Survival Guide dummy by Jorge Duarte

LAC + USC DEM Survival Guide 2010

Editors Feier Borquez

CONTENTS ABC’s Resus Stocking Simplified Adult ACLS Tachycardia Bradycardia PEA Hypothermia Shock Sepsis RSI basics Hypertensive emergency Dyspnea Stridor

2 3 4 7 8 9 11 13 15 17 18 27

Pediatrics Formulas Crashing Neonate Peds fever <29 days Peds fever 2-24 months

Gyn Pelvic pain Pregnant VB (<20 weeks)

29 30 33 35 38 41 44

Common shoulder reductions Detailed hand exam Low back pain Joint pain

89 90 91 93

Random References DEM empiric antibiotic grid Needlestick protocol Billing and coding 101 Off-service rotation summary sheet Resident pagers VOIP list

Medicine Altered Mental status HA Seizure and Status Procedural Sedation & Code Green Vertigo Weakness EKG reading basics Chest pain Lytics – Stroke, PE, MI Syncope Abdominal Pain Acute Scrotum Acid base algorithm DKA basics Toxidromes EKG Toxicology

85 87

Ortho

Trauma CT Head reading C-Spine reading C-Spine algorithm Neck trauma Penetrating Chest Burns Pregnancy

79 81 83 84

45 47 49 50 51 53 55 57 64 65 67 73 75 76 77 78

95 100 102 103 104 105

Great care was taken to try to ensure the completeness and correctness of this guide, but errors are certain. Also they are not a substitute for common sense or clinical judgment nor do they represent a consensus view of management. And yes, you can still be M&M’d even if you follow it to the letter. Welcome to County. Thanks to all the USC DEM faculty – many of whose lectures are summarized here. In particular thanks to Drs. McCollough and K. Newton for their work on the empiric antibiotic guide, crashing Neonate, Gyn referral guide, needle-stick protocol and contact information. Dr. Tabatabai for his work on the pediatric formulae and drugs. Drs. Herbert and Masri for their tachydysrhythmia lectures. Dr. Swadron for his RSI lecture, CT Head reading lecture and images, and EKG pearls (also from Dr. Tabas’ lecture series). Dr. Hedayati & Mallon for their status epilepticus lectures. Dr. Votey for his DKA pearls. Drs Moulin, Wittenberg & Soifer for their work on the original guide.

Resus Stocking Taken from the old County survival guide Replace the word C-Booth with Resus Booth The junior resident in C-Booth is responsible for stocking as soon as sign-outs are taken. The utmost importance should be on the airway trays so that they are always ready. Airway trays: two laryngoscope handles with functioning lights one blade of each size, Miller 3 & 4 and Mac 3 & 4 ETTâ&#x20AC;&#x2122;s size 6.5 â&#x20AC;&#x201C; 8.0 (several of each) with stylets inserted and shaped into "J" be sure to attach syringes and test balloons a size 4 and 6 Shiley with disposable Cric kits McGill forceps an easily accessible Bougie a bag-valve-mask set up O2 supply with valve and "Christmas tree" should be tested a non-rebreather mask available Oral airways, nasal airways, surgilube, scalpels, and 14 gauge needles clean suction set up and tested including tubing and yankauers set up DEM Procedure trays: Two Chest-tube (thoracostomy) trays should be set up on Mayo stands at either end of C-Booth. Sterile trays are prepared by Central Supply and stored under the work counter near the sink. Open the top flap and place the following inside: syringe full of 1% Lidocaine with sticker labeled with date, time and your initials package of sterile gloves (your size) disposable scalpel suture 36Fr or 40Fr chest tube package of Vaseline gauze package of 0-Silk suture two packages of sterile 4x4 gauze tape on tray betadine bottle on tray Thoracotomy trays: They can be placed under procedure trays or nearby on shelf. Central line kits (Cordis): Place these on top of procedure trays and/or on side shelves. Taped to the top of each tray should be a dead head, an op-site, and a flush. Cricothyrotomy kits: At least one sterile Cric kit on the back counter

SIMPLIFIED ADULT ACLS

Airway, √ Pulse

Pulse Other orders: BS, ABG, RSI drugs, CXR Central line NS Bolus

No Pulse Bag, CPR, O2, IV Monitor, defibrillator

-CPR until defib arrives -Defib biphasic 200J monophasic 360J immediately resume CPR CPR x 5 cycles (30:2) x 5 after shock and before rechecking the rhythm

√ Rhythm

Bradycardic

√ Stability: CP, MS, BP

O2, IV Monitor, defibrillator EKG

O2, IV Monitor

√Rhythm VF/VT

Tachycardic

Asys or PEA

Stable -CPR x 5 -Vasopressin 40U x1 -Epi 1mg IV q3min -Atropine 1mg if slow PEA or asystole

Unstable +/- sedation

Go to Stable Tachycardia Algorithm

Synchronized Cardioversion Biphasic 120, 200J.

Adequate

Inadequate

Monitor √ Rhythm & pulse

Atropine 0.5mg IV repeat to total of 3mg.

- Shock -200J - CPR x 5 - 1mg Epi q3min

Effective

√ Rhythm

- Shock- 360 - CPR x 5 - Amio 300mg x1 then 150mg x1 - Mag 2 grams

Check perfusion: CP, MS, BP

Differentials Hypovolemia Hypothermia H+ (Acidosis) Hyperkalemia Hypoxia Hypoglycemia Toxins Tamponade Tension Pneumo Trauma Thrombosis

Orders Bolus Warming Bicarb Ca++, Bicarb, insulin, D50 O2 D50 Digibind, Glucagon… U/S,needle pericardiocentesis Needle decompression, chest tube IVF, Blood products. tPA.

Ineffective

- Pacing -Transvenous pacer. -alternative agents: epi 2-10 ug/min dopamine 210 ug/kg/min

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RAPID SEQUENCE INTUBATION GENERAL FORMULAS

General formula

Asthma variation (example)

Preparation, preoxygenate, pretreat: O2 Paralysis and induction Etomidate 0.3mg/kg Succinylcholine 1.5mg/kg Protection, placement, postintubation management.

Preparation, preoxygenate, pretreat Lido 1.5mg/kg, (If time allows) Paralysis and induction Ketamine 1.5mg/kg & Succinylcholine 1.5mg/kg Protection, placement, postintubation management .

Pediatrics < 8yo

Dialysis, Burns, HyperK+

Preparation, preoxygenate, pretreat Atropine 0.02mg/kg Paralysis and induction Etomidate 0.3mg/kg Succinylcholine 1.5mg/kg Protection, placement, postintubation management .

Preparation, preoxygenate, pretreat Paralysis and induction Etomidate 0.3mg/kg Rocuronium 1mg/kg (0.6-1.2) Protection, placement, postintubation management .

PARALYTIC AGENTS. Depolarizing Succinylcholine 1.5mg/kg

Nondepolarizing Rocuronium 1mg/kg Vecuronium

Onset

Duration

Pros

10s

Fast on and off

30s 1m

30-60m 45-60m

Cons Contra-indindicatied in: Hyperkalemia Burns >1d Denervation Disorder Malignant hyperthermia Maseter spasm Relatively slow. Will not be able to do neuro exam for >30m

INDUCTION AGENTS Name/dose Etomidate 0.3mg/kg

On/Off 40s/9m

Thiopental 3-5mg/kg Propofol 2mg/kg Ketamine 2mg/kg

40s/10m

Midazolam 0.07-0.3mg/kg

2m/1h

The good Rapid on/off Agent of choice Stable storage BP neutral

The bad Adrenal axis suppression with repeat admin.

40s/5m 60s/30m

Good for asthma & penetrating neck trauma (maintain airways if not using paralytic) Good for procedural sed.

REFERENCE: Swadron, EM Corecontent, Rapid sequence intubation.

↓BP not great conditions ↓BP storage/allergy probs not great conditions can cause psychosis can cause laryngospasm ↓BP, usually underdosed (dose=0.3mg/kg)

RSI - NOTES

I - Basics: 1) Indications Imminent failure of oxygenation, ventilation or airway protection 2) Advantages ↑success, ↓aspiration ↓IOP, ↓ICP, ↓pain. 3) Disadvantages Prolonged intubation, adverse drug effects (which ↑with multiple drugs), may force crash airway. 4) Contraindications. Full arrest (don’t need drugs), if you can’t do 2 out of 3 airway management techniques (BVM, ETT or Cric)

ii. prior to second dose of succinylcholine iii. Know that controversy exists (Fastle Ped Emer Care 20(10) 651-5 2004 & McAuffe Can J Anaesth 43(7) 754-5 1996.) c)

Defasciculating dose (optional) – i. Small dose of paralytic given 3 min before paralytic. ii. Traditionally thought to blunt ICP rise, ↓aspiration, ↓muscular pain. iii. Considered optional Clancy Emer Med Journal 18 (5) 373-5 2001. iv. Contraindicated in the case of pulmonary exhaustion/respiratory failure (COPD, Asthma…) v. Doses: Rocuronium 0.6mg/kg IVP. Vecuronium 0.01mg/kgIVP Pancuronium 0.01mg/kg

Opioids (Fentanyl) (don’t use) i. Traditionally used to blunt hemodynamic response to intubation and ↓pain. ii. Very limited role currently, don’t use

II - 7 Ps of RSI 1) Preparation a) Ask: can I bag, tube and cric? (should be able to do at least 2 / 3) b) Can I tube?: Mallampati, 3-3-2 rule, obstruction, neck mobility. 2) Preoxygenation a) Don’t bag unless sats drop. b) If you do bag, use the sellick maneuver.

4) Paralysis and Induction. a) See preceding drug list.

3) Pretreatment LOAD: Lidocaine, Opiods Atropine and Defasciculating. a) Lidocaine (optional) Was used to tx tight brains (lower ICP) and tight lungs (would decrease bronchospasm) but shown not to be true. (Robinson Emer Med Journal 18 (6) 453-7 2001 & Maslow Anesth. 93(5) 1198-1204 2000). Now consider optional.

Protection and position Sellick maneuver & C-spine precautions

Placement and protection

b) Atropine (0.01-0.02mg/kg IVP) standard of care for: i. all children age <8yo (susceptible to bradycardia)

Post intubation management. i. Confirm intubation: Auscultation & litmus capnography. ii. Secure Tube iii. Check CXR -Just makes sure tube is not in mainstem, but doesn’t confirm postion

Hypertensive Emergency 1 End Organ

Drugs

Comments

20-25% reduction in MAP over 2-3h (but keep DBP >100mmHg) BP no lower than 220/120 over 24h

SNP, FD, Labetalol, nicardipine

Treatment may worsen neuro function

SNP 0.25–10 µg/kg/min IV † infusion (maximum dose for 10 min only)

Labetalol

‫ڣ‬SNP, FD and NTG

Intracranial Hemorrhage

SBP 140-160mmHg (or pre-stroke level

Labetalol, SNP, nicardipine

Monitor for worsened neuro function while lowering BP

Labetalol 20 mg IV bolus over 2 min, followed q 10 min by 40 mg, then up to 3 doses of 80 mg; or 0.5–2 mg/min IV infusion See above Nicardipine gtt 5–15 mg/h IV

Subarachnoid hemorrhage

Generally withheld; if patient alert, consider treatment to decrease re-bleed risk

Nimodipine to prevent spasm +/labetalol

‫ڣ‬Avoid SNP, FD and

DBP ≤ 100 mmHg or resolution of symptoms

SNP plus NTG plus diuretic

DBP ≤ 100 mmHg or resolution of symptoms

NTG, β-blocker, Add SNP if DBP remains elevated

Avoid negative inotropes in LV dysfunction. Search for myocardial ischemia. In CAD or Peripheral Artery Disease search for renal artery stenosis

Hypertensive Encephalopathy

Ischemic stroke

Pulmonary edema

MI or unstable angina

Aortic dissection

Goal

SBP 100-12- or MAP 80 mmHg (watch urine output)

Sympathomimetic OD (cocaine, amphetamine)

DBP 100-105 (but ≤ 25% reduction in presenting BP) over 26h.

Pregnancy (eclempsia)

DBP 90-105 or MAP ≤ 126 mmHg

Acute renal insufficiency.

DBP 100-105 (but ≤ 25% reduction in presenting BP)

SNP: Sodium nitroprusside FD: Fenoldopam β-B : Beta-blocker NTG: Nitroglycerin

may increase ICP. Goal of 185-110 if thrombolytic given

SNP or FD plus β-B or labetalol

Benzodiazepines. Phentolamine (first) then β-B or labetalol.

Hydralizine, labetalol, nifedipine. Magnesium FD, Ca++ channel blocker, SNP

NTG (vasodilatation increases ICP)

Doses

Nimodipine 60mg PO/NGT q4h

See above NTG gtt 5–100 µg/min IV

See NTG and Labetalol above

0$ Start with betablocker to decrease wall shearing and blunt reflex tachycardia you will get with the afterload reducer ‫ڣ‬DO NOT give βblockers alone (will get unopposed alpha stimulation). Restart clonidine if withdrawing. PO: methyldopa. Avoid SNP, ACE-I.

Avoid diuretics.

Esmolol 250–500 µg/kg/min for 1 min, then 50–100 µg/kg/min for 4 min; may repeat sequence SNP – See above

Phentolamine 5–15 mg IV

Hydralizine 10–40 mg IV

Fenoldepam 0.1–0.3

µg/kg/min IV infusion; maximum dose 1.6 µg/kg/min

Reference: Table is adpted from Tarascon Internal medicine and rd Critical Care 3 edition, p 37 and the Merck Manual http://www.merck.com/mmpe/sec07/ch071/ch071c.html

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INDUCTION AGENTS Name/dose Etomidate 0.3mg/kg

On/Off 40s/9m

Thiopental 3-5mg/kg Propogol 2mg/kg Ketamine 2mg/kg

40s/10m

Midazolam 0.070.3mg/kg

2m/1h

The good Rapid on/off Agent of choice Stable storage BP neutral

40s/5m 60s/30m

Good for asthma & penetrating neck trauma (maintain airway s if not using paralytic) Good for procedural sed.

The bad Adrenal axis suppression with repeat admin. #BP not great conditions #BP storage/allergy probs not great conditions can cause psychosis can cause laryngospasm #BP usually underdosed (dose=0.3mg/kg)

PARALYTIC AGENTS. Depolarizing Succinylcholine 1.5mg/kg

Nondepolarizing Rocuronium 1mg/kg Vecuronium 0.1-0.3mg/kg

Ons et

Duration

Pros

10s

Fast on and off

30s 1m

30-60m 45-60m

Cons Contra-indindicatied in: Hyperkalemia Burns >1d Denervation Disorder Malignant hyperthermia Maseter spasm Relatively slow. Will not be able to do neuro exam for >30m

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6$"+/7"8/) M03+#)%H!9%K#+&,)$%+,0(! % J$-0\!U$+()%@!b^^^!9%),-!E6!Ph^9%),-F;@R!f!d]h^!9%),-F'!Pdh9%),-F;@F'R! % Y$+*!577\!enV_^!-0&! • U8I!M03+#)%! % G$%,#+)%()&+,)$%-\!-0C0#0!$:0-),<H!#0%+*!K+)*=#0!PA($-0!+(l=-,/0%,RH!B,je^;@! % J$-0\!d/@F;@!1W!a!d]'! • 7'#$/:$*<,)&-A!P./!Q!2/0#@!80(!]^^mc]_\heVmbR! % G+#()+&!+##0-,\!)/3#$C0!>T1G!+%(!)/3#$C0!-=#C)C+*! % 8+--)C0!52!P1"5jm^R!(0&#0+-0!#)-;!$K!(0+,'!+%(!#0&=##0%,!52! % 1=:/+--)C0!52!! " J0K)%0\!-,+:*0!'0/$(<%+/)&-!B),'!>6!(<-K=%&,)$%!P,#$3$%)%H!"45H!2GMTR! % 4$#/+*!MJ!B),'!0C)(0%&0!$K!>6!(<-K=%&,)$%!P?0/#7+2/;+@)%#*'&!]^^bcAA\_nnV__dR! " )%&$%&*=-)C0! % 1,+:*0\!%$!:0%0K),!)%!3+,)0%,-!B),'!-,+:*0!MJ!+%(!%$#/+*!>6!K=%&,)$%! =&%>0%&/&08\!.(/),!K$#!+,!*0+-,!]e!'!:0&+=-0!$K!!!#+,0!$K!&$/3*)&+,)$%-!+%(!#0&=##0%&0! ! ! •

1)Airway Emergency?

2)Emergent diagnosis? Epiglottitis

Bacterial Tracheitis

RPA

Foreign body

3)Congenital cause?

4)Croup

• • • •

Racemic epi Nebulized steroids Steroids IV Emergent intubation?

Stridor-Upper Respiratory

H&P

W/U and Tx

• • • • •

Drooling Dyspnea Dysphonia Dysphagia !fever

• Lateral Xray#thumbprint • Airway management#in OR • Avoid anxiety • Gentle op exam • Antibiotics/Admit

• Age: 6m-8y • Season: fall/winter • Present similar to Epiglottitis/Croup • Cough

• • • •

Toxic !fever Resp distress No response to treatment

• Frontal Xray#?steeple • Airway management#OR • Antibiotics • Admit

• Age: 6-12m • Torticollis (stiff neck?) • Dysphagia • Trismus

• Toxic • !fever • !neck extension

• Lateral Xray#soft tissue swelling • CT neck, U/S • ENT C/S • Antibiotics • Airway management

• Age: Infants/toddlers • Classic Triad (wheeze + cough + "BS) present in only 1/3

Symptoms (3 stages) • Violent cough • Asymptomatic interval • Complications

Xrays (nl in 2/3) • Bilateral decubitus • Insp/Exp Position of comfort Po ENT

• • • • •

Age: 2-8yo Season:winter Viral type prodrome Toxic, irritable Tripod position, hyperextended neck

Stridor present since birth? • Laryngomalacia • Vascular ring • Subglottic stenosis • Webs • Vocal cord paralysis • Papillomas

• • • • •

• !fever/toxic#rare • Croup score?

Age: 6m-4y Season: fall-winter Viral prodrome Barky cough Hoarse

• Frontal Xray#steeple sign • Mist • Decadron • Racemic Epi

General Types of stridor: Inspiratory"subglottic; Expiratory"supraglottic; Biphasic"subglottic, glottic; Sonorous"nasal

Epiglottitis • •

•

General: acute inflammation of epiglottis and surrounding structure"serious, life threatening, airway emergency Diagnosis ! Lateral neck" “thumbprint sign” negative in up to 20% of cases. (Prim care 1990;17(2):335-45) ! Diagnosis made on visualization of inflamed epiglottis Treatment ! Avoid agitation of child as this can worsen the airway (no IV, oral examination) ! If emergent airway needed"use tube size 0.5-1 smaller than age ! Ideal airway should be obtained in the OR, controlled conditions ! Antibiotics (3rd gen Ceph)

Bacterial Tracheitis-(croup-like illness + toxic + not respond to therapy) • • • •

General: laryngeotracheobronchitis, subglottic edema and membranous secretions Clinical: vs epiglottitis"tracheitis children have a cough, comfortable lying down, no drool (J Otolaryngol 1989;18(3):101-4) Diagnosis"endoscopic visualization of normal supraglottic structures and subglottic inflammation, ulcers, secretions Treatment ! Emergent airway"use tube size smaller than age ! Ideally intubated , diagnosed, cultured in the OR, optimal conditions ! Antibiotics"anti-staph

Retropharyngeal abscess (looks like meningitis with normal mental status) • •

General: deep neck space infection, can spread through neck"danger space"cause mediastinitis Clinical: ! Age: 50% of cases occur between 6-12mos, 96% occur before 6 years of age (Arch Dis Child 1991;66:1227-30) # Lymph nodes of Rouviere that drain the retropharyngeal space atrophy after this age ! Typical presentation is child with neck in neutral, difficulty extending neck and uses eyes to look up, vs !neck flexion (meningitis). (Pediatrics 2003;111:1394-8)

Foreign Body • only 50% diagnosed in first 24h"usually asymptomatic in ED, therefore must elicit a choking/coughing episode • Complications: Obstruction, infection, fever, cough

Croup • • •

•

• •

General: Peak incidence in 1-2yo Organisms: Parainfluenza I (most common), II and III, M. pneumoniae, RSV, Influenza A, B, adenovirus Clinical ! Sx peak over 2 days and resolve over 1 week ! Croup score: mild (0-4), mild/mod (5-6), moderate (7-8), severe (9-14), terminal (15) Treatment ! Cool mist: sooths inflamed mucosa # Multiple studies show minimal efficacy in treating croup (JAMA 2006;295(11):274) ! Steroids!all croup in the ED? 0 1 2 3 # Multiple studies show efficacy, associated with a decrease in ED stay Cyanotic Cyanotic nl Dusky Color and ED bounce backs (Ann Emerg Med 2002;30(3):353) on o2 # Efficacious for even mild croup, lees likely to return for croup Nl Mild! Mod! Marked! Air mvmt related care (NEJM 2004;351(13):1306) Mild Mod Sever Retractions None # Dose: 0.15mg/kg vs 0.3mg/kg vs 0.6mg/kg?? equally efficacious PO Nl Restless Lethargic Obtunded Mentation or IM or inhaled (Acad Emerg Med 2003;10:16) None Mild Mod severe ! Racemic epinephrine!mod/severe croup; stridor at rest Stridor # Dose: 0.25-0.5ml of 2.25% soln with saline 3ml, can substitute with epinephrine 0.5ml /kg of 1:1000, 5ml max with equal efficacy (Pediatrics 1992;89(2):302) # Use"stridor at rest, can help reduce need for emergent intubation # Rebound phenomenon"not need admission for observation, if significantly improved-can be safely discharged after 3 hours (Ann Emerg Med 1995;25(3):331-7) ! Summary: may give cool mist, steroids for all kids in ED, epinephrine only if they have stridor Discharge: well appearing, nl color, no stridor at rest, no aloc Admit: Moderate croup score, toxic appearing, respiratory distress

Head CT Reading Checklist

Step 1: Soft tissue & Bone Pos-traumatic changes in soft tissue structures – hematomas, lacs, foreign bodies Skull for fractures and metastases in the bone window.

