When to use vancomycin
The most common use for vancomycin is in invasive Gram positive infections
You need to consider
- Infection site
- Patient weight
- Kidney function
- Pathogen susceptibility
- Vancomycin has bad oral bioavailability so it’s almost never used as a pill
- Occasionally it is orally to supplement C. diff infections (because that’s going on in the GI tract)
- Volume of distribution: IV serum 0.4-1 L / kg
- Normally vancomycin doesn’t cross the blood brain barrier very well, but in the setting of meningitis the inflamed meninges increases permeability
- Redman syndrome: A histamine-like flushing during or immediately after dose. Occurs mostly on the face and neck. This is NOT life threatening
- Treatment: anti-histamine, pause infusion, then restart at a slower rate
- If the reaction is severe, stop the infusion, give antihistamines, wait until symptoms resolve before restarting. When you restart, give the infusion reaaaalllllly slooooooowly (over more than 4 hours)
This is where vancomycin can get tricky, because you are aiming for a target trough (between dose) serum concentrations.
- Generally the target is 10 mcg/ml, but this may need to be higher for treating MRSA or osteomyelitis
- Trough concentrations should be measured 30 minutes before the 4th dose any time a course of vanco is started or the dose is changed
- Monitor creatinine at least once a week (remember that whole nephrotoxicity bit)
Starting dose should be 15-20 mg/kg (based on actual not ideal body weight) every 12 hours. This usually works out to 1-2 g IV Q12H. If the kidneys are not working well, reduce the dose.
- UpToDate.com “Vancomycin: Parenteral dosing, monitoring, and adverse effects in adults”
Sore throats (pharyngitis) are a common complaint in primary and emergency care settings. Most of the time, pharyngitis is caused by viral infection (most commonly rhinovirus).
Streptococcus pyogenes, aka Lancefield group A streptococci, (GAS) is the most common bacterial cause of pharyngitis. The possible complications of GAS infection include:
- Rheumatic fever
- Post-streptococcal glomerulonephritis
- Peritonsillar/retropharyngeal abscess
- Otitis media
- Pediatric autoimmune neuropsychiatric disorder associated with Group A streptococci (PANDAS) *controversial!
Signs and symptoms
GAS pharyngitis may also include fever, chills, malaise, headache, nausea, vomiting, abdominal pain, or maculopapular rash (scarlet fever). Cough, coryza/rhinitis, and conjunctivitis are uncommon symptoms for GAS pharyngitis. However, clinically diagnosing GAS pharyngitis based on history and physical is incredibly unreliable, so patients with a convincing presentation would benefit from laboratory confirmation (i.e., throat culture, rapid antigen detection test of throat swab). The Centor and McIsaac criteria are useful for helping rule out GAS pharyngitis, but shouldn’t be used exclusively to diagnose it.
The Centor criteria are scored based on the presence of:
- Fever (subjective or >38 C)
- Lack of cough
- Tender lymphadenopathy (anterior cervical)
- Tonsillar exudate
The MacIsaac criteria add an extra point for patients < 14 years old (since this age group is more prone to GAS pharyngitis) and subtract a point if >45 years old. A low score on these criteria help to exclude GAS pharyngitis, but higher scores indicate a need for lab tests.
The first-line treatment for GAS pharyngitis is penicillin. Other antimicrobial agents vary between different guidelines. Guidelines vary about whether empiric treatment should be considered before lab results have confirmed a diagnosis.
- Aalbers J et al. 2011. Predicting streptococcal pharyngitis in adults in primary care: A systematic review of the diagnostic accuracy of symptoms and signs and validation of the Centor score. BMC Medicine: 9;67.
- Kociolek LK, Shulman ST. 2012. Pharyngitis. In: Annals of Internal Medicine: In the Clinic (Cotton D, Taichman D, Williams S, Eds.). ITC3-1.
- Weber R. 2014. Pharyngitis. Primary Care Clinics in Office Practice: 41;91.
- Wessels MR. 2011. Streptococcal pharyngitis. New England Journal of Medicine; 364:648.
- Worrall G. 2011. Acute sore throat. Canadian Family Physician: 57;791.
BUY THIS AS A STUDY CARD
A kid without a rash just isn’t a kid.
- Incubation: 10-21d, infective until crusted over
- Rash: vesicles on macules (dewdrops on rosepetals),
- Very pruritic!
- Other symptoms: 1-3d prodrome of fever and respiratory symptoms
- Treatment: supportive, acyclovir for severe disease, VZIG for post-exposure prophylaxis
- Complications: 1st or 2nd trimester = congenital varicella syndrome
- Incubation: 5-15d
- Rash: pink macules and maculopapules, starts on neck.
- Other symptoms: HIGH FEVER, cough, respiratory symptoms, erythematous pharynx, tonsils & TMs
- Treatment: supportive
- Complications: febrile seizures
- * Generally affects kids <5 years old
- Incubation: 10-14d, dx with measles IgM
- Rash: maculopapular, starts on face.
- Other symptoms: the 3 Cs
- 1) Cough 2) Coryza (runny nose) 3) Conjunctivitis
- Koplik spots in mouth 1-2d before rash
- Treatment: supportive, prophylactic Ig
- Complications: secondary bacterial infection, encephalitis (1:1000), subacute sclerosing panencephalitis (1:100000)
Rubella aka German Measles
- Incubation: 14-21d, infective 5d before rash and 7d after
- Rash: pink maculopapular, starts on face.
