Tag Archives: pharma

Stress Dose Steroids

WHEN IS STRESS DOSE STEROIDS INDICATED?

  • depends on history of steroid intake and likelihood of HPA supression + type and duration of surgery
  • NONSUPPRESSED HPA AXIS: 
    • < 3 weeks of steroids at any dose
    • prednisone <5mg/daily for any duration
    • prednisone <10mg every other day
    • PLAN:  continue same regimen perioperatively; no need for cosyntropin test or stress dose steroids
  • SUPPRESSED HPA AXIS
    • prednisone >20mg/day x 3 weeks or more OR Cushingoid appearance
    • PLAN:
      • give stress dose steroids based on type and duration of surgery (see below)
  • INTERMEDIATE HPA SUPPRESSION (Unknown HPA Axis suppression, previous 3 or more intraarticular or spinal steroid injections within 3 mos prior to suregery)
    • PLAN
      • evaluate HPA axis 
        • check AM cortisol (8a.m.) after 24h off steroids
        • if <5 ug/dL – likely suppressed axis; give stress dose steroids
        • if >10 ug/dL – likely no supression; continue current dose on day of surgery
        • if 5-10 ug/dL – ACTH stim test or empiric stress dose steroids
      • ACTH stim test (standard is 250 ug):
        • if serum cortisol <18 ug/dL 30 mins after ACTH – give stress dose steroids
        • if >serum cortisol >18 ug/dL 30 mins after ACTH – no stress dose steroids

 

STEROIDS BASED ON TYPE AND DURATION OF SURGERY

MINOR PROCEDURES / LOCAL ANESTHESIA – stress dose not necessary, take AM steroids

MODERATE SURGICAL STRESS: (eg. LE revascularization, total joint replacement)

  1. take AM steroids
  2. hydrocortisone 50mg IV prior to procedure, 25mg IV q8h x 24h
  3. resums usual dose after

MAJOR SURGICAL STRESS (e.g open heart surgery, proctocolectomy, esophagogastrectomy)

  1. take AM steroids
  2. hydrocortisone 100mg IV before induction of anesthesia
  3. hydrocortisone 50mg q8h x 24h
  4. taper by half per day to maintenance dose

 

 

 

Reference:

Uptodate.com. (2018). UpToDate. [online] Available at: http://www.uptodate.com/contents/the-management-of-the-surgical-patient-taking-glucocorticoids?search=stress+dose+steroids&source=search_result&selectedTitle=1~60#H6 [Accessed 25 Mar. 2018].

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Treatment of Native Vertebral Osteomyelitis (IDSA, 2015)

Parenteral Antimicrobial Treatment of Common Microorganisms Causing Native Vertebral Osteomyelitis

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Reference:

Berbari, Elie F. et al. “2015 Infectious Diseases Society Of America (IDSA) Clinical Practice Guidelines For The Diagnosis And Treatment Of Native Vertebral Osteomyelitis In Adults”. Clinical Infectious Diseases 61.6 (2015): e26-e46. <PDF link>

 

Sulfa Allergy

Drugs to avoid in patients with sulfonamide allergy:

Antimicrobials

  • Sulfamethoxazole
  • Sulfamerazine
  • Sulfamethizole
  • Sulfamoxole
  • Sulfamethazine
  • Sulfoxazole
  • Sulfapyridine

Nonantimicrobials (diuretics, triptans, oral hyopglycemics, antiinflammatories)

  • Bumetanide
  • Furosemide
  • Celecoxib
  • Acetazolamide
  • Sumatriptan
  • Hydrochlorothiazide Diazoxide
  • Glyburide
  • Sulfasalazine

 

Reference:

 

Uptodate.  “Sulfonamide allergy in HIV-uninfected patients.” Accessed 03/13/2017.

Antibiogram (LHH-Year 2015)

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LHH Antibiogram

Medications Used to Treat Seizures and Status Epilepticus in Adult ICU Patients

AEDs in the ICU.

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From ENLS:


Mechanism of action

  1. Benzodiazepines – stimulates GABA A receptor subunits, leads to inhibition of transmission through chloride channel-induced hyperpolorization of resting cells embrane, at high levels Benoza function in a manner similar to phenytoin

 

Neurocritical Care Society provided dosing cards for IV and PO AEDs in their website for free.  See links below for PDF files.