Step 2: CSF & ICP Normal contour of qudrigeminal and basal cistern? (risk of brainstem herniation) Normal size of ventricles and CSF spaces appropriate to the patient’s age? Any blockage to flow of CSF (obstructive hydrocephalus) or signs of brain edema (effaced sulci)? Look evidence of elevated ICP: Mass effect with a midline shift ≥3 mm Collapsed third ventricle Hydrocephalus Effacement of sulci with evidence of significant edema Abnormal mesencephalic cisterns

Step 3: Brain tissue & arteries Evaluate cerebral arteries for regularity Find areas of hyperdense foci and calcifications. Common areas of calcification are choroids plexus and pineal body. Paraventricular white matter and cortex inconspicuous and well defined? Any focal lesions or local edema? Basal ganglia and internal capsule intact? (common areas of infarction). Brainstem, pons and cerebellum normal? REFERENCES Text adapted from: CT Teaching Manual: A Systematic Approach To CT Reading 2nd Edition by Matthias Hofer Images all from Swadron’s CT head lecture. CT findings of elevatd ICP Acad Emerg Med. 2003 Apr;10(4):376-

C-SPINE CHECKLIST LATERAL QA: C1 to Top of T1 are visible Lines: 1) Arcs of anterior spinal, posterior spinal and spinolaminar lines should be smooth. Limit of overriding of vertebral bodies is 2.5 mm 2) Posterior cervical line Spinolaminar line of C2 should be w/I 2mm anterior or posterior to this line Vertebral bodies: look for cortical defects and uniform height. Atlanto-dens interval AKA Predental space: ≤3mm adults, <5mm peds Prevertebral soft tissues: 1) C2 Prevertebral space/ retropharyngeal space ≤6mm adults 2) C6 Retrotracheal space ≤22mm in adults 3) Prevertebral fat stripe should no bulge out Pseudosubluxation: anterior displacement of C2 on C3 of up to 4 mm or 40% displacement. Normal in <8yo. Should not be associated with prevertebral soft tissue swelling. Use Swischuk’s line to see if pseudosubluxation is pathological.

AP Spinous processes: in a straight line and spaced equally. A unilateral facet dislocation causes rotational displacement of the adjacent vertebrae in turn causing misalignment of the processes. Anterior cervical dislocation causes a wideing of the interspinous spaces. No single space should be >50% than the one immediately adjacent.

ODONTOID Dens fractures – types I (through upper dens, rare, good prognosis) type II (through the . junction of odontoid with body of axis, unstable especially if posteriorly displaced) , III (thorough the body of the axis). Displacement of the margin of either of the lateral mases of C1 away from the corresponding margin of C2 (ie overhanging lateral margins of C1 on C2). Unequal or increased space between the dens and lateral mass of C2. Combined lateral mass displacement > 7 mm suggests that transverse ligament is torn

References: http://www.aafp.org/afp/990 115ap/331.html Tarascon Pediatric emergency pocketbook 4th ed p 167 http://www.wheelessonline. com/ortho/pseudosubluxatio n_of_the_c_spine

GLOSSARY OF MISC. MEASUREMENT TOOLS 1) 2) 3) 4)

Powers ratio. X÷Y. Normal is 0.7. 0.7 -1.0 suggests anterior subluxation of atlanto-occipital (AA) joint. Atlanto-occipital dislocation. Line from anterior margin of foramen magnum to the tip of the odontoid should be <12mm. If greater, atlantooccipital dislocation may be present. Wackenheim line – line along posterior clivus (clivus base line=D) usually intersects tip of odontoid tangentially. If displaced suspect atlanto-occipital joint laxity. Swischuk' Line line is drawn from the anterior aspect of C1-C3 spinous processes; this line should be within 2 mm of the anterior C2 spinous process;

Accident & Emergency Radiology 2nd edition. http://www.ispub.com/xml/j ournals/ijn/vol4n1/cervicalfig1.jpg

UNSTABLE C-SPINE FRACTURES Flexion

Flexion-Rotation

Flexion teardrop Anterior displacement of wedge-shaped fragement of anteroinf. Portion of vertebral body. Commonly assoc. with ligamentious and nerve injury. Subluxation Ligamentous complex rupture w/o associated bony injury. The degrees of ligamentous injury produce 1) Subluxation of vertebral body 2) Perched facet 3) Locked facets (At least 50% subluxation)

Rotary atlantoaxial dislocation Asymmetry in the relationship of the lateral masses of c1 to the odontoid process. Rotation causes the one lateral mass to appear larger

Extension Posterior neural arch C1 fracture Compression of the posterior elements between the occiput and the spinous process of the axis (C2) during forced extension

Normal relationships of facet jointsInferior articulating facet of body above (blue arrow) lies posterior to superior facet of body below (red arrow)

Extension teardrop Abrupt extension causes the ant longitudinal ligament to pull the anterointeroir corner of the vertebral body away from the remainder of the vertebra.

Bilateral facet dislocation â&#x20AC;&#x201C;inferior articulating facets of the upper vertebra pass up and over the superior facets of the lower vertebra. Very unstable. Body of C4 is subluxed anteriorly on C5. The inferior facet of C4(blue arrow) lies anterior to the superior facet of C5 (red arrow).

Atlanto-occipital dislocation Anterior atlantoaxial dislocation

Odontoid fracture with lateral displacement fracture

Increase in the distance between the anterior surfaceof the dens and the posterior surface of the C1 tubercle (blue arrow). The imaginary line connecting the spinolaminarlines (white line) shows that the body of C1 (red arrow) is displaced anteriorly relative to the remainder of the spine.

Hangmanâ&#x20AC;&#x2122;s Trumatic spondylolysis of C2 (with or without anterior subluxation of C2 on C3) caused by extreme hyper extension.

Bilateral C2 pars (common) or Pedicle (less common) Now seen most commonly in head-on MVA patients.

Posterior atlantoaxial dislocation

Verticle compression Jefferson burst C1 Compression force drives the lateral masses outward resulting in fractures of the anterior and posterior arches of the atlas and disruption of the transverse ligament

STABLE C-SPINE FRACTURES Flexion Wedge Diminished height and increased concavity of the anterior border of the vertebral body. Increased density of the vertebral body and prevertebral STS.

Clay Shoveler’s An avulsion of the spinous process of the lower cervical vertebrae, classically C7, is known as a clay-shoveler´s fracture.

Because the posterior column remains intact this injury is usually stable, unless there is >50% of height loss or there are mult. Adjacent fractures.

An isolated clay shoveler´s fracture is mechanically stable. Conservative treatment with ice, analgesia, rest, and early referral is indicated.

Intense flexion against contracted posterior erector spinal muscles causes avulsion of the spinous process.

Transverse process

Although stable, there are case reports of vertebral-basilar artery stroke

Flexion-Rotation Unilateral facet dislocation Involves both flexion and rotation causing one facet to function as a fulcrum and the contralateral facet to dislocate. This locks the dislocated articular mass in place, making it a stable fracture. The Lateral shows forward displacement of the dislocated segment on the vertebra belos (<50% of the AP diambeter) T The AP shows spinous processes displaced from the midline.

Vertical compression Verticle compression causes the Burst fracture nucleus pulposus of the disk into the vertebral body which is of the vertebral shattered outward. body The fracture is stable because all ligaments remain intact. However, fracture fragment may impinge on or penetrate the spinal cord causing an anterior cord compartment syndrome

Isolated articular pillar

burst fracture

articular pillar fracture

C-Spine Clearance Clinical Clearance? 1. 2. 3. 4. 5.

NEXUS

No midline tenderness No focal neuro deficit Normal level of alertness No intoxication No distracting injury

Yes

Clinical Clearance

Radiography (see Step 2)

+/High risk factor? • Age > 65 • Dangerous mechanism • Paresthesias

CCR

Yes

No Low risk factor? • • • • •

Simple rear-end MVC Sitting position in ED Ambulatory any time Delayed neck pain No midline tenderness

Radiography (see Step 2)

Unable

Yes Actively rotate neck 45 left/right

Clinical Clearance

Radiographic Clearance • CT + MRI entire C-spine • Neurosurg C/S

Neuro deficit

risk

C-spine Xrays (3 views) • Adequate films? • Completely negative? • Low risk patient?

Yes Radiographic Clearance

No neuro deficit !risk

CT C-spine • Negative with recons • High risk pt. • Inadequate/abnormal Xrays

Yes

C-Spine Clearance NEXUS •

Definitions Midline posterior bony cervical-spine tenderness is present if the patient reports: √ pain on palpation of the posterior midline neck from the nuchal ridge to the prominence of the first thoracic vertebra, or √ if the patient evinces pain with direct palpation of any cervical spinous process. Patients should be considered intoxicated if they have either of the following: √ a recent history provided by the patient or an observer of intoxication or intoxicating ingestion, or √ evidence of intoxication on physical examination such as an odor of alcohol, slurred speech, ataxia, dysmetria, or other cerebellar findings, or √ any behavior consistent with intoxication. √ Patients may also be considered to be intoxicated if tests of bodily secretions are positive for alcohol or drugs that affect the level of alertness. An altered level of alertness can include any of the following: √ a Glasgow Coma Scale score of 14 or less; √ disorientation to person, place, time, or events; √ an inability to remember three objects at five minutes; √ a delayed or inappropriate response to external stimuli; or other findings. A focal neurologic deficit is any focal neurologic finding on motor or sensoryexamination. No precise definition of a painful distracting injury is possible. √ This category includes any condition thought by the clinician to be producing pain sufficient to distract the patient from a second (neck) injury. √ Such injuries may include, but are not limited to, any long-bone fracture; a visceral injury requiring surgical consultation; a large laceration, degloving injury, or crush injury; large burns; or any other injury causing acute functional impairment. √ Physicians may also classify any injury as distracting if it is thought to have the potential to impair the patient’s ability to appreciate other injuries.

•

Evidence NEXUS validation study (NEJM 2000;343:94-9) √ Cervical Spine injury (Sens 99%, NPV 99.8%) √ Clinically significant injury (Sens 99.6%, NPV 99.9%) CCR vs Nexus study (NEJM 2003;349:2510-8) retrospective study done by developers of Canadian rule √ Sensitivity 90.7% for NEXUS vs 99.4% for CCR Do we need each of the 5 criteria? (Ann Emerg Med 2001;38:22-25) √ A substantial number of patients (29%) with clinically significant CSI met only one of the criteria √ Posterior mid-line tenderness was the only criteria present in 61% of these patients √ Distracting injury was sole criterion present in 45/578 of patients with clinically significant CSI

Canadian C-spine rules •

Definitions For patients with trauma who are alert (as indicated by a score of 15 on the Glasgow Coma Scale) and in stable condition and in whom cervical-spine injury is a concern, the determination of risk factors guides the use of cervical spine radiography. A dangerous mechanism is considered to be: √ a fall from an elevation !3 ft or 5 stairs; √ an axial load to the head (e.g., diving); √ a motor vehicle collision at high speed (>100 km/hr) or with rollover or ejection; √ a collision involving a motorized recreational vehicle; √ or a bicycle collision. A simple rear-end motor vehicle collision excludes being pushed into oncoming traffic, being hit by a bus or a large truck, a rollover, and being hit by a high-speed vehicle.

•

Evidence CCR validation study (JAMA 2001;286:1841-1848) √ Senstivity 100%

Radiographic Clearance •

•

Plain Xrays (Ann Emerg Med 2001;38:1-7) Role: Screening radiography to detect evidence of injury then other modalities (CT, MRI) can be used to evaluate the injury. Cervical Spine Xrays (3 views, adequate, no abnormality) missed 0.07% of fractures (23 missed/34,069 total pts), NPV 99.9% Only 3 of these injuries were potentially unstable (0.008% of all blunt trauma patients) CT C-spine Multiple studies show high sensitivity (100%) of if done with lateral reconstructions (to eval alignment) Straight to CT? (no plain films?) √ High risk patient (>1 Nexus criteria, bad mechanism of injury) √ Low likelihood of adequate films: DJD, obese, ALOC

Airway Control

Bleeding Control

• • • •

ABCs Emergent airway? Procedure of choice! RSI Back-up plan?: LMA, nasotracheal, fiberoptic, cric, direct tracheal • C-collar! ?remove for airway eval if neuro intact

• • • • •

Direct pressure No clamps, No ties (except EJ) Platysma violated? Resuscitation: IVF, blood transfusion Unstable! OR

Evaluate Injury

Airway

Vascular

Hard signs

Soft signs • • • •

• Severe active bleeding • Expanding hematoma • Peripheral pulse absent/ diminished (ABIs) • Bruit/Thrill • Unexplained hypotension/shock

• Small/moderate hematoma • Minor bleeding • Proximity wound • CNS/peripheral ischemia

• Color flow Doppler • CT angio (4 vessel) • Angiography

• None

• Painful swallowing • SQ emphysema • Hematemesis

• Barium swallow • Flexible endoscopy • Rigid endoscopy

• None

Work-up Hard signs

Selective Work-up

• Respiratory distress • Air bubbling through wound • Major hemoptysis

Digestive tract

Neurologic

Penetrating Neck Trauma

• • • •

SQ emphysema/air Hoarseness Minor hemoptysis Trachea deviated

Spinal cord deficit Cranial nerve deficit Horner’s syndrome Brachial plexus injury

• CXR/ soft tissue neck • CT neck • Bronchoscopy

• C-spine series • CT C-spine • Vascular eval

Xray: CXR, AP/lateral soft tissue neck

OR!surgical exploration Selective Management

Soft signs

Asymptomatic

• Zone I!CT angio, bronch, endoscopy • Zone II!CT angio, bronch, endoscopy vs exploration • Zone III!CT angio, CT Head

Observation vs selective management 35

Airway management • •

Indications for emergent airway: Hypoxia, Unable to prtotect airway (loss of gag, "secretions…), AMS, shock Emergent airway (Mandavia et al, Ann Emerg Med 2000;35:221-5) ! 11% needed emergent airway management ! 100% successful with RSI if clinician deemed airway to be RSI capable Suggested References

Control Bleeding • • •

Persistent bleeding from Zone I injury!possible subclavian artery injury ! May temporarily tamponade bleed by inserting foley into entrance wound Impaled objects!do not remove, to be removed in OR Cardiac arrest ! ED thoracotomy, cross clamp aorta and treat for air embolism " Trendelenburg and attempt to aspirate air from right ventricle

• EM:RAP August 2006 (S. Coluciello) • CMEDownload Resuscitation 2006 (K. Inaba) • Review: Emerg Med Clin N Am 2007;25:679-94

Injury Evaluation •

•

Airway injury trachea, esophagus, great Zone I clavicles! ! Physical exam vessels, thoracic duct, upper inferior cricoid " Hoarseness!likely laryngeal fracture/injury or recurrent mediastinum, lung apices cricoid cartilage carotid and vertebral arteries, Zone II laryngeal nerve injury !angle of jugular veins, pharynx, larynx, " Hemoptysis! ask patient to cough to evaluate for hemoptysis mandible esophagus, trachea ! Work-up Zone III angle of distal carotids and vertebral " Plain films (CXR, AP/lat neck)! cervicofacial emphysema, mandible! arteries, jugular veins mediastinal emphysema base of skull " MDCT! extrapulmonary air, tracheal disruption " Bronchoscopy! gold standard Vascular Injury ! Physical exam " Zone I! check ABI of each arm, if <0.9, assume vascular injury " Bruit/thrill! 50% of carotid injuries have bruits, pathognomonic of AV fistula that needs repair " Normal PEX and CXR showed NPV 100% for vascular injury in one series (J Trauma 2000;48:208-13) ! Work-up " CT angio! sensitivity 90-100% Digestive tract ! Physical exam " SQ emphysema! can be esophageal or tracheal injury ! Work-up (Am J Surg 1987;54:619-22) " Esophageal injury, most commonly missed injury!early diagnosis and treatment is critical " CT !not sensitive enough to detect all esophageal injuries; if "suspicion, need further work-up " Combination rigid endoscope + barium swallow ! 100% sensitivity for esophageal injuries Nerve injury ! Physical Exam " Lower cranial nerves i CN 9 (glossopharyngeal)!say aaahhhhh, is palate rising, midline ii CN 10 (vagus, recur laryng n.) !hoarseness iii CN 11 (Accessory nerve)! shrug shoulders iv CN 12 (hypoglossal)! tongue midline " Spinal Cord injury i Moving all extremities, sensation in all extremities, rectal tone, priapism ii Unstable C-spine fx? ! can clear c-collar? (a) Stab wounds!no reports of unstable fractures (b) GSW!all unstable c-spine fx patients also presented with neurological signs (Spine 2005;30:2274-9) " Horner’s syndrome!Carotid injury i Ptosis, miosis anhidrosis " Brachial Plexus injury i Increased in Zone I injuries • Median n.!fist • Musculocutaneous n. ! flex forearm • Radial n.!wrist extension • Axillary n.!abduction of arm • Ulnar n.!finger abduction/adduction ! Work-up!Plain films for C-spine fracture, CT angio to evaluate carotids

No role for steroids in penetrating spinal cord injury (Neurosurgery 1997;41:576-83

Work-up • • •

Absolute indications for OR (Hard signs): shock, uncontrolled bleeding, absent radial pulse, resp distress Symptomatic with soft signs ! Directed evaluation based on symptoms and zone of injury Asymptomatic patients (Demetriades et. al. World J Surg 1997;21:41-48) ! Absence of signs/symptoms suggestive of vascular or aerodigestive excluded significant injury (NPV 100% for both)

Blunt neck injury •

•

Clothesline injury! ? transection of trachea ! Consider fiberoptic or awake intubation (RSI causes loss of muscle tone and "risk of soft tissue intubation) ! Work-up! CT scan Blunt Carotid injury! dissection, pseudoaneurysm !Stroke ! Seatbelt sign " Not an isolated finding; If no hard findings! not need work-up ! Horner’s syndrome ! Expanding hematoma ! Bruit/ thrill ! Stroke findings ! Treatment! Heparin and Coumadin Vertebral artery injury ! Can embolize to ipsilateral or contralateral side ! Clinical: HA + neck pain +/- Brainstem sx (vertigo, ataxia, CN findings) Strangulation ! Injuries: larynx, hyoid, trachea, rare cervical spine injury (only in judicial hangings, "height) ! Pitfall: well appearing on arrival!hypoxic lung inury and florid pulmonary edema after 4-6 hours " Check for petechiae to face and neck " CXR prior to discharge for pulmonary edema ! Work-up: CT neck (especially if hoarse, crepitus) " CXR prio

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Trauma in Pregnancy1 ≥ 24 weeks No

Algorithm adapted from from Rosen’s Emergency Medicine. 6th Edition. Mosby-Elsevier

Test Vaginal bleed

Yes

Watery discharge Crystallization Test Bimanual

Rupture of membranes

Continuous FHM with OBRN to look at toco Rh

Late Decelerations Loss of beat to beat variability Rh- RhoGAM

Kleihauer-Betke

Fetal-Maternal hemorrage anti-D immunoglobulin, Placental/Uterine injury

Focus on the mother Intermittent fetal monitoring

Maternal 1˚ Trauma Survey & FHT Unstable

Maternal 2˚ Survey eval fetal distress 2 FHT stable

Maternal Arrest -FHT

Stop

Stable

Maternal Resus

+FHT

FHT unstable

Perimortum C-section5

Emergent OB Gyn C/S 4

Monitor3

Looking for Placental abruption

DIC panel

Bony pelvic injury

Placental abruption is known to occur 48hrs after an event. Range of recommended monitoring is 4-48 hours Monitor for 4 hours, but if any of the following are present, extend to 24hrs Frequent contractions ≥ 3/h Abdominal/uterine tenderness Vaginal bleeding Evidence of hypovolemia Abnormal fetal tracing. Pearlman MD Tintinalli JE Am J Obstet Gynecol 162: 1502, 1990 Discharge instructions: < 4 fetal movements/h goes to OB for NST& RTED for preterm labor, membrane rupture, bleeding & pain

Emergent OB Gyn C/S Indications: Fetal distress, Uterine rupture, Fetal malpresentation during premature labor Begin 4 minutes after arrest. Continue maternal resus during cesarean. If thoracotomy is done, do not cross clamp aorta before cesarean. Henderson SO, Mallon SK Trauma in Pregnancy EM Clinics of North America Vol 16 Num 1 Feb 1998. No infant survives if FHT are absent before emergent cesarean begins. Ann Surg 223:481, 1996 Morris JA Jr

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Hypo/Hypernatremia Uremia Hepatic Encephalopathy Toxidrome/Toxic OD (CO, ASA, EtOHs), withdrawal, Serotonin Syndrome

LP !

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Hypertensive Encephalopathy • Acute organic brain syndrome to failure of cerebral auto-regulation • MAPs> 150! failure of autoregulation, endothelial dysfunction and vasogenic edema • If not treated! leads to coma and death Symptoms • HA, Mental status changes (confusion!lethargy!coma), Visual changes (cortical blindness, scotoma, hemmianopsia) • Rare: seizures, focal neuro deficits, papilledema Diagnosis • Diagnosis of exclusion#Consider: SAH, ICH, SDH, EDH, infection (meningitis/encephalitis), drug ingestion/withdrawal, uremia Management • Fluid resuscitation#Usually volume depleted 2/2 pressure induced natriuresis ("renin/Angiotensin/Aldosterone) • BP reduction#Decrease BP by 25% in first 2 hours $ 1st hour: decrease BP by 10-15%; 2nd hour: decrease BP by an additional 10% $ If BP reduction >40%! neurologic event!!! • Medication route# IV titratable medication should be used $ SL, transdermal, oral route should not be used! can cause precipitous decline that can not be reversed • Dosing $ Not recommended: clonidine (CNS depressant effects), diuretcs (volume depleted already), Hydralazine (can give sharp decline in BP; ok for eclampsia), Nitroprusside (linked to "ICP, CN toxicity), Nicardipine, Enalapril $ Labetalol 20mg IV and double dose every 5-15 minutes $ Nicardipine gtt (5-15 mg/h) $ Fenoldopam

1. Emergency HAs K I L L E R S

Intracranial hemorrhage SAH

Mass Lz (tumor, abscess, chronic SDH)

IIH M A I M E R S

Hx • • • • •

(Pseudotumor Cerebri)

Temporal Arteritis

• • •

• •

Fever Neck stiffness AMS

•

Hx • • • • • • •

• •

CT LP Tx:

Focal neuro deficit Meningismus (70%) Retinal/vitreal bleed

Focal neuro exam HIV/Immunocomp

PEX • •

Progressive, exertional HA Morning HA New onset Sz HIV

• •

Obese, young female HA x weeks/months Visual disturbances

Papilledema Causal Meds?

