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 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.
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 stare. MC 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
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?
b. Hepatic failure
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.
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
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
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)
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.
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.
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.
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.
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)
DKA (cn hv asso’d cerebral edema esp during peds fluid resusc-see below)
INH, Iron OD
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.
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/
- 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 age. T highest risk is in children <age 5 yrs and it increased exponentially in infants*** i.e., those <1 yr f age. T 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/
- 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 ICP. Most 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.
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!
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