Here is my last typical week of writing medicine notes/questions in preparation for teaching…this is one week of doing this for decades…this is how I memorize. …and these few pgs r [are] not quite finished–but close…I call it Density. It dcres’s T time it takes to reread. If you can read the notes and are not a physician you should be…T [the] world wd [would] be a better place. You will notice that mny [many] Density [D] terms r [are] defined like what you see here in brackets as you read…so you learn it as you read it…easy! :)

CV EMERGENCIES

Which of the following is incorrect about CV [cardiovascular] disorders?

a.  One in three American adults has one or more types of CV disease.

b.  Chest pain is the second most common ED presentation in adults.

c.  A GI cocktail cannot distinguish between cardiac or gastrointestinal cause of chest pain.

d.  Shortness of breath requires the most medical decision making of any chief complaint.

e.  Missed thomboembolism does not meet the current standard for missed AMI at time of ED discharge.

Answer:  E.  Missed thromboembolism.  T currnt EM goal is to reduce T likelihd f missing serious causes f CP to ≤1-2% or having a 30-d adverse event.  DUE TO RAPID , SENSITIVE CARDIAC BIOMARKER RESULTS, & othr factors THIS GOAL Z ACHIEVABLE FOR AMI (ACS).**     [AHN Ed6 CH6 CP]/T7 p  ]  dwight page number

Pts w/either CP of cardiac etiol or GI etiol may respond to either or both a GI cocktail and/or NTG; T response to either does nt prove T etiol.

In general, a response to NTG is slower for esophageal than cardiac pain. (but as isolat’d data by itslf, it z NOT clin reliabl to r/o a cardiac etiol)!

**DUE TO CONT’D PROBS W/T COMPLEXITY DXGNSNG PE, & OCCULT PRSNTATNS THIS GOAL Z STILL VRY PROBLEMATC FR MNY HOSPS, & ESP NURSING HOMES.

PE z call’d-T SILENT KILLER: LESS THAN HALF R DX’D PRIOR TO DEATH! 

REF:  Pineda LA, Hathwar VS, Grant BJ. Clinical suspicion of fatal pulmonary embolism. Chest 2001;120:791–795.

>50% f all Dxed PE n T US ocr n pts bth n hosps or nursing homes.

REF:  Heit JA, O’Fallon WM, Petterson TM, Lohse CM, Silverstein MD, Mohr DN, Melton LJ 3rd. Relative impact of risk factors for deep vein thrombosis and pulmonary embolism: a population-based study. Arch Intern Med 2002;162:1245–1248.

IN US–POSIBLY >1 million people hv a PE per yr, w/100,000 -> 200,000 being fatal.

REF:  Anderson FA Jr, Wheeler HB, Goldberg RJ, Hosmer DW, Patwardhan NA, Jovanovic B, Forcier A, Dalen JE. A population-based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism. The Worcester DVT Study. Arch Intern Med 1991;151:933–938

REF:  Dalen JE, Alpert JS. Natural history of pulmonary embolism. Prog Cardiovasc Dis 1975;17:257–270.

A 2007 report est’d >12 million pts (31% of all D/Cd frm US hosps) r @ rsk f PE!

REF:  Anderson FA Jr, Zayaruzny M, Heit JA, Fidan D, Cohen AT. Estimated annual numbers of US acute-care hospital patients at risk for venous thromboembolism. Am J Hematol 2007;82:777–782.

Ref:  Reasons for Emergency Room Use Among U.S. Adults Aged 18–64: National Health Interview Survey, 2013 and 2014 by Renee M. Gindi, Ph.D., M.P.H.; Lindsey I. Black, M.P.H.; and Robin A. Cohen, Ph.D., Division of Health Interview Statistics; National Health Statistic Reports, Number 90, February 2016 [Ths report lists T %age f adults 18–64 yrs using an ED n T past 12 mos & T reasons fr their mst recent ED visit].

Ths Ref notes:  20% f adults present to US EDs annuly & ths hs nt chng’d n T last decade:

T 3 1° reasons categoriz’d per pt responses fr those ED visits were list’d in a hierachical system f 3 choices:

Cat 1 (Seriousness of T med prob):  Summary:  Health provider advis’d pt to go to ED/tht care needed requir’d a hospital; pts MC arriv’d by ambulance

Cat 2 (Doctors office/clinic was not open

Cat 3 (Lack of access to other providers (list’d as: “either ER was closest provider, pt didn’t have another place to go, pt gets most of their care in ER”)

KEY CONCEPT:  If u look at this data & allow it to affect you, your clinical ED practice will include bias tht will lead to ncrs’d clinical errors.

“Labelling” pts is a dangerous practice, but it is an omnipresent issue.  It is a REAL PROBLEM; it z possibly 1 f T greatst medical probs of ALL!

Best practice: b a professional:

My definitn of a professional–one who does do not bring their emotions to work.  They manage T pt’s illness.

Look at this:

CP (for myocardial ishemia) is list’d as T 2nd MC CC in pts presenting to T ED (AH-Nuss Ed CH6 Ed 6 p 414): howevr, “CP equivalents” i.e., all conditions tht might also represent myocard ischem r list’d as T MC ED presentatn:  [these include ALL SXS of serious presentatns of CP: such Dxs nclude–PE, Ao dissctn, all forms of ACS [acute coronary syndromes] [includes sxs of all myocardial ischemia, UA, NSTEMI, STEMI, pericarditis, TPX, Pneumonia, esoph rupture]

Bcaus thes r most cmn presntatns/oftn highly fatal, u shd plan on a lot f testing re these topics!  

ACS: T7 def: CP <24 h;

Lists 3 presntatns:

UA: Nl or nonspecif EKG & no elevtn f biomarker.

NSTEMI: not true ST elev criteria but hv [+] biomarker

STEMI: hv bth clin signif ST elevatn + elvat’d biomarker.

REINFORCMNT–T MC ED presntatn bar none:  a sx or sxs of potentially serious chest pain, i.e., “CP equivalent” is T MC ED presentatn!

NCLUDES many nonspecific sxs: neck pain, back pain; SOB [shortness of breath] see below**

**SOB:  is used here as “Density terminololgy” but I advise against evr writing it n a chart.  

Write fully:  shortness of breath; “SOB” cn & hs bn used to hv [-] connotatn in litigation.  

**More compelling reasons:  SOB as a CC z a highly lethal presntatn & requires T most MDM of any serious CC!  

**SOB IS OFTN RAPIDLY FATAL [SOB SHD B TRIAG’D AS HIGHEST ACUITY UNTIL PROVIDER DECIDES OTHERWISE]

COMN SERIOUS ERRORS w/PE*

Lack of risk factor(s): does not r/o PE

Not recognizing atypical presntatn(s):  syncope in elderly

Failure to recognize PE in pts w/o convincing alternative Dx (esp if + for dyspnea, tachyp, or pleuritic CP)

Mis’d findings on plain CXR:  elevat’d hemidiaph present in 49% (others are atelectais or signs of pneumonia, ie., problematic mimickers of other disz jst bcaus thy r nonspecifc)

Fail to understand tht PE cn recur in fully anticoag pt (esp cancer pts)

*Also: Not using PERC/D-Dimer to avoid unnec cost/radiatn

At time f ED presntatn: PE as a dx z bth COMPLICATED/oftn rapidly fatal [both pt/provider delays]

PERC (Pul embolism r/o criteria) rule 8 elements [all must b true] to be TRUE PERC NEG:

Age 50 yrs or less

HR <100 bpm

RA sat >94%

No Hx DVT/PE

No recent trauma/surgery

No hemoptysis

No exog estrogen

Clinically no sign(s) of DVT

If none r present, in pt w/low to low-mod pretest probablitiy, T risk f PE or death ~same as of pts w/neg V/Q or CT angio

Kline JA, Mitchell AM, Kabrhel C, et al. Clinical Criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost. 2004;2(8):1247-1255”: pts w/PERC score of 0 & low-low-mod probabliity (risk <15%) using gestalt or clin decin rule do NOT need further test for PE!  [Kline et al study cited on pp 2366 and 2379 AHN ed6].

Ruling out DVT: 2-23 out of 100 pts with DVT will b missed w/a DVT Wells score alone: thus, this test must be used in conjunction with another test: e.g., Doppler US.

10 elements in newer 2 level Wells score; it is 96% sensitive in cancer pts so it would miss only 4%; but is too nonspecific (specificity 26%) to confirm DVT in cancer pts though.  

[Back in 1986:  T3 cited: up to 12% had PE: of those w/neg V/Q plus low pretest clin prob for PE]  

D-Dimer only useful if negative with low pretest clin prob pt: excludes DVT/PE.

Multipl subtle presentatns

Mandatory Intervntns for PE:

Risk-stratify all pts [lw,mod, hi probabil] bs’d on Hx, Exam, prelim lab

Aticoag pts w/hi clin suspicn fr PE/DVT bfor dfinitiv studies bcause signif Tx delays caus signif neg outcomes

Admin thrombolytic fr PE w/hemodynam instabli (BP <90mmHg).