Other clinical features • Jaw/tongue claudication • Vision change

Dx (need 3/5) • Age >50 • New HA • Temp art tender/ decr pulse • ESR>50 • biopsy→vasculitis/granuloma

• •

Eye pain,N/V, blur vision Conj hyperemia

• •

CO Poisoning

• • •

Exposure? Multiple pts/similar location/similar sx HA c N/V/syncope

• • •

Acute Sinusitis Obstructive hydrocephalus Benign Exertional HA

Corneal edema mid-dilate, non react pupil

• • •

Neurosurg C/S Nimodipine Coil vs clip

• •

CT? LP

• •

Dexamethasone Antibiotics

•

Resp iso

CT (+contrast?)

Focal neuro papilledema

Acute Glaucoma

2. Urgent HAs

Work-up/Tx

PEX Onset: sudden onset (thunderclap) Quality: qualitative different HA than previous Severity: +/- worst HA Assoc sx: N/V, syncope, ALOC, diplopia Risk factors: HTN, EtOH, smoking, FamHx

H&P

Meningitis

Headache

Red Flags

LP?

CT LP (Opening press. 20-40) Tx • Wt control, Steroids • Acetazolamide • Serial LPs • Ophtho/Neuro C/S

• • •

ESR Temp art bx Empiric Prednisone (1mg/kg/d)?

• •

IOP elevated Timolol/glaucoma Rx

• •

CoHb level* O2 (NRM vs HBO)*

Post-Traumatic Drug/Food Related Cranial Neuralgias

3. Primary HAs Common Migraine • Severe, throbbing, unilat HA • Photo/Phonophobia • Hours to days

Classic Migraine • Preceded by aura • +/- GI distress

• • • •

Compazine IV IVF Triptans NSAIDS

Middle aged men Sudden onset HA Unilateral blur vision/nasal congest/lacrimate/salivate/ sweat

•

Cluster HA

• • •

•

Last hours, recur same time of day PPT by exertion/stress

• • • •

O2 Symptomatic Intranasal lidocaine Neuro referral

Tension HA

• •

Frontal/occipital/band-like No preceding event

•

No assoc sx

Symptomatic relief (NSAIDS, Tylenol)

Migraine HA

Headache

General Approach: • • •

Emergency department evaluation relies on excluding life-threatenting causes of HA, specifically SAH and meningitis. Then consider other serious causes of headache that can debilitatie the patient (the maimers) When these have been excluded, we can then diagnose primary headache syndromes.

SAH •

• •

The clinical presentation of SAH lies on a spectrum. The classic (middle of the spectrum) presentation is that of sudden onset and distinct HA, worst of their life associated with neck pain, N/V. a On the extreme end, they can present with focal neuro deficit and ALOC. b On the subtle end 1/3 present with only HA without neuro deficits, and are likely to be misdiagnosed.1 Maximum severity is reached instantaneously in 50% and within 1-5 minutes in 19% of patients with SAH.2 Sudden severe HA: a ¼ will have SAH, 40% will have benign thunderclap HA, and the rest will have another primary or secondary HA.3 b Therefore, all patients with sudden severe HA need to be worked-up for SAH CT scans miss about 2% of SAH within 12 hours and 7% by 24 hours Therefore anyone with suspected SAH and normal CT requires an LP LP results depends on timing of HA4: <12h: Xanthochromia +/- present; large RBCs should be present a Incompletely clearing RBCs??(if suspected traumatic tap→repeat at different interspace) 12h-2weeks: Xanthochromia highly suggestive; large RBC +/- present >2weeks: Both may be absent.

Meningitis •

•

• •

•

Clinical Presentation Classic triad in bacterial meningitis of fever, neck stiffness and AMS present in only 44% a 95% patients had 2 out of 4 of: HA, fever, neck stiffness and AMS5 Do I need a CT before LP? (2 studies say not always). OMIT if: Hasbun et. al.: age<60, no immunocompromised/CNS disease/seizure within 1 week and has a non-focal neuro exam6 Gopal et al: Absence of AMS, focal neuro exam, papilledema and favorable clinical impression by doctor 7 Dexamethasone 10mg IV q 6 hour for 4 days 15 minutes prior to or with first dose of antibiotics8 Reduced risk of unfavorable outcome (RR 0.59) and reduced mortality (RR 0.48) Benefits seen mostly in patients with S. pneumoniae Predisposing Common Bacterial Pathogen Antimicrobial Therapy Antibiotics should be administered as soon as Factor possible; multiple studies have shown an association 16–50 yr Neisseria meningitidis, Streptococcus Vancomycin plus a thirdpneumoniae generation cephalosporin between time of antibiotic administration and poor >50 yr S. pneumoniae, N. meningitidis, Vancomycin plus a thirdoutcome (greater than 4-6 hours) Listeria monocytogenes, generation cephalosporin Antimicrobial Choice:9 (see table) aerobic gram-negative bacilli plus ampicillin Special Case: HA and HIV (CD4<200?) Presence of a risk S. pneumoniae, L. monocytogenes, Vancomycin plus a thirdCT w/wo contrast: r/o mass lesion, toxo, factor Haemophilus generation cephalosporin lymphoma influenzae plus ampicillin LP: r/o cryptococcal meningitis (if serum crypto Ag(-)→not need LP) IIH (Idiopatic Intracranial Hypertension, Pseudotumor cerebri) Diagnostic criteria for IIH:10 1. S/Sx of elevated intracranial pressure 4. Increased CSF pressure (nonobese>200; obese>250 mm water) 2. Non focal neuro exam (except abducens nerve paresis) 5. No other cause of increased intracranial pressure (CNS tumor, 3. Normal Neuroimaging study (CT or MRI) encephalitis, right heart failure) Vision loss secondary to papilledema is the only serious complication of IIH, is avoidable with appropriate treatment. Temporal arteritis begin empiric prednisone if medium or high suspicion. Consider IV steroids if visual loss (AION)

Emerg Med Clin N Am 2003;21:73-87 J Neurol Neurosurg Psychiatry 1998;65:791-3 Lancet 1994:344:590-3 4 J Emerg Med 2002;23:67-74 5 NEJM 2004;351:1849-59 6 NEJM 2001;345:1727-1733 7 Ann Int Med 1999;159:2681-2685 8 NEJM 2002;347:1549-1556 9 NEJM 2006;354:44-53 10 Am J Emerg Med 1999;17:517-521 2 3

Status Epilepticus ABCs Rapidly reversible causes?

Benzos (repeat 2-3X)

I n t u b a t i o n

Phenytoin

Phenobarbital

Maintain airway protection IV/O2/Monitor Intubation?

Glucose ck or give empirically (2-4ml/kg/dose) Opioid Naloxone 2mg (0.1mg/kg/dose) Pyridoxine Neonates/INH tox (50-100mg/dose)

Ativan (0.05-0.1mg/kg IV/IM (long duration of action) Valium 0.2-0.4mg/kg IV or 0.5-1mg/kg PR (quicker onset, short duration)

Versed 0.05-0.1mg/kg IV or 0.1-0.2 mg/kg IM (if no IV access) • •

Benzos terminate 75-90% of seizures Versed IM and Valium IV same efficacy and time to seizure cessation (Ind J Ped 2005;72:667)

Phenytoin 10-20mg/kg IV slower than 50mg/min Fosphenytoin 10-20PE/kg slower then 150mg/min • Onset: 10-30min, duration 24h • No seation/resp depression; +hypotension with rapid administration (propylene glycol)

Phenobarbital 20mg/kg IV over 5-10 min • +sedation, resp depression, hypotension • Onset 15-30 min, duration 48h

Valproic acid 30 mg/kg over 15 min

Valproate

• Equal or greater efficacy vs PHT as primary or secondary agent (Neurology 2006;67:340–342; Seizure 2007;16:527)

MgSO4 2-6 gm, then 1-2gm/h gtt

MgSO4 Lidocaine NaHCO3

• •

Consider in female→eclampsia or EtOH withdrawal Resp depression at high doses (level >12)

Lidocaine 100mg (1mg/kg) IVP • Used in neoneates and some efficacy in adults (Epilepsia 1998;29:584)

NaHCO3-50ml of 7.5% soln •

Empiric treatment for hyponatremic seizures, TCA overdose

Pyridoxime

Pyridoxime (B6) 1gm Pyr:1gm INH or 5gm if unknown

Refractory Status!

• • • • •

•

Empiric treatment for INH overdose

Intubation/Ventilation General Anesthesia/Coma (pentobarb, propofol, versed gtt) Paralysis Continuous EEG Consults (Neuro/ICU/Anesthesia)

PROCEDURAL SEDATION DRUGS Class Opiate

Drug Fentanyl

Dose 2-3 mcg/kg IV 2-5 mcg/kg IM

Onset 1-2min

Duration

Benzo

Midazolam (Versed)

0.05-0.1mg/kg IV 0.05-0.15mg/kg IM

1-2min IV 2-5 min IM

Barb

Methohexital (Brevital)

0.75-1mg/kg IV

Pentobarbital (Nembutal) Ketamine (Special K)

Phencyclidine

Complication Rigid chest, vomiting

Solution

Other Notes

30min IV 30-60 IM

Respiratory depression

<30sec

5-10min

Respiratory depression

Flumazenil (but do not use if chronically uses benzos or etoh!!) For laryngospasm, push more, if that doesn’t work, paralyze and intubate.

2.5 mg/kg IV/IM

<<30s

Varies

Apnea

Intubation

1-2 mg/kg IV 3-4 mg/kg IM

30-60s IV

Hypersalivation emesis, or recovery agitation. Laryngospasm

For emergence reaction, some pre-treat with versed.

Classic cocktail: 2 versed, 100 fentanyl Hepatic metabolism, renal excretion.

Good sedation, anxiolysis and amnesia but poor analgesia. Push FAST (lipophilic) >50% report apnea ↓ sz threashold Good for peds head CT Excellent amnestic/sedative no analgesia Atropine 0.01 mg/kg Glycopyrrolate 5mcg/kg IV According to APLS “Ketamine might have the greatest margin of dosing safety of all procedural sedation meds” APLS p512

Carboxylated imidazole derivative

Etomidate

RSI: 0.2-0.4mg/kg IV Sed: 0.05-0.1 mg/kg IV

30-60s

5-10 min

Alkylphenol

Propofol (Diprivan) (Milk of amnesia)

Bolus: 1mg/kg then 0.5mg/kg miniboluses Gtt:0.21mg/kg/min (210mcg) then 50100mcg/kg/min

<1 min

8-10 min

Resp. depression any myoclonus

More etomidate, benzos or wait and use something else

Anecdotally, IVDA’ers report painful injection, tend to have worse myoclonus. Excellent amnestic/ sedative, no analgesia. Egg and soybean solution.

CODE GREEN DRUGS Drug Versed

IM (mg) 5

Good for Coke/meth, etoh w/d

Zyprexa & Olanzapine wafer

5mg wafer

Psychotic/agitated, but somewhat cooperative

Haldol

5-10

Acute psychotic episode, withdrawal

Ativan

2-4

Meth

Bad for Etoh intoxication apnea

Stiff, Fever (NMS), Lithium, Anticholinergic, Cocaine, PCP, Meth, Long QT Etoh apnea

Notes Fastest on Believed to precipitate DKA in some Onset 10min

Much longer acting than versed.

•

Vertigo

1) True Vertigo?

• • • •

Syncope/presyncope Hypoglycemia Orthostatic Psych Cardiac

Peripheral

2) Central vs Peripheral

Central

Onset: sudden, severe Duration: seconds, minutes

1. Sx

Onset: gradual Duration: continuous

2. Nystagmus Not vertical Usually bilateral Latency: long Duration: transient Intensity: mild to severe Fatigability: yes Suppressed None

Any Direction (Vertical=Central) Unilateral or bilateral Latency: short Duration: sustained Intensity: mild Fatigability: no

Fixation

Not suppressed, may be enhanced Usually present (5Ds)

3. Neurologic sx 4. Auditory sx 5. Head thrust test

May be present, +/- tinnitus Positive

Peripheral

Direction Lateralization Position

none negative

3) Differential Diagnosis

Central

Vestibular Neuritis A) Acute Prolonged Vertigo?

+ auditory sx

A) Acute Sx

• •

VBI Cerebellar CVA Brainstem CVA

• •

•

Cancer Abscess MS

• • •

TIA Migraine Sz

Acute Labyrinthitis + Fistula test

B) Progressive Sx

Perilymph fistula + neuro sx

Labyrinth infarct*

B) Paroxysmal attacks? C) Recurrent attacks?

• • • •

Rx: Benzos, Epley Admit: unable to walk D/C:significant improved F/U ENT: acoustic neuroma, perilympatic fist.

C) Recurrent/ Transient Sx

BPPV

Meniere’s

4) Work-up & Dispo

• • •

CT/MRI Neuro C/S Admit

Vertigo

True Vertigo •

•

General Dizziness: 4 different etiologies Lightheadedness/ Presyncope Dysequilibrium (neuromuscular disorder) Vertigo Psychiatric Definition: True Vertigo→disorientation in space combined with a sense of motion. Hallucination of movement of self (subjective vertigo) or of environment (objective vertigo) (Rosen’s Emerg Med, 6th ed. Ch 13. 2006)

Central vs Peripheral •

•

General Approach: for vertigo is differentiating benign peripheral vertigo from life-threatening central vertigo, using the 5 criteria Neuro exam: 5Ds of an abnormal neuro exam: diplopia, dysphagia, dysarthria, dysmetria, and dysphonia Head thrust test: bedside test of horizontal VOR (vestibuloocular reflex) [NEJM Video] (NEJM 2003;348:1027-32) Start: Head turned to one side and eyes turned 10º from center to same side Motion: Apply brief high accel head turn so that eyes end looking at examiner’s nose Test: Catch up saccades on one side, but not the other indicates peripheral vestibular lesion on that side

Peripheral Vertigo • •

•

• • •

•

Prolonged vertigo definition: continuous vertigo lasting more than a few hours Vestibular Neuritis develops over hours and resolves over days, usually post-viral. May mimic infarct type symptoms Treatment : General (Antihistamines, anticholinargics, antiemetics, benzodiazepines) a Directed treatment: Dexamethasone, Valacyclovir Acute Labyrinthitis 3 subtypes: Toxic: usually medication induced, has auditory sx and tinnitus Serous: associated ENT infection, ?fever Suppurative: severe sx, febrile, toxic→Admit, IV Abx, ENT C/S Labyrinthine infarct: abrupt onset, h/o vascular dz, associated with neuro signs (also considered central type vertigo) Perilymphatic fistula: associated with trauma, lifting, coughing, sneezing Fistula test: Vertigo and nystagmus induced by pressure in the external ear canal BPPV: Free floating debris in posterior semicircular canal Clinical: Abrupt onset of vertigo seconds after change in head position, lasting less than a minute. Dix Hallpike: for diagnosis, presence of paroxysmal positional nystagmus is most reliable finding in patients with BPPV (Am J Otol 1995;16:806-10) a Start: Seated with head turned 45º to side being tested b Motion: Quickly lower to supine position with head angled backward 45º off bed c Test: Nystagmus with affected side down, can continue to Epley from this position Canalith Repositioning Maneuvers (Epley and Semont) ( Ann Emerg Med 2001;37:392-8) a See reference or EMRAPTV Episode 9 on http://cmedownload.com Meniere’s: Attacks of vertigo preceded/accompanied by reduced hearing, tinnitus and pressure in ear. Attacks followed by residual hearing loss. Treatment: Dietary restrictions (salt, caffeine, tobacco), lasix, betahistine, ENT referral Other causes: ear canal foreign body, trauma (labyrinth concussion), otitis media, medication (aminoglycosides)…

Central Vertigo •

•

Cerebellar stroke: may simulate sx of vestibular neuritis (VN) and present with isolated vertigo Cerebellar CVA vs VN (Neurology 2006;67:1178-83) a 10% isolated cerebellar infarct pts present with isolated vertigo (VN sx) b No patients with cerebellar infarct had a positive head thrust test MRI is indicated if there are associated neurologic signs/symptoms, if the onset is sudden in a patient with risk factors for stroke, or if there is a new, severe HA accompanying the vertigo (NEJM 1998;339:680-5).

1) UMN v LMN

Weakness

CVA

Central

DTR-dec Muscle tone-dec Atrophy/fasic-yes Babinski-neg

DTR-inc Muscle tone-inc Atrophy/fasic-no Babinski-pos

Myelopathy

Peripheral

2) Symmetry? Symmetric

Asymmetric

3) Motor/Sesory S>M

M>S

Pure Motor

M&S

4) Pattern/ Distribution DSPN (periph neuropathy) •

stocking glove distibution

NMJ

AIDP/CIDP(GBS) •

Ascend weakness

•

Variable sensory

• • • •

MG (ocular) LambEat (proximal musc) Botulinism (descend) Tick (ascend)

Radiculopathy Plexopathy (nerve root/ plexus dist)

Myopathy • •

Poly/Dermatomyositis (proximal weakness) Periodic Paralyses (Extremity weakness)

Mononeuropathy Dist of periph n. (ulnar, radial, median, sciatic…)

Mononeuropathy multiplex

Ant Horn cell

Dist: distal, patchy

(ALS)

(+)=positive (UMN) type sx, (-)=negative (LMN) type sx

Focal Weakness

Other

Symmetry

Motor

I Anterior Horn cell (ALS)

Asym

(+)fasiculations/cramps (-)weakness/atrophy

Distal Patchy, asymmetric

• UMN (positive sx) and LMN signs (negative sx)

II. Nerve root

Asym

(+)fasiculations/cramps (-)weakness/atrophy

Distal/Proximal Nerve root distribution

• DDx: Compression v Systemic disease

Asym

(+)fasiculations/cramps (-)weakness/atrophy

(+) pain (-)paresthesia/ hyp/ anesthesia (+) pain (-)paresthesia/ hyp/ anesthesia

Distal/Proximal

• Sx of radiculopathy, but not in same distribution

AIDP/CIDP (GBS)

Sym

(-) weakness motor sx predominate

variable

Distal→proximal (ascending weakness)

DSPN

Sym

(-) weakness

Sensory sx predominate:

Distal

• • • • •

(Radiculopathy)

III. Plexus (Plexopathy)

Sensory

Pattern/Dist

eripheral Nerve (Neuropathy)

dorsiflex big toe→foot drop→steppage gait

(Distal Symmetric Polyneuropathy)

Mononeuropathy

Asym

(+)fasiculations/cramps (-)weakness/atrophy

Stocking glove distribution, ascending

initial (+) then (-)sx

(+) pain (-)paresthesia/ hyp/ anesthesia (+) pain (-)paresthesia/ hyp/ anesthesia

Distal Distribution of peripheral nerve:

• 2/2 compression of peripheral nerve (radial,

Distal Patchy, unorganized distribution

• DDx: vasculitis, DM, neoplastic, infectious, sarcoid, Lyme

• • • • • • • •

Asym

(+)fasiculations/cramps (-)weakness/atrophy

Myasthenia Gravis

Sym

(-)weakness/atrophy

Descending? Ocular sx: ptosis, diplopia, blurred (85%)

Lambert-Eaton

Sym

(-)weakness/atrophy

Proximal muscle weakness (rise

Botulinism

Sym

Tick Paralysis

Sym

(-)weakness/atrophy

Sym

(-)weakness/atrophy

Sym

(-)weakness/atrophy

Mononeuropathy multiplex

DTR(-) Autonomic sx: hypotension Resp sx: intubate at FVC 10-12mk/kg MF variant: weakness begins in CN, descends DDx: DANG THERAPIST (DM, EtOH, Lyme, HIV. Etc…) median, ulnar, sciatic, lat fem cut.)

V. NMJ

from chair, climb stairs, lift hands)

(-)weakness/atrophy

Descending flaccid paralysis (like GBS MF variant, MG)

Bulbar/CN involved Ascending flaccid paralysis (like GBS)

Fatigable, improves c rest Resp sx (17%)→intubation? Tensilon test, Ice test Myasthenic vs Cholinergic crisis Sx improve with use Malignancy? Pupils: fixed/dilated (vs MG) Anticholinergic sx

• Pupils: fixed/dilated (vs MG) • Anticholinergic sx • REMOVE TICK!!!

VI Muscle (Myopathy)

Inflammatory (PM/DM) Metabolic

Proximal muscle weakness-like LE (rise from chair, climb stairs, lift hands) Distal Extremity weakness

• Pain,tender muscles • Malar rash? • Lytes v periodic paralyses

EKG READER STEP 1 RATE AND RHYTHM 1) 2) 3)

Calculate rate by boxes: 300, 150, 100, 75, 60, 50, 43, 37 Regular or irregular? P before each QRS? Yes= sinus, No= Junctional or ventricular

Tachydysrhythmias Regular Narrow -SVT -Aflutter with 2:1 block -Sinus Tachycardia Wide -V tach - WPW -SVT with aberrancy -Sinus tach with BBB

Irregular -Afib with RVR -Aflutter with variable block -Multifocal atrial tachycardia - Afib with WPW - Torsades - Afib with BBB

STEP 2 INTERVALS AND AXIS 4) 5)

Are the intervals and axis normal? Are the PR intervals constant or changing? Constant= no block, 1st degree block or Mobitz II Changing= Mobitz I or complete block.

