The Elective Rotation: A Critical Care Hospital Pharmacy Podcast

Show notes at pharmacyjoe.com/episode70. In this episode I ll discuss the treatment of severe alcohol withdrawal.

Show notes at pharmacyjoe.com/episode70

In this episode I’ll discuss the treatment of severe alcohol withdrawal.

Symptoms

Symptoms of alcohol withdrawal are the result of an increase in autonomic activity and sympathetic outflow, as well as psychomotor agitation. Commonly this manifests as diaphoresis, nausea, vomiting, tremor, and anxiety.

Severe alcohol withdrawal may progress to seizures and/or delirium tremens.

Treatment

The goal of treatment is to reduce the severity of symptoms and prevent progression to delirium tremens.

It is widely accepted that the best way to treat alcohol withdrawal in hospitalized patients is with symptom triggered benzodiazepine therapy. Such treatment results in equivalent outcomes and less benzodiazepine use compared with scheduled benzodiazepine therapy.

The use of symptom-triggered therapy has yet to be studied prospectively in patients requiring intensive care for severe alcohol withdrawal.

Evidence for treating severe alcohol withdrawal is limited to retrospective pre/post intervention reviews. From the available evidence, it appears that

Show notes at pharmacyjoe.com/episode69. In this episode I’ll: 1. Discuss an article about whether aspirin affects mortality in staph aureus bloodstream infection 2. Answer the drug information question “Why is phenylephrine such a bad vasopressor to use in sepsis?” 3. Share a resource for finding medical information on social media

Show notes at pharmacyjoe.com/episode69

In this episode I'll:

1. Discuss and article about whether aspirin affects mortality in staph aureus bloodstream infection

2. Answer the drug information question "Why is phenylephrine such a bad vasopressor to use in sepsis?"

3. Share a resource for finding medical information on social media

Article

Low-Dose Acetylsalicylic Acid Treatment and Impact on Short-Term Mortality in Staphylococcus aureus Bloodstream Infection: A Propensity Score–Matched Cohort Study

Lead author: Michael Osthoff

Published in Critical Care Medicine April 2016

Background

Experimental and observational studies provide evidence of a direct antistaphylococcal effect of aspirin. Several studies have analyzed the association between aspirin use and outcomes in intensive care patients with systemic inflammatory response syndrome and the prevention of catheter associated S. aureus bloodstream infections.

Methods

The investiators' goal was to estimate the effect of low-dose aspirin therapy on mortality in bloodstream infections caused by S. aureus compared with Escherichia coli. The study was a retrospective cohort study of 838 and 602 episodes of S. aureus and E. coli bloodstream infection in a Swiss tertiary referral center. Adult patients with S. aureus and E. coli bloodstream infection, respectively, were categorized according to low-dose aspirin therapy use and non-use before bacteremia.

Results

S. aureus bloodstream infection cases and controls were equally matched for relevant confounders except treatment with statins, which was strongly associated with a low-dose aspirin use. At day 30, 12.1% of cases and 27.4% of controls had died. Low-dose aspirin use was associated with a reduced 30-day all-cause mortality in multivariate analysis of matched patients and also of the entire cohort after adjustment. In contrast, low-dose aspirin use was not associated with the primary endpoint in patients with E. coli bloodstream infection.

Conclusion

The authors concluded that

Show notes at pharmacyjoe.com/episode68. In this episode I’ll discuss whether sugammadex can rescue your patient from a can t intubate, can t oxygenate scenario.

Show notes at pharmacyjoe.com/episode68

In this episode I'll discuss whether sugammadex can rescue your patient from a “can’t intubate, can’t oxygenate” scenario.

Now that sugammadex has made it to the US market, the push to add it to formulary has begun. I discussed the approval of sugammadex in episode 33. Sugammadex may have a role in the OR/PACU setting - I’ll leave that to others to determine.

One argument I’ve heard for adding sugammadex to formulary is for reversal of rocuronium or vecuronium if rapid sequence intubation unexpectedly fails and the patient cannot be intubated or ventilated.

Context for determining whether sugammadex might work in this scenario is important. For the purpose of this episode, the context is in a critically ill patient undergoing non-elective intubation for actual or impending respiratory failure.

Imagine that rapid sequence intubation was performed using rocuronium and etomidate. An airway could not be established, and the patient’s oxygen saturation is falling rapidly despite attempts at bagging the patient. There are just moments left before the patient experiences severe hypoxia and anoxic injury.

