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Osteomyelitis, AKI - Coggle Diagram
Osteomyelitis
Pharmacologic Treatment
Cephalosporins
Cefazolin
Adult: 2 g q8h IV
Children: 25-100 mg/kg/day divided every 8 hours (MAX 6 g/day)
1st generation
Cefuroxime
Adult: 1.5 g IV or IM q8h
Children: 50 mg/kg IV or IM q8h (MAX 1500 mg/dose)
2nd generation
MOA: inhibit bacterial cell wall synthesis
3rd- or 4th generation used in combination with vancomycin for empiric treatment
Ceftriaxone
3rd generation
Adult: 2 g q24h (generally x 6 weeks)
Children: 50-75 mg/kg once daily (MAX 1 g/day)
Vancomycin
Treatment of choice when >10% of local S. aureus isolates are methicillin resistant
Adult: 15 mg/kg IV q12 h
Children: 60 mg/kg/day in 4 equally divided doses
TDM: trough 15 mg/L or AUC of 400
MOA: Inhibits bacterial cell wall synthesis by binding the D-ala D-ala portion of the cell wall precursor unit to block plymerization
ADE: Anaphylaxis, C. diff infection, reversible nephrotoxicity, irreversible ototoxicity, red man syndrome (infuse slowly)
PK/PD: large Vd, 55% protein binding, eliminated unchanged in urine
Linezolid
Adult: 600 mg IV or PO q12h
Children: 30 mg/kg/day in 3 equal doses (MAX dose 1.2 g for no more than 28 days)
Long term use can lead to cytopenias
MOA: Inhibits bacterial protein synthesis by
binding to bacterial 23S ribosomal RNA of the 50S subunit
.
Gram + infection: AUC/MIC goal: >~105, higher AUC targets may be needed for bone infection
ADE: diarrhea, vomiting, headache, decrease platelet counts,decrease white blood cells
Clindamycin
Adult: 400 IV q8-12h OR 300-600 mg PO q6h
Children: 40 mg/kg/day in 4 equal doses (MAX dose is 3 g daily)
Recommended as second line for sensitive staphylococcal infection
MOA: Reversibly binds to 50S ribosomal subunits preventing peptide bond formation thus inhibiting bacterial protein synthesis; bacteriostatic or bactericidal depending on drug concentration, infection site, and organism
BBW: C.Diff-associated diarrhea
PD/PK
Must be hydrolyzed in the GI tract before it is active
Metabolized by CYP3A4
ADE: injection site pain (IV), diarrhea, GI upset, metallic taste
Doxycycline
Adult: 100 mg PO BID
ADE: Esophagitis, esophageal ulcer, and/or esophageal stenosis, skin photosensitivity rxn, teeth staining, diarrhea, GI upset
MOA:
Inhibits protein synthesis by binding with the 30S
and possibly the 50S ribosomal subunit(s) of susceptible bacteria
PD/PK:
Absorbed in the GI track
Partially inactivated by chelation formation
Excreted in feces (30%) and urine (23 to 40%)
Sulfamethoxazole-trimethoprim
MOA: interferes with bacterial folic acid synthesis and growth
Dose: Adult: 5-10 mg/kg PO q24h (1 DS tablet = 160 mg) or 8-20 IV mg/kg/day, Children: 6-12 mg/kg/day PO or IV q12h
PK/PD: hepatic metabolism (CYP2C9)
Most S. aureus strains are susceptible
Empiric Therapy
: Vancomycin PLUS third- or fourth- gen. cephalosporin (MRSA plus gram negative coverage)
Targeted Therapy: perform bone biopsy or blood culture for HO
Treatment duration
is 4-6 weeks
Pathophysiology
Hematogenus osteomyelitis
HO in neonates:
involves multiple bones
bridging vessels go across the epiphyseal plate from the metaphysis into the epiphysis.