INTERVALS PR

QRS

preexitation =WPW normal 1st deg AVB <120 >120 normal Predispose to VT/Vfib

AV BLOCKS

<120 120-200 >200 normal LBBB, RBBB <470 >470

1 Degree ↑ PR interval>200 st

2nd degree a) Type 1/Wenkeback progressively longer, then drops b) Type 2/NonWenkebach random drops 3 degree complete block rd

BUNDLE BRANCH BLOCKS DIAGNOSTIC CRITERIA Multiple definitions. These are from A. Mattu p62, 140 & Marriot’s 10th ed pages 101, 103 and 108 RBBB LAFB V1 M-shaped QRS or aVL qR pattern (small q rSR pattern big R) any QRS ≥0.12 III rS complex I, V6 Wide S in Lateral Axis Leftward QRS axis leads Assoc w LAC ischemi LPFB aVL & I III Axis

AXIS Normal -30 to +99 LAD = <-30 RAD = >+99

rS complex qR complex Rightward QRS axis Associated with RAD ischemia (rare b/c has dual blood supply)

LBBB I VI V6

Monophasic R, no Q QS or rS Late intrinsicoid, no Q waves, monophasic R Intrinsicoid= time between start of QRS and peak of R wave.

AXIS DEVIATION DIFFERENTIAL DIAGNOSIS Rightward axis ddx Leftward axis ddx LPFB LAFB Lateral MI LBBB RVH Inferior MI Acute lung dz ie PE LVH Chronic lung dz ie COPD Ventricular Ectopy Ventricular ectopy Paced beats Hyperkalemia WPW Na channel blocker OD ie TCA

STEP 3 MORPHOLOGY DDX 6)

Is the QRS wide or narrow? Narrow =supraventricular origin Wide= ventricular origin or aberency present. 7) Is there more than one population of QRSs? 1 = ectopy or aberrancy. >1 implies multifocal ectopy. 8) Look at the QRS, PR & ST segments, T wave morphology.

WIDE QRS - 6 causes Ventricular Rhythm Bundle Branch Block Paced Rhythm Hyperkalemia Drugs WPW AMI!!!!

ST Depression - 6 causes Posterior MI Reciprocal Changes Subendocardial Infarct (Non-STEMI) Subendocardial Ischemia LVH with strain Digoxin Effect Hypokalemia

The Rule of Appropriate Discordance The appropriate relationship of the ST segment to the T wave in the LBBB pattern is one of discordance ( i.e.,the major terminal portion of the QRS complex and the ST segment/T wave complex must be on opposite sides of the iso-electric baseline). RBBB LBBB Paced Rhythms PVC’s LVH

Big T waves – 6 causes Hyperacute T’s of AMI Hyperkalemia Benign Early Repolarization Acute pericarditis BBB Pre-exitation syndromes

ST Elevation - 6 causes Acute MI Prinzmetal’s Angina Benign Early Repolarization Pericarditis LV Aneurysm Left Ventricular Hypertrophy (LVH) Pericarditis stages I. A) Diffuse concave-upward ST-segment elevation with concordance of T waves; B) ST-segment depression in aVR or V1; C) PR-segment depression; low voltage; D) absence of reciprocal ST-segment changes II. ST segments return to baseline; T-wave flattening II. TWI III. Gradual resolution of TWI Benign early repol features Am JEM. 1998 Oct;16(6):592-7. 1)Diffuse ST segment elevation 2)Upward concavity of the initial portion of the ST segment 3)Notching / slurring of terminal QRS 4)Concordant large amplitude T’s

Inverted T waves - 3 causes Acute Ischemia (Wellen’s syndrome) Pulmonary Embolism (Right Heart Strain) “CNS” T waves 6 Causes of Sudden Cardiac Death QTc Prolongation Brugada Syndrome Pulmonary Embolism WPW IHSS / HOCM ; Classic “Needle” Q waves, LVH, LBBB, Normal (Thick Chest Wall) Critical AS QTc prolongation Drugs Antiarrhythmics Class Ia, Ic, III Macrolides (Erythromycin) Antifungals (Ketoconazole) Prokinetics (Reglan) Antipsychotics (CPZ, Droperidol) Congenital: Romano-Ward Lange-Jervil Other Ischemia Hypo K, Mag, Ca++, thermia, thyroid Elevated ICP (usually w inverted TW’s) Syncope killers Ischemia WPW Dysrythmia Brugada Long QT syndrome Hypertrophic cardiomyopathy

1) Consider Emergent Dx

Hx •

Ao Dissection

•

Chest Pain

PEX

• • •

US, CXR CT Chest CT Surg C/S

• • • •

D-dimer CT PA V/Q scan LE Duplex

• •

EKG !ESR

H/O EtOH, blunt trauma, caustic ingestion

• •

CXR Esophogram/ Esophagoscopy

Decreased/absent breath sounds Dyspnea H/O COPD, asthma, CF, PCP

• •

CXR Chest tube vs Heimlich

• • •

Sudden onset severe tearing CP Risks: h/o Marfan, HTN

New murmur Pulse deficit Focal neuro deficit

STEMI (below) •

•

Pericarditis

Boerhave’s

PTX

• •

Sharp. pleuritic pain Preceded by URI, underlying dz (SLE, uremia)

•

Abrupt pan. pain preceded by vomiting

•

Acute pleuritic pain Asthenic body, h/o trauma

•

• •

Sudd onset Sudden et pleuritc le it CP, SOB ? risk factors

2) Consider ACS?

Well’s score SOB algorithm

•

• • •

Worse supine, improves on sitting up

Risk stratify (Low vs High) • • • •

• • • •

CAD risks risk CP story EKG Troponin

ACP TIPI ACP-TIPI TIMI risk score Braunwald Gestalt

Low Risk

High Risk

Empiric Tx

Low risk therapies • • • • •

• •

R/O MI

NSTEMI/UA

ASA Beta-blockers? Nitrates O2 Morphine

!"#$%&'()*' +%#,$%-' .%#/"#012#34'

• • • •

•

STEMI

• • • • •

Low risk therapies ies Heparin/LMWH Clopidogrel? GPI? PCI: Selective vs Early (high risk)

Low risk therapies Heparin/LMWH Clopidogrel? GPI? PCI vs Lytics stat

Non-invasive testing No

R/O UA

• •

Inpatient 72h output

!"#$%&'()*+)#' VS

3) Very Low Risk/No ACS

Non-Cardiac • • •

• Consider other causes • No ACS rule-out

GERD Costochondritis Pneumonia

• • •

PUD Psych Abdominal causes

"#$%&'!()*+,!

General Approach: • • • •

Always think about emergent/immediately life-threatening conditions first. After those are ruled out by H&P, EKG, CXR or more advance testing!then begin work-up to r/o ACS. Patients are stratified into low or high risk ACS using certain criteria!then give empiric treatment based on their risk level. If not concerned for ACS (young, no risk factors, atypical story), then think of other causes of chest pain and give appropriate treatment

•

Mortality increases 1-2% per hour if unrecognized!!!

Aortic Dissection •

General " " "

•

Type A (80%)-ascending dissection +/- descending (10% mortality at 24 hours) Type B (20%)- descending dissection (10%mortality at 30 days) Risk factors: HTN, Marfan’s, Pregnancy, Coarctation, bicuspid aortic valve, trauma, cocaine/meth

History and Physical (JAMA 2002;287(17):2262-2272) " "

" " " "

" " "

Abdominal pain + Chest pain!Be highly suspicious if pain above and below diaphragm Stroke presentation # 95% of patients with a stroke and dissection have some type of chest pain or back pain. # Caution with giving thrombolytics to a stroke patient!consider aortic X-ray feature dissection Wide aortic contour # Screening CXR? Wide mediastinum Isolated neurologic symptoms: altered, seizure, unable to move legs Tracheal displacement Chest pain and leg pain-down to iliac vessels Displaced calcification Paralysis!no pain and presents like spinal cord injury T10-T12 Aortic kinking Opacified pulm window (Compromise of spinal artery) Blurred aortic contour Syncope IRAD Study (JAMA 2000;283:897-903) # 13% of patients with aortic dissection had syncope as their only symptom # no CP/back pain/abdominal pain # Consider bedside U/S to screen for pericardial effusion Myocardial Infarction • Dissection flap that comes down into R coronary ostia! inferior MI • CP that radiates to back with "ST II, III, aVF Abdominal pain after cocaine use!Usually young males (Type B dissections) Cardiac arrest (Resuscitation 60 (2004) 143–150) # Evaluated patients with aortic dissection or AAA that presented as PEA arrest # Thoracic dissection! only 48% patients had chest pain # AAA rupture ! abdominal pain in only 52% # Bedside U/S diagnostic of their process (effusion, free fluid) Malperfusion syndromes # Cardiothoracic surgeon will not operate on patients with that have end organ ischemia! Mortality 100% # Must improve perfusion to end organ (kidney, spinal cord, intestines…) prior to operating on dissection # May need to involve IR, Vascular surgery, or transfer patient Increased likelihood of Ao dissect HTN Hx Marfan syndrome Pulse deficit Focal neuro deficit

•

Suggested References CMEdownload.com • UCSF High risk 2009 (Snoey, Slovis) • Resus 2009 (Tabas) EM:RAP 4/08 (R.Rogers)

(+)LR 1.6 4.1 5.7 6.6-33

Decreased likelihood of Ao dissect Absence of sudden onset CP Absence of HTN hx

(+)LR

(-)LR

3.2 2.2 ns 5.6 10.2 2.3 ns

0.4 0.6 ns 0.9 0.6 0.8 ns

(-)LR 0.3 0.5

Chest X-ray "

Sensitivity of 64% and Specificity of 86% for diagnosis of Ao dissection (Am J Med 2004;116:73-77) Pooled Data: combining 1)absence of immediate onset tearing/ripping CP 2)nl CXR and 3) absence of pulse/BP deficit yielded probability of 7% for Ao dissection!not good enough? (Arch Intern Med. 2000;160:2977-2982) D-dimer (EM:RAP 1/2008) " Sens 100%, Specificity 68% in one study (Eur Heart J. 2007;28:3067-75) "

•

" "

•

Other studies show sens as low as 85%!not all dissection involves clotting cascade, may dissect through false lumen (Ann Emerg. Med. 2008;52:339-43) Currently NOT recommended as screening test for dissection

Treatment (Stop extension of dissection) "

#-blockers # most important medication to give!can give empirically if high suspicion

" "

# Labetalol IV, Esmolol IV Vasodilators # Nitroprusside (agent of choice) # Fenoldopam (new)!Dopamine agonist, titratable Goal: <120/80 (as low as possible) and pain under control Variant management scenarios # AI: gentle rate control, early surgery # Pericardial tamponade: IVF, early surgery, (pericardiocentesis!worse outcome!!) # MI: gentle rate control, (no ASA, thrombotics!) Consultation # Usually after CT is done showing dissection # Type B!usually medically managed vs IR (grafts, stents, fenestrations) # Type A Proximal Dissection? (CT surgery consult prior to CT) • Pulse deficit • Pericardial effusion • Aortic diastolic murmur • Dramatic EKG changes (inferior MI)

Pericarditis • •

•

Causes: Idiopathic up to 80%, viral 1-10%, Bacterial, TB, Inflammatory, metabolic, Neoplastic EKG changes " Stage 1: (Acute pain) diffuse ST elevation (except depressed in aVR and V1), PR depression " Stage 2: (days later) ST returns to baseline with flattening of T waves " Stage 3: T waves inverted " Stage 4: (weeks-months) EKG returns to patients baseline, +/- TWI persisting (chronic pericarditis) Work-up: Most cases are viral or idiopathic!extensive w/u not needed " H&P!exclude medical/surgical condition associated with pericarditis (TB, uremia, recent MI, cardiac surgery) " Echocardiography!exclude cardiac tamponade (bedside) Dispo? " Admit!High risk features? (fever, subacute onset, immunosuppression, trauma, anticoagulants, myopericarditis, severe effusion(>20mm), cardiac tamponade, not respond to outpatient tx?) Treatment: based on underlying cause and evidence of effusion/tamponaaade " Viral/Idiopathic: NSAIDs (Indomethacin 50mg po q 8h, Ibuprofen)

PE (see SOB algorithm) STEMI (see below) Pneumothorax! see Dyspnea algorithm Boerhave’s

ACS Risk Stratification (Low vs High) •

Histrory (JAMA 2005;294:2623-2629) Increased likelihood of AMI Radiation Worse with exertion N/V/diaphoresis Similar to previous MI Pressure

•

Limited clinical value in diagnosing ACS in the ED setting, especially >40yo Age Pt <40yo: CAD screening can help (Ann EM 2007;49:145-152) # No risk factors!negative LR 0.17 (95% CI 0.04-0.66) # 4 or more risk factors!positive LR 7.39 (95% CI 3.09-17.67)

Troponin "

•

Decreased likelihood of AMI Pleuritic Positional Sharp Reproducible

CAD Risk factors " " "

•

(+)LR 4.5 2.4 2 1.8 1.3

Mortality increases as peak troponin rises

EKG "

Insensitive but specific

(-)LR 0.2 0.3 0.3 0.3

•

"#$%&'!()*+,! # Up to 55% ACS have normal/non-diagnostic EKGs!when negative, not very helpful (Ann Emerg Med. 1989;18:741-746.) # 7% AMI have completely normal EKG # Specificity$80% (when positive, they’re helpful) Prognosis # ACS(suspected) + nondiagnostic ECG=1.1%mortality # ST depression=4-6X death/MI/ischemia rate

Risk Scores (combine all of the above) "

TIMI Risk Score=14 day event rate (JAMA Aug 2000; 284:835-842) # Historical: (age %65, %3 CAD risk factors, prior stenosis % 50%, %2 anginal episodes in prior 24h, ASA in prior 7 days) # Presentation: (ST deviation on EKG, elevated trops) # Graph: 14 day event rate (MI, death, revascularization) vs number of TIMI risk factors # Prospective validation yielded similar results, but still unable to rule-out ACS !TIMI score 0/7 had 1.7% risk of adverse outcomes (Ann Emerg Med. 2006;48:252-259) # http://www.mdcalc.com/ for plug-in TIMI score Braunwald Risk stratification (Heart Disease:Braunwald 2004, p 1248) # Low risk= TIMI score<3 + nondiagnostic EKG + nl trop • 30 day death rate is 1.7% (pretty low?) # High risk=TIMI score>3 OR ST depression OR troponin positive

Low Risk Work-up •

Rule out AMI (non-ST-segment elevation AMI) " Cardiac serum markers # ACEP Clinical Policy (Level B ACEP recommendation . Ann Emerg Med. 2006;48:270-301) • Single negative CK-MB or Troponin 8-12 hours after sx onset • Negative myoglobin + negative CK or Troponin at baseline and 90 min if <8 hours of sx onset • Negative 2hour delta CK-MB and 2 hour delta Troponin if <8 hours of sx onset # ACC/AHA Guidelines 2007 ( J Am Coll Cardiol 2007;50:e1-e157) • Single negative marker 12h after sx onset • Negative marker on arrival and 6 hr later # Clinical Chemistry Society Guidelines (Circulation 2007;115:e356-375) • Low risk pt!negative marker >6h after onset • Mod/High risk pt.!negative markers 12h after onset " Serial EKGs (Level B ACEP recommendation) # Initial EKG in patients with AMI can be normal/non-diagnostic up to 55% of the time. Rule-out Unstable Angina! Non-invasive stress testing " Prior Stress Test (Am J Emerg Med 2007;25:39-44) # Previous positive! increases admission and adverse events # Previous negative! does not change admission rate or adverse events (not reassuring) " ED Treadmill Study (n=1000 ED patients with acute chest pain, J Am Coll Cardiol 2002;40:251– 6) # Negative ETT: 0.2% cardiac event rate at 30 days!can d/c these patients home # Non-diagnostic ETT(>85%MPHR, >6mets…): 3.6% event rate!further work-up and risk stratification # Positive ETT: 14% event rate!Admission " Outpatient Stress test!within 72 hours (Ann Emerg Med 2006;47:427-435) # Kaiser study: Safe strategy in low risk patients after AMI ruled out # ACC/AHA recommendation!Non-invasive testing within 72 hours

•

Low Risk Therapies •

ASA " " " " "

•

Dose: 162 or 325mg, chewed if they can Indications: if they have a chest!! (except dissect or allergy) Decrease death rate by 50% NNT to prevent 1 death/MI = 16 Bottom Line: Chest Pain=ASA, ASA=Chest Pain

NTG " " "

Short term benefit unknown? Long term!no decrease in mortality (ISIS-4) Dose: # PO! 400mcg SL (getting 50-100mcg/min!) # IV!start 10mcg/min and go up to max 200, 250 mcg/min (so must titrate IV dose up quickly for same effect as po)

Contraindications: hypotension, Viagra use, Right sided MI

•

Morphine! Dose: 1-5mg increments

•

O2!Just give it

•

Beta-blockers " "

•

Indication: ACS and sick Benefits: lower HR, lower O2 requirement, decrease arrhythmic events, lower potential for myocardial rupture (day 2-3, esp if given lytics) " Contraindications: brady, heart blocks, COPD/Asthma (decrease dose) " Dose: Metoprolol 5mg IV q 5min x 3 " STEMI: very bad, esp in CHF with systolic dysfunction (COMMIT trial-see below) " NSTEMI: # UA/NSTEMI Guidelines (Circulation 116 (7): 803) • Beta-blockers should be given in first 24 hours orally for ACS!&VF and sudden death # COMMIT trial (Lancet 2005; 366: 1622–32) • #-blocker group! no difference in mortality • slight reduction in reinfarction and V-fib but increased risk of cardiogenic shock # Gusto I • Early IV #-blockers associated with increased death, CHF, shock, recurrent ischemia, need for pacemakers # Final Recs • No urgency to give Beta-blockers in ED!give orally within first 24h (no longer a CMS quality measure) " Long term (secondary prevention): effective " Low risk in ED: may give but may interfere with treadmill? Calcium-Channel Blockers?? " Indications: need rate lowering (dilt, verapamil) and contraindication to beta-blocker

Specific Therapies-High Risk •

Heparin " " " " "

•

Clopidogrel (Plavix) "

•

Good: Mortality/MI benefit $ 2.5% (NNT$40) Bad: Severe bleeding complications $1% (NNH$100) Dose: 60Units/kg bolus(max 4000 U) + 12 Units/kg/h(max 100 U) # aPTT in 6 hours (goal 1.5-2.5x control) All benefit limited to high risk patients only LMWH vs UFH (JAMA 2004;292:55-64) # Meta-analysis combining 6 trials # 17% relative risk reduction in death /MI at 30 days # Bleeding rates similar # Bottom line: LMWH works a little better and easier to use Lovenox IV? (JACC 2003;42:424) # Brings ANTI-Xa levels up almost immediately # Dose: 0.5mg/kg IV bolus + 1mg/kg SQ q 12h • age > 75: no IV bolus and decrease to 0.75mg/kg SQ • CrCL<30: 0.5mg/kg IV and 1mg/kg q 24h CURE trial (NEJM 2001;345:494) # Good: 2% (11.4!9.3) absolute risk reduction in composite of death,MI,stroke (no significant reduction in death alone!) • 25% of effect seen in first 24h (maybe 4 hrs!!) • Get it on board early??? # Bad: increased bleeding (major bleed 2.7!3.7%) • Cost per MI saved: $40,000 Special Situation: might go to CABG? (Circulation 2004;110:1202-1208) # Absolute CABG bleeding risk$1.4% (NNH=77) # CABG rate$5% in NSTE-ACS # Conclusion: 1 patient/3000 will have excess CABG bleeding due to Clopidogrel!ok to give # AHA Scientific statement (Circulation 2005;111:2659) Special Situation: STEMI (Clarity TIMI 28 trial NEJM 2005;352:1179) # Good: Composite endpoint risk reduction 21.7!15 (NNT=16) # Bad: bleeding risk similar as placebo # Dose: may be increasing loading dose? (JACC 2005;46:906) • 75mg peak effect!5 days • 600mg peak effect!2 hours!! • 900mg!even faster!!! (Albion trial) • No increased bleeding with increased loading doses Bottom Line?: Class I rec for high risk NSTE-ACS and STEMI +/- PCI, lytics or CABG

Statins "

MIRACL study (JAMA 2001;285:1711)

"#$%&'!()*+,!

