• May is Stroke Awareness Month;  Health care provider and patient education about how to prevent stroke is at least as important as treating it with cutting-edge therapies.
• Studies have shown that up to 80% of strokes could be prevented through recognition and management of risk factors, lifestyle changes, and compliance with recurrent stroke prevention treatments.
• Even in the emergency department, the opportunity to educate patients about the following stroke risk factors should be seized when possible:

              --  Hypertension                        

              --  Diabetes

              --  Atrial Fibrillation

              --  Hypercholesterolemia

              --  Physical Inactivity

              --  Tobacco Use

              --  Alcohol Use

              --  Obesity

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PRBC Transfusions in Neurocritical Care

• Historically, neurocritical care textbooks have favored a more liberal PRBC transfusion strategy, as the brain is very sensitive to decreases in oxygen delivery.
• Despite these recommendations, limited studies have failed to show a mortality benefit to PRBC transfusion in critically ill patients with neurologic illness.
• Postulated reasons for the lack of morbidity or mortality benefit center around the injured brain's response to attempts to increase oxygen delivery through transfusion.
  • TBI: PET studies have shown an overall lower level of metabolic activity along with a lower oxygen extraction and loss of autoregulation
  • SAH: transfusion may increase the risk of vasospasm in SAH and worsen flow
• Although the evidence is not overwhelming, current recommendations from SCCM-Eastern Society for the Surgery of Trauma recommend a restrictive PRBC transfusion threshold (Hgb < 7 gm/dL) even in neurocritical care patients.

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Some considerations in the patient with a penetrating vascular injury (gunshot, stab):

• Obtain ankle-brachial index on all patients and document
• An ABI <0.9 indicates the need to perform an arterial study
• Traditional approach to penetrating extremity injury has been to perform angiography
• Recent (good) studies have shown that CTA of the involved extremity is just as good if not better than angiography, and a lot of centers have moved to CTA
• Obtain vascular surgery consultation if there is any concern for an arterial injury. Never hurts to err on the side of caution. 

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The most likely considerations for a regular, narrow complex tachycardia are sinus tachycardia (ST), atrial flutter with 2:1 conduction, and supraventricular tachycardia (SVT, a generic terms that encompasses a few remaining rhythms originating above the ventricle). Atrial flutter is diagnosed when one sees atrial beats at a rate of 250-350/minute.

The distinction between ST and SVT can be difficult at very rapid rates. Here are a few clues that may help in this distinction:
1. Generally the maximal sinus rate that a patient produces will be 220-age. That means that a 20 year old can possibly have a ST up to 200 beats/min, but a 70 year old can only have a ST has fast as 150 beats/min. Rates that exceed that simple formula are extremely unlikely to be ST.
2. If the rate varies with respiration, with positional changes, with relaxation, or with fluid administration, these all favor ST.
3. If the rate reduces slowly, it favors ST. SVT, on the other hand, tends to "break" suddenly.
4. SVT generally will either have no P-waves visible or there may be P-waves just after the QRS complexes. These are referred to as retrograde Ps.
5. History, history, history. Is there a reason for tachycardia, for example a history consistent with dehydration or anxiety? That favors ST. If the patient reports palpitations or other symptoms that were of abrupt onset, that favors SVT.
6. Valsalva maneuvers may gently slow down ST but will either not affect SVT or will abruptly break the SVT....SVT shouldn't gently slow down.

Conservative Treatment of Back Pain:

Muscle relaxanats and benzodiazipnes are often used in the non-operative management of sciatica and non-specific low back pain.  In fact, a 2003 Cochrane review concluded that muslce relaxanats were effective in the management of non-specific low back pain. However, a recent analysis of randomized trials reported little efficacy or only  minor benefits with the use of benzodiazapines in treatment of low back pain.

A recent prospective, randomized, placebo-controlled, double-blinded trial conducted in Germany that enrolled a total of 60 patients found that the use of diazepam was equivilant to placebo in the reduction of distance of referred pain at day 7 of treatment.  Diazepam was also noted on average to increase the length of stay of those patients hospitalized by 2 days (median hospital days of 8 for placebo versus 10 for diazepam), and the probablility of pain reduction on a visual analog scale by more than 50% was twice as high in the placebo group (p< 0.0015).  Placebo reduced the patients pain more than diazepam.

Though the sample size was small; this study should really make one reevaluate the use of diazepam in the treatment of back pain.  Early movement and discouraging bed rest have been associated with decreased back pain, so one mechanism by which  benzodiazepines may make things work is by causing enough sedation to prevent early movement.

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It is likely that you will be asked questions about the huge recall by McNeil..

It stems from complaints received of black particles found in the pediatric liquid formulation, which are manufactured at one facility in Fort Washington, PA.  The FDA inspected the plant and found inadequate quality standard testing and facilities. Either there were potential bacteria in one of the raw products (which did not make it to the final product), or the final concentrations were stronger than specified.

McNeil recalled forty-three formulations of pediatric liquid tylenol, zyrtec, motrin and benadryl. Generic versions are unaffected.

Complete recall information:

www.mcneilproductrecall.com

For more information and links:

http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm210442.htm

• May is National Stroke Awareness Month.  It is an important opportunity to foster education of the public and health care providers, which is a key component of stroke management.  Awareness hastens recognition and optimized management.

• Clinicians can take part in public health initiatives by educating patients about the following signs and symptoms of acute stroke:

              1.  Walk; Is their balance off?
              2.  Talk; Is their speech slurred or face droopy?
              3.  Reach; Is one side weak or numb?
              4.  See; Is their vision all or partly lost?
              5.  Feel; Is their headache severe?

• This month, public education campaigns, through mechanisms such as billboard and mass transit advertisement, will be heightened, and can be used as additional tools for patient education.

In the ICU, diabetes insipidus (DI) develops in patients with pituitary surgery, brain trauma, intracranial hypertension and brain death.  Criteria include the following:

• urine output >200 ml/hr or 3 ml/kg/hr
• urine osmolality <150 mOsm/kg
• serum sodium>145 mEq/L
• urine specific gravity<1.005

In the ICU, patients are typically unable to consume free water to compensate for urinary losses, and dehydration, hypotension and hypernatremia occur.  Clinical signs may not appear until sodium levels surpass 155-160 mEq/L or serum osmolality surpsses 330 mOsm/kg. 

Symptoms include confusion, lethargy, coma, seizures and cerebral shrinkage associated with subdural or intraparenchymal hemorrhage. 

Treatment includes

• controlling polyuria with vasopressin (antidiuretic, vasoconstrictive effects) and desmopressin (DDAVP - antidiuretic effect)
• calculate and replace free water loss
• TBW deficit (L) = body weight (kg) x 0.6 x (Na-140)/Na
• monitor and replace urine losses hourly (using gastric access if possible)
• monitor serum sodium and adjust therapy every 4 hours closely monitor for hyperglycemia and treat to prevent osmotic diuresis due to glucosuria

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Slight revisions have been made in what is considered to be normal QRS duration.
In children < 4yo, a normal QRS duration is < 90ms.
In children 4-16yo, a normal QRS duration is < 100ms.
Above the age of 16, a normal QRS duration is < 110m.

Consider these numbers when evaluating patients for aberrant conduction (e.g. toxicologic reasons as well) and when defining conduction blocks.

Reference:
Surawicz B, Childers R, Deal BJ, et al. AHA/ACCF/HRS Recommendations for the standardized interpretation of the electrocardiogram, Part III: Intraventricular conduction disturbances. A scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. J Am Coll Cardiol 2009;53(11):976-981.

