Aftercare (what do you tell your patients!!)

- Ointment (antibiotic for example) and dressing immediately after lac repair: Not much out there evidence wise what I could find indicates doing this

• Moisture promotes re-epithelialization
• Xeroform with gauze isn’t a bad idea
• REMINDER: if u closed the lac with tissue adhesives DO NOT use topical ointments caue they loosen the adhesive

- Wrap large scalp wounds, small ones can be left open

- Leave the wound covered for 24 hours after which it can be open to air.

- Non-absorbable sutures (nylon, prolene etc) can be gently washed with soap and water after 24 hours – recommend the patient continue to place ointment 2 times a day until the sutures are removed (decreases scab formation)

• While patient’s with non-absorbable sutures can shower recommend they don’t soak the area (like go swimming, take a long bath) until the sutures are removed

- Absorbable should be kept dry with minimal exposure to water as it will expedite suture breakdown

Prophylactic Antibiotics

- Not necessary in healthy patients with non-bite laceration (a very good lac clean out works just fine)

- Definitely need to be given for animal and human bites, water exposure, open fractures or wounds with exposed tendons/joints (simple hand lacs no good data as of yet, one article recommending a RCT – any takers!)

•  probably also in those with excessive contamination, immunocompromised or with vascular insufficiency.

TETANUS—don’t forget to update their tetanus

Wound Check

- Most don’t need a wound check except for those with high risk features (high risk patient, high risk wound or don’t seem capable of identifying signs of infection)

- Reasons to return include fever, redness/swelling around the wound, pus drainage or the stitches open up

Suture removal- when should they come back or even better go their PCP for suture removal:

Face – 5 days (eyelids and neck even earlier 3-4 days)

Scalp 7-14 days (usually 10 works)

Trunk- 7 days

Upper Extremities- 7-10 days (hand  more like 10)

Lower Extremities- 8-10 days  (foot closer to 12 days)

• Sutures over joints on in the hands should stay in for 10-14 days because of the tension they are under.
• If you used tissue adhesives let tell your patient to expect it to slough off in 5-10 days

Interrupted suture- most commonly used in ED to close percutaneous wound

• Wound edges must be everted
• Needle enters skin @ 90 degrees with the suture loop as wide as it is deep to the skin surface
• Try and get similar width and depth on both sides
• Placed close enough so you don’t have a gap in the wound edges (approx distance between sutures = distance from wound edge around .5-1 cm)
• For most traumatic Lacs we see start with a bite in the center suturing out (clean linear sharp cuts can start at the far edge but we dont usually see these

Dermal/buried suture- used to approximate dermis below the skin (reduces tension and closes deep tissue spaces making it easier to close percuteanously)

Absorbable sutures must be used and the knot (less than 3 ideally) buried so as not to inhibit healing. Avoid in highly contaminated wounds

Running suture: rapid percutaneous long wound closure ideal for long wounds with already goo edge approximation (distributes tension evenly along the length of the wound)

• Final bite made 90 degrees in direction of previous bite left as a loose loop to act as a free end for knot tying.
• Disadvantage is if the suture breaks the entire wound will open and you cannot remove just a few sutures at a time.

Vertical Mattress-  good for wounds under tension or whose edges tend to invert

• Far-Far suture acts as a deep/dermal stitch and near-near stitch acts to evert edges
  

  vertical mattress suture

Horizontal Mattress- also serves to evert wound edges and distribute tension good for pulling wound edges over larger distances or to as an initial suture to anchor two wound edges

• Also good for holding fragile skin together
  

  Horizontal mattress

Corner stitch- used to approximate angled skin flaps (avoids needing to put in multiple sutures to hold a corner down leaving the tip intact).

Corner stitch

sources: utdol.com; http://www.aafp.org/afp/2002/1215/p2231.html, Rich Wong and google of course!

• Monofilament – stronger, low tissue drag and harbor less infection. But DO NOT handle as easily and multifilament
• Multifilament- handles easily but promotes tissue infection and reactivity as it acts as a capillary allowing liquids an bacteria to travel along the strand easily
• Tensile strength- Higher number of zeros the smaller the size and less strong the suture is (general guide below:)’

5-0 to 6-0 : face, eyebrow, nose, lip, eyelid, ear, penis

4-0 to 5-0:  hand

3-0 to 5-0:  Scalp, torso, extremities, foot/sole

2-0 : Chest tube securing  (good luck finding it so we at Elmhurst use 5 Silk)

Absorbable:

• Fast-absorbing/plain/chromic Gut- strength retention 7 days and absorbs in 10-14 (chromic a little longer). Fast- absorbing less tensile strength than plain gut.