Q:  What is the most specific sign of pulmonary embolims when viewing a CT or CT angiogram

A:  Visualization of Intraluminal clot is the only truly specific sign of PE.  Cut-off signs and areas of vessel narrowing cn be due to local inflammatn (ex: pneumonia), or tumor compressn-regional decreased pul bld flow cn also b seen w/atelectasis.  However, atelectasis is also associat’d w/pul embolism.

Q:  True or false, finding McConnell’s sign using a transthoracic apical 4-chamber US view is highly specific for Pulmonary embolism.

A:  This is false.  This finding is a nonspecific finding found in both acute and chronic causes of pulmonary HTN of many causes: COPD, vasculitis, chronic LV dysfunctn that leads to pul HTN, acute severe bronchospasm, and acute PTX [pneumothorax]

On bedside transthoracic ultrasound for PE: using T apical 4 chamber view:  acute dilatn f T RV chamber w/hypokinesis f T RV free wall w/RV apical sparing is McConnell’s sign; At times the apex may even b hyperkinetic.  This finding ma b  seen w/PE (frm acute RV/pul a. HTN); Howevr, McConnell’s Sign IS NOT specific for acute RV strain 2° to PE!  

Various causes f acute or chronic cor pulmonale produce RV strain (& thus) ths sign: 

REF:  J Emerg Med. 2015 Sep;49(3):301-4. doi: 10.1016/j.jemermed.2014.12.089. Epub 2015 May 16.

McConnell’s Sign is Not Specific for Pulmonary Embolism: Case Report and Review of the Literature.  

This is a case report of a woman w/chronic pul HTN [ 2° to lupus & chronic COPD] w/no PE on CT angio & neg venous dopplers for DVT; She presnt’d to ED w/cough, SOB, leg swelling.  Only pos finding ws a minor nonspecifc elevatn f D-dimer.

Which of the following has not been found to increase T D-Dimer?

a.  Increased age especially ≥80 yrs

b.  Acute aortic syndromes including aortic dissection

c.  Cardiac arrest and after cardiopulmonary resuscitation

d. Severe infection or circulatory shock state

e.  Pneumonia but not ARDS

Answer:  E.  Any severe infection (e.g., pneumonia, and ARDS are both assocd w/an increased D-Dimer.  D-Dimer

T specificity f this test = poor!  All of T above incrs D-Dimers as well as:  very early minor elevation(s) n AMI due to intra-coronary clot [bt ths z not clin useful compared to standard trop biomarker elevatns; D-Dimer elvatns r proprtnl to amt of clot = small in intracoronary vsl oclns].

Patho:  Other situatns tht incrs D-Dimers:  DIC, malig, preg, p acut traumatic injury or hemorrhg, & p surgery.  T test is now more often used to consider acute aortic syndrs, not only acute aortic dissectn, but also any process tht ma invlv clot formatn-degradatn whn there z damage to T integrity f T aortic wall (thus intramural hematoma, aortic ulceration are includd).

Prev, their 1° use ws T findng f a [-] D-Dimer in a pt w/clin low pretest probability for PE/DVT to r/o these conditns.  D-Dimers r vry sensitiv for venous VTE [venous thromboembolism: both DVT/PE; time is importnt fr mgmt w/pos outcomes for many serious CP presentatns & a [-] tst ma exclude as many as ~30% of pts w/suspicion fr PE [it is an excellent rapid non-invasive triage test (biomarker)–whn neg useful to r/o life-threats f acute acut Ao syndr’s; T problm z a [+] result–comn fr all T aforment’d scenarios n T tst Q/patho abov.   Whn there z a [+] result, it z NOT specific for 1 entity–[thus, othr tsts som noninvasiv–> echo, & som invasiv->CT angio, r thus often nec employ’d for rapid Dx whn a serious etiol fr non-cardiac thorcic pain z considrd ].

D-Dimers: r produc’d n bld whn fibrin is cleaved during plasmin-mediated fibrinolysis (dissolutn of bld clot).  This correlates w/turnover of fibrin: again bcaus f T high [-] predictiv valu f ths highly sens tst, invasive tsts ma b avoidd, whn suspecting specifically PE/acute Ao syndrs.

T MC EKG rhythm/finding with PE is sinus tachycardia.  [good TI]

On EKG:  S1Q3T3:  Oftn list’d as evidence f PE [dates back mny decades); alone ths finding = nonspecifc & indicates of pul HTN/cor pulmonale: i.e., an S wave in lead I, a Q wave in lead III and an invert’d T wave in lead III

Acute cor pulmonale = acutly ncrs’d vol/presur w/n T RV from causes of acute pul HTN: PTX, ARDS, bronchospasm, PE cn all produce this finding.  Chronic COPD is a leading cause of chronic cor pulmonale mentioned abov n T case report.

When ths pattern z seen w/signs of acute RV strain, ths combinatn is mch mor indcativ f a vry acute process like acut PE: RV strain is seen in leads V1-V3 as “too tall” R waves in combinatn w/invert’d coving T waves.   Below–a gd EKG ex f S1Q3T3 plus RV strain (the R wave in lead II shd nvr b as tall as in V3 as it is here).  Both Post wall AMI & RV strain (any cause f acute sever cor pulmonale) cn produce ths finding.  T t wave inversns f post infartn r mch mor square plus invert’d: T R waves n post AMI becom too tall esp in V1-V2 because there is LOSS of directly post vectors in post AMI [usu most prominent n V2 bcaus T loss f post vector is directly post to T AV node (in T transverse axis)–it aligns most w/lead V2.  T V leads “look” at T electrical activity, “axis” of T hrt in 6 positns n this plane.  V1/V2 r T most rt-wrd & thus mst rel to T RV f all 6 V leads.

             S1Q3T3plus RV strain-more suggestiv f PE than just S1Q3T3 alone.

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PEDIATRIC EMERGENCIES

Which of the following is incorrect about seIzure disorders?

a.  Convulsive syncope is a minor form of seIzure disorder.

b.  Absence seizures are generalized, and may have a post-ictal period.

c.  Secondary generalized seizures are a form of partial seizure

d.  Complex partial seizures are psychomotor-temporal lobe seizures

e.  Complex partial seizures may present with mental and psychological symptoms including visual hallucinations.

Answer:  A.  Choice A Z NOT a true seizure*; it is often seen as brief twtching motor activity p cardioinhibitory syncope (i.e., a simple faint); it is of no clinical significance.  [a simpl faint = a Dx of exclusion in any pt 40 y or older-i.e., r/o serious occult pathology-e.g., always prfrm CV w/u to r/o occult CV event, (eg., AMI ) bfor dxing smpl fainting n ths age grp].  Chck med list: comn fr pts takng HTN meds to faint from sudn standing (ths is a comn Dx but shd always follow a basic w/u also for an accult CV or CNS event [AMI/TIA/CVA).  T pt wil hv an entirly nl exam p simpl faint n T ED–nl nero xam, nvr post ictal & no tongue biting (lab/EKG also nl).  *A variant of cnvlsiv syncpe z micturatn syncpe (faintng p/or durng voidng; also assoc’d w/brief twitchng).

Bth cnvlsiv-/micturatn syncpe r rel cmn; again, neithr z a tru szr nor f clin sgnifcnc

AS [Absence szrs]: r gnraliz’d szrs/caus an altratn n mental status w/o notabl (if any) motor actvity.  Clasic dscrptn:  sudn brief imobility w/blnk stareMC age:  5-10 y-olds (uncomn p 15 yrs) & ave last ~10 s; rarely DO HV a postictal state.

PS [Partial szrs]-subdividd rel to assoc’d altr’d consciousnes. Simpl PS hv brief sens or motor manifestatns w/o impair’d consciousness & categoriz’d rel to clin presntatn.  CPS [Complx partial szs] produce alter’d consciousness.  These szrs typically involv T temporal lobe & presnt w/mental and/or psychological sxs e.g., change(s) in affect (mood), confusion, or evn hallucinatns. [Aka psychomotor szrs].

NEW OR RECURRENT SZR IN A CHILD

Incidnc:  4-6% of ALL chldrn by age 16 [TI BCAUS SZR Z T MC NEUROLGC PED CNDITN]!

Often frightening to obsevers. Hence -> cmn ED Vist!

PATHO:  Abnl electrical discharges f cerebral neurons

Observers ma see:  temp involvmnt f cognitn, awareness/awakness, concsciousness, motor/behavioral activity, & altr’d autonomic fnctn .

Thus 2* fall/njury ma ocr.  If pt hs known szr hx, chk fr med noncomplianc, other meds or conditns known to alter particulr szr drug lvl or effect.  These vary w/each szr med: ex [example]:  these dcrs Dilantin (phenytoin) lvl-this list z 1° relevnt to adults bcaus mst r agents used in adults: also pregnancy cn increase szr activity by lowering phyentoin lvl:

1.  Chronic ethanol (esp abuse), chronic benzo (esp diazepam).  Othr antiepileptics: phenobarb, valproic acid, valproate sodium [thz cn actually ncrs OR dcrs dilantin lvls: i.e., their efcts r VARIABLE!

2.  antineoplastics but esp combinatin of antineoplastics: Cisplatin, Bleomycin, carboplastin, doxorubicin, methotrexate.