• seizure disorder occuring in infants and children <1 year of age
• mostly occur between ages 4-8 months
• classic spasm is sudden, simultaneous flexion of the head and trunk with felxion and adduction of the extremities (salaam attack Blitz-krampf)
• occurs in clusters of diminishing severity
• initiated or aggrevated by transition from sleep to wakefulness or emotions
• EEG demonstrates hypsarrhythmia: high-voltage, irregular, slow waves occuring out of synch with multiple foci
• most resolve over time without therapy, but most children have some level of mental retardation or other seizure disorder

• The terms pseudotumor cerebri, benign intracranial hypertension, and idiopathic intracranial hypertension (IIH), are all synonymous terms which describe a condition of elevated intracranial pressure (ICP), but the latter is the preferred term of use.
• IIH almost ubiquitously presents with a generalized headache and papilledema (i.e. fundoscopic examination imperative!).  Visual disturbance and non-specific symptoms such as dizziness may also be present.
• Elevated ICP and papilledema are clinical emergencies until the presence or absence of an intracranial mass is confirmed. 
• The following conditions must be met in order to diagnose IIH:

1. Non-focal neurologic examination (except for 6th nerve palsy in some cases)
2. Elevated opening pressure on lumbar puncture, > 20 to 25 mmH2O (perform only after risk for herniation assessed!)
3. Normal cytologic and chemical cerebrospinal fluid analysis
4. Small, symmetric brain ventricles on neuroimaging
5. Exclusion of other sources of IH such as venous sinus thromboses by obtaining an MRI/venographic study of the head

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PRBC Transfusion Threshold for Patients with Cardiac Disease

• As previously discussed, the PRBC transfusion threshold for the general population of critically ill patients is a Hgb < 7 gm/dL.
• Traditional teaching has been to maintain a Hgb > 10 gm/dL in patients with a history of CAD.
• This threshold stems from a 1950s cohort of Jehovah's Witness patients, and several observational studies, that demonstrated increased perioperative mortality in patients whose Hgb was < 10 gm/dL.
• Recent studies, however, have found that patients with a history of CAD tolerate lower Hgb levels without increases in morbidity or mortality.  In fact, current cardiovascular surgery guidelines favor a conservative Hgb threshold (7 gm/dL) for patients with CAD.
• Importantly, the Hgb threshold of < 7 gm/dL for PRBC transfusion applies to patients with simply a history of CAD and not to patients with evidence of an acute coronary syndrome (STEMI, NSTEMI, unstable angina).  Guidelines continue to recommend a Hgb > 10 gm/dL for patients with ACS.

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A review of the PERC rule...

The "PERC Rule"  is used to assess a patient's risk for probability of PE in the emergency department. It involves evaluating the presence or absence of 8 clinical criteria to arrive at a pretest probability.  And remember, this rule is supposed to be used for patients with really low pretest probability where you weren't concerned about PE to begin with. Some experts claim that "PERC negative" on the chart proves you considered PE in the differential diagnosis. But the test isn't designed to be used on EVERY patient as a means to rule out PE. Only use if you thought about the disease in a low risk patient and didn't plan on getting a d-dimer or further testing. 

The criteria are (all must be YES):

age < 50 years

heart rate less than 100 beats per minute

room air oxygen saturations 95% or greater

no prior deep venous thrombosis [DVT] or PE

no recent trauma or surgery (4 weeks)

no hemoptysis

no exogenous estrogen

no clinical signs suggestive of DVT (Unilateral leg swelling on visual inspection

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Three common herbal supplements are reported to be associated with clinically significant hypokalemia: aloe vera, gossypol (used as a male contraceptive), and licorice.

Another popular herbal supplement is reported to be associated with clinically significant hyperkalemia: oleander.

Always ask your cardiac patients (especially those on digoxin) if they are taking any of these herbal supplements!


[Tachjian A, Maria V, Jahangir A. Use of herbal products and potential interactions in patients with cardiovascular diseases. J Am Coll Cardiol 2010;55:515-525.]