Fast-absorbing good for peds lacerations where removal might be difficult

• Vicryl- synthetic absorbable braided suture. 2 weeks of 65% tensile strength. Complete absorption 60-90 days

Great for buried suture to approximate wound edges and gain strength to keep wound closed; also great for nail bed closure

• Vicryl rapide- synthetic absorbable multifilament. 50% tensile strength at 5 days with 0% at 2 weeks. Absorption/falling off by 2 weeks.

Non-absorbable

• Nylon (Ethilon, Dermalon)- first synthetic suture/monofilament – high tensile strength (at 2 weeks), low $ and minimal tissue reactivity. Has poor memory so you need more knots to hold suture in place
• Prolene –synthetic/monofilament- similar to nylon in high tensile strength and low tissue reactivity. Plasticity noted allowing it to stretch and accommodate wound edema. Is slippery so requires extra throws to secure the knot.
• Silk- natural/braided – low tensile strength, evokes significant inflammatory response but with good knot security– rarely used cause we have nylon and prolene

Needles- 3 parts to a needle eye where the suture attaches; body where you hold on to; point tip to maximum cross section of body.

Points:

•  Cutting- 2 opposing cutting edges – ideal for skin sutures that must pass through dense irregular thick dermal tissue
• Conventional cutting- have a 3^rd cutting edge on the inside concave curvature of the needle (track faces wound edge so risk of cutting tissue)
• Reverse cutting- 3^rd cutting edge on the outer convex curvature decreasing tissue cutout. Used for thick skin like palms and soles.
• Blunt – dull point used for friable tissue (fascia)

Finally a quick literature review comparing Absorbable v. non-absorbable (limited literature on this, not much at all looking at adults/elderly)

• 1997 J Emerg Med (Shetty, Dicksheet, Scalea) 5 year retrospective study of hand lacerations repaired with 5-0 vicryl or nylon and no complications or infections reported in study group and scar was comparable at 6 months in both group
• 2004 – Academic Emergency Medicine ( Karounis, Gouin, Eisman, Chalut, Pelletier, Williams) Randomized clinical trial comparing peds traumatic lacerations closed with absorbable plain gut sutures v. nonabsorbable nylon found comparable cosmetic outcomes
• 2008- Pediatric emergency medicine (Luck, Flood, Eyal, Saludades, Hayes, Gaughan)-  Facial lacerations on pediatric population compared fast-absorbing cat gut v. nylon sutures – small study but showed no significant difference in scar appearance/parental satisfaction, infection rate, wound dehiscence or keloid formation.
• 2007 Pediatric Emergency Care (Al-Abdullah, Plint, Fergusson) meta analysis – lack of large/RCT evaluating absorbable v. nonabsorbable. However from the data reviewed appears non-absorbable sutures seem no better than absorbable in wound repair.

Vitals: 101.7  128  140/91 19  96%   FS 143

PE remarkable for an agitated male, AOx1 not following basic commands. Laceration to forehead, Pupils dilated but equal and reactive. Tachycardic but regular rate; Lungs CTAB. Abdomen with decreased bowel sounds but SNT. Skin hot and dry. Neuro exam non-focal

EKG ST @ 137; Qtc 475; incomplete RBBB

Initial labs remarkable for WBC 19 (89% PMN); Lactate 6.2. Foley placed 1200 cc urine voided with UA WNL. CXR and Head CT WNL

Just in time the cousin arrives with an empty bottle of Benadryl (just as the patient was being turned to set up for an LP!). This patient has an Anticholinergic picture of Bendaryl OD.

Anticholinergic OD: Red as beet; Dry as a bone; Hot as a hare; Blind as a bat; Mad as a Hatter (seizures as with this patient possible); Full as a flask . tachycardia (earliest sign of OD), decreased Bowel sounds

Rx: ABCs of course!!   Charcoal can be given within first 2 hours of ingestion if patient can tolerate it; Sodium Bicarb for QTc and QRS prolongation (given in this case in anticipation of continued absorption and lengthening of already prolonged QTc); Benzo’s for seizures and agitation, Physostigmine.