" "

•

# Atorvastatin 80mg given w/in 24-96h of admission # Significant improvement in composite endpoint, recurrent ischemia and stroke at 16 weeks. ACS:Statin (Lancet 2001;357:1063) # Decreased death/MI at 6 months Use: for secondary prophylaxis and doesn’t matter if given in ED

GPIs (Reopro, Integrelin, Agrastat)!another antiplatelet! "

NSTEMI # Clear benefit in PCI for ACS # Without PCI!questionable (meta-analysis) • Good: O.R. death/MI=0.91 • Bad: major bleed increased 1% • Limitations: subgroup effect (limited to highest risk population!refractory ischemia, +trop, dynamic EKG's, planned/probable MI). # Should we give in ED? • ACUITY-Timing Trial (JAMA 2007;297:591-602) (a) Upstream (in ED) use had fewer ischemic complications, but more bleeding. • No advantage in giving upstream vs selective use in the lab

PCI •

•

NSTEMI (Routine vs Selective PCI) " TACTICS-TIMI-18 trial (JAMA 2000;284:835) # Low risk (TIMI 0-2) patients did worse with invasive therapy (cath) # Intermediate (TIMI 3-4) and high risk (TIMI 5-7) did better with invasive therapy on 6 month composite outcome " ICTUS trial (NEJM March 2007) # Immediate PCI vs Intensive medical therapy with selective PCI for breakthrough ischemia # Results: early PCI had more MIs but fewer hospitalizations " Bottom line: Early PCI (6-48h) vs selective strategy # 33% RRR angina/rehospitalization at 6-12mos # 2X increase peri-procedural MI # No mortality benefit until 2-5 yrs # Benefit limited to high risk patients STEMI: PCI vs Lytics " Problem with lytics? # Major bleeding 1% (usually intracranial) # Only 50% of STEMIs recover with full patency (TIMI-3 flow) # 15% of those that recover patency!will re-occlude " 2004 AHA Guidelines # If optimal conditions (present <3h, door to needle<30min, door to balloon<90min)!no preference for either strategy. " Pathophysiology made simple # 0-3 hours (time dependent) • Myocardial salvage • Decreased Mortality!!! # 3-12 hours (Time independent)!PCI • Plaque stabilization (PCI) • Perfuse hibernating myocardium • Prevent infarct expansion " CAPTIM trial (Circulation 2003;108:2851) # Pre-hospital fibrinolysis superior mortality trend (p=0.58) vs PCI when T<2h # Pre-hospital fibrinolysis equivalent to PCI when T<3h " Lancet 2003;361:13 # PCI had improved composite outcome and less bleeding (T<4.6h) over in-hospital fibrinolysis " PCI as standard? # 80% of US hospitals have no PCI capability • 37% of STEMI got PCI<90 min at PCI capable hospital • 4% of transferred STEMI got PCI<90min # Does delay matter? (JAMA June 2000;283:2941-7) • 90 minute delay!42% increase relative mortality • 2 hour delay!62% increase mortality STEMI: Facilitated PCI?: (Drip and Ship) " Early 90s studies mostly negative " ASSENT 4 PCI trial (Lancet 2006;367:569) # Equivalent TIMI-3 flow post PCI in both groups of primary PCI and Fibrinolysis + PCI (facilitated PCI) # Facilitated PCI group did worse in all other outcomes (death, shock, strokes, bleeds) vs primary PCI

•

Summary " Consider lytics over PCI if… # Time from onset < 1hour # Time from symptom onset <3h and PCI delay>90-120 min (in lieu of PCI) # Time from symptom onset <3h and PCI delay>90 and high risk MI • Facilitated PCI?!rescue PCI after lytics given # Allergy to contrast dye " Consider PCI if… # Time from onset >3hours # High risk ICH (age >75, female, small, HTN) # High risk MI (CHF, hypotension/shock, MR) # Lytics fail!rescue PCI

LYTICS 1

Stroke

MI Indications: Thrombolytic therapy should be provided within 30 minutes of ED presentation to all patients diagnosed with an acute myocardial infarction exhibiting a ST segment elevation as long as there is no contraindication.

Inclusion criteria for rt-PA Administration1: □ Ischemic stroke. □ Patient presentation within 3 hours of symptom onset (some studies show a benefit within 6 hours of symptom onset). □ Clearly define time of symptom onset. □ CT scan negative for hemorrhage.

Contraindications □ Any CNS bleed (past or present, known or suspected) □ Substantial edema, mass effect or midline shift on CT scan. □ Intracranial surgery in past 3 months. □ Intracranial neoplasm. □ Subarachnoıd hemorrhage or hx of ICH. □ MI in past 3 months □ Recent spinal tap. □ Uncontrolled hypertension >190 mm Hg systolic and > 100mm Hg diastolic. □ Non-compressible arterial puncture last 7 days □ Non-CNS surgery in the past 14 days □ GU or GI bleeding in past 21 days □ Blood glucose <50 or >400mg/dl □ Platelet count <75,000. □ Seizure at onset of stroke □ AV malformation or aneurysm. □ Known bleeding diathesis and prolonged PT and PTT. □ Heparin use within the last 48 hours. □ Rapidly improving deficit or mild isolated deficit. □ Pregnancy Administer:rt-PA 0.9 mg/kh, 10% as a bolus with the remainder given over 60 minutes (maximum dose of 90 mg).

PE 1 Treat with heparin, 80 units/kg bolus, followed by continuous IV infusion at 18 units/kg/h.

Absolute Contraindications : □ Any prior intracranial hemorrhage (ICH □ Known structural cerebral vascular lesion (eg AVM) □ Known malignant intracranial neoplasm (primary or metastatic) □ Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours □ Suspected aortic dissection □ Active bleeding or bleeding diathesis (EXCEPT MENSES) □ Significant closed head trauma or facial trauma within 3 months. Relative contraindications 3: □ History of chronic, severe, poorly controlled HTN □ Severe HTN at presentation (SBP >180 or DBP >110) □ History of prior ischemic stroke greater than 3 months, dementia or known intracranial pathology not covered in contraindications. □ Traumatic or prolonged CPR (>10 minutes) or major surgery (<3 weeks) □ Recent (within 2-4 weeks) internal bleeding □ Noncompressible vascular puncture □ Pregnancy □ Active peptic ulcer □ Current use of anticoagulants □ For Streptokinase/anistreplase: prior exposure (>5 days ago) or prior allergic reaction. Some Suggested Guidelines: Alteplase: >67 kg: 15 mg initial IV bolus, 50 mg infused over the next 30 minutes, 35 mg infused over the next 60 minutes. <67 kg: 15 mg initial IV bolus, 0.75 mg/kg infused over the next 30 minutes, 0.50 mg/kg infused over the next 60 minutes (max. dose is 100 mg). Streptokinase: 1.5 million units infused over 60 minutes. No heparin is required.

Use thrombolysis or embolectomy on patients with hypotension requiring vasopressors and with angiographically documented PE. May be considered empirically for a patient in extremis.

Anistreplase (APSAC, Eminase): Infused 30 units IV over 5 minutes. There is no need for heparin.

t-PA, 100 mg over 2 hours or streptokinase, 250,000 IU load over 30 minutes, followed by 100,000 units/h for 24 hours, or urokinase, 4,400 IU/kg load over 10 minutes, followed by 4,400 IU/kg/h for 12 to 24 hours. STAT thoracic surgery consult for consideration of embolectomy.

Reteplase (r-PA, Retavase, Reptilase): Derivative of rt-PA that is effective as rt-PA and may work more quickly. Infuse 10 units IV over 2 minutes followed by a repeat dose in 30 minutes. Heparin must be used to prevent reclosure. Tenecteplase (TNKase): < 60 kg: 30 mg IV over 5 seconds. >60

kg–69 kg: 35 mg IV over 5 seconds. 70 kg—79 kg: 40 mg over 5 seconds. 80 kg–89 kg: 45 mg IV over 5 seconds. >90 kg: 50 mg IV over 5 seconds.

References: 1) Gossman, Plantz Emergency Medicine Oral Board Review: Pearls of Wisdom, Fifth Edition 2) Tarascon EM 3rd Edition page 111, 3) AHA Handbook of Emergency Cardiovascular Care 2005 p. 36

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General •

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Approach: ! Chief objective in syncope w/u is distinguishing life-threatening cardiac causes from benign causes using the History, Physical, and EKG. ! Patients are risk stratified and high risk patients are then admitted for monitoring and further work-up ! Usually unable to establish exact diagnosis/cause of syncope in the ED. Differential (NEJM 2002;347(12):878-884) ! Non cardiac: Vasovagal (21%), Orthostatic (9.4%), Unknown (36.6%)"1 year mortality 2-4% ! Cardiac: Arrythmia, Myocardial ischemia, Outflow obstruction"1 year mortality 18-33%

R/O pseudosyncope: • •

Syncope definition: sudden transient loss of consciousness with a loss of postural tone with a return to preexisting neurologic function Syncope mimics can usually be ruled out by history. ! Hypoglycemia-usually not transient event, sx resolve after glucose ! Vertigo-pt elicits spinning sensation, no LOC ! Seizure-convulsive movements, post-ictal period ! Stroke-focal deficit, usually no LOC ! Drop attacks-falls without loss of consciousness

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R/O Cardiac Causes (9%) •

• •

Hx ! Preceding events: during exertion suggests outflow obstruction; abrupt onset, occurrence while sitting/supine, longer duration suggests cardiac cause ! During: tonic/clonic movements, bowel/bladder incontinence, fall/trauma as a result of syncope? ! Postsyncopal: post-ictal state? PEX: evidence of CHF (arrythmia risk) or murmur suggesting outflow obstruction, complete neuro exam EKG (emcorecontent.com) ! STEMI, EKG changes suggesting ischemia, arrythmias or prolonged intervals ! Brugada syndrome: RBBB pattern with ST elevations ! WPW: delta wave with short PR ! Long QT syndrome (medications vs congenital?) ! IHSS/HCM: LVH, LBBB, needle Q waves Labs: to be considered on clinical situation, although of limited use Disposition ! San Francisco Syncope Rule (Ann Emerg Med 2004;43:224-32) (a) Derivation study sensitivity of 96% and specificity of 62% in predicting a serious outcome in 7 days (b) Compared to physician judgment, SFSR has potential to decrease admissions by 10% in low risk group and still predict serious outcomes. (Am J Emerg Med 2005;23:782-6) (c) Internal Validation of SFSR was able to predict serious outcomes at 30 days with sensitivity of 98% and decrease admissions by 24%. (Ann Emerg Med. 2006;47:448-454) (d) External validation cohort of the San Francisco rules, sensitivity and specificity were found to be 89% and 42%, respectively. (Ann Emerg Med. 2007;49:420-427) ! ACEP Guidelines (Ann Emerg Med 2001;37:771-6, Ann Emerg Med 2007;49:431-444) (a) Retrospective study showed for level B recs sensitivity and specificity were 100% and 81% respectively. (b) Level B + C sensitivity and specificity were 100% and 33% respectively, offering no further advantage over level B recs. (Am Heart J 2005;149(5):826-31) ! Cardiac Monitor: for most patients, monitoring >24h unlikely to detection of arrhythmias ! Admission W/U (thinking ahead) (a) Echo "r/o mechanical causes, CHF (b) ETT/Cath "r/o ischemia (c) Monitor/Holter/EPS studies"r/o arrhythmia

Other Causes • •

Vasovagal: appropriate stimulus upon standing"pallor, dizzy, nausea, diaphoresis, #vision Orthostatic syncope: secondary to volume depletion, meds, autonomic dysfunction

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ACID-BASE & ABG ALGORITHM 1

STEP 2 CHECK pCO2

<40 ACIDOSIS

<7.36 STEP 1 CHECK PH

7.36 - 7.44

>40

Metabolic Acidosis Respiratory Acidosis

pC02<36 HCO3 <21

Mixed Resp Alk & Met Acidosis

pC02>44 HCO3 >27

Mixed Resp. Ac. & Met Alkalosis

>7.44

Metabolic Alkalosis ALKALOSIS

>40 <40

Respiratory Alkalosis

STEP 3 CHOOSE FORMULA

STEP 4 Identify mixed disorders

pCO2= 1.5[HCO3 -] + 8

Compare the values of the ABG to the calculated values of the formulas. If they match then a pure disorder is present. If they do not, then a mixed disorder is present.

For every ∆ of 10 in pCO2: pH decreases by: 0.08 (Acute) 0.03 (Chronic) HCO3 – increases by 1mEq/L (Acute) 4 mEq/L (chronic)

STEP 5 Check Anion Gap [Na+] – [Cl- + HCO3 -] STEP 7 Check Urine pH/Lytes

pCO2= 0.9[HCO3 -] + 16 For every ∆ of 10 in pCO2: pH increases by: 0.08 (Acute) 0.03 (Chronic) HCO3 – decreases by 2 mEq/L (Acute) 5 mEq/L (Chronic)

STEP 8 Generate a DDX STEP 9 Check the A-a gradient A-a O2 Gradient = PAO2 – PaO2

Metabolic Acidosis GAP Methanol/Etoh Ethanol Uremia DKA Paraldehyde Ischemia Lactic acidosis Ethylene glycol Salicylates

Non-GAP Diarrhea Ureteral diversion RTA Acetazolamide Pancreatic fistula Cholestyramine

W/u of Anion Gap Metabolic Acidosis2 It is possible to have two distinct metabolic disorders and a respiratory disorder ie “triple ripple” To identify, check the delta-delta. ∆∆ = ∆ HCO3 - - ∆ anion gap ∆ HCO3 = change from normal HCO3 – = 24 – measured HCO3 – ∆ AG= Expected – calculated anion gap. Expected anion gap= [albumin] x 2.5 Calculated anion gap [Na+] – [Cl- + HCO3 -] If ∆ HCO3 = ∆ AG pure AG metabolic acidosis If ∆ HCO3 > ∆ AG simultaneous nonAG acidosis If ∆ HCO3 < ∆ AG simultaneous metabolic alk

W/u of Non-Anion Gap Metabolic Acidosis2 1) √ Urine gap UAG = [ UNa + UK] - UCl 2) UAG is an indirect measure of NH4+ as an unmeasured cation 3) Negative UAG= increased NH4 excreation as in type II RTA, GI losses 4) Positive UAG = failure to excreate NH4 as in Type I or IV RTA, ARF.

PAO2= [(FiO2) * (Patm - PH2O) – (PaCO2/0.8) ] PaO2 = PaO2 from ABG

References 1) 2)

High-Yield Acid-base. Pocket Medicine 2nd edition.

DKA: Some Basics Diagnostic criteria Glucose > 250 mg/dl pH < 7.30 Bicarbonate < 18 mEq/L Ketonemia STEP 1: Resus 1) ABC’s 2) Fluid Replacement a. Deficit is typically 50-100ml/kg (5-10L) b. Initially use NS (start with 1/2NS if Na>150) c. 1st L over 30-60 min, then 1-2L over next 2 hours. d. Switch to ½ NS @250cc/h as vitals, exam and U/O normalize and as chloride reaches >105 (prevent rebound hyperchloremic metabolic acidosis) 3) For peds: a. Avoid excessive fluids (<50mL/kg in first 4h) b. No insulin bolus c. No bicarb. 4) Identify and treat precipitating cause 5I’s a. ICON, MI, Cerebral Infarct, Infection, Insulin noncompliance. STEP 2 : Electrolyte Management 1) 2) 3) 4) 5)

Most patients in DKA are K+ depleted even if initial K is elevated. Do not give insulin until K+ is known. If K < 3.5 give K prior to insulin If K 3.5-5, give K in maintenance IV, OK to start insulin concurrently Remember to give 2 grams Mag when replacing K.

STEP 3: Insulin therapy 1) 2) 3) 4)

IV insulin gtt is standard of care (SC is poorly absorbed when dehydrated/ in shock) Recommended initial infusion rate is 0.1 units/kg/hr Can decrease insulin 50% when acidosis resolving (bicarb >15 or gap <12). No evidence exists that bolus benefit (but if you do use do 0.1 units/kg) and some consider dangerous due to K+ shifting. 5) Switch to SC insulin when tolerating PO’s and DKA resolved (ie bicarb >19, acidosis & gap resolved) 6) Start SC insulin before stopping IV insulin (15minutes for Humalog or Novolog and 60 minutes for Regular)

References 1) Grand Rounds Scott Votey USC Grand Rounds 8/21/08 www.emcorecontent.com/

TOXIDROMES & Toxic Alcohols SUMMARY VERSION Temp

↑

Anticholinergic Benadryl, TCAs, Atropine Cholinergic Acetylchol Est. Inhibitors Pesticide, Nerve agents Sympathomimetic Cocaine Ecstasy Opiates

↑

Skin Dry

Bowel & Bladder Retention

↑

↓

Wet

Urination & diarrhea

↑

Wet

↓

Dry

Constipation

Eyes

Syndrome

Symptoms

Common Causes

Anticholinergic

Tachycardia, hyperthermia, mydriasis, warm and dry skin, urinary retention, ileus, delirium (“mad as a hatter, blind as a bat, red as a beet, hot as a hare, and dry as a bone”*)

Antihistamines Atropine Belladonna alkaloids Jimson weed

Mushrooms (some) Psychoactive drugs Scopolamine Tricyclic antidepressants

Cholinergic, muscarinic

SLUDGE syndrome (salivation, lacrimation, urination, defecation, GI cramps, and emesis), miosis, bronchorrhea, wheezing, bradycardia

Carbamates Mushrooms (some) Organophosphates

Physostigmine Pilocarpine Pyridostigmine

Cholinergic, nicotinic

Tachycardia, hypertension, fasciculations, abdominal pain, paresis

Black widow spider bites Carbamates

Insecticides (some) Nicotine

Opioid

Hypoventilation, hypotension, miosis, sedation, possibly hypothermia

Opioids heroin, methadone

morphine pentazocine

Sympathomimetic

Tachycardia, hypertension, mydriasis, agitation, seizures, diaphoresis, hyperthermia, psychosis (after chronic use)

Amphetamines Caffeine Cocaine Ephedrine

MDMA (Ecstasy) Phenylpropanolamine Theophylline

Withdrawal

Tachycardia, hypertension, mydriasis, diaphoresis, agitation, restlessness, seizures, hyperreflexia, piloerection, yawning, abdominal cramps, lacrimation, hallucinations

Withdrawal of any of the following: Alcohol Barbiturates

Benzodiazepines Opioids Sedatives (some)

http://www.merck.com/mmpe/sec21/ch326/ch326b.html#BGBGFFEC

Toxic Alcohols Review1

Ethanol

Isopropran olol AKA Isopropyl Alcohol Ethelene Glycol

Methanol

Classic Source 40 oz

Anion / Osmolar gap +/- / Yes

Lab

Rubbing alcohol

Yes < Yes

Ketones Normal to mild ↓pH

Antifreeze

Yes / Yes

Hypocalcemia Long QT

Wood alcohol, solvents

Yes / Yes

Complications & distinuguishing features Can result in ETOH ketoacidosis if binge occurs in starving state Hemorragic gastritis GIB Peripheral vasodilation ↓ BP Hemolysis Rhabdo Calcium oxalate precipitaes Neprhotoxic ARF Hypocalcemia long QT Is converted to formate which in turn inhibits cytochrome oxidase causing lactic acidosis and blindness

Treatment 1) 2) 3) 1) 2)

1) 2) 3)

1) 2) 3) 4)

Banana bag D5 NS or ½ NS No bicarb Supportive care HD if hypotension despite tx.

Bicarb (↓ precipitation) Ca gluconate, Mag Dialysis if anuria, acidosis, level>50mg/dl Bicarb Fomepizole Ethanol HD if visual symptoms, CNS depression, level >50mg/dl, severe acidosis

EKG Toxicology Cardiac action potential review 0 1 2 3 4

0 – Na channel blocker.

open fast Na channels Na in close fast Na channels open Ca and K channels balance of Ca in, K out Ca channels close K out Channels all closed. Na/K ATPase pumps sodium out of and potassium in to maintain a negative electric potential

Molecular & EKG effects

Clinical effects

Management

Examples.

Create delay in NA influx

Bradycardia may occur because of slowed depolarization of pacemaker cells that depend on entry of sodium ions.

Bicarb to goal serum pH=7.5

But because many of the Na channel blocking agents are also anticholinergic or sympathomimetic agents, bradydysrhythmias are rare.

Hypotension is likely due to adrenergic agonism – therefore treat with phenylephrine or methoxamine.

Carbamazepine Class IA antidysrhythmics (Disopyramide, Quinidine, Procainamide) Class IC antidysrhythmics (Encainide, Flecainide, Propafenone) Cocaine, Cyclic antidepressants, Amitriptyline, Diltiazem (also CCB) Diphenhydramine, Propranolol, Quinine, Verapamil Antihistamines (Diphenhydramine) Antipsychotics (Haloperidol…) Class IA, IC, III antidysrhythm. Cyclic antidepressants (Amitriptyline) Fluoroquinolones Macrolides (Erythromycin) Dihydropyridines (Nicardipine, Nifedipine, Isradipine, Amlodipine, Felodipine, Nimodipine) Verapamil, Diltiazem, Bepridil

QRS widening and may mimic bundle branch block - Ventricular dysrhythmias Sine wave.

In Na channel blocker poisoning by anticholinergic and sympathomimetic drugs (ie TCAs!!) the combination of a wide QRS complex and bradycardia is an ominous sign and my indicate that the Na channel blockade is so profound that tachycardia does not occur, despite clinical muscarinic antagonism (ie Hot as a hare..) or adrenergic agonism.

2-K efflux blocker

Prolong the cardiac cycle action potential QT prolongation

Sinus tachycardia can occur because of the anticholinergic effect of these medications and from the reflex tachycardia induced by alpha-adrenergic blockade in the peripheral vasculature.

Mag, overdrive pacing.

Decreased intracellular calcium within the myocardial cells results in slowing of conduction, decreased contractility, and decreased cardiac output. Blockade of calcium influx within the vascular smooth muscle cells results in vasodilation. Decreased cardiac output coupled with vasodilation can result in profound hypotension, shock, pulmonary edema.

atropine, calcium, glucagon, insulin, sodium bicarbonate,or various catecholamines

QRS complex widening can occur as a result of Na channel blockade (see later discussion).

2 &3 Ca channel blocker. 4- Na/K ATPase

sinus bradycardia, AV block (first-, second-, and third-degree) and junctional and ventricular bradydysrhythmias on ECG. A widening of the QRS complex may be encountered. This may be caused by ventricular escape rhythms or by CCBinduced sodium channelblockade causing a delay of phase 0 of depolarization. Cellular effects: ↑ extracellular K, ↑ intracellular Na Decreases the transmembrane Na gradient and subsequent increased activity of the Na–Ca2 exchanger. ↑This intracellular calcium concentration ↑ augments myofibril activity in cardiac myocytes 0 ↑inotropy

Additionally, The ECG may demonstrate findings associated not only with cardiac glycoside toxicity but also with hyperkalemia. Acute toxicity most closely correlates with hyperkalemia as the Na/K ATPase is inhibited and extracellular K increases. In chronic toxicity, hyperkalemia may not be seen because of the slower increase in K, allowing for renal compensation.

