UMEM Educational Pearls

• The majority of those afflicted with bell palsy experience neurapraxia or a local nerve conduction block, which usually predicts a prompt and full recovery.  80% to 90% of Bell Palsy patients experience recovery without any noticeable disfigurement within 6 weeks to 3 months.

• Some Bell Palsy patients experience axonotmesis, disruption of the axons, which increases their risk of an incomplete recovery.

• One is at higher risk of developing sequelae in the following scenarios: 

          --  Age greater than 60 years

          --  Diabetes

          --  Decreased taste or salivary flow on the affected side

          --  Complete paralysis

• Common post-Bell Palsy sequelae that you may see clinically include:

          --  Synkinesis - abnormal contracture of facial muscles with smiling or

               closing eyes; may cause slight chin movement with blinking, eye closure

               with smiling, contracture around mouth with blinking.

          --  Crocodile tears - lacrimation while eating.

          --  Hemifacial muscle spasms - tonic contractures of affected side of face, 

               rare, often seen during times of fatigue, stress, or while sleeping.

 

NICE-SUGAR and Glucose Control in the Critically Ill

• Hypergycemia is associated with increased morbidity and mortality in hetergeneous populations of critically ill patients.
• Over the past few years there has been great interest in aggressively controlling glucose through the use of continuous insulin infusions.
• Results of recent trials and meta-analyses, however, question the benefit of tight glucose control and highlight the marked increase in severe hypoglycemia rates.
• Recently, the results of the NICE-SUGAR study were published, the largest trial to date (6000 patients)evaluating intensive vs. conventional glucose control in the critically ill.
• Investigators found an INCREASED mortality among adults randomized to intensive glucose control
• Given the lack of benefit, potential harm, risks of severe hypoglycemia, and resource utilization, intensive glucose control should not be a therapy routinely implemented in the ED.

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Transvenous pacing

We had a very interesting case the other day in the ED. A 60 yo male presented after a syncopal episode. After arriving in the ED he was awake (with a pulse of 50) but then became asystolic, without warning. He then woke up and 10 minutes later became asystolic again. He then woke up again. So, we decided to put in a transvenous pacer.

Some considerations when putting in a transvenous pacer:

• You need to use a small cordis (e.g. 6 French)
• Right IJ is the preferred approach so that when the balloon is inflated you will have easy entry into the right heart
• You will need transvenous pacing wires, obviously.
• Once you open the wire kit, you will find 2 adaptors that fit over the two ports of the pacemaker wire. Snap them on, then these connect to the ventricular leads of the pacer box-ignore the atrial side. Here is the key: the POSITIVE lead connects to the PROXIMAL port on the pacemaker (PROXIMAL=POSITIVE) and the distal lead connects to the distal port.
• Turn the pacer on then set rate to 80 or so. And start the mAmp at 20.
• Advance the wire through the Cordis and after the wire has cleared the Cordis, blow up the balloon with a syringe and lock it.
• The key is in determining capture: While the patient is on the monitor, and as the wire is being slowly advanced, look for pacer spikes and the development of wide complexes. This indicates electrical capture. Be sure to check for mechanical capture by checking the patient's pulse.
• After capture, the mAmps can be turned down to the capture point.
• DON'T forget that transcutaneous pacing is clearly the first option as this is easy to initiate.

 

Post-cardiac arrest care of patients is a hot topic in the resuscitation literature and is gaining increasing attention. We've discussed induced hypothermia; another important intervention is to apply the concepts of goal-directed therapy for these patients. The goal is to optimize MAP (> 65 mm Hg) and provide IVF and pressors when needed. Look for more literature on this in the coming year. Also, for more on this topic, be sure to listen to the June EM Cast, in which Dr. Evie Marcolini will be discussing post-cardiac arrest care of patients.

Elbow Dislocation

• The elbow is the second most commonly dislocated joint after the shoulder in adults. 
• It is the most commonly dislocated joint in children.
• 90% of all elbow dislocation are posterior.  A considerable amount of force is required to dislocate the elbow so be highly suspicous for associated fractures of the radial head, or coronoid process of the ulna. 
• The combination of a radial head fracture, coronoid process fracture and elbow dislocation is known as the terrible elbow.
• Anterior elbow dislocations can be associated with injuries to the brachial artery, median and ulnar nerves. 