3.  *Other antiepileptics:  vigabatrin, carbemazepine

4.  Antivirals:  Fosamprenavir, nelfinavir, retonavir

5.  Diazoxide

6.  Folate

7.  Reseripine/theophylline (both not commonly in use today in medicine)

8.  OTCs: esp St John’s Wort-ths effect cn b highly variable depending on the product.

*Note that whenever >one antiepileptic agent z used n T same pt: dilantin cn cause unpredictable lvl of phenobarb, sodium valproate, and valproic acid (this cd incrs szr activity or dcrse it!  Always start w/ABCs and short acting benzo; chk elytes (esp hypo-Na+ and othr agent(s) tht promote hypo-Na+)ex’s: ethanol/loop diuretics; Risk of szr inrcs greatly w/s-Na+ <115 mEq/L.  Initial tx: stop inciting cause and limit fluids, [hypotonic fluids r contraindicat’d]; limiting fluids alone may allow s-Na+ to increase.  Therapeutic intervntn to ncrs s-Na shd b ltd to a s-Na of 125 mEq/L to avoid T complictn of central pontine mylenolysis (CPS): ths irreversibl complicatn z MC seen in alcoholic adults nt in peds.  Gen Rule to follow:  t rate of an elyte prob shd b correct’d at t rate whch it ocr’d.  

Never admin dilantin routinely fr szrs bcaus DILANTIN TOXICITY CN PRESENT AS SZR(s):  there is a progresn f sxs w/dilantin tox: slurr’d speech, H/A, dizzy=> obvious cerebellar sxs (ataxia/vertigo), twitching, tremor, dyskinesia, clonus, nystagmus, somnolence=>AMS=>SZR.  These r also oftn iatrogenic: during admin by IV chck for hypotn, resp depresn, cv instability (need constant EKG monitoring); in peds do NOT admin > 1-3 mg/kg/min or 50 mg/kg whchevr z less.  

There is a long list of meds that cause phenytoin toxicity as well as in those w/renal/hepatic impairment esp hypoalbuminemia (here best to check free phenytoin lvl [TI]):  

1.  Antacids:  H2 blockers-e.g., cimetidine, omeprazole

2.  Antidepresnts:  Fluoxetine, fluvoxamine, sertraline

3.  Antiepileptics:  Ethosuximide, felbamate, oxcarbazepine, methsuximide, topiramate

4.  Antineoplastic:  5-FU, Capecitabine 

4.  Azoles:  fluconazole, itraconazole, ketoconazole, miconazole, variconazole

5.  Sulfas:  SMP-TMZ, sulfamethoxazole, sulfadiazine & other sulfas

         (because it is a comn used agent: expect this type of list as a TI!)

Which of the following would be least likely related to phenytoin toxicity?

a.  Diarrhea

b.  Hepatic failure

c.  Nausea

d.  Vomiting

e.  Hyperglycemia

Answer:  A.  Constipation is associat’d but not diarrhea.  The rest are all assoc’d.  There are numerous other adverse effects:  Also atrial and ventricular conductn disturbances (depressn of conductn); multipl effects on bld cell line productn (bone marrow supressn):  leukopenia to agranulocytosis,, thrombocytopenia lupus, decrsd T3T4 w/incrsd TSH but w/o clinical hypothyroidism, incrsd alk phos, GGT, s-gluc.  Ginginval hyperplasia (reverses when the drug is D/C’d).  Also, benign lymph node hyperplasia/lymphadenopathy to pseudolymphoma as well as lymphoma and Hodgkin’s disz!

Such simply-worded fact questns are comn to all exams.  In part, they prove you have read the core material.

PATHO KEY ASSESS & TX IN ED EARLY:

INcrs’d O2/gluc utilizatn (key-assess/provide early [A->B->C->D]

1* Survey shd take only 30s! (Neonates-3 y-o (D10%/4y-o 2-4 mL/kg D25%;8 y-o or> D50%-Tx as an adult)

Of the following which is the most approptiate initial dose of dextrose to administer to a 17 kg child with hypoglycemic seizure?

a. 20 mL D10W

b. 20 mL D 12.5W

c. 34 mL D25W

d. 60 mL D25W

e.  34 mL D50W

Answer:  C.  The correct answer is 17 x2 = 34 Ml = 2 to 4 ML/kg of 25% dextrose. 10% glucose is used in infants. The Jose is 0.5 to 1 mg per kilogram per dose. But those can always be repeated as should the bedside blood sugar.  Infants more commonly need continuous glucose infusions.  A classic example would be in the treatment of Reyes syndrome.

Reye’s syndrome is a rare, serious conditn tht causes hepatomegaly, hypoglycemia, & cerebral edema.  It mst often affects children & teens recovering from a viral infctn, esp T flu, chickenpox &, rotavirus infctn (gastroenteritis).  Risk of Reye’s syndr ncreas’s whn salicylate was used for fever or these viral illnesses.

Signs/sxs: repetitive vomiting, confusion, SZRs, and coma.  All are nonspecific;but hepatomegaly is found in 50% and may be helpful w/a detailed Hx & lab evidence of elevatd ammonia & LFTs.  These pts require a comprehensive approach to r/o othr life-thretening conditns (some rare).  Treatment includes a continuous glucose infusion as well as intensive, supportive care.  T incidence hs decreased w/educatn f T public about asprin use in chldrn.

Easy math u mst kno: For all ages provide: .5-1G glucose/kg per bolus; may repeat (shd b bas’d on rapid bedside testing); if nt immed avail, always just give T gluc!

PERCENT =% ALWAYS MEANS  #G/100 mL 

[Ths z tru for all solns list’d as %] 

D5W means 5G gluc/100 mL ; another useful ex: 20% magnesium sulfate [20% = 20 G/100 mL-adult preparatn].  A standard adult dose = 4 G.  Since 4G is 1/5 of 20G, [divide T denominator by 5], give 100/5 = 20 mL of a 20% soln to admin 4G.  Ths z dilut’d in 150 ML of D5W & administer’d ovr 15 min intravenously.  

PEDS Ex:  One would give standard peds dose for mild-severe hypomag:  dose range-frm 25-200 mg/kg; lets choose 100 mg/kg as our dose; it is available as a 1% soln.

Using 1% soln, our rule says 1% always means 1G/100mL.  Since 1G = 1000 mg.  we can rewrite that as 1% means 1000 mg = 100mL The latter is the same as 100 mg = 10 mL.  Meaning to give 100 mg magnesium sulfate per kg body wt, we just need 10 mL per kg body wt of a 1% soln.

Finally, since a 1 y-o weighs 10 kg, give 10  x 10 mL = 100 mL of that 1% solution to provide 100 mg per kg of body wt.

ABSOLUTELY RQUIR’D:  

U shd hv concept for all peds wts by age; whenevr non-life thrt circmstnc, all peds pts shd b weigh’d.  NB:  3.5kg; 7 mos = 7kg (doubled BW); 1 Yr = 10 kg (tripl’d BW); 2 Y = 12 kg (there is a 2 in 12); 3 Yr = 15 kg (both odd #s & 3 is midway from 1-5 when body wt doubles); 4 Yr =17 kg (1/4th a 70 kg adult); 5 Yr 20 kg (double a 1 yr-old); from age 4 to 10 yrs add 3kg for each yr of life: 5 Yr = 20 kg, 6 Yr 23 kg, 7 Yr 26 kg, 8 Yr 29 kg, 9 Yr, 32 kg; 10 Yr 35 kg (10 yr old is ½ of a “standard 70 kg adult).  All of this shd b comn knowledge for all providers because ALL PEDS MED ADMIN, evn glucose, based on body wt in kg!   (Classic TI questn; but no Abx doses; must always know ACLS, PALS, anaphylaxis & anaphylactoid med doses; again, it will always be a TI!).  Thus, mst  kno: epi, atropine, bicarb, steroid (cortisone, methylpred, prednisolone, and dexameth doses) for all EP board exams and clin practice.  Review this every week of your life until it is perm knowledge.  Write it, draw it, write it on a white t shirt…you wear.  Live IT and Fluid Tx:  becaus this is wht u do that saves lives!  Boards expect u to know all approp abx’s for each type of T Most serious nfctns including those based on age rec’s: e.g., meningitis list of abx’s bas’d on age.     

Classic TI u shd plan for over and over for PALS/ACLS: dosing

Which of the following is a correct intervention?

a.  0.02 mg atropine IV for asystole in a child

b.  0.05 mL of 1:10,000 epinephrine IM in an adult for anaphylaxis repeat every 5 min in 

c.  Administer enough potassium and bicarbonate to create a pH of 7.55 and a potassium of 5.5 mEq/L for acute 300 mg/kg salicylate ingestion

d.  Defibrillate with 100 J for Torsades de Pointes

e.  Administer 5mg/kg Amiodarone to small adult with ventricular tachycardia

Answer:  C.  Up to 30 mEq/hour of potassium intravenously plus IV bicarbonate [2 amps in 1 L 0.9NS] may be required to alkalinize the urine (to ion trap the salicylate anion in the urine).  T3 has the best chapter written by Steven Curry.  This was published in 1986 and this chapter still has the best description of treatment.  