I think it is risky to say that sugammadex is the treatment that should be relied on to save such a patient from anoxic injury.

The hope is that reversing the paralytic will allow the patient to be ventilated with a bag-valve mask. But it is also possible that airway edema from the failed attempt at intubation is responsible for the “can’t oxygenate” part of this scenario. If so, sugammadex would be of no help and precious time would be wasted preparing and administering the medication instead of securing the airway.

If the patient needed an airway, even after rocuronium is reversed with sugammadex, they will still need an airway. Instead of using sugammadex, the next step in the provider’s failed airway algorithm (such as cricothyrotomy) should be initiated.

Some published case studies illustrate how sugammadex may not be able to reverse a “can’t intubate can’t oxygenate” scenario:

Show notes at pharmacyjoe.com/episode67. In this episode I ll: 1. Discuss an article about using dexmedetomidine for agitated delirium when haloperidol doesn t work. 2. Answer the drug information question Should I use a loading dose when initiating a dexmedetomidine infusion?” 3. Share a resource I created for calculating the time to wait after the last dose [...]

Show notes at pharmacyjoe.com/episode67

In this episode I’ll:

1. Discuss an article about using dexmedetomidine for agitated delirium when haloperidol doesn’t work

2. Answer the drug information question “Should I use a loading dose when initiating a dexmedetomidine infusion?"

3. Share a resource I created for calculating the time to wait after the last dose of a non-vitamin K antagonist oral anticoagulant before a low or high risk surgical procedure.

Article

Dexmedetomidine for the Treatment of Hyperactive Delirium Refractory to Haloperidol in Nonintubated ICU Patients: A Nonrandomized Controlled Trial

Lead author: Genís Carrasco

Published online February 2016 in the journal Critical Care Medicine.

Background

Agitated delirium in the ICU setting complicates the management of critically ill patients.

Methods

The study was a non-randomized controlled trial in a 13 bed medical-surgical ICU setting. 132 consecutive ICU patients with a diagnosis of agitated delirium were included. Numerous exclusion criteria were applied including history of substance abuse, Parkinson’s, bradycardia, and QTc interval prolongation at baseline. Despite the exclusion criteria, only 18 of 154 patients evaluated were excluded for these reasons. This is a very low number and speaks well to the generalizability of the results. Haloperidol was titrated as follows:

All patients received IV haloperidol bolus doses of 2.5–5 mg, with intervals of 10–30 minutes, until control of agitation (RASS score, 0 to −2) or until reaching the maximum cumulative daily dose of 30 mg.

The patients were then split into “responder” and “non-responder” groups. Patients in the responder group were given a haloperidol infusion of 0.5-1mg/hr to maintain a RASS of 0. Patients in the non-responder group were given a dexmedetomidine infusion starting at 0.2 mcg/kg/hr titrated to a maximum of 0.7 mcg/kg/hr to maintain a RASS of 0.

Results

86 patients responded to

Show notes at pharmacyjoe.com/episode66. In this episode I’ll discuss diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS).

Show notes at pharmacyjoe.com/episode66

In this episode I'll discuss diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS).

Definition

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the most serious acute complications of diabetes. These diabetic crises cause thousands of deaths annually in the US.

DKA and HHS differ clinically according to the presence of ketoacidosis and the degree of hyperglycemia.

In DKA metabolic acidosis is often the major finding. The serum glucose is below 800 mg/dL and usually in the 350-500 mg/dL range. DKA usually evolves rapidly.

In HHS, there is little or no ketoacidosis and the serum glucose concentration frequently exceeds 1000 mg/dL. HHS usually evolves over a period of several days.

Overlap between DKA and HHS occurs in more than one-third of patients.

Pathogenesis

Insulin deficiency/resistance and glucagon excess are responsible for the development of DKA and HHS.

The deficiency in insulin (either absolute or relative deficiency) is more severe in DKA compared with HHS.

In HHS the residual insulin secretion and its systemic activity minimizes the development of ketoacidosis but is not adequate to control hyperglycemia.

In patients with absolute or relative insulin deficiency, DKA and HHS are usually precipitated by a stressor such as infection or discontinuation of / inadequate insulin therapy.

Treatment

The treatment of DKA and HHS involves the correction of fluid and electrolyte abnormalities, followed by the administration of insulin.

Specific treatment protocols include: