UMEM Educational Pearls

Pregnancy is a risk factor for AMI, increasing the risk 3-4-fold. The risk is accentuated with age, especially in women > 40 yo in whom the risk is 30-fold higher. Overall, heart disease is the biggest [non-obstetric-related] killer of pregnant women in the developed world, surpassing even thromboembolic disease. [Roos-Hesselink, et al. Pregnancy in high risk cardiac conditions. Heart 2009;95:680-686.]

Glucose-6-Phosphate Dehydrogenase Deficiency

• G6PD Deficiency is a genetic disorder which can cause hemolytic anemia when people with the disorder come into contact with drugs, food and other substances which cause oxidative stress.
• It is the most common genetic enzyme deficiency.
• G6PD is an inherited disorder with over 400 different known variants.
• Oxidative stress can cause the premature distruction of RBC's due to the lack of the enzyme reduced glutathione which G6PD helps produce.
• Drugs that are at high risk for causing hemolytic anemia in those with G6PD deficiency are:
  • NSAIDS (Asprin, Tylenol, Ibuprophen)
  • Quinolones
  • Sulfa drugs
  • Drugs metabolized known to cause blood or liver related problems or hemolysis
  • Primaquine
  • Nitrofurantoin
  • Glyburide
  • Dapsone

Also make sure that you are not G6PD deficiency if you are eating with Hannibal Lecter as Fava beans and other legumes can also cause an episode of hemolysis.

A good reference for G6PD deficiency is http://g6pddeficiency.org/index.php

Overdoses of insulin glargine (Lantus) are rarely reported in the literature.  In fact, there are only 6 case reports.  We recently had a patient in our ED who was hypoglycemic from insulin glargine.  The hypoglycemic episode was quite prolonged (> 24 hours) in the ED before being the patient was transferred to the MICU.  Here are a few points to remember:

• Insulin glargine does not peak; it was designed to mimic basal islet cell insulin secretion.
• In the therapeutic setting, its effects can last up to about 24 hours.  In overdose the hypoglycemic effects have been reported to last up to 60-130 hours!
• Be prepared to give IV dextrose 5% or 10% infusion for the duration of the patient's hypoglycemic effect.  This can be supplemented with food.
• Octreotide will be ineffective for exogenous insulin poisonings because its effect comes from its ability to suppress insulin secretion from the pancreas.

• One may wonder how to determine whether a patient has limb ataxia in the setting of limb weakness when scoring the NIH Stroke Scale (NIHSS).

• The component of the NIHSS that tests for limb ataxia asks that the patient perform finger to nose and shin to heel testing.

• A patient who does not exhibit any ataxia would receive a score of 0 (zero), which is the best score.

• If the patient does not exhibit any ataxia because he/she has neuromuscular weakness and therefore can't perform the tasks at all, they would also receive a score of 0 (zero) on this component of the NIHSS.

Ventilation in the Brain-injured Patient

• As we have discussed in previous pearls, the ARDSnet trial forms the basis for ventilatory management in the ICU.  A primary component to current ventilatory management is the focus on maintaining lower and safer distending pressures through the use of lower tidal volumes.
• Similar to last week's pearl on the obstetric patient, these ventilatory settings may not be applicable to all patients.
• Recall that the use lower tidal volumes results in lower minute ventilation.  This leads to the accumulation of CO₂, termed permissive hypercapnia.  In general, we tolerate higher levels of CO₂ in favor of lower plateau pressures.
• For the brain-injured patient, however, increases in CO₂ may increase intracranial pressure (ICP) causing adverse effects.
• Current recommendations for mechanical ventilation in the brain-injured patient include maintaining a P_aCO₂ between 35 - 40 mm Hg.  Thus, you need to be more vigilant at following P_aCO₂ in this patient population.

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The One Minute Preceptor-Microskills in Teaching

Most clinical teaching takes place in the context of busy clinical practice where time is at a premium. Microskills enable teachers to effectively assess, instruct, and give feedback more efficiently. This model is used when the teacher knows something about the case that the learner needs or wants to know.

Most of already do this on a daily basis when a learner (student or resident) presents a case to us.

 

• Get a commitment (Make them commit to a diagnosis and/or management strategy)
• Probe for supporting evidence (why do they think this patient with CP has an MI?)
• Teach general rules
• Reinforce what was right
• Correct mistakes

One of the biggest pitfalls in teaching, particularly to medical students, is the first skill, getting a commitment. Let (i.e. make) the student commit to a diagnosis and treatment plan and avoid spoonfeeding them.

