Critical Care Pharmacy

Introducing The Elective Rotation With Pharmacy Joe, A Critical Care and Hospital Pharmacy Podcast

Episode 2 Code Response And ACLS Algorithm Review

Patients Die Less Often When Pharmacists Respond To Code Blue Calls

Why should Pharmacy Nation respond to Code Blue Calls?

It's simple.
 
Patients will die less often.  To the tune of 12,880 reduced deaths in 2007, p=0.009 according to:
 
Bond, C. A. and Raehl, C. L. (2007), Clinical Pharmacy Services, Pharmacy Staffing, and Hospital Mortality Rates. Pharmacotherapy, 27: 481–493. doi: 10.1592/phco.27.4.481
 
Even without any data I still think you should be there at the codes Pharmacy Nation!
A code is a high-stress situation with rapid decisions being made about medications - why shouldn't a pharmacist be involved?
 
You wouldn't jump from a plane without a parachute despite a lack of evidence that parachutes prevent death from gravitational challenge would you?
 
Roles and expectations of a pharmacist at a code:
  
Role 1 - Assume responsibility for the provision of pharmacotherapy
Locate/obtain necessary medications quickly and easily
Calculate doses, rates, concentrations correctly
Prepare and label medications appropriately
Provide IV compatibility information
 
Role 2 - Actively participate in medical decision making
Make treatment recommendations
Determine the cause of deterioration
 
Role 3 - Anticipate patient and provider needs and prepare in advance to meet those needs
Be the pessimist in the room and always plan for "what is the worst thing that could go wrong right now?"
Role 4 - Function as a knowledgeable team member 
Make an effort to know the purpose and location of the non-drug contents of the code cart
Be aware of what is going on around you
Other team members you can expect at the code:
 
Patient's nurse
Critical care nurse
Respiratory therapist
Patient care technician
Physician(hospitalist/intensivist/cardiologist/other)
 
How to respond
 
Remain calm!
Each code will be a different scenario; be alert and pay attention
You will become more comfortable each time you attend a code
 
At my institution, notification will come via the overhead page system and code beeper
Take stairs when possible to reach the site of the code.  The elevator will slow you down too much.

When you enter room/area identify yourself to staff already in attendance.
 
Make your initial observations:
 
What does the patient look like?
Are chest compressions being performed?
Respiratory distress?
Unresponsive?
Alert?
What other team members are present?
Get to work:
 
If the medication tray has not been removed from the cart, remove it, place it on a flat surface, and open the plastic wrapping
 
If the medication tray has been removed already, offer to assume responsibility for the medications
 
Identify the physician running the code
Identify the nurse recording events
Identify the nurse administering medications
 
Stand by the medication tray in sight of the physician running the code
 
If possible, be in view of the ECG monitor
 
At the start of the code open and assemble an epinephrine syringe
Obtain 6 NS flushes and prepare them for immediate use
Attach a needle to a 10 mL syringe
 
Locate additional supplies as necessary for requested medications
Stay focused on the physician running the code
 
 
We’ll continue this discussion in the next episode
 
Please subscribe on Android, iTunes, or your favorite pod catcher.

Episode 1 The Elective Rotation

Welcome!  Today we are talking about pharmacist participation on rapid response teams.  According to the wikipedia definition (don't tell my professors I referenced that site!):

A rapid response team (RRT) is a team of health care providers that responds to hospitalized patients with early signs of clinical deterioration on non-intensive care units to prevent respiratory or cardiac arrest.

Episode 3 Rapid Response

Shock is the syndrome that results when the cardiovascular system fails to maintain adequate tissue perfusion.

The goal is to maintain hemodynamics while the cause of shock can be addressed.  Fluids, vasopressors, and inotropes are the essential parts of the treatment of shock.  Today we'll focus on the vasopressors norepinephrine, vasopressin, epinephrine, dopamine, and phenylephrine.

Before we dive into discussing each vasopressor, lets talk dosing and administration.

Starting dose

My starting rate always depends on how close to dead the patient is.  If they are in extremis I will start at the maximum rate and titrate down.  If they are stable then I will start at the bottom and work up.