EKG effects 1) Abnormal inverted or flattened T waves 2) ST segment depression – 3) sagging or scooped ST segment/T wave complex. 4) QT interval shortening as a result of decreased ventricular repolarization time, 5) PR interval lengthening as a result of increased vagal activity, 6) Increased U-wave amplitude with toxicity

Digoxin-specific antibody (Fab) fragments are the first-line

Bufadienolides, Digoxin, Digitoxin, Foxglove, Lily of the valley, Oleander, Red squill

Atropine in AV block If pacing is needed care should be exercised as the pacing wire itself may induce ventricular fibrillation

References: Emerg Med Clin N Am 24 (2006) 159–177, Current Critical Care Diagnosis and Treatment 3rd p765,

PEDIATRIC SURVIVAL GUIDE VITALS SBP (min, 5th %)

WT (kg) = 2 x AGE + 10 Nb-3kg, 1y-10kg, 5y-20kg, 10y-30kg

HR (max)

0-1month = 60mmHg 1month-1year= 70 Ages 1-10yo= 70 + (AGEx2) Ages >10yo= 90

Nb-6mo-180-190 1yr-2yr-150 3yr-6yr-120-140 7yr-12yr- 110

Newborn-50 1yr-40 3yr-30 5yr-25, 10yr-20

AIRWAY ETT Age/4 + 4 PREMIS: <28wks - 2.5 28-32wks - 3.0 32-36wks - 3.5

LARYNGOSCOPE Miller/Mac 1: <2yo, Miller/Mac 2: <8-10yo, Miller/Mac 3: >10yo

VENT SETTINGS Press support, TV: 610cc/kg, Rate 20 (30 if <1yr old)

MISC NGT/Foley: 2xETT Chest Tube: 3-4xETT

BREATHING INTUBATION Atropine (<8yo)= 0.02mg/kg, min 0.1mg, max 0.5mg) Etomidate= 0.3 mg/kg IV Succinylcholine= 2 mg/kg IV Vecuronium= 0.1-0.2 mg/kg IV Rocuronium= 1mg/kg IV

ANAPHYLAXIS Epi 1/1,000= 0.01mg/kg IM q15min PRN(MAX dose 0.5mg) OR IV/IO 1/10,000=0.01 mg/kg q3-5min (max 1mg) if hypotension, then 0.1-1 ug/kg/min IV if refractory hypotension after IM/IVF Benadryl 1-2 mg/kg IV q4-6h (max 50mg) Ranitidine 1mg/kg IV

ASTHMA Albuterol 0.15mg/kg (MAX 5mg) Atrovent <12yo=250mcg, >12yo=500mcg Magnesium: 50 mg/kg (max 2g) over 20 min Epi (1/1000) 0.01mg/kg IM q15min PRN (0.5mg MAX) Terb: IV- 10mcg/kg bolus THEN 0.1mcg/kg/min gtt OR .01mL/kg SUBQ

Steroids 1mg/kg/day Steroids: Prednisone( 15mg/5cc) 1mg/kg/day PO or Methylprednisone 2mg/kg IV/IM(Max 80mg) THEN 0.5mg/kg IV/IO q6h (max 120mg/day)

CIRCULATION BOLUS 20cc/kg

MAINTENANCE 0-10kg=4cc/kg/hr, 11-20kg=add 2cc/kg/hr, >20=add 1cc/kg/hr

BLOOD, FFP, platelets 10cc/kg

ACLS DRUGS CODE DRUGS

SHOCK

SVT

CODE ADJUNCTS

(Infants: HR >220, Kids >180, no p-waves, not-variable) or VTAC

EPI 1/10,000= 0.01mg/kg in Unstable Brady, PEA, VF/VT (=0.1cc/kg) ** ETT dose 0.1cc/kg of 1:1,000 = 0.1mg/kg Atropine= .02mg/kg in Brady, only if Prim AV block or vagal DEFIB (AED only if >1yo): 2 J/kg then 4 J/kg

Adenosine= 0.1mg/kg (Max first dose=6mg), may double 2nd dose Synchronized CV= 0.5-1 J/kg, may inc to 2 J/kg Amio 5mg/kg IV over 2060min Procainamide 15mg/kg IV over 30-60 min

Dopamine 2-20mcg/kg/min Levophed 0.05-2 mcg/kg/min Phenylephrine 0.1-0.5 mcg/kg/min Dobutamine 2-20 mcg/kg/min

Calcium Chloride: 20 mg/kg IV/IO (max 1,000mg) Glucose: 0.5-1 g/kg, 4 cc/kg D25 5 cc/kg D10 10 cc/kg D5 Narcan: 0.1mg/kg Flumazenil: 0.01 mg/kg (MAX 2mg) [1-5ug/kg if partial]

Magnesium 25-50 mg/kg IV/IO (MAX 2g) for Torsades

Mannitol: 0.5-1 g/kg

OTHER DRUGS PROCEDURAL SEDATION Ketamine 1-2mg/kg IV 2-4 mg/kg IM Propofol 0.5-2.0 mg/kg Brevital 1 mg/kg

SEIZURE

ANTIPYRETICS & ANTIBIOTICS

Ativan (lorazepam): 0.1mg/kg IV (max 4mg)

Tylenol 80mg/0.8cc or 160mg/5cc=15mg/kgq6,

Valium (diazepam): 0.1-0.3 mg/kg IV (max 10mg)

Benadryl 12.5mg/5cc=1mg/kg q6

Versed (midazolam): 0.1 mg/kg IV, 0.3 mg/kg IM

Etomidate: 0.15 mg/kg

Motrin 100mg/5cc=10mg/kg q6,

Ampicillin 50mg/kg Amoxicillin(125 or 250mg/5cc) 80mg/kg/day divided q8-12 Cefotaxime 50mg/kg Augmentin(200mg or 400mg/5cc) 40mg/kg/day divided q12

Phenytoin (dilantin): 20 mg/kg Phenobarbitol: 20 mg/kg

Ceftriaxone 50-100mg/kg Keflex(125mg or 250mg/5cc)25-100mg/kg/day divided q6h Gentamycin 4mg/kg (q24h)

Depakote (Valproate): 15-20 mg/kg IV

Bactrim(40mg/5cc)TMP 6-12mg/kg/day divided q12 Vancomycin 15mg/kg

Pyridoxine(INH Tox): 1gIV/IM q30min, dose 1g for each gram of INH ingested

Zithro (100mg/5cc)10mg/kg(day 1) 5mg/kg (day 2-5) Rifampin 20mg/kg Clinda (75mg/5cc)10-30mg/kg/day divided q6-8

)*+( "# "#$%&$'()*+(,! ")+-./+*()0! ")

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P8-2(94! 6/@!F/! >(N! D*8*!

• Benzos • Phenobarb

• Dilantin

• D10 • Ca-gluconate 10% (1-3ml/kg)

• Pyridoxine (50-100mg

if refractory)

Cyanotic (blue) • • •

! )F:(

1-2 weeks Cyanosis Hypoxia-O2 not correct

E: E:;4,(N*/!+49+! /2*C(9*9! /2

CV collapse (grey)

• • • •

QR90!GTUV<2A$5A$<*)!"#W! X(;/<*)4$X(.-+/<*)4! ")+-./+*()0! I4C9!9-,A4,:Y!

1.N!G1<;@!P4)+!@!F8*)C/W! Q#P*(D6"-(*%$%C(

• • • •

Pale, shocky Sudden circulatory collapse Acidosis !pulses LE (coarc)

G'%#*%,'$B( :,*$*%#"(

• • •

1.C(<4)!C*9+4)+*()! #(<*+!-"##'(A,B#C( D8-4!/.C(<4)!

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• • • • •

E$%!9*.8*)A!C4/+39! #(<*+$C43:C,/+*()! F67!9:<;+(<9! E4;/+(<4A/8:! %C(,!G9B4/+@!<-9+:@!H,-*+:!

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• • • •

67$XVT! XVT!Z!67!VU[O&N!</*)+! 6I%! EF%\0!G*H!;E]^UV!H(,!(,A/)*2! /2*C4<*/W!

• • • •

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General Approach (CME Download lectures: (McCollough M, Sharieff GQ, Brown, L), www.cmedownload.com) • • • • •

Definition: Full-term newborn, born well and d/c home by pediatrician!returns in first month looking sick, hypotensive and dehydrated. Always begin with ABCs and decide whether or not to emergently intubate. Then begin fluid resuscitation if not in overt CHF and check/correct hypoglycemia, which is invariably present. Then, think about and rule-out emergent causes starting with focused H&P, labs and possibly imaging. At minimum, these neonates will get a septic work-up including labs, antibiotics and possibly LP!then admission.

Reversible Causes • Hypoglycemia always present!treat early with D10

Seizure • •

Present with atypical movements!usually not tonic-clonic Ddx large: CNS, Infection, Metabolic, Drug withdrawal, Toxins, fam hx ! Hypoxic-Ischemic encephalopathy (50-65%), IVH/SDH/SAH (15%), Other"IEM, Sepsis, metabolic, toxin (10%)

•

Labs: check labs even if seizures have stopped

(Common Complaints in the First 30 Days of Life. Emerg Med Clinics North Am 2002;20(1):27-48)

Congenital Heat Disease (3 varieties based on color of pt) (Pediatric Emergency Medicine: A Comprehensive Study Guide. McGrawHill. 2002:235-245)

•

PGE1 ! Side effects!, hypotension, fever, apnea (may need to intubate)

Acyanotic

Cyanotic

Color Path Examples

Pink (!PBF) L!R shunt VSD, PDA

Grey ("PBF) Ductal dependent cardiac failure Coarc, AS, Hypoplastic LV

Present Sx

First 6 months, gradual-not sick Poor feeding, sweating, dyspnea, cough, #resp infxn Resp distress, rales, hepatomegaly

1-2 weeks, sudden Sudden circulatory collapse, hypotension, acidosis CHF, "LE pulses

PEX PDA Tx

CHF treatment (lasix, dig)

Need PDA for systemic blood flow PGE1

Blue R!L shunt "PBF: TOF, Tricusp atresia, #PBF: TA, TAPVR, TGA 1-2 weeks, sudden Cyanotic, hypoxia not responsive to O2 Cyanotic Need PDA for pulm blood flow PGE1

Intestinal Emergencies (Volvulus, Incarcerated hernia, Diaphragmatic hernia, Nec Enterocolitis) •

•

Volvulus (cogenital malrotation)!irritable, vomit..gastroenteritis sx ! KUB!”double-bubble”; UGI!corkscrewing of intestine ! Tx!Antibiotics, Surgical emergency! ! Complete volvulus can lead to bowel necrosis in 1-2 hours! (Emerg Med Clinics North Am 2002;20(1):139-153) ! Unexplained Bilious Vomiting in young infant=Malrotation and Midgut Volvulus until 2-&' ()*+,#"' proven otherwise Necrotizing enterocolitis ! Premies, present similar to volvulus !"#$%&#&' ! KUB!pneumotosis intestinalis -3-4+5-$' 7)-+'82"3-'$-9-"5' ! Tx: Bowel rest, ABx /%'

/01'

Inborn errors of metabolism (IEM) •

Biochemical defect that causes accumulation of toxic metabolite (NH4, ketones, lactic acid) usually in the brain

/6'

CAH (Congenital Adrenal Hyperplasia) • •

Deficiency in cortisol and aldosterone; accumulation of androgens 21-hydroxylase deficiency (90%)"not screened for in all states

!.#,%'+"#$'$-9-"5' :;)#,-'<#5=')-$;"#,*'

Fever (<29 days old) Fever F ev ver ((<29 <22299 d days ays oold) lld) d Temp>100.4

Work up • • • •

!"!#$"%&&'$!(#$$ )*+),($-./01$ 23$$ !456$$

Antibiotics Ampicillin 50mg/kg/dose IV/IM + Gentamicin 2.5mg/kg/dose IV/IM OR Cefotaxime 50mg/kg/dose Consider: Vanco 15mg/kg/dose Acyclovir 20mg/kg/dose

Admit

General Ge al Pediatric Fever F • • •

20% of febrile children have fever without an apparent source of infection (FWS) after history and physical exam. A response to antipyretic medication does not change the likelihood of a child having a serious bacterial infection and should not be used for clinical decision-making (Level A ACEP recommendation Ann Emerg Med 2003;42:530-545 ). If parents report a fever at home but is afebrile in the ED, the child should still be considered as having had a fever

Fever < 29days General •

Using low risk criteria (Rochester) does not apply to the neonate (birth-29d) because too many serious bacterial infections can be missed, and therefore admission and further w/u is advised. • Infants between 1 and 28 days old with a fever should be presumed to have a serious bacterial infection (Level A ACEP recommendation Ann Emerg Med 2003;42:530-545) Work-up • If the infant is critically ill, may postpone LP. ! Positioning for LP may suppress respiratory drive"will need continuous pulse ox; sitting position may decrease risk of respiratory depression • CXR required only if resp sx present (tachypnea, retractions, grunting, abn lung exam or pulse ox). Antibiotics • Consider cefotaxime especially if CSF is suspicious or positive for meningitis • Consider Vancomycin if infant critically ill, mother or child previously treated for Group B Strep • Consider Acyclovir if infant critically ill, seizing or if mother has history of Herpes

Fever (29-60 days) Ill Appearing

1) Well Appearing?

Admit + Sepsis w/u • • • •

Well

• • •

CBC, BCX Udip/Ucx CXR LP

Cefotaxime 50-100mg/kg +Ampicillin 100mg/kg +/-Acyclovir 20mg/kg

Well, not Low risk

2) Low risk?

Admit

No • •

• •

BCx CXR

LP Antobiotics

Low risk criteria •

Yes

• •

Clinical criteria Previously healthy, term infant Non-toxic No focal bacterial infxn on exam

• • • •

Lab criteria WBC 5-15,000; <1500 bands, B/N <0.2 UA: gm stain(-), LE/Nitrate(-), <5WBC/hpf Diarrhea if present:<5 WBC/hpf stool CSF (optional): <8 WBC/mm3

Well,, Low risk Outpatient Management

3) Outpatient Tx ?

4) Follow-up (24h)

Observation option • CBC, BCX • Urine dip/CX • Reevaluate in 24h

• • • • •

Empiric ABx option CBC, BCX Urine dip/CX LP Ceftriaxone 50mg/kg IV/IM Reevaluate in 24h

AT 24 hours: Bl Blood Cx positive: "Admit for sepsis w/u and IV ABx Urine Cx positive: Ur • Afebrile/well: outpatient antibiotics • Persistent fever: Admit for sepsis w/u and IV ABx

Generall Approach Ge Ap ch •

•

In this age group, can use low risk criteria (Rochester, Boston, Philadelphia) to identify a cohort of infants that can safely be treated on an outpatient basis and separate those patients from those that have a higher risk of Serious Bacterial Illness (SBI) that includes UTI, occult bacteremia, bacterial enteritis and bacterial meningitis Risk of SBI in the three groups:1)Ill appearing 22.2% 2)Well and not low risk 12.3% 3)Well and low risk 1% (Jaskiewcz Pediatrics 1994;94:390-6)

Low Risk Work-up •

•

Using the above low risk criteria, rate of SBI across multiple studies is 0.9% (Baraff, LJ Ann Emerg Med 2000;36:602-614). ! When using less conservative criteria (WBC<20, urine dipstick w/o UA, no stool examination) rate of SBI increased to 5.4% (Baskin MN J Pediatr 1992;120:22-27). ! If the infant fails to meet low risk criteria, then they are at higher risk for SBI (up to 25%) and should be admitted for sepsis w/u ! Sensitivity of low risk criteria (Philadelphia) > 98% for identifying febrile children at low risk for SBI (Baker NEJM 1993;329:1437-1441) Lumbar Puncture ! Lumbar Puncture is optional if the child is well appearing, has normal lab values and no other sources of infection found. Most experts still recommend an LP in the 4-8wk old despite well appearance ! LP is indicated if discharging home on empiric antibiotics ! LP is indicated if another source of infection is found (i.e. UTI) because infants in this age group have difficulty containing infections to one organ system. There are two treatment options for the well appearing low risk child: ! Observation option: hold antibiotics until cultures become positive and re-evaluate in 24h or ! Empiric antibiotics option: can treat empirically x2 doses in 48h (this option requires an LP be done prior to Abx) 84 Also consider admission if parents unreliable and not able to follow up in 24h.

Acute Pelvic Pain

ABC IV/O2 IVF Pain Rx

1) Initial Resuscitation

(Nonpregnant)

2) R/O Non-GYN causes

GU causes

UTI/Pyelo Ureteral colic

UA U/S CT stone protocol

GI causes

Appendicitis Diverticulitis Hernia, Obstruction, other

Labs CT A/P? Surgery C/S

Other

3) Emergent Gyn H&P

Ovarian Torsion

TOA

PID

4) Non-Emergent Gyn

• • • • •

• • • •

W/U and Tx

Risk factors: (Reproductive age, pregnant, infertility tx, vigorous activity) Acute severe unilateral pelvic pain Bilateral (25%) Radiation back, flank, groin N/V

Abd/Pelvic pain H/O PID/ PID sx CMT/adnexal pain

Hx: • • • •

Abd/Pelvic pain Vaginal d/c Fever STD risk factors

• Palpable mass • Fever • !WBC

U/S • • •

Cystic/solid mass (>70%) Free fluid (>50%) Doppler (Art/venous flow, whirlpool sign)

GYN C/S OR

U/S • Homogenous, cystic mass • A/F levels, septations

Tx • Antibiotics • IR guided drainage • OR

PEX • CMT/Adnexal tender • Febrile • WBC/ESR

Ruptured corpus luteum cyst Hemorrhagic cyst Mittleschmerz Endometriosis Leiomyoma

U/S • • Tx •

R/O TOA Diagnostic of PID? Treat empirically?

Acute Pelvic Pain

General Approach: • • • •

(Nonpregnant)

The approach to the woman with pelvic pain is to start with the initial resuscitation and pain control. Then expand the differential to think about non-gynecologic causes from GU or GI origin, most commonly appendicitis. Then, the focus should be on emergent gynecologic disease, such as ovarian torsion and PID/TOA. If that work-up is negative, consider treating empirically for PID, and think about other causes of pelvic pain.

Non-Gyn Causes • See abdominal pain algorithms for more detailed explanation of GI and GU causes of abdominal pain

Ovarian Torsion • •

•

Definitive diagnosis of ovarian torsion is based on surgical findings Difficult diagnosis correct pre-operative diagnosis made in only 38% of cases (J Reprod Med 2000;45:831) U/S: Cyst/Mass found in >94% of torsion cases (Clin Exp Obstet Gynecol 2004;31:34) √ Normal ovaries (absence of cyst/mass) does not completely rule-out torsion √ Normal ovaries found in 6% of adult cases and over 50% of children under age 15. ( Arch Pediatr Adolesc Med. 2005;159:532-535) Doppler blood flow √ Predictive of non-viability of the ovary √ Blood flow preserved in early/incomplete torsion √ Whirlpool sign (J Ultrasound Med 2004; 23:1643–1649) √ Sonographic appearance of twisted vascular pedicle √ Earliest and most definitive sign for torsion Therefore, the presence of normal flow does not exclude torsion, and if high clinical suspicion (persistent pain) may need laparoscopy despite negative ultrasound. Treatment: Gyn Consult for likely surgery

TOA • • • •

•

Etiology: PID (most common), pelvic surgery, intra-abdominal process Micro: same as PID, polymicrobial, anaerobes Diagnosis: consider in any woman suspected of PID U/S: Sensitivity and Specificity almost 100% (Am J Surg 1982;143:582) Differentiates vs TOC (tuboovarian complex) perfused inflammatory living tissue without abscess wall, amenable to medical therapy Treatment: Trial of medical therapy (antibiotics) IR guided drainage Operative drainage

PID

Criteria for hospitalization: (MMWR Recomm Rep 2006;55:1)

• Unable to follow or tolerate an • Surgical emergencies (e.g., Path: represents a spectrum of disease from endometritis to fatal outpatient oral regimen; appendicitis) cannot be excluded intraabdominal sepsis • Severe illness, nausea and vomiting, • Pregnant • Diagnosis or high fever; and • Does not respond clinically to Difficulty in diagnosis, potential for damage to the reproductive oral antimicrobial therapy; • Tubo-ovarian abscess health of women, and evidence of mild/subclinical PID CDC has issued a minimum set of criteria of treatment of PID for women with abdominal pain and at least one of the following: (MMWR Recomm Rep 2006;55:1) • CMT or uterine/adnexal • Vaginal secretions with tenderness WBC on saline microscopy • Temp>101 • Elevated ESR • Leukocytosis/left shift • Elevated CRP • Abnormal cervical/vaginal discharge • Treatment: Antibiotics (see Sanford guide)

•

Non-Emergent Gyn •

•

Cyst rupture: sudden onset, unilateral abdominal pain, +/-vaginal bleeding, +/- peritoneal signs (blood irritating peritoneum). Uncomplicated (follicular or corpus luteum cyst)•follow expectantly for enlarging hemoperitoneum Complicated: may need operative control of bleeding→treat like ectopic pregnancy Mittleschmerz: midcycle pain from rupturing of follicle during ovulation

AB ABCs IV/O2/Monitor IV IVF IV Transfusion? Stat GYN C/S?

1) Initial Resuscitation

Pregnant Vaginal Bleed <20 WKS

2) R/O Ectopic U/S:

(+) IUP

Indeterminate

(+) Ectopic

ß<DZ DZ • •

ß-HCG:

•

ß>DZ

Non-Diagnostic

No Ect Ectopic ic Heterotopic? (infertility drugs?...) Eval for SAB (below)

• •

Abnormal Pregnancy

• •

GYN N C/S Serial ß-HCG(48h)

• •

GYN N C/S MTX vs Surgery

GYN C/ C/S Expectant mgt vs MTX vs Surgery

3) Eval for SAB OS:

Threatened • •

POC:

Inevitable • •

Os closed No POC

Complete

Incomplete • •

Os open No POC

Os open POC

• •

Os closed POC expelled

• • •

• •

Expectant mgmt D/C Home GYN F/U

GYN C/S D&C (1-3d if stable)

• • •

Remove POC GYN C/S D&C

• • •

Expectant mgmt D/C Home GYN F/U

RhoGAM if Rh(-)

4) Rh Status 5) Other Dx

• • •

Exclude Vaginal/Cervical/Uterine Pathology Molar pregnancy Physiologic/Implantation Bleeding (Dx of exclusion)

Abbreviations: DZ=Discriminatory Zone, IUP=intrauterine pregnancy, SAB=spontaneous abortion, POC=products of conception, r/o=rule-out, C/S=consult, GYN=Gynecology, Dx=diagnosis, MTX=methotrexate, D&C=dilation and curettage, w/u=work-up, r/o=rule-out

General Approach • • • •

Start with initial resuscitation and ABCs depending on stability of the patient. Then rule-out ectopic pregnancy using pelvic ultrasound and HCG level. If ultrasound shows IUP and no concern for ectopic, then evaluate for SAB based on os and POC on exam. Final steps are to consider RhoGAM and other benign causes for vaginal bleeding.