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Adenosine is everyone's favorite drug for SVTs, and it is often even used as a diagnostic maneuver in some tachydysrhythmias of uncertain origin. BUT there are some definite cautions of which we must all be wary:

1. Adenosine CAN convert some types of ventricular tachycardia to sinus rhythm. This "adenosine sensitive VT" is very well reported in the cardiology literature. Don't use adenosine as a diagnostic method of distinguishing VT from SVT (with aberrant conduction).

2. Atrial fibrillation with WPW can sometimes mimic SVT if one doesn't look closely and notice the irregularity. If you misdiagnose these patients as having SVT and give adenosine, you will likely induce VFib. Not good, Mav, not good!

3. Adenosine causes some histamine release (thus the flushing and hot sensation that patients report). That's bad for patients that have reactive airway disease (RAD). Adenosine should be avoided in patients with severe RAD by history (asthma, COPD) or if patients have active wheezing.

4. Concurrent use of adenosine in patients on digoxin or patients that have received digoxin or verapamil has been reported to cause VFib in rare cases.

5. The effects of adenosine appear to be potentiated by dipyridamole and carbamazepine. Lower the dose of adenosine in patients that take these medications.

6. The effects of adenosine are antagonized by methylxanthines such as caffeine or theophylline. You will probably need higher doses of adenosine in these patients.

7. There are rare cases of adenosine inducing atrial fibrillation. I'm not sure what to say about this, except don't be surprised if your patients goes from SVT into atrial fibrillation. Rare, fortunately.

8. And finally...always remember to push adenosine very quickly and follow immediately with saline BOLUS flush (don't just open up the IVF...you must PUSH 10-20cc of NS); and warn your patient that for ~10 seconds they are going to feel like they are about to die while the adenosine takes effect. If you don't warn them, they will never trust you or the drug again.

9. And finally finally...always have your code cart ready to go when you are using potent cardiac drugs such as adenosine. Don't let yourself be unprepared for a side effect.

Bad luck only happens when you are unprepared!

AM

Radial Head Fractures:

Radial head fractures are more common in adults, where radial neck fractures are more common in children.  Remember to look for fat pads to help make the diagnosis if it is not obvious on plain films.  On plain films, a line drawn down the middle of the radial head should always line up with the capitellum of the humerus.  If this does not occur the radial head is dislocated and/or fracture.

Orthopaedics use the Mason classification to help guide treatment, and break down fractures into 3 different types.

• Type I - is undisplaced, generally treated nonoperatively. 
  • Early mobilization prevents chronic elbow stiffness.
• Type II - a single fragment is displaced.
  • May be treated nonoperatively if the displacement is minimal.
  • The rule of threes is used. Nonsurgical treatment can be considered if the fracture involves less than one third of the articular surface, less than 30° of angulation, and if displacement is less than 3 mm
• Type III  - is comminuted.
  • Usually require operative intervention.

 

 

Hemolytic-uremic syndrome (HUS)

• Characterized by hemolytic anemia (pallor on exam), acute renal failure (oliguria or anuria by history), and thrombocytopenia (petechiae).
• HUS is one of the most common causes of acute renal failure in children.
• Two types: diarrhea-associated (shiga toxin+ or D+) which is more common and has a more favorable prognosis, and non diarrhea-associated (atypical or sporadic or D-).
• Most common age at presentation is during infancy or young childhood.
• Pediatric HUS is a true medical emergency.
  • Resuscitation with blood products frequently is required, but it is crucial to provide volume carefully because renal function may be severely compromised.
  • Dialysis is required if anuria persists for 12+ hours or for severe hyperkalemia (>6.5mEq/L) Some patients may benefit from plasmapheresis, but full renal recovery is not certain.

Classical illicit recreational drugs like cocaine, ecstacy, and marajuana are sometimes difficult for teens to acquire. As a result, many are turning to their parents medicine cabinets as a source for recreational drugs.

[From the website drugabuse.gov] In 2008, 15.4 percent of 12th-graders reported using a prescription drug nonmedically within the past year. This category includes:

• amphetamines
• sedatives/barbiturates
• tranquilizers
• opiates other than heroin
  • hydrocodone, oxycodone

When adolescent patient presents to the ED, consider the possibility of a poly-pharmacy overdose. Always query parents about the presence of OTC and Rx medications in their home, and what is within reach of their kids.