Maximum dose

Maximum doses vary greatly between institutions.  It is likely that your hospital has arbitrarily set a maximum dose for each vasopressor.  I wouldn't get too hung up on it as long as there is agreement across disciplines on your institutional max.  Maximum doses were invented to be exceeded, so don't be shocked when your doc squeezes the IV bag in while trying to stabilize that young OD patient long enough for ECMO to be started.

Peripheral vs. central line

Any port in a storm

Let's be realistic.  Many patients would suffer organ damage from profound hypotension if you waited for a central line to be placed to give them vasopressors.  If you are using vasopressors in a peripheral line, you should choose a small bore in the largest vein possible.  If the need for vasopressors persists, a central line should be placed ASAP.  In a Cochrane review the average infusion duration that resulted in complications was 55 hours.  This is especially important given the phentolamine shortage.  I wouldn't count on phentolamine alternatives (terbutaline and topical nitro paste) if I were you.

Episode 5 Vasopressor Review

Phentolamine is no longer manufactured.

Phentolamine has now made ASHP's list of drugs no longer available.

This information is critical to communicate to emergency medicine and critical care practitioners, as the risk:benefit of peripheral vasopressor therapy changes without the availability of this extravasation antidote.

This doesn't change my any port in a storm philosophy of peripheral vasopressor use, but it will make me advocate for the placement of a central line sooner in patients where I see peripheral vasopressor use continuing for more than a few hours.

The alternatives to phentolamine for extravasation from phenylephrine, norepinephrine, epinephrine, dopamine, and dobutamine are:

Apply heat proximal to site of extravasation.
Elevation of the site of extravasation.
Topical nitroglycerin 2%, apply a 1-inch strip to the site of ischemia q8 hrs prn; monitor for hypotension.
Dilute 1 mg terbutaline in 10 ml NS.  Inject locally across symptomatic sites.
The alternatives to phentolamine for extravasation from vasopressin and methylene blue are:

Apply heat proximal to site of extravasation.
Elevation of the site of extravasation.
Topical nitroglycerin 2%, apply a 1-inch strip to the site of ischemia q8 hrs prn; monitor for hypotension.
The alternatives to phentolamine for extravasation from epinephrine autoinjector are:

Watchful waiting
Topical nitroglycerin 2%, apply a 1-inch strip to the site of ischemia q8 hrs prn; monitor for hypotension.
Dilute 0.5 to 1 mg terbutaline in 1 ml NS.  Inject locally across symptomatic sites (it is usually the finger).

Episode 6 Alternatives To Phentolamine

So much of antibiotic selection has to do with local resistance patterns, and it cannot be protocolized or generalized without that knowledge.

That said I believe there are some principles of antibiotic selection in the ICU that are worth discussing in general terms.  A big shout out to pharmacist Sokhak & physician Mary for suggesting this topic.  If you would like to suggest a topic for the show head on over here.

Today we will talk about:

Source identification and control
Knowing the antibiotic spectrum of activity
Selecting empiric therapy against likely pathogens
Renal dose adjustment of initial empiric therapy

critical care pharmacy

Episode 8 Empiric Antibiotics

Today I’m going to pull the curtain back and show you how I trained myself to have successful verbal communications with physicians, and get my interventions accepted.
 
We’ll go over: 
Expected acceptance rates
First impressions of your conversation
Planning out your conversation
What to do when the physician comes to you with a question

pharmacy podcast

Episode 9 How To Talk Like A Physician And Get A Physician To Listen Like A Pharmacist

Bonus Full RT Pete Interview

Show notes at pharmacyjoe.com/episode31

In this episode, I will:

Review an article about monitoring vancomycin by trough levels
Answer a drug information question:  Why do some of my trauma patients get heparin and some enoxaparin for DVT prophylaxis?
Share sleep hygiene resources that I personally use.
Article

Vancomycin Trough Concentration as a Predictor of Clinical Outcomes in Patients with Staphylococcus aureus Bacteremia: A Meta-analysis of Observational Studies

Author:  John P. Prybylski

Published in Pharmacotherapy October 24, 2015

Background

Can you believe vancomycin is over 50 years old and we still don’t know the best way to dose it?

