Classic Cerebrospinal Fluid Characteristics

• Bacterial Meningitis >> Milky CSF with increased protein, decreased glucose, high WBC's, few RBC's, mildly increased opening pressure, normal % gamma globulin.

• Viral Meningitis >> Cloudy CSF with increased protein, normal glucose, increased WBC's (lymphocyte predominant), no RBC's, normal opening pressure, normal % gamma globulin.

• Herpes Simplex Encephalitis >>  Cloudy CSF with increased protein, normal glucose, increased WBC's (lymphocyte predominant), few RBC's, increased opening pressure, normal % gamma globulin.

• Subarachnoid Hemorrhage >> Yellow CSF with increased protein, normal glucose, few WBC's, inumerable RBC's, mildly increased opening pressure, normal % gamma globulin.

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Increasing literature demonstrates ICU delirium is bad. Delirium in mechanically ventilated patients is an independent predictor for long-term cognitive defects (e.g., managing money, following detailed instructions, reading maps, and developing dementia). The cited study found 80% of patients with ICU delirium had cognitive dysfunction at three months, and 70% had residual dysfunction at one year (33% had severe dysfunction).

You must be aggressive to prevent delirium:

-         Implement daily assessment tools (e.g., CAM-ICU)

-         Daily awakening and spontaneous breathing trials

-         Early patient mobilization

-         Aggressive pharmacological treatment of delirium

-         For more information: www.icudelirium.org

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Magnesium is considered a mainstay of treatment of prolonged QT syndrome leading to torsade de pointe, including those cases caused by drugs. The exact mechanism of action is unknown, though it is thought to stabilize the myocardium. Interestingly, magnesium infusions will not necessarily change the heart rate or QT interval on ECG.

The dose is 2 g IV followed by an infusion (similar to treatment of eclampsia/preeclampsia). The bolus should be given slowly if the patient is relatively stable, but can be pushed over 1 minute in a patient with ongoing torsade that is not responding to electricity.
 

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Epidural compression syndrome encompasses spinal cord compression, cauda equina syndrome, & conus medullaris syndrome.

Causes include:

1. massive midline disc herniation (most commonly), usually at the L4 to L5 level.
2. tumor
3. epidural abscess
4. spinal canal hematoma.

Measurement of a post-void bladder residual volume tests for the presence of urinary retention with overflow incontinence (a common, though late finding) (sensitivity of 90%, specificity of 95%).  Large post-void residual volumes (>100 mL) indicate a denervated bladder with resultant overflow incontinence and suggest significant neurologic compromise. The probability of cauda equina syndrome in patients without urinary retention is approximately 1 in 10,000.

Use this in your daily practice!!

The administration of glucocorticoids can minimize ongoing neurologic damage from compression & edema until definitive therapy can be initiated. The optimal initial dose and duration of therapy is controversial, with a recommended dose range of dexamethasone anywhere from 10 to 100 mg intravenously. Consider traditional dosing (dexamethasone 10 mg)  for those with minimal neurologic dysfunction, & reserve the higher dose  (dexamethasone 100 mg) for patients with profound or rapidly progressive symptoms, such as paraparesis or paraplegia.

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Colic

• excessive, unexplained paroxysms of crying in an otherwise well-nourished normal infant
• lasts >3 hours/day, and occurs >3 days/week...ughh!
• usually occurs at the same time of the day or evening
• usually resistant to most attempts to quell it
• infant may have excess flatus and draw legs up during episodes (but don't change formulas)
• beings in first week of life and ends by 4 months of age

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• A broadly-accepted, standard definition of concussion, also known as mild traumatic brain injury (MTBI), does not exist and is still a work in progress. 

• Historically, the diagnosis of concussion has been based upon the presence of three findings:  (1) Loss of consciousness (usually for less than 30 seconds), (2) post-traumatic amnesia (usually for less than 24 hours), and (3) a Glascow Coma Scale score of 13 to 15.                  

• Today, many experts question whether loss of consciousness is inherently associated with concussion, but rather that any change in consciousness, such as that related to amnesia, suffices.  

• Patients with the following symptoms should be screened, typically with head CT, for more serious injury:  loss of/deteriorating consciousness, persistent headache, dizziness, vomiting, disorientation/confusion, seizure, and unequal pupil size.

• Treatment of concussion consists of monitoring and rest.  Symptoms usually spontaneously resolve within 3 weeks, but may persist for up to around 3 months.