While sedatives and analgesics are concerning, be alert for overdoses of more mundane medications like beta blockers and calcium-channel blockers which often pose a much more lethal threat. Consider overdose in adolescent patients with:

• GI or respiratory complaints
• Altered mental status (combative or somnolent)
• Abnormal vital signs
• History of depression or psychiatric illness

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Monitoring the Future Study: Trends in Prevalence of Various Drugs for 8th-Graders, 10th-Graders, and 12th-Graders

2005-2008 (in percent)*

	8th-Graders				10th-Graders				12th-Graders
	2005	2006	2007	2008	2005	2006	2007	2008	2005	2006	2007	2008
Any Illicit Drug Use
Lifetime Past Year Past Month	21.4 15.5   8.5	20.9 14.8   8.1	[19.0] [13.2]   7.4	19.6 14.1   7.6	38.2 29.8 17.3	36.1 28.7 16.8	35.6 28.1 16.9	34.1 26.9 15.8	50.4 38.4 23.1	48.2 36.5 21.5	46.8 35.9 21.9	47.4 36.6 22.3

Full chart available by clicking link in references.

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• With regard to following commands, the NIH Stroke Scale (NIHSS) assesses this level of consciousness in part 1C by asking the patient to do the following two things:

          1.  "Close your eyes and now open them."

          2.  "Make a fist and now open it."

• You may repeat the command no more than twice in order to avoid the bias of coaching the patient.

• It's fine to provide some prompting by performing the task yourself while asking the patient to do the same.
   
• This component of the NIHSS is scored as follows:

          0 = performs both tasks correctly.
          1 = performs one task corectly.
          2 = performs neither task correctly.

Mechanical Ventilation of the Obstetric Patient

• In previous pearls, we have discussed ventilatory settings to avoid excessive volumes and limit plateau pressures to < 30 cm H₂O
• Importantly, these settings have not be extensively evaluated in pregnant patients
• Some important pearls when ventilating the pregnant patient:
  • Avoid hyperventilation, as this adversely affects uterine blood flow
  • Optimize oxygenation to ensure adequate fetal oxygen delivery (us 100% F_iO₂)
  • In the presence of adequate oxygenation, P_aCO_s values <= 60 mm Hg do not appear to be detrimental to the fetus

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Nitroprusside-Friend or Foe?

Nitroprusside is a direct venous and arteriolar vasodilator and is very effective at lowering blood pressure. It has been used for the treatment of hypertensive emergencies for many years and most of are comfortable with using it.

The problems with the drug:

• May cause precipitous drops in BP and lead to overshoot of BP target goals
• The drug is inactivated by light so the infusion bag and tubing must be protected  from light
• Frequently causes nausea, vomiting, and muscle twitching
• Most importantly, cyanide (CN) is released from nitroprusside in a dose-dependent fashion and may cause clinical toxicity
• Good alternatives exist: Fenoldopam as an example. Just as effective and without any of these side effects.

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Patients with catastrophic cardiovascular conditions often manifest with JVD + hypotension. The DDx for this combination is therefore critical to know:

1. large LV MI
2. right ventricular MI
3. cardiac tamponade
4. tension PTX
5. massive PE
6. acute mitral regurgitation
7. acute aortic regurgitation

You can make a diagnosis clinically among these 7 entities by:

1. Listening to the lungs
2. Listening for murmurs
3. Getting an ECG.

Of course if you have bedside U/S, it becomes even easier. ECG is almost always diagnostic with either the large LV MI or RV MI. Wet lungs found in large LV MI, acute MR, and acute AR. Murmur found in MR (systolic) and AR (diastolic).

Hamate Fractures:

• Typically the result of a direct blow, and the hook of the hamate is commonly fractured in batters or golfers.
• Like the scaphoid, the hook is at risk for avascular necrosis and non-union of the hook.
• Fractures of the body are more common than fracture of the hook of the hamate
• On exam you will typically find:
  • Increased pain with axial loading of ring (4th) and little finger (5th) metacarpals
  • Most patients complain of pain and tenderness on ulnar side of palm or on the dorsoulnar aspect of the wrist.
  • Pain also aggravated by grasping items.
• Diagnosis
  • Fracture often missed on routine AP & lateral films
  • Most fractures can be diagnosed by plain films if you as for the "Carpal tunnel view"
  • CT scan can also be used to see the fracture
• Treatment
  • Good Immobilization will often prevent avascular necrosis and allow early healing
    • Volar splint or short arm cast are usually adequate.
  • Excision of the hook of the hamate provides similar results as an ORIF in those that have non-union or displaced fractures.
  • Refer to orthopedics