Joint guidelines on dosing vancomycin were published by the Infectious Disease Society of America and the Association of Health Systems Pharmacists in 2009.

In these guidelines the authors recommend attaining a trough of 15-20 mg/L when treating serious infection due to Staphylococcus aureus.

This trough goal of 15-20 mg/L in serious infection was controversial when it came out in 2009 and remains so today.

This goal was proposed as a way to ensure that patients achieve the ideal 24-hour area under the concentration-time curve to minimum inhibitory concentration ratio (AUC:MIC) of at least 400 hours.  However, analyses have demonstrated that patients with adequate renal function can typically achieve the AUC:MIC goal with a more conservative trough 

Episode 31 Vanco Dosing By AUC - MIC, Heparin Vs LMWH, And Sleep Hygiene Resources

Show notes at pharmacyjoe.com/episode34

In this episode I’ll:
1. Review how to recognize severe hyperkalemia
2. Review the 3 categories of hyperkalemia treatments and the order which they should be used
3. Discuss the nuances of each treatment

Recognizing hyperkalemia

Severe hyperkalemia can be recognized by cardiac conduction abnormalities on ECG, muscle weakness / paralysis, or a serum potassium value greater than 7. In a patient without chronically high potassium, a value lower than 7 may still have severe consequences.

While a patient with severe hyperkalemia can progress from any level of ECG change to ventricular tachycardia / ventricular fibrillation / asystole, in general a peaked T wave with shortened QT interval is the earliest change , followed by progressive lengthening of the PR interval and QRS duration. The P wave may disappear, and ultimately the QRS widens further to a sine wave until asystole occurs.  Don't bother trying to learn at which level of potassium the ECG changes occur - the changes do not correlate well with the serum potassium concentration.

critical care

Episode 34 Severe Hyperkalemia Treatment

Show notes at pharmacyjoe.com/episode45

In this episode I'll:

1. Review an article about using melatonin to decrease the need for sedation in the ICU
2. Answer the drug information question "How long can I take NSAIDs before I need to take GI prophylaxis?
3. Share a resource I use when taking care of a patient with myasthenia gravis

Article

Melatonin reduces the need for sedation in ICU patients: a randomized controlled trial

Lead Author: Giovanni Mistraletti

Published in the journal Minerva Anestesiologica December 2015

Background

Critically ill patients suffer from physiological sleep deprivation and have reduced blood melatonin
levels.

Purpose

The purpose of this study was to determine whether nocturnal melatonin supplementation would reduce the need
for sedation in critically ill patients.

Methods

This double-blind randomized placebo-controlled trial was carried out in a mixed medical-surgical Intensive Care Unit in Milan, Italy.  Of 1158 patients admitted to ICU, 82 critically-ill patients with mechanical ventilation >48 hours and Simplified Acute Physiology Score II > 32 points were randomized 1:1 to receive melatonin 3 mg at eight p.m. and midnight, or placebo from the third ICU day until ICU discharge.  The primary outcome was the total amount of enteral hydroxyzine administered (more about this interesting outcome later).  

Results

Melatonin treated patients received a lower amount of enteral hydroxyzine. Other neurological indicators
(the amount of neuroactive drugs, pain, agitation, anxiety, sleep observed by nurses, need for restraints, need for
extra sedation, and nurse evaluation of sedation adequacy) seemed improved, with reduced cost for neuroactive drugs.
Post-traumatic stress disorder prevalence did not differ between groups, nor did ICU or hospital mortality. Study
limitations include the differences between groups before intervention, the small sample size, and the single-center
observation.

Conclusion

The authors concluded that long-term enteral melatonin supplementation may result in a decreased need for sedation, with improved
neurological indicators and cost reduction. Further multi-center evaluations are required to confirm these
results with different sedation protocols.

Episode 45 Melatonin Decreases Need For ICU Sedation, NSAIDS & GI Prophylaxis, & Myasthenia Gravis

Show notes at pharmacyjoe.com/episode46

In this episode I'll review the pharmacologic treatments for anaphylaxis.