Atropine is not used in asystole (only epi + ACLS/PALS VENT/CHEST COMPRESNS).  Epi is administered: 0.3-0.5 mL 1:1000 dilution repeated q5-15 min for anaphylaxis.  A common error is to administer a ß-agonist and fail to administer the epi FOR FEAR OF CAUSING CARDIAC DISTURBANCE or failure to recognize true anaphylaxis…The former error is VERY FLAWED THINKING BUT STILL PERVASIVE PROBLEM.  Urticaria plus wheezing is enough to make the Dx; other findings: all of these are low: CO, CVP, SVR in anaphylactic shock.  For anaphylaxis with BP <90mmHg, intravenous epi may be required (as well as IV hydration):  epi infusion dose:  5- 15ug/min by continuous infusion titrated for the alpha effect to raise the BP.   The dose of amiodarone listed in the choice e is the pediatric dose.  Adult dose is 150-300 mg IV bolus depending on the scenario.  (300 mg for VF; 150 mg for VT).   The Tx of Torsades is overdrive pacing and magnesium sulfate.  If defibrillation is attempted higher doses are required than listed in choice d; start with no less than 200 J.    

BACK TO SZRS:  

SZR-ASSOC’D ISOLAT’D FINDINGS

Tongue biting

Postictal state

Hypoxemia

Hypo- or hyperglycemia

Lactic acidosis (W/brief szr resoves in 60 s)*

Leukocytosis w/o Lt shift

CSF pleocytosis [up to 10 WBC/microL]

SZR-ASSOC’D END-ORGAN OR SYSTEMIC FINDINGS

Cardiac arrhyth

DIC [disseminated intravascular coagulatn]

Hyper-K (usu in assoc w/rhabdo

HTN -> HPOTSN

Generaiz’d cerebral edema

Generaliz’d pul edema [form of noncardiogenic pul edema]

Fxs and dislocatns

Key TI [szr or falls esp in acholic adult-highly asso’d w/POST SHOULDER DISLOCATN)

SE (status epilepticus): progressive LA [lactic acidosis], hyperK esp w/rhabdo, abnl hypothal fnctn (hyperthermia).

SE ma lead to perm CNS njury.

Most r brief-isolated/usu good short/long term cerebral fnctn.

Key Def:  SE-recurrent or continuous szr activity >30 min w/o period(s) f baseline fnctn.  Most experts-continuous or recurnt szr(s) >5 minutes = SE!

B wary f those whch don’t resolv spont or ovr brief period!  ~10% w/new onset szr present in SE. [A BIG #-why we mst b confidnt  n acut szr mgmt->eval->dispo)

BASIC F CLASSIFICATN

1st:  gen [generalized] or partial* = latter r focal!

Gen’d szrs-convulsive vs nonconvulsive/almost always ass’d w/by ALC [altered lvl f consciousness].  Cn b atonic (no motor activity-ma b flaccid)

Partial ma spread from site f origin to 1 then both hemispheres (termed secondary convulsive generalz’d szr)-Proven by finding focal lesion on CT/MRI)

LOCATN/FURTHR CLASSIFICATN

PC szrs-3 categories & their alteratns cn overlap or combine:

Motor:  tonic, clonic, tonic–clonic, or myoclonic (jerking) activity.

Sensory:  perceptual distrtns (evn hallucinatns-includes “psychic szrs”)-these r asso’d w/temporal lobe involvement

Autonomic:  sweating/piloerection; repetitive, uniq movmnt(s) or isolatd behaviors (bicycling movemnts n infants; also, nonstop crying; lip smacking, clicking sounds, blinking-uo to >100/min n chldrn)

(Pseudoszrs): not tru szrs, bt pts oftn hv abnl EEG.

ED PRESENTATION

many hv spontan ceased.

If not having a szr p primary survey, T MOST IMPORTANT 1st step is to obtain a thorough history and physical.  At this time cn determine if a postictal state is present, if loss of bowel and/or bladder control occurred, or if a focal neuro deficit remains.  All help determine if true szr occurr’d.

T info determines if further w/u is warranted.

Ex:   a hemiparesis (Todd paralysis) or other focal neuro, deficit is a key localizing sign suggesting tht T szr hd a focal component.

Todd’s paralysis:

If focal deficit is new/persistent, neuroimaging is indicat’d to ID potential CNS lesion.

When a child presents w/risk for szr, T most important issue is to determine if there is ongoing szr.  If yes, addressing T ABCs + terminating T szr r T 1st two priorities.

DIFFERENTIAL DIAGNOSIS

Seizures have many potential causes, which vary with age

TX OF SZRS

Seizures have many etiologies; to stop t szr t etiol mst b addressed

Ex:  delivery is t definitive tx for szr’s assoc’d w/eclampsia.

List of meds tht cause szrs: very long: CAs

Also drug w/d: esp CAs, benzos, and both if pt takes either & is administered

Szr Meds: list in progress…complete this Dwight. 

Oxygen

Dextrose

Ca

Mg

Specific antidote, e.g., pyridoxine for INH OD

Benzo -> gen anesth

Tx infctn: e.g., tx meningitis: S-ACLS:  ABx->CT->LP->(Steroid bfore Abx)

Atropine + 2PAM-Insectcide poisoning (szrs stage 5: very poor prognosis)

Thiamine: esp for malnourishe/cancer pts not just to prevent Wernick’es encephalopathy.  If u admin gluc 1st yes thiamine is used in both glycolysis and gluconeogenesis; it is also needed for the TCA cycle and the pentose phosphate shunt. T tim relative to glucose admin and whn you admin 100 mg of thiamine z NT an issue! Just remember to give thiamine to all alcoholics, hypothermics, malnourish’d cancer pts in the ED.   If u did wait days…yes that cd b a real problem!  Wernicke’s and Korsakoff syndrs are PERMANENT!  Not good…Wernicke’s is a true type of stroke.  On pathology you will find multipl tiny hemorrhagic infarctns in the ant hypothalamus…so yes your pt will also have probs w/temperature control…i.e., they become poikilothermic…like a lizard!

Acidosis is list’d as physiologic response to szrs & SE.  Yet exog [TOXIN-INDUC’D-e.g., INH [Isoniazid] O.D., Cocaine] or ENDOG ACIDOSIS (inborn error of metabolism) MAYB T ETIOL OF SZRs esp SE…I modified a cmn list u must kno:  T one for AG [anion gap] met acidosis.  In theory, any of these cd produce Szr’s or SE; note, T author in T5 comment’d tht ethanol, prev list’d n anothr versn f ths mnemonic z NOT a real cause f AG met acidosis:  A MUDPILES CT:

_________________________________________________________________________________________

Acetone (the toxin whch produces T highest acetone lvls is metaboliz’d isopropanol)

Methanol

Uremia

DKA (cn hv asso’d cerebral edema esp during peds fluid resusc-see below)

Paraldehyde

INH, Iron OD

LA

Ethylene glycol

Salicylate(s)

CO, CN

Toluene

_________________________________________________________________________________________

DKA & SZR:

During a fluid resusc fr ped DKA a ℅ H/A = an ominous sign of ongoing cerebral edema.

It mandates T fluid resuscitatn shd b stop’d bcause cerebral herniatn & sudn death r list’d as rapid onset events relat’d to IV fluid resusc in peds DKA. Head elevatn/othr stndrd measur’s for incrs’d ICP shd b considered as well as evn neuro-surg consultatn.

Which of the following is incorrect about febrile seizures?

a.  They occur in up to 20% of children.

b.  Electrolyte abnormalty is not an element of a complex febrile seizure

c.  Complex febrile seizures last more than 15 minutes, but are not associated with a CNS infection

d.  Simple febrile sezure is brief and generalized

e.  Complex febrile seizures may be focal

Answer:  A.  FS occur in just 2-5% of all chldrn; always maintain a high index of suspicion for meningitits; T 1st LP ma b nl!  Repeat LP ma b needed.

FEBRILE SZR’S [SEIZURES] [FS]

FS = MC szr’s f chldrn

Key Def: Szr in assoc w/febrile illness, bt w/o CNS infctn, no prior afeb szr, knwn brain abnormality, or abnl elyte(s).

Clasic age:   6 mos->5 y.

peak @ ~18 mos.

FS R Simpl or Complx

Complex: focal, last >15 min or multipl (>1 in 24 h).

Simple =(mjority of all)-mst b brief, singular, & generaliz’d.

FS Patho unclear:

Implict’d:  viral infctn, immunizatn, genetics.

Mortality rare!

Morbidity:  no difference in cognitn after a FS, evn if prolong’d.

FS-ALWAYS A DX OF EXCLUSN!

Must r/o meningitis, encephalitis, abnl elyte [e.g., hypoNa+, or any acute CNS disz. LP: is debated as requir’d Dxstic tst for FS; more widely used for:  younger age < 12 mos, has AMS (or prolonged postictal period) any petechial rash, recent visit to PCP, repeat szr’s in ED, appears ill/lethargic/toxic, recent prescrib’d abx’s.

