Tag Archives: ID

Wound prophylaxis – Should lip lacs get antibiotics (and few others)?

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During my review for 72 hour returns we had a through and through lip laceration come in that returned with a wound infection a few days later.  This prompted me to look up current recommendations as I’m pretty sure that I haven’t been giving antibiotic prophylaxis for this.

Searching literature, Tintinalli and UpToDate…… Most superficial wounds do not require prophylaxis, however, through and through lip lacerations were an area of uncertainty and debate….

Tintinalli  – “matter of provider preference.”

UptoDate – no clear clinical evidence to say that these wounds should receive antibiotic prophylaxis , however, due to the pathogens of the oral cavity, they recommend prophylaxis.

Current literature – Review article in 2008, Annals of Emergency Medicine, Mark DG et al – review of studies do not show a statistically significant benefit; however, the only double-blinded randomized control trial showed a trend toward benefit in patient’s that were compliant with therapy.

Some other stats – Rate of infection in wound treated in the ED (Tintinalli)

Head and neck 1-2%

Upper extremity 4%

Lower extremity 7%

Oral wounds – 9-27%

If giving prophylaxis then Pen VK or Clindamycin is recommended for 3-5 days.

For other oral wounds, <1cm, no need to close. Close if large gap susceptible to food getting trapped, and counsel on good oral hygiene.  Dental and OMFS usually recommend d/c with chlorhexidine gluconate oral rinse (0.12%) (Peridex) and will have patients swish and spit after meals to keep the wound from contamination with food particles.

My take away from this is strongly consider antibiotic prophylaxis with through and through oral wounds as they are higher risk for infection with oral flora; however, not an absolute must based on the current evidence.  Be sure to emphasize good oral hygiene, and as always, close follow up with good return precautions.

Other wounds to strongly consider prophylaxis due to increased risk for infection are mammalian and human bite wounds, crush injury, puncture wounds, and wounds with either fresh or salt water contamination, or patients who are immunocompromised, asplenic, advanced liver disease, associated edema (according to the IDSA).

Open fractures and wounds with joint capsule violation should receive antibiotic prophylaxis.

Reminder: Update Tetanus and simple lacerations do not need antibiotic prophylaxis.

Facial Edema

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This was an interesting presentation from a Peds shift.

15 y/o AAM with no significant medical history who presents with facial swelling. Patient noticed significant swelling to the left side of his face upon awakening in the morning. The swelling involved his entire left cheek, inferior lid of his left eye, upper lip and part of his right cheek. The patient denies any pain, tongue swelling, voice change, difficulty breathing or swallowing, fevers, recent ill symptoms (cough, congestion, vomiting, diarrhea), dysuria, hematuria, rectal bleeding, sore throat, ear complaints. He denies any new exposures including new medications, new soaps, detergents, animal exposures, environmental exposures, recent travel, insect bites.

PMH:none. PShx: had 4 wisdom teeth removal 1 month prior (finished antibiotics), no other recent surgeries or dental work. No EtOH, drugs. No current medications. No known allergies.

Vitals: 97.8, 90, 110/70, 18, 99 % on RA

Exam: HEENT- moderate swelling of the left buccal area, inferior lid of the left eye, upper lip. Mild swelling to the right buccal area. No erythema or palpable areas of fluctuance. No swelling surrounding the right eye. No conjunctival injection. No erythema within the ears, TMs normal. No mastoid tenderness. No lingual swelling, no erythema within the mouth or palpable areas of fluctuance. No signs of infection from previously removed wisdom teeth. No posterior oropharyngeal swelling or uvular deviation. No lymphadenopathy.

Heart- normal. Lungs- clear, no wheezing or stridor. Abdomen- normal. No CVA tenderness.

Treatment started with Benadryl for possible allergic reaction. Basic labs obtained and urine for possible nephrotic syndrome. WBC-17, otherwise normal. Urine with 200 protein, no RBC or WBC- nephrology consulted and recommended repeat POC labs as outpatient and follow-up in clinic, but no intervention at this time. Patient had mild improvement with Benadryl. Discharged home with Benadryl and steroids.