Quick clinical clues that the elbow is dislocated:

• Posterior dislocation typically will have a prominent olecranon process, the arm is flexed at the elbow, and the forearm will appear shortened.
• Anterior dislocation typically present with the arm in extension and the forearm will appear elongated.

• Bell Palsy is the most common cause of unilateral facial weakness.

• It is caused by edema and ischemia causing compression of the facial nerve (cranial nerve seven).

• While Bell Palsy is by definition an idiopathic facial palsy, the etiology is often infact discovered and attributed to conditions such as Lyme Disease, Herpes Simplex Virus, and HIV.

• Classic symptoms of Bell Palsy include:

          -- acute onset of unilateral upper and lower facial paralysis (over 48 hr. period)

          -- posterior auricular pain

          -- decreased tearing

          -- hyperacusis (due to stapedius muscle weakness)

          -- taste disturbances

• Bell Palsy is a diagnosis of exclusion.  If the facial paralysis is isolated to the lower face, if there is associated contralateral weakness, and/or if there is diplopia, a central cause for the symptoms, rather than Bell Palsy, must be strongly considered.

Platelet Transfusions and the Critically Ill

• Current literature suggests that platelets are given too frequently and inappropriately
• Recall that approximately 50% of platelet transfusions fail to increase counts
• In addition, bacterial contamination of units is a special concern, with sepsis occurring 10x more frequently than with PRBCs
• In general, platelet transfusions in nonbleeding patients can be withheld untl the count reaches 10 x 10³/mm³
• A transfusion trigger of 50 x 10³/mm³ should be used for invasive procedures

Multiple Myeloma + Altered Mental Status=Hyperviscosity Syndrome

Although the differential diagnosis of altered mental status is quite extensive, a patient with multiple myeloma and altered mental status should prompt consideration of one important, albeit not too common, condition.....hyperviscosity syndrome.

Some important pearls:

• This syndrome occurs when excessive amounts of protein (immunoglobulin) are secreted by myeloma (plasma) cells.
• Excessive circulating protein leads to sludging and ischemia in lung and brain tissue, lesding to hypoxia and altered mental status, respectively.
• You will only pick up this diagnosis by thinking about it, so multiple myeloma + altered mental status = hyperviscosity syndrome
• Treatment is with IVF and plasmapheresis (heme onc consult)
• And don't forget common stuff, like stroke, subdural hematomas, meningitis, etc.

There are multiple causes of electrocardiographic ST-segment elevation which are well-known to mimic STEMI and often are a cause of misdiagnosis of STEMI.  These are:

• Benign early repolarization
• Pericarditis
• Left ventricular aneurysm
• Brugada syndrome
• Left ventricular hypertrophy
• Left bundle branch block
• Paced rhythms
• Hyperkalemia

Whenever there is doubt regarding whether you are dealing with a STEMI or a mimic, look for reciprocal ST-depression. Most of these will not produce ST-depression (LVH, LBBB, Pacers, and hyperkalemia WILL). The other key intervention is to perform serial ECGs and look for evolving changes, which strongly points to the presence of a true STEMI.

Trimallelor Fractures:

Bimallelor fracture involve both the medial mallelous of the tibia and the distal fibula.  The third malleloi is the posterior tip of the articular surface of the tibia. Can result in instability in the posterior and lateral directions along with external rotation.

Some indications for Open Reduction Internal Fixation when the posterior mallelous is fractured are:

• > 25% of the posterior articular surface being involved.
• Fractures that allow posterior subluxation of the talus
• Fractures that are displaced more than 2 mm
• Fractures that can not be reduced satisfactorily.

 

Classic presentation:  breastfeeding failure with umbilical stump and gastrointestinal bleeding by postnatal day 7.  Oozing from circumcision, venipuncture, and heel sticks is also common.  Beware bleeding into the scalp or intracranial space.

Due to essential vitamin K deficiency which exists at birth as the fetus receives little vitamin K from the uteroplacental circulation.  It is responsible for impaired neonatal clotting function (deficiency of factors II, VII, IX, and X).

Prevented by a single intramuscular dose of 1mg vitamin K in the first few hours following delivery.

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Your patient presents unresponsive with an empty bottle of alprazolam (Xanax). You order a urine and blood toxicology screen. The blood comes back negative for benzodiazepines but the urine test is positive. How do you interpret this result?