Also, LP for nuchal rigidity i.e., + Kernig, + Brudzinsky signs, bulging fontanelle + Abx Tx fr meningitis shd nevr b delay’d! SEQUENCE: A, C, LP:  Abx’s->CT->LP!

It is rare for a child w/meningitis to have a single simple seizure as a presenting sx.  Comorbid finding of otitis media + fever + szr shd always raise index f suspicion for meningitis.

EXCLUSNS:  most r r/o by a proper Hx/PE. (e.g., signs f shaken baby syndr: UE grip marks + retinal hemorr’s/Head CT proves that Dx).

AAP recs:  in chldrn who present with FS: <12 mos of age, an LP shd b considered  (signs/sxs of meningitis ma b absent); 12-18 mos, an LP shd b considered bcaus  signs f meningitis ma b less obvious in ths age grp; any w/their 1st complex febrile seizure, an LP shd b strongly considered if there has been recnt or current antibiotic Tx.  By itself, a complex FS, IS NOT an indicatn for a LP in a well-appearing child.

Which of the following is not a contraindication for performing lumbar puncture?

Which of the following patients has the most significant need for immediate emergency brain CT in a pediatric patient?

a.  A persistently crying 9 month-old with a simple febrile seizure and petechiae on the left thigh.

b.  A persistently fussy 13-month-old without fever or any known problem who then has a 20 minute generalized seizure in the ED.

c.  A well-appearing 14-month-old with a first simple febrile seizure.  The history and physical examination are unremarkable.

d.  A well-appearing 5-year-old with a first complex febrile seizure.

e.  A well-appearing 12-year-old male who has a right Bell’s palsy, a supple neck and recent history of a tick bite over the right temporal scalp.

A.  Answer:  B.  The choice B patient should be considered for shaken baby syndrome or other intracranial pathology.  Examination of the anterior and posterior fontanelles will likely not be helpful (both will likely be closed).  An ophthmologist should perform a fusduscopic exam for pathonomonic retinal hemorrhages.  The upper extremities may display grip marks (bruising from severe sagittal shaking).  Choice A first needs emergency antibiotic treatment for suspected meningitis! This is followed by CT (only if there is risk of increased ICP or predisposing conditions (listed below) that increase the likelihood of an abnormal study) and then, LP. (The order may vary depending on other findings and physician preference.  Choices C and D likely need a period of observation and discharge home with detailed instructions.  Choice E should be examined for rash, site of the tick bite and treated for Lyme disease.  Bilateral Bell’s palsy is highly pathognomonic of Lyme disease.

 

Whn Is Brn [Brain CT] Indicatd Fr Peds Szr?

1° uses: physician decides to r/o bleed, or midline shift (e.g., space occupying mass of higher risk).

Just bcaus CT can b easily ordered empirically, this does not make such use for any szr approp…this alone [do it because we can] is quakery since brain CT isn’t absolutely benign: 2 risks:  1. Acutely frm consc sedatn; 2.  Long-term risks: a very publicly known and debated subject: radiatn risk.

BRAIN RADIATION RISK DISCUSSN:  For ths subject:  2 recent lrg human cohort studies of chldrn [ref: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4470427/

RESULTS:  T strongest data is frm 2 human cohort studies,5,31 both report data frm head/brn CTs & 1 report’d results after facial & neck/spine CT.

  1. Reported incidence rate ratios suggest’d a significnt ncrease n incidence f thyroid malignancy after neck/spine CT & significant bt near borderline increases n risk f all cancers after either facial or neck/spine CT.  Results for brain cancers p [after] brain CT were reportd in more detail in both studies; 1 estimatd tht if every excess brain cancer after brain CT ws attributable only to imaging, thn ~1 in 4000 brain CTs in chldrn wd b followed by 1 malignancy (mean estimatd brain dose 40 mSv per scan).31 T additional cohort study5 estimatd tht risk in T 10 yrs following CT was 1 brain tumor per 10,000 pts exposed to a 10 mGy scan at <10 y of ageT highest risk is in children <age 5 yrs and it increased exponentially in infants*** i.e., those <1 yr f ageT age dependence in younger pt is expectd to have some highr risk bcaus f incrsd yrs of future life & bcaus n younger pts T dose rel to body size as well as inherent age-specific risks per unit dose is incrsd.     ***REF GRAPH for risk related to age https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4470427/figure/F3/
  2. Radiation effects r f 2 types: cumulative & stochastic.49 Cumulative efcts (deterministic effects) occur w/a high dose in a short period.  Consider an extreme circumstance, e.g., radiation Tx, it may be assocd w/tissue necrosis. Ths effect expected based on a threshold dose & are typically nt seen w/radiological interventions (testing)Stochastic effects, in contrast, ocr in low doses over a long period of time.  T effects ma b seen over a wide range f doses, & T severity f effect isn’t clearly relatd to a threshold dose.  [Implies there is no “safe” dose & this is why EP decision-making for risk-benefit is key!…e.g., we must ask how T study affects our subseqnt interventns/decisions in this pt & wht is T risk of no study in this pt?]  In today’s practice we cn assess T ant fontanelle for ICP in infants and treat meningitis immediately w/o CT.  We can use othr tests (latex agglutination and other Ag immuno-assys on spinal fluid-and evn urine), Abx inhibitors in cultures to prove a bacterial etiol f meningitis if T risk of CT is high for anticipated complicatn: listed below in detail**).     

Ref 5. Pearce MS, Salotti JA, Little MP, et al. Radiation exposure from CT scans in childhood and subsequent risk of leukaemia and brain tumours: a retrospective cohort study. Lancet. 2012;380:499–505.[PMC free article] [PubMed]

Ref 31. Mathews JD, Forsythe AV, Brady Z, et al. Cancer risk in 680 000 people exposed to computed tomography scans in childhood or adolescence: data linkage study of 11 million Australians. BMJ (Clinical research ed.) 2013;346:f2360. [PMC free article] [PubMed]

 

Gen consensus:  a complex febrile seizure is not automatically an indicatn for brain CT & clin eval shd determine need fr brain CT.  A comn exampl of an indicatn fr brain CT would be clin evidence of incrsd ICP.  Conversely:  Importnt to note tht ncrsd ICP is NOT always clin evident; papilledema and papillitis  have an identical apperance & only T former indicates ncrsd ICPMost EPs admit thy cannot visualize fundi well enough to use T exam!  (my personal questioning of 12,000 EPs over 30 years for oral exam simulations).  Majority state they only assess for red reflex.  Editorial comment DDC, MD.   Likewise, older EPs who have decades of experience & no cases of adverse outcome from LP: they cite funduscopic exam is more useful n older children /adults if they can cooperate w/t exam.  Today ocular US cn b used to chck for ncrs’d ICP (easy to learn techniq).  Ths z a measurmnt f T subarach spac around T optic nv. 

PHOTOPHBIA CN B USED AS A FINDING OF INTRACRANIAL CONDITNS W/T CAVEAT THAT MIGRAINE IS STILL T MCC OF PHOTOPHOBIA.  IF U CN EXCLUDE MIGRANE THN PHOTOPHOBIA BCOMS A USEFUL SIGN F AN INTRACRANIAL CONDITN:

Intracranial conditns such as meningeal irritatn frm meningitis, SAH, or pituitary tumors or CVA caus photophobia->due to irritation f T basal meninges esp around T diaphragma sellae. This pain z mediated by branches f T 1st division trigeminal nv whch innervates T meninges.

REF:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485070/

Migraine is T MC neurologc disordr causing photophobia, whch = 1 f T major Dxnostic criteria fr migraine per T International Classificatn f H/A Disorders–Up to 80% f migrainers hv photophobia during an attack. T ID Migraine validatn study suggestd tht T presenc f photophobia, disability, & nausea predict’d migraine ~98% f T time!

REF:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485070/

In a study focusing on complex febrile szrs by Teng et al tht involvd a cohort f 71 chldrn, all of whom had complex FSs, 79% appeared well, 19% appeared “unclear” based on gen appearanc, 3% appeard lethargic or inconsolabl.  In ths study, 24% hd focal szrs/14% had prolonged multipl or isolatd szrs.  LP ws performd on 10 chldrn; ALL were () fr meningitis!  Brn CT ws also obtaind in 10; NONE hd intracran pathology.  NONE f T 71 pts w/a complex FS had an intracranial abscess & none presentd w/any signif intracran patho requiring emerg attentn. A brn MRI ws obtained w/in a wk p presentatn on 36 additional subjcts; those MRIs were also () for pathology.

Teng stdy-conclusion: emergncy neuroimaging (brn CT) frm ED isn’t indicatd for well-appearing peds pts who present w/a 1st-time complex FS. 

AAP current rec:  chldrn w/1st simple FS: emergency neuroimaging need not be perform’d in ED. 

Brn [Brain] CT & T Afebrile Peds Szr

1 lrg retrospectv study [Sharma et al1] look’d @ ED Brn CT fr 1st-evr (nw onset) unprovokd, afebrile szr in 500 pts–1st conclusion: CT usu nt indictd! 