Physostigmine- once part of the “coma cocktail” for AMS now not often used.

A carbamate acetylcholinesterase inhibitor that binds reversibly to inhibit acetylcholinesterase increasing amounts of acetylcholine to overcome anticholinergic blockade.

Should not be given if TCA OD is suspected (more sedated than agitated anticholinergic picture) especially if patient has wide QRS cause can lead to asystole

Superior to Benzos for the AMS/agitation of anticholinergic OD

Can be used diagnostically if unclear picture as administration of physostigmine in AC OD should result in improvement of clinical picture. Repeat dosing can be done every 20-30 minutes for continued agitation/delirium.

Reminders for the oral boards:  altered patients need all 6 vitals HR, BP, RR, O2 Sat, Temp and FS. Always order Tylenol for patients with fevers and tetanus for patient with lacerations.

Thank you Raashee for interesting morning report!

]]> http://www.sinaiem.org/wellness/2013/05/16/yoga-524/feed/ 0 http://www.sinaiem.org/pearls/2013/05/13/1939/ http://www.sinaiem.org/pearls/2013/05/13/1939/#comments Mon, 13 May 2013 13:19:29 +0000 tali http://8.1939 22 y/o F 35 weeks gestation being treated with magnesium sulfate for preeclampsia in your ED awaiting transfer to nearby hospital for definitive care. You go to re-evaluate the patient and find her somnolent, decreased respiratory drive and decreased deep tendon reflexes. After managing the airway what is the next step in management:

1. Dexamethasone
2. Lidocaine
3. Labetolol
4. Calcium gluconate
5. Atropine

Answer:  Calcium gluconate. This patient has signs and symptoms of magnesium toxicity. Although uncommon in women with good renal function toxicity is related to serum magnesium levels. Symptoms include loss of deep tendon reflexes, respiratory paralysis and cardiac arrest at higher doses. Calcium gluconate (1gm IV over 5-10 minutes) antagonizes the affects of magnesium and can counteract these life threatening side effects.

Less concerning but other side affects of Magnesium infusion at rapid rates include diaphoresis, flushing and warmth (likely due to peripheral dilation) nausea, vomiting, HA and palpitations.

Pre-eclampsia as a reminder is new onset HTN and proteinuria after 20 weeks gestation in a previously normotensive woman. Magnesium is used to prevent eclampsia (seizures) intrapartum. The mechanism of how it prevents seizures is not well understood. Recommendation is to begin infusion at onset of labor or prior to c-section.

Bethamethasone, not Dexamethasone, is administered to women to promote fetal lung maturation in prematurity (unrelated to pre-eclampsia but possibly a complicating factor).

Labetolol along with Hydralazine are 1^st line therapies in hypertensive women during pregnancy that might present to the ED (Nifedipine, Nicardipine and nitroglycerin are also safe to use). Remember though that treating hypertension does not alter the pre-eclampsia disease process nor does it reduce morbidity or mortality surrounding pre-eclampsia.

Source of question: www.1000emergencymedicinequestions.com

56 y/o F with acute organophosphate overdose, severe bronchorrhea, bradycardia and coma. She is intubated for airway protection and atropine therapy initiated. After 10 mg Atropine her HR is 130, BP 160/90 and secretions are still copious. Which of the following is the most appropriate next step in management?

1. Stop Atropine, start Epinephrine
2. Stop Atropine, start Vasopressin
3. Stop Atropine, Start Pralidoxime
4. Continue Atropine therapy alone
5. Continue Atropine therapy and add Pralidoxime

Answer: E

Organophosphates bind to and inhibit Acetylcholinesterase causing a cholinergic syndrome (Sludge- Salivation, lacrimation, Urination, Defecation, GI distress and Emesis – as well as Bronchorrhea with variable effects on HR). Mortality from organophosphate OD is usually attributed to hypoxia from bronchorrhea. Treatment includes high doses of Atropine (endpoint being reduction of bronchial secretions, not HR or BP control). Over time the bond between Acetylcholinesterase and organophosphates becomes irreversible (aging) so Pralidoxime has to be given as it acts to break the complex bond between the two and reverse symptoms further.