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Serotonin is a neurotransmitter that has central and peripheral effects. It regulates the secretion of ADH from the hypothalamus and also controls the chemoreceptive trigger zone (CTZ) which induces emesis. Here are a list of medications categorized by the way they affect serotonin. Remember, any combination of these agonists could precipitate serotonin syndrome:

Enhance 5-HT synthesis: L-tryptophan

Direct HT agonists: Ergots, metoclopramide, sumatriptan, buspirone

Increase 5-HT release: amphetamines, cocaine, dextromethorphan, MDMA, L-dopa

Inhibit 5-HT breakdown: MAOIs, Linezolid

Inhibit 5-HT re-uptake: SSRIs (paxil), amphetamines, carbamazapine, tramadol, TCAs, citalopram, trazodone, lamotrigine, meperidine

 

• The first part of the NIH Stroke Scale assesses level of consciousness in 3 parts, 1A, 1B, and 1C.

• Part 1B assesses orientation by having the patient tell the examiner (1) their age and (2) the month.

• Part 1B is scored in the following manner:

          -- Answers both questions correctly = 0

          -- Answers one of the two questions correctly = 1

          -- Answers neither question correctly = 2

• If patient is unable to speak due to being intubated, having orotracheal trauma, dysarthria, a language barrier, or any other reason other than truly being aphasic, a score of 1 should be assigned.

Parainfluenza viruses (types 1, 2, 3) account for more than 65% of all cases. The different serotypes have seasonal patterns, with type 1 and 2 occuring in the autumn and being the most common pathogens associated with croup while type 3 is more frequent in the spring and summer and is associated with pneumonia and bronchiolitis.

Infections are rarely associated with high fever and usually last 4 to 5 days. There are no distinctive laboratory abnormalities, and diagnosis is generally made clinically.  Chest and neck xray may demonstrate a “steeple sign” from narrowing of the subglottic region.  Viral cultures and immunofluorescent rapid antigen identification can be obtained from respiratory secretions.  Specific antiviral therapy is not available. Aerosolized epinephrine can be given to severely affected, hospitalized patients to decrease airway obstruction.  Parental (>0.3mg/kg) and oral ((0.15mg/kg) dexamethasone have been demonstrated to lessen the severity and duration of symptoms and hospitalization in patients with moderate to severe croup.  
 

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Critical Illness-Related Corticosteroid Insufficiency (CIRCI)

• CIRCI is defined as inadequate corticosteroid activity for the severity of illness of a patient
• CIRCI arises due to steroid tissue resistance and inadequate circulating levels of free cortisol
• Hypotension refractory to fluids and requirement of vasopressors is the primary manifestation of CIRCI
• In contrast to chronic adrenal insufficiency, hyponatremia and hyperkalemia are uncommon
• Consider CIRCI in all critically ill patients requiring vasopressor support

So, which critically ill patients do you treat with steroids?  Current literature suggests the indications for steroid treatment include vasopressor dependent septic shock and persistent ARDS despite supportive therapy and lung protective ventilation.  A patient who requires only an hour or two of a vasopressor while being fluid resuscitated is unlikely to benefit.  An accepted dosing schedule is hydrocortisone 50 mg IV every 6 hours.

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Documentation of the Chest Pain Patient

Chest pain is a high risk entity in emergency medicine. And since many patients we see with chest pain are eventually discharged, we should consider what our charts should look like should we discharge a patient who has a missed life-threatening diagnosis. In other words, what would an attorney look for?

Considerations for the chart:

• Consider documenting some type of medical decision making in the chart. What were you thinking? Why didn't you think the patient needed cardiac enzymes, a CT, or admission? The chart should support your decision to send the patient home.
• Document a thorough history...enough said
• Document risk factors for the deadliy causes of chest pain (ACS, PE, dissection, etc.). This is frequently missing on charts.
• Consider documenting important, pertinent negative "chest pain physical exam findings," such as a normal leg exam (frequently missing on missed PE charts), no murmurs, equal pulses. Comments like this in the chart prove that you were thinking about a differential diagnosis. A question to ask yourself is, "Does my physical exam look like I was searching for the bad players of chest pain?"