Othr Main Conclusn:  Gave Two 1° critria fr hi-rsk cln signif abnl stdy (indicatns to do CT): 

1.  Any focal szr pt age <33 mos.

2.  Presence of a predisposng cnditn [order CT]:

1.  Focal szr, focal neuro deficit(s) or prolong’d szr [any status:  pt ma evn b atonic]

2.  VP shnt

3.  Sign of ncrsd ICP or Signs of neurocutaneous disorder

4.  Known travel to area endemic for cysticercosis

5.  Immunocompromis’d (HIV)/cancer pt/malnourish’d

6.  “Hypercoag” pts (thrombophilia pts):  Cancer pt; SS disz; prot C/S deficiency & othrs [some present @ birth/othrs acquir’d], lupus, antiphospholipid abs, elevat’d homocysteine (vit B12/folate deficits), antithrombin III defic, Factor V Leiden Mutation, othr vasculitis]–any are good as TI [Test item]

7.  “Bleeding disordrs”-e.g. factor VIII/IX deficiency, therapeutic anticoagulatn

8.  Closd head njury (if the head injury ws assocd w/loss f consciousns)

9.  Recent visit to any health care (implies acut or chronicaly medically ill)

10. Any AMS (GCS <15); (always consider suspct shakn baby syndr)-Test item [TI]

11.  Vomiting (in all literature 2 or more episodes is an indicatn to study w/acut head njury)

12.  Close temporal relation to T szr

T Sharma study1 concluded:  children w/these high risk conditns shd hv emergency brain CT from ED. T study also concluded tht those who met low risk criteria and were well appearing cd be safely sent home as long as f/u cd b assur’d.

If EP bliev’s meningits z cz f a FS [febrile szr], LP shd b dn!  [Note:  Szr, in general, z Nt a comn prsntatn fr meningits!]

REPETITION IS GOOD

Brn CT prior to LP?–Mst studies:  CT isn’t usful bfr LP! [still many EPs worry abt ncrs’d ICP/ordr CT out f routine (often prior to proper hx/complete exam): ths z discourag’d!  It is still not uncommon for a unit secretary to order such a test: very unethical practice.  

REPETITION IS GOOD

Again, order CT:  Imunocmprms’d (e.g., suspct brn abscs), (vomiting, new anisocoria, dilated sluggish pupils and/or obtund’d, focality exam or papiledma* =>ncrsd ICP), suspct endocarditis => brn emboli, [+] sun-settng sign = eyes down/inward w/smal pupils => pretectal ncrsd ICP @ p

*Papilledema is not distinguishable frm papillitis as in MS (MS is NOT usu a peds Dx)

NEONAT:  ED emrg brn CT/emerg cranl US n neonat eval: fr szr lks fr njury/or bleed [e.g., shkn baby sndr; AVM, othr anomaly; acute unexplaned AMS w/vomiting esp w/ sluggish, dilated, unequal or sunset pupils)

Brain MRI Fr Ped Szr

Emerg brn MRI isn’t indictd n initial ped szr eval n ED/nt usu avail to EP. (1 xcptn:  acut CES [cauda equina syndr]-a true neurosurg emerg! [a TI!]

MRI vs CT: betr to dtct [detect] epileptogenic site, to find abnl gry/whit matr d’vlpmnt & fr DAI [diffuse axonal njury].

MRI z mr time cnsumng thn CT:  prolng’d ped sedtn hs 1° risk -> mrbdity to death [need manpowr fr monitorng/resusc equip].

Brn MRI approp p admt’d:  fr congenitl-genetic isu’s.

Well doctors that is an example just one week every week for most of my medical career…this is how you can avoid needing to walk around with an app like UTD…and you grow your brain…this is part of the 7th ed of Pearls…still writing it.  The week of 2/11/2018-2/18/2018…these will also bcom convertd to slides in my lectures and then I add the images/art/layering effects.  I hv bn doing ths since befor cmputrs xist’d…thnk God fr Cmputrs!  Have a nice week..hope some of these reminders were helpful…and if you are just getting started in medicine just write it for 15 min a day…read it and write it…everyday…DDC  

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Digital currency is also very private and it is up to the individual to report their capital gains earnings. Money can’t be devalued in digital form because you have no government able to print it at will for the needs of the government(s). This has in the past diluted the value of paper money. This process cannot happen with digital currencies. All over the globe computers know who has the money and this prevents errors including double spending. When 10 or more computers agree that a person who is making a transaction owns that money they are confirming the validity of the transaction and then money is sent via the internet. Each person generates a key and a password so their transactions are secure. This is done at the moment of the transaction. So when you buy with digital currency even if there is a computer falure somewhere in the world, there are plenty more computers that can verify the transaction is valid and avoid middle men charges. Those who manage the computers get a small fee which is much more reasonable that the banks (up to 6 taking fees for every transaction) has now been reduced so a person is not paying so much in fees. These transactions are private. There is nothing cryptic in the world of cryptocurrencies because all the coders who manage the computers can see the code. They design it to perform functions that solve problems. It is still important to note that cryptocurrencies other than the well known ones such as DASH, designed for rapid transactions, BTC, Etherium, and just a few others are safe to use…however, the majority are scams, ie., like Ponzi schemes. So how do you start to use these digital currencies start with an allocation of about 10 percent of your portfolio and by cryptocurrencies. Also get FREE coins by mining them. I have a way for you to earn them for FREE called FREE MINING. You will need a link to open mutiple mines to double, triple, quadruple…and so on, increase your mining rate…again…all of for FREE. First open FREE mining accounts, one at each of these links. I will give you detailed insturctions how to do all of this. I will show you how by getting your friends to open free accounts that they can help you increase your rate of mining. It is important to note that as of Dec 14 bitcoin has reached an all-time high of over 17,000 dollars. If you think you are late to the earnings well you are wrong and there is planty of room for you to become unbelievable wealthy if you simply act and follow these instructions. You can even protect yourself from hackers because you can buy a cold storage device (a usb hard drive…designed for this purpose). When you take your bitcoin or other currency out of your wallets and transfer it to you hard drive, it is “unhackable. Even if the power goes out, or in the case of some severe attack against our cities (like an EMP strike), your money is safe on the hard drive. There are many companies who sell these drives on company you may want to look into for this and consider purchasing the Ledger Nano S device. It is easy to use and attaches to your computer using a USB connection. Go to Ledgerwallet.com for more information. So to recap: step one is to open a wallet as it provides your secret adresses and you generate them by pressing a button, and they are much like a random number but consist of multiple number and symbols too long for anyone to memorize. You should use each one address only once and if you create them in BTC wallet an application you can get for your phone, then you have a way to create as many addresses as you would like. Next, you go to the links I have listed for you. Each one will open a new account at the vault for bitcoin mining. Enter your address into the screen by cutting and pasting it so you don’t make any mistakes. Repeat this process for every affiliate website adressess link . On the PC it will be called your referral link but it is the same as the affiliate link: Then you will have mining for each link that will begin. Once you have 0.0005 bitcoin you can have that money sent back to your address in your wallet. I would also suggest you open an account at www.COINBASE and move your coins to that site. There you can also purchase other coins like litecoin and ethermium. Then take 90% of the value of your coins and put it on your hard drive cold storage and do not convert it to US dollars unless you need to spend it; as BTC and other cryptos are going to increase in value why dollars do the opposite over time. Since I began writing about BTC the value has gone from 14,000 per coin to now over $17000.00 per coin. It is estimated that one coin in 5 years could be worth hundreds of thousands of dollars or as high as one million percoin. There aer several ways to increase your mining capacity: invest in a faster mining program by paying the mine in BTC, by having friends sign up visit the site and buy mining. It is still affordable to increase your mining rate.                                                                                                                                                                                                                                                                                                                                                                                      I will write more and add some graphics so you will have no difficulty in earning FREE BTC asap! this is a way to hedge against swings in the stock market.

Edit Post ‹ EMedNation.com — WordPress.com  BTC update! Today Nov each coin is worth >$17.000.00 …Litecoin & Etherium are also increasing & T latter >3000% since Summer!  U [you] r NOT too LATE to get huge GAINS IN T COMING YRS!  THR R MANY MOR ADVANTAGES TO USING THESE 3 KEY WELL-ACCEPTD CURRENCIES….I WILL PRESNT SOME BASICS & WILL GET INTO some DETAILS!  I HV ALSO ADDED A SECTION BELOW TO MOTIVATE U TO STUDY W/ME FOR ALL ER BOARD EXAMS…I TEACH FOR ALL T EXAM & I AM THE ONLY PERSON IN T WORLD WHO HAS BOTH TRAINED EXRS X 10 YRS WHILE ALSO PREPARING CANDIDATES/T BOARDS HV REVIEWED ALL OF MY MATERIAL AND ARE HAPPY THAT I ALLOWED THIS TO SHOW THEM THAT MY WORK IS ORIGINAL & BASED ON STATISTICAL ANALYSIS OF WHAT IS MST IMPORTANT, MST SERIOUS IN OUR DAY-TO-DAY CARE OF IT.  PERSONALLY I PREFER TO WORK WITH THE MOST ILL PATIENTS.  I FIND THIS THE MOST PLEASING AND REWARDING.  I HAVE OFTEN THOUGHT OF GOING BACK INTO TRAINING TO COMPLETE MY SURGICAL TRAINING IN PLASTIC AND CARDIOTHORACTIC SURGERY.  IT IS STIL A POSSIBILITY, BUT MY IMMEDIATE GOALS ARE TO HELP ALL OF U: TO HELP U REGAIN SOME FINANCIAL INDEPENDENCE (BCAUS MST OF U SPENT 10 – 15  TO GET UR MEDICAL DEGREE THAN I DID/I WANT TO HELP U!  ALSO, LIFESTYLE IMPROVEMENTS, TO TEACH YOU THE IMPORTANCE OF MUCH YOUR HEALTH WILL DETERMINE THEALHY OF YOUR FAMILY, “THE HEALTHY OF UR WORK”.  