Source:  www.1000emergencymedicinequestions.com

Labs: alcohol (271), ASA (wnl), Tylenol (wnl)

Initial VBG: pH 7.34, PCO2 55, PO2 40 lactate 1.5

Carboxyhemoglobin 0.9

EKG- NSR 79, no STT changes. Incomplete RBBB. Flattening T waves laterally

CO poisoning

CO – colorless, odorless gas formed from hydrocarbon combustion that binds to Hgb at much higher affinity (240x) than O2 forming COHb à results in impaired oxygen transportation and utilization

-          Once it binds to the heme moiety it changes the heme so that it cant unload the three oxygen binding sites to the peripheral tissue and also interferes with cytochrome oxidase

Symptoms depend on duration of exposure and CO levels.

-          Cardiac: myocardial ischemia, MI , dysrhythmias, cardiac arrest

-          Brain: Stroke like symtpoms , Seizures Syncope,  Leukoencephalopathy, DNS

• DNS (delayed neuro sequlea)- not well understood  – theorized that involved lipid peroxidation by toxic oxygen species- when you recover from CO exposure you have a similar phenomenom to ischemia-reperfusion injury and exposure to hyperoxia may exacerbate oxidvative damage

-          Skin- cherry red skin – usually only present in excessive exposure (fatal levels)- also can see cutaneous bullae but uncommon as well

Workup

A+B – hypoventilation, high flow O2 via NRB With resevor – remember SPO2 wont change much

ECG (MI, dysrhythmia), cardiac monitor, volume resuscitation

Mental status / mini mental

Get an exposure history—duration, soursc, other exposures, other people exposed…

VBG- Initial respiratory alkalosis (compensation for reduced delivery); later anion gap metabolic acidosis  due to elevated lactate

CO-oximetry – levels correlate poorly with degree of poisoning and do not predict DNS (normal CO levels in a non-smoker up to 3%; smoker 10-15%)

-          Children are more likely to be affected cause they have a higher RR so they get higher doses of the poison;

Treatment: supplemental oxygen (NRB) or hyperbaric oxygen (JACOBI hospital)

-          Hyperbaric oxygen – 100% oxygen pressurized –not used to expedite removal of blood CO but to stop tissue level destruction

-           Indications for HBO (recommendations, not criteria): Syncope, Coma, Sz, AMS/confusion, COHb > 25% (even if asymptomatic), pregnant woman and children, abnormal cerebellar exam

-          Should be considered up to 24 hours after exposure

Hyperbaric fellow consulted on this patient but determined due to other causes of AMS (alcohol) and low levels not a candidate for hyperbaric at that time.

Thanks to Dr. Hernandez for this case!

Initial venous blood gas revealed pH of 7.21, pco2 40, lactate 2.1 and glucose of 20.

Initial ER venous revealed Na of 140, K 5.1, Cl 109, CO2 23, Bun 19, Cr 1.1 and glu 20.

Patient has a non-anion gap acidosis. Helpful mnemonic for differential in this category is HARDUP.

• Hyperalimentation
• Acetazolamide or other carbonic anhydrase inhibitors
• Renal Tubular Acidosis
• Diarrhea
• Ureteroenteric fistula
• Pancreaticoduodenal fistula

Of these, RTA is most likely given her history and physical. Which RTA however?

RTA type 1

• Affects distal tubules
• Hypokalemia 2/2 H+ secretion

RTA type 2

• Affects proximal tubules
• Hypokalemia 2/2 failed hco3 reabsorption from the urine by the proximal tubular cells

RTA type 4

• Affects adrenal glands
• Hyperkalemia 2/2 aldosterone deficiency

So this patient has RTA type 4, treat with dextrose for the hypoglycemia, hydrocortisone for glucocorticoid and fludrocortisone for the mineralcorticoid activity.

Thanks to Jake Isserman for his informative morning report.

What is the next initial management after starting IV TMP-SMX?

A. Corticosteroids

B. Intubate

C. Continue supportive care

D. Start antiretroviral therapy

Severe PCP is defined as arterial PaO2<60 mmHg on air. Moderate PCP is defined as: PaO₂ between 60 and 80 mmHg on air. Corticosteroid therapy should be considered in patients with paO2 below 70 mmHg. ART should be initiated after two weeks of initial dose of TMP-SMX for ART naive patients. ART in patients already on their course should continue.