• The benzodiazepine toxicology screen typically looks for oxazepam. If it is present in sufficient quantity, the test will be positive.
• Three benzodiazepines are detected by this test: oxazepam (Serax), diazepam (Valium), and chlordiazepoxide (Librium); [diazepam and chlordiazepoxide are metabolized to oxazepam].
• Other benzodiazepines such as clonazepam, lorazepam, and alprazolam will generally test negative unless there is cross-reactivity or large quantity.
• The urine and blood immunoassays are exactly the same. For this patient, there was probably a low overall quantity of alprazolam in the blood but a concentrated amount in the urine. Therefore, the positive urine and negative blood.

• Neurologic complications affect 30 to 60% of allograft organ transplant recipients.
   
• Many of these complications are related to immunosuppresant medication neurotoxicity.
   
• Calcineurin inhibitors such as tacrolimus (FK-506 or Fujimycin) and cyclosporin are classically associated with the following neurologic disorders:
  • Cranial Nerve Palsy:  Tacrolimus toxicity can cause reversible  internuclear ophthalmoplegia.
  • Movement Disorders:  Tacrolimus and cyclosporin often cause tremor, which can be further compounded by the development of asterixis should the patient also have significant renal or hepatic insufficiency.
  • Visual Abnormalities:  Cortical blindness, visual disturbances, hallucinations, retinal toxicity, and optic neuropathies have all been attributed to calcineurin inhibitor toxicity.  Opsoclonus (rapid, involuntary, uncontrolled, multivectorial eye movements) has specifically been associated with cyclosporin neurotoxicity. 
     

• Neurotoxicity related to immunosuppresant drug therapy is most likely to occur early after transplantation and during a rejection episodes, times at which medication doses are typically at their highest.  Dose adjustment often results in resolution of symptoms.
   
• Be sure to check drug levels of immunosuppresant medications, particularly when a transplant patient presents with a neurologic disorders.

 

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Risk of PE/DVT in patients with microalbuminuria....another risk factor to consider??

Microalbuminuria (protein in the urine) is a known risk factor for arterial thromboembolic disease, and recent studies suggest that arterial thromboembolism and venous thromboembolism (VTE) have common risk factors. In a prospective community-based cohort study in the Netherlands, researchers enrolled 8574 adults (age range, 28-75) who were followed for 9 years. People with insulin-dependent diabetes or pregnancy were excluded.

Of 129 identified episodes of VTE, roughly half were deep venous
thromboses, and half were pulmonary embolisms. The annual VTE incidence
rate was 0.12% in patients with normoalbuminuria (<30 mg/24 hours)
versus 0.40% in those with microalbuminuria. After adjustment for known VTE
risk factors and other factors (including hypertension, known coronary arterydisease, and elevated C-reactive protein level), the hazard ratio for
VTE in people who had microalbuminuria, compared with those who had
normoalbuminuria, was 2.0.

Comment: The importance of this study is not in the clinical value of
usingmicroalbuminuria as a marker for VTE risk, because the absolute risk
conferred by microalbuminuria is very low, and the therapeutic
implicationsare unclear. Rather, this study suggests that microalbuminuria is a
marker for endothelial dysfunction in both arterial and venous systems, and it
suggests a mechanism for how statins interact with the endothelium to
prevent VTE (JW Cardiol Mar 29 2009).

So, does this affect us as emergency physician? Unclear. But it may very well mean that we might be dealing with a new risk factor that needs to be taken into consideration when evaluating patients with chest pain or SOB. Obviously, we might need medical records to find this risk factor...can you imagine asking a patient if they have microalbuminuria?

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Ultrasound of the IVC for Volume Assessment

• In a recent pearl, I discussed that a 15% variation in IVC collapsibility could be used as a marker of hypovolemia
• As a follow up and since % variation is sometimes difficult to calculate at the bedside, consider the following numbers:
  • The normal diameter of the IVC is 1.6 - 1.75 cm
  • Patients with hypovolemia typically have an IVC diameter < 0.8 - 1.0 cm
  • In general, the IVC diameter should increase 1 mm for every 100 ml of isotonic fluid

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Cardiocerebral resuscitation is a new approach to CPR which has demonstrated improvements in survival and neurological recovery. The main focus is early defibrillation and good compressions with an early dose of EPI, but with a strong de-emphasis on early intubation or bagging. Most patients with sudden cardiac arrest don't need early oxygenation anyway, and the previous emphasis on ventilations only serves to take time and effort away from the important chest compressions. Intubation is deferred for 6-8 minutes after the cardiac arrest in favor of simple passive oxygenation with a non-rebreather.