- Other symptoms: non-specific
- Treatment: supportive
- Complications: congenital rubella syndrome (very bad*), first four months of pregnancy highest risk (this is why we check rubella immunity status in prenatal screening)
* Congenital Rubella Syndrome
“Blueberry muffin baby” (purpura). Cataracts/congenital glaucoma, congenital heart disease, hepatosplenomegaly, jaundice, microcephaly, developmental delay
Fifth Disease aka Erythema Infectiosum
- Incubation: 4-14d, infective prior to onset of rash
- Rash: slapped cheeks (raised uniform maculopapular lesions on cheeks), may appear on extensor surfaces
- Usually not pruritic
- Other symptoms: flu-like illness ~3d prior to rash
- Treatment: supportive, blood transfusions if aplastic crisis
- Complications: arthritis (10%), vasculitis
- Aplastic crisis: reticulocytopenia, not bad in normal people, very bad anemia if you already have chronic hemolytic anemia
- During pregnancy: fetal hydrops/fetal loss
* This is a good one to actually know the virus name! PARVOVIRUS B19
Other rash descriptors to think about
- Sandpaper rash: scarlet fever (Group A Strep), they also have strawberry tongue, fever and sore throat
- Pink macules with central clearing: erythema marginatum (one of the major Jones criteria for rheumatic fever)
- Palpable purpura: Henoch-Schonlein Purpura
- Non-blanching petechiae: BAD (meningococcal disease), could be other things too, but need to rule out meningitis
Suppurative (infectious) flexor tenosynovitis is a medical emergency because the tendon sheath is a closed space and too much swelling can lead to compartment syndrome and necrosis.
* You can’t really get these complications in extensor tendons as it is an open space (no tendon sheath)
There are 4 cardinal signs of flexor tenosynovitis (Kanavel’s Signs)
- Tenderness along the whole tendon sheath (late sign)
- Finger held in flexion
- Fusiform swelling (sausage finger)
- Pain with passive extension *this is the earliest finding
It is usually caused by some sort of inoculation, but this can be something very small and the patient may not be aware that he/she had ever been injured (can also be caused by local or hematogenous spread). It’s not unreasonable to get an x-ray to rule out other things and if there’s a fever or they seem very unwell, you can do blood cultures. You also probably want to start the patient on some broad spectrum antibiotics such as vancomycin + ciprofloxacin (or ceftriaxone).
Treatment is tendon sheath drainage and debridement as well as antibiotics.
Meningitis is very literally inflammation of the meninges. Something swollen in a closed space is never good, so it’s important to not miss meningitis when it presents.
Classic triad of meningitis
- Neck stiffness
- Mental status change – in babies this can be an increase in somnolence or irritability (unconsolably crying)
- E. coli*
- GBS (Group B strep)*
- Neisseria meningitidis
- Strep pneumoniae
- Staph aureus
- Gram neg bacilli
- Haemophilus influenza
- Viral (“aseptic”)
* These are the common ones in the neonatal period
- Positive Gram stain
- CSF white blood cell (WBC) count >1000/uL with a predominance of neutrophils
- Low CSF glucose concentration <40 mg/dL (2.2 mmol/L)
- Empiric treatment: high doses of a 3rd generation cephalosporin (cefotaxime, ceftriaxone) and vancomycin (this covers antibiotic-resistant S. pneumoniae, N. meningitidis, and Hib)
Hand, foot and mouth syndrome (or disease to all you lay people out there) is a common viral illness, most often caused by coxsackie virus. Generally it affects daycare-aged children (the 1-10ish age group), mostly under the age of 6. The big thing is the fever with a rash on, you guessed it, the palms, soles and in the mouth. Sometimes the rash can also present on the trunk or back as well. The worst part is that the vesicles in the mouth are VERY painful, so it’s not uncommon for kids to want to stop eating or drinking when they have it.
The danger zone on the face is a little triangle from the corners of the mouth up to the bridge of the nose. The reason it has such an epic name is because due to its venous drainage (from the facial veins and pterygoid plexus) there’s the possibility of infection traveling from that area into the cavernous sinus.
The cavernous sinuses (there’s one on each side) is an area posterior to the maxillary sinuses and lateral to the pituitary. It receives blood from the superior and inferior ophthalmic veins, superficial cortical veins and the basilar plexus. The blood then drains into the petrosal sinuses (you guessed it, there’s a superior and inferior one of those too) and then those drain into the internal jugular vein.
The thing about the cavernous sinuses a whole lot of important stuff passes through it.
- CN III (occulomotor)
- CN IV (trochlear)
- CN V1 (ophthalmic branch of trigeminal)
- CN V2 (maxillary branch of trigeminal)
- CN VI (abducens)
- Internal carotid (and the sympathetic fibres on the carotid)
This means that if you are so unfortunate as to have infection tract back into it, there can be some nasty consequences like meningitis and cavernous sinus thrombosis which will generally present as problems involving those nerves.
The abducens and carotid are more medial and thought to be more bathed in the warm loving venous drainage meaning these are generally the first to show signs of a problem a-brewin’.
With bites you need to consider not only the ton of different bacteria inhabiting the mouth of whatever/whoever was the biter, but also the flora of whatever part of the body was bitten. Mouths tend to be a schmogourbord of Gram positives and negative, aerobes and anaerobes. The two bugs to specifically keep in mind when thinking about bites are Eikenella in human bites and Pasturella in animal bites (especially cat bites).
Amox-clav is a fairly good choice for bites (of both the human and animal variety) but you need to remember that if the bite if say, on the ear, you’ll also need coverage for pseudomonas. To make matters a little more confusing Eikenella is resistant to clindamycin, macrolides, metronidazole, and fluoroquinolones. So if the bitten person is allergic to penicillins, clindamycin just won’t do.