There z a time to sew & a time to reap & it z key to regain T balance to regardn \

U ma hv had bt lost T sUMAY HV HAD bt lost to T forces tht act on u everyday IN WHT SEEMS AN “ATTACK.”  I FACE IT TWO BUT BY STUDYING SUCCESSFUL PEOPLE I CN BRING UR THEIR INSIGHT HOW TO SOLVE HUMAN probs.  VIRTUALLY 95% OF THE CASES WE SEE IN THE ED.  WHEN U R STRESSED & FEEL “UNDER ATTACK” U SAY YOU FEEL THS STRESS OR IF U R MALE (YES MALES & FEMALES ON NOT WIRED T SAME IN THEIR BRAINS). MALES usu SUBLIMATE STRESS UNTIL THY ‘EXPLODE’ WHILE FEMALES TEND TO TALK AB THEIR STRESS (THESE, ARE GENERALIZATNS & DONT FIT EVERY PERSON OR PERSONALIY TYPE).  IT IS IMPORTNT TO HOWTO DISTRACT/DEFLECT T PEOPLE/WHO.U FEEL CAUSE U STRESS AS T ADRENERIC SURGE WILL, OVER TIME, LEAD TO YOUR EARLY DEMISE.  YOU WILL LEARN THT ALL OF T “FOG” YOU FEEL IN YOUR MIND WILL LIFT WHEN YOU GAIN CONTROL OF THIS  & THT U CAN PERFORM.  IT IS CRITICAL TO TEACH THS SKILL TO CHILDREN BEFORE THY R-8-YRS-OLDOTHERWISE, THEY WILL CARRY THT PROB FOREVER.  

ONE DICTUM TO FOLLOW IS STRESS IS TRULY THAT ONLY  IF YOU MAKE IT THAT…THIS MEANS, IF, U HEAR SOMETHING U DON’T LIKE.  WHAT DID U JUST DO?  U INTERPRETATED INFORMATION.  S IS HARD FOR MANY TO ACCPET BUT U R T ONLY PERSON WHO CN MAKE U ANGRY FR T MOST PART.  OF COURSE, THERE IS JUSTIFIED ANGER WHN SOMEONE IS INJURED OR VIOLATED.  THT Z DIFFERENT.  DAY-TO-DAY IT IS OUR INTERPRETATN F MERE SOUND WAVES PRODUCED BY ANOTHER’S VOCAL CORDS THT PASS THROUGH T AIR WE RECEIVE AS INPUT AND WE must intrprt thm as thy cause T eardrum to A MESG TO OUR MIND.  OUR CORTICAL BRAIN, COMMAND CONTROL CNTR N T FRONTAL LOBE DECIDES IF T STRESS IF “GOOD STRESS OR BAD STRESS (SIMPLIFIED TERMS YES I KNOW)

IT REQUIRES SOMTHING > AN EDUCATIONAL PROGRM.  IT REQUIRES  A TRUE “TRAINING PROGRAM” W/REPETITION, REINFORCEMENT OF THT/REHEARSAL OF VARIOUS WAYS TO PRESENT OR UNDERSTAND T SAME KNOWLEDGE.

Your brain is hardwired to work this way.  I will show you how to control ur mind in ways you thought not possible.  There is a duplicated system in the brain that dates back THOUSANDS OF millenia and is a reflex system designed for your survival.  It was then based on man living with fierce wild animals that would attack early humans and decimate them if they could not defend themselves or flee and is T basis for the flight of  fight phenomenon part of the sympathetic nervous system.

Today mostly this mechanism isnt nec bcause we r not running frm wild saber tooth tigers & bcaus it can produce adrenergic surge (sudden release of epinorepi) which now does more harm than good.  These substances  actually damage brain and cardiac muscle cells-even kill them…to mention a few & u need to have the control of what you experience much of this in day-to-day practice to keep this reflex in check.  We’re all still hard wired this way.  So bilaterally, you have a hippocammpus which has subsegmental regions and each is “hard-wired” directly to your emotional brain.  Each memory center is storing both long and short term memories.  Th[emotial experiences u hav had an u will likely recall all of the events but realize tht you nevr tried to memorize T details of T events.  This is ur mechanism for long term memory to remember how dangerous wild animals are.  But today we have a different stress.  It is purely based on our interpretatio nof our feelings not our overall circumstances most of the time.  It is easy to lose perspective in a situation and feel all is bleak.  This is purely the mechanism that is built into each of us and it can be controlled by learning to control it with practice.  So one of my staff members was right; she often said, “stress is only stress if you make it stress.”

No 1 Cn predict absolute outcome of a situatn, if u learn to not react to any situatn & let it play ur best efforts to make it work out well it usually does.  All the emotions were for nothing but harm you.  This is why long-term truly angry people die younger and have more health problems.  Children suffer immensely from this if they are not trained to “manage” stress.  One of the best ways is to simply realize that anything negative someone says about you is not gong to impact your life and they are trying to get you to have an emotional response.  You must resist the urge to do that and just let it pass through you.  Your body will thank you/ yrs from now. ”U must realize it is almost comical to think that other’s can “make us aWe have to interpret their words whch ar; just vibrating molecules of air % thus  are getting angry over that…jst some nitrogen & oxygen an\\d a little carbon dioxide bumping into you inner ear which then sends electrical impulses to the brain but you cannot feel the pressure they exert.  So our realities are just how we decide to interpret all that is around us.  If it is interpreted as ok or good…we have no negative emotion.  No adrenergic surge and we remain much more functional  we are not killing heart of brain cells.  Ths science  real/well doc’d.  It is amazing how whn T brain z happy & healthy T body follows

EACH Hs a hippocammpus on either side                                                                                                     F T BRAIN FR REDUNDANCY.  Each serves T same functn.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

brain and the duplicated system serves muliptle purposes.

On each side of

 

 