R/O Ectopic •

•

• •

•

R/O Ectopic: based on results of U/S!3 possibiltites: " If U/S shows ectopic, call Gyn for operative vs conservative management. " If U/S shows IUP and no concern for heterotopic, eval for SAB. " If U/S indeterminate, classify into non-diagnostic or abnormal pregnancy based on ß-HCG level U/S criteria for IUP (see below for normal u/s appearance in pregnancy) " Gestational sac + “double decidual sac” sign is earliest sign of pregnancy, although some believe it is the yolk sac " Pitfall!Pseudosacs are false sacs that can be confused with gestational sacs; pseudosacs can occur in 10-20% of ectopic pregnancies # (centrally located) compared to Table 1: Normal ultrasound findings and ß-HCG levels vs gestational eccentric location of true gestational ageError! Bookmark not defined. sacs Gestational Transabdominal Transvaginal !-hCG Level U/S signs suggestive of ectopic pregnancy (Ma Age Landmarks Landmarks (mIU/mL) OJ, Mateer JR. First Trimester Pregnancy. In: Emergency 4–5 weeks ± Gestational sac Gestational sac 1000 st Ultrasound 1 ed. McGraw Hill. 2003, pp. 239-278) 5 weeks Gestational sac ± Gestational sac with 1000–2000 " Definite: Extrauterine embryo with cardiac yolk sac, ± fetal pole yolk sac activity (seen in 15-20% of EPs) 6 weeks Yolk sac and fetal Yolk sac and fetal pole 10,000–20,000 " Suggestive: Free pelvic/Intraperitoneal fluid, tubal ring, complex adnexal mass Incidence of heterotopic in " general population: 1:4,000-30,000 " Incidence in assisted reproduction: 1 in 100, therefore cannot exclude ectopic and further work-up needed in this population Discriminatory zone for ß-HCG for transvaginal U/S is usually 1,000-1,500 (depending on institution) Non Diagnostic: Indeterminate U/S below DZ: " Ddx: early viable IUP vs nonviable IUP vs ectopic " If pt stable: can d/c home, obtain serial ß-HCG, repeat U/S when ß-HCG above DZ after GYN consult " Pitfall!U/S should still be obtained if ß-HCG is below discriminatory zone because may still be able to diagnose both IUP and ectopic (Level C ACEP Recommendation) Abnormal pregnancy: Indeterminate U/S above the discriminatory zone: " Ddx: recent spontaneous AB or ectopic pregnancy is likely (86-100%) " Indeterminate U/S + ß-HCG> 2,000 virtually diagnostic of ectopic pregnancy (Fertil Steril 1998;70:972-981) " Follow-up needed in abnormal pregnancy because of increased likelihood of ectopic (Level B ACEP Recommendation Ann Emerg Med 2003;41:123) " Thinking 2 steps ahead:! Standard approach for serial ß-HCG is looking for a rise of 66% of 48hours, considered normal, although: # A normal rise may be seen in up to 15% of ectopics and an abnormal rise (<66%) may be seen in 15% of IUPs (Obstet Gynecol 1981;58:162-6)

•

Serial ß-HCG values at 48h: (Level B ACEP Recommendation Ann Emerg Med 2003;41:123) • 66%: IUP, EP(15%) • Plateau: nonviable IUP, EP • <66: EP, SAB, nl IUP (15%) • Decreasing: SAB, tubal AB Ectopic pregnancy can resolve spontaneously by tubal abortion or regression, but >90% of women with ectopic and ß-HCG>2,000 will require surgery (CMAJ 2005;173(8);905-912)

Indications for Medical Therapy of Ectopic Pregnancy

Evaluate for SAB and further work-up •

Evaluate for Spontaneous abortion in the patient with an IUP and vaginal bleeding • Hemodynamically stable " Classify into type of SAB based on OS and POC • Patient desires future fertility Incidence of miscarriage: (BMJ 1997;315:32-4) • Ability to return for follow-up • No contraindications to MTX " 21% bleed before 20th wk • Unruptured mass <3.5cm " 57% of those will miscarry • No fetal cardiac activity " 80% of those will miscarry before 12 weeks • Quantitative ß-hCG < 6-15,000 • After detection of fetal cardiac activity, <5% of pregnancies with normal sonographic appearance will abort (Ann Emerg Med 2003;41:123,) • RhoGAM 50 mcg for Rh(-) women at loss of first trimester pregnancy (Level B ACEP Recommendation Ann Emerg Med 2003;41:123,) " No recommendations for after first trimester, but standard dose is 300 mcg IM • Other Dx " Molar pregnancy dx by U/S showing “snowstorm” pattern or cystic structures " Implantation bleeding is spotting from implantation of embryo around the time normal period occurs

Kocherâ&#x20AC;&#x2122;s

Some Common Shoulder Reduction Techniques for Anterior dislocations Bend the arm at the elbow, press it against the body, rotate outwards until resistance is felt. Lift the externally rotated upper part of the arm in the sagittal plane as far as possible forwards and finally turn inwards slowly

Milch

With the patient lying on the back, the arm is raised by the side and externally rotated. The therapistâ&#x20AC;&#x2122;s thumb is used to gently push the head of the humerus back in place. A modified version of this technique is applied to patients lying on their abdomen.

Stimson technique

The patient lies prone on the bed with the dislocated arm hanging over the side. Traction is provided by up to 10 kg of weight attached to the wrist or above the elbow. Apply gentle internal/external humeral rotation. Reduction may take 2030 minutes.

Scapular rotation

This less traumatic technique has success rates of more than 90% in experienced hands, often without sedation. With the patient lying prone, apply manual traction or 5-15 lb of hanging weight to the wrist. After relaxation, rotate the inferior tip of the scapula medially and the superior aspect laterally. Alternatively, the patient can be seated while an assistant provides traction-countertraction by pulling on the wrist with one hand and bracing the upper chest with the other. The same scapular rotation is then performed.

Tractioncountertraction:

While the patient lies supine, apply axial traction to the arm with a sheet wrapped around the forearm and the elbow bent at 90Â°. An assistant should apply countertraction using a sheet wrapped under the arm and across the chest while the shoulder is gently rotated internally and externally to disengage the humeral head from the glenoid

Extrinsic muscles

The Detailed Hand Exam

Flexors

Nerve

Test

1) History: Hand dominance, occupation, hobbies, prior injury, time & location on trauma, mechanism of injury, posture of the hand at the time of injury. 2) Joints above: shoulder, elbow ROM. Pronation/supination. 3) Inspection: Skin: Color, swelling, edema, integrity, moisture, tenderness. Nailbed and fingertip: 4) Muscle testing:

F. Pollicis Longus (FPL)

Median

Bend the tip (IPJ) of the thumb

F. Digitorum Profundus

F Digitorum Superficialis

Median & Ulnar Median

Bend the tip (DIPJ) of each finger while holding the PIPJ of the finger Bend the PIPJ of the finger while holding the other fingers in extension.

Rapid screening

F. Carpi Radialis

Median

Radial Median

F. Carpi Ulnaris

Ulnar

Palmaris Longus

Median

Pronator Quadratus

Median

Abductor Pollicus Longus (APL)

E. Pollicus Brevis (EPB)

E. Carpi Radialis Longus (ECRL) E. Carpi Radialis Brevis (ECRB) E. Pollicus Longus (EPL)

Ulnar

Wrist extension 1st and 5th fingertip opposition. Finger abduction and adduction.

Nerve Radial

Median

Ulnar

Sensory Dorsal aspect of the second and third web space

Distal, palmar surface of the second digit Distal, palmar surface of the fifth digit

Extensors

Motor Proximal limb radial nerve lesions will cause wrist drop

Notes Superficial radial nerve, as it courses through the hand, is sensory only. Apply resistance and palpate the thenar eminence for contraction of the abductor pollicis brevis Challenging the interosseous muscles best tests ulnar motor function. Place the hand on a surface with the fifth digit down and the thumb pointing at the ceiling. Then, the patient abducts the second finger (spreading the fingers) against resistance. Document weakness and palpate the first interosseous muscle to verify contraction

11 12

13 14

E. Digitorum Communis (EDC) E. Indicis Proprius (EIP)

E. Digiti Minimi (EDM)

E. Carpi Ulnaris

Thenar group

Nerve

Test

Opponens Pollicis (OP)

Abductor Pollicis Brevis (APB) Flexor Pollicis Brevis (FPB)

Usually innervated by the motor branch of median, but in some, the ulnar.

Oppose tips of 1 and 5 digits. Place hand on dorsum of the hand on the table and raise the thumb up 90°

Hypothenar group 4 5 6 7

Opponens digiti minimi (OPM). Abductor digiti minimi (ADM) Flexor digiti minimi (FDM) Adductor pollicus

Ulnar

Intraosseous

Ulnar

Lumbricals

Median (index and long fingers). Ulnar

Radial

Bring the thumb out to the side of the hand while palpating each tendon. As above. The palmar border of the snuff box. Make of fist and extend the thumb against resistance

Palm flat on the table, lifting the thumb only off the table. Is the dorsal part of the snuff box. Straighten out the fingers after making a fist. Make a fist, then extend ONLY the index finger. Make a fist, then extend ONLY the little finger finger. Palpate the tendon as there is wrist extension and ulnar deviation.

5) Sensory - 2 point discrimination is more critical than sharp/dull and temperature. a) Static 2PD test (>6mm = abnormal) using a “Disk-Criminator” b) Moving 2PD test (>3mm = abnormal)

Intrinsic muscles

Flex the wrist while each of these fingers is palpated.

Move the little finger in the ulnar direction while palpating the muscle, noting a dimpling of the hypothenar skin. Place a piece paper between the thumb and radial side of the index finger and attempt to pull out. Froment’s sign: the IPJ of the thumb flexes. Spread the fingers: Palmar interossei adduct Dorsal interossei abduct. Hold a piece of paper between the 4th and 5th digits. Flex the MCPJs and extend the PIPJs and DIPJs of the fingers.

Muscles

Root Level

Nerve

Interossei

C8, T1

Ulnar

ADP

C8>T1

Ulnar

FCU

C8>C7

Ulnar

FDP (4 and 5)

C8 >C7

Ulnar

FDP (2 and 3)

C8> C7

AIN

FPL

T1,C8

AIN

APB

C6,C7

Median

FCR

C7,C6

Median

Pronator Teres

C7> C6

Median

EDC

C6 C7 C8

EPL

C6 C7 C8

ECRL

C6 C7

Radial

Triceps

C5 T1

Radial

Biceps

C5>C6

Musculocutaneous

http://www.wheelessonline.com/ortho/hand_motor_and_tendon_exam AIN = Anterior intraosseos branch of median nerve PIN = posterior intraosseos nerve 7)

Nerve Roots

Tendons Flexors: FPL FDP FDS FCR FCU PL

Extensors: EPL EDC ECRB ECRL ECU

Vascular a) Radial/ulnar pulses b) Cap refill, Pulse oximetry

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•

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1) Peri-articular?

2) Fracture?

3) Septic Joint?

Tendonitis Bursitis Cellulitis

• •

Trauma/Fall? X-ray

Joint Pain

H&P •

Non-GC

• • •

Labs • • •

Acutely painful swollen joint Risk factors Fever Minimal ROM

WBC ESR, CRP Synovial fluid WBC, PMN Gm stain, Culture

•

H&P

Gonococcal

• • • • •

Labs

Young, healthy sex active F>M Migratory polyarthralgia Tenosynovitis Dermatitis Fever

• • •

Gm stain(+) <10% Cx (+) <50% GU Cx (+)70-90%

4) Arthritis? Monoarticular

• • • •

OA Gout Pseudogout TB/Fungal

Polyarticular

• •

RA Seronegative Spondyloarthropathies Lyme dz Viral

• •

• • • •

Antibiotics Ortho C/S Culture results Admit

•

Pan-Cx every orifice Antibiotics Admit

• •

General Approach • • •

The first step in evaluating a patient with joint pain is to ensure that the pain is in the joint and not the surrounding structures Then, rule out critical diagnoses such as fracture and septic arthritis We are then left with important, but non life/limb threatening causes of acute arthritis

Fracture •

Rule out with X-ray if clinically indicated

Septic Arthritis-Non Gonocoocal !JAMA. 2007;297:1478-1488) •

• •

•

General: (Lancet 1998;351:197-202) ! Irreversible loss of joint function"25-50% patients Risk Factor LR+ ! Case fatality rate 5-15% Age >80 3.5 ! Must consider in any patient with an acutely swollen, painful joint DM 2.7 Risk Factors:""(Arthritis Rheum. 1995;38:1819-1825) RA 2.5 Clinical Exam: classic exam is painful, swollen, red hot joint but: recent joint surgery 6.9 ! Joint pain"Sens 85% hip/knee prosthesis 3.1 ! Joint swelling"Sens 78% Skin infection 2.8 ! Fever had Sens 57%"absence of fever does not rule-out infection Hip/knee prosthesis + skin 15 Laboratory eval (Am J Emerg Med. 1997;15:626-629) infxn ! Peripheral WBC, CRP, ESR have limited diagnostic utility because of low specificity HIV 1.7 ! Peripheral WBC>10,000"Sens 90%, LR+ 1.4 ! ESR>30"Sens 95%, LR+1.3 Synovial fluid analysis ! Because of history, physical and lab tests are unable to reliably change the pre-test probability (8-27%) that an acutely painful joint is septic arthritis"further work-up with arthrocentesis and synovial WBC/diff are needed. ! Synovial WBC: # Progressively higher WBC counts increase likelihood of septic arthritis # Can still have septic arthritis with very low synovial WBC counts. Synovial analysis Specificity LR+ (Acad Emerg Med 2004;11:276-280) WBC>100,000 99% 28 • 10% had synovial WBC counts < 10,000 WBC>50,000 92% 7.7 • Lowest value"168 WBC>25,000 73% 2.9 ! Gm stain positive in only 50%, Culture positive in over 90% PMN"90% 79% 3.4 Decision rule? (Acad Emerg Med 2004;11:276-280) ! Retrospective study found that 100% of patients with septic arthritis had abnormality in at least one of the three tests (peripheral WBC, ESR, synovial WBC) ! If all 3 normal"very low likelihood of septic arthritis (Sensitivity 100%) Treatment ! Antibiotics"empirically vs S.aureus & Strep or based on gram stain result ! Joint Drainage? Needle aspiration, arthroscopy, or open surgical drainage

Septic Arthritis-Gonococal •

•

Clinical (Rosens 6th ed. Ch 114) ! Bacteremic Phase (2-3 days)"malaise, fever, polyarthralgias with the triad of: # Tenosynovitis"acute, asymmetric, on dorsum of wrists, hands and fingers # Arthritis"asymmetric migratory polyarthralgia (most common presenting sx of disseminated GC) # Dermatitis"pustular, macular, hemorrhagic on distal extremities; spares face, palms, soles ! Suppurative phase (3-6 days) # !Articular findings, joint fluid purulent Diagnosis ! Synovial fluid Cx positive <50%, Blood cultures almost always negative"need to culture other sites ! Collect samples from endocervix (90% positive), urethra (50%), pharynx, skin lesions and rectum Treatment"Antibiotics (ceftraixone 1gm) and admission to await Cx results

Oher arthritides •

•

Gout: negative birefringent crystals in UA vs pseudogout (positively birefringent crystals) ! NSAIDS for acute attack (Indomethacin 50mg tid and taper) ! Colchicine: effective in first 24h (0.6mg po q 1 hour until:pain controlled, GI sx, or max 6mg) Lyme dz (Med Clin North Am 2002;86(2):297-309) ! Clinical dx based on history of tick bite (weeks-years prior), rash (ECM), endemic area, joint fluid (inflammatory with PMNs) ! If suspicion"start empiric treatment (Doxy 100mg bid) prior to results of serologic tests"shorten dz & prevent later disease Others"OA, RA.. ! Treat symptomatically with Tylenol, NSAIDS & appropriate referral (PMD, Rheum)

LAC+USC MEDICAL CENTER DEPARTMENT OF EMERGENCY MEDICINE Empiric Antibiotic Recommendations 2010 These are the agents generally preferred for first-line empiric therapy at LAC+USC Department of Emergency Medicine Circumstances of individual cases may dictate different antibiotic choices * denotes antibiotics require dosing adjustments in renal impaired patients

Site Abdomen

Diagnosis

Likely Pathogens

Outpatient N/A

Initial Treatment Regimens Inpatient ceftriaxone 2g iv q24h or cefotaxime* 2g iv q8h

Spontaneous bacterial peritonitis (paracentesis WBC > 500 or neutrophils > 250)

E.coli Streptococci Enterobacteriacea Enterococci Klebsiella

Localized abdominal infection (e.g., localized appendicitis,) Perforated appendicitis (gangreneous, contained and ruptured abscess) Abdominal sepsis peritonitis, shock

E. coli Enterobacteriaceae Enterococci Anaerobes

N/A

ceftriaxone 2g iv q24h + metronidazole 500mg iv q8h

E. coli Enterobacteriaceae Enterococci Anaerobes

N/A

piperacillin/tazobactam* 3.375g iv q6h

E. coli Enterobacteriaceae Enterococci Anaerobes E. coli Enterobacteriaceae Enterococci Anaerobes

N/A

piperacillin/tazobactam* 3.375g iv q6h + gentamicin* 5-7mg/kg iv q24h ceftriaxone 1g iv q24h + metronidazole 500mg iv q6h

Diverticulitis

ciprofloxacin* 750 mg po bid + metronidazole 500 mg po q6h x 7-10 days

Cholecystitis â&#x20AC;&#x201C; acute without cholangitis Cholecystitis â&#x20AC;&#x201C; acute with cholangitis

N/A

No antibiotics

N/A

Pancreatitis

N/A

cefoxitin* 2g iv q8h or ceftriaxone 2g iv q24h + metronidazole 500mg iv q8h or piperacillin/tazobactam* 3.375g iv q6h No antibiotics unless patient has CT proven necrotizing pancreatitis Necrotizing pancreatitis - doripenem* 500mg iv q8h

Cultures Peritoneal fluid

Comments E.coli sensitivity: 92% to ceftriaxone PCN allergy: ciprofloxacin* 400mg iv q12h PCN allergy: metronidazole 500mg iv q8h + ciprofloxacin* 400mg iv q12h PCN allergy: metronidazole 500mg iv q8h + ciprofloxacin* 400mg iv q12h

Blood culture x 2

PCN allergy: metronidazole 500mg iv q8h + ciprofloxacin* 400mg iv q12h

Site

Diagnosis

Likely Pathogens

Initial Treatment Regimens Outpatient Inpatient ciprofloxacin* 750mg po x 1 ciprofloxacin* 400mg iv q12h or 500mg po bid x 3 days

Infectious diarrhea: fever > 38.5, bloody stool

Shigella Salmonella Campylobacter E. coli

Antibiotic associated diarrhea

C. difficile

metronidazole 500mg po tid x 7-14 days

metronidazole 500mg po q8h (iv if pt cannot tolerate po)

CNS

Meningitis

S. pneumoniae N. meningitidis (Listeria in elderly, HIV, immunosuppressed; Group B Strep or E. coli in neonates)

N/A

Endocarditis native valve

S. aureus Strep. viridans Enterococci

N/A

ceftriaxone 2g iv q12h + vancomycin* 15mg/kg iv q12h if bacterial meningitis confirmed/ suspected. ( + ampicillin* 2g iv q6h if elderly, pregnant, AIDS or immunosuppresed) vancomycin* 15mg/kg iv q12h (if MRSA suspected) + gentamicin* 1mg/kg q8h (for resistant strep. viridans)

Endocarditis prosthetic valve

S. epidermidis S. aureus Strep viridans Enterococci Enterobacteriaceae (rarely)

N/A

ENT

Acute sinusitis

S. pneumoniae H. flu Moraxella

Cervicitis/ urethritis

N. gonorrheae Chlamydia

amoxicillin* 500mg po tid x 10-14 days or amoxicillin/clavulanic acid* 875/125mg po q12h or 500/125mg po q8h cefixime 400mg po x 1 dose + azithromycin 1g po x 1 dose

vancomycin* 15mg/kg iv q12h + gentamicin* 1mg/kg q8h + rifampin* 300mg po/iv q8h ceftriaxone 1g iv q24h

Cultures

Comments

Stool cultures not routinely needed for diarrhea only if fever, blood, or suspected outbreak. Check C. diff toxin if prolonged or severe C. difficile toxin (NOT culture)

Most diarrhea does not require cultures or antibioticsâ&#x20AC;&#x201D;treat with fluids + anti-motility agents

Blood and CSF cultures prior to abx. If unable to get CSF cultures prior to abx, then obtain blood culture

If fail metronidazole then vancomycin 125mg po qid x 14 days Before 1st dose abx, consider dexamethasone 10mg iv q6h or 0.4mg/kg iv q12h (D/c if gram stain negative for bacteria)

Blood culture x 3 (total volume is most importantâ&#x20AC;&#x201D; should be > 30ml for adults) Blood culture x 3

S. pneumo sensitivity: levofloxacin 100% penicillin 100% cefotaxime 100%

cervical/urethral swab-GC, chlamydia. Consider RPR, HIV

Complete STD public health report form.

Site

Diagnosis Pelvic inflammatory disease Cystitis – uncomplicated

Pyelonephritisuncomplicated

Pyelonephritiscomplicated (present of Foley catheter or other instrumentation etc.)