Patient re-presents 6 hours later (just came back for my shift the next day)

Facial swelling has worsened. Now involves bilateral buccal areas, bilateral lower eyelids and upper lip. No fevers, no difficulty breathing, no dysphagia. Patient had taken 1 repeat dose of Benadryl at home and had not started steroids yet. No other changes in HPI except patient mentions some bleeding from the inside of his upper lip. Upon exam, patient has some bleeding and purulent drainage from the gumline of his left central incisor. No palpable fluctuance, but able to express drainage with pressure to upper lip.

Labs obtained: WBC 17, CRP 1.6, ESR 41. UA- minimal protein. All other labs unremarkable. CT face with contrast obtained showing left central incisor periapical abscess with cortical erosion as well as extensive cellulitis of the midface. Also some concern for phlegmon within the paranasal sinus. ENT, OMFS, and finally pediatric dentistry consulted. Patient admitted for IV clindamycin, Unasyn for cellulitis and dentistry consult for possible root canal versus tooth extraction.

Bottom line: Odontogenic infections can cause orofacial infections and rarely but more importantly peripharyngeal space infections as well as jaw osteomyelitis. If concerned about deep facial infection, CT face is warranted. Treatment includes draining of pus from abscesses (either through I&D or needle aspiration) and culture as well as antibiotic therapy. Common regimens include a penicillin plus metronidazole, clindamycin, augmentin, or unasyn depending on disposition. Dentistry should be involved whether through consult or outpatient follow-up for root canal versus tooth extraction.

Sepsis-3

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I’m sure you guys have heard about the new sepsis definitions unveiled at the SCCM conference last week which were originally published in JAMA (2016;315(8):801-810); if not you’re in luck because I’ve outlined them for you below.  Keep in mind the sepsis definition has not been updated since most of you were still in high school- or middle school- I’m showing my age, in 2001, with Sepsis-2.

Sepsis-3:

New Terms and Definitions

  • Sepsis: Life-threatening organ dysfunction caused by a dysregulated host response to infection
  • Organ dysfunction: Acute change in total SOFA score ≥2 points consequent to the infection
  • Identification of patients likely to have poor outcomes:
    • ICU Patients: SOFA score ≥2: Overall mortality risk of approximately 10% in a general hospital population with suspected infection
    • ED patients: qSOFA score >2 (SBP < 100 mm Hg, RR > 22, or altered mental status)
      • These patients are likely to have a prolonged ICU stay or to die in the hospital
    • Septic shock: Sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥65 and a serum lactate level >2 mmol/L despite adequate volume resuscitation
      • Hospital mortality is in excess of 40%
    • The term “severe sepsis” has been abandoned

Antibiotic review

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Maybe it’s because an overhead projector slide scanned and inserted into a powerpoint presentation comprised my medical school antibiotics curriculum (you know what I’m talking about if you went to U of L), but I’ve never really felt comfortable with the nuances of antibiotics. For those who want to understand them a little better, here’s a great review.

The bar is set, Chrissy!

Acute Cholecystitis, Classic

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Interesting case from a couple weeks ago.

20ish yo white male, no significant past medical diagnoses. Overweight. Family history of gallbladder disease. No OTC or Rx medications. Patient smokes, does not drink, and has used IV drugs in the past.

Here in the ER due to RUQ abdominal pain for one week, was coming and going and is now constant. On further questioning, admits that his mom made him come because of her history of gallstones and cholecystectomy. On exam patient has jaundiced sclera and urine on table is dark brown, pain in right upper quadrant of abdomen is exquisite. States he has been vomiting especially after eating and all food makes him sick. No documented fevers, but feeling chills.