infection is able to spread from under the periosteum directly to the joint
HO in 12-18 month:
Involves one bone - likely to infect long bones: femur, tibia, humerus, and tibula
likely to occur due to trauma
sequestrum: subperiosteal abscess impairs blood flow to the outer portion of the cortical bone resulting in dead bone
involucrum: raised boen growing overtop of the infection
HO in adults: remains intramedullary - periosteum is tightly bound to the cortex, which is thick, causing it to hardly infiltrate to other parts of the body
Vertebral osteomyelitis
usually monomicrobial
common in adults > 50yo - lumbar + thorasic regions are the most infected locations
usually in vascular areas near the subchondral plate region of the vertebral body
Direct inoculation Osteomyelitis
direct entrance of organisms from sources outside the body - i.e. trauma, orthopedic surgery, open fractures, nail punctures in foot
Contiguous spread Osteomyelitis
polymicrobial
anaerobic osteomyelitis pre-disposing factors: vascular disease, peripheral neuropathy, trauma, bites, abcess
Causative pathogens:
S. Aureus >80% of cases (VO and HO)
Streptococci (HO)
E. coli (VO and HO)
Enterobacteriaceae (VO)
Klebsiella pneumoniae (VO)
Kingella kingae in children 3 months- 4 years old
Treatment Goals
Resolve infection: afebrile, decrease in ESR
Prevent long-term sequelae
Return patient to pre-morbid functional status
Prevent dissemination of disease
Clinical Presentation
Symptoms: significant tenderness, swelling, fever, chills, decreased motion, and malaise
Lab values: elevated erythrocyte sedimentation rate, C-reactive protein, positive blood cultures
Bone changes observed on radiographs 10-14 days after onset; magnetic resonance imaging and technetium scans positive as early as 1 day after onset
Nonpharmacologic Treatment
Joint drainage
Joint rest
Sequestrum resection
Monitoring
Resolution of sx (eg. pain, limb/joints swelling, instability
Presence of adverse effects (eg. cytopenias, diarrhea, hypersensitivity rxn)
Pts' adherence to treatment plan
Outpatient Parenteral Antimicrobial Therapy (OPAT)
Inclusion criteria: receiving stable treatment, motivated to participate, have good venous access, support from family/neighbors, and the means to store drugs safely
Exclusion criteria: poor eyesight or dexterity, or recent hx of IV drug abuse
Patients must undergo training in the following areas to utilize OPAT: aseptic technique, proper catheter care, and administration techniques
Special populations
IV drug users: >50% of infections will occur in the vertebral column; infections are not common in the extremities; MRSA is more commonly seen in this population; gram-negative species are more common
Hemoglobinopathies: 2/3 of infections are caused by Salmonella species; osteomyelitis can be relatively advanced when found due to inaccurate initial dx of sickle cell crisis
AKI
Diagnosis
SCr used to estimate CrCL and eGFR
Limitations: it is affected by age, gender, race, muscle mass, diet and hydration status (eg. low muscle mass -> low values)
When source is unclear - imaging techniques (abdominal radiography, CT, ultrasonography may be helpful)
BUN
Limitations: urea production
and renal clearance are heavily influenced by extrarenal factors such as critical illness, volume status, protein intake, and medications
Urine Output
Pathophysiology
Intrinsic AKI: Direct damage to the renal vasculature (uncontrolled HTN), glomeruli (lupus), tubules (nephrotoxins like contrast dyes), or interstitium
Postrenal AKI: Obstruction at any level of the urinary collection system: prostatic hypertrophy, improperly placed catheter, crystal deposition in tubules
Prerenal AKI: prolonged hypoperfusion of the renal tissue either (1) with systemic hypotension caused by hemorrhage, dehydration, diuretics, etc. or (2) without systemic hypotension caused by renal artery occlusion
Treatment Goals
Minimizing the degree of insult to the kidney
Reducing external complications
Expediting the pt's recovery of kidney function
Prevention
Critical - there is no treatment to reverse the insult once it has developed
Statins: have anti-inflammatory, antioxidant, and endothelium protective effects
Glycemic control
Medications that can induce AKI
Prerenal AKI
: vasodilators, NSAIDs, COX-2 inhibitors, cyclosporine, tacrolimus, ACEIs, ARBs
Intrinsic AKI
: ahminoglycosides, amphotericin B, antiretrovirals, amtibicrobials, COX-2 inhibitors, NSAIDs, PPIs, HRAs, lithium, mercury, hydralazine
Postrenal AKI
: sulfonamides, antiretrovirals, methotrexate, triamterene, large doses of vitamin C
Pharmacologic Treatments
Currently, no drugs for treatment
Adjust doses of any meds the pt is taking to account for changes in SCr / CrCl
Clinical Presentation
Sx highly variable due to dependence on underlying etiology
Common signs: abnormal urine output, urine discoloration, edema, electrolyte imbalance, sudden weight gain, or severe abdominal/flank pain
Imbalance in patient's volume can be indication
Volume overload signs: elevated JVD, pitting edema, ascites, pulmonary crackles
Volume depletion signs: postural HTN, decreased jugular venous pressure (JVP), dry mucous membranes
Lab values to assess: BUN, serum creatinine (>1.5 x baseline in 7 days), urine sediment, urinary RBC, urinary WBC, urine Na, FENa, and urine specific gravity
Monitoring
Fluid in and outs, Weight, Electrolytes (Na, Cl, Ca, Mg), BUN. SCr, Glucose, TDM of renally cleared drugs, hemodynamics (BP, HR)
Nonpharmacologic Treatments
IV fluids to maintain blood volume
Crystalloid
Indications: SBP <100 mmHg, HR >90 bpm, hypovolemia, anuria; oliguria
Composition: 0.9% saline most commonly used
Dose/Rate: 1-3 L bolus over 15 minutes with monitoring of clinical response, maintenance isotonic fluids at 75 mL/hour
ADE: edema
chloride restrictive fluids have been associated with lower hospital mortality and decreased incidence of AKI
KDIGO recommends using isotonic crystalloids int he absence of hemorrhage.
Colloid
Indications: hemorrhagic shock, cirrhosis, advanced hepatic failure
Composition: albumin most commonly used
Dose/Rate: 500 mL of albumin 5% every 30 minutes
ADE: extravascular extravasation; anaphylaxis; pruritus, edema
Contraindicated in fluid overload or HF
Monitoring: HR; BP (MAP 65-70 mmHg, no greater than 70 mmHg); urine output (should be >0.5 mL/kg/hour); skin turgor; mucus membrane integrity; mental status, SCr, proteinuria