Prevention of desaturation during intubations

A great article in this month's Annals of Emergency Medicine from Scott Weingart and Richard Levitan: "Preoxygenation and Prevention of Desaturation During Emergency Airway Management."

Recommendations for improving oxygenation and preventing desaturation during ED intubations:

1.  Preoxygenate patient using standard reservoir facemask with highest possible flow rate of O2, head-up position, when possible.

2.  If possible, preoxygenate for 3 minutes or have patient take 8 maximal inhalation/exhalation breaths.

3.  For patients who cannot achieve saturations > 93-95% with high FiO2, consider preoxygenation with PEEP, including CPAP masks, noninvasive positive-pressure ventilation, or PEEP valves on a bag-valve-mask device.  

4.  Provide passive oxygenation during RSI (using high-flow O2 via nasal cannula after sedatives and paralytics given) to increase duration of safe apnea in ED tracheal intubations.

6.  Ventilate hypoxemic patients during onset phase of muscle relaxants in RSI prior to tracheal intubation.  For fully oxygenated patients at low risk for desaturation, ventilation is not required during the onset phase of muscle relaxants.

7.  Position patients to maximize upper airway patency using ear to sternal notch positioning.


References:
1.  Weingart, S and Levitan, R.  Preoxygenation and Prevention of Desaturation During Emergency Airway Management.  Annals of Emergency Medicine 2012;59:165-75.

Normal ESR values by age

Rule for correcting erythrocyte sedimentation rate (ESR) by age:

Men:  Age in years  /  2
Women:  Age in years + 10  /  2


References:
1.  Miller A, Green M, Robinson D.  Simple rule for calculating normal erythrocyte sedimentation rate.  BMJ 1983; 286:266.  

What are the top causes of small bowel obstruction?

Upright abdominal film showing multiple air-fluid levels.

Most common causes of small bowel obstruction in adults:

#1.  Adhesions after abdominal surgery (60%)
#2.  Malignancy (20%)
#3.  Hernia (10%)
#4.  Inflammatory bowel disease (5%)

Intussusception is the most common cause of small bowel obstruction in children.

References:  
1.  Nobie, BA.  Small-Bowel Obstruction.  Emedicine.  Available at http://emedicine.medscape.com/article/774140-overview#aw2aab6b2b3.  Accessed March 3, 2012.

What are appropriate antibiotics for PID?

Pelvic inflammatory disease (PID), refers to infection and inflammation of the female genital tract, including endometritis, salpingitis, tubo-ovarian abscess, and pelvic peritonitis.  PID is believed to be initiated by ascending infection from the vagina and cervix (often Chlamydia trachomatis), but is often polymicrobial.

The CDC recommends empiric treatment for PID in sexually active young women and other women at risk for STDs if no cause for symptoms can be found and the patient has at least one of the following:

1.  Cervical motion tenderness
OR
2.  Adnexal tenderness
OR
3.  Uterine tenderness

The following criteria enhance specificity and further support the diagnosis of PID:
1.  Temp > 101 F
2.  Abnormal mucopurulent cervical or vaginal discharge
3.  Presence of abundant leukocytes on wet prep
4.  Elevated ESR
5.  Elevated CRP
6.  Laboratory evidence of C. trachomatis or N. gonorrhea cervical infection

For patients with mild to moderate PID who can be managed as outpatients, the CDC recommends:

Patient who don't respond to oral therapy within 72 hours should be reevaluated both to confirm the diagnosis and to initiate parenteral therapy.

For patients with severe illness, tubo-ovarian abscess, pregnancy, or lack of response to oral agents, the CDC recommends inpatient therapy.  Recommended parenteral regimes include the following:

References:
1.  CDC Sexually Transmitted Disease Treatment Guidelines, 2010.  Available at http://www.cdc.gov/std/treatment/2010/STD-Treatment-2010-RR5912.pdf.  Accessed Feb. 9, 2012.

Dog bites: When should you use prophylactic antibiotics?

Dog bites are the most common mammalian bite injury seen in the United States, followed by cat bites and human bites.  Management of minor dog bite wounds includes copious irrigation with normal saline (>150 mL through an 18 or 19 gauge plastic catheter), debridement of any devitalized or crushed tissue, assessment for underlying tendon or bone injury, updating tetanus status when indicated, and assessment of rabies risk.  Primary closure of bite wounds is controversial, but it is generally accepted that wounds can be sutured unless they are high risk or already infected.  High risk wounds should be closed with delayed primary closure 72 hours later.  Wounds to the face are usually sutured for optimal cosmetic results, and infection is rare due to copious irrigation, excellent blood supply, and use of antibiotic prophylaxis.

There is a lack of consensus about which type of wounds require antibiotic prophylaxis.  Risk factors for infection include location on hand, foot, or over a major joint, puncture wounds and crush injuries, treatment delay > 12 hours, and systemic factors such as advanced age, immunosuppression, asplenism, diabetes, and vascular disease.  Griego et al list the following indications for prophylactic antibiotics:

There is no clear consensus on the appropriate antibiotic choice for infection prophylaxis.  When infections do develop from dog bites, they are usually polymicrobial with both aerobic and anaerobic species.  Staphylococcus, Streptococcus, and Corynebacterium are the most common aerobic species isolated, with Bacteriodes fragilis, Prevotella, Peptostreptococcus, and Fusobacterium among common anaerobic isolates.  A rare, but potentially fatal infection associated with dog bites is Capnocytophaga canimorsus. Patients who develop this infection usually have a predisposing condition, such as splenectomy.