Definition

Anaphylaxis is a potentially fatal allergic reaction with a rapid onset.

Immunoglobulin E (IgE)-mediated allergic reactions to food, insect stings and medications are the most common triggers for anaphylaxis.

As a result of the IgE reaction, mast cells release histamine and other mediators of anaphylaxis. If not properly treated, it will progress to respiratory arrest and cardiovascular collapse.

Diagnostic criteria

According to World Allergy Organization guidelines, anaphylaxis is highly likely when any one of the following three criteria is fulfilled:

1. Acute onset of an illness (within minutes to several hours) with involvement of the skin, mucosal tissue, or both (eg, generalized urticaria, itching or flushing, swollen lips-tongue-uvula)
AND AT LEAST ONE OF THE FOLLOWING:
A) Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)
B) Reduced blood pressure or associated symptoms of end-organ dysfunction (eg. hypotonia [collapse], syncope, incontinence)

2. Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (within minutes to several hours)
A) Involvement of the skin-mucosal tissue (eg, generalized urticaria, itch-flush, swollen lips-tongue-uvula)
B) Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)
C) Reduced blood pressure or associated symptoms (eg, hypotonia [collapse], syncope, incontinence)
D) Persistent gastrointestinal symptoms (eg, crampy abdominal pain, vomiting)

3. Reduced blood pressure after exposure to known allergen for that patient (within minutes to several hours)
A) Infants and children: low systolic blood pressure (age-specific) or greater than 30% decrease in systolic blood pressure
B) Adults: systolic blood pressure of less than 90 mm Hg or greater than 30% decrease from that person's baseline
Treatment of anaphylaxis

Epinephrine, IV fluids, and airway management are the main treatments for anaphylaxis.

Epinephrine

Epinephrine is the drug of choice for anaphylaxis.  Epinephrine has no absolute contraindications to use in the treatment of anaphylaxis.

Epinephrine stabilizes mast cells, prevents or reverses obstruction to airflow in the upper and lower respiratory tracts and prevents or reverses cardiovascular collapse.

Intramuscular (IM) injection is the preferred route of administration for the treatment of anaphylaxis.  Several different preparations of epinephrine are available - take care to select the correct one!   The epinephrine preparation for intramuscular injection contains 1 mg per mL and will also be labeled as epinephrine 1:1000.

The recommended adult dose of epinephrine (1 mg per mL) is 0.3 to 0.5 mg per single dose, injected IM into the mid-outer thigh. If needed, this dose may be repeated every 5 to 15 minutes.

Occasionally patients with extreme anaphylactic reactions do not adequately perfuse muscle tissue and therefore do not respond well to IM injection of epinephrine.  If this occurs, administer epinephrine via an infusion pump at a rate of 2 to 10 mcg /minute (or 0.1 mcg / kg / minute).

Episode 46 Pharmacologic Treatments For Anaphylaxis

Show notes at pharmacyjoe.com/episode55

In this episode I’ll:

1.  Discuss an article that found an increase in mortality when succinylcholine was used for rapid sequence intubation in patients with traumatic brain injury.
2.  Answer the drug information question "Do antibiotics need to be stopped prior to fecal microbiota transplantation (FMT) to treat clostridium difficile infection?"
3. Share a resource I use during in-hospital medical emergencies.

Article

Succinylcholine Is Associated with Increased Mortality When Used for Rapid Sequence Intubation of Severely Brain Injured Patients in the Emergency Department.

Lead author:  Asad Patanwala
Published in the journal Pharmacotherapy January 2016

Background

The "Sux vs Roc" debate over whether to use succinylcholine or rocuronium in the setting of rapid sequence intubation (RSI) has been going on for a long time.  I gave my opinion on the matter back in episode 14.  

Purpose

The purpose of this article was to compare mortality in patients with traumatic brain injury (TBI) who received either succinylcholine or rocuronium for rapid sequence intubation.

