EMDoc

Archive for December, 2010|Monthly archive page

Leg Pain

In EM2 on December 24, 2010 at 12:35 pm

70yo M presenting with R groin and RLE pain x2days. Patient had a cardiac cath 5days ago, access via R groin. States the pain started shortly post cath but intensified 2days ago after he had a vigorous cough. Now with difficulty ambulating. No other associated symptoms. PMHx: DM, HTN, CAD, arthritis. SgHx -prior cardiac cath with stents. PE(pertinent): +femoral and distal pulses in both lower extremities. R groin with 10cm area of old bruising, palpable induration and pain on palpation over the artery, 1+ non-pitting edema in RLE. 

US groin – 3.8cm partially thrombosed pseudo-aneurysm in R femoral artery with small AV fistula between the R femoral artery and vein

Outcome: Pt sent to IR, sent back without intervention secondary to AV fistula. Surgery consulted, Pt admitted for observation, serial H/H and repeat US in AM. 

Teaching Points: Access Site Complications

DDX: pseudo-aneurysm, hematoma, DVT, acute vessel occlusion, AV fistula, Neurogenic

1. Pseudo-aneurysm(PSA): Most common access site complication. It is an arterial rupture of one or more layers of its walls, contained by overlying fibromuscular tissue, which communicates with an artery by a neck or sinus tract. 8% of femoral artery catheterizations and can result in distal embolization, extrinsic compression on neurovascular structures, rupture and hemorrhage. Patient presents with groin pain. +/-pulsatile groin mass +/-audible bruit

Workup: US groin – looking for extra-arterial flow or ‘to and fro’ doppler waveform via neck of PSA. Large PSA (>3 cm) that are symptomatic, expanding or those associated with large hematomas are generally thought the most prone to rupture. 

Consults: IR Vs. Vascular Surgery consult.

Rx:  Ultrasound-guided thrombin injection for PSA. Potential complications of thrombin injection include leakage of thrombin causing thrombosis of the femoral artery and distal embolization.Contraindication for thrombin injection includes PSA with a wide, short neck, and associated arteriovenous fistula.  
 

2. Acute vessel occlusion: the patient may complain of pain, pallor, parenthesis or decreased movement in the respective limb. Clinical examination may reveal a cold ischemic limb with absent pulses

 

Consults: Surgery ASAP; Rx: percutaneous vs surgical 

3. Hematoma: Local Vs. Retroperitoneal.

a. Local: Duplex ultrasound of the groin should be performed if the hematoma is pulsatile, expansile, has a bruit or exquisitely tender to exclude a PSA or arteriovenous fistula.

b. Retroperitoneal: Clinically, look for signs of hypotension, lower abdominal or flank pain, acute drop in hematocrit and a high puncture at the site of arterial access (typically above the inguinal ligament) which predispose to a higher risk of retroperitoneal bleeding. 

Workup: H/H, CT abd/pelvis

If stable, Admit for serial H/H, close monitoring, transfusion and anticoag reversal if indicated. If unstable, Volume resuscitation, Vascular Sg consult and urgent angiography 

4. AV fistula.

Clinically: high index of suspicion is warranted in patients with a new femoral bruit, thrill, fresh hematoma or pain in the lower limbs on the following day after sheath removal. Confirmed by color Doppler ultrasonography demonstrating an AVF with continuous systolic and diastolic flow

Plan: Conservative VS surgical management. Simple observation and ultrasound guided compression have been suggested as first line therapies in the management of post-catheterization femoral AVF because of their noninvasive nature. Contraindications for conservative management include associated large PSA, hemorrhage, expanding mass, compromised cardiac output, arterial or venous occlusion, and leg edema. 

5. DVT – need i say more?

6. Neurogenic complications may arise due to the proximity of the femoral nerve and the more laterally located lateral cutaneous nerve of the thigh to the common femoral artery. Clinically: hypoesthesia, dysesthesia and hypalgesia of the thigh can be caused by compression of either of the above two nerves as a result of hematoma from the femoral artery access site. Symptoms usually subside over a number of days but symptoms have been reported up to 6 months.