Urine: Large bilirubin, otherwise normal

Pertinent blood: WBC 8.4, Hgb 14.2, Plt 430. Alk Phos 140, AST 734, ALT 1417, Total Bili 9.5. Lipase 22. Tylenol neg.

Didn’t expect this guys ‘acute chole’ to cause liver failure.  Either way, he was getting further imaging to find out more. No ultrasound coverage at 5am so CT for now, then ultrasound at 7am. Added tox screens and hepatitis panel at this time.

CT abdomen/pelvis with contrast: “Markedly thickened/edematous wall of the gallbladder indicating cholecystitis. No calcified stone visualized. Additional imaging maybe obtained with ultrasound.” Also, normal liver.

The results of the ultrasound showed a “nondistended gallbladder with marked wall thickening, edema and a positive sonographic Murphy sign. Given lack of clear visualization of the posterior wall, highly worrisome for complicated cholecystitis, possibly gangrenous or with a focal posterior perforation.” Normal liver and mildly dilated bile duct.

Now with labs showing liver failure and two forms of imaging showing acute cholecystitis, it had to be. Admitted to the general surgery team though the ‘acalculous cholecystitis’ with liver failure was enough to peak my interest in follow-up.

Hepatitis panel comes back later same day showing reactivity for Hep C. Discharge 5 days later, no surgery, no acute interventions, with down-trending liver function panel and follow-up with the GI clinic.

While most commonly associated with cholecystitis, a quick literature search reveals multiple reasons besides cholecystitis to have gallbladder wall thickening… congestive heart failure (right sided), gallbladder carcinoma, adenomyomatosis (chronic gallbladder inflammation or degeneration), renal failure, pancreatitis, cirrhosis and other forms of liver failure.

Fever from Africa…..

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Just stop right there. It’s not ebola.

It’s malaria (unless the patient is uncontrollably vomiting blood or has participated in the cultural burial practices of West Africans within the past couple of weeks).

Seeing as I’ve had two patient’s with malaria, I thought it’d be nice to share some of the great resources I’ve come across (had med students look up), while treating these guys.

1. First off is the CDC malaria map: http://cdc-malaria.ncsa.uiuc.edu

You can see where malaria is endemic, and you click on different countries to see speciation and resistance.

2. Next is the CDC treatment recommendations: http://www.cdc.gov/malaria/resources/pdf/treatmenttable.pdf

Get a good history and know where the patient has travelled. This has doses for adults and children, so it can be useful at Kosair or out in the community too.

3. Clinical Pearls

  • Transmitted by the Anopheles Mosquito
  • Classically will have fevers/symptoms spiking every 24/48 hours
  • Severe Malaria (ICU admission): AMS, severe anemia, DIC, parasitemia >5%, metabolic acidosis, AKI/liver injury, hypoglycemia
  • Probably best to admit/observe all patients until you have a viral load and get treatment started at the hospital. Some of the antimalarials can be hard to come by and these patient’s can get sick.

Golden Hour

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Below is the LITFL summary of another look at the importance of early ABx administration in septic patients. Septic and especially severely septic patients should be taken to room 9, obtain blood cultures promptly, and initiate antibiotics as early as possible.

 

Ferrer R et al. Empiric antibiotic treatment reduces mortality in severe sepsis and septic shock from the first hour: results from a guideline-based performance improvement program. Crit Care Med 2014; 42: 1749-55. PMID: 24717459

  • This retrospective analysis of prospective surviving sepsis data of patients admitted to the ICU with severe sepsis found that delays in antibiotic administration resulted in a concomitant increase in hospital mortality. Though the results are compelling with a linear relationship between time to administration and hospital mortality discovered it is key to interpret this study with caution as the data are uncontrolled for the antibiotic administration to time metric primarily studied by this paper. Multiple potential confounders exist that might account for the observed relationship that should be studied prospectively. In the meantime it makes reasonable sense to administer antibiotics as soon as possible after the actual discovery of real sepsis.  
  • Recommended by: William Paolo