Amoxicillin/clavulanate is often prescribed due its dual aerobic and anaerobic coverage. Alternative regimens include clindamycin plus ciprofloxacin, TMP/SMX, and second- or third-generation cephalosporins such as cefuroxime.  Duration should be 5-7 days.  It is recommended that patients have an initial follow-up visit at 24-48 hours to assess wound healing and presence of infection.





References:
1.  Griego RD et al.  Dog, cat, and human bite wounds:  A review.  J Am Acad Dermatol 1995;33:1019-29.
2. Smith PF, Meadowcroft AM, May DB.  Treating mammalian bite wounds.  Journal of Clinical Pharmacy & Therapeutics.  2000;25:85-99 

To bolus or not to bolus in DKA

IVF and insulin drip

I recently saw an adult patient with diabetic ketoacidosis.  She was treated with intravenous fluids and an insulin drip and admitted to the ICU. There was some questioning among the nursing staff about whether or not she needed to receive an insulin bolus first.  I decided to look for some literature to share with the nursing staff, as well as educate myself.  Here is what I found:

In children with diabetic ketoacidosis, an insulin bolus is NOT recommended.  It is one of the factors that has been linked to increased risk of cerebral edema.  Do not bolus insulin in kids with DKA.

In adults the guidelines are less clear.  A recent review in Annals of Internal Medicine says that either a bolus followed by drip can be given, (regular insulin at 0.1 U/kg IV bolus followed by 0.1 U/kg/hr as continuous IV infusion), or simply an infusion started.  Tintinalli recommends just starting insulin infusion at 0.1 U/kg/hr.

A few pearls:
1.  Always give fluids before anything else, while awaiting lab results.  The average adult with DKA has a water deficit of 5-10 L.
2.  Wait for potassium level before starting insulin.  Many patients with DKA have a profound potassium deficit, even though serum levels can initially be normal or even high.  This is because the acidosis drives potassium out of cells in exchange for hydrogen ions, falsely elevating the potassium level. If initial [K+] level is <3.3, give potassium-containing fluids BEFORE starting insulin.  Otherwise life-threatening hypokalemia can result.
3.  Bicarbonate therapy is controversial due to risk of worsening hypokalemia, worsening intracellular acidosis.  Bicarbonate should not be routinely given, but should be considered for severe acidosis (pH < 6.9).
4.  Remember to look for precipitants of DKA, and treat any underlying conditions.



References:
1.  Rosenbloom, AL.  The management of diabetic ketoacidosis in children.  Diabetes Therapy 2010. 1:103-120.
2. From Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7th Ed. Tintinalli, JE, Ed, et al.  New York: McGraw Hill, 2011: p. 442-445.
3.  Wilson et al.  In clinic:  Diabetic ketoacidosis.  Annals Internal Medicine 2010.  152(1):ITC1-1.




The management of diabetic ketoacidosis in children.Source:Diabetes Therapy [1869-6953] Rosenbloom yr:2010 vol:1 iss:2 pg:103 -120

Beta blocker overdose

Sinus bradycardia with HR of 50

A 70 yo female presents with lightheadedness and feeling "crummy."  She was started on metoprolol yesterday by her PCP for an elevated heart rate.  Initial vital signs reveal HR of 31, BP 121/85, RR of 15, and T 37.  She had been having intermittent burning substernal chest pain but denies any currently.  On physical exam she is awake and alert but looks pale and uncomfortable.  Pupils are PERRL, CV exam reveals bradycardia with regular rhythm, there is no respiratory distress, lungs are clear to auscultation bilaterally, abdomen is soft and nondistended, neuro exam is intact.  Skin is warm and dry.  EKG shows sinus bradycardia with T wave inversions in leads II, III, and aVF.

The differential for bradycardia is broad and includes vasovagal response, sick sinus syndrome, myocardia ischemia involving right coronary artery, atrioventricular block, increased intracranial pressure (seen with elevated BP in Cushing's reflex), hypokalemia, hypothermia, hypothyroidism, and medications (beta blockers, calcium channel blockers, digoxin, clonidine).  Bradycardia can also be a normal finding, often seen in well-conditioned athletes.

The key branch point for management of bradycardia is whether or not signs of adequate perfusion are present.  If the bradycardia is leading to hypoperfusion, according to ACLS guidelines, transcutaneous pacing should be initiated while reversible causes (H's and T's) are investigated.  If the bradycardia is not causing hemodynamic compromise, patients can be monitored and observed.

While transcutaneous pacing is being set up, atropine 0.5 mg IV push should be given (repeat for total dose of 3 mg).  Dopamine is a second-line agent for when atropine is not effective.  Dose is 2-10 mcg/kg/min infusion.  Epinephrine is a third-line agent, dose 2-10 mcg/min infusion.  If beta blocker overdose is suspected, glucagon 1-5 mg IV should be given.  If heart rate responds, a glucagon infusion should be started.

Pacer pads were placed on the patient, but because she was maintaing her blood pressure and mentating well, transcutaneous pacing was not required.  She was given a fluid bolus as well as atropine 0.5 mg IV x 2 doses without improvement.  Because beta blocker overdose was a consideration, she was given glucagon 3.5 mg IV.  Because of possible ischemic changes on EKG, an aspirin was administered and cardiology was consulted.