Read More HERE

Nose Bleeds

In EM2 on December 24, 2010 at 3:39 am

2 Cases:

52yo M presenting with nose bleed for about 4hours. Pt has a history of bleeds, usually self resolving, However, this episode has been continuous even after packing his nose with cotton wool. On exam, +epistaxsis from the Right nare, No identified bleeding vessel in anterior nose. BP 120 systolic. Patient instructed to maintain sniffing position, avoid blowing his nose and hold pressure.

Shortly after, called in by the nurse because patient became pre-syncopal. briefly unresponsive, pale, with increasing bleeding from the nare.

Outcome: Patient was responsive and awake but pale on exam. a rhino-rocket was quickly inserted in the R nare with resolution of bleeding. ENT consulted. Admitted. Planned to goto OR.

48yo M hx of ESRD on Dialysis presenting with nosebleed for about 3hours. +history of nosebleeds. On exam, no identifiable bleeding vessel in anterior nose. bleeding seemed controlled initially. However restarted shortly after. Rhino-rocket was inserted in R nare but still with bleeding thru nare. Labs – Hgb 9.4 (dropped from 13 -3weeks prior)

Outcome: ENT consulted. Scope in the ED revealed no bleeding in posterior pharynx. Repacked nose with rhinorocket and recommended dispo home if stable after few hours of observation. About an hour later, patient still bleeding. Admitted for observation and ENT f/u in the AM.

Teaching Point: Management of Posterior Nose Bleeds.

H/p tip: Ask specifically about NSAID, warfarin, heparin, or aspirin use. Alcohol or cocaine abuse, trauma, prior head and neck procedures, as well as a personal and family history of coagulopathy, should all be addressed.

Remember Kiesselbach?

1. 90% of epistaxsis are anterior bleeds, originating from little’s area – an anastimosis of arteries.

What can you do?!

a. Direct Nasal Pressure.

  • avoid blowing nose
  • may use nasal afrin + 4% lidocaine solution via an atomizer to provide both nasal analgesia and vasocontriction

b. Chemical Cauterization

  • cauterize if you see the source of bleeding.
  • Just roll the tip of the silver nitrate stick until a grey eschar forms
  • Never cauterize both sides of the septum. Increase chances of nasal perforation.

c. Anterior Packing

  • multiple strategies available. Rapid Rhino, Vaseline gauze
  • See info on Anterior Packing Here

Dispo is Home with ENT f/u in 2-3days, Abx to prevent sinusitis/staph-TSS

2. When is it a Posterior Nose bleed?! (usually originating from the sphenopalatine artery)

Generally, a posterior hemorrhage suspected in the ED if there’s acquired or inherited coagulopathy, a significant amount of hemorrhage visible in the posterior nasopharynx, hemorrhage from bilateral nares, or epistaxis uncontrolled with either anterior rhinoscopy or an anterior pack.

If you don’t have any fancy double baloon packing equipment, a good ol’ foley will do. Lubricate, insert, visualize at the back of the mouth(posterior oropharynx), inflate ballon with about 10cc water, pull back gently until its in posterior nasopharynx. Pack the anterior nose with a rhino rocket or other device.

See info on posterior packing Here

Dispo: Posterior bleed typically warrant admission cause posterior packing may lead to airway compromise and reflex bradydysrythmia. .

Labs are typically not indicated in general unless there’s heavy or symptomatic bleeding.

an ‘Atrial Fibrillation’ kinda day

In EM2 on December 23, 2010 at 1:50 am

Two Patients:

50yo F sent in from cardiologist office (routine visit) for AF with RVR @150. Completely asymptomatic. denies any CP, sob, nausea, vomitting, palpitations or other complaints. PMHx – recent STEMI 2months ago with drug eluting stent in LCx, on asa and plavix. Outcome – Pt given 20mg Diltiazem, no major response. Given another 20mg bolus and started on Diltiazem drip (started at 5mg/hr, got up to 15mg/hr) for HR between 95-110, BP @108/67. Heparin gtt. Still asymptomatic. Trop negative. Seen by cardiologist, Admitted to Telemetry.