Carpal Tunnel Syndrome (CTS):

• A compressive neuropathy of the median nerve at the wrist as it travels through the carpal tunnel. 
• Median nerve is bound on three sides by carpal bones and anteriorly by the transverse carpal ligament.  Surgical repair typically consists of cutting this ligament to allow decompression of the nerve.
• The neuropathy results in:
  • parasethesia of the thumb, index and middle fingers
  • weaknesss of the thumb and thenar muscles.
• NO physical exam test has great senstivity or specificity for CTS. The two most common are:
  • Phalen's test: hyperflexion of the wrist. Need to hold for 60 seconds.  Sensitivity ~68% and Specificity ~73%
  • Tinel Sign: tapping over cubital tunnel to produce parasthesia along the median nerve. Sensitivity ~50% and Specificity ~77%.
• Increased risk in those patients with:
  • Diabetes
  • Rheumatoid arthritis
  • hypothyroidism
  • amyloidosis

• also known as acute cerebellitis of childhood
• most commonly affects children 2-6 years old
• about 50%  have a history of recent URI or viral GI illness
• abrupt onset of ataxia which may be mild to severe, and findings usually include hypotonia, tremor, horizontal nystagmus, and dysarthria
• child often is irritable with nausa/vomiting
• sensory exam and DTR's are normal
• CT and MRI are normal
• CSF usually demonstrates an increase in WBC, with a predemonance of lymphocytes
• 90% recover without any specific therapy in 6-8 weeks (steroids are not indicated).

• The Brachial Plexus is a bundle of nerve roots arising from C5, C6, C7, C8, and T1.
• Brachial plexus injuries (BPI) result from severe traction forces on the limb.
• The most common sources of BPI are motorcycle accidents and birth palsy (i.e. Erb or Duchenne Palsy) affecting the upper part of the plexus (C5, C6) and causing shoulder and biceps muscle weakness.
• Injury to C7 >>> wrist weakness.
• Injury to C8 and T1 >>>  forearm and intrinsic hand muscle weakness.
• Injury to stellate ganglion or cervical sympathetic trunk >>> Horner's Syndrome.
• MRI of the upper extremity is the standard imaging modality used to make the diagnosis.

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It is true, 1/3 of Americans are obese.  There is conflicting evidence regarding the mortality risk of obesity (defined as BMI>30 kg/m²) in critically ill patients. 

It has been shown that abdominal fat has greater consequences than peripheral obesity, and based on this, a recent study has utilized the sagittal abdominal diameter (SAD) in ICU patients to show that abdominal obesity (as differentiated from BMI) poses an independent risk of death.  The SAD detects visceral fat, which has been shown to have metabolic and immune health consequences, including the following:

-incidence and severity of certain infections is higher

-excess adipocytes are associated with elevated levels of proinflammatory factors that favor insulin resistance, diabetes, dyslipidemia and hypertension, all of which lead to microcirculatory dysfunction

-rates of required renal replacement therapy and abdominal compartment syndrome correlate to increased SAD

-there is also a trend toward a longer length of ventilator weaning

See you at the gym.

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Secondary Hypertension...say what?

We obviously see tons of patients in the ED with hypertension, and we are very comfortable with both symptomatic and asymptomatic presentations. Most of these patients have essential or primary hypertension. Some patients, however, may have secondary hypertension (i.e. something is causing it). Although we will refer patients to a primary care physician for further management and workup it is worth discussing when to suspect other diagnoses as the cause of the hypertension. Is it out job necessarily to diagnose these conditions in the ED? No. 

Causes of secondary hypertension to consider:

• Obstructive sleep apnea
• Renal disease
• Renal artery stenosis (think older person with HTN and abdominal bruit)
• Coarctation (young person with HTN-ever wonder why pediatricians palpate upper and lower extremity pulses in the office?)
• Cushing's disease (excess cortisol-patient may have new diabetes, have abdominal striae, and easy bruising)
• Hyperaldosteronism (due to an adrenal tumor)...think about if a patient comes to the ED and is repeatedly hypokalemic and hypertensive
• Pheochromocytoma (episodes of flushing, hypertension, palpitations, etc.)
• Hypothyroidism (not myxedema coma or storm)...commonly causes elevated diastolic BP. 
• Hyperthyroidism 

Consider the ABCDE mnemonic:

A-Accuracy (is it really htn?), Apnea, Aldosteronism

B-Bruits, Bad Kidneys

C-Catecholamines, Coarctation, Cushing's 

D-Drugs, Diet

E-Endocrine

Aren't you glad you didn't do a Medicine residency???

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