tachycardia, hypertension, restlessness

Other: anorexia, weight loss, poor concentration, anxiety

Usual presentation is prolonged underperformance despite adequate rest and recovery (weeks to months).