80yo F hx HTN brought in by fire/rescue for witnessed syncope. On arrival to ED found to be in Afib with RVR @130, BP146/77. Asymptomatic. Doesn’t remember syncopal episode. denies Hx of Afib or cardiac issues. PERC score 2/8, Wells score for PE – 1.5 = low risk for PE. Outcome – 20mg Diltiazem ordered, nurse gave 10mg first, HR decreased to 78, BP @98/57. still asymptomatic. (Labs pending at time of signout). Plan for Admit.

Teaching Point: Management of AFib.

Quick Review: For tachyarrythmias always think:

1. Chant your mantra – IV, O2, Monitor.

2. Stable or unstable?

3. Pwaves present?

4. Regular or Irregular?

5. Narrow or Wide?

Afib – Narrow, Irregular, both of these patients were stable. GREAT! Now what do you do?

1. Cardiovert (i.e Rhythm control)

– if patient is unstable, SHOCK ‘EM.  If patient is stable, <48hrs from onset of new/paroxysmal Afib – You may SHOCK ‘EM.

REMemeber to sedate the awake and stable patient.

2. Rate control – CaChannelBlocker or Bblocker or IV Magnesium

-anedoctally alot of EM physicians used Diltiazem as preffered rate controller in AF. Cardiologist typically used Bblocker. Use whatever floats your Boat!

– Diliazem – ACLS dosing is 20mg bolus over 2mins, if not successful then 25mg bolus, then Diltiazem gtt 5-15mg/hr. 20mg might be much in the little old lady with a BMI of 19. Its ok to Low-ball and then titrate up the bolus. STAND BY THE BEDSIDE. Donot give a 5mg bolus and walk away. Wait for it. Diltiazem is a long acting agent but with a quick onset of action. Try the 2.5mg/min bolusing method. Our 1st patient needed 40mg + a gtt to be rate controlled, The 2nd stayed HR<100 after just 10mg. This is where medicine becomes more art than science.

-Some attendings suggest a PO diltiazem dose (eg 60mg) after the HR is reduced to <100 (after the initial bolus of cardizem)

-Metoprolol 5-15mg IV over 5-15min

-Magnesium IV – 2g over 2mins (Rosens Chpt 78, pg 1233; 6th Edition)

3. Anti-coagulate!

See a pretty good lecture on Tachyarrythmias here

 

Crack is whack! (Cocaine Chest pain)

In Uncategorized on December 23, 2010 at 1:33 am

52yo M hx htn, hl, ‘fluid in lungs’ presenting with CP + SOB x1week. Incidentally pt was assaulted with fist in an attempted robbery yesterday AM, states CP is now worse and he was SOB all nite. 7/10 substernal sharp intermittent pain, radiating to R shoulder, associated with mild SOB. denies other symptoms asides from mild HA, R shoulder and elbow pain from assault.

PMHx as stated. SurgHx -cardiac cath years ago at OSH, he doesn’t remember details

SHx – no etoh, no tobacco, +Crack – last use 4days ago.

PE: heart and lungs are unremarkable – no murmurs, rales.

Mild TTP at R shoulder and elbow, mild decrease ROM 2/2 pain.

neuro – 5/5 upper and lower motor, normal sensory

EKG: sinus Tachycardia with T wave inversions laterally(v4-v6). No old EKG for comparison.

CXR: mild pulmonary vasculature congestion, normal size heart.

Labs – trop 0.19, myoglobin 200’s, BNP 1200, UA +cocaine, other baseline labs within normal range.

Outcome: Pt was given aspirin, SL NTGx3 -with relief of CP to 3/10; started on NTG gtt. IV Ativan. Heparin ordered. Cardiology consulted – they questioned administration of heparin since we “know the etiology of his CP”…(I thought to myself…really?!). Admission.