The bottom line is that when facing a patient in cardiac arrest, the traditional mantra in emergency medicine of "A-B-C" needs to now be changed to emphasize the "C" coming first, second, and third.

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Knee Dislocations:

Are relatively rare injuries, but can result in loss of the limb if missed.  Patients will sometimes say they dislocated their knee when they actually mean their patella, so a good history where they describe what their knee looked like, and what they were doing at the time will help differentiated the two.

Some signs that you are dealing with a spontanously reduced knee dislocation are:

• Varus or valgus instability in full extension of the knee is suggestive of a grossly unstable knee
• Pain out of proportion to injury
• Absent or decreased pulse

The loss of limb is due to unrecognized injury to the popiteal artery which as be estimated to occur 7-45% of the time. 

• Normal pulses and a normal capillary refill does NOT rule out as significant vascular injury. 
• Arteriograms are no longer mandatory in all cases, but it is generally recommended that you perform an ankle-brachial index and get a vascular duplex scan of the popiteal artery to exclude dissections, tears, aneurysms and psuedo-anuerysms that can all occur as a result of the dislocation.

If you would like to see some videos of knee injuries in the making follow this link www.csmfoundation.org/Educational_Lower_Extremity.html

• Recently, a study was published which compared adverse drug events in patients who had received either fomepizole or ethanol for ethylene glycol or methanol poisoning.
• Importantly, this is the first trial which has compared these events head to head.
• Retrospectively, 172 charts over a 9 year period were reviewed. Toxicologists identified at least 1 ADR in 74 of 130 ethanol treated cases (57%) versus 5 of 42 fomepizole treated cases (12%).
• Severe ADRs occurred in 20% of ethanol treated patients vs 5% fomepizole treated patients.
• This adds further data to support the use of choosing fomepizole over alcohol for treatment of toxic alcohol poisonings

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• Akathisia is an adverse effect sometimes associated with the administration of medications such as neuroleptic anti-psychotics (i.e. chlorpromazine (Thorazine); haloperidol (Haldol); ziprazidone (Geodon)) and dopamine-blocking anti-emetics (i.e. metoclopramide (Reglan); prochlorperazine (Compazine)).

• This unpleasant symptom complex consists of restlessness and agitation, the severity of which correlates with the dose of the causative agent.

• Treatment classically consists of stopping or decreasing the dose of the causative agent and administering diphenhydramine (Benadryl).

• Benzodiazepines, beta blockers, and the antihistamine cyproheptadine have also been used with success.

• The following instrument, a modified version of the Prince Henry Hospital Scale of Akathisia, can be used to clinically assess for akathisia in a standardized fashion:

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Subjective Findings Do you feel restless or the urge to move especially in th legs? 0=No (none)     1=Some times (mild)    2=Most times (mod)    3=All times (severe) Objective Findings Observe patient for 2 full minutes on stopwatch: For how much time were they off their stretcher? 0=None   1=1 to 30 sec.     2=31 to 60 secs.     3=61 to 108 secs.    4=Whole time For how much time do they have purposeless or semi-purposeless leg or foot movement? 0=None   1=1 to 30 sec.     2=31 to 60 secs.     3=61 to 108 secs.    4=Whole time Diagnosis requires an elevation of 1 grade or more in the reported severity of subjective findings between the baseline and follow-up assessment (i.e. from none to mild, mild to mod.), with objective corroboration.

 

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New Perspectives on Clostridium difficile

• In the past 5 years, C.difficile infection rates have doubled and the overall disease severity appears to be worsening.
• Particularly concerning is the increase in community acquired infections in young patients without antibiotic or nosocomial exposure.
• These epidemiologic changes are likely due to a new strain of C.difficile characterized by increased virulence and quinolone resistance.
• Importantly, the efficacy of metronidazole has waned in recent years.  In fact, > 25% of patients with moderate to severe disease do not respond to metronidazole therapy.
• As a result, vancomycin has become first-line therapy for any critically ill patient with C.difficile.

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