programs both teach thse

This site links I listed below….it is the best site to have FREE BTC BitCoins MINED FOR YOU! NOTE I AM NOT A LICENSED FINANCIAL PLANNER SO THIS IS FOR EDUCATIONAL PURPOSES ONLY. TALK TO A FINANCIAL PLANNER AND I SUGGEST NOT PUTTING MORE THAN ANY OF YOUR ASSETS IN MORE THAN 10% OF THE WELL ACCEPTED (NONSCAM COINS I.E., BTC, LTC, ETHERIUM AND ET-C [THE LESS EXPENSIVE FORM OF ETHERIUM BECAUSE 98% OF CRYTPOCURRENIES AFTER THESE 3 EXCLUDING DASH AND A FEW OTHERS ARE SCAMS! OVER 100,000 PEOPLE ARE INVESTING INTO BTC DAILY BY REGISTERING AT WWW. COINBASE.COM AND HUNDREDS OF THOUSANDS OF BUSNESSNIESS WORLD WIDE ARE ACCEPTING IT FOR PAYMENT NOW! I WLL ACCEPT IT FOR MY ORAL BOARD TUTORIAL! AND ALL OF MY BOARD PREP PROBRAMS NOW AS WELL AS PRIVATE TUTORIING.  THIS EARLY SPRING IF AMAZON BEGINS ACCEPTING BTC FOR PAYMENT YOU WILL SEE BTC VALUE SOAR…DONT MISS OUT! IT IS EXPECTED TO HAPPEN IN FEBRUARY 2018.
BTC IS DESIGNED TO SOLVE A PROBELM. I AM HOPING I CAN CONVINCE EXPERTS TO SET UP A COIN THAT WILL HELP THE MEDICAL AND SCIENTIFIC COMMUNITY SOLVE ANOTHER PROBLEM!  PLEASE BUY MY ART!   IT IS GREATLY DISCOUNTED AND IT HELPS KEEP THIS WEBSITE PUBLISHED; I AM HOPING YOU WILL FIND SOMETHING YOU LIKE.
THANK YOU. DONATIONS ARE WELCOME TOO AND CAN BE SENT TO EMedNation.COM ℅ DWIGHT COLLMAN MD. I REALLY NEED your help and you need MINE!
ANY AMOUNT WILL HELP BUT OUR GOAL IS TO RAISE $100,000.00 By January 31 2018.
I WILL TUTOR YOU AT A DISCOUNT FOR EMERGENCY MEDICINE BOARDS IF YOU DO THIS.  REMEMBER IN LIFE YOU GET WHAT YOU PAY FOR … DONT RISK YOUR BOARD CERTIFICATION WITH PEOPLE WHO RUN A COURSE A FEW TIMES  A YEAR OF LESS.  THIS IS MY LIFE’S WORK.  I KNOW WITHOUT QUESTIONS WHAT YOU WILL BE TESTED….THE BOARDS ARE MORE THAN FINE WITH THIS THEY ARE HAPPY BECAUSE I AM REINFORCING WHAT YOU MAY NEED HELP WITH SINCE YOU COMPLETED THOSE STUDIES.
EACH PROGRAMS IS $3000.000/I WILL OFFER IT WITH PRIVATE TUTORING on Skype AND YOU WILL HAVE ALL OF THE TEST ITEMS YOU NEED TO PASS INSERVICE AND EM BOARD EXAMS…I PROMISE! YOU WILL GET ALL OF MY LECTURES AND ALL OF MY CASE SUDIES THAT ARE WELL KNOWN TO HIGHLY EXACTLY SIMULILATE THE LIVE ABEM AOBEM AND BCEM EXAMS. I HAVE WORKED FOR THESE ORGANIZATIONS TO TRAING THEIR EXAMINERS AND I HAVE JUST REWITTEN THE TEST ITEMS SO I DONT VIOLATE ANY RULES (AS I HAVE DONE FOR OVER 3 DECADES AND I HAVE TRAINED RECENTLY RESIDENTS FOR MIDWESTERN UNIVERISTY IN CLINICAL PROCEDURE AND HAVE TWO LETTER SO THANK YOU INVITING ME BACK TO /4TEACH FOR THEM AGAIN.
“I TRAINED BOTH CLINICAL BEDSIDE HX/PE EXAM TEACHINIQUES, PEARLS, AND ALL EM PROCEDURES INCLUDING MY LECTURE PRESENTATION AND BESIDE USE OF ULTRASOUND FOR WHCH I USE IT IN 30% OF MY CLINICAL PRACTICE FROM EFAST TO IVC (FLIUID STATUS) TO NERVE BLOCKS, AND DVT BEDSIDE STUDIES DOWN TO THE TRIFURCATION).”  YOU CAN LEARN THIS AND ABDOMINAL ULSTRASOUND IN DETAIL (GU, AORTA, BLADDER, PROSTATE, OBGYN STUDIES AT THE BESDISE).  THIS IS TO SUPPLANT AND EXPEDITE YOUR PATIENTS IN THE ED!”
BECOMING AN EXPERT AT NERVE BLOCKS SAVES PATIENTS ENORMOUS AMOUNTS OF PAIN AND HELPS TO EXPEDITE THEIR CARE WITH FEWER COMPLICATIONS.  “I USE BEDSIDE US IN ABOUT ⅓ OR MORE OF MY SICK PATIENTS AND ALSO IN THE WELL PATIENTS WHO JUST WANT A QUCK SCAN TO SHOW THEY HAVE NO PATHOLOGY.  FLUID STATUS IS A CRITICAL ISSUE TO LEARN WITH BEDSIDE ULTRASOUND; IT IS VERY VERY HELPFUL IN THOSE WHO ARE MORBIDLY OBESE WHERE STANDARD 70 KG FORMULAS DO NOT APPLY AND IN THOSE WHO ARE ON VENTILATORS OR HAVE INTRINSIC HEART DISEASE LIKE VALVULAR HEART DISEASE, CARDIOMYOPATHIES (ALL 4 TYPES IHSS, DILATED, RESTRICTIVE AND IDIOPATHIC RV CARDIOMYOPATHY), TAKASUBO’S CARDIOMYOPATHY AKA “SAD HEART SYDNROME” WHICH CAN LEAD TO DEATH ESP IN WOMEN.
DR COLLMAN IS AN EXPERT IN TEACHING BESIDE ULTRASOUND ALSO IN THE AREA OF PLACING CENTRAL LINES AND PACEMAKERS.  HIS BACKGROUND IS HEAVILY WEIGHTED IN THE AREAS OF PROCEDURES SINCE HE IS AN ARTIST AND SURGICALLY TRAINED, HAS WON NUMEROUS AWARDS FOR CONCEPTUALIZING AND BUILDING THE FIRST HEART LUNG MACHINE FOR PREMATURE INFANTS AND HE DID ALL OF THIS PRIOR TO FORMALLY MATRICULATING INTO UNIVERSITY.  HE IS A WORLD-RENOWNED EDUCATOR AND HAS TRAINED PERSONALLY OVER 12,000 EMERGENCY PHYSICIANS AND OTHER HEATH-CARE PROVIDERS IN OTHER SPECIALITIES SINCE THE 1980S.  HE TRAINED IN GENERAL SURGERY WITH AN EMPHASIS ON POST OP CARE, PREOP ASSESSMENT AND SURGICAL PLANNING, TRAUMA SURGERY AND WAS THE FIRS TTO ILLUSTRATE AN INTRACRANIAL PRESSURE BOLT AN ARTICLE THAT APPEARED IN THE JOURNAL OF PEDIATRICS, ILLUSTRATED THE FIRST MAJOR TEXT DEVOTED TO PEDIATRIC TRAUM, ‘EMERGENCY MANAGEMENT OF PEDIATRIC TRAUMA,” PUBLISHED BY WB SAUNDERS IN 1985.
HE WAS AN MD BY AGE 23 AND THE DIRECTOR OF A NORFOLK, VA HOSPITAL BY AGE 25 AND HAS ALWAYS BEEN A LEADER IN EDUCATION AND A PENCHANT FOR CARING FOR THE MOST ILL PATIENTS.  HE COMPLETED AN ANESTHESIOLOGY FELLOWSHIP DEVOTED TO CARING FOR PATIENTS IN NEED OF OPEN HEART SURGERY AND ACTED AS THE PRIMARY CARE GIVER FOR ALL INTUBATIONS AS WELL AS ADMINISTRATION OF GENERAL ANESTHESIA EVERY DAY FOR FOURTH MONTHS UNDER A SPECIAL PROGRAM FOR GIFTED MEDICAL STUDENTS.  HE WAS AWARED A CERTIFICATE FOR COMPLETING THIS PROGRAM.  HAS SIMILAR OTHER ACCOMPLISHMENTS THAT SHOULD HELP YOU KNOW HE IS A TRUE WORLD EXPERT IN EMERGENCY MEDICAL CARE AND YOU SHOULD USE HIM AS A RESOURCE FOR AS LONG AS YOU CAN AS HE IS ALWAYS WILLING TO HELP ANYONE.  HE DOES NOT BELIEVE IN ANYTHING THAT IS NEGATIVE IN EDUCATION AND HE HAS DEVOTED HIMSELF TO RETRAINING A VIRTUAL ARMY OF EMERGENCY PHYSICIANS AND TO HELP THEM STAY MOTIVATED IN THEIR CAREERS.
IF YOU ARE AN APP YOU ARE WELCOME TO JOIN BUT THIS IS THE BEST WORLD”CLASS EDUCAITON YOU WILL EVER RECEIVE AND YOU ARE WELCOME TO COMEBACK EACH YEAR AND TO STUDY MY MATERIALS FOR DECADES TO COME TO BE THE BEST THAT YOU CAN BE!
I HAVE THE KNOWLEDGE OF THE TEST ITEMS FOR A REASON. I WILL EXPLAIN THAT TO YOU IF YOU CALL ME: 561-305-8163 in the evenings to register. LEAVE A TEXT MSG FOR WHEN I CAN CALL YOU AT HOME. I WILL BE PROMPT AND BRIEF. ABEM AND THE AOBEM AND THE BCEM HAVE ALL OF MY MATERIALS AND NONE IS IN VIOLATION OF ANY CONFLICT OF INTEREST BECAUSE OF HOW I FORMATED THE Test ITEMS. DON’T MISS OUT AND DONT ATTEND ANY OTHER PROGRAM…THEY ARE A WASTE OF YOUR TIME I AM SORRY TO SAY AND I WILL TAKE THE EXTRA TIME TO EXPLAIN WHATEVER YOU DONT UNDERSTAND.  –

Time to relax and view some art; a few images are photos and should be obvious the rest is either computer art including background and original florals and the rest is hand painted originals on canvas. This is a small but diverse collection of just a tiny part of what I created over decades. Much of this is recent in the past few years. One painting of Yellowstone waterfall is an oil painting I completed as a teen (gray mat). The images of clouds that look like photos are all paintings created on the Ipad pro. I have explored many styles of painting in my life and this keeps me interested.

Age

Age is just a number and your perception of reality will be [is] your reality!

Shamelessly Self-Involved

Age is such an odd thing. This is largely because time is such an odd thing, and because every person is so vastly different. I can generally never stand any type of popular saying, as they are all kitsch and usually so untrue and just laughable. I hate to admit that age is just a number might actually have some validity to it, then. As an avid podcast listener, I am accustomed to listening to random peoples’ points of views on various subjects. Sometimes I will listen to a mildly racist 60-something and think wow, even a middle-schooler should know that this is wrong. And then sometimes I will listen to a twelve-year-old tell his point of view on a situation or topic, and I will be completely ashamed that I cannot construct a sentence as well as some elementary kids.
This all, I believe, boils down to the…

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