Likely Pathogens Chlamydia N. gonorrhoea E. coli Strep Anaerobes E. coli Enterobacteriaceae Enterococci Staph. saprophyticus

E. coli Enterobacteriaceae Staph. saprophyticus

E. coli Enterobacteriacea Enterococci

Initial Treatment Regimens Outpatient Inpatient cefoxitin* 2g iv q6h ceftriaxone 250mg IM x 1 + + doxycycline* 100mg iv q12h doxycycline* 100mg po bid x 10-14 days cephalexin* 500mg po tid x 7 ceftriaxone 1g iv qday days ± ® Macrobid * 100mg po bid x 37 days (avoid if CrCl < 60 ml/min) cephalexin* 500mg po tid or qid x 14 days or amoxicillin/clavulanic acid* 875/125mg po q12h x 14 days or 500/125mg po q8h x 14 days cephalexin* 500mg po qid x 14 days or amoxicillin/clavulanic acid* 875/125mg po q12h x 14 days or 500/125mg po q8h x 14 days

ceftriaxone 1g iv qday

ceftriaxone 1g iv q24h + gentamicin* 3-5mg/kg iv q24h or piperacillin/tazobactam* 3.375g iv q6h

Cultures GC, chlamydia cultures. Also test VDRL, HIV

Comments Complete STD public health report form.

PCN allergy: ciprofloxacin* 400mg iv q12h

Urine culture only Blood culture not necessary

Urine culture after removal of catheter if catheter is no longer indicated. If foley catheter is still indicated, obtain urine culture after replacement of catheter. Consider blood culture if appear septic

Change to PO after afebrile for 48 hours PCN allergy: ciprofloxacin* 400mg iv q12h Long term foley catheter present without signs or symptoms of infection (no fever, no increase in WBC) – may just be colonized, consider not to treat

Site

Diagnosis

Likely Pathogens

Joint

Septic arthritis

N. gonorrhoeae S. aureus Streptococci

Lung

Communityacquired pneumonia (CAP) – (Non-ICU)

S. pneumoniae H. flu C. pneumoniae Mycoplasma

Severe communityacquired pneumonia (ICU)

S. pneumoniae S. aureus Klebsiella Enterobacteriaceae

Nosocomial/ nursing home acquired pneumonia (HAP or VAP or HCAP) Acute exacerbation of chronic bronchitis

Enterobacteriaceae S. aureus Pseudomonas

Cellulitis (No pus)

Strep S. aureus

Cellulitis with abscess or purulent drainage

S. aureus including MRSA

Skin

S. pneumoniae H. influenzae Chlamydia Mycoplasma

Initial Treatment Regimens Inpatient ceftriaxone 2g iv q24h + vancomycin* 15mg/kg iv q12h ceftriaxone 2g iv q24h Otherwise healthy with no co+ morbidities: azithromycin 500mg po x 1 day azithromycin 500mg iv q24h) or then 250mg po days 2-5 levofloxacin* 750mg iv daily With co-morbidities: levofloxacin* 750mg po daily x 5 days N/A ceftriaxone 2g iv q24h + levofloxacin* 750mg iv q24h ± vancomycin* 15mg/kg iv q12h (if suspect MRSA) N/A cefepime* 2g iv q8h + levofloxacin* 750mg iv q24h + vancomycin* 15mg/kg iv q12h Outpatient N/A

azithromycin 500mg po daily x 3 days or levofloxacin* 750mg po 7 days cephalexin* 500mg po qid ± Bactrim DS* 10mg/kg/day po in two to three divided doses or clindamycin 300mg po q6h x 10 days Drainage first Bactrim DS* 10mg/kg/day po in two to three divided doses or clindamycin 300mg po q6h x 10 days

Cultures Joint fluid gram’s stain and culture Blood cultures Tap pleural fluid if present

Blood cultures and sputum culture. If intubated, obtain endotracheal aspirate or miniBAL Blood cultures and sputum culture. If intubated, obtain endotracheal aspirate or miniBAL

azithromycin 500mg iv q24h or levofloxacin* 750mg iv q24h cefazolin 1g iv q6h

Drainage first vancomycin* 15mg/kg iv q12h or clindamycin 900mg iv q8h

Wound culture

Comments

If HIV is suspected, then TMP/SMX 5mg/kg IV q8h for PCP. Room air pO2<70mmHg or A-a gradient >35mmHg initiate Prednisone 40mg po q12h within 72 hrs

Site

Diagnosis

Likely Pathogens

Bite infections

Pasteurella (cat, dog) Eikenella (human) Streptococci S. aureus Anaerobes Group A strep S. aureus GNB Anaerobes

Necrotizing fasciitis

Systemic

Initial Treatment Regimens Outpatient Inpatient amoxicillin/clavulanic acid* ampicillin/sulbactam* 3g iv q6h 875/125mg po bid x 10 days or cefoxitin 2g iv q8h Give clindamycin first

Diabetic foot ulcer - uncomplicated

Polymicrobic GPC GNB Anaerobes

amoxicillin/clavulanic acid* 875/125mg po q12h or clindamycin 300mg po qid + ciprofloxacin* 750mg po bid

Diabetic foot ulcer - complicated (with leukocytosis & fever)

Polymicrobic – GPC GNB Anaerobes

N/A

Neutropenic fever

E. coli Pseudomonas Klebsiella Strep Staph Candida

sepsis – immunocompetent. No obvious source

meets SIRS criteria

clindamycin 900mg iv q8h + piperacillin/tazobactam* 3.375g iv q6h + vancomycin* 15mg/kg iv q12h ceftriaxone 2g iv q24h + metronidazole 500mg iv q8h ± vancomycin* 15mg/kg iv q12h

Cultures Wound culture

PCN allergy: doxycycline 100mg po bid

Wound culture Blood cultures

PCN allergy: clindamycin 900mg iv q8h + levofloxacin* 750mg iv q24h + vancomycin* 15mg/kg iv q12h PCN allergy: ciprofloxacin* 400mg iv q12h + metronidazole 500mg iv q8h + vancomycin* 15mg/kg iv q12h PCN allergy: ciprofloxacin* 400mg iv q12h + metronidazole 500mg iv q8h + vancomycin* 15mg/kg iv q12h

Wound culture

vancomycin* 15mg/kg iv q12h + piperacillin/tazobactam* 3.375g iv q6h

Bone biopsy or deep wound cultures

cefepime* 2g iv q8h + amikacin* 7.5mg/kg q12h (add vancomycin* 15mg/kg iv q12h if febrile after 48 hours on cefepime + amikacin) vancomycin* 15mg/kg iv q12h + piperacillin/tazobactam* 3.375g iv q6h

Blood culture x 2 urine culture

Comments

Blood culture x 2 urine culture

Needlestick Injury Protocol UPDATED MAY 09 – see website for most recent. During office hours: refer to Employee Health if patient is an LAC+USC employee/student/USC staff.

n. Consider ancillary meds for gi toxicity associated with PEP (antiemetic, antimotility) Do not write for PEP meds beyond a four-day supply. The employee/student/USC staff will receive the remainder of their medications at their follow up visit in employee health (or with their own employer or physician). Initial dose of PEP medications will be given in DEM; remainder of 4-day supply can be obtained at pharmacy once employee/student is discharged from DEM. Employee Health will write for ongoing PEP medications at the first visit.

After hours: Register as a County patient and get a PF#. DEM ANM and attending/two star resident to be immediately informed of patient’s arrival Nursing to request STAT Ident immediately upon arrival. PFS to STAT ED Register with IA Carrier Code Nursing to escort employee/student/staff directly to West Pod for stat 2Star or Attending physician evaluation. Fire and Police personnel should be registered as a County patient; follow-up for them should be through THEIR employee health. Patients who are not employees (bystander helping at the scene of an accident who gets exposed to blood) should be registered as a regular patient (not IA Carrier Code). Follow-up for them should be through the normal patient process.

LIVER TOXICITY RISK: The employee/student/USC staff should be counseled that these HIV prophylaxis medications have some risk of liver toxicity. The employee/student/USC staff should be offered the option of having LFTs drawn in the ED prior to starting the HIV medication. The decision to draw LFT’s prior to PEP meds will be left up to the employee/student/USC staff. Employees/students/USC staff at risk for liver disease should be encouraged to have their LFTs checked prior to starting to medication. If LFTs are drawn, the PF# given to the employee/student/USC staff by PFS will be used. These lab results will be in Affinity. The DEM does NOT have access to the confidential patient file numbers ie: HSN #s that Employee Health uses. SPECIAL CIRCUMSTANCE: If source is known HIV and on PEP medications, provider should immediately consult ID fellow or HIV specialist for specific PEP medication recommendations.

HIV Prophylaxis – Resources: ED Physician to counsel employee/student/USC staff regarding the need for HIV prophylaxis and potential side effects of PEP. For more information refer to: CDC guidelines The National Clinician’s 24 hour Hotline is 1-888448-4911 Daytime hours: LAC-USC HIV Clinic at 1-323-3438255 Daytime hours: LAC-USC Employee Health Clinic 323 226-5236 (Dr. Zuk) After hours: Consider ID Fellow consultation for unique questions (pager available through county pager operator x 323 226-4906) PEP Medication Recommendations: All attempts will be made to administer PEP meds immediately following patient’s decision to take them (ideally within a 3 hour window from exposure) Our standard HIV prophylaxis Rx is as follows:

Kaletra two tablets PO BID x 4 days (#16) PLUS Truvada one tablet PO daily x 4 days (#4)

PREGANCY: Combivir and Kaletra are recommended for pregnant patients. The recommended dose of Kaletra is higher in pregnant w o Combivir one tablet PO BID x 4 days (#8) m PLUS e Kaletra 3 tablets PO BID x 4 days (#24)

CHARTING/CHART DISTRIBUTION: The DEM physician completes the chart describing exposure, treatment, counseling, etc. The completed chart will be given to DEM Charge Nurse - this chart goes to Employee Health NOT to Medical Records. EMPLOYEE/STUDENT/USC staff (Exposed Person) LABS TO BE ORDERED: LFTs should be ordered in affinity with the standard PF number (do NOT use the special HSN employee number) LIVER TOXICITY RISK: PEP Medications can cause liver toxicity, so the employee/student should be counseled that these risks. The employee/student/USC staff should be offered the option of having LFTs drawn in the ED prior to starting the HIV medication. The decision to draw LFT’s prior to PEP meds will be left up to the

100

employee/student/USC staff. Employees/students/USC staff at risk for liver disease should be encouraged to have their LFTs checked prior to starting to medication. If LFTs are drawn, they should be ordered in affinity using the assigned PF# given to the employee by PFS so the treating provider can access the LFT and make recommendations. These lab results will be in Affinity. The DEM does NOT have access to the confidential patient file numbers ie: HSN #s that Employee Health assigns for the labs that will eventually be sent from employee health. All other labs (except for LFTs prior to PEP medication) to be drawn by Employee Health the next business day Long 3-4 day weekend – OK to have bloods drawn on the following business day. Employees/students/USC staff will not seroconvert during that time (even over a 4 day weekend). LFTs do not need to be drawn in DEM if the employee/student/USC staff is not going to begin PEP meds.

SOURCE LABS: All source orders go through affinity only with the exception of the rapid HIV test! Rapid HIV test is ordered using the paper request Source person: The Primary Team is responsible for obtaining the Source Panel if the source person is an inpatient. The DEM is responsible for obtaining the Source Panel if the source is still in the DEM. Source Labs to be drawn: RPR, Rapid HIV, Hep B Surf Antigen, and Hep C. Please send 3 Gold top tubes.

What if the source person is unable to consent? (Comatose or dead and no close family available to give consent)? Administrative Approval is needed. Note: If source blood has already been drawn (or was being drawn during the exposure), then this blood can used with administrative approval for a Source Panel and rapid HIV. What if the source person refuses to consent? If the blood has already been obtained (even if during the course of the exposure), Administrative Approval would be needed. What if BLOOD HAS NOT YET BEEN DRAWN on the source patient and the source patient is either unable to consent or refuses to consent? Hospital Administration has not addressed this situation. Again, contact Dr. Zuk, his M.D. designee (daytime only) or the M.O.D on-call. Make sure the source patient understands it is his or her legal right not to know the results of the test. This may convince some to allow the HIV test to be drawn. What if the source person is a minor? Typically a minor cannot give consent unless emancipated. This topic has not been specifically addressed at the time this policy was being written. What if the source person is a juvenile ? Often a parent is available by phone when a juvenile is brought in to the ED. This topic has not been specifically addressed at the time this policy was being written. When will Administrative Approval NOT be given? (1) if the exposure occurred outside of the window for early medication therapy, or (2) when the employee/student/USC staff states that he or she will take the prophylaxis medication regardless of the HIV results, or (3) the employee/student/USC staff states he/she will NOT take the medication regardless of the HIV results.

DISCHARGE INSTRUCTIONS: CONSENT/ORDERING HIV TEST (Scenarios): Rapid HIV test (with patient permission or The employee/student/USC staff is to follow-up with administrative approval) should be ordered on the Employee Health the next business day at in the “Requisition for HIV Testing” form. IRD room 320. Phone: 323 226-5236. Verbal consent for HIV testing must be documented Fire or Police Personnel should follow-up the next on the chart by the provider as well as any business day with their own Employee Health. consultation given to the employee/student/USC Employee Health takes responsibility for drawing staff. and sending the appropriate labs for the Written consent for HIV per state law is not required. Employee/student. Please note: Administrative Approval can only be Employee Health has its own computers and HSN # obtained from: (prohibiting DEM from accessing results of any lab 1. Office Hours: Dr. Zuk, Director of Employee tests excluding LFT’s if drawn in the DEM). Employee Health provides the necessary counseling Health, or his M.D. designee in Employee and follow-up for the employee/student/USC staff. Health 323 226-5236 during business hours only (not after-hours) 2. After Hours: The MOD on call (call pager operator x94906) 3. The N.O.D. and the A.O.D. cannot give Administrative Approval for HIV testing. Source person willing to consent to HIV test: A rapid HIV test can be ordered once the source person has given permission and been verbally 101 consented.

BILLING & CODING BASICS CODING LEVELS Level 1 2

H&P Problem-focused Expanded problem-focused

MDM Straightforward Low complexity

Expanded problem-focused

Moderate

4 5

Detailed High complexity

Moderate complexity High complexity

STEP 1: HISTORY DEFINITIONS HPI Brief ≤3 elements Extended ≥4 elements or the status of at least 3 chronic or inactive conditions. ROS ProblemOnly the system pertinent related to the problem Extended 2-9 systems Complete ≥ 10 systems PFSH Pertinent 1 item in any of three Past, history areas Family Complete 1 item from 2 of 3 & Social history areas

LEVEL 1 2 3

HPI

ROS

PFSH

Yes Yes Yes

Brief Brief Brief

No Pertinent Pertinent

No No No

Yes

Extended

Pertinent

Yes

Extended

Complete

SUMMARY OF ELEMENTS NEEDED LEVEL HPI ROS PFSH 1 ≤3 0 0 2 ≤3 1 0 3 ≤3 1 0 4 ≥4 2-9 1 5 ≥4 ≥10 ≥2

STEP 2: EXAM

STEP 3: MDM

SUMMARY OF ELEMENTS NEEDED Body area(s) or Elements in each organ systems(s) Problem ≥1 1-5 elements Focused Expanded ≥1 ≥6 elements Problem Focused Detailed ≥6 ≥ 2 elements for each system OR ≥2 ≥ 12 elements total Compreh. ≥9 ≥ 2 elements for each system

102

SUMMARY OF ELEMENTS NEEDED MDM Level Dx/Mgmt Data Risk 0-1 0-1 Minimal Straightforward Low

element 2 elements

Moderate

3 elements

High

≥4 elements

elements 2 elements 3 elements ≥4 elements

Low Moderate High

Off-Service Rotation Basics

Rotation Ortho

Where do I go? OEA

Psych ER

EMS

Base station, across from Resus

Anesthesia

5/F, Pre-op area

MICU

4A Low

Medicine

Varies, work rounds depend on the senior 4D/4M

CCU

SICU

C5L100 Jackie Stout’s office – p/u TTA pager and both Red and Blue trauma books

Who do I report to? PGY-2 on call. Go to amion.com, pw is USC ortho. Attending on shift, usually Dr Barker Gloria Tolle, scheduled ride-alongs and base station days Dr Amaya

What time? Pass on’s @ 0600 on 6/F conference rm 0800 0800 in base station, varies for ride-alongs 0730

Your team’s fellow. Go 0730 is fellow to amion.com, pw is USC rounds. You’ll pulm need to pre-round. Get sign out from intern. Senior resident. Go to Usually 07300745 for work rounds. Senior resident. Highly variable. Amion.com, pw is Show up at 0730 USCIM on 1st day. 5B High, find 1 of the 2 Around 0730 to trauma fellows round, Attending rounds @ 0930

103

What do I need? Trauma shears

A pen and stethoscope Donuts or other food for the firemen Make sure you’re wearing county scrubs Need Eclipsys login, ask the charge RN for access. You’ll need to preround. Get sign out from intern. You’ll need to preround. Get sign out from intern. Need Eclipsys login, ask the charge RN for access

Department of Emergency Medicine Resident Pagers 2010-2011 GY-4

Pager

GY-3

Pager

GY-2

Pager

GY-1

Pager

Beckham,

213-919-0130

Abrishamian,

213- 919-1491

Burke,.

213-919-9739

Abdi,

Bhatt,

213-919-7161

Ballinger,

213- 919-1490

Cheng,.

213-919-9742

Cardena, Coyne,

213 717-0116

Doane,

213 919-0131

Huang,

213 919-6174

Johnson,

213 919-8990

Knox,

213 717-4930

Kohanteb,

213 704-3958

Leicher,

213 919-9012

Marzec,

213 919-9013

Mestres,

213 919-0141

Milano,

213 704-3931

Peabody,

213 704-3934

Sicalo,

213 717-7140

Sikora,

213 217-0269

213 717-0115 213 704-3956

Burner,

213-919-0486

Bowns,

213- 919-1099

Eng,

213-919-1477

Goldberg,

213-919-9910

Cannis,

213- 919-1484

Goodman,

213-217-0344

Hooker,

213-717-7154

Chacko,

213- 919-1489

Greco,

213-919-1481

Jamehdor,

213-919-7185

Morato,

213- 919-8987

Hemak,

213-919-9740

Jhun,

213-208-0151

Naima,

213- 919-2925

Johanson,

213-919-0642

Lemus,

213-704-3911

Olaes,

213- 919-8998

Lopez,

213-919-1479

Loza,

213-919-0699

Osterman,

213- 919-9896

Majoewsky,

213-919-1483 213-919-7181

Lucas,

213-717-7158

Palmisano,

213- 919-7191

McCormick,

Martin,

213-919-3921

Probst,

213- 919-0085

McGarry,

213-919-0960

Seif,

213-919-9887

Reverte,

213- 919-2024

Meeks

213-919-1486

Spangler,

213-919-0525

Rice,

213- 919-0062

Moran,

213-919-1488

Vasquez,

213-717-7169

Sanko,

213- 919-0322

Myatt,

213-919-1493

Wagner,

213-717-7152

Sporty,

213- 919-0375

Schlesinger, Vijverberg,.

213-919-1487

Walker,

213-717-7195

Vu,

213- 919-0522

Washington,

213-919-0488

Wendler,

213- 919-0626

Wilkes,

213-717-7173

Wu,

213- 919-0942

213-919-1482 Wyler,

104

213-919-1492

NOTES

105

NOTES

106

CONTACT LISTS TRANSLATION Language line

Sign

VOIPS TRIAGE

1) Put your VOIP phone on speaker by hitting the button on the upper right side. 2) Dial 8-226-3600 3) Client ID 201609 4) Personal code 1350 5) Say the name of the desired language or hit the button when prompted. 7) If system failure call 800-874-9426 800-633-8883

409-1700 EFC EMERG FLOW COORD 409-1637 DEM CMA COORDINATOR 409-1605 CMA COORDINATOR MED MED CONSULT 409-1644 409-1688 & 1699 ER ANM 409-1699 ER ANM

AMBULANCE RAMP 409-1623 409-1612 409-1613

CONSULTS Consult Acute Care Surg Burns Cardiology CT Surgery Cath Lab Dermatology EKGs, old Endocrine ENT Epidemiology GI Hematology Infectious Dis. Medicine Neurology Neurosurgery OB-GYN OMF Oncology Ophthalmology Orthopedics Palliative Pediatrics Plastics Psychiatry Pulmonary Renal Rheumatology Reimplant Stroke Team TB control Thoracic/Foregut Trauma Urology VIP –sexual assault

Day 97728 97991 97111 Pgr op. 94906 95783 213-717-2626 97467 Pgr. Op 94906 213-919-7000 96645 Pgr Op 94906 8-226-6969 Pgr op 94906 213-919-9218 97405 97405 VOIP x94198 95051 (clinic) 8-226-6395 (MF) 213-919-9254 213-919-3487 98534 93601 Pgr op. 94906 97085 8-226-7926 8-226-7307 8-226-7889 213-919-3487 97405 8-226-7962 213-919-6417 97728 213-919-2156 8-226-3961

Night Same Same Same Same Same 213-919-9578 Same Same Same Same Same Same Same VOIP 91644 Same Same Same 97309 94021

AMBULANCE TRIAGE MICN AMBULANCE TRIAGE LEAD BASE/MICN

RESUS 409-1610 409-1615 409-1617 409-1619 409-1611 409-1616

RESUS ATTENDING RESUSC TWO STAR RESUS RESIDENT RESUS RESIDENT RESUS CHARGE RN RESUS HMA

409-1620 409-1630 409- 1666 409-4125 409-1621 409-1680

NORTH A ATTENDING NORTH B ATTENDING NORTH TWO STAR DAY NORTH TWO STAR NIGHT NORTH CHARGE RN NORTH-EAST HMA

409-1670

RESIDENT

NORTH

JAIL WEST

Same or 8-865-3000 Same Same Same same Same Pgr op. 94906 Pgr op. 94906 Same Same Same Same Same Same same same

409-1646 409-3750 409-1631

WEST ATTENDING WEST BACK ROOM WEST CHARGE RN

409-1650 409-1651 409-1652

PEDS ATTENDING PEDS CHARGE RN PEDS TRIAGE DESK RN

409-1660 409-1665

PSYCH ATTENDING PSYCH CONSULT

PEDS

PSYCH

107