Methods

The study examined a retrospective cohort in an academic emergency department (ED) in the United States. The cohort consisted of adult patients with TBI who underwent rapid sequence intubation (RSI) in the ED with rocuronium or succinylcholine between October 2010 and October 2014. The main outcome of interest was in-hospital mortality. Subjects were stratified based on severity of injury using head abbreviated injury scores. The high-severity group had a severe or critical head injury (score 4 or higher); the low-severity group had a less than severe head injury (score lower than 4).

Results

A total of 233 patients were studied; 149 received succinylcholine and 84 received rocuronium.  In patients who received rocuronium, mortality was

Episode 55 Sux Vs Roc In Brain Injury, Stopping Antibiotics In Fecal Microbiota Transplant & more

Show notes at pharmacyjoe.com/episode64

In this episode I'll discuss how I identify drug fever.

Background

Drug fever is a common condition that coincides temporally with the administration of a drug and disappears after discontinuation of the medication. Unfortunately it is usually an unclear diagnosis, often made by exclusion.

It is just as valuable to the healthcare team for the pharmacist to identify a drug that might be causing fever as it is to identify when medications are not involved in causing a fever.

An excellent review of drug fever was published by Ruchi Patel in Pharmacotherapy 2010.

A fever often leads clinicians to suspect and treat infection. For this reason drug fever can lead to over-utilization of antibiotics, putting a patient at risk of adverse effects and the development of antimicrobial resistance.

Drug fever that occurs during the course of treating an infection may mislead clinicians into believing that the patient is not responding to treatment for the infection.

Drug fever may precede or accompany more serious adverse drug reactions.

A key feature that differentiates drug fever from fever of other causes is that it disappears once the offending drug is discontinued.

Many medications have been implicated in drug fever. I discussed in episode 27 how dexmedetomidine has been associated with drug fever. In episode 40 I discussed severe hyperthermia from serotonin syndrome, malignant hyperthermia, and neuroleptic malignant syndrome.

The most frequent drugs implicated are antimicrobials, anticonvulsants (carbamazepine and phenytoin), anti-arrhythmic agents (procainamide and quinidine), and other cardiac agents.  Here is a list of other medications that may cause drug fever.

Identification of drug fever

Identifying drug fever is complicated because fever can be a characteristic of many disease processes other than infection, including malignancy, thromboembolic disease, cerebrovascular accidents, collagen vascular diseases, acute gout, surgery, and trauma.

To identify drug fever, I

Episode 64 How To Identify Drug Fever

Show notes at pharmacyjoe.com/episode73

In this episode I'll:

1. Discuss an article about calcium correction in the ICU
2. Answer the drug information question "What weight should be used to calculate an initial dose of IV immune globulin (IVIG)?"
3. Share a resource about open access medical journals.

Article

Ionized Calcium in the ICU: Should It Be Measured and Corrected?

Author: Scott Aberegg
Published in CHEST March 2016

Shout out to “Intensivist Anna” for bringing this review article to my attention.

Calcium is vital for many functions, including muscle contraction and coagulation (it is also called clotting factor IV!).

Abnormal calcium levels in ICU patients are a common occurrence, but these levels are not usually due to a disorder in calcium homeostasis.

Routine monitoring and correction of calcium levels is commonplace in many ICUs, including my institution. However routine efforts to correct the serum calcium level only treat the laboratory number; there is no evidence that replacement has an effect on patient morbidity and mortality.

The author of this review article makes the point that

Episode 73 Calcium Correction In The ICU, IVIG Dosing Weight, & Open Access Medical Journals

Show notes at pharmacyjoe.com/episode74

In this episode I'll discuss monitoring continuous infusions of neuromuscular blocking agents.

The non-depolarizing neuromuscular blocking agents (NMBAs) cisatracurium, rocuronium, and vecuronium are occasionally given as a continuous infusion in critically ill patients.

These medications paralyze all skeletal muscle, including the diaphragm muscle.

Adverse effects

NMBAs, especially the steroid-based rocuronium and vecuronium are associated with reports of prolonged recovery and myopathy. For this reason it is critical to use the lowest possible NMBA dose for the shortest possible duration.