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Reference:

Tesoro, Eljim P. and Gretchen M. Brophy. “Pharmacological Management Of Seizures And Status Epilepticus In Critically Ill Patients”. Journal of Pharmacy Practice 23.5 (2010): 441-454. Web.

Manno, in The Neurohospitalist

Medication Dosing Cards | NCS. (2019). Retrieved from https://www.pathlms.com/ncs-ondemand/courses/2653/sections/12865

 

tPA Dosing Chart + Flowsheets post-tPA

Total Dose = 0.9 mg/kg (maximum dose =90 mg): give 10% of dose as IV bolus over 1minute; infuse remainder over 1 hour
(Reconstitute Activase 100 mg vial with 100 ml sterile water = 1mg/ml)

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<click here for MSWord document>

IV-tPA-Dosing-Chart

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tPA Dosing Chart

References:

“Acute Stroke Protocol”. Boston Medical Center. N.p., 2017. Web. 16 Jan. 2017.

Strokecarenow.com. (2017). [online] Available at: http://www.strokecarenow.com/wp-content/uploads/IV-tPA-Dosing-Chart.pdf [Accessed 18 Nov. 2017].

Ketamine in Status Epilepticus

Problem:  prolonged status epilepticus leads to upregulation of NMDA receptors, glutamate-mediated excitotoxicity and resistance to conventional antiepileptics.
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Definitions:

1.  Refractory status epilepticus – either generalized or complex partial status epilepticus that fails to respond to first and second line therapies

2.  Superrefractory status epilepticus – status epilepticus that remains unresponsive despite 24 hours of therapy with general anesthesia
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Mechanisms of conventional AEDs:
  1. GABA agonist – cortical inhibition / reduction of epileptogenicity and lateral spread; e.g. benzodiazeipne, valproate, propofol, barbiturates, clonazepam, clobazam, vigabatrin, and topiramate
  2. Na blockers – phenytoin, carbamazepine, lamotrigine, oxcarbazepine, zonisamide, and rufinamide
  3. Ca blockers – gabapentin and pregabalin,

 

Molecular Changes in Prolonged Status Epilepticus:

  1. GABA A downregulation – depletes receptors for benzodiazepines, etc, also subunit alterations in GABAA receptor lead to impaired binding –> resistance to GABA-mediated AEDs
  2. p-glycoprotein molecular transporter upregulation – occurs at the level of BBB ~20 to 30 minutes into status epilepticus; these transporters export phenytoin and phenobarbital molecules and efficacy of phenytoin and phenobarbital is greatly diminished
  3. upregulation of NMDA receptors – leads to glutamate-mediated activation of these receptors, leads to intracellular calcium influx and excitotoxicity
  4. proinflammatory mediators can also alter BBB permeability and induce neuronal damage which can lead to AED resistance and excitotoxicity

 

Advantages of Ketamine in RSE / SRSE:

  • NMDA receptor antagonists target a receptor known to be upregulated during SE/RSE/SRSE
  • NMDA receptor antagonists provide neuroprotection (studied in TBI population)
  • drug is readily available and cheap
  • sympathomimetic properties = vasopressor sparing effects
  • side effect profile low

 

Possible Complications:

  • arrhythmias
  • hypersalivation
  • mild hypertension
  • hallucinations
  • ICP elevation? – old literature, should not be factored in

 

Notes:

  • Effectivity:  110 patients = 56.5% responded (cessation of SE)
  • Duration of Treatment:  16 hours to 140 days
  • Usual dosing: bolus 0.5 to 5 mg/Kg then continuous infusion 0.12 to 10mg/kg/hr, duration of 2h to 27d
  • most common duration: 7 days, most responding within 48-72h
  • Start ketamine within 24-48 hours of SE onset, after failure of first trial with anesthetics of choice (midazolam, propofol, pentobarbital)
  • Suggested dosing:  bolus 3mg/kg, followed by continuous infusion up to 10mg/kg/hr, duration up to 7 days

 

Reference:

Zeiler, F. A. “Early Use Of The NMDA Receptor Antagonist Ketamine In Refractory And Superrefractory Status Epilepticus”. Critical Care Research and Practice 2015 (2015): 1-5.