UMEM Educational Pearls

While breastfeeding is still the preferred source of infant nutrition by the AAP, a little-known fact is that breastfeeding may expose the nursing infant to environmental pollutants to which they might not normally be exposed.  If you have a mother that appears ill due to exposure to any of these agents, don't forget to have the infant examined as well for signs of intoxication.

• Breastmilk can contain approximately 20% of the maternal toxin load, which can produce more severe effects in the infant due to the vastly different dose/weight ratio
• Toxin load is usually due to the lipid solubility of agents
• Formulas are safe due to the nature of their fat sources;  cows usually have a much lower exposure rate to pollutants, and those that are ingested are much more dilute due to the volume of milk produced in comparison to a human female;  also, with non-cows'-milk formulas, the lipid components are usually plant-derived and thus also with a lower risk of exposure
• Common offending agents include:  DDT, PCBs, Dioxin, hexachlorobenzene, Halothane, carbon disulfide, nicotine, lead, methylmercury, Heptachlor, Chlordane, and tetrachloroethylene

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• Should patients continue to seize even after administration of a benzodiazepine (i.e. lorazepam, diazepam) plus phenytoin, additional high-dose phenytoin should first be considered.

• While the standard loading dose for IV phenytoin is 10-20 mg/kg, it is recomended that up to 30 mg/kg of phenytoin be given for refractory status epilepticus prior to using another anti-epileptic, such as phenobarbital, pentobarbital infusion, or propofol infusion.

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Severe mitral regurgitation (MR) after MI, accompanied by cardiogenic shock carries a poor prognosis.

Severe MR in many cases is due to infarction of the posterior papillary muscle, and in these cases the area of infarction tends to be less extensive than in those with MR due to severe left ventricular dysfunction. 

Take Home Pearl:

The presence of pulmonary edema and/or cardiogenic shock in a patient with an inferior STEMI should prompt consideration for acute MR due to papilary muscle rupture. Get an echo as fast as you can to confirm or r/o the diagnosis. Treatment is afterload reduction, inotropic support, and urgent surgical repair. 

Don't forget about pheochromocytoma as a possible cause of severe hypertension...especially in those patients that are recalcitrant to "normal" medications. A few important points:
1. Incidence may be as high as 0.2% of patients with hypertension...sounds very rare, but statistically we'll all see some during our career.
2. Mortality may be as high as 10% if unrecognized; but if recognized and treated, excellent prognosis.
3. Suspect this in patients with intermittent episodes of flushing, palpitations, diaphoresis, headaches, and hypertension.
4. Treatment with beta blockers alone (including labetalol) may induce unopposed alpha-activity and worsen BP.
5. Treat with nitroprusside or phentolamine (an alpha blocker). Phentolamine is 5 mg IV, can be repeated every 5-10min as needed.
6. After phentolamine is given, there may be reflex tachycardia. NOW you can add beta blockers.

The most important thing is to keep the diagnosis in mind. It's out there! But you'll miss 100% of the diagnoses you don't consider.

AC Joint Dislocations

The acromioclavicular (AC) Joint is commonly injured when a person falls onto their shoulder.

The AC Joint consists of three ligaments:

• acromioclavicular ligament (AC)
• coracoacromial ligament (CA)
• coracoclavicular ligament (CC)

Injuries to this joint are classified as Type I – Type VI and involve sprain or tears of the AC or CC ligaments

• Type I – Is a sprain of the joint without complete tear of either the AC or CC ligament
• Type II – Does not show significant elevation of the lateral end of the clavicle but is due to a tear of the AC ligament.
• Type III – Results from tears in the AC and CC ligament. Noted by > 5 mm elevation of the AC joint.
• Types IV – VI : are associated with complications of a Type III injury.

• although newborn screening for PKU has been routine throughout North America since the 1960's, it is not routine in undeveloped countries (beware immigrants, foreign visitors)
• PKU is caused by phenylalanine hydroxylase (PAH) deficiency which catalyzes the conversion of phenylalanine to tyrosine
• neonates with PKU typically show no physical signs of hyperphenylalaninemia
• children with untreated PKU have impaired brain development with poor brain growth, seizures, behavior problems, and severe mental retardation
• affected individuals exude a pungent, musty odor due to elevated phenylalanine levels which also causes skin conditions such as eczema
• because there is absent tyrosine production with reduced tyrosinase, the hair and skin are very lightly pigmented
• early diagnosis and management with a low-phenylalanine diet eliminates these complications; and once treated, affected children are healthy and do not require hosopitalizations

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Aripiprazole (Abilify): a new atypical antipsychotic partially agonizes D2 and serotonin receptors though its compelte mechanism is not known. Used in schizophrenia, in overdose you may see the following symptoms (from a retrospective study done over 4 years worth of calls to a PCC):

• Somnolence 89 (56%)
• Tachycardia 32 (20%, heart rate 102-186)
• Nausea/vomiting 29 (18%)
• Dystonic reactions 21 (13%)

The study was with over 255 patients. Though QT prolongation is listed, it is not common with this medication.