Indications

Continuous infusions of neuromuscular blocking agents are usually given to critically ill patients for 1 of 2 reasons:

1. To facilitate mechanical ventilation
2. To prevent movement

To facilitate mechanical ventilation

When given to facilitate mechanical ventilation, NMBAs prevent dysynchrony with the ventilator, stop spontaneous respiration and muscle movement, and improve gas exchange.

To prevent movement

When given to prevent movement, NMBAs are used in patients with

Episode 74 Monitoring Continuous Infusions Of Neuromuscular Blocking Agents (NMBAs)

Show notes at pharmacyjoe.com/episode75

In this episode I'll discuss the drug ciraparantag.

Shout out to Pharmacy Lawrence on Twitter for requesting this topic!

If you are not on Twitter you should consider it. I believe it is the best social media platform to use for education and collaboration with other healthcare providers. For more information listen to episode 69 where I discuss using twitter hashtags for free open access medication education. You can find me on twitter as @PharmacyJoe.

Ciraparantag or PER977 is a broad spectrum anticoagulant reversal agent under fast track review at the FDA.

Ciraparantag is reported to antagonize the effects of all anticoagulants except warfarin and agratroban - even enoxaparin and fondaparinux!

Not much is published on the exact mechanism of action for PER977. According to a letter to the editor published in NEJM November 2014: 	

Episode 75 When Will The FDA Approve Ciraparantag  PER977

Show notes at pharmacyjoe.com/episode76

In this episode I’ll discuss how to use dexmedetomidine for sedation in the ICU. If you are wondering about the use of dexemedetomine in agitated delirium or alcohol withdrawal, check out episodes 67 & 70.

Mechanism of action

Dexmedetomidine is a selective a2-adrenoceptor agonist. I like to think of it as an intravenous version of clonidine. As a sedative, dexmedetomidine is unique in that it:

1. Does not suppress the respiratory center
2. Acts as an analgesic adjunct, reducing the dose of opioids required

Cost

Despite having recently been made available as a generic medication in the US, dexmedetomidine has the highest drug cost when compared to propofol or midazolam.

Adverse effects

Dexmedetomidine commonly causes bradycardia and hypotension at rates that are similar to those of 

Episode 76 How To Use Dexmedetomidine For ICU Sedation And Ventilator Weaning

Show notes at pharmacyjoe.com/episode77

IIn this episode I'll:

1. Discuss an article that looks at the incidence of acute kidney injury in ICU patients receiving vancomycin and piperacillin-tazobactam
2. Answer the drug information question "Should 2.5% dextrose ever be infused?"
3. Share a resource about G6PD deficiency

Article

Comparative Incidence of Acute Kidney Injury in Critically Ill Patients Receiving Vancomycin with Concomitant Piperacillin-Tazobactam or Cefepime: A Retrospective Cohort Study

Lead author: Drayton Hammond
Published online in Pharmacotherapy April 2016

Background

Beta-lactam antibiotics are usually

Episode 77 Acute Kidney Injury With Vancomycin And Piperacillin - Tazobactam, Hypotonic Dextrose

Show notes at pharmacyjoe.com/episode78

In this episode I’ll discuss My secret to learning, recalling, and applying pharmacotherapy knowledge to patient care: correlating mechanism of action to the pathophysiology of disease.

Earlier in my career, I noticed that most physicians and some other more experienced clinicians seem to have this natural ability to apply their knowledge to any patient scenario, no matter how complex.

I often wondered, “How can I do that?” So, I began to observe, talk with, and study these clinicians and how they analyze and act when caring for a patient.

After careful study, I have arrived at a method to learn, recall, and apply pharmacotherapy knowledge to patient care. I call this method 

Episode 78 Correlating Mechanism Of Action To Pathophysiology Of Disease

Show notes at pharmacyjoe.com/episode79

If you haven’t been hit by the methylprednisolone shortage yet, get ready…it looks like it may be coming to a pharmacy near you!

According to the ASHP drug shortage bulletin, 40 and 125 mg vials of methylprednisolone are in short supply. Pfizer appears to be experiencing a manufacturing delay, and Fresenius Kabi states the reason for the shortage is increased demand.