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Ketamine for RSI in Hemodynamically Unstable ED Patients

• Recall that ketamine acts as a sympathomimetic resulting in increases in heart rate, blood pressure, and ultimately cardiac output.
• Because of its rapid transport across the blood-brain barrier, its sympathomimetic effects, and lack of significant adverse effects, ketamine is recommended by many organizations as a first line agent for RSI in unstable patients.
• Important contraindications to ketamine include an acute coronary syndrome, aortic dissection, and acute heart failure.
• Take Home Point: Consider using ketamine the next time you need to intubate a hypotensive, critically ill ED patient.

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ECG early repolarization (or sometimes referred to as "benign early repolarization" or BER) is a common finding on ECGs, especially in young patients. It is a common "confounding" pattern when trying to identify STEMI. Here are some pearls that help in distinguishing BER vs. true STEMI. Remember at the outset, though, nothing in medicine is 100%....and that getting old ECGs or getting serial ECGs can be incredibly helpful.

1. BER is ONLY allowed to have STE that is concave upwards. If you ever see STE that is convex upwards (like a tombstone) or horizontal, it MUST be a STEMI.
2. BER should not have ST-segment depression, except maybe in aVR and V1. If there is ST depression in any of the other 10 leads, it is almost definitely a STEMI.
3. If you see STE in the inferior leads, compare the STE in lead II vs. lead III. If the STE in lead III is greater than the STE in lead II, it rules out BER....gotta be STEMI.
4. STE from BER is usually maximal in the mid precordial leads. You CAN have STE in the inferior leads with BER also, but you really shouldn't have STE isolated to the inferior leads. In other words, BER can have (1) STE in the precordial leads alone, or (2) STE in the precordial + inferior leads, but it should never have STE isolated to the inferior leads, and also the STE in the precordial leads should be more prominent than the STE in the inferior leads.
5. BER should usually not have STE > 5 mm. However, I've seen some occasional exceptions when the patient has large voltage QRS complexes.

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Subungual Hematomas:

• Subungual hematomas are collections of blood that form under the nail with injuries to the distal phalanx. 
• Those that are < 25% of the nailbed can be drained via trephination and heal well.
• Up to 94%  of subungual hematomas that are are associated with a distal phalanx fracture have a nailed laceration.  It is commonly taught this hematomas should have the nail removed and the nailbed repaired.  However  studies from the 1990's have shown that as long as the nail is attached to the nailbed or paronychia and is not displaced; trephination alone can be done to achieve similar outcomes.

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You may already love ondansetron, but consider using it ORALLY followed by PO hydration in children with vomiting.

• Improve ORT success
• Decrease IV placements
• Decrease admission rates
• NOT cause any significant difference in the number of missed serious alternate diagnoses 

The size of the study that showed this: N of just under 35,000.

But don't skimp on dosing.  The dose is 0.1 - 0.15mg/kg, and you don't reach a max until 8mg.  To put this in perspective, a scrawny 115lb (about 53kg) middle school tennis player would get 8mg, an initial dose often reserved for chemo patients in the adult ED.

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Emerging evidence supports using intravenous fat emulsion (Intralipid) therapy for various drug overdoses, particularly those that are lipophilic.  Within seconds to minutes of administration, toxic cardiovascular effects are reversed, including return of spontaneous circulation in cardiac arrest patients.  Central nervous system effects also tend to improve.

Lipophilic agents for which there has been success include:

• Calcium channel blockers (verapamil, diltiazem, amlodipine)
• Beta blockers
• Bupropion
• Quetiapine
• Lamotrigine
• Sertraline
• TCA's
• Diphenhydramine

Bottom line: Consider intralipid therapy early in the course of a hemodynamically unstable patient with suspected overdose.  Give a bolus of 1.5 mL/kg of 20% lipid emulsion over 1-2 minutes.

• When emergently managing stroke, be vigilant about anticipating potential complications and recognizing them with expediency, regardless of whether the patient receives tPA therapy.

• The following are associated with greater risk of developing cerebral edema and/or post-tPA hemorrhage:

              ---  High NIH Stroke Scale scores.

              ---  Large areas of infarct.

              ---  Cerebellar infarcts.

              ---  Extended time to tPA administration.

              ---  Previous stroke.

              ---  Older age.
 

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Heliox is a mixture of oxygen and helium resulting in a gas less dense than air. In asthma, airway resistance causes turbulent airflow which increases the work of breathing. Heliox reduces airway resistance by increasing laminar airflow. 

Benefits: 

Better lung mechanics

Improved nebulizer delivery

Few known side-effects/complications

Drawbacks:

Expensive

Contraindicated in hypoxemic patients.

Paucity of large prospective randomized trials.