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• Indications and timing of head CT scans in patients with a first-time seizure (FTS), who have returned to a normal baseline, are controversial.

• The range of such patients with abnormal head CT's is broad, at 3 to 41%.
   
• A retrospective study found that 22% of patients with a FTS and normal neurologic exams, had an abnormal head CT (Hennemen, et al).

• Another study found that in patients with suspected alcohol withdrawal seizures, 58% had an abnormal head CT, 16% of which were clinically significant findings (Earnest, et al).

• When feasible, neuroimaging of the brains of patients presenting with a FTS should be performed in the emergency department.  Deferred outpatient neuroimaging may be used when reliable follow-up is ensured. (Level B Recommendation).

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Mechanically Ventilated ED Patients and Secretion Mobilization

• As more of our intubated ED patients remain in the ED for longer periods of time, some may develop problems with secretion management (thick/copious amounts of sputum).
• The preferred method of secretion mobilization is heated humidification.
• If you anticipate the duration of intubation to be at least 96 hours, have your respiratory therapist set up a heated humidifier.
• Commonly, clinicians and nurses will instill 5-10 ml of isotonic saline to thin secretions.
• The use of saline to thin secretions is unsupported by the literature and carries a small risk of dislodging the bacterial laden biofilm that covers the endotracheal tube.

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Herpes Encephalitis-When to Consider

Herpes encephalitis is a potential lethal condition with high morbidity. Obviously our job in the ED is to rule-out bacterial meningits. So, when should we consider the diagnosis of herpes encephalitis?

• High wbc in the CSF with a negative gram stain
• Lymphcytic predominance in the CSF
• Altered patient and abnormal CSF
• And, just about any of the softer "rule-out aseptic meningitis" patients

Although no great guidelines exist, consider ordering a herpes PCR when sending studies on the "rule-out meningitis" patient. What about emperically treating a patient with Acyclovir? Again, no great data. Consider treating with 10 mg/kg IV q 8 hours for patients with abnormal CSF (in addition to the Ceftriaxone/Vanc, etc.) if you are worried about them, if they are altered (or encephalopathic), and if the CSF is abnormal (elevated wbc) with a negative gram stain. Acyclovir can always be discontinued when the PCR returns negative.

Systemic lupus erythematosus produces a significant predisposition towards premature atherosclerosis. Although the exact mechanism for what causes this is uncertain, premature CAD is at least partially (or largely) caused by systemic inflammation, which can produce endothelial damage and initiates the process of atherogenesis.

The literature indicates that there is a 9X increased risk of CAD in patients with lupus, and the risk increases to 50X higher in women 35-44 years of age! In general, patients with lupus develop their first MI 20 years earlier than age-matched non-lupus counterparts. 

[Mattu A, Petrini J, Swencki S, et al. Premature atherosclerosis and acute coronary syndrome in systemic lupus erythematosus. Am J Emerg Med 2005;23:696-703.]

Beware of your online contributions, they can come back to hurt you in legal settings. You must remember that there is a digital trail of everything you post online. Discovery rules vary state to state. It is best to practice save surfing. What you may perceive as paranoia is really just good practice.

The following guidelines apply to:

• Email
• Online chats: google chat, IRC, AOL AIM, MSN
• Social networks: Facebook, Mypage, Medical networking pages, etc
• Any online medium, forum, discussion site

General guidelines

• Do not reference any patient cases with dates (regardless of hipaa identifiers)
• Do not provide any medical advice for specific cases online
  • Add a disclaimer for general advice (see the disclaimers for these pearls as example)
• Do not discuss any potential or ongoing legal cases with peers PERIOD, especially electronic methods with a record.
• Do not document ethically questionable behavior online
  • ie: "that time in vegas when you got sooooo drunk"

Assume that whenever you hit send, your message will be available to a plaintiff attorney who will twist it to suit his/her needs. The only potential exception is direct email communication to your personal legal counsel. Please verify that local laws protect this form of communication before making an assumption of privacy.

[This pearl is a review of published general recommendations on privacy practices and should not be interpreted as, or replace competent legal advice.]