This isn’t the first time we’ve faced a shortage of methylprednisolone. In 2011 and 2014 similar problems occurred.

Can an equivalent dose of another corticosteroid be substituted? Dexamethasone is probably the steroid most similar to methylprednisolone.

Compared to methylprednisone, dexamethasone also has no mineralcorticoid activity but is a bit longer acting. Finding a steroid equivalency chart is the easy part. In this episode I’ll review the evidence behind some alternative corticosteroids.

COPD

For patients with a COPD exacerbation, methylprednisolone was compared to

Episode 79 Methylprednisolone Shortage Alternatives

Show notes at pharmacyjoe.com/episode80

In this episode I’ll discuss the drug phenytoin.

Indications

Common indications for the use of phenytoin are:

Control of generalized tonic-clonic and complex partial (psychomotor, temporal lobe) seizures

Prevention and treatment of seizures occurring during or following neurosurgery

Prevention of early (within 1 week) post-traumatic seizures following traumatic brain injury

Initial dose

The initial dose of phenytoin is a loading dose of 15-20 mg/kg, followed by a maintenance dose of 5-6mg/kg/day.

How can I tell if the phenytoin concentration is therapeutic?

To determine if a patient has a therapeutic phenytoin level, I look at 4 things in the following order:

Episode 80 Phenytoin Dosage, Adjustment, And Monitoring

Show notes at pharmacyjoe.com/episode81

In this episode, I’ll:

1. Discuss an article about using tigecycline for clostridium difficile infection.
2. Answer the drug information question “Has mycophenolate ever been associated with avelor hemorrhage?"
3. Share a resource that can be used to determine a patient’s warfarin dose.

When tigecycyline first arrived on the market it was called a - 1st in class antibiotic - a glycycycline. The drug was accompanied by tigers walking next to doctors in the advertisements, and a black-box warning about increased mortality after a meta-analysis of phase 3&4 trials. This prompted me to look closer at tigecycline. I noticed that tigecycline is structurally identical to minocycline, with an extra 4-carbon chain dangling off one end. I immediately thought:

Episode 81 Tigecycline For Clostridium Difficile, Mycophenylate Induced Aveolar Hemorrhage,

Show notes at pharmacyjoe.com/episode82

In this episode I'll discuss cyanide toxicity.

Cyanide is a rapidly lethal toxin. It causes death within minutes to hours of exposure.

Cyanide inhibits oxidative phosphorylation in the mitochondria, shutting down aerobic metabolism. Oxygen supply remains adequate but cells are unable to utilize the oxygen.

Cyanide is present in low background levels in the environment and is safely metabolized to thiocyanate by the liver. The capacity to metabolize cyanide is limited, and just ~0.5mg/kg is enough to be fatal.

Cyanide toxicity is relatively rare. Domestic fires, industrial accidents, and sodium nitroprusside are more common possible causes of cyanide poisoning.

Fabrics, upholstery, and melamine (often used as a coating on shelves and cabinets) can all give off cyanide when burned.

Cyanide is used in the extraction of gold and silver, and the production of nylon.

The antihypertensive sodium nitroprusside contains cyanide. Cyanide toxicity may occur in patients who receive prolonged infusions of sodium nitroprusside, have chronic renal failure, or in pediatric patients. Significant toxicity has resulted from rates higher than

Episode 82 Cyanide Poisoning

The Elective Rotation

Episode 177: Vitamin C, hydrocortisone, and thiamine for severe sepsis and septic shock

The Elective Rotation - the #1 Hospital Pharmacy podcast in iTunes - is created for YOU Pharmacy Nation!  If you are a Pharmacy Student, Resident, Pharmacist, or Critical Care Practitioner in a hospital, intensive care unit (ICU) or emergency department looking to improve your practice, The Elective Rotation delivers expert critical care and hospital pharmacy content from a Board Certified Pharmacotherapy Specialist. Episodes are published every Monday and Thursday at 3AM EST. Find the show notes at pharmacyjoe.com. 

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