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Previous pearls have described tips for smart and safe documentation of typical ED complaints such as chest pain.  Properly assessing and documenting orthopedic complaints is likewise very important.  No evaluation or chart is complete if it does not include include the following 7 components:

The joint above

The joint below

Motor

Sensory

Vascular

Skin

Compartments

The joint above/below is important in cases of shoulder and hip pain actually being radicular pain (from the neck and back respectively).  Also, hip pain from trauma may be due to a femur fracture for example.

For motor and sensory evaluation, test the most distal isolated innervation of a particular nerve (L5 - great toe dorsiflexion for example).

Note distal pulses and check ABIs for injuries with potential subtle vascular  findings.

Note intact skin especially in cases where the joint will be covered by a splint.

Note "soft" compartments especially in cases of forearm and lower leg fractures.

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EMS in Maryland has REMOVED endotracheal medication administration from its ADULT protocols

This is due to:

• Unclear efficacy and need for a much higher dosage
• Ability to administer drugs via IO route
• Decrease reliance on intubation
  • chest compressions only CPR
  • BiPAP use
• Note this does not pertain to PEDIATRICS, where it is still included in its protocols

• Emergency department evaluation of diplopia is largely based on a comprehensive history and should always include the following questioning with documented findings:

1. Does the diplopia resolve by covering one eye?  (Differentiates binocular diplopia (disappears when one eye covered; most common) from monocular diplopia (persists with one eye covered; usually related to a focal, ocular problem).
2. Does the degree of diplopia change with direction of gaze and/or head position?  (Determines whether deficit related to cranial nerve innervation, helps localize associated paretic muscle).
3. Is the diplopia horizontal (i.e. two objects side by side) or vertical (i.e. two objects one on top of the other)?  (Horizontal diplopia suggests cranial nerve III or VI deficit (i.e. lateral gaze function); vertical diplopia suggests cranial nerve IV deficit (i.e. elevator or depressor gaze function).
4. Is there associated pain? (Suggests possible foreign body or extraocular muscle entrapment).
5. Was there associated trauma? (Blow-out fractures can be associated with diplopia).
6. Is there associated weakness, headache, confusion, or dizziness?  (Imaging usually indicated to rule out intracranial processes such as stroke or increased intracranial pressure).

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Respiratory Distress in the Ventilated ED Patient

• In the ventilated patient with respiratory distress, evaluation of peak and plateau pressures can help to identify the cause.
• Isolated increases in peak pressure suggest increased resistance to airflow and should prompt consideration of the following:
  • kinked or twisted ET tube
  • patient biting ET tube
  • obstructed ET tube
  • bronchospasm
  • lower airway obstruction
• Increases in plateau pressure suggest decreased pulmonary compliance and should prompt consideration of the following:
  • unilateral intubation
  • pneumothorax
  • pulmonary edema
  • worsening pneumonia
  • abdominal HTN/compartment syndrome

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Chest pain is a very high risk chief complaint in emergency medicine. And although we are told by the experts what we should write on the chart, we often struggle with finding time to do so.

Given that we can't pick up every MI, dissection, and PE, what things can we document in the chart that prove we are thorough and that we have thought about a diagnosis? And how can we document a "protective thought process" without taking too much time to do so?

Consider documenting these on your chest pain charts:

• Risk factors present/absent for ACS/MI, dissection, and PE
• Good family history
• Don't be sloppy with the history and physical exam. Doesn't matter if they help or not. Attorneys will have a field day discussing how sloppy the history and exam was. If the history and physical examination are bad get out the checkbook. 
• Pulses in upper and lower extremity
• Any leg swelling?
• Any diastolic murmur?

Documenting key pertinent negative comments in the chart shows that you are thinking (and considering MI, Aortic Dissection, and PE), and whenever this can be shown in a chart, there is more ammunition for the defense attorney. 

The traditional teaching has always been to use supplemental high-flow oxygen routinely for patients with acute MI. I recall specifically being taught in residency by EM, IM, and cardiology attendings that every acute MI patient should receive a minimum of 6 liters of supplemental oxygen via nasal canula, if not 100% oxygen, regardless of the initial pulse oximetry.

Mounting evidence, however, is demonstrating that the use of supplemental oxygen in patients that are "normoxic" (i.e. the production of "hyperoxia") is detrimental. Studies are demonstrating that there is no improvement in mortality or prevention of dysrhythmias; and in fact a trend towards increased mortality when patients are hyperoxic. This detrimental effect is likely the result of coronary vasoconstriction which occurs through several different mechanisms, all induced by hyperoxia. Oxygen, it turns out, is a vasoactive substance.

The takeaway point is very simple: if an AMI patient is not hypoxic, don't go overboard with the supplemental oxygen!

[Moradkhan R, Sinoway LI. Revisiting the role of oxygen therapy in cardiac patients. J Am Coll Cardiol 2010;56:1013-1016.]

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