Teaching point: Etiology and Management of Cocaine-CP.

Cocaine causes MI via:

(1) increasing myocardial oxygen demand by increasing heart rate, blood pressure, and contractility (via its sympathomimetic effect)

(2) decreasing oxygen supply via vasoconstriction

(3) inducing a prothrombotic state by stimulating platelet activation and altering the balance between procoagulant and anticoagulant factors

(4) accelerating atherosclerosis.


FYI –Cocaine use is reported as positive when the level of benzoylecgonine is above a standard cut-off value (usually 300 ng/mL). As benzoylecgonine has a urinary half-life of 6 to 8 hours, it can be detected in the urine for about 24 to 48 hours after cocaine use. Always ask for drug hx in CP pt. check UA if suspicious, cant get a hx or hx is unreliable even if the pt SWEARs ‘they’ve never seen cocaine ever”

Management:

1. Avoid BetaBlockers!!!! (a discussion for another day )

2. GIVE IV benzodiazepines early – will improve chest pain and hemodynamics while controlling anxiety!

3.”We recommend aspirin be routinely administered and unfractionated heparin or low-molecular-weight heparin be given to patients with cocaine-associated MI unless there is a contraindication.” -AHA guidelines for mgt of cocaine-CP/MI.

In summary for Cocaine-CP/MI, think of the way u’d manage a classic ACS(STEMI, NSTEMI or UA) case, add IV benzo, subtract IV Bblockers!

1. oxygen 2. aspirin 3. IV benzo 4. Nitroglycerin -for pain relief and BP control -will also reduce vasospasm/constriction; if SL NTG doesn’t work, move to nitro drip 5. Heparin -unfractionated or LMWH 6. Call your cardiologist, Admit the patient.

See references HERE


The Lady and her EKG

In Uncategorized on December 23, 2010 at 1:28 am

68yo F hx HTN, GERD, MI presenting with substernal burning pain since yesterday. took her prilosec with good relief of her symptoms. ran out of her prilosec today, so pain has persisted. worse with exertion. non-radiating. associated with diaphoresis. denies sob, nausea, vomitting, or other symptoms. states she’s CP free currently. states her prior MI was ‘silent’ and didn’t know when she had it.

PMHx: htn, gerd, mi, ‘enlarged heart’

FHx -neg, SHx -no tobacco, ETOh, drugs. No prior Sg.

Last cardiac stress 2yrs ago – ?borderline. No prior cardiac cath.

PE: afebrile, HR@115, BP@148/68, RR@12, 98% on RA;

CV/Pulm: no murmurs, no wheezing or rales, good bs. No overt signs of fluid overload.

EKG: wat do u see?

CXR: enlarged heart, no pulmonary edema.

Labs: Trop 0.12. (cbc, bmp otherwise normal)

Outcome: Pt was CP free. Given asa. Cardiology c/s. Transferred to CCU. Started on heparin and integrillin gtt. Planned cath for the next day. *Next day, trop peaked at 0.4*

Teaching point: ST elevation in aVR.

ST Elevation of more than 1mm in aVR in the setting of Acute Coronary syndrome is:

  • associated with left mainstem (LMCA) disease and 3 vessel disease.
  • suggests urgent angiography is necessary.
  • associated with an increase in mortality.
  • Probably not an indication for emergent angiography @ 3am unless the patient is not settling with standard medical therapy.

LMCA stenosis is bad – 70 % mortality without surgery / PTCA

In summary, if you see an EKG with ischemic changes, ALWAYS LOOK AT aVR for ST Elevation!!!!!!!!!! This means baddness!


Listen to Dr. Amal Mattu talk abt STE in aVR HERE

See reference HERE, visit another blog with similar presentation and cool EKG HERE


 

 

Hello world!

In Uncategorized on December 23, 2010 at 1:02 am

Welcome to WordPress.com. This is your first post. Edit or delete it and start blogging!