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• Although rare, it is a serious life threatening entity of pediatric emergency medicine
• Must be in the differential of those with signs of increased intracranial pressure or focal deficit and hx of sinusitis, mastoiditis or cyanotic congenital heart disease.
• Investigation and diagnosis primarily with CT scan
• CSF studies demonstrate sterile fluid with elevated protein, and mildly elevated WBC
• Antibiotic coverage should be broad Naficillin/Vanc + Ceftriaxone + Metronidazole, until speciation and susceptibilities obtained from surgical specimen
• Steroids reserved only in cases of imminent herniation
• Controversy exists over prophylactic anticonvulsants
• Mortality recently <10% attributed to early diagnosis and appropriate antibiotic coverage.

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You've probably long been taught that Sickle Cell Trait is an irrelevant piece of the PMH, unless you are a genetic counselor.  Well, thanks to Dr. Rolnick and a literature search, I (and now you) know that that is incorrect.

Though Sickle Cell Trait (SCT) does not cause exactly the same pathologies as Sickle Cell Disease (SCD), there are believed to be a variety of RBC abnormalities associated with HgbS (such as measurably lower RBC deformability, and low levels of sickling under extreme heat and exercise conditions) which contribute to increased exercise-related sudden death.  In one NEJM study of all deaths among 2 million (MILLION) military recruits over a 4 year period, the relative risk of otherwise unexplained sudden death for black recruits with HgbAS vs. black recruits without HgbS was 27.6 (p<0.001), and 39.8 (p<0.001) for all recruits (HgbAS vs. no HgbS).

I must say that this topic is not controversy-free, however, I should also note that my search for "Sickle Cell Trait and Sudden Death" turned up quite a few articles directed at plaintiff's attorneys. 

The take-home point is that SCT is likely not a benign condition, and you must be cautious in telling patients that it is.  Again, this phenomenon is best described in patients undergoing extreme physical exertion, but hopefully this will change how you think about SCT.

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• The classic triad of fever, meningismus (stiff neck), and altered mental status only occurs in 44% of cases of acute bacterial meningitis (ABM).

• Headache is a much more common presenting complaint with ABM.

• The sensitivity and specificity of Kernig and Brudzinski signs are suboptimal, making their presence or absence of little diagnostic value.

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Daptomycin and MRSA

• Several new antibiotics are approved for the treatment of infections due to MRSA: linezolid, daptomycin, and tigecycline.
• Although most are familiar with linezolid, it seems that both daptomycin and tigecycline are being used more frequently.
• A few pearls on daptomycin:
  • administered IV once daily
  • dose needs to be adjusted in patients with renal failure
  • exerts its effect through a calcium-dependent binding to the bacterial membrane resulting in cell death
• Importantly, daptomycin is inactivated by pulmonary surfactant and therefore should not be given in patients with suspected MRSA pneumonia.

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Elderly patients are at higher risk of barotrauma with positive pressure ventilation (e.g. CPAP, BiPAP, and especially after intubation) because of decreased vital capacity and lung compliance. Watch those plateau pressures closely!

If an elderly patient develops hypotension within minutes of endotracheal intubation, always consider tension PTX (and don't forget about hypovolemia, as we've discussed before).

     Most hand sanitizers contain ethanol, while some contain isopropyl alcohol. The concentration of alcohol in these products varies from 45% to 95%, with the most commonly used products containing 62%.  How much would a 15 kg child have to ingest to obtain a blood alcohol concentration of 100 mg/dL (or 0.1%)?

     Assuming a volume of distribution of 0.6 L/kg and 100% bioavailability, only 15-20 mL is required to produce this toxic level.  That is equivalent to 3-4 teaspoons or approximately 8-10 “squirts” of hand sanitizer!

The following symptoms of phenytoin toxicity typically present initially, once plasma concentrations reach the listed levels below:

• Nystagmus (on lateral gaze, at 20 mcg/mL)
• Ataxia (at 30 mcg/mL)
• Dysarthria and lethargy (at over 40 mcg/mL)

Other associated symptoms include tremor, hyper-reflexia, nausea, and vomiting.

Complications of Resuscitation

• CPR, defibrillation, endotracheal intubation, and cannulation of peripheral and central veins are common procedures during resuscitation of cardiac arrest patients
• Although not obvious immediately, complications from these procedures can develop and manifest several hours after successful return of spontaneous circulation
• Not surprisingly, the most common complications are rib and sternal fractures
• Additional complications to recall include:
  • tracheal mucosal lesions (almost 20%)
  • retropharyngeal bleeding
  • liver/spleen injuries
  • rhabdomyolysis (post-defibrillation)
  • air embolism (central venous access)
  • gastric rupture (very rare; due to continuous air